Hematology Flashcards
Microcytic anemia
Iron deficiency
Thalassemia
Sideroblastic anemia
Anemia of chronic disease
Macrocytic anemia
Bone marrow failure (aplastic anemia, diamond-Blackfan anemia)
Megaloblastic anemia (B12/folate deficiency)
Drugs
Dyserythropoeisis
Normocytic anemia
Haemolytic Anemia of chronic disease Sequestration Bleeding Malnutrition
Definition of hemolytic anemia
There’s and increased RBC destruction. Can be caused by intrinsic abnormalities of RBC or by extrinsic factors, such as the presence of antibodies on their surface, that lead to early destruction. An enlarged spleen sequesters and destroys RBC more rapidly than normal.
Symptoms and Signs of anemia
Fatigue, drowsiness Pallor Poor feeding, anorexia Poor growths Dyspnea on exertion Rarely stomatitis or koilonychia
Hemolytic disease of newborn
Def + types
It is an hemolytic anemia. Rh negative mothers have been sensitised to rh positive previous baby. If new baby is + igG may cross placenta and cause fetal and neonatal hemolysis
Mild: mild ha with reticulocytosis
Moderate: erythroblastosis fetalis
Severe: Hydrops fetalis
Hemolytic disease of newborns
Clinical diagnosis and treatment
Clinical: anemia and hyperbilirubinemia with ongoing hemolysis secondary to persistent maternal IgG
Diagnosis: direct and indirect Coombs
Treatment: anti D Ig, phototherapy, exchange transfusion
ABO incompatibility
Increases RBC destruction witch is immune mediated
Usually occurs with 0 mothers
Clinical: less severe than that causes by Rh sensitisation: anemia and hyperbilirubinemia
Diagnosis: direct Coombs test
Autoimmune hemolytic anemia
Def
Warm type
Def: hemolytic anemia causes by autoAB that react with RBC at certain degrees
Warm > 37 MCC OF AIHA
IgG attached to RBC –> destroyd in spleen
Etiology: primary/idiopathic, secondary: CLL, SLE, RA, penicillin
Hemolysis occurs in SPLEEN, clinical: HA +- fever chest pain syncopy. Diagnosis spherocytes direct Coombs test. Treatment: corticosteroids and splenectomy
AIHA COLD TYPE
RBC membrane disorder
Hereditary spherocytosis and elliptocytosis
Etiology and clinical
MOST COMMON CAUSE OF HEREDITARY HA!
Etiology: AD. Abnormal shape of RBC, leading to decreased deformability and early removal by spleen
Clinical: anemia and hyperbilirubinemia in newborn, hypersplenism, biliary gallstones, susceptible to aplastic crisis
RBC membrane disorder
Hereditary spherocytosis and elliptocytosis
Diagnosis and treatment
Diagnosis: blood smear: spherocytes, CBC + other lab: increased reticulocytes, and increased bilirubin, inc MCHC, hb 6-10
splenomegaly,
Treatment; transfusion, splenectomy after 5-6 yrs, folate
RBC enzyme disorder
G6PD def
Most common RBC enzymopathy
Def, pathomec
XLR. Common in Mediterranean
HA due to decreased glutathione which is needed to protect the RBC from oxidative stress. This oxidative stress produced Heinz bodies (globin precipitate, is dissociated from heme). Damaged RBC are removed by spleen. One peripheral smear the damaged RBC are called bite cells
RBC enzyme disorder
G6PD def
Most common RBC enzymopathy
Clinical
Diagnosis
Treatment
Clinical: after ingestion of an oxidant (asa, sulfa drugs, antimalarials, favs beans) or infection or stress –> rapid drop in hb, hemoglobinuria and jaundice
Diagnosis: measurement of G6DP activity, Heinz bodies, bite cells
Treatment: prevention, hydration (to protect kidneys) transfusion in acute episodes