Pharm Test 4 / Final Part 1

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cholesterol and fats become soluble in water when they combine with

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blood protein

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cholesterol, fat, protein combo called

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lipoprotein

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lipoprotein function

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transport lipids

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triglyceride composed of

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3 fatty acids and 1 glycerol

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HDL

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high density lipoprotein

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LDL

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low density lipoprotein

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VLDL

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very low density lipoprotein

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HDL function

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remove cholesterol from arteries and carry to liver

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LDL function

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carry cholesterol to tissues, inc. risk for CAD

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VLDL function

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deliver triglycerides to adipose tissue and muscle

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VLDL composed mostly of

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triglycerides

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TCL

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total cholesterol levels

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TCL children

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< 170

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TCL adults desirable

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< 200

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TCL borderline high

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200-239

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TCL high

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>240

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HDL level positive risk

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<35

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HDL level negative risk

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>60

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VLDL level

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3-32

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optimal TCL

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<100

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desirable LDL level

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<130

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borderline LDL level

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130-159

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high risk LDL level

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>160

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triglyceride normal level

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<150

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triglyceride borderline high level

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150-199

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triglyceride high level

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200-499

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triglyceride very high

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>500

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cholesterol first line management methods

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diet management, exercise, risk factor reduction

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diet management for cholesterol management

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calories, tansfat/saturatedfat, cholesterol

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exercise for cholesterol management

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lowers LDL, increases HDL

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risk factor reduction for cholesterol management

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modifiable, nonmodifiable

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many lipid lowering agents require

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healthy liver

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HMG-CoA inhibitor aka

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statins

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statins

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rebound effect, watch liver

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rebound effect

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dont stop taking suddenly

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bile sequestering agents

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usually in combination with statins

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fibric acid derivatives

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very highly protein bound

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cholesterol absorption inhibitor aka

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CAI

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CAI

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2nd most common, keeps body from absorbing cholesterol in small intestine, given in combination with statins

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nicotinic acid

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lots of side effects

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lipid lowering agents

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nicotinic acid, bile sequestering agents, CAI, statins, fibric acid derivatives

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arteriosclerosis aka

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atherosclerosis

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CAD results from progression of

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arteriosclerosis

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artery of arteriosclerosis

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thick, hard, loss of elasticity

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leading cause of death in US is

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arteriosclerosis

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precursor to atherosclerosis

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fatty streaks

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fatty streaks appearance

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thin, flat, yellow on artery wall

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fatty streaks commonly found in

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children

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first progressive stage of ateriosclerosis

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damaged endothelium

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causes for damaged endothelium

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HTN, smoking, diabetes, high LDL

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damaged endothelium steps

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injured cells inflame > macrophages adhere to injured areas > release enzymes and oxygen radicals > oxidation of LDLs > macrophage engulf oxidized LDL and penetrate intima

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steps of fibrous plaque formation

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smooth muscle cells proliferate and make collagen > migrate over fatty streak forming fibrous plaque > endothelial cell dysfunction

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manifestations of endothelial cell dysfunction

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narrowing of lumen, increased stiffness, necrosis of vessel tissue

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steps to complicated lesion

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ulcerated or rupture of plaque > platelet adherence to the lesion > initiate coagulation > rapid thrombus formation > complete vessel occlusion

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complete vessel occlusion

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tissue ischema, infarction

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most common cause of CAD

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ateriosclerosis

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no symptoms of CAD until

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60% blood occlusion

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if plaque forms slowly what may develope

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colateral arteries

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why do occlusion symtoms vary

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depending on the artery involved

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common CAD symptoms

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pain (from ischema), discoloration (pale)

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nonmodifiable CAD risk factors

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men >45 yrs, women > 55 yrs, family hx

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modifiable CAD risk factors

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smoking, HTN, high LDL, diabetes mellitus, dietary deficiency of antioxidants, obesity

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how does peripheral resistance affect BP

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opposition of blood flow caused by friction of vessel walls

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short term regulation of BP

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baroreceptors, chemoreceptors

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baroreceptors

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respond to pressure changes

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chemoreceptors

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respond to pH, CO2, and H+ ions

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long term BP regulation

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humoral regulation, RAAS

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HTN numbers

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systolic > 140 or diastolic > 90

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precursor to HTN

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systolic > 120

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HTN cure

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there is none,

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HTN treatment

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life long

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prehypertension numbers

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systolic 120-139

diastolic 80-89

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stage 1 HTN numbers

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systolic 140-159

diastolic 90-99

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stage 2 HTN numbers

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systolic > 160

diastolic > 100

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hypertensive crisis

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systolic > 180

diastolic > 110

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most people have what kind of hypertension

