Hypertension
Q: What is hypertension?
A: A chronic elevation of systemic arterial blood pressure, usually defined as ≥140/90 mmHg (or per current guideline cutoffs).
Q: What is a thrombus?
A: A blood clot that forms within a vessel or the heart and remains attached to the site where it formed.
Q: What is peripheral artery disease (PAD)?
A: Atherosclerotic occlusive disease of arteries supplying the extremities, most commonly the legs.
Q: What is superior vena cava (SVC) syndrome?
A: Obstruction of the superior vena cava that impairs venous return from the head, neck, and upper extremities.
Q: What is a myocardial infarction (MI)?
A: Necrosis (death) of heart muscle caused by prolonged ischemia, usually from acute blockage of a coronary artery by a ruptured atherosclerotic plaque and thrombus.
Q: What is the difference between primary and secondary hypertension?
A: Primary (essential) hypertension has no identifiable single cause; secondary hypertension is due to an identifiable underlying condition (e.g., kidney disease, endocrine disorders).
Q: What is an embolus?
A: A thrombus or other material (e.g., fat, air) that has broken loose and travels through the bloodstream to lodge in a distant vessel.
Q: What is the hallmark symptom of PAD?
A: Intermittent claudication—leg pain or cramping with exertion that is relieved by rest.
Q: What are common causes of SVC syndrome?
A: Malignancies in the mediastinum (e.g., lung cancer, lymphoma) and intravascular thrombosis around central venous catheters.
Q: What are the classic symptoms of an acute MI? Name 4
A: Prolonged chest pain or pressure (often radiating to arm, neck, jaw, or back), shortness of breath, diaphoresis, nausea/vomiting, and a sense of impending doom; symptoms may be atypical in women, older adults, and diabetics.
Q: How does long‑standing hypertension damage target organs?
A: It causes vascular remodeling and atherosclerosis leading to heart failure, stroke, chronic kidney disease, retinopathy, and peripheral vascular disease.
Q: What is a thromboembolism?
A: An embolus that originated from a thrombus, often causing obstruction at a distant site (e.g., pulmonary embolism from a DVT).
Q: What complications can severe PAD cause?
A: Critical limb ischemia, non‑healing ulcers, gangrene, and possible limb loss.
Q: What are typical clinical signs of SVC syndrome?
A: Swelling of the face, neck, and upper limbs; distended neck and chest veins; dyspnea; and headache.
Q: Which cardiac biomarkers are most important in diagnosing MI?
A: Cardiac troponins (I or T) are the most specific and sensitive; CK‑MB may also rise but is less specific.
Q: What are major risk factors for developing hypertension? Name 3
A: Family history, age, obesity, high sodium intake, smoking, excessive alcohol, sedentary lifestyle, diabetes, and dyslipidemia.
Q: What is deep vein thrombosis (DVT)?
A: A blood clot that forms in a deep vein, usually in the legs, which can embolize to the lungs.
Q: What physical assessment findings may indicate advanced peripheral artery disease (PAD) in the lower extremities?
A: Diminished or absent peripheral pulses, cool and pale skin, shiny hairless legs, delayed capillary refill, and in severe cases dependent rubor and non-healing ulcers on toes or feet.
Q: How do ECG changes in NSTEMI/unstable angina differ from those in STEMI?
A: NSTEMI/unstable angina typically show ST‑segment depression and/or T‑wave inversion without persistent ST‑segment elevation or development of pathologic Q waves.
Q: What is the main difference between STEMI and NSTEMI?
A: STEMI involves full‑thickness (transmural) myocardial injury with ST‑segment elevation on ECG; NSTEMI involves subendocardial injury with elevated troponins but no persistent ST‑segment elevation.
Q: What is arteriosclerosis?
A: A general term for thickening, hardening, and loss of elasticity of arterial walls.
Q: What classic triad (Virchow’s triad) predisposes to thrombosis?
A: Endothelial injury, stasis or turbulent blood flow, and hypercoagulability.
Q: Why does elevating the legs worsen symptoms in patients with PAD?
A: Elevation further reduces arterial blood flow to already ischemic tissues, increasing pain and pallor; blood flow (and pain relief) often improve when the legs are placed in a dependent (dangling) position.
Q: What are the classic ECG changes seen in a STEMI (transmural myocardial infarction)?
A: ST‑segment elevation in the leads overlying the injured area, often with reciprocal ST depression in opposite leads, followed later by T‑wave inversion and development of pathologic Q waves.
Q: Why is “time is muscle” an important concept in MI management?
A: The longer coronary blood flow is blocked, the more myocardium becomes irreversibly damaged, so rapid reperfusion (PCI or thrombolytics) greatly improves outcomes.