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  #1  
Old 10-26-2010
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Help Some Confusing Questions about Nitropresside and Framshift mutations

I have some questions/differentials that are confusing me. I hope somebody could shed some light on them.
  1. Nitroprusside infusion can cause cyanide toxicity (ttt is Na thiosulfate). It can also cause methemoglobinemia (ttt is IV methylene blue and cyanide(?). Is this correct? Can somebody explain this.
  2. In frameshift mutation, there's deletion of a number not divisible by 3 of bases or nucleotides?
  3. How to differentiate between Fibroadenoma and Fibroadensosis (clinically, and by biopsy)?
Thanks in advance.
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Originally Posted by Haisook View Post
[*]In frameshift mutation, there's deletion of a number not divisible by 3 of bases or nucleotides?[/LIST]Thanks in advance.

I'll just answer this 1 first b/c it will take the least amount of time

Frameshift mutation = nucleotide addition or deletion, when they say not divisible by 3, they just mean that the whole picture moves, if you add or delete 3 then you delete 1 whole gene codon, it wouldn't mess up the rest of the sequence because the rest of those proteins will still be accounted for, however if you add or delete 1 or 2 nucleotides....then you change the whole frame....for example.

AAA BBB CCC
when you add or delete 1 or 2 nucleotides, you will have (in this case delete)
AAA BBC CC

now the BBB and BBC per say will not code for the same protein....etc, etc

nucleotide = Base + Sugar + PO4
Base = just the Nucleobase i.e A, T, C, G, U
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I figured out point 1.

Nitrites can cause methemoglobinemia by oxidation of Fe2+ to Fe3+. MetHb is treated with methylene blue.

Surprisingly, this toxicity can also be used as a treatment in cyanide poisoning. MetHb loves CN more than oxygen. So, providing MetHb in CN poisoning will lead to formation of MetHb-CN complexes. At this point, Na thiosulfate is given to bind these complexes and excrete them in the kidneys.
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Originally Posted by Haisook View Post
I figured out point 1.

Nitrites can cause methemoglobinemia by oxidation of Fe2+ to Fe3+. MetHb is treated with methylene blue.

Surprisingly, this toxicity can also be used as a treatment in cyanide poisoning. MetHb loves CN more than oxygen. So, providing MetHb in CN poisoning will lead to formation of MetHb-CN complexes. At this point, Na thiosulfate is given to bind these complexes and excrete them in the kidneys.

hmmm, maybe I just didn't understand ur question right! but yeah all of this is mentioned in Goljan
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Quote:
Originally Posted by Haisook View Post
I have some questions/differentials that are confusing me. I hope somebody could shed some light on them.
  1. Nitroprusside infusion can cause cyanide toxicity (ttt is Na thiosulfate). It can also cause methemoglobinemia (ttt is IV methylene blue and cyanide(?). Is this correct? Can somebody explain this.
I started Biochemistry today ... so i thought i should add some points...

As u already know, exposure to any oxidizing agent can cause methemoglobinemia common drugs involved are antibiotics (trimethoprim, sulphonamides & dapsone), nitrates & local anesthetics (benzocaine etc).

Sodium nitroprusside contains an iron molecule coordinated to five cyanide molecules and one molecule of nitric oxide.

The nitric oxide molecule is rapidly released during infusion, whereas the cyanide molecules are liberated gradually. So treatment with nitroprusside can cause both cyanide toxicity & methemoglobinemia.

Now methemoglobin can be protective in cyanide poisoning as cyanide and methemoglobin combine to form cyanomethemoglobin, a safe but non-oxygen-carrying form of hemoglobin.
Due to this reason the Cyanide Antidote Kit (CAK) has Amyl nitrite, sodium nitrite & sodium thiosulphate.
Hydroxycobalamin can also be used which converts cyanide into cyanocobalamin (vitamin B-12)

Cyanide is so common in nature that body has an enzyme called rhodonase that detoxifies cyanide by converting it to thiocyanate. So, cyanide poisoning is usually not an issue during the routine treatment of hypertensive emergencies. It should be anticipated in pts who have rapid infusions of nitroprusside for prolonged periods of time.

I hope this helps....
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I have some questions/differentials that are confusing me. I hope somebody could shed some light on them.

3. How to differentiate between Fibroadenoma and Fibroadensosis (clinically, and by biopsy)?

Thanks in advance.
Now its really a confusing question.....

The combined term for these conditions & a few others is called ANDI Abbretions of Normal Development & Involution. I think it would be difficult to differentiate between them both clinically & pathologically.

Anyways a few points are.....

For fibroadenoma usually, the chief complain is breast lump. Clinically its a solitary, firm, mobile & well circumscribed lump. It is difficult to differenciate between these two only on the basis of FNA.. i guess excision of the lump can give a definitive diagnosis.

On the other hand for fibroadenosis generally the chief complain is breast pain (mastalgia) and/ or breast lump. Important point in history is that pain is cyclical varying in intensity though the menstrual cycle. FNA is inconclusion & even excision is inconclusive some time. At surgery instead of a definite lump, an indurated area is often found.

I hope this is of any help....
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In med school I was taught that Fibroadenosis is ANDI, the most common breast disease in young women, and that it presents with tender breasts with or without lumps, and the tenderness varies according to the menstrual cycle. On the other hand, Fibroadenoma is a discrete localized firm mass, which is movable "mouse in breast", and is not tender.

First Aid and UW mentions that fibroadenoma is also tender and the tenderness varies with the menstrual cycle. The pathology for both is the same: sclerosing adenosis and ductal epitheliosis.

I got a couple of questions wrong because I thought it was fibroadenosis, and it was not.

I noticed the question-writers favor fibroadenoma. According to First Aid, fibroadenoma is the most common breast lesion in women < 25 yrs old, while fibroadenosis (ANDI) is most common in those > 25 years.

Still kinda confused.
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Originally Posted by Haisook View Post
In med school I was taught that Fibroadenosis is ANDI, the most common breast disease in young women, and that it presents with tender breasts with or without lumps, and the tenderness varies according to the menstrual cycle. On the other hand, Fibroadenoma is a discrete localized firm mass, which is movable "mouse in breast", and is not tender.
Well i think both fibroadenoma & fibroadenosis are included in the term ANDI which was proposed to cover the whole spectrum of benign breast disorders.

Quote:
Originally Posted by Haisook View Post
First Aid and UW mentions that fibroadenoma is also tender and the tenderness varies with the menstrual cycle. The pathology for both is the same: sclerosing adenosis and ductal epitheliosis.
Well although both can manifest cyclical mastalgia but its a predominat feature of the fibroadenosis...

Quote:
Originally Posted by Haisook View Post
I noticed the question-writers favor fibroadenoma. According to First Aid, fibroadenoma is the most common breast lesion in women < 25 yrs old, while fibroadenosis (ANDI) is most common in those > 25 years.

Still kinda confused.

Fibroadenoma is mainly the probem of abberant developed of the breast tissue. This would explain why it is most common in women during the period of breast development (15 to 25 years old). Fibroadenoma resembles the hyperplastic nodules commonly found in normal breasts

On the other hand fibroadenosis is thought to be a more severe form of the cyclical changes that take place in a woman's breasts monthly under the influence of sex hormones. This would explain why fibroadenosis is common in women during their reproductive age (25 to 35 years old).
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