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Pharmacology > Drugs Acting on the Cardiovascular System > Flashcards

Drugs Acting on the Cardiovascular System Flashcards

1
Q

Part of the heart that receive deoxygenated blood from the circulation

A

Right atrium

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2
Q

Part of the heart that pumps blood to the lungs through the pulmonary artery for gas exchange

A

Right ventricle

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3
Q

Part of the heart that receives oxygenated blood

A

Left atrium

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4
Q

Part of the heart that pumps blood into the aorta for systemic circulation

A

Left ventricle

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5
Q

What are the 3 Layers of the Heart Wall

A
  1. Endocardium
  2. Myocardium
  3. Epicardium
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6
Q

The layer of the heart wall that lines the inner chambers of the heart, valves, chordate tendinae and papillary muscles.

A

Endocardium

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7
Q

The layer of the heart wall that is a muscular layer, middle layer, responsible for the major pumping action of the ventricles.

A

Myocardium

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8
Q

The layer of the heart wall that has a thin covering (mesothelium), covers the outer surface of the heart.

A

Epicardium

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9
Q

It is a fibrous covering that protects the heart from injury and infection

A

Pericardium

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10
Q

2 parts of the Pericardium

A

Visceral – attached to the exterior of the myocardium

Parietal – attached to the great vessels and diaphragm

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11
Q

It arises from the endocardial and myocardial surfaces of the ventricles and attach to the chordae tendinae

A

Papillary muscle

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12
Q

It attaches to the tricuspid and mitral valves and prevent eversion during systole; “heartstrings

A

Chordae tendineae

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13
Q
  • permit blood flow in only one direction
  • Open and close in response to the movement of blood and pressure changes within the chambers
A

Heart Valves

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14
Q

Name at least 3 Heart Valves

A
  • Tricuspid
  • Pulmonic
  • Mitral/Bicuspid
  • Aortic
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15
Q

Found on the Right Coronary Artery
- supplies the SA node

A

SA nodal branch

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16
Q

Found on the Right Coronary Artery
- supplies the right border of the heart

A

Right marginal branch

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17
Q

Found on the Right Coronary Artery
- supplies the AV node

A

AV nodal branch

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18
Q

Found on the Left Coronary Artery
- supplies SA node in 40% of people

A

Circumflex branch

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19
Q

Found on the Left Coronary Artery
- supplies the left ventricle

A

Left marginal branch

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20
Q

Found on the Left Coronary Artery
- supplies both ventricles and interventricular septum

A

Anterior interventricular branch aka left anterior descending (LAD)

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21
Q

Found on the Left Coronary Artery
- terminates in a surface of the heart

A

Lateral branch

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22
Q

What are the 3 Coronary Veins

A
  • Coronary Sinus
  • Great cardiac vein
  • Oblique vein
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23
Q

main vein of the heart

A

Coronary Sinus

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24
Q

main tributary of the coronary sinus

A

Great cardiac vein

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25
Q

remnant of SVC, small and insignificant

A

Oblique vein

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26
Q

amount of blood ejected with each heartbeat

A

Stroke volume

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27
Q

amount of blood pumped by the ventricles per minute

A

Cardiac Output

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28
Q

degree of stretch of the cardiac muscle fibers at the end of diastole

A

Preload

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29
Q

ability of the cardiac muscle to shorten in response to an electric impulse

A

Contractility

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30
Q

the resistance to ejection of blood from the ventricle

A

Afterload

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31
Q

the percent of end-diastolic volume with each heartbeat

A

Ejection Fraction

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32
Q

Total blood collected in the ventricles at the end of diastole; determined by the length of diastole and venous pressure

A

End diastolic volume (EDV)

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33
Q

Blood left over in the ventricle at the end of contraction (not pumped out); determined by the force of ventricle contraction and arterial blood pressure

A

End systolic volume (ESV)

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34
Q

Average blood EDV

A

120 ml

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35
Q

Average blood ESV

A

50 ml

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36
Q

What law states that A greater EDV increases the contractile strength of the ventricles and will increase SV

Increased EDV = Increased Preload = More stretched sarcomeres = Increased sensitivity to Ca2+ channels = More contraction force = Increased SV

A

Frank-Starling Law of the Heart

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37
Q

increases heart rate (maintains stroke volume which leads to increased Cardiac Output)

A

Sympathetic – NOREPINEPHRINE (NE

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38
Q

decreases heart rate

A

Parasympathetic

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39
Q

parasympathetic inhibition of inherent rate of SA node, allowing normal HR

A

Vagal Tone

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40
Q

monitor changes in blood pressure and allow reflex activity with the autonomic nervous system

A

Baroreceptors, pressoreceptors

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41
Q

hormone released by adrenal medulla during stress; increases heart rate

A

Epinephrine

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42
Q

hormone released by thyroid; increases heart rate in large quantities; amplifies effect of epinephrine

A

Thyroxine

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43
Q

increased K+ level; KCI used to stop heart on lethal injection

A

Hyperkalemia

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44
Q

lower K+ levels; leads to abnormal heart rate rhythms

A

Hypokalemia

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45
Q

depresses heart function

A

Hypocalcemia

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46
Q

increases contraction phase

A

Hypercalcemia

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47
Q

HIGH Na+ concentration; can block Na+ transport and muscle contraction

A

Hypernatremia

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48
Q

Factors Affecting Heart Rate

A

Exercise – lowers resting heart rate (40-60)

Heat – increases heart rate significantly

Cold – decreases heart rate significantly

Tachycardia – higher than normal resting heart rate (over 100); may lead to fibrillation

Bradycardia – lower than normal resting heart rate (below 60); parasympathetic drug side effects; physical conditioning; sign of pathology in non-healthy patient

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49
Q

Heart pumps deoxygenated blood from the R ventricle through the pulmonary artery to the lungs

A

Pulmonary Circulation

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50
Q

aka Peripheral Circulation

Heart pumps blood from the left ventricle to the aorta and into the general circulation

A

Systemic Circulation

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51
Q
  • Naturally-occurring cardiac glycoside
  • Obtained from the purple and white foxglove plant.
  • Used since 1200 AD
    In 1978 – used by William Withering of England to alleviate “dropsy” (now known as edema) caused by kidney and cardiac insufficiency
  • Later known to be effective in treating heart failure
A

Digitalis

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52
Q

pathologic increase in stretching and thickening of ventricular walls allowing greater filling pressure associated with a weakened heart

A

Increased preload

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53
Q

additional pressure or force in the ventricular wall caused by excess resistance in the aorta

A

Increased afterload

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54
Q

Left-Sided Heart Failure Risk Factors

A

Mitral Valve Stenosis (RHD) – 90%
Aging
Myocardial Infarction
Ischemic Heart Disease
Hypertension
Aortic Valve Stenosis

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55
Q

Right-Sided Heart Failure Risk Factors

A

Tricuspid Valve Stenosis
COPD
Pulmonary Embolism
Pulmonic Stenosis
Left sided heart failure

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56
Q

Identify What NYHA Class
-No limitation of physical activity. Ordinary activities do not cause undue fatigue, palpitations, or dyspnea.

A

Class I

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57
Q

Identify What NYHA Class
- Slight limitation of physical activity. Comfortable at rest, but ordinary activities cause fatigue, palpitations, or dyspnea.

A

Class II

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58
Q

Identify What NYHA Class
- Marked limitation of physical activity. Comfortable at rest; less than ordinary activity causes fatigue, palpitations, or dyspnea.

A

Class III

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59
Q

Identify What NYHA Class
- Symptoms occur at rest; any physical activity increases discomfort.

