Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology Test 2 > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Cholesterol precursor for

A
  • steroid hormones
  • bile acids
  • vitamin D
    (end of cholesterol pathway)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Rate limiting step in Cholesterol Synthesis

A

HMGCR

- target of statins

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

Coronary Heart Disease and Risk Factors

A
  • high blood cholesterol/triglycerides
  • high blood pressure
  • high blood sugar/type II diabetes
  • smoking
  • gender/age/family history
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Low LDL-C

time

A

the longer and lower the reduction in circulating LDL-C, the lower the incidence of CHD
** duration of LDL-C reduction v. important **

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

Familial-Hypercholesterolemia

A
  • Lack of LDL receptors

- IDL & LDL not taken up; excess amount in system

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

VLDL

A

Very low density lipoprotein

- synthesized by liver

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

IDL

A

Intermediate density lipoprotein

VLDL remnants

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

LDL

A

Low density lipoprotein

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

HDL

A

High density lipoprotein

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

FFA

A

Free Fatty Acids

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

LPL

A

Lipoprotein lipase

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

SREBP

A
  • sterol regulatory element binding protein
  • transcription factor
  • MASTER REGULATOR OF CHOLESTEROL LEVELS IN CELL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Low-cholesterol diet

A

SREBP activated

  • increased cholesterol biosynthesis
  • increased receptor mediated LDL endocytosis from plasma (cholesterol uptake into cell)
  • decreased plasma LDL
  • increased transcription of
  • – LDL receptors
  • – HMGCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

High-cholesterol diet

A 
SREBP not activated
- decreased cholesterol biosynthesis
- decreased LDL receptors
*** plasma LDL remains high ***
(higher cholesterol in blood)
  • fewer LDL receptors
  • decreased HMGCR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Adipose Lipolysis

A
  • inhibits adipose glycolysis

- less fat released

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

Statins

A

HMG-CoA Reductase Inhibitors

  • most effective and best-tolerated
  • agents for treating dyslipidemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

HMG-CoA Reductase Inhibitors

A

Statins

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

PCSK9 Inhibitors

A

-mab

monoclonal antibody

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

Cholesterol Absorption Inhibitor

A

Ezetimibe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Bile Acid Sequestrants

A

Resins

Chol-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Acid Citrate Lyase Inhibitor

A

Bempedoic Acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Geranylgeranyl-PP

Farensyl-PP

A

Prenylated Proteins

  • heme a
  • dilichol
  • ubiquinone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Total serum cholesterol should be lower than

A

200

24
Q

Chylomicrons

A
  • synthesized by the intestine
  • converted to remnants by hydrolysis
  • rapidly cleared from plasma by the liver
25
Q

Apo B100

A

how lipoproteins are taken up by peripheral tissues

- cause plaque

26
Q

Cholesterol delivery to cells

A
  • ribosomes make LDL receptors
  • transported golgi -> membrane
  • LDL bind to LDL receptor and are taken in
  • – clathrin coated pit -> vesicle -> endosome
  • ** LDL -> Lysosome ***
  • ** LDL receptors recycled back to membrane ***
27
Q

LDL Receptors V Important

A

without LDL & IDL will NOT be taken up; excess amounts will be in circulation
(occurs when receptors genetically defective)

28
Q

Bempedoic Acid

A
  • inhibits Acetyl CoA synthesis
29
Q

HMG-CoA reductase

rate

A
  • rate limiting step

- inhibited by statins

30
Q

Mevalonate Synthesis

A
  • inhibited by statins

- inhibit HMG CoA reductase

31
Q

PCSK9 Inhibitors

A
  • inhibit degradation of LDL receptors
32
Q

Niacin

A
  • inhibit adipose lipolysis

- less fat released

33
Q

Fibrates

A
  • stimulate PPARa

- increase LDL (upregulate)

