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Laz questions > Haem > Flashcards

Haem Flashcards

1
Q

Define haemolytic anaemia

A

Anaemia caused by shortened RBC survival

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2
Q

List some e.g.s of extravascular haemolysis

A

AI haemolytic anaemia

Hereditary spherocytosis

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3
Q

List some e.g.s of intravascular haemolysis

A 
Malaria (most common worldwide)
G6PD deficiency
Pyruvate kinase deficiency
Mismatched blood transfusion
MAHA
Paroxysmal nocturnal haemoglobinuria
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4
Q

What is paroxysmal nocturnal haemoglobinuria caused by>

A

Acquired defect in GPI anchor which is 1 of 2 mechanisms by which cells attach proteins to their surface

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5
Q

List some consequences of haemolytic anaemia

A 
Anaemia
Erythroid hyperplasia
Increased folate demand
Susceptibility to parvovirus B19 infection
Propensity to gallstones
Increased risk of Fe overload
Increased risk of osteoporosis
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6
Q

Why is parvovirus B19 infection dangerous in patients with haemolytic anaemia?

A

Infects erythroid cells in bone marrow & arrests their maturation
If this happens in someone with shortened RBC survival, can cause dramatic drop in Hb (aplastic crisis)
N.B: Can be identified by observing low reticulocyte count

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7
Q

Why do people with haemolytic anaemia have increased risk of developing gallstones?

A

Increased generation of bilirubin

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8
Q

Co-inheritance of which condition with haemolytic anaemia could further increase risk of gallstones?

A

Gilbert’s syndrome

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9
Q

Describe genetic cause of Gilbert’s syndrome

A

Caused by UGT TA7/TA7 genotype
Instead of usual 6TA repeats, extra dinucleotide on each allele - associated with reduced transcription of UGT 1A1
Reduced production of enzyme in liver
Less efficient bilirubin conjugation

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10
Q

Why is there an increased risk of Fe overload with haemolytic anaemia?

A

Increased intestinal Fe absorption (also due to transfusions)

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11
Q

List some clinical features of haemolytic anaemia

A 
Pallor
Jaundice
Splenomegaly
Family history
Pigmenturia
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12
Q

List some lab features of haemolytic anaemia

A 
Anaemia
Increased reticulocytes
Polychromasia
Increased LDH (intracellular enzyme released when RBCs destroyed)
Increased bilirubin
Reduced/absent haptoglobins
Haemoglobinuria
Hemosiderinuria
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13
Q

What is polychromasia?

A

RBC take up both eosinophilic & basophilic dye giving them bluish appearance - due to presence of reticulocytes

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14
Q

What is increased LDH a marker of?

A

Increased LDH suggests intravascular haemolysis

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15
Q

What are haptoglobins? What is the significance of reduced haptoglobins?

A

Haptoglobins are proteins in bloodstream that bind to & remove free Hb from bloodstream
Low haptoglobins suggests lots of free Hb in bloodstream

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16
Q

Which stains used for haemosiderinaemia?

A

Perl’s stain

Prussian blue stain

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17
Q

What does presence of haemoglobinuria & haemosiderinuria imply?

A

Intravascular haemolysis

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18
Q

RBC lipid membrane rests on a cytoskeleton made of what?

A

Spectrin

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19
Q

Describe the inheritance of hereditary spherocytosis

A

75% family history (autosomal dominant)
25% de novo mutations

N.B: Most common defect of RBC cytoskeleton

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20
Q

What is the hallmark feature of RBC in hereditary spherocytosis?

A

Osmotic fragility - RBC show increased sensitivity to lysis in hypotonic saline

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21
Q

What is another test for hereditary spherocytosis?

A

Reduced binding to eosin 5-maleimide (dye)

Shown by flow cytometry

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22
Q

Describe appearance of blood film in hereditary spherocytosis

A

Cells lack central area of pallor because have lost biconcave shape
Cells are small & more densely stained
May be polychromatic cells (due to presence of young RBC population)

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23
Q

Outline the blood film & FBC features of hereditary elliptocytosis

A

RBC elliptical but no polychromasia & blood count likely to be normal because there is little haemolysis

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24
Q

What is the homozygous form of elliptocytosis called?

A

Hereditary pyropoikilocytosis

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25
Q

Describe appearance of blood film in hereditary pyropoikilocytosis

A

Fragmentation of RBC & lot of variation in shape of RBC (poikilocytosis)
Can cause severe haemolytic anaemia

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26
Q

Describe the inheritance pattern of G6PD deficiency

A

X-linked recessive

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27
Q

Outline the importance of G6PD in RBCs

A

G6PD catalyses 1st step in pentose phosphate pathway
This reaction generates NADPH which is required to maintain intracellular glutathione
Glutathione protects RBCs against oxidative stress
Lack of G6PD means RBCs at increased risk of oxidative damage

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28
Q

List possible clinical effects of G6PD deficiency

A

Neonatal jaundice
Acute haemolysis
Chronic haemolytic anaemia (rare)

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29
Q

List some triggers for haemolysis in G6PD deficiency

A

Drugs (antimalarials, abx, dapsone, Vit K)
Infections
Fava beans
Naphthalene mothballs

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30
Q

Describe appearance of blood film in G6PD deficiency during acute haemolysis

A

Contracted cells
Nucleated RBCs
Bite cells
Hemighosts (Hb retracted to one side of cell)

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31
Q

What is a Heinz body? What is it suggestive of?

What stain is used to look for them?

A

Denatured Hb
Suggestive of oxidative haemolysis

Methylviolet

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32
Q

What is a characteristic blood film feature of pyruvate kinase pathway?

