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Block 2: Pharmacology > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

(Heart: Preload, Contractility and Afterload)
Preload (Blood filling Heart from Veins)?

A

Passive stretching of muscle fibers in ventricles. This stretching results from blood volume in ventricles at end of diastole. The more the heart muscles stretch during diastole, the more forcefully they contract during systole

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2
Q

(Heart: Preload, Contractility and Afterload)
Contractility (Force of Heart)?

A

Refers to the inherent ability of myocardium to contract normally. Contractility is influenced by preload. The greater the stretch the more forceful the contraction

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3
Q

(Heart: Preload, Contractility and Afterload)
Afterload (Resistance)?

A

Refers to pressure that the ventricular muscles must generate to overcome higher pressure the aorta to get blood out of Heart

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4
Q

(Mechanisms for Controlling Blood Pressure)
Arterial BP is regulated within a narrow range?

A

(120/80) To perfusion of the tissues without damaging to the vascular system (want 120/80 to oxygen tissue and not rupture BV)

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5
Q

(Mechanisms for Controlling Blood Pressure)
Arterial BP is directly proportional to?

A

Cardiac Output and Peripheral Vascular Resistance

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6
Q

(Mechanisms for Controlling Blood Pressure)
Cardiac Output and Peripheral Resistance are controlled mainly by?

A

2 Overlapping Mechanisms:
-Baroreflexes (Sympathetic Nervous System)
-Renin-Angiotensin-Aldosterone System (RAAS)

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7
Q

(Mechanisms for Controlling Blood Pressure)
Most Antihypertensive Drugs reducing?

A

Cardiac Output and/or Decreasing Peripheral Resistance

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8
Q

Baroreceptors?

A

(Fast)
-Activate SNS

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9
Q

Renin?

A

(Slow)
-Fluid Retention

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10
Q

(Baroreceptors RAAS)
(Decrease in BP)
Rapidly?

A

Increase Sympathetic Activity via Baroreceptors –> Activate A1 (increase Ven return and Resistance) and B1 (increase contractility, increase CO, release Renin) –> increase BP

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11
Q

(Baroreceptors RAAS)
(Decrease in BP)
Long Term?

A

Decrease in renal blood flow –> release Renin –> increase Angiotensin 2 –> increase Aldosterone –> increase water/Na retention –> increase blood volume –> increase CO –> increase BP

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12
Q

(Baroreceptors RAAS)
2 Ways to Release Renin?

A

-B1
-Low renal BF

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13
Q

(Renin-Angiotensin-Aldosterone System)
Angiotensinogen?

A

Liver

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14
Q

(Renin-Angiotensin-Aldosterone System)
Renin?

A

Kidney

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15
Q

(Renin-Angiotensin-Aldosterone System)
ACE?

A

Lungs

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16
Q

(Renin-Angiotensin-Aldosterone System)
Angiotensinogen –(Renin)–> ?

A

ANG1 –ACE–> ANG2 (increase sympathetic, tub reabsorption, aldosterone and ADH increase) ALL leads to increase BP

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17
Q

(Cardiac myocyte contraction and relaxation)
Sympathetic Activation –> ?

A

Release NE –> binds to B1 rec. –> Gs increases cAMP –> increase Pka –> increase CA release extracellular –> intracellular Ca release from SR –> binds to troponin –> actin can bind to myosin –> contraction

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18
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
Contraction in VSM can be initiated by?

A

Mechanical, Electrical and Chemical stimuli

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19
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
Passive stretching of VSM can cause?

A

Contraction termed a myogenic response

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20
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
Electrical depolarization of VSM by?

A

Opening voltage dependent Ca+ channels, causing an increase in intracellular concentration of calcium

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21
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
A number of chemical stimuli such as Norepinephrine, Angiotensin II, Vasopressin, Endothelium-1, and Thormboxane A2 can cause?

A

Contraction

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22
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
Stretch, Depolarization, or Chemical can cause?

