Free NEET PG & INI-CET Question Bank & Practice MCQs

Explanation

The upper trunk is formed by C5 and C6, and traction that widens the head-to-shoulder angle stretches it at Erb point. Loss of the deltoid, supraspinatus, infraspinatus and biceps leaves the limb adducted, medially rotated, extended and pronated. C8 and T1 injury instead produces a claw hand from intrinsic muscle paralysis.

Explanation

The axillary nerve winds around the surgical neck, so a fracture there is its classic injury site. It supplies deltoid, the main abductor beyond the first 15 degrees, and gives the upper lateral cutaneous nerve of the arm to the regimental badge area. Supraspinatus, supplied by the suprascapular nerve, initiates abduction, which is why the first few degrees are preserved.

Explanation

The radial nerve lies directly against bone in the spiral groove of the humeral shaft, so mid-shaft fractures injure it. It supplies all the extensors of the wrist and fingers, and losing them gives wrist drop. Its cutaneous territory includes the dorsal skin of the first web space, which is the small area most reliably affected.

Explanation

The ulnar nerve passes in a groove behind the medial epicondyle, where it is subcutaneous and easily struck. It supplies most intrinsic hand muscles, and losing the lumbricals to the fourth and fifth digits leaves the metacarpophalangeal joints extended and the interphalangeal joints flexed. Sensation over the medial one and a half digits is also ulnar territory.

Explanation

The long thoracic nerve arises from the C5, C6 and C7 roots and runs superficially on serratus anterior along the chest wall, which puts it at risk during axillary surgery. Serratus anterior holds the medial border of the scapula against the thorax and protracts it. Without it the medial border lifts away, most obviously when the arm pushes forward against resistance.

Explanation

The three trigeminal divisions exit in order from front to back and top to bottom: V1 through the superior orbital fissure, V2 through foramen rotundum and V3 through foramen ovale. Foramen spinosum carries the middle meningeal artery, not a nerve division. Remembering the sequence rotundum then ovale for V2 then V3 covers most questions on the topic.

Explanation

Foramen ovale transmits the mandibular division, V3, along with the accessory meningeal artery and the lesser petrosal nerve. V3 is the only trigeminal division carrying motor fibres, which is why a lesion here weakens the muscles of mastication. The facial nerve leaves through the stylomastoid foramen instead.

Explanation

The jugular foramen transmits cranial nerves IX, X and XI along with the internal jugular vein. Glossopharyngeal loss removes the afferent limb of the gag reflex, vagal loss gives hoarseness through the recurrent laryngeal branch, and accessory loss weakens trapezius and sternocleidomastoid. The hypoglossal canal carries only CN XII, so tongue deviation without these features points there instead.

Explanation

The superior orbital fissure carries the three ocular motor nerves, III, IV and VI, the branches of V1 and the superior ophthalmic vein. The optic nerve takes a separate route through the optic canal, accompanied by the ophthalmic artery. That separation explains why an optic canal lesion can spare eye movements while abolishing vision.

Explanation

The trochlear nerve is unique in leaving the brainstem dorsally, just below the inferior colliculus, and it decussates before doing so. It therefore supplies the superior oblique of the opposite side and has the longest intracranial course, which makes it vulnerable in head injury. Superior oblique depresses and intorts the adducted eye, so patients complain of vertical diplopia going down stairs.

Explanation

Cranial nerves III, IV, V1 and V2 run within the lateral wall of the cavernous sinus, while the abducent nerve runs free in the sinus alongside the internal carotid artery. Being surrounded by blood rather than protected by dura, it is the first to suffer when pressure rises. The result is a lateral rectus palsy with failure of abduction.

Explanation

The femoral triangle is bounded above by the inguinal ligament, laterally by the medial border of sartorius and medially by the medial border of adductor longus. Its floor is formed by iliopsoas, pectineus and adductor longus. From lateral to medial its contents run nerve, artery, vein and lymphatics, which the mnemonic NAVEL preserves.

Explanation

The femoral sheath is a downward prolongation of the abdominal fascia and contains three compartments: lateral for the artery, intermediate for the vein and medial for the femoral canal with its lymph node. The femoral nerve lies lateral to the sheath, outside it, deep to the fascia iliaca. This is why a femoral hernia through the canal presents medial to the vessels.

Explanation

The adductor canal transmits the femoral artery, the femoral vein, the saphenous nerve and the nerve to vastus medialis. The saphenous nerve is purely sensory, the terminal cutaneous branch of the femoral nerve, and it leaves the canal without piercing the adductor hiatus. It then supplies skin along the medial leg down to the medial malleolus.

Explanation

The common peroneal nerve winds around the neck of the fibula where it is subcutaneous and lies against bone, making it the most commonly injured nerve in the lower limb. It supplies the dorsiflexors and evertors through its deep and superficial branches, so injury gives foot drop with a high-stepping gait. Sensation over most of the dorsum of the foot is lost as well.

Explanation

The sciatic nerve leaves the pelvis through the greater sciatic foramen, and in roughly 85 per cent of people it passes below piriformis as a single trunk. Variants where a division pierces the muscle are the anatomical basis proposed for piriformis syndrome. The lesser sciatic foramen transmits the tendon of obturator internus and the pudendal neurovascular bundle re-entering the perineum.

Explanation

The thoracic duct ascends from the cisterna chyli, crosses to the left at about the level of T5, and empties at the junction of the left internal jugular and left subclavian veins. It therefore drains the whole body except the right upper limb and the right side of the head, neck and thorax. That remaining territory drains through the right lymphatic duct on the opposite side.

Explanation

The right lymphatic duct drains only the right upper limb and the right half of the head, neck and thorax. Everything below the diaphragm, including both lower limbs, drains into the cisterna chyli and then the thoracic duct. The common error is to assume that a right-sided structure must use the right duct, which holds only above the diaphragm.

Explanation

The left anterior descending artery runs in the anterior interventricular groove and gives septal perforators to the anterior two thirds of the septum. It also supplies the anterior wall of the left ventricle and the apex, which is why its occlusion is the most consequential coronary lesion. The posterior third of the septum comes from the posterior interventricular artery.

Explanation

The sinuatrial nodal artery arises from the right coronary artery in about 60 per cent of hearts and from the circumflex in the remainder. The atrioventricular node is likewise usually right coronary territory, supplied at the crux of the heart. This is why an inferior infarct from right coronary occlusion so often produces bradycardia and heart block.

Explanation

Roughly 85 per cent of hearts are right dominant, meaning the posterior interventricular artery arises from the right coronary artery. About 8 per cent are left dominant, with the branch coming from the circumflex, and the remainder are codominant. Dominance matters because it determines which vessel supplies the inferior wall and the atrioventricular node.

Explanation

The azygos vein arches forward over the right lung root at about the level of the sternal angle, which corresponds to the T4 and T5 disc. The same plane marks the start and end of the aortic arch, the bifurcation of the trachea and the division between superior and inferior mediastinum. Grouping these landmarks at one level is far more efficient than memorising them separately.

Explanation

The deep ring is a defect in the transversalis fascia, lying about midway between the anterior superior iliac spine and the pubic symphysis, just lateral to the inferior epigastric vessels. The superficial ring by contrast is a triangular gap in the external oblique aponeurosis above the pubic tubercle. The internal spermatic fascia the cord picks up at the deep ring is derived from transversalis fascia.

Explanation

The inferior epigastric vessels are the landmark that separates the two inguinal hernias: indirect sacs come through the deep ring lateral to them, direct sacs push through the weak posterior wall medial to them. Direct hernias are acquired and rarely enter the scrotum, whereas indirect ones follow the cord and often do. A femoral hernia lies below the inguinal ligament and lateral to the pubic tubercle.