A

Echinocytes - RBCs with lots of short projections
N.B: As cells decrease in size due to dehydration, RBCs will resemble spherocytes. Number of echinocytes usually increases post-splenectomy

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33
Q

Describe how pyrimidine 5-nucleotidase deficiency leads to haemolytic anaemia

A

Defect in nucleotide metabolism

Normal:

  • Pyrimidine nucleotides are toxic to the cell but the cell must recycle purines
  • RBCs have mechanism for selectively eliminating pyrimidines
  • This mechanism dependent on pyrimidine 5-nucleotidase

Deficiency of pyrimidine 5-nucleotidase leads to accumulation of toxic pyrimidines

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34
Q

What is a characteristic blood film feature of pyrimidine 5-nucleotidase deficiency?

A

Basophilic stippling

N.B: Also seen in lead poisoning because lead inhibits pyrimidine 5-nucleotidase

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35
Q

What are Ham’s test & flow cytometry for GPI-linked proteins used for?

A

Paroxysmal nocturnal haemoglobinuria

N.B: Ham’s test looks at sensitivity of RBCs to lysis by acidified serum

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36
Q

What investigations are used for malaria?

A

Thick & thin blood film

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37
Q

Outline the principles of management of haemolytic anaemia

A

Folic acid supplementation
Avoidance of triggers in G6PD deficiency
Blood transfusions/exchange
Immunisations against blood-borne viruses
Monitor for chronic complications (e.g. gallstones)
Splenectomy if needed

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38
Q

List some indications for splenectomy

A 
Pyruvate kinase deficiency
Hereditary spherocytosis
Severe eliptocytosis/pyropoikilocytosis
Thalassaemia symptoms
AI haemolytic anaemia
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39
Q

What is the main risk of splenectomy?

A

Overwhelming sepsis due to susceptibility to encapsulated bacteria (e.g. pneumococcus)
N.B: Risk can be reduced by using penicillin prophylaxis & immunisations

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40
Q

List some specific criteria for splenectomy

A 
Transfusion dependence
Growth delay
Physical limitation
Hypersplenism (where causes pooling & physical symptoms)
3< Age <10
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41
Q

What is Hb Hammersmith (HH)?

A

Severe unstable Hb variant that produces a Heinz body haemolytic anaemia

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42
Q

Which chromosomal duplications are most commonly associated with AML?

A

8 & 21 (hence Down’s syndrome predisposition)

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43
Q

List some RFs for AML

A 
Familial
Constitutional (e.g. Down's syndrome)
Anticancer drugs
Irradiation
Smoking
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44
Q

What are type 1 & type 2 abnormalites with regards to leukaemogenesis?

A

Type 1: Promotes proliferation & survival (anti-apoptosis)
Type 2: Blocks differentiation
N.B: Leukaemogenesis in AML requires multiple genetic hits

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45
Q

Give an e.g. of how disruption of a transcription factor can lead to leukaemogenesis

A

Core binding factor (CBF) = master controller of haemopoiesis
Translocation 8;21 fuses RUNX1 with RUNX1T1 leading to formation of fusion gene that drives leukaemia
Fusion transcription factor binds to co-repressors leading to differentiation block

Inversion of Chr16 also affcts CBF in a similar way

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46
Q

Which chromosomal aberration causes APML?

What fusion gene does this produce?

A

Translocation 15;17

PML-RARa (type 1 mutation)

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47
Q

What is a characteristic feature of APML?

Why does this occur?

A

Haemorrhage - because APML is associated with DIC & hyperactive fibrinolysis

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48
Q

In what way are the promyelocytes in APML abnormal

A

Contain multiple Auer rods - these are pathognomonic of myeloid leukaemias
(Large, crystalline cytoplasmic inclusion bodies)

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49
Q

Describe how the variant version of APML is different from the original variation

A

Variant form has granules that are below the resolution of a light microscope
Also tend to have bilobed nuclei

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50
Q

Give a type 1 & type 2 mutatation for APML

A

Type 1: FLT3-ITD

Type 2: PML-RARa

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51
Q

Which stain can be used to distinguish myeloid leukaemias from other leukaemias?
What other similar stains that are not used as frequently?

A

Myeloperoxidase

Less frequent:
Sudan black
Non-specific esterase

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52
Q

List the clinical features of AML?

A

Bone marrow failure (anaemia, neutropaenia, thrombocytopaenia)
Local infiltration (splenomegaly, hepatomegaly, gum infiltration, lymphadenopathy, CNS, skin)
Hyperviscosity if WBC very high (can cause retinal haemorrhages & exudates)

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53
Q

Outline the tests that may be used to diagnose AML

A 
Blood film
- Neutrophilia
- Myeloblasts
Bone marrow aspirate
Cytogenic studies (done in every patient)
Molecular studies & FISH
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54
Q

What is aleukaemic leukaemia?

A

When there are no leukaemic cells in the peripheral blood but the bone marrow has been replaced them

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55
Q

Outline the supportive care given for AML

A 
RBCs
Platelets
FFC/cryoprecipitate in DIC
Abx
Allopurinol (prevent gout)
Fluid & electrolyte balance
Chemotherapy
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56
Q

What are the principles of treatment in AML?

A 
Damage the DNA of the leukaemic cells
Leave normal cells unaffected
Combination chemo always used
Usually given as 4-5 courses (2x remissin induction + 2/3x consolidation)
Treatment usually lasts around 6mths
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57
Q

List some determinants of prognosis in AML

A 
Patient characteristics
Morphology
Immunophenotyping
Cytogenetics
Response to treatment
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58
Q

Outline clinical features of ALL

A

Bone marrow failure

Local infiltration

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59
Q

What is a key difference in the origin of B-lineage & T-lineage ALL?

