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PHRM 844 Exam 5 LOs > Hockerman Dyslipidemia > Flashcards

Hockerman Dyslipidemia Flashcards

1
Q

what are the major classes of lipoproteins?

A
  1. chylomicrons
  2. VLDL
  3. IDL
  4. LDL
  5. HDL
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2
Q

what are chylomicrons and what is its size and composition like compared to other lipoproteins?

A
  1. involved in transport of dietary lipids from gut to liver and adipose tissue
  2. they are the biggest
  3. they are mostly triglycerides
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3
Q

what are VLDLs and what is its size and composition like compared to other lipoproteins?

A
  1. secreted by liver into blood as a source of triglycerides
  2. the second biggest particle
  3. mae mostly of triglycerides and cholesterol
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4
Q

what are LDLs and what is its size and composition like compared to other lipoproteins?

A
  1. main cholesterol form in blood
  2. third biggest
  3. mostly cholesterol
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5
Q

what are HDLs and what is its size and composition like compared to other lipoproteins?

A
  1. secreted by the liver & acquire cholesterol from peripheral tissues & atheromas (reverse cholesterol transport)
  2. smallest
  3. mostly protein and equal balance of phospholipids and cholesterol
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6
Q

what are IDLs?

A

triglyceride-depleted VLDLs

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7
Q

what are the important apolipoproteins?

A
  1. ApoA-1
  2. ApoB-48
  3. ApoE
  4. ApoC2
  5. ApoB-100
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8
Q

what is ApoA-1 and what does it do? where is it produced?

A
  1. In HDL; mediates reverse cholesterol transport
  2. liver and intestine
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9
Q

what is ApoB-48 and where is it produced?

A
  1. chylomicrons and in intestine
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10
Q

what is ApoE and where is it produced?

A
  1. LDL ligand; reverse cholesterol transport with HDL
  2. liver and intestine
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11
Q

what is ApoC2 and what does it do?

A
  1. in chylomicrons and VLDL
  2. binds to lipoprotein lipase to enhance TG hydrolysis
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12
Q

what does the exogenous pathway do for lipid absorption transport?

A
  1. fat & cholesterol get absorbed from lumen into intestine
  2. this forms chylomicrons
  3. those travel through circulation and get broken down by FFAs
  4. distributed to tissues
  5. chylomicron remnants get taken back up into the liver
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13
Q

what does the endogenous pathway do for lipid absorption transport?

A
  1. starts in liver and secreted VLDL
  2. VLDL is broken down by LPL
  3. this can get distributed to cells and form into LDLs
  4. VLDL in circulation turn into FFAs
  5. LDLs in the peripheral tissues get taken back up into the liver via LDL receptor
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14
Q

What are the two factors the play a role in lipid metabolism via absorption and transport?

A

ApoE and ApoB mediated

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15
Q

What is the central role of the liver in the cholesterol synthesis and distribution?

A

the liver synthesis of de novo synthesis is the major source of cholesterol into LDLs. This happens in the liver to total body burden

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16
Q

what are the two diseases associated with lipoprotein disorders?

A
  1. hyperlipoproteinemia
  2. hypertriglyceridemia
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17
Q

what is associated with hyperlipiproteinemia?

A
  1. atherosclerosis
  2. premature CAD
  3. stroke - neurologic disease
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18
Q

what is associated with hypertriglyceridemia?

A
  1. pancreatitis
  2. xanthomas
  3. increased risk of CHD
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19
Q

How does atherosclerosis occur?

A
  1. stress or oxidative damage to endothelium –> infiltration of monocytes into lumen
  2. causing upregulation of endothelial molecules
  3. monocytes stick to endothelium
  4. they move to inima
  5. turn into macrophages –> leads to foam cells
  6. oxidized LDL can release cytokines that stimulate the proliferation and hypertrophy of smooth muscle cells into intima forming foam cells
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20
Q

What drugs are in the BAR class?

A

colestipol (Colestid)
cholestyramine (queastran)

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21
Q

what is the MOA, target, and SEs for BARs?

A

MOA: inhibit reabsoprtion of bile acids from the intestine by binding to them and forming insoluble complex excreted in feces
TARGET: up-regulate LDL receptors in liver
SEs: constipation & bloating and may inc. TG

22
Q

what is Ezetimibe (zetia)? what is the MOA, target, and SEs?

A
  1. cholesterol absorption inhibitor
  2. inhibits NPC1L-1
    –> enterocytes in liver
  3. AEs: low incidence of liver/skeletal muscle damage
23
Q

What drug class is statins?

