Lower GI — Disease Index & Clinical Criteria

Written by Betra Youhanna, a medical student and not a doctor — check every detail against your own teaching.

Disease Index · 33 entries across 8 categories · deck-derived, finals-triage

Criteria & Scores · 65 scoring systems, classifications, comparison tables, frameworks

C/P — Clinical Presentation

Inves — Investigations

Mng — Management

Special — Pathognomonic / disease-unique

IBD & Colitides

5 entries

Ulcerative Colitis (UC)

C/P

Relapsing bloody mucoid diarrhoea, lower abdominal cramps relieved by defaecation
Proctitis: blood mixed with stool, urgency, tenesmus
Acute attack: 10–20 liquid stools/day, nocturnal, urgency, incontinence
Malaise, lethargy, anorexia; fluid/electrolyte imbalance
Peak onset 20–25 yr and 70–80 yr; no gender preference; mainly Whites
Extra-intestinal: arthropathy, ankylosing spondylitis (HLA-B27), uveitis/episcleritis/conjunctivitis, pyoderma gangrenosum, erythema nodosum, PSC (more common in UC), clubbing, sacroiliitis

Inves

FBC + iron studies — assess anaemia (chronic blood loss + inflammation)
WBC / platelets / ESR / CRP — activity + severity markers
Albumin — malnutrition + severity (Truelove & Witts criterion)
pANCA — supports UC over CD (contrast: ASCA in CD)
Stool cultures — exclude infective mimics (CMV, C. difficile) before immunosuppression
AXR — assess colonic dilatation (toxic megacolon), wall thickening
USS — non-invasive screen for wall thickening + free fluid
Colonoscopy — confirm continuous rectal-proximal inflammation, friable mucosa, pseudopolyps + biopsy; DO NOT scope in severe attack (perforation risk)
Cancer surveillance colonoscopy + random biopsies if total UC ≥ 10 yr — detect dysplasia
Histology — confirm superficial (mucosa/submucosa) inflammation, crypt abscesses, goblet cell depletion, glandular distortion, Paneth metaplasia, flask-shaped ulceration

Mng

Step-up: 5-ASA (mesalamine) → corticosteroids → AZA/6-MP → biologics (infliximab, adalimumab) → surgery
Mild proctitis: 5-ASA enema; moderate: oral 5-ASA; severe: IV 5-ASA
Acute severe: admit, IV hydrocortisone 100 mg 6-hrly, IV fluids, enteral nutrition, azathioprine if recurrent
Topical: hydrocortisone foam, prednisolone enema, mesalazine enema, budesonide enema
Resistant proctitis: oral steroids ± azathioprine
Surgery curative: proctocolectomy + IPAA or Brooke ileostomy; indications — severe attack failing 48 h IV steroids, toxic megacolon, perforation, massive haemorrhage, dysplasia/cancer, steroid-dependent

Special

Backwash ileitis — distal terminal ileum (≤ 25 cm of ileocaecal valve)
Pseudopolyps — islands of regenerating mucosa, strongly suggestive of UC
Toxic megacolon — colon > 5.5 cm (X-ray > 5 cm thin-walled gas-filled with mucosal islands); urgent colectomy if not resolved in 48 h; mortality 15–25%; precipitated by antidiarrhoeals
Lead-pipe colon on barium (loss of haustration)
Cancer risk: extensive UC > 8–10 yr; dysplasia 5% at 10 yr, 25% at 20 yr; high-grade dysplasia → colectomy

physiology · background · low-yield

Epidemiology/Risk

60% have mild disease; 97% have at least one relapse per 10-year period

Crohn's Disease (CD)

C/P

Diarrhoea (80% — bloody only in Crohn's colitis), abdominal pain, weight loss
Constitutional: malaise, anorexia, nausea/vomiting, low-grade fever
Steatorrhoea (small bowel, bile-acid malabsorption)
Anal/perianal disease (fissures, fistulae) often precedes intestinal symptoms
Enteric fistulae (to bladder, skin)
Peaks teens–20s and 50–69; Whites (HLA-DR1/DQw5), Jews, smokers
20% abrupt onset mimics acute appendicitis or bowel perforation
Extra-intestinal: migratory polyarthritis, sacroiliitis, ankylosing spondylitis, erythema nodosum, clubbing, PSC (less than UC)

Inves

FBC + iron/folate/B12 — chronic disease anaemia + terminal-ileum malabsorption
ESR / CRP / WBC — inflammation activity
Albumin — nutritional + severity marker
ASCA positive, pANCA usually negative — favours CD over UC
Faecal calprotectin — neutrophil marker of intestinal inflammation; predicts treatment response; monitor relapse
CDAI — objective activity score (guides therapy escalation)
Colonoscopy — confirm patchy aphthoid → deep cobblestone ulcers, skip lesions, strictures + biopsy
MR enterography — small-bowel imaging (assess extent, strictures, fistulae)
High-resolution USS + spiral CT — bowel wall, mesentery, intra-abdominal abscess
Rectal USS / MRI — map perianal disease (fistula tracks, abscess)
Histology — confirm transmural inflammation, lymphoid aggregates, non-caseating sarcoid-like granulomas (50–60%, epithelioid + Langhans'), pyloric/Paneth metaplasia, focal cryptitis

Mng

Stop smoking (major risk factor)
Symptomatic: loperamide / codeine; cholestyramine for bile-acid diarrhoea post-ileal resection; treat anaemia (B12, folate, iron)
Induction: systemic steroids (prednisone) or budesonide (ileal/proximal colonic)
Maintenance: 5-ASA (Crohn's colitis only); azathioprine/6-MP (6–8 wk to work, FBC monitoring); methotrexate IM/IV (steroid-resistant); mycophenolate
Biologics — infliximab / adalimumab (anti-TNF); ustekinumab; first-line moderate-severe and first-line for fistulae and perianal disease
Antibiotics: ciprofloxacin + metronidazole for perianal CD / abscesses
Surgery NOT curative (recurrence common); 2/3 require ≥1 op; limited resections, fistulectomies, abscess drainage
Surgical indications: recurrent intestinal obstruction (commonest) · perforation · failed medical therapy · intestinal fistula · fulminant colitis · malignant change · perianal disease
Surgical options: ileocaecal resection (commonest) · segmental resection (fistulising > stricturing) · colectomy + IRA (rectal sparing) · emergency colectomy (toxic megacolon, ~8%) · total proctocolectomy + Brooke (rectum involved, refractory, anorectal disease) · temporary loop ileostomy (acute distal / severe perianal) · strictureplasty (preserve bowel length) · anal disease — drain abscess + draining seton (avoid aggressive fistulotomy)
Strictureplasty types: Heineke-Mikulicz (short, 5–10 cm; longitudinal incision antimesenteric → transverse closure; metal clip marker) · Finney (medium up to 15 cm) · Side-to-side isoperistaltic (Michelassi) (long > 15 cm)

Special

Skip lesions — sharply demarcated affected segments with intervening normal bowel
Cobblestone appearance — deep + transverse + linear ulcers
String sign on barium (stricture)
Creeping fat — mesenteric fat wraps around bowel; bacteria migrate into fat to "plug leaks"; contributes to fibrosis
Fat-wrapping, serositis, fistulae, transmural lymphoid aggregates, non-caseating granulomas, deep fissures — all favour CD over UC
Rectal sparing usual; preferential right-sided; terminal ileum + ascending colon most common
B12 deficiency unusual despite terminal ileum involvement
Fistula surgical management (asymptomatic = no surgery; internal fistulae 5–10% of CD): Gastrocolic → colonic resection + wedge of stomach · Enterovesical → resect bowel + repair bladder · Enterovaginal (below sphincter) incise/drain or excise · (trans/above sphincter) proctectomy · Enteroenteric → resection-anastomosis

physiology · background · low-yield

Mechanism

Creeping-fat protective response has no 'off' switch → contributes to severe intestinal scarring / fibrosis, which occurs in ~40% of Crohn's patients

Background

Also called regional enteritis — because it affects sharply delineated segments

Epidemiology/Risk

Prevalence ~3 per 100,000 (primarily Western populations)

Indeterminate Colitis

C/P

Mixed / atypical IBD presentation that cannot be classified

Inves

Endoscopy + biopsy — attempt to distinguish UC from CD (features overlap)
Colectomy specimen — if surgery required, definitive histology may still be indeterminate

Mng

Treat as severe IBD; most evolve to a definite diagnosis at follow-up

Special

5–15% of IBD cases; up to 30% of paediatric
Originally tied to fulminant colitis requiring urgent colectomy where classic features were obscured
Not a specific disease entity — no diagnostic criteria
Indication for ileo-rectal anastomosis (not pouch) in surgery

Microscopic Colitis

C/P

Chronic or fluctuating watery diarrhoea

Inves

Colonoscopy — macroscopically normal (rules out visible IBD / neoplasia)
Random biopsies — the diagnostic step (histology abnormal despite normal appearance)

Mng

Symptomatic — deck does not specify

Special

Three forms: microscopic ulcerative colitis, microscopic lymphocytic colitis, microscopic collagenous colitis

Other chronic colitides

C/P

— context-specific (see individual conditions)

Inves

— biopsy-based

Mng

— underlying cause

Special

Diversion colitis · Diverticulitis / segmental colitis · Pouchitis

Polyps & Precancer

8 entries

Hyperplastic Polyp

C/P

Asymptomatic; no malignant potential

Inves

Colonoscopy — incidental finding (most common colonic polyp 75–90%)
Size 1–5 mm (rarely ≥ 1 cm); left colon, especially rectum; often multiple; age ≥ 50
Biopsy — mandatory (cannot differentiate from adenoma by endoscopy alone; histology rules out neoplasia)

Mng

None required (no malignant potential)

Special

Histology: hyperplastic glands, absent atypia

Adenomatous Polyps (Tubular / Tubulovillous / Villous)

C/P

Often asymptomatic; rectal bleeding; vague abdominal discomfort
Conventional adenomas more common in left colon

Inves

Colonoscopy — detect polyp; assess morphology + size (screening-detected or symptomatic)
Polypectomy specimen — histology confirms adenoma (vs hyperplastic) + grades dysplasia
Gross morphology (endoscopy) — pedunculated (with stalk), sessile (flat-based), or flat
Architecture on histology — Tubular (< 25% villous, commonest); Tubulo-villous (25–75%); Villous (> 75%, papillary fronds, ~1%); villous ↑ with size + malignant potential
Hallmark on histology = epithelial dysplasia (nuclear hyperchromasia, stratification, elongation)
Grade of dysplasia — determines follow-up interval + endoscopic vs surgical sufficiency
Low-grade: stratification doesn't reach luminal border; minimal-moderate mitosis
High-grade: full-thickness stratification reaching luminal border; enlarged hyperchromatic nuclei, prominent nucleoli
Intramucosal carcinoma — invasion into mucosa/muscularis mucosae but NOT beyond = no metastatic potential (mucosa lacks lymphatics); polypectomy curative
Adenoma (even high-grade) = no invasion through muscularis mucosae into submucosa → endoscopic clearance sufficient

