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GIT Patho Flashcards

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1
Q

What is a polyp?

A

Fleshy protuberant growth on an epithelial surface

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2
Q

What are the 2 growth patterns of polyps?

A

1) Pedunculated
2) Sessile (no stalk)

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3
Q

(Pedunculated/sessile) polyps can be removed by looping a snare to cauterise the stalk.

A

Pedunculated (have stalk)

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4
Q

(Pedunculated/sessile) polyps can be removed by injecting saline into the submucosa to elevate the poly and facilitate snaring.

A

Sessile (no stalk, need to elevate)

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5
Q

What are 5 categories of polyp/lesions?

A

1) Neoplastic (carcinoid, adenomatous carcinoma)

2) Hyperplastic/inflammatory (eg. gastritis, sites of repair, cardiac, inflammatory fibroid)

3) Hamartomatous/development (eg. pancreatic heterotopia, fundic-gland polyp, peutz-jeghers)

4) Mesenchymal (eg. native cell type tumours)

5) Misc. (eg. xanthoma, lymphoma, hemangioma)

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6
Q

Fundic gland polyps are (benign/malignant) and consist of which 2 types?

A

Benign
1) Sporadic (eg. PPI Rx)
2) Familial (eg. FAP, Gardner’s syndrome)

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7
Q

What are the macroscopic and microscopic features of fundic gland polyps?

A

Macro: 1/multiple bumps

Microscopic:
1) Dilated glands
2) Microcysts lined by oxyntic epithelium
3) Shortened foveola
4) ↑smooth muscle bundles in LP
5) no proliferation of foveolar epithelium

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8
Q

What are 2 associations of fundic gland polyps?

A

1) ↓acidity
2) Hypergastrinemia → oxyntic-glandular hyperplasia

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9
Q

Hyperplastic polyps are often (benign/malignant) and are very common in px in their 50s-60s, preceding _________, formed as a regenerative response to injury.

A

Benign
Precedes chronic erosive gastritis

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10
Q

What are the macroscopic and microscopic features of hyperplastic polyps?

A

Macroscopic:
1) Bumps (<1cm)
2) Surface erosions ±bleeding
3) multiple polyps in gastric atrophy

Microscopic:
1) Elongated/ tortuous/ dilated gastric foveolae w pyloric/fundus glands
2) LP has inflammatory cells, scattered smooth muscles bundles, edema, patchy necrosis
3) Surface mucosa regenerative changes due to ulceration

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11
Q

What is a gastric adenocarcinoma?

A

Malignant neoplasm showing GI glandular epithelial differentiation

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12
Q

True or false: Gastric carcinoma is
* Commoner in Asia than in the West
* Ave. age of diagnosis is 7th decade of life
* One of the leading causes of cancer deaths
worldwide due to tendency for late clinical
presentation and poor response to
conventional chemotherapy
* 5 year survival is 10-15% overall; but 95% for
subset of surgically treated early gastric
carcinoma

A

True

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13
Q

What are 5 symptoms of gastric adenocarcinoma?

A

1) WL
2) Abdo pain
3) Anorexia
4) Vomiting
5) Altered bowel habits
Less common
6) Dysphagia
7) Anaemic symptoms
8) Haemorrhage

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14
Q

How is early gastric cancer differentiated from late?

A

Invaded no more deeply than the submucosa, irrespective of lymph node metastasis

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15
Q

What does the prognosis of gastric carcinoma depend on?

A

1) Depth of invasion
2) Extent of nodal and distant metastasis

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16
Q

What is the standard treatment option for gastric carcinoma?

A

Surgical resection

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17
Q

What are 3 macroscopic growth patterns of gastric carcinoma (evident at both early and advanced stages)?

A

1) Exophytic (protrusion of mass into lumen)
2) Flat/depressed (no obvious mass in mucosa)
3) Excavated (erosive crater present in wall of stomach)

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18
Q

How is a gastric carcinoma different from a bleeding/chronic peptic ulcer macroscopically?

A

Peptic ulcer:
- flat ulcer edge level w remaining stomach
- Straight vertical edges
- haemorrhage/flat clean base

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19
Q

What are the 3 subtypes of GI adenocarcinomas?

A

1) Intestinal (53%)
- associated w chronic atrophic gastritis, severe intestinal metaplasia, dysplasia

2) Diffuse (33%)
- younger px
- proximal stomach
- poorly differentiated carcinomas

3) Unclassified (14%)

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20
Q

What is the main histological feature of intestinal type adenocarcinoma?

A

Well formed glands lined by cuboidal/columnar epithelial

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21
Q

Where do intestinal type adenocarcinomas arise from?

A

Majority from complete-type intestinal metaplasia
(pattern of genetic alterations resembles colonic carcinoma)

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22
Q

What is the main histological feature of diffuse type adenocarcinoma?

A

1) Individual/poorly formed nests of cells growing in an infiltrative pattern

2) Signet ring cells

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23
Q

Where do diffuse type GIT adenocarcinomas arise from?

A

Directly from gastric foveolar epithelium

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24
Q

What is the main macroscopic feature of diffuse type adenocarcinoma?

A

“Leather bottle” appearance
- extensive infiltration of malignancy, creating a rigid, thicken linitis plastica

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25
Q

Which parts of the stomach are gastric carcinomas most common?

A

Pylorus and antrum > Cardia
Lesser curve > Greater

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26
Q

What is the most important prognosis factor for gastric carcinomas?

A

Depth of invasion

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27
Q

Where do gastric carcinomas most often spread to?

A

1) Oesophagus (proximal carcinoma)
2) Duodenum (distal carcinoma)
3) Omentum, colon, pancreas, spleen

Death by widespread seeding to:
4) Peritoneum
5) Lung/Liver
6) Adrenal gland, ovary, spleen

First clinical manifestation:
7) Supraclavicular nodes (Virchow’s nice, Trousseau’s sign)

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28
Q

What is the difference between hamartomatous and adenomatous polyp?

A

Hamartomatous
- Non-cancerous growths.
- Arise from disorganized overgrowth of normal tissue.
- Typically do not progress to cancer.
- Often associated with genetic syndromes.

Adenomatous Polyps:
- Considered pre-cancerous growths.
- Arise from glandular tissue in the colon or rectum.
- Have the potential to develop into colorectal cancer if left untreated.

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29
Q

What is Peutz-Jeghers syndrome?

A

Genetic condition of hamartomatous polyps
- associated with ↑pigmentation around lips, genitalia, buccal mucosa, feet and hands
- polyps carry very little malignant potential

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30
Q

What are GI adenomas?

A

Benign epithelial neoplastic polyps composed of proliferating neoplastic glands.

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31
Q

What are 3 growth patterns of GI adenomas?

