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Pharmacology > UNIT 3 > Flashcards

UNIT 3 Flashcards

1
Q

can work in various ways. depends on the route
-can interfere with microorganism such as germs and destroy abnormal cell

A

Drug

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2
Q

pumps blood from the heart to the lungs to get the oxygen

A

Cardiovascular system/circulatory system

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3
Q

denses deoxygenated blood through the arteries to the rest of the body

A

Heart

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4
Q

Carry oxygen, pour blood back to the heart to start the circulation process over

A

Veins

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5
Q

Is critical to healthy organs, muscles, and tissue

A

Circulatory system

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6
Q

Oxygenated;___
Unoxygenated

A

Artery ; Vein

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7
Q

defined as a persistent systolic pressure of greater than 140 mm Hg and/or a diastolic pressure greater than 90 mm Hg, affects approximately 50 million people in the United States and approximately 1 billion people worldwide, designating it as the most common disease state.

A

Hypertension

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8
Q
  • Major risk factor for coronary artery disease, cardiovascular disease, and the death resulting from the cardiovascular causes
  • Most important factor for stroke and heart failure, renal failure
A

Hypertension

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9
Q

Is determine by the product of the cardiac output (dapat 4-8L / min) and systemic vascular resistance

A

blood pressure

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10
Q

Is the amount of blood ejected from the left ventricle and is measured in liters per minute (svr)
- is the resistance to blood flow determined by the diameter of blood vessel
-It is calculated by the blood pressure divided by the cardiac output

A

Cardiac output

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11
Q

ANTI HYPERTENSIVE AGENT TABLE
Under cardiac output there are:

A

Cardiac factors and circulating volume

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12
Q

ANTI HYPERTENSIVE AGENT TABLE Under cardiac factors there are

A

Heart rate and contractibility

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13
Q

ANTI HYPERTENSIVE AGENT TABLE Drugs under Cardiac factors

A

Beta blockers, Calcium channel blockers, Centrally acting adrenergics

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14
Q

ANTI HYPERTENSIVE AGENT TABLE Under circulating volume there are:

A

Salt and aldosterone

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15
Q

ANTI HYPERTENSIVE AGENT TABLE Drugs under circulating volume

A

ACE inhibitors and diuretics

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16
Q

ANTI HYPERTENSIVE AGENT TABLE Under systemic vascular resistance there are:

A

Hormones, Peripheral sympathetic receptors, CNS, and Local

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17
Q

ANTI HYPERTENSIVE AGENT TABLE Under hormones there are:

A

Vasodilators and vasoconstrictors

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18
Q

ANTI HYPERTENSIVE AGENT TABLE Drugs under hormones

A

Vasodilators, prostaglandins, ACE inhibitors, calcium channel blockers, Angiotensin II blockers

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19
Q

ANTI HYPERTENSIVE AGENT TABLE Drugs under peripheral sympathetic receptors

A

Alpha Alpha1 blockers and Beta Beta blockers

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20
Q

ANTI HYPERTENSIVE AGENT TABLE
CNS; __ Local; ____

A

Centrally acting adrenergic ; Peripherally acting adrenergic

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21
Q

CATEGORIES AND SUBCATEGORIES OF ANTIHYPERTENSIVE DRUGS

A
  • Adrenergic drugs
  • Angiotensin-converting enzyme inhibitors, Angiotensin II Receptor Blockers, Calcium Channel blockers
  • Diuretics
    -Vasodilators
    -Direct Renin Inhibitors
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22
Q

Usually are large group of anti-hypertensive drugs

A

Adrenergic drugs

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23
Q

Contraindications of Adrenergic drugs

A

drug allergy and may also include acute heart failure, concurrent use of monoamine oxidase inhibitors, severe mental depression, peptic ulcer, and severe liver or kidney disease

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24
Q

adverse effects of Adrenergic drugs

A

bradycardia with reflex tachycardia, postural and postexercise hypotension, dry mouth, drowsiness, dizziness, depression, edema, constipation, and sexual dysfunction

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25
Q

Interactions of Adrenergic drugs

A

additive CNS depression when taken with alcohol, benzodiazepines, and opioids.

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26
Q

Indications Adrenergic drugs

A

used primarily for the treatment of hypertension, either alone or in combination with other antihypertensive drugs. Various forms of glaucoma may also respond to treatment with some of these drugs.

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27
Q

How many ace inhibitors available for clinical use?

A

10

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28
Q

Mechanism of Action and Drug Effect of Angiotensin-Converting Enzyme (ace) Inhibitors

A

Kininase is an enzyme that normally breaks down bradykinin, a potent vasodilator in the human body

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29
Q

5 examples of ACE inhibitors

A

benazepril
captoril
enalapril
fosinopril
ramipril

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30
Q

Indications of Angiotensin-Converting Enzyme (ace) Inhibitors

A

They are excellent antihypertensives and adjunctive drugs for the treatment of heart failure

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30
Q

Explain the development of ACE inhibitors

A

The development of ACE inhibitors was because of the discovery of an animal substance found to have beneficial effects to humans. This substance was the venom of the south american viper

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31
Q

Contraindications of Angiotensin-Converting Enzyme (ace) Inhibitors

A

allergy, especially a previous reaction of angioedema (e.g., laryngeal swelling) to an ACE inhibitor. Patients with a baseline potassium level of 5 mEq/L or higher may not be suitable candidates for ACE inhibitor therapy because it promotes HYPERKALEMIA, Lactating women

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32
Q

Adverse effect of Angiotensin-Converting Enzyme (ace) Inhibitors

A

fatigue, dizziness, mood changes, and headaches, cough.

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33
Q

The most pronounced symptom of an overdosed ACE inhibitors

A

Hypotension

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34
Q

Interaction of Angiotensin-Converting Enzyme (ace) Inhibitors

A

Nonsteroidal antiinflammatory drugs (NSAIDs), such as ibuprofen, can reduce the antihypertensive effect of ACE inhibitors

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35
Q

Mechanism of Action and Drug Effect
Angiotensin II Receptor Blockers

A

The ARBs block the binding of AII to type 1 AII receptors.

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36
Q

Indications
Angiotensin II Receptor Blockers

A

The therapeutic effects of ARBs are related to their potent vasodilating properties

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37
Q

Contraindications.
Angiotensin II Receptor Blockers

A

drug allergy, pregnancy, and lactation

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38
Q

Adverse Effects
Angiotensin II Receptor Blockers

A

The most common adverse effects of ARBs are upper respiratory infections and headache. Occasionally dizziness, inability to sleep, diarrhea, dyspnea, heartburn, nasal congestion, back pain, and fatigue can occur.

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39
Q

Adverse Effects

A

The most common adverse effects of ARBs are upper respiratory infections and headache. Occasionally dizziness, inability to sleep, diarrhea, dyspnea, heartburn, nasal congestion, back pain, and fatigue can occur.

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40
Q

may be used to treat angina, dysrhythmias, and hypertension and help to reduce blood of blood vessels. If calcium is not present, then the smooth muscle of the blood vessels cannot contract.

A

CALCIUM CHANNEL BLOCKERS

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41
Q

Mechanism of Action and Drug Effect CALCIUM CHANNEL BLOCKERS

A

Calcium plays an important role in the excitation-contraction coupling process that occurs in the heart and vascular smooth muscle cells, as well as in skeletal muscle..

