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FRACS study > Appendix to Anus > Flashcards

Appendix to Anus Flashcards

1
Q

Anatomy of the appendix

A

Midgut organ

Variable length 2-25cm

3 Taeniae coli coalesce to form a complete longitudinal muscle layer over appendix

Lined by colonic type columnar epithelium, neuroendocrine and mucin producing goblet cells

Blood supply from posterior caecal from ileocolic

Lymphatics to ileocolics

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2
Q

Appendicitis pathophysiology

A

Luminal obstruction

Increased intraluminal pressure from continued cellular mucus and bacterial gas production

Distension

Bacterial overgrowth

Venous stasis

Ischaemia

Perforation, either local or free

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3
Q

Bacteriology of appendicitis

A

Colonic flora- mixed anaerobic and anaerobic cultures

Aerobes

  • E coli
  • Enterococci
  • pseudomonas

Anaerobes

  • Bacteroides (fragilis)
  • Bilophila wadsworthia
  • peptostreptococci
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4
Q

List cystic lesions of the appendix

A

Non- Neoplastic

  • Simple mucocoele (retention cyst)

Neoplastic

  • Serrated Appendiceal polyps
  • Low Grade Mucinous Neoplasms
  • High Grade Mucinous Neoplasms
  • Mucinous Adenocarcinoma
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5
Q

LAMN vs HAMN

A

Differentiated only by degree of dysplasia

HAMNs show high grade nuclear features: enlarged, pleomorphic, hyperchromatic. high mitotic activity

Neither invade the muscularis mucosa but both can have mucin forced into or through the wall or rupture the appendix and lead to PMP

LAMN staged as in situ disease

HAMN as invasive disease T1-T4

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6
Q

Appendiceal neuroendocrine neoplasms

A

Usually incidental/unexpected at appendicectomy

Most commonly submucosal in distal 3rd

Broadly grouped into

  • Well differentiated (NETs)
    • Divided into grades
      • Low
      • Intermediate
      • High
    • mutations in MEN1, DAXX and ATRX are entity defining
  • Poorly differentiated
    • Divided into
      • small cell type
      • large cell type
    • TP53 or RB1

Major adverse prognostics

  • Size >2cm
  • Grade 3
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7
Q

List the primary appendiceal neoplasms

A

Epithelial derived

  • LAMN
  • HAMN
  • Adenocarcinoma (mucinous, signet ring or intestinal)
  • Goblet cell adenocarcinoma (mixed NET and adeno features- manage as adenoca)

Neuroendocrine derived

  • NET (well vs poorly differentiated)
  • MiNEN (mixed neuroendocrine-non neuroendrocrine) tumours (manage as poor diff. NET)
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8
Q

Borders of fore, mid and hindgut

A

Defined by vascular supply

Foregut

  • Oesophagus to duodenal ampullla- Coeliac

Mid gut

  • Ampulla to distal third of transverse colon- SMA

Hindgut

  • Distal transverse to rectum- IMA
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9
Q

Colon lengths

A

Total colorectal length ~150cm

  • Caecum 10cm
  • Ascending 15cm
  • Transverse 45cm
  • Descending 25cm
  • Sigmoid 40cm
  • Rectum 15cm
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10
Q

Vertebral heights for the origins of the non paired visceral branches of the aorta

A

Coeliac T12

SMA L1

IMA L3

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11
Q

What is the arc of Riolan

A

Inconstant arterial communication between the proximal IMA and Proximal SMA

Flow may be in either direction

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12
Q

What is the relationship of the SMV to the SMA

A

The vein sits on the right of the artery and behind its arterial branches to the colon

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13
Q

What are the levels of the colonic lymph nodes

A

Epicolic- along bowel wall and in appendica epiploicae

Paracolic- Marginal artery

Intermediate- along main branches

Primary- SMA and IMA

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14
Q

Sympathetic supply of colon

A

T6-T12 preganganglionic sympathetics synapse in preaortic ganglia then travel with SMA branches to right and transverse colon

L1-L3 preganglionic sympathetics form preaortic ganglion above bifurcation then runs with IMA, lower fibers involved in inf. hypogastric plexus also

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15
Q

Parasympathetic supply of colon

A

Right (posterior) vagus supplies SMA distribution

Pelvic Splancnics S2,3,4 through inf hypogastric plexus to bowel to supply IMA distribution

Synapse at the organ

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16
Q

Primary energy source of the colonocyte

A

Short chain Fatty acids from bacterial fermentation of complex carbohydrate.