A

1) Tubular adenoma (tubular invaginations)
2) Villous adenoma (finger-like projections)
3) Tubulovillous adenoma

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32
Q

What are serrated polyps?

A

Polyps with saw-toothed microscopic appearance
- arise in colon
- may become cancerous
- small in distal (hyperplastic polyps): rarely malignant
- large: precancerous and difficult to remove

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33
Q

What are 3 major molecular pathways that lead to colorectal cancer via adenomatous polyps?

A

1) Oncogene/TS gene mutation (eg. APC, KRAS, BRAF, TP53)

2) Microsatellite instability (MMR deficiency)

3) CpG island methylation pathway (CIMP)

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34
Q

What are 3 gross findings of colorectal cancer?

A

1) Polypoidal, fungated, ulcerated appearance
2) Larger tumours predominated in proximal colon
3) Circumferential growth/apple core lesions in distal colon

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35
Q

Colorectal cancer tumours in the proximal colon tend to grow as ______________ masses that extend along 1 wall of capacious cecum and ascending colon (obstruction is uncommon).

A

Colorectal cancer tumours in proximal colon
→ polypoid, exophytic masses

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36
Q

When carcinomas in the distal colon are discovered, they tend to be _____________ lesions that produce _____________________ constrictions of the bowel.

A

Carcinoma in distal colon
→ annular, encircling lesions
→ produce napkin-ring constrictions

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37
Q

What are 9 clinical presentations of colorectal cancer?

A

1) Abdo pain

2) Altered bowel habits

3) Per-rectal bleeding

4) Asymptomatic

5) Fistulation

6) Weakness

7) Anemia

8) Weight loss

9) Obstruction

10) Others

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38
Q

What are 4 histological findings on CRC?

A

1) Well to poor differentiated of tubule formation
2) prominent desmoplastic (fibrotic tissue) response
3) Abundant intraluminal eosinophilic necrotic debris (outgrowth vascular supply)
4) Extracellular mucin pools (mucinous type carcinoma)

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39
Q

What is the most common type of GI cancer?

A

Colon adenocarcinoma

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40
Q

True or false: Colon adenocarcinomas:
* begins in the cells of colonic crypts and spreads first through the wall of the colon and potentially into the lymphatic system and other organs.
* Colon adenocarcinoma can be treated, with 50% of
patients surviving for at least five years.
* Early-stage colon cancers have 5 yr survival rates of
70 to 80%.
* These tend to present as cancers arising in
polyps and be cured but surgical resection.

A

True

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41
Q

What are 2 genetic conditions that predispose an individual to colon adenocarcinoma?

A

FAP and Gardner’s syndrome
(↑ polyps → ↑risk)

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42
Q

How does a normal mucosa progress to a carcinoma?

A

1) Normal mucosa:
- 1st hit: germline/somatic mutation of TS genes (eg. APC @ 5q21)

2) Mucosa @ risk:
- Methylation → inactivation of TS/protooncogenes (eg. APC, ß-catenin)

3) Early adenoma:
- Protooncogene mutation (KRAS @ 12p12)

4) Late adenoma:
- LOH @ 18q21 (SMAD 2 and 4)

5) Carcinoma:
- homozygous loss of TS genes (TP 53)

6) Tumour progression + metastasis
- additional mutations
- gross chromosomal alterations

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43
Q

What is the difference in the criteria for invasive stomach vs colonic carcinomas?

A

Stomach: invasion beyond basement membrane
Colon: invasion beyond muscular mucosae

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44
Q

True or false: Familial adenomatous polyposis:
* AD inheritance of APC gene (5q21)
* M=F
* Incidence 1:100,000
* 80-100% gene penetrance
* >95% of colonic polyposis by
age 35 - bleeding
* >90% chance of cancer by age
50 if untreated by colectomy

A

True

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45
Q

What is the name for neuroendocrine cell tumours in the GIT?

A

Carcinoids

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46
Q

Carcinoids are growths that look like (low/high) grade cancers but (frequently/infrequently) spread to other parts of the body.

A

Low grade
infrequently spread

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47
Q

What is carcinoid syndrome?

A

Overproduction of substances + metastasis of carcinoid into systemic circulation:
1) Flushing
2) Diarrhoea/+freq. of mvt
3) Bronchoconstriction
4) R cardiac valvular disease
5) Abdo cramps
6) Peripheral oedema

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48
Q

What are the gross appearance of Gastrointestinal Stromal Tumours?

A

Polypoidal intramural tumours
- ulcerate overlying GI mucosa
- rarely: separate masses in mesentery

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49
Q

What is the most common type of sarcoma in the GIT?

A

GISTs (made up of spindled cells)

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50
Q

What is used to diagnose GISTs?

A

IHC biomarkers:
1) CD117
2) CD34
3) DOG1

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51
Q

Where is the upper and lower GIT separated?

A

Duodenal-jejunum junction

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52
Q

What are 4 cardinal symptoms of GIT diseases?

A

1) Abdo/chest pain
2) Altered ingestion of food (eg. nausea, vomiting, dysphagia, anorexia)
3) Altered bowel movements (eg. diarrhoea, constipation)
4) GIT bleed

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53
Q

What are 4 common acute complications of GIT diseases?

A

1) Dehydration
2) Sepsis
3) Bleeding
4) Obstruction/Perforation

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54
Q

What is the main chronic complication of GIT diseases?

A

Malabsorption (malnutrition, deficiency states)

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55
Q

What is an ulcer?

A

Local defect of an organ/tissues surface produced by sloughing of inflamed necrotic tissue → breach in continuity of covering epithelium

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56
Q

What are the mucosal changes in an ulcer?

A

Patch-like w colour change

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57
Q

What are 6 causes of oral ulcers?

A

V
I - Candidiasis, HSV, HFMD
T - lip-biting, ill-fitting dentures
A - mucocutaneous disorders (eg. lichen planus, erythema multiforme), SLE, IBD
M
I - Aphthous ulcers
N - dysplasia, squamous cell carcinoma
C
D - cytotoxic chemo, B12/folate deficiency
E

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58
Q

What are aphthous ulcers (canker sores)?

A

Iatrogenic, common, small, painful, shallow ulcer
- superficial erosion, grey-white exudate w erythematous rim
- self-limiting

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59
Q

Oral candidiasis usually presents as ________________________, caused by ______________ and only leads to pathology when ________________________. In severe cases, it can __________________.

A

Oral candidiasis:
- adherent white, curd-like plaque on tongue→ underlying granular erythematous inflammatory base
- by Candida albicans
- only pathogenic in immunocompromised
- severe → spread to oesophagus/haematogenously

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60
Q

Herpetic stomatitis usually presents as _________________________, caused by __________________.
It is usually (symptomatic/asymptomatic) as ________________________. In severe cases, it can ___________.
It can be treated with __________________.