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42
Q

Contraindications of CALCIUM CHANNEL BLOCKERS

A

drug allergy, acute MI, secondor third-degree AV block (unless the patient has a pacemaker), and hypotension

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43
Q

They act directly on arteriolar and venous smooth muscle to cause relaxation

A

Vasodilators

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44
Q

Indications CALCIUM CHANNEL BLOCKERS

A

considered first-line drugs for the treatment of such conditions as angina, hypertension, and supraventricular tachycardia. Often effective for the treatment of coronary artery spasms (vasospastic or Prinzmetal angina).

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45
Q

Adverse effects CALCIUM CHANNEL BLOCKERS

A

Hypotension, palpitations, tachycardia or bradycardia, constipation, nausea, dyspnea, rash, flushing, peripheral edema

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46
Q

TOXICITY AND MANAGEMENT WITH VASODILATORS

A

hypotension- treatment is administration of iv fluid and beta blockers

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47
Q

How do ARBs work?

A

by blocking the binding of angiotensin at the receptors; the end result is a decrease in blood pressure.

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48
Q

ACE inhibitors work by blocking a critical enzyme system responsible for the production of AII (angiotensin II; a potent vasoconstrictor)

A

They (1) prevent vasoconstriction caused by AII, (2) prevent aldosterone secretion and therefore sodium and water resorption, and (3) prevent the breakdown of bradykinin (a potent vasodilator) by AII.

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49
Q

A thorough nursing assessment includes

A

determining whether the patient has any underlying causes of hypertension, such as renal or liver dysfunction, a stressful lifestyle, Cushing’s disease, Addison’s disease, renal artery stenosis, peripheral vascular disease, or pheochromocytoma.

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50
Q

REMEMBER

A

Always assess for the presence of contraindications, cautions, and potential drug interactions before administering any of the antihypertensive drugs. Contraindications include a history of MI or chronic renal disease. Cautious use is recommended in patients with renal insufficiency or glaucoma. Drugs that interact with antihypertensive drugs include other antihypertensive drugs, anesthetics, and diuretics.

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51
Q

Hypertension is managed by ____ AND ____ . Patients need to consume a diet low in fat, make any other necessary modifications in their diet (such as possibly decrease the intake of sodium and increase fiber intake), engage in regular supervised exercise, and reduce the amount of stress in their lives.

A

both pharmacologic and nonpharmacologic measures

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52
Q

useful for heart failure
-wherein the heart is not able to effectively pump the blood towards diff. body organ

A

Cardiotonic agents

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53
Q

are drugs used to increase the contractility of the heart. Included below is a pharmacology guide for nurses on the various effects of cardiotonic-inotropic agents.

A

Cardiotonic agents

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54
Q

is a syndrome characterized by dysfunction of cardiac muscles.
-can occur with the number of heart condition that can result to overworking of the heart

A

Heart failure

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55
Q

Insufficient blood supply for the myocardium
-also the most common cause of heart failure (HF)

A

Coronary Artery Disease (CAD)

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56
Q

Enlargement of the heart and nagkaroon ng myocardial fatigue

A

Cardiomyopathy

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57
Q

Reflux, overloading of blood to the ventricles which over stretches the myocardium

A

Valvular Heart Disease

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58
Q

Primarily reflects pulmonary manifestations because the left ventricle cannot push blood towards the peripheral systems.

A

Left-sided HF

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59
Q

Occurs when the right side of the heart has the need to exert more force in order to push blood towards the pulmonary circulation.
- neck veins become distended, liver and spleen are enlarged

A

Right-sided HF

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60
Q

They exert their effects on the cardiac muscles by affecting levels of intracellular calcium. In turn, the contractility of the muscles is increased.

A

Cardiac Glycosides

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61
Q

Therapeutic Action Cardiac Glycosides

A

Allows more calcium to enter during contraction, therefore increasing the force of contraction – positive inotropic effect.

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62
Q

This drug can increase the strength of contractility without increasing the rate of contraction

A

Cardiac Glycosides

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63
Q

Indications Cardiac Glycosides

A

Primarily indicated for decreasing workload of the heart and relieving HF.

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64
Q

For atrial flutter, fibrillation
- widely use for children but the dosage should be calculated

A

Digoxin

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65
Q

notes for digoxin

A

Walang caution sa lactating women, pero proven na humahalo sya sa gatas kaya ingat pa rin. Mas susceptible sa older people

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66
Q

Contraindications Cardiac Glycosides

A

Allergy to any component of digitalis preparation,Ventricular tachycardia or fibrillation, Heart block (sick sinus syndrome),
Idiopathic hypertrophic subaortic stenosis (IHSS),
Acute myocardial infarction (MIRenal insufficiency, Can cause potential adverse effects to the fetus or neonate.

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67
Q

Pharmacokinetics Cardiac Glycosides

A

Oral: 30-120 min, 2-6 h peak, 6-8 days duration
IV: 5-30min, 1-5 h peak, 4-5 days duration

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68
Q

Adverse Effects Cardiac Glycosides

A

CNS: headache, weakness, drowsiness, vision changes (most commonly reported is seeing yellow halo around objects)
CV: arrhythmias
GI: GI upset, anorexia

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69
Q

NURSING ALERT! Signs and symptoms of digitalis toxicity

A

anorexia, nausea, vomiting, malaise, depression, irregular heart rhythms (e.g. heart block, heart arrhythmias, and ventricular tachycardia)

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70
Q

Interactions Cardiac Glycosides

A

Digoxin immune Fab or DigiFab: antidote; these antibodies bind molecules of digoxin, making them unavailable at site of action. Used when serum digoxin is >10 ng/mL and serum potassium is >5 mEq/L.
Verapamil, amiodarone, quinine, erythromycin, tetracycline, cyclosporine: increased therapeutic and toxic effects of digoxin. Combination of digoxin with any of these drugs would warrant decrease in dose of digoxin to prevent toxicity.
Potassium-losing diuretics: increased risk of cardiac arrhythmias
Thyroid hormones, metoclopramide, penicillamine: decreased therapeutic effects of digoxin. Increasing the dose of digoxin is important.
Cholestyramine, charcoal, colestipol, antacids, bleomycin, cyclophosphamide, methotrexate: decreased absorption of digoxin. In this case, digoxin must be taken 2-4 hours after taking any of these drugs.
St. John’s wort, psyllium: decreased therapeutic effect of digoxin
Ginseng, hawthorn, licorice: increased risk of digoxin toxicity

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71
Q

Nursing Considerations Cardiac Glycosides

A

IMPORTANT! Count apical pulse for one full minute before administering drug to monitor for adverse effects.
Drug is withheld if pulse is less than 60 beats per minute in adults and 90 beats per minute in infants.
Apical pulse is taken after one hour and if it remains low, nurse must document it, withhold the dose, and inform doctor.

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72
Q

aid in increasing force of myocardial contractility through their enzyme-blocking effect. This in turn, increases the flow of calcium into the myocardial cells.

