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Pharmacology > Module 3 Hypertension > Flashcards

Module 3 Hypertension Flashcards

1
Q

what are classes of drugs used in the treatment of hypertension

A

calcium channel blockers
angiotensin converting enzyme inhibitors
angiotensin receptor blockers
thiazide diuretics
alpha 1 adrenergic antagonists

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2
Q

what percentage of americans are hypertensive

A

15% and largely asymptomatic

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3
Q

what is considered hypertension

A

above 120/80 is prehypertensive
140/90 is stage 1 hyper tensive
160/100 is stage 2 hypertnesive

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4
Q

what is the etiology of hypertension

A

unknown (primary or essential)
known (secondary) less than 5 %
-chornic renal or vascular disease
-endocrine (pheochromocytoma, primary aldoseronism)
-drugs/food (glucocorticoids, sympathomimetic amines)
-white coat

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5
Q

what is pheochromocytoma

A

neoplasia of chromatin cells causing the over production of catecholamines

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6
Q

glucocorticoids do what

A

sodium retinaing action

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7
Q

Blood pressure is the equation of what

A

TPR x CO
total peripheral resistance x cardiac output

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8
Q

cardiac output is the equation of what

A

cardiac output = Heart Rate x Stroke Volume

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9
Q

what are the two mechanisms to decrease blood pressure

A

decrease total peripheral resistance (relax vasucalr smooth muscle) (decrase TPR)
-calcium channel blockers
-antiotensin converting enzyme (ACE) inhibitors
-angiotensin receptor blockers (ARBs)
-alpha 1 adrenergic antagonists

decreaes the amount of blood pumped from the heart per beat (decrease co) (Strookve volume)
-thiazide diuretucs

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10
Q

contraction of vascular smooth muscle is done how

A

initiated by depolarization of the cell membrane potential and actiivation of voltage gated calcium channels
-this causes calcium ions to come into the smooth muscle an causes additional cacium release from a sarcoplasmi reticulum
calcium then binds to protein calmodiun
the calcium calmodiun compelx then stimulate the enzume myosin light chain kinase that phosphrylates the mysotin lifght chain of the contractile protins
this bnds myosin light chain to aciin and brings about smooth msucle contraction

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11
Q

drugs taht block the calcium channel do whay

A

inhibit contraction adn this decrase peripheral resistance

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12
Q

what are examples of calcium channel blockers

A

amlodipine and nifedipine
act to block smooth msucle calcium channels and inhibit contraction

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13
Q

amlodipine is used when in hypertension

A

stage 1 and in combinationn for stage 2
first line therapy - mroe effective in african americans and geriatric aptients

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14
Q

what are side effects of amlodipine and nifedipine

A

hypotension and relfex tachycarida
lower leg edema
risk of orthostatic hypotension

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15
Q

what is reflex tachycarida

A

with a fall in blood pressure the body compensates by increasing heart rate

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16
Q

what happens with a fall in blood pressure normally in kidneys

A

kineyes secrete enzyme called renin
renin converts angiotensinogen (peptide made in the liver) to angiotensin 1
in the blood, enzume called angiotensin convertin enzyme convers angiotensin I to angiotensin II
antiotension II causes vasoconstriction thus increasing total peripheral resistance
increaes aldosterone production by the adrenal gland
aldosterone increases sodium reabsorptin by the kidneys and potassium excretion
increase in na absorption means and increase in water reabsoptin which increases blood volume
ace also breaks down bradykinin to inactive peptides

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17
Q

how do ace inhibitors work

A

ace inhibitors decrease angiotnein II productin and this decrease antiogensin II indicued vasocontriction
-they inhibit aldosterone syntehsis resulting in less blood volume
decrease potassium excretion
so tehy increase blood potassium (hyperkalemia)
-also increase bradykinin which has a proinflamatory action which can result in dry cough that is non productive and angioedema

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18
Q

how do arbs (angiotensin receptor blocker) work

A

inhibit vasoconstriction and aldosterone syntheis do not affect bradykinin breakdown
so couhg and angioedema is not a side effect of arbs

