Free NEET PG & INI-CET Physiology MCQs

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.

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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.

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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.

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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.

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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.

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

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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.

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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.

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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.

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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.

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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.

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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.

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

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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

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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.

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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.

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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.