A

Class IV

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60
Q

They Inhibit Na-K pump
which increase in intracellular sodium
which results in the influx of calcium
resulting to efficient contraction of heart muscle

A

CARDIAC GLYCOSIDES

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61
Q

3 effect of Digitalis on heart muscles

A
  1. Positive inotropic action - ↑ myocardial contraction SV
  2. Negative chronotropic action - ↓ heart rate
  3. Negative dromotropic action - ↓ conduction of heart cells
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62
Q

Nonpharmacologic Measures to Treat Heart Failure

A

Limit salt intake to 2g/day (1tsp)

Avoid or decrease alcohol intake to 1 drink/day

Restrict fluid intake
Avoid smoking

Mild exercises such as walking or bicycling

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63
Q

Secondary drug for heart failure (First-line drugs are dopamine, dobutamine, and milrinone)

Used to correct atrial fibrillation (rapid uncoordinated contraction of atrial myocardium) and atrial flutter (rapid contractions of 200-300bpm)

A

Digoxin (Lanoxin)

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64
Q

This drug’s pharmacokinetics is …..

Absorption
- Oral – 70%
- Liquid and capsule 90%

Protein binding – 30%

Half-life – 30-40hours; Risk for toxicity

Metabolized in the liver; 50-70%, Excreted in the urine

Dose should be decreased in hypothyroidism and increased in hyperthyroidism

A

Digoxin (Lanoxin)

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65
Q

This drug’s Pharmacodynamics is…

In heart failure – increases myocardial contraction which will have increased cardiac output and improved circulation and tissue perfusion

Decreased heart rate
Therapeutic serum level – 0.8-2ng/mL

A

Digoxin (Lanoxin)

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66
Q

What is the Therapeutic Serum level range of Digoxin (Lanoxin)

A

0.8-2ng/mL

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67
Q

Its s/sx is Anorexia, diarrhea, nausea and vomiting, bradycardia, premature ventricular contractions (PVCs), cardiac dysrhythmias, headaches, malaise. Blurred vision, visual illusions (white, green, yellow halos around objects), confusion, and delirium

A

Digitalis (Digoxin) Toxicity

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68
Q

It is the antidote for Digitalis (Digoxin) Toxicity binds with digoxin to form complex molecules that can be excreted in the urine

A

Digoxin immune Fab (ovine, Digibind)

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69
Q

Which drug has an interaction with Digoxine that matches the description below

Diuretics = loss of potassium = hypokalemia = increased effect of digoxin at the myocardial cells = digitalis toxicity

A

Furosemide (Lasix), Hydroclorthiazide (Esidrix, Microzide)

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70
Q

Which drug has an interaction with Digoxine that matches the description below

  • Promote sodium retention and potassium excretion
  • Advise patient to eat K-rich food or take K+ supplements
A

Cortisone

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71
Q

Which drug has an interaction with Digoxine that matches the description below

  • Can decrease digitalis absorption if taken together
  • Doses should be staggered
A

Antacids

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72
Q

Prevents degradation of cAMP and cGMP, thus causing a positive inotropic effect and vasodilation resulting to increased stroke volume and cardiac output

A

Phosphodiesterase Inhibitors

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73
Q

What is the AE of Phosphodiesterase Inhibitors

A

severe cardiac dysrhythmia

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74
Q

enzyme that degrades cAMP and cGMP promoting smooth muscle and vessel contraction

A

Phosphodiesterase

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75
Q

It decreases venous blood return to the heart which causes decreased cardiac filling, ventricular stretching, and oxygen demand on the heart

A

Vasodilators

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76
Q

What are the 3 ways vasodilators act?

A
  1. Reduce cardiac afterload which causes increased cardiac output
  2. Dilate the arterioles of the kidneys which causes improved renal perfusion and increased fluid loss
  3. Improve circulation to the skeletal muscles
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77
Q

They
- Dilate venules and arterioles causing improved renal blood flow and decreased blood volume

  • Moderately decrease the release of aldosterone causing reduced Na and fluid retention
  • Can increase K+ levels; serum K+ levels must be monitored
A

Angiotensin Converting Ezyme (ACE) Inhibitors

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78
Q

Enumerate at least 3 ACE inhibitors

A

Captopril
Enalapril
Lisinopril
Perindopril

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79
Q

Given to patients who cannot tolerate ACEi

A

Angiotensin II receptor blockers (ARBs)

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80
Q

Enumerate at least 3 ARBs

A

Valsartan, Candesartan, Losartan

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81
Q

They are

  • Potassium-sparing diuretic
  • Used to treat moderate to severe HF
  • Blocks the production of aldosterone causing decreased excretion of potassium and magnesium causing improved heart rate variability and decreased myocardial fibrosis
A

Spironolactone (Aldactone)

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82
Q

What is the recommended dose of Spironolactone (Aldactone)

A

12.5-25mg/day

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83
Q

They are

  • Previously contraindicated for patients with HF due to reduction in cardiac contractility
  • Now shown to improve cardiac performance.
  • Dose should be initially low and gradually increased
A

Beta Blockers

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84
Q

Enumerate at least 3 Beta Blockers

A

Carvedilol, Metoprolol, Bisprolol

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85
Q
  • An Atrial natriuretic peptide that inhibits ADH by increasing urine sodium loss
  • Promotes vasodilation, natriuresis, and diuresis
  • Useful in acute decompensated HF with dyspnea
A

Neseritide (Natrecor)

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86
Q
  • A Combination of hydralazine (for blood pressure) and isosorbide dinitrate (dilator to relieve heart pain)
  • FDA approved for treating HF especially in African Americans
A

BiDil

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87
Q
  • Used to treat angina pectoris
  • Increase blood flow by 1.) increasing O2 supply or 2.) decreasing O2 demand by the myocardium
A

ANTIANGINAL DRUGS

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88
Q

acute cardiac pain caused by inadequate blood flow to the myocardium due to plaque occlusions within or spasms of the coronary arteries

A

angina pectoris

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89
Q

tightness, pressure in the center of the chest, and pain radiating down the left arm; referred pain in the neck and left arm

A

Anginal pain

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90
Q

Name 3 types of Angina Pectoris

A

Classic (stable)
Unstable (Preinfarction)
Variant (Prinzmetal, vasospastic)

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91
Q

What type of Angina Pectoris
- occurs with predictable stress or exertion

A

Classic (stable)

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92
Q

What type of Angina Pectoris
- Occurs frequently with progressive severity unrelated to activity; unpredictable regarding stress/exertion and intensity
- Often indicates and impending MI

A

Unstable (Preinfraction)

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93
Q

What type of Angina Pectoris occurs during rest

A

Variant (Prinzmetal, vasospastic)

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94
Q

Nonpharmacologic Measures to Control Angina : Enumerate at least 3

A

Avoid heavy meals, smoking, extreme weather changes, strenuous exercise, and emotional upset

Proper nutrition, moderate exercise (only after consulting with physician), adequate rest, and relaxation techniques

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95
Q
  • Developed in 1840s
  • Cause generalized vascular and coronary vasodilation causing increased blood flow through the coronary arteries
  • Reduces myocardial ischemia but can cause hypotension
A

Nitrates/Nitroglycerin

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96
Q

2 Examples of Nitrates/Nitroglycerin

A

Isosorbide dinitrate (Isordil)

Isosorbide mononitrate (Imdur)

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97
Q
  • Given sublingually, 0.4mg following cardiac pain; effect lasts 10mins
  • Decompose when exposed to heat
  • Dispensed in screw-cap tops that are not childproof for easy opening during an anginal attack
  • Also available in topical, translingual, oral ER capsule and tablet, aerosol spray and IV
A

