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NUR370 Pathophysiology and Pharmacology > Medications for Cardiovascular Diseases > Flashcards

Medications for Cardiovascular Diseases Flashcards

1
Q

Goals of Dyslipidemia Therapy

A

a. increase HDL
b. lower LDL and TG

reduce CAD

TARGET LDL levels <2.0 mmol/L
or
>50% decrease in LDL

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2
Q

HMG-CoA Reductase Inhibitor (Statins)

A

= inhibit rate limiting enzyme in cholesterol synthesis
- most effective agents to #lowering LDL, also #^HDL and #lowers TG

Onset: 2 weeks, max efficacy in 4-6 weeks
Dose: once daily at bedtime, PO only

Prototype: ATORVASTATIN (Lipitor)

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3
Q

Statins Side Effects

A

a. hepatotoxicity (~1%)
contraindicated in liver disease, monitor LFTs
site of metabolism is liver, usually occurs early on

b. myopathy (0.5%)
muscle ache or weakness, monitor creatine kinase (CK)

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4
Q

Statins Drug Interactions

A

some statins metabolized by CYP450

  • CYP450 inhibitors may increase risk of statin accumulation and myopathy
  • avoid grapefruit juice

fibrates, niacin
- increases risk of myopathy

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5
Q

Fibric Acid Derivative (Fibrates)

A

= increases breakdown of TG and facilitate HDL formation, enhances cholesterol elimination in bile
- most effective agent in #lowering TG, also #^HDL, small effect on LDL

Onset: 3-4 weeks
Dose: once daily with meal for absorption, PO only

Prototype: FENOFIBRATE (LipidilMicro)

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6
Q

Fibrates Side Effects

A

a. gallstones
- due to increased cholesterol saturation of bile

b. GI effects
- nausea, dyspepsia, diarrhea

c. myopathy
d. rash
e. hepatotoxicity

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7
Q

Fibrates Drug Interactions

A

statin
- increased risk of myopathy

warfarin
- increased risk in bleeding, monitor INR

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8
Q

Bile Acid Sequestrants (Resins)

A

= resins bind bile acids in gut to increase excretion
= increase bile acid production in liver to remove cholesterol from blood, cholesterol is building block for bile acid
- modest #lowering of LDL, #small ^HDL and TG
- mainly used in combination with statin

Onset: 1 week, max effect in 4 weeks
Dose: take 30-60 mins prior to meal
- mix powder or granules with fluid, cannot take in dry form due choking hazard

Prototype: CHOLESTYRAMINE (Questran)

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9
Q

Resins Side Effects

A 
GI upsets (nausea, constipation, bloating, abdo pain, flatulence)
- not absorbed in blood stream, eliminated in feces
  • only agent safe in pregnancy
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10
Q

Resins Drug Interactions

A

can reduce absorption of other drugs:

a. fat soluble vitamins (ADEK)
b. some anionic drugs (digoxin, warfain, levothyroxine, thiazides, fibrates)

GENERAL RULE: administer all other meds 1 hour before or 4 hours after resin

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11
Q

Key Concepts of Dyslipidemia Therapy

A
  • statins are most effective
  • onset of action is weeks
  • lifestyle intervention enhances therapeutic effects
  • contraindications:
    a. only resins safe in pregnancy
    b. avoid statin and caution with fibrates with liver disease
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12
Q

Determinant of Oxygen Supply and Demand

A

Supply
- myocardial blood flow via coronary vessels

Demand

  1. heart rate
  2. myocardial contractility
  3. cardiac preload
  4. cardiac afterload
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13
Q

Key Principle of Pharmacotherapy for CAD

A

a. CAD leads to imbalance between myocardial oxygen supple and demand
b. drug therapy for angina is aimed at reducing oxygen demand

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14
Q

Determinants of Blood Pressure

A

Arterial pressure = Cardiac Output x Peripheral Resistance

Cardiac Output:
- heart rate, contractility, preload, afterload

Peripheral Resistance:
- arteriolar constriction

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15
Q

Beta-blockers

A

Indications: prevent anginal attack, acute MI, HF, HTN, dysrhythmias
Dose: PO once or twice daily, some IV forms available

