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Pharmacology Test 2 > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Cholesterol precursor for

A
  • steroid hormones
  • bile acids
  • vitamin D
    (end of cholesterol pathway)
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2
Q

Rate limiting step in Cholesterol Synthesis

A

HMGCR

- target of statins

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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
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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 **

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5
Q

Familial-Hypercholesterolemia

A
  • Lack of LDL receptors

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

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6
Q

VLDL

A

Very low density lipoprotein

- synthesized by liver

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7
Q

IDL

A

Intermediate density lipoprotein

VLDL remnants

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8
Q

LDL

A

Low density lipoprotein

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9
Q

HDL

A

High density lipoprotein

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10
Q

FFA

A

Free Fatty Acids

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11
Q

LPL

A

Lipoprotein lipase

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12
Q

SREBP

A
  • sterol regulatory element binding protein
  • transcription factor
  • MASTER REGULATOR OF CHOLESTEROL LEVELS IN CELL
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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
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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
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15
Q

Adipose Lipolysis

A
  • inhibits adipose glycolysis

- less fat released

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16
Q

Statins

A

HMG-CoA Reductase Inhibitors

  • most effective and best-tolerated
  • agents for treating dyslipidemia
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17
Q

HMG-CoA Reductase Inhibitors

A

Statins

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18
Q

PCSK9 Inhibitors

A

-mab

monoclonal antibody

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19
Q

Cholesterol Absorption Inhibitor

A

Ezetimibe

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20
Q

Bile Acid Sequestrants

A

Resins

Chol-

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21
Q

Acid Citrate Lyase Inhibitor

A

Bempedoic Acid

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22
Q

Geranylgeranyl-PP

Farensyl-PP

A

Prenylated Proteins

  • heme a
  • dilichol
  • ubiquinone
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23
Q

Total serum cholesterol should be lower than

24
Q

Chylomicrons

A
  • synthesized by the intestine
  • converted to remnants by hydrolysis
  • rapidly cleared from plasma by the liver
25
Apo B100
how lipoproteins are taken up by peripheral tissues | - cause plaque
26
Cholesterol delivery to cells
- 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
LDL Receptors V Important
without LDL & IDL will NOT be taken up; excess amounts will be in circulation (occurs when receptors genetically defective)
28
Bempedoic Acid
- inhibits Acetyl CoA synthesis
29
HMG-CoA reductase | rate
- rate limiting step | - inhibited by statins
30
Mevalonate Synthesis
- inhibited by statins | - inhibit HMG CoA reductase
31
PCSK9 Inhibitors
- inhibit degradation of LDL receptors
32
Niacin
- inhibit adipose lipolysis | - less fat released
33
Fibrates
- stimulate PPARa | - increase LDL (upregulate)
34
Gemfibrozil
fibrate
35
Ezetimibe
- cholesterol absorption inhibitor | - inhibits cholesterol absorption into body from gut
36
Cholestyramine
- bile acid resin | - inhibits bile acid resorption from gut
37
Effect of statins on LDL receptors and circulating LDL levels
- 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
Statins | mechanism of action
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
Statins (therapeutic use) - contraindication
- 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
Atorvastatin & Rosuvastatin
- longest t1/2 - most efficacious for sever hypercholesterolemia - more TG lowering activity compared to other statins
41
Statins | toxic/adverse effects
- hepatotoxicity (rare and unpredictable) - Diabetes mellitus - -- slight risk of new on-set; outweighed by statin benefits for patients with cardiovascular risk - myopathy: reversible
42
Increased Simvastatin plasma levels =>
increased risk of myopathy
43
PCSK9 Inhibitors
- 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
Evolocumab
STRONGEST - PCSK9 inhibitor - t1/2: 11-17 days
45
Alirocumab
- PCSK9 inhibitor | - t1/2 12 days
46
Ezetimibe
- cholesterol absorption inhibitor - blocks NPC1L1 cholesterol transporter * ** blocks uptake of cholesterol micelles from intestine ***
47
Ezetimibe | mechanism of action
- 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
Bile Acid Sequestrants
- resins | - take up bile salts
49
Bile Acid Sequestrants | mechanism of action
- 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
Resin induced bile production leads to increase in hepatic TG synthesis
USE EXTREME CAUTION OR AVOID in patients with sever hypertriglyceridemia
51
Bile Acid Sequestrants | take with
- 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
Bile Acid Sequestrants | adverse effects
GI Symptoms
53
Kepone & Brodifacoum
eliminated by bile acid sequestrants
54
Nexletol
Bempedoic Acid
55
Bempedoic Aid
``` 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)

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