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Cardio Module > anti-hypertensive drugs > Flashcards

anti-hypertensive drugs Flashcards

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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?

Study These Flashcards
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
amlodipine is a _______
dihydropyridine calcium channel blocker
26
indications of calcium channel blockers
- mild to moderate HTN - reduces TPR - cardiac ischemia
27
main adverse effects of dihydropyridines... why?
- 2.5 fold incrased risk of death with short acting (quick releasing) dihydropyridines because of sympathetic reflex
28
What two compounds are broken off of nitrovasodilators by enzymatic activities... what is their fate?
1. cyanide -- thiolated then sent to renal for elimination | 2. nitric oxide- vasodilation
29
indications of sodium nitroprusside
- Hypertensive emergencies TO REDUCE AFTERLOAD - reduce bleeding during surgery - acute cardia ischemia (to decrease preload and afterload, and thus decrease cardiac work
30
what is the toxicity of sodium nitroprusside
- CN poisoning when high infusion rates overwhelm SCN synthesis
31
T/F tolerance does not occur with inorganic nitrates like sodium nitroprusside
- False... just different mechanism
32
Name the two centrally acting sympatholytic drugs
1. methyldopa | 2. clonidine
33
both methyldopa and clonidine are _____ receptor selective agonists... what's the difference between them?
alpha-2; methyldopa is a prodrug, clonidine is direct
34
give prodrug pathway for methyldopa
methyldop --> methyldopamine --> methylnorepinephrine
35
what is the overall goal of clonidine and methyldopa?
- inhibiting sympathetic outflow from brainstem
36
indications of methyldopa/clonidine
- HTN when resistant to other treatments | - decrease TPR and reduce CO
37
side effects of methyldopa/clonidine
- dampens sympathetic reflexes (sympathectomy) - sedation - nausea - Withdrawal syndrome almost makes them seem sicker than they are because of side effects
38
What is the prototypical sympatholytic and what does it do generally?
- trimethaphan (non-depolarizing inhibitors of ganglionic nicotinic cholinergic receptors)
39
indications of trimethaphan
1. create controlled hypotension | 2. dampen spinal autonomic reflex during spinal cord injury
40
What is the classic alpha-1 andrenergic anatagonist and what does it generally do?
- prazosin | - blocks vasoconstrictor effect of sympathetic tone to reduce TPR
41
indications of alpha-1 blocker uses
- monotherapy for mild to moderate HTN | - symptomatic prostate hypertrophy
42
Side effects of alpha-1 blocker uses
1. first-dose phenomenon --> postural hypotension ... worsens and impairs recovery from orthostatic hypotension
43
describe why postural hypotension occurs
- 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
name the non-selective beta receptor antagonist beta -1 selective mixed alpha1-AR, beta-AR antagonist
- propranolol - metoprolol - carvedilol
45
mechanism of antihypertensive action of betablockers
- negative inotropic and chronotropic effect in heart to reduce cardiac output
46
what's the secondary effect of beta blockers
- inhibits sympathetic mediated renin release to indirectly lower TPR
47
______ is gold standard anti-HTN therapy
- propranolol
48
________ is better for asthmatics
- metoprolol
49
side effects of beta blockers
- exercise intolerance, so non-ideal drug for active people (because reduciton of cardiac output) Impotence
50
The only cells that produce ACTIVE renin are ______
JG- cells... renal juxtaglomerular
51
what are triggers of renin-angiotensin system?
- low pressure - low sodium in distal tubule or low flow - increased sympathetic nervous system activity
52
what does renin do?
- converts angiotensinogen to angiotensin I
53
how is Angiotensin II formed? what else does this do?
- via ACE... also inactivates bradykinin
54
what is role of angiotensin II
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
Name 3 renin-angiotensin system inhibitors
1. renin inhibitors --> aliskren 2. ACE inhibitor --> "Prils" --> LISINOPRIL 3. AT1-R antagonist ... sartans (LOSARTAN)
56
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
1. all 2. all 3. all 4. only ACE inhibitors (because you increase bradykinin levels, which causes cough)
57
Name 3 main diuretics used for HTN... what is the gold standard? when do you use the other 2
1. thiazide (GOLD STANDARD FOR MILD HTN) 2. K+ sparing (adjuvant) 3. Loop diuretics (only in refractory HTN)
58
why do you get sustained antihypertensive effect from diuretics?
- decrease total peripheral resistance... not really because of change in plasma volume or cardiac output TPR lowering is the mechanism, although unknown
59
two examples where you don't use thiazide
- 1. post myocardial infarction | 2. chronic kidney disease (because kdineys aren't working well anyway

Cardio Module (25 decks)

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