Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology part B > Lipid disorders > Flashcards

Lipid disorders Flashcards

1
Q

define atherosclerosis

A

abnormal deposition of cholesterol in arteries

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

3 sites to decrease cholesterol

A

decrease GI uptake
decrease LDL levels
decrease endogenous cholesterol synthesis

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

how can you decrease GI uptake of cholesterol

A

decrease dietary intakes, reabsorption of bile acids, and absorption of cholesterol

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

what class of drugs are the statins, what does that do

A

HMG-CoA reductase inhibitors which is the rate limiting step in cholesterol synthesis causing an increase in LDL receptors

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

what effect do the statins have

A

decrease LDL levels and triglyceride levels

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

when should you give statins

A

at night because that is when you are not eating and the body would be synthesizing its own cholesterol

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

adverse effects of statins

A

myalgia, muscle weakness
increase inplasma aminotransferase
first pass metabolism

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

statins contraindicated in

A

pregnancy

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

why is grapefruit juice bad

A

inhibits CYP3A4

which will result in increase of statin bioavailability

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

what strength of stain should be used

A

10mg, any increase doesnt result in much more efficacy

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

example of cholesterol absorption inhibitor

A

ezetimibe

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

how do cholesterol absorption inhibitors work

A

inhibit cholesterol transport protein NPC1L1, inhibiting dietary and biliary cholesterol absorption

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

where does ezetimibe work

A

at the intestinal brush border

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

what is the downfall of cholesterol absorption inhibitors

A

less cholesterol absorbed from the gut so there is an increase in the amount that the liver produces

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

potential side effects of ezetimibe

A

myalgia
hepatitis
rhabdomyolysis
acute pancreatitis

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

examples on bile binding resins

A

cholestyramine
colestipol
colesevelum

17
Q

how do bile acid binding resins work

A

anion exchange resin that binds to bile in intestinal lumen and doesnt allow it to be recirculated

18
Q

how does preventing bile reabsorption decrease cholesterol

A

liver has to increase LDL receptors to take up cholesterol to synthesize new bile salts and synthesize de novo cholesterol

19
Q

adverse effects of bile acid binding resins

A 
increase VLDL
decrease absorption of fat soluble vitamines
nausea, constipation 
unpleasant taste/texture 
absorption of drugs altered
20
Q

why combine statin and ezetimibe

A

ezetimibe decrease cholesterol uptake in the gut but mechanisms increase synthesis in the liver. the HMGCoA reductase inhibito blocks the increased synthesis in the liver

21
Q

reasons of failure to achieve target LDL-C

A 
poor adherence 
high baseline LDL-C
high cholesterol diet or absorption 
variable statin response 
inability to tolerate higher dose statins
22
Q

what is the new expensive therapy

A

inject human monoclonal antibody to PCSK9 to increase LDL receptors on the liver

23
Q

how does the PCSK9 antibody work

A

causes the LDL receptor to be recyled rather than degraded and then be expressed at the surface

24
Q

potential sites to decrease triglycerides

A

decrease dietary triglycerides
increase lipoprotein lipase activity
decrease VLDL secretion from the liver

25
Q

non pharm to decrease triglycerides

A

eat more fiber

26
Q

examples of fibric acid derivatives

A

fenofibrate

gemfibrozil

27
Q

fibrates mechanism

A

increased VLDL clearance due to increased lipoprotein lipase activity
decreased VLDL secretion

28
Q

side effects of fibrates

A

flu like
muscle crampls
myopathy

29
Q

contraindications of fibrates

A

hepatic or renal dysfunction
oral anticoagulants
cyclosporine

30
Q

how do fibrates increase the amount of lipoprotein lipase

A

bind to receptor and increase transcription of LPL

31
Q

what effects does nicotinic acid have

A

low doses increases HDL levels

higher doses decrease VLDL and triglyceride levels

32
Q

how does niacin decrease hepatic VLDL production

A

activates niacin receptors in adipocytes decreases cAMP which decrease triglyceride hydrolysis causing less fatty acid in circulation to be taken up by liver(which means less converted to TG and secreted as VLDL)

33
Q

how does niacin increase VLDL clearance

A

increases lipoprotein lipase activity

34
Q

adverse effects of niacin

A

skin flushing and itching

increase aminotransferase or alkaline phosphatase

35
Q

contraindications of niacin

A

peptic ulcer

diabetes due to glucose intolerance

Pharmacology part B (17 decks)

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