A

Herpetic stomatitis:
- small vesicles/blisters contain clear fluid around lips
- caused by HSV 1»»2
- asymptomatic in most adults as dormant within mouth ganglia, reactivated by fever, sun, cold, URTI, trauma and immunocompromised
- severe: multiple vesicles throughout oral cavity, lymphadenopathy, viraemia
- Treat w anti-virals eg. acyclovir

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61
Q

Lichen planus usually presents as ____________________, caused by ______________. It is treated with _______________________.

A

Lichen planus:
- Wickham striae, erosions, ulceration

  • Inflammatory, uncertain aetiology ?T-cell mediated autoimmune
  • Treatment: Steroids, immunosuppressants
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62
Q

Pemphigus vulgaris usually presents as ____________________, caused by ______________. It is treated with _______________________.

A

Pemphigus vulgaris:
- ulcers on the mouth

  • Autoantibodies to desmosomal proteins → blisters
  • Treatment: Steroids, immunosuppressants
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63
Q

What 3 types of mucosal change appearances in the mouth?

A

1) Leukoplakia
- whitish, well-defined mucosal patch (caused by epidermal thickening/hyperkeratosis)

2) Erythroplakia
- thin, friable, atropic mucosa with red, granular appearance

3) Speckled mucosa (red + white)
- “Combined” leuko-erythroplakia mucosal changes

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64
Q

Leukoplakia:
- (clinical/histological) syndrome
- presents as ______________
- most (benign/malignant)

A

Leukoplakia:
- clinical syndrome

  • White patch or plaque that cannot be scraped off or characterized as any other disease, Vermilion border of lower lip, buccal mucosa, hard and soft palates
  • most benign (3-25 % undergo transformation to invasive carcinoma)
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65
Q

What are 3 histological features of leukoplakia?

A

1) Banal hyperkeratosis without epithelial dysplasia
2) Mild to severe dysplasia/ Carcinoma in-situ
3) Invasive carcinoma

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66
Q

What are 3 things leukoplakia are most commonly associated with?

A

1 Tobacco
2) chronic friction
3) alcohol abuse

> common in older men

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67
Q

Erythroplakia:
- presents as ______________

A
  • Red, velvety, often granular areas, may or may not be elevated
  • Usually occurs at thin squamous mucosal sites: Lateral-ventral tongue, floor of mouth, palatine arch, retromolar trigone
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68
Q

What are 3 implications of erythroplakia?

A

1) Severe epithelial dysplasia
2) carcinoma-in-situ
3) invasive squamous cell carcinoma (majority)

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69
Q

What are 3 histological features of erythroplakia?

A

1) Epithelial dysplasia (> 50%)

2) Absence of keratin production and a reduced number of epithelial cells.

3) Since the underlying vascular structures are less hidden by epithelium,
erythroplakia appears red clinically.

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70
Q

What are 2 tumours that can arise from the oral/oropharyngeal surface squamous epithelium?

A

Benign: Squamous cell papilloma
Malignant: Squamous cell carcinoma

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71
Q

Oral/oropharyngeal squamous cell papilloma:
- most common (benign/malignant) epithelial neoplasm
- associated with ________virus
- found on ________________

A

Oral/oropharyngeal squamous cell papilloma:
- most common benign epithelial neoplasm
- associated with HPV virus
- found on uvula, palate, tongue, gingiva, lower lips, buccal mucosa

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72
Q

How is squamous cell papilloma treated?

A

local excision

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73
Q

What are the macroscopic features of squamous cell papilloma?

A

Solitary/multiple exophytic, warty, cauliflower-like lesions

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74
Q

What are the microscopic features of squamous cell papilloma?

A

Papillary projections of delicate fibrovascular cores surfaced by mature squamous epithelium

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75
Q

Oral/oropharyngeal squamous cell carcinoma:
- 95% of oral cavity cancers
- usually affect __________
- found on ________________

A

Oral/oropharyngeal squamous cell carcinoma:
- 95% of oral cavity cancers
- usually affect 50-70 years, 90% men
- found on floor of mouth, tongue, hard palate, base of tongue (areas constantly bathed in saliva and with thin non-keratinized squamous epithelium)

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76
Q

What are 5 factors that ↑the risk of squamous cell carcinoma and 1 factor that ↓ risk?

A

↓: fruit and veg consumption

↑:
1) Smoking
2) alcohol
3) tobacco chewing
4) betel chewing
5) HPV (esp. type 16)

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77
Q

What are the macroscopic features of squamous cell carcinoma?

A

Masses with necrosis, ulcers and rolled borders; induration is relatively specific for invasion

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78
Q

What are the microscopic features of squamous cell carcinoma?

A

May have keratinizing growth pattern, but moderate/marked atypia at base, irregular and infiltrative stromal invasion

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79
Q

What are 4 causes of sialadenitis?

A

1) Trauma
2) Viral: Mumps
3) Bacterial: Staph aureus, strep viridans
4) Autoimmune: Sjögren syndrome (dry mouth and eyes)

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80
Q

What are 4 association of Sialolithiasis: Calculi causing ductal obstruction (mostly in submandibular glands)?

A

1) Dehydration
2) trauma
3) smoking
4) gum disease

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81
Q

What are 6 neoplasms of the salivary glands?

A

(parotid>submandibular>sublingual and minor)

Benign: Pleomorphic adenoma (50%) >
Warthin tumor (5-10%)

Malignant:
Mucoepidermoid carcinoma (15%) > Adenocarcinoma (10%) >
Adenoid cystic carcinoma (5%) >
Acinic cell carcinoma (5%)

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82
Q

Pleomorphic adenoma:
- Benign epithelial tumor (______ tumor)

  • Most common tumor of salivary
    glands (10x more common in parotid)
  • Average age of presentation: _____
  • clinical presentation:__________
  • (prone/not prone) to recurrence
  • malignant transformation (rare/common)
A

Pleomorphic adenoma:
- Benign epithelial tumor (mixed tumor)

  • Most common tumor of salivary glands (10x more common in parotid)
  • Average age of presentation: 40
  • clinical presentation: Painless, slow-growing mass in front of and below the ear (parotid)
  • Prone to recurrence (no true capsule; avoid enucleation)
  • Rarely can have malignant transformation (carcinoma ex-pleomorphic adenoma)
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83
Q

What are the macroscopic features of a pleomorphic adenoma?

A

Lobulated, solid mass with chondroid (firm, cartilaginous) and myxoid (soft, gelatinous) areas

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84
Q

What are the microscopic features of a pleomorphic adenoma?

