Cardio Mod 5 Flashcards

Question

Clinical for PAD

Answer 1

• MC in lower vs upper extremities • Symptoms: (i) Intermittent claudication = most common 1. Pain/cramping/tightness/uncomfortable, or fatigue in the legs that occurs during exercise (walking) and is relieved by rest. a. this exertional pain pattern is similar to stable angina pectoris (reversible ischemia) 2. Common in the calves but may experience symptoms in feet or proximal LE (thighs/ hips/buttocks) 3. DDx - neurogenic vs intermittent claudication a. neurogenic: “positional” relief b. vascular (intermittent) claudication: “exertional” relief 4. As severity of peripheral plaques progress then exercise tolerance diminishes as noted by an earlier onset of symptoms with walking/exercise. (ii) Rest pain 1. usually worse distally, is aggravated by leg elevation (often causing pain at night), and lessens when the leg is below heart level. 2. The pain may be burning, tightening, or aching, although this finding is nonspecific. (iii) “Asymptomatic” patients with PAD 1. Estimated that 20% of patients with PAD are asymptomatic due to CAD limitations a. i.e. patients simply aren’t active enough to provoke LE claudication

Answer 2

* Inflammation of peripheral arteries | * STRONGLY associated with tobacco use (95% of cases related to smoking)

Answer 3

(i) Inflammatory response (ii) Thrombi and arterial vasospasm may be present (iii) Potential to damage small arteries (iv) NO atherosclerotic changes in effected blood vessels

Answer 4

(i) Common regions: 1. Arteries of distal extremities (ii) Common symptoms: 1. Distal extremity ischemic pain of involved region at rest 2. Distal extremity ischemic ulcers (iii) Intervention strategies: 1. eliminate tobacco exposure 2. pharmaceuticals to improve circulation (vasodilators, etc..)

Answer 5

* Vasospasms of small arteries/arterioles in distal UE (occasionally distal LE) * Abnormal temperature tolerance/responses

Answer 6

(i) Dysfunction of NO (nitric oxide) and sympathetic feedback mechanisms for blood vessel dilation/constriction (ii) Genetic predisposition

Answer 7

(i) Raynaud Phenomenon (secondary Raynaud) 1. Secondary complication of other systemic conditions a. scleroderma, chemotherapy, malignancy, hypothyroidism, etc… (see text for list) (ii) Raynaud Disease (primary Raynaud) 1. Primary vasospastic disorder – etiology not clear 2. Primary Raynaud is not usually as severe as secondary

Answer 8

(i) Raynaud Phenonmenon (secondary) 1. address primary condition/disease causing the Raynaud’s (ii) Raynaud Disease (primary) 1. pharmaceutical strategies to optimize blood flow (vasodilators) 2. avoid vasocontricting triggers (nicotine, cold, stress, etc…)

Answer 9

• Normal < 120/80 mmHg • Pre-hypertension: systolic = 120-139 or diastolic = 80-89 • Stage 1 = systolic = 140-159 or diastolic = 90-99 • Stage 2 = systolic >160 or diastolic > 100 b. Elevated systolic can be most damaging to organs in the long run c. Diagnosed on two or more separate readings of HTN

