Medicine I

Medicine Marking Scheme →

https://drive.google.com/file/d/1THMyD_hWmjdxYzDAUCrnWmI7EGaqFd3S/view?us
p=sharing

Answers are from the following books - - Archith Boloor : Exam Preparatory Manual
for Undergraduates - Manthappa : Manipal Prep Manual of Medicine - Matthew :
Medicine Prep Manual for Undergraduates.

Cardiovascular System
HYPERTENSION
Discuss role of non-pharmacological measures in management of systemic
hypertension
Recommended for all patients with hypertension and pre-hypertension. A reduction
in systolic blood pressure of 5 mmHg has been associated with about 10% reduction
in mortality caused by stroke and heart disease.
Modification Recommendation Approximate
reduction in
systolic BP
Weight reduction Maintain normal body weight (BMI 18.5-24.9) 5-20 mmHg/10 kg
weight loss
Adopt DASH diet Consume a diet rich in fruits, vegetables and low-fat dairy products 8-14 mmHg
plan with a reduced content of saturated and total fats
Dietary sodium Reduce dietary sodium intake to no more than 100 mEq/day (2.4 g 2-8 mmHg
restriction sodium or 6 g NaCl)
Physical activity Engage in regular aerobic physical activity such as brisk walking (at 4-9 mmHg
least 30 minutes a day, most days of the week)
Moderation of Limit consumption to no more than two drinks per day (1 oz or 30 2-4 mmHg
alcohol ml ethanol e.g. 24 oz beer, 10 oz wine, or 3 oz 80- proof whisky) in
consumption most men, and no more than one drink per day in women and
lighter-weight persons
Complete
cessation of
smoking
Discuss secondary causes of hypertension // Mention four causes of secondary
hypertension
The secondary causes of hypertensions are -
Coarctation of aorta
clinical features → radio-femoral delay, upper limb hypertension, systolic murmur
over spine
investigations → CXR (rib notching)
Pheochromocytoma
clinical features → paroxysmal headaches, palpitations
investigations → 24 hour urinary catecholamine, metanephrines, VMA levels
Chronic pyelonephritis
clinical features → chronic back pain, undiagnosed fever, recurrent UTIs
PKD
clinical features → enlarged palpable kidneys
investigations → USG, IV urogram
Renal artery stenosis
clinical features → bruit over abdomen
investigations → Captopril-enhranced radionuclide scan, doppler USG, CT
angiogram, MR angiogram, renal arteriogram
Cushing's syndrome
clinical features → characteristic facies and habitus
investigations → Dexamethasone suppression test, 24 hour urinary cortisol, late night
salivary cortisol, plasma cortisol levels
Hypo/Hyperthyroidism
Hyperparathyroidism
Primary Hyperaldosteronism
investigations → Serum potassium (hypokalemia), aldosterone levels (high), renin
(low)
Mention four antihypertensive drugs with correct dosage and 1 side effect each
Chlorthalidone → 12.5 - 25 mg OD. Impotence, postural hypertension, allergic rash,
marrow depression, hyperuricemia, hypercalcemia
Furosemide → 10-40 mg BD. Hypocalcemia, Hypomagnesemia, Hypokalemia,
Metabolic alkalosis, Interstitial nephritis
Propranolol → 20-80 mg BD. Gastric disturbances, bardycardia, cardiac failure,
bronchospasm, tiredness, bad dreams, cold hands, muscle weakeness
Captopril → 12.5 - 50 mg. Dry cough, angio-edema, postural hypotension, rashes,
blood dyscrasias
A 20 yr old student is admitted with dizziness. O/E his blood pressure is
230/140 mm of Hg. What clinical features and investigations will aid in making
a diagnosis? Enumerate four antihypertensive drugs, with dosage and side
effects
CLINICAL FEATURES
Due to hypertension
majority are asymptomatic, detected on routine examination
acute hypertension → transient headache and polyuria
chronic hypertension → left ventricular hypertrophy and heaving apical impulse
left atrial hypertrophy
auscultation → S4 audible, A2 accentuated, very short early diastolic murmur
fundal changes
Due to different causes of hypertension
Coarctation of aorta → radio-femoral delay, upper limb hypertension, systolic
murmur over spine
Pheochromocytoma → paroxysmal headaches, palpitations
Chronic pyelonephritis → chronic back pain, undiagnosed fever, recurrent UTIs
PKD → enlarged palpable kidneys
Renal artery stenosis → bruit over abdomen
Cushing's syndrome → characteristic facies and habitus
Hypothyroidism → fatigue, weight gain, reduced appetite, menstrual abnormalities
Hyperthyroidism → irritability, weight loss, increased appetite, menstrual
abnormalities
Hyperparathyroidism → nausea/vomiting, polydipsia, polyuria
Primary Hyperaldosteronism → fatigue, headache, muscle-weakness
INVESTIGATIONS
general investigations
Urine analysis for protein, blood and glucose, and microscopic examination for casts
or pus cells
Blood urea and creatine
Serum electrolytes
Fasting and postprandial blood glucose
Serum cholesterol and triglycerides
Serum calcium and uric acid
ECG
CXR
to determine the cause of secondary hypertension
Coarctation of aorta → CXR (rib notching)
Pheochromocytoma → 24 hour urinary catecholamine, metanephrines, VMA levels
Chronic pyelonephritis → urine culture, urine analysis
PKD → USG, IV urogram
Renal artery stenosis → Captopril-enhranced radionuclide scan, doppler USG, CT
angiogram, MR angiogram, renal arteriogram
Cushing's syndrome → Dexamethasone suppression test, 24 hour urinary cortisol,
late night salivary cortisol, plasma cortisol levels
Hypo/Hyperthyroidism → Thyroid function tests (TSH, T3, T4)
Hyperparathyroidism → Serum calcium, phosphate levels, PTH levels
Primary Hyperaldosteronism → Serum potassium (hypokalemia), aldosterone levels
(high), renin (low)
DRUGS
Chlorthalidone → 12.5 - 25 mg OD. Impotence, postural hypertension, allergic rash,
marrow depression, hyperuricemia, hypercalcemia
Furosemide → 10-40 mg BD
Propranolol → 20-80 mg BD. Gastric disturbances, bardycardia, cardiac failure,
bronchospasm, tiredness, bad dreams, cold hands, muscle weakeness
Captopril → 12.5 - 50 mg. Dry cough, angio-edema, postural hypotension, rashes,
blood dyscrasias
Emergency treatment of malignant hypertension

ATRIAL FIBRILLATION
65 year old male is admitted for evaluation of irregular palpitations of recent
onset. On examination he has irregularly irregular pulse of 123 per minute.
Cardiovascular examination shows varying intensity of 1st heart sound and no
murmur. Other systems are normal a. What is the likely arrhythmia patient is
suffering from? And give one differential diagnosis and mention all causes of
this arrhythmia. b. How do you evaluate this patient for arrhythmia? c. Discuss
the management of this case
Atrial Fibrillation. Differential Diagnosis → Atrial flutter w/ variable block
Causes
Cardiac
Rheumatic heart disease (mitral valvular disease)
Ischemic heart disease (acute MI)
Congenital heart disease (ASD)
Cardiomyopathy
Pericardial disease
Non-cardiac
Hypertension
Alcohol
Thyrotoxicosis
Electrocution
Pulmonary embolism
Evaluation
Symptoms
palpitations, fatigue, syncope, angina
symptoms of cardiac failure → dyspnea, peripheral edema
symptoms of thromboembolism → altered mental status, abdominal pain, vision
problems
Signs
Pulse → Irregularly irregular pulse, varying volumes of pulse, apex-pulse deficit
Auscultation→
Varying intensity of first heart sound
Disappearance of pre-systolic accentuation (PSA) of mid-diastolic murmur of MS
Disappearance of fourth heart sound
JVP → Absent a waves
Hypotension
ECG
Irregularly Irregular rhythm of QRS complexes
No discernible P waves
Small, irregular waves (fibrillary waves) at a rate of 350-600/ min that are difficult to
see on ECG (fine atrial fibrillation)
At lower rates of 150-300, coarse fibrillary waves are seen (coarse atrial fibrillation)
Management
If patient hemodynamically unstable (presence of hypotension, angina, syncope,
pulmonary edema or altered sensorium) → Immediate synchronized cardioversion
starting at 100 J is the treatment of choice
If patient hemodynamically stable : Treatment is in two steps
Rate control
Goal : To achieve ventricular rate less than 100/min
Drugs used :
Diltiazem: 10 mg intravenously over 2 minutes; repeat same dose in 15 minutes if
required; start an infusion at 10-15 mg/hour to maintain ventricular rate below
100/minute.
Verapamil: 5-10 mg intravenously over 2 minutes; repeat in 30 minutes if required.
Propranolol: 1 mg intravenously over 2 minutes; repeat every 5 minutes up to a
maximum of 5 mg.
Digoxin: 0.25-0.5 mg intravenously, then 0.25 mg after 4-6 hours and another dose
after another 12 hours. Peak effect not seen for hours and, therefore, less commonly
used at present.
Amiodarone: 150 mg over 10 minutes, followed by 1 mg/minute over 6 hours and
then 0.5 mg/minute for next 18 hours.
Drug of choice in stable patients with known ejection fractions of less than 40%.
Less likely to produce fall in blood pressure compared to other drugs.
However, it may convert atrial fibrillation to normal rhythm that may lead to
embolism
Rhythm control
Pharmacological cardioversion to sinus rhythm with quinidine, ibutilide, flecainide,
propafenone or amiodarone.
The dose of amiodarone 5-7 mg/kg intravenously over 1 hour followed by 1.2-1.8
g/24-hour infusion
If medical cardioversion fails, electric cardioversion is performed after 3 weeks of
warfarin therapy that is continued for another 4 weeks after cardioversion
If cardioversion successful (sinus rhythm restored), prevent recurrence by →
amiodarone, dronedarone, flecainide, propafenone, or sotalol.
In patients in whom cardioversion unsuccessful or in whom atrial fibrillation is likely
to recur, treatment consist of following
Allowing the patient to remain in atrial fibrillation but reduce the ventricular rate by
digitalis, diltiazem, verapamil or propranolol. Goal is to achieve a resting heart rate of
80/minute.
Chronic anticoagulation
Anticoagulation therapy
If atrial fibrillation has been present for less than 48 hours → Medical/electrical
cardioversion can be done without prior anticoagulation therapy
If duration of atrial fibrillation exceeds 48 hours or is unknown
Do a TEE (transesophageal echocardiography) first
If no atrial thrombi observed : Heparin → immediate cardioversion → Warfarin for 4
weeks
If atrial thrombi seen : Warfarin for 3 weeks → Cardioversion → Warfarin for 4 weeks
If cardioversion unsuccessful and patient remains in atrial fibrillation, or cardioversion
is not planned → Long term warfarin therapy recommended if
���2��2−����CHA2DS2−VASc score is ≥ 2.

Drugs used for anticoagulation → warfarin, dabigatran (direct thrombin inhibitor) or

apixaban (direct factor Xa inhibitor)
With warfarin an INR should be maintained between 2 and 3 (between 2.5 and 3.5 if
underlying valvular lesion present)
Refractory cases →
anti-tachycardia pacemakers
inducing complete heart block by radiofrequency ablation of bundle of His followed
by permanent pacemaker implantation
Note on management of a case of atrial fibrillation
If patient hemodynamically unstable (presence of hypotension, angina, syncope,
pulmonary edema or altered sensorium) → Immediate synchronized cardioversion
starting at 100 J is the treatment of choice
If patient hemodynamically stable : Treatment is in two steps
Rate control
Goal : To achieve ventricular rate less than 100/min
Drugs used :
Diltiazem: 10 mg intravenously over 2 minutes; repeat same dose in 15 minutes if
required; start an infusion at 10-15 mg/hour to maintain ventricular rate below
100/minute.
Verapamil: 5-10 mg intravenously over 2 minutes; repeat in 30 minutes if required.
Propranolol: 1 mg intravenously over 2 minutes; repeat every 5 minutes up to a
maximum of 5 mg.
Digoxin: 0.25-0.5 mg intravenously, then 0.25 mg after 4-6 hours and another dose
after another 12 hours. Peak effect not seen for hours and, therefore, less commonly
used at present.
Amiodarone: 150 mg over 10 minutes, followed by 1 mg/minute over 6 hours and
then 0.5 mg/minute for next 18 hours.
Drug of choice in stable patients with known ejection fractions of less than 40%.
Less likely to produce fall in blood pressure compared to other drugs.
However, it may convert atrial fibrillation to normal rhythm that may lead to
embolism
Rhythm control
Pharmacological cardioversion to sinus rhythm with quinidine, ibutilide, flecainide,
propafenone or amiodarone.
The dose of amiodarone 5-7 mg/kg intravenously over 1 hour followed by 1.2-1.8
g/24-hour infusion
If medical cardioversion fails, electric cardioversion is performed after 3 weeks of
warfarin therapy that is continued for another 4 weeks after cardioversion
If cardioversion successful (sinus rhythm restored), prevent recurrence by →
amiodarone, dronedarone, flecainide, propafenone, or sotalol.
In patients in whom cardioversion unsuccessful or in whom atrial fibrillation is likely
to recur, treatment consist of following
Allowing the patient to remain in atrial fibrillation but reduce the ventricular rate by
digitalis, diltiazem, verapamil or propranolol. Goal is to achieve a resting heart rate of
80/minute.
Chronic anticoagulation
Anticoagulation therapy
If atrial fibrillation has been present for less than 48 hours → Medical/electrical
cardioversion can be done without prior anticoagulation therapy
If duration of atrial fibrillation exceeds 48 hours or is unknown
Do a TEE (transesophageal echocardiography) first
If no atrial thrombi observed : Heparin → immediate cardioversion → Warfarin for 4
weeks
If atrial thrombi seen : Warfarin for 3 weeks → Cardioversion → Warfarin for 4 weeks
If cardioversion unsuccessful and patient remains in atrial fibrillation, or cardioversion
is not planned → Long term warfarin therapy recommended if
���2��2−����CHA2DS2−VASc score is ≥ 2.

Drugs used for anticoagulation → warfarin, dabigatran (direct thrombin inhibitor) or

apixaban (direct factor Xa inhibitor)
With warfarin an INR should be maintained between 2 and 3 (between 2.5 and 3.5 if
underlying valvular lesion present)
Refractory cases →
anti-tachycardia pacemakers
inducing complete heart block by radiofrequency ablation of bundle of His followed
by permanent pacemaker implantation
Clinical features and complications of atrial fibrillation
Clinical features
Symptoms
palpitations, fatigue, syncope, angina
symptoms of cardiac failure → dyspnea, peripheral edema
symptoms of thromboembolism → altered mental status, abdominal pain, vision
problems
Signs
Pulse → Irregularly irregular pulse, varying volumes of pulse, apex-pulse deficit
Auscultation→
Varying intensity of first heart sound
Disappearance of pre-systolic accentuation (PSA) of mid-diastolic murmur of MS
Disappearance of fourth heart sound
JVP → Absent a waves
Hypotension
Complications
Hypotension
Angina
Thromboembolism
Syncope
Precipitation/worsening of cardiac failure
Precipitation of pulmonary oedema in mitral stenosis
What are the causes and complications of atrial fibrillation?
Causes
Cardiac
Rheumatic heart disease (mitral valvular disease)
Ischemic heart disease (acute MI)
Congenital heart disease (ASD)
Cardiomyopathy
Pericardial disease
Non-cardiac
Hypertension
Alcohol
Thyrotoxicosis
Electrocution
Pulmonary embolism
Complications
Hypotension
Angina
Thromboembolism
Syncope
Precipitation/worsening of cardiac failure
Precipitation of pulmonary edema in mitral stenosis
ISCHEMIC HEART DISEASE, ANGINA and MYOCARDIAL
INFARCTION
What are risk factors for Ischemic heart disease? How do you investigate and
treat chronic stable angina? Write the complications of acute myocardial
infarction // Write a note on treatment of chronic stable angina pectoris
RISK FACTORS FOR IHD
Modifiable
Smoking
Cholesterol
Arterial hypertension
Diabetes mellitus
Physical inactivity
Dietary factors
Coagulation factors
Obesity
Stress factors
Non-modifiable
Geographic influences : More common in Asian countries
Family history of premature CAD
Age
Genetic factors
INVESTIGATIONS FOR CHRONIC STABLE ANGINA
ECG
Normal at rest and in between attacks
During attack : Reversible ST depression or elevation with or without T wave
inversion
Stress myocardial perfusion scanning using radioactive thallium or technetium. If a
patient cannot perform exercise pharmacological challenge is performed using
dipyridamole, adenosine or dobutamine.
ECHO and radionuclide blood pool scanning provide information about ventricular
function
Coronary arteriography : Extent and site of coronary artery stenosis
TREATMENT OF CHRONIC STABLE ANGINA
General measures
Education of the patient regarding their condition
Evaluate the risk factors and take steps to correct them
Correction of precipitating underlying conditions, e.g. anemia, hyperthyroidism,
valvular disease, arrhythmia, aortic stenosis, hypertrophic cardiomyopathy, control of
hypertension and diabetes
Lipid management - Treat with diet and drugs
Healthy diet
Saturated fatty acids < 10% of total energy intake
Limit salt intake to less than 5 g per day
Consume 30-45 grams of fiber per day
Limit consumption of alcohol
Anti-anginal drug treatment
Nitrates
Glyceryl-trinitrate
Metered dose aerosol (400 mcg per spray) or as a tablet (300-500 mcg)
Action: Relieves attack of angina in 2-3 minutes
Isosorbide dinitrate
Dose: 10-20 mg BD or TID orally
Beta-blockers
Cardioselective beta-blockers are preferred
Include slow release metoprolol (50-200 mg daily), bisoprolol (5-15 mg daily)
Carvedilol (3.125-25 mg BD) has additional antiarrhythmic properties
Calcium channel blockers
DHP CCBs → Nifedipine, Amlodipine, Nicardipine. Can cause reflex tachycardia
Non-DHP CCBs → Verapamil, Diltiazem. They may reduce the cardiac output so
shouldn’t be used with impaired ventricular function.
Second line anti-anginal drugs
Nicorandil → K channel opener → Smooth muscle relaxation → Arterial and venous
dilation. Dose 10-30 mg twice daily
Ivabradine → Funny sodium channel antagonist. Should be used in bradycardia
causing conditions like AV block, sick sinus syndrome
Ranolazine → Inhibits late sodium channel. Drug of choice in bradycardic and
hypertensive patients
Anti-platelet therapy - To reduce the risk of adverse effects such as MI
Low dose aspirin (75-150 mg)
P2Y12 antagonists
Clopidogrel - 75 mg daily
Prasugrel
Ticagrelor
Statins
Invasive surgical treatment (Revascularization)
PCI
Percutaneous coronary intervention (PCI) includes angioplasty (PTCA) or stent
placement in coronary artery
Types of stents - bare metal stents and drug eluting stents
Indications for PCI
Ideal for single-vessel or two vessel coronary disease without significant lesion in the
proximal LADA, with normal LV function, with high risk of noninvasive testing and
large area of viable myocardium
Undergone prior PCI with either recurrence of stenosis or high risk on noninvasive
testing.
Failure of medical therapy and with acceptable risk for PCI. Treatment of choice for
unstable angina (UA) when rest pain recurs in spite of full medical treatment.
No diabetes
Coronary Artery Bypass Grafting
Indications
Significant left main coronary disease.
Triple vessel disease/two blood vessel disease with reduced left ventricular function
(left ventricular ejection fraction is <50%).
Two vessel disease with significant proximal left anterior descending artery disease
and either LVEF <50% or demonstrable ischemic on noninvasive testing.
Failure of medical therapy and with acceptable risk for CABG
Diabetes
Prior CABG, PCI (percutaneous coronary interventions) with recurrent re-stenosis
Abnormal stress test.
COMPLICATIONS OF ACUTE MYOCARDIAL INFARCTION (DARTH VADER)
Death
Arrhythmias : Sinus bradycardia, sinus tachycardia, ventricular ectopic beats,
ventricular tachycardia, atrial tachycardia, atrial fibrillation, ventricular fibrillation,
heart blocks
Rupture of interventricular septum leading to VSD
Tamponade : Due to ventricular free wall rupture
Heart failure manifesting as pulmonary edema
Valvular disease : Infarction of the mitral papillary muscle (posteromedial most
commonly) causing MR
Aneurysm of ventricle
Dressler’s syndrome
Embolism : Cerebral and peripheral thromboembolism
Recurrence
A 40 year old male presents with acute onset retrosternal chest pain of 30
minutes. What is your diagnosis? Discuss the diagnosis, management and
enumerate the complications of the same. // Discuss the clinical features,
investigations, complications and management of Acute Myocardial infarction.
// Discuss cardiac biomarkers in acute coronary syndrome // Changes in Plasma
cardiac biomarkers in acute myocardial infarction // Describe clinical features
(symptoms and signs) of acute myocardial infarction // ECG changes in acute anterior
wall myocardial infarction // ECG changes in acute myocardial infarction // Mention
list of investigations required for a case of ST segment elevation myocardial
infarction.
The diagnosis is acute myocardial infarction.
Clinical features
Symptoms
Retrosternal chest pain
Character - squeezing, crushing, tightening, heaviness
Radiates to left arm, or throat, back, jaw, chin etc.
Severe and prolonged as compared to anginal pain
Maybe absent in elderly, prior stroke, diabetes mellitus, females etc.
Breathlessness, syncope, vomiting, and extreme tiredness are common
Signs
General appearance → Pallor, sweating
Pulse → Tachycardia or bradycardia, narrow pulse pressure, irregularly irregular pulse
JVP → Raised
Precordium
Palpation → Diffuse apical impulse
Auscultation →
Soft S1
S3 present
Pericardial friction rub
Systolic murmur due to MR or VSD
Pulmonary auscultation → Basal crepitations
Investigations
ECG
Should be done within 10 minutes of arrival
Typical changes seen in infarcts
ST elevation (with reciprocal depression in opposite leads)
Leads V2-V3
≥ 2 mm in men
≥ 1.5 mm in women
Other contiguous chest leads ≥ 1 mm
Appearance of new left bundle branch block
Appearance of pathological Q waves i.e. initial negative deflections of 0.04 seconds
or more in leads other than aVR and V1
In very early MI → T waves become tall and peaked
ST depression in ≥ 2 precordial leads (V1-V4) may indicate STEMI of posterior wall.
Left main or proximal LADA occlusion → Multilead ST depression with co-existent ST
elevation in aVR
ECG and location of MI
Inferior wall MI - changes in leads II, II, aVF
Anterior wall MI - changes in leads V1 to V6, I and aVL
Anteroseptal MI - changes in leads V1 to V2
Anterolateral MI - changes in leads V4 to V6, I and aVL
Posterior wall MI - tall R and ST depression in leads V1 and V2
Right ventricular infarction - changes in V4R
Cardiac markers
Creatine Kinase (CK) : CK-MB more specific for heart
starts to rise : 4-6 hours
peaks : 12 hours
falls to normal : 48-72 hours (utility in re-infarction)
Aspartate aminotransferase (AST)
starts to rise : 12 hours
peaks : 1st or 2nd day
Lactate dehydrogenase (LDH)
starts to rise : 12 hours
peaks : 2-3 days
remains elevated : for 1 week
Myoglobin
starts to rise : 2-6 hours
remains elevated : 7-12 hours
Troponins (troponin I and troponin T)
starts to rise : 4-6 hours
remains elevated : 100-200 hours
Other investigations
Leukocytosis on day 1
Raised ESR and CRP
CXR : Evidence of pulmonary edema may be present
Radionuclide scan : Shows site of necrosis and impairment of ventricular function
ECHO : Wall motion abnormalities and reduced EF
Management
Initial treatment
Attach a cardiac monitor
Secure an IV line
Oxygen by nasal prongs or face mask (2-4 liters/min for 6-12 hours after infarction)
Aspirin 325 mg oral and clopidogrel 300 mg oral loading dose should be given and
continued at lower doses later
Sublingual glyceryl trinitrate 0.4 mg. Repeat at 5 min intervals up to 3 doses.
IV heparin for all patients unless there is as contraindication
Injection morphine 2-5 mg IV, improves chest pain and control anxiety
IV beta blocker e.g. metoprolol 5 mg every 2 to 5 mins for a total of three doses.
Confirm diagnosis
ECG
If available, do cardiac markers testing CK-MB and troponins
Reperfusion therapy
Percutaneous coronary intervention (PCI)
Treatment of choice, if facility available
Preferred when
Maximum acceptable delay from presentation to balloon inflation is
90 minutes if a patient presents directly to a PCI-enabled hospital (door-to-balloon
time)
120 minutes if a patient is referred from another hospital with door-in door-out time
in the first hospital < 30 minutes
Door-to-balloon time minus door-to-needle time is ≤ 60 minutes
Door-to-balloon time is ≤ 90 minutes
Types
Primary PCI
Rescue PCI
Facilitated PCI
Fibrinolysis
Initiated within 30 minutes (door-to-needle time). Highest benefit is if done within 1
to 3 hours of onset of symptoms.
Preferred when
Early presentation (≤3 hours from symptom of onset)
In patients where primary PCI cannot be done because of the following
Catheterization lab occupied
Vascular access difficulties
Lack of access to a skilled PCI lab
Delay to primary PCI
Door-to-balloon time minus door-to-needle time is > 60 minutes
Door-to-balloon time is greater than 90 minutes
Thrombolytic Agents and their doses

MOA : Lyse thrombi/clot to recanalize occluded vessel

Coronary artery bypass grafting
Recommended in
Failed PCI with persistent pain or hemodynamic instability with coronary anatomy
suitable for surgery
Persistent or recurrent ischemia refractory to medical therapy in patients with
coronary anatomy suitable for surgery, and are not candidates for PCI or fibrinolytic
therapy
Patients with STEMI at the time of operative repair of mechanical defects
Management of complications
Ventricular dysfunction : ACE inhibitors and nitrates
Cardiogenic shock : IV vasopressors, intra-aortic balloon pump
Right ventricular infarction : Volume expansion to maintain adequate right ventricular
preload
Pericarditis : Aspirin 650 mg QID and withhold anticoagulants
Aftercare and rehabilitation
Physical activity : To be restricted for 4-6 weeks because replacement of infarct by
fibrous tissue takes 4-6 weeks.
Lifestyle and risk factor modifications :
Control obesity
Regular exercises
Cessation of smoking
Control of plasma lipids by diets and drugs
Secondary prevention and drug therapy
Aspirin and clopidogrel : Low dose aspirin (75 mg daily) and clopidogrel (75 mg
daily) to be continued for 12 months, particularly after stent placement
Beta-blockers : Continued indefinitely unless contraindicated. Metoprolol, carvedilol,
bisoprolol are given.
ACE inhibitors (e.g. enalapril 10 mg BD or ramipril 2.5-5 mg BD) is found to
counteract ventricular remodeling, prevent onset of heart failure, and reduce
recurrent MI
Statin therapy : To improve plasma lipid profile
Warfarin : In patients with high risk of thromboembolism due to atrial fibrillation,
mural thrombus, CCF, previous embolization.
Short acting nitrates for chest pain when beta-blockers alone are unsuccessful or
contraindicated
Aldosterone antagonists (e.g. eplerenone) is given in patients with LVEF ≤40%,
despite optimum dose of ACE inhibitors and β-blockers, and have either CHF or
diabetes.
Complications (DARTH VADER)
Death
Arrhythmias : Sinus bradycardia, sinus tachycardia, ventricular ectopic beats,
ventricular tachycardia, atrial tachycardia, atrial fibrillation, ventricular fibrillation,
heart blocks
Rupture of interventricular septum leading to VSD
Tamponade : Due to ventricular free wall rupture
Heart failure manifesting as pulmonary edema
Valvular disease : Infarction of the mitral papillary muscle (posteromedial most
commonly) causing MR
Aneurysm of ventricle
Dressler’s syndrome
Embolism : Cerebral and peripheral thromboembolism
Recurrence
Management of NSTEMI
Hospitalize
Aspirin 325 mg oral and clopidogrel 300 mg oral loading dose should be given and
continued at lower doses later
Sublingual glyceryl trinitrate 0.4 mg. Repeat at 5 min intervals up to 3 doses.
If pain persists or patient develops heart failure, or remains hypertensive,
administration of IV NTG should be initiated.
Injection morphine 2-5 mg IV, improves chest pain and control anxiety
IV beta blocker e.g. metoprolol 5 mg every 2 to 5 mins for a total of three doses.
CCBs (Verapamil / Diltiazem) may be used if beta-blockers are contraindicated.
ACE inhibitors for patients with hypertension despite treatment with nitroglycerine
and a beta-blocker, and with LV systolic dysfunction or CHF.
Thrombolytic agents are contraindicated
Management based on risk status
High risk
IV nitroglycerine if chest pain continues
Anticoagulation using
IV heparin (60 U/kg as bolus and then 12 U/kg/h infusion with aPTT monitoring
(maintain between 1.5-2 times the control)
SC LMWH (e.g. enoxaparin)
If invasive strategy is planned → Use bivalirudin
Platelet GPIIb/IIIa receptor antagonists are recommended in patients in whom
invasive strategy is planned. These drugs include tirofiban and abciximab.
Statins : Should be started regardless of baseline cholesterol levels
If patient becomes pain free → Consider early coronary angiography and re-
vascularization
If patient does not become pain free → Immediate angiography and
revascularization
Intermediate risk group
Reclassify as low or high risk by diagnostic evaluation
Low risk group
After appropriate period of observation and assessment these patients may be
discharged and brought for outpatient follow-up
Medication including aspirin, beta-blocker, ACE inhibitors and statins should be
started.
CONGESTIVE CARDIAC FAILURE
Enumerate the etiology (any four), discuss the clinical features and
investigations in a case of Congestive cardiac failure. Add a note on its
management
ETIOLOGY of Left Heart Failure
Pressure overload of ventricle → Systemic hypertension , aortic stenosis
Volume overload of ventricle → AR, VSD, PDA
Inflow obstruction of ventricle → Mitral stenosis
Impaired ventricular function → MI, Myocarditis, Cardiomyopathy
CLINICAL FEATURES
Symptoms
Dyspnea
Orthopnea
PND
Cardiac asthma / Wheezing
Nocturia
Cerebral symptoms → Confusion, difficulty in concentration, memory impairment,
headache
Signs
Vitals →
Sinus tachycardia
Diminished pulse pressure due to reduced stroke volume
Pulsus alternans
JVP is raised
Cheyne-stokes repiration → A type of periodic breathing with alternate periods of
apnoea and hyperventilation seen in advanced heart failure
Cyanosis
Auscultation →
Acute pulmonary edema → Bibasilar coarse crepts
S3, S4 heart sounds
Per abdomen → Tender hepatomegaly due to stretching of capsule of liver
INVESTIGATIONS
CXR →
Cardiomegaly
Cephalization of pulmonary vessels
Kerley B lines - engorged peripheral lymphatics seen in lower lobe
Phantom tumour → Fluid in horizontal or oblique fissures of lungs, disappears with
diuretics
Pleural effusion
ECG → Biventricular hypertrophy, arrhythmias, conduction abnormalities, previous MI
BNP → BNP > 400 pg/mL is highly suggestive of acute heart failure
ECHO → Assesment of EF, valvular functions, and chamber size and shape
Ambulatory holter monitoring if arrhythmias are suspected
MANAGEMENT
Control of excessive fluid
Low salt diet and fluid restriction
Diuretics :
Loop diuretics (furosemide, torsemide)
Thiazides
K sparing diuretics (spironolactone, eplerenone, amiloride)
Prevention of deterioration of myocardial function (Prevention of ventricular
remodeling)
Done by blocking the adrenergic nervous system and the renin-angiotensin-
aldosterone system (RAAS)
ACE inhibitors
MOA → Blocks angiotensin converting enzyme, thereby inhibiting conversion of
angiotensin 1 to angiotensin 2
Drugs → Captopril, enalapril, ramipril, lisinopril
Side effects → dry cough, angioedema, AKI in patients with bilateral renal artery
stenosis, hyperkalemia
Angiotensin receptor blockers
MOA → Blocks angiotensin receptors, hence do not allow angiotensin 2 to act
Drugs → Candesartan, valsartan, losartan, telmisartan
Side effects → hyperkalemia, angioedema
Aldosterone antagonists
Drugs → Spironolactone, eplerenone
Beta-blockers
Drugs → Atenolol, carvedilol, bisoprolol
Side effects → Sinus bradycardia, nightmares, bronchospasm
Vasodilators
Drugs → Sodium nitroprusside, nitroprusside, hydralazine and nesiritide (BNP
analogue)
Enhancement of myocardial contractility
Cardiac glycosides → Digitalis and digoxin
Sympathomimetic amines → Dopamine, dobutamine
PDE inhibitors → Milrinone, enoximone
Circulatory assist devices / cardiac transplantation
Required in class IV heart failure or refractory heart failure
Antiarrhythmics
Premature ventricular beats and episodes of asymptomatic ventricular tachycardia
are common in advanced heart failure. Amiodarone, a class III anti-arrhythmic may
be used.
Anticoagulation
Warfarin may be used in patients with previous thromboembolic events
Define congestive cardiac failure. Discuss etiology, clinical features and
management of acute left heart failure (Acute pulmonary edema). // Heart
failure treatment
Heart failure or cardiac failure is defined as a state in which the ventricles at normal
filling pressures (i.e. adequate intravascular volume) cannot maintain an adequate
cardiac output to meet the metabolic needs of peripheral tissues or can do so only
with an elevated filling pressure. It results from any structural or functional
impairment of ventricular filling or ejection of blood
ETIOLOGY of Left Heart Failure
Pressure overload of ventricle → Systemic hypertension , aortic stenosis
Volume overload of ventricle → AR, VSD, PDA
Inflow obstruction of ventricle → Mitral stenosis
Impaired ventricular function → MI, Myocarditis, Cardiomyopathy
CLINICAL FEATURES
Symptoms
Dyspnea
Orthopnea
PND
Cardiac asthma / Wheezing
Nocturia
Cerebral symptoms → Confusion, difficulty in concentration, memory impairment,
headache
Signs
Vitals →
Sinus tachycardia
Diminished pulse pressure due to reduced stroke volume
Pulsus alternans
JVP is raised
Cheyne-stokes repiration → A type of periodic breathing with alternate periods of
apnoea and hyperventilation seen in advanced heart failure
Cyanosis
Auscultation →
Acute pulmonary edema → Bibasilar coarse crepts
S3, S4 heart sounds
Per abdomen → Tender hepatomegaly due to stretching of capsule of liver
MANAGEMENT
Control of excessive fluid
Low salt diet and fluid restriction
Diuretics :
Loop diuretics (furosemide, torsemide)
Thiazides
K sparing diuretics (spironolactone, eplerenone, amiloride)
Prevention of deterioration of myocardial function (Prevention of ventricular
remodeling)
Done by blocking the adrenergic nervous system and the renin-angiotensin-
aldosterone system (RAAS)
ACE inhibitors
MOA → Blocks angiotensin converting enzyme, thereby inhibiting conversion of
angiotensin 1 to angiotensin 2
Drugs → Captopril, enalapril, ramipril, lisinopril
Side effects → dry cough, angioedema, AKI in patients with bilateral renal artery
stenosis, hyperkalemia
Angiotensin receptor blockers
MOA → Blocks angiotensin receptors, hence do not allow angiotensin 2 to act
Drugs → Candesartan, valsartan, losartan, telmisartan
Side effects → hyperkalemia, angioedema
Aldosterone antagonists
Drugs → Spironolactone, eplerenone
Beta-blockers
Drugs → Atenolol, carvedilol, bisoprolol
Side effects → Sinus bradycardia, nightmares, bronchospasm
Vasodilators
Drugs → Sodium nitroprusside, nitroprusside, hydralazine and nesiritide (BNP
analogue)
Enhancement of myocardial contractility
Cardiac glycosides → Digitalis and digoxin
Sympathomimetic amines → Dopamine, dobutamine
PDE inhibitors → Milrinone, enoximone
Circulatory assist devices / cardiac transplantation
Required in class IV heart failure or refractory heart failure
Antiarrhythmics
Premature ventricular beats and episodes of asymptomatic ventricular tachycardia
are common in advanced heart failure. Amiodarone, a class III anti-arrhythmic may
be used.
Anticoagulation
Warfarin may be used in patients with previous thromboembolic events
List important factors known to worsen chronic stable cardiac failure.
Increased cardiac workload: Activities that increase the workload on the heart, such
as physical exertion or stress, can worsen cardiac failure.
Fluids accumulation: If the heart is not able to pump blood effectively, fluid can
accumulate in the lungs and other parts of the body, which can worsen cardiac
failure.
Medication nonadherence: Failing to take medications as prescribed by a healthcare
provider can worsen cardiac failure.
Poor diet: Eating a diet high in salt, saturated fat, and cholesterol can contribute to
the development of cardiac failure and worsen existing symptoms.
Alcohol consumption: Excessive alcohol consumption can increase the risk of
developing cardiac failure and worsen existing symptoms.
Smoking: Smoking can damage the heart and blood vessels and increase the risk of
developing cardiac failure.
Treatment of Chronic Heart Failure

