Colorectal Flashcards
1
Q
Peutz Jegher’s Syndrome
A
-
Definition:
- Autosomal dominant disorder in which hamartomatous polyps can occur throughout the gastrointestinal tract.
-
Pathophysiology:
- STK11 gene; chromosome 19,
- Tumour suppressor gene
- [St Kilda – luna park 1911]. 50% cases inherited and 50% sporadic
-
Clinical manifestations:
- mucocutaneous pigmentation, SB intussuception, colorectal polyps or bleed, malignant transformation
-
Macroscopic features:
- Large pedunculated polyps, ?cherry-red
-
Microscopic features:
- Non neoplastic hamartomas, connective tissue and smooth muscle covered by hyperplastic epithelium, Frond-like polyp with all three components of mucosa: (Muscosal epithelium (melanotic mucosa, goblet cells), Lamina propria, M. mucosae.)
-
Investigations:
- To get genetic testing (2 out of 3 needed)
- GI hamartomatous Polyps
- Pigmentation
- Family history
- To get genetic testing (2 out of 3 needed)
-
Risk of malignancy and surveillance:
- GI malignancy 57%, baseline gas, colon, MRE age 8 or earlier, if polyps then 3 yearly if no polyps then start again age 18
- Colorectal 39%
- No prophylactic surgery
- Breast: 45%
- Consider bilateral mastectomy, age 30 annual imaging
- Pancreas: 20%
- 2 yearly MRCP or EUS age 35
- Testicle/cervix:
- Annual exam
2
Q
pseudomembranous colitis pathophysiology
A
-
Organism:
- Clostridium difficile
- Spore forming anaerobic gram positive
- Clostridium difficile
-
Pathophysiology
- Antiobiotic therapy–> disruption of colonic microflora–> C difficile exposure and colonisation –> release of toxin A (enterotoxin) and B (cytotoxin) –> mucosal injury and inflammation
- C Diff. Toxin A/B mediated ribosylation of small GTPases, leads to disruption of the epithelial cytoskeleton, tight junction barrier loss, cytokine release (IL-8,TNF), and apoptosis
-
Pseudomembranes microscopic appearance
- Bacteria
- Fibrin
- Mucus
- Neutrophils
- Crypt erosions
3
Q
Anatomy of the anal canal
A
-
Definition
- Begins at levator ani, opens to the anal verge
- I.e. Anorectal junction (top of puborectalis) to the squamous mucocutaneous junction
- 2.5-5cm in length, longer in men
-
Columns of mogagni
- Mucosal folds above the dentate line
- In between the columns are the anal crypts into which drain the anal glands – site of cryptoglandular disease
-
Embyrology
- The lining of the upper part of the anal canal is embryologically derived from the cloaca, i.e. it is endodermal;
- The lower part is from the proctodeum or anal pit and is ectodermal
- The dividing line between these territories is usually considered to be at the pectinate (dentate) line (anal membrane remnant)
-
Blood supply
- Arterial
- Inferior anal canal
- Inferior rectal artery (from the internal iliac artery pudendal artery)
- Superior anal canal
- Superior rectal or middle rectal artery if present
- Inferior anal canal
- Venous
- Drainage corresponds to the arteries
- Upper anal canal IMV
- Lower anal canal can drain to external iliac vein
- Drainage corresponds to the arteries
- Arterial
-
Lymphatic
- Upper portion drains to inferior mesenteric LN
- Lower portion drains to superficial iliac LN
-
Histology
- Lacks a peritoneal covering
- Three histologic types:
- glandular (proximal)
- transitional (also called intermediate, cloacogenic)
- keratinized or nonkeratinized squamous (distal)
- Notes: ganglion cells are normally absent 1 – 2 cm above dentate line (important for Hirschsprung’s disease biopsies)
- Proximal colorectal zone:
- Top of puborectalis to dentate line, 1 – 2 cm long
- Rectal glandular mucosa (columnar)
- Similar to rectal mucosa but with shorter more irregular crypts, more smooth muscle fibers in lamina propria
- Anal transitional zone (ATZ):
- 0.3 cm to 1.1 cm
- Zone between uninterrupted columnar mucosa above and uninterrupted squamous epithelium below
- Wrinkled, glistening appearance
- Transitional epithelium resembles urothelium (small basal cells with nuclei perpendicular to basement membrane, columnar, cuboidal, polygonal or flat) with 4 – 9 cell layers, minimal mucin production
- Contains anal glands in submucosa, also endocrine cells, rare melanocytes
- Lower distal zone:
- Dentate line to squamous mucocutaneous junction: nonkeratinizing squamous epithelium without skin appendages, without glands
- Contains melanocytes
- Anal papillae contain squamous mucosa that joins rectal mucosa
- Squamous mucosa merges with perianal skin (with keratin, hair follicles and apocrine glands) at anal verge / anal margin
-
Innervation
- Pudenal nerve is important in rectal sensation (needed for rectal defaecation)
4
Q
Anatomy of anal sphincters
A
The outer longitudinal muscular fibres run between the internal and external anal sphincters
- Internal sphincter
- Thickened extension of the inner circular smooth muscle layer
- 5mm thick
- mainly parasympathetic (pelvic splanchnic nerves), 75% of resting tone of the sphincter
- External sphincter
- Continuation of the pubrectalis muscle which blends with the longitudinal muscular fibres (maybe)
- In the middle posteriorly it is attached to the coxxyx and perineal body, anocoxygeal ligament
- Extends below the internal sphincter
- Skeletal muscle, pudenal nerve innervation, voluntarily control to defer defaecation
5
Q
Anatomy of the Pelvic Floor
A
- A combination of muscles (eg, levator ani, coccygeus) and fascia that support the pelvic organs of the lower abdominal cavity (eg, rectum, bladder, uterus). It separates the true pelvis from the perineum.
- Levator ani (3 parts)
- Puborectalis (U shaped sling around the anorectal junction)
- Pubococcygeus muscle
- iliococcygeus muscle
- The muscles arise from the posterior aspect of the pubis, a white tendinous condensation of the obturator and the ischial spine and insert into the …
- Coccygeus
- Consider it the ischo-coccygeus
- Origin ischial spine and insertion coccyx and lower sacrum
- Levator ani (3 parts)
- Surface anatomy:
- Urogenital triangle
- Pubic symphysis anteriorly
- Ischial tuberosity bilaterally
- Anal triangle
- Ischial tuberosity bilaterally
- Coccyx posteriorly
- Ischial spine is palpable on vaginal examination palpated at about a finger-length into the vagina, at 4 and 8 o’clock. They are felt as bony prominences.
