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Nursing Semester 2 > Monica - Exam 4: Anti-lipemics > Flashcards

Monica - Exam 4: Anti-lipemics Flashcards

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1
Q

What is coronary artery disease?

A

progressive blood vessel disorder caused by the hardening of arteries

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2
Q

major cause of CAD

A

atherosclerosis - deposits of lipids within the epithelium that harden with time

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3
Q

Explain the disease progression of an artery with atherosclerosis.

A

Soft fat deposits within the epithelium. It hardens into plaques. Macrophages are activated to consume the bad cholesterol causing inflammation. The plaques and inflammation lead to stenosis (narrowing) of the artery that can cause occlusion and generate clots.

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4
Q

non-modifiable risk factors for CAD

A
  • age and gender: greatest risk for white middle-aged man; risk increased for females >65
  • ethnicity: african-american (2x risk), native-american (<35yo 2x mortality)
  • genetic predisposition/family hx
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5
Q

Why does the risk for CAD increase after menopause?

A

lack of estrogen. estrogen helps maintain higher HDL and lower LDL.

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6
Q

modifiable risk factors

A
  • elevated blood pressure: HTN
  • DM
  • tobacco use
  • physical inactivity
  • obesity: linked to bad lipid levels
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7
Q

T/F - HTN accelerates the deposition of plaque in the arteries.

A

True

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8
Q

How does tobacco use increase the risk of CAD?

A

Increased heart rate and vasoconstriction lead to elevated BP. Toxins cause vessel inflammation.

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9
Q

How does physical inactivity increase the risk of CAD?

A

decreased fat metabolism, decreased good cholesterol, increased cardiac workload

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10
Q

triglycerides

A
  • come from excess calories
  • excess triglycerides are stored in fat
  • source of energy available in the bloodstream but high levels are associated with atherosclerosis
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11
Q

cholesterol

A
  • naturally occurring
  • secreted by the liver
  • fx: manufacture hormones, cell membranes, bile acids, insulate nerve fibers
  • found in animal sources
  • promotes atherosclerosis
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12
Q

Biosynthesis of cholesterol is higher at what time?

A

During the night - that is why anti-lipemics are scheduled qHS

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13
Q

What are lipoproteins?

A

Lipid+protein molecules that mobilize and transport lipid.

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14
Q

How are lipoproteins classified?

A

composition, size, and weight

HDL, LDL, VLDL

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15
Q

HDLs are mainly composed of:

A

protein, thus heavier/more dense

“good” cholesterol

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16
Q

LDLs are mainly composed of:

A

cholesterol

“bad”

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17
Q

VLDLs are mainly composed of:

A

triglycerides

“bad”

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18
Q

Why are HDLs considered “good cholesterol”?

A

They transport LDL away from tissues and arteries, protecting the arteries from lipid accumulation.
Increased HDL leads to decreased risk of CVD

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19
Q

HDL is manufactured in the _____ and _____.

A

liver and small intestine

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20
Q

Why is LDL considered “bad cholesterol”?

A

It transports cholesterol from liver to tissues and organs contributing to fatty deposits in arteries.

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21
Q

lab values:

total cholesterol

A

optimal: <200
borderline in between
high: >240

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22
Q

lab values:

LDL

A

optimal: <100
near optimal in between
high: >130

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23
Q

lab values:

HDL

A

optimal: >60

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24
Q

lab values:

VLDL

A

optimal: 5-30

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25
Q

lab values:

tryglycerides

A

normal: <150
borderline in between
high: >200

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26
Q

Dietary approaches to lowering cholesterol:

A

DECREASE intake of: calories, cholesterol, saturated fat
AVOID: trans-fat
INCREASE: mono- and poly-unsaturated fats, omega-3 fatty acids, fiber

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27
Q

examples of saturated fats

A

beef, butter, cheese, tropical oils

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28
Q

examples of trans-fats

A

fried foods, margarine, donuts

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29
Q

examples of mono- and poly-unsaturated fats

A

avocado, nuts/seeds, olive oil

30
Q

examples of omega-3 fatty acids

A

fish, soybeans, flaxseed

31
Q

How does increased fiber affect lipid levels?

A
  1. Fiber increases fullness, reducing calories.

2. It binds to cholesterol and eliminates it. Poop it out!

32
Q

Hydroxymethylglutaryl CoEnzyme-A (Hmg CoA) Reductase inhibitors are also called:

A

statins

33
Q

prototypical statin:

A

atorvastatin

34
Q

Statins are metabolized by the ______

A

liver

35
Q

statins:

action

A

Inhibits enzyme needed for cholesterol synthesis.