Answer 10

``` a. Primary HTN • “essential HTN” or “idiopathic HTN” • MC form of HTN 90 -95% individuals with HTN b. Secondary HTN • HTN 2° to a primary disease process • Ex: renal or endocrine disorders ```

Answer 11

1. increased HR 2. increased vascular resistance a. chronic vascular remolding (“new normal” vasoconstriction) 3. promote insulin resistance a. insulin plays role in NO production/signaling 4. promotes coagulation a. increased vasospasm and thrombus formation

Answer 12

1. RAAS responds to decreased pressure/volume and encourage renal retention of salt and H2O 2. Dysfunction of RAAS can result in: a. increased blood volume (salt and water retain via kidney) b. promotes vasoconstriction c. promotes insulin resistance

Answer 13

1. ANP/BNP respond to elevated pressure/volume and encourage renal excretion of salt and H2O 2. Normal pressure response equilibrium of these hormone feedback mechanisms can be disrupted by: a. excessive intake of sodium or insufficient intake other electrolytes (potassium, calcium, magnesium) b. obesity 3. Dysfunction of natriuretc peptide homeostasis can result in: a. Increased vascular tone and promotes increased blood volume/pressure

Answer 14

a. Age & gender • younger men and older women …men < 55 and women > 74 b. Race • African American c. High dietary intake of sodium and low intake potassium, calcium and magnesium d. Glucose intolerance (insulin resistance) e. Cigarette smoking • Nicotine acts as vasoconstrictor f. Obesity • metabolic syndrome (HTN, CAD and glucose intolerance) g. Excessive alcohol intake • 3 drinks per day elevates likelihood of HTN however, moderate alcohol 2- 4 drinks per week appear to do better than non-drinkers

Answer 15

(i) Normal inflammatory response 1. cytokines (histamine, prostoglandins) signal cascade of events leading to vasodilation/permeability changes 2. these changes promote healthy healing response to acute injury (ii) Chronic inflammatory response = negative endothelial response 1. vasoconstriction: abnormal vascular remodeling/smooth muscle contraction 2. Note: atherosclerotic plaque development causes chronic inflammatory response

Answer 16

(i) Healthy individual: 1. Insulin plays role in endothelial function (constriction/dilation mechanisms) 2. Insulin promotes NO production (ii) Insulin resistance: 1. Abnormal response to insulin is altered in viscous cycle a. cells become less sensitive to insulin (receptors or insulin itself) b. feedback mechanism to pancreas result in increased insulin secretion (hyperinsulemia) c. hyperinsulinemia promotes more insulin resistance 2. Insulin resistance = less NO production and endothelial dysfunction 3. Insulin resistance is pathological consequence of diabetes however: a. Insulin resistance can be identified in 50% individuals with HTN and are non-diabetic

Answer 17

a. Lifestyle changes b. Pharmaceuticals aimed at the specific mechanisms of cardiac pump mechanics or blood volume/sodium excretion pathways • Ex: ACE inhibitors, angiotensin II blockers, aldosterone receptors blockers, beta blockers, calcium channel blockers, renin inhibitors, diuretics (many act at different points in the kidney filtration system), central and peripheral adrenergic antagonist (sympathetic inhibition), endothelial vasodilators, etc… c. If secondary HTN – address primary pathology + functional pressure/volume/pump changes

Answer 18

1. Decreased systolic, diastolic or both from supine to upright position change a. Normal pressure compensation with standing: • Increased HR and venous/arteriole vasoconstriction (i) Stretch receptors stimulus of increased sympathetic response • Mechanical systems – muscular pump, valve function b. Orthostatic hypotension is dysfunction of one of these mechanisms

Answer 19

a. BP changes within 3 minutes of standing | • Systolic decrease > 20 mmHg or diastolic decrease > 10 mmHg

Answer 20

* temporary decrease of BP requires patient to take a few extra minutes to transfer from supine to stand (usually supine to sit, wait, sit to stand) * medications, chronic bed rest/immobility, anatomical/physiological anomaly, starvation/dehydration, venous pooling (pregnancy, varicose veins/CVI, etc…)

Answer 21

• Disease causing orthostatic hypotension (i) Endocrine, metabolic, CNS/PNS disorders • Idiopathetic orthostatic hypotension (i) No known cause

Answer 22

a. Inflammatory/immune process | b. Exact pathological mechanisms continue to be debated

Answer 23

(i) Endothelial injury (ii) Fatty streaks (iii) Fibrous plaque formation (iv) Complicated plaques or unstable plaque

Answer 24

• Initial damage to endothelial lining causes inflammatory response (i) allows cascade of events to progress to atherosclerotic plaque…“opens the door” to development of fatty streak

Answer 25

(i) Endothelial cells can’t produce anti-thrombotic and vasodilator cytokines 1. sets the stage for thrombus formation and vasoconstriction (ii) Excessive release of inflammatory mediators (cytokines) 1. TNF-alpha, IL-1, Interferon-gamma (IFN), oxygen radicals, heat shock proteins (iii) Growth factors are released that will promote smooth muscle proliferation (iv) Macrophages accumulate and adhere to injury 1. Macrophages release enzymes that oxidize LDL and add to endothelial damage a. LDL oxidation is critical step in atherosclerosis i. Diabetes, hypertension, smoking all associated with increased LDL oxidation (i.e. “oxidative stress”) 2. Macrophages ingest oxidized LDL and “become” foam cells

Answer 26

(i) Smoking and other infectious toxins (ii) Hyperglycemia (diabetes) (iii) Hypertension and other changes in blood flow dynamics (iv) Dyslipidemia (elevated LDL, low HDL, elevated TG’s) (v) Elevated homocysteine levels (vi) Additional factors 1. insulin resistance 2. elevated CRP (C reactive protein) 3. oxidative stress (LDL oxidation) – promote free radicals 4. infection/periodontal disease 5. elevated fibrinogen

Answer 27

• Fatty streak is “earliest” gross pathological lesion in atherosclerosis (i) Accumulation of foam cells (“packed full” of LDL) results in fatty streak (ii) Other events accompanying the growth of fatty streaks 1. Platelets attach to the damaged endothelium 2. Migration of smooth muscle into the area (iii) Fatty streaks promote more endothelial damage/inflammatory responses which turns into a viscous cycle of negative pathology • Current lifestyle of our society – observation of fatty streaks at younger ages

Answer 28

• Smooth muscle continues to proliferate in area and then produce collagen • Collagen forms a fibrous plaque over the fatty streak (i) Growth factors released initially promote smooth muscle and collagen formation • The fibrous plaque may, or may not, calcify • Plaque and blood flow (i) Impair laminar flow (aka create turbulent flow) (ii) If large enough – may occlude blood flow • Fissures may develop

Answer 29

• Ruptured plaque = complicated plaque (i) Some plaques can be prone to “rupture” (ii) Clinical concern regardless of size (iii) Hemorrhaging within the plaque leads to rupture • Bleeding from rupture leads to: (i) Platelet adhesion, clotting factor cascade and quick thrombus formation • “New” thrombus may abruptly occlude blood flow causing ischemia or infarction

Answer 30

a. Atherosclerotic plaque formation the coronary arteries

Answer 31

• Age • Gender (i) males > females (ii) females after menopause • Family history: MI, cardio revascularization or sudden death (i) 1st degree male relative: 55 yrs or younger (ii) 1st degree female relative: 65 yrs or younger (iii) 1st degree = father, mother, brother or sister

Answer 32

