Platelets - all of the following are true
Alpha granules contain Fibrinogen and VWF, and dense granules contain ADP and serotonin
Aspirin is a weak platelet inhibitor
Platelet glycoprotein GP1b adheres to VWF at the exposed sub endothelial tissue
None of the above are true about platelet
VWF deficiency
Type I most common - decreased amount of VWF
Type II - normal amounts but abnormal intracellular transport or abnormal binding
Type III - Severe deficiency of the factor
Least common inherited bleeding disorder
Platelet aggregation is mediated by binding of GPIIb /IIIa with fibrinogen - this process is inhibited by Plavix
Regarding blood clotting
Blood clotting proteases are homologous to digestive enzyme chymotrypsin, all belonging to the class of cysteine proteases
Calcium ions form connection between the carboxylated glutamate of the clotting factors and the negatively charged surface of the platelet
Vitamin K is required for carboxylation of glutamate residues
Warfarin is a Vitamin K Antagonist whereas Heparin stimulated anti thrombin
Thrombin
Formed by the activation of Prothrombin via Xa:Va
Thrombin with thrombomodulin activates protein C which binds with protein S and inactivated Va and VIIIa
Factor Leiden is a point mutation in Fibrinogen
Thrombin in turn activates fibrinogen to fibrin
All of the following are true statements except
Antithrombin is a serpin (serine protease inhibitor) which irreversibly inactivates serine protease - stimulated by heparin
Firbinolysis removes clots during wound healing
tPA and uPA promote clot formation
anti thrombin's main targets Xa and Thrombin
All of the following about DIT (Diet Induced Thermogenesis) from protein are true except?
Na linked AA transport
AA supported gluconeogenesis
Salvage/recycling of purines
Detoxification of ammonia via Urea cycles
None of the above
All AA are absorbed via Na linked cotransport except Branched chain and aromatic AA
1st step in AA Catabolism
Transamination (PLP co factor)
Oxidative Deamination (NAD cofactor)
Both of the above
none of the above
Glutamate is the only AA that can accept free ammonia via glutamine synthetase
Catabolism of BCAA is predominantly in the liver
Glucose-Alanine cycle consist of
Removal of amino group from alanine
Removed amino group is collected as glutamate
Alanine in the liver is converted to pyruvate
Pyruvate is converted into Acetyl CoA
The toxicity of ammonia is due to pH changes in osmotic gradients
Treat urea cycle failure patients with benzoate,phenylacetate or phenybutyrate
Histidine degradation
Results in Proline production
Deficiency of formimino transferase results in accumulation of FIGLU in the urine
Histidinemia is most prevalent inborn error in Japan
Irreversible
Methionine degradation
Results in SAM
SAM degraded into Homocysteine
Homocysteine further degraded into Cystathione which breaks into cysteine and alpha ketobutyrate
Homocysteine is methylated back to Methionine and uses both B9 and B12 as cofactors
Carbon skeleton for cysteine comes from Methionine and SH group from serine
Cysteine degrades into taurine
Lysine is important in the synthesis of carnitine and it is also ketogenic
Tryptophan degradation
Results in Alanine - gluconeogenic
Acetoacetate - Ketogenic
Pyridoxine - Vitamin B synthesis
All of the above
The only AA created by reductive amination is glutamate
The only AA disorder due to defective Lysosomal transporter is Cystinosis
Heme synthesis
Heme allosterically inhibits ALA synthase in Bone marrow
Succinly CoA, Glycine and Iron are the essential components of heme
Lead inhibits ALA dehydratase and Ferrochelatase
All of the above are correct