A

Phosphodiesterase inhibitors

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73
Q

Therapeutic Action Phosphodiesterase Inhibitors

A

By blocking the enzyme phosphodiesterase, cyclic adenosine monophosphate (cAMP) increases. cAMP stimulates flow of calcium towards the myocardium and thereby, increases force of cardiac contractility. This leads to three major effects: vasodilation, increase oxygen consumption, arrhythmias

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74
Q

Indications Phosphodiesterase Inhibitors

A

Only indicated for short-term treatment of patients not responding to cardiac glycosides, vasodilators, and diuretics.

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75
Q

t OR F
Phosphodiesterase Inhibitors ARE SAFE FOR CHILDREN

A

F. NOT SAFE

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76
Q

Contraindications Phosphodiesterase Inhibitors

A

Allergy to phosphodiesterase inhibitors and bisulfites.
Severe aortic or pulmonary valvular disease.
Acute MI.
Conditions with fluid volume deficit.

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77
Q

Adverse Effects Phosphodiesterase Inhibitors

A

CV: ventricular arrhythmias, ventricular fibrillation, hypotension, chest pain
GI: nausea, vomiting, GI upset, abdominal pain
Hema: thrombocytopenia
Associated hypersensitivity reactions: vasculitis, pericarditis, pleuritis, and ascites
Burning at intravenous injection site

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78
Q

Nursing Considerations Phosphodiesterase Inhibitors

A

Assess for the mentioned contraindications to this drug (e.g. fluid volume deficit, acute MI, hypersensitivity, etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Obtain baseline status for weight while noting recent manifestations that increases or decreases to determine patient’s fluid status.
Assess closely patient’s heart rate and blood pressure to identify cardiovascular changes that may warrant change in drug dose.
Determine urinary pattern and output to assess gross indication of renal function.
Obtain baseline electrocardiogram (ECG) to identify heart rate and rhythm.
Monitor serum electrolyte, complete blood count, and renal and hepatic function test results to determine whether changes in drug dose is needed or not.

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79
Q

Examples of anti-anginal drugs

A

Nitrates and nitrites
Beta-Adrenergic Blockers
Calcium- channel blockers

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80
Q

is the narrowing ofbloodvessels supplying oxygen and nutrients to the heart, primarily due to the development of fatty tumors (atheromas) in the lumen of blood vessels in a process called atherosclerosis.

A

Coronary Artery Disease (CAD)

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81
Q

This pathologic process attracts platelets andclottingfactors to the area, causing a much larger obstruction to the vessels. The vessels also lose their natural ability to be elastic, resulting to inability to dilate and constrict. The heart stimulates the blood vessels to deliver more blood but blood delivery is limited by narrow vessel diameter, resulting to low oxygen supply of the heart.

A

Coronary Artery Disease (CAD)

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82
Q

As a consequence of hypoxia,____ is felt.

A

pain(angina)

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83
Q

Two types of angina:

A

classic angina (of exercise), & vasospastic/Prinzmetal’s/variant angina

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84
Q

type of angina which occurs due to diminished coronary blood flow to the heart

A

classic angina (of exercise),

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85
Q

type of angina which is caused by reversible vasospasm even at rest. Both types decrease oxygen supply of the heart.

A

vasospastic/Prinzmetal’s/variant angina

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86
Q

Provides FAST ACTION to directly relax smooth muscles and depress muscle tones without affecting the nerve activity
-dilates veins & oxygen

A

Nitrates and nitrites

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87
Q

Therapeutic Action

A

-The main effect is drop in systemic blood pressure.
-It compensates by increasing blood flow to healthy arteries and veins because affected vessels already lose their elasticity.

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88
Q

Indications Nitrates and Nitrites

A

Children:May be used only for congenital heart defects and cardiacsurgerybecause they can cause potentially dangerous changes in blood pressure.
Adults:Should be educated on drug’s various forms and their proper administration, storage, effectiveness, and manifestations that would warrant prompt medical help.
Older adults:Safety measures should be instituted as they areproneto adverse effects like arrhythmias andhypotension.

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89
Q

Contraindications Nitrates and Nitrites

A

Allergyto nitrates; Severeanemia–decreased cardiac output; Head trauma and cerebralhemorrhage; Pregnancy and lactation – potential harm to fetus; Conditions that can limit CO (e.g.hypovolemia,hypotension, etc.

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90
Q

Adverse Effects Nitrates and Nitrites

A

CNS: throbbing headache, dizziness, weakness
GI: nausea, vomiting, incontinence
CV: hypotension, reflex tachycardia, syncope
EENT: pallor, flushing, sweating\
Large dose leads to methemoglobinemia and cyanosis.

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91
Q

Interactions Nitrates and Nitrites

A

Ergot derivatives: risk for hypertension; decreased antianginal effect\
Heparin: decreased therapeutic effect of nitrates
PDE-5 inhibitors: risk for severe hypotension

92
Q

Nursing Considerations Nitrates and Nitrites

A

Presence of mentioned contraindications and cautions
Skin color and integrity, especially for transdermal or topical forms of nitrates
Pain and activity level
Neurological status (level of consciousness, affect, reflexes, etc.)
Cardiopulmonary status (BP; take heart rate in full minute)
Electrocardiogram as ordered
Laboratory tests (e.g. CBC, liver and kidney function tests, etc.)

93
Q

The most effective for recurrent variant of angina

A

Sublingual nitroglycerines

94
Q

for unstable angina

A

Continuous transfusion or transdermal patch

95
Q

are drugs which block or lyse the effects of sympathetic stimulation. Hence, they are also called as sympatholytics.

A

Beta-Adrenergic Blockers

96
Q

Therapeutic Action Beta-Adrenergic Blockers

A

Decrease in blood pressure, contractility or heart rate by blocking beta receptors in the heart. Reduce the oxygen demand of the heart.

97
Q

Indications Beta-Adrenergic Blockers

A

Nadolol is used for management of chronic angina. It is the drug of choice in angina patients with hypertension.
Propranolol is the prototype drug of this class. It is used for treatment of angina and syncope.
Nebivolol, the newest adrenergic blocking agent does not produce the same adverse effects seen in propranolol.

98
Q

is used for management of chronic angina. It is the drug of choice in angina patients with hypertension.

A

Nadolol

99
Q

is the prototype drug of this class. It is used for treatment of angina and syncope.

A

Propranolol

100
Q

, the newest adrenergic blocking agent does not produce the same adverse effects seen in propranolol.

A

Nebivolol

101
Q

Contraindications Beta-Adrenergic Blockers

A

Bradycardia, heart block, and cardiogenic shock – blocking effect of drugs exacerbates these conditions
Pregnancy and lactation – potentially harmful effects to the fetus or neonate
Diabetes, chronic obstructive pulmonary disease (COPD), thyrotoxicosis, and peripheral vascular diseases – blocking effect prevents maintaining homeostatic requirements of these diseases

102
Q

Adverse Effects Beta-Adrenergic Blockers

A

CNS: emotional depression, dizziness, fatigue, sleep disturbances
GI: gastric pain, nausea, vomiting, colitis, diarrhea
CV: heart failure, reduced cardiac output, arrhythmia
Respiratory: dyspnea, cough, bronchospasm

103
Q

Interactions Beta-Adrenergic Blockers

A

Clonidine: increased rebound hypertension
NSAIDs: decreased antihypertensive effects
Epinephrine: hypertension followed by bradycardia
Ergot alkaloids: peripheral ischemia
Insulin and oral hypoglycemic agents: alteration in blood glucose levels without the patient experiencing manifestations of hypo- or hyperglycemia

104
Q

Nursing Considerations Beta-Adrenergic Blockers

A

Assess for presence of mentioned contraindications and cautions.
Assess neurological status to determine presence of neurological adverse effects. Focus on level of orientation and sensory function.
Monitor blood pressure and heart rate accurately. Be sure to count the heart rate in one full minute.
Auscultate lungs to determine presence of possible respiratory adverse effects.
Check color and sensation of extremities. Measure capillary refill. This is to evaluate presence of insufficiencies in the peripheral vascular system.
Monitor laboratory test results (e.g. electrolyte levels and renal function tests) to ascertain risk for arrhythmia and discern whether dose adjustment is needed.

