Clinical Exam Notes

Clinical Teaching and Communication Skills
Taking a Cardiovascular History

At the end of this session you should be able to:
1.
2.
3.
4.
Take a detailed cardiovascular history from a patient.

Complete a full history.
Complete a systems review.
Present and summarize the case.
Introduce yourself to patient and find out patients name, age and where they
are from. Ask them what brought you to hospital.
Presenting Complaint
Chest pain
Site of pain - central/retrosternal

Radiation jaw, left arm
Onset gradual/sudden
Periodicity intermittent/constant
Duration minutes, hours, days
Character- crushing/heaviness
Severity out of 10
Aggravating factors - exertion/stress, pain at rest may indicate unstable angina
Relieving factors rest/GTN
Associated features
Nausea
Vomiting
Sweating [diaphoresis]
Anxiety
Dyspnoea
Palpitations
Syncope
Fatigue
Intermittent claudication
Ankle swelling
With angina, pain may initially occur with exertion, getting progressively worse
over time and eventually leading to pain at rest [Unstable angina], or
myocardial infarction.
Canadian cardiovascular society (CCS) classification of angina

-
Class I
No angina/ mild angina at strenuous exertion.
Class II
angina with moderate exertion (walking > 2 blocks on
level or climbing > 1 flight of stairs).
Class III
angina with mild exertion (walking 1-2 blocks on
level or climbing 1 flight of stairs).
Class IV
angina at rest.
New York Heart Association (NYHA) functional classification

- Class I
no SOB with activity/ exertion.
- Class II
SOB at moderate activity/ exertion.
- Class III
SOB at mild activity/ exertion.
- Class IV
SOB at rest.
Cardiovascular Risk Factors

1. Hyperlipidaemia high cholesterol/triglycerides (? medication)
2. Smoking (duration/number per day)
3. Hypertension (? medication)
4. Family History of CAD
5. Diabetes mellitus (type/duration/medication)
6. Obesity [BMI]
7. Age
8. Gender
9. Physical activity
Relevant background
History of angina
Previous myocardial infarction
History of palpitations
Previous cardiac investigations
Previous cardiac surgery/interventional procedures
Recent dental work [endocarditis]
Rheumatic fever in past
Ask all the relevant questions to presenting complaint (If chest pain ask all
pain questions, etc.)
Other cardiovascular symptoms

Shortness of breath (SOB)/ Dyspnoea
-
Exertional? Relieved by rest?

Acute vs. chronic?
Worsening?
Associated wheeze (cardiac wheeze)?
Orthopnoea
-
How many pillows at night when sleeping?

Using more pillows lately?
Characterise as 1,2, 3 or 4 pillow orthopnoea.
Paroxysmal nocturnal dyspnoea (PND)

-
patient wakes from sleep gasping for air

Due to acute left ventricular failure.
Palpitations
1) Aim to get a good description of the palpitations
-
Describe the palpitation/ unexpected awareness of heart beat?

Slow/fast; regular or irregular; sensation of a skipped beat or an extra
beat?
Ask the patient to try tapping out the rhythm
When did they start?
Increasing in frequency or the same?
Duration of palpitations when they occur?
Sudden onset/ termination? Or gradual onset?
Associated symptoms with the palpitations? Eg pain, symptoms of
heart failure
2) What is causing the palpitations?

- Obvious triggering factors? Alcohol? Caffeine intake? Symptoms of
hyperthyroidism? Known hyperthyroidism? Illicit drugs? Stress?
- Previous cardiac history precipitating palpitations?
- Family history of arrhythmia?
- Medications causing palpitations eg salbutamol
3) Effect of the palpitations
- Syncope
3
Heart failure etc
Syncope/ pre-syncope
-
Transient loss of consciousness due to cerebral anoxia.

Is dizziness postural?
Sudden onset vs. gradual?
Warning signs? (Nausea, vomiting, sweaty, dizziness, palpitations,
chest pain, headache, etc).
Collateral history if loss of consciousness (LOC) - (seizure activity?).
Length of LOC?
Symptoms when recovered from LOC (palpitations, pain, etc.?).
Ankle swelling
-
Symmetric?
Worsening?
Past Medical/Surgical History

-
Other medical/surgical problems.

Mention dates of surgery and previous medical diagnosis (dates of
bypass surgery? how many grafts?)
Previous percutaneous coronary intervention? How many stents? Dates
of procedure and where it was done?
Medication
-
Prescribed and over the counter.

Always use generic names of medication.
Mention dosing regimen (i.e. OD, BD, etc.).
State type of drug and indication
To any medication
Allergies
Document the reaction which occurred, e.g. nausea/ vomiting / rash/ wheeze/
bronchospasm/ loss of consciousness.
Social History
Marital status
Children
Employment
Home situation
Alcohol intake [count units]
Smoking (quantity of cigarettes per day, and duration of smoking must be
documented)
o Activities of daily living? Home help?
o
o
o
o
o
o
Family History
4
Relevant family history MI / PVD / stroke, Hypertension, Diabetes

mellitus, High cholesterol/triglycerides.
Onset of cardiovascular disease in first degree relatives? Age at initial
diagnosis with CVD
Family history sudden cardiac death?
Complete Systems Review

- Refer to Talley and OConnor for questions in systems review.
Summarize History
Refer to Talley & OConnor for further reading on cardiovascular history taking.
The above notes are NOT intended as a replacement for the book. Practice makes
perfect!
Clinical teaching - Cardiovascular Examination

To begin examination
Student must introduce themselves to patient.
Find out patients name.
Explain to patient what they are going to do.
Exposing the patient

The patient must be put lying at 45 degree angle and be comfortable.
Chest must be exposed [take off shirt/top/pyjamas/vest].
General inspection
For all systems initial inspection is done from the end of the bed
Look at general state of health. Does patient appear ill?

Rapid/laboured respiration (tachypnoea)
Cachectic [severe loss of weight and muscle wasting]. Severe cardiac failure may have this
effect.
Comment on chest asymmetry/scars/pulsations.
Pacemaker
Comment on intravenous lines/any equipment around bed
Hands
Ask patient to hold out their hands. Note if cold, clammy or well perfused. Check
capillary refill.
Tar staining
Indicative of a history of cigarette smoking
Clubbing
Inspect for loss of nail angle between the nail bed and the finger.
Grade 1: Fluctuation and softening of the nail bed
This can be examined for by compressing nail bed with your fingers and
rocking it.
Grade 2: Loss of the nail-bed angle
Grade 3: Increased curvature of the nail
Grade 4: Fingertip develops a clubbed (drumstick) appearance
Grade 5: Hypertrophic pulmonary osteoarthropathy (HPOA).
Cardiovascular causes of clubbing
1.
2.
3.
Cyanotic congenital heart disease

Infective endocarditis
Atrial myxoma
[The cause of clubbing is not known there are several theories]
Pallor - Pallor of the palmar creases/palm of hand
This may indicate underlying anaemia.

Anaemia from any cause may result in cardiovascular symptoms eg chest pain due
to lack of oxygen supply to the myocardium
Anaemia related to cardiovascular disease is usually normochromic, normocytic
anaemia
Causes
1. Haemolytic anaemia ( prosthetic heart valves)
2. Infective endocarditis (chronic inflammation)
Splinter haemorrhages
Linear haemorrhages of the nail bed may be caused by infective endocarditis or
vasculitis.
Osler Nodes
Red raised tender nodules on the pulps of the fingers, thenar and hypothenar eminences in
infective endocarditis
Janeway Lesions
Non-tender erythematous maculo-papular lesions containing bacteria on palms or
pulps of fingers in infective endocarditis
Xanthomata
Yellow deposits of lipid occur in hyperlipidaemia.
Arterial Pulse
Palpate radial pulse using pulp of forefinger and middle finger.
Rate
Normal pulse: 60-100 beats per minute [Bradycardia < 60/minute, Tachycardia >
100/minute]
Rhythm
Regular or irregular [Atrial fibrillation is an example of an irregularly irregular
rhythm]
Radio femoral Delay
Palpate radial pulse and femoral pulse at the same time. A delay in the arrival of
femoral pulse suggests
coarctation of the aorta. Femoral pulse is located below the inguinal ligament one
third of the way between the pubic tubercle and the anterior superior iliac spine
Radial-radial inequality
Palpate both radial pulses together
Inequality in timing or volume usually due to large arterial occlusion or aneurysm
Character and Volume
Collapsing pulse of aortic incompetence. Otherwise character and volume better
assessed at the carotid
Blood Pressure
Systolic BP - Peak pressure that occurs in the artery following ventricular systole
Diastolic BP - Level to which arterial blood pressure falls during ventricular diastole
Face
Jaundice
8
Severe congestive cardiac failure leads to hepatic congestion, causing intra-hepatic

jaundice.
Xanthelasma
Intracutaneous yellow cholesterol deposits around the eyes may indicate
hyperlipidaemia.
Arcus senilis/Corneal arcus

Cholesterol deposits in the corneal stroma result in a white/grey opaque ring
surrounding the cornea. It is associated with hyperlipidaemia and with ageing.
Malar flush
Rosey cheeks with a bluish tinge. Associated with pulmonary hypertension and severe
mitral stenosis.
Mouth
High arched palate
This is a feature of Marfan Syndrome. This is an autosomal dominant connective
tissue disease. It is associated with cardiac complications, in particular, aortic
regurgitation and dissection. Patients have a distinctive physical appearance tall and
thin, with an arm span that exceeds height (arachnodactyly).
Tooth decay
This may be a source of endocarditis infection.
Petechiae
May be present in infective endocarditis
Lips
Peripheral cyanosis associated with cyanotic congenital heart disease. It affects the
distal extremities and circumoral or periorbital areas. It is caused by increased tissue
oxygen extraction.
Tongue
Central cyanosis ask patient to open their mouth and look under their tongue. It is
caused by decreased arteriolar oxygen saturation.
Cyanosis is a bluish discoloration of the tissues that results when the absolute level of
reduced hemoglobin in the capillary bed exceeds 3 g/dL.
The Neck
Carotid Arteries
10
Medial to the sternomastoid muscles

Provides information about aorta and left ventricular function
Evaluate the pulse wave form [collapsing pulse of aortic regurgitation]
o Anacrotic
Aortic stenosis (small volume slow uptake)
o Plateau
Aortic stenosis (Slow upstroke)
o Bisferiens
Anacrotic and collapsing in AS and AR
o Collapsing
Aortic regurgitation
Hyperdynamic circulation
PDA
Peripheral AV fistula
o Small volume
Aortic stenosis and
Pericardial effusion
Jugular Venous pressure
Provides information regarding right atrial and right ventricular function

Internal jugular vein is medial to sternomastoid muscle
External jugular vein is lateral to sternomastoid muscle
External jugular vein has more tortuous course, the internal jugular vein is
more reliable
The column of blood in the internal jugular vein extends into the right atrium
The right atrium is about 5cm below the sternal angle
It enables us to observe pressure changes in the right atrium
The JVP is measured as the vertical distance between the sternal angle and the
top of the venous column.
Gentle pressure at the base of the neck may abolish visible pulsations and may
make a vein visible by causing distension above the occlusion
11
When the JVP is more than 3cm above the zero point then right heart filling
pressure is raised.
Features of Jugular Venous Pressure

It is a multi-wave form.
It is visible, not palpable.
It is occludable.
It fills from above.
It decreases with inspiration.
It increases with pressure on the abdomen (hepatojugular reflux).
Hepatojugular Reflux
Abdominal compression increases venous return and pressure and facilitates analysis
of the JVP
Apply firm sustained pressure over upper abdomen
It is a simple way of confirming the venous nature of a pulsation in the neck.
Causes of elevated JVP
Renal failure - fluid overload

Right ventricular Failure
Tricuspid regurgitation
Tricuspid stenosis
Constrictive pericarditis
Cardiac tamponade
Superior Vena Caval Obstruction
The Praecordium
Inspection
Scars
Sternotomy [A cut down the middle of the sternum - CABG and valve surgery]
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Thoracotomy [mitral valvotomy - a stenosed mitral valve is opened through an

incision made in the left atrium]
Skeletal abnormalities
Marfans Syndrome may cause pectus excavatum/kyphoscoliosis. Severe deformity
may cause
distortion of the position of the heart and great vessels and
also interfere with pulmonary function]
Visible apex beat

Heaves/abnormal pulsations
Pacemaker or Inmplanted Cardiac Defibrillator (ICD) Box
[Under the left pectoral muscle easily palpable]
Palpation
Apex beat
1. Assess Position
This is the most lateral, inferior point at which the palpating fingers are raised with
each systole. Its normal position is in the fifth left intercostal space midclavicular line.
13
Begin palpation in axilla and move medially until apex beat is located.
Once you have located the apex beat count down the number of intercostal spaces to
confirm its position. The second intercostal space lies just below the manubriosternal
angle. The apex beat may be displaced laterally or inferiorly or both. This usually
indicates ventricular dilatation but may be due to chest wall deformity.
The apex beat is best located with the patient in the left lateral position, in order to
position the apex closer to the chest wall. Note any apical thrills (palpable murmurs)
2.Character
Normal
Heaving LV hypertrophy 2ry to pressure overload (hyperkinetic) 2ry to
Systemic hypertension
Aortic stenosis
Coarctation of the aorta
Thrusting LV dilatation 2ry to volume overload (hyperdynamic) 2ry to
Aortic regurgitation
Mitral regurgitation
VSD
Tapping mitral stenosis causing a loud & palpable S1
Double impulse HOCM
Causes of an impalpable apex beat
1.
2.
3.
4.
5.
Obesity
Emphysema (hyperexpansion)
Shock
Dextrocardia
Causes of a displaced apex beat

3.
4.
5.
6.
7.
Left ventricular dilatation

Right ventricular dilatation
Cardiomegaly
Chest wall deformities
Mediastinal mass
Parasternal heave may be palpable when the heel of the hand is rested just to the left
of the sternum. The fingers can also be used. This is present in right ventricular
enlargement/hypertrophy.
Thrills
Thrills are palpable murmurs. Palpate for thrills with the flat of the hand. Palpate over
the apex, left sternum and base of the heart (sitting forward in full expiration for base
of heart).
Percussion
14
Little additional information is gained and therefore is not helpful.
Auscultation
1. Begin in the mitral area [over the apex beat]

Listen with the bell (low pitch sounds such as diastolic murmur of mitral stenosis.
Then listen with the diaphragm for mitral regurgitation.
2. Listen in tricuspid area with diaphragm [fifth left intercostal space]
3. Listen in the pulmonary area with diaphragm [second left intercostal space]
4. Listen in aortic area with diaphragml [second right intercostal space]
The bell amplifies low pitched sounds i.e. mitral stenosis. The diaphragm is best
for higher pitched sounds i.e. mitral incompetence. The bell must be applied
lightly to the chest wall as forceful application will stretch the skin so it forms a
diaphragm.
NB. Palpation of carotid pulsation will indicate the timing of systole and allow heart
sounds to be identified.
The first heart sound - S1
Mitral and Tricuspid valve closure.
The second heart sound - S2
Aortic and pulmonary valve closure

Marks the end of systole
Lower pitch
The second heart sound has two components, the aortic (A2) and the
pulmonary (P2). This occurs because the pressures in the pulmonary
circulation are lower than those in the systemic circulation, leading to a delay
in the closing of the pulmonary valve.
Cardiac Murmurs
Pansystolic Murmur: Audible throughout systole
15
Causes
1. Mitral regurgitation
2. Tricuspid regurgitation
3. VSD
Ejection Systolic Murmur: Audible best at midsystole.
Causes
1. Aortic stenosis
2. Pulmonary stenosis
3. Hypertrophic Obstructive Cardiomyopathy (HOCM)
Early Diastolic Murmur: Loudest at the beginning of diastole.
Causes
1. Aortic Regurgitation
2. Pulmonary Regurgitation
Mid Diastolic Murmurs: begin later in diastole.
Causes
1. Mitral Stenosis
2. Tricuspid Stenosis
Continuous murmurs
Causes
1. Patent Ductus Arteriosus
2. Arteriovenous fistula
Grade Murmurs 1-6
1/6: very soft

2/6: soft
3/6: moderate [no thrill]
4/6: loud, palpable thrill
5/6: very loud, thrill easily palpable
6/6: very, very loud (audible without stethoscope)
Extra heart sounds the third heart sound is a low pitched mid-diastolic sound
that is best appreciated by listening for a triple rhythm. It is often called a gallop
rhythm. A pathological S3 is due to reduced ventricular compliance so that a
filling sound is produced even when diastolic filling is not rapid.
Presentation of auscultation
Heart sounds 1&2 Normal or abnormal? Loud, soft, splitting?
Any extra heart sounds? Eg 3rd or 4th heart sounds
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Any additional sounds? Friction rub, opening snap, clicks

Any murmurs
Timing
Area of greatest intensity
Grade
Radiation
Effect of dynamic manoevres
o Systolic (early, midsystolic or pansystolic)
o diastolic (early or late diastolic)
o Continuous
Dynamic manoeuvres
Lesions on the left side of the heart are best elicited on listening in full
expiration.
Lesions on the right side of the heart are best elicited on inspiration.
Mitral Stenosis: Listen over mitral area using bell with patient in left lateral position.
Aortic Regurgitation: Lean patient forward in full expiration and listen at lower left sternal
border with diaphragm.
Mitral Regurgitation: Radiates to axilla, listen with diaphragm

Aortic Stenosis: Radiates to carotid arteries, listen with diaphragm or bell if patient
small/thin. Best heard leaning forward in full expiration|
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We also listen over the carotid arteries for a bruit which will be audible with carotid
stenosis
The Back
Auscultation of the lung bases for pulmonary oedema crackles/crepitations

(often due to congestive cardiac failure) or pleural effusion may be identified
Check for sacral oedema
The Abdomen
The liver may be enlarged [hepatomegaly] and/or tender due to congested hepatic
veins caused by right-heart failure.
A pulsatile liver is a feature of tricuspid regurgitation.
The Legs
Check for pedal oedema
Palpate distal shaft of tibia. Compress the area for at least 15 seconds with the thumb.
*Area often tender be gentle*
Pitting oedema - Skin is indented and only slowly refills.

Note upper level of oedema, abdominal wall and scrotum may be
involved.
Palpitations
18
Palpitations are the perception of cardiac activity. They are often described as a
fluttering, racing, or skipping sensation.
Differential diagnosis
1) Some patients simply have heightened awareness of normal cardiac activity,
particularly when exercise, febrile illness, or anxiety increases heart rate.
2) Arrhythmia
Common arrhythmias include
Premature atrial contractions (PACs)

Premature ventricular contractions (PVCs)
Both usually are harmless.

Other common arrhythmias include
Paroxysmal supraventricular tachycardia (PSVT)

Atrioventricular nodal reentrant tachycardia
Atrial fibrillation or flutter
Ventricular tachycardia
Bradyarrhythmias and heart block
May occur spontaneously or due to an underlying disorder.

Cardiac Disorders Precipitating Arrhythmia
myocardial ischemia,
congenital heart disease,
valvular heart disease,
conduction system disturbances (eg, disturbances that produce bradycardia or
heart block).
Patients with orthostatic hypotension commonly sense palpitations caused by
sinus tachycardia upon standing.
Noncardiac Disorders Precipitating Palpitations
thyrotoxicosis
pheochromocytoma
anxiety
anaemia
hypoxia
hypovolemia
electrolyte abnormalities eg K+
Other Precipitants of palpitations

19
Stress/Anxiety
Caffeine
Nicotine
Alcohol
Medications
o Salbutamol
Pathophysiology
The mechanisms responsible for the sensation of palpitations are unknown.
Ordinarily, sinus rhythm at a normal rate is not perceived, and palpitations thus
usually reflect changes in cardiac rate, rhythm, or contractility. It is the abnormal
movement of the heart within the chest that is felt. In cases of isolated extrasystoles,
the patient may actually perceive the augmented post-extrasystolic beat as the
skipped beat rather than the premature beat itself, probably because the extrasystole
blocks the next sinus beat and allows longer ventricular filling and thus a higher
stroke volume.
The clinical perception of cardiac phenomena is highly variable. Some patients are
aware of virtually every premature ventricular beat, but others are unaware of even
complex atrial or ventricular tachyarrhythmias. Awareness is heightened in sedentary,
anxious, or depressed patients and reduced in active, happy patients. In some cases,
palpitations are perceived in the absence of any abnormal cardiac activity.
Consequences:
Many arrhythmias that cause palpitations have no adverse physiologic

consequences of their own (ie, independent of the underlying disorder).
However, bradyarrhythmias, tachyarrhythmias, and heart blocks can be
unpredictable and may adversely affect cardiac output and cause hypotension,
heart failure or death.
Ventricular tachycardia sometimes degenerates to ventricular fibrillation and
cardiac arrest.
The History
3 tasks in presenting complaint and history of presenting complaint
1) Aim to get a good description of the palpitations
- Describe the palpitation/ unexpected awareness of heart beat?
- Slow/fast; regular or irregular; sensation of a skipped beat or an extra
beat?
- Ask the patient to try tapping out the rhythm
- When did they start?
- Increasing in frequency or the same?
- Duration of palpitations when they occur?
- Sudden onset/ termination? Or gradual onset?
20
Symptoms associated with the palpitations? Eg pain, symptoms of

heart failure, syncope, light-headedness, tunnel vision, dyspnoea, and
chest pain. Give clues regarding aetiology and potential seriousness.
2) What is causing the palpitations? (See above also)

- Obvious triggering factors? Alcohol? Caffeine intake? Symptoms of
hyperthyroidism? Known hyperthyroidism? Illicit drugs? Stress?
Anaemia, Blood loss, etc
- Previous cardiac history precipitating palpitations?
- Recent chest pain/progressive dyspnoea suggesting ischaemia
- Family history of palpitations, arrhythmia, sudden death or thyroid
problems?
- Medications causing palpitations eg salbutamol
3) What were the consequences of the palpitations?
None
Syncope
Heart failure symptoms
What was the trigger for presenting to the doctor?
Red flags: Certain findings raise suspicion of a more serious aetiology of palpitations:
Light-headedness or syncope (particularly if injury occurs from syncope)

Chest pain
New onset of irregularly irregular heart rhythm
Heart rate >120 beats/min or < 45 beats/min while at rest
Significant underlying heart disease
Family history of sudden death
Suggestive Historical Findings with Palpitations

Finding
Possible Cause
Occasional skipped beats
PACs, PVCs
Rapid, regular palpitations with sudden PSVT, atrial flutter with 2:1
onset and termination
atrioventricular block, ventricular
tachycardia
Often history of recurrence
Syncope following palpitations
Sinus node dysfunction, atrioventricular

bypass tract, such as in the WolffParkinson-White syndrome, congenital
long QT syndrome
21
Palpitations during exercise or an

emotional episode
Healthy person: Sinus tachycardia

History of coronary artery disease:
Ventricular arrhythmia from exerciseinduced ischemia
Palpitations following episodic drug use Drug-induced cause

Sense of doom, anxiety, or panic
Suggests (but does not confirm) a

psychologic cause
Postoperative patient
Sinus tachycardia (eg, due to infection,

bleeding, pain)
Recurrent episodes since childhood
Supraventricular arrhythmia (eg,

atrioventricular nodal re-entrant bypass
tract, Wolff-Parkinson-White syndrome)
Congenital long QT syndrome (usually
manifests during adolescence)
Family history of syncope or sudden

death
Brugada syndrome, long QT syndrome,

inherited dilated or hypertrophic
cardiomyopathy
Peripheral Vascular Disease

History
Presenting Complaint/History of Presenting Complaint
Medication
Allergies
Social History
Family History
Systems review
Respiratory
Cardiovascular
Gastrointestinal
Genitourinary
Musculoskeletal
Neurological
Pain History
10 points that should be elucidated in taking a pain history
22
1. Time course
2. Mode of onset
3. Pattern
4. Site
5. Radiation
6. Character
7. Severity
8. Aggravating factors
9. Relieving factors
10. Associated symptoms
Symptoms of peripheral vascular disease
Gradual arterial obstruction, particularly in the lower limbs, presents as Intermittent
Claudication
Intermittent Claudication
Ischemic cramp-like pain usually in the calves during exercise and relieved by
rest.
Pain may be in one or both calves but can also occur in thighs or buttocks.
Claudication distance
Determine how long patient can walk prior to onset of pain. The distance they can
walk prior to onset of pain is called the Claudication distance. The claudication
distance may be shorter when patient is walking up a hill.
Can they walk to shop?

To local church?
To bus stop?
To the end of the garden?
Across the room?
**Both limbs often affected, usually one more severely than the other**
Rest pain
Severe chronic arterial insufficiency may cause rest pain. This may be felt deep in the
limb or superficially. Usually described in the dorsum of the foot. There may be
altered cutaneous sensation and there may be a feeling of burning. The patient may
attempt to relieve discomfort by letting the leg hang over the side of the bed at night,
outside the bed clothes.
In severe cases the patient may even report sleeping in a chair.
Rest pain is indicative of severe peripheral vascular disease and of critical limb
ischemia.
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Ulceration, gangrene and tissue loss

In very severe cases, patients may actually present with ulceration and gangrene due
to insufficient blood supply. These are also indicative of critical limb ischemia.
Risk factors for vascular disease
Smoking
Diabetes mellitus
Hypertension
Hypercholesterolemia
Family history of arterial disease
Differential Diagnosis
1.
2.
3.
4.
5.
6.
7.
8.
9.
Spinal stenosis (pain on getting up, improves on walking)

Sciatica
Lumber spondylosis
Arthropathy (osteo/rheumatoid/gout)
Varicose veins
DVT
Compartment syndrome
Infections / cellulitis
Abdominal aneurysm
Acute Ischemic Limb

Causes sudden onset of severe pain
This can be the result of:
1. Embolism [sudden blockage of an artery by material brought
to the site of the obstruction in the blood stream e.g. clot]
2. Thrombosis [clotting of blood within an artery so that the
blood flow is reduced or impeded]
3. Injury.
Peripheral arterial embolism usually arises from thrombus in the heart, where it is
often secondary to,
Myocardial infarction
Atrial fibrillation
Infective endocarditis
Acute arterial occlusion of a major peripheral limb artery results in the six Ps,
Painful
Pale
Pulseless
Paralysed limb
Perishing Cold
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Paresthesia
Venous Insufficiency
Varicose Veins
DVT
Varicose Veins:
Causes:
Previous DVT
Venous HTN from prolonged standing
Pregnancy
Uterine Fibroids
Pelvic Malignancy
Exam:
Trendelenberg test
Tourniquet test
DVT
Risk Factors:
Immobility
Surgery
Pregnancy
Malignancy
OCP
Vascular examination of the lower limb

The lower limbs should be fully exposed.
All examinations begin with inspection.
Inspection
Look for;
Leg pallor
Dry skin
Absence of hairs
Thickened atrophic toenails
Ulceration
Gangrene
Students should comment of each of these findings when inspecting limb [presence or
absence of].
Describe an ulcer
Site
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Size
Shape
Surface
Edge
Base
Surrounding skin
Arterial ulcers
Due to critical limb ischemia
Painful
Punched out
Relatively deep [tendon may be visible]
Occur where arterial supply poorest:
Tips of toes
Dorsum of foot
Heel
Middle of shin
Venous Ulcers
Superficial
Painless
Medial or lateral malleolus
Can undergo malignant change
Beer bottle leg
Brawny oedema
Dermatoliposclerosis (sub cut fat replaced by collagen)
Palpation
Feel for temperature of limbs.
Compare temperature of limbs
Capillary refill
Oedema (Pitting or non-pitting if present)
Palpate for lower limb/peripheral pulses

Femoral Artery
Femoral pulse is felt at the mid inguinal point which is halfway between the
anterior superior iliac spine and the pubic symphysis
The femoral artery lies halfway between the pubic symphysis and the
anterior superior iliac spine.
It cannot be felt satisfactorily through clothing.
Examine both femoral arteries by palpating and then auscultating.
A bruit may be heard if the artery is narrowed.
[Bruit will not be heard over smaller arteries]
26
Popliteal Artery
Popliteal pulse is felt in the popliteal fossa between the two heads of
gastronemius against the tibial plateau
popliteal
posterior to
Palpate for the popliteal artery behind the knee.

The patient should be lying supine with the knee slightly flexed.
Press with the finger tips [use both hands] in the middle of the
fossa.
The artery is one of the deepest structures in the fossa and lies
the knee joint.
With practice it can nearly always be detected unless there is proximal
obstruction.
Posterior Tibial Artery

The Posterior Tibial pulse is felt in a groove half way between the medial
maleollus and the Achilles tendon
Palpate behind the medial maleollus.
Dorsalis Pedis Artery
The Dorsalis Pedis pulse is felt two thirds is the way along a line drawn
from the midpoint of the two maleolli and the first interdigital cleft
Palpate on the forefoot.
Lateral to extensor hallucis longus tendon on the dorsum of the foot.
In the elderly the Dorsalis Pedis artery and the posterior tibial artery
may not be palpable.
Buerger's test is used to assess the adequacy of the arterial supply to the leg. It is
performed in two stages.
With the patient supine, elevate both legs to an angle of 45 degrees and hold for one
to two minutes.
Observe the color of the feet. Pallor indicates ischemia. It occurs when the peripheral
arterial pressure is inadequate to overcome the effects of gravity. The poorer the
arterial supply, the less the angle to which the legs have to be raised for them to
become pale.
Then sit the patient up and ask them to hang their legs down over the side of the bed
at an angle of 90 degrees.
Gravity aids blood flow and colour returns in the ischemic leg. The skin at first
becomes blue, as blood is deoxygenated in its passage through the ischemic tissue,
and then red, due to reactive hyperemia from post-hypoxic vasodilatation.
Both legs are examined simultaneously as the changes are most obvious when one leg
has a normal circulation.
27
Investigations
Specific:
ABPI
0.9
0.71 0.90
0.41 0.70
0.00 0.40
Normal
Mild Obstruction
Moderate Obstruction
Severe Obstruction
Doppler / Duplex Ultrasound

Arteriogram
MRA
Others:
FBC
Renal Profile
Fasting Glucose
HbA1C
Fasting Lipids
ECG
Management
Must be able to identify acute limb ischemia. Requires heparin infusion if no absolute
contraindications and seek expert help straight away. 6 hour window period from time
of onset.
Decrease risk factors
Stop smoking
Treat DM
Treat Hypertension
Lower cholesterol
Weight loss
Regular exercise encourages development of collateral vessels.

