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Medicine - Finals > Haematology > Flashcards

Haematology Flashcards

1
Q

Heinz Bodies

A

G6PD deficiency

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2
Q

Mechanism of action: Dabigatran

A

Direct thrombin inhibitor

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3
Q

Mechanism of action: Heparin

A

Antithrombin III

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4
Q

Mechanism of action: Rivaroxiban/Apixaban

A

Direct factor Xa inhibitor

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5
Q

Mechanism of action: Warfarin

A

Inhibits clotting factors II, VII, IX and X

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6
Q

In which 2 conditions is spherocytes found

A

autoimmune haemolytic anaemia as well as hereditary spherocytosis

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7
Q

EMA blood testing

A

hereditary spherocytosis

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8
Q

direct Coombs test

A

autoimmune haemolytic anaemia

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9
Q

Indirect Coombs test

A

Rhesus haemolytic disease of the newborn

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10
Q

‘Tear-drop’ poikilocytes

A

Myelofibrosis

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11
Q

Howell-Jolly bodies

A

hyposplenism

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12
Q

Anaemia caused by cytoplasmic defects. MCV. Causes.

A

Microcytic Anaemia - caused by a shortage of Hb components

  • Iron deficiency
  • Porphyrin deficiency
  • Congenital Sideroblastic Anaemia
  • Thalassaemia
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13
Q

Anaemia caused by nuclear defects. MCV. Causes.

A

Macrocytic Anaemia

Megaloblastic - large nucleated RBCs
- B12 and folate deficiency

Non-megaloblastic - alcoholic, liver disease hypothyroidism, marrow failure

Spurious - macrocytosis

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14
Q

Alpha thalassaemia with 3 defected genes

A

HbH disease (Hb with 4x B globin chains –> golf ball appearance)

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15
Q

Alpha thalassaemia with 4 defected genes

A

Hb barts hydrops fetalis

  • Hb barts (4x gamma chains), and
  • HbH (4x B globin chains –> golf ball appearance)

incompatible with life

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16
Q

High HbA2; low MCV

A

Beta Thalassaemia trait

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17
Q

Presentation of Major Beta Thalassaemia

A

Presents at 6-24 months (as HbF falls) with pallor and failure to thrive

requires transfusions

Skull X-ray –> “hair on end” appearance

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18
Q

Skull X-ray –> “hair on end” appearance

A

Major Beta Thalassaemia

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19
Q

What is HPLC used for?

A

Thalassaemia diagnosis

B trait –> excess HbA2
B major –> Some HbF, Some HbA2, No HbS, No HbA
A trait –> normal (use DNA testing)
Sickle Cell –> HbS

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20
Q

Aetiology, Features and Management of sickle cell crisis

A

Caused by hypoxia, infection or stress

features incl.

  • hyposplenism caused by infarcts
  • chronic haemolysis
  • widespread infarcts

Manage with oxygen, analgesia, antibiotics (if there is an infection), transfusion

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21
Q

Diagnosis of autoimmune haemolysis

A

Coomb’s test

  • Warm (IgG) e.g., SLE, Penicicllins, infection, CLL
  • Cold (IgM)e.g., TB, EBV
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22
Q

Features of haemochromatosis

A

Weakness, Arthritis, Arthralgia, Fatigue, Impotence, Cirrhosis, Diabetes, Cardiomyopathy

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23
Q

Causes of prolonged Prothrombin Time

A

Mild Liver disease
Vitamin K deficiency
Factor VII deficiency
Anticoagulation therapy with warfarin

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24
Q

Causes of prolonged APTT

A 
Factor VIII/XI deficiency 
Haemophilia A (VIII deficiency) or B (IX deficiency)
vWF deficiency 
Anti-phospholipid syndrome
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25
Q

Causes of both prolonged PT and APTT

A

Severe liver disease
FI/II/V/X deficiency
DIC

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26
Q

What does vitamin K do?

A

Carboxylates FII(prothrombin), VII, IX, X

Remember… Factors 2, 7, 9, 10

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27
Q

Management of DIC

A

Platelets, FFP (clotting factors), Cryoprecipitate (fibrinogen and factor VIII)

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28
Q

Inheritance of Haemophilia

A

X-linked

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29
Q

Knee Haemarthrosis with no Hx of trauma - investigate for …

A

Haemophilia

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30
Q

Management of Haemophilia

A

Lifelong IV factor concentrates

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31
Q

When would you screen for thrombophilia?

