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PATHOLOGY > haematology cases > Flashcards

haematology cases Flashcards

1
Q

summarise where myeloblasts usually are

A

<5% is normal in marrow
5-10% = myelodysplasia in marrow
>20% AML

never in peripheral blood - if there it is likely AML or leucoerythroblastic

may havbe Auer rods - AML

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2
Q

summarise where lymphoblasts usually are

A

they are precurser lymphoid cels - never in peripheral blood

<5% is normal in marrow
>20% - ALL

lymphoblasts are TdT +ve - no Auer rods

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3
Q

2 causes of low MCV

A

iron deficiency
haemoglobinopathies

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4
Q

2 causes of mod high MCV

A

alcohol
hypothyroidism
combined iron and folic acid deficiency

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5
Q

2 causes of super high MCV

A

B12 def
folate def

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6
Q

what are the b cell markers and what are they used for

A

CD19 - epitope for CAR T cells - used for lympoblastic leukaemia or lymphoma
CD20 - epitope for rituximab moab - chemo for lymphoma, and rheumatoid

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7
Q

what are the T cell markers

A

CD3 - all mature
CD4 (helper)
CD8 (cytotoxic)
CD5 - normal in peripheral blood, not in B cells

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8
Q

markers of lymphoid differentiation ie maturity

A

TdT - marker of immature T and B lymphoblasts - ie immature
* surface Ig marker of matyre B cels and plasma cells

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9
Q

differentiate these features for myeloma and normal

A
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10
Q

causes of raised polyclonal Ig

A

HIV, infection, SLE

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11
Q

how to approach interpreting blood results

A
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12
Q
A

haemolytic anaemia - because of hx likely SLE with autoimmune haemolytic anaemia
Borderline raise in MCV - because reticulocytes around

BR - want to know if conjugated or unconjugated

LDH released from haemolysing red cells

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13
Q

haemolytic anaemia and get these results

A

Liver is normal othe than raised unconjugated BR - so pre-hepatic jaundice

LDH released from haemolysing red cells

spherocytes - smaller than normal erythrocytes and no central pallor

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14
Q

causes of spherocytes

A

hereditroy spherocytosis

autoimmune haemolytic anaemia

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15
Q

where is the defect for inherited haemolytic anaemia

A

defect of the red cells

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16
Q

where is the defect for acquired haemolytic anaemia

A

the env/toxins in env

red cell is normal - although morphological damage may occur

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17
Q

causes of hereditory haemolytic anaemia and how you would diagnose them

A
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18
Q

causes of acquired haemolytic anaemia and how you would dx them

A

non immune eg malaria, damage from metal valve, drugs, MAHA

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19
Q
A

Anaemia of inflammation
Normal HbA2 excludes beta thal trait - HbA2 would be raised

Ferritin is an inflammatory protein

Transferrin is normal

20
Q

differentiate anaemia of inflammation (ACD) from IDA

A

transferrin is the key - will be high in IDA, and low/normal in ACD

ferritin low = confirms IDA, but can be high if also have inflammation - because it is an inflammatory protein

21
Q

summarise anaemia of chronic disease

A

anaemia if inflammation- mediated by high hepcidin levels

body iron stores are sequested and unavailable for erythropoeisis
high hepcidin inhiobits GI absorption of iron and sequesters it in macrophage and kuppfer cells

hepcidin is an anti-bacterial/inflammatory response protein - removing iron from blood deprives bacteria of iron needed for proliferaton

22
Q

causes of isolated single lineage cytopenia with otherwise normal FBC

A

often poeripheral destruction/shortened survival
* immune destruction
* non immune - infection (malaria), mechanical (DIC), consumption sequestration (splenomegaly)

failure of production
* haematinics - iron only required for Hb - isolated anaemia. B12 and folate needed for DNA synth - can affect all lineages
* drugs - agranulocytosis

23
Q
A

B12 deficiency
Get pancytopenia because B12 needed for DNA synth - so get reduced in all lineages