Care to avoid trauma/infection.
Surgery
Balloon dilatation/angioplasty/stenting
Bypass grafts
Amputation-severely ischemic/gangrene
Taking a Gastrointestinal History

28
Abdominal pain
The following questions must be asked, when enquiring about any pain:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Site
Radiation where the pain moves
Character sharp/dull/ache
Severity score from 1 to 10, 1 being very mild, 10 being worst pain
ever experienced.
Onset sudden/gradual
Periodicity constant/intermittent
Duration minutes/hours/days
Aggravating precipitants/makes it worse
Relieving eases
Associations other symptoms that accompany the pain, e.g. nausea,
vomiting, diarrhoea etc.
Site/radiation
Ask the patient to point to the site of pain

o Pancreatitis Back
o Epigastric oesophagitis, gastritis, peptic ulcer
disease, pancreatitis
o Right Upper Quadrant gallstones, cholangitis,
cholecystitis
o Central Abdominal irritable bowel syndrome,
inflammatory bowel disease
o Suprapubic diverticular disease, irritable
bowel syndrome, inflammatory bowel disease
o Flank renal colic
o Right Iliac Fossa appendicitis, hernia, ovarian
cyst
Ask about radiation of pain
Appendicitis pain commonly begins in the periumbilical

region, later radiating to and then localising in the RIF
Pancreatitis pain can radiate from the epigastric region
through to the back
Gall bladder pain can radiate around into the flank and
the back
Renal pain can radiate down along the ureters and into
the groin
Pain associated with subdiaphragmatic irritation (gall
stones, perforated ulcer) can also be felt in the right
shoulder and tip of the scapula.
29
Onset/periodicity/duration
Onset - When did the pain start? Sudden or gradual

Periodicity - How often it occurs
Duration How long does / did it last?
Acute/chronic
Character and severity

Sharp/burning/dull/gnawing
Colicky pain comes in waves e.g. from obstruction of bowel
Associated features
Loss of appetite/weight
Ask about any change in appetite
Determine from patient how much weight loss has occurred, and over
what period, i.e. 6 kg over two months
Nausea and vomiting
Acute - gastrointestinal infection e.g. Food poisoning [staphylococcus aureus]
Ask about contents old food e.g. Gastric outlet obstruction
Blood [haematemesis] gastric/oesophageal - ulceration/malignancy
Other causes
Small bowel obstruction
Pregnancy
Medications e.g. opioids, chemotherapy,
antibiotics
Infections gastrointestinal, any systemic sepsis
Bulimia
Pancreatitis
Cholecystitis
Peptic ulcer disease
Heartburn/acid regurgitation
Regurgitation of stomach contents into the oesophagus
Heartburn burning or discomfort in retrosternal area
Acid regurgitation Sour or bitter tasting fluid coming up into the mouth
In reflux disease the lower oesophageal sphincter muscle is usually weak
Dysphagia
Difficulty swallowing, usually solids initially, progressing to dysphagia with liquids
Causes
30
Oesophageal spasm
Oesophageal stricture
Oesophageal Carcinoma
Mediastinal mass
Neurodegenerative disorder
Change in bowel habit

Diarrhoea
Diarrhoea refers to a decrease in faecal consistency. It may refer to an
increased volume or frequency, or change in consistency, of the stool.
Constipation
Constipation is generally understood as a delay or difficulty in defaecation, but
the interpretation of the term "delay" varies broadly.
Determine what patient means by constipation.
Causes
Hypothyroidism
Hypokalaemia
Anorexia
Pregnancy
Multiple sclerosis
Low-fibre diet
How often would your bowels normally move?
How often are they moving now?
How long has this been going on for?
Alternating diarrhoea and constipation
Suspicious for underlying colonic malignancy
Gastrointestinal Bleeding
Haematemesis: vomiting blood [bleeding from upper GIT]
Melaena: passage of dark black tarry stools [bleeding from upper GIT/
right side colon/small bowel lesions]
Bright red blood per rectum: usually indicates bleeding from lower GIT
Causes of upper GIT bleeding

Oesophageal varices
Oesophageal/Gastric neoplasm
Arteriovenous malformations
Mallory-Weiss tears
Causes of lower GIT bleeding

31
Cancers/polyps
Colitis/ulcers (including Inflammatory bowel disease and
infectious)
Anorectal (hemorrhoids, fissures, and rectal ulcers)
Diverticular disease
Jaundice
Yellow discoloration of the sclera or skin
Due to the presence of excess bilirubin
Have you noticed your skin or your eyes looking a little yellow?
Has anyone else commented on it?
Has your urine been any darker (obstructive jaundice)?
How about your stools are they paler than usual (obstructive jaundice)?
Causes of jaundice
1.
Increased bilirubin production

Haemolysis [unconjugated bilirubin]
2.
Congenital hyperbilirubinaemia
Gilberts syndrome [unconjugated bilirubin]
3.
Cholestatic jaundice
Intra-hepatic (Liver disease)
Viral
Alcohol
Drug
Pregnancy
Cirrhosis any type
Extra-hepatic
Common duct stones
Carcinoma head of pancreas/ampulla/bile duct
Pancreatitis/pseudocyst
Biliary stricture
Abdominal distension
32
Bowel obstruction
Pregnancy
Constipation
Irritable Bowel Syndrome
Liver disease (ascites)
History of Presenting Complaint

Previous diagnosis of:
Irritable bowel syndrome
Jaundice
Hepatitis
GIT malignancy
Inflammatory Bowel Disease
Previous abdominal surgery
Previous OGD/colonoscopy

Other medical/surgical problems
Medication
Determine what medication patient is taking prescribed/over-the-counter
Anti-diarrhoeal agents
Laxatives
Anti-emetics
Analgesics, especially paracetamol (can cause liver damage)
and Non Steroidal Anti-Inflammatory Drugs (cause peptic
ulcer disease/GIT bleeds)
Allergies
To any medication ask about type of reaction
Social History
Married/children
Employed
Home situation
Alcohol - Excessive alcohol use can cause liver problems [cirrhosis]
Smoking
High risk behaviour for Hepatitis transmission travel/sexual behaviour/Intravenous drug usage
Family History
Bowel cancer
33
Inflammatory bowel disease

Liver disease, e.g. haemochromatosis
CVS
RESP
GI
GU
Musculoskeletal
Neuro
Preparation: 4Es
Environment
Warm and private
Good light
Explain that you are going to examine their abdomen and ask their permission.
General Inspection
From the end of the bed
General Appearance
Jaundice
Yellow discoloration of the skin and sclera
Cachexia and wasting
GIT malignancy and malabsorption
Malnutrition in alcoholic patients
Mental state
Hepatic encephalopathy due to decompensated liver disease

Patients eventually become stuporous and comatosed
The hands
Look at patients hands, initially palmar surface and then ask patient to turn hands
over.
Clubbing
Cirrhosis
Coeliac disease
34
Leuconychia
White discoloration of the nails due to hypoalbuminaemia
Koilonychia
Thin, brittle, concave finger nails
May result from iron deficiency anaemia
Palmar erythema
Reddening of the thenar and hypothenar eminences
Attributed to raised oestrogen
Can also occur with pregnancy/thyrotoxicosis/polycythaemia/rheumatoid
arthritis
Anaemia
Inspect palmar creases for pallor [blood loss/malabsorption B12 and folate]
Dupuytrens contracture
Thickening and contraction of the palmar fascia causing permanent flexion
most often of the ring finger [associated with alcoholism, manual work also
familial]
Hepatic Flap/Asterixis
Ask patient to stretch out the arms in front, seperate the fingers and extend
wrists
Look for jerky, irregular flexion-extension movement at the wrist and
metacarpophalangeal joints
Also present with cardiac, respiratory and renal failure
35
The arms
Bruising
Absorption of vitamin k and therefore clotting factors 2, 7, 9 and 10
Scratch marks
Obstructive or cholestatic jaundice may cause pruritis
Commonly the presenting feature of primary biliary cirrhosis
Petechiae [pinhead sized bruises]
Excessive alcohol consumptionbone marrow
depressionthrombocytopenia
Splenomegaly [portal hypertension] hypersplenismthrombocytopenia
Spider naevi
Central arteriole from which radiates numerous small vessels.
Distribution is in the area drained by the superior vena cavaarms, neck and
chest wall
More than 2 spider naevi is abnormal, attributed to oestrogen excess
Acanthosis nigricans
Brown/black velvety elevations of the epidermis due to confluent papillomas
Usually found in the axillae and the nape of the neck
Rarely associated with GIT carcinoma, lymphoma, acromegaly, DM
The face
Eyes
Sclerae
For signs of jaundice and anaemia
Kayser-Fleischer rings
Brownish green rings at the periphery of the cornea
Due to deposits of excess copper found in Wilsons diseasecopper storage
disease which causes cirrhosis and neurological disturbances
Xanthelasma
Cholestasis is associated with cholesterol
Xanthelasma are common in patients with primary biliary cirrhosis
36
Parotids/Parotidomegaly
Clench the teeth and palpate the masseter muscle
Parotid is best felt behind the masseter muscle and in front of the ear
Associated with alcoholism rather than liver disease
The Mouth
Ulcers
Aphthous ulceration: Cause unknown
Other causes of mouth ulcers: Crohns/Ulcerative colitis/Herpes
Simplex/Autoimmune disorders
Fetor hepaticus
Rather sweet smell of the breath
Indication of severe hepatocellular disease
Leukoplakia
White coloured thickening of the mucosa of the tongue and the mouth
This condition is premalignant
Macroglossia/Enlargement of the tongue
Downs Syndrome/Acromegaly/tumour infiltration/Amyloidosis
Candidiasis
Creamy white curd-like patches in the mouth
Associated with immunosuppressionsteroids/chemotherapy/AIDS
May spread to involve oesophagus causing dysphagia
Peutz-Jeghers Syndrome
Freckle-like spots on the buccal mucosa, fingers and toes are associated with
hamartomas of the bowel
Incidence of GIT adenocarcinoma is increased
Autosomal dominant condition
The Neck and Chest

Palpate the cervical lymph nodes
Particularly important to feel for supraclavicular lymph nodes especially on
the left
These may be involved with gastric and other GIT malignancy
Troisiers sign
Presence of a large left supraclavicular/ Virchows node in combination with
carcinoma of the stomach
Examination bed
Patient flat with head at 15-20 degrees i.e. one pillow under head (abdominal
muscles are not stretched and remain relaxed)
Rest arm by the side

37
Exposure
Nipple to pubic symphysis
Gynaecomastia
Occurrence in the male of breasts resembling those of the sexually mature
female
Sign of chronic liver disease
Changes in the oestradiol to testosterone ratio may be responsible
Spironolactone used to treat ascites is also a common cause
Position of examiner:
Clean warm hands
Hand & forearm horizontal plane with abdominal wall
Kneel beside the patient
Inspection:
Asymmetry
Shape: Flat, distended, obvious mass,
Scars, Sinuses, Distended veins, Pulsation, striae, Cullens, grey
turners
Cough impulse
Scars: Previous surgery/trauma.
1 2 3 4 5 6 7 8 9
1.
2.
3.
4.
5.
6.
7.
8.
Subcostal/Kocher's
Choleocystectomy
Right Paramedian
Laparotomy
Midline
Laparotomy
Nephrectomy/Loin
Renal surgery
Gridiron
Appendectomy
Laparoscopic
Choleocystectomy
Appendectomy
Colectomies
Left Paramedian
Anterior rectal resection
Transverse suprapubic/Pfannenstiel
Hysterectomy
Other pelvic surgery
9. Inguinal hernia
Hernia repair
38
Palpation:
Ask for pain; go from non tender to tender region
Light palpation in nine areas
Deep palpation
Hand held still during inspiration an advanced on expiration
Eyes on pts face
Guarding: contraction of abdominal muscles, tenderness or anxiety,
voluntary or involuntary
Rigidity: constant involuntary contraction of the abdominal muscles,
associated with tenderness, indicates peritonitis
Rebound tenderness: strongly suggests peritonitis, compress abdominal
wall slowly and release rapidly, sudden stab of pain
Abdominal mass: Any intra-abdominal mass must be carefully
described.
Site/Size [may be measured]/Shape/Surface [regular or
irregular]
Consistency [hard or soft]
Tenderness
Mobility [move with inspiration]
Pulsatile or not
Get above mass
Liver:
Begin RIF
Hand parallel to right costal margin
If the liver edge is identified surface of liver should be felt (hard, soft,
tender, non tender, regular, irregular, pulsatile or non-pulsatile)
Measure total liver span: percuss down along right mid clavicular line
until the liver dullness is detected. The normal upper border is 5th rib
and normal span is less than 12.5cm.
Gallbladder: Murphys Sign: Hand at the right costal margin, on taking a deep
breath the patient catches breath when inflamed gallbladder presses on
examiners hand.
Courvoisiers law: If the gallbladder is enlarged and the patient is jaundiced
the cause is unlikely to be gallstones. Carcinoma of the pancreas of the
pancreas or lower biliary tree is likely to be present. The gallbladder
with stones is fibrosed and is incapable of enlargement.
Spleen:
Enlarges inferiorly and medially
Begin RIF moving to left costal margin
If not palpable move the patient slightly on to the right side towards the
examiner and palpation with two hand technique.
Splenomegaly is detectable if the spleen is one and half to two times enlarged
Kidneys:
Both kidneys move downward with inspiration
Bimanual method: Left hand slides underneath the back in the area of
renal angle, right hand is placed over the upper quadrant, fingers flex at
metacarpophalangeal joints.
Ballotting: press over the renal angle by flexing the fingers of the posterior
hand, the kidney can be felt to float upward and strike the anterior
hand.
39
AAA: Place two hands along the midline just above the umbilicus and feel expansile
pulsation
Hernial Orifices:
At rest and when the patient coughs (inguinal, femoral &
umbilical)
Lymph nodes:
Supraclavicular and inguinal
External Genetalia: Scrotum, testes
Rectal Exam: The abdominal examination is not complete without the performance
of a rectal examination. It is covered in practical skills sessions in detail.
Percussion
Liver
The right side of the abdomen should be percussed from the right iliac fossa to the
right costal margin along the mid clavicular line. Dullness defines the livers lower
border. Define the upper border of the liver by percussing along the mid clavicular
line from above. Normally the upper level of liver dullness is the fifth rib in the right
mid clavicular line.
Kidneys
We do not percuss the kidneys as there will usually be a resonant area due to
overlying gas.
Bladder
Percuss from the umbilicus to the pubic symphysis. An area of suprapubic dullness
may indicate the upper border of an enlarged bladder or pelvic mass.
Ascites
2-3 litres of ascites are present before this is clinically detected. Usually the
percussion note over the abdomen is resonant due to air in the bowel. When peritoneal
fluid [ascites] collects, this accumulates in the flanks due to gravity in a supine
patient. When 2-3 litres of ascites is present the abdomen will be dull to percussion in
the flanks. As fluid accumulates abdominal distension and umbilical eversion occur.
The dullness is then detectable closer to the midline.
Shifting dullness:
Percuss out to the left flank until dullness is reached. Keeping your finger over this
area ask the patient to roll towards you. Gravity will cause the fluid to move to the
right side of the abdomen [wait 15-20 seconds].
Percussion is repeated and shifting dullness is present if the area of dullness has
changed to become resonant.
Fluid thrill:
This may be present when very large amounts of ascites are present. One of the
examiners hands is placed flat on the patients flank.
The other hand then flicks the other flank. A shock wave is transmitted to the
palpating hand. The patient can be asked to help by placing a hand in the midline of
the abdomen to prevent any ripple from passing through the fat of the anterior
abdominal wall.
Auscultation
40
Place the diaphragm of the stethoscope just below the umbilicus on the right and left
side. Bowel sounds can be heard intermittently. They should be described as either
present or absent. Normal bowel sounds are low pitched and gurgling occurring every
15-30 second period. No bowel over 30 seconds indicates paralytic ileus. Distension
of the bowel leads to high pitched tinkling sounds caused usually by mechanical
obstruction.
Succussion splash: In pyloric stenosis or obstruction the stomach is distended with
fluid and gas. Hold the patients from hips and shake the abdomen from side to side,
splashing sounds are heard.
Clinical Teaching and Communication Skills

Taking a Respiratory History
RESPIRATORY CURRICULUM SC2

CORE KNOWLEDGE
The following topics must be known well.
Also student should have taken at least one history from patient with
each of following conditions.
Chronic Bronchitis
Emphysema
Asthma
Resp Failure
Sepsis
Pneumonia
Lung Ca
Sarcoid
TB
Occupational Lung Disease
DVT/PE
Sleep Studies
Pneumothorax
Pleural Effusions
Cystic Fibrosis
Lung Transplant
Clinical Criteria for ICU admission
SYMPTOMS
(Student must be capable of taking directed history and exam and be
able to order and interpret relevant investigations)
Cough (productive and non productive)
Shortness of breath (acute and chronic)
Wheeze
Stridor
41
Haemoptysis
Pleuritic chest pain
Pyrexia
Asymptomatic nodules found on routine Chest X Ray
Pleural fluid on CXR
At the end of this session you should be able to:
5. Take a detailed respiratory history from a patient.
6. Complete a full history.
7. Complete a systems review.
Introduce yourself to patient and find out patients name, age and where they
are from.
Allow the patient to describe their problem in their own words and in their
own way. Beginning the interview with an open question may bring valuable
information, which will help in making a diagnosis:
Do you want to tell me about the problem?
Explore the presenting complaint fully, asking questions to ensure you are
clear about all aspects of the problem.
Many of the questions pertaining to pain may be adapted for any symptom,
e.g. onset, periodicity, duration, aggravating factors, relieving factors,
associations.
Ask about all the respiratory symptoms remember that the patient may not
realise the relevance of certain symptoms or the association between them.
Cough
Duration
Nature of cough ( dry, barking etc)
Change in character ( if chronic cough)
When does the cough occur? ( Night, post meals)
Associated symptoms (fever, wheeze)
Sputum producton?
Some causes of Cough Acute cough

1. Infection
2. Allergy
3. Asthma/COPD
Chronic cough
1. Smoking
2. Asthma/COPD
3. Post-nasal drip
4. Lung Carcinoma
42
5. TB
Sputum
How much are you bringing up in a day? (tsp, tbsp, cup etc)
What colour is it?
If chronic then how much would you usually produce and what colour is it
normally? Vs How much are you producing now and what colour?
Have you ever seen blood / pink discoloration in it?
Can you comment on the taste / smell?
Can you describe the consistency? (thick, sticky, watery, frothy)
Do you have trouble getting it up?
What time of the day is it worse classically much worse in early morning
with bronchiectasis.
Sputum production
Copious amounts of purulent sputum are characteristic of an infective exacerbation
of COPD. Large amounts of frothy-white/pink sputum are seen in cardiac failure.
Some causes of sputum production
1.
2.
3.
4.
5.
6.
7.
Infection
Smoking
COPD
Bronchiectasis
Lung CA
TB
Pulmonary oedema
Haemoptysis
Have you ever coughed up blood / bloodstained sputum?

Can you describe it? (blood flecks, bright / dark red, pink & frothy, clots)
How long is this going on for?
How many times has it happened?
How much on each occasion?
Some causes of haemoptysis 1.

2.
3.
4.
5.
6.
Lung carcinoma
Pulmonary embolism
TB
Pneumonia
Bronchiectasis
Cystic Fibrosis
Dyspnoea
How long have you been feeling breathless?

Is it getting worse? Severity
What brings it on?
How far can you run / walk / climb before it happens?
43
Are you ever breathless at rest?

Do you ever feel breathless in bed?
Timing of onset (acute, subacute, chronic)
Duration and variability. Eg dry cough at night in asthma
Ask about associated factors eg wheeze
How is it affecting your life?
Ask about baseline vs current level of dyspnoea.
Some causes of dyspnoea

1. COPD
2. Asthma
3. Pneumonia
4. Pneumothorax
5. Lung carcinoma
6. Pulmonary embolism
7. Pulmonary fibrosis
8. Cystic Fibrosis
9. Pleural effusiom
10. Left ventricular failure
Wheeze
What brings it on? (allergens, exercise, cold air, stress, smoke, dust)
How often do you get an attack?
Is this more often than usual?
How do you relieve it? Does this help?
How often do you take you inhaler (if on one)?
Do you check peak flows at home? What is your average usually? What is it
now?
How is it affecting your life?
Have you ever had to attend A&E with an attack?
Were you ever ventilated?
Some causes of wheeze Acute
Respiratory infection
Foreign body aspiration
44
Chronic
Asthma
Chronic infection
Cystic Fibrosis
Bronchiectasis
Mediastinal masses
Cardiac wheeze (LVF)
Chest pain
How long have you had this chest pain?

Is it worse on taking a deep breath?
Was it of gradual or sudden onset?
Ask all the pain questions SOCRATES - Site, Onset, Character, Radiation,
Associated symptoms, Timing, Exacerbating and relieving factors, Severity.
If pain is pleuritic in nature, it is usually localised, sharp and made worse by deep
inspiration and coughing.
Fever
Is patient febrile?
Are they getting chills or rigors?
Are they checking their temperature? What is it?
Hoarseness
Is this a new problem?

How long is it going on?
Night sweats
How long is it going on?

Does it happen every night?
Do they have to change their night clothes and bed sheets?
Weight loss
ASK
If they were trying to lose weight?

Is there a change in appetite?
How much weight was lost and over what time period?
Weight loss may be associated with Respiratory neoplasm or Chronic infection, e.g.
COPD/Cystic Fibrosis

45
Previous respiratory illness [asthma, pneumonia, TB, COAD, Tumour] and all
relevant details about that?
o In COPD ask when diagnosed and how, smoker or not? History of
recurrent chest infections? How many exacerbations per year requiring
antibiotics, how many hospitalisations per year, when was the last
exacerbation? Every in ITU or intubated?, Every do pulmonary
rehabilitation? Baseline dyspnoea, exercise tolerance and sputum
(colour and volume), effect on mobility and life in general. Home
oxygen use or not. Nebuliser use or not.
o In asthma when diagnosed and how, current control, how often
attacks and what triggers, what inhalers, compliance and technique,
what is baseline peak flow and what is current peak flow? Every
hospitalised with asthma, every in ITU or intubated?
Risk factors for respiratory disease eg smoking, family history,
Abnormal CXR?
Any chest problems as a child?
Any allergies, hayfever, eczema or other atopy increase risk of asthma?
Previous admissions?
Previous operations?
o
o
o
o
Video Assisted Thoracoscopy for biopsy

Chest drain insertion
Lobectomy
Pneumonectomy

Medication
Prescribed and over the counter
Bronchodilators/inhalers
Home nebuliser
Home oxygen
Antihistamines
Antibiotics
Steroids
Allergies
To any medication
Document the reaction which occurred, e.g. true allergy or adverse reaction.
nausea/vomiting/rash/wheeze/bronchospasm/loss of consciousness.
Social History
46
Marital status/children
Employment effect of condition on employment status
Home situation Independent or needs help with ADLs, any adjustments
made to the home, how mobilise? home help? Meals on wheels? Who is at
home? Are there people/family nearby who help?
Alcohol intake [count units per week]
Smoking history
a.
b.
c.
d.
e.
f.
Do you smoke? / Have you ever smoked?

How many cigarettes do you smoke in a day?
Have you ever smoked more / less?
Have you ever tried to give up?
Were you successful?
Passive smoking in work place/at home
Occupational History
Exposure to dust in mining industry/factories [asbestos/coal]

Exposure to mouldy hay [allergic alveolitis]
Exposure to birds [psittacosis]
Family History
Any family history of respiratory disease
Asthma
Cystic Fibrosis
Emphysema
Alpha-1-anti-trypsin deficiency
Any other illness in family
CVS
RESP
GI
GU
Musculoskeletal
Neuro
Respiratory Examination
47
Exposing the patient

Patient should be undressed to the waist. Patient can be sitting in bed, over the edge of
the bed or on a chair.
General Appearance/Inspection
All examinations begin with a general inspection of the patient and their immediate
surroundings.
This is done from the end of the bed.
Is the patient comfortable?
Dyspnoea at rest [shortness of breath]
Tachypnoea - rapid respiratory rate, count respiratory rate

[Should not exceed 14 breaths/min @ rest]
Are accessory muscles of respiration being used?

- Sternomastoid, scalenes, trapezius, platysma muscles
increasing chest expansion
- Abdominal muscles
- Splinting may also be seen where the arms are fixed to
allow use of the pectoral and other muscles to assist in
breathing
Character of cough
Productive Excess bronchial secretions pneumonia/chronic bronchitis
Dry cough Asthma/bronchial Ca/LVF
Sputum production
Volume/purulent/blood
Haemoptysis quantity/duration
Wheeze On expiration Asthma/COAD

48
Stridor [obstruction of larynx, trachea, and large airways,

rasping noise loudest on inspiration i.e. foreign body/tumour]
Hoarseness [Listen to voice]

Recurrent laryngeal nerve palsy,
E.g. Carcinoma of the lung
Laryngeal cancer
Laryngitis
Comment on equipment O2 delivery, IV access, ECG monitor, and catheter bag

Comment on bedside table inhalers, sputum pot
Mobility walking frame, wheel chair
Cyanosis
Haemoglobin molecule changes colour from blue to red when oxygen is added to it in
the lungs. Cyanosis is a blue coloration of the skin and mucous membranes due to the
presence of greater than, or equal to, 5 g/dL of deoxygenated hemoglobin in blood
vessels near the skin surface
Peripheral Cyanosis
Blood supply to a certain part of the body is reduced and the tissues extract more
oxygen than normal i.e. the lips in cold weather may appear blue.
Central Cyanosis
Abnormal amount of deoxygenated haemoglobin in the arteries causes a blue
discoloration in parts of the body with good circulation [the tongue]
Examination of the Hands

Clubbing
Inspect for loss of angle between the nail bed and the finger.
It can be graded:
Grade 1 fluctuation and softening of the nail bed. This can be examined for
by compressing nail bed with your fingers and rocking it [swelling of the
subcutaneous tissues over the base of the nail]
Grade 2 loss of the nail-bed angle
Grade 3 increased curvature of the nail [swelling of the subcutaneous tissues
involves the nail bed]
Grade 4 fingertip develops a clubbed (drumstick) appearance [swelling of the
pulp of the fingers in all dimensions]
Early clubbing
Increased sponginess of the proximal nail bed [There is fluctuation of the nail bed]
This can be examined for by compressing nail bed with your fingers and rocking it.
The next change is loss of the nail angle.
49
Late clubbing
Eventually the distal phalanx becomes enlarged due to soft tissue swelling [drum
sticking]
[The cause of clubbing is not known there are several theories]
In a few cases Hypertrophic Pulmonary OsteoArthropathy [HPOA] may develop

causing pain and swelling of the hands, wrists, knees, feet and ankles, with
radiographic evidence of subperiosteal new bone formation
Causes of clubbing
Cardiovascular
Cyanotic congenital heart disease
Subacute infective endocarditis
Atrial myxoma
Respiratory
Bronchial carcinoma [squamous cell]
Bronchiectasis
Lung abscess
Cystic Fibrosis
Empyema
Pulmonary fibrosis [fibrosing alveolitis]
Mesothelioma
Asbestosis
Gastrointestinal
Cirrhosis
Coeliac disease
Thyroid acropachy hyperthyroidism
Familial
50
Idiopathic
NB Chronic bronchitis and emphysema do not cause clubbing
**Clubbing is a sign that is looked for as part of the CVS, Respiratory,

Gastrointestinal and Thyroid exam. It is frequently asked in exams. You must know
the causes and stages of clubbing. **
Tar Staining
Sign of cigarette smoking
Pulse
Tachycardia is a common feature of infection, and is a side-effect of beta-agonist
therapy for obstructive airway disease.
Bradycardia may occur in very severe sepsis/asthma.
Atrial fibrillation may be caused by pneumonia and lung carcinoma.
Mention that you would also like to take the blood pressure.
Wasting and weakness
Compression and infiltration by a peripheral lung tumour of a lower trunk of the
brachial plexus results in wasting of the small muscles of the hands
Flapping tremor/Asterixis
51
Dorsiflex the wrists with the arms outstretched and spread out the fingers. With severe
carbon dioxide retention a flapping tremor may occur.
Causes of Asterixis
1. CO2 retention Respiratory failure
2. Liver disease usually associated with hepatic encephalopathy in
cirrhosis or acute liver failure
3. Acute renal failure
Signs of CO2 Narcosis
1.
2.
3.
4.
5.
Bounding pulse
Asterixis
Chemosis collection of fluid under the conjunctiva
Altered consciousness
Kussmauls breathing deep sighing respiration
Examination of the Face

Anaemia
Examine conjunctiva anaemia/chemosis
Horners Syndrome
Ptosis, miosis, anhydrosis and enophthalmos [sunken eye]
Partial ptosis/Constricted pupil/Loss of sweating [ipsilateral]

Interruption of the sympathetic innervation of the eye at any
point
E.g. Apical lung tumour compressing sympathetic nerves in the neck
52
Abnormal right eye in right-sided Horners syndrome

Central Cyanosis
Examine tongue
Upper Respiratory tract infection
Reddened pharynx
Enlarged tonsils
Pus on tonsils
Pneumonia
Lung abscess
Tooth Decay
Sinusitis
Tenderness over sinuses
Nose
Note any obvious septal deviation or polyps. A nasal speculum can be used to inspect
for polyps or engorged nasal turbinates
Facial plethora/oedema
Superior vena caval obstruction

53
Prominent veins in superior vena cava obstruction
Trachea
Is the trachea central or is it deviated from the midline? Explain to the patient that you
are going to press gently on their neck and that it may be a little uncomfortable.
Use the forefinger of the right hand to palpate for the position
of the trachea above and
backwards from the suprasternal
notch.
If displacement of trachea is
present its edge rather than its
middle will be palpated and a
larger space will be present on
one side than the other.
Causes of tracheal deviation

Towards the lesion
1. Upper lobe fibrosis
2. Upper lobe collapse
3. Pneumonectomy
Away from the lesion
1. Tension pneumothorax
2. Massive pleural effusion
Tracheal tug is present when the finger resting on the trachea moves inferiorly with
each inspiration. This is a sign of gross overexpansion of the chest.
Lymph node examination
Cervical - Examine patient sitting up from behind for submental, submadibular,
jugular chain, supraclavicular, posterior triangle, occipital, postauricular and
preauricular. If enlarged comment on site, size, consistency, tenderness, fixation,
overlying skin.
The Chest
54
Examine anteriorly and posteriorly by inspection, palpation, percussion and

auscultation. Compare left and right sides.
INSPECTION
Is the chest moving with respiration?
Is the movement equal and symmetrical on both sides?
A large effusion, pneumothorax, area of collapse etc in one lung can cause
asymmetrical movement.
Kyphoscoliosis
Kyphosis-forward curvature of spine

Scoliosis-lateral curvature of spine
Severe kyphoscoliosis may reduce lung capacity and increase the work of breathing.
Pectus Excavatum
Depression of lower end of sternum.

A developmental defect.
In severe cases lung capacity may be restricted.
Pectus Carinatum
Prominence of sternum and costal cartilages.

Can occur with chronic childhood respiratory illness and rickets.
Barrel-shaped
Anteroposterior diameter is increased compared with the lateral diameter.

This indicates hyperinflation.
Severe asthma and emphysema
Scars
From previous thoracic operations.

Chest drains.
Thoracotomy scars.
Traumatic scars.
55
Thoracoplasty
An operation performed in the past for tuberculosis.

It involved removal of a large number of ribs on one side of the chest to
achieve permanent collapse of the affected lung.
No longer required due to antituberculous medication.
Radiotherapy
Marks on chest wall.

Skin may appear erythematous and thickened over irradiated area.
Lung Cancer and lymphoma
Subcutaneous emphysema
Swelling of chest wall and neck due to tracking of air from lungs as in
pneumothorax.
May also be due to rupture of the oesophagus.
It is felt as a crackling sensation on palpating the skin of the chest or neck.
Movement of chest wall
Look for asymmetry of chest wall movement anteriorly and posteriorly.

Unilateral reduction in chest wall movement may be due to
consolidation/pleural effusion/pneumothorax.
Bilateral reduction of chest wall movement indicates a diffuse abnormality
such as COAD/diffuse pulmonary fibrosis.
Palpation
Chest expansion
Measuring chest expansion provides
information on a number of things.
Is expansion equal on both sides?
If the patient has a
pneumothorax or an area of
consolidation on one side,
expansion will be decreased on
that side.
In patients with COPD,
because their chest is
hyperinflated, chest expansion
is decreased overall.
Expansion will also be decreased with diffuse pulmonary fibrosis.
56
Place hands over upper anterior chest wall and get patient to take a deep
breath in and out. Chest movement should be equal on both sides. This is checking
anterior expansion. The hands can also be wrapped around the lower chest to
measure outward expansion.
Place hands on lower posterior chest wall with fingers extending
around the sides of the chest. The thumbs are lifted slightly off the chest
and should almost meet in the midline. On inspiration the thumbs should
move symmetrically apart at least 5cm. This will assess lower lobe
expansion.
Take a breath in, and let it all the way out please. When they are in full expiration,
place your hands over the lower ribs and stretch your thumbs out until they meet in
the midline. Take a deep breath in please The distance your thumbs move apart is
measured in centimetres
Vocal fremitus
Palpate the front and back of the chest with the hand in two comparable
positions as the patient repeats 'ninety-nine'.
Differences in vibration on the chest wall can be detected. The causes of

change in vocal fremitus are the same as those for vocal resonance [checked as
part of auscultation] e.g. consolidation. Over consolidated lung the
sound/vibration is transmitted better.
This sign may be difficult to interpret.
Ribs
Compress the chest wall anteroposteriorly and laterally.

Localised pain suggests a fracture.
Percussion
Position the patient sitting up with the arms folded in front of the chest. Put
left hand on the chest wall with fingers slightly separated and aligned with the
ribs.
The middle finger is pressed firmly against the chest. Other fingers are raised
slightly off the chest wall
With the pad of the right middle finger strike firmly the middle phalanx of the
middle finger of the left hand.
The percussing finger must be held slightly flexed and a loose swinging
movement should come from the wrist. The percussing finger should be held
off the middle phalanx at the end of percussion. Ending percussion with the
percussing finger held on the middle phalanx will result in a falsely dull
percussion note.
Percussion of symmetrical areas of the anterior, posterior and axillary regions
is necessary.
57
If the underlying structure contains air, the sound produced will be resonant.
If the underlying structure is solid, the sound produced will be dull.
As the lungs contain air, we expect to hear a resonant note throughout all lung fields.
Begin with percussion in the supraclavicular fossa over the apex of the lung.
Percuss the clavicles directly.
On percussion posteriorly, the scapulae should be moved out of the way by
asking the patient to move their elbows forward. This rotates the scapulae
anteriorly.
Dull Percussion over solid structure i.e. consolidated area of lung.