Explanation

At the lower oesophagus the left gastric vein of the portal system anastomoses with oesophageal veins draining into the azygos system, which is systemic. When portal pressure rises, flow reverses through this channel and the submucosal veins distend into varices. The other classic sites are the anorectal junction, the periumbilical region giving caput medusae, and the retroperitoneum.

Explanation

The coeliac trunk supplies foregut structures from the lower oesophagus to the second part of the duodenum, as far as the entry of the bile duct. Beyond that point the midgut takes over with the superior mesenteric artery. The transition at the ampulla is also where the arterial, venous, lymphatic and autonomic supply all change, which makes it a favourite examination landmark.

Explanation

The superior mesenteric artery is the midgut vessel, supplying from just beyond the bile duct entry in the duodenum to about two thirds of the way along the transverse colon. The hindgut from that point to the upper rectum belongs to the inferior mesenteric artery. The junction near the splenic flexure is a watershed zone and a common site for ischaemic colitis.

Explanation

From front to back the hilum contains the renal vein, then the renal artery, then the renal pelvis continuing as the ureter. The vein lies most anterior because it drains forward into the inferior vena cava, which sits ahead of the aorta. The left renal vein is the longer of the two and crosses in front of the aorta beneath the superior mesenteric artery.

Explanation

Each pharyngeal arch keeps its own nerve however far its muscles migrate. Arch one takes V3 and gives the muscles of mastication, mylohyoid, the anterior belly of digastric, tensor tympani and tensor veli palatini. Arch two takes the facial nerve, arch three the glossopharyngeal, and arches four and six the vagus.

Explanation

Stapedius is a second arch muscle and is therefore supplied by the facial nerve, the nerve of that arch. This is why facial nerve palsy proximal to the nerve to stapedius produces hyperacusis, since the muscle can no longer damp stapes movement. Tensor tympani, by contrast, is a first arch muscle supplied by V3.

Explanation

Arch four is supplied by the superior laryngeal branch of the vagus and arch six by the recurrent laryngeal branch. All the intrinsic laryngeal muscles except cricothyroid derive from arch six and are therefore recurrent laryngeal territory. Cricothyroid is the arch four exception, supplied by the external branch of the superior laryngeal nerve.

Explanation

Meckel diverticulum is the persistent proximal part of the vitellointestinal duct, which normally obliterates in the seventh week. It is a true diverticulum containing all bowel layers, arises from the antimesenteric border of the ileum, and may contain ectopic gastric or pancreatic tissue. The ectopic gastric mucosa is what causes painless bleeding in children.

Explanation

The ductus arteriosus connects the pulmonary trunk to the aortic arch in fetal life and closes functionally within hours of birth, leaving the ligamentum arteriosum. The left recurrent laryngeal nerve hooks under this ligament, which explains its long course in the chest. The umbilical vein becomes the ligamentum teres and the ductus venosus becomes the ligamentum venosum.

Explanation

The notochord regresses in the vertebral bodies but persists between them as the nucleus pulposus, the only adult remnant of the structure. The surrounding anulus fibrosus and the vertebral bodies themselves come from sclerotome. Chordoma, a tumour of notochordal remnants, arises for the same reason at the sacrococcygeal and clival ends of the axis.

Explanation

The trachea is lined by pseudostratified ciliated columnar epithelium with goblet cells, the classic respiratory epithelium. Every nucleus sits at a different height, which makes it look layered, but all cells reach the basement membrane. The cilia and mucus together form the mucociliary escalator that clears particles upward.

Explanation

Transitional epithelium, or urothelium, lines the urinary tract from the renal calyces to the proximal urethra. Its umbrella cells flatten as the bladder fills, letting the lining stretch without breaking, and its tight junctions keep urine from leaking into tissue. The oesophagus by contrast is stratified squamous non-keratinised.

Explanation

Type II pneumocytes are cuboidal cells that make and secrete surfactant, and they also act as the progenitor for both alveolar cell types after injury. Type I pneumocytes are thin squamous cells that cover about 95 per cent of the alveolar surface and handle gas exchange. Surfactant lowers surface tension and prevents alveolar collapse at end expiration.

Explanation

Purkinje fibres are modified cardiac myocytes that are larger and paler than working muscle, packed with glycogen and relatively sparse in myofibrils. That structure suits conduction rather than contraction and gives them the fastest conduction velocity in the heart. They remain cardiac muscle, so they keep their intercalated discs and striations.

Explanation

Adjacent Sertoli cells are joined by tight junctions that divide the seminiferous tubule into a basal and an adluminal compartment. This isolates developing germ cells from the immune system, which matters because meiotic cells express antigens the body has never seen. Leydig cells sit outside the tubule in the interstitium and secrete testosterone.

Explanation

Three structures pass through the parotid, and their depth is fixed: the facial nerve is most superficial, the retromandibular vein lies deep to it, and the external carotid artery is deepest. The nerve divides within the gland into its five terminal branches without supplying the gland itself. Its superficial position is why superficial parotidectomy carries a real risk of facial weakness.

Explanation

The recurrent laryngeal nerve runs in the tracheo-oesophageal groove and has a variable relationship to the branches of the inferior thyroid artery, passing in front, behind or between them. Ligating that artery close to the gland rather than on the main trunk keeps the dissection away from the nerve. The superior thyroid artery has the same problem with the external laryngeal nerve, which is why it is ligated close to the upper pole.

Explanation

The posterior triangle is bounded in front by the posterior border of sternocleidomastoid, behind by the anterior border of trapezius, and below by the middle third of the clavicle. The inferior belly of omohyoid crosses it and subdivides it into occipital and supraclavicular parts. The accessory nerve crosses the triangle superficially and is at risk during lymph node biopsy here.

Explanation

The carotid sheath contains the common and internal carotid arteries, the internal jugular vein and the vagus nerve, with the vein lateral, the artery medial and the nerve between and behind them. The sympathetic chain lies behind the sheath, embedded in prevertebral fascia, not inside it. That separation is why a sheath lesion need not cause Horner syndrome.

Explanation

The lingual nerve loops under the submandibular duct, passing from lateral to medial as it descends and then ascending on its medial side to reach the tongue. It is one of the few places where a nerve spirals around a duct rather than running alongside it. The relationship matters in surgery for submandibular calculi, where the nerve lies directly in the operative field.

Explanation

The lenticulostriate arteries are small perforating branches of the middle cerebral artery that supply much of the internal capsule and basal ganglia. They arise at right angles from a large vessel, which exposes them to high pressure and makes them the classic site of hypertensive haemorrhage and lacunar infarction. Because corticospinal fibres are densely packed there, a tiny lesion can cause a dense contralateral hemiplegia.

Explanation

About 85 per cent of corticospinal fibres cross in the pyramidal decussation at the lower medulla and descend as the lateral corticospinal tract. The uncrossed remainder forms the anterior corticospinal tract and decussates segmentally. Because the crossing is above the cord, a cortical or capsular lesion causes weakness on the opposite side of the body while a cord lesion causes it on the same side.

Explanation

The dorsal columns carry fine touch, vibration and proprioception without synapsing until the medulla. Fibres from below T6 travel in the medially placed fasciculus gracilis and relay in the nucleus gracilis, while those from above T6 use the laterally placed fasciculus cuneatus. Second order fibres then cross as the internal arcuate fibres to form the medial lemniscus.

