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🏥 CLINICAL CASES - 1st Year MBBS Exam Notes

Bold text = examiner-highlighted lines (high-scoring points) Format: Mixed tables + bullets for quick revision

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💪 SECTION 1: NERVE-MUSCLE

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1. MYASTHENIA GRAVIS

• Antibodies bind and destroy ACh receptors at motor end plate
• Reduces number of functional receptors
• Each nerve impulse releases less effective ACh signal
• Result: muscle fatigability with repeated use

• Ptosis (drooping eyelid) - most common presenting feature
• Diplopia (double vision)
• Fatigability - weakness worsens with activity, improves with rest
• Dysphagia, dysarthria (bulbar muscles)
• Myasthenic crisis: respiratory failure (life-threatening)

• Tensilon (Edrophonium) test - GOLD standard
• Anti-AChR antibody titre (positive in 85%)
• EMG: decremental response on repetitive stimulation
• CT chest: thymoma in 15%

• Anticholinesterases: Neostigmine, Pyridostigmine (first-line)
• Thymectomy (especially if thymoma present)
• Immunosuppressants: steroids, azathioprine
• Plasmapheresis / IV Ig for crisis

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2. DUCHENNE MUSCULAR DYSTROPHY (DMD)

• Absence of dystrophin protein (links actin cytoskeleton to extracellular matrix)
• Muscle fibre membrane becomes fragile and ruptures
• Progressive fibre necrosis → replaced by fat and fibrous tissue
• Result: progressive proximal muscle weakness

• Gower's sign - child uses hands to "climb up" own legs to stand (proximal weakness)
• Pseudohypertrophy of calf muscles (replaced by fat/fibrous tissue - looks big but weak)
• Waddling gait
• Progressive proximal muscle weakness (pelvic girdle first)
• Lordosis, scoliosis
• Cardiomyopathy in later stages

• Serum CK (creatine kinase) - markedly elevated (10-100x normal)
• Muscle biopsy - absence of dystrophin on immunostaining (gold standard)
• EMG: myopathic pattern
• Genetic testing: deletion in dystrophin gene

• No cure; management is supportive
• Corticosteroids (prednisolone) - slow progression
• Physiotherapy, orthoses
• Cardiac management
• Gene therapy (emerging)

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🔬 SECTION 2: REPRODUCTION

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3. MALE INFERTILITY

• Pre-testicular: Hypogonadotrophic hypogonadism, hyperprolactinaemia, thyroid disorders
• Testicular (most common): Varicocele, cryptorchidism, mumps orchitis, Klinefelter syndrome (47,XXY)
• Post-testicular: Obstruction (vas deferens), erectile dysfunction, retrograde ejaculation

• Inability to father a child
• Signs of underlying cause: small testes (Klinefelter), varicocele ("bag of worms")

• Spermatogenesis requires 2-4°C lower than body temperature (reason for scrotal position)
• Any factor raising testicular temperature, blocking ducts, or reducing gonadotropins impairs sperm production

• Semen analysis - FIRST investigation
  • Normal: count >15 million/mL, motility >40%, normal morphology >4% (Kruger)
  • Azoospermia = no sperm; oligospermia = low count
• FSH, LH, testosterone, prolactin levels
• Testicular biopsy if needed
• Karyotype (to rule out Klinefelter)

• Treat underlying cause
• Varicocele repair, hormonal therapy
• Assisted reproduction: IUI, IVF, ICSI (intracytoplasmic sperm injection)

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4. PREGNANCY (Physiological Changes)

• Cardiac output increases by 40-50% (increased HR + stroke volume)
• Blood pressure falls in first two trimesters
• Blood volume increases by 40-50%
• Physiological anaemia of pregnancy (plasma increases more than RBCs - dilutional)

• Tidal volume increases (progesterone stimulates respiratory centre)
• Minute ventilation increases
• FRC decreases (diaphragm pushed up)

• GFR increases by 50% → glycosuria and proteinuria can be normal
• Urinary frequency (uterus compresses bladder)

• WBC increases (physiological leukocytosis)
• Hypercoagulable state (increased clotting factors - DVT risk)
• ESR elevated

• hCG produced by trophoblast - basis of pregnancy test
• Progesterone maintains pregnancy (corpus luteum → placenta)
• HPL (human placental lactogen) causes insulin resistance

