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Haematology > Haematology > Flashcards

Haematology Flashcards

1
Q

How does essential thrombocythaemia present?

A
  • Thrombosis
  • Bleeding
  • Erythromelalgia
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2
Q

Investigations for essential thrombocythaemia

A
  • FBC: Increased platelets >600
  • Film: increased megakaryocytes
  • Bm Bx: hypercellular,
  • Genetics: JAK2 +ve
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3
Q

Management of essential thrombocythaemia

A
  • Aspirin

- Hydroxycarbamide

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4
Q

How does polycythaemic vera present?

A
  • Plethoric face
  • Headaches
  • Tinnitus
  • Thrombosis
  • Erythromelalgia
  • Pruritis after a hot bath
  • Splenomegaly
  • Hepatomegaly
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5
Q

Investigations for polycythaemia vera

A
  • Bloods: raised RBC and Hct
  • Bone marrow: hypercellular with erythroid marrow
  • Genetics: JAK2 +ve
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6
Q

Management of polycythaemia vera

A
  • Venesection
  • Aspirin
  • Hydroxycarbamide
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7
Q

Myelofibrosis presentation

A
  • Anaemia - fatigue
  • Infections
  • Bleeding tendency
  • Splenomegaly
  • Hepatomegaly
  • FLAWS
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8
Q

Myelofibrosis investigations

A
  • Bloods: Cytopenias
  • Film: tear-drop poikilocytes
  • Bone marrow biopsy: not possible (Dry tap), so need to do a trephine biopsy
  • Genetics: JAK2 +ve
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9
Q

Myelofibrosis management

A
  • Supportive e.g. transfusions
  • EPO, G-CSF
  • Allogeneic BMT
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10
Q

Causes of aplastic anaemia

A
  • Congenital: Fanconi syndrome
  • Infections: Parvovirus
  • Drugs: sulphonamides,
  • Radiation
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11
Q

Management of aplastic anaemia

A
  • Supportive: transfusions
  • Anti-thymocyte globulin
  • BMT
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12
Q

Myelodysplasia presentation

A
  • Patients >60y
  • Fatigue
  • Infections
  • Bleeding risk
  • Splenomegaly
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13
Q

Myelodysplasia investigations

A
  • Bloods: cytopenias
  • Blood film: Pelger-huet cells
  • BM Bx: hypercellular marrow, ringed sideroblasts
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14
Q

Myelodysplasia management

A
  • Supportive: transfusions, EPO, G-CSF
  • BMT
  • Anti-thymocyte globulin
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15
Q

What murmur can anaemia give?

A

Flow murmur - apical ESM

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16
Q

Sideroblastic anaemia - blood film

A
  • Ringed sideroblasts

- Pappeheimer bodies

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17
Q

When does beta thalassemia present?

A

3-6 months- when HbF falls

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18
Q

Beta thalassemia - HPLC

A
  • Raised HbA2
  • Raised HbF
  • No HbA
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19
Q

How does HUS present?

A
  • MAHA
  • Thrombocytopenia
  • Renal failure
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20
Q

How to mx HUS

A

Usually resolves spontaneously

May need dialysis/exchange transfusion

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21
Q

How does TTP present?

A
  • MAHA
  • Thrombocytopenia
  • Renal failure
  • Fever
  • CNS signs
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22
Q

How to manage TTP?

A
  • Plasmapheresis
  • Immunosuppression
  • Splenectomy
23
Q

How to tx HS?

A
  • Folate

- Splenectomy (after childhood)

24
Q

G6PD deficiency - blood film

A
  • Irregularly contracted cells
  • Heinz bodies
  • Bite cells
  • Ghost cells
25
Q

How to treat HS?

A
  • Folate

- Splenectomy

26
Q

How to treat G6PD Deficiency?

A
  • Stop precipitants

- Supportive treatment

27
Q

How does autoimmune haemolytic anaemia present?

A
  • Extravascular haemolysis (splenomegaly)

- Jaundice

28
Q

Warm AIHA - key points

A
  • IgG
  • 37 degrees
  • Tx with immunosuppression, splenectomy
29
Q

Cold AIHA - key points

A
  • IgM
  • <4 degrees
  • Tx by avoiding cold, rituximab
30
Q

What is paroxysmal cold haemoglobinuria associated with?

