[Hyperkalemia]

◼ Causes:

A - Pseudohyperkalemia (hemolyzed sample) M.C.C

B - Oliguric renal failure, Type 4 RTA

C – Trauma, Thrombocytosis, Leucocytosis

D – Addison’s , Hypoaldosteronism, Congenital adrenal hyperplasia, Nelson Syndrome

E – Shifting K out of cells → 1- Acidosis 2- Rhabdomyolysis 3- tumor lysis $ 4- Insulin deficiency

F – Drugs: K-Sparing diuretics (Spirinolactone, amiloride, Trimetrine), Digoxin, B-Blocker, NSAID ,

ARB, ACEI , Cyclosporine, heparin, succinylcholine, trimethroprim

◼ Clinical Features:
A- Cardiac:
a. ECG: Low or absent P, Prolonged PR, Wide QRS, Peaked T wave
b. Sine wave in severe hyperkalemia
c. Cardiac arrhythmias
B- Neuromuscular effect:
a. Muscular weakness
b. Flaccid muscular paralysis
c. Paresthesia
C- GIT:
a. Nausea
b. Intestinal colic
c. Diarrhea

◼ Treatment:
A- Cardiac monitoring and accurate intervention if arrhythmias occur
B- Restrict potassium diet
C- Stabilize cell membrane: calcium gluconate (Cardio protective)
D- Shift K to intercellular: Insulin, B-Agonist, Sodium bicarbonate
E- Remove K by kidneys: Furesemide injection, Dialysis if refractory hyperkalemia
F- Remove K by GIT: kayexalate, Calcium resonium
[Hypokalemia]

◼ Causes:
A- Inadequate intake: low K+ diet
B- Intracellular shift: Alkalosis, Insulin, B-agonist, Barium intoxication, HCO3
C- Renal loss:
a. Diuretic therapy
b. RTA type 1 + 2
c. Cushing and conn’s (Hyperaldosteronism)
d. Genetic: Barter, liddle Syndromes
e. Hypomagnesemia
f. Refeading Syndrome
g. DKA
D- GI loss:
a. Vomitting: Pyloric obstruction, pronged gastroduodenal suction
b. Diarrhea: UC, Villous adenoma, lactulose
c. Ileostomy, Uretrosigmoidostomy
d. Villous adenoma of rectum
E- Drugs:
a. Theophylline
b. Ethacrynic acid
c. Cortison, CCB , Cisplastin , Chloithalidone
d. Amphotercin
e. Diuretics like Furesemide and thiazide
◼ Clinical Features:
A- Fatigue, Weakness, cramps, anorexia, nausea, vomiting
B- Decreased bowel mobility (ileus)
C- Hyperglycemia due to suppressed insulin
D- Restless legs
E- Rhabdomyolysis
F- Arrhythmias
G- Hypotension d.t decreased peripheral resistance
H- ECG changes: (High P wave, Depressed ST, Broad flat T wave, U wave)
I- Metabolic Alkalosis
◼ Treatment:
A- Potassium-rich diet (Banana, Orange, Tomato, Potato, Milk)
B- Potassium supplement (Oral or IV according to the cause)
[Hyponatremia]

◼ Causes:
A- Hypovolemic:
a. Diuretics
b. Diarrhea
c. Peritonitis
d. Pancreatitis (Acute abdomen)
e. Burn, Fever, Sweating
f. Adrenal insufficiency
B- Euvolemic:
a. SIADH
b. Addison’s
c. Hypothyroidism
d. Psychogenic polydipsia
C- Hypervolemic:
a. Congestive heart failure
b. Chronic liver failure/ liver cirrhosis
c. CRF/ARF/ Nephrotic
d. Pregnancy
◼ Clinical features:
The more the acute the Hyponatremia the more the severe the symptoms
a. Nausea
b. Lethargy
c. Disorientation
d. Seizures
e. mental status changes
f. Irritability
g. Increase ICP
h. Coma
◼ Treatment:
Correction should not exceed 8-12 mEq/l every day to avoid central pontine myelonsis
If asymptomatic, SIADH or post op hyponatremia → Restrict fluids
If moderate symptoms (minimal confusion) → Saline + loop diuretics
If severe (Coma) → Hypertonic solution
[Hypernatremia]

◼ Causes:
A- Water deprivation
B- Excessive water loss: (Hyperventilation, Massive burn, Fever)
C- Burn
D- Watery diarrhea
E- Polyuria (Diabetes inspidius, Diuretic use)
◼ Clinical Features:
A- Thirst, Dry tongue
B- Weakness, restlessness
C- Changes in consciousness up to coma
◼ Treatment:
A- Treatment of the cause
B- Fluid replacement

[Hypermagnesemia]

◼ Causes:
A- Renal failure
B- Iatrogenic (MgSo4 in treatment of preeclampsia)
◼ Clinical features:
A- Decrease deep tendon reflexes → 1st sign so monitor reflexes is best monitor for Mg toxicity
B- ECG like hyperkalemia (Peaked T wave, Wide QRS)
◼ Treatment:
A- Calcium gluconate or calcium chloride ( both best and cardioprotective)
B- Dialysis if severe
[HyperCalcemia]