``` Dyslipidemia HTN Obesity Smoking DM (increase insulin resistance) ```

Answer 33

(i) Elevated plasma lipoprotein levels (lipids, phospholipids, cholesterol, TG’s all bind to carrier proteins hence “lipo”protein) (ii) “Major risk” of CAD = combination of elevated LDL (> 160) with low HDL (<40)

Answer 34

1. LDL cholesterol (mg/dl) a. 240 - “High” 3. Triglycerides a. > 200 - “high” 4. HDL cholesterol a. > 60 - ideal b. < 40 - undesirable

Answer 35

(i) Primary and secondary both ↑ CAD risk (ii) Risks may ↓ by as much as 50% within first year of quitting (iii) Smoking contributes to 1. decreased HDL, elevated LDL and LDL oxidation 2. endothelial inflammation/thrombus formation

Answer 36

(i) Numerous negative effects on cardiovascular system (ii) Impaired fasting glucose (delayed GTT) (iii) Insulin dependent vs non-insulin dependent

Answer 37

(i) Infections (ii) Elevated C-reactive protein and other inflammation markers (iii) Elevated homocysteine levels 1. Homocysteine – what is it? a. Amino acid that is similar to the A.A. cysteine (it is homolgue therefore…the name homo-cysteine.) b. It is a temporary A.A. molecule that occurs naturally in a cascade of protein metabolic pathways c. Requires B6 (pyridoxine), B9 (folic acid) & B12 to avoid accumulating in the blood stream

Answer 38

a. lack of enzyme that breaks down homocysteine | b. dietary deficiencies – some of the B vitamins (B6 pyrydoxine, B9 folate, B12 cobalamin)

Answer 39

a. Inhibits a key enzyme in collagen and elastin production

Answer 40

a. ↑ CAD risk – d/t damaged blood vessels | b. ↑ risk of fractures in elderly

Answer 41

atheroclerosis in form of CAD • Initially – impairment may only be evident under increased demand (exercise, stress, etc..) • As pathology progresses impairment becomes evident at low levels of demand (rest, ADL’s, etc..)

