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Y4 Cancer Care > GI, breast and lung > Flashcards

GI, breast and lung Flashcards

1
Q

What types of cancer are breast cancer?

A
  • 95% adenocarcioma
  • these are divided into invasive and insitu
  • can be lobular or ductal
  • other types inc tubualr, papillary, mucinous
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2
Q

What is DCIS?

A
  • ductal carcinoma in situ
  • neoplastic cells limited to ducts and lobules by basement membrane- myoepithelial cells preserved
  • cannot met and kill pt
  • can transform to become invasive (esp if high grade) so usually removed
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3
Q

What is pagets disease of the breast?

A

The neoplastic cells can extend to the nipple without crossing the BM, and cause unilateral, red, crusting of the nipple. It is often mistaken for eczema

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4
Q

Is lobular carcinoma in situ concerning?

A
  • no, not considered cancerous
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5
Q

What type of breast cancer is often underestimated on initial imaging?

A
  • invasive lobular adenocarcinoma
  • if biopsy confirms this type, an MRI is done for accurate sizing
  • tend to be more aggressive
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6
Q

give 8 RFs for breast cancer

A
  • gender (female)
  • age 50+
  • uninterrupted menses// no pregnancy
  • late menopause
  • late age of 1st pregnancy
  • never breast feeding
  • obesity and high fat diet
  • exogenous oestrogens (HRT, some debate about long term COCP use)
  • geography (affluent countries)
  • atypical changes (ductal or lobar hyperplasia) on previous biopsy and previous breast cancer
  • radiation exposure
  • BRCA1 and 2 mutations
  • FHx
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7
Q

Describe the possible clinical features of breast cancer

A
  • Hard, craggy, fixed, non tender palpable masses are most worrying
  • But any palpable mass could be cancer
  • Mammogram abnormalities
  • Nipple discharge (esp if bloody or serous and spontaneous and unilateral)
  • Breast pain
  • Redness or pitting of skin over breast
  • Nipple changes such as inversion
  • Change in contours of the breast
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8
Q

Give 3 non cancerous differentials for breast cancer and the age each most commonly occurs

A
  • fibroadenoma (if age <30)
  • fibrocystic change (age 20-60)
  • cysts (age 40-60)
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9
Q

What are the 2WW refferal criteria for breast cancer

A
  • any unexplained breast lump with or without pain if age >30
  • unilateral discharge, retraction or other nipple changes in woman >50
  • age >30 and unexplained axillary lump
  • any skin changes suggestive of cancer
  • non urgent referral if under 30 and unexplained breast lump with or without pain
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10
Q

Describe the triple assessment of breast lumps

A
  • history and examination
  • radiography (bilateral mammography and USS of breast and regional LNs)
  • Biospy (USS guided core needle or open for non palpable lesions, excision biopsy or incisional biopsy (when >4cm) if palpable, rarely FNA as no receptor status or grade
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11
Q

Describe the staging investigations for cancers picked up on triple assessment (7) and when is it done?)

A
  • MRI if dense breast, lobular carcinomas and for high risk screening
  • Full staging only done where chemo is an option and when higher risk/ suspicion of mets
  • ER and progesterone receptor status using monoclonal antibody assay
  • epidermal GF and HER2 receptor status
  • LFTs and other routine bloods
  • CXR for lung mets
  • CT if mets suspected (abnormal CXR, neuro symptoms, hepatosplenomegaly, lymphadenopathy, LFT derangement)
  • bone scintigraphy if distant mets, bone pain, LN mets
  • PET scan if distant mets suspected (often fails to detect mets <5mm)
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12
Q

name and describe the staging system for breast cancer

A

bloom richardson staging
EARLY: T1-2= up to 5cm, N0 or N1 (up to 3 nodes)
LOCALLY ADVANCED= T3= >5 cm or T4= fixed to skin or chest wall, N2= 4 or more nodes, or fixed nodes or N3= nodes other than in axilla
METASTATIC= M1 (mets)

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13
Q

What prognostic indicators are there for breast cancer?

A
  • blood richardson stage
  • axillary node status
  • tumour size
  • tumour grade
  • lymphatic or vacular grade
  • pt age and BMI
  • ER and PR status are weak prognostic factors
  • oncotype dx: microarray to look at 21 genes gives indicator of chance of re- occurrence after mastectomy and guides decision to give chemo
  • PREDICT tool online, NPI (cancer size x 0.2 + grade + node stage)
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14
Q

Where does breast cancer spread to and how?

