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NUR311 > Exam III > Flashcards

Exam III Flashcards

1
Q

What type of angina is caused by coronary spasm?

A

Variant

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2
Q

What kind of angina does not respond to beta-blockers?

A

Variant

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3
Q

Nitrates predominately vasodilate which vessels in low doses? Prevent spasm where?

A

Veins. Coronary arteries.

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4
Q

Headaches due to nitrates can be expected to do what over time?

A

Diminish

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5
Q

What adverse effect is triggered by baroreceptors in response to venous dilation?

A

Reflex tachycardia

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6
Q

What drugs are contraindicated in men who are taking nitrates?

A

Phosphodiesterase type 5 inhibitors

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7
Q

Which nitrate formulation is recommended for intermittent angina treatment at home?

A

SL nitroglycerin

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8
Q

How are SL nitroglycerin tablets taken?

A

1 Tablet (0.3-0.6 mg) every 5 minutes x 3, Emergency department if angina persists 5 min

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9
Q

What must the nurse check before administering nitroglycerin?

A

Blood pressure and pulse

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10
Q

Why should nitroglycerin paste be removed at night?

A

Prevent tachyphylaxis (tolerance)

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11
Q

How would a dry mouth affect the absorption of nitroglycerin?

A

Slows absorption

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12
Q

Nitrates in low doses decrease afterload or preload? Arterioles or veins?

A

Preload. Veins.

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13
Q

Selective beta-blockers block which receptors at low doses?

A

Beta-1

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14
Q

Beta-blockers decrease three parameters. What are they?

A

Heart rate, blood pressure, contractility

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15
Q

What may beta-blockers mask in diabetes and during allergy shots?

A

Signs of hypoglycemia and allergic reactions.

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16
Q

Which drug given for allergic reactions may be inhibited by beta-blockers?

A

Epinephrine

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17
Q

In asthmatics, beta-blockers may cause what symptom? Block what receptor?

A

Bronchoconstriction. Beta-2.

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18
Q

Beta-blockers with verapamil or diltiazem can severely decrease which vital sign parameter?

A

Heart rate

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19
Q

Abrupt cessation of beta-blockers can lead to excitation or depression of the beta-adrenergic receptors?

A

Excitation

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20
Q

Do not give beta-blockers if the pulse is below ____ or the systolic BP is below____.

A

Pulse 50, SBP 90

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21
Q

What is the family of calcium-channel blockers which does not include verapamil or diltiazem?

A

Dihydropyridines

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22
Q

Calcium-channel blockers vasodilate which blood vessels?

A

Arterioles

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23
Q

Calcium-channel blockers decrease afterload or preload?

A

Afterload

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24
Q

Dihydropyridines may cause what side effect which can be treated with beta-blockers?

A

Reflex tachycardia

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25
Q

Swelling of extremities may be caused by what 2 classes of antihypertensive agents?

A

Nitrates & calcium-channel blockers

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26
Q

Calcium-channel blockers are used for what kinds of angina?

A

Stable and variant

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27
Q

Vasodilation of arteries reduces afterload or preload?

A

Afterload

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28
Q

How does ranolazine (Ranexa) work?

A

The drug decreases sodium and calcium in the myocardial cells, which allows the cells to use energy more efficiently.

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29
Q

How does ranolazine (Ranexa) cause torsades de pointes?

A

The drug prolongs the QT interval.

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30
Q

Digoxin (Lanoxin) is used in heart failure primarily for what effect?

A

Positive inotropic effect

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31
Q

What should the nurse do before giving digoxin?

A

Take the apical pulse for 1 minute.

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32
Q

What electrolyte competes with digoxin for the receptor?

A

Potassium

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33
Q

What are some signs of digitalis toxicity?

A

Anorexia, nausea, vomiting, arrhythmias, weakness, yellow vision, halos around lights, blurred vision

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34
Q

What is the antidote for digoxin toxicity?

