Pilot exam question.

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Psiquis

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Hi, guys,

I'm looking at the Pilot exam and there is a question that is driving me crazy.

Q. 334 says:
- Following prophylactic administration of Amox., a patient becomes hypotensive and itchy and is having difficulty breathing. Which of the following is MOST probably occuring?

a) CD4 lymph are secreting lymphokines resulting in edema.
b) Amoxi. reacts with IgE and activates cytotoxic T-cells to relase lymphokines.
c) IgG and complements are inducing the chemotaxis of neutrophils out of vessels.
d) IgE bound to antigen results in histamine relase from mast cells.

Answer is given as b.

As far as I know, the mast cells (or basoph) are the ones that react with IgE-antigen complex, causing their degranulation in Hypersensitivity type I reaction.
Did I miss something? I just don't understand.
Can anyone explain why is B the right answer?
 
Hi, guys,

I'm looking at the Pilot exam and there is a question that is driving me crazy.

Q. 334 says:
- Following prophylactic administration of Amox., a patient becomes hypotensive and itchy and is having difficulty breathing. Which of the following is MOST probably occuring?

a) CD4 lymph are secreting lymphokines resulting in edema.
b) Amoxi. reacts with IgE and activates cytotoxic T-cells to relase lymphokines.
c) IgG and complements are inducing the chemotaxis of neutrophils out of vessels.
d) IgE bound to antigen results in histamine relase from mast cells.

Answer is given as b.

As far as I know, the mast cells (or basoph) are the ones that react with IgE-antigen complex, causing their degranulation in Hypersensitivity type I reaction.
Did I miss something? I just don't understand.
Can anyone explain why is B the right answer?


Hi
i hav read in one solved paper,there the ans z 'D'

any one plz correct me if i m wrong.
Thank u.
 
answr D is for allergy-histamine release triple response
answr B is anaphylaxis caused by amox

Hi, redroulette...
Could you, please, be more specific?
I didn't know anything about "allergy-histamine release triple response, nor anaphylaxis caused by amox".
Right now I'm like: "whatttttt?"😱

If you can explain that, I'll be really grateful.
 
The answer is to find the difference between an anaphylactic reaction and an allergic reaction
Both are not exactly similar..thats the answer for the above Q .
Hints: Anaphylaxis - cardiovascular collapse by trigerring ?
(Roitt- Textbook of immunology)
 
The answer is to find the difference between an anaphylactic reaction and an allergic reaction
Both are not exactly similar..thats the answer for the above Q .
Hints: Anaphylaxis - cardiovascular collapse by trigerring ?
(Roitt- Textbook of immunology)

Well, that's the point. I don't have Roitt.
I do have First Aid, Kaplan and Mosby, but even though I have been reading those books for a long time, they say nothing about cardiovascular collapse due to anaphylaxis.

Thanks for the hint... I'll google it right now.
 
Please post if you found the difference between allergic reaction and analphlaxis.


Hi, guys,

I'm looking at the Pilot exam and there is a question that is driving me crazy.

Q. 334 says:
- Following prophylactic administration of Amox., a patient becomes hypotensive and itchy and is having difficulty breathing. Which of the following is MOST probably occuring?

a) CD4 lymph are secreting lymphokines resulting in edema.
b) Amoxi. reacts with IgE and activates cytotoxic T-cells to relase lymphokines.
c) IgG and complements are inducing the chemotaxis of neutrophils out of vessels.
d) IgE bound to antigen results in histamine relase from mast cells.

Answer is given as b.

As far as I know, the mast cells (or basoph) are the ones that react with IgE-antigen complex, causing their degranulation in Hypersensitivity type I reaction.
Did I miss something? I just don't understand.
Can anyone explain why is B the right answer?
 
Please post if you found the difference between allergic reaction and analphlaxis.

Actually I didn't.... funny note is that the exact Q. is repeated in other released exam, and the answer is given as IgE/mast.
I couldn't find the Roitt... so... I have no idea.
Also, as far as it's concerned, other textbooks point to mast and basoph as causative agents of anaphylaxis.

But, as I said, I have not idea.

Good luck! (I need it!) 😉
 
The answer is to find the difference between an anaphylactic reaction and an allergic reaction
Both are not exactly similar..thats the answer for the above Q .
Hints: Anaphylaxis - cardiovascular collapse by trigerring ?
(Roitt- Textbook of immunology)

wrong.
 
ansewr is correct.
because amoxicilin is oral route.. so doesn't affect to systemic reaction as type I allergy reaction called anaphylatic shock.
It will act like delay hypersensitivity(type 4)- cell mediated.

But If ampicilin, the answer will be "D". coz it usally given by IV. so it means it will go systemic~~.

anything wrong, correct me pls~!!
 
ansewr is correct.
because amoxicilin is oral route.. so doesn't affect to systemic reaction as type I allergy reaction called anaphylatic shock.
It will act like delay hypersensitivity(type 4)- cell mediated.

But If ampicilin, the answer will be "D". coz it usally given by IV. so it means it will go systemic~~.

anything wrong, correct me pls~!!

Anaphylaxis, a type I hypersensitivity rxn, can occur with oral ingestion of the offending antigen. Example, peanut/seafood allergies can result in anaphylaxis if the antigen (peanut/seafood) is orally ingested. Hypersensitivity type I rxns don't really depend on the route of administration, but rather, on the antigen's ability to mass-bind IgE antibodies bound to the surface of mast cells. In "atopic" (allergic) individuals, for whatever reason, IgE is hypersecreted by plasma cells in response to a sensitizing antigen. These excess IgE levels then "arm" the surface of mast cells in higher proportions than they do in non-atopic individuals.

Hypersensitivity type IV rxns, on the other hand, are induced by antigens that tend to be processed and presented by APC's. Contrast this to hypersensitivty type I antigens which more likely bind to surface IgE's. The APC's will present their antigens to CD4 T cells, which will then "superactivate" macrophages via the release of IFN-g and also activate CD8 cytotoxic T cells. It is the combination of CD8 T cells and superactivated macrophage mediated immune response against the antigen that results in the clinical symptoms commonly associated with this rxn.
 
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