Mng

Polypectomy + microscopic exam of every adenoma (adenoma-carcinoma sequence)

Special

Malignant potential factors (highest → lowest): high-grade dysplasia · villous architecture · size (> 2 cm) · multiple
74% of adenomas < 1 cm → 1% contain invasive cancer
35% of adenomas > 2 cm show malignant change
Pathology report MUST include size + grade of dysplasia
Adenoma-carcinoma sequence: ~10% inherited, 90% sporadic

Familial Adenomatous Polyposis (FAP) + Variants

C/P

18-year-old with abdominal discomfort, rectal bleeding
Colon "carpeted" / studded with hundreds–thousands of polyps
Mean age of polyp development: 16 years

Inves

Colonoscopy — visualise carpet of polyps (diagnostic)
Genetic testing for APC mutation — up to 100% accuracy; confirms diagnosis + cascade family screening
At-risk children — colonoscopy every 1–2 yr from age 10–12 yr for early polyp detection
Biopsy strategy — sample every polyp suspicious for carcinoma (large, fixed, eroded, irregular); otherwise representative polyps every 10 cm to detect focal high-grade / invasion
Upper GI endoscopy — screen for duodenal / ampullary adenomas (2nd-most common CA after CRC in FAP)

Mng

Prophylactic colectomy in late 2nd / early 3rd decade (late teens / early 20s)
Family screening — colonoscopy + APC genetic testing

Special

Autosomal dominant
APC gene on chromosome 5q21 (tumour suppressor — "gatekeeper")
100% develop adenocarcinoma by 40–45 yr if untreated
Two-hit: first hit often inherited; second hit = LOH; allows replicating cells to heap up + further K-ras, p53 mutations
APC regulates cell adhesion via β-catenin and migration
Variants: Gardner (osteomas + dental + soft-tissue tumours) · Turcot (CNS tumours, e.g. medulloblastoma) · Attenuated FAP (AAPC) (~30–35 polyps, ~36 yr, proximal/right colon)

Lynch Syndrome (HNPCC)

C/P

Familial clustering of cancers at younger ages than sporadic
CRC often right colon / proximal (60–70%)

Inves

Tumour IHC for MLH1 / MSH2 / MSH6 / PMS2 — rapid screen for MMR deficiency (loss = MSI-H phenotype)
MSI testing (PCR / NGS) — confirms MSI-H, guides Lynch workup + immunotherapy eligibility
BRAF V600E + MLH1 promoter methylation — distinguishes sporadic MSI-H (methylation) from Lynch (germline)
Germline MMR gene testing — confirms Lynch diagnosis + cascade family screening
Colonoscopy every 1–2 yr from age 20–25 — surveillance (right-sided predilection, faster adenoma→cancer)
Gynae surveillance (endometrial biopsy, TVUS) — endometrial CA is most common non-colon Lynch tumour
More common than FAP; ~3–5% of all colonic adenocarcinomas

Mng

Surveillance + colectomy if cancer — deck does not specify protocol details

Special

Autosomal dominant; DNA Mismatch Repair (MMR) genes — "caretaker"
Main genes: hMSH2 (chr 2, 31%), hMLH1 (chr 3, 33%), hPMS1/hPMS2 (2 + 7, 2% + 4%)
Faulty MMR → Microsatellite Instability (MSI-H)
Cancer cluster: colorectum, endometrium (most common non-colon), stomach, ovary, ureters, brain, small bowel
Synchronous or metachronous; high grade / poorly differentiated; mucinous or medullary; intense lymphocytic infiltrate
Despite high grade — better prognosis than sporadic

Juvenile Polyposis

C/P

Tens–hundreds of mucus-filled hamartomatous polyps in colorectum

Inves

Colonoscopy — identify hamartomatous polyps (macroscopic diagnosis)
Biopsy — histology confirms hamartoma (mucus-filled), rules out adenomatous change / carcinoma
Genetic testing (SMAD4, BMPR1A) — if familial pattern; SMAD4 also links to HHT

Mng

Surveillance; resection of polyps

Special

1/3 inherited autosomal dominant
Up to 1/5 develop colorectal cancer before age 40

Peutz-Jeghers Syndrome

C/P

Hamartomatous polyps (typically small bowel)
Mucocutaneous pigmentation — lips, buccal mucosa, palms, soles

Inves

Colonoscopy + small-bowel imaging (capsule / MR enterography) — hamartomas often small-bowel
Histology — confirms hamartoma with arborising smooth-muscle core (pathognomonic)
STK11 genetic testing — confirms diagnosis + cascade family screening
Multi-organ surveillance — small bowel, colon, breast, pancreas, ovary (elevated risk each)

Mng

Surveillance + resection

Special

Autosomal dominant
Mutations in STK11 serine-threonine kinase gene (19p)
Increased risk of small bowel + colonic adenocarcinoma; also breast, pancreas, ovary

11b

Serrated Polyposis Syndrome (WHO)

C/P

Multiple serrated polyps; ↑ CRC risk via serrated pathway (BRAF mutation, CpG island methylator phenotype)

Inves

Colonoscopy — identify serrated polyps + confirm WHO criteria (count, size, location)
Biopsy of all serrated lesions — distinguish sessile serrated lesion (dysplastic potential) from hyperplastic
BRAF + CIMP testing — supports serrated pathway (research / atypical cases)

Mng

Surveillance colonoscopy 1–3 yearly; polypectomy; colectomy if dysplasia / cancer

Special

WHO criteria (any one): (1) ≥ 5 serrated polyps proximal to sigmoid, ≥ 2 of which > 10 mm · (2) any serrated polyps proximal to sigmoid with family history of serrated polyposis · (3) > 20 serrated polyps of any size across the colon
Sessile serrated lesions (right colon, BRAF-mutant) — main precursor

11c

Other Hamartomatous / Polyposis Syndromes

C/P

Cowden — GI hamartomas + breast/thyroid (follicular)/endometrial cancers; mucocutaneous trichilemmomas
Cronkhite-Canada — GI hamartomas + alopecia + nail dystrophy + hyperpigmentation
Turcot — polyposis + CNS tumour

Inves

Cowden — PTEN germline testing; thyroid US, mammography surveillance
Cronkhite-Canada — clinical + histology (hamartomas + ectodermal features); nutritional labs (protein-losing)
Turcot — colonoscopy + brain MRI + APC/MMR testing to distinguish variant

Mng

Surveillance + targeted resection

Special

Cowden — autosomal dominant, PTEN mutation
Cronkhite-Canada — non-hereditary; ectodermal features distinguish from PJS
Turcot: FAP variant → medulloblastoma; Lynch variant → glioblastoma

Colorectal & Anal Cancer

3 entries

Colorectal Cancer (Colon)

C/P

Change in bowel habit (74%) — most common
Rectal bleeding + change in bowel habit (51%)
Rectal / abdominal mass (12.5–24.5%); iron deficiency anaemia (9.6%); abdominal pain (3.8%)
Asymptomatic (screening-detected); intestinal obstruction
Globally — 3rd commonest in males, 2nd in females
Uncommon < 40 yr; incidence rises 40–50
Virchow's node (left supraclavicular LN) on general examination — sign of metastatic spread
Narrowed stool calibre — pencil-like / ribbon-like stools (constricting left-sided / rectosigmoid lesion)

Inves

Colonoscopy = gold standard — direct visualisation + biopsy + assess synchronous polyps
Biopsy — histology confirms adenocarcinoma; grade + margin assessment
Serum CEA (> 5 ng/mL = adverse prognostic threshold) — preop baseline + postop recurrence surveillance
Tissue CDX-2 IHC — confirms colorectal origin (important in metastatic workup)
CT colonography — alternative when colonoscopy incomplete (obstructing tumour)
Barium enema — apple-core sign (mostly historical / limited-resource)
FIT / gFOBT — population screening (asymptomatic detection)
Staging CT abdomen + chest — assess M status (liver + lung mets), local extent, LN spread
pT layers (inner → outer): mucosa → submucosa → muscularis propria → subserosa → peritoneal elastic lamina → mesothelium — histological depth defines pT
Site distribution: rectum ~30% · sigmoid ~25% · caecum ~15% · ascending ~10% · descending/transverse remainder
FBC — detect iron-deficiency anaemia (right-sided occult bleed)
LFTs — screen for hepatic metastases

Mng

Stage 0 (Tis): polyp removal
Stage I (T1/T2 N0): surgical resection alone
Stage II (T3/T4 N0): surgery
Stage III (any T, N1/N2): surgery + adjuvant chemotherapy
Stage IV (M1): chemo (1st–3rd line) + anti-angiogenic + anti-EGFR ± radiation (rectal)
Metastasis options: peritonectomy + HIPEC (Sugarbaker, peritoneal); SIRT (yttrium-90 microspheres, liver); RFA (unresectable liver); VATS (resectable lung mets)
Marginal safe zone = 2 cm
Resection by site: caecum/ascending → right hemicolectomy; hepatic flexure → extended right; splenic flexure → extended left; descending → left hemicolectomy; sigmoid → rectosigmoid resection
Obstruction (resectable): Hartmann's / elective resection / primary anastomosis / SEMS
Obstruction (unresectable): ascending → ileocolic bypass; upper-left → transverse loop colostomy; pelvic → sigmoid loop colostomy

