Hematology Flashcards
Site of BM aspiration in adults? (1)
Iliac crest (posterior superior)
Tibia may be used for neonate
MCV, MCH, MCHC calculation? (3)
MCV = HCT / RBC
80~100 fL (10^-15 L)
MCH = HB / RBC
27~31 pg (10^-12 g)
MCHC = HB / HCT
32~36 g/dL
In FR, what makes you suspect EDTA Dependent Pseudothrombocytopenia? (2) What is the etiology behind? (1), suggest ways to correct this. (5)
PLT aggregation without fibrin
CA chelation by EDTA exposes PLT antigen, which trigger immune response, causing PLT aggregation
Frequency: 0.1%
Solution:
3 min vortex
Excess EDTA
Kanamycin
Use Plain tube / Citrate tube
Use MgSO4
Why do we use EDTA instead of heparin for CBC? (1)
Heparin acts on antithrombin & thus prevents coagulation, but not PLT aggregation
EDTA acts by CA chelation, preventing both coagulation & PLT aggregation
Effect of sample clot on PT/APTT? (2)
Shorten due to factor activation
Prolong due to factor consumption
What are the effects of underfilling & overfilling EDTA tubes for CBC? (2)
Underfilling causes excess EDTA and thus RBC shrinkage, decreasing HCT
Overfilling causes insufficient EDTA and thus blood clotting
Can I interpret reticulocyte % directly to assess RBC proliferation? (2)
No. Anaemic patient has higher RETIC%, and proliferation is not linear with degree of anemia, so patient HCT & Maturation correction based on that should be account for before interpretation
RI = [(RETIC%*Patient/Normal HCT ratio)] / Maturation Correction
RI > 2 = hyperproliferation (destruction problem)
-AIHA, SCD
RI < 2 = hyperproliferation (production problem)
-CKD, aplastic
When is Osmotic fragility increased / decreased? (2)
Increased in HS
Decreased in SCD / other poikilocytosis
Why do we use Wright-Giemsa for BM but Wright for FR? (2) Why pH 6.8 is critical? (1)
Both uses methylene blue & eosin
Wright-Giemsa is basophilic to facilitate nuclear content inspection, while Wright is relatively eosinophilic
For acidic pH the slide would be eosinophilic, reverse would be basophilic
Why do Heinz Bodies and bite cells exist in G6PD deficient patients? (3) Can we see Heinz bodies in Wright stain? (1)
- Normally, G6PD forms NADPH to reduce H2O2 with Glutathione peroxidase
- G6PD deficiency causes H2O2 accumulation and thus oxidative damage to HB
-Also oxidation of Fe2+ to Fe3+ (Methemoglobin) - Splenic macrophage remove denatured HB, so bite cell is formed
-Absence of bite cell, suspect hyposplenic
Heinz bodies is detected with supravital stain (NMB / BCB)
What is Howell-Jolly’s body? (1) Why does it exist in SCD? (1)
Basophilic nuclear remnant of RBC
Normally removed by splenic macrophages
Exist in cases of hyposplenic (functional hyposplenic in SCD or HS)
What CBC & Chem result would you suspect malaria? (2) Why does a patient with malaria have a fixed interval of fever? (1) How can you tell the difference between different types of Malaria? (5)
Result matching hemolytic anaemia, LR failure, as well as low PLT
Fever occurs during hemolysis, and temporarily stop when invasion of new RBC is completed
falciparum:
>=2 rings, Banana shaped gametocytes
ovale & vivax:
Large infected RBC
malariae:
band form
knowlesi:
>=2 rings, band form
Suggest factors that affect ESR result (3)
Increase: FIB, IgG (MM)
Decrease: anisocytosis, poikilocytosis
When MCHC > 37, what would you do? (3)
MCHC = HB / HCT
Why MCHC is high:
1. Cold agglutinin causes RBC clumping, decreasing HCT
2. Lipaemic causes HB falsely high
3. HS is true MCHC high as spherocyte has smaller cell volume
rule of 3 (RBC3=HB3=HCT) violated:
1. Warm 20min rerun to remove Cold agglutinin
2. Spin down for plasma blanking to compensate for Lipaemic
rule of 3 (RBC3=HB3=HCT) not violated:
1. perform FR, Spherocytosis 3+ suggest HS
2. check for hypoNa induced RBC aggregation causing by altered RBC zeta potential
Why can a patient with high sO2 still be ischemic? (2)
- 2,3 DPG facilitate O2 unloading from HB
When PHOS is Low OR in transfused RBC, 2,3 DPG is deficient, increasing O2 affinity of HB - Oxyhaemoglobin portion is high but O2 delivery is compromised, so tissue hypoxia still occurs
Acidosis also facilitate O2 unloading, so the same condition can occur when patient is having alkalosis
Which leukocyte is in majority in patients with aplastic anemia? (1)
Lymphocyte
In aplastic anemia, pancytopenia (HB,N,PLT) occurs, but lymphoid lineage is less affected.
