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Anti-Anaemic Drugs

Deficiency Iron
Oral iron:

Type

Dosage
200- 400mg oral elemental iron daily (25% absorbed ,so 50-100mg iron can be incorporated in Hb).

Treatment
Treatment should be continue for 3-6 months, to correct the anaemia & replenish iron stores. (Hb should reach normal level in 1-3 months).

Adverse Effect
Nausea, epigastric discomfort, abdominal cramps, constipation, diarrhea, black stool.

A) Ferrous sulfate - 325mg 65mg elementaliron Inadequate dietary. B )Ferrous gluconate - 320mg In w omen heavy 37mg elem.iron menstruation. Iron requirement increase C) Ferrous fumarate - 325mg 106mg elem.iron in pregnancy and in grow ing children. Malabsorption. Parenteral iron: Iron dextran Micrositic hypochromic (ferric hydrox ide + dex tran) anaemia

50mg elemental iron/ml

Route of administration: I/M, or by I/V infusion in 1-2 hours.

Local pain, tissue staining ( brow n discoloration of tissues overlying the inj. site), headache, fever, arthralgia, nausea, vomiting, bronchospasm, urticaria, anaphylax is, and death

Oral Iron Toxicity


Its seen in young children w ho have ingested a no. of iron tablets ( more than 10 tablets). Adults are able to tolerate large doses of iron.

Acute Toxicity:
Necrotizing gastroenteritis, vomiting, abdominal pain, bloody diarrhea, dyspnea, metabolic acidosis, coma and death.

Acute Treatment:
Whole bow el irrigation Deferoxamine Supportive therapy for GIT bleeding , metabolic acidosis and shock

Chronic toxicity:
Hemochromatosis, w hen excess iron is deposited in different organs cause organ failure and death. It occurs in patients w ith inherited hemochromatosis (excessive iron absorption in pts. Who receive many red cell transfusions for long period

Chronic Treatment:
Intermittent phlebotomy, 1 unit of blood removed/w eekly Deferoxamine ( I/V or I.M) It is metabolized and excreted in urine (turn urine color orange red).

Chronic Treatment Adverse effects:


Rapid I/V administration hypotension. Idiosyncratic response such as flushing, erythema, intestinal irritation, urticaria. Acute respiratory distress syndrome w hen I/V infusion lasts > 24 hours. Neurotox icity after long term therapy of iron overload condition

Vit B12
Stored in liver, a normal individual has enough to last 5 years. It is available in 2 forms 1. cyanocobalamine, 2. hydroxy cobalamine has a longer circulating half life.

Pharmacokinetics:
Vit B12 is produced only by bacteria. It is absorbed from the GIT in presence of intrinsic factor, a product of the parietal cells of stomach. Plasma transport is accomplished by binding to transcobalamin II

Pharmacodynamics:
Vit B12 IS ESSENTIAL IN 2 REACTIONS 1.Conversion of methyl malonyl coenzyme A(co A) to succinyl co A 2.conversion of homocystein to methionine. The second reaction is linked to folic acid metabolism and synthesis of deoxythymidylate (d TMP), a precursor required for DNA synthesis

Vit B 12 deficiency:
Megaloblastic Anaemia Folates accumulates as N methyl tetrahydrofolate, the supply of tetrahydrofolate is depleted; and the production of RBCS slow s.Giving folic acid w ith Vit B12 deficiency helps refill the tetrahydrofolate pool folic acid does not correct the neurologic defects of Vit B12 deficiency

Folic acid:
Dietary insufficiency and malabsorption. Megaloblastic Anaemia

Pharmacokinetics:
Folic acid is readily absorbed from GIT. Only modest amount are stored in the body, so a decrease in dietary intake is follow ed by anemia w ithin few months

Pharmacodynamics
Folic acid is converted to tetrahydrofolate by the action of dihydrofolate reductase

Folic Acid Importance


One important set of reactions involving tetrahydrofolate and dihydrofolate constitutes the dTMP cycle, w hich supplies the dTMP required for DNA synthesis. Rapidly dividing cells are highly sensitive to folic acid deficiency. For this reason,

Treatment
Easily treated by oral folic acid. folic acid supplementation is recommended prior during pregnancy antifolate drugs are useful in treatment of infections and cancers

Erythropoietin
Produced by kidney Reduction in its synthesis is responsible for anemia of renal failure

How it w orks
Activation of receptors on erythroid progenitors in the bone marrow , it stimulates the production of red cells and increases their release from B. M

Clinical Uses
Erythropoietin is used for anemia associated w ith renal failure and some time effective for patients w ith other forms of anemia eg. primary bone marrow disorder or anemia secondary to cancer chemotherapy or HIV treatment ,bone marrow transplantation, AIDS or cancer

Toxicity
Thrombosis ,cardiovascular events w hen used along w ith some other erythropoietic agents

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