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Advanced Nursing Pharmacology > Module 6 cardiac > Flashcards

Module 6 cardiac Flashcards

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1
Q

What are the risk factors for CV disease?

A

gender, age cigarette smoking, DM, HTN, dyslipidemia

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2
Q

Which lipoproteins are associated with hyperlipidemia?

A

Decreased amount of High-density lipoproteins (HDL-C)

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3
Q

At which point in the cholesterol synthesis pathway do the statins intervene?

A

HMG CoA- inhibits this step to decrease the amount of endogenous cholesterol in our body

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4
Q

What does the LDL-C do? And what are the important aspects to remember?

A

“Bad” cholesterol
60% of total cholesterol in body
transports cholesterol to peripheral cells
excess initiates atherosclerosis
predictor for CV disease
Primary target of cholesterol lowering therapy

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5
Q

What is HDL-C and what does it do?

A

“Good” cholesterol
20-30% of cholesterol in body
transports cholesterol from peripheral tissues and vessels to liver and kidneys for removal

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6
Q

What is VLDL-C and what is its purpose?

A

Made up of triglycerides
produced by liver
precursor to LDL

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7
Q

There are primary and secondary causes of hyperlipidemia. What are the primary causes?

A

genetics

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8
Q

There are primary and secondary causes of hyperlipidemia. What are the secondary causes?

A

Diet (high fat)
Underlying disease (DM, Liver disease, CRF, alcoholism)
Medications (estrogens, protease inhibitors, steroids, thiazides, beta blockers)

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9
Q

What effect does estrogen have on cholesterol?

A

decreases LDL
increases HDL
but increases triglycerides

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10
Q

What determines the patient’s LDL goal?

A

Coronary hear disease risk assessment

Risk factor status

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11
Q

What are the determinants of the CHD risk assessment?

A 
MI
Myocardial ischemia
angina
coronary angioplasty
coronary artery surgery
DM
Peripheral arterial disease
AAA
Carotid artery disease
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12
Q

What are the risk factors to count after the CHD risk assessment is complete?

A

Cigarette smoking
Hypertension (140/90)
Low HDL (45, women =/> 55)

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13
Q

After completing the Framingham scoring, your patient has a 10year risk of >20%, what is their LDL-C goal?

A

<100mg/dl

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14
Q

After completing the Framingham scoring, your patient has a 10year risk of </= 20%, what is their LDL-C goal?

A

<130 mg/dl

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15
Q

For those patients with 0-1 risk factor and no need for further risk factor assessment, what would their LDL-C goal be?

A

<160 mg/dl

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16
Q

What are the items to score in the Framingham risk assessment?

A 
Age
Total cholesterol
Smoking status
HDL level
Systolic blood pressure
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17
Q

What is the normal/accepted HDL range?

A

40-60 mg/dl

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18
Q

What is the accepted/normal level for total cholesterol?

A

<200 mg/dl

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19
Q

What does a lipoprotein analysis include?

A

total cholesterol
LDL-C
HDL-C
triglycerides

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20
Q

What is the accepted/normal for triglycerides?

A

<150 mg/dl

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21
Q

What is considered the “cornerstone” in LDL-lowering therapy?

A

Lifestyle changes

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22
Q

What are the 4 lifestyle modifications encouraged in lowering LDL levels?

A

Reduce intake of cholesterol
soluble fiber intake of 10-25g/d
Weight reduction
Increased physical activity

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23
Q

Describe the progression of drug therapy in primary prevention of hyperlipidemia.

A
  1. Initiate statin or bile acid sequestrant or nicotinic acid
  2. In 6 weeks, if goal not acheived, intensify same medications
  3. In 6 weeks, if goal acheived, treat other lipid risk factors. If goal not acheived, refer to specialist.
  4. Monitor Q4-6 months
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24
Q

What is the main concern in increasing the lipid lowering medications?

