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Cardio Week 3 > ICL 3.5: HTN Pharmacology > Flashcards

ICL 3.5: HTN Pharmacology Flashcards

1
Q

what is the formula for MAP?

A

MAP = CO x PR

CO = SV x HR

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2
Q

what are the 3 control mechanisms used to control BP?

A
  1. rapid, moment-to-moment, baroreceptor reflexes mediated by ANS
  2. slower, longer-term regulation of blood volume and resistance by RAAS
  3. local release of vasoactive substances from vascular endothelium (endothelin-1, NO)
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3
Q

what are diuretics?

A

they lower BP by removing sodium from the body; water follows sodium out, reducing blood volume

ex. thiazides, loop diuretics, K sparing diuretics

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4
Q

what are drugs that affect the RAAS?

A

they alter the ability of this system to regulate blood volume and systemic vascular resistance, (thereby influencing cardiac output and arterial pressure)

ex. ACE inhibitors, AT II receptor blockers, direct renin inhibitors, aldosterone inhibitors

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5
Q

what are drugs that are direct vasodilators?

A

they cause larger vessel diameter which decreases resistance (arteries) and/or increases capacitance (veins), these effects decrease blood pressure

ex. Ca channel blockers, nitrates

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6
Q

what are SNS depressants?

A

drugs in this group all decrease sympathetic nervous system effects on vessel resistance, cardiac output, renin stimulation, etc.

ex. alpha and beta blockers. clonidine

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7
Q

what are the 3 main drug approaches for treating HTN?

A
  1. thiazide-type diuretics
  2. ACE inhibitors/ARBs
  3. Ca channel blockers
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8
Q

what are the basics of renal physiology?

A

renal tubule: removes waste and mediates filtration & secretion (blood –> lumen), and reabsorption (lumen –> blood) of fluid and ions, to maintain homeostasis

ion transporter systems vary along the segments of the renal tubule

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9
Q

what are the main uses of diuretics

A
  1. edema
  2. heart failure
  3. renal failure

most diuretics act at specific transporters to increase excretion of Na and water, which reduces blood volume and BP

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10
Q

which drugs are thiazide and thiazide-type diuretics?

A
  1. hydrochlorothiazide

2. chlorthalidone

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11
Q

what is the MOA of thiazide drugs?

A

Na/Cl symporter moves Na and Cl from the lumen into the blood

so thiazides selectively inhibit the Na+/Cl- co-transporter (NCC) on luminal side of DCT and also has mild vasodilator effects

blocking sodium reabsorption into blood reduces water movement into blood (decreases blood volume)

only 5% of filtered Na is reabsorbed by the NCC though so thiazides aren’t the strongest diuretics but hydrochlorothiazide is long lasting and first-line treatment for HTN

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12
Q

what are some of the side effects of thiazides?

A
  1. increased blood sugar and cholesterol/LDL
  2. hypercalcemia & hyperuricemia (–> gout)
  3. K+ wasting; requires monitoring for hypokalemia
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13
Q

which drugs are loop diuretics?

A

furosemide

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14
Q

what is the MOA of loop diuretics?

A

the thick ascending limb (TAL) has a cotransporter that reabsorbs sodium, potassium and 2 chloride into the blood

so loop diuretics inhibit luminal Na+/K+/2Cl- transporter (NCCL2) in the thick ascending loop of Henle

they also induces synthesis of renal prostaglandins that inhibits salt transport in the TAL

blocking Na+ reabsorption into blood reduces water movement into blood (decreases blood volume)

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15
Q

which diuretics are the most powerful?

A

loop diuretics

NCCL2 reabsorbs ~25% of the filtered Na+ load so blocking them has a much bigger effect and are used in severe HTN

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16
Q

what are some of the side effects of loop diuretics?

A
  1. Increased loss of Ca2+, Mg+, K+, H+ in urine (indirect consequence of blocking NCCL2)
  2. hyperuricemia (↑ uric acid in blood)
  3. allergic reactions (sulfonamide structure)
  4. ototoxicity (dose-related, reversible)
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17
Q

which drugs are K+ sparing diuretics?

A
  1. spironolactone

2. eplerenone

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18
Q

what is the MOA of K+ sparing diuretics?

A

ion transport in the DCT and collecting duct is regulated by aldosterone, a mineralocorticoid hormone

aldosterone binds to intracellular receptors, then diffuses into the nucleus to increase expression of ENaC (reabsorbs Na into blood) and an ATP-dependent K+ pump (secretes K+ into lumen)

so K sparing diuretics are antagonists at aldosterone receptors in collecting tubule; they reduce expression of ENaC sodium channels and ATP-dependent K+ pumps

so they increase loss of Na+ which pulls water out of blood and decreases excretion of K+ and H+

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19
Q

what are the side effects of K sparing diuretics?

A
  1. hyperkalemia
  2. gynecomastia
  3. antiandrogenic effects (spironolactone only)
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20
Q

how good of a diuretic are K sparing diuretics?

A

weak diuretic effects

but can be added to other diuretics to reduce K+ wasting

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21
Q

what is the net effect of activating RAAS?

