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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
What does an increase in bradykinin result in?
Vasodilation Cough Angioedema (adverse effect and bad)
26
ACE inhibitors - adverse effects
First-dose hypotension Fetal injury Cough Angioedema Hyperkalemia Dysgeusia and rash Renal failure Neutropenia
27
ACE inhibitors - drug interactions to watch out for or avoid
Diuretics Anti-hypertensive agents Drugs that raise potassium levels Lithium NSAIDs
28
How should ACE inhibitors be administered?
Orally (except for Enalprilat)
29
ARBs - mechanism of action
Prevents the action of angiotensin 2 at the AT1 receptor site Prevents angiotensin 2 from inducing pathological changes in cardiac structure
30
ARBs - pharmacological effects
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
31
ARBs - therapeutic uses
Hypertension Heart failure (valsartan, candesartan) Diabetic neuropathy (irbesartan, losartan) Myocardial infarction (valsartan) Stroke prevention Migraine headache
32
ARBs - adverse effects
Angioedema Fetal harm Renal failure *lowers the risk for cough and hyperkalemia*
33
Aldosterone Antagonists Eplerenone [Inspra]
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*
34
Aldosterone agents Spironolactone [Aldactone]
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
35
How do drugs affecting the RAAS work?
Vasodilation leads to a decrease in blood volume This decrease creates less work for the heart
36
What should the nurse monitor for drugs working on the RAAS?
Blood pressure ECG Adverse effects Labs
37
What are the principal determinants of blood pressure with cardiac output?
Arterial pressure Heart rate Myocardial contractility Blood volume Venous return
38
What systems help to regulate blood pressure?
Sympathetic baroreceptor reflex Renin-angiotensin-aldosterone system Renal regulation of blood pressure
39
Antihypertensive mechanisms: sites of drug action
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
40
What are the types of diuretics used for hypertension?
Thiazide diuretics [HCTZ] Loop diuretics [Lasix] Potassium-sparing diuretics [Aldactone]
41
What are the types of anti-adrenergic drugs used for hypertension?
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
42
What are the fundamentals of hypertension drug therapy?
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
43
What are some way to minimize the adverse effects of anti-hypertensive drugs?
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
44
What are someways in which adherence can be promoted?
Educate the patient Teach self-monitoring Minimize side effects Establish a collaborative relationship Simplify the regimen Other measures
45
What drugs are used for hypertensive emergencies?
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
46
What are the symptoms of heart failure?
Feeling short of breath Fatigue or weakness Coughing Swelling and weight gain Difficulty sleeping when lying flat
47
What does structural heart disease refer to?
Conditions which affect your heart’s valves, walls, chambers, or muscles
48
What are the four major goals when it comes to managing heart failure?
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
What happens during heart failure?
Ventricular dysfunction Reduced cardiac output Insufficient tissue perfusion Fluid retention
50
How does Digoxin affect the heart during CHF?
51
How does cardiac remodeling affect the body?
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
What is the goal of therapy in cardiac remodeling with heart failure?
Stop the cycle or at least slow it down
53
What drugs should be avoided in the treatment of heart failure?
Anti-dysrhythmic agents Calcium channel blockers NSAIDs
54
What drugs are used for the treatment of heart failure?
Diuretics ACE inhibitors ARBs ARNI’s Aldosterone antagonists Beta blockers Digoxin and other cardiac glycosides Inotropic agents Vasodilators
55
What are the hemodynamic benefits of ACE inhibitors?
Arteriolar dilation Venous dilation Suppression of aldosterone release
56
What are the adverse effects of ACE inhibitors in heart failure?
Hypotension Hyperkalemia Intractable cough Angioedema
57
What is the action of beta blockers in heart failure?
Can improve cardiac remodeling (CAREFUL CONTROL OF DOSAGE) Protection from excessive sympathetic stimulation Protection against dysrhythmias
58
What are the adverse effects of beta blockers in heart failure?