“-olol”

a. Non-selective agents =PROPRANOLOL=
block both b1 and b2 receptors

b. Cardioselective agents =METOPROLOL=
block b1 only

c. vasodilating beta-blockers =CARVEDILOL=
block alpha1-adrenergic receptors and beta receptors

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16
Q

b-blockers: mechanism of action

A

a. block b1 receptors
b. decrease renin release by blocking b1 receptors in kidney
c. decrease peripheral vascular resistance
d. blunt reflex tachycardia from HTG and other vasodilators

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17
Q

b-blockers: side effects

A

a. bradycardia
assess HR before administration

b. reduce cardiac output

c. bronchoconstriction
b2 receptor blockade

d. hypoglycemia
b2 receptor blockade prevent glycogenolysis in liver, suppress glucose production

e. CNS effects (sleep disturbances, fatigue, depression)

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18
Q

b-blockers: drug interactions

A

combined with CCB may cause excessive cardiosuppression

do not stop abruptly
- rebound cardiac excitation can cause tachycardia, dysrhythmia, angina or MI

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19
Q

Alpha1-adrenergic Blockers

A

Indications: #hypertension and benign prostatic hyperplasia (BPH)
Dose: once daily, preferably at bedtime
- start low go slow

“-osin”

=TERAZOSIN=

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20
Q

a1-adrenergic blockers: mechanism of action

A

block a1 receptors on arterioles and veins, preventing vasoconstriction

21
Q

a1-adrenergic blockers: side effects

A

a. orthostatic hypotension
can be severe especially with first dose
dizziness, lightheadedness, fainting
dose at night

b. increased reflex HR to compensate
c. nasal congestion

d. sexual dysfunction
inhibition of ejaculation

22
Q

Angiotensin Converting Enzyme (ACE) Inhibitors and Angiotensin Receptor Blockers

A

Indications: HTN, HF, acute MI, prevent CV events in high risk patients
Dose: once or twice daily, PO (only exception enalaprilat IV)
- start low, go slow

ACE inhibitor =RAMIPRIL=
“-pril”

ARBs =LOSARTAN=
“-sartan”

  • ARB if pt develops cough on ACE inhibitor
  • rare to see pt on both ACE and ARB, risk of renal dysfunction
23
Q

ACE Inhibitors: mechanism of action

A

a. inhibit angiotensin II production
- decreased angiotensin II leads to vasodilation, which leads to increased cardiac output
- reduce aldosterone release and promotes excretion
- prevent cardiac and vascular remodelling by decreasing sympathetic transmission, thereby reducing O2 demand

b. blockade of bradykinin breakdown

24
Q

ARBs: mechanism of action

A

a. blockade of angiotensin II receptors
- prevent vasoconstriction
- prevent aldosterone release
- decrease blood volume
- prevent cardiac remodelling, reduce O2 demand

*do not prevent breakdown of bradykinin

25
Q

ACE inhibitors and ARBs: side effects

A

a. first dose hypotension
start low, go slow

b. decrease glomerular filtration pressure
small increase in serum creatinine, small decrease in GFR (rarely clinically significant)

c. hyperkalemia
reduced K+ excretion, avoid potassium supplements

d. fetal harm
contraindicated in pregnancy

SPECIFIC TO ACE INHIBITORS ONLY

e. inhibition of ACE increases bradykinin, histamine-like compound
- dry, irritating, non-productive cough(~10%) (subsides when d/c ACE inhibitors)
- angioedema (1%), swelling of lower layer of skin and muscous membrane

26
Q

ACE inhibitors and ARBs: drug interactions

A

a. diuretics
intensifies first dose hypotension

b. other anti-hypertensives
avoid additive effects

c. drugs that increase K+

d. NSAIDs: Na+ retention, vasoconstriction
reduces effect of ACE inhibitors, counterproductive

