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Pharmacology > Calcium Channel Blockers; ACE-I, & ARBS > Flashcards

Calcium Channel Blockers; ACE-I, & ARBS Flashcards

1
Q

Calcium Channels are important in what 4 areas of the cardiovascular system?

A
  1. Vascular smooth muscle
  2. Cardiac muscle
  3. SA node
  4. AV node
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2
Q

Of the areas that calcium channel blockers impact, Which is the main target of drug therapy?

A

Vascular smooth muscle

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3
Q

What effect does calcium have on vascular smooth muscle?

A

Calcium channels determine caliber of blood vessels, how tightly the vascular smooth muscle will be contracted or relaxed

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4
Q

What is the SA node important for?

A

the electrical timing of signals in heart

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5
Q

Calcium channel blockers (CCB) are the primary treatment for _____________ and the secondary treatment for _______

A

Calcium channel blockers (CCB) are the primary treatment for ARRHYTHMIA and the secondary treatment for HTN

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6
Q

Calcium Channel Blockers (CCB)

  • ________________ calcium is required for contraction of cardiac and vascular smooth muscle.
  • Skeletal muscle contraction is NOT contingent on extracellular calcium so our drugs have _________ effect
A
  • EXTRACELLULAR calcium is required for contraction of cardiac and vascular smooth muscle.
  • Skeletal muscle contraction is NOT contingent on extracellular calcium so our drugs have NO effect
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7
Q

What are 3 main uses for calcium channel blockers? What are 2 less common uses?

A

Main:

  1. Angina pectoris (chest pain)
  2. Arrhythmias
  3. HTN

Less common:

  1. Raynaud’s syndrome
  2. migraines
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8
Q

What are the 2 classes of calcium channel blockers?

A
  1. Dihydropyridines

2. Non-dihydropyridines

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9
Q

What class of calcium channel blockers are these drugs?

  • Nifedipine (procardia)
  • Felodipine (plendil)
  • Isradipine (DynaCirc)
  • Nisoldpine (Sular)
  • Nicardipine (Cardene)
  • Amlodipine (Norvasc)
  • Clevidipine (Cleviprex)
A

Dihydropyridines (DHPs)

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10
Q

Effects of Dihydrophyridines (DHPs)

  1. Marked __________ in peripheral vascular resistance (dilates ________, not ________)
  2. Decrease ___________
  3. Little ___________ effect on HR or force of contraction (exception is Nifedipine)
  4. Reduced myocardial ___________ demand
  5. Potential to cause ________________ (exception is Amlodipine)
    * Every recent __________ or ________ patient should be put on one of these
A
  1. Marked DECREASE in peripheral vascular resistance (dilates ARTERIES, not VEINS)
  2. Decrease AFTERLOAD
  3. Little DIRECT effect on HR or force of contraction
  4. Reduced myocardial OXYGEN demand
  5. Potential to cause REFLEX TACHYCARDIA (exception is Amlodipine)
    * Every recent CHF or MI patient should be put on one of these
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11
Q

Why is Amlodipine (a DHP) not associated /c reflex tachycardia?

A

b/c of a slower onset of action; no sudden vasodilation or drop in BP

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12
Q

AMLODIPINE (NORVASC)

  • Used for ________ and _________
  • Adverse drug reaction = ______________________
  • Most _________ used DHP d/t decreased risk of reflex tachycardia
A
  • Used for HTN and ANGINA
  • Adverse drug reaction = PERIPHERAL EDEMA
  • Most COMMONLY used DHP d/t decreased risk of reflex tachycardia
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13
Q

NIFEDIPINE (PROCARDIA, ADALAT)

- What are 4 uses for nifedipine?

A
  1. HTN
  2. Angina
  3. Pulmonary artery HTN
  4. Raynaud’s Syndrome
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14
Q

NIFEDIPINE (PROCARDIA, ADALAT)

- What should be avoided when on nifedipine d/t a P450 metabolism issue?

