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MRCP Part 1 > Haem > Flashcards

Haem Flashcards

1
Q

Burkitt’s lymphoma translocation

A

Burkitt’s lymphoma - t(8:14)
c-myc gene translocation

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2
Q

t(8:14)

A

Burkitt’s lymphoma
the c-myc gene translocation

EBV virus

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3
Q

chronic myeloid leukaemia translocation

A

Translocation t(9;22) - philadelphia chromosome

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4
Q

follicular lymphoma translocation

A

The t(14;18) translocation causes increased BCL-2 transcription

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5
Q

warm AIHA antibody

A

IgG

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6
Q

cold AIHA antibody

A

IgM

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7
Q

G6PD deficiency drugs

A

Some drugs causing haemolysis:
anti-malarials: primaquine
ciprofloxacin
sulph- group drugs: sulphonamides, sulphasalazine, sulfonylureas

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8
Q

The presence of DIC without any underlying cause in a young patient suggests what disease

A

Acute promyelocytic leukaemia - t(15;17)

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9
Q

stain for sideroblastic anaemia

A

perl’s

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10
Q

Benign ethnic neutropaenia is common in which ethnic group?

A

black African and Afro-Caribbean ethnicity

  • requires no treatment
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11
Q

commonest inherited thrombophilia

A

factor v leiden

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12
Q

most common bacteria causing neutropenic sepsis

A

staph epidermis (from lines)

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13
Q

biochemical findings in tumour lysis syndrome

A

high potassium
high phospate
low calcium

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14
Q

reducing risk of tumour lysis syndrome

A

high risk - rasburicase
low risk - allopurinol

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15
Q

treatment of tumour lysis syndrome

A
  1. IV fluids
  2. rasburicase
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16
Q

test for hereditary spherocytosis

A

EMA test

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17
Q

most reliable screening test for hereditary angioedema

A

Low C4

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18
Q

What is the single most important factor in determining whether cryoprecipitate should be given?

A

low fibrinogen

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19
Q

inheritance pattern of hereditary angioedema

A

autosomal dominant

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20
Q

deficient in patients with hereditary angioedema?

A

C1-INH deficiency

C4 is the best screening test for hereditary angioedema in between attacks. A result of low C4 would support the diagnosis.

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21
Q

Meig’s syndrome

A

an ovarian fibroma associated with a pleural effusion and ascites

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22
Q

Woman with bone metastases-, most likely to originate from?

A

breast ca

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23
Q

Direct antiglobulin test

A

specific for autoimmune haemolytic anaemia

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24
Q

red cell abnormalities in lead poisoning

A

including basophilic stippling and clover-leaf morphology

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25
Q

Mantle cell lymphoma translocation

A

t(11;14) translocation

overexpression of cyclin D1, a protein that regulates cell cycle progression, leading to uncontrolled proliferation of B-cells in the mantle zone of lymph nodes.

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26
Q

reed sternberg cells

A

hodgkin’s lymphoma

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27
Q

Disproportionate microcytic anaemia -

A

beta-thalassaemia trait

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28
Q

most common symptom of super vena cava obstruction?

A

dyspnoea

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29
Q

mx of ITP vs TTP

A

ITP - steroids, IvIg, splenectomy

TTP - plasma exchange, steroids,

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30
Q

Acute promyelocytic leukaemia presentation

A

young people
DIC
thrombocytopenia

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31
Q

Acute promyelocytic leukaemia translocation

A

t(15;17) translocation

32
Q

what is mesna?

A

given with cyclophosphamide
to decrease its risk of causing haemorrhagic cystitits

33
Q

gold standard test for paroxysmal nocturnal haemoglobinuria

A

Flow cytometry for CD59 and CD55

34
Q

on what chromosome is alpha haemoglobin coded for?

A

16

35
Q

how does heparin work?

A

Heparins generally act by activating antithrombin III. Unfractionated heparin forms a complex which inhibits thrombin, factors Xa, IXa, XIa and XIIa.

