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Pharmacology > Hypertension, Heart Failure, and Ischemic Heart Disease > Flashcards

Hypertension, Heart Failure, and Ischemic Heart Disease Flashcards

1
Q

What are the steps of the RAAS?

A

In response to decreased BP or volume, renin is released by the kidneys.
Renin acts on the liver which causes the release of Angiotensinogen that is cleaved by the renin resulting in Angiotensin I which is converted via the lungs by ACE to Angiotensin II which stimulates the adrenal cortex to release Aldosterone. Aldosterone acts on the distal portion of the nephron to increase Na K ATP pumps to increased the reabsorption of Na and H2O=increased blood volume and BP

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2
Q

Hydrochlorothiazide: Class, site of action, MOA, AE

A

Class: Thiazide diuretic
Site of action: Distal tubule
MOA: Competitive antagonism of Na+Cl- cotransporter (by inhibiting the transporter= inhibit Na+Cl- reabsorption into the blood)
AE: hypokalemia, hyperuricemia (incr. gout), hyperglycemia, dehydration

**Less effective of CrCl <30ml/min

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3
Q

Triameterene/amiloride: Class, site of action, MOA, AE

A

Class: K sparing diuretics
Site of action: Collecting duct
MOA: Na+ channel blockade, increased reabsorption of K
AE: hyperkalemia

**Mild as monotherapy, used with thiazide drugs. Ex- Maxide is an HCTZ/TMT combo drug

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4
Q

Furosemide, bumetanide, torsemide: Class, site of action, MOA, AE

A 
Class: Loop diuretics 
Site of action: Loop of Henle
MOA: Inhibits Na-K-Cl cotransporter 
AE: hypokalemia, hypomagnesemia, hypocalcemia, dose related ototoxicity
CI: sulfa allergy

**Management of s/s of congestive HF

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5
Q

Spironolactone, eplerone: Class, Site of action, MOA, AE

A

Class: Aldosterone Antagonist
Site of action: Distal tubule and collecting duct (decreases K+/Na+ exchange here)
MOA: Competitive antagonist at aldosterone receptors, inhibits mineralcorticoid receptors
AE: hyperkalemia (caution with renal dysfx)

***Spironolactone- used in the management of HF, known mortality reduction. Also inhibits mineralcorticoids AND androgen receptors (gynecomastia, impotence)
Eplerone- more selective for mineralcorticoids, less AE

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6
Q

Beta-blockers antagonize ________ at __-receptors.

A

Catecholamines at B-receptors

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7
Q

Beta-Blockers effects on the body include:

A
  • Decrease CO by decreasing HR and contractility (=decreased BP)
  • Initial compensatory increase in PVR
  • Decreases peripheral resistance by inhibition of B-receptors in kidney which decreases renin
  • Produce resting bradycardia
  • Reduce exercise-induced tachycardia
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8
Q

AE of Beta-Blockers include:

A
  • Acute asthma, wheezing (inhibits bronchial muscle relaxation)
  • Symptomatic bradycardia
  • Fatigue and Depression (lipid soluble BB’s enter CNS)
  • Hypoglycemia (avoid in diabetics)
  • Sexual dysfunction
  • Lipid profile changes

**Avoid sudden withdrawal of agent

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9
Q

What type of patient should not be on a non-selective beta blocker and why?

A

Asthmatics. Non-selective beta blockers can inhibit bronchial muscle relaxation leading to an acute asthma attack

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10
Q

Why might a Beta-blocker be avoiding in diabetics?

A

Can cause hypoglycemia as well as mask the s/s of the hypoglycemia which could result in decreased detection and more profound hypoglycemia

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11
Q

Propranolol: Class, MOA, CI, metabolization

A

Class: Non- selective beta blocker
MOA: antagonizes catecholamines at b1 and b2 receptors, inhibition of sympathetically induced renin secretion
CI: asthmatics
Met: Hepatic; CYP2D6, 2C19

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12
Q

Selective B-Blockers include:

A

B1 Selective:
Metoprolol(Lopressor), atenolol, bisoprolol, esmolol
Dose dependent cardiac selectivity, may affect B2 in some doses

Atenolol is less lipid soluble and renally excreted (don’t use with renal impairment, OK with hepatic impairment)
Metoprolol is hepatically metabolized by CYP2D6