A

B-lineage starts in the bone marrow

T-lineage can start in the thymus (which may be enlarged)

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60
Q

List some investigations used in the diagnosis of ALL

A

FBC & blood film
Bone marrow aspirate
Immunophenotyping
Cytogenetic/molecular analysis

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61
Q

What are the 4 phases of chemo for ALL?

A

Remission induction
Consolidation & CNS therapy
Intensification
Maintenance

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62
Q

How long does chemo for ALL usually take? Why is it longer in M?

A

2-3yrs

Longer in M because testes are site of accumulation of lymphoblasts

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63
Q

Who receives CNS-directed chemo? How can this be given?

A

All patients

Can be given intrathecally or high dose of chemo can be given that penetrates BBB

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64
Q

Outline the supportive care for ALL

A

Blood products
Abx
General medical care (central line, gout management, hyperkalaemia management, sometimes dialysis)

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65
Q

Which factors are procoagulant?

Which are anticoagulant?

A

Procoagulant:

  • Platelets
  • Endothelium (products & subendothelium)
  • vWF
  • Coagulation cascade

Anticoagulant:

  • Fibrinolysis
  • Antithrombins
  • Protein C/S
  • Tissue factor pathway inhibitor
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66
Q

Which 3 responses are stimulated by vessel injury?

A 
Vasoconstriction
Platelet activation (forms primary haemostatic plug)
Activation of the coagulation cascade
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67
Q

What are the 2 main functions of the endothelium?

A

Synthesis of prostacyclin, vWF, plasminogen activators, & thrombomodulin
Maintain barrier between blood & procoagulant subendothelial structures

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68
Q

How many platelets are produced by each megakaryocyte?

What is the life span of platelets?

A

4000 produced

10 days
N.B: This is important because means the effect of antiplatelet drugs lasts for 10 days after stopping the drug

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69
Q

What are glycoproteins?

A

Cell surface proteins through which platelets can interact with the endothelium, vWF, & other platelets

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70
Q

What do dense granules contain?

A

Energy stores (ADP, ATP) - found in platelets

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71
Q

Which features of platelets enable them to massively expand their SA?

A

Open cannalicular system & microtubules & actomyosin

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72
Q

What are the 2 ways in which platelets can adhere to subendothelial structures

A

Directly - Via GlpIa

<b> Indirectly - Via binding of GlpIb to vWF </b>

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73
Q

Which factors, released by platelets after adhesion, promote platelet aggregation?

A

ADP

Thromboxane A2

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74
Q

How do platelets bind to each other?

A

GlpIIb/IIIa

Also binds to fibrinogen via this receptor

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75
Q

Describe the effects of aspirin & other NSAIDs on the arachidonic acid pathway

A

Aspirin = irreversible COX inhibitor

Other NSAIDs reversibly inhibit COX

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76
Q

What is the rate-limiting step for fibrin formation?

A

Factor Xa

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77
Q

What are the effects of thrombin?

A

Activates fibrinogen
Activates platelets
Activates profactors (FV & FVIII)
Activates zymogens (FVII, FXI, FXIII)

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78
Q

Name the complex that is responsible for activating prothrombin to thrombin

A

Prothrombinase complex

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79
Q

Outline the initiation phase of the clotting cascade

A

Damage to the endothelium results in exposure of tissue factor binds FVII -> FVIIa
TF-FVIIa complex activates FIX & FX
FXa binds to FVa resulting in the first step of the coagulation cascade

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80
Q

Outline the amplification phase of the clotting cascade

A

FVa & FXa result in production of small amount of thrombin
This thrombin activates platelets
Thrombin also activates FXI which activates FIX, and FVIII which recruits more FVa
FVa, FVIIIa, FIXa will bind to the activated platelet

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81
Q

Outline the propogation phase of the clotting cascade

A

FVa, FVIIIa, FIXa recruit FXa
Results in generation of large amount of thrombin (thrombin burst)
Enables formation of stable fibrin clot

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82
Q

Why is the prothrombinase complex important?

A

Allows prothrombin activation at a much faster rate

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83
Q

What is required for adequate production/absorption of Vit K?

A

Bacteria in gut produce Vit K

Fat-soluble so bile needed for Vit K to be absorbed

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84
Q

What is the most common cause of Vit K deficiency?

A

Warfarin

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85
Q

Name 2 factors that convert plasminogen to plasmin

A

Tissue plasminogen activator

Urokinase

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86
Q

Name a factor that inhibits tissue plasminogen activator & urokinase

A

Plasminogen activater inhibitor 1 & 2

87
Q

Name 2 factors that directly inhibit plasmin

A

Alpha-2 antiplasmin

Alpha-2 macroglobulin

88
Q

What is the role of thrombin-activatable fibrinolysis inhibitor (TAFI)?

A

Inhibitor of fibrin breakdown

89
Q

Describe the action of antithrombins

A

Bind to thrombin 1:1 & this complex excreted in urine

90
Q

What is the most thrombogenic hereditary condition?

A

Antithrombin deficiency

91
Q

Outline the role of protein C & protein S

A

Trace amounts of thrombin generated at start of clotting cascade activate thrombomodulin
Allows protein C to bind to thrombomodulin through endothelial protein C receptor
Protein C then fully activated in presence of protein S
Fully activated protein C will inactivate FVa & FVIIIa

92
Q

State & explain 2 causes of activated protein C resistance

A 
Mutated FV (e.g. FV Leiden) - resistant to breakdown by protein C
High levels of FVIIIa
93
Q

What is the role of tissue factor pathway inhibitor?

A

TFPI neutralises TF-FVIIa complex once it has initiated the clotting cascade

94
Q

What is the difference between immediate & delayed bleeding with regards to the underlying pathological process?