Butyrate is the most common

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17
Q

How much ileal effluent enters the caecum per 24 hours

A

1000-1500mL

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18
Q

How do antibiotics cause diarrhoea

A

Decreased colonic bacteria

Decreased fermentation

Decreased Butyrate production

Decreased active transport of sodium from lumen

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19
Q

What are the layers of the enteric nervous system

A

Subserosal, myenteric (Auerbach) plexuses

Submucusal (Meissner) plexuses

Mucosal plexuses

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20
Q

Normal bacteriology of the colon

A

Bacteroides most common (Anaerobe)

E. Coli most common aerobe

Pseudomonas

Enterococcus

Proteus

Klebsiella

Streptococci

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21
Q

What is used for bowel prep

  • What are the benefits of this agent

Name some alternative agents

A

Polyethylene glycol and electrolyte solutions

  • High molecular weight polymer and balanced electrolyte solution
    • Isosmotic
  • e.g Klean prep
  • 4 sachets in 1L of water each
    • Consume 250ml every 10 mins
  • Does not injure the colonic mucosa
  • Does not induce major fluid shifts (although this has been rarely reported anyway)

Alternatives

  • All hyperosmotic
    • Sodium picosulphate (picoprep)
    • Sodium phosphate
    • Magnesium citrate
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22
Q

Oral antibiotics for elective bowel surgery

A

Not used routinely in my institution but there is evidence from RCTs that shows reduced SSI rates and similar C. diff rates

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23
Q

Appropriate stoma siting

A

Consultation with stoma therapist is optimal

Away from creases

Visible

Easily accessible

Through Rectus

In a normal size patient usually below umbo and at the apex of the natural curvature if the abdomen

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24
Q

Delineate the Hinchey Classification

A

I- Localised pericolonic or mesenteric abscess

II- Pelvic walled off abscess

III- Purulent peritonitis

IV- Faeculent peritonitis

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25
Q

Causes of pseudoobstruction

A

Opiates

Neuroleptic meds

Retroperitoneal haematoma

Autonomic disruption (true Ogilvie’s)

DM

Severe metabolic illness

Electrolyte disturbance

Hyperparathyroidism

Parkinsonism

Scleroderma

Systemic lupus erythematosis

Uraemia

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26
Q

Pathophysiology of colonic pseudoobstruction

A

Signs and symptoms consistent with a large bowel obstruction without mechanical cause.

Multiple underlying aetiologies and often multifactorial.

Results ultimately from an imbalance of sympathetic and parasympathetic nervous supply to the colon.

Likely related to sympathetic overactivity vs parasympathetics.

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27
Q

Treatment of pseudoobstruction

A

First: Neostigmine

  • 2.5mg IV over 3 mins
  • Bradycardia- cardiac monitoring on and atropine ready

Second: Spinal epidural

  • Block sympathetics- effective

Third: Colonoscopy

  • Caution re: insufflation and perforation,
  • Higher recurrence rates

Operate if needed or unable to resolve

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28
Q

Features of UC

A

Clinical features

  • Bleeding and diarrhoea more prominent than Crohn’s
  • Perianal disease rare

Microscopy

  • Inflammation of mucosa and submucosa only
  • Crypt abscesses (also seen in Crohn’s and infection)

Endoscopic

  • Continuous
  • Hyperaemic friable mucosa
  • (ulceration is actually rare)
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29
Q

Features suggestive of malignancy in UC strictures

A

Prolonged UC (0%<10 years, 60%>20 years)

Proximal to splenic flexure

LBO

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30
Q

Extraintestinal Manifestations of IBD

A

Joints

  • Arthritis
  • Ankylosing Spondylitis

Skin

  • Erythema Nodosum
  • Pyoderma Gangrenosum

Eyes

  • Primary
    • episcleritis
    • uveitis
  • Secondary
    • cataracts (steroid)

Hepatic

  • Primary Sclerosing Cholangitis

Manifestations which may respond to surgical management of the affected bowel:

  • Skin
  • Eye
  • Arthritis

Manifestations which do not respond to surgical management affected bowel:

  • Ankylosing spondylitis
  • PSC
    • colitis often less severe with PSC associated phenotype but colon cancer risk is 5x that of UC alone
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31
Q

UC ECCO guidelines for UC management

A

Mild-moderate proctitis-

  • 5ASA, topical,
  • If resistant add oral 5ASA initially

More proximal involvement-

  • enema and oral

Refractory- steroids, cyclosporin, biologics

Severe colitis-

  • Steroid for 3 days-
  • if no/inadequate response- either cyclospirin, infliximab or surgery
  • if rescue therapy given then surgery if no/inadequate response by further 4-7 days

NB methotrexate is out

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32
Q

Truelove and Witts criteria for severe colitis in UC

(used by ECCO)

A
  • Bloody diarrhoea at least 6x per day

AND any of:

  • Pulse >90
  • Temp> 37.8
  • Hb <105
  • ESR >30
  • CRP>30
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33
Q

Indications for surgery in UC

A

Acute

  • Toxic megacolon
  • Non response to therapy
  • Bleeding

Chronic

  • Dysplasia
  • Stricture (presume malignancy)
  • Cancer
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34
Q

Risk factors for Crohn’s

A

Smoking

Jewish descent

Away from the equator (Scotland, Scandinavia)

Prev. Abx use

OCP

FHx

Mycobacterium paratuberculosis?

