Formative Flashcards

1
Q

What does an isolated prolonged APTT reflect?

A

Deficiency of factors in the intrinsic pathway of coagulation;
Factor 8, 9 = haemophilia
Heparin
APS

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2
Q

What does an isolated prolonged PT time reflect?

A

Deficiency of factors in the extrinsic pathway
Factor 7 and vWF
Warfarin

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3
Q

What is DIC?

A

Consumptive coagulopathy due to abnormal activation of coag system with deposition of thrombi in micro and macro vasculature

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4
Q

In blood tests, how will DIC present?

A

Prolonged PT
Prolonged APTT
Low platelets
Low fibrinogen

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5
Q

What causes TRALI?

A

Anti-leucocyte antibodies in donation that bind to the patients white cells and cause an acute lung injury

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6
Q

What mutation is present in those with myeloproliferative polycythaemia?

A

JAK2 gene

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7
Q

What should be investigated in someone with a high Hb with no history to suggest secondary polycythaemia?

A

Polycythaemia rubra vera

JAK 2 gene

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8
Q

What does rituximab target?

A

CD20 - expressed on B cells and B cell lymphomas

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9
Q

What does imatinib target?

A

BCR-ABL 1 tyrosine kinase

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10
Q

What do bence jones protein reflect?

A

The excretion of monoclonal (kappa or lambda) immunoglobulin light chains

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11
Q

What is the appearance of an eosinophil?

A

Bi-lobed (spectacle) shaped nuclei

Red stained cytoplasmic granules

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12
Q

What is AML?

A

Bone marrow based malignancy where there is a block in differentiation and an excess of primitive cells

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13
Q

What ic CLL?

A

NO block on differentation but a failure of cell death resulting in a steady accumulation of cells
Seen as an excess of small mature lymphocytes in the blood (often smear cells)

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14
Q

How is a diagnosis of CLL confirmed?

A

Peripheral blood immunotyping

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15
Q

Why will pancytopenia occur in megaloblastic anaemia?

A

B12 is required for nuclear maturation in all 3 haemopoietic lineages

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16
Q

What will the blood film show in megaloblastic anaemia?

A

Macroovalocytes

Hypersegmented neutrophils

17
Q

Why does marrow failure occur in AML?

A

Excessive proliferation of primitive cells (myeloblasts)

18
Q

What is an auer rod?

A

PATHOGNOMONIC OF AML

Abnormalities of granulation in blasts

19
Q

What is essential thrombocythaemia?

A

Chronic myeloproliferative disorder characterized by excess production of platelets in the bone marrow and an increased risk of thrombosis

20
Q

What causes HbS?

A

Point mutation in codon 6 resulting in a substitution of glutamic acid to valine in the beta chain

21
Q

What is a different way to describe a spherocyte?

A

Red cells that have lost central pallor

22
Q

What is the treatment for autoimmune haemolytic anaemia?

A

Steroid (1 mg/kg of pred per day)

Folic acid

23
Q

What is the mode of action of clopidogrel?

A

Selectively inhibits binding of ADP to platelet receptor and the subsequent ADP mediated activation of glycoprotein GP2b/3a complex therefore inhibiting platelet activation

24
Q

What is the mode of action of aspirin?

A

Irreversible inactivates cyclooxygenase 1

25
Q

What is the mode of action of rivaroxaban?

A

Competitively inhibits factor 10a

Factor 10 along with 5a form the prothrombinase complex which converts prothrombin to thrombin

26
Q

What is the treatment for a sickle chest crisis?

A

Exchange transfusion

27
Q

What is vWF deficiency?

A

Disorder of primary haemostasis due to deficiency of vWF which bridges platelets to sub-endothelial collagen following endothelial injury
This affects platelet adhesion at the site of injury

28
Q

What causes myelodysplasia?

A

Stem cell malignancy that results in ineffective haematopoiesis

29
Q

What can myelodysplasia progress to?

A

AML