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Cardio Module > Drug therapy in the treatment of hyper lipoproteinemias > Flashcards

Drug therapy in the treatment of hyper lipoproteinemias Flashcards

1
Q

what are two roles of apolipoproteins

A
  • ligands for cellular receptors… act as almost a zip code mechanism
  • cofactors for various enzymes involved in lipoprotein metabolism
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2
Q

Name some physiologic functions of lipoproteins

A
  1. help to transport lipids, triglycerides, and cholesterol in the circulatory system
  2. supply energy to muscle
  3. provide cholesterol for synthesis of steroid hormones, bile acids, and cell membrane synthesis
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3
Q

Biggest lipoprotiens have the ____density

A
  • lowest
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4
Q

Name the important lipoproteins from least to most dense

A
  • Chylomicrons
  • VLDL
  • LDL
  • Lp(a)
  • HDL
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5
Q

what lipoprotein is the most involved in disease?

A
  • LDL
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6
Q

Hyperlipoproteinemas are associated with what condition?

A
  • atherosclerosis
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7
Q

atherosclerosis is related to what two conditions?

A
  • coronary heart disease

- stroke

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8
Q

LDL does not contain a lot of ____ but contains a lot of ______

A
  • Triglycerides; cholesterol
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9
Q

give the pathophys of hyperlipidemia with LDL

A
  • LDL oxidized in subendothelial space to give inflammatory response via activation of foam cells
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10
Q

How does HDL lower cholesterol?

A
  • binds cholesterol and promotes reverse cholesterol transport from tissues to liver
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11
Q

What three beneficial properties does HDL have?

A
  1. anti-inflammatory
  2. anti-oxidant
  3. anti-thrombotic
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12
Q

What enzyme is responsible for breaking down lipoproteins?

A
  • Lipoprotein lipase, into free fatty acids and either remnants in the exogenous, or IDL in the endogenous
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13
Q

what are two fates of LDL in normal metabolism?

what would be a pathological fate

A
  1. uptake into liver
  2. uptake into extra hepatic tissue

accumulation of LDL in the subendothelial space

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14
Q

what is LDL-receptor gene regulated by?

A
  • amount of cholesterol and other sterols in the body
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15
Q

Describe role of SCAP?

A
  • sterol sensing domain; cholesterol inhibits SCAP-SREBP complex to golgi for processing to active transcription factor; if sterol is present, no processing to become an active transcription factor
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16
Q

Name 4 challenged in pharmacotherapy of hyperlipediemias?

A
  1. inadequate changes in lipid profiles ( so just the efficacy of the drug)
  2. patient tolerance of drug (toxicity)
  3. variations in genotype
  4. multiple dyslipeidemias
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17
Q

What is the most common inhibitor of cholesterol synthesis

A
  • Statins ( reversible competible inhibitor of HMG CoA reductase )
18
Q

What is the result biochemically of statins

A
  • no mevalonate from HMG CoA… lower cholesterol synthesis so you decrease VLDL levels
19
Q

what is the result of stains on LDL receptors?

A
  • Statins inhibit cholesterol synthesis; decrease C levels in the liver and you get more LDL receptors TO INCREASE LDL RECEPTORS!
20
Q

what specific statin is the best at LDL lowerin?

A
  • Crestor (rosuvastatin)
21
Q

what is the result of statins in HDL?

A
  • increases it
22
Q

what are the side effects of statins

A
  • muscle complaints (from myalgia to rhabdomyolysis)
  • memory loss
  • Type II diabetes
23
Q

What other factors besides HMG-CoA reductase inhibition might affect ability of individual statins to lower LDL (3 of them)

A
  1. dose limiting adverse reactions
  2. differentaial hepatic uptake via SLCO1B1
  3. metabolism/bioavailability
24
Q

What is hte main inhibitor of LDL-R degradatin?

A

PCSK9 inhibitor

25
Q

what are the indications of PCSK9 inhibitor

A
  • therapeutic monoclonal antibody indicated for:
  1. heterozygous familial hypercholesterolemia
  2. pts with stroke/heart attack
  3. pts who can’t tolerate statins or they don’t work well
26
Q

what is the result of statins (at higher doses) to PCSK9?

A
  • Increases levels
27
Q
  • mechanism of action of PCSK9 inhibitor?
A
  • PCSK9 binds to LDL-R on hepatocyte surface to direct them to lysosome for degradation and prevent LDL-R recycling
  • by inhibiting them, you don’t get as much directing for lysosome degradation, so more LDL receptors are available
28
Q

what is the main agent used for inhibition of bile acid absoprtion

A

bile acid seqestrants (Cholestyramine)

29
Q

mechanism of action of cholestyramine

secondary effects on LDL?

A
  • reduce hepatic bile acid fuel and make you use more cholesterol to make more bile acid, which decreases intraheaptic cholesterol pool

Increase LDL receptors, Increase LDL clearance
Decrease LDL in plasma

30
Q

what is side effect of cholestyramien and why?

A
  • decrease drug and fat soluble vitamin absorption because of nonspecificity.. .and can even bind other drugs to make drug-drug intearctions
31
Q

WHat is the prototype cholesterol uptake inhibitor?

A
  • Ezetimibe
32
Q

mechanism of action of zetia

A
  • inhibits cholesterol uptake through NPC1L1 from the diet to decrease serum LDL
33
Q

why combine with statin

A
  • because if you aren’t getting cholesterol from diet, the liver will want to make more cholestrowl.. .stop this with statin
34
Q

Hypertriglyceridemia is a(n) ______ risk factor for CV disease

A
  • independent
35
Q

What is a major inhibitor of trigylceride synthesis? and give MOA

A
  • Niacin (vitamin B3)
  • acts on GPCR at fat cells to inhibit triglyceride breakdown in adiposte tissue
  • also inhibits DGAT2 at liver to decrease TG synthesis
  • without ttis, you don’t have VLDL, and VLDL is needed to make LDL so you have a lowering of LDL (AKA Reduce VLDL production and secretion by liver)
36
Q

what is the effect of niacin on HDL?

A
  • elevates it via inhibition of Apo-A1 clearance
37
Q

Side effects of niacin

A
  1. intense flushing
  2. HYPERURICEMIA
  3. impaired insulin sensitivity
38
Q

What do fibrate derivates do?

A
  • bind to PPARalpha (nuclear receptor) so that you cannot do transcription that is required for lipoprotein metabolism, as well as inflammatory responses
39
Q

What is the role of omega-3 polyunstaurated fatty acids

A
  • serve as ligands for the nuclear receptor PPARalpha… act like fibrate derivates by binding to PPARalpha and decreasing TG count and inflammatory response
40
Q

When do we typically think about using fibrate derivates/omacor?

A
  • when TG levels are greater than 500 mg/dL
41
Q

Give 3 effects of Omacor for cholesterol synthesis in body

A
  1. inhibits TG synthesis
  2. stimulates fatty acid oxidation
  3. Reduces VLDL production/secretion

Cardio Module (25 decks)

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