Lower GI disease Flashcards
Examples of congenital disorders affecting the large bowel
- atresia/stenosis
- hirschsprung’s
- duplication
- imperforate anus
most common hirschsprung’s
What is the congenital abnormality in hirschsprung’s disease?
absence of ganglionic cells in the myenteric plexus
causes failure of dilatation of the distal colon
Which patient group does hirshcsprung’s affect?
80% affects male babies
Presentation of hirschsprung’s disease
constipation with overflow diarrhoea
abdominal distension
vomiting
Associations of hirschsprung’s disease
- down’s syndrome
- RET proto-oncogene
Diagnosis of hirschsprung’s disease
full thickness biopsy
hypertrophy of nerve cells but absence of ganglion cells
Treatment of hirschsprung’s disease
Resection of affected (constricted) segment
Ano-rectal pull through
Which parts of the bowel are affected by volvulus? (small intestine vs large intestine)
Children: small intestine: Midgut volvulus
Elderly and pregnant women: sigmoid colon (sigmoid > caecal)
*think children are younger; more proximal part is affected
- NOTE: psychiatric patients also get this (?medication related)
3 types of volvulus
- caecal
- midgut
- sigmoid
AXR findings of sigmoid vs caecal volvulus
sigmoid: coffee bean sign
caecal: embryo sign
Associated factors for diverticular disease
Age (>60 years)
Chronic Constipation
Diet:
Low Fibre
Rich in fatty food or red meat
Difference between pseudodiverticulum and true diverticulum
pseudodiverticulum: caused by high intraluminal pressure eg due to straining –> causes outpouchings. does not involve all layers of the bowel wall
true diverticulum: caused by traction/pulling forces –> involves all layers of the bowel wall
Which side of the colon is most affected by diverticular disease?
90% are left sided
**maybe because constipation commonly causes faecal impaction on the left side??
Diagnosis of diverticular disease
CT with contrast
colonoscopy is contraindicated in acute diverticulitis due to risk of perforation
Which drugs can cause c diff colitis?
4Cs:
cephalosporins
ciprofloxacin
clindamycin
co-amoxiclav
can also be precipitated by antacids/PPIs, cytotoxic drugs and non-surgical procedures eg NG tubes
Histological appearance of c difficile colitis
pseudomembraneous colitis
looks like volcano exploding - bits on the surface are necrotic pseudomembranous regions full of pus and inflammatory cells
CRP in C difficile colitis
CRP may be low
even though WCC is high
C difficile treatment
- moderate severity: metronidazole –> vancomycin if no response
- severe: vancomycin first, can add on metronidazole
Which ribotype of c difficile is associated with increased toxicity?
Ribotype 027
caused an outbreak in June 2005
as it produces more toxins
Which genetic mutation can predispose to crohn’s?
NOD2 mutation
present in 30% of people with crohn’s
**NOD2 is expressed in myeloid cells
Characteristic features of crohn’s disease
Crow’s NESTS
N: no blood or mucous
E: entire GI tract can be affected (most common in terminal ileum and large bowel- caecum)
S: skip lesions
T: transmural inflammation
S: smoking is a risk factor
Histological features:
- non-caseating granulomas
- rose thorn ulcers
Management of Crohn’s disease
Inducing remission:
1st line: corticosteroids (PO–>IV)
2nd line: immunosuppressants
Maintaining remission:
immunosuppressants
Which is more common: crohn’s or UC?
UC is slightly more common
Key features of ulcerative colilitis
- Extends proximally from rectum
- Continuous inflammation
- Inflammation confined to the mucosa → bowel wall is normal thickness
- Usually does not affect the small intestine unless severe pancolitis causes backwash ileitis
- Extensive superficial broad ulcers
- No granulomas/ fissures/ fistulae/ strictures
- Islands of regenerating mucosa bulge into lumen → pseudopolyps
- can fuse to form mucosal bridges
- May see appendiceal involvement
Extraintestinal manifestations of ulcerative colitis
Arthritis
Myositis
Uveitis/ iritis
Erythema nodosum
pyoderma gangrenosum
Primary sclerosing cholangitis
**pretty much the same as crohn’s disease except PSC
Management of ulcerative colitis
Inducing remission:
1) Mild:
- prednisolone
- mesalazine (5-ASA)
2) Moderate:
- prednisolone
- 5-ASA mesalazine
- steroid enema bd
3) Severe:
- Admit
- NBM
- IV fluids
- IV hydrocortisone
- rectal steroids
- Maintain remission:
- 1st line: 5-ASA - mesalazine
- 2nd line: azathioprine
Maintain remission
- 5-ASA
- immunosuppressants
What is the most common vascular disorder of the GI tract?