Stony dull Percussion over fluid-filled area i.e. pleural effusion.
Resonant Percussion over normal lung.
Hyper-resonant Percussion over hollow structures i.e. pneumothorax
Auscultation
Start using the bell of the stethoscope applied above the clavicles to listen to
the lung apices.
Auscultate using the diaphragm over the anterior, lateral and posterior chest
wall.
58
It is important to compare each side with the other and to listen over enough
areas.
Ask the patient to

Breathe in and out through your mouth please
Listen over the same areas you percussed, again comparing right & left sides at
each level.
Listen for the quality and intensity of breath sounds and the presence of additional
sounds.
Quality of breath sounds
Vesicular breath sounds
Normal vesicular breath sounds are produced in the airways.
There is no gap between inspiratory and expiratory sounds.
Bronchial breath sounds
Bronchial breath sounds are due to turbulence in the large airways. They have a
hollow and blowing quality.
Often a gap is present between inspiration and expiration.
Heard over areas of - consolidation [pneumonia]
- pleural effusion [above the fluid]
- collapsed lung [i.e. adjacent to a pleural effusion]
Intensity of breath sounds
Normal or Reduced
Causes of reduced intensity
COAD [especially emphysema]

Pneumothorax
Pleural effusion
Pneumonectomy
Pulmonary fibrosis
Added sounds:
Note the stage in the respiratory cycle at which the added sounds occur: inspiration/
expiration, early/mid/late/pan.
Wheeze
Wheeze may be heard on inspiration or expiration or both.
They imply significant airway narrowing.
They tend to be louder on expiration.
An inspiratory wheeze implies severe airway narrowing.
Usually the result of acute [asthma] or chronic [COAD]
59
Airflow limitation may be due to

Bronchial spasm
Mucosal oedema
Excessive secretions
Crackles/Crepitations
Crackles [crepitations] are probably the result of small
peripheral airways collapsing on expiration.
Fine Crackles similar to hair rubbed between the fingers i.e. pulmonary
fibrosis
Medium Crackles i.e. LVF
Coarse Crackles Characteristic of pools of retained secretions and have an
unpleasant gurgling quality.
They tend to change with coughing.
i.e. bronchiectasis/pneumonia
Pleural rub
Due to thickened, roughened pleural surfaces rubbing together as the lungs expand
and contract - grating sound.
I.e. Pulmonary infarction/pneumonia
Vocal resonance
Auscultating while a patient speaks gives further information about the

lungs ability to transmit sounds.
Ask the patient to repeat 'ninety-nine' and listen over each part of the
chest.
Over consolidated lung the numbers are clearly audible while over
normal lung the sound is muffled.
Whispering pectoriloquy
Vocal resonance is increased to such an extent that whispered speech is

distinctly heard.
Ask the patient to whisper 'ninety-nine' and listen over each part of the
chest.
Aegophony
Consolidated lung tends to transmit high-pitched sounds so that speech

heard through the stethoscope takes on a bleating quality. When a
patient says 'e'[bee] it sounds like 'a' [bay].
Listen over each part of the chest as the patient repeats e, e, e
To complete the examination

60
LOUD P2
If loud pulmonary component to 2nd heart sound [P2] heard in second left intercostal
space pulmonary hypertension should be suspected.
Pulmonary hypertensive heart disease [cor pulmonale] may be due to:
COAD
Pulmonary fibrosis
Pulmonary thromboembolism
PEMBERTONS SIGN occurs in superior vena cava obstruction.
Raise arms over head

Facial plethora [redness]
Inspiratory stridor
Non pulsatile elevation of JVP
ABDOMEN
Enlarged liver due to secondary deposits in cases of lung cancer
FEET
Oedema [right heart failure]
DVT
Diabetic History and Examination

History
Presenting complaint
A diabetic patient can present in a number of ways.
1) Subacute symptoms of hyperglycaemia
Polyuria
Polydipsia/thirst
Blurred vision
Hyperphagia
Weight loss
Tiredness / fatigue
Irritability / Difficulty concentrating
Infections - genital candidiasis and cutaneous infections.
The classical symptoms of, polyuria, polydipsia and weight

loss are more common in type 1 diabetes.
2) Acute diabetic emergency
Diabetic Ketoacidosis : Type 1 Diabetes

61
DKA
Thirst
Nausea and vomiting
Abdominal pain
Confusion / Drowsiness / Coma
Blurred vision
Weakness
is the first presentation of a new diabetic in 20 %
of cases.
In an established diabetic it usually occurs in the
context of intercurrent
illness such as infection (60%)
or ommision of insulin dose (30 %).
Non Ketotic hyperosmolar diabetic coma

-
Marked drowsiness / coma

Thirst
Symptoms of hyperviscosity such as blurred
vision, headache, stroke
Hypoglycaemia
- FIRST:
Adrenergic symptoms (sweating,
tremor, palpitations, anxiety, nausea, weakness)
- THEN:
Neuroglycopoenic symptoms (speech
difficulty, confusion, drowsiness, convulsions,
coma).
WHY DOES IT OCCUR LIKE THAT? From Harrisons Principles Of

Internal Medicine, 17th ed, 2008:
TABLE 339-2. PHYSIOLOGIC RESPONSES TO DECREASING
PLASMA GLUCOSE CONCENTRATIONS
Response Glycemic
Physiologic Role in the Prevention or
Threshold, Effects
Correction of
mmol/L
Hypoglycemia (Glucose
(mg/dL)
Counterregulation)
Insulin
4.4-4.7 (80Ra ( Rd)
Primary glucose regulatory
85)
factor/first defense against
hypoglycemia
Glucagon 3.6-3.9 (65Ra
Primary glucose
70)
counterregulatory
factor/second defense
against hypoglycemia
Epinephri 3.6-3.9 (65Ra, Rc
Third defense against
ne
70)
hypoglycemia, critical when
glucagon is deficient
Cortisol
3.6-3.9 (65Ra, Rc
Involved in defense against
and growth 70)
prolonged hypoglycemia,
62
hormone
Symptoms
not critical
2.8-3.1 (50- Recognition Prompt behavioral defense
55)
of
against hypoglycemia (food
hypoglycemi ingestion)
a
Cognition <2.8 (<50)
(Compromises behavioral
defense against
hypoglycemia)
Note: Ra, rate of glucose appearance, glucose production by the liver
and kidneys; Rc, rate of glucose clearance, glucose utilization
relative to the ambient plasma glucose concentration; Rd, rate of
glucose disappearance, glucose utilization by the brain (which is
unaltered by the glucoregulatory hormones) and by insulin-sensitive
tissues such as skeletal muscle (which is regulated by insulin,
epinephrine, cortisol, and growth hormone).
Copyright 2008 by The McGraw-Hill Companies, Inc. All rights
reserved.
In people with diabetes, hypoglycaemia occurs in the context of
treatment and an accurate history of treatment, home
circumstances and depression, should be taken.
3) Presentation with complications
Microvascular disease
-
Retinopathy: Visual loss is a late symptom, which

is why screening is required.
Neuropathy: Peripheral and autonomic
Nephropathy: May progress to renal failure
Macrovascular disease
-
Peripheral vascular disease

Cardiovascular disease
Cerebrovascular disease
Infection
4) Detection on screening with little or no symptoms
History of presenting complaint
1. When was diabetes first diagnosed? How? Symptoms?
2. Recent glycaemic control
a. Symptoms of hyperglycaemia
b. Home glucose reading diary?
c. Recent HbA1C? Does patient knows what it is?
3. Diet carbohydrates? Portions? Fats? Sweets?
63
4. Exercise patients with diabetes should exercise for at least

30 min daily
5. Early signs of complications
a. Macrovascular: Any chest pain/SOB when walking? Any
calf pain when walking?
b. Microvascular:
i. Any vision deterioration? (retinopathy, cataracts)
ii. Any pins/needles/numbness/pain/altered sensation
anywhere? (peripheral neuropathy?)
iii. Any change in bowel motions pattern/ diarrhoea/
constipation/ incontinence? Early satiety?
Dysphagia? (GI autonomic neuropathy)
iv. Any dizziness when standing up? (CVS autonomic
neuropathy)
v. Any urinary incontinence? (bladder neuropathy)
vi. For men: any difficulty getting or keeping an
erection? Any symptoms of retrograde
ejaculation?
6. If on hypoglycaemics (sulphonylurea, insulin)
a. Any symptoms of hypoglycaemia? How often? When?
After exercise/not enough food/ insulin dose increase?
Any serious hypoglycaemia (LOC) that required family to
administer glucagon?
7. If type 1, any admissions for DKA?
8. If type 2, any admission for HHS (hyperglycaemic
hyperosmolar state)?
9. Any recent infections (genital candidiasis trush, balanitis;
UTIs, URTI & LRTIs)? Any skin infections?
Glucometer reading
Medication / Diabetic treatment /Allergies

-
What treatment the patient is on for their

diabetes (diet, oral hypoglycaemics, insulin),
doses and any recent changes in treatment
Insulin pens
64
Modification of co-morbidities: ACE inhibitors,

Angiotensin receptor blockers, Statins, Aspirin
It is important to assess if the patient is undergoing regular

ophthalmic review and foot care
Past medical/surgical history / History of co-morbidities
1.
2.
3.
4.
5.
6.
7.
Hypertension
Dyslipidaemia
Obesity
Pancreatitis
Obstetric history of macrosomia
Heart disease/ strokes/TIA/PVD
In type 1, ask for other autoimmune conditions or their
symptoms (thyroiditis with hypothyroidism or Graves' disease
with hyperthyroidism, Addisons, primary hypogonadism,
myasthenia gravis, celiac disease, pernicious anemia,
alopecia, vitiligo, and serositis all components of
autoimmune polyglandular syndrome II)
Social history
-
Marital status/children
Very important to assess home situation,

especially in elderly
with regards to
compliance with treatment, dietary regulation,
and emergency assistance in the event of a diabetic emergency
-
Occupation
SMOKING !!!
Alcohol consumption
Diabetes
Hypertension
Ischaemic heart disease or stroke
If type 1, any other autoimmune diseases (see
above)?
Family history
65
Review of systems - as in every systemic disease, should be

done as part of HPC.
Examination
General inspection
glucose load
Dehydration osmotic diuresis caused by
[Dry mouth, loss of skin turgor, sunken

eyes]
Weight loss glycosuria
Obesity NIDDM
Level of consciousness- ask time person and

place
Endocrine facies such as Cushings

syndrome/acromegaly
Pigmentation: Yellow brown skin

discolouration can be associated with haemochromatosis
which can be associated with secondary diabetes
Have a look at the patients surroundings

and make note of medications by the bedside, urinalysis
samples, IV fluids, insulin, antibiotics, diabetic drinks and
diabetic diet sign.
Vital signs
possible metabolic acidosis
Hyperventilation is a sign of
Blood pressure, check both lying

and standing. Look for postural drops of more than 20/10 mmHg
which is a sign of autonomic neuropathy, or severe dehydration,
in an acutely unwell patient
Hands:
o Look for signs of carpal tunnel syndrome (median nerve
entrapment)
o Thenar wasting
o Tinels sign
o Phelans sign
o Look for ulnar nerve entrapment signs
o Hypothenar wasting
Eyes (obligatory in annual review)
66

Check visual acuity which
could be impaired in a diabetic due to retinopathy, temporarily
disturbed because of changes in the shape of the lens associated
with hyperglycaemia or permanently, due to cataracts
Check 3rd, 4th and 6th

cranial nerves. Diabetic third nerve palsy from ischaemia, usually
spares the pupil
Fundoscopy:
Use the ophthalmoscope

first at arms length, to check for
o rubeosis iridis (new blood vessel
formation in the iris which can lead to
glaucoma)
o cataracts (due to sorbitol deposition in

the lens) retina will be red and
cataract black
then come close to the eye, find optic disc

and look in all four retinal quadrants, following four retinal
arteries
Non proliferative changes: Caused directly by ischaemia
Microaneurysms (appear as dot haemorrhages, they

originate in the inner retinal layer.
Blot haemorrhages (Occur more superficially in the
nerve fibre layer)
Soft exudates (cotton wool spots)
Hard exudates (Due to lipid and protein deposition)
Venous beading
67
Proliferative changes:
Changes in the blood vessels in response to retinal ischemia and are
associated with new vessel formation (neovascularisation), scar
formation and eventually retinal detachment.
Mouth
-
Check for ketotic fetor which smells like acetone

(in DKA)
Look for candida infection
Auscultate the carotid arteries for bruits
Neck
Chest
Respiratory
o Signs of infection
Cardiovascular
o Resting tachycardia (>100) sign of autonomic
neuropathy
o Beat-to-beat HRV (not done routinely in clinic, but
described here FYI)
With the patient at rest and supine (not having
had coffee or a hypoglycemic episode the night
before), heart rate is monitored by ECG or
autonomic instrument while the patient breathes
in and out at six breaths per minute, paced by a
metronome or similar device. A difference in heart
rate of >15 bpm is normal, <10 bpm is abnormal.
68
Abdomen
Hepatomegaly fatty infiltration or haemochromatosis
If taking insulin, look for fat atrophy/ lipohypertrophy
areas and advise avoiding them
Legs
Diabetic foot exam:
Inspection
Assessment of foot pulses
Testing for loss of protective sensation
Inspection:
Hairless
Atrophy [ischaemia]
Calluses describe where, how thick; if present, podiatry
referral needed
Ulcers at pressure points (mixed vascular / neuro)
Fungal infection (skin or nails or both)
Cellulitis
Make note of the following about ulcer, if present. It is good
practice to include a drawing.
o Site
o
o
o
o
Always check between toes for even the slightest

skin defect which can rapidly ulcerate in a diabetic
with vascular compromise and poor wound
healing.
Size
Base (? granulation)
Edges (sloping, punched out, overhanging)
Surrounding skin (cellulitis)
Thighs and shins:
69
Necrobiosis lipoidica diabeticorum - red / brown /

yellow, raised and often ulcerated patches usually
on shins [rare]
Muscle:
Check for wasting of quadriceps muscle due to
femoral nerve mononeuropathy ( Diabetic
amyotrophy)
Vessels:
Know how to palpate peripheral pulses a. dorsalis pedis and
a. tibialis posterior
Temperature of the feet
Capillary refill
ABI + toe pressures
o If symptomatic or pulses not palpable
o As screening - in patients over 50 years of age
considered in patients <50 with PAD risk factors
(e.g., smoking, hypertension, hyperlipidemia, or
duration of diabetes >10 years) (ADA consensus
2003)
Neurology:
All patients with diabetes should be screened annually for DPN
by checking any of the five tests (use of a 10-g monofilament,
vibration testing using a 128-Hz tuning fork, tests of pinprick
sensation, ankle reflex assessment, and testing vibration
perception threshold with a biothesiometer), but usually:
10-g monofilament plus testing any one of:
70
o
o
o
o
vibration using 128-Hz tuning fork

pinprick sensation
ankle reflexes
vibration perception threshold
(Diabetic Neuropathy, American Diabetes Association Statement,

Diabetes Care 2005.)
Charcot joint is a medical emergency! : A severely distorted

and deformed joint caused by recurrent unnoticed injury as a
result of loss of proprioception and pain sensation
Urinalysis
Examination is not complete without urinalysis for
1. microalbuminuria (albumin/creatinine ratio) for assessment
of ?nephropathy
2. protein, glucose and ketones
a. if present, urine culture and sensitivity
Exercise within 24 h, infection, fever, CHF, marked hyperglycemia,
and marked hypertension may elevate urinary albumin excretion
over baseline values.
Examination of Thyroid
The aim of this tutorial is to complete examination of the thyroid gland.
All students should get an opportunity to complete the exam and students should
practice on each other during the class.
The normal thyroid consists of 2 lateral lobes joined together by a central

isthmus.
The normal thyroid may be just visible in a thin young person below the
cricoid cartilage
The thyroid gland is ensheathed by the pretracheal fascia and moves on
swallowing
Look at the front and sides of the neck and decide if there is localised or
general swelling of the gland.
The lateral lobes of the thyroid should have a volume no greater than the
patients terminal phalanges of the thumbs.
GOITRE: enlarged gland

71
Often noticed as a cosmetic defect by patient, relatives and friends

Most are painless but pain/discomfort can arise in acute varieties [thyroiditis
subacute or rarely suppurative]
Goitres can produce dysphagia and difficulty in breathing, implying
oesophageal or tracheal compression
Inspection
The presence of a goitre is best observed with the neck slightly extended and
identified by its movement when the patient swallows
Look for scars, a thyroidectomy scar forms a ring around the base of the neck
in the position of a high necklace
Ask the patient to swallow sips of water and watch the neck swelling carefully.
Take a sip of water and hold it in your mouth
Look at the neck
Now swallow
A goitre or a thyroglossal cyst [cyst formed in remnant of thyroglossal duct]
will rise during swallowing
Swallowing allows the shape of the gland to be seen
Check whether the base of the gland can be seen as it rises [implying the
absence
of retrosternal
extension]
Gland is usually symmetrical
Rarely redness of the skin over the gland occurs in cases of suppurative
thyroiditis
Look for prominent veins. Dilated veins over the upper part of the chest wall,
often accompanied by filling of the external jugular vein. This suggests
retrosternal extension of the goitre [thoracic inlet obstruction]
Palpation
Ask the patients permission to feel the neck and then approach patient from
behind
Slightly flex the head to relax the sternomastoids
With the right middle and index finger feel for the cricoid cartilage
Below this palpate the isthmus of the thyroid gland which lies over the trachea
Then palpate the 2 lobes of the thyroid gland which extend laterally behind the
sternomastoid muscle using the pulps of the fingers over the gland
72
Palpation: Posterior Approach

Determine:
Size feel for the lower border as its absence

suggests retrosternal extension
Tenderness [thyroiditis subacute or rarely

suppurative]
Whether it is soft [normal] / firm [simple

goitre] / hard [carcinoma]
Whether it is smooth, nodular or diffusely enlarged
If a single nodule is present describe its location, size, consistency, tenderness

and
mobility. Determine if other nodules are present
[multinodular goitre]
Whether it moves on swallowing [carcinoma may tether the gland]
Ask the patient to swallow again while you palpate the thyroid; ensure the neck is
slightly flexed to ease palpation
If goitre/nodules palpated anterior approach can also be used
Lymph nodes
Palpate laterally for lymph nodes, if you find lymph node enlargement in the neck
check
Supraclavicular nodes
Submandibular nodes
Postauricular nodes
Suboccipital nodes
Enlarged lymph nodes near goitre will suggest the possibility of carcinoma of the
gland
particularly if they are firm or hard
73
Describe lymph node findings

{Complete examination of lymphatic system to be completed later in semester 2}
Percussion
The upper part of the manubrium can be percussed

A change from resonant to dull indicates possibility of a retrosternal goitre,
but this is not a very reliable sign
Auscultation
Auscultate over the thyroid for evidence of

increased vascularity which may occur in
hyperthyroidism
Listen over each lobe for a bruit
Differential diagnosis includes carotid bruit
Pembertons sign
Ask the patient to raise both arms over their head
Wait and then look for;
Facial congestion [plethora]

Facial cyanosis
Respiratory distress
Inspiratory stridor
Dilated veins over the upper chest and filling of the external jugular vein
Ask the patient to take a deep breath through the mouth and listen for stridor
These signs suggest restrosternal extension and thoracic inlet obstruction [also can
be caused by any retrosternal mass]
If there is any evidence of thyroid disease begin to examine for thyroid status
Thyrotoxicosis/Hypothyroidism
This is covered in clinical skills
The symptoms and signs of endocrine disease

Hyperthyroidism
The commonest cause
74
in young people Graves disease, an autoimmune disorder where circulating

immunoglobulins stimulate TSH receptors on the surface of thyroid follicular
cells
in older people multinodular goitre
History
Weight and appetite: weight loss despite normal or increased appetite

Bowel habit: Diarrhoea
Increased sweating, nervousness, irritability and anxiety
Tremors
Heat intolerance [preference for cooler surrounds]
Palpitations (Atrial fibrillation)
Change in facial appearance: Exophthalmos, Lid retraction with thyroid stare
Amenorrhoea
Muscle weakness
Lump in neck: Toxic multinodular goitre with or without a dominant nodule,
Graves disease (diffuse enlargement), toxic adenoma or carcinoma
Examination
General Inspection
Check for agitation, anxiety, irritability
Weight loss
Vital signs
Heart rate: Thyrotoxicosis is a cause of sinus tachycardia and atrial fibrillation

(an irregularly irregular heart rhythm)
Blood pressure: Hypertension is common in thyrotoxicosis
75
Hands
-
Check for a fine resting tremor [due to sympathetic overactivity]. It is often

useful to ask the patients to stick their hands out palms down and place a sheet
of paper on the back of the hands. This will make even the slightest tremor
very obvious.
- Thyroid Acropachy (clubbing): Specific to Graves disease

[This looks like clubbing and is clubbing, rarely seen in Graves disease but not
with other causes of thyrotoxicosis]
Onycholysis [Plummers nails] separation of the distal nail from the nail bed
Palmar erythema - [Also in RA, liver disease, pregnancy]

Feel the palms for warmth and sweatiness sympathetic overactivity
Arms
- Proximal Myopathy (Proximal muscle weakness)
[Ask the patient to raise arms over head]
- Reflexes may be brisk.
Face
Eyes and periorbital region
76
Examine the eyes for exophthalmos protrusion of the eyeball out of the
orbit
It occurs only in Graves diesease
Due to inflammatory infiltrate of the orbital contents not the globe
If not obvious look at the sclerae which in exophthalmus are not covered by
the lower eye lid
Next look from behind over the patients forehead. If exophthalmus is present,
the eye will be visible anterior to the superior orbital margin
Examine for complications of proptosis, conjunctivitis, chemosis [oedema of
the conjunctivae], corneal ulceration [due to inability to close eye lids], and
opthalmoplegia [paralysis of eye muscles] as well as pain on eye movement
Thyroid opthalmopathy
Related to sympathetic overactivity and not specific to graves disease
Thyroid stare - frightened expression

Lid retraction sclera visible above the iris
Lid lag ask patient to follow your finger as it descends from the upper to the
lower part of the visual field, descent of the upper lid lags behind descent of
the eyeball
** Note: Must look for exophthalmos/proptosis from above
77
Neck
Examination of the Thyroid gland
Chest
-
Auscultate the heart for systolic flow murmur
Legs
- Pretibial myxoedema bilateral firm elevated dermal nodules and plaques
caused by mucopolysaccharide accumulation
78
Occurs only in Graves disease
Proximal myopathy (Ask patient to squat)
Reflexes which may be brisk
Hypothyroidism
Primary disease of the thyroid or secondary due to pituitary/hypothalamic failure
Myxoedema implies a more severe form of hypothyroidism;
mucopolysaccsaccharides accumulate in the ground substance of tissues including the
skin.
History
-
Lethargy, physical and mental slowing

Weight gain
Bowel habit: Constipation
Cold intolerance - preference for warmer weather
Skin and hair changes: Dry pale skin with thinning hair
Decreased pigmentation: Hashimoto thyroiditis [autoimmune mediated]
Lump in neck: Goitre (thyroiditis, non functioning adenoma)
Change in facial appearance: Puffy face swelling of eyelids [oedema]
Hoarseness of voice
Menorrhagia/amenorrhoea
Symptoms and signs of heart failure in severe cases due either to bradycardia
or pericardial effusion: Shortness of breath, ankle swelling
Symptoms of anaemia: chest pain, shortness of breath
79
Examination
Inspection
-
Mental and physical sluggishness

General CNS slowing is common with stupor or coma in severe cases
Weight gain
Hoarse voice
The hands/ arms

Cyanosis due to reduced cardiac output
Palmar crease pallor anaemia due to:
Chronic disease
Folate deficiency bacterial overgrowth
in bowel
Vitamin B12 deficiency due to
pernicious
anaemia [associated
autoimmune
disorder]
Iron deficiency menorrhagia
Pulse small volume and slow bradycardia (slow heart rate below 60 beats per
minute)
Tinels sign tap over flexor retinaculum, carpal tunnel thickened in myxoedema, this
may cause paraesthesia in the distribution of the median nerve
Blood pressure: Hypotension
Proximal Myopathy
Reflexes hung up or slow to relax
Face
80
Skin may be thickened

Alopecia hair loss
Vitiligo - associated autoimmune disorder
Skin but not sclera may appear yellow due to hypercarotenaemia [due to slowing of
hepatic carotene
metabolism]
Periorbital oedema
Loss/thinning of outer third of eyebrows
Xanthelasma due to associated hypercholesterolaemia
Ask the patient to speak and listen for coarse, croking, slow speech
Neck
Observe patient for any surgical scars in the neck (often concealed by wrinkles)
81
Examination of the Thyroid gland: Goitre
Check for an elevated JVP: Right heart failure can be associated with
hypothyroidism specifically in relation to pericardial effusion.
Chest
-
Check for pleural or pericardial effusion.
Legs
Ask the patient to kneel on a chair with the ankles exposed. Tap the Achilles tendon
with a reflex hammer. There is normal contraction followed by delayed relaxation of
the foot
Reflexes are hung up or slow to relax
-
Peripheral oedema: Sign of right heart failure
Acromegaly
Acromegaly is caused by excessive secretion of growth hormone from the pituitary
gland most often due to an adenoma.
Gigantism is the result of growth hormone hypersecretion occuring before puberty
and fusion of the epiphyses. It results in massive skeletal and soft tissue growth.
Acromegaly occurs when the growth plates have fused, so that only soft tissue and
flat bone enlargement is possible.
History
Symptoms due to local mass effects of the tumor
82
Symptoms depend on the size of the intracranial tumor.

Headaches and visual field defects are the most common symptoms.
Visual field defects depend on which part of the optic nerve pathway is compressed.
The most common manifestation is a bitemporal hemianopia due to pressure on the
optic chiasm. This often presents with a patient bumping into things accidentally due
to loss of temporal peripheral vision.
The pituitary mass may cause headaches by direct invasion of adjacent
structures. Headache may also be caused by interruption of the flow of cerebrospinal
fluid. Pituitary tumours may also promote vascular headaches such as migraines.
Headache may also be caused by hypertension, which is a very common finding in
patients with acromegaly.
Loss of end organ hormones is due to diminished anterior pituitary
secretion of corticotropin (ie, adrenocorticotropic hormone [ACTH]), gonadotropins
(luteinizing hormone [LH], follicle-stimulating hormone [FSH]), and thyrotropin
(thyroid-stimulating hormone [TSH]). Hyperprolactinaemia may also occur and in
this setting oligomenorrhoea / amenorrhoea and galactorrhoea may occur in females
while impotence may occur in males
Symptoms due to excess of GH
-
Soft tissue swelling and enlargement of extremities

Increase in ring and/or shoe size.
Symptoms of carpal tunnel syndrome including pain and parasthesia in the
hands.
Hyperhydrosis (Increased sweating)
Coarsening of facial features with frontal bossing and prognathism (protrusion
and squaring of the jaw). Patients often notice this themselves or have it
commented to them by someone else. Old photographs are very useful in
highlighting these changes.
Macroglossia (enlargement of the tongue)
Arthritis (particularly osteoarthritis of the knees)
Symptoms of heart failure including exertional dyspnoea, and peripheral
oedema. This occurs due to uncontrolled hypertension which is very common
in patients with acromegaly and due to cardiomyopathy attributable to excess
growth hormone.
Examination
General Inspection
-
Blood pressure: Hypertension is a very important sign in acromegaly
The facial and body habitus features of acromegaly mentioned below may be
quite obvious on initial inspection from the end of the bed
Hands
83
Large / wide / spade like / Doughy hands. This is due to soft tissue and bony
enlargement. Check if any finger rings have been moved to a smaller finger or
cut to a new fit.
-
The hands are often notably warm and sweaty. This is due to increased
metabolic rate.
Wrist
Test for carpal tunnel syndrome using Tinels sign. The symptoms of pain and
parasthesia are reproducible by tapping on the flexor retinaculum.
Arms
Proximal Myopathy (weakness of the proximal upper limb muscles)
Check the BP for hypertension
Axilla
Skin overgrowth skin tags (molluscum fibrosum)

Greasy axillary skin
Acanthosis nigricans: Velvety discoloration
Face
84
Frontal bossing, large supraorbital ridge, squaring of jaw (progmathia)
Mouth: Large tongue/Splayed and separated teeth

Eyes: Examine visual fields: Bitemporal hemianopia may be noted if the pituitary
tumour is large.
Fundoscopy:
Hypertensive or diabetic changes: Hypertension and diabetes
are
common in patients with acromegaly.
Papilloedema: Due to increased intracranial pressure with large
tumour
Optic atrophy: Due to nerve compression
Chest
Signs of heart failure, cardiomegaly
Abdomen
Hepatic, splenic, renal enlargement

Testicular atrophy: Gonadotrophin deficiency which can be associated with an
enlarging pituitary tumour
Legs

Foot drop due to peroneal nerve entrapment
Signs of osteoarthritis especially of the knees and hips
Back
Kyphosis
Test the urine for glucose as GH is diabetogenic [glycosuria]
Cushings syndrome
Due to chronic excess of glucocorticoids

Cushings disease is specifically pituitary ACTH overproduction
Cushings syndrome is due to excessive steroid hormone production
from any cause
It is very important to enquire about a history of steroid therapy
Features
Change in body form, particularly central obesity, weight gain in the face that
is referred to as moon like facies (never mention moon face in front of a
patient!) Limbs appear thin
85
Skin changes with easy bruising [due to loss of perivascular supporting tissue],
purplish stretch marks, called stria, and red cheeks (plethora). Acne is also
common.
Look for excessive pigmentation on the extensor surfaces [because of MSHlike activity in the ACTH molecule]
Buffalo hump due to fat deposition over interscapular area (but never call it
that in front of a patient!!!)
Bony tenderness due to crush fractures of the vertebral bodies from

osteoporosis [steroid effect on bone]
Excess hair growth on face, neck, chest, abdomen and thighs
Overall weakness and fatigue

86
Loss of muscle bulk ask the patient to squat to test for proximal myopathy
[due to mobilisation of muscle tissue or excessive urinary potassium loss]
Menstrual disorders/decreased fertility and/or libido
Hypertension including headache, chest pain, symptoms of heart failure
Symptoms of diabetes which is common in patients with Cushings syndrome
Depression with wide mood swings as well as steroid induced psychotic

features.
Examination
General Inspection
The patient should be undressed to underpants.

Look for bruising
Look for poor wound healing
Look for increased pigmentation: Primary adrenal insufficiency or Cushings
disease where the excess ACTH has MSH-like activity.
Face
-
Moonlike facies: Due to disproportionate fat deposition in the upper part of the
face
Plethora
Acne and hirsutism can be observed if androgen production from the adrenal
glands is also increased.
Eyes:
tumour
-
Examine visual fields: Bitemporal hemianopia with large pituitary

in Cushings disease.
Fundoscopy:
Hypertensive and diabetic changes may be present.
87
Optic atrophy and papilloedema where there is an increase in

intracranial pressure in cases of Cushings disease
due to a
pituitory tumour.
Axilla and Chest

-
Acanthosis nigricans
Note supraclavicular fat pads
Buffalo hump - Fat deposition
Abdomen
-
Purple striae: These are caused by weakening of collagen fibres in the dermis
leading to exposure of vascular subcutaneous tissue
Central obesity: Due to marked disproportionate fat deposition
Palpate for an adrenal mass, which may rarely be detected in cases of adrenal
carcinoma.
Legs
-
Proximal myopathy
Bruising, poor wound healing.
Peripheral oedema [salt and water retention]
Urinalysis
Test the urine for sugar [as steroids are diabetogenic]
Hypertension
Hypertension is common due to salt and water retention
Primary Hyperparathyroidism
Due to excess parathyroid hormone which results in increased serum calcium, loss
of phosphate in the urine and increased formation of 1, 25dihydroxycholecalciferol.
Hyperparathyroidism causes problems with stones, bones, moans and abdominal
groans
Symptoms of hypercalcaemia (hyperparathyroidism)
Kidney stones
Osteopenia, leading to an increased risk of fractures
Abdominal pain (Due to peptic ulcer disease, stone disease, pancreatitis and
constipation)
Increased thirst and urination due to increased excretion of calcium in urine
(hypercalciuria)
88
Nausea, vomiting or loss of appetite

Confusion or poor memory
Severe hypercalcaemia may cause coma or convulsions
Muscle weakness or fatigue
Examination
General Inspection
Mental status: Hypercalcaemia-reduced level of consciousness if severe
Hydration status: Dehydration due to hypercalciuria
Face
Band keratopathy (Calcium corneal deposition usually at the 3 or 9 oclock
positions relative to the iris):
Body and limbs
Palpate shoulders, sternum, ribs, spine and hips for bony tenderness, deformity
or evidence of fractures
Test for proximal muscle myopathy
Test blood pressure as hypertension may occur
Test for blood in the urine - haematuria [renal stones]
Hypoparathyroidism
Symptoms of hypocalcaemia (hypoparathyroidism)
This results in hypocalacemia with neuromuscular consequences [tetany].
It is usually a postoperative complication following throidectomy.
Trousseaus sign with a blood pressure cuff on the arm, raise the pressure
above the systolic pressure. Contraction of the hand occurs within 2 minutes
when hypocalcaemia has caused neuromuscular irritability
Positive trousseaus sign
89
Chevsteks sign - tap gently over the facial nerve [seventh cranial nerve]
below
the ear. The nerve is hyperexcitable in hypocalcaemia and a brisk
muscular twitch occurs on the same side of the face.
Hyper-reflexia due to neuromuscular irritability

Nails fragile and monilial infection
Dry skin
Deformity of the teeth
Tingling (paresthesias) in the fingers, toes and lips
Muscle aches or cramps affecting the legs, feet, abdomen or face
Fatigue or weakness
Anxiety or nervousness
Always enquire about a history of thyroid surgery
Blood pressure: Hypertension is a very important sign

Observe for general features of hypothyroidism (post thyroidectomy)
90
91
92
93
94
95
96
General inspection
1. Non physiological asymmetry
2. Skin changes
- Dimpling
97
o Tumor pulling on skin directly

o Or close to coopers ligament
- Gross edema- peu dorange
3. Nipple changes
- Abscesses in or around nipple
- Eczema rash around the nipple- pagets disease
- Discharge
Palpation
- Most tumors in the upper outer quadrant- feel axillary tail of Spence
The patient history- book
Renal History
Infection
Acute renal failure
Chronic renal failure
Dialysis
Post transplant
Not all of the questions outlined below will be relevant in all cases but use your
judgement as to which are appropriate.
Renal stones, GU tumours and prostate will be covered by surgeons.
General symptoms
Change in urinary appearance
Red discolouration:
Haematuria
Haemoglobinuria (due to haemolysis)
Drugs such as Rifampicin
Note: With suspected haematuria ask about whether the patient means frank distinct
blood in the urine or a general tea coloured urine, whether it is painful or painless
(more sinister). Is the blood totally mixed in? (from bladder or above). Also ask if the
patient has noticed if the haematuria occurs early or late in the urinary stream or if it
is uniform throughout. The later in the stream the higher up the urinary tract the
pathology is likely to be. Are there blood clots? (cannot be from the kidney)
Causes of haematuria
Colour
(Bloody, coca cola, frothy, cloudy). Cloudly in infection (may also be foul smelling).
Concentrated in dehydration and some type of renal failure. Very light colour and
large volume in recovery phase of acute tubular necrosis or in other states of impaired
renal concentrating capacity.
Changes in urinary volume
98
Polyuria (over 3 L of urine per day): Can be a feature of acute renal

failure due to acute tubular necrosis, diabetes mellitus, diabetes
insipidus, psychogenic polydipsia
- Oliguria (less than 400 ml of urine per day): Due to renal failure or
dehydration.
- Anuria (less than 50 ml of urine in 24 hours)
You must rule out urinary retention by asking about suprapubic pain/discomfort
feeling of needing to pass urine. In some patients urinary retention is asymptomatic
apart from anuria particularly in neurological conditions and is retention is chronic. In
these patients a palpable bladder will be present and if still concerned, do a bedside
bladder scan.
Frequency
o (Identify the patients norms)
o
o
o
How often passing urine and how much on each occasion.

