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Pharmacology Exam 2 > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

What are the 5 major risk factors for CVD?

A 
smoking
hypertension (>140/90 or on meds)
low HDL (45, women >55)
Fam hx of early CHD
Age (men >45, women >55)
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2
Q

LDL goal - “high risk” (CHD)

A

<70)

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3
Q

LDL goal - “moderately high risk” (2+ risk factors)

A

<130

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4
Q

LDL goal - “moderate risk” (2 risk factors)

A

<130

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5
Q

LDL goal - “lower risk” (0-1 risk factors)

A

<160

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6
Q

Risks factors for metabolic syndrome

A 
3 or more:
abdominal obesity (men >40, women >35)
tg >150
low HDL (men 130/>85)
fasting glucose >110
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7
Q

What is the treatment approach for hyperlipidemia?

A
  1. initiate TLCs
  2. Treat secondary causes (DM, meds, etc.)
  3. Treat LDL to goal
  4. When LDL is to goal, treat high tg (>200)
  5. Attempt to increase HDL if <40
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8
Q

What are the TLCs (therapeutic lifestyle changes) for LDL lowering?

A
  1. TLC diet (low fat, low cholesterol), plant stanols/sterols, fiber
  2. weight reduction
  3. increased physical activity
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9
Q

*What part of the cholesterol panel do statins mostly act on?

A

LDL reduction

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10
Q

*What part of the cholesterol panel do bile-acid resins mostly act on?

A

LDL reduction

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11
Q

*What part of the cholesterol panel do fibric acid derivatives mostly act on?

A

decrease triglycerides

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12
Q

*What part of the cholesterol panel do omega-3 fatty acids mostly work on?

A

decrease triglycerides

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13
Q

*Statins - MOA

A

inhibit HMG CoA reductase –> decrease in cholesterol production (up regulation of LDL receptors and enhanced clearance)
*only works if receptors are not defective

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14
Q

Statins - time of day to administer

A

usually at night so it peaks when cholesterol synthesis is the highest (2-4am)

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15
Q

Side effects are low with statins but include:

A

elevated liver enzymes
myopathy
rabdomyolysis

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16
Q

DDI - Statins (because of CYP450)

A

gembibrozil
Protease inhibitors
itraconazole/ketoconazole/voriconazole
emycin/clarithromycin

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17
Q

Which 2 statins reduce LDL the most?

A

Atorvastatin (Lipitor) 60%

Rosuvastatin (Crestor) 60+%

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18
Q

What level are we getting under control first in drug therapy for high cholesterol?

A

LDL

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19
Q

What level do we treat next after lowering LDL?

A

Triglycerides

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20
Q

What drug can reduce total cholesterol/LDL, Apo B, non-HDL or TG and increase HDL in patients where mono therapy is not adequate?

A

Niacin extended release/Simvastatin (Simcor)

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21
Q

As you increase the dose of statin, you increase the risk of _______.

A

Myopathy

22
Q

What level is considered very high LDL?

A

> 190mg/dl

23
Q

What can be added to statins for very high LDL?

A

ezetimibe +/- nicotinic acid

bile acid sequestrates +/- nicotinic acid

24
Q

What class are: cholestyramine (Questran), colestipol (Colestid) and Colesevelam (Welchol)?

A

bile acid binding resins

25
Q

What time of day are bile acid binding resins given?

A

with meals (acts on bile acid that is present during digestion)

26
Q

*Bile acid binding resins - side effects

A

GI (bloating, constipation, gas), increase in liver enzymes, increase in TG
hard to tolerate

27
Q

Bile acid binding resins - DDI

A

fat soluble vitamins (binds)

give 1 hr before or 4 hrs after meal

28
Q

What is the selective cholesterol absorption inhibitor?

A

Ezetimibe (Zetia)

combo agent simvastatin + ezetimibe (Vytorin)

29
Q

What is the nicotinic acid derivative used for hyperlipidemia?

A 
ER Niacin (Niaspan)
IR Niacin (available OTC)
30
Q

Nicotinic acid derivative dosing considerations

A 
start out low and titrate b/c of side effects
effective range 1500-2000 mg/day
take at night (b/c of flushing)
take ASA or NSAID 30 min before
avoid ETOH
31
Q

*Nicotinic acid - side effects

A 
flushing
hepatotoxicity (esp. at higher doses)
glucose homeostasis/insulin resistance 
blurry vision
gout
32
Q

Classification of serum TG

A

normal <150
borderline high 150-199
high 200-499
very high 500+

33
Q

What is the secondary target of therapy for hyperlipidemia?

A

non-HDL (VLDL + LDL)

34
Q

At what level do you treat TG?

A

> 200

35
Q

Treatment of triglycerides

A
  1. treat underlying factors
  2. niacin
  3. fibric acid derivative “fibrates”
  4. fish oil
  5. therapeutic phlebotomy
36
Q

What are the underlying factors for elevated triglycerides?

A

diet, ETOH, DM, hypothyroidism, antiretrovirals, steroids,

37
Q

What is the treatment goal for very high triglycerides (>500)?

A

prevent acute pancreatitis

38
Q

*What are the two formulations for fibrates?

A

Fenofibrates and Gemfibrozil

*Fenofibrates are favored b/c of dosing (no restriction with food timing)

39
Q

*Fibrates - clinical issues

A

gall stones

Gemfibrozil can increase LDL and fenofibrates can decrease LDL

40
Q

Fibrates - DDI

A

protein bound so can displace other meds: warfarin, ASA, glyburide, statins, niacin

41
Q

Fibrates - ADE

A

contraindication: hepatic or renal dysfunction and preexisting gall bladder disease

42
Q

How much fish oil is needed/day to reduce TG?

A

2-4 grams

43
Q

Fish oils should be discontinued if what occurs?

A

acute bleeding episode such as hemorrhagic stroke

44
Q

Causes of low HDL (<40 mg/d)

A

physical inactivity
type 2 diabetes
smoking
genetic

45
Q

What med is the DOC for low HDL treatment?

A

Niacin

46
Q

Red yeast rice - active ingredient

A 
Monacolin K (comparable to Lovastatin)
can lower cholesterol
47
Q

Red yeast rice - dosage

A

600 mg po bid

48
Q

Risk factors for statin induced myopathy

A

female
65+
kidney disease
hypothyroidism

49
Q

Red yeast rice - effects on levels

A

lowers TC, TG and LDL

increases HDL

50
Q

Ezetimibe (Zetia) - MOA

A

(selective cholesterol absorption inhibitor)

blocks niemann Pick C1 like 1 peptide (NPC1L1) in the small intestine

51
Q

At what level should triglycerides be treated before LDL?

A

> 500

Pharmacology Exam 2 (9 decks)

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