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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
What is the main apo-protein for LDL
B100 - functions as ligand for LDL receptor
26
What is LDL receptor regulated by? What condition is absence of LDL receptor?
internal cholesterol balance (by HMG CoA reductase) Absence of LDL receptor --> familial hypercholesterolemia
27
What is the reverse cholesterol transport?
Process by which cholesterol is transported from peripheral cells to the liver
28
How is HDL produced in reverse cholesterol transport? (3 steps)
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
How does Nascent HDL get converted to mature HDL in reverse cholesterol transport? purpose?
through esterification of free cholesterol by lecithin-cholesterol acyltransferase (LCAT) - A-1 activates LCAT Purpose - to pick up more cholesterol
30
What is the role of cholesteryl ester transfer protein in reverse cholesterol transport? What happens to HDL after?
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
What is the overall process of reverse cholesterol transport?
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
What is familial hypercholesterolemia: class IIa hyperlipidemia classified as?
Downregulation in LDL receptors --> increase in LDL levels
33
Which type of class IIa hyperlipidemia is more common
heterozygous FH homozygous has higher LDL and more dangerous
34
What does FH class IIa hyperlipidemia susceptible to?
Early onset of CHD - Due to higher susceptibility for oxidation and deposition of plaque in vascular sites
35
What are physical findings of heterozygous FH? (3)
1. tendinous xanthomas - deposit in achilles or extensor tendons 2. Xanthelasmas - cholesterol deposits in the eyelids 3. Arcus cornealis - deposit around corneal rim
36
What does FH class IV hypertriglyceridemia classified by?
Mutations in the LPL gene - VLDL elevation - moderate elevations in triglyceride (removes FFA from triglycerides)
37
What is the best treatment for familial hypertriglyceridemia
Fibrates
38
What is the most common form of dyslipidemia?
Polygenic hypercholesterolemia
39
What are some causes of Polygenic hypercholesterolemia? (4)
- 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
What is the physical presentation of Polygenic hypercholesterolemia?
None
41
What diseases are secondary causes of lipoprotein disorder metabolism
- Anorexia - Hypothyroidism - Obesity - Cushing's - Diabetes - Renal/hepatic disorders - Sedentary lifestyle
42
What drug causes are secondary causes of lipoprotein disorder metabolism
- HIV meds - cyclosporine (inc LDL) - Carbamazepine (inc LDL) - glucocorticoids - isotretinoin - progestins - thiazide diuretics - beta-blockers (NON-SELECTIVE) - anabolic steroids
43
What is the progression of atherosclerosis? (3)
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
How does dyslipidemia lead to atherosclerosis?
1. Elevated LDL -> goes under endothelium 2. Damage to endothelium causes LDL to be oxidized -> 3. Attracts monocytes (WBCs) 4. Endocytosis of oxidized LDL 5. Oxidized LDL becomes foam cells 6. Attraction of smooth muscle cells 7. Smooth muscle proliferation (and apoptosis) -> plaque forms -> fibrous cap is formed 8. Core lipid Plaque + fibrous cap grows bigger towards the lumen -> causes the endothelium to bulge -> narrowing of the lumen of the artery
45
How is dyslipidemia diagnosed?
Risk assessment of CHD/CVD is basis of diagnosis
46
Who to screen for dyslipidemia?
Over 40+ or conditions regardless of the age - diabetes - hypertension - cigarette smoking - CKD - obesity - ED - COPD
47
How to screen for dyslipidemia (5)
- history and physical examination - standard lipid profile - FPG or A1C - eGFR - liporotein(a) 0 - once in a patient's lifetime
48
Define Fatty streaks
thickening of the intima with lipid + foam cells
49
Define Vasa vasorum
micro-vessels that supply outer layer of vessel wall. Extend from adventitia through the media toward the thickened intima and can rupture/bleed
50
Define fibrous cap
if it is thin -> vulnerable -> Acute coronary syndrome
51
Define advanced lesions
necrotic lipid-rich core, calcified regions
52
What is recommended for lipid and lipoprotein testing? Fasting/non-fasting? What is the effect
non-fasting - minimal non-HDL change - slight decrease in LDL - slight inc in TG

IPFC 3 Final (6 decks)

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