Answer 42

• Narrowing of coronary artery (>50%) will result in impairment of cellular metabolism • Myocardial cells become ischemic within 10 seconds of blood flow occlusion • Attempt to rely on myoglobin O2 stores for first 6 – 10 seconds • After 2-3 minutes (i) Loss of contractility followed by drop in cardiac output (ii) Conduction abnormalities (EKG changes, etc…) leading to dysrhythmias (iii) Anaerobic metabolism is only mechanism to provide energy with lactic acid accumulation • If flow is restored then return to aerobic metabolism, contractility returns followed by cellular repair • If flow is not restored then myocardial infarction occurs (damage and/or potential tissue necrosis)

Answer 43

(i) Coronary spasm (prinzmetal angina) (ii) Hypotension (iii) Arrhythmias (iv) Decreased O2 capacity of the blood (anemia, hypoxemia, altitude)

Answer 44

(i) Tachycardia and exercise - (both more work for the heart) (ii) Hypertension (more work to overcome increased afterload) (iii) Cardiac hypertrophy (bigger muscle demands more O2) (iv) Valve dysfunction/disease

Answer 45

(i) Transient episode of blood flow impairment in relation to O2 demand of the cardiac muscle (ii) This scenario is usually the individual with gradual narrowing of the lumen and stable plaque development within the blood vessel walls (iii) Recurrent episodes lasting 3-5 minutes (iv) Onset usually some form of exercise/exertion or stress (v) Pain is often relieved with rest (vi) S/S include 1. “Angina pectoris” - substernal chest discomfort (heaviness – pressure – pain) a. Pain vs discomfort – “open ended” questioning 2. Other “classic” signs/symptoms (see text) (vii) Discuss patient interview: pain vs discomfort (viii) Other classic myocardial ischemia s/s

Answer 46

(i) Myocardial ischemia that does not cause obvious signs/symptoms (ii) Common following conditions/surgical procedures that may impair innervation 1. Ex: heart transplant, CABG (coronary artery bypass graft surgery), emotional stress, diabetes, etc…

Answer 47

• UA - Thrombus breaks up before cell death, allows return of blood flow (perfusion) • “Reversible” myocardial ischemia – no cell damage • Occurrence of UA increases the likelihood of MI within “relative” near future (i) 20% of patients with UA will have MI or death from MI within 30 days

Answer 48

1. 6 – 10 seconds of impaired blood flow the cell becomes ischemic (cooler and cyanotic) 2. Anaerobic metabolism attempts to supply ATP for muscle contraction…can’t supply adequate amount compared to aerobic metabolism 3. Lactic acid and H+ ions accumulate as a result of anaerobic metabolism…acidic environment impairs conductivity 4. Electrolytes disturbances also occur due to the lack of blood flow (potassium, calcium and magnesium) – alter conduction. 5. Myocardial cells release catecholamines (EPI and NE)

Answer 49

1. Promotes vasoconstriction and sodium retention a. obviously counterproductive….systemically it increases BP and work demand on heart 2. Angio-2 also stimulates smooth muscle proliferation coronary vasoconstriction/spasm 3. Promotes catecholamine release – sympathetic response 4. Clinical a. ACE inhibitors (limit the Angio response) and Beta blockers (limit the sympathetic response)

Answer 50

(i) Inflammatory response (immediately first 4 days) 1. leukocytes/proteolytic enzymes accumulate to remove damaged/necrotic cells 2. glycogenolysis and FFA release to increase fuel availability during recovery (ii) Soft scar formation (4-10 days) 1. weak soft collagen matrix forms 2. potential for re-injury (iii) Mature scar tissue formation (6+ weeks) 1. soft scar replaced by mature collagen formation 2. mature scar a. not susceptible to “mechanical” injury b. however it DOES NOT contract – cardiac wall function permanently impaired

Answer 51

(i) Myocardial stunning – transient (hours – days) loss of contractility (ii) Hibernating myocardium - ischemic tissue goes into metabolic survival state to survive until return of blood flow (iii) Myocardial remodeling 1. Hypertrophy and loss of contractility of myocardial cells throughout heart in response to infarction 2. Stimulated by angio-2, aldosterone, catecholamines and inflammatory cytokines 3. Clinical goal to limit via restoration of blood flow and pharmaceuticals aimed at the above

Answer 52

(i) Arrhythmias 1. cellular and mechanical response to MI may trigger arrhythmic patterns 2. V-fib and re-entrant patterns (ii) Pericarditis 1. inflammatory responses may lead to pericarditis (iii) Ventricular wall aneurysm 1. mechanical changes from scar formation/weakened wall lead to structural displacement

Cardio Mod 5 Flashcards

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