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19
Q

what are examples of ace inhibitors

A

captopril and enalapril

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20
Q

what are examples of arbs

A

losartan and valsartan

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21
Q

what are the therapeutic uses of ace inhibiotrs and arbs

A

-hypertension stage 1 and in combination for stage 2
-more effective in Caucasian and young people (less so in geriatric)
-congestive heart failure
-diabetic neuropathy

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22
Q

what are side effects of ace inbitors

A

hyperkalemia
caution with k+ supplements
dry cough and andioedema
contraindicated in all trimesters of pregnancy

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23
Q

what are side effects of arbs

A

hyperkalemia
caution with k+ supplemnts
contraindicated in all tirmestsof pregnancy’s
felta hypotension and potential kidney damage.,

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24
Q

what do diuretics do inblood pressure

A

decraese blood volume by increasing water exrestion frin the kiney

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25
Q

what are exmaples of diuretics

A

furosemide
hydrochlorothiazie

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26
Q

where does furosemide act

A

acts on teh loop of henle in the kidney and is the most efficacious direetct
also used in the treatment of congestive heart failture

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27
Q

where does hydrocholothiazide work

A

actrs on teh distal tubule and is used in treatment of hypertension

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28
Q

what is the action of hydrochlorothiazide

A

kidney diuretic action
increaes urine output thus reducing blood volume and this stroke volume
smooth msucle relaxation reducing TPR

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29
Q

what are the therapeutic uses of hydrochlorothiazide

A

first line therapy
african and geriatirc patients
-used in monotherapy or combined with calcium channel blcokers, ace inhib or arbs

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30
Q

what are the side effects of hydrochlortiazide

A

hypokalemia - offset acei/arb
sulfonamide sensitivity (such as sulfa abx)
caution in pregnany

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31
Q

contrction of vascular smooth mscule occurs by binding of norepi to what

A

binding to alpha 1 adrenegic receptors

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32
Q

increase in heart rate is from binding of norpi to what

A

to cardiac beta 1 receptors

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33
Q

what happens when alpha 1 recetpor is stimulated by epi or norepi

A

the production of ip3 through gq protein
ip3 then causes calcium release from the sarcoplasmic reticulum
the relase calcium then binds to calmodium leading to the phosphyrlation fo mysoin light chain kinase and myosin light chaain and contraction

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34
Q

what does alpha adrenergic blocker (antagonist) do

A

causes venous dilation thus reducing vascualr resistance
inhiibits catecholamine induced vascualr constirction

35
Q

example of alpha adrenergic blocker

A

prazosin

36
Q

what is the therapeudic use of prazosin

A

essential hypertension used in combination for stage 1 and 2
not commonly used anymore
benign prostatic hyperplasia relieving obstructive symptoms

37
Q

how does prazosin releive urinary obstruction

A

reducing the tone of the prostate by relaxing teh uretra increaing the urnary stream

38
Q

what is heart failure

A

patholoogicl state in which the heart is unable to pump blood at a rate necessary to meet the requirements of teh body
the resuling symptoms fatigue, shortnes sof rbeath, pulmonary congestion and edema results from inadequate perfusion of tissue and retention of fluid

39
Q

what is afterload

A

the arterial resistance that the heart needs to pump against
increases with vascualr constirction (hypertension)

40
Q

what is preload

A

the amount of stretch of the cardiac ventricular chamber referred to as end diastoluc pressure (EDV)
increased venous return of blood to the ventrilce (blood volune) increases EDV

41
Q

what is contractillity

A

the force of cardiac contraction

42
Q

what is cardiac output

A

amount of bloood ejected from heart over time

43
Q

what is stroke volume

A

amount of blood ejected from heart during one beat

44
Q

what factors effect stroke volume

A

contractility
afterload
heart rate
cardiac output
lv wall integrity
valvular competnece
preload