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🧠 SECTION 3: CNS

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5. DYSDIADOCHOKINESIA

• Definition: Inability to perform rapid alternating movements
• Cause: Cerebellar lesion (most commonly)
• Examples: rapid pronation/supination of hand, tapping fingers rapidly
• Associated signs: Intention tremor, ataxia, nystagmus, dysmetria
• DANIAN mnemonic for cerebellar signs: Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Atonia, Nausea
• Pathophysiology: Cerebellum coordinates timing/force of movements; damage impairs smooth rapid movements

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6. PARKINSONISM

• Substantia nigra → basal ganglia (striatum) via dopaminergic pathway
• Dopamine normally inhibits excessive motor activity
• Loss of dopamine → imbalance: dopamine (inhibitory) ↓, acetylcholine (excitatory) ↑
• Result: rigidity, tremor, bradykinesia

• T - Tremor: resting "pill-rolling" tremor (4-6 Hz), disappears on movement
• R - Rigidity: "cogwheel" rigidity (jerky resistance throughout range)
• A - Akinesia/Bradykinesia: slowness of movement
• P - Postural instability
• Mask-like (expressionless) face (hypomimia)
• Festinant gait (shuffling, short steps, forward-leaning)
• Micrographia (small handwriting)
• Monotonous speech

• Levodopa + Carbidopa (FIRST LINE) - Levodopa crosses BBB; carbidopa inhibits peripheral decarboxylation
• Dopamine agonists: bromocriptine, ropinirole
• MAO-B inhibitors: selegiline
• Anticholinergics: benztropine (for tremor)
• Deep Brain Stimulation (DBS) for advanced cases

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7. HUNTINGTON'S DISEASE

• Mutant huntingtin protein is toxic to GABA neurons in striatum
• Loss of GABAergic inhibitory output → disinhibition of thalamus → excess motor activity
• Neurodegeneration progressive; no cure

• Chorea - involuntary, irregular, dance-like movements (hallmark)
• Progressive dementia (cognitive decline)
• Psychiatric symptoms: depression, personality changes
• Dysphagia, dysarthria in late stages

• Genetic testing - >36 CAG repeats confirms diagnosis (gold standard)
• MRI: caudate nucleus atrophy ("box-car" ventricles)

• No disease-modifying treatment
• Tetrabenazine (for chorea - depletes dopamine)
• Antipsychotics, antidepressants
• Genetic counselling is essential

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8. ALZHEIMER'S DISEASE

• Amyloid precursor protein (APP) cleaved abnormally → beta-amyloid plaques (extracellular)
• Tau protein hyperphosphorylation → neurofibrillary tangles (intracellular)
• Cholinergic neurons in nucleus basalis of Meynert are preferentially lost
• Progressive cortical atrophy (hippocampus first)

• Short-term memory loss - EARLIEST feature (hippocampus affected first)
• Progressive cognitive decline
• Language problems (aphasia), disorientation
• Apraxia, agnosia, personality changes
• Late: bedridden, incontinence

• Clinical (MMSE score); PET scan: amyloid imaging
• CSF: decreased amyloid-beta, increased tau
• MRI: hippocampal and cortical atrophy
• Definitive: post-mortem brain histology (senile plaques + NFTs)

• Cholinesterase inhibitors: donepezil, rivastigmine, galantamine (mild-moderate)
• Memantine (NMDA antagonist) for moderate-severe
• No cure; supportive care

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9. BROWN-SEQUARD SYNDROME

• Half the spinal cord is cut → motor tracts (uncrossed at cord level) and sensory tracts (some crossed, some uncrossed) are differentially affected

• Ipsilateral (same side as lesion):
  • Upper Motor Neurone (UMN) weakness (corticospinal tract - uncrossed in cord)
  • Loss of proprioception and vibration sense (dorsal column - uncrossed in cord)
• Contralateral (opposite side):
  • Loss of pain and temperature sensation (spinothalamic tract - crosses at cord level)
• At the level of lesion:
  • Ipsilateral LMN weakness and all sensory loss

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10. HEMIPLEGIA

• Lesion in contralateral motor cortex or internal capsule (posterior limb)
• Internal capsule lesion is most common - compact area, small lesion causes large deficit
• Upper motor neurone (UMN) lesion

