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Cardiovascular system Rx Flashcards

1
Q

What is the mechanism of action of Diuretics?

A

Ion transport inhibitors, impacting reabsorption of electrolytes => water follows electrolytes to maintain osmotic pressure gradient
NOT WATER TRANSPORT INHIBITORS

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2
Q

Where do Thiazide diuretics work?

A

luminal (inner) surface of proximal convoluted tubule= Na+, Cl-, and K+ excretion
requires adequate renal perfusion to work

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3
Q

What are adverse effects of diuretics?

A

Dry mouth/mucous membranes
Electrolyte imbalances
Can potentiate drugs that cause ototoxicity and nephrotoxicity

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4
Q

What is a unique adverse effect of thiazide diuretics?

A

Potentiate uric acid retention => gout

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5
Q

What lab evaluations are important for diuretics?

A

serum electrolytes- especially K+
renal function- BUN/creatinine
Thiazides- additionally Na+ and uric acid if hx of gout

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6
Q

What is the mechanism of action of Beta Adrenergic Antagonists?

A

1) “Beta Blockers” prevent sympathetic stimulation of the heart =>block action of epinephrine
2) prevent renin release from glomerulus => decrease outflow and water retention in kidney
* Cardio-selective or noncardio-selective

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7
Q

Cardioselective beta blockers

A 
-selective for B1 receptors =>cardiac effect only; may lose selectivity in high doses
Atenolol (Tenormin)
Acebutolol (Sectral)
Esmolol (Brevibloc)
Metoprolol (Lopressor)
Penbutolol (Levatol)
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8
Q

Non-cardioselective beta blockers

A 
-Also block B2 receptors of smooth muscle => inhibits smooth muscle relaxation=>vasocontriction, bronchospasm
Lebetolol (Trandate)
Nadolol (Corgard)
Propranolol (Inderal)
Pindolol (Visken)
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9
Q

What are the Third Generation Beta Blockers?

A
  • combination agents that produce vasodilation and beta blockade
  • Nebivolol (Bystolic) and Carvedilol (Coreg)
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10
Q

What are the common adverse effects of Beta Blockers?

A

Bradycardia, hypotension
B2 receptor inhibition => bronchospasm, inability to present sympathetic response, weakness/fatigue, erectile dysfunction

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11
Q

What is the mechanism of action of Alpha adrenergic antagonists (alpha blockers)?

A

block alpha receptors => relaxation of arterial and venous smooth muscle => decrease peripheral vascular resistance and lower BP

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12
Q

Name Alpha adrenergic antagonists

A

“-zosin”
Prazosin (Minipress)
Terazosin
Doxazosin

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13
Q

What are common adverse effects of Alpha adrenergic antagonists?

A 
Orthostatic hypotension
HA
drowsiness
N/V
impotence
*NSAIDs block antiHTN effect
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14
Q

What is the mechanism of action of ACE inhibitors?

A

Angiotensin Converting Enzyme Inhibitors
- block conversion of Angiotensin I to Angiotensin II in RAAS=> decreases aldosterone release, ADH release, and vasoconstriction => less Na + water retention and vasodilation

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15
Q

Name ACE inhibitors

A

“-pril”

Captopril, Lisinopril, Ramipril, Benazepril, Fosinopril, Quinapril, Enalapril, Perindopril

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16
Q

What are common adverse effects of ACE inhibitors?

A

HA/dizziness; tachycardia
neutropenia/agranulcytosis
*angioedema
*cough; maculopapular rash

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17
Q

What lab evaluations are considered for ACE inhibitors?

A

-WBC with diff @ baseline
-baseline urine protein
-renal function studies
Lab interference- may produce false ANA titers; transient BUN/creat. elevations; increase K, prolactin and LFTs; may decrease fasting blood glucose

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18
Q

What is the mechanism of action of ARBs?

A

Angiotensin II Receptor Blockers => block vasoconstrictive effect of angiotensin II at receptor site => decrease periph vascular resistance

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19
Q

Name ARBs

A 
"-sartan"
Losartan potassium
valsartan
irbsartan
candesartan
telmisartan
eprosartan
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20
Q

What are common adverse effects for ARBs?