◼ Causes: ABCDEFGHI MTS

A- Acromegaly, Addison, Aluminium
B- Barter Syndrome
C- Cron’s disease, Ca supplentation IV, Cushing’s
D- Digitalis toxicity and lithium
E- Eosteoporosis
F- Familial benign hypercalcemia Familial ,hypocalciuric hypercalcemia
G- Gastrinoma, granulomatous disease
H- Hyperparathyroidism, Hyperplasia of parathyroid, hypermagnesemia, hypervitaminosis A+D
I- Immobility, Increase bone turnover + paget’s disease of bone

M- Multiple myeloma, Malignancy, Metastasis to bone, Milk alkali syndrome

T- Thiazide, thyrotoxicosis, T.B

S- Sarcoidosis, Syphilis

◼ Clinical features:
A- Usually asymptomatic
B- Psychiatric: Confusion, Depression, Psychosis
C- GI: Constipation, abdominal pain, Pancreatitis
D- Bone pain
E- Cardio: Short QT syndrome, Hypertension, Osborn wave also seen In hypothermia
F- Renal: nephrolithiasis, DI, Renal insufficiency
◼ Treatment:
A- Saline hydration
B- Biphosphonates
C- Treatment of the cause
[Hypocalcemia]

◼ Causes: CBP HOSAM FIRED $

C. CF, Celiac disease, Calcitonin

B. Blood transfusion , Biphosphonates

P. Phenytoin toxicity

H. Hypoparathyroidism, Hypomagnesemia, Hypogonadism, Hyperphosphatemia

O. osteomalacia

S. Short bowel $, Sepsis , Steroid

A. Acute pancreatitis, ACEI , Amiloride, Aminoglycosides

M. Medullary thyroid CA, Mercury poisoning, Metabolic alkalosis

F. Foscarent

I. Intestinal malabsorption, intestinal bypass

R. RF, refeeding $, Rickets, respiratory alkalosis, rhabdomyolosis

E. exposure to sun decreased

D. Di-george $, Vit. D deficiency, Diuretics (Spirinolactone, furosemide)

$. Nephrotic and tumor lysis syndromes

◼ Clinical features:
A-In children: carpopedal spasm, stridor, convulsions
B-In adults: tingling in hand and feet + around the mouth, muscle cramps, psychosis, abd. Cramps
C-Signs:
a. Trousseaus sign (carpal spasm after inflation of cuff on the arm
b. Chvostek’s sign (twitching of facial muscles after facial nerve tapping)
c. Peroneal sign (taping on peroneal nerve results in dorsflexion and abduction of foot)
d. Erb’s sign (motor nerve can be stimulated by low current < 5milliamperes)
e. Prolonged QT interval ECG
◼ Treatment:
A- IV Calcium gluconate
B- If no improvement → I.V MgSO4
C- Correction of alkalosis
[Causes of gynecomastia]

A- Idiopathic (M.C.C)
B- Physiological (2nd M.C.C): Neonate, pubertal , old age
C- Chronic disease: CRF, Liver failure, Cystic fibrosis
D- Endocrine: Hypogonadism, hyperthyroidism, Hyperprolactinemia, Acromegaly
E- Tumor: Breast CA, Testicular CA, Bronchogenic CA, Adrenal CA, Chemotherapy
F- Genetic: Kleinfelter $, Marfan $, Androgen resistant $ , Kallman $
G- Starvation and refeeding
H- Orchitis , autoimmune gonadal failure
I- Drugs:
a. Flutamide & bicalutamide
b. CCB, Methyldopa
c. Ketoconazol
d. Tricyclic antidepressant
e. Cemetidine
f. Spirinolactone
g. Digitalis
h. HIV medication & Steroids
i. Opioids

[Causes of Hirsutism] I-DOHA

1. Idiopathic M.C.C
2. Drugs: (DMPC) Danzol, Diazoxide, minoxidile, Progestron, Phenytoin, Cyclosporin, Cortison
3. Ovarian: Theca lutein cyst, PCOS, Ovarian tumor, Sertoli leydig tumor, Hilus cell tumor, luteoma
4. Hypothyroidism and obesity
5. Acromegaly, Adrenal causes ( adrenal tumor, cushing$, CAH)

N.B → Rapid hirsutism caused by adrenal or ovarian tumor, PCOS doesn’t cause rapid onset of hirsutism

[Causes of polyuria]

A- Hypokalemia, hypercalcemia, hyperthyroidism, hyperparathyroidism, hyperglycemia,

hyperaldosteronism (Conn’s), Hypopituitarism, hypoxia + hemochromatosis
B- Acromegaly
C- Migraine
D- Pregnancy, pheochromocytoma
E- Sickle cell anemia
F- Osmotic diuretic as in DM, RF , IV manitol
G- Lithium, demeclocycline
H- Dietary, DI , Diffuse renal disease (MM, Sarcoidosis, Amyloidosis)
[Hypoglycemia causes]