- Urogenital triangle
Innervation:
- Perineal branches of S3-4
- Inferior rectal branch of the pudendal nerve (external sphincter)
Relevance to operations:
- Relevance in both APR, fistula in-ano and perianal sepsis
6
Q
Pudendal nerve
A
- S2-3-4 nerve roots
- Emerges from just deep to the ischial tuberosity inferior to the sacrospinous ligament)
- Supplies external anal sphincter
7
Q
Anatomy Ureter
A
-
Definition:
- Bilateral, 25cm long, retroperitoneal muscular tubes that carry urine from the kidney to the bladder
- Narrows in 3 places: pelviureteric junction, pelvic brim and vesicoureteric junction
-
Embryology:
- The kidneys ascend from the pelvis to the lumbar region as the embryo lengthens, the ureter grows to length with them from the ureteric bud
- The ureteric bud is derived from caudal mesonephric duct at the base of the urogenital sinus which will become the trigone of the bladder
- Males (relation to vas)
- The vas deferens is also derived from the caudal mesonephric duct but more medially and caudally (think about where prostate lies in relation to bladder)
- As the kidney “ascends” along the posterior wall of the lumbar region, the gonads “descend” anteriorly and medial to the ureters
- Thus the vas are draped over the insertion of the ureters into the trigone
-
Surface anatomy:
- The right ureter is found at the pelvic brim as it crosses the iliac artery bifurcation
-
Surrounding structures and relations:
- Course:
- Arises from the renal pelvis and descends inferiorly towards the bladder/pelvis on the anterior surface of the psoas major muscle.
- The ureters cross the pelvic brim then run posteroinferiorly on the lateral walls of the pelvis, and curve anteromedially to enter the posterior aspect of the bladder at the VUJ
- The ureter is divided into abdominal and pelvic parts. The abdominal part lies retroperitoneal on the medial part of the psoas major muscle and is crossed by the gonadal vessles
- It enters the pelvis by crossing the division of the common iliac vessels. The pelvic part runs downward on the lateral pelvic sidewall, along the anterior border of the sciatic notch. It lies anterior to the hypogastric artery?, and medial to the obturator nerve. It inclines medially to enter the bladder at the lateral angles of the trigone
- In females the ureters pass under the uterine arteries (water under the bridge)
- In males, the ureters pass under the vas deferens
- Relations
- Anterior
- Right
- Duodenum (D2)
- R gonadal artery
- R colic artery
- Ileal mesentery, SMA
- Left
- L gonadal
- L colic
- Sigmoid mesentery
- Right
- Posterior
- Psoas muscle
- Genitofemoral nerve
- SI joint
- Bifurcation of CIA
- Medial
- Right
- IVC
- Right
- Anterior
-
Arterial supply:
- Segmental from the renal, gonadal, common iliac, vaginal, hypogastric and inferior vesicle
- Venous drainage:
- Innervation:
- Lymphatics:
- Structure within the organ and cell types:
-
Relevance to operations:
- Females
- Looking from posteriorly (like laparoscopic) from top down (A->P) around the uterus
- Bladder
- Round ligament
- Tubes draped over by broad ligament (which covers everything below)
- Uterusligament of ovaryovarysuspensory ligament (of ovary) containing ovarian (gonadal) vessels
- Cardinal ligament (transverse cervical ligament – containing uterine artery*)
- Ureter
- Uterosacral ligament
- *At the midplane of the pelvis, the ureter is crossed superior by the uterine artery travelling from anterior to posterior (from proximal to distal/lateral to medial & relative to the ureter). Here it tunnels into the cardinal ligament, approximately 1.5 to 2.0 cm lateral to the cervix near the internal cervical os and vaginal fornices as it enters into the trigone of the bladder
- Looking from posteriorly (like laparoscopic) from top down (A->P) around the uterus
- Females
8
Q
Innervation of the GIT
A
- The gut has dual innervation with intrinsic and extrinsic components
- It is able to function independently with the intrinsic enteric nervous system but is modulated by the extrinsic autonomic nervous system
- ANS synapses with the Enteric nervous system
-
Enteric nervous system consists of myenteric and submucosa plexus
- Myenteric plexus is situated between the outer longitudinal and middle circular layers, co-ordinates muscular contractions
- Submucosal plexus, co-ordinates blood flow/secretion/absorption
-
ANS Parasympathetic nerves
- Generally stimulatory to GIT smooth muscle but inhibitory to sphincters
- 2 different pathways (1 each for fore-midgut & hindgut)
- Foregut/midgut receive preganglionic nerve fibres from the medulla (dorsal motor nucleus of vagus) which travel along the right vagus nerve, via the coeliac/(+/- SM) ganglion (actually the para aortic plexus – they don’t synapse in the ganglion) and blood vessels to synapse with the postganglionic neurons in the enteric plexus
- Hindgut receive preganglionic nerve fibres from the IML (Intermediolateral nucleus) of the S2-4 spinal cord** which travel from anterior/ventral rami along **the pelvic splanchnic nerves (nervi ergentes) via the inferior hypogastric plexus (bilateral) to synapse with the enteric plexus, some fibres pass to the left colon via the superior hypogastric plexus
-
ANS Sympathetic nerves
- Generally inhibitory to GIT smooth muscle but stimulatory to sphincters
- 2 different pathways (1 each for fore-midgut & hindgut)
- Foregut/midgut receives preganglionic fibres from intermediate lateral horn of thoracolumbar spinal cord via sympathetic trunk and lesser splanchnic nerves which synapse with postganglionic splanchnic nerves in the coeliac/(+/- SM) ganglion whose fibres travel with blood vessels to synapse with the enteric plexus
-
Hindgut
- Distribution of IMA blood vessels
- Receives preganglionic fibres from the lumbar part of the sympathetic trunk via the lumbar splanchnic nerves which travel to the inferior mesenteric ganglion and post ganglionic fibres travel onward with the IMA to synapse with the enteric plexus
- Distribution of middle rectal from internal iliac
- Receives preganglionic fibres from the lumbar part (L1-3) of the sympathetic trunk which travel to the inferior hypogastric plexus (via superior hypogastric plexus - L & R pelvic nerves) post ganglionic fibres travel with the parasympathetic nervi ergentes
- Distribution of IMA blood vessels
9
Q
Defaecation physiology
A
- Colonic mass movements and peristalsis move intestinal contents distally into the rectum
- Rectal filling activates mechanoreceptors in the rectal wall causing awareness of the need to defecate
- As stool reaches the rectum, a small amount is allowed to pass through to the anal canal by an involuntary relaxation of the internal anal sphincter. This action, known as the rectoanal inhibitory reflex, is necessary for anal sampling, which is the process of determining if the rectal contents are of the gaseous, solid, or liquid form.
