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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

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2
Q

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

A

LPL or apoCII → ↑ chylomicrons

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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

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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

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5
Q

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

A

↑ LDL and ↑ VLDL due to overproduction of VLDL

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6
Q

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

A

ApoE; type 3 familal dysbetalipoproteinemia

“apo E type threeee”

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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)

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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

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9
Q

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

A

hypertriglyceridemia

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10
Q

what the the secondary factors that can lead to hypercholesterolemia

A
  • hypothyroidism (both)
  • glucocorticoids (both)
  • nephrotic syndrome
  • obstructive liver disease
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11
Q

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

A

statins

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12
Q

can statins ↓ the incidence of death?

A

yes

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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
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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)

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15
Q

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

A

intracellular cholesterol;

↑ HMG CoA reductase and ↑ LDL receptors

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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

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17
Q

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

A

TG: ↓
LDL: ↓ ↓
HDL: small ↑

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18
Q

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

A

Rosuvastatin> atorvastatin > simvastatin > lovastatin, pravastatin > fluvastatin

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19
Q

statins are contraindicated in ______

A

pregnancy

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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

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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
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22
Q

what LDL level is associated with giving them statins

A

LDL above 190 mg/dL

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23
Q

Pleotropic effects of statins:

A
  • improves endothelial function
  • ↓ platelet aggregation
  • stabilize atherosclerotic plaque
  • reduce inflammation
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24
Q

AE of statins?

