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Year 3 > Haematology > Flashcards

Haematology Flashcards

1
Q

What do both the extrinsic and intrinsic pathways activate

A

Activate factor X

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2
Q

What does the activation of factor X lead to?

A

The conversion of prothrombin into thrombin

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3
Q

What does thrombin do

A

Converts fibrinogen to fibrin which triggers activation of factor XIII to stabilise clot

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4
Q

What is a stable clot formed by?

A

Activated platelets, fibrin and factor XIIIa

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5
Q

What factors does haemophillia type A and type B affect?

A

Type A- factor VIII
Type B- factor IX

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6
Q

How would haemophillia effect a coagulation screen?

A

Cause an isolated increase in APTT

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7
Q

What mutation is on the most common thrombophillia?

A

Factor V mutation which causes resistance to inactivation by protein C.

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8
Q

What factor does Von Willebrand factor transport

A

Transports factor 8

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9
Q

Treatment for febrile non-haemolytic transfusion reactions

A

Slow the transfusion and give 1mg paracetamol

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10
Q

When does the intrinsic pathway become activated?

A

When blood is exposed to collagen (due to vascular damage), the intrinsic pathway is initiated and factor XII is converted to ‘activated Factor XII’ (factor XIIa)

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11
Q

When does the extrinsic pathway become activated?

A

When tissue factor comes into contact with blood, activating factor VII

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12
Q

What can cause ferritin to rise?

A

Acute infection/illness

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13
Q

Describe hepcidin and its function?

A

A major regulator of iron uptake, produced in the liver in response to iron load and inflammation.
Binds to ferroportin and causes degradation

Iron therefore trapped in duodenal cells and macrophages

Hepcidin levels decrease when iron deficient

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14
Q

What is the treatment for autoimmune haemolytic anaemia

A

Corticosteroids

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15
Q

Treatment for Von Willebrand’s disease?

A

Desmopressin- causes the release of VwF

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16
Q

How long is treatment for an unprovoked DVT?

A

6 months

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17
Q

How long is treatment for a provoked DVT?

A

3 months

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18
Q

How long is treatment for DVT in patients with active cancer?

A

3-6 months

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19
Q

What do Howell-Jolly bodies suggest?

A

Represent DNA material of red cells usually removed by the spleen so show hyposplenism

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20
Q

When are target cells seen?

A

Obstructive liver disease, haemoglobinopathies, and post splenectomy

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21
Q

What does G6PD deficiency cause?

A

Haemolytic anaemia

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22
Q

What inheritance pattern is G6PD deficiency?

A

X-linked recessive

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23
Q

How do you reverse the effects of warfarin?

A

IV vit K and prothrombin complex

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24
Q

What is the inheritance pattern of Haemophilia A?

A

X linked recessive

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25
Q

What are heinz bodies seen in?

A

G6PD deficiency (heinz beans -> fava beans -> G6PD)

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26
Q

When is there likely a polyclonal increase in plasma cells?

A

Infection

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27
Q

When is there likely a monoclonal increase in plasma cells?

A

Malignancy eg multiple myeloma

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28
Q

What are smudge cells seen in?

A

Chronic Lymphocytic Leukaemia

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29
Q

How can you tell the difference between chronic and acute myeloid leukaemia

A

Acute= thrombocytopenia
Chronic= normal or raised platelets

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30
Q

Characteristics of chronic myeloid leukaemia?

A

Massive splenomegaly
Raised RBC, WBC and platelets

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31
Q

Which vitamin can vegans be deficient in?

A

B12

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32
Q

What kind of drug is methotraxate

A

Folate antagonist so should always be prescribed with folic acid supplements

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33
Q

What are teardrops seen in?

A

Myelofibrosis

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34
Q

Where does extravascular haemolysis occur?

A

In the spleen

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35
Q

1st line treatment for VwF disease?

A

Desmopressin

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36
Q

Why could you get you frontal bossing and hepatosplenomegaly in Beta Thal major in children?

