MLT GlobeBasic Pathology: Hemodynamic disorders – page 5
153 Basic Pathology MCQs on Hemodynamic disorders with answers and explanations.
Occlusion of a venous outflow, as in testicular torsion, or infarction in loose spongy tissue such as the lung typically produces which infarct?
Venous occlusion, dual circulation, loose tissue or reperfusion allow blood to collect in the infarcted zone, making it red. White infarcts follow arterial occlusion in solid organs.
Regardless of its cause, shock is fundamentally a state of:
Shock is circulatory failure causing widespread tissue hypoperfusion, from reduced cardiac output or reduced effective circulating blood volume. Single-organ ischaemia is infarction, not shock.
A trauma patient who has lost two litres of blood becomes hypotensive and tachycardic. The type of shock is:
Loss of blood or plasma volume, from haemorrhage, burns or severe fluid loss, reduces venous return and causes hypovolaemic shock. Cardiogenic shock results from pump failure.
Untreated shock evolves through stages. Which sequence is correct?
Shock begins with a compensated non-progressive phase, moves to a progressive phase with hypoperfusion and acidosis, and ends in an irreversible phase with lethal cellular injury.
A patient with an extensive myocardial infarction develops ventricular free-wall rupture and severe hypotension. The type of shock is:
Cardiogenic shock results from pump failure due to myocardial damage, rupture, arrhythmia or tamponade. Massive pulmonary embolism is now usually classed separately as obstructive shock.
Two days after a femoral shaft fracture, a young man becomes breathless and confused, with petechiae over the chest and axillae. The most likely diagnosis is:
Fat globules from fractured marrow enter the circulation 1–3 days after long-bone fracture, causing respiratory insufficiency, neurological symptoms and a petechial rash. Petechiae are not a feature of thromboembolism.
An elderly nursing-home resident arrives hypotensive (70/30 mm Hg), febrile and breathing rapidly. Her leukocyte count is 22 × 10⁹/L with marked neutrophilia, and her urine is teeming with Gram-negative rods. What type of circulatory collapse best explains her condition?
A urinary Gram-negative infection with fever, neutrophilia and hypotension points to sepsis; endotoxin-driven vasodilation causes septic shock. Nothing suggests pump failure, fluid loss or an allergic trigger.
A man immobilised in cervical traction after a neck injury develops a swollen, red, painful calf one week later; Doppler confirms deep vein thrombosis. Which element of Virchow's triad is chiefly responsible?
Prolonged bed rest slows venous return in the legs, and stasis is the dominant factor in DVT of immobilised patients. There was no calf trauma to injure endothelium.
A healthy bank cashier notices painless ankle and foot swelling after standing at her counter for a full shift. Which mechanism explains this oedema?
Prolonged standing pools blood in leg veins, raising capillary hydrostatic pressure and pushing fluid into tissues. She has no liver, kidney or lymphatic disease to cause the other mechanisms.
After a road accident with heavy bleeding, a man is unconscious with BP 60/40 mm Hg, a fast thready pulse and cold, clammy, bluish skin. Which form of shock is present?
Major blood loss lowers circulating volume, triggering sympathetic vasoconstriction (cold, clammy skin) and tachycardia. Neurogenic shock typically causes warm skin and bradycardia; septic shock needs infection.
Shock is best defined as:
Shock is systemic hypoperfusion from reduced cardiac output or effective circulating volume, leading to cellular hypoxia. Tachycardia is typical.
At autopsy, a brain shows flattened gyri, narrowed sulci and compressed ventricles after a large infarct. Which process explains these findings?
Brain edema may be localized (around an abscess or tumor) or generalized. Generalized swelling flattens gyri, narrows sulci and compresses ventricles; atrophy does the opposite.
A patient with long-standing heart failure has congested organs with scattered hemosiderin-laden macrophages, fibrosis and parenchymal cell loss. These findings indicate:
Long-term venous congestion causes chronic hypoxia, cell death, fibrosis and small hemorrhages that leave hemosiderin in macrophages.
In liver cirrhosis, which mechanism specifically lowers plasma oncotic pressure and so contributes to edema and ascites?
The cirrhotic liver makes less albumin, causing hypoalbuminemia. Urinary albumin loss is the mechanism in nephrotic syndrome; portal hypertension and sodium retention add to ascites.
According to Starling forces, which force mainly pulls fluid back from the interstitium into the venular end of capillaries?
Hydrostatic pressure pushes fluid out, while plasma oncotic pressure (mainly albumin) draws it back. Lymphatics remove the small excess.
A 30-year-old man with a femoral shaft fracture becomes suddenly breathless and confused on the third day after injury, with petechiae over his chest. The most likely cause is:
Fat embolism syndrome typically appears 1-3 days after long-bone fractures with respiratory insufficiency, neurologic signs, anemia and thrombocytopenia with petechial rash.
Which description does NOT apply to a typical arterial thrombus?
Arterial thrombi form under high flow on damaged endothelium, are pale, adherent and show lines of Zahn. Red, stasis-type thrombi are typical of veins.
Which of the following is NOT a recognized risk factor for deep venous thrombosis?
Immobility, heart failure (stasis), malignancy, advanced age and recent myocardial infarction all raise venous thrombosis risk. Early ambulation reduces stasis and lowers risk.
At autopsy of a patient with sudden left heart failure, the lungs show blood-filled alveolar capillaries with alveolar septal edema and focal intra-alveolar hemorrhage. The diagnosis is:
Acute pulmonary congestion shows engorged alveolar capillaries, septal edema and focal hemorrhage. Chronic congestion adds septal fibrosis and hemosiderin-laden 'heart failure cells'.
In which type of shock are widespread peripheral vasodilation and pooling of blood the principal mechanisms?
In septic shock, microbial products and cytokines cause systemic vasodilation and pooling. Hypovolemic shock is volume loss; cardiogenic shock is pump failure.