Exam 4 (Week 13) Flashcards

(68 cards)

1
Q

What is the pharmacological class of Nifedipine (procardia)?

A

Calcium channel blocker: dihydropyridine

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2
Q

What is therapeutic class of Nifedipine (procardia)?

A

antianginal/antihypertensive

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3
Q

MOA of Nifedipine (procardia):

A

blocking calcium channels in vascular smooth muscle

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4
Q

MOA of Nifedipine (procardia) - direct hemodynamic effects:

A

Direct hemodynamic effects:

  1. vasodilation of peripheral arterioles
  2. lowering of arterial pressure
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5
Q

MOA of Nifedipine (procardia) - indirect hemodynamic effects:

A

because it lowers bp…

1. activation of baro reflex which causes sympathetic stimulation of heart

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6
Q

MOA of Nifedipine (procardia) - net effects

A
  1. vasodilation

2. reflex cardiac stimulation

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7
Q

What does reflex cardiac stimulation do with Nifedipine (procardia)?

A
  1. lowers bp
  2. increases heart rate
  3. increases contractile force
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8
Q

Uses of Nifedipine (procardia):

A
  1. angina pectoris

2. hypertension

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9
Q

ADE of Nifedipine (procardia):

A
  1. flushing
  2. dizziness
  3. headache
  4. peripheral edema
  5. gingival hyperplasia
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10
Q

What does Nifedipine (procardia) pose a risk for in older adults?

A

chronic exemetous rash

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11
Q

1 nursing implication Nifedipine (procardia):

A

signs of edema

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12
Q

Pharmacological class of Verapamil (Calan):

A

Calcium channel blocker: phenylakylamine

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13
Q

Therapeutic class of Verapamil (Calan):

A

Antianginal/antihypertensive/antidysrhythmic

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14
Q

MOA of Verapamil (Calan):

A

acts by blocking calcium channels in blood vessels and in the heart.

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15
Q

4 direct hemodynamic effects MOA of Verapamil (Calan):

A
  1. blockade at peripheral arterioles causing dilation
  2. blockade at arteries and arterioles of the heart
  3. blockade at the SA and AV nodes of the heart
  4. blockade in the myocardium
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16
Q

indirect hemodynamic MOA of Verapamil (Calan):

A

indirectly activates the baroreceptor reflex causing increase firing of sympathetic nerves to the heart

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17
Q

Net hemodynamic MOA of Verapamil (Calan):

A
  1. vasodilation
  2. reduced arteriole pressure
  3. increased coronary perfusion
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18
Q

3 uses of Verapamil (Calan):

A
  1. angina pectoris
  2. essential hypertension
  3. cardiac dysrhythmias
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19
Q

7 ADE of Verapamil (Calan):

A
  1. constipation
  2. dizziness
  3. facial flushing
  4. headache
  5. edema of ankles and feet
  6. gingival hyperplasia
  7. heart block
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20
Q

1 nursing implication of Verapamil (Calan):

A

educating the patient that constipation can be minimized by increasing fluid and fiber.

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21
Q

Pharmacological class of Hydralazine (Apresoline):

A

Vasodilator: selective dilation of arterioles

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22
Q

Therapeutic class of Hydralazine (Apresoline):

A

Antihypertensive/Heart failure

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23
Q

MOA of Hydralazine (Apresoline):

A

direct action on vascular smooth muscle causing selective dilation of arterioles

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24
Q

Uses of Hydralazine (Apresoline):

