Histo path - lower GI Flashcards
Atresia/stenosis
Normal anus but small rectum and anal canal without stool, dilated proximal bowel
Common in Down’s - Hirschprung’s Disease
Absence of ganglionic cells in myenteric plexus
biopsy: hypertrophied nerve fibres w/out ganglia. RET pro-oncogene resection of affected area (frozen section)
Partial or complete doubling of a variable length of bowel, very cystic
Duplications
No anal canal, rectum ends above levator ani muscle
Imperforate anus
Causes severe obstruction
● Associated with anomalies in vertebrae and urinary tract, defective innervation of pelvic muscles, fistulas from rectum to bladder, urethra or vagina
Serosa-based fibrous bands of scar tissue that cause colon to connect and adhere to nearby structures, typically other viscera
Adhesions
Typically due to injury, such as prior surgical procedures, infection (i.e. peritonitis), or radiation damage
blind pouch leading off alimentary tract, lined by mucosa that communicates with gut lumen
Multiple, small, flasklike invaginations present along prominent taeniae coli, filled with mucin or stool but easily emptied, may bulge into serosa
Diverticula
cramping, discomfort, constipation, distention, sensation of inability to completely empty rectum; alternating constipation and diarrhea
No muscle layer around diverticula except for residual bundles of muscularis mucosa
Intramucosal ganglion cells are common
protrusion of a viscus through the wall in which it is normally contained
Herniation
Complete twisting of loop of bowel around its mesenteric base of attachment, causing obstruction and infarction
Usually involves cecum or sigmoid
Volvulus
Colon may be ischemic or gangrenous
24 year old man, with bloody diarrhoea with stringy mucus with pains/cramps that are relieved on defecation.
usually limited to colon, diffuse continuous disease from rectum proximally
Affects primarily mucosa and submucosa, except in most severe cases
Ulcerative Colitis
Affects primarily mucosa and submucosa (shallow ulcers), except in most severe cases
Bowel wall normal thickness (not thickened)
No granulomas, no fissures, no transmural inflammation (except in fulminant cases), no submucosal edema or inflammation, no neuronal hyperplasia
Complications: perforation, toxic megacolon, adenocarcinoma 20-30x risk, worse than Crohns
What are some extra-abdominal complications of UC?
Arthritis
Uveitis/Iritis (iritis affects sight, uveitis doesn't) Skin lesions Erythema nodosum Pyoderma gangrenosum Primary Sclerosing Cholangitis (5.5% in patients with pancolitis)
Abdominal pain, watery or bloody diarrhea
Sudden onset, early fever, often with numerous (greater than 6) bowel movements daily
Signs of systemic illness
Infective colitis
Essentially Gastroenteritis
Hx of Abx use (cipro, clari, co-am, cef)
Acute colitis with adherent inflammatory exudate (pseudomembrane) overlying sites of mucosal injury, usually after broad spectrum antibiotics
Yellow-white mucosal plaques, ‘mushroom cloud exudate’, neutrophil infiltration, ‘inflammatory slough’
Pseudomembraneous Colitis
Sudden onset abdominal pain and bleeding
Vascular, DM, bowel obstruction
Splenic flexure (upper left) (SMA and IMA at risk) Rectosigmoid (lower middle) (IMA and internal iliac artery)
Ischaemic Colitis
Hallmarks of ischemic bowel are necrotizing phlebitis and thrombi formation
Thrombophlebitis morphology differs in viable bowel (lymphocytic) and ischemic bowel (necrotizing lesions)
petechial hemorrhages, edematous and fragile mucosa, segmental erythema, scattered erosion, longitudinal ulcerations, sharply defined segment of involvement
Ulceration (may be discrete or serpiginous) with possible cobblestone pattern resembling Crohn’s disease or pseudopolyps resembling ulcerative colitis
Ischemic changes may be mucosal, mural (due to hypoperfusion) or transmural (major vessels involved)
Episodic mild diarrhea, fever, pain, weight loss
Sharply delimited and typically transmural involvement of bowel by an inflammatory process with mucosal damage, noncaseating, non-confluent, sarcoid-like granulomas (60%) in involved and non-involved bowel, fissuring (30%) deep into muscularis propria with formation of fistulas and strictures
Crohn’s Disease
Discontinuous, transmural granulomatous disease from oral cavity to anus, usually involves small intestine and colon
‘Cobblestone appearance’
5x Adenocarcinoma risk (UC is 30x)
Complications:
● Fibrosing strictures (common in terminal ileum), fistulas to loops of bowel, bladder, vagina, perianal skin
Small adenomatous lesion, usually < 1 cm and pedunculated but may be sessile. However, it is still well-differentiated and circumscribed, without invasion of the stalk, and is benign. Glands are rounded - ‘test tube appearance’
Darker color than surrounding mucosa
Asymptomatic, with a bit of occult bleeding
Tubular Adenoma
Form after ‘first hit’ APC gene mutation
90% of GI tubular adenomas occur in colon; also stomach and small intestine
50% are single
Mostly asymptomatic so need regular surveillance if over 3.4cm 45% malignant change .
