Drugs Acting on the Cardiovascular System Flashcards

(292 cards)

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
remnant of SVC, small and insignificant
Oblique vein
26
amount of blood ejected with each heartbeat
Stroke volume
27
amount of blood pumped by the ventricles per minute
Cardiac Output
28
degree of stretch of the cardiac muscle fibers at the end of diastole
Preload
29
ability of the cardiac muscle to shorten in response to an electric impulse
Contractility
30
the resistance to ejection of blood from the ventricle
Afterload
31
the percent of end-diastolic volume with each heartbeat
Ejection Fraction
32
Total blood collected in the ventricles at the end of diastole; determined by the length of diastole and venous pressure
End diastolic volume (EDV)
33
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
End systolic volume (ESV)
34
Average blood EDV
120 ml
35
Average blood ESV
50 ml
36
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
Frank-Starling Law of the Heart
37
increases heart rate (maintains stroke volume which leads to increased Cardiac Output)
Sympathetic – NOREPINEPHRINE (NE
38
decreases heart rate
Parasympathetic
39
parasympathetic inhibition of inherent rate of SA node, allowing normal HR
Vagal Tone
40
monitor changes in blood pressure and allow reflex activity with the autonomic nervous system
Baroreceptors, pressoreceptors
41
hormone released by adrenal medulla during stress; increases heart rate
Epinephrine
42
hormone released by thyroid; increases heart rate in large quantities; amplifies effect of epinephrine
Thyroxine
43
increased K+ level; KCI used to stop heart on lethal injection
Hyperkalemia
44
lower K+ levels; leads to abnormal heart rate rhythms
Hypokalemia
45
depresses heart function
Hypocalcemia
46
increases contraction phase
Hypercalcemia
47
HIGH Na+ concentration; can block Na+ transport and muscle contraction
Hypernatremia
48
Factors Affecting Heart Rate
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
49
Heart pumps deoxygenated blood from the R ventricle through the pulmonary artery to the lungs
Pulmonary Circulation
50
aka Peripheral Circulation Heart pumps blood from the left ventricle to the aorta and into the general circulation
Systemic Circulation
51
- 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
Digitalis
52
pathologic increase in stretching and thickening of ventricular walls allowing greater filling pressure associated with a weakened heart
Increased preload
53
additional pressure or force in the ventricular wall caused by excess resistance in the aorta
Increased afterload
54
Left-Sided Heart Failure Risk Factors
Mitral Valve Stenosis (RHD) – 90% Aging Myocardial Infarction Ischemic Heart Disease Hypertension Aortic Valve Stenosis
55
Right-Sided Heart Failure Risk Factors
Tricuspid Valve Stenosis COPD Pulmonary Embolism Pulmonic Stenosis Left sided heart failure
56
Identify What NYHA Class -No limitation of physical activity. Ordinary activities do not cause undue fatigue, palpitations, or dyspnea.
Class I
57
Identify What NYHA Class - Slight limitation of physical activity. Comfortable at rest, but ordinary activities cause fatigue, palpitations, or dyspnea.
Class II
58
Identify What NYHA Class - Marked limitation of physical activity. Comfortable at rest; less than ordinary activity causes fatigue, palpitations, or dyspnea.
Class III
59
Identify What NYHA Class - Symptoms occur at rest; any physical activity increases discomfort.