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13
Q

Acebutolol, carteolol, penbutolol, pindolol: Class, MOA

A

Partial B-blockers
(mixed agonist/antagonist)
MOA: Intrinsic Sympathomimetics Activity (= can increase sympathetic tone in addition to B blocking)
-Less decrease in HR and CO
-Agonist when sympathetic tone is low= less resting bradycardia
-Antagonist when sympathetic tone is high = blocks exercise-induced tachycardia

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14
Q

Labetolol: Class, uses

A

Mixed a1/B1/B2 blocker
3:1 B to a antagonism (orally)
Used IV to treat hypertensive crisis

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15
Q

Carvedilol (Coreg): Class, uses

A

Mixed a1/B1/B2 blocker
S(-) isomer- non selective B blockade
R(+) isomer- a-blockade
Primary use is in HF

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16
Q

Prazosin: Class, MOA, precautions, uses, met

A

a-1 blocker
MOA: Inhibitor of peripheral vasomotor tone, reducing vasoconstriction and decreasing SVR
Precautions: ‘first dose effect’ postural hypotension.
Na+ H2O retention when given w/o diuretics
Uses: BPH
Met: Hepatically non-CYP

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17
Q

Centrally acting a-2 agonists: MOA, AE

A

MOA: Reduce sympathetic outflow from vasopressor centers in the brain stem
AE: Sedation, impaired concentration, nightmares, depression, vertigo, EPS(extrapyramidial s/s), lactation in men

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18
Q

Methyldopa (Aldomet): Class, MOA, uses

A

Centrally acting a-2 agonist
MOA: Converted to alpha-methyldopamine and alpha methylnorepinephrine in CNS. Stimulates central a-2 centers leading to reduction in the activity of the vasomotor center
Renal blood flow maintained = good in renal insufficiency
**Recommended for pregnant women

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19
Q

Clonidine: Class, SOA, uses, met

A

Centrally acting a-2 agonist
Site: CNS non-adrenergic binding sites and a a2 receptor agonism
=BP reduction d/t decreased CO d/t decreased HR and peripheral resistance

  • Block effects of TCA
  • Rebound hypertension with abrupt cessation (d/t downregulation of a-2 receptors while using drug= less feedback inhibition)
  • 50/50 hepatic/renal metabolism
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20
Q

ACE Inhibitors act where in the RAAS?

A

Block conversion of Angiotensin I to Angiotensin II

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21
Q

Lisinopril, captopril, ramipril, enalapril, fosinopril, quinapril, benazepril: Class, Site of action, MOA, prodrugs?

A

ACE Inhibitors
Site: ACE in endothelium
MOA: blocks ACE conversion of AI to AII, blocks inactivation of bradykinin (ACE usu. breaks down bradykinin)
Prodrugs: ramipril, enalapril, benazepril, fosinopril

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22
Q

Besides ACEI antihypertensive properties, what else could they be used for and in whom?

A

Diabetics with proteinuria

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23
Q

AE of ACEI:

A

Hyperkalemia
Angioedema (bradykinin)
Dry cough (bradykinin)

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24
Q

What type of drug can interfere with ACEI?

A

NSAIDs (block bradykinin-mediated vasodilation)

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25
Q

CI of ACEI:

A

Pregnancy and renal artery stenosis

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26
Q

Where do Angiotensin Receptor Blockers(ARBs) work?

A

A II receptors

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27
Q

Losartan, valsartan, candesartan, irbesartan, telmisartan, eprosartan: Class, Site, MOA

A

ARBs
Site: A II receptors
MOA: Competitive binding results in decreased peripheral vasoconstriction

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28
Q

ARBs AE and CI

A

AE: Hyperkalemia
No effect on ACE or bradykinin (no cough or angioedema)
CI: Pregnancy

29
Q

Aliskiren (Tekturna): Class, site, MOA, CI

A

Direct Renin Inhibitors
Site: Renin binding pocket
MOA: prevents conversion of Angiotensiogen to AI by renin
CI: Pregnancy

30
Q

What are the two types of Calcium Channel Blockers?