How much is the patient drinking? (alcohol or otherwise)
Caffeine can also cause bladder irritation and lead to frequency.
Nocturia
Does the patient wake frequently at night to pass urine? Clarify how many
times per night and volume of urine passed each time
Urinary obstruction
Common symptom in elderly men [prostatism]
Hesitancy - difficulty starting micturition
Poor stream - cannot hit wall
Post micturition dribbling
Double voiding/ Incomplete emptying (needing to pass urine soon after
micturition)
Nocturia - an objective increase in the frequency of waking up at night to void
urine
Frequency urine passed more often without increase in volume
Complete obstruction/Overflow incontinence
Retention inability to pass urine with suprapubic discomfort and pain.
Pain
SOCRATES
Dull/continuous renal angle pain due to tumour or large polycystic kidneys

Renal colic is severe pain radiating down to groin [renal calculus/clot]
Kidney - Loin or lower back - Renal angle pain due to pyelonephritis is
associated with fever/rigors/dysuria [pain passing urine]
Ureter - Upper abdo, groin or genitals Renal stone colic classically radiates loin to
groin.
Bladder - Central & suprapubic
Timing of the day, (worse day, afternoon, night?)
Dysuria (Painful micturition) Causes inflammation cystitis, stones, trauma, bladder
Ca
99
Prostatitis [inflammation of prostate e.g. bacterial infection]

Remember full pain questionnaire - onset, site, radiation, severity, character, time
course, aggravating and relieving factors, associated symptoms
Incontinence
Stress incontinence - when sneezing, laughing [multiparous female]
Urgency - strong desire to pass urine may be followed by incontinence
[Gynaecological prolapse or bladder instability]
Overflow incontinence
Spinal cord lesion, bladder will fill and then empty reflexly
Pneumaturia
Passing bubbles in the urine [vesico-colic fistula e.g. crohns disease]
Oedema
Ankle oedema, ascites, puffy face and eyes (nephrotic syndrome results in large
amounts of protein loss in the urine and loss of fluid into the tissues).
Dyspnoea, orthopnoea and paroxysmal nocturnal dyspnoea from fluid overload due to
failure of the kidneys to excrete enough fluids.
Symptoms of urinary tract infection
Fever, general malaise, poor appetite, nausea and vomiting.

Dysuria (pain/stinging passing urine suggestive of a bladder or urethral infection)
Foul smelling cloudy urine,
Haematuria may be present,
Loin pain and rigors suggestive of pyelonephritis (infection of the kidney itself).
Previous or recurrent infections including in childhood.
If so any previous imaging and any anatomical abnormalities found.
In men any prostatic symptoms or any symptoms of bladder outlet obstruction as
stagnation of urine in the bladder leads to increased risk of infection.
Sexual history.
Any urethral discharge?
100
Hygiene - Pass urine after intercourse reduces UTIs in women. Wiping from front to
back after using the toilet? Double voiding to ensure bladder fully empty?
Volume of water drinking
Symptoms of infection
Acute renal failure/Acute kidney injury:

Sudden and often reversible loss of renal function developing over days to weeks
How it presents?
Asymptomatic or minimally symptomatic discovered on routine blood test. (eg

noted post op)
Urine
o
Anuria - failure to pass more than 50mls of urine daily
o
o
o
Oliguria - < 400mls urine daily

Less frequent urination with dark coloured urine
Polyuria, nocturia and frequency inability of kidneys to concentrate urine
normally (urine usually pale)or nocturia and frequency may be due to bladder
outflow obstruction such as in prostatism.
Colour
Haematuria
Foamy or bubbly urine if high protein concentration.
Fatigue, Generally unwell
Fluid overload or hypoalbuminaemia

o Oedema, dyspnoea, PND, Orthopnoea
o Facial, periorbital and limb oedema classically in nephrotic syndrome with
resultant hypoalbuminaemia
Symptoms of uraemia
o Fatigue, Lethargy
o Weight loss
o Hiccuping
o Nausea and vomiting tends to be worse in the morning
o Pruritis
o Easy bruising and bleeding due to uraemia interfering with haemostatic
mechanisms.
o Chest pain and fever from uraemic pericarditis
o
o
o
o
Headache.
Weakness.
Restless legs
Poor concentration
101
o
o
o
o
Poor sleep,
Drowsiness,
Seizures
Coma.
Hyperkalaemia
o asymptomatic
o vague symptoms including:
o nausea,
o fatigue,
o muscle weakness,
o tingling sensations.
More serious symptoms of hyperkalemia include slow heartbeat and weak pulse (may
manifest with palpitations or sensation of skipped beats). Severe hyperkalemia can result in
fatal cardiac arrest. Generally, a slowly rising potassium level (such as with chronic kidney
failure) is better tolerated than an abrupt rise in potassium levels.
Ask about symptoms of potential causes of acute renal failure

The first thing to rule out is a post renal cause such as urinary retention as this is an
easily reversible cause. Then rule out prerenal causes and then consider intrinsic renal
causes.
Pre renal
Impaired renal blood flow due to
Fluid loss
o Blood (Haemorrhage)
o Plasma (Burns)
o Water and electrolytes (diarrhoea, vomiting and dehydration)
Hypotension
o MI
o Heart failure
o Septicaemic shock
o Drugs
Increased renal vascular resistance

o liver failure (hepatorenal syndrome)
Renovascular disease
o renal artery occlusion embolism, dissection, atheroma
o ACE inhibitors precipitating renal artery stenosis
Intrinsic Renal Failure
Acute tubular necrosis

o Hypovolaemia leading to ischaemia
o Toxins and drugs
102
o
o
Aminoglycosides
Contrast media
Heavy metals and many more
Rhabdomyolysis
Haemoglobinuria
Glomerular disease
Interstitial disease- drugs (sulphonamides,ciclosporin A), poisoning, component of
systemic multisystem disease
Vasculitis or scleroderma
Myeloma
Post renal
Always consider urinary retention as a cause of renal failure and rule it out
immediate.
Urethra
o Calculus
o Blood clot
o Phimosis or paraphimosis
Bladder neck
o Calculus
o Blood clot
o Prostatic hypertrophy or cancer
o Obstruction by stones, prostate or tumour
Urethers
o Intrauretheric
Clot
Pyogenic
Debris
Calculi
Extraureteric
Retroperitoneal fibrosis
Pelvic tumour or surgery
Uterine prolapsed
A thorough medication history is extremely important including any medications

taken over the past few weeks that may have precipitated renal failure. It is also
important as any nephrotoxic drugs that are currently being taken should be stopped
and drugs which are excreted by the kidneys may need to be dose adjusted or changed
to other medications.
Irreversible deterioration in renal function which develops over a period of months to
years. Initially manifests as only as a biochemical abnormality.
Most often asymptomatic at diagnosis and progresses insidiously.
103
When diagnosed? How and by who?

Cause if know
o
Diabetes
Hypertension
Glomerular disease
Interstitial disease
Renal artery stenosis
Chronic urinary retention
Nephrolithiasis
Systemic Inflammatory Diseases
Polycystic kidney disease
Amyloid and myeloma
Vasculitis
Medications very important to take a thorough history as outlined above.
And many others
Ask about symptoms of possible causes.

Ask about urine symptoms, overload, uraemic symptoms and hyperkalaemia as in
acute renal failure above.
In addition ask about
Bone disease (Secondary hyperparathyroidism), Bone pain due to renal bone disease
caused by secondary hyperparathyroidism which is compensating for vitamin D
deficiency caused by the renal failure. Fractures? Osteomalaecia (vitamin d
deficiency) or osteoporosis (also important as depending on condition patients may be
on steroids. On alfacalcidol, calcium supplements, phosphate binders? Low
phosphate diet?
Symptoms of anaemia (Due to declining erythropoietin levels) Healthy kidneys
produce the hormone erythropoietin which stimulates the bone marrow to make
oxygen-carrying red blood cells. As the kidneys fail, they produce less erythropoietin,
resulting in decreased production of red blood cells to replace the natural breakdown
of old red blood cells resulting in anaemia. On EPO? On iron?
Hypertension Symptoms, Do they check it regularly. How good is control?
Hypertension can be both a cause a result of renal failure.
Any known parathyroid problems?
Hypercalcaemia (Tertiary hyperparathyroidism)
o Bones, stones, groans, psychic moans
104
Abdomen pain
Vomiting
Constipation
Anorexia
Weight loss
Tiredness
Weakness
Hypertension
o
o
o
o
o
o
Depression
Confusion
Pyrexia
Renal stones
Renal failure
Polyuria
Polydipsia
o
o
o
o
o
Cardiovascular disease and stroke

o
Much higher incidence in renal disease
Patients with chronic renal failure have tendency to hypercholestrolaemia

particularly hypertriglycerideaemia in nephrotic syndrome
Caution with statins as many are renally excreted
Polycystic kidney disease, which causes large, fluid-filled cysts on the kidneys
and sometimes the liver, can cause pain in the back or side
Abnormally dark skin
Gout
Myopathy
Peripheral neuropathy
Low level of sexual interest and impotence
Menstrual periods stop (amenorrhea)
Sleep problems, such as insomnia, restless leg syndrome, and obstructive sleep
apnoea
Clotting problems due to platelet dysfunction due to uraemia. In dialysis platelet

dysfunction can be due to the process of dialysis itself also. Also anticoagulation with
heparin is used during dialysis which transiently increases bleeding risk.
Dehyration, sodium loss and hypotension due to loss of renal concentrating ability in
some cases (usually recovery phase of acute tubular necrosis but can also occur in
others)
Metabolic acidosis due to failure of renal excretion of acids
Kausmall breathing
Confusion
In nephrotic syndrome
105
Increased risk of thromboembolism
Increase in clotting factors and platelet abnormalities
Hyperlipidaemia
Particularly hypertriglyceridaemia
Thought to be due to hepatic lipoprotein synthesis in response to low

oncotic pressure
Increased susceptibility to infection
Loss of immunoglobulins in urine
Diet - Renal failure patients must be questioned about diet - Protein, fluid and salt
restriction, low phosphate diet and use of phosphate binders. Diet tailored to
individual patient needs.
Ask about Renal replacement therapy (see below)
Are they on the transplant list?
If on dialysis
When started on dialysis?
What was cause of renal failure?
Summary of symptoms on presentation and how the renal failure progressed as

above.
Still producing urine or not and how much?
Method of dialysis currently

o
Haemodialysis fistula (needle or button) or line
Peritoneal dialysis
Previous methods of dialysis and why changed? Previous fistulas or catheters.
For haemodialysis
o
How many times per week dialysed and for how many hours each session?
What is your dry weight? (ie The weight that is aimed for post dialysis)
How much weight do you gain between dialysis sessions and how much fluid
is taken off on dialysis?
Are you on fluid restriction?
Every considered for home haemodialysis?
106
Intraperitoneal dialysis
o
CAPD or APD?
How many exchanges per day in CAPD?
HIV, CMV Hepatitis status checked prior to dialysis patient may or may not know
this.
Have they had their hep B vaccine and annual flu vaccine?
Previous methods of dialysis and why changed? Previous fistulas or catheters.
Diet restrictions
Phosphate binders, calcium and alfacalcidol?
EPO?
IV iron?
Ask about complications of haemodialysis
Line infections or blockage or line falling out.
Fistula
o
thrombosis, aneurysms, stenosis, infections, ischaemia, steal syndromes
Hypotension due to excess fluid removal or in some patients it becomes chronic due
to failure of BP control mechanisms. Ask about dizziness on standing or during
dialysis.
Disequilibrium syndrome
o
Nausea, vomiting, headache, altered consciousness and rarely seizures or

coma due to rapid changes in in placma osmolality and cerebral oedema on
initial dialysis
Pulmonary oedema due to fluid overload Dyspnoea, Orthopnoea, PND.
Cardiac arrhythmia due to potassium shifts palpitations or collapse. Paplitations

may also be due to haemodynamic shifts.
Haemorrhage due to anticoagulation
Dialyser hypersensitivity (allergy to dialysis membrane)
Air embolism
Systemic sepsis
Cardiovascular
107
IHD
Stroke
Cardiac failure ar all more common in dialysis patients
Hypertension persists in 25-30% on dialysis
Anaemia
o
Combination of underlying condition and dialysis
Treated with EPO and iron if also iron deficient. Iron given IV at time of
dialysis.
Transfusions avoided if possible if on transplant list as antibodies would be

produced reducing the possibility of successful transplant.
Renal bone disease as above
B2 microglobulin amyloidosis
Carpal tunnel syndrome
Arthralgia
Fractures
Acquired renal cysts which may lead to bleeding and haematuria
Ask about complications of peritoneal dialysis
Peritonitis fever, rigors, unwell, abdomen discomfort or pain.
Problems with tenchkoff catheter placement. Can become blocked if moves high in
the peritoneal cavity. More likely if patient becomes constipated so ask about bowel
habit.
Tenchkoff exit site infections
Hernias
Back pain
Feeling of bloating
How it affects life? Job? Study? Finance?

On transplant list?
Any previous transplants?
Post transplant patient
What was primary diagnosis?
Were you on dialysis prior to transplant and for how long? Ask about complications
of chronic renal failure eg bone disease.
108
When was transplant?

Cadaveric, living related donor, living unrelated donor?
After the operation
Did you produce urine immediately or was production delayed?
What volume of urine was produced?
What was your Creatinine post op and what is it now? Most patients will know this.
Did your creatinine normalise quickly?
What immunosuppressant, anti-fungals and antibiotics were you on initially and what
regime are you on now?
Any post op complications such as infections (wound, urine or systemic),

haematomas, urine leaks from the newly anastomosed urether with formation of a
urocele around the new kidney.
Any episodes of rejection post transplant? Any renal biopsies needed?
Did you need any dialysis after the transplant? (suggestive of delayed function)
Was it the first transplant? If not the first transplant ask
When the first transplant was?
Cadaveric or living related donor or unrelated living donor?
How long did the kidney function for?
If known what was the cause of the rejection?
CMV status may or may not know this

Transplant compatibility may or may not know this
Any opportunistic infections? Eg candida. Any UTIs? Any other infections
If it has been some time since the transplant ask about any skin lesions that have
appeared or if there have been any skin lesions removed? High risk of skin
malignancy post transplant due to immunosuppression.
Have they had the flu vaccine?
Medications
Immunosuppressant
Tacrolimus side effects of tremor and renal impairment
Cyclosporin
Steroids
Antifungals
Antibiotics
109
Past medical history

Ask about conditions predisposing to renal failure and pre-existing renal conditions,
Bladder Ca, surgery, dialysis, catheters, UTI as a child, stones, gynae/obs history.
Hypertension. Hypercholestrolaemia, heart disease, stroke
Drug History & Allergies
A very careful drug history is important to screen for potential nephrotoxic
medications that may have causes the renal failure. It is also important to stop
nephrotoxic drugs even if they were not the original culpit as they may worsen the
situation. Drugs which are renal excreted may need to be dose adjusted or changed to
a different medication. Rifampicin discolours the urine turning it orange. Diuretics
can result in pre renal renal failure and polyuria and frequency.
Family History
Family history of prostate Ca or kidney stones, heart disease, diabetes or high blood
pressure, polycystic kidneys or any other renal problems
Social History
Smoking. Alcohol. Travel. Effects of symptoms on ADL, work and finances. Renal
disease can have devastating effect on peoples lives and this is an important
consideration.
Review of systems
A full review of all systems should be carried out
The genitourinary examination

If renal disease is suspected or known to be present then certain signs must be sought.
The purpose of clinical examination is to assess clinical status as well as trying to
elucidate the cause of the renal failure.
Inspection
General inspection remains crucial.
Hyperventilation underlying metabolic acidosis
Hiccupping can be a sign of terminal uraemia
Sallow complexion dirty brown appearance in chronic renal failure [impaired
excretion of urinary pigment]
110
Anaemia of chronic disease/poor nutrition/erythropoietin

deficiency/haemolysis/bone marrow depression (pallor, palmar crease pallor,
conjunctival pallor)
Terminal renal failure
Level of consciousness - drowsy/coma - due to nitrogen/toxin retention
Muscle twitching/tetany/epileptic seizures due to low serum calcium level and to
nitrogen retention
The hands
Leuconychia white transverse opaque lines in hypoalbuminaemia [nephrotic
syndrome]
Terrys lines/ half and half nails distal brown arc occurring in 20% of renal failure
patients
Anaemia palmar crease pallor

Asterixis may be present in terminal chronic renal failure [Dorsiflex the wrists with
the arms outstretched and spread out the fingers, a flapping tremor may occur as in
liver failure]
Hydration
dehydration can cause acute renal failure
over hydration can result from intravenous infusion of fluids to correct renal
failure
fluid overload can result from renal failure [pedal oedema/pulmonary oedema]
Fluid balance and hydration can be assessed from BP, postural BP drop, pulse,
skin turgor, mucous membranes, eyes, daily weight, level of oedema, is the
patient thirsty?
The arms
1) Arteriovenous fistula used for haemodialysis [Make sure this is palpated for
thrill and auscultated for bruit to assess function of the fistula]
111
Brachio-cephalic, radiocephalic?
Bruising nitrogen retention causes abnormal platelet aggregation

Skin pigmentation failure to excrete urinary pigments
Scratch marks pruritis due to uraemia and calcium deposition
Blood pressure hypertension may be the cause of renal disease or a complication
Peripheral neuropathy/ myopathy
The face
Anaemia conjunctival pallor
Jaundice nitrogen retention can cause haemolysis
Uraemic fetor due to breakdown of urea to ammonia in the saliva
Mucosal ulcers underlying connective tissue disease i.e. SLE
Gingival hyperplasia due to immunosuppressant therapy [cyclosporin]
Rash - underlying connective tissue disease i.e. SLE
The neck
Central line for dialysis
Jugular venous pressure to assess hydration [elevated JVP in fluid overload/CCF]
Carotid artery bruits there may be generalised atherosclerosis [renal artery stenosis]
The chest
112
Cardiac
- CCF due to fluid retention in chronic renal failure
- Hypertension sodium and water retention and excess renin production
- Pericarditis due to retained metabolic toxins and can cause a pericardial rub
Lungs
- Pulmonary oedema [volume overload]
- Percuss for effusions
- Infection due to immunosuppression in renal transplant patients
The abdominal examination

As done previously but particular attention must be paid to the following;
Peritoneal dialysis scar- either on right or left next to the umbilicus
Inspection
Nephrectomy scar - look at loin and lumbar regions
Nephrectomy tube - draining wound
Nephrostomy tube - draining urine directly from kidney into a bag
Renal transplant scar right or left iliac fossa

Transplanted kidney bulge under scar in RIF/LIF
Catheter for peritoneal dialysis
Small scars from catheter placement near midline or the lower abdomen
Suprapubic catheter to allow drainage of urine directly from bladder
Distension polycystic kidneys/ascites [nephrotic syndrome]/dialysis fluid
Palpation
The kidneys bimanual method
113
To palpate the right kidney the examiners left hand is placed underneath the back. The
left fingers flex at the metacarpophalangeal joints in the area of the renal angle. The
examiners right hand is placed over the RUQ. The kidneys are felt by balloting, the
renal angle is pressed by the flexing fingers of the posterior hand and the anterior
hand is used to palpate the kidney.
To palpate the left kidney the left hand is stretched over the abdomen and placed
posteriorly over the renal angle. The right hand feels for the left kidney anteriorly.
Deep palpation in the renal angle can elicit tenderness suggesting pyelonephritis.
To distinguish a large left kidney from splenomegaly:
1. Spleen has no palpable upper border
2. Spleen has a notch
3. Spleens moves inferomedially on inspiration, kidney
moves inferiorly
4. Spleen is not ballottable unless gross ascites present
5. Percussion note is dull over the spleen resonant over
kidneys
6. Friction rub may be heard over the spleen but never
over the kidney as it is too posterior
Unilateral renal mass
Renal cell carcinoma
Hydronephrosis
Polycystic kidneys [asymmetrical enlargement]
Acute pyelonephritis
Abscess
Bilateral renal mass
Polycystic kidneys
Bilateral hydronephrosis
Bilateral renal carcinoma
Early diabetic nephropathy
Infiltrative disease i.e. lymphoma/amyloid
Transplanted kidney palpable in LIF or RIF. Note size, tenderness, presence of any
bruits.
Hepatomegaly - from hepatic cysts may be present in PCKD
Bladder empty bladder is impalpable. If there is urinary retention the full bladder
may be palpable above the pubic symphysis. It is typically regular, smooth, firm and
oval shaped. It may reach as high as the umbilicus or even higher in severe urinary
retention. It must be differentiated from any swelling arising from the pelvis. The
bladder can be emptied by insertion of a urinary catheter.
Percussion
Ascites shifting dullness [nephrotic syndrome]
Enlarged bladder percuss down from the epigastrium towards the pubic symphysis.
Dullness will be heard over the bladder
Auscultation
114
Renal bruits best heard just above the umbilicus about 2 cms to the left or right of
the midline. Listen with the diaphragm of the stethoscope. Its presence suggests renal
artery stenosis due to atherosclerosis or fibromuscular dysplasia. The absence of
hypertension makes a diagnosis of renal artery stenosis less likely.
Rectal and pelvic examination
Examination of external genitalia for evidence of STI
Prostatomegaly in males and Frozen pelvis from cervical cancer in females: These
may cause urinary tract obstruction and renal failure
The back
Sacral oedema fluid overload/CCF
Bony tenderness strike the vertebral column gently and may elicit tenderness. This
may be due to renal osteodystrophy or secondary hyperparathyroidism
The legs
Oedema
Pigmentation
Scratch marks
Gouty tophi in feet
The fundi
Diabetic changes
Hypertensive changes
Male genital examination and per rectum examination will be covered by the
surgeons.
Female genital examination will be covered in gynaecology next year.
Renal replacement therapy background information
For patients with end-stage renal disease, renal replacement therapy is achieved by
dialysis (haemodialysis or peritoneal dialysis) or renal transplantation. Although true
replacement of renal function is not provided by dialysis, this modality is lifesustaining since it removes metabolic wastes and excess body water.
The guidelines for instituting renal replacement therapy in renal failure are as
follows:
-
Urea > 30 mmol/l [2.5-8.5 mmol/L]

Creatinine > 600 umol/L [50-120 umol/L]
Hyperkalaemia: K > 6 mmol/L [3.2-5.2 mmol/L]
Metabolic acidosis
PH [7.35 - 7.45]
HCO3 [23.0 31.0 mmol/L]
- Fluid overload and pulmonary oedema
- Uraemic encephalopathy or pericarditis
In acute renal failure haemodialysis is used for renal replacement therapy.
115
In chronic renal failure preparation for renal replacement therapy is begun usually
about a year before predicted start date of dialysis as GFR begins to decline below 30
ml/min [Normal GFR is approximately 100 ml/min].
The options for renal replacement in chronic renal failure are haemodialysis (70%),
and peritoneal dialysis (30%). All patients are considered for renal transplantation
unless there is a contraindication such as an active malignancy, active vasculitis or
severe ischaemic heart disease.
Haemodialysis:Haemodialysis takes place usually over three to four hours, three times a week. To
perform this type of dialysis it is necessary to gain access to the blood stream so that
the blood can be taken and given back. The type of access used will depend upon the
patient and how long the dialysis will be needed.
AV fistulas are typically constructed with an end-to-side vein-to-artery
anastomosis between an artery and vein. The most commonly used fistulas are created
by anastomosing the radial artery and cephalic vein (radiocephalic or wrist fistula).
This requires an operation. Although some fistulas mature within weeks, others
require up to six months before they provide reliable haemodialysis access.
AV fistulas
Double-lumen tunneled cuffed catheters

Alternatively, a special catheter may be used which is placed into one of the large
veins in the neck and hidden under the skin so that only the end is exposed on the
chest. Needles are not required for haemodialysis or blood sampling with this
catheter.
Catheters are most commonly placed in the internal jugular vein and tunneled
superficially to exit on the upper, anterior chest. The catheter should be positioned
under fluoroscopy such that the tip rests in the right atrium.
116
Tunneled cuffed venous catheters are primarily used as intermediate-duration vascular

access to allow maturation of grafts. Central venous catheters can also provide
chronic dialysis access when haemodialysis is required for less than one year,
arteriovenous access is contraindicated, and when patients refuse permanent access.
The primary advantage is the ability to provide immediate access, while the main
disadvantages are the risk of infection and malfunction.
The preferred type of access is a fistula because they have the lowest risk of
complications, lowest need for intervention, and the best long-term patency.
117
Peritoneal Dialysis
An alternative to haemodialysis is peritoneal dialysis where the patient's peritoneum
acts as a blood filter. A catheter is surgically inserted into the patient's abdomen.
During treatment, the catheter is used to fill the abdominal cavity with dialysate.
Waste products and excess fluids move from the patient's bloodstream into the
dialysate solution. After a waiting period, the waste-filled dialysate is drained from
the abdomen, and replaced with clean dialysate.
Peritoneal dialysis:
Does not take blood from the body to be filtered

Uses the lining of the abdomen (peritoneum) to filter blood
Is flexible as can be done almost anywhere
Peritoneal dialysis works by using the patients peritoneum as a filter. There are three
stages to a dialysis cycle (or exchange):
The abdomen is filled with dialysis fluid (dialysate). The amount of

fluid varies but is usually 2 litres
The dialysis fluid stays in the abdomen for a period of time. During
this time, waste products and chemicals pass into the fluid.
The 'used' dialysis fluid is drained from the body and discarded.
118
Types of peritoneal dialysis

There are two main types of peritoneal dialysis:
Continuous Ambulatory Peritoneal Dialysis (CAPD)

Automated Peritoneal Dialysis (APD).
CAPD - This is the most commonly used form of peritoneal dialysis and works by
using gravity. It is carried out manually throughout the day. A bag of fluid is warmed
to body temperature (using a special heating machine) and placed at a high enough
level to allow the fluid to drain into the abdomen through a tube. When it has filtered
the blood of waste products, chemicals and water, an empty bag is placed at a low
enough level to allow the fluid to drain out of the abdomen through the tube. It takes
around 30 to 40 minutes to carry out a 'bag change' as above and patients can stick to
their normal routine between bag changes. Between bag changes dialysate is left in
abdominal cavity for several hours. Between 3 and 5 exchanges are usually required
every day.
APD - This system is used during the night, so that patients do not have to change
bags during the day. A machine warms the fluid and delivers it through the tube. The
machine leaves the fluid in the abdomen for a specified time and then drains it out of
the abdomen through the tube. This 'cycle' is then repeated according to a pre-set
programme. In the morning patients can disconnect from the machine and go about
their normal routine.
Before dialysis a procedure is required to insert a soft tube (catheter) into the
abdomen. In many cases, the catheter can be placed with just a local anesthetic, but
for some people, surgery is necessary.
119
Peritoneal dialysis has the advantage of being carried out in the patients home.
Haemofiltration
This can be used to treat ARF patients in ITU setting. Haemofiltration is less likely
than haemodialysis to cause acute hypotension in patients with septicaemia or with
poor myocardial function. Large volumes of plasma water are removed and replaced
by a sterile electrolyte solution. Although like haemodialysis it can be carried out
intermittently using a machine it is usually performed as CAVH continuous arteriovenous haemofiltration. Its main advantage is in controlling fluid and electrolyte
balance.
Continuous venovenous haemofiltration [CVVH] can be carried out using central
venous lines but requires a blood pump for circulation.
A further variation is to combine continuous dialysis with continuous haemofiltration
[CAVHD]. In this blood is ultrafiltered and dialysed.
For CAVH and CAVHD cannulas are inserted into a major artery [usually the radial
artery] and a vein to form an AV shunt. Frequent assessment of fluid balance is
required.
The Genitourinary History

Pain
Questionnaire:
11.
12.
Site
Radiation where the pain moves
Renal Pain: felt in the Loin Renal Angle (angle between the 12th rib & the edge of
erector spinae muscle)
Ureteric Colic: felt along the line of the ureter loin to groin (starts in the loin &
radiates down around the waist just above the inguinal ligament to the base of penis,
scrotum or labia)
Bladder pain: Dull suprapubic ache worse by micturation
120
Prostatic pain: felt deep in the pelvis, between the legs in the perineum patient
often thinks the pain is coming from rectum
13.
14.
15.
16.
17.
18.
19.
20.
Character sharp/dull ache/colicky

Severity score from 1 to 10, 1 being very mild, 10 being worst pain
ever experienced.
Onset sudden/gradual
Periodicity constant/intermittent
Duration minutes/hours/days
Aggravating precipitants/makes it worse
Relieving eases
Associations other symptoms that accompany the pain, e.g. nausea,
vomiting, diarrhoea, urinary symptoms etc.
Associated Features:
1.
2.
3.
4.
Anorexia
Weight loss
Nausea & Vomiting
Fever and chills
Do you feel feverish or sweaty?

Simple urinary tract infections generally dont lead to a pyrexia, however if left for some time, the
patient may develop pyelonephritis resulting in fever, malaise and occasionally vomiting. Also an
obstructing renal calculus may lead to pyrexia, rigors and vomiting due to obstruction of the ureter lead
to superimposed infection, an emergency. A RCC may present as pyrexia of unknown origin, beware!
5. Changes in urinary appearance

6. Changes in urinary volume
7. Symptoms suggesting Urinary Obstruction

Haematuria:
Frank distinct blood in the urine or a general tea

coloured urine)
Painful or painless (more sinister)
If the haematuria occurs early or late in the urinary
stream or if it is uniform throughout. The later in the
stream the higher up the urinary tract the pathology is
likely to be.
Kidney/bladder tumour,
Bleeding from prostate,
Infection
Calculi
Other causes of red discolouration of urine:
Haemoglobinuria (due to haemolysis)
Drugs such as Rifampicin
When did you first notice passing blood in the water?
121
Essential to establish whether this is an acute or chronic presentation.

Acute presentations with large volumes of blood can lead to acute urinary retention secondary to clot
formation in the bladder, which could be from a bladder neoplasm.
Many older men may give a history of many months or even a couple of years of blood loss.
New onset haematuria in the younger person is generally a UTI a renal calculus, or trauma.
Is the blood bright red or dark coloured?

Bright red blood is a fresh bleed, from either inflammation, trauma, infection or the sloughing of some
tumour in the renal tract. Dark blood is possibly from a ruptured renal cyst into the collecting system
and will appear as altered stale blood with some flecks of bright red.
Is the blood at the start of the stream or at the end?

Urethral inflammation, trauma or, prostatic disease can cause haematuria at the beginning of
micturition which then clears, or haematuria only at the end of micturition.
Do you have any pain?

Painless haematuria raises the question a renal tract neoplasm.
In the younger person pain resulting in frequency and urgency points towards a urinary tract infection
and cystitis suprapubic pain/discomfort, or a renal calculus, which gives a colicky type pain mainly
in the flank.

