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The Science of Lipidology: Lipid Metabolism, Pathogenesis of Atherosclerosis and Genetic Disorders > Module 1: Deck3/Cards 16-20 > Flashcards

Module 1: Deck3/Cards 16-20 Flashcards

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1
Q

Common causes of low HDL? 12

A
  1. Visceral obesity (often associated with physical inactivity
  2. insulin resistance)
  3. type 2 diabetes and
  4. HIV.
    (But wouldn’t expect severe)
  5. High carbohydrate, low-fat diets
  6. Diet rich in polyunsaturated fats
  7. Hypertriglyceridemia
  8. Metabolic syndrome
  9. Cigarette smoking
  10. Severe stress states i.e. sepsis or burns
  11. Liver disease
  12. Renal insufficiency
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2
Q

Drugs associated with low HDL? 6

A
  1. Isotretinoin
  2. Sirolimus
  3. Protease inhibitors
    Lower by causing hypertriglyceridemia
  4. Androgenic steroids
  5. Nonselective beta-blockers
  6. Recombinant interleukin-2
    Lower by directly altering HDL metabolism by activation of hepatic lipase.
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3
Q

Severe HDL deficiency, defined as below 20mg/dL, may be cause by genetic defects affecting HDL metabolism including mutations of what?

How do they cause low HDL?

A
  1. apo A-I deficiency
  2. ABCA1
  3. LCAT deficiency

inability to form mature HDL particles

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4
Q

What medications can cause idiosyncratic reactions causing low HDL (high TG)? 2

A
  1. thiazolidinediones (TZDs, Rosiglitazone, Pioglitazone)
  2. fibrates

Also separately paraproteinemias.

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5
Q

Causes of severe HDL deficiency? 16

A
  1. Moderate to severe hypertriglyceridemia
  2. Critical illness, including sepsis, burns, small bowel exclusion
  3. Anabolic steroid
  4. Acquired L cat deficiency (possibly decreased ApoA-I synthesis)
  5. Severe cholestasis
  6. Cholestatic liver disease with liver failure
  7. Alcoholic hepatitis
  8. Acute viral hepatitis
  9. Alcoholic cirrhosis
  10. Cholesterol deficiency
  11. Partial hepatectomy
  12. Recombinant interleukin-2 therapy
  13. Disappearing HDL syndrome
  14. Paraproteinemia
  15. True deficiency
  16. Artifactual deficiency
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6
Q

What mutation is associated with marked HDL reduction with HDL concentrations less than 5 mg/dL?

A

a mutation of the ABC-binding cassette transporter-A1

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7
Q

How does LCAT Deficiency result in very low HDL C levels?

A

Prevents adequate lipidation of HDL particles

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8
Q

Patients with which of the following have been reported to have dysfunctional HDL particles?

A

psoriasis

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9
Q

There is evidence that HDL particles in patients with (4), carry different proteins as compared to those who do not have these condition.

A
  1. chronic inflammatory states
  2. end-stage renal disease
  3. diabetes
  4. coronary artery disease
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10
Q

Phospholipid depletion and enrichment with pro-inflammatory proteins include (2) and others may generate dysfunctional HDL particles, regardless of the HDL-C concentration?

A
  1. serum amyloid A proteins

2. apolipoprotein C-III

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11
Q

List the known functions for ApoA-I: 4

What inflammatory states affect this apolipoprotein? 3

A
  1. major protein of HDL
  2. lipid binding and transport
  3. Cofactor of LCAT
  4. Anti-oxidative properties
  5. ESRD decreases Apo A-I
  6. psoriasis, RA, decrease ApoA-1
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12
Q

List the known functions for ApoA-II: 2

What inflammatory states affect this apolipoprotein? 3

A
  1. 2nd major protein of HDL
  2. Inhibitor of hepatic lipase
  3. decreased in ESRD
  4. decreased in DM
  5. increased in psoriasis
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13
Q

