Cancer care and Haematology Flashcards

Emergencies ✔ Complications of tx ✔ Haem ✔ Treatments - Gynae ca - colorectal ca -

1
Q

What are poor prognostic features in AML?

A

> 60 y/o
20% blasts after first course of chemo
Cytogenetics- deletion of chromosome 5 or 7

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2
Q

What conditions can progress to AML?

A

Myeloproliferative disorder
CML can convert to AML

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3
Q

What is the common pc of AML?

A

Related to bone marrow failure. Most common sign is bleeding e.g. of the gums

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4
Q

What is a classic sign of AML on myeloperoxidase staining?

A

Auer rods

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5
Q

What chromosome is commonly present in patients with CML, and why?

A

Philadelphia chromosome
Due to translocation(9:22)

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6
Q

At what age do people tend to present with CML?

A

Median is middle aged, 40-50

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7
Q

What is the first line management of CML?

A

Imatinib (TK inhibitor)

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8
Q

What gene does the philadelphia chromosome code for?

A

BCR-ABL
Codes for a fusion protein that has excessive tyrosine kinase activity

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9
Q

What are the most common signs of CML?

A

B symptoms
Massive splenomegaly
Bleeding
Gout

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10
Q

What finding on blood film indicates a diagnosis of CLL?

A

Smudge cells/ smear cells

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11
Q

What is Richter’s transformation?

A

CLL -> non hodgkins lymphoma
Leukaemia cells enter the lymph node and change into a high grade lymphoma, often diffuse large b cell

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12
Q

How does Richter’s transformation present?

A

Pt becomes very unwell, quickly.
Lymph node swelling
Fever without infection
Weight loss and night sweats
N+V
Abdo pain

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13
Q

What are the possible complications of CLL?

A

Anaemia
Hypogammaglobulinaemia causing recurrent infections
Warm autoimmune haemolytic anaemia
Richter’s transformation

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14
Q

What haematological cancer is most common in children?

A

ALL
Acute lymphoblastic leukaemia

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15
Q

What are the risk factors for Hodgkin’s lymphoma?

A

HIV
EBV

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16
Q

What does alcohol induced lymph node indicate a diagnosis of?

A

Hodgkin’s lymphoma
Although it is present in <10% of pts

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17
Q

What are the risk factors for ALL?

A

Down’s syndrome
Klinefelter’s syndrome
Fanconi anaemia
Ionizing radiation

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18
Q

Is CNS involvement more commom in ALL or AML?

A

ALL>AML
E.g. CN palsies, meningism

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19
Q

What are the similarities and differences between aplastic anaemia and ALL?

A

Both lead to pancytopenia.
Aplastic anaemia- bone marrow is hypocellular
ALL- bone marrow is hypercellular with lymphoblasts

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20
Q

How is ALL treated and response measured?

A

Combined chemo plus maintenance chemo for 2 years
Blast count in bone marrow
Using PCR of bone marrow cells to assess minimal residual disease (MRD)

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21
Q

How are the CNS symptoms of ALL treated/prevented?

A

Intrathecal chemo
Intrathecal CNS prophylaxis

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22
Q

What are the poor prognostic factors in ALL?

A

Age <1 or >10
Male
Higher pretreatment WCC
CNS disease
T ALL worse than B ALL

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23
Q

What are the similarities and differences between aplastic anaemia and AML?

A

Both lead to pancytopenia.
Aplastic anaemia- bone marrow is hypocellular
ALL- bone marrow is hypercellular with myeloid blasts

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24
Q

What is CLL?

A

Chronic lymphocytic leukaemia
Mature B cell neoplasm characterised by the accumulation of monoclonal B lymphocytes in the blood, bone marrow, and lymphoid tissues.
They accumulate as they survive a long time and crowd out other cells, not due to rapid proliferation.

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25
Q

How does CLL present?

A

Usually asymptomatic - incidental finding of lymphocytosis
Can have b symptoms, hepatosplenomegaly and non tender lymphadenopathy etc.
Bone marrow failure features are less common

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26
Q

What are some differentials for CLL?

A

Hairy cell leukaemia
Small lymphocytic lymphoma

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27
Q

How are smudge cells created?

A

Cells are damaged as the film is made because they lack a cytoskeletal protein

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28
Q

What are the consequences of a very high white cell count, and in what haematological cancer is this most common?

