Brainscape's Knowledge GenomeTM

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


See full index

PATHO/PHARM II > Dyslipidemia & Agents > Flashcards

Dyslipidemia & Agents Flashcards

Kaplan Pharm

1
Q

Lipoproteins: What are there functions?

A

Lipid transport (not H2O soluble)

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

Classes of ”chylomicrons”

A

VLDL, LDL, HDL

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

Classes of ”chylomicrons”: Very-Low-Density Lipoproteins VLDL

What are they made up of?

A

Lipid core = TGs

VLDL particles contain triglycerides as their major component, along with cholesterol and other lipids.

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

Classes of ”chylomicrons”: Very-Low-Density Lipoproteins VLDL

What are they responsible for?

A

Responsible for transporting triglycerides synthesized in the liver to various tissues in the body for energy or storage.

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

Classes of ”chylomicrons”: Very-Low-Density Lipoproteins VLDL

What is the risk with elevation of VLDL?

A

Increased VLDL ~ increase in TGs

Link to atherosclerosis not firmly established

> 500mg/dL ~ pancreatitis

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

Classes of ”chylomicrons”: Low-Density Lipoproteins LDLs

A

By-products of VLDL metabolism

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

Classes of ”chylomicrons”: Low-Density Lipoproteins LDLs:

What are they directly related to?

A

Directly related to ASCVD risk, target of TX

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

Classes of ”chylomicrons”: Low-Density Lipoproteins LDLs:

What are they directly related to?

A

Directly related to ASCVD risk, target of TX

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

Classes of ”chylomicrons”: High-Density Lipoproteins HDLs:

What are they directly related to?

A

Reduces ASCVD risk

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

Dyslipidemia: Complications

A

Atherosclerosis

HTN, CAD, PVD

Stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Dyslipidemia: Familial dyslipidemia

A

↑ liver production of cholesterol

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

Approach to Drug Therapy for Dyslipidemia:

A

Primary target ↓ LDL

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

Approach to Drug Therapy for Dyslipidemia:

Primary target ↓ LDL: What med is initiated first?

A

HMG-CoA reductase inhibitors initiated 1st

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Approach to Drug Therapy for Dyslipidemia:

Primary target ↓ LDL: What med is an add on?

A

Add-on bile acid sequestrant

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

Approach to Drug Therapy for Dyslipidemia:

What are fibrates used for?

A

Fibrates primarily for TGs, not LDL

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

Drug Classes Used for Dyslipidemias & ASCVD PX include:

A

HMG-CoA Reductase Inhibitors (Statins)

Bile-Acid Sequestrants

Ezetimibe

Fibric Acid Derivatives (Fibrates)

PCSK 9 Inhibitors (Monoclonal Antibodies)

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

HMG-CoA Reductase Inhibitors end in?

A

(Statins)

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

HMG-CoA Reductase Inhibitors: What are they most effective for?

A

Most effective for ↓ LDL & total cholesterol

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

HMG-CoA Reductase Inhibitors: What can they aid in?

A

Evidence for possible benefits for osteoporosis

20
Q

HMG-CoA Reductase Inhibitors: When is cholesterol synthesis greatest in the day? What does this mean about when med should be taken?

A

increases Cholesterol synthesis @ night ~ QHS

21
Q

HMG-CoA Reductase Inhibitors:

MOA: What does it inhibit?

A

Inhibition of HMG-CoA reductase (enzyme for cholesterol synthesis)

22
Q

HMG-CoA Reductase Inhibitors:

MOA: What does it increase?

A

Increase hepatocyte production of LDL receptors

23
Q

HMG-CoA Reductase Inhibitors:

MOA: What does it decrease?

A

↓ production of apolipoprotein B-100 ~  VLDL & TGs

24
Q

HMG-CoA Reductase Inhibitors (Statins)

ADEs:

A

Generally well tolerated-Transient HA, rash, GI disturbances

Hepatotoxicity

Cataracts

Myopathy

Rhabdomyolysis

Teratogenic

25
Q

HMG-CoA Reductase Inhibitors (Statins)

ADEs: Myopathy

What is a sign of this?

A

Muscles aches, tenderness, weakness

26
Q

HMG-CoA Reductase Inhibitors cont.