A

increasing blood volume and systemic vascular resistance, which together increase CO and arterial pressure

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22
Q

what is the RAAS pathway?

A

in response to signals, the kidney releases renin, which cleaves circulating angiotensinogen into angiotensin I – ACE in the lungs converts that to angtiotensin II

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23
Q

what are the effects of angiotensin II?

A
  1. acting at AT1 receptors to constrict resistance vessels, increasing systemic vascular resistance and arterial pressure
  2. stimulating sodium reabsorption at renal tubular sites, which increases Na+ and water retention
  3. stimulating adrenal cortex to release aldosterone, which in turn acts on the kidneys to increase Na+ and water retention
  4. stimulating pituitary to release vasopressin (antidiuretic hormone, ADH), which increases fluid retention by the kidneys
  5. stimulating thirst centers within the brain
  6. enhancing sympathetic function by stimulating norepinephrine release and inhibiting norepinephrine re-uptake
  7. stimulating cardiac hypertrophy and vascular hypertrophy (cardiac remodeling)
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24
Q

which drugs are ACE inhibitors?

A
  1. lisinoprl
  2. enalapril

prodrugs = need to metabolize them to turn them into their active forms

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25
Q

what is the MOA of ACE inhibitors?

A

inhibits ACE, thereby:

  1. preventing production of ATII
  2. increasing levels of bradykinin because ACE normally inhibits bradykinin –> a potent vasodilator because it increases prostaglandin synthesis which are vasodilators

they lower BP mainly by decreasing PVR via inhibition of the RAAS and stimulation of the kinin system

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26
Q

what is the main use of enalapril?

A

it’s an ACE inhibitor

it is directly given IV to treat hypertensive emergency

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27
Q

what are the main uses of ACE inhibitors?

A
  1. CHF
  2. diabetes
  3. post-MI
  4. first line in HTN!!!
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28
Q

what are the major side effects of ACE inhibitors?

A

these are all really important!!!

  1. initial hypotension
  2. acute renal failure (rare), hyperkalemia
  3. dry cough (common) and angioedema –-> both result from increased bradykinin levels because it sensitizes the cough reflex
  4. teratogenic effects –> contraindicated in pregnancy due to fetal mortality, renal defects (2nd /3rd trimester) and likely CV and CNS (1st trimester) defects
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29
Q

what does ARB stand for?

A

ATII receptor blockers

30
Q

which drugs are ARBs?

A

losartan

several agents in class; all names end in “-sartan”

31
Q

what is the MOA of ARBs?

A

they are selective angiotensin II receptor antagonist

lowers BP mainly by decreasing PVR via inhibition of RAAS –> so you’re still making ATII but you’re blocking its receptors

no effects on kinin system though!!

32
Q

what are the side effects of ARBs?

A
  1. Initial hypotension, hyperkalemia (like ACEIs)
  2. teratogenesis – contraindicated in pregnancy (like ACEIs)

no cough/angioedema (unlike ACEIs, no effect on kinins)

33
Q

what are the uses of ARBs?

A
  1. CHF
  2. post-MI (because ATII can prevent cardiac remodeling)
  3. 2nd choice in HTN if ACEI can’t be tolerated or used
34
Q

which drugs are direct renin inhibitors?

A

aliskerin

35
Q

what is the MOA of direct renin inhibitors?

A

renin antagonist; binds at renin’s active site

effects HTN by:
1. arterial & venous dilation (reduces preload, afterload)

  1. decreasing blood volume
  2. depression of SNS activity
36
Q

what are the side effects are direct renin inhibitors?

A
  1. generally mild; headache, diarrhea

2. contraindicated in pregnancy due to similarities with ACEIs and ARBs, but not teratogenic in animal models

37
Q

how is vascular tone regulated?

A

vascular tone is regulated by numerous competing mechanisms that directly or indirectly relax or contract smooth muscle surrounding blood vessels

some vasodilator drugs can selectively alter the tone of arteries (resistance vessels) vs. veins (capacitance vessels)

extrinsic (systemic) – SNS, ATII, atrial natriuretic peptide, etc.

intrinsic (local) – NO, endothelin, histamine, etc.

38
Q

what are calcium channel blocker drugs?

A

CCB drugs used in hypertension act at L-type calcium channels

these voltage-gated channels are found at several sites, where they mediate specific effects:
1. nodal tissue – conduction velocity

  1. cardiomyocytes – contractility
  2. vascular smooth muscle – vasoconstriction
39
Q

which drugs are dihydropyridines?

A

nifedipine

several agents in the dihydropyridine class; all end in “-dipine”

Ca channel blockers

40
Q

what are dehydropyridines?

A

blocking L-type calcium channels

more selective for those on arterial vascular smooth muscle

mainly reduction of systemic vascular resistance and arterial pressure

many are formulated to be long-acting sustained release –> less side effects because less reflex responses

41
Q

what are the major side effects od dehydropyridine CCBs?

A
  1. flushing
  2. headache
  3. excessive hypotension
  4. edema
  5. reflex tachycardia
  6. gingival hyperplasia
42
Q

what are the uses of dihydropyridine?