A

Visual disturbance
Confusion
Priapism
Deafness
Most common (WCC>500) in CML

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29
Q

What are some differentials for CML?

A

Reactive leukocytosis (no philadelphia chromosome)
Polycythemia vera (mainly affects RBC)

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30
Q

What is the most important premalignant paraproteinaemia?

A

MGUS- monoclonal gammopathy of unknown significance

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31
Q

What is a paraprotein?

A

An abnormal protein that is produced by clonal plasma cells in the bone marrow. Usually an intact immunoglobulin (IgM/G/A more common).

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32
Q

What are the risk factors for myelodysplastic syndrome?

A

Advance age- most significant rf
Genetic predisposition
Chemo or radiation therapy
Toxins e.g. benzene - rubber/printers/gas station etc.

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33
Q

What is myelodysplasia?

A

AKA myelodyplastic syndrome
Group of bone marrow disorders characterized by ineffective haematopoiesis, leading to cytopaenias and dysplastic changes in blood cells

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34
Q

How is MDS managed?

A

Supportive- blood transfusions, abx when needed, growth factors
Stem cell transplant
Hypomethylating agents may slow progression to AML

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35
Q

What is multiple myeloma?

A

Plasma cell dyscrasia characterised by abnormal clonal proliferation of plasma cells (post germinal b cells)

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36
Q

What are the clinical features of MM?

A

CRABBI
Calcium >2.6 (normal ALP)
Renal failure
Anaemia
Bone pain and lytic lesions
Bleeding
Infection

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37
Q

How is a diagnosis of myeloma confirmed?

A

Plasma cells >10% in bone marrow

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38
Q

What may be seen on blood film to indicate MM?

A

Rouleaux- stacked RBC

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39
Q

What may cause acute SOB in a patient with existing cancer?

A

Anxiety
Pneumonia
Lung collapse
Pleural effusions
Radiation pneumonitis
Anaemia
PE
SVCO

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40
Q

What may cause N+V in a patient with existing cancer?

A

Treatment related - chemo, RT
Progression of disease e.g. causing bowel obstruction
Inner ear problems
Metabolic disturbance- uraemia, hypercalcaemia, hyperuricaemia
Infection
Anxiety/Anticipatory vomiting

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41
Q

What may cause confusion in a patient with existing cancer?

A

Metabolic disturbance- hypercalcaemia, hypoglycaemia
Infection - LRTI, UTI
Anaemia
Mets to brain
Intense pain
ADR of pain medication

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42
Q

What types of obstruction can be caused by a tumour

A

Bowel
Biliary tree- jaundice, ascites
Ureteric- hydronephrosis=AKI
Urethra- LUTS
Bronchial- SOB
Lymph node- lymphoedema of arms or legs

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43
Q

How is bowel obstruction managed (in a pt with cancer)

A

Usually drip and suck and surgical removal
Alt:
Antiemetics- cyclizine slows upper GI, hyoscine butylbromide reduced secretions, ocreotide reducd secretions
Dexamethasone 16mg reduces oedema short term

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44
Q

How can cancer cause GI bleed?

A

Perforation of obstruction
Infiltration of GI tract blood vessels
N+V leading to mallory weiss tear
Oesophageal varices bleed

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45
Q

How does hypercalcaemia present?

A

Painful Bones
Renal Stones
Thrones- polyuria, constipation
Abdominal Groans - GI symptoms: Nausea, Vomiting, Constipation, Indigestion
Psychiatric Undertones– Effects on nervous system: lethargy, fatigue, memory loss, psychosis, depression

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46
Q

How is hypercalcaemia managed?

A

IV fluids
Bisphosphonates (caution in low eGFR)
Symptom control- haloperidol

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47
Q

What can cause ascites in the context of cancer?

A

Peritoneal spread
Liver spread or primary tumour

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48
Q

What investigations are done in suspected MSCC?

A

Urgent whole spine MRI within 24 hours
B12/folate
Bladder scan

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49
Q

How is MSCC managed?

A

Alert MSCC team
Surgical decompression within 48 hours of presenting.
Dexamethasone 16 mg STAT and then daily (with PPI cover) is indicated, if high clinical suspicion, or confirmed on MRI.
Ask the patient not to move until the spine is confirmed to be stable on MRI.
Palliative radiotherapy if surgical decompression inappropriate.