A

Avoid grapefruit juice

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15
Q

NIFEDIPINE (PROCARDIA, ADALAT)

- What are 6 adverse drug reactions of nifedipine?

A
  1. Reflex tachycardia - very prominent, so drug is usually avoided
  2. Peripheral edema
  3. Hypotension
  4. Flushing
  5. Dizziness
  6. HA
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16
Q

NICARDIPINE (CARDENE)

  • Used for ________ HTN and _________ HTN in patients /c _____________ (Drug of choice)
  • Relatively quick onset (_______ min.)
  • Avoid ________________ d/t drug interactions
  • What are 6 adverse drug reactions?
A
  • Used for ACUTE HTN and ARTERIAL HTN in patients /c ACUTE STROKE (Drug of choice)
  • Relatively quick onset (10 - 20 min.)
  • Avoid GRAPEFRUIT JUICE d/t drug interactions
  • 1) reflex tachycardia, 2) hypotension, 3) syncope, 4) peripheral edema, 5) flushing, 6) HA
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17
Q

FELODIPINE (PLENDIL), ISRADIPINE (DYNACIRC), NISOLDIPINE (SULAR)

  • Only approved for ________
  • all _______ drugs, not _______ much at all
  • Same ADR profile (reflex tachycardia, peripheral edema, hypotension, flushing, HA)
  • No real advantages over ____________
A
  • Only approved for HTN
  • all OLDER drugs, not USED much at all
  • Same ADR profile (reflex tachycardia, peripheral edema, hypotension, flushing, HA)
  • No real advantages over AMLODIPINE
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18
Q

What do all Dihydropyridines (DHPs) end in?

A

“-dipine”

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19
Q

What are the two non-Dihydropyridines?

A
  1. Verapamil (Calan, Isoptin, Verelan)

2. Diltiazem (Cardizem, Cartia, Taztia, Tiazac)

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20
Q

VERAPAMIL (CALAN, ISOPTIN, VERELAN)

  • Vasodilation thought be much less ________ than dihydropyridines (____________ is thus minimal)
  • Slows __________ through the SA and AV nodes (decreases _______ and force of ___________) — negative __________ (force) and negative ____________ (rate)
  • **do NOT use this drug in pts /c ___________
A
  • Vasodilation thought be much less POTENT than dihydropyridines (REFLEX TACHYCARDIA is thus minimal)
  • Slows CONDUCTION through the SA and AV nodes (decreases HR and force of CONTRACTION) — negative INOTROPES (force) and negative CHRONOTROPES (rate)
  • **do NOT use this drug in pts /c CHF
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21
Q

VERAPAMIL (CALAN, ISOPTIN, VERELAN)

- What are 3 uses for verapamil?

A
  1. Arrhythmias
  2. Angina
  3. HTN
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22
Q

VERAPAMIL (CALAN, ISOPTIN, VERELAN)

- What are 5 adverse drug reactions of verapamil?

A
  1. Constipation
  2. Headaches
  3. Peripheral edema (less than /c DHPs)
  4. Hypotension
  5. Bradycardia
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23
Q

VERAPAMIL (CALAN, ISOPTIN, VERELAN)

  • lots of drug _______________
  • Contraindicated in those /c certain __________, & _______
A
  • lots of drug INTERACTIONS

- Contraindicated in those /c certain ARRHYTHMIAS, & CHF

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24
Q

DILTIAZEM (CARDIZEM, CARTIA, TAZTIA, TIAZAC)

  • Exhibits _________ dependent block of calcium channels
  • causes ___________ to a lesser extent than DHPs
  • Slows __________ through the SA and AV nodes (negative inotropes, negative chronotropes)
  • Can see an ________ reflex tachycardia
  • inhibits heart function less than _____________ but still more than _______________
A
  • Exhibits FREQUENCY dependent block of calcium channels
  • causes VASODILATION to a lesser extent than DHPs
  • Slows CONDUCTION through the SA and AV nodes (negative inotropes, negative chronotropes)
  • Can see an INITAL reflex tachycardia
  • inhibits heart function more than VERAPAMIL but still more than DHP
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25
Q

DILTIAZEM (CARDIZEM)

  • What are 3 uses for Diltiazem?
  • Diltiazem is the drug of choice for what 2 things?
A

Uses:

  1. HTN
  2. Arrhythmias
  3. Angina

Drug of Choice:

  1. atrial fibrillation (a-fib)
  2. Atrial flutter
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26
Q

DILTIAZEM (CARDIZEM)

- What are 4 adverse drug reactions of diltiazem?