Nitrates/Nitroglycerin

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98
Q

Pharmacokinetics

SL – absorbed rapidly in the IJV and the right atrium

40-50% absorbed through the GI tract

A

Nitrates/Nitroglycerin

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99
Q

Pharmacodynamics
Act on the smooth muscles of BVs causing relaxation and dilation

Decreases preload and afterload, and reduces myocardial O2 demand

Onset of action
*SL and IV – 1-3 minutes
*Transdermal – 30-60 minutes
*Transdermal patch – 24h; must be removed nightly to allow 8-12hr nitrate-free interval
*Ointment – 6-8 hours

A

Nitrates/Nitroglycerin

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100
Q

What drug has an SE and AE as stated below

  • Headaches – most common SE (Give paracetamol)
  • Hypotension, dizziness, weakness, faitness
  • Doses must be tapered over several weeks to prevent rebound effect of severe pain caused by myocardial ischemia
  • Reflex tachycardia – if given too rapidly; due to overcompensation of the CV system
A

Nitrates

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101
Q

most common SE of Nitrates

A

Headaches

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102
Q

Enumerate 3 examples of Beta Blockers

A

Metoprolol, Propranolol, Atenolol (“olols”)

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103
Q

This type of beta blocker - Decreases heart rate and cause bronchoconstriction

  • Pharmacodynamics
    *Onset: 30 mins
    *Peak: 1-1.5hrs
    *Duration: 4-12hrs
A

Nonselective beta blockers (block b1 and b2)

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104
Q

These Beta Blockers
- Act more strongly on b1 receptors
- Decreases heart rate but avoids bronchoconstriction

  • Choice for controlling angina pectoris
  • Pharmacodynamics
    *Onset: 15 - 60 mins
    *Peak: 2-4hrs
    *Duration: 6- 24hrs
A

Selective (cardioselective) beta blockers ( block b1 only)

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105
Q

Identify

Pharmacodynamics
- Decrease the force of myocardial contractions causing decreased O2 demand by the myocardium

A

Beta Blockers

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106
Q

Beta Blockers: Side Effects and Adverse Reactions

A

Bradycardia, Hypotension

Nonselective b-blockers – bronchospasm, behavioral or psychotic response, and impotence

Dose should be tapered for 1-2 weeks

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107
Q
  • Block β1 and β2 adrenergic receptors
  • Blocks the action of epinephrine and norepinephrine causing decreased heart rate, myocardial contractility, and blood pressure causing reduced O2 demand causing reduced anginal pain
  • Most useful for classic (stable) angina
  • Should be tapered to avoid reflex tachycardia
A

Beta Blockers

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108
Q

They
- Block Ca2+ influx in the cell causing decreased cardiac contractility, thus decreasing cardiac O2 demand

  • Used in variant and classic angina
A

Calcium Channel Blockers

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109
Q

Pharmacokinetics
- 80-90% absorbed through the GI
- Highly protein bound
- Half-life: 2-9hrs

A

Calcium Channel Blockers

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110
Q

Pharmacodynamics
*Verapamil – bradycardia

*Nifedipine – most potent; vasodilation  hypotension

*Onset: verapamil – 10mins; nifedipine and diltiazem – 30min

*Duration: verapamil – 3-7hrs; nifedipine and diltiazem – 6-8hrs

A

Calcium Channel Blockers

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111
Q

Identify what SE and AE is caused below

  • Headache, hypotension, dizziness, flushing of the skin
  • Peripheral edema – nicardipine, nifedipine, verapamil
  • Liver and kidney function changes; check serum liver enzymes periodically
  • Nifedipine (immediate-release form) – sudden cardiac death in high doses
A

Calcium Channel Blockers (CCBs)

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112
Q

Nursing Interventions: Antianginals

A
  • Do not use fingers when applying ointment; use tongue blade/gloves
  • Do not touch medication portion of nitro patch
  • Do not apply ointment or patch in any area near the vicinity of defibrillator-cardioverter paddle placement.
  • Explosion and skin burns may result
  • Administer SL nitroglycerin tablet if chest pain occurs. If pain has not subsided or has worsened in 5mins, seek immediate medical attention
  • Advise pt not to ingest alcohol while taking nitroglycerin
  • Notify HCP if chest pain is not completely alleviated
  • Inform pt not to d/c b-blockers and CCBs without consulting with HCP
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113
Q

Deviation from the normal rate or pattern of the heartbeat
Causes: MI, hypoxia, hypercapnia, thyroid dse., CAD, cardiac surgery, excess catecholamines, electrolyte imbalance

A

Cardiac Dysrhythmias

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114
Q

Prevent proper filling of the ventricles and decrease CO by 33%

A

Atrial Dysrhythmia

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115
Q
  • It is Life-threatening
  • Causes Ineffective filling and pumping of the ventricles  decreased or absent CO
A

Ventricular Dysrhythmia

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116
Q
  • Primary pacemaker of the heart
  • At the junction of the SVC and the right atrium
  • Firing rate: 60 to 100 impulses/min
A

Sinoatrial Node

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117
Q
  • Coordinates incoming electrical impulses from the atria, and after a slight delay, relays the impulse to the ventricles
  • Firing rate: 40 to 60 impulses/min
A

Atrioventricular Node (AV Node)

118
Q
  • Provides for ventricular conduction system
  • Fastest conduction among cardiac tissues
    Right and Left bundle
A

Bundle of His/Purkinje Fibers

119
Q

3 physiologic characteristics of the nodal cell and Purkinje cell

A

Automaticity
Excitability
Conductivity

120
Q

Identify which physiologic characteristics is being identified below

  • ability to initiate an electrical impulse
A

Automaticity

121
Q

Identify which physiologic characteristics is being identified below

  • ability to respond to an electrical impulse
A

Excitability

122
Q

Identify which physiologic characteristics is being identified below

  • ability to transmit an electrical impulse from one cell to another
A

Conductivity

123
Q

The repeated cycle of depolarization and repolarization

A

Cardiac Action Potential

124
Q

electrical activation of a cell caused by the influx of sodium into the cell while potassium exits the cell

A

Depolarization

125
Q

return of the cell to the resting state caused by re-entry of potassium into the cell while sodium exits

A

Repolarization

126
Q

What are the 5 phases of Cardiac Action

A
  1. Cellular Depolarization Phase
  2. Repolarization Phase
  3. Plateau Phase
  4. Repolarization Phase
  5. Resting Phase
127
Q
  • Used as local anesthetic, and still used for this purpose
  • Later discovered to have antidysrhythmic properties
  • Slows conduction velocity and decrease action potential amplitude
  • Class I drug
128
Q
  • Decrease conduction velocity, automaticity, and recovery time
  • More frequently prescribed for dysrhythmias than sodium channel blockers
  • A class II
A

Beta Blockers

129
Q
  • Increases refractory period and prolongs action potential duration
  • Used in the emergency treatment of ventricular dysrhythmias when other antidysrhythmics are ineffective
  • A Class III: Class that Prolong Repolarization
A

Amiodarone

130
Q
  • slow channel blocker causing a decreased excitability and contractility of the myocardium
  • increases refractory period of the AV node causing a decreased ventricular response
  • contraindicated for pts with AV block or heart failure
  • A class IV drug: Calcium Channel Blockers
131
Q

2 examples of Class IV Calcium Channel Blockers

A

Verapamil, diltiazem

132
Q

Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described

  • nausea, vomiting, diarrhea, confusion, hypotension, heart block, and neurologic and psychiatric symptoms
133
Q

Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described

  • less cardiac depression than quinidine
A

Procainamide

134
Q

Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described

  • CV depression, bradycardia, hypotension, seizure, blurred vision, and double vision, dizziness, lightheadedness, and confusion; used in caution in liver disease and HF; contraindicated in advanced AV block
135
Q

Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described

  • similar to lidocaine
A

Mexiletine and Tocainide

136
Q

Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described

  • bradycardia and hypotension
A

Beta blockers

137
Q

Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described

  • nausea, vomiting, hypotension, neurologic symptoms
A

Bretylium and Amiodiarone

138
Q

Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described

  • nausea, vomiting, hypotension, and bradycardia
139
Q

Nursing Interventions: Antidysrhythmics

Enumerate Nursing Interventions at least 3

A
  • Monitor VS
  • Administer IV route over a period of 2-3minutes
  • Monitor ECG
  • Teach pt to take drugs as prescribed
  • Provide specific instructions for each drug
  • Tell pt to report SE and AE
  • Advise pt to avoid alcohol, caffeine, and tobacco
140
Q

What are the 2 main purposes of diuretics

A
  1. Decrease hypertension
  2. Decrease edema in heart failure and renal or liver disorders
141
Q

This drugs mechanism of action is Inhibition of sodium and water reabsorption from the kidney tubules causing increased urine flow/diuresis

142
Q

What are the 5 Diuretic sites of action
(M.A.L.T.S)

A

M-annitol
A- cetazolamide
L - oop diuretics
T - hiazide diuretics
S - pironolactone

143
Q

Name 2 examples of THIAZIDES AND THIAZIDE-LIKE DIURETICS

A

Chlorothiazide
Hydrochlorothiazide

144
Q
  • Act on the distal convoluted renal tubule
  • Promotes sodium, chloride, and water excretion
  • Used to treat hypertension and peripheral edema
    NOT effective for immediate diuresis and should NOT be used in pts with severe renal dysfunction
  • Can cause Na, K, and Mg loss; promote Ca2+ reabsorption leading to hypercalcemia
  • Can affect glucose tolerance leading to hyperglycemia; should be used with caution in patients with diabetes
A

Chlorothiazide Hydrochlorothiazide

145
Q

Diuretics that should be used with caution in patients with diabetes

A

Chlorothiazide
Hydrochlorothiazide

146
Q

Pharmacokinetics
- Well absorbed in the GI tract

  • Moderate protein-binding
  • Half-life: longer than loop diuretics; should be administered in the morning to avoid nocturia and sleep interruption
A

THIAZIDES AND THIAZIDE-LIKE DIURETICS

147
Q

Pharmacodynamics
- Act directly on the arterioles causing vasodilation causing lower BP

  • NaCL and H2O excretion causing ↓vascular fluid volume causing ↓ CO and BP
  • Onset: 2hrs; Peak: 3-6hrs; Duration: 12-24h
A

THIAZIDES AND THIAZIDE-LIKE DIURETICS

148
Q

What diuretics has the following SE and Adverse Reactions

  • Electrolyte imbalance, hyperglycemia, hyperuricemia, hyperlipidemia
  • Dizziness, headache, nausea, vomiting, constipation, urticaria, hives, blood dyscrasias
  • Hypokalemia – monitor serum K+ levels; K+ supplements may be needed
  • Hyperuricemia – monitor serum uric acid levels
  • Hyperlipidemia – lipid-lowering drug might be needed
A

THIAZIDES AND THIAZIDE-LIKE DIURETICS

149
Q

what are the contraindications of THIAZIDES AND THIAZIDE-LIKE DIURETICS

A

Renal failure – may cause oliguria, elevated BUN and serum creatinine

150
Q

What is the THIAZIDES AND THIAZIDE-LIKE DIURETICS drug interaction with Digoxin

A

hypokalemia and hypocalcemia may enhance action of digoxin and can cause digitalis toxicity

151
Q

Enumerate at least 3 Nursing Interventions for THIAZIDES AND THIAZIDE-LIKE DIURETICS

A
  • Assess VS, weight, urine output, serum chemistry values for baseline levels
  • Check for edema
  • Obtain a drug history
  • Monitor VS and serum electrolytes
  • Observe for s/sx of hypokalemia (muscle weakness, leg cramps, cardiac dysrhythmias)
  • Monitor weight daily (1kg gain = 1L of body fluids)
  • Note urine output (Adult: 0.5-1.5cc/kg/hr or 30cc/hr)
  • Emphasize adherence to treatment regimen
  • Suggest to take in early morning
  • Keep out of children’s reach
  • Instruct to change position slowly from lying to standing
  • Advise prediabetics to have blood sugar checked regularly
  • Suggest use of sunblock when in direct sunlight for photosensitivity
  • Advise to eat potassium-rich food
  • Advise to take with food
152
Q

What are 3 examples of LOOP (HIGH CEILING) DIURETICS

A

Ethacrynic acid
Furosemide (Lasix)
Bumetamide

153
Q

These diuretics

  • Act on the thick ascending loop of Henle
    Inhibits chloride transport of sodium into the circulation causing inhibition of passive reabsorption of sodium causing loss of Na, H20, K, Ca2+, Mg
  • Extremely potent and can cause marked depletion of water and electrolytes
  • Less effective as antihypertensive agents
  • Should NOT be prescribed if a thiazide could alleviate body fluid excess; may be given together with a thiazide
  • Usually administered orally in the morning
  • Can increase renal blood flow up to 40%
  • Furosemide - given for patients with renal dysfunction
  • Unlike thiazides, causes Ca2+ excretion
A

LOOP (HIGH CEILING) DIURETICS

154
Q

LOOP (HIGH CEILING) DIURETICS Pharmacokinetics

A
  • rapidly absorbed in the GI tract
  • highly protein-binding
  • Half-life: 30mins – 1.5hrs
155
Q

LOOP (HIGH CEILING) DIURETICS Pharmacodynamics

A
  • Saluretic (NaCl-losing) or natriuretic (Na-losing) effect
  • Cause rapid diuresis causing decreased vascular fluid volume causing decreased CO and BP
  • Vasodilatory effect
  • Onset: 30-60mins;
  • Duration: shorter than thiazides
156
Q

Identify which diuretics have these SE and Adverse Reactions found below

  • Fluid and electrolyte imbalance (K, Na, Ca2+, Mg, Cl)
  • Hypochloremic metabolic alkalosis – worsens hypokalemia
  • Orthostatic hypotension
    Thrombocytopenia, skin disturbance, transient deafness - rare
A

LOOP (HIGH CEILING) DIURETICS

157
Q

What is LOOP (HIGH CEILING) DIURETICS reaction with Digoxin

A

hypokalemia may cause toxicity, as with thiazides

158
Q

Name at least 3 Nursing Interventions for LOOP (HIGH CELING) DIURETICS

A
  • Obtain drug history
  • Asses VS, s . electrolytes, weight, urine output for baseline levels
  • Assess hypersensitivity to sulfonamides
  • Monitor urine output
  • Notify HCP if urine output does not increase
  • Weigh pt
  • Monitor VS
  • Administer IV slowly;
    hearing loss may occur
  • Observe for s/sx of hypokalemia; monitor s. K levels
  • Advise to take in the morning to avoid sleep disturbance and nocturia
  • Teach to rise slowly from lying to sitting to standing
  • Suggest taking with food
159
Q

Name 2 examples of Osmotic Diuretics

A

Mannitol, Urea

160
Q

This type of drugs

  • Increase osmolality and sodium reabsorption in the proximal tubule and loop of Henle
  • Na, Cl, and K (to a lesser degree), and water are excreted
  • Used to prevent kidney failure, decrease intracranial pressure, and decrease intraocular pressure
  • Potent osmotic potassium-wasting diuretic
  • Frequently used in emergency situations like ICP and IOP
  • Diuresis occur within 1-3hours after IV administration
A