A

Vascular Constriction

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23
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
Contraction?

A

An increase in free intracellular Ca+ (through Ca+ channels or by release from internal stores (SR))

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24
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
(Contraction)
Free Ca+ binds to?

A

Calmodulin (CM). Calcium-calmodulin activates myosin light chain kinase (MLCK), an enzyme that phosphorylates myosin light chains (MLC) in the presence of ATP

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25
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
(Contraction)
Myosin Light Chain phosphorylation leads to?

A

Cross-bridge formation between myosin heads and actin filaments –> VSM contraction

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26
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
(Contraction)
Pathway?

A

Ca –> CM –> MLCK –> Phosphorylation MLC –> Contraction

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27
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
VSM?

A

Reduced phosphorylation of MLC

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28
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
VSM can result from?

A

-Reduced release of Ca+
-Inhibition of MLCK by increased intracellular concentration of cAMP (Gs-R pathway)
-MLC dephosphorylation (nitric oxide (NO) –> cGMP pathway)

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29
Q

(Vascular Smooth Muscle (VSM) Contraction and Relaxation)
Decrease Ca, increase cAMP, or Dephosphorylation via NO/cGMP = ?

A

Vasodilation

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30
Q

(Direct-Acting Vasodilators: Pharmacodynamics)
Capacitance Venules?

A

Determines Preload

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31
Q

(Direct-Acting Vasodilators: Pharmacodynamics)
Resistance Arterioles?

A

Determines Afterload

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32
Q

(Drugs to Know and Love)
Nitrates?

A

-Isosorbide denigrate
-Nitroglycerine
-Nitroprusside

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33
Q

(Drugs to Know and Love)
Hydralazine?

A

Hydralazine

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34
Q

(Drugs to Know and Love)
Phosphodiesterase V Inhibitors?

A

Slidenafil

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35
Q

(Drugs to Know and Love)
Calcium Channel Blockers (CCBs) (non-dihydropyridine, non-DHP)?

A

-Diltiazem
-Verapamil

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36
Q

(Drugs to Know and Love)
Calcium Channel Blockers (CCBs) (dihydropyridine, DHP)?

A

-Amiodipine
-Nifedipine

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37
Q

Nitric Oxide Donors: Mechanisms of Action and Pharmacology?

A

-Release NO when metabolized
-Relax smooth muscle (vascular, corpora cavernosa, short-lived in others (ex. bronchial, GI))
-Inhibit platelet aggregation

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38
Q

(Nitric Oxide Donors)
Organic Nitrites and Nitrates?

A

-Amyl Nitrate (1 NO)
-Isosorbide dinitrate (2 NO)
-Nitroglycerin (3 NO)
(metabolized in vein, short half-life, ONLY in vein)

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39
Q

(Nitric Oxide Donors)
Inorganic NO Donors?

A

-Nitroprusside (1 NO)
-Metabolized in blood cells
-Cyanide toxicity
-Targets both veins and vein

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40
Q

(Organic NO Donors: Pharmacodynamics)
Nitrites and Nitrates target is?

A

Vein

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41
Q

(Organic NO Donors: Pharmacodynamics)
Less blood in Heart to?

A

Pump, More Blood supplying Heart

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42
Q

(Organic NO Donors: Pharmacodynamics)
Preload?

A

-Decreased oxygen demand
-Improved collateral flow

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43
Q

(Organic NO Donors: Pharmacodynamics)
Increase blood flow to?

A

Coronary Arteries

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44
Q

(Organic NO Donors: Pharmacodynamics)
Increase capacitance in?

A

Vein

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45
Q

(Organic NO Donors: Pharmacodynamics)
Decrease?

A

Preload (Heart won’t work as hard)

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46
Q

(Inorganic NO Donors: Pharmacodynamics)
Nitroprusside?

A

Reduce Preload and Afterload
(works both in veins and arteries)

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47
Q

(O2 Supply and Demand)
(Arterial: Vein)
AV Oxygen Difference, Regional Myocardial Distribution, Coronary Blood Flow?

