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Pharm > CV drugs and antihypertensives 53/54/55 > Flashcards

CV drugs and antihypertensives 53/54/55 Flashcards

1
Q

anti-HTN:

A

Diuretics
Beta blockers
Calcium channel blockers
RAAS inhibitors

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2
Q

Antihyperlipidemics

A

Bile acid binding resins
HMG-CoA reductase inhibitors
Fibrates
Niacin

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3
Q

Antidiabetics

A

Insulin
Sulfonylureas
Biguanides
Thiazolidinediones

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4
Q

Antianginals

A

Nitrates
Calcium channel blockers
Beta blockers

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5
Q

Drugs for CHF

A 
Cardiac glycosides
Non-glycoside inotropes
ACE inhibitors
Diuretics
Vasodilators
Beta blockers
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6
Q

Antiarrhythmics

A

Sodium channel blockers
Potassium channel blockers
Calcium channel blockers
Beta blockers

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7
Q

Hydrochlorothiazide (Microzide)

A

thiazide Diuretic

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8
Q

Chlorthalidone (Thalitone)

A

thiazide Diuretic

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9
Q

Indapamide

A

thiazide Diuretic

direct dilator action on vascular smooth muscle

lesser propensity to raise serum cholesterol (even though it is longer acting)

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10
Q

Furosemide (Lasix)

A

loop diuretic

short-acting. Often given two or three times a day

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11
Q

Triamterene (Dyrenium)

A

K+ sparing diuretic

inhibitor of renal Na+ channels

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12
Q

Spironolactone (Aldactone)

A

K+ sparing diuretic

competitively block binding of aldosterone

interferes with sex-steroid receptors (non-sp)

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13
Q

Eplerenone (Inspra)

A

K+ sparing diuretic

competitively block binding of aldosterone

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14
Q

Reserpine

A

Peripheral Adrenergic Neuron Blocker

Depletes storage of the peripheral neurotransmitter: NE in vesicles of sympathetic nerve endings, thereby reducing amount of NE released with each nerve impulse

dec. both CO and TPR–>dec. BP
* irreversible*: persistent effect, need to make new vesicles
- do not get rebound HTN

used in standard HTN pt: cheap!

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15
Q

Methyldopa

A

Central Adrenergic Neuron Blocker

prodrug which is converted into methylnorepinephrine

alpha2 adrenergic AGONIST in the central vasomotor centers, dampening sympathetic neural outflow

  • dec. in TPR*- main effect
    dec. in renin
    dec. in CO

HTN during pregnancy
not used as much anymore

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16
Q

Clonidine (Catapres)

A

Central Adrenergic Neuron Blocker

sim. to Methyldopa, influence CNS imidazoline rec

patch for transdermal absorption: moother BP control with fewer side effects although many show local skin reactions

primary HTN

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17
Q

Prazosin (Minipress)

A

α1-Adrenergic Receptor Blocker
3x day
more severe first-dose postural hypotension

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18
Q

Doxazosin (Cardura)

A

α1-Adrenergic Receptor Blocker

1x day

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19
Q

Terazosin (Hytrin)

A

α1-Adrenergic Receptor Blocker

1x day

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20
Q

important pgs to learn

A

skip pgs 5-7 (mostly pathology)

know pgs: 11-25
sections 13-23

after: sections 24-34 not as important

36-38: important tables

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21
Q

Propranolol (Inderal-LA)

A

β1 and 2-Adrenergic Receptor Blocker

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22
Q

Nadolol (Corgard)

A

β1 and 2-Adrenergic Receptor Blocker

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23
Q

Timolol

A

β1 and 2-Adrenergic Receptor Blocker

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24
Q

Pindolol

A

β1 and 2-Adrenergic Receptor Blocker (with ISA)

*partially stimulates B2, so contributes to vasodilation, lowering TPR–>lowering BP

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25
Q

Atenolol (Tenormin)

A

β1-Adrenergic Receptor Blocker

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26
Q

Metoprolol (Toprol-XL)

A

β1-Adrenergic Receptor Blocker

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27
Q

Acebutolol (Sectral)

A

β1-Adrenergic Receptor Blocker

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28
Q

Labetalol (Trandate)