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35
Q

Mechanism of action of Infliximab

A

Anti TNF-a

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36
Q

Clostridioides Difficile risk factors

A

Antibiotic use (esp Clinda)

Hospitalisation

Age

Comorbid illness

Acid suppression

IBD

Cirrhosis

GI surgery

Immunosuppression

Obesity

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37
Q

Clostridioides difficile microbiology

A

Gram positive spore forming, toxin producing anaerobic bacillus

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38
Q

Pathophysiology of C. Diff

A

Interruption of normal flora

Colonisation

Toxin production

  • Toxin A (enterotoxin) and B (cytotoxin) enter colonocytes and interrupt Rho GTPases
  • Toxin A also direct neutrophil recruitment and activation of macrophages

Colonocyte death and direct toxin A effects lead to inflammation

  • mediated by IL-1,6,8, TNF, substance p causing:

Further colitis and colonocyte death.

Toxin B is a potent cytotoxin, ? necessary to pathogenesis

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39
Q

Classification of ischaemic colitis

A

By depth and cause

Partial thickness

  • transient
  • stricturing

Full thickness with gangrene

Occlusive

Non occlusive

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40
Q

The adenoma-carcinoma pathway

A

Normal Colonocyte

  • APC/Beta-catenin (tumour suppressor)

Tumour Initiation (abnormal crypt foci and early adenoma)

  • KRAS

Adenoma formation and growth

  • DCC/SMAD4/SMAD2

Late adenoma

  • p53

Carcinoma

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41
Q

What is the APC gene

A

Tumour suppressor gene

Chromosome 5q21

APC mutation leads to increased intracytoplasmic pool of Beta Catenin and Wnt signalling pathway disruption

It is the underlying genetic mutation in FAP and the initial mutation in the sporadic adenoma-carcinoma pathway in 80%

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42
Q

Gardner syndrome

A

Original description is FAP with extraintestinal manifestations

  • Mandibular osteomas
  • Desmoids
  • Periampullary neoplasms

More recently recognised associations

  • papillary thyroid cancer
  • medulloblastoma
  • gastric fundic gland polyps
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43
Q

MYH associated polyposis (MAP)

A

Autosomal recessive polyposis and cancer

Mutation in MYH gene encodes oxidative repair of DNA genes

Mutation promotes APC mutation

MAP phenotype is variable

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44
Q

p53

A

Tumour Supressor gene

Induces either:

  • Apoptosis or:
  • G1 cell cycle arrest allowing DNA repair-

in response to cellular injury

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45
Q

HNPCC

A

Lynch syndrome

Autosomal dominant, 80% penetrance

Accounts for 3% of colon cancers

Mutation in DNA MMR genes

  • MLH1, PMS2, MSH2, MSH6, EPCAM
  • MLH1 and MSH2 account for 90% of detected known mutations

50% of clinical Lynch syndrome (on family history) will not have an identifiable genetic mutation

MMR defects induce microsatellite instability

  • Errors in S phase of DNA replication- resulting in vast increase in rate of mutation

Associated malignancies-

  • Classically
    • Colon
    • ovarian
    • endometrial
    • urothelial
    • gastric.
  • Others
    • HPB
    • gliomas
    • sebaceous skin cancers
    • Breast cancers
      • in some studies but this finding is variable
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46
Q

Define invasive colon cancer

A

Breach of the muscularis mucosae

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47
Q

Haggitt Classification for Malignant polyps

A
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48
Q

Kikuchi

A
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49
Q

Paris Polyp Classification

A
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50
Q

Kudo Pit Pattern

A
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51
Q

Tattooing in colonoscopy

A

Use pure carbon black

Polyps >1cm- 1 spot

Worrisome polyp (suspect malignancy)- 3 spots

Cancer- 3 spots

Not usually caecum/ascending (caecum is reliable endoscopic landmark) or rectum

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52
Q

Risk Factors to consider in malignant polyps:

ACPGBI 2013

A
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53
Q

Malignant polyp risk factors

A

Haggit 4

SM2-3

Positive margin

LVI +

Width of cancer >4mm

Depth of cancer >2mm

Tumour budding

Cribriform

Poor differentiation

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54
Q

FAP expression and clinical outcomes

A

100% penetrance

Autosomal Dominant

Average age of presentation with new diagnosis 29

Average age of Malignancy 39

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55
Q

FAP UGI Surveillance recommendations

A

No firm guidelines, initial endoscopy at ~30 years

Suggest endoscopy based on Spigleman stage

  • Stage 0: Every four years
  • Stage I: Every two to three years
  • Stage II: Every one to three years
  • Stage III: Every 6 to 12 months
  • Stage IV: In the absence of surgery (duodenectomy), surveillance every six months
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56
Q

Muir-Torre syndrome

A

Rare

Autosomal dominant

Phenotypic variant of HNPCC

At least:

  • 1 sebaceous skin tumour and:
  • 1 visceral tumour
    • colon
    • endometrial
    • urothelial
    • ovarian

Same Mutations as HNPCC

  • MLH1
  • PMS2
  • MSH2
  • MSH6
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57
Q

Sporadic MSI in colon cancer

A

Results from hypermethylation of MLH1 promoter region and is strongly associated with the BRAF V600E mutation.