A
  1. management of essential hypertension
  2. hypertensive crisis
  3. heart failure
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25
3 ADE of Hydralazine (Apresoline):
1. reflex tachycardia 2. increased blood volume 3. acute rheumatoid syndrome that closely resembles SLE (systemic lupus eryth.)
26
1 nursing implication of Hydralazine (Apresoline):
prevent falls
27
Pharmacological class of Minoxidil (Loniten):
Vasodilator: selective dilation of arterioles
28
Therapeutic class of Minoxidil (Loniten):
Antihypertensive: Severe hypertension
29
MOA of Minoxidil (Loniten):
selective dilation of arterioles
30
What is unique about Minoxidil (Loniten)?
more intense vasodilation than hydrazine but also causes more severe adverse reactions
31
Pharmacological class of sodium nitroprusside (nitropress)
Vasodilator: dilation of veins and arterioles
32
Therapeutic class of sodium nitroprusside (nitropress)
Antihypertensive: Hypertensive emergencies
33
Is nitroprusside (nitropress) potent or not?
potent
34
true or false: sodium nitroprusside (nitropress) is slower than any vasodilator
faster than any other vasodilator
35
What does nitroprusside (nitropress) cause?
venous and arteriolar dilation
36
Pharmacological class of Lovastatin (altoprev)
HMG-CoA reductase inhibitor
37
Therapeutic class of Lovastatin (altoprev)
Antihypercholesterolemia
38
MOA of lovastatin (altoprev):
by inhibiting hepatic HMG-CoA reductase
39
What is HMG-CoA reductase with Lovastatin (altoprev)?
rate limiting enzyme in cholesterol synthesis
40
What does MOA of Lovastatin (altoprev) depend on?
depends on increasing the number of LDL receptors on hepatocytes or liver cells
41
Statins like lovastatin (altoprev) decrease what? causing what?
decrease the production of certain apolipoproteins, which lowers VLDL and triglyceride levels
42
4 uses of Lovastatin (altoprev)
1. hypercholesterolemia 2. primary and secondary prevention of cardiovascular events 3. post-myocardial infarction therapy 4. diabetes
43
4 ADE of Lovastatin (altoprev):
1. headache 2. rash 3. memory loss 4. GI disturbances
44
Rare and significant ADE of Lovastatin (altoprev):
1. myopathy 2. rhabdomyolysis 3. hepatotoxicity
45
1 nursing implication of Lovastatin (altoprev):
inform patients that dosing in the evening is preferred for all statins
46
Pharmacological class of Colesevelam (welchol)
Bile-acid sequestrant
47
Therapeutic class of Colesevelam (welchol)
antihypercholesterolemia
48
MOA of Colesevelam (welchol):
binds or sequesters bile acids and other substances in the GI tract preventing their absorption and promoting their excretion
49
How does Colesevelam (welchol) affect LDL?
lowers LDL cholesterol and is also dependent on increasing the number of available LDL receptors on hepatocytes.
50
Use of Colesevelam (welchol):
1. adjutant therapy to diet and exercise | 2. use of statins
51
ADE of Colesevelam (welchol):
not absorbed from the GI tract: 1. constipation 2. bloating 3. indigestion 4. nausea
52
1 nursing implication of Colesevelam (welchol):
administer other medication 1 hour before taking sequestrates, or 4 hours after
53
Pharmacological class of ezetimibe (zetia):
Inhibits cholesterol absorption
54
Therapeutic class of ezetimibe (zetia):
antihypercholesterolemia
55
MOA of ezetimibe (zetia):
blocks cholesterol absorption
56
What are the most effective drugs for lowering triglyceride or TG levels?
fibrates
57
What can fibrates raise? What do fibrates have little to no effect on?
HDL cholesterol levels, but little to no effect on LDL cholesterol levels
58
Pharmacological class of gemfibrozil (lopid):
fibric acid derivative "fibrate"
59
Therapeutic class of gemfibrozil (lopid):
Antihypertriglyceridemia
60
what levels does gemfibrozil (lopid) lower?
decreases plasma triglyceride levels by lowering vLDL levels
61
MOA of gemfibrozil (lopid):
1. work by interacting with specific receptor subtype present in the liver and brown adipose tissue 2. activation of these receptor leads to increase of synthesis of lipoprotein lipase and reduced production of certain apolipoproteins.
62
Uses of gemfibrozil (lopid):
1. high levels of triglycerides or vLDLs | 2. raise HDL
63
5 ADE of gemfibrozil (lopid):
1. rash 2. GI disturbances 3. Gallstones 4. myopathy 5. liver injury
64
1 nursing implication of gemfibrozil (lopid):
advise patients to report any signs of muscle pain, tenderness, or weakness, or any other pain.
65
What is the most common complication of pregnancy?
hypertension
66
Chronic hypertension is usually what in pregnancy?
benign
67
What are 2 conditions that are life-threatening to a patient and the fetus?
1. pre-eclampsia | 2. eclampsia
68
true or false: antihypertensive drugs can be used in both patient's with pre-eclampsia and eclampsia
true