A

rare- hyperkalemia
no cough issues and fewer renal issues
contraindications- caution if on diuretics or with renal impairments
drug interactions- issues with K+ in drugs

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21
Q

Aliskiren (Tekturna)

A
  • Renin Inhibitor
  • Direct renin inhibitor- decreases conversion of angiotensinogen to angiotensin I and plasma renin activity not increased
  • Indicated for HTN
  • Adverse effects similar to ACE inhibitors- angioedema, cough, diarrhea
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22
Q

Entresto

A
  • Entresto (valsartan/sacubitril)- combination agent of ACE I with Neprilysin Inhibitor
  • Indicated for CHF
  • Adverse effects: hypotension, hyperkalemia, cough
  • do not administer with ACE I or with pregnancy/planning pregnancy
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23
Q

How do HCN channel blockers work?

A

ivabradine (Corlanor)

Inhibits funny current in SA node => lowers HR by slowing depolarization in SA node

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24
Q

What is the mechanism of action of Calcium Channel Blockers?

A

Blocks Ca entry into cell => inhibits constriction => vasodilation => lower BP

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25
Name Calcium Channel Blockers
"-dipines" | Amlodipines, isradipine, nicardipine, nifedipine, nisoldipine, clevidipine, verapamil
26
What are the adverse effects of calcium channel blockers?
r/t vasodilation - HA, dizziness, hypotension constipation - peripheral edema - AV block
27
What are other vasodilators?
``` -directly relax arterial smooth muscle Sodium Nitroprusside (Nipride) Hydralazine (Apresoline) Minoxidil (Rogaine) Diazoxide (Hyperstat) ```
28
What is the mechanism of action of Clonidine?
centrally acting antiadrenergic derivitive activates alpha2 receptors in CNS to sympathetic nervous centers => decrease plasma norepi => inhibits renin release from kidney
29
What adverse effects are related to Clonidine?
CNS depression | Caution with recent MI, SA node dysfuntion, CKD, depression
30
What lab evaluations are important for Clonidine?
May decrease urinary aldosteron, catecholamines, and VMA (mask pheochromacytoma)
31
What are the first line drugs for hypertension?
1) Thiazide diuretics 2) ACE inhibitors or ARBs 3) CCBs
32
What are the first line drugs for hypertension in the Black population?
Thiazides and DHP CCBs
33
What is the drug class of choice for CKD patients with Hypertension?
ACE I or ARBs
34
In general, when are patients treated for HTN?
BP >130/80- pts with comorbid disease or high risk | BP>140/90- general population
35
How is hypertension treatment managed?
If goal is not readed after 1 month, increase dose or add 2nd agent => continue to assess and modify until goal reached => add third agent if necessary
36
What is the goal of treatment for coronary artery disease (CAD)?
increase oxygenation or decrease workload to equalize supply and demand => decrease preload or afterload and dilate coronary arteries
37
What are the drugs of choice for CAD?
Beta blockers- decrease workload by decreasing contractility and HR
38
What drugs are often used to manage CAD?
Beta blockers- decrease workload by decreasing contractility and HR CCBs- decrease contractility and inhibit vascular constriction Nitrates- vasodilate coronary arteries, decreases preload Ranolazine (Ranexa)- decreases episodes of angina
39
What are Nitrates?
cause direct vasodilation of coronary arteries to increase oxygenation to heart; venodilate and can dilate arteries in high doses isosorbide dinitrate- used for acute anginal attack isosorbid mononitrate- long acting
40
How is CAD treatment managed?
1) beta blocker 2) CCB 3) long acting nitrites 4) angiography/angioplasty
41
What is Ranolazine (Ranexa)
"Metabolic modulator" for chronic angina unresponsive to other drugs CYP450 substrate and prolongs QT Decreases episodes of angina and increases exercise tolerance (small benefit)
42
What is are the management strategies for congestive heart failure?
1) correct underlying problem- CO insufficient to meet metabolic demands 2) decrease workload of heart (preload/afterload) 3) increase contractility of heart
