HistoPath - Lower GI Flashcards

(52 cards)

1
Q

Give examples of congenital disorders of the lower GI tract

A

Atresia
Stenosis
Duplication
Imperforate anus

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2
Q

What is Hirschsprung’s disease (pathophysiology, associations)

A

Most common congenital abnormality of the lower GI tract
Absence of ganglions in the myenteric plexus
Starts in the rectum → distal colon fails to dilate
80% in male babies
Associated with Down’s syndrome and RET proto-oncogene Cr10

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3
Q

How does Hirschsprung’s disease present and what would investigations show

A

Failure to pass meconium
Constipation, overflow diarrhoea
Non-bilious vomiting
Abdominal distention

Full thickness biopsy of affected segment: Hypertrophied nerve fibres but NO ganglia

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4
Q

What is the management for Hirschprung’s disease

A

Resection of affected (constricted) segment (this is a frozen section) and pull through the normal part (known as a anorectal pull through)

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5
Q

What can mechanical obstruction of the bowel be caused by

A

Constipation
Diverticular disease
Adhesions
Herniation
External mass e.g. foetus, aneurysm, foreign body
Volvulus (infants → small bowel, elderly → sigmoid > caecal)
Intussusception

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6
Q

What is volvulus and what is the difference in the usual site of volvulus between children and adults

A

Complete twisting of a loop of bowel at the mesenteric base, around a vascular pedicle
This can lead to intestinal obstruction and infarction, with the tissue becoming necrotic
In CHILDREN- usually affects the small bowel
In the ELDERLY- usually affects the sigmoid colon

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7
Q

What is diverticular disease and where does it occur

A

Outpouchings of the bowel
High intraluminal pressure → herniation of the bowel mucosa through weak points (usually at points of entry of nutrient vessels) → mucosa pushes out → ballooning
90% occur in ht left colon (mostly sigmoid)

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8
Q

What are the risk factors for diverticular disease

A

Western cultures
Low-fibre diet

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9
Q

What can be seen on imaging and histology for diverticular disease

A

Contrast AXR: can see the outpouchings
Endoscopy: can see the extra lumens where there are outpouchings

Histology: outpouchings visualised

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10
Q

What are the complications of diverticular disease

A

Adhesion → erosion → fistula formation (bowel, bladder, vagina)
Perforation → peritonitis
Pain
Diverticulitis
Obstruction

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11
Q

What are the inflammatory disorders of the bowel

A

Acute Colitis
- Infection: CMV (most common),Salmonella, entamoeba histolytica, candida
- Drug/ toxin (especially antibiotics)
- Chemotherapy
- Radiotherapy

Chronic Colitis
- Crohn’s disease
- Ulcerative colitis
- TB
- Basically anything that inflames the bowel

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12
Q

What is pseudomembranous colitis and what is the treatment

A

Antibiotic-associated colitis
Acute colitis with pseudomembrane formation - no epithelium, membrane is made up of inflammatory cells
Caused by protein exotoxins of C. difficile

Tx: metronidazole +/- vancomycin

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13
Q

What is seen on investigation for pseudomembranous colitis

A

“volcanoes exploding out of the surface”
Necrotic pseudomembranous regions full of pus and inflammatory cells

Toxin stool assay → C. difficile toxin detected

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14
Q

Describe ischaemic disease of the bowel and how is it treated

A

Ischaemic colitis - acute or chronic
Narrowing of the mesenteric arteries → gut ischaemia
Occurs in watershed zones
May be mucosal, mural, or transmural → perforation, infarction and bowel disintegrating

Tx: resection of necrotic bowel

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15
Q

What are the watershed zones

A

Splenic flexures (SMA and IMA)
Rectosigmoid (IMA and internal iliac artery)

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16
Q

What are the causes of ischaemic colitis

A

Arterial (atheroma, thrombosis) or venous (thrombosis), occlusion, small vessel disease (DM, cholesterol), low flow states (e.g. due to hypovolaemic shock), obstruction (hernia, volvulus, adhesion)
RF: smoking

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17
Q

What is the epidemiology of Crohn’s disease

A

More common in Western populations
Peak onset is in early 20s
More common in White people (2-5 x more)
Higher incidence in Jewish population
RF: smoking

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18
Q

What is the pathophysiology of Crohn’s disease

A

Can affect the whole GI tract from mouth to anus - most commonly terminal ileum and large bowel (caecum)
Transmural inflammation
Skip lesions: normal and inflamed bowel interspersed → cobblestone mucosa
Fat wrapping
Thick, “rubberhose”-like wall
Non-caseating granulomas