A

rhabdomyolosis

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25
Q

What are the four drug classifications used in treatment of dyslipidemia?

A

HMG CoA Reductase Inhibitors (Statins)
Bile acid sequestrants
nicotinic acid (Niacin)
Fibric acids

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26
Q

What are the contraindications in using HMG CoA Reductase inhibitors?

A

Liver disease (absolutely do not use)
CYP450meds
Antifungals
macrolides

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27
Q

Name the HMG CoA Reductase inhibitors.

A 
lovastatin (Mevacor)
pravastatin (Pravachol)
simvastatin (Zocor)
fluvastatin (Lescol)
atorvastatin (Lipitor)
rosuvastatin (Crestor) newest
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28
Q

When do the HMG CoA Reductase inhibitors work best?

A

when taken before bed

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29
Q

What are the major side effects of HMG CoA reductase inhibitors?

A

Myopathy

increased liver enzymes

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30
Q

Are bile acid sequestrants systemic acting?

A

No

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31
Q

What effect do bile acid sequestrants have on triglycerides?

A

increases triglyceride levels

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32
Q

What are the side effects of bile acid sequestrants?

A

GI distress/constipation

decreased absorption of other drugs (HCTZ, warfarin, digoxin, thyroid meds, BBs, statins)

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33
Q

When is the use of bile acid sequestrants contraindicated?

A

TG level of more than 400

dysbetalipoproteinemia (increases TG = acute pancreatitis)

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34
Q

What are the common bile acid sequestrants used?

A

cholestyramine (Questran)
colestipol (Colestid)
colesevelam (Welchol)

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35
Q

Which medication is used to raise the HDL level once the LDL goal has been reached?

A

Nicotinic acid

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36
Q

What does nicotinic acid do?

A

decreases the production of VLDL which eventually becomes LDL and raises HDL

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37
Q

What are the side effects of nicotinic acid?

A

flushing, hyperglycemia, hyperuricemia, upper GI distress, hepatotoxicity

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38
Q

When is nicotinic acid contraindicated?

A

liver disease
severe gout
peptic ulcer

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39
Q

What is an important aspect in patient education regarding nictonic acid?

A

Side effects lessen over time

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40
Q

What is the major drug interaction in using fibric acids?

A

Warfarin - more warfarin is available in blood, increasing anticoagulant effect

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41
Q

What do fibric acids do?

A

decreases hepatic TG production and VLDL synthesis

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42
Q

Name the 2 fibric acids used.

A

gemfibrozil (Lopid)

fenofibrate (Tricor)

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43
Q

What does ezetimibe (Zetia) do?

A

inhibits the absorption of cholesterol by the small intestine

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44
Q

What drug interactions are of concern in using ezetimibe (Zetia)?

A

fibric acids and cyclosporines block the absorption of Zetia

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45
Q

What is the purpose of taking fish oil (omega-3 fatty acids)?

A

decreases TG/VLDL

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46
Q

What are the main risks associated with a triglyceride level > 500?

A

pancreatitis, increased risk for atherosclerosis

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47
Q

What is the treatment for hypertriglyceridemia?

A 
dietary fat restriction
 ETOH restriction
 weight reduction
treat coexisting conditions
medications: fibric acids, niacin, fish oil, statins
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48
Q

What are the four types of medications used in treating Coronary Artery Disease?

A

Nitrates
Beta Blockers
Calcium Channel Blockers

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49
Q

What do nitrates do?

A

Reduce cardiac preload

Dilate coronary arteries

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50
Q

What are the 3 nitrates commonly prescribed?

A

Nitroglycerin
isosorbide dinitrate
isosorbide mononitrate

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51
Q

What is the timeframe that a patient being treated with nitrates should be nitrate FREE?

A

8-12 hours

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52
Q

What is the first line nitroglycerin agent?

A

Sublingual nitroglycerin

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53
Q

What do beta blockers do?