Explanation

The oculomotor nerve runs beside the posterior communicating artery, so an aneurysm there compresses it. The parasympathetic pupilloconstrictor fibres travel on the outside of the nerve, which is why compression blows the pupil early while ischaemic third nerve palsies from diabetes typically spare it. Unopposed lateral rectus and superior oblique action leaves the eye down and out.

Explanation

The palmar cutaneous branch of the median nerve leaves the trunk about 5 cm proximal to the wrist and crosses superficial to the flexor retinaculum rather than through the tunnel. Compression under the retinaculum therefore spares the skin of the thenar eminence while affecting the lateral three and a half digits. Preserved thenar sensation with numb fingers is a useful sign that the lesion is at the tunnel rather than higher.

Explanation

The scaphoid forms the floor of the anatomical snuffbox, so tenderness there after a fall on the outstretched hand suggests its fracture. Its nutrient vessels enter near the distal pole and run backwards through the bone, so a waist fracture cuts off the proximal fragment. That retrograde supply is why avascular necrosis and non-union are common and why suspected fractures are immobilised even with normal initial films.

Explanation

The Na+/K+ ATPase extrudes three sodium ions and imports two potassium ions per ATP hydrolysed, making it electrogenic. It maintains the resting membrane potential and cell volume.

Explanation

Total body water is about 60% of body weight, or 42 litres. Two-thirds is intracellular, around 28 litres, and one-third extracellular, around 14 litres, of which plasma is about 3 litres and interstitial fluid about 11 litres.

Explanation

The resting membrane is most permeable to potassium, so the resting potential of about -70 mV lies close to the potassium equilibrium potential predicted by the Nernst equation.

Explanation

Albumin is the most abundant plasma protein and, being smallest, contributes 75 to 80% of plasma oncotic pressure. Hypoalbuminaemia reduces oncotic pressure and causes oedema.

Explanation

Intestinal glucose uptake uses the sodium-glucose cotransporter SGLT1, a secondary active transport that harnesses the sodium gradient set up by the Na+/K+ ATPase. GLUT2 then moves glucose out basolaterally.

Explanation

The upstroke results from opening of voltage-gated sodium channels and rapid sodium influx. Repolarisation follows from potassium efflux as sodium channels inactivate.

Explanation

Acetylcholine is released at the neuromuscular junction and acts on nicotinic receptors on the motor end plate, triggering muscle depolarisation. It is broken down by acetylcholinesterase.

Explanation

Calcium binds troponin C, causing tropomyosin to shift and expose actin's myosin-binding sites, allowing cross-bridge formation. This is the trigger step of excitation-contraction coupling.

Explanation

In the sliding filament model, the I band and H zone shorten during contraction while the A band, the length of the thick filament, stays constant. The sarcomere shortens as filaments slide past each other.

Explanation

A-alpha fibres are the largest and most heavily myelinated, giving the fastest conduction for motor function and proprioception. Unmyelinated C fibres, carrying slow pain and temperature, are the slowest.

Explanation

In the absolute refractory period, voltage-gated sodium channels are inactivated and cannot reopen until the membrane repolarises, so no stimulus, however strong, can trigger another action potential.

Explanation

The 'a' wave reflects right atrial contraction. It is absent in atrial fibrillation and becomes a large cannon wave in complete heart block, when the atrium contracts against a closed tricuspid valve.

Explanation

Cardiac output is stroke volume multiplied by heart rate, about 5 litres per minute at rest. Stroke volume depends on preload, afterload and contractility.

Explanation

The Frank-Starling mechanism means greater end-diastolic volume, or preload, stretches cardiac muscle, increasing contractile force and stroke volume. This matches output to venous return.

Explanation

The QRS complex represents ventricular depolarisation. The P wave is atrial depolarisation, the T wave is ventricular repolarisation, and the PR interval reflects AV nodal conduction delay.

Explanation

Baroreceptors in the carotid sinus and aortic arch sense increased pressure and increase parasympathetic while decreasing sympathetic outflow, lowering heart rate and causing vasodilation to restore normal pressure.

Explanation

The SA node has the fastest intrinsic firing rate, about 60 to 100 per minute, and sets the heart rhythm. If it fails, lower pacemakers in the AV node and His-Purkinje system take over at slower rates.

Explanation

S1 is produced by closure of the atrioventricular, mitral and tricuspid, valves at the start of systole. S2 results from closure of the aortic and pulmonary semilunar valves.

Explanation

A right shift, meaning easier oxygen unloading, is caused by increased 2,3-BPG, carbon dioxide, temperature and hydrogen ions, that is a low pH. This is the Bohr effect.

Explanation

Residual volume, the air remaining after maximal expiration, cannot be measured by spirometry and needs body plethysmography or helium dilution. Consequently functional residual capacity and total lung capacity cannot be measured directly either.

Explanation

Obstructive disease such as asthma and COPD reduces the FEV1/FVC ratio because airflow is limited. Restrictive disease reduces both FEV1 and FVC proportionally, keeping the ratio normal or high.

Explanation

Surfactant reduces alveolar surface tension, increasing compliance and preventing alveolar collapse at end-expiration. Its deficiency in premature infants causes respiratory distress syndrome.

Explanation

Central chemoreceptors respond to CSF hydrogen ion changes driven by arterial PaCO2, the most powerful normal respiratory stimulus. Hypoxic drive via peripheral chemoreceptors becomes important only at low PaO2 or in chronic carbon dioxide retainers.

Explanation

About 70% of carbon dioxide is carried as bicarbonate, formed via carbonic anhydrase in red cells, about 23% as carbaminohaemoglobin and about 7% dissolved. The bicarbonate system also buffers blood pH.

Explanation

Carbon monoxide poisoning causes anaemic, or haemic, hypoxia by binding haemoglobin with about 240 times the affinity of oxygen, reducing oxygen-carrying capacity. It also shifts the dissociation curve left, worsening tissue delivery.

Explanation

Inulin is freely filtered and neither reabsorbed nor secreted, so its clearance equals GFR. Clinically creatinine clearance is used as an approximation, while PAH clearance estimates renal plasma flow.

Explanation

Efferent arteriolar constriction raises glomerular capillary hydrostatic pressure, increasing GFR up to a point. This is why angiotensin II supports GFR in low-flow states, and why ACE inhibitors can reduce it.

Explanation

The proximal convoluted tubule reabsorbs nearly all filtered glucose and amino acids and about two-thirds of sodium and water. Glucose appears in urine only when the reabsorptive transport maximum is exceeded.

Explanation

ADH, or vasopressin, acts on V2 receptors to insert aquaporin-2 water channels into the collecting duct's apical membrane, increasing water reabsorption and concentrating urine.

Explanation

A low pH with low bicarbonate indicates metabolic acidosis, and the low PaCO2 shows respiratory compensation through hyperventilation. Causes include diabetic ketoacidosis, lactic acidosis and renal failure.

Explanation

The loop of Henle acts as a counter-current multiplier, creating a hypertonic medullary interstitium. The vasa recta act as counter-current exchangers to preserve this gradient, enabling urine concentration.

Explanation

Parietal, or oxyntic, cells secrete hydrochloric acid and intrinsic factor. Chief cells secrete pepsinogen and G cells secrete gastrin. Proton pump inhibitors block the parietal cell H+/K+ ATPase.

Explanation

Secretin, released from duodenal S cells in response to acid, stimulates pancreatic and biliary bicarbonate secretion to neutralise chyme. Cholecystokinin stimulates enzyme secretion and gallbladder contraction.

Explanation

Parietal cells secrete intrinsic factor, which binds vitamin B12 for absorption in the terminal ileum. Loss of intrinsic factor, as in pernicious anaemia, causes B12 deficiency.

