Long Answer Questions
Q.1 Discuss the Clinical Features, Diagnosis, Complications & Management of H1N1 Influenza.
+1.CLINICAL FEATURES OF H1N1 INFLUENZA
H1N1 influenza presents similarly to seasonal flu.
(a) Common Symptoms:
• Fever and chills
• Fatigue
• Cough and sore throat
• Headache and body aches
• Digestive symptoms: diarrhea and vomiting
(b) Clinical Deterioration:
• Primary viral pneumonia (destroys lung tissue, not responsive to antibiotics)
• Multiorgan dysfunction (heart, kidneys, liver)
• Severe disease symptoms include:
– Dyspnea
– Cyanosis
– Dehydration
– Altered mental status
2. DIAGNOSIS
• Real-time RT-PCR is the recommended test for confirmation of H1N1 cases.
• Sample taken from nose or throat swab.
3. COMPLICATIONS
(A) Pulmonary Complications
Most commonly due to secondary bacterial superinfection by:
• Streptococcus pneumoniae
• Staphylococcus aureus
• Other bacterial pathogens
May lead to:
• Severe pneumonia
• Respiratory failure
• ARDS
(B) Rare Extrapulmonary Manifestations
Musculoskeletal: Myositis
Cardiac: Myocarditis, Pericarditis
Neurological:
• Reye’s syndrome (typically in children, especially with aspirin use)
• Encephalitis
• Transverse myelitis
4. MANAGEMENT
1. Supportive Therapy
(a) Isolate the patient to prevent transmission.
(b) Provide bed rest, plenty of fluids, cough suppressants, antipyretics, and analgesics
(e.g., acetaminophen, NSAIDs) for fever and muscle pain.
(c) Severe cases may require:
• IV hydration
• Ventilator support
2. Antiviral Treatment
(a) Used for serious or high-risk patients.
First-line drugs:
• Oseltamivir (Tamiflu) → 75 mg twice daily for 5 days
• Zanamivir → 10 mg inhaled twice daily for 5 days
(b) Best started within 48 hours of symptom onset.
(c) Action → Inhibit neuraminidase, reducing viral release & spread.
(d) Helps reduce risk of pneumonia & hospitalization.
(e) High-risk groups (pregnancy, underlying illness) should receive antivirals immediately — even before lab confirmation.
3. Preventing Spread of Infection
(a) Self-isolate for 7 days after symptoms begin or 24 hours after recovery.
(b) Infection control measures:
• Frequent handwashing with soap and water
• Use face mask, especially within 6 feet of others or while visiting healthcare
• Call physician before hospital/clinic visit
(c) Antiviral prophylaxis for high-risk contacts:
• Household contacts with chronic illness, pregnancy, age <5 or >65
• High-risk school children
• Healthcare workers exposed without protection
(d) Not recommended for healthy individuals.
(e) School closures & avoiding public gatherings may be required during outbreaks.
4. Vaccination
(a) Stimulates active immunity.
Available formulations:
• Intramuscular (IM) — inactivated, 0.5 mL
• Children <10 years → 2 doses
• Adults & children ≥10 years → 1 dose
• Intranasal — live vaccine, 0.2 mL (0.1 mL/nostril)
• Quadrivalent vaccine — H1N1 + 3 other strains
(b) Recommended for pregnant women, adults & children >6 months.