A

Immediate - issue with the primary haemostatic plug (platelets, endothelium, vWF)
Delayed - issue with the coagulation cascade

95
Q

Describe the key clinical differences between platelet disorders (immediate bleeding) & coagulation factor disorders (delayed bleeding)

A

Platelet disorders

  • Bleeding from skin & mucous membranes
  • Petechiae
  • Small, superficial ecchymoses
  • Bleeding after cuts & scratches
  • Bleeding immediately after surgery/trauma
  • Usually mild

Coagulation factor disorders

  • Bleeding into soft tissues, joints, & muscles
  • No petechiae
  • Large, deep ecchymoses (typical lesion in coagulation disorders)
  • Haemarth roses
  • No bleeding from cuts & scratches
  • Delayed bleeding from surgery & trauma
  • Often severe
96
Q

When is treatment for platelet disorders required?

A

Platelet count <30x10^9/L (associated with spontaneous haemorrhage)

97
Q

Why is it important to look at platelets under the microscope in thrombocytopaenia?

A

To distinguish from pseudothrombocytopaenia (platelets clumped together giving erroneously low result)
Also allows identification of other abnormalities (e.g. Grey platelet syndrome - large platelets)

98
Q

What can cause a decrease in platelet number?

What can cause defective platelet function?

A

Number

  • Decreased production
  • Decreased survival (ITP)
  • Increased consumtpion (DIC)
  • Dilution

Function

  • Acquired (e.g. aspirin)
  • Congenital (e.g. thombasthaenia)
  • Cardiopulmonary bypass
99
Q

What can cause immune-mediated thrombocytopaenia?

A 
Idiopathic
Drug-induced e.g. quinine, rifampicin
Connective tissue disorder e.g. SLE
Lymphoproliferative disorder
Sarcoidosis
100
Q

List 2 non-immune mediated conditions that cause thrombocytopaenia

A

DIC

MAHA

101
Q

Describe the pathophysiology of ITP

A

Auto-Ab generated against platelets

Platelets tagged by auto-Ab then destroyed by reticuloendothelial system (liver, spleen, bone marrow)

102
Q

What are the main differences between acute & chronic ITP

A

Acute

  • Mainly children
  • Usually preceding infection
  • Abrupt onset of symptoms
  • Lasts 2-6wks
  • Spontaneously resolves

Chronic

  • Mainly occurs in adults
  • More common in F
  • Can be abrupt or indolent
  • Doesn’t resolve spontaneously
103
Q

How is ITP treated?

A

Mainly with steroids & IVIG based on the platelet count

104
Q

Give some e.g.s of thrombocytopaenia that can be diagnosed by blood film

A

Vit B12 deficiency

Acute leukaemia

105
Q

What clotting study abnormality would be seen in haemophilia?

A 
Prolonged APTT
(Intrinsic & common pathway - FVIII (a) & FIX (b) most common)
106
Q

What is the most common coagulation disorder? What is its inheritance pattern?

A

Von Wilebrand disease
Autosomal dominant - type 1 & 2
Autosomal recessive - type 3

107
Q

Describe the relationship between vWF & FVIII

A

Binding of FVIII to vWF protects FVIII from being destroyed

N.B: Type 3 vWD has very similar phenotype to haemophilia A (because absent vWD leads to low FVIII)

108
Q

What is vitamin K required for?

A

Synthesis of FII, VII, IX, & X

Synthesis of protein C, S, & Z

109
Q

List some causes of Vit K deficiency

A

Malnutrition
Biliary obstruction
Malabsorption
Abx therapy

110
Q

Outline the pathophysiology of DIC

A

Release of thromboplastic material into circulation causes widespread activation of coagulation & fibrinolysis
Results in increased vascular deposition of fibrin, which leads to thrombosis of small & mid-size vessels with organ failure
Depletion of platelets & coagulation factors leads to bleeding

111
Q

List some causes of DIC

A

Sepsis (most common)
Trauma (e.g. fat embolism)
Obstetric complications (e.g. amniotic fluid embolism)
Malignancy
Vascular disorders
Reaction to toxin
Immunological (e.g. transplant rejection)

112
Q

Describe the typical clotting study results in DIC

A 
Prolonged APTT & PT
Decreased fibrinogen
Increased fibrin degradation products
Decreased platelets
Schistocytes (due to shearing of RBCs as pass through fibrin mesh)
113
Q

Outline treatment of DIC

A 
Treat underlying cause
Anticoagulation with heparin
Platelet transfusion
FFP
Coagulation inhibitor concentrate
114
Q

Describe how liver disease leads to bleeding disorders

A

Decreased synthesis of FII, VII, IX, X, XI, & fibrinogen
Dietary Vit K deficiency
Dysfibrogenaemia
Enhanced haemolysis (decreased alpha-2 antiplasmin)
DIC
Thrombocytopaenia due to hypersplenism

115
Q

Outline the treatment of:

  • Prolonged PT/APTT
  • Low fibrinogen
  • DIC
A

Prolonged PT/APTT

  • Oral Vit K
  • FFP infusion

Low fibrinogen
- Cryoprecipitate

DIC
- Replacement therapy

116
Q

What may need to be given in severe warfarin overdose?

A

Prothrombin complex concentrate (PCC) - contains Vit K-dependent clotting factors

117
Q

What are Janus Kinases?

A

Family of 4 tyrosine kinase receptors associated with haemopoietic cell growth factor receptors
Have a kinase domain & a catalytically inactive pseudokinase domain with regulatory function

118
Q

Describe what happens when growth factors bind to Janus Kinase receptors

A

Binding of growth factors leads to JAK activation, which activates STAT pathway
STAT = transcription factor that moves to nucleus & promotes transcription of genes associated with cell growth & proliferation

119
Q

What is a chronic myeloproliferative disorder?

