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Pharmacology > Pharm E2 > Flashcards

Pharm E2 Flashcards

1
Q

-sartan

A

ARBs - used to lower hypertension

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2
Q

-darone

A

Anti-arrhythmic

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3
Q

-dipine

A

Calcium channel blocker
lowers hypertension

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4
Q

-ide

A

Diuretic
Lowers hypertension

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5
Q

-lol

A

Beta blockers
Lower hypertension

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6
Q

-oxin

A

Anti-arrhythmic medications

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7
Q

-phrine

A

Vasopressor
Increase vasoconstriction and increase cardiac contractility

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8
Q

-pril

A

ACE inhibitor
Lowers hypertension

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9
Q

-statin

A

Cholesterol reducer

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10
Q

-zosin

A

BPH
Lowers hypertension

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11
Q

What is the antidote for aspirin?

A

Sodium bicarbonate

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12
Q

What is the antidote for beta blockers?

A

Glucagon

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13
Q

What is the antidote for calcium channel blockers?

A

Glucagon, insulin, or calcium

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14
Q

What is the antidote for digoxin?

A

Digibind, digoxin immune fab

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15
Q

What is the antidote for heparin?

A

Protamine sulfate

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16
Q

What is the antidote for a hypersensitive crisis?

A

Phentolamine injection

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17
Q

What is the antidote for iron?

A

Deferoxamine

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18
Q

What is the antidote for warfarin?

A

Vitamin K

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19
Q

What is the antidote for thrombolytics?

A

Aminocaproic acid

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20
Q

Explain the process of the Renin-Angioensin-Aldosterone System.

A

The RAAS detects a drop in blood pressure and stimulates the sympathetic nervous system —> the juxtaglomerular cells of the kidney release renin —> angiotensinogen enters circulation and converts to angiotensin 1 in the liver —> ACE produces angiotensin 2 —> angiotensin 2 leads to vasoconstriction which raises blood pressure
The kidneys retain sodium and water with the help of aldosterone; potassium is released

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21
Q

What are the actions of aldosterone?

A

Regulation of blood volume and blood pressure
Uptake and retention of sodium and water
Excretion of potassium
Pathological cardiovascular effects

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22
Q

ACE inhibitors - mechanism of action

A

Reduce the levels of angiotensin 2 produced
Increasing levels of bradykinin

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23
Q

ACE inhibitors - therapeutic uses

A

Hypertension
Heart failure
Myocardial infarction (MI)
Diabetic and non-diabetic neuropathy
Prevention of cardiovascular incidents

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24
Q

What does a drop in angiotensin 2 result in?

A

Vasodilation
Lowers blood volume
Decreases cardiac and vascular remodeling
Retains potassium
Fetal injury

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25
Q

What does an increase in bradykinin result in?

A

Vasodilation
Cough
Angioedema (adverse effect and bad)

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26
Q

ACE inhibitors - adverse effects

A

First-dose hypotension
Fetal injury
Cough
Angioedema
Hyperkalemia
Dysgeusia and rash
Renal failure
Neutropenia

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27
Q

ACE inhibitors - drug interactions to watch out for or avoid

A

Diuretics
Anti-hypertensive agents
Drugs that raise potassium levels
Lithium
NSAIDs

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28
Q

How should ACE inhibitors be administered?

A

Orally (except for Enalprilat)

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29
Q

ARBs - mechanism of action

A

Prevents the action of angiotensin 2 at the AT1 receptor site
Prevents angiotensin 2 from inducing pathological changes in cardiac structure

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30
Q

ARBs - pharmacological effects

A

Causes dilation of arterials and veins
Reduces excretion of potassium
Decreases release of aldosterone
Increases renal excretion of sodium and water
Does not inhibit kinase 2
Does not increase levels of bradykinin

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31
Q

ARBs - therapeutic uses

A

Hypertension
Heart failure (valsartan, candesartan)
Diabetic neuropathy (irbesartan, losartan)
Myocardial infarction (valsartan)
Stroke prevention Migraine headache

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32
Q

ARBs - adverse effects

A

Angioedema
Fetal harm
Renal failure

lowers the risk for cough and hyperkalemia

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33
Q

Aldosterone Antagonists
Eplerenone [Inspra]

A

MOA: selective blockade of aldosterone receptors
Therapeutic uses: hypertension, heart failure
Pharmacokinetics: absorption not affected by food
Adverse effects: hyperkalemia, gynecomastia, menstrual irregularities, impotence, hirsutism, deepening of the voice
Side effects: extreme tiredness, increased urination, upset stomach

use with caution when combined with lithium

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34
Q

Aldosterone agents
Spironolactone [Aldactone]

A

MOA: blocks aldosterone receptors and binds with receptors of other steroid hormones
Therapeutic uses: hypertension, heart failure
Adverse effects: hyperkalemia, gynecomastia, menstrual irregularities, impotence, hirsutism, deepening of the voice
Side effects: extreme tiredness, increased urination, upset stomach

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35
Q

How do drugs affecting the RAAS work?