A
  1. Hypotension
  2. Syncope
  3. Peripheral edema
  4. Headache
27
Q

DILTIAZEM (CARDIZEM)

- What population is Diltiazem contraindicated in?

A

Those /c CHF

28
Q

Summary:

  • DHPs affect _______________ (increasing vasodilation)
  • Non-DHPs have an inhibitory effect on ______ and __________ contractility in addition to vasodilation
A
  • DHPs affect VASCULATURE (increasing vasodilation)

- Non-DHPs have an inhibitory effect on HR and MYOCARDIAL contractility in addition to vasodilation

29
Q

RENIN-ANGIOTENSIN SYSTEM

  • regulated by the __________ and is responsible for _____________ control via many different control points
  • HTN is considered to be a _______ disease
  • System is triggered via a decrease in _____ which causes ______ (an enzyme) release
  • A negative feedback loop exists to slow renin release as BP __________ to normal or above normal
A
  • regulated by the KIDNEY and is responsible for BLOOD PRESSURE control via many different control points
  • HTN is considered to be a RENAL disease
  • System is triggered via a decrease in BP which causes RENIN (an enzyme) release
  • A negative feedback loop exists to slow renin release as BP INCREASES to normal or above normal
30
Q

What are the 3 ways to regulate the Renin-Angiotensin System?

A
  1. NaCl reabsorption at the kidney level
  2. BP sensors in pre-glomerular vessels
  3. Beta-1 receptor activation in Kidney
31
Q

RENIN-ANGIOTENSIN SYSTEMS — NaCl reabsorption at the kidney level

  • As Na+ reabsorption decreases, water reabsorption ___________ and blood pressure will __________.
  • This sends a signal to release _______
  • Diuretics function to excrete Na+/H2O — explains why diuretics often _____ control HTN adequately as monotherapy
A
  • As Na+ reabsorption decreases, water reabsorption DECREASES and blood pressure will DECREASE.
  • This sends a signal to release RENIN
  • Diuretics function to excrete Na+/H2O — explains why diuretics often CANNOT control HTN adequately as monotherapy
32
Q

RENIN-ANGIOTENSIN SYSTEMS — BP sensors in pre-glomerular vessels
- When ______ BP is detected, they send a message to release renin

A
  • When LOW BP is detected, they send a message to release renin
33
Q

Renin - Angiotensin System

- What does Renin do?

A

converts angiotensinogen to angiotensin I

34
Q

Renin - Angiotensin System

- How is angiotensin I (inactive form) converted to angiotensin II (active form)?

A

Angiotensin Converting Enzyme (ACE)

35
Q

Renin - Angiotensin System

- What is responsible for vasoconstriction and aldosterone release?

A

Angiotensin II

36
Q

Renin - Angiotensin System

- What does aldosterone lead to?

A

Na+ and water retention

37
Q

Renin - Angiotensin System

- Angiotensin II is then converted to ______________ which causes more aldosterone release and some vasoconstriction

A
  • Angiotensin II is then converted to ANGIOTENSIN III which causes more aldosterone release and some vasoconstriction
38
Q

Renin - Angiotensin System: Effects of Angiotensin II that are associated /c RAPID VASOCONSTRICTION

  • Direct _______________
  • Enhanced action of peripheral ________________ (increased synaptic release, reduced reuptake)
  • Increased __________ discharge
  • Release of ___________ from adrenal glands
A
  • Direct VASOCONSTRICTION
  • Enhanced action of peripheral NOREPINEPHRINE (increased synaptic release, reduced reuptake)
  • Increased SYMPATHETIC discharge
  • Release of EPINEPHRINE from adrenal glands
39
Q

