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Cardio Module > anti-hypertensive drugs > Flashcards

anti-hypertensive drugs Flashcards

1
Q

Name 5 complications of hypertension

A
  1. atherosclerosis
  2. diabetes
  3. blindness
  4. renal failure
  5. aneurysm and stroke
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2
Q

what is primary htn

A

aka essential

  • unknown origin
  • MUCH more common (85%)
  • usually asymptomatic
  • treatable BUT NOT CURABLE
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3
Q

what is secondary hypertension

A
  • rapid in onset
  • more severe
  • symptomatic
  • endocrine disorders, medications, renal disease, obesity, congenital heart defects, lifestyle
  • CURABLE POTENTIALLY (solve acute case)
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4
Q

What is goal of htn therapy

A
  • noramlize blood pressure and prevent end organ damage
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5
Q

Give systolic/diastolic for:

normal

pre-HTN

Stage 1

Stage 2

A

120/80

120-139/80-89

140-159/90-99

> 160/>100

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6
Q

Name the 5 clases of anti-HTN drugs

A
  1. vasodilators
  2. sympatholytics
  3. alpha-1 and beta adrenergic blockers
  4. angiotensin inhibitors
  5. diuretics
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7
Q

What drugs affect the heart most?

A
  • beta blockers
  • peripherally acting sympatholytics
  • cardioselective calcium channel blockers
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8
Q

What drugs affect the kidney most

A
  • diuretics
  • angiotensin inhibitors
  • beta blockers
  • peripherally acting sympatholytics
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9
Q

what drugs affect the vessels most

A
  • alpha-1 blockers
  • angiotensin inhibitors
  • diuretics
  • direct vasodilators
  • calcium channel blockers
  • peripherally acting sympatholytics
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10
Q

what drugs affect brain most

A
  • beta blockers

- centrally acting sympatholytics

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11
Q

What anti htn meds affect co

A
  • beta blockers
  • angiotensin inhibitors
  • diuretics
  • sympatholytics
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12
Q

what anti htn meds affect TPR

A
  • beta blockers (INDIRECTLY..?)
  • angiotensin inhibitors
  • diuretics (unknown why)
  • sympatholytics
  • vasodilators
  • alpha-1 blockers
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13
Q

how does calcium regulate smooth muscle tone

A
  • calmodulin and MLC kinase is inactive; calcium binding makes it activeand can phosphorylate the myson light chain which can then go through actin-myosin crossbridging to get contraction of muscle scell and the constriciton of the blood vessel
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14
Q

what are the 3 relaxation pathways?

A
  1. cAMP (PKA)
  2. endothelium dependent (cGMP and PKG)
  3. hyperpolarization ( K+ efflux inhibits L-type CA2+ channel activity)
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15
Q

vasodilator drugs directly only reduce _____

A

tpr

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16
Q

what is the indirect effect of vasodilators

A
  • compensatory reflex (sympathetic reflex
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17
Q

describe how the compensatory reflex comes about

A
  • vasodilator –> VSMC relaxation –> decrease TPR –> Decreased BP

kidneys sense decrease bp to increase renin and incrase aldosterone, which decreases na+ excretion to increase volume and increase CO while incresaeing bloop pressure

  • Barosensors from decreased BP also increase sympathetic tone to increase TPR and to increase the renin

VASODILATORS STILL HAVE A NET WINNING EFFECT EVEN WITH THE COMPENSATORY REFLEX

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18
Q

What are the 3 classes of vasodilator drugs

A
  1. potassium channel blockers
  2. organic and inorganic nitrates
  3. calcium channel blockers
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19
Q

Prototypicak potassium channel opener and its target

A
  1. minoxidil –> Katp channels
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20
Q

give mechanism of minoxidil

A
  • open potassium channels to lead to potassium efflux, cell hyperpolarization… inhibits voltage sensitive L-types to reduce ca2+ and cause relaxation
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21
Q

why are hydralazine and diazoxide unique

A
  • Very direct and very strong vasodilators
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22
Q

main indication of potassium channel openers

A
  • HTN uncontrolled by other drugs
  • HTN emergency
  • severe HTN
  • research
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23
Q

Main side effects of drugs of potassium channel blockers

A
  • strong inducers of sympathetic reflex

- increases volume retention and cardiac rate and contractility… can reveal myocardial ischemia and arrythmia

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24
Q

what are dihydropyridines not good at? why?

A
  • don’t bind well to L-type channels in heart
  • because binding is voltage dependent… VSMC RMP are more positive, which dihydropyridines can bind well in… but cardiomyocytes are less polar, and dihydropyridines can’t bind well
25
Q

amlodipine is a _______

A

dihydropyridine calcium channel blocker

26
Q

indications of calcium channel blockers

A
  • mild to moderate HTN
  • reduces TPR
  • cardiac ischemia
27
Q

main adverse effects of dihydropyridines… why?

A
  • 2.5 fold incrased risk of death with short acting (quick releasing) dihydropyridines because of sympathetic reflex
28
Q

What two compounds are broken off of nitrovasodilators by enzymatic activities… what is their fate?

