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MCQ knowledge > Haematology > Flashcards

Haematology Flashcards

1
Q

What are Bence Jones protein?

A

Lambda light chains secreted in the urine.

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2
Q

True/False: patients with multiple myeloma typically have macroglobulins.

A

False.

This fits with Waldenstrom’s macroglobulinamia, excess of IgM (high molecular weight) from lymphocyte proliferation.

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3
Q

Young patient known to have sickle cell anaemia presents with malaise and rapidly increasing SOB. FBC reveals Hb 51 and low reticulocytes.

What is the diagnosis?

What is the likely pathogen?

A

Aplastic crisis in sickle cell anaemia.

Pathogen = parvovirus B19.

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4
Q

Patient presents with fever and confusion, his bloods reveal renal impairment and low platelets. Blood film reveals shistocytes.

What is the diagnosis?

A

TTP (Thrombotic Thrombocytopenic Pupura) - schistocytes suggest microangiopathic haemolysis.

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5
Q

Blood film reveal schistocytes - what are the DDx?

A
  1. Microangiopathic haemolysis (TTP-HUS, DIC)

2. Traumatic haemolysis (AS, prosthetic valves)

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6
Q

Patient presents with an isolated thrombocytopenia and purpuric rash. What is the likely diagnosis?

A

ITP (Immune Thrombocytopenic Pupura)

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7
Q

What are the causes of ITP?

Which of these causes is the most common?

A
  • Idiopathic (most common)
  • Autoimmune disorder (SLE)
  • Viral infections (CMV, VZV, Heb C, HIV)
  • H. pylori
  • Medications (heparin, penicillin, phenytoin)
  • Lymphoproliferative disorders
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8
Q

FBC suggests low platelets, low WCC and high MCV. What deficiency may cause this?

A

Folate.

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9
Q

Elderly patient presents for a routine blood test and is noted to have a high protein level and a low albumin level.

What could this be? What screen should be done?

A

Myeloma screen for a surreptitious monoclonal gammopathy.

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10
Q

What is a myeloma screen (4-5 things)?

A
  1. Serum calcium
  2. Immunoglobulins
  3. EPG / iEPG
  4. Urinary EPG / Bence Jone protein
  5. +/- skeletal survey
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11
Q

What are the clinical hallmarks of sickle cell disease (2)?

A
  1. Vasoocclusive phenomena (acute painful episodes)

2. Haemolysis

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12
Q

T/F: persistent and painful erections is complication of sickle cell disease.

A

True

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13
Q

What 3 features of a blood film are consistent with sickle cell disease?

A
  1. Sickle cells
  2. Increased reticulocytes hence polychromasia
  3. Howell-Jolly bodies (hyposplenism)
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14
Q

What 5 vaccinations should be considers in a patient with sickle cell disease (SHHIN)?

A 
Streptococcus pneumoniae
Haemophilus influenza
Hepatitis B
Influenza (seasonal)
Neisseria Meningitidis
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15
Q

What type of eye complication do patients with sickle cell disease get?

When should monitoring begin?

A

Proliferative retinopathy

Retinal assessment after the age of 10yrs

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16
Q

Patient with known sickle cell disease presents with venoocclussive phenomena.

  1. How should the pain be treated?
  2. What prophylaxis needs to be considered?
A
  1. Pain: PO/IVF rehydration and IV opioids (avoid non-opioids)
  2. DVT prophylaxis
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17
Q

T/F: GCSF is routinely used in the management of sickle cell disease.

A

False - risk of multi-organ failure and death.

May be considered on rare occasions if benefit > risk

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18
Q

What is the only cure for sickle cell anaemia?

A

Allogeneic stem cell transplant

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19
Q

Patient has thallasaemia intermedia, what bacterial pathogen is this patient susceptible to?

A

Yersinia

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20
Q

In treatment Ph+ naive CML which of the following has a ‘superior’ response; nilotinib vs. imatinib.

What type of drugs are they?

A

Nilotinib

Both are BCR-ABL1 -tyrosine-kinase INHIBITORS

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21
Q

Patient with AML requires allogeneic stem cell transplant.

What type of donor transplant is associated with the GREATEST risk of AML relapse?

A

Identical twin donor

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22
Q

What is found within cryoprecipitate?

When is it indicated?

A
  • Fibrinogen
  • F8 and vWF
  • F13
  • Fibronectin

Used primarily in fibrinogen deficiency

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23
Q

What clotting regulatory factors does warfarin affect?