A

VTE in <45yo

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32
Q

Monitoring for LMWH

A

Anti-Xa Assay

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33
Q

Monitoring for Unfractionated Heparin

A

APTT

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34
Q

Monitoring for Warfarin

A

INR and PT

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35
Q

Mechanism of Aspirin

A

COX-1 inhibitor

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36
Q

Mechanism of Clopidogrel

A

ADP receptor (P2Y12) antagonist

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37
Q

Mechanism of Dipyridamole

A

Phosphodiesterase inhibitor

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38
Q

Mechanism of Abciximab

A

GPIIb/IIIa inhibitor - used in cardiac surgery

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39
Q

Macro-ovalocytes

A

Megaloblastic Anaemia (B12/Folate deficiency)

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40
Q

Hyper-segmented Neutrophils

A

Megaloblastic Anaemia (B12/Folate deficiency)

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41
Q

Cigar or Pencil Cells

A

Iron Deficiency

42
Q

Blood film. ‘rouleaux formation’

A

Myeloma

43
Q

Features of Myeloma (CRAB)

A

C - calcium raised
R - renal failure
A - anaemia (technically a pancytopenia)
B - bone pain

44
Q

When should lithium levels be checked after a dose change?

A

7 days; 12 hours since last dose

45
Q

Reed-Sternberg cell AKA ‘mirror image nuclei’

A

Hodgkin’s Lymphoma

46
Q

Features of histological aggression

A 
increased N:C 
open chromatin
more primitive cells
larger cells 
prominent nucleoli 
rapid proliferation
47
Q

itch without a rash and alcohol induced pain

A

Hodgkin’s disease

48
Q

Hard tender lymphadenopathy with skin inflammation

A

bacterial

49
Q

Hard tender lymphadenopathy with no skin inflammation

A

viral

50
Q

Hard non-tender irregular lymphadenopathy

A

Metastatic carcinoma

51
Q

Soft rubbery non-tender lymphadenopathy

A

Lymphoma

52
Q

What is the difference in immunohistochemistry and immunophenotyping with respect to investigating haematological malignancies?

A

Immunohistochemistry - analysis of surface proteins to classify lymphoma

Immunophenotyping - used for cells in liquid phase e.g., leukaemia, Burkitt’s Lymphoma

53
Q

CD30+ Lymphoma

A

Hodgkin’s Disease

54
Q

CD20+ Lymphoma

A

Non-Hodgkin’s Lymphoma

55
Q

Biological treatment for NHL

A

Ibrutinib

56
Q

Subtypes of Non-Hodgkin’s Lymphoma

A

T-cell (10%)

B-cell (90%)

57
Q

Features of Pancytopaenia

A

Anaemia - fatigue, shortness of breath
Neutropaenia - infections (particularly Gram -‘ve)
Thrombocytopenia (bleeding, purpura, petechiae)

58
Q

Fanconi’s Anaemia. features

A

Short stature, skin pigmentation, GI/Renal/CV and haematological abnormalities
presents around 7 years old with bone marrow failure
high risk of leukaemia

59
Q

What does myelodysplastic syndrome put you at risk of?

A

AML

60
Q

Causes of hypercellular marrow?

A

Myelodysplastic Syndrome
B12/Folate deficiency
Hypersplenism

61
Q

Causes of hypocellular marrow?

A

Aplastic anaemia

62
Q

What gives rise to immunoglobulin variability?

A

VDJ recombination

63
Q

Features of Myeloma (CCRABI)

A

Use the mnemonicCRABBI:

Calcium
Hypercalcaemia occurs as a result of increased osteoclast activity within the bones
This leads to constipation, nausea, anorexia and confusion

Renal
Monoclonal production of immunoglobulins results in light chain deposition within the renal tubules
This causes renal damage which presents as dehydration and increasing thirst
Other causes of renal impairment in myeloma include amyloidosis, nephrocalcinosis, nephrolithiasis

Anaemia
Bone marrow crowding suppresses erythropoiesis leading to anaemia
This causes fatigue and pallor

Bleeding
bone marrow crowding also results in thrombocytopenia which puts patients at increased risk of bleeding and bruising

Bones
Bone marrow infiltration by plasma cells and cytokine-mediated osteoclast overactivity creates lytic bone lesions
This may present as pain (especially in the back) and increases the risk of fragility fractures

