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3rd Year > Haematology > Flashcards

Haematology Flashcards

1
Q

Blood production in foetus:
Just after conception
After 2 months
In adults

A

Yolk sac
Liver and spleen
Bone marrow

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2
Q

What % of the marrow is producing white cells

A

75%

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3
Q

Hormone that stimulate neutrophils, basophils and eosinophils

A

Granulocyte colony stimulating factors (G-CSF)

Produced by the endothelium and macrophages

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4
Q

Idiopathic thrombocytopenia purpura

A

Antibodies against glycoprotein IIb/IIIa complex or Ib-V-IX complex

Acute form:
Children following infection/vaccination
Self limiting over 1-2 weeks

Chronic:
Young middle aged women
Relapsing remitting

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5
Q

Evans syndrome

A

ITP in associated with autoimmune haemolytic anaemia

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6
Q

Platelet survival
RBC survival
Neutrophil survival

A

7 days
120 days
24 hours

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7
Q

Hb in pregnancy

A

Decreased

RBC increases but plasma increases more

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8
Q

Prevalence of anaemia in UK

A

4-5%

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9
Q

Methaemaglobin

A

Fe3+ is oxidised to Fe2+

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10
Q

Microcytic anaemia causes

A

Iron deficiency
Thalassaemia
Chronic bleeding

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11
Q

Normocytic anaemia

A 
Chronic disease
Haemolysis
Acute blood loss
Bone marrow infiltration
Combined haematinic deficiency
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12
Q

Macrocytic anaemia causes

A 
Haemolysis
B12/folate deficiency (megaloblastic)
Hypothyroidism
Liver disease
Alcohol excess
Myelodysplasia
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13
Q

TIBC in:
Pregnancy
Anaemia of chronic disease
Iron deficiency anaemia

A

Increased
Decreased
Increased

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14
Q

RBC survival in anaemia of chronic disease

A

105 days

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15
Q

B12 source

A

Animal products

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16
Q

Folate source

A

Nuts vegetables cereals

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17
Q

Clinical features of b12 And folate deficiency

A

Glossitis
Jaundice
Neurological deficit - paresthesia and cognitive decline

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18
Q

Replacing B12 and folate

A

IM B12 then
Oral folate
Otherwise get subacute degeneration of the spinal cord

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19
Q

Hyposplenism blood film

A

Holly-Jowel bodies

Pappenheimer bodies

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20
Q

G6PDH

Inheritance

A

Enzyme cause of haemolytic anaemia
Mediterranean and middle eastern boys
Ciprofloxacin is a trigger

X-linked recessive

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21
Q

PK deficiency

A

Enzyme cause for haemolytic anaemia

Northern european children

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22
Q

Warm autoimmune haemolytic anaemia immunology

A

IgG mediated haemolysis occurring in spleen at body temperature.

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23
Q

Warm AIHA cause

A

SLE

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24
Q

Warm AIHA treatment

A

Steroids immunosuppression and splenectomy

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25
Q

Cold AIHA immunology

A

IgM and complement mediated haemolysis occurring at 4 degrees (e.g. In hands on cold day)

Responds less well to steroids`

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26
Q

Diagnosis of AIHA

A

Coombs’ test

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27
Q

Clinical features of haemolytic anaemia

A 
Jaundice
Anaemia
Gallstones (if chronic)
Haemoglobinuria (if intravascular)
Splenomegaly (if extravascular)
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28
Q

Chromosomes of globin chain

A 
A = 16 2 genes
B = 11 1 gene
Y = 11 2 genes
D = 11 1 gene
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29
Q

Clinical features of beta thalassaemi major

A 
Normal foetal life
Anaemia in first few months
Jaundice
Medullary hyperplasia --> frontal bossing and hair on end appearance of cranium on xray
Hepatosplenomegaly
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30
Q

Blood film of beta tahallasaemia major

A

Few RBC
Hypochromia
Target cells
Uncleared red cells

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31
Q

Barts syndrome

A

When all 4 of your alpha genes are mutated –> hydrops featalis and death as you cant make HbF

