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Y3 MedEd > Cancer and Bleeding Disorders > Flashcards

Cancer and Bleeding Disorders Flashcards

1
Q

Which cells are granulocytes (3)

A

Basophils, eosinophils, neutrophils

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2
Q

Which cells are myeloid cells (5)

A

Granulocytes (basophils, eosinophils, neutrophils) platelets and RBC

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3
Q

What triad do acute leukaemias cause

A

Anaemia (↓ Hb): fatigue, pallor, breathlessness

Neutropenia (↓ neutrophils): recurrent infections

Thrombocytopenia (↓ platelets): bleeding and easy bruising

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4
Q

What are the effects of bone marrow failure

A

Anaemia (↓ Hb): fatigue, pallor, breathlessness

Neutropenia (↓ neutrophils): recurrent infections

Thrombocytopenia (↓ platelets): bleeding and easy bruising

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5
Q

RF AML (4)

A

Down’s, irradiation, anti-cancer drugs, age (incidence ↑ with age)

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6
Q

Which disease shows Auer rods on a blood film

A

AML

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7
Q

What is seen on blood film in AML (2)

A

Auer rods and accumulation of myeloblast cells

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8
Q

What is promyelocytic leukaemia a subtype of

A

Subtype of AML

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9
Q

What is promyelocytic leukaemia associated with

A

DIC

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10
Q

What is the most common type of ALL

A

¾ are B cell ALL

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11
Q

Which cells are particularly deficient in AML

A

Granulocytes (neutrophils, basophils, eosinophils)

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12
Q

Which cells are particularly deficient in ALL (4)

A

B lymphocytes (and plasma cells), T lymphocytes and NK cells but most ALL’s are B lymphocyte form

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13
Q

Which is the commonest cancer of childhood

A

ALL

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14
Q

What does ALL present with

A

Bone marrow failure symptoms
Organ infiltration:
hepatosplenomegaly, enlarged lymph notes, swollen testes

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15
Q

When does ALL present with a thymus mass

A

T cell ALL

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16
Q

What are the blood results of ALL (3)

A

↑↑ WCC, ↓ Hb, ↓ plts

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17
Q

What is seen in the BM film of ALL

A

BM film: >20% lymphoblasts

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18
Q

What accumulates in CLL

A

Accumulation of mature incompetent lymphocytes (unable to undergo apoptosis)

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19
Q

What happens in the bone marrow of CLL patients

A

BM becomes infiltrated by small, nomoformic B cells, meaning patients will start to develop symptoms and signs of BM failure

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20
Q

Symptoms of CLL

A

Symptoms of BM failure: recurrent infections (including herpes zoster), sx of anaemia, easy bruising/bleeding

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21
Q

Examination of CLL (2)

A

O/E: enlarged non-tender lymphadenopathy, hepatosplenomegaly

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22
Q

Blood results of CLL (4)

A

Bloods: ↑ lymphocytes, ↓ Hb, ↓ neutrophils, ↓ platelets

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23
Q

Blood film of CLL

A

smear/smudge cells

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24
Q

In which disease is smear/smudge cells seen in

A

CLL

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25
Q

Associations of CLL

A

AI thrombocytopenia and anaemia (Evan’s syndrome)

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26
Q

What is Evan’s syndrome

A

AI thrombocytopenia and anaemia

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27
Q

What can CLL become

A

aggressive NHL = Richter’s syndrome

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28
Q

What happens in CML

A

Uncontrolled proliferation of granulocyte precursors in BM but slower progression than AML

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29
Q

Symptoms of CML (think about the ways it manifests (3))

A

Up to 50% are asymptomatic
Hypermetabolic symptoms: weight loss, malaise, sweating
Hyperviscosity symptoms: visual disturbance, headaches, thrombotic event
Gout
Same triad: anaemia, thrombocytopenia, neutropenia