A

1) Circumscribed, lobulated but unencapsulated

2) Epithelial (tubular structures) and stromal (greyish chondromyxoid stroma) components

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85
Q

Warthin tumour:
- (benign/malignant)

  • 2nd most common salivary gland tumour (Almost exclusively in parotid gland, superficial lobe)
  • Average age of presentation: _____
  • more common in ______________
A

Warthin tumour:
- benign

  • 2nd most common salivary gland tumour (Almost exclusively in parotid gland, superficial lobe)
  • Average age of presentation: 50-70
  • more common in M smokers
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86
Q

What are the macroscopic features of a warthin tumour?

A

Ovoid, encapsulated mass

  • Cut sections show a solid-cystic interior that contains viscous yellow-brown fluid “motor oil”
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87
Q

What are the microscopic features of a warthin tumour?

A

1) well circumscribed mass
2) Dense lymphoid stroma
3) Tubular and papillary projections of epithelium, lined by 2 distinctive layers of oncocytic (abundant eosinophilic cytoplasm) cells

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88
Q

Oesophageal congenital disorders such as _________________________ and ___________________:
- present when?
- treat how?
- complications (3)

A

Oesophageal atresia, tracheo-oesophageal fistula
- present shortly after birth: regurgitation on feeding
- treatment: surgical repair
- complications:
1) Aspiration pneumonia
2) suffocation
3) fluid & electrolyte imbalances

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89
Q

Diaphragmatic hernia is __________________________________________ and can lead to: _____________________.

A

Incomplete formation of diaphragm → abdominal viscer herniate into thoracic cavity

Severe: pulmonary hypoplasia

90
Q

How do oesophageal motility disorders (eg. nutcrack esophagus, corkscrew esophagus, achalasia) present?

A

1) Heartburn
2) Dysphagia
3) Frequent coughing/choking

91
Q

What are 3 examples of esophageal motility disorders?

A

1) Nutcracker esophagus
2) Corkscrew esophagus
3) Achalasia

92
Q

What is a nutcracker esophagus?

A

High amplitude, uncoordinated contractions of inner circular and outer longitudinal smooth muscle

93
Q

How is a nutcracker esophagus diagnosed?

A

Manometry

94
Q

What is a corkscrew esophagus?

A

Diffuse esophageal spasm:
Uncoordinated peristalsis with repetitive, simultaneous contractions (normal amplitude) of the distal oesophageal smooth muscle

95
Q

What is achalasia?

A

Triad of incomplete lower oesophageal sphincter relaxation, increased lower oesophageal sphincter tone, and aperistalsis of the oesophagus

96
Q

How is achalasia treated?

A

1) Myotomy
2) Pneumatic balloon dilatation
3) Botox injection

97
Q

What are 3 causes of achalasia?

A

Primary:
1) Degenerative

Secondary
2) Chagas disease
3) Diabetic autonomic neuropathy

98
Q

What are 2 examples of esophageal lacerations?

A

1) Mallory-Weiss tears:
- Longitudinal superficial mucosal tears near the GEJ
- a/w severe retching or vomiting secondary to acute alcohol intoxication
- no need surgical intervention
- present w: Haematemesis

Boerhaave syndrome:
- Less common, more severe barogenic injury due to sharp increase in intraluminal pressure
- Transmural tearing and rupture of the distal oesophagus
- Leads to severe mediastinitis and usually require surgery
- present w: Severe chest pain, tachypnea and shock

99
Q

How are Mallory-Weiss tears and Boerhaave syndrome differentiated clinically and why is it important?

A

Mallory-Weiss: hematemesis
- no need surgery

Boerhaave syndrome: Severe chest pain, tachypnea, shock
- need surgery

100
Q

What are oesphageal varices and how do they form?

A

Dilated tortuous vessels, usually submucosal, within the lower oesophagus and proximal stomach.

Pathogenesis:
Portal hypertension (eg. liver cirrhosis)
→ ↑ portal venous P → collateral channels @ portal-systemic anastomoses
→ congestion and dilatation

101
Q

What are 2 possible complications of esophageal varices?

A

1) Hematemesis
2) Melena

102
Q

What are 5 forms/etiologies of esophageal inflammation?

A

1) Reflux esophagitis (GERD)
2) Chemical
3) Infectious
4) Eosinophilic
5) Iatrogenic injury

103
Q

What is the most common cause of esophagitis?

A

GERD

104
Q

How does GERD present and what are 4 associated risk factors?

A

Clinical presentation:
1) Heartburn
2) Dysphagia
3) Postprandial regurgitation of sour-tasting gastric contents
4) Sore throat and cough

Risk factors:
1) Abrupt ↑ in abdo P (eg. coughing, bending)
2) Alcohol, tobacco
3) Obesity, pregnancy
4) Hiatus hernia

105
Q

What is the possible complication for GERD?

A

Barrett esophagus in chronic GERD

106
Q

What are 4 macroscopic and 4 microscopic features of GERD?

A

Macroscopic:
1) Normal
2) Hyperaemia
3) Erosions
4) Strictures

Microscopic:
1) Basal zone hyperplasia
2) Elongation of LP papillae
3) Erosions
4) Intraepithelial eosinophils

107
Q

What is eosinophilic esophagitis and 3 macroscopic features?

A

Eosinophil-dominated inflammation a/w atopic disease

Macroscopic:
1) Feline esophagus
2) Linear furrows
3) Strictures

108
Q

What is Barrett esophagus and what is it a/w?

A

Intestinal metaplasia in esophageal squamous mucosa (complication of chronic GERD)

  • a/w ↑ risk of dysplasia and adenocarcinoma
109
Q

What are 2 diagnostic criteria for barrett esophagus?

A

Endoscopy: Metaplastic columnar mucosa above GEJ

Microscopy: Intestinal-type metaplasia w goblet cells

110
Q

What is the typical macroscopic appearance of barrett esophagus?

A

Tongues of red, velvety columnar mucosa extending upward from the GEJ, alternating with smooth, white squamous mucosa.

111
Q

What are 5 malignant neoplasia of the esophagus?

A

1) Carcinomas: SCC, adenocarcinoma
2) Neuroendocrine carcinoma
3) Melanoma
4) Lymphoma
5) Sarcoma

112
Q

What is an example of a benign esophageal neoplasm?

A

Leiomyoma (mesenchymal)

113
Q

What are 3 clinical presentations of esophageal SCC?

A

1) Mass effect/Stricture: Dysphagia, odynophagia, obstruction

2) Ulceration: Haemorrhage, anaemia, sepsis

3) Systemic: Weight loss (impaired nutrition and tumour cachexia)

114
Q

What are 2 macroscopic features of esophageal SCC?

A

Most common on middle to upper 2/3 of esophagus
1) Polyploid and exophytic
2) Ulcerating and diffusely infiltrative

115
Q

What are 4 areas/methods esophageal SCC can spread?