• Spasticity (clasp-knife rigidity)
• Hyperreflexia (exaggerated deep tendon reflexes)
• Extensor plantar response (Babinski sign)
• Clonus
• Muscle weakness (not wasting)

• Stroke (ischaemic/haemorrhagic) - most common
• Brain tumour, brain abscess
• Multiple sclerosis, trauma

• Treat underlying cause (thrombolysis for ischaemic stroke if <4.5 hours)
• Physiotherapy, rehabilitation
• Spasticity: baclofen, tizanidine

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11. HYDROCEPHALUS

• CSF produced by choroid plexus (500 mL/day); normal volume ~150 mL
• Obstruction or impaired reabsorption by arachnoid villi → increased CSF volume → raised ICP

• Non-communicating (obstructive): Blockage within ventricular system (aqueduct stenosis, tumour)
• Communicating: CSF flows freely but reabsorption impaired (meningitis, subarachnoid haemorrhage)
• Normal pressure hydrocephalus (NPH): Special type in elderly

• In infants: Enlarged head circumference (above 97th percentile)
• "Sunset sign" (eyes deviated downward - raised ICP compresses tectal plate)
• Bulging fontanelle
• In adults/older children: Headache, vomiting, papilloedema (signs of raised ICP)
• NPH triad: "wet, wobbly, wacky" - urinary incontinence, gait disturbance, dementia

• CT/MRI scan - shows ventricular enlargement (key investigation)
• Skull X-ray (infants): "beaten copper" appearance

• Ventriculo-peritoneal (VP) shunt - DEFINITIVE treatment
• Endoscopic third ventriculostomy (ETV)
• Treat underlying cause

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12. APHASIA

• Broca's area = Brodmann area 44, 45 (inferior frontal gyrus)
• Wernicke's area = Brodmann area 22 (superior temporal gyrus)
• Both connected by arcuate fasciculus
• Aphasia ≠ dysarthria (dysarthria is motor speech problem, language intact)

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13. HEAT STROKE

• Failure of thermoregulation: heat production > heat loss
• Hypothalamus fails to regulate body temperature
• High temperature causes cellular protein denaturation, enzyme dysfunction
• Multi-organ failure: brain, kidney, liver, muscle (rhabdomyolysis)
• Anhidrosis (absence of sweating) in classic type - skin is hot and DRY

• Core temperature >40°C
• CNS dysfunction: confusion, seizures, coma (distinguishes from heat exhaustion)
• Hot, dry skin (classic type)
• Tachycardia, hypotension
• Rhabdomyolysis → myoglobinuria → acute renal failure

• Clinical + rectal temperature measurement
• Labs: elevated CK, LFTs, creatinine, DIC panel

• RAPID COOLING is the priority
• Ice-water immersion (most effective method)
• Cold IV fluids
• Fan + mist cooling
• Treat complications (seizures, renal failure)
• DO NOT use antipyretics (no role - it's not fever but thermoregulatory failure)

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14. CEREBELLAR ATAXIA

• D - Dysdiadochokinesia
• A - Ataxic (wide-based) gait
• N - Nystagmus (horizontal)
• I - Intention tremor (worsens as hand approaches target)
• A - Atonia (hypotonia)
• N - Nausea

• Past-pointing (dysmetria) on finger-nose test
• Romberg's test negative (ataxia WORSE with eyes open - unlike sensory ataxia)
• Scanning (staccato) speech
• Heel-shin test abnormal

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🦋 SECTION 4: ENDOCRINE

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15. GOITRE

• Definition: Enlargement of the thyroid gland
• Causes:
  • Simple/Endemic (most common worldwide): Iodine deficiency → low T3/T4 → TSH ↑ → thyroid hyperplasia
  • Multinodular goitre
  • Autoimmune (Hashimoto's, Graves' disease)
  • Neoplasia
• Iodine deficiency - most common cause globally
• Clinical: Neck swelling (moves with swallowing), dysphagia, stridor if large
• Investigation: TFTs, ultrasound, FNAC (fine needle aspiration cytology for nodules)
• Treatment: Iodine supplementation (prophylaxis), thyroxine, surgery if large

