This is a real-world medical entrance exam question, please give the true answer based on the question and selection. Topic name: None, Subject name: Pathology
[{'content': 'True about shock -a) In early stage cardiac output and BP are maintainedb) There is decreased sympathetic activityc) Renin secretion may be increased d) Aldosterone secretion is decreased \nSelect and explain. \nA. a, B. bc, C. ac, D. b', 'role': 'user'}, {'content': 'Answer: C \nExplanation: Stages of shock \n\nShock tends to evolve through three general phages : -\n\nA. Non progressive (Initial or compensated reversible) shock\nIn the early stage of shock, there is activation of compensatory mechanisms that attempt to maintain adequate perfusion of the heart and brain, and to maintain adequate cardiac output and blood pressure.\nThese compensatory mechanisms include : -\n\t1. Due to decrease perfusion pressure, baroreceptors are stimulated that leads to increased sympathetic discharge & catecholamines release with reduced vagal activity. All these cause : -\n\ta)\xa0Peripheral vasoconstriction Cool clammy extrimities (In hyperdynamic stage of septic shock and in neurogenic shock the extrimities are warm due to vasodilatation).\n\tb)\xa0Tachycardia\n\t2. Decreased renal perfusion and sympathetic stimulation cause increased renin release from the kidney and activation of renin angiotensin system. So that : -\nAngiotensin II causes vasoconstriction and release of aldosterone.\nAldosterone causes fluid and salt conservation by kidney.\nIn this stage patient can be managed by correcting the underlying cause, e.g., fluid therapy in hypovolemic. Shock and control of infection in septic shock.\n\nB. Progressive (Decompensated reversible) shock\nDue to continued tissue hypoxia, aerobic respiration replaced by anaerobic glycolysis that leads to formation of lactic acid →\xa0Lactic acidosis & pH.\nAcidosis (↓ pH) causes blunting of venoconstrictor effect of catecholamine → Venodilatation → Pooling of blood in peripheral veins. As there is arteriolar constriction ( ↑ peripheral resistance) and venodilatation (↓ venous return) → Cardiac output is decreased.\nPeripheral pooling of blood and decreased cardiac output cause anoxic injury to endothelial cells that may cause DIC.\nDecreased perfusion to vital organs like brain causes mental confusion & drowsiness and decreased perfusion to kidney causes decline in urinary output.\nIn this stage patient can be managed but more aggresive management is required i.e., along with correction of underlying cause; intropic agent, vasopressor, oxygen and resuscitation may be required.\n\nC. Irreversible shock\nUnless there is intervention in previous stages, the process enters in an irreversable stage in which there is multiple organ damage.\nIn this stage survival is not possible even after intervention.', 'role': 'assistant'}]