BMED 450 - MIDTERM 1 EXAM
QUESTIONS WITH VERIFIED CORRECT
ANSWERS 2025-2026
loss of homeostasis CORRECT ANSWER overwhelming challenge
abnormal response or gene expression
thrombocytes CORRECT ANSWER cause vasoconstriction
(thromboxane) adhere to connective tissue under endothelium
form platelet plug
coagulation proteins CORRECT ANSWER activated by tissue factor from damaged ETCs
platelet phospholipids activate thrombin
thrombin CORRECT ANSWER activates fibrinogen to form fibrin clot
fibrinolysis proteins CORRECT ANSWER plasmin breaks down
clot ETCs release tissue plasminogen activator (t-PA)
relaxed endothelium CORRECT ANSWER anticoagulant NO
vasodilates prostacyclin (PGI2) dilates and inhibits platelet aggregation
inflammatory state CORRECT ANSWER endothelium produces
endothelin less PGI2 and NO = vasoconstriction
tissue factor
platelets produce thromboxane A2
B lymphocytes CORRECT ANSWER produce antibodies that coat pathogens
, helper T lymphocytes CORRECT ANSWER activate macrophages and lymphocytes
cytotoxic T lympocytes CORRECT ANSWER cause infected cells to apoptose
innate immunity components CORRECT ANSWER neutrophils,
granulocytes coagulation factors limit spread
complement reactants
3 factors that initiate thrombosis CORRECT ANSWER endothelial injury (prothrombotic molecules)
abnormal blood flow (turbulence or stasis)
hypercoagulability (genetic or acquired)
infective endocarditis CORRECT ANSWER Strep
viridans toxins kill endocardial and myocardial cells
dead cells cause stenosis
autonomic control of heart rate and contractility CORRECT ANSWER SNS: beta adrenergics
increase PNS: acetylcholine decrease
autonomic control of peripheral resistance CORRECT ANSWER SNS: alpha adrenergic contract
shock CORRECT ANSWER hypoperfusion
vasodilation
low blood volume
MAP <50mmHg
septic shock CORRECT ANSWER
bacterial lipopolysaccharide (LPS) endotoxin binds to TLR4 on macrophages and neutrophils = cytokine
storm
QUESTIONS WITH VERIFIED CORRECT
ANSWERS 2025-2026
loss of homeostasis CORRECT ANSWER overwhelming challenge
abnormal response or gene expression
thrombocytes CORRECT ANSWER cause vasoconstriction
(thromboxane) adhere to connective tissue under endothelium
form platelet plug
coagulation proteins CORRECT ANSWER activated by tissue factor from damaged ETCs
platelet phospholipids activate thrombin
thrombin CORRECT ANSWER activates fibrinogen to form fibrin clot
fibrinolysis proteins CORRECT ANSWER plasmin breaks down
clot ETCs release tissue plasminogen activator (t-PA)
relaxed endothelium CORRECT ANSWER anticoagulant NO
vasodilates prostacyclin (PGI2) dilates and inhibits platelet aggregation
inflammatory state CORRECT ANSWER endothelium produces
endothelin less PGI2 and NO = vasoconstriction
tissue factor
platelets produce thromboxane A2
B lymphocytes CORRECT ANSWER produce antibodies that coat pathogens
, helper T lymphocytes CORRECT ANSWER activate macrophages and lymphocytes
cytotoxic T lympocytes CORRECT ANSWER cause infected cells to apoptose
innate immunity components CORRECT ANSWER neutrophils,
granulocytes coagulation factors limit spread
complement reactants
3 factors that initiate thrombosis CORRECT ANSWER endothelial injury (prothrombotic molecules)
abnormal blood flow (turbulence or stasis)
hypercoagulability (genetic or acquired)
infective endocarditis CORRECT ANSWER Strep
viridans toxins kill endocardial and myocardial cells
dead cells cause stenosis
autonomic control of heart rate and contractility CORRECT ANSWER SNS: beta adrenergics
increase PNS: acetylcholine decrease
autonomic control of peripheral resistance CORRECT ANSWER SNS: alpha adrenergic contract
shock CORRECT ANSWER hypoperfusion
vasodilation
low blood volume
MAP <50mmHg
septic shock CORRECT ANSWER
bacterial lipopolysaccharide (LPS) endotoxin binds to TLR4 on macrophages and neutrophils = cytokine
storm
