CVS - Lipid homeostatis Flashcards

1
Q

What is hyperlipidaemia?

A

high cholesterol, means you have too many lipids (fats) in your blood

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2
Q

hypercholesterolemia

A

high cholesterol content.

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3
Q

hyperapobetalipoproteinemia

A

high levels of apolipoprotein B, which is part of LDL cholesterol.

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4
Q

What is bad cholestrol called?

A

LDL

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5
Q

What is the genetic type of hyperlipidaemia?

A

hyperlipidaemia
hypercholestrerolemia
hyperapobetaliprotieinemia

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6
Q

What is the secondary type of hyperlipidaemia caused by
?

A
  • obesity
    smoking
    high fat diet
    alochol
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7
Q

LIPID-LOW
means

A
  1. Cholesterol synthesis inhibition
  2. Intestinal absorption
  3. Lipoprotein lipase activity
  4. HDL
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8
Q

Cholesterol synthesis inhibition:

A
  • statins competitively inhibit the HMG-CoA reductase > reduced cholesterol

-Then liver recruits MORE LDL from circulation > LDL clearance from the blood

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9
Q

What are CYP inhibitors?

A
  • grapefruit juice
  • diltiazem
  • amlodipine
  • macrolide antibiotics

worsen statin adverse effects

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10
Q

What are the 1st line therapy for CVD?

A
  • atorvastatin
  • pravastatin
  • rosuvastatin
    -simvastatin
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11
Q

How does cholesterol absorption inhibition work? give an example

A
  • anion exchange resins:
    binds with bile salts (insoluble complex) > excreted in faeces

EZETIMDE - block the transport protein Niemann-Pick C1 (in gut wall)

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12
Q

What is the outcome of cholesterol absorption inhibition?

A

reduced intestinal

cholestrol absorption

cholestrol directed to

compensate for bile loss
LDL cholestrol clearance

Ezetimibe - reduces intestinal cholestrol absorption, without affecting bile

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13
Q

coronary thrombosis

A

myocardial infarction (MI)

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14
Q

Cholesterol

A

an essential component that makes the cell membrane and modulates membrane fluidity, and critical for cell growth and viability; Precursor for steroid hormones, vitamin D and bile salts

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15
Q

Triglycerides

A

largely through diet, but synthesised in the liver as well. supply energy/fuel to muscle and other tissues

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16
Q

How is cholesterol absorbed and transported to the liver?

A

absorbed by micelles into intestinalw all throigh identified protein channels
bile EMULSIFIES dietery lipids (incl cholestrol), facilitates absorption, salts are recycled via hepatic portal vein (entero-hepatic circulation)

SOME chol. pumped out fo body > away into intestinal lumen by heterodimeric ATP- binding cassette transporter protein complex

17
Q

Conversion of HMG-CoA to mevaolnate can be stopped, how?

A

by blocking enzyme, stop secretion of cholestrol

18
Q

are chol and triglycerides soluble of insoluble in water?

A

INSOLUBLE - require carrier protein

19
Q

Characteristics of lipoproteins

A

central core containing cholesterol esters (hydrophobic)
triglycerides surrounded by free cholesterol, phospholipids (amphophilic)
apolipoproteins, facilitate lipoprotein formation and function
AMPOPHILIC – MIXTURE OF HYDROPHOBIC AND HYDROPHILIC
In core phobic, out phobic – this is how it can move in the blood

20
Q

Chylomicrons

A

triglyceride-rich particles made byintestine, transports triglycerides/choletsrol to PERIPHERL tissues and liver

21
Q

Chylomicron remnants

A

removal of trigloyceride from chylomicrons by peripheral tissues results in smaller

22
Q

Intermediate-density lipoproteins (IDL; VLDL remnants)

A

removal of triglycerides from VLDL by MUSCLE and adipsose tissue results in formation of iDL particles – enriched in cholesterol

23
Q

sLDL particles

A

decreased affinity for the LDL receptor resulting in a prolonged retention time in the circulation

24
Q

How does sLDL get trapped in arterial wall?

A

easily enters the arterial wall and binds more avidly to intsa-arterial proteoglycans

25
Q

are sLDL suitable for oxidation?

A

yes > results in an enhanced uptake by macrophages

26
Q

HDL, good or bad?

A

good
- antiapoptotic
- dec, expression of adesion molecules (anti-inflammatory)
- dec LDL oxidation
- ameliorates endothelial function

27
Q

what do HDL particles contain?

A

cholestrol and phospholipids

apo A-I is the core structural protein and each - HDL particle may contain multiple Apo A-I moleucles

high levels of Apo-I + atherosclerosis

28
Q

Pathophysiology of atherosclerosis

A

1) endothelial dysfunction
2) formation of lipid layer or fatty streak within the intima
3) migration of leukocytes and smooth muscle cells into the vessel wall
4) foam cell formation
5) degradation of extracellular matrix

29
Q

Increased LDL

A

plaque rupture

30
Q
A