27
Q

Aldosterone Receptor Blockers

A

Indications: HTN and HF
Dose: once daily, PO
Onset: 48 hrs

a. non-selective =SPIRONOLACTONE=
aldosterone antagonist

b. selective =EPLERENONE=

28
Q

aldosterone receptor blockers: mechanism of action

A

aldosterone stimulates synthesis of Na+/K+ exchange pumps in distal tube
aldosterone blockade causes Na+ excretion, which lowers blood volume and pressure

29
Q

aldosterone receptor blockers: side effects

A

a. hyperkalemia

b. endocrine effect (spironolactone only)
binds to steroid hormone receptors causing gynecomastia, menstrual irregularities, impotence and hirsutism

30
Q

aldosterone receptor blockers: drug interactions

A

a. caution with other drugs that increase K+
ACE inhibitors, ARBs, K+ supplements, K+ sparing diuretics

b. some CYP450 inhibitors can increase eplereone

31
Q

Diuretics

A

Indications: HTN, HF (often first line therapy)
Dose: once or twice daily, AM and afternoon, PO
- IV furosemide

a. Thiazide =HYDROCLOROTHIAZIDE=
site of action: distal convoluted tubule, sodium delivery to distal tube causes K+ loss
*renal impairment affects Na+ travelling to distal tubule
Onset: 2 hr

b. Loop =FUROSEMIDE=
site of action: thick ascending loop of Henle, K+ loss at proximal tubule
*more powerful diuretic, causes vasodilation, second-line
Onset: 1 hr PO, 5 min IV

c. Potassium-sparing =TRIAMTERENE, AMILORIDE=
- non-aldosterone antagonists, aldosterone antagonists
site of action: late distal tubule and collecting duct
*usually an add-on, used to counteract potassium loss
Onset: 2-3 hrs

used alone or combined with other agents
generally inexpensive

32
Q

diuretics: mechanism of action

A

a. block reabsorption of Na+ and Cl- in renal tubules, salt and water excretion
b. increase urine flow
c. decrease blood volume thereby decreasing bp

33
Q

diuretics: side effects

A

a. nocturia
avoid dosing at night, dose AM

b. decreased K+ using thiazide and loop
combine with K+ sparing agent or K+ supplement

c. dehydration
loop diuretics cause decrease Na+, decreased Mg2
ototocity in high IV doses

d. hyperkalemia, leg crames, dizziness, blue urine
K+ sparing agents such as triamterene

34
Q

diuretics: drug interactions

A

a. NSAIDs
causes salt and water retention (counterproductive)

b. loop and thiazide
increase risk of digoxin toxicity

c. K+ sparing agents
avoid ACE inhibitors, ARBs, potassium supplements (risk of hyperkalemia)

35
Q

Calcium channel blockers (CCBs)

A

Indications: angina, HTN, arrhythmias

a. agents that affect blood vessels, dihydropyridines
=AMLODIPINE=
Dose: once or twice daily

b. agents that affect heart and blood vessels, non-dyhrdopyridines
=DILTIAZEM, VERAPAMIL=
Dose: long-acting formulations, once daily

36
Q

CCBs: mechanism of action

A

a. calcium channels regulate contraction of arterioles
- blockade causes arteriolar dilation, decreases afterload
- biggest effect with dihydropyridines

b. calcium channels in myocytes regular contractility and conduction, heart rate
- blockade causes decreased contractility and HR, suppress conduction through AV node
- biggest effect with non-dihydropyridines