1- Insulin overdose
2- Factitious insulin injection (Munchausen $)
3- Oral hypoglycemic medication (Sulfonylurea)
4- Infant of diabetic mother , late pregnancy , DI
5- Born error of metabolism (galactosemia)
6- Postprandial hypoglycemia → dumping $
7- Liver diseases: viral hepatitis, hepatic congestion & alcohol
8- Adrenal insufficiency, hyperprolactinemia
9- Hypopituitarism, GH deficiency, Hypothyroidism
10- Glycogen storage disease, CAH, Reye syndrome
11- Insulinoma
12- Sepsis, Endotoxic shock
13- Prolonged fasting
14- Drugs (B-blocker, ASA, paracetamol , Quinine)

[Hyperglycemia causes]

1- DM & obesity
2- Gestational DM
3- Endocrine (Pheochromocytoma, Cushing, Conn’s, Acromegaly
4- Thyrotixicosis, Cystic fibrosis, PCO
5- Chronic renal failure
6- Glucagonoma, Somastostatinoma, Chronic pancreatitis, Pancreatic tumor
7- Phenylketonuria, mucopolysachride
8- Infection ,stress ,TPN,
9- Drugs (Drugs that induce DM): Cortison, OCP , THaizide, B-Blocker, Lasix, Anti-TB, Anti-HIV

Cushing’s $ Conn’s $
Hypertension Hypertension, no edma
Hypokalemia Hypokalemia
hypercalcemia Hypernatremia
Hypomagnesemia
Hyperglycemia Hyperglycemia
Hyperchostrolemia Metabolic alkalosis
Weight gain rapid Low renin
Pheochromocytoma Hypoaldosteronism CAH Hyperparath. Hypoparath. Pseudohypoparat
h.
HTN Hypotension Hypotension ↑Ca ↓Ca ↑ PTH, ALP
Headache ↑K ↑K ↑active vit D ↓active vit D ↑Po4-
Hyperglycemia ↓Na ↓ Na ↓PO4- ↑Po4- ↓Ca
tachycardia M.acidosis ↓glucose ↑ PTH, ALP ↓PTH & ALP
Dyspnea ↓ renin Acidosis ↑ CL
Anxiety, Vomit Caused by DM, Skin
ACE, Heparin, pigment,
Spirinolactone, weakness
NSAID
pallor dehydration

Addison disease Addison crisis

Hypotension All same but severe
Hyponatremia Hypotension up to shock
Hypoglycemia Hypoglycemia up to confusion
Hyperkalemia in 1ry only Unexplained fever and acute abdomen
Hypercalcemia
Hyperpigmentation and weight loss
Autoimmune ass.: Vitiligo, Graves
N.B

Prolactine antagonist Dopamine

Dopamine antagonist Phenothiazine
Growth hormone antagonist Somatostatin
ADH antagonist Demeclocyline
Cortison receptor antagonist Mifepriston
Aldosteron antagonist Spirinolactone

Hypothyroidism Hyperthyroidism
Bradycardia Tachycardia , arrhythmia, A-fib
Cold intolerance, heat preference Heat intolerance, cold preference
Weight gain with less appetite Weight loss with more appetite
Constipation Diarrhea
Hyporreflexia Hyperreflexia
Increase cholesterol Decrease cholesterol
Dry skin (decrease sweating), coarse hair Moist skin, increase sweating, fine hair
Hypothermia Fever
Fatigue, depression, lethargy, coma Anxiety, restlessness, nervousness
Menorrhagia, infertility Oligomenorrhea, infertility
Diastolic HTN Systolic HTN
Increase sleep Decrease sleep
 Features Crohn’s disease Ulcerative Colitis
Male to female Equal Male more affected
Involvement Any site, Skip lesion present, full Start at rectum, no skip lesion,
thickness no inf. Beyond submucosa
Features Non-bloody diarrhea, Weight Bloody diarrhea, no oral or anal
loss, palpable abd. Mass in RIF, involvement, LIF pain , no vit
malabsorption of vit D+B12, malabsorption, crypt abscess
crypt abscess
M.C site Terminal ileum then colon Rectum
Non caseating granuloma Present Absent
Extraintestinal manifestations -Seronegative arthritis -Seronegative arthritis
-Erythema nodosum -Erythema nodosum
-Pyoderma gangrenosum -Pyoderma gangrenosum
-Gallstones -Ankylosing spondylitis
-Liver cirrhosis -Episcleritis, Uveitis
-Pericarditis
Complications -Stricture -Toxic megacolon
-Fistula -Cholangitis
-Malabsorption -more risk of colorectal CA
-1ry sclerosing cholangitis
Smoking relation Increase by smoking Decrease by smoking
Serum marker ASCA pANCA