  • Detection of BRAF V600E almost completely excludes lynch syndrome
58
Q

MSI status prognosis and management

A

True Lynch have favourable stage for stage prognosis

MSI high (MMR deficient) cancers are resistant to 5-FU based chemotherapy and there is no or little survival advantage

MSI high cancers may be sensitive to irinotecan, mytomycin and checkpoint inhibitors e.g pembrolizumab

59
Q

Peutz-Jeghers syndrome

A

Rare autosomal dominant syndrome

Congenital hamartomatous polyposis of GI tract and hyperpigmentation of buccal mucosa, lips and digits

STK11 tumour supressorgene

2-10% GI cancer risk (panenteric)

Associated cancers

  • GI
  • Breast
  • Cervix
  • Testicle
  • Ovary
  • Pancreas
60
Q

Juvenile polyposis syndrome

A

Rare

Autosomal dominant

High penetrance

SMAD4 tumour suppressor

Variable phenotype

Predominantly hamartomas but also adenomas and increased colorectal cancer risk

Colonic and extraintestinal cancers

61
Q

Syncronous Colorectal cancer rate

A

3%

62
Q

Dukes staging

A
63
Q

Colorectal Staging:

Tumour (overview)

A

T1: tumor invades submucosa

T2: tumor invades muscularis propria

T3: tumor invades through the muscularis propria into the pericolorectal tissues

T4:

  • T4a: tumor invades through the visceral peritoneum
    • including gross perforation of the bowel through tumor
  • T4b: tumor directly invades or adheres to other adjacent organs or structures
64
Q

Non TNM prognostic variables in colorectal cancer

A
  • CEA
  • MSI
  • Tumour deposits
  • Satellite deposits (? obliterated LN’s)
  • Tumour regression grade
  • CRM
  • Resection margin
  • Perineural invasion
65
Q

Assessing neoadjuvant response in colorectal cancer

A

Multiple scoring systems, AJCC advocates/uses the:

  • Modified Ryan tumour regression score
    • 0- No viable tumour cells (complete response)
    • 1- Single cells or rare small groups of cells (near complete response
    • 2- Residual cancer with evident regression (desmoplastic response)
    • 3- No evident response
66
Q

5 year survival by stage in colorectal cancer

A

From SEER 1998-2005

I- 90%

II- 75%

III- 50%

IV- <5%

One suspects outcomes have improved from these though

67
Q

Surveillance post colorectal cancer

A
68
Q

Adjuvant chemotherapy in colorectal adenocarcinoma

A

Stage 2 and above with at least 1 poor prognostic factor should be considered

  • Treatments are 5F-U based
    • Either infusiional 5-FU or capecitabine
      • Capecitabine may infact be superior as it is activated by an enzyme universally overexpressed by tumour cells
  • addition of Oxaliplatin (FOLFOX) or Irinitecan (FOLFIRI) or both (FOLFIRINOX) is beneficial in stage III and IV disease
    • possibly in stage II also

Consider MoABs

  • Bevacizumab- VEGF inhibitor
  • Cetuximab- EGFR inhibitor
    • Not in RAS gene mutations
    • Not in BRAF mutations

Checkpoint inhibitors

  • Pembrulizumab, nivolumab
    • Only in dMMd/MSI-h cancers
69
Q

What is the appropriate distal margin in rectal cancer

A

Heald et al descrided tumour deposits 4cm distal to the cancer, more contemporary series show 3cm.

5cm is consider the appropriate distal margin

70
Q

Muscles of levator ani

A

Pubococcygeus

Ileococcygeus

Puborectalis

71
Q

Components of anorectal physiology testing

A

Anal resting and squeeze pressures

  • Manometry

Anal reflexes

Pudendal nerve conduction velocities

electromyographic muscle fibre recruitment

72
Q

Risk factors for rectal propapse

A

Age

Female gender (6:1)

Chronic constipation

More common in young institutionalised psychiatric men also

Parity deserves a mention but may not actually be that important (35% nulliparous)

73
Q

Macroscopic features differentiating rectal prolapse from prolapsed haemorrhoids

A

Concentric mucosal rings vs deep radial grooves

74
Q

Abdominal vs perineal rectal prolapse repairs

A
75
Q

Solitary rectal ulcer syndrome

A

Anteriorly based 4-12cm from anal verge

1/3 related to fullthickness rectal prolapse

  • Respond well to surgery

If related to mucosal prolapse- less well

Topical 5ASA, pelvic floor physio and dietary management resolve most episodes

76
Q

Chagas Disease

A

Rare

Protozoan parasite disease

Trypanosoma Cruzi

South america

Denervation of both myenteric (Auerbach) and submucosal (Meissner) plexuses secondary to immune mediated cross reactivity

Oesophageal (differential for Achalasia) and colonic (progressive dilatation, megacolon and slow transit) are the most common manifestations of the gut

Also causes cardiomyopathy

77
Q

Biopsies for Hirschprungs

A

Suction or punch biopsy

3cm (in adults) above the dentate line (below this is usually aganglionic anyway)

Histology by ACh shows an increased number of large brown nerve fibres

78
Q

Musculature and innervation of the anal canal

A

4cm in length, variable shorter in multiparity

Tube within a cone

  • External sphincter continuous with levator ani
    • Skeletal muscle
    • S2, Pudendal, somatic innervation
  • Internal sphincter continuous thickened portion of internal circular muscular layer of colon
    • Visceral smooth muscle
    • Sympathetic fibres maintain contraction (pelvic plexus L1,2)
    • Parasympathetics relax (pelvic sphlancnic)
79
Q

