Cardiac Dyslipidemic Flashcards Preview

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Flashcards in Cardiac Dyslipidemic Deck (30)
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1
Q

Microsomal triglyceride transfer protein (MTP) inhibitor

Decreases VLDL secretion and accumulation of LDL in plasma

A

Lomitapide

2
Q

Lomitapide SE (2)

A

Inc TAG in liver

Inc transaminase

3
Q

Antisense oligonucleotide targeting APOB-100 (liver)

A

Mipomersen

4
Q

Mipomersen SE (2)

A

Mild to mod injection site reaction

Flu-like symptoms

5
Q

Inhibits transporter that mediated GI uptake of cholesterol and phytosterol

A

Ezetimide

For hypercholesterolemia
Phytosterolemia

6
Q

Ezetimibe SE

A

Hepatotoxicity if combined with HMG COA

7
Q

Dec LDL cholesterol by 20% (monotherapy)

More effective when combined with HMG COA reductase inhibitors but inc hepatotoxicity

A

Ezetimibe

8
Q

Activates signaling pathway that dec HORMONE SENSITIVE LIPASE activity

Dec plasma FA and TG level

Inc clearance of VLDL by lipoprotein lipase dec VLDL

Dec catabolic rate of HDL inc HDL

A

Niacin

For hypercholesterolemia

Hypertriglyceridemia

Low HDL CHOLESTEROL

9
Q

Drug for hypertriglyceridemia and low HDL

A

Niacin

10
Q

Niacin SE (2)

A
Cutaneous flushing - NSAID
Hyperuricemia
GI
Pruritus
Hepatotoxicity
Hyperglycemia
11
Q

Dec circulating fibrinogen

Inc tissue plasminogen activator

A

Niacin

12
Q

Act as ligand for peroxisome proliferator-activated receptor alpha (PPAR-a) protein

A

Fibric acid
Gemfibrozil
Fenofibrate

For hypertriglyceridemia

13
Q

Gemfibrozil
Fenofibrate SE

(5)

A
Inc risk of gallstone
Inc risk of myopathy with statin
Rashes gemfibrozil only
Nausea
Leukopenia, Anemia, Potentiate anticoag
14
Q

Dec TAG, VLDL

Inc HDL

No effect on LDL

But inc LDL in patients with familial combined hyperlipoprotinemia

A

Fibric Acid derivatives
Gemfibrozil
Fenofibrate

15
Q

Inhibits rate limiting step in cholesterol synthesis

A

HMG COA reductase inhibitors

16
Q

Rate limting step in cholesterol synthesis

A

Conversion of hydroxymethylglutaryl coenzyme A to mevalonate

by

HMG COA reductase

17
Q
Dec LDL dramatically
Dec risk of coronary events and MI
Dec risk of ischemic stroke
Dec TAG and
Inc HDL
A

Statins

18
Q

Statin SE (4)

A

Hepatotoxicity (inc transaminase)
Inc Crea kinase
Rhabdomyolysis (severe pain)
Teratogenic

19
Q

Statins do not work in hypercholes familial bec

A

They need functional LDL receptor to work which is impaired

20
Q

Why is there risk for hepatotoxicity and rhabdomyolysis in statin

A

Bec it inhibits CYP450 inc conc of drugs

21
Q

Large nonabsorbable polymers that bind bile acid and similar steroids in intestine and prevent their absorption

Diverts cholesterol to synthesis of new bile acid

A

Cholestyramine
Colestipol
Colesevelan
Bile Acid Binding Resins

22
Q

For hypercholesterolemia

To dec pruritus in patients with cholestasis and bile salt accum

A

Cholestyramine
Colestipol
Colesevelam

23
Q

Bile acid binding SE (4)

A

Impaired absorption of fat and vitamins
Unpleasant gritty taste
Bloating
Constipation

24
Q

Dec LDL
Inc TAG and VLDL
No effect on HDL

Interferes with absorption of HMG COA reductase i

A

Bile acid binding resin

25
Q

deficiency in LPL and apoC-II

inc chylomicron, VLDL

A

Primary chylomicronemia

Type I

26
Q

Dec clearance of VLDL
Inc VLDL, chylomicrons

Inc VLDL, chylomicrons
Inc production VLDL

A

Familial hypertriglyceridemia severe

Moderate

27
Q

Inc hepatic apoB and VLDL production

Inc VLDL, LDL

A

Familial combined hyperlipoproteinemia

28
Q

Inc VLDL chylomicron remnants

Deficient apoE

A

Familial dysbetalipoproteinemia

Type III

29
Q

Inc LDL

Defect in LDL receptors

A

Familial hypercholesterolemia

Type II

30
Q

Statins are used in (3)

A

Familial combined hyperlipoproteinemia
Familial dysbetalipoproteinemia III
Familial hypercholesterolemia II