Q.2 WRITE THE CLINICAL FEATURES & MANAGEMENT OF DIABETIC KETOACIDOSIS (DKA)
+CLINICAL FEATURES
A. FEATURES DUE TO HYPERGLYCEMIA
I. Earliest Symptoms
a. Polyuria
b. Polydipsia
c. Weight loss
II. Neurological Symptoms (due to ↑ osmolality)
a. Lethargy
b. Confusion or focal neurological deficits
c. Obtundation → may progress to coma
III. Visual Changes
a. Blurred vision
• Due to osmotic change in lens refractive power
B. FEATURES DUE TO DEHYDRATION
I. Physical Signs
a. Reduced skin turgor
b. Dry tongue & cracked lips
c. Sunken eyeballs
II. Circulatory Features
a. Tachycardia
b. Hypotension
c. Cold extremities & peripheral cyanosis
C. FEATURES DUE TO METABOLIC ACIDOSIS
I. Respiratory
a. Deep, rapid breathing — Kussmaul respiration
II. Breath Odor
a. Fruity/acetone smell
III. GIT Symptoms
a. Nausea
b. Vomiting
c. Abdominal pain
• Caused by acidosis & electrolyte imbalance
D. OTHER ASSOCIATED FEATURES
I. With Precipitating Illness
a. Fever in infections
b. Signs of pneumonia / consolidation
c. Any illness triggering metabolic disturbance
MANAGEMENT OF DKA
A. PRINCIPLES
I. Main Targets
a. Correct dehydration
b. Correct hyperglycemia
c. Correct electrolyte imbalance
II. Additional Requirements
a. Identify & treat precipitating cause
b. Frequent monitoring required
B. INITIAL ASSESSMENT
I. Clinical Evaluation
a. ABCs: Airway, Breathing, Circulation
b. Vital signs + GCS
c. IV access
II. Investigations
a. Blood glucose, electrolytes, ketones
b. ABG/VBG, BUN/Cr, ECG
c. Search cause: infection, missed insulin, MI, stroke
C. FLUID RESUSCITATION (FIRST & MOST IMPORTANT)
I. Initial Fluid
a. Start 0.9% Normal Saline — 1L in first hour (adjust to BP/hydration)
II. After Stabilization
a. Shift to 0.45% saline if sodium high/normal
III. When Glucose Reaches 200–250 mg/dL
a. Add 5–10% dextrose
• Prevents hypoglycemia while ketosis resolves
D. INSULIN THERAPY
I. Start After Checking Potassium
a. IV regular insulin 0.1 units/kg/hr continuous infusion
II. Target
a. Reduce glucose 50–75 mg/dL per hour
III. Continue Until
a. pH > 7.3
b. HCO₃⁻ > 18
c. Anion gap normalizes
• Not just when glucose normalizes
E. POTASSIUM REPLACEMENT
I. Indications
a. Start only if K⁺ < 5.3 mEq/L
b. If K⁺ < 3.3 → hold insulin, give K⁺ first
II. Target
a. Maintain K⁺ 4–5 mEq/L
• Continuous ECG monitoring advised
F. BICARBONATE THERAPY
I. Indication
a. Only if pH < 6.9
• Not routinely recommended
G. TREAT UNDERLYING CAUSE
I. Common Triggers
a. Infection (UTI/Pneumonia)
b. Missed or inadequate insulin dose
c. MI/Stroke/Pancreatitis
d. New onset diabetes
H. MONITORING
I. Regular Assessment
a. Hourly glucose
b. Electrolytes + ABG/VBG every 2–4 hrs
c. Urine output + fluid balance
d. Mental status
e. Watch for cerebral edema (especially in children)
Q.3 Acute Glomerulonephritis
+AETIOLOGY
Post-infectious glomerulonephritis (most common – Post-streptococcal)
- Occurs after Group A β-hemolytic Streptococcal throat or skin infection.
- Other causes: Hepatitis B, Hepatitis C, HIV, CMV, Syphilis, Malaria, SBE, Infectious Mononucleosis.
Primary Glomerular Diseases
- Diffuse Proliferative GN
- Membranoproliferative GN (MPGN)
- Rapidly Progressive / Crescentic GN (RPGN)
- IgA Nephropathy
Secondary to Systemic Diseases
- SLE
- ANCA-associated vasculitis
- Goodpasture Syndrome (Anti-GBM)
- Henoch–Schönlein Purpura (IgA Vasculitis)
- Polyarteritis Nodosa
Others
- Serum sickness, Malignant HTN, Eclampsia, Malignancy, Drug-induced
PATHOGENESIS
Mostly immune-mediated.
1. In situ Antibody Deposition
- Antibodies against GBM (e.g., Goodpasture disease)
2. Circulating Immune Complex Deposition
- Classic in Post-streptococcal GN (Type III Hypersensitivity).
- → Complement activation → ↓C3
- → Cytokine release & neutrophil influx
- → Glomerular damage → ↓GFR
CLINICAL FEATURES
Common in children 5–15 yrs, more in boys.