Do you need to pass water more often than usual?
Urethritis, Cystitis of any cause, UTI, prostatitis and heavy blood loss leading to clot retention can give
symptoms of frequency and urgency and also dysuria.
Polyuria (over 3 L of urine per day):

Acute renal failure due to acute tubular necrosis,
Diabetes mellitus,
Diabetes insipidus,
Psychogenic polydipsia
Oliguria (less than 400 ml of urine per day):
Renal failure
Dehydration.
Anuria (less than 50 ml of urine in 24 hours):
Renal failure
Dehydration
Urinary obstruction

122
Post micturition dribbling stream is weak and dribbles down to nothing as it

finishes
Straining - to push or strain to begin urination
Double voiding/ Incomplete emptying - needing to pass urine soon after
micturition
urine
Retention inability to pass urine
Urinary Incontinence
Urgency/urge incontinence urge to pass urine as soon as desire arises

Overflow incontinence uncontrollable leakage and dribbling of urine from
urethra
Pneumaturia
Urethral Discharge
-
Colour
Consistency
Quantity
Painful or burning micturition
Fever
Chills
Perineal fullness
Sexual problems in the male

-
Erectile dysfunction / impotence (inability to maintain an erection adequate for

satisfactory sexual intercourse)
Premature Ejaculation
Loss of libido
Haemospermia (trauma/infection)
Sexual problems in the female
Frequency, regularity and duration of menses, LMP

Blood loss, clots suggest menorrhagia, heavy menstrual loss
Dysmenorrhoea
Primary/secondary amenorrhoea
Post menopausal or post coital bleeding
OCP/HRT
Dyspareunia
123
Vaginal/urethral discharge STD [e.g. gonorrhoea]

Pregnancies number and complications
Infertility

Have you had any kidney or bladder problems in the past?
As transitional cell carcinoma of the renal tract represents field change, meaning the entire
urothelium has potentially been affected by TCC and strict surveillance is mandatory. A previous
cautery or resection of a TCC ( transurethral resection of a bladder tumour (TURBT)) again raises
suspicion of recurrence.
Those with a history of renal calculi may have multiple recurrent episodes through their life time.
Past transurethral resection of the prostate (TURP) does not exclude the prostate as the origin of
haematuria as remaining tissue may undergo neoplastic change.
- History of recurring UTIs or renal calculi

- Previous haematuria or proteinuria
- History of DM/gout
- Hypertension may cause renal impairment and is a complication of renal
disease
- Previous renal biopsy
- Childhood UTIs/VUR, childhood GU surgery (congenital anomalies, e.g
ureteric
aplasia

Medication
Do you have any medical problems? Are you taking any medication?
Recent treatment with Rifampicin can colour the urine red similar to haematuria. Radiation to the
pelvis may lead to radiation cystitis and haematuria, which still needs to be investigated. Many patients
with longstanding atrial fibrillation or valvular disease may not volunteer anticoagulants as
medications: Its imperative that you ask!
Any anticoagulant, aspirin, plavix, warfarin can lead to haematuria, and may in fact be the only cause.
Any coagulopathies should be asked about also.
Steroids/immunosuppressants
NSAIDS (Analgesic nephropathy)
Anticoagulant: aspirin, plavix, warfarin
Allergies
Social History
Do you smoke? What type of work do/did you do?
Transition cell carcinoma has a very strong association with smoking, 4 fold increase in urothelial
tumours; it is important not only to illicit current smoking habits but also previously. Work such as coal
mining, dye factories, and those working with benziolene and naphthylamine are associated with a 20
124
60 fold increase in development of tumours as they are renaly excreted and result in prolonged
exposure of the urothelium.
Marital status/children, employment, alcohol [count units], smoking

If patient has chronic renal failure ask how they are coping with illness/dialysis.
If the patient is on dialysis ask about travel times and expenses, effect on
quality of life, home management of polypharmacy
Family History
Is there any family history of problems with the water, or any cancers in the
family?
Family history of urological malignancies is important. Also benign pathology such as renal cysts and
polycystic kidney disease may direct you to the cause.
Some forms of renal disease are inherited ie polycystic kidney disease is

autosomal dominant
Renal stones
Other relevant family history diabetes/hypertension

Important questions to be asked in history
-
When did you first begin noticing urinary symptoms?

Have your urinary symptoms been continuous, or occasional?
Have your symptoms gradually worsened over time, or did they come on
suddenly?
How bothersome are your symptoms?
How often do you urinate during the day?
How often do you need to get up at night to urinate?
Do you start and stop when urinating, or feel like you have to strain to urinate?
Do you have difficulty starting urination?
Do you ever leak urine? If so, when?
Do you have a frequent or urgent need to urinate?
Do you feel you arent able to completely empty your bladder?
125
Do you ever have blood in your urine?

Have you had urinary tract infections?
Is there any burning when you urinate?
How do you know when you have a urinary tract infection?
Do you have type 2 diabetes?
Do you have any problems getting and maintaining an erection (erectile
dysfunction) or any other sexual problems?
Do you feel pain in your bladder area?
Have you ever had surgery or another procedures that involved insertion of an
instrument through the tip of your penis into the urethra?
Do any of you blood relatives (such as your father or brother) have a history of
enlarged prostate, or prostate cancer, or kidney stones?
What medication do you take, including any over the counter medications or
herbal remedies?
Are you on any blood thinners such as aspirin, warfarin (Coumadin) or
clopidogrel (plavix)?
The Genitourinary History and examination

-
Red discolouration: - Haematuria

- Haemoglobinuria (due to haemolysis)
-Drugs such as Rifampicin
Note: With suspected haematuria ask about whether the patient means
frank distinct blood in the urine or a general tea coloured urine, whether
it is painful or painless (more sinister). Also ask if the patient has noticed
if the haematuria occurs early or late in the urinary stream or if it is
uniform throughout. The later in the stream the higher up the urinary tract
the pathology is likely to be.
Kidney/bladder tumour,
Bleeding from prostate,
Infection
Calculi
-
Polyuria (over 3 L of urine per day): Can be a feature of acute renal

failure due to acute tubular necrosis, diabetes mellitus, diabetes
insipidus, psychogenic polydipsia
Oliguria (less than 400 ml of urine per day): Due to renal failure or
dehydration.
Anuria (less than 50 ml of urine in 24 hours)
Urinary obstruction
126

Post micturition dribbling
Double voiding/ Incomplete emptying (needing to pass urine soon after
micturition)
urine
Complete obstruction/Overflow incontinence
Retention inability to pass urine
Pain
Renal angle pain due to pyelonephritis is associated with fever/rigors/dysuria

[pain passing
urine]
Dull/continuous renal angle pain due to tumour
Renal colic is severe pain radiating down to groin [renal calculus/clot]
Prostatitis [inflammation of prostate e.g. bacterial infection]

Remember full pain questionnaire - onset, site, radiation, severity, character, time
course, aggravating and relieving factors, associated symptoms.
Incontinence

Urgency - strong desire to pass urine may be followed by incontinence
[Gynaecological prolapse]
Overflow incontinence
Spinal cord lesion, bladder will fill and then empty reflexly
Pneumaturia
Symptoms of renal failure
Anuria failure to pass more than 50mls of urine daily

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Oliguria < 400mls urine daily

Nocturia/Polyuria inability of kidneys to concentrate urine normally
Anorexia/vomiting/fatigue/hiccup
Pruritis general itchiness of the skin
Oedema due to fluid retention
Symptome of hyperkalaemia (muscle weakness, cardiac arrhythmia)
Bone pain due to renal bone disease caused by secondary
hyperparathyroidism which is compensating for vitamin D deficiency
caused by the renal failure.
Symptoms of anaemia (Due to declining erythropoietin levels)
Altered level of consciousness( drowsy/forgetful/coma), in acute renal
failure
Dyspnoea, due to pleural effusions/ pericardial effusions / cardiac
failure
Renal failure patients must be questioned about renal replacement therapy:Dialysis:What type, how long, urinary output, weight gain between sessions,
fluid restriction
Haemodialysis:-
Peritoneal dialysis
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Renal transplant
Ask about function of graft, rejection episodes

Other renal transplants
Complications of drugs such as steroids and other
immunosuppressants
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Renal failure patients must be questioned about diet:Protein, fluid and salt restriction
Sexual problems in the male
Lack of libido/inability to achieve or maintain an erection/trouble with
ejaculation
Penile discharge/STD
Sexual problems in the female
Frequency, regularity and duration of menses, LMP
Blood loss, clots suggest menorrhagia, heavy menstrual loss
Dysmenorrhoea
Primary/secondary amenorrhoea
Post menopausal or post coital bleeding
OCP/HRT
Dyspareunia
Vaginal/urethral discharge STD [e.g. gonorrhoea]
Pregnancies number and complications
Infertility

- History of recurring UTIs or renal calculi
- Previous haematuria or proteinuria
- History of DM/gout
- Hypertension may cause renal impairment and is a complication of renal
disease
- Previous renal biopsy
- Childhood UTIs/VUR, childhood GU surgery (congenital anomalies, e.g
ureteric
aplasia
Medication
Prescribed and over the counter

Steroids/immunosuppressants
NSAIDS (Analgesic nephropathy)
Allergies
To any medication
Social History
Marital status/children, employment, alcohol [count units], smoking

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If patient has chronic renal failure ask how they are coping with illness/dialysis.
If the patient is on dialysis ask about travel times and expenses, effect on
quality of life, home management of polypharmacy)
Family History
Some forms of renal disease are inherited ie polycystic kidney disease is

autosomal dominant
Other relevant family history diabetes/hypertension
The genitourinary examination
If renal disease is suspected or known to be present then certain signs must be sought.
Inspection
General inspection remains crucial.
Hydration
dehydration can cause acute renal failure

over hydration can result from intravenous infusion of fluids to correct renal
failure
fluid overload can result from renal failure [pedal oedema/pulmonary oedema]
Hyperventilation underlying metabolic acidosis

Hiccupping can be a sign of terminal uraemia
Sallow complexion dirty brown appearance in chronic renal failure [impaired
excretion
of urinary pigment]
Anaemia of chronic disease/poor nutrition/erythropoietin
deficiency/haemolysis/bone
marrow
depression
Terminal renal failure
Level of consciousness -drowsy/coma - due to nitrogen/toxin retention
Muscle twitching/tetany/epileptic seizures due to low serum calcium level and to
nitrogen retention
The hands
Leuconychia white transverse opaque lines in hypoalbuminaemia [nephrotic
syndrome]
131
Terrys lines/ half and half nails distal brown arc occurring in 20% of renal failure
patients
Anaemia palmar crease pallor

Asterixis may be present in terminal chronic renal failure [Dorsiflex the wrists with
the
arms outstretched and spread out the fingers, a flapping tremor may occur
as
in liver failure]
The arms
2) Arteriovenous fistula used for haemodialysis [Make sure this is palpated for
thrill and auscultated for bruit to assess function of the fistula]
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Bruising nitrogen retention causes abnormal platelet aggregation

Skin pigmentation failure to excrete urinary pigments
Scratch marks pruritis due to uraemia and calcium deposition
Blood pressure hypertension may be the cause of renal disease or a complication
Peripheral neuropathy/ myopathy
The face
Anaemia conjunctival pallor
Jaundice nitrogen retention can cause haemolysis
Uraemic fetor due to breakdown of urea to ammonia in the saliva
Mucosal ulcers underlying connective tissue disease i.e. SLE
Gingival hyperplasia due to immunosuppressant therapy [ciclosporin]
Rash - underlying connective tissue disease i.e. SLE
The neck
Central line for dialysis
Jugular venous pressure to assess hydration [elevated JVP in fluid overload/CCF]
Carotid artery bruits there may be generalised atherosclerosis [renal artery stenosis]
133
The chest
Cardiac - CCF due to fluid retention in chronic renal failure
- Hypertension sodium and water retention and excess renin production
- Pericarditis due to retained metabolic toxins and can cause a pericardial
rub
Lungs - Pulmonary oedema [volume overload]
- Infection due to immunosuppression in renal transplant patients
The abdominal examination

As done previously but particular attention must be paid to the following;
Inspection
Nephrectomy scar - look at loin and lumbar regions
Nephrectomy tube - draining wound
Renal transplant scar right or left iliac fossa

Transplanted kidney bulge under scar in RIF/LIF
Catheter for peritoneal dialysis
Ileostomy connection from bladder to abdominal wall, to allow drainage of urine
directly from bladder to stoma bag.
Small scars from catheter placement near midline or the lower abdomen
Distension polycystic kidneys/ascites [nephrotic syndrome]/dialysis fluid
Palpation
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The kidneys bimanual method
To palpate the right kidney the examiners left hand is placed

underneath the back. The left fingers flex at the metacarpophalangeal joints in the area
of the renal angle. The examiners right hand is placed over the RUQ. The kidneys are
felt by balloting, the renal angle is pressed by the flexing fingers of the posterior hand
and the anterior hand is used to palpate the kidney.
To palpate the left kidney the left hand is stretched over the abdomen
and placed posteriorly over the renal angle. The right hand feels for the left kidney
anteriorly.
Deep palpation in the renal angle can elicit tenderness suggesting pyelonephritis.
To distinguish a large left kidney from splenomegaly:
7. Spleen has no palpable upper border
8. Spleen has a notch
9. Spleens moves inferomedially on inspiration, kidney
moves inferiorly
10. Spleen is not ballottable unless gross ascites present
11. Percussion note is dull over the spleen resonant over
kidneys
12. Friction rub may be heard over the spleen but never
over the kidney as it is too posterior
Unilateral renal mass
Renal cell carcinoma

Hydronephrosis
Polycystic kidneys [asymmetrical enlargement]
Acute pyelonephritis
Abscess
Bilateral renal mass

Polycystic kidneys
Bilateral hydronephrosis
135
Bilateral renal carcinoma

Early diabetic nephropathy
Infiltrative disease i.e. lymphoma/amyloid
Transplanted kidney palpable in LIF or RIF

Hepatomegaly - from hepatic cysts may be present in PCKD
Bladder empty bladder is impalpable. If there is urinary retention the full bladder
may
be palpable above the pubic symphysis. It is typically regular, smooth, firm
and oval shaped. It may reach as high as the umbilicus. It must be
differentiated from any swelling arising from the pelvis. The bladder can be
emptied by insertion of a urinary catheter.
Percussion
Ascites shifting dullness [nephrotic syndrome]
Enlarged bladder
Auscultation
Renal bruits best heard just above the umbilicus about 2 cms to the left or right of
the
midline. Listen with the diaphragm of the stethoscope. Its presence
suggests renal artery stenosis due to atherosclerosis or fibromuscular
dysplasia. The absence of hypertension makes a diagnosis of renal
artery
stenosis less likely.
Rectal and pelvic examination
Examination of external genitalia for evidence of STI
Prostatomegaly in males and Frozen pelvis from cervical cancer in females:
These may cause urinary tract obstruction and renal failure
The back
Sacral oedema fluid overload/CCF
Bony tenderness strike the vertebral column gently and may elicit tenderness. This
may
be due to renal osteodystrophy from osteomalacia or secondary
hyperparathyroidism
The legs
Oedema
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Pigmentation
Scratch marks
Gouty tophi in feet
The fundi
Diabetic changes
Hypertensive changes
The Neurological History

A thorough neurologic history allows the clinician to define the patient's problem
and, along with the result of physical examination, assists in making a diagnosis.
Solid knowledge of the basic principles of the various disease processes is essential
for obtaining a good history.
The history of the presenting illness or chief complaint should include the following
information:
Symptom onset: Acute onset symptoms (minutes to hours) suggest vascular or

convulsive problems and may be preceded by an aura. Subacute onset (hours
to days) occurs with inflammatory pathology such as that associated with
meningitis, Guillian-Barre syndrome. Chronic onset (weeks to months) may
indicate malignant aetiology; and onset in the order of months to years is
associated with degenerative disease.
Duration
Course of the condition (eg, static, progressive, or relapsing and remitting)
Associated symptoms, such as pain, headache, nausea, vomiting, weakness,
and seizures
Symptoms may be localized or diffuse and a logical assessment of the nervous
system level of pathology can be made on this basis. Is the pathology
occurring at the level of the cerebral hemispheres, posterior fossa, spinal cord,
peripheral nervous system?
Important miscellaneous factors of the history include the following:
Results of previous attempts to diagnose the condition

Any previous therapeutic intervention and the response to those treatments
A complete history often defines the clinical problem and allows the examiner to
proceed with a complete but focused neurologic examination
Presenting symptoms
1) Headache
Obtain details on all 10 characteristics of pain (outlined below).
137
The typical symptoms of the commonest causes of headaches are outlined. These are
the commonest features, but every patient is different.
Tension
Site
Generalised
Radiations
Character
Severity
Onset
Periodicity
Duration
Aggravating
neck(occasional
)
Ache
subjective
Gradual
variable
Hours
stress/posture
Relieving
rest/analgesia
Associations
Migraine
Unilateral/
near eyes
Cluster
variable
sharp or ache
subjective
gradual
variable
hours
light
rest/analgesi
a
forehead/cheek
ache
subjective
gradual
recurring bouts
intermittent
pollen/allergens
Nausea/aura
vomiting
Lacrimation
rhinorrhoea
Over one eye
SAH
Local,then
generalised
Neck
thunderclap
worst ever
sudden
persistent
decongestant
neck
stiffness
Other causes of headache

Meninges
meningitis
Intra- cranial
Trauma
Tumour / abscess / congenital malformation
(Any space-occupying lesion, which can cause raised intra-cranial pressure)
Systemic
Asociated with infection, connective tissue disease, etc

Vascular
Acute cerebral artery/vein thrombosis

Temporal arteritis
Carotid aneurysm
138
Sinuses, middle or inner ear

2) Faints
Syncope is defined as a transient loss of consciousness with an inability to maintain
postural tone that is followed by spontaneous recovery. The term syncope excludes
seizures, coma, shock, or other states of altered consciousness. Dizziness (faintness) is
the symptom which precedes syncope.
Causes of syncope
Cardiac syncope:
Vascular disease, cardiomyopathy, arrhythmia, or valvular dysfunction
Noncardiac syncope:
Vasovagal syncope is the most common type in young adults but can
occur at any age. It usually occurs in a standing position and is precipitated
by fear, emotional stress, or pain (eg, after a needlestick). Autonomic
symptoms are predominant. Classically, nausea, diaphoresis, blurred or
faded vision, epigastric discomfort, and light-headedness precede syncope
by a few minutes. Syncope is thought to result in decreased peripheral
vascular resistance. It is not life threatening and occurs sporadically.
Dehydration and decreased intravascular volume contribute to
orthostasis. Orthostatic syncope describes a causative relationship between
orthostatic hypotension and syncope.
Situational syncope is essentially a reproducible vasovagal syncope with a
known precipitant. Micturition, defaecation, and carotid sinus syncope are
types of situational syncope. These stimuli result in autonomic reflexes,
ultimately leading to transient cerebral hypotension.
Neurologic syncope may have prodromal symptoms such as vertigo,
dysarthria, dysphagia, diplopia, and ataxia. Syncope results from
preexisting bilateral vertebrobasilar insufficiency with some superimposed
acute process. Consider a transient ischemic attack as an alternative
diagnosis.
A detailed account of the event must be obtained from the patient. The account must
include the circumstances surrounding the episode: the precipitant factors, the
patient's activity involved in prior to the event and the patient's position when it
occurred.
Physicians should specifically inquire to identify symptoms, such as chest

pain, dyspnoea, palpitations, severe headache, focal neurologic deficits,
diplopia, ataxia, or dysarthria prior to the syncopal event.
139
Patients should be asked to estimate the duration of their loss of

consciousness. Syncope is associated with patient estimates ranging from
seconds up to 1 minute in most cases. To discriminate from seizures, patients
should also be asked if they remember being confused about their
surroundings after the event or whether they have oral trauma [tongue biting]
or incontinence.
A detailed account of the event must also be obtained from any available
witnesses. Witnesses can aid the clinician in differentiating among syncope,
altered mental status, and seizure.
3) Fits
Seizure: a sudden change in behaviour that is the consequence of brain dysfunction.
Epileptic seizures: sudden change in behaviour due to abnormal electrical activity in
the brain (cerebral cortex). Electrical activity can be measured using an EEG.
Non epileptic seizures: sudden change in behaviour, without abnormal electrical
activity in the brain.
Characteristics of seizure
Altered/loss of consciousness
Involuntary movements jerking
Incontinence
Tongue-biting
Preceded by an aura (abnormal visual/auditory/olfactory sensation)
Weakness following fit (Todds paralysis)
Types of Epileptic Seizures
Simple no loss of consciousness

Complex loss of consciousness
Generalised abnormal activity widespread in brain
Partial abnormal activity in focal part of brain
Causes of Epileptic Seizures (damage to CNS)
Brain injury( trauma/haemorrhage)

Stroke
Intracranial infection
Congenital malformation
Tumour
Causes of Non Epileptic Seizures (These are generalized seizures)
Metabolic hypo/hyperglycaemia, hypothyroidism, hypercalcaemia,

hyponatraemia.
140
Hypoxia infection, blood loss, cardiac dysfunction

Renal failure/ Liver failure
Drugs/medications alcohol, sedatives
4) Dizziness/vertigo
Vertigo is an illusion of movement, caused by disease of the inner ear, the eighth
cranial nerve, or the central connections of the eighth cranial nerve.
In true vertigo, there is a sensation of rotation
Associations: Nausea, vomiting, unsteadiness, pallor, weakness.
Causes of Vertigo
Inner Ear Causes

Otitis interna
Acute labyrinthitis
CN 8 Causes
Acoustic neuroma (tumour of CN 8)
Central Connection Causes ( disease in the pons, origin of CN 8)

Tumour
Vascular disease
Multiple Sclerosis (demyelination)
5) Deafness
Impaired hearing can be due to damage/ obstruction of the ear canal, or due to damage
to the nerve supplying the ear. (CN 8, vestibulocochlear nerve)
Ear Canal Causes
Middle ear infection ( otitis media)

Wax (cerumen)
Nerve Causes
Noise exposure
Trauma (skull fracture)
Drugs (alcohol)
Congenital infections (rubella)
6) Visual disturbances
141
Diplopia double vision
Weakness of intra-ocular muscles or damage to nerves/blood supply of intra-ocular

muscles
Amblyopia blurred vision
Photophobia light intolerance (migraine/ meningitis)
Visual field loss These patterns are discussed in the clinical tutorials
Visual loss
a) Acute visual loss damage to the eye/ nerve supply/blood supply/brain
Stroke
Haemorrhage
Multiple Sclerosis
Retinal vascular occlusion
b) Chronic progressive visual loss damage to the eye/nerve
supply/blood supply/brain
Cataracts (ageing/DM/glaucoma/steroids)
Diabetes Mellitus (damages blood supply and nerves and causes cataracts)
Ageing (macular degeneration)
7) Gait
Many neurological conditions can impair walking. Gait can be abnormal due to
disease of
brain/ spinal cord (CNS)

nerves to the leg muscles (PNS)
leg muscles
joints
systemic disease
Types of impaired gait
Cerebellar disease unsteady, reeling

Stroke hemiplegic gait , dragging of one side
Parkinsons disease- small steps, shuffling, slow
8) Disturbed sensation
142
With regards to temperature sensation, patients can be asked whether they have any
problems detecting water temperature. Failure to notice cuts, wounds after injury due
to lack of sensation. For fine touch discrimination, patients can be asked whether they
have problems pulling the correct coin or other objects out of their pockets. Position
sense can be explored by asking whether patients have problems knowing where their
feet are on the car accelerator and brake pedals.
One should also inquire about pins and needles which can result from nerve
entrapement or peripheral neuropathy
Causes of Sensory Neuropathy include
Diabetes Mellitus
Vitamin B12 deficiency
Hereditary syndromes
9) Weakness
Weakness may be local one arm or leg, or may be generalised.
Enquire as to whether it is constant or intermittent.
Causes
Central Nervous System

Following CVA
Cerebral tumour
Spinal cord injury
Peripheral nervous system

DM
Toxins
Anterior horn cell

Motor Neuron Disease
Neuromuscular junction
Myasthenia gravis
Muscle
Alcohol
Medications (steroids)
Connective tissue diseases (SLE)
143
Endocrine (thyroid disease, Cushings, acromegaly)

10) Tremor and Involuntary movements
Distinguish between resting (visible at rest), postural (present throughout movement)
and intention (increases toward target).
Causes of Tremor include
Parkinsons disease
Cerebellar disease
Hyperthyroidism
Anxiety
Medications (inhalers, e.g. Ventolin)
11) Speech
Dysarthria difficulty with articulation
Causes of dysarthria
Cerebellar disease ( slurred speech)

Local oral disease mouth ulcers, cleft palate
Dysphasia difficulty with communication
Caused by disease of the dominant cortical hemisphere
Receptive dysphasia: where the patient cannot understand the spoken or

written word. Speech is fluent but disorganised. Ask patient to follow
commands, unable to do so.
Expressive dysphasia: the patient understands but cannot answer

appropriately. Ask to name objects, repeat words.
Nominal dysphasia: patient cannot name objects. Point to your pen, watch
and ask patient to name them.
Other Higher Centre Functions include:
Frontal lobe personality

Temporal lobe memory, speech
Parietal lobe performing tasks, speech
Occipital lobe vision
Past Medical and Surgical history

Start with the OPEN ENDED enquiry first. Have you ever been admitted to hospital
for any reason? is a good way to start. Follow this with Do you have any medical
144
conditions or health problems of any kind? and Have you ever had any operations
no matter how minor before?
In this part of the history it is helpful to ask the open ended question in a number of
ways because what you and the patient consider a past medical history does not
always coincide.
Then you can focus on specifics. If the answer is yes to any of these, ask what the
treatment has been, any changes in treatment and how successful any treatment has
been.
History of trauma / injury

History of meningitis / encephalitis
History of epilepsy / convulsions
History of Diabetes If no, ask whether blood sugars have actually been
checked
History of high cholesterol Also ask if this has been checked specifically.
History of hypertension Again, ask if it has been checked recently
History of heart disease or peripheral vascular disease
History of Atrial fibrillation or any other arrhythmia
History of rheumatic fever or endocarditis
Medications/Allergies
Are you on any medications?

How about over the counter medications
Any herbal remedies?
Enquire about allergies and whether any medication has made the patient unwell
before. Ask what the patient means by allergy?
Relevant specifics:
Anticoagulants and / or anti platelet agents

Anti convulsants
Antihypertensive agents
Treatment for high cholesterol
Oral contraceptive pill
Social History
Home circumstances: Including who is with the patient at home and the
general health of that person, home modifications and home layout.
Occupation
Smoking (how much and how long?).
Alcohol intake (Long term alcohol use is associated with dementia,
neuropathy, cerebellar degeneration, encephalopathy)
145
Family History
Again, OPEN ENDED enquiry first. Are there any medical conditions that
run in the family?
Then more specific if suitable (i.e. not in an 85 year old patient): Are your
parents still alive? How is their health? or What was the cause of their
passing?
The same for siblings
Then Any relatives with a neurological condition?
Family history of heart disease, stroke, hypertension, diabetes, high
cholesterol, epilepsy
Systems review
Start with Is there anything else you would like to add or Do you have any
other symptoms to report
Then ask about general wellbeing, weight and appetite.
Then 4-5 questions about each body system in quick point form.
WARD TUTORIAL
Cranial nerve examination
The aim of this tutorial is for students to begin examination of the cranial nerves.
A student should volunteer for demonstration and then students should work in
pairs
Position the patient sitting over the edge of the bed
Look at the head, face and neck
Inspection
Craniotomy scars
Ptosis drooping of the upper eyelid
Proptosis abnormal protrusion of the eyeball
The first [Olfactory] Nerve

Purely sensory nerve
This nerve is not tested routinely, ask patient have they any difficuty with their sense
of smell. If the answer is no, move to the second cranial nerve.
If patient c/o loss of smell [anosmia] test each nostril separately with bottles
containing essences of familiar smells such as coffee.
The second [Optic] Nerve

Purely sensory nerve which begins in the retina
Visual acuity is tested with the patient wearing his or her glasses
146
Ask patient do they have any difficulty with their vision

Can you see the clock on the wall?
Can you read the newspaper?
Each eye should be tested separately
A portable Snellens chart will enable you to perform a more formal test
A patient who is having visual problems should be asked to count fingers held up in
front of each eye in turn, and if this is not possible then perception of hand movement
should be assessed. Failing this light perception only may be present.
Visual fields are assessed by positioning yourself in visual confrontation about a
metre away. Always remove the patients glasses. Test the visual fields of your
patient against your own.
Ask patient to cover his right eye with his right hand and close your left eye
Ask patient to keep looking at my eye
Test his left temporal vision against your right temporal vision by moving your
wagging finger from the periphery towards the centre
Tell me when you see my finger move
The temporal field should be tested in the horizontal plane and in the upper and lower
temporal quadrants.
Change hands and repeat on the nasal side
Any areas of field defect are mapped out
The visual fields of his right eye are assessed in the same way.
Bitemporal hemianopia: optic chiasm lesion, pituitory tumour
Unilateral field loss: optic nerve lesion, tumour/vascular
Homonymous hemianopia: optic tract to occipital cortex, vascular/tumour
The blind spot there is a small area close to the centre of the visual fields where
there is no vision. This is the area where the optic disc is seen on fundoscopy and is
the point where the optic nerve joins the retina.
The blind spot enlarges with papilloedema eg raised intracranial pressure with brain
tumour
Central scotoma or loss of central macular vision is tested for with a redheaded
hat pin.
As before move the red-headed pin from the temporal periphery through the central
field to the nasal periphery, asking the patient can you see the head of the pin?
Eg demyelination of the optic nerve in multiple sclerosis can cause loss of central
vision
Colour vision Tests of colour vision are not carried out routinely
They may reveal subtle defects of the retina or optic nerve
Ishihara plates are used. Checking patients eyes separately plates made up of
coloured dots containing numerical shapes are presented to patient who is asked to
discern the numbers shown in each pattern.
Fundoscopy Use the right eye to look in patients right eye and vice versa
Look first at the cornea, iris and lens. Then look at the fundus.
Search first for the optic disc then look at the four quadrants of the retina
147
The Third [Oculomotor], Fourth [Trochlear] and Sixth [Abducens]

The pupils
The size of the pupils depends on a balance of parasympathetic and sympathetic
innervation. The parasympathetic innervation of the eye is supplied by the EdingerWestphal nucleus of the third nerve [stimulation causes pupillary constriction]
The pupillary reflexes depend on the optic nerve for their afferent limb
Ask the patient to look at an object at an intermediate distance
Examine the pupils for size, shape, equality and regularity
Light reflex: with a pocket torch shine the light from the side [so the patient does not
focus on the light and accomadate] into one of the pupils to assess its reaction to light
Normally the pupil into which the light is shone constricts briskly this is the direct
light reflex
Simultaneously the other pupil constricts in the same way, this is the consensual light
reflex
Repeat this procedure on the other side
Afferent pupillary defect/Marcus Gunn pupillary sign: Move the torch from pupil
to pupil
If an eye has optic atrophy or severely reduced visual acuity from another cause the
affected pupil will dilate paradoxically after a short time
This occurs because afferent impulses are reduced so the light reflex is markedly
reduced in the eye with decreased acuity
Accomodation: Ask the patient to look into the distance and then to focus on your
finger held near the patients nose
There is normally constriction of both pupils, the accomodation response
Absent light reflex with an intact accomodation reflex occurs in Argyll Robertson
pupil in syphilus affecting the nervous system
Eye movements
Assess for eye movement, diplopia [double vision] and nystagmus
Look at my finger; follow it with your eyes
Ask the patient to look laterally left and right, continue moving the finger to complete
H pattern.
The third nerve supplies all the ocular muscles except;
Superior oblique fourth nerve
Lateral rectus sixth nerve
The lateral rectus and medial rectus abduct and adduct the eyes
When the eye is abducted the elevator is the superior rectus [third nerve] while the
depressor is the inferior rectus [third nerve].
148
When the eye is adducted the elevator is the inferior oblique [third nerve] while the
depressor is the superior oblique [fourth nerve]
Third nerve also supplies Levator palpebrae superioris
Tell the patient to inform you if they see double images [diplopia]
Diplopia is an early sign of ocular muscle weakness
The false image is usually paler, less distinct and more peripheral than the real one
Features of a third nerve lesion
1. Complete ptosis
2. Eye down and out
3. Dilated pupil which is not responsive to light and accomadation
Features of fourth nerve lesion
Usually associated with a third nerve palsy
Double vision going down stairs
Ask patient to turn the eye in and then to look down
Superior oblique paralysis
Features of sixth nerve lesion
Failure of lateral movement
Nystagmus
Ask patient to follow your finger to each side
The direction of nystagnus is defined as that of the fast [correcting] movement
Vestibular lesion nystagmus away from the side of the lesion
Cerebellar lesion nystagmus to the side of the lesion
Internuclear ophthalmoplegia abducting eye has greater nystagmus than the
adducting eye. There is dissociation of conjugate eye movements.
It suggests MS with a lesion in the medial longitudinal bundle
WARD TUTORIAL
Cranial nerve examination
The aim of this tutorial is for students to complete examination of the cranial
nerves.
A student should be asked to volunteer and students should work in pairs.
The fifth [trigeminal] nerve

This nerve contains both sensory and motor fibres
There are 3 sensory divisions
149
Ophthalmic: supplies forehead, cornea and conjunctiva

