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Haematology > Hemolytic anaemia with emphasis on lab diagnosis > Flashcards

Hemolytic anaemia with emphasis on lab diagnosis Flashcards

1
Q

What is hamolysis

A

premature destruction of RBCs

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2
Q

How do hemolytic anemias arise

A

When the RBCs are being destroyed at a faster rate than the body can compensate for

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3
Q

What is a hemolytic disorder

A

A condition that leads to the reduction in mean lifespan of RBCs

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4
Q

Haemolytic anemia is silent until

A

Mean lifespan of RBC is about 30 days

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5
Q

What is erythroid hyperplasia

A

increased activity of the bone marrow in order to compensate for increase in destruction of RBCs

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6
Q

Breakdown of haemoglobin

A

haemoglobin

  1. haem group—-> Iron and protoporphyrin ring
  2. globin group—–> Amino acids
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7
Q

Iron in haem group function

A

Iron is ferried to erythroblasts via transferrin and used in the formation of red blood cells. It is reused

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8
Q

Protoporphyrin ring is made up of

A

bilirubin and Co2

CO2 leave the body via expiration

Bilirubin is conjugated by the liver and expelled as stercobilin through feces and urobilinogen in urine

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9
Q

Why do RBCs rely on glycolysis for energy

A

Because they lack mitochondria they rely on glycolysis for materials required to prevent oxidative damage. Limitations in glycolysis however make them more susceptible to oxidative damage

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10
Q

Classification of hemolytic anemias

A

Site of hemolysis
site of defect
inherited or acquired

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11
Q

What are the types of hemolysis that occur at a site

A

intravascular hemolysis

extravascular hemolysis

combination of both intra and extravascular hemolysi

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12
Q

What is intravascular hemolysis

A

Release of broken down RBC into vascular space or blood stream. This causes the release of free Hb into the system,which on its own is toxic to the body

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13
Q

How does free Hb cause toxicity in the body

A

Free Hb binds to haptogloblin

Haptoglobin binding prevents the binding of heam and albumin from happening

, If this doesnt happen, Free Hb oxidizes and releases heam group which binds to albumin or hemopexin

this causes increased methemalbumin and oxidative stress

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14
Q

What is extravascular hemolysis

A

This is when macrophages of reticular endothelial system destroy RBCs

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15
Q

Lab signs of extravascular hemolysis

A

erythroid hyperplasia

hemosiderosis ( collection of iron deposits on tissues)

hyperbilirubinemia

increased excretion of bilirubin

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16
Q

Clinical states that present with extravascular hemolysis

A 
Autoimmune hemolysis
Hereditary spherocytosis
haemoglobinopathies i.e SSD, thalassemia
Delayed hemolytic transfusion reactions
Hypersplenism
17
Q

Clinical states associated with intravascular hemolysis

A 
Sepsis
severe burns
paroxysmal nocturnal hemoglobinuria
acute hemolytic transfusion reactions
severe microangiopathic reactions
physical trauma
18
Q

Site of defect types

A
  1. defect found in red cell- intrinsic defect.
    i. e in sickle cell disease there is a problem wrong with Hb
  2. defect found in RBC environment, nothing fundamentally wrong with RBC- extravascular defect
    i. e antibodies cause destruction of RBCs
19
Q

inherited hemolytic anemia are usually

A

intrinsic in nature

20
Q

Acquired hemolytic anemias

A

are usually extrinsic in nature

21
Q

This acquired hemolytic anemia is intrinsic in nature

A

Paroxysmal nocturnal hemoglobinuria

22
Q

Conditions that cause inherited hemolytic anemia

A
  1. Membrane defects
    i. e hereditary spherocytosis
  2. Metabolic defects
    i. e G6PD deficiency
  3. Hb defects
    i. e Sickle cell anemia
23
Q

Conditions that cause acquired hemolytic anemia

A 
Paroxysmal nocturnal hemoglobinuria
Chemical and physical agents
infections
march hemoglobinuria
red cell fragmentation syndromes
Immune conditions i.e autoimmune hemolytic anemia
24
Q

How to diagnose hemolytic anemia

A
  1. family history
  2. history of infections,behaviours
  3. Ethnic origin i.e G6PD deficiency very common in chinese
  4. Past history i.e neonatal jaundice
25
Q

Clinical features of hemolytic anemia

A 
pallor of mucus membrane
jaundice
splenomegaly
dark urine due to hb in urine
pigment gall stones
ulcers around ankle; due to hb mopping up vasodilator NO--> vasoconstriction--> decreased blood and nutrient supply--> tissue necrosis
hypertrophic skeletal changes i.e bone marrow overworks and enlarges
growth retardation
aplastic changes
26
Q

Lab features of increased red blood cell breakdown

A 
increased urine urobilinogen
increased fecal stercobilinogen
raised serum bilirubin
reduced serum hemopexin
increased free haptoglobin, because haptoglobins are produced in excess to bind free Hb which is toxic in its free form
increased lactate dehydrogenase
27
Q

Peripheral blood film features of hemolytic anemia

A
  1. normocytic/macrocytic cells
  2. polychromasia–bluish young RBC mixed with pinkish older RBC. Staining done with Leishman stain
  3. Nucleated RBCs– young RBCs are nucleated before losing it as they grow. Due to increased production of young RBC into blood stream, cells are seen as nucleated
  4. Schistocytes-red cell fragments
  5. Micro spherocytes - spherical instead if biconcave hence will lose area of central pallor
  6. Elliptocytes
  7. Helment cells i.e. in G6PD deficiency
  8. Reticulocytes -young RBCs. Staining done with supravital stains
  9. Howell Jolly bodies
28
Q

Heinz bodies in G6PD deficiencies

A

are bitten off to look like helments

29
Q

Tests for hemolytic anemia

A

coombs test

osmotic fragility test

30
Q

Stain for reticulocytes

A

cresyl blue

methylene blue

31
Q

Dark urine is a feature of

A

intravascular hemolysis

blood rich in free Hb is filtered by kidney–>Hb present in urine

32
Q

Lab features of intravascular hemolysis

A

hemoglobinuria
hemoglobinemia- increased Hb in plasma
hemosiderinuria - iron deposits in urine
methemoglobin - Hb plus albumin complex. Detected by schumms test

33
Q

Autoagglutiation

A

A form of autoimmune hemolytic anemia, where red cells stick together

Haematology (29 decks)

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