LMWH however Forms a complex that only increases the action of antithrombin III on factor Xa

36
Q

blood film finding in CLL

A

blood film: smudge cells (also known as smear cells)

37
Q

most commonn leukaemia in adults?

A

CLLp

38
Q

pathophysiology of TTP

A

1) abnormally large and sticky multimers of von Willebrand’s factor cause platelets to clump within vessels

2) in TTP there is a deficiency of ADAMTS13 (a metalloprotease enzyme) which breakdowns (‘cleaves’) large multimers of von Willebrand’s factor

39
Q

Features of TTP

A

rare, typically adult females
fever
fluctuating neuro signs (microemboli)
microangiopathic haemolytic anaemia
thrombocytopenia
renal failure

40
Q

porphyria cutanea tarda (PCT) is associated with which virus?

A

hep C

41
Q

Systemic mastocytosis features

A

Systemic mastocytosis results from a neoplastic proliferation of mast cells

Features
urticaria pigmentosa - produces a wheal on rubbing (Darier’s sign)
flushing
abdominal pain
monocytosis on the blood film

Diagnosis
raised serum tryptase levels
urinary histamine

42
Q

reversal for bleeding on dabigatran?

A

idarucizumab to reverse

43
Q

reversal of apixaban or rivaroxaban.

A

Andexanet alfa is used for factor Xa inhibitors

44
Q

how to reverse heparin

A

Protamine is used

45
Q

what causes haemolytic uraemic syndrome?

A

E.coli O157: H7 is the strain causing haemolytic uraemic syndrome

46
Q

management PE/DVT in pregnancy?

A

LMWH

47
Q

Ann-Arbour Staging

A

Stage
I: single lymph node
II: 2 or more lymph nodes/regions on the same side of the diaphragm
III: nodes on both sides of the diaphragm
IV: spread beyond lymph nodes

Each stage may be subdivided into A or B
A = no systemic symptoms other than pruritus
B = weight loss > 10% in last 6 months, fever > 38c, night sweats (poor prognosis

48
Q

Hodgkin’s lymphoma management

A

1) chemotherapy is the mainstay of treatment. Two combinations may be used:
- ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine): considered the standard regime
- BEACOPP (bleomycin, etoposide, doxorubicin, cyclophosphamide, vincristine, procarbazine, and prednisone): alternative regime with better remission rates but higher toxicity

2) radiotherapy

3) combined modality therapy (CMT)
chemotherapy followed by radiotherapy

4) hematopoietic cell transplantation
may be used for relapsed or refractory classic Hodgkin lymphoma

49
Q

blister cells

A

G6PD defiency (also bite cells)

50
Q

Waldenstrom’s macroglobulinaemi features

A

Features
systemic upset: weight loss, lethargy
hyperviscosity syndrome e.g. visual disturbance
the pentameric configuration of IgM increases serum viscosity
hepatosplenomegaly
lymphadenopathy
cryoglobulinaemia e.g. Raynaud’s

51
Q

CD markers for hodgkins

A

Reed-Sternberg cells are classically CD15 and CD30 positive.

52
Q

low ADAMTS13 level

A

A low ADAMTS13 level would confirm the diagnosis of TTP.

53
Q

TRALI is differentiated from TACO by?

A

hypotension = TRALI
hypertension = TACO

54
Q

Drug-induced thrombocytopenia

A

quinine
abciximab
NSAIDs
diuretics: furosemide
antibiotics: penicillins, sulphonamides, rifampicin
anticonvulsants: carbamazepine, valproate
heparin

55
Q

he development of necrotic skin lesions in this patient after being switched to warfarin

A

warfarin-induced skin necrosis (WISN). WISN is characteristically associated with Protein C deficiency.

56
Q

before starting the patient on eculizumab for paroxysmal nocturnal hemoglobinuria, what supportive measure must be given

A

eculizumab, a monoclonal antibody that inhibits terminal complement activation (C5-C9) which prevents complement-mediated intravascular haemolysis.

C5-9 deficiency predisposes to Neisseria meningitidis infections

give vaccine for Neisseria meningitidis

57
Q

APML is treated with ?