Mannitol
Urea

161
Q

What type of Diuretics has the SE and Adverse reactions described below

  • Fluid and electrolyte imbalance
  • Pulmonary edema – rapid shift of fluids
  • Nausea, vomiting, tachycardia, acidosis
  • Crystallization of vial when exposed to low temperature; should be warmed to dissolve crystals; DO NOT use when crystals are present and have not been dissolved
A

OSMOTIC DIURETICS

162
Q

What is the Contraindications of Osmotic Diuretics

A

Given with extreme caution in patients who have heart disease and HF

163
Q

facilitates conversion between CO2 and H2O from carbonic acid (H2CO3) and its dissociative ions, HCO3 and H+

A

Carbonic anhydrase

164
Q

Name at least 3 examples of CARBONIC ANHYDRASE INHIBITORS

A

Acetazolamide, dichlorphenamide, ethoxzolamide, methazolamide

165
Q
  • Block the action of carbonic anhydrase causing an increase Na, K, and HCO3 excretion
    Metabolic acidosis may occur with prolonged use
  • Used primarily to decrease IOP in pts with open-angle glaucoma
A

CARBONIC ANHYDRASE INHIBITORS

166
Q

What Diuretic has SE and Adverse Reactions being described below

  • Fluid and electrolyte imbalance, metabolic acidosis. Nausea vomiting, anorexia, confusion, orthostatic hypotension
A

CARBONIC ANHYDRASE INHIBITORS

167
Q

These Diuretics

  • Weaker than thiazides and loop diuretics
  • Act in the collecting duct and late distal tubule to promote Na and H2O excretion and potassium retension
  • Serum K+ may increase; K+ should be regularly monitored
  • Blocks the action of aldosterone and inhibits the Na-K pump
  • Heart rate is more regular, and the possibility of myocardial fibrosis decreased
  • Should NOT be taken with ACE inhibitors and ARBs
A

POTASSIUM-SPARING DIURETICS

168
Q

Enumerate 3 examples of POTASSIUM-SPARING DIURETICS

A

Spironolactone (Aldactone)
amiloride
triamterene
eplerenone

169
Q

effective antihypertensive

A

Amiloride and eplerenone

170
Q

useful in edema caused by HF or liver cirrhosis

A

Triamterene

171
Q

This type of Diuretic has the following side effects and Adverse Reactions

  • Hyperkalemia – pts should NOT take K+ supplements, unless s. K+ is low.
  • Caution in renal dysfunction
  • Life-threatening when given with ACEi
  • GI disturbances
A

POTASSIUM-SPARING DIURETICS

172
Q

Enumerate at least 3 Nursing Interventions for POTASSIUM-SPARING DIURETICS

A
  • Obtain drug history
  • Take baseline values
  • Note half-life of spironolactone; usually given 1-2x a day
  • Monitor urine output
  • Record VS
  • Observe for s/sc of hyperkalemia
  • Administer in the morning to avoid nocturia
  • Take with or after meals
  • Do not d/c without informing HCP
  • Caution to avoid direct sunlight exposure
  • Advise to take K-rich food
173
Q

2 types of Hypertension

A

Primary and Secondary Hypertension

174
Q

Identify the type of Hypertension

  • Most common, 90%
  • Unknown etiology
  • Risk factors: family history, hyperlipidemia,
  • African-American background, diabetes, aging, stress, excessive alcohol ingestion, smoking, obesity
A

Primary (Essential) Hypertension

175
Q

Identify the type of Hypertension

  • 10%
  • Related to renal and endocrine disorders
A

Secondary Hypertension

176
Q

Name 3 examples of Regulators of Blood Pressure

A

Kidneys
Blood Vessels
Other hormones

177
Q

Selected Regulators of Blood Pressure

  • Renin-Angiotensin-Aldosterone System
178
Q

Selected Regulators of Blood Pressure

  • Baroreceptors in the aorta and carotid sinus
  • Vasocenter in the medulla
  • Epinephrine and norepinephrine – vasoconstriction
A

Blood Vessels

179
Q

Selected Regulators of Blood Pressure

  • ADH, atrial natriuretic peptide, brain natriuretic peptide
A

Other hormones

180
Q

Name at least three NONPHARMACOLOGIC CONTROL OF HYPERTENSION

A

Stress-reduction techniques

exercise

salt restriction

decrease alcohol ingestion

smoking cessation

181
Q
  • Most frequently prescribed diuretic for BP control
  • Can be used alone for recently diagnosed HPN or mild HPN or with another fantihypertensive drugs
  • NOT for pts with renal impairment
A

Hydrochlorothiazide

182
Q

what are the 5 SYMPATHOLYTICS (SYMPATHETIC DEPRESSANTS)

A
  1. beta-adrenergic blockers
  2. Centrally-acting alpha2 agonists
  3. Alpha-adrenergic blockers
  4. Adrenergic neuron blockers
  5. Alpha1 and beta2 adrenergic blockers
183
Q

What are the effects of Alpha 1 and 2 receptors to Blood Vessels?

A

Constriction

184
Q

What are the effects of Beta 2 receptors to Blood Vessels?

185
Q

What is the effect of Beta 1 receptors on the heart

A

Tachycardia; increased contractility

186
Q

What is the effect of alpha 1 receptors on the heart

A

increased contractility

187
Q

What are the effects of Beta 2 receptors to Bronchi?

A

Relaxation

188
Q

What is the effect of alpha 2 receptors on thrombocytes

A

Aggregation

189
Q

What are the effects of Alpha 1 and 2 receptors to Kidneys?

A

Vasoconstriction

190
Q

What are the effects of Beta 1 and 2 receptors to Kidneys?

A

Renin Release; inhibition tubular sodium reabsorption

191
Q

What is the effect of alpha 2 receptors to Adipocytes

A

Inhibition lipolysis

192
Q

What is the effect of Beta 1,2, and 3 receptors to Adipocytes

193
Q

African-American pts DO NOT respond well to these drugs; can be combined with diuretics

A

Beta-Adrenergic Blockers

194
Q
  • They Decrease the sympathetic response from brainstem to the peripheral vessles
  • Stimulate the alpha2 receptors causing decreased sympathetic activity, increased vagus activity, decreased cardiac output, decreased serum epi and NE, and renin release
A

Centrally-Acting Alpha2 Agonists

195
Q

Examples of Centrally-Acting Alpha2 Agonists

A

Methyldopa, Clonidine, Guanfacine

196
Q

Identify which Centrally-Acting Alpha2 Agonists is being described

  • Can cause Na and H2O retention in high doses
  • DO NOT use in pts with liver impairment
A

Methyldopa

197
Q

Identify which Centrally-Acting Alpha2 Agonists is being described

  • Can cause Na and H2O retention in high doses
  • Available in transdermal preparation – replaced within 7 days and may be left while bathing
198
Q

Identify which Centrally-Acting Alpha2 Agonists is being described

  • Similar to clonidine
  • Long half-life
A

Guanfacine

199
Q

Name 3 SE Centrally-Acting Alpha2 Agonists

A
  • Drowsiness, dry mouth, dizziness, and bradycardia
  • Doses must be tapered to prevent rebound hypertension; if needed to be stopped immediately, another antihypertensive drug is prescribed
  • Peripheral edema
    Avoid clonidine during pregnancy; use methyldopa instead
200
Q

They
- Cause vasodilation and decreased BP

  • Useful in treating pts with lipid abnormalities; decrease VLDL and LDL, increase HDL
  • Safe for pts with diabetes
  • Do not affect respiratory function
A