Features of Nephritic Syndrome
- Hematuria — cola/tea-colored urine, RBC casts
- Proteinuria — mild/moderate (<3g/day)
- Oliguria — reduced urine output
- Edema — periorbital → generalized
- Hypertension — due to fluid retention
Associated symptoms:
- Fever, malaise, anorexia, headache, flank pain
- Subclinical cases → microscopic hematuria only
Investigations
- ↓Complement C3 (normalizes in 6–8 weeks)
- ↑ASO titre in Post-streptococcal GN
- Urine: RBC casts, pyuria, mild proteinuria
- ↑Serum Creatinine, ↑Urea
MANAGEMENT
Supportive Treatment
- Salt & fluid restriction
- Diuretics (Furosemide) for edema
- Antihypertensives (ACEI/CCB)
- Dialysis if severe renal failure/hyperkalemia/pulmonary edema
If Streptococcal infection suspected
- Treat patient + close contacts
- Penicillin V/Amoxicillin 10 days
- (Alternatives: Cephalosporins, Macrolides, Clindamycin)
Immunosuppressive Therapy
- Not used in typical PSGN
- Indicated in RPGN, SLE, Anti-GBM disease
PROGNOSIS
- Excellent in children — complete recovery within weeks
- Microscopic hematuria may persist months
- CKD is uncommon
Q.4 Acute Rheumatic Fever
+PATHOGENESIS
Acute rheumatic fever is a delayed immune-mediated response to Group A Streptococcal infection. Streptococcal antigens cross-react with cardiac myosin and sarcolemmal proteins, leading to autoimmune inflammation of endocardium, myocardium, pericardium, joints and skin.
Histology: fibrinoid degeneration in connective tissues; Aschoff nodules (pathognomonic) seen only in heart → multinucleated giant cells, macrophages and T-lymphocytes.
DIAGNOSIS
Jones Criteria
Major manifestations:
- Carditis
- Polyarthritis
- Chorea
- Erythema marginatum
- Subcutaneous nodules
Minor manifestations:
- Fever
- Arthralgia
- Raised ESR/CRP
- Previous rheumatic fever
- Leucocytosis
- First-degree AV block
Plus — evidence of preceding streptococcal infection:
Recent scarlet fever, ↑ASO/streptococcal antibodies, positive throat culture.
Diagnosis requires: 2 major OR 1 major + 2 minor with evidence of streptococcal infection.
LABORATORY FINDINGS
- Mild normocytic normochromic anemia
- Polymorphonuclear leukocytosis
- Elevated ESR, CRP
Evidence of Streptococcal Infection:
- ASO, anti-DNase B, antihyaluronidase, antistreptozyme test
- ASO ↑ in ≥80% patients (Adults >200 Todd units/ml, Children >320).
- Rising titres more significant.
ECG
- Persistent sinus tachycardia
- PR interval prolongation
- AV conduction defects, atrial flutter/fibrillation
- Low QRS voltage if pericardial effusion present
Echocardiography
- Mitral valvulitis, annular dilation
- Thickened valves, nodular lesions
- Mitral regurgitation
- Heart failure
ENDOMYOCARDIAL BIOPSY
Limited role. Shows Aschoff nodules, interstitial mononuclear infiltrates, myocyte necrosis.
MANAGEMENT
Acute Episode
Strict bed rest until fever, ESR, pulse & ECG normalize.
Management of Heart Failure
- Diuretics, ACE inhibitors, beta-blockers
- Digoxin cautious in myocarditis
- Mitral valve repair/replacement if severe
Antibiotics (eradicate residual streptococci)
- Benzathine penicillin G 1.2 million units IM single dose
- Phenoxymethylpenicillin 250 mg QID × 10 days
- If allergic: erythromycin / cephalosporins
Prophylaxis (prevent recurrence)
- Phenoxymethylpenicillin 250 mg BID
- OR Benzathine penicillin G 1.2 million units IM monthly
- If allergic → sulfadiazine or erythromycin
Prophylaxis duration:
Usually stop at age 21.
Continue longer if recent attack (<5 yrs), high exposure risk, or residual heart disease (up to age 40 or 10 yrs after last attack).
Aspirin
- Symptomatic relief within 24 hrs
- Dose: 60 mg/kg/day in divided doses (adult up to 100 mg/kg/day)
- Toxicity: nausea, tinnitus, deafness; severe → vomiting, acidosis
- Continue until ESR normal, then taper
Glucocorticoids
- Indicated in carditis or severe arthritis
- Prednisolone 1–2 mg/kg/day
- Taper when ESR normal
- Provides rapid improvement, no long-term benefit
Short Answer Questions
Q.1 Clinical Features of Hypothyroidism
+General:
Weight gain, fatigue, somnolence, cold intolerance, hoarseness of voice, slurred speech, puffy face, loss of eyebrows.
Skin:
Dry, cold and pale skin, decreased sweating, non-pitting edema (myxedema), carotenemia, coarse hair and hair loss, xanthelasma.