- At this time, if defecation is not socially acceptable or convenient, the rectal wall relaxes (defer), and the need to defecate subsides temporarily.
- If it is a proper time to defecate, the person generally either sits or squats depending on their environment (When defecation is desired, the anorectal angle is voluntarily straightened (which is facilitated by squatting or sitting), and abdominal pressure is increased by straining)
- Next, contraction of the abdominal muscles and performing the Valsalva maneuver while simultaneously relaxing the external anal sphincter and puborectalis muscle will expel feces from the body due to the pressure gradient generated between the rectum and anal canal.
- After fecal expulsion, the closing reflex occurs, which involves the external anal sphincter regaining its tone to maintain continence at rest
10
Q
A beautiful picture of splenic flexure mobilisation
A
11
Q
What is the rectum?
A
- Rectum
- Starts from the:
- S3 (6cm distal to sacral promontory)
- Taenia coli fuse/coalesce into a continuous layer
- Absence of epiploic appendages
- No haustra/sacculations
- No intraperitoneal mesentery
- And continues to the levator ani
- Starts from the:
- 15cm – final 3cm is anal canal
- Internal valves of Huston (3 semi lunar lateral curves)
- Upper part to the right
- Middle to the left
- Lower to the right
- Peritoneal reflections
- Proximal 1/3 anterolateral covered
- Middle 1/3 anterior covered
- Distal 1/3 extraperitoneal
- Mesorectum
- Layer of fat around the outside of the rectum
- Contained by the mesorectal fascia
- Continuous with the sigmoid mesentery
- Contains vessels and lymphatics
- Tapers to finish at the levator muscles
- Waldeyes fascia
- Posterior strong fascia that overlies the sacrum and the coccyx
- Denonvillers fascia
- Anterior to the rectum in men and covers the seminal vesicles and prostate
- Lateral “ligament”
- Middle rectal vessels
12
Q
Carcinogenesis of colorectal cancer
A
- 3 main known pathways
- Chromosomal instability
- 75% of cancers and those with FAP
- Classic mucosa-adenoma-carcinoma pathway
- Cumulation of mutations
- Sporadic Inactivation of tumour suppressor genes APC and p53
- Constitutive activation of oncogenes RAS and RAF
- Adenomatous polyps (85%), sporadic and FAP
- Multiple cumulative genetic changes happen that progress the adenoma into a carcinoma and onto metastatic
- Inactivation in the APC gene, this causes early adenoma
- KRAS mutation (50% of CRC will have this and can be targeted by epidermal growth factor inhibitors)-> progress early adenoma into intermediate adenoma
- SMAD2-4 and CC mutation intermediate into late adenoma
- TP53 mutation late adenoma into a carcinoma
- Jevon Puckett “A KRASzy Disease Process”
- APC
- KRAS
- DCC (deleted in colorectal cancer) or SMAD4
- P53
- Microsatellite instability & Hypermethylation/(CIMP) CpG Island Methylator Phenotype
- 15% of cancers
- Sporadic or familial mutation in DNA mismatch repair genes
- BRAF mutation
- Chromosomal instability
13
Q
Pathology report CRC (RCPA)
A
-
Macroscopic
- Operative procedure
- Specimen length
- Tumour site
- Tumour dimensions
- Distance to the closest cut end
- Perforation
- Rectal
- Distance to the non peritonealised circumferential margin
- Relationship to the anterior peritoneal reflection
- Specimen quality (Quirke grade)
- Plane of mesorectal excision
- N/A
- 3 Mesorectal fascia (complete)
- Intramesorectal (near complete)
- 1 Mucscularis propria (incomplete)
- Plane of sphincteric excision
- Extralevator – sphincteric – intersphincteric
- Plane of mesocolic excision
- Mesocolic plane – intramesocolic – muscularis propria
- Plane of mesorectal excision
- Peritoneum
- Tumour invades to peritoneal surface
- Discrete nodule along the serosal surface
-
Microscopic features
-
Histological subtypes
- Common:
- Adenocarcinoma not otherwise specified
- Medullary
- Sheets of epithelioid neoplastic cells
- Pushing border
- Tumour infiltrating lymphocytes
- Associated with lynch
- Good prognosis
- Signet ring cell adenocarcinoma
- <1% of adenocarcinomas
- At least 50% of tumour cells to show signet cell features
- Poorly differentiated, high grade
- Associated with lynch
- Mucinous adenocarcinoma
- 10% of adenocarcinomas
- >50% tumour volume of extracellular mucin, if less than 50% then called a mucinous component
- Poorly differentiated, high grade
- Others:
- Micropapillary
- Serrated
- Cribiform
- Comedo
- Adenosquamous
- Spindle cell
- Undifferentiated
- Common:
-
Histological subtypes
- Histological tumour grade
- Meaning gland formation differentiation (only used in adenocarcinoma NOS and mucinous adenocarcinoma)
- Low grade >50%
- High grade <50%
- Meaning gland formation differentiation (only used in adenocarcinoma NOS and mucinous adenocarcinoma)
- Depth of invasion
- T stage
- Measurement of invasion beyond muscularis propria (T3 tumours)
- Inflammatory cell infiltrate
- Lymphovascular (actually lymph and venous) invasion
- Poor prognostic feature
- Small (lymphatic, capillary or venular) vs large vessel (vein intra or extra mural)
- Perineural invasion
- Lymph node status
- Number examined
- Number involved
- Apical node involvement
- Ratio of involved to examined
- Discontinuous extramural deposits not associated with lymph nodes
- Tumour budding
- For non-mucinous and non-signet
- Tumour budding is defined as single cells or clusters of up to four tumour cells at the invasive front of carcinomas. It is considered to be the morphological manifestation of epithelial mesenchymal transition
- Budding score
- 1 low (0-4 buds)
- 2 intermediate (5-9 buds)
- 3 high (10+ buds)
- Adverse prognostic feature
- Response to neoadjuvant (modified AJCC )
- No treatment
- Complete response (score 0)
- Near complete response (score 1)
- Partial response (score 2)
- Poor or no response (score 3)
- Margins
- Longitudinal
- Circumferential
- Distant metastasis
- Co existent pathology
- Polyps, synchromous carcinoma, other
- Microscopic residual tumour status (completeness of resection)
- R0-R2
- Ancillary findings
- BRAF V600E
- Mutation common in sporadic MMR deficient tumours
- Rare in Lynch
- MLH1 promoter methylation testing
- MMR status by MSI testing
- MS, MSI low, MSI high
- RAS
- Mutated or wild type
- Needed when metastatic disease
- Neuroendocrine markers
- BRAF V600E
- ———– below additional notes———
Patients with KRAS mutation - unlikely to benefit from anti EGFR therapy
Patients with BRAF mutation - unlikely to benefit from anti EGFR therapy
Patients with BRAF mutation - but would benefit from BRAF inhibitors