Lining of the anal canal

A

divided by the dentate (pectinate line) approx 1/3 from anorectal margin and intersphincteric groove inferiorly

  • Above dentate line:
    • GRADUAL transition between columnar rectal mucosa and stratified squamous epithelium
    • up to 12 anal columns
    • at the base of these are the anal valves transversely which constitute the visual dentate line
    • Anal sinuses above valves, between columns
      • Anal glands open into sinuses
  • Pecten extends from dentate line to intersphincteric groove
    • stratified squamous epithelium
      • Non keratinising
      • No follicles or sweat glands
  • Below intersphincteric groove is histologically typical skin
    • keratinizing squamous epithelium
    • sebaceous, sweat glands and hair follicles present
80
Q

Blood and lymphatic supply of the anus

A

Arterial

  • Upper part from superior rectal artery from IMA
  • lower part from inferior rectal artery from internal pudendal from internal iliac

Venous

  • correspond to arteries but partake in the rectal venous plexus (which is actually anal)
  • Internal venous plexus form cusions at 3,7,11
    • Contributes to continence and development of haemorrhoids

Watershed “as per the vascular supply” in lasts but not totally correct

  • Upper part usually drains with the internal pudendal supply to the internal iliacs
  • lower part via anastomoses with superficial external pudental (from femoral) to the medial superficial inguinal group
81
Q

Factors contributing to anal continence

A

Pressure differential between rectum and anus

  • anus ~90cm H2O

Haemorrhoidal cushions

Anorectal angle

  • 75-90º at rest
  • Angle opens out with relaxation of puborectalis
82
Q

Management of anal incontinence

A

Medical

  • Konsyl D- Bulking
  • Loperamide- Decrease transit

Physiotherapy

  • Pelvic floor physiotherapy
  • Biofeedback training

Surgery

  • Sphincter repair
  • Prostheses-
    • Bulking (collagen, silicone)
    • Artificial sphincter
  • Sacral nerve stimulation
  • Diversion
  • Dynamic graciloplasty
83
Q

Internal haemorrhoid grading

A
84
Q

Rectocoele definition

A

2cm anterior to the anterior line of the anal canal on DPG

85
Q

Haemorrhoid management

A

Lifestyle

  • Water supplementation
  • Fibre supplimentation

Office procedures (best suited for grade 1-2, consider in 3)

  • Banding
    • Failure predicted by >4 bandings
  • Sclerotherapy

Surgery

  • Open (Milligan-Morgan)
  • Closed (Fergusson)
    • Use of an energy device probably decreases post operative pain.
  • Stapled
    • Increased recurrence rate
86
Q

Risks post haemorrhoidectomy

A

Urinary retention 30%

Faecal incontinence 2%

Infection 1%

Haemorrhage 1%

Stricture 1%

87
Q

Anal fissure differentials

A

Consider esp if atypical position (non midline)

TB

Crohns

HIV

Syphillis

Carcinoma

88
Q

Classification of fistula in ano

A

Parks Classification

  1. intersphincteric
  2. Trans-sphincteric
  3. suprasphincteric
  4. extrasphincteric
89
Q

Percentage risk of fistula in ano after abscess.

What can be done to reduce this risk

A

up to 40%

Am. J. Surg. 2019 metanalysis showed reduction in fistula from 25% to 16% with an oral 5-10 day post operative antibiotic course but that study was pretty shit, a retrospective cohirt study was included and the 2 RCTS actually showed quite different outcomes and the better one trended toward harm

90
Q

Goodsalls rule

A
91
Q

Risk factors for pilonidal disease

A

Male sex

Ages 18-45

Obesity

Trauma

Sedentary lifestyle

Deep natal cleft

Hirsuit

Family history

92
Q

Evidence based pilonidal abscess management

A

deroofing and curretage is superior to simple excision

Pit excision is not beneficial

Depilation decreases recurrence and number of procedures with laser, wax, creams- razor may increase recurrence

93
Q

Evidence based pilonidal surgery

A

Secondary intention has long healing times but lower recurrence rates

For primary closure, off midline procedures are superior to midline

Thats pretty much it

94
Q

Surgical options for pilonidal repair

A

Simple excision with primary or secondary intention healing

Bascome 1 (pit picking)

Bascome cleft lift

Rhomboid flap (inferiorly based)

Karydakis flap

95
Q

AJCC anatomic regions in perianal neoplasia

A

Anal canal

  • Not visible externally or incompletely with light external traction

Perianal

  • completely visible, arising within5cm of the anal opening

Skin

  • >5cm from the anus
96
Q

HPV viral subtype pathologic predilections

A

Benign condyloma

  • HPV-6, HPV-11

Dysplasia and increased cancer risk

  • HPV-16, HPV-18
97
Q

Anal and genital tract squamous intraepithelial neoplasia nomenclature

A

AJCC recommends the use of Squamous Intraepithelial Lesion (SIL) rather than Anal Intraepithelial neoplasia (AIN)