Class IV
60
They Inhibit Na-K pump which increase in intracellular sodium which results in the influx of calcium resulting to efficient contraction of heart muscle
CARDIAC GLYCOSIDES
61
3 effect of Digitalis on heart muscles
1. Positive inotropic action - ↑ myocardial contraction SV 2. Negative chronotropic action - ↓ heart rate 3. Negative dromotropic action - ↓ conduction of heart cells
62
Nonpharmacologic Measures to Treat Heart Failure
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
63
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)
Digoxin (Lanoxin)
64
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
Digoxin (Lanoxin)
65
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
Digoxin (Lanoxin)
66
What is the Therapeutic Serum level range of Digoxin (Lanoxin)
0.8-2ng/mL
67
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
Digitalis (Digoxin) Toxicity
68
It is the antidote for Digitalis (Digoxin) Toxicity binds with digoxin to form complex molecules that can be excreted in the urine
Digoxin immune Fab (ovine, Digibind)
69
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
Furosemide (Lasix), Hydroclorthiazide (Esidrix, Microzide)
70
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
Cortisone
71
Which drug has an interaction with Digoxine that matches the description below - Can decrease digitalis absorption if taken together - Doses should be staggered
Antacids
72
Prevents degradation of cAMP and cGMP, thus causing a positive inotropic effect and vasodilation resulting to increased stroke volume and cardiac output
Phosphodiesterase Inhibitors
73
What is the AE of Phosphodiesterase Inhibitors
severe cardiac dysrhythmia
74
enzyme that degrades cAMP and cGMP promoting smooth muscle and vessel contraction
Phosphodiesterase
75
It decreases venous blood return to the heart which causes decreased cardiac filling, ventricular stretching, and oxygen demand on the heart
Vasodilators
76
What are the 3 ways vasodilators act?
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
77
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
Angiotensin Converting Ezyme (ACE) Inhibitors
78
Enumerate at least 3 ACE inhibitors
Captopril Enalapril Lisinopril Perindopril
79
Given to patients who cannot tolerate ACEi
Angiotensin II receptor blockers (ARBs)
80
Enumerate at least 3 ARBs
Valsartan, Candesartan, Losartan
81
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
Spironolactone (Aldactone)
82
What is the recommended dose of Spironolactone (Aldactone)
12.5-25mg/day
83
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
Beta Blockers
84
Enumerate at least 3 Beta Blockers
Carvedilol, Metoprolol, Bisprolol
85
- An Atrial natriuretic peptide that inhibits ADH by increasing urine sodium loss - Promotes vasodilation, natriuresis, and diuresis - Useful in acute decompensated HF with dyspnea
Neseritide (Natrecor)
86
- A Combination of hydralazine (for blood pressure) and isosorbide dinitrate (dilator to relieve heart pain) - FDA approved for treating HF especially in African Americans
BiDil
87
- Used to treat angina pectoris - Increase blood flow by 1.) increasing O2 supply or 2.) decreasing O2 demand by the myocardium
ANTIANGINAL DRUGS
88
acute cardiac pain caused by inadequate blood flow to the myocardium due to plaque occlusions within or spasms of the coronary arteries
angina pectoris
89
tightness, pressure in the center of the chest, and pain radiating down the left arm; referred pain in the neck and left arm
Anginal pain
90
Name 3 types of Angina Pectoris
Classic (stable) Unstable (Preinfarction) Variant (Prinzmetal, vasospastic)
91
What type of Angina Pectoris - occurs with predictable stress or exertion
Classic (stable)
92
What type of Angina Pectoris - Occurs frequently with progressive severity unrelated to activity; unpredictable regarding stress/exertion and intensity - Often indicates and impending MI
Unstable (Preinfraction)
93
What type of Angina Pectoris occurs during rest
Variant (Prinzmetal, vasospastic)
94
Nonpharmacologic Measures to Control Angina : Enumerate at least 3
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
95
- Developed in 1840s - Cause generalized vascular and coronary vasodilation causing increased blood flow through the coronary arteries - Reduces myocardial ischemia but can cause hypotension
Nitrates/Nitroglycerin
96
2 Examples of Nitrates/Nitroglycerin
Isosorbide dinitrate (Isordil) Isosorbide mononitrate (Imdur)
97
- 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
Nitrates/Nitroglycerin
98
Pharmacokinetics SL – absorbed rapidly in the IJV and the right atrium 40-50% absorbed through the GI tract
Nitrates/Nitroglycerin
99
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
Nitrates/Nitroglycerin
100
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
Nitrates
101
most common SE of Nitrates
Headaches
102
Enumerate 3 examples of Beta Blockers
Metoprolol, Propranolol, Atenolol (“olols”)
103
This type of beta blocker - Decreases heart rate and cause bronchoconstriction - Pharmacodynamics *Onset: 30 mins *Peak: 1-1.5hrs *Duration: 4-12hrs
Nonselective beta blockers (block b1 and b2)
104
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
