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HIV and STIs — KMTC Medicine Study Notes

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PART 1: HIV/AIDS

1. Overview & Epidemiology

• ~39 million people worldwide living with HIV (2022); ~630,000 deaths/year
• Sub-Saharan Africa bears ~67% of global HIV burden — Kenya included
• ART has transformed HIV from a fatal disease into a manageable chronic illness
• UNAIDS 95-95-95 targets (by 2030): 95% know their status → 95% on ART → 95% virally suppressed
• Five countries already achieved this: Botswana, Eswatini, Rwanda, Tanzania, Zimbabwe
• First-line ART in low/middle-income countries now costs <$45/patient/year (down from >$10,000 in 2000)

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2. The Virus — Structure & Classification

• HIV-1 (predominant globally) and HIV-2 (West Africa)
• Retrovirus — carries RNA genome; uses reverse transcriptase to make DNA
• Key surface glycoproteins: gp120 (binds CD4) and gp41 (membrane fusion)
• Core contains: RNA genome, reverse transcriptase, integrase, protease

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3. Pathogenesis

Entry & Transmission

• Sexual contact (most common)
• Mother-to-child (vertical) — antenatal, intrapartum, breastfeeding
• Contaminated needles/blood products
• Healthcare worker needlestick

Mechanism of CD4+ T-cell Destruction

1. HIV binds CD4 receptor + co-receptor (CCR5 on macrophages/memory T cells; CXCR4 on T cells)
2. Virus enters, reverse transcriptase converts RNA → DNA
3. Viral DNA integrates into host genome (provirus) via integrase
4. Cell machinery produces new virions; protease cleaves viral precursors
5. Infected CD4+ T cells are killed — progressive immunodeficiency

Cellular Reservoirs

CNS Involvement

Natural History of HIV Infection

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4. WHO Clinical Staging

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5. AIDS-Defining Opportunistic Infections

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6. Diagnosis of HIV

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7. Antiretroviral Therapy (ART)

Drug Classes & Mechanism

Kenya First-Line ART (Adults)

• Alternative: AZT + 3TC + EFV (if DTG unavailable or contraindicated)

When to Start ART

• All HIV-positive patients regardless of CD4 count — "Treat All" policy (WHO 2015 onward)
• Start as early as possible after diagnosis and readiness counseling
• In OI co-infection: treat OI first, then start ART (except TB — start ART within 2–8 weeks)

Monitoring on ART

• Viral load at 6 months, 12 months, then annually — goal: undetectable
• CD4 count — baseline, then annually
• Clinical monitoring: weight, symptoms, drug toxicity

Common ART Side Effects

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8. Prevention of Mother-to-Child Transmission (PMTCT)

• Without intervention: transmission rate ~25–45%
• With full ART: transmission <1–2%
• Kenya PMTCT protocol: All HIV+ pregnant women start lifelong ART (Option B+)
• Infant receives NVP syrup for 6 weeks (prophylaxis)
• EID at 6 weeks (DNA PCR)
• Exclusive breastfeeding for 6 months if mother is on ART with VL suppressed

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9. Pre-Exposure Prophylaxis (PrEP) & Post-Exposure Prophylaxis (PEP)

• Preferred: TDF + 3TC + DTG × 28 days
• Must start as soon as possible; not effective if started >72 hours post-exposure

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10. HIV/TB Co-infection

• HIV is the strongest risk factor for TB reactivation
• CD4 <50: start ART within 2 weeks of TB treatment
• CD4 >50: start ART within 8 weeks
• Monitor for IRIS
• Cotrimoxazole Preventive Therapy (CPT): TMP-SMX daily — all HIV+ patients with CD4 <200 (prevents PCP, toxoplasma, isospora)

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PART 2: SEXUALLY TRANSMITTED INFECTIONS (STIs)

1. Overview

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2. Common STIs — Summary Table

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3. Syndromic Management (KMTC/Kenya Focus)

Urethral Discharge Syndrome (Male)

• Likely: Gonorrhea + Chlamydia
• Tx: Ceftriaxone 500 mg IM + Azithromycin 1g PO (single dose)
• Partner notification and treatment

Vaginal Discharge Syndrome

• Likely: Trichomoniasis + BV (± Gonorrhea/Chlamydia in high-risk)
• Tx: Metronidazole 2g stat (or 400 mg BD × 7 days)
• If cervicitis signs: add Ceftriaxone + Azithromycin

