About Danil Hammoudi.MD Expertise I can answer your questions in hematology including anemias, and cancer, hematopathology, I can not treat you just advise you.
Experience Lectures, publication, Board certified surgeon and general pathology instructor
I was given two cases for my biochemistry assignment as follows:
CASE I:
M.J. is a male of 25 years of age, of African-American dissent, who was traveling in the region when he began to notice a persistent headache, nausea, and severe backache with bouts of shivering. On admission to the hospital, his temperature was noted to be 40'C. Malaria was suspected, and later confirmed by blood analysis. For treatment, the patient was prescribed primaquine by his doctor. Three days later, he began to complain of weakness, abdominal pain, and vomiting. His sclera (white part of eye) became yellow during this period, and his urine became dark. An examination of the blood revealed that in addition to normal red blood cells, reticulocytes and red blood cells which showed Heinz bodies were observed. The patient was somewhat anemic [Hb (normal) – 14-18 g/dl, M.J. – 9.5 g/dl, RBC count (normal) - 5x1012 / l, M.J. 3.7x1012/l]
A 1. What is the medical disorder that the patient is suffering from following primaquine treatment? (hint: not malaria)
2. The patient's sclera were observed to be yellow.
Explain. In other words:
[A] what is it that is making the sclera yellow, and
[B] what are the biochemical / metabolic step which occur to generate this “pigment”?
[C] How does this the presence and placement of this “pigment” related to the patient's condition?.
[D] Where is this pigment normally formed for the majority of healthy people, and how does the body get rid of it (i.e. what is the mechanism of its catabolism and exactly how does it leave the body?)
3. The patient noted that his urine began to become dark, and eventually became almost black. Why? How is this effect related to the patient's disorder?
4. What is the probable source of the patient's indicated anemia?
5. What are reticulocytes and why do they arise in the patient's blood as a result of his condition?
6. What are Heinz bodies? What are they composed of?
7. Even while the patient is undergoing treatment with primaquine for 7 days (i.e. prior to stopping primaquine therapy altogether), you note that many of the patient's symptoms seem to be slightly improving. To confirm your suspicions, you order a test to examine the patient's blood levels of the key enzyme which you feels is connected to the symptoms he is experiencing. Sure enough, you see that the patient's level of this enzyme has risen slightly. How is this possible?
8. In performing a general physical on the patient, it was noted that he has a cataract in one eye. Is this feature related to the patient's current illness, and if so, how?
CASE II:
A family's 2 year old child Max has been brought in to the hospital because, he has been vomiting, exhibits constipation, and is pale in color. Prior to this the child was otherwise healthy, was not on any medication, and has no known metabolic errors of metabolism. The family was living in a condemned house which had not been painted in many years. The parents confided that Max had a habit of nibbling on the house furnishings such as doors. X-rays taken of Max's long bones revealed areas of increased density seen on the X-ray in growing areas of the bone (metaphyses). A blood smear taken from Max showed that he was anemic, and staining of red cells with methylene blue revealed numerous reticulocytes and RBC's with (methylene blue) stippling. Analysis of the urine revealed a puzzling elevation in gamma-aminlaevulinic acid.
9. What is wrong with Max?
10. Why is Max anemic? (what is the precise biochemical mechanism of his anemia?)
11. Why do Max's long bones look abnormal at their ends?
12. It was suggested that Max should be given a solution of calcium ethylene diamine tetraacetic acid intravenously. Why this chemical, and why intravenously? (as opposed to other routes of administration)
13. During analysis of Max's red blood cells, it was found that they exhibit heightened sensitivity to pharmaceutical agents which generate free radicals in RBC's. What is the probable mechanism of this deficiency?
14. It was fortunate that the family did not delay in bringing Max in, as doctors begun to detect the beginning of nerve damage Max's peripheral nerves (which can be repaired in time). What is the mechanism of this effect?
I know that in the first case is hyperbilirubinemia that's making his sclera yellow. But I am not sure about how this is related to the black urine and his condition (anemia and presence of reticulocytes). As well, I need help on question 7 and 8.
I think case 2 has something to do with iron overdose but I am not sure what it has to do with his abnormal metaphyses and how it's going to affect his peripheral nerves.
I know this is a long question but thanks so much for your help.
Sincerely,
Carol
Answer too long to answer in details and really time to do so
case1:
A 1. What is the medical disorder that the patient is suffering from following primaquine treatment? Methemoglobinemia
Nausea, vomiting and stomach cramps occasionally occur, with anemia
2. The patient's sclera were observed to be yellow.
Explain. In other words:
[A] what is it that is making the sclera yellow, : bilirubin impregnation [read about jaundice]
[B] what are the biochemical / metabolic step which occur to generate this “pigment”? increase bilirubin in the blood [read bilirubin cycle]
[C] How does this the presence and placement of this “pigment” related to the patient's condition?. see above same mechanism
[D] Where is this pigment normally formed for the majority of healthy people, and how does the body get rid of it (i.e. what is the mechanism of its catabolism and exactly how does it leave the body?)conjugated : liver unconjugated : red cells
The patient noted that his urine began to become dark, and eventually became almost black. Why? How is this effect related to the patient's disorder? either from urobiliuria [see bili cycle] or the methomeglobuneria but I think in this case from uro
4. What is the probable source of the patient's indicated anemia? lab
5. What are reticulocytes and why do they arise in the patient's blood as a result of his condition? red cells babies [still have nuclei, increase in case of regenerative anemia [see causes of anemia]
6. What are Heinz bodies? What are they composed of? particles in the red cells ,aggregates of denatured, precipitated hemoglobin within red blood cells (RBC)resulting in premature destruction in the spleen. The spleen also removes membrane-bound Heinz bodies from red cells resulting in "blister" or "bite" cells.
email me the rest when I have a minute I will answer
sinoe@earthlink.net
thanks
