Anemia and Its Classification by Dr Bashir Ahmed Dar a Sopore Kashmir 1228039135310976 9

8/2/2019 Anemia and Its Classification by Dr Bashir Ahmed Dar a Sopore Kashmir 1228039135310976 9

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ANEMIA

By Dr Bashir Ahmed Dar

Chinki pora sopore kashmir

Associate professor of Medicine


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Classification of Anemia

I. Etiologic Classification

1. Impaired RBC production

2. Excessive destruction

3. Blood lossII. Morphologic Classification

1. Macrocytic anemia

2. Microcytic hypochromic anemia

3. Normochromic normocytic anemia


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Impaired RBC Production

1. Abnormal bone marrow

1.1 Aplastic anemia1.2 Myelophthisis : Myelofibrosis, Leukemia,

Cancer metastasis2. Essential factors deficiency

2.1 Deficiency anemia : Fe, Vit. B12, Folic acid, etc2.2 Anemia in renal disease : Erythropoietin

3. Stimulation factor deficiency3.1 Anemia in chronic disease3.2 Anemia in hypopituitarism3.3 Anemia in hypothyroidism


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Excessive Destruction of RBC(cont.)

Hemolytic anemia

1. Intracorpuscular defect

1.1 Membrane : Hereditary spherocytosis

Hereditary ovalocytosis, etc.

1.2 Enzyme : G-6PD deficiency, PK def., etc.

1.3 Hemoglobin : Thalassemia, Hemoglobino-

pathies


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Excessive Destruction of RBC

2. Extracorpuscular defect

2.1 Mechanical : March hemolytic anemia

MAHA (Microangiopathic HA)

2.2 Chemical/Physical

2.3 Infection : Clostridium tetani

2.4 Antibodies : HTR, SLE

2.5 Hypersplenism


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Blood Loss

1. Acute blood loss : Accident, GI bleeding

2. Chronic blood loss : Hypermenorrhea

Parasitic infestation


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Macrocytic AnemiaMCV > 94

MCHC > 31

1. Megaloblastic dyspoiesis

1.1 Vit. B12 deficiency : Pernicious anemia

1.2 Folic acid deficiency : Nutritional megaloblas-

tic anemia, Sprue, Other malabsorption

1.3 Inborn errors of metabolism : Orotic aciduria,etc.

1.4 Abnormal DNA synthesis : Chemotherapy,

Anticonvulsant, Oral contraceptives


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Microcytic Hypochromic AnemiaMCV < 80MCHC < 31

1. Fe deficiency anemia : Chronic blood loss,

Inadequate diet, Malabsorption, Increaseddemand, etc.

2. Abnormal globin synthesis : Thalassemia with or

without Hemoglobinopathies

3. Abnormal porphyrin and heme synthesis :

Pyridoxine responsive anemia, etc.

4. Other abnormal Fe metabolism :


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Normocytic Normochromic AnemiaMCV 82 - 92MCHC > 30

1. Blood loss

2. Increased plasma volume : Pregnancy, Overhydration

3. Hemolytic anemia : depend on each cause

4. Hypoplastic marrow : Aplastic anemia, RBC aplasia

5. Infiltrate BM : Leukemia, Multiple myeloma,

Myelofibrosis, etc.6. Abnormal endocrine : Hypothyroidism, Adrenal

insufficiency, etc.

7. Kidney disease / Liver disease / Cirrhosis


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Hemolytic Anemia


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What is Hemolysis

- Premature destruction of dead cells.

- Causes hereditary and acquired disorders.

- Hemolysis occurs at two sites:


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Intravascular

- Hemolysis occurs within systemic

circulation.

- Hemoglobin is released into plasma.

- Hemoglobin is lost through kidneys orcatabolized in the liver.


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Extravascular- Trapping of red cells in spleen or liver

sinuses.

- Lyses of trapped red cells.

- Release of lysed hemoglobin and

catabolism within the sequestering organ.


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Classification of Hereditary

Hemolytic Anemia Based on side effect:

- Metabolic defect

- Membrane defect

- Hemoglobin defect


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A) Metabolic defect:- Defect in hexose monophosphate shunt: G-

6-PD deficiency.

- Defects of glycolysis; pyrovate kinase def.,glucose phosphate isomerase def.

- Defects in red cell nucleotide metabolism:pyramidine-5-nucleotidase def.