Infection
a reduction in the production of normal immunoglobulins results in increased susceptibility to infection

64
Q

Features of MGUS

A

benign paraproteinaemia , precursor to myeloma, asymptomatic but may have demyelinating neuropathy,

protein <30g/L

65
Q

Most common myeloma subtype

A

IgG

66
Q

Congo red staining -> apple-green birefringence

A

Amyloidosis

67
Q

Most common adult leukaemia

A

CLL

68
Q

Smudge cells on blood film

A

CLL

69
Q

Richter’s transformation

A

CLL->NHL high grade

70
Q

BCR-ABL1+ (Philadelphia Chromosome)

A

CML

71
Q

Biological treatment of CML

A

TK inhibitors e.g., Imatinib

72
Q

Myeloproliferative disorders

A

BCR-ABL1 -ve

  • Myelofibrosis
  • Polycythaemia Rubra Vera
  • Essential Thrombocytopaenia

BCR-ABL1 +ve
- CML

73
Q

Pruritis after hot bath

A

Polycythaemia Rubra Vera

74
Q

JAK2 positive in 95%

A

PRV

75
Q

Management of polycythaemia rubra vera

A

venesection (until Hct <0.45) is first line
could add aspirin
could add hydroxyurea(hydroxycarbamide)

76
Q

burning sensation in the hands + thrombosis + haemorrhages

A

Essential Thrombocytosis

77
Q

Teardrop poikilocytes

A

Myelofibrosis

78
Q

Management of Myelofibrosis

A

Supportive - JAK 2 inhibitor e.g. ruloxitinib

Definitive - stem cell transplantation

79
Q

Investigations show a prolonged bleeding time and increased APTT. Normal PT and platelet count.

A

vWF disease

80
Q

Management of acquired haemophilia

A

Steroids

81
Q

Main difference between TRALI and TACO?

A

TACO - hypertensive

TRALI - hypotensive

82
Q

Management of TACO

A

Slow or stop transfusion

Consider intravenous loop diuretic (e.g. furosemide) and oxygen

83
Q

Which haematological condition occurs in 30% of individuals with coeliac disease?

A

Acquired Hyposplenism

84
Q

Blood smear results associated with hyposplenism

A

target cells and howell-jolly bodies

85
Q

Causes of a Acidosis with a normal anion gap

A

Remember: H.A.R.D

Hyperchloraemia
Addison’s disease
Renal tubular acidosis
Diarrhoea

86
Q

Biochemistry seen in early myeloma

A

High calcium, normal phosphate, normal ALP

87
Q

Management of Warfarin: Major Bleeding

A

Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate - if not available then FFP*

88
Q

Management of Warfarin: INR > 8 with minor bleeding

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0

89
Q

Management of Warfarin: INR > 8 with NO bleeding

A

Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0

90
Q

Management of Warfarin: INR 5.0-8.0

Minor bleeding

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR < 5.0

91
Q

Management of Warfarin: INR 5.0-8.0

with NO bleeding

A

Withhold 1 or 2 doses of warfarin

Reduce subsequent maintenance dose

92
Q

Management of VWF disease

A

tranexamic acid for mild bleeding
desmopressin (DDAVP): raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells
factor VIII concentrate

93
Q

Prolonged bleeding time, normal platelets, prolonged APTT

A

VWF disease

94
Q

Fatigue, prolonged bleeding and thrombocytopaenia

A

Immune thrombocytopenic purpura (ITP)

95
Q

Management. Immune thrombocytopenic purpura (ITP)

A

Oral Prednisolone

pooled normal human immunoglobulin (IVIG) - for active bleeding

96
Q

Monitoring for LMWH e.g. Dalteparin

A

Anti Factor Xa

97
Q

Adverse effects of Heparin

A

bleeding
thrombocytopenia
osteoporosis and an increased risk of fractures
hyperkalaemia - this is thought to be caused by inhibition of aldosterone secretion

98
Q

Which blood product is most likely to result in septicaemia?

A

Platelets - stored at room temperature

99
Q

Features of Factor V Leiden

A

Most common thrombophilia (5% in UK)

Protein C resistance

100
Q

Characteristic iron study profile in haemochromatosis

A

Raised transferrin saturation
Raised ferritin
Low TIBC

Medicine - Finals (21 decks)

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