Alpha-Adrenergic Blockers

201
Q

Examples of Alpha-Adrenergic Blockers

A

Prazosin
terazosin
doxazosin
phentolamine
phenoxybenzamine

202
Q

Identify which Alpha-Adrenergic Blockers is being described

  • Commonly prescribed
  • DO NOT take with alcohol or another antihypertensive
203
Q

Identify which Alpha-Adrenergic Blockers is being described

  • Longer half-lives
  • Given once at bedtime
A

Terazosin and doxazosin

204
Q

Identify which Alpha-Adrenergic Blockers is being described

  • Used for hypertensive crisis and severe hypertension from pheochromocytoma
A

Phentolamine and phenoxybenzamine

205
Q

Alpha-Adrenergic Blockers

Pharmacokinetics

A
  • absorbed through the GI
  • Large portion is Slost during hepatic first-pass metabolism
  • Should be administered 2x a day
    Highly protein-bound
206
Q

Alpha-Adrenergic Blockers Pharmacodynamics

A
  • Dilation of arterioles and venules causing decreased peripheral resistance causing decreased BP
  • Onset: 30mins-2 hrs; duration; 10 hours
207
Q

Alpha-Adrenergic Blockers SE

A

Prazosin, doxazosin, terazosin – orthostatic hypotension, nausea, headache, drowsiness, nasal congestions, edema, weight gain

Phentolamine – hypotension, reflex tachycardia, nasal congestion, GI disturbance

208
Q

Alpha-Adrenergic Blockers Drug Interactions

A

Anti-inflammatory drugs – intensified peripheral edema

  • Nitroglycerin – syncope/ faintness
209
Q

Nursing Interventions Alpha-Adrenergic Blockers

A
  • Monitor VS
  • Check daily for fluid retention and weight gain
  • Advise pt to comply with drug regimen
  • Inform pt that orthostatic hypotension may occur
  • Teach pt to self-monitor daily weights
  • Caution pt that dizziness, lightheadedness, and drowsiness may occur
  • Inform male pt that impotence may occur in high doses
  • Tell pt to report if edema is present in the morning
  • Inform pt not to take cold, cough, or allergy OTC medications without informing HCP
210
Q
  • They Block norepinephrine release from the sympathetic nerve endings causing decreased NE causing a decreased BP
  • SE and AE: orthostatic hypotension; vivid dreams, nightmares, suicidal ideation; sodium and water retention
  • Last choice for treatment of chronic hypertension
A

Adrenergic Neuron Blockers (Peripherally Acting Sympatholytics)

211
Q

Example of Adrenergic Neuron Blockers (Peripherally Acting Sympatholytics)

212
Q

They

  • Alpha1 > beta1; decreased BP, moderately dec. heart rate
  • Alpha1 receptor blocking – vasodilation causing decreased blood flow resistance causing decreased BP
  • Beta2 receptor blocking – decreased HR and AV contractility
    Large doses can block beta2 receptors causing inc. airway resistance
  • Large doses should not be taken by asthmatic patients
A

Alpha1- and Beta1-Adrenergic Blockers

213
Q

They

  • Relax the smooth muscles of the blood vessels causing vasodilation causing increased blood flow to the brain and kidneys causing decreased BP and sodium and water retention
  • SE: orthostatic hypotension, reflex tachycardia, palpitations, edema, nasal congestion, headache, dizziness, GI bleeding, lupus-like symptoms, numbness, tingling, excess hair growth
A

DIRECT-ACTING ARTERIOLAR VASODILATORS

214
Q

Examples of DIRECT-ACTING ARTERIOLAR VASODILATORS

A

Hydralazine, minoxidil, nitropurusside

215
Q

They

  • Inhibits ACE causing inhibition of AngII causing blockage of aldosterone release causing sodium and water excretion, potassium retention
  • African Americans – do not respond to ACEi
  • NOT given to during pregnancy d/t reduced placental blood flow
  • Reduce dose with renal insufficiency
A

ANGIOTENSIN-CONVERTING ENZYME INHIBITORS

216
Q

Examples of ANGIOTENSIN-CONVERTING ENZYME INHIBITORS

A

Benazepril, captopril, enalapril, fosinopril, lisinopril, perindopril, quinapril, ramipril, trandolapril

217
Q

Nursing Interventions for ANGIOTENSIN-CONVERTING ENZYME INHIBITORS

A
  • Monitor BP
  • Monitor lab tests relation to renal function
  • Watch for hypoglycemic reaction in patients with DM
  • Report to HCP occurrences of bruising, petechiae, and/or bleeding
  • Warn pt not to abruptly d/c use of captopril
  • Inform pt not to take OTC drugs w/o informing HCP
  • Teach pt to rise slowly
218
Q

They…

  • Act on the renin-angiotensin-aldosterone system (RAAS) to prevent release of aldosterone
  • Cause vasodilation and decrease peripheral resistance
  • Do not cause irritated cough compared to ACEi
    Contraindicated in pregnancy
    t1/2 – 6-9hours
  • Can be taken with or without food
  • Suitable for pts with mild hepatic insufficiency
A

ANGIOTENSIN II RECEPTOR BLOCKERS

219
Q

Examples of ANGIOTENSIN II RECEPTOR BLOCKERS

A

Losartan, Valsartan, Irbesartan, Candesartan, Eprosartan, Olmesartan, Telmisartan

220
Q

They…

  • Binds with renin causing reduction of Ang1, Ang2, and aldosterone levels
  • Effective for mild to moderate hypertension
  • Can be used alone or with another antihypertensive agent
  • Additive effect when combined with a thiazide or ARB
A

DIRECT RENIN INHIBITOR

221
Q

Examples of DIRECT RENIN INHIBITOR

A

Aliskiren (“ALIS Ka RENin”)

222
Q

They…

  • aka calcium antagonist and calcium blockers
  • Free Ca2+ increases muscle contractility, peripheral resistance, and BP
  • Block the Ca2+ channel in the vascular smooth muscle, promoting vasodilation
  • Large central arteries are not as sensitive to CCBs as coronary and cerebral arteries
A

CALCIUM CHANNEL BLOCKERS

223
Q

Examples of CALCIUM CHANNEL BLOCKERS

A

Amlodipine, Nifedipine, Verapamil, Diltiazem

224
Q

Identify which CALCIUM CHANNEL BLOCKERS is being described below

  • used to treat chronic HPN, angina pectoris, and cardiac dysrhythmias
225
Q

Identify which CALCIUM CHANNEL BLOCKERS is being described below

  • used to prevent ischemic brain injury due to vasospasms that often accompanies subarachnoid hemorrhage
A

Nimodipine

226
Q

Identify which CALCIUM CHANNEL BLOCKERS is being described below

  • decrease BP in older adults and those with low serum renin values; immediate-release form has been assoc. with increased incidence of sudden cardiac death (prescribed only as PRN in the hospital setting)
A

Nifedipine

227
Q

formation of clot in an arterial or venous vessel caused by blood stasis, platelet aggregation, or blood coagulation

A

Thrombosis

228
Q

dislodged thrombus that move through the bloodstream

229
Q

How clots form

A
  1. Blood vessel injury
  2. Platelets adhere to broken surface
  3. Synthesis of thromboxane A2
  4. Fibrin clot production
  5. Increased activation of GP IIb/IIIa
  6. Inhibition of blood flow
  7. Tissue ischemia
230
Q

They…

  • Inhibit clot formation
  • DO NOT dissolve clots that have already formed, unlike thrombolytics
  • Used in patients with DVT, pulmonary embolism, coronary thrombosis, or myocardial infarction, presence of artificial heart valves, and cerebrovascular accidents
A