A

Group of clonal disorders of haemopoietic stem cells characterised by overproduction of 1/> mature myeloid cellular elements in the blood
Trend towards increased fibrosis in bone marroww
Some cases will develop into acute leukaemia

120
Q

Outline the usual presentation of myeloproliferative disorders

A

Preponderance to thrombosis
Splenomegaly
Hepatomegaly

121
Q

List some chronic myeloproliferative disorders

A 
Polycythaemia vera
Essential thrombocythaemia
Idiopathic myelofibrosis
Idiopathic erythrocytosis
Chronic granulocytic leukaemia
122
Q

What are the key differences between:

  • Myeloproliferative disorder
  • Leukaemia
  • Myelodysplastic syndrome
A

Myeloproliferative disorder
- Proliferation with full differentiation

Leukaemia
- Proliferation with little/no differentiation

Myelodysplastic syndrome
- Abnormal proliferation & abnormal differentiation

123
Q

What is polycythaemia vera?

A

Myeloproliferative disorder characterised by increased RBC production (independent of normal control mechanisms) with compensatory increase in plasma vol
Often accompanied by a degree of increased platelets & granulocytic cells

124
Q

Describe the clinical presentation of polycythaemia vera

A

Incidental finding
Symptoms of hyperviscosity (headaches, visual disturbances, fatigue, dyspnoea)
Increased histamine release (aquagenic pruritis, peptic ulceration)
Splenomegaly
Plethora
Erythromelalgia (red, painful extremities)
Thrombosis
Retinal vein engorgement
Gout

125
Q

Outline the typical investigation findings polycythaemia vera including bone marrow biopsy appearance and a diagnostic investigation finding

A

High Hb, Hct, MCV, plasma vol, & platelets
No circulating immature cells

Bone marrow biopsy:

  • Increased cellularity (mainly erythroid cells)
  • Slight reticulin fibrosis & megakaryocyte abnormalities

Diagnostic investigation finding:
- Presence of JAK2 V617F mutation

126
Q

What is pseudopolycythaemia?

A

Reduced plasma vol in presence of normal amount of Hb results in apparently raised Hb

127
Q

On which exon is JAK2 V617F found?

Which other JAK mutation is a significant finding & which condition is it associated with?

A

Exon 14

Other:

  • Exon 12 mutation
  • Associated with idiopathic erythrocytosis - isolated erythrocytosis with low EPO
128
Q

What are some causes of JAK2 V617F -ve polycythaemia?

A

Pseudopolycythaemia

True polycythaemia secondary to increased EPO (e.g. hypoxia, renal disease, tumours)

129
Q

Outline the principles of treatment of polycythaemia vera

A 
Reduce viscosity & keep Hct <45%
- Venesection
- Cytoreductive therapy
Aim to reduce risk of thrombosis
- Aspirin
- Keep platelets <400x10^9/L (same as essential thrombocythaemia treatment)
130
Q

Outline the prognosis of idiopathic erythrocytosis & polycythaemia vera

A

Idiopathic erythrocytosis - no adverse prognosis if Hct maintained

Polycythaemia vera - most survive 10yrs, causes of death include thrombosis, leukaemia, & myelofibrosis

131
Q

What is essential thrombocythaemia?

How does it typically present?

A

Myeloproliferative disorder mainly involving megakaryocyte lineage (platelet count >600x10^9/L)

Typical clinical presentation:

  • Incidental finding
  • Thrombosis (e.g. stroke, DVT, gangrene)
  • Bleeding
  • Headaches, dizziness, visual disturbances
132
Q

What proportion of essential thrombocythaemia patients have JAK2 mutations?

A

50%

133
Q

Outline the treatment options for essential thrombocythaemia?

A

Aspirin
Anagrelide (specific inhibitor of platelet formation - may accelerate myelofibrosis)
<b> Hydroxycoarbamide </b> - may be leukaemogenic
Alpha-interferon - may be used in patients <40yo

134
Q

What factor is important in determining risk level in essential thrombocythaemia?

A

Age (> -> higher risk)

Also platelet count & whether symptomatic or not

135
Q

Describe the prognosis of essential thrombocythaemia

A

Normal life span
Leukaemic transformation in about 5% after 10yrs
Myelofibrosis uncommon

136
Q

Define chronic idiopathic myelofibrosis

Describe the typical clinical presentation

A

Clonal myeloproliferative disease with proliferation mainly of megakaryocytes & granulocytic cells, associated with reactive bone marrow fibrosis & extramedullary haemopoiesis

Typical presentation

  • Incidental finding
  • Cytopaenias
  • Thrombocytosis
  • Splenomegaly (can be massive)
  • Hepatomegaly
  • FLAWS
  • Gout
137
Q

Describe the 2 stages of myelofibrosis

A 
Pre-fibrotic = mild blood changes with hypercellular marrow
Fibrotic = splenomegaly, blood changes, dry tap, prominent fibrosis, & later osteosclerosis
138
Q

Describe the appearance & features of myelofibrosis on blood film

A

Leukoerythroblastic picture
Tear drop poikilocytes

Dry tap
Trephine biopsy will show increased reticulin or collagen fibrosis, prominent megakaryocyte hyperplasia & new bone formation

139
Q

Outline the treatment options for myelofibrosis

A

Symptomatic treatment (e.g. transfusions for anaemia)
Splenectomy
Cytoreductive therapy (hydroxycarbamide & thalidomide)
Bone marrow transplant (in younger patients)

140
Q

Describe the prognosis of myelofibrosis

A

Median 3-5yr survival

141
Q

What effect does JAK2 V617F mutation have on janus kinases?

