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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
CI of ACEI:
Pregnancy and renal artery stenosis
26
Where do Angiotensin Receptor Blockers(ARBs) work?
A II receptors
27
Losartan, valsartan, candesartan, irbesartan, telmisartan, eprosartan: Class, Site, MOA
ARBs Site: A II receptors MOA: Competitive binding results in decreased peripheral vasoconstriction
28
ARBs AE and CI
AE: Hyperkalemia No effect on ACE or bradykinin (no cough or angioedema) CI: Pregnancy
29
Aliskiren (Tekturna): Class, site, MOA, CI
Direct Renin Inhibitors Site: Renin binding pocket MOA: prevents conversion of Angiotensiogen to AI by renin CI: Pregnancy
30
What are the two types of Calcium Channel Blockers?
Dihydropyridines (more arterial) | Non-dihydropyridines (more cardiac)
31
Amlodopine, felodipine, nifedipine ER, nicardipine, nimodipine: Class, MOA, AE, Met
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
Verapamil, diltiazam: Class, MOA, AE,
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
Vasodilators initiate what 2 compensatory mechanisms and how can this be countered?
Tachycardia, counter with beta blocker Activation of RAAS, counter with diuretic Vasodilators also cause NO formation, open K+ channels, and D1 stimulation
34
Hydralazine: Class, MOA, AE, Met
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
Nitroprusside: Class, MOA, AE
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
Fenoldopam: Class, MOA
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
Monoxidil: Class, MOA, AE
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
What can HF trigger?
Renin secretion and activation of the RAAS
39
Systolic dysfunction is descriptive of HF with an EF of:
<40%
40
Drugs used to reduce preload in non ischemic HF patients:
Diuretics Aldosterone antagonists Venodilators
41
Drugs used to reduce afterload in non ischemic HF patients:
ACEI B-blockers Vasodilators
42
Drugs used to increase intropy (myocardial contractility) in non ischemic HF patients:
Cardiac glycosides Sympathomimetic amines Phosphodiesterase inhibitors
43
Which diuretics are better used for hypertension management and which are better used for HF?
HTN: thiazides HF: loop diuretics
44
What drug is sometimes administered with loop diuretics if the GFR is reduced?
Metolazone | avoid loop diuretics in patients with serum Cr 2-2.5
45
Nitroglycerin: Class, MOA
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
How do ACEI's help to treat HF?
- 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
How do ARBs help to treat HF?
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
How do B-blockers help to treat HF?
- 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
What is Bidil and what population has increased mortality benefit with its use?
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
What is the MOA of Digoxin?
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
How is 90% of digoxin excreted?
Renally
52
What is a therapeutic level for digoxin, its onset of action, its half life, and how long dose it take to reach steady state?
0.5-1.2ng/ml Onset of action- 30-60mins Half-life: 36hrs Steady state: takes 7 days
53
AE of Digoxin:
Hypokalemia AV block Ventricular ectopy
54
Antidote for Digoxin:
Digoxin immune Fab (Digibind, DigiFab)
55
Pharmacodynamic interactions that can occur with Digoxin:
- Increased risk of AV block with B-blockers | - B-blockers and CCB's decrease contractility
56
Pharmacokinetic interactions that can occur with Digoxin:
- 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
Dobutamine:
Stimulation of B1 increases cardiac contractility Stimulation of B2 causes arterial vasodilation and reduced afterload Short term treatment of acute decompensated HF
58
Milrinone
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
Nesiritide(Natrecor):
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
Drugs used to treat CAD:
``` B-blockers CCB Nitrates ASA Lipid-lowering agents ```
61
Management of unstable angina, NSTEMI vs. STEMI:
Antianginal drugs Heparin, ASA GPIIb, IIIa antagonists Thienopyridines STEMI- All of above + thrombolytics
62
Nitrates MOA:
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
Modes of nitrate delivery include: (3)
Sublingual (Oral-Isosorbide dinitrate, and isosorbide mononitrate=100% bioavailability) Topical IV
64
How is nitroglycerin usually metabolized and what are the advantages of sublingual and transdermal administration?
90% degraded by the liver to inactive metabolites during first pass. Sublingual and transdermal administration bypasses the liver and avoids first pass metabolism
65
Most common AE of nitroglycerin?
HA
66
Nitrate tolerance can be avoided using___________
nitrate free intervals
67
Nitrate drug interactions include:
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
The ABCDE's of stable Angina include:
``` ASA, antianginals Blood pressure, B-blockers Cholesterol, cigarettes Diet, DM Education, exercise ```

Pharmacology (48 decks)

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