A

Dihydropyridines (more arterial)

Non-dihydropyridines (more cardiac)

31
Q

Amlodopine, felodipine, nifedipine ER, nicardipine, nimodipine: Class, MOA, AE, Met

A

Dihydropyridine CCB
MOA: Block entry of extracellular Ca which is necessary for contraction (selectivity of smooth arterial muscle over cardiac and skeletal muscle unaffected)
AE: peripheral edema, dizziness, HA, flushing, reflex tachycardia
Met: CYP3A4

32
Q

Verapamil, diltiazam: Class, MOA, AE,

A

Non-dihydropyridine CCB
MOA: Block entry of extracellular Ca in SA and AV nodal tissue, other cardiac and smooth muscle tissue
AE: Dilt-HA, brady, edema, worsen HF
Verapamil: constipation, dizziness, worsen HF
Met: CYP3A4, also inhibit CYP3A4**

33
Q

Vasodilators initiate what 2 compensatory mechanisms and how can this be countered?

A

Tachycardia, counter with beta blocker
Activation of RAAS, counter with diuretic

Vasodilators also cause NO formation, open K+ channels, and D1 stimulation

34
Q

Hydralazine: Class, MOA, AE, Met

A

Vasodilator
IV/PO
MOA: Stimulates NO synthesis from endogenous sources in endothelial cells. Dilates ONLY arterioles
AE: SLE-like s/s with high doses
Met: well absorbed but rapidly metabolized by first-pass (fast aceylators= very rapid met)
Used in hypertensive crisis

35
Q

Nitroprusside: Class, MOA, AE

A

Vasodilator
IV
MOA: Gives of NO itself which then enter smooth muscle causing both arterial and venous dilation (short duration of action)
AE: cyanide toxicity (use caution with hepatic/renal insuff)
Used in hypertensive crisis

36
Q

Fenoldopam: Class, MOA

A

Vasodilator
MOA: D1-dopamine receptor agonism. Decreased PVR and increased renal blood flow, diuresis, natriuresis
Minimal adrenergic effects (unlike dopa)
Used in hypertensive crisis.

37
Q

Monoxidil: Class, MOA, AE

A

Vasodilator
PO
MOA: K channel opener. Produce hyperpolarization of smooth muscle membrane reducing excitation and contraction=vasodilation
Half-like of 4hrs but active metabolite can causes persistence of hypotensive effect for 24hrs (QID)
AE: hypertrichosis

38
Q

What can HF trigger?

A

Renin secretion and activation of the RAAS

39
Q

Systolic dysfunction is descriptive of HF with an EF of:

A

<40%

40
Q

Drugs used to reduce preload in non ischemic HF patients:

A

Diuretics
Aldosterone antagonists
Venodilators

41
Q

Drugs used to reduce afterload in non ischemic HF patients:

A

ACEI
B-blockers
Vasodilators

42
Q

Drugs used to increase intropy (myocardial contractility) in non ischemic HF patients:

A

Cardiac glycosides
Sympathomimetic amines
Phosphodiesterase inhibitors

43
Q

Which diuretics are better used for hypertension management and which are better used for HF?

A

HTN: thiazides
HF: loop diuretics

44
Q

What drug is sometimes administered with loop diuretics if the GFR is reduced?

A

Metolazone

avoid loop diuretics in patients with serum Cr 2-2.5

45
Q

Nitroglycerin: Class, MOA

A

Venodilator
Increases venous capacitance which reduces venous return to the heart.
Decreased myocardial oxygen demand
Alleviate ischemia which improves diastolic relaxation
Improved LV compliance in addition to preload reduction

46
Q

How do ACEI’s help to treat HF?

A
  • Reverse vasoconstriction and volume retention that is causes by RAAS activation
  • Reduces afterload which increases SV, increases GFR, increases natriuresis and diuresis
  • Reversal of aldosterone related volume retention = decreases preload

**Significant mortality benefit

47
Q

How do ARBs help to treat HF?

A

Similar to ACEI
Lack of bradykinin-related vasodilation
Mortality benefit- use when ACEI CI, may be additive when used with ACEI

**Combo of ACEI, ARB, and aldosterone antag not recommended

48
Q

How do B-blockers help to treat HF?