Vitamin deficiency Signs and symptoms

B1 (thiamin) Wet beriberi: SOB, LL edema, HF
Dry beriberi (Wernicke’s encephalopathy):
Paralysis, Confusion, Nystagmus
B3 (Niacin) Pellagra (Dementia, Diarrhea, dermatitis,
depression, death)
B6 (pyridoxine) Skin rashes, cracked lips, Sore tongue, depression,
irritability , weak immunity, lethargy, Seizures
B9 (Folic acid) Megaloblastic anemia withOUT neuro. Manifest.
B12 (Cobalamin) Megaloblastic anemia with neuro. Manifestations
C (ascorbic acid) Scurvy: Sore arms, sore legs, gum bleeding
D Rickets, Osteomalacia
K Bleeding tendancy, High INR
[Causes of watery diarrhea]

A- Vibrio cholera
B- C. difficile
C- Giardiasis
D- Bacillus cereus
E- Staph aureus
F- Enteropathogenic E.coli
G- Enterotoxigenic E. coli
H- Clostridium botulinum

[Causes of bloody diarrhea]

A- Enteroinvasive E.Coli
B- Enterohemorrhagic E.Coli
C- Campylobacter jejuni
D- Entameba histolytica
E- Salmonella
F- Shigella
G- Yersinia enterolitica
H- Divirticulitis
I- CMV
J- Schistomiasis

[Causes of peripheral Cyanosis]

A- Cold exposure
B- Obstruction
C- LVF and shock
D- Decreased cardiac output

[Causes of central cyanosis]

A- Polycythemia
B- High altitude
C- Lung diseases
D- Metsulfhemoglobinemia
E- Shunt
[Causes of Chest pain]

A- Cardiac:
a. MI
b. Angina
c. Pericarditis
d. Aortic dissection
B- Respiratory:
a. PE
b. Pneumothorax
c. Pneumonia
C- GI:
a. Esophageal spasm
b. GERD
c. Pancreatitis
d. Peptic ulcer
D- Muskuloskeletal:
a. Costochondriasis
b. Trauma

[Causes of Epigastric pain]

A- Biliary:
a. Cholecystitis
b. Cholelithiasis
c. Cholangitis
B- Cardiac:
a. MI
b. Pericarditis
C- Gastric:
a. Esophagitis
b. Gastritis
c. Peptic ulcer
D- Vascular
a. Aortic dissection
b. Mesenteric ischemia
Causes of splenomegaly Causes of massive splenomegaly
Malaria CML
Leukemia Agnogenic myeloid metaplasia
HF Polycythemia vera
Cirrhosis Hairy cell leukemia
Tumor in spleen or spread to spleen B-Thalassemia major
Infections Visceral leishmaniasis
Inf. Diseases as SLE or RA Malaria
SCA Gaucher disease

[Causes of hepatosplenomegaly]

A- Infection:
a. Acute viral Hepatitis
b. Infectious mononucleosis
c. CMV
d. Brucella
e. Hyperactive malaria $
f. Leishmeniasis
g. Typhoid fever
h. Schistosomiasis
i. Histoplasmosis
B- Hematologic:
a. Myeloproliferative disease
b. Leukemia
c. Lymphoma
d. Pernicious anemia
e. SCA
f. Thalassemia
g. Myelofibrosis
C- Metabolic disease:
a. Gaucher’s disease
b. Hurler’s $
D- Chronic liver disease and portal hypertension
E- Amyloidosis
F- Acromegaly
G- SLE
H- Sarcoidosis
I- Trypanosomiasis
J- Obesity
Anti-TB drug Adverse effect Treatment
Rifampicin Red or orange colored body No need for treatment
secretions
Isoniazid Peripheral neuropathy Prophylactic with pyridoxine
Decreased B6
Pyrazinamide Hyperuricemia Treat if symptomatic only
Hepatotoxicity
Ethambutol Optic neuritis, color vision Adjust dose in Renal failure
Streptomycin Ototoxic, Nephrotoxic Dose adjustment

[Pneumonia]

◼ Criteria for hospitalization: CURB 65

a. Confusion
b. Urea > 7
c. RR > 30
d. BP < 90/60
e. Age > 65
0-1 ttt at home , 2-3 Hospitalization , 4-5 ICU
◼ M.C.C Typical pneumonia is Strept. Pneumonia (Rusty Sputum)
◼ M.C.C Atypical pneumonia is mycoplasma (Ass. With ear drum inf.) (ttt by erythromycin)
◼ M.C.C Hosp. acq. Pneum. Is Staph aureus (purulent sputum)
◼ M.C.C aspiration pneumonia is anaerobe (ttt by clindamycin)
◼ M.C.C in air condition workers is legionella (ass with Hyponatremia and
lymphopenia)(macrolides is the ttt)
◼ M.C.C in bronchiectasis and CF is pseudomonas (Green sputum)
◼ M.C.C in alcoholics and DM pt. is klebsiella (red current jelly sputum)
◼ M.C.C in HIV CD4 < 200 is PCP (TTT by cotrixamazole)
◼ M.C.C in HIV CD4 < 100 is mycobacterium

[Features massive PE]