Explanation

Bile salts emulsify dietary fats into micelles, increasing the surface area for pancreatic lipase and aiding absorption of fats and fat-soluble vitamins. They are recycled via the enterohepatic circulation.

Explanation

Insulin stimulates translocation of GLUT4 transporters to the cell membrane in skeletal muscle and adipose tissue, increasing glucose uptake. GLUT2 in liver and pancreas and GLUT1 for basal uptake are insulin-independent.

Explanation

T3 is several times more potent than T4 at target tissues. Most circulating T3 is produced by peripheral deiodination of T4, which acts largely as a prohormone.

Explanation

PTH raises calcium by resorbing bone, increasing renal calcium reabsorption and activating vitamin D to boost gut absorption. It decreases rather than increases renal phosphate reabsorption, causing phosphaturia.

Explanation

Glucagon, along with ACTH, PTH and beta-adrenergic hormones, acts via Gs-protein-coupled receptors that raise cAMP. Insulin uses tyrosine kinase, while steroid and thyroid hormones use intracellular nuclear receptors.

Explanation

Aldosterone, from the zona glomerulosa, acts on the distal nephron to increase sodium reabsorption and potassium excretion, regulating extracellular volume and blood pressure. It is controlled by the renin-angiotensin system.

Explanation

Depolarisation opens voltage-gated calcium channels, and calcium influx triggers vesicle fusion and neurotransmitter release into the synaptic cleft. This is the calcium-dependent step of synaptic transmission.

Explanation

The lateral spinothalamic tract carries pain and temperature, crossing near the level of entry. The dorsal columns carry fine touch, vibration and proprioception, crossing in the medulla.

Explanation

About 85 to 90% of corticospinal fibres cross at the pyramidal decussation in the medulla to form the lateral corticospinal tract, which controls voluntary movement of the limbs on the opposite side.

Explanation

The patellar reflex is a monosynaptic stretch reflex: muscle spindle afferents synapse directly on alpha motor neurons, causing quadriceps contraction. It tests the L2 to L4 spinal segments.

Explanation

Cerebellar lesions cause intention tremor, ataxia, dysmetria, dysdiadochokinesia and nystagmus, with signs ipsilateral to the lesion. Resting tremor and rigidity instead suggest basal ganglia, or Parkinsonian, pathology.

Explanation

Alpha waves at 8 to 13 Hz dominate in an awake, relaxed adult with eyes closed. Beta waves appear with mental activity, delta waves occur in deep sleep, and theta waves appear in drowsiness and in children.

Explanation

Most postganglionic sympathetic fibres release noradrenaline. An exception is sweat glands, which use acetylcholine. All preganglionic autonomic fibres and postganglionic parasympathetic fibres use acetylcholine.

Explanation

A-delta fibres are thinly myelinated and carry fast, sharp, well-localised first pain. Unmyelinated C fibres carry slow, dull, poorly localised second pain and temperature.

Explanation

Cones mediate colour vision and high-acuity central vision in bright, photopic conditions and are concentrated at the fovea. Rods handle dim-light, scotopic vision and are more sensitive but do not detect colour.

Explanation

The hypothalamus regulates body temperature, hunger, thirst and circadian rhythms, and links the nervous and endocrine systems via the pituitary. It is central to homeostasis.

Explanation

Km is the substrate concentration at half-maximal velocity. A low Km means the enzyme reaches half of Vmax at low substrate concentration, indicating high affinity for its substrate.

Explanation

A competitive inhibitor competes for the active site, raising the apparent Km through reduced affinity, while Vmax is unchanged because high substrate concentrations overcome the inhibition.

Explanation

Cardiac troponins T and I are the most specific and sensitive markers of myocardial injury, rising within hours and remaining elevated for days. CK-MB is an older marker.

Explanation

Thiamine pyrophosphate, from vitamin B1, is a coenzyme for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and transketolase. B1 deficiency impairs these and causes beriberi and Wernicke encephalopathy.

Explanation

HMG-CoA reductase catalyses the rate-limiting step of cholesterol synthesis and is the target of statins. HMG-CoA lyase, by contrast, is involved in ketone body formation.

Explanation

Transferases move functional groups such as amino or phosphate groups between substrates; the aminotransferases ALT and AST are examples. Oxidoreductases handle redox reactions and hydrolases cleave bonds using water.

Explanation

PFK-1 is inhibited by ATP and citrate, both signals of energy abundance, and activated by AMP and fructose-2,6-bisphosphate. This makes it the main control point of glycolysis.

Explanation

Glycolysis takes place in the cytoplasm and does not require oxygen. It converts glucose to pyruvate with a net yield of 2 ATP and 2 NADH per glucose molecule.

Explanation

The citric acid cycle occurs in the mitochondrial matrix. Each turn generates 3 NADH, 1 FADH2 and 1 GTP, feeding electrons into the electron transport chain for ATP production.

Explanation

The liver is the main site of gluconeogenesis, producing glucose from lactate, glycerol and amino acids to maintain blood glucose during fasting. The kidney contributes during prolonged starvation.

Explanation

The HMP shunt produces NADPH, for reductive biosynthesis and antioxidant defence, and ribose-5-phosphate for nucleotide synthesis. It does not generate ATP directly.

Explanation

In the Cori cycle, muscle lactate travels to the liver, where it is converted back to glucose via gluconeogenesis and returned to muscle. This recycles lactate and supports glucose supply during exercise.

Explanation

Molecular oxygen is the final electron acceptor at complex IV, being reduced to water. This maintains electron flow and the proton gradient that drives ATP synthesis; without oxygen the chain halts.

Explanation

GLUT4 is the insulin-responsive transporter in skeletal muscle and adipose tissue, and insulin promotes its translocation to the cell membrane. GLUT2 is in liver and pancreatic beta cells, and GLUT5 transports fructose.

Explanation

Carnitine shuttles long-chain fatty acids across the inner mitochondrial membrane via the carnitine palmitoyltransferase system. Carnitine deficiency impairs fatty-acid oxidation, causing muscle weakness and hypoglycaemia.

Explanation

HDL carries out reverse cholesterol transport, moving cholesterol from peripheral tissues to the liver, and is protective against atherosclerosis. LDL delivers cholesterol to tissues and is atherogenic.

Explanation

Apo C-II activates lipoprotein lipase on capillary endothelium, releasing free fatty acids from triglyceride-rich lipoproteins. Apo A-I activates LCAT and Apo B-100 is the ligand for the LDL receptor.

Explanation

Ketone bodies, namely acetoacetate, beta-hydroxybutyrate and acetone, are made in liver mitochondria from acetyl-CoA during fasting or diabetic ketoacidosis. Peripheral tissues, including the brain in prolonged fasting, use them for energy.

Explanation

Linoleic acid, an omega-6, and alpha-linolenic acid, an omega-3, are essential because humans cannot synthesise them. They are precursors of arachidonic acid and other signalling molecules.

Explanation

Familial hypercholesterolaemia results from defective LDL receptors, impairing LDL clearance and causing very high LDL, tendon xanthomas and premature atherosclerosis. It is inherited in an autosomal dominant pattern.

Explanation

The urea cycle occurs in the liver, partly in mitochondria and partly in cytoplasm, converting toxic ammonia to urea for excretion. Enzyme defects cause hyperammonaemia and encephalopathy.

Explanation

Pyridoxal phosphate, from vitamin B6, is the coenzyme for aminotransferases such as AST and ALT, transferring amino groups between amino acids and keto acids.