A
  • Inhibition of renin relases
  • Reduction of cytotoxic and signaling effects of circulating catecholamines
  • Prevent ACS

**DO NOT used for uncompensated HF, mortality benefits for chronic compensated HF (bisoprolol, carvedilol, metoprolol ER)

49
Q

What is Bidil and what population has increased mortality benefit with its use?

A

Vasodilator
Combo of hyralazine (arterial dilator) and isosorbide (venodilator)
Generally used when patient can’t take ACEI or ARBs
Mortality benefits in African-Americans

50
Q

What is the MOA of Digoxin?

A

Na-K adenosine triphosphatase inhibitor

In vagal afferent fibers sensitizes cardiac baroreceptors causing decreased sympathetic outflow
Increases parasympathetic outflow
Decreased conduction velocity, Increased AV refractor period
Decreases HR, preload, afterload
Increases intracellular Ca
Decreased renal tubule absorption of Na+

51
Q

How is 90% of digoxin excreted?

A

Renally

52
Q

What is a therapeutic level for digoxin, its onset of action, its half life, and how long dose it take to reach steady state?

A

0.5-1.2ng/ml
Onset of action- 30-60mins
Half-life: 36hrs
Steady state: takes 7 days

53
Q

AE of Digoxin:

A

Hypokalemia
AV block
Ventricular ectopy

54
Q

Antidote for Digoxin:

A

Digoxin immune Fab (Digibind, DigiFab)

55
Q

Pharmacodynamic interactions that can occur with Digoxin:

A
  • Increased risk of AV block with B-blockers

- B-blockers and CCB’s decrease contractility

56
Q

Pharmacokinetic interactions that can occur with Digoxin:

A
  • Abx increase absorption (less broken down by normal bacteria in gut= more systemically absorbed)
  • Verapamil, quinidine, amiodarone increase dig levels by affecting Vd and/or decreasing renal clearuance
57
Q

Dobutamine:

A

Stimulation of B1 increases cardiac contractility
Stimulation of B2 causes arterial vasodilation and reduced afterload

Short term treatment of acute decompensated HF

58
Q

Milrinone

A

Phosphodiesterase inhbitor
Inhibits degradation of cAMP in cardiac myocytes which increase intracellular Ca( incr. contractility)
Arterial and venous dilation decreases afterload and preload

Short term treatment of acute decompensated HF

59
Q

Nesiritide(Natrecor):

A

Recombinant B-type natriuretic peptide
Counter regulates RAAS= promotes vasodilation, natriuresis, diuresis
AE: hypotension esp. with ACEI, renal toxicity

Short term treatment of acute decompensated HF

60
Q

Drugs used to treat CAD:

A 
B-blockers
CCB
Nitrates
ASA
Lipid-lowering agents
61
Q

Management of unstable angina, NSTEMI vs. STEMI:

A

Antianginal drugs
Heparin, ASA
GPIIb, IIIa antagonists
Thienopyridines

STEMI- All of above + thrombolytics

62
Q

Nitrates MOA:

A

Venodilators
Decrease venous return
Decrease preload and wall tension
Increase concentration of nitric oxide in smooth muscle cells
Leads to activation of cGMP
Smooth muscle relaxation (coronary arteries)

63
Q

Modes of nitrate delivery include: (3)

A

Sublingual (Oral-Isosorbide dinitrate, and isosorbide mononitrate=100% bioavailability)
Topical
IV

64
Q

How is nitroglycerin usually metabolized and what are the advantages of sublingual and transdermal administration?

A

90% degraded by the liver to inactive metabolites during first pass.
Sublingual and transdermal administration bypasses the liver and avoids first pass metabolism

65
Q

Most common AE of nitroglycerin?

A

HA

66
Q

Nitrate tolerance can be avoided using___________

A

nitrate free intervals

67
Q

Nitrate drug interactions include:

A

Sildenafil (Viagra), Tadalafil (Cialis) vardenafil (Levitra), and phophodiesterase 5 inhibitors

Additive effects can causes significant hypotension
Treat with phenylephrine (potent a-agonist) to causes vasoconstriction

68
Q

The ABCDE’s of stable Angina include:

A 
ASA, antianginals
Blood pressure, B-blockers
Cholesterol, cigarettes
Diet, DM 
Education, exercise

Pharmacology (48 decks)

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