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Y5 Pathology > HistoPath - Lower GI > Flashcards

HistoPath - Lower GI Flashcards

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
Q

What are the clinical features of ulcerative colitis

A

Bloody diarrhoea and mucous
Crampy abdominal pain that is relieved by defecation

26
Q

What are the complications of ulcerative colitis

A

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
Q

What is the management for ulcerative colitis

A

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
Q

What are the extra-GI manifestations of IBD

A

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
Q

What investigations should be done for IBD

A

Stool culture
ESR/CRP: raised
CXR
Crohn’s: endoscopy, barium contrast
UC: rectal biopsy, flexible sigmoidoscopy/colonoscopy

30
Q

What are the tumours of the colon and rectum

A

Non-neoplastic polyps
Neoplastic epithelial lesions
Adenoma
Adenocarcinoma
Carcinoid tumour (NETs)
Mesenchymal lesions
Stromal tumours
Lipoma
Sarcoma
Lymphoma

31
Q

Describe non-neoplastic polyps

A

Hyperplastic-scarring type of response
Proliferation of folds of mucosa - “fjords of Norway”
Completely benign, will not lead to cancer

32
Q

What are the types of non-neoplastic polyps

A

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
Q

Describe neoplastic polyps and what are the types

A

These increase the risk of getting carcinoma (adenoma-carcinoma sequence)
Three types:
Tubular adenoma
Tubulovillous adenoma
Villous adenoma

34
Q

What are adenomas and what is their prevalence

A

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
Q

What is the histology of tubular and villous adenomas

A

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
Q

What is the adenoma → carcinoma sequence

A
  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
Q

What are the risk factors for polyps transforming into cancer

A

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
Q

Which syndromes affecting the lower GIS are familial

A

Peutz Jeghers
Familial Adenomatous Polyposis: Gardner’s, Turcot
Hereditary non-polyposis colon cancer (HNPCC)

39
Q

What is Peutz-Jeghers

A

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
Q

What is juvenile polyposis

A

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
Q

What is familial adenomatous polyposis (FAP)

A

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
Q

What is Gardner’s syndrome

A

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
Q

What is Turcot’s syndrome

A

Same as Gardner’s syndrome + brain tumour

44
Q

Describe Hereditary Non-Polyposis Colorectal Cancer (HNPCC)

A

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
Q

What is the epidemiology of colorectal cancer

A

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
Q

What are the risk factors for colorectal cancer

A

Dietary - low fibre, high fat diet
Lack of exercise
Obesity
Familial syndromes
Chronic IBD

(Note: NSAIDs protective)

47
Q

What are the clinical features of colorectal cancer

A

Right sided tumours: Fe def. anaemia, weight loss
Left sided tumours: Change in bowel habit, crampy LLQ pain

48
Q

What investigations should be done for colorectal cancer

A

FBC, CEA (monitor and response)
CT/MRI
Proctoscopy, sigmoidoscopy, colonoscopy
Barium enema

49
Q

How is colorectal cancer staged

A

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
Q

What is the management for colorectal cancer

A

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
Q

What is carcinoid syndrome and how is it investigated/managed

A

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
Q

What are the symptoms of carcinoid syndrome and carcinoid crisis

A

Syndrome: bronchoconstriction, flushing, diarrhoea
Crisis: life-threatening vasodilation, hypotension, tachycardia, bronchoconstriction, hyperglycaemia

Y5 Pathology (71 decks)

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