A

As the beta chains are defective, fetal haemoglobin in made to compensate and this is made in abnormal locations such as the skull or spleen

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37
Q

What does G6PD deficiency present as?

A

Acute haemolytic anaemia

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38
Q

What are target cells seen in?

A

Beta Thal
Sickle Cell
Hyposplenism
Liver disease

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39
Q

What is seen in biopsy of Hodgkin’s lymphoma?

A

Reed-sternberg cells

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40
Q

What are spherocytes seen in?

A

Hereditary spherocytosis
Autoimmune haemolytic anaemia

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41
Q

What are howell-jolly bodies seen in

A

Hyposplenism

42
Q

What are Heinz bodies seen in?

A

G6PD deficiency
Alpha thal

43
Q

What are schistocytes seen in?

A

Intravascular haemolysis
Mechanical Heart valve
DIC

44
Q

How does sideroblastic anaemia happen?

A

A red cell fails to completely form haem leading to iron deposits in the mitochondria

Sufficient iron but ineffective erythropoiesis causes deposition of iron in multiple organs.

45
Q

What is a common cause of sideroblastic anaemia

A

alcohol

46
Q

What is the investigation for autoimmune haemolytic anaemia?

A

Coombs test

47
Q

What triggers G6PD deficiency crises?

A

Jaundice and anaemia after medication, infection or eating fava beans

48
Q

Which ethnicities is G6PD most common?

A

Middle Eastern, Mediterranean and african

49
Q

What is the Ann Arbor staging system used to classify?

A

Hodgkin’s Lymphoma

50
Q

What are Auer rods seen in?

A

Acute Myeloid Leukaemia

51
Q

What are smudge cells seen in?

A

Chronic lymphocytic leukaemia. In CLL lymphocytes are fragile so damage easily on prep

52
Q

What blood cancer can present asymptomatically with a high WCC?

A

chronic lymphocytic leukaemia

53
Q

What is the first factor to be activated in the intrinsic pathway?

A

Factor 12

54
Q

What is the first factor to be activated in the extrinsic pathway?

A

Factor 7. Has the shortest half life of all the factors of the coag cascade

55
Q

What can cause anaemia of chronic disease?

A

Inflammatory conditions such as rheumatoid arthritis, diabetes

56
Q

What is microscopic haemolytic anaemia? (MAHA)

A

Haemolytic anaemia caused by factors in small blood vessels eg HUS, DIC, TTP

57
Q

What does Waldenström macroglobulinaemia present with?

A

Signs of hyperviscosity: headaches, blurred vision, papilloedema, ischaemic stroke, venous thromboembolism
Signs of anaemia
Signs of thrombocytopenia
B symptoms

58
Q

What are macroovalocytes and hypersegmented neutrophils seen in?

A

Vitamin B12 or folic acid deficiency

59
Q

How can TACO lead to pulmonary oedema?

A

When patients with chronic oedema and high cardiac output are given a large volume overload = pulmonary oedema

60
Q

How does TRALI occur?

A

Anti- leucocyte antibodies present in donation bind to the patients white cells and degranulation of the affected neutrophils in the lungs causing lung injury. Pulmonary infiltrates are seen on CXR.

61
Q

What are red cells that have lost their central pallor?

A

Spherocytes

62
Q

How does a aplastic crisis arise?

A

Patients with sickle cell <16 as result of parvovirus B19 reducing erythropoiesis

63
Q

What typically cause HUS?

A

Shiga toxin

64
Q

What is polycythaemia rubra vera characterised by ?

A

Erythrocytosis so increased Hb

65
Q

Management of Waldenstrom’s

A

Plasmapharesis to filter IgM

66
Q

Which blood type is the universal donor

A

O negative because no antigens (A,B or D)

67
Q

Which blood type is the universal recipient?

A

AB+ because no antibodies

68
Q

Diagnostic test for multiple myeloma?

A

Bone marrow aspirate and trephine biopsy

69
Q

How could total biliary obstruction lead to bleeding/prolonged INR?

A

Deficiency in fat soluble vitamins eg K,D,E,A and fat malabsorption so greater INR

70
Q

Best diagnostic test for polycythaemia rubra vera?

A

Jak 2 mutation status

71
Q

Which antibodies in cold autoimmune haemolytic anaemia?

A

IgM

72
Q

An acute haemolytic transfusion reaction is mediated by which antibody?

A

IgM -> activate the complement system

73
Q

Treatment for warm autoimmune intravascular haemolysis?

A

Prednisolone

74
Q

Which antibodies in warm autoimmune haemolytic anaemia?

A

IgG

75
Q

Where is most iron absorbed and in what state?

A

In the duodenum in the Fe2+ state (ferrous form)

76
Q

What is aplastic anaemia?

A

Normochromic, normocytic anaemia with pancytopenia and hypoplastic bone marrow

77
Q

In both B12 and folate deficiencies which one must be treated first?

A

Vit B 12 to avoid subacute degeneration of the spinal cord

78
Q

Management of B12 deficiency?

A

1mg IM hydroxocobalamin 3 times each week for 2 weeks then once every 3 months

79
Q

What is a sequestration crisis?

A

Blood pool in organs due to sickling eg splenomegaly, causes worsening anaemia due to loss of blood in vasculature and increase in reticulocytes as body compensates for loss

80
Q

What would bloods show in an aplastic crisis?

A

Sudden drop in Hb with pancytopenia

81
Q

What does haptoglobin do?

A

Bind to free haemoglobin so low haptoglobin level in haemolysis

82
Q

Hypersegmented neutrophils are seen in what disease?

A

Megaloblastic anaemia

83
Q

What is imatinib and what is it used for?

A

A tyrosine kinase inhibitor- first line treatment of CML

84
Q

What can be used for patients with repeated painful sickle cell crises?

A

Hydroxyurea

85
Q

ADAMTS-13 is associated with what?

A

Thrombotic thrombocytopenic purpura

86
Q

TACO symptoms?

A

SOB and hypertension

87
Q

Target action of ritixumab?

A

Monoclonal antibody that targets CD20. Important in the maturation of B cells into plasma cells

88
Q

Why are blood products irridiated?

A

To avoid transfusion associated graft vs host disease

89
Q

Most common organism implicated in neutropenic sepsis?

A

Staph epidermidis- gram positive coag negative

90
Q

Primary AL amyloidosis is due to what?

A

Protein deposition due to excess production of monoclonal immunoglobulin light chains

91
Q

Secondary AA amyloidosis is due to what?

A

Associated with inflammatory conditions involving chronic inflammation/infection.
Protein deposition due to excess production of serum amyloid A an acute phase protein

92
Q

Pentad of symptoms in thrombotic thrombocytopenic purpura?

A

Fever, haemolytic anaemia, thrombocytopenia, acute renal failure and neurological symptoms

93
Q

What does prothrombin complex replace?

A

Vit K clotting factor used in bleeding on warfarin

94
Q

Lymph node presentation of hodgkin’s lymphoma?

A

Painless, rubbery cervical nodes

95
Q

When does LDH increase?

A

In haemolytic anaemia due to increased response by bone marrow to increase red cell production

96
Q

What is serum iron

A

Measures the serum iron levels in the blood- represents iron almost completely bound to transferrin

97
Q

What is TIBC

A

Measures the blood’s ability to attach itself to iron and transport it around the body

98
Q

What is serum ferritin

A

The bodies ability to store iron

99
Q

How does LMWH work?

A

Activates anti-thrombin-> activates factor Xa -> stops conversion of prothrombin to thrombin-> which stops fibrinogen to fibrin to reduce blood clotting

100
Q

What are pappenheimer bodies seen in?

A

Sideroblastic anaemia

Year 3 (12 decks)

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