Chapter 15_2 flashcards

Question 1

Hyperlipidemia: Definition & Significance

Answer 1

Elevated levels of lipids (cholesterol, triglycerides) in bloodstream. Major condition leading to atherosclerosis. High LDL and low HDL are key concerns.

Question 2

Familial Hypercholesterolemia (FH): Definition & Genetics

Answer 2

Genetic condition causing elevated LDL-C from birth, leading to premature atherosclerotic CVD. Most common genetic cause of CVD (~1 in 220 persons). Commonly polygenic (LDLR, APOB, APOE, PCSK9 gene variants).

Question 3

Hyperlipidemia: Risk Factors

Answer 3

Familial hypercholesterolemia, Diabetes mellitus, Obesity, Hypothyroidism, Sedentary lifestyle, Diet high in saturated/trans fats, Medications (progestins, corticosteroids).

Question 4

Hyperlipidemia: Signs & Symptoms (Overt)

Answer 4

Often lacking. May include: Xanthoma (cholesterol deposits under skin), Xanthelasma (cholesterol deposits around eyes), Arcus senilis (yellow-white ring around cornea).

Question 5

Hyperlipidemia: Diagnosis (Lipid Panel - Desirable Levels)

Answer 5

Total Cholesterol: <200 mg/dL (optimal); <150 mg/dL (ideal for high ASCVD risk). LDL: <100 mg/dL (optimal); <70 mg/dL (ideal for high ASCVD risk). HDL: >60 mg/dL (ideal/cardioprotective). Triglycerides: <150 mg/dL (ideal). Also assess hs-CRP, homocysteine.

Question 6

Hyperlipidemia: Treatment (Lifestyle & Medications)

Answer 6

Lifestyle: Diet low in cholesterol (<300mg/day) & saturated/trans fats, regular physical activity. Medications: Statins (HMG-CoA reductase inhibitors - first line, e.g., atorvastatin), Bile acid sequestrants (cholestyramine), Fibrates (gemfibrozil for high TGs), Ezetimibe, PCSK9 inhibitors (monoclonal antibodies like evolocumab).

Question 7

Hypertension (HTN): Definition & General Criteria

Answer 7

Elevated Blood Pressure. “Silent killer.” General criteria: 2 or more BP readings of DBP >80 mmHg or SBP >130 mmHg on separate visits.

Question 8

Hypertension: Categories (AHA/ACC 2017)

Answer 8

Normal: <120/80. Elevated: 120-129 SBP AND <80 DBP. Stage 1 HTN: 130-139 SBP OR 80-89 DBP. Stage 2 HTN: =140 SBP OR =90 DBP. Hypertensive Crisis: >180 SBP AND/OR >120 DBP.

Question 9

Hypertension: Primary vs. Secondary

Answer 9

Primary (Essential) HTN: 95% of cases, etiology unknown. Secondary HTN: Due to underlying disease (e.g., kidney disease, Cushing’s, pheochromocytoma).

Question 10

Hypertension: Risk Factors

Answer 10

Age, African American ethnicity, obesity, family history, diabetes mellitus, tobacco use, stress, excessive alcohol, high sodium/low potassium diet, high renin secretor, angiotensin II hypersensitivity.

Question 11

Hypertension: Pathological Effects on Arteries & Heart

Answer 11

Arteries: High shearing stress on arterial walls -> endothelial injury -> atherosclerosis; damage to retina, kidneys, brain, lower extremities. Heart: LV hypertrophy (LVH) due to increased afterload -> coronary blood supply may become inadequate -> ischemia/MI risk.

Question 12

Hypertension: Assessment & Diagnosis

Answer 12

Often no symptoms. Assess for target organ damage (headaches, chest pain, vision changes, dizziness). Measure BP correctly (seated 5min, no recent caffeine/exercise/smoking, 2 readings averaged on 2 separate days). Fundoscopic exam for retinopathy. Check PMI for LVH. Listen for bruits. Rule out secondary causes. ECG, urinalysis (proteinuria), CBC, electrolytes, glucose.

Question 13

Hypertension: Treatment (Lifestyle & Medications)

Answer 13

Lifestyle: DASH diet (low sodium, low fat, rich in fruits/veg/whole grains), stress reduction, physical activity, smoking cessation. Medications: Diuretics, ACE inhibitors, ARBs, Calcium channel blockers (CCBs), Beta-adrenergic blockers. Specific choices based on patient profile (e.g., JNC-8 recs for African Americans, diabetics).