List the known functions for SAA1/SAA2 : 2

What inflammatory states affect this apolipoprotein? 5

A
  1. major acute phase protein
  2. pro-inflammatory properties
  3. increases in ESRD
  4. increases in HD
  5. Increases in ACS
  6. Increases in psoriasis
  7. Increases in RA
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14
Q

List the known functions for Complement C3 : 3

What inflammatory states affect this apolipoprotein?3

A
  1. Cleaved into C3A and C3B
  2. C3a: Mediator of local inflammation
  3. C3b: Opsonizing factor
  4. Increases in CAD
  5. Increases in psoriasis
  6. Increases in RA
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15
Q

List the known functions for hemoglobin/haptoglobin : 2

What inflammatory states affect this apolipoprotein? 4

A
  1. Oxygen transport
  2. Hemoglobin pending
  3. Increases in ES RD
  4. Increases in psoriasis
  5. Increases in RA
  6. Increases in CAD
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16
Q

List the known functions for ApoAI-IV : 2

What inflammatory states affect this apolipoprotein? 2

A
  1. Modulates LPL
  2. Activator of LCAT
  3. Increases in ESRD
  4. Increases in stage
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17
Q

List the known functions for ApoC-II : 2

What inflammatory states affect this apolipoprotein? 1

A
  1. Activates LPL
  2. Inhibitor LCAT
  3. Decrease his ESRD
18
Q

List the known functions for ApoC-III : 3

What inflammatory states affect this apolipoprotein? 2

A
  1. Inhibits LPL and HL
  2. Delays TGR L catabolism
  3. Ligand of TLR2
  4. Increases in ESRD
  5. Increases CAD
19
Q

List the known functions for ApoM: 2

What inflammatory states affect this apolipoprotein? 3

A
  1. Lipid transport
  2. Binds S1P and fatty acids
  3. Decreases in ESRD
  4. decreases in diabetes
  5. decreases in stress
20
Q

List the known functions for Clusterin: 2

What inflammatory states affect this apolipoprotein? 2

A
  1. ATP independent chaperone
  2. Inhibits apoptosis
  3. Decreases in CAD
  4. decreases in diabetes
21
Q

List the known functions for PON1 activity: 1

What inflammatory states affect this apolipoprotein? 6

A
  1. hydrolyzes lactones, aromatic carboxylic acid esters, organophosphates
  2. decreases in ESRD
  3. decreases in diabetes
  4. decreases in CAD, ACS
  5. decreases in RA
  6. decreases in psoriasis
  7. decreases in heart disease
22
Q

List the known functions for Lp-PLA2 activity: 3

What inflammatory states affect this apolipoprotein? 2

A
  1. hydrolyzes PAF
  2. Ca2+ independent PLA2
  3. Phospholipid binding
  4. increases in psoriasis
  5. increases in ESRD
23
Q

Patients with which of the following have been reported to have dysfunctional HDL particles?

A

psoriasis

24
Q

What is associated with very low HDL levels but no increased risk of ASCVD?

A

Apo A-I Milano

25
Q

Process of cholesterol efflux capacity is complex because of multiple mediators involved and issues and accurate measurement of the process. There are several propose measures for cholesterol efflux in humans. Which of the following measures has the greatest evidence bases being the most important in protection of ASCVD events.

A

Non- macrophage arterial wall efflux

26
Q

How do HDL particles reduce the process of atherosclerosis? 4

A
  1. Mediation of macrophage cholesterol reflux
  2. Antioxidant capacity
  3. Anti-inflammatory properties
  4. Nitric oxide promoting activity
27
Q

HDL: Multiple components are involved in the process of reverse cholesterol transport including:
7

A
  1. Macrophage specific arterial wall efflux
  2. Nonmacrophage arterial wall reflux
  3. Nonarterial wall reflux
  4. Lipoprotein transport
  5. Hepatic cholesterol uptake (hepatobiliary excretion)
  6. Direct excretion into the small intestine
  7. Fecal excretion
28
Q

The measure of cholesterol efflux capacity felt to be most closely linked to atheroprotection is ?

