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HISTOPATHOLOGY PATH GUIDE > GI > Flashcards

GI Flashcards

1
Q

What type of epithelium is found in the oesophagus?

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 is the commonest cause of oesophagitis?

A

Reflux oesophagitis (GORD).

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3
Q

What are the complications of reflux oesophagitis?

A

Ulceration, haemorrhage leading to haematemesis/melaena, Barrett’s oesophagus, stricture, perforation.

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4
Q

How is GORD classified

A

Los Angeles Classification of severity

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5
Q

How is reflux oesophagitis (GORD) managed?

A

Lifestyle changes (stop smoking, weight loss), PPI/H2 receptor antagonists.

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6
Q

What is Barrett’s oesophagus?

A

Intestinal metaplasia of