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Chemical Pathology > Haematology > Flashcards

Haematology Flashcards

1
Q

What is flow cytometry?

A

Tests for types of proteins on surface of the cell, size + complexity ie type of cell

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2
Q

What’s the difference between serum and plasma

A

Plasma = coag factors and protein rich
Serum = no coag factors and proteins (clot using them up)

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3
Q

What does haematocrit refer to

A

The % of RBC’s column over total

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4
Q

Causes of low reticulocyte count

A

Iron def
Marrow diseases
Lack of erythropoietin
Decreased O2 consumption
Ineffective erythropoeisis
Chronic inflam or malig disease

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5
Q

Causes of neutropenia

A

> increased destruction = hyperspace sim, immune mediated destruction
decreased production = bone marrow failure (aplastic anaemia, chemo, acute leukaemia), specific neutrophil dysfunction (congenital/ drug induced)

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6
Q

Causes of neutrophil leukocytosis

A

> bacterial infection
tissue necrosis
pregnancy
acute haemorrhage
drugs
asplenia

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7
Q

What is a leukaemoid reaction

A

When mature and immature leukocytes are found in the peripheral blood in response to a severe infection

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8
Q

Causes of leukoerythroblastic blood film (nuclei in RBC’s)

A

> acute/chronic myeloid leukaemia
severe megaloblastic anaemia
myeloma/lymphoma
Severe haemolysis
primary myelofibrosis

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9
Q

Causes of eosinophilia NB

A

> allergic disease
parasitic disease
recovery from acute infection
certain skin diseases eg psoriasis
drug sensitivity
metastatic malignancy

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10
Q

What’s the difference between chronic and acute leukaemia

A

Acute - immature cells proliferate (aggressive)
Chronic - mature cells don’t die

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11
Q

What pattern of bleeding does thrombocytopenia give you

A

Mucocutaeous bleed (gums, nose etc)

Joint/muscle bleed = coag factor deficiency

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12
Q

Causes of deranged platelet counts

A

Thrombocytopenia
> decreased production
>increased destruction
>hypersplenism
>dilutional

Thrombocytosis
>reactive (acute haemorrhage, chronic infections, post splenectomy
>endogenous (myeloproliferative disorders)

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13
Q

Indications for bone marrow aspiration NB

A

> unexplained cytopenias
lymphoma staging
suspecting infiltration by TB or malignancy
leukaemia follow ups

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14
Q

Risk factors for thrombosis

A

Increased age
Pregnancy
Surgery

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15
Q

Arterial thrombosis risk factors

A
  • male
  • hyperlipidaemia
  • family history
  • diabetes
    -hypertension
  • gout
  • smoking
  • polycytaemia
  • lupus
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16
Q

Venous thrombosis risk factors

A

VIRCHOWS TRIAD
- age
- obesity
- lupus
- immobility
- lupus
- trauma
- surgery
- hormone replacement therapy
- previous thrombosis

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17
Q

What’s ironic about antiphospholipid syndrome

A

High PTT when tested in the lab, but the patient thrombosis

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18
Q

What are the symptoms of paroxysmal nocturnal haemaglobinuria

A

> dark urine in the morning from haemolysis
fatigue, dizziness, blood clots
can lead to aplastic anaemia

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19
Q

What tests would you run for a thrombophilia screen?

A

> FBC (platelets), diff and smear (fragments)
Clotting profile
Vit K
aPTT and PT (lupus antibody)
ESR (inflammation)
APS = antiphospholipid screen
thrombin time
Fribrinogen
antithrombin, protein C and s
PNH screen (paroxysmal nocturnal haemaglobinuria)

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20
Q

How long do you treat a patient who has clotted?

A

Provoked =3 months
Unprovoked = lifelong

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21
Q

Who do you test and who do you not test for thrombophilia?

A

TEST
>VTE in unusual location, unprovoked
>DVT/PE high risk of recurrence

CONSIDER
>VTE pt request
>family of strong thrombophilia in index pt
>arterial thrombosis in young, unexplained

NO TEST
>pregnancy loss (UNLESS >2 MISCARRIAGES >15 WEEKS →antiphospholipid)

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22
Q

What are the strong thrombophilia?

A

APLS
Protein C def
Protein S def
Antithrombin def

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23
Q

What do you do before you test for thrombophilia?

A

Wells score probability of having a PE or DVT

> 4 = high probability

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24
Q

What’s the difference between therapeutic and prophylactic anticoagulant treatment?

A

Therapeutic dose is higher

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25
Q

How do you treat thrombophilia?

A

Initiate LMWH parenteral and VitKA (warfarin) = bridging therapy

Warfarin also inhibits natural anticoagulants

When INR>2 then you can stop LMWH

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26
Q

What is a complication of not using bridging therapy?

A

Warfarin induced Skin necrosis

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27
Q

High INR indicates

A

Longer time to clot (pt bleeds)

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28
Q

What are the advantages of direct oral inhibitors?

A

Fixed dose
Few drug/food interactions
No monitoring
No need for bridging

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29
Q

What are disadvantages of direct oral inhibitors?

A

No reversal agents
Can’t miss a dose as short acting
Hepatic and renal effects
Less experience

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30
Q

What are the advantages of warfarin?

A

Long acting
Reversible
Long experience
Monitoring encourages compliance
Safe in renal failure

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31
Q

Disadvantages of warfarin

A

Monitoring frequency
Food and drug interactions
Variable dose
Narrow therapeutic range
Slow onset

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32
Q

What is heparin induced coagulopathy and treatment

A

Heparin binds to platelet factor and forms complex (removes platelets from plasma)
Antibodies attack complex and activate platelets to form throng = thrombocytopenia with clots

If this happens, stop heparin and find alternative.

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33
Q

Indications for ordering haemostasis tests?

A

> to ID pts who are acutely bleeding who have a correctable bleeding tendency
to ID pts with acute clots who have a correctable clotting tendency
monitoring anticoagulant medication
prognostication of liver failure pts
screening for DIC

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34
Q

Why do you need to fill the citrate tube to the top?

A

So that the ratio of plasma to anticoagulant is 1:9

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35
Q

What are the conventional tests for haemostasis?

A

Platelet count
PTT
PT/INR
Fibronogen
D-dimer

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36
Q

What may cause pseudothrombocytopenia?

A

Platelet trapping clots in tube from not mixing properly
EDTA dependent agglutinates

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37
Q

Causes of thrombocytosis? NB

A

Reactive: infection, post-surgery, post-splenectomy,malignancy, acute blood loss

Myeloproliferative

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38
Q

Causes of thrombocytopenia?

A

Decreased production: bone marrow disease, nutritional deficiencies

Increased destruction: autoimmune disease, DIC, medications, alcohol, HIV

Hypersplenism

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39
Q

Isolated increased PT/INR indicates…

A

VII deficiency

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40
Q

Increased INR + other coagulation abnormalities could be …

A

Vit K deficiency
Vit K antagonist
Malabsorption
Liver disease
Dilutional coagulopathy
High conc unfractionated heparin

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41
Q

How to prepare sample for PT measurement

A

> centrifuge
discard RBC’s
add calcium, thromboplastin (phospholipid and tissue factor)
fibrin clot

42
Q

How to conduct aPTT test in lab?

A

> centrifuge
remove RBC’s
add calcium, partial thromboplastin (phospholipid with no tissue factor) and silica =activating agent
fibrin clot

43
Q

Causes for isolated elevated aPTT

A

Factor XII, XI, IX and VII deficiency
Contact factor deficiency
Acquired clotting factor inhibitors

44
Q

Prolonged aPTT and PT

A

Vit K deficiency
Liver disease due to malabsorption, decreased synthesis of clotting factors,
DIC
Multiple clotting factor deficiencies
Direct thrombin inhibitors
Dilutional coagulopathy

45
Q

Causes of increased PTT +- increased PT

A

UFH
Antiphospholipid antibodies
Acquired clotting factor inhibitors

46
Q

What causes high fibrin levels?

A

Acute phase reactant
Pregnancy

47
Q

What causes low fibrin levels?

A

Liver failure (synthesised in the liver)
DIC

48
Q

What is mixing studies and how does it help?

A

Take pt plasma and normal pt plasma and mix them. If clotting corrects then factor deficiency. If it doesn’t correct then there is a factor inhibitor.
Helps decide treatment

49
Q

What is D-dimer?

A

A fibrin degradation product.

50
Q

Causes of high D-dimer

A

PE
DVT
Arterial clot
Severe sepsis
Malignancy
Recent surgery or trauma
Liver disease
Pregnancy
DIC

51
Q

Reasons for an artefactual abnormal result?

A

Pts haematocrit
Pt fasting state
Time between sample collection and test
Concentrate of citrate in tube

52
Q

Define blood transfusion

A

Safe transfer of blood components from a donor to a recepient

53
Q

What is acute normovolaemic haemodilution?

A

Remove blood from pt once under anaesthesia and replace with acellular fluid. Return as detected by intracellular loss.

54
Q

How is platelet rich plasma formed?

A

4 huffy coat units and 1 plasma unit

55
Q

Pre-transfusion tests of recipient?

A

Crosshatch
ABO and are blood ground
Antibody screen

56
Q

Red cell concentrate indications

A

Acute blood loss
Anaemia symptomatic
Obs haemorrhage
Surgery

57
Q

Platelet transfusion indications

A

Bone marrow failure
Massive transfusion
Acute DIC
Congenital disorders of platelets

58
Q

Contraindications of platelet transfusion

A

Immune thrombocytopenia unless bleeding
Thrombotic thrombocytopenia purpura
Heparin induced thrombocytopenia

59
Q

FFP indications

A

Replacement of inherited single factor deficiencies
Multiple coag deficiency
Thrombotic thrombocytopenia purpura
Reversal of warfarin if active bleeding
Vit K deficiency
Haemolytic disease of the newborn

60
Q

What is leukodepletion?

A

Removal of majority of WBC’s from transfused blood products

61
Q

Indications for leukodepletion

A

Pts on chronic transfusion regimens
Risk of CMV infection (intracellular)
Organ and stem cell transplant patients
Infant <1y
Pts undergoing cardiac surgery

62
Q

What is gamma-irradiation

A

Kills off T lymphocytes to prevent graft vs host disease

63
Q

Indications for gamma irradiation

A

Transfusion from relatives
HLA matched platelets
Intrauterine transfusions
Exchange transfusion
Congenital immunodeficiency states
Post allogenic transplants
Hodgkin lymphoma
Pts treated with purine analogue

64
Q

Early complications of blood transfusions

A

Haemolytic reaction
Anaphylaxis
bacterial contamination
Allergic reaction
Febrile non-haemolytic transfusion
Electrolyte imbalances
Transfusion related acute lung injury

65
Q

Late complications of blood transfusion

A

Graft vs host disease
Purpura
Alloimmunisation
Transmission of infection

66
Q

Clinical features of haemolytic anaemia

A

Anaemia
Jaundice
Splenomegaly
Ankle ulcers(sickle cell)
Pigment gallstones
Bone expansion in children due to marrow expansion

67
Q

Lab features of haemolytic anaemia

A

→/↑ Hb
↑ unconjugated bilirubin
↓ Haptoglobin
↑ LDH
↑reticulocytes
Increased urin + plasma Hb

68
Q

How can you measure lifespan of RBC’s

A

Radioactive chromium labelling

69
Q

Causes of intravascular haemolysis

A

Mismatched blood transfusion
Red cell fragmentation syndromes
Autoimmune haemolytic anaemia
Drug/infection induced
G6PD deficiency

70
Q

Hereditary spherocytosis

A

Abnormal RBC membrane proteins = lipid bilateral unsupported = dehydration and K loss

71
Q

Clinical features of hereditary spherocytosis

A

Increased haemolysis during infection
Splenomegaly, mild anaemia, mild jaundice,gallstones, iron overload, lower leg ulcers

72
Q

Lab features hereditary spherocytosis

A

Hb varies
MCHC increased
Microspherocytes
Polychronasia
Osmotic fragility

73
Q

Treatment of hereditary spherocytosis

A

Folic acid
Blood transfusion
Splenectomy
Cholecystectomy

74
Q

G6PD enzyme deficiency clinical picture

A

Haemolysis 1-3 days after drug exposure
Dark urine, backache
Neonatal jaundice
Heinz bodies appear and Hb decreases rapidly