Special

Two pathogenic pathways: (1) Adenoma-carcinoma sequence (Vogelgram: APC/MCC → hyperplasia → K-ras → adenoma → DCC → late adenoma → p53 → carcinoma → metastasis); (2) Inflammation-dysplasia sequence (IBD — UC > CD)
Risk: age, low-fibre, refined carbs, low vit A/C/E, excess fat (→ bile-acid carcinogens via flora), FAP (APC), HNPCC (MMR), IBD, alcohol, obesity, smoking, abdominal radiation
Protective: physical activity, fibre, folic acid, vit B6/D, calcium/dairy, vegetables, garlic, fish, aspirin/NSAIDs
Hepatic metastasis — multiple nodules ("cannonball")
Grade 1 well-diff (looks like origin); Grade 4 undifferentiated (no glands, sheets)
Macroscopic: ulcerative (raised rolled edges) · fungating/polypoid (cauliflower) · annular (stenosing, rectosigmoid) · papilliferous · colloid
MSI-H phenotype (Lynch + some sporadic) — mucinous, right-sided, lymphocytic infiltrate, better prognosis, responds to immunotherapy (anti-PD1)
Signet ring cell carcinoma — worst-prognosis histologic variant
Additional risk factors — prior cholecystectomy (bile-acid exposure), ureterosigmoidostomy
Postop mortality causes (ranked): anastomotic leak / sepsis · MI · PE

physiology · background · low-yield

Background

Colonic lymph node tiers (spread order): Epicolic (bowel wall) → Paracolic (marginal vessels) → Intermediate (major SMA/IMA branches) → Principal (origin of SMA/IMA)

Exam technique

Palpable mass by site: caecal → right iliac fossa; transverse colon → epigastric; rectosigmoid → left lumbar (often with faecal impaction)

Rectal Cancer

C/P

Bleeding — small dark red streak on stool
Mucus expressed in liquid motion (diarrhoea-like)
Change in bowel habit → constipation
High annular cancers cause alternating constipation + diarrhoea
75% in lower rectal ampulla, 25% upper; 90% palpable on DRE
Progression to painful tenesmus signifies nerve invasion / advanced disease
Copious mucus from cauliflower tumour → hypokalaemia + perianal irritation / incontinence

Inves

DRE — 90% of rectal cancers palpable; assess size, distance from anal verge, fixity, sphincter involvement
Proctoscopy — direct visualisation of low/mid-rectal tumour
Colonoscopy + biopsy — histological confirmation + rule out synchronous colonic lesions
Endorectal sonography (ERUS) — best for local T + N staging in early tumours (superficial layers)
MRI pelvis — assesses CRM + mesorectal extension → determines neoadjuvant chemoradiation need
CT chest/abdomen — distant staging (liver, lung mets)
CEA — baseline + recurrence surveillance

Mng

T1 N0 → local excision; T1–2 N0 → transabdominal; T3 N0 or any T + N1/N2 → pre-op chemoradiotherapy → surgery
AR — upper 3rd (~11–15 cm), above peritoneal reflection; 2 cm distal margin safe
LAR — middle 3rd (~7–11 cm), below peritoneal reflection
ULAR — lower 3rd (< 7 cm), pelvic floor; uses intersphincteric plane to preserve external sphincter
ISR — total / partial — preserves external sphincter
APR — distal rectal cancer involving sphincter or sphincter-sparing unsound; abdominal + perineal; removes sigmoid + rectum + anal canal; permanent end colostomy
ELAPE — wider plane for very low rectal cancers
Local excision (T1): transanal · transsphincteric · transcoccygeal (posterior wall) · TEM (middle-lower 3rd)
Anastomosis: hand-sewn / double-stapled / single-stapled
Anal canal involvement: ULAR if no sphincter; APR if poorly differentiated low rectal cancer OR < 1 cm from dentate line

Special

Key margins — Distal (DRM) + Circumferential (CRM, mesorectal + lateral pelvic wall)
TME named planes — Holy Plane (Heald) = avascular areolar plane between visceral mesorectal fascia + parietal pelvic fascia; Denonvilliers fascia = anterior (rectoprostatic / rectovaginal); Waldeyer fascia = posterior (rectosacral)
Mesorectum = visceral endopelvic fascia containing rectum + perirectal fat + lymphovascular tissue; TME = sharp dissection in the mesorectal plane
Pelvic exenteration: APR + posterior vaginectomy (vagina); posterior pelvic exenteration (rectum + uterus + cervix + vagina); total pelvic exenteration (rectum + bladder + prostate)
Lymphatic spread along IMA pedicle
Pelvic autonomic nerve injury during rectal/pelvic dissection — damage to nervi erigentes (pelvic splanchnic) & hypogastric plexus → erectile dysfunction, retrograde ejaculation, bladder dysfunction

physiology · background · low-yield

Background

Detailed lymphatic spread: upper/middle third → superior haemorrhoidal → IMA nodes; lower third → middle rectal → internal iliac; inguinal nodes involved only if tumour invades the dentate line

Anal Cancer

C/P

Bleeding per rectum (most common); pain, tenesmus, pruritus
Mass palpable in anus; inguinal mass (metastatic LNs)
Anal canal (anorectal ring → anal verge) — 3–4× commoner than anal margin
Less common than rectal cancer

Inves

DRE — assess size, location (canal vs margin), fixity, sphincter involvement
Proctoscopy — direct visualisation + guide biopsy
Inguinal LN examination — anal canal drains to inguinal chain (unlike rectal → mesorectal)
Pelvic exam — rule out other HPV-associated cancers (cervical, vaginal, vulvar) in field of same HPV exposure
Biopsy from mass — histology confirms SCC (vs adenoCa, melanoma, GIST)
FNAC of inguinal LNs — confirm N status → alters radiation field
CT abdomen/pelvis — regional spread + distant mets
MRI pelvis — best for soft-tissue local staging (sphincter involvement)
Transanal USS — local T staging in early tumours
CT chest — pulmonary mets
HIV test — high co-prevalence; affects prognosis + tolerance to chemoradiation

Mng

AIN: local surgery / photodynamic therapy / topical imiquimod
Invasive cancer: Nigro regime — chemoradiotherapy (5-FU + mitomycin OR 5-FU + cisplatin)
Good response → may excise local remnant; obvious residual → APR

Special

HPV-16 — very high risk SCC; types 18, 31, 33, 35 moderate
HIV — all categories ↑ risk; Tobacco — 5-fold ↑ risk
Benign anal pathology (fistula, fissure, haemorrhoid) does NOT increase risk
Pathology: AIN precursor; SCC 70% (also adenoCa, mucinous, small cell); basaloid / cloacogenic / transitional = SCC variants
Anal margin: mostly SCC; also basal cell, Paget disease, Bowen disease (intra-epidermal SCC), verrucous carcinoma (SCC variant)

Diverticular

1 entry

Diverticular Disease / Diverticulitis

C/P

80–90% asymptomatic diverticulosis; 10–20% develop diverticulitis
Rising in Western world with ageing; > 80% by age 80; 60% by 50; 5% by 40
South-east Asians — right-sided; Caucasian — left-sided (sigmoid 50%, sigmoid+descending 40%, whole colon 5–10%)
Demographics > 60 yr; no sex predilection; men more bleeding, women more fistula
Younger < 50 — chronic/recurrent diverticulitis
Females need surgery 5 yr later than males
Acute simple: LIF pain, anorexia, fever, altered bowel habit, tachycardia, LIF tenderness/guarding, tender mass
Complicated: + perforation, tachycardia, hypotension (Hinchey applies)
Chronic atypical: LLQ intermittent low-grade, no systemic; Chronic typical: + systemic + phlegmon
Complex: fistula, stricture, obstruction
Fistula types: colovesical, colocutaneous, coloenteric, colovaginal

Inves

FBC + CRP — inflammation activity (raised WBC + CRP in acute diverticulitis)
CT abdomen/pelvis — main investigation in acute; confirms diverticulitis, stages Hinchey severity, excludes malignancy + other DDx
Colonoscopy — for chronic (contraindicated in acute — perforation risk); confirms diverticulosis + excludes malignancy
Follow-up colonic imaging ~ 6 weeks post-acute (colonoscopy / barium enema / CT colonography) — confirms diverticulosis, rules out cancer / IBD mimicking as diverticulitis
DDx of acute to keep in mind (imaging targets): PID, appendicitis (right-sided redundant sigmoid), Crohn's colitis, ischaemic colitis, perforated colonic CA, pyelonephritis
Hinchey classification — grades complicated acute diverticulitis → guides drainage vs surgery
Urinalysis — pneumaturia / faecaluria points to colovesical fistula
Cystoscopy / CT cystography — confirms colovesical fistula

Mng

Hinchey I–II (abscess): IV antibiotics + radiological (CT/USG) percutaneous drainage; aim to resolve sepsis, avoid emergency surgery
Follow-up imaging 3–5 days after drainage; colonoscopy after acute → resection of diseased sigmoid + colorectal anastomosis
Hinchey III–IV (peritonitis): surgical exploration after resuscitation; cross-sectional imaging to exclude malignancy
Surgical: Hartmann's (conventional, sigmoid resection + colostomy, high morbidity/mortality); laparoscopic wash-out; resection + primary anastomosis (selected cases, on-table antegrade colonic lavage); damage control
Conservative: rifaximin (weak), fibre (weak)
Elective resection indications: recurrent complicated diverticulitis · persistently symptomatic post-acute · fistula/stricture
Fistula mng: excise diverticular segment + repair organ defect + primary anastomosis; rule out Crohn's, malignancy
Obstruction: resection + primary anastomosis / Hartmann's / stenting (if inoperable)

Special

True diverticulum = all layers; False (pseudodiverticulum) = lacks a layer; colonic = mucosa through muscle = pseudodiverticula = pulsion (intraluminal pressure)
Sigmoid narrowest → highest pressure (up to 90 mmHg, 9× normal)
Herniation at vasa recta brevia — mesenteric side of antimesenteric taenia
Often embedded in appendices epiploicae
Muscular hypertrophy (circular + taenia coli) precedes diverticula
Elastosis precedes diverticulosis; not found in other inflammatory colonic conditions
Saint's triad — diverticulosis + hiatus hernia + gallstones (concurrent age-related connective-tissue change)
Right-sided diverticula — Asian, congenital, true (all layers), solitary; left-sided — Western, acquired, false, multiple
Giant colonic diverticulum — > 4 cm, usually sigmoid, perforation risk

physiology · background · low-yield

Epidemiology/Risk

Progression cascade: 10–20% of diverticulosis → diverticulitis; 10–20% of these hospitalised; 20–50% of admitted need surgery; overall < 1% ultimately require operative management

Background

Non-inflammatory diverticulitis subtype — a postoperative diagnosis, probably a healed microabscess

Appendix

4 entries

Acute Appendicitis

C/P

Dull, colicky periumbilical pain → migrates to RIF / McBurney's point (parietal peritoneum)
Anorexia (important in children), nausea, vomiting
Pyrexia; localised RIF tenderness, muscle guarding, percussion tenderness
Discomfort moving, walking, coughing
Uncommon: micturition frequency, diarrhoea, microscopic haematuria