A

Digibind

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35
Q

What common drug classes can precipitate digoxin toxicity?

A

Loop and thiazide diuretics

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36
Q

What are the effects of alpha-1 activation by catecholamines?

A

Vasoconstriction of arterioles in skin, viscera, & mucous membranes and in veins.

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37
Q

What are the effects of beta-1 activation by catecholamines?

A

Increased heart rate, contractility, and conduction rate. Renin release.

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38
Q

What are the effects of beta-2 activation in the lungs and liver?

A

Bronchodilation & glycogenolysis.

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39
Q

What are the renal effects of dopamine activation?

A

Renal blood vessel dilation.

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40
Q

Which IV continuous drug is used to increase contractility without causing vasoconstriction?

A

Dobutamine (Dobutrex).

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41
Q

Common drug ending -olol

A

Beta-adrenergic blocker (ex: Metoprolol)

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42
Q

Common drug ending -dipine

A

Calcium channel blocker (ex: Amlodipine)

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43
Q

Common drug ending -zosin

A

Alpha-adrenergic blocker (ex: Prazosin)

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44
Q

Common drug ending -pril

A

Angiotensin-converting enzyme (ACE) inhibitor (ex: Lisinopril)

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45
Q

Common drug ending -sartan

A

Angiotensin-receptor blocker (ex: Losartan, Candesartan)

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46
Q

Common drug ending -statin

A

HMG-CoA reductase inhibitor (ex: Atorvastatin)

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47
Q

Common drug ending -ase, -plase

A

Thrombolytic (ex: Alteplase)

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48
Q

Common drug ending -parin

A

Anticoagulant (ex: Enoxaparin)

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49
Q

Common drug ending -xaban

A

Direct Factor Xa Inhibitor (ex: Rivaroxaban)

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50
Q

What should the nurse check before administering antihypertensives?

A

Blood pressure and pulse

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51
Q

Antihypertensive agents should be given for what period of time?

A

Lifelong

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52
Q

What is the systolic blood pressure range for prehypertension?

A

120-139

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53
Q

What side effect may occur with the coadministration of an antihypertensive drug with another antihypertensive drug or diuretic?

A

Hypotension

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54
Q

Which drug classification is the first-line therapy for hypertension?

A

Thiazides.

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55
Q

How do thiazide diuretics affect blood vessels?

A

Arteriole dilation.

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56
Q

What are three effects of beta-blockers on the heart?

A

Decreased heart rate, AV block, decreased contractility

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57
Q

Name two ways beta-blockers affect diabetic patients.

A

Block glycogenolysis. Mask symptoms of hypoglycemia.

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58
Q

What hormone do beta1-blockers block?

A

Renin

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59
Q

Alpha1-blockers cause what? What disease may they be used for and why? Why are they seldom used?

A

Vasodilation of arterioles and veins. Benign prostatic hypertrophy, because it relaxes the smooth muscle of the prostatic capsule and bladder neck. Increased number of CV events.

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60
Q

By what mechanism do alpha2-agonists decrease blood pressure? What side effects disappear over time?

A

Decrease sympathetic outflow from brainstem and decrease norepinephrine release. Dry mouth and sedation.

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61
Q

Which alpha2-agonist is commonly-used for hypertension that starts during pregnancy?

A

Methyldopa (Aldomet).

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62
Q

Direct-acting vasodilators may cause what two important adverse effects? What drug category is used to prevent this?

A

Reflex tachycardia and renin release. Treat with beta-blockers.

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63
Q

Which calcium channel blockers should not be given with beta-blockers? Why?

A

Diltiazem and verapamil. Suppresses heart function in persons with heart disease.

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64
Q

How does grapefruit juice affect calcium channel blocker serum levels? What are the effects?

A

Raise calcium channel blocker serum levels. Raise heart rates in dihydropyridines and decrease heart rates with verapamil or diltiazem.

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65
Q

Direct renin inhibitors prevent what? Why is it used?