Explanation

Lysine is essential and must be obtained from the diet. Others include leucine, isoleucine, valine, threonine, methionine, phenylalanine, tryptophan and histidine. Alanine, glutamate and serine are non-essential.

Explanation

Vitamin C, or ascorbate, is a cofactor for prolyl and lysyl hydroxylases, essential for stable collagen triple-helix formation. Deficiency, or scurvy, causes fragile collagen, poor wound healing and bleeding gums.

Explanation

Secondary structure refers to local folding patterns such as the alpha-helix and beta-sheet, stabilised by hydrogen bonds. Primary is the amino-acid sequence, tertiary is the overall three-dimensional fold and quaternary is the assembly of subunits.

Explanation

Negative nitrogen balance means nitrogen loss exceeds intake, reflecting net protein catabolism as seen in starvation, trauma, sepsis or severe illness. Positive balance occurs during growth, pregnancy and recovery.

Explanation

Thiamine deficiency causes Wernicke encephalopathy, with confusion, ophthalmoplegia and ataxia, and if untreated Korsakoff psychosis. Give thiamine before glucose to avoid precipitating Wernicke encephalopathy.

Explanation

Vitamin B12 deficiency causes megaloblastic anaemia with hypersegmented neutrophils plus neurological features, namely subacute combined degeneration. Folate deficiency gives the same haematology but without neurological signs.

Explanation

Vitamin C deficiency, or scurvy, impairs collagen synthesis, causing bleeding gums, perifollicular haemorrhages, poor wound healing and corkscrew hairs. Vitamin C is a cofactor for collagen hydroxylation.

Explanation

Vitamin D is hydroxylated first in the liver to 25-hydroxyvitamin D and then in the kidney to 1,25-dihydroxyvitamin D, or calcitriol, the active form. Calcitriol increases intestinal calcium and phosphate absorption.

Explanation

Vitamin A, as retinal, is required for rhodopsin in the retina; deficiency causes night blindness, then xerophthalmia and Bitot spots. Vitamin A also maintains epithelial integrity.

Explanation

Vitamin K is essential for gamma-carboxylation of clotting factors II, VII, IX and X, as well as proteins C and S. Warfarin inhibits this by blocking vitamin K epoxide reductase.

Explanation

Pellagra, with dermatitis, diarrhoea and dementia, results from niacin deficiency. It can also occur in Hartnup disease and carcinoid syndrome, where tryptophan, a niacin precursor, is diverted or lost.

Explanation

Southern blotting detects DNA, Northern detects RNA and Western detects protein. Western blot has been used, for example, as a confirmatory HIV test.

Explanation

PCR uses heat-stable Taq DNA polymerase to amplify DNA through repeated cycles of denaturation, annealing and extension. Taq's thermostability allows it to survive the high denaturation temperatures.

Explanation

DNA polymerase I uses its 5' to 3' exonuclease activity to remove RNA primers and fills the gaps with DNA. DNA ligase then seals the remaining nicks between Okazaki fragments.

Explanation

The code is degenerate, or redundant, because most amino acids are specified by more than one codon. This buffers the effect of some point mutations, especially at the third wobble position.

Explanation

Transcription is the synthesis of mRNA from a DNA template by RNA polymerase. Translation then converts the mRNA sequence into protein at the ribosome.

Explanation

A nonsense mutation changes a codon to a premature stop codon, truncating the protein. A missense mutation changes one amino acid, a silent mutation causes no amino-acid change and a frameshift shifts the reading frame.

Explanation

Von Gierke disease, glycogen storage disease type I, is due to glucose-6-phosphatase deficiency, blocking the final step of gluconeogenesis and glycogenolysis. This causes fasting hypoglycaemia, hepatomegaly and lactic acidosis.

Explanation

McArdle disease, glycogen storage disease type V, results from muscle glycogen phosphorylase deficiency, causing exercise intolerance, cramps and myoglobinuria, with a characteristic second wind as fatty acids are recruited.

Explanation

Phenylketonuria is caused by phenylalanine hydroxylase deficiency, leading to phenylalanine accumulation, a musty odour, fair pigmentation and intellectual disability if untreated. Management is a phenylalanine-restricted diet.

Explanation

Alkaptonuria is due to homogentisate oxidase deficiency, causing accumulation of homogentisic acid. Urine darkens on standing, and pigment deposits in connective tissue cause ochronosis and arthritis.

Explanation

Classic galactosaemia results from galactose-1-phosphate uridyltransferase deficiency. Galactose-1-phosphate accumulates, causing liver damage, cataracts and, if untreated, sepsis. Treatment is a galactose-free diet.

Explanation

Tay-Sachs disease is caused by hexosaminidase A deficiency, leading to GM2 ganglioside accumulation, neurodegeneration and a cherry-red macular spot. Unlike Niemann-Pick disease, there is no hepatosplenomegaly.

Explanation

Gaucher disease is the most common lysosomal storage disorder, due to glucocerebrosidase deficiency. Gaucher cells, lipid-laden macrophages with a crumpled tissue paper appearance, accumulate and cause hepatosplenomegaly and bone disease.

Explanation

Maple syrup urine disease is due to deficient branched-chain ketoacid dehydrogenase, causing accumulation of leucine, isoleucine and valine. It presents with a characteristic urine odour, poor feeding and neurological decline.

Explanation

Wilson disease is a disorder of copper metabolism with low ceruloplasmin, causing copper accumulation in the liver, brain and cornea, where it forms Kayser-Fleischer rings. Treatment uses copper chelators such as penicillamine.

Explanation

G6PD deficiency, an X-linked disorder, reduces NADPH and leaves red cells vulnerable to oxidative stress. Triggers such as fava beans, infections and drugs like primaquine cause haemolysis with bite cells and Heinz bodies.

Explanation

Homocystinuria, most often from cystathionine beta-synthase deficiency, causes a marfanoid habitus, downward lens dislocation, thromboembolism and intellectual disability. In Marfan syndrome the lens dislocates upward and there is no thrombotic tendency.

Explanation

Irreversible injury is marked by severe mitochondrial damage with loss of ATP production, plasma membrane damage and lysosomal rupture. Cellular swelling and fatty change are features of reversible injury.

Explanation

Apoptosis is programmed, ATP-dependent cell death with cell shrinkage and no inflammation, since membrane integrity is preserved. Necrosis involves swelling, membrane rupture and inflammation.

Explanation

Caseous (cheese-like) necrosis is characteristic of tuberculosis, appearing as amorphous granular debris within granulomas. Coagulative necrosis follows ischaemia in most organs, and liquefactive necrosis occurs in the brain and in abscesses.

Explanation

Superoxide dismutase converts superoxide to hydrogen peroxide, which catalase and glutathione peroxidase then detoxify to water. These antioxidant systems limit free-radical-mediated cell injury.

Explanation

Dystrophic calcification occurs in injured or necrotic tissue despite normal serum calcium. Metastatic calcification occurs in normal tissue when serum calcium is elevated.

Explanation

The liver is the main site of fat metabolism, so fatty change is most common there, classically from alcohol. It is reversible but can progress to steatohepatitis and cirrhosis with continued injury.

Explanation

Neutrophils are the first responders in acute inflammation, dominating the first 24 hours. Macrophages take over after 24 to 48 hours. Chronic inflammation is dominated by lymphocytes, plasma cells and macrophages.

Explanation

Granulomas are collections of epithelioid cells, activated macrophages with abundant pink cytoplasm, often with multinucleated giant cells. Causes include tuberculosis, sarcoidosis, leprosy and fungal infections.

Explanation

Histamine, released mainly from mast cells, causes early vasodilation and increased vascular permeability, the immediate transient response. Other mediators include prostaglandins, leukotrienes and bradykinin.