Inves

Clinical — largely a clinical diagnosis; scores (Alvarado, PAS, AIR) formalise it
FBC — leukocytosis + left shift; WBC > 20,000 → gangrenous or perforated
CRP — raised; normal WBC/CRP + normal neutrophil % should make you think twice
Urinalysis — mild pyuria/haematuria possible (bladder irritation); exclude UTI
Pregnancy test — mandatory in reproductive-age women (rule out ectopic; guides imaging)
U&E — baseline (rehydration + preop)
Supine AXR (selective) — rarely diagnostic; may show fecalith, sentinel loop
USS first-line in children + pregnancy (no radiation) — appendix ≥ 7 mm AP, thick-walled, blind-ending, non-peristaltic, non-compressible + periappendiceal fluid
CECT (helical, IV contrast) — imaging of choice per SIS/IDSA when clinical unclear or intervention high-risk; higher sens/spec than USS; also excludes DDx
Children with equivocal exam → CT abdomen
Elderly → early CT (atypical presentation, malignancy DDx)
Pregnancy → USS first; if equivocal, MRI (avoid CT radiation to fetus)
Diagnostic laparoscopy — women of childbearing age with inconclusive USS/CT (rules out gynae DDx + treats in same op)

Mng

Surgical — open or laparoscopic appendicectomy
Pre-op antibiotics; spinal or general anaesthesia; reexamine abdomen after anaesthesia
Laparoscopic preferred: obese, women of childbearing age, diagnostic uncertainty
Other approaches: SILS, NOTES (transvaginal/transgastric)
Pregnancy: proceed to appendicectomy (don't observe); fetal-loss risk relates to severity
Intraop scenarios: normal appendix → still remove (look for mesenteric lymphadenitis, Meckel's, tubo-ovarian); tumour < 2 cm → appendicectomy, > 2 cm → right hemicolectomy; abscess with lump → drainage + local toileting + IV antibiotics (don't separate)

Special

Clinical signs: Dunphy's (cough); Rovsing's (RLQ pain on LLQ palpation); Obturator (internal hip rotation — pelvic appendix); Iliopsoas (right hip extension — retrocaecal appendix)
McBurney's point tenderness minimal/absent in retrocaecal/pelvic/postileal, obese, 2nd/3rd-trimester pregnancy, high-up caecum, long appendix
Positions: retrocaecal 74% · pelvic 21% · paracaecal 2% · subcaecal 1.5% · preileal 1% · postileal 0.5%
Perforation ≥ 48 h; perforated signs: seriously ill, fever, tachycardia, rebound
Risk factors perforation: extremes of age, immunosuppression, DM, previous abdominal surgery
Obstruction causes: fecalith · hyperplastic lymphoid follicles · parasites (Oxyuris vermicularis / pinworm) · caecal carcinoma
Organisms: E. coli, Strep viridans, Pseudomonas, Bacteroides
Left-sided pain — possible if intestinal malrotation (left-sided caecum)
DDx children: pre-school — intussusception, Meckel's, gastroenteritis; school-age — mesenteric lymphadenitis, gastroenteritis
DDx childbearing women: ruptured ectopic, Mittelschmerz, ovarian cyst/torsion, PID
Postop unwell check: wound (abscess), rectal exam (pelvic abscess), lungs, legs (DVT), liver + rigors (pylephlebitis), urine (pyelonephritis), suspect subphrenic abscess

physiology · background · low-yield

Other

Fecalith composition: inspissated faecal material + calcium phosphates + bacteria + epithelial debris

Microbiology

Additional organisms found in a few patients (beyond E. coli / Strep viridans / Pseudomonas / Bacteroides): Peptostreptococcus, Lactobacillus, Fusobacterium nucleatum

Appendicular Mass (Lump)

C/P

Features of acute appendicitis + lump in lower abdomen; lump = perforated appendix + omentum + intestinal loops

Inves

USS / CT (CT preferred) — confirm mass, define components, exclude abscess needing drainage
FBC + CRP — monitor response to conservative regimen
Serial exams (pulse, temp, mass size) — decide continue vs escalate

Mng

Ochsner-Sherren regimen:
Conservative + IV fluids + IV antibiotics; monitor pulse / temperature / lump size
If responds → continue conservative → interval appendicectomy (~6 weeks)
If not responding → exploration as early as possible
Criteria to stop conservative: rising pulse · increasing/spreading pain · increasing mass size

Special

Explore early if signs of deterioration

Appendiceal Carcinoid Tumour (Argentaffinoma)

C/P

Often presents as recurrent appendicitis

Inves

Appendicectomy specimen histology — usually incidental discovery post-op
Chromogranin B IHC positive — confirms neuroendocrine origin
Chromogranin A + urinary 5-HIAA — baseline for functional monitoring (metastatic disease)
CT / MRI — assess base/mesoappendix involvement + mesenteric/nodal spread (decides right hemicolectomy)
Colonoscopy — screen for second GI primary

Mng

Tumour < 2 cm → appendicectomy
Tumour > 2 cm OR involves base of appendix or mesoappendix → right hemicolectomy
Screen for second primaries (GI + GU) — colonoscopy

Special

Most common neoplasm of the appendix
Neuroendocrine tumour (NET) from Kulchitsky cells of crypts of Lieberkühn
Most at the tip of the appendix
Appendiceal carcinoid rarely metastasises

Mucinous Neoplasm / Pseudomyxoma Peritonei (PMP)

C/P

Appendix tumour producing copious mucin; rupture spills mucin + tumour cells into abdomen

Inves

CT abdomen/pelvis — peritoneal cavity full of jelly-like mucin coating organs; classic "scalloping" of liver capsule = pathognomonic sign
USS — free mucinous ascites, ovarian masses (drop metastases)
Tumour markers — CEA, CA 19-9, CA 125 (baseline + monitoring)
Appendicectomy specimen histology — grades LAMN (low-grade appendiceal mucinous neoplasm) vs high-grade → guides HIPEC decision

Mng

— deck does not specify treatment

Special

Literally "false mucus tumour of the peritoneum"
Coats liver, uterus, intestines; CT scalloping appearance

Non-septic Anorectal

5 entries

Internal Haemorrhoids

C/P

Painless, bright red bleeding per rectum during defecation (dripping / squirting)
Prolapse during defecation; mucoid discharge
Pain not usual except in thrombosed external
Grades: I bleeding only; II spontaneously reduces; III manual reduction; IV irreducible

Inves

Positioning (left lateral / knee-elbow / lithotomy) — enables adequate perianal exposure
Inspection — visualise external component + prolapse on straining
DRE — assess sphincter tone + exclude anorectal mass (piles themselves are not palpable)
Proctoscopy — essential for diagnosis + grading internal haemorrhoids
Sigmoidoscopy — excludes proximal inflammation / neoplasia mimicking piles
Colonoscopy — mandatory if symptoms don't correspond, age > 40, or CRC risk factors (don't blame bleeding on piles without ruling out cancer)
FBC — chronic blood loss anaemia if prolonged bleeding

Mng

1st-degree (Conservative): dietary fibre, fluid, avoid straining, stool softeners
2nd-degree (Non-operative): rubber band ligation (Barron's) — band at base, ischaemic necrosis + fibrosis; do NOT place at/distal to dentate line (severe pain); sclerotherapy — phenol 5% in almond oil submucosa; infrared photocoagulation
3rd + 4th-degree (Operative): haemorrhoidectomy
Open (Milligan-Morgan) — V-incision, wound left open; closed (Park's / Ferguson) — submucosal, closed with running absorbable suture
Newer: Stapled (PPH) — circumferential 3–4 cm strip excised + circular stapler; Doppler-guided artery ligation
Post-op complications: pain, acute retention, reactionary haemorrhage; late — secondary haemorrhage, stricture, fissure, incontinence

Special

Definition: downward sliding of one or more anal cushions causing symptoms
Anal cushions = vessels + smooth muscle (Treitz's muscle) + elastic CT; between anorectal ring and dentate line; at 3, 7, 11 o'clock (left lateral, right posterior, right anterior)
Prolapse: loss of anchoring muscle fibres (longitudinal muscle of rectum → internal sphincter) due to ageing, constipation/straining, pregnancy
Internal — above dentate line, transitional + columnar epithelium
Complications: strangulation + thrombosis, ulceration, gangrene, portal pyaemia, fibrosis
Carcinoma pitfall — frequent miss (don't blame bleeding on piles)

physiology · background · low-yield

Other

Sclerotherapy alternative agents to phenol 5% in almond oil: sodium morrhuate, quinine urea

External / Thrombosed Haemorrhoids

C/P

External — below dentate line, squamous epithelium
Thrombosed: painful perianal mass with throbbing pain
Self-limiting (4–5 days); thrombus in capillaries

Inves

Clinical inspection — visible tender purple perianal mass = diagnostic
Palpation — hard, exquisitely tender (thrombosed) vs soft, tender (non-thrombosed)
Proctoscopy after acute pain settles — assess coexisting internal haemorrhoids

Mng

Haemorrhoidectomy for symptomatic external / large mixed
Thrombosed: clot removed via elliptical incision over the mass
Aims: relieve severe pain · prevent recurrence · manage residual skin tag

Special

Pain hallmark of thrombosed external (vs painless internal bleed)

Anal Fissure (Fissure-in-Ano)

C/P

Pain — predominant symptom: sharp, agonising, starts during defecation, lasts hours ("more pain, less bleeding")
Bleeding — slight streaks on stool / toilet paper
Constipation — fear of pain → cycle
Mild discharge
Posterior midline most common (vascular watershed posteriorly); anterior midline — common in females
Ectopic location → think Crohn's, hidradenitis suppurativa, STD
Classic chronic triad: sentinel pile · fissure (linear ulcer with exposed internal sphincter) · hypertrophied anal papilla internally

Inves

Gentle buttock traction → eversion of anus — visualises the fissure (avoids painful internal exams)
Avoid proctoscopy + DRE in acute fissure — pain + sphincter spasm make it useless and cruel; delay internal exam 4–6 weeks
Chronic fissure → DRE + proctoscopy OK (pain settled; look for sentinel pile, exposed internal sphincter, hypertrophied papilla)
Ectopic (lateral / multiple) fissure → colonoscopy + biopsy — rule out Crohn's, HIV, syphilis, TB, malignancy
EUA — if diagnosis uncertain or sphincter spasm prevents exam