A

Vasodilation leads to a decrease in blood volume
This decrease creates less work for the heart

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36
Q

What should the nurse monitor for drugs working on the RAAS?

A

Blood pressure
ECG
Adverse effects
Labs

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37
Q

What are the principal determinants of blood pressure with cardiac output?

A

Arterial pressure
Heart rate
Myocardial contractility
Blood volume
Venous return

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38
Q

What systems help to regulate blood pressure?

A

Sympathetic baroreceptor reflex
Renin-angiotensin-aldosterone system
Renal regulation of blood pressure

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39
Q

Antihypertensive mechanisms: sites of drug action

A

Brainstem
Sympathetic ganglia
Terminals off adrenergic nerves
Beta 1 adrenergic receptors on the heart
Alpha 1 adrenergic receptors on blood vessels
Vascular smooth muscle
Renal tubules
Beta 1 receptors on juxtaglomerular cells
Angiotensin-converting enzyme
Angiotensin 2 receptors
Aldosterone receptors

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40
Q

What are the types of diuretics used for hypertension?

A

Thiazide diuretics [HCTZ]
Loop diuretics [Lasix]
Potassium-sparing diuretics [Aldactone]

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41
Q

What are the types of anti-adrenergic drugs used for hypertension?

A

Beta-blockers
Alpha 1 blockers
Alpha/beta blockers
Centrally acting alpha 2 agonists
Adrenergic neuron blockers
Direct-acting vasodilators
Calcium channel blockers
ACE inhibitors
ARBs
Aldosterone antagonists

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42
Q

What are the fundamentals of hypertension drug therapy?

A

Treatment algorithm
Initial drug selection: patients WITHOUT or WITH compelling indications
Adding drugs to regimen: rationale for drug selection, benefits of multidrug therapy
Dosing
Step-down therapy

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43
Q

What are some way to minimize the adverse effects of anti-hypertensive drugs?

A

Educate patients on monitoring blood pressure
Hypotension: drink at least 500 mL of water and lay down
Side effects and adverse effects to monitor for
When to call the HCP

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44
Q

What are someways in which adherence can be promoted?

A

Educate the patient
Teach self-monitoring
Minimize side effects
Establish a collaborative relationship
Simplify the regimen
Other measures

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45
Q

What drugs are used for hypertensive emergencies?

A

Sodium nitroprusside
Fenoldopam - causes vasodilation and promotes sodium excretion via dopamine receptors along the nephron (less than 4 minutes)
Labetalol - IV push; rapid drop
Diazoxide - potent K+ channel activator causing relaxation of smooth muscles

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46
Q

What are the symptoms of heart failure?

A

Feeling short of breath
Fatigue or weakness
Coughing
Swelling and weight gain
Difficulty sleeping when lying flat

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47
Q

What does structural heart disease refer to?

A

Conditions which affect your heart’s valves, walls, chambers, or muscles

48
Q

What are the four major goals when it comes to managing heart failure?

A

Relief of pulmonary and peripheral congestive symptoms
Improve functional capacity and quality of life
Slow cardiac remodeling and progression of LV dysfunction
Prolong life

49
Q

What happens during heart failure?

A

Ventricular dysfunction
Reduced cardiac output
Insufficient tissue perfusion
Fluid retention

50
Q

How does Digoxin affect the heart during CHF?

A
51
Q

How does cardiac remodeling affect the body?

A

Reduces the cardiac output which activates the “compensatory symptoms” and these increase heart rate, venous pressure, and arterial pressure

  1. Cardiac dilation
  2. Activation of the sympathetic nervous system
  3. Activation of the RAAS
  4. Retention of water and increased blood volume
52
Q

What is the goal of therapy in cardiac remodeling with heart failure?

A

Stop the cycle or at least slow it down

53
Q

What drugs should be avoided in the treatment of heart failure?

A

Anti-dysrhythmic agents
Calcium channel blockers
NSAIDs

54
Q

What drugs are used for the treatment of heart failure?

A

Diuretics
ACE inhibitors
ARBs
ARNI’s
Aldosterone antagonists
Beta blockers
Digoxin and other cardiac glycosides
Inotropic agents
Vasodilators

55
Q

What are the hemodynamic benefits of ACE inhibitors?

A

Arteriolar dilation
Venous dilation
Suppression of aldosterone release

56
Q

What are the adverse effects of ACE inhibitors in heart failure?

A

Hypotension
Hyperkalemia
Intractable cough
Angioedema

57
Q

What is the action of beta blockers in heart failure?