A

Inactivates pseudokinase domain thereby removing inhibition of activation so it becomes constitutively activated

142
Q

How can lymphoma cause jaundice?

A

Direct liver involvement
Compression of the bile duct
Causing AI haemolytic anaemia

143
Q

Which types of anaemia can be caused by cancer?

A

Fe deficiency (occult blood loss e.g. GI cancers, urinary tract cancers)
Anaemia of chronic disease
Haemolytic anaemia
Leucoerythroblastic anaemia

144
Q

Which types of cancer are associated with causing secondary polycythaemia?

A

Renal cell carcinoma
Liver cancer

Due to production of EPO

145
Q

What are the typical lab findings of Fe deficiency anaemia?

A

Low ferritin
Low transferrin saturation
High TIBC

146
Q

What is leucoerythroblastic anaemia

A

Anaemia characterised by RBC & white cell precursors

147
Q

What are the morphological features of leucoerythroblastic anaemia seen on blood film?

A

Teardrop RBCs (aniso- & poikilocytosis)
Nucleated RBCs
Immature myeloid cells

148
Q

What does leucoerythroblastic anaemia tend to be caused by?

A

Bone marrow, infiltration (leukaemia, lymphoma, myeloma, solid tumours, myelofibrosis, miliary TB, severe fungal infection)

149
Q

What are the 2 main groups of haemolytic anaemia? List some e.g.s

A

Inherited (defects with cell)

  • Hereditary spherocytosis (membrane problem)
  • G6PD (enzyme problem)
  • Sickle cell disease, thalassaemia (Hb problem)

Acquired (defects with environment)

  • Immune-mediated
  • Non-immune mediated e.g. infection (e.g. malaria), MAHA
150
Q

Which test distinguishes immune-mediated & non-immune mediated haemolytic anaemia?

A

DAT or Coombs’ test

DAT +ve means haemolytic anaemia mediated through immune destruction of RBCs

151
Q

What morphological change is seen on the blood film of patients with AI haemolytic anaemia?

A

Spherocytes

152
Q

List some systemic diseases that can cause AI haemolytic anaemia

A

Cancer involving immune system (e.g. lymphoma)
Diseases of immune system (e.g. SLE)
Infections (disturb immune system)

153
Q

List some key features of MAHA

A

Usually caused by underlying adenocarcinoma
RBC fragments
Low platelets
DIC/bleeding

154
Q

Outline the mechanism of MAHA

A

Underlying adenocarcinoma produces procoagulant cytokines that activate clotting cascade
Leads to DIC & formation of fibrin strands in various parts of microvasculature
RBCs pushed through these fibrin strands & fragment
N.B: Always consider underlying adenocarcinoma in any patient presenting with MAHA

155
Q

List some causes of secondary polycythaemia

A

Cancer (renal, hepatocellular, bronchial)
High altitude
Hypoxic lung disease
Congenital cyanotic heart disease

156
Q

List some causes of neutrophilia

A 
Corticosteroids (due to demargination)
Underlying neoplasia
Tissue inflammation (e.g. colitis, pancreatitis)
Myeloproliferative/leukaemia disorder
Infection
157
Q

List some infections that typically don’t cause neutrophilia

A

Brucella
Typhoid
Many viral disease

158
Q

List some key features of reactive neutrophilia on blood film

A

Band cells (immature neutrophils - presence of band cells show bone marrow has been signalled to release more WBCs)
Toxic granulation
Clinical signs of infection/inflammation

159
Q

List some causes of monocytosis

A

Bacteria: TB, Brucella, typhoid
Viral: CMV, VZV
Sarcoidosis
Chronic myelomonocytic leukaemia

160
Q

List some causes of reactive eosinophilia

A

Parasitic infection
Allergy (e.g. asthma, rheumatoid arthritis)
Underlying neoplasms (e.g. Hodgkin’s lymphoma, T cell lymphoma, NHL)
Drug reaction (e.g. erythema multiforme)

161
Q

Which gene mutation causes chronic eosinophilic leukaemia?

A

FIP1L1-PDGFRa fusion gene

162
Q

Which type of virus typically causes basophilia?

A

Pox viruses

163
Q

List some causes of reactive lymphocytosis

A 
Infection (EBV, CMV, toxoplasmosis, rubella, HSV)
AI disease (N.B: More likely to cause lymphopaenia)
Sarcoidosis
164
Q

How would the lymphocytes seen on blood film due to viral infection be different from leukaemia/lymphoma?

A

Viral infection: Reactive or atypical lymphocytes (EBV)

CLL or NHL: Small lymphocytes & smear cells1

165
Q

What is light chain restriction?

A

Individual B cells will either express kappa or lambda light chains (not both)
In response to infection, will get polyclonal B cell response so will be roughly even mixture of kappa & lambda light chains
In lymphoproliferative disorders, monoclonal proliferation of B cell expressing only 1 type of light chain (e.g. kappa) will mean proportion of kappa to lambda will increase (e.g. showing overwhelming majority of kappa)

166
Q

What are the consequences of thromboembolism?

A

Death (5% mortality)
Recurrence
Thrombophlebitic syndrome (recurrent pain, swelling, & ulcers)
Pulmonary HTN

167
Q

What are the components of Virchow’s triad?

A

Blood composition (viscosity - Hct, protein/paraprotein)
Vessel wall
Blood flow

168
Q

List some anticoagulant molecules produced by endothelium

A 
Thrombomodulin
Endothelial protein C receptor
Tissue factor pathway inhibitor
Heparans
N.B: Doesn't normally produce tissue factor
169
Q

What antiplatelet factors are produced by endothelium?

