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4 - Y5 a Path lectures 2021/22 > ChemPath 2S: Lipoproteins > Flashcards

ChemPath 2S: Lipoproteins Flashcards

1
Q

What are Atherosclerotic plaques formed of?

A
  • Atherosclerotic plaques are formed of a
    • necrotic core (dead macrophages) of cholesterol crystals surrounded by foam cells (macrophages)
    • all topped with a fibrous cap
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2
Q

Name some plasma lipoproteins

A
  • Chylomicron (high TGs)
  • vLDL (high TGs)
  • LDL
  • HDL
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3
Q

What are the concentrations in fasting plasma – Cholesterol & Triglycerides of the following plasma lipoproteins:

  • Chylomicron (high TGs)
  • VLDL (high TGs)
  • LDL
  • HDL
A
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4
Q

What are the types of dyslipidaemia?

A
  • hypercholesterolaemia
  • hypertryglyceridaemia
  • mixed hyperlipidaemia
  • hypolipidaemia
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5
Q

Describe cholesterol absorption, metabolism, transport

A
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6
Q

Describe triglyceride absorption, metabolism, transport

A
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7
Q

Where is cholesterol solubilised into mixed micelles?

A

intestines

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8
Q

Which transporter transports cholesterol across the intestinal epithelium?

A
  • NPC1L1 (main determinant of transport)
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9
Q

Which 2 transporters Two transporters can transport cholesterol back into the lumen of the intestines?

A
  • ABC G5
  • ABC G8
  • – a balance between these transporters determines the net amount of cholesterol absorbed)
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10
Q

Where are bile acids reabsorbed?

A

terminal ileum

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11
Q

Which enzyme does cholesterol downregulate the activty of? and what does this enzyme do?

A
  • HMG CoA reductase
  • (the main enzyme to create cholesterol from acetate and mevalonic acid) at the liver –
  • i.e. the amount of cholesterol synthesised in the liver is dependent on the amount of cholesterol absorbed in the small intestines
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12
Q

What happens to cholesterol cholesterol brought to the liver (produced IN the liver or absorbed and transported)?

A
  • Hydroxylation by CYP7A1 enzyme, 7a-hydroxylase –> bile acids –> excreted via bile ducts
  • Esterified by ACAT –> cholesterol esters and combined with TG and apoB into VLDL (precursor to LDL)
    • ACAT = Acyl-CoA: cholesterol acyltransferase
    • MTP = Microsomal Triglyceride Transfer Protein (used to package cholesterol esters)
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13
Q

What happens to LDLs after circulation?

A

LDLs will bind to LDL receptor on the liver

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14
Q

What are HDLs responsible for?

A

picking up excess cholesterol from the periphery

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15
Q

Which transporter is important in packaging free cholesterol from the periphery into HDLs?

A

ABC A1

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16
Q

What does CETP (cholesteryl ester transfer protein) do?

A

mediates the movement of:

  • Cholesterol from HDL to VLDL
  • Triglyceride from VLDL to HDL
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17
Q

What does the receptor SR-B1 do?

A

Some of the HDLs will be taken up by the liver via SR-B1

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18
Q

What are the types of Hypercholesterolaemia (primary)?

A
  • Familial hypercholesterolaemia
  • Polygenic hypercholesterolaemia –
  • Familial hyper-a-lipoproteinaemia
  • Phytosterolaemia
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19
Q

Which mutations are implicated in Familial hypercholesterolaemia (FH)?

A

dominant mutations in:

  • LDL receptor
  • apoB or
  • PCSK9

rarely, recessive mutations in:

  • LDLRAP1
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20
Q

Which mutations are implicated in Polygenic hypercholesterolaemia

A
  • NPC1L1,
  • HMG-CoA Reductase,
  • CYP7A1 polymorphisms
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21
Q

What is the cause of Familial hyper-a-lipoproteinaemia?

A

lots of causes, but sometimes. CETP deficiency

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22
Q

What is Familial hyper-a-lipoproteinaemia ?

A

increase in HDL

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23
Q

Which mutations are implicated in Phytosterolaemia?

A

ABC G5 & G8 mutations (in small intestine)–> premature atherosclerosis

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24
Q

What is the Pathophysiology of Hypercholesterolaemia (primary)?

A

normally:

  • LDL binds to LDL-R (on coated pits of the liver)
  • undergoes endocytosis
  • taken to lysosome for processing and degradation

pathophysiology:

  • many LDL-R mutations identified –> less LDL binds to LDL-R –> less is degraded in lysosome –> high [serum LDL]
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25
Q

What are the signs/symptoms seen in homzygotes with Hypercholesterolaemia (primary)?

A
  • corneal arcus,
  • atheroma of aortic root
26
Q

What are the signs/symptoms seen in heterozygotes with Hypercholesterolaemia (primary)?

A
  • corneal arcus,
  • xanthomas (eye [xanthelasma], tendon)
27
Q

What is the function of Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9)?

A
  • bind to LDL-R and aid its degradation
    *
28
Q

Describe the rare cause of FH, related to a mutation in PCSK9

A
  • autosomal dominant mutation
  • gain-mutation in PCSK9 –> increased LDL-R degradation
  • (–> less LDL binds to LDL-R –> less LDL is degraded –> high [serum LDL])
29
Q

What are the types of Hypertriglyceridaemia (primary)?

