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Pathology ICSM COPY > Chemical Pathology 2 - Lipoprotein metabolism, CVD and obesity > Flashcards

Chemical Pathology 2 - Lipoprotein metabolism, CVD and obesity Flashcards

(49 cards)

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1
Q

How is cholesterol transported in the fasting plasma?

A
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2
Q

What are the sources of cholesterol

A

Diet and bile

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3
Q

Where is cholesterol and bile resorbed?

A

Cholesterol - jejunum

Bile acids - terminal ileum

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4
Q

What is the role of HDL?

A

Picks up excess cholesterol from the periphery and transports it to liver

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5
Q

What controls the amount of cholesterol resorbed into the intestine?

A

Balance of 2 enzymes: NPC1L1 and ABC G5/G8

NPC1L1: out of jejunum (to enterocyte?)

ABC G5 and G8: cholesterol into jejunum

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6
Q

How is cholesterol synthesised in the liver, and what is it downregulated by?

A

HMG CoA reductase

Gut resorption of cholesterol

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7
Q

Which enzyme converts cholesterol to cholesteryl ester?

A

ACAT

also makes VLDL

add MTP enzyme with apoB TG

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8
Q

What is the function of 7-alpha hydroxase in cholesterol metabolism?

A

Which enzyme converts cholesterol to bile acids

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9
Q

Which enzyme converts cholesterol to bile acids

A

What is the function of 7-alpha hydroxase in cholesterol metabolism?

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10
Q

How is Cholesterol-ester taken up in the liver?

A

SR-B1

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11
Q

What is the role of the enzyme CETP in cholesterol metabolism?

A

HDL to VLDL conversion

VLDL → TG → HDL

HDL → cholesterol-ester → VLDL

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12
Q

How is LDL taken up in the liver?

A

LDL receptor

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13
Q

What is the function of LDL vs HDL

A

LDL cholesterol from liver to periphery

HDL cholesterol from periphery to liver with ABC A1

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14
Q

What is VLDL constituted of?

A

ApoB, cholesteryl ester and triglyceride

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15
Q

What is the main component of mixed micelles?

A

Bile acids

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16
Q

Where are bile acids resorbed?

A

Terminal ileum

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17
Q

How are triglycerides transported in the fasting plasma?

A
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18
Q

What is the main source of triglycerides?

A

Diet and small intestine

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19
Q

REcall the steps in triglyceride metabolism

A
  1. Broken down into fatty acids then resynthesised into triglycerides
  2. Transported via chylomicrons into plasma
  3. Chylomicrons hydrolysed in plasma into free fatty acids using lipoprotein lipase (LPL)
  4. FFAs taken up by liver and adipose tissue
  • Liver resynthesises FFAs into triglyerides
  • Exported as VLDL → LPL → FFA
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20
Q

What is the inheritance pattern of familial hypercholesterolaemia type II?

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A

Heterozygous dominant

21
Q

What mutations are present in familial hypercholesterolaemia (type2)?

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A

LDL receptor

apoB

PCSK9 gene

RARE: LDLRAP1, autosomal recessive

22
Q

Which mutations are present in polygenic hypercholesterolaemia?

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A

NPC1L1

HMGCR

CYP7A1

23
Q

What name is given to an inherited predeliction to high HDL, and what mutation causes this?

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A

Familial hyper alpha lipoproteinaemia
= CETP deficiency

24
Q

What condition is caused by ABC G5/G8 mutation?

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A

Phytosterolaemia

25
What is phytosterolaemia?
Inherited condition that allows plant sterols to enter the plasma freely, which are more athrogenic than cholesterol itself
26
Recall the function of PCSK9
Binds LDL R and promotes degradation
27
What is the implication of a gain of function/loss of function mutation of PCSK9?
**Gain of function mutation** ↑LDL R degradation **Loss of function mutation** ↓LDL R degradation
28
What deficiency is responsible for familial type 1 hypertriglyceridaemia?
Lipoprotein lipase/apoC II deficiency
29
What deficiency is responsible for familial type 4 hypertriglyceridaemia?
Increased TG synthesis
30
What deficiency is responsible for familial type 5 hypertriglyceridaemia?
apoA V deficiency
31
Recall some examples of primary mixed hyperlipidaemia
Familial combined hyperlipidaemia Familial hepatic lipase deficiency Familial dysβlipoproteinaemia (type III)
32
An ApoE mutation is associated with which condition?
Familial dysβlipoproteinaemia (type III) ApoE4 - a/w Alzheimer's
33
What is A-beta-lipoproteinaemia?
MTP deficiency causing hypolipidaemia
34
What is Hypoβ-lipoproteinaemia?
truncated apoB (dominant)
35
What is Hypoalpha-lipoproteinaemia?
apoA-I mutations causing hypolipidaemia
36
What is Tangier disease?
HDL deficiency caused by ABC AI mutations -\> hypolipidaemia
37
Recall 3 clinical signs of hypercholesterolaemia
Xanthalasma Arcus Tendon xanthoma
38
what clinical sign is this picture showing?
corneal arcus and xanthelasma (also in PBC)
39
Which clinical signs is this picture showing?
eruptive xanthoma
40
What clinical sign is this picture showing?
palmar striae - yellow palmar crease
41
How can you examine for tendon xanthoma?
Feel back of ACL
42
What are the different types of primary hypertriglyceridaemia?
Familial type 1, 4, 5
43
Recall 3 inherited conditions that can cause hypolipidaemia
A-beta-lipoproteinaemia Hypo-beta-lipoproteinaemia Tangier disease (HDC deficiency)
44
What is the effect of statins on cholesterol levels?
Very effective at reducing LDL, also reduce triglyceride and HDL
45
What is the effect of fibrate drugs on cholesterol levels?
Very effective at reducing triglycerides, also reduces LDL
46
What is the mechanism of action of statins?
HMG coA reductase inhibition
47
Recall some treatment options for obesity
* hypocaloric diet and exercise * bariatric surgery if BMI \> 40 (gastric banding, gastric bypass, biliopancreatic diversion) * iatrogenic malabsorption (Orlistat)
48
Recall some novel forms of LDL lowering therapy
microsomal triglyceride transfer protein (MTP) inhibitor e.g. lomitapide Anti-PCSK9 monoclonal antibody (REGN727) Anti-sense apoB oligonucleotide (mipomersen)
49
Recall some alternatives to statins
* nicotinic acid * gemfibrozil * ezetimibe * colestyramine

Pathology ICSM COPY (90 decks)

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