Selective (cardioselective) beta blockers ( block b1 only)
105
Identify Pharmacodynamics - Decrease the force of myocardial contractions causing decreased O2 demand by the myocardium
Beta Blockers
106
Beta Blockers: Side Effects and Adverse Reactions
Bradycardia, Hypotension Nonselective b-blockers – bronchospasm, behavioral or psychotic response, and impotence Dose should be tapered for 1-2 weeks
107
- 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
Beta Blockers
108
They - Block Ca2+ influx in the cell causing decreased cardiac contractility, thus decreasing cardiac O2 demand - Used in variant and classic angina
Calcium Channel Blockers
109
Pharmacokinetics - 80-90% absorbed through the GI - Highly protein bound - Half-life: 2-9hrs
Calcium Channel Blockers
110
Pharmacodynamics *Verapamil – bradycardia *Nifedipine – most potent; vasodilation  hypotension *Onset: verapamil – 10mins; nifedipine and diltiazem – 30min *Duration: verapamil – 3-7hrs; nifedipine and diltiazem – 6-8hrs
Calcium Channel Blockers
111
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
Calcium Channel Blockers (CCBs)
112
Nursing Interventions: Antianginals
- 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
113
Deviation from the normal rate or pattern of the heartbeat Causes: MI, hypoxia, hypercapnia, thyroid dse., CAD, cardiac surgery, excess catecholamines, electrolyte imbalance
Cardiac Dysrhythmias
114
Prevent proper filling of the ventricles and decrease CO by 33%
Atrial Dysrhythmia
115
- It is Life-threatening - Causes Ineffective filling and pumping of the ventricles  decreased or absent CO
Ventricular Dysrhythmia
116
- Primary pacemaker of the heart - At the junction of the SVC and the right atrium - Firing rate: 60 to 100 impulses/min
Sinoatrial Node
117
- 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
Atrioventricular Node (AV Node)
118
- Provides for ventricular conduction system - Fastest conduction among cardiac tissues Right and Left bundle
Bundle of His/Purkinje Fibers
119
3 physiologic characteristics of the nodal cell and Purkinje cell
Automaticity Excitability Conductivity
120
Identify which physiologic characteristics is being identified below - ability to initiate an electrical impulse
Automaticity
121
Identify which physiologic characteristics is being identified below - ability to respond to an electrical impulse
Excitability
122
Identify which physiologic characteristics is being identified below - ability to transmit an electrical impulse from one cell to another
Conductivity
123
The repeated cycle of depolarization and repolarization
Cardiac Action Potential
124
electrical activation of a cell caused by the influx of sodium into the cell while potassium exits the cell
Depolarization
125
return of the cell to the resting state caused by re-entry of potassium into the cell while sodium exits
Repolarization
126
What are the 5 phases of Cardiac Action
0. Cellular Depolarization Phase 1. Repolarization Phase 2. Plateau Phase 3. Repolarization Phase 4. Resting Phase
127
- 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
Lidocaine
128
- Decrease conduction velocity, automaticity, and recovery time - More frequently prescribed for dysrhythmias than sodium channel blockers - A class II
Beta Blockers
129
- 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
Amiodarone
130
- 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
Verapamil
131
2 examples of Class IV Calcium Channel Blockers
Verapamil, diltiazem
132
Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described - nausea, vomiting, diarrhea, confusion, hypotension, heart block, and neurologic and psychiatric symptoms
Quinidine
133
Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described - less cardiac depression than quinidine
Procainamide
134
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
Lidocaine
135
Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described - similar to lidocaine
Mexiletine and Tocainide
136
Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described - bradycardia and hypotension
Beta blockers
137
Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described - nausea, vomiting, hypotension, neurologic symptoms
Bretylium and Amiodiarone
138
Identify which Antidysrhythmic: Side Effects and Adverse Reactions is being described - nausea, vomiting, hypotension, and bradycardia
CCBs
139
Nursing Interventions: Antidysrhythmics Enumerate Nursing Interventions at least 3
- 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
What are the 2 main purposes of diuretics
1. Decrease hypertension 2. Decrease edema in heart failure and renal or liver disorders
141
This drugs mechanism of action is Inhibition of sodium and water reabsorption from the kidney tubules causing increased urine flow/diuresis
DIURETICS
142
What are the 5 Diuretic sites of action (M.A.L.T.S)
M-annitol A- cetazolamide L - oop diuretics T - hiazide diuretics S - pironolactone
143
Name 2 examples of THIAZIDES AND THIAZIDE-LIKE DIURETICS
Chlorothiazide Hydrochlorothiazide
144
- 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
Chlorothiazide Hydrochlorothiazide
145