A

α1/β1,2 Blocker

partial agonist @ B2
BP falls mainly from a decrease in peripheral resistance (due to the alpha block, partial vascular beta-2 stimulation and less renin release) but with some decrease in CO

severe primary HTN (oral)
HTN emergency (IV)
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29
Q

Nebivolol (Bystolic)

A

NO-releasing β1 Blocker

“vasodilating powerhouse” (Also decreases NO degradation)

decrease in BP is due to vasodilator effect (dec. TPR) as well as dec. CO:
β 1 -blocking action decreases renin release, HR and contractility
Increase in endothelial NO dilates vascular smooth muscle

good for HTN pts w. imparied endothelial cell function
good for mild-mod primary HTN

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30
Q

Hydralazine

A

Direct Arteriolar Dilator

release NO from arteriole endothelium–>vasodilate–>dec. TPR

partly inactivated by acetylation in the liver: “rapid” acetylators in the population show much smaller drug effects than “slow” acetylators (adjust dosing)

added as 3rd drug if not responding to diuretic and 2nd drug (i.e. B-blocker), but being used less due to SEs

SE: lupus-like rxn (also edema described elsewhere)

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31
Q

Minoxidil

A

Direct Arteriolar Dilator

opens ATP-sensitive K+ channels in arteriolar smooth muscle cells (via active sulfate metabolite)

added as 3rd drug if not responding to diuretic and 2nd drug (i.e. B-blocker), but being used less due to SEs

use for severe HTN
esp. effective treating renal insufficiency (good renal arteriolar dilator)

SE: hair growth (also edema described elsewhere)

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32
Q

Verapamil (Calan)

A

Calcium Channel Blocker (CCB)
-block in heart

older: short acting (3x/day)

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33
Q

Diltiazem (Cardizem)

A

Calcium Channel Blocker (CCB)
-block in heart

older: short acting (3x/day)

SEs: nausea, headache
directly suppressed heart rate and A-V conduction

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34
Q

Nifedipine (Procardia - XL)

A

Calcium Channel Blocker (CCB)
-block in vasculature

older: short acting (3x/day), original prototype, pts were dying from rapid effects
* tx for primary pulmonary HTN*

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35
Q

Felodipine

A

Calcium Channel Blocker (CCB)
-block in vasculature

longer-acting with slow onset (safer)

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36
Q

Amlodipine (Norvasc)

A

Calcium Channel Blocker (CCB)
-block in vasculature
only “dipine” not effected/enhanced by grapefruit juice (metabolism in liver)

longer-acting with slow onset (safer)

37
Q

Captopril (Capoten)

A

ACE Inhibitor

prototype ACE inhibitor (NOT prodrug)

SEs: sulfydryl group: rash, loss of taste, and possibly (though seldom) some renal abnormalities causing loss of protein in urine.

38
Q

Enalapril (Vasotec)

A

ACE Inhibitor

prodrug that is activated by deesterification to enalaprilat (need adequate liver function)

39
Q

Lisinopril (Prinivil, Zestril)

A

ACE Inhibitor

active derivative to enalaprilat (NOT prodrug)

40
Q

Fosinopril (Monopril)

A

ACE Inhibitor

long-acting, prodrug activated primarily by *liver

“smartdrug”:
Active liver metabolite which has balanced route of elimination which shifts toward liver if the kidneys are damaged (useful in HTN pts with renal insufficiency)

41
Q

Quinapril (Accupril)

A

ACE Inhibitor

long-acting, prodrug activated primarily by *liver

42
Q

Ramipril (Altace)

A

ACE Inhibitor

long-acting, prodrug activated primarily by *liver

43
Q

Losartan (Cozaar)

A

Angiotensin II Receptor Blocker (ARB)

44
Q

Valsartan (Diovan)

A

Angiotensin II Receptor Blocker (ARB)

45
Q

Candesartan (Atacand)

A

Angiotensin II Receptor Blocker (ARB)

46
Q

Aliskiren (Tekturna)

A

Renin Inhibitor

47
Q

HTN def

A

sustained systemic arterial blood pressure (BP) levels above 140/90 mmHg (systolic/diastolic)
>1 reading

Isolated systolic hypertension (ISH), usually seen over age 65, is defined by some as a systolic blood pressure (SBP) > 160.

