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Dunedin RACP Study Course > Lab Haematology > Flashcards

Lab Haematology Flashcards

(59 cards)

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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

Study These Flashcards
A

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

25
Normocytic anaemia causes
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
Where does extra-vascular haemolytic occur
mostly the spleen
27
Is intra or extra-vascular haemolysis more common
extra
28
Tests for AIHA
Anaemia Reticulocytes Blood film - Spherocytes Bilirubin (unconjugated) Haptoglobin - low Direct antiglobulin test (DAT; aka Coombs)
29
Post-splenectomy blood cell changes
Howell Jolly bodies (nuclear remnant), target cells, spherocytes, odd cells
30
Things that can mutate to cause spherocytosis
Ankyrin, Band 3, Spectrin, and Protein 4.2 AD disease
31
Causes for acquired hyposplenism
* 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
Test for spherocytosis
DAT of look at FHX +/- genetic studies
33
Hereditary spherocytosis consequences
* Anaemia * Pigment gallstones * Splenectomy may be needed for cases with symptomatic anaemia - kids not growing
34
Inheritance of G6PD def
X-linked recessive
35
Cells in G6PD deficiency (and why)
bite cells / keratocytes Due to Heiz bodies (precipitant DNA)
36
Drugs that cause drug induced oxidate haemolysis
* Sulphonamides * Dapsone - see commonly even though not used much * Antimalarials * Co-trimoxazole * Naphthalene * etc
37
Causes for rouleux bodies
High globulins / fibrinogen * Chronic infection or inflammation * Monoclonal proteins
38
Causes of reactive lymphocytes
* EBV * CMV * Toxoplasmosis * Other viruses occasionally - don't cause so much lymphocytosis
39
Causes for cold agglutination
* EBV * Mycoplasma * Lymphoma
40
Test for lymphoma
– Morphology * usually of a lymph node but sometimes blood, spleen, marrow, skin – Immunophenotyping * Immunohistochemistry and/or * Flow cytometry – FISH/cytogenetics occasionally
41
smudge/ smear cells in?
CLL
42
clefted and cerebriform cells in?
Sezary syndrome / peripheral T cell lymphoma
43
granular lymphocytes in?
arge granular lymphocyte leukaemia (associated with neutropenia and RA - Felty's)
44
starry sky cells in?
Burkitt lymphoma
45
owl eye looking cells in?
Hodgkin's
46
Cell surface markers B cells
* CD19 * CD20 * Kappa * Lambda
47
Cell surface markers for T cells
* CD3 * CD4 * CD8 * CD5
48
Increased VWF in?
Thrombotic microangiopathies * Multimers not cleaved (TTP) * Too much VWF secreted from toxin-stimulated kidney endothelium (HUS)
49
Decreased VWF in?
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
no ADAMTS 13 =
TTP
51
Clinical features TTP
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
TTP treatment
* plasma exchange to replace the ADAMTS13 and to remove antibodies (Reduces mortality from ~90% to ~20%)
53
Main cause of HUS?
* ~ 90% of cases caused by Shiga-toxin producing E. coli * Strep pneumoniae HUS (SP-HUS) ~ 5% * Atypical HUS (aHUS) ~ 5% (Genetic)
54
Type of VW disease
* 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
Tests for T2 VWD
* 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
What is Heyde's syndrome?
acquired VW syndrome d/t valvular disease
57
acquired VW syndrome causes
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
Diagnostic criteria APLS
59
Clinical features APLS
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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