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16. CUSHING'S SYNDROME

• Excess cortisol → protein catabolism (thin limbs, striae), fat redistribution (central obesity), gluconeogenesis (diabetes), Na+/water retention (hypertension)

• "Lemon on toothpicks" - central obesity with thin limbs
• Moon face, buffalo hump (fat deposition)
• Purple striae on abdomen
• Hypertension, diabetes, osteoporosis, amenorrhoea
• Proximal muscle weakness
• Thin skin, easy bruising
• Hirsutism (excess cortisol → adrenal androgens)

• 24-hour urinary free cortisol (screening)
• Low-dose dexamethasone suppression test (LDST) - cortisol not suppressed
• High-dose DST: to distinguish pituitary (suppresses) vs ectopic/adrenal (does not suppress)
• ACTH levels: high in Cushing's disease, low in adrenal tumour

• Remove the cause (stop steroids if iatrogenic)
• Pituitary adenoma: transsphenoidal surgery
• Adrenocortical tumour: adrenalectomy
• Medical: metyrapone, ketoconazole

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17. CRETINISM

• Absence of T3/T4 → failure of neuronal myelination, CNS maturation, and skeletal ossification
• Irreversible mental retardation if untreated (T3 essential in first 3 years of life for brain development)

• Mental retardation (intellectual disability) - most serious consequence
• Short stature (dwarfism)
• Umbilical hernia
• Coarse facies, large tongue (macroglossia), hoarse cry
• Delayed bone age, delayed dentition
• Constipation, hypothermia, jaundice (prolonged neonatal)
• Pot-belly, dry skin

• Neonatal screening: heel-prick TSH test (within 5 days of birth)
• Low T4, high TSH
• X-ray: delayed bone age, epiphyseal dysgenesis

• Levothyroxine (T4) - start immediately, lifelong
• Early treatment prevents mental retardation (critical window < 3 years)

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18. MYXOEDEMA

• Deficiency of T3/T4 → ↓ metabolism in all cells
• Accumulation of glycosaminoglycans (hyaluronic acid) in dermis → non-pitting oedema

• Non-pitting oedema (myxoedema) - periorbital puffiness, puffy face, hands
• Weight gain, cold intolerance, constipation
• Bradycardia, dry coarse skin, hair loss
• Delayed relaxation of deep tendon reflexes ("hung-up reflex" - pathognomonic)
• Hoarse voice, macroglossia
• Menorrhagia
• Myxoedema coma (hypothermia, coma) - medical emergency

• TSH elevated (most sensitive test)
• Free T4 low
• Anti-TPO antibodies (Hashimoto's)

• Levothyroxine (thyroxine) - start low, go slow (especially in elderly/cardiac patients)
• Lifelong treatment

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19. ADDISON'S DISEASE

• Destruction of adrenal cortex → deficiency of cortisol AND aldosterone (AND androgens)
• ↓ Cortisol → ↑ ACTH (pituitary negative feedback removed)
• ↑ ACTH → hyperpigmentation (ACTH cross-reacts with MSH receptor)
• ↓ Aldosterone → Na+ loss, K+ retention, water loss → hypotension

• Hyperpigmentation (buccal mucosa, skin creases, pressure areas) - PATHOGNOMONIC
• Postural hypotension, weakness, fatigue
• Hyponatraemia, hyperkalaemia, hypoglycaemia
• Anorexia, nausea, weight loss
• Addisonian crisis: Acute life-threatening collapse with hypotension, hypoglycaemia (precipitated by stress/infection)

• Short Synacthen (ACTH stimulation) test - gold standard (cortisol fails to rise)
• Low cortisol, high ACTH
• Electrolytes: Na↓, K↑
• Anti-adrenal antibodies (autoimmune)

• Hydrocortisone (cortisol replacement) - LIFELONG
• Fludrocortisone (aldosterone replacement)
• Double/triple dose during illness/stress (sick day rules)
• Crisis: IV hydrocortisone + IV saline + glucose

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20. THYROTOXICOSIS (Hyperthyroidism)

• TSH receptor antibodies (TSI) stimulate thyroid → excess T3/T4 production
• Excess T3/T4 → increased metabolic rate, sympathetic nervous system overstimulation