  • Low-grade squamous intraepithelial lesions (LSIL)
    • AIN I, low grade
  • High-grade squamous intraepothelial lesions (HSIL)
    • AIN II, moderate grade
    • AIN III, high grade
98
Q

Management of AIN

A

LSIL

  • May spontaneously regress
  • HSIL may be found but likely arises seperately
  • Biopsy anything concerning or excise for symptoms (e.g condylomata) but does not specifically need treatment
  • Follow up every 6/12

HSIL

  • Recommend treatment
  • Unlikely to regress
  • ablate the tissue somehow
    • cautery, excision, imiquimod, 5-FU
  • Surveillance required- high recurrence rate
99
Q

Buschke-Lowenstien tumour AKA

A

Giant condylomata accumenatum

Verrucous carcinoma

100
Q

Anal SCC risks

A

Anal canal 5x more common than perianal disease

Risk factors include:

  • HPV
  • HSIL
  • HIV
  • Receptive anal intercourse
  • Smoking
  • Lifetime number of sexual partners
101
Q

List perianal and anal canal neoplasms

A

Squamous derived

  • Benign
    • Condylomata accumenatum
  • Premalignant
    • LSIL/HSIL
  • Malignant
    • SCC
    • BCC
    • Melanoma
    • Extramammary Paget’s disease

Columnar derived

  • Adenocarcinoma

Soft tissue

  • Sarcoma
102
Q

Anal SCC staging

A

CT CAP

MRI Pelvis

CT PET for T2 (2cm) or greater or node positive disease

103
Q

Anal SCC management

A

Definitive chemorads

  • 5-FU and Mitomycion C.
  • 45Gy initially, up to 59 if needed as second dose or in high risk disease
  • Continued response for 6 months, therefore:
    • Initial assessment at 10 weeks
      • Complete response
        • Monitor every 3-6 months for 2 years then less frequent
      • Partial response
        • Monitor out to 6 months then salvage if persistent disease beyind that
      • Progressive disease
        • Get histological confirmation before considering salvage
  • Salvage is with APR
104
Q

Anal melanoma

A

Rare

Very poor prognosis

Often amelanotic

Manage by obtaining R0 resection, more aggressive surgery i.e APR doesn’t seem to improve survival

105
Q

Colorectal cancer screening

A

NZ uses Faecal Immunochemical Test

  • Age 60-75
  • Single test (c/w Guaic acid-3 days)- highest uptake
  • every 2 years

Screening has been shown in RCTs to decrease mortality

Most international guidelines recommend screening from age 50

Other screening options range from stool based tests to CTC, to flex sig to colonoscopy

Main risks are psychological and related to colonoscopy

106
Q
A

Melanosis coli

Benign

Pigmentation of colon (and small bowel) caused by lipofuscin deposition in macrophages

Associated with long term laxative use/abuse

107
Q

Incidental finding of crohns with normal appendix at laparoscopy

A

ESMO guidelines recommend not resecting either the small bowel or appendix

High rates of abscess and fistula from appendicectomy

small bowel can be treated medically if crohns but the differential would still be broad.

108
Q

Interval appendicectomy for perforated appendicitis

A

JAMA surg paper 2019 RCT of interval appendicectomy vs MRI surveillance showed 20% rate of neoplasm in patients managed with perc drain for perforated appendicitis.

The study was terminated early and all patients offered interval appendicectomy

33% of the MRI group had already required interval appendicectomy for recurrence

109
Q

Antibiotics after perianal abscess drainage

A

2019 meta-analysis showed of 5 days of cipro/metronidazole or Augmentin reduced the risk of fistula from 24% to 16%

The studies included were at some risk of bias

110
Q

Management of appendiceal NETs

A
111
Q

Colorectal Staging:

N1

A

N1: metastasis in 1 - 3 regional lymph nodes

  • N1a: metastasis in 1 regional lymph node
  • N1b: metastasis in 2 - 3 regional lymph nodes
  • N1c: no regional lymph nodes are positive but there are tumor deposits in the subserosa, mesentery or nonperitonealized pericolic or perirectal / mesorectal tissues
112
Q

Colorectal cancer staging:

N2

A

Metastasis in 4 or more regional lymph nodes

  • N2a: metastasis in 4 - 6 regional lymph nodes
  • N2b: metastasis in 7 or more regional lymph nodes

There is no N3 for colorectal cancer

113
Q

Colorectal cancer staging:

T1

A

Tumour invades submucosa

114
Q

Colorectal cancer staging:

T2

A

Tumor invades muscularis propria

115
Q

Colorectal cancer staging:

T3

A

Tumor invades through the muscularis propria into the pericolorectal tissues

116
Q

Colorectal cancer staging:

T4

A

T4a

  • tumor invades through the visceral peritoneum
  • including gross perforation of the bowel through tumor

T4b

  • tumor directly invades or adheres to other adjacent organs or structures
117
Q

What is the optimal timing for colonoscopy prep

A

Optimal preprocedural preparation depends on timing of procedure

  • Morning procedures should have split dosing
    • Improved rates of adequate prep, adenoma detection and patient tolerance
  • Afternoon procedures single dose appears to be better

