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Haematology > The Haemolytic Anemias > Flashcards

The Haemolytic Anemias Flashcards

1
Q

Most hemoglobin degradation occurs in the

A

Macrophages of the spleen

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2
Q

Indirect indicators of erythrocyte destruction

A

Blood bilirubin
Urobilinogen concentration in the urine

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3
Q

Bilirubin is conjugated in the liver with

A

Glucoronic acid
Enzyme-Glucoronyl transferase

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4
Q

Haemolysis is associated with (bilirubin)

A

High concentrations of UNCONJUGATED BILIRUBIN

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5
Q

Evidence of increased haemolysis: Biochemical consequences

A

Hyberbilirubinemia(unconjugated)
Reduced serum haptoglobin

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6
Q

Evidence of increased haemolysis: intravascular haemolysis

A

Haemoglobinemia
Reduced serum haptoglobulin
Reduced serum hemopexin
Haemoglobinuria
Haemosiderinuria
Methalbuminemia (Schumm’s test)

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7
Q

Evidence of damaged red cells

A

Micro-spherocyte
Red cell fragments
Sickle cells

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8
Q

Evidence of increased red cell production

A

Polychromasia
Nucleated red cells

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9
Q

Clinical presentations of haemolysis

A

Jaundice
Anemia

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10
Q

Clinical features of haemolysis states

A
  1. Jaundice
  2. Pallor
  3. Pigment stones
  4. Splenomegaly
  5. Expansion of marrow cavities in congenital HA
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11
Q

Laboratory evidence of increased erythropoietic activity

A
  1. Reticulocytosis (polychromasia)
  2. Erythroblastaemia (nucleated rbcs)
  3. Macrocytosis (High MCV)
  4. Erythroid hyperplasia (Bone marrow)
  5. Reduced myeloid/erythroid ratio (Bone marrow)
  6. Changes in the skull and tubular bones
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12
Q

Evidence of red cell damage

A

Spherocytes
Fragment cells

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13
Q

Reticulocyte count is increased/decreased in hemolysis

A

Increased

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14
Q

Hemosiderinuria and Hemoglobinuria are present in

A

INTRAVASCULAR hemolysis

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15
Q

Complications of Hemolysis

A
  1. Aplastic crisis
  2. Leg ulcers; chronic haemolytic states
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16
Q

Diagnosis of hemolysis

A
  1. Demonstration of a hemolytic state
  2. Demonstration of its aetiology
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17
Q

Haemolytic states

A

Polychromasia +/- NRBC
Reticulocytosis
Erythroid hyperplasia

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18
Q

Treatment of haemolysis

A

Treat the underlying cause
Give folic acid
Red cell concentrates

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19
Q

Structure of the red cell membrane

A

Trilaminar
Outermost (glycolipids, glycoproteins)
Central (cholesterol, phospholipids)
Inner (cytoskeleton)

20
Q

Most common congenital hemolytic anemia

A

Hereditary Spherocytosis

21
Q

Inheritance is

A

Autosomal recessive/Autosomal dominant

22
Q

Clinical features of Hereditary spherocytosis

A

Asymptomatic
Episodic jaundice
Variable splenomegaly
Gall stones

23
Q

Laboratory features of hereditary spherocytosis

A
  1. Negative antiglobulin test
  2. Variable degree of spherocytosis
  3. Floe cytometric analysis for EMA binding to detect spherocytes
  4. Membrane protein defect test -
    SDS-PAGE, RIA or EIA
24
Q

Diagnosis of hereditary spherocytosis

A

Can be missed till adulthood

25
Q

Molecular defect of Hereditary Spherocytosis

A
  1. RBC membrane loss is due to defective vertical protein linkage between membrane skeleton and lipid bilayer
  2. Caused by molecular defects in genes encoding for proteins (spectrin, ankyrin, band 3 and protein 4.2)
26
Q

Molecular defect of hereditary Elliptocytosis

A

Most common defect is in soectrin

27
Q

Clinical features of hereditary elliptocytosis

A

Asymptomatic
Anemia
No splenomegaly

28
Q

Differentials of H.E

A

Iron deficiency
Artifacts
Myelodysplasia

29
Q

Inheritance of G6PD deficiency

A

X linked, recessive (commoner in males)

30
Q

Feature of G6PD Deficiency episodic haemolysis

A

Acute haemolysis induced by increased oxidant stress

31
Q

G6PD Deficiency: Triggers of acute haemolysis

A
  1. Antimalarials, sulphonamides, nitrofurans
  2. Favism
  3. Infections
32
Q

Clinical features of G6PD Deficiency

A

Acute haemolysis
Neonatal jaundice (most common cause)

33
Q

Laboratory features of G6PD deficiency

A

Anisocytosis
Bite cells
Heinz bodies

34
Q

Treatment of G6PD deficiency

A
  1. Stop precipitating drug or treat the infection
  2. Acute transfusions, if possible
35
Q

Types of immune haemolytic anaemia

A

Autoimmune
Alloimmune

36
Q

Types of autoimmune haemolytic anaemia

A

Warm IHA
Cold IHA
Drug induced IHA

37
Q

Causes of Warm AI Haemolysis

A

50% Idiopathic
SECONDARY
1. Lymphoid neoplasm e.g CLL, Lymphoma, Myeloma
2. Solid tumors eg Lung, Kidney
3. Connective tissue ds e.g Lupus, RA
4. Drugs e.g Alpha methyl DOPA, Penicillin, Quinine, Chloroquine
5. Misc e.g UC, HIV

38
Q

Types of CAHA

A

Cold agglutinin syndrome (CAD)
Paroxysmal cold hemoglobinuria

39
Q

Causes of secondary CAD

A

Mycoplasma
Infectious mono
LPD

40
Q

Causes of secondary Paroxysmal Cold Hemoglobinuria

A

Measles
Mumps
Syphilis

41
Q

Who is affected by Warm AI Haemolysis

A

More females than males
All age groups

42
Q

P smear of Warm AI Hemolysis

A

Micro-spherocytosis
Nucleated RBCs

43
Q

Confirmation of Warm AI Haemolysis

A

Coombs test
Antiglobulin test

44
Q

Treatment of Warm AI haemolysis

A

Correct underlying cause
1. Prednisolone
2. Transfusion; for severe occasions
3. Splenectomy (if steroids don’t work)
4. Immunosuppressives: Azathioprine, Cyclophosphamide

45
Q

Clinical features of CAD

A

Acrocyanosis

46
Q

IgM with specificity to I or IAg is seen in what disease

A

Cold AI Haemolysis

47
Q

Examples of Mechanical trauma to red cells in Non immune HA

A
  1. Abnormalities to heart and large vessels
  2. Microangiopathic HA - HUS, TT, DIH
  3. March haemoglobinemia

Haematology (3 decks)

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