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302 Scientific basis of medicine > Metabol 4) Lipid disorders > Flashcards

Metabol 4) Lipid disorders Flashcards

1
Q

Where do lipids come from?

A

Exogenous - from gut to tissues (ingested lipids)
Endogenous - from liver to tissues (synthesised lipids)
Lipids in blood
- fatty acids - bound to albumin
- cholesterol and triglyceride form lipoprotein complex

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2
Q

Why are lipoprotein particles water soluble?

A

Apoplipoproteins and other amphipathic molecules have detergent-like properties so they surround lipids to create lipoproteins

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3
Q

What affects a lipoproteins size and flotation density?

A

Triglyceride content
Cholesterol conent
Apo-lipoprotein content
Stage in circulation through body

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4
Q

What are the 5 major classes of lipoproteins?

A 
Chylomicrons
Very low-density lipoproteins
Intermediate density lipoproteins
Low density lipoprotein
High density lipoprotein
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5
Q

What is the function of the Al apoliprotein?

A

Lecithin: cholesterol acyl transferase activation

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6
Q

What is the function of apolipoprotein B-100?

A

LDLR ligand

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7
Q

What is the function of apoliproprotein B-48?

A

Principal apoprotein in chylomicron

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8
Q

What is the function of the apolipoprotein Cll?

A

Lipoprotein lipase inhibitor

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9
Q

What is the function of the apolipoprotein Clll?

A

LPL activator

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10
Q

What is the function of the apolipoprotein E?

A

Chylomicron remnant R ligand

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11
Q

What is the role of the liver in chylomicron metabolism?

A

Endogenous:

  • synthesis of triglyceride
  • export as VLDL
  • take up particles when triglyceride is removed
  • LDL delivers cholesterol to peripheral cells

Exogenous:
- liver produces bile acids and cholesterol which are involved in creation of micelles for lipid absorption from gut

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12
Q

Describe the stages of the exogenous lipid pathway

A

1) cholesterol and fatty acids from digestion are absorbed into intestinal mucosa cells
2) Re-esterified to cholesterol esters and triglycerides and packaged with phospholipids and lipoproteins
3) Secreted into lymphatic systems as chylomicrons
4) Enter systemic circulation via thoracic duct
5) Lipoprotein lipase from capillary walls hydrolyse triglycerides to fatty acids and glycerol
6) Fatty acids taken up by adipose or muscle cells and glycerol is processed by the liver –> reutilised to make triglyceride or converted to glucose
7) Chylomicron remnant is taken up by LDL receptors on the liver

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13
Q

What are normal serum lipid concentrations?

A

5.0mmol/L in individuals without cardiovascular disease

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14
Q

What are the healthy limits for fasting serum triglycerides?

A

1.7mmol/L

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15
Q

What are the healthy limits for HDL-C?

A

Lower limit is 0.9mmol/L for men and 1.2mmol/L in women

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16
Q

Give an example of a primary dyslipidaemia?

A

Familial hypercholesterolaemia

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17
Q

What is familial hypercholesterolaemia?

A

Autosomal dominant disorder of lipid metabolism

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18
Q

What are the features of familial hypercholesterolaemia?

A

Raised blood cholesterol (especially LDL-C)

Tendon and skin xanthomata (deposits of cholesterol)

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19
Q

Why is it difficult to diagnose familial hypercholesterolaemia?

A

Due to overlapping levels of cholesterol

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20
Q

What genetic mutations are implicated in familial hypercholesterolaemia?

A

APOB
PCSK9
LDLR

21
Q

What is APOB?

A

Protein that binds to LDL receptor

22
Q

What is PCSK9?

A

Protein involved in receptor degradation

23
Q

What are some examples of secondary dyslipidaemia?

A

Hypertriglyceridaemia

Hypercholesterolaemia

24
Q

What can cause hypertriglyceridaemia?

A 
Obesity
Diabetes mellitus
Excess alcohol
Renal failure
Gout
Drug treatments - thiazides, beta blockers, retinoid acid derivatives, oestrogen therapy
25
Q

What can cause hypercholesterolaemia?

