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Pathology (Guide) > Histopathology - GI Disease > Flashcards

Histopathology - GI Disease Flashcards

1
Q

What is normal oesophageal histology?

A

Squamous stratified epithelium (NO GOBLET CELLS), separated from columnar epithelium of the stomach via squamo-columnar junction/Z-line

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2
Q

What are the charcteristics, complications and treatment of Reflux oesophagitis/GORD?

A
  • Commonest cause of oesophagitis
  • Los Angeles Classification of Severity
  • Cx: Ulceration, Haemorrhage (leads to haematemesis/meleana), Barrett’s oesoophagus, strictures, perforation
  • Tx: Lifestyle changes (stop smoking, weight loss), PPI/H2 receptor antagonists
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3
Q

What is Barrett’s Oesphagus, it’s characteristics and complications?

A

Intestinal metaplasia of squamous mucosa to columnar epithelium (have goblet cells) following chronic GORD - upwards migation of the squamo-columnar junction

  • 10% of symptomatic GORD pts
  • Cx: Adenocarcinoma (metaplasia -> dysplasia -> Cancer)
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4
Q

What confers a higher risk of developing cancer in a patient with Barrett’s oesophagus?

A

Presence of goblet cells (Intestinal metaplasia)

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5
Q

Where is oesophageal adenocarcinoma most commoly seen, and its risk factors?

A

Distal 1/3 Oesophagus (due to Barrett’s oesophagus)

RFs:
- Barrett’s oesophagus
- Smoking
- Obesity
- Prev. radiation therapy
- Caucasian
- M»F

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6
Q

What are some RFs of Squamous cell oesophageal carcinoma?

A

Ethanol use + smoking

  • Achalasia of cardia
  • Plummer-Vinson syndrome
  • Nutritional deficiencies
  • Nitrosamines
  • HPV
  • Afro-caribbean
  • M>F
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7
Q

Where is squamous cell oesophageal carcinoma most commonly found?

A
  • Middle 1/3 = 50%
  • Upper 1/3 = 20%
  • Lower 1/3 = 30%
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8
Q

What is the presentation of squamous cell oesophageal carcinoma?

A
  • Progressive dysphasia
  • Odynophagia (pain)
  • Anorexia
  • Severe weight loss
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9
Q

What are varices, its presentation and treatment?

A

Engorged dilated veins, usually due to portal HTN (back pressure)

  • Sx: Pt vomits large volumes of blood
  • Tx: Emergency endoscopy = sclerotherapy/banding
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10
Q

What is the spread of squamous cell oesophageal carcinoma?

A
  • Rapid growth
  • Early spread to LNs, liver, + proximal structures (results in palliative care)
  • Invades mucosa and creates keratin + intracellular bridges
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11
Q

What is the normal histology of the stomach?

A

Lined by gastric mucosa (NO GOBLET CELLS), columnar epithelium (mucin secreting) + glands

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12
Q

What are some causes of acute gastritis?

A
  • Aspirin
  • NSAIDs
  • Corrosives (bleach)
  • Acute H. pylori
  • Severe stress
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13
Q

What are some causes of chronic gastritis?

A
  • H-pylori (Antral)
  • Autoimmune (e.g. pernicious anaemia)
  • Ethanol
  • Smoking
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14
Q

What are some complications of gastritis?

A
  • Chronic –> Gastric ulcer formation
  • Chronic from H. pylori may induce lymphoid tissue in stomach + increase future risk of mucosa associated lymphoid tissue (MALT) Lymphoma
  • Intestinal metaplasia –> Dysplasia –> Cancer
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15
Q

What is a gastric ulcer and its symptoms?

A

Breach through muscularis mucosa into submucosa (deoth of tissue loss goes beyond mucosa)

  • Epigastric pain +/- weight loss
  • Pain worse with food + relieved by antacids
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16
Q

What are some RFs, Ix and Cx for gastric ulcer?

A

RFs:
- H. pylori
- Smoking
- NSAIDs
- Stress
- Delayed gastric emptying
- Elderly

Ix:
- Biopsy (Punched out lesion with rolled margins)

Cx:
- Anaemia - IDA (massive haemorrhage)
- Perforation (erect CXR)
- Malignancy

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17
Q

What are some charactertistics of gastric cancer?

A
  • Highest incidence: Japan/China (more fermented/pickled foods eaten)
  • > 95% = adenocarcinomas
  • Intestinal or diffuse
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18
Q

What are the histological differences between intestinal and diffuse gastric cancers?

A

Intestinal:
- Well differentiated
- Goblet cells present following intestinal metaplasia

Diffuse:
- Poorly differentiated
- No gland formation
- Includes signet ring cell carcinoma

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19
Q

What is gastric lymphoma (MALT) and it’s treatment?

A

Chronic inflammation + B-lymphocyte driven
- Caused by H.pylori

Tx: Remove cause
- H. pylor = triple therapy (PPI, clarythromycin + amoxicillin)

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20
Q

What are some features of a duodenal ulcer, its RFs and complications?

A
  • 4x more common than gastric ulcer
  • Epigastric pain, worse at night
  • Pain relieved by food + milk
  • Occurs in younger adults

RFs:
- H. pylori
- Drugs
- Aspirin
- NSAIDs
- Steroids
- Smoking
- Increased drug use
- Acid secretion

Cx:
- IDA
- Perforation (CXR)

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21
Q

What is coelia diseaase + its presentation?

A

T-cell mediated autoimmune disease (DQ2, DQ8 HLA status)

Presentation:
- Young children (paeds) + irish women

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22
Q

What are some symptoms of coeliac disease (malabsorption)

A
  • Steatorrhoea
  • Abdo pain
  • Bloating
  • N+V
  • Weight loss
  • Fatigue
  • IDA
  • Failure to thrive
  • Rash (dermatitis herpetiformis)
  • Hyposplenism
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23
Q

What are some complications of coeliac disease?

A
  • MALT
  • Hyposplenism
  • Osteoporosis
  • Subfertility
  • IDA
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24
Q

What is a differential diagnosis for coeliac disease?

A

Tropical sprue

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25
Q

What are the serological tests + results for coeliac disease?

A
  • Anti-endomysial Ab (Best sensitvity + specificity)
  • Anti-Tissue transglutaminase (IgA)
  • Anti-gliadin (poor marker of disease control)
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26
Q

What is the gold standard investigation for coeliac disease and what is seen on histology?

A
  • Upper GI endoscopy + duodenal biopsy (while eating gluten)
  • Villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes
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27
Q

What is a normal villous:crypt ratio?

A

2:1

28
Q

What is the treatment for coeliac disease?

A

Gluten-free diet

29
Q

What are some congenital GI diseases?

A
  • Atresia
  • Stenosis
  • Duplication
  • Imperforate anus
  • Hirschsprung’s disease
30
Q

What is the most common congenital GI abnormality?

A

Hirschsrprung’s disease

31
Q

What is Hirschsrpung’s disease and how does it present?

A

An absence of ganglion cells in myenteric plexus

  • Sx + signs of obstruction in young babies (constipation, abdominal distension, overflow diarrhoea)
  • Mostly male
  • Failure to pass meconium within first 48hrs
32
Q

What are some RFs for Hirschprung’s disease?

A
  • Down’s syndrome (2%)
  • Males
  • RET proto-oncogene Cr10+ (genetics)
33
Q

What is the gold-standard investigation and treatment for Hirschprung’s disease?

A

Ix:
- Full thickness biopsy of affected segment
- Hypertrophied nerve fibres, no ganglia

Tx:
- Insufflation
- Resection of affected segment + pull-through of normal functioning bowel

34
Q

What are some causes of an obstruction?

A
  • Constipation
  • Diverticular disease
  • Adhesions
  • Herniation
  • External mass
  • Volvulus
  • Intussusception
35
Q

What is a volvulus?

A

The complete twisting of bowel loop at mesenteric base around vascular pedicle
- Small bowel (infants)
- Caecum (elderly)

36
Q

What are some inflammatory bowel diseases?

A

Acute colitis:
- Infection
- Drug/toxin
- Chemo/radiotherapy

Chronic colitis:
- IBD
- TB

37
Q

What is a Clostridium difficle infection, its causes, diagnosis + treatment?

A

Pseudomembrane formation

  • Causes: (4C’s) Ciprofloxacilin, Cephalosporins, Clindamycin, Co-amoxiclav
  • Dx: Exotoxins (toxin stool assay)
  • Tx: Side room + vancomycin + metronidazole
38
Q

What are some causes of ischaemic colitis?

