A detailed medical educational poster about Thalassemia with the following sections clearly laid out: TITLE: THALASSEMIA - A Complete Medical Guide DEFINITION section: "Thalassemia is an inherited (autosomal codominant) disorder caused by mutations in globin genes (α or β) that reduce hemoglobin synthesis, resulting in microcytic hypochromic anemia, hemolysis, and tissue hypoxia. The word 'thalassa' means sea in Greek - originally described in Mediterranean populations." CAUSE / GENETICS section: - β-Thalassemia: Point mutations on Chromosome 11 reducing/abolishing β-globin synthesis - α-Thalassemia: Gene deletions on Chromosome 16 reducing α-globin synthesis - Autosomal codominant inheritance - Endemic in Mediterranean, Middle East, Africa, India, Asia (malaria belt) CLASSIFICATION table: β-Thalassemia Major (Cooley's Anemia) | Homozygous | Severe anemia, needs transfusions β-Thalassemia Intermedia | Variable | Moderate anemia β-Thalassemia Minor (Trait) | Heterozygous | Mild/asymptomatic α-Thalassemia Silent Carrier | 1 gene deleted | No symptoms α-Thal Trait | 2 genes deleted | Mild microcytosis HbH Disease | 3 genes deleted | Moderate-severe hemolysis Hydrops Fetalis | 4 genes deleted | Fatal in utero SIGNS & SYMPTOMS section: - Severe microcytic hypochromic anemia (Hb <7 g/dL) - Pallor, fatigue, weakness - Jaundice (hemolysis) - Hepatosplenomegaly (extramedullary hematopoiesis) - Thalassemia facies: frontal bossing, prominent cheekbones, flat nasal bridge (skull X-ray: "hair on end" appearance) - Growth retardation, delayed puberty - Iron overload (hemosiderosis): cardiac, liver, endocrine failure - Leg ulcers, gallstones INVESTIGATIONS section: - CBC: Low Hb, low MCV, low MCH, microcytic hypochromic picture - Peripheral blood smear: target cells, tear-drop cells, nucleated RBCs, basophilic stippling - Hb Electrophoresis (KEY test): ↑HbA2 in β-thal minor; ↑HbF; absent/reduced HbA in major - Serum ferritin & iron: elevated (iron overload) - Skull X-ray: "Hair on end" / "crew cut" appearance - Bone marrow: erythroid hyperplasia - Genetic/DNA analysis: confirms mutations - Prenatal: CVS, amniocentesis TREATMENT section: - Regular blood transfusions (every 2-4 weeks, target Hb >10 g/dL) - for Thal Major - Iron chelation therapy: Desferrioxamine, Deferasirox (prevent iron overload) - Folic acid supplementation - Splenectomy (if hypersplenism) - Bone Marrow / Stem Cell Transplantation - CURATIVE - Gene therapy (emerging treatment) - Hydroxyurea (increases HbF) - NO IRON supplements PREVENTION section: - Genetic counseling - Carrier screening (premarital) - Prenatal diagnosis Use a clean medical infographic style with a dark navy blue and white color scheme, red and orange accent colors for section headers, clear icons for each section, and organized layout with distinct boxes for each section. Professional, clinical, and easy to read.

A detailed medical educational poster about Thalassemia. Clean infographic style, dark navy blue background, white text, red and orange accent colors for section headers. Organized into clearly labeled boxes. TITLE at top: THALASSEMIA - Complete Medical Guide 6 sections in grid layout: 1. DEFINITION: Inherited autosomal codominant disorder. Mutations in globin genes (alpha or beta) reduce hemoglobin synthesis. Results in microcytic hypochromic anemia, hemolysis, tissue hypoxia. "Thalassa" = sea in Greek. Common in Mediterranean, Middle East, Africa, India, Asia. 2. CAUSES / GENETICS: Beta-Thalassemia - point mutations on Chromosome 11. Alpha-Thalassemia - gene deletions on Chromosome 16. Types: Beta Major (Cooley anemia) homozygous severe; Beta Minor heterozygous mild; HbH disease 3 gene deletions; Hydrops Fetalis 4 gene deletions fatal. 3. SIGNS AND SYMPTOMS: Severe pallor and fatigue. Jaundice. Hepatosplenomegaly. Thalassemia facies - frontal bossing, flat nose. Growth retardation. Iron overload - cardiac and liver failure. Gallstones. Leg ulcers. 4. INVESTIGATIONS: CBC - low Hb, low MCV microcytic hypochromic. Blood smear - target cells, nucleated RBCs, tear drop cells, basophilic stippling. Hb Electrophoresis - raised HbA2 and HbF, reduced HbA. Serum ferritin raised. Skull X-ray - hair on end appearance. Bone marrow - erythroid hyperplasia. DNA analysis for mutations. 5. TREATMENT: Regular blood transfusions every 2-4 weeks. Iron chelation - Desferrioxamine, Deferasirox. Folic acid supplements. Splenectomy for hypersplenism. Bone marrow stem cell transplant - curative. Gene therapy emerging. Hydroxyurea increases HbF. NO iron supplements. 6. PREVENTION: Genetic counseling. Premarital carrier screening. Prenatal diagnosis - CVS or amniocentesis.