MSI high patients - likely to benefit from PD-1 inhibitor (pembrolizumab)
HER2 overexpressors- may benefit from targeted HER2 therapy (trastuzumab)
- CK20, CK7, CDX2, SATB2+ staining positive
- BRAF or KRAS mutation
- BRAF
- Familial lynch (wildtype) vs sporadic cancer (mutated from hypermethylation of MLH1 via serrated pathway)
- KRAS – important because Cetuximab unable to used for EGFR if this is mutated in the setting of metastatic disease
- BRAF
- MSI histology
- MMR immunohistochemistry MLH1 MSH2 MSH6 PMS2 proteins
- if under age 70 and proteins missing then PCR test for MSI for germline testing (lynch)
- Typically poorly differentiated
- Crohns like inflammatory reaction
- Lots of tumour infiltrating leukocytes (TILs)
- No precursor lesion seen
- Some subtypes such as mucinous/signet/medullary are MSI-H
14
Q
TNM staging colorectal
A
T; depth of tumour invasion
T1; into submucosa
T2; into muscularis propria
T3; through muscularis propria into surrounding pericolic tissues
T4a; penetrates through the adventitia (retroperitoneal) or visceral peritoneum/serosa (<-same thing)
T4b; into surrounding organs or structure
–
N0
N1; 1-3
N2; 4+
–
M0
M1; distant site or peritoneal surface
15
Q
Prognosis in CRC
A
Rectal cancer prognosis 5 year overall survival rates
- Stage1 92%
- Stage 2 84%
- Stage 3 64%
- Stage 4 11%
- Break into clinical, pathological, molecular, treatment
- Clinical
- Obstruction/perforation
- High preoperative stage
- High CEA >5ng/ml
- Pathological
- Right side worse than left
- Stage
- Poor differentiation
- Extramural vascular/venous invasion
- Prescence of mucin
- <12 LN harvested
- Absence of Peritumoral lymphocytes and crohns like aggregates (seen in MSI H tumours which have a better prognosis)
- Residual tumour
- Anterior location and low tumour position
- CRM <1mm
- Molecular
- Mutations of KRAS BRAF (don’t respond to immunotherapy
- dMMR MSI-H (better prognosis)
- Treatment
- Poor response to neoadjuvant
- Modified Ryan Scale
- 0 Complete response
- 1 Near complete response
- 2 Partial response
- 3 Poor or no response
- Modified Ryan Scale
- Poor response to neoadjuvant
- Clinical
- MSI and BRAF mutation screening:
- This approach would allow almost all cases to be categorized and managed appropriately
- Lynch syndrome patients would need screening for other Lynch syndrome–associated malignancies and counselling of family members
- Patients with sporadic MSI would be apprised of their superior prognosis and potential lack of response to 5-FU chemotherapy
- MSS cases could plan for a poorer prognosis but could also potentially take advantage of 5-FU
- Circulating tumour DNA (ctDNA)
- Big deal in prognosis
16
Q
Define TME
A
Enbloc resection of the mesorectum intact mesorectal fascia, removal of the regional LNs, decreases regional recurrence by 2/3s
Defintion of TME: a precise, sharp dissection between the visceral and parietal layers of the endopelvic fascia to ensure en bloc resection of the mesorectal envelope, lymphatics, and vascular/perineural tumor deposits with the primary rectal cancer
17
Q
Steps anterior resection
A
- Abdominal exploration
- Medial to lateral dissection
- IMV high at inferior border of pancreas
- Mobilisation splenic flexure and L colon for length
- IMA high
- Pelvic dissection TME
- 2cm distal to cancer margin (2cm fresh, 1cm fixed), >1mm CRF radial margin
- Tension free well vascularized anastomosis
- Diverting ileostomy (neoadjuvant, low or difficult, consider patient and bowel) – reversed at 6 weeks if well (check anastomosis with contrast enema)
18
Q
Dukes classification
A
A; limited to the muscular wall
B; through the muscular wall
C; involved lymph nodes
D; distant metastasis
19
Q
Liver metastasis (background stats, resectability)
A
Stats
- 20% of patients present with liver metastasis synchronously
- 2/3 of CRC patients develop distant metastasis
- Over half of colorectal patients will develop liver metastasis at some point
- Rectal cancer metastasis (liver 70%, Lung 50%, bone 12%, CNS 8%)
- Most recurrence occur within 3 years
- Most liver metastasis are not resectable (80-90%)
Resectability (patient, oncological & technical factors)
- Patient factors
- Fitness for surgery (age, cardiopulmonary status)
- Preference
- Oncological factors
- Primary cancer
- Resectable for cure
- Extrahepatic disease
- Limited extrahepatic disease amenable to surgical resection or long-term control with adjuvant therapies may be considered for a hepatic resection. (lung mets better than portal or retroperitoneal nodes)
- Intrahepatic disease
- Primary cancer
- Technical factors
- Old guidelines more strict (ESMO 2013 Steele et al)
- Newer guidelines less conservative (SSO 2006, AHPBA 2013, NCCN 2021)
- R0 resection achievable (aim >1mm MD Anderson study)
- Adequate functional of future liver remnant (FLR)
- 2 contiguous segments
- Preserved vascular inflow & outflow, biliary drainage
- FLR normal >20(27)%, chemotherapy injured 30%, cirrhosis 40%
- If borderline; appropriate regenerative response post PVE
20
Q
Principles of screening test
A
- Important health problem
- Detectable in early stage
- Well understood biology
- Acceptable treatable for disease in the early stage
- Accurate screening method
- Better prognosis with early detection
- Non invasive method/acceptable to population
- Agreement on the screening population
- Affordable – screening should decrease total healthcare expenditure
- Continuous process
21
Q
FIT
A
- Tests directly for human globulin
- Positive predictive value (true test positive/total test positive) 16% = 1 in 6 for advanced adenoma or cancer
- Negative predictive value (true test negative/total test negative) 97.5% for advanced adenoma/cancer, cancer 0.1% or 1:1000 negative tests will actually have an invasive cancer
- The current NBCSP (iFOBT screening every 2 years) requires 56 colonoscopies to prevent one colorectal cancer death, assuming 100% adherence to screening recommendations
22
Q
FAP
A
Familial Adenomatous Polyposis syndrome
-
Definition:
- Autosomal dominant inherited condition
- Characterized by multiple colonic polyps, high risk of colorectal and other cancers
- – classically diagnosed as >100 colonic polyps – still useful because only 80% demonstrate APC gene mutation
- Garners syndrome (polyps, epidermoid cysts, osteomas)
- Turcotts (colonic polyps and brain tumours)
-
Incidence/epidemiology:
- <1% of all CRC
-
Aetiology & risk factors:
- 80% familial, 20% sporadic
-
Pathophysiology:
- Adenomatous Polyposis Coli (APC) gene mutation q5
- Tumour suppressor gene
