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P&T Block 1 > L24 > Flashcards

L24 Flashcards

1
Q

Receptor for HDL on liver for steroidogenic tissues

A

SR-B1

Scavenger receptor

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2
Q

What drug class is the most effective at reducing LDL

A

Statins

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3
Q

Statin mechanism of lowering cholesterol

A

X HMG co-reductase
- No cholesterol synthesis
More LDL-R expression b/c less LDL in circulation - sensitizes the system

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4
Q

Statin mechanism for CV benefits

A

Anti-inflam

Anti-thrombogenic

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5
Q

How are most statins metabolized? Exceptions?

A

First pass extraction in liver via CYP enzymes
Except
- Prava
- Rosuva only slightly metab by liver

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6
Q

Statin adverse SEs

A
  1. Hepatitis that presents as flu-like sickness
  2. Rhabdomyolysis - can progress to kidney failure
  3. New onset diabetes
  4. Teratogenic - don’t give to pregnant women
  5. Peripheral neuropathy
  6. cP450 drug ints
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7
Q

What 2 enzyme levels are you going to monitor for pts on statins

A

Serum liver transaminases

Creatinine

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8
Q

Should you give statins to diabetic pts?

A

Yes
Higher risk of experiencing a cardiac event or death if diabetic
But benefits&raquo_space; risk

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9
Q

When should pts take their statins?

A

Before bed

Cholesterol levels highest at night

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10
Q

What are the 3 1st gen statins?

A

Simvastatin
Pravastatin
Lovastatin

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11
Q

What are the 2, 2nd gen statins?

A

Atorvastatin
Rosuvastatin
More potent forms

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12
Q

What is the mechanism of bile acid binding resins?

A

Bile acids contain cholesterol
- Usually recycled to preserve cholesterol stores
Instead, bind them and excrete them
Force the liver to use cholesterol to make more
Less cholesterol in circulation, reflex increase LDL-R expression

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13
Q

Which pts should you NOT give bile acid binders to?

A

High TGs

Bide acid binders also increase VLDL for unknown reasons –> increases TGs

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14
Q

Bind acid binder SEs

A

GI

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15
Q

Name the 2 bile acid binding resins

A

Cholestyramine

Colesevelam

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16
Q

Which cholesterol absorption inhibitor do you need to know

A

Ezetimibe

17
Q

Ezetimibe mechanism

A 
Blocks cholesterol and plant sterol GI absorption via X NPC1L1
Acts on dietary AND biliary cholesterol
Decreases serum:
- Cholesterol
- LDL
No change to TGs
18
Q

How is ezetimibe excreted

A

Feces - with whatever it bound!

19
Q

Evidence shows ezetimibe acts best when added to which statin specifically

A

Simvastatin

20
Q

3 PCSK9 inhibitors you need to know

A

Alirocumab

Evolocumab

21
Q

PCSK9 inhibitor mechanism

A

PCSK9 = internalization of LDL-R

Give w/ statins b/c when you ↑LDL-R, you also ↑PCSK9 levels

22
Q

What is a gain of function PCSK9 mutation associated with?

A

FHyperlipidemia

23
Q

What disease is secondarily benefited by ↓LDL

A

Metabolic syndrome

24
Q

Fibrates mechanism

A

Ligand for peroxisome proliferator-activated receptor (PPAR)
= nuclear receptors
↓TG + ↑HDL

25
Q

2 fibrates you need to know

A

Gemfibrozil

Fenofibrate

26
Q

Use of fibrates

A

BEST method to ↓TGs

↓CV events

27
Q

Which drug interaction should you keep in mind with fibrates?

A

Warfarin

Adjust dosing since fibrates bind plasma proteins warfarin would otherwise bind

28
Q

Fibrates SEs

A

GI

↑risk gallstones b/c ↑biliary cholesterol

29
Q

Which drug will give the largest ↑HDL

A 
Nicotinic acid (this is the active form)
Also some ↓LDL & TGs
30
Q

Nicotinic acid mechansim

A

Activates Niacr1 on adipose tissue

X lipolysis –> no FFAs toliver for TG or VLDL synthesis

31
Q

Is there a benefit to combining niacin w/ statins?

A

No - niacin goal is not for LDL reduction

Use alone to ↓TGs

32
Q

Niacin SEs

A

Skin flushing
- Prostaglandin vasodilation of skin
- ↓if use time release forms
Makes diabetes worse

P&T Block 1 (43 decks)

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