Maxillary: supplies the middle of the face
Mandibular: supplies the lower jaw
Facial sensation
Test in the three divisions of the nerve comparing each side with the other
FOREHEAD - Ophthalmic
MAXILLA - Maxillary
LOWER JAW Mandibular
Test for pain using sharp object.
Ask patient does it feel sharp or dull.
Test for light touch using cotton wool
The patient should be instructed to say yes each time the touch of the cotton wool is
felt. Do not stroke the skin touch it.
Motor division
Inspect for wasting of the temporal and masseter muscles
Ask patient to clench their teeth and palpate for contraction of the masseter muscles
Ask patient to open their mouth and hold it open while the examiner attempts to force
it shut [pterygoid muscles]. A unilateral weakness of the motor division causes the
jaw to deviate towards the weak side.
If weakness is suspected patients should be asked to move the jaw laterally against
resistance. The jaw can be moved towards the affected muscle but cannot move
towards the normal side.
Jaw jerk
The afferent and efferent pathways are supplied by the fifth nerve
The patient lets his mouth fall open slightly
The examiners finger is placed on the jaw
The finger is tapped lightly with a tendon hammer
The reflex response comprises brisk closure of the jaw
It is often not visible and can be difficult to determine if it is present
Corneal reflex
The afferent part of the reflex arc is the first division [ophthalmic nerve] of the fifth
nerve
The efferent arc is supplied by facial nerve
Each fifth nerve communicates with both seventh nerves and therefore both eyes close
when each cornea is stimulated
Lightly touch the cornea with a wisp of cottonwool
Reflex blinking of both eyes is a normal response
The seventh [facial] nerve

Supplies: The muscles of facial expression
150
Stapedius muscle
Chorda tympani contains taste fibres from anterior two-thirds of the tongue
Inspection: for facial asymmetry
Unilateral drooping of the corner of the mouth
Smoothing of the wrinkled forehead
Smoothing of the nasolabial fold
Muscle power
Ask patient to look up and wrinkle his forehead
Feel for muscle strength by pushing down on forehead
This movement is preserved on the side of an upper motor neurone lesion [a lesion
which occurs above the level of the brainstem nucleus], because of bilateral cortical
representation of these muscles
The remaining muscles of facial expression are usually affected on the side of an
UMN lesion.
In a LMN lesion all muscles of facial expression are affected on the side of the lesion.
Ask the patient to shut the eyes tightly
Observe and try to force open each eye
Ask the patient blow out cheeks
Ask the patient to show their teeth
Compare the nasolabial grooves which are smooth on the weak side
If a lower motor neuron lesion is detected [weakness on one side of face], check for
ear and palatal vesicles of herpes zoster of the geniculate ganglion the Ramsay Hunt
syndrome
Examining for taste of the anterior two-thirds of the tongue is not usually required
**Left upper motor neurone seventh nerve lesion leads to drooping of the corner
of the mouth, flattened nasolabial fold, and sparing of the forehead on the left
side**
The Eighth [Vestibulocochlear] nerve

There are two components:
Vestibular containing afferent fibres for balance
Cochlear with afferent fibres for hearing
Examination for hearing
Ask the patient do they have any problems with their hearing
Cover one of the patients ears with your hand and whisper into the other ear
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If deafness is suspected perform Rinnes test and Webers test

Rinnes test
A vibrating tuning fork is placed on the mastoid process behind the ear. When
the sound is no longer heard it is placed in line with the external meatus. Normally the
sound is audible at the external meatus. With nerve deafness the note is audible at the
external meatus, as air and bone conduction are reduced equally, so that air
conduction is better as is normal. This is termed Rinne-positive.
With conduction [middle ear] deafness no note is audible at the external
meatus. This is termed Rinne-negative.
Webers test
A vibrating tuning fork is placed on the centre of the forehead. Normally the
sound is heard in the centre of the forehead. With nerve deafness the sound is
transmitted to the normal ear. With conduction deafness the sound is heard louder in
the abnormal ear.
Audiometry
Patients with defective hearing should be referred for audiometry. This
measures the degree of hearing loss at different sound frequencies.
Examination of vestibular function
This cannot effectively be evaluated at the bedside.
The ninth [Glossopharyngeal] and Tenth [Vagus] nerves

Get the patient to open their mouth and inspect the palate with a torch. Note
any displacement of the uvula. Ask the patient to say Ah. If the uvula is drawn to
one side this indicates a unilateral tenth nerve palsy. The uvula is pulled towards the
normal side.
Now test gently for the gag reflex
Ninth is the sensory component
Tenth is the motor component
Touch the back of the pharynx on each side with a spatula. Ask the patient if the touch
of the spatula is felt each time. Normally there is reflex contraction of the soft palate.
The ninth nerve supplies taste from the posterior two-thirds of the tongue this is not
routinely tested for.
The eleventh [Accessory] nerve

It supplies motor fibres to the trapezius and sternomastoid muscles
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Ask the patient to shrug their shoulders and feel the bulk of the trapezius
muscles and attempt to push the shoulders down.
Ask the patient to turn their head against resistance and feel the bulk of the
sternomastoids. Feel for the sternomastoid on the side opposite to the turned head.
There will be weakness on turning the head away from the side of a muscle whose
strength is impaired.
The twelth [Hypoglossal] nerve

It is the motor nerve for the tongue
Inspect for wasting and fasciculations. These indicate a lower motor neurone
lesion
Ask the patient to stick out their tongue. It will deviate towards the weaker
side if there is a unilateral lower motor neuron lesion.
Having completed the cranial nerve examination complete a full examination from
1-12 getting all students to participate
Inspection: take a good general look at the patient; in particular the face.
[1] Do you have any difficulty with your sense of smell?
[2] Visual acuity Do you have any difficulty with your vision?
Can you see the clock on the wall? Can you tell me what time it is?
[Glasses should be worn and test each eye seperately]
Can you read this line of your newspaper/book?
Check visual fields and check for central scotoma with red-headed hat pin
Fundoscopy
[3, 4, 6] Check direct and consensual light reflex and accomadation
Eye movements
Nystagmus
[5] Facial sensation
Masseter, temporal and pterygoid muscles
Corneal reflex
Jaw jerk
[7] Facial movement
[8] Hearing/Rinnes/Webers test
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[9, 10] Inspect/Check gag

[11] Trapezius and sternomastoid muscles
[12] Tongue
Gait, cerebellar function and MMSE

At the end of this session students should be able to examine gait, examine cerebellar function and
complete MMSE
Gait
Ability to stand and walk normally is dependent on input from several systems,
including: visual, vestibular, cerebellar, motor, and sensory.
A lot of information about neurological (and other) disorders can be gained from
simply watching a patient stand and then walk. Ask the patient to stand. If they are
very weak or unsteady, make sure that you are in a position and capable of catching
and supporting them if they fall. Enlist the help of a colleague if you need an extra
pair of hands. If you are still unsure as to whether standing/walking can be performed
safely, skip this area of testing. No test result is worth a broken hip!
Have the patient stand in one place. This is a test of balance, incorporating input
from the visual, cerebellar, proprioceptive, and vestibular systems. If they are able
to do this, have them close their eyes, removing visual input. This is referred to as
the Romberg test. Loss of balance suggests impaired proprioception, as it is this
pathway which should provide input that allows the patient to remain stable with
eyes closed.
Romberg test is positive when unsteadiness increases with eye closure.
Ask the patient to walk across the room, turn around quickly, and come back
towards you. Pay particular attention to:
a. Balance: Do they veer off to one side or the other as might occur with
cerebellar dysfunction? Disorders affecting the left cerebellar
hemisphere (as might occur with a stroke or tumor) will cause patients
to fall to the left. Right sided lesions will cause the patient to fall to the
right. Diffuse disease affecting both cerebellar hemispheres will cause
a generalized loss of balance.
b. Rate of walking: Do they start off slow and then accelerate, perhaps
losing control of their balance or speed (e.g. as might occur with
Parkinsons disease)? Are they simply slow moving secondary to
pain/limited range of motion in their joints, as might occur with
degenerative joint disease?
c. How do they hold their arms and legs? Is there loss of movement and
evidence of contractures as might occur after a stroke?
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Heel to Toe Walking: Ask the patient to walk in a straight line, putting the heel of
one foot directly in front of the toe of the other. Difficulty with this can be a sign
of a midline cerebellar lesion. This may be difficult for older patients (due to the
frequent coexistence of other medical conditions) even in the absence of
neurological disease.
Ask the patient to then walk on the toes [an S1 lesion will make this impossible]
and then walk on the heels [an L4 or L5 lesion causing footdrop will make this
impossible].
Test for proximal myopathy by asking the patient to squat and then stand up, or
sit in a low chair and then stand.
Gait disorders
Hemiplegia - The foot is plantar flexed and the leg is swung in a

lateral arc.
Spastic paraparesis Scissors gait
Parkinsons disease Hesitation, shuffling, freezing
Cerebellar Wide based; the patient staggers towards the affected
side
Footdrop High stepping gait
Proximal myopathy Waddling gait
The cerebellar examination

Causes of cerebellar disease
Alcohol: Characteristically spares the upper limbs

Unilateral cerebellar signs:
Bilateral cerebellar signs:
Space occupying lesion (Tumour, abscess)

Ischaemia (Vertebrobasilar disease)
MS
Trauma
Drugs (Phenytoin)
Alcohol
Friedreichs ataxia
Hypothyroidism
Paraneoplastic syndrome
MS
Large space occupying lesion
Midline
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Paraneoplastic lesion
Midline tumour
Examination for cerebellar signs
The cerebellum provides an important feedback loop for coordination of muscle
activity by integrating the functions of the cortex, basal ganglia, vestibular apparatus,
and spinal cord. Midline cerebellar dysfunction results in ataxia of gait with
abnormal heel-toe walking and difficulty in maintenance of upright posture.
Cerebellar hemispheric lesions result in additional signs outlined below.
General inspection
Patients level of consciousness

Abnormal posture or gait
Asymmetry (limbs, face)
Involuntary movement
Scars
Skin (Rash Vasculitis, neurofibromas, caf au lait spots)
Hearing aid
Walking aid
Head and neck
Check for nystagmus usually jerky horizontal nystagmus

This occurs in the direction of the cerebellar lesion (toward the lesion).
Assess speech for cerebellar dysarthria (scanning speech)
Keep in mind that dysarthria is not a disorder of speech content or language

(dysphasia dominant hemispheric deficit) but difficulty with speech
articulation.
Dysarthria is usually a sign of diffuse involvement of the cerebellum.
Cerebellar dysarthria is jerky, slurring, explosive and loud with irregular
separation of syllables.
Test for dysarthria by asking the patient to say British constitution or west
register street.
Upper limbs
- Upper limb drift: When the arms are extended they drift upwards due to
hypotonia.
- Upper limb rebound: The patient is asked to raise the arms quickly from their
sides and stop suddenly mid motion. Inability to stop is called rebound and it is
caused by loss of coordination between agonist and antagonist muscular action
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- Test tone
Finger to nose testing:

a. With the patient seated, position your index finger at a point in space in
front of the patient.
b. Instruct the patient to move their index finger between your finger and
their nose.
c. Reposition your finger after each touch.
d. Then test the other hand.
The patient should be able to do this at a reasonable rate of speed, trace a
straight path, and hit the end points accurately
Interpretation: You need to look for the following which are signs of ipsilateral
cerebellar disease:
Past-pointing: Overshooting the target (the examiners finger)
Intention tremor as the patients finger approaches the examiners
Rapid Alternating finger Movements:

a. Ask the patient to touch the tips of each finger to the thumb of the
same hand.
b. Test both hands.
Interpretation: The movement should be fluid and accurate. Inability to do this,

known as dysdiadochokinesis, may be indicative of cerebellar disease ipsilaterally.
Rapid Alternating Hand Movements:

a. Direct the patient to touch first the palm and then the dorsal side of one
hand repeatedly against the palm of the other hand.
b. Then test the other hand.
Interpretation: The movement should be performed with speed and accuracy.

Inability to do this, known as dysdiadochokinesis, may be indicative of cerebellar
disease ipsilaterally.
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Lower limbs
Test tone
Heel to Shin Testing:
a. Direct the patient to move the heel of one foot up and down along the
top of the other shin.
b. Then test the other foot.
Interpretation: The movement should trace a straight line along the top of the shin
and be done with reasonable speed. Failure to do this indicates loss of lower limb
coordination and suggests ipsilateral cerebellar disease.
Ask the patient to lift the big toe up to touch the examiners finger. Look for
intention tremor and past pointing
The cerebellar gait and station

When walking the patient staggers toward the side of the cerebellar lesion if the lesion
is unilateral. These patients preferentially adopt a wide spaced gait to avoid falling to
one side.
Difficulty with heel to toe walking is a sign of balance loss and suggests a midline
cerebellar lesion.
The station is the ability to stand still upright with the feet pushed in together.
Cerebellar disease is suggested if the patient is unable to do this with the eyes open or
closed. Loss of this ability only on closing the eyes suggests a proprioceptive deficit.
Truncal ataxia is a station abnormality characterized by an inability to maintain
upright position with a tendency to fall backwards. It is due to a midline cerebellar
lesion.
Students must realise that other organ system problems can affect performance of any
of these tests. If, for example, the patient is visually impaired, they may not be able to
see the target during finger to nose pointing. Alternatively, weakness due to a
primary muscle disorder might limit the patients ability to move a limb in the fashion
required for some of the above testing. Thus, other medical and neurological
conditions must be taken into account when interpreting cerebellar test results.
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Dementia
Definition Evidence from the history and mental status examination that
indicates major impairment in learning and memory as well as at least one of the
following:
- Impairment in handling complex tasks
- Impairment in reasoning ability
- Impaired spatial ability and orientation
- Impaired language
The cognitive symptoms must significantly interfere with the individual's work
performance, usual social activities, or relationships with other people
This must represent a significant decline from a previous level of functioning
The disturbances are of insidious onset and are progressive, based on evidence
from the history or serial mental-status examinations
The disturbances are not occurring exclusively during the course of delirium
The disturbances are not better accounted for by a major psychiatric diagnosis
The disturbances are not better accounted for by a systemic disease or another
brain disease
Diagnosing Dementia
Patients and close family/friends are often uncertain about the onset of symptoms
since the appearance of dementia is insidious. Useful questions for the patient and
family/friends are, "When did you first notice the memory loss?" and "How has
the memory loss progressed since then?" The physician can ask when the patient
stopped driving or managing finances.
Spouses, relatives, and friends take care of people with dementia. As symptoms
progress care of patients in the home becomes more difficult and 24 hour care
in a nursing home may be necessary. Students must be aware of the impact
such a diagnosis has on family and friends.
Mental Status Examination
Level of alertness
No special testing is required to determine the level of alertness. While taking the
history and examining the patient, observe whether the patient is alert, attentive,
sleepy, or unresponsive.
orientation
Person what is your name?
Place - where are you/do you know where you are?
Time what day/date/month/year is it?
Delirium: acute and reversible confusional state [infection in the elderly]
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Dementia: chronic and irreversible confusional state [Alzheimers disease]
Language
1) Fluency No special testing is required to assess fluency. Assess
whether the patient's phrases and sentences are of normal length during
conversation, are spoken effortlessly and at a normal rate, and have
normal grammatical structure. Fluency is independent of content;
speech can be completely fluent and still be incomprehensible.
2) Comprehension Comprehension is often adequately assessed
through the routine history and physical but can be tested explicitly.
Give the patient progressively more complex commands, such as one step
(eg, "Touch your nose."), two steps (e.g. "Touch your nose and then stick
out your tongue"), and three steps (e.g. "Touch your nose, then stick out
your tongue and then raise your right foot"). Commands that require a
body part to cross the midline (e.g. "Touch your right ear with your left
thumb") are more complex than those that do not. Increasingly complex
grammatical structures can also be used (e.g. "Touch the coin with the
pencil"; "With the comb, touch the coin"). Ask the patient progressively
more complex questions (e.g. "Does a stone sink in water?" "Do you put
on your shoes before your stockings?").
3) Repetition Ask the patient to repeat phrases or sentences of

progressively greater length and complexity (e.g. "It is cold outside";
"We all went over there together"; "The lawyer's closing argument
convinced the jury").
4) Naming Observe whether the patient frequently pauses and
struggles to think of words during routine conversation. Test naming
explicitly by asking the patient to name items as you point to them
(e.g., shirt, shoe, phone, and collar). Less common objects are
generally harder to name; parts of an object are harder to name than the
entire object.
5) Reading Ask the patient to follow a written command. This can be
one of the same commands used to test comprehension of spoken
language.
6) Writing Ask the patient to write an original sentence and to write a
sentence from dictation. Look for omitted or added words, or for word
substitutions.
Memory
1) Immediate Ask the patient to repeat a string of seven digits
immediately after you complete it. Lengthen or shorten the string until
you find the longest string the patient can repeat correctly. Despite its
categorization as "immediate memory," this is really more
appropriately considered "attention."
2) Short-term Ask the patient to memorize three unrelated words (e.g.
baseball, horse, purple), distract him or her for five minutes (usually by
performing other parts of the examination), then ask the patient to
recall the list. Give clues if an item is missed (e.g. "One was an
animal"); offer a multiple choice if this is not enough (e.g. "It was a
cat, a bear, or a horse").
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3) Long-term Long-term memory includes both recent and remote

memory.
a) Assess recent memory by testing orientation to time (e.g., day, date, month,
season, year), place (e.g. state, city, building), person, and by asking
questions about events of the past few days or weeks, (e.g. "Who are the
current candidates for president?" or, assuming an independent source is
available for verification, "What did you have for breakfast this
morning?").
b) Remote memory can be tested by asking about important historical events
and dates. The patient can also be asked about details of personal life such
as birth date, names and ages of children and grandchildren, and work
history, assuming independent verification is available.
Calculation
Ask some straightforward computation problems (e.g. 5 + 8; 6 x 7; 31 - 18).
Construction
Ask the patient to draw a clock, including all the numbers, and to place the hands at
4:10. Ask the patient to draw a cube; for patients who have trouble doing so, draw a
cube and ask them to copy it.
Abstraction
Ask the patient to explain similarities, "What do an apple and an orange have in
common?"; "a basketball and a grapefruit?"; "a tent and a cabin?"; "a bicycle and an
airplane?" and differences "What is the difference between a radio and a television?"
and "a river and a lake?"
Mini-Mental State Examination

The Mini-Mental State Exam (MMSE) is the most widely used cognitive test for
dementia. The examination takes approximately seven minutes to complete. It tests a
broad range of cognitive functions including orientation, recall, attention, calculation,
language manipulation, and constructional praxis.
A total maximal score on the MMSE is 30 points. Generally a score of less than 24
points is suggestive of dementia or delirium. The test is not sensitive for mild
dementia, and scores may be influenced by age and education, as well as language,
motor, and visual impairments.
161
Tutor should demonstrate to class how to complete this examination with a

volunteer.
Class should work in pairs to complete task.
MMSE on hospital patients are usually completed by Interns
162

Lower limb
Gait
Begin by testing gait if this is possible
Make sure the patients legs are clearly visible.
Now ask the patient to walk normally for a few metres and then to turn around quickly and
walk back.
Ask the patient to walk heel-to-toe [midline cerebellar lesion].
Ask the patient to walk on the toes [S1 lesion will make this impossible].
Ask the patient to walk on the heels [L4/L5 lesion causing footdrop will make this
impossible].
Ask the patient to squat and then stand up [proximal myopathy].
Ask the patient to stand erect with the feet together and the eyes open. Once the patient is
stable ask them to close the eyes. Compare steadiness shown with eyes open then closed.
Marked unsteadiness with the eyes closed is seen with cerebellar or vestibular dysfunction.
The Romberg test: a tendency to sway or fall while standing upright with the feet to-gether,
the arms outstretched and the eyes closed. A positive Rombergs sign suggests loss of
proprioceptive sensation.
Inspection
Inspect the legs with the patient lying in the bed and the legs and thighs entirely exposed.
If a urinary catheter is present this may indicate a spinal cord lesion.
The Motor system

Tone/Power/Coordination/Reflexes
163
Inspect for muscle wasting and fasciculation
Tone
Resistance felt when a joint is moved passively.
Patient must be relaxed lying on the bed.
Place your hands on the right leg below the knee and rock the leg gently from side to side.
The passive movements of the ankle are observed. Repeat on left side.
Place your hand under the knee and flex and extend the knee joint. Feel for resistance to
muscle stretch. When the patient is relaxed this should occur without resistance.
Normal tone can be assessed by repeated examination of normal people.
Tone may be increased [hypertonia] or decreased [hypotonia].
Now test for clonus.
Ankle clonus
This is sustained rhythmical contraction of the muscles when put under sudden
stretch. It is due to hypertonia from an upper motor neuron lesion.
Hold the leg with the knee bent and sharply dorsiflex the foot. When ankle clonus is present,
recurrent ankle plantar flexion movement occurs. This may persist for as long as the
examiner sustains dorsiflexion of the ankle.
Patellar clonus
To test for patellar clonus place your hands on the lower part of the quadriceps
with the knee extended and move the patella down sharply. Sustained rhythmical contraction
of the quadriceps occurs as long as the downward stretch is maintained.
Power
A measure of muscle strength
Age, gender and build should be taken into account
0 Complete paralysis
1 Flicker of contraction possible
2 Movement is possible when gravity is excluded [sideways]
3 Movement is possible against gravity but not if any further
resistance is added
4 Movement is possible against gravity and some resistance
6 Normal power
If power is reduced decide if it is symmetrical or asymmetrical and whether it is proximal,
distal or general.
Hip
Flexion
Ask patient to lift up their straight leg. Place your hand on the leg above the knee and attempt
to push the leg down saying to the patient do not let me push down your leg.
164
Extension
Ask the patient to keep the leg down and not to let you pull it up.
Abduction
Ask the patient to abduct the leg and not to let you push it in.
Adduction
Ask the patient to keep the leg adducted and not to let you push it out.
Knee
Flexion
Ask the patient to bend the knee and not to let you straighten it.
Extension
With the knee bent ask the patient to straighten the knee and not to let you bend it.
Ankle
Plantar flexion
Ask the patient to push the foot down and not to let you push it up.
Dorsiflexion
Ask the patient to bring the foot up and not to let you push it down.
Eversion
With the foot in complete plantar flexion ask the patient to evert the foot against resistance.
Inversion
Ask the patient to invert the foot against resistance
Toes
Plantar flexion
Ask the patient to plantar flex the big toe and not to let you push it up.
Dorsiflexion
Ask the patient to bring the big toe up and not to let you push it down.
Coordination
The cerebellum plays an integral role in coordinating voluntary movement. A number of tests
are used to test coordination.
Toe-finger test
Ask the patient to raise the foot with the knee bent and touch the examiners finger with the
big toe. Look for intention tremor.
Heel-shin test
165
Ask the patient to place one heel on the opposite knee and to slide the heel accurately down
the front of the shin to the ankle and back again at a moderate pace.
Foot-tapping test
Ask the patient to tap the sole of the foot quickly on the examiners hand; this movement is
slow and clumsy in cerebellar disease.
Reflexes
Make sure the patient is resting comfortably
Knee jerk
Slide the left arm under the knees so they are slightly bent and supported.
The tendon hammer is allowed to fall on to the infrapatellar tendon.
Contraction of the quadriceps causes extension of the knee.
pull
If the knee jerk appears to be absent it should be tested again following a

reinforcement manoeuvre. Ask the patient to interlock the fingers and then to
apart hard at the moment before the hammer strikes the tendon [Jendrassik
manoeuvre].
Ankle jerk
Have the foot in the mid-position at the ankle with the knee bent and thigh externally rotated.
The hammer is allowed to fall on the Achilles tendon. The normal response is plantar flexion
of the foot with contraction of the gastrocnemius muscle.
Plantar reflex
Use a blunt object such as a key. This is drawn slowly along the lateral border of the foot
from the heel towards the little toe until a response is elicited.
The normal response is flexion of the big toe at the metatarsophalangeal jointThe extensor
response is abnormal [Babinski response] and indicates an upper motor neurone lesion.
The reflexes can be recorded as follows:
0 Absent reflexes
+ Reduced reflexes
++ Normal reflexes
+++ Exaggerated reflexes
++++ Exagerated reflexes and clonus
Sensation
Light touch
Some fibres travel in the posterior columns [ipsilaterally] and the rest cross the midline to
travel in the anterior spinothalamic tract [contralaterally]
Use cotton wool to test for light touch. Initially touch the anterior chest wall [normal area];
this is to demonstrate to the patient how it feels.
Ask the patient to close their eyes and begin proximally on the upper leg and test in each
dermatome [memorise dermatomes] comparing right with left.
Ask
patient to tell you when they feel something.
166
Pain
Spinothalamic pathway fibres enter the spinal cord and cross a few segments higher to the
opposite spinothalmic tract.
Using a sharp object touch the patients anterior chest wall [normal area], this is to
demonstrate to the patient how it feels sharp.
Ask the patient to close their eyes and begin proximally on the upper leg and test in each
dermatome comparing right with left. Ask patient if they can
feel
object and if it feels sharp or dull.
Map out any area of dullness. Always do this by moving from area of dullness to the area of
normal sensation.
Vibration and proprioception

These fibres enter and ascend ipsilaterally in the posterior columns of the spinal cord to the
nucleus gracilib and nucleus cuneatus in the medulla, where they decussate.
Vibration
The base of a vibrating tuning fork is placed on the anterior chest wall. It should be explained
to the patient that it is the sensation of vibration and not cold or touch which is being
detected.
The base of the vibrating tuning fork is then placed on the dorsum of the terminal phalanx.
The patient is asked can they feel it vibrate and to indicate when vibration stops.
They are then asked to repeat this with their eyes closed. Stop the tuning fork
vibrating by touching it and the patient should be able to say exactly when this occurs.
Compare one side with the other.
Should vibration sense be lost or impaired distally then the tuning fork should be moved
proximallly in order to establish the level at which it is normally appreciated.
[Lateral malleolus, upper part of tibia, iliac crest, costal margin]
Proprioception
Grasp the distal phalanx from the sides and move it up and down to demonstrate these
positions. Then ask the patient to close the eyes while these manoeuvres are repeated.
Normally movement through even a few degrees is detectable, and should be reported
correctly.
If there is an abnormality, proceed to test the ankles and knees similarly.
Sensory level
If there is peripheral sensory loss attempt to map out the upper level.
This may involve testing over the abdominal or even the chest dermatomes.
Establishing a sensory level on the trunk indicates the spinal cord level that is affected.
The abdominal reflexes
167
Test these by lightly stroking the abdominal wall diagonally towards the umbilicus in each of
the four quadrants of the abdomen. Reflex contractions of the abdominal wall are
absent in upper motor neurone lesions above the segmental level.
They are also absent in patients who have had surgical operations interrupting the
nerves.
Ward tutorial
Upper limb
Inspection
Arms and shoulder girdles should be completely exposed.
Inspect the upper limbs and look for abnormal posture.
Look for muscle wasting and compare one side with the other.
Also look for abnormal movements such as a tremor in the wrist or arm.
General
Ask the patient to hold out both hands with the arms extended and the eyes closed.
Watch the arms for evidence of drifting [movement of one or both arms from the initial
neutral position].
Upper motor neurone lesion the drifting of the limb is due to muscle
weakness. The drifting downwards starts distally with the fingers and spreads
proximally.
Cerebellar disease the drift is due to hypotonia and is usually upwards.
Loss of proprioception the drift is due to loss of joint position sense and can
be in any direction.
Ask the patient to relax arms and rest them on their lap. Inspect for fasciculations. These are
irregular contractions of small areas of muscle which have no rhythmical pattern.
If present with weakness and wasting, fasciculation indicates degeneration of the lower motor
neurone e.g. motor neurone disease.
The Motor system

Tone/Power/Coordination/Reflexes
Tone
Resistance felt when a joint is moved passively.
Tone is tested at the wrists and elbows.
The patient should be told to relax and to allow the examiner to move the joints freely.
Flexion and extension of the elbow and wrist joint is performed passively.
Normal tone can be assessed by repeated examination of normal people.
Tone increased - hypertonic, as in an upper motor neurone lesion.
Tone decreased - hypotonic, as in a lower motor neurone lesion.
168
Power
A measure of muscle strength
Age, gender and build should be taken into account
0 Complete paralysis
1 Flicker of contraction possible
2 Movement is possible when gravity is excluded [sideways]
3 Movement is possible against gravity but not if any further
resistance is added
4 Movement is possible against gravity and some resistance
5 Normal power
If power is reduced decide if it is symmetrical or asymmetrical and whether it is proximal,
distal or general.
Shoulder
Abduction
With the elbows flexed ask the patient to abduct the arms.
The patient should resist the examiner pushing them down.
Adduction
The patient should adduct the arms with the elbows flexed.
The patient should resist the examiner separating them.
Elbow
Flexion
Ask the patient to bend the elbows and not to let you straighten it.
Extension
With the elbow bent ask the patient to straighten the elbow and not to let you bend it.
Wrist
Flexion
Ask the patient to flex the wrist and not to let you straighten it.
Extension
Ask the patient to extend the wrist and not to let you bend it.
Fingers
Flexion
The patient squeezes two of the examiners fingers.
Extension
The patient should straighten the fingers and not allow the examiner to push them down.
Abduction
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The patient should spread the fingers and not allow the examiner to push them together.
Coordination
The cerebellum plays an integral role in coordinating voluntary movement. A number of tests
are used to test coordination.
Finger-nose test
Ask the patient to touch their nose with the index finger and then to touch the examiners
outstretched finger at nearly full extension. The test should be done a number of times with
the patients eyes open and then closed.
Look for: 1] Intention tremor, which is tremor increasing as the target is
approached [cerebellar disease].
2] Past-pointing, where the patients finger overshoots the target
[cerebellar disease].
Rapidly alternating movements
Ask the patient to pronate and supinate their hand on the dorsum of the other hand as rapidly
as possible. In cerebellar disease this movement is slow and clumsy and is called
dysdiadochokinesis
Rebound
Ask the patient to lift rapidly the arms from the sides and then stop. Hypotonia from
cerebellar disease causes delay in stopping the arms.
Reflexes
Make sure the patient is resting comfortably
Biceps jerk
Place one forefinger on the biceps tendon and tap this with the tendon hammer. The hammer
should be held distally. There is brisk contraction of the biceps muscle with flexion of the
forearm.
If the biceps jerk appears to be absent it should be tested again following a
reinforcement manoeuvre. Ask the patient to clench their teeth tightly just
before you
let the hammer fall. Sometimes normal reflexes can only be elicited after
reinforcement, but they should be symmetrical.
Triceps jerk
Support the elbow with one hand and tap the triceps tendon. Triceps contraction results in
forearm extension.
Brachioradialis jerk
Place your first two fingers over the lower end of the radius just above the wrist. Strike the
fingers. Contraction of the brachioradialis causes flexion of the elbow.
The reflexes can be recorded as follows:
0 Absent reflexes
170
+ Reduced reflexes
++ Normal reflexes
+++ Exaggerated reflexes
++++ Exagerated reflexes and clonus
Sensation
Light touch
Some fibres travel in the posterior columns [ipsilaterally] and the rest cross the midline to
travel in the anterior spinothalamic tract [contralaterally]
Use cotton wool to test for light touch. Initially touch the anterior chest wall [normal area];
this is to demonstrate to the patient how it feels.
Ask the patient to close their eyes and begin proximally on the upper arm and test in each
dermatome [memorise dermatomes] comparing right with left.
Ask patient to tell you when they feel something.
Pain
Spinothalamic pathway fibres enter the spinal cord and cross a few segments higher to the
opposite spinothalmic tract.
Using a sharp object touch the patients anterior chest wall [normal area], this is to
demonstrate to the patient that it feels sharp.
Ask the patient to close their eyes and begin proximally on the upper arm and test in each
dermatome comparing right with left.
Ask patient if they can feel object and if it feels sharp or dull.
Map out any area of dullness. Always do this by moving from area of dullness to the
area of normal sensation.
Vibration and proprioception