34
Q

Gemfibrozil

A

fibrate

35
Q

Ezetimibe

A
  • cholesterol absorption inhibitor

- inhibits cholesterol absorption into body from gut

36
Q

Cholestyramine

A
  • bile acid resin

- inhibits bile acid resorption from gut

37
Q

Effect of statins on LDL receptors and circulating LDL levels

A
  • HMGCR inhibited -> inhibits cholesterolgenesis
  • increase expression of LDL receptors
  • Increase removal of LDL (VLDL, IDL) from blood
  • decrease hepatic CLDL production
  • SREBP is upregulated because of inhibition of HMGCoA reductase which lowers cholesterol which is made in cell, and increases cholesterol absorbed from blood
38
Q

Statins

mechanism of action

A

Competitive inhibitors of HMG-CoA Reductase

  • inhibit cholesterolgenesis
  • increase expression of LDL receptors
  • increase removal of LDL (VLDL, IDL) from blood
  • decrease hepatic VLDL production

LDL-C levels lowered by 20-55%

39
Q

Statins
(therapeutic use)
- contraindication

A
  • alone or in combination with resins or ezetimibe
  • CONTRAINIDCATED in women who are/want to be pregnant
  • some indicated in children with familial hypercholesterolemia
40
Q

Atorvastatin & Rosuvastatin

A
  • longest t1/2
  • most efficacious for sever hypercholesterolemia
  • more TG lowering activity compared to other statins
41
Q

Statins

toxic/adverse effects

A
  • hepatotoxicity (rare and unpredictable)
  • Diabetes mellitus
  • – slight risk of new on-set; outweighed by statin benefits for patients with cardiovascular risk
  • myopathy: reversible
42
Q

Increased Simvastatin plasma levels =>

A

increased risk of myopathy

43
Q

PCSK9 Inhibitors

A
  • monoclonal antibodies against PCSK9 protein
  • injected
  • with PCSK9, LDL receptor directed to lysosome => degraded (rather than recycled back to surface)
  • ** when PCSK9 INHIBITORS LDL receptors are saved and recycled back to surface, thus decreasing plasma LDL levels)
44
Q

Evolocumab

A

STRONGEST

  • PCSK9 inhibitor
  • t1/2: 11-17 days
45
Q

Alirocumab

A
  • PCSK9 inhibitor

- t1/2 12 days

46
Q

Ezetimibe

A
  • cholesterol absorption inhibitor
  • blocks NPC1L1 cholesterol transporter
  • ** blocks uptake of cholesterol micelles from intestine ***
47
Q

Ezetimibe

mechanism of action

A
  • selectively inhibits intestinal cholesterol absorption
  • targets NPCL1 transport
  • – decreases intestinal delivery of cholesterol to the liver
  • – increases expression of hepatic LDL receptors
  • – decreases cholesterol content of atherogenic particles
  • average reduction in LDL-C is ~18%
  • – with statins: additional 25%
48
Q

Bile Acid Sequestrants

A
  • resins

- take up bile salts

49
Q

Bile Acid Sequestrants

mechanism of action

A
  • increase bile acid excretion; less bile acid absorbed
  • – highly + charge binds - charged bile and makes too large to be absorbed
  • increase hepatic bile-acid synthesis (because less amount taken up by blood)
  • – hepatic cholesterol content declines
  • – LDL receptors increased in hepatocytes
  • – increased LDL clearance from plasma
  • net effect: decrease of LDL-C
  • HMG-CoA reductase upregulated
  • increased cholesterol synthesis partially offsets reduction in LDL-C
  • coadministered with statin
50
Q

Resin induced bile production leads to increase in hepatic TG synthesis

A

USE EXTREME CAUTION OR AVOID in patients with sever hypertriglyceridemia

51
Q

Bile Acid Sequestrants

take with

A
  • meal or no effect (need bile present in order to be able to bind to it)
  • ** take at least 4 hours before or after other medications (can interfere with absorption) ***
52
Q

Bile Acid Sequestrants

adverse effects

A

GI Symptoms

53
Q

Kepone & Brodifacoum

A

eliminated by bile acid sequestrants

54
Q

Nexletol

A

Bempedoic Acid

55
Q

Bempedoic Aid

A 
ATP Citrate Lyase Inhibitor
- used in combo with statins
- indication: adjunct to diet and maximally tolerated statin therapy
ORAL (advantage over PCSK9 Inhibitors)
- 12-18% reduction in LDL-C

Pharmacology Test 2 (8 decks)

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