• Weight loss despite increased appetite
• Heat intolerance, sweating
• Tachycardia, palpitations, atrial fibrillation
• Tremor (fine), anxiety, irritability
• Diarrhoea
• Goitre
• Specific to Graves': Exophthalmos (proptosis), pretibial myxoedema, thyroid acropachy (triad)
• Thyroid storm (crisis): fever, extreme tachycardia, confusion, life-threatening

• TSH suppressed (most sensitive), free T3/T4 elevated
• TRAb (TSH receptor antibodies) - Graves' specific
• Technetium thyroid scan: diffuse uptake

• Anti-thyroid drugs: Carbimazole (first-line), Propylthiouracil (PTU, pregnancy)
• Beta-blockers (propranolol) for symptomatic control
• Radioiodine (I-131) - definitive for non-pregnant adults
• Surgery: thyroidectomy
• Thyroid storm: high-dose propylthiouracil, iodine (Lugol's), beta-blockers, steroids

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21. PHAEOCHROMOCYTOMA

• Tumour secretes excess adrenaline and noradrenaline (catecholamines)
• Catecholamines → paroxysmal hypertension, tachycardia, hyperglycaemia

• Classic triad: Headache, Sweating, Palpitations (paroxysmal)
• Paroxysmal hypertension (crises lasting minutes to hours)
• Pallor, anxiety
• Hyperglycaemia
• Hypertensive crisis may be triggered by surgery, drugs (beta-blockers alone)

• 24-hour urinary catecholamines, metanephrines, VMA (vanillylmandelic acid) - best screening
• Plasma metanephrines (most sensitive)
• CT/MRI abdomen: locate tumour
• MIBG scan (functional imaging)

• Pre-operative: Alpha-blocker first (phenoxybenzamine), THEN beta-blocker (NEVER beta-blocker alone - causes hypertensive crisis)
• Surgical removal (adrenalectomy) - DEFINITIVE

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22. DIABETES MELLITUS (DM)

• Type 1: Autoimmune T-cell mediated destruction of islets of Langerhans → absolute insulin deficiency
• Type 2: Insulin resistance (cells don't respond to insulin) + progressive beta-cell failure → relative deficiency

• Polyuria, Polydipsia, Polyphagia (the three Ps)
• Weight loss (Type 1)
• Recurrent infections (UTI, skin, candidiasis)
• Blurred vision
• Type 2: often asymptomatic, discovered incidentally

• Fasting plasma glucose ≥7 mmol/L (126 mg/dL)
• Random glucose ≥11.1 mmol/L (200 mg/dL) with symptoms
• HbA1c ≥48 mmol/mol (≥6.5%) - reflects 3-month glycaemic control
• OGTT: 2-hour glucose ≥11.1 mmol/L

• Type 1: Insulin (mandatory)
• Type 2: Lifestyle → Metformin (first-line) → Add-on agents (SGLT2i, GLP-1 RA, insulin)
• Monitoring: HbA1c, glucose, BP, lipids, renal function, eye/feet exam

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23. DIABETIC KETOACIDOSIS (DKA)

• No insulin → cells cannot use glucose → starvation state
• Fat mobilisation → fatty acids → ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone)
• Ketones are acidic → high anion gap metabolic acidosis
• Osmotic diuresis → dehydration, electrolyte loss

• Polyuria, polydipsia, vomiting, abdominal pain
• Kussmaul breathing (deep, sighing respirations) - compensating for acidosis
• Fruity/acetone breath (acetone excreted via lungs)
• Dehydration, hypotension
• Altered consciousness, coma

• Glucose >11 mmol/L, ketones >3 mmol/L or ++/+++ on urine dipstick, pH <7.3
• Arterial blood gas: metabolic acidosis (low pH, low bicarbonate, low pCO2)
• High anion gap = Na - (Cl + HCO3) > 12

• Insulin (IV infusion 0.1 units/kg/hr)
• IV Fluids (normal saline - rapid rehydration)
• Potassium replacement (K+ falls as insulin drives K+ into cells)
• Identify and treat precipitant (infection)

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24. HYPERGLYCAEMIC COMA (Hyperosmolar Hyperglycaemic State - HHS)

• Relative insulin deficiency → extreme hyperglycaemia but enough insulin to prevent ketosis
• Profound hyperosmolality → cellular dehydration → CNS dysfunction
• Extreme dehydration (deficit 8-10 litres)