Explanation

Vitamin C is a cofactor for prolyl and lysyl hydroxylase in collagen synthesis. Deficiency, or scurvy, causes poor wound healing, bleeding gums and fragile vessels.

Explanation

Labile cells such as surface epithelia, bone marrow and gut mucosa divide continuously and regenerate well. Neurons and cardiac myocytes are permanent cells with little regenerative capacity, healing by scar.

Explanation

Exudates are protein-rich fluids with high specific gravity above 1.020 and contain cells, resulting from increased vascular permeability in inflammation. Transudates are protein-poor ultrafiltrates from altered hydrostatic or oncotic pressure.

Explanation

AFP is raised in hepatocellular carcinoma and yolk-sac (endodermal sinus) tumours. PSA marks prostate cancer, calcitonin marks medullary thyroid cancer and CA-125 marks ovarian cancer.

Explanation

CA 19-9 is used to monitor pancreatic carcinoma and some biliary and gastrointestinal cancers. CA 15-3 relates to breast cancer, PSA to prostate, and beta-hCG and AFP to testicular tumours.

Explanation

Psammoma bodies occur in papillary thyroid carcinoma, serous ovarian carcinoma, meningioma and papillary renal cell carcinoma. They are not a feature of hepatocellular carcinoma.

Explanation

Signet-ring cells are classic of diffuse-type gastric adenocarcinoma, or linitis plastica, associated with loss of E-cadherin. They may also appear in some breast and colonic cancers.

Explanation

Metastasis is the single most reliable indicator of malignancy; benign tumours never metastasise. Malignant tumours also show rapid growth, invasion, poor differentiation and lack of a capsule.

Explanation

p53, the guardian of the genome, arrests the cell cycle to allow DNA repair or triggers apoptosis if damage is irreparable. Loss of p53 function permits damaged cells to proliferate; it is the most commonly mutated gene in human cancer.

Explanation

Carcinomas, being epithelial cancers, typically spread first via lymphatics to regional nodes. Sarcomas characteristically spread haematogenously. Knowing this pattern guides staging and nodal assessment.

Explanation

Low serum ferritin is the most specific indicator of iron deficiency, the commonest cause of microcytic hypochromic anaemia. Ferritin is normal or high in thalassaemia and in anaemia of chronic disease.

Explanation

Hypersegmented neutrophils with more than five lobes, together with macro-ovalocytes, are hallmarks of megaloblastic anaemia from B12 or folate deficiency. B12 deficiency additionally causes neurological signs, namely subacute combined degeneration.

Explanation

The Reed-Sternberg cell, CD15 and CD30 positive, is pathognomonic of classical Hodgkin lymphoma. Its classic form has two mirror-image nuclei giving an owl-eye appearance.

Explanation

Chronic myeloid leukaemia is defined by t(9;22) producing BCR-ABL, a constitutively active tyrosine kinase. This is the target of imatinib, a tyrosine kinase inhibitor.

Explanation

Auer rods are crystallised azurophilic granules containing myeloperoxidase, seen in acute myeloid leukaemia and especially in acute promyelocytic leukaemia with t(15;17). They are not seen in lymphoid leukaemias.

Explanation

Burkitt lymphoma shows a starry-sky pattern of tingible-body macrophages amid rapidly dividing cells, and t(8;14) juxtaposing c-MYC with the immunoglobulin heavy-chain locus. It is one of the fastest-growing human tumours.

Explanation

Hereditary spherocytosis results from red-cell membrane protein defects in spectrin or ankyrin, producing spherocytes with increased osmotic fragility, splenomegaly and jaundice. Splenectomy is curative for the anaemia.

Explanation

DIC consumes platelets and clotting factors, giving low fibrinogen, prolonged PT and aPTT and thrombocytopenia, while fibrinolysis raises D-dimer. It is a secondary process driven by sepsis, obstetric complications or malignancy.

Explanation

Aschoff bodies, foci of fibrinoid necrosis surrounded by Anitschkow cells, are pathognomonic of rheumatic carditis, a sequel to group A streptococcal infection.

Explanation

Fatty streaks, lipid-laden foam cells in the intima, are the earliest lesions and can appear even in childhood. They may progress to fibrous plaques and to complicated plaques with rupture and thrombosis.

Explanation

Minimal change disease is the leading cause of nephrotic syndrome in children, showing normal light microscopy but podocyte foot-process effacement on electron microscopy. It responds well to corticosteroids.

Explanation

Mallory-Denk bodies are eosinophilic cytoplasmic inclusions of damaged intermediate filaments, classically seen in alcoholic hepatitis though not specific to it. They reflect hepatocyte injury.

Explanation

Alpha-1 antitrypsin deficiency causes panacinar emphysema with basal predominance, because unopposed elastase destroys alveolar walls. It also causes liver cirrhosis. Smoking-related emphysema is typically centriacinar and upper-zone.

Explanation

Helicobacter pylori, a urease-producing gram-negative organism, causes most chronic gastritis and peptic ulcers and increases the risk of gastric carcinoma and MALT lymphoma.

Explanation

Papillary thyroid carcinoma shows optically clear Orphan Annie eye nuclei, nuclear grooves and psammoma bodies. It is the commonest thyroid cancer and spreads via lymphatics with a good prognosis.

Explanation

Anaphylaxis is a Type I, IgE-mediated hypersensitivity with mast-cell degranulation. Type II is antibody-mediated cytotoxicity, Type III is immune-complex-mediated and Type IV is T-cell-mediated delayed hypersensitivity.

Explanation

Amyloid stains with Congo red and shows apple-green birefringence under polarised light because of its beta-pleated sheet structure. Types include AL from light chains and AA from serum amyloid A in chronic inflammation.

Explanation

Anti-double-stranded DNA and anti-Smith antibodies are highly specific for SLE. ANA is sensitive but not specific. Anti-dsDNA titres also correlate with disease activity, especially in lupus nephritis.

Explanation

The Mantoux reaction is a Type IV delayed hypersensitivity mediated by sensitised T cells and macrophages, peaking at 48 to 72 hours. Contact dermatitis and granuloma formation share this mechanism.

Explanation

HIV infects and depletes CD4 T helper cells. A CD4 count below 200 cells per microlitre defines AIDS and predisposes to opportunistic infections such as Pneumocystis pneumonia and cryptococcal meningitis.

Explanation

S-100 and HMB-45 mark melanocytic tumours. CD20 marks B cells, desmin marks muscle and cytokeratin marks epithelial or carcinoma cells. Immunohistochemistry helps classify poorly differentiated tumours.

Explanation

Bacterial meningitis gives a neutrophilic pleocytosis with high protein and low glucose, as bacteria consume glucose. Viral meningitis shows lymphocytes with normal glucose, and tuberculous meningitis shows lymphocytes with very low glucose.

Explanation

Prussian blue, the Perls stain, colours iron and haemosiderin blue and is useful in haemochromatosis and haemosiderosis. Congo red stains amyloid, Ziehl-Neelsen stains acid-fast bacilli and PAS stains glycogen and fungi.

Explanation

ABO-incompatible transfusion causes a Type II hypersensitivity: preformed IgM antibodies bind donor red cells and activate complement, causing intravascular haemolysis. It is a medical emergency.

Explanation

In sickle cell disease, glutamate is replaced by valine at position 6 of the beta-globin chain. Deoxygenated HbS polymerises, deforming red cells into sickles that cause vaso-occlusion and haemolysis.