A

1) Circumferential and longitudinal spread

2) Local invasion into adjacent structures:
- Respiratory tree (tracheo-oesophageal fistula) → aspiration pneumonia
- Aorta → catastrophic exsanguination
- Mediastinum → mediastinitis

3) Lymph node metastasis
- Upper third → cervical lymph nodes
- Middle third → mediastinal, paratracheal and tracheobronchial nodes
- Lower third → gastric and coeliac nodes

4) Distant metastasis

116
Q

What are 3 risk factors and 1 protective factor for esophageal adenocarcinoma?

A

Risk factors:
1) Chronic GERD
2) Radiation
3) Tobacco

Protective:
Fruits and veg

117
Q

What are 3 clinical presentations of esophageal adenocarcinoma?

A

1) Mass effect: Dysphagia, odynophagia, obstruction

2) Ulceration: Haemorrhage, anaemia, sepsis

3) Systemic: Weight loss (impaired nutrition and tumour cachexia)

118
Q

What are the macroscopic features of adenocarcinoma?

A

Lower third of esophagus (may invade cardia)

Flat/raised patches → large mass or ulcerate, infiltrate
diffusely

119
Q

What are 3 microscopic features of esophageal adenocarcinoma?

A

Mucin-producing, gland-forming:
1) Usually intestinal-type
2) Signet ring cells, poorly differentiated
3) Barrett’s (intestinal metaplasia) in the background

120
Q

What are 2 causes of acquired pyloric stenosis?

A

Benign: antral gastritis/peptic ulcers close to pylorus

Malignant: Carcinoma of distal stomach/pancreas (via infiltration/fibrosis)

121
Q

What are 3 risk factors for congenital hypertrophic pyloric stenosis?

A

1) FHx
2) Turner syndrome
3) Trisomy 18
4) Erythromycin/Azithromycin exposure

122
Q

How does congenital hypertrophic pyloric stenosis present (i) clinically and (ii) on PE?

A

Clinical presentation: 3-6wk
- new onset regurgitation
- projective non-bilious vomiting after feeds
- frequent demands for refeeding

PE:
- Firm ovoid 1-2cm mass in epigastric region
- visible peristalsis

123
Q

How is congenital hypertrophic pyloric stenosis treated?

A

Myotomy

124
Q

What is the difference between gastritis and gastropathy?

A

Gastritis: + inflammation
- neutrophil infiltration

Gastropathy: - no inflammatory cells

125
Q

What is are 2 ways that acute gastritis can present?

A

1) Asymptomatic:
- epigastric pain
- nausea and vomitting

2) Mucosal erosion, ulceration, hemorrhage → hematemesis, melena, Iron deficiency anemia

126
Q

What are 6 causes of acute gastritis/peptic ulcers?

A

1) Age → ↓mucin and HCO3

2) Uraemia/H. pylori → ↓HCO3 by NH4+

3) Direct cellular dmg (eg. alcohol, tobacco, stress, radiation, chemo)

4) Local ischaemia (eg. HTN, vasoconstrictors, stress-induced splanchnic vasocontriction)

5) Chemotherapy → ↓epithelial renewal

6) NSAIDs → ↓PGEs

127
Q

What is the main cause of acute erosive haemorrhagic gastritis?

A

Ingestion of medications, alcohol

128
Q

What are the 2 macroscopic and 4 microscopic features of acute erosive hemorrhagic gastritis?

A

Macroscopic:
1) Diffuse hyperemic edematous mucosa
2) Surface erosions

Microscopic:
1) Superficial mucosal defects
2) Fibrinous exudate
3) Neutrophilic infiltrate
4) Corkscrew profiles (tortuosity and mucin depletion → regenerative foveolar hyperplasia)

129
Q

What are 3 pathogeneses of stress-related mucosal injury?

A

1) HTN, stress-induced splanchnic vasoconstriction → release of vasocontrictors → local ischaemia

2) Intracranial injury → vagal stimulation → gastric acid hypersecretion

3) Systemic acidosis → ↓pH of mucosal cells → ↓acid secretion

130
Q

What are 3 names for different types of stress-related mucosal injury?

A

1) Stress ulcers: shock, sepsis, trauma

2) Curling ulcers: proximal duodenal ulcers (a/w burns and trauma)

3) Cushing ulcers: gastric, duodenal, esophageal ulcers (a/w brain injury and ↑ intracranial P)

131
Q

What is the macroscopic and microscopic appearance of stress-related mucosal injury?

A

Macroscopic:
- multiple erosions or ulcers, in the stomach, sharply demarcated, rounded, <1 cm

Microscopic:
- Lack chronic features in PUD such as scarring and blood vessel thickening

132
Q

How does chronic gastritis present clinically?

A

Less severe than acute but more persistent:
- nausea
- epigastric pain

133
Q

What are 4 causes of chronic gastritis?

A

1) H. pylori
2) Radiation injury
3) Chronic bile reflux
4) Autoimmune atrophic gastritis
5) Uncommon:
- Eosinophilic, lymphocytic, granulomatous

134
Q

True or false: H. pylori infections of the GIT are typically acquired in childhood present clinically in both acute and chronic infections.

A

False.
Infection typically acquired in childhood and persists for life without treatment.
Acute infection minimal symptoms, most present with symptoms of chronic gastritis

135
Q

What are 4 virulence factors of H. pylori that aid in causing gastritis?

A

1) Flagella → motile in viscous mucous
2) Urease → generate ammonia → ↑pH for survival
3) Adhesins → ↑adherence to surface foveolar cells
4) Toxins → eg. CagA

136
Q

What are 3 pathogenesis/sequelae of H. pylori gastritis?

A

1) Antral inflammation → ↑gastrin → ↑acid → ulcers

2) Chronic infection → atrophic gastritis → ↓parietal cells + intestinal metaplasia → ↓ ulcer risk but ↑adenocarcinoma risk

3) Lymphoid aggregates w germinal centers → MALT → MALT lymphoma

137
Q

What are 2 microscopic features of H. pylori gastritis?

A

1) Abundant subepithelial plasma cells in superficial LP
2) Lymphoid aggregates w germinal centers

138
Q

What are 4 ways H. pylori gastritis can be diagnosed?

A

1) Tissue biopsy → rapid urease, culture, PCR
2) Serology for anti-H. pylori Abs
3) Urea breath test
4) Fecal bacteria detection

139
Q

What is the pathogenesis of autoimmune atrophic gastritis?

A

CD4+ T cells against parietal cell components
→ loss of parietal cells
→ ↓acid and IF production

140
Q

What are 3 sequelae/direct consequences of autoimmune atrophic gastritis?

A

1) Achlorhydria → hypergastrinemia + G cell hyperplasia → neuroendocrine cell hyperplasia

2) ↓IF → defective ileal B12 abs → pernicious anemia

3) ↓chief cells via gastric gland destruction → ↓serum pepsinogen I

141
Q

How does autoimmune atrophic gastritis typically present?

