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Renal II, Exam 3 > ACEI's, ARBS, vasodilators and sympathoplegics! > Flashcards

ACEI's, ARBS, vasodilators and sympathoplegics! Flashcards

1
Q

-epril

A

ACE inhibitors

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2
Q
  • sartan
A

ARBs

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3
Q

list of ACE inhibitors

A 
Benazepril
***Captopril
***Enalapril - IV admin
Enalaprilat
Fosinopril
Lisinopril
Moexipril
Perindopril
Quinapril 
Ramipril
Trandolapril
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4
Q

list of ARBs

A 
Azilsartan
Candesartan
Eprosartan
Irbesartan
***Losartan
Olmesartan
Telmisartan
***Valsartan
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5
Q

drugs that block renin secretion?

A
  • clonidine

- propanolol

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6
Q

Renin inhibitors

A

Aliskiren

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7
Q

RAAS system

A

drop in sodium/blood pressure –> renin secretion from kidneys

renin goes to liver and converts ANG –> ANG I

ANGI is converted to ANG II by ACE in the liver

ANGII results in:

  • sodium retenion, H20 retenteion in kidneys
  • release of corticotropin and adiuretin and thirst stimulation in brain
  • increased production of aldosterone in adrenals
  • increased vasoconstriction and increased blood pressure of blood vessels
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8
Q

3 major effects of ANG II?

A
  1. altered peripheral resistance: cause direct vasoconstriction, increased symp discharge –> rapid pressor response
  2. altered renal function: direct increase of sodium reabsorption in proximal tubule, release of ALDO and renal vasoconstriction –> Slow pressor response
  3. altered cardiovascular structure: vascular and cardiac hypertrophy and remodelling (increased ECM proteins, growth factors and proto-oncogenes)
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9
Q

strategies to decrease RAAS?

A 
Diuretics 
Aldosterone receptor (MR) antagonists

ACE inhibitors (ACEIs)
Angiotensin II receptor blockers (ARBs)
Renin inhibitors

β-blockers

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10
Q

captopril/enalapril MOA

A

inhibit the conversion of angiotensin I to the more active angiotensin II; also prevent degradation of bradykinin and other vasodilator peptides

** thus it downregulates a vasoconstrictor and UPREGULATES a vasodilator

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11
Q

indications of ACE inhibitors?

A

hypertension, heart failure, left ventricular dysfunction, prophylaxis of future cardiovascular events (e.g., MI, CAD, stroke) and nephropathy (+/- diabetes)

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12
Q

benefits of ACE inhibitors in HTN?

A

Lowers TPR and mean, diastolic, and systolic BP

Cardiac function in patients with uncomplicated hypertension is little changed

Stroke volume and cardiac output may increase slightly with sustained treatment

Baroreceptor function and cardiovascular reflexes are not compromised

Responses to postural changes and exercise are little impaired

Evidence that ACEIs are superior in treating HTN in patients with diabetes

Improve endothelial function and reduce CV events more so than CCBs or diuretic and β-blocker combo

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13
Q

Adverse effects of ACE inhibitors?

A

Hypotension
*Cough (caused by reduced metabolism of bradykinin)
*Angioedema
*Hyperkalemia – avoid K+-sparing diuretics
Acute renal failure – particularly in patients with renal artery stenosis
Fetopathic potential (teratogen) – **contraindicated in pregnancy
Proteinuria
Skin rash
Dysgeusia (altered sense of taste)

Drug interactions: antacids, capsaicin, NSAIDs, K+-sparing diuretics, digoxin, lithium, allopurinol

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14
Q

type 1 diabetics with renal disease?

A

ACEIs prevent/delay the progression of renal disease in type 1 diabetics and in patients with nondiabetic nephropathies (results mixed in type 2 diabetics)

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15
Q

ACEIs role on renal vasculature?

A

ACEIs vasodilate efferent arterioles > afferent arterioles
Reduces back pressure on the glomerulus and reduces protein excretion
ACEIs usually improve renal blood flow and Na+ excretion rates in CHF

In rare cases, ACEIs can cause a rapid decrease in GFR, leading to acute renal failure
Can occur anytime during therapy, even after months or years of uneventful ACEI treatment

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16
Q

risk factors for ACEIs?