A

Lymph node- to axially nodes
Blood- to bone, liver and lung commonly but can go anywhere
Directly- into chest wall and skin

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15
Q

What surgeries are available for breast cancer and how is the type used chosen?

A
  • mastectomy or wide local excision

- type depends on pt choice, size of tumour relative to breast, number of nodes, site of tumours

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16
Q

How are lobar carcinomas in situ managed?

A
  • usually picked up incidentally on biopsies as usually asymptomatic and doesnt cause micro-calcifications visible on mammogram
  • usually only monitored and bilateral prophylactic mastectomy offered if BRAC1 or 2 +ve
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17
Q

How are DCIS managed?

A

mastectomy or wide local excision then radiotherapy

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18
Q

What is sentinel node biopsy?

A

Dye injected to breast, first node it drains to is taken
Other option is node sampling where you remove 4-5 node randomly for testing. You then do axillary node clearance if they’re involved.

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19
Q

When is radiotherapy used in breast cancer?

A
  • always after wide local excision (given to breast)

- given to chest wall after mastectomy if poor prognostic group

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20
Q

Give 3 side effects of radiotherapy for breast cancer

A

skin reaction, chest wall pain and fatigue acutely.

fibrosis, atrophy of breast and telangiectasia later. Brachial plexopathy is rare now

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21
Q

When is chemotherapy given to breast cancer pts

A
  • Sometimes before surgery to shrink

- After surgery if high risk invasive cancers to reduce reoccurrence risk

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22
Q

What chemo regime is used for breast cancer

A

FEC- T
5FU, epirubicin, cyclophosphamide +/- docetaxel
(probs dont need to know this)

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23
Q

What drug is given to a HER2 +ve breast cancer

A

Herceptin- particularly effective and given for 1 yr

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24
Q

Name an aromatase inhibitor and state how they work

A

Anastrozole, letrozole

Inhibits aromatase so and so production of oestrogen in peripheral fat

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25
Q

How does tamoxifen work

A

Selectively blocks oestrogen (SERM) in breast tissue but increases oestrogens effect in bones, endometrium and blood (so prothombotic)

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26
Q

When are aromatase inhibitors used over tamoxifen and what are the risks and benefits of each?

A

Aromatase inhibitors used in post menopausal women, lower risk of DVT but higher risk of osteoporosis so bone protection is given with it.
Tamoxifen used in pre and post menopausal women, less expensive but slightly less effective. It increases DVT and endometrial ca risk but is bone protective.

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27
Q

how long are oestrogen therapies given for in breast cancer

A

5-10 years

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28
Q

Describe the screening programme for breast ca?

A
  • 2 view mammograms every 3 years for women age 47-73
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29
Q

What types of lung cancer are there and which are most/ least common?

A

Small cell carcinoma- 12% (from neuroendocrine tissue)
Non small cell carcinoma
- squamous cell (40%)
- adenocarcinoma (35%)
- large cell (5%)
The remaining 5% are rarer tumours like carcinoid tumours

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30
Q

Give 5 RFs for lung cancer

A
  • smoking
  • airflow obstruction
  • increasing age
  • FHx
  • exposure to carcinogens like asbestos
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31
Q

Describe the clinical features of lung cancer caused by the primary tumour

A
  • Cough (lasting >3 weeks)
  • SOB
  • Haemoptysis
  • Wheeze
  • SVC obstruction (SOB, distended neck veins and JVP, headache/ fullness, blurred vision, odema arms/ face, confusion, syncope)
  • Persistent/ recurrent infections
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32
Q

Describe the clinical features of lung cancer caused by mets

A
  • Fatigue
  • Weight loss
  • Night sweats
  • Lymph node enlargement (supraclavicular)
  • Liver mets- anorexia, mass, jaundice, abdo pain, ascites
  • Adrenals- addisons (bronze pigment, hypoglycaemia, postural hypotension, weight loss, GI disturbance, weakness, crises)
  • Bone- pathological fractures, bone pain
  • Pleura- effusions
  • CNS- cord compression, focal neurological signs
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33
Q

Describe the possible clinical features of lung cancer caused by paraneoplastic syndromes

A
  • Horners syndrome (partial ptosis, unilateral anhidrosis, miosis)
  • Clubbing
  • Hypercalcaemia
  • Anaemia
  • SIADH
  • Cushings
  • Lambert eaton myasthenic syndrome (muscle weakness, fatigue, pain, reduced reflexes, walking difficulty, speech impairment and swallowing problems)
  • VTE
  • Thrombocytosis
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34
Q

Describe the referral criteria for lung cancer

A
  • age >40 w/ unexplained haemopytsis or suspicious CXR= 2WW

- age >40 + 2 of : cough, fatigue, SOB, chest pain, weight loss or appeitite loss or 1 if smoker = 2WW CXR

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35
Q

Describe how suspected lung cancer is investigated initially

A
  • CXR (routine or urgent)
  • If CXR suspicious then get CT chest same day or within 72 hrs
  • If no lesion seen on CXR by high clinical suspicion then CT same day/ within 72hrs
36
Q

What further investigations are done for lung cancer?

A
  • bloods: fbc, u&e, bone profile, lft, inr
  • CT spine, thorax, upper abdomen for staging
  • PET CT if surgical candidate and inital CT suggests low stage
  • biopsy
37
Q

What options are available for lung biopsy and when are each indicated

A
  • US guided FNA for cytology is lymphadenopathy
  • Bronchoscopy- endobronchial, transbronchial or endobronchial ultrasound (if mediastinal lymphadenopathy)
  • CT guided biopsy (if peripheral (scope only goes so small))
  • Thoracoscopy if pleural effusion present
38
Q

Describe the TNM staging of lung cancer

A

Tis= carcinoma in situ
T1: a= <1cm, b=1-2cm, c= 2-3cm
T2= 3-5cm or involvement of main bronchus
T3= 5-7cm or involving chest wall, pericardium, prenhic nerve
T4= >7cm or mediastinum, diaphragm, heart, great vessel, recurrent nerve, trachea, oesophagus, spine
N1= ipsilateral peribronchial and/ or hilar nodes and intrapulmonary noes
N2= ipsilateral mediastinal and/ or subcarnial nodes
N3= contralateral nodes
M1= distant mets

39
Q

When is surgery indicated in lung cancer management

A
  • need good performance status
  • can be curative
  • stage 0- IIIa
  • mostly only for NSCLC as small cell usually too advanced at diagnosis
  • surgeries can be lobectomy, wedge resection or segmentectomy
40
Q

When is radiotherapy used in lung cancer

A
  • often used to reduce size and for palliation
  • can be used for curative intent (continious hyperfractionated accelerated radiotherapy (CHART) where surgery is not an option but pt still relatively fit and stage only I or II
  • can be curative in 10% of small cell after chemotherapy
41
Q

When is chemotherapy used in lung cancer

A
  • usually 1st line in SCLC as often responds well- can be used to buy time or with view to surgery/ radiotherapy if effective
  • can be given before radio or surgery to shrink tumour or help control symptoms in NSCLC
  • immunotherapies such as pembrolizumab starting to be used to good effect esp for NSCLC
42
Q

What chemotherapy agents are used in lung cancer

A

1st- cisplatin
2nd- doxetaxcel (for relapse with good PS)
probs dont need to know this

43
Q

What causes cushings syndrome in lung cancer (inc which type)

A
  • ACTH related peptide from small cell tumours causing increased cortisol release
  • also get hyperpigmentation (usually seen in addisons) as high ACTH = high a MSH= more melanin production
44
Q

What tumour causes SIADH and what is this

A
  • Small cell tumours
  • Secrete ADH
  • causing hyponaturarmia due to increased water reabsorption, diluting blood
45
Q

What type of lung cancer can cause hyperparathyroidism?

A
  • squamous cell carcinomas
  • can produce PTHrp causing increase Ca2+ release
  • hypercalcaemia may also be caused by osteolytic bone mets
46
Q

How can lung cancer cause a hoarse voice

A

Tumours can impinge on the left recurrent laryngeal nerve can paralyse the posterior cricoaryetnoid muscle, causing paralysis of the left vocal cord, leading to vocal changes

47
Q

How can lung cancer cause anaemia

A

Similar mechanism to anaemia of chronic disease: tumour causes macrophage activation, causing hepcidin release (directly and via cytokines acting on liver this reduces iron absorbtion and release from stores, idea is to starve bacteria in blood of iron) leading to functional iron deficiency

48
Q

How can lung cancer cause VTE

A

Inflammatory cytokines activate procoagulant pathways.

Ca cells can also produce procoagulant proteins, fibrinolysis inhibitors and microparticles also

49
Q

What is lamber eaton myasthenic syndrome, what cancer is it associated with?

A

Autoimmune destruction of the neuromuscular junction (VGSC). Presents similarly to myasthenia gravis- but transient improvement in symptoms and EMG with exercise. 50% is associated with small cell lung cancer.

50
Q

What genetic disorders are associated with carcinoid tumours?

A

MEN1 and neurofibromatosis

51
Q

Describe the clinical features of carcinoid tumours

A
  • vague abdo pain
  • n+v
  • abdo distension
  • bowel obstruction
  • unintentional weight loss
  • carcinoid syndrome: cells over secrete serotonin (as well as prostaglandins and gastrin), this causes flushings (classically exacerbated by alcohol or coffee), abdo pain, diarrhoea, wheezing and palpitations
52
Q

What biomarkers are used to detect carcinoid tumours?

A
  • chromogranin A and 5HIAA levels
53
Q

What imaging is used to look for carcinoid primaries and mets?

A

primaries: endoscopy for colorectal, CT enteroclysis for small bowel
- for mets: whole body somatostatin receptor scintigraphy (SSRS)

54
Q

How are carcinoid tumours managed?

A
  • Surgery + adjuvant chemo is curative if localised but mets common at presentation so surgery often palliative
  • type of surgery depends on location of the tumour
  • Somatostatin analogues like octreotide can give symptom control if functional tumour
  • innterferon alpha inhibits protein, hormone synthesis and angiogenesis and stimulates immune system- is primary treatment for low proliferating tumours
  • cytotoxic chemo for high proliferating tumours and large tumour burden
  • radiotherapy only used if brain or bone mets
55
Q

What is carcinoid crisis and how is it avoided?

A
  • this is where overwhelming release of hormones from the primary tumour causes resistant hypotension.
  • somatostatin analogues can be used for prophylaxis pre and post op if carcnoid syndrome
56
Q

What types of colorectal cancer is there and which is commonest?

A
  • adenocarcinoma is commonest: most arise from adenoma- carcinoma sequence (this takes ~10 yrs)
  • other rarer ones inc lymphoma, carcinoid and sarcoma
57
Q

What two genetic conditions cause colorectal cancer?

A
  • Adenomatous polyposis coli (APC) gene is a tumour surpressor gene. Mutation of which causes familial adenomatous polyposis
  • Hereditary non polyposis colorectal cancer (HNPCC) is caused by DNA mismatch repair gene mutation, and commonly accounts for familial risk associated with colorectal cancer
58
Q

What are the risk factors for colorectal cancer?

A
  • age >60
  • fhx
  • idb
  • low fibre diet
  • high processed meat intake
  • smoking
  • high alcohol intake
  • worth noting that up to 75% have no risk factors
59
Q

Describe the clinical features of right and left sided colorectal cancer

A
  • RIGHT SIDED: vague abdo pain, anaemia, mass in RIF, faecal occult blood/ faecal immunochemical test +ve presents later
  • LEFT SIDED: rectal bleeding, change in bowel habit or tenesmus, LIF mass (usually on PR), blood or mucus in stool
  • Colorectal cancer anywhere can present with change in bowel habit, rectal bleeding, weightloss, abdo pain and iron deficiency (microcytic anaemia)
  • Weight loss is only present if there is mets, as opposed to upper GI malignancy
60
Q

Who is screened for colorectal cancer and how?

A
  • faecal occult blood home testing

- sent out to those age 60-75 every 2 yrs

61
Q

Give 3 differentials for colorectal ca

A
  • IBD: avg onset is younger, typically presents with bloody or mucus in diarrhoea
  • Haemorrhoid: bright red rectal bleeding covering surface of stool, rarely presents with abdo pain, altered bowel habit, weightloss
  • Diverticulitis: can present with blood in stool, abdo pain and change in bowel habit but unlikely to cause systemic features of inflammation such as weight loss
62
Q

Describe the 2WW referral criteria for colorectal ca

A
  • 40+ and abdopain and unexplained weight loss
  • 50+ and unexplained rectal bleeding
  • 60+ and iron deficiency anaemia or change in bowel habit
63
Q

How should suspected colorectal ca be investigated? (initial and further investigations?)

A
  • FBC, U&E, LFT, coagulation screen
  • CEA- not used for diagnosis but for disease progression and reocurrance
  • colonoscopy with biopsy is gold standard but in some places CT colography is used (cheaper and same detection rate) and can be used if too frail or dont tolerate
  • If +ve colonscopy: CT CAP (for mets and invasion), MRI rectum (if rectal ca, for depth and invasion) and endo- anal USS (for early rectal ca to assess suitability for trans anal resection)
64
Q

How is colorectal ca staged and what are the most important prognostic factors?

A
  • Dukes staging: A-D based on level of invasion into mucosa (T1-4), regional lymph nodes or distant mets
  • surgical margins, CEA levels and obstruction are also important prognostic factors
  • BRAF and KRAS gene mutations give poor prognosis
  • mucinious adenocarcinoma, signet ring cell and small cell carcinoma have worse prognosis
65
Q

Describe the surgical procedures for tumours in the: caecal/ ascending colon, transverse colon, descending colon, signmoid colon, high rectum and low rectum

A
  • Caecal/ ascending tumours: right hemi
  • transverse colon: extended right hemi
  • descending colon tumours: left hemi
  • sigmoid colon tumours: sigmoid colectomy
  • high rectal (upper 1/3 rectum/>5cm from anus): anterior resection (leaves rectal sphincter intact)
  • low rectal: low anterior resection (leaves anal sphincter intact) if can get 2cm margin, Abdominal- perineal (AP) resection if cant get 2cm margin - excision of distal colon, rectum, analsphincters, resulting in permanent colostomy
66
Q

What is a hartmanns procedure and when is it used?

A

complete resection of recto- sigmoid colon with formation of end colostomy and closure or rectal stump, used in emergencies such as bowel obstruction or perforation

67
Q

When are radiotherapy and chemotherapy used in colorectal ca?

A
  • chemo used in metastatic disease
  • neo- adjuvant radiotherapy can be used in rectal cancer (but not colon as risk of small bowel damage)
  • palliative care is late stage, endoluminal shunts or stomas can be used to relieve acute large bowel obstruction
68
Q

What are the two types of oesphageal cancer and whats the difference between their location and aetiology?

A
  • Squamous cell carcinoma: typically occurs in middle- upper oesophagus and strongly associated with smoking and excessive alcohol consumption
  • Adenocarcinoma: typically occurs in lower oesophagus and due to barretts oesophagus from reflux
  • Other types are rare and inc leiomyosarcoma, rhabdomyosarcoma and lymphoma
69
Q

Describe the clinical features of oesphageal cancer

A
  • dysphagia: progressive, solids then liquids- all dysphagia is ca until proven otherwise
  • weight loss
  • odynphagia
  • hoarse voice
  • weight loss, upper abdo pain, dyspepsia and refluc also qualify for 2WW OGD
70
Q

Give 4 differentials for dysphagia

A

Mechanical (benign strictures, tumours, extrinsic compression, pharngyeal pouch, foreign body) or neuromuscular (stroke, achalasia, oesphagea spasm, myasthenia gravis)

71
Q

How should oesphageal ca be investigated? (initial and further)

A
  • Urgent upper GI endoscopy (oesphago-gastro- duodenoscopy or OGD) and biopsy for histology
  • CT CAP and PET CT to look for mets
  • Endoscopic USS to measure penetration into the oesophageal wall (t staging) and assess and biopsy mediastinal lymph nodes
  • Laparoscopy is often used to look for intraperitoneal mets if the tumour has an intra abdominal component
  • Bronchoscopy may be warrented if hoarseness or haemoptysis
72
Q

How is oesphageal cancer managed?

A
  • most palliative as often presents with advanced disease
  • palliative care inc stents, radio, chemo, nutritional support, thickened fluids
  • SCC: chemo usually only choice as upper oesphagus too difficult to operate on, lower SSCs may get surgery and neoadjuvant chemoradio
  • adenocarcinoma: neoadjuvant chemo and oesphageal resection if very fit, surgery only if fit
  • surgery is massive and includes opening chest and abdomen, deflating a lung for 2 hrs, recover is 6-9 months, 30 day mortality is 4%
73
Q

What is the common types and causes of liver cancer?

A
  • 90% are mets
  • 10% hepatocellular carcinoma (HPCC)
  • HPCC arises from chronic inflammation due to viral hepatitis, chronic alcoholism, hereditary haemochromatosis, primasry biliary cirrhosis
  • other rfs: age >70, aflatoxin exposure, fhx
74
Q

How does of liver cancer present?