Fluid retention Fatigue Hypotension Bradycardia or heart attack
59
What are the physiologic adaptations that occur with reduced cardiac output?
Cardiac dilation Increased sympathetic tone Water retention and increased blood volume Natriuretic peptides
60
What drugs are used to treat heart failure?
Diuretics ACE inhibitors and ARBs ARNIs Aldosterone antagonists Beta-blockers Digoxin and other cardiac glycosides Inotropic agents Vasodilators
61
What drugs should be avoided when treating heart failure?
Anti-dysrhythmic agents Calcium channel blockers NSAIDs
62
What are the hemodynamic benefits of ACE inhibitors?
Arteriolar dilation Venous dilation Suppression of aldosterone release
63
What are the adverse effects of ACE inhibitors?
Hypotension Hyperkalemia Intractable cough Angioedema
64
What actions do beta blockers perform in heart failure?
Can improve cardiac remodeling Protect against excessive sympathetic stimulation Protects against dysrhythmias
65
What are the two positive inotropic actions in heart failure?
Increase of force of contraction Slowing heart rate (AV node - negative chronotropic effect)
66
What are second-line agents for treating heart failure?
Dobutamine Dopamine Milrinone Amrinone
67
What do digoxin and other cardiac (digitalis) glycosides do to the heart in heart failure?
Increase myocardial contractility Increase cardiac output
68
What is the adverse effect of Digoxin and other cardiac (digitalis) glycosides in heart failure?
Can cause severe dysrhythmias
69
What is the relationship of potassium to inotropic action of Digoxin?
Potassium levels must be kept within their normal range
70
What are the hemodynamic benefits of Digoxin in heart failure?
Increased cardiac output - decreased sympathetic tone, increased urine production, decreased renin release
71
What are the neuro-hormonal benefits of Digoxin in heart failure?
Modulate the activity of neuro-hormonal system of the heart Suppress renin release in the kidney Increases the sensitivity of cardiac baroreceptors
72
What are the electrical effects of Digoxin in heart failure?
Increases the firing rate of vagal fibers Increases the responsiveness of the SA node to acetylcholine Slows depolarization rate in AV node
73
What are the non-cardiac adverse effects of Digoxin in heart failure?
Anorexia Nausea Vomiting Fatigue
74
What measures can be taken to reduce the adverse effects of Digoxin in heart failure?
Levels between 0.8-2.0 ng/mL Check pulses
75
What drug interactions should be avoided with Digoxin in heart failure?
Diuretics ACE inhibitors and ARBs Sympathomimetic agents Quinidine Verapamil
76
Inotropic sympathomimetic agents: Dopamine [Intropin]
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
Inotropic sympathomimetic agents: Dobutamine
Synthetic catecholamine Selective activation of beta 1 - adrenergic receptors
78
What are examples of phosphodiesterase inhibitors in heart failure?
Inamrinone - inodilator Milrinone [Primacor]
79
What do vasodilators consist of?
Isosorbide dinitrate and hydralazine
80
What are the three intravenous vasodilators used in acute care for heart failure?
Nitroglycerin Sodium nitroprusside [Nitropress] Nesiritide [Natrecor]
81
What are the principal adverse effects of nitroglycerin in heart failure?
Hypotension Resultant reflex tachycardia
82
What is the adverse effect of sodium nitroprusside [Nitropress] in heart failure?
Profound hypotension
83
What is the principal adverse effect of nesiritide [Natrecor] in heart failure?
Symptomatic hypotension
84
What devices can be used to manage heart failure?
Implanted cardioverter-defibrillators (AICD) Cardiac resynchronization
85
What three classes are relevant to coronary atherosclerosis?
Very-low-density lipoproteins (VLDL) - triglycerides Low-density lipoproteins (LDL) - cholesterol, greatest contributor to CAD High-density lipoproteins (HDL) - cholesterol
86
What factors are considered in the risk assessment for CHD?
