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Dunedin RACP Study Course > Lab Haematology > Flashcards

Lab Haematology Flashcards

1
Q

utility of haemltocrit (non USA)

A

use for target for polycythaemia venesection

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2
Q

utility of MCHC?

A

Goes down if dehydrated - heridatry spherocytosis.

Otherwise pretty much constant and kind of useless

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3
Q

utility of basophil count?

A

increased in CML (until further results come back)
otherwise not very useful

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4
Q

Portion of T vs B cells in blood

A

70-80% T cells

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5
Q

Microcytic anaemia causes

A
  • Thalassaemia
  • Anaemia of of chronic disease (of inflammation - changing its name, not CKD)
  • Iron deficiency
  • Lead poisoning (rare)
  • Rare: congenital sideroblastic anaemia
  • Hyperthyroidism (rare)
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6
Q

Hepcidin release process

A

endotoxin
-> stimulates Kupffer cell
-> IL-6 release
-> hepcidin release from liver

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7
Q

characteristic RBC feature of lead poisoning?

A

basophilic stippling

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8
Q

Classic appearance of RBCs in thalassaemia

A

Target cell

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9
Q

Main types of Hb in adults

A

HbA

HbA2 < 3.5%

HbF < 1%

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10
Q

Naming of alpha thalasaemia by number of genes

A

One gene deletion
– (silent carrier)

  • Two gene deletion
    – alpha trait
  • Three gene deletion
    – (HbH disease)
  • Four gene deletion
    – (Barts hydrops fetalis)
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11
Q

Characteristic RBC appearance in alpha thalasaemia

A

golf ball appearance

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12
Q

testing for alpha thalassaemia

A

do a RAT test type thing these days - pretty good

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13
Q

naming of 2 gene alpha deletion

A

Either α-/α- or - - /αα
(α+/α+ or α0 /α)

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14
Q

Reason for maternal complications hydros faetalis

A

complications due to large placenta (toxaemia, post-partum haemorrhage)

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15
Q

nomenclature for beta thalasaemia genes

A

– reduced expression (β+ )

– absent expression (β0 )

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16
Q

most reliable test for beta thalassaemia

A

Increased HbA 2(α2δ2)

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17
Q

nomenclature for beta thalasaemia disease

A
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18
Q

how much central pallor should you have in a RBCs

A

1/3 at most

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19
Q

Definition of beta thalassaemia major

A

dependent on transfusions

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20
Q

Test for hydros faetalis?

A

test parents genetics

chorionic villous sampling

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21
Q

Clinical phenotype HbE + betal thal

A

variable but more severe than beta that
- since few or no normal β chains
- 30-50% require regular transfusion
- 20-50% require splenectomy

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22
Q

Clinical phenotype HbS + betal thal

A

worsens sickle trait – closer to sickle disease

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23
Q

Main causes for macrocytosis

A

Etoh (smoking more rare)
MDS (myeloma more rarely)
Liver disease - cholestatic in particular (mech unknown)
B12 (folate more rare)
Meds
Retics
Haemachromatosis (fertilising Fe)

Less common
- aplastica anaemia (pancytopaenic normally)
- anorexia
- COPD
- hypothyroid
- familial
- preggers - ?folate ?Fe supplements

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24
Q

Major meds causing macrocytosis

A

Anti-biotic (trimethoprim)
Anti-virals
Anti-Epileptic (phenytoin)
Anti-Cancer (cytotoxics)

25
Q

Normocytic anaemia causes

A

Decreased production – decreased reticulocytes
* Lack of erythropoietin (CKD) (normocytic)
* Infiltration of bone marrow (normocytic)
* Chemotherapy
* Inflammatory process (tends toward microcytic)
* Lack of nutrients (can be macro, microcytic)
* Marrow disease such as MDS (often macrocytic)

Increased loss or destruction – increased reticulocytes
* Acute bleeding
* Haemolysis (sometimes macrocytic)

26
Q

Where does extra-vascular haemolytic occur

A

mostly the spleen

27
Q

Is intra or extra-vascular haemolysis more common

A

extra

28
Q

Tests for AIHA

A

Anaemia
Reticulocytes

Blood film - Spherocytes

Bilirubin (unconjugated)

Haptoglobin - low

Direct antiglobulin test (DAT; aka Coombs)

29
Q

Post-splenectomy blood cell changes

A

Howell Jolly bodies (nuclear remnant),
target cells,
spherocytes,
odd cells

30
Q

Things that can mutate to cause spherocytosis

A

Ankyrin, Band 3, Spectrin, and Protein 4.2

AD disease

31
Q

Causes for acquired hyposplenism

A
  • Infarction
    – Sickle cell, Essential thrombocythaemia, Polycythaemia vera
  • Atrophy/Hypofunction
    – Coeliac, dermatitis herpetiformis, IBD, Autoimmune (SLE, RA, GN, PBC, Sjogren’s, MCTD, thyroiditis), irradiation
    – Bone marrow transplantation & GVHD
    – HIV/AIDS
  • Infiltration
    – Amyloid, sarcoidosis, leukaemia, myeloproliferative, etc
32
Q