A
  • Arterial or venous occlusion
  • Small vessel disease (DM / Vasculitides)
  • Low flow rates (hypovolaemic shock -> hypoperfusion)
  • Obstruction
39
Q

What is the epidemiology and aetiology of Crohn’s disease?

A

Epi:
- Western populations
- Peak onset = 20s
- F>M
- White 2-5x > non-white
- Smoking worsen Sx

Aetiology:
- Unknown
- MZ twin concordance 50%

40
Q

What is the pathophysiology of Crohn’s disease?

Distribution, nature of lesions, bowel + first lesion

A

Distribution:
- Affects whole GI tract (mouth to anus)
- Terminal ileum + caecum
- SKIP LESIONS
- COBBLESTONE APPEARNCE (areas of healthy mucosa lie above diseased mucosa)

Nature of lesions:
- TRANSMURAL INFLAMMATION
- Non-caseating granulomas

Bowel:
- Thick bowel wall
- Narrow lumen

First lesion = aphthous ulcer
- Ulcers, fissures + abscesses

41
Q

What is the epidemiology + aetiology of Ulcerative colitis?

A

Epi:
- More common than Crohn’s
- White > non-white
- Peak age = 20-25yrs
- Smoking is protective factor

Aetiology:
- Unknown
- MZ twin concordance = 15%

42
Q

What is the pathophysiology of Ulcerative Colitis?

Distribution, nature of lesions + bowel

A

Distribution:
- Proximal extension from rectum + colon
- CONTINUOUS involvement of mucosa
- BACKWASH ILEITIS

Nature of lesions:
- Inflammation of superficial
- Confined to mucosa
- Shallow ulcers

Bowel:
- Normal bowel thickness

  • Pseudopolyps
43
Q

What are the clinical featuers of Crohn’s + Ulcerative colitis?

A

Crohn’s
- Intermittent diarrhoea
- Pain
- Fever

Ulcerative Colitis:
- Bloody diarrhoea
- Mucus
- Crampy abdominal pain, relieved by defecation

General:
- Angular stomatitis
- Anterior uveitis
- Erythema nodosum
- Pyoderma gangrenosum
- Arthritis

44
Q

What are some complications, investigations and management options for Crohn’s disease?

A

Cx:
- Strictures
- Fistulae
- Abscess formation
- Perforation

Ix:
- Systemic markers of inflammation
- ESR/CRP, Barium contrast, Endoscopy

Tx:
- Prednisolone (Mild attack)
- IV hydrocortisone + metronidazole (Severe attacks)
- Azathioprine, methotrexate, infliximab (additional)

45
Q

What are some complications, investigations + management options for ulcerative colitis?

A

Cx:
- Toxic megacolon
- Severe haemorrhage
- Adenocarcinoma (20-30x risk)

Ix:
- Rectal biopsy
- Flexible sigmoidoscopy
- AXR
- Stool Culture

Tx:
- Prednisolone + Mesalazine (Mild)
- Prednisolone + 5-ASA + Steroid enema BD (Moderate)
- Admit + NBM + IV fluids + IV hydrocortisone + rectal steroids (severe)
- 5-ASA first-line OR azathioprine second-line (remission)

46
Q

What are some features of diverticular disease?

A
  • High incidence in west (low fibre diet)
  • 90% = left colon
  • Asymptomatic +/- PR bleed
  • Presence of diverticulae = diverticulosis
  • Barium enema CT/endoscopy = BOWEL OUTPOUCHINGS (at weak points of bowel)
47
Q

What are some complications fo diverticular disease?

A
  • Divertculitis: Fever + peritonism
  • Gross perforation
  • Fistula
  • Obstruction
48
Q

What is carcinoid syndrome?

A
  • Diverse group of tumours of enterochromaffin cell origin
  • Produce 5-HT (serotonin)
  • Commonly found in bowel
  • Slow growing
49
Q

What symptoms are characteristic of carcinoid syndrome versus a carcinoid crisis?

A

Syndrome:
- Bronchoconstriction
- Flushing
- Diarrhoea

Crisis:
- Life threatening vasodilation
- Hypotension
- Tachycardia
- Bronchoconstriction
- Hyperglycaemia

50
Q

What are the investigations and management for carcinoid syndrome?