Enumerate four drugs used in the treatment of cardiac failure, mentioning the
dosage and 1 side effect for each
Furosemide
Dosage - 20-40 mg OD or BD
Side effects - Interstitial nephritis, Hypokalemia, Hypomagnesemia, Hypocalcemia,
Metabolic alkalosis
Enalapril
Dosage - 2.5 mg BD to 10-20 mg BD
Side effects - Angioedema, Dry Cough, Teratogenic
Bisoprolol
Dosage - 1.25 - 2.5 mg OD
Side effects - Bradycardia, dry mouth, breathing problems
Spironolactone
Dosage - 12.5-25 mg OD
Side effects - Impotence, Gynecomastia, Metabolic acidosis
PULMONARY EMBOLISM
An obese woman aged 45 years suddenly develops acute severe dyspnea and
hypotension 2 days after undergoing a cholecystectomy. There is mild jugular
venous distension with prominent A waves. The lung fields are clear. ECG shows
sinus tachycardia with a right bundle-branch block a. What is your diagnosis?
Justify your diagnosis b. List the common risk factors for this condition c. List the
investigations and mention abnormalities expected d. How will you treat this patient?
Pulmonary Embolism with features of acute right heart failure most probably
secondary to deep vein thrombosis post surgical immobilization, current unstable.
Risk Factors
Primary (genetic)
Antithrombin III deficiency
Protein C and S deficiency
Factor V Leiden
Prothrombin 20210a
Secondary (acquired)
Surgery : Major abdominal/pelvic, hip/knee surgery
Obstetrics : Pregnancy, postpartum
Cardiorespiratory disease : COPD, CCF
Lower limb conditions : Fracture, varicose veins
Malignancy : Abdominal/pelvic, advanced/disseminated cancers, concurrent
chemotherapy
APLA
Misc. : Increased age, prolonged bed rest, prolonged immobilization, trauma
Investigations
Polymorphonuclear leukocytosis and raised ESR with pulmonary infarction
ECG → Tachycardia, Chances of acute pulmonary hypertension and right ventricular
enlargement
ABG → Hypoxemia, hypocapnia and respiratory alkalosis
Elevated D-dimer (500 ng/mL)
Pulmonary CT angiography → If normal then PE is ruled out. However, if abnormal,
could be due to PE or any underlying lung pathology. V/Q scan has to be done in
such cases
Doppler USG → Failure to compress the vascular lumen
Ascending contrast venography
Impedance plethysmography → Detects above knee thrombi
Radiofibrinogen method → Very accurate in calf vein and lower thigh thrombi
Radiological Features

Management
Supportive measures
Bed rest in acute stages
High flow oxygen (60-100%)
IV administration of inotropic agents (dopamine and noradrenaline)
Anticoagulation :
Either unfractionated heparin or LMWH can be used
Unfractionated heparin
Unfractionated heparin at initial dose of 80 units/kg IV followed by maintenance
For maintenance, heparin is administered using an infusion pump at rate of 18
units/kg/h
Heparin therapy is monitored with clotting time and activated plasma
thromboplastin time (aPTT) which is maintained at 1.5-2 times the control value
IV heparin has to be continued for 5-7 days
LMWH (e.g. enoxaparin, dalteparin) may be used. Monitoring in not required in case
of LMWH.
Oral warfarin should be started with an intention of keeping INR at 2.5-3.0
Anticoagulation is maintained for at least 6 months
Thrombolytic therapy
Indicated in patients with massive PE with hemodynamic compromise such as
hypotension
Streptokinase (2.5 lakh units by IV infusion over 30 minutes, followed by 1 lakh units
IV hourly for up to 12-72 hours) or urokinase or tPA can be used
Surgery
Surgical pulmonary embolectomy may be appropriate in patients who have massive
embolism occluding the main or proximal branches could be considered in all
patients if they are not able to maintain and cannot receive thrombolytic therapy.
IVC filters
In patients with contraindications to anticoagulation and recurrent embolism while
on anticoagulant therapy.
Risk factors for pulmonary thromboembolism
Primary (genetic)
Antithrombin III deficiency
Protein C and S deficiency
Factor V Leiden
Prothrombin 20210a
Secondary (acquired)
Surgery : Major abdominal/pelvic, hip/knee surgery
Obstetrics : Pregnancy, postpartum
Cardiorespiratory disease : COPD, CCF
Lower limb conditions : Fracture, varicose veins
Malignancy : Abdominal/pelvic, advanced/disseminated cancers, concurrent
chemotherapy
APLA
Misc. : Increased age, prolonged bed rest, prolonged immobilization, trauma
Extras
PULMONARY EDEMA
A chronic smoker, hypertensive and diabetic male patient aged 60 years
presents with acute onset dyspnea, cough and pink frothy sputum to the
emergency room a. What is the likely diagnosis based on the presenting symptoms?
b. What are the likely etiological possibilities? c. What other symptoms and signs you
would like to elicit? d. Outline the investigations and treatment of this case
Acute Pulmonary Edema
Likely etiological possibilities
Cardiogenic pulmonary edema
Left ventricular systolic/diastolic dysfunction
Arrhythmias
LV hypertrophy and cardiomyopathies
Myocardial infarction
LV outflow obstruction
Non-cardiogenic pulmonary edema
Direct injury to the lung - Chest trauma, pneumonia, pulmonary embolism
Indirect injury to the lung - Sepsis, Transfusion related acute lung injury (TRALI),
pancreatitis
Other symptoms and signs to be elicited
Symptoms
Chest pain, palpitations, orthopnea or PND
Bluish discoloration of skin
Leg pain, erythema or warmth (DVT)
Bilateral pedal edema
Epigastric pain radiating to the back relieved on bending forward
Syncope / Pre-syncope
Altered mental status
Signs
Cool extremities may indicate low cardiac output
Thready pulse
Lung auscultation → Bibasilar crepitations or wheeze
CVS auscultation → S3, Accentuation of pulmonic component of S2
JVD
Anasarca
Dependent edema (Both legs)
Patients with RV failure → hepatomegaly, sustained hepatojugular reflex and
peripheral edema
Investigations
CXR → Cardiomegaly, Batwing appearance, pleural effusion, cephalization of
pulmonary vessels, Kerley B lines
CT scan → Diffuse consolidation with air bronchograms, bullae, pleural effusions,
pneumomediastinum and pneumothorax
Electrocardiography → Reveals MI, active ischemia, ventricular hypertrophy,
arrhythmias
Stress ECG → Helps in assessing the viability in dysfunctional myocardium
Radionuclide Angiography → Reveal myocardial prefusion and viability
Cardiac Catheterization → Measuring pulmonary capillary wedge pressure can help
differentiate between cardiac and pulmonary causes of acute pulmonary edema
BNP - elevated in heart failure
Arterial blood gas analysis - PaO2 / FiO2 ratio
Treatment
Initial management consists of resuscitation of patient and maintaining the airway,
breathing and circulation.
Continuous monitoring of cardiac rhythm, BP and pulse oximetry.
Sit the patient up (Reduces preload)
Give high flow oxygen (Corrects hypoxia)
Ensure continuous positive airway pressure (CPAP) of 5-10 mmHg by tight fitting
mask (Reduces preload and pulmonary capillary hydraulic gradient)
Administer nitrates - IV glyceryl trinitrate (10-200 mcg/min) or Buccal glyceryl
trinitrate (2-5 mg) - The dose of nitrate should be titrated upwards until there is an
improvement or systolic blood pressure is less than 110 mmHg. (Nitrates reduce
both preload and afterload)
Administer a loop diuretic - Furosemide (50-100 mg IV) - (This combats fluid
overload)
Insertion of an intra-aortic balloon pump may be beneficial in patients with acute
cardiogenic pulmonary edema and shock.
After treatment of acute episode additional measures must be taken to control heart
failure in long term. These include -
General measures
Education
Diet
Good general nutrition and weight reduction in obese
Avoidance of high-salt foods and added salts
Alcohol - Moderation or elimination of alcohol consumption
Smoking cessation
Exercise - Regular moderate aerobic exercise within limits of symptoms
Vaccination - Consideration of influenza and pneumococcal vaccine
Drug treatments
Oral diuretics - Along with regular monitoring of weight and dose to be increased if
the weight increases suddenly since it might be indicative of edema due to
insufficient dosage. ACE inhibitors/ARBs and Spironolactone antagonists have an
additional benefit of prevention of remodeling of heart and thereby reduce mortality.
Neprilysin inhibitor → Sacubitril inhibits neprilysin, an enzyme that degrades ANP
and BNP. It is used along with the ARB valsartan.
Vasodilators → Useful when ACE inhibitors and ARBs are contraindicated. These
include nitrates, hydralazine.
Beta blockers → Prevent cardiac remodeling and thus provide mortality benefits.

Digoxin → used to provide rate control in patients with heart failure and atrial
fibrillation. Has no effect on long term survival.
Non-pharmacological treatment
Implantable cardiac defibrillators - indicated in symptomatic ventricular arrhythmias
and heart failure
Resynchronization devices
Coronary revascularization - in patients where heart failure was precipitated due to
MI
Cardiac transplantation - in patients with intractable cardiac failure
Ventricular assist devices - in patients with intractable cardiac failure and no donors
available for transplantation
Treatment of acute pulmonary edema
Treatment
Initial management consists of resuscitation of patient and maintaining the airway,
breathing and circulation.
Continuous monitoring of cardiac rhythm, BP and pulse oximetry.
Sit the patient up (Reduces preload)
Give high flow oxygen (Corrects hypoxia)
Ensure continuous positive airway pressure (CPAP) of 5-10 mmHg by tight fitting
mask (Reduces preload and pulmonary capillary hydraulic gradient)
Administer nitrates - IV glyceryl trinitrate (10-200 mcg/min) or Buccal glyceryl
trinitrate (2-5 mg) - The dose of nitrate should be titrated upwards until there is an
improvement or systolic blood pressure is less than 110 mmHg. (Nitrates reduce
both preload and afterload)
Administer a loop diuretic - Furosemide (50-100 mg IV) - (This combats fluid
overload)
Insertion of an intra-aortic balloon pump may be beneficial in patients with acute
cardiogenic pulmonary edema and shock.
VALVULAR PATHOLOGIES
A female patient aged 25 years presents with dyspnea and palpitation. On
examination she has irregularly irregular pulse, tapping apical impulse and mid-
diastolic murmur at apex. What is the likely diagnosis? What is the
pathophysiological basis for her symptoms and signs? What are the
complications of this condition? How do you investigate and treat this patient?
Mitral Stenosis complicated by Atrial Fibrillation
Pathophysiology of Symptoms
Mitral stenosis → Increase in LA pressure → Pulmonary Venous Hypertension →
Pulmonary Venous congestion → Fluid leak from pulmonary capillaries into
interstitium → Reduced lung compliance → Increased work of breathing → DYSPNEA
Mitral Stenosis → Increase in LA pressure → LA dilatation → Atrial Fibrillation →
PALPITATIONS
Pathophysiology of Signs
Mitral Stenosis → Increase in LA pressure → LA dilatation → Atrial Fibrillation →
IRREGULARY IRREGULAR PULSE
Mitral Stenosis → Increase in LA pressure → Increased transmitral pressure gradient
→ Failure of mitral valve to come into semi-closed position at the end of atrial
diastole → LV needs a higher pressure to close the mitral valve → Rapid apposition of
leaflets → Loud palpable S1 → TAPPING APICAL IMPULSE
Mitral stenosis → Diseased mitral valve → Murmur during blood flow through
diseased valve → MID DIASTOLIC MURMUR
Complications
Investigations

Treatment
A 20 year old male presented with history of hemoptysis of about 100 ml since
2 days. On examination he had irregular pulse and mid-diastolic murmur in the
mitral area. a. What is your likely diagnosis? b. Describe relevant investigations
to arrive at diagnosis c. Describe the management.
Mitral stenosis complicated by pulmonary venous hypertension leading to
hemoptysis
Investigations
ECG →
Left atrial enlargement (P Mitrale)
Enhanced second hump in lead II
Increased negative deflection in V1
Right ventricular hypertrophy
AFib
ECHO →
Mitral stenosis and the valve orifice size
Size of cardiac chambers
Pulmonary artery pressure
Calcification of mitral valve
TEE
Improved image of mitral valve anatomy
Clot in left atrium
CXR
Left atrial enlargement → Straightening of the left heart margin (mitralisation) due to
enlargement of left atrial appendage, widening of carinal angle and elevation of left
main stem bronchus, indentation of esophagus on barium swallow
Pulmonary venous hypertension → Cephalization of pulmonary vessels (Stag’s
Antlers Sign), Kerley A (hilum) and Kerley B (costophrenic angles) lines
Mitral valve calcification
Management
MEDICAL →
For complications like
Atrial Fibrillation → Anti-coagulants, digoxin, verapamil
Right ventricular failure → Salt restriction, diuretics
Infective endocarditis prophylaxis if prosthetic valve present
Rheumatic fever prophylaxis
SURGICAL
Balloon mitral valvotomy (BMV) also known as percutaneous balloon valvuloplasty
(PBV) in young patients without extensive valvular calcification or thickening, no atrial
thrombus and no or mild mitral regurgitation
Mitral valve replacement is performed if significant mitral regurgitation is present, if
leaflets are immobile, heavily calcified or if there is severe subvalvular scarring
Mechanical prosthetic valves → Require lifelong anti-coagulation
Bioprosthetic valves → Low incidence of thrombosis. Because of rapid deterioration
of valve, it is not used in patients < 35 years of age
34 year old male presented with fever of 3 weeks duration and dyspnea on
exertion since 2 weeks. On examination patient had pallor and pan systolic
murmur in mitral area. What are the possible diagnosis? Describe in detail
investigations and outline the management of this patient
Acute Mitral Regurgitation secondary to
Infective endocarditis
Acute Rheumatic Fever with carditis
Investigations -
ECG → Look for atrial fibrillation
CXR → Calcification of mitral valve
ECHO → Vegetations, Valvular defects, Degree of regurgitation, Clues regarding
etiology
CBC → Leukocytosis, anemia
ESR and CRP → Elevated
Procalcitonin → High
Blood culture → 3 samples, different sites, 1 hr apart
Medical Management
Restriction of physical activity
Evaluation and modification of coronary artery risk factors to prevent its
development
Treatment of heart failure with salt restriction, digoxin, diuretics, ACE inhibitors, beta-
Blockers, aldosterone antagonists and vasodilators
Nitrates and diuretics to reduce preload
Rheumatic Fever prophylaxis
Drug used → Benzathine Penicillin G 1.2 million units deep IM (buttocks) every
month or every 3 weeks (more effective)
Duration of prophylaxis
Category of patient Duration
Rheumatic fever without carditis For 5 years after last attack or up to 21 years of age
(whichever is longer)
Rheumatic fever with carditis but no residual For 10 years after last attack or up to 21 years of age
valvular disease (whichever is longer)
Rheumatic fever with persistent valvular disease For 10 years after last attack or up to 40 years of age or
visible on ECHO sometimes lifelong
Infective endocarditis prophylaxis
Qualifying cardiac conditions for prophylaxis
Prosthetic valves
Previous infective endocarditis
Congenital heart disease -
Unrepaired cyanotic CHD
Completely repaired CHD with prosthetic material or device, during the first 6
months after procedure
Repaired CHD with residual defects at the site or adjacent to the site of prosthetic
device (which inhibits endothelialization)
Cardiac transplant recipients with cardiac valvular diseases
Qualifying procedures for prophylaxis
Dental procedures that require manipulation of gingival tissue or the periapical
region of teeth or perforation of oral mucosa
Invasive procedures of the respiratory tract that involve incision or biopsy of the
respiratory mucosa, such as tonsillectomy or adenoidectomy
Surgical procedures that involve infected skin, skin structure, or musculoskeletal
tissue
Drugs used for prophylaxis
Situation Agent and dose (single dose 30-60 mins before procedure)
Able to take oral meds Amoxicillin 2 g
Unable to take oral meds Ampicillin 2 g IM
Allergic to penicillin and able to take orally Cephalexin 2 g or Clindamycin 600 mg
Allergic to penicillin and unable to take orally Cefazolin or Ceftriaxone 1 g IV or IM
Surgical management
Re-construction of mitral valve apparatus by mitral valvuloplasty or mitral
annuloplasty.
MVR with a prosthesis if the above is not feasible. Prophylactic infective endocarditis
antibiotics after MVR to be started.
Causes and clinical features of aortic stenosis

Symptoms
Decreased exercise tolerance is usually the first symptom and occurs due to angina in
the compensated phase
Exertional dizziness and syncope
Exertional breathlessness, orthopnea and PND due to heart failure which occurs in
decompensated phase
Hematemesis and melaena from AV malformations of right colon, small intestine and
stomach (Heyde's syndrome)
Signs
Pulsus tardus is a slow rising arterial pulse best felt in carotids (delayed carotid
upstroke) due to prolongation of ejection phase. The classic anacrotic pulse is seen in
severe aortic stenosis
Low systolic blood pressure ( < 100 mmHg).
In congenital supravalvular aortic stenosis, systolic blood pressure is usually higher
by approximately 30 mmHg in right arm than in left arm
Normal jugular venous pulse; however prominent a waves may be present due to
reduced right ventricular compliance produced by hypertrophy of interventricular
septum.
Heaving apical impulse.
No cardiomegaly in the initial stages of concentric hypertrophy. Cardiomegaly
develops later, with left ventricular dilatation and failure.
Auscultation
A2 delayed → Narrow splitting of second heart sound in mild to moderate cases,
paradoxical splitting in severe cases
S3 heard in case of ventricular failure
S4 due to vigorous atrial contraction
Ejection systolic mumur best heard at aortic area, conducted to carotids. It is best
heard with patient sitting up, leaning forwards with breath held in expiration
Gallavardin phenomenon → In calcific aortic stenosis, the murmur is loud and harsh
in the aortic area, but it has a musical quality along the left sternal border and at
apex. This difference in quality of the same murmur at two different sites is referred
to as "Gallavardin phenomenon". It may be confused with murmur of mitral
regurgitation. However, the murmur of aortic stenosis at apex is musical and high
pitched while that of mitral regurgitation is harsh holosystolic murmur
Extras
Aortic Regurgitation
Causes
Acute AR : Infective endocarditis, trauma, aortic dissection
Chronic AR : Ehlers-Danlos syndrome, Osteogenesis imperfecta, Marfan’s syndrome
Rheumatic heart disease, Syphilis, Congenital bicuspid aortic valve, large vessel
vasculitis
Symptoms
Dyspnea on exertion
Angina : Due to decreased diastolic perfusion → Decreased coronary perfusion
Signs
Murmur : Diastolic decrescendo, heard best at left sternal border, increases on
squatting and hand gripping, decreases on Valsalva maneuver
Widened pulse pressure
De Musset’s sign : Head bobbing
Quincke’s pulse : Pulsating nail bed (flushing and blanching)
Muller’s sign : Pulsations of uvula with heartbeat
Pistol shot murmur : femoral artery
Water-hammer (Corrigan’s) pulse : Rapid rise and fall of carotid pulse
CARDIOMYOPATHIES
Hypertrophic cardiomyopathy (HOCM) clinical features and treatment
Symptoms
Many patients are asymptomatic
Family history of sudden death may be positive
Dyspnea, fatigue, angina, syncope or near syncope
Sudden death during or after physical exertion
Signs
Arrthythmias are common
Rapidly rising carotid pulse
Bisferiens pulse
Double apical impulse
Loud S4
Harsh ejection systolic mumur best heard at the lower left sternal border. The
murmur increases during standing and valsava manoeuvre (reduces preload) but
decreases during squatting or sustained hand grip (increases afterload), and also by
leg raising (which increases preload)
Pansystolic murmur at mitral area due to mitral regurgitation
Treatment
Beta-blockers → Improves ventricular relaxation, increases diastolic filling time and
reduces susceptibility to ventricular and supraventricular arrhythmias
Amiodarone for controlling arrhythmias
CCBs w/o significant vasodilatory effect are also beneficial
If beta-blockers alone are not sufficient, disopyramide (which also has a negative
inotropic effect) along with 13-blockers are helpful to reduce outflow tract
obstruction
Surgical myotomy or myectomy of hypertrophied septum
Digoxin, diuretics, nifedipine, nitrates and beta-agonists should be avoided since
they increase outflow tract obstruction
Implantable cardioverter-defibrillator in high-risk patients
Septal alcohol ablation is being increasingly used.
Evaluation of family members
RHEUMATIC HEART DISEASE
Jones Criteria for diagnosis of Acute Rheumatic Fever

Acute rheumatic fever diagnosis and management // Treatment of acute rheumatic

fever
INFECTIVE ENDOCARDITIS
40 year old lady, known case of valvular heart disease presents with fever and
joint pain. On examination there is clubbing mild splenomegaly. There is a
systolic murmur in mitral area. What is your diagnosis? How do you evaluate
the case? How do you treat the same?
Clinical features, investigations and treatment of infective endocarditis
Clinical features
Evidence of infection
Vague symptoms such as unusual tiredness, fatigue, lassitude, loss of appetite and
weight
Persistent or intermittent low-grade or high-grade fever with night sweats, chills and
rigor
Clubbing
Splenomegaly
Evidence of new valve lesion
New murmur - particularly a diastolic murmur is the diagnostic feature
Changing murmurs
Evidence of embolism
Cutaneous manifestations
Purpura and petechiae
Subconjunctival or Subungual splinter hemorrhages
Janeway lesions - Erythematous, non-tender nodules on palms and soles
Roth spots - flame shaped hemorrhages
Septic infarcts
Spleen - painful splenomegaly
Kidney - loin pain, hematuria, and renal failure
Brain - Convulsions, hemiplegia, aphasia, loss of vision, cerebellar disturbances
Lungs - Pulmonary infarction, pleurisy and pleural effusion
Mycotic aneurysms
Evidence of immunological phenomena
Osler’s node - Tender, small, painful, swollen subcutaneous nodules in pulp pf distal
fingers due to hypersensitive angiitis
Focal segmental glomerulonephritis
Investigations
Microbiological investigations
Blood cultures - At least three sets of blood samples for cultures should be taken
from different venipuncture sites
Serological tests - useful when cultures are negative such as in Coxiella, Bartonella,
Legionella and Chlamydia
ECG - Complications like AB block and MI due to emboli can be detected
CXR - Evidence of cardiac failure, cardiomegaly, pulmonary edema
ECHO - identify the presence and size of vegetations, assess valve damage, abscess
formation, assess cardiac functions
Transthoracic
Transesophageal - greater sensitivity and specificity
CBC → Increased WBC counts, Normocytic normochromic anemia
Urea and Creatinine - May be increased due to glomerulonephritis
Liver biochemistry - ALP may be increased
CRP/ESR increased
Urine Analysis - Proteinuria and hematuria
Treatment
Medial treatment
Collect blood cultures before starting treatment.
If source of infection is identified, it should be removed as soon as possible
Empirical treatment regimen
No suspicion of Staphylococci → Benzylpenicillin IV 1.2 g 4 hourly, 4-6 weeks +
Gentamicin IV 80 mg 12 hourly, 2-6 weeks
Suspicion of Staphylococci (IVDU, recent intravascular devices or cardiac surgery) →
Vancomycin IV 1 g 12 hourly for 6 weeks + Gentamicin IV 80-120 mg 8 hourly, 1-2
weeks.
In prosthetic wall endocarditis → Add Rifampicin 20 mg/kg/day in two divided doses
Surgical treatment → In selected patients only. Cardiac surgery consists of
debridement of infected material and valve replacement. Antibiotic therapy should
be started before surgery
Investigations of bacterial endocarditis
Investigations
Microbiological investigations
Blood cultures - At least three sets of blood samples for cultures should be taken
from different venipuncture sites
Serological tests - useful when cultures are negative such as in Coxiella, Bartonella,
Legionella and Chlamydia
ECG - Complications like AB block and MI due to emboli can be detected
CXR - Evidence of cardiac failure, cardiomegaly, pulmonary edema
ECHO - identify the presence and size of vegetations, assess valve damage, abscess
formation, assess cardiac functions
Transthoracic
Transesophageal - greater sensitivity and specificity
CBC → Increased WBC counts, Normocytic normochromic anemia
Urea and Creatinine - May be increased due to glomerulonephritis
Liver biochemistry - ALP may be increased
CRP/ESR increased
Urine Analysis - Proteinuria and hematuria
Treatment of infective Endocarditis
Treatment
Medial treatment
Collect blood cultures before starting treatment.
If source of infection is identified, it should be removed as soon as possible
Empirical treatment regimen
No suspicion of Staphylococci → Benzylpenicillin IV 1.2 g 4 hourly, 4-6 weeks +
Gentamicin IV 80 mg 12 hourly, 2-6 weeks
Suspicion of Staphylococci (IVDU, recent intravascular devices or cardiac surgery) →
Vancomycin IV 1 g 12 hourly for 6 weeks + Gentamicin IV 80-120 mg 8 hourly, 1-2
weeks.
In prosthetic wall endocarditis → Add Rifampicin 20 mg/kg/day in two divided doses
Surgical treatment → In selected patients only. Cardiac surgery consists of
debridement of infected material and valve replacement. Antibiotic therapy should
be started before surgery
Duke’s criteria

