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aldosterone
hormone that promotes sodium and fluid reabsorption
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angiotension
potent vasoconstrictor that is produced when the renin-aldosterone-angiotensin system (RAAS) is activated
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angiotensin-converting enzyme (ACE)
enzyme that catalyzes the conversion of angiotensin I to angiotensin II
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body mass index (BMI)
- measure of human body size and proportion.
- weight(kg)/ height (m2)
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cardiac output (CO)
volume of blood ejected from the left ventricle in 1 minute
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diastolic blood pressure (DBP)
measure of BP when the heart is at rest (diastole)
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diuretic
drug that produces diuresis (urination)
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gynecomastia
painful breast enlargement in men
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hirsutism
excessive hair growth in women
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hyperkalemia
excessive serum potassium levels
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hypokalemia
deficient serum potassium levels
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hypernatremia
excessive serum sodium levels
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hyponatremia
deficient serum sodium levels
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hypertension (high BP)
elevated diastolic or systolic blood pressure
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hyperuricemia
increased uric acid levels in the blood that is produced by some diuretics and can aggravate gout
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metabolioc syndrome
important risk factor of hypertension that promotes the development of atherosclerosis and cardiovascular disease
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nocturia
nighttime urination
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orthostatic hypotension
sudden drop in BP that occurs when arising from lying down or sitting or standing
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photosensitivity
increased sensitivity to sun exposure that can result in sunburn
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preeclampsia
sudden rise in BP, excessive weight gain, generilized edema, proteinuria, severe headache, and visual disturbances occurring in late pregnancy
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prehypertension
systolic BP ranging between 120-139 mm Hg and diastolic BP ranging 80-89 mm Hg
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peripheral vascular resistance (PR)
resistance to the flow of blood in peripheral arterial vessels that is associated with blood vessel diameter, vessel length, and viscosity
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RAAS
renin-aldosterone-angiotensin system
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RAAS:
system that is activated when there is a drop in renal blood flow that increases blood volume, blood flow to the kidney, vasoconstriction, and BP
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systolic BP (SBP)
measure of the pressure when the heart's ventricles are contracting (systole)
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BP is necessary to circulate blood, O2, and nutrients to body organr and to remove CO2 and waste products
without BP shock, circulatory collapse, and death would result
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BP is measured using sphygmomanometer (aneroid or mercury), or and electronic BP measuring device
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average normal BP is
120/80 (systole/diastole)
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formula for determining BP
BP = CO x PR
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Cardiac output (CO) is determined by measuring the HR and multiplying it by the stroke volume (vol. of blood injected by the ventricles)
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body sensors monitor blood, when decreases are detected, regulatory mechanisms are "switched on"
sites for BP control are the kidneys, heart, blood vessels, CNS, and sympathetic nerves
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when the kidney detects a drop in renal blood supply, the RAAS is activated
causes levels of aldosterone (endocrine hormone) and angiotensin to rise
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aldosterone and angiotensin act to ______ blood volume, blood flow, vasoconstriction, and BP
increase
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heart controls the CO by increasing or decreasing rate of contractions
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when CNS senses drop in BP, it signals sympathetic nerves to release neurotransmitters that control heart rate and blood flow through the arteries
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sympathetic nerves release NE, which causes vasoconstriction and increased peripheral vascular resistance (PR)
when PR increases, BP increases.
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if blood thickness (viscosity) increases, BP will also rise
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hypertension is the most diagnosed medical condition in the US, affecting more the 65 million Americans (25% if adult population). in canada:
affects 3 million canadians (10% of pop.)
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by age 60, ______ or people have hypertension
30-40%
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______ hypertension is the predominant form of hypertension before age 50.