• Gradual onset over days
• Severe dehydration, polyuria, polydipsia
• CNS: confusion, seizures, coma
• No Kussmaul breathing (no acidosis)

• Slow, careful rehydration (risk of cerebral oedema if too fast)
• IV insulin (lower doses than DKA)
• Low-molecular-weight heparin (LMWH) - high thrombosis risk
• Identify precipitant

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25. ACROMEGALY

• Excess GH → increased IGF-1 (insulin-like growth factor 1) → soft tissue and bone overgrowth (periosteal, not epiphyseal)
• GH also causes insulin resistance → diabetes

• Enlarged hands, feet (ring size increase, shoe size increase)
• Coarse facial features: enlarged nose, prognathism (jaw protrusion), prominent brow ridges
• Macroglossia, widely spaced teeth
• Hyperhidrosis (excess sweating), oily skin
• Hypertension, diabetes, carpal tunnel syndrome
• Bitemporal hemianopia (tumour compresses optic chiasm)
• Arthralgia, visceromegaly

• Oral Glucose Tolerance Test (OGTT): GH fails to suppress (gold standard)
• IGF-1 level elevated (best screening test)
• MRI pituitary: adenoma

• Transsphenoidal surgery (first-line)
• Somatostatin analogues: octreotide, lanreotide
• Dopamine agonists: cabergoline
• GH receptor antagonist: pegvisomant
• Radiotherapy

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26. GIGANTISM

• Same pathophysiology as acromegaly but occurs in childhood/adolescence before epiphyses close
• Excess GH → linear bone growth at epiphyseal plates → abnormal increase in height
• Clinical: Abnormal tall stature, delayed puberty, features of acromegaly may coexist
• Same investigations and treatment as acromegaly + management of underlying cause
• Surgery (transsphenoidal) is first-line

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27. PROLACTINOMA

• Women: Amenorrhoea, galactorrhoea (milk secretion), infertility - classic triad
• Men: Erectile dysfunction, infertility, galactorrhoea, hypogonadism
• Large tumours: headache, bitemporal hemianopia (optic chiasm compression)

• Excess prolactin inhibits GnRH → suppresses LH/FSH → hypogonadism
• Prolactin stimulates lactation (galactorrhoea even without pregnancy)

• Serum prolactin level elevated
• MRI pituitary
• Visual field testing

• Dopamine agonists: Cabergoline (first-line), Bromocriptine (dopamine inhibits prolactin)
• Surgery: transsphenoidal (if medical therapy fails or large tumour)
• Medical treatment often shrinks tumour - unique among pituitary tumours

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28. HYPOTHYROIDISM

• Most common cause adults: Hashimoto's (autoimmune) + iodine deficiency (worldwide)
• TSH ↑, Free T4 ↓
• Treatment: Levothyroxine

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29. HYPERTHYROIDISM

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30. HYPERPARATHYROIDISM

• PTH raises serum calcium: bone resorption ↑, renal Ca2+ reabsorption ↑, gut absorption ↑ (via Vit D activation)
• Result: Hypercalcaemia

• Bones: Bone pain, osteitis fibrosa cystica, pathological fractures, "brown tumours"
• Stones: Renal stones (nephrolithiasis) - calcium oxalate/phosphate
• Groans (GI): Nausea, vomiting, peptic ulcer, pancreatitis, constipation
• Psychic moans: Depression, confusion, psychosis
• Muscle weakness

• Serum calcium ↑, PTH ↑ (in primary)
• Serum phosphate ↓ (PTH causes phosphaturia)
• X-ray: subperiosteal bone resorption (radial side of middle phalanx - pathognomonic), "pepper pot skull"
• Sestamibi scan: localise adenoma

• Primary: Parathyroidectomy (surgical removal) - definitive
• Secondary: Treat underlying renal failure + phosphate binders, Vit D, calcimimetics (cinacalcet)
• Hypercalcaemic crisis: IV fluids, bisphosphonates, furosemide

