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4TH YEAR - CSIM2 > Cancer > Flashcards

Cancer Flashcards

1
Q

What causes cannonball lung mets?

A
  1. Testicular cancer
  2. Choriocarcinoma
  3. Renal carcinoma
  4. Thyroid cancer
  5. Melanoma
  6. Osteosarcoma
  7. Metastatic adenocarcinoma
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2
Q

What is the difference between ionising and non-ionising radiation?

A

Ionising

  • High energy
  • From x-rays, gamma rays
  • Has the ability to displace electrons from atoms

Non-ionising

  • Lower energy
  • From UV radiation (particularly B)
  • Has the ability to excite electrons, leading to a chemical change in the tissue
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3
Q

Which tissues are particularly susceptible to ionising radiation?

A

Breast, thyroid and bone marrow

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4
Q

What is xeroderma pigmentosum?

A

A condition in which the repair pathway for non-ionising radiation is faulty, leading to multiple melanomas from UVB exposure at a very young age

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5
Q

What will happen if you give a 16 year old radiotherapy for lymphoma?

A

She is likely to develop breast cancer later in life, due to the exposure to ionising radiation at a young age

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6
Q

What are the 3 steps of carcinogenesis?

A

INITIATION - mutation in key regulatory pathways
PROMOTION - selective growth advantage induced in the initiated cells (NB usually without mutation)
PROGRESSION - multiple mutations from genetic instability leading to further degrees of invasiveness

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7
Q

What cancers do tobacco smoke cause?

A

Anywhere!! Often lung, bladder

NOT endometrial

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8
Q

What cancers do dye/rubber cause?

A

Bladder cancer

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9
Q

What cancer does chemotherapy sometimes lead to?

A

AML

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10
Q

What cancer is schistoma associated with?

A

Bladder cancer

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11
Q

What cancer is malaria and EBV associated with?

A

Burkitts lymphoma

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12
Q

Which environmental factors can cause cancer?

A
  • Radiation
  • Chemicals
  • Infections
  • Hormones
  • Diet (most important RF?)
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13
Q

What cancer is related to:

a) prolonged oestrogen exposure
b) more ovulatory cycles

A

a) endometrial cancer, breast cancer

b) ovarian cancer

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14
Q

What is a germline mutation?

A

A mutation in a germ cell (testes/ova) at embryogenesis which can be passed on to future generations, and affects all cells.

eg. Hereditary cancer syndromes

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15
Q

What is a somatic mutation?

A

A mutation in any cell except a germ cell, at any point during a persons lifetime. This mutation will only affect the direct cell lineage, and will not be passed on to future generations.

eg. Sporadic tumours

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16
Q

What is Knudsons hypothesis?

A

If a gene has a faulty allele (ie. a germline mutation) , is only takes one mutation to become cancerous. In this way it is genetically predisposed to cancer

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17
Q

What is an oncogene?

A

A gene that promotes cell proliferation by mimicking growth signals and should be switched on in embryonic life but switched off in adult tissue.

protoonco = switched off

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18
Q

Give an example of where a ‘gain of function’ mutation has switched back on a proto-oncogene in cancer

A

RET gene on chr 10q11
If turned back on, it leads to MULTIPLE ENDOCRINE NEOPLASIA TYPE 2

NB with oncogenes only 1 gene copy needs to be affected (dominant)

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19
Q

What cancers are associated with MEN2?

A

MEN2a: thyroid/parathyroid/phaeochromocytoma (adrenal gland)

MEN2b:
mucosal neuromas in eye, mouth and endocrine glands

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20
Q

What is a tumour suppressor gene?

A

A gene that protects the cell from proliferating

NB with tumour suppressor genes both copies need to be affected (recessive)

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21
Q

Give 3 examples of where a ‘loss of function’ mutation in a tumour suppressor gene has lead to cancer

A

Mutation in RB1 - retinoblastoma
Mutation in BRCA1/2 - breast/ovarian/prostate
Mutation in APC - FAP

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22
Q

What is a mismatch repair gene?

A

A gene that produces proteins that detect mismatch and directs repair machinery towards it

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23
Q

By which 3 ways can cell death occur in normal tissue ?

A
  1. Apoptosis
  2. Necrosis
  3. Autophagy
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24
Q

Describe apoptosis

A
  • Regulatory elements sense apoptotic signals (activation of cyclin E, removal of IL-3/IGF-1)
  • Nuclear fragmentation
  • Chromosomal condensation
  • Cell shrinkage
  • Bleb formation
  • Phagocytosis of blebs

This is programmes cell death.

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25
Q

Describe 4 ways in which cancer cells can evade apoptosis

A
  1. Loss of p53 tumour suppressor function
  2. Increased survival signals (Bcl-2/xl)
  3. Decreased bax, bim, puma
  4. Short circuited ligand-induced death pathway
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26
Q

Describe autophagy

A

Lysosomes degrade cellular contents in response to stresses, allowing the metabolites to be recycled

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27
Q

How does cancer evade autophagy?

