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Cardiology > Antihypertensive drug therapy > Flashcards

Antihypertensive drug therapy Flashcards

1
Q

Describe the neuroendocrine reflexes that occur with vasodilation.

A
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2
Q

5 classes of antihypertensive drugs

A
  1. diuretics (thiazide)
  2. Calcium channel antagonists (CCBs)
  3. inhibition of the RAAS: ACEIs, ARBs, MR-antagonists
  4. Sympatholytics
  5. Direct vasodilators
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3
Q

Where do diuretics act?

A

distal convoluted tubule of the nephron: 5-8% of filtrate is reabsorbed activel via Na/Cl cotransporter in apical cell membrane

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4
Q

Acute effect, compensatory mechanism, and long term effect of diuretics

A

Acute: Na loss= fluid loss, decrease blood volume, decreased CO, decrease blood pressure

Compensatory: decrease plasma volume triggers renin and aldosterone release= K loss and Na retention to increase distal fluid reabsorption; this is our body’s attempt to restore blood volume, but the net effect is hypotensive! (responders vs. nonresponders)

Long-term: proposed decrease PVR secondary to increased NO production

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5
Q

Explain the NO hypothesis in long-term diuretic use

A

-diuretcs cause volume depletion and subsequent decrease in BP. This causes renin release and activation of RAAS to try to compensate. Due to this, with time we see that renin causes Na reabsorption and water as well to increase intravascular volume. Yet despite all of this, we still see a decrease in BP…how? Well it is thought that this comes from a decrease in SVR potentially through NO mediation.

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6
Q

3 -etic properties of thiazide diuretics

A

-diuretic, naturetic, and kaliretic

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7
Q

Excretion and duration of action of thiazide diuretics

A
  • renal excretion–use with care in elderly
  • 24 hr duration–LONG!
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8
Q

Different degrees of response in thiazide diuretics

A
  • AA and elderly are most responsive (AA have salt sensitive HTN)
  • response depends on vigor of adaptation process
  • response reduced in CRI
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9
Q

Thiazide diuretics toxicities to remember

A

sulfa allergy

hypoK

promote insulin resistance (increase plasma glucose)

increase TG and LDL cholesterol

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10
Q

Diuretics are first line tx for “uncomplicated HTN” in whom?

A
  • elderly patients with isolated systolic hypertension
  • AA patients
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11
Q

Calcium role in VSMCs

A
  • Ca2+ influx through L-type channels and binds to calmodulin
  • Cal-Ca2+ complex activates MLCK
  • MLCK phosphorylates myosin and activates it
  • activated myosin combined with actin to cause contraction
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12
Q

Role of Calcium and cardiac myocytes

A
  1. Ca influx through L-type channels after initial depolarization
  2. Ca influx causes release of Ca from SR
  3. Ca binds troponin eliminating tropomyosin’s inhibitory effects on actin and myosin= contraction occurs
    - In SA and AV node Ca2+ influx is also important in spontaneous depolarization
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13
Q

Sources of calcium in contraction in 3 muscle types

A
  1. VSMCs: mostly Ca2+ influx
  2. Cardiac: Ca2+ influx and intracellular stores
  3. skeletal: almost exclusively on intracellular Ca2+ stores
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14
Q

Which channels do CCAs mostly affect? Consequently, which tissues are these most active on?

A
  • majority of CCAs affect only L-type channels (found on all muscle membranes)
  • cardiac and smooth muscle rely on INFLUX of Ca2+ through these channels, they are most affected by these agents
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15
Q

Classes of CCAs and examples

A
  1. Non-Dihydropyridine: verapamil (isoptin) and diltiazem (cardizem-used in anti arrhythmia, not HTN))
  2. Dihydropyridines: nifedipine (procardia) and amlodipine (norvasc); can cause reflex tachycardia
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16
Q

All CCAs interfere with Ca2+ entry into cells by blocking L channels. However, each class preferentially _________.