Explanation

PT assesses the extrinsic pathway and factor VII, while aPTT assesses the intrinsic pathway. Isolated PT prolongation points to factor VII deficiency or early warfarin effect, as factor VII has the shortest half-life.

Explanation

Plasmodium falciparum shows characteristic banana or crescent-shaped gametocytes and causes the most severe disease, including cerebral malaria. It parasitises red cells of all ages, producing high parasitaemia.

Explanation

PSA is a glycoprotein produced by prostate epithelium; levels rise in prostate carcinoma and also in benign prostatic hyperplasia and prostatitis. It is used for screening, with known limitations, and to monitor treatment response.

Explanation

Virchow's triad comprises endothelial injury, stasis or turbulent flow, and hypercoagulability. These factors underlie venous and arterial thrombosis and guide risk assessment for conditions such as deep vein thrombosis.

Explanation

Anaemia of chronic disease shows low serum iron but normal or high ferritin, because hepcidin sequesters iron, together with a low TIBC. This distinguishes it from iron deficiency, where ferritin is low and TIBC is high.

Explanation

Acute lymphoblastic leukaemia is the commonest childhood leukaemia. Blasts are TdT positive and B-ALL commonly expresses CD10. With modern therapy the prognosis in children is generally favourable.

Explanation

Bioavailability is the fraction of an administered dose reaching the systemic circulation unchanged. Intravenous administration bypasses absorption entirely, so its bioavailability is defined as 100% and is the reference against which other routes are measured.

Explanation

Sublingual absorption drains into the systemic circulation via the superior vena cava, bypassing the portal vein and hepatic first-pass metabolism. This is why sublingual nitroglycerin acts rapidly and reliably.

Explanation

Phenytoin, ethanol and high-dose aspirin follow zero-order kinetics because their metabolising enzymes saturate at therapeutic concentrations. A small dose increase can then cause a disproportionate rise in plasma level and toxicity.

Explanation

A competitive inhibitor competes for the active site, raising the apparent Km (lower affinity) but leaving Vmax unchanged, since the inhibition can be overcome by increasing substrate concentration.

Explanation

The insulin receptor is a receptor tyrosine kinase. Ligand binding triggers autophosphorylation of tyrosine residues, activating downstream signalling. Insulin-like growth factor and several growth factor receptors work the same way.

Explanation

Digoxin, lithium, warfarin, phenytoin and theophylline have narrow therapeutic indices, meaning the toxic dose is close to the therapeutic dose. They require plasma level monitoring to avoid toxicity.

Explanation

It takes about 4 to 5 half-lives to reach 94 to 97% of steady-state concentration, and the same number to eliminate a drug after stopping it. This principle guides dosing intervals and loading-dose decisions.

Explanation

Atropine is a competitive muscarinic (cholinergic) antagonist. It causes tachycardia, mydriasis, dry mouth and reduced secretions, and is used in bradycardia and organophosphate poisoning.

Explanation

Metoprolol, atenolol, bisoprolol and esmolol are beta-1 selective (cardioselective), causing less bronchoconstriction than non-selective agents such as propranolol. Selectivity is relative and is lost at high doses, so caution still applies in asthma.

Explanation

Tamsulosin is a selective alpha-1A blocker that relaxes smooth muscle in the prostate and bladder neck, improving urine flow in BPH. Finasteride works differently, by inhibiting 5-alpha-reductase.

Explanation

Pyridostigmine and neostigmine inhibit acetylcholinesterase, increasing acetylcholine at the neuromuscular junction and improving muscle strength in myasthenia gravis. Neostigmine also reverses non-depolarising muscle blockade.

Explanation

Adrenaline reverses anaphylaxis through alpha-1 mediated vasoconstriction (raising blood pressure and reducing mucosal oedema) and beta-2 mediated bronchodilation, while beta-1 effects support cardiac output. It is the first-line drug, given intramuscularly.

Explanation

Succinylcholine can cause hyperkalaemia (dangerous in burns, crush injury and denervation) and can trigger malignant hyperthermia in susceptible individuals, treated with dantrolene. It also causes transient fasciculations.

Explanation

ACE also degrades bradykinin. ACE inhibitors raise bradykinin levels, producing the characteristic dry cough and, rarely, angioedema. Switching to an ARB, which does not affect bradykinin, resolves the cough.

Explanation

Warfarin inhibits vitamin K epoxide reductase, reducing synthesis of the vitamin K dependent factors II, VII, IX and X. It is monitored by PT/INR and reversed with vitamin K or, urgently, prothrombin complex concentrate.

Explanation

Unfractionated heparin is monitored by aPTT; it acts by activating antithrombin III. Warfarin is monitored by PT/INR. The antidote to heparin is protamine sulphate.

Explanation

Verapamil, quinidine and amiodarone reduce digoxin clearance and displace it from tissue binding, raising serum levels. Hypokalaemia also worsens toxicity. Digoxin-specific antibody fragments treat toxicity rather than causing it.

Explanation

Labetalol, methyldopa and nifedipine are safe in pregnancy. ACE inhibitors and ARBs are teratogenic, causing fetal renal damage, and are contraindicated especially in the second and third trimesters.

Explanation

Amiodarone is iodine-rich and lipophilic, causing pulmonary fibrosis, thyroid dysfunction (both under- and over-active), corneal deposits, hepatotoxicity and blue-grey skin discolouration. Baseline and periodic thyroid, liver and lung function testing is required.

Explanation

Statins (HMG-CoA reductase inhibitors) can cause myopathy ranging from myalgia to rhabdomyolysis, especially alongside fibrates or CYP inhibitors. They also raise liver transaminases. Muscle symptoms with a high CK warrant stopping the drug.

Explanation

Intravenous lorazepam, a benzodiazepine, is first-line for status epilepticus because of its rapid onset and longer duration than diazepam. Longer-term control follows with phenytoin, fosphenytoin or valproate.

Explanation

Ethosuximide is first-line for absence seizures, acting on T-type calcium channels in thalamic neurons. Valproate is an alternative, especially when other seizure types coexist. Carbamazepine and phenytoin can worsen absence seizures.

Explanation

The triad of miosis, respiratory depression and reduced consciousness indicates opioid overdose. Naloxone, a competitive opioid antagonist, reverses it rapidly, though repeat dosing may be needed because of its short half-life.

Explanation

Thiazides reduce renal lithium clearance by increasing proximal reabsorption, raising lithium into the toxic range. NSAIDs and ACE inhibitors do the same. Lithium has a narrow therapeutic index and needs level monitoring.

Explanation

Clozapine can cause agranulocytosis and requires regular white cell and absolute neutrophil count monitoring. It is reserved for treatment-resistant schizophrenia and also carries risks of myocarditis and seizures.

Explanation

MAC is the alveolar concentration preventing movement in 50% of patients in response to a stimulus. A low MAC means high potency. MAC correlates with lipid solubility, the Meyer-Overton hypothesis.

Explanation

Isoniazid increases pyridoxine excretion, causing a deficiency neuropathy. Prophylactic pyridoxine prevents it, particularly in those at risk such as diabetics, people with alcohol dependence and pregnant women.

Explanation

Aminoglycosides accumulate in renal proximal tubule cells (nephrotoxicity, usually reversible) and in cochlear and vestibular hair cells (ototoxicity, often permanent). Once-daily dosing and level monitoring reduce the risk.

Explanation

Ethambutol causes dose-dependent retrobulbar (optic) neuritis with reduced acuity and red-green colour blindness. It is usually reversible on stopping the drug; visual acuity and colour vision should be checked before and during treatment.