Diuretics that should be used with caution in patients with diabetes
Chlorothiazide Hydrochlorothiazide
146
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
THIAZIDES AND THIAZIDE-LIKE DIURETICS
147
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
THIAZIDES AND THIAZIDE-LIKE DIURETICS
148
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
THIAZIDES AND THIAZIDE-LIKE DIURETICS
149
what are the contraindications of THIAZIDES AND THIAZIDE-LIKE DIURETICS
Renal failure – may cause oliguria, elevated BUN and serum creatinine
150
What is the THIAZIDES AND THIAZIDE-LIKE DIURETICS drug interaction with Digoxin
hypokalemia and hypocalcemia may enhance action of digoxin and can cause digitalis toxicity
151
Enumerate at least 3 Nursing Interventions for THIAZIDES AND THIAZIDE-LIKE DIURETICS
- 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
What are 3 examples of LOOP (HIGH CEILING) DIURETICS
Ethacrynic acid Furosemide (Lasix) Bumetamide
153
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
LOOP (HIGH CEILING) DIURETICS
154
LOOP (HIGH CEILING) DIURETICS Pharmacokinetics
- rapidly absorbed in the GI tract - highly protein-binding - Half-life: 30mins – 1.5hrs
155
LOOP (HIGH CEILING) DIURETICS Pharmacodynamics
- 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
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
LOOP (HIGH CEILING) DIURETICS
157
What is LOOP (HIGH CEILING) DIURETICS reaction with Digoxin
hypokalemia may cause toxicity, as with thiazides
158
Name at least 3 Nursing Interventions for LOOP (HIGH CELING) DIURETICS
- 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
Name 2 examples of Osmotic Diuretics
Mannitol, Urea
160
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
Mannitol Urea
161
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
OSMOTIC DIURETICS
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What is the Contraindications of Osmotic Diuretics
Given with extreme caution in patients who have heart disease and HF
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facilitates conversion between CO2 and H2O from carbonic acid (H2CO3) and its dissociative ions, HCO3 and H+
Carbonic anhydrase
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Name at least 3 examples of CARBONIC ANHYDRASE INHIBITORS
Acetazolamide, dichlorphenamide, ethoxzolamide, methazolamide
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- 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
CARBONIC ANHYDRASE INHIBITORS
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What Diuretic has SE and Adverse Reactions being described below - Fluid and electrolyte imbalance, metabolic acidosis. Nausea vomiting, anorexia, confusion, orthostatic hypotension
CARBONIC ANHYDRASE INHIBITORS
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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
POTASSIUM-SPARING DIURETICS
168
Enumerate 3 examples of POTASSIUM-SPARING DIURETICS
Spironolactone (Aldactone) amiloride triamterene eplerenone
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effective antihypertensive
Amiloride and eplerenone
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useful in edema caused by HF or liver cirrhosis
Triamterene
171
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
POTASSIUM-SPARING DIURETICS
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Enumerate at least 3 Nursing Interventions for POTASSIUM-SPARING DIURETICS
- 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
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2 types of Hypertension
Primary and Secondary Hypertension
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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
Primary (Essential) Hypertension
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Identify the type of Hypertension - 10% - Related to renal and endocrine disorders
Secondary Hypertension
176
Name 3 examples of Regulators of Blood Pressure
Kidneys Blood Vessels Other hormones
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Selected Regulators of Blood Pressure - Renin-Angiotensin-Aldosterone System
Kidneys
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Selected Regulators of Blood Pressure - Baroreceptors in the aorta and carotid sinus - Vasocenter in the medulla - Epinephrine and norepinephrine – vasoconstriction
Blood Vessels
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Selected Regulators of Blood Pressure - ADH, atrial natriuretic peptide, brain natriuretic peptide
Other hormones
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Name at least three NONPHARMACOLOGIC CONTROL OF HYPERTENSION
Stress-reduction techniques exercise salt restriction decrease alcohol ingestion smoking cessation
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- 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
Hydrochlorothiazide
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what are the 5 SYMPATHOLYTICS (SYMPATHETIC DEPRESSANTS)
1. beta-adrenergic blockers 2. Centrally-acting alpha2 agonists 3. Alpha-adrenergic blockers 4. Adrenergic neuron blockers 5. Alpha1 and beta2 adrenergic blockers
183
What are the effects of Alpha 1 and 2 receptors to Blood Vessels?