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👁️ SECTION 5: SPECIAL SENSE

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31. HEARING LOSS

• Rinne Test: Compare air conduction (AC, tuning fork near ear) vs bone conduction (BC, tuning fork on mastoid)
  • Normal/SNHL: AC > BC (Rinne positive)
  • Conductive: BC > AC (Rinne negative)
• Weber Test: Tuning fork on vertex of skull
  • Conductive loss: sound louder on AFFECTED side
  • SNHL: sound louder on NORMAL side

• Conductive: Remove wax, treat infection, hearing aids, surgery (stapedectomy for otosclerosis)
• Sensorineural: Hearing aids, cochlear implant (severe/profound)

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32. MYOPIA (Short-sightedness)

• Pathophysiology: Light rays from distant objects converge before reaching retina (focal point falls in front of retina)
• Clinical: Squinting, difficulty reading blackboard
• Treatment: Concave lens (spectacles/contact lens), LASIK surgery
• Complication of high myopia: Retinal detachment risk

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33. PRESBYOPIA

• Physiological ageing process; universal
• Accommodation = ability to change lens shape to focus near objects
• Presbyopia ≠ hypermetropia (different mechanism; presbyopia is dynamic loss of accommodation)

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34. VISUAL PATHWAY LESIONS (HIGH EXAMINER FAVOURITE!)

• Optic chiasm: nasal fibres cross → bitemporal defect with central lesion
• Post-chiasmal lesions: homonymous defects (same half of visual field lost in both eyes)
• Macular sparing in occipital lesions (dual blood supply of macula)

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35. ASTIGMATISM

• Regular astigmatism: principal meridians at 90° - corrected with cylindrical lens
• Irregular astigmatism: keratoconus (cone-shaped cornea) - may need rigid contact lens/corneal graft
• Clinical: Blurred vision at all distances, distortion, eyestrain/headache
• Diagnosis: Keratometry (corneal curvature), retinoscopy
• Treatment: Cylindrical spectacle lens, toric contact lens, LASIK

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📋 QUICK REVISION TABLE - Exam Favourites

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⭐ EXAMINER'S TOP PICKS (These Lines Score Maximum Marks)

These points, when written clearly, almost always earn marks in 1st year MBBS viva and theory:

1. "Myasthenia Gravis is caused by IgG antibodies against nicotinic ACh receptors - diagnosed by Tensilon test"
2. "DMD is X-linked recessive; Gower's sign + pseudohypertrophy of calf are pathognomonic"
3. "In Parkinsonism: Lewy bodies in substantia nigra; TRAP signs; treated with Levodopa + Carbidopa"
4. "Huntington's: Autosomal dominant CAG repeat expansion; chromosome 4; caudate atrophy; chorea"
5. "Alzheimer's: Amyloid-beta plaques (extracellular) + Neurofibrillary tangles (intracellular); cholinesterase inhibitors"
6. "Brown-Sequard: Ipsilateral UMN weakness + proprioception loss; Contralateral pain + temperature loss"
7. "DKA triad: hyperglycaemia + ketones + metabolic acidosis; Kussmaul breathing; treat with insulin + saline + K+"
8. "Cushing's: Moon face, buffalo hump, purple striae; Low-dose DST; transsphenoidal surgery for pituitary adenoma"
9. "Addison's: Hyperpigmentation (ACTH/MSH); Na↓ K↑; Synacthen test; hydrocortisone + fludrocortisone lifelong"
10. "Pituitary tumour compressing optic chiasm → Bitemporal hemianopia (nasal fibres cross at chiasm)"
11. "Phaeochromocytoma: Rule of 10s; alpha-blocker BEFORE beta-blocker (phenoxybenzamine); 24h urinary metanephrines"
12. "Cretinism = congenital hypothyroidism; mental retardation + dwarfism; neonatal TSH screening; early T4 prevents MR"
13. "Myopia = concave lens; Presbyopia = convex lens (age >40, loss of accommodation)"
14. "Rinne negative (BC>AC) = conductive loss; Weber lateralises to bad ear in conductive, good ear in SNHL"
15. "HHS vs DKA: HHS has higher glucose, no ketones, no acidosis, older Type 2 patient; treat with slow rehydration"

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Study tip: For each condition, make sure you can write a 5-mark answer covering: Definition/Cause → Pathophysiology (mechanism) → Clinical features (3-5 key ones) → Key investigation → Treatment. The bold lines above are what examiners specifically look for and tick off during marking.