105
Q

are drugs which block heart contraction by inhibiting movement of calcium ions, thereby altering arterial and cardiac muscle action potentials.

A

Calcium-Channel Blockers

106
Q

Therapeutic Action Calcium-Channel Blockers

A

blocking the contractions, loss of muscle tone and vasodilation occur. Decreasing peripheral resistance. It relieves various spasm in variant angina

107
Q

Indications Calcium-Channel Blockers

A

Treatment of variant angina, chronic angina and effort-associated angina

108
Q

Contraindications

A

Allergy to drugs
Heart block and sick sinus syndrome – conduction problems in these disease may be exacerbated by slow conduction effect of drugs
Renal and hepatic dysfunctions – alteration with metabolism and excretion of drugs
Heart failure – worsened by decreased cardiac output effect of the drug

109
Q

Adverse Effects Calcium-Channel Blockers

A

CNS: dizziness, lightheadedness, fatigue, and headache
GI: nausea, hepatotoxicity effect of the drug
CV: hypotension, bradycardia, peripheral edema
EENT: flushing, rash

110
Q

Interactions Calcium-Channel Blockers

A

Cyclosporine with diltiazem: increased serum level and toxicity of cyclosporine
Cyclosporine with verapamil: heart block and digoxin toxicity. Verapamil increases level of digoxin.
Digoxin with verapamil: depressed myocardial conduction
General anesthesia with verapamil: serious respiratory distress

111
Q

Nursing Considerations Calcium-Channel Blockers

A

Assess for presence of mentioned contraindications and cautions.
Inspect skin color and integrity to determine presence of adverse effects on skin.
Assess the patient’s complaint of pain and the activity level prior to and after the onset of pain to aid in identifying possible contributing factors to the pain and its progression.
Monitor cardiopulmonary status closely as the drug can cause severe effects on these two body systems`

112
Q

Antiarrhythmics address arrhythmia by altering cells’ automaticity and conductivity.

A

Antiarrhythmics

113
Q

is the term applied for disruptions that interfere with generation of impulses and conduction of these impulses to the myocardium.

A

Arrhythmia

114
Q

T or F
All cells in the heart are capable of undergoing spontaneous contractions (automaticity). Therefore, these cells are capable of generating excitatory impulses.
Disruptions in the conduction of these impulses affect contractility of the heart as well as the volume of blood pumped by the heart each minute (cardiac output).

A

T

115
Q

Examples of antiarrhythmic

A

I, II, III, IV,

116
Q

Also called dysrhythmia, involves changes in automaticity and the conductivity of the heart cells

A

Arrhythmia

117
Q

is the property of the heart cells to transmit spontaneous impulses starting from the sinoatrial (SA) node, activating all parts of the heart muscle almost spontaneously.
-is the basis of cardiac contraction and relaxation, allowing the heart to beat.

A

Conductivity

118
Q

____ – impulse generation of 60-100 impulses per minute
____ – 40-50 impulses per minute
_____ – 10-20 impulses per minute

A

SA node ; AV node ; Ventricular muscle cells

119
Q

Different areas of the specialized conductive system include:

A

SA node
AV node
Ventricular muscle cells –

120
Q

is the property of the heart cells to undergo spontaneous depolarization during relaxation

A

Automaticity

121
Q

Here are the five phases of action potential:

A

Phase 0 – depolarization phase; This phase is characterized by open sodium gates and sodium ions rushing towards the cell leading to action potential.
Phase 1 – a very short period wherein concentration of sodium equalizes inside and outside of the cell
Phase 2 – plateau phase; stage in which cell is trying to go back to its resting stage (repolarization).
Phase 3 – rapid repolarization phase
Phase 4 – resting phase; stage in which sodium-potassium pump restores the cell’s resting membrane potential in preparation for the next action potential.

122
Q

Types of arrhythmias

A

Depending on factors causing them, here are different types of arrhythmias:

Changes in rate: tachycardia, bradycardia
Stimulation from ectopic focus: premature atrial contractions (PACs), premature ventricular contractions (PVCs), atrial flutter and/or fibrillation (AF), ventricular fibrillation
Alterations in conduction through the muscle: heart blocks, bundle branch block
It can be triggered by the following: electrolyte disturbances, decreased oxygen supply to the cells, structural damage of the conduction system, drug effects, acidosis, and lactic acid accumulation.

123
Q

This class blocks sodium channels in the cell membrane during action potential. Subgroup under this class is based on their mechanism in blocking sodium channels.
These class are local anesthetics and membrane-stabilizing agents because of their ability to bind more quickly to sodium channels.

A

Class I antiarrhythmics

124
Q

Therapeutic Action Class I antiarrhythmics

A

Class I antiarrhythmics stabilize cell membrane by depressing phase 0 of action potential. They bind to sodium channels and change the duration of action potential of the cells.
Class Ia drugs depress phase 0 and prolong duration of action potential.
Class Ib drugs somewhat depress phase 0 and shorten duration of action potential.
Class Ic drugs markedly depress phase 0 and extremely slows conduction but has little effect on the duration of action potential.

125
Q

Indications Class I antiarrhythmics

A

Primarily indicated for decreasing workload of the heart and relieving HF
Digoxin is especially indicated for atrial flutter, atrial fibrillation, and paroxysmal atrial tachycardia.

126
Q

Class Ia drugs ____

A

Class Ia drugs depress phase 0 and prolong duration of action potential.

127
Q

Class Ib ____

A

Class Ib drugs somewhat depress phase 0 and shorten duration of action potential.

128
Q

Class Ic ____

A

drugs markedly depress phase 0 and extremely slows conduction but has little effect on the duration of action potential.

129
Q

t OR F antiarrhythmics IS SAFE FOR PREGNANT WOMEN

A

antiarrhythmics NOT SAFE F IT IS PROHIBITED

130
Q

T OR F antiarrhythmics SUSCEPTIBLE TO ADULTS

A

T

131
Q

Contraindications Class I antiarrhythmics

A

Allergy to Class I antiarrhythmics. Prevent severe hypersensitivity reactions.
Bradycardia, heart block. Unless an artificial pacemaker is in place, the conduction-altering effect of drug can lead to total heart block.
HF, hypotension, shock. Exacerbated by effects of drug on action potential.
Electrolyte imbalance. Can alter drug effectiveness
Renal, hepatic dysfunction. Interfere with drug bioavailability and excretion
Pregnancy and lactation. Can cause potential adverse effects to the fetus or neonate.