A

HMG-CoA reductase inhibitor

24
Q

where did statins get their structure from?

A

mavalonic acid

25
Q

what statins are prodrugs?

A

lovastatin and simvastatin

26
Q

what statin was isolated from aspergillus terreus?

A

lovastatin

27
Q

why do statins bind to HMG-CoA reductase?

A

it is the rate-limiting enzyme in cholesterol synthesis

28
Q

what are the indications for statins?

A
  1. hypercholesterolemia
  2. initiate after MI
29
Q

what statins are given in the evening? why?

A

short HL drugs to inhibit nocturnal cholesterol synthesis

30
Q

what statins interact with CYP3A4 and what are examples?

A
  1. simvastatin, atrovastatin, lovastatin
  2. grapefruit juice
31
Q

what statins interact with CYP2C9 and example?

A

fluvastatin and rosuvastatin
1. amiodarone

32
Q

what statin interacts with sulfation?

A

pravastatin

33
Q

what statin undergoes enterohepatic recirculation and excreted unchanged in the bile?

A

pitavastatin

34
Q

what are the AEs of statins?

A
  1. rhabdomyolysis
  2. hepatotoxicity
  3. increased T2DM risk
35
Q

What is this statin?

A

atorvastatin

36
Q

what is bempedoic acid (nextolol)? (use and side effects)

A
  1. adjunct to statin
  2. ATP-citrate lyase inhibitor (ACL)
  3. reduced LDL with statin for patients with HeFH or ASCVD
  4. GOUT is side effect
37
Q

what is the mechanism of PSCK9 inhibitors?

A

they promote degradation of LDL receptors in the liver

38
Q

what are PSCK9 inhibitor drugs, what do they do?

A
  1. Praluent (alirocumab)
    –> q2wks
  2. Repatha (evolocumab)
    –> q2wks or 4wks
  3. they increase LDLr # and reduce serum LDL-c levels
39
Q

what is special about leqvio (inclisiran) what is its use?

A
  • siRNA- hybridizes PSCK9 mRNA and directs degradation in hepatocytes
  • used in adjunct to statins for HeFH & ASCVD
40
Q

why are drugs that lower cholesterol beneficial in patients with HeFH?

A
  1. LDL-r function reduced
  2. B100 binding to LDLR reduced
  3. PSCK9 activity increased
41
Q

what is Juxtapid (lomitapide)? what is its mechanism and incdication?

A
  1. inhibits ApoB synthesis in BOTH liver and intestine
  2. interferes with chylomicrons and VLDL
  3. used for HeFH- LDL-R mutation
    * does not require LDL-R
42
Q

what is mipomersen (kynamro)? What is it used for? what is a severe risk?

A
  1. inhibits ApoB synthesis
    –> it is a anti-sense inhibitor
  2. for HeFH
  3. can cause hepatic steatosis(rx program)
    * only liver no intestine effect
43
Q

what is evinacumab (evkeeza)? What is its mechanism? what is its use?

A
  1. inhibits Angiopoietin-like protein 3
  2. HeFH tx
  3. does not require LDL-R
    – mechanism is through ANGPTL3 in an LDL-R independent manner through the remnant receptor
44
Q

what are drugs that are fibrate derivatives?

A
  1. gemfibrozil
  2. fenofibrate
45
Q

what are fibric derivatives doing? what is their effect on a lipid panel? what are interactions and SEs?

A
  1. PPARa
    –> regulate gene transcription along the RXR.
  2. PANEL
    –> LDL: reduce
    –> HDL: elevate
    –> TGs: reduce
  3. SEs: rhabdomyolysis (use in caution in statins)
  4. DI: warfarin
46
Q

which fibrate is a prodrug?

A

fenofibrate

47
Q

What class is this?

48
Q

what is niacin?

A
  1. reduce triglycerides by decreasing FFA by directly inhibiting DGAT2
49
Q

what are the three targets for niacin? What do they do at each?

A
  1. adipose tissue –> decrease FA transport to liver
  2. liver –> reduce TG export via VLDL & inc. HDL level and reverses transport
  3. macrophages –> dec. CE content via HDL-mediated reverse transport
50
Q

what is the indication for niacin and its adverse effects?

A

Indication
– raising HDL levels (15-35%)
Adverse Effects
– flushing, itching, HA
–> by prostaglandin mediation so use aspirin or NSAID

PHRM 844 Exam 5 LOs (4 decks)

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