A
  • ↑ aminotransferases even though there is not evidence of liver damage
  • myopathy and rhabdomyolysis
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25
how can statins cause renal injury?
an AE is rhabdomyolysis and that can cause myoglobinuria --
26
_____ and _____ are used to monitor the potential adverse effects you see with statins
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
27
Niacin is the most effect agent for _________
increasing HDL and is the one one that can reduce lipoprotein A
28
what is the effect of niacin on the different lipid levels
↓ VLDL, ↓ LDL, ↓ Lp(a) | ↑ HDL
29
what is the only drug that can reduce Lp(a)
Niacin
30
what is the most effective agent for ↑ HDL
Niacin
31
is niacin associated with reduced mortality and morbidity?
NO
32
Niacin inhibits ______ through activation of what type of G protein in adipocytes leading to the inhibition of _______
adenyl cyclase in Gi proteins; inhibits hormone sensitive lipase ↓ cAMP → PKA inactive
33
what is the effect of niacin on the liver?
inhibits senses and esterification of fatty acids → VLDL production ↓ and as a result will ↓ LDL
34
MOA of niacin:
- ↑ LPL activity | - ↓ catabolic rate of HDL
35
a person takes a antihyperlipidemia drug and develops intense cutaneous flush. what is this drug and wha can be used to reduce this flushing?
flushing is seen with giving niacin and will have to give aspirin to reduce it because the flushing is prostaglandin mediated
36
the cutaneous flushing associated with niacin is ______ mediated
prostaglandin
37
what are the adverse effects niacin?
- cutaneous flushing - pruritus rashes and dry ski - acanthosis nigricans - nausea and abdominal discomfort - hepatotoxicity and hyperglycemia (most serious) - ↑ uric acid levels → gout
38
what are the most serious adverse effects of niacin?
- hepatotoxicity and hyperglycemia due to insulin resistance
39
gout is an adverse effect of what antihyperlipidemic drug
niacin
40
fibrates: ______ and ______ are given to lower ______ and increase _____
gemfibrozil and fenofibrate; | ↓ VLDL ↑ HDL
41
fibrates _________ the ___________ receptor that is found in liver and brown adipose tissue
activates the peroxisome proliferator-activated receptor α (PPAR-α)
42
what is the mechanism of the ↓ in TG levels due to fibrates
- ↑ expression of lipoprotein lipase - ↓ hepatic expression of apoC-III - ↑ hepatic oxidation of fatty acids
43
fibrates may increase _____ if the TG level is greater than 400 mg/dL
LDL; | if TG is very high, then LDL can be underestimated because everything is measured directly except LDL
44
what is the DOC for the SEVERE hypertriglyceridemia?
fibrates
45
what are the best drugs in descending order to treat high TG
fibrates > niacin> omega 3 fatty acids > statins > ezetimibe
46
gallstones is a AE of _____
fibrates because they ↑ biliary cholesterol excretion
47
what are some adverse effects of fibrates?
- mild GI ditruabes - myositis (inflammation of muscles) especially in patients with renal insufficiency - rhabdomyolysis - lithiasis (gallstones)
48
which fibrate when given with statin will increase BOTH levels in the body? why?
gemfibrozil + statins because they both compete against each other for the glucuroronysl transferase which metabolizes both
49
administering gemfibrosil with statins will increase the risk of ________
rhabdomyolysis
50
gemfibrosil is a _______ drug that competes with statin for _________
fibrate | glucuronosyl transferase
51
what are the fibrates and their drug interactions
- gemfibrosil: ↑ statin concentration leading to ↑ risk of rhabdomyolysis - fenofibrate: no drug interactions
52
which drug class ↑ the biliary excretion of cholesterol leading to _______
fibrates; gallstone formation (lithiasis)
53
what are the bile acid binding resins (3) and when are they given
- cholestyramine - colestipol - colesevalam used when there is only ↑ LDL
54
MOA of bile acid binding resins
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
_____ and _____ are drug classes that cause an ↑ in LDL receptor expression
statins, bile acid binding resins, ezetimibe (cholesterol absorption inhibitor)
56
how do bile acid binding reins such as: ______, ______ and _____ lead to the up regulation of LDL receptors?
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
functional LDL receptors are required in the use of what drugs?
statins and bile acid binding resins
58
bile acid binding resins are not used in mono therapy but are usually used with _____ or ____
statins or niacins to ↓ LDL
59
pregnant or child with ↑ LDL what drug would you give them?
bile acid binding resins (colesevelam) because they are not absorbed so they don't have many adverse effects
60
which bile acid binding resins has the least GI adverse effects?
colesevelam
61
what drug is contraindicated in patients with hypertryglyceridemia?
bile acid binding resins
62
what type of drug is ezetimibe and what is its effect?
inhibits intestinal absorption of cholesterol → primary clinical effect is to lower LDL
63
reduced delivery of intestinal cholesterol to the liver by ________ leads to _______
ezetimibe (inhibits the intestinal transport protein NPC1L1) up regulation of LDL reception enhancing LDL clearance from plasma
64
if a patient cannot tolerate statins, what is the first non-statin drug that should be given?
ezetimibe (only time that it is used as mono therapy, otherwise usually given with statins to achieve a good ↓ in LDL)
65
_______ should not be given with ezetimibe
bile acid binding resins because they inhibit the absorption of ezetimibe
66
what are the two effects of omega 3 fatty acids (DHA and EPA)
- ↓ TG synthesis - ↑ fatty acid oxidation (modest ↑ in HDL)
67
which class of antihyperlipidemic drugs has the potential to ↑ LDL levels?
``` fibrates and omega 3 fatty acids, fibrates is the class that can ↓ TG levels the most ```
68
_____ class of antihyperlipidemic drugs ↑ TG levels
bile acid binding resins
69
______ ↑ HDL the most
niacin
70
______ ↓ TG the most
fibrates
71
statin is the initial drug given for which lipid profiles
- ↑ LDL - ↑ LDL and ↑ TG - low HDL
72
what are the initial drugs given for isolated severe hypertriglyceridemia and what is the additional drug given
fibrate (or niacin or omega 3) and then give statin if levels don't ↓ enough
73
drug therapy for ↑ LDL only
statin + niacin, resin, ezetimibe
74
drug therapy for ↑ LDL and TG
statin + niacin, fibrate, omega 3
75
______ is a category X and is absolutely contraindicated in pregnancy
statins
76
what antihyperlipidemic drugs are contraindicated in pregnancy?
- statins - fibrates - niacin - ezetimibe - cholestyramine and colestipol
77
_______ is a bile acid binding resin that can be used in pregnant patients and kids
colesevalam

PCM Exam 2 (32 decks)

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