A

Oxygen Supply

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48
Q

(O2 Supply and Demand)
Contractility, Heart Rate, Preload, Afterload?

A

Oxygen Demand

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49
Q

(O2 Supply and Demand)
We want to increase?

A

Oxygen supply and decrease demand

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50
Q

(O2 Supply and Demand)
Heart isn’t getting enough Blood can cause?

A

Angina (No O2 to Heart so pain) if left too long will lead to MI
(Ischemia (20 minutes) Infarct (Cell Death))

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51
Q

(O2 Supply and Demand)
Can increase Coronary Blood Flow and give Heart more?

A

O2

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52
Q

(O2 Supply and Demand)
Reduce Preload?

A

Less O2 Demand

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53
Q

(O2 Supply and Demand)
Organic NO donor?

A

Increase O2 supply, decrease oxygen demand

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54
Q

(O2 Supply and Demand)
Organic NO donor?

A

Increase O2 supply, decrease oxygen demand

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55
Q

Classes of Angina?

A

-Stable Angina
-Unstable Angina
-Variant Angina

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56
Q

(Classes of Angina)
Stable Angina?

A

Exertion
(when you work hard and have heart pain)
(organic NO Donors)

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57
Q

(Classes of Angina)
Unstable Angina?

A

Plaque
(severe atherosclerosis –> coronary at blocked by platelet)
(reducing preload won’t help so organic doesn’t work)

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58
Q

(Classes of Angina)
Variant Angina?

A

Spasm
(contracts and blocks blood flow)
(reducing preload won’t help so organic doesn’t work)

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59
Q

(Clinical Uses of Nitric Oxide Donors)
Isosorbide denigrate/mononitrate?

A

Stable Angina
(Organic)

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60
Q

(Clinical Uses of Nitric Oxide Donors)
Nitroglycerin?

A

-Acute decompensated heart failure
-Acute myocardial infarction
-Angina
-Hypertensive emergency
-Hypotension induction
-Perioperative hypertension
-Acute pulmonary hypertension
(Not for chronic treatment of HTN)
(Organic)

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61
Q

(Clinical Uses of Nitric Oxide Donors)
Nitroprusside?

A

Hypertensive emergency
(Inorganic)

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62
Q

(Clinical Uses of Nitric Oxide Donors)
PK?

A

Onset fast, Half-Life Short (fast effect to get to the hospital)

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63
Q

Organic Nitrate/Nitrite Tolerance?

A

-Continuous 24 hour plasma levels of organic nitrates results in insurmountable tolerance (tachyphylaxis)
-Nitrate-free period of >10 hours are necessary to prevent or attenuate tolerance
-Tolerance is not developed to nitroprusside

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64
Q

(Nitric Oxide Donors: Adverse Effects, Contraindications, and Interactions)
(Adverse Effects)
Isosorbide dinitrate/mononitrate and Nitroglycerin?

A

-Hypotension (decrease BP)
-No blood to Brain
-Dizziness
-Headache
-Flushing
-Syncope (fainting)

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65
Q

(Nitric Oxide Donors: Adverse Effects, Contraindications, and Interactions)
(Precautions/Contraindications)
Isosorbide dinitrate/mononitrate and Nitroglycerin?

A

-Tolerance
-Increased intracranial pressure
-Pregnancy category C

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66
Q

Which Nitrate has no tolerance?

A

Nitroprusside

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67
Q

Which Nitrate is inorganic?

A

Nitroprusside

68
Q

Which Nitrate can be used for Stable Angina?

A

Isosorbide, NG

69
Q

Do we use Nitrates for Systemic HTN?

A

No

70
Q

What is the importance of MLCP? MLCK?

A

We want to increase MLCP and decrease MLCK to treat Angina and HTN

71
Q

Compare Nitrates to Physiological NO?

A

NO is produced in endothelial, so if injured can’t have NO, nitrates provide NO and skip endothelial step

72
Q

(Nitric Oxide Donors: Adverse Effects, Contraindications, and Interactions)
(Interactions)
Isosorbide dinitrate/mononitrate and Nitroglycerin?

A

Slidenafil (Viagra, this will kill you)

73
Q

(Nitric Oxide Donors: Adverse Effects, Contraindications, and Interactions)
(Adverse Effects)
Nitroprusside?

A

-Hypotension (decrease BP)
-No blood to Brain
-Dizziness
-Headache
-Flushing
-Syncope (fainting)
-Cyanide toxicity

74
Q

(Nitric Oxide Donors: Adverse Effects, Contraindications, and Interactions)
(Precautions/Contraindications)
Nitroprusside?

A

-Prolonged infusion
-Pregnancy category C

75
Q

(Phosphodiesterase V Inhibitors: Pharmacodynamics)
(Smooth Muscle)
Can’t breakdown?

A

cGMP

76
Q

(Phosphodiesterase V Inhibitors: Pharmacodynamics)
(Smooth Muscle)
Slidenafil?

A

(can’t PDE V)
-cGMP goes to Actin + Myosin-LC-PO4
-Becomes Actin and Myosin-LC
-Actin leads to relaxation

77
Q

(Phosphodiesterase V Inhibitors: Pharmacokinetics and Clinical Uses)
Drugs?

A

-Slidenafil
-Tadalafil
-Vardenafil

78
Q

(Phosphodiesterase V Inhibitors: Pharmacokinetics and Clinical Uses)
Slidenafil?

A

-Clinical Use: Erectile Dysfunction; Pulmonary arterial hypertension
-Pregnancy/Lactation: Category B
-SE/AR: Severe hypotension and death if combined with nitrates, priapism

79
Q

Slidenafil and Nitrates both increase?

A

cGMP
(this would lead to severe dilation and hypotension so severe it can cause death)

80
Q

Pulmonary Artery Vascular Tone Regulation Pathways?

A

1) Prostacyclin pathway
2) Endothelin pathway
3) Nitric Oxide pathway

81
Q

(Pulmonary Artery Vascular Tone Regulation)
Prostacyclin pathway?

A

Intravenous drug, not good for chronic PA hypertension disease
(oral available are much better)

82
Q

(Pulmonary Artery Vascular Tone Regulation)
Endothelin pathway?

A

Severe toxicity associated with drug

83
Q

Hydralazine: Mechanisms of Action and Pharmacology?

A

-Mechanism of action unknown
-Requires NO from endothelium (mainly reduces afterload)
(if endothelial not working, Hydralazine will NOT work)

84
Q

(Hydralazine: Mechanisms of Action and Pharmacology)
If Endothelial is not working?

A

Hydralazine will NOT work

85
Q

(Hydralazine: Clinical Uses)
(Clinical Use)
Hydralazine?

A

-Hypertension
-Hypertensive emergency in pregnancy
-Heart failure

86
Q

(Hydralazine: Clinical Uses)
(Side Effects/Adverse Reactions)
Hydralazine?

A

Dizziness, headache, angina, tachycardia, peripheral edema, nausea, lupus-like syndrome

87
Q

(Effects of Hydralazine on Organic Nitrate Tolerance)
Hydralazine caused tolerance to disappear, NOT used for?

A

Angina (but can be administered with nitrate to decrease tolerance)

88
Q

(Effects of Hydralazine on Organic Nitrate Tolerance)
BiDil?

A

Prescription medicine used to treat Heart Failure (HF)

89
Q

(Effects of Hydralazine on Organic Nitrate Tolerance)
BiDil is a fixed-dose combination of?

A

Isosorbide denigrate (vasodilation with effects on both arteries and veins) and Hydralazine hydrochloride (arterial vasodilator

90
Q

(Coronary Steal Phenomenon)
Hydralazine will vasodilation?