Mng

Aim: break pain → spasm → ischaemia cycle
Symptomatic: warm sitz bath + bulking agents / softeners
GTN 0.2% ointment — NO donor, relaxes internal sphincter; SE = headache
Diltiazem 2% — CCB; SE = headache, flushing
Nifedipine 0.3% — CCB, vasodilatation
Botulinum injection — prevents ACh release → paresis → breaks spasm cycle
Arginine (NO donor); bethanecol (muscarinic agonist)
Surgical: Lateral Internal Sphincterotomy (LIS) — most common (closed: cataract blade in intersphincteric plane / open); anal advancement flap
Anal stretching (Lord) — no longer performed (incontinence risk)

Special

Ischaemic ulcer in midline anal canal
Cycle: trauma → tear + pain → internal sphincter spasm → ischaemia → chronic ulcer; ↑↑ resting anal pressure

Pruritus Ani

C/P

Common; perianal itch

Inves

Perianal inspection — skin disease, threadworm perianal tape test, discharge signs
Proctoscopy — exclude discharging pathology (haemorrhoids, fistula, malignancy)
Skin scrapings / swabs — fungal / bacterial infection
HbA1c — rule out diabetes as underlying driver

Mng

Treat cause if possible; symptomatic mainstay

Special

Causes: skin diseases, parasites (threadworm), anal discharge, allergies, diabetes

Solitary Rectal Ulcer Syndrome (SRUS)

C/P

Commonly young females
Chronic constipation, digital disimpaction, bleeding, mucus
Lesion on anterior wall of rectum, 4–12 cm from anal verge
Crater-like ulcer → polypoidal growth

Inves

Defecography (MR / dynamic) — the diagnostic study — identifies underlying internal intussusception / full-thickness prolapse (mechanism of SRUS)
Colonoscopy + biopsy — exclude Crohn's, malignancy, CMV mimicking SRUS
Anorectal manometry — sphincter dysfunction / paradoxical puborectalis contraction
Histology — fibromuscular obliteration of lamina propria + smooth muscle in-growth (SRUS-specific)

Mng

Conservative: high fibre, pelvic floor retraining, topical mesalamine
Surgical: rectopexy (if conservative fails)

Special

Commonly associated with internal intussusception

Septic Anorectal

2 entries

Anorectal Abscess

C/P

Perianal abscess: dull perianal discomfort, pruritus; erythematous, defined, fluctuant subcutaneous mass
Ischiorectal: large swelling over the buttock
Intersphincteric / supralevator: clinical exam alone cannot diagnose; needs imaging / EUA

Inves

Clinical — perianal and ischiorectal abscesses are clinical diagnoses (inspection + palpation)
Imaging only for deep/complex abscess (intersphincteric, supralevator, horseshoe) — clinical exam misses them
Anal endosonography (endoanal USS) — maps deep abscesses + concurrent fistula tracks
MRI pelvis — investigation of choice in complex / recurrent anorectal sepsis (defines all extensions)
Proctosigmoidoscopy — exclude primary drivers (IBD, malignancy breakdown, pelvic sepsis)
Pus culture + sensitivity — guides antibiotics; gut flora → suspect cryptoglandular / fistula; skin flora → superficial
FBC + CRP — sepsis severity + monitor response
Glucose / HbA1c — diabetic patients over-represented

Mng

Don't wait for fluctuation; antibiotics alone delay drainage → chronic infection
Drainage under anaesthesia; pus for culture and sensitivity
Perianal: cruciate-shaped incision, corners excised
Ischiorectal: cruciate incision at maximum swelling; break locules (finger then gauze); biopsy wall
Intersphincteric: transverse incision inside anal canal below dentate line
Submucous: open mucosa above swelling
Supralevator (least common): from intersphincteric → drain via rectal route; from ischiorectal → via ischiorectal fossa; abdominal pathology → transabdominal/rectal/ischiorectal
Horseshoe: ischiorectal — posterior drainage + counter-incision both fossae; intersphincteric — divide internal sphincter; supralevator — both ischiorectal fossae

Special

Causes: cryptoglandular infection (commonest), local anorectal pathology (Crohn's, malignancy), pelvic pathology (extraperitoneal abscess — appendicular/diverticular/Crohn's)
Cryptoglandular: anal gland ducts open at dentate line; mucus-secreting; reach intersphincteric space (natural tunnel)
Gram-negative organisms (colon content); contrasts with gram-positive in hidradenitis suppurativa
Primarily originates in intersphincteric plane then extends vertically (supralevator / perianal) or horizontally (ischiorectal / submucous)

Anal Fistula (Fistula-in-Ano)

C/P

Purulent discharge around anus / from canal
Pain cycle: gradually increasing intensity → discharge starts with immediate relief (repeats)
History of previous abscess operations
Solitary anterior close to margin → simple fistula
Multiple openings ("watering can") → TB, Crohn's, STD
Track palpable as cord of induration
Crucial to locate internal opening

Inves

Clinical — external opening + cord of induration on palpation
Proctoscopy — identify internal opening (missed internal opening = recurrence)
Goodsall's rule — predicts internal opening from external location
Fistulogram — not helpful (largely abandoned)
CT — not for fistula anatomy, useful for associated abscess
MRI pelvis — investigation of choice in complex fistula — maps tract, sphincter relation, secondary tracks + Parks classification
Endoanal USS — high resolution, can be used intra-op to define track ± peroxide injection
St James's University Hospital MRI Classification (Grades 0–5) — standardises MRI reporting
Biopsy of tract — if suspicion of Crohn's, TB, malignancy, actinomycosis

Mng

Asymptomatic — no treatment; symptomatic — surgery (spontaneous healing rare)
Techniques: fistulotomy, seton, fistulectomy, fibrin glue, mucosal advancement flap
Principles: drainage of intersphincteric primary focus; manage primary tract across EAS + secondary tracks
Fistulotomy: lay open; for intersphincteric + low transsphincteric; marsupialisation; CI if > 1/3 sphincter, anterior fistula in women, impaired continence
Draining seton: prevents closure; anterior fistula in female, elderly, multiple
Cutting seton: slowly cuts; scarring prevents muscle separation; high transsphincteric, complex
Fistulectomy: excision; useful when histology needed; larger wound
Mucosal advancement flap: extrasphincteric + suprasphincteric; cover internal opening with advanced mucosa from above
By Parks: intersphincteric → excision + fistulotomy; low trans → excision + fistulotomy; high trans → distal fistulotomy + seton; suprasphincteric → distal fistulotomy + seton; extrasphincteric → excision + rectal advancement flap

Special

Most arise from anal gland sepsis at dentate line
Low (below anorectal ring, < 1/3 sphincter) vs High (above anorectal ring, upper 2/3 EAS or more)
Parks Classification: 1. Intersphincteric (commonest) 2. Transsphincteric (2nd) 3. Suprasphincteric 4. Extrasphincteric (NOT cryptoglandular)
Goodsall's Rule: anterior to transverse anal line → straight radial; posterior → curved, opens midline posteriorly; exceptions: anterior openings > 3 cm from anal margin OR multiple openings → complex

Other

5 entries

Pilonidal Sinus

C/P

Most hirsute (dark hairs) + obese; males more affected
Typical: midline pits ~5 cm posterior to anus, overlying sacrum/coccyx
Secondary openings: granulation tissue + seropurulent discharge
Hairs protruding from pits

Inves

Clinical inspection — midline pits + protruding hairs in intergluteal cleft = diagnostic
PR palpation for mass/tenderness + proctoscopy — exclude communication with anal canal (rule out cryptoglandular fistula mimicking pilonidal)
MRI — only for complex/recurrent disease to map tract extent
Culture of discharge — rarely needed; identifies organisms if superimposed cellulitis

Mng

Conservative: remove all hairs, clean track, frequent washing, avoid long sitting
Surgical: Bascom's technique · Karydakis method · Z-plasty
By scenario: abscess — wide incision (away from midline), superficial excision of pits short of base; simple chronic midline — excision of pits + marsupialisation OR Bascom's (lateral drainage) OR Karydakis (elliptical excision + primary closure away from midline); complex — open / graft / flap (Z-plasty, advancement, myocutaneous for large)
Cleft obliteration for deep buttocks

Special

Latin pilus = hair + nidus = nest; "jeep disease" (1935–45 jeep riders)
Bascom's theory (acquired): folliculitis → abscess; gluteal-crease movement → suction → hair drawn into cavity
Karydakis's theory: loose hair shaft inserts into natal cleft → foreign-body reaction → infection
Other locations: finger web (Barber's), axilla, perineum, umbilicus, breast
Occupational: sheep shearers, dog beauticians, hairdressers

Meckel's Diverticulum

C/P

Painless bleeding
Typical: children with currant jelly stool (more often intussusception than direct Meckel's)

Inves

Technetium-99m pertechnetate scan (Meckel scan) — detects ectopic gastric mucosa (bleeding source)
Colonoscopy — usually normal (bleed source above the colon)
CT / MR enterography — assess wall thickening, associated intussusception

Mng

Diverticulectomy (surgical resection); prophylactic removal if incidentally found in children < 40 with rule-of-2 features

Special

Aetiology: incomplete obliteration of vitelline duct
Incidence 0.3–3.0%
Ectopic mucosa: 50% ileal; 50% gastric, pancreatic, colonic
Complications include intussusception
Cause of LGIB particularly in children and adolescents

Angiodysplasia

C/P

LGIB; more on the right side; degenerative

Inves

Colonoscopy — direct visualisation (small red fern-like vascular lesions in caecum / ascending colon); allows haemostasis (APC, clips)
Angiography — active bleed shows tuft of small vessels + early filling vein (diagnostic + therapeutic — embolisation)
Tagged RBC scan (99mTc-labelled) — detects slow / intermittent bleeds ≥ 0.1 mL/min
CT angiography — active bleeds ≥ 0.5 mL/min; localises + plans intervention
Capsule endoscopy — for small-bowel lesions when colonoscopy negative
FBC — chronic occult bleed → iron-deficiency anaemia

Mng

Embolisation; endoscopic therapy (per LGIB algorithm)

Special

Acquired mucosal/submucosal telangiectasia of degenerative origin
Dilated, tortuous vessels; walls lack smooth muscle
Pathogenesis: chronic intermittent low-grade colonic contraction → obstruction of mucosal venous drainage → AVM
~3% of LGIB

Radiation Proctitis

C/P

Bleeding; endoscopic telangiectasias

Inves

History — prior pelvic radiotherapy (prostate, cervical, rectal CA) points to diagnosis
Sigmoidoscopy / proctoscopy — friable rectal mucosa + telangiectasias = diagnostic
Biopsy — cautious (radiated tissue heals poorly, fistula risk); use only if malignancy suspected
FBC — chronic anaemia from ongoing blood loss