A
  • Measles, mumps and chickenpox
31
Q

What antibodies are seen in Paroxysmal cold haemoglobinuria?

A

Donath Landsteiner (IgG)

32
Q

How does paroxysmal nocturnal haemoglobinuria present?

A
  • Thrombosis
  • Dark urine (haemoglobinuria)
  • Jaundice
33
Q

Tx of PNH

A
  • anticoagulation

- Eclulizumab

34
Q

What are the immediate transfusion reactions?

A

HIT OAF

  • Haemolytic
  • Infection
  • TRALI
  • Overload
  • Allergic
  • Febrile
35
Q

How to treat allergic transfusion reaction

A

STOP THE TRANSFUSION

- IV chloramphenicol

36
Q

Cause of haemolytic transfusion reaction

A

ABO incompatability

37
Q

How to treat haemolytic transfusion reaction?

A

Stop the transfusion, tell the lab
IV normal saline
Treat complications e.g. AKI, DIC

38
Q

How does CLL present?

A
  • Symmetrical painless lymphadenopathy
  • Anaemia
  • Thrombocytopenia
  • Purpura
  • Hepatosplenomegaly
  • FLAWS
39
Q

Ix for CLL

A
  • Bloods: Raised WCC with raised lymphocytes

- Blood film: smear cells

40
Q

What is Richter transformation?

A

When CLL develops into large B-cell lymphoma

41
Q

How does CML present?

A
  • Bloods: Raised WCC with raised PMNs

- Chromosomal analysis: BCR:ABL fusion gene in 80%

42
Q

CML Tx

A

Imatinib (tyrosine kinase inhibitor)

43
Q

How does Non-Hodgkin Lymphoma present?

A
  • Symmetrical painless lymphadenopathy
  • Splenomegaly
  • FLAWS
44
Q

What is the staging system for Lymphoma?

A

Ann-Arbor

  1. One group of LNs affected
  2. Multiple groups of LNs on same side of diaphragm
  3. Multiple groups on LNs on different sides of diaphragm
  4. Extranodal involvement e.g. splenomegaly

Plus

A - No B-symptoms
B - B-symptoms present (FLAWS)

45
Q

Different types on Non-Hodgkin lymphoma

A

B-cell NHL

  • Diffuse large B-cell (most common; can arise from CLL)
  • Burkitts (EBV, starry sky)
  • Follicular
  • Small cell lymphocytic
  • Marginal zone (MALTomas)

T-cell NHL

  • ATLL (HTLV1, Caribbean and Japanese people)
  • Enteropathy-associated T-cell lymphoma: coeliac disease
  • Cutaneous T-cell lymphoma
  • Anaplastic large cell
46
Q

Hodgkin Lymphoma presentation

A
  • Painless asymmetric lymphadenopathy
  • Massive splenomegaly
  • Pain after drinking alcohol
  • FLAWS
47
Q

How does multiple myeloma present?

A
  • Hypercalcaemia
  • Renal insufficiency
  • Anaemia
  • Bone pain

Plus
- Recurrent infections

48
Q

Investigations for MM

A
  • Bloods: normocytic normochromic anaemia, high Ca, normal ALP
  • Urine electrophoresis: Bence-jones proteins
  • Film: rouleaux
  • Serum electrophoresis: all kappa or all lambda
  • Skeletal survey
49
Q

Poor prognostic factors in MM

A

Low albumin

High b2-microglobulin

50
Q

Definition of MGUS

A

Serum monoclonal protein or BM plasma cells >10% without CRAB

51
Q

What happens in tumour lysis syndrome?

How is it prevented?

A
  • Massive cell destruction
  • High K and urate
  • Renal failure

Preventative tx: fluid intake and allopurinol

52
Q

Causes of Splenomegaly

A

Haematological

  • Myeloproliferative disease (CML, myelofibrosis)
  • Lymphoma
  • Leukaemia
  • Extravascular haemolysis: hereditary spherocytosis

Abdominal
- Portal HTN due to cirrhosis, Budd-Chiari

Infective

  • EBV
  • Malaria
53
Q

Causes of massive splenomegaly

A

4 M’s

  • cML
  • Myelofibrosis
  • Malaria
  • leichManiasis
54
Q

Features on blood film after splenectomy

A
  • Howell Jolly bodies
  • Target cells
  • Pappenheimer bodies

Haematology (1 decks)

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