D236 Pathophysiology - Set 5 - Part 3

Correct Answer: Hyperuricemia complex

Rapid tumor cell lysis releases uric acid, potassium, and phosphate causing hyperuricemia, hyperkalemia, and hyperphosphatemia requiring urgent treatment.
Option a is incorrect because while hypocalcemia occurs from phosphate binding, multiple metabolic abnormalities occur simultaneously described.
Option c is incorrect because glucose typically remains normal; the syndrome involves uric acid and electrolyte abnormalities.
Option d is incorrect because sodium isn't primarily affected; potassium, phosphate, and uric acid elevations characterize this syndrome.

Correct Answer: Antibody types

Different autoantibodies characterize each condition with anti-Jo-1 in polymyositis and anti-Mi-2 in dermatomyositis among others distinguishing them.
Option a is incorrect because both affect proximal muscles similarly; antibody profiles and skin involvement distinguish them primarily.
Option c is incorrect because age ranges overlap; the antibody patterns and skin changes distinguish these myositis types.
Option d is incorrect because treatment approaches are similar; antibody profiles help distinguish and predict clinical course.

Correct Answer: Decreased metabolism

Reduced metabolic rate during hypothermia decreases oxygen demand, providing protection during reduced perfusion or cardiac arrest.
Option a is incorrect because metabolism decreases, not increases; this reduction provides the protective effect described here.
Option c is incorrect because glucose production changes aren't the protective mechanism; reduced metabolic demand provides protection.
Option d is incorrect because protein synthesis decreases; the overall metabolic reduction protects against ischemic damage described.

Correct Answer: Tetanospasmin

Tetanospasmin blocks inhibitory neurotransmitter release causing unopposed muscle contraction and characteristic spastic paralysis in tetanus infection.
Option b is incorrect because botulinum toxin blocks acetylcholine causing flaccid paralysis, opposite of tetanus spasms described.
Option c is incorrect because diphtheria toxin affects protein synthesis causing cardiac and neural damage, not spastic paralysis.
Option d is incorrect because cholera toxin causes secretory diarrhea through cyclic AMP, not the muscle spasms described.

Correct Answer: Podocyte foot processes

Podocyte foot process effacement disrupts glomerular filtration barrier causing selective proteinuria while basement membrane appears normal microscopically.
Option a is incorrect because basement membrane appears normal in minimal change disease; podocyte changes cause proteinuria described.
Option c is incorrect because mesangial cells aren't primarily affected; podocyte foot process fusion causes the proteinuria.
Option d is incorrect because tubular damage causes different problems; glomerular podocyte changes cause nephrotic syndrome described.

Correct Answer: Myelin degradation

B12 deficiency causes posterior column demyelination affecting proprioception and vibration while motor function remains initially preserved.
Option a is incorrect because myelin damage occurs before axonal degeneration in B12 deficiency neuropathy described here.
Option c is incorrect because neurons survive initially; the myelin degradation causes the sensory deficits described first.
Option d is incorrect because synaptic function remains; the myelin loss in posterior columns causes position sense loss.

Correct Answer: Membrane defect

PNH involves defective GPI-anchored proteins making red cells sensitive to complement-mediated lysis, worse during sleep-related acidosis.
Option a is incorrect because PNH isn't antibody-mediated; it's an intrinsic membrane defect causing complement sensitivity described.
Option c is incorrect because enzyme deficiencies cause different hemolytic patterns; PNH involves membrane anchor defects specifically.
Option d is incorrect because hemoglobin is normal in PNH; the membrane protein defect causes complement-mediated hemolysis.

Correct Answer: Massive dilation

Toxic megacolon involves severe colonic dilation with systemic toxicity risking perforation, requiring urgent surgical intervention typically.
Option a is incorrect because while perforation risk exists, the massive dilation itself defines toxic megacolon requiring intervention.
Option c is incorrect because strictures cause obstruction over time; toxic megacolon involves acute severe dilation described.
Option d is incorrect because fistulas are different complications; toxic megacolon specifically involves dangerous colonic dilation described.

Correct Answer: ADH production

Central DI lacks ADH production while nephrogenic DI has normal ADH but kidney resistance, requiring different treatments.
Option a is incorrect because both cause polyuria; the distinction is ADH deficiency versus resistance to ADH.
Option c is incorrect because both can cause hypernatremia; ADH production versus response distinguishes these conditions clearly.
Option d is incorrect because both cause polydipsia; the mechanism of ADH deficiency versus resistance distinguishes them.

Correct Answer: Receptor desensitization

Chronic opioid exposure causes receptor desensitization and downregulation requiring higher doses for equivalent analgesic effect over time.
Option a is incorrect because receptors aren't destroyed; they become less responsive through desensitization mechanisms described here.
Option c is incorrect because mutations don't occur; the receptors undergo functional desensitization with chronic stimulation described.
Option d is incorrect because receptor numbers typically decrease, not increase; desensitization reduces response to opioids.