OTHERS
Define these terms: preload, afterload, hypoxia, hypercarbia
Preload → Refers to the pressure that fills the left ventricle during diastole. It is
measured either directly as the left-ventricular end-diastolic pressure, or indirectly
and more commonly as the pulmonary artery wedge pressure (PAWP). Main
determinants of preload are left ventricular compliance and venous return
Afterload → Refers to the pressure against which the left ventricle contracts and is
measured as the mean aortic pressure. Main determinants of afterload are total
peripheral resistance and left ventricle size
Hypoxia → Hypoxia is defined as a condition where the oxygen supply is inadequate
either to the body as a whole (general hypoxia) or to a specific region (tissue
hypoxia)
Hypercarbia → Hypercapnia, defined as an elevation in the arterial carbon dioxide
tension, is commonly encountered during the evaluation of patients with dyspnea
and/or altered sensorium
Clinical features of right heat failure
Symptoms
Anorexia, nausea, vomiting (due to gastric mucosal congestion)
Right hypochondrial pain (due to liver congestion)
Signs
Peripheral edema
Raised JVP
Ascites, pleural effusion
Right ventricular S3 and S4 gallop
Treatment
Salt restriction
Digoxin
Diuretics
Phlebotomy when hematocrit is more than 60%
Vasodilator therapy to reduce afterload with hydralazine and nifedipine
Sildenafil (PDE4 inhibitor) may be used in treatment of pulmonary hypertension
Bosentan, an endothelin-1 receptor blocker, has some role in idiopathic pulmonary
hypertension
Four etiology of syncope
Vasovagal syncope → Emotional stress, warm overcrowded room, sudden pain, mild
blood loss, anemia, fever and fasting
Cardiac syncope → Complete heart block, Paroxysomal tachycaridas, Sick sinus
syndrome, Acute massive MI, Aortic stenosis
Orthostatic syncope → Physiological, antihypertensive drugs, diabetic neuropathy,
tabes dorsalis
Syncope associated with cerebrovascular disease → Occlusion of large arteries in the
neck (Carotid stenosis)
A 60 year old male presents with h/o recurrent episodes of syncope since 2 months.
His pulse rate is 36/minute, regular. Neck shows occasional canon waves.
Cardiovascular examination except for bradycardia is normal. What is the diagnosis
and how to investigate and treat him?
Cardiac syncope due to complete heart block (Stokes Adams Morgagni Syndrome)
Investigations → ECG → Complete AV dissociation. Constant P-P and R-R intervals.
Management
IV atropine (0.6 mg) that may be repeated every 3-5 minutes for a total of 3 mg
If bradycardia is unresponsive to atropine, IV infusion of beta-agonists with rate-
accelerating effects (dopamine, epinephrine) or transcutaneous pacing can be
effective while the patient is prepared for emergent transvenous temporary pacing
Chronic complete heart block should be treated by the implantation of a permanent
pacemaker.
A 25 years old male with chronic rheumatic mitral valve disease presents with
acute onset right sided hemiplegia a. Mention three differential diagnosis. b.
Mention the specific history, clinical features and investigations to differentiate
each of them. c. Discuss the specific treatment of any one of them.
Explain four complications of congenital heart diseases
Infective endocarditis
Cardiac Failure
Pulmonary Hypertension and Eisenmenger’s syndrome
Paradoxical embolism
Write a note on clinical features (symptoms and signs) of acute pericarditis.
Symptoms
Pericardial pain → Sharp, retrosternal chest pain which radiates to shoulder and neck
Relieved by leaning forward
Aggravated by deep breathing, movement and change of position, coughing
Non-specific symptoms
Low grade fever and malaise
Large pericardial effusion can compress adjacent bronchi and lung and produce
dyspnea (Ewart’s sign)
Signs
Pericardial friction rub
High pitched superficial scratching sound produced by movement of inflamed
pericardium.
Best heard by applying firm pressure with diaphragm of stethoscope at the lower left
sternal edge at the end of expiration with the patient sitting upright and leaning
forward
Pulsus paradoxus - weakness/disappearance of pulse during inspiration (due to
reduced systolic BP)
Cardiac tamponade
Constrictive pericarditis
Constrictive pericarditis
Etiology
Tuberculosis
Rheumatoid arthritis
Hemopericardium
Idiopathic
Clinical features
Raised JVP with rapid y descent
Pulse is rapid and of low volume
Pulsus paradoxus
Kussmaul’s sign : inspiratory augmentation of JVP
Hepatomegaly
Ascites and pedal edema
Pericardial knock
Investigations
CXR : Small sized heart with calcification of pericardium
Ascitic fluid : Transudative
ECG : Confirms the diagnosis. Normal QRS axis, low voltage, T wave
flattening/inversion.
Treatment
Manage the underlying cause
Pericardiectomy
Atorvastatin
Complete heart block
In complete heart block, none of the atrial impulses reach the ventricles. The atria are
thus activated by one pacemaker, usually the sinus pacemaker. The ventricles are
activated by another pacemaker situated either in the bundle of His or ventricles.
Paroxysmal nocturnal dyspnea
Definition - Episode of sudden onset of dyspnea 2–2.5 hours after sleep
Timing - Patient wakes up from rapid eye movement (REM) sleep
Method of relief - Sits up with legs hanging down, stands up, air hunger, self
ventilates to comfort
Mechanism - Depressed respiratory center. Sympathetic over activity during REM →
catecholamine surge resulting in tachycardia → interstitial pulmonary congestion →
respiratory center lags behind → perceived as acute dyspnea. There is sudden
transient increase in PCWP
Associated symptoms - Angina, perspiration, palpitations
Oxygen saturation - Transient hypoxia
D/D → Nightmares, Panic attacks, Obstructive sleep apnoea
Mention the causes of acute onset of dyspnea in a 50 year old male. Discuss the
differential diagnosis.
Hyperacute onset (Minutes to Hours)
Airway causes
Anaphylaxis
Triggers → food, medications, insect stings
C/F → Angioedema, hypotension, wheezing, urticaria
Foreign body
CXR → Unilateral air trapping
Pulmonary causes
Pneumothorax
C/F → Pleuritic chest pain, increased resonance to percussion, diminished breath
sounds on affected side
CXR → Absence of lung markings on the side of collapse. Visible white pleural line.
Deviation of mediastinum to opposite side.
Pulmonary embolism
C/F → concomitant tachycardia, pleuritic chest pain and leg pain/swelling from DVT,
prolonged immobilization, recent surgeries, OCP use
CT scan
Cardiac causes
Acute myocardial infarction
C/F → Anginal chest pain, diaphoresis
ECG → ST segment changes
Cardiac biomarkers → Troponins, CK-MB
Arrhythmias
C/F → Palpitations, irregularly irregular pulse
Cardiac tamponade
C/F → Beck’s triad (elevated JVP, hypotension, muffled heart sounds)
ECHO
Others
Panic attack
Acute onset (hours to days)
Pulmonary causes
COPD exacerbation
Triggers → Respiratory infection, smoking
C/F → Worsening dyspnea, cough, sputum
ABG → Hypercapnia, acidosis
Asthma
Triggers → Respiratory infection, smoking
C/F → History of atopy
ABG → Hypercapnia, acidosis
Pneumonia
C/F → Fever, productive cough, pleuritic chest pain, crackles on lung auscultation
CXR → Focal consolidation
CBC → Leukocytosis
Lung cancer
C/F → Significant smoking history, weight loss, hemoptysis
CXR → Mass lesion
ARDS
C/F → Features of sepsis, bibasilar crepitations (pulmonary edema)
CXR → Bilateral infiltrates
Cardiac causes
Heart failure
C/F → Pink frothy sputum, bibasilar crepitations, wheezing, lower extremity edema
and JVD, S3 audible, heart murmurs
BNP levels elevated
ECHO may show valvular pathologies
Others
Toxins → OP poisoning, botulinum toxin
Causes of Pulmonary Hypertension
Clubbing
Clubbing is enlargement of soft tissues in the terminal phalanges leading to both
transverse and longitudinal curving of the nails. Longitudinal curving leads to loss of
angle between the nail and nail bed. Normally this angle is 180 degrees. In clubbing
it is more than 180 degrees.
Grades
Grade I: Softening of nail bed. Fluctuation is present at this stage.
Grade II: Loss of angle between the nail and nail bed.
Grade III: Parrot beak appearance nail or drumstick appearance of the digit
Swelling of fingers in all dimensions associated with hypertrophic pulmonary
osteoarthropathy
Mechanism
It is believed that chronic hypoxia is the main triggering factor for the development
of clubbing. Chronic hypoxia leads to opening of arteriovenousfistulas which increase
the blood supply to digits and toes leading to soft tissue hypertrophy
Causes of clubbing
Respiratory
Pulmonary TB
Lung abscess
Bronchiectasis
Bronchogenic carcinoma
Mesothelioma
Interstitial lung disease
Empyema thoracis
Cystic fibrosis
CVS
Infective endocarditis
Cyanotic congenital heart diseases
Atrial myxoma
Aneurysms
GIT
Inflammatory Bowel Diseases
Primary biliary cirrhosis
Hepatocellular carcinoma
Endocrine
Acromegaly
Myxedema
Unilateral clubbing - Pancoast tumor, SC artery aneurysm
Unidigital clubbing - Trauma, nerve injury
Idiopathic
Central chest pain- etiology and evaluation
Etiology
Cardiac causes - ECG, ECHO, Cardiac Markers, BNP
Acute coronary syndrome
Stable angina
Vasospastic angina
Stress indued cardiomyopathy
Aortic dissection
Cardiac tamponade
Acute pericarditis
Respiratory causes - Sputum culture
Pneumonia
Pulmonary embolism
Pleuritis
Pneumothorax
Gastrointestinal causes - Esophageal manometry, Upper GI Endoscopy
GERD
Esophageal dysmotility disorder
Esophagitis
Hiatal hernia
Esophageal spasm
Esophageal rupture (mediastinitis)
Others
Costochondritis

Respiratory System incl. Tuberculosis

TUBERCULOSIS
A 30 year old driver presents with 2 weeks history of fever, cough, and loss of
appetite. What are the four differential diagnosis? Discuss the investigation of
this patient and management of one cause of this condition.
Tuberculosis
Pneumonia
Acute sinusitis
Acute bronchitis
General Investigations to identify the cause
CXR
Tuberculosis : Apical infiltrates, cavitary lesions, calcified lesions and pleural
effusion/thickening
Pneumonia : Focal consolidation
PNS X-ray
Acute sinusitis : Collection of fluid in sinus. May also show a nasal polyp or DNS
CT head and neck
Sputum culture
To aid in the diagnosis of TB or pneumonia by identifying the organism
CB-NAAT
Provides a quick diagnosis of TB along with rifampicin sensitivity information
Management of tuberculosis
Anti-tubercular therapy
Drug sensitive TB
As per the latest recommendations from NTEP, treatment of TB is now based
primarily on drug susceptibility testing. This is irrespective of new cases, previously
treated cases or recurrent TB cases.
All cases of TB are treated with drug sensitive TB regimen, as long as patients is
sensitive to isoniazid and rifampicin.
It consist of the following
Intensive phase → HRZE x 2 months
Continuation phase → HRE x 4 months
Drug Daily Dose Max Dose
Isoniazid (H) 5 mg/kg 300 mg
Rifampicin (R) 10 mg/kg 600 mg
Pyrazinamide (Z) 25 mg/kg 2 g
Ethambutol (E) 15 mg/kg
H mono/poly drug resistant TB
The following drugs for a duration of 6 months are given
Pyrazinamide (Z)
Ethambutol (E)
Rifampicin (R)
Levofloxacin (Lfx)
MDR TB/ Rifampicin Resistant TB
Shorter MDR TB regimen (9-10 months)
Intensive phase (4-6 months)
Clofazimine (Cfz)
High dose Isoniazid (Hh)
Moxifloxacin (Mfx)
Bedaquiline (Bdq) - 6 months
Pyrazinamide (Z)
Ethionamide
Ethambutol
Continuation Phase (5 months)
Clofazimine
Moxifloxacin
Pyrazinamide
Ethambutol
All oral longer MDR TB regimen (18-20 months)
Bedaquiline (6 months or longer)
Levofloxacin
Linezolid (Dose reduced at end of 6 months)
Clofazimine
Cycloserine
35-year-old male presented with history of fever and cough for 3 weeks
duration. He had lost 10 kilos in the last 2 months. He had exposure to multiple
commercial sex workers in the past. On examination, he had oral candidiasis
and multiple cervical lymph nodes. Vitals were stable. Respiratory system -
suprascapular and supraclavicular region crepitations were present. Rest of
systemic examination was unremarkable a. What is the clinical diagnosis? b.
Outline the list of investigations. c. Outline treatment plan in detail d. Mention
common side effects of the drugs used in the treatment
Post-primary (Secondary) Pulmonary tuberculosis and Oral candidiasis possibly due
to retroviral disease (HIV infection)
Investigations
Blood examination
Anemia - moderate degree
WBC count - Usually normal or below normal
ESR - raised
Investigations for TB
Radiological
Chest X-ray → Apical infiltrates, cavitary lesions, calcified lesions and pleural
effusion/thickening
CT chest → Tree in bud appearance
Specific
Direct sputum examination
Two samples - one spot and one morning sample taken
Stained using Ziehl-Neelsen staining.
Presence of acid fast bacilli
Culture of sputum
Liquid culture - Middlebrook 7H12 or MGIT (1-3 weeks)
Solid media - Lowenstein-Jensen slopes (4-6 weeks)
CB-NAAT (GeneXpert)
Sputum sample used
Results within 90 minutes
Also tests rifampicin sensitivity
IGRA (Interferon Gamma Release Assay)
Investigations for HIV
HIV RNA levels can be detected earliest by 12th day of infection
p24 antigen can be detected by average of 16th day infection
4th generation antigen antibody combined assay is being done now - These assays
detect p24 capsid antigen and IgG antibodies against HIV 1/2
If a patient comes negative - patient doesn’t have HIV
If the patient comes positive - look specifically for antibodies against HIV 1/2
CD4 counts to detect the severity of disease
Treatment → First start Antitubercular therapy and then add Anti-retroviral therapy
to prevent SIRS
Anti-tubercular therapy
Drug sensitive TB
As per the latest recommendations from NTEP, treatment of TB is now based
primarily on drug susceptibility testing. This is irrespective of new cases, previously
treated cases or recurrent TB cases.
All cases of TB are treated with drug sensitive TB regimen, as long as patients is
sensitive to isoniazid and rifampicin.
It consist of the following
Intensive phase → HRZE x 2 months
Continuation phase → HRE x 4 months
Drug Daily Dose Max Dose
Isoniazid (H) 5 mg/kg 300 mg
Rifampicin (R) 10 mg/kg 600 mg
Pyrazinamide (Z) 25 mg/kg 2 g
Ethambutol (E) 15 mg/kg
H mono/poly drug resistant TB
The following drugs for a duration of 6 months are given
Pyrazinamide (Z)
Ethambutol (E)
Rifampicin (R)
Levofloxacin (Lfx)
MDR TB/ Rifampicin Resistant TB
Shorter MDR TB regimen (9-10 months)
Intensive phase (4-6 months)
Clofazimine (Cfz)
High dose Isoniazid (Hh)
Moxifloxacin (Mfx)
Pyrazinamide (Z)
Bedaquiline (Bdq) - 6 months
Ethionamide
Ethambutol
Continuation Phase (5 months)
Clofazimine
Moxifloxacin
Pyrazinamide
Ethambutol
All oral longer MDR TB regimen (18-20 months)
Bedaquiline (6 months or longer)
Levofloxacin
Linezolid (Dose reduced at end of 6 months)
Clofazimine
Cycloserine
Anti-retroviral therapy
It consists of three drug combination
Nucelotide Reverse Transcriptase Inhibitor
Nucleoside Reverse Transcriptase Inhibitor (NRTI)
Integrase inhibitor
The current regimen followed is TED regimen
Tenofovir disoproxil (300 mg OD)
Emtricitabine (200 mg OD)
Dolutegravir (50 mg OD)
NACO regimen
Tenofovir disoproxil (300 mg OD)
Lamivudine (300 mg OD)
Dolutegravir (50 mg OD)
Treatment for Oral Candidiasis
Oral nystatin
Fluconazole
Side effects

List the manifestations of tuberculosis in the chest. Discuss the clinical features
of pneumothorax, and the management of tension pneumothorax.
Clinical manifestations of pulmonary tuberculosis
Primary pulmonary TB
Symptoms
Majority are asymptomatic
Few patients - self limiting febrile illness which may last no more than 7-14 days
Clinical disease only occurs if there is progressive infection.
History of contact with a case of active TB
Signs
Sometimes few crepitations may be heard over lung parenchyma involved by the
primary complex
Erythema nodosum may be seen on shins
Secondary pulmonary TB
Symptoms
Generalized symptoms
Localized secondary TB may remain asymptomatic
Onset is usually insidious, with symptoms developing slowly over weeks or months
Non-specific - Malaise, anorexia, loss of appetite and weight
Low grade fever - remittent (appearing late each afternoon and then subsiding -
commonly known as evening rise of temperature) and night sweats
Respiratory symptoms
Chronic cough - most consistent symptom
Hemoptysis
Sputum - classical sputum is described as numular
Pain in the chest - due to pleurisy
Breathlessness - in advanced disease
Signs
General signs
Fever, tachycardia and tachypnea
Pallor and cachexia
Clubbing
Chest
Fine crepts in the upper part of one or both lungs. Better heard on taking a deep
breath after coughing (post-tussive crepitations)
Cavernous bronchial breathing
Classical signs of consolidation (dullness to percussion), cavitation, fibrosis,
bronchiectasis, pleural effusion or pneumothorax may be present
Pneumothorax
Clinical features
Symptoms
Sudden onset pleuritic chest pain and breathlessness (dyspnea)
Severity depends on extent of lung collapse and amount of pre-existing lung disease
Tension pneumothorax - distressed patient, rapid labored respiration, cyanosis,
marked tachycardia, profuse diaphoresis
Signs
General - cyanosis, tachypnea, peripheral pulses may be feeble and hypotension may
be present
Respiratory
Inspection and Palpation
Accessory muscle usage
Trachea and mediastinal shift to the unaffected side
On the affected side -
fullness of chest
diminished respiratory movements
increase in size of hemithorax
increased spino-scapular distance
markedly diminished vocal fremitus
subcutaneous emphysema may be present
Percussion - Hyper-resonant note over affected hemithorax
Auscultation -
Markedly decreased/absent breath sound and vocal resonance
Absence of adventitious sounds
Open pneumothorax with bronchopulmonary fistula, there may be amphoric
bronchial breathing
Management of tension pneumothorax
Acute medical emergency
Insertion of large-bore needle into the pleural space through second anterior
intercostal space
Diagnosis is confirmed if large amounts of air escape through the inserted needle.
Needle should be kept in place till a thoracostomy tube can be inserted
Cover the open end of the needle with glove finger
Outline clinical features, risk factors, investigations and management of sputum
positive tuberculosis. Add a note on common side effects of first line
antitubercular drugs.
Clinical features
Primary pulmonary TB
Symptoms
Majority are asymptomatic
Few patients - self limiting febrile illness which may last no more than 7-14 days
Clinical disease only occurs if there is progressive infection.
History of contact with a case of active TB
Signs
Sometimes few crepitations may be heard over lung parenchyma involved by the
primary complex
Erythema nodosum may be seen on shins
Secondary pulmonary TB
Symptoms
Generalized symptoms
Localized secondary TB may remain asymptomatic
Onset is usually insidious, with symptoms developing slowly over weeks or months
Non-specific - Malaise, anorexia, loss of appetite and weight
Low grade fever - remittent (appearing late each afternoon and then subsiding -
commonly known as evening rise of temperature) and night sweats
Respiratory symptoms
Chronic cough - most consistent symptom
Hemoptysis
Sputum - classical sputum is described as numular
Pain in the chest - due to pleurisy
Breathlessness - in advanced disease
Signs
General signs
Fever, tachycardia and tachypnea
Pallor and cachexia
Clubbing
Chest
Fine crepts in the upper part of one or both lungs. Better heard on taking a deep
breath after coughing (post-tussive crepitations)
Cavernous bronchial breathing
Classical signs of consolidation (dullness to percussion), cavitation, fibrosis,
bronchiectasis, pleural effusion or pneumothorax may be present
Risk Factors
HIV
Diabetes mellitus
Malnutrition
Hodgkin’s lymphoma
Immunosuppression
Alcoholism
Chronic lung disease (eg. silicosis)
Chronic renal failure
Investigations
Blood examination
Anemia - moderate degree
WBC count - Usually normal or below normal
ESR - raised
Investigations for TB
Radiological
Chest X-ray → Apical infiltrates, cavitary lesions, calcified lesions and pleural
effusion/thickening
CT chest → Tree in bud appearance
Specific
Direct sputum examination
Two samples - one spot and one morning sample taken
Stained using Ziehl-Neelsen staining.
Presence of acid fast bacilli
Culture of sputum
Liquid culture - Middlebrook 7H12 or MGIT (1-3 weeks)
Solid media - Lowenstein-Jensen slopes (4-6 weeks)
CB-NAAT (GeneXpert)
Sputum sample used
Results within 90 minutes
Also tests rifampicin sensitivity
IGRA (Interferon Gamma Release Assay)
Anti-tubercular therapy
Drug sensitive TB
As per the latest recommendations from NTEP, treatment of TB is now based
primarily on drug susceptibility testing. This is irrespective of new cases, previously
treated cases or recurrent TB cases.
All cases of TB are treated with drug sensitive TB regimen, as long as patients is
sensitive to isoniazid and rifampicin.
It consist of the following
Intensive phase → HRZE x 2 months
Continuation phase → HRE x 4 months
Drug Daily Dose Max Dose
Isoniazid (H) 5 mg/kg 300 mg
Rifampicin (R) 10 mg/kg 600 mg
Pyrazinamide (Z) 25 mg/kg 2 g
Ethambutol (E) 15 mg/kg
H mono/poly drug resistant TB
The following drugs for a duration of 6 months are given
Pyrazinamide (Z)
Ethambutol (E)
Rifampicin (R)
Levofloxacin (Lfx)
MDR TB/ Rifampicin Resistant TB
Shorter MDR TB regimen (9-10 months)
Intensive phase (4-6 months)
Clofazimine (Cfz)
High dose Isoniazid (Hh)
Moxifloxacin (Mfx)
Bedaquiline (Bdq) - 6 months
Pyrazinamide (Z)
Ethionamide
Ethambutol
Continuation Phase (5 months)
Clofazimine
Moxifloxacin
Pyrazinamide
Ethambutol
All oral longer MDR TB regimen (18-20 months)
Bedaquiline (6 months or longer)
Levofloxacin
Linezolid (Dose reduced at end of 6 months)
Clofazimine
Cycloserine
Side effects of first line anti-TB drugs

65 year old male treated for tuberculosis 5 years back was admitted with massive
hemoptysis. How do you evaluate and manage the case?
INVESTIGATIONS
CXR :
Pneumonia : Focal consolidation
Tuberculosis : Apical infiltrates, cavitary lesions
Bronchiectasis : Tram track appearance, and peribronchial cuffing
CT chest :
Bronchiectasis : Thickened airways filled with secretions
ECG : Mitral stenosis, Pulmonary embolism and pulmonary hypertension
Bronchoscopy : Most important diagnostic procedure
Total leukocyte count with differential count : Raised leukocyte count and shift to left
indicates upper and lower respiratory tract infection
Hemoglobin and Hematocrit : Decreased in anemia
Platelet count : Reduced in thrombocytopenia
PR and aPTT : Disorders of coagulation, drugs
Arterial blood gas : Hypoxia, hypercarbia
d-Dimer : Raised in pulmonary embolism
Sputum
Gram stain and culture and sensitivity : Klebsiella pneumoniae, identify organism in
acute exacerbation of chronic bronchitis, bronchiectasis and lung abscess
AFB and culture : Pulmonary TB
Cytological examination : Bronchial carcinoma
Tuberculin test : Positive in TB
ESR : Increased in infection, and auto-immune conditions (Wegner’s granulomatosis,
SLE, Goodpasture’s syndrome) and malignancy
Urine microscopy : RBC and red cell casts in hemorrhagic diathesis and
Goodpasture’s syndrome
ANCA levels : Microscopic polyangiitis (p-ANCA), eosinophilic granulomatosis with
polyangiitis (p-ANCA) and granulomatosis with polyangiitis (c-ANCA)
Anti-glomerular basement membrane antibody : Goodpasture’s syndrome
TREATMENT
Medical
ET tube - Position of the patient in sitting or bleeding side down
Large bore IV line for fluids, blood transfusion
Supplemental oxygen / mechanical ventilation
Avoid cough suppressants
Surgical
Emergency resection for bronchogenic mass after patient stabilizes
Surgical resection for aspergilloma
Endobronchial
Identify : Source, rate and to slow/arrest bleeding
Rigid bronchoscope (preferred) : enables blood to be aspirated more easily
Fiberoptic bronchoscope : Cold saline lavage, which sometimes arrests bleeding
Balloon catheter : Inflated proximal to bleeding bronchus. Isolates the source of
bleeding from rest of the lung and contralateral lung, thereby preventing
asphyxiation
Endovascular
Most cases bleeding is from bronchial arteries than pulmonary arteries
Transcatheter embolization is effective in immediate control of massive hemoptysis
First line antitubercular drugs with dosage and one toxicity for each
Anti-tubercular therapy
Drug sensitive TB
As per the latest recommendations from NTEP, treatment of TB is now based
primarily on drug susceptibility testing. This is irrespective of new cases, previously
treated cases or recurrent TB cases.
All cases of TB are treated with drug sensitive TB regimen, as long as patients is
sensitive to isoniazid and rifampicin.
It consist of the following
Intensive phase → HRZE x 2 months
Continuation phase → HRE x 4 months
Drug Daily Dose Max Dose
Isoniazid (H) 5 mg/kg 300 mg
Rifampicin (R) 10 mg/kg 600 mg
Pyrazinamide (Z) 25 mg/kg 2 g
Ethambutol (E) 15 mg/kg

Latent tuberculosis—detection and management

In majority of individuals infected by Mycobacterium tuberculosis, the immune system
contains thee infection and the patient develops cell mediated immune memory to
the bacteria. These individuals currently do not have active tubercular disease. This is
termed latent tuberculosis. About 5-10% of these patients have a lifetime risk of
developing tuberculosis.
Screening for latent tuberculosis
Tuberculin skin test
T-cell IGRAs
To prevent development of active tuberculosis - Isoniazid preventive therapy (IPT) is
given
Isoniazid at the dose of 5mg/kg/day (Max 300 mg/day) for 6-12 months is used for
chemoprophylaxis
Exclude active tuberculosis by history, physical examination, chest radiograph and if
necessary, by other tests before starting chemoprophylaxis
Clinical manifestations of Cryptic tuberculosis
Cryptic TB is a type of miliary TB
Age: Usually in the elderly
Symptoms
Prolonged low grade pyrexia
Lassitude, weight loss and general debility
Signs
Hepatosplenomegaly may occur
Chest is usually normal
Choroidal tubercles are rare
DOTS (directly observed treatment short course) therapy for tuberculosis
Anti-tubercular therapy
Drug sensitive TB
As per the latest recommendations from NTEP, treatment of TB is now based
primarily on drug susceptibility testing. This is irrespective of new cases, previously
treated cases or recurrent TB cases.
All cases of TB are treated with drug sensitive TB regimen, as long as patients is
sensitive to isoniazid and rifampicin.
It consist of the following
Intensive phase → HRZE x 2 months
Continuation phase → HRE x 4 months
Drug Daily Dose Max Dose
Isoniazid (H) 5 mg/kg 300 mg
Rifampicin (R) 10 mg/kg 600 mg
Pyrazinamide (Z) 25 mg/kg 2 g
Ethambutol (E) 15 mg/kg
H mono/poly drug resistant TB
The following drugs for a duration of 6 months are given
Pyrazinamide (Z)
Ethambutol (E)
Rifampicin (R)
Levofloxacin (Lfx)
MDR TB/ Rifampicin Resistant TB
Shorter MDR TB regimen (9-10 months)
Intensive phase (4-6 months)
Clofazimine (Cfz)
High dose Isoniazid (Hh)
Moxifloxacin (Mfx)
Pyrazinamide (Z)
Bedaquiline (Bdq) - 6 months
Ethionamide
Ethambutol
Continuation Phase (5 months)
Clofazimine
Moxifloxacin
Pyrazinamide
Ethambutol
All oral longer MDR TB regimen (18-20 months)
Bedaquiline (6 months or longer)
Levofloxacin
Linezolid (Dose reduced at end of 6 months)
Clofazimine
Cycloserine
A patient is on DOTs category I ATT for pulmonary tuberculosis. After 3 weeks of
treatment, patient presented with decreased appetite. On examination he had mild
jaundice. How do you manage this patient?
If a patient on DOTS Category I ATT for pulmonary tuberculosis presents with
decreased appetite and mild jaundice after 3 weeks of treatment, it may be indicative
of liver toxicity, a known side effect of some of the drugs used in tuberculosis
treatment. The management of this patient would involve the following steps:
Assess the severity of symptoms: Mild jaundice and decreased appetite can be
managed conservatively, but it's important to assess the patient's overall health and
evaluate if there are any other symptoms present that might indicate a more serious
condition.
Monitor liver function tests: Regular monitoring of liver function tests (such as ALT,
AST, bilirubin, etc.) can help determine if the patient's liver is being affected by the
drugs and to what extent.
Adjust the treatment regimen: Depending on the severity of liver toxicity, the
physician may consider adjusting the dose or switching to an alternative drug.
Provide symptomatic treatment: If the patient is experiencing discomfort due to
decreased appetite or jaundice, providing symptomatic treatment such as
antiemetics or pain relief can help.
BRONCHIAL ASTHMA
18 year old girl with occasional dust allergy, comes to emergency with acute
breathlessness of 2 days duration. She is barely able to complete her sentences,
on examination, she is tachypneic, cyanosed. Pulse 110, BP-130/80, JVP not
elevated, chest-extensive ronchi, CVS normal. Spo2 - 88 (room air). What is the
likely diagnosis? How will you investigate and treat her? Briefly discuss the
usual triggers and long term management plan for the above condition.
Acute severe asthma
Treatment
Assess peak expiratory flow rate
Give high concentration of oxygen (40-60%)
Albuterol (salbutamol) nebulization 2.5-5 mg every 20 minutes for three doses
Four to eight puffs by metered dose inhalers every 20 minutes
If not improving,
Add 500 mcg ipratropium for nebulization
IV hydrocortisone 100 mg STAT
If still not controlled
IV Magnesium Sulphate 2g over 20 minutes
Failure → Non-invasive ventilation → Invasive ventilation
If symptoms controlled
Taper hydrocortisone
Oral steroids for 5 to 7 days
Investigations
Pulmonary function tests
Spirometry - Greater than 15% improvement in FEV1 or PEFR following inhalation of
bronchodilator is diagnostic of asthma
Peak Expiratory Flow Rate → The diurnal variation in PEFR of more than 20% is
considered diagnostic
Methacholine bronchial provocation test to detect the presence of airway
hyperresponsiveness in patients whose main symptom is cough only
Imaging
CXR → Normal between attacks. During an acute episode or in severe chronic disease
there may be hyperinflated lungs.
HRCT → May show areas of thickening of bronchial walls (bronchiectasis) as a
complication
Measurement of allergic status
Skin prick test
Elevated serum IgE levels
Blood and sputum tests → Eosinophilia
Trial of corticosteroids
Patients with severe airflow limitation are given prednisolone 30 mg orally/day for 2
weeks with lung function measured before and immediately after the course.
An improvement of FEV1 by more than 15% indicates the presence of reversible
airway obstruction and indicates that the administration of corticosteroids will be
helpful.
Arterial blood gas analysis
Hypoxia and hypocarbia during attack
Hypercarbia during acute severe asthma
Usual Triggers