A
  1. mainly for treatment of HTN (systemic & pulmonary)
  2. some use in angina
  3. Raynaud’s phenomenon
43
Q

which drugs are non-dihydropyridine CCBs?

A
  1. verapamil

2. diltiazem

44
Q

what is the MOA of non-dihydropyridine CCBs?

A

they bind nonselectively to L-type calcium channels on vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue

more “cardioselective” than DHP CCBs

arterial > venous effects

cardiac depressant effects (decreased HR, CO), reduction of systemic vascular resistance and arterial pressure

class IV antiarrhythmics!

45
Q

what are the major side effects of non-dihydropyridine CCBs?

A
  1. excessive bradycardia
  2. impaired electrical conduction
  3. depressed contractility
  4. constipation
  5. hyperprolactinemia
46
Q

what are the uses of non-dihydropyridine CCBs?

A

angina and arrhythmias

47
Q

which drugs are nitrate vasodilators?

A
  1. nitroglycerin

2. sodium nitroprusside

48
Q

what is the MOA of nitrate vasodilators?

A

formation or release of NO to dilate venous (nitroglycerin) or arterial (nitroprusside) vessels

NO increases cGMP, which (1) inhibits Ca++ entry into the cell –> smooth muscle relaxation and (2) stimulates a kinase that activates myosin light chain phosphatase –> relaxation

NO also activates K+ channels –> hyperpolarization, relaxation

49
Q

what are the clinical uses of nitrate vasodilators?

A
  1. angina!!

2. hypertensive emergency (because can be given IV)

50
Q

what are the side effects of nitrate vasodilators?

A
  1. headache
  2. flushing
  3. reflex tachycardia
  4. cyanide toxicity
51
Q

which drugs are direct vasodilators?

A
  1. hydralazine
  2. minoxidil
  3. fenoldopam
52
Q

what is hydralazine?

A

direct vasodilator; releases NO which dilates arterioles (not veins)

used adjunct in HTN treatment and heart failure

rapid acetylators clear the drug more rapidly = lower drug effect –> you’ll see a difference between how well it works for people

you can use this in pregnancy!!!

53
Q

what are the side effects of hydralazine?

A
  1. headache
  2. nausea
  3. palpitations
  4. reflex tachycardia
  5. reversible SLE-like syndrome
54
Q

what is minoxidil?

A

opens K+ channels in smooth muscle, polarizing effect reduces likelihood of contraction –> dilates arterioles, not veins

used for HTN and hair loss!

55
Q

what are the side effects of minoxidil?

A
  1. headache
  2. sweating
  3. hair growth
  4. compensatory effects –> SNS stimulation, fluid and sodium retention –> treat with B blockers and loop diuretics
56
Q

what is fenoldopam?

A

D1 agonist

short-term use in severe hypertension

57
Q

what are the adverse effects of fenoldopam?

A
  1. dose related tachycardia
  2. hypokalemia
  3. increased IOP in glaucoma
58
Q

what is the main use of alpha 1 antagonists?

A

benign prostatic hyperplasia

59
Q

for patients with mild HTN and no indication for a specific drug, what monotherapy would you use?

A
  1. thiazides
  2. ACEI/ARBs
  3. CCBs

these produce target response in 30-50% of patients with mild HTN

trying different single agents have 60-80% response rate

consider two-drug initial therapy when BP is >20/10 mmHg above goal

60
Q

which drug class should you use to treat HTN in people with angina?

A
  1. B blockers

2. CCBs

61
Q

which drug class should you use to treat HTN in people with Afib/flutter?

A
  1. B blockers

2. non-DHP CCBs

62
Q

which drug class should you use to treat HTN in people with HF/post-MI?

A
  1. ACEI/ARBs
  2. B blockers
  3. non-DHP CCBs
63
Q

which drug class should you NOT use to treat HTN in people with asthma/COPD?

A
  1. B blockers

2. ACEI

64
Q

which drug class should you use to treat HTN in people who are pregnant?

A
  1. labetalol
  2. nifedipine
  3. hydralazine
  4. methyldopa
65
Q

which drug class should you NOT use to treat HTN in people who are pregnant?

A
  1. ACEI/ARBs

2. DRIs

66
Q

which drug class should you use to treat HTN in african americans? not use?

A
  1. CCBs
  2. thiazide diuretics

don’t use B blockers or ACEIs

67
Q

which drug class should you NOT use to treat HTN in people who have diabetes?

A

B blockers

they can mask hyperglycemia

use ACEI/ARBs

68
Q

why give drugs IV instead of oral for hypertensive emergency?

A

they are immediately present in the blood

69
Q

which HTN drugs trigger reflex tachycardia? how can you treat it?

A

hydralazine, minoxidil, fenoldopam tend to trigger reflex tachycardia

this can be treated with β blockers

70
Q

which HTN drugs trigger RAAS activation?

A

vasodilators and SNS-targeted drugs (except BB) trigger RAAS activation that produces fluid retention

can be treated with diuretics or ACEIs

Cardio Week 3 (13 decks)

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