(mostly concerned with large arteries, capillaries and veins also involved)

48
Q

?? may be the most popular drugs for therapy of chronic primary hypertension

A

Thiazides and thiazide-like drugs (e.g. hydrochlorothiazide, chlorthalidone, indapamide)

indapamide with a lesser propensity to raise serum cholesterol

49
Q

thiazide diuretic mechanism in HTN

A

In lowering BP, initially diuretics induce a natriuresis which shrinks blood volume thus reducing cardiac output (within 2-3 days).
[This activates mechanisms responsible for maintenance of fluid volume, particularly (RAAS) which may then limit the degree of volume reduction and the degree of ↓ BP]. –>tends to eventually return to normal

Continued diuretic use leads to a fall in TPR (and return of cardiac output toward normal, within 6-8 weeks), which is the reason for continued antiHTN effect. This may be due to an autoregulatory phenomenon and/or to direct relaxant actions of the drugs on vascular smooth muscle (indapamide may do the latter via calcium channel blockade)- direct dilator action (as well as inhib. Na+ retention)

50
Q

autoregulatory phenomenon

A

decreased perfusion leading to vasodilation

51
Q

thiazides have ??? on BP and blood chemistry

A

flat dose response curve

i. e. increasing dose does not significantly increase therapeutic response
- typically good enough for mild hypertensive pts

52
Q

HTN pts may have
high-normal or
low-normal renin

why would it be low?

tx these pts with what ??

A

it is suppressed

makes sense to tx these high volume pts with diuretics (“volume dependent” HTN)
i.e. elderly, Afr. Americans

53
Q

Resistance to thiazides

A

Overly vigorous diuretic therapy may activate the RAAS excessively–>pressure-raising mechs
-vasoconstrictive effect of angiotensin and aldosterone-mediated exchange of K for Na (tending to retain Na and waste more K)

overwhelming load of dietary Na or an intrinsically impaired renal capacity to excrete Na to begin with

the reduction in BP by direct vasodilation–>inc. hydrostatic press–>edema
may lead to intense Na retention, mandating use of additional diuretic

54
Q

Thiazide SEs

A

Hypokalemia: K+ wasting
–>ventricular ectopic activity, sudden cardiac death

Hypercholesterolemia (be careful in high cholesterol pts)

Glucose Intolerance with hyperglycemia (be careful with DM pts)

55
Q

how to minimized hypokalemia from thiazides

A

use of small doses and/or use of only moderately long-acting diuretics rather than very long-acting ones

combine K+ sparers with the diuretic and/or add drugs that suppress the RAAS.

reduce dietary Na+ intake and increase dietary K+ intake

56
Q

loop diuretic: Furosemide

A

loop diuretics may exert a natriuretic effect near 25 percent of the filtered Na load (much more than thiazide diuretics) by blocking NaCl reabsorption in the thick ascending limb of the loop of Henle

better for v. low GFR and severe edema

indicated for patients with reduced renal Na excretory function

57
Q

Reserpine SEs

A

sedation, migraine and mental depression: depletes NT; deplete serotonin (does get into brain!)

postural hypotensive symptoms (deplete NE in vasc. smooth musc)
bradycardia (deplete NE in SA node)
systemic fluid retention
nasal congestion

GI: PUD, diarrhea (unopp. parasymps)

58
Q

Methyldopa SEs

A

peripheral fluid retention
and centrally-mediated sedation and dry mouth.