ADEs: Rhabdomyolysis

What are risk factors?

A

Advanced age, small body frame, frailty
Multisystem DX ~ chronic renal insufficiency & DM
High doses & rosuvastatin
**Low vitamin D & coenzyme Q, supplement **
Concurrent fibrates
Concurrent agents that  statins

27
Q

HMG-CoA Reductase Inhibitors cont.

Drug interactions:

A

Concurrent lipid-lowering drugs

CYP-3A4 inhibitors

28
Q

HMG-CoA Reductase Inhibitors cont.

Drug interactions: CYP-3A4 inhibitors:

A

increase lovastatin & simvastatin
increase atorvastatin

29
Q

Bile-Acid Sequestrants:

What do they do to LDLs? VLDL (what does this mean for people with very high VLDLs)?

A

decrease LDL ~ 20%

Mild transient increases VLDL in some (Avoid if VLDL already high)

30
Q

Bile-Acid Sequestrants:

Mode of Action:

A

Bile acids –> intestine –> XX –> reabsorbed

increases bile acid secretion excretion –> increase synthesis (requires cholesterol)

increases LDL receptors on hepatocytes = increase LDL uptake from plasma

31
Q

Bile-Acid Sequestrants

ADE

A

Mainly issues w/ cholestyramine, colestipol

Constipation

decrease uptake of fat-soluble vitamins ADEK

GI upset bloating, indigestion, nausea

32
Q

Bile-Acid Sequestrants

Interactions

A

Insoluble complex w/ PO meds

33
Q

Bile-Acid Sequestrants

Interactions: How should it be taken with thiazides, digoxin, warfarin, certain antibiotics?

A

Thiazides, digoxin, warfarin, certain ABX
1h before, 4h after

34
Q

Ezetimibe: How is it used?

A

Used as add-on w/ statin, or monoTX

35
Q

Ezetimibe:

MOA: Actions on brush border cells (small intestine)

A

Inhibits dietary cholesterol absorption

Inhibition of cholesterol reabsorption secreted in the bile

36
Q

Ezetimibe:

MOA: Lipoprotein effects

A

decrease total cholesterol, LDL, TGs, apolipoprotein B.

Small increase in HDL

No evidenced of decrease ASCVD

37
Q

Ezetimibe:

ADE: Who should it be avoided in?

A

Avoid in moderate-severe hepatic impairment

37
Q

Ezetimibe:

ADE:

A

Gallstones ~ increase bile cholesterol

38
Q

Fibric Acid Derivatives (Fibrates) ~ -fibr

Effects on lipoproteins?

A

Most effective for decreasing TG 40-55%

Can increase HDL 6-10%
Little or no effect on LDL (may actually increase)
No evidenced of decreasing ASCVD

39
Q

Fibric Acid Derivatives (Fibrates) ~ -fibr:

When is it used?

A

Considered 3rd line

40
Q

Fibric Acid Derivatives (Fibrates) ~ -fibr

A

Activation of PPAR-alpha receptor (liver & brown adipose tissue)

Accelerated clearance of VLDLs ~ increases TGs

Increase apolipoproteins A-I & A-II ~increasing HDL

41
Q

Fibric Acid Derivatives (Fibrates) ~ -fibr

ADEs:

A

Gallstones

Myopathy

Hepatotoxicity ~ periodic LFTs

42
Q

Fibric Acid Derivatives (Fibrates) ~ -fibr

Interactions

A

Displacement of warfarin from albumin

43
Q

PCSK9 Inhibitors- end in what?

A

mab

44
Q

PCSK9 Inhibitors-

MOA:

A

Monoclonal antibodies that inhibit PCSK9 (protein)

“Frees-up” receptor for LDL uptake ~ decrease in plasma LDL

45
Q

Fish Oil & Omega-3 Agents

A

Contains omega-3 fatty acids ~ EPA & DHA

Reduces risk of CAD progression & PX arrythmia

45
Q

Contains omega-3 fatty acids ~ EPA & DHA: What is it not effective for?

A

OTC Fish oil is NOT effective for
Lowering LDL
Direct protection for ASCVD

PATHO/PHARM II (27 decks)

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