A

Vit-K dependent factors:

  • 2, 7, 9 and 10
  • protein C and S
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24
Q

Which factors fall initially in warfarin commencement?

A

F7 reduced initially then protein C falls (exacerbated by reduction in protein S) within 36h, so for 3-5 day patient is paradoxically pro-thrombotic until F2 reduction occurs.

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25
Q

What is the % platelet drop suggestive of HITTS?

A

50%

26
Q

When does HITTS usually occur after heparin commencement?

A

5-10 days, if greater than 10 days, consider other causes.

27
Q

What is the main complications of HITTS: bleeding or thombosis?

A

Thrombosis (DVT in 50%)

28
Q

What is the typical range of thrombocytopenia in HITTS?

A

40-80 x10^9/L

Rarely below 20 x10^9/L

29
Q

Which type of heparin is more likely to causes HITTS?

A

Unfractionated heparin (rather than LMWH)

30
Q

What is the normal function of platelet factor 4 (PF4)?

A
  • PF4 is released during platelet activation, binds anionic glycosaminoglycans on cell surfaces.
  • This Inhibits the formation of megakaryocytes and angiogenesis + modulate immune response.
  • PF4 is released after trauma, inflammation, and in cancer
31
Q

How is PF4 implicated in HITTS?

A

2 Types of HITTS:

HITTS Type I (benign)

  • Heparin binds to PF4 causes decreased cAMP then mild platelet aggregation and thrombocytopenia
  • platelets rarely below 100 x 10^9/L and self-limiting

HITTS Type II

  • Formation of a PF4/heparin complex that triggers an immune response
  • IgG binds to PF4/heparin complexes causing clustering of platelet Fc-receptors and platelet activation
  • Results in arterial and venous thrombosis
32
Q

In HITTS, aside from the PF4 mechanism of thrombus formation, what are 2 other mechanisms of thrombosis?

A
  1. HIT-Ab (heparin-PF4 Ab) may bind to the Fc receptor of monocytes leading to thrombosis.
  2. Endothelial damage may increase vWF and thrombomodulin causing thrombosis.
33
Q

T/F: HIT-Ab may often be positive in absence of HITTS.

A

True.

Only 20% of patients with HIT-Ab will develops HITTS.

34
Q

T/F: Negative HIT-Ab is highly suggestive that HITTS may be excluded.

A

True.

HIT-Ab not helpful with ruling-in HITTs but high NPV renders it useful for excluding HITTS

35
Q

T/F: Treatment of HITTs is targeted at the bleeding risk.

A

False - aim is to reduce thrombotic risk

36
Q

T/F: warfarin is the first-line therapy in HITTS

A

False.

Warfarin may cause skin necrosis in HITTS - AVOID

37
Q

What is an antidote for heparin?

A

Protamine

38
Q

What is an alternative to heparin for anticoagulation if a patient develops HITTS?

A

Factor Xa inhibitors or Direct thrombin inhibitors

In Australia: Danaparoid (factor Xa inhibitor)

39
Q

Is it advisable to transfuse platelets in HITTS?

A

No - avoid.

40
Q

What are the current CD20 antibodies available?

What type of Ab are they?

A

Mouse analogues: Ibritu-momab and Tositu-momab

Chimeric Ab: Ritu-ximab

Humanise Ab: Ibinutu-zumab

Human mAb: Ofatum-umab

41
Q

During anaemia of chronic inflammation, what happens to the renal release of EPO?

A

EPO is suppressed by the inflammatory cytokine which contributes to the anaemia.

42
Q

How does rituximab destroy B-cells?

A

Attaches to CD20, which then attract NK-cells that kill it.

43
Q

What is the MOA of Eculizumab?

Indication?

A

C5 mAb that prevents activation of the C5-C9 termminal complement complex elements.

Used in ‘atypical HUS’ to inhibit complement-mediated MAHA

44
Q

Graft-versus-host-disease:

  1. Is a consequence of tissue destruction from which donor cells?
  2. T/F: incidence increases with donor and recipient age
  3. When does is occur post-transplant?
  4. T/F: Affect oral cavity but rarely skin
A
  1. Is a consequence of tissue destruction from which donor cells?
    T-cells
  2. T/F: incidence increases with donor and recipient age
    True
  3. When does is occur post-transplant?
    LESS than 100 days
  4. T/F: Affect oral cavity but rarely skin
    True
45
Q

Regarding RBC:

  1. What intervention has lead to less febrile non-haemolytic reactions?
  2. What optimal temperature should they be stored?
  3. What effect does storage have upon 2,3 DPG levels
  4. What is the effects of lowered pH upon oxygen delivery by Hb?
  5. Patient treated with fludarabine require what special intervention to the packed cells?
A
  1. What intervention has lead to less febrile non-haemolytic reactions?
    Leucodepletion at point of donation
  2. What optimal temperature should they be stored?
    4 degrees celcius
  3. What effect does storage have upon 2,3 DPG levels?
    Decreases 2,3 DPG levels
  4. What is the effects of lowered pH upon oxygen delivery by Hb?
    During sepsis i.e. low pH, oxygen delivery is increased
  5. Patient treated with fludarabine require what special intervention to the packed cells?
    Irradiated packed cells
46
Q

For the following forms of haemachromatosis, give the inheritance pattern:

  1. Hemojuvelin
  2. HFE
  3. TfR2
  4. Ferroportin
A

Autosomal recessive:

  1. Hemojuvelin
  2. HFE
  3. TfR2

Autosomal Dominant
4. Ferroportin

47
Q

What is Factor V Leiden?

A
  • Clotting disorder - most common hereditary
  • Factor V Leiden can NOT be inactivated by protein C
  • Homozygous patient all need treatment (DVT prophylaxis or full anticoagulation if at risk)
48
Q

What is the MOA of Bortezomib?

2 Indications?

A

Proteosome inhibitor

Indications:

  1. Relapsed multiple myeloma
  2. Mantle cell lymphoma
49
Q

MOA of DDAVP?

A

Induces the release of vWF from endothelial cells

50
Q

What are the 4 types of Hodgkin’s Lymphoma?

Rank these in terms of prognosis (best, good, worst).

What are the frequencies?

A

Lymphocyte predominant (70%) - best prognosis

Mixed cellularity (20%) - good prognosis

Nodular sclerosing (5%) - good prognosis

Lymphocyte deplete (rare) - worst prognosis

51
Q

Patient has a grossly elevated APTT. What are the 3 DDx?

A
  1. Heparin therapy
  2. Haemophilia
  3. Antiphospholipid syndrome
52
Q

Patient has CML (chronic myeloid leukaemia), which chromosomal translocation is found in 95%?

A

Philadelphia chromosome - t(9;22)

53
Q

In a patient with escalated BEACOPP curative chemotherapy for HL, which of the main clinical benefit of prophylactic use of G-CSF?

A

It will reduce the risk of febrile neutropenia.

54
Q

Patient with AML is noted to have a TP3 mutation. What is the significance of this?

A

TP53 suggests a high risk molecular lesion.

55
Q

Auer rods are found in the bone marrow of most AML patients. If these are noted to abundant - which condition is suggested?

A

APML (acute promyelocytic leukaemia)

56
Q

Patient has AMl with positive TP53 mutation. What is the treatment?

A

Induction chemotherapy (for cytoreduction) followed by allogeneic HSCT.

57
Q

Patients with SLE and elevated homocysteine levels have higher risk of arterial or venous thrombus formation?

A

Arterial thrombosis.

58
Q

What % of immune thrombocytopenia case are idiopathic?

A

80%

59
Q

What is the relative risk of VTE in the following scenarios:

  1. Prothrombin gene mutation
  2. Hyperhomocysteinaemia
  3. Protein C or S deficiency
  4. Factor V Leiden (heterozygous)
  5. AT deficiency
  6. Malignancy
  7. Antiphospholipid antibodies
  8. Hospitalisation
  9. Post-partum
  10. Factor V Leiden (homozygous)
A
  1. Prothrombin gene mutation = 2
  2. Hyperhomocysteinaemia = 2
  3. Protein C or S deficiency = 3
  4. Factor V Leiden (heterozygous) = 5
  5. AT deficiency = 5
  6. Malignancy = 7
  7. Antiphospholipid antibodies = 9
  8. Hospitalisation = 10
  9. Post-partum = 14
  10. Factor V Leiden (homozygous) = 24
60
Q

Immunocompromised patient develops red cell aplasia leading to aplastic anaemia.

Which pathogen do you suspect?

A

Parvovirus B19

61
Q

Elderly patient presents with fever, weight loss and anorexia. She has splenomegaly. Bloods indices are unremarkable. Blood film is leukoerythroblastic and shows teardrop cells with occasional blasts.

Diagnosis?

A

Myelofibrosis - suggested by splenomegaly and tear drop cells.

62
Q

Elderly patient presents with fever, weight loss and anorexia. Bloods reveals increased basophils and myelocytes.

Diagnosis?

A

CML

MCQ knowledge (22 decks)

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