Why pancytopenia should be reviewed by hematologist? (8)
Pancytopenia can occur in:
1. Sepsis
2. aplastic anaemia
3. megaloblastic anemia (B12 deficiency)
4. S: SLE, SS
5. M: MDS, MM
6. A: AML, ALL
7. P: PNH, PMF (not in PV, ET)
8. splenomegaly caused by cirrhosis induced portal-hypertension
When would you consider an inverted differential to be physiological? (1)
In patient<4y, due to relative neutropenia
Why should monocytes >1.5 be reviewed? (1)
It can be a case of CML / abnormal Lymph
Morphology resembling monocyte have to be reviewed microscropically
What would you suspect when you see an Auer rod? (1) What is an Auer rod? (1)
Myeloid leukaemia (AML / CML)
Auer rod is a linear projection of primary azurophilic granules
Why is pancytopenia related to leukaemia? (1)
Leukemic cell accumulate in bone marrow, causing BM failure
What clinical detail would be expected for a patient with Acute monocytic leukaemia? (1) How about ALL? (1)
M5: Skin / Gum hyperplasia
ALL: lymphadenopathy
The patient is a child and you see blast in FR, what would you consider first? (1)
ALL
The patient has prolonged PT/APTT with high D-dimer, and you see blast in FR, what would you consider first? (1)
APL as DIC is a common complication of APL due to release of thromboplastic substances
What would you check for BM slides? (1)
M/E ratio, > 6 = Leukaemia, reverse = erythroid leukemia (M6)
Stain to determine lineage? (2)
AML:
Sudan Black B (PL of organelles)
peroxidase (in primary granules)
ALL:
PAS (intracellular glycogen, B-cell ALL -)
TdT (B-cell ALL -)
What defines Acute leukaemia? (1)
Blast > 20%
HCT is high, how can you tell if it is PV or 2nd Polycythemia? (1) How about Relative polycythemia? (1) Why do PV patients usually have IDA? (1)
Splenomegaly & Pancytosis in PV only
Relative polycythemia is reduced plasma volume, EPO is normal
Phlebotomy is used to remove HCT back to ~45%
PLT is high in ET, does it mean that the patient won’t have bleeding risk? (1)
No. The PLT produced is dysfunctional, so patient has both thrombotic and bleeding risk
You see teardrop cells in FR, what would you suspect? (1)
MF
What is LAP score? (1)
Measure of granule maturity, which increases in infection & decreases in CML
Ph+ CML prognosis? (1)
Better than Ph-
Basophil is high, what would you consider? (1)
CML
WBC high with different stages of granulocyte present, what would you consider? (1)
CML
What clinical detail helps differentiate AML from CML? (1)
Splenomegaly, 90%CML, not characteristic for AML
What clinical detail helps differentiate MM from WM? (3)
Osteolytic lesions, happens in MM
Leukocytosis, happens in WM
Check IgM (WM) & IgG (MM) helps
For infant CBC, what would you expect? (3)
Infant WBC, HCT & MCV are physiologically higher
Why should Mono High be confirmed by FR? (2)
A. Lymph in Infectious mononucleosis & Blast cell in CML may be misclassified as Mono
WBC High, N, metaMYE, MYE, consider? (1)
CML
Perform DC with for sample with low WBC? (2)
- Prepare more slides
- Prepare Buffy coat slides
Elderly, High Lymphocyte, smudge cells, consider? (1)
CLL
Normal CBC with Elliptocyte 3+? (1)
HE, relatively common, hemolysis only in severe form
High MCHC not corrected with warming & plasma blanking
HS, proceed to osmotic fragility test
MCV & MCH Low, IDA or THAL? (1)
see RBC, MCV/RBC<13 = THAL (RBC increase in THAL)
MCV & MCH Low, target cell, NRBC+, consider? (1)
Hb diseases, not beta THAL trait due to NRBC+
Differentiate ALL, CML, AML, CLL with Age & lab tests. (4)
What are their treatment? (4)
How to tell if CML case is progressed to AML? (1)
ALL: ~10, TdT+, Cytarabine
CML: ~40, Ph [t(9,22)], Imatinib
AML: ~50, Auer rod & MPO+, ATRA
CLL: ~80, Smear cell, Nothing
CML»_space; 20% Blast»_space; AML