"autoimmune" disorders and may cause
parkinsonian signs (possibly due to accumulation of methyldopamine in CNS dopamine neurons) not seen with the other central alpha2 drugs.

surprisingly not much postural hypotension

not much rebound HTN as it is a pro-drug, so active form takes time to disappear

59
Q

clonidine SEs

A

patch may cause local skin reactions

rebound hypertension may occur (though less with patch vs. oral drug)

60
Q

a1-adrenergic receptor blockers:

doxazosin, prazosin and terazosin

A

Blockade of arterial vascular alpha1- receptors competitively inhibits binding of sympathetically-released NE–>dec. vasoconstriction–>dec. TPR–>dec. BP

primary HTN

affects vv as well as aa (some dec. in CO as well)

may improve glucose tolerance (but don’t want to use in pts with autonomic neuropathy–>impaired postural reflex)

lower cholesterol and triglyceride levels, increase HDL

61
Q

a1-adrenergic receptor blocker SEs

A

severe first-dose postural hypotension
postural dizziness

stress-induced urinary incontinence (esp. old ladies)

Reflex tachycardia and systemic fluid retention (less than other vasodilating drugs)

62
Q

B-blockers reduce BP how ??

A

B1 action:

reduce CO (↓ contractility and possibly by ↓ HR)

inhibit the release of renin from the renal JG cells

63
Q

non-selective (B1 and B2) blockers

A

remove the normal physiologic level of beta2-mediated vasodilation

tends to offset the decrease in total peripheral vascular resistance expected from the inhibition of renin release, thus limiting the overall antihypertensive effectiveness

but work well, so still used

64
Q

metabolism of B-blockers

A

more lipid soluble–>metabolized by liver and more enters brain

less lipid soluble–>excreted thru kidney, less enters brain (less CNS effects, better pt compliance)

65
Q

B blockers won’t work as well in ??

useful in pts with ??

A

elderly and African- American patients
pts with lower plasma renin

Chinese pts are MORE sensitive

HTN associated with tachycardia and high CO
HTN accompanied by other cardiovascular conditions which can also be tx with B-blockers: e.g. angina, arrhythmia

66
Q

B-blocker CV SEs

less SEs with partial agonist activity (ISA)

A

bradycardia (if little/no ISA) -20% lower!

reduced exercise ability and easier fatigue

slow A-V conduction and suppress ventricular contractility too much

Rebound HTN

67
Q

B-blocker pulmonary SEs

less SEs with partial agonist activity (ISA) and with selective B1 blockers

A

Bronchoconstriction

inhibition of airway β2 receptors (Especially a problem in patients who need to inhale beta2-agonists to maintain open airways) (try to chose a more selective B1 blocker for these pts)

68
Q

B-blocker metabolic SEs

less SEs with partial agonist activity (ISA) and selective B1 blockers

A

insulin-induced hypoglycemia may be longer in duration and/or more severe in the presence of especially nonselective beta-blockers without ISA

ALL B-blockers mask an important warning sign of such hypoglycemia, i.e. tachycardia (sweating still occurs)

aggravate insulin resistance with glucose intolerance

Hypertriglyceridemia and a fall in HDL-cholesterol

69
Q

B-blocker central SEs

A

Bad dreams, even hallucinations

-much less likely with lipid insoluble agents

70
Q

combined a1/B adrenergic receptor blocker (Labetalol) SEs

A

a-blockade:
postural dizziness which B- blockade can not correct

B-blockage:
bradycardia
A-V block at high doses Obviously, little chance of reflex tachycardia otherwise expected with regular alpha-1 blockers!

71
Q

NO-releasing B1 receptor blocker (Nebivolol) SEs

A

Similar to other β 1 -blockers though less rebound HTN upon sudden complete withdrawal

headache and fatigue (FYI- due to inc. NO in cerebral blood vessels (paradoxical?))

72
Q

selective arteriolar vasodilators:

(Hydralazine, Minoxidil) major SE

A

if taken ALONE: markedly dilate resistance arterioles leading to ↑ capillary hydrostatic pressure with ↑ filtration of fluid into the interstitial spaces (edema) plus renal retention of Na and H2O

fall in arterial BP markedly activates sympathetic and renal compensatory reactions causing considerable release of catecholamines and renin resulting in stimulation of the heart and much more retention of Na and water

use with B-blocker and diuretic to inhibit compensatory reactions

don’t effect vv as much, so little postural hypotension

73
Q

CCBs that end in “dipine” block Ca2+ channels in the ??