Whereas iron is only required for haem synthesis - gives isolated anaemia- no impact on anything else

Organ specific autoimmune conditions - if have one organ specific autoimmune disorder likely to get another one eg pernicious anaemia

MCV would also be high in haemalytic anaemia because of the reticulocytes - woulndt be this high

Unconjugated BR - because ineffective red cell production in bone marrow -> more death -> high unconjugated BR

24
Q
A

Leucoerythroblastic anaemia
Due to prostate cancer met to bone marrow

Pancytopenia
Myeloma and leukaemia don’t usually cause these sx - urine and haematuria

Leucoerythroblastic blood film - tear drop red cell

Precursers which are present - nuceated red cells - should only be present in the marrow

25
Q

summarise pancytopenia

A
26
Q
A

For philidelphia chr - with rtPCR or cytogenetics

Healthy person

Chronic myeloid leukemia - Leukaemia with excess prolifeation - ie a myeloproliferative disorder, proliferation with retained maturation
Retained maturation

WCC very high - much higher than would expect in any type of infection

film - Heterogenous - All mainly myeloid

27
Q

summarise CML

A

Hx - lethargy/hypermetabolism/thrombotic event: monocular blindness CVA, bruising, bleeding
o/e - massive splenomegaly +- hepatomegaly

FBC - Hb and plts preserved/raised, massive leucocytosis

blood film - neutrophils and myelocytes (not blasts if chronic phase), basophilia

28
Q

how can we use leukaemia markers in treatment

A

use rtPCR to see ratio of cells with just abl gene vs those with bcr-abl

29
Q
A

Imatinib - abl kinase inhibitor

30
Q
A

Transform to become acute leukaemia - refractory or resisntant to drugs - acquired new mutations and is a blast crisis

31
Q
A

JAK2V617F mutation analysis
Pruritis withheat - typical of polycythaemia vera

32
Q

what result would you expect

A

expression of CD5 in B cell population

33
Q

what is the likelu dx and why

A

CLL

Leukocytoiss
All leukocytes
Rest are preserved - favours chronic

Normal mature lymphocytes
Smudge cells - artefact

34
Q

cell based prognostic factors for CLL

A

IgHV mutation status
CLL FISH cytogenetic panel
TP53 mutation status (Chr 17p del and/or TP3 point mutation)

35
Q

clinical staging system for CLL

A

Binet or Rai
CLL IPI score

based on lymphocytosis, lymphadenopathy, pancytopenia

36
Q

clinical staging system for CLL

A

Binet or Rai
CLL IPI score

based on lymphocytosis, lymphadenopathy, pancytopenia

37
Q

what are the clinical issues with CLL

A
38
Q

what is B cell targetted therapy

A

Bruton’s X linked agammaglobinopathy (inherited condition)
* abnormal B cell tyrosine kinbase gene - pre B cells cannot develop to mature B cells
* abscence of mature B cells
* No circulating Ig after 3 mo

ibrutinib tries to mimic this condition - inhibit bruton tyrosine kinase

39
Q

what is ruxolotinib

A

JAK2 tyrisine kinase inhibitor

40
Q

treatment options in CLL

A
41
Q
A

Myeloma

Riased IgA
Immune paresis

Low hb - bone marrow infiltration by plasma cells

42
Q

problem with dx myeloma

A

a lot of sx are general complaints of the elderly -> late dx
can be catastrophic - spinal cord compression or established renal failure

43
Q
A

No
Havent exclude dlight chain only myeloma - don’t impact full IgG or IgA - need to check serum free light chains

44
Q
A

Super high serum free light chain - high level of circ light chain - pass trhough basement membrane of kidney -> cast nephropathy

45
Q
A

blood - O rhD -ve Can give men and postmenopausal women RhD +ve - would sensitise but only relevant in pregnancy

FFP - AB RhD-ve

46
Q
A

Use cryoprycippitate
It is the fibrinogen that is low

PATHOLOGY (94 decks)

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