MASSIVE splenomegaly in 90%

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30
Q

Which cancer is the Philadelphia chromosome associated with

A

CML

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31
Q

Do you see splenomegaly in acute leukaemias and why

A

Splenomegaly does not have time to form in acute leukaemias

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32
Q

What is seen in the FBC of CML

A

↑↑ WCC (often >100 x109)

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33
Q

What happens in Hodgkin’s lymphoma

A

Malignant proliferation of lymphocytes, accumulate in LNs  lymphadenopathy

34
Q

Age of presentation of Hodgkin’s lymphoma

A

Bimodal age distribution peaks in 20-30 and >50y

35
Q

What is Hodgkins lymphoma associated with

A

50% of cases associated with EBV infection

36
Q

Presentation of Hodgkin’s lymphoma (5)

A

Painless enlarging mass (most often in neck, occasionally axilla or groin)
May become painful after alcohol ingestion
B symptoms

37
Q

What are B symptoms (3)

A

fevers >38, night sweats, weight loss (>10% in last 6 months)

38
Q

What is seen on examination of Hodgkins lymphoma (3)

A

non tender firm rubbery lymphadenopathy, splenomegaly +/- hepatomegaly

39
Q

Ix for Hodgkins lymphoma

A

Lymph node biopsy under microscopy = Reed Sternberg cells

40
Q

What type of cell is seen in Hodgkins lymphoma

A

Reed-Sternberg

41
Q

What are Reed-Sternberg cells seen in

A

Hodgkins lymphoma

42
Q

What is non-Hodgkins lymphoma

A

Malignancy of lymphoid cells originating in LNs without Reed Sternberg cells

43
Q

Which cells are involved in non-Hodgkins lymphoma

A

85% are B cell

15% are T cell or NK cell

44
Q

Associations of non-Hodgkins’ lymphoma (5)

A

Associated with EBV, HIV, SLE, Sjogren’s

↑ with age

45
Q

Age of non-Hogkins lymphoma

A

Increases with age

46
Q

Presentation of non-Hodgkins lymphoma

A

Painless enlarging mass in neck, axilla or groin
Systemic symptoms (less common than in HL): weight loss, night sweats, fever
Organ involvement (more common than in HL): skin rashes, headache hepatosplenomegaly, sore throat, cough
Signs of BM failure: anaemia, neutropenia, thrombocytopenia

47
Q

Differences between HL and NHL

A

No Reed-Sternberg cells in NHL
Hodgkins - pain after drinking
NHL is also associated with HIV, SLE and Sjogrens as well as EBV (HL is only EBV)
Systemic symptoms (less common in NHL than in HL):
Organ involvement (more common NHL than in HL)

48
Q

What is Burkitt’s lymphoma

A

Subtype of NHL (B cell):

African child

Large LN in the jaw (fast-growing)

Under microscopy: starry sky appearance

49
Q

What happens in MM

A

Haematological malignancy characterised by proliferation of plasma cells + production of a monoclonal immunoglobulin (usually IgG or IgA)

50
Q

MM epidemiology - age and race

A

> 70 years. Afrocarribeans > Caucasians > Asians

51
Q

RFs of MM (4)

A

ionizing radiation, HIV, agricultural work, occupational chemical exposure e.g. benzene, herbicides

52
Q

S/s symptoms of MM (4)

A

↑ Ca  tired, thirsty, polyuria, nausea, constipation

Renal impairment  Ig and its fragments (light chains) deposit in the kidney – present in 20% at diagnosis (associated with worse prognosis)

Anaemia (+ neutropenia, thrombocytopenia) due to marrow infiltration by plasma cells. Also get recurrent bacterial infections due to low levels of other Ig

Bone pain/lesions: increased osteoclast activation due to myeloma cell signaling  back/rib pain

53
Q

What is MGUS

A

Monoglonal gammopathy of unknown significance:

Pre-malignant condition – accumulation of some monoclonal plasma cells
1% acquire additional mutations  MM