Long term management plan

General measures
Avoidance of active and passive smoking
Control obesity
Avoid identified allergens such as pets, moulds or certain foodstuff
Follow proper inhalation techniques
Classification of asthma severity
Intermittent Mild persistent Moderate Persistent Severe persistent
Daytime ≤ 2 days/week > 2 days/week but not Daily Multiple times
symptoms daily throughout the day
Nocturnal ≤2 > 2 times/month but At least once every week Daily
awakenings times/month not weekly but not daily
Treatment
Intermittent asthma - SABA whenever needed
Mild persistent - Low dose ICS daily + SABA whenever needed
Moderate persistent asthma -
Low dose ICS daily + LABA daily + SABA as needed (more effective)
Moderate dose ICS daily + SABA as needed (less effective)
Severe persistent asthma - Medium dose ICS daily + LABA daily + SABA as needed
SABA - Short acting beta-2-agonist
Salbutamol: Two puffs of 100 mcg each as required
Terbutaline: Two puffs of 100 mcg each as required
LABA - Long acting beta-2-agonist
Salmeterol: Two puffs of 25 mcg each two to three times a day
Formoterol: Tow puffs of 6 mcg each one to three times a day
ICS - Inhaled corticosteroid → Usually given twice daily
Beclomethasone: 200 mcg
Fluticasone: 125 mcg
Additional treatment options
Leukotriene Receptor Antagonists → Montelukast, Zafirlukast
Methylxanthines - Theophylline
5-LOX inhibitors - Zileuton
Monoclonal antibodies - Omalizumab
Mention four causes of recurrent attacks of wheezing with eosinophilia. Discuss
the clinical features, management and complications of Acute Severe Asthma
Bronchial asthma
Eosinophilic pneumonia
Allergic Bronchopulmonary Aspergillosis
Tropical Pulmonary Eosinophilia
Acute Severe Asthma
Clinical features
Severe dyspnea
Unproductive cough
Patients prefer an upright position fixing the shoulder girdle to assist the accessory
muscles of respiration
Physical signs
Sweating
Central cyanosis
Tachycardia
Pulsus paradoxus
Cyanosis
Management
Assess peak expiratory flow rate
Give high concentration of oxygen (40-60%)
Albuterol (salbutamol) nebulization 2.5-5 mg every 20 minutes for three doses
Four to eight puffs by metered dose inhalers every 20 minutes
If not improving,
Add 500 mcg ipratropium for nebulization
IV hydrocortisone 100 mg STAT
If still not controlled
IV Magnesium Sulphate 2g over 20 minutes
Failure → Non-invasive ventilation → Invasive ventilation
If symptoms controlled
Taper hydrocortisone
Oral steroids for 5 to 7 days
Complications
Pneumonia
Collapse of part or all of the lung
Respiratory Failure
Status asthmaticus
Long term management plan
General measures
Avoidance of active and passive smoking
Control obesity
Avoid identified allergens such as pets, moulds or certain foodstuff
Follow proper inhalation techniques
Classification of asthma severity
Intermittent Mild persistent Moderate Persistent Severe persistent
Daytime ≤ 2 days/week > 2 days/week but not Daily Multiple times
symptoms daily throughout the day
Nocturnal ≤2 > 2 times/month but At least once every week Daily
awakenings times/month not weekly but not daily
Treatment
Intermittent asthma - SABA whenever needed
Mild persistent - Low dose ICS daily + SABA whenever needed
Moderate persistent asthma -
Low dose ICS daily + LABA daily + SABA as needed (more effective)
Moderate dose ICS daily + SABA as needed (less effective)
Severe persistent asthma - Medium dose ICS daily + LABA daily + SABA as needed
SABA - Short acting beta-2-agonist
Salbutamol: Two puffs of 100 mcg each as required
Terbutaline: Two puffs of 100 mcg each as required
LABA - Long acting beta-2-agonist
Salmeterol: Two puffs of 25 mcg each two to three times a day
Formoterol: Tow puffs of 6 mcg each one to three times a day
ICS - Inhaled corticosteroid → Usually given twice daily
Beclomethasone: 200 mcg
Fluticasone: 125 mcg
Additional treatment options
Leukotriene Receptor Antagonists → Montelukast, Zafirlukast
Methylxanthines - Theophylline
5-LOX inhibitors - Zileuton
Monoclonal antibodies - Omalizumab
Discuss the precipitating factors, clinical features and management of acute
severe asthma. Add a note on prevention of asthma
Precipitating factors

Clinical features
Severe dyspnea
Unproductive cough
Patients prefer an upright position fixing the shoulder girdle to assist the accessory
muscles of respiration
Physical signs
Sweating
Central cyanosis
Tachycardia
Pulsus paradoxus
Cyanosis
Management
Assess peak expiratory flow rate
Give high concentration of oxygen (40-60%)
Albuterol (salbutamol) nebulization 2.5-5 mg every 20 minutes for three doses
Four to eight puffs by metered dose inhalers every 20 minutes
If not improving,
Add 500 mcg ipratropium for nebulization
IV hydrocortisone 100 mg STAT
If still not controlled
IV Magnesium Sulphate 2g over 20 minutes
Failure → Non-invasive ventilation → Invasive ventilation
If symptoms controlled
Taper hydrocortisone
Oral steroids for 5 to 7 days
Prevention of asthma
Avoid triggers: Identify and avoid things that trigger your asthma symptoms, such as
tobacco smoke, dust, and pets.
Get vaccinated: Get vaccinated against the flu and pneumonia, as these infections
can trigger asthma attacks.
Exercise regularly: Exercise can help improve lung function and reduce risk of asthma.
However, be sure to warm up before exercising and have inhaler with in case the
person experience symptoms.
Eat a healthy diet: A healthy diet rich in fruits, vegetables, and whole grains can help
reduce your risk of asthma and other respiratory conditions.
Stay indoors on high pollution days: Pollution and other environmental factors can
trigger asthma symptoms.
Follow your treatment plan: If you have been diagnosed with asthma, it's important
to follow your treatment plan as directed by your doctor. This may include taking
prescribed medications, such as inhalers, and avoiding triggers that can worsen your
symptoms.
Quit smoking: If you smoke, quitting can significantly reduce your risk of developing
asthma and other respiratory conditions.
What is the treatment of acute severe asthma? // Treatment of status asthmatics
Assess peak expiratory flow rate
Give high concentration of oxygen (40-60%)
Albuterol (salbutamol) nebulization 2.5-5 mg every 20 minutes for three doses
Four to eight puffs by metered dose inhalers every 20 minutes
If not improving,
Add 500 mcg ipratropium for nebulization
IV hydrocortisone 100 mg STAT
If still not controlled
IV Magnesium Sulphate 2g over 20 minutes
Failure → Non-invasive ventilation → Invasive ventilation
If symptoms controlled
Taper hydrocortisone
Oral steroids for 5 to 7 days
45 year old male is admitted with acute severe asthma. How do you manage the
case?
Treatment
Assess peak expiratory flow rate
Give high concentration of oxygen (40-60%)
Albuterol (salbutamol) nebulization 2.5-5 mg every 20 minutes for three doses
Four to eight puffs by metered dose inhalers every 20 minutes
If not improving,
Add 500 mcg ipratropium for nebulization
IV hydrocortisone 100 mg STAT
If still not controlled
IV Magnesium Sulphate 2g over 20 minutes
Failure → Non-invasive ventilation → Invasive ventilation
If symptoms controlled
Taper hydrocortisone
Oral steroids for 5 to 7 days
Long term management plan
General measures
Avoidance of active and passive smoking
Control obesity
Avoid identified allergens such as pets, moulds or certain foodstuff
Follow proper inhalation techniques
Classification of asthma severity
Intermittent Mild persistent Moderate Persistent Severe persistent
Daytime ≤ 2 days/week > 2 days/week but not Daily Multiple times
symptoms daily throughout the day
Nocturnal ≤2 > 2 times/month but At least once every week Daily
awakenings times/month not weekly but not daily
Treatment
Intermittent asthma - SABA whenever needed
Mild persistent - Low dose ICS daily + SABA whenever needed
Moderate persistent asthma -
Low dose ICS daily + LABA daily + SABA as needed (more effective)
Moderate dose ICS daily + SABA as needed (less effective)
Severe persistent asthma - Medium dose ICS daily + LABA daily + SABA as needed
SABA - Short acting beta-2-agonist
Salbutamol: Two puffs of 100 mcg each as required
Terbutaline: Two puffs of 100 mcg each as required
LABA - Long acting beta-2-agonist
Salmeterol: Two puffs of 25 mcg each two to three times a day
Formoterol: Tow puffs of 6 mcg each one to three times a day
ICS - Inhaled corticosteroid → Usually given twice daily
Beclomethasone: 200 mcg
Fluticasone: 125 mcg
Define bronchial asthma. What are the factors precipitating asthma? Outline
the management of acute severe asthma.
Asthma is a chronic inflammatory disorder of the airways (bronchial tree) in which
breathing is periodically rendered difficult by widespread narrowing of the bronchi
(reversible bronchoconstriction).
It is clinically, characterized by recurrent episodes (paroxysms) of wheezing,
breathlessness (dyspnea), tightness of the chest, and cough.
Factors precipitating asthma

Management of acute severe asthma

Assess peak expiratory flow rate
Give high concentration of oxygen (40-60%)
Albuterol (salbutamol) nebulization 2.5-5 mg every 20 minutes for three doses
Four to eight puffs by metered dose inhalers every 20 minutes
If not improving,
Add 500 mcg ipratropium for nebulization
IV hydrocortisone 100 mg STAT
If still not controlled
IV Magnesium Sulphate 2g over 20 minutes
Failure → Non-invasive ventilation → Invasive ventilation
If symptoms controlled
Taper hydrocortisone
Oral steroids for 5 to 7 days
Long term management plan
General measures
Avoidance of active and passive smoking
Control obesity
Avoid identified allergens such as pets, moulds or certain foodstuff
Follow proper inhalation techniques
Classification of asthma severity
Intermittent Mild persistent Moderate Persistent Severe persistent
Daytime ≤ 2 days/week > 2 days/week but not Daily Multiple times
symptoms daily throughout the day
Nocturnal ≤2 > 2 times/month but At least once every week Daily
awakenings times/month not weekly but not daily
Treatment
Intermittent asthma - SABA whenever needed
Mild persistent - Low dose ICS daily + SABA whenever needed
Moderate persistent asthma -
Low dose ICS daily + LABA daily + SABA as needed (more effective)
Moderate dose ICS daily + SABA as needed (less effective)
Severe persistent asthma - Medium dose ICS daily + LABA daily + SABA as needed
SABA - Short acting beta-2-agonist
Salbutamol: Two puffs of 100 mcg each as required
Terbutaline: Two puffs of 100 mcg each as required
LABA - Long acting beta-2-agonist
Salmeterol: Two puffs of 25 mcg each two to three times a day
Formoterol: Tow puffs of 6 mcg each one to three times a day
ICS - Inhaled corticosteroid → Usually given twice daily
Beclomethasone: 200 mcg
Fluticasone: 125 mcg
Additional treatment options
Leukotriene Receptor Antagonists → Montelukast, Zafirlukast
Methylxanthines - Theophylline
5-LOX inhibitors - Zileuton
Monoclonal antibodies - Omalizumab
Outpatient treatment outline of a Bronchial asthma case.
Answered above
Name any two inhaled glucocorticoids used in treatment of asthma along with any
two devices used to deliver these medications
Two inhaled corticosteroids used in the treatment of asthma (Usually given twice
daily)
Beclomethasone (200 mcg)
Budesonide (200 mcg)
Fluticasone (125 mcg)
Devices
Metered Dose Inhaler
Dry Powder inhaler
Nebulizer
Write salient differences in pulmonary function testing between Bronchial asthma
and Pulmonary fibrosis.
Parameter Bronchial asthma Pulmonary fibrosis
Forced expiratory volume in 1 second (FEV1) Reduced Reduced
Forced vital capacity (FVC) Normal or reduced Reduced
FEV1/FVC Reduced Normal
Peak expiratory flow (PEF) Reduced Normal or reduced
Diffusing capacity for carbon monoxide (DLCO) Normal or reduced Reduced
COPD
Discuss the etiology, Clinical features and management of Chronic obstructive
Pulmonary disease
Etiology
Smoking : Cigarette smoking is a major risk factor. 95% of cases are smoking-related,
typically > 20 pack years (1 pack year is 20 cigarettes smoked per day for 1 year)
Airway hyperresponsiveness : Patients with increased airway responsiveness are more
likely to develop COPD
Occupational exposures : Severe occupational exposures like coal mining, gold
mining, cotton textile dust etc., are all risk factors for COPD
Air pollution
Genetic factors : alpha1-antitrypsin deficiency
Pathogenesis
All three components of lung affected - large airways, small airways and lung
parenchyma
Large airways :
mucous gland enlargement, and goblet cell hyperplasia.
The Reid index, which indicates the ratio of thickness of the submucosal glands to
that of the bronchial wall, is thus increased.
Squamous metaplasia of mucous membrane which predisposes to cancer
development and impairs muco-ciliary clearance.
Small airways
Goblet cell metaplasia
Loss of surfactant releasing Clara cells
Smooth muscle hypertrophy
Chronic inflammation and fibrosis
Lung parenchyma
Destruction of gas exchanging air spaces i.e. the respiratory bronchioles, alveolar
ducts, and alveoli leading to emphysema. Two types of emphysema
Centriacinar : Due to smoking (ciagrettes). Often affects upper lobes (ceiling)
Panacinar : Seen in patients with alpha1-antitrypsin deficiency. Affects lower lobess
Clinical features
Symptoms
Cough
Sputum production
Exertional dyspnea
Episodes of exacerbation precipitated by respiratory tract infections
Signs
Signs of smoking : Odor of smoke, tobacco staining of teeth or nicotine staining of
finger nails
General appearance :
Cyanosis may be present (if predominantly chronic bronchitis)
Wasting and loss of subcutaneous fat
Respiratory examination
Inspection
Accessory muscle usage
Speaking in short sentences
Tripod positioning
Prolonged expiration
Wheezing
Barrel shaped chest
Breathing with pursed lips (emphysema)
Palpation
Obliteration of cardiac dullness
Percussion
Tidal percussion : Decreased movement of diaphragm as it is pushed down already
Advanced COPD
Right heart failure (cor pulmonale) : Peripheral edema, raised JVP, congestive
hepatomegaly
Investigations
Pulmonary function tests
Reduction in FEV1/FVC
DLCO may be reduced in emphysema
ABG : Hypoxemia
Hematocrit : High
ECG : Right ventricular hypertrophy
CXR
Emphysema : Bullae, flattening of diaphragm and hyperlucency
Chronic bronchitis : Increased broncho-vascular markings
Serum alpha1-antitrypsin levels
Treatment
To alter the course of COPD
Smoking cessation
Bupropion and nicotine (patches, gums etc.) may help
Oxygen therapy
Decreases pulmonary hypertension and prolongs life.
Can be given during the day or night at home
Using it for 12 hours or more has been shown to provide significant benefit
Symptomatic relief
Bronchodilators
Beta2-agonists : Salbutamol (200 mcg 6 hourly), terbutaline (500 mcg 6 hourly)
Methylxanthines : Theophylline
Muscarinic antagonists : Ipratropium bromide (40-80 mcg 6 hourly), tiotropium
bromide (18 mcg OD)
Glucocorticoids : Reduce the frequency of exacerbations. Beclomethasone,
budesonide, fluticasone can be used
PDE-4 inhibitor : Roflumilast
Other measures
IV alpha1-antitrypsin in patients with deficiency
Vaccination : H. influenzae and pneumococcal vaccines
Lung transplantation
Pharmacological treatment of COPD

Clinical features (symptoms & Signs) of Emphysema.

Symptoms
Dyspnea
Cough and expectoration of scanty mucoid sputum
Weight loss, weakness, anorexia and lethargy
Signs
General → Body built is asthenic, short and thick neck, neck veins may appear to
distend during expiration and collapse during inspiration. Tripod posture while sitting
Respiratory
Inspection
Distressed, tachypneic, hypertrophy of accessory muscles of respiration
Length of trachea above the suprasternal notch is reduced
Apical impulse is invisible or feeble
During inspiration: Trachea descent exagerrated (Campbell’s sign), excavation of the
suprasternal and supraclavicular fossa
Expiration: Prolonged through pursed lips
Chest: Barrel shaped chest
Dahl sign - Above the knee patches of hyperpigmentation or bruising due to
constant tenting position of hands or elbows
Hoover’s sign - Subcostal angle paradoxically decreased during inspiration
Harrison’ sulcus - A horizontal groove where the diaphragm attaches to the ribs
Percussion
Hyperresonant note over lungs
Reduced cardiac and liver dullness
Tidal percussion is negative
Auscultation
Diminished intensity of breath sound
Breath sounds are vesicular with prolonged expiration
High pitched end-expiratory rhonchi may be audible
BRONCHIECTASIS
Define bronchiectasis. Discuss etiopathogenesis, clinical features, complications
and management of bronchiectasis
Bronchiectasis is defined as an irreversible (permanent), abnormal dilation of the
cartilage-containing airways, bronchi or bronchioles
Etiology
Congenital
Cystic fibrosis
Ciliary dysfunction syndromes
Primary ciliary dyskinesia
Young’s syndrome - Azoospermia, Bronchiectasis, Chronic sinusitis
Kartagener’s syndrome - Bronchiectasis, Chronic sinusitis, Dextrocardia (Situs
inversus)
Alpha-1 antitrypsin deficiency
Acquired
Children
Pneumonia (complicating whooping cough or measles)
Primary TB
Inhaled foreign body
Adults
Pulmonary TB
MAC
ABPA
Suppurative pneumonia
RA, Sjogren’s syndrome, SLE, IBD
Pathogenesis
Pressure of secretion theory (Obstruction): Secretions → mechanical obstruction of
lungs → impaired clearing mechanisms of lung → results in accumulation of
secretions distal to obstruction → leading to secondary infection → inflammation →
weakens and dilates airway
Infection theory: Chronic persistent necrotizing infection and inflammation in the
bronchi and bronchioles → increased bronchial secretions → obstruction of airways
by secretion → inflammation and fibrosis of airway walls → weakening and dilation of
airways
Traction theory: Traction of the bronchi walls secondary to fibrosis/scarring
Atelectasis theory: Negative intrapleural pressure resulting in collapse and bronchial
dilation
Clinical Features
Symptoms
Severe persistent productive cough
Foul smelling sputum
Hemoptysis
Pleuritic chest pain
Infective exacerbation
Bronchiectasis sicca - occasionally the patient is asymptomatic or has dry cough
Situs inversus is found in 50% cases of ciliary dyskinesia
Signs
General examination - Anemia, clubbing, halitosis, fever, weight loss and sinusitis
Respiratory system
Nasal polyps and signs of chronic sinusitis
Auscultation - Reveals bilateral coarse leathery crepitations and wheezing
Complications
Septicemia
Empyema
Metastatic abscess
Aspergilloma
Pneumonia
Hemoptysis
Osteomyelitis
Respiratory failure
Generalized edema
Cor pulmonale
Generalized amyloidosis
Lung abscess
Microbial resistance to antibiotics
Investigations
Blood - Anemia, raised ESR and leukocytosis
ABG - Respiratory alkalosis or hypoxemia
Sputum
If collected in conical flask and allowed to stand forms three layers (three-layered
sputum)
CXR - Tram track opacities, Peri-bronchial cuffing
CT scan
Thickened dilated airways (Tram tracks or signet ring sign)
Absence of bronchial tapering in the periphery of chest
Sinus X-rays
Pulmonary Function Tests - Initially obstructive pattern but later may shift to
restrictive as the disease evolves
Sweat electrolytes: Measurement of sodium and chloride concentration is useful in
the diagnosis of cystic fibrosis
Muco-ciliary clearance testing by nasal clearance of saccharin
Treatment
Improvement in secretion clearance and bronchial hygiene
To reduce the microbial load within airways and minimize the risk of repeated
infections
Methods - Chest physiotherapy (postural drainage), hydration, mucolytic
administration, aerosolization of bronchodilators
Bronchoscopic removal of secretions
Antibiotics therapy
For Pseudomonas: Oral ciprofloxacin (500-750 mg twice daily) or ceftazidime by IV
injection or infusion (1-2 g three times daily) for 7-10 days
Suppressive antibiotics after resolution of acute infection - Inhaled antibiotics are
safe and effective. eg. tobramycin, gentamicin
Antibiotics for exacerbation: Depends on the results of culture and sensitivity of
sputum
Anti-inflammatory therapy
Inhaled or oral steroids can reduce the rate of progression of bronchiectasis.
Macrolide antibiotic: They have immunomodulatory action
Reversal of airflow obstruction
Bronchodilators (β-adrenoreceptor agonists, anticholinergics)
Inhaled corticosteroids may be useful in some patients
Surgical treatment
The procedure involved is excision of bronchiectatic areas. It is usually done in cases
where the bronchiectasis is restricted to a single lobe or segment on CT
Lung transplantation is considered in patients with advanced disease and respiratory
failure
Treatment of hemoptysis
Blood transfusion is given if necessary.
Occasionally, fiberoptic bronchoscopy is needed to detect the source of bleeding.
If the hemoptysis continues, embolization of bronchial artery is the treatment of
choice.
Surgical resection may be needed if embolization fails
Other measures
Graded exercise, routine deep breathing, good nutrition
Vaccination
Prompt treatment of sinusitis
Clinical features of bronchiectasis
Clinical Features
Symptoms
Severe persistent productive cough
Foul smelling sputum
Hemoptysis
Pleuritic chest pain
Infective exacerbation
Bronchiectasis sicca - occasionally the patient is asymptomatic or has dry cough
Situs inversus is found in 50% cases of ciliary dyskinesia
Signs
General examination - Anemia, clubbing, halitosis, fever, weight loss and sinusitis
Respiratory system
Nasal polyps and signs of chronic sinusitis
Auscultation - Reveals bilateral coarse leathery crepitations and wheezing
Complications of bronchiectasis
Complications
Septicemia
Empyema
Metastatic abscess
Aspergilloma
Pneumonia
Hemoptysis
Osteomyelitis
Respiratory failure
Generalized edema
Cor pulmonale
Generalized amyloidosis
Lung abscess
Microbial resistance to antibiotics
Radiological findings and etiology of bronchiectasis
Radiological findings
CXR - Tram track opacities, Peri-bronchial cuffing
CT scan
Thickened dilated airways (Tram tracks or signet ring sign)
Absence of bronchial tapering in the periphery of chest
Sinus X-rays
Etiology
Congenital
Cystic fibrosis
Ciliary dysfunction syndromes
Primary ciliary dyskinesia
Young’s syndrome - Azoospermia, Bronchiectasis, Chronic sinusitis
Kartagener’s syndrome - Bronchiectasis, Chronic sinusitis, Dextrocardia (Situs
inversus)
Alpha-1 antitrypsin deficiency
Acquired
Children
Pneumonia (complicating whooping cough or measles)
Primary TB
Inhaled foreign body
Adults
Pulmonary TB
MAC
ABPA
Suppurative pneumonia
RA, Sjogren’s syndrome, SLE, IBD
RESPIRATORY FAILURE
Define respiratory failure? Discuss causes, pathophysiology and management of
different types of respiratory failure?
Respiratory failure is the term used when pulmonary gas exchange fails to maintain
normal arterial oxygen and carbon dioxide levels
Causes
Type I Respiratory Failure → Hypoxemic (PaO2 < 60 mmHg)
Failure of oxygen exchange
Increased shunt fraction (Qs/Qt)
Occurs due to alveolar flooding
Hypoxemia refractory to supplementary oxygen

Management
Acute Type I respiratory failure
Treat the underlying condition
High concentrations ( 40-60%) of oxygen through oronasal mask.
Most patients recover with treatment of underlying disease and oxygen therapy, but
a few very ill patients may require artificial ventilation
Chronic Type I respiratory failure
Treat the underlying cause
Oxygen therapy, which may be intermittent or at times long term.
Artificial ventilation may be tried, but in general the prognosis is poor.
Venesection to reduce hematocrit in patients with severe secondary polycythemia.
Diuretics to reduce peripheral oedema.
Type II Respiratory Failure → Hypercapnic (PaCO2 > 45 mmHg)
Failure to exchange or remove carbon dioxide
Decreased alveolar minute ventilation
Often accompanied by hypoxemia that corrects with supplemental oxygen

Management
Acute Type II respiratory failure
Treatment of the underlying condition.
Oxygen therapy to be started with 24% oxygen and adjusted further based on serial
measurements of ABG levels.
Removal of secretions by coughing or emergency bronchoscopic aspiration.
Bronchodilators in severe airflow obstruction.
Assisted ventilation (invasive or non-invasive) must be considered in selected cases
Chronic Type II respiratory failure
Treatment of the underlying causes.
Oxygen therapy carries the risk of causing depression of ventilation if respiratory
drive has been dependent on hypoxemia. Correction of hypoxemia will then cause a
further rise in PaC02 resulting in confusion, drowsiness or loss of consciousness.
Think carefully before prescribing oxygen to such patients. However, oxygen is
indicated in selected cases. Note the following points on oxygen therapy:
Measure ABG levels before oxygen therapy.
Do not give more than 24% oxygen initially.
Give oxygen continuously and not intermittently. It is preferable to give oxygen at a
rate of 1-2 L/minute.
Oxygen therapy should be monitored by serial ABG measurements and/or pulse
oximetry. In selected cases, oxygen concentration can be increased to 28-32%.
Respiratory stimulants like doxapram hydrochloride can increase or maintain
ventilation for a short time, at most 24 hours. However, its role is controversial.
Mechanical ventilation is reserved for selected cases who fail to respond to all other
measures.
Supportive treatment includes antibiotics for respiratory infection, nebulized
bronchodilators, clearing secretions by coughing, suction, chest physiotherapy, etc.
and diuretics for edema.
Type III Respiratory failure → Perioperative respiratory failure
Increased atelectasis due to low FRC in the setting of abnormal abdominal wall
mechanics
Often results in type I or type II respiratory failure
Type IV Respiratory Failure → Shock
Describes patients who are intubated and ventilated in the process of resuscitation
for shock
Respiratory Failure
Answered above
PNEUMONIA
Discuss the etiology, clinical features, complications and management
complications of community acquired pneumonia (x2)
Etiological agents

Clinical features
Systemic features → Sudden onset fever, rigors, shivering and malaise
Pulmonary symptoms
Cough
Initially short, painful and dry
Later productive with expectoration of mucopurulent sputum
Rusty sputum in S. pneumoniae
Currant jelly sputum in Klebsiella pneumoniae
Pleuritic chest pain
Breathlessness
Extrapulmonary features

Signs
Fever
Respiratory and Pulse rate may be raised and the BP low
Tachycardia is common. Relative bradycardia in Legionnaire’s pneumonia
Oxygen saturation on air may be low
Chest examination
Percussion: Dull note
Auscultation:
Tubular bronchial breath sounds over areas of consolidation
Bronchophony
Whispering pectoriloquy
Coarse crackles
Complications
General Complications

Local complications
Lung abscess
Organizing pneumonia → Delayed and incomplete resolution can cause ingrowth of
granulation tissue into the alveolar exudate. The intra-alveolar plugs of granulation
tissue are known as organizing pneumonia. Gradually, increased alveolar fibrosis
leads to a shrunken and firm lobe and is called as cornification.
Spread of infection to pleural cavity
Pleuritis
Parapneumonic pleural effusion
Pyothorax
Pneumothorax
Investigations
CBC -
WBCs →
Very high (>20,000/cu.mm) in bacterial pneumonia
Very low (<4000/cu.mm) in viral and atypical pneumonias
Neutrophilic leukocytosis suggests bacterial pneumonia
Hemolytic anemia (occasionally complicates Mycoplasma)
Urea and electrolytes
Uremia - Marker for severity
Hyponatremia - marker of severity. may occur in Legionnaire’s disease
Liver function tests
Abnormal transaminitis, raised bilirubin when basal pneumonia inflames liver or in
atypical pneumonia
Hypoalbuminemia - Marker of severity
ESR/CRP - elevated
CXR
Lobar pneumonia - Patchy opacification evolves into homogenous consolidation of
the affected lobe
Bronchopneumonia - Patchy and segmental shadowing
Complications - Para-pneumonic effusion, Intrapulmonary abscess or empyema
Pleural aspirate and culture when present in more than trivial amounts
Blood culture - Bacteremia is marker of severity
Serological and antigen detection tests
Cold agglutinins - Positive in 50% patients of Mycoplasma
Arterial blood gas - Measure when SaO2 < 93% or when severe clinical features
present
HIV testing
Sputum testing - for tuberculosis (ZN staining and visualization of acid-fast bacilli)
Oropharyngeal swab - PCR for Mycoplasma pneumoniae and other atypical
pathogens
Urine - Pneumococcal and/or Legionella antigens
Treatment
Assess severity → Assessed by the CURB 65 score. It is used in the community where
serum urea level is not usually available.
General management of pneumonia
Check airway, breathing and circulation
Oxygen
Indicated in all patients with tachypnea, hypoxemia, hypotension or acidosis.
Aim is to maintain oxygen saturation between 94-98%.
In patients with known COPD, high concentrations (35% or more) preferably
humidified oxygen should be used to maintain saturation between 88-92%.
If hypoxia continues or patient develops increasing hypercapnia, ventilate the patient
mechanically
IV fluids
Used in patients with severe illness, older patients and those who are vomiting.
Antibiotics
Empiric antibiotics → To be started as as soon as the diagnosis of pneumonia is
made preferably within 4 hours of presentation in hospital. The following antibiotics
are given empirically
Duration of therapy: Min 5 days (usually 7-10 days). Duration is 10-14 days for
patients with Mycoplasma and Chlamydia pneumonia.
Mild analgesics for pleuritic chest pain - Paracetamol, Codeine or NSAIDs
Clinical signs in suppurative pneumonia
General signs
Fever
Clubbing
Halitosis
Anemia
Oronasal sepsis
Respiratory Examination
Early stages - May be normal
Later
Signs of consolidation -
Palpation : Increased vocal fremitus
Percussion : Dullness
Auscultation : Vocal resonance, bronchial breathing, crepitations and pleural rub
Signs of cavitation - Once the abscess opens into a bronchus, signs of cavitation like
cavernous or amphoric bronchial breathing and coarse post-tussive crepitations
are heard on auscultation.
Write the etiology and treatment of community acquired pneumonia
Etiological agents

Treatment
Assess severity → Assessed by the CURB 65 score. It is used in the community where
serum urea level is not usually available.
General management of pneumonia
Check airway, breathing and circulation
Oxygen
Indicated in all patients with tachypnea, hypoxemia, hypotension or acidosis.
Aim is to maintain oxygen saturation between 94-98%.
In patients with known COPD, high concentrations (35% or more) preferably
humidified oxygen should be used to maintain saturation between 88-92%.
If hypoxia continues or patient develops increasing hypercapnia, ventilate the patient
mechanically
IV fluids
Used in patients with severe illness, older patients and those who are vomiting.
Antibiotics
Empiric antibiotics → To be started as as soon as the diagnosis of pneumonia is
made preferably within 4 hours of presentation in hospital. The following antibiotics
are given empirically

Duration of therapy: Min 5 days (usually 7-10 days). Duration is 10-14 days for
patients with Mycoplasma and Chlamydia pneumonia.
Mild analgesics for pleuritic chest pain - Paracetamol, Codeine or NSAIDs
Nosocomial pneumonia // Hospital acquired pneumonia
Hospital-acquired pneumonia (HAP) or nosocomial pneumonia is a new episode of
pneumonia developing in hospital in a patient who is beyond 2 days (more than 48
hours) of their initial admission to hospital, which was not incubating at the time of
admission.
Most common mechanism of nosocomial pneumonia is aspiration
Most common organism is Staphylococcus aureus.
The most common multidrug-resistant Gram-negative bacilli (MDR-GNB) causing
HAP/VAP: P. aeruginosa.
Criteria / Clinical features
Two of the following clinical features (fever > 38 C, leukocytosis/leukopenia, purulent
secretions)
Positive culture of sputum or tracheal aspirate
New lung infiltrate
Investigations
Blood cultures
CBC
Urea and electrolytes
ESR and CRP
Arterial Blood Gas analysis
CXR
Management
Similar to community acquired pneumonia - Adequate oxygenation, fluids and
antibiotics
Early onset HAP (within 4 days of hospitalization) - usually due to drug sensitive
bacteria
Not received antibiotics before → Treated with (amoxicillin + clavulanic acid) or with
cefuroxime
Received a course of recent antibiotics → Treated with Piperacillin/Tazobactam or a
third generation cephalosporin
Late onset HAP (after 4 days of hospitalization)
Antipseudomonal cover by carbapenem (meropenem) or a third generation
cephalosporin combined with an aminoglycoside
MRSA can be covered by vancomycin or linezolid
Complications of Pneumonia.
General Complications
Local complications
Lung abscess
Organizing pneumonia → Delayed and incomplete resolution can cause ingrowth of
granulation tissue into the alveolar exudate. The intra-alveolar plugs of granulation
tissue are known as organizing pneumonia. Gradually, increased alveolar fibrosis
leads to a shrunken and firm lobe and is called as cornification.
Spread of infection to pleural cavity
Pleuritis
Parapneumonic pleural effusion
Pyothorax
Pneumothorax
40 year old patient who was being treated for acute flaccid paralysis develops
hemoptysis and breathing discomfort after 1 week of hospital stay. Identify the most
probable medical complication patient developed and how would you investigate
this patient (any three)?
Hospital-acquired pneumonia (HAP) or nosocomial pneumonia is a new episode of
pneumonia developing in hospital in a patient who is beyond 2 days (more than 48
hours) of their initial admission to hospital, which was not incubating at the time of
admission.
Most common mechanism of nosocomial pneumonia is aspiration
Most common organism is Staphylococcus aureus.
The most common multidrug-resistant Gram-negative bacilli (MDR-GNB) causing
HAP/VAP: P. aeruginosa.
Criteria / Clinical features
Two of the following clinical features (fever > 38 C, leukocytosis/leukopenia, purulent
secretions)
Positive culture of sputum or tracheal aspirate
New lung infiltrate
Investigations
Blood cultures
CBC
Urea and electrolytes
ESR and CRP
Arterial Blood Gas analysis
CXR
Management
Similar to community acquired pneumonia - Adequate oxygenation, fluids and
antibiotics
Early onset HAP (within 4 days of hospitalization) - usually due to drug sensitive
bacteria
Not received antibiotics before → Treated with (amoxicillin + clavulanic acid) or with
cefuroxime
Received a course of recent antibiotics → Treated with Piperacillin/Tazobactam or a
third generation cephalosporin
Late onset HAP (after 4 days of hospitalization)
Antipseudomonal cover by carbapenem (meropenem) or a third generation
cephalosporin combined with an aminoglycoside
MRSA can be covered by vancomycin or linezolid
What is CURB 65 Score and what is the clinical relevance?