These fibres enter and ascend ipsilaterally in the posterior columns of the spinal cord to the
nucleus gracilis and nucleus cuneatus in the medulla, where they decussate.
Vibration
The base of a vibrating tuning fork is placed on the anterior chest wall. It should be explained
to the patient that it is the sensation of vibration and not cold or touch which is being
detected.
The base of the vibrating tuning fork is then placed on one of the distal interphalangeal joints.
The patient is asked can they feel it vibrate and to indicate when vibration stops.
They are then asked to repeat this with their eyes closed. Stop the tuning fork
vibrating by touching it and the patient should be able to say exactly when this occurs.
Compare one side with the other.
171
Should vibration sense be lost or impaired distally then the tuning fork should be moved
proximally in order to establish the level at which it is normally appreciated.
[Ulnar head at wrist, olecranon at elbow and then the shoulders]
Proprioception
Grasp the distal phalanx from the sides on the patients index finger and move it up and down
to demonstrate these positions. Then ask the patient to close the eyes while these
manoeuvres are repeated. Normally movement through even a few degrees is
detectable, and should be reported correctly.
If there is an abnormality, proceed to test the wrists and elbows similarly.
UMNL
Increased(hypertonic)+/clonus
Spasticity
Weak abductors/extensors
in upper limb
Tone
Power
Reflexes
Other
Increased(hyperreflexia)
Muscle wasting rare
LMNL
Decreased(hypotonic)
Flaccidity
Distal muscles
weakened more than
proximal
Decreased
Muscle wasting
Fasciculation
WARD TUTORIAL
Rheumatological history
The rheumatologic system includes diseases of the joints, tendons and muscles.
Some causes of Monoarthritis
Septic arthritis
Trauma
Gout
Haemarthrosis [haemophilia]
Some causes of polyarthritis
Rheumatoid arthritis
Connective tissue disease [systemic lupus erythematosus]
Infection viral
Spondylarthropathies :
1. Psoriatic arthropathy
2. Enteropathic arthropathy
3. Ankylosing spondylitis
4. Reiters Disease
Primary osteoarthritis
Gout
Pseudogout
Adult Stills disease
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History
Presenting complaint/history of presenting complaint
Ask about joint pain and swelling.
Arthralgia is the presence of joint pain.
1. Determine what joints are involved
2. Determine the pattern of joint involvement [bilateral, symmetrical,
migrating]
3. Are symptoms acute or chronic in nature?
4. Is pain getting worse or better? [progression]
5. Any precipitating factors [trauma]?
6. Ask about the presence of early morning stiffness and the length of
time that this stiffness lasts [morning stiffness can occur in
rheumatoid arthritis and other inflammatory arthropathies].
7. Enquire about the functional capacity of the patient - can they dress,
make a cup of tea [with rheumatoid arthritis of the hands function can
be severely limited].
8. Enquire about the impact of the illness on work, social life, mood,
9. Ask about systemic symptoms
10. Fatigue [connective tissue diseases]
11. Rash [SLE, facial butterfly rash]
12. Fever [connective tissue diseases]
13. Weight loss [scleroderma]
14. Diarrhoea [scleroderma]
15. Mucosal ulcers [rheumatoid arthritis/SLE]
Associations
Ask about Raynauds phenomenon
Disorder of the small arteries of the fingers and toes
Exposure to cold causes these arteries to narrow and decreased blood flow causes
digits to become cold and white
The pallor is followed by blueness [cyanosis]
Redness results as the arteries open and the blood flow returns
173
Raynauds phenomenon
Primary RP Primary RP or idiopathic Raynauds disease describes those

patients without a definable cause for their vascular events. Primary RP has an
age of onset between 15 and 30 years of age, is more common in women, and
may occur in multiple family members
Secondary RP Secondary RP refers to those patients with RP in whom an

associated disease or cause may underlie the attacks. More correctly termed
Raynauds Syndrome. Causes include:
1. Scleroderma
2. Systemic Lupus Erythematosus
3. Other connective tissue diseases (mixed connective tissue
disease, polymyositis, dermatomyositis, rheumatoid
arthritis, Sjgren's syndrome and vasculitis)
4. Occlusive vascular disease (arteriosclerosis,
atheroemboli, and thromboangiitis obliterans)
5. Drug-induced (amphetamines, beta-blockers, nicotine)
6. Haematological (Cold agglutinin disease,
cryoglobulinemia, paraproteinemia, and polycythemia)
7. Vibration-induced (pneumatic drills and hammers)
Ask about dry eyes (xerophthalmia) and mouth (xerostomia)

In Sjogrens syndrome, decreased exocrine gland function leads to the "sicca
complex", a combination of dry eyes (xerophthalmia) and dry mouth (xerostomia). In
addition, a wide variety of extraglandular disease features can occur in SS. Dry eyes
can result in conjunctivitis/corneal ulcers. Dyspareunia may also occur, due to vaginal
dryness. Dry cough and enlargement of the salivary glands may also be present.
Ask about red eyes
This can occur with:
1. iritis which may complicate seronegative spondyloarthropathies [psoriatic
arthritis, Reiters disease, ankylosing spondylitis]
174
2. scleritis [ RA, SLE]

3. scleromalacia Scleral thinning due to chronic scleritis [RA]
Septic arthritis
Trauma
Gout
Haemarthrosis [haemophilia]
o Inflammatory bowel disease can result in arthritis
o
o Psoriasis can cause psoriatic arthropathy
175
Arthritis mutilans in psoriatic arthropathy
o Tick bite may indicate Lyme disease
o
o History of STI [gonorrhoea monoarthritis]
o Enquire about physiotherapy/joint surgery
o Previous endocarditis/pericarditis [SLE]
o Heart failure [due to valvular disease in SLE, right-sided heart failure due
to advanced pulmonary fibrosis]
o Respiratory disease [pulmonary fibrosis in RA/SLE, pulmonary
hypertension, pleurisy in SLE]
o Renal disease [proteinuria, nephritic syndrome secondary to
gold/penecillamine, glomerulonephritis in SLE, renal vascular disease in
scleroderma]
o HTN- can complicate RA, SLE, scleroderma if renal involvement
Medication/Allergies
Anti-arthritic medications:
1. Analgesics NSAIDs
2. Steroids oral, intra-articular
3. DMARDS azathioprine, gold, penecillamine, captopril
4. Anti-TNF alpha agents
Anti-ischaemic agents [SLE accelerates coronary heart disease]
Social History
If the patient has a chronic disabling arthritis determine the patients domestic
setup/support
Bungalow/two-storey
Bedroom/bathroom - upstairs/downstairs
Stairs access rails, chairlift, etc.
Walking aids
176
Ramps/wheelchair access
Modified bath/walk-in shower
Modified domestic tools, grooming instruments
Smoking history poor prognostic indicator in Rheumatoid Arthritis

Alcohol history
Home supports carers, specialist nurse, outpatient physiotherapy, occupational
therapy.
Recent foreign travel [tick-infested regions, Lyme disease]
177
Sexual history [gonococcal septic arthritis]

Intravenous drug use [Increased risk of staphylococcal aureus septic arthritis]
Family History
Ask about family members with diseases associated with arthritis
Gout
Osteoarthritis
Spondylarthropathies
Other autoimmune disease
Review of Systems
Many rheumatological disorders can have varied and extensive systemic manifestations.
A thorough review of systems is necessary to elicit the severity and extent of any extraarticular disease.
CVS symptoms of heart failure/endocarditis
Respiratory dry cough, dyspnoea [fibrosis], pleuritic chest pain [pleurisy]
CNS Dysphasia, motor or sensory disturbance, unsteadiness indicative of TIAs/Strokes
[thromboemboloic phenomenon increased in SLE, due to antiphospholipid syndrome and
cerebral vasculitis in SLE/RA]. Seizures, cognitive impairment [SLE]
GIT Dysphagia, constipation, diarrhoea, abdominal pain [scleroderma], Oral ulcers
[palatal ulcers in SLE, aphthous ulcers in UC, secondary to drugs used in RA [gold,
steroids], ulcers due to Reiters disease
GUT dysuria, haematuria, circinate balanitis [Reiters disease], and calculi [associated
with gout]
Endocrine symptoms of DM, thyroid disease, Addisons disease [autoimmune in origin]
BACK PAIN
LEARNING OBJECTIVES:
At the end of this tutorial you should be able to:
1. Define back pain
2. List the risk factors for back pain
3. Take a history from a patient with back pain, addressing the points
which will help to narrow the differential
4. Perform physical examination focussing on the features which may
be associated with each of the likely differentials.
5. Choose and justify appropriate investigations of the patient with
back pain.
DEFINITION: (also known as "dorsalgia") is pain felt in the back that usually
originates from the muscles, nerves, bones, joints or other structures in
thse spine.
DIFFERENTIAL DIAGNOSIS:
Trauma
o Strain/sprain
o Whiplash injury
o Falls
178
Mechanical/Degenerative
o Hypermobility Ehlers Danlos syndrome, Marfans syndrome
o Scoliosis/kyphosis
o Sacroiliitis
o Spinal stenosis
o Rheumatoid arthritis
o Osteoarthritis
Malignancy
o Primary bone tumours
o Metastatic
Infection/inflammation
o Osteomyelitis S. aureus, tuberculosis, brucellosis
o Spinal epidural abcess
o Septic disk
o Meningitis
o Lumbar arachnoiditis
Metabolic
o Osteoporosis hyperparathyroidism, immobility
o Osteosclerosis Pagets disease
Vascular
o Abdominal aortic aneurysm
o Vertebral artery dissection
Others
o Referred pain from visceral disease
o Postural
o Sickle cell crisis
o Psychogenic, malingering, chronic pain syndrome
o Urinary tract infection/Pyelonephritis
o Pelvic inflammatory disease
o Herpes zoster
Red flags" for a potentially serious underlying cause for low back pain
Preceding episode of trauma
Unintentional weight loss
History of malignancy
IV drug abuser
Immunosuppressives therapy, osteoporosis
Age >70 years
Progressive or disabling neurological deficit
(2)
5 Types of Back Pain:
Local pain due activation of pain nerve-endings from

tears/stretching
Referred pain usually abdominal or pelvic origin, pain unaffected
by spine movement
Radicular pain radiates from spine to the leg. Coughing,
sneezing, lifting heavy objects or straining may elicit pain
Pain of spine origin restricted to the back and referred to the
lower limb. Diseases originating from the upper lumbar spine refer
179
pain to upper lumbar region, groin or anterior thighs. Diseases of

lower lumbar spine refer pain to buttocks or posterior thighs.
Pain associated with muscle spasm accompanied by taut
paraspinal muscles.
HISTORY:
Onset of pain acute/progressive, post-trauma

Location and exact point of the pain
Character of the pain sharp, shooting, dull constant
Radiation of pain/discomfort
Timing of pain
Severity of pain (scale out of 10), associated disability
Relieving factors
Associated symptoms extra-articular symptoms,
constitutional/systemic symptoms
The impact of the pain in patients daily activities, functional
capacity
Medications history steroids treatment
Symptoms
Back pain radiating down the buttock and
below the knee
Back pain at night, unrelieved by rest or

change in position/posture
Back pain aggravated by activity and

improves with rest
Back pain that worsens with rest and
improves with activity
Pathology
-Herniated disk causing nerve
root irritation
-Sacroiliitis
-Facet joint degenerative
arthritis
-Spinal stenosis
-Sciatic nerve irritation
-Malignancy (either a
vertebral body metastasis or
cauda equina tumour)
-Compression fractures
(multiple myeloma,
osteoporosis)
-degenerative bone diseases
-Ankylosing spondylitis
-Seronegative
spondyloarthropathies
EXAMINATION:
Inspection look for abnormality of posture i.e. scoliosis or
kyphosis, scars, skin lesions
Passive range of motion - flexion and extension, adduction,
abduction
Palpation of the back - to elicit vertebral or soft tissue
tenderness, bony deformities
Straight leg raising - The test is considered positive when the
sciatica is reproduced between 10 and 60 degrees of elevation. A
positive straight leg test is sensitive, but not specific, for herniated
disc.
180
Neurologic testing if prolapsed disc is suspected, neurologic

testing should be performed
L5 motor nerve root testing evaluates strength of ankle and
great toe dorsiflexion. L5 sensory nerve root damage would
result in numbness in the medial foot and the web space
between the first and second toe.
The S1 nerve root is tested by evaluating ankle reflexes and
sensation at the posterior calf and lateral foot. S1 radiculopathy
may cause weakness of plantar flexion, but is difficult to detect
until quite advanced. One strategy is to have the patient rise up
on tip-toe three times in a row, on one foot alone and then the
other.
Observe the gait pattern
antalgic gait
wide-based gait (suggests unsteadiness)
leaning forwards/stiff legged (spinal stenosis)
shuffling (Parkinsonism)
foot-drop (suggest L5 or S1 nerve root compression)
flat-feet, hind feet valgus and genu recurvatum on stance
phase might suggest hypermobility associated with various
low back lesions
INVESTIGATIONS:
Blood tests (CBC, ESR, CRP) raised WCC, ESR and CRP in
spinal infection or malignancy
Blood culture if infection is suspected as the cause of back
pain
Plain radiographs fractures, malignant infiltrations,
osteomyelitis, narrowed disc spaces, degenerative changes and
spondylolidthesis
Tumour markers raised tumour markers with underlying
malignancies
Serum Ca raised calcium in myeloma, hyperparathyroidism
MRI or CT urgent when the clinical examination suggests
underlying cord compression. MRI is a better initial test for most
patients with low back pain who require advanced imaging,
though CT scan gives better definition of bony structures.
Myelogram - useful in patients with multiple disc abnormalities,
multilevel radiculopathies, extruded free disc fragments, a disc
fragment in the lateral recess, or previous lumbar surgery
DIAGNOSTIC ALGORITHM
FOR
LOW BACK PAIN
181
Algorithm taken from http://www.uptodate.com/online/content/image.do?

imageKey=PC%2F22468
WARD TUTORIAL
Rheumatological examination 2
The rheumatological system includes diseases of the joints, tendons and muscles.
Temporomandibular joints
Look just in front of the ear for swelling.
Palpate by placing a finger just infront of the ear and ask the patient to open and close
their mouth. The head of the mandible is palpable as it slides forwards when the jaw
is opened.
Rheumatoid arthritis commonly affects the temporomandibular joint and may cause
clicking, grating and tenderness of the joint.
182
The Back
With the patient standing and wearing only underwear look for abnormal
posture/deformity.Look from the back, front and the sides.
1.
2.
3.
4.
5.
Cervical spinous process C1

Lumbar spinous process, L2
L3/L4 intervertebral space
Iliac crests
Sacro-iliac joints (dimple of Venus)
Note loss of the normal thoracic kyphosis and lumbar lordosis.

Look for scoliosis [spinal deformity, a lateral curvature of the spine]
Palpate each vertebral body for tenderness. Gentle percussion with the fist may elicit
it.
Actively assess movement

Flexion; ask the patient to touch their toes with the knees straight.
Extension; ask the patient to lean backwards.
Lateral flexion/bending; ask the patient to slide their right hand down the right leg as
far as possible without bending forward and then to do the same on the left side.
Rotation; with the patient sitting ask them to rotate the head and shoulders as far as
possible to each side.
Measure the lumbar flexion with Schobers test
183
A mark is made at the level of the sacro-iliac joints on the vertebral column [approx
L5, no 2 in image]
One finger is placed 5cm below the mark and another 10cm above the mark.The
distance between these two marks is then measured.The patient is then asked to touch
their toes.
An increase of less than 5cm in the distance between the 2 fingers indicates limited
184
Straight leg raising

With the patient lying down lift the patients straight leg.
The test should be performed slowly and the patient told to report as soon as it
becomes painful.
Normally 90 degrees of flexion at the hip should be possible.
This will be limited by pain when the nerve root is stretched round or over a prolapsed
disc.
Lasegues Test
When the limit of straight leg raising has been achieved, further tension on the root is
caused by dorsiflexing the ankle. If positive the pain is aggravated and is felt in the
back of the leg, radiating into the lumbar region in some instances. This is usually dur
to sciatic nerve compression.
Femoral Stretch Test

With the patient lying prone, flex the knee to its limit of movement. In a positive test,
the patient will feel pain in the ipsilateral anterior thigh, i.e. the distribution of the
femoral nerve.
185
Sacro-iliac joints
These are involved in an early stage of ankylosing spondylitis.
Ask the patient to lie on their stomach.
Firm palpation with both palms overlying each other may elicit tenderness in
sacroiliitis.
The Hips
Pain arising from the hip is most commonly situated in the groin, but may radiate
down the thigh to the knee or be present in this joint alone.
Move the hip joint passively with the patient lying on their back.
The pelvis must be immobilised to ensure that movement being measured is coming
from the hip alone and not also from the pelvis on the spine.
Flexion
The iliac crest is stabilised with one hand while the other grasps the leg.
Flex the patients knee and move the thigh towards the chest.
Rotation is tested with the knee and hip flexed.
The foot is moved medially - external rotation of the hip.
The foot is moved laterally internal rotation of the hip.
Abduction
The right hand holds the heel of the right foot while the left hand is placed over the
opposite anterior iliac crest to steady the pelvis. The leg is then moved outward as far
as possible.
Adduction
The leg is carried immediately in front of the other limb.
Extension
Ask the patient to roll over on to their stomach.
Place one hand over the sacroiliac joints while the other hand raises each leg.
Trendelenburgs Test
Ask the patient to stand.
Now ask them to stand first on one leg and then on the other.
When the normal subject stands on one leg, the abducters contract so that the opposite
side of the pelvis is tilted slightly up. If the patient stands on the affected leg when the
186
actions of the abducters are deficient, the opposite side of the pelvis will tilt
downward and balance can be maintained only by leaning over towards the side of the
lesion.
The test is performed with the patients back to the examiner.
This test is useful in the late stages of congenital dislocation of the hip and in
poliomyelitis affecting the lower leg.
Measurement of leg length
True leg length from the anterior superior iliac spine to the medial malleolus
The cause of
the apparent leg length difference is the contracture ( permanent shrinkage) of the soft
tissues and of the abductor musculature (the gluetus and tensor fasciae muscles
When true shortening is present the normal limb must be measured in a comparable
position to the abnormal one, in respect to abduction or adduction for accuracy.
Apparent leg length from the umbilicus to the medial malleolus
187
Where a fixed deformity of the hip joint is present and the legs are brought parallel,
the limbs will apparently be unequal in length. The amount of apparent shortening is
measured from the umbilicus to the medial malleolus.
Fracture of the neck of the femur the limb is externally rotated, adducted and
shortened. This is common in the elderly, especially women.
The knee
With the patient lying down expose both legs.
Look for wasting of the quadriceps and swelling and deformity of the knee joint.
Swelling of the synovium is usually seen medial to the patella and in the joints
suprapatellar extension.
Palpate the quadriceps for wasting and the knee joint for warmth and tenderness.
The patellar tap
This is used to confirm the presence of a moderate/large effusion.
One hand lies over the lower part of the quadriceps and compresses the suprapatellar
bursa which is emptied.(milking the suprapatellar pouch). The other hand pushes the
patella downwards. The sign is positive if there is sufficient fluid to allow the patella
to tap off the femur.
The active range of movement is tested first in the normal and then in the abnormal
knee.
Passive movement is then tested in the same way. Place a hand on the knee to detect
the presence of crepitus.
188
Tests of stability
The lateral and medial collateral ligaments
The patients ankle is held between the examiners elbow and side.
This leaves both hands free to abduct and adduct the tibia on the femur while keeping
the knee straight. Normally no movement should be present.
The cruciate ligaments
Anterior Drawer Test
With the knee flexed to a right angle the examiner sits on the patients foot, or enure
the foot is stabilised, and in the neutral position.
To test the anterior cruciate the tibia is grasped just below the knee and is drawn
forward (anteriorly).
Excessive anterior movement is due to laxity of the anterior cruciate.
Lachmans test.
This is the most sensitive test for anterior cruciate ligament injury.
The examiner uses the right hand to place anterior force on the lower leg while
simultaneously using the left hand to place posterior force on the distal thigh. A good
end point should be felt. Hands are reversed to test the left knee. Excessive laxity
indicates an anterior cruciate ligament tear.
189
Posterior Drawer Test

To test the posterior cruciate, this movement is reversed.
Excessive posterior movement is due to laxity of the posterior cruciate.
Stability of the patella

With the knee extended the patella is grasped and moved from side to side.
The ankles and feet

Look for swelling, deformity and muscle wasting.
Hallux valgus fixed lateral deviation of the main axis of the big toe.
Ankle dorsiflexion raise the foot up

Plantar flexion push foot down
Hip examination
HISTORY
190
It is important to bear in mind the following points when performing a hip examination:
Age of the patient

o Younger patients - traumatic injuries, osteonecrosis and developmental dysplasia of
the hip are more prevalent
o Older patients - hip fractures and osteoarthritis are more common
Mechanism of injury
Duration of problem
CLINICAL EXAMINATION
Follow the scheme below:
Inspection
Palpation
Measurment
Movement
Before starting
Introduce yourself
Explain what the examination entails
Ask permission to perform examination
Expose the patient appropriately - from waist down exposing both the lower limbs, but leaving
the underwear on
Preserve dignity by using a blanket appropriately
Tell the patient to let you know if anything you do is uncomfortable
Remember - always watch the patients face
Inspection
General observation
o Does the patient look well?
o Is there a walking stick? Frame?
o Is there a shoe raise?
o Hands (Rheuamtoid arthritis?)
Patient Standing
Remember to inspect from all sides (front, laterally and from behind):
o Skin
Scars (previous injuries or surgical scars)
Sinuses (secondary to TB or infected hip replacements)
Colour - discolouration?
o Deformity
Abduction / adduction contracture
Fixed flexion deformity
Limb shortening
Limb rotation
Scoliosis
Lumbar lordosis
o Swelling (the hip joint is deep and thus swelling is not generally seen)
o Muscle wasting - look at the gluteal folds
gluteals? quadraceps?
o Pelvic obliquity (anterior superior iliac spines (ASIS) not horizantal)
Is there a leg length discrepancy?
Is there a fixed deformity?
191
Patient Walking
Observe the patient walking.

o Gait pattern. There are different types of gait:
Stiff hip (pelvis swing)
Antalgic (short stance phase)
Short leg
Trendelenburg (Lurching gait, watch the shoulders)
Drop foot gait
Broad based gait (ataxia)
o Stride length
o Use of a walking aid
Patient Lying down - supine with one pillow under the head
Observe the patient climb onto the examination couch

Deformity
o Rotational deformity is common in osteoarthritis (observe the position of the patella
and foot on either side)
o Fixed flexion deformity (look at the angle between the thigh and the bed). Perform
Thomas's test at this stage (see below)
o Abduction / Adduction deformity (adduction deformity - tilted pelvis and apparent
shortening of that leg)
Detailed check:
o Skin - scars
Palpation
Ask the patient.."Does it hurt anywhere?"
Skin temperature (use dorsal surface of your hand to compare temperatures over both hips)
Is there tenderness over the bony landmarks?
o Anterior and posterior superior iliac spines
o Ischial Spine
o Greater Trochanters (trochanteric bursitis)
o Iliac crests
o Ischial tuberosity (hamstring tear)
o Pubic Tubercle
Is there tenderness of the soft tissues?
o Muscles
o Femoral triangle
Joint line tenderness (beneath the mid inguinal point)
Measurement
Before measuring, if a fixed deformity of one leg has been observed, the unaffeted leg should be placed
in the same position as the one affected to make them identical.
The different types of measurements to be taken are:
Apparent length - the distance between the xiphi-sternum (a fixed point) and the medial
mallelous.
True length - the distance between the ASIS and the medial malleolus
Circumference of the quadriceps at a fixed point (from the tibial tuberosity).
If a difference has been observed in true leg length measurements, it is important to determine whether
the shortening is above (femoral) or below (tibial) the knee:
192
Having asked the patient to bend their knees, keeping their ankles together, compare the
position of both knees.
Movement
These should be performed both actively and passively for both legs. When assessing hip movements,
it is important to fix the pelvis and prevent any movement taking place at this anatomical structure. This
is done either by dropping one leg over the edge of the couch and assessing movements of the other
leg, or by placing one forearm between the ASIS's.
Active movement
Flexion (0-130o)- "Can you bring your heel to your bottom?"

Extension (0-10o) - Having asked the patient to lie prone, ask them to raise each leg off the bed
with the knee straight.
Abduction (0-45o) - "Can you move your leg away from the bed?"
Adduction (0-30o) - "Can you move your leg across your other leg"
Passive movements
Repeat the above movements but additionally testing for hip rotation.
Rotation - With each leg in turn, flex both hip and knee to 90o , and having stabilised it with one
hand, move the heel first outwards (internal rotation - 0-45o) and inwards (external rotation - 045o) with the other hand.
Special Tests
There are two special tests:
Trendelenburg test - test of abductor function (gluteus medius weakness)
Stand behind the patient and identify the iliac crests

Have another person in front of the patient for balance
Ask the patient to stand on the normal and then the affected leg by flexing the knee rather than
flexing the hip. This is for testing the abductors on the opposite side.
Watch for the patients' response in terms of balance (truncal position) and pelvic tilt
Negative test (normal)
o If pelvis stays level or rises slightly, with the trunk staying over the pelvis (i.e. staying
over the centre of gravity), AND can be maintained for 30 seconds.
Positive test (abnormal)
o The patient is unable to hold pelvis level and maintain this for 30 seconds.
o The patient leans over to the affected side, in order to keep their centre of gravity over
their foot
For further information about performing a Trendelenburg test, please Click Here.
Thomas' test - test for fixed flexion deformity
With the palm up, place your hand beneath the lumbar spine
Passively flex the unaffected hip until the hollow of the lumbar spine is eliminated
The affected leg rises up from the bed, if there is a fixed flexion deformity present.
Repeat for the other side
Finally
Check distal neurovascular supply.
193
Examination of the patient with Rheumatoid Arthritis (RA)

The general principles of examining a joint:
1) Inspect from the front, back and sides:
Skin
Erythema: Suggests active inflammation or infection
Scars: Previous joint replacement or tendon repair.
Rash: Psoriasis is associated with Psoriatic arthritis, an
important differential diagnosis for RA.
A vasculitic rash is associated with multisystem inflammatory
conditions including RA, SLE, and Sjogrens syndrome etc.
Psoriasis
Joint
Vasculitis
Swelling: Can be due to hypertrophy of the synovial

membrane, effusion or bony swelling caused by overgrowth of
the bony joint margins.
Deformity: See below for individual joints.
Abnormal bony alignment: Dislocation or subluxation (partial
dislocation)
Muscle wasting
2) Palpate the joint

You must at all times watch the patients face while palpating, looking for
signs of discomfort
Warmth: A sign of active synovitis, infection or crystal arthritis such as

Gout.
Tenderness: Remember to watch the face.
Swelling
Synovial swelling is boggy or spongy
Joint effusion swelling is fluctuant. The fluid can be shifted
within the joint
194
Bony swelling is hard.

3) Move the joint
Passive movement
Check for limitation of movement in any direction (fixed
flexion or fixed extension deformity). Measurement of
movement range is also useful.
Check for crepitus: A grating sensation from the joint as it is
moved. It indicates irregularity in the articular surfaces.
Check joint stability: This tests the integrity of the joint and
surrounding ligaments. It is tested by gentle attempt to move
the joint in abnormal directions.
Active movement is used to assess integrated joint function.
Rheumatoid Arthritis (RA) patient

Rheumatoid arthritis eventually affects the peripheral joints in almost all patients.
Involvement of axial and central joints, such as the atlantoaxial joint of the neck,
acromioclavicular, sternoclavicular, temporomandibular, cricoarytenoid joints, and
shoulders and hips is less common.
General inspection
Obvious deformity or asymmetry

Posture
Characteristic appearance such as Cushingoid facies
Rashes (as above)
Eye involvement may be evident ( Red eye due to iritis or scleritis)
Walking aides
The hands
Inspection: With patients hands supported by a white pillow for comfort.
Start with the dorsal aspect from proximal to distal looking at skin and nails and
check for swelling, erythema, skin atrophy, deformity, abnormal bony alignment,
muscle wasting, rash, scars and nail changes.
-
Vasculitic changes around the nail folds 1-2mm lesions due to skin
infarction
Splinter haemorrhages due to vasculitis
195
Wasting of the small muscles of the hands wasting of intrinsic muscles

with hollow ridges between the metacarpal bones
Joint swelling - Photo shows swelling and early damage from rheumatoid
arthritis
Wrist
-
Ulnar styloid prominence
Metacarpophalangeal joints
Ulnar deviation deviation of the phalanges at the
metacarpophalangeal joints towards the medial [ulnar] side of the
hand.
Volar subluxation [palmar subluxation of the fingers]
Proximal and distal interphalangeal joints
196
Changes due to joint destruction and tendon dysfunction
Swan neck deformity

Boutonniere deformity
Z thumb deformity
Palmar aspect of the hands
Palmar erythema: Also occurs with liver disease, polycythemia,

thyrotoxicosis, pregnancy.
Palmar crease pallor: Anaemia (Anaemia of chronic disease,

associated pernicious anaemia, secondary to GI bleeding due to
NSAIDS, due to disease modifying drugs used to treat RA, due to
hypersplenism).
Surgical incisions (tendon repair)
Muscle wasting
Palpation (Palpate joints from proximal to distal with the palms down): Feel
all joints in the hand individually.
Tenderness, heat, and the character of the swelling observed. Note that
synovial inflammation feels boggy, effusion is fluctuant.
Move the joint
Passive movement first
197
Move all joints gently in their normal plane of movement. Start from the wrist
and move distally.
Check for tenderness on movement, limitation of movement, and

crepitus.
Test for trigger finger. The distal interphalangeal joint gets stuck in
flexion.
Test for volar subluxation (partial dislocation) of the
metacarpophalangel joints (MCPs). This is done by flexing the joint
with the proximal phalanx held between the thumb and forefinger.
Test for carpal tunnel syndrome tap over flexor retinaculum [Tinels
sign]
Active movement and functionality of the hand
Test all joints active movement in normal planes starting with the
wrist, MCP, PIP, DIP joints.
Test thumb movements independently as it is a major cause of
disability when impeded.
Hand function tests include:
Grip strength (Ask patient to squeeze your first two fingers)
Opposition strength (Ask patient to hold piece of paper
between thumb and forefinger and prevent you from pulling it
free)
Key grip
Thumb opposition to other fingers
Practical tasks like writing and buttoning up shirt.
Examination of the hands is not complete without feeling for subcutaneous nodules
near the elbows.
The arms
Inspection
Scars, erythema, rash.

Rheumatoid nodules: The examination of the rheumatoid hands is incomplete
without checking for rheumatoid nodules at the elbows. They occur in
approximately 25% of patients with RA. They are hard to touch and can be
differentiated from gouty tophi in that the latter appear yellow under the skin.
198
Examination of the elbow and shoulder joints (These will be demonstrated in

class, only point notes are included here).
Remember: Look, feel, move.