132
Q

Adverse Effects Class I antiarrhythmics

A

CNS: dizziness, drowsiness, fatigue, twitching, mouth numbness, slurred speech, vision changes, tremors
CV: arrhythmias, hypotension, vasodilation, potential for cardiac arrest
Respiratory: respiratory depression
Hema: bone marrow depression
EENT: rash, hypersensitivity reactions, hair loss

133
Q

Interactions
Class I antiarrhythmics

A

Digoxin, beta-blockers: increased risk for developing arrhythmias
Quinidine with digoxin: quinidine competes with digoxin at renal transport sites so it can increase chances of developing digoxin toxicity
Cimetidine: increased Class Ia toxicity
Anticoagulants: increased risk of bleeding

134
Q

This class interferes with action potential by blocking beta receptors in the heart and kidneys. This, in turn, blocks phase 4 of action potential.
are beta-adrenergic blockers.

A

Class II antiarrhythmics

135
Q

Therapeutic Action Class II antiarrhythmics

A

Class II antiarrhythmics engage in competitive inhibition of beta receptors specifically found in the heart and kidneys. For this reason, there is decreased in heart rate, excitability, and cardiac output. Conduction through AV node also slows down. In the kidneys, release of renin is decreased.
These effects decrease blood pressure and the stabilize the highly-excitable heart. As a result, workload of the heart is lessened.

136
Q

Indications Class II antiarrhythmics

A

This class is specifically indicated for treatment of supraventricular tachycardia and premature ventricular contractions (PVCs).
Children: antiarrhythmics are not often used for this age group
Adults: usually indicated for emergency cases. Evaluation of drug regimen should be done carefully and regularly to ensure effectiveness and patient safety. Drug safety for pregnant women not established. This drug can enter breast milk and has been associated with various side-effects. Antiarrhythmics I, III, and IV are strictly prohibited to lactating women.
Older adults: are more susceptible to drug toxicity because of underlying conditions that would interfere with metabolism and excretion of drug. Renal and hepatic function should always be monitored.

137
Q

Contraindications Class II antiarrhythmics

A

Sinus bradycardia (<45 beats per minute), heart block. Exacerbated by the therapeutic effects of the drug.
HF, cardiogenic shock, asthma, respiratory depression. Exacerbated by blocking beta receptors.
Pregnancy and lactation. Can cause potential adverse effects to the fetus or neonate.
Diabetes, thyroid dysfunction. Altered by blockade of beta-receptors
Renal, hepatic dysfunction. Interfere with bioavailability and excretion of drugs.

138
Q

Adverse Effects Class II antiarrhythmics

A

CNS: dizziness, fatigue, dreams, insomnia
CV: arrhythmias, hypotension, bradycardia, AV blocks, alteration in peripheral perfusion
Respiratory: bronchospasm, dyspnea
GI: anorexia, diarrhea, constipation, nausea, vomiting
Other: loss of libido, decreased tolerance to exercise, alterations in blood glucose level

139
Q

Interactions Class II antiarrhythmics

A

Verapamil: increased adverse drug effects
Insulin: increased hypoglycemia

140
Q

This class prolongs and slows down the outward movement of potassium during phase 3 of action potential. These drugs act directly on the heart muscles to prolong repolarization and refractory period.
All of these drugs are proarrhythmic and have the possibility of inducing arrhythmias.

A

Class III antiarrhythmics

141
Q

Indications Class III antiarrhythmics

A

Amiodarone is the drug of choice for ventricular fibrillation and pulseless ventricular tachycardia.
Children: antiarrhythmics are not often used for this age group
Adults: usually indicated for emergency cases. Evaluation of drug regimen should be done carefully and regularly to ensure effectiveness and patient safety. Drug safety for pregnant women not established. This drug can enter breast milk and has been associated with various side-effects. Antiarrhythmics I, III, and IV are strictly prohibited to lactating women.
Older adults: are more susceptible to drug toxicity because of underlying conditions that would interfere with metabolism and excretion of drug. Renal and hepatic function should always be monitored.

142
Q

Therapeutic Action Class III antiarrhythmics

A

Class III antiarrhythmics’ ability to prolong refractory period and repolarization increases the threshold for ventricular fibrillation.
These are used to treat life-threatening arrhythmias for which no other drugs have been effective.
This class can also act on peripheral tissues to decrease peripheral resistance..

143
Q

Contraindications
Class III antiarrhythmics

A

AV Block. Ibutilide and dofetilide exacerbate this health condition.
Renal, hepatic dysfunction. Interfere with bioavailability and excretion of drugs.
Shock, hypotension, respiratory depression, prolonged QT interval. Depressed action potentials can worsen these health problems.

144
Q

Adverse Effects Class III antiarrhythmics

A

CNS: weakness, dizziness
CV: arrhythmias, HF
GI: nausea, vomiting, GI distress
Amiodarone is associated with liver toxicity, ocular abnormalities, and very serious cardiac arrhythmias.

145
Q

Interactions Class III antiarrhythmics

A

Digoxin, quinidine: increased toxic drug effects
Antihistamines, phenothiazines, tricyclic antidepressants: increased risk of proarrhythmias
Dofetilide combined with ketoconazole, verapamil, cimetidine: increased risk for adverse drug effects
Sotalol combined with antacids, NSAIDs, and aspirin: loss of effectiveness of sotalol

146
Q

Include two calcium-channel blockers, namely: diltiazem and verapamil.
This class blocks the movement of calcium towards the cell membrane..

A

Class IV antiarrhythmics

147
Q

Therapeutic Action Class IV antiarrhythmics

A

Class IV antiarrhythmics depress action potential generation and slows down phases 1 and 2 of action potential. This action slows down both conduction and automaticity.

148
Q

Indications
Class IV antiarrhythmics

A

Other uses of diltiazem and verapamil include treatment for hypertension and angina.
Children: antiarrhythmics are not often used for this age group
Adults: usually indicated for emergency cases. Evaluation of drug regimen should be done carefully and regularly to ensure effectiveness and patient safety. Drug safety for pregnant women not established. This drug can enter breast milk and has been associated with various side-effects. Antiarrhythmics I, III, and IV are strictly prohibited to lactating women.
Older adults: are more susceptible to drug toxicity because of underlying conditions that would interfere with metabolism and excretion of drug. Renal and hepatic function should always be monitored.

149
Q

Contraindications Class IV antiarrhythmics

A

Allergy to calcium-channel blockers. Prevent hypersensitivity reactions.
Heart block (sick sinus syndrome). Unless an artificial pacemaker is in place, heart blocks can be exacerbated by the effects of the drug.
HF, hypotension. Exacerbated by hypotensive effect of the drug.
Pregnancy, lactation. Potential adverse effects to neonate or fetus.
Renal, hepatic dysfunction. Interfere with bioavailability and excretion of drugs.

150
Q

Adverse Effects Class IV antiarrhythmics

A

CNS: weakness, dizziness, fatigue, depression, headache
CV: hypotension, shock, edema, HF, arrhythmia
GI: nausea, vomiting, GI distress.