Mng

Conservative — sucralfate enema, mesalamine
Argon plasma coagulation (APC) — endoscopic ablation of telangiectasias (main definitive therapy)
Formalin application, cryotherapy — refractory cases
Surgery (rare) — refractory bleeding / fistula / stricture

Special

Cause of LGIB; associated with telangiectasias + bleeding

Lower GI Bleeding (Syndrome Approach)

C/P

Abnormal intraluminal blood loss distal to Ligament of Treitz
Massive LGIB criteria: ≥ 4 U blood / 24 h, instability + shock, Hb ≤ 6 g/dL, > 3 days, rebleed < 1 week
Guaiac positive — occult, low volume; Melena — tarry, UGI; Hematochezia — bright red, colonic (UGI if brisk)
Colour by location: bright red — rectum/anal canal; dark red — ascending/transverse/descending/sigmoid; black — small intestine or higher
Site proportions: colon 80–85% · small intestine 0.7–9% · UGI 10%
Adult aetiology: diverticular 60% · IBD/colitis 13% · benign anorectal 11% · neoplasia 9% · coagulopathy 4% · AVM 3%
Paediatric: intussusception (commonest), polyps (JP, PJ, FAP), IBD, Meckel's
DDx: diverticulosis (#1 large-volume painless), angioectasia, haemorrhoids, colitis, neoplasm, post-polypectomy, Dieulafoy's
Relation of blood to stool localises source: mixed with faeces → proximal to sigmoid (soft stool allows mixing); on surface of faeces → rectum / anal canal; on toilet paper → anal-skin bleed (fissure-in-ano, external haemorrhoids); separate from faeces (blood ± mucus then urge to defecate) → rectal cancer, diverticular disease, UC, polyp

Inves

FBC — anaemia baseline; initial Hct can under-read acute whole-blood loss
U&E — ↑ urea:creatinine ratio hints at UGIB (protein reabsorbed as blood transits gut)
LFTs — screen for chronic liver disease (varices, coagulopathy)
Coag profile / INR — guides FFP + reversal of anticoagulation
Group and cross-match — anticipate transfusion; lactate for tissue hypoxia
NG tube if severe haematochezia + unsure UGIB vs LGIB; positive (blood/coffee grounds) → UGIB; negative 15–20% of UGIB
ATLS Class I–IV shock classification — guides resuscitation intensity
Endoscopic: proctoscopy / sigmoidoscopy, colonoscopy, video capsule, double balloon, intraoperative
Radiological: AXR / CT (MDCT), angiography, radionuclide scintigraphy (Tc Sulfur Colloid or 99mTc-RBC)
Barium studies — NO role in LGIB
Colonoscopy — after stabilisation; diagnostic + haemostatic; needs bowel prep
Angiography — diagnostic + therapeutic; needs ≥ 0.5–1.0 mL/min bleed rate; for massive unstable; embolisation (microcoils, gelfoam); complications — bowel infarction, renal failure
Video capsule endoscopy — visualises whole GIT for obscure bleeding; no intervention capability
Double-balloon endoscopy — real-time whole GIT; treats obscure small-bowel bleeds
Intraoperative endoscopy — transfusion-dependent obscure overt bleeding with no source identified
Radionuclide scintigraphy — 0.1 mL/min sensitive; non-invasive; screen before angio; major false localisation
MDCT / CT angio — 0.5 mL/min; ER-quick; localises + identifies aetiology; guides embolisation; no therapy

Mng

Core: stabilise → determine source → stop active bleeding → treat underlying → prevent recurrence
Large-bore peripheral IVs; crystalloids first
Transfusion threshold: Hb ≤ 7 g/dL; 1 U PRBC ≈ ↑ Hb 1 g/dL (Hct 3%)
Coagulopathy: vit K (slow); FFP (fast) — 1 U FFP per 4 U PRBC
Acute LGIB algorithm: resuscitate + DRE + anoscopy + NG tube; intermittent → colonoscopy; moderate → 99mTc-RBC → angio/segmental; massive → mesenteric angiography (positive → embolisation; negative → intraop endoscopy or subtotal colectomy)

Special

Rectal carcinoma as LGIB source: 75% lower ampulla, 25% upper; 90% palpable on DRE; ulcerating commonest
Diverticulosis bleeding: more on the right; eroded artery in mouth of diverticulum

physiology · background · low-yield

Exam technique

Pain-based bleeding DDx: with pain — fissure-in-ano, fistula-in-ano, anal-canal carcinoma, ruptured perineal haematoma / anorectal abscess, endometriosis, injury; without pain — blood alone (polyp, villous adenoma, diverticular disease), blood after defecation (haemorrhoids), blood + mucus (UC, Crohn's, intussusception, ischaemic colon), blood streaked on stool (rectal carcinoma)

Diagnostic Criteria

4 entries

Truelove & Witts — Severe Attack of UC

Parameter	Threshold
Stool frequency	> 6 stools/day with blood +++
Fever	> 37.5 °C
Tachycardia	> 90 bpm
ESR	> 30 mm/hr
Anaemia	Hb < 10 g/dL
Albumin	< 30 g/L

Severity comparison

Severity	Bowel motions	Blood
Mild	< 4 / day	small
Moderate	4–6 / day	moderate
Severe	> 6 / day	+++

Massive LGIB Criteria

Transfusion ≥ 4 units blood / 24 h
Haemodynamic instability + shock
Hb drop to ≤ 6 g/dL
Bleeding > 3 days
Significant rebleed within 1 week

UC Definitive Diagnosis (Pathology)

Diffuse disease limited to colon
Rectal involvement with continuous proximal extension
No skip lesions
No deep fissural ulcers
No transmural sinus tracts
No transmural lymphoid aggregates or granulomas

CD Definitive Diagnosis (Pathology)

Terminal ileum inflammation
Fistulas / sinus tracts
Serositis
Fat wrapping
Transmural lymphoid aggregates
Non-necrotising granulomas
Skip lesions, linear ulcers, mucosal cobblestone

Anatomical / Severity Classifications

7 entries

Hinchey Classification — Acute Complicated Diverticulitis

Grade	Perforation Effect
I	Confined pericolic or mesenteric abscess
II	Pelvic or retroperitoneal abscess
III	Non-communicating perforated diverticulitis causing purulent peritonitis
IV	Communicating perforated diverticulitis causing faecal peritonitis

Application: I + II → IV antibiotics + CT/USG percutaneous drainage; III + IV → surgical exploration after resuscitation (Hartmann's / lap wash-out / resection + anastomosis / damage control)

Grades of Internal Haemorrhoids

Grade	Description	Presentation
I	Enlarged, do not prolapse	Bleeding only
II	Prolapse, spontaneously reduce	Prolapse during defecation, reduces spontaneously
III	Prolapse, require manual reduction	Prolapse, manual reduction
IV	Irreducible prolapse	Cannot be reduced

Application: I → conservative; II → rubber band / sclerotherapy / IR photocoagulation; III + IV → haemorrhoidectomy

Parks Classification — Anal Fistula

Based on relation to external sphincter:

Intersphincteric — most common
Transsphincteric — second commonest
Suprasphincteric
Extrasphincteric — NOT cryptoglandular (rectal/abdominal origin)

Type	External Opening	Track	Internal Opening
Intersphincteric	Close to anal orifice	Intersphincteric plane	At dentate line
Low transsphincteric	Lateral to intersphincteric	Intersphincteric → between subcutaneous + superficial EAS	At dentate line
High transsphincteric	Away from anal orifice	Between superficial + deep EAS	At dentate line
Suprasphincteric	Away from anal orifice	Between puborectalis + deep EAS	At dentate line
Extrasphincteric	Away from anal orifice	Into ischiorectal fossa, may pierce levator	Rectum or supralevator

St James's University Hospital MRI Classification — Anal Fistula

Grade	Description
0	Normal appearance
1	Simple linear intersphincteric fistula
2	Intersphincteric fistula with abscess or secondary track
3	Transsphincteric fistula
4	Transsphincteric fistula with abscess or secondary track in ischiorectal fossa
5	Supralevator and translevator disease

Goodsall's Rule — Anal Fistula Tract Direction

Anterior to transverse anal line → straight radial tract running directly into anal canal
Posterior to transverse anal line → curved tract, likely opens midline posteriorly

Exceptions (complex / non-simple)

Anterior openings > 3 cm from anal margin → likely complex or high tract
Multiple fistulous openings → branching / complex network

Montreal Classification — IBD

Ulcerative Colitis (extent)

E1 — Proctitis (limited to rectum)
E2 — Left-sided / distal (up to splenic flexure)
E3 — Extensive / pancolitis (proximal to splenic flexure)

Crohn's Disease

Age at diagnosis (A) — A1 ≤ 16 yr · A2 17–40 yr · A3 > 40 yr
Location (L) — L1 terminal ileum · L2 colon · L3 ileocolon · L4 isolated upper GI (modifier)
Behaviour (B) — B1 non-stricturing/non-penetrating · B2 stricturing · B3 penetrating · "p" suffix for perianal disease

Anorectal Disease Classification

Malignant: rectal cancer (upper · mid · low) · anal cancer (canal · margin)
Benign — Non-septic: haemorrhoids · fissure · rectal prolapse · obstructed defaecation · incontinence
Benign — Septic: abscess · fistula · pilonidal disease (partially related)

Toxic Megacolon — Definition + Features

Colon diameter > 5.5 cm (X-ray > 5 cm thin-walled gas-filled with mucosal islands)
Most severe / life-threatening complication of UC
Common in transverse colon
Also in bacterial / pseudomembranous / amoebic colitis
Precipitated by antidiarrhoeal drugs
Pathophys: inflammation extends from mucosa to submucosa + muscular → paralysis → dilatation → wall thinning
Mortality 15–25%
Mng: IV fluids, blood, antibiotics, steroids; plain X-ray; emergency subtotal colectomy + Brooke ileostomy with rectum preserved
Urgent surgery if not resolved within 48 h

TNM & Staging

8 entries

TNM Colorectal Cancer

Primary Tumour (T)

Tis — carcinoma in situ
T1 — invades submucosa
T2 — invades muscularis propria
T3 — invades till subserosa
T4 — invades visceral peritoneum ± nearby tissue/organ

Regional Lymph Nodes (N)

N0 — no LN metastasis
N1 — 1–3 pericolic / perirectal nodes
- N1a — 1 node
- N1b — 2–3 nodes
- N1c — tumour deposits in subserosa/mesentery, no positive nodes
N2 — ≥ 4 pericolic / perirectal nodes
- N2a — 4–6 nodes
- N2b — ≥ 7 nodes
N3 — any nodes along major blood vessels (high tie nodes)

