Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what percentage of americans are hypertensive

A

15% and largely asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is pheochromocytoma

A

neoplasia of chromatin cells causing the over production of catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

glucocorticoids do what

A

sodium retinaing action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Blood pressure is the equation of what

A

TPR x CO
total peripheral resistance x cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cardiac output is the equation of what

A

cardiac output = Heart Rate x Stroke Volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

drugs taht block the calcium channel do whay

A

inhibit contraction adn this decrase peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are examples of calcium channel blockers

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are side effects of amlodipine and nifedipine

A

hypotension and relfex tachycarida
lower leg edema
risk of orthostatic hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is reflex tachycarida

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are examples of ace inhibitors

A

captopril and enalapril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are examples of arbs

A

losartan and valsartan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what do diuretics do inblood pressure

A

decraese blood volume by increasing water exrestion frin the kiney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what are exmaples of diuretics
furosemide hydrochlorothiazie
26
where does furosemide act
acts on teh loop of henle in the kidney and is the most efficacious direetct also used in the treatment of congestive heart failture
27
where does hydrocholothiazide work
actrs on teh distal tubule and is used in treatment of hypertension
28
what is the action of hydrochlorothiazide
kidney diuretic action increaes urine output thus reducing blood volume and this stroke volume smooth msucle relaxation reducing TPR
29
what are the therapeutic uses of hydrochlorothiazide
first line therapy african and geriatirc patients -used in monotherapy or combined with calcium channel blcokers, ace inhib or arbs
30
what are the side effects of hydrochlortiazide
hypokalemia - offset acei/arb sulfonamide sensitivity (such as sulfa abx) caution in pregnany
31
contrction of vascular smooth mscule occurs by binding of norepi to what
binding to alpha 1 adrenegic receptors
32
increase in heart rate is from binding of norpi to what
to cardiac beta 1 receptors
33
what happens when alpha 1 recetpor is stimulated by epi or norepi
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
34
what does alpha adrenergic blocker (antagonist) do
causes venous dilation thus reducing vascualr resistance inhiibits catecholamine induced vascualr constirction
35
example of alpha adrenergic blocker
prazosin
36
what is the therapeudic use of prazosin
essential hypertension used in combination for stage 1 and 2 not commonly used anymore benign prostatic hyperplasia relieving obstructive symptoms
37
how does prazosin releive urinary obstruction
reducing the tone of the prostate by relaxing teh uretra increaing the urnary stream
38
what is heart failure
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
what is afterload
the arterial resistance that the heart needs to pump against increases with vascualr constirction (hypertension)
40
what is preload
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
what is contractillity
the force of cardiac contraction
42
what is cardiac output
amount of bloood ejected from heart over time
43
what is stroke volume
amount of blood ejected from heart during one beat
44
what factors effect stroke volume
contractility afterload heart rate cardiac output lv wall integrity valvular competnece preload
45
what are factors that decrase stroke volume
-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
when cardiac output falls, a number of compensatory systems are activated including what
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
what are the long term consequenses of compensatory systems in heart failure
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
to treat heart failure, what does digoxin do
directly incrases the force of cardiac contraction or other ionotropic agents
49
to treat heart failure what do beta blockers do
beta adrenergic antagoists or beta blockers will protect the heart from damage caused by catecholamies
50
vasodialators, angiotension converting enzume inhibitors and angiotensin recetpor antatognistsdoes what to heart failiure
reduce afterload and ventricular wall stres
51
what do diuretic do in heart failutre
reduced preload and reduce edema
52
what do ionotropic drugs do
increase cardiac contractility increase in intracellualr calcium
53
what are the three groups of iontropuic drugs
dobutamine inathrionine digonxin
54
what is dobutamine and its action
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
what is inamrionone and its action
a phosphodiesterade inhibitior phosphodiesterase enzymes break down cyclic amp by inhibiting breakdwon of clyclic amp inamrionr increases intracellular camp increaesing ca
56
what is digoxin adn what does it do
binds to and inhibits the sodium potassium atpase this increaes intraceulular soudium whihc then increases inctracellular calcium
57
what is the pharmacology of digoxin
increase contraction which is positive inotrophy increasing cardiac output decreases preload, end diasolic voliume and heart oxygen demand increases cholinteric activity slowing heartrate
58
if there is an increase in cardiac output then what doe sthis do to compensatory ssytems
decrease compensations so decrease preload, edv anbd heart ocygen demand increaes parasymp activity slows heart rate
59
what is the therapeutic use of digozin
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
what are side effects of digoxin
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
life threatenign digoxin toxicity is treated with what
atropine and digoxin antibodies (muscarinin antagonist) and bind to digoxin in boood and remove from body
62
dobutamine is considered what
beta adrenerigc receptor agonist
63
inamrinon is considered what
pde inhibitor
64
what is the pharmacology of dobutamine and inamrinon
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
what is used for patient in icu for treating pt w/ acute heart failure
nitroglycerin an na nitroprusside
66
nitroglycerin and na nitroprusside are considered what
direct acting vasodilators
67
what is the pharmacology of direct acting vasodulators (nitroglycerin and na nutroprusside
venous dilation (nitrogly) decrease preload (edv) reduign pulmonary edema and improving breathing arterial and venous sialtion afterload and preload decreased (na nitroprusside)
68
what are side effects and considerations of nitroglycerin and na nitroprusside
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
what is now considered first line drugs in treating congestive heart failure
ace inhibitor and arbs
70
both ace inhibtiors and arbs decrease afterload andn preload and this do what
increase cardiac output increasing water excretion reducing edema
71
ace i and arbs are given with what when heart failture is first diagnosed
beta blockers
72
what is the pharmacology of ace i and arbs in heart failure
first line therapy in chf pt reducing mortality both decrease afterload and preload increasing cardiac output both decrease aldosterone syntheiss decreasing edema
73
what are the side effects of abrs and aceinhib
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
diureticsc decrase preload how
by decreaing blood volume
75
what is the pharmacology of furosemide and hydrochlorothiazide
reduce plasma volume decreasing preload loop direetc furosemide prefered bc greater diuretic action decrease pulmonary (dyspenia) and peripheral edema
76
what are side effects of diuretics
electrolyte K+ loss is major concern hypokelemia
77
what do beta blockers do
decrease contraction and this decrease cardiac output
78
what are examples of beta blockers
metoprolol and carvedilol beta adrenergic receptor blockers
79
what is the therapeutic use of bta blockers
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
what are the side effects of beta blockers
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
entresto does what
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
nitric ozxide does waht
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
what does brain naturtic peptide (BNP) receptor do
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

Pharmacology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions