Anemia Classification Chart PDF

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Summary

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Description

Anemia Classification Chart Type of Anemia

Clinical Presentation

Space Occupying Lesion

Etiology -

Anemia of Renal Failure

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Aplastic Anemia

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kidney damage

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Fanconi Anemia

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Pure Red Blood Cell Aplasia

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Folic Acid/Vitamin B12 Deficiency (Megaloblastic or Macrocytic Anemia)

Hypoplasia of kidney/spleen Bone abnormalities in thumbs/radius

B12 ONLY: Neuropsych manifestations B12 and Folic Acid Anemia sx Glossitis

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Granulomas Fibrosis in bone marrow malignancy kidney damage  dec EPO  dec RBC production Idiopathic Infections (EBV, CMV, Rubella, Viral hepatitis) Chemical (benzene) Inherited (Fanconi Anemia – see below) Drug Toxicity Autosomal recessive

Immune-mediated Drug Tumors (thyoma, large granular lymocytic leukemia Parvovirus B19 Asynchronous growth – nucleus doesn’t mature, cytoplasm does mature B12: Nutritional Malabsorption Gastrectomy Ileal resection Tropical sprue (flattening of the intestinal wall) Transcobalamin deficiency NO abuse Competition for vitamin B12 with fish tapeworm or bacterial overgrowth Chronic pancreatitis

Blood Work

PBS

Bone Marrow

Treatment Treat underlying cause

Leukoerythroblastosis -tear drop RBCs -immature cells

Recombinant Epogen

Pancytopenia -anemia -thrombocytopenia -leukopenia

Hypocellular

Bone marrow transplant immunosuppression

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Treat underlying cause Immunosuppression

B12: increased methylmalonic acid and homocysteine Folic Acid: increased homocysteine ONLY CBC: macrocytes

-Macrocytes -Ovalocytes -Hypersegmented PMNs -Giant bands -Metamyelocytes

Megaloblasts from ineffective hematopoiesis

Hypercellular with megaloblastosis

Supplementation

Iron Deficiency Anemia

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Anemia sx Glossitis Esophageal webs Angular chelitis Koilonychia Pallor Pica Plummer Vinson Syndrome (glossisitis, esophageal varices, microcytic, hypochromic anemia presents at 6-9 months failure to thrive as infant hemolytic anemia  jaundice hepatosplenomegaly increase in HbF May be asymptomatic Increase in HbA2

Alpha Thalassemia: Silent Carrier

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Alpha Thalassemia Trait

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Beta Thalassemia Major

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Beta Thalassemia Minor

Alpha Thalassemia: HbH Disease

Folic Acid: Decreased intake (alcoholics, elderly, diet) Increased requirement (pregnancy) Blood loss Dec diet intake Increased requirements (pregnancy, growth spurt) Impaired absorption (sprue) inflammation

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CBC: dec RBC, H&H, MCV, RI; inc RDW Iron studies: low serum iron, high TIBC, low ferritin, low hepcidin, high sTfR

Hypochromic Microcytic Anisocytosis (target/tearshaped)

Heterozygous

Asymptomatic

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Loss of 1 copy

May be asymptomatic

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Loss of 2 copies

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Loss of 3 copies  HbH tetramers

Treat underlying cause Supplement with oral iron

hypercellular

Transfusion dependent

Homozygous Bone marrow expansion Ineffective hematopoiesis

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No iron on Prussian Blue Stain

Hypochromic Microcytic Bastophilic stippling Nucleated RBC Anisocytosis Poikilocytosis Hypochromic Microcytic Bastophilic stippling Nucleated RBC Anisocytosis Poikilocytosis Hypochromic Microcytic Bastophilic stippling Nucleated RBC Anisocytosis Poikilocytosis

See HbH tetramers on methylene blue stain

Alpha Thalassemia: Hydrops Fetalis Anemia of Chronic Disease

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Sickle Cell Anemia

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Hereditary Spherocytosis

G6PD Deficiency

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Lethal in utero/shortly after birth

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Loss of 4 copies  HbBarts tetramers

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Cancer Infections Autoimmune diseases Body hiding iron in ferritin form Point mutation Glu  Val

Iron studies: low serum iron, low/normal TIBC, high ferritin, high hepcidin

Normochromic (hypo) Normocytic (micro)

Adequate iron stores seen with Prussian blue stain

Hemolytic anemia Reticulocytosis Jaundice Increased LDH Chronic leg ulcers Pigment gallstones Kidney damage Avascular necrosis Salmonella osteomyelitis Children: skeletal deformities from bone marrow expan, splenomegaly, splenic sequestration crisis, stroke from large vessel thrombosis Adults: infarcted spleen – functional asplenia or autosplenectomy Aplastic crisis Vaso-occlusive crisis Acute chest syndrome Stroke priapism Hemolytic anemia Jaundice Splenomegaly Pigment gallstones Folic acid deficiency Asplastic crisis during parvovirus infection Hemolytic crisis

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Autosomal dominant – mutation sin ankyrin, spectrin, band 3, band 4.2

High MCHC

Spherocytes Howell-Jolly Bodies

Splenectomy Blood transfusions

Asymptomatic Episodic hemolytic anemia from some triggers After exposure, symptoms occurs 1-2 days later

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X-linked recessive

mild normocytic anemia

Normocytic Bite Cells Heinz Bodies

Stop offending agent

Folic acid supplementation Prophylactic Ab against encapsulated microorganisms Hydroxyurea

G6PD Levels

Supportive care

Paroxysmal Nocturnal Hemoglobinuria

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Immunohemolytic Anemia

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Intravascular hemolysis Paroxysmal – episodic or chronic Nocturnal – happens more at night Hemoglobinemia Hemoglobinuria Hemosiderinuria Increased risk for thrombosis Smooth muscle spasm  abdominal pain, difficulty swallowing Leukemia, myelofibrosis, myelodysplasia, aplastic anemia Hemolytic anemia

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Microangiopathic Hemolytic Anemia (MAHA)

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Acquired somatic mutations  inactivate PIGA and affect complement activity  increase hemolysis

Primary idiopathic Secondary idiopathic (SLE, lymphoid, malignancies, drugs) – IgG Ab Post-Infectious – IgM Ab; Cold Agglutinin Disease Post-Viral Infections in Children – IgG Ab Disease small vessels due to formation of fibrin or platelet aggregation  mechanical/traumatic injury and fragmentation  schistocytes Artificial heart valuves Trauma Diseases that damage small vessels (DIC, TTP, HUS, malignant htn, SLE)

Eculizumab Immunosuppressive therapy Bone marrow transplant...