A

Healthy veins and even less O2 will go through constricted vessel leading to angina

91
Q

(Effects of Hydralazine on Organic Nitrate Tolerance)
Hydralazine is NOT used for?

A

Angina

92
Q

(Vasodilators: Effects on distinct vascular beds)
Nitrates?

A

(Veins)
Venous Vasodilator

93
Q

(Vasodilators: Effects on distinct vascular beds)
Nitroprusside?

A

(Both; Veins and Arteries)
Venous Vasodilator and Arterial Vasodilator

94
Q

(Vasodilators: Effects on distinct vascular beds)
Hydralazine?

A

(Artery)
Arterial Vasodilator

95
Q

Calcium-Channel Blocks (CCB): Mechanisms of Action and Pharmacology?

A

-Block calcium channels
-Decrease calcium influx into cells (decrease ER/SR calcium loading
-Effects depend on selectivity

96
Q

No extracellular Ca = ?

A

No intracellular Ca = No constriction

97
Q

(Calcium Channel Blockers: Pharmacodynamics)
Non-DHP?

A

(Heart)
-Reduce CO
-Reduce AL
(decrease rate and force)

98
Q

(Calcium Channel Blockers: Pharmacodynamics)
Non-DHP?

A

(Heart)
-Reduce CO
-Reduce AL
(decrease rate and force)

99
Q

(Calcium Channel Blockers: Pharmacodynamics)
Kidneys?

A

-Decreased resistance
-Increased GFR
-Increase Diuresis

100
Q

(Vasodilators: Effects on distinct vascular beds)
Ca2+ Channel Blocks?

A

(Mainly Arteries)
Arterial Vasodilator

101
Q

Diltiazem Verapamil?

A

Non-DHP target both Heart and Vasculature

102
Q

DHPs?

A

Targets JUST Vasculatures

103
Q

(Relative Vascular and Cardiac Effects of CCBs)
DV?

A

Non-DHP = Heart + Vasculature

104
Q

(Relative Vascular and Cardiac Effects of CCBs)
DHPs have limited?

A

To no effect on Heart

105
Q

(Relative Vascular and Cardiac Effects of CCBs)
Dipine?

A

DHP

106
Q

(Relative Vascular and Cardiac Effects of CCBs)
Non-DHP (DV) cause?

A

Vasodilation and decrease HR/Contractility

107
Q

(Relative Vascular and Cardiac Effects of CCBs)
DHP (Dipine)?

A

Just effect Vasculature

108
Q

(Relative Vascular and Cardiac Effects of CCBs)
DHP (Dipine)?

A

Just effect Vasculature

109
Q

(Calcium Channel Blockers: Pharmacokinetics)
Diltiazem?

A

-Onset of Action: (<3 min (IV)) (>30 min (PO))
-Plasma Half-Life: (3-4 hours)

110
Q

(Calcium Channel Blockers: Pharmacokinetics)
Verapamil?

A

-Onset of Action: (<1.5 min (IV)) (30 min (PO))
-Plasma Half-Life: (6 hours)

111
Q

(Calcium Channel Blockers: Pharmacokinetics)
Amlodipine?

A

-Onset of Action: (24-48 hours)
-Plasma Half-Life: (30-50 hours)

112
Q

(Calcium Channel Blockers: Pharmacokinetics)
Nifedipine?

A

-Onset of Action: (< 1 min (IV)) (5-20 min (SL, PO))
-Plasma Half-Life: (4 hours)

113
Q

(Calcium Channel Blockers: Pharmacokinetics)
Amlodipine takes longer to work but?

A

(More daily use)
Lasts longer

114
Q

(Calcium Channel Blockers: Pharmacokinetics)
Nifedipine has a quick onset but?

A

(More chronic use)
Doesn’t last long

115
Q

(First Line Treatment of Adults with Systolic/Diastolic Hypertension without other Compelling Indications)
Will Need Mix of 4?

