Haematology Flashcards

1
Q

When is anti-D administered?

A

Weeks 28 + 34 + < 72 hours following birth

+ if there is a sensitising event

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2
Q

Why can ABO incompatibility occur with a first pregnancy?

A

Maternal anti-A/B antibodies are present from birth

These are usually IgM antibodies but may also be IgG antibodies which can cross the placenta​

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3
Q

What % of newborns with ABO compatibility are symptomatic?

A

5-10%

Maternal antibodies are usually IgM and cannot cross the placenta

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4
Q

How does the Coombs test help distinguish ABO and Rhesus incompatibility?

A

+ve in Rhesus

  • ve or weakly +ve in ABO
  • A and B antigens are less well developed in neonates than in older children and adults*
  • Antigenic sites are fewer and farther apart on neonatal RBCs*
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5
Q

How does a peripheral blood smear differentiate ABO and Rhesus incompatibility?

A

Spherocytosis in ABO incompatibility due to partial membrane loss

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6
Q

How is haemolytic disease of the newborn and foetus treated prenatally?

A

Intrauterine blood transfusion

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7
Q

What are the harms of iron deficiency in an infant

A

Long-term effects on neurodevelopment and behaviour

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8
Q

What is involved in a haemolytic screen?

A

Reticulocyte count

Direct antiglobulin test (whether red cells have been coated in antibodies and/or complement)

Lactate dehydrogenase

Bilirubin

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9
Q

What is the most common bleeding disorder of childhood?

A

Idiopathic thrombocytopenic purpura

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10
Q

When is the peak age for ITP?

A

4-8 years

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11
Q

What is the pathophysiology of ITP?

A

Antiplatelet antibodies attach to platelets → platelets are destroyed by splenic macrophages

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12
Q

What is the prognosis of ITP in infants?

A

Benign, 80% recover by 6 months

Platelets usually return to normal in 1-3 weeks

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13
Q

Why can excess milk cause iron deficiency?

A

Calcium inhibits iron absorption

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14
Q

How is hyperbilirubinaemia in infants with haemolytic disease of the infant and newborn treated?

A

Phototherapy

UV oxidises and breaks down bilirubin

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15
Q

What is the triad of HUS?

A
  1. Low platelets (petechiae)
  2. Microangiopathic haemolytic anaemia (jaundice, fatigue, pallor)
  3. Impaired renal function (oliguria)
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16
Q

What are the most common causative agents in HUS?

A

Enterohaemorrhagic E. coli (shiga-like toxin)

Shiga toxin (Shigella dysenteriae)

Streptococcus pneumoniae infection

17
Q

Atypical lymphocytosis is characteristic of which disease?

A

Infectious mononucleosis

18
Q

What are the most common causes of haemolytic uremic syndrome?

A

Bacterial exotoxins (Shiga toxin; Shiga-like toxin (enterohaemorrhagic E. coli, usually from food poisoning)

Streptococcus pneumoniae

19
Q

Which age group does HUS predominantly affect?

A

Children < 5

20
Q

What laboratory test best differentiates HSP from HUS?

A

HSP - elevated platelets

HUS - low platelets

21
Q

What classically preceedes HSP?

A

Infection

Most commonly an URTI caused by group A Streptococcus

22
Q

What is the pathophysiology of HSP?

A

Antigen → IgA production → IgA immune complexes → complement activation → vascular inflammation and damage

23
Q

What murmur is associated with a PDA?

A

Loud continuous murmur

Best heard in the left infraclavicular region

24
Q

Hypersegmented polymorphonuclear cells are characteristic of which condition?

A

Megaloblastic anaemia

25
Q

What clotting factor is deficient in haemophilia A?

A

VIII

26
Q

Which clotting factor is deficient in haemophilia B?

A

IX