Genital Ulcer Syndrome

• Likely: Syphilis + Chancroid (± Herpes)
• Tx: Benzathine Penicillin 2.4 MU IM + Azithromycin 1g stat
• If herpes suspected: add Acyclovir

Lower Abdominal Pain in Women (PID)

• Likely: Gonorrhea + Chlamydia + Anaerobes
• Outpatient Tx: Ceftriaxone 500 mg IM stat + Doxycycline 100 mg BD × 14 days + Metronidazole 400 mg BD × 14 days
• Inpatient Tx: Cefoxitin/Clindamycin + Gentamicin IV

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4. Pelvic Inflammatory Disease (PID) — Detail

• Inflammation of upper female genital tract: endometritis, salpingitis, tubo-ovarian abscess, pelvic peritonitis
• Caused by ascending infection from cervix
• Pathogens: N. gonorrhoeae, C. trachomatis → secondary invasion by Bacteroides, Gram-negatives, Group B Strep
• Minimum clinical criteria: lower abdominal tenderness + adnexal tenderness ± cervical motion tenderness
• Complications:
  • Tubal-factor infertility: 7% after 1 episode, 28% after ≥3 episodes
  • Ectopic pregnancy risk ↑ 7–10 fold
  • Chronic pelvic pain
  • Tubo-ovarian abscess (Fitz-Hugh–Curtis if perihepatitis)

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5. Neonatal Infections from STIs

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6. HIV and STIs — Interconnection

• STIs increase HIV transmission 2–5 fold — ulcerative STIs (syphilis, herpes, chancroid) disrupt mucosal barriers; inflammatory STIs recruit CD4+ T cells to genital mucosa
• HIV+ patients have more severe/atypical STI presentations
• STI treatment is a key HIV prevention strategy
• All patients diagnosed with an STI should be offered HIV testing
• Concurrent testing for Gonorrhea, HIV, and Syphilis recommended with any Chlamydia diagnosis

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7. STI Prevention (5 Cs)

1. Counseling — risk reduction, behaviour change
2. Condom use — male and female condoms
3. Contact tracing — partner notification and treatment
4. Compliance — adherence to full treatment courses
5. Check-up — follow-up and screening (test of cure for Gonorrhea)

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8. Special Populations

• Tetracyclines and quinolones are contraindicated
• Chlamydia: Azithromycin 1g stat (preferred over doxycycline)
• Gonorrhea: Ceftriaxone 250 mg IM
• Syphilis: Benzathine Penicillin (no alternative — desensitize if allergic)
• Screen for: HIV, Syphilis (RPR), Hepatitis B at first ANC visit

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9. Key Investigations Summary

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Quick Revision — High-Yield Points for KMTC Exams

📌 HIV enters via CD4 receptor + CCR5/CXCR4 co-receptors 📌 AIDS defined as CD4 <200/μL OR presence of an AIDS-defining illness 📌 First-line ART in Kenya: TDF + 3TC + DTG (once daily) 📌 PEP must start within 72 hours of exposure 📌 Window period = time between infection and detectable antibodies (~3–12 weeks) 📌 Most common STI worldwide: Chlamydia trachomatis 📌 Painless chancre = Primary syphilis; Palm/sole rash = Secondary syphilis 📌 PID minimum criteria: lower abdominal + adnexal tenderness 📌 Syndromic management: treat without waiting for lab results 📌 STIs increase HIV transmission 2–5 fold 📌 PMTCT reduces MTCT from ~35% to <2% with full ART

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🫁 RESPIRATORY SYSTEM — EXAM QUESTION SET

KMTC Medicine | Key Topics | Questions with Model Answers

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SECTION A: PNEUMONIA

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The causative agent is identified in only about half of CAP cases.

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• Symptoms: Fever (often high-grade), chills/rigors, productive cough (rusty/purulent sputum), pleuritic chest pain, dyspnoea
• Signs:
  • Tachypnoea, tachycardia
  • Reduced chest expansion on affected side
  • Dull percussion note (consolidation)
  • Bronchial breath sounds
  • Increased vocal fremitus/vocal resonance
  • Crepitations (crackles)
• Atypical features (Mycoplasma, Chlamydia): Gradual onset, dry cough, minimal signs, extrapulmonary features (rash, haemolytic anaemia, diarrhoea)

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• C — Confusion (new)
• U — Urea >7 mmol/L
• R — Respiratory rate ≥30/min
• B — BP (systolic <90 mmHg or diastolic ≤60 mmHg)
• 65 — Age ≥65 years