A

induced acute renal failure

MAP insufficient for adequate renal perfusion

  • Poor cardiac output
  • Low systemic vascular resistance

Volume depletion (diuretic use)

Renal vascular disease
- Bilateral renal artery stenosis
- Stenosis of dominant or single kidney
- Afferent arteriolar narrowing (HTN, cyclosporin A)
- Diffuse atherosclerosis in smaller renal vessels
Vasoconstrictor agents (NSAIDs, cyclosporine)

***All cause renal hypoperfusion

don’t combine ACE, ARB or renin inhibitor –> ARF

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17
Q

ANG II Receptor blockers

A
  • LOSARTAN, VALSARTAN

MOA: selectively block AT1 receptors, which leads to
↓ contraction of vascular smooth muscle
↓ aldosterone secretion
↓ pressor responses
↓ cardiac cellular hypertrophy and hyperplasia

No effect on bradykinin metabolism

Therapeutic uses: hypertension, diabetic nephropathy, HF, HF or left ventricular dysfunction after AMI, and prophylaxis of cardiovascular events

Adverse effects similar to ACEIs but less cough and edema; contraindicated during pregnancy

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18
Q

ACEI’s vs ARBs?

A

ARBs reduce activation of AT1 receptors more effectively than do ACE inhibitors

ARBs permit activation of AT2 receptors (vasodilation)

ACE inhibitors increase the levels of a number of ACE substrates, including bradykinin (vasodilation)

Unknown whether or not these pharmacological differences result in significant differences in therapeutic outcomes

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19
Q

aliskiren

A

MOA: inhibits renin and blocks the conversion of angiotensinogen to angiotensin I

Does not increase bradykinin

Rise in plasma renin levels but decreased plasma renin activity (ACEIs, ARBs, and diuretics raise plasma renin levels and activity via feedback loop)

Studies show effectiveness comparable to ACEIs and ARBs

AEs similar to ACEIs and ARBS; contraindicated in pregnancy

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20
Q

clonidine

A

(1) MOA: an agonist of α2-receptors in the brainstem
(2) When stimulated, α2-receptors cause inhibition of sympathetic vasomotor centers, resulting in a centrally mediated reduction in renal sympathetic nerve activity
(3) Ultimate effect is a reduction of renin secretion.

Pharmacodynamics: lowers blood pressure by reducing cardiac output (decreased heart rate and relaxation of capacitance vessels) and reducing peripheral vascular resistance

Adverse Effects: sedation, dry mouth, depression, sexual dysfunction

(1) transdermal preparation is associated with less sedation than oral, but may cause skin reaction
(2) Abrupt withdrawal can lead to life-threatening hypertensive crisis

Clinical Use:
Essential hypertension (rarely used)
Adjunct for narcotic, alcohol, & tobacco withdrawal (unlabeled)

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21
Q

Propanolol

A

(and other β-blockers)

(1) MOA: nonspecific antagonist of adrenergic β-receptors
(2) Act on juxtaglomerular cells by blocking β1-receptor stimulated release of renin and thereby decreases blood pressure (also decreases BP by decreasing cardiac output and decreasing sympathetic outflow from the CNS)

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22
Q

-dipine

A

dihydropyridine CCB: ex. amlodipine, nifedipine

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23
Q

amlodipine

A

DHP CCB

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24
Q

Nifedipine

A

DHP CCB

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25
Q

non-dihydropyridines?

A

Diltiazem, verapamil

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26
Q

Diazoxide (Hyperstat IV)

A

potassium channel openers

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27
Q

Fenoldopam

A

dopamine agonist - thus ensures adequate renal blood flow

MOA: peripheral arteriolar dilator; natriuretic

Use: administered IV for HTN emergencies and post-op HTN

Adverse effects: Tachycardia, h/a flushing

CI: patients with glaucoma due to increases in intraocular pressure

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28
Q

Minoxidil

A

potassium channel opener

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29
Q

hydralazine

A

NO modulator

=Oral drug, dilates arterioles but not veins

MOA: Releases nitric oxide from endothelium

Clinical Uses:

  • controls longer term outpatient HTN
  • First-line therapy for hypertension in pregnancy, with methyldopa
  • Combination with nitrates is effective in heart failure and should be considered in patients, especially African-Americans, with both hypertension and heart failure

Adverse effects:

