MLT GlobeBasic Pathology: Hemodynamic disorders – page 8
153 Basic Pathology MCQs on Hemodynamic disorders with answers and explanations.
Months after severe postpartum haemorrhage, a woman has failure of lactation, amenorrhoea and lethargy. The pituitary damage is best explained by:
In Sheehan syndrome, the pituitary enlarged in pregnancy becomes ischaemic during hypovolaemic shock and undergoes infarction, causing hypopituitarism.
In neurogenic shock following spinal cord injury, the hypotension is primarily due to:
Interruption of sympathetic outflow causes arterial and venous dilation, pooling of blood and hypotension, often with bradycardia and warm skin. Blood loss causes hypovolaemic shock.
A young woman with jaundice and ascites has hepatic vein thrombosis. Liver biopsy shows markedly dilated, blood-filled sinusoids around the central veins. This reflects:
Blocked hepatic veins (Budd–Chiari) prevent blood leaving the liver, so it pools in centrilobular sinusoids: passive congestion. Active hyperaemia is arteriolar dilation that increases inflow.
A woman with recurrent epistaxis and heavy periods has normal PT, APTT and platelet count but low von Willebrand factor activity. Which haemostatic step is primarily defective?
VWF bridges platelet GPIb to exposed subendothelial collagen; its deficiency impairs adhesion. Aggregation depends on GPIIb/IIIa and fibrinogen, which are normal here.
Shortly after acute heart failure, the liver shows distended central veins and sinusoids, with some centrilobular hepatocyte loss, while periportal cells are spared. This is:
In acute hepatic congestion, blood distends central veins and sinusoids; centrilobular hepatocytes may become ischemic while better-oxygenated periportal cells survive.
Factor XII deficiency prolongs the APTT but causes no bleeding tendency. This is because in vivo coagulation is started by:
Physiologically, exposed tissue factor binds factor VIIa to launch coagulation; the contact pathway is important in vitro only.
In pure hypovolaemic shock, the lungs are relatively spared because they are resistant to:
The lungs resist hypoxia and are unaffected in uncomplicated hypovolaemic shock; lung damage (ARDS) is more typical of septic shock.
At autopsy, which feature distinguishes a postmortem clot from an antemortem venous thrombus?
Postmortem clots are gelatinous, unattached, with dark red lower and yellow 'chicken fat' upper portions. Antemortem thrombi are firmly attached, friable and may show lines of Zahn.
Systemic arterial emboli most frequently lodge in which site?
About three-quarters of systemic emboli lodge in the lower limbs and about 10% in the brain; kidneys, intestine, spleen and upper limbs are less often affected.
In platelets, P-selectin (CD62P) is stored until activation within:
P-selectin sits in platelet alpha granules (and endothelial Weibel-Palade bodies) and moves to the surface on activation; flow cytometry for CD62P is a marker of platelet activation. Dense granules hold ADP, serotonin and calcium.
Bacterial superantigens cause massive cytokine release because they:
Superantigens bind outside the peptide groove, linking MHC II to T-cell receptor Vβ chains and activating up to 20% of T cells polyclonally, causing a cytokine storm.
Pro-inflammatory cytokines such as TNF and IL-1 promote coagulation in sepsis mainly by increasing endothelial and monocyte expression of:
TNF and IL-1 induce tissue factor and reduce natural anticoagulants, contributing to DIC in sepsis. Thrombomodulin, t-PA and antithrombin are antithrombotic.
As shock enters its progressive stage, why does blood begin to pool in the microcirculation?
In progressive shock, anaerobic metabolism causes lactic acidosis; the low pH blunts the vasomotor response, arterioles dilate and blood pools, worsening output and hypoxia. Reflex compensation belongs to the earlier non-progressive stage.