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Y3 MedEd > Cancer and Bleeding Disorders > Flashcards

Cancer and Bleeding Disorders Flashcards

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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
Associations of CLL
AI thrombocytopenia and anaemia (Evan's syndrome)
26
What is Evan's syndrome
AI thrombocytopenia and anaemia
27
What can CLL become
aggressive NHL = Richter’s syndrome
28
What happens in CML
Uncontrolled proliferation of granulocyte precursors in BM but slower progression than AML
29
Symptoms of CML (think about the ways it manifests (3))
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%
30
Which cancer is the Philadelphia chromosome associated with
CML
31
Do you see splenomegaly in acute leukaemias and why
Splenomegaly does not have time to form in acute leukaemias
32
What is seen in the FBC of CML
↑↑ WCC (often >100 x109)
33
What happens in Hodgkin's lymphoma
Malignant proliferation of lymphocytes, accumulate in LNs  lymphadenopathy
34
Age of presentation of Hodgkin's lymphoma
Bimodal age distribution peaks in 20-30 and >50y
35
What is Hodgkins lymphoma associated with
50% of cases associated with EBV infection
36
Presentation of Hodgkin's lymphoma (5)
Painless enlarging mass (most often in neck, occasionally axilla or groin) May become painful after alcohol ingestion B symptoms
37
What are B symptoms (3)
fevers >38, night sweats, weight loss (>10% in last 6 months)
38
What is seen on examination of Hodgkins lymphoma (3)
non tender firm rubbery lymphadenopathy, splenomegaly +/- hepatomegaly
39
Ix for Hodgkins lymphoma
Lymph node biopsy under microscopy = Reed Sternberg cells
40
What type of cell is seen in Hodgkins lymphoma
Reed-Sternberg
41
What are Reed-Sternberg cells seen in
Hodgkins lymphoma
42
What is non-Hodgkins lymphoma
Malignancy of lymphoid cells originating in LNs without Reed Sternberg cells
43
Which cells are involved in non-Hodgkins lymphoma
85% are B cell | 15% are T cell or NK cell
44
Associations of non-Hodgkins' lymphoma (5)
Associated with EBV, HIV, SLE, Sjogren’s | ↑ with age
45
Age of non-Hogkins lymphoma
Increases with age
46
Presentation of non-Hodgkins lymphoma
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
Differences between HL and NHL
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
What is Burkitt's lymphoma
Subtype of NHL (B cell): African child Large LN in the jaw (fast-growing) Under microscopy: starry sky appearance
49
What happens in MM
Haematological malignancy characterised by proliferation of plasma cells + production of a monoclonal immunoglobulin (usually IgG or IgA)
50
MM epidemiology - age and race
>70 years. Afrocarribeans > Caucasians > Asians
51
RFs of MM (4)
ionizing radiation, HIV, agricultural work, occupational chemical exposure e.g. benzene, herbicides
52
S/s symptoms of MM (4)
↑ 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
What is MGUS
Monoglonal gammopathy of unknown significance: Pre-malignant condition – accumulation of some monoclonal plasma cells 1% acquire additional mutations  MM
54
Ix for MM (5)
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
What is seen in the blood film of MM
Rouleaux
56
What disease is rouleaux seen in in the blood film
MM
57
What is seen in the bloods of MM (5)
ESR, ↑CRP, ↑ urea/Cr, ↑ Ca, ALP normal
58
What is pathognomic of MM
Bence Jones serum/urine electrophoresis
59
What is the difference in bloods between MM and malignancy
In malignancy you get high Ca with HIGH ALP MM high calcium with NORMAL ALP
60
Which factor is deficient in Haemophilia A
Factor 8
61
Which factor is deficient in Haemophilia B
Factor 9
62
What form of inheritance are haemophilias
X-linked recessive - typically affects boys
63
When do haemophilias present
Early in life or after surgery trauma
64
What is a haematoma
painful bleeding into muscles (increased pressure can lead to compartment syndrome or nerve palsies)
65
What can haematomas lead to
increased pressure can lead to compartment syndrome or nerve palsies
66
What is a haemarthrosis
after minimal trauma  swollen painful joints
67
S/s of haemophilias
``` Haemarthrosis Haematomas Haematuria Excessive bruising/bleeding Bruises Joint deformity from haemarthrosis Signs of IDA ```
68
Is the APTT checking the intrinsic or extrinsic pathway
Intrinsic
69
Is the PT checking the intrinsic or extrinsic pathway
Extrinsic
70
Ix for haemophilias
prolonged APTT (intrinsic pathway); factor assay confirms diagnosis
71
What does vWF do (3)
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
What receptor does vWF attach to platelets through
Gp1b
73
Which factor does vWF bind to and what does it do to it
Binds to factor 8 and prevents its degradation
74
What are 3 types of vWD and what are the inheritance types
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
Ix for wVD (6)
↑ APTT, ↑ bleeding time, ↓ vWF levels, N plts, normal PT, (↓ factor 8)
76
Presentation of vWD
More superficial bleeding compared to haemophilias Bruising, epistaxis, menorrhagia Increased gum bleeding post tooth extraction Prolonged bleeding from minor wounds
77
When does DIC occur (4)
Occurs in sepsis (esp children with meningococcal septicaemia), trauma, obstetric complications, malignancy
78
What should you be careful of in children with meningococcal septicaemia
DIC
79
Signs of chronic DIC
signs of deep venous or arterial thrombosis or embolism
80
Signs of acute DIC (7)
petechiae, purpura, ecchymoses, epistaxis, mucosal bleeding, hemorrhage, respiratory distress
81
Ix for DIC (6)
FBC (↓ plts, ↓ Hb) Clotting (↓ fibrinogen, ↑ PT/APTT, ↑ fibrin degradation products) Peripheral blood film: schistocytes (MAHA)
82
What is seen in the blood film of DIC
schistocytes

Y3 MedEd (34 decks)

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