Distant Metastasis (M)

M0 — no distant metastasis
M1 — distant metastasis
- M1a — confined to one organ (liver, lung, ovary, non-regional LN)
- M1b — > 1 organ / peritoneum

pT Staging Layers (inner → outer)

Mucosa → Submucosa → Muscularis propria → Subserosa → Peritoneal elastic lamina → Mesothelium

pT1 = submucosa
pT2 = muscularis propria
pT3 = subserosa
pT4 = perforates peritoneum / mesothelium

TNM Stage Grouping

Stage	Tumour	Treatment
Stage 0	Tis (HGD)	Polyp removal
Stage I	T1/T2 N0 M0	Surgical resection alone
Stage IIA	T3 N0 M0	Surgery
Stage IIB	T4a N0 M0	Surgery
Stage IIC	T4b N0 M0	Surgery
Stage IIIA	T1–2 N1/N1c, or T1 N2a	Surgery + adjuvant chemo
Stage IIIB	T3–4a N1/N1c, T2–3 N2a, T1–2 N2b	Surgery + adjuvant chemo
Stage IIIC	T4a N2a, T3–4a N2b, T4b N1–N2	Surgery + adjuvant chemo
Stage IVA	Any T, Any N, M1a	Chemo + biologics ± radiation (rectal)
Stage IVB	Any T, Any N, M1b	Chemo + biologics ± radiation (rectal)

Modified Dukes' Staging & 5-Yr Survival

Dukes	TNM	Development	Treatment	5-Yr Survival
A	T1 N0 M0	Confined to bowel wall	Surgery	95%
B1	T2 N0 M0	Into but not through MP	Surgery	~85%
B2	T3/T4 N0 M0	Through muscularis propria	Surgery	80%
C1	Any T, N1/N2, apical node negative	Pericolic nodes only	Surgery + chemo	~60%
C2	Any T, N1/N2, apical node positive	Apical/high-tie node positive	Surgery + chemo	~30%
D	M1	Has metastasis	Surgery + chemo (± radiation rectal)	5%

Rectal Cancer General Guidelines (Treatment by TNM)

T1 N0 → local excision (transanal / transsphincteric / transcoccygeal / TEM)
T1–2 N0 → transabdominal surgery (AR / LAR / ULAR by tumour height)
T3 N0 or any T + N1/N2 → pre-op chemoradiotherapy → surgery

Anterior Resection by Tumour Height (from anal verge)

Distance	Anastomosis Level	Procedure
~11–15 cm (Upper 3rd)	Above peritoneal reflection	Anterior Resection (AR)
~7–11 cm (Middle 3rd)	Below peritoneal reflection	Low AR (LAR)
< 7 cm (Lower 3rd)	Pelvic floor	Ultra-Low AR (ULAR)

Colonic Resection by Tumour Site

Tumour Location	Procedure	Vessels Ligated
Caecum / ascending	Right hemicolectomy	Ileocolic, right colic, right branch MCA
Hepatic flexure	Extended right hemicolectomy	Ileocolic, right colic, MCA
Splenic flexure	Extended left hemicolectomy	Left colic, left branch MCA
Descending colon	Left hemicolectomy	Left colic, sigmoid vessels
Sigmoid	Sigmoidectomy / Rectosigmoid resection	IMA after origin of left colic

Marginal safe zone = 2 cm

Key Rectal Cancer Resection Margins

Distal Resection Margin (DRM)
Circumferential Resection Margin (CRM) — mesorectal incisions + lateral pelvic wall dissections

Risk & Screening

13 entries

CRC Risk Assessment

Average risk: general population

High / increased risk

History of polyps on prior colonoscopy
History or family history of CRC
History or family history of familial polyposis syndromes
Inflammatory bowel disease
Received abdominal radiation for childhood malignancy

CRC Risk Factors

Age — uncommon < 40, rises 40–50
Familial: FAP (APC), Gardner, Turcot, AAPC; Lynch/HNPCC (MMR) — AD, 3–5% of all colonic adenoCa
Personal/family history of sporadic CRC or adenomatous polyps
Alcohol, obesity, smoking, IBD

Protective

Physical activity · fibre · folic acid · vit B6 / D · calcium + dairy · vegetables · garlic · fish · aspirin / NSAIDs

Adenoma Malignant Potential — Risk Factors

High-grade dysplasia (highest)
Villous architecture
Size (especially > 2 cm)
Multiple adenomas

74% of adenomas < 1 cm → 1% contain invasive cancer
35% of adenomas > 2 cm show malignant change

ACG Screening — Family History

Scenario	Recommendation
Single 1st-degree relative dx ≥ 60 yr with CRC or advanced adenoma	Colonoscopy every 10 yr from age 45
Single 1st-degree relative dx < 60 yr OR ≥ 2 1st-degree with CRC/adenoma at any age	Colonoscopy at age 40 or 10 yr before youngest relative's dx; repeat every 5 yr

Average-Risk Population Screening

Start with FOBT (positive → colonoscopy)
gFOBT uses guaiac (affected by food/drugs); requires eliminating red meat 3 days; vit C < 250 mg/day; avoid NSAIDs 7 days
FIT uses antibodies to human Hb; very good sensitivity; no dietary restrictions; annual (US), every 2 yr (UK), every 3 yr (Holland)
gFOBT may be less effective than FIT for detection of CRC and advanced adenoma
Starts age 50 or 60; every 1–2 yr

UK National Screening Programme (CRC)

Age 50–74 yr offered FIT
Positive → colonoscopy
Negative → repeat every 2 yr

CRC Screening Methods (Overview)

Stool-based: FIT · gFOBT · multi-target stool DNA test + FIT
Endoscopic: colonoscopy · sigmoidoscopy · sigmoidoscopy + FIT · colon video capsule
Radiologic: CT colonography
Blood tests: liquid biopsy (other markers, tumour markers)

Anal Cancer Risk Factors

HPV-16 — very high risk for anal SCC; types 18, 31, 33, 35 moderate
HIV — all exposure categories ↑ risk (receptive anal intercourse highest)
Tobacco — 5-fold ↑ risk
Benign anal pathology (fistula, fissure, haemorrhoid) does NOT increase risk

Risk Factors for Appendiceal Perforation

Extremes of age (paediatric + geriatric)
Immunosuppression
Diabetes mellitus
Previous abdominal surgery (restricted greater omentum spread)

28a

Alvarado Score (MANTRELS) — Acute Appendicitis

Finding	Points
Migratory RIF pain	1
Anorexia	1
Nausea / vomiting	1
Tenderness RIF	2
Rebound tenderness	1
Elevated temperature	1
Leukocytosis (WBC ≥ 10 × 10⁹/L)	2
Shift to left (neutrophilia)	1
Total	/10

Interpretation

< 3 — low possibility; discharge / observe
4–6 — equivocal; further imaging (CT / USS)
≥ 7 — high possibility; appendicectomy

28b

Pediatric Appendicitis Score (PAS)

Finding	Points
Migration of pain	1
Anorexia	1
Nausea / vomiting	1
RLQ tenderness	2
Cough / hopping / percussion tenderness RLQ	2
Increased temperature	1
Leukocytes > 10,000/μL	1
Polymorphonuclear neutrophilia > 75%	1
Total	/10

Interpretation

1–3 — negative for appendicitis
4–7 — further diagnostic testing
8–10 — positive

28c

Appendicitis Inflammatory Response (AIR) Score

Refines on Alvarado by including CRP concentration as well as WBC / neutrophilia
Better predictive performance than Alvarado in adults

Indications for Surgery in UC

Emergency

Acute severe colitis unresponsive to IV steroids
Toxic megacolon with impending perforation
Perforation
Massive haemorrhage
Total obstruction from stricture

Detailed (highest in 1st year)

Severe/fulminating disease failing medical therapy
Chronic disease with anaemia, frequent stools, urgency, tenesmus
Steroid-dependent disease
Risk of neoplastic change (severe dysplasia on colonoscopy)
Extra-intestinal manifestations
Rarely: severe haemorrhage or stenosis causing obstruction

Elective Surgical Options for UC

Total proctocolectomy + Brooke ileostomy
Total proctocolectomy + Kock's pouch
Total proctocolectomy + Ileal Pouch-Anal Anastomosis (IPAA) — gold-standard restorative
Total colectomy + ileorectal anastomosis (IRA) + rectal mucosectomy
Total colectomy + IRA (most favoured; preserves continence; needs proctoscopy follow-up)

Decision tree

IRA → failure to thrive · young · indeterminate colitis
Restorative pouch (IPAA) → good sphincter · young
Brooke ileostomy → old age · poor sphincter · patient choice

Ileostomy Types

End Ileostomy (Brooke's) — non-continent; after total proctocolectomy (UC, Hirschsprung's, occasionally CD, carcinomas); right iliac fossa through right rectus; spout ≥ 4 cm above skin; acts in 48 h; complications: prolapse, stenosis, haemorrhage, retraction, skin maceration
Loop Brooke's — temporary; critically ill, multiple ileal perforations, gangrene, distal fistulas, sepsis
Kock's — continent intra-abdominal pouch

31a

Ileal Pouch Configurations (after restorative proctocolectomy)

Pouch	Loops	Notes
J-pouch	2	Most popular; easiest with linear stapler; standard IPAA
S-pouch	3	Long efferent spout → evacuation difficulty
W-pouch	4	Larger reservoir → less bowel frequency

Pouch usually 10–20 cm; apex must reach below symphysis pubis for tension-free IPAA
Anastomosis: stapled (EEA — anvil in pouch + circular through rectal cuff) OR hand-sewn (after mucosectomy for distal neoplasia, poorer function)

31b

Pouchitis

Most common late complication of IPAA
Symptoms: ↑ stool frequency, urgency, bloody diarrhoea, perianal pain, fever
Treat: metronidazole / ciprofloxacin; refractory → biologics; recurrent → redo or conversion

31c

Kock Continent Ileostomy — Technique

30 cm ileal reservoir + intussuscepted spout valve below skin
Patient empties pouch with catheter through valve (continent — no bag needed)
Complications: early leak / fistula · late valve subluxation (slippage)
Rarely done now (largely superseded by IPAA)

31d

Subtotal Colectomy vs Proctocolectomy (UC — Emergency vs Elective)