1. Arterial hypotension
2. Cardiogenic shock (oliguria, lactic acidosis, cool extremities, altered level of conciousnesss)
3. Circulatory collapse in pt. with syncope or undergoing CPR
[Rheumatoid arthritis]

RA is a chronic symmetrical polyarthritis of unknown cause, also characterized by extra-articular feature

F>M 3:1, Associated with HLA-DR4

M.C.C of death in RA is CAD

Associated with caplan’s syndrome (RA + pneumoconiosis + lung nodules)

Diagnosis:

A- High ESR & CRP

B- Anti-CCP (Most specific)
C- RF (70% positive, can be +ve in 10% of normal population)

Treatment:

A- Analgesia (NSAID is first line of treatment)

B- DMARD (Methotrexate is most used, others like sulfalazine, lefunomide, hydroxychloroquine)
S.E methotrexate = liver toxicity, Bone marrow suppression, Pulmonary toxicity
S.E hydroxychloroquine = Retinal toxicity
S.E Sulfalazine = Bone marrow toxicity, Hemolysis in G6PD deficiency, Rash
C- TNF-inhibitors (etanercept)
S.E = Reactivation of T.B, Infection
D- Rituximab (Anti-CD20 monoclonal antibodies) S.E = Infection
E- Physiotherapy
F- Surgery

[PseudoGout]

Known as calcium pyruvate deposition disease

May be associated with hemochromatosis, Hyperparathyroidism, hypothyroidism & True gout

Clinical features:

A- Acute synovitis (Hotness, redness, tenderness, pain, swelling)

B- Chronic arthritis (pain + morning stiffness + functional impairment)
C- The knee joint is most common site, DIP & PIP not affected

Treatment:

A- NSAID (Best initial treatment)

B- Intraarticular steroid if NSAID resistant
C- Joint aspiration to relieve swelling & pain, colchicine for prophylaxis
[Systemic lupus erythematous]

SLE is an autoimmune disorder with a number of autoantibodies

Clinical features:

A- General symptoms (fever, fatigue, malaise)

B- Arthritis with early morning stiffness and tenosynovitis
C- Serositis
D- Raynaud’s phenomenon
E- Skin manifestations (malar butterfly rash, discoid lupus rash)
F- Renal: typically proliferative glomerulonephritis –nephritic
G- Cardio (Pericarditis M.C in SLE, Libman-sacks endocarditis)
H- Respiratory: (pleuritis, pleural effusion, pulmonary fibrosis, alveolitis)
I- Neuro: carpel tunnel syndrome, chorea, lymphocytic meningitis)
J- Hematological: neutropenia, lymphopenia, thrombocytopenia, anemia
K- GI: oral ulcer, mesenteric vasculitis
M.C presentation is arthralgia with arthritis & raynaud’s phenomenon

Treatment:

A- For mild disease: NSAID, hydroxychloroquine, Prednisolone)

B- For severe disease: I.V methylprednisolone combine with I.V cyclophosphamide
C- Maintenance therapy: Azathiprine, Methotrexate

[Septic Arthritis]

Most common site is(knee & wrist), In I.V drug users (Spine & Sacroiliac joint is more common)

M.C.C is staph aureus , Gonorrea in sexually active, pseudomonas after deep wounds,salmonella in SCA

Clinical features:

A- Sudden joint pain aggravated by movement

B- Hotness, redness, tenderness of affected joint
C- Fever, fatigue & malaise

Diagnosis: Joint aspiration with cytology & culture (Best), leukocytosis

Treatment:

A- Analgesia
B- Antibiotics (Ceftriaxone & vancomycin are best initial empirical therapy
C- Joint drainage may be needed
D- If prosthetic joint → remove joint then treat with Ab, then replace joint after 6-8 weeks
[Gout]

Disease of uric acid metabolism which leads to accumulation of sodium urate crystals

Causes:

A- Idiopathic
B- Increased cell turnover (Cancer, Hemolysis, Chemotherapy)
C- Enzyme deficiency (Lesch-nyhan syndrome, glucagon storage disease)
D- Renal insufficiency
E- Ketoacidosis or lactic acidosis
F- Drugs as thiazide and aspirin

[Peptic Ulcer]

Ulceration of lower eseophagus, stomach or duodenum

It can occur in the ileum adjacent to Meckel’s diverticulum

M.C site of gastric ulcer is lesser curvature, Blood group A is a risk factor

Causes:

A- H-Pylori M.C.C , more in duodenal

B- NSAID’s 2nd M.C.C
C- Stress induced (any illness, RTA, Burn)
D- Zollinger Ellison Syndrome
E- Crohn’s disease
F- Idiopathic

Clinical features:

A- Recurrent episodes of epigastric pain related to meal (GU ↑ with food, DU ↓ with food)
B- PUD is M.C.C UGIB
C- Vomiting may be present
D- Dyspepsia is M.C symptom

Diagnosis: UGI endoscopy is most accurate test, biopsy from ulcerated mucosa

Management:

A- Stop smoking and alcohol

B- Identify the cause ,Treat the cause to prevent recurrence
C- PPI effective in 95% of cases

Complications of peptic ulcer: Perforation, chronicity, bleeding, anemia, malignant, transformation,

gastric outlet obstruction. Never malignant
[Hepatitis A]

◼ HAV & HEV have fecal oral route

◼ HAV never become chronic
◼ HAV infection give lifelong immunity but vaccine gives 10 years immunity
◼ HAV symptoms are more severe in adults than in children
◼ IgM is antigen for HAV

[HBV]

◼ HBV is strongly associated with polyarthritis nodosa and associated with increased risk of HCC as
well as hepatoma
◼ HBV HDV transmitted by blood transfusion, saliva, sex, vertical ( from mother to fetus)
◼ HDV is preventable by HBV vaccine, as it require HBsAg for entry to hepatocyte
◼ HBV has 3 antigens (HBsAg,HBcAg, HBeAg)
◼ HBV vaccination has only HBsAg
◼ If HBsAg positive → HBV infection
◼ AntiHbc IgM positive with HBsAg negative
◼ Anti-Hbc if positive indicates active replication
◼ If anti-HBs positive, patient is vaccinated
◼ Treated by lamivudine and tenofovir

[Facts about Hepatitis]

◼ All hepatitis virus are RNA except HBV is DNA

◼ HCV transmission is like HBV but less likely by sex
◼ HBV & HCV can cause chronic hepatitis and increased risk of HCC
◼ HAV & HBV have vaccinations but HCV & HEV don’t
◼ Interferons can be used in ttt of HCV & HBV , S.E is flu like symptoms
◼ HCV is m.c hepatitis transmitted in blood transfusion
◼ In infected needle stick, risk of infection is → HBV30%, HCV3% , HIV0.3%

[Causes of Lower GI bleeding]

A- Diverticular disease ( diverticulosis, diverticulitis)

B- Colitis
C- Hemorrhoids
D- Neoplasms as colorectal cancer
E- Angiodysplasia
F- Rectal varices
G- Coagulopathy
H- Anal fissures
I- NSAIDS
[Hepatic Encephalopathy]

Risk factors:

A- Trauma
B- Infection
C- Heavy protein meal
D- GI bleeding
E- Hepatotoxic drugs (Narcotics, sedation)
F- Constipation
G- Dehydration and hypokalemia and alkalosis
H- TIPS

Grades:

A- Grade 1: Insomnia(1st symptom), slurred speech, slow mentation

B- Grade 2: Drowsy, aggressive behavior
C- Marked confusion, sleepy, respond to pain
D- Coma, unresponsiveness

[Spontaneous Bacterial peritonitis]

Bacterial infection in patient with ascites but without perforation of bowel, E.Coli is most common

Symptoms:

A- Asymptomatic in 30% but may worsen hepatic encephalopathy

B- Abd. Pain, fever, chills, hypotension

Diagnosis:

A- All pt. with ascites should have paracentesis to rule out SBP as 30% are asymptomatic
B- High ANC in ascites → best initial test
C- Culture 80% sensitive not needed for diagnosis but most accurate test

Prophylaxis indications:

A- Cirrhosis or GI bleeding: IV ceftriaxone daily or norfloxacin bidx 7d

B- Previous SBP: long term prophylaxis with daily norfloxacin or TMP/SMX

Treatment:

A- Antibiotics: Cefotaxime or Ceftriaxone

B- Albumin: decreases mortality and decreases risk of renal failure

Complications: AKI, Encephalopathy

[Bronchial Asthma]

Clinical picture:

A- Usually worse at night and vary overtime

B- Cough M.C symptom
C- Dyspnea, expiratory wheezing, tachypnea, tachycardia, chest tightness
D- Pulsus paradoxus
E- Reversible obstruction on PFT

Signs severe asthma

1. PEFR 33-50% 2. RR> 25 3. Pulse > 110 4.Can’t complete a sentence

Signs life threatening asthma

1.PEFR<33% 2.O2 Sat<92% 3. Silent chest 4.Cyanosis 5.Bradycardia

6. Hypotension 7.Confusion 8.Coma

Treatment of acute asthma and status asthmaticus:

A- Oxygen
B- 1st step: SABA nebulizer or MDI (Salbutamol, albuterol, levalbuterol)
C- 2nd step: SAMA
D- 3rd step: steroid (oral and IV are equivelant)
E- 4th step: MgSO4 IV
F- 5th step: if no response IV salbutamol
G- Intubation and mechanical ventilation can be helpful

[Clinical picture of hypercapnia]

A- Headache
B- Tremor (Asterixis)
C- Large pulse volume
D- Vasodilatation (warm extremities)
E- High ICP → Papilloedema
F- Decreased level of consciousness → Coma
[Bronchiectasis]

M.C.C is pseudomonas aeruginosa

Causes:

A- Cystic fibrosis is M.C.C

B- Obstruction (Foreign body, tumor)
C- Infection
D- Kartagener’s syndrome (Ciliary dysfunction)
E- Hypogammaglubinemia

