Plasma Proteins Notes
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Plasma Proteins Revision
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Plasma proteins Synthesised in the liver Functions
-Colloid osmotic pressure
-Defence Examples a) Albumin b) Transport proteins e.g Transferrin/Transcobalamin c)Protease inhibitors: alpha1-antitrypsin d) Clotting factors: Prothrombin, Factors 7,9,10, Fibrinogen 1) Albumin Plasma concentrations = 40g/L Synthesis= 12g/day Function: Transportation of:
-Long chain fatty acids: mobilised from the adipose tissue
-Bilirubin: prevents liver intoxicity
-Copper 2) Catbolism of Haeme Haeme consists of a prophyrin ring made up of four pyrollic groups joined together by methine bridges. The porphyrin ring is chelated to Fe 2+ at the centre
-Catbolism of Haeme produces bilirubin which comes from the
-80% senescent RBC, 20% cytochromes, myoglobin, catalase
-The initial reaction is ring cleavage by ER by Haeme oxygenase with Fe2+/NADPH Long linear molecule
-Bilirubin: Lipophilic molecule so is highly insoluable in water, bright yellow compound- transported in the blood by binding to albumin. The binding site on albumin is also used by various drugs (sulphonamides- antibiotics)
-Excretion of bilirubin i) Liver cells:
-Transported to liver bound to albumin. Within the cytoplasm they bind to protein ligandin
-Propionyl side gropus are conjugated with glucuronic acid (hydrophilic) to form bilirubin monoglucuronides and bilirubin diglucoronides- more water soluable. These are excreted into Bile canaliculi by specific transport mechanisms.
-In the gut the conjugated bilirubin is mostly not reabsobed and is degraded by gut bacteria to colourless urobilinogens (Unconjugated)
-These are absorbed and re-excreted in bile whih small fraction excreted in the kidney
-Some of the urobilinogens are oxidised to urobilins-give colour to urine and faeces Toxicity of bilirubin Hyperbilirubinaemia and jaundice a) Excess unconjugated bilirubin
-Unconjugated bilirubin is highly lipophic- can cross the blood brain barrier- affects mostly the cochlear nucli, hippocampus, basal ganglia, brain stem, cerebral nuclei of the brain
-Excess unconjugated bilirubin results in kernicterus- occurs in neonates/infantssymptoms are hypotonia, loss of refexes, athetoid movements, high pitched cry, reflex opisthotonus, lethargy, atonia, death
-survivors may be deaf and have athetosis SYMPTOM: Unconjugated bilirubin is not excreted in urine as it is not water soluable, so urine is colourless, CAUSE:
-immaturity of the conjugating enzymes-physiological jaundice of the neonate
-Increased bilirubin load due to haemolytic anaemias- life span of RBC shorter, so constant release of Haeme, constant generation of bilirubin
-Genetic defects of conjugating enzymes- Gilbert's syndrome b) Excess conjugated biliribin CAUSE:
-Hepatocellular disease such as viral hepatitis A
-Intra/Extra hepatic biliary obstruction so can't enter the gut
-Genetic defects of bilirubin excretion- Rotor syndromes
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