Ischaemic colitis/ifarction
**can be acute or chronic
Where do diverticulae usually form?
At points where nutrient arteries penetrate the GI tract
–> taenia coli
Which areas of the bowel does ischaemic colitis affect?
Watershed areas - receive dual blood supply.
a) rectosigmoid
b) splenic flexure
Small bowel vs large bowel ischaemia
Histological findings of ischaemic colitis
- thickening of bowel wall
- necrotic ulceration confined to mucosal layers
Types of non-neoplastic polyps in. the bowel
- hyperplastic
- most common
- rectosigmoid
- rare- malignant potential - hamartomous
- isolated or as part of syndromes eg peutz-jeghers, juvenile - inflammatory
- associated with inflammatory bowel disease
- aka pseudopolyps (ulcerative colitis)
Definition of adenoma
Excess epithelial proliferation with dysplasia
3 types of adenoma
- tubular
- lowest malignant potential - villous
- highest malignant potential
(V for violent)
- tubulovillous
- intermediate malignant potential
Description of villous adenoma
sessile cauliflower-like mass covered by dysplastic columnar epithelium in the rectum
Risk factors for adenoma progressing to cancer
- size
- villous content
- degree of dysplastic changes
Adenoma carcinoma sequence
What electrolyte abnormality may be seen in colorectal adenoma?
hypokalaemia
**because the adenoma leaks potassium
**also causes hypoproteinaemia
Which area of the bowel is most commonly affected by adenocarcinoma?
rectosigmoid
Left vs right colon cancer presentation
left: obstruction
right: anaemia
What staging is used for colorectal adenocarcinoma?
Duke’s staging
A = confined to bowel wall
B = through bowel wall
C = lymph node metastases
D = distant metastases
Name 3 familial syndromes characterised by intestinal polyps
- peutz jeghers
- HNPCC
- FAP
Which type of polyps in peutz jegher’s?
Hamartomous polyps
Which genes are mutated in HNPCC? Mode of inheritance?
MSH2 and MLH1
Autosomal dominant
rare
Where do you get tumours in HNPCC? Type?
Proximal to splenic flexure
Tend to be mucinous adenocarcinomas
Which other type of tumour does HNPCC predispose to?
Ovarian tumours
–>endometroid and mucinous (think mucinous - tend to form mucinous tumours in the GIT also)
(early onset- more bc of HNPCC than BRCA)
Mode of inheritance of FAP
Which gene is affected?
autosomal dominant
Mutation in APC tumour suppressor gene on chromosome 5q21
Two forms of FAP
- Gardener’s
* bony and soft tissue tumours - Turcots
- gliomas
- medulloblastoma
Between crohn’s and UC which one has higher monozygotic twin concordancy?
Crohns: 50%
Which cells does carcinoid syndrome originate from?
Enterochromaffin cells
produce 5-HT (serotonin)
Where do carcinoid tumours arise from?
Commonly in bowel
but also lung, ovaries and testes
Carcinoid syndrome vs carcinoid crisis
Ivx and treatment of carcinoid tumours
Investigation: 24hr urine 5-HIAA (main metabolite of serotonin) Treatment: Octreotide (somatostatin analogue
Juvenile vs peut-jeghers syndrome
2nd commonest cause of cancer deaths in UK
colorectal cancer
What drug is protective against colorectal cancer?
NSAIDS - as a lot of tumours express COX-2
Tumour marker of colorectal carcinoma
Carcinoembryonic antigen
What is gardner’s syndrome?
– like FAP with extra intestinal features eg: osteoma’s, dental caries
complciations of diverticular disease
- Pain
- Diverticulitis
- Perforation >>> peritonitis
- Fistula (bowel, bladder, vagina)
- Obstruction
