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Pharm exam 5 > Antihyperlipidemics > Flashcards

Antihyperlipidemics Flashcards

1
Q

Lipid digestion products associate with bile salts to form ______ (transport poorly soluble products to surface of enterocyte)

A

micelles

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2
Q

what is choelsterol absorbed thruogh

Monoglycerides and fatty acids diffuse across plasma membrane

A

NPC1L1 (Niemann-Pick C1 like 1) transporter

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3
Q

synthesis of chylomicrons (exogenous metabolism)

A
  1. SI mucosal cells secrete TAG-rich chylomicrons
  2. Apo C-ll and E are transferred from HDL to nascent chylomicron
  3. chylomicron –> systemic circulation
  4. Lipoprotein lipase (Apo C-II activates it) degrades TAG in CM in capillaries –> FA to tissues and glycerol to liver
  5. Apo E is receptor on liver that allows take up of chylomicron remnants
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4
Q

Endogenous synthesis/metabolism of VLDL, IDL, LDL

A
  1. Apo B attachd to Tag-rich VLDL particles in liver
  2. secretes and Apo C-II and E are added to VLDL
  3. VLDL enters capillaries and lipoprotein lipase degrades –> FA to tissues and glycerol to liver –> IDL –> LDL
    (can be converted to LDL or taken up by liver)
  4. LDL binds to receptors on extrahepatic tissue
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5
Q

what is apoE important for

A

important for chylomicron elemetns to be taken up and LDL

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6
Q

How is excess cholesterol gotten rid of

A

HDL takes it up

HDL binds to A-1 and SR-BI in liver

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7
Q

what apolipoprotein is ligand for LDL

what happens if inactivated

A

Apo B-100

increase in LDL

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8
Q

what apolipoprotein is cofactor for LPL

what happens if inactivated

A

Apo C-II

increase chylomicrons and VLDL

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9
Q

what apolipoprotein is Ligand for IDL to bind to LDL receptor and chylomicron remnants to bind to remnant receptors

what happens if inactivated

A

ApoE

increase IDL and chylomicrons

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10
Q

what happens if LPL is inactivated

A

increase in chylomicrons and VLDL

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11
Q

what happens if LDL-receptor is inactivated

A

increase LDL

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12
Q

what are the statins target?

A

HMG CoA reductase inhibitors

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13
Q

what are the fibrates (PPAR activators)?

A

gemfibrozil

fenofibrate

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14
Q

what are the bile acid sequestrants

A

Colesevelam

Colestipol

Cholestyramine

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15
Q

what is a cholesterol absorption inhibitor

A

Ezetimibe

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16
Q

what is fibric acid derivatives used to treat

A

hypertriglyceridemia

17
Q

adverse effects of fibrates

A

Rarely cause rashes, gastrointestinal symptoms, and myopathy

Risk of myopathy increases with combination with statins

18
Q

Gemfibrozil is contraindicated with what drug

A

statins

Use caution when combining fenofibrate with statins

19
Q

what do bile acid-binding resins treat

A

hypercholesterolemia - for patients whom statins do not provide sufficient LDL reduction

20
Q

MOA of bile acid-binding resins

A

***Bind to bile acids and bile salts in intestine

Disrupt enterohepatic circulation of bile acid and bile salts

Liver has to increase synthesis of bile acid to replace lost bile acids and salts

Requires increased liver uptake of cholesterol
Elevation of liver LDL-receptors

21
Q

MOA of fibrates

A

activates PPAR receptor

22
Q

Bile acid-binding resins:

↓ 1
However, can increase plasma 2
Should not generally be used in patients with 3
Can cause 4 and constipation

A
  1. LDL
  2. TG
  3. hypertriglyceridemia
  4. bloating
23
Q

Drug of choice to lower cholesterol in children and women who are pregnant or lactating
(not systemically absorbed)

A

Bile acid-binding resins

24
Q

MOA of niacin

A

Inhibit VLDL synthesis & secretion by liver

25
Q

what does niacin treat

A

Can be useful in treatment of all hypertriglyceridemias and hypercholesterolemia

26
Q

SE of niacin

A

Cutaneous flushing and itching (most common side effect)

  • due to prostacyclin from skin released
  • pretreat with NSAID

Hyperuricemia (induce gout attacks in susceptible individuals)

Hepatotoxicity (slight risk)

Slightly increases risk of statin-induced myopathy

Safest combination is niacin with fluvastatin and highest risk is with lovastatin

27
Q

what is the safest combo for niacin and a statin to decrease risk of statin-induced myopathy

what is the highest risk combo

A

niacin with fluvastatin

highest risk = lovastatin

28
Q

what drug inhibits cholesterol absorption at jejunum

A

Ezetimibe

29
Q

Ezetimibe (Zetia) blocks intestinal absorption of cholesterol by inhibiting ___

A

*** Niemann-Pick C1-like 1 protein

Blocks uptake of both dietary cholesterol and reabsorption of cholesterol excreted in bile

Reduces incorporation of cholesterol into chylomicrons

Reduced chylomicron remnants delivered to liver increases expression of hepatic LDL receptors

Reduces plasma LDL levels by 15-20%

30
Q

What can ezetimibe tx

A

hypercholesterolemia

31
Q

what statin is least potent and what are most potent

A

Least: Fluvastatin

Most: atorvastin and rosuvastatin

32
Q

MOA of statins

A

**inhbit HMG CoA reductase –> decrease concentration of cholesterol in cells

low cholesterol –> stimulates synthesis of LDL receptros –> uptake of LDL from blood

low intracellular cholesterol decreases VLDL

33
Q

what drugs greatly reduce CV risk and mortality

A

statins

34
Q

SE of statins

A

Myopathy

  • Patients with an inherited variant in a anion transporter are at higher risk for myopathy
  • Baseline creatine kinase measurements recommended

Rarely rhabdomyolysis occurs

*Liver toxicity in low percentage of patients

35
Q

clinical indictions for statins

A

Indications
Elevated LDL, CVD, and elevated CVD risk

Used to lower plasma cholesterol levels in many types of hyperlipidemias

Given to patients with clinically evident atherosclerotic disease or at high risk

36
Q

first line tx of hypercholesterolemia

if pts do not respond adequately then what?

A

Statins

Add cholesterol absorption inhibitors and/or bile acid binding resins

37
Q

what is niacin often useful for

A

both hypercholesterolemia and hypertriglyceridemia

38
Q

what is often used for Hypertriglyceridemia (generally elevated VLDL and/or chylomicrons)

A

fibrates

Niacin

Pharm exam 5 (9 decks)

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