  • Can induce fluid and sodium retention
  • Headache, nausea, anorexia, sweating, flushing, palpitations
  • Reflex tachycardia can provoke angina in patients with ischemic heart disease
  • Lupus-like syndrome (reversible on drug withdrawl)
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30
Q

sodium nitroprusside

A

NO modulator
- Used to treat hypertensive emergencies, heart failure, & angina (nitrates)

  • Pharmacodynamic effects
    Dilates both arterial and venous vessels—decreases TPR and venous return
    Decreases both preload & afterload

Mainly relaxation of large veins –> decreased venous return –> decreased preload –> decreased O2 demand (major effect), smaller decrease in afterload

Adverse effects
Nitroprusside: excessive hypotension, cyanide poisoning

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31
Q

nitroglycerine

A

organic nitrate NO modulator
* prototype* - cause release of NO via enzymatic action

  • Used to treat hypertensive emergencies, heart failure, & angina (nitrates)
  • Pharmacodynamic effects
    Dilates both arterial and venous vessels—decreases TPR and venous return
    Decreases both preload & afterload

Mainly relaxation of large veins –> decreased venous return –> decreased preload –> decreased O2 demand (major effect), smaller decrease in afterload

Nitrates: orthostatic hypotension, syncope, throbbing headache

Compensatory responses contributing to the development of tolerance: tachycardia, increased cardiac contractility, retention of salt and water

CI: intracrnail pressure is elevated

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32
Q

-olol

A

Beta blockers

33
Q

-zosin

A

alpha 1 antagonists

34
Q

clonidine

A

alpha 2 agonist

35
Q

guanabenz

A

alpha 2 agonist

36
Q

guanfacine

A

alpha 2 agonist

37
Q

methyldopa

A

alpha 2 agonist

Pharmacodynamics: lowers blood pressure by reducing peripheral vascular resistance; variable reduction in heart rate and cardiac output

Pharmacokinetics: Methyldopa is an analog of L-dopa; it is converted to α-methylnorepinephrine by an enzymatic pathway that directly parallels synthesis of norepinephrine from L-dopa

Adverse Effects: sedation, dry mouth, lack of concentration, sexual dysfunction

38
Q

dihydropyridines vs. nonDHPs?

A

i) Dihydropyridines (DHPs)
(1) Prototypes: Nifedipine, Amlodipine
(2) MOA: Blocks vascular L-type calcium channels > cardiac channels

ii) Non-Dihydropyridines
(1) Prototypes: Verapamil, Diltiazem
(2) MOA: Nonselective block of vascular and cardiac L-type calcium channels

39
Q

PD of CCB’s?

A

i) All CCBs block L-type calcium channels (voltage-gated), which are responsible for Ca++ flux into smooth muscle cells, cardiac myocytes, and SA and AV nodal cells in the heart.
iv) Effects on smooth muscle: All CCBs cause vasodilation, which decreases peripheral resistance. Arterioles are more sensitive than veins; orthostatic hypotension is not usually a problem. Relaxation of arteriolar smooth muscle leads to decreased afterload and decreased O2 demand by the heart. (thus work as anti-anginal agents)
v) Effects on cardiac muscle include reduced contractility throughout the heart and decreases in SA node pacemaker rate and AV node conduction velocity.

40
Q

how do CCPs affect cardiac mm?

A

CCBs can produce a negative inotropic effect
In myocytes, Na+ entry through “fast” channels in the primary carrier of current in the depolarization event, but Ca++ entry through “slow” channels (L-type) is an additional component
Ca++ entry may also induce Ca++ release from SR
Ca++ binds to troponin, relieving troponin inhibition of the contractile apparatus, and allows actin-myosin contraction
Inotropic effects of Verapamil > Diltiazem > DHPs

41
Q

why do DHPs not affect cardiac mm?

A

DHPs relax vascular smooth muscle at lower concentrations than required for direct action on the heart

Greater vasodilation with DHPs elicits reflex increase in sympathetic tone that overcomes the negative inotropic effects

42
Q

what could cause heart block?

A

use of beta blockers with non-DHP CCB’s

43
Q

how do non-DHP’s affect the heart?

A

Verapamil & diltiazem block channel, delay recovery of channel, & are frequency dependent
Therefore, verapamil & diltiazem  the rate of SA node depolarization + slow AV nodal conduction
These properties makes them useful for treatment of supraventricular tachyarrhythmias but dangerous in patients with slowed nodal conduction

44
Q

PK properties of CCBs?