A

Can improve cardiac remodeling (CAREFUL CONTROL OF DOSAGE)
Protection from excessive sympathetic stimulation
Protection against dysrhythmias

58
Q

What are the adverse effects of beta blockers in heart failure?

A

Fluid retention
Fatigue
Hypotension
Bradycardia or heart attack

59
Q

What are the physiologic adaptations that occur with reduced cardiac output?

A

Cardiac dilation
Increased sympathetic tone
Water retention and increased blood volume
Natriuretic peptides

60
Q

What drugs are used to treat heart failure?

A

Diuretics
ACE inhibitors and ARBs
ARNIs
Aldosterone antagonists
Beta-blockers
Digoxin and other cardiac glycosides
Inotropic agents
Vasodilators

61
Q

What drugs should be avoided when treating heart failure?

A

Anti-dysrhythmic agents
Calcium channel blockers
NSAIDs

62
Q

What are the hemodynamic benefits of ACE inhibitors?

A

Arteriolar dilation
Venous dilation
Suppression of aldosterone release

63
Q

What are the adverse effects of ACE inhibitors?

A

Hypotension
Hyperkalemia
Intractable cough
Angioedema

64
Q

What actions do beta blockers perform in heart failure?

A

Can improve cardiac remodeling
Protect against excessive sympathetic stimulation
Protects against dysrhythmias

65
Q

What are the two positive inotropic actions in heart failure?

A

Increase of force of contraction
Slowing heart rate (AV node - negative chronotropic effect)

66
Q

What are second-line agents for treating heart failure?

A

Dobutamine
Dopamine
Milrinone
Amrinone

67
Q

What do digoxin and other cardiac (digitalis) glycosides do to the heart in heart failure?

A

Increase myocardial contractility
Increase cardiac output

68
Q

What is the adverse effect of Digoxin and other cardiac (digitalis) glycosides in heart failure?

A

Can cause severe dysrhythmias

69
Q

What is the relationship of potassium to inotropic action of Digoxin?

A

Potassium levels must be kept within their normal range

70
Q

What are the hemodynamic benefits of Digoxin in heart failure?

A

Increased cardiac output - decreased sympathetic tone, increased urine production, decreased renin release

71
Q

What are the neuro-hormonal benefits of Digoxin in heart failure?

A

Modulate the activity of neuro-hormonal system of the heart
Suppress renin release in the kidney
Increases the sensitivity of cardiac baroreceptors

72
Q

What are the electrical effects of Digoxin in heart failure?

A

Increases the firing rate of vagal fibers
Increases the responsiveness of the SA node to acetylcholine
Slows depolarization rate in AV node

73
Q

What are the non-cardiac adverse effects of Digoxin in heart failure?

A

Anorexia
Nausea
Vomiting
Fatigue

74
Q

What measures can be taken to reduce the adverse effects of Digoxin in heart failure?

A

Levels between 0.8-2.0 ng/mL
Check pulses

75
Q

What drug interactions should be avoided with Digoxin in heart failure?

A

Diuretics
ACE inhibitors and ARBs
Sympathomimetic agents
Quinidine
Verapamil

76
Q

Inotropic sympathomimetic agents:
Dopamine [Intropin]

A

Catecholamine
Activates beta 1 - adrenergic receptors in the heart, kidney, and in the blood vessels
Increases heart rate
Dilates renal blood vessels
Activates alpha 1 receptors

77
Q

Inotropic sympathomimetic agents:
Dobutamine

A

Synthetic catecholamine
Selective activation of beta 1 - adrenergic receptors

78
Q

What are examples of phosphodiesterase inhibitors in heart failure?

A

Inamrinone - inodilator
Milrinone [Primacor]

79
Q

What do vasodilators consist of?

A

Isosorbide dinitrate and hydralazine

80
Q

What are the three intravenous vasodilators used in acute care for heart failure?

A

Nitroglycerin
Sodium nitroprusside [Nitropress]
Nesiritide [Natrecor]

81
Q

What are the principal adverse effects of nitroglycerin in heart failure?

A

Hypotension
Resultant reflex tachycardia

82
Q

What is the adverse effect of sodium nitroprusside [Nitropress] in heart failure?

A

Profound hypotension

83
Q

What is the principal adverse effect of nesiritide [Natrecor] in heart failure?

A

Symptomatic hypotension

84
Q

What devices can be used to manage heart failure?

A

Implanted cardioverter-defibrillators (AICD)
Cardiac resynchronization

85
Q

What three classes are relevant to coronary atherosclerosis?

A

Very-low-density lipoproteins (VLDL) - triglycerides
Low-density lipoproteins (LDL) - cholesterol, greatest contributor to CAD
High-density lipoproteins (HDL) - cholesterol

86
Q

What factors are considered in the risk assessment for CHD?