Constriction
184
What are the effects of Beta 2 receptors to Blood Vessels?
Dilation
185
What is the effect of Beta 1 receptors on the heart
Tachycardia; increased contractility
186
What is the effect of alpha 1 receptors on the heart
increased contractility
187
What are the effects of Beta 2 receptors to Bronchi?
Relaxation
188
What is the effect of alpha 2 receptors on thrombocytes
Aggregation
189
What are the effects of Alpha 1 and 2 receptors to Kidneys?
Vasoconstriction
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What are the effects of Beta 1 and 2 receptors to Kidneys?
Renin Release; inhibition tubular sodium reabsorption
191
What is the effect of alpha 2 receptors to Adipocytes
Inhibition lipolysis
192
What is the effect of Beta 1,2, and 3 receptors to Adipocytes
Lipolysis
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African-American pts DO NOT respond well to these drugs; can be combined with diuretics
Beta-Adrenergic Blockers
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- 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
Centrally-Acting Alpha2 Agonists
195
Examples of Centrally-Acting Alpha2 Agonists
Methyldopa, Clonidine, Guanfacine
196
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
Methyldopa
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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
Clonidine
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Identify which Centrally-Acting Alpha2 Agonists is being described - Similar to clonidine - Long half-life
Guanfacine
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Name 3 SE Centrally-Acting Alpha2 Agonists
- 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
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
Alpha-Adrenergic Blockers
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Examples of Alpha-Adrenergic Blockers
Prazosin terazosin doxazosin phentolamine phenoxybenzamine
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Identify which Alpha-Adrenergic Blockers is being described - Commonly prescribed - DO NOT take with alcohol or another antihypertensive
Prazosin
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Identify which Alpha-Adrenergic Blockers is being described - Longer half-lives - Given once at bedtime
Terazosin and doxazosin
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Identify which Alpha-Adrenergic Blockers is being described - Used for hypertensive crisis and severe hypertension from pheochromocytoma
Phentolamine and phenoxybenzamine
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Alpha-Adrenergic Blockers Pharmacokinetics
- absorbed through the GI - Large portion is Slost during hepatic first-pass metabolism - Should be administered 2x a day Highly protein-bound
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Alpha-Adrenergic Blockers Pharmacodynamics
- Dilation of arterioles and venules causing decreased peripheral resistance causing decreased BP - Onset: 30mins-2 hrs; duration; 10 hours
207
Alpha-Adrenergic Blockers SE
Prazosin, doxazosin, terazosin – orthostatic hypotension, nausea, headache, drowsiness, nasal congestions, edema, weight gain Phentolamine – hypotension, reflex tachycardia, nasal congestion, GI disturbance
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Alpha-Adrenergic Blockers Drug Interactions
Anti-inflammatory drugs – intensified peripheral edema - Nitroglycerin – syncope/ faintness
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Nursing Interventions Alpha-Adrenergic Blockers
- 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
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- 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
Adrenergic Neuron Blockers (Peripherally Acting Sympatholytics)
211
Example of Adrenergic Neuron Blockers (Peripherally Acting Sympatholytics)
Reserpine
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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
Alpha1- and Beta1-Adrenergic Blockers
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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
DIRECT-ACTING ARTERIOLAR VASODILATORS
214
Examples of DIRECT-ACTING ARTERIOLAR VASODILATORS
Hydralazine, minoxidil, nitropurusside
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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
ANGIOTENSIN-CONVERTING ENZYME INHIBITORS
216