diastolic
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after age 50, ______ is predominant form of hypertension
systolic
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in more than 90% of cases, the actual cause of hypertension are UNKNOWN. (rick factors for chronic elevated high BP are known)
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metabolic syndrome is an important risk factor for hypertension, promoting the development of athersclerosis and cardiovascular disease
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hypertension risk factors
- age: >55 in men, >65 in woman
- diabetes mellitus
- family history
- metabolic syndrome
- obesity
- smoking
- no exercise
- increase total LDL or low HDL
- diet high in salt and sat. fats
- excessive alcholol consumption
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drugs that increase BP
- NSAIDS (COX2 Inhibitors)
- cocaine
- decongestants
- diet pills
- oral contraceptives
- glucocorticosteriods(prednisone, hydrocortisone, methylprednisone)
- cyclosporin and tacrolimus
- mineralcorticoids (aldosterone)
- erythropoietin
- licorice
- herbals(ma huang, ephedra, bitter orange)
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medical conditions known to produce hypertension
chronic kidney disease, thyroid disease, Cushing's syndrome, sleep apnea
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reduction of BP to normal levels is beneficial for persons with prehypertension with and without preexisting disease
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drug therapy should be added to the treatmet program in people who have diabetes or kidney disease if lifestyle modifications do not bring BP down
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stage 1 hypertension
SBP range 140-159 mm Hg, DBP range 90-99mm Hg
managed thru lifestyle change
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stage 2 hypertension
SBP >= 160mm Hg
DBP>= 100mm Hg
managed thru lifestyle changes and drug therapy
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BP > 180/110mm Hg is a medical emergey and should be treated immediatly
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gestational hypertension typically occurs after 20 weeks of pregnancy in susceptible women
can progress to preeclampsia and cause premature delivery and fetal growth retardation
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approx 25% of pregnant woman who have chronic hypertension for more than 4 years will develop preclampsia during pregnancy
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white coat hypertension
abnormally high BP when taken by medical professional, but BP measurements taken at nonclinic setting are within normal range
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hypertension sometimes called "silent killer" because it can cause damage to body without obvious symptoms
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high BP can cause damage to kidney, heart, brain, arteries, and eyes
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hypertension can weaken arteries and cause aneurysms that can bleed and cause death if they occur in the brain, aorta, or abdomen
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hypertension can cause blindness when blood vessels in the retina are damaged and scarred
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for each 20mm Hg increase in SBP and 10mm Hg in DBP there is a two-fold increase in risk for death due to ischemic heart disease (IHD) and stroke
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hypertension is categorized as a chronis disease of lifestyle because is it associated with obesity, excessive dietary sodium intake, reduced physical activity, excessive alcohol consumption, and inadequate consumption of fruits and vegetables
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lifesyle modification is an important strategy and is the first step in treatment and prevention of hypertension
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drugs in the treatment of hypertension work at the sites of blood presure regulation:
the kidney, heart, blood vessels, brains, and sympathetic nerves
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the kidney plays a major role in regulating BP and diuretics exert their effects on the kidney
they increase the elimination of water, sodium, and selected electrolytes (K+, Cl+, HCO3-), depending on their location of action in kidney
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tech note!!
natural licorice may aggravate hypertension and interfere with the affective of antihypertensive drugs, it increases Na and water retension and K depletion
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diuretics lower BP by decreasing PR and CO, lower PR by lowering blood volume
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classifications of diuretics
- thiazide
- loop
- potassium sparing
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aldosterone antagonists
ometimes classified as diuretics because their location of action is the kidney
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most thiazide diuretices share the common ending:
"-thiazide"
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hydrochlorothiazide is commonly abbreviated HCTZ
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thiazide diuretics promote elimination of
water, Na+, K+, Mg2+, and Cl-
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thiazides act at the distal convoluted tubule where they block the Na+Cl- cotransporter, interfering with Ca2+ transport into arterioles, decreasing vasoconstriction.
PR and BP are lower
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thiazide diuretics should be used cautiously in patients with _______
gout and diabetes
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diuretics should be used in the morning to avoid the need to urinate in the middle of the night (nocturia)
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thiazides are weak acids and are highly protein bound
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thiazide ADRs
dehydration, hyponatremia, hypokalemia, hypomagnesia, hypochloremia, hyperuricemia, GI upset, impotence, photosensitivity
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effect of thiazides and loop diuretics reduced when taken with NSAIDS
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Loop diuretics also block sodium-potassium transporter in the ascending loop of Henle.
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loop diuretics are the most potent diuretics because they inhibit the reabsorption of 20-30% of Na load, whereas thiazides inhibit only 5-10% and K-sparing diuretics inhibit only 1-3%.
