B.
Administration of hyperosmolar agents (e.g., mannitol) or hypertonic saline to reduce cerebral edema.
✓
A.
Peripheral neuropathy.
✓
B.
Bacterial colonization and vegetation on heart valves, potentially leading to septic emboli and systemic infection.
✓
C.
Autoimmune response.
✓
D.
Valvular calcification.
✓
A.
Increased cerebral blood flow.
✓
B.
Cerebral vasoconstriction due to decreased PCO2? and decreased ionized calcium.
✓
C.
Decreased oxygen levels.
✓
D.
Increased heart rate.
✓
A.
Direct kidney damage.
✓
B.
Severe renal vasoconstriction in the setting of advanced liver disease, without primary kidney pathology.
✓
D.
Glomerular inflammation.
✓
A.
Excess catecholamines.
✓
B.
Deficiency of cortisol and aldosterone, leading to volume depletion and vascular collapse.
✓
C.
Increased blood pressure.
✓
B.
To urgently achieve reperfusion of the ischemic myocardium to limit infarct size and preserve cardiac function.
✓
C.
To prevent infection.
✓
D.
To reduce fluid overload.
✓
A.
Increased bone formation.
✓
B.
Impaired calcium and phosphate homeostasis, leading to bone remodeling abnormalities.
✓
C.
Decreased parathyroid hormone.
✓
D.
Increased Vitamin D activation.
✓
A.
Increases insulin secretion.
✓
B.
Inhibits sodium-glucose co-transporter 2 in the renal tubules, leading to increased glucose excretion in the urine.
✓
C.
Decreases hepatic glucose production.
✓
D.
Increases insulin sensitivity.
✓
B.
Deep vein thrombosis (DVT), requiring urgent anticoagulation to prevent pulmonary embolism.
✓
A.
Localized clot formation.
✓
B.
Widespread activation of coagulation and fibrinolysis, leading to simultaneous thrombosis and bleeding.
✓
C.
Platelet destruction only.
✓