A

vasculature

*not pure distinction, some crossover at high doses

74
Q

dihydropyridine (“dipines”) CCB actions

A

reduce calcium entry into arterial vascular smooth muscle cells through arterial L-type calcium channels
–>decrease in free intracellular calcium –>reduces arterial vascular tone–>dec. TPR and BP

(little suppressive effect upon ventricular contractility at
standard therapeutic doses)

intrinsic natriuretic capability (not as much edema)

75
Q

Diltiazem and verapamil actions

A

↓ calcium entry through ventricular L-type calcium channels–>reduces ventricular contractility–>suppresses CO

May be some ↓ in HR and some ↓
arterial tone, via inhibition of similar channels in cardiac SA node and arterial smooth
muscle

76
Q

CCBs are used for ??

particularly useful for ??

A

virtually all types of primary systemic hypertension (versatile)

elderly and African-American hypertensive patients
also work well in the face of high Na intake, irrespective of the degree of Na sensitivity.

77
Q

dihydropyridine CCB SEs

A

reflexively (indirectly) increased heart rate due to peripheral vasodilation–>increased risk MI (incr. sympathetic activity)

nausea, headache, tachycardia, slight postural dizziness, ankle edema

78
Q

Verapamil SEs

A

nausea, headache, constipation
directly suppressed heart rate and A-V conduction
(verapamil > diltiazem)
serious myocardial depression like excessive bradycardia and excessive A-V nodal dysfunction

79
Q

ACE inhibitors end in ??

action ??

A

“pril”

inhibit production of the active form of angiotensin (angiotensin II)

inactivates the vasodepressor hormone bradykinin
–>increase availability of bradykinin and related PG vasodilators which can further ↓ BP by ↓ TPR

80
Q

ACE inhibitors are eliminated primarily by the ??; dose should be reduced in patients with ??

A

kidneys

renal insufficiency

(also note the prodrugs are metabolized/activated by the liver)

81
Q

MOA of RAAS inhibitors:
Renin inhibitors (prevent angiontensinogen–>AngI)
ACE inhibitors
ARBs

A

Ang-II mediated vasoconstriction is obviously overcome and TPR and BP then falls

A-II mediated synthesis of aldosterone is inhibited, thereby Na and H2O retention potentially reduced

also inhibits positive feedback of RAAS

82
Q

good candidates for of RAAS inhibitors

A

“normal renin” as well as in “high renin” patients with primary HTN and/or with diuretic-induced renin-related resistance

HTN secondary to diabetic nephropathy

83
Q

pts who should not get RAAS inhibitors

A

patients with fully established bilateral (efferent and afferent) renovascular hypertension (GFR is very low) , wherein abnormally “super” high levels of A-II keep renal GFR from falling too low beyond the stenoses by constricting the efferent arterioles; these patients may experience more loss of GFR with these drugs

(still sometimes used in these pts because of v. high systemic HTN)

84
Q

AngII is more effective at vasoconstricting the ?? arterioles

A

efferent (vs. afferent)

therefore RAAS inhibitors decrease GFR by preventing efferent vasoconstriction

85
Q

RAAS inhibitor SEs:

higher bradykinin levels with ACE inhibitors (less with ARBs or the renin inhibitor), may cause ??

A

nonproductive cough

Angioedema: localized, potentially fatal (asphyxiation)

86
Q

RAAS inhibitor SEs

A

hyperkalemia (may become worse with addition of a K-sparing diuretic or K supplements)

too much hypotension
teratogenic!!
hepatotoxicity

87
Q

??These drugs?? may impair the antihypertensive effects of ACE inhibitors by blocking ??

A

NSAIDs

bradykinin-mediated vasodilation because it is, at least in part, prostaglandin mediated

88
Q

CASE: middle-aged male, HTN, start on diuretic hydrochlorothiazide (25mg: intermediate dose)

  • adequately maintained
  • comes in few mos later with severe hypokalemia, what is next most appropriate step??

a. lowering dose of hydrochlorothiazide
b. add on captopril (ACE inhib)
c. add on K+ sparing diuretic
d. add on other powerful diuretic

A

a. NO: would increase BP
b. NO: while it would raise the K+, it would lower BP too much (he is currently adequately controlled)
c. YES: would raise K+ without affecting BP much (these are weak diuretics, less effect on BP)
d. NO: would lower BP too much (remember: he is adequately controlled)

Pharm (45 decks)

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