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IPFC 3 Final > Dyslipidemia pathophysiology > Flashcards

Dyslipidemia pathophysiology Flashcards

1
Q

What leads to Acute coronary syndrome ACS after atherosclerosis and plaque growth?

A
  1. Vulnerable plaque (thin fibrous cap)
  2. Plaque rupture –> thrombus
    - coagulation cascade starts
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2
Q

What leads to stable angina after atherosclerosis and plaque growth?

A
  1. Stable plaque (thick fibrous cap)
  2. Stable ischemia
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3
Q

Where do patients with chronic stable angina classify in (primary/secondary prevention)

A

Usually considered PRIMARY prevention
- but at higher risk than others in this group
- can sometimes be included as 2ndary prevention in some trials

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4
Q

What are the lowest density lipoproteins characterized by? Ex.?

A

Highest triglycerides, lowest protein
Chylomicrons

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5
Q

What are the functions of apolipoproteins? (3)
What are they?

A
  1. Provide the physical structure of lipoproteins
  2. Ligands for cell surface receptors
  3. Regulate enzyme activity

proteins that bind to lipids -> to form lipoproteins

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6
Q

What kind of properties to lipoproteins have? hydrophilic/hydrophobic

A

Hydrophilic properties

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7
Q

Which lipoproteins carry most of the plasma cholesterol? (2)

A

LDL
VLDL
HDL

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8
Q

Which lipoproteins carry most of the plasma triglycerides? (2)

A

Chylomicrons
VLDL

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9
Q

Which lipoproteins have the apolipoprotein of B-100? (3) function (3)? Major site of synthesis (1)

A

VLDL
IDL
LDL

All 3 functions
- Ligand for LDL receptor
- necessary for assembly and secretion of VLDL from the liver
- structural protein

Major site of synthesis: Liver

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10
Q

Which lipoprotein have the apolipoprotein of B-48 (1)? Function (1)? Major site of synthesis (1)

A

Chylomicron

Necessary for assembly and secretion of chylomicrons from the SI
- regulate enzyme

Major site of synthesis: intestine

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11
Q

Which lipoproteins have the apolipoprotein of A-1? (2) Function? (2) Major site of synthesis (2)

A

Chylomicrons
HDL

  • Cofactor with lecithin-cholesterol acetyltransferase (LCAT)
  • ligand for HDL receptor

Major site of synthesis: Liver, intestine

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12
Q

Which lipoproteins have the apolipoprotein of C-II? (3) Function? Major site of synthesis (1)

A

Chylomicrons
VLDL
HDL

Activator of lipoprotein lipase (LPL)
Major site of synthesis: Liver

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13
Q

Which lipoproteins have the apolipoprotein of Apo-E? (4) Function (1)? Major site of synthesis (1)

A

Chylomicrons
VLDL
IDL
HDL

Ligand to LDL and LDL-related protein (LRP) “remnant receptor”, possibly to a separate hepatic apo E receptor

Major site of synthesis: liver

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14
Q

Where does the exogenous pathway start? what is absorbed?

A

Starts in intestinal cell
- absorbs dietary cholesterol and fatty acids

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15
Q

What are the steps for chylomicron assembly and secretion in the intestine in EXOGENOUS pathway? (3)

A
  1. Glycerol + FFA –> triglycerides
    - Diglyceride acyltransferase (DGAT):
  2. Cholesterol esterification –> Cholesterol ester
    Acyl-coenzyme A:cholesterol acyltransferase (ACAT)
  3. Apolipoprotein B-48 is used for assembly and secretion of chylomicrons
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16
Q

What occurs to the chylomicrons in the circulation (on the way to the liver) in EXOGENOUS pathway?
What activates the enzyme used (cofactor)?
What are the products used for?

A

Chylomicrons –> chylomicron remmants + FFA
- LPL lipoprotein lipase

C-II activates LPL
FFA is used as an energy source or stored as fat

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17
Q

What occurs to the chylomicron remnant when it reaches the liver in EXOGENOUS pathway?
What is the ligand here?

A

LDL and LRP receptors in the liver (hepatocytes) absorb chylomicron remnants
- Apo E “remnant receptor”: the ligand on chylomicrons that allow entry to liver

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18
Q

Where does the endogenous pathway begin? What gets synthesized?

A

In the liver

synthesis of VLDL

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19
Q

What does the microsomal tryglyceride transfer protein MTP do in the ENDOGENOUS pathway? (3)

A

Lipids (mainly TG) + B-100 –> nascent VLDL

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20
Q

What happens to nascent VLDL?
What is transferred to VLDL

A

Apo-A,C-II, C-III, E: mature the Nascent VLDL -> VLDL
- transferred from HDL

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21
Q

What happens to mature
VLDL in the endogenous pathway?

A

Apo-CII actiabtes Lipoprotein Lipase (LPL): releases FFAs from VLDL -> VLDL remnant + FFA

22
Q

What are the 2 options that can happen to the VLDL remnants?

A
  1. VLDL remnants –> Clearance by the liver
    - LDL receptors
  2. VLDL remnants –> LDL
    - hepatic lipase
23
Q

What are options that can happen to the LDL after conversion from VLDL remnants (2)

A
  1. LDL receptors convert LDL to bile acids, sent to intestinal lumen
    OR
  2. LDL is sent to the peripheral tissues
24
Q

What happens when LDL is sent to peripheral tisues (2)

A

GOOD use: hormone production, cell membrane synthesis, storage

BAD use: LDL is oxidized, attracts monocytes (WBCs) -> foam cells -> contributes to atheromatous plaques
- This is the major contributor to plaque formation

25
Q

What is the main apo-protein for LDL

A

B100
- functions as ligand for LDL receptor

26
Q

What is LDL receptor regulated by?
What condition is absence of LDL receptor?