A

B12 deficiency:
- megaloblastic anemia
- atrophic glossitis
- malabsorptive diarrhoea
- subacute degeneration of spinal cord

142
Q

Which part of the stomach is spared in autoimmune atrophic gastritis?

A

Antrum (no parietal cells)

143
Q

What are consequences specific to autoimmune atrophic gastritis?

A

1) Progression to low-grade neuroendocrine tumours

2) Atrophy and intestinal metaplasia → ↑risk of adenocarcinoma

144
Q

What are the macroscopic features of autoimmune atrophic gastritis?

A

Body and fundus mucosa appears thinned and rugal folds are lost (atrophic)

145
Q

What are 4 microscopic features of autoimmune atrophic gastritis?

A

1) Deeper inflammation centered on gastric glands
2) paucity of oxyntic glands
3) intestinal metaplasia (checkerboard pattern)
4) pseudopyloric metaplasia
5) neuroendocrine cell
hyperplasia

146
Q

What is eosinophilic gastritis?

A

Tissue damage associated with dense infiltrates of eosinophils in the mucosa and muscularis,
usually in the antral/pyloric region

  • a/w peripheral eosinophilia and ↑serum IgE l
  • Food allergies (e.g. cow’s milk, soy, immune disorders, parasitic infections, H. pylori infections, Crohn’s disease
147
Q

What is lymphocytic gastritis?

A

Marked increase in intraepithelial T-lymphocytes
- women
- Idiopathic, a/w coeliac disease

148
Q

What is granulomatous gastritis?

A

Any gastritis that contains granulomas

  • Idiopathic, Crohn’s disease, sarcoidosis, infections (mycobacteria, fungi, CMV, H. pylori)
149
Q

What are 4 complications of chronic gastritis?

A

1) Peptic ulcer disease

2) Mucosal atrophy and metaplasia → ↑adenocarcinoma risk

3) Inflammation and free radical dmg proliferative stimuli → regenerative response to injury + gastrin production (mitogen) → accumulation of genetic alterations → dysplasia

4) Gastritis cystica

150
Q

What is peptic ulcer disease?

A

Chronic mucosal ulceration in duodenum or stomach that penetrates the muscularis mucosae and deeper

151
Q

What are 4 PUD risk factors?

A

1) H. pylori infection
2) NSAID (low-dose aspirin synergises with H. pylori for gastric PUD)
3) Cigarette use
4) Cardiovascular disease
5) COPD
6) Illicit drugs (e.g. cocaine reduces mucosal blood flow)
7) Alcoholic cirrhosis (primarily duodenal PUD)
8) Endocrine cell hyperplasia (stimulate parietal cell growth)
9) Zollinger-Ellison syndrome (ulcers also occur in distal duodenum and jejunum)

152
Q

What is the most susceptible site for PUD?

A

1) Proximal duodenum
2) Lesser curve near the interface of body and antrum

153
Q

What are the macroscopic features of PUD?

A

Solitary, Round to oval, sharply demarcated, punched-out defect, Usually level with surrounding mucosa

  • Variable depth
  • Base is smooth and clean
  • Scarring and puckering of the wall
154
Q

What are the microscopic features of PUD?

A

1) Fibrinopurulent/ inflammatory exudate
2) Necrotic debris
3) Granulation tissue
4) Fibrosis

155
Q

What are 4 clinical features of PUD?

A

1) Epigastric burning or aching pain
- Pain occurs 1-3 hours after food, worse at night, relieved by alkali or food
- Penetrating ulcers can cause referred pain to back, left upper quadrant, chest

2) Nausea and vomiting
3) bloating
4) belching
5) weight loss

156
Q

What are 4 complications of PUD?

A

1) Bleeding
2) Perforation
3) Obstruction (2° to edema and scarring)
4) Transformation to cancer

157
Q

What are 3 ways PUD is treated?

A

1) H. pylori eradication
2) Neutralisation of gastric acid with PPI
3) Withdraw offending agents that may interfere with mucosal healing

158
Q

What 3 examples of vascular gastropathies?

A

1) Gastric antral vascular ectasia (GAVE)
2) Portal hypertensive gastropathy
3) Dieulafoy lesion

159
Q

What are 3 macroscopic features of gastric antral vascular ectasia?

A

1) Longitudinal stripes of oedematous, erythematous
mucosa that alternated with less severely injured, paler
mucosa

2) “watermelon stomach”

3) Erythematous stripes caused by ectatic mucosal vessels

160
Q

What are 2 microscopic features of gastric antral vascular ectasia?

A

1) Reactive gastropathy
2) Dilated capillaries containing fibrin thrombi

161
Q

What is portal hypertensive gastropathy?

A

Portal hypertension secondary to hepatic cirrhosis

162
Q

What is the macroscopic appearance of portal hypertensive gastropathy?

A

Mosaic pattern, resembling snake skin or cherry-red spots

163
Q

What are 2 microscopic appearance of portal hypertensive gastropathy?

A

Most prominent in corpus:
1) Reactive gastropathy
2) Congested, dilated mucosal capillaries without fibrin thrombi

164
Q

What is a dieulafoy lesion?

A

Abnormal caliber-persistent artery in the submucosa
- Most commonly found in the lesser curvature, near the GEJ
- Erosion of mucosa → recurrent bleeding

165
Q

What are 2 hypertrophic gastropathies?

A

1) Menetrier disease
2) Zollinger-Ellison Syndrome

166
Q

What is Menetrier disease and what are its (i) macroscopic and (ii) microscopic presenations?

A

Hypertrophic gastropathy due to excessive secretion of TGF-alpha:

i) Macroscopic: Irregular enlargement of gastric rugae in body and fundus, sparing the antrum

ii) Microscopic: Foveolar hyperplasia with focally dilated glands

167
Q

What is Zollinger-Ellison Syndrome and what are its (i) macroscopic and (ii) microscopic presenations?

A

Gastrin-secreting neuroendocrine tumours (gastrinoma) in small intestine or pancreas; sporadic or MEN1 → duodenal ulcers or chronic diarrhoea:

i) Macroscopic: marked ↑ in oxyntic mucosal thickness

ii) Microscopic: Massive parietal cell hyperplasia, mucous neck and neuroendocrine cell hyperplasia

168
Q

What is the difference between a true and a meckel diverticulum?

A

Meckel → vestigial remnant of vitelline duct (anti-mesenteric border of ileum)

True → blind outpouching communicating w lumen (all 3 layers of wall)

169
Q

What are 3 congenital pathologies of the intestine?

A

1) Meckel diverticulum
2) Hirschsprung disease
3) Anorectal atresia

170
Q

How does Meckel diverticulum present clinically (3)?