37
Q

CCBs: side effects

A

a. reflex increase in HR, edema, flushing, headache
- due to arteriolar dilation
- especially with dihydropyridines, combine with b-blocker to minimize effect on HR

b. bradycardia
- non-dihydropyridines

c. constipation with verapamil
blockade of calcium channels in gut smooth muscle

38
Q

CCBs: drug interaction

A

a. increased cardiosuppression
b-blockers with non-dihydropyridines

b. both diltiazem and verapamil
increases digoxin levels
cardiosuppression effect counteract digoxin’s inotropic action

c. grapefruit juice
will increase levels of non-dihydropyridines

39
Q

Digoxin

A

Indications: HF, dysrhythmias
Dose: long half life (~1.5 days), once daily, PO or IV
- may use loading dose to reach therapeutic range quickly for dysrhythmia

positive inotrope
- increase contractility, increase cardiac output

negative chronotrope
- decrease heart rate

NARROW THERAPEUTIC INDEX, needs TDM

40
Q

Digoxin: mechanism of action

A 
blocks Na+/K+ exchange pump on myocytes
>>
increase Ca2+ levels in myocytes
>>
increase contractility and cardiac output
41
Q

digoxin: side effects

A

may signal toxicity

a. GI, anorexia
b. fatigue, visual disturbances

c. arrhythmias
due to electrolyte disturbances, namely decreased K+
- caution use with diuretics or vomiting/diarrhea

*K+ and digoxin bind to the same site, therefore, decreased K+ means more digoxin get bound

42
Q

digoxin: drug interactions

A

a. diuretics (loop and thiazides)
risk of toxicity due to K+ loss

b. ACE inhibitors, ARBs, K+ sparing diuretic
counteracts therapeutic response because it binds to same sites

c. verapamil (CCB)
increase in digoxin counteracts inotropic actions

d. sympathomimetics (i.e. dopamine)
further increase contractility and heart rate

43
Q

Nitrates

A

Indications: angina
Dose: SL or transdermal

=NITROGLYCERIN=
nitroglycerin is highly lipid soluble, half-life is 5-7 mins
if given orally, rapidly inactivated by liver (first pass effect)

*mainly effects veins instead of arteries

44
Q

nitrates: mechanism of action

A

nitrate taken up by VSM, gets converted to nitric oxide (NO) in the presence of sulfhydryl groups

NO acts on VSM causing #vasodilation

45
Q

nitrates: side effects

A

a. headache
decreases with time, managed with acetaminophen

b. orthostatic hypotension
due to relaxation of VSM, blood pools in veins

c. reflex tachycardia
prevent with b-blocker or CCB

46
Q

nitrates: drug interactions

A

a. b-blockers, some CCBs suppress NTG-induced tachycardia
b. increase effects of other anti-hypertensives

c. viagra or similar agents
intensify NTG-induced vasodilation
- do not take within 24 hours of any nitrate

d. alcohol
vasodilatory effects, may decrease blood pressure

47
Q

nitrate administration

A

= dosage forms aimed to prevent hepatic metabolism and to prolong therapeutic effects

  1. rapid acting to treat angina
  2. long acting to prevent angina

a. Sublingual
- direct absorption, no FP effect
- to treat angina: rapid onset (1-3 min), last 1 hr
- for chest pains: 1 tab q5min prn x 3 doses
- SL tabs or spray, chemically unstable, storage condition important

b. Transdermal patch
- slow release, absorbed directly, no FP effect
- used to prevent angina only
- onset: 30-60min, effect lasts as long as patch on
- apply new patch daily to hairless area, rotate site

  • intermittent schedule to prevent tolerance and maintain efficacy, nitrate-free 10-12 hr
48
Q

Multi-drug therapy for hypertension

A
  • use of drugs with different mechanisms to improve success
  • use lower doses of individual agents to reduce frequency and intensity of side effects
  • one agent may offset adverse effects of another
  • non-adherence is the major cause of treatment failure
  • HTN is often asymptomatic
  • therapeutic response is not apparent but side effects are
49
Q

Drugs that cause HTN

A
  • oral contraceptives
  • sympathomimetics
  • corticosteriods
  • immunosuppressants
  • some antidepressants (MAOIs)
  • thyroid hormone excess
  • illicit drugs
  • NSAIDs
  • caffeine, alcohol, licorice

NUR370 Pathophysiology and Pharmacology (20 decks)

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