Hematology Flashcards

1
Q

Microcytic anemia

A

Iron deficiency
Thalassemia
Sideroblastic anemia
Anemia of chronic disease

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2
Q

Macrocytic anemia

A

Bone marrow failure (aplastic anemia, diamond-Blackfan anemia)
Megaloblastic anemia (B12/folate deficiency)
Drugs
Dyserythropoeisis

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3
Q

Normocytic anemia

A
Haemolytic
Anemia of chronic disease 
Sequestration 
Bleeding 
Malnutrition
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4
Q

Definition of hemolytic anemia

A

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.

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5
Q

Symptoms and Signs of anemia

A
Fatigue, drowsiness 
Pallor
Poor feeding, anorexia 
Poor growths 
Dyspnea on exertion
Rarely stomatitis or koilonychia
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6
Q

Hemolytic disease of newborn

Def + types

A

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

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7
Q

Hemolytic disease of newborns

Clinical diagnosis and treatment

A

Clinical: anemia and hyperbilirubinemia with ongoing hemolysis secondary to persistent maternal IgG
Diagnosis: direct and indirect Coombs
Treatment: anti D Ig, phototherapy, exchange transfusion

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8
Q

ABO incompatibility

A

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

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9
Q

Autoimmune hemolytic anemia
Def
Warm type

A

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

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10
Q

AIHA COLD TYPE

A
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11
Q

RBC membrane disorder
Hereditary spherocytosis and elliptocytosis
Etiology and clinical

A

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

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12
Q

RBC membrane disorder
Hereditary spherocytosis and elliptocytosis
Diagnosis and treatment

A

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

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13
Q

RBC enzyme disorder
G6PD def
Most common RBC enzymopathy
Def, pathomec

A

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

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14
Q

RBC enzyme disorder
G6PD def
Most common RBC enzymopathy

Clinical
Diagnosis
Treatment

A

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

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