A
  1. cyanide – thiolated then sent to renal for elimination

2. nitric oxide- vasodilation

29
Q

indications of sodium nitroprusside

A
  • Hypertensive emergencies TO REDUCE AFTERLOAD
  • reduce bleeding during surgery
  • acute cardia ischemia (to decrease preload and afterload, and thus decrease cardiac work
30
Q

what is the toxicity of sodium nitroprusside

A
  • CN poisoning when high infusion rates overwhelm SCN synthesis
31
Q

T/F tolerance does not occur with inorganic nitrates like sodium nitroprusside

A
  • False… just different mechanism
32
Q

Name the two centrally acting sympatholytic drugs

A
  1. methyldopa

2. clonidine

33
Q

both methyldopa and clonidine are _____ receptor selective agonists… what’s the difference between them?

A

alpha-2; methyldopa is a prodrug, clonidine is direct

34
Q

give prodrug pathway for methyldopa

A

methyldop –> methyldopamine –> methylnorepinephrine

35
Q

what is the overall goal of clonidine and methyldopa?

A
  • inhibiting sympathetic outflow from brainstem
36
Q

indications of methyldopa/clonidine

A
  • HTN when resistant to other treatments

- decrease TPR and reduce CO

37
Q

side effects of methyldopa/clonidine

A
  • dampens sympathetic reflexes (sympathectomy)
  • sedation
  • nausea
  • Withdrawal syndrome

almost makes them seem sicker than they are because of side effects

38
Q

What is the prototypical sympatholytic and what does it do generally?

A
  • trimethaphan (non-depolarizing inhibitors of ganglionic nicotinic cholinergic receptors)
39
Q

indications of trimethaphan

A
  1. create controlled hypotension

2. dampen spinal autonomic reflex during spinal cord injury

40
Q

What is the classic alpha-1 andrenergic anatagonist and what does it generally do?

A
  • prazosin

- blocks vasoconstrictor effect of sympathetic tone to reduce TPR

41
Q

indications of alpha-1 blocker uses

A
  • monotherapy for mild to moderate HTN

- symptomatic prostate hypertrophy

42
Q

Side effects of alpha-1 blocker uses

A
  1. first-dose phenomenon –> postural hypotension … worsens and impairs recovery from orthostatic hypotension
43
Q

describe why postural hypotension occurs

A
  • normally, you have sympathetic activation kicking in after standing up to correct postural hypotension
  • with alpha blockers… you’re dropping your blood pressure more AND you can’t get reflex as much.. so you can’t repair as well
44
Q

name the non-selective beta receptor antagonist

beta -1 selective

mixed alpha1-AR, beta-AR antagonist

A
  • propranolol
  • metoprolol
  • carvedilol
45
Q

mechanism of antihypertensive action of betablockers

A
  • negative inotropic and chronotropic effect in heart to reduce cardiac output
46
Q

what’s the secondary effect of beta blockers

A
  • inhibits sympathetic mediated renin release to indirectly lower TPR
47
Q

______ is gold standard anti-HTN therapy

A
  • propranolol
48
Q

________ is better for asthmatics

A
  • metoprolol
49
Q

side effects of beta blockers

A
  • exercise intolerance, so non-ideal drug for active people (because reduciton of cardiac output)

Impotence

50
Q

The only cells that produce ACTIVE renin are ______

A

JG- cells… renal juxtaglomerular

51
Q

what are triggers of renin-angiotensin system?

A
  • low pressure
  • low sodium in distal tubule or low flow
  • increased sympathetic nervous system activity
52
Q

what does renin do?

A
  • converts angiotensinogen to angiotensin I
53
Q

how is Angiotensin II formed?

what else does this do?

A
  • via ACE… also inactivates bradykinin
54
Q

what is role of angiotensin II

A
  1. binds to AT1 receptor and activates it (at arterioles and adrenal gland_)… you get synthesis of aldosterone at adrenal gland… and you increase resistance at arteries

** aldosterone increases sodium/h20 reabsorption to increase blood pressuer

55
Q

Name 3 renin-angiotensin system inhibitors

A
  1. renin inhibitors –> aliskren
  2. ACE inhibitor –> “Prils” –> LISINOPRIL
  3. AT1-R antagonist … sartans (LOSARTAN)
56
Q

Out of ACE inhibitors, AT-1 antagonists, and Renin inhibitors, which:

  1. are teratogenic
  2. disrupt electrolyte homeostasis
  3. Reduce GFR with renal artery stenosis
  4. angiodema/cough
A
  1. all
  2. all
  3. all
  4. only ACE inhibitors (because you increase bradykinin levels, which causes cough)
57
Q

Name 3 main diuretics used for HTN… what is the gold standard? when do you use the other 2

A
  1. thiazide (GOLD STANDARD FOR MILD HTN)
  2. K+ sparing (adjuvant)
  3. Loop diuretics (only in refractory HTN)
58
Q

why do you get sustained antihypertensive effect from diuretics?

A
  • decrease total peripheral resistance… not really because of change in plasma volume or cardiac output

TPR lowering is the mechanism, although unknown

59
Q

two examples where you don’t use thiazide

A
    1. post myocardial infarction

2. chronic kidney disease (because kdineys aren’t working well anyway

Cardio Module (25 decks)

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