- Deactivation of the protein which normally regulates b catenin-> increased b catenin which increases cellular growth processes->inappropriate cell growth-> polyps
- Autosomal dominant
- Can be sporadic
- 3 phenotypes
- Mutation Codon 157-1595 – 100% lifetime risk
- (attenuated) mutation 5 prime and 3 prime ends – 70% risk of right colon cancer
- Mutation 1309 codon mutation – 100% lifetime risk
-
Clinical manifestations:
-
Polyposis syndromes should typically be considered in patients with
- Greater than 20 lifetime adenomas, or
- Desmoid tumour or other extracolonic manifestations of FAP, or
- Family members of individuals with known FAP, AFAP, or MAP
- Testing for: known family history, personal history polyps 10 under 30 or 20 any age
- 3 phenotypes
- 100-1000 colonic adenomas (culumulative)
- 10-100
- >1000 adenomas
-
Polyposis syndromes should typically be considered in patients with
-
Macroscopic features:
- Extracolonic polyps
- Stomach
- Fundic gland polyps (similar to PPI)
- Rarely adenomas
- Duodenum
- Adenomatous
- Premalignant
- Form later in life
- Stomach
- Extracolonic manifestations
- Congenital hypertrophy of the retinal pigment epithelium (CHRPE)
- 75% present
- Bilateral
- Congenital hypertrophy of the retinal pigment epithelium (CHRPE)
- Extracolonic polyps
- Multiple osteomas
- Mandible, skull, tibia
- Extracolonic cancers:
- Duodenal
- Desmoid tumours (20% will develop) – see own topic!
- 2nd greatest cause of death after CRC
- Soft tissue tumours
- Sites: SB mesentery, retroperitoneum and the abdominal wall
- Intraabdominal 50%
- Abdominal wall 45%
- Trunk/extremities 5%
- Rarely metastasis but can be invasive
- Usually arises at site of trauma thus problem at prophylactic colectomy
- Thyroid cancer
- Hepatoblastoma
- Young males
- Extrahepatic biliary tree cancers
- Adrenal tumours
- Benign adenomas non functional
- Brain tumours
- Astroblastomas or gilalblastomas
- Epidermoid inclusion cysts
- Multiple adenomatous polyps
- Throughout colon and rectum
- Childhood begins
- Microscopic features:
-
Investigations:
- Surveillance (eviQ guidelines check)
- Gastroscopy
- Spigelman Staging System
- Rates duodenal polyps by number, max size, histology and dysplasia
- Categories (points 1-3)
- Number: 1-4, 5-20, >20
- Max size: 1-4, 5-10, >10
- Histology: tubular, tubulovillous, villous
- Dysplasia: mild, mod, severe
- Score >7 = high risk for invasive cancer (2%); particularly 9-12 points –> risk 36%.
- Zero = scope 4 yearly
- 1 = 3 years
- 2 = 1-3 years
- 3 = 6-12 months +/- EUS
- 4 = EUS and consider surgery
- Normal gastroscopy + side viewing scope to look at ampulla
- Spigelman Staging System
- Lower endoscopy
- If known mutation
- Flexi sigmoidoscopy annual from age of 10 years then change to colonoscopy once adenoma found (mean age 15 first polyps)
- Colonoscopy 1 yearly until prophylactic colectomy
- Gastroscopy
- Surveillance (eviQ guidelines check)
-
Treatment:
- Non operative
- No role for chemoprevention
- Operative
- All FAP patients, 15-25 years old depending on phenotype and patient preferences
- Consider leaving completion proctectomy until after family done, need to check rectal stump frequently
- Non operative
23
Q
MAP
A
MUTYH
-MAP (MUTYH-Associated Polyposis)
-
Definition:
- MUTYH-associated polyposis is a recessively inherited predisposition to adenomatous colorectal polyps and early onset colorectal cancer due to biallelic mutations in the MUTYH gene
- Autosomal recessive- the only one
-
Incidence/epidemiology:
- 1-2% of the general population carry 1 gene mutation
- Biallele expression of MUTYH mutation is <1% of CRC
- Aetiology & risk factors:
-
Pathophysiology:
- MUTYH gene mutation, gene responsible for base excision repair
- Germline MUTYH mutations predispose to developing somatic APC and KRAS mutations
- Prevents DNA repair development of polyps and cancers
- Autosomal recessive
-
Clinical manifestations:
- Colonic polyps 20-100 but can have >100
- If tested for FAP but no APC mutation found
- Family history
- Synchronous or early onset cancer (under 50)
-
Macroscopic features:
- Extracolonic cancers
- Duodenal
- ?Breast
- Colonic
- 10-100 cumulatively
- Occurs older age
- Extracolonic cancers
-
Microscopic features:
- Colonic
- tubular or tubovillous adenomas
- Colonic
-
Investigations:
- Surveillance colonoscopy every 2 years from age of 18
-
Treatment:
- Non operative
- Genetic testing if cumulatively more than 20 polyps
- Operative
- No prophylactic colectomy, unless unable to manage polyps endoscopically then ileorectal anastomosis with surveillance of rectum
- Non operative
-
Prognosis:
- CRC
- 80% cancer risk
- Later presentation
- If monoallelic MUTYH mutations are present in 1 to 2% of the population and may confer, on average, a 1.5- to 2-fold increase in the risk of colorectal cancer
- CRC
24
Q
Familial Juvenile Polyposis syndrome
A
-
Definition:
- Autosomal dominant inherited condition multiple hamartomatous polyps with histology characteristic of juvenile polyps occur in the gastrointestinal tract
- 5 juvenile polyps in the colorectum or juvenile polyps elsewhere in the gastrointestinal tract
- Or any juvenile polyps with family history
- Incidence/epidemiology:
- Aetiology & risk factors:
-
Pathophysiology:
- 50% SMAD4 gene mutation, chromosome 10
- BMPR1A mutation
- TGFb signalling pathway
- Can become adenomatous and therefore carcinoma risk
- Associated with hereditary haemorrhagic telangectasia
- Associated with other congenital problems including malrotation, hydrocephaly and cardiac problems
-
Clinical manifestations:
- Intussusception and bleeding
- Rectal bleeding in child
- Clubbing
-
Macroscopic features:
- 100s of polyps throughout GI tract, usually right colon
- Cherry red
-
Microscopic features:
- Harmatomatous polyps
- Inflammatory stromal tissue with mucus-filled cystic glands
-
Investigations:
- Screening colonoscopy from 12-15 years, annual if polyps found or 3 yearly until polyps found
- Gastroscopy
-
Treatment:
- Non operative
- Operative
- Colectomy not indicated, unless unable to manage endoscopically
- Total colectomy or proctocolectomy
-
Prognosis:
- Gastric duodenal and pancreatic cancer risk also
- 30-40% lifetime CRC risk
25
Q
Serrated polyposis syndrome
A
-
Definition:
- Criteria
- ≥ 5 serrated polyps ≥5mm proximal to the rectum, with ≥ 2 of these being >10mm
- Any number of serrated polyps proximal to the sigmoid colon in an individual who has a first-degree relative with serrated polyposis syndrome
- > 20 serrated polyps of any size, but distributed throughout the colon.