A

Decrease heart rate
reduce blood pressure
decrease contractility

54
Q

What is the treatment plan for CAD?

A
  1. Initiate aspirin
  2. Sublingual NTG
  3. NTG vs. CCB vs BB
  4. Maximize single agent
  5. combination treatment
55
Q

90% of patients with HTN havethis type of HTN.

A

Essential

56
Q

According to JNC 8, how is a non-black patient treated with blood pressure >140/90?

A

Thiazide type diuretic and ACEI, ARB, or CCB

57
Q

According to JNC 8, how is a black patient treated with blood pressure >140/90?

A

Thiazide type diuretic or CCB

58
Q

Which drugs affect heart rate and contractility?

A

BBs
CCBs
Centrally acting adrenergics

59
Q

What effects does the parasympathetic system have on the cardiac system?

A

Stimulates smooth muscle, cardiac muscle and decreases heart rate

60
Q

What effects does the sympathetic system have on the cardiac system?

A

Stimulates the heart rate, vasoconstricts vessels in skin and visceral and vasodilates vessels in skeletal muscle

61
Q

What is the mechanism of action for adrenergic drugs?

A

decreased BP, HR, venous return, CO, and cardiac workload

62
Q

What are the centrally acting alpha2-receptor agonists?

A

clonidine (Catapres)

methyldopa (Aldomet)

63
Q

What are the 5 types of adrenergic drugs?

A

Centrally and peripherally acting adrenergic neuron blockers
Centrally acting alpha2-receptor blockers
peripherally acting alpha1-receptor blockers
Peripherally acting beta-receptor (beta blockers)
both cardioselective (beta1) and nonselective(beta1 and beta2)
Pheripherally acting dual alpha1 and beta-receptor blockers

64
Q

What type of drugs are the -zosin’s?

A

Adrenergic: peripheral alpha1-vlockers

65
Q

Describe the mechanism of action in peripheral alpha1-blockers.

A

Decreased BP, peripheral resistance
Promotes vasodilation
No change in CO

66
Q

What are the beta blockers mechanism of action?

A

reduces BP by reducing HR
reduces renin secretion
decreases myocardial contractility
results in decreased HR, BP, CO, SVR, and cardiac workload

67
Q

What is the mechanism of action in dual action alpha1 adn beta-receptor blockers?

A

Decreased HR
vasodilation
results in decreased BP, HR, SVR, and improves CO
also useful in CHF

68
Q

What is clonidine and when is it useful?

A

central acting alpha2-receptro agonist

among other things, useful in management of withdrawal symptoms of opioid or nicotine dependent persons

69
Q

What are the most common side effects of adrenergic drugs?

A

Dry mouth
Drowsiness, sedation
constipation

70
Q

Which drugs end in -olol or -lol?

A

Beta blockers

71
Q

Which drugs end in -pril?

A

ACE inhibitors

72
Q

What are ACE inhibitors used for?

A

used for first line therapy in CHF and HTN

73
Q

What are ACE inhibitors sometimes combined with?

A

CCBs or thiazide diuretics

74
Q

Once ACE converts angiotensin I to angiotensin II, what does angiotensin II do?

A

Potent vasoconstrictor that causes aldosterone secretion from the adrenal glands

75
Q

What are the effects of ACE inhibitors?

A

decreased afterload
systemic vasodilation
decreases Na and H2O reabsorption
decreases BP

76
Q

Name the most common ACEIs

A

captopril (Capoten)
enalapril (Vasoec)
lisinoptil (Prinivil and Zestril)
quinapril (Accupril)

77
Q

Which ACEI is used in diabetic patients, and why?

A

captopril (Capoten)

It is renal protective

78
Q

Which ACEIs are newer with long half-lives and require once a day dosing?

A

lisinopril (Prinivil and Zestril)

quinapril (Accupril)

79
Q

Which ACEI may be used in patients with liver dysfunction?