A

all-trans retinoic acid (ATRA) to force immature granulocytes into maturation to resolve a blast crisis prior to more definitive chemotherapy.

58
Q

Dentistry in warfarinised patients -

A

check INR 72 hours before procedure, proceed if INR < 4.0§

59
Q

Leukaemoid reaction vs Chronic myeloid leukaemia reaction

A

Leukaemoid reaction:
high leucocyte alkaline phosphatase score
toxic granulation (Dohle bodies) in the white cells
‘left shift’ of neutrophils i.e. three or fewer segments of the nucleus

Chronic myeloid leukaemia:
low leucocyte alkaline phosphatase score

60
Q

The most common malignancy associated with acanthosis nigricans
is

A

gastrointestinal adenocarcinoma

61
Q

haemophilia types and deficiencies

A

Haemophilia A is due to a deficiency of factor VIII whilst in haemophilia B (Christmas disease) there is a lack of factor IX

62
Q

Myelofibrosis - most common presenting symptom -

A

lethargy

63
Q

acute vaso-occlusive crisis in sickle cell disease - diagnosis

A

clinical

64
Q

Screening for haemochromatosis
general population

A

transferrin saturation

65
Q

CLL investigation of choice

A

immunophenotyping with flow cytometry

66
Q

with recurrent DVT/PE, when to consider inferior vena caval filters

A

increasing target INR to 3-4 for long term high-intensity oral anticoagulant therapy
or
switching treatment to LMWH.’

67
Q

Polycythaemia rubra vera progresses to?

A

around 5-15% progress to myelofibrosis or AML

68
Q

Hodgkin’s lymphoma - most common type

A

nodular sclerosing

69
Q

mx
Essential thrombocytosis

A

myeloproliferative disorder

hydroxyurea (hydroxycarbamide) is widely used to reduce the platelet count\

interferon-α is also used in younger patients

low-dose aspirin may be used to reduce the thrombotic risk

70
Q

inheritance of haemophilia

A

X-linked recessive condition

71
Q

CML Indications for treatment

A

progressive marrow failure: the development or worsening of anaemia and/or thrombocytopenia

massive (>10 cm) or progressive lymphadenopathy

massive (>6 cm) or progressive splenomegaly

progressive lymphocytosis: > 50% increase over 2 months or lymphocyte doubling time < 6 months

systemic symptoms: weight loss > 10% in previous 6 months, fever >38ºC for > 2 weeks, extreme fatigue, night sweats

autoimmune cytopaenias e.g. ITP

basically, if asymptomatic, no need to treat

72
Q

what kind of autoimmune haemolytic anaemia occurs in with chronic lymphocytic leukaemia

A

Warm autoimmune haemolytic

73
Q

Philadelphia translocation, t(9;22) impact on prognosis

A

Philadelphia translocation, t(9;22) - good prognosis in CML, poor prognosis in AML + ALL

74
Q

CD Receptor for Epstein-Barr virus

A

CD 21

75
Q

differentiating Hodgkin’s lymphoma from non-Hodgkin’s

A

NonHodgkin’s lymhpoma is more common - extra nodal disease more common

** except in younger females, Hodgkins is more common!

Hodgkin’s lymphoma can experience alcohol-induced pain in the node

‘B’ symptoms typically occur earlier in Hodgkin’s lymphoma and later in non-Hodgkin’s lymphoma

76
Q

lymphoma in mediastinum is most likely to be which subtype

A

hodgkins

77
Q

anti phospholipid syndrome mx

A

primary thromboprophylaxis
low-dose aspirin

secondary thromboprophylaxis
initial venous thromboembolic events: lifelong warfarin with a target INR of 2-3

recurrent venous thromboembolic events: lifelong warfarin; if occurred whilst taking warfarin then consider adding low-dose aspirin
increase target INR to 3-4
arterial thrombosis should be treated with lifelong warfarin with target INR 2-3

LMWH if planning pregnancy

MRCP Part 1 (21 decks)

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