A

Nitrous oxide

Prostacyclin

170
Q

Describe the mechanism by which stasis promotes blood flow

A

Leads to accumulation of activated factors which promotes platelet adhesion & promotes leucocyte adhesion & transmigration
Hypoxia has inflammatory effect on endothelium

171
Q

Which drugs can be used to achieve immediate anticoagulation?
Name an anticoagulant that has a delayed effect

A

Immediate

  • Heparin
  • Direct acting anti-Xa & anti-IIa

Delayed
- Warfarin (2-3 days)

172
Q

What is the mechanism of action of heparin?

What is the antidote for heparin?

A

Increases anticoagulant activity by potentiating antithrombin III

Antidote: Protamine

173
Q

List some disadvantages of heparin

A

Administered by injection
Risk of osteoporosis
Variable renal dependence

174
Q

List some anti-Xa DOACs

Name an anti-IIa DOAC

A

Anti-Xa

  • Rivaroxaban
  • Apixaban
  • Edoxaban

Anti-IIa
- Dabigatrin

175
Q

List some properties of DOACs

A 
Oral administration
Immediate action (peak = 3-4hrs)
Useful in long-term
Short 1/2 life
No monitoring needed
176
Q

Outline the mechanism of action of warfarin

A

Vit K epoxide reductase inhibitor meaning inhibits gamma-carboxylation of FII, VII, IX, X
Also causes reduction in protein C & protein S (initially a bit procoagulant)

177
Q

How is warfarin monitored?

How can the action of warfarin be reversed?

A

Monitoring: INR

Administering Vit K - takes 12hrs
Giving FII, VII, IX, X - immediate

178
Q

List some methods of thromboprophylaxis

A

LMWH (e.g. tinzaparin 4500U, clexane 40mg OD)
TEDS
Flotron (intermittent compression)
Sometimes DOAC with/without aspirin (orthopaedics)
N.B: All hospital admissions should be risk assessed for VTE & receive heparin prophylaxis unless C/I

179
Q

Outline DVT/PE treatment including life-threatening DVT/PE

A

Start LMWH (e.g. tinzaparin 175U/kg) + warfarin
Stop LMWH when INR >2 for 2 days
Alternative: Start a DOAC
Should be continued for 3-6mths

Life-threatening: Thrombolysis (used sparingly as increases risk of intracranial haemorrhage (4%) although reduces risk of post-phlebitic syndrome)

180
Q

Define myelodysplastic syndrome

A

Biologically heterogeneous group of acquired haematological stem cell disorders

Development of clone of marrow stem cell with abnormal maturation resulting in functionally defective blood cells & reduction in cell counts
- Leads to cytopaenia, functional abnormalities of cell maturation & increased risk of transformation to leukaemia

181
Q

How do myelodysplastic syndromes typically present?

A

Symptoms/signs of bone marrow failure developing over wks/mths

182
Q

List & describe some blood & bone marrow features of the following myelodysplastic syndromes

A

Pelger-Huet anomaly (bilobed neutrophils)
Dysgranulopoiesis of neutrophils (failure of granulation)
Dyserythropoiesis of RBC (lack of separation between RBC precursors, presence of abnormal ring of cytoplasm around nucleus of precursor RBCs)
Dysplastic megakaryocytes (micromegakaryocytes)
Increased proportion of blast cells in bone marrow (normally <5%)

183
Q

What might you see by staining with Perl’s stain the bone marrow in myelodysplastic syndrome?

A

Ringed sideroblasts (accumulation of Fe around the nuclei or RBC precursors)

184
Q

What is the presence of myeloblasts with large crystalline cytoplasmic inclusions suggestive of?

A

Acute myeloid leukaemia

The crystalline structures are Auer rods

185
Q

What are the 5 prognostic variables used to calculate prognostic risk using the Revised International Prognostic Scoring System (IPSS-R) for myelodysplastic syndromes?

A 
Bone marrow blast %
Karyotype
Hb
Platelets
Neutrophils
N.B: High risk considered >6, low risk <= 1.5
186
Q

What are the usual causes of death in patients with myelodysplasia?

A

1/3 infection
1/3 bleeding
1/3 leukaemia

187
Q

What are the 2 treatments that can prolong life in myelodysplastic syndromes?

What other treatments may be used?

A

Allogeneic stem cell transplantation
Intensive chemotherapy
N.B: As most MDS patients elderly, often cannot tolerate treatment

Others:
Supportive care (blood products, antimicrobials, growth factors (e.g. EPO, GM-CSF))
Biological modifiers
- Immunosuppression
- Azacytidine (hypomethylating agent)
- Decitabine
- Lenalidomide (used in 5q minus syndrome)
Oral chemo (e.g. hydroxyurea)
Low-dose chemo (SC low-dose cytarabine)
188
Q

List some causes of primary bone marrow failure

A

Fanconi anaemia (multipotent stem cell)
Diamond-Blackfan syndrome (RBC progenitor)
Kostmann syndrome (neutrophil progenitor)
Acquired: Idiopathic aplastic anaemia (multipotent stem cell)

189
Q

List some secondary causes of bone marrow failure

A 
Marrow infiltration
Haematological malignancies
Solid tumours spreading to bone marrow
Radiation
Drugs
Chemicals (e.g. benzene)
AI
Infection (e.g. parvovirus B19)
190
Q

List some inherited causes of aplastic anaemia, including the most common inherited cause

What is the most common cause overall?

A

Fanconi anaemia (most common inherited)
Schwachman-Diamond syndrome
Dyskeratosis congenita

Most common cause: idiopathic (70-80%)

191
Q

What are some investigative features of aplastic anaemia?