A

internal cholesterol balance
(by HMG CoA reductase)
Absence of LDL receptor –> familial hypercholesterolemia

27
Q

What is the reverse cholesterol transport?

A

Process by which cholesterol is transported from peripheral cells to the liver

28
Q

How is HDL produced in reverse cholesterol transport? (3 steps)

A
  1. produced by liver (hepatocytes) and gut (enterocytes) in the form of Nascent HDL (A-I)
  2. Nascent HDL obtains apolipoproteins from chylomicron and VLDL remnants
  3. Nascent HDL is then sent to the peripheries to pick up cholesterol to take back
29
Q

How does Nascent HDL get converted to mature HDL in reverse cholesterol transport? purpose?

A

through esterification of free cholesterol by lecithin-cholesterol acyltransferase (LCAT)
- A-1 activates LCAT

Purpose
- to pick up more cholesterol

30
Q

What is the role of cholesteryl ester transfer protein in reverse cholesterol transport?
What happens to HDL after?

A

transfers esterfied cholesterol to LDL and VLDL to be cleared by liver in the form of bile acids

HDL is then cleared by the liver

31
Q

What is the overall process of reverse cholesterol transport?

A

HDL takes cholesterol from peripheral tissue, esterfies it, and transfers it to LDL + VLDL to be secreted in the gut in the form of bile acids

32
Q

What is familial hypercholesterolemia: class IIa hyperlipidemia classified as?

A

Downregulation in LDL receptors –> increase in LDL levels

33
Q

Which type of class IIa hyperlipidemia is more common

A

heterozygous FH

homozygous has higher LDL and more dangerous

34
Q

What does FH class IIa hyperlipidemia susceptible to?

A

Early onset of CHD
- Due to higher susceptibility for oxidation and deposition of plaque in vascular sites

35
Q

What are physical findings of heterozygous FH? (3)

A
  1. tendinous xanthomas
    - deposit in achilles or extensor tendons
  2. Xanthelasmas
    - cholesterol deposits in the eyelids
  3. Arcus cornealis
    - deposit around corneal rim
36
Q

What does FH class IV hypertriglyceridemia classified by?

A

Mutations in the LPL gene
- VLDL elevation
- moderate elevations in triglyceride (removes FFA from triglycerides)

37
Q

What is the best treatment for familial hypertriglyceridemia

A

Fibrates

38
Q

What is the most common form of dyslipidemia?

A

Polygenic hypercholesterolemia

39
Q

What are some causes of Polygenic hypercholesterolemia? (4)

A
  • Abnormal genotype/phenotype of LDL metabolism
  • Mild defects in LDL receptor structure/function (LDL elevated)
  • Flawed Apo-B-100
  • Increased Apo-B + other Apo-E4 phenotype synthesis
40
Q

What is the physical presentation of Polygenic hypercholesterolemia?

A

None

41
Q

What diseases are secondary causes of lipoprotein disorder metabolism

A
  • Anorexia
  • Hypothyroidism
  • Obesity
  • Cushing’s
  • Diabetes
  • Renal/hepatic disorders
  • Sedentary lifestyle
42
Q

What drug causes are secondary causes of lipoprotein disorder metabolism

A
  • HIV meds
  • cyclosporine (inc LDL)
  • Carbamazepine (inc LDL)
  • glucocorticoids
  • isotretinoin
  • progestins
  • thiazide diuretics
  • beta-blockers (NON-SELECTIVE)
  • anabolic steroids
43
Q

What is the progression of atherosclerosis? (3)

A
  1. Elevated LDL-c plus endothelial damage
  2. Oxidation of LDL-c inside the vessel wall
  3. WBCs migrate into vessel wall and engulfs oxidzed LDL-c (to become foam cells), eventually form the plaque
44
Q

How does dyslipidemia lead to atherosclerosis?

A
  1. Elevated LDL -> goes under endothelium
    1. Damage to endothelium causes LDL to be oxidized ->
    2. Attracts monocytes (WBCs)
    3. Endocytosis of oxidized LDL
    4. Oxidized LDL becomes foam cells
    5. Attraction of smooth muscle cells
    6. Smooth muscle proliferation (and apoptosis) -> plaque forms -> fibrous cap is formed
  2. Core lipid Plaque + fibrous cap grows bigger towards the lumen -> causes the endothelium to bulge -> narrowing of the lumen of the artery
45
Q

How is dyslipidemia diagnosed?

A

Risk assessment of CHD/CVD is basis of diagnosis

46
Q

Who to screen for dyslipidemia?

A

Over 40+

or conditions regardless of the age
- diabetes
- hypertension
- cigarette smoking
- CKD
- obesity
- ED
- COPD

47
Q

How to screen for dyslipidemia (5)

A
  • history and physical examination
  • standard lipid profile
  • FPG or A1C
  • eGFR
  • liporotein(a) 0 - once in a patient’s lifetime
48
Q

Define Fatty streaks

A

thickening of the intima with lipid + foam cells

49
Q

Define Vasa vasorum

A

micro-vessels that supply outer layer of vessel wall. Extend from adventitia through the media toward the thickened intima and can rupture/bleed

50
Q

Define fibrous cap

A

if it is thin -> vulnerable -> Acute coronary syndrome

51
Q

Define advanced lesions

A

necrotic lipid-rich core, calcified regions

52
Q

What is recommended for lipid and lipoprotein testing?
Fasting/non-fasting?
What is the effect

A

non-fasting
- minimal non-HDL change
- slight decrease in LDL
- slight inc in TG

IPFC 3 Final (6 decks)

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