It is very useful to watch the patient remove top here as it gives an idea of
limitation of movement and functionality as well as discomfort.
Elbow
Inspection:
Subcutaneous nodules (RA, gout).
Enlarged bursa (fluid).
Colour of nodules (yellow: gout).
Swelling (joint effusion).
Psoriasis on elbows (psoriatic arthritis).
Palpation:
Warmth.
Lateral epicondyle tenderness (tennis elbow).
Medial epicondyle tenderness (golfer's elbow).
Enlarged bursa (fluid).
Nodules: hard (RA) or firm (gout).
Motion:
Flexion [normal: 150]
Shoulders
Inspection:
Swelling.
Palpation:
Warmth.
Tenderness: localized or diffuse.
Swelling.
Axillary nodes (RA).
Motion, asking if painful:
Abduction [normal: 90].
Adduction [normal: 50].
Flexion [normal: 180].
Extension [normal: 60].
External rotation [normal: 60].
Internal rotation [normal: 90].
Pain during movement:

All directions [intra-articular]
One direction [inflamed tendon]
No pain, only weakness [lesion to tendon or nerve]
The head
Eyes:
199
Anaemia
Cataracts (Occur in this setting secondary to long-term steroid treatment)
Dry eyes (Sjogrens syndrome occurs in about 10% of RA cases)
Scleritis and episcleritis (Scleral redness secondary to rheumatoid lesions
affecting the sclera ( Purple / red lesions which are pathologically rheumatoid
nodules)
Scleromalacia (Due to scleral thinning in severe cases).
Fundus ( Hyperviscosity can lead to venous or arterial occlusion)
Mouth:
Dry mouth (Sjogrens syndrome)

Ulcers (Drug treatment with Gold)
Face:
Parotid gland swelling (Sjogrens syndrome)

Examination of the temporomandibular joint:
Look for swelling in front of the ear
Palpation with the examiner standing behind the patient: Feel for
tenderness, crepitus when the patient opens and closes the mouth.
The neck
Examination of the cervical spine

Inspect and note any postural abnormalities.
Palpate the individual spinous processes. Feel for
tenderness and uneven spacing of the processes.
200
Ask the patient to move the neck actively, note any

limitation.
Touch your chest with your chin (flexion), Look up at ceiling (extension), Touch each
shoulder with ear (lateral bending) and finally rotation.
Cervical spine involvement can produce upper limb

neurological deficit. So neurological exam of the upper
limb is part of the neck assessment.
The chest
Heart:
Pulsus paradoxus (Constrictive pericarditis)

Elevated JVP (Constricitve pericarditis)
Impalpable apex beat (Constricive pericarditis)
Auscultate for
Pericardial friction rub (Acute
pericarditis)
Distant heart sounds (pericardial
effusion)
Regurgitant murmurs especially of aortic
valve.
Peripheral oedema ( Constricive pericarditis)
Lungs:
Palpation:
Limitation of chest expansion (Fibrosis)
Unequal expansion (Fibrosis or effusion)
Tracheal deviation (towards fibrosis away from effusion)
Percussion: Assess for stony dullness (effusion)
Auscultation:
Reduced or absent breath sounds in the base (effusion)
Fine pan inspiratory or late inspiratory crackles (Fibrosis)
[Caplans syndrome is the presence of rheumatoid lung nodules in combination

with pneumoconiosis]
Pulmonary fibrosis on CXR
201
The abdomen
Splenomegaly (Occurs in 10% of patients with RA and may

Feltys syndrome)
suggest
Feltys syndrome: Triad of RA, splenomegaly, and

granulocytopenia. Although many patients are asymptomatic,
some develop serious and life-threatening infections secondary
to granulocytopenia.
Hepatomegaly ( May occur secondary to treatment with

Methotrexate)
The lower limbs
Inspect for rashes, erythema, scars, muscle wasting and joint swelling
Examine the hips, knees and foot joints (hips and knee examination
to be covered in ward tutorials)
Look for foot drop [peroneal nerve entrapment or vasculitis] and
examine the ankle joint for limitation of movement.
Signs of cord compression due to anterior dislocation of the first
cervical vertebra or subluxation of the odontoid process. Here upper
motor neuron signs occur in the lower limbs mixed with lower motor
neuron signs in the upper limbs.
CLINICAL FEATURES
OF
RHEUMATOID ARTHRITIS
At the end of this tutorial, you should be able to:
1. Define rheumatoid arthritis
2. List the diagnostic criteria for rheumatoid arthritis
3. Form a differential diagnosis for rheumatoid arthritis
4. Examine patients with RA, in order to:
1. Assess disease severity
2. Look for complications
deforming arthropathy.
202
DEFINITION:
Rheumatoid arthritis (RA) is a chronic, systemic, inflammatory disease of
unknown aetiology involving not only the joints but other organs. The
pattern of joint involvement is typically symmetrical, may be remitting and
can lead to destruction of joints due to erosion of cartilage and bone which
leads to deformity (1).
Diagnostic criteria
The American College of Rheumatology has defined the following criteria
for the classification of rheumatoid arthritis (2):
Morning stiffness of >1 hour most mornings for at least 6 weeks.
Arthritis and soft-tissue swelling of >3 of 14 joints/joint groups
present for at least 6 weeks
Arthritis of hand joints, present for at least 6 weeks
Symmetric arthritis, present for at least 6 weeks
Subcutaneous nodules in specific places
Positive rheumatoid factor titre
Radiological changes suggestive of joint erosion
At least four criteria have to be met for classification as RA
Osteoarthritis typically affecting larger joints, asymmetrical
distributions
Gouty arthritis tender joints especially the metatarsophalangeal
joints, crystal deposits over the small joints of the hands, pinna,
Achilles tendon
Psoriatic arthropathy scaly silvery plaques, asymmetrical
distributions, telescoping of interphalangeal joints in severe disease
Chronic juvenile arthiritis radial deviation, negative rheumatoid
factors
Infectious arthritis Infectious arthritis is usually monoarticular,
but polyarthritis can occur.
Paraneoplastic disease Joint pain or frank polyarthritis can occur
in association with malignancy
HISTORY:
Age, occupation, sex (RA commoner in women)
Presenting symptoms
Joints
o Degree of pain
o Duration of morning stiffness and pattern
of distribution, swelling, loss of function
Extra-articular/systemic symptoms
o signs such as fever, anorexia, malaise,
weight loss, lethargy (due to anaemia)
o skin palmar erythema, Raynauds
phenomenon, rheumatoid nodules
o painful eyes (scleritis)
Disease modifying drugs, NSAIDS
EXAMINATION:
Inspection
203
Face - Cushingoid from steroids treatment

Eyes - Conjunctival pallor, episcleritis, uveitis, dry eyes
(Sjogrens syndrome), scleromalacia, cataracts (steroid or
chloroquine therapy)
o Mouth xerostomia (Sjogrens syndrome)
o Skin - rheumatoid nodule, vasculitis (microinfarcts around the
nailfolds), livedo reticularis, pyoderma gangrenosum,
erythema nodosum, scars, atrophy of digital skin, diffuse
thinning (rice paper skin), and skin fragility (often worsened
by corticosteroid use), Raynauds phenomenon,
o Joints swelling, erythema, ulnar deviation, boutonniere
deformity,
swan
neck
deformity
and "Z-deformity"
(hyperextension of the interphalangeal joint, and fixed flexion
and subluxation of the metacarpophalangeal joint), muscle
wasting, ulcers,
Palpation
o Enquire patient whether any joint is tender
o Assess degree of joint tenderness and tissue swelling
o Palpate for tenderness and rheumatoid nodules (radius)
Movement
o Active and passive joint movement
and the range of
movement noted
o Joint instability should be sought during passive joint
movement
o Function asses function by asking patient to unbutton shirt,
hold a pen/tea cup, writing.
Lungs
o Crepitations from lung fibrosis (fibrosing alveolitis) and
pleural effusions (stony dullness to percussion, reduced air
entry over effusion, bronchial breathing above the level of
effusions)
Liver/spleen
o Palpable spleen from Feltys syndrome
Neurological
o Peripheral neuropathy and mononeuritis multiplex
o Carpal tunnel syndrome caused by compression of the
median nerve by swelling around the wrist (Tinels sign)
o
o
INVESTIGATIONS
CBC
Anaemia of chronic disease, iron deficiency anaemia,
megaloblastic anaemia
Thrombocytosis - platelets are acute phase reactants, and their
levels typically rise in a variety of inflammatory conditions
Thrombocytopenia - hepersplenism
Leukocytosis Leukocytosis can be a manifestation of active
RA, but infection or treatment with glucocorticoids can also be
responsible for this finding.
Rheumatoid factors occur in 70 to 80 percent of patients with RA
ESR /CRP not specific for RA however useful for distinguishing
inflammatory conditions, of which RA is one, from noninflammatory
disorders.
204
Antinuclear antibody (ANA) A positive antinuclear antibody test is

present in 30 to 40 percent of patients with RA, most commonly
those with more severe, chronic disease
Joint aspiration Synovial fluid examination typically reveals a
leukocytosis with a predominance of polymorphonuclear cells, low
glucose, low C3 and C4 complement levels
Joint x-rays joint/bony erosions, deformity
MRI detect bone erosions earlier in the course of the disease than
is possible with plain films
Ultrasound another alternative for estimating the degree of
inflammation and the volume of inflamed tissue
CLINICAL FEATURES
OF
OSTEOARTHRITIS
1. Define osteoarthritis
2. List the risk factors for osteoarthritis.
3. Take a history from a patient with deforming arthropathy,
addressing the points which will help to narrow the differential
4. Perform physical examination focussing on the features which may
be associated with each of the likely differentials.
deforming arthropathy.
DEFINITION:
Osteoarthritis is a form of degenerative bone disease characterized
by progressive deterioration and loss of articular cartilage
accompanied by proliferation of new bone and soft tissue in and
around involved joint (1).
There are recognized associations between OA, aging and trauma.
Risk Factors (4)
Age - Advanced age is one of the strongest risk factors associated
with osteoarthritis
Female sex there is a female preponderance in severe disease
Obesity - the strongest modifiable risk factor
Occupation
Sports activities
Previous injury/trauma
Muscle weakness
Proprioceptive deficits (peripheral neuropathy)
Genetic elements
Acromegaly
Calcium crystal deposition disease
PATHOGENESIS:
Two principal mechanisms are thought to initiate osteoarthritis
Damage to normal articular cartilage by injury and trauma.
Chondrocytes react to this injury by releasing degradative enzymes
and elaborating inadequate repair responses.
205
Defective cartilage. Examples include a type II collagen gene defect

or ochronotic cartilage that fails because of deleterious pigment
deposition.
There are multiple factors that contribute to the development of OA. These
include abnormalities in biochemical forces and the cartilage mixed with
multiple risk factors (such as obesity, aging, mineral deposition, systemic
hormones, and abnormalities in neurogenic control).
Types of Osteoarthritis:
1. Idiopathic osteoarthritis Idiopathic OA can be categorized into

localized or generalized forms of the disease.
a. Localized OA - commonly affects the hands, feet, knee, hip,
and spine. Other joints are less commonly involved (shoulder,
temporomandibular, sacroiliac, ankle, and wrist joints).
b. Generalized OA consists of involvement of three or more joint
sites.
2. Secondary osteoarthritis
a. Trauma
b. Congenital or developmental disorders
c. Calcium pyrophosphate dihydrate deposition disease (CPPD)
d. Other bone and joint disorders (osteonecrosis, rheumatoid
arthritis, gouty arthritis, septic arthritis, and Paget disease of
bone)
e. Other diseases such as
i. Diabetes mellitus
ii. Acromegaly
iii. Hypothyroidism
iv. Neuropathic (Charcot) arthropathy
v. Inflammatory diseases (such as Perthes disease),
Lyme disease
vi. Ligamentous instability
vii. Marfans syndrome
viii. Obesity
ix. Alkaptonuria
x. Haemochromatosis
xi. Wilsons disease
Calcium pyrophosphate crystal deposition disease
Infectious monoarticular disease
HISTORY:
Pain
o
Deep boring pain typically exacerbated by activity and

relieved by rest.
o It is often worse at night (increased body temperature
increased blood flow increased stimulation of pain
receptors).
206
Painful joints are not usually tender, except in the active

Heberdens or Bouchards nodes.
Stiffness is also a common complaint in patients with OA. Morning
stiffness typically resolves less than thirty minutes after a patient
awakens, but may recur following periods of inactivity, a
phenomenon termed articular or inactivity gelling
Crackling noise (joint "crepitus") when the affected joint is moved or
touched, muscle spasm and contractions in the tendons
Loss of function
Osteoarthritis is typically not associated with any systemic /
constitutional symptoms
o
EXAMINATION:
Inspection
o Skin - scars, hair distribution, coarse doughy skin from
Acromegaly
o Joints
swelling,
erythema,
deformity
of
distal
interphalangeal joint, and fixed flexion and subluxation of the
metacarpophalangeal joint and muscle wasting
Palpation
o Enquire patient whether any joint is tender
o Commonly affected joints
First carpometacarpal joint
Proximal interphalangeal joint
Distal interphalangeal joint
Cervical and lumbar spine
Knee
Hip
Subtalar joint
First metarsophalangeal joint
o Uncommonly affected joints shoulder, wrist, elbow,
metacarpophalangeal joints
o Assess degree of joint tenderness and tissue swelling
Hands osteoarthritic enlargements of the distal and
proximal interphalangeal joints - Heberden's and
Bouchard's nodes. The first carpometacarpal joint is
also a common area affected in OA. Enlargement of
this joint result in a squared appearance to the hand
Feet the first metatarsophalangeal joint - hallux
valgus or hallux rigidus.
Knees osteophytes,
effusions,
crepitus,
and
limitation of range of motion, malalignment (genu
varus or genu valgus), varus angulation ("bow-legged")
occurs more commonly than valgus ("knock-kneed").
Femerotibial malalignment may be a risk factor for
more rapid progression of OA of the knee. A fluctuant
swelling along the posterior aspect of the knee, or
Baker's cyst, is a common complication
Hips pain around the hip is common in patients with
OA. It may be due to OA of the hip or to pain referred
to the hip area from other structures, such as the
lumbosacral spine
207
Spine most common at spinal levels C5, T8, and L3,

which represent the areas of greatest spinal flexibility.
Spondylolisthesis, a slipping of one vertebral body on
another, typically affecting the apophyseal joints at L4
to L5, may occur with severe OA.
Shoulders glenohumeral joint (anterior shoulder
pain), involvement of the acromioclavicular joint may
cause vague shoulder pain. Osteophytes located along
the undersurface of the acromioclavicular joint may
result in rotator cuff tendonitis or tears due to the
juxtaposition of tendons with the inferior portion of the
acromioclavicular joint
Movement
and the range of
movement noted
movement
INVESTIGATIONS:
Blood investigations
CBC WCC level (raised in infection/inflammation), normal in OA
Erythrocyte sedimentation rate (ESR) raised in inflammation,
normal in OA
Rheumatoid factor titre
Joint aspiration -The presence of leukocytosis may help to distinguish an
inflammatory from a noninflammatory process. In OA there is good
viscosity of fluid with normal mucin clot.
Synovial fluid analysis
Clear fluid
WBC <2000/mm3
Normal viscosity
Bursal aspiration - Bursal aspiration is performed to distinguish bursitis
due to trauma, crystal deposition disease (gout), or infection
Joint x-rays - Joint space narrowing, subchondral sclerosis, marginal
osteophyte (spur) formation, subchondral cysts, deformity
MRI - is not necessary for most patients with suggestive symptoms of OA
however MRI of the knee has a diagnostic role in patients with joint pain
and symptoms such as locking, popping, or instability that suggest
meniscal or ligamentous damage
CLINICAL FEATURES
OF THE
VASCULITIDES
1. Define vasculitides
2. Outline the pathogenesis of vasculitides
3. Describe the clinical and laboratory features of the common
vasculitides
4. Outline and justify investigations for diagnosis of vasculitides
208
DEFINITION: Vasculitis is characterized by inflammation of and damage to

blood vessels, compromise of vessel lumen and resulting ischaemia due to
an underlying clinicopathological process.
PATHOGENESIS: clinical manifestations depend on the size and location of the
affected vessel. Most vasculitic syndromes appear to be immunemediated. This may be due to primary or sole manifestation of a disease
or secondary to another disease process (1).
CLASSIFICATION:
Large vessels includes the aorta and its largest branches
subclavian, carotid and femoral arteries.
o Takayasu arteritis
o Giant cell arteritis
Medium vessels
o Polyarteritis nodosa
o Kawasaki disease
Small vessels
o Churg-Strauss syndrome
o Kawasaki disease
o Wegeners granulomatosis
o Microscopic polyangiitis
o Henoch-Schonlein purpura
o Mixed essential cryoglobulinaemia
o Vasculitis secondary to connective tissue disorders
HISTORY:
1. Patients age - mean age at onset for Wegener granulomatosis and
polyarteritis nodosa 45 and 50, HSP and Takayasu arteritis 17
and 25, Giant cell arteritis - >60 years.
2. Sex Takayasu and Giant cell arteritis occur primarily in women
3. Vasculitic disorders commonly present with constitutional
symptoms:
a. Henoch-Schnlein purpura - low-grade fever (38C), purpura,
joint pains (usually in the ankles and knees), abdominal pain,
bleeding in the digestive tract and boys with HSP often have
inflammation of the testicles
b. Kawasaki disease - high fever (40C), strawberry tongue and
cracked lips, conjunctivitis, irritability, loss of appetite, the
peeling of skin from the finger tips
c. Polyarteritis nodosa - fever, loss of appetite, weight loss, and
pain in the abdomen, joint pain or skin rashes
d. Takayasu arteritis - fever, weight loss, pain caused by lack of
blood supply such as aching in the legs while walking or
cramping sensations in the abdomen after meals
e. Wegener's granulomatosis symptoms from the upper
respiratory tract, the eyes, ears, kidneys, and skin, recurrent
ear infections that are slow to heal, inflammation of the
tissues inside the eye, inflamed sinuses, nosebleeds,
coughing up blood and saddle nose, which is a deformity
caused by the collapse of cartilage inside the nose. The
patient may also have joint pains, loss of appetite, skin
lesions, and fever.
209
4. Past medical history

a. Connective tissue diseases are commonly associated with
vasculitis (systemic lupus erythematosus, scleroderma,
antiphospholipid
syndrome,
Raynauds
disease,
dermatomyositis).
b. Hepatitic B and C are strongly associated with mixed
cryoglobulinaemia.
c. infective
endocarditis
may
present
with
vasculitic
lesions(splinter haemorrhages, Roths spots).
5. Medications certain drugs can cause hypersensitivity vasculitis or
rash.
EXAMINATION:
A careful physical examination helps to determine the extent of
vascular lesions, the distribution of affected organs, and the
presence of additional disease processes.
Presence of radial-radial delay with a collapsing pulse suggest
Takayasu arteritis as one of the differential causes.
Photophobia or reduced vision with tender scalp and jaw suggest
Giant Cell Arteritis.
Mononeuritis multiplex and palpable purpura are highly suggestive
of an underlying vasculitic process.
Look
specifically
for
distribution
of
rash/vasculitis,
lymphadenopathy, muscle weakness, diminished peripheral pulses,
oral ulcers and any signs of bleeding.
INVESTIGATIONS:
Laboratory tests help ascertain the type of vasculitis, and the
degree and types of organs affected.
Basic investigations
o CBC low Hb, increased WCC, eosinophilia (in Churg-Strauss
syndrome)
o Serum urea & creatinine (impaired function in renal
involvement)
o CPK levels (raised in myopathic disorders)
o Liver function test (elevated liver transaminases in viral
hepatitis)
o ESR/CRP raised due to inflammation
o ANA - A positive antinuclear antibody test suggests the
presence of an underlying connective tissue disorder,
particularly systemic lupus erythematosus
o Serum complements level - low serum complement levels
may be present in mixed cryoglobulinemia and SLE (low
C3/C4)
o Viral Hepatitis Serology positive Hepatitis B/C titres in
mixed cryoglobulinaemia
o ANCA - cANCA strongly suggests a diagnosis of Wegener
granulomatosis, while pANCA favuors a diagnosis of
microscopic polyangiitis
o Urinalysis haematuria, casts, proteinuria
o Chest x-ray (pulmonary haemorrhage in Wegeners
granulomatosis)
210
o Electromyography - useful if a systemic vasculitis is
suspected and neuromuscular symptoms are present, such

as a mononeuritis multiplex
o Tissue biopsy - biopsy examination of the most clinically
involved tissue is essential for diagnosis.
o Arteriography - helpful in identifying and characterizing a
vasculitis of large and medium-sized arteries, such as
polyarteritis nodosa, Takayasu arteritis, and giant cell
arteritis with an aortic arch syndrome
o Angiograms of mesenteric or renal arteries in polyarteritis
nodosa may show aneurysms, occlusions, and vascular wall
irregularities
o Skin biopsy IgA deposition in HSP
JOINT SWELLING
At the end of this tutorial, you should be able to:
1. Define joint swelling
2. Form a differential diagnosis for the aetiology of joint swelling.
3. Outline the causes of joint swelling.
4. Take a history from patients with joint swelling, looking for features
which may assist in narrowing the differential.
5. Examine patients with joint swelling to elicit features suggestive of
underlying aetiology.
joint swelling.
INTRODUCTION: Joint swelling is one of the four classical signs of inflammation
(heat, pain, redness, and swelling). Joint swelling is commonly
accompanied by pain.
Common
o Trauma meniscal tear, fracture, osteonecrosis
o Rheumatoid arthritis
o Osteoarthritis
o Infection
bacterial
(gonnococcal,
meningococcal,
tuberculosis, Lyme disease), viral
o Gout/pseudogout
o Haemarthrosis/hematoma Hemophilia, Sickle cell,
Anticoagulants
o Neoplastic
metastatic
disease,
osteosarcoma,
chondrosarcoma
Uncommon
o Psoriatic arthropathy
o Reiters syndrome
o Enteropathic arthritis (inflammatory bowel disease)
o Connective tissue disease SLE, MCTD, scleroderma
o Sarcoidosis
211
HISTORY
Musculoskeletal emergencies Hot or swollen joints may suggest
infection
Constitutional symptoms (high-grade fever, weight loss, malaise)
raise the suspicion of infection or sepsis.
Weakness may be a symptom of a compartment syndrome or an
acute myelopathy.
Burning pain, numbness, or paraesthesia with joint swelling may
suggest an acute myelopathy, radiculopathy, or neuropathy.
Presence of a rash may suggest a vasculitic process including
connective tissue diseases (SLE, Rheumatoid arthritis).
Take a detailed history on

o Symptom onset (sudden or gradual), progression (constant,
intermittent, improving or worsening) and duration (acute or
chronic).
o distribution of swelling, number of joints involved, symmetry
o progression of swelling over time
o duration and time of onset
o associated
symptoms
pain,
redness,
warmth,
discharge/punctum,
joint
stiffness,
extra-articular
manifestations, weakness (suggest neurological or muscle
problems)
o pain character, quality, time of onset, exacerbating/remitting
factors, duration
o preceding history of trauma( fracture, meniscal tear,
haemarthrosis) and travel history to endemic areas (infective
causes-Lyme disease, tuberculosis, parasitic infection)
o past medical history previous diagnosis of joints disorder,
gout, blood disorder, medications lists, malignancy, GI or
genitor-urinary complaints
o a history of prior joint pain or swelling (single or multiple,
symmetric or asymmetric, migratory or additive, small or large
joints) should be ascertained
EXAMINATION
General appearance a general inspection of the patient should
determine whether the patient is ill or well appearing. Check for
temperature and vital signs for any evidence of sepsis.
Inspection Enquire patient whether any joint is tender. Assess
degree of joint tenderness and tissue swelling. Each joint should be
examined in comparison with its symmetrical partner. Look for rash
(SLE, infection), at the nails (psoriatic nail changes, splinter
haemorrhages in infective endocarditis, clubbing in inflammatory
bowel disease), scars, bruises from trauma and discoloration
(Raynauds phenomenon). Look for any joint deformity that may
suggest RA, OA or psoriatic arthritis.
Palpation the initial step in palpation is to detect any changes in
the temperature of the skin overlying the affected joint. Increased
warmth of the affected joint compared to the unaffected side could
indicate inflammation due to infection or rheumatologic disorder.
Palpate and locate carefully for any points of tenderness.
212
Movement
and the range of
movement noted
movement
Proceed with examination of other systems to determine the cause of
the joint swelling.
INVESTIGATIONS:
Joint x-ray
Patients who presented with prior fall or trauma should have
radiographs to rule out a fracture or tumor.
Chondrocalcinosis, tophaceous erosions, joint space narrowing,
subchondral sclerosis, marginal osteophytes, subchondral cysts can
be appreciated on joint radiographs
Joint aspiration should be attempted in all patients who have an
effusion or signs suggesting inflammation with the joint swelling. The main
purpose of synovial fluid analysis is to evaluate whether the effusion is
inflammatory, infected, bloody, contains crystals, or is bland (1)
Visual inspection for xanthochromia (suggestive of a recent
haemorrhage due to a fracture or other trauma, or a coagulopathy),
and clear (noninflammatory) versus cloudy fluid (inflammatory)
Total leukocyte count and differential
Gram stain and culture
Crystal analysis utilizing polarizing microscopy
Blood investigations The patient with bloody synovial fluid and no
evidence of trauma, should have a prothrombin (PT), INR and platelet
count.
Blood cultures should be performed in patients with signs and
symptoms of sepsis
Others:
ESR &CRP - elevated in infection, inflammatory states, and
malignancy.
ANA - high sensitivity but low specificity for systemic lupus
erythematosus (SLE).
Serum dsDNA more specific for SLE
Serum rheumatoid factor (RF) positive in rheumatoid arthritis
CBC & LFTs - should be considered if a multisystem disease is
suspected based upon the history and physical examination. Raised
WCC suggests infection and inflammatory causes.
Other tests such as HLA-B27 and Lyme serologies should be ordered
only when the clinical suspicion is high for a spondyloarthropathy or
Lyme infection, respectively.
Examination of patients with

Systemic Lupus Erythematosus (SLE)
And Scleroderma
1) SLE
213
General inspection and vital signs

Blood pressure (hypertension may result from renal involvement)
Temperature (pyrexia can occur due to infection due to leucopenia
or due to the systemic inflammation itself)
Mental state (neuropsychiatric manifestation is frequent either due
to the disease itself or steroids)
Weight loss
Cushingoid appearance
Obvious deformity, postural abnormality or Rashes (especially in
sun exposed areas indicating photosensitivity)
Scan the patients surroundings and note any walking aids, gloves
(raynauds), urine sample
Hands
Look:
Nails: Look for signs of vasculitis around the nail bed which
may manifest as small punctuate lesions or telangiectasia.
Skin on dorsum: Look for photosensitive rash
214
Look for Raynauds Phenomenon (An abnormal responser to

cold which manifests as a tricolor change sequentially from
white to blue to red. Also look for digital ulcers.)
Skin on palmar aspect: Rashes again

Palmar crease pallor
Joints for swelling and deformity: Small-joint arthritis of the
hands and wrists is most frequent. Jaccouds arthropathy is the
term for the nonerosive hand deformities due to chronic
arthritis and tendonitis that develop in 10% of patients with
SLE. This may mimic rheumatoid arthritis (RA) - ulnar
deviation and phalangeal subluxations.
Muscle wasting
Palpate the joints making note of tenderness and swelling
characteristics
Move the joins actively and passively making note of limitation of
movement, tenderness and crepitus. Hand function should be tested
with active movement.
Arms
Skin:
Livedo reticularis (describes a lacy, mottled,
erythematous skin pattern that develops in some
patients with SLE)
215
Purpura (Vasculitis or due to

thrombocytopenia)
Muscle: Check for proximal myopathy
Nerves: Sensory loss due to peripheral sensory neuropathy
Head and neck

Skin and scalp:
Look for alopecia which occurs in about 60% of patients. Often
affects the temporal regions or creates a patchlike pattern of
hair loss, note also the presence of thin, short and broken hairs
just above the forehead. These are called lupus hairs.
Butterfly rash (erythematous rash over the cheeks and bridge
of nose.
Discoid lupus rash: plaquelike lesions with follicular plugging

and scarring. They may be part of systemic lupus or may
represent discoid lupus without organ involvement, which is a
separate diagnostic entity.
216
Eyes:
Red eyes in SLE can occur due to dryness (Sjogrens), scleritis,
episcleritis.
Look for signs of anaemia (conjunctival pallor): Usually anaemia
of chronic disease
Look for signs of jaundice which may occur due to autoimmune
haemolysis.
Mouth:
Oral ulcers may be noted, with palatal ulcers being
most specific for SLE.
Oral purpura may indicate thrombocytopenia or a sign
of vasculitis
Palpate for cervical lymphadenopathy
Check for cranial nerve lesions (neuropathy)
Chest
Heart: Pericardial friction rub
Also look for signs of heart failure due to pericardial
constriction or myocarditis (SEE RA TUTORIAL NOTES)
Lungs: Look for signs of pleuritis (pleural rub on auscultation),
pleural effusion, pulmonary fibrosis, collapse. (SEE RA
TUTORIAL NOTES)
In a haemodynamically unstable patient with SLE think of
pulmonary embolus which may indicate the presence of anti
phospholipid syndrome
217
Abdomen
Abdominal pain in SLE is significant because it may be directly
related to active lupus, including peritonitis, pancreatitis,
mesenteric vasculitis, and bowel infarction
Hepatomegaly
Splenomegaly
Ascites (Due to nephrotic syndrome)
Lower limbs
Skin: Look again for vasculitic rash.
Check also for ulceration over the malleoli or on the toes
(Vasculitis)
Nerves: Check for sensory loss due to peripheral sensory
neuropathy
Cerebellar ataxia
Hip joint: Avascular necrosis of the femoral head may occur
(either due to SLE vasculitis or steroids) leading to tenderness with
limitation of movement which spares extension.
2) Scleroderma
General inspection and vital signs
Blood pressure (Hypertension due to renal involvement)
Pyrexia (Infection)
Weight (Cachexia may result from oesophageal motility disturbance or
from malapsorption)
Comment on obvious features if present (such as bird like facies)
Hands
Look
218
Nails: Look for dilated capillary loops in the nail folds due to
Raynauds phenomenon.
Skin:
Calcinosis ( Palpable calcific nodules in the
subcutaneous tissues of the fingers)
Telangiectasia on the fingers

Raynau
ds phenomenon which can also lead to a) atrophy
of the subcutaneous tissues of the pulps of the
fingers and b) digital infarcts
Sclerodactyly (Tapering of the fingers due to skin

tightening): The skin of the hands may be oedematous
or indurated early in the disease, and the patient may
initially report this as puffy changes. This oedematous
stage precedes the sclerotic stage; longer time to
progression to the sclerotic phase indicates a better
prognosis. A rapid progression of sclerosis is associated
with a worse prognosis and, often, more extensive and
aggressive visceral organ involvement with an increased
risk of renal crisis development. In the sclerotic phase,
the skin may appear tight and shiny, with a
characteristic loss of hair, decreased sweating, and loss
219
of the ability to make a skin fold. This process of

thickening generally begins distally on the fingers.
Structures such as skin creases and dorsal veins begin to
fade. The skin induration usually progresses proximally
in a continuous symmetrical fashion.
Joints and deformity

Joint swelling due to arthropathy of the small
joints in the hands
Fixed flexion deformity of the fingers due to
both arthropathy and skin tightening
Palpate the pulps of the fingers for calcific lesions, and palpate the
joints for swelling and tenderness
Movement is very important actively for the assessment of hand
function given the sclerodactyly and flexion deformity.
Ask the patient to perform the following test of function:
Grip strength (Ask patient to squeeze your first
two fingers)
Thumb opposition to other fingers
Opposition strength (Ask patient to hold piece of

paper between thumb and forefinger and prevent
you from pulling it free)
Key grip
Practical tasks like writing and buttoning up shirt
Arms
Skin
Check for oedema (early) and skin thickening / tightening
(extension of the thickened skin beyond the hands suggests
limited scleroderma if it extends only to the elbows and diffuse
scleroderma if it extends to the arms and trunk)
Pigmentation: Salt and pepper pigmentation
Vitiligo
220
Head and neck

Scalp: Alopecia
Face: General appearance can sometimes be described as bird like due to
skin thickening with beaking of the nose, puckering of the mouth, and loss of
normal skin folds
Ask the patient to close their eyes: This may be

incomplete due to skin tightening
Ask the patient to open mouth: Abnormal restriction is

defined by inability to achieve 3cm between incisors
(microstomia)
Skin:
Scleroderma:
facial changes
Telangiectasia
Malar telangiectasia
Eyes:
Loss of eyebrows
Red eyes: Dryness due to associated Sjogrens syndrome
221

Look also for conjunctival pallor (anaemia due to
chronic disease, haemolysis, GI bleeding from oesophagitis or
drugs) and jaundice (Haemolytic anaemia).
Chest
Heart: Look for signs of pericarditis
Right heart failure may occur due to cor pulmonale secondary
to pulmonary fibrosis. Look for pedal oedema, elevated JVP,
Loud pulmonary second heart sound, pericardial friction rub.
Left heart failure suggests myocardial involvement by the
disease itself.
Check for bibasal crackles on auscultation of the lung fields.
Lungs: Check for signs of pulmonary fibrosis
Lower limbs
As in upper limbs examine the skin for evidence of vasculitis including
rash and ulcers
Check for skin tightening.
Check for proximal myopathy
Clinical cases
Case 1
A 40-year-old woman with a 2-year history of Raynaud's phenomenon presented
because the skin on her hands was beginning to feel tight. Five weeks earlier, her
hands had been swollen, erythematous, and pruritic, but these symptoms resolved
without treatment. The patient also described flu like symptoms during this same
period of time. The review of systems was significant for slight dyspnoea without
chest pain, heartburn, difficulty swallowing pills, bloating, and abdominal distension.
Case 2
A 19-year-old female was admitted to hospital with dyspnoea, easy fatigability,
palpitations, anorexia, weight loss, dry cough and episodic attacks of fever every three
to four months with night sweats for the last two years. Five days prior to admission
she developed pain in various large and small joints with swelling in interphalangeal
and right wrist joints and described features of Raynaud's phenomenon.
222

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Clinical Teaching and Communication Skills

Taking a Cardiovascular History

Take a detailed cardiovascular history from a patient.

Site of pain - central/retrosternal

Canadian cardiovascular society (CCS) classification of angina

New York Heart Association (NYHA) functional classification

Cardiovascular Risk Factors

Other cardiovascular symptoms

Exertional? Relieved by rest?

How many pillows at night when sleeping?

Paroxysmal nocturnal dyspnoea (PND)

patient wakes from sleep gasping for air

Describe the palpitation/ unexpected awareness of heart beat?

2) What is causing the palpitations?

Heart failure etc

Transient loss of consciousness due to cerebral anoxia.

Past Medical/Surgical History

Other medical/surgical problems.

Prescribed and over the counter.

Relevant family history MI / PVD / stroke, Hypertension, Diabetes

Complete Systems Review

Clinical teaching - Cardiovascular Examination

Exposing the patient

Look at general state of health. Does patient appear ill?

Comment on chest asymmetry/scars/pulsations.

Comment on intravenous lines/any equipment around bed

Indicative of a history of cigarette smoking

Cyanotic congenital heart disease

[The cause of clubbing is not known there are several theories]

Pallor - Pallor of the palmar creases/palm of hand

This may indicate underlying anaemia.

Severe congestive cardiac failure leads to hepatic congestion, causing intra-hepatic

Arcus senilis/Corneal arcus

Medial to the sternomastoid muscles

Jugular Venous pressure

Provides information regarding right atrial and right ventricular function

Features of Jugular Venous Pressure

Renal failure - fluid overload

Thoracotomy [mitral valvotomy - a stenosed mitral valve is opened through an

Visible apex beat

Causes of a displaced apex beat

Left ventricular dilatation

Little additional information is gained and therefore is not helpful.

1. Begin in the mitral area [over the apex beat]

Aortic and pulmonary valve closure

Grade Murmurs 1-6

1/6: very soft

Any additional sounds? Friction rub, opening snap, clicks

Mitral Regurgitation: Radiates to axilla, listen with diaphragm

Auscultation of the lung bases for pulmonary oedema crackles/crepitations

Pitting oedema - Skin is indented and only slowly refills.

Premature atrial contractions (PACs)

Both usually are harmless.

Paroxysmal supraventricular tachycardia (PSVT)

May occur spontaneously or due to an underlying disorder.

Noncardiac Disorders Precipitating Palpitations

Other Precipitants of palpitations

Many arrhythmias that cause palpitations have no adverse physiologic