The need to hospitalize (severity) a patient is commonly assessed by CURB 65 or the

CRB 65 score (Table 6.74). The CRB 65 score is used in the community where the
serum urea level is not usually available.
PNEUMOTHORAX
Clinical features of tension pneumothorax
Clinical features
Symptoms
Sudden onset pleuritic chest pain and breathlessness (dyspnea)
Severity depends on extent of lung collapse and amount of pre-existing lung disease
Tension pneumothorax - distressed patient, rapid labored respiration, cyanosis,
marked tachycardia, profuse diaphoresis
Signs
General - cyanosis, tachypnea, peripheral pulses may be feeble and hypotension may
be present
Respiratory
Inspection and Palpation
Accessory muscle usage
Trachea and mediastinal shift to the unaffected side
On the affected side -
fullness of chest
diminished respiratory movements
increase in size of hemithorax
increased spino-scapular distance
markedly diminished vocal fremitus
subcutaneous emphysema may be present
Percussion - Hyper-resonant note over affected hemithorax
Auscultation -
Markedly decreased/absent breath sound and vocal resonance
Absence of adventitious sounds
Open pneumothorax with bronchopulmonary fistula, there may be amphoric
bronchial breathing
Management of tension pneumothorax
Management of tension pneumothorax
Acute medical emergency
Insertion of large-bore needle into the pleural space through second anterior
intercostal space
Diagnosis is confirmed if large amounts of air escape through the inserted needle.
Needle should be kept in place till a thoracostomy tube can be inserted
Cover the open end of the needle with glove finger
Clinical features of right sided hydropneumothorax
Symptoms
Sudden onset pleuritic chest pain and breathlessness (dyspnea)
Severity depends on extent of lung collapse and amount of pre-existing lung disease
Tension pneumothorax - distressed patient, rapid labored respiration, cyanosis,
marked tachycardia, profuse diaphoresis
Signs
General - cyanosis, tachypnea, peripheral pulses may be feeble and hypotension may
be present
Respiratory
Inspection and Palpation
Accessory muscle usage
Trachea and mediastinal shift to the unaffected side
On the affected side -
fullness of chest
diminished respiratory movements
increase in size of hemithorax
increased spino-scapular distance
markedly diminished vocal fremitus
subcutaneous emphysema may be present
Percussion -
Hyper-resonant note over the upper air-containing part and stony dull over the
lower fluid containing part
Straight line dullness. Shifting dullness can be elicited
Auscultation -
Markedly decreased/absent breath sound and vocal resonance
Absence of adventitious sounds
Open pneumothorax with bronchopulmonary fistula, there may be amphoric
bronchial breathing
Coin test positive over the upper air-containing part
Succussion splash can be elicited on the affected side
PLEURAL EFFUSION
Note on Investigations and their interpretation in a case of pleural effusion.

List typical clinical signs expected in case of left sided moderate pleural effusion.
Symptoms - Breathlessness
Signs
Inspection: Tachypnea. Shift of trachea to the normal side (here right side)
Palpation
Shift of trachea and mediastinum to normal side
Reduced chest movements on affected side, bulging of intercostal spaces and
fullness of affected chest
Markedly reduced vocal fremitus
Diminished chest expansion
Increased size of the affected hemithorax
Increase in spino-scapular distance
Percussion
Stony dullness over the fluid
Small effusion
Left sided - Obliteration of Traube’s space
Right sided - Detectable by Tidal percussion
Moderate to large effusions - Percussion reveals a triangular area of dullness or
impaired note over the back of chest on the contralateral (normal) side of the
effusion. It may be due to shift of posterior mediastinum to the opposite side by
effusion
Auscultation
Breath sounds are markedly diminished or absent over the fluid
Vocal resonance is markedly diminished over the fluid
Bronchial breathing or crackles the level of pleural effusion
Grocco’s sign - Triangular area of paravertebral dullness on the side opposite to
pleural effusion. The boundaries are
Medial boundary - Midspinal line from the upper level of effusion down to the level
of tenth thoracic vertebrae
Lower boundary - A horizontal line extending laterally from the tenth thoracic
vertebrae along the lower limit of lung resonance
Lateral boundary - Curved line connecting the above two lines
Exudative pleural effusion
Mention 4 causes for exudative pleural effusion. Mention 4 points which help in
differentiating transudate from exudate
Causes of exudative pleural effusion
Tuberculosis
Bacterial pneumonia
Malignancy
Pulmonary infarction
SLE, RA
Acute pancreatitis
Dressler’s syndrome
Hemothorax
Chylothorax
Intra-abdominal abscess
Differentiation of exudative vs transudative pleural effusion
Light’s criteria (if any of the following is true it indicates exudative pleural effusion)
Pleural fluid protein to Serum protein ratio > 0.5
Pleural fluid LDH to serum LDH > 0.6
Pleural fluid LDH > 2/3 the upper limit for normal serum LDH levels
Other points of differentiation
ARDS
Write a note on Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) is a sudden and progressive form of
acute respiratory failure in which the alveolar capillary membrane becomes damaged
and more permeable to intravascular fluid resulting in severe dyspnea, hypoxemia
and diffuse pulmonary infiltrates
Etiology
Sepsis
Aspiration of gastric contents
Pneumonia
Blunt chest trauma
Near drowning
Massive blood transfusion
Pancreatitis
Narcotic drug overdose - Heroin, morphine, methadone
Phases
Exudative phase (1-7 days)
Proliferative phase (3-7 days)
Fibrotic phase (>10-14 days)
Clinical Features
Acute dyspnea and hypoxemia within hours to days
Tachypnea and Tachycardia
Febrile or hypothermic
Bilateral crepitations
Exclude cardiogenic pulmonary edema by excluding signs of CHF or intravascular
fluid overload, including jugular venous distension, cardiac murmurs, gallops,
hepatomegaly and edema
Investigations
CXR → Diffuse, bilateral alveolar infiltrates
Arterial blood gas analysis
PaO2/FiO2 ratio

Initially may show respiratory alkalosis which progresses to respiratory acidosis

ARDS occurring the context of sepsis, a metabolic acidosis may be seen with or
without respiratory compensation
To exclude cardiogenic pulmonary edema - ECG, BNP
Management
Treat the precipitating cause
Maintain adequate oxygenation
Positive end-expiratory pressure (PEEP) between 5-20 cm of H2O
Lung protective mechanical ventilation
Low tidal volume ventilation (LTVV)
Initial tidal volume set to 8 mL/kg of ideal body weight
Reduce tidal volume to 7 mL/kg IBW then 6 mL/kg IBW over the next 1–3 hour
Permissive hypercapnia (50-75 mmHg) is used to maintain adequate minute
ventilation
Fluid management
Prone position ventilation - About 2/3 of patients with ARDS improve their
oxygenation after being placed in prone position
Experimental therapy
Surfactant replacement therapy
Ketoconazole
PULMONARY EOSINOPHILIC SYNDROMES
What are the causes of eosinophilia, and how is tropical pulmonary eosinophilia
treated?
Causes of eosinophilia
Allergic bronchopulmonary aspergillosis
Bronchial asthma
Churg-Strauss Syndrome
Drug and toxin-indued pulmonary eosinophilic syndrome
Chronic eosinophilic pneumonia
Tropical pulmonary eosinophilia
Loeffler’s syndrome (Simple Pulmonary Eosinophilia)
Idiopathic acute eosinophilic pneumonia
Idiopathic hypereosinophilic syndrome
Diagnosis
History of long residence in endemic area
Peripheral blood
Absence of microfilariae
Marked peripheral eosinophilia in excess of 3000/mL
Chest X-ray: Miliary mottling
Serological findings
High titers of anti-filarial antibodies
Elevated levels of IgE
Therapeutic response to DEC (6mg/kg/day for 3 weeks) within 7-10 days of initiating
therapy
Treatment
Diethylcarbamazine in a dose of 2 mg/kg orally three times a day for 14–21 days or
for as long as 4 weeks. It is directly filaricidal to both adult worms and microfilariae.
Tropical Pulmonary Eosinophilia // Clinical features, diagnosis and treatment of
tropical pulmonary eosinophilia
Tropical pulmonary eosinophilia is an occasional atypical host response
(hypersensitivity reaction) of an individual to a mosquito-borne filarial infection by
tissue-dwelling human nematode (microfilariae) Wuchereria bancrofti and Brugia
malayi
Clinical Features
Paroxysmal dry cough, fever, malaise, anorexia, weight loss, dyspnea or wheeze and
miliary pulmonary infiltrates
Other features
Presentation can be similar to status asthmaticus
Chest pain, muscle tenderness, pericardial and CNS involvement
Chest Examination: Coarse crackles and rhonchi
Generalized lymphadenopathy and hepatosplenomegaly may be present
Diagnosis
History of long residence in endemic area
Peripheral blood
Absence of microfilariae
Marked peripheral eosinophilia in excess of 3000/mL
Chest X-ray: Miliary mottling
Serological findings
High titers of anti-filarial antibodies
Elevated levels of IgE
Therapeutic response to DEC (6mg/kg/day for 3 weeks) within 7-10 days of initiating
therapy
Treatment
Diethylcarbamazine in a dose of 2 mg/kg orally three times a day for 14–21 days or
for as long as 4 weeks. It is directly filaricidal to both adult worms and microfilariae.
LUNG CANCER
Pancoast tumor
Pancoast tumor is a tumor at the apex of lung which may invade the neural
structures around the first rib, subclavian vessels and the cervical sympathetic plexus.
Clinical Features
Shoulder pain which radiates in the distribution of ulnar nerve of the arm (i.e. along
the C8-T1 distribution).
Wasting of the small muscles of the hand from due to C8-T1 nerve involvement.
Pain and tenderness over the first and second ribs and radiological evidence of rib
destruction due to local invasion by tumor.
Horner’s syndrome (enophthalmos, ptosis, miosis, and anhidrosis) on the same side
as the tumor due to involvement of the sympathetic pathway as it passes through
the T1 root.
Investigations
CT scan
Fine needle aspiration
MRI
Treatment
Combined chemoradiotherapy and surgery
Preoperative radiotherapy along with chemotherapy (cisplatin and etoposide) is
given followed by en-bloc resection of the tumor.
Non metastatic manifestations of bronchogenic carcinoma. (x3)
OTHERS
Describe the causes of wheezing

Mention four clinical findings of right upper lobe collapse

Depends on the underlying cause, the degree of volume loss within the lung, and
rate of volume loss.
No symptoms may develop when atelectasis develops slowly.
Chronic atelectasis may be a nidus of chronic purulent infection. This may damage
bronchial wall leading to bronchiectasis.
Physical examination:
Reduced chest movement during breathing on the involved region.
Deviation of trachea and apex beat toward affected side.
Dullness over the involved region
Absence of breath sounds over involved region. No added sounds.
Mention important imaging modalities used in patient with respiratory diseases.
Chest X-ray: This is a commonly used imaging test that produces detailed images of
the organs and structures inside the chest, including the lungs, heart, and blood
vessels.
Computed tomography (CT) scan: This test produces detailed, cross-sectional images
of the chest using X-rays and a computer. It can be helpful in identifying
abnormalities in the lungs and other chest structures.
Magnetic resonance imaging (MRI): This test uses a strong magnetic field and radio
waves to produce detailed images of the chest. It can be useful in evaluating certain
types of lung diseases, such as interstitial lung diseases.
Positron emission tomography (PET) scan: This test uses a small amount of
radioactive tracer to produce detailed images of the body's tissues and organs. It can
be helpful in identifying the extent and severity of certain types of lung cancer.
Bronchoscopy: This is a procedure in which a flexible tube with a camera attached
(bronchoscope) is inserted through the nose or mouth and into the airways. It can be
used to obtain tissue samples, remove foreign objects, or assess the inside of the
airways.
Lung ultrasound: This is a non-invasive test that uses sound waves to produce
images of the lungs. It can be helpful in evaluating certain types of respiratory
diseases, such as pneumonia.
Cyanosis
Bluish discoloration of the skin and mucous membrane. It results from an increased
concentration of reduced hemoglobin/deoxyhemoglobin (>5 g/dL) or abnormal
hemoglobin derivatives (e.g. methemoglobin, sulfhemoglobin, etc.) in the capillary
blood perfusing the area. Cyanosis is normally detected when the oxygen saturation
(SaO2) is <85%.
Causes
Central cyanosis
Cardiac -
Cyanotic congenital heart diseases:
Transposition of great vessels,
Tetralogy of Fallot,
Truncus arteriosus,
Total anomalous pulmonary venous return,
Eisenmenger’s Syndrome,
Ebstein’s anomaly
Acute pulmonary edema
Pulmonary
Acute severe asthma
Acute PE
COPD
Cor pulmonale
Tension pneumothorax
High altitude
Peripheral cyanosis
CHF
Cold, frostbite, Raynaud’s phenomenon, shock
PVD
SVC syndrome
Differential diagnosis of cough with sputum with clubbing
Chronic obstructive pulmonary disease (COPD): COPD is a group of lung conditions
that cause breathing difficulties. It is often caused by smoking and is characterized by
a persistent cough with phlegm and shortness of breath.
Bronchiectasis: This is a condition in which the bronchi (airways in the lungs) become
damaged and dilated, leading to an accumulation of mucus in the lungs. It can cause
a chronic cough with sputum and is often associated with recurrent respiratory
infections.
Cystic fibrosis: This is a genetic disorder that affects the respiratory, digestive, and
reproductive systems. It can cause a chronic cough with thick, sticky mucus and
clubbing of the fingers and toes.
Pulmonary fibrosis: This is a lung condition characterized by scarring of the lung
tissue, which can lead to breathing difficulties and a persistent cough with sputum.
Lung cancer: A cough with sputum and clubbing can also be a symptom of lung
cancer. Other symptoms may include shortness of breath, chest pain, and weight
loss.

Infectious Diseases and Tropical Medicine

A college student aged 22 years brought to the emergency department with
history of 5 days of high grade fever, chills and rigors. On examination he was
febrile, drowsy and jaundiced. His pulse was 130/min, BP was 90/60 mmHg and
respiratory' rate was 45. Pulse oximeter displayed Sa02 of 85%. What are the
differential diagnosis? How will you manage (investigation and treatment) this
patient?
Pyrexia of Unknown Origin
Define pyrexia of unknown origin (PUO). A 30 year old salesman presents with
high grade fever and weight loss of 5 kg over 1 month duration. How do you
evaluate him clinically (history and examination)? How do you investigate a
case of PUO in general?
Classic pyrexia of unknown origin (PUO) is classically defined as:
Duration: Fever of at least 3 weeks duration.
Temperature: Daily temperature persistently elevated above 101°F (38.3°C).
Remains undiagnosed despite after a thorough history-taking, physical examination,
and obligatory investigations (or at least three outpatient visits or 3 days in hospital).
No known immunocompromised state (e.g. HIV or other immunosuppressing
conditions)
History Taking
Onset:
Acute: Malaria, pyogenic infection
Gradual: TB, typhoid fever
Character: High grade fever is seen in urinary tract infections (UTI), malaria,
thrombosis, drug fever.
Pattern:
Sustained/persistent: Typhoid fever, drugs
Intermittent fever:
Daily spikes: Malaria, abscess, tuberculosis (TB), Schistosomiasis
Double quotidian, Twice-daily spikes: Leishmaniasis, gonococcal endocarditis, adult
onset Still’s disease
Saddle back fever: Leptospirosis, dengue, borrelia
Relapsing/recurrent fever: Non-falciparum malaria, brucellosis, Hodgkin’s lymphoma
Antecedents: Prior to onset of fever
Dental extraction: Infective endocarditis
Urinary catheterization: UTI, bacteremia
Associated symptoms:
Chills and rigors: Bacterial, rickettsial and protozoal disease (malaria), influenza,
lymphoma, leukemia, drug-induced
Night sweats: TB, Hodgkin’s lymphoma
Loss of weight: Malignancy, TB
Cough and dyspnea: Miliary TB, multiple pulmonary emboli, AIDS patient with PCP
(Pneumocystis pneumonia), CMV (Cytomegalovirus)
Headache: Giant cell arteritis, typhoid fever, sinusitis, meningitis, drug fever
Joint pain: Rheumatoid arthritis, systemic lupus erythematosus (SLE), vasculitis, adult
onset Still’s disease
Abdominal pain: Cholangitis, biliary obstruction, perinephric abscess, Crohn’s disease,
dissecting aneurysm, gynecological infection
Bone pain: Osteomyelitis, lymphoma
Sore throat: Infectious mononucleosis, retropharyngeal abscess, streptococcal
infection
Dysuria, rectal pain: Prostatic abscess, UTI
Altered bowel habit: Inflammatory bowel disease (IBD), typhoid fever,
schistosomiasis, amebiasis
Skin rash: Gonococcal infection, polyarteritis nodosa (PAN), nonHodgkin’s lymphoma
(NHL), dengue fever, connective tissue disorders.
Review past medical history: Malignancy (e.g. leukemia, lymphoma, hepatocellular
carcinoma), HIV infection, diabetes mellitus, inflammatory bowel disease, collagen
vascular disease [e.g. systemic lupus erythematosus (SLE), rheumatoid arthritis (RA)],
giant cell arteritis, tuberculosis, heart disease (e.g. valvular heart disease)
Past surgical history: Post-splenectomy/post-transplantation, prosthetic heart valve,
catheter, AV fistula, recent surgery/operation
Drug history
Immunosuppressive drug/corticosteroid
Anticoagulants
Before the fever: Drug fever occur within 3 months after starting, taking drugs may
cause hypersensitivity and low grade fever, usually associated with rash.
Due to the allergic reaction, direct effect of drug which impairs temperature
regulation (e.g. phenothiazine), antiarrhythmic drug (e.g. procainamide, quinidine);
anti-microbial agent (e.g. penicillin, cephalosporin, hydralazine), phenytoin.
After the fever: May modify clinical pictures, mask certain infection, e.g. subacute
bacterial endocarditis (SBE), antibiotic allergy.
Family history: Whether anyone in family has similar problem (e.g. tuberculosis,
familial Mediterranean fever)
Social history
Travel: Amebiasis, typhoid fever, malaria, schistosomiasis
Residential area: Malaria, leptospirosis, brucellosis
Occupation
Farmers, veterinarian, slaughter-house workers = Brucellosis
Workers in the plastic industries = polymer-fume fever
Contact with domestic/wild animal/birds : Brucellosis, psittacosis (pigeons),
leptospirosis, Q fever, toxoplasmosis
Diet history
Unpasteurized milk/cheese = Brucellosis
Poorly cooked pork = Trichinosis
IVDU (intravenous drug user) = HIV-AIDS related condition, endocarditis
Sexual orientation = HIV, sexually transmitted disease (STD), pelvic inflammatory
disease (PID)
Close contact with TB patients
Physical Examination
Investigations
Covid-19
Preventive measures in Covid -19 infection
Wearing a mask: Wearing a mask over the nose and mouth can help reduce the
spread of respiratory droplets that may contain the virus. It is important to wear a
mask properly, covering both the nose and mouth and securing it under the chin.
Practicing physical distancing: Keeping a distance of at least 6 feet from others can
help reduce the risk of respiratory droplets being transmitted from person to person.
Washing hands frequently: Regular hand washing with soap and water for at least 20
seconds can help reduce the risk of transmission by removing the virus from the
hands.
Disinfecting frequently touched surfaces: Cleaning and disinfecting frequently
touched surfaces such as doorknobs, tables, and keyboards can help reduce the risk
of transmission.
Getting vaccinated: COVID-19 vaccines have been developed and are being
distributed globally. Getting vaccinated can help protect you and those around you
from getting sick.
Clinical features of Covid 19 (SARS Corona virus 2) infection
Fever: A fever, defined as a body temperature of 100.4°F (38°C) or higher, is a
common symptom of COVID-19.
Dry cough: A dry cough, which means a cough that does not produce phlegm or
mucus, is a common symptom of COVID-19.
Fatigue: Many people with COVID-19 experience fatigue, or extreme tiredness, as a
symptom.
Shortness of breath: Shortness of breath, or difficulty breathing, is a common
symptom of COVID-19, particularly in severe cases.
Body aches: Some people with COVID-19 experience body aches, or pains in the
muscles and joints.
Loss of sense of smell or taste: Some people with COVID-19 experience a loss of
sense of smell or taste, or a change in the way things taste or smell.
Malaria
Treatment of Vivax malaria (x2) // Treatment of uncomplicated vivax malaria with
dosage
INVESTIGATIONS
Diagnosis of malaria
Peripheral smear examination : Demonstration of asexual forms of the parasites.
Smears are stained by Giemsa or Leishman’s stain. Both thin and thick smears should
be examined
Bone marrow aspirate : IF peripheral blood smears are negative (due to partial
antimalarial treatment).
Quantitative buffy coat analysis : Centrifuged buffy coat is stained with flurochrome
(e.g. acridine orange) that ‘light up’ (microtube concentration methods with acridine
orange staining) malarial parasites
Serological techniques : ELISA and IFA. Not specific and hence not done routinely
PCR testing
Other lab findings
Blood :
Normochromic normocytic anemia, thrombocytopenia
TLC is low to normal
Acute phase reactants : Elevated ESR and CRP
Coagulation study : In severe infections, PT and aPTT may be prolonged
Other findings in severe malaria
Metabolic acidosis
Low plasma concentration : glucose, sodium bicarbonate, calcium and albumin
Elevated : lactate, BUN, creatinine, muscle and liver enzymes, bilirubin and gamma
globulin
Neuroimaging in cerebral malaria : Brain swelling, cortical infarcts and hyperintense
areas in white matter
TREATMENT
Most cases of vivax malaria are sensitive to chloroquine.
Chloroquine is the drug of choice for suppressive therapy
Dose
Day 1 → 10 mg/kg
Day 2 → 10 mg/kg
Day 3 → 5 mg/kg
Primaquine is used for radical cure (elimination of hypnozoites in liver)
Dose → 0.25 mg/kg for 14 days
Supportive measures
Adequate hydration (IV fluids)
Bed rest
Antipyretics
45 year old male is admitted with 2 weeks history of fever and jaundice. Give
four possible differential diagnoses. Discuss in details steps to arrive diagnosis
in this case. Write briefly treatment of Falciparum Malaria.
Differential Diagnosis
Viral Hepatitis
Malaria
Leptospirosis
Scrub typhus
Treatment of uncomplicated falciparum malaria
All over India (except NE states)
Day 1 → Artesunate (200 mg) + Sulfadoxine (1500 mg) + Pyrimethamine (75 mg)
Day 2 → Artesunate (200 mg) + Primaquine (45 mg)
Day 3 → Artesunate (200 mg)
North-Eastern States
Day 1 - 3 → [Artemether (80 mg) + Lumefantrine (480 mg)] BD
Write a prescription for uncomplicated falciparum malaria / Treatment of falciparum
malaria
All over India (except NE states)
Day 1 → Artesunate (200 mg) + Sulfadoxine (1500 mg) + Pyrimethamine (75 mg)
Day 2 → Artesunate (200 mg) + Primaquine (45 mg)
Day 3 → Artesunate (200 mg)
North-Eastern States
Day 1 - 3 → [Artemether (80 mg) + Lumefantrine (480 mg)] BD
Mention two severe complications of falciparum malaria and outline the treatment of
severe falciparum malaria
Cerebral edema
Algid malaria (Circulatory Collapse)
Complications of Falciparum Malaria (x4)
Cerebral edema
Anemia
Renal Failure
Hypoglycemia
Non-cardiogenic pulmonary edema
Circulatory collapse (Algid malaria)
Malarial hemoglobinuria (Black water fever)
Tropical splenomegaly syndrome
Quatran Malarial nephropathy
Burkitt’s lymphoma
Management of severe falciparum malaria (x2)

Dengue
Clinical features of dengue shock syndrome
Clinical Features
Dengue Fever
Fever
Headache
Retro-orbital pain
Myalgia
Arthralgia
Rash
Dengue Hemorrhagic Fever - I
Hemorrhagic manifestations
Evidence of plasma leakage
Dengue Hemorrhagic Fever - II
Spontaneous bleeding
Dengue Hemorrhagic Fever-III (Dengue Shock Syndrome)
Circulatory failure (Weak pulse, narrow pulse pressure, Hypotension, restlessness)
Dengue Hemorrhagic Fever-IV (Dengue Shock Syndrome)
Undetectable BP and Pulse
Dengue shock syndrome
According to WHO severe dengue (Fig. 4.17) is defined by one or more of the
following:
Plasma leakage that may lead to shock (dengue shock) and/or fluid accumulation,
with or without respiratory distress.
Severe bleeding.
Severe organ impairment
Mechanism of Dengue Shock
Time of occurrence → Day 4 or Day 5 of illness
Mechanism of shock: Progression of increased vascular permeability leads to
worsening of hypovolemia and results in shock
Consequences: Initially compensatory mechanisms try to correct the process, but
once they fail it goes into the decompensatory phase and organ dysfunction sets in.
When major bleeding develops, it is always associated with profound shock,
hypotension, thrombocytopenia, hypoxia and acidosis.
Clinical Features
Dengue Fever
Fever
Headache
Retro-orbital pain
Myalgia
Arthralgia
Rash
Dengue Hemorrhagic Fever - I
Hemorrhagic manifestations
Evidence of plasma leakage
Dengue Hemorrhagic Fever - II
Spontaneous bleeding
Dengue Hemorrhagic Fever-III (Dengue Shock Syndrome)
Circulatory failure (Weak pulse, narrow pulse pressure, Hypotension, restlessness)
Dengue Hemorrhagic Fever-IV (Dengue Shock Syndrome)
Undetectable BP and Pulse
Diagnosis
Increased Hb, hematocrit, leucopenia, thrombocytopenia and raised liver enzymes
Isolation of dengue virus from the blood (within first 5 days of onset of symptoms)
by tissue culture
Detection of serum NS1 antigen
Detection of virus specific IgM antibodies
In severe dengue : CXR to look for pleural effusion
Treatment of severe dengue
Admit to a hospital with ICU facilities and blood transfusion
Administer IV fluids judiciously
Replacement of plasma losses with isotonic crystalloid solution or in the case of
hypotensive shock by colloid solutions.
Start intravenous fluid resuscitation with isotonic crystalloid solutions at 5–10
mL/kg/hour over 1 hour. Then reassess the patient’s condition (vital signs, capillary
refill time, hematocrit, urine output). If no improvement or shock worsens, fluid
infusion rate can be increased. Vasopressors and inotropes need to be added.
Treatment of hemorrhagic complications
Avoid IM injections
NSAIDs, anti-platelet drugs, anticoagulation to be withheld temporarily
What are the clinical features and complications of dengue fever? How will you
investigate a 29 year old man with suspected dengue fever?
Clinical Features
Dengue Fever
Fever
Headache
Retro-orbital pain
Myalgia
Arthralgia
Rash
Dengue Hemorrhagic Fever - I
Hemorrhagic manifestations
Evidence of plasma leakage
Dengue Hemorrhagic Fever - II
Spontaneous bleeding
Dengue Hemorrhagic Fever-III (Dengue Shock Syndrome)
Circulatory failure (Weak pulse, narrow pulse pressure, Hypotension, restlessness)
Dengue Hemorrhagic Fever-IV (Dengue Shock Syndrome)
Undetectable BP and Pulse
Complications
DHF and DIC
Dengue Shock Syndrome
Cerebral hemorrhage or edema
Hepatitis, encephalitis, myocarditis, aseptic meningitis, GB syndrome, cortical venous
thrombosis
Diagnosis
Increased Hb, hematocrit, leucopenia, thrombocytopenia and raised liver enzymes
Isolation of dengue virus from the blood (within first 5 days of onset of symptoms)
by tissue culture
Detection of serum NS1 antigen
Detection of virus specific IgM antibodies
In severe dengue : CXR to look for pleural effusion
Treatment of severe dengue
Admit to a hospital with ICU facilities and blood transfusion
Administer IV fluids judiciously
Replacement of plasma losses with isotonic crystalloid solution or in the case of
hypotensive shock by colloid solutions.
Start intravenous fluid resuscitation with isotonic crystalloid solutions at 5–10
mL/kg/hour over 1 hour. Then reassess the patient’s condition (vital signs, capillary
refill time, hematocrit, urine output). If no improvement or shock worsens, fluid
infusion rate can be increased. Vasopressors and inotropes need to be added.
Treatment of hemorrhagic complications
Avoid IM injections
NSAIDs, anti-platelet drugs, anticoagulation to be withheld temporarily
Gonorrhea
Write a note on clinical features and treatment of gonorrhea
Clinical features
Men → Acute urethritis is the most common manifestation. It presents with
Urethral discharge
Dysuria usually without urinary frequency or urgency
On examination - Mucopurulent discharge from urethra and erythema of urethral
meatus
Women → Gonococcal cervicitis and vaginitis
Scant vaginal discharge
Dysuria
Anorectal and pharyngeal gonorrhea are usually asymptomatic
Ocular gonorrhea → Gonococcal conjunctivitis. It may present with purulent
discharge from the eye(s), inflammation of conjunctivae and edema of the eyelids,
pain and photophobia.
Disseminated gonococcal infection → Occurs in women with asymptomatic genital
infection. It presents as
Asymmetric migratory arthritis
Pustular skin lesions
Fever
Tenosynovitis
Acute perihepatitis (Fitz-Hugh-Curtis Syndrome) → Rare complication of PID, and is
thought to occur through direct extension of N. gonorrheae from fallopian tube to
liver capsule and peritoneum along the paracolic gutters. Patients present with sharp,
pleuritic right upper quadrant pain
Treatment