A

-Thiazide/thiazide-like
-ACEI
-ARB
-CCB

115
Q

(First Line Treatment of Adults with Systolic/Diastolic Hypertension without other Compelling Indications)
Will Need Mix of 4?

A

-Thiazide/thiazide-like
-ACEI
-ARB
-CCB

116
Q

(First Line Treatment of Adults with Systolic/Diastolic Hypertension without other Compelling Indications)
Target?

A

<130/80 mmHg (automated measurement method)

117
Q

(First Line Treatment of Adults with Systolic/Diastolic Hypertension without other Compelling Indications)
If more than 20 mmHg above target?

A

Dual Target

118
Q

(Important Facts About CCBs)
Calcium channel inhibitors are particularly useful for treating hypertension in?

A

Low renin producer such as African-Americans and elderly patients

118
Q

(Important Facts About CCBs)
Calcium channel inhibitors are particularly useful for treating hypertension in?

A

Low renin producer such as African-Americans and elderly patients

119
Q

(Important Facts About CCBs)
Dihydropyridine CCBs have less effect on exercise performance than?

A

B-blockers and will not affect electrolytes like diuretics

120
Q

(Important Facts About CCBs)
Long duration of action provides?

A

Superior long-term outcomes (also applicable to other anti-HTN meds)

121
Q

(Important Facts About CCBs)
Long duration of action provides?

A

Superior long-term outcomes (also applicable to other anti-HTN meds)

122
Q

ACEI/CCB will?

A

Decrease risk

123
Q

(What are preferred antihypertensive combinations)
Preferred?

A

-ACE I or ARB + Thiazide
-AC
-CT

124
Q

(What are preferred antihypertensive combinations)
(Preferred)
AC?

A

ACE I or ARB + CCB

125
Q

(What are preferred antihypertensive combinations)
(Preferred)
CT?

A

CCB + Thiazide (black population)

126
Q

(What are preferred antihypertensive combinations)
Acceptable?

A

-CT
-BDT
-Thiazide + K sparing diuretic
-ALTC

127
Q

(What are preferred antihypertensive combinations)
(Acceptable)
CT?

A

CCB + Thiazide (non-black population)

128
Q

(What are preferred antihypertensive combinations)
(Acceptable)
BDT?

A

Beta-blocker + DHP CCB or thiazide

129
Q

(What are preferred antihypertensive combinations)
(Acceptable)
ALTC?

A

Aliskiren + Thiazide or CCB

130
Q

(What are preferred antihypertensive combinations)
Not Preferred?

A

-ACEI + ARB
-Beta-blocker + ACEI or ARB (preferred only post-MI or HF)
-Beta-blocker + Non-DHP CCB
-Beta-blocker + Central acting (ex. clonidine, etc.)

131
Q

(What are preferred antihypertensive combinations)
(Not Preferred)
Both will decrease Heart Rate, Too Much?

A

Beta-blocker + Non-DHP CCB

132
Q

(Treatment of Isolated Systolic Hypertension without Other Compelling Indications)
Target?

A

<130 mmHg

133
Q

(Treatment of Isolated Systolic Hypertension without Other Compelling Indications)
If more than 20 mmHg above target?

A

Dual Therapy

134
Q

(Treatment of Isolated Systolic Hypertension without Other Compelling Indications)
No ACE if just?

A

Systemic HTN

135
Q

(O2 Supply and Demand)
Non-DHPs?

A

Affect Heart

136
Q

(O2 Supply and Demand)
DHPs?

A

Do not affect Heart

137
Q

(O2 Supply and Demand)
Factors that contribute to Oxygen Supply?

A

-AV Oxygen Difference
-Regional Myocardial Distribution
-Coronary Blood Flow

138
Q

(O2 Supply and Demand)
Factors that contribute to Oxygen Demand?

A

-Contractility
-Heart Rate
-Preload
-Afterload

139
Q

Classes of Angina?