A

DHPs with long plasma half-lives are prefered to minimize reflex cardiac effects and extend release preparations are available

ex. amlodopine

45
Q

clinical use of CCBs?

A

long-term outpatient therapy for hypertension, hypertensive emergencies and angina (due to reduction of O2 demand)

46
Q

adverse effects of CCBs?

A

ii) Dihydropyridines: excessive hypotension, dizziness, headache, peripheral edema, flushing, tachycardia, rash, gingival hyperplasia
iii) Non-Dihydropyridines: Dizziness, headache, peripheral edema, constipation (especially verapamil), AV block, bradycardia, heart failure, lupus-like rash with diltiazem. Pulmonary edema, coughing, and wheezing are possible.

47
Q

nifedipine?

A

iv) Some studies reported increased risk of MI, stroke, or death in patients receiving short-acting nifedipine for HTN; therefore short-acting DHPs should not be used for management of chronic HTN; Slow-release and long-acting DHPs are preferred to minimize reflex cardiac effects.

Nifedipine does not decrease AV conduction and therefore can be used more safely than the non-DHPs in the presence of AV conduction abnormalities.

48
Q

MOA of Diazoxide?

A

Opens potassium channels in smooth muscle

(1) Increased potassium permeability hyperpolarizes the smooth muscle membrane, reducing the probability of contraction
(2) Arteriolar dilator resulting in reduced systemic vascular resistance and mean arterial pressure

relatively long acting - 4-12 hours after injection

typically administered as 3-4 injections

49
Q

diazoxide?

A

Arteriolar vasodilation
Diminishing use in hypertensive emergencies due to adverse effects:
Excessive hypotension can cause stroke and MI
Hyperglycemia

50
Q

Minoxidil?

A

= potassium channel opener

= Arteriolar vasodilation, more effacacious than hydralazine

Clinical uses include severe hypertension thats not responding to other tx and baldness (topical)

Adverse effects:
Headache, sweating
Hypertrichosis
Reflex tachycardia & edema – must be used with β-blocker & diuretic to avoid these effects

51
Q

Propanolol

A

non-selective Beta blocker

52
Q

Carvedilol

A

non selective Beta blocker and alpha 1 blocker

used to reduce mortality of heart failure- administration may worsen acute CHF

53
Q

Labetalol

A

nonselective beta blocker and alpha 1 blocker

54
Q

nadolol

A

non selective beta blocker

55
Q

timolol

A

non selective beta blocker

56
Q

carteolol

A

non selective beta blocker

57
Q

penbutolol

A

non selective beta blocker

58
Q

pindolol

A

non selective beta blocker

59
Q

Metoprolol

A

B1 selective blocker

most common used for HTN

used to reduce mortality of heart failure- administration may worsen acute CHF

60
Q

atenolol

A

B1 selective blocker

most common used for HTN

61
Q

Esmolol

A

B1 selective blocker

Very rapid onset & short duration of action

Used as IV infusion for peri-operative tachycardia and hypertension, hypertensive emergencies, arrhythmias

Used in electroconvulsive therapy

62
Q

Bisoprolol

A

B1 selective blocker

used to reduce mortality of heart failure- administration may worsen acute CHF

63
Q

betaxolol

A

B1 selective blocker

64
Q

Acebutolol

A

B1 selective blocker

65
Q

nebivolol

A

B1 selective blocker

66
Q

Doxazosin

A

alpha1 blocker

67
Q

prazosin

A

** alpha1 blocker

  • prevents vasoconstriction of aa. and vv; blood pressure is reduced by lowering peripheral vascular resistance
  • relaxes smooth mm. in prostate
  • results in retention of salt and water when used w/out diuretic

Adverse Effects:

  • generally well tolerated but may cause orthostatic hypotension, dizziness, palpitations, h/a
  • less incidence of reflex tachycardia than non selective adrenergic blockers

clinical use:
- used in men w/ concurrent HTN and BPH

68
Q

Terazosin

A

alpha1 blocker

69
Q

why use propanolol?

A
    • propanolol
  • treat HTN by decreasing the CO –> decreased mortality after MI
  • especially useful in preventing the reflex tachycardia that often results from tx w/ direct vasodilators
  • blockade of B1 receptors inhibits renin release

contraindication: asthma

70
Q

Adverse effects of propanolol?