A 
Hypothyroidism
Nephrotic syndrome
High saturated fat diet
Cholestatic liver disease
Anorexia nervosa
26
Q

What is the BMI of obese class I?

A

30.0-34.9

27
Q

What is the BMI of overweight?

A

25-29.9

28
Q

What is the BMI of obese class II?

A

35-39.9

29
Q

What is the BMI of obese class III?

A

≥40

30
Q

How is BMI calculated?

A

Weight (kg) / height^2 (m2)

31
Q

What molecules does adipose tissue release?

A 
Leptin
TNF-alpha
PAI-1, haptoglobin, serum amyloid A
IL-1 beta, IL-6, IL-10, TGF-beta
NGF
MCP-1, MIF, IL-8
Adiponectin
VEGF
32
Q

Why does high visceral fat increase cardiovascular risk?

A

Increased triglycerides
Decreased HDL-cholesterol
Increased glucose
Increased insulin

33
Q

What are the factors in metabolic syndrome?

A 
Reduced glucose tolerance
Hyperinsulinaemia
Visceral oebsity
Haemostatic disorders
Hypertension
Lipid disorders
 - elevated triglycerides
 - LDL-C normal or moderately elevated
 - HDL-C diminished
34
Q

What is the waist circumference for identifying metabolic syndrome?

A

Men >94cm

Women >80cm

35
Q

How is metabolic syndrome identified according to IDF criteria?

A

Waist circumference
+ 2 of:
- fasting serum triglycerides ≥1.7mmol/L
- serum HDL-C cholesterol lowered
- BP ≥130/85mmHg
- fasting glucose ≥5.6mmol/L or diagnosis of diabetes mellitus

36
Q

What are some further consequences of visceral obesity?

A 
Brain health
 - stroke, necrosis
 - brain size
 - cognitive function
 - dementia
Respiratory diseases
Heart diseases
 - heart failure
 - CHD
 - valve diseases
 - arrhythmias
Diabetes
Cancers
Bone density
PCOS
HIV
37
Q

What are some risk factors for coronary heart disease?

A 
Lipid profile
Obesity
Inflammation / infection
Blood pressure
Socio-economic status
Genetic factors
Metabolic
Smoking habit
38
Q

What factors does the Framingham risk score include?

A 
Age
Total serum cholesterol / HDL cholesterol
Systolic BP
Smoking status
Sex
Left ventricular hypertrophy
T2DM
39
Q

What factors does the Q risk 2 score include?

A 
Age
Total serum cholesterol / HDL cholesterol
Systolic BP
Smoking status
Sex
Left ventricular hypertrophy
T2DM
BMI
Family history
Deprivation score
Ethnicity
AF
Renal disease
Rheumatoid arthritis
40
Q

What drug classes can be used for lipid management in dyslipidaemia?

A 
Statins
Bile acid sequestrant
Cholesterol absorption inhibitor
PCSK inhibitors
Fibric acid derivatives
Fish oil
41
Q

What is the mode of action of statins?

A

HMG-CoA reductase inhibitor

42
Q

What is the mode of action of bile acid sequestrants?

A

Bind bile salts

43
Q

What is the mode of action of PCSK inhibitors?

A

Block LDLR catabolism

Inhibit PCSK9 –> blocks PCSK9-LDL-R interaction –> increases LDL-R expression –> increases LDL-C clearance

44
Q

What is the mode of action of fibric acid derivatives?

A

LPL stimulation

45
Q

What statin should be used if there is low risk of CHD?

A

Lovastatin

46
Q

What statin should be used with high risk of CHD (high cholesterol)

A

Pravastatin

47
Q

What statin should be used for secondary prevention?

A

Simvastatin

48
Q

What anti-atherogenic effects does a high HDL-C have?

A

Anti-inflammatory
Antithrombotic
Pro-endothelial

302 Scientific basis of medicine (28 decks)

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