A

captopril (Capoten)

lisinopril (Prinivil and Zestril)

80
Q

What are the adverse effects of ACEIs?

A 
Fatigue
Dizziness
HA
Mood changes
Impaired taste
Possible hyperkalemia
Dry, nonproductive cough
Angioedema (rare but potentially fatal)
First dose hypotension
81
Q

What is the suffix associated with ARBs?

A

-sartan

82
Q

What is special about ARBs in reference to its side effects, as compared with ACEIs?

A

No dry cough

Less likely to cause hyperkalemia

83
Q

Name the most common ARBs.

A

losartan (Cozaar, Hyzaar)
valsartan (Diovan)
sprosartan (Teveten)
irbesartan (Avapro)

84
Q

What is the mechanism of action in calcium channel blockers (CCBs)?

A

causes smooth muscle relaxation by blocking the binding of calcium to its receptors, preventing muscle contraction

85
Q

What are the effects of CCBs?

A

decreased peripheral smooth muscle tone
decreased systemic vascular resistance
decreased BP
decreased HR

86
Q

What are the suffixes associated with CCBs?

A
  • zem
  • mil
  • dipine
87
Q

Name the most common CCBs.

A

benzothiazepines: diltiazem (Cardizem)
phenylalkamines: verapamil (Calan)
dihydropyridines: amlodipine (Norvasc)
nifedipine (Procardia)

88
Q

What are the indications for use of CCBs?

A 
angina
HTN
dysrhythmias
migraines
Raynauds disease
89
Q

What are the adverse effects of CCBs?

A 
hypotension
papitations
tachycardia
worsening of CHF
constipation, nausea
rash
flushing
peripheral edema
dermatitis
90
Q

What are the effects of diuretics?

A 
decreased preload
decreased CO
decreased total peripheral resistance
which results in 
decreased workload on the heart and BP
91
Q

What are the most common vasodilators?

A

diazoxide (Hyperstat)
hydralazine HCl (Apresoline)
minoxidil (loniten)
sodium nitroprusside (Nipride, Nitropress)

92
Q

What are the 3 types of diuretics?

A

thiazide
loop
potassium-sparing

93
Q

What are the most common thiazide and thiazide-like drugs used?

A 
thiazides:
HCTZ
all end in -zide
thiazide-like:
metolazone (Zarozolyn)
94
Q

What is the mechanism of action in thiazide/thiazide-like drugs?

A

action primarily in the distal convouted tubule
inhibits tubular reabsorption of Na, Cl, K ions
results in systemic vascular resistance

95
Q

What is the minimum creatinine clearance for use of thiazides?

A

30-50 ml/min

metolazone: 10 ml/min

96
Q

What are the adverse effects of thiazide diuretics?

A 
dizziness
HA
blurred vision
paresthesias
decreased libido
anorexia
n/v/d
impotence
urticaria
photosensitivity
hypokalemia
hyperglycemia
97
Q

Name the common loop diuretics.

A

bumetanide (Bumex)
furosemide (Lasix)
torsemide (Demedex)

98
Q

How do loop diuretics work?

A

act directly on the ascending limb of the loop of Henle to inhibit Cl and Na resorption
Increases renal prostaglandins, resulting in the dialtion of blood vessels and reduced peripheral vascular resistance

99
Q

Loop diuretics adverse effects are similar to thiazides except for what?

A

No decreased libido, no impotence/photosensitvity

risk for hematologic concerns

100
Q

Name the potassium sparing diuretics.

A

also known as aldosterone inhibiting diuretics:
amiloride (Midamor)
spironolactone (Aldactone)
triamterene (Dyrenium)

101
Q

When are potassium supplements not recommended when using diuretics?

A

when potassium levels exceed 3 mEq/L

102
Q

Name some foods high in potassium.

A 
bananas
oranges
dates
apricots
raisins
broccoli
green beans
potatoes
meats
fish
legumes
103
Q

What drug toxicity is of concern with diuretic drug therapy?

