MLT GlobeBasic Pathology: Hemodynamic disorders – page 3
153 Basic Pathology MCQs on Hemodynamic disorders with answers and explanations.
After a blow to the thigh, blood collects within the soft tissue as a palpable mass. This is a:
A haematoma is a localised collection of blood within tissue, which may be trivial or, if large, clinically important.
The clinical importance of a haemorrhage depends mainly on:
Rapid loss of 20% or more of blood volume can cause shock, while a small bleed in the brainstem can be fatal.
Deficiency of which vitamin causes perifollicular haemorrhages and bleeding gums from weak vessel walls?
Vitamin C is needed for collagen hydroxylation; scurvy weakens vessel support, causing petechiae and bleeding despite normal clotting tests.
Which thrombi seldom embolise but cause local pain, swelling and congestion?
Superficial (e.g., saphenous) vein thrombi rarely embolise. Deep vein thrombi are the main source of pulmonary emboli.
The most common inherited bleeding disorder is:
vWD affects about 1% of people, mostly type 1 with autosomal dominant inheritance. Haemophilia A is the commonest serious X-linked disorder.
Which of the following is NOT one of the three components of Virchow's triad for thrombosis?
Virchow's triad comprises endothelial injury, abnormal blood flow (stasis or turbulence) and hypercoagulability. Raised capillary permeability produces oedema, not thrombosis.
The prothrombin time (PT) evaluates the integrity of which part of the coagulation cascade?
PT uses tissue factor (thromboplastin) and detects deficiencies of factors VII, X, V, II and fibrinogen. The aPTT assesses the intrinsic and common pathways.
A thrombus adhering to the wall of a dilated left ventricle or to the aortic lumen is called a:
Thrombi attached to the wall of heart chambers or the aorta are mural thrombi. Vegetations are thrombi on heart valves; phlebothrombosis refers to venous thrombi.
In infective endocarditis, thrombi attached to the heart valves are known as:
Thrombi on cardiac valves are called vegetations; in infective endocarditis they contain microbes and may embolise. Mural thrombi attach to chamber walls.
A large pulmonary embolus found straddling the bifurcation of the main pulmonary artery is called:
A saddle embolus lodges across the bifurcation of the pulmonary trunk; it can cause sudden death from acute right heart failure.
Deep venous thrombi of the leg most commonly embolise to:
Venous emboli travel through the right heart to the pulmonary circulation. Reaching the systemic circulation requires a right-to-left shunt (paradoxical embolism).
The main consequence of an embolus that occludes a systemic artery is:
Arterial emboli block blood supply, causing ischaemic necrosis (infarction) of the territory supplied. Collateral circulation may lessen the damage.
A diver who ascends too quickly develops painful joints and muscles due to nitrogen bubbles in the tissues. This condition is called:
In decompression sickness, nitrogen comes out of solution; bubbles in muscles and around joints produce the bends, whereas lung involvement causes the chokes.
The most common inherited cause of hypercoagulability results from a point mutation in:
Factor V Leiden resists inactivation by activated protein C, and is the commonest inherited thrombophilia in populations of European descent; prothrombin G20210A is second.
An embolus is a detached mass carried from its point of origin to a distant site by:
An embolus is any detached intravascular solid, liquid or gaseous mass transported by the blood to a distant site, where it may cause infarction.
Arterial and intracardiac thrombi typically begin at sites of:
Endothelial damage exposes subendothelial collagen and tissue factor, initiating platelet adhesion and coagulation; it is the dominant factor in arterial and cardiac thrombi.
Alternating pale layers of platelets and fibrin with darker layers of red cells, seen microscopically in a thrombus formed in flowing blood, are called:
Lines of Zahn indicate that a thrombus formed in flowing blood before death, helping distinguish it from a postmortem clot.
Sudden, widespread formation of fibrin thrombi in the microcirculation, with consumption of platelets and clotting factors, is known as:
DIC causes microvascular thrombosis and consumption of platelets and factors, leading to bleeding; labs show prolonged PT/aPTT, low fibrinogen and raised D-dimer.
Damaged tissue initiates the extrinsic coagulation pathway by exposing:
Tissue factor on subendothelial cells binds factor VIIa to activate factor X, starting the extrinsic pathway. Fibrinogen is the substrate converted to fibrin at the end.
Platelet adhesion to exposed subendothelial collagen is mediated chiefly by:
vWF bridges platelet glycoprotein Ib to collagen. Deficiency of vWF or GPIb (Bernard-Soulier) impairs adhesion and causes mucocutaneous bleeding.