L8 Anaemia Treatment Drugs(2)

They inhibit the enzymes that convert folic acid to tetrahydrofolic acid (folinic).

Recombinant erythropoietin.

Nausea, vomiting, epigastric pain, abdominal cramps, constipation or diarrhea.

Cyanocobalamin and hydroxocobalamin.

To properly treat anemia.

Anticonvulsants (e.g., phenytoin & phenobarbital), oral contraceptives, long-term use of aspirin, and caffeine.

To stimulate the production of red blood cells.

Impaired marrow production and nutritional deficiencies (iron, vitamin B12, and folic acid).

Treatment of megaloblastic anemia due to folate deficiency.

Increased risk of hypertension, stroke, myocardial infarction, heart failure, and death.

Oral or parenteral, depending on the severity of anemia and absorption adequacy.

Meat, dates, nuts, and green leafy vegetables.

A reduction in the concentration of hemoglobin (Hgb) that results in reduced oxygen-carrying capacity of the blood.

Because increased RBC synthesis will need iron.

Headache, back pain, arthralgia, fever, lymphadenopathy, and anaphylactoid reactions.

For hemoglobin, myoglobin, and enzymes.

Necrotizing gastroenteritis, nausea and vomiting, hematemesis, and bloody diarrhea.

Tetracyclines, levothyroxine, and ciprofloxacin.

By administering both Vitamin B12 and folic acid.

To replace the iron necessary for red blood cells (RBCs).

Inadequate erythropoiesis, increased hemolysis, and blood loss.

Myelosuppressive drugs, irradiation, infection, cancer, chronic kidney diseases, chronic immune-related diseases, and chronic inflammation.

It may improve symptoms if due to folate deficiency, but neurological lesions from B12 deficiency will persist.

1 - 2 months.

Failure of oral iron therapy or persistent chronic causes like chronic severe anemia or chronic renal disease on hemodialysis.

Administer an initial test dose and observe the patient for allergic reactions.

To reduce excess iron in the absence of anemia.

Initial intramuscular intensive treatment phase, followed by lifelong maintenance therapy.

B12 and/or folic deficiency.

Cell replication, hematopoiesis, and myelin synthesis.

Through GI microorganism synthesis.

Using deep injection with a Z technique.

Accidental ingestion of iron tablets.

They are degraded by reticuloendothelial cells.

Organ failure, including bronzed diabetes.

To manage iron overload.

Prophylaxis for folic or iron deficiency anemia and for pregnant women.

Vegetarian diet.

Erythropoiesis stimulating agents.

Essential for DNA synthesis and cell proliferation.

Ferrous sulfate, ferrous gluconate, and ferrous fumarate.

100 - 200 mg given per day in divided doses.

Susceptible individuals such as pregnant women, premature infants, and those with severe chronic hemolytic anemia.

Via exfoliation of intestinal cells in stool, bile, urine, and sweat.

Supportive treatment for gastrointestinal bleeding, acidosis, and shock.

It is used to treat megaloblastic anemia.

In cases of excessive blood loss, heart failure, or when immediate replenishment is required.

Synthetic proteins that mimic erythropoietin, including Recombinant human EPO (epoetin alfa) and epoetin β (pegylated form).

They should be given with iron, B12, and folic supplements to support erythropoiesis.

Fe3+.

They help convert ferric iron to ferrous iron, enhancing absorption.

Slow IV infusion in 500 ml saline over 1 - 2 hours.

It combines with cyanide to form harmless cyanocobalamin in the blood.

Gastrectomy and malabsorption.

It leads to decreased erythropoietin production.

By taking iron after meals and using enteric-coated sustained-release iron preparations.

Orally (p.o.), parenterally, or as sublingual (SL) or nasal spray.

Transferrin.

Increased blood transfusion leading to excess iron accumulation.

Celiac disease is one example.

It is especially used for diabetic neuropathy.

Iron therapy.

Peptic ulcer (PU) and menorrhagia.

1. Anemia of chronic renal failure. 2. Bone marrow suppression (e.g., cancer chemotherapy or zidovudine for AIDS).

From the upper small intestine (SI).

From the distal ileum after binding to intrinsic factor (IF).

IF is secreted from parietal cells with HCl and is necessary for B12 absorption.

Hemochromatosis.

Ferric iron increases, leading to decreased absorption.

It is an iron chelating compound used to treat iron toxicity.

Treatment of the cause.

Pregnancy and premature babies.

Dietary meats, dairy products, and eggs.

Pain, inflammation, and brown staining with intramuscular injection.

To reduce gastric distress caused by iron.

Vitamin B12 deficiency leading to pernicious anemia.

It returns to plasma or is stored, with small amounts excreted.

Gastric lavage using phosphate or carbonate solutions.

Megaloblastic anemia (macrocytic).

Methotrexate, trimethoprim, and pyrimethamine.

Deficiency of Erythropoietin, which is essential for RBC formation in the bone marrow.

It is given intravenously or subcutaneously 1-3 times per week to target Hb levels between 10-12 gm/dL.

As ferritin.

No, it is very rare but can occur.

Iron absorption increases with higher requirements and decreases with higher iron stores.

To prevent toxicity of antifolate drugs.

Tannic acid from tea, phytates from plant origin, and carbonates.

Decrease intake (vegetarians), malabsorption, gastrectomy (IF), tapeworm infection, pernicious anemia.

4 - 6 months.

Only IV with less hypersensitivity.

Based on hemoglobin deficit, usually 1 - 2g (20 - 40 ml) of iron dextran.

Continued cell growth occurs without DNA synthesis.

Because B12 cannot combine with intrinsic factor.

Neural tube defects, such as cleft lip, cleft palate, and spina bifida.

They form non-absorbable complexes with iron, decreasing absorption.

It acts as a co-factor to convert dihydrofolic acid to active folinic acid.

Colchicine, neomycin, chronic heavy alcohol intake, and drugs that decrease HCl.