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B) Membrane defect:- Heriditary spherocytosis

- Heriditary elliptocytosis

- Hereditary pyropoikilocytosis


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C) Hemoglobin defect:

- Thalassemias

- Sickle cell anemia

- Hemoglobin C disease

- HemoglobinE

disease

- Unstable hemoglobin


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Laboratory Findings Chemistry

Hyperbilirubinemia, predominantly unconjugated bilirubindue to breakdown of heme ring by reticuloendothelial cellsin the liver.

elevated LDH: released from destroyed cells.

Hemoglobinemia: free hemoglobin level increases inhemolysis esp. intravascular hemolysis: levels of 10-20mg/dl gives plasma amber color and 50-100 gm/dl reddishcolor.


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Hemoglobinuria: red-brown color of urine due to freehemoglobin and methamoglobin.

Decreased Heptaglobin level: it is a alpha-2-globin producedin the liver. It binds free hemoglobin thus level is reduced inhemolysis.

Hemosidrinuria: it reflects extensive hemolysis for a

prolonged period of time.When hemoglobin is filtered bynephron, proximal tubular cells metabolize hemoglobin andiron accumulate in the cells. Cells then exfoliate in the urineand iron can be detected by Prussian blue reaction.


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Drug-Induced Acute Hemolysis Drugs that have been linked to G6PD:

Primaquine (an antimalarial)

Sulphonamide antibiotics

Sulphones (e.g. dapsone, used against leprosy) Other sulphur-containing drugs: glibenclamide (an anti-diabetic drug)

Nitrofurantoin (an antibiotic often used forurinary tract infections)

Vitamin K analogues

Several others

Henna can cause a hemolytic crisis in G6PD deficient infants


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Acquired hemolytic anaemia


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Immune haemolytic anaemiasAre caused by AB production by the body

against its own red cells.

Divided into 1) warm 37c

2) cold

4 c


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Warm AIHA

IgG alone ,Bind at 37c


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Cold AIHA

Usually IgM

Bind to red cell at 4c


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Coombs TestCoombs Test

Antiglobulin TestAntiglobulin Test

RBCRBC

Red cell withRed cell with

bound antibody tobound antibody to

membrane antigenmembrane antigen

++

AntiAnti--immunoglobulinimmunoglobulin


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Coombs TestCoombs Test

Antiglobulin TestAntiglobulin Test

RBCRBC RBCRBC

AgglutinationAgglutination


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NonNon--Immune Hemolytic AnemiasImmune Hemolytic Anemias

Hemolytic anaemias due to mechanisms or agentsHemolytic anaemias due to mechanisms or agents

other than antibodies +/or complement e.g.:other than antibodies +/or complement e.g.:

Mechanical (traumatic)Mechanical (traumatic)

ToxinsToxins InfectionsInfections

Splenomegaly (hypersplenism)Splenomegaly (hypersplenism)

Burn (physical)Burn (physical)

Renal failure and liver failureRenal failure and liver failure

ChemicalChemical


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Mechanical (Traumatic)Mechanical (Traumatic)

(Fragmentation)(Fragmentation)This is due to direct trauma (stress) to the RBCsThis is due to direct trauma (stress) to the RBCscausing fragmentation of the RBCs & intracausing fragmentation of the RBCs & intra--vascular hemolysis. The fragmented cells canvascular hemolysis. The fragmented cells canbe seen on peripheral blood smears & are calledbe seen on peripheral blood smears & are called

(schistocytes).(schistocytes).

Due to:Due to:

1.1. Prosthetic valvesProsthetic valves

2.2. PatchesPatches

3.3. Valvular diseasse e.g., stenosisValvular diseasse e.g., stenosis

Cont


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Mechanical (Traumatic)

(Fragmentation)(cont)2.2. Microangiopathic:Microangiopathic: mechanical hemolysis due tomechanical hemolysis due to

contact between the RBCs & the abnormal intemacontact between the RBCs & the abnormal intemaof thrombosed, narrowed, necrotic small vessels orof thrombosed, narrowed, necrotic small vessels or

fibrin strand formation.fibrin strand formation.Caused by many diseases e.g., DIC (disseminatedCaused by many diseases e.g., DIC (disseminatedintravascular coagulation), malignant hypertension,intravascular coagulation), malignant hypertension,disseminated malignancies especially mucindisseminated malignancies especially mucin

secreting adenocarcinomas, TTPsecreting adenocarcinomas, TTP(thrombocytopenic purpura), hemolytic uremic(thrombocytopenic purpura), hemolytic uremicsyndrome (HUS).syndrome (HUS).


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Anemia and Its Classification by Dr Bashir Ahmed Dar a Sopore Kashmir 1228039135310976 9

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