Small adenomatous lesion, usually < 1 cm and pedunculated but may be sessile. However, it is still well-differentiated and circumscribed, without invasion of the stalk, and is benign. Round glandular look with villous projections.
Darker color than surrounding mucosa
Tubulovillous adenoma
Increased villous component increases risk of malignant change.
Dark colour shows dysplasia
Soft, usually large and sessile with papillary villous projections, large base and no stalk. Long fronds of papillary / villous projections arising directly from mucosal surface.
“Like fingers”
Villous adenoma
More cancerous as more villi. Hypokalaemia as they leak proteins and K
Small (< 5 mm), sessile, usually on top of mucosal folds, multiple and same color as surrounding mucosa
Hyperplastic polyps
90% of all polyps. Due to delayed shedding of epithelial cells
Inflamed regenerating mucosa surrounded by ulcerated tissue; also granulation tissue overlying epithelium. Smooth hyperemic or hypervascular appearance; variable surface erosion
Pseudopolyp
caused by IBD
Child <5, some rectal bleeding (maybe), lesion has red granular or glistening surface
Juvelile hamartomatous polyp
Up to 100 found in Juvenile Polyposis (AD) - may require colectomy to stop bleeding
Many polyps, monocuaneous hyperpigmentation, freckles around mouth, palms and soles
Peutz-Jeghers syndrome (AD - LKB1)
Have increased risk of intussusception and of malignancy regular
surveillance of GI tract, pelvis and gonads.
65 year old man presents with painless rectal bleeding, fatigue and weight loss. There is a palpable mass in his rectum. Histology shows invasion through muscularis propria, hyperchromatic cells and disordered architecture. Cells have ‘necrotic debris’.
Invasion
through Muscularis propria/externa.
Hyperchromatic, big nuclear: cytoplasmic ratio Increased mitotic activity Atypical mitotic forms Disordered architecture Invasion with reactive stromal changes
Colorectal adenocarcinoma
45% in rectum, 98% are adenocarcinoma
Right sided tumours: Fe def. anaemia, weight loss
Left sided tumours: change in bowel habit, crampy LLQ pain
Investigations: Proctoscopy, sigmoidoscopy, colonoscopy, barium enema, bloods e.g. FBC, CT/MRI Carcinoembryonic antigen (CEA) – monitor disease
Most commonly mutated genes include APC, TP53, and KRAS
Colorectal adenocarcinoma has invaded the muscularis propria but not externa, there is LN metastasis. What is the stage according to Duke’s criteria?
C1
1 = musc prop 2 = intramural B= no LN C = LN
A: confined to mucosa (5yr survival >95%)
B1: extending into muscularis propria (5yr survival 67%)
B2: transmural invasion, no lymph nodes involved (5yr survival 54%)
C1: extending to muscularis propria, with LN metastases (5yr survival 43%)
C2: transmural invasion, with lymph node metastases (5yr survival 23%)
D: distant metastases (5yr survival <10%)
12 year old, has 100 adenomatous polyps
Familial adenomatous polyposis (FAP)
− 70% AD mutation in APC gene (C5q1), 30% AR mutation in DNA mismatch
repair genes
− Present 10-15yrs - >100 adenomatous polyps required for diagnosis, usually
100-1000s seen. ALL will adenocarcinoma if left untreated by 30yrs therefore
most have prophylactic colectomy.
FAP like presentation but also has extra intestinal features such as osteoma’s and dental carries. Will have cutaneous skin involvement
Gardner’s Syndrome
Autosomal genetic condition that predisposis to colorectal, endometrial and ovarian cancers
Hereditary non-polyposis colorectal cancer/Lynch syndrome (HNPCC)
− AD mutations in DNA mismatch repair genes
− Carcinomas usually in right colon, few polyps but fast progression to malignancy
therefore present usually <50yrs
− Associated with endometrial, ovarian, small bowel, transitional cell and stomach
carcinoma.