Symptoms: Episodes of lung infection with HIGH volume of foul smelling sputum, Hemoptysis, Clubbing,
recurrent infections

Diagnosis:

A- High resolution CT (Best)

B- CXR (Tram-track appearance)
C- PFT obstructive pattern
D- Investigations of cause

Treatment: TTT of cause, Ab for acute, Chest physiotherapy, ICS, Hydration, Bronchial hygiene V.Imp

[Lung abscess]

M.C.C is staph aureus

RF: Stroke, Intoxication, Endotracheal intubation

Clinical features:

A- Large volume of foul smelling sputum

B- Weight loss
C- Clubbing finger

Diagnosis:

A- Cavity with air fluid level appears on imaging

B- Lung biopsy is the best to determine the pathogen
C- Sputum culture is not beneficial

Treatment: Clindamycin or Penicillin, Surgical drainage only if failed medical treatment

[Causes of dullness on percussion]

A- Effusion
B- Pleural thickening
C- Collapse
D- Fibrosis
E- Consolidation

[Causes of increased TVF]

A- Cavity
B- Consolidation
C- Collapse

[Red flags of headache]

A- Sudden onset , Age >50

B- Vomiting
C- Continuous
D- Symptoms of Increased intracranial pressure
E- Signs of focal neurological disorder ( monoplasia, diplopia)

[Multiple Sclerosis]

Autoimmune demyelinating disease of the CNS, more common in white women in cold climates

Common presentation:

A- Visual symptoms: Optic neuritis, Optic atrophy, intraocular ophthalmoplegia

B- Sensory: Numbness, trigeminal neuralgia, Lhermitte’s sign)
C- Motor: Weakness, most commonly in legs
D- Cerebral: Ataxia, tremor
E- Urinary and sexual: incontinence, impotence
F- Depression and suicide is common

Treatment:

A- Acute relapse: I.V Methylprednisolone for 5 days

B- Disease modifying drugs (Beta interferon, Fingolimod)

Good prognosis: Female, relapsing remitting type, optic neuritis, few attacks, young age onset

Bad prognosis: Male, progressive type, paraplegia, Old > 50 at onset, DM

[Acute stroke]

Causes:

A- Ischemic stroke(85%)
a. Thrombosis M.C
b. Embolism
B- Hemorrhagic stroke
a. M.c.c is HTN
b. 2nd mcc is amyloidosis

-M.C site of bleeding is putamen

Presentation:

A- Middle cerebral artery stroke:

a. Weakness and sensory loss in opposite site
b. Loss of visual field on the opposite side
c. Aphasia
B- Anterior cerebral artery stroke:
a. Cognitive defect
b. Urine incontinence
c. Weakness in leg more than arm
C- Posterior cerebral artery stroke:
a. Ipsilateral sensory loss of face
b. Contralateral sensory loss of limbs
c. Limb ataxia

Treatment:

A- Ischemic stroke less than 3 hours since onset: TPA

B- Ischemic stroke more than 3 hours since onset: Aspirin
C- Recurrent TIA: Carotid endarterectomy and angioplasty
D- Ischemic stroke in patient already on aspirin: add dipyridamole or switch to clopidogrel
E- Hemorrhagic stroke: control vital signs only
[Premature ventricular contractions PVC]

Ectopic beats arise from ventricular foci

Causes: Hypoxia, fibrosis, electrolyte disturbance and hyperthyroidism

Treatment: treat underlying cause, if symptomatic then B-Blockers

Alarming signs: Multifocal (risk of Vent. Fib), Recurrent, R’ on T

[Atrial fibrillation]

Absent Twave, irregular RR interval , M.C sustained arrhythmia, but might predispose to stroke

Causes: IHD, pneumonia, HTN, Thyrotixicosis, pericarditis, alcohol

Types: Paroxysmal , persistant , permanent

Treatment:

A- If unstable: DC cardioversion
B- If stable + elderly: rate control with B-Blocker or verapamil or Digoxin
C- If stable + young: rhythm control with felcainide, propafenone, amiodarone, sotalol

[Mitral stenosis]

M.C.C is RF

Symptoms: pulmonary edema, pulmonary HTN, hemoptysis, malar flush, loud S1, late-diastolic murmur
or presystolic murmur, opening snap

Can be complicated with atrial fibrillation

[Mitral regurgitation]

M.C.C is RF

Can be caused by MI, LV dilatation

Symptoms: Pulmonary edema, atrial enlargement, pan-systolic murmur, soft s1, split s2, s3 if severe

Treatment: diuretics + ACEI + surgery if severe

[Aortic stenosis]

Causes: Bicuspid aortic valve (M.C), RF , HOCM, calcification in elderly or fibrosis in young patient

Symptoms: chest pain, dyspnea, syncope, narrow pulse pressure, slow rising pulse, systolic ejection
murmur , S4

Treatment: No need if asymptomatic, if asymptomatic: valve replaced for elders, balloon valvuloplasty in
young