*most potent drug class, favored by health care providers

36
Q

statins:

effect

A

DECREASED:

  • formation of plaque
  • LDL and triglycerides
  • risk of MI and stroke

Slight increase: HDL level

37
Q

statins:

adverse effects

A

C: abdominal cramps, constipation, diarrhea, flatus, heartburn
LT: rhabdomyolysis

38
Q

What is rhabdomyolysis?

A

breakdown of muscle protein

sxs: muscle pain, weakness, dark urine

39
Q

What increases the risk of rhabdomyolysis with use of statins?

A
  • grapefruit

- concurrent use w/ other anti-lipemics (except cholestyramine and ezetimibe)

40
Q

How can rhabdomyolysis be reversed?

A

by discontinuing the statin medication

41
Q

prototypical bile acid sequestrant:

A

cholestyramine

42
Q

bile acid sequestrant:

indication

A

management of hypercholesteremia

43
Q

bile acid sequestrant:

action and effect

A

A: binds to bile acids in the small intestine and forms insoluble complex that is excreted in feces
E: decreased cholesterol and LDLs

44
Q

bile acid sequestrant:

adverse effects

A

abdominal discomfort, constipation, nausea

45
Q

implementation of cholestyramine:

A
  • dissolved thoroughly in water or applesauce to prevent choking
  • before meals
  • take other meds 1 hour before OR 4 hours after cholestyramine
46
Q

prototypical nicotinic acid derivative:

A

niacin

47
Q

niacin:

action and effect

A

In large doses: decreases VLDL, LDL levels and triglyceride synthesis; may increase HDL level

48
Q

niacin:

adverse effects

A

flushing of the face and neck, pruritus, GI upset

*intense side effects

49
Q

Davis Drug Guide recommends taking _______ 30 min before each dose of ______

A

ASA 300mg
niacin
* to treat the side effects
* slow release available to minimize AEs

50
Q

T/F: Niacin is commonly used as a monotherapy.

A

FALSE - rarely!

51
Q

prototypical fibric acid derivative:

A

gemfibrozil

52
Q

gemfibrozil:

indication

A
  • management of hyperlipidemia W/O CAD

- previously attempted diet, exercise, weight loss or other agents

53
Q

gemfibrozil:

action and effect

A

DECREASES: VLDL level; triglyceride synthesis in liver
INCREASES: HDL level

54
Q

gemfibrozil:

adverse effects

A

abdominal pain, diarrhea, epigastric pain

55
Q

prototypical cholesterol absorption inhibitor:

A

ezetimibe

56
Q

ezetimibe:

indication, action

A

I: use alone or with statins for hypercholesteremia to lower cholesterol
A: inhibits absorption of cholesterol in the small intestine by about 50%

57
Q

ezetimibe:

AEs

A

no common ones

58
Q

What is troponin?

A
  • myocardial protein

- biomarker for MI dx

59
Q

normal troponin ranges

A

<0.05 ng/mL

60
Q

troponin range: suspected MI

A

0.05-2.3 ng/mL

61
Q

troponin range: MI

A

> 2.3 ng/mL

62
Q

Troponin levels rise __-___ hours after MI onset.

A

4 - 6 hours after MI

63
Q

Peak troponin levels are __-__ hours after MI.

A

10 - 24 hours after MI

64
Q

Troponin returns to baseline in __-__ days.

A

10 - 14 days

65
Q

What is a “cardiac series” and why is it ordered?

A
  • serial sampling q6-8hrs for 24 hrs to see the troponin trends (peak) and determine the severity of the cardiac event
  • also looks at creatine kinase trends
66
Q

What is creatine kinase?

A
  • enzyme in skeletal muscle, brain and nervous system, and heart
  • increases after muscle injury or certain medications
  • NONspecific marker for muscle injury
67
Q

CK-MB is specific to ________

A

myocardium

68
Q

CK-MB ranges for males and females:

A

M: 50-204 units/L
F: 36-160 units/L

69
Q

CK-MB rises __-__ hours after onset of MI.

A

3-6 hours after onset

70
Q

CK-MB peaks __-__ hours after MI.

A

12 - 24 hours

71
Q

CK-MB returns to baseline after __-__ hours.

A

12 - 48 hours

Nursing Semester 2 (7 decks)

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