A
  • binds during a specific functional state of the channel
  • non-HDPR: bind while channel is open; therefore if the frequency of stimulation to the cell is increased (rapid arrhythmias), the blockade is increased
  • DHPRs: bind during the resting state
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17
Q

Important side effect of using dihydropyridine CCAs

A

-reflex tachycardia

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18
Q

MOA of CCAs in cardiac myocytes

A
  • myocytes and conduction tissue, CAAs decrease contractility (resulting in reduced O2 demand) and they also induce coronary vasodilation; Verapamil > diltiazem > nifedipine
  • slow impulse through SA and AV nodes to reduce HR and intracardiac conduction; verapamil > diltiazem > nifedipine
  • ideal use: paroxysmal SupraV dysrhythmias in setting of HTN or angina
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19
Q

Which class of CCas is most effective in VSMCs and why?

A
  • in PV SMCs, the channels are infrequently activated (due to latch state), so DHPRs bind best since they act mostly during the resting state of L channels
  • result in arterial vasodilation including the coronary arteries
  • Nifedipine >> verapamil >> diltiazem
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20
Q

Verapamil

A
  • predominantly myocardial effects: contractility, blood flow, and conduction
  • effective tx of paroxysmal SVT and in rx of angina (decrease O2 demand and increase coronary blood flow), HTN (reduces SVR)
  • most notable side effect is constipation
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21
Q

Diltiazem

A

lowest side effect incidence

effective in rx of SVT

not great anti HTN drug

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22
Q

Nifedipine

A
  • mainly peripheral vasodilatory effects
  • effective antihypertensive, may be used in conjunction with B-blocker to prevent reflex tachycardia
  • contraindicated in post MI, CHF
  • greatest side effects related to MOA: facial flushing, headaches, dizziness, palpitations, ankle swelling
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23
Q

Dihydropyridines and reflex tachycardia. How and why do we care?

A
  • DHPRs cause profound peripheral vasodilation and limited direct myocardial effects
  • they may produce a reflex tachycardia and increase myocardial contractility
  • this increases myocardial workload and has been demonstrated to be detrimntal in patients who are at high risk of having a MI!! Be care in patients with cardiac dz!!
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24
Q

Summarize CV effects of CCBs: verapamil, diltiazem, nifedipine

A
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25
Q

4 drug classes involved in inhibition of RAAS

A
  • ACEIs
  • ARBs
  • Aldosterone antagonists
  • Direct renin inhibitors (DRIs)
26
Q

Peripheral vasodilators and examples

A
  • drugs that produce a direct relaxation of VSMCs that is not dependent upon innervatio and their effect is not medaited by known receptors
  • venous: nitrates
  • Arterial: hydralazine, minoxidil
  • Both: nitroprusside
27
Q

Are vasodilators effective, even in light of their profound neuroendocrine responses?

A

-yes!! in fact, sometimes you have to give an anti-hypotensive in addition

28
Q

Hydralazine

A
  • unknown MOA
  • Pharm effect: direct arteriolar dilation (no venous effect), preferentially effects renal, peripheral, splanchnic, and coronary arteries; net decrease in BP due to decrease in PVR
  • toxicity: excessive vasodilation (flushing, sweating, palpitations, hypotension, angina); SLE-link syndrome of arthralgia, myalgia, fever, and rash (may be reversible when drug stopped)
29
Q

Who do we see the SLE-line sydrome in with hydralazine?

A

-women who are slow acetylators who have been on high doses for > 6 mos

30
Q

Utility of hydralazine

A
  • limited: frequently used for hypertension during pregnancy including preeclampsia
  • typically used in combination with B adrenergic antagonist to blunt reflex SNS activation
31
Q

Minoxidil

A
  • activates ATP-modulated K+ channel in arteries allowing K to leave the cell= hyperpolarization and relaxation
  • effects: direct arteriolar vasodilation with no venous effect, decrease PVR and also BP, reflex SNS activation, Na retention and increase renin production which return BP to baseline
  • can be blunted with concommitant use of B blockers and diuretics
  • used in outpt setting unlike hydralazine
32
Q

Side effect seen of minoxidil

A

-increase in hair growth–hypertrichosis

33
Q

Sodium nitroprusside

A
  • metabolized directly by SMCs into NO which activation GC to make cGMP=SMC relaxation and vasodilation
  • vasodilates arterioles and veins = decrease PVR and venous return (afterload and preload)
  • easily titrated so good in pts with arteritis
  • coupled with thiosulfate to breakdown the cyanide byproduct
34
Q

When is Na Nitroprusside the drug of choice?