Hematologic:
Anemia, macrocytosis.
CVS:
Diastolic hypertension, bradycardia, reduced cardiac output, angina, pericardial effusion.
RS:
Hypoventilation, sleep apnea, exertional dyspnea, pleural effusion.
GIT:
Enlarged tongue, constipation (↓ gut motility), ileus, decreased taste sensation, ascites.
Reproductive system:
Oligomenorrhea, amenorrhea or menorrhagia, decreased fertility, increased risk of abortion, decreased libido, erectile dysfunction, delayed ejaculation.
Neuropsychiatric:
Encephalopathy, myxedema coma, mental retardation in children, carpal tunnel syndrome, cerebellar ataxia, depression, psychosis, myotonia, delayed relaxation of tendon reflexes.
Musculoskeletal:
Slow movements, myalgia, arthralgia, aches, stiffness.
Metabolic:
Hyperuricemia, hyponatremia, hyperlipidemia.
Q.2 Eating Disorders
+Eating disorders mainly include Anorexia Nervosa (AN) and Bulimia Nervosa (BN), with about 90% of cases occurring in females. Many individuals also show disordered eating patterns not meeting full criteria, such as binge eating disorder.
1. Diagnostic Features
Anorexia Nervosa:
- Weight loss >15% or BMI ≤ 17.5
- Avoidance of high-calorie food
- Body image distortion (believes overweight despite being underweight)
- Amenorrhoea ≥3 months
Bulimia Nervosa:
- Recurrent binge eating with loss of control
- Compensatory behaviours → vomiting, laxatives, strict dieting
- Weight usually within normal range
2. Medical Consequences
- Cardiac: Bradycardia, arrhythmias, prolonged QT, T-wave/ST changes
- Haematological: Anaemia, thrombocytopenia, leucopenia
- Endocrine: Amenorrhoea, pubertal delay, short stature, euthyroid sick syndrome
- Metabolic: Osteoporosis, renal calculi, uraemia
- Gastrointestinal: Constipation, abnormal LFTs
3. Management
- Nutritional rehabilitation with gradual weight restoration
- Cognitive Behavioural Therapy (CBT) is first-line for AN & BN
- Family-based therapy (FBT) effective in adolescents with AN
- Fluoxetine beneficial in BN, especially in higher doses
Q.3 Pneumocystis jiroveci
+Pneumocystis jiroveci is an opportunistic fungal pulmonary pathogen, previously called P. carinii. Although classified as a fungus, it lacks ergosterol, making it resistant to conventional antifungals. It is globally distributed and exposure commonly occurs in childhood.
Pathogenesis
Occurs mainly in immunocompromised individuals.
High-risk groups:
- HIV with CD4+ <200/µL
- Immunosuppressive therapy
- Primary immunodeficiency
- Premature malnourished infants
Infection process:
- Inhalation → alveoli → attaches to type I alveolar cells
- Normal immunity → cleared by macrophages
- Immunosuppression → proliferation → alveolar damage + surfactant loss
- ↑ alveolar-capillary permeability → foamy exudate
- Severe disease → interstitial edema, fibrosis, hyaline membranes
Clinical Features
- Incubation: 1–2 months
- Symptoms: Fever, dyspnea, dry cough (symptoms > signs)
- Findings: Tachypnea, tachycardia, cyanosis, occasional pneumothorax
- May disseminate (rare): liver, spleen, lymph nodes, bone marrow, eye (choroiditis like CMV)
Investigations
- CXR: Bilateral diffuse perihilar infiltrates
- ABG: ↓PaO2, respiratory alkalosis, ↑A–a gradient (>35 mmHg poor prognosis)
- PFT: ↓DLCO
- Serum LDH ↑
Diagnosis
- Induced sputum → methenamine silver / toluidine blue stain
- BAL sensitivity >90%
- Biopsy if uncertain
Treatment
- Start treatment immediately when suspected.
- Drug of choice: Trimethoprim–Sulfamethoxazole (TMP–SMX)
- Duration: 14 days (non-HIV), 21 days (HIV)
- Alternatives: Clindamycin, Pentamidine, Trimetrexate
- Steroids indicated in severe HIV-PCP (use cautiously due to TB/fungal co-infection risk)
Q.4 Clinical Characteristics of Different Types of Leprosy
+1. Tuberculoid (TT) Leprosy
High cell-mediated immunity; common in brown/black-skinned individuals.