- Criteria
- Incidence/epidemiology:
-
Aetiology & risk factors:
- Unknown
- Family history
-
Pathophysiology:
- Unknown mutation at the moment
- Clinical manifestations:
- Macroscopic features:
- Microscopic features:
-
Investigations:
- Colonoscopy every 1 to 3 years with the aim to remove all polyps ≥ 5mm.
- Age 40 or 10 years younger than the youngest age of serrated polyposis syndrome diagnosis in the family, whichever comes first
-
Treatment:
- Non operative
- Operative
- if the number and size of polyps make it impossible endoscopically control, colectomy and ileorectal anastomosis should be considered
-
Prognosis:
- More polyps = more cancer
26
Q
PTEN
A
-
Definition:
- Autosomal dominant inherited mutation caused by PTEN mutation, multiple hamartomatous polyps and associated with colorectal, breast, endometrial and thyroid cancer
- Cowden syndrome
- Colorectal
- Incidence/epidemiology:
- Aetiology & risk factors:
-
Pathophysiology:
- Mutation in tumour suppressor gene chromosome 10
-
Clinical manifestations:
- Multiple hamartomatous polyps in stomach and colon
- Extracolonic mucocutaneous lesions
- Gylcogenic acanthosis of the oesophagus (if extensive, otherwise is probably benign)
-
Macroscopic features:
- Colonic polyps
- Mucocutaneous lesions include trichilemmoma, acral keratosis and oral papilloma
- Macrocephaly; dysplastic gangliocytoma of cerebellum (Lhermitte-Duclos disease)
- Breast fibroadenoma, fibrocysttic disease and carcinoma
- Thyroid goiter
-
Microscopic features:
- Colon polyps: nondysplastic epithelium, dilated glands, expanded stroma; histologically similar to juvenile polyps; may also show intramucosal lipomas
-
Investigations:
- ?unclear how frequent colonoscopy
- Cleveland clinic risk calculator to help determine genetic testing
-
Treatment:
- Non operative
- Operative
-
Prognosis:
- 15-25% risk CRC
- 30-50% breast cancer risk
- 5% thyroid cancer (follicular)
- CNS/cerebellar gangliocytoma
- Endometrial cancer
- Adenomas or MN goitre thyroid
- Fibrocystic change in breast
27
Q
Revised Amsterdam criteria?
A
- Lynch
- 3+ HNPCC associated family cancer:
- CRC
- Endometrium
- SB
- Upper urinary tract (ureter or renal pelvis)
- 2 successive generations
- 1 CRC needs to be <50
- 0 FAP i.e needs to be excluded
- 3+ HNPCC associated family cancer:
28
Q
Mismatch repair genes?
A
- Autosomal dominant inherited MMR gene mutation 2p or 3p (MLH1, MSH2, MSH6, PMS2)
- MMR chromosome 2p or 3p or epCAM gene (MSH2 gene) mutation
- Tumour suppressor genes: DNA mismatch repair (MMR) gene.
- MMR corrects errors that spontaneously occur during DNA replication, such as single base mismatches or short insertions and deletions. The proteins involved in MMR correct polymerase errors by forming a complex that binds to the mismatched section of DNA, excises the error, and inserts the correct sequence in its place.
- Cells with abnormally functioning MMR are unable to correct errors that occur during DNA replication and consequently accumulate errors. This causes the creation of novel microsatellite fragments.
- NOT THE (Hypermethylation inactivation of promotor region of MLH ) pathway – they normally have BRAF
29
Q
CRC features of lynch, surveillance and treatment
A
- Loss of MMR, lymphocytic reaction, mucinous with medullary growth pattern, right sided, signet, R side, synchronous
- Surveillance
- Annual colonoscopy from 25 or from 5 years younger than age of family member
- Gastroscopy annual from 30 years
- Urine analysis for cytology
- Consider TAHSBO
-
Treatment:
- Non operative
- Aspirin 75-100mg/day from 25 years of age for chemoprophylaxis
- Operative
- No prophylaxis unless multiple advanced adenoma (right side if elderly and total if young) – if doing segmental resection for cancer consider doing total colectomy [Europena guidelines – only for MLH1 & MSH2, MSH6 & PMS2 not necessarily]
- TAHSBO
- Non operative
-
Prognosis:
- 80% risk of CRC
- MSH6 or PMS2 20% risk
- Endometrial cancer 33%
- 9% ovarian
- 6% gastric
- <3 urothelial and SB tumours
- 80% risk of CRC
30
Q
Operative indications for malignant polyps
A
- Indications for resection
- Haggit 4, SM2-3
- Poorly differentiated
- Incomplete margin <1mm
- Piecemeal removal
- LVI
- Tumour budding
- St Mark’s LN risk calculator
- Patient factors
- Low-risk malignant polyps have all of the following features:
- Superficial submucosal invasion (<1000 microns i.e. 1mm)
- Moderate or well differentiated histology
- No lymphovascular invasion
- Clear margins
- No other risk features:
- Malignant invasion depth >2mm
- Invasion width >3mm
- Tumour budding and cribriform architecture
- In these cases, where the endoscopist is certain that the lesion has been completely removed, then the neoplasm should be considered cured by endoscopic polypectomy.
