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Medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

Sites of extramedullary haematopoiesis

A

Liver + spleen

also in utero

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2
Q

Types of bone marrow

A

Red + yellow (can convert into red)

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3
Q

Causes of splenomegaly

A

Infections: bacterial, viral, parasitic
Haem: haemoglobinopathes, haemolytic anaemias
Haem malignancies
Congestive: liver cirrhosis, RVF, thrombosis of portal/ hepatic/ splenic veins
Trauma: intracapsular haematoma
Infiltrative

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4
Q

Effects of hypersplenism

A

-poenias and release of immature blood cells

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5
Q

Which microbes are asplenic patients vulnerable to? Why?

A

Encapsulated bacteria (Neisseria meningitides, Strep pneumoniae, Haemophilus influenzae)

Spleen main site of IgM site for opsonisation of encapsulated organisms

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6
Q

Interventions for asplenic patients

A 
Pneumococcal (boosters every 5-10 years)
Haemophilus influenzae course
Meningococcal vaccines
Influenza (annually)
Lifelong prophylactic abx, eg Pen V or erythromycin
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7
Q

Causes of microcytic anaemia

A

Iron deficiency (hypochromic)
Anaemia of chronic disease (sometimes normocytic)
Thalassaemia

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8
Q

How long should iron supplements be taken for?

A

3 months+ to replenish stores

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9
Q

Causes of megaloblastic anaemia

A

Folate and B12 deficiencies - must be co-administered

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10
Q

Which has smaller supplies: B12 or folate?

A

Folate

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11
Q

What is usually damaged in pernicious anaemia?

A

Gastric parietal cells (causing failure of IF secretion)

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12
Q

Common causes of B12 deficiency in elderly

A

Malabsorption as pH of stomach too high (eg PPI, H.pylori)

Metformin use

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13
Q

Most common anaemia in hospitals

A

Anaemia of chronic disease (usually normocytic, normochromic). Can be microcytic.

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14
Q

extravascular vs intravascular haemolysis

A

Extra: enhanced rate of RBC breakdown (eg hyperspelenism) - usually less severe, more gradual

Intra: destruction of RBCs within circulatory system, cytoskeletal defects

Both show increased bili, increased reticulocytes

Intravas also causes haemoglobinuria, haemosiderin in urine

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15
Q

What does sickle cell provide protection against?

A

Plasmodium falciparum

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16
Q

Why is it important to diagnose beta-thalassaemia trait?

A

May wrongly be diagnosed with Fe-deficiency anaemia: inappropriate Fe therapy

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17
Q

Why does thalassaemia cause hair on end skull appearance?

A

Extramedullary haemopoiesis causes (hepatosplenomegaly and) expansion of marrow cavities in cortical bone. also causes more fractures

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18
Q

What are myeloproliferative disorders?

A

Excessive proliferation of one or more specific cell lines from myeloid pregenitor. These cells retain ability to mature and differentiate normally.
Usually indolent course.
E.g. polycythaemia rubra vera

NON-MALIGNANT (but have potental to evolve into AML)

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19
Q

Which gene mutation is present in myeloproliferative disorders?

A

JAK2 gene mutation (can differentiate from secondary polycythaemia)

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20
Q

Presentation of polycythaemia rubra vera

A

Plethora
Splenomegaly/ hepatomegaly
Risk of thrombosis

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21
Q

Define myelodysplastic disorders

A

Clonal proliferation of myeloid cells that mature abnormally/ incompletely
(usually disease of elderly)

22
Q

What is acute vs chronic in terms of haem malignancies?

A

Acute: immature blast cells
Chronic: more mature cells

23
Q

Why do leukaemias often cause cytopenias?

A

Marrow being taken up

24
Q

Most common adult acute leukaemia?

A

AML

25
Q

Most common childhood cancer?

A

ALL

26
Q

Which malignancy causes alcohol-induced pain?

A

Pathognomic for Hodgkins

27
Q

Reed-Sternberg cells are associated with

A

Hodgkins

28
Q

Most common adult leukaemia

A

CLL

29
Q

Clinical features of multiple myeloma (and mnemonic)

A 
CRAB
Calcium
Renal (impairment): dehydration, NSAIDs for bone pain, hypercalcaemia, Bence-Jones...
anaemia (normochromic, normocytic)
Bones
30
Q

Blood tests you might request in haem malignancies

A

Serum lactate dehydrogenase

Serum urate

31
Q

Why give FFP instead of packed red cells?

A

Clotting factors

32
Q

In which transfusion reaction can you continue infusing?

A

Febrile non-haemolytic: fever/ rigors in hours - slow and give paracetamol

33
Q

What is classed as anaemia

A

under 13g/dl men, 12 g/dl women

34
Q

triad in plummer-vinson syndrome (aka Paterson-Kelly-Brown)

A

iron-deficiency anaemia, oesophageal webs, dysphagia

replace fe and endoscopic dilatation

higher risk of developing oesophageal ca

35
Q

why should you be careful interpreting iron results in hospital

A

ferritin is an acute phase protein so may be falsely elevated

36
Q

what is sideroblastic anaemia

A

congenital or acquired form of anaemia with dysfunctional erythropoiesis
iron deposition in RBC precursors leads to formation of ringed sideroblasts

iron studies will show high Fe

37
Q

antifolate drugs

A

phenytoin, methotrexate, trimethoprim

38
Q

how to replace folate and B12

A

folate: 5 mg daily for 3 weeks, followed by weekly dose

B12: loading regime of 6 doses.
then 1 mg every week for 2 weeks
then 1 mg every 3 months

39
Q

when do you see Heinz bodies?

A

G6PD deficiency

40
Q

when do you see prickle cells?

A

Pyruvate kinase deficiency

41
Q

what blood abnormality can be caused by heparin?

A

thrombocytopenia

42
Q

what will be abnormal in bloods of haemophilia A?

A

prolonged APTT

reduced factor VIII

43
Q

which factor is low in haemophilia B?

A

factor IX

44
Q

what do bloods show in vWB disease?

A

prolonged APTT and PT

45
Q

what do bloods show in vit K deficiency?

A

prolonged APTT and PT

46
Q

when are Auer rods seen?

A

Aml

47
Q

when are smudge cells seen?

A

cml

48
Q

in anaemia, rate for prescribing packed cells?

A

1 unit at a time, usually over 2h

49
Q

rate for infusing unit of FFP, cryoprecipitate or platelets

A

30 mins

50
Q

universal donor for FFP

A

AB Rh -

Medicine (30 decks)

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