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Therapeutics 2 - Fall 2017 > Dyslipidemia (Wendt & Gonzalvo) > Flashcards

Dyslipidemia (Wendt & Gonzalvo) Flashcards

1
Q

Apoplipoproteins Role:

ApoA-1

A

(structural in HDL)

mediates reverse of cholesterol transport

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2
Q

Apoplipoproteins Role:

ApoB-100

A

structural in VLDL; IDL; LDL; LDL receptor ligand made in liver

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3
Q

Apoplipoproteins Role:

ApoB-48

A

produced in intestines/structural in chylomicrons

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4
Q

Apoplipoproteins Role:

ApoE

A

does reverse cholesterol transport with HDL;

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5
Q

Apoplipoproteins Role:

ApoCIII

A

inhibits LPL and interferes w/ ApoB and ApoE binding to hepatic receptors

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6
Q

ApoB48 will be found on ______

A

chylomicrons

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7
Q

ApoB-100 will be found on _______

A

VLDLs; IDLs; LDLs

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8
Q

Ratio of what two things is important for assessing CVD risk (per Wendt lecture)

A

ratio of Total Cholesterol: HDL cholesterol

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9
Q

Diseases assoc. with Hypertriglyceridemia

A

Pancreatitis
Xanthomas
Increased risk in CHD

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10
Q

Diseases assoc. w/ Hypoerlipoproteinemia

A

Atherosclerosis
Premature CAD
Neurologic disease- stroke

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11
Q

What TC:HDL ratio is considered increase risk for CVD

A

> 4.5

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12
Q

There are ____ receptors on endothelial cells - helps lead to atherosclerosis

A

LDL

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13
Q

Atheroslerosis

LDL in blood gets into ________ which leads to ______ cells then _______

A

monocytes; foam cells; fatty streak

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14
Q

How Statins Increase LDL Receptors:

Statins cause there to be less ______ in the blood, therefore the _______ are no stuck anymore and can go _______

A

cholesterol(sterols); proteases (arent stuck anymore); go cleave transcription factors (that will increase LDL receptor transcription)

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15
Q

which statins should be taken in the evening with meals (for absorption)

A

Simvastatin and Lovastatin

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16
Q

which statins have CYP3A4 metabolism?

A

Simvastatin; Lovastatin; Atorvastatin

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17
Q

which statin does not have metabolism via CYP enzyme? and how is it metabolized?

A

pravastatin; sulfation!

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18
Q

what is Zetia’s MOA?

A

inhibits NPC1L1 – aka will inhibit intestinal absorption of cholesterol from dietary sources and reabsorption of cholesterol in the bile

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19
Q

what drugs inhibit Apo B lipoprotein synthesis

A

Lomitapide; Mipomersen

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20
Q

what is the fibrate class of drugs’ MOA?

A

fibrate binds to PPAR-alpha and aso RXR; all of that binds to PPRE with drives LPL expression! it also increase expression of ApoA1 (aka HDL expression)

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21
Q

what is PSCK9s normal job (not talking about drugs)

A

PCSK9 = promotes degradation of LDL receptors in the liver

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22
Q

MOA for Omega 3 fatty acids

A

inhibits synthesis of TGs in liver –bc it is a poor substrate for enzymes that make TGs

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23
Q

Niacin will reduce TGs by:

  • increase ______ activity to increase _____ clearance
  • decrease _______ production
  • strongly increase _______ levels
A

increase Lipase; increase VLDL clearance

decrease VLDL production

increase HDL levels

24
Q

Niacin works in ______ tissue and which organ?

A

adipose; liver

25
Q

Niacin:

works in adipose tissue by decreasing Fatty Acid transport to liver by _________

A

inhibiting TG lipolysis by hormone sensitive lipase

26
Q

Niacin:

works in liver by inhibiting ________ and ______

A

fatty acid synthesis and esterification

27
Q

what things can reduce HDL

A
  • smoking
  • T2DM
  • Obesity
  • Malnutrition
  • Drugs (anabolic steroids and Beta blockers)
28
Q

what things can lead to elevated LDL

A
  • hypothyroidism
  • nephrotic syndrome
  • cholestasis
  • anorexia nervosa
  • Drugs: Thiazides; cyclosporine; tegretol
29
Q

steps for Pathogenesis of Atherosclerosis:

A
  • endothelial injury
  • inflamm. response
  • macrophage infiltraiton
  • platelet adhesion
  • smooth muscle proliferation
  • extracellular muscle accumulation
30
Q

Common signs for dyslipidemia

A
  • pancreatitis
  • eruptive xanthomas
  • peripheral polyneuropathy
  • increased BP
  • Waise Size
    (> 40 in in men; > 35 in women)
  • BMI > 30 kg/m^2)
31
Q

Common Sx of Dyslipidemia

A
  • chest pain/palpitations
  • Sweating/anxiety/SOB
  • Loss of consciousness
  • Difficulty w/ speech or movement
  • abdominal pain
  • sudden death
32
Q

how to calculate LDL

A

LDL = TC - HDL - TG/5

33
Q

what lab parameters are used for dyslipidemia

A

HDL; TC; TG; LDL

34
Q

what things are needed for BOTH Framingham and Pooled cohort eqns

A
  • gender
  • age
  • HDL
  • Systolic BP
  • Tx for HTN
  • Smoking
  • Total Cholesterol
35
Q

what things are needed for pooled cohort eqn and NOT framingham

A

race; diabetes

36
Q

Statins and Muscle Injury:

if CK is ______ times the upper limit - stop the statin!

A

10

37
Q

why is grapefruit juice a possible issue with statins

A

grapefruit juice is a CYP3A4 inhibitor - will elevate statin levels — higher risk of muscle injury

38
Q

when to monitor Statins?

A

baseline
4 - 12 weeks after starting statin initiation
every 3 - 12 months as clinically indicated

39
Q

ADEs of Bile acid resins

A

impaired absorption of fat soluble vitmains
hypernatremia
hyperchloremia
GI obstruction

40
Q

Niacin will
_____ LFTs
and lead to _____uricemia and ______glycemia
_____ statin levels

A

increase;
hyper; hyper;
increase

41
Q

Fibrates will increase the levels of what drugs

A
  • statins
  • zetia
  • sulfonylureas
  • warfarin
42
Q

which lipid drug is an oligonucleotide inhibitor of ApoB-100 synthesis

A

Mipomerson

43
Q

which lipid drug is an inhibitor of a triglyceride transfer protein

A

lomitapide

44
Q

what are guidelines used for Lipid therapy

and in the order they were implemented

A 
NECP
ACC/AHA
NLA
ACC - non statin
NLA - PCSK9
45
Q

what are 4 statin benefit groups

A
  • Clinical ASCVD
  • LDL > 190
  • Diabetes and ages 40 - 75
  • ASCVD risk > 7.5% and ages 40 - 75
46
Q

if someone has clinical ASCVD what type of statin should they be on

A

if > 75 yo - moderate intensity

if < 75 yo - high intensity

47
Q

if someone is b/w ages 40 - 75 and has diabetes what type of statin should they be on

A

if ASCVD risk > 7.5% - high intensity

if ASCVD risk < 7.5% - moderate intensity

48
Q

if someone has an LDL > 190 and has diabetes what type of statin should they be on

A

high intensity

49
Q

what are the high intensity statins

A

ator. 40 - 80

rosuv 20 - 40

50
Q

what are the major risk factors for ASCVD (for NLA statin)

A
  • Age: M > 45; W > 55
  • HDL: M < 40; F: 50
  • HTN?
  • Smoker?
  • FH of early CHD: first degree relative —- M: < 55; F < 65
51
Q

goals for NON- HDL and LDL if put into NLA VERY high risk group

A

NON-HDL < 100

LDL < 70

52
Q

goals for NON- HDL and LDL if put into NLA low, mod, or high risk group

A

NON-HDL < 130

LDL < 100

53
Q

NLA Guidelines:

Who is low risk

A

0 - 1 major risk factor

54
Q

NLA Guidelines:

who is mod risk

A

2 major risk factors + ASCVD risk b/w 5 - 15%

55
Q

NLA Guidelines:

who is very high risk

A

Clinical ASCVD
OR
DM with 2+ Risk Factors

56
Q

NLA Guidelines:

who is high risk

A
  • CKD 3B/4
  • LDL > 190
  • DM w/ 0 - 1 risk factors
  • 3+ risk factors
  • 2 risk factors + (pooled: > 15%; framingham >10%)

Therapeutics 2 - Fall 2017 (22 decks)

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