Clear fluids should be ceased at least 2 hours prior to procedure to facilitate sedation

118
Q

Predictors of poor preparation in colonoscopy

A
  • Prior inadequate preparation
  • History of constipation
  • Use of medications associated with constipation
    • e.g tricyclic antidepressants and opioids
  • Dementia or Parkinson disease
  • Male sex
  • Low health literacy of cognitive function
  • Low patient engagement
  • Obesity
  • Diabetes mellitus
  • Cirrhosis
119
Q

Effect on colonoscopy outcomes due to poor prep

A
  • Increase the risk of adverse events related to the procedure
  • Lengthen the insertion time and overall procedure time
  • Necessitate reducing the interval between procedures
  • Lower caecal intubation rates
  • Lower adenoma detection rates
120
Q

Colorectal cancer genetic changes can be broadly grouped into which 3 pathways

  • What are their relative frequencies in CRC
A

MSI-high phenotype

  • 15-20% of CRCs
  • loss of DNA mismatch repair genes
    • Sporadic (BRAF associated)
    • HNPCC (~3%)

Chromosomal instability (CIN)

  • 70-85% of CRCs
  • Wnt/beta-catenin pathways
    • Most frequently APC

Global genomic hypermethylation

  • inactivation of tumour suppressor genes
    • CpG island methylator phenotype (CIMP)
      • Often results in MLH1 mutation leading to dMMR
      • Frequently associated with serrated polyps
        • progress to MSI-h sporadic CRC (BRAF V600E associated)
121
Q

Hyperplastic polyps

  • What are the recommendations for colonoscopy surveillance if identified?
A

Most common non neoplastic polyp of the colon

  • Most common in rectum and rectosigmoid
    • Unclear if associated with increased risk of more proximal neoplasia
  • Guidelines
    • consensus of US multidisciplinary taskforce Am J gastro 2020 recommends colonoscopy in
      • 10 years for:
        • <20 polyps in rectum and sigmoid all <10mm
        • <20 polyps proximal to rectosigmoid all <10mm
      • 3-5 years for
        • >10mm
      • 1 year for
        • serrated polyposis syndrome
          • diagnosis requires both of:
            • >20 sessile polyps distributed throughout the colon
            • > at least 5 proximal to the rectum of which 2 or more are >10mm
    • NZ and Aus just say return to baseline screening if hyperplastic polyps
      • No further delineation of risk (both NZGG and Australian Cancer Council)
122
Q

Serrated polyposis syndrome

A

Rare syndrome (formerly called hyperplastic polyp syndrome)

Genetic testing not recommended due to unknown genetics and heterogeneity

Diagnosis is endoscopic (use carmine blue!)

  • requires both of (WHO):
    • >20 sessile polyps distributed throughout the colon
    • > at least 5 proximal to the rectum of which 2 or more are >10mm

Lifetime risk of cancer is ~50%

123
Q

Features to encourage formal right hemicolectomy in appendiceal NETs

A
  • R1
  • G3
  • Mesoappendiceal invasion >3mm
  • Size >2cm (definate)
  • Size 1-2cm (if high risk features)
    • Tumour at base of appendix (even R0)
    • LVI
    • G2
124
Q

What is the rate of appendicitis in pregnancy

A

~1 in 1000 pregnancies

  • It is unclear if appendicitis is more or less common in pregnancy, if anything it is probably less common
  • Appendiceal rupture occurs more frequently in pregnant women especially in the third trimester
125
Q

What is the recommended management of appendicitis in pregnancy

A

Operative

  • this is considered the standard of care in appendicitis and there is insufficient data to support non operative management in pregnant patients
  • A higher negative appendicectomy rate in pregnant women is generally accepted
126
Q

How should appendicitis with abscess or inflammatory mass be managed

A

This is usually from late or missed appendicitis

  • management depends on the clinical condition of the patient primarily
    • well patient
      • drainable- drain
      • not drainable- antibiotics only
      • the role of interval appendicectomy should be considered especially in those over 40 as there is a risk of rare but clinically important diagnoses such as NETS
        • Overall this risk and the risk of relapse are low
          • in some series the risk or relapse is up to 40%
    • unwell patient
      • operate on initial presentation
127
Q

Familial risk in colon cancer; recommendations on colonoscopy

Category 1

A
128
Q

Familial risk in colon cancer; recommendations on colonoscopy

Category 2

A
129
Q

Familial risk in colon cancer; recommendations on colonoscopy

Category 3

A
130
Q

KPI in colonoscopy:

Adenoma detection rate

A

20% in women

30% in men

Adenoma detection rates correlate with the risk of interval colorectal cancer

Recent paper in the gastroenterology literature suggests that overall polyp detection rate may be a reasonable surrogate marker for ADR

131
Q

Outcome numbers in bowel screening with FIT testing

A

50/1000 will obtain a positive result

  • 35/1000 will have adenomatous polyps
  • 3-4/1000 will have colorectal cancer
132
Q

In Lynch syndrome what are the major associated risks other than colon cancer.

