Serum Proteins 2 Flashcards
what are 3 types of lipid
fatty acids
phospholipids
cholesterol
what are the functions of lipids
Major component of cell membranes Solubilise fat soluble vitamins Biosynthetic precursors (steroid hormones e.g. testosterone) Protection and insulation Major energy source
Lipids are Hydrophobic- how are they transported round the body?
They combine with (are “packed inside”) proteins to form lipoprotein particles.
They have a hydrophilic surface monolayer, and hydrophobic core.
what is classification of lipoproteins based on?
Classification is based on their density (NMR spectrum) and electrophoretic mobility.
what are the 4 classes of lipoproteins?
Chylomicrons (CM)
Very low density lipoproteins (VLDL)
Low density lipoproteins (LDL)
High density lipoproteins (HDL)
what are Apolipoproteins
the proteins associated with lipoproteins
describe the exogenous pathway of lipid metabolism
Comes from diet
The liver produces bile acids to emulsify fats, absorbed through small intestine, and either used or recycled
(NOT FULL EXPLANATION OBVS)
Describe the endogenous lipid metabolism
Cholesterol is produced by liver, packaged from liver in VLDL, travels around blood, broken down to produce heat energy, free fatty acids stored in adipose tissue, lose fats (IDL), lose more (LDL), HDL can take tryglycerides from IDL.
(NOT FULL EXPLANATION OBVS)
who is LDL removed, and what happens if there is too much
LDL is removed from circulation by peripheral cells via LDL receptors which recognise ApoB-100.
If there is an excess of LDL this results in downregulation of receptor and high concentration of circulating LDL.
what is atherosclerosis
Chronic inflammatory response to deposition of LDL causing two main problems:
- narrowing of arteries (stenosis)
- thrombus breaks from main plaque causing infarction
what are cadiovascular risk factors
male sex, age, smoking, high plasma cholesterol, low plasma HDL, hypertension, obesity, sedentary lifestyle, diabetes
describe HDL and reverse cholesterol transport
Nascent HDL removes free cholesterol from macrophage and returns it to the liver (“reverse” cholesterol transport).
50% of cholesterol in HDL is transferred to VLDL, IDL and LDL by CETP for ongoing “forward” transport
why do we need hemostais
Blood is the transport system for oxygen, nutrients, hormones, minerals, metabolic products.
Must limit loss via day to day accidents.
Mechanism must stem flow but not occlude vessels at site of origin (thrombosis) or downstream (embolsm).
A careful balance is needed.
what are the 4 stages of Haemostasis
- Vasoconstriction
- Platelet aggregation and plug formation
- Blood coagulation (clotting)
- Permanent repair and clot dissolution (fibrinolysis)
describe platelet plugs
Minor vessel injuries can be plugged by platelets alone.
Platelets adhesion to collagen fibers is stabilized by von Willebrand factor, an adhesive glycoprotein.
Healthy cells produce nitric oxide to prevent platelets binding.
what are the 3 parts of coagulation
- Intrinsic - Initiated by contact activation (-vely charged surfaces)
- Extrinsic – involves tissue factor which is released when tissues are damaged
- Common pathway – allows amplification of the cascade
what can happen if you have deficiencies in any of the 14 factors in the coagulation cascade
Deficiencies in any factor can cause excess bleeding.
how does warfarin inhibit coagulation
Vitamin K is a co-factor for the enzyme g-glutamyl carboxylase (cannot function without vitamin K).
Post-translational carboxylation required for activity of factors II VII IX X
The presence of Warfarin leads to accumulation of non-carboxylated and therefore inactive clotting factors
why does warfarin need constant monitoring
Warfarin has a narrow therapeutic window therefore constant monitoring is required:
• Dose too low - Ineffective
• Dose too high - Risk of bleeding (esp in brain)
how does aspirin work as an anti-coag.?
inhibits the production of Thromboxane-A2 which is produced by activated platelets to signal to other platelets for the initial aggregation
how does haemophilia affect clotting
lack of clotting resulting in prolonged bleeding and internal haemorrhage