Brucellosis
Diagnosis and treatment of brucellosis
Clinical features
Incubation period : 1 week to several months
Acute or insidious onset of fever which is low or high grade, remittent or intermittent
with chills and sweats.
Anorexia, fatigue, weakness, malaise and weight loss
Splenomegaly and lymphadenopathy
History of contact with animals or animal products
Investigations
LFT : sometimes elevated
Leukocyte counts : Normal or low with relative lymphocytosis
Mild anemia and thrombocytopenia
ESR elevated
Blood, bone marrow and lymph node culture may grow organisms
Serological tests : Demonstrates antibodies to brucella
In endemic areas > 1:320 - 1:640 are considered diagnostic
In non-endemic areas > 1:360 is considered significant
PCR
Treatment
Streptomycin + Doxycycline x 6 weeks OR
Rifampicin + Doxycycline x 6 weeks
In pregnancy TMP-SMX can be used
Surgery in case of infection of prosthetic valves and prosthetic joints.
Enteric Fever (or something GI related)
Discuss the etiology, clinical features, complications, investigations and
treatment of Enteric Fever.
Etiology
Agent → Salmonella typhi and Salmonella paratyphi
Source of infection
Humans are the only natural reservoir - Patients suffering from disease, chronic
carriers
Mode of transmission - Ingestion of contaminated food or water, Feco-oral spread
Clinical Features
Symptoms
Insidious onset
Fever → The temperature rises in a step-ladder fashion (step-ladder fever) to 40–41
°C for 4 or 5 days in some cases. The hallmark of typhoid fever is continuous,
persistent fever, often lasting 4–8 weeks in untreated patients
Constipation for one week which is then succeeded by diarrhea and abdominal
distension with tenderness in right iliac fossa. The stools are loose and greenish
characteristically described as pea-soup.
Signs
Abdominal tenderness
Mild hepatosplenomegaly
Lymphadenopathy
Rose spots (Maculopapular rash)
Relative bradycardia
Complications

Investigations
TLC → Leukopenia with relative lymphocytosis
Isolation of bacilli
Blood culture → Maximum positivity in first week of fever and remains positive in
second week till fever subsides. Rapidly becomes negative on treatment with
antibiotics.
Stool cultures → Becomes positive in the third week
Urine culture → Becomes positive by third week
Widal test → Lacks sensitivity and specificity. Positive from the end of first week till
fourth week.
Molecular tests like PCR to detect flagellin, somatic gene and Vi gene
Treatment
General management → Bed rest, isolation and maintenance of nutrition and fluid
intake
Antibiotic therapy
Ceftriaxone 75 mg/kg/day x 7-14 days
Ciprofloxacin 500-750 mg BD x 14 days
Azithromycin 1 g OD x 7 days
Corticosteroids
Indicated in patients with severe toxemia, CNS manifestations and DIC
IV Dexamethasone 3 mg/kg loading dose followed by 1 mg/kg every 6 hourly for 24
hours
Discuss the etiology, clinical features, complications and management of
Typhoid fever
Etiology
Agent → Salmonella typhi
Source of infection
Humans are the only natural reservoir - Patients suffering from disease, chronic
carriers
Mode of transmission - Ingestion of contaminated food or water, Feco-oral spread
Clinical Features
Symptoms
Insidious onset
Fever → The temperature rises in a step-ladder fashion (step-ladder fever) to 40–41
°C for 4 or 5 days in some cases. The hallmark of typhoid fever is continuous,
persistent fever, often lasting 4–8 weeks in untreated patients
Constipation for one week which is then succeeded by diarrhea and abdominal
distension with tenderness in right iliac fossa. The stools are loose and greenish
characteristically described as pea-soup.
Signs
Abdominal tenderness
Mild hepatosplenomegaly
Lymphadenopathy
Rose spots (Maculopapular rash)
Relative bradycardia
Complications
Investigations
TLC → Leukopenia with relative lymphocytosis
Isolation of bacilli
Blood culture → Maximum positivity in first week of fever and remains positive in
second week till fever subsides. Rapidly becomes negative on treatment with
antibiotics.
Stool cultures → Becomes positive in the third week
Urine culture → Becomes positive by third week
Widal test → Lacks sensitivity and specificity. Positive from the end of first week till
fourth week.
Molecular tests like PCR to detect flagellin, somatic gene and Vi gene
Treatment
General management → Bed rest, isolation and maintenance of nutrition and fluid
intake
Antibiotic therapy
Ceftriaxone 75 mg/kg/day x 7-14 days
Ciprofloxacin 500-750 mg BD x 14 days
Azithromycin 1 g OD x 7 days
Corticosteroids
Indicated in patients with severe toxemia, CNS manifestations and DIC
IV Dexamethasone 3 mg/kg loading dose followed by 1 mg/kg every 6 hourly for 24
hours
Write a note on treatment of Enteric fever
Treatment
General management → Bed rest, isolation and maintenance of nutrition and fluid
intake
Antibiotic therapy
Ceftriaxone 75 mg/kg/day x 7-14 days
Ciprofloxacin 500-750 mg BD x 14 days
Azithromycin 1 g OD x 7 days
Corticosteroids
Indicated in patients with severe toxemia, CNS manifestations and DIC
IV Dexamethasone 3 mg/kg loading dose followed by 1 mg/kg every 6 hourly for 24
hours
Write a note on investigations done in a suspected case of Enteric fever
TLC → Leukopenia with relative lymphocytosis
Isolation of bacilli
Blood culture → Maximum positivity in first week of fever and remains positive in
second week till fever subsides. Rapidly becomes negative on treatment with
antibiotics.
Stool cultures → Becomes positive in the third week
Urine culture → Becomes positive by third week
Widal test → Lacks sensitivity and specificity. Positive from the end of first week till
fourth week.
Molecular tests like PCR to detect flagellin, somatic gene and Vi gene
Clinical features of typhoid fever (x2)
Clinical Features
Symptoms
Insidious onset
Fever → The temperature rises in a step-ladder fashion (step-ladder fever) to 40–41
°C for 4 or 5 days in some cases. The hallmark of typhoid fever is continuous,
persistent fever, often lasting 4–8 weeks in untreated patients
Constipation for one week which is then succeeded by diarrhea and abdominal
distension with tenderness in right iliac fossa. The stools are loose and greenish
characteristically described as pea-soup.
Signs
Abdominal tenderness
Mild hepatosplenomegaly
Lymphadenopathy
Rose spots (Maculopapular rash)
Relative bradycardia
Complications
Complications of Typhoid fever
Complications

Traveler’s diarrhea
Traveler’s diarrhea is the leading cause of illness in travelers. Usually a short-lived and
self-limited illness
Etiological Agents
Bacteria → E. coli and enteroaggregative E. coli, Shigella, Campylobacter jejuni,
Salmonella
Viruses → Norovirus, Rotavirus
Parasites → Giardia lamblia, Cryptosporidium, Entamoeba histolytica
Clinical features
Involves intercontinental travelers
Symptoms
Abrupt onset
Watery diarrhea lasting 2-5 days
Abdominal cramps
Nausea
Vomiting
Anorexia
Fever
Signs → Diffuse tenderness over abdomen
Treatment
Self-limiting usually
Dehydration correction by ORS
Drugs
Anti-diarrheal agents and antibiotics are rarely required
If fever or bloody diarrhea present → Use norfloxacin / ciprofloxacin
If non-invasive bacterial pathogen suspected → Rifaximin is used
Prevention
Doxycycline 100 mg/day for few weeks. Norfloxacin/ciprofloxacin/rifaximin once a
day.
Probiotics
What are the organisms causing acute gastroenteritis? Mention the treatment for
each
Leptospirosis
Clinical features and complications of leptospirosis
Clinical Features
Leptospiremic phase → Nonspecific features
Fever → High grade with chills and rigors
Severe headache → Retro-orbital or occipital
Myalgia → The muscles of the thighs and lumbar areas (calf and back) show severe
tenderness and may show cutaneous hyperesthesia (causalgia).
Conjunctival suffusion
Anorexia, nausea, vomiting, abdominal pain, hepatosplenomegaly
Immune phase → In many patients, the first (leptospiremic) phase is followed by a
period of apparent recovery, after which the symptoms worsen again for another 2–5
days (immune phase)
Altered mental status
CN palsies
Iridocyclitis
Dilatation of the gallbladder and cholecystitis
Meningitis → Headache, neck stiffness, fever may suggest meningitis
Weil’s syndrome (COMPLICATIONS)
Jaundice
Renal Failure → Oliguria or anuria
Hemorrhagic manifestations → Purpura, petechiae on mucosal surfaces, epistaxis,
hemoptysis, malena, hematemesis
Pulmonary manifestations → ARDS, Pulmonary hemorrhage, Pneumonia, effusion
CNS → Meningoencephalitis, Sub-arachnoid hemorrhage, seizures
Other features → DIC, Hemolytic anemia, myocarditis, arrhythmias and MODS
Clinical features of severe leptospirosis.
Weil’s syndrome (Severe leptospirosis)
Jaundice
Renal Failure → Oliguria or anuria
Hemorrhagic manifestations → Purpura, petechiae on mucosal surfaces, epistaxis,
hemoptysis, malena, hematemesis
Pulmonary manifestations → ARDS, Pulmonary hemorrhage, Pneumonia, effusion
CNS → Meningoencephalitis, Sub-arachnoid hemorrhage, seizures
Other features → DIC, Hemolytic anemia, myocarditis, arrhythmias and MODS
Syphilis
Clinical features of congenital syphilis
Early congenital syphilis — presents before two years
Snuffles
Hepatosplenomegaly
Syphilitic pemphigus
Late congenital syphilis (Hutchinson’s triad) — presents after two years
Hutchinson’s incisors : notched incisors
Sensorineural hearing loss
Interstitial keratitis
Others
Higoumenaki’s sign : Unilateral periostitis of sternal end of clavicle
Sabre tibia : Periostitis of tibia
Mulberry molars
Saddle nose
Rhagades (radiating scars around mouth, nose and anus)
Bossing of frontal and parietal bones
Salt and pepper scars on retina (choroiditis)
Clinical recognition and treatment of primary syphilis
Clinical features
Primary chancre
Location → Site of inoculation
Males → Penis or scrotum (heterosexual males) anal canal (homosexual males)
Females → Cervix, vulva and vaginal wall
Characteristics of the lesion → Single, firm, non-tender, slightly raised, red papule up
to several centimeters in diameter. It rapidly becomes eroded to create a clean-based
shallow ulcer. Because of the induration surrounding the ulcer, it is termed as hard
chancre.
Regional lymphadenitis → Firm, rubbery, mobile, non-suppurative, painless and non-
tender
Treatment
Injection Benzathine Penicillin G 2.4 million IU single dose IM
In patients allergic to penicillin
Doxycycline 100 mg BD x 14 days
HIV / AIDS
A known case of retroviral disease on irregular treatment presents with few days
history of fever, cough and severe breathlessness. His chest X-ray shows bilateral
perihilar opacities. His CD4 lymphocyte count is 120/mm3? What is the diagnosis and
outline the treatment?
Pneumocystis jiroveci pneumonia possibly due to non-adherence to treatment of
retroviral disease
Diagnosis
Chest X-ray →
Bilateral interstitial infiltrates spreading out from hilar region
Pneumatoceles may occur and rupture leading to pneumothorax
HRCT → Ground-glass interstitial infiltrates
Arterial blood gas → Hypoxemia with an increased A-a gradient and respiratory
alkalosis
Serum LDG → Elevated
Pulmonary Function tests → Restrictive pattern with reduced diffusion capacity
Diagnosis made by
Examination of induced sputum stained with methenamine silver (stains cyst wall)
and Giemsa stain (stains wall of trophozites and sporozoites)
PCR
Immunofluorescence of BAL
Treatment
Instruction to follow the proper ART regimen prescribed
Treatment of PJP
Trimethoprim 5mg/kg 6 hourly + Sulphamethoxazole 25 mg/kg 6 hourly orally
Pentamidine 4 mg/kg/day IV
Prevention
Trimethoprim 160 mg + Sulphamethoxazole 800 mg/day
Aerosolized pentamidine 300 mg once a month
What are the infections common in a HIV positive patient with CD4 of 56
cells/cumm? How will you prevent these infections in him?

Prevention of the infections

Treatment of HIV - Reduce viral load, transmission and improve the CD4 counts
Anti-retroviral therapy
It consists of three drug combination
Nucelotide Reverse Transcriptase Inhibitor
Nucleoside Reverse Transcriptase Inhibitor (NRTI)
Integrase inhibitor
The current regimen followed is TED regimen
Tenofovir disoproxil (300 mg OD)
Emtricitabine (200 mg OD)
Dolutegravir (50 mg OD)
NACO regimen
Tenofovir disoproxil (300 mg OD)
Lamivudine (300 mg OD)
Dolutegravir (50 mg OD)
Prophylaxis against opportunistic infections
CD4 < 200
Start prophylaxis against Pseudomonas jiroveci pneumonia using Trimethoprim 160
mg + Sulphamethoxazole 800 mg OD.
This also prevents toxoplasmosis
Prophylaxis against TB (Isoniazid Preventive Therapy)
Isoniazid 5 mg/kg/day for 6-12 months
CD4 < 150
Start prophylaxis against histoplasmosis using itraconazole
CD4 < 50
Azithromycin prophylaxis against Mycobacterium avium complex
A 30 year old male, known case of HIV infection, on antiretroviral therapy
presented with fever, headache and vomiting since 25 days. On examination he
had neck stiffness. Describe the differential diagnosis and investigations.
Describe the treatment of any one of these conditions.
25 year old lorry driver comes with history of fever of 5 days duration with
chills, loss of appetite and distaste for food. He also complains of passing high
colored urine and abdominal pain. a. What is the likely diagnosis? b. What are
the lab investigations for evaluation? c. Write briefly on principles of
management.
Pulmonary manifestations of AIDS
Acute bronchitis and sinusitis -
Presents as fever, nasal congestion and headache
Etiological agents: H. influenzae and Streptococcus pneumoniae
Pneumonia
Etiological agents: H. influenzae and Streptococcus pneumoniae
Presents as fever, chills, rigors, pleuritic chest pain, dyspnea in severe cases
Pulmonary tuberculosis
Etiological agent: Mycobacterium tuberculosis
Presents as evening rise of temperature, night sweats, loss of weight and appetite
Pneumocystis jirovecii pneumonia
Etiological agent: Pneumocystis jirovecii
Key presenting feature is progressive dyspnea. Fever and dry cough may also be
present
Atypical Mycobacterial infections
Etiological agent: Mycobacterium avium complex
Presents as disseminated disease with fever, weight loss and night sweats, abdominal
pain, diarrhea, massive splenomegaly
Invasive aspergillosis
Etiological agent: Aspergillus fumigatus
Presents as pseudomembranous tracheobronchitis
Indications for starting ART in HIV infection

Mention any four opportunistic infections in HIV positive patient with CD4 count less
than 200.

CD4 count
A CD4 count is a blood test that measures the number of CD4 cells in your body.
CD4 cells, also known as T cells, are a type of white blood cell that play a key role in
the immune system. They help the body fight off infections and diseases.
A CD4 count is often used to monitor the immune system in people with HIV, the
virus that can lead to AIDS. HIV attacks and destroys CD4 cells, which can lead to a
weakened immune system and an increased risk of infections and other health
problems. A low CD4 count can be a sign of HIV infection or that the HIV infection is
progressing.
A normal CD4 count for an adult ranges from about 500 to 1,500 cells per
microliter (cells/µL) of blood. A count below 200 cells/µL is considered to be low
and may indicate a weakened immune system. A CD4 count above 500 cells/µL is
generally considered normal.

HIV positive man is admitted with CD 4 count 45. How do you give prophylaxis
against opportunistic infections in this patient?
Treatment of HIV - Reduce viral load, transmission and improve the CD4 counts
Anti-retroviral therapy
It consists of three drug combination
Nucleotide Reverse Transcriptase Inhibitor
Nucleoside Reverse Transcriptase Inhibitor (NRTI)
Integrase inhibitor
The current regimen followed is TED regimen
Tenofovir disoproxil (300 mg OD)
Emtricitabine (200 mg OD)
Dolutegravir (50 mg OD)
NACO regimen
Tenofovir disoproxil (300 mg OD)
Lamivudine (300 mg OD)
Dolutegravir (50 mg OD)
Prophylaxis against opportunistic infections
CD4 < 200
Start prophylaxis against Pseudomonas jiroveci pneumonia using Trimethoprim 160
mg + Sulfamethoxazole 800 mg OD.
This also prevents toxoplasmosis
CD4 < 150
Start prophylaxis against histoplasmosis using itraconazole
CD4 < 50
Azithromycin prophylaxis against Mycobacterium avium complex
Prophylaxis against TB (Isoniazid Preventive Therapy)
Isoniazid 5 mg/kg/day for 6-12 months
HAART Therapy (x2)
HAART, or highly active antiretroviral therapy, is a combination of medications used
to treat HIV, the virus that causes AIDS. HAART is designed to suppress the
replication of HIV in the body, which can help to prevent the progression of HIV to
AIDS and also reduce the transmission of HIV to others.
HAART typically consists of a combination of three or more antiretroviral drugs from
at least two different drug classes. HAART has been shown to be effective in reducing
the viral load (the amount of HIV in the blood) to undetectable levels in many people
with HIV, and it can also help to improve immune function.
Anti-retroviral therapy
It consists of three drug combination
Nucelotide Reverse Transcriptase Inhibitor
Nucleoside Reverse Transcriptase Inhibitor (NRTI)
Integrase inhibitor
The current regimen followed is TED regimen
Tenofovir disoproxil (300 mg OD)
Emtricitabine (200 mg OD)
Dolutegravir (50 mg OD)
NACO regimen
Tenofovir disoproxil (300 mg OD)
Lamivudine (300 mg OD)
Dolutegravir (50 mg OD)
Post exposure prophylaxis of HIV
Decontamination
Wash the area with soap and water
Avoid squeezing or milking the wound
Initiating postexposure prophylaxis
Start within 72 hours
The following drug should be given once a day for a period of 28 days
Tenofovir disoproxil (300 mg)
Emtricitabine (200 mg)
Dolutegravir (50 mg)
Monitoring the exposed healthcare worker
Monitored for any serious side effects of the drugs
CBC and renal and hepatic function tests should be done at baseline and then two
weeks after initiating chemoprophylaxis
Baseline HIV-antibody test and test for hepatitis B and C infections should be done
that are repeated at 6 weeks, 12 weeks and 6 months postexposure.
Two antiviral drug regimens used in HIV infected individuals and one side effect of
each regimen
The current regimen followed is TED regimen
Tenofovir disoproxil (300 mg OD)
Side effects → Renal insufficiency, proteinuria, glycosuria, acute tubular necrosis
Emtricitabine (200 mg OD)
Side effects → Minimal toxicity, hyperpigmentation
Dolutegravir (50 mg OD)
NACO regimen
Tenofovir disoproxil (300 mg OD)
Lamivudine (300 mg OD)
Side effect → Minimal toxicity, severe acute exacerbation of hepatis may occur with
HBV coinfection upon discontinuation, pancreatitis
Dolutegravir (50 mg OD)
Cholera
Describe mode of transmission, incubation period and pathogenesis of cholera.
Mode of transmission
Feco-oral route
Stools or vomitus of symptomatic patients
Contaminated drinking water is a major source
Incubation period → 12-48 hours
Pathogenesis
Vibrio cholerae proliferates in small intestine and produces cholera toxin that acts on
Gs receptor which increases the concentration of cAMP in the cells
An increase in cAMP opens CFTR channel which increases Chloride ion secretion into
the intestinal lumen
This results in decreased sodium absorption from the lumen and hence water
diffuses into the lumen
This causes watery diarrhea (rice-water stools)
Write a note on treatment of Cholera
Appropriate and effective rehydration therapy
IV therapy if there is severe dehydration. Ringer lactate is the best fluid for IV
replacement. It should be administered till the patient becomes hemodynamically
stable.
Oral rehydration → Once the vomiting stops and the patient is hemodynamically
stable, fluid should be given orally up to 500 mL hourly. Oral rehydration solutions
(ORS) are based on the observation that glucose (and other carbohydrates) increases
absorption of sodium and water in the small intestine, even in the presence of
secretory loss due to toxins
Antibiotics → A single dose of doxycycline 300 mg or ciprofloxacin 1 g in adults or
cotrimoxazole one tablet daily reduces the duration or excretion of V. cholerae. It
also reduces the total volume of fluid required for replacement.
Zinc supplementation in children
Leishmaniasis
Treatment of visceral leishmaniosis // Write a note on diagnosis and treatment of
Kala Azar
Investigations
Direct evidence
Demonstration of amastigotes (Leishman-Donovan bodies) in crushed tissue smears
Sample taken from aspirates of bone marrow, spleen, liver, lymph nodes or buffy
coat of peripheral blood
Donovan bodies are seen as closed safety pin appearance on Giemsa stain
Culture: Aspirated material can be cultured in the Novy-MacNeal-Nicolle medium
Indirect evidence
CBC → Pancytopenia
Biochemical findings → Hypoalbuminemia and Polyclonal hypergammaglobulinemia
LFTs → Mildly elevated bilirubin, AST/ALT and ALP may be seen
Leishmanin (Montenegro) skin test → Delayed type hypersensitivity reaction
Napier’s aldehyde test and Chopra’s antimony test
Detection of specific antibody
PCR
Antigen detection
Treatment
Blood transfusions to correct severe anemia
Sodium stibogluconate (Pentavalent antimonial compound) is the mainstay of
treatment. The dose is 20 mg/kg IV or IM for 40 days
Amphotericin B deoxycholate is the primary drug of choice in Bihar. The dose is 0.75
- 1mg/kg given once daily or on alternated days for a total of 15-20 infusions
Miltefosine is the first highly effective oral drug. The dose is 50 mg BD for a duration
of 28 days.
Amebiasis
A male patient aged 60 year presents with symptoms of loose stools with blood and
mucus associated with severe tenesmus 2 weeks after returning from pilgrimage.
One week later he develops right upper abdominal pain and high grade fever. How
to investigate and treat this patient
Seeing the history, the clinical features are suggestive of liver abscess secondary to
intestinal amebiasis
Diagnosis
Blood → Polymorphonuclear leukocytosis
Liver function tests
Raised ALP
AST reflects severity of disease
CXR → Raised right hemidiaphragm, right sided pleural effusion, right basal
pneumonitis
USG
Serological tests
Amebic fluorescent antibody test
Nested multiplex PCR
Aspiration of amebic liver abscess → Anchovy-sauce or chocolate-brown pus
Treatment
Metronidazole 800 mg TID x 7-10 days or Tinidazole 2 g OD x 5 days
Chloroquine (300 mg BD x 2 days followed by 150 mg BD x 19 days) is used in those
patients who do not respond to metronidazole
Therapeutic aspiration of abscess
Percutaneous drainage
Clinical features of amebic liver abscess
Fever, anorexia, weight loss and malaise
Insidious onset
Pain in right hypochondrium due to stretching of liver capsule
Past history of dysentery
Physical examination
Tender hepatomegaly
Upward extension of liver dullness on percussion
Bulging of intercostal spaces
Discuss the etiology, clinical feature and management of Amoebic liver abscess
Etiology
Agent → Entamoeba histolytica
Trophozoites from the base of an amoebic ulcer in colon may reach through portal
circulation
Clinical features
Fever, anorexia, weight loss and malaise
Insidious onset
Pain in right hypochondrium due to stretching of liver capsule
Past history of dysentery
Physical examination
Tender hepatomegaly
Upward extension of liver dullness on percussion
Bulging of intercostal spaces
Diagnosis
Blood → Polymorphonuclear leukocytosis
Liver function tests
Raised ALP
AST reflects severity of disease
CXR → Raised right hemidiaphragm, right sided pleural effusion, right basal
pneumonitis
USG
Serological tests
Amebic fluorescent antibody test
Nested multiplex PCR
Aspiration of amebic liver abscess → Anchovy-sauce or chocolate-brown pus
Treatment
Metronidazole 800 mg TID x 7-10 days or Tinidazole 2 g OD x 5 days
Chloroquine (300 mg BD x 2 days followed by 150 mg BD x 19 days) is used in those
patients who do not respond to metronidazole
Therapeutic aspiration of abscess
Percutaneous drainage
Herpes
Herpes zoster (x2)
Herpes zoster refers to reactivated VZV infection which persisted in the dorsal root
ganglion of sensory nerves
Clinical features
Common in elderly
Skin rash followed by discrete vesicles accompanied by severe pain in the affected
dermatome
Most commonly the thoracic dermatome or ophthalmic division of trigeminal nerve
is involved
Ramsay Hunt Syndrome
Due to geniculate ganglion involvement
Cranial nerve 5 and 7 involved
Triad of ipsilateral facial paralysis, ear pain and vesicles/rash in external auditory
canal and auricle
Postherpetic neuralgia → Persistent pain for 1-6 months
Treatment →
Herpes zoster :
Acyclovir 800 mg five times a day x 2 weeks or
Valacyclovir 1 g TID or
Famciclovir 500 mg TID
Postherpetic neuralgia : Analgesics + Amitriptyline 25-100 mg daily. Capsaicin cream
may be of some help.
Prevention → Herpes zoster vaccine single dose SC 0.65 mL
Fungal
Name any four invasive fungal infections
Candida
Aspergillosis
Nocardiosis
Cryptococcosis
Mucormycosis
What are the risk factors and treatment of tenia corporis?
Tinea corporis refers to dermatophytic infection of the body (smooth skin)
Risk factors
Warm moist environments
Athletes
Treatment
Topical → Clotrimazole, Miconazole
Oral → Terbinafine, Itraconazole
Parasites
Cysticercosis
It is the condition in which human tissue is invaded by the larval form of Taenia
solium
Mode of infection
Human cysticercosis results from ingestion of eggs of T. solium from contaminated
water or vegetable
Feco-oral autoinfection
Reversal of peristaltic movements of the intestine
Clinical features
Intestinal infection → Presence of adult tapeworm in the intestine do not produce
any symptoms.
Cysticercosis
Superficially placed cysts
Cause few or no symptoms
Produce palpable or visible nodule under the skin or mucosa
They die and undergo dystrophic calcification
Resulting in muscular pain, weakness, fever and eosinophilia
Neurocysticercosis
Cysts in brain
Meningoencephalitis, epilepsy, personality changes, staggering gait, space occupying
lesion, stroke
Diagnosis
Stool examination → Eggs and proglottids
Radiological
Radiographs of involved soft tissue (buttocks and thigh) may show calcified cysts
(cigar-shaped/rice grain calcification) in muscles
CT scan of brain may show calcified cysticerci, small hypodense ring enhancing lesion
Serological tests
Histological examination of excised subcutaneous nodule
Treatment
Intestinal infection → Niclosamide 2 g as a single dose
Neurocysticercosis → Albendazole 15 mg/kg/day for 2-4 weeks
Corticosteroids → Successful treatment is accompanied by increased local
inflammation. Hence, prednisolone is given
Larva Migrans
Cutaneous larva migrans (CLM) is a creeping eruptions in the skin caused by the
filariform larvae which aimlessly wander through the skin for weeks or months
producing a reddish itch papule along the path of travel of the larvae
Etiological agents: Ancylostoma braziliense and A. caninum
Sites affected → Dorsum and sole of feet, buttocks, pelvic waist, legs and shoulders
Clinical features → Skin shows multiple, clearly defined, intensely pruritic, linear and
serpiginous tracts
Treatment → Ivermectin single dose of 150-200 mcg/kg
Swine Flu
Swine flu // H1N1 infection
Etiological agent → H1N1 virus (Orthomyxovirus endemic to pig populations)
Clinical Features

Complications
ARDS
MODS
Diagnosis
RT-PCR
Virus culture from swabs (Oral, nasal secretions)
Treatment
Mainly supportive and consists of bed rest, increased fluid consumption, cough
suppressants, antipyretics and analgesics
Severe cases may need intravenous hydration and other supportive measures
Neuraminidase inhibitors like oseltamivir and zanamivir may be used. They work by
decreasing the release of virus from infected cells and thus decrease the spread
of virus
Amantadine and Rimantadine (M2 inhibitors) were used earlier but current strains
are resistant to them
Vaccination → Yearly vaccination with season specific strain before the annual flu
season is recommended
Misc.
Ceftriaxone
Two mechanisms of Antibiotic resistance in bacteria and any two steps to contain it
Differential diagnosis of fever with Rash with jaundice of 1 week duration
Twenty five year old boy, who had no premorbid illness was admitted with
fever, rash and jaundice of 5 days duration. On examination he had
hypotension, red spots over the body and hepatomegaly. a. Name four
differential diagnoses for above problem. b. What other relevant history and
clinical examination will help in diagnosis? c. How do you investigate the
problem to confirm diagnosis d. Add a note on management of the conditions.
Mention four causes of 2 weeks of fever with splenomegaly. Discuss the clinical
features, investigations, treatment and complications of any one of them.
Causes -
Malaria
Scrub Typhus
Leptospirosis
Infectious mononucleosis
Malaria
Clinical features
Fever
P. malariae → Every fourth day (quartan)
P. vivax/ovale → Every third day (tertian)
P. falciparum → Everyday
Anemia
Mild jaundice
Hepatosplenomegaly
Investigations
Peripheral smear examination - Thin and thick smears stained with Giemsa stain
could be used to visualize the parasites
Quantitative buffy coat analysis
Serological methods - IFA and ELISA
PCR
Other findings
ESR/CRP → High
Blood → Normochromic normocytic anemia and thrombocytopenia
Treatment
Vivax malaria
Most cases of vivax malaria are sensitive to chloroquine.
Chloroquine is the drug of choice for suppressive therapy
Dose
Day 1 → 10 mg/kg
Day 2 → 10 mg/kg
Day 3 → 5 mg/kg
Primaquine is used for radical cure
Dose → 0.25 mg/kg for 14 days
Falciparum malaria
All over India (except NE states)
Day 1 → Artesunate (200 mg) + Sulfadoxine (1500 mg) + Pyrimethamine (75 mg)
Day 2 → Artesunate (200 mg) + Primaquine (45 mg)
Day 3 → Artesunate (200 mg)
North-Eastern States
Day 1 - 3 → [Artemether (80 mg) + Lumefantrine (480 mg)] BD
Complications
Cerebral edema
Hypoglycemia
Anemia
Non-cardiogenic pulmonary edema
Renal Failure
Circulatory collapse (Algid malaria)
Malarial hemoglobinuria (Black water fever)
Tropical splenomegaly syndrome
Quatran Malarial nephropathy
Burkitt’s lymphoma