Test for spherocytosis

A

DAT

of look at FHX

+/- genetic studies

33
Q

Hereditary spherocytosis consequences

A
  • Anaemia
  • Pigment gallstones
  • Splenectomy may be needed for cases with symptomatic anaemia - kids not growing
34
Q

Inheritance of G6PD def

A

X-linked recessive

35
Q

Cells in G6PD deficiency (and why)

A

bite cells / keratocytes

Due to Heiz bodies (precipitant DNA)

36
Q

Drugs that cause drug induced oxidate haemolysis

A
  • Sulphonamides
  • Dapsone - see commonly even though not used much
  • Antimalarials
  • Co-trimoxazole
  • Naphthalene
  • etc
37
Q

Causes for rouleux bodies

A

High globulins / fibrinogen

  • Chronic infection or inflammation
  • Monoclonal proteins
38
Q

Causes of reactive lymphocytes

A
  • EBV
  • CMV
  • Toxoplasmosis
  • Other viruses occasionally - don’t cause so much lymphocytosis
39
Q

Causes for cold agglutination

A
  • EBV
  • Mycoplasma
  • Lymphoma
40
Q

Test for lymphoma

A

– Morphology
* usually of a lymph node but sometimes blood, spleen, marrow, skin

– Immunophenotyping
* Immunohistochemistry and/or
* Flow cytometry

– FISH/cytogenetics occasionally

41
Q

smudge/ smear cells in?

A

CLL

42
Q

clefted and cerebriform cells in?

A

Sezary syndrome / peripheral T cell lymphoma

43
Q

granular lymphocytes in?

A

arge granular lymphocyte leukaemia (associated with neutropenia and RA - Felty’s)

44
Q

starry sky cells in?

A

Burkitt lymphoma

45
Q

owl eye looking cells in?

A

Hodgkin’s

46
Q

Cell surface markers B cells

A
  • CD19
  • CD20
  • Kappa
  • Lambda
47
Q

Cell surface markers for T cells

A
  • CD3
  • CD4
  • CD8
  • CD5
48
Q

Increased VWF in?

A

Thrombotic microangiopathies

  • Multimers not cleaved (TTP)
  • Too much VWF secreted from toxin-stimulated kidney endothelium (HUS)
49
Q

Decreased VWF in?

A

Genetic: von Willebrand disease

Acquired: von Willebrand syndrome
* Aortic stenosis and LV assist devices
* Essential thrombocythaemia – VWF depleted by very high platelet numbers
* Immune mediated, malignancy, hypothyroidism

50
Q

no ADAMTS 13 =

A

TTP

51
Q

Clinical features TTP

A

All patients have:
- thrombocytopenia
- microangiopathic haemolytic anaemia.

Most common symptoms are nonspecific:
- abdominal pain, nausea, vomiting, and weakness (microvascular thrombi in many organs).

Neurological signs occur in about half.
Renal failure can occur.
Fever uncommon

52
Q

TTP treatment

A
  • plasma exchange to replace the ADAMTS13 and to remove antibodies

(Reduces mortality from ~90% to ~20%)

53
Q

Main cause of HUS?

A
  • ~ 90% of cases caused by Shiga-toxin producing E. coli
  • Strep pneumoniae HUS (SP-HUS) ~ 5%
  • Atypical HUS (aHUS) ~ 5% (Genetic)
54
Q

Type of VW disease

A
  • Type 1 – reduced level of VWF protein
  • Type 2 – reduced function
  • activity < 70% of expected for protein level
  • different subtypes depending on the position of the mutation
  • Type 3 – very low levels (both alleles affected)
55
Q

Tests for T2 VWD

A
  • VWF activity assay
    OR
  • Ristocetin co-factor activity (VWF:RCo)
  • ristocetin alters conformation (mimicking shear forces) induces platelet binding
  • Collagen binding assay (VWF:CB)
  • Factor VIII levels
56
Q

What is Heyde’s syndrome?

A

acquired VW syndrome d/t valvular disease

57
Q

acquired VW syndrome causes

A

In certain conditions, large VWF multimers are broken/proteolysed leading to loss of HWM forms = Acquired type 2a VWD.

  • Valvular disease (Heyde syndrome), ventricular assist devices, congenital heart disease: shear-stress-induced proteolysis
  • Essential thrombocythaemia, polycythaemia vera: excessive binding to abnormal platelets + proteolysis

Autoantibody-mediated loss of function in myeloma/lymphoma and SLE

58
Q

Diagnostic criteria APLS

A
59
Q

Clinical features APLS

A

Haematologic
* Thrombocytopenia
* Haemolytic anaemia

Dermatologic
* Livedo reticularis or racemosa Livedoid vasculopathy (recurrent, painful skin ulcerations)

Neurologic
* Cognitive dysfunction (in the absence of stroke)
* Subcortical white-matter changes

Renal
* Acute thrombotic microangiopathy
* Chronic vaso-occlusive lesions

Cardiac
* Valve vegetations or thickening

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