151
Q

Interactions Class IV antiarrhythmics

A

Verapamil with beta-blockers: increased risk of cardiac depression
Digoxin: additive slowing of AV node conduction
Atracurium, pancuronium, vecuronium: increased respiratory depression
Increased risk of cardiac depression if IV preparation of these drugs were given 48 hours within administration of IV beta-adrenergic blockers.
Diltiazem can increase serum level of cyclosporine.

152
Q

Nursing Considerations for Antiarrhythmics

A

These are the important things the nurse should include in conducting assessment, history taking, and examination:

Assess for the mentioned contraindications to this drug (e.g. renal dysfunction, heart blocks, hypersensitivity, etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Assess patient’s neurological status to determine potential CNS drug effects.
Assess cardiac status closely (e.g. blood pressure, heart rate and rhythm, heart sounds, ec.) to determine whether change in drug dose is imperative.
Monitor respiratory rate, rhythm, and depth to assess for respiratory depression and detect changes associated with development of HF.
Monitor laboratory test results including complete blood count, renal and liver function tests to determine the need for possible change in dose and identify toxic effects.

153
Q

lower serum levels of cholesterol and various lipids. They are also called as lipid-lowering agents; these drugs provide effective treatment for hyperlipidemia (increased lipid level in the blood).

A

lipid lowering agents/ antihyperlipidemic drug

154
Q

Due to various reasons, fatty streaks begin to develop in the endothelium of coronary arteries. Over time, these fatty streaks develop into plaques (atheromas) and injure the lining of blood vessels. The inflammatory reaction begins, and it attracts white blood cells and platelets to the area. These cells collect on the injured vessels and cause the atheroma to grow bigger, further narrowing the diameter of blood vessels, and therefore, limiting the blood flow.
The injury decreases the flexibility of the vessels, rendering it less distensible and less reactive to neurochemical stimuli. Coronary arteries are now unable to balance oxygen demand and blood supply.
If not acted promptly, this can lead to total vessel blockage and vessel rupture. CAD is the leading cause of death worldwide, and its incidence is high in people with hyperlipidemia.
The cause of CAD remains unknown, but certain risk factors were identified, and these include increasing age, male gender, sedentary lifestyle, smoking, obesity, high-fat diet, high-stress levels, menopause, and medical conditions like hypertension, gout, and diabetes.

A

Coronary Artery Disease (CAD)

155
Q

Examples of lipid lowering agents

A
  • Bile Acid Sequestrants
  • HMG-CoA Reductase Inhibitors
  • Cholesterol Absorption Inhibitors
156
Q

These drugs are used to normalize high serum level of cholesterol.

A

Bile Acid Sequestrants

157
Q

Therapeutic Action Bile Acid Sequestrants

A

Bile acid sequestrants exert their effect in the intestines by binding into bile acids which contain a high level of cholesterol.
The resultant insoluble complex formed by this combination is then excreted through feces.
As this happens, more LDL segments from the circulation will be absorbed by the intrahepatic circulation to make more bile acids.

158
Q

Indications Bile Acid Sequestrants

A

Bile Acid Sequestrants are used as the treatment for primary hypercholesterolemia (high cholesterol and high LDL) as an adjunct to diet and exercise.
Cholestyramine is also used to treat pruritus associated with partial biliary obstruction.
Children: limited because lipids are important for development
Adults: combination with ChMg

159
Q

Pharmacokinetics Bile Acid Sequestrants

A

Not absorbed systemically and is excreted in the feces.

160
Q

Contraindications Bile Acid Sequestrants

A

Allergy to bile acid sequestrants. Prevent severe hypersensitivity reactions.
Complete biliary obstruction. Prevent bile from being secreted into the intestines.
Abnormal intestinal function. Aggravated by the presence of bile acid sequestrants.
Pregnancy and lactation. Potential decrease in absorption of fat and fat-soluble vitamins can be detrimental to fetus or neonate

161
Q

Adverse Effects Bile Acid Sequestrants

A

CNS: headache, anxiety, fatigue, drowsiness
GI: GI upset, constipation, fecal impaction, nausea, aggravated hemorrhoids
Hema: increased bleeding time, decreased production of clotting factors
Musculoskeletal: muscle aches, muscle pains
Other: rash, fat-soluble vitamin deficiencies

162
Q

Interactions Bile Acid Sequestrants

A

Bile acid sequestrants delay the absorption of thiazide diuretics, corticosteroids, digoxin, warfarin, and thyroid hormones. Therefore, if needed, these drugs are taken 1 hour before or 4-6 hours after a meal.

163
Q

Nursing Considerations Bile Acid Sequestrants

A

Assess for the mentioned contraindications to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy and evaluate potential adverse effects.
Obtain baseline status for weight while noting recent manifestations that increases or decreases to determine patient’s fluid status.
Assess neurological status, particularly orientation and alertness to determine any CNS effects.
Assess bowel elimination patterns, including frequency of stool passage and stool characteristics to monitor the development of constipation and possible fecal impaction.
Assess closely patient’s heart rate and blood pressure to identify cardiovascular changes that may warrant change in drug dose
Inspect abdomen for distention and auscultate bowel sounds to assess for changes in GI motility.
Monitor results of laboratory tests, particularly serum cholesterol and lipid levels to evaluate the effectiveness of drug therapy.

164
Q

This drug group increases the cell absorption of LDL by blocking the enzyme (HMG-CoA reductase) regulating the rate-limiting step in the synthesis of cholesterol. With this alteration in fat metabolism, HDL increases slightly.
-chemically modified from the products of fungi

A

HMG-CoA Reductase Inhibitors

165
Q

Therapeutic Action HMG-CoA Reductase Inhibitors

A

These are primarily indicated as adjunct medicine with diet and exercise for treatment of high cholesterol and LDL levels in the blood.

166
Q

Indications HMG-CoA Reductase Inhibitors

A

Pravastatin, lovastatin, and simvastatin are indicated for patients with documented CAD to slow progression of the disease.
Together with these three agents, atorvastatin is used as prophylaxis for first myocardial infarction attack for patients with multiple risk factors for CAD.
PREGNANCY CATEGORY X For women who are pregnant, this drug class is contraindicated (pregnancy category X).

167
Q

Contraindications HMG-CoA Reductase Inhibitors

A

Allergy to HMG-CoA reductase inhibitors. Prevent severe hypersensitivity reactions.
Active liver disease. Exacerbated by drug’s therapeutic effect and has potential to lead to severe liver failure.
Pregnancy, lactation. Potential for drug adverse effects to fetus or neonate.
Impaired endocrine function. Problems can arise due to alteration in the formation of steroid hormones.
Renal impairment. Caution is given to patients taking other statins and close monitoring in instituted. Atorvastatin is not affected by renal diseases.

168
Q

Interactions HMG-CoA Reductase Inhibitors

A

Cyclosporine, erythromycin, gemfibrozil, niacin, antifungal drugs: increased risk for rhabdomyolysis
Digoxin, warfarin: increased serum levels and resultant toxicity of HMG-CoA reductase inhibitors
Oral contraceptives: increased serum estrogen
Grapefruit juice: increased serum levels and resultant toxicity

169
Q

HMG-CoA Reductase Inhibitors Adverse Effects

A

CNS: headache, dizziness, insomnia, fatigue, blurred vision, cataract development
CV: increased risk for cardiovascular effects with simvastatin started at 80 mg for new patients
GI: flatulence, nausea, vomiting, cramps, abdominal pain, constipation
Hepatobiliary: increase liver enzymes, acute liver failure with use of atorvastatin and fluvastatin

170
Q

Nursing Considerations HMG-CoA Reductase Inhibitors

A

Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, pregnancy etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Obtain baseline status for weight while noting recent manifestations that increases or decreases to determine patient’s fluid status.
Assess neurological status with particular focus on consciousness, reflexes, and affect.
Assess closely patient’s heart rate and blood pressure to identify cardiovascular changes that may warrant change in drug dose.
Assess bowel patterns to determine possibility of developing constipation and resultant fecal impaction.