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• Mild (outpatient): Amoxicillin 500 mg TDS × 5–7 days OR Azithromycin 500 mg OD × 5 days (atypical cover)
• Moderate (inpatient): IV Amoxicillin-clavulanate + Azithromycin OR Ceftriaxone 1–2g IV OD + Azithromycin
• Severe (ICU): Ceftriaxone + Azithromycin OR Piperacillin-tazobactam + Azithromycin
• Atypical pneumonia: Azithromycin, Doxycycline, or Fluoroquinolone (Levofloxacin)
• PCP (HIV patient): Co-trimoxazole (TMP-SMX) high dose + Prednisolone if PaO₂ <70 mmHg
• Supportive: O₂ supplementation, IV fluids, analgesics (pleuritic pain)

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SECTION B: TUBERCULOSIS (TB)

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• Transmitted by airborne droplet nuclei (inhalation of particles from coughing/sneezing)
• Primarily affects the lungs (pulmonary TB) but can affect any organ (extrapulmonary TB)

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• Persistent cough (productive or non-productive) — most common symptom
• Fever and night sweats
• Weight loss and fatigue
• Loss of appetite (anorexia)

• Haemoptysis (in advanced disease)
• Pleuritic chest pain
• Dyspnoea

• Post-tussive rales (crackles) in upper lung zones
• Amphoric breath sounds (cavitary lesion)
• Lymphadenopathy (more in primary TB)

Note: Up to 25% of culture-confirmed pulmonary TB patients do not report cough.

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• R — Rifampicin
• I — Isoniazid (INH)
• P — Pyrazinamide
• E — Ethambutol

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• MDR-TB (Multi-Drug Resistant TB): Resistant to at least Isoniazid AND Rifampicin
• XDR-TB (Extensively Drug Resistant TB): MDR-TB + resistance to any fluoroquinolone AND at least one injectable second-line drug
• Treatment: Second-line drugs for 18–24 months (Bedaquiline, Linezolid, Clofazimine, etc.)
• Risk factors: Prior inadequate treatment, non-adherence, contact with MDR-TB case, HIV co-infection

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SECTION C: ASTHMA

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• Airway hyperresponsiveness
• Reversible bronchoconstriction
• Airway inflammation and remodelling

1. Early phase (immediate) — within minutes of exposure:
   • Allergen binds IgE on mast cells → degranulation → histamine, leukotrienes, prostaglandins released → bronchoconstriction, mucosal oedema, mucus secretion
2. Late phase — 4–12 hours later:
   • Recruitment of eosinophils, T-lymphocytes → sustained inflammation
   • Th2 cytokines (IL-4, IL-5, IL-13) are key mediators
   • Eosinophil products (major basic protein) → airway damage
3. Airway remodelling (chronic):
   • Subbasement membrane thickening
   • Hypertrophy of bronchial smooth muscle and glands
   • Can add an irreversible component over time

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• Allergens: Dust mites, pollen, animal dander, moulds
• Respiratory infections (viral — commonest trigger, especially in children)
• Exercise (Exercise-induced asthma)
• Cold air
• Air pollutants: Cigarette smoke, fumes
• Drugs: NSAIDs/Aspirin (Aspirin-exacerbated respiratory disease), Beta-blockers
• GERD (gastro-oesophageal reflux)
• Emotional stress
• Occupational exposures (isocyanates, flour, latex)

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• History: Episodic symptoms, atopy (eczema, allergic rhinitis, family history)
• Spirometry: Obstructive pattern — ↓FEV₁, ↓FEV₁/FVC (<0.7)
• Reversibility: ≥12% AND ≥200 mL improvement in FEV₁ after bronchodilator (salbutamol) → confirms asthma
• Peak Expiratory Flow (PEF): Diurnal variation >20% over ≥3 days
• Bronchial provocation test: Methacholine/histamine challenge (if spirometry normal)
• Skin prick test / serum IgE: Identifies allergic triggers
• CXR: Usually normal; hyperinflation in severe attack

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1. Sit upright; O₂ — high-flow via face mask (target SpO₂ 94–98%)
2. Salbutamol (SABA) — nebulised 2.5–5 mg every 20 min for 1 hour (back-to-back)
3. Ipratropium bromide — nebulised 0.5 mg (add to salbutamol in severe)
4. Systemic corticosteroids — Prednisolone 40–50 mg oral or Hydrocortisone 100 mg IV
5. IV Magnesium sulphate — 1.2–2 g IV over 20 min (life-threatening)
6. Monitor: ABG, SpO₂, PEFR, clinical response
7. ITU/intubation: Exhaustion, worsening PaCO₂ (rising CO₂ = ominous sign — patient tiring)