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loop diuretics readily absorbed in GI tract and 98% protein bound
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most loop diuretics share the same common ending:
"-semide"
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loop diuretic bumetandine partially metabolized in liver, 50% is excreted unchanged in urine
thorsemide's metabolismn in liver is greater and 20% elimated in urine
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potassium-sparing diuretics inhibit sodium reabsorption while avoiding potassium loss
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potassium-sparing diuretics effects are less than loop and thiazide, but can be increased with a thiazide
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fixed dose potassium-sparing combinations currently available:
- amiloride
- +
- hydrochlorothiazide
- triamterene
- +
- hydrochlorothiazide
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hyperkalemia is the most common ARD for K-sparing diuretics, risk increased if prescribed with ACE inhibitors
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K-sparing diuretics should be used cautiously in patients with congestive heart failure who are taking digoxin
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______ is a hormone that is released when the kidney perceives a drop in blood flow and BP
aldosterone
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aldosterone causes sodium and water reabsorption
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spironolactone is a competitive antagonist of aldosterone, blocks the effects of aldosterone on Na channels, decreases Na reabsorption, and inhibits K elimination
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spironolactone is sometimes classified as a k-sparing diuretic
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hyperkalemia is a serious ADR caused by spironolactone
other ADRs are nausea, unpleasant aftertaste, gynecomastia (breast enlargement in males), hirsutism, impotence, and menstraul irregularities.
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Angiotension-converting enzyme inhibitors (ACEIs) share the common ending:
"-pril"
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ACEIs lower SBP and DBP by their blocking action on ACE.
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ACE converts angiotensin I to angiotensin II
When angiotensin II levels rise, BP increases because angiotensin II is a vasoconstrictor, stimulates the release of aldosterone, and promotes the release of NE from sympathetic neurons
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ACEIs inhibit the activity of ACE, reducing angiotensin II and aldosterone levels
- decrease reabsorption of sodium in the renal tubules
- cause accumilation of bradykinins reducing PR, further lowering BP
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ACEIs would not be drug of choice for people with liver function because prodrugs have limited activity until they undergo metabolism
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Fosinopril is a good choice for patients with decreased kidney function beacuse it is eliminated by the liver (50%) and the kidney (50%).
All other ACEIs are 90% eliminated by the kidney and can accumulate if kidney disease is present
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dry cough is a common side effect of ACEIs
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ACEIs are contraindicated in pregnancy because they can interfere with fetal development of the kidneys and fetal death has been reported
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Angiotensin II receptor blockers (ARBs) are competitive antagonists at the angiotensin II receptor site
they lower BP by blocking the bindng of angiotensin and inhibit growth of smooth muscle stimulated by angiotensin II, reducing ventricular and arterial hypertophy that is associated with chrons hypertension
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Angiotensin II receptor blockers (ARBs) share a common ending:
"-sartan"
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ARBs are similar to ACEIs in effectiveness but no not produce dry cough, perhaps because they do not increase bradykinen levels like ACEIs
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Losartan is one of the first ARBs to be marketed
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ARBs adverse reactions are
fatigue, abdominal pain, dizziness, dry mouth, constipation, impotence, and muscle cramps
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ARBs are contraindicated in the second and third trimester of pregnancy because they can interfere with fetal development of the kidneys and fetal death has been reported
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β-blockers lower BP by decreasing HR and PR
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β-blockers used in the treatment off hypertension may be selective (β1) or nonselective (β1,β2)
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all β-blockers decrease BP, but selective β1-blockers are less likely to produce bronchospasms
selectivitiy is higher when doses are higher
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all β-blockers decrease HR, especially during exercise, and decrease force of contractions in the heart lowering CO
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β-blockers are contraindicated in asthma and diabetes
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β-blocers should not be discontinued abruptly because this may cause the onset of arrythmias or angina.
important drug interactions exist between β-blockers and cimetidine and salicylates
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administration of α1-blockers produces vascular relaxation, which reduces PR and lowers BP
α1-blockers also reduce LDL cholesterol levels, making them useful in the treatment of IHD
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α1-blockers share a common generic name ending:
"-zosin"
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α1-blockers have ability to reduce urethral resistance and increase urine flow, making them effective in the treatment of benign prostatic hyperplasia (BPH)
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CCBs are effective at lowering BP beacuse of their ability to relax blood vessels, decreasing PR.
also decrease HR and rate of contractions, lowering CO.
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methyldopa is a prodrug that mimics the autoinhibitory effects of NE.
when methyldopa binds to receptors, efferent sympathetic activity is reduced, blood vessels dialate, and PR is decreased
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clonidine inhibits NE release from CNS and peripheral sites, and reserpine depletes neuronal stores of NE at CNS and peripheral sites
prolonged use results in decreases in HR and CO, further reducing BP
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hydralzine and minoxidil decrease PR and reduce BP by relaxing vascular smooth muscle
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hydralazine is recommended for hypertensive emergencies (parenteral use) and is safe for the treatment of preeclampsia in pregnant women
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hydralazine can cause lupus-like syndrome
minoxidil causes facial hair growth, has been reformulated for topical use for treatment of baldness
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