A

Most asymptomatic
1) painless rectal bleeding
2) obstruction (intussuception)
3) meckel diverticulitis (clinically similar to acute appendicitis)

171
Q

EXTRA: What is the rule of 2s

A

Rule of 2s for meckel diverticulum:
- 2% of the population
- Twice as common in males
- Within 2 feet of the ileocecal valve
- 2 inches in length
- 2 types of heterotopic mucosa (pancreas and gastric tissue)
- Presentation before age of 2

172
Q

What is an anorectal atresia?

A

Congenital anorectal malformation (ARM)
where a normal anal opening is absent at
birth

  • Failure of the cloacal diaphragm to involute
  • Spectrum of anomalies which can involve
    anus alone or also a segment of rectum
173
Q

How does anorectal atresia present clinically (2)?

A

1) Abdominal distension
2) not passing meconium (baby’s first poop!)
- usually recognised @ birth upon visual inspection

174
Q

What is Hirschsprung disease?

A

Congenital megacolon:
Failure of neural crest-derived ganglion cells to migrate into the distal colon (mutation in the receptor tyrosine kinase RET)

  • Distal intestinal segmentlacks both Meissner submucosal plexus and the Auerbach
    myenteric plexus (aganglionosis) → Failure of aganglionic segment to relax → absence of coordinated peristalsis →
    functional obstruction → proximal dilatation (megacolon)
  • Defect always begins at the rectum but extends proximally for variable lengths
175
Q

How does Hirschsprung disease present clinically (3)?

A

1) Failure to pass meconium
2) Abdominal distension
3) Bilious vomiting

176
Q

What are 3 complications of Hirschsprung disease?

A

1) Fluid and electrolyte imbalances
2) Perforation
3) Enterocolitis
4) Peritonitis

177
Q

How is Hirschsprung disease diagnosed and treated?

A

Diagnosed via histology (ganglion cells absent)

Treatment: resection of aganglionic segement

178
Q

What are 4 risk factors for bowel ischaemia?

A

1) Arterial thrombosis (eg. atherosclerosis)
2) Arterial embolism (eg. aortic athroma)
3) Venous thrombosis
4) Non-occlusive ischaemia (eg. HF, shock, vasoconstrictors)
5) Misc. (eg. radiation, mechanical obstruction)

179
Q

What differentiates the pathogenesis of intestinal mucosal/mural infarction and transmural infarction in ischaemic bowel disease?

A

Mucosal/Mural: extensive narrowing/occlusion

Transmural: sudden occlusion of main artery

180
Q

What are 5 effects/sequelae of ischaemic bowel disease?

A

1) F(x)-al obstruction → vomiting, distension

2) Muscle ischaemia → abdominal angina (pain after meals)

3) Mucosal necrosis → exudate and hemorrhage → bloody diarrhoea

4) Muscle necrosis → ↓peristalsis ↓bowel sounds

5) Transmural necrosis → perforation → peritonitis

6) Gram -ve bacteremia → endotoxic shock

181
Q

Why is the colon the most common site for ischaemic bowel disease?

A

Watershed zones (supplied by terminal branches)

182
Q

What are the macroscopic features of ischaemic bowel disease?

A

Depends on type but infarcted area: dusky, congested to purple-red

(acute, transmural → sharp demarcation/transition)

183
Q

What are the microscopic features of ischaemic bowel disease (3)?

A

1) Mucosal change
- atrophy
- hyperproliferative crypts
- fibrous scarring of LP in chronic ischaemia

2) Mural changes
- ulceration
- coagulative necrosis
- serositis (w purulent exudates)

3) bacterial superinfection → pseudomembrane formation

184
Q

How does (i) acute and (ii) chronic ischaemic bowel disease present?

A

i) Acute:
- sudden onset cramping, abdo pain, hematochezia
- ↓ bowel sounds, guarding, rebound tenderness
- shock

ii) chronic
- Intermittent bloody diarrhoea interspersed with periods of healing
- Rarely, stricture formation
- Mimic inflammatory bowel disease

185
Q

What is pseudomembranous colitis caused by?

A

Clostridioides difficile
- a/w AB use → disruption normal microbiota → C. diff overgrowth

186
Q

What are 4 risk factors for pseudomembranous colitis?

A

1) AB use (esp. clindamycin and cephalosporins)
2) Age
3) Hospitalisation
4) Immunosuppression

187
Q

How is pseudomembranous colitis diagnosed and treated?

A

Diagnosed via histology (C. diff toxin)

Tx: Metronidazole and Vancomycin

188
Q

What are the clinical features (4) and complication of pseudomembranous colitis?

A

Clinical features:
1) Fever
2) Leukocytosis
3) Abdo pain
4) Watery diarrhoea → dehydration

Complication:
- toxic megacolon

189
Q

What are the (i) macroscopic and (ii) microscopic featuresd of pseudomembranous colitis?

A

Macroscopic:
- Colon coated with pseudomembranes made up of adherent layer of inflammatory cells/debris

Microscopic:
- Mucopurulent exudate that erupts from damaged crypts to form “volcano” lesions

190
Q

What are 2 ways in such intestinal TB can occur?

A

1) Primary:
- Ingestion of M. bovis (raw milk)

2) Secondary:
- sputum ingestion from active pulmonary TB
- hematogenous spread from distant focus
- lymphatic spread through infected nodes
- direct extension from contiguous site

191
Q

How does intestinal TB present clinically (5)?

A

1) Abdo pain
2) Fever
3) Altered bowel habits
4) Obstruction
5) WL
6) Lymphadenopathy
7) Pulmonary involvement → pulmonary symptoms

192
Q

What are the macroscopic (3) and microscopic (1) features of intestinal TB?

A

Macroscopic:
1) sharply-defined ulcers (circumferential/transverse)
2) inflammatory polyploid masses
3) strictures, bowel wall thickening

Microscopic:
- caseating granulomas
(will stain red w ZN stain)

193
Q

What are the macroscopic (3) and microscopic (1) features of amoebiasis?

A

Macro:
1) Flask-shaped ulcers
2) Amoeboma (inflammatory mass like tumour)
3) Diffuse colitis

Micro:
- trophozoites w round dense nuclei and ingested RBCs

193
Q

How does intestinal amoebiasis occur?

A

Entamoeba histolytica
- ingested cyst pass through stomach and colonise colon (have wall R to acid)
- release trophozoites → invade colonic epithelium

193
Q

How does intestinal amoebiasis present clinically (3)?

A

1) Hematochezia + mucus
2) abdo pain
3) fever (amoebic colitis)

193
Q

What other organ is affected in intestinal amoebiasis?

A

Liver (form abscess)
- embolise via portal circulation

194
Q

How does acute appendicitis present clinically (5)?