Renin - Angiotensin System: Effects of Angiotensin II that are associated /c SLOWER PRESSOR RESPONSE

  • Direct effects to increase _______ reabsorption in proximal tubule (promoting water reabsorption)
  • Synthesis and release of ____________ causing retention of Na+ and water
  • Renal ______________
A
  • Direct effects to increase SODIUM reabsorption in proximal tubule (promoting water reabsorption)
  • Synthesis and release of ALDOSTERONE causing retention of Na+ and water
  • Renal VASOCONSTRICTION
40
Q

Renin - Angiotensin System: Effects of Angiotensin II that are associated /c VASCULAR & CARDIAC HYPERTROPHY AND REMODELING

  • Increase in ___________ and _________
  • Increase in __________ wall tension
A
  • Increase in PRELOAD and AFTERLOAD

- Increase in VASCULAR wall tension

41
Q

Renin-Angiotensin System: A review of Cardiac Remodeling

  • Referring to the process whereby cardiac and vascular muscle become _________, more ________, resulting in decreased efficiency of ___________
  • Thought to be the major contributing factor in _______
  • Thus these drugs slow that process and have potential to prolong the life of a patient /c _______ or a patient that is post- _____________
A
  • Referring to the process whereby cardiac and vascular muscle become THICKER, more FIBROTIC, resulting in decreased efficiency of CONTRACTION
  • Thought to be the major contributing factor in CHF
  • Thus these drugs slow that process and have potential to prolong the life of a patient /c CHF or a patient that is post- ACUTE MYOCARDIAL INFARCTION (AMI)
42
Q

What are 3 Drug categories that are used to target the renin-angiotensin system?

A
  1. Direct renin inhibitors
  2. Angiotensin converting enzyme inhibitors (ACE-I)
  3. Angiotensin receptor blockers (ARBs)
43
Q

What drug class do these belong to?

  • Enalapril (Vasotec)
  • Lisinopril (Zestril, Prinivil)
  • Ramipril (Altace)
  • Benazepril (Lotensin)
  • Quinapril (Accupril)
  • Captopril (Capoten)
  • Fosinopril (Monorail)
  • Moexipril (Univasc)
  • Perindopril (Aceon)
  • Trandolapril (Mavik)
A

Angiotensin Converting Enzyme Inhibitors (ACE-I)

44
Q

What do all ACE-I end in?

A

“-pril”

45
Q

What are 4 Clinical uses of ACE-inhibitors?

A
  1. HTN
  2. Left ventricular systolic dysfunction (CHF)
  3. Coronary artery disease (CAD)
  4. Diabetic nephropathy
46
Q

ACE-I: Use for HTN

  • ACE-I are ______ line therapy for HTN
  • 50% __________ rate; 90% when ________ are added
  • _________ systemic vascular resistance
  • _________- stress or reflex induced stimulation (sympathetic NS)
  • __________ on heart rate
  • __________ sodium excretion
A
  • ACE-I are FIRST line therapy for HTN
  • 50% RESPONSE rate; 90% when DIURETICS are added
  • DECREASES systemic vascular resistance
  • DECREASES- stress or reflex induced stimulation (sympathetic NS)
  • NO EFFECT on heart rate
  • INCREASES sodium excretion
47
Q

ACE-I: Used for CHF

  • __________ vascular resistance (Afterload)
  • To prevent cardiac ___________. An absolute must for ALL patients /c CHF regardless of baseline _______.
A
  • DECREASED vascular resistance (Afterload)

- To prevent cardiac REMODELING. An absolute must for ALL patients /c CHF regardless of baseline BP.