A

Renin from binding with the receptor. Hypertension.

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66
Q

What is a common electrolyte disturbance caused by ACEIs?

A

Hyperkalemia

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67
Q

The patient on an ACEI asks you whether he should use salt or salt substitute. What do you say?

A

Check to make sure that the salt substitute does not have potassium, which may increase potassium levels to an unsafe level.

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68
Q

ACEIs cause vasodilation of which blood vessels? Which vasodilates the most?

A

Arterioles and veins. Arterioles.

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69
Q

RAAS drugs are the only hypertensive drugs contraindicated for what?

A

Pregnancy

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70
Q

Why would a patient be encouraged to lie down prior to the first dose of an ACEI?

A

First dose hypotension

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71
Q

What category of diuretics should a person on ACEIs avoid?

A

Potassium-sparing diuretics

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72
Q

What side effect of ACE inhibitors commonly leads to the discontinuation of these drugs?

A

Persistent, nonproductive cough

73
Q

How do ARBs work?

A

Block angiotensin II receptors.

74
Q

What are the adverse effects of angiotensin II receptor blockers (ARBs)?

A

Hypotension, fatigue, headache, dizziness, diarrhea, rare angioedema.

75
Q

How does spironolactone (Aldactone) work?

A

Blocks aldosterone receptors

76
Q

Spironolactone (Aldactone) may cause gynecomastia by interfering with what?

A

Steroid hormones like progesterone, androgens, corticosteroids

77
Q

Spironolactone (Aldactone) may cause what electrolyte disturbance?

A

Hyperkalemia

78
Q

How does blocking aldosterone affect the sodium stores of the body? How might this influence lithium?

A

Promotes sodium loss which lowers body sodium stores. Prevents excretion of lithium.

79
Q

Sodium nitroprusside (Nitropress) vasodilates which blood vessels?

A

Arterioles and veins

80
Q

Why is nitroprusside (Nitropress) used?

A

Emergency treatment of severely elevated blood pressure

81
Q

What blood levels are monitored with sodium nitroprusside (Nitropress) use?

A

Thiocyanate levels

82
Q

When should diuretics be taken?

A

In the morning if daily, morning and 2 pm if bid

83
Q

Where does the most reabsorption take place?

A

Proximal convoluted tubule

84
Q

Where is 20% of the sodium reabsorbed?

A

Ascending loop of Henle

85
Q

Which diuretics have the greatest potential for diuresis? Why?

A

Osmotic diuretics followed by loop diuretics.

They block sodium reabsorption at sites where more sodium is normally reabsorbed.

86
Q

Large dose of loop diuretics may adversely affect what organ?

A

Ear, ototoxicity

87
Q

What permanent adverse effect may occur with ethacrynic acid (Edecrin)?

A

Ototoxicity

88
Q

What change in calcium may occur with loop diuretics?

A

Hypocalcemia

89
Q

What class of diuretics does not cause calcium loss?

A

Thiazides

90
Q

What change in blood sugar may be seen with loop diuretics?

A

Hyperglycemia

91
Q

Thiazide diuretics are contraindicated with an allergy to what?

A

Sulfonamides

92
Q

When might thiazide diuretics be ineffective?

A

When the glomerular filtration rate (GFR) is below 15-20 mL/min

93
Q

What are some signs of electrolyte imbalance?

A

Muscle weakness, twitching, nausea and vomiting, dysrhythmias, dry mouth and thirst, confusion, etc.

94
Q

Loop diuretics decrease which electrolytes?

A

K+, Na+, Cl-, Ca2+, Mg2+

95
Q

The coadministration of digoxin (Lanoxin) and diuretics may precipitate what condition?

A

Digoxin toxicity with dysrhythmias.

96
Q

Potassium-sparing diuretics should not be used with which three antihypertensive drug categories that may raise potassium levels? Name two common potassium-sparing diuretics.

