Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PCM Exam 2 > Antihyperlipidemic Drugs > Flashcards

Antihyperlipidemic Drugs Flashcards

1
Q

what is the lipid profile and the etiology of Type I Familial hyperchylomicronemia

A

↑ chylomicrons due to deficiency in LPL or apoCII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

type I familial hyperchylomicronemia is due to a deficiency in ____ or _____

A

LPL or apoCII → ↑ chylomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the lipid profile and the etiology of type 2A familial hypercholesterolemia

A

↑ LDL due to ↓ or no functional LDL receptor expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

↑ in ONLY VLDL is seen in what familial disease and what is the etiology?

A

Type 4 familial hypertriglyericidemia and is due to the overproduction of VLDL or its impaired catabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the lipid profile and the etiology of type 2B familial hypercholesterolemia

A

↑ LDL and ↑ VLDL due to overproduction of VLDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

an abnormal _____ leads to the ↑ in IDL and is seen in type _____

A

ApoE; type 3 familal dysbetalipoproteinemia

“apo E type threeee”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the lipid profile and the etiology of type 5 familial mixed hyper triglyceridemia

A

↑ chylomicrons
↑ VLDL
due to the ↑ production or ↓ clearance of VLDL and chylomicrons

(type 1 + 4 = type 5)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the most important and most common familial lipidemia disorders?

A

type 2B (↑ VLDL and LDL) and type 4 (↑ VLDL)

these two make up 80% of the hyperlipidemia disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diabetes mellitus is a secondary factor that can lead to: hypertriglyceridemia / hypercholesterolemia

A

hypertriglyceridemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what the the secondary factors that can lead to hypercholesterolemia

A
  • hypothyroidism (both)
  • glucocorticoids (both)
  • nephrotic syndrome
  • obstructive liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the first choice for treatment in lowering lipids in patients with atherosclerotic cardiovascular disease

A

statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

can statins ↓ the incidence of death?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the 5 different classes of antihyperlipidemic drugs

A
  • HMG CoA reductase inhibitors (statins)
  • Niacin
  • bile acid binding resins
  • fibrates
  • cholesterol absorption inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

______ is a antihyperlipidemic drug that can reduce morbidity and mortality and acts by inhibiting______

A

Statins; competitively inhibit HMG CoA reductase (first step in cholesterol synthesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

statins cause the depletion of _____ leading to the upregulation of _______ and ________

A

intracellular cholesterol;

↑ HMG CoA reductase and ↑ LDL receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

upregulation of the LDL receptors as a result of ____ drugs causes _____

A

statins; results in ↑ clearance of LDL from the blood → ↓ LDL levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the effect of statins on TG, LDL, and HDL

A

TG: ↓
LDL: ↓ ↓
HDL: small ↑

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

list the statin drugs in order of most potent to least potent:

A

Rosuvastatin> atorvastatin > simvastatin > lovastatin, pravastatin > fluvastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

statins are contraindicated in ______

A

pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

statins would have significantly less treatment benefits for what type of people?

A

for people who don’t have a functional LDL receptor (those who have homozygous familial hypercholesterolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what type of patients with NORMAL LDL levels would you give statins?

A
  • patients with atherosclerotic coronary vascular disease or those with diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what LDL level is associated with giving them statins

A

LDL above 190 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Pleotropic effects of statins:

A
  • improves endothelial function
  • ↓ platelet aggregation
  • stabilize atherosclerotic plaque
  • reduce inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

AE of statins?

A
  • ↑ aminotransferases even though there is not evidence of liver damage
  • myopathy and rhabdomyolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how can statins cause renal injury?

A

an AE is rhabdomyolysis and that can cause myoglobinuria –

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

_____ and _____ are used to monitor the potential adverse effects you see with statins

A

aminotransferase (measure baseline and then 1-2 months after statin use and then ever 6-12 months)
CK: for muscles; measure baseline and only again when patient complains of muscle pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Niacin is the most effect agent for _________

A

increasing HDL and is the one one that can reduce lipoprotein A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the effect of niacin on the different lipid levels

A

↓ VLDL, ↓ LDL, ↓ Lp(a)

↑ HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is the only drug that can reduce Lp(a)

A

Niacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the most effective agent for ↑ HDL

A

Niacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

is niacin associated with reduced mortality and morbidity?

A

NO

32
Q

Niacin inhibits ______ through activation of what type of G protein in adipocytes leading to the inhibition of _______

A

adenyl cyclase in Gi proteins; inhibits hormone sensitive lipase

↓ cAMP → PKA inactive

33
Q

what is the effect of niacin on the liver?

A

inhibits senses and esterification of fatty acids → VLDL production ↓ and as a result will ↓ LDL

34
Q

MOA of niacin:

A
  • ↑ LPL activity

- ↓ catabolic rate of HDL

35
Q

a person takes a antihyperlipidemia drug and develops intense cutaneous flush. what is this drug and wha can be used to reduce this flushing?

A

flushing is seen with giving niacin and will have to give aspirin to reduce it because the flushing is prostaglandin mediated

36
Q

the cutaneous flushing associated with niacin is ______ mediated

A

prostaglandin

37
Q

what are the adverse effects niacin?

A
  • cutaneous flushing
  • pruritus rashes and dry ski
  • acanthosis nigricans
  • nausea and abdominal discomfort
  • hepatotoxicity and hyperglycemia (most serious)
  • ↑ uric acid levels → gout
38
Q

what are the most serious adverse effects of niacin?

