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Author8 Posts
  #1

what are the main point to differentiate these two on exam?sad

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  #2

in g6pd heinz bodies are seen but not in pk deficiency

there is inc 2,3-BPG in PK defcn. but not in g6pd.also g6pd has a defective NADP oxidase sysytem leading to chr. granulomatous disease

  #3

what about inheritence patterns?

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  #4

Easier way to figure this out.. G6PD deficiency cannot make NADPH and the severity of this deficit is variable among individuals, MOST of these patients have a moderate deficit and only have symptoms while they are under oxidative stress situations.. Infections, drugs, fava beans.. All of these situations increase O2 free radicals which make these patients have hemolytic crisis, Heinz bodies viewed with supravital stains and so on. They dont have enough NADPH to feed glutathion peroxidase pathway so their RBCS cannot clear these newly formed free radicals. Severe cases of G6PD def may be related to a severe absence of NADPH, there would be no substrate for NADPH oxidase (which is normal in these individuals), and it may act as a chronic granulomatous dzs in a way. PK deficiency you dont have the enzyme to make PEP to pyruvate, therefore you cannot make anaerobic glycolysis (lactate) from pyruvate. These patients have a persistent hemolytic anemia and the glycolytic pathway ends up doind 2,3 BPG shifting the curve to the right.. An accumulation of NADH will eventually stop glycolisis and the RBCs will lyse persistently and not periodically..

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  #5

G6PD X linked recessive, PK dont know

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  #6

mazinger isnt PK deficiency reccesive ds??

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  #7

Id say PK is autosomal reccesive

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  #8

... thx guys didnt know that

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