A

ACE inhibitors, Angiotensin II receptor blockers, direct renin inhibitors.
Spironolactone (Aldactone) and triamterene (Dyrenium)

97
Q

Diuretics and antihypertensive drugs can cause what adverse effect?

A

Additive hypotension

98
Q

Why are osmotic diuretics used in renal failure?

A

To maintain urine flow through the tubule.

99
Q

Why are osmotic diuretics used for cerebral edema?

A

Used to reduce intracranial pressure

100
Q

What is added to deter patients from taking diphenoxylate (Lomotil) for analgesic effects?

A

Atropine, causes dry mouth and tachycardia.

101
Q

Name 2 contraindications for Diphenoxylate (Lomotil)?

A

Infectious diarrheas and pseudomembranous colitis.

102
Q

What are the mechanisms of action for bulk-laxatives?

A

Form nondigestible gel that expands with bacterial action. The enlarged fecal size triggers peristalsis.

103
Q

List contraindications for laxatives. Why?

A

Abdominal pain, nausea, cramps, appendicitis, bowel obstruction, diverticulitis, ulcerative colitis, enteritis.
Worry about bowel perforation.

104
Q

Why must a bulk laxative be administered with a full glass of fluids?

A

To prevent bowel obstructions.

105
Q

What are the mechanisms of action for surfactant laxatives?

A

Decrease surface tension allowing water to penetrate stool, inhibit fluid absorption in gut, and increase water and electrolyte secretion into gut.

106
Q

What is the difference between Docusate sodium (Colace) and Peri-Colace?

A

Peri-Colace includes a stimulant laxative, sennosides.

107
Q

What are the mechanisms of action for stimulant laxatives?

A

Increase peristalsis, inhibit fluid reabsorption in gut, and increase water and electrolyte secretion in gut.

108
Q

What food substance and drug category may not be taken within 1 hour of bisacodyl (Dulcolax), a stimulant laxative? Why?

A

Milk and antacids. They dissolve the enteric coating meant to protect the stomach from the drug.

109
Q

What harmless urinary side effect is caused by senna, a stimulant laxative?

A

Yellowish-brown or pinkish urine.

110
Q

What are the mechanisms of action for saline laxatives?

A

Attracts water that stretches the gut and causes peristalsis.

111
Q

What is a non-GI contraindication to magnesium hydroxide? Why?

A

Renal disease. Magnesium accumulates and causes CNC toxicity.

112
Q

What are the mechanisms of action for lactulose?

A

The disaccharide is metabolized into acid by gut bacteria. The acids cause an osmotic action.

113
Q

Name a non-GI use for lactulose?

A

High ammonium blood levels.

114
Q

What are the mechanisms of action for glycerin suppositories? Where do they work?

A

Softens and lubricates stool. Stimulates rectal contraction. Rectum.

115
Q

What is the most important indication of constipation?

A

Hard, pellet-like feces.

116
Q

What is a possible effect of laxatives during pregnancy?

A

Initiation of labor.

117
Q

Discuss the use of laxatives during lactation.

A

The drug may be found in breast milk.

118
Q

What are the indications for lubiprostone?

A

Idiopathic constipation, irritable bowel syndrome in women older than 18, and opioid induced constipation

119
Q

How often should adults be screened for high cholesterol?

A

Every 5 years

120
Q

Cholesterol is mainly produced when?

A

At night

121
Q

Which lipoproteins are the “bad” lipoproteins?

A

LDL

122
Q

The triglycerides are carried by which lipoproteins?

A

VLDL

123
Q

Carbohydrates should be restricted to 50-60% of the caloric intake because they can form what?

A

Triglycerides

124
Q

Saturated fats should be what percent of the caloric intake?

A

< 7%

125
Q

How do HMG-CoA Reductase Inhibitors work?

A

Reduce synthesis of cholesterol by inhibiting the enzyme. And increasing the number of LDL receptors in the liver.

126
Q

When should statins be taken?