A

Cancers can survive stress (such as chemo/radio) and can shrink to a reversible dormancy, enabling regrowth after removal of stress

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28
Q

Describe necrosis

A

Unprogrammed chaotic cell death from noxious stimuli, involving inflammatory immune cells

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29
Q

How do cancer cells use necrosis to their selective advantage?

A

Necrosis of tumour cells leads to angiogenesis, cellular proliferation and tissue invasion, as it stimulates neighbouring cells in an uncontrolled way

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30
Q

How do tumour suppressor genes affect the cell cycle?

A

They inactivate cyclin-CDK complexes, which halts the cell cycle

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31
Q

Which cell cycle checkpoint is sometimes lost in cancer?

A

G1 checkpoint- this means that there is no ‘checking’ of the damaged cancerous genome before DNA synthesis (S phase)

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32
Q

Give an example of where cancer can cause increased expression of growth factor receptors

A

EGFR overexpression in GI/lung cancer
HER2 overexpression in breast cancer

This both activate Ras-Raf-MAP kinase causing cell proliferation

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33
Q

Give an example of where cancer can cause ‘ligand independent signalling’

A

RAS mutations - activate MAP kinase in the absence of a binding of a growth factor ligand

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34
Q

Give 3 ways in which cancer cells can evade growth suppression

A
  1. Lack of response to p53 and Rb inhibitory signals
  2. Loss of contact inhibition
  3. Mutations in tumour suppressor genes (Rb, tp53, tp21/27)
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35
Q

How do cancer cells enable replicative immortality?

A

They possess a telomerase enzyme that adds nucleotides to telomeres to allow continued cell division

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36
Q

How do cancer cells induce and maintain angiogenesis? How are these blood vessels different to normal ones?

A
  1. Production of growth factors (VEGF, PDGF)
  2. Suppression of angio inhibitors (TSP1)
  3. Maintenance of vasculature by pericytes and myeloid cells (although vessels are much more leaky and likely to haemorrhage)

Tumour cells cannot grow beyond 1mm cubed without their own blood supply

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37
Q

Name 2 therapies that target cancer-induced angiogenesis

A

Bevacizumab - VEGF antibody

Sunitinib - PDGF inhibitor

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38
Q

What does cadherin-1 do, and how is this involved in metastasis?

What is the name of this transition?

A

Cadherin-1 is a protein that usually organises cell tissue sheets.

In cancer, a mutation or downregulation of CDH1 gene means the cell becomes more disorganised and more motile, invasive and aggressive.

This is known as the epithelial-mesenchymal transition

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39
Q

Following the epithelial-mesenchymal transition, how do the new mesenchymal cells stimulate invasive behaviour?

A

They produce CCLs, which together with IL2 and IFNgamma, induce WBC infiltration.

Macrophages degrade the matrix with enzymes, allowing for invasion of the basement membrane

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40
Q

What is aerobic glycolysis and how is it involved in cancer?

ie. how do cancer cells reprogram energy metabolism?

A

It is the ability to to limit energy production to glycolysis, even when oxygen is present. (Usually cells use oxidative phosphorylation when oxygen is present)

This is helpful because the intermediates from glycolysis are necessary for production of new cancer cells

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41
Q

How can inflammation influence tumour development?

A

Once leucocytes have moved into tissue, they release reactive oxygen species, which are mutagenic to surrounding tissue.

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42
Q

How do tumour cells evade immune destruction?

A

They can recruit T helper and suppressor cells that enable them to not be recognised by immune cells.

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43
Q

Why are HIV patients predisposed to cancer?

A

Deficiency of CD4 cells means that their immune systems will not be strong enough to identify and destroy cancerous cells

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44
Q

What is the pathology of familial adenomatous polyposis?

A

Mutation in the APC gene, involved in the tumour suppressor pathway. This leads to a cascade of mutations leading to a ‘multistep carcinogenesis’

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45
Q

What are the two main types of FAP?

A
  1. Classical - 1000s of adenomas, 100% risk of malignancy (do colectomy)
  2. Attenuated - 100s of adenomas, increased but not certain risk of malignancy
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46
Q

What are the symptoms of FAP?

A

Blood in stool
Change in bowel habits >6wks
Abdo pain

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47
Q

What are the extracolonic features of FAP?

A
  • You get polyps all over the gut
  • Retinal pigmentation
  • Childhood hepatoblastoma
  • Thyroid cancer
  • Sebaceous/jaw cysts
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48
Q

A patient has retinal pigmentation, bloody stools and change in bowel habits. His dad had to have a colectomy when he was young. What condition are you worried about, and what screening should they have?

A

FAP

Annual screening (colonoscopy) from age 11

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49
Q

A patient with known FAP presents with an osteoma and a soft tissue tumour. What are you worried about?

A

Gardners syndrome

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50
Q

A patient with known FAP presents with confusion and CT scan shows brain tumour. What are you worried about?

A

Turcot syndrome

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51
Q

What is the pathology of Lynch Syndrome (aka HNPCC)

A

Mutation in MLH1 mismatch repair gene, leading to a cascade of mutations that cannot be repaired.
This will occur at areas of repeated DNA sequences known as microsatellites.
This leads to a frameshift mutation and a new truncated peptide.

This has two actions:

  1. Generation of adenomas
  2. The body mounts an inflammatory response against this foreign peptide
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52
Q

What is micro satellite instability?

A

Failure to repair repetitive sequences of DNA, due to faulty mismatch repair genes. This is characteristic of lynch syndrome and is rarely seen in sporadic colorectal cancer

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53
Q

What are the symptoms of lynch syndrome?

A

Usually none!!

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54
Q

What are the complications of lynch syndrome?

A

Colorectal cancer

Endometrial cancer

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55
Q

What is the Amsterdam Criteria (321)?

A

It says that lynch syndrome is likely if there are
3 colorectal tumours
across 2 generations
with at least 1 diagnosed before 50

If it fulfils this, do colonoscopy every 2 years after the age of 25

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56
Q

How can biopsy differentiate between Lynch syndrome and sporadic colon cancer?

A

Do a biopsy of tumour tissue and do MSI and BRAF test.

MSI high - lynch syndrome
BRAF high - sporadic cancer

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57
Q

How is lynch syndrome managed?

A
  1. Surveillance
  2. Chemoprophylaxis with low dose aspirin
  3. Surgical prophylaxis (colectomy)
  4. Family cascade testing
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58
Q

A person with known lynch syndrome presents with sebaceous skin tumours. What are you worried about?

A

Miur Torre Syndrome

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59
Q

A patient presents with mucosal neuromas on the tongue, long fingers and skin pigmentation. Her father had to have his adrenal gland removed. What are you worried about?

A

MEN2b - mutation of RET gene associated with those features + phaemochromocytoma + thyroid cancer

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60
Q

What exam finding would in hereditary retinoblastoma give you?

A

White pupillary reflex
Two different coloured eyes with ‘flash’

Hereditary - more likely to be bilateral

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61
Q

What are Wilsons Criteria for evaluating a screening programme?

A
  • Important health problem
  • Understood natural history of condition
  • Easy to perform test
  • Recognised treatment
  • Treatment more effective if started early
  • Policy on who should be treated
  • Diagnosis and treatment cost effective
  • Continuous case-finding
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62
Q

What are the features of Peutz-Jeghers syndrome?

A

Wine coloured lip staining

Cancers of pancreas, lungs, liver, breast ovary and uterus

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63
Q

How are people with known PJ syndrome screened?

A

Screening every 6 months by OGD/capsule, from 8 years

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64
Q

Describe the genetics of PJ syndrome

A

Mutation of STK11 gene tumour suppressor

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65
Q

What is a CUP and why is it difficult to manage?

A

Cancer of unknown primary

  • More aggressive
  • Early dissemination
  • Unpredictable metastatic pattern
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66
Q

What approach do you use to manage a CUP?

A
  1. Search for primary site
  2. Rule out potentially treatable/curable cancers
  3. Treat with curative or palliative intent
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67
Q

What is the gold standard for a diagnostic work up of a CUP?

A

Immunohistochemistry

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68
Q

What are the five main subtypes of CUP?

A
  1. Moderately well differentiated adenocarcinoma (better prognosis)
  2. Poorly or undifferentiated adenocarcinoma
  3. Squamous cell carcinoma
  4. Undifferentiated carcinoma
  5. Carcinoma of neuroendocrine differentiation
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69
Q

What is the main predictor of suitability for chemo?

A

Performance status

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70
Q

What are the symptoms of lung cancer?

A

Respiratory - Cough, dyspnoea, chest pain, haemoptysis, recurrent chest infections

Systemic - fever, weight loss, fatigue

Specific - dysphagia, hoarsness

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71
Q

Why do you get dysphagia in some lung cancers?

A

Extrinsic oesophageal compression by the primary tumour

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72
Q

Why do you get hoarseness in some lung cancers?

A

Invasion of the recurrent laryngeal nerve

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73
Q

What are the 4 characteristcs of clubbing?

A
  1. Increased curvature
  2. Soft tissue swelling
  3. Nail fluctuance
  4. Loss of nail bed angle
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74
Q

What are the signs of lung cancer?

A

Nicotine staining, clubbing, retention flap
Pulmonary collapse/effusion/consolidation
Lymphadenopathy, SVC obstruction

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75
Q

For a pleural effusion what is the:

a) expansion
b) mediastinum
c) vocal fremitus
d) percussion
e) breath sounds
f) air entry

And what other 2 features do you often hear?

A

a) reduced
b) central
c) reduced
d) reduced
e) dull
f) reduced

Whispering pectoliruquy - loud on whispering
Pleural rub

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76
Q

What is acanthosis nigricans?

A

A paraneoplastic syndrome causing velvety dark patches, particularly under the arms, associated with lung cancer

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77
Q

What is Pancoats syndrome, and what 4 features does it cause?

A

Apical malignant neoplasm (usually sq) that invades the brachial plexus and cervical sympathetic nerves causing:

  1. Chest/shoulder pain at T1
  2. Horners syndrome
  3. Atrophy of hand and arm muscles
  4. SVC obstruction
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78
Q

What are the features of Horners syndrome?

A
  1. Meiosis
  2. Anhydrosis
  3. Ptosis
  4. Enopthalmous
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79
Q

Why is T1 level significant?

A

It is the most common place for NSCLC to metastasize and will cause chest/shoulder pain

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80
Q

What investigations should be done in someone with suspected lung cancer?

A

BEDSIDE - sputum, sats
BLOODS - FBC (can get anaemia), CRP, LFTs, U&Es, bone profile, LDH
IMAGING - CXR, bronchoscopy, transthoracic needle biopsy, CT (always couple imagine with biopsy)
SPECIAL - pleural tap (exudative)

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81
Q

What further investigations should be done in someone with confirmed lung cancer?

A 
Pulmonary function tests
V/Q
MRI
USS
Scope

These are to assess metastatic spread and operability of cancer/performance status

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82
Q

What blood test should always be done in a patient with unexplained confusion?

A

CRP - most common cause of confusion in the elderly is UTI

Calcium

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83
Q

What is the main type of lung cancer? What are the subtypes?

A

Non small cell carcinoma (85%)

  • Adenocarcinoma (40%)
  • Squamous (30%)
  • Large cell carcinoma
  • Broncheoalveolar carcinoma
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84
Q

Describe an adenocarcinoma NSCLC

A
  • Peripheral lung
  • Slow growing but metastatic
  • Asbestos
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85
Q

Which NSCLC is most common in non-smokers and women?

A

Adenocarcinoma

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86
Q

Describe a squamous NSCLC

A
  • Central, cavitating lesion (can haemorrhage)
  • Proximal bronchi
  • Slow growing
  • Smoking association
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87
Q

Describe some CXR changes with lung cancer

A

Mass lesion (nb if patient has pneumonia, repeat in a month)
Pleural Effusion
Diaphragm

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88
Q

Describe a large cell NSCLC

A
  • Very large peripheral mass
  • Subtle initital symptoms (due to peripheral location)
  • Fast -growing
  • Incurable once LN are involved
  • Mucus secreting
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89
Q

What is the fastest growing NSCLC?

A

Large cell

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90
Q

Describe a broncheolaveolar carcinoma NSCLC

A
  • Multiple bilateral nodules
  • Non-invasive
  • Frothy pink sputum
  • Drug resistant
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91
Q

A patient has drug resistant lung cancer with frothy pink sputum. What is the mst likely diagnosis?

A

Broncheoalveloar carcinoma

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92
Q

Describe a small cell carcinoma

A
  • Found all over the lung
  • Hilar/mediastinal lymphadenopathy
  • Highly metastatic
  • Fast-growing
  • Responds well to therapy

OFTEN PARANEOPLASTIC (as they originate from neuroendocrine cells)

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93
Q

A patient with lung cancer has an xray showing mediastinal/hilar lymphadenopathy. What is the diagnosis? What paraneoplastic syndrome are you worried about?

A

Small cell carcinoma

Cushings (ACTH)
SIADH (ADH)

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94
Q

Describe a malignant mesothelioma

A
  • Arises from the pleura (of any organ!)
  • Manifests as unilateral pleural effusion
  • Restrictive defect
  • Asbestos
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95
Q

What CXR finding is seen in malignant mesothelioma?

A

Unilateral pleural effusion

96
Q

What are the complications of local invasion of lung cancer?

A
  • SVC obstruction

- Pleural effusion

97
Q

What are the features of SVC obstruction?

A
  • Facial oedema
  • Non pulsative JVP
  • Demarcations around the nipples
  • Aggravated by bending down
98
Q

What causes SVC obstruction?

A

Compression of superior mediastinum, most commonly by lung cancer

99
Q

Where do lung cancers metastatize?

A
  1. Brain
  2. Liver
  3. Bones
  4. Adrenals
100
Q

What are some signs of brain mets ? How can they be investigated? How can they be treated?

A

Headache, cognitive impairment, seizures

Do CT/PET

Surgery most effective
Steroids for oedema
Anticonvulsants
Radio 
Chemo (rarely passes BBB)
101
Q

What are the 2 reasons that you get hypercalcemia in lung cancer?

A
  1. Bony mets

2. Ectopic production of PTH, particularly from NSCLC (squamous)

102
Q

How is hypercalcemia diagnosed?

A

Ca > 2.7
Increased phosphate
Decreased PTH/Cl

103
Q

How is hypercalcemia managed?

A

IV fluids

IV bisphosphonates

104
Q

What is the most common endocrine paraneoplastic syndrome?

A

SIADH

cause by lung, prostate, thymic, pancreatic cancers and lymphoma

105
Q

What

paraneoplastic conditions do you get with lung cancer?

A

Endocrine -

  1. SIADH (SCLC)
  2. Ectopic ACTH (SCLC)
  3. Raised gonadotrophins
  4. Hypercalcemia

Dermatological
- Dermatomyositis

Neuro

  • Lambert Eaton
  • Encephalomyopathy
106
Q

A patient has loss of short term memory and hallucinations. He was diagnosed with SCLC a few months ago. What is going on? How can this complication be diagnosed?

A

He is suffering from an encephalomyopathy.

Diagnosis with raised protein in CSF and anti-HUantibody in serum

107
Q

A patient has proximal muscle weakness and symptoms like myasthenia gravis, without any bulbar involvement. He was diagnosed with SCLC a few months ago. What is going on? How can this complication be diagnosed?

A

Lambert-Eaton syndrome - reduced calcium dependent Ach release at the neuromuscular junction
Diagnosis with low amplitude muscle action potential on EMG

108
Q

What are the complications of chemotherapy?

A
  • Neutropenic sepsis

- Anaemia

109
Q

What is the definition of neutropenic sepsis?

A 
Pyrexia >38C or >37.5 twice in one hour
OR
Rigors
OR
Unexplained tachycardia/hypotension

in a patient with neutrophils <1 x 10^9/L

110
Q

How is neutropenic sepsis managed?

A
  1. Do blood cultures
  2. COMPENCE BROAD ABX (TAZOCIN)
  3. Do further investigations
111
Q

What are the components of a sepsis/infection screen?

A

Cultures, MSU, CXR, swabs

112
Q

What should not be done in suspected neutropenic sepsis?

What are the signs of poor prognosis?

A

PV/PR - infection dissemination
Paracetamol - may affect fever

Diarrhoea
Hypotension
Coagulopathy
Organ failure

113
Q

What is radiation pneumonitis?

A

Shortness of breath, dry cough, fever, chest tightness and pain, secondary to radiotherapy for chest malignancies

114
Q

In germ cell tumours, markers can be diagnostic. Which tumour markers should be done in suspected germ cell tumour?

A

AFP
b-HCG
(these are also good for monitoring)

LDH

115
Q

What cancers give a raised AFP?

A

Germ cell tumour
Hepatocellular carcinoma

NB - it is normally present in very low levels as it is made my the liver and intestine

116
Q

What could give you a false positive AFP?

A

Alcohol

117
Q

What could give a raised b-HCG?

A

Germ cell tumour (high sensitivity for NSGCT and choriocarcinoma)
Pregnancy
Molar pregnancy

118
Q

What could give you a false positive bHCG?

A

Cannabis

119
Q

Why do you get raised LDH?

A

It is an enzyme released from cell necrosis, so represents a high cell turnover

120
Q

High levels of LDH are a predictor of…

A

Tumour lysis syndrome

121
Q

When should AFP. bHCG and LDH be measured?

A

At diagnosis - if high they can be used to measure outcome
Pre-orchidectomy, 24hr after and weekly after until normal

When normal, the cancer has likely gone.

122
Q

Other than tumour markers, what investigations should be done in a patient with suspected testicular cancer?

A

Scrotal USS
Bloods
Imaging

123
Q

What are the risk factors for testicular cancer?

A 
Klinefelters syndrome (47XXY)
Downs syndrome (trisomy 21)
Testicular maldescent
Infertility
Infant hernia
Genetics
124
Q

What are the 2 main subtypes of testicular cancer?

A

Seminoma

Non seminomatous germ cell tumour

125
Q

Describe the pathology of a seminoma

A

Cancer of sheets of uniform cells that resemble primitive germ cells

126
Q

Describe the spread of a seminoma

A

Spreads locally to rete testis
Lympathically to para-aortic nodes
Rarely haematogenously

127
Q

Describe the pathology of NSGCT.

Give 2 examples

A

Cancers of a variety of appearances

  • teratoma
  • choriocarcinoma

These have an earlier onset and lower survival rate

128
Q

Describe the spread of an NSGCT

A

Spreads locally to rete testis
Lymphatically to para-aortic nodes
Haematogenously to the lungs

129
Q

What therapy do seminoma and NSGCT respond to?

A

Seminoma - responds well to chemo/radio
NSCGT - responds to cisplatin

They have a good prognosis generally!!

130
Q

What are the complications of testicular cancer:

a) local
b) metastatic
c) non-metastatic

A

a) SVC obstruction, ureteric obstruction
b) brain, lung, liver, nodes
c) tumour lysis, pulmonary emboli

131
Q

A 20yo male undergoing chemo presents with vomiting, diarrhoea, muscle cramps and weakness. What is happening?

A

Tumour lysis syndrome - rapid cell turnover causing rapid release of urate which is toxic (corresponds with high LDH)

132
Q

What are the RF for tumour lysis syndrome?

A

Large, sensitive tumours eg. burkitts, sarcoma, germ cell
Renal impairment
Male <25

133
Q

What electrolyte abnormalities are seen in tumour lysis syndrome?

A

Hyper K/urea/phosphate

Hypo calcemia

134
Q

What are the complications of tumour lysis syndrome?

A
  • cardiac arrest
  • renal failure
  • DIC
135
Q

How can tumour lysis syndrome be prevented?

A
  1. Adequate hydration
  2. Allopurinol and raspuricase
  3. Alkalise urine
136
Q

How can tumour lysis syndrome be managed?

A
  1. Electrolyte replenishment
  2. Haemodialysis
  3. Allopurinol oral/IV
137
Q

What are some complications of treatment for germ cell tumours?

A
  • Tumour lysis syndrome
  • Neutropenic sepsis
  • Infertility
  • Psychosexual issues
  • Secondary malignancies
  • Pulmonary fibrosis from belomycin
  • CVS risk from nephrotoxic chemo
138
Q

How might a testicular tumour present?

A
  • Dragging sensation
  • Scrotal pain
  • Painless, unilateral mass
  • Decreased testicular size
  • Systemic (weight loss, fatigue etc)
  • Advanced disease (urinary changes, mets)
139
Q

Describe the ways in which breast cancer might present?

A
  • Discolouration
  • Oedema
  • Peau d’orange (skin puckering from local invasion)
  • Pagets disease (eczematous rash, bloody discharge)
  • Nipple retraction
  • Discharge
  • Assymetry
140
Q

What proportion of breast cancer pts have a family history?

A

10%

141
Q

In terms of family history, what presentation is the strongest indicator of familial breast cancer?

A

First degree relative with bilateral breast disease for breast cancer

142
Q

What are the RF for breast cancer?

A
  • Family hx
  • Oestrogen exposure (not COCP!)
  • Previous benign breast disease
  • Smoking/alcohol/obesity
143
Q

What lymph node involvement indicated poor prognosis in breast cancer?

A

Supraclavicular

144
Q

What examination findings may be present in someone with breast cancer?

A
  • Breast changes
  • Lymphadenopathy
  • Respiratory compromise - consolidation
  • Distant mets
145
Q

What are the components of the 2WW triple assessment for breast cancer?

A
  1. Clinical exam
  2. Mammography (or MRI/USS)
  3. FNA/core biopsy
146
Q

What features on mammography would be suggestive of malignancy?

A
  • Asymmetry
  • Microcalcifications
  • Mass (can detect before palpable)
  • Architectural distortion
147
Q

When is USS imaging helpful for breast cancer diagnosis?

A

Can distinguish between solid and cystic, especially if the lesion is non-palpable

148
Q

When is MRI imaging useful for breast cancer diagnosis?

A

Patients who already have fibroadenomas or excessive lumpiness, in which palpation is very difficult
Used especially in high risk or younger patients

149
Q

Why is FNA used as part of the triple assessment?

A

Allows doctor to obtain matieral for cytology and aspirate masses to look for blood

150
Q

When is breast biopsy indicated? Describe the two types?

A

If FNA shows blood, or unsure about diagnosis

  1. Excisional biopsy - removes entire abnormal area
  2. Wire excision biopsy
151
Q

What tumour marker can be done in suspected breast cancer? How useful is it?

What other cancer is it elevated in?

A

CA-153 - low specificity and sensitivity so not suitable for screening/diagnosis but can be good for risk of recurrence

Gynae cancers

152
Q

What are the main pathological subtypes of breast cancer?

A 
Ductal carcinoma (70%)
Lobular carcinoma (30%)

Both can be in situ or invasive

153
Q

What is the most common location for breast cancer?

A

Left breast

Upper outer quadrant and retroareolar region

154
Q

What are BRCA1/2?

A

Tumour suppressor genes that have ‘loss of function’ mutations in familial breast cancer

155
Q

What cancers involve BRCA1 mutation?

A

Breast cancer (most common in younger women)
Peritoneal cancer
Pancreatic cancer
Prostate cancer

156
Q

What population have a high rate of BRCA1/2 mutations?

A

Ashkenazi Jews

157
Q

What cancers involve BRCA2 mutation?

A

Male breast cancer
Prostate cancer
Pancreatic cancer

158
Q

What are the characteristics of BRCA associated cancer?

A
  • Younger age of onset
  • Frequent bilateral occurence
  • Worse histological features (aneuploidy, higher grade, proliferation)
159
Q

Describe the ER status of BRCA1 and what this means for management

A

ER negative - this means tamoxifen won’t work as its a hormone therapy for people with ER+ cancer

160
Q

Describe the ER status of BRCA2 and what this means for management

A

ER positive so responds to tamoxifen

161
Q

Describe breast screening for people with BRCA mutations

A

Annual screening from age 30

162
Q

What is Li Fraumeni syndrome?

A

Autosomoal dominant mutation in p53 tumour suppresor gene, causing 100% risk of breast cancer

163
Q

Describe breast screening for people with Li Fraumeni syndrome

A

Annual screening from age 20 to at least 49, followed by annual mammography

164
Q

A patient has multiple hamartomas all over her skin. What is she at risk of?

A

Breast cancer

patient has Cowden Syndrome

165
Q

What is the name of the condition that give you ‘spider veins’, loss of motor control and an increased risk of breast cancer?

A

Ataxia telangectasia

166
Q

What is HER2 status?

A

Presence of human epidermal growth factor 2. Overexpression of this receptor can lead to breast cancer and it is an indication of severity

167
Q

How do you determine someones HER2 status?

A

FISH test

168
Q

How are HER2 cancers treated?

A

Herceptin

169
Q

What staging system is used in breast cancer?

A

TNM

170
Q

What investigations for mets should be done:

a) in all patients
b) if suspected mets

A

a) CXR, USS, bone scan

b) CT, MRI

171
Q

What treatment is used for breast cancer?

A

Premenopausal - Tamoxifen (depending on ER status)
Postmenopausal - Aromatoase inhibitors (anastrozole)
Radiotherapy
Chemotherapy

SURGERY DOESNT HELP DUE TO MICROCALCIFICATIONS

172
Q

What are the side effects of tamoxifen?

A

Increased risk of DVT and endometrial cancer

173
Q

How can breast cancer be prevented in those with known risk factors?

A

Masectomy
Ovarian ablation (no oestrogen production)
Tamoxifen??
Surveillance and screening

174
Q

What are the local complications of breast cancer?

A

Lymphoedema

Pleural effusion

175
Q

Where does breast cancer metastasise?

A
  • Bones - do radioisotope scan
  • Brain - do CT/PET (second most common after lung cancer)
  • Liver
  • Lung
176
Q

What are the four components in management of bony mets?

A
  1. Pain relief
  2. Preservation of function
  3. Skeletal stabilization
  4. Local tumour control (release impingement)
177
Q

What cancer is the main cause of spinal cord compression?

A

Breast cancer

178
Q

What is the investigation of choice for spinal cord compression?

A

MRI (diagnosis is clinical but confirmation by MRI)

179
Q

In SCC, what is the strongest predictor of treatment outcome?

A

Degree of pre-treatment neurological dysfunction

180
Q

What cancer is most likely to give brain mets?

A

Lung cancer

181
Q

How is spinal cord compression managed?

A

Steroids, etc etc

182
Q

What are the symptoms of ovarian cancer?

A 
ASYMPTOMATIC 'the silent killer'
Bloating, ascites and abdo pain
Vaginal bleeding after menopause
GORD
Early satiety
183
Q

Why do patients with ovarian cancer sometimes present with PE?

A

Many of the ovarian cancers, particularly clear cell, are pro-thrombotic. This is known as Trousseaus syndrome

184
Q

What are the RF for ovarian cancer?

A

MORE OVULATORY CYCLES (low parity, IVF, HRT)
Chemicals (talc, smoking)
Diet (lactose, fatty foods)
Family history

185
Q

What is the biggest RF for ovarian cancer?

A

Family history

186
Q

Which genetic mutations are involved in ovarian cancer?

A

BRCA1
BRCA2
HNPCC (mutation in MLH1/2)

187
Q

What are some protective factors for ovarian cancer?

A
  • Combined pill
  • High parity
  • Breastfeeding
  • Hysterectomy
188
Q

What investigations should be done for a patient with suspected ovarian cancer?

A

Bedside - urine dip, obs
Bloods - FBC, U&E, LFT, bone profile TFTs, tumour markers
Imaging - USS, CXR

189
Q

Which tumour markers are used in ovarian cancer?

A

Ca-125
CEA

bHCG, AFP and LDH in younger women

190
Q

How effective is Ca-125 as a tumour marker? When is it best used?

A

It is sensitive but non specific, as it released from inflammation of any peritoneal surface.

Best used in presentation of a women with a pelvic mass

191
Q

What is the first line imaging for ovarian cancer and what does it show?

A

USS diagnosis:

  • Cyst >5cm in perimenopausal women
  • Any cyst in postmenopausal
192
Q

What extra imaging can be done if USS is not adequate, and why are they each useful?

A

CT - determines operability
MRI - cyst surveillance
Explorative laparotomy
Endometrial sampling

193
Q

Which investigation is contraindicated in ovarian cancer?

A

Paracentesis/needle biopsy - could cause seeding

194
Q

How do you calculate the risk of malignancy index?

A

Ultrasound appearance x menopausal status x Ca-125

USS - max 3 of (multilocular, solid areas, bilateral, ascites, mets)

Men status - (perimenopausal 1, postmenopausal 3)

195
Q

What RMI would give you high risk for ovarian cancer?

A

> 250 (if >200 refer to specialist centre)

196
Q

Why do more ovulatory cycles increase the risk of ovarian cancer?

A

Increased rate of ovarian repair by dividing cells, translating to an increased mutation rate

197
Q

What are the two main types of ovarian cancer?

A 
Type 1 (low histological grade)
Type 2 (high histological grade)
198
Q

Give some examples of Type 1 ovarian cancer

A

Endometrioid
Mucinous
Clear cell

199
Q

Give some examples of Type 2 ovarian cancer?

A

Serous

Carcinosarcoma

200
Q

Name 5 types of epithelial ovarian cancer (most common)

A 
Serous
Mucinous
Endometrioid
Clear cell
Transitional (brenner)
201
Q

Which epithelial ovarian cancer type is associated with:

a) UTI
b) endometriosis
c) colon cancer
d) beginning in fallopian tube
e) very aggressive course with no raised Ca125

A

a) Transitional
b) Endometrioid
c) Mucinous
d) Serous
e) Clear cell

202
Q

90% of ovarian cancers are epithelial. What are the other 10%?

A

Sex cord stromal tumours (granulosa)
Sarcoma
Germ cell tumours (teratomas)

203
Q

Which ovarian cancer subtype is most likely to occur in young women?

A

Teratoma

204
Q

What is a krukenburg tumour?

A

A secondary tumour, usually met from GI tract, with a poor prognosis

205
Q

Describe some local effects of ovarian cancer

A 
Pleural effusion
Vaginal discharge
Bowel obstruction
Lymphoedema
Malignant ascites
206
Q

What is malignant ascites?

A

Ascites that indicates malignant peritoneal involvement, aka a poorer prognosis

207
Q

How is malignant ascites diagnosed and managed?

A

Diagnosis - clinical, USS/CT/MRI, cytology
Management - drainage

DO NOT USE DIURETICS

208
Q

Which cancers are likely to cause dermatomyositis/polymyositis?

A

NSCLC, SCLC, breast, ovary, GI tract

209
Q

A patient presents with gottrans papules, proximal myopathy and joint pain. What investigations should be done to diagnose this condition?

A

Dermatomyositis

BLOODS - LDH, CK, aldolase high
SPECIAL - muscle biopsy and EMG

210
Q

How do you treat malignant dermatomyositis?

A

Treat tumour
Steroids
Azathioprine (immunosuppresant)

211
Q

How can ovarian cancer be treated?

A

Surgical
Chemo - usually adjuvant, cisplatin
Radiation - localised

212
Q

What is lead time bias?

A

The length of time between disease detection and its usual clinical presentation

ie. early diagnosis may not prolong life but it will seem like it because it is being picked up earlier

213
Q

What is length time bias?

A

The fact that screening is more likely to detect slow growing tumours (as aggressive ones are not asymptomatic for long), and therefore it will seem like screening appears to improve survival

214
Q

What are the 3 cancer screening programmes in the UK?

A

Breast cancer
Colon cancer
Cervical cancer

215
Q

Describe breast cancer screening

age, when, how?

A

Ages 50-70, every 3 years, mammography

216
Q

Describe colon cancer screening

age, when, how?

A

Ages 60-74, every 2 years, faecal occult blood and flexi sig

217
Q

Describe cervical cancer screening

age, when, how?

A

Age 25-29 every 3 years, biopsy for CIN

Age 30-64 every 5 years

218
Q

What is Meigs syndrome?

A

Triad of

  • Benign ovarian tumour
  • Ascites
  • Pleural effusion
219
Q

What is lights criteria?

A

A pleural effusion is likely to be exudative if

Pleural protein/plasma protein >0.5 (or LDH >0.6)

220
Q

Describe the aspirate of an exudate?

A 
Straw coloured/turbid
High protein content (>3g/dl)
High lymphocytes/neutrophils (malignancy/infection)
Low glucose
ph <7.2
221
Q

Describe the aspirate of a transudate?

A 
Clear
Few lymphocytes
Low protein (<3g/dl)
High glucose (>40mg/dl)
ph normal
222
Q

What causes raised calcitonin?

A

Medullary thyroid

223
Q

What causes raised ALP?

A

Osteosarcoma/bone mets/myeloma

224
Q

What causes raised CEA?

A

Colorectal, ovarian

225
Q

What causes a raised Ca199?

A

Pancreatic cancer

226
Q

Patient >60 with symptoms of bowel cancer, what investigation?

A

Urgent 2WW colonoscopy

227
Q

What is adjuvant therapy?

A

Chemo/radio given AFTER surgery

228
Q

What is neoadjuvant therapy?

A

Chemo/radio given BEFORE surgery

229
Q

What is radical therapy?

A

Chemo/radio with curative intent

230
Q

What is brachytherapy?

A

Chemo/radio which is placed within or adjacent to the area requiring treatment.

231
Q

Which cancers are the most metastatic?

A

BLT PR

Breast, lung, thyroid, prostate, renal

232
Q

Which cancer patients are particularly at risk of hypercalcemia and how do you treat it?

A

Multiple myeloma - give saline + pamidronate

233
Q

How do you treat hypercalcemia generally?

A

SALINE

If there is a metastatic cause, also give IV bisphosphates (eg. pamidronate)

234
Q

A patient has a bad headache and is vomiting. They were diagnosed with small cell lung cancer 3 months ago. What investigation is the most urgent?

A

CT head - might have brain mets

235
Q

If you suspect colon cancer, what is the next step?

A

ENDOSCOPY + COLONOSCOPY

you need to do both if you are unaware where the bleeding/malignancy is coming from

236
Q

What is extravasation of chemotherapy?

A

Accidentally putting chemo into the surrounding tissues rather than the vein, causing an erythematous rash around the injection site

237
Q

What causes acanthosis nigricans?

A
  • GI cancer
  • PCOS
  • Diabetes
  • Thyroid dysfunction

4TH YEAR - CSIM2 (20 decks)

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