Haematology Flashcards

1
Q

How would you further investigate a microcytic anaemia?

A

haematinics (iron studies, B12 and folate)
coeliac screen - TTG antibodies

consider endoscopy and colonoscopy if old or RF for bowel CA

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

what results of blood tests would you expect a patient suffering from DIC to have?

A

low platelets
low fibrinogen
high PT and APTT
high D-dimer and fibrin degradation products

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

what are hereditary causes of haemolytic anaemia?

A

hereditary spherocytosis
hereditary elliptocytosis

G6PD deficiency, pyruvate kinase deficiency

sickle cell disease, thalassaemia

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

what are acquired causes of a haemolytic anaemia?

A

autoimmune (SLE)
some drugs
infection
MAHA

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

What would be the differential for a patient present with backache with hypercalcaemia, low PT and normal ALP ?

A

multiple myeloma

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

What features do patients with multiple myeloma have?

A

CRAB

Calcium is high
Renal impairment
Anaemia
Bone (pain/ache or fracture)

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

What might patients with polycythaemia present with?

A

headache
pruritis post hot bath
blurred vision
tinnitus
thombosis
grangrene
choreiform movements

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

what causes a low reticulocyte count?

A

parvovirus B19 infection (-> aplastic crisis)

aplastic crisis 2nd to sickle cell
blood transfusion

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

What is the most common cause of aplastic anaemia?

A

idiopathic acquired aplastic anaemia

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

What are some secondary causes of aplastic anaemia?

A

infection - parvovirus B19
cytotoxic drugs

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

What do Heinz bodies suggest?

A

oxidized Hb

GLUCOSE-6-PHOSPHATE DEHYDROGENASE

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

causes of macrocytosis

A

B12/folate deficiency
alcoholism
myelodysplastic disorders
hypothyroidism
liver disease

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

What does a positive Coombs test indicate?

A

confirms the presence of antibodies to RBC indicating a autoimmune haemolytic anaemia

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

What do Burr cells indicate?

A

uraemia

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

what do target cells indicate?

A

IDA

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

What do reed-sternberg cells indicate?

A

hodgkin’s lymphoma

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

What is the philadelphia chromosome associated with?

A

CML

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

What does a positive Hams test indicate?

A

paroxysmal nocturnal haemoglobinuria

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

what is paroxysmal nocturnal haemoglobinuria?

A

acquire RBC defect making them more susceptible to being destroyed by complement

PC: abdo pain, haemolytic anaemia, dark coloured urine at night or early morning

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

What are hyperviscosity symptoms?

A

blurry vision from retinal haemorrhages
headaches
bleeding
severe pruritus post bath

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

what is the tumour marker for a seminoma?

A

beta-HCG

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

What cancer is EBV a RF for?

A

lymphoma

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

what is haemophilia?

A

an inherited deficiency in clotting factors leading to a bleeding disorder

rarely an acquired form may occur whereby an individual makes autoantibodies to clotting factors

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

What are the main types of haemophilia?

A

haemophilia A - factor 8 deficiency
haemophilia B - factor 9 deficiency
haemophilia C - factor 11 deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is the most common type of haemophilia?

A

haemophilia A

26
Q

Epidemiology of acute lymphoblastic leukaemia?

A

most common malignancy in children
peak incidence 2-5 years of age
second peak of incidence in the elderly

27
Q

what are the stages of CML?

A
  1. relatively stable chronic phase (4-6 years)
  2. accelerated phase (3-9 months)
  3. acute leukaemia phase characterised by blast transformation
28
Q

Describe the ann arbor staging system for lymphoma

A
I = single LN region 
II = 2+ LN regions on one side of diaphragm 
III = LN regions on both sides of diaphragm 
IV = extranodal involvement 
A = no B symptoms 
B = B symptoms 
S = spleen involvement
29
Q

Give features of Hodgkin’s lymphoma

A

15% of all lymphomas
Reed-sternberg cells are diagnostic
EBV infection is a risk factor
bimodal incidence - 20-30s and >50s
M>F

30
Q

What are some presenting features of Hodgkin’s lymphoma?

A

enlarged mass in neck/axilla/groin which may spontaneously enlarge or reduce in size
mass painful post alcohol
pruritis, cough, SOB

B symptoms: fever, night sweats, weight loss

31
Q

what are the B symptoms?

A

fever, night sweats, weight loss

32
Q

is extra nodal involvement more common in Hodgkin’s or non-Hodgkin’s?

A

non hodgkin’s

33
Q

RF for Non-hodgkin’s lymphoma

A

radiotherapy, immunosuppresion, chemotherapy, HIV, HBV, HCV, oncogenic viruses (EBV)

34
Q

Presentation of non-Hodgkin’s lymphoma

A

painless enlarged mass in neck/axilla/groin
systemic symptoms (FLAWS)
extra-nodal - skin rash, headache, sore throat, abdo pain, testicular swelling
BM failure -> anaemia, infections, bleeding

hypercalcaemia

35
Q

what is multiple myeloma?

