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302: Scientific basis of medicine > Lipid disorders and metabolic syndrome > Flashcards

Lipid disorders and metabolic syndrome Flashcards

1
Q

Transport of lipids in the blood

A

Fatty acids
- Bound to albumin

TG and cholesterol
- Lipoprotein complexes.

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2
Q

Lipoproteins

A

Amphiphatic complex that transports lipids in water-like fluids.

Classes

  • Chylomicrons (CM)
  • Very low density lipoprotein (VLDL)
  • Intermediate density lipoprotein (IDL)
  • Low density lipoprotein (LDL)
  • High density lipoprotein (HDL)
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3
Q

Apo-lipoproteins

A

Amphipathic proteins that form lipoprotein complex by binding to lipids.

Types:

  • AI
  • AII
  • B-100
  • B-48
  • CII
  • CIII
  • E
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4
Q

Apolipoprotein A1

A

Major component of HDL

Co-factor for Lectin cholestero-acyl-transferace (LCAT)
- Forms cholesterol esters

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5
Q

ApoB-100

A

Receptor ligand for LDL

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6
Q

ApoB-48

A

Ligand for Chylomicrons

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7
Q

ApoC-1

A

Lipoprotein lipase inhibitor

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8
Q

ApoC-2

A

Lipoprotein lipase activator

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9
Q

ApoE

A

Chylomicron remnant R ligand

- Interacts with LDL receptor on liver.

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10
Q

Exogenous lipid cycle.

A
  1. Lipids are absorbed in the small bowel.
    - Facilitated by bile acids produced from liver.
  2. Chylomicrons transport TG and cholesterol to peripheral tissue via lymphatic system (thoracic duct) from the gut.
  3. CM is broken down by lipoprotein lipase to release TG in peripheral tissue.
    - TG is broken down into FA+ glycerol in tissue.
  4. As CM loses TG, it becomes ‘CM remnant’ which is taken up by the liver via LDL-Receptor.
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11
Q

Endogenous lipid cycle

A
  1. Synthesis occurs when CHO available exceeds that required for energy demand.
  2. Liver synthesises TG and cholesterol which is exported via VLDL to peripheral tissue.
  3. VLDL is broken down by lipoprotein lipase which releases TG–> FA and glycerol..
  4. IDL is formed when TG is removed for VLDL.
    - IDL taken up by liver
    - IDL loses more TG to become LDL which transports cholesterol to periphery
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12
Q

Regulation of cholesterol synthesis

A

N-SREBP transcription factor in liver stimulates production of LDL-receptors.

Increases of this, decreases cholesterol synthesis?

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13
Q

Lipoprotein lipase

  • Location
  • Function
  • Substrate
  • Co-factor
  • Regulation
A

Enzyme found in capillary walls that hydrolyses TG into FA and glycerol.

Substrate
- VLDL, CM

Co-factor
- Apo-CII

Allows uptake of fats into peripheral tissue like muscles and adipose tissue.

Glycerol is processed in liver to make more TG or make glucose.

Regulation

  • Feeding
  • Fasting
  • Exercise
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14
Q

Hepatic lipase

  • Location
  • Function
  • Substrate
  • Regulation
A

Enzyme found in liver, adrenal gland.

Breaks down TG into DG and FFA.

Substrate

  • IDL–> release of FFA turns it to LDL
  • HDL

Regulation
- Endocrine

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15
Q

Healthy serum cholesterol levels

A

5 mmol/L

After 5, risk of CHD doubles at least.

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16
Q

Healthy fasting serum TG levels

A

1.7 mmol/L

17
Q

Serum HDL-C, healthy levels

A

Men
- >0.9

Women
- >1.2

HDL levels inversely correlates with heart disease risk

18
Q

Familial hypercholesterolaemia

  • Genetics
  • Prevalence
  • Signs and symptoms
A

Type of primary dyslipidaemia

Genetics
- Autosomal dominant
- Genes mutated: APOB (binds to LDL-R), PCSK9 (degrades LDL-R), LDL-R
Prevalence
- 1 in 200

Signs

  • Raised cholesterol, especially LDL
  • Tendon and skin xanthoma
  • Xanthalamsa/ corneal arcus.
19
Q

Secondary causes of hypertriglyceridaemia

A
  • Obesity
  • DM
  • Gout
  • Renal failure
  • Drugs: Thiazides, beta-blockers, retionic acid, oestrogens.
  • Excess alcohol consumption
20
Q

Metabolic syndrome

  • Features
  • Classification
A

Reduced glucose tolerance

Hyperinsulinaemia

Hypertension

Visceral obesity

Haemostatic disroders

Dyslipidaemia: raised TG, LDL-C, low HDL-C.

Classification
- Waist circumference
>96cm Men
>80cm women

\+ any 2
- Fasting serum TG >1.7
- Serum HDL-C 
<1.03 men
<1.29 women
- BP > 130/85
- Fasting glucose >5.6mmol/L
21
Q

Risk factors in framingham risk score

A

Age

Total serum cholesterol/ HDL-C

Systolic BP

Smoking

Sex

LVHT

T2 DM

22
Q

Statins

  • Lipid effects
  • Mode of action
A

Reduces LDL by 60%

Inhibits HMG CoA reductase

23
Q

Bile acid sequestrants

  • Lipid effects
  • Mode of action
A

Reduces LDL by 25%

Binds bile salts= less fats absorbed

24
Q

Ezetimibe

  • Lipid effects
  • Mode of action
A

Reduces LDL by 20%

Blocks cholesterol absorption

25
Q

PCSK inhibitors

  • Lipid effects
  • Mode of action
A

Reduces LDL by 50%

- Blocks LDL-R breakdwon

26
Q

Fibrates

  • Lipid effects
  • Mode of action
A

Reduces TG by 35%, LDL by 20%

- Stimulates LPL

27
Q

Fisk oil

  • Lipid effects
  • Mode of action
A

Reduces TG by 25%

- Reduces hepatic synthesis of TG

28
Q

Lipoprotein a

  • Structure
  • Elevated levels
A

Consists of

  • LDL
  • ApoB
  • Apo(a)

When elevated= increased CVD risk

  • Prothrombotic/ anti-fibrinolytic
  • Plasminogen and plasmin structural effects but no fibrinolytic activity
  • Initimal deposition of Lipo(a), accelerates artherogenesis

302: Scientific basis of medicine (28 decks)

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