[Aortic regurgitation]

Causes: Aortic dissection, bicuspid aortic valve, RA, SLE, Syphilis, HTN

Signs:

A- Short rumbling diastolic murmur

B- Wide pulse pressure
C- Water hammer pulse
D- Easily palpable popliteal and dorsalis pedis pulse
E- Hill’s sign
F- Quincke’s sign
G- Corrigan’s sign
H- De musset’s sign
I- Muller’s sign
J- Rosenbach’s sign
K- Traube’s sign
[Hypertension]

Risk factors: Family history, Smoking, CKD, High salt diet, obesity, increasing age, male sex, sedentary life
style

Emergency HTN:

A- HTN encephalopathy
B- Intracranial hemorrhage
C- ACS, LV failure
D- Acute aortic dissection
E- Eclampsia

Causes of secondary HTN:

A- Renal artery stenosis

B- CKD, Glomerulonephritis
C- Hormonal (Pheochromocytoma, cushing’s, hyperaldosteronism, hyperparathyroidism)
D- Obstructive sleep apnea
E- Liddle syndrome: mutation of aldosterone receptors on nephron

Treatment:

A- If patient < 65 start with ACEI

B- If patient > 65 start with CCB
Patient category The drug of choice
HTN + DM ACEI/ARB
HTN + CAD B-Blocker/ CCB
HTN + pregnancy Methyldopa, labetalol, hydralazine
HTN + BPH Alpha-Blockers
➢ 50% of HTN pt will improve with lifestyle modifications without treatment
➢ Target BP we treat for is < 140/90
➢ In emergency HTN don’t decrease BP rapidly, ( don’t use diuretics)
➢ In conn’s aldosterone will be high but low in liddle syndrome
➢ Complications of HTN include: retinopathy, nephropathy, encephalopathy, Brain Hemorrhage,
LVF
➢ [Congestive heart failure]

Symptoms:

A- Symptoms of Low cardiac output: Hypotension, syncope, cold extremities

B- Left side heart failure symptoms: dyspnea, orthopnea, PND, Pulmonary edema, pleural effusion,
cardiomegaly, Left side s3/s4 gallop rhythm
C- Right side heart failure symptoms: peripheral & lower limb edema, liver congestion,
hepatojugular reflux, ascites, High JVP, Right syde s3/s4 gallop rhythm
[DM complications]

A- Microvascular complications:
a. Retinopathy – Visual symptoms (after 5 years of DM)
b. Nephropathy – Renal impairment ( after 10 years of DM)
c. Neuropathy – sensory and autonomic can be affected ( after 15 years of DM)
d. Diabetic foot – Ulceration, infection → amputation
B- Macrovascular complications:
a. CAD – M.C.C of death
b. PAD – Peripheral arterial disease
c. CVA
C- Others:
Cataract, Infections

[Nephritic Syndrome]

1. Hematuria (RBC casts in the urine) M.C sign, hallmark of disease

2. Mild proteinuria <3.5 g/day
3. HTN usually diastolic
4. Mild edema
5. Uremia = Azotemia = increased KFT = oliguria = decreased GFR

M.C.C in children is PSGN

M.C.C in adult is IgA nephropathy

[Nephrotic Syndrome]

1. Massive proteinuria >3.5 g/day

2. Hypoalbuminemia, albumin < 30g/l
3. Massive edema (M.C sign) hallmark
4. Hyperlipidemia
5. No HTN, No hematuria, no uremia, normal KFT

M.C.C of 1ry nephrotic in adult ➔ Membranous Glomerulpathy/ FSGS

M.C.C of 1ry nephrotic in children ➔ Minimal change → TTT by steroids

[Chronic renal failure]

Progressive loss of renal function over a period of months or years

M.C.C is DM then HTN then GN (M.C renal cause)

Clinical features:

A- 2ry HTN, CHF, pericarditis

B- Increased BUN and creatinin
C- Hyperkalemia, Hyponatremia, Hyperphosphatemia, Hypocalcemia, hypermagnesemia
D- Sexual: ↓Testosterone in males, Amenorrhea and infertility in females
E- Uremic seizures, lethargy, weakness, asterexis, hyperreflexia
F- Decrease Vit D3
G- 2ry hyperparathyroidism with increased PTH
H- Renal osteodystrophy
I- Metabolic acidosis
J- Anemia (Decreased erythropoietin)
K- Peripheral neuropathy
L- Azotemia → itching , encephalopathy

N.B→ Kidney in CRF is small except: amyloidosis, MM, SS , polycystic K, DM

M.C.C of death in pt with CKD ➔ CVS Disease and increased susceptibility to infection

First lab finding in CKD is proteinuria

[Indications of dialysis in CKD] AEIOUC

A- Acid base imbalance: PH<7.2(Acidosis)

B- Electrolyte: Refractory Hyperkalemia >7meq/l
C- Intoxication
D- Overload: Fluid overload
E- Uremia: uremic symptoms (pericarditis, encephalitis, bleeding, convulsion)
F- Creatinin > 10