45
Q

what are factors that decrase stroke volume

A

-coronary artery diease, MI, arrhythias affect contractility decrasing it
-hypertension increases the resistnacne the heart needs to pymp against thus increasing afterload
-direct damage to walls and values of the heart (mitral valve stenosis)
-venous constrition and increased venous return to heart will increase preload, increase myocaridal wall stress

46
Q

when cardiac output falls, a number of compensatory systems are activated including what

A

increased sympathetic activirt will increaes heart rate and contraction (sympathetic stimulation of the veins increaes venous return to the heart and this increases diasolic volume
this is accompanied by an increase in the heart 0 cardiac hypertrophy

47
Q

what are the long term consequenses of compensatory systems in heart failure

A

vasocoonstriction of the synpathetic system increases afterloaf which increases the resistance against which the heart pumps
-there is also an increase in diasolic volume
-the resuction in renal blood flow activates the renin angiotensino II system leaving to further fascular contriction and increase in aferload
-the also increases aldosterone release from the adrenal gland resuling in an increase in sodium and water reabsrption
this further increasses end diasolic volume
-the increased wall stress can impair caridac contractin resuling in a further drop in cardiac output
-catecholamies such as epinephrine directly damage the heart

48
Q

to treat heart failure, what does digoxin do

A

directly incrases the force of cardiac contraction or other ionotropic agents

49
Q

to treat heart failure what do beta blockers do

A

beta adrenergic antagoists or beta blockers will protect the heart from damage caused by catecholamies

50
Q

vasodialators, angiotension converting enzume inhibitors and angiotensin recetpor antatognistsdoes what to heart failiure

A

reduce afterload and ventricular wall stres

51
Q

what do diuretic do in heart failutre

A

reduced preload and reduce edema

52
Q

what do ionotropic drugs do

A

increase cardiac contractility
increase in intracellualr calcium

53
Q

what are the three groups of iontropuic drugs

A

dobutamine
inathrionine
digonxin

54
Q

what is dobutamine and its action

A

a beta 1 adrenergic receptor agonist
increases cyclinc amp and stmulates camp dependent protien kinase
this increases calcium influc throguh ca channel into the myocyte enhanxcing contraction

55
Q

what is inamrionone and its action

A

a phosphodiesterade inhibitior
phosphodiesterase enzymes break down cyclic amp
by inhibiting breakdwon of clyclic amp inamrionr increases intracellular camp increaesing ca

56
Q

what is digoxin adn what does it do

A

binds to and inhibits the sodium potassium atpase
this increaes intraceulular soudium whihc then increases inctracellular calcium

57
Q

what is the pharmacology of digoxin

A

increase contraction which is positive inotrophy increasing cardiac output
decreases preload, end diasolic voliume and heart oxygen demand
increases cholinteric activity slowing heartrate

58
Q

if there is an increase in cardiac output then what doe sthis do to compensatory ssytems

A

decrease compensations
so decrease preload, edv anbd heart ocygen demand
increaes parasymp activity slows heart rate

59
Q

what is the therapeutic use of digozin

A

second line drug in treating heart failure
low output heart failure with accompanying atrial fibrillation
end stage heart failure

acei, arbs, beta blocker first line of defense

60
Q

what are side effects of digoxin

A

k+ and digondn compete for same biiding site on na/k atpase
caution with k wastering diruretics (furosemide) enhanced digozin toxicity
less k = more digoxin binding
narrow therapeutic infex (easy to reach toxin blood level)
cardiac arrhythmias
gi anorexia, nausea, vomiting
cns fatigue, weakness and confusion
mostly eliminated unchanged by kindey so caution in kidney damage pt

61
Q

life threatenign digoxin toxicity is treated with what

A

atropine and digoxin antibodies (muscarinin antagonist) and bind to digoxin in boood and remove from body

62
Q

dobutamine is considered what

A

beta adrenerigc receptor agonist

63
Q

inamrinon is considered what

A

pde inhibitor

64
Q

what is the pharmacology of dobutamine and inamrinon

A

only used in late stage heart failure since they increase mortality
increaes contraction (increase co)
use limited to advanced heart failure (ICU)
may increase mortality in chf patients
parasoxical use of beta blockers