43
What drugs are used to manage CHF?
Loop diuretics- for acute, symptomatic HF to immediately decrease preload *ACE I/ARB- decrease afterload by inhibiting vasoconstriction *Beta Blocker- Carvediolol, Metroprolol, Bisoprolol Entresto- Neprilysin inhibitor/ACE I Aldosterone Antagonist- for severe disease (spironolactone); watch K closely HCN channel blockers- if on max beta blocker, stable but symptomatic, HR >70 Hydralazine/Nitrates- esp in African Americans Cardiac Glycosides- slows HR, but increases contraction Dobutamine and Dopamine- increase HR and BP Vasodilators- decrease preload Phosphodiesterase Inhibitors- increase contractility
44
What is the mechanism of action of cardiac glycosides?
Digoxin inhibit Na-K pump => increase release of Ca => increase force of contraction increases sensitivity of AV node to vagal stimulation =>slows conduction of impulse
45
What are adverse effects of cardiac glycosides?
Dig. toxicity (very narrow therapeutic range) Fatigue, muscle weekness, nausea, AV block Contraindications- hypokalemia, acute MI
46
What labs are important for cardiac glycosides?
Digoxin levels, K (watch for hypokalemia)
47
How do Dopamine and Dobutamine work?
Dopa- catecholemine that is precursor to norepi; acts like epi in high doses; stimulates B1 receptors of heart and A1 receptors of arteries => increase contractility and vasoconstriction Dobut- B1 agonist and dopamine receptor agonist increase HR and BP
48
What are adverse effects of dopamine and dobutamine?
angina, palpitations, HA Contraindicated for HTN and pheochromacytoma Beta blockers and Alpha blockers- block effects
49
What are Phosphodiesterase Inhibitors?
Amrinone, Milrinone, Cilostazol inhibits breaking of cAMP =>increases smooth muscle contraction => increases heart contractility Adverse effects- hypotension, dysrhythmias Contraindications- severe valve disease, hypokalemia, dehydration
50
How is CHF treatment managed?
symptomatic CHF- loop diuretic chronic CHF: ACE I/Neprilysin Inhib. and beta blocker; HCN channel blocker, Aldosterone antagonist, cardiac glycoside Severe, inpatient CHF- loop diuretic, morphine, inotropes, vasodilators
51
What are adverse effects and contraindications of Nitrites?
Adverse effects- H/A, dizziness, flushing; postural hypotension, palpitations Contraindications- increased ICP, glaucoma, hypotension, hyperthyroidism
52
What medication can interfere with effectiveness of antihypertensives?
Ibuprofen
53
Nebivolol (Bystolic)
- Third generation beta blocker - extremely cardioselective - increases nitric oxide release - only approved for HTN
54
Carvedilol (Coreg)
- not cardioselective | - indicated for *CHF, HTN, LV dysfunction after MI
55
What contraindications are there for beta blockers?
symptomatic SB >1st degree heart block RAD
56
What drug interactions are there for beta blockers?
antacids- decrease absorption | anticholinergics- increase absorption
57
What are contraindications are there for ACE Inhibitors?
``` B/L renal artery stenosis *pregnancy *renal impairment on immunosuppressants collagen vascular disease severe salt/volume depletion ```
58
What are Neprilysin Inhibitors?
Metabolizes to LBQ657 => inhibits neprilysin => increases circulating amounts of vasoactive peptides => promotes natriuresis, diuresis, vasodilation, attenuates cardiac fibrosis *Used in Entresto- combination with ACE I
59
Ivabradine (Corlanor)
- HCN Channel Blocker - Indications: - reduce hospitalizations for stable symptomatic CHF with LVEF <35% - beta blockers on max doses - resting HR >70 - Contraindicated for decompensated CHF, SBP <90, A. Fib
60
DHP vs non-DHP calcium channel blockers
Non-dihydropyridines (nonDHP)- primary site of action @ cardiac monocyte; best choices for CAD; Diltiazem, verapamil DHP- primary site of action @ arterial smooth muscle; best choice for HTN; "-dipines"
61
Contraindications and drug interactions for CCBs
``` Contraindications: *>1st degree heart block severe CHF sick sinus syndrome SBP <90 *aortic stenosis Drug interactions- beta blockers increase CHF risk; CCBs potentiate other antihypertensives ```

Advanced Pharmacology (9 decks)

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