75
Q

Lab features G6DP deficiency

A

Polychromatic
Acute ingravascular haemolysis
Heinz bodies on supravital staining

76
Q

Management of G6DP deficiency

A

Stop offending drug
Treat infection
Transfuse red cells
Consider splenectomy

77
Q

What is thalassaemia

A

Reduced synthesis of alpha or beta glob in chain subunit of Hb

78
Q

Clinical features of thalassaemia

A

Anaemia
Failure to thrive, inter current infection, mild jaundice
Iron overload

79
Q

Lab findings thalassaemia

A

Hypochromic microcytic anaemia
Raised RCC
Hyper cellular bone marrow

80
Q

Management of thalassaemia

A

Keep Hb >9-10
Iron chelation therapy
Immunise for hep B
Splenectomy
Bone marrow transplant

81
Q

What is iron stored as in the body?

A

Haemosiderin and ferritin

82
Q

Iron deficiency vs iron deficiency anaemia

A

In the latter, there is depletion of the iron stores in the presence of anaemia

83
Q

What is functional iron deficiency?

A

Insufficient mobilisation of iron for the purpose of erythropoiesis.

84
Q

Iron restricted erthropoiesis

A

Reduced iron supply for the purpose of erythropoiesis, regardless of the level of iron stores.

85
Q

Symptoms of iron deficiency anaemia

A

Pallor
Fatigue
Dizziness
Headache
Dyspnoea
Dry and damaged hair
Cardiac murmur
Tachycardia
Dry and rough skin

86
Q

Lab features of iron deficiency anaemia

A

Microcytic hypochromic RBC’s
Reticulocytopenia
Pencil shaped poikilocytes
Target cells

87
Q

What does S-ferritin levels tell us

A

Decreased in iron and Vit C deficiency

Increased in chronic disease from haemolysis after organ damage and inflammation

88
Q

What does s-transferrin receptor levels tell us

A

Increased in iron deficiency anaemia (but not in chronic disease)

Influenced by change in rate of erythropoiesis

89
Q

How does reticulocyte haemaglobin content help us?

A

Decreased in iron deficiency anaemia <27,2
But also in thalassaemia

90
Q

Causes of iron tx failure

A

Non compliance
Continuing haemorrhage
Mixed deficiency
Another cause
Malabsorption
Wrong diagnosis

91
Q

Expected response to iron supplements

A

Increase in Hb by 2g/dl every 3 weeks

92
Q

What is iron refractive iron deficiency anaemia

A

Inherited disorder of both absorption and utilisation of iron

Partially responsive to parenteral, nonresponsive to oral

93
Q

Causes for macrocytosis

A

Pregnancy
Reticulocytosis
Alcohol
Smoking
Liver disease
Myxoedema
Myeloma
Cytotoxic drugs

94
Q

What are the effects of VitB12 deficiency and folate deficiency?

A

Megaloblastic anaemia
Macrocytosis of epithelial cell
Neuropathy
Sterility
Decreased osteoblast activity
Neural tube defects in fetus

95
Q

Causes of ViB12 deficiency

A

Malabsorption
>pernicious anaemia
>gastrectomy

Abuse of nitric oxide
Inherited metabolic
>impaired ability to transport VitB12

Dietary deficiency

96
Q

Pathophysiology of pernicious anaemia

A

Autoimmune gastritis = gastric atrophy = reduced acid and intrinsic factor

97
Q

Clinical features of pernicious anaemia

A

Gradual onset with features of anaemia
Mild jaundice
Glossitis
Angular stomatitis
Purpura
Reversible melanin pigmentation
Progressive neuropathy

98
Q

Lab findings of pernicious anaemia

A

Low reticulocyte count
Oval macrocytes
Hypersegmented neutrophils
Decreased leukocyte and platelet count

99
Q

Treatment for Vit B12 deficiency

A

IM hydroxocobalamin 1000micrograms
6 doses over 2-3 weeks and then 1 dose every 3 months

100
Q

Treatment for folate deficiency

A

5mg oral folic acid daily for 4 months (if chronic condition = lifelong tx)

Chemical Pathology (8 decks)

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