Nephrology
NEPHRITIC SYNDROME
Post streptococcal glomerulonephritis
Etiology
Occurs almost two weeks after a streptococcal throat or skin infection
immune complex deposition in the glomerular basement membrane (Type III HSR)
Clinical features
Hematuria (Smoky or cola colored urine)
Hypertension
Oliguria
Periorbital edema
Peripheral edema
Investigations
Blood : Raised ASO titers, Reduction in C3 levels, Elevated urea and creatinine
Urinary findings : Oliguria, Mild proteinuria, Hematuria
Urine microscopy : Dysmorphic RBCs, RBC casts
Renal biopsy :
Light microscopy : Hypercellular glomerulus with neutrophils
Immunofluorescence : Granular deposits of IgG and C3
Electron microscopy : Dense deposits in subepithelial aspects of capillary walls
Treatment
Supportive : Salt restriction, diuretics and antihypertensives
Severe oliguria, fluid overload or hyperkalemia : Dialysis
If recovery slow or RPGN develops : Methylprednisolone may be of some help
IgA nephropathy
Most common type of primary glomerulonephritis in adults
Characterized by deposition of IgA immune complexes in glomeruli
Pathogenesis
Increased IgA production, defective IgA glycosylation causing increased binding to
mesangial cells, decreased clearance, a defective mucosal immune system and
overproduction of cytokines stimulating mesangial cell prolfieration
Clinical features
Symptoms usually occur 1-2 days following a respiratory or GI tract infection
Gross painless hematuria (recurrent)
Frothy urine (Proteinuria)
Hypertension
Investigations
Urine analysis : RBCs, RBC casts, proteinuria
Renal biopsy : Mesangial deposition of IgA and complement C3 of
immunofluorescent staining.
Treatment
Mild disease : Monitor at 6-12 months interval
Progressive disease : Methyl prednisolone 1 g daily for three consecutive days
Persistent proteinuria : ACE inhibitors
Additional : Omega-3 fatty acids supplements
A 16 year old boy presents with history of facial puffiness following an episode of
sore throat. On examination blood pressure is 170/ 106 mm Hg. What is the
provisional diagnosis? Describe the investigation and treatment of this condition
Poststreptococcal glomerulonephritis
Investigations
Blood : Raised ASO titers, Reduction in C3 levels, Elevated urea and creatinine
Urinary findings : Oliguria, Mild proteinuria, Hematuria
Urine microscopy : Dysmorphic RBCs, RBC casts
Renal biopsy :
Light microscopy : Hypercellular glomerulus with neutrophils
Immunofluorescence : Granular deposits of IgG and C4
Electron microscopy : Dense deposits in subepithelial aspects of capillary walls
Treatment
Supportive : Salt restriction, diuretics and antihypertensives
Severe oliguria, fluid overload or hyperkalemia : Dialysis
If recovery slow or RPGN develops : Methylprednisolone may be of some help
Causes and Clinical features of focal segmental Glomerulosclerosis
Causes
Primary (idiopathic)
Secondary
Viruses - HIV
Drugs - Heroin addiction
Sickle Cell Disease
Massive obesity
Congenital - unilateral agenesis
Acquired - reflux nephropathy
Hereditary - podocin, alpha-actinin 4 gene mutations
Clinical features
Heavy proteinuria
Hypertension
Hyperlipidemia
Lipiduria
Write a note on Rapidly Progressive Glomerulonephritis.
Rapidly progressive glomerulonephritis (RPGN) is a syndrome, characterized by rapid
and progressive loss of renal function (usually a 50% reduction in the GFR within 3
months) associated with severe oliguria and signs of nephritic syndrome. If not
treated death occurs due to renal failure within weeks to months
Classification
Type I - Linear deposits of IgG and C3
Goodpasture syndrome
Type II - Immune complex deposition (granular deposits)
IgA nephropathy
Membranous glomerulopathy
Lupus nephritis
PSGN
Henoch-Schonlein Purpura
Type III - Pauci-immune (no deposits)
Granulomatosis with polyangiitis
Eosinophilic granulomatosis with polyangiitis
Microscopic polyangiitis
Clinical features
Hematuria with RBC casts in urine
Moderate proteinuria
Variable hypertension and edema
Oliguria and uremia
Investigations
Blood urea and creatinine levels raised
Urinanalysis - Moderate proteinuria, microscopic hematuria, RBC and WBC casts
Circulating anti-GBM antibodies
ANCA
USG - normal sized kidenays
Renal biopsy - shows crescents
Treatment
Supportive therapy
Control of infection
Control of volume status
Specific therapy
Plasma exchange to remove circulating antibodies in patients presenting with life-
threatening pulmonary hemorrhage
Steroids methylprednisolone 500-1000 mg/day for 3 days to suppress inflammation
Immunosuppressive therapy such as cyclophosphamide
Infliximab and Rituximab
CHRONIC KIDNEY DISEASE
Enumerate various causes & clinical features of chronic kidney disease (CKD) // Four
clinical features of chronic kidney disease and four important investigations //
Metabolic abnormalities in chronic renal failure
CAUSES
Primary glomerular disease
IgA nephropathy
Focal and segmental glomerulosclerosis (FSGS)
Membranoproliferative glomerulonephritis (MPGN)
Membranous nephropathy
Secondary glomerular disease
Collagen-vascular disease
Hypertension
Amyloidosis
Diabetic nephropathy
Sickle cell nephropathy
HIV associated nephropathy
Postinfectious glomerulonephritis
Tubulointerstitial nephritis
Idiopathic
Heavy metals
Analgesic nephropathy
Reflux/chronic pyelonephritis
Drugs
Obstructive nephropathies
BPH
Calculus
Tumor
Retroperitoneal fibrosis
Vascular disease
Renal artery stenosis
Vasculitis
Hereditary diseases
Medullary cystic diseases
Alport ’s syndrome
PKD
CLINICAL FEATURES / METABOLIC ABNORMALITIES IN CHRONIC RENAL
FAILURE
Fluid and electrolyte imbalance
Retention of sodium and water leading to fluid overload —
Peripheral edema, ascites, pleural and pericardial effusions
Hypertension
Rarely : Dilutional hyponatremia
Hyperkalemia (K excretion impaired)
Acid-base disturbance
Metabolic acidosis
RS: Deep breathing (Kussmaul’s respiration)
GI : Anorexia, nausea, vomiting, hiccups
Skin : Pruritus
MSK : Muscular twitching
NS : Fits, drowsiness and coma
Uremia
GI : Anorexia, nausea, vomiting
CNS : Altered mental status, seizures and coma
PNS: Peripheral neuropathy
CVS : Pericarditis (Friction rub)
RS : Pleural effusion
Hematological : Platelet dysfunction
Growth retardation
Disturbance in calcium and phosphate metabolism
Renal osteodystrophy
Diminished 1, 25-dihyroxycholecalciferol (active vitamin D)
Hyperphosphatemia
Hypocalcemia
Stimulate PTH production (Secondary hyperparathyroidism)
Increased bone resorption leading to osteitis fibrosa cystica
Marrow fibrosis and bone cysts
Anemia : Due to low EPO production. Normocytic normochromic
Hypertension : Due to volume expansion and RAAS activation
Dyslipidemia and atherosclerosis : Elevated triglycerides and cholesterol levels
Endocrine dysfunction
Growth hormone : End organ resistance to GH leading to increased levels of IGF
binding proteins → Growth retardation
Thyroid function : Low T3 and T4, normal TSH (Sick-euthyroid syndrome)
Gonadal hormones :
Males : Low testosterone and elevated LH and FSH
Females : Low estrogen and elevated LH and FSH. Loss of pulsatile patter of LH
leading to anovulation.
Investigations
Urinanalysis
Physical examination - Fixed specific gravity around 1.010
Chemical examination
Hematuria
Proteinuria
Glycosuria
Urine microscopy
White cells indicate bacterial urinary infections. Sterile pyuria suggests papillary
necrosis or renal tuberculosis
Eosinophils indicate allergic tubulointerstitial nephritis or cholesterol embolization
Red-cell casts are suggestive of glomerulonephritis.
Granular casts indicate active renal disease.
Broad casts are seen in CRF
Urine culture
Urine biochemistry
24 hour creatine clearance to know severity
Urine osmolality is a measure of concentrating ability
Urine electrophoresis for the detection of light chains in myeloma
Serum biochemistry
Serum urea and creatinine
Electrophoresis for myeloma
Hematology
Anemia
Eosinophilia indicate allergic tubulointerstitial nephriti
Peripheral smear with fragmented red cells (Burr cells) and/or thrombocytopenia
suggestive of intravascular hemolysis due to accelerated hypertension, hemolytic
uremic syndrome or thrombotic thrombocytopenic purpura.
Immunology
Low complement proteins - active glomerular disease
Autoantibody screening
Antibodies to streptococcal antigens
Antibodies to HBV and HCV
Antibodies to HIV
Radiological examination
USG → Assess renal size and exclude hydronephrosis
Plain abdominal radiograph and CT → To exclude renal stones
Renal biopsy
What are the indications for renal replacement therapy in chronic kidney disease?
Indications for hemodialysis
A: Acidosis (severe) — pH < 7.1
E : Electrolyte disturbance —
Resistant hyperkalemia (> 6.5 mEq/L)
Severe hyperphosphatemia (> 12 mg/dL)
I : Ingestion of toxins, drugs
Dialyzable drugs (SLIMe)
Salicylates
Lithium
Isopropyl (ethylene) glycol
Methanol
O : Fluid overload that is refractory to diuretics
U : Uremia — Plasma urea > 180 mg/dL and creatinine > 6.8 mg/dL
Complications of uremia - pericarditis, encephalopathy, neuropathy
Tumor lysis syndrome
Anuria > 12 hours
Indications for continuous renal replacement therapy → ARF with combined
hemodynamic instability, cerebral edema, severe fluid overload and encephalopathy
Indications for peritoneal dialysis
Preferred mode of dialysis for infants and young children
Patients with difficult vascular access
Patients with severe hemodynamic instability on hemodialysis
Mention the investigations which distinguish between acute and chronic renal failure.
// Mention the key features to distinguish between acute kidney injury and chronic
kidney disease
Finding Comment
Previously documented elevation of serum Most reliable evidence of CKD
creatinine
Small kidney on USG Seen in CKD
Normal or enlarged kidneys on USG Favors AKI. Some forms of CKD (diabetic
nephropathy, PKD, RPGN, amyloidosis, infiltrative
diseases)
Oliguria, daily increase in serum creatinine and BUN Favors AKI
Complications : Hyperphosphatemia, hypocalcemia, Favors CKD
neuropathy, osteodystrophy, band keratopathy
Presence of anemia Favors CKD
Renal osteodystrophy (x3)
The term ‘renal osteodystrophy’ (bone mineral disorder), constitutes various forms of
bone disease that may develop alone or in combination in chronic renal failure
Pathogenesis
Chronic renal failure → Decreased calcium and increased phosphate → Increased PTH
(Secondary hyperparathyroidism) → Increased bone resorption (Osteitis fibrosa
cystica)
Long-standing secondary hyperparathyroidism → hyperplasia of glands and
autonomy of glands (tertiary hyperparathyroidism)
Clinical features
Bone pain
Acute arthritis
Recurrent fractures
Calciphylaxis - Soft tissue and vascular calcification which includes the coronary
arteries
Skeletal deformities (e.g. genu valgum)
Investigations
X-ray
Rugger Jersey Spine: Alternating bands of sclerotic and porotic appearance
Brown tumors: radiolucent cystic lesions within cortical bone
Osteopenia
Laboratory
Calcium: Decreased
PTH: Increased
Phosphate: Increased
ALP: Increased
Treatment
Correction of electrolyte abnormalities
Lowering phosphate by dietary restriction to 800-1200 mg/day and by phosphate
binders such as calcium carbonate or calcium acetate
Treatment of hypocalcemia by calcium tablets, calcitriol
Cinacalcet decreases secretion of serum PTH through stimulation of calcium-sensing
receptors in parathyroid gland
Parathyroidectomy for tertiary hyperparathyroidism
Causes of end stage renal failure (ESRD)
Primary glomerular disease
IgA nephropathy
Focal and segmental glomerulosclerosis (FSGS)
Membranoproliferative glomerulonephritis (MPGN)
Membranous nephropathy
Secondary glomerular disease
Collagen-vascular disease
Hypertension
Amyloidosis
Diabetic nephropathy
Sickle cell nephropathy
HIV associated nephropathy
Postinfectious glomerulonephritis
Tubulointerstitial nephritis
Idiopathic
Heavy metals
Analgesic nephropathy
Reflux/chronic pyelonephritis
Drugs
Obstructive nephropathies
BPH
Calculus
Tumor
Retroperitoneal fibrosis
Vascular disease
Renal artery stenosis
Vasculitis
Hereditary diseases
PKD
Medullary cystic diseases
Alport’s syndrome
ACUTE RENAL FAILURE
Causes of acute renal failure // Four causes of acute deterioration of kidney functions
Etiology and treatment of acute renal failure

Management
Advisable to restrict fluid intake to about 400 mL/day
Sodium is restricted to avoid volume expansion and overhydration
Hyperkalemia is the leading cause of death in ARF
If severe acidosis, give IV sodium bicarbonate.
Hypocalcemia and Hypercalcemia both can be observed in maintenance phase of
ARF and not serious clinical problems
Phosphate retention can be controlled with Aluminum hydroxide, lanthanum
carbonate, sevelamer, calcium acetate or calcium bicarbonate
Diet
Restrict dietary proteins to 40 g/day
Restrict salt intake
Vitamin supplements
Systemic complications
Infectious → Should be treated by appropriate antibiotics
GI bleed → PPIs and gastroprotective agents
Nephrotoxic drugs should be avoided
Identification and treatment of underlying cause
Postrenal obstruction requires urgent relief of obstruction
Drug-induced acute tubulo-interstitial nephritis usually recovers after stopping the
drug
If conservative measures fail, dialysis and hemofiltration may be necessary
Indications for dialysis and hemofiltration
A: Acidosis (severe) — pH < 7.1
E : Electrolyte disturbance —
Resistant hyperkalemia (> 6.5 mEq/L)
Severe hyperphosphatemia (> 12 mg/dL)
I : Ingestion of toxins, drugs
Dialyzable drugs (SLIMe)
Salicylates
Lithium
Isopropyl (ethylene) glycol
Methanol
O : Fluid overload that is refractory to diuretics
U : Uremia — Plasma urea > 180 mg/dL and creatinine > 6.8 mg/dL
Complications of uremia - pericarditis, encephalopathy, neuropathy
Tumor lysis syndrome
Anuria > 12 hours
Indications for hemodialysis. (x2) // Indications for dialysis in acute kidney injury
A: Acidosis (severe) — pH < 7.1
E : Electrolyte disturbance —
Resistant hyperkalemia (> 6.5 mEq/L)
Severe hyperphosphatemia (> 12 mg/dL)
I : Ingestion of toxins, drugs
Dialyzable drugs (SLIMe)
Salicylates
Lithium
Isopropyl (ethylene) glycol
Methanol
O : Fluid overload that is refractory to diuretics
U : Uremia — Plasma urea > 180 mg/dL and creatinine > 6.8 mg/dL
Complications of uremia - pericarditis, encephalopathy, neuropathy
Tumor lysis syndrome
Anuria > 12 hours
Etiology and treatment of acute tubular necrosis
Etiology
Ischemia - hypotension, sepsis, shock, hemorrhage, heart failure
Drugs - aminoglycosides, radiocontrast agents, lead, cisplatin, myoglobinuria,
hemoglobinuria
Crush injuries - myoglobinuria
High level of uric acid - Tumor lysis syndrome
Treatment
INFECTIOUS CONDITIONS
Acute pyelonephritis.
Refers to infection of renal parenchyma
Etiology
Ascending infection from bladder. Rarely hematogenous spread due to bacteremia
Pre-existing renal damage (e.g. cysts) facilitate infection
Clinical features
Triad :
Costovertebral angle (renal angle) pain : Acute onset, unilateral or bilateral and may
radiate to iliac fossa and suprapubic area. May be associated with tenderness and
guarding in the lumbar region
Fever : High grade with chills and rigor
Tenderness over the kidneys
Investigations
CBC : Leukocytosis
UA : pus cells (neutrophils), organisms, RBCs and tubular epithelial cells
Urine culture and sensitivity
Blood culture
Renal USG
CT scan
Complications
Emphysematous pyelonephritis : Seen in diabetics. It is a severe necrotizing form of
pyelonephritis with gas formation and extension of infection through renal capsule
Renal and perinephric abscess formation
AKI
CKD
Sepsis/MODS
Management
Adequate fluid intake, if necessary by IV route
Antibiotic therapy :
Uncomplicated pyelonephritis : Oral trimethoprim sulfamethoxazole (TMP-SMX) or a
fluoroquinolone
Complicated pyelonephritis : PIP-TAZ, cefepime, meropenem
Duration : 7-14 days
Surgery : If abscess formation
Causes of recurrent urinary tract infections
Anatomical abnormalities
Poor hygiene
Risky sexual behavior
Hormonal changes - menopause
Pregnancy
Bladder catheterization in chronic bed ridden patients
Diabetes mellitus
NEPHROTIC SYNDROME
Minimal lesion nephrotic syndrome -diagnosis and treatment
Diagnosis
Anemia, Leucocytosis
ESR - raised
Urine
Proteinuria → 4+
Hematuria → +/-
WBC to rule out UTI
Serum albumin < 2.5 g%
Serum cholesterol > 250 mg%
Serum BUN and Creatinine
Minimal change disease → normal
Others → Increased
Management
Diet →
Salt and Fluid restriction
Maintenance of protein
Specific
Initial episode
Prednisolone 2mg/kg/day x 6 weeks
Prednisolone 1.5 mg/kg/day - alternate days x 6 weeks
Four components of nephrotic syndrome
Nephrotic syndrome is characterized by
Massive/heavy proteinuria (>3.5 g of protein/24 hours)
Hypoalbuminemia
Generalized edema
Hyperlipidemia and lipiduria
Definition and causes of nephrotic syndrome
Nephrotic syndrome is characterized by
Massive/heavy proteinuria (>3.5 g of protein/24 hours)
Hypoalbuminemia
Generalized edema
Hyperlipidemia and lipiduria

Causes of nephrotic syndrome

Definition and investigations of nephrotic syndrome
Nephrotic syndrome is characterized by
Massive/heavy proteinuria (>3.5 g of protein/24 hours)
Hypoalbuminemia
Generalized edema
Hyperlipidemia and lipiduria
Investigations
Urine examination
Proteinuria - 24 hour protein estimation
Microscopy - RBC and Waxy casts
Serum albumin - reduced
Serum cholesterol - raised
Renal biopsy
Complications of nephrotic syndrome (x2)
OTHERS
Clinical significance of different types of casts in the Urine
Diagnosis of diabetic renal disease and its prevention
Screening for microalbuminuria
Measurement of albumin-to-creatine ratio on spot urine test. A ratio > 30 mg
albumin/g creatine is consider elevated
Albumin from a 24 hour urine collection (>30 mg/day is diagnostic)
Prevention
Meticulous control of diabetes can reverse microproteinuria in some patients
Stop smoking and control dyslipidemia
Management
ACE inhibitors or Angiotensin Receptor Blockers can retard the progression at this
stage
Avoid oral hypoglycemic agents partially excreted via kidney (e.g. glibenclamide and
metformin)
Aggressive control of hypertension
The BP should be decreased to less than 140/90 mmHg
Aldosterone inhibitors can be added with ACE inhibitors
Low protein diets (0.8 g/kg/day) may be beneficial
Once the azotaemic phase is reached the management is similar to other forms of
chronic renal failure
Causes of hematuria
Write a note on Adult Polycystic Kidney Disease (APKD). // Write a note on clinical
features of adult polycystic kidney disease.
ADPKD is genetically heterogeneous disorder caused by mutations in either PKD1 on
chromosome 16 (85% of cases) or PKD2 gene on chromosme 4
It characterized by multiple thin-walled, spherical cysts in cortex and medulla of both
kidneys.
Clinical features
Onset - May be at any age from the second decade and majority of patients remain
asymptomatic until the fourth decade of life
Acute loin/flank pain
Hematuria
UTIs
Urinary tract stone formation
Renal colic
Subarachnoid hemorrhage due to rupture of berry aneurysms
Hypertension
Complications of associated liver cysts
Bilateral large abdominal masses of irregular kidneys
Investigations
USG - visualization of cystic masses
MRI - small cysts
Treatment
No treatment to alter the rate of progression of renal failure
Control of hypertension
Control of pain
Treatment of infection
Renal dialysis or transplantation
Clinical Features and investigations of renal artery stenosis
Clinical features
Most common cause is atherosclerosis
In women < 35 years old it can be due to fibromuscular dysplasia - neurological
symptoms
Resistant hypertension
Recurrent flash pulmonary edema
Polycythemia
Abdominal bruit
Investigations
MRI
Renal isotope scan
Renal angiography
What are the causes of proteinuria and what drugs are used to decrease proteinuria?
Causes
Diabetes mellitus
Essential hypertension
Atherosclerosis
Pregnancy
Nephrotic syndrome - Minimal change disease, FSGS, Membranous nephropathy
Drugs used to decrease
ACE inhibitors/ ARBs
Control of diabetes mellitus and blood pressure
Causes and clinical features of urinary tract infection
Etiological agents
E. coli is the most common organism
Proteus, Klebsiella, Enterobacter and Pseudomonas
In immunocompromised patients viruses such as CMV and adenovirus
Clinical features
Fever with chills and rigors
Micturition abnormalities
Increased frequency
Dysuria
Urgency
Strangury
Suprapubic pain and tenderness
Renal causes of secondary hypertension
Renal artery stenosis
Autosomal Dominant Polycystic kidney disease
Nephritic syndrome
PSGN
RPGN
Nephrotic syndrome
FSGS
IgA nephropathy
Renal cell carcinoma
Renal cell carcinoma (RCC) is the most common malignant tumor of the kidney in
adults. It is an adenocarcinoma and arises from renal tubules
Risk factors
Smoking
Obesity
Use of phenacetin
Acquired cystic disease in dialysis patients
VHL syndrome
Exposure to radio-opaque dyes, asbestos, cadmium, petroleum products
Clinical features
Sex : Male to female ratio is 2:1
Age : 50-70 years of age
Most common manifestation : Gross or microscopic hematuria
Loin pain, abdominal mass may be present
Paraneoplastic syndromes : Hypercalcemia, anemia, thrombocytosis, neuropathy
Investigations
Ultrasound abdomen : Distinguishes between solid tumor and cysts
CT abdomen and chest : Extent and staging of tumor
Biopsy of lesion
Management
Radical nephrectomy is preferred wherever possible. This includes the removal of
kidney
perirenal fascial envelope and
ipsilateral para-aortic lymph nodes.
Radical nephrectomy should be considered even when metastases are present,
because this leads to reduction of systemic effects and regression of metastases
Immunotherapy : Interferon and IL-2
Resistant to radiotherapy and chemotherapy

Electrolytes, Water and Acid Base

Disorders
Enumerate the investigations for metabolic encephalopathy with one etiology of
each
Calcium
Mention FOUR important causes for hypercalcemia and write a note on initial /
emergency treatment of hypercalcemia.
Causes
Hyperparathyroidism
Paraneoplastic syndrome - Squamous cell carcinoma of lung
Multiple myeloma
Sarcoidosis
Management
Intravenous normal saline
4–6 L may be required over first 24 hours
Bisphosphonates: Inhibit bone resorption
Zoledronic acid 4 mg IV over 30 min
Pamidronate 60–90 mg IV over 2–4 hours
Ibandronate 2 mg IV over 2 hours
Calcitonin: Increases calcium excretion
100 U; 3 times/day; IM/SC for first 24–48 hours
Gallium nitrate
200 mg/m2
IV daily for 5 days
Alternative to bisphosphonate
Dialysis
Treatment of hypercalcemia.
Management
Intravenous normal saline
4–6 L may be required over first 24 hours
Bisphosphonates: Inhibit bone resorption
Zoledronic acid 4 mg IV over 30 min
Pamidronate 60–90 mg IV over 2–4 hours
Ibandronate 2 mg IV over 2 hours
Calcitonin: Increases calcium excretion
100 U; 3 times/day; IM/SC for first 24–48 hours
Gallium nitrate
200 mg/m2
IV daily for 5 days
Alternative to bisphosphonate
Dialysis
Tetany
It is characterized by muscle spasms due to increased excitability of peripheral nerves
Causes
Clinical features
In children: Triad of carpopedal spasm, stridor and convulsion
In adults: Tingling in the hands, feet and around the mouth
Signs
Chvostek’s sign → Tapping the skin over the facial nerve in front of external auditory
meatus causes an ipsilateral contraction of facial muscles
Trousseau’s sign → Inflating BP cuff on arm >20 mmHg over systolic BP for 3-5
minutes causes a carpopedal spasm
Cardiac manifestations
Prolonged QT interval in ECG
Treatment
Control of tetany
Calcium gluconate (10%) 20 mL slow IV over 10 minutes
Magnesium: if not relieved by above
Correction of alkalosis
If due to persistent vomiting: IV isotonic saline and potassium
Hysterical hyperventilation: May be controlled by rebreathing expired air from a
suitable bag
Causes and treatment of hypocalcemia
Causes
Treatment
Treated with calcitriol or alphacalcidol and calcium supplementation
Serum calcium level should be monitored to avoid hypercalcemia. Oral calcium
carbonate also decreases the bioavailability of dietary phosphates
Sodium
Treatment of Hypernatremia
CAUSES
Hypovolemia → Corrected by isotonic saline
Diarrhea
Vomiting
Sweating
Osmotic diuretics
Euvolemic → Corrected by D5W or DNS
Insensible water losses
Diabetes insipidus
Hypervolemic → Treated using loop diuretics
Primary hyperaldosteronism
Salt administration
Cushing’s syndrome
TREATMENT
First calculate water deficit
����� �������=������ ��
�������������−140140×����� ����
�����WaterDeficit=140PlasmaNaConcentration−140
×Totalbodywater
Rapid correction is dangerous because sudden decrease in osmolality can lead to
rapid shift of water from extracellular to intracellular compartment leading to
cerebral edema
Treatment
Hypovolemic hypernatremia → Isotonic saline
Euvolemic hypernatremia → Dextrose 5% or DNS
Hypervolemic hypernatremia → Diuretics
Treatment of diabetes insipidus
Central diabetes insipidus
Desmopressin
Injection : 1-2 mcg BD or QID
Intranasal : 10-20 mcg BD or TID
Other drugs : Clofibrate, chlorpropamide, carbamazepine
Nephrogenic diabetes insipidus
Low sodium diet and thiazide diuretics
Other drugs - Lithium, amiloride, NSAIDs
What are the causes of hyponatremia? Mention principles of sodium correction in
chronic hyponatremia
Causes and treatment
Hypertonic Hyponatremia
Hyperglycemia
IV mannitol
Isotonic hyponatremia
Sorbitol
Pseudohyponatremia - Waldenstrom’s macroglobulinemia, Multiple myeloma
Hypotonic hyponatremia
Hypovolemic → Treated with isotonic saline
Extrarenal losses
Thiazide Diuretics (Renal losses)
1° Adrenal insufficiency
Euvolemic → Treated using salt tablets and water restriction. ADH antagonists
may be used
2° & 3° Adrenal insufficiency
Psychogenic polydipsia
Hypothyroidism
SIADH
Beer potomania
Pregnancy
Hypervolemic → Treated by water and salt restriction. Loop diuretics may be
used
Heart Failure
Cirrhosis
Nephrotic syndrome
Renal impairment
The principles of sodium correction in chronic hyponatremia involve balancing the
need to correct the hyponatremia with the potential risks of overcorrection. The
following are some key principles to consider:
Assess the severity of the hyponatremia: The rate of sodium correction should be
based on the severity of the hyponatremia. More severe hyponatremia (sodium <
120 mmol/L) requires more cautious correction.
Use isotonic or hypertonic saline: Isotonic saline (0.9% NaCl) is generally
recommended for correcting chronic hyponatremia because it does not cause
significant shifts in water or electrolyte balance. Hypertonic saline (3% NaCl) may be
used in more severe cases, but it can cause water shifts that may lead to
complications.
Correct slowly: The rate of sodium correction should be slow, typically no more than
8-10 mmol/L in the first 24 hours and no more than 18-20 mmol/L in the first 48
hours. Rapid correction can lead to osmotic demyelination syndrome (ODS), a
potentially serious complication.
Monitor closely: Sodium levels should be monitored frequently during correction,
with adjustments made as needed based on the patient's response.
Water deprivation test
SIADH (x3)
Normal : Hypotonicity of ECF → ADH decreases → Decreased free water retention
(increase water excretion) → Tonicity increases → Normal plasma osmolality
maintained
SIADH : Hypotonicity → ADH still high (doesn’t decrease) → Free water retention
continues → Tonicity doesn’t increase → Plasma remains hypotonic
Cardinal features
Hyponatremia due to excessive water retention
Urine osmolality inappropriately high ( > 100 mOsm/L)
Plasma osmolality < 270 mOsm/L
Plasma urea and creatine are normal or low
Continued urinary sodium excretion (> 40 mEq/L)
Clinically normal intravascular volume (euvolemia)
Causes
Pulmonary : Small cell carcinoma of lung, pneumonia, TB, COPD
CNS : Meningitis, tumors, head injury, stroke
Drugs : Cyclophosphamide, carbamazepine, chlorpropamide, SSRIs
Clinical features : Nausea, irritability, confusion, seizures and coma. No edema
Treatment
Underlying cause to be corrected
Fluid intake restricted to 500-1000 mL/day
Demeclocycline may be given at a dose of 600-1200 mg/day
Severe hyponatremia : Slow infusion of hypertonic saline and furosemide
Rapid correction may cause central pontine myelinolysis
Diagnosis of SIADH
Hyponatremia due to excessive water retention
Urine osmolality inappropriately high ( > 100 mOsm/L)
Plasma osmolality < 270 mOsm/L
Plasma urea and creatine are normal or low
Continued urinary sodium excretion (> 40 mEq/L)
Clinically normal intravascular volume (euvolemia)
Search for underlying conditions that may lead to SIADH

How do you investigate and treat SIADH

Investigations
Hyponatremia due to excessive water retention
Urine osmolality inappropriately high ( > 100 mOsm/L)
Plasma osmolality < 270 mOsm/L
Plasma urea and creatine are normal or low
Continued urinary sodium excretion (> 40 mEq/L)
Clinically normal intravascular volume (euvolemia)
Treatment
Correction of underlying cause e.g. lung pathologies
Fluid intake restriction to 500 mL - 1000 mL/day
ADH antagonists like demeclocycline at a dose of 600-1200 mg/day
Slow infusion of hypertonic saline and furosemide may be rarely required in severe
hyponatremia
What is anion gap? What is its clinical utility?
Potassium
A patient of diabetic nephropathy admitted with pulmonary edema. ECG-tall T waves,
ABG - pH-7.1, p02-64, pCo2-20, HC03- 8, Na+-128, K+-6.8. How will you treat his
acute condition?
Hyperkalemia