A

haematological malignancy characterised by proliferation of plasma cells causing increased monoclonal immunoglobulin production (usually IgG or IgA)

36
Q

what monoclonal immunoglobulin is most commonly implicated in multiple myeloma?

A

IgG
accounts for 2/3 of cases

37
Q

What would the blood results and blood film show for a patient with multiple myeloma?

A

low Hb
high creatinine
high calcium
high ALP

rouleux formation on blood film

38
Q

what might you find in urine analysis of a multiple myeloma patient?

A

serum paraprotein
BENCE JONES PROTEIN

39
Q

what is myelofibrosis?

A

obliteration of the bone marrow with fibrosis due to increased fibroblast activity

40
Q

what conditions are associated with myelofibrosis?

A

30% of myelofibrosis patients have a Hx of polycythaemia rubra vera or essential thrombocytopenia

41
Q

What are the symptoms and signs of myelofibrosis?

A

weight loss, fever, loss of appetite, night sweats, pruritis

splenomegaly, hepatomegaly, symptoms of BM failure

42
Q

what are the symptoms of polycythaemia?

A

headache, blurred vision, tinnitus
SOB
pruritis after a hot bath
burning pain in fingers and toes
night sweats
thrombotic events

43
Q

what are the signs of polycythaemia?

A

splenomegaly
plethoric complexion [red and ruddy]
scratch marks from ithcing
HTN

44
Q

what is the inheritance pattern of thalassaemia?

A

autosomal recessive

45
Q

what does the impaired Hb synthesis in thalassaemia patients lead to?

A
  1. impaired erythropoiesis
  2. haemolysis
  3. anaemia
  4. extramedullary haematopoiesis
46
Q

how does alpha thalassaemia 3 gene deletion present?

what signs on blood film are there?

A

severe anaemia, splenomegaly, jaundice and abnormal RBC indices

very early life

HEINZ BODIES

47
Q

how does beta thalassaemia major present?

A

3-6 months of age when foetal haemoglobin becomes adult Hb

failure to thrive, recurrent infections, anaemia

48
Q

what are the signs of major beta thalassaemia?

A

pallor, malaise, SOB, mild jaundice, frontal bossing, thalassaemia facies, hepato-splenomegaly

49
Q

what is the pentad of thrombotic thrombocytopenic purpura?

A

MAHA
thrombocytopenia
renal involvement (impairment)
neurological abnormalities
fever

note majority of patients with TTP don’t have the pentad

50
Q

what are the causes of TTP?

A

idiopathic (40%)
autoimmune e.g. SLE
cancer
pregnancy or post-partum (10-25%)
malignancy
drug related (quinine)
bloody diarrhoea prodrome type (progression of HUS from E.coli infection)

51
Q

what are the symptoms and signs of TTP?

A

epistaxis, bruising, petechiae, haematuria, menorrhagia
NEURO: confusion, headache, vision changes, aphasia, fits

fever, pallor, myalgia, chest/abdo pain

purpura, jaundice (2nd to haemolysis), severe HTN, splenomegaly

52
Q

what are the functions of vWF?

A
  1. binds to exposed subendothelium
  2. aids platelet activation and binding to one another
  3. stabilises factor VIII preventing it’s degradation
53
Q

what are the type of von willebrands disease

A

type 1 = most common, autosomal dominant, deficiency in vWF

type 2 = 2nd most common, abnormal vWF, autosomal dominant

type 3 = undetectable vWF levels, autosomal recessive

54
Q

what clotting factor abnormalities do vWF disease patients have ?

A

low VIII
vWF abnormality/deficiency
prolonged clotting time (high APTT)

55
Q

What malignancy are auer rods associated with?

A

acute myeloid leukaemia

56
Q

what is aplastic anaemia?

A

it is a global pancytopenia where cells are normal in morphology but deficient.

BM biopsy shows hypocellular marrow
at least 2 peripheral deficiencies must be detected of either: Hb < 100, platelets < 50 or neutrophil < 1.5 x 10^9

57
Q

what are some acquired causes of aplastic anaemia?

A

parvovirus B19
medications such as methotrexate
chemicals such as benzene or DDT
paroxysmal nocturnal haemoglobinuria

58
Q

what are inherited causes of aplastic anaemia?

A

fanconi’s anaemia

59
Q

what is the diagnosis of DIC based on?

A

presence of > 1 known underlying condition causing DIC + abnormal global coagulation tests

  • reduced paltelet count
  • increased PT
  • increased fibrin-related marker (d-dimer, fibrin degradation production)
  • decreased fibrinogen levels
60
Q

what drugs trigger G6PD deficiency?

A

sulpha drugs

  • sulphonamides - trimethoprim, sulfasalazine
  • sulphasalazine
  • sulphonylureas - glipizide, gliclazide, glimepiride
61
Q

who gets irradiated transfusion and who gets CMV -ve

A