Question 14

Atherosclerosis: Definition & Pathophysiology Stages

Answer 14

Gradual process of atherosclerotic plaque buildup on arterial walls, initiated by endothelial injury. Stages: 1. Endothelial injury & inflammation (WBCs/platelets attracted). 2. LDL deposition; WBCs (macrophages) engulf LDL -> foam cells. 3. Foam cells release lipids -> fatty streaks. 4. Fibroblasts invade -> fibrous plaque, arterial wall stiffens/narrows, vasodilation capacity decreases. 5. Plaque calcifies, becomes fragile (atheroma). 6. Plaque rupture -> thrombus formation -> embolism/occlusion.

Question 15

Atherosclerosis: Risk Factors (Modifiable & Nonmodifiable - Table 15-4)

Answer 15

Nonmodifiable: Age, gender (males earlier, postmenopausal women catch up), race/ethnicity (African Americans higher risk), family history. Modifiable: Diet (high sat fat/cholesterol/salt, low K+/folate), physical inactivity, obesity, smoking, excessive alcohol, stress, HTN, diabetes.

Question 16

Atherosclerosis: Clinical Manifestations & Diagnosis

Answer 16

Often asymptomatic until organ dysfunction. Signs of CVD (obesity, SOB, cyanosis, rapid pulse, high BP, weak peripheral pulses, bruits, retinal changes). Diagnosis: Lipid profile, hs-CRP, homocysteine. Imaging: Calcium CT scan, cardiac angiography (gold standard for CAD), intravascular ultrasound.

Question 17

Atherosclerosis: Treatment

Answer 17

Same as hyperlipidemia (lifestyle, statins, etc.). Revascularization procedures for significant blockages: Coronary Artery Bypass Graft (CABG) or Percutaneous Coronary Intervention (PCI) like angioplasty with stent.

Question 18

Peripheral Arterial Disease (PAD): Definition & Common Site

Answer 18

Arteriosclerosis/atherosclerosis outside coronary arteries, most often in lower extremities. Most common site: femoral artery above knee.

Question 19

PAD: Risk Factors & Key Symptom

Answer 19

Same as atherosclerosis (diabetes accelerates). Key Symptom: Intermittent claudication (cramping leg pain with exertion, relieved by rest). Pain at rest indicates critical limb ischemia.

Question 20

PAD: Assessment & Diagnosis

Answer 20

Examine for diminished/absent pulses (compare bilaterally), palpable coolness, paresthesias, pallor, delayed capillary refill (<2s normal). Ankle-Brachial Index (ABI): Compares ankle SBP to brachial SBP. Normal =1; <1 indicates PAD; <0.4 severe PAD. Ultrasound, angiography.

Question 21

PAD: Treatment

Answer 21

Lifestyle modification (exercise for collateral circulation). Medications (cholesterol-lowering, antihypertensives, platelet inhibitors like aspirin/clopidogrel, vasodilators like cilostazol). Thrombolytics for acute occlusion. Revascularization: Endovascular (angioplasty, stent) or open surgical bypass graft.

Question 22

Aneurysm: Definition & Common Locations

Answer 22

Weakening in an arterial wall causing localized bulging or dilation, susceptible to rupture and thrombus formation. Common locations: Cerebral arteries (“berry aneurysms” on circle of Willis), Aorta (most common: Abdominal Aortic Aneurysm - AAA).

Question 23

Aneurysm: Types (True vs. False; Fusiform vs. Saccular)

Answer 23

True: Involves all 3 vessel wall layers. False: Hematoma where clot is outside arterial wall. Fusiform: All layers dilate equally (spindle shape). Saccular: Weakness on one side, pouchlike bulge.

Question 24

Aneurysm: Risk Factors & Presentation

Answer 24

Risk: Atherosclerosis, smoking, HTN, genetic predisposition (Marfan’s, Ehlers-Danlos, ADAMTS2 variant for cerebral, fibrillin-1 for aortic). Presentation: Often asymptomatic until rupture. AAA: abdominal/back pain, pulsatile mass (in thin patient), bruit. Cerebral: headache, cranial nerve dysfunction; rupture -> SAH (“thunderclap” headache).

Question 25

Aneurysm: Diagnosis & Treatment

Answer 25

Diagnosis: Often incidental. AAA: Ultrasound (choice for detection/follow-up), CT, MRA. Cerebral: MRA, CT angiography. Treatment: Smoking cessation, BP regulation. AAA: Monitor; surgery (endovascular repair/graft) if >4.5 cm or symptomatic. Cerebral: Microsurgical clipping, endovascular coiling.