A

macrophage specific arterial wall efflux

29
Q

A 60-year-old asymptomatic Japanese woman presents for consultation in the lipid clinic. She saw her primary care provider for routine physical exam and was noted to have the following results on her lipid panel. TC 260: HDL 100: TG 60: And LDL-C 148. She does not drink alcohol and takes no medication. She walks 30 minutes daily. Her family history is unknown as she was adopted. She has no history of high blood pressure, diabetes or cigarette smoking. BMI is 26. And systolic blood pressure is 140. Which of the following options were presents the current best advice to provide to the patient new primary care provider.

A

dietary intervention

30
Q

Hyperalphalipoproteinemia is characterized by what?

A

Elevated levels of apolipoprotein’s A–1 and A–2 and of HDL over 60 mg/dL.

31
Q

The differential diagnosis for hyper alpha lipoproteinemia includes? 6

A
  1. Familial hyperalphalipoprotein anemia as a primary disorder or related to deficiencies of cholesteryl ester transfer protein or hepatic lipase
  2. LCAT overexpression or APO A1 up regulation
  3. Sustained regular high intensity aerobic exercise
  4. Regular substantial alcohol intake
  5. Primary biliary cirrhosis
  6. Various medications including high-dose niacin, phenytoin, fibrate and rarely statins
32
Q

What medications can cause increased HDL? 4

A
  1. high dose niacin
  2. phenytoin
  3. fibrates
  4. statins
33
Q

Synthesis of fatty acids and cholesterol is activated by gene transcription factors called (1) . Genes encoding for the following enzymes are involved in (2).

Synthesis of fatty acids and cholesterol is required for the formation of and growth of (3). Cholesterol biosynthesis is also required for the production of (4).

Fatty acid synthesis which is driven primarily by the availability of (5), occurs in lipogenic organs such as the liver and adipose tissue. Cholesterol biosynthesis is carefully regulated by a feedback system, the purpose of which is to maintain (6).

A
  1. sterile element binding proteins (SREBPs)
  2. lipogenesis
  3. cell membranes
  4. bile acids and steroid hormones
  5. carbohydrates and hormonal factors such as insulin
  6. cellular cholesterol levels.
34
Q

The synthesis of fatty acids and cholesterol are controlled by a common family of transcription factors called SREBPs. SREBPs enter the (1) of the cell and activate transcription of genes involved in cholesterol and fatty acid synthesis by (2). SREBP target genes are all involved in lipid synthesis and are categorized as (3)

A
  1. nucleus
  2. binding the steroid regulatory elements
  3. lipogenic enzyme genes or cholesterol synthetic genes.
35
Q

SREBP-1 regulates the enzymes involved in (1).

A
  1. triglyceride and phospholipids synthesis
36
Q

SREBP-1: Its expression is down regulated by (1).

A
  1. polyunsaturated fats such as omega-3 fatty acids, a possible explanation for the triglyceride lowering effect of fish oils.
37
Q

SREBP-1: It is likely that hyperinsulinemia, by increasing SR EBP–1C expression, causes hepatic lipogenesis, resulting in (2)?

A
  1. hepatic steatosis and

2. increased secretion of the LDLs

38
Q

SREBP-2: Regulates the enzymes associated with 2.

A

cholesterol synthesis and LDL receptor expression

39
Q

SREBP-2: Reduction in hepatic cholesterol synthesis by statin therapy results in what?

A

SR ED P–2 mediated up regulation of LDL receptors

40
Q

Conversely, SR EBP–2 expression is decreased in what, resulting in decreased LDL receptor expression

A

hypothyroidism

41
Q

Genes regulated by SREBP-2 and SREBP-1c see picture

A

add figure

42
Q

The genes encoding for ATP citrate lyase, squalene synthase and lanosterol synthase are all involved in (1). The genes encoding for acetyl CoA carboxylase are involved with biosynthesis of (2)

A
  1. cholesterol synthesis
  2. triglycerides and phospholipids.

add figure

The Science of Lipidology: Lipid Metabolism, Pathogenesis of Atherosclerosis and Genetic Disorders (5 decks)

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