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32
Q

HbH disease

A

3/4 alpha genes are mutated
Commonly mistaken for iron deficiency anaemia as you get a microcytic hypochromia anaemia.
Dont give iron or you’ll make then worse. Usually live normal lives with the occasional transfusion

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33
Q

Inheritance pattern of thalassamieas and suckling disorders

A

AR

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34
Q

Prevalence of sickle cell anaemia

A

1 in 10,000

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35
Q

Specific mutation for HbS

A

6th amino acid of beta globin gene

Glutamic acid –> Valine

36
Q

Rbc survival in sickle cell

A

<20 days

37
Q

Sickle cell crises

A
  1. Thrombotic crisis - painful occlusion causing widespread infarction. Precipitated by dehydration, infection, deoxygenation. Acute chest syndrome can occur
  2. Sequestration crisis - spleen rapidly enlarges, pooling blood and causing anaemia but with high reticulocyte count
  3. Aplastic crisis - parvovirus infection leading to a sudden drop in Hb
  4. Haemolytic crisis - rare. Also causes sudden drop in Hb
38
Q

Lab tests for sickle cell

A

High pressure liquid chromatography

Sickle cell solubility test ( goes cloudy in phosphate buffers)

39
Q

First line treatment for neutropaenic sepsis

A

Tazocin

40
Q

Definition of CLL

A

B cell >5x10’9 per litre for more than 3 months

If its raised but below the threshold its called a monoclonal B cell lymphocytosis

41
Q

Smear cells

A

CLL

42
Q

Flow Cytometry of CLL

A

T cell marker CD5

43
Q

Survival of CLL

A

11 years

Pretty good considering diagnosis is around 72!

44
Q

Somatic hypermutation, good or bad in CLL

A

Good

Un-somatically hypermutated CLL forms have a worse prognosis

45
Q

Basal cell carcinoma is associated with which leukaemia

A

CLL

46
Q

Presentation of CML

A

Early satiety (splenomegaly pushes on stomach)
Weight loss and sweats (hypermetabolic state)
SOB, priapism, eye problems (leucostasis)

47
Q

Mainstay of management for myeloproliferative disorders

A 
Track them
Aspirin to reduce clotting
Lifestyle factors to reduce clotting
Hydroxycarbamide can be used as cytoreductive therapy
In PRV --> venesection
48
Q

Other treatment for JAK2 negative myelofibrosis

A

JAK2 inhibitors

Last line is transplant

49
Q

Tear drop cells

A

Myelofibrosis

50
Q

Chromosomal abnormality predisposing you to ALL/AML

A

Downs syndrome

51
Q

Prognostic indicators for AML

A

Age (younger patients do better)
Genotype (FLT-3 neg/NPM-1 pos is better)
Cytogenetics - you know this

52
Q

Treatment for very bad prognosis AML

A

BMT

53
Q

Bone marrow histology for AML/ALL

A

Blasts must be >20% of nucleated cells for diagnosis

54
Q

Clinical syndrome of ALL

A

Similar to AML: anaemia, thrombocytopenia, high blast

Dissimilar to AML: CNS symptoms, lymphadenopathy, bone pain.

55
Q

Reasons for 20% mortality of BMT

A

Neutropenic sepsis

Graft versus host disease

56
Q

Incidences of lymphomas

A 
Hodgkin = bimodal
Non-hodgkin = elderly
57
Q

Ann Arbor staging

A 
1 = 1 node
2 = 2 nodes same side of diaphragm
3 = 2 nodes different side of diaphragm
4 = involvement of major organs
\+
A = no B symptoms
B = B symptoms (drenching night sweats, fevers >38, weight loss >10% in 6 months)
58
Q

Types of hodgkin lymphoma

A

Nodular sclerosing. 70%. F>M. Lacunar cells. Good prognosis.

Mixed cellularity. 20%. Many reed sternberg cells. Good prognosis.

Lymphocyte predominant. 5%. Best prognosis.

Lymphocyte depleted. <1%. Worst prognosis.

59
Q

Burrkits lymphoma

A

High grade B cell neoplasm.
C-myc t(8.14) mutation
Starry sky appearance on microscopy
Common cause of tumour lysis syndrome

Two types:

Endemic - Africa, EBV, mandible
Sporadic - iléocaecal tumour

60
Q

RF for hodgkin

A

EBV

Smoking

61
Q

RF for non-hodkin

A

Autoimmune diseases
HIV/AIDS
HTLV1 infection
Smoking

62
Q

Treatment of non-hodgkin

A

Low grade - nothing

High grade - RCHOP
1a –> 4 rounds every 3 weeks
Others –> 6-8 rounds every 3 weeks

RCHOP = rituximab, cyclophosphamide, hydroxydanunorubicin, oncovin, prednisolone.

63
Q

Treatment of Hodgkin

A

ABVD +/- radiotherapy

64
Q

Criteria for myeloma

A

> 30g/l paraproteinin blood
10% B cells in marrow
End organ damage CRABI

65
Q

Monitoring for MGUS

A

Every 6 months

66
Q

Monitoring for smouldering myeloma

A

Every 3 months

67
Q

Treatment for myeloma

A

Chemo
Steroids
Thalidomide
Proteasome inhibitors

68
Q

Whats in the blue blood test tube

A

Citrate to chelate all the calcium and prevent clotting in the tube

69
Q

VWD inheritance

A

AD

70
Q

Haemophilia inheritance

A

X-linked recessive

71
Q

Management of haemophiliacs

A

Recombinant factor concentrate

72
Q

Treatment of von willebrand disease

A

Tranexamic acid for mild bleeding

Desmopressin (DDAVP) raises levels of vWF by inducing releases f vWF from Weibel-

Palade bodies in endothelial cells
VWF/F8 concentrate if severe (v expensive)

73
Q

Biliary obstruction leading to clotting problem?

A

Less bile and less vitamin K absorption so less 2 7 9 10

74
Q

When to treat deranged PT aPTT platelet and fibrinogen levels in blood in someone with liver disease

A

Only if there are symptoms

75
Q

What are thrombotic microangipathies

A

Thrombotic features + bleeding

DIC TTP HUS pre-eclampsia

76
Q

Blood film in TTP

A

Thrombocytopenia and red cell fragments

77
Q

Warfarin targets for first DVT

Recurrent DVT

A
  1. 5

3. 5

78
Q

Length of warfarin treatment for
Provoked DVT
Unprovoked DVT

A

3months

6 months

79
Q

What is factor V leiden

Prevalence

A

AD mutation in F5 gene making you 4x more likely to develop DVT

Activated protein C resistance

1 in 20

80
Q

Peri-operative management of warfarin

A

Stop it 5 days before surgery
If INR <1.5 on the days, surgery can continue

Stratify into low, medium, high risk groups:
Low = no bridging therapy
High risk = prophylactic dose LMWH
Very high risk = treatment dose LMWH

81
Q

Classic features of haemolytic transfusion reaction

A

Within minutes there is massive intravascualr haemolysis
Fever and tachycardia
Backache
Dark urine

–> DIC and renal failure

82
Q

Management of acute haemolytic transfusion reaction

A

Termination of transfusion, generous fluid resuscitation and inform the lab

83
Q

Allergic reaction to transfusion
Mild
Severe

A

Within minutes –> wheeze, urticaria, angiooedema etc

Simple urticaria = mild –> antihistamine and discontinue transfusion until symptoms have subsided and then can continue

Anything more = IM adrenaline, antihistamine, hydrocortisone

84
Q

Over how long can you give red cells

FFP?

A

4 hours

30mins

85
Q

Deferiprone

A

Iron chelation to prevent iron overload e.g. Haemophiliacs

3rd Year (9 decks)

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