  • What are the lifetime risks
  • What are the associated screening recommendations
  • Risk reduction strategies
A

Endometrial and ovarian cancers

  • both have an increased risk and have an earlier onset in Lynch syndrome

Endometrial cancer

  • lifetime risk is 25-70% depending on the mutation
  • mean age ~50
  • screening:
    • women should be counselled for the increased risk and have dynfunctional bleeding promptly investigated
    • annual endometrail sampling should begin at the age of 30-35 or 5-10 years earlier than the earliest family member

Ovarian cancer

  • lifetime risk is 10-25% depending on the underlying mutation
  • mean age ~45
  • screening:
    • annual TVUS at the age of 30-35 or 5-10 years earlier than the earliest family member
    • CA125 every 6-12 months
      • all screening has a high rate of false positives and potential harm in ovarian cancer

Risk reduction

  • ultimately prophylactic TAH and BSO from age 35-45 is warranted
    • it is reasonable to wait until child bearing is complete
    • earlier if there is a family history of early onset of cancers
133
Q

What criteria for family history are used to diagnose Lynch syndrome?

A

Amsterdam II criteria

  • There should be at least three relatives with any Lynch syndrome-associated cancer (colorectal cancer, cancer of the endometrium, small bowel, ureter, or renal pelvis)
  • One should be a first-degree relative of the other two
  • At least two successive generations should be affected
  • At least one should be diagnosed before age 50
  • Familial adenomatous polyposis should be excluded in the colorectal cancer case(s), if any
  • Tumors should be verified by pathological examination
134
Q

What guidelines are used to guide testing for MSI

A

The revised Bethesda guidelines

  1. Colorectal cancer diagnosed in a patient who is less than 50 years of age.
  2. Presence of synchronous, metachronous colorectal, or other HNPCC-associated tumors regardless of age.
  3. Colorectal cancer with the MSI-H-like histology diagnosed in a patient who is less than 60 years of age
  4. Colorectal cancer diagnosed in a patient with one or more first-degree relatives with an HNPCC-related tumor, with one of the cancers being diagnosed under age 50 years.
  5. Colorectal cancer diagnosed in a patient with two or more first- or second-degree relatives with HNPCC-related tumors, regardless of age.
135
Q

What is the lifetime risk of colorectal cancer in Lynch syndrome

A

This depends on the genetic mutation

  • MLH1 and MSH2 are higher risk
    • 35-45%
  • MSH6 and PMS2 are lower risk
    • 15-25%
136
Q

When should screening colonoscopy in Lynch syndrome begin

A

At age 25

137
Q

What anatomic classification may be used for rectovaginal fistulae

  • what is the anatomical entry point for each
  • what are the common causes of each
A

Divided into three anatomic classes

  • forniceal
    • enter high, through the posterior fornix of the vagina
      • common causes:
        • crohns
        • bowel cancer
        • diverticular
        • radiation to gynaecological cancers
        • post operative from bowel anastomosis
  • septal
    • pass through the rectovaginal septum (middle third of the vagina) and are suprasphincteric
      • common causes:
        • rectal cancer
        • crohns
        • radiation
        • cervical cancer
        • obstructed labour with pressure necrosis
  • perineal
    • pass through the sphincter mechanism
      • common causes
        • crypotoglandular infections
        • obstetric tears
        • crohns
        • surgery
138
Q

Familial GI cancer risk:

who is at a mildly increased risk of colorectal cancer

What are the guidelines for colonoscopy

A

the risk of colorectal cancer is mildly increased in patients with 1 first degree relative with bowel cancer over the age of 55

colonoscopy should begin at age 50

139
Q

Familial GI cancer risk:

who is at a moderately increased risk of colon cancer

what are the guidelines for colonoscopy

A

Either

  • 1 FDR with colon cancer under the age of 55 or
  • 2 FDR with colon cancer at any age

Colonoscopy should begin at 50 or 10 years before the first family member

140
Q

Familial GI cancer risk

who is at a high risk?

what are the recommendations on colonoscopy

A

There are multiple risk groups in the NZGG document:

  • those with a known genetic mutation
    • taylor recommendations to that syndrome
  • those with polyps
    • 1 FDR or SDR with cancer and multiple polyps
    • 1 FDR with multiple polyps
  • those with FDR with colon cancer
    • 1 FDR plus 2 other FDR or SDR with cancer any age
    • 2 FDR and one has any of:
      • cancer age <55
      • multiple cancers
      • extracolonic cancer suggestive of a syndrome
    • 1 FDR <50
      • esp. if dMMR
141
Q

What is our local protocol for neoadjuvant treatment of rectal cancer where there is not a need for downstaging?

A

Our local protocol is for short course radiotherapy only, without chemosensitization.

  • 25 in 5
  • surgery within 1 week of cessation
142
Q

What is our local protocol for dneoadjavant treatment in rectal cancer where there is a need for downstaging

A

Patients receive long course radiotherapy with 5-FU sensitization.

  • Post treatment surgery is based on the mercury study
    • MRI at 1 month
      • if there is progressive or non responsive disease then progression to surgery within the week
        • if there is response then surgery is undertaken 6-12 weeks post neoadjuvant therapy

FRACS study (13 decks)

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