ANTICOAGULANTS

231
Q
  • Introduced in 1938 as a natural substance in the liver that prevents clot formation
  • First used in blood transfusions to prevent clotting
  • Indicated for a rapid anticoagulant effect when a thrombosis occur because of a DVT, pulmonary embolism, or an evolving stroke
  • Also used in open-heart surgery to prevent blood from clotting and the critically ill patient with disseminated intravascular coagulation
  • Combines with antithrombin III causing inhibition of factor Xa and thrombin causing fibrinogen is not converted to fibrin causing fibrin clot formation is prevented
  • Poorly absorbed orally due to heparinase found in the liver
  • Given SQ for prophylaxis or IV for acute thrombosis
  • Prolongs clotting time
  • PTT and aPTT tests are used to monitor heparin therapy
  • Can decrease platelet count
232
Q

What is the antidote for Heparin

A

Protamine sulfate (1mg for every 100 units of heparin or LMWH given)

233
Q

They…

  • Inactivate the Xa factor, but it is less able to inactivate thrombin (aPTT monitoring is not necessary)
  • Prevent DVT and acute pulmonary embolism after orthopedic or abdominal surgery
  • Can be administered at home, SQ once or twice daily, usually in the abdomen
    t1/2 is 2-4x longer that that of heparin
  • Instruct pt NOT to take antiplatelet drug while taking LMWH or heparin
A

Low-Molecular-Weight Heparins

234
Q

What are the contraindications for Low-Molecular-Weight Heparins

A
  • Strokes, peptic ulcer, and blood anomalies
  • Eye, brain, or spinal surgery
235
Q

They…

  • Directly inhibits thrombin from converting fibrinogen to fibrin
  • very expensive
  • Class II Prenteral Anticoagulants
A

Direct Thrombin Inhibitors

236
Q

Examples of Direct Thrombin Inhibitors

A

Argatroban, Bivalirudin, Lepirudin, Dabigatran, Desirudin

237
Q

They…

  • Rivaroxaban (Xarelto) and Apixaban (Eliquis) – Xa inhibitors (do not require routine coagulation monitoring; given OD or BID)
  • Inhibit hepatic synthesis of Vitamin K, thus affecting the clotting factors II, VII, IX, and X
  • Used to prevent thromboembolic conditions such as thrombophlebitis, pulmonary embolism, and embolism formation caused by atrial fibrillation
  • Prolong clotting time; monitored by
  • Prothrombin time test (performed immediately before administering the next drug dose until the therapeutic level has been reached
A

Oral Anticoagulants

238
Q

An Oral Anticoagulants used in rodenticides to kill rats causing hemorrhage

A

Warfarin (Coumadin)

239
Q

The antidote for Oral Anticoagulants

240
Q

SE of Oral Anticoagulants

241
Q

Drug Interactions of Oral Anticoagulants

A

Aspirin, NSAIDs, sulfonamides, phenytoin, cimetidine, allopurinol, and oral hypoglycemic drugs - increase action

242
Q
  • A Warfarin antagonist
  • Given 1-10mg OD
  • Fresh whole blood or fresh frozen plasma or platelets are given if it fails to control bleeding
  • An Anticoagulant Antagonists
A

Vitamin K (Phytonadione)

243
Q

Nursing Interventions for Warfarin and Heparin

A
  • Obtain history of abnormal clotting or blood clotting problems
  • Obtain a drug and herbal history
  • Obtain baseline PT and INR values
  • Monitor VS, PT or INR (warfarin), and aPTT (heparin)
  • Examine mouth, nose, urine, and skin for bleeding
  • Check stools periodically for occult blood
    Keep anticoagulants antagonists available
  • Inform dentist when taking anticoagulants
  • Use soft toothbrush
  • Shave with electric razor
  • Have PT or INR performed
  • Carry medical ID card or wear MedicAlert bracelet
  • Encourage pt not to smoke
  • Check with HCP before taking OTC drugs
  • Teach how to control external hemorrhage (direct pressure for at least 5-10mins with a clean, dry abdorbsent material
  • Avoid large amounts of green leafy vegetables, legumes, soy bean oil (rich in Vit K), coffee, tea, cola, excessive alcohol, and certain herbs and nutritional supplements
244
Q

They…

  • Prevent thrombosis in the arteries by suppressing platelet aggregation
  • For prophylaxis in
    *Prevention of MI or stroke
    *Prevention of stroke for pts having transient ischemic attacks (TIAs)
A

ANTIPLATELET DRUGS

245
Q

Identify which ANTIPLATELET DRUGS is being described

  • Long-term, low-dose therapy – effective and inexpensive treatment
  • Inhibits COX resulting in inhibition of thromboxane A2 synthesis
  • Should be discontinued at least 7 days before surgery
246
Q

Identify which ANTIPLATELET DRUGS is being described

  • frequently used after MI or stroke to prevent a second event
A

Clopidogrel

247
Q

Identify which ANTIPLATELET DRUGS is being described

  • Inhibits platelet aggregation and a vasodilator
  • Used for intermittent claudication
A

Cilostazol

248
Q

Identify which ANTIPLATELET DRUGS is being described

  • Taken in conjunction with aspirin 75-100mg in a maintenance regimen
A

Ticagrelor

249
Q

A peripheral artery disease that causes pain on the thigh and calf muscles when active and stops when at rest due to narrowed or blocked arteries reducing blood flow

A

Intermittent Claudication

250
Q

They

  • Used since the early 1980s to promote fibrinolytic mechanism
  • Thrombus disintegrates within 4 hours of thrombolytic administration in acute MI
  • Should be administered within 3 hours of a thrombolic stroke
A

THROMBOLYTICS

251
Q

Examples of THROMBOLYTICS

A

Urokinase, streptokinase, alteplase tPA, reteplase rPA, tenecteplase

252
Q

A THROMBOLYTICS that is…

  • aka tissue plasminogen activator (tPA)
  • Binds to the fibrin surface of a clot, promoting conversion of plasminogen to plasmin (enzyme that digests the fibrin clot)
253
Q

What is the SE and AE of THROMBOLYTICS

A

Anaphylaxis – more common in streptokinase

Hemorrhage – major complication

254
Q

What is the antidote for Thrombolytics

A

Aminocaproic acid (Amicar) - antithrombolytic

255
Q

Nursing Interventions for THROMBOLYTICS

A
  • Assess baseline VS
  • Check baseline CBC, PT or INR
  • Obtain a medical and drug history
  • Monitor VS
  • Observe for S/Sx of active bleeding
  • Examine pt for active bleeding for 24h after thrombolytic therapy has been discontinued (q15min x 1 hr, then q30min x 8 hrs, then hourly)
    Observe for signs of allergic reaction
  • Avoid administering aspirin or NSAIDs for pain or discomfort
  • Monitor ECG
  • Avoid venipuncture/arterial sticks
256
Q

excess of one or more lipids in the blood

A

Hyperlipidemia or hyperlipoproteinemia

257
Q
  • “friendly” or “good” lipoprotein
  • Smallest, most dense; contains more protein and less fat
  • Remove cholesterol from the bloodstream and deliver it to the liver for excretion in bile
A

High-density lipoprotein (HDL)

258
Q
  • “bad” lipoprotein
  • Contains 50-60% cholesterol in the bloodstream
  • Elevated LDL = greater risk for developing atherosclerotic plaques and heart disease
A

Low-density lipoprotein (HDL)