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19
Q

What are the clinical features of Crohn’s disease

A

Intermittent diarrhoea
Abdominal pain
Fever
Anaemia
Weight loss
Extra-intestinal manifestations

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20
Q

What are the complications of Crohn’s disease

A

Perforation
Strictures
Fissures
Sinus/fistula formation
Linear ulcer
Abscesses

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21
Q

What is the management for Crohn’s disease

A

Mild attack: Prednisolone
Severe attacks: IV hydrocortisone, metronidazole
Additional therapies: Azathioprine, methotrexate, infliximab

22
Q

What is the epidemiology of ulcerative colitis

A

Slightly more common than Crohn’s
White > non-whites
Peak age is 20-25 yrs
Smoking improves symptoms/protective

23
Q

What is the MZ twin concordance of inflammatory bowel disease

A

Crohn’s: 50%
UC: 15%

24
Q

What is the pathophysiology of ulcerative colitis

A

Starts in the rectum and extends proximally
Backwash ileitis → small bowel involvement
Continuous mucosal involvement
Inflammation is superficial and confined to the mucosa
No granulomas/ fissures/ fistulae/strictures
Pseudopolyps: islands of regenerating mucosal bulging into the lumen → fuses to form mucosal bridges

25
What are the clinical features of ulcerative colitis
Bloody diarrhoea and mucous Crampy abdominal pain that is relieved by defecation
26
What are the complications of ulcerative colitis
Severe haemorrhage Toxic megacolon →perforation (damage to muscularis propria w/disruption of neuromuscular function → colonic dilatation) 30% require colectomy within 3yrs for uncontrollable symptoms Adenocarcinoma (20-30x risk)
27
What is the management for ulcerative colitis
Mild: Prednisolone + mesalazine (5 ASA) Moderate: Prednisolone + 5-ASA + steroid enema bd Severe: Admit, NBM IV fluids and IV hydrocortisone, rectal steroids For remission: All 5-ASA (1st line), azathioprine (2nd line)
28
What are the extra-GI manifestations of IBD
Malabsorption & Fe def. Anaemia → angular stomatitis Eyes: Anterior uveitis (iris & ciliary body), conjunctivitis Skin: Erythema nodosum (tender bruise-like swellings on shins), pyoderma gangrenosum, erythema multiforme, Digitial clubbing Joints: Migratory asymmetrical polyarthropathy of large joints (15%), sacroiliitis, myositis, ankylosing spondylitis Liver: Pericholangitis, primary sclerosing cholangitis (UC>CD), steatosis
29
What investigations should be done for IBD
Stool culture ESR/CRP: raised CXR Crohn's: endoscopy, barium contrast UC: rectal biopsy, flexible sigmoidoscopy/colonoscopy
30
What are the tumours of the colon and rectum
Non-neoplastic polyps Neoplastic epithelial lesions Adenoma Adenocarcinoma Carcinoid tumour (NETs) Mesenchymal lesions Stromal tumours Lipoma Sarcoma Lymphoma
31
Describe non-neoplastic polyps
Hyperplastic-scarring type of response Proliferation of folds of mucosa - "fjords of Norway" Completely benign, will not lead to cancer
32
What are the types of non-neoplastic polyps
Inflammatory (pseudopolyps)- where you have inflammation and regeneration of the mucosa e.g. IBD Hamartomatous (juvenile, Peutz-Jeghers) Hyperplastic: 50-60yo from shedding of epithelium Sessile Serrated lesions - has architectural abnormalities, may show dysplasia → cancer Stalk: pedunculated polyp
33
Describe neoplastic polyps and what are the types
These increase the risk of getting carcinoma (adenoma-carcinoma sequence) Three types: Tubular adenoma Tubulovillous adenoma Villous adenoma
34
What are adenomas and what is their prevalence
Excessive epithelial proliferations with dysplasia It has lost control but it has NOT invaded yet (potential to become cancerous) 40-50% prevalence > 60 years
35
What is the histology of tubular and villous adenomas
Tubular: stalk seen | dark colour (chromatin), tightly packed, irregular dysplasia | no BM invasion Villous: dysplastic | pokes out | pink = good, purple = bad → hypoproteinaemic hypokalaemia (leaks large amounts of protein and K+)
36
What is the adenoma → carcinoma sequence