A

1) Periumbilical pain → localised to right iliac fossa
2) Nausea and vomiting
3) fever
4) Leukocytosis
5) mild neutrophilic leukocytosis
6) McBurney sign

195
Q

What are 3 ddx for acute appendicitis?

A

1) Mesenteric lymphadenitis
2) Acute salpingitis
3) Ectopic pregnancy

196
Q

What is the pathogenesis of acute appendicitis?

A

Luminal obstruction
→ ↑ intraluminal P
→ ↓venous outflow, bacterial proliferation, acute inflammation, ischaemia

197
Q

How can acute appendicitis complicate?

A

Perforation → peritonitis

198
Q

What are the macroscopic (4) and microscopic (2) features of acute appendicitis?

A

Macro:
1) Edema
2) Turgidity
3) Congestion
4) Hemorrhage
5) Fibrinopurulent exudate

Micro:
1) Neutrophilic infiltration of muscularis propria
2) ulceration
3) Necrosis

199
Q

What is the difference between a true and false diverticulum?

A

Both outpouching of gut wall
True: all layers of wall (congenital)

False: Mucosa/submucosa only (pulsion: P>wall strength)

200
Q

Diverticulum usually form at weak spots of the gut wall liek where ____________ penetrate.

A

Vasa recta

201
Q

What are 4 risk factors for diverticular disease?

A

1) Age
2) Low fibre
3) Low stool volume
4) Reduced activity

202
Q

How does diverticular disease present clinically (3)?

A

1) Asymptomatic
2) Bleeding → anemia
3) Diverticulitis (pain, fever, leukocytosis)

203
Q

What are 4 complications of diverticular disease?

A

1) Pericolic abscess, fibrosis, adhesions
2) Colovesical fistula
3) Stricture → obstruction
4) Perforation → peritonitis

204
Q

What are the macroscopic (1) and microscopic (2) features of diverticular disease?

A

Macro:
- small outpouches in rows betwen taenia coli

Micro:
1) transmural neutrophilic infiltrate
2) Abscess

205
Q

What are 2 forms of inflammatory bowel disease?

A

1) Crohn’s disease
- any part of GIT
- transmural skip lesions

2) Ulcerative colitis
- only colon and rectum
- continuous
- limited to mucosa and submucosa

206
Q

What are 5 factors that contribute to the pathogenesis of inflammatory bowel disease?

A

1) Genetic predisposition (eg. NOD2 polymorphisms → 10x risk of CD)
2) Environmental
3) Mucosal immune regulation
4) Autophagy and cellular stress response
5) Host-microbial interactions (gut microbiome)

207
Q

How does Crohn’s disease present clincally (3)?

A

Variable, intermittent
1) hematochezia
2) fever
3) Abdo pain

208
Q

What are the macroscopic (5) and microscopic (5) features of crohn’s disease?

A

Macro:
1) Multiple, separate, sharply delineated areas of disease → skip lesions

2) Elongated, serpentine ulcers oriented along the axis of the bowel

3) Ulceration with sparing of interspersed normal mucosa (patchy distribution) → cobblestone mucosa

4) Fissures/fissuring ulcers → fistula, perforation

5) Transmural inflammation, fibrosis → stricture, creeping fat

Micro:
1) Active inflammation - Neutrophilic cryptitis, crypt abscess

2) Chronicity changes – crypt architectural distortion, epithelial metaplasia (pseudopyloric metaplasia, Paneth cell metaplasia in left colon)

3) Patchy distribution of inflammatory changes

4) Transmural chronic inflammation with lymphoid follicles

5) Non-caseating granulomas in any layer of intestinal wall, draining mesenteric lymph nodes

209
Q

What are 6 extraintestinal manifestations of crohn’s disease?

A

1) Uveitis
2) Migratory polyarthritis
3) Sacroileitis
4) Ankylosing spondylitis
5) Erythema nodosum
6) Cutaneous granulomas
7) Finger clubbing
8) Pericholangitis and primary sclerosing cholangitis (more common in UC)

210
Q

Crohn’s disease and ulcerative colitis both cause and increase risk of _____________________ in long-standing disease.

A

Colonic adenocarcinoma

211
Q

How does ulcerative colitis present clinically (2)?

A

1) Relapsing attacks of bloody diarrhoea with stringy mucoid material
2) abdo pain, cramps that are temporarily relieved by defaecation

212
Q

What are the macroscopic (5) and microscopic (5) features of ulcerative colitis?

A

Macro:
1) Red, granular mucosa
2) Broad-based ulcers, aligned along long axis of colon
3) Isolated islands of regenerating mucosa bulge into lumen to form pseudopolyps, which may fuse to form mucosal bridges
4) Mucosal atrophy
5) NOT transmural - colon wall is not thickened, serosal surface normal, strictures do not occur

Micro:
1) Active inflammation - Neutrophilic cryptitis, crypt abscess
2) Chronicity changes – crypt architectural distortion, epithelial metaplasia (pseudopyloric metaplasia, Paneth cell metaplasia in left colon)
3) Diffuse distribution of inflammatory changes
4) Inflammation mostly limited to the mucosa and submucosa
5) Granulomas NOT present

213
Q

What are 6 extraintestinal manifestations of ulcerative colitis?

A

1) Uveitis
2) Migratory polyarthritis
3) Sacroileitis
4) Ankylosing spondylitis
5) Erythema nodosum
6) Pericholangitis and primary sclerosing cholangitis (more common in UC)

214
Q

How does intestinal obstruction present clinically (3)?

A

1) Abdo pain
2) distention
3) vomiting
4) constipation

215
Q

Intestinal obstruction:
________________ most often involved due to narrow lumen

80%: (4)

20%: (3)

A

Small bowel most often involved due to narrow lumen

80%: Hernia, adhesion, volvulus, intussusception

20%: Tumours, infarctions, strictures

216
Q

How does adhesion lead to intestinal obstruction?

A

Surgical procedures, infection or other causes of peritoneal inflammation
→ fibrous adhesions between bowel segments, abdominal wall, or operative sites
→closed loop → internal herniation

217
Q

How does volvulus lead to intestinal obstruction?

A

loop of bowel twists about its mesenteric point of attachment
→ luminal and vascular compromise

218
Q

How does intussusception lead to intestinal obstruction?

A

segment of intestine, constricted by a wave of peristalsis, telescopes into the immediate distal segment

219
Q

What are 2 complications of hernias?

A

1) Pressure at the neck of the hernia impairs venous drainage → stasis and oedema → ↑ in bulk of herniated loop → permanent entrapment ‘incarceration’ → arterial and venous compromise → ‘strangulation’ and infarction

2) Constriction of bowel lumen produces IO

GIT (14 decks)

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