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Confusion ; (

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AngelT
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07/03/07 - 09:07 PM

A researcher develops a specific antibody to the complement component C3b. Assume that IV administration of the Ab prevents the biological effects of C3b. Which of the following disease conditions would be most likely to be ameliorated by the administration of this Ab to a patient?

A-Acute Glomerulonephritis
B-Hashimoto Thyroiditis
C-Lupus Erythematosus
D-Myasthenia Gravis
E-Tuberculosis

silver
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07/03/07 - 09:25 PM

A-Acute Glomerulonephritis

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AngelT
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07/04/07 - 10:06 AM

The answer is C. But I still didnt understand why it could not be A???

silver
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07/04/07 - 10:35 AM

can you post the expln. that is given for this question? where is it from?

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po
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07/04/07 - 11:13 AM

A-Acute Glomerulonephritis-type 2cytotoxic
B-Hashimoto Thyroiditis-type 2 cytotoxic

C-Lupus Erythematosus-immune complex type 3

D-Myasthenia Gravis-type 2 cytotoxic

E-Tuberculosis-cell mediated type 4

Am I right?can this some clue?just thinking.

AngelT
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07/04/07 - 12:34 PM

GNDA- type III
GoodPasture- type II cytotoxic
Myasthenia gravis- type II not cytotoxic
Tuberculosis- type IV
Hashimoto - type IV

The confusion is about the letter A that could be II or III depending on the type of glomerulonephritis.

AngelT
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07/04/07 - 12:34 PM

LES- type III

paheli
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08/09/07 - 01:30 PM

in SLE, there is excess Ag-Ab complexes that is deposited in various parts of the body. suppressing the action of C3 in that, incl opsonication etc will result in decreased deposition of the complexes.

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doc179
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08/09/07 - 02:49 PM

right, the immunecomplexes activate the classic complement pathway and hence when you inhibit the c3b you prevent damage to self tissue and ameliorate the disease

MALUKO
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08/14/07 - 03:02 PM

#10

Type III hypersensitivity in SLE is characterized by deposition of immune complexes specially in the kidney. If you block the function of C3b you will with withdraw the process of getting rid of the immune complexes from the body. So, you will probably end up with an increased amount of immune complexes.

C3b is an opsonin and will mediate phagocytosis of the immune complex and vasodilation.

Correct me if I'm wrong.

MALUKO
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08/14/07 - 03:09 PM

#11

doc179 wrote:
right, the immunecomplexes activate the classic complement pathway and hence when you inhibit the c3b you prevent damage to self tissue and ameliorate the disease

I think the damage is due to the immune-complex themselves and the not the action of c3b which is to prevent the immune-complex depositions.

doc179
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08/14/07 - 07:05 PM

#12

damage is not due to the deposition of immunecomplexes but because of the activation of the classic complement pathway by them which attracts the PMNs and other defense mechansims to get rid of them, hence when you block C3b , you basically alleviate the immune response towards the immunecomplexes and hence decrease damage to the tissue.

yoga
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08/15/07 - 04:36 AM

#13

E

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yoga
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08/15/07 - 04:40 AM

#14

? DONT WE HAVE IMMUNE COMPLEX DEPOSITION IN GLOMERULONEPHRITIS ALSO?

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ok07
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08/28/07 - 11:29 PM

#15

C ?

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hope4dabest
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08/30/07 - 12:35 PM

#16

Pathophysiology: Glomerular lesions in acute glomerulonephritis are the result of glomerular deposition or in situ formation of immune complexes. On gross appearance, the kidneys may be enlarged up to 50%. Histopathologic changes include swelling of the glomerular tufts and infiltration with polymorphonucleocyte. Immunofluorescence reveals deposition of immunoglobulins and complement
SOURCE--eMEDICINE

AGREED WITH CHOICE C BUT CAN SOMEBODY PLZZ EXPLAIN Y ITS NOT CHOICE A ALSO????

sfk
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08/30/07 - 06:46 PM

#17

angel, where from is this question? and whats the explanation given?

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tompat
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09/10/07 - 01:01 AM

#18

may be because u need few c3b to be free to cause damage in AGN but in SLE u require more of c3b.
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