171
Q

are one of the new class of drugs approved (2003) to lower serum cholesterol levels.
- contreversy, fail to show its effects, further studies need to validate this

A

Cholesterol Absorption Inhibitors

172
Q

Therapeutic Action Cholesterol Absorption Inhibitors

A

Acting on the brush border of intestines, cholesterol absorption inhibitors block the absorption of dietary cholesterol. Consequently, less cholesterol goes to the liver and it increases the cholesterol clearance to make up for the drop..

173
Q

Indications Cholesterol Absorption Inhibitors

A

Adjunct to diet and exercise as a monotherapy or in combination with HMG-CoA inhibitors or bile acid sequestrants.
Used in combination with statins to treat homozygous familial hypercholesterolemia.

174
Q

Contraindications Cholesterol Absorption Inhibitors

A

Allergy to cholesterol absorption inhibitors. Prevent severe hypersensitivity reactions.
Liver disease, pregnancy, lactation: not used if combined with statins because of the effects of statins to these health conditions. Effect of this class to fetuses and neonates is not known.

175
Q

Adverse Effects Cholesterol Absorption Inhibitors

A

CNS: headache, dizziness, fatigue
Respiratory: upper respiratory tract infection (URI)
GI: mild abdominal pain, diarrhea
Musculoskeletal: muscle aches and pains, back pain

176
Q

Interactions Cholesterol Absorption Inhibitors

A

Cholestyramine, fenofibrate, antacid, gemfibrozil: elevated serum level of cholesterol absorption inhibitors
Cyclosporine: increased toxicity of cholesterol absorption inhibitors
Fibrates: increased risk for development of cholelithiasis
Warfarin: increased serum warfarin levelsy

177
Q

Nursing Considerations Cholesterol Absorption Inhibitors

A

Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, pregnancy etc.). To prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy. To establish baseline status, determine effectivity of therapy and evaluate potential adverse effects.
Assess neurological status. Give with a particular focus on orientation and reflexes to determine CNS drug effects.
Assess closely patient’s heart rate and blood pressure. To identify cardiovascular changes that may warrant a change in drug dose.
Assess bowel patterns. To determine the possibility of developing constipation and resultant fecal impaction.
Monitor laboratory test results of serum cholesterol, LDL, and liver function. To determine the potential for drug adverse effects and monitor effectiveness of therapy.

178
Q

These groups of drugs affect clot formation and resolution by hindering different steps in clotting formation which include altering the formation of platelet plug (antiplatelet drugs), interfering the clotting cascade and thrombin formation (anticoagulant drugs), and stimulating the plasmin system to break down the formed clot (thrombolytic agents).

A

Drugs Affecting Coagulation

179
Q

Examples of Drugs Affecting Coagulation

A
  • Antiplatelet Agents
  • Anticoagulants
  • Thrombolytic Agents
180
Q

Disorders that directly affect coagulation process

A

Thromboembolic and Hemorrhagic Disorders

181
Q

Disorders that directly affect coagulation process are divided into two main categories:

A

thromboembolic disorders and hemorrhagic disorders

182
Q

which involve overproduction of clots

A

thromboembolic disorders

183
Q

which is characterized by ineffective clotting process leading to excessive bleeding.

A

hemorrhagic disorders

184
Q

include medical conditions (e.g. CAD) which involve overproduction of clots which result into decreased blood flow and total vessel occlusion. Manifestations include hypoxia, anoxia, and even necrosis. These disorders are treated by drugs that interfere with normal coagulation process to prevent formation of clots.

A

Thromboembolic disorders

185
Q

Antiplatelet Agents

A

This drug class exerts its action by decreasing the responsiveness of platelets to stimuli that cause it to clump or aggregate. Through this, formation of platelet plug is decreased.

186
Q

Therapeutic Action Antiplatelet Agents

A

By blocking receptor sites on the platelet membrane, platelet adhesion and aggregation is inhibited.
Also, platelet-platelet interaction as well as interaction of platelets to clotting chemicals are prevented.

187
Q

Indications Antiplatelet Agents

A

Primarily indicated for cardiovascular diseases that have potential for development of vessel occlusion.
Other indications include maintenance of arterial and venous grafts, preventing cerebrovascular occlusion, and including them as adjunct to thrombolytic therapy for treatment of myocardial infarction.
One drug, anagrelide, blocks the production of platelets in the bone marrow.

188
Q

Contraindications Antiplatelet Agents

A

Allergy to antiplatelet agents. Prevent severe hypersensitivity reactions.
Known bleeding disorder. Increased risk of excessive blood loss
Recent surgery. Increased risk of bleeding in unhealed blood vessels
Closed head injuries. Increased risk of bleeding in injured blood vessels of the brain
History of thrombocytopenia. Anagrelide decreased bone marrow production of platelets.
Pregnancy, lactation. Generally inadvisable because of potential adverse effects to fetus or neonate

189
Q

Adverse Effects Antiplatelet Agents

A

Adverse Effects
CNS: headache, dizziness, weakness
GI: GI distress, nausea
Skin: skin rash
Hema: bleeding (oftenly occurs while brushing the teeth)

190
Q

Interactions Antiplatelet Agents

A

Increased risk of bleeding if combined with another drug that affects blood clotting.

191
Q

Nursing Considerations Antiplatelet Agents

A

Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, pregnancy etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Obtain baseline status for complete blood count and clotting studies to determine any potential adverse effects.

192
Q

By interfering with clotting cascade and thrombin formation, anticoagulants are able to interfere with the normal clotting process.

A

Anticoagulants

193
Q

Indications Anticoagulants

A

Among the many indications for this drug class include: stroke and systemic emboli risk reduction, nonvalvular atrial fibrillation, and deep vein thrombosis.
Heparin is used for prevention of blood clots in blood samples, dialysis, and venous tubing. It also does not enter breastmilk so it is the anticoagulant of choice for lactating women.
Antithrombin is a naturally-occurring anticoagulant and is a natural safety feature in the clotting system.

194
Q

Therapeutic Action Anticoagulants

A

Warfarin, an oral agent in this class, reduces Vitamin K-dependent clotting factors. As a result, clotting process is prolonged.
Two new oral agents, dabigatran and rivaroxaban, directly inhibits thrombin (last step in clotting process) and factor Xa, respectively.
Heparin and antithrombin block formation of thrombin from prothrombin.

195
Q

Contraindications Anticoagulants

A

Allergy to anticoagulants. Prevent severe hypersensitivity reactions.
Known bleeding disorder, recent trauma/surgery, presence of indwelling catheters, threatened abortion, GI ulcers. These conditions can be compromised by increased bleeding tendencies.
Pregnancy, lactation. Warfarin is a contraindication.