A
  • Familial T-I
  • Familial T-IV
  • Familial T-V
30
Q

What is the cause of Hypertriglyceridaemia (primary) Familial T-1?

A
  • lipoprotein lipase or apoC II deficiency
  • –> Less breakdown of chylomicrons
31
Q

What is the cause of Hypertriglyceridaemia (primary) Familial T-IV?

A

increased synthesis of Triglyceride (unknown cause)

32
Q

What is the cause of Hypertriglyceridaemia (primary) Familial T-V?

A

apoA V deficiency

33
Q

What does the picture show?

A
  • eruptive xanthomas
  • seen in primary hyperlipidaemia Familial T-I
34
Q

Which particles are seen in each of the Hypertriglyceridaemia (primary) Familial types?

  • Familial T-I
  • Familial T-IV
  • Familial T-V
A
  • Familial T-I = chylomicrons
  • Familial T-IV = vLDLs
  • Familial T-V = vLDLs (with some chylomicrons)
35
Q

Match each of the pictures with one of the below Hypertriglyceridaemia (primary) types:

  • Familial T-I
  • Familial T-IV
  • Familial T-V
A
  • Familial T-1 = left (chylomicrons in plasma)
  • Familial T-IV = middle (vLDLs in EDTA blood)
  • Familial T-V = right (majority vLDLs with some chylomicrons in plasma)
36
Q

What is mixed hyperlipidaemia?

A
  • high [serum LDL]
  • high [serum triglyceride]
    • low [serum HDL]
37
Q

What are the types of Mixed hyperlipidaemia (primary)?

A
  • Familial combined hyperlipidaemia
  • Familial hepatic lipase deficiency
  • Familial dys-B-lipoproteinaemia (type III hyperlipoproteinemia)
38
Q

What is the cause of the Familial combined hyperlipidaemia type of primary Mixed hyperlipidaemia?

A

unknown cause

39
Q

What is the cause of the Familial hepatic lipase deficiency type of Mixed hyperlipidaemia (primary)?

A

hepatic lipase deficiency

40
Q

What is the cause of the Familial dys-B-lipoproteinaemia type of Mixed hyperlipidaemia (primary)?

A
  • ApoE2 polymorphism
41
Q

What are the diagnostic signs of Familial dys-B-lipoproteinaemia?

A
  • Yellow palmar crease (LEFT),
  • xanthomas on elbow (RIGHT)
42
Q

What is the link between ApoE2 polymorphism and Alzheimer’s?

A
  • ApoE2 = less Alzheimer’s (ApoE2 implicated in Familial dys-B-lipoproteinaemia)
  • ApoE3 = normal
  • ApoE4 = increase Alzheimer’s
43
Q

What is secondary hyperlipidaemia?

A

non-genetic cause of increased [serum lipids]

44
Q

What are some causes of secondary hyperlipidaemia?

A
45
Q

Name some types of hypolipidaemia

A
  • A-β-lipoproteinaemia: RARE
  • Hypo-β-lipoproteinaemia
  • Tangier disease: orange tonsils
  • Hypo-α-lipoproteinaemia
46
Q

What is A-β-lipoproteinaemia?

A
  • hypolipidaemia disorder
  • MTP deficiency (AR) –
  • RARE
  • –> very low LDL and vLDL
47
Q

What is MTP?

A
  • mitosomal triglyceride transfer protein
48
Q

What is hypo-β-lipoproteinaemia?

A
  • type of hypolipidaemia
  • truncated apoB
  • (AD)
  • –> Low LDL
49
Q

What is Tangier’s disease?

A
  • Tangier disease: orange tonsils
  • ABC A1 mutations
  • –> HDL deficiency
50
Q

What is the cause of hypo-a-lipoproteinaemia?

A

sometimes due to mutations of apoA-1

51
Q

What is the relationship between lipids and cardiovascular disease?

A
  • CVD is associated with serum cholesterol à deaths
    • HDL = protective; LDL = deleterious
52
Q

What is the pathophysiology of atherosclerosis?

A
53
Q

Name some lipid-regulating drugs

A
  • atorvastatin
  • gemfibrozil
  • ezetimibe
  • colestyramine
54
Q

Which lipid regulating drug is the most effective at reducing LDL?

A

atorvastatin

55
Q

Which lipid-regulating drug is the most effective at reducing triglycerides?

A

Gemfibrozil

56
Q

Name some novel lipid-regulating drugs

A
57
Q

What is Lp(a) (lipoprotien A) used as a marker for?

A

CVD risk factor marker

58
Q

How is Lp(a) used?

A
  • Should be measured once with intermediate-high CVD/CHD risk (inc. FH)
59
Q

What is a desirable Lp(a) level? What is the Tx if this is too high?

A
  • Desirable Lp(a) = <500mg/L
  • Tx is nicotinic acid 1-3g/day
60
Q

What is the Tx for obesity?

A
  • Low-calorie diet & exercise
  • Iatrogenic malabsorption (Orlistat, 120-360 mg, OD)
  • Bariatric surgery (BMI >40Kg/m2) – e.g. gastric banding, bypass, biliopancreatic bypass
61
Q

What are the risks and benefits of bariatric surgery used to treat obesity?

A
  • Success –> 50% loss in weight, 72% reduction of diabetes risk, reduced TG, increased HDL, reduced fatty liver, reduced HTN
  • Post-op mortality = 0.1-2%

4 - Y5 a Path lectures 2021/22 (37 decks)

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