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pharm exam 2 > cardiac > Flashcards

cardiac Flashcards

1
Q

differences between JNC 7 and JNC 8

A
  • JNC 8 (2014): for targeted BP management: recommend use of 4 different meds (removed beta blockers)
  • JNC 7 (2004): 5 different meds (added beta blockers)
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2
Q

Post JNC 8 Evidence

A
  • SPRINT Trial
  • NIH funded multicenter RCT
  • Lower systolic BP (<=120) greatly decreases CV complications and death in older adults
  • decreased risk of death by 25% and decreased rate of cardiac morbidity by 1/3
  • there are few advances in medicine that truly warrant an immediate change in practice, but the SPRINT trial appears to be one such study
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3
Q

stage 1 HTN

A
  • systolic 130-139 or diastolic 80-90
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4
Q

stage 2 HTN

A

systolic >/ 140 or diastolic >/90

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5
Q

lifestyle recommendations to reduce BP

A
  • DASH eating
  • exercise
  • reduce sodium dietary intake
  • moderate alcohol
  • weight loss
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6
Q

hypertensive crisis

A

systolic: higher than 180
diastolic: higher than 120

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7
Q

calcium channel blockers: MOA

A

blocking the inward movements of calcium through the cell membranes of cardiac and smooth muscle cells
This results in:
* decreased cardiac muscle contraction
* decreased cardiac conduction between AV & SA nodes
* vasodilation of coronary arteries and peripheral arterioles

which leads to
* decreased CO, HR, and coronary artery spasms

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8
Q

CCBs uses

A
  • arrthymias (verapamil, diltiazem)
  • angina (verapamil, diltiazem, nifedipine, amlodipine, felodipine)
  • hypertension (all)
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9
Q

CCBs common side effects

A
  • nifedipine and diltiazem: pedal edema (r/t peripheral artery vasodilation), headache
  • nifedipine: flushing, dizziness
  • verapamil: constipation
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10
Q

CCBs prescribing considerations

A
  • what am I treating? which sub-class of CCB is most appropriate?
  • how old is my patient?
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11
Q

CCBs contraindications

A
  • hx of heart failure or MI
    -giving med that decreases contraction of heart will worsen HF and AMI
  • hepatic impairment (since all drugs are metabolized by liver)
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12
Q

pt education CCBs

A
  • do not stop the medication abruptly
    -rebound effects (HTN, tachycardia
    -may cause increased severity and duration of chest pain
  • monitor for & report signs of hypotension and CHF
  • Do not take with grapefruit juice (CYP-450 inhibitor)
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13
Q

ACE-I (-prils): MOA

A
  • block angiotensin converting enzyme from converting angiotensin I to angiotensin II- a potent vasoconstrictor
  • inhibit the breakdown of bradykin0 a potent vasodilator
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14
Q

ARBs (-sartan): MOA

A
  • block the binding of angiotensin II to its receptors
  • do not affect bradykin levels
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15
Q

uses of ACE-I and ARBs

A
  • HTN
  • CHF
  • acute/post MI
  • left ventricular dysfunction
  • diabetic nephropathy–ACE I first line to tx diabetes
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16
Q

side effects of ACE-I and ARBs

A
  • cough (ACE-I only) most common
    -can persist 2-6 weeks (even if switched to ARB)
  • dizziness
  • hyperkalemia
  • elevated renal function tests
  • angioedema
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17
Q

prescribing considerations: ACE-I and ARBs

A
  • what am I treating?
  • age of pt–> older patients caution with polypharmacy ex K-sparing meds- check med list
  • pregnant or of childbearing age–birth defects
  • hx of renal insufficiency–check baseline RFTs and Na/K
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18
Q

education ACE-I and ARBs

A
  • well tolerated
  • if cough develops with ACE-I then switch to ARB–may persist 2-6 weeks even after switch
  • monitor renal function and electrolytes periodically (3-6 months after starting), esp with dose change
  • some pts have a precipitous drop in BP with the first dose of ACE-I, esp pts on also diuretics
    -take while sitting down
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19
Q

beta blockers: MOA

A

block beta receptors resulting in:
- ↓ the workload of the heart through decreases in heart rate (chronotropy)
-↓ strength of myocardial contraction (ionotropy
- Blocks epinepherine/norepinephrine leading to vasodilation