Examples of ANGIOTENSIN-CONVERTING ENZYME INHIBITORS
Benazepril, captopril, enalapril, fosinopril, lisinopril, perindopril, quinapril, ramipril, trandolapril
217
Nursing Interventions for ANGIOTENSIN-CONVERTING ENZYME INHIBITORS
- 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
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
ANGIOTENSIN II RECEPTOR BLOCKERS
219
Examples of ANGIOTENSIN II RECEPTOR BLOCKERS
Losartan, Valsartan, Irbesartan, Candesartan, Eprosartan, Olmesartan, Telmisartan
220
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
DIRECT RENIN INHIBITOR
221
Examples of DIRECT RENIN INHIBITOR
Aliskiren (“ALIS Ka RENin”)
222
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
CALCIUM CHANNEL BLOCKERS
223
Examples of CALCIUM CHANNEL BLOCKERS
Amlodipine, Nifedipine, Verapamil, Diltiazem
224
Identify which CALCIUM CHANNEL BLOCKERS is being described below - used to treat chronic HPN, angina pectoris, and cardiac dysrhythmias
Verapamil
225
Identify which CALCIUM CHANNEL BLOCKERS is being described below - used to prevent ischemic brain injury due to vasospasms that often accompanies subarachnoid hemorrhage
Nimodipine
226
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)
Nifedipine
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formation of clot in an arterial or venous vessel caused by blood stasis, platelet aggregation, or blood coagulation
Thrombosis
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dislodged thrombus that move through the bloodstream
Embolus
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How clots form
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
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
ANTICOAGULANTS
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- 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
Heparin
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What is the antidote for Heparin
Protamine sulfate (1mg for every 100 units of heparin or LMWH given)
233
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
Low-Molecular-Weight Heparins
234
What are the contraindications for Low-Molecular-Weight Heparins
- Strokes, peptic ulcer, and blood anomalies - Eye, brain, or spinal surgery
235
They... - Directly inhibits thrombin from converting fibrinogen to fibrin - very expensive - Class II Prenteral Anticoagulants
Direct Thrombin Inhibitors
236
Examples of Direct Thrombin Inhibitors
Argatroban, Bivalirudin, Lepirudin, Dabigatran, Desirudin
237
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
Oral Anticoagulants
238
An Oral Anticoagulants used in rodenticides to kill rats causing hemorrhage
Warfarin (Coumadin)
239
The antidote for Oral Anticoagulants
Vitamin K
240
SE of Oral Anticoagulants
Bleeding
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Drug Interactions of Oral Anticoagulants
Aspirin, NSAIDs, sulfonamides, phenytoin, cimetidine, allopurinol, and oral hypoglycemic drugs - increase action
242
- 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
Vitamin K (Phytonadione)
243
Nursing Interventions for Warfarin and Heparin
- 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
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)
ANTIPLATELET DRUGS
245
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
Aspirin
246
Identify which ANTIPLATELET DRUGS is being described - frequently used after MI or stroke to prevent a second event
Clopidogrel
247
Identify which ANTIPLATELET DRUGS is being described - Inhibits platelet aggregation and a vasodilator - Used for intermittent claudication
Cilostazol
248
Identify which ANTIPLATELET DRUGS is being described - Taken in conjunction with aspirin 75-100mg in a maintenance regimen
Ticagrelor
249
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
Intermittent Claudication
250
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
THROMBOLYTICS
251
Examples of THROMBOLYTICS
Urokinase, streptokinase, alteplase tPA, reteplase rPA, tenecteplase
252
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)
Alteplase
253
What is the SE and AE of THROMBOLYTICS
Anaphylaxis – more common in streptokinase Hemorrhage – major complication
254
What is the antidote for Thrombolytics
Aminocaproic acid (Amicar) - antithrombolytic
255
Nursing Interventions for THROMBOLYTICS
- 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
excess of one or more lipids in the blood
Hyperlipidemia or hyperlipoproteinemia