Emergency Management
ECG changes in Hyperkalemia

Etiology and treatment of hyperkalemia // Treatment of hyperkalemia. // Mention

four causes of Hyperkalemia and discuss the treatment
Causes
Transcellular shift
Metabolic acidosis
Insulin deficiency
Tissue breakdown (Crush injuries, Rhabdomyolysis)
Medications - Non-selective beta blockers, digoxin, succinylcholine
Renal
Oliguric AKI
CKD
Hypoaldosteronism
Hyporenemic Hypoaldosteronism - Diabetic nephropathy, NSAIDs, Calcineurin
inhibitors
Normal renin - Primary adrenal insufficiency, ACEi/ARBs, heparin and LMWH
Aldosterone resistance
K sparing diuretics
TMP-SMX
Treatment
IV calcium gluconate (10%) 10 mL over 2-3 mins
Sodium bicarbonate 1-2 mmol/kg over 10-15 minutes
100 ml of 50% dextrose with 10-12 units of insulin over 15-20 minutes
Hyperventilation
Diuretics like furosemide and thiazides to enhance excretion
Cation exchange resins : Sodium polystyrene sulfonate and patiromer bind to K in
gastrointestinal tract which is excreted in stool
Salbutamol nebulization
Peritoneal or hemodialysis
Acid/Base
30 year old male presents with deep sighing respiration. He complains of fatigue.
ABG shows pH 7.10, PO2 95mmHg, PCO2 30mmHg, HCO3 12mmol/L. O2 Saturation
98% on room air. What is the metabolic abnormality? What are the three differential
diagnosis?
ABG in metabolic acidosis, enumerate four causes of metabolic acidosis
Metabolic acidosis // Enumerate the causes of metabolic acidosis
Causes
High anion gap (MUDPILES)
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets / Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates
Normal anion gap
Gastrointestinal bicarbonate loss - Diarrhea
Renal acidosis
Hypokalemia - Proximal RTA (type 2), Distal (classic) RTA (type 1)
Hyperkalemia
Drugs - K sparing diuretics, Trimethoprim, ACEi, ARBs
Clinical features
Hyperventilation
Kussmaul’s breathing
Lethargy, disorientation, stupor, muscle twitching
Treatment
Correct underlying disorder
Sodium bicarbonate may be administered
Tromethamine can be used alternatively
Dialysis may be necessary in renal failure
Classify shock. Mention the clinical features and management of septic shock //
Definition and clinical features of septic shock
Shock is defined as an acute clinical syndrome characterized by hypoperfusion and
severe dysfunction of vital organs. There is a failure of the circulatory system to
supply blood in sufficient quantities or under sufficient pressure necessary for the
optimal function of organs vital to survival.
Classification
Hypovolemic
Hemorrhagic
Non-hemorrhagic
Cardiogenic
Distributive
Septic shock
Anaphylactic shock
Neurogenic shock
Adrenal insufficiency
Obstructive
Clinical features
Low systemic vascular resistance (peripheral vasodilation) and ventricular dysfunction
resulting in persistent hypotension
Generalized tissue hypoperfusion may lead to cellular dysfunction, lactic acidosis and
ultimately multiorgan failure
Early phases of septic chock may produce evidence of hypovolemia such as dry
mucous membrane, and cold clammy skin
After resuscitation with fluids, however, the clinical picture is typically more
consistent with hyperdynamic shock. This includes tachycardia, bounding pulses with
a widened pulse pressure, a hyperdynamic precordium on palpation and warm
extremities
Signs of possible infection - fever, localized erythema, or tenderness, consolidation
on chest examination, abdominal tenderness, guarding, rigidity and meningismus
Signs of end organ hypoperfusion includes tachypnea, cyanosis, mottling of the skin,
digital ischemia, oliguria, abdominal tenderness and altered mental status
Management of septic shock
Removal of the septic foci e.g. resection of gangrenous bowels, closure of
perforation, appendicectomy
Early empirical antibiotic therapy
Supportive care - Oxygenation, and if necessary ET intubation and mechanical
ventilation
IV fluids →
Crystalloids, such as isotonic saline or Ringer’s lactate, may be used.
Large amounts may be required and may contribute to tissue oedema.
Colloids restore intravascular volume faster and remain longer in the central
circulation.
However, they are expensive and are more often used in patients where there is a
high risk of pulmonary oedema due to cardiac dysfunction and thus, may not
tolerate large volume of fluids
Vasoactive agents such as norepinephrine to produce vasoconstriction and raise the
systemic vascular resistance to normal, may be used. Dopamine, dobutamine or
adrenaline may be added.
Measure and monitor lactic acidosis. Aim to eliminate lactic acidosis with fluid
resuscitation and better perfusion

Poisoning
Principles of management of a case of poisoning
Clinical features and treatment of scorpion bite
Clinical features
In case of hemolytic venom → Similar to viper snake bit
Local features
Rapid swelling at bite site
Discoloration
Blister formation
Bleeding from bite site
Pain
Systemic features
Generalized bleeding - epistaxis, hemoptysis, hematemesis, bleeding gums
Lateralizing neurological symptoms - asymmetric pupils, intracranial bleed
Hypotension
Low back pain - indicative of early renal failure
Muscle pain - Rhabdomyolysis
Parotid swelling
Conjunctival edema, subconjunctival hemorrhage
In case of neurotoxic venom → Similar to Elapidae (Cobra/Krait) snake bite
Preparalytic stage → Vomiting, headache, giddiness, weakness and lethargy
Paralytic stage →
Eye → Ptosis, ophthalmoplegia
CNS → Drowsiness, convulsions, Bulbar paralysis
Respiratory failure
Death
Neck muscle weakness (Broken neck sign)

Write a note on clinical features and treatment of multiple bees sting

Clinical features
Uncomplicated stings cause pain, a wheal-and-flare reaction and local edema that
subsides within hours
Multiple stings can lead to vomiting, diarrhea, generalized edema, dyspnea,
hypotension, rhabdomyolysis, renal failure and death
Serious reaction occur within 10 min after the sting and include upper airway edema,
bronchospasm, hypotension, shock and death.
Treatment
Stingers embedded in skin should be removed promptly by grasping with forceps or
scraping with a blade.
The site should be disinfected and ice packs applied to slow the flow of venom
Elevation of the bite site and administration of analgesic, oral histamines and topical
calamine lotion may ease symptoms
Anaphylaxis is treated with epinephrine 0.3 mL 1:1000 solution, given SC.
Patients with a history of allergy to insect stings should carry a sting kit and seek
medical attention immediately after the kit is used
What are the indications for anti snake venom and what are the complications of the
same
Acute renal failure
Myoglobinuria/hemoglobinuria
Neurotoxicity
Bleeding/Coagulopathy : WBCT (whole blood clotting test) > 20 mins
Cardiac toxicity
Local edema involving more than half of the bitten limb
Rapid extension of swelling
Development of enlarged lymph node draining the bitten limb
Complications

Snake bite
Classification of poisonous snakes
Elapidae (Neurotoxic) → Common cobra, King Cobra, Krait
Viperidae (Vasculotoxic) → Pitiless vipers (Russel and Saw-scaled vipers) and Pit
vipers
Clinical features of neurotoxic snake bite
Local features (Milder than viperine bite)
Fang marks
Burning pain
Swelling and Discoloration
Serosanguinous discharge
Systemic features
Preparalytic stage → Vomiting, headache, giddiness, weakness and lethargy
Paralytic stage →
Eye → Ptosis, ophthalmoplegia
CNS → Drowsiness, convulsions, Bulbar paralysis
Respiratory failure
Death
Neck muscle weakness (Broken neck sign)
Clinical features of vasculotoxic snake bite
Local features
Rapid swelling at bite site
Discoloration
Blister formation
Bleeding from bite site
Pain
Systemic features
Generalized bleeding - epistaxis, hemoptysis, hematemesis, bleeding gums
Lateralizing neurological symptoms - asymmetric pupils, intracranial bleed
Hypotension
Low back pain - indicative of early renal failure
Muscle pain - Rhabdomyolysis
Parotid swelling
Conjunctival edema, subconjunctival hemorrhage
Lab investigations
Prothrombin time, Fibrin Degradation Products and Fibrinogen levels
CBC, Serum creatine, Serum amylase, Serum CPK
ABG and electrolytes
ECG
Management - Do it RIGHT
R = Reassure the patient
I = Immobilize in the same way as fractured limb. Do not compress by tight ligatures
GH = Get to hospital immediately
T = Tell the physician about any specific symptoms that may develop on way to
hospital
Specific treatment is Anti-snake venom which is to be ideally administered within 4
hours but is effective, if given within 24 hours
Dose
Mild cases → 5 vials (50 mL)
Moderate cases → 5-10 vials
Severe cases → 10-20 vials
Mode of administration → Slow IV injection or infusion at rate of 2 mL/min after
diluting with normal saline (5-10 mL/kg body weight)
Supportive therapy for coagulopathy → Fresh frozen plasma, cryoprecipitate, fresh
whole blood, platelet concentrate
Supportive therapy for bulbar paralysis and respiratory failure
ASV alone is not sufficient
Tracheostomy, ET intubation and mechanical ventilation
Inj Neostigmine → 50-100 mcg/kg/4hr continuous infusion
Glycopyrrolate → 0.25 mg can be given before neostigmine
Neurotoxic snake bite // Cobra bite- clinical features and management // Outline the
treatment of cobra bite
Neurotoxic snakes consists of snakes belonging to the family Elapidae. Theses
include common cobra, King Cobra and Krait
Clinical features of neurotoxic snake bite
Local features (Milder than viperine bite)
Fang marks
Burning pain
Swelling and Discoloration
Serosanguinous discharge
Systemic features
Preparalytic stage → Vomiting, headache, giddiness, weakness and lethargy
Paralytic stage →
Eye → Ptosis, ophthalmoplegia
CNS → Drowsiness, convulsions, Bulbar paralysis
Respiratory failure
Death
Neck muscle weakness (Broken neck sign)
Lab investigations
Prothrombin time, Fibrin Degradation Products and Fibrinogen levels
CBC, Serum creatine, Serum amylase, Serum CPK
ABG and electrolytes
ECG
Management - Do it RIGHT
R = Reassure the patient
I = Immobilize in the same way as fractured limb.
GH = Get to hospital immediately
T = Tell the physician about any specific symptoms that may develop on way to
hospital
Specific treatment is Anti-snake venom which is to be ideally administered within 4
hours but is effective, if given within 24 hours
Dose
Mild cases → 5 vials (50 mL)
Moderate cases → 5-10 vials
Severe cases → 10-20 vials
Mode of administration → Slow IV injection or infusion at rate of 2 mL/min after
diluting with normal saline (5-10 mL/kg body weight)
Supportive therapy for bulbar paralysis and respiratory failure
ASV alone is not sufficient
Tracheostomy, ET intubation and mechanical ventilation
Inj Neostigmine → 50-100 mcg/kg/4hr continuous infusion
Glycopyrrolate → 0.25 mg can be given before neostigmine
Viper bite // Complications of viper bite
Clinical features/Complicatons
Local features
Rapid swelling at bite site
Discoloration
Blister formation
Bleeding from bite site
Pain
Systemic features
Generalized bleeding - epistaxis, hemoptysis, hematemesis, bleeding gums
Lateralizing neurological symptoms - asymmetric pupils, intracranial bleed
Hypotension
Low back pain - indicative of early renal failure
Muscle pain - Rhabdomyolysis
Parotid swelling
Conjunctival edema, subconjunctival hemorrhage
Lab investigations
Prothrombin time, Fibrin Degradation Products and Fibrinogen levels
CBC, Serum creatine, Serum amylase, Serum CPK
ABG and electrolytes
ECG
Management - Do it RIGHT
R = Reassure the patient
I = Immobilize in the same way as fractured limb. Do not compress by tight ligatures
GH = Get to hospital immediately
T = Tell the physician about any specific symptoms that may develop on way to
hospital
Specific treatment is Anti-snake venom which is to be ideally administered within 4
hours but is effective, if given within 24 hours
Dose
Mild cases → 5 vials (50 mL)
Moderate cases → 5-10 vials
Severe cases → 10-20 vials
Mode of administration → Slow IV injection or infusion at rate of 2 mL/min after
diluting with normal saline (5-10 mL/kg body weight)
Supportive therapy
Coagulopathy → Fresh frozen plasma, cryoprecipitate, fresh whole blood, platelet
concentrate
Write a note on Organophosphorus poisoning.
Clinical Features (Triphasic illness)
Acute Cholinergic Syndrome
Occurs within first 24 hours
Garlic like odor in breath/vomit/clothes, bradycardia, miosis, fasciculations, twitching,
convulsions, flaccid paralysis of limbs and extraocular muscles
Intermediate syndrome
Occurs 24-96 hours after poisoning
Proximal neck muscle weakness leading to respiratory distress and failure.
Without intervention cyanosis, coma and death occur rapidly
OP-induced delayed polyneuropathy
Occurs 1-3 weeks after exposure
Cramps in the legs, numbness and paresthesia in upper and lower limbs, shuffling
gait, wrist drop and foot drop
Diagnosis
Clinical features
Lab
Red cell cholinesterase
Plasma cholinesterase
ECG - prolonged QTc and sinus tachycardia
ABG - hypoxemia
Treatment
Initial steps
Assess and record GCS
Measure pulse rate and blood pressure and auscultate the lungs
Make patients lie down in the left lateral position
Start oxygen
Intubate if patient has respiratory distress. Start atropine quickly to reduce
bronchorrhea responsible for respiratory distress.
Set-up an infusion of 0.9% normal saline. Aim at systolic blood pressure 80 mm Hg
and urine output >30 mL/h
Remove the contaminated clothes and thoroughly wash the skin with soap and water
Perform gastric decontamination with gastric lavage once the patient is stabilized
and within two hours of ingestion. Skin exposure would require irrigation of the skin
with copious amounts of water and liberal use of soap. Eye exposure should be
irrigated with copious amount of normal saline.
Drugs used
Atropine
Inject 1.8-3 mg of atropine bolus
Check pulse, blood pressure and chest crepitations
If the condition does not improved double the dose of atropine every five minutes
If there is persistent and satisfactory improvement in the condition atropine infusion
can be planned
Calculate total dose of atropine required for rapid atropinization.
Start hourly atropine infusion at 10–20% of total dose of atropine required for
atropinization.
Use three-point checklist (secretions, heart rate, pupils) to reduce infusion rate by
20% every 4 hourly once the patient is stable
Target end points for atropine infusion

Pralidoxime
Bolus dose → 30 mg/kg in 100 mL NS over 15-30 minutes
Maintenance dose → Continuous IV infusion 8-12 mg/kg/hr
Benzodiazepines
Diazepam 10 mg slow IV push for agitation and seizures
Complications of organophosphorus poisoning
Respiratory distress and failure
Coma
Extrapyramidal manifestations
OP-induced delayed polyneuropathy
Treatment of Organophosphorus poisoning (x3)
Treatment
Initial steps
Assess and record GCS
Measure pulse rate and blood pressure and auscultate the lungs
Make patients lie down in the left lateral position
Start oxygen
Intubate if patient has respiratory distress. Start atropine quickly to reduce
bronchorrhea responsible for respiratory distress.
Set-up an infusion of 0.9% normal saline. Aim at systolic blood pressure 80 mm Hg
and urine output >30 mL/h
Remove the contaminated clothes and thoroughly wash the skin with soap and water
Perform gastric decontamination with gastric lavage once the patient is stabilized
and within two hours of ingestion. Skin exposure would require irrigation of the skin
with copious amounts of water and liberal use of soap. Eye exposure should be
irrigated with copious amount of normal saline.
Drugs used
Atropine
Inject 1.8-3 mg of atropine bolus
Check pulse, blood pressure and chest crepitations
If the condition does not improved double the dose of atropine every five minutes
If there is persistent and satisfactory improvement in the condition atropine infusion
can be planned
Calculate total dose of atropine required for rapid atropinization.
Start hourly atropine infusion at 10–20% of total dose of atropine required for
atropinization.
Use three-point checklist (secretions, heart rate, pupils) to reduce infusion rate by
20% every 4 hourly once the patient is stable
Target end points for atropine infusion
Pralidoxime
Bolus dose → 30 mg/kg in 100 mL NS over 15-30 minutes
Maintenance dose → Continuous IV infusion 8-12 mg/kg/hr
Benzodiazepines
Diazepam 10 mg slow IV push for agitation and seizures
Discuss Treatment of a patient who has consumed 20 grams of paracetamol tablet 2
hours back // Treatment of Paracetamol Overdosage
Treatment
Activated charcoal
Within 4 hours of ingestion
May reduce absorption by 50-90%
Single oral dose of 1g/kg body weight
Gastric lavage→ Only for massive ingestions (e.g. > 600 mg/kg)
Antidote: N-acetylcysteine
MOA → Glutathione precursor that limits the formation of NAPQI (Toxic
intermediate)
Dosage
IV infusion or oral tablets
150 mg/kg over 15 minutes; 50 mg/kg over next 4 hours; 100 mg/kg over next 16
hours up to 36 hours
Oral N-acetylcysteine treatment regimen consists of a 72-hour oral course given as a
140 mg/kg loading dose followed by 17 doses of 70 mg/kg every four hours (total
dose 1330 mg/kg)
Liver transplantation
Indications (King’s College Criteria)
Acidosis (pH < 7.3)
PT > 100 seconds
Creatine > 3.4 mg/dL
Grade 3 encephlopathy
Paracetamol poisoning
Treatment
Activated charcoal
Within 4 hours of ingestion
May reduce absorption by 50-90%
Single oral dose of 1g/kg body weight
Gastric lavage→ Only for massive ingestions (e.g. > 600 mg/kg)
Antidote: N-acetylcysteine
MOA → Glutathione precursor that limits the formation of NAPQI (Toxic
intermediate)
Dosage
IV infusion or oral tablets
150 mg/kg over 15 minutes; 50 mg/kg over next 4 hours; 100 mg/kg over next 16
hours up to 36 hours
Oral N-acetylcysteine treatment regimen consists of a 72-hour oral course given as a
140 mg/kg loading dose followed by 17 doses of 70 mg/kg every four hours (total
dose 1330 mg/kg)
Liver transplantation
Indications (King’s College Criteria)
Acidosis (pH < 7.3)
PT > 100 seconds
Creatine > 3.4 mg/dL
Grade 3 encephalopathy
Salicylate poisoning. // Clinical features and management of Salicylate Poisoning
Clinical features (ASPIRIN)
Altered mental status
Sweating/Diaphoresis
Pulmonary edema
Increased vital signs (Hypertension, Tachypnea, Tachycardia)
Ringing in the ears
Irritable
Nausea and vomiting
Management
Decreasing absorption
Activated charcoal - Given in those who have taken more than 250 mg/kg body
weight less than 1 hour ago
Gastric lavage - It is advised in patients who have taken more than 500 mg/kg body
less than 1 hour ago.
Increasing elimination
Urinary alkalinization
Alkalinizing urine from pH 5 to 8 increases renal elimination of ASA from 1.3 mL/min
to 100 mL/min
This is done by infusion of sodium bicarbonate
Hemodialysis → Used in severe life threatening dose
Endosulfan poisoning
Endosulfan is an organochlorine compound. It has the following features
Acute organochlorine poisoning
Prodromal symptoms → Tremor, ataxia, myoclonus, dizziness, confusion, paresthesia
of mouth, nausea and vomiting
Typical presentation → Status epilepticus followed by respiratory failure, cardiac
arrhythmias, rhabdomyolysis and acute renal failure
Treatment → Control seizures using benzodiazepines, phenobarbital and phenytoin
Subacute organochlorine poisoning
Hyperexcitability stage → Tachycardia, tremor, hyperreflexia
Treatment → Anxiolytics; Cholestyramine to enhance elimination
Chronic organochlorine poisoning
Interferes with endocrine and reproductive symptoms
Manifestations → Low sperm count and motility, infertility and abortion
Forced alkaline diuresis
Forced alkaline diuresis is a medical treatment that involves increasing the pH of the
urine to enhance the excretion of certain toxic substances, such as salicylates or
heavy metals. This is achieved by administering alkaline substances, such as sodium
bicarbonate, and increasing fluid intake to increase urine output
Used for
Barbiturate poisoning
Uric acid excretion in tumor lysis syndrome (Controversial as it may worsen
hypocalcemia)
Methotrexate poisoning
Salicylate poisoning
Plumbism.
Etiology
Occupational : Batteries, solder, ammunitions, paint, card radiators, cable and wires
tec.
Lead containing bullets lodged in the body
Pathogenesis
Inhibits sulfhydryl-dependent enzymes such as gamma-aminolaevulinic acid
dehydratase (ALA-D) and ferro-chelatase which are important for heme synthesis
Interferes with mitochondrial and various nerve functions
Can also affect DNA and RNA
Clinical features
GI : Constipation, colicky abdominal pain
MSK : Muscle aches, joint pains, motor neuropathy (e.g. wrist drop).
CNS : Difficulty concentrating, deficits in short term memory. Coma and convulsions
in severe cases
Hematological : Anemia
Nephropathy
General : Headaches, decreased libido
Bluish lead line at the gum-tooth line
Investigations
Whole blood lead
Levels > 10 mcg/dL → Toxic
Levels > 50 mcg/dL → Headache, irritability, subclinical neuropathy, colicky
abdominal pain
Levels > 70 mcg/dL → Severe poisoning and acute encephalopathy
Microcytic anemia : Basophilic stippling
Elevated free erythrocyte protoporphyrin
X-ray fluorescence : Rapid, noninvasive measurements of lead in bone
Treatment
Maintain airway and treat coma and convulsions in severe poisoning
Avoid further exposure — if a large lead containing object has been ingested, it
should be removed by cathartics, whole bowel irrigation, endoscopy or even surgical
removal to prevent subacute lad poisoning
Chelation therapy —
patients with severe intoxication (encephalopathy or levels greater than 70 mcg/dL)
should receive calcium EDTA
Dimercaprol (BAL) can be used in addition to EDTA
Succimer can be used in children

Environmental Medicine
Extremes of Temperature
Write a note on clinical features and treatment of Heat Stroke // Heat stroke (x2)
Clinical features
Rise in body temperature from apparent baseline
Three cardinal sings
CNS dysfunction -
Confusion, aggressive behavior, delirium, convulsions and pupillary constriction. May
rapidly progress to coma
Cerebellar signs including ataxia and dysarthria
Hyperpyrexia (>40 C)
Hot dry skin - Pink or ashen depending upon circulatory state
Tachycardia, dysrhythmias
Hypotensive or normotensive with wide pulse pressure
Extreme tachypnea with RR > 60/minute
Pulmonary edema : Crackles and cyanosis
Rhabdomyolysis
Acute renal failure
DIC
Investigations
Temperature recording
CBC : Leukocytosis
UA: Myoglobinuria (due to rhabdomyolysis)
RFT: Elevated urea and creatine
ABG : Respiratory alkalosis, Metabolic acidosis
Blood indices : Hemoconcentration
LFT : Elevated liver enzymes
ECG : Non-specific ST depression and T wave inversion
Treatment
First aid
Remove victim to cooler location, out of the sun
Loosen or remove clothing, if possible immerse the victim in very cold water
If immersion cannot be done, cool victim with water
Use cold compress mainly in the region of the head and neck, armpits and groin
Do not use antipyretics
NPO
Hospital care
Cooling by the following methods (ICES)
Immersion
Ice cold IV fluids
Cooling blankets
Evaporative
Strategic ice packs
Supportive
IV volume replacement
Inotrope: Dobutamine
Urgent treatment of hyperkalemia
Small dose of mannitol may benefit patients with rhabdomyolysis
Avoid following medications
Paracetamol: Increases hepatic dysfunction and may create toxicity.
ASA: Uncouples oxidative phosphorylation and increases temperature
Dantrolene
Hypothermia
Hypothermia is defined as a core temperature below 35 °C
Clinical features
Mild cases
Normal mental status
Shivering
Tachycardia, tachypnea
Moderate cases
Altered mental status
No shivering
Stupor
Bradycardia, Bradypnea
Decreased BP
Pupils dilated
Severe cases
Unconscious
Investigations
Blood indices: Hemoconcentration
Electrolytes : Hyperkalemia
Arterial blood gas (ABG) analysis : low pAO2 and metabolic acidosis
SGOT and CK may be elevated due to muscle damage
Serum amylase may be elevated due to pancreatitis
ECG
J or Osborn wave
Prolongation of RR, PR, QT
Treatment
Support of airway, breathing and circulation
Prevention of further heat loss
Initiation of rewarming
Passive - Endogenous by shivering, metabolic rate, TSH, sympathetic activity
Active
Heat to body surfaces
Heating blankets
Air blankets
Radiant warmers
Warm IV fluids
Warm humid oxygen
Treatment of complications like hypotension, arrhythmia, hyperkalemia,
hypoglycemia, bladder atony and bleeding diathesis
Dermatology
Psoriasis
Psoriasis // Clinical features and treatment of psoriasis. // Clinical features of psoriasis
vulgaris // Treatment of psoriasis
T-cell mediated inflammatory skin disease
Etiology
Genetics → HLA-CW6 and HLA-B27
Infection → Group A beta hemolytic streptococci (Guttate psoriasis)
Winter season
Drugs → NSAIDs, Lithium, Anti-malarial medications, Beta-blocker, Systemic steroids
Clinical features
Skin, scalp and nails involved
Skin lesion are well defined pink-red, sharply demarcated macules, papules or
round plaques, that are usually covered with silvery scales with a whitish halo
around lesions (Woronoff’s sign)
On removal of the lesion using a microscopic slide, multiple pin-point bleeding
points may be observed (the Auspitz sign/Grattage test)
Predominantly affects the extensor surfaces and scalp
Nail pitting : Coarse, deep, irregular pitting
Diagnosis → The diagnosis can be made based on the history and physical
examination alone. Biopsy is seldom necessary
Management
Topical treatments
Emollients/Moisturizers
Topical corticosteroids → E.g. betamethasone 0.5%
Coal tar and anthralin
Calcipotriene and Calcitriol (Vitamin D3 analog)
Tazarotene (Vitamin A derivative)
Topical calcineurin inhibitors (Tacrolimus)
Phototherapy
UVB radiation (295-320 nm)
UVB-Narrow band (311 nm)
PUVA → Photochemotherapy with oral psoralen followed by exposure to UV-A
radiation (320-400 nm)
Regimen
Goeckerman regimen → UVB + Coal tar
Ingram regimen → UVB + Coal tar + Dithranol
Systemic therapy
Methotrexate
Acitretin
Cyclosporine
Biologics
Etanercept and Infliximab (TNF-alpha inhibitors)
Brodalumab (IL-17 inhibitor)
Secukinumab and Ixekizumab (IL-17a inhibitor)
Tildrakizumab, Guselkumab, Risankizumab (IL-23 inhibitors)
Guttate psoriasis
Guttate psoriasis is a type of psoriasis that is characterized by small, drop-like
lesions on the skin. It typically occurs in children and young adults and is often
triggered by a bacterial infection, such as streptococcal throat infection.
The clinical features of guttate psoriasis may include:
Small, red, scaly lesions on the skin, usually on the arms, legs, and trunk
Lesions that are usually less than 1 cm in diameter
Rapid onset of symptoms, with the development of multiple lesions over a short
period of time
Itching or burning sensations on the affected skin
Treatment → Same as above
Leprosy
Treatment of Leprosy

Steven Johnson Syndrome (x3)

Stevens-Johnson syndrome (SJS) is a rare, acute and life-threatening mucocutaneous
disease with systemic involvement and is nearly always drug-related
Classification
SJS → Minor form of TEN (Toxic epidermal necrolysis). < 10% body surface area
involved
SJS-TEN → Overlap (Moderate form). 10-30% BSA involved
TEN → Severe form. > 30% BSA involved
Clinical features
Cutaneous
Initial phase : Erythematous, dusky red, flat, atypical targetoid macules
Late phase : Lesions progressively coalesce and evolve into flaccid blisters,
detachment of epidermis
Location : face, trunk, proximal part of limbs
Mucous membrane
Ocular : Edema of eyelid, redness, photophobia, discharge, lacrimation, corneal
scarring
Buccal : Erosive hemorrhagic lesions, greyish-white
Genital : Erosive hemorrhagic lesions, painful ulceration
Extracutaneous
Fever, pain, weakness
Respiratory distress
GI : Diarrhea, nausea, malabsorption, perforation of colon, malena
Renal : Proteinuria, hematuria, micro-albuminuria
Management
Stop the offending drug
Maintain the fluid and electrolyte balance
Manage oral lesions with mouthwashes. Topical anesthetics may reduce pain and
allow the patient to take fluids
Systemic steroids are contraindicated
IVIG 2-3 g/kg over a period of 2-5 days may improve prognosis
Lichen planus
Lichen Planus (x2)
Clinical features
Skin lesions (5 P’s)
Pruritic
Planar
Purple
Polygonal
Papules/Plaques
Fine lacy reticular white pattern on surface of lesion (Wickham’s striae)
Koebner’s phenomenon
Nail involvement - Longitudinal ridges which may progress to complete loss of nail
plate (dorsal pterygium)
Mucous membranes are generally involved
Diagnosis
Histopathology of the lesions
Hypergranulosis
Hyperkeratosis
Bank like T-cell infiltrate at dermo-epidermal junction
Colloid or civatte bodies which are necrotic keratocytes in upper dermis
Treatment
Symptomatic
Topical steroids → Clobetasol propionate 0.05%, Triamcinolone ointment 0.1%
Systemic steroids → Oral prednisolone 30 mg daily for 2-4 weeks
Pyoderma
Furuncle
A furuncle, also known as a boil
Skin infection that is caused by bacteria, typically Staphylococcus aureus.
Clinical features
Lesion : a red, swollen, tender bump on the skin that is filled with pus.
Location : can occur anywhere on the body, but they are most common on the face,
neck, armpits, and buttocks.
Furuncles are often caused by the bacteria entering the skin through a cut or other
opening. They may also occur in areas where the skin is repeatedly rubbed or chafed,
such as under a bra strap.
Treatment :
Draining the pus and keeping the area clean
This can be done by a healthcare professional, or in some cases, the furuncle may be
able to be drained at home using warm compresses.
Antibiotics may be prescribed if the infection is severe or if there is a risk of the
infection spreading.
It's important to keep the area clean and avoid picking at or squeezing the furuncle
to prevent the spread of infection.
Histamine mediated disorders
Urticaria
Urticaria (also known as hives) is produced due to localized edema of dermis
secondary to a temporary increase in capillary permeability. The term
angioedema is used if edema involves subcutaneous or submucosal layers
Clinical features
They are well-circumscribed wheals, pink to light red in color, with erythematous
raised serpiginous borders blanched center. Size of the lesions vary from one
millimeter to several centimeters.
Almost always pruritic and individual wheals come and go within 24 hours and
those lesions lasting up to 6 weeks are called as acute urticaria. If the urticaria
recurs over a period of 6 weeks or more it is known as chronic urticaria.
Management
Mild urticaria limited to the skin: Antihistamines (diphenhydramine) or the newer
nonsedating agents (terfenadine, cetirizine, loratadine).
Severe urticaria: Short-term corticosteroids (up to 1 mg/kg).
Chronic urticaria: Finding the cause and remove the causative antigen. Antihistamines
and cyclosporine at doses of 3 mg/kg or higher for 8 to 16 weeks may be beneficial.
Angioedema
Angioedema is defined as a well-demarcated localized edema involving the
deeper layers of the skin, including the subcutaneous tissue and submucosal
tissues.
Etiology
IgE mediated disorder
C1 esterase inhibitor deficiency (Hereditary angioedema)
Clinical features
Well-defined, non-pitting swelling, usually non-pruritic.
Angioedema up to 6 weeks is called acute and if it lasts beyond 6 weeks is called
chronic.
Often affects periorbital area, lips and genital area
Involvement of gastrointestinal system may produce abdominal colic, with or without
nausea and vomiting
Management
Identification and removal of offending agent
Antihistamines to control the lesions, e.g. diphenhydramine, cetirizine, desloratidine
Observe for any evidence of airway obstruction
During severe attacks of hereditary angioedema due to C1 esterase inhibitor
deficiency, fresh frozen plasma is lifesaving as it provides C1-esterase inhibitor.
Danazol is useful to prevent episodes of hereditary angioedema.
Newer therapy for hereditary angioedema:
Purified C1 inhibitor concentrate
Recombinant C1 esterase inhibitor - Conestat alfa
Bradykinin receptor antagonist—Icatibant
Kallikrein inhibitor—Ecallantide.
Scabies
Clinical features and management of Scabies
Scabies is an intensely itchy rash caused by the ectoparasitic, mite, Sarcoptes scabiei
var hominis
Clinical features
Itchy red papules
Itching worse at night and after hot shower
Site of lesions (Circle of Hebra)
Between web spaces of fingers
Palms and soles
Wrists and ankles
Male genitalia
Nipples, areola, axillae, elbow flexures
Pathognomic sign → Linear or curved skin burrows where the mites live
Diagnosis
Clinical grounds
Identify the scabietic burrow and visualizing the mite
Treatment
Topical scabicides (Be CaLM)
Benzyl benzoate 10-25%
Crotamiton 10%
Lindane 1%
Malathion 0.5%
Precipitate sulfur 2-10%
Permethrin 5%
They are applied thinly and thoroughly over all skin below the neck. They are
reapplied after one week
Oral therapy is by ivermectin single dose 200 mcg/kg
Differential diagnosis of Erythema Nodosum