54
Q

Ix for MM (5)

A

Serum/urine electrophoresis
Bence Jones proteins

Bloods
↑ ESR, ↑CRP, ↑ urea/Cr, ↑ Ca, ALP normal

Blood film: rouleax formation

Serum MONOCLONAL protein >30g/L

BM aspirate = ↑ plasma cells (>10%)

55
Q

What is seen in the blood film of MM

A

Rouleaux

56
Q

What disease is rouleaux seen in in the blood film

A

MM

57
Q

What is seen in the bloods of MM (5)

A

ESR, ↑CRP, ↑ urea/Cr, ↑ Ca, ALP normal

58
Q

What is pathognomic of MM

A

Bence Jones serum/urine electrophoresis

59
Q

What is the difference in bloods between MM and malignancy

A

In malignancy you get high Ca with HIGH ALP

MM high calcium with NORMAL ALP

60
Q

Which factor is deficient in Haemophilia A

A

Factor 8

61
Q

Which factor is deficient in Haemophilia B

A

Factor 9

62
Q

What form of inheritance are haemophilias

A

X-linked recessive - typically affects boys

63
Q

When do haemophilias present

A

Early in life or after surgery trauma

64
Q

What is a haematoma

A

painful bleeding into muscles (increased pressure can lead to compartment syndrome or nerve palsies)

65
Q

What can haematomas lead to

A

increased pressure can lead to compartment syndrome or nerve palsies

66
Q

What is a haemarthrosis

A

after minimal trauma  swollen painful joints

67
Q

S/s of haemophilias

A 
Haemarthrosis
Haematomas
Haematuria
Excessive bruising/bleeding
Bruises
Joint deformity from haemarthrosis
Signs of IDA
68
Q

Is the APTT checking the intrinsic or extrinsic pathway

A

Intrinsic

69
Q

Is the PT checking the intrinsic or extrinsic pathway

A

Extrinsic

70
Q

Ix for haemophilias

A

prolonged APTT (intrinsic pathway); factor assay confirms diagnosis

71
Q

What does vWF do (3)

A

vWF is a protein involved in blood clotting:
Forms the bridge between the damaged subendothelium and the platelets (via the GP1b receptor)
Makes platelets bind to each other
Binds to factor 8 and prevents its degradation

72
Q

What receptor does vWF attach to platelets through

A

Gp1b

73
Q

Which factor does vWF bind to and what does it do to it

A

Binds to factor 8 and prevents its degradation

74
Q

What are 3 types of vWD and what are the inheritance types

A

Type 1: reduced levels of normal vWF (AD)
Type 2: defective vWF (AD)
Type 3: complete lack of vWF and highly reduced factor 8 (AR)

75
Q

Ix for wVD (6)

A

↑ APTT, ↑ bleeding time, ↓ vWF levels, N plts, normal PT, (↓ factor 8)

76
Q

Presentation of vWD

A

More superficial bleeding compared to haemophilias
Bruising, epistaxis, menorrhagia
Increased gum bleeding post tooth extraction
Prolonged bleeding from minor wounds

77
Q

When does DIC occur (4)

A

Occurs in sepsis (esp children with meningococcal septicaemia), trauma, obstetric complications, malignancy

78
Q

What should you be careful of in children with meningococcal septicaemia

A

DIC

79
Q

Signs of chronic DIC

A

signs of deep venous or arterial thrombosis or embolism

80
Q

Signs of acute DIC (7)

A

petechiae, purpura, ecchymoses, epistaxis, mucosal bleeding, hemorrhage, respiratory distress

81
Q

Ix for DIC (6)

A

FBC (↓ plts, ↓ Hb)
Clotting (↓ fibrinogen, ↑ PT/APTT, ↑ fibrin degradation products)
Peripheral blood film: schistocytes (MAHA)

82
Q

What is seen in the blood film of DIC

A

schistocytes

Y3 MedEd (34 decks)

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