A

Risk factors
10-year risk
Risk equivalents: diabetes, atherosclerotic disease, Framingham risk score greater than 20%

87
Q

What are lifestyle changes an individual can make to minimize the risk for developing CHD or to help maintain it?

A

DASH diet
Weight control
Exercise
Smoking cessation

88
Q

What are the secondary treatment targets in high-cholesterol?

A

High blood glucose
High triglycerides - 200 mg/dL
High apolipoprotein B
Low HDL
Small LDL particles
Pro-thrombotic state
Pro-inflammatory state
Hypertension
Metabolic syndrome

89
Q

What do HMG-COA reductase inhibitor (statins) do?

A

Inhibit an enzyme which is responsible for catalyzing an early step in the synthesis of cholesterol

90
Q

What are the non-lipid beneficial cardiovascular actions of HMG-COA reductase inhibitors?

A

Reduce risk of CV events
Increased bone formation

91
Q

What are the therapeutic uses of HMG-COA reductase inhibitors?

A

Hypercholesterolemia
Primary and secondary prevention of CV events
Diabetes

92
Q

What are the adverse effects of HMG-COA reductase inhibitors?

A

Headache
Rash
GI disturbances
Myopathy/rhabdomyolysis (rare)
Hepatotoxicity (rare)
Muscle fatigue

93
Q

What drug/other interactions should be avoided with HMG-COA reductase inhibitors?

A

Fibrates and ezetimibe
Agents that inhibit CYP3A4
Use in pregnancy

94
Q

What are the pharmacokinetics of HMG-COA reductase inhibitors?

A
95
Q

Nicotinic Acid [Niacin]

A

Reduce LDL and triglyceride levels
Increase HDL levels better than any other drug
Decreases production of VLDLs

96
Q

What are the therapeutic uses of Nicotinic acid [Niacin]?

A

Lowering triglyceride levels
Elevating HDL cholesterol

97
Q

What are the adverse effects of nicotinic acid [Niacin]?

A

Flushing, itching
Gastrointestinal
Hepatotoxicity
Hyperglycemia
Gouty arthritis

98
Q

Bile acid-binding resins:
Cholestyramine [Questran]
Colestipol [Colestid]

A

Reduction in LDL cholesterol
Increase VLDL levels in some patients

99
Q

Bile acid-binding resins - mechanism of action

A

Increases LDL receptors
Prevents absorption of bile-acids

100
Q

Bile acid-binding resins - adverse effects

A

Constipation
Decreased uptake of fat-solube vitamins

101
Q

Fibric acid derivatives [fibrates] - example

A

Gemifibrozil [Lopid]

102
Q

Fibric acid derivatives [fibrates] - effects on plasma lipoproteins

A

Decreases plasma triglyceride content
Lowers VLDL levels
Raises HDL cholesterol

103
Q

Fibric acid derivatives [fibrates] - mechanism of action

A

Unknown

104
Q

Fibric acid derivatives [fibrates] - adverse effects

A

Rashes
Gastrointestinal
Gallstones
Myopathy
Liver injury (hepatotoxic)

105
Q

Ezetimibe [Zetia] - mechanism of action

A

Inhibit cholesterol absorption

106
Q

Ezetimibe [Zetia] - therapeutic use

A

Reducing total cholesterol, LDL cholesterol, and apolipoprotein B

107
Q

Ezetimibe [Zetia] - adverse effects

A

Myopathy
Rhabdomyolysis
Hepatitis
Pancreatitis
Thrombocytopenia

108
Q

Ezetimibe [Zetia] - drug interactions

A

Statins
Fibrates
Bile-acid sequestrants
Cyclosporine

109
Q

What drug combinations are used to alter plasma lipid levels?

A

Niacin/Lovastatin
Simvastatin/ezetimibe
Pravastatin/aspirin
Atorvastatin/amlodipine

110
Q

What other products can be used to alter plasma lipid levels?

A

Fish oil
Plant stanol and sterol esters
Estrogen
Cholestin

111
Q

How do calcium-channel blockers work?

A

Prevent calcium ions from entering cells
Called calcium antagonists
Also called slow calcium blockers
Greatest effects on the heart and blood vessels

112
Q

How do calcium-channel blockers affect vascular smooth muscle?

A

Regulate contractions
No significant effect on veins

113
Q

How do calcium-channel blockers affect the heart?

A

Myocardium
SA and AV node - slow action potential
Coupling of cardiac calcium-channels to beta 1 - adrenergic receptors

114
Q

What is an example of and the site of action of dihydropyridines?

A

Nifedipine [Procardia]
Action mostly affects arterial vascular smooth muscle and lowers blood pressure by causing vasodilation

115
Q
A

Pharmacology (5 decks)

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