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Advanced Pharmacology > Cardiovascular system Rx > Flashcards

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
Q

Name Calcium Channel Blockers

A

“-dipines”

Amlodipines, isradipine, nicardipine, nifedipine, nisoldipine, clevidipine, verapamil

26
Q

What are the adverse effects of calcium channel blockers?

A

r/t vasodilation

  • HA, dizziness, hypotension constipation
  • peripheral edema
  • AV block
27
Q

What are other vasodilators?

A 
-directly relax arterial smooth muscle
Sodium Nitroprusside (Nipride)
Hydralazine (Apresoline)
Minoxidil (Rogaine)
Diazoxide (Hyperstat)
28
Q

What is the mechanism of action of Clonidine?

A

centrally acting antiadrenergic derivitive
activates alpha2 receptors in CNS to sympathetic nervous centers => decrease plasma norepi => inhibits renin release from kidney

29
Q

What adverse effects are related to Clonidine?

A

CNS depression

Caution with recent MI, SA node dysfuntion, CKD, depression

30
Q

What lab evaluations are important for Clonidine?

A

May decrease urinary aldosteron, catecholamines, and VMA (mask pheochromacytoma)

31
Q

What are the first line drugs for hypertension?

A

1) Thiazide diuretics
2) ACE inhibitors or ARBs
3) CCBs

32
Q

What are the first line drugs for hypertension in the Black population?

A

Thiazides and DHP CCBs

33
Q

What is the drug class of choice for CKD patients with Hypertension?

A

ACE I or ARBs

34
Q

In general, when are patients treated for HTN?

A

BP >130/80- pts with comorbid disease or high risk

BP>140/90- general population

35
Q

How is hypertension treatment managed?

A

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
Q

What is the goal of treatment for coronary artery disease (CAD)?

A

increase oxygenation or decrease workload to equalize supply and demand => decrease preload or afterload and dilate coronary arteries

37
Q

What are the drugs of choice for CAD?

A

Beta blockers- decrease workload by decreasing contractility and HR

38
Q

What drugs are often used to manage CAD?

A

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
Q

What are Nitrates?

A

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
Q

How is CAD treatment managed?

A

1) beta blocker
2) CCB
3) long acting nitrites
4) angiography/angioplasty

41
Q

What is Ranolazine (Ranexa)

A

“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
Q

What is are the management strategies for congestive heart failure?

A

1) correct underlying problem- CO insufficient to meet metabolic demands
2) decrease workload of heart (preload/afterload)
3) increase contractility of heart

43
Q

What drugs are used to manage CHF?

A

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
Q

What is the mechanism of action of cardiac glycosides?

A

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
Q

What are adverse effects of cardiac glycosides?

A

Dig. toxicity (very narrow therapeutic range)
Fatigue, muscle weekness, nausea, AV block
Contraindications- hypokalemia, acute MI

46
Q

What labs are important for cardiac glycosides?

A

Digoxin levels, K (watch for hypokalemia)

47
Q

How do Dopamine and Dobutamine work?

A

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
Q

What are adverse effects of dopamine and dobutamine?

A

angina, palpitations, HA
Contraindicated for HTN and pheochromacytoma
Beta blockers and Alpha blockers- block effects

49
Q

What are Phosphodiesterase Inhibitors?

A

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
Q

How is CHF treatment managed?

A

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
Q

What are adverse effects and contraindications of Nitrites?

A

Adverse effects- H/A, dizziness, flushing; postural hypotension, palpitations
Contraindications- increased ICP, glaucoma, hypotension, hyperthyroidism

52
Q

What medication can interfere with effectiveness of antihypertensives?

A

Ibuprofen

53
Q

Nebivolol (Bystolic)

A
  • Third generation beta blocker
  • extremely cardioselective
  • increases nitric oxide release
  • only approved for HTN
54
Q

Carvedilol (Coreg)

A
  • not cardioselective

- indicated for *CHF, HTN, LV dysfunction after MI

55
Q

What contraindications are there for beta blockers?

A

symptomatic SB
>1st degree heart block
RAD

56
Q

What drug interactions are there for beta blockers?

A

antacids- decrease absorption

anticholinergics- increase absorption

57
Q

What are contraindications are there for ACE Inhibitors?

A 
B/L renal artery stenosis
*pregnancy 
*renal impairment 
on immunosuppressants
collagen vascular disease
severe salt/volume depletion
58
Q

What are Neprilysin Inhibitors?

A

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
Q

Ivabradine (Corlanor)

A
  • 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
Q

DHP vs non-DHP calcium channel blockers

A

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
Q

Contraindications and drug interactions for CCBs

A 
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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