A
  • HTN emergencies because of rapid onset of action (1-2 min) and consistent response
  • intiate tx with B blocker prior to discontinuing the infusion
35
Q

Type, location and normal function of a1, a2, B1 and B2 adrenergic receptors

A

a1: vascular smooth muscle=constriction
- GU smooth muscle: constriction
a2: vascular smooth muscle: constrict

B1: heart myocardium=inotropy and conduction tissue=chronotropy; kidney= renin release

B2: vascular smooth muscle: dilation, airway smooth muscle: dilation

36
Q

4 categories of sympatholytic antihypertensive drugs

A
  1. B blocker: selective or non
  2. Peripheral a1 and a2 adrenergic blockers
  3. centrally acting a2 adrenergic agonists
  4. adrenergic NT release blockers
37
Q

B adrenergic antagonists commonly used in rx of hypertension

A
  • propanolol
  • metoprolol
  • atenolol
38
Q

MOA of B blockers in HTN

A

-reduce HR and reduce renin release

39
Q

classification schemes of B blockers

A
  1. selectivity
  2. lipid solubility
  3. duration of action
  4. intrinsic sympathomimetic activity
40
Q

Compare metoprolol, atenolol, propanolol on B selectivity, use in pts with lung dz, lipophilicity, duration of action

A
41
Q

Prototypical peripheral a-adrenergic antagonists and their MOA

A
  • prazosin: a1 and a2
  • doxazosin and terazosin: pure a1

MOA: antagonist the peripheral vasoconstrictor actions at a receptors; end result is vasodilation and reduction in PVR

42
Q

When are peripheral a antagonists used?

A
  • 3rd line rx in HTN
  • also used to rx BPH
43
Q

2 combination a and B receptor antagonists and their MOA

A
  • labetolol and carvedilol
  • antagonize a1=vasodilation and reduction in PVR
  • nonselective B antagonist= reduce heart rate and renin release
44
Q

Centrally acting a2 adrenergic AGONISTS: example and MOA

A
  • clonidine: administered by mouth with 12 hour duration of action; can use transdermal patches with 1/week to improve compliance
  • MOA:STIMULATE preganglionic a2 receptors on adrenergic neurons in vasomotor center in medulla to REDUCE NE release

this results in decrease sympathetic tones: decrease in PVR, HR< CO, and BP

45
Q

Clonidine is the first line treatment in which patient subgroup?

A

-patients with autonomic neuropathy

46
Q

Adverse effects of centrally acting a2 agonists

A
  • adverse effects are due to unopposed vagal tone
  • dry mouth, orthostatic hypotension, bradycardia, somnolence
  • rebound HTN with discontinuation =a real problem
47
Q

Adrenergic NT blockers

A
  1. reserpine: depletes peripheral NE from storage vesicles in sympathetic nerve endings and therefore decreases PVR; takes 2-3 weeks to be max effective; major side effect of depression!

–rarely used due to profound decrease in QOL

  1. guanethidine: decrease release of NE from peripheral SNS nerve endings
48
Q

Summary of sites of action of major classes of antihypertension drugs

A
49
Q

7 steps in treating a pt with HTN

A
  1. make the dx
  2. determine if there are concomitant dx (DM or CKD)
  3. decide upon rx goal (age)
  4. initiate therapeutic lifestyle change (TLC)
  5. pick right drug (for ethnicity)
  6. adjust dose or add additional meds to achieve goals and side effect profile; dont forget about cost!!!
  7. monitor efficacy and tolerability of therapy
50
Q

Why are ARBs and ACEIs less effective in AAs?

A

-they have lowest RAAS contribution to HTN; use these only if they have kidney disease

51
Q

Lifestyle modifications to prevent and manage HTN

A
  • reduce weight
  • increase physican activity
  • moderate consumption of alcohol, Na, saturated fat, cholesterol
  • maintain adequate intake of K, Ca, Mg (DASH diet)
  • avoid tobacco
52
Q

Pick drugs that appropriately target organ damage due to HTN. What are these targets?

A
53
Q

Selection of classes of drugs based on comorbid conditions: HF, MI, high CAD risk, DM, CKD, recurrent stroke prevention

A
54
Q

3 dosing strategies for BP meds

A
  1. state 1 drug, reach maximum and then add 2nd
  2. start 1 drug and add second before reaching max
  3. begin 2 drugs at the same time
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Cardiology (27 decks)

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