Explanation

Rifampicin colours urine, sweat and tears orange-red, which is harmless but alarming if unwarned. It is also a potent CYP450 inducer, reducing the effect of oral contraceptives, warfarin and many other drugs.

Explanation

Vancomycin is first-line for serious MRSA infections, with linezolid and daptomycin as alternatives. It can cause red man syndrome with rapid infusion and is nephrotoxic at high trough levels.

Explanation

Fluoroquinolones are associated with tendinitis and tendon rupture, and cause cartilage damage in animal studies, so they are avoided in children and pregnancy. They can also prolong the QT interval.

Explanation

Amphotericin B binds ergosterol in the fungal cell membrane, forming pores that cause leakage of ions and cell death. Azoles instead inhibit ergosterol synthesis and echinocandins block beta-glucan synthesis. Amphotericin is notably nephrotoxic.

Explanation

Beta-lactams bind penicillin-binding proteins and inhibit transpeptidation, the cross-linking step of peptidoglycan cell wall synthesis, leading to bacterial lysis. Resistance often occurs through beta-lactamase enzymes.

Explanation

Cyclophosphamide's metabolite acrolein irritates the bladder, causing haemorrhagic cystitis. Mesna binds and inactivates acrolein in the urine, preventing this. Adequate hydration also helps.

Explanation

Doxorubicin, an anthracycline, causes dose-dependent cardiotoxicity and cardiomyopathy through free-radical generation, and dexrazoxane is cardioprotective. Bleomycin causes pulmonary fibrosis, vincristine causes neuropathy and cisplatin causes nephrotoxicity.

Explanation

Vincristine, a vinca alkaloid that inhibits microtubule formation, characteristically causes peripheral neuropathy, its dose-limiting toxicity. Notably it produces relatively little myelosuppression, unlike vinblastine.

Explanation

Methotrexate inhibits dihydrofolate reductase. Folinic acid (leucovorin) bypasses the blocked enzyme, rescuing normal cells from toxicity while the tumour effect is preserved with correct timing.

Explanation

Insulin lispro, aspart and glulisine are rapid-acting analogues with onset within 15 minutes, used at mealtimes. Glargine and detemir are long-acting basal insulins, and NPH is intermediate-acting.

Explanation

Metformin, a biguanide, rarely causes lactic acidosis, especially in renal impairment, and is withheld around contrast studies and surgery. Unlike sulfonylureas it does not cause hypoglycaemia when used alone, and it is weight-neutral.

Explanation

Corticosteroids raise blood glucose and are diabetogenic, so hypoglycaemia is not expected. Chronic use causes osteoporosis, Cushingoid features, immunosuppression, cataracts and adrenal suppression on withdrawal.

Explanation

Propylthiouracil is preferred in the first trimester because methimazole and carbimazole are associated with fetal malformations such as aplasia cutis and choanal atresia early in pregnancy. Radioactive iodine is contraindicated in pregnancy.

Explanation

Aspirin irreversibly acetylates cyclooxygenase, blocking thromboxane A2 synthesis in platelets. Because platelets cannot synthesise new enzyme, the antiplatelet effect lasts the platelet's lifespan of 7 to 10 days.

Explanation

Colchicine relieves acute gout by inhibiting microtubule formation and neutrophil migration into the joint. Allopurinol and febuxostat lower urate for long-term prevention and can worsen an acute attack if started during one.

Explanation

First-generation H1 antihistamines cross the blood-brain barrier and cause sedation and anticholinergic effects. Second-generation agents such as cetirizine, loratadine and fexofenadine are less sedating because they penetrate the CNS poorly.

Explanation

Gastric mucosal prostaglandins, produced via COX-1, promote mucus and bicarbonate secretion and mucosal blood flow. NSAIDs inhibit their synthesis, reducing protection and predisposing to ulcers. Misoprostol, a prostaglandin analogue, is protective.

Explanation

Organophosphates inhibit acetylcholinesterase, causing a cholinergic crisis (DUMBELS). Atropine blocks the muscarinic effects while pralidoxime reactivates the enzyme if given before ageing of the enzyme-inhibitor complex.

Explanation

N-acetylcysteine replenishes hepatic glutathione, allowing conjugation and clearance of the toxic metabolite NAPQI. It is most effective within 8 hours of ingestion and prevents hepatic necrosis.

Explanation

Fomepizole inhibits alcohol dehydrogenase, preventing conversion of methanol to toxic formic acid, which causes the visual loss and acidosis. Ethanol is an alternative competitive substrate, and haemodialysis removes methanol in severe cases.

Explanation

Glucagon raises intracellular cAMP through a receptor independent of the beta adrenergic receptor, restoring heart rate and contractility in beta blocker overdose refractory to atropine. High-dose insulin-euglycaemia therapy is an adjunct.

Explanation

Gram-positive bacteria retain the crystal violet-iodine complex in their thick peptidoglycan wall and appear purple. Gram-negatives lose it during decolourisation and take up the safranin counterstain, appearing pink.

Explanation

Standard autoclaving uses saturated steam at 121 degrees C and 15 psi for 15 minutes, killing bacteria, viruses, fungi and spores. Moist heat denatures proteins more effectively than dry heat.

Explanation

The Ziehl-Neelsen stain identifies acid-fast bacilli such as Mycobacterium tuberculosis, whose mycolic-acid-rich walls retain carbol fuchsin despite acid-alcohol decolourisation, appearing red on a blue background.

Explanation

Cell-wall-active antibiotics such as beta-lactams work best in the log phase, when bacteria are actively dividing and synthesising peptidoglycan. Dormant cells in stationary phase are less susceptible.

Explanation

Lowenstein-Jensen, an egg-based medium, is used to grow Mycobacterium tuberculosis. Thayer-Martin is for gonococci, Loeffler for diphtheria and Bordet-Gengou for pertussis.

Explanation

Ethylene oxide gas sterilises heat- and moisture-sensitive items such as endoscopes and plastics. It is effective but toxic, requiring adequate aeration before the item is used.

Explanation

Both toxins ADP-ribosylate elongation factor-2, halting protein synthesis and killing the cell. Diphtheria toxin also produces a pseudomembrane in the throat and can cause myocarditis.

Explanation

Tetanospasmin blocks release of the inhibitory neurotransmitters GABA and glycine from spinal interneurons, causing unopposed motor activity with rigidity and spasms such as lockjaw and opisthotonos. Botulinum toxin by contrast blocks acetylcholine release, causing flaccid paralysis.

Explanation

Cholera toxin ADP-ribosylates the Gs protein, permanently activating adenylate cyclase and raising cAMP. This drives massive chloride and water secretion into the gut lumen, producing rice-water stools.

Explanation

Staphylococcus aureus is coagulase-positive, distinguishing it from coagulase-negative staphylococci such as S. epidermidis. All staphylococci are catalase-positive, which separates them from streptococci.

Explanation

Group A streptococcus, S. pyogenes, is beta-haemolytic, producing complete clearing on blood agar, and is bacitracin-sensitive. S. pneumoniae and viridans streptococci are alpha-haemolytic, giving partial greenish haemolysis.

Explanation

In neonates, Group B Streptococcus, Escherichia coli and Listeria monocytogenes are the leading causes of meningitis. In older children and adults, S. pneumoniae and N. meningitidis predominate.

Explanation

The high mycolic-acid content of the mycobacterial cell wall makes it acid-fast, resisting decolourisation by acid-alcohol. This waxy wall also confers resistance to many disinfectants and to drying.

Explanation

H. pylori produces urease, which splits urea into ammonia and neutralises gastric acid locally. The urea breath test detects this activity by measuring labelled carbon dioxide produced from ingested urea.