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20
Q

beta blockers indications

A
  • CAD – all patients should be on BB post MI unless contraindicated
  • Angina
  • Heart Failure
  • Arrhythmias
  • HTN
    -The effect of the beta-blockers on BP is minimal but rapid (~1 week
  • Other: migraine prophylaxis, essential tremor, hyperthyroid, pregnancy induced hypertension (labetalol)
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21
Q

contraindications beta blockers

A
  • 2nd/3rd degree heart block – do EKG before starting
  • Decompensated heart failure
  • Symptomatic bradycardia
  • Do not combine with non-DHP CCBs (2 meds decreasing HR)
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22
Q

side effects beta blockers

A

Bradycardia, worsened HF, fatigue/drowsiness, depression, dizziness, decreased HDL, bronchoconstriction, erectile dysfunction

23
Q

use caution: beta blockers

A
  • Use caution in patients with DM
    -Can increase insulin resistance and decrease insulin release from the pancreas = hyperglycemia
    -Can mask s/s of hypoglycemia
24
Q

avoid: beta blockers

A
  • Avoid abrupt discontinuation
    -Increases risk of MI
    -Titrate down slowly
25
Q

Cardioselectivity of Beta Blockers:

A
  • Cardioselective beta blockers preferred – especially in asthma/lung disease
    -Atenolol
    -Esmolol
    -Metoprolol
    -Bisoprolol
    -Nebivolol
  • Even cardioselective BBs can result in some bronchospasm
26
Q

alpha blockers: MOA

A

Blocks the alpha 1 adrenergic receptor on vascular (arteriole and venule) smooth muscle and ↓ vascular resistance

27
Q

alpha blockers common drugs

A
  • Doxazosin (CARDURA)
  • Prazosin (MINIPRESS)
  • Terazosin (HYTRIN)
28
Q

side effects of alpha blockers

A
  • No sexual side effects
  • Increased risk of hypotension/ hypotension related side effects
29
Q

adverse reactions alpha reactions

A
  • First-dose phenomenon - hypotension
  • Reflex tachycardia
  • Orthostatic hypotension
  • Dizziness, palpitations, headache
  • Priapism (prolonged erection in men)
  • Stress incontinence in women
    -Generally avoided in women
30
Q

ALLHAT Collaborative Research Group (2000). JAMA, 283: 1967.

A
  • Increased incidence of heart failure in pts treated with doxazosin
  • Use is therefore limited to compelling indications such as BPH, sexual dysfunction
31
Q

alpha blockers use

A

Generally, 3rd or 4th line except in patients with BPH

32
Q

Sympatholytics: MOA

A

Inhibit the actions of the central nervous system
* Beta blockers
* Alpha Blockers
* Centrally acting agents (clonidine, methyldopa)

33
Q

Diuretics in Heart Failure

A
  • Furosemide is the most prescribed loop diuretic in heart failure
    -BUT: study stating torsemide is better—more improvement in functional status and lower cardiac mortality/hospitalizations in patients w/ HF
34
Q

loop diuretics: MOA

A

inhibit Na/K/Cl cotransporter in the Loop of Henle which inhibits reabsorption of sodium and chloride leading to increased water excretion

35
Q

Loop diuretics: indications

A

o Edema/fluid overload 2/2 CHF, cirrhosis, renal disease – most common use
o Hypertension (in those with renal insufficiency)

*Less effective at BP lowering and more effective at diuresis than thiazides

36
Q

common loop diuretics

A

Furosemide, torsemide, bumetanide (PO or IV)

37
Q

high oral bioavailability

A

Torsemide and bumetanide - oral and IV

38
Q

adverse effects of loop diuretics

A

Diuresis related
* Risk of hypokalemia, hypocalcemia, hypomagnesemia, hyponatremia
* Hyperuricemia
* Metabolic acidosis

Hypersensitivity reactions
* Furosemide, torsemide, bumetanide are sulfonamides – risk for rash or acute interstitial nephritis (rare)
* Minimal allergic cross reactivity with sulfonamide abx
* Ethacrynic acid – non sulfonamide loop diuretic