1. Normal colon → first hit mutation in first copy of APC gene (FAP have this mutation) → at risk mucosa 2. Second hit mutation to the remaining APC gene → adenoma 3. Activation of KRAS, LOF mutations of p53 → carcinoma
37
What are the risk factors for polyps transforming into cancer
Size of polyp (> 4cm= 45% invasive risk) - most important Proportion of villous component (more villousy) Degree of dysplastic change within a polyp (increased dysplasia)
38
Which syndromes affecting the lower GIS are familial
Peutz Jeghers Familial Adenomatous Polyposis: Gardner’s, Turcot Hereditary non-polyposis colon cancer (HNPCC)
39
What is Peutz-Jeghers
Hamartomous polyp Autosomal dominant - LKB1 Multiple polyps, mucocutaneous hyperpigmentation, freckles around mouth, palms and soles. Increased risk of intussusception and of malignancy → regular surveillance of GI tract, pelvis and gonads.
40
What is juvenile polyposis
Focal malformations of mucosa and lamina propria Mostly <5yo Mostly in the rectum → bleeding Autosomal dominant juvenile polyposis → up to 100 polyps → may require colectomy to stop haemorrhage
41
What is familial adenomatous polyposis (FAP)
Autosomal dominant: APC tumour suppressor gene on chromosome 5q21 (FAP) (some in DNA mismatch repair genes) Average age of onset 25yo Large numbers of adenomatous polyps (mostly colorectal): min. 100, average 1000 100% will develop cancer within 10-15 years (each polyp = 1% chance) → risk of duodenal cancer
42
What is Gardner's syndrome
Same clinical, pathological and aetiological features of FAP with a high cancer risk Distinctive extraintestinal manifestations: - Multiple osteomas of the skull and mandible - Epidermoid cysts - Desmoid cysts - Dental caries, unerupted supernumerary teeth - Post-surgical mesenteric fibromatoses
43
What is Turcot's syndrome
Same as Gardner's syndrome + brain tumour
44
Describe Hereditary Non-Polyposis Colorectal Cancer (HNPCC)
Lynch syndrome Autosomal dominant condition: numerous DNA replication errors (not directly oncogenic) Accounts for 3-5% of colorectal cancers → onset at an early age Poorly differentiated and mucinous carcinomas, usually proximal to the splenic flexure Multiple synchronous cancers, including extra-colonic (e.g. endometrium, prostate, breast, stomach)
45
What is the epidemiology of colorectal cancer
2nd commonest cause of cancer deaths in the UK Age 60-79 yrs If found <50yrs: consider familial syndrome Commoner in western population 98% are adenocarcinoma, 45% in rectum
46
What are the risk factors for colorectal cancer
Dietary - low fibre, high fat diet Lack of exercise Obesity Familial syndromes Chronic IBD (Note: NSAIDs protective)
47
What are the clinical features of colorectal cancer
Right sided tumours: Fe def. anaemia, weight loss Left sided tumours: Change in bowel habit, crampy LLQ pain
48
What investigations should be done for colorectal cancer
FBC, CEA (monitor and response) CT/MRI Proctoscopy, sigmoidoscopy, colonoscopy Barium enema
49
How is colorectal cancer staged
TNM used presently Duke's used before: A= confined to bowel wall (5 year survival >95%) B= through wall of bowel - 1: extends to muscularis propria - 2: transmural invasion C= lymph node metastases - 1: extends to muscularis propria - 2: transmural invasion D= distant metastases (5 year survival <10%)
50
What is the management for colorectal cancer
Rectal/low sigmoid: - <1-2cm above anal sphincter → abdomino-perineal resection - >1-2cm above anal sphincter → anterior resection Sigmoid → sigmoid colectomy Descending colon and distal transverse → left hemicolectomy Caecum, ascending colon, proximal transverse → right hemicolectomy Transverse colon → extended R hemicolectomy + post-op radiotherapy, chemotherapy in palliation (5-FU)
51
What is carcinoid syndrome and how is it investigated/managed
Group of slow-growing tumours of enterochromaffin cell origin, produces 5-HT (serotonin) Found in the bowel, lung, ovaries, testes Investigation: 24hr urine 5-HIAA Tx: ocreotide (somatostatin analogue)
52
What are the symptoms of carcinoid syndrome and carcinoid crisis
Syndrome: bronchoconstriction, flushing, diarrhoea Crisis: life-threatening vasodilation, hypotension, tachycardia, bronchoconstriction, hyperglycaemia