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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
lab values: | tryglycerides
normal: <150 borderline in between high: >200
26
Dietary approaches to lowering cholesterol:
DECREASE intake of: calories, cholesterol, saturated fat AVOID: trans-fat INCREASE: mono- and poly-unsaturated fats, omega-3 fatty acids, fiber
27
examples of saturated fats
beef, butter, cheese, tropical oils
28
examples of trans-fats
fried foods, margarine, donuts
29
examples of mono- and poly-unsaturated fats
avocado, nuts/seeds, olive oil
30
examples of omega-3 fatty acids
fish, soybeans, flaxseed
31
How does increased fiber affect lipid levels?
1. Fiber increases fullness, reducing calories. | 2. It binds to cholesterol and eliminates it. Poop it out!
32
Hydroxymethylglutaryl CoEnzyme-A (Hmg CoA) Reductase inhibitors are also called:
statins
33
prototypical statin:
atorvastatin
34
Statins are metabolized by the ______
liver
35
statins: | action
Inhibits enzyme needed for cholesterol synthesis. | *most potent drug class, favored by health care providers
36
statins: | effect
DECREASED: - formation of plaque - LDL and triglycerides - risk of MI and stroke Slight increase: HDL level
37
statins: | adverse effects
C: abdominal cramps, constipation, diarrhea, flatus, heartburn LT: rhabdomyolysis
38
What is rhabdomyolysis?
breakdown of muscle protein | sxs: muscle pain, weakness, dark urine
39
What increases the risk of rhabdomyolysis with use of statins?
- grapefruit | - concurrent use w/ other anti-lipemics (except cholestyramine and ezetimibe)
40
How can rhabdomyolysis be reversed?
by discontinuing the statin medication
41
prototypical bile acid sequestrant:
cholestyramine
42
bile acid sequestrant: | indication
management of hypercholesteremia
43
bile acid sequestrant: | action and effect
A: binds to bile acids in the small intestine and forms insoluble complex that is excreted in feces E: decreased cholesterol and LDLs
44
bile acid sequestrant: | adverse effects
abdominal discomfort, constipation, nausea
45
implementation of cholestyramine:
- dissolved thoroughly in water or applesauce to prevent choking - before meals - take other meds 1 hour before OR 4 hours after cholestyramine
46
prototypical nicotinic acid derivative:
niacin
47
niacin: | action and effect
In large doses: decreases VLDL, LDL levels and triglyceride synthesis; may increase HDL level
48
niacin: | adverse effects
flushing of the face and neck, pruritus, GI upset | *intense side effects
49
Davis Drug Guide recommends taking _______ 30 min before each dose of ______
ASA 300mg niacin * to treat the side effects * slow release available to minimize AEs
50
T/F: Niacin is commonly used as a monotherapy.
FALSE - rarely!
51
prototypical fibric acid derivative:
gemfibrozil
52
gemfibrozil: | indication
- management of hyperlipidemia W/O CAD | - previously attempted diet, exercise, weight loss or other agents
53
gemfibrozil: | action and effect
DECREASES: VLDL level; triglyceride synthesis in liver INCREASES: HDL level
54
gemfibrozil: | adverse effects
abdominal pain, diarrhea, epigastric pain
55
prototypical cholesterol absorption inhibitor:
ezetimibe
56
ezetimibe: | indication, action
I: use alone or with statins for hypercholesteremia to lower cholesterol A: inhibits absorption of cholesterol in the small intestine by about 50%
57
ezetimibe: | AEs
no common ones
58
What is troponin?
- myocardial protein | - biomarker for MI dx
59
normal troponin ranges
<0.05 ng/mL
60
troponin range: suspected MI
0.05-2.3 ng/mL
61
troponin range: MI
>2.3 ng/mL
62
Troponin levels rise __-___ hours after MI onset.
4 - 6 hours after MI
63
Peak troponin levels are __-__ hours after MI.
10 - 24 hours after MI
64
Troponin returns to baseline in __-__ days.
10 - 14 days
65
What is a "cardiac series" and why is it ordered?
- 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
What is creatine kinase?
- enzyme in skeletal muscle, brain and nervous system, and heart - increases after muscle injury or certain medications - NONspecific marker for muscle injury
67
CK-MB is specific to ________
myocardium
68
CK-MB ranges for males and females:
M: 50-204 units/L F: 36-160 units/L
69
CK-MB rises __-__ hours after onset of MI.
3-6 hours after onset
70
CK-MB peaks __-__ hours after MI.
12 - 24 hours
71
CK-MB returns to baseline after __-__ hours.
12 - 48 hours

Nursing Semester 2 (7 decks)

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