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• ICS = Inhaled Corticosteroid (Beclomethasone, Budesonide, Fluticasone)
• SABA = Short-Acting Beta₂ Agonist (Salbutamol) — reliever
• LABA = Long-Acting Beta₂ Agonist (Salmeterol, Formoterol) — not used alone without ICS

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SECTION D: COPD

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• COPD: A preventable, treatable disease characterised by persistent, irreversible (or poorly reversible) airflow limitation (FEV₁/FVC <0.7 post-bronchodilator), usually due to significant exposure to noxious particles/gases.
• Emphysema: Permanent enlargement of air spaces distal to terminal bronchioles due to destruction of alveolar walls (loss of elastic tissue by neutrophil proteases). Result: ↓gas exchange surface, air trapping.
• Chronic Bronchitis: Defined clinically as productive cough for ≥3 consecutive months in ≥2 consecutive years without other cause.
  • Mechanism: Hyperplasia of mucus-secreting glands, goblet cell metaplasia, chronic bronchiolitis → airway obstruction

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• Cigarette smoking (major; dose-dependent — pack-years)
• Biomass fuel combustion (cooking fires in enclosed spaces — common in Kenya/Africa)
• Occupational dust (mines, grain, cotton)
• Childhood respiratory infections → impaired lung growth
• α1-antitrypsin deficiency (genetic; causes panacinar emphysema — lower lobes; onset in young non-smokers)
• Air pollution

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• Smoking cessation — most important intervention (slows FEV₁ decline)
• Pulmonary rehabilitation
• Nutritional support
• Avoid biomass/occupational exposures
• Vaccinations: Influenza (annual), Pneumococcal

• Indicated if: PaO₂ ≤7.3 kPa (≤55 mmHg) at rest; OR PaO₂ 7.3–8 kPa with polycythaemia/cor pulmonale
• ≥15 hours/day; improves survival in severe COPD with respiratory failure

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SECTION E: PLEURAL EFFUSION

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1. Pleural fluid protein / serum protein >0.5
2. Pleural fluid LDH / serum LDH >0.6
3. Pleural fluid LDH >⅔ of upper limit of normal serum LDH (Sensitivity and specificity >98% when all three criteria are considered)

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• Failure — Congestive Heart Failure (most common; often bilateral, R > L)
• Albuminaemia low — Nephrotic syndrome, liver cirrhosis (hypoalbuminaemia)
• Infarction — Pulmonary embolism (can be either, usually exudate)
• Liver — Cirrhosis, ascites (hepatic hydrothorax)

• Malignancy (lung, mesothelioma, metastases) — most common in adults >40 yrs
• Abscess/Pneumonia (parapneumonic effusion, empyema)
• Pulmonary TB
• Lupus (SLE), Rheumatoid arthritis
• Empyema (pus in pleural space; pH <7.2)
• Trauma, Pancreatitis

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• CXR: Blunting of costophrenic angle (>200 mL); meniscus sign; mediastinal shift (large)
• USS chest: Confirms fluid; guides thoracentesis
• CT chest: Characterises effusion; identifies underlying lesion
• Thoracentesis (pleurocentesis): Aspiration of 30–50 mL for diagnosis
  • Send for: Protein, LDH, glucose, pH, cytology, AFB, M/C/S
  • Remove up to 1–1.5 L for symptom relief (>1.5 L risks re-expansion pulmonary oedema)

• Treat underlying cause
• Therapeutic thoracentesis (symptomatic relief)
• Chest drain (ICD) — for empyema, haemothorax, large symptomatic effusion
• Pleurodesis — recurrent malignant effusion (talc)

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SECTION F: PNEUMOTHORAX

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• Severe respiratory distress, tachycardia, hypotension
• Absent breath sounds on affected side
• Tracheal deviation away from affected side
• Distended neck veins (JVP elevated)
• Tracheal deviation + absent breath sounds + haemodynamic instability = DO NOT wait for CXR

1. Needle decompression — 2nd intercostal space, midclavicular line, large-bore (14G) needle — converts tension to open pneumothorax
2. Chest drain (ICD) — 4th/5th ICS, anterior axillary line → definitive treatment
3. High-flow O₂ (100%)
4. IV access, fluids if haemodynamically unstable

