Dr. Soban sadiq

Oral Therapy:Ferrous SulphateFerrous FumarateFerrous Gluconate

Parenteral Therapy:Iron DextranIron-sucrose complex Iron sodium gluconate complex

Iron deficiency anemia in Infants Pregnant and lactating women Children during rapid growth periods

Common 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 no

clinical significance in itself but may obscure the diagnosis of

continued gastrointestinal blood loss

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

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

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.

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

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

ELIMINATION :

Trace amounts of vitamin B12 are normally lost

in urine and stool.

Significant amount of vitamin B12 are excreted

in urine (when large amounts are givenparenterally)

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

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

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 folicacid so replacement is required

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

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