Hyperlipidaemia and atherosclerosis Flashcards
What is hyperlipidaemia
elevated levels of triacylgylceride (TAG) and cholesterol in blood
Define chylomicrons
Chylomicrons
Transport exogenous fats from intestines to tissues
VLDL, IDL & LDL
Transport endogenous fats from liver to tissues
HDL
Transport endogenous cholesterol from tissues to liver
Difference between primary and secondary hyperlipidaemia
- Primary hyperlipidaemia - mainly due to genetic deficiency
- Secondary hyperlipidaemia – due to lifestyle and other metabolic diseases.
Explain the structure of lipoprotein
- Nonpolar core:
triacylglycerols and cholesteryl esters - Amphiphilic surface:
Apoproteins, phospholipid & cholesterol.
Outline causes of hyperlipiademia
nutrition, genetics, medications & metabolic diseases. Genetic causes include; increased sensitivity to dietary cholesterol,
how is hyperlipaemia diagnosed
- Blood test under fasting conditions
Describe treatment for hyperlipidaemia
- Healthy balance diet : replace saturated nfats diet with fruits and vegetables
- regular exercise
- limit alcohol, ,
- avoid smoking
Medications
- stains: inhibits cholesterol biosynthesis (take for lifelong, if stopped can reverse the cholesterol
-Aspirin: inhibit platelet activation (prescribe at low dose)
periodic test to check liver functionats
- Ezetimibe: Blocks the absorption of cholesterol from food and bile. Taken as a combination with statins if the level is not reduced
- Bile acid sequestrants:
- Fibrates:
- Nicotinic acid or niacin or vitamin B3: Inhibits lipolysis in adipocytes and reduce lipid synthesis in the liver
Usually high concentrations are required
side effects include skin rash, hepatotoxicity and hyperglycaemia
what is the difference between atherosclerosis and arteriosclerosis
Atherosclerosis is hardening of arteries due to plague while
arteriosclerosis is hardening of arteries due to non-plaque factors
What is the major cause of atherosclerosis
hyperlipidaemia
Describe the different stages of progression of atherosclerosis
- Endothelial cell injury
- High LDL levels, smoking and high blood pressure can cause
- cause irritation or damage or dysfunction to endothelial cells - Migration of LDLs
- Endothelial dysfunction allows the migration of excessive LDL into intima
- LDLs get oxidised to form oxidised LDL - Adhesion, migration & transformation of monocytes
- Damage to endothelium expresses signalling molecules that attract monocytes to the damaged site.
- Monocytes binds to endothelial cells and then transform into macrophages - Engulfing ox-LDLs
- Macrophages engulf all the oxidised LDLs and become foam cells
- Macrophages & Foam cells release growth factors - Migration and proliferation of SMCs
- Growth factors enhance the migration and proliferation of SMCs
- Dead cells release the lipid core - Expansion and occlusion
- Initially the plaque grows towards the Tunica externa
- Then grows towards the lumen
- At a final stage, plaque can rupture and activate platelets and lead to thrombosis
What are the risk factors of atherosclerosis
Family history Physical inactivity
genetic factors Poor diet (high calorie, fat)
Ageing Heavy stress
Gender (male) Alcohol
Modifiable factors
- Hyperlipidaemia
- Metabolic diseases (e.g. DM & obesity)
- Smoking
- Hypertension
How is atheroclerosis diagnosed
- Blood test
- Electrocardiogram
How is atherosclerosis treated
SAME as hyperlipidaemia
- Anti-hypertensives: ACE inhibitors, calcium channel blockers & diuretics
- Anti-platelet drugs to prevent thrombosis
- Surgical procedures (coronary angioplasty, carotis angioplasty)