Setting	Operation	Reason
Emergency (toxic megacolon, perforation, refractory acute severe colitis)	Subtotal colectomy + Brooke ileostomy + rectal stump preservation	Avoids pelvic dissection in hostile environment; preserves ileocolic arterial arcade for later pouch; large specimen for pathology; off all drugs
Elective	Total proctocolectomy + IPAA / Brooke / Kock / IRA ± mucosectomy	Definitive cure

Adverse Outcomes in Colorectal Resection

↑ Circumferential margin (CRM) involvement
Intra-operative specimen perforation

Comparison Tables

9 entries

UC vs Crohn's — Pathology

Feature	UC	Crohn's
Distribution	Diffuse & continuous	Segmental (sharp demarcation)
Rectum	Always affected (adults)	Occasional / spared
Severity	Increasing distally	Variable / patchy
Ileum	Backwash ileitis (≤ 25 cm of ileocaecal valve)	Often affected
Location (depth)	Superficial (mucosal)	Transmural
Fissures	Rare / superficial	Deep
Sinus / fistulas	Absent	Present
Mural thickening	Absent	Present
Mucosa	Pseudopolyps	Cobblestones
Granulomas	If crypts ruptured	Present, not crypt-related
Radiology	Lead-pipe colon	String sign

UC vs Crohn's — Clinical / Endoscopic

Feature	Crohn's	UC
Location	Any GI (mouth → anus)	Continuous from rectum; colon only
Thickness	Transmural	Mucosa + submucosa only
Colonoscopy	Skip lesions, cobblestoning, ulcerations, strictures	Pseudopolyps, continuous, loss of vascular pattern
Anaemia	+ (chronic disease)	++ (more bleeding)
Abdominal pain	++ (colicky, strictures)	+ (cramping, with defecation)
Rectal bleeding	+ (Crohn's colitis only)	++ (hallmark)
Colon cancer risk	++ (less than UC)	+++ (especially pancolitis)

UC vs Crohn's — Surgical

Feature	UC	Crohn's
Affected part	Mainly colon + rectum	Whole GI, commonly terminal ileum
Layer	Mucosa	Full thickness
Pattern	Continuous	Skip lesions
Stricture & fistulation	Less common	More common
Granulomas	Absent; +ve crypt abscesses	Common
Perianal disease	Less common	More common
Mimics appendicitis	No	Yes
Resection	Curative	Recurrence common

FAP vs HNPCC

Feature	FAP ("Gatekeeper")	HNPCC ("Caretaker")
Gene	APC (tumour suppressor)	MSH2 / MLH1 (DNA repair)
Pathway	Adenoma-carcinoma sequence	DNA mismatch repair → MSI
Polyps	Thousands of typical adenomas (tubular/villous)	Fewer polyps (often sessile)
Tumour	Typical adenocarcinoma	Mucinous adenocarcinoma + lymphocytic infiltrate
Inheritance	Autosomal dominant	Autosomal dominant

Hereditary CRC Syndromes

Syndrome	Inheritance	Gene	Key Feature
FAP	AD	APC (5q21)	100% adenocarcinoma by 40–45; mean polyp age 16
HNPCC / Lynch	AD	MMR (MSH2, MLH1, etc.)	Right colon, younger age, MSI-H
Juvenile polyposis	1/3 AD	—	Mucus-filled hamartomas; CRC in 20% before 40
Peutz-Jeghers	AD	STK11 (19p)	Hamartomas; ↑ small bowel + colonic adenoCa

Crohn's Endoscopy Findings

Discontinuous distribution of longitudinal ulcers
Cobblestone appearance
Small aphthous ulcers in longitudinal array
Strictures
Fat-wrapping, creeping fat, fistulae, sinus tracts
Dull granular serosa, thick rubbery wall

Crohn's Microscopic Features

Superficial OR deep ulceration with granulation tissue → deep submucosa or below
Transmural inflammation with lymphoid aggregates throughout bowel wall
Sarcoid-like, non-caseating, poorly formed granulomas in all tissue layers
Focal — intervening normal mucosa
Initially focal neutrophils in epithelium + lymphoid aggregates + plasmacytosis → cryptitis → crypt abscesses
Fibrosis, thickened bowel wall; variable Paneth cells + pyloric metaplasia; aphthous ulcers

UC Microscopic Features

Affects mucosa + submucosa (except fulminant — transmural)
Diffuse mononuclear inflammatory infiltrate in lamina propria
Crypt abscesses + cryptitis
Chronic: architectural glandular disarray, reactive epithelial changes (nuclear enlargement, mitotic activity, reduced mucin), glandular atrophy, hypertrophic muscularis mucosae, Paneth cell metaplasia, flask-shaped ulceration

Why Anti-TNF in IBD

Activated macrophages + T-lymphocytes produce excess TNF-α → recruits more immune cells (vicious cycle)
Anti-TNF (infliximab, adalimumab) blocks signal → breaks cycle
FDA-approved for both UC and CD

Other Frameworks

14 entries

Pilonidal Sinus — Theories of Development

Bascom's theory (acquired)

Folliculitis → leads to → abscess
Movement of gluteal crease creates suction
Hair enters abscess cavity via suction
Locations also: finger web (Barber's), axilla, perineum, umbilicus, breast
Occupational risk: sheep shearers, dog beauticians, hairdressers

Karydakis's theory

Shaft of loose hair inserts into depth of natal cleft
Foreign-body reaction → infection
Secondary opening via self-propelling ability of hair + spontaneous abscess rupture
Shows primary sinus (midline) + secondary sinus (lateral)

Pilonidal Sinus — Surgical Choice Framework

Pilonidal abscess: wide incision (away from midline); superficial excision of pits short of sinus base; ellipse one side of midline
Simple chronic midline sinus:
- Excision of pits + marsupialisation
- Excision of pits + lateral drainage = Bascom's technique
- Elliptical excision + primary closure away from midline = Karydakis's technique
Complex sinuses + fistulae:
- Open: staged I&D / excise primary pits + curettage of tracks
- Excision with graft
- Excision with flap: small → advancement or Z-plasty; large → myocutaneous

ATLS Shock Classification (used in LGIB)

Parameter	Class I	Class II	Class III	Class IV
Blood loss (mL)	< 750	750–1500	1500–2000	> 2000
Blood vol loss	< 15%	15–30%	30–40%	> 40%
Heart rate	< 100	> 100	> 120	> 140
SBP	No change	Orthostatic	Reduced	Very low, supine
Urine output (mL/hr)	> 30	20–30	10–20	< 10
Mental status	Alert	Anxious	Aggressive / drowsy	Confused / unconscious

Acute LGIB Algorithm

Aggressive volume resuscitation AND DRE + anoscopy (positive → treat anorectal bleeding) AND NG tube (positive → EGD for UGIB)
If DRE + NG negative — check bleeding status:
- Intermittent → colonoscopy
- Moderate → 99mTc-RBC scintigraphy (positive → mesenteric angio or segmental resection)
- Massive → mesenteric angiography (positive → embolisation; negative → intraoperative endoscopy or subtotal colectomy if source unknown)

IBD Step-up vs Step-down Therapy

Step-up (ACG): 5-ASAs / antibiotics → corticosteroids → immunomodulators → anti-TNF → surgery

Step-down: surgery / anti-TNF → immunomodulators → corticosteroids → 5-ASAs

Default: step-up unless very severe or specific patient (athletes, business people, etc.)

Anal Cancer — Nigro Regime

Chemoradiotherapy: 5-FU + mitomycin (or 5-FU + cisplatin) + RT
Good response → may excise local remnant
Obvious residual tumour → APR

Indications for APR (Rectal Cancer)

Tumour involves pelvic floor or external sphincter complex (cannot excise without incontinence)
Restorative procedures (LAR/ULAR) are oncologically unsound · technically impossible · produce unfavourable functional results
Poorly differentiated low rectal cancer
Tumour encroaches < 1 cm from dentate line

Indications for Pelvic Exenteration

APR + posterior vaginectomy — locally advanced low rectal involving vagina
Posterior pelvic exenteration — recurrent rectal invading vagina + cervix (rectum + uterus + cervix + vagina)
Total pelvic exenteration — locally advanced rectal involving prostate + bladder (rectum + bladder + prostate)

Genetic Mutations in Sporadic Adenoma-Carcinoma Sequence (Vogelgram)

Normal mucosa → APC/MCC loss → Hyperplasia → altered DNA methylation → Early Adenoma → K-ras mutation → Intermediate Adenoma → DCC loss → Late Adenoma → p53 loss → Carcinoma → other genetic alterations → Metastasis

APC, MCC, DCC, p53 = tumour suppressor genes
K-ras = oncogene

Inflammation-Dysplasia Sequence (IBD Pathway)

Chronic colitis → epithelial damage → ↑ cell turnover → mutations → dysplasia → adenocarcinoma
Differs from sporadic: Normal → Chronic Colitis → Dysplasia (often flat) → Carcinoma

CRC Tumour Markers

Serum: CEA (Carcinoembryonic Antigen)
Tissue: CDX-2

IBD Aetiology Triad

Genetic susceptibility (e.g. HLA-B27)
Host immune response
Environmental factors (gut microenvironment, nutrition)

Lining of Anal Canal

Above dentate line: rectal mucosa (plum coloured)
At dentate line: transition zone
Below dentate line: anal canal skin (white) → true anal skin (pigmented)
Lower part lined by sensitive squamous epithelium
Blood supply: superior, middle, inferior rectal vessels
Lymphatic drainage of lower half of anal canal → inguinal LNs
Internal sphincter: circular non-striated involuntary; autonomic
External sphincter: striated voluntary; pudendal nerve; fuses superiorly with puborectalis (anorectal angle for continence)

Diverticulitis — Clinical Subtypes

Feature	Acute simple	Acute complicated	Chronic atypical	Chronic typical recurring	Chronic typical persistent	Complex
Pain	LLQ acute persistent	LLQ + maybe generalised	LLQ intermittent low-grade	LLQ intermittent low-grade	LLQ persistent low-grade	LLQ + other symptoms
Systemic	Present	Present + tachycardia + hypotension if generalised peritonitis	No systemic	Present	Present	Present
GIT	No N/V	Vomiting	Antidating	Antidating, more constipation	Antidating, more constipation	More constipation, subacute obstruction
Signs	Local tenderness	Tenderness + mass; psoas/obturator; maybe peritonitis	Maybe phlegmon	Maybe phlegmon	Maybe phlegmon	Phlegmon or obstruction signs
Main inves	CT	CT	Colonoscopy + contrast; CT for DDx	Colonoscopy + contrast; CT for DDx	Colonoscopy + contrast; CT for DDx	CT