196
Q

Adverse Effects Anticoagulants

A

Warfarin is associated with alopecia, dermatitis, bone marrow depression, and less frequently with prolonged and painful erections.
Direct drug toxicity is characterized by nausea, GI upset, diarrhea, and hepatic dysfunction

197
Q

Interactions Anticoagulants

A

Anticoagulants, salicylates, penicillin, cephalosporin: increased bleeding if combined with heparin
Nitroglycerin: decreased anticoagulation if combined with heparin
Cimetidine, clofibrate, glucagon, erythromycin: increased bleeding if combined with warfarin
Vitamin K, phenytoin, rifampin, barbiturates: decreased anticoagulation if combined with warfarin
Antifungals, erythromycin, phenytoin, rifampin: alteration in metabolism of dabigatran and rivaroxaban

198
Q

Nursing Considerations Anticoagulants

A

Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, pregnancy etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Obtain baseline status for complete blood count and clotting studies to determine any potential adverse effects.

199
Q

agents promote clot resolution, the process of activating the plasmin system to break down the thrombus or clot that has been formed.

A

Thrombolytic Agents

200
Q

Indications Thrombolytic Agents

A

For treatment of acute MI, pulmonary embolism, and acute ischemic stroke.
Also for clearing of occluded intravenous catheters and central venous access devices.

201
Q

Therapeutic Action Thrombolytic Agents

A

The conversion of plasminogen to plasmin is the body’s natural anticlotting system. Thrombolytic agents’ action to activate this promotes breakdown of fibrin threads and dissolution of formed clots.
It is necessary to prevent vessel occlusion and therefore, to deliver adequate blood flow to body systems.

202
Q

Contraindications Thrombolytic Agents

A

Allergy to thrombolytics. Prevent severe hypersensitivity reactions.
Known bleeding disorder, recent trauma/surgery, acute liver disease, cerebrovascular accident within 2 months, GI ulcers. These conditions can affect normal clotting factors and normal plasminogen production.
Pregnancy, lactation. Potential adverse effects to fetus or neonate.

203
Q

Adverse Effects Thrombolytic Agents

A

CV: cardiac arrhythmias, hypotension
Hema: bleeding (most common)
Hypersensitivity reaction (uncommon) is characterized by rash, flushing, and bronchospasm.

204
Q

Interactions Thrombolytic Agents

A

Anticoagulant, antiplatelet: increased risk of bleeding

205
Q

Nursing Considerations Thrombolytic Agents

A

Assess for the mentioned contraindications to this drug (e.g. hypersensitivity, acute liver disease, CVA within 2 months, etc.) to prevent potential adverse effects.
Conduct thorough physical assessment before beginning drug therapy to establish baseline status, determine effectivity of therapy, and evaluate potential adverse effects.
Obtain baseline status for complete blood count, fecal occult blood test (FOBT), and clotting studies to determine any potential adverse effects.

206
Q

Condition slowly arising all across country.
-hemoglobin concentration is lower than normal
-not specific disease state

A

Anemia

207
Q

results from the inability of bone marrow to produce adequate numbers of red blood cells.

A

Hypoproliferative anemia

208
Q

Premature destruction of erythrocytes that results the liberation of hemoglobin from the erythrocytes

A

Hemolytic anemia

209
Q

The formation of new blood cells is one of the primary functions of bones. This process is known as

A

hematopoiesis, and it includes the production of erythrocytes (red blood cells, or RBCs), as well as leukocytes (white blood cells) and thrombocytes (platelets)

210
Q

is a mineral that is essential for the proper function of all biologic systems in the body. It is stored in many sites throughout the body (liver, spleen, and bone marrow). Deficiency of this mineral is the principal nutritional deficiency resulting in anemia.

A

IRON

211
Q

Therapeutic Action IRON

A

is an oxygen carrier in both hemoglobin and myoglobin (oxygen-carrying molecule in muscle tissue) and is critical for tissue respiration. Iron is also a required component of a number of enzyme systems in the body and is necessary for energy transfer in the cytochrome oxidase and xanthine oxidase enzyme systems

212
Q

IRON Indications

A

Supplemental iron contained in multivitamins plus iron or iron supplements alone are indicated for the prevention or treatment of iron-deficiency anemia.

213
Q

Adverse Effect IRON

A

Nausea, constipation, epigastric pain, black and tarry stools, vomiting, diarrhea, temporarily discolored tooth enamel, eyes pain on injects

214
Q

Contraindications IRON

A

Contraindications to the use of iron products include known drug allergy, hemochromatosis (iron overload), hemolytic anemia, and any other anemia not associated with iron deficiency.

215
Q

Interactions IRON

A

The absorption of iron can be enhanced when it is given with
ascorbic acid and decreased when it is given with antacids and
calcium. Iron preparations can decrease the absorption of certain antibiotics, including tetracyclines and quinolones.

216
Q

is a water-soluble B-complex vitamin. It is also referred to as folate, the name of its anionic form.

A

FOLIC ACID

217
Q

Therapeutic Action FOLIC ACID

A

Folic acid is converted in the body to tetrahydrofolic acid, which is used for erythropoiesis and for synthesis of nucleic acids (DNA and ribonucleic acid [RNA]).

218
Q

Adverse Effect FOLIC ACID

A

Adverse effects associated with folic acid use are rare. Allergic
reaction or yellow discoloration of urine may occur.

219
Q

Indications FOLIC ACID

A

Folic acid is primarily used to prevent and treat folic acid deficiency. Anemias caused by folic acid deficiency can be treated by exogenous supplementation of folic acid.

220
Q

Contraindications FOLIC ACID

A

Contraindications to the use of folic acid include known allergy to a specific drug product and any anemia not related to folic acid deficiency (e.g., pernicious anemia). Folic acid is not to be used to treat anemias until the underlying cause and type of anemia have been determined.

221
Q

Interactions FOLIC ACID

A

No significant drug interactions occur with folic acid.

222
Q

OTHER ANEMIA DRUGS

A

Cyanocobalamin (vitamin B12)

223
Q

used to treat pernicious anemia and other megaloblastic anemias. It can be given orally or intranasally to treat vitamin B12 deficiency but is usually given by deep intramuscular injection to treat pernicious anemia. Once remission of the anemia is seen, cyanocobalamin can be dosed once a
month.

A

Cyanocobalamin (vitamin B12)

224
Q

are ineffective without adequate body iron stores.

A

Erythropoiesis-stimulating agents

225
Q

are very important in the treatment of many disorders and diseases (e.g., malignancies) to achieve RBC and hemoglobin formation that is as adequate as possible and to help prevent nutritional deficits that can affect all body systems, especially the immune system

A

Iron and folic acid

226
Q

are often used in the treatment of pernicious anemia, malabsorption syndromes, hemolytic anemias, hemorrhage, and renal and liver diseases.

A

Blood-forming drugs

227
Q

T or F
Instruct patients to take iron products exactly as ordered. Parenteral dosage forms may cause anaphylaxis and orthostatic hypotension.

A

T

228
Q

The primary treatment for heart failure (HF) is ___________.

A

Increasing contractility so the heart will be able to pump more blood

Pharmacology (12 decks)

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