65
Q

what is used for patient in icu for treating pt w/ acute heart failure

A

nitroglycerin an na nitroprusside

66
Q

nitroglycerin and na nitroprusside are considered what

A

direct acting vasodilators

67
Q

what is the pharmacology of direct acting vasodulators (nitroglycerin and na nutroprusside

A

venous dilation (nitrogly) decrease preload (edv) reduign pulmonary edema and improving breathing
arterial and venous sialtion afterload and preload decreased (na nitroprusside)

68
Q

what are side effects and considerations of nitroglycerin and na nitroprusside

A

used in icu in acute heart failure indlucing pulmonary edema (difficulty breathing and extreme fatigue and swelling of legs and ankles)
nitroprusside is convered to cyanide and thiocyanate (cyanide toxicity)

69
Q

what is now considered first line drugs in treating congestive heart failure

A

ace inhibitor and arbs

70
Q

both ace inhibtiors and arbs decrease afterload andn preload and this do what

A

increase cardiac output increasing water excretion reducing edema

71
Q

ace i and arbs are given with what when heart failture is first diagnosed

A

beta blockers

72
Q

what is the pharmacology of ace i and arbs in heart failure

A

first line therapy in chf pt reducing mortality
both decrease afterload and preload increasing cardiac output
both decrease aldosterone syntheiss decreasing edema

73
Q

what are the side effects of abrs and aceinhib

A

hyperkalemia because inhibit aldosterone sysntheiss
dry cough and andioendema in ace inhibitors
both contrainsidcaed in prengnacy
both contraindicated in pt with bilateral renal stenosis bc these pt need angiotensin II in order to maintain normal kidney function

74
Q

diureticsc decrase preload how

A

by decreaing blood volume

75
Q

what is the pharmacology of furosemide and hydrochlorothiazide

A

reduce plasma volume decreasing preload
loop direetc furosemide prefered bc greater diuretic action
decrease pulmonary (dyspenia) and peripheral edema

76
Q

what are side effects of diuretics

A

electrolyte K+ loss is major concern
hypokelemia

77
Q

what do beta blockers do

A

decrease contraction and this decrease cardiac output

78
Q

what are examples of beta blockers

A

metoprolol and carvedilol
beta adrenergic receptor blockers

79
Q

what is the therapeutic use of bta blockers

A

parasoxical benefical action and decrease mortality
mechanism to decrease catecholamine induced apoptosis of cardiac myocytes (exact mech not known) - with remodeling there are changes in the expression of ion channels and contractile protiens in the heart
use with ace i or arbs and diuretics

80
Q

what are the side effects of beta blockers

A

cardiac contraction and excitatoin depression (prevent the binding of catecholamines to beta 1 recepotr in heart
they caase depression of cardiac contractio and exxcitation in heart
-asthma and copd as pt needed catecholamine simulation of b2 in the lungs - need to use beta 1 selective drug such as metorprolol
-masking hypoglcemia in diabetes - mask effect of catecholamine release from hypoglycemia (increase hr and dizziness) so may not realize have hypo

81
Q

entresto does what

A

is a new drug that acts partially by increasing blood levels of BNP
it has been shown to reduce mortality and hosptual visits with pt w heart failure

82
Q

nitric ozxide does waht

A

is a chemical released from teh endothrlisum assocuated with vasulcar smooth muscle
it enters into smooth muscle and stimualted the prodiction fo cgmp
cgmp activates cgmp dependent protien kinase that caues a relaxation of vasular smooth msucel

83
Q

what does brain naturtic peptide (BNP) receptor do

A

is a cell membrane glynylele cyclase
binding of bnp to the receptor incrases cgmp in vascular smooth muscle
this results in decrreases in arterial resistance afterlaod and pulmary congestion from preload

84
Q
A

Pharmacology (6 decks)

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