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High yield Flashcards

1
Q

What are D1 and D2 gastrectomies

A

Adequate resection of gastric cancer mandates removal of 4 cm of healthy tissue on proximal and distal margin of resection along with harvest of at least 15 lymph nodes.

D1 gastrectomy involves R0 resection of stomach and removal of peri gastric (lesser and greater curve nodes) nodes (stations 1-6)

D2 gastrectomy involves R0 resection, all D1 nodes (stations 1-6) plus left gastric, common hepatic, coeliac, splenic and splenic hilar nodes (station 7-11)

There is controversy regarding the appropriate degree of lymphadenectomy. D2 is an oncologically superior resection but has more morbidity. The spleen should be preserved even on D2 resections unless it is involved.

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2
Q

What proportion of biopsy confirmed DCIS are diagnosed with invasive cancer after excision? When would you perform SNB for DCIS?

A

Up to 20% patients with DCIS are found to have invasive cancer after excision, rates of positive sentinel node would be much lower (approx 4-5%). By definition DCIS should not involve nodes.

I would perform SNB for DCIS in

  • patients undergoing mastectomy
  • I would offer it to patients with suspicious features i.e. palpable mass or DCIS>5cm, but this is controversial. Alternative would be to perform SNB if final histology confirms invasive cancer.
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3
Q

Indications for adjuvant radiotherapy for breast cancer

A

POST BCS

  • most patients with invasive ca
    • controversial in >65yrs with <3cm ca, ER+/HER2-ve and No nodal involvement - here the benefits are marginal and a nuanced discussion with the patient is needed (2014 metanalysis shows some benefit in reduction of local recurrence 2.2% vs 6.4%, with NNT of 24; but no benefit in OS)
  • After DCIS usually if Van Nuys Prognostic score 7-9

POST MASTECTOMY

  • T4
  • T2/T3 with high-risk features (triple negative, high grade, LVI) - controversial

NODAL DISEASE (without AND)

  • N2 (4 or more nodes)
  • Macroscopic N1 (controversial. In BCS* EORTC and MA20 studies show decrease recurrence but no difference in OS; in *Mastectomy - EBCTCG (early breast cancer collaborative group) systematic review shows decrease in recurrence)

NODAL DISEASE POST AND

  • Extracapsular extension, large proportion (50%) of involved nodes, axillary fat invasion

POST NAC

  • Stage 3 disease
  • residual nodal disease post NAC
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4
Q

What are the cancers associated with Lynch syndrome?

A

Large bowel (30-75%)

Endometrial (30-75%)

Ovarian (10%)

Stomach (10%)

urothelial (renal pelvis, ureter bladder) (5%)

Others (SB, panc, brain) (5%)

Skin (Muir-Torre) sebaceous adenoma, sebaceous carcinoma, epithelioma and keratoacanthoma

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5
Q

how are pancreatic neuroendocrine tumors graded?

A

Several systems exist. I use the WHO system which uses degree of differentiation, Ki67 and mitotic index.

Well differentiated

  • Pan NEN Grade 1 (low) - Ki 67 <3%, Mitotic index (per 50 hpf) <2
  • Pan NEN Grade 2 (intermediate) - Ki 67 3- 20%, Mitotic index 2-20
  • Pan NEN Grade 3 (high) - Ki 67 >20%, mitotic index >20

Poorly differentiated

  • Pan NEC Grade 3 (high) Ki 67 >20%, mitotic count >20
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6
Q

What is Barretts esophagus and what are the symptoms?

A

Barrett’s is a histopathological diagnosis where by the stratified squamous epithelium of the lower oesophagus undergoes columnar metaplasia due to acid reflux.

(American definition requires presence of goblet cells, UK definition doesn’t)

Barrett’s usually doesn’t cause any symptoms and most patients are diagnosed during investigation of GERD. In advanced cases patients may complain of odynophagia and can have strictures and ulceration

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7
Q

What chemotherapeutic agents used for colorectal cancer?

A

The options are

5 FU - this is IV form, oral form is capecitabine. This is main stay but not very effective in MSI patients (patients with MMR mutation).

Folinic acid (also called leucovorin) - potentiates 5FU

Oxaliplatin - further reduces recurrence when added to 5FU

Other agents used to potentiate 5FU particularly in metastatic disease - Irinotecan (IRI)

EGFR inhibitors (monoclonal antibodies) - e.g. bevacizumab (Avastin), Cetuximab - these bind to EGFR which are expressed in 60-80% of all colorectal cancers. These are not good in presence of KRAS mutation and have increased risk of perforation when used with stents in situ.

For rectal cancer there is lack of consensus for adjuvant chemo. But recommendations are extrapolated from colon cancer and are broadly the same. Adjuvant chemo is poorly tolerated in rectal cancer and many patients never finish the recommended course due to multiple factors like - treatment delay (longer convalescence after rectal surgery than colon surgery); presence of defunctioning stoma increases severity of diarrhoea.

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8
Q

Duke’s and TNM staging for colorectal cancer

A

Dukes A = muscularis propria

Duke’s B = through muscle laer but No nodes

Duke’s C = node positive (Same as Stage 3 cancer)

T1 = submucosal invasion

T2 = muscularis propria

T3 = subserosa

T4 = perforates serosa

N0 = no nodes

N1 = <3 nodes

N2 = 4 or more nodes

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9
Q

Investigations for gynaecomastia

A

In neonates - no investigation

Pubertal - review in 6 months

Adults -

LFT/Renal function/AFP/LDH

bHCG/estradiol/testosterone/LH/FSH

Mamo + US

US of liver/testis (if needed)

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10
Q

polyp surveillance protocol

A
  • Low Risk = 5 yrs
    • <2 small adenomas (<1cm)
    • low grade dysplasia
  • Intermediate = 3 yrs
    • 3-4 small adenomas
    • 1 adenoma >1cm
    • villous adenoma
    • High grade dysplasia
  • High risk = 1 yr
    • 5 or more small adenomas
    • >3 adenomas with 1 >1cm
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11
Q

Pathogenesis and treatment for radiation proctitis

A

Acute - mucosal damage

chronic - endarteritis obliterans -> chronic mucosal damage

Treatment

  • hydration
  • antidiarrheals
  • Bleeding
    • sucralfate enema
    • Argon plasma coag
  • Pain
    • Sucralfate
  • Obstruction
    • stool softeners
    • endoscopic dilatation
  • surgery
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12
Q

How are esophageal motility disorders classified, what are the manometric/ imaging abnormalities and what are the treatment options

A

Chicago classification

  • Gastroesophageal outflow obstruction
    • Achalasia types I – III (hellers myotomy + anti-reflux procedure)
    • Hypertensive lower oesophageal sphincter (balloon dilation or surgery)
  • Major motility disorders
    • Absent motility
    • Diffuse oesophageal spasm (uncoordinated contraction, medical therapy)
    • Hypercontractile (nutcracker) oesophagus (normal LES relaxation, very high amplitude coordinated contraction, medical therapy)
  • Minor
    • Ineffective/fragmented contractions
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13
Q

Child Pugh score

A

classifies severity of liver disease according to the

  • albumin
  • bilirubin
  • INR
  • Ascites
  • Encephalopathy

score of 5 to 6 is considered Child-Pugh class A (well-compensated disease);

7 to 9 is class B (significant functional compromise)

10 to 15 is class C (decompensated disease).

These classes correlate with one- and two-year patient survival: class A: 100 and 85%; class B: 80 and 60%; and class C: 45 and 35%

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14
Q

Describe the lymph node levels in neck? What are radical, modified radical and selctive neck dissection?

A

There are 7 levels

  1. submental (1a) and submandibular (1b)
  2. Upper third of IJV (hyoid to base of skull (2a = anterior to XI nv; 2b = posterior to XI nerve)
  3. midddle third of IJV (Hyoid to Cricoid)
  4. Lower third of IJV (Hyiod to clavicle)
  5. posterior to SCM (5a= above cricoid; 5b = below cricoid)
  6. Central (between carotids and innnominate)
  7. Superior mediastinum

Radical neck dissection = removal of all fibrofatty tisssue on levels 1 -5 plus SCM, IJV and XI nerve

Modified radical = all fibrofatty tissue in levles 1-5 but any or all of SCM, IJV and XI preserved

Selective neck dissection = dissection of all fibrofatty structures ina selected compartment, preserving all critical structures

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15
Q

How are enterocutaneous fistula classified based on output volume?

A

Low <200mls/day

Moderate 200-500 mls/day

High >500 mls/day

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16
Q

What are some commonly used chemotherapy options for gastric cancer?

A

Neoadjuvant

  • FLOT - 5FU, Leucovorin, oxaliplatin, docetaxel - for fit patients who can tolerate intense chemo
  • ECF - Epirubicin, cisplatin, 5FU - used in MAGIC trial for fit patients
  • FOLFOX - 5FU, folic acid, oxaliplatin - less fit patients
  • CAPOX - capecitabine (oral FU) and oxaliplatin - less fit patient

Adjuvant

  • ECF
  • FOLFOX
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17
Q

How are gastric cancers staged?

A

CT CAP

EUS +/- FNA

  • assess T stage and N stage, perform FNA of lymph nodes and biopsy gastric lesion if needed

PET/CT

  • if no mets seen on CT CAP

Staging Laparoscopy

  • if >T1a and no mets seen on PET/CT and patient being considered for neoadjuvant/ surgical therapy
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18
Q

Outline the treament for patients with Lynch syndrome

A

This depends on whether patient is being assessed for prophylactic vs therapeutic intervention.

Prophylactic

  • For colon -
    • Non-operative (adds 13.5 yrs life expectancy)
      • 1-2 yearly high-quality colonoscopy with chromoendoscopy
      • High dose aspirin (600 mg/d) CAPP2 RCT demonstrated substantial reduction in CRC rates
    • Operative
      • ​Restorative Proctocolectomy (adds 15.6 years life expectancy)
      • TAC-IRA (adds 15.3 yrs) - cancer risk in retained rectum 1-1.5% per year
  • For Tubes and ovaries
    • ​Non-operative - annual TVS scan and endometrial sampling
    • Operative - TAH + BSO

Therapeutic treatment

  • Segmental colectomy / TAC-IRA / RPC (particularly if rectal Ca) - discuss risks of metachronous tumour 16% @10 yrs
  • Adjuvant - 5FU less effective but otherwise indications and regimes are similar as sporadic CRC
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19
Q

What are the endoscopic features of GIST? how are they identified immunohistochemically? Outline investigation and treatment

A

Endoscopic features - smooth submucosal nodule with central ulceration.

Immmunohisto - c-kit positive (95%), CD34 (70%), and DOG1 (discovered in Gist- 1)

GISTs are sarcomatous tumors of GI tract that arise from interstitial cells of Cajal. They Can occur anywhere in GI tract but most common in stomach and SB. Histologically they have polymorphic spindle cells.

Can be asymptomatic but may present with abdo pian / bleeding.

Diagnosis is usually incidental on endoscopy or imaging.

Investigation:

Endoscopy and biopsy (often negative due to submucosal nature) - well biopsy has better yield.

EUS - and FNA

Immunohistochemistry - c-kit

CT - staging

Difficult to differentiate benign vs malignant (size >10 cm and mitosis >5 per 50 hpf are predictors along with obvious invasion)

TREATMENT

<2cm no high risk features - can be monitored

<2cm with high risk features or >2cm- resect (with no tumour on ink)+ adjuvant imatinib (Gleevac) tyrosine kinase inhibitor (for 1 year). Sunitinib is used for lesions that progress on imatinib. Radiation and chemotherapy do not have significant affect.

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20
Q

Surgical options for perf. DU

A

Perf < 1cm >> Graham Patch

Perf > 3cm

  • Jejunal serosal patch + pyloric exclusion
  • Antrectomy and Bilroth II
  • Tube drainage of duodenum
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21
Q

MELD score

A

Statistical score that was originally used to predict mortality after TIPS but studies have validated it use as a reliable scoring system for selecting patients for liver transplant and risk prediction for other surgical interventions in patients with cirrhosis.

Components

  • Bilirubin
  • INR
  • Creatinine
  • more recently Na has been added

It has been suggested that patients with a MELD score below 10 can undergo elective surgery, those with a MELD score of 10 to 15 may undergo elective surgery with caution, and those with a MELD score >15 should not undergo elective surgery

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22
Q

What are some important branch points (based on T stage) in gastric cancer treatment?

A

>T1a

  • staging lap (unless proven mets)

T1b

  • straight up surgery (usually vs neoadjuvant for T2)

T2

  • Neo-adjuvant (chemotherapy). Multimodal therapy better than surgery alone
  • Chemoradiation (rather than chemo alone) used for oesophageal and cardia tumours

T3 or N1

  • Adjuvant (chemoradio vs chemo)
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23
Q

What factors are used to prognosticate GIST

A

Prognosis depends on

  1. Tumour size (<2cm vs >10 cm)
  2. Mitotic count (<5 per 50HPF vs >50)
  3. Location (SB worse than stomach)
  4. Obvious metastatic disease
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24
Q

Which part of the intestine absorbs which nutrient?

A
  1. Carbohydrate, protein and water soluble vitamins - upper 200 cm of jej
  2. Fat and fat soluble vitamins - entire SB
  3. Bile salt/ acid - terminal ileum
  4. Iron, calcium and other minerals - duodenum
  5. Water and sodium - entire SB and colon
  6. K and short chain fatty acid - colon
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25
Q

Factors that will prevent a fistula from healing

A

FRIEND

F - foreign body

R - radiation

I - infection/ inflammation

E - epithelialization

N - neoplasia

D - distal obstruction

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26
Q

what are the antireflux mechanisms?

A

LES - not a structural sphincter but a dynamic high pressure zone

Diaphragmatic sphincter - right crus fibres make a pinchcock

Distal esophageal compression - by abdo pressure closes lumen

Acute angulation of OGJ - acts as a flap valve

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27
Q

Who should be referred for genetic testing for breast cancer?

A

Assess risk using CanRisk or Manchester score. Refer anyone over CanRisk score >10% (EVIQ guidelines)

KNOWN GENETIC HISTORY - Adult untested relatives of

  • BRCA1 (breast, ovarian, tubes, pancreas, peritoneal)
  • BRCA2 (all BRCA1 plus prostate, AML)
  • P53 (Li Fraumeni - sarcoma, breast, brain, leukaemia)
  • PTEN (Cowden - breast, thyroid, hamartomatous polyp)
  • STK11 (Peutz-Jehgers)

PERSONAL HISTORY OF

  • triple negative cancer at age <50
  • any breast ca <40yrs
  • 2 primary breast with first at age <50
  • Breast and ovarian primary any age
  • High grade non-mucinous ovarian, tubal or peritoneal ca
  • male breast ca
  • Lobular Ca PLUS fam h/o lobular or diffuse stomach ca
  • Breast Ca plus fam H/o
    • Peutz Jehgers
    • Li Fraumeni
    • PTEN

FAMILY HISTORY - 2 first- or second-degree relatives with breast or ovarian cancer plus

  • additional breast/ovarian ca
  • one relative with breast Ca <50yrs
  • >1 breast ca in same person
  • breast and ovarian ca in same person
  • male breast ca
  • Ashkenazi (eastern European) Jews
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28
Q

What are the phases of recovery from intestinal failure

A
  1. Hypersecretory phase - high stoma output, can last up to 2 months
  2. Adaptive phase - histological changes increasing adaptive surface - 3-12 months
  3. Stabilization phase - 1-2 years
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29
Q

Which extra intestinal manifestation of UC responds to colectomy?

A

RESPONDS

  • Peripheral arthropathy
  • Erythema nodosum
  • Iritis

MAY RESPOND

  • Pyoderma Gangrenosum

DOES NOT RESPOND

  • Axial arthropathy
  • Uveitis, episcleritis
  • PSC
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30
Q

for IPMN that are not being resected, how would you follow up?

A

Clinical follow-up

  • yearly review
    • abdo pain
    • jaundice
    • wt loss
    • pancreatitis

Imaging

<1cm cyst - 2-3 yrly CT/MR

1-2 cm cyst - annual CT/MR x2 and then lengthen interval

2-3cm - 3-6 EUS then lengthen interval with alternating MR–> consider surgery instead

>3cm - 3-6 monthly EUS alternating with MR -> considr surgery instead

Note: tumor markers are currently not recommeded for follow up.

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31
Q

Describe broadly the treatment of Gallbladder cancer

A

Staging investigations

  • CT chest abdo pelvis for nodes, vascular and peritoneal disease
  • MRI - for liver parenchyma and bile duct
  • Blood to check for jaundice (poor prognostic indicator - do not offer surgery straight up without MDM discussion)
  • Diagnostic laparoscopy
  • PET CT - controversial, use only when CT/MRI findings equivocal

Regional nodes: cystic, hepatoduodenal, hepatic artery and portal vein nodes

Non- regional nodes - para-aortic, peri-caval, SMA, coeliac nodes - involvement of these denote metastatic disease and is unresectable

Margin = 2 cm, plus clear margin on cystic duct end.

Criteria for unresectabitly:

  • unresectable hepatic mets
  • Distant mets (including non-regional nodes)
  • Peritoneal disease
  • Extensive involvement of hepatic artery, portal vein or hepatoduodenal ligament.

Treatment: surgery is the only curative treatment, but it is only offered if curative surgery can be achieved with clear margins. There is no role for palliative debulking surgery. treatment depends on the stage of disease

T1a (invades lamina propria) - cholecystectomy only

T1b (invades Muscle layer) - Controversial. Although T1b means tumour not through muscularis propria, studies have reported up to 20% LN involvement. If patient is fit then extended cholecystectomy (2cm margin on liver with non-anatomical resection of segments IVb and V) + regional lymphadenectomy

T2-3 (T2 - invades perimuscular layer T3 perforates visceral peritoneum or invades into 1 surrounding organ) - Extended chole + regional lymphadenectomy +/- bile duct resection (if negative margins can’t be achieved with chole on cystic duct stump on frozen section)

T4 (invades 2 or more surrounding organs)- palliative chemo +/- radiation

Jaundiced patient - relative contraindication to surgery due to poor prognosis - should be discussed in MDM, jaundice can be relieved with stenting post staging.

Palliative chemo -

  • gemcitabine
  • capox
  • folfox

Radio

  • EBRT + 5FU

Biliary drainage

relieve bowel obstruction - palliative bypass

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32
Q

OUTLINE THE MANMAGEMENT options for PERIANAL FISTULAS

A

Simple fistula -> fistulotomy (>90% healing, low incontinence in well selected patients)

Complex fistula -> seton + sphincter preserving procedure

  • Cutting seton (80% success, 30% incont)
  • LIFT (90% success, rare incon)
  • Advancement flap (70% heal, 12% incont, 0-40% recur)
  • Modified Hanley procedure (90% heal, no incon)
  • Diversion
  • Proctectomy
  • Fibrin glue (up to 70% recur, useful adjunct to flap)
  • Fistula plug (up to 70% recur)
33
Q

Causes of stone disease after bowel resection/ malfunction

A
  1. Oxalate stones - SB resection -> increased fatty acid delivery to colon due to a) loss of length and b) disruption of enterohepatic circulation -> fatty acid increases colonic permeability to oxalate and preferentially binds to calcium leaving oxalate free -> oxalate stones
  2. Gallstones - terminal ileal resection/ disease -> disruption of enterohepatic circulation -> decreased bile acid –> increased cholesterol in bile -> cholesterol stone
  3. Uric acid stone - Colon rection -> bicarbonate rich ileal effluent and volume contraction -> formation of concentrated acidic urine -> uric acid crystallises out due to already acidic urine
34
Q

Describe risk stratification for colorectal cancers

A

CATEGORY 1 - no specific surveillance

  • 1st degree x 1 >55yrs

CAT 2 - 5 yearly cols from 50 or 10 yrs earlier than earliset cancer

  • 1st deg x 1 <55
  • 1st deg x 2 any age

CAT 3

  • familial CRC
  • 2 x 1st deg with one <55yrs
  • 3 rels with 1 st degree
  • personal history or rel with CRC and multiple bowel polyps
35
Q

How are anal squamous intraepithelial lesions treated?

A
  1. Prevention - Education, Contact tracing, HPV vaccination
  2. Check for HIV since conversion rates much higher
  3. Asymptomatic LSIL treatment is optional, but patients should undergo High resolution anoscopy to rule out HSIL/Anal cancer
  4. Treatment of HSIL -
  5. Medical options:
  • Podophyllin cream
  • Imiquimod (5FU) application 3-4 times a week for 16 weeks
  • cryotherapy
  1. Surgical excision
  2. Follow up with Anoscopy with anal mapping and acetic acid staining plus biopsy usually 4-6 months until lesion clearance.
36
Q

How is Barrett’s graded endoscopically?

A

It is graded using the Prague C&M system

C - circumferential extent (distance from incisors at GEJ - distance to proximal circumferential Barrett’s)

M - maximal extent (distance from incisors at GEJ - distance to max proximal extent of Barrett’s)

37
Q

What is the pathognomonic ERCP sign of IPMN?

A

Mucin protruding from widely open papilla

38
Q

How can you predict the risk of residual disease after resection of a malignant colorectal polyp?

A

A combination of Haggit, Kikuchi, resection margin and other high-risk features are used to predict the chance of residual malignancy after resection of a malignant colorectal polyp. Even when dealing with high-risk polyp, the final resection specimen will be devoid of malignancy in 80-90% of cases.

High risk:

Haggit 4 = 20%

Kikuchi SM3 = 20%

Sessile polyp = 20%

Resection margin <1mm = 20%

Poor differentiation = 15%

Moderate risk

Kikuchi SM2 = 10%

LVI = 10%

Low risk

Tumour budding = 5%

Resection margin 1-2 mm = 5%

39
Q

Classify the options for breast reconstruction

A

Can be divided into

Autologous

  • ​Free
  • Pedicled e.g LD falp

Implant based

  • Immediate
  • Delayed

Combination of Autologous and implant based

40
Q

Indications for neo-adjuvant imatinib in GIST

A
  1. Borderline resectable GIST
  2. Potentially resectable metastatic GIST (liver, peritoneal mets)
  3. Gist in
    1. esophagus
    2. EG junction
    3. duodenum
    4. lower rectum

Total recommended duration for imatinib is not clear, US FDA advised a total of 3 years

41
Q

Surveillance in Lynch

A

Colonoscopy - 1-2 yearly from 25 yrs (or 5 yrs < youngest rel)

Screening for extra colonic cancer varies from centre to centre and there is no strong evidence of benefit but it is still recommended.

Gynae - annual TV scan and endometrial sampling

  • annual Ca 125

Stomach - 2 yrly Gastroscopy

Skin - annual skin check

Panc - yearly Ca19-9 and LFT

Urothelium - annual US imaging of KUB

annual urine cytology

42
Q

Treatment options for FAP. When is surgery performed?

A

Chemoprevention: long term data ar missing hence no strong recommendations are present. Agents used in small studies includes: Sulindac, Cox2 inhibitors, omega 3 fish oils.

Surveillance - colonic and extra colonic, but given APC has 100% penetrance, patients will need surgical prophylaxis

Surgical options

  • TAC IRA - particularly for attenuated FAP
  • RPC or pan-proctocolectomy plus end ileostomy
    • patient preference
    • rectal cancer
    • mutation in codon 1309 of APC gene which manifests with florid rectal polyposis

TIMING OF SURGERY

  • Elective- Early teens. When social and academic impact will be minimum e.g. GAP year. In patients with sparse or small adenomas resection can be deferred to late teens or early 20s
  • Non -elective
    • ​presence of cancer/dysplasia/multiple polyps >6mm
    • multiple/ dense polyposis making surveillance difficult
    • bleeding
    • marked increase in polyps between subsequent exams

UPPER GI SURGERY

  • endoscopic therapy for Spiegelman 3, prophylactic pancreaticoduodenectomy for Spiegelman 4.
43
Q

How is esophagitis classified?

A

it is classified by LA grade on endoscopy

A - < 5mm not across folds

B- > 5 mm not across folds

C- across 2 or more folds but < 75% circumference

D - > 75% circumference

44
Q

Indications for neo-adjuvant therapy in breast cancer

A

NAC is usually indicated in

  • Stage 3 or T3 breast cancer
  • Stage 2 HER2+ and triple negative cancers
  • patients with temporary contraindications to surgery e.g., pregnancy

NAC is sometimes considered in

  • downstaging axillary disease especially cN1 disease to avoid axillary dissection (SNB done if response)
  • downstage breast disease in early breast cancer where tumour to breast ratio prevents BCS and patient desires BCS
  • select early breast cancer (T1c i.e. >1cm but <2cm) if they are triple negative or HER2 +ve can also given NAC particularly given that their cancers typically respond well to NAC and they will need chemotherapy at some stage of treatment for thier current tumor.
45
Q

colonoscopic surveillance in UC

A

Risk 2% at 10 yrs and 1 % per year thereafter. In PSC patients risk is higher 30% at 20 yrs and 40 % 30 yrs.

Start colonoscopy (ideally chromoendoscopy - indigocarmine dye spray) at 8-10 yrs after pancolitis and in absence of any lesion perform quadrantic biopsy every 10 cm (around 33 biopsies of normal appearing mucosa needed to detect LGD with 90% confience)

PSC - col on diagnosis and yearly thereafter

LGD - 24% upgrade rate on resection - resect vs observe

HGD - resect (up to 44 % upgrade rate even with complete excision due to field affect of colitis)

46
Q

What are the relative roles of investigation for reflux?

A

Endoscopy

  • rules out cancer
  • if it shows reflux, then severity grading can be done and, pH studies are not needed

pH studies (Use pre-op or for uncertain diagnosis)

  • establish presence of reflux
  • Can help establish casualty

Impedance

  • to diagnose non-acid reflux e.g. bile reflux, post prandial reflux

Manometry (Used pre-op)

  • to rule out motility disorder before surgery

Imaging

  • Not used routinely but can help establish motility or show hiatus hernia
47
Q

Indications for surgery in Crohn’s and the main pre-op priorities

A

Emergency

  • Perforation with peritonitis
  • Toxic megacolon
  • Massive bleeding
  • Failure of medical therapy (typically after at least 7 days)

Elective

  • Failure to wean off steroids
  • Failure to thrive/ growth retardation
  • Fistula
  • Symptomatic stricture
  • localised obstructive ileocecal disease with no inflammation

Pre-op prep

  • Control sepsis (Perc drain collection >5cm)
  • Optimize nutrition
  • Assess disease with scope and cross-sectional imaging
  • Plan procedure
48
Q

Indications for neo-adjuvant therapy in rectal cancer

A

Absolute

  1. T3/T4 rectal cancers (this is the only indication that is supported by a number of RCTs)

Relative

  1. Node positive T1/T2 cancers
  2. Threated CRM (disease within 1-2 mm of mesorectal fascia)

controversial

  1. T1/T2 Node negative low rectal cancer that need APR - neoadjuvant is sometimes administered to downstage tumour so LAR can be performed rather than APR
49
Q

Classify hiatus hernia

A

Type 1 (sliding) - GEJ lies above hiatus

Type 2 - (rolling) - part of stomach herniates past GEJ which remains intra-abdominal

Type 3 - combined type 4 - other organs herniate. Most commonly transverse colon Giant - where >50% of stomach has herniated.

Types 2-4 need surgical correction

50
Q

What is the colorectal cancer risk in UC and what factors influence it?

A

Colorectal cancer risk is about 2% at 10 years after onset of disease and rises by 1% per year thereafter.

Risk is increased by

  • continuous active disease
  • severe disease
  • diffuse involvement (pancolitis)
  • prolonged disease
  • PSC
  • Dysplasia (LGD increases CRC risk by 9 times and can directly progress to cancer bypassing the high grade state - nearly 25% of patients with LGD harbour either HGD or invasive cancer elsewhere)
51
Q

Haggit classification for malignant polyps

A

4 levels depending on level of malignant transformation

Haggit 1 - head

2 - neck

3 - stalk

4 - base

LN involvement - 1-3 = 3%; 4 = 20%

52
Q

how do you classify gastric cancer?

A
53
Q

What are the CT landmarks for identifying the level of esophageal cancer

A
  1. Cricopharyngeus (15 cm from incisors) - cerv esophagus starts
  2. Sternal notch (20cm) - upper thoracic esophagus starts
  3. Azygous vein (25cm) - mid part of thoracic esophagus starts
  4. Inferior pulm vein (30 cm) - lower thoracic esophagus starts
  5. GEJ (37cm) - abdominal esophagus starts
54
Q

Treatment for anal SCC

A

Nigro protocol (aka Combined modality treatment) - mainstay 80% respond

  • Mitomycin
  • radiation with 5FU sensitization (45gy)

APR

  • Salvage APR may be necessary for residual disease (t3/4 disease).
  • recurrence
  • fistula
  • incontinence
55
Q

Neoadjuvant options for esophageal cancer

A
  1. Chemorad (for fit patients)
    1. (CROSS) Carboplatin and paclitaxel + 50 gy radiation
  2. Chemotherapy
    1. FLOT
    2. ECF (MAGIC trail)
56
Q

How is H. Pylori infection diagnosed

A

Invasive tests

  • Rapid Urease test (>90% sensitivity and 99-100% specificity)
  • Microscopy with HE stain
  • Culture (80% sensitive, allows antibiotic sensitivity testing)

Non-invasive tests

  • Urea Breath test (sensitivity and specificity >95%), samples entire stomach
  • serology (sens 90%, spec 75-95%) - titres are positive up to an year after infection
  • Stool antigen (sens and spec >90%) - cheap and easy to assess eradication
57
Q

What are the high-risk features and worrisome features for IPMN

A

HIGH RISK FEATURES

  • Jaundice
  • Main duct >10mm diameter
  • Enhancing solid component

WORRISOME FEATURES

  • Pancreatitis
  • cyst >3cm
  • wall enhancement
  • non-enhancing mural nodule
  • Duct 5-9 mm
  • abrupt calibre change in duct with distal pancreatic atrophy
  • Lymphadenopathy
58
Q

Outline the management of bleeding oesophageal varices

A

Management can be broadly classified under the following categories:

  • Resuscitative and temporising measures
  • Pharmacologic
  • Endoscopic
  • Interventional
  • Surgical

RESUSCIATION AND TEMPORISING MEASURES

  • Airway and O2
  • hemodynamic resus
  • correct coagulopathy
  • Antibiotics (ceftriaxone 1g x 7 days)
  • Balloon compression
    • Intubate before starting
    • Check position with fluoroscopy before full balloon inflation
    • can be left in situ for 24-48 hrs before necrosis
    • start with oesophageal pressure 35-40 mmhg, once bleeding stops bring down by 5 mm to 25 mm
    • Can be repeated if bleeding restarts

Pharmacology

  • Terlipressin 2mg iv q 4hrs

Endoscopy

  • Within 12 hrs of admission
  • EVL better than sclerotherapy
  • Cyanoacrylate better for gastric varices
  • If rebleeding occurs - repeat once more then go to TIPS or surgery

INTERVENTIONAL

  • TIPS if no contraindication
  • Attempt after 2 failed endoscopic attempts

SURGICAL (50% mortality due to encephalopathy, sepsis and renal failure - hence TIPS is favoured)

  • Shunt
    • Nonselective (portocaval shunt) - quickest but most encephalopathy
    • Selective (distal splenorenal)
    • Partial non-selective (portocaval interposition graft - decompresses portal system and allows hepatic flow)
  • Non-shunt
    • Oesophageal transection and reanastamosis after ligation of varices
    • Devascularization of GEJ (Sugiura procedure)
59
Q

What are the Hard signs and soft signs of vascular injury?

A

HARD SIGNS (Immediate intervention)

  • pulsatile bleeding
  • expanding hematoma
  • bruit/thrill over artery
  • distal ischaemia (5 Ps)

SOFT SIGNS

  • Bleeding at scene
  • stable hematoma
  • Injury close to major artery
  • Neurological deficit
  • weak pulse distally
  • Altered doppler signal
  • reduced ABPI
60
Q

What are the mechanisms / causes of intestinal failure

A

Multifactorial

  • Loss of actual length - 100 cm of SB or 50 cm of SB and colon is usually the minimum needed to come off TPN
  • Loss of functional length - fistulas e.g., enterocutaneous or Crohn’s fistula
  • Loss of absorptive capacity - IBD, coeliac, radiation
  • Loss of function - ileus, gastroparesis, pseudo-obstruction
61
Q

What genetic cancers can affect the stomach?

A

CDH1 mutation

  • diffuse stomach cancer, young females, also have ILC of breast

Le Fraumeni

  • p53 mutation (tumour suppressor gene) - multiple other malignancies, most commonly soft tissue and bony sarcomas, brain tumours, breast tumours, GI tract tumours, Lung, thyroid.

Lynch

  • colon cancer (MMR gene)

FAP

  • APC gene, colon cancer

Peutz Jeghers

Juvenile polyposis (SMAD4)

62
Q

What are the extracolonic manifestations of FAP

A

ECTODERMAL

  • Epidermoid cyst
  • Pilomatrixoma
  • CNS tumour
  • CHRPE (congenital hypertrophy of retinal pigment epithelium)

MESODERM

  • desmoid tumours, excessive adhesions
  • Bone - osteoma, exostosis
  • dental - unerupted/extra teeth, odontoma

Endodermal

  • adenoma and carcinoma - stomach, duo, SB, Biliary tree, thyroid, adrenal cortex
  • fundic gland polyp
  • hepatoblastoma
63
Q

HOW CAN YOU CLASSIFY BLEEDING PEPTIC ULCER

A

This is done during endoscopic evaluation.

FORREST CLASSIFICATION

1 - actively bleeding (a= spurting, b = ooze)

2 - recent bleed (a = naked vessel, b = clot, c = pigment spot)

3 - No bleeding (clean ulcer base)

64
Q

What are the types of phyllodes tumor?

A

Classified into benign, borderline or malignant based on

  • stromal cellularity and atypia
  • mitosis per 10 hpf
  • infiltrative margins
  • stromal overgrowth

Benign - mild to moderate stromal cellularity and atypia, pushing margins, mitosis <5 per 10 hpf, no stromal overgrowth

borderline - more stromal cellular atypia, mitosis 5-9 per 10 hpf, no stromal overgrowth, microscopic infiltrative margins

Malignant - marked atypia, macroscopic infiltrating margins, mitosis >10 per 10 hpf, stromal overgrowth present

65
Q

Treatment of Barretts

A

GENERAL MEASURES

  • PPI - once daily
  • weight loss
  • quit smoking
  • quit alcohol

METAPLASIA

  • discuss surveillance (0.5% cancer risk per year but 30 times the basal risk but still low risk). ongoing surveillance related issues and scope related complications plus therapeutic procedures as needed
  • Surveil every 3-5 yrs with 2 cm quadrantic biopsies

LOW GRADE DYSPLASIA

  • expert pathology review
  • surveillance every 6 months with quadrantic biopsies every 1 cm until 2 negative dysplasia. then increase interval to 2-3 yrs (>3cm) or 3-5 yrs (<3cm)

INDEFINITIE FOR DYSPLASIA

  • Repeat endoscopy in 2 months with 1 cm quadrantic biopsies

HIGH GRADE DYSPLASIA

  • expert pathology review
  • treat with EMR/RFA and resect any irregular areas of metaplasia.
66
Q

Describe Siewert classification of esophageal cancers

A

Siewert classification is used for cancers of the GEJ.

S1 - 5cm to 1 cm proximal to GEJ

S2 - 1 cm prox to 2 cm distal to GEJ

S3 - 2 cm - 5 cm distal to GEJ

S1 and S2 treated as distal esophageal cancers

S3 treated as gastric cardiac cancer

67
Q

What is Van Nuys prognostic score and it’s utility?

A

VN prognostic score is used for DCIS prognostication and is based on tumor grade, tumor size, age, margins.

Tumor grade

  • 1 = low grade, no necrosis
  • 2 = low grade + comedo necrosis
  • 3 = high grade

Size

  • 1 = <15mm
  • 2 = 16 -40 mm
  • 3 = >40 mm

Age

  • 1 = <60
  • 2 = 40 -60
  • 3 = <40

Margins

  • 1 = >1cm
  • 2 = 1-9 mm
  • 3 = <1mm

Recommendation:

4-6 = low risk

7-9 = consider radiation

10-12 = consider mastectomy

68
Q

What are the adjuvant therapy options for melanoma

A

Depends on local protocols/ availability/ tumour characters.

Adjuvant therapy is indicated in stage 3 - 4 disease (nodes or mets)

Surgery

  • Oligometastatic disease that is resectable (best outcome)

Targeted therapy

  • ​**MAPK pathway - _(_BRAF+MEK - inhibitors if mutation present)
  • KIT - inhibitors (If mutated)

Immune therapy

Immune checkpoint therapy - blocks natural checkpoint for T-cell productions thereby unleashes massive number of T cells. Combination of CTLA4 + PD1 is recommended.

  • ​CTLA4 blockers - Ipilimumab (Yervoy)
  • PD-1 blocker - Pembrozulimab (keytruda), Nivolumab (Opdivo)

Isolated limb infusion using Melphalan

  • Papaverine used as vasodilator and heparin used as anticoagulant before melphalan infusion.

limited availability, no survival benefit but improves local control.

Radiotherapy

  • Palliative control of local disease

Chemotherapy

  • Limited role due to poor outcomes
69
Q

Severity assessment of pancreatitis

A

There are several ways to assess severity of pancreatitis. I use the Multiple organ dysfunction score as advised in the consensus Atlanta classification. Other methods like Glasgow score, CRP are also widely used.

Timing - On admission, and then at 24 hrs, 48 hrs and 7 days)

Mild

  1. No organ failure
  2. No local complication

Moderate

  1. Transient organ failure (<48 hrs)
  2. Local complication present

Severe

  1. Persistent organ failure (>48 hrs) (single or multiple)
70
Q

What are the endoscopic and histological features of Crohn’s vs UC?

A

Endoscopy - Crohn’s vs UC =

  1. Skip lesion vs continuous
  2. Rectum usually spared vs involved
  3. SB may be involved vs never involved
  4. Perianal disease may be present vs never present
  5. Strictures may be present vs no strictures
  6. Crohn’s also has linear ulcers not seen with UC

Histologically Crohn’s vs UC =

  1. Transmural vs mucosal/submucosal inflammation
  2. Granulomas (deep non-caseating granulomas and intra-lymphatic granulomas) present vs absent
  3. Goblet cell mucin preserved vs depleted
71
Q

Classify liver incidentalomas

A

Congenital

  • simple cysts
  • Polycystic liver disease
  • Haemangioma

Infective

  • Pyogenic liver abscess
  • Hydatid cyst

Neoplastic

  • Benign
    • FNH
    • Adenoma
    • Cystadenoma
    • Haemangioma
  • Malignant
    • Primary
      • HCC
      • Intrahepatic Cholangiocarcinoma
      • Cystadenocarcinoma
      • Hemangiosarcoma
    • Mets
    • Lymphoma
    • Melanoma
72
Q

Describe the genetics of Lynch syndrome

A

Lynch results from autosomal dominant germline mutation in mismatch repair gene (MMR). Vast majority of the mutations are in MLH1, MSH2, MSH6, PMS2 or EPCAM gene.

When there is MMR mutation it leads to errors in coding for microsatellite which is known as Microsatellite instability (MSI). MSI high tumours are usually due to Lynch.

However, some sporadic CRC can also exhibit MLH1 or PM2 mutation. In these cases it is important to know if these are sporadic vs Lynch (they will also have MSI due to MMR mutations by promoter methylation and occur in older age).

MLH1 or PM2 mutation + BRAF mutation -> not lynch

MLH1 or PM2 + no BRAF mutation -> do methylation studies:

  • Methylation present = Not lynch
  • Methylation absent = Likely Lynch -> genetic testing
73
Q

Benign breast disease that may need excision after core biopsy

A
  1. Fibroepithelial lesion suspected fibroadenoma -> excise -> To rule out phyllodes
  2. Radial scar/CSL >>>Vacuum/ excise>>>Associated with DCIS/Ca
  3. Phyllodes >>> excise >>> 1cm margin for malignant phyllodes, clear margin for benign
  4. ADH >>> Excise to clear margin >>> Associated with DCIS/Ca
  5. ALH/LCIS >>> No need to excise unless pleomorphic LCIS … LCIS = increased cancer risk
  6. Papilloma >>> Vacuum/excise >>> Core cannot differentiate benign vs malignant
  7. Granular cell tumour >>> Excise to clear margin >>> Uncertain imaging and histological features
  8. Desmoid >>> Excise to clear margin >>> Locally invasive
74
Q

Flow chart for assessment of reflux

A

Filter out atypical reflux and refer for investigation to other specs as needed.

Typical symptoms >>> trial PPI (if no alarm signs) >>> endoscopy (if it shows reflux changes pH not needed) otherwise >>> pH studies (if if confirms causality then impedance not needed) >>> impedance (if reflux still not diagnosed then diagnose functional GORD and don’t operate) otherwise >>> manometry >>> swallow only if concern about motility or hiatus hernia >>> assess for surgical suitability

75
Q

Outline the complications of acute pancreatitis

A

Early

  1. Local
    1. Peripancreatic fluid collection -> pseudocyst
    2. Necrotic collection -> WON
    3. Gastric outlet obstruction
    4. Splanchnic venous thrombosis (treat only symptomatic patients i.e. hepatic symptoms or SB symptoms with splenic V or SMV thrombus – optimise management of panc, start anticoagulation)
    5. Colonic necrosis
  2. Systemic
    1. Exacerbation of pre-existing disease
    2. Transient (<48hrs) and persistent organ failure (>48 hrs)
    3. SIRS
    4. DVT/PE

Late

  1. Pseudocyst
  2. Chronic pancreatitis
76
Q

Classify anal fistula

A

Parks classification (attached image)

  • submucosal
  • intersphincteric
  • trans-sphincteric
  • supra-sphincteric
  • Extra-sphincteric

SIMPLE FISTULA

  • Submucosal
  • intersphincteric
  • trans <30% ext sphincter involvement

COMPLEX

  • LOCATION
    • Transsphincteric >30% involvement
    • suprasphincteric
    • extrasphincteric
    • colovaginal
    • Horse shoe
  • pathology
    • Crohns
    • cancer
    • radiation
    • recurrent
    • multiple fistula tract
77
Q

Nutritional and pathophysiological consequence of 60cm terminal ileal resection

A

NUTRITIONAL

  • vit B12 deficiency (absorbed with intrinsic factor)
  • Vt ADEK - fat soluble vitamin

PATHOPHYSIOLOGICAL

  • Cholesterol stone (decreased bile acid pool secondary to enterohepatic circulation disruption)
  • Oxalate stone (decreased bile acid -> increases oxalate absorption)
  • colonic secretomotor diarrhoea (increased bile acid loss)
  • decreased fluid absorption in response to bolus hyperosmolar meals
  • Ileum better than jejunum at adaptation - loss of ileum increases risk of short bowel syndrome with future resection
78
Q

Diagnostic features of non IPMN panc cysts

A

SCA (resect only if symptomatic)

  • Can involve any part of panc
  • associated with other cystic disease e.g. VHL
  • Microcystic pattern
  • central calcification (sunburst)
  • No duct connection
  • EUS-FNA
    • Viscosity <1.6
    • Lipase >6000
    • CEA low (<5ng/ml)
  • Molecular marker - VHL +, GNAS-ve, Kras -ve

MCN (always resect, however newer studies suggest resecting >3cm like BD-IPMN)

  • mainly in body or tail
  • No connection to duct
  • Macrocystic pattern
  • Peripheral (egg cell calc) - marker of malignancy
  • Ovarian stroma present - differentiates from IPMN
  • viscosity >1.6
  • CEA high >190
  • Genetic marker - Kras +ve

Pseudocyst

  • Thick inflammatory wall
  • History of pancreatitis or pancreatic trauma
  • Connected to the duct
  • viscosity <1.6
  • Lipase >6000
  • CEA low (usually <5 but if >480 - repeat EUS in 3-6 months)

SOLID PSEUDOPAPILLARY TUMOR

  • Young females <35 yrs
  • solid and cystic components +/- calcifications
  • Body and tail
  • no definitive markers
  • Resect due to high malignant potential
79
Q

Describe the staging of breast cancer and significant branch points in management

A

FRACS Revision (12 decks)

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