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SECTION G: LUNG CANCER

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• NSCLC (Non-Small Cell Lung Cancer) — 85% of all lung cancers
  • Adenocarcinoma — most common overall; commonest in women, never-smokers, <45 yrs; peripheral location; EGFR mutations
  • Squamous cell carcinoma — central; associated with smoking; causes hypercalcaemia (PTHrP); cavitates
  • Large cell carcinoma — undifferentiated; peripheral; poor prognosis
• SCLC (Small Cell Lung Cancer) — 15%; central; strongly associated with smoking; neuroendocrine origin; early metastasis; responds to chemotherapy; paraneoplastic syndromes

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• Persistent cough, haemoptysis, dyspnoea, wheeze, recurrent chest infections
• Pleuritic pain, pleural effusion

• Superior Vena Cava (SVC) obstruction — facial/arm oedema, dilated neck veins, headache
• Pancoast tumour (apex) — shoulder/arm pain, Horner syndrome (ptosis, miosis, anhidrosis)
• Recurrent laryngeal nerve palsy — hoarseness of voice
• Phrenic nerve palsy — raised hemidiaphragm on CXR
• Pericardial involvement — pericardial effusion, arrhythmias

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SECTION H: RESPIRATORY FAILURE

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• PaO₂ <60 mmHg (8 kPa) on room air ± PaCO₂ >45 mmHg (6 kPa)

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• High-flow O₂ (10–15 L/min via non-rebreather mask)
• Treat underlying cause (e.g., antibiotics for pneumonia, diuretics for pulmonary oedema)
• Non-invasive ventilation (NIV) if severe
• Intubation and mechanical ventilation if deteriorating

• Controlled O₂ — target SpO₂ 88–92% (avoid hypercapnic drive suppression)
  • Start at 28% Venturi mask; titrate up
• NIV (BiPAP) — first choice for COPD-related Type 2 failure:
  • IPAP (inspiratory pressure) + EPAP (expiratory pressure)
  • Reduces need for intubation, lowers mortality
• Treat cause: Bronchodilators, steroids, antibiotics
• Invasive ventilation (ETT + mechanical ventilator) — if NIV fails or contraindicated

⚠️ Critical: Giving high-flow O₂ to a Type 2 COPD patient can suppress hypoxic drive → worsen hypercapnia → CO₂ narcosis → coma

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SECTION I: SHORT NOTES / HIGH-YIELD ONE-LINERS

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• Definition: Permanent, abnormal dilatation of bronchi due to destruction of bronchial wall
• Causes: Recurrent infections (TB — commonest in Kenya), cystic fibrosis, post-measles, hypogammaglobulinaemia, Kartagener syndrome (immotile cilia)
• Features: Chronic productive cough with copious purulent sputum (>100 mL/day), haemoptysis, recurrent chest infections; finger clubbing
• Diagnosis: HRCT chest (gold standard) — "signet ring sign" (bronchus wider than adjacent artery), tram-track shadows
• Treatment: Chest physiotherapy (postural drainage), antibiotics for exacerbations, bronchodilators; surgery for localised disease

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• Definition: Occlusion of pulmonary artery/branches by thrombus (usually from DVT in leg veins)
• Risk factors: Virchow's triad — stasis (immobility, heart failure), hypercoagulability (OCP, cancer, thrombophilia), endothelial injury (surgery, trauma)
• Features: Sudden dyspnoea, pleuritic chest pain, haemoptysis; tachycardia, tachypnoea; hypoxia
• Massive PE: Haemodynamic collapse, RV failure, raised JVP, S₁Q₃T₃ on ECG
• Diagnosis: D-dimer (screening), CTPA (gold standard), V/Q scan
• Treatment: Anticoagulation (LMWH → Warfarin/DOAC); Thrombolysis for massive PE; IVC filter if anticoagulation contraindicated

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• ARDS (Acute Respiratory Distress Syndrome) — life-threatening form of Type 1 respiratory failure
• Berlin Definition:
  • Onset within 1 week of known insult
  • Bilateral opacities on CXR/CT (not fully explained by effusion or collapse)
  • PaO₂/FiO₂ <300 mmHg (mild), <200 (moderate), <100 (severe)
  • Not primarily due to cardiac failure/fluid overload
• Causes: Pneumonia, sepsis, trauma, aspiration, pancreatitis, major surgery
• Pathophysiology: Diffuse alveolar damage → capillary leak → non-cardiogenic pulmonary oedema → refractory hypoxia
• Treatment: Treat underlying cause; lung-protective ventilation (low tidal volumes 6 mL/kg, PEEP, prone positioning); fluid restriction; dexamethasone

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QUICK EXAM REVISION TABLE

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