48
Q

ACE-I: Used for CAD

  • Similar to CHF, all these patients must have ________
A
  • Similar to CHF, all these patients must have ACE-I
49
Q

ACE-I: Used for Diabetic nephropathy

  • ________ afferent and efferent renal arterioles
  • Decreases ____________ pressure
  • ACE-I is a must for all patients /c diabetes to _______ disease progression
A
  • DILATES afferent and efferent renal arterioles
  • Decreases GLOMERULAR CAPILLARY pressure
  • ACE-I is a must for all patients /c diabetes to SLOW disease progression
50
Q

ACE-I are often used in combination /c

  • Hydrochlorothiazide (diuretic)
  • Amlodipine (DHP)
  • Felodipine
  • Verapamil
A
51
Q

ACE-I Pharmacokinetics

  • All given ________
  • Most have long enough half life for _______ daily dosing
  • Most eliminated via _______ excretion
A
  • All given ORALLY
  • Most have long enough half life for ONCE daily dosing
  • Most eliminated via RENAL excretion
52
Q

What are 4 adverse drug reactions of ACE-I?

A
  1. Hypotension
  2. Dry, non-productive cough (resolves 1 - 4 weeks)
  3. Hyperkalemia
  4. Angioedema
53
Q

ACE-I: How does angioedema present and how is it treated?

A

Presents as anaphylaxis - swelling of nose, mouth, and throat

Treated /c epinephrine

54
Q

What are 2 contraindications for ACE-I?

A
  1. Pregnancy

2. Renal Artery Stenosis

55
Q

ACE-I Summary

  • Incredibly effective for ________ and invaluable for their role in preventing cardiac ________
  • Some of the most commonly prescribed drugs for patients /c a variety of ______________ diseases
  • For the most part, well tolerated /c a few ____________ of concern (albeit rare)
  • All ________ medications, ___________
A
  • Incredibly effective for HTN and invaluable for their role in preventing cardiac REMODELING
  • Some of the most commonly prescribed drugs for patients /c a variety of CARDIOVASCULAR diseases
  • For the most part, well tolerated /c a few ADRs of concern (albeit rare)
  • All OLDER medications, INEXPENSIVE
56
Q

What drug class are these from?

  • Losartan (Cozaar)
  • Valsartan (Diovan)
  • Olmesartan (Benicar)
  • Candesartan (Atacand)
  • Telmisartan (Micardis)
  • Azilsartan (Edarbi)
A

Angiotensin Receptor Blockers (ARBs)

57
Q

What do all ARBs end in?

A

“-artan”

58
Q

What is the mechanism of action for ARBs?

A

Selectively block angiotensin II receptors (end result similar to that of ACE-I)

59
Q

What are 3 clinical uses for ARBs?

A
  1. HTN
  2. CHF
  3. Diabetic nephropathy
60
Q

What drug class is similar to ACE-I and prevents cardiac remodeling?

A

ARBs

61
Q

Angiotensin Receptor Blockers (ARBs)

  • Though ARBs work via a different MOA when compared to ACE-I, they generally are ________ used in combination
  • Usually go-to drug when patients cannot tolerate _________ (usually d/t cough or angioedema)
  • Similar to ACE-I, many of these are available commercially as combo products /c ____________, _________, _______
A
  • Though ARBs work via a different MOA when compared to ACE-I, they generally are NOT used in combination
  • Usually go-to drug when patients cannot tolerate ACE-I (usually d/t cough or angioedema)
  • Similar to ACE-I, many of these are available commercially as combo products /c AMLODIPINE, HYDROCHLOROTHIAZIDE, ALISKIREN
62
Q

Pharmacokinetics for ARBs

  • Only available ________
  • All should be used cautiously in severe ______ impairment
A
  • Only available ORALLY

- All should be used cautiously in severe RENAL impairment

63
Q

What are the 2 main adverse drug reactions of ARBs? What are 2 ADRs that exist to a lesser extent in ARBs than in ACE-I?

A

Main

  1. Hypotension
  2. Hyperkalemia

Lesser extent

  1. Dry cough
  2. Angioedema
64
Q

What are 2 contraindications for ARBS? (hint: same as /c ACE-I)

A
  1. Pregnancy

2. Renal artery stenosis

Pharmacology (10 decks)

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