Ototoxicity
* Transient or permanent deafness
* Highest risk with high dose IV therapy or lower doses in patients with kidney impairment or concurrent use of other ototoxic drugs such as aminoglycosides
* Ethacrynic acid – higher risk of ototoxicity
* Rate of administration is important – continuous infusion less risky than bolus

39
Q

potassium sparing diuretics (spironolactone): MOA

A
  • Blocks Na+ movement in & also prevents K+ movement out of cells
    -Acts on collecting tubule—mild diuretic effect
40
Q

Potassium-sparing diuretics (Spironolactone): common uses

A
  • Edema: especially related to chronic liver failure (combo with loop diuretic)
  • CHF, when hypokalemia is a problem (earlier stage)
  • Drug resistant HTN
    -Not first line but may be added to a thiazide
  • Hyperaldosteronism (Spironolactone & eplerenone)
  • Anti-androgen properties
  • PCOS
  • Hirsutism
  • Acne
  • Female pattern hair loss
41
Q

Common Drugs: potassium sparing diuretics

A

Amiloride, triamterene, spironolactone

42
Q

contraindications potassium sparing diuretics

A
  • Caution with other meds that may increase K
  • Caution in renal impairment
  • Caution in women of childbearing age
    -Ensure adequate contraception
  • Caution in men
    -Risk for gynecomastia, impotence, loss of libido
  • Lab monitoring controversial in young healthy persons
43
Q

diuretics

A
  • Most powerful of these classes= one acting on ascending loop of Henle (loop diuretics)
  • Second powerful: thiazide
  • Least powerful class: acting on collecting tubule & duct (spironolactone, amiloride, triamterene)
44
Q

thiazide direutics: MOA

A

Inhibit Na and Cl transport reduces blood volume and CO reduces peripheral resistance

45
Q

thiazide diuretics: most common

A

hydrochlorothiazide (most common), chlorthalidone, indapamide

46
Q

Contraindications: thiazide diuretics

A
  • Renal/hepatic disease
  • Gout
  • Hypokalemia
  • Sulfa drug allergy (contains sulfa molecule)
47
Q

indications of thiazide diuretics

A

Hypertension
* Decrease risk of CVA and MI in hypertension
* Often considered first-line therapy in hypertension (effective, safe and cheap)
* Increasing dose does not increase efficacy and increases risk for side effects

Edema
* Related to CHF, cirrhosis, CKD, corticosteroids, nephrotic syndrome

48
Q

adverse effect thiazide diuretics

A
  • Dose-Dependent
    -Higher dose–> more side effects
  • Hypokalemia (monitor K+)
  • Dehydration
    -Particularly in the elderly
    -Leads to orthostatic hypotension (dangle feet prior to getting off bed)
  • Hyperglycemia
    -possibly because of impaired insulin release 2º hypokalemia
  • Hyperuricemia
    -thiazides compete with urate for tubular secretion
  • Hyperlipidemia
    -Mechanism unknown but cholesterol increases usually trivial (1% increase)
  • Impotence
  • Hyponatremia
    -Due to thirst, sodium loss, inappropriate ADH secretion (can cause confusion in the elderly), usually after prolonged use
49
Q

Thiazide like vs. Thiazide type diuretics

A

Thiazide like = same physiologic properties but different chemical structure

50
Q

Thiazide like (chlorthalidone/indapamide)

A
  • Longer half-life = more pharmacologic effect
    -12% additional risk reduction for CV events
    -21% additional risk reduction for HF
  • Reduce platelet aggregation and vascular permeability
  • Possible increased risk of hypokalemia
  • Dosage: 25-50mg (similar to HCTZ)—don’t need to know
51
Q

Thiazide type (HCTZ)

A
  • More commonly prescribed in the US
  • Dosage: Recommend 12.5-25 mg , no significant benefit over 25mg
    -Start at lower doses
52
Q

dihydropyridines–nifedipine

A

decrease output: minimally
decrease HR: minimally
increase vasodilatio: significantly

53
Q

phenylakylamines–verapamil

A

decreased CO: significantly
decreased HR: significantly
increased vasodilation: moderately

54
Q

benzothiazepines–diltiazem

A

decreased CO: moderately
decreased HR: significantly
increased vasodilation: moderately

pharm exam 2 (3 decks)

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