anemia pharmaco slaytı

What is anemia?

A reduction in hemoglobin, hematocrit, or red blood cell mass resulting in decreased oxygen-carrying capacity.

What is the WHO definition of anemia in men?

Hb <13 g/dL

What is the WHO definition of anemia in women?

Hb <12 g/dL

What are the three major mechanisms of anemia?

Decreased RBC production, increased RBC destruction, blood loss.

What does MCV <80 fL indicate?

Microcytic anemia.

What does MCV >100 fL indicate?

Macrocytic anemia.

What type of anemia is iron deficiency anemia?

Microcytic hypochromic anemia.

What does MCHC indicate?

Hemoglobin concentration within RBCs.

What does a high reticulocyte count suggest?

Hemolysis or acute blood loss.

What does a low reticulocyte count suggest?

Decreased RBC production.

What is ferritin?

The major iron storage protein.

What is transferrin?

The iron transport protein in plasma.

What is TIBC?

Total iron-binding capacity of transferrin.

How is ferritin affected in iron deficiency anemia?

Decreased.

How is TIBC affected in iron deficiency anemia?

Increased.

How is ferritin affected in anemia of inflammation?

Normal or increased.

How is TIBC affected in anemia of inflammation?

Normal or decreased.

What is hepcidin?

The master regulator of iron metabolism.

Where is hepcidin produced?

Liver.

What does hepcidin bind to?

Ferroportin.

What happens when hepcidin increases?

Decreased iron absorption and iron release from stores.

When does hepcidin increase?

Inflammation and iron overload.

When does hepcidin decrease?

Iron deficiency and increased erythropoiesis.

What is the mechanism of anemia of inflammation?

IL-6 ↑ → Hepcidin ↑ → iron trapped in storage sites.

Where is iron mainly absorbed?

Duodenum and proximal jejunum.

Which form of iron is best absorbed?

Fe²⁺ (ferrous iron).

What are the main causes of iron deficiency anemia?

Blood loss, increased demand, decreased intake, malabsorption.

Which oral iron preparations are commonly used?

Ferrous sulfate, ferrous fumarate, ferrous gluconate.

What enhances iron absorption?

Vitamin C (ascorbic acid).

What reduces iron absorption?

Tea, coffee, calcium-containing products.

What are the most common adverse effects of oral iron?

Nausea, vomiting, constipation, diarrhea, dark stools.

What is the earliest sign of response to iron therapy?

Reticulocytosis.

When is reticulocyte response seen after iron therapy?

7–10 days.

When does hemoglobin usually increase after iron therapy?

2–4 weeks.

Why is iron therapy continued after Hb normalizes?

To replenish iron stores.

What are indications for IV iron therapy?

Oral intolerance, malabsorption, CKD, need for rapid replacement.

Which route is preferred for parenteral iron?

Intravenous infusion.

Why is IM iron generally avoided?

Pain, local reactions, skin staining.

Which IV iron preparation has the highest hypersensitivity risk?

Iron dextran.

What is the first-line treatment for hereditary hemochromatosis?

Therapeutic phlebotomy.

Name three iron chelators.

Deferoxamine, deferasirox, deferiprone.

What are the most common causes of megaloblastic anemia?

Vitamin B12 deficiency and folate deficiency.

What is the classic blood smear finding in megaloblastic anemia?

Hypersegmented neutrophils.

How is homocysteine affected in vitamin B12 deficiency?

Increased.

How is methylmalonic acid (MMA) affected in vitamin B12 deficiency?

Increased.

How is MMA affected in folate deficiency?

Normal.

What is the most important distinguishing feature of vitamin B12 deficiency?

Neurologic manifestations.

Do neurologic symptoms occur in folate deficiency?

No.

What causes pernicious anemia?

Autoimmune destruction of parietal cells leading to intrinsic factor deficiency.

Which cells produce intrinsic factor?

Gastric parietal cells.

Where is vitamin B12 absorbed?

Terminal ileum.

What neurologic findings are seen in vitamin B12 deficiency?

Paresthesia, ataxia, loss of vibration sense.

What is the preferred treatment for severe vitamin B12 deficiency?

Parenteral vitamin B12.

What is the antidote for methotrexate toxicity?

Leucovorin (folinic acid).

What is the primary role of folate?

DNA synthesis.

What is the active form of folate?

Tetrahydrofolate (THF).

What is the daily folate requirement in adults?

400 mcg/day.

What is the daily folate requirement during pregnancy?

600 mcg/day.

Why is folic acid given during pregnancy?

To prevent neural tube defects.

Name two neural tube defects.

Spina bifida and anencephaly.

Where is erythropoietin (EPO) produced?

Kidney.

What is the effect of EPO?

Stimulates erythroid progenitor cells and RBC production.

How does hypoxia affect EPO production?

Increases EPO production.

What does ESA stand for?

Erythropoiesis-Stimulating Agent.

Name two ESAs.

Epoetin alfa and darbepoetin alfa.

What is the advantage of darbepoetin alfa over epoetin alfa?

Longer half-life.

What is the major indication for ESA therapy?

Anemia of chronic kidney disease.

What are the major adverse effects of ESAs?

Hypertension and thrombosis.

Name two HIF-PHIs.

Daprodustat and vadadustat.

How do HIF-PHIs work?

Stabilize HIF and increase endogenous EPO production.

What is luspatercept?

An erythroid maturation agent.

What are the major indications of luspatercept?

Beta-thalassemia and lower-risk MDS.

What does G-CSF stimulate?

Neutrophil production.

Name two G-CSF agents.

Filgrastim and pegfilgrastim.

What is the most common adverse effect of filgrastim?

Bone pain.

What is GM-CSF?

A growth factor stimulating neutrophils, monocytes, and eosinophils.

Name a GM-CSF drug.

Sargramostim.

What does thrombopoietin (TPO) stimulate?

Megakaryocyte maturation and platelet production.

Name four TPO receptor agonists.

Romiplostim, eltrombopag, avatrombopag, lusutrombopag.

What is the major indication for romiplostim?

Chronic immune thrombocytopenia (ITP).

Which minerals interfere with eltrombopag absorption?

Calcium, iron, magnesium, aluminum.

What is a major adverse effect of eltrombopag?

Hepatotoxicity.

What is oprelvekin?

Recombinant IL-11.

What is the effect of oprelvekin?

Increases platelet production.

What is the most important adverse effect of oprelvekin?

Fluid retention.

What hematologic abnormalities occur in copper deficiency?

Anemia and leukopenia.

What is pyridoxine (vitamin B6) used to treat?

Sideroblastic anemia.

What is the treatment for isoniazid-induced sideroblastic anemia?

Pyridoxine (vitamin B6).

Which drugs are used for anemia of CKD?

Epoetin alfa, darbepoetin alfa, daprodustat, vadadustat.

Which drug is used for transfusion-dependent beta-thalassemia?

Luspatercept.

Which drug is used for chemotherapy-induced neutropenia?

Filgrastim.

Which drugs are used for chronic ITP?

Romiplostim and eltrombopag.