A

In the evening

127
Q

What are two severe adverse effects of statins?

A

Hepatoxicity and myopathy

128
Q

What are two contraindications for statins?

A

Liver disease and pregnancy

129
Q

How do bile-acid sequestrants lower cholesterol?

A

They inhibit reabsorption of bile and cause the liver to use LDLs in the blood to make more bile. The liver increases the number of LDL receptors in the liver.

130
Q

What deficiencies can be caused by bile-acid sequestrants?

A

Vitamin A, D, E, K

131
Q

A patient must wait how long after the administration of a bile-acid sequestrant before taking another medication?

A

4 hours

132
Q

Bile-acid sequestrants are taken to lower what?

A

LDL

133
Q

Fibrates (or fibric acid derivatives) are the most effective drug for lowering what?

A

Triglycerides

134
Q

Fibrates can cause what gastrointestinal dysfunction?

A

Gallstones, nausea, diarrhea, and abdominal pain

135
Q

What major risk increases when fibrates are coadministered with statins?

A

Risk of myopathy. (Also liver injury and kidney disease)

136
Q

Do fibrates increase or decrease the effect of warfarin?

A

Increase by displacing warfarin from the albumin.

137
Q

How does ezetimibe (Zetia) work?

A

Blocks reabsorption of dietary and biliary cholesterol

138
Q

What are the side effects of ezetimibe (Zetia)?

A

Myopathy, rhabdomyolysis, pancreatitis, hepatitis, thrombocytopenia.

139
Q

Lovaza is used to decrease which lipid?

A

Triglycerides.

140
Q

What are the two stages of hemostasis?

A

Formation of platelet plug, reinforcement of platelet plug with fibrin (coagulation).

141
Q

How does heparin work as an anticoagulant?

A

Assists antithrombin in inactivating thrombin & factor Xa

142
Q

How does warfarin work as an anticoagulant?

A

Decreases synthesis of clotting factors dependent on vitamin K

143
Q

How do thrombolytic drugs work?

A

Promote conversion of plasminogen to plasmin

144
Q

Arterial thrombi cause what kind of injury?

A

Local injury

145
Q

Venous thrombi cause what type of injury

A

Distal injury

146
Q

Name the three categories of drugs for thromboembolic disorders? Where in the vascular system do they work?

A

Anticoagulants - veins
Antiplatelet agents - arteries
Thrombolytics – veins or arteries

147
Q

What factors does heparin deactivate? What does this prevent?

A

Assists antithrombin in deactivating thrombin & factor Xa to prevent more venous thrombi.

148
Q

What factor do low molecular weight anticoagulants deactivate?

A

Factor Xa

149
Q

Which anticoagulant can be given during pregnancy?

A

Heparin

150
Q

What is the antidote for heparin?

A

Protamine sulfate

151
Q

Which lab is used to monitor heparin? What is the recommended range?

A

aPTT 1.5-2X the control

152
Q

What potentially-fatal disorder occurs with heparin?

A

Heparin induced thrombocytopenia (HIT)

153
Q

List contraindications to heparin.

A

Thrombocytopenia; uncontrollable bleeding; surgery of eye, brain, or spinal cord; lumbar puncture or regional anesthesia

154
Q

List signs and symptoms indicative of bleeding?

A

Decreased BP, increased HR, gum bleeding, bruises, petechiae, hematomas, red or black/tarry stools, discolored/cloudy urine, pelvic pain from ovaries, headache or faintness, lumbar pain from adrenal gland

155
Q

Discuss the proper administration of heparin SubQ.

A

Lower abdomen, rotate sites; no rubbing; no aspiration; 2” from umbilicus; 25-26 gauges, 1/2 to 5/8 needle; gentle, firm pressure for 1-2 min after.

156
Q

List drugs which may increase bleeding with heparin.

A

ASA, antiplatelet drugs, NSAIDS, glucocorticoids

157
Q

What is the antidote for low molecular weight anticoagulants?