A
  • hepatotoxicity and hyperglycemia due to insulin resistance
39
Q

gout is an adverse effect of what antihyperlipidemic drug

A

niacin

40
Q

fibrates: ______ and ______ are given to lower ______ and increase _____

A

gemfibrozil and fenofibrate;

↓ VLDL ↑ HDL

41
Q

fibrates _________ the ___________ receptor that is found in liver and brown adipose tissue

A

activates the peroxisome proliferator-activated receptor α (PPAR-α)

42
Q

what is the mechanism of the ↓ in TG levels due to fibrates

A
  • ↑ expression of lipoprotein lipase
  • ↓ hepatic expression of apoC-III
  • ↑ hepatic oxidation of fatty acids
43
Q

fibrates may increase _____ if the TG level is greater than 400 mg/dL

A

LDL;

if TG is very high, then LDL can be underestimated because everything is measured directly except LDL

44
Q

what is the DOC for the SEVERE hypertriglyceridemia?

A

fibrates

45
Q

what are the best drugs in descending order to treat high TG

A

fibrates > niacin> omega 3 fatty acids > statins > ezetimibe

46
Q

gallstones is a AE of _____

A

fibrates because they ↑ biliary cholesterol excretion

47
Q

what are some adverse effects of fibrates?

A
  • mild GI ditruabes
  • myositis (inflammation of muscles) especially in patients with renal insufficiency
  • rhabdomyolysis
  • lithiasis (gallstones)
48
Q

which fibrate when given with statin will increase BOTH levels in the body? why?

A

gemfibrozil + statins because they both compete against each other for the glucuroronysl transferase which metabolizes both

49
Q

administering gemfibrosil with statins will increase the risk of ________

A

rhabdomyolysis

50
Q

gemfibrosil is a _______ drug that competes with statin for _________

A

fibrate

glucuronosyl transferase

51
Q

what are the fibrates and their drug interactions

A
  • gemfibrosil: ↑ statin concentration leading to ↑ risk of rhabdomyolysis
  • fenofibrate: no drug interactions
52
Q

which drug class ↑ the biliary excretion of cholesterol leading to _______

A

fibrates; gallstone formation (lithiasis)

53
Q

what are the bile acid binding resins (3) and when are they given

A
  • cholestyramine
  • colestipol
  • colesevalam

used when there is only ↑ LDL

54
Q

MOA of bile acid binding resins

A

does NOT bind to a receptor;

charge- charge phenomenon: bind to the anionic bile acids in the intestinal lumen and present their reabsorption and so now the insoluble resin-bile acid complex is excreted in the feces

55
Q

_____ and _____ are drug classes that cause an ↑ in LDL receptor expression

A

statins, bile acid binding resins, ezetimibe (cholesterol absorption inhibitor)

56
Q

how do bile acid binding reins such as: ______, ______ and _____ lead to the up regulation of LDL receptors?

A

cholestyramine, colestipol, and colesevalam;
↓ bile acid causes the liver to covert more cholesterol into bile acid → ↓ intracellular cholesterol → up regulation of LDL receptors and up regulation of HMG-CoA reductase to synthesize more cholesterol

57
Q

functional LDL receptors are required in the use of what drugs?

A

statins and bile acid binding resins

58
Q

bile acid binding resins are not used in mono therapy but are usually used with _____ or ____

A

statins or niacins to ↓ LDL

59
Q

pregnant or child with ↑ LDL what drug would you give them?

A

bile acid binding resins (colesevelam) because they are not absorbed so they don’t have many adverse effects

60
Q

which bile acid binding resins has the least GI adverse effects?

A

colesevelam

61
Q

what drug is contraindicated in patients with hypertryglyceridemia?

A

bile acid binding resins

62
Q

what type of drug is ezetimibe and what is its effect?

A

inhibits intestinal absorption of cholesterol → primary clinical effect is to lower LDL

63
Q

reduced delivery of intestinal cholesterol to the liver by ________ leads to _______

A

ezetimibe (inhibits the intestinal transport protein NPC1L1)
up regulation of LDL reception enhancing LDL clearance from plasma

64
Q

if a patient cannot tolerate statins, what is the first non-statin drug that should be given?

A

ezetimibe (only time that it is used as mono therapy, otherwise usually given with statins to achieve a good ↓ in LDL)

65
Q

_______ should not be given with ezetimibe

A

bile acid binding resins because they inhibit the absorption of ezetimibe

66
Q

what are the two effects of omega 3 fatty acids (DHA and EPA)

A
  • ↓ TG synthesis
  • ↑ fatty acid oxidation
    (modest ↑ in HDL)
67
Q

which class of antihyperlipidemic drugs has the potential to ↑ LDL levels?

A 
fibrates and omega 3 fatty acids,
fibrates is the class that can ↓ TG levels the most
68
Q

_____ class of antihyperlipidemic drugs ↑ TG levels

A

bile acid binding resins

69
Q

______ ↑ HDL the most

A

niacin

70
Q

______ ↓ TG the most

A

fibrates

71
Q

statin is the initial drug given for which lipid profiles

A
  • ↑ LDL
  • ↑ LDL and ↑ TG
  • low HDL
72
Q

what are the initial drugs given for isolated severe hypertriglyceridemia and what is the additional drug given

A

fibrate (or niacin or omega 3) and then give statin if levels don’t ↓ enough

73
Q

drug therapy for ↑ LDL only

A

statin + niacin, resin, ezetimibe

74
Q

drug therapy for ↑ LDL and TG

A

statin + niacin, fibrate, omega 3

75
Q

______ is a category X and is absolutely contraindicated in pregnancy

A

statins

76
Q

what antihyperlipidemic drugs are contraindicated in pregnancy?

A
  • statins
  • fibrates
  • niacin
  • ezetimibe
  • cholestyramine and colestipol
77
Q

_______ is a bile acid binding resin that can be used in pregnant patients and kids

A

colesevalam

PCM Exam 2 (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions