Methemoglobinemia

Question: What do argyria and methemoglobinemia have in common? How is the main supposed visible symptom in each really brought about?

Answer: type your question in yahoo and go to where it says emedicine:argyria something and to emedicine:methemoglobinemia somethig some

Question: In methemoglobinemia what happens to the proteins and actiive sites. Also-? also- explain in general terms what effect the mutation must have on diaphorase 2.

Answer: In general, methemoglobinemia is malfunction of the synthesis of the completed form protein hemoglobin (Hb). Congenital methemoglobinemia is generally the result of a deficiency of the enzyme diaphorase, which results in high levels of Met-Hb, which does not transport oxygen. Congenital methemoglobinemia can also be caused by formation of the abnormal hemoglobins HbM and HbH, which are very poor carriers of oxygen. I don't know of any direct effect on diaphorase II, but diaphorase II can be utilized to treat methemoglobinemia. Diaphorase II normally does not have too much to do with red blood cell reducing capacity, but it can be activated by methylene blue to 5 times its normal level of activity, which can be very helpful. Chronic low-level methemoglobinemia can be treated using oral methylene blue daily. Severe methemoglobinemia can be treated using intravenous methylene blue.

Question: How frequently does methemoglobinemia happens?

Answer: You can look into this website to know more about the disease and or the frequency that it happens: http://www.answers.com/topic/methemoglob… Good luck to youl.

Question: Methemoglobinemia, aka "Blue People"? Methemoglobinemia is a condition where the skin literally is blue, but it can be cured through daily tablets of methylene blue (ironic, I know). My question is, has anybody been able to find a true photo of a person with methemoglobinemia? Like of the Fugates of Troublesome Creek? The only picture I can find doesn't even look like a real picture- it looks more like a drawing.

Answer: Here is one; http://www.healthsystem.virginia.edu/internet/medtox/cct/consult.cfm

Question: Genetic disorder methemoglobinemia (blue person disease)? Is methemoglobinemia a chromosomal disorder or a gene disorder? i can't tell....any doctors or biology experts out there? lol

Answer: It's caused by a recessive gene, but it manifests itself in a chromosomal error. So the answer is, yes....it's a chromosomal and genetic disorder.

Question: Summarize methemoglobinemia. What is it?

Answer: methemoglobinemia is a disease caused when cytokins such as necrosis factor-alpha (TNF-alpha) and interleukin-1 are produced via the photochemical addition of cyclic endoperoxides to glucocorticoids in the gluconeogenesis process of carbohydrate metabolism. As a result, the globin proteins in the blood inflame because the arachidonic acid forms carbon radicals from cyclooxygenase-1-enzyme (COX-1). This inflamation causes the patient to suffer from fatigue. It is often treated by binding catalytic gamma subunits of AMP to the protease inhibitor proteins. This action, blocks the production of arachidonic acid and thus, inhibits the carbon radical formation. Without the high energy radicals, inflamation is non existent.

Question: which is worse - 50% carboxyhemoglobinemia or 50% methemoglobinemia?

Answer: I hope this is not a personal question. Neither is good. Carboxyhemoglobin is carbon monoxide that is attatched to the hemoglobin. 50% is severe poisoning that can cause death. Remember that carbon monoxide binds to hemoglobin 200% more than oxygen. You can get CO poisoning from house fires, furnaces, and car fumes to name a few. Methemo is is when you have red blood cells and the oxygen can't bibind to it. At 50% a coma, seizures and other symptoms can occur. 70% is the fatal range. All in all, both are extremely bad.

Question: who discovered Methemoglobinemia? i need this for my biology project. aka blue offspring syndrome and blue fugates disease

Answer: Dr. James Deeny The 'blue men of Lurgan' were a pair of Lurgan men suffering from what was described as 'familial idiopathic methaemoglobinaemia' who were treated by Dr. James Deeny in 1942. Deeny, who would later become the Chief Medical Officer of the Republic of Ireland, prescribed a course of ascorbic acid and sodium bicarbonate. In case one, by the eighth day of treatment there was a marked change in appearance and by the twelfth day of treatment the patient's complexion was normal. In case two, the patient's complexion reached normality over a month-long duration of treatment. http://en.wikipedia.org/wiki/Methemoglob…

Question: Methemoglobinemia Mutations? Using your knowledge of the general structure of proteins and specificity of active sites of enzymes, explain in general terms what effect the mutation must have on Diaphorase II

Answer: Methemoglobinemia mutations typically cause a deficiency of the enzyme diaphorase I (NADH methemoglobin reductase), resulting in a rise of methemoglobin levels rise, such that the blood of met-Hb sufferers has reduced oxygen-carrying capacity, often manifested by a brownish blood coloration and a bluish cast in the skin color of white victims of methemoglobinemia. Methemoglobinemia can be treated with supplemental oxygen and methylene blue 1% solution (10mg/ml), where methylene blue 1-2 mg/kg solution is administered intravenously slowly, over a five minute session, followed by an IV flush with normal saline. Methylene blue restores the iron in hemoglobin to its normal (reduced) oxygen-carrying state. This is achieved through the enzyme inducing effect of methylene blue on levels of diaphorase II (NADPH methemoglobin reductase). Diaphorase II normally contributes only a small percentage of the red blood cells' reducing capacity, but is pharmacologically activated by exogenous cofactors, such as methylene blue, to 5 times its normal level of activity. Genetically induced chronic low-level methemoglobinemia may be treated with oral methylene blue daily. Also, vitamin C can occasionally reduce cyanosis associated with chronic methemoglobinemia, but has no role in the treatment of acute acquired methemoglobinemia.

Question: If Methemoglobinemia has been ruled out ... what next? If you have blood gas results (Co-Oximetry), that are the following: O2Hb 66% MetHb 20% COHb 1% HHb 13% You were given methylene blue via IV x 2 occassions, and the MetHb is not affected, what would be the next step in evaluating this patient?

Answer: I think your logical step is to suspect Sulfhemoglobinemia (SHb) ... which would probably have to be sent off to some large diagnostic lab .. you see ... SHb has the same absorption spectra as MetHb ... approx. 626 nm. Thus automated blood gas analyzers with spectrophotometers are unable to accurately differentiate between the two species ... I know some labs that will add cyanide to the assay ... where the MetHb turns to cyanomethemoglobin and changes absorption characteristics ... and the SHb is an irreversible hemichrome, and unaffected by cyanide, thus when the measurements are made ... the measured MetHb ... actually represents the SHb ... After you have established this rare diagnosis ... generally ... with SHb .. the oxyhemoglobin curve shifts to the right ... which will actually ameliorate the effects of reduced oxygen binding capacity and enhances oxygen delivery to the tissues .. How do you get rid of it? Actually, they usually allow the natural churn over rate of RBC's (57 to 60 days ... I forget) ... unless the SHb is huge ... then I guess you have to consider a transfusion (never seen that done)