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YEAR 5: Histopathology - PK Edited > Histo: Lower GI Disease > Flashcards

Histo: Lower GI Disease Flashcards

1
Q

List some congenital disorders of the GI tract.

A
  • Atresia/stenosis
  • Duplication
  • Imperforate anus
  • Hirschsprung disease (MOST COMMON)
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2
Q

What is Hirschsprung disease?

A
  • Caused by the absence of ganglion cells of the submucosa & myenteric plexus results in failure of dilatation of the distal colon
  • Presents with: constipation, abdominal distension, vomiting and overflow diarrhoea
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3
Q

List some genetic associations of Hirschsprung disease.

A
  • Down syndrome
  • RET proto-oncogene Cr10
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4
Q

How is Hirschsprung disease diagnosed?

A
  • Clinical impression
  • Full thickness rectal biopsy
  • Shows hypertrophied nerve fibres but no ganglia
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5
Q

How is Hirschsprung disease treated?

A

Resection of affected (constricted) segment

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6
Q

What is a volvulus?

A

Twisting of a loop of bowel at the mesenteric base around a vascular pedicle

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7
Q

Which part of the intestines tend to be affected by volvulus in children and the elderly?

A

Children - small bowel

Elderly - sigmoid colon > caecal

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8
Q

Describe the pathophysiology of diverticular disease.

A

High intraluminal pressure (e.g. due to poor diet) leads to herniation of the bowel mucosa through weak points in the bowel wall (usually sites of entry of nutrient vessels)

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9
Q

List some causes of acute colitis.

A
  • Infection
  • Drugs/toxins
  • Chemotherapy
  • Radiotherapy
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10
Q

List the effects of infection on the colon.

A
  • Secretory diarrhoea (due to toxin)
  • Exudative diarrhoea (due to invasion and mucosal damage)
  • Severe tissue damage and perforation
  • Systemic illness
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11
Q

What can cause pseudomembranous colitis?

A

Exotoxins by C. difficile

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12
Q

How can C. difficile colitis be diagnosed?

A

Toxin stool assay

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13
Q

How is pseudomembranous colitis treated?

How is H.pylori infection treated?

A

C.diff (lower GI) - Metronidazole or vancomycin

H.pylori (upper GI) - triple therapy (PPI, amox, clarythro)

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14
Q

Where in the intestines does ischaemic colitis tend to occur?

A

Watershed zones (e.g. splenic flexure, rectosigmoid)

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15
Q

List some causes of ischaemic colitis.

A
  • Arterial occlusion (e.g. embolism)
  • Venous occlusion (e.g. thrombus)
  • Small vessel disease (e.g. diabetes mellitus)
  • Low flow states (e.g. CCF)
  • Obstruction (e.g. hernia, intussusception)
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16
Q

List some characteristic micro/macro histiological features of Crohn’s disease.

A
  • Can occur anywhere from mouth to anus
  • Skip lesions
  • Transmural inflammation
  • Non-caseating granulomas
  • Sinus/fistula formation
  • Mostly affects large bowel and terminal ileum
  • Thick rubber hose-like wall
  • Cobbelstone mucosa
  • Narrow lumen, strictures

rosethorn ulcers which can form fistulas

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17
Q

List some extra-intestinal features of inflammatory bowel disease.

A
  • Arthritis
  • Uveitis
  • Polyarthritis
  • Stomatitis/cheilitis
  • Skin lesions (pyoderma gangrenosum, erythema multiforme, erythema nodosum)
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18
Q

List some characteristic macro and micro histiological features of ulcerative colitis.

A
  • Involves rectum and colon in a continuous fashion
  • May see backwash ileitis (involvement of the terminal ileum)
  • Inflammation is confined to the mucosa
  • Bowel wall is normal thickness

no granulomas/fissures/fistulae/strictures

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19
Q

List some complications of ulcerative colitis.

A
  • Severe haemorrhage
  • Toxic megacolon
  • Adenocarcinoma (20-30x increased risk)
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20
Q

Which liver condition is associated with UC?

A

Primary sclerosing cholangitis

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21
Q

List some types of neoplastic epithelial lesions that occur in the GI tract.

A
  • Adenoma
  • Adenocarcinoma
  • Carcinoid tumour
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22
Q

List some types of stromal lesions that occur in the GI tract.

A
  • Stromal tumours
  • Lipoma
  • Sarcoma
  • Other: lymphoma
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23
Q

List three types of non-neoplastic polyp and explain their subtypes/associated conditions

A
  • Hyperplastic
  • hyperplastic polyps
  • sessile serated lesions (subtype)
  • Inflammatory (pseudopolyp)
  • IBD
  • Haemartomatous
  • juvenile polyposis (autosomal dominant)
  • Peutz-Jeghers (autosomal dominant) multiple polyps and periorbital pigmentation
24
Q

List three types of neoplastic polyp.

A
  • Tubular adenoma
  • Tubulovillous adenoma
  • Villous adenoma (most likely to turn to adenocarcinoma)
25
Q

What is an adenoma?