Risk factors 10-year risk Risk equivalents: diabetes, atherosclerotic disease, Framingham risk score greater than 20%
87
What are lifestyle changes an individual can make to minimize the risk for developing CHD or to help maintain it?
DASH diet Weight control Exercise Smoking cessation
88
What are the secondary treatment targets in high-cholesterol?
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
What do HMG-COA reductase inhibitor (statins) do?
Inhibit an enzyme which is responsible for catalyzing an early step in the synthesis of cholesterol
90
What are the non-lipid beneficial cardiovascular actions of HMG-COA reductase inhibitors?
Reduce risk of CV events Increased bone formation
91
What are the therapeutic uses of HMG-COA reductase inhibitors?
Hypercholesterolemia Primary and secondary prevention of CV events Diabetes
92
What are the adverse effects of HMG-COA reductase inhibitors?
Headache Rash GI disturbances Myopathy/rhabdomyolysis (rare) Hepatotoxicity (rare) Muscle fatigue
93
What drug/other interactions should be avoided with HMG-COA reductase inhibitors?
Fibrates and ezetimibe Agents that inhibit CYP3A4 Use in pregnancy
94
What are the pharmacokinetics of HMG-COA reductase inhibitors?
95
Nicotinic Acid [Niacin]
Reduce LDL and triglyceride levels Increase HDL levels better than any other drug Decreases production of VLDLs
96
What are the therapeutic uses of Nicotinic acid [Niacin]?
Lowering triglyceride levels Elevating HDL cholesterol
97
What are the adverse effects of nicotinic acid [Niacin]?
Flushing, itching Gastrointestinal Hepatotoxicity Hyperglycemia Gouty arthritis
98
Bile acid-binding resins: Cholestyramine [Questran] Colestipol [Colestid]
Reduction in LDL cholesterol Increase VLDL levels in some patients
99
Bile acid-binding resins - mechanism of action
Increases LDL receptors Prevents absorption of bile-acids
100
Bile acid-binding resins - adverse effects
Constipation Decreased uptake of fat-solube vitamins
101
Fibric acid derivatives [fibrates] - example
Gemifibrozil [Lopid]
102
Fibric acid derivatives [fibrates] - effects on plasma lipoproteins
Decreases plasma triglyceride content Lowers VLDL levels Raises HDL cholesterol
103
Fibric acid derivatives [fibrates] - mechanism of action
Unknown
104
Fibric acid derivatives [fibrates] - adverse effects
Rashes Gastrointestinal Gallstones Myopathy Liver injury (hepatotoxic)
105
Ezetimibe [Zetia] - mechanism of action
Inhibit cholesterol absorption
106
Ezetimibe [Zetia] - therapeutic use
Reducing total cholesterol, LDL cholesterol, and apolipoprotein B
107
Ezetimibe [Zetia] - adverse effects
Myopathy Rhabdomyolysis Hepatitis Pancreatitis Thrombocytopenia
108
Ezetimibe [Zetia] - drug interactions
Statins Fibrates Bile-acid sequestrants Cyclosporine
109
What drug combinations are used to alter plasma lipid levels?
Niacin/Lovastatin Simvastatin/ezetimibe Pravastatin/aspirin Atorvastatin/amlodipine
110
What other products can be used to alter plasma lipid levels?
Fish oil Plant stanol and sterol esters Estrogen Cholestin
111
How do calcium-channel blockers work?
Prevent calcium ions from entering cells Called calcium antagonists Also called slow calcium blockers Greatest effects on the heart and blood vessels
112
How do calcium-channel blockers affect vascular smooth muscle?
Regulate contractions No significant effect on veins
113
How do calcium-channel blockers affect the heart?
Myocardium SA and AV node - slow action potential Coupling of cardiac calcium-channels to beta 1 - adrenergic receptors
114
What is an example of and the site of action of dihydropyridines?
Nifedipine [Procardia] Action mostly affects arterial vascular smooth muscle and lowers blood pressure by causing vasodilation
115

Pharmacology (5 decks)

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