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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does an isolated prolonged PT time reflect?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is DIC?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

In blood tests, how will DIC present?

A

Prolonged PT
Prolonged APTT
Low platelets
Low fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What causes TRALI?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What mutation is present in those with myeloproliferative polycythaemia?

A

JAK2 gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does rituximab target?

A

CD20 - expressed on B cells and B cell lymphomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does imatinib target?

A

BCR-ABL 1 tyrosine kinase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do bence jones protein reflect?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the appearance of an eosinophil?

A

Bi-lobed (spectacle) shaped nuclei

Red stained cytoplasmic granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is AML?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is a diagnosis of CLL confirmed?

A

Peripheral blood immunotyping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why will pancytopenia occur in megaloblastic anaemia?

A

B12 is required for nuclear maturation in all 3 haemopoietic lineages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
What is the mode of action of rivaroxaban?
Competitively inhibits factor 10a | Factor 10 along with 5a form the prothrombinase complex which converts prothrombin to thrombin
26
What is the treatment for a sickle chest crisis?
Exchange transfusion
27
What is vWF deficiency?
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
What causes myelodysplasia?
Stem cell malignancy that results in ineffective haematopoiesis
29
What can myelodysplasia progress to?
AML