257
- “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
High-density lipoprotein (HDL)
258
- “bad” lipoprotein - Contains 50-60% cholesterol in the bloodstream - Elevated LDL = greater risk for developing atherosclerotic plaques and heart disease
Low-density lipoprotein (HDL)
259
Carries mostly triglycerides and less cholesterol
Very low-density lipoprotein
260
Large particles that transport fatty acids and cholesterol to the liver
Chylomicrons
261
Identify at least 3 Nonpharmacologic Methods for Cholesterol Reduction
- 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
What are the 3 types of fats
Trans Fat Saturated Fat Unsaturated Fat
263
Identify which type of fat - Hydrogenated vegetable oils - fast foods - cakes and pastries - Chocolate - Deep Fried Food
Trans Fats
264
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
Saturated Fats
265
Identify which type of fat - Polyunsaturated Fats *Corn oil *Soybean oil *Sunflower oil *Seeds *Cold water fish
Unsaturated Fats
266
Identify which type of Lipids is being described - Increased chylomicrons and increased triglycerides - uncommon
Type I
267
Identify which type of Lipids is being described - Increased Low density lipoprotein and increased cholesterol - Common
Type IIA
268
Identify which type of Lipids is being described - increased very low density lipoprotein, increased Low density Lipoprotein, increased cholesterol and triglycerides - very common
Type IIB
269
Identify which type of Lipids is being described - Moderately increased cholesterol and triglycerides - Uncommon
Type III
270
Identify which type of Lipids is being described - Increased very low density lipoprotein and markedly increased triglycerides - very common
Type IV
271
Identify which type of Lipids is being described - Increased chylomicrons, VLDL, and Triglycerides - uncommon
Type V
272
Enumerate at least 3 ANTIHYPERLIPIDEMICS
Bile Acid Sequestrants Nicotinic acid or niacin (Vitamin B3) Cholesterol absorption inhibitor Statins
273
Identify which ANTIHYPERLIPIDEMICS is being described - reduces LDL cholesterol levels by binding with bile acids in the intestine
Bile Acid Sequestrants
274
Examples of Bile Acid Sequestrants
- 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
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
Nicotinic acid or niacin (Vitamin B3)
276
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
Cholesterol absorption inhibitor (Ezetimibe)
277
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
Statins
278
Examples of Statins
Atorvastatin, fluvastatin, lovastatin, pravastatin, simvastatin, rosuvastatin
279
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
High-sensitivity C-reactive protein
280
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
Homocysteine
281
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
Cholestyramine
282
Identify which ANTIHYPERLIPIDEMICS has the SE and Adverse Reactions stated below - GI disturbances, skin flushing, abnormal liver function, hyperglycemia, hyperuricemia
Nicotinic acid
283
Identify which ANTIHYPERLIPIDEMICS has the SE and Adverse Reactions stated below - dose-related increase in liver enzyme levels, rhabdomyolysis
Statins
284
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
- 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
They... - Increase blood flow to the extremities - Used in peripheral vascular disorders of venous and arterial vessels such as Raynaud’s disease
PERIPHERAL VASODILATORS
286
characterized by numbness and coolness of extremities, intermittent claudication, and possible leg ulcers
Peripheral arterial disease
287
Examples of PERIPHERAL VASODILATORS
Papaverine (direct-acting vasodilator), prazosin (alpha blocker), Nifedipine (calcium channel blocker), cilostazol
288
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
Statins
289
Identify which Peripheral Vasodilators are being described - and ACEi; hypertensive pts with PAD receive improvement for both conditions when administered
Ramipril
290
Identify which Peripheral Vasodilators are being described - an antiplatelet and vasodilator
Cilostazol
291
Identify which Peripheral Vasodilators are being described - taken with an antiplatelet drug, is used to treat intermittent claudication; has an antioxidant effect
Gingko biloba
292
Nursing Interventions for Cilostazol
- 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