A

Ix:
- 24hr urine 5-HIAA (main metabolite of serotonin)

Tx:
- Octreotide (somatostatin analogue)

51
Q

What is the classification for gastric (neoplastic polyps) adenomas and their occurrence?

A
  • Tubular appearance (>75%)
  • Tubulovillous (25-75%)
  • Villous (>75%)
52
Q

What are some features of gastric adenomas?

A
  • Benign dysplastic lesions
  • Precursors to most adenocarcinomas
  • 50% of >50yrs in Western world
  • Mostly asymptomatic
53
Q

What are RFs for malignancy in a gastric adenoma?

A
  • Large size (>3.4cm)
  • Degree of dysplasia
  • Increased villous components
  • No. of polyps
54
Q

What proto-oncogenes require activation for the transformation of gastric adenomas to carcinomas?

A
  • KRAS
  • LOF mutations (p53)
55
Q

What are some non-neoplastic polyps?

A
  • Hamartomatous polyp
  • Hyperplastic polyp
  • Inflammatory
56
Q

What is the epidemiology + aetiology of colorectal cancer?

A

Epi:
- 2nd most common cause of cancer deaths in UK
- 60-79yrs
- IF <50yrs consider familial syndrome
- Western population
- 98% adenocarcinomas
- 45% in rectum

Aetiology:
- Diet (reduced fibre, increased fat)
- Lack of exercise
- Obesity
- Chronic IBD
- Familial syndromes

57
Q

What are protective against the development of colorectal cancer?

A

NSAIDs

58
Q

What are some clinical features and investigations for colorectal cancer?

A

Right sided tumours:
- IDA
- Weight loss

Left-sided tumours:
- Change in bowel habit
- Crampy LLQ pain

Ix:
- Proctoscopy/sigmoidoscopy/colonoscopy
- Barium enema
- Bloods

59
Q

What is used to monitor disease + response to therapy in colorectal cancer?

A

Carcinoembryonic antigen (CEA)

60
Q

What staging system is used in Colorectal cancer and what are the different types?

A

Duke’s Staging
- A: Confined to mucosa
- B1: Extends into muscularis propria
- B2: Transmural invasion
- C1: Extends to muscularis propria with LN metastasis
- C2: Transmural invasion with LN metastasis
- D: Distant metastasis

61
Q

What is the management of colorectal cancer?

A

SURGERY
- Rectal cancer/low sigmoid cancer <1-2cm above anal sphincter = abdomino-perineal resection
- Rectal cancer/low sigmoid cancer >1-2cm above anal sphincter = anterior resection
- Sigmoid cancer = sigmoid colectomy
- Descending colon = Left hemicolectomy
- Ascending colon = Right hemicolectomy
- Transverse colon = Extended right hemicolectomy

RADIOTHERAPY
CHEMOTHERAPY (in palliation): 5-FU - fluorouracil

62
Q

What is familial adnemomatous polyposis and its features?

A
  • Lots of polps ~1000
  • 70% AD mutation in adenomatous polyposis coli (APC) gene
  • 30% AR mutation in DNA mismatch repair genes
  • 100% will get cancer (adenocarcinoma) in 10-15yrs
63
Q

Where is the APC gene found and what type of gene is it?

A
  • Adenomatous Polyposis Coli
  • C5q1
  • Tumour suppressor gene
64
Q

What is Gardners syndome and its features?

A
  • Subtype of FAP (familial adenomatous polyposis)
  • AD
  • Has extra-intestinal features (e.g. osteomas of skull, dental caries, epidermoid cysts, desmoid tumours, unerupted supernumary teeth)
65
Q

What is Hereditary Non-Polyposis Colorectal Cancer/Lynch Syndrome (HNPCC) + its features?

A
  • AD mutation in DNA mismatch repair genes
  • Carcinomas usually in right colon
  • Fast progression to malignancy
  • Onset <50yrs
  • A/w extra-colonic cancers: Endometrial, Ovarian, Small bowel, stomach etc.
  • Fewer polyps than FAP
66
Q

What is the general treatment for familial syndromes causing colorectal cancer?

A
  • Regular monitoring
  • Total colectomy (eventually)

Pathology (Guide) (84 decks)

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