A
  • most presents with cirrhosis: weight loss, fatigue, lethargy
  • dull ache in RUQ is uncommon, but characteristic feature of HPCC
  • advanced disease may present with liver failure: ascites, jaundice, portal HTN, clotting derangement
  • O/e: irregular, hard craggy and tender liver
75
Q

How should suspected liver cancer be investigated?

A
  • LFTs (AST:ALT >2 = likely alcoholic liver disease, if around 1 more likely viral hepatitis), FBC (platelets may be low), clotting screen (may be prolonged), alpha fetoprotein (raised in 70%)
  • USS: if mass >2cm and AFP raised this is basically diagnostic
  • CT scan for staging and further evaluation
  • MRI liver may be used if diagnosis unsure
  • Biopsy or percutaneous fine needle aspiration may be performed to confirm but last resort due to difficulties in setting of ascites, deranged clotting and risks associated with tumour seeding
  • Cirrhosis risk scores: MELD and child- Pugh scores can be used to predict likelihood of pt tolerating a liver transplant
76
Q

How is primary liver cancer managed?

A
  • surgical: liver resection if cirrhosis with good baseline health status, transplant if they fulfil the milan criteria (one lesion <5cm or many <3cm, no extra hepatic manifestations, no vascular infiltration)
  • image guided ablation: if early HCC, ultrasound or microwave probes placed in tumour mass to induce necrosis
  • alcohol ablation if small inoperable tumour
  • transarterial chemoembolisation if BCLC stage B (large mutlinodular)- high conc chemo injected into hepatic artery then embolising agent added to induce ischaemia in area of tumour
77
Q

How are secondary liver malignancies managed?

A
  • most commonly from bowel, breast, pancreas, stomach and lung
  • biopsy not advised if tumour operable as may lead to seeding
  • surgery indicated if mets confined to liver and primary is under control
78
Q

What type of cancer are most gastric cancers and what are the major RFs?

A
  • 90% adenocarcinoma

- male, h. pylori, increasing age, smoking, alcohol

79
Q

How does gastric cancer present?

A
  • dyspepsia, dysphagia, nausea, vomiting, malaena, haematemesis, anorexia, weight loss, anaemia
80
Q

How should gastric cancer be investigated?

A
  • CAE can be used for monitoring disease progression but not for diagnosis
  • OGD and biopsy for diagnosis
  • HER2/ neu protein expression is tested for mAb testing
  • CT CAP and staging laparoscopy needed for all pts
  • PET CT rarely used as dont take up tracer well
81
Q

How should gastric cancer be managed?

A
  • proximal cancer: total gastrectomy
  • distal cancer: subtotal gastrectomy
  • if pt fit enough thell get neoadjuvant and adjuvant chemo also
  • most pts get palliative management as tends to present very late
82
Q

Where do cholangiocarcinomas most commonly arise from and what are the RFs?

A
  • arise from bifucation of left and right hepatic ducts most commonly
  • RFs: primary sclerosing cholangitis, UC, toxins, alcohol, diabetes
83
Q

How does cholangiocarcinoma present?

A
  • Post hepatic jaundice due to mass effect: pruritis, pale stools, dark urine, sometimes RUQ pain, weight loss, anorexia, malaise
  • if jaundice and enlarged or palpable gallbladder then strongly suspect biliary tree malignancy (couvoisers law)
84
Q

Give 4 differentials for post hepatic jaundice

A
  • obstructive choledochlithiasis
  • bile duct strictures
  • choledochal cysts
  • pancreatic tumours
  • biliary cirrhosis
  • primary sclerosis cholangitis
85
Q

What blood would you expect in post hepatic jaundice?

A
  • elevated bilirubin and conjugated bilirubin (unconjugated level is normal), raised ALP/ ALT/ AST and gamma GT, CAE may also be elevated
86
Q

How should cholangiocarcinoma be managed?

A
  • USS to demonstrate obstructive cause, MRCP optimal for diagnosis and CT for staging looking for mets
  • definitive management complete surgical resection but many are inoperable at time of presentation so palliative with radio +/- chemo, ERCP stents and bypassing of obstructions
  • complications inc biliary sepsis, secondary biliary cirrhosis and long term prognosis is poor
87
Q

give 4 complications of mastectomy and breast conserving surgery

A
  • flap necrosis
  • infrction
  • shoulder dysfunction
  • injury/ thrombosis of axiallry vein
  • seroma/ lymph node collection
  • axillary nerve injury
  • arm swelling- lymphodema
  • haematoma

Y4 Cancer Care (6 decks)

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