A
  • Excess epithelial proliferation with dysplasia but does NOT disrupt the BM
  • NOTE: there are three types - tubular, tubulovillous and villous
26
Q

List some features of an adenoma that are associated with increased risk of becoming a carcinoma.

A
  • Size of polyp (>4cm = 45%)
  • Proportion of villous component (i.e. villous more dangerous than tubulous)
  • Degree of dysplastic change within a polyp
27
Q

List some observations that have given rise to adenoma-carcinoma sequence theory.

A
  • Areas with a high prevalence of adenomas have a high prevalence of carcinoma
  • Adenomas tend to appear 10 years before a carcinoma
  • Risk of cancer is proportional to the number of adenomas
28
Q

List some familial syndromes that are characterised by intestinal polyps.

A
  • Peutz-Jegher’s syndrome
  • FAP (Gardner’s, Turcot)
  • HNPCC
29
Q

What is the inheritance pattern of FAP?

A

Autosomal dominant

30
Q

Which gene is mutated in FAP?

A

APC gene - chromosome 5q21

APC - adenomatous polyposis coli gene!

NOTE: almost 100% will develop cancer in 10-15 years

31
Q

What is Gardner’s syndrome?

A

Same features of FAP but with extra-intestinal manifestations: multiple osteomas of the skull and mandible, epidermoid cysts, desmoid tumours and supernumerary teeth

32
Q

What is the inheritance pattern of HNPCC?

A

Autosomal dominant

33
Q

Which gene mutation is associated with HNPCC?

A

1 of 4 DNA mismatch repair genes is mutated

34
Q

Where do carcinomas in HNPCC tend to occur?

A

Proximal to the splenic flexure

NOTE: poorly differentiated and mucinous cancers are more common. Polyps do not necessarily precede the cancer.

35
Q

Outline Dukes’ staging of colorectal cancer.

A

A - confined to bowel wall

B - through the bowel wall

C - lymph node metastases

D - distant metastases

36
Q

define fistula?

A

communication between two hollow viscera

37
Q

four layers of the bowel?

A

the mucosa (epithelium, lamina propria, and muscular mucosae)
the submucosa
the muscularis propria (inner circular muscle layer, intermuscular space, and outer longitudinal muscle layer)
and the serosa

38
Q

what causes ischemia in volvulus?

A

venous not arterial obstruction

39
Q

organisms that cause infection in acute colitis?
and specific drugs?

A

salmonella
CMV (particularly in IBD!)

checkpoint inhibitors

40
Q

What causes chronic colitis?

A

crohn’s and uc

tb

41
Q

what layer of the bowel dies first in ischaemic colitis?

A

mucosa first (as blood supply comes through the other way)

42
Q

why are watershed areas vulnerable to ischaemia?

A

splenic flexure - SMA transition to IMA

rectosigmoid - IMA transition to internal iliac

43
Q

conditions associated with HLA B27 and UC

A

Ank spond, JIA

44
Q

Marker of active disease (acute on chronic) in UC/crohns

A

Crypt abscesses

45
Q

2 cancers people with UC are at risk of?

A

colorectal adenocarcinoma (x20-30)
and cholangio (from PSC!)

46
Q

antibiotics that put you at risk of c.diff psuedomembranous colitis?

A

4Cs - ciprofloxacin, cephalosporins, co-amox and clinda

47
Q

what differentiates diverticula to pseudodiverticulum and which is meckel’s and acquired?

A

true diverticulum (meckel’s) - goes through mucosa, submucosa, muscularis and serosa

pseudo - diverticulosis - just goes through muscosa / submucosa

48
Q

rule of 2 for diverticulum

A

2% pop, 2ft proximal from ileocaecal valve, 2:1 M:F

49
Q

what is carcinoid syndrome

A

group of neuroendocrine tumours of enterochromaffin origin which produce 5ht (serotonin)

50
Q

symptoms of carcinoid

A

dirrhoea, flushing

51
Q

Ix and Mx of carcinoid

A

24hr urine 5-HIAA

Octreotide (somatostatin analogue)

52
Q

key difference between dysplastic mucosa and normal?

A

Dysplastic has a raised nuclear:cytoplasmic ratio

53
Q

Tell me the difference in histological appearance between the two types of hyperplastic polyps?

A

Hyperplastic polyps - sawtoothed and serrated

Sessile serated lesions = hyperplastic polyp + architectural abnormalities (crypts at base are horizontal not vertical!)

54
Q

Tell me about the 2 conditions related to hamartomatous polyps?

A

Juvenile polyposis (AD)
- <5yrs old

Peutz-Jeghers syndrome (PJS) (AD)
- periorbital pigmentation
- regular surveillance requried

55
Q

Marker for colorectal Ca?

A

CEA

56
Q

difference between grade and stage of CRC?

A

grade - how differentiated
stage - how far spread

TNM or duke

57
Q
A

YEAR 5: Histopathology - PK Edited (29 decks)

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