A

-Stable Angina
-Unstable Angina
-Variant Angina

140
Q

(Classes of Angina)
Stable Angina?

A

Exertion
(all CCBs + organic nitrates)

141
Q

(Classes of Angina)
Unstable Angina?

A

Plaque
(non-DHP CCBs)
(blocked vessel. Non-DHP decrease HR/contraction so will decrease O2 demand)

142
Q

(Classes of Angina)
(Unstable Angina)
Blocked vessel, Non-DHP decrease?

A

HR/contraction so will decrease O2 demand

143
Q

(Classes of Angina)
Variant Angina?

A

Spasm
(all CCBs)

143
Q

(Classes of Angina)
Variant Angina?

A

Spasm
(all CCBs)

144
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Adverse Effects)
Diltiazem?

A

(Non-DHP)
-Headache
-Dizziness
-Constipation
-Edema
-AV block
-Bradycardia
-Hypotension

145
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Adverse Effects)
Verapamil?

A

(Non-DHP)
-Headache
-Dizziness
-Constipation
-Edema
-AV block
-Bradycardia
-Hypotension

146
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Adverse Effects)
Amlodipine?

A

(DHP)
-Headaches (7.5%)
-Edema
-Hypotension
-Palpitations
-Nocturia/polyurea

147
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Adverse Effects)
Nifedipine?

A

(DHP)
-Headaches (7.5%)
-Edema
-Hypotension
-Palpitations
-Nocturia/polyurea

148
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Precautions/Contraindications)
Diltiazem?

A

(Non-DHP)
-Sick sinus syndrome
-Heart failure
-2nd/3rd heart block
-Hypotension

149
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Precautions/Contraindications)
Verapamil?

A

(Non-DHP)
-Sick sinus syndrome
-Heart failure
-2nd/3rd heart block
-Hypotension

150
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Precautions/Contraindications)
Amlodipine?

A

(DHP)
-Hypotension

151
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Precautions/Contraindications)
Nifedipine?

A

(DHP)
-Heart failure
-Hypotension

152
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Interactions)
Diltiazem?

A

(Non-DHP)
-Beta-blockers
-Grapefruit (inhibits metabolism, can increase concentration)

153
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Interactions)
Verapamil?

A

(Non-DHP)
-Beta-blockers
-Grapefruit (inhibits metabolism, can increase concentration)

154
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Interactions)
Amlodipine?

A

(DHP)
Beta-blocker withdrawal Grapefruit

155
Q

(CCB: Adverse Effects, Contraindications, Interactions)
(Interactions)
Nifedipine?

A

(DHP)
Beta-blocker withdrawal Grapefruit

156
Q

(CCB: Adverse Effects, Contraindications, Interactions)
If you drink Grapefruit it will?

A

Breakdown Beta-Blockers

157
Q

(Labeled Clinical Uses of CCBs: Summary)
Non-DHP Drugs?

A

-Diltaizem
-Verapamil

158
Q

(Labeled Clinical Uses of CCBs: Summary)
DHP Drugs?

A

-Amlodipine
-Nifedipine
-Nimodipine

159
Q

(Labeled Clinical Uses of CCBs: Summary)
(Clinical Use)
Non-DHP?

A

-Effort, variant and unstable angina
-Hypertension
-Atrial fibrillation and atrial flutter (injection)
-Paroxysmal supra ventricular tachycardia (PSVT)

160
Q

(Labeled Clinical Uses of CCBs: Summary)
(Clinical Use)
(DHP)
Amlodipine?

A

-Hypertension
-Effort and variant angina

161
Q

(Labeled Clinical Uses of CCBs: Summary)
(Clinical Use)
(DHP)
Nifedipine?

A

-Hypertension
-Effort and variant angina

162
Q

(Labeled Clinical Uses of CCBs: Summary)
(Clinical Use)
(DHP)
Nimodipine?

A

Subarachnoid hemorrhage

Block 2: Pharmacology (5 decks)

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