gm sir
DESCRIPTION
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HEMATINICS
TREATMENT
Oral Therapy:Ferrous SulphateFerrous FumarateFerrous Gluconate
Parenteral Therapy:Iron DextranIron-sucrose complex Iron sodium gluconate complex
Clinical uses
• Iron deficiency anemia in • Infants• Pregnant and lactating women• Children during rapid growth periods
ADVERSE EFFECTS –ORAL IRONCommon adverse effects:• Nausea• Epigastric discomfort• Abdominal cramps• Constipation/diarrhea
These effects are usually dose-related and can often beovercome by lowering the daily dose of iron or by taking thetablets immediately after or with meals
Patients taking oral iron develop black stools; this has noclinical significance in itself but may obscure the diagnosis ofcontinued gastrointestinal blood loss
PARENTERAL IRON THERAPY
Parenteral therapy should be reserved for patients who
are unable to tolerate or absorb oral iron and forpatients with extensive chronic blood loss .
Postgastrectomy conditions Small bowel resection Inflammatory bowel disease(proximal small bowel) Malabsorption syndromes
VITAMIN B12....
Essential in two reactions:1.Conversion of methylmalonyl-coenzyme A to
Succinyl-CoA2.Conversion of Homocysteine to Methionine
The second reaction is linked to folic acidmetabolism and synthesis of deoxythymidylate(dTMP)
dTMP is a precursor for DNA synthesis
VITAMIN B12.....
In Vitamin B12 deficiency, folate accumulatesas N-Methyltetrahydrofolate
The supply of tetrahydrofolate is depleted
This slows production of RBCs
Folic acid replacement can correct B12deficiency anemia, but not the neurologicalmanifestation of B12 deficiency.
VITAMIN b12...Absorption:
Vitamin B12 binds to Intrinsic factor (secreted bygastric parietal cells)
It prevents digestion of B12
In bound state ,it binds to receptors on brushborder of mucosa
These receptors are located in ileum
Bound intrinsic factor and B12 are absorbed withpinocytosis
VITAMIN B12....
DISTRIBUTION:
Vitamin B12 is distributed to various cellsbound to a plasma glycoprotein,Transcobalamin
II
STORAGE:Excess vitamin B12 (upto 300-500 microgram) isstored in liver
VITAMIN B12
ELIMINATION :
Trace amounts of vitamin B12 are normally lostin urine and stool.
Significant amount of vitamin B12 are excretedin urine (when large amounts are givenparenterally)
FOLIC ACID.....ABOSRPTION:Form:
Dietary folates in polyglutamate forms; first undergo hydrolysis by conjugase (present in brush border of intestinal mucosa) and form monoglutamate
Site: Proximal jejunum
Only modest amounts of folic acid are stored inbody,therefore a decrease in diet will lead toanemia in few months
Folic acid
Distribution:Widely distributed through out the body viablood stream
Storage:Normally, 5-20 mg is stored in liver and othertissues
Elimination:Excreted in urine and stool, and also destroyedby catabolism
CLINICAL USES OF VIT B12 AND FOLIC ACID
These are used in anemia (megaloblastic)
Pernicious anemia ( Vitamin B12, basically IF)
Prophylaxis for neural tube defects (folic acidbefore conception)
Neuropathy (Vitamin B12)
Cancer chemotherapyCertain drug therapies lead to deficiency of folic
acid so replacement is required
VITAMIN B12 PREPARATIONS
Tablet and syrup forms:Cyanocobalamin, Hydroxycobalamin
Parenteral:I/M, I/V.
Use: To corrects major depletion of B12 quickly If patient is unable to take orally Required in patients with pernicious anemia(IF deficiency)
Parenteral therapy can lead to pain at injection site
VITAMin B12 and folic acid
Both are very well toleratedThere are no remarkable adverse effects oftherapy
• The side effect which primarily limits acceptability of oral iron therapy is
• Black stools• Epigastric pain and bowel upset• Staining of teeth • Metallic taste
• Choose the correct statement about iron therapy
• Iron is given in megaloblastic anemia• Iron must be given orally except in pernicious
anemia• Prophylactic iron therapy must be given during
pregnancy• Infants on breast feeding do not require
medicinal iron
• A 23 year old pregnant woman is referred by her obstetrician for evaluation of anemia.If this woman has macrocytic anemia,an increased serum concentration of vitamin B12,the most likely cause of her anemia is deficiency of ,
• Cobalamin• Erythropoietin• Folic acid• Intrinsic factor• Iron
• If the patient had folic acid deficiency,her infant would have a higher than normal risk of
• Cardiac abnormality• Kidney damage• Limb deformity• Neural tube defect
• A pregnant patient is found to have microcytic anemia.Optimal treatment of microcytic anemia is
• A high fibre diet• Erythropoietin injections• Ferrous sulphate tablet• Folic acid supplements• Hydroxocobalamin injections
• The iron stored in intestinal mucosal cells is complexed to
• Intrinsic factor• Transcobalamin II• Transferrin• Ferritin
• An important biochemical consequence of vitamin B12 deficiency is accumulation of
• Dihydrofolate• dTMP • Folic acid• Tetrahydrofolate• Methyltetrahydrofolate
• Mr. Abid, 25 years of age was suffering from chronic lethargy and weakness On examination he was very pale and he had signs of neuropathy as well. His Laboratory tests showed megaloblastic type of anemia. His physician performed Schilling’s test, which was positive. Choice of management would be:
• • Cyanocobalamin orally• Folic acid orally• Vitamin B12, I/V• Folic acid+Vitamin B12 orally• Intrinsic factor orally