A

digitalis

104
Q

Which type of heart failure is most common?

A

Systolic

105
Q

What are the common causes of chronic heart failure (CHF)?

A 
HTN
CAD
idiopathic
valvular disease
viral 
genetic abnormalities
drug induced: anticancer, ETOH, cocaine, immunomodulating drugs
106
Q

What are the first line agents used for CHF?

A

ACEIs

107
Q

What do positive inotropic drugs do?

A

increase the force of myocardial contraction

108
Q

What do negative chronotropic drugs do?

A

decrease HR

109
Q

What do negative dromotropic drugs do?

A

slows cardiac conduction through the tissue

110
Q

What are the common drug classes used in treatment of CHF?

A 
ACEIs
Angiotensin II receptor blockers (ARBs)
Beta blockers
Aldosterone blocking agents
cardiac glycosides
111
Q

What is the therapeutic level for digoxin?

A

0.5 - 2 ng/ml

112
Q

Name the therapy used in digoxin toxicity.

A

Digoxin immune Fab (Digibind)

113
Q

Name the conditions that predispose a patient to digoxin toxicity.

A

hypokalemia, hypomagnesemia, hypercalcemia
cardiac pacer
hepatic dysfunction
dysrhythmias
hypothyroid, respiratory, or renal disease
advanced age

114
Q

When would you hold digoxin?

A

apical pulse less than 60 or greater than 120

s/s toxicity

115
Q

What foods should be avoided while taking digoxin and why?

A

High fiber

fiber binds with digitalis

116
Q

What are the contraindications for the use of warfarin?

A 
pregnancy
psychosis/senility
alcoholism
hepatic disease
high bleeding risk
117
Q

What is the length of treatment for warfarin for the use of cardioversion?

A

3 weeks prior to cardioversion

118
Q

What is the initial dosing for warfarin?

A

5mg every day for 2-3 days

119
Q

What is the target INR in warfarin therapy for most patients? for those with a mechanical heart valve?

A

2-3

2.5-3.5

120
Q

What is the antidote for warfarin in the case of toxicity?

A

Vitamin K

121
Q

What is the general rule for monitoring INR in warfarin therapy?

A

Monitor INR twice weekly, till patients have 2 consecutive INRs in range, then may monitor every 4 weeks as stable. Remember that an INR today is the dose change 3-5 days ago.

122
Q

The average change in INR due to amiodarone when taken with warfarin is what?

A

increase of 44%

123
Q

How much would you need to decrease the warfarin dose if a patient would need to take amiodarone?

A

50% reduction

124
Q

Name the medications that interact with warfarin (increases INR).

A 
antiobiotics
amiodarone
zafirlukast
sulfa/trimeth
flagyl
HMG CoA Reductase inhibitors
fibric acid derivatives
125
Q

What effect does chronic alcoholism have on warfarin therapy?

A

decreases INR

126
Q

What are the effects of vitamin K, herbals, and ASA on warfarin therapy.

A

vitamin K: decreases INR
herbals: increase INR
ASA: increases INR

127
Q

Weekly dose changes should be approximately how much in warfarin therapy?

A

5-20% of total weekly dose

128
Q

JNC-7 recommends which diagnostic tests before initiating treatment form HTN?

A 
12 lead EKG
urinalysis with albumin
blood glucose and hematocrit
serum potassium
creatinine and GFR
serium calcium
lipid profile
129
Q

When treating HTN pharmacologically, what is the drug of choice for patients with DM, CHF, and MI?

A

ACEIs

130
Q

Which HTN medication may make cognitive dysfunction and dementia worse?

A

central alpha2 agonists

131
Q

What is preeclampsia?

A

HTN and proteinuria after 20 weeks

132
Q

HTN is higher in which ethnic/racial group?

A

African Americans

Advanced Nursing Pharmacology (6 decks)

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