Question 26

Aortic Dissection: Definition & Pathophysiology

Answer 26

Tear in tunica intima of aorta -> blood flows between layers (intima and media), splitting them, forming a false lumen. Potentially lethal. Stanford Type A (ascending aorta, proximal) vs. Type B (arch/descending aorta, distal).

Question 27

Aortic Dissection: Etiology, Symptoms & Diagnosis

Answer 27

Etiology: HTN (>70% cases), arteriosclerosis, connective tissue disorders (Marfan's), genetic (MYLK, ACTA2). Symptoms: Sudden, severe "ripping" or "tearing" chest/back pain. Pallor, tachycardia, variable BP (may differ between arms >20mmHg). Signs of aortic regurgitation or cardiac tamponade. Neurological deficits (syncope). Diagnosis: ECG, Chest x-ray, CT scan, MRI. Transesophageal echocardiogram (TEE) best for arch.

Question 28

Vasculitis: Definition & Classification

Answer 28

Inflammation of arterial walls, often autoimmune. Classified by vessel size: Large (Temporal Arteritis, Takayasu Arteritis), Medium (Polyarteritis Nodosa, Kawasaki Disease), Small (Raynaud's Disease, Thromboangiitis Obliterans).

Question 29

Temporal Arteritis (Giant Cell Arteritis): Characteristics & Complication

Answer 29

Inflammation of superficial temporal arteries (and other large/medium). >50 yrs, European descent, women > men. Most common symptom: new-onset headache. Complication: Blindness (ophthalmic artery involvement). Associated with Polymyalgia Rheumatica (PMR). Diagnosis: Elevated ESR/CRP, temporal artery biopsy. Treatment: Steroids, low-dose aspirin.

Question 30

Takayasu Arteritis: Characteristics

Answer 30

Inflammation of aorta and major branches. Young women (<50 yrs), Asian/Indian descent. 3 stages: Flulike -> Arterial inflammation (stenosis, aneurysms, ischemia) -> Fibrotic changes (remission/relapse). Diagnosis: Elevated ESR/CRP, angiography. Treatment: Corticosteroids, cytotoxic agents, anti-TNF/IL-6 agents.

Question 31

Polyarteritis Nodosa (PAN): Characteristics

Answer 31

Necrotizing inflammation of small/medium arteries (often at bifurcations), entire arterial wall affected. Leads to aneurysms, thrombosis, ischemia. Associated with viral infections (HBV). Symptoms: Vague flu-like, TIAs, neuropathy, skin lesions, GI pain, renal involvement (HTN). Diagnosis: Angiography, biopsy. Treatment: Corticosteroids, immunosuppressants.

Question 32

Kawasaki's Disease: Target Population & Arteries Affected

Answer 32

Vasculitis affecting children, predominantly coronary arteries. Associated with infections. Death may occur from MI.

Question 33

Kawasaki's Disease: Stages & Symptoms

Answer 33

4 Stages: Acute (high fever, conjunctivitis, hand/foot erythema/edema, strawberry tongue, lymphadenopathy), Subacute (fever abates, desquamation, thrombocytosis, coronary aneurysms develop - highest risk for sudden death), Convalescent (resolution of signs), Chronic (cardiac complications persist). Diagnosis: Clinical criteria, echocardiogram for aneurysms. Treatment: IV immunoglobulin (IVIg), aspirin.

Question 34

Raynaud's Disease/Phenomenon: Characteristics

Answer 34

Vasospasm in arterioles of hands (sometimes feet), often triggered by cold/stress. Disease (primary) vs. Phenomenon (secondary to other conditions e.g. autoimmune). Thought to be exaggerated SNS response, low NO, high endothelin. Signs: Classic triad of color change in digits - pallor (white), cyanosis (blue), rubor (red).

Question 35

Thromboangiitis Obliterans (TAO / Buerger’s Disease): Characteristics

Answer 35

Inflammatory disorder of small/medium arteries and veins of hands/feet (vasospasm, thrombus). Young adult males who smoke. Symptoms: Deep red skin, coolness, claudication of hands/feet, ischemic ulcerations, gangrene. Diagnosis: Angiogram ("corkscrew" collaterals). Treatment: Smoking cessation (critical), vasodilators, exercise.

Question 36

Arterial Ulcers: Characteristics & Location

Answer 36

Ischemic skin wounds from lack of blood flow (PAD). Extremity pale, diminished pulses, delayed capillary refill. Ulcers usually located distally: tips of toes, heel, lateral malleolus. Painful, worsened by elevation.