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primary

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primary (essential) HTN classified as

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benign or malignant

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which primary HTN is slowly progressive

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benign

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which primary HTN is rapid

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malignant

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malignant primary HTN results in

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severe organ damage

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long standing HTN of either type produces

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structural changes of arterioles throughout body, characterized by fibrosis of vessel walls

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cause of primary HTN

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cannot be identified

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primary HTN is what type of disorder

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chronic and progressive

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when do HTN sypmtoms occur

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long after has occured

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risk factors for primary HTN

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elderly, black, postmenopausal women, obesity, smoking, alcoholism, gender, high sodium intake, low K Ca Mg, diabetes, visceral fat

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visceral fat

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really bad because inhibits organs

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several hypotheses for onset of primary HTN

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oxygen free radicals, increase blood volume, inappropriate autoregulation, overstimulation of sympathetic nerve fibers in heart and vessels, water and sodium retention by kidneys

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overstimulation of sympathetic nerve fibers in heart and vessels causes

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vasoconstriction

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HTN known as

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silent killer

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clinical manifestations of HTN

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headache, fatigue, activity intolerance

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HTN headache from

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vasoconstriction, lack of blood flow

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HTN fatigue from

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overworked body, poor heart function

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HTN activity intolerance from

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poor heart function

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HTN organ damage

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heart (CAD), renal (ESRF), eyes (retinal damage), brain (CVA), liver (engorgement), peripheral vasculature (peripheral vascular disease)

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cause of secondary HTN

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is identified

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examples of causes of secondary HTN

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chronic renal disease, cushing syndrome, pheochromocytoma, COA, oral contraceptives

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big cause of secondary HTN

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oral contraceptives - cause sodium retention

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how to correct secondary HTN

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correct cause = correct HTN

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lifestyle changes to correct secondary HTN

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wt reduction, sodium restriction, alcohol restriction, exercise, smoking cesation

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wt loss can reduce blood pressure in what % of individuals

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60-80% of overwt individuals

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sodium restriction no more than

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no more than 2 g / day

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alcohol can do what to BP

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increase it

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regular exercise can reduce BP by how much

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10 mm Hg

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smoking contributes to what

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heart disease

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pharmacologic therapy for HTN

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diuretic, beta blocker, ACE inhibitor, Ca channel blocker, vasodilator

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diuretics do what

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vasodilate arterioles

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who does not respond well to single beta blocker therapy and what do these people need

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blacks, need combination therapy

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beta blocker therapy prefered

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cardioselective

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Ca channel blocker mechanism of action

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inhibit release of intracellular Ca decreasing contraction force preventing Ca entry into smooth muscle decreasing arteriolar constriction decreasing PVR and BP

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Ca channel blockers SE

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hypotension, worsen CHF because decreasing contractility, bradycardia

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Ca channel blocker NI

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monitor orthostatic BP, monitor SnS CHF, hold if HR < 60

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ACE inhibitors block what

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RAAS

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ACE inhibitor block RAAS how

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inhibiting conversion of angiotensin I into II, decreasing aldosterone secretion, competing with angiotensin II to block effects

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ACE inhibitor SE

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hypotension, hyperkalemia, tachycardia, cough

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ACE inhibitor cough

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will subside

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ACE inhibitor NI

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monitor orthostatic BP, monitor K level, avoid foods high in K, monitor HR, monitor CBC (assess for infection)

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sympatholytics mechanism of action

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inhibit stimulation of sympathetic nervous system

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sympatholytics SE

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hypotension, dry mouth, constipation, sedation

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sympatholytics NI

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monitor orthostatic BP, treat SE

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vasodilator SE

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hypotension, rebound HTN

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vasodilator NI

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monitor BP q 5-15 min, use pump, must protect light, nipride and apressoline

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NI for HTN meds

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monitor BP, I & O, teach to check BP at home, report wt inc. of 2-3 lbs in 2-3 days, orthostatic BP, compliance, avoid OTC cold meds, check renal function

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NI for antihypertensive drugs

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pt may need more than 1 drug, do not stop drugs abruptly, life long therapy, avoid alcohol, slow position changes, promote compliance, assess and teach to report adverse affects

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pt recognition of adverse affects of antihypertensive drugs

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pt do not always relate SnS to drug therapy

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examples of adverse affects of antihypertensive drugs

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sedation, dizziness, orthostatic hypotension, sexual dysfunction

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HMG CoA reductase inhibitor decrease cholesterol by (4 ways)

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preventing bile acid absorption in small intestine, promote bile acid production, inhibiting enzyme that helps produce cholesterol, binding to cholesterol in small intestine to prevent absorption