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50
Q

What are the differentials for a cancer pt presenting with back pain?

A

MSCC
Pathological #
MSK pain
Bone mets

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51
Q

What can cause raised ICP in a cancer pt?

A

Brain mets
SVCO
Cavernus sinus thrombosis

52
Q

What can cause status epilepticus in a cancer pt?

A

Brain mets
Raised ICP
Tumour lysis - raised urea and hypocalcaemia

53
Q

What is the eponymous test for SVCO?

A

Pemberton’s test

54
Q

What are the signs and symptoms of SVCO?

A

SOB
Facial plethora- red and swollen face and arm
Dilated/engorged veins
Headache
Vision changes due to raised ICP and papilloedema

Hypotension

55
Q

How is SVCO managed?

A

Dexamethasone 16mg STAT
Stenting
Radiotherapy

56
Q

How is DVT/PE managed in active cancer?

A

Oxygen
DOAC (used to be LMWH) to prevent further/multiple PEs
Lifelong treatment

57
Q

What are the different WHO performance classifications?

A

0: able to carry out all normal activity without restriction
1: restricted in strenuous activity but ambulatory and able to carry out light work
2: ambulatory and capable of all self-care but unable to carry out any work activities; up and about more than 50% of waking hours
3: symptomatic and in a chair or in bed for greater than 50% of the day but not bedridden
4: completely disabled; cannot carry out any self-care; totally confined to bed or chair.

58
Q

What conditions does MEN1 predispose to?

A

Hyperparathyroidism
Endocrine pancreatic tumours
Pituitary tumours- prolactinoma

59
Q

What are the different pancreatic endocrine tumours and the cells affected?

A

G cell- gastrinoma (Zollinger-Ellison)
A Islets- glucagonoma
B Islets- Insulinoma
δ(delta) Islet- somatostatinoma
Non islets- vasoactive intestinal peptidoma

60
Q

What is the tumour marker for pancreatic cancer? And how is it used?

A

CA 19-9
(best for monitoring response to treatment, poor specificity for initial diagnosis)

61
Q

What is the curative management of pancreatic cancer?

A

Radical resection
Head of pancreas- Whipple’s/pancreaticoduodenectomy
Body or tail- distal pancreatectomy and splenectomy

62
Q

What genetic mutations can predispose individuals to colorectal cancer?

A

FAP- mutation of APC gene
HNPCC- DNA mismatch repair gene leads to Lynch syndrome

63
Q

What are the risk factors for colorectal cancer?

A

Increasing age
Male
FMH
IBD
Low fibre diet
Smoking
Alcohol
High processed meat intake

64
Q

Who should be referred for bowel cancer 2WW?

A

> /=40 with weight loss and abdo pain
/=50 with PR bleed
/=60 with change in bowel habit or anaemia

65
Q

How may a colorectal cancer presenting with bowel obstruction be relieved?

A

Decompressing colostomy
Endoscopic stenting

66
Q

What are the risk factors for anal cancer?

A

HPV infection (16 and 18)
HIV
Increasing age
Smoking
Immunosuppression
Crohn’s disease

67
Q

What is the MoA of tranexamic acid?

A

Inhibits plasminogen activation and reduces fibrinolysis

68
Q

What are the causes of aplastic anaemia?

A

Idiopathic
Inherited e.g. fanconi anaemia
Acquired:
Viral infection e.g. hepatitis
Autoimmune
Pregnancy
Environmental exposures e.g. benzene
Medications e.g. phenytoin, chloramphenicol

69
Q

What are the two main long term managements of sickle cell disease?

A

Hydroxyurea/hydroxycarbamide (increase fetal Hb), prophylaxis of acute episodes
Pneumococcal vaccine every 5 yrs

70
Q

What is seen on blood film in B12 deficiency?

A

Hypersegmented polymorphs

71
Q

What is VWf and what are the functions of Von Willebrand factor?

A

Glycoprotein that promotes platelet adhesion to damaged endothelium
Carried molecule for factor VIII

72
Q

What does a low reticulocyte count indicate?

A

Bone marrow suppression

73
Q

What are the complications of sickle cell disease?

A

Vaso-occlusive crisis
Aplastic crisis
Acute chest crisis
Hyposplenism
CKD
Retinopathy

74
Q

What are the types of inherited haemolytic anaemias?

A

membrane: hereditary spherocytosis/elliptocytosis
metabolism: G6PD deficiency
haemoglobinopathies: sickle cell, thalassaemia

75
Q

What are the types of acquired, Coombs +ve, haemolytic anaemias?

A

COOMBS +ve = immune causes
Autoimmune
Alloimmune- transfusion reaction, haemolytic disease of the newborn
Drugs- methyldopa, penicillin

76
Q

What are the types of acquired, Coombs -ve, haemolytic anaemias?

A

Coombs -ve = non immune causes
Microangiopathic haemolytic anaemia- TTP/HUS, DIC, malignancy, pre-eclampsia
Prosthetic heart valves
Paroxysmal nocturnal haemoglobinuria
Infections: malaria
Drug: dapsone
Alcohol binge

77
Q

What is the MoA of clopidogrel?

A

Inhibits ADP receptors, irreversibly acting on P2Y12 receptors on platelets
Prevents platelet aggregation

78
Q

What is the MoA of heparin?

A

Activates antithrombin
Inc inaction of factor IIa, IXa, Xa

79
Q

What is the MoA of warfarin?

A

Competitively inhibits vitamin K

80
Q

What clotting factors are vitamin K dependent?

A

Factors II, VII, IX, X, protein C and S

81
Q

What does isolated rise in GGT in the context of a macrocytic anaemia suggest?

A

Alcoholism as cause

82
Q

What is a complication and a c/i of hydroxycarbamide?

A

Increased risk of infection
Advised not to take in pregnancy

83
Q

What do Target cells and Howell-Jolly bodies indicate?

A

Hyposplenism

84
Q

What are some of the differences between G6PD deficiency and hereditary spherocytosis (Hx, blood film, Ix)?

A

Both: hx of gallstones

G6PD deficiency:
X linked recessive
Hx of infection/drugs/fava beans precipitating haemolysis.
Blood film- heinz bodies
Diagnosis- measure activity of G6PD enzymes (3 months after acute haemolysis)
Hereditary spherocytosis:
Autosomal dominant
Hx of splenomegaly
Blood film spherocytes
Diagmosis with EMA binding test

85
Q

In patients with both vitamin B12 and folate deficiencies, what should be replaced first and why?

A

B12
To avoid subacute degeneration of the cord

86
Q

What is a typical blood picture in DIC (platelets and clotting)

A

Platelets reduced
Fibrinogen reduced
PT prolonged
APTT prolonged

87
Q

What may be seen on blood film in DIC?

A

Schistocytes

88
Q

What are the risk factors for developing tumour lysis syndrome?

A

Haematological malignancy
Large tumour burden
Chemosensitive tumours
Recent chemotherapy

89
Q

What are the electrolyte imbalances seen in tumour lysis syndrome?

A

Increased:
Uric acid
Phosphate
Potassium
Creatinine

Decreased:
Calcium

90
Q

What does the tumour marker CA19-9 represent?

A

Raised in
Pancreatic cancer
Gastric cancer
Hepatobiliary cancer

91
Q

What is a specific ADR of bleomycin?

A

Pulmonary fibrosis

92
Q

What are specific ADRs of platinum agents?

A

Cisplatin- Nephrotoxicity and ototoxicity
All platinum agents e.g. carboplatin- peripheral neuropathy and sensorineural hearing loss

93
Q

What are specific ADRs of cyclophosphamide?

A

Haemorrhagic cysts- mild freq, frank haematuria
TCC of the bladder

94
Q

What chemotherapy drugs cause cardiomyopathy?

A

Doxorubicin, anti HER2 mabs e.g. herceptin

95
Q

What are specific ADRs of methotrexate?

A

Nephrotoxic
Myelosuppression

96
Q

What is a specific ADR of vincristine?

A

Peripheral neuropathy

97
Q

What is a specific ADR of asparagine?

A

Neurotoxicity

98
Q

What are some early ADRs of radiotherapy?

A

Fatigue- most common
N+V
Hair loss
Oral mucositis
Cystitis
Proctitis
Dermatitis
Oesophagitis
Pneumonitis (-itis can be late signs, present up to 18 months after RT)

99
Q

What are some late ADRs of radiotherapy?