A

Protamine sulfate

158
Q

How does warfarin work?

A

Interferes with synthesis of Vitamin K-dependent clotting factors

159
Q

Where in the vascular system does warfarin work?

A

Veins

160
Q

How is warfarin distributed? Can it enter the placenta or breast milk?

A

Highly-protein bound, crosses placenta and enters breast milk

161
Q

What lab is used to monitor warfarin therapy? What is the suggested range?

A

PT & INR; INR 2-3 (3-4.5 if mechanical heart valve)

162
Q

Which anticoagulant is Pregnancy Category X?

A

Warfarin (Coumadin)

163
Q

What is the antidote for warfarin?

A

Vitamin K (phytonadione), fresh frozen plasma (FFP)

164
Q

List contraindications to warfarin.

A

Active bleeding; severe thrombocytopenia; decreased synthesis of vitamin K (alcoholism, Vitamin K deficiency, liver disease); surgery of eye, brain, & spinal cord; lumbar puncture or regional anesthesia; pregnancy & lactation

165
Q

What would you tell a patient on warfarin who wants to take Tylenol?

A

Need to monitor INR - 4 325 mg tablets a day for one week can increase risk of elevated INR by 10X (May need to lower warfarin dose)

166
Q

What two drugs increase the synthesis of Vitamin K-dependent clotting factors?

A

Vitamin K, oral contraceptives

167
Q

What foods are high in vitamin K?

A

Spinach, kale, lettuce, turnips, greens, cabbage, watercress, peas, asparagus, broccoli, oats, whole wheat, green tea, mayonnaise, canola oil, soybean oil.

168
Q

How does dabigatran (Pradaxa) work?

A

Directly binds thrombin, which prevents fibrin formation and activation of factor VIII.

169
Q

What are the advantages of dabigatran (Pradaxa) over warfarin? Disadvantages?

A

Less bleeding, faster onset, no blood work, fewer food interactions, fixed dosing, reversal agent Praxibind. GI distress, less experience, BID dosing, must give on time.

170
Q

How does rivaroxaban (Xarelto) work?

A

Directly inhibits Factor Xa in clots and serum and inhibits prothrombinase, which prevents fibrin formation.

171
Q

How does apixaban (Eliquis) work? What is the approved use?

A

Directly inhibits Factor Xa in clots and serum and inhibits prothrombinase, which prevents fibrin formation.
Prevention of stroke and systemic embolization in nonvalvular atrial fibrillation.

172
Q

In what part of the vascular system do antiplatelet agents work?

A

Arteries

173
Q

List three classes of antiplatelet agents.

A

ASA, P2Y12ADP receptor antagonists, glycoprotein IIb/IIIa receptor antagonists

174
Q

How does aspirin work? How long are platelets affected? How many days before surgery should aspirin be stopped?

A

Inhibits COX-1, decreasing platelet aggregation, and inhibits COX-2, decreasing vasoconstriction. 7-10 days. 7 days.g

175
Q

How do ADP receptor antagonists work? How long are platelets affected?

A

Block ADP receptors and prevents platelet aggregation (clopidogrel- Plavix). 7-10 days, take off 5days prior to surgery.

176
Q

What is a significant adverse blood dyscrasia that may be caused by the ADP receptor antagonist, clopidogrel (Plavix)? What drugs may prevent its action?

A

Thrombotic thrombocytopenia purpura (TTP). Proton inhibitors may inhibit CYP2C19, which activates clopidogrel (Plavix).

177
Q

How do GP IIb/IIIa receptor antagonists work? Size of effect?

A

Blocks GP IIb/IIIa receptors & prevents fibrinogen bridges. Large effect, because final step in platelet aggregation.

178
Q

What is the major adverse effect of thrombolytic therapy?

A

Serious bleeding.

179
Q

Which thrombolytic drug is administered as a single IV bolus?

A

Tenectaplase (TKNase)

NUR311 (7 decks)

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