31
Q
Risk of lymph node metastasis in malignant colorectal polyp
A
-
Haggit classification
- Level of invasion into a pedunculated polyp
- Sessile polyps are level 4
- Risk of LN metastasis
- Level1-3: very low
- Level 4 only: 12-25% (need resection)
-
Kikuchi level (see diagram below)
- Used for sessile polyps
- Submucosa divided up into thirds (sm1,2,3)
- SM1: 2%
- SM2: 8%
- SM3: 28%
- Note above [2 + 8 = 28] for Kikuchi & Level 4 is the same as Kikuchi, so it depends, but is up to 28%
32
Q
Hamartomatous polyps
A
- Juvenile & Hamartoma
- Associated with
- Peutz Jaghers disease
- Familial juvenile polyposis
- Cowdens syndrome or PTEN syndrome
- Rounded, pedunculated, abnormal colour (cherry-red)
- Connective tissue, smooth muscle, lamina propria, inflammatory cells
- Anywhere throughout the GI tract (SB intussuception)
- Autosomal dominant
- Associated with
33
Q
Demoid tumours
A
-
Definition:
- Well differentiated mesenchymal (myofibroblasts) tumour that is locally invasive
- Also known as aggressive fibromatosis
-
Incidence/epidemiology:
- Rare 0.5 per 100,000
- Peak age 30-40
- 10% associated with FAP, note 20% of FAP will develop
-
Aetiology & risk factors:
- FAP
- High oestrogen states
- Trauma
-
Pathophysiology:
- Genetic mutation
- 85% have a mutation in the CTNNB1 encoding beta-catenin pathway
- FAP APC mutation
- Cause displacement/obstruction i.e. hydroureter, SBO
- Desmoid tumours are a type of soft-tissue tumor that come from fibrous tissue. They are related to connective tissue cancers called sarcomas, but desmoid tumors are not cancer because they do not spread to other parts of the body.
- Genetic mutation
-
Clinical manifestations:
- Abdominal wall
- Enlarging mass, smooth
- Intra-abdominal
- SB obstruction
- Hydroureter
- Extra-abdominal
- Mass
- Abdominal wall
-
Macroscopic features:
- Firm, rubbery, ill-defined, infiltrative masses
-
Microscopic features:
- Differentiated fibroblasts and myofibroblasts within collagenous stroma
- Uniform spindle cells resembling myofibroblast
- Histology: long, sweeping fascicles with thin walled vessels and microhaemorrhages; bland cells with mild to moderate cellularity and minimal atypia
- Immunohistochemistry: SMA+ (smooth muscle actin) and nuclear beta catenin+
- Molecular: CTNNB1 and APC mutations may be seen
- Spindle, beta-catenin
-
Investigations:
- Imaging
- MRI & CT
- Endoscopy for ?FAP
- Biopsy
- Imaging
-
Staging of Desmoids
- Size, doubling rate, location
- 0 = minimal lesion, doubling rate unknown
- 1 = <5cm, >24m doubling rate, extra-abdominal
- 2 = 5-10cm, 12-24m doubling, abdo wall
- 3 = 10-20cm, 6-12m doubling, mesentery without obstruction
- 4 = >20cm, 1-6m doubling, mesentery with obstruction.
-
Treatment: (this area is super difficult)
- Operative
- Surgical resection
- May need SB transplant
- Abdominal wall reconstruction
- Complex..
- Surgical resection
- Non operative
- NSAID
- SERM (tamoxifen)
- Cytotoxic (chemotherapy)
- Targeted (Tyrosine Kinase Inhibitors)
- Sorafenib (multiple targets)
- Imatinib (c kit)
- Operative
-
Prognosis:
- 2nd leading cause of death for FAP patients
- Locally recurrent but do not metastasize
- 10% will spontaneously regress
34
Q
Causes of appendiceal neoplasm, mucocele and PMP
A
-
Neoplasm by cell lineage [epithelial vs neuroendocrine]
- Epithelial
- Mucinous
- Low-grade appendiceal mucinous neoplasm (LAMN) (also called cyst adenoma)
- High-grade appendiceal mucinous neoplasm (HAMN)
- Serrated polyp
- Mucinous adenocarcinoma
- Non mucinous
- Adenoma
- Adenocarcinoma
- Goblet cell adenocarcinoma*? Are these neuroendocrine?
- Mucinous
- Non epithelial
- Neuroendocrine
- Well differentiated neuroendocrine tumours (previously called carcinoid)
- Poorly differentiated neuroendocrine carcinoma
- Lymphoma
- Sarcoma
- Neuroendocrine
- Epithelial
-
Mucocele causes [non neoplastic vs neoplastic]
- Non neoplastic
- Simple mucocele/retention cyst
- Neoplastic
- Serrated polyp
- Low-grade appendiceal mucinous neoplasm (LAMN)
- High-grade appendiceal mucinous neoplasm (HAMN)
- Mucinous adenocarcinoma
- Non neoplastic
-
Pseudomyxoma peritonei (PMP)
- LAMN
- HAMN
- Mucinous adenocarcinoma
- Ovarian mucinous neoplasm (rare)
35
Q
PMP pathophysiology
A
- As the lesion grows and occludes the lumen, mucus accumulates and the appendix ruptures or the mucin dissection of mucin through periappendiceal connective tissues onto the serosal surface with/without atypical epithelium.
- The peritoneum is then seeded with mucus-producing cells, which continue to proliferate and produce mucus.
- The progressive accumulation of copious amounts of mucinous fluid gradually fills the peritoneal cavity, resulting in the characteristic “jelly belly”.
- Inevitably, this condition progresses to intestinal obstruction, which is fatal without treatment.
- A distinctive feature of PMP is the redistribution phenomenon. The mucus and the cells it contains follow the normal flow of peritoneal fluid and are “redistributed” within the peritoneal cavity to sites of fluid absorption through lymphatic lacunae and lymphoid aggregates. Consequently, the tumor tends to spare mobile loops of small intestine but accumulates in other sites such as the pelvis, paracolic gutters, omentum, and liver capsule. Bulky accumulations can form as the mucus is absorbed and epithelial cells “filtered out” and concentrated. Peristalsis and mobility of the SB excludes it till later.