A

Skin pigmentation changes
Pulmonary fibrosis
Infertility
Secondary cancers
Constrictive pericarditis
Dysphagia
Pulmonary fibrosis
Bowel strictures/adhesions/fistulas

100
Q

What cells do head and neck cancers most commonly arise from?

A

Squamous cells

101
Q

What are the risk factors for H+N cancers?

A

Tobacco use
Alcohol
HPV
EBV

102
Q

What are the symptoms that warrant a 2WW referral for suspected laryngeal cancer?

A

Persistent unexplained hoarseness
Unexplained lump in neck, over 45

103
Q

What are the symptoms that warrant a 2WW referral for suspected oral cancer?

A

Persistent, unexplained ulceration >3wks
A red or red and white patch in the oral cavity (erythro/erythroleukoplakia)
Unexplained lump in the neck

104
Q

What are the symptoms that warrant a 2WW referral for suspected thyroid cancer?

A

Unexplained thyroid lump

105
Q

What can cause a raised PSA?

A

Prostate cancer
UTI
Prostatitis
BPH
Acute urinary retention

106
Q

What are the risk factors for TCC of the bladder?

A

Smoking
Aromatic amines
Cyclophosphamide

107
Q

What are the risk factors for SCC of the bladder?

A

Schistosomiasis infection
Long term catheterisation
Recurrent bladder stones

108
Q

What are the management options for muscle invasive bladder cancer?

A

Stage T2 and above:
Radical cystectomy with urinary diversion (ileal conduit or neobladder)

109
Q

What are the management options for non muscle invasive bladder cancer?

A

CIS, Ta, T1:
TURBT
Mitomycin C chemo
BCG immunotherapy

110
Q

What are the initial imaging investigations for bladder ca?

A

CT urogram
Flexible cystoscopy

111
Q

What are the tumour markers in testicular cancer?

A

AFP (specific to seminomas)
bHCG
LDH

112
Q

Q
What are the most common types of testicular cancer and in what age groups?

A

Seminoma. Seen in ~35y/o
Non seminoma- Teratoma most common. Seen in ~25 y/o

113
Q

What are the risk factors for cervical cancer?

A

HPV 16 and 18
Early first sex
Multiple partners
Smoking
HIV
Non compliance with cervical screening

114
Q

What are the risk factors for ovarian cancer?

A

Obesity
Early menarche/late menopause
Nulliparity
Unopposed oestrogen e.g. Tamoxifen
Family history
Previous breast or ovarian cancer
BRCA ½
Endometriosis

115
Q

What are the risk factors for endometrial cancer?

A

(excessive oestrogen = overstim endometrium)
Obesity
Early menarche/late menopause
Nulliparity
PCOS
Unopposed oestrogen e.g. Tamoxifen
Previous breast or ovarian cancer
BRCA ½
Endometrial polyps
Diabetes Mellitus
Parkinson’s

116
Q

What factors are protective for endometrial cancer?

A

Continuous combined HRT
COCP
Smoking
Physical activity

117
Q

What factors are protective for ovarian cancer?

A

COCP
Pregnancy
Breast feeding
Hysterectomy
Oophorectomy

118
Q

What are the risk factors for vulvar cancer?

A

HPV
Herpes Simplex Virus Type 2
Smoking
Immunosuppression
Chronic vulvar irritation
Conditions such as Lichen Sclerosus

119
Q

What is the most common type of non invasive breast cancer, and what does it show on mammogram?

A

DCIS
Macrocalcifications

120
Q

What are the risk factors for breast cancer?

A

Female
Increased age
BRCA1/2
FMH - first degree relatives
Obesity
Alcohol
Unopposed oestrogen (early menarche, late menopause, nulliparity, COCP or HRT)

121
Q

What is a triple assessment in breast cancer?

A

-history and examination
-imaging
-histology

122
Q

What is the most common type of breast cancer?

A

Invasive ductal carcinoma

123
Q

What is the most common type of thyroid cancer?

A

Papillary thyroid cancer

124
Q

What are the routes in which a tumour may metastasize?

A

Haematogenous
Local spread
Lymphatic

125
Q

What are the possible complications of heparin infusion?

A

Haemorrhage
Heparin induced thrombocytopenia
Osteoporosis with long term use

126
Q

What clotting factors are involved in the intrinsic pathway?

A

VIII, IX, XI, XII
8,9,11,12

127
Q

What clotting factors are involved in the extrinsic pathway?

A

III and VII
3, 7