Skin lesions:
- Few hypopigmented macules/plaques
- Sharply demarcated, erythematous/raised borders
- Loss of sensation (hypoaesthetic)
- Dry, scaly, anhidrotic
Nerve involvement:
- Early, localized; nerves thickened & tender
- Common: ulnar, posterior auricular, peroneal, posterior tibial
Investigations:
- Histology: granulomas with macrophages, lymphocytes, giant cells
- Smears: absent/very few AFB
- Lepromin test: Positive
2. Lepromatous (LL) Leprosy
Occurs in deficient CMI; common in white-skinned people.
Skin lesions:
- Multiple, symmetrical, poorly defined macules/plaques/nodules
- Diffuse infiltration → leonine facies
- Loss of eyebrows (lateral first)
Nasal involvement:
- Bridge collapse, epistaxis, septal perforation
Nerve involvement:
- Late, diffuse; distal symmetrical neuropathy
- Burns, trophic ulcers, deformities, digit resorption
Systemic involvement:
- Lymph nodes, liver, spleen, testes (gynecomastia), bacillemia
Investigations:
- Smear: numerous AFB
- Lepromin test: Negative
Slow progressive course; death from renal failure, amyloidosis or infection possible.
3. Borderline Leprosy Spectrum
Intermediate features; unstable form.
- BT: Near TT → fewer lesions, may show satellite lesions
- BL: Near LL → more numerous, poorly defined
- BB: Mid spectrum → mixed TT/LL features
4. Primary Neuritic Leprosy
- Nerve involvement only, no skin lesions
- Nerves thickened & tender, sensory loss
- May present with facial palsy
5. Indeterminate Leprosy
- Usually single hypopigmented macule, may be hypoesthetic
- AFB may or may not be present
- Unstable → may progress to TT or LL
Very Short Answer Questions
Q.1 Stages of Lupus Nephritis
+Six classes of lupus nephritis (ISN/RPS classification):
Class I – Minimal mesangial
Class II – Mesangial proliferative
Class III – Focal (<50% glomeruli)
Class IV – Diffuse (>50% glomeruli, most severe)
Class V – Membranous
Class VI – Advanced sclerosing (end-stage)
Q.2 Causes of Metabolic Acidosis
+Diabetic ketoacidosis (DKA)
Lactic acidosis
Renal failure (reduced acid excretion)
Diarrhea (loss of bicarbonate)
Q.3 Ectopic Hormones Produced by Tumors
+Ectopic hormone production by tumours:
| Hormone | Consequence | Tumours |
|---|---|---|
| ACTH | Cushing’s syndrome | Small cell lung carcinoma (SCLC) |
| Erythropoietin | Polycythaemia | Kidney tumour, hepatoma, cerebellar haemangioblastoma, uterine fibroids |
| FGF-23 | Hypophosphataemic osteomalacia | Mesenchymal tumours |
| PTHrP | Hypercalcaemia | NSCLC (squamous), breast cancer, kidney cancer |
| Vasopressin (ADH) | Hyponatraemia | Small cell lung carcinoma (SCLC) |
Q.4 Medicines for Scabies
+Permethrin 5% cream
Ivermectin (oral) 200 μg/kg
Benzyl benzoate lotion
Crotamiton cream or lotion
Q.5 Neurological Features of Vitamin B12 Deficiency
+Peripheral neuropathy (numbness/tingling)
Subacute combined degeneration of spinal cord
Ataxia / impaired vibration & proprioception
Cognitive changes (memory loss, dementia)
Q.6 Sexually Transmitted Infections with Genital Ulcers
+Herpes genitalis – Herpes Simplex Virus (HSV)
Syphilis – Treponema pallidum
Chancroid – Haemophilus ducreyi
Lymphogranuloma venereum (LGV) – Chlamydia trachomatis (L1–L3)
Q.7 Anti-retroviral Drugs
+Zidovudine (AZT)
Lamivudine (3TC)
Nevirapine
Efavirenz
Q.8 Opportunistic Infections in HIV
+Pneumocystis jirovecii pneumonia (PCP)
Tuberculosis (TB)
Oral and esophageal candidiasis
Cytomegalovirus (CMV) infection
Q.9 Causes of Delirium in the Elderly
+Infections – UTI, pneumonia
Medications – polypharmacy, sedatives, anticholinergics, opioids
Metabolic/electrolyte disturbances – dehydration, hyponatremia, hypoglycemia
Post-operative or acute medical illness – surgery, trauma, stroke
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