A

Asthma/COPD: blocks the B2 receptors causing to bronchospasm

Diabetes: glycogenolysis is inhibited after B2 blockade

Cardiac arrythmias: see fatigue and bradychardia

drug interactions with CCBs can cause heart block

71
Q

why use beta blockers?

A 
HTN
Heart failure
Ischemic heart disease
cardiac arrythmias
glaucoma

B1 selectivity advantageous in treating patients w/ comorbid asthma, diabetes or peripheral vascular disease

72
Q

alpha 2 agonists

A

clonidine, methyldopa

General MOA: reduce sympathetic outflow from vasomotor centers in the brainstem but allow these centers to retain or even increase their sensitivity to baroreceptor control

i) Agonists at central α2 receptors
ii) Slight variations in hemodynamic effects of clonidine and methyldopa suggest that these two drugs may act at different populations of central neurons

Clinical Uses
i) With the exception of clonidine, these agents are rarely used today; methyldopa is used for hypertension during pregnancy (see below)

73
Q

acute management of severe HTN in pregnant women?

A

(1) Labetalol (IV): effective, rapid onset of action, good safety profile
(2) Hydralazine (IV)
(3) Calcium Channel Blockers: sustained release nifedipine or immediate release nicardipine; nicardipine can also be given IV; data is more limited for use in pregnancy compared to labetalol and hydralazine
(4) Nitroglycerin (IV)

74
Q

long term oral therapy management of HTN in pregnant women?

A

(1) Methyldopa: long-term safety for the fetus has been demonstrated; mild antihypertensive of limited efficacy; sedative effect is bothersome to already fatigued patients
(2) Labetalol: more rapid onset of action than methyldopa; alternatives in this category include pindolol and long-acting metoprolol
(3) Nifedipine (extended release)
(4) Hydralazine: Due to reflex tachycardia, monotherapy with oral hydralazine is not recommended; hydralazine may be combined with methyldopa or labetalol if needed as add-on therapy

75
Q

contraindications of antihypertensives and pregnancy?

A

i) ACE inhibitors, ARBs, direct renin inhibitors: these drugs are associated with significant fetal renal and cardiac abnormalities
ii) Nitroprusside: possible fetal cyanide poisoning if used for more than a few hours

76
Q

vasodilators used for tx of HTN emergencies?

A

(1) Sodium nitroprusside: considered the most effective parenteral drug for hypertensive emergencies; potential for cyanide toxicity limits prolonged use
(2) Nitroglycerin: frequently used in patients with cardiac ischemia or after coronary bypass surgery
(3) Nicardipine: parenteral formulation of this DHP-CCB is available for rapid effect
(4) Clevidipine: parenteral formulation of this DHP-CCB is approved only for hypertensive emergencies
(5) Fenoldopam: maintains or increases renal perfusion by dilating renal arteries; possibly a good choice for patients with renal dysfunction
(6) Hydralazine: often used for hypertensive emergencies in pregnancy related to eclampsia (see above)

77
Q

adrenergic antagonists used for HTN emergencies?

A

(1) Phentolamine: α-blocker used to treat patients with hypertension due to elevated catecholamines (cocaine intoxication, pheochromocytoma)
(2) Esmolol: rapid but short-acting β1-blocker used to treat aortic dissection or postoperative hypertension
(3) Labetolol: combined α- and β-blocker that may be safe in patients with active coronary disease

78
Q

choice of therapy in essential HTN?

A

General classes typically employed as initial monotherapy:

i) Thiazide diuretics
ii) ACE Inhibitors/ARBs
iii) Calcium channel blockers (long-acting)
iv) Beta-blockers are NOT typically used in the absence of a specific indication

Exhibit roughly equal efficacy, but some patients will respond to one drug and not to another
i) Some predictable differences, e.g., black patients respond better to thiazide diuretics and CCBs, and respond poorly to ACE inhibitors and beta-blockers

79
Q

common HTN drug combinations?

A

i) ACEIs and calcium channel blockers (trandolapril/verapamil)
ii) ACEIs and diuretics (benazepril/hydrochlorothiazide)
iii) ARBs and diuretics (valsartan/hydrochlorothiazide)
iv) β-blockers and diuretics (propranolol/hydrochlorothiazide)
v) Centrally acting agent and diuretic (reserpine/chlorothiazide)
vi) Diuretic and diuretic (spironolactone/hydrochlorothiazide)

Renal II, Exam 3 (9 decks)

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