- Omentum has lots of phagocytic cells that trap the tumour cells, thus preferentially involved with omental caking
36
Q
histo features neuroendocrine appendix
A
- Poorly differentiated neuroendocrine carcinoma
* High grade (G3): > 20 mitoses / 2 mm2 or > 20% Ki67 index
* Note that 10 HPF is eqivolent to 2mm2 these days but not previously when HPF meant x40 magnification
Well differentiated neuroendocrine tumour- Stains: serotonin, chromogranin A, synap-to-physin
- Nests surrounded by palisading cells on the periphery and separated by trabecula
- Stippled/salt & pepper chromatin, nucleoli small
- Grading systems for neuroendocrine tumors of the midgut (jejunum, ileum, appendix and cecum):
- Low grade (G1): < 2 mitoses / 2 mm2 and < 3% Ki67 index
- Intermediate grade (G2): 2 - 20 mitoses / 2 mm2 or 3 - 20% Ki67 index
- Poorly differentiated neuroendocrine carcinoma
37
Q
LAMN/HAMN TNM staging
A
- LAMNs that are confined to the appendiceal wall without invasion or loss of the muscularis propria are classified as Tis(LAMN)
- This is to reflect the excellent outcome for confined LAMNs. The T1 and T2 stages are not used for LAMNs (but are for HAMN).
- LAMNs that demonstrate involvement with either acellular mucin or mucinous epithelium of the subserosa or serosa are classified as T3 or T4a, respectively.
- Acellular mucin involving the appendiceal serosa or mesoappendix is classified as T4a, while mucin involvement of distant peritoneal sites is classified as M1.
- In order to address the improved outcome for cases in which peritoneal dissemination is limited to acellular mucin only, these cases are classified as M1a. Other metastatic categories are M1b, which refers to metastases confined to the peritoneum only, and M1c, which refers to metastases outside the peritoneum.
38
Q
Management of appendiceal lesions
A
Mucocele - depends on underlying pathology
- Adenocarcinoma = right hemicolectomy
- LAMN/HAMN = appendicectomy +/- caecectomy, mucin cytology, PCI calculation and washout - referral to peritonectomy unit for discussion on surveillance
- Neuroendocrine tumour
- Criteria to encourage formal oncological right hemicolectomy
- R1
- G3
- Base (opposed to tip or middle)
- Mesoappendix invasion >3mm
- Size >2cm (definite)
- Size 1-2cm with high risk features
- R1
- G2
- LVI
- For appendiceal NETs ≤2 cm without high-risk features (nodal metastases, lymphovascular invasion, mesoappendiceal invasion, intermediate- or high-grade or mixed histology) that are confined to the appendix and treated with simple appendectomy, we do not recommend routine follow-up
- Criteria to encourage formal oncological right hemicolectomy
49
Q
Colonoscopy in IBD
A
- 8 years after the symptoms of IBD colonoscopy surveillance
- chromendocopy preferable
- Random biopsies less good, 2-4 bx every 10cm
50
Q
Management of Crohns complications
A
- Strictures
- Inflammatory or fibrotic
- Endoscopic dilation (<5cm, 50% will avoid surgery after 5 years), 5% risk of bleeding or perforation
- If long, inaccessible, refractory then surgery
- Bypass (duodenal or distal gastric)
- Resection with 2cm margin normal bowel
- End-end (easier to dilate) vs side-side (wider)
- Plasty
- SB strictures
- Contraindicated in fistula, sepsis, cancer
- Colonic strictures are treated with resection and reanastomosis (stricturoplasty contraindicated)
- Types
- [stupid way of remembering these stupid eponymous names
- Heineke-miculicz; easiest to do, hardest to say
- Finney; fin, end, blind ended
- McLassey; side to side SS spooning
- Heineke-miculicz
- <5cm
- Incise antemesenteric side of bowel 1cm proximal and distal, close transersely
- Finney
- 10-20cm
- Incise antemesenteric
- Fold in half and close in two layers i.e. side to side anastomosis
- McLassey
- >20cm
- If >20cm then probably do resection (leak rate 2%)
- [stupid way of remembering these stupid eponymous names
- SB strictures
- Abscess
- Perc drain and IVABx (1/3 will fail)
- Surgery
- Perforation
- Resection of the disease segment and either end stoma or diverted anastomosis
- Haemorrhage
- Typically from SB mucosal ulceration, can be managed with angiography
- Laparotomy
- Fistula disease (intraabdominal)
- Perforation/obstruction/phlegmon
- Remove the disease segment of bowel (or both bits of disease bowel if enteroenteric) and the secondarily involved organ will resolve with primary closure
- If fistula is going to the duodenum then may require a patch or a roux repair as the primary repair may breakdown
- Colonic crohns
- Extent, symptoms, systemic wellness
- Segmental resection vs subtotal/end ileostomy
- [CH] If one segment then do segment, if 2+ then subtotal
- If doing a proctectomy then don’t need to do TME resection and therefore will avoid the pelvic nerves
- Pelvic pouch
- Perianal disease
- Non operative
- Best to avoid operative intervention
- Multidiscipinary approach due to the complexity
- Best medical management
- Inflixamab therapy – monoclonal AB TNFa
- Fissures
- Don’t respond that well to botox, diltizem or lateral sphincterotomy
- Skin tags
- Don’t excise them because they reoccur – can be removed for diagnostic purposes (30% have granulomas of CD)
- Operative
- Draining sepsis
- Incision and drainage
- Vessel loop for fistula
- May need mushroom drain/malecot if deep cavity
- Give antibiotics, ciprofloxacin and metronidazole
- Preserve sphincter function
- Fistula
- Seton
- If active disease then need to do medical management
- For me, if they aren’t responding with draining seton I would be refering them to a colorectal surgeon for more definitive surgery
- Options surgically
- Fistulotomy
- Fibrin glue and plug
- Endorectal advancement flap
- Ligation of Intersphincteric Flap LIFT
- Faecal diversion (high likelihood this would be permanent)
- Proctectomy
- Draining sepsis
- Operative
64
Q
Location of diverticulae within the bowel wall
A
- 4 defined sites around the bowel wall, all on the mesenteric side (see diagram)
67
Q
Appendicitis Alvarado score - mneumonic
A
MANTRELS
72
Q
Pruitis ani causes
A
- 75% of cases coexisting underlying cause
- Faecal incontinence or seepage
- Excessive cleaning or topical creams
- Malignancy
- Rectal cancer or rectal adenomas, anal scc, melanaoma, extramammary pagets
- Inflammation
- Haemorrhoids, fissures, fistulas, rectal prolapse, radiation proctitis and UC
- Dermatitis, lichen simplex, lichen planus, lichen atrophicus
- Infectious
- Condylomata, candida, syphilis, HSV, anal pinworm
73
Q
Surgical sieve for differential diagnosis
A
VINDICATE
78
Q
How to categorise polyp aetiology?
A
- Neoplastic
- Non Neoplastic
83
Q
Scoring tool for severity of lower GI bleed
A
Oakland score
Recommended by the british gastro and colorectal surgeons
92
Q
Fistula in ano classification
A
94
Q
Essential principals of ERAS
A