A

Peripheral blood - cytopaenia

Bone marrow - hypocellular

192
Q

List some differential diagnoses for pancytopaenia & hypocellular bone marrow

A 
Hypoplastic MDS/AML
Hypocellular AML
Hairy cell leukaemia
Atypical mycobacterial infection
Anorexia nervosa
ITP (although Hb & RBC will be normal)
193
Q

What is the Camitta criteria for severe aplastic anaemia?

A

2 out of 3 peripheral blood features:

  • Reticulocytes <1% (<20x10^9/L)
  • Neutrophils <0.5x10^9/L
  • Platelets <20x10^9/L

Bone marrow cellularity <25%

194
Q

Outline the management approaches used for bone marrow failure

How does age influence management decisions?

A

Seek & remove cause
Supportive (blood products, abx, Fe chelators)
Immunosuppressive therapy (antithymocyte globulin, steroids, ciclosporin A)
Drugs that promote bone marrow recovery (oxymetholone (androgen), thrombopoietin receptor agonist (eltrombopag))
Stem cell transplantation
Alemtuzumab (T cell depletion) - for refractory cases

Immunosuppressive therapies tend to be used for older patients
Stem cell transplantation tends to be used in younger patients (80% cure rate)

195
Q

List some complications that occur after immunosuppressive therapy for aplastic anaemia

A

Relapse (35% in 15yrs)
Clonal haematological disorders - 20% risk in 10yrs (myelodysplasia, leukaemia, paroxysmal nocturnal haemoglobinuria)
Solid tumours (3% risk)

196
Q

What is the inheritance pattern of Fanconi anaemia?

A

Autosomal recessive or X-linked recessive

197
Q

List some somatic abnormalities seen in Fanconi anaemia

What proportion of patients would be expected to have these abnormalities?

A 
Short stature
Hypopigmented spots/cafe -au-lait spots
Abnormality of thumbs
Microcephaly or hydrocephaly
Hypogonadism
Developmental delay

Only present in 70% patients

198
Q

List some complications of Fanconi anaemia

A 
Aplastic anaemia (90%)
Myelodyspolasia
Leukaemia
Cancer (epithelial)
Liver disease
199
Q

What are the characteristic features of dyskeratosis congenita?

A

Bone marrow failure
Cancer predisposition
Somatic abnormalities

200
Q

What are the 3 main somatic features of dyskeratosis congenita?

A

Abnormal skin pigmentation
Nail dystrophy
Leucoplakia

201
Q

Which genes are involved in dyskeratosis congenita & what are the inheritance patterns?

A

X-linked recessive (most common) - DKC1 gene
Autosomal dominant - TERC
Autosomal recessive - no mutation identified

N.B: Abnormal telomeric structure & function heavily implicated in dyskeratosis congenita

202
Q

What are the different prevalences of Hodgkin’s lymphoma & Non-Hodgkin lymphoma?

A 
NHL = 80%
Hodgkin = 20%
203
Q

Outline the processes by which immunoglobulins & T cell receptors become capable of identifying a wide variety of Ags

A

Germline VDJ genes undergo recombination in bone marrow to generate wide repertoire of specificities
In germinal centres, 2nd stage of DNA alteration involving isotype switching & somatic hypermutation (point mutations) generates even more diversity

204
Q

What is main downside of the processes that generate variety in immunoglobulins & T cell receptors?

A

Recombination errors & new point mutations can occur
Lymphocytes are reliant on apoptosis to keep their massive proliferation under control (90% lymphocytes die in germinal centres)
If mutation turns off apoptosis, can lead to malignancy or AI

205
Q

List some oncogenes implicated in lymphoma/leukaemia

A

Bcl2
Bcl6
Cyclin D1
c-Myc

206
Q

List some e.g.s of how constant antigenic stimulation can lead to lymphoma

A

H. pylori -> gastric MALT marginal zone NHL of stomach
Sjogren syndrome -> marginal zone NHL of parotid
Coeliac disease -> small bowel T cell lymphoma, enteropathy-associated T cell non-Hodgkin’s lymphoma

207
Q

List 2 e.g.s of viral infections that can lead to lymphoma

A

Direct viral integration: HTLV1

  • HTLV1 infects T cells by vertical transmission
  • May cause adult T cell leukaemia/lymphoma (very aggressive)
  • Caused by viral genome integrating into T cell genome & driving proliferation

EBV infection & immunosuppression

  • EBV established latent infection in B cells which kept in check by cytotoxic T cell (kill EBV Ag-expressing B cells)
  • Loss of T cell function (e.g. HIV, post-transplant immunosuppression) can lead to EBV-driven lymphoma
208
Q

What are the main markers used for B & T cells?

A

T cell:

  • CD3
  • CD5

B cell:
- CD20

209
Q

Why is non-Hodgkin lymphoma often disseminated at presentation?

A

Neoplastic lymphoid cells circulate in blood leading to disseminated disease at presentation
N.B: Lymphoid neoplasms can disrupt normal immune functioning leading to immunodeficiencies

210
Q

Give an e.g. of chromosomal translocation diagnostic of lymphoma

A

11;14 = Mantle cell lymphoma

211
Q

Give an e.g. of chromosomal translocation that is prognostic in lymphoma

A

2;5 = anaplastic large cell lymphoma

212
Q

List some types of low-grade lymphoma

Name a type of intermediate-grade lymphoma

Name a type of high-grade lymphoma

A

Low-grade

  • Follicular lymphoma
  • Small lymphocytic lymphoma (CLL)
  • Marginal zone lymphoma
  • Mantle cell lymphoma

Intermediate-grade
- Burkitt’s lymphoma

High-grade
- Diffuse large B cell lymphoma

213
Q

How does follicular lymphoma typically present?

A

Lymphadenopathy in middle-aged or elderly patients

N.B: Usually indolent but can transform into high-grade lymphoma

Laz questions (2 decks)

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