Haematology Flashcards

1
Q

incidental finding of thrombocytopenia
normal PT and APTT
petechiae, fatigue

A

immune thrombocytopenic purpura

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

Mx of ITP

A

self limiting, if severe: prednisolone

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

petechiae, neurological symptoms, anaemia

A

thrombotic thrombocytopenic purpura

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

Mx of TTP

A

plasmapheresis

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

polycythaemia rubra vera Px

A

itching after hot shower, redder skin
low erythropoetin
high MCV high haematocrit

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

polycythaemia mutation

A

JAK2 mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ALL Px

A

children, bone marrow failure, testicular enlargement, hepatosplenomegaly

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

ALL Ix

A

Blast cells

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

AML Px

A

bone marrow failure, hepatosplenomegaly

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

AML Ix

A

Auer rods

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

CML Px

A

weight loss, fever, massive splenomegaly, gout

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

CML Ix

A

Philadelphia chromosome, mature myeloid cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CLL Px

A

Asymptomatic, old males

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

CLL Ix

A

smudge cells, increased lymphocytes

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

Complication of CLL

A

can transform into non-hodgkins lymphoma (Richter transformation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Symptoms of lymphoma

A

lympadenopathy (rubbery tender lymph nodes)
fever, weight loss, night sweats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

differentiating Hodgkins vs non-Hodgkins

A

Hodgkins has Reed-Sternberg cells (owls)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Burkitt’s lymphoma: associated with, Ix

A

Epstein Barr virus
Malaria
HIV

Starry sky appearance on lymph node biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MALT lymphoma Px

A

affected area: around stomach
associated with H pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

paraprotein spike, bence jones protein

A

multiple myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

dark urine in the morning, fatigue, dyspnea.
Ix:

A

paroxysmal nocturnal haemogloninuria
flow cytometry for CD55 and CD59

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

most common cause of aplastic crisis in pts with sickle cells

A

parvovirus b19 infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

anaemia, bone pain, hypercalcaemia, renal failure
lytic lesions

A

multiple myeloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

positive coombs test?

A

autoimmune haemolytic anaemia

25
Q

iron deficiency anaemia, high ferritin and iron. pappenheimer bodies

A

sideroblastic anaemia

26
Q

haemophilia A inheritance

A

x linked recessive

27
Q

Dx of haemophilia A

A

prolonged APTT normal PT

28
Q

Pathophis of haemophilia A

A

factor 8 deficiency

29
Q

Mx fo haemophilia A in mild vs severe bleeds

A

mild: desmopressin and tranexamic acid
severe: recombinant factor 8

30
Q

post partum haemorrhage, prolonged APTT and PT, low Hb, low fibrinogen

A

DIC

31
Q

investigation for multiple myeloma

A

urine electrophoresis to look for Bence-Jones protein

32
Q

hereditary haemochromatosis

A

iron deposition in the tissues
Px: diabetes mellitus, hyperpigmentation, testicular enlargement, erectile dysfunction, weakness

33
Q

hereditary haemochromatosis Ix

A

low TIBC, high ferritin, high transferrin

34
Q

rouleaux, when does it occur

A

stacks of RBC
multiple myeloma, waldrens macroglobulinemia

35
Q

howell jolly bodies

A

nuclear remnants found in RBC
hyposplenism

36
Q

schistocytes

A

jagged fragments of RBC
haemolysis

37
Q

tear drop cells

A

abnormality of bone marrow function (myelofibrosis)

38
Q

nocturnal haemoglobinuria cause

A

defect in phosphotidylinitol glycan A

39
Q

Ix findings in anaemia of chronic disease

A

increased ferritin
decreased TIBC
normal transferrin

40
Q

features of hodgkins lymphoma

A

Reed sternberg cells (B cells with multi lobed nuclei)
B symptoms
Cervical/mediastinal lymph nodes
Lymph nodes hurt with alcohol
SVC obstruction, dysnpnoea

41
Q

chemo for hodgkins lymphoma

A

ABVD

42
Q

Diffuse large b cell lymphoma

A

high grade NHL
layers of Large B cells growing in sheets
CLL can turn into this
Assoc with Hepatitis C

43
Q

Burkitt lymphoma associated with

A

EBV

44
Q

2 variants of Burkitt lymphoma

A

endemic/african variant. Risk factor is co infection of EBV and malaria
Massive Jaw tumour

Sporadic variant: ileocecal tumour

45
Q

Staging system for lymphoma

A

Ann Arbor

1: one node
2: spread on same side of diaphragm
3: both sides of diaphragm
4: extra nodal

46
Q

Symptoms of ALL

A

bone marrow failure
infiltration (lymphadenopathy, splenomegaly, orchidomegaly, CNS involvement)

47
Q

CNS involvement common in which leukaemia?

A

ALL
lymphocytes cross the blood brain barrier more readily

48
Q

what is diagnostic of ALL

A

> 20% blast cells on bone marrow aspirate

49
Q

3 phases of chemo for ALL and AML

A
  1. remission induction
  2. remission consolidation
  3. maintenance therapy
50
Q

what should be added for management for CNS involvement

A

intrathecal chemotherapy

51
Q

what is diagnostic of AML

A

> 20% blast cells and Auer rods

52
Q

what is t(9:22)

A

Philadelphia chromosome
associated with CML
indicates poor risk for ALL

53
Q

what is t(15:17)

A

Acute Promelanocytic Leukaemia (APML).

The PML gene fuses with the RAR alpha gene (retinoic acid receptor alpha) to make a PML-RAR fusion. This causes arrest of promelanocyte differentiation.

Retinoic acid ATRAs are effective in targeting this gene fusion, and then restoring differentiation.

54
Q

important gene in CML + management

A

Fusion gene encoding the BCR-ABL protein, which enhances Tyrosine kinase activity

Imatinib is a tyrosine kinase inhibitor, inhibits phosphorylation

55
Q

3 Phases of CML development:

A
  1. Chronic
  2. Accelerated
  3. Blastic (transforms to acute leukaemia)
56
Q

CLL diagnostic criteria

A

smear cells

57
Q

mx of non-diet related B12 deficiency

A

1mg hydroxycobalamin IM 3x week for 2 weeks
1mg IM every three months

58
Q
A