259
Q

Carries mostly triglycerides and less cholesterol

A

Very low-density lipoprotein

260
Q

Large particles that transport fatty acids and cholesterol to the liver

A

Chylomicrons

261
Q

Identify at least 3 Nonpharmacologic Methods for Cholesterol Reduction

A
  • Reduce saturated fats and cholesterol in diet
  • Total fat intake should be <30% or less of caloric intake
  • Cholesterol intake should be 300mg/d or less
  • Choose lean meats, especially chicken and fish
  • Exercise
  • Avoid smoking
262
Q

What are the 3 types of fats

A

Trans Fat
Saturated Fat
Unsaturated Fat

263
Q

Identify which type of fat

  • Hydrogenated vegetable oils
  • fast foods
  • cakes and pastries
  • Chocolate
  • Deep Fried Food
A

Trans Fats

264
Q

Identify which type of fat

  • Vegetable Fats
    *Coconut
    *Palm Oil
    *3 in 1 and 2 in 1 beverages
    *creamer
    *condensed milk
  • Animal Fats
    *Poultry Skin
    *Fatty Meat
    *Butter
    *Ghee
    *Tallow/Lard
    *Full Cream Dairy Products
A

Saturated Fats

265
Q

Identify which type of fat

  • Polyunsaturated Fats
    *Corn oil
    *Soybean oil
    *Sunflower oil
    *Seeds
    *Cold water fish
A

Unsaturated Fats

266
Q

Identify which type of Lipids is being described

  • Increased chylomicrons and increased triglycerides
  • uncommon
267
Q

Identify which type of Lipids is being described

  • Increased Low density lipoprotein and increased cholesterol
  • Common
268
Q

Identify which type of Lipids is being described

  • increased very low density lipoprotein, increased Low density Lipoprotein, increased cholesterol and triglycerides
  • very common
269
Q

Identify which type of Lipids is being described

  • Moderately increased cholesterol and triglycerides
  • Uncommon
270
Q

Identify which type of Lipids is being described

  • Increased very low density lipoprotein and markedly increased triglycerides
  • very common
271
Q

Identify which type of Lipids is being described

  • Increased chylomicrons, VLDL, and Triglycerides
  • uncommon
272
Q

Enumerate at least 3 ANTIHYPERLIPIDEMICS

A

Bile Acid Sequestrants

Nicotinic acid or niacin (Vitamin B3)

Cholesterol absorption inhibitor

Statins

273
Q

Identify which ANTIHYPERLIPIDEMICS is being described

  • reduces LDL cholesterol levels by binding with bile acids in the intestine
A

Bile Acid Sequestrants

274
Q

Examples of Bile Acid Sequestrants

A
  • Cholestyramine, Colestipol, Colesevelam HCl -effective against hyperlipidemia type II
  • Gemfibrozil – more effective at reducing triglyceride and VLDL levels than LDL; effective in hyperlipedemia type IV
275
Q

Identify which ANTIHYPERLIPIDEMICS is being described

  • Reduces VLDL and LDL
  • Very effective at lowering cholesterol levels
  • Only 20% of pts can initially tolerate niacin due to its numerous side effects and large doses required
A

Nicotinic acid or niacin (Vitamin B3)

276
Q

Identify which ANTIHYPERLIPIDEMICS is being described

  • Acts on the cells in the small intestine to inhibit cholesterol absorption
  • Decreases cholesterol from dietary absorption, reducing serum cholesterol, LDL, triglycerides, and apoB levels
  • Causes only a small increase in HDL
  • Must be combined with a statin for optimum effect
A

Cholesterol absorption inhibitor (Ezetimibe)

277
Q

Identify which ANTIHYPERLIPIDEMICS is being described

  • Inhibit HMG CoA reductase in cholesterol biosynthesis, thereby decreasing cholesterol, LDL, and slightly increases HDL
  • Reduction of LDL may be seen as early as 2 weeks after initiating therapy
  • Cholesterol and LDL levels return to pretreatment levels once therapy is withdrawn
278
Q

Examples of Statins

A

Atorvastatin, fluvastatin, lovastatin, pravastatin, simvastatin, rosuvastatin

279
Q

Identify which laboratory tests for ANTIHYPERLIPIDEMICS is being described

  • N: <0.175 mg/L
  • Produced in the liver in response to tissue injury or inflammation
  • Highly sensitive in detecting the inflammatory protein that can be associated with CV and peripheral vascular disease
  • Can detect an inflammatory process caused by the buildup of atherosclerotic plaque in the arteries
  • Ordered frequently along with cholesterol screening test
A

High-sensitivity C-reactive protein

280
Q

Identify which laboratory tests for ANTIHYPERLIPIDEMICS is being described

  • N: 4-17 mmol/L (fasting)
    by-product of protein
  • Found in eggs, chicken, beef, and cheddar cheese
  • High levels has been linked to CV disease, stroke, and the possibility of Alzheimer’s disease
  • May promote blood clotting
A

Homocysteine

281
Q

Identify which ANTIHYPERLIPIDEMICS has the SE and Adverse Reactions stated below

  • constipation and peptic ulcer; instruct pt to increase fluids and take foods high in fiber
A

Cholestyramine

282
Q

Identify which ANTIHYPERLIPIDEMICS has the SE and Adverse Reactions stated below

  • GI disturbances, skin flushing, abnormal liver function, hyperglycemia, hyperuricemia
A

Nicotinic acid

283
Q

Identify which ANTIHYPERLIPIDEMICS has the SE and Adverse Reactions stated below

  • dose-related increase in liver enzyme levels, rhabdomyolysis
284
Q

Nursing Interventions for ANTIHYPERLIPIDEMICS

  • Assess VS and baseline serum chemistry values
  • Obtain a medical history
  • Monitor blood lipid levels every 6-8 weeks for the first 6 months after statin therapy, then every 3-6 months
  • Monitor liver function tests
  • Observe for s/sx of GI upset
  • Instruct pt to have annual eye examination and report changes in visual acuity
A
  • Advise pt taking gemfibrozil that it may increase risk for bleeding when taking together with oral anticoagulant
  • Instruct pts with DM or those at risk to monitor blood glucose levels if they are taking gemfibrozil
  • Instruct pt to take nicotinic acid with meals
  • Teach pt to mix cholestyramine/colestipol powder well in water or juice
285
Q

They…

  • Increase blood flow to the extremities
  • Used in peripheral vascular disorders of venous and arterial vessels such as Raynaud’s disease
A

PERIPHERAL VASODILATORS

286
Q

characterized by numbness and coolness of extremities, intermittent claudication, and possible leg ulcers

A

Peripheral arterial disease

287
Q

Examples of PERIPHERAL VASODILATORS

A

Papaverine (direct-acting vasodilator), prazosin (alpha blocker), Nifedipine (calcium channel blocker), cilostazol

288
Q

Identify which Peripheral Vasodilators are being described

  • pts with PAD and hyperlipidemia may get improvement for intermittent claudication and decrease in serum lipids when this is administered
289
Q

Identify which Peripheral Vasodilators are being described

  • and ACEi; hypertensive pts with PAD receive improvement for both conditions when administered
290
Q

Identify which Peripheral Vasodilators are being described

  • an antiplatelet and vasodilator
A

Cilostazol

291
Q

Identify which Peripheral Vasodilators are being described

  • taken with an antiplatelet drug, is used to treat intermittent claudication; has an antioxidant effect
A

Gingko biloba

292
Q

Nursing Interventions for Cilostazol

A
  • Obtain baseline VS
  • Assess for signs of inadequate blood flow to the extremities
  • Inform pt that a desired therapeutic response may take 1.5-3mos
  • Advise pt not to smoke
  • Instruct pt to use aspirin or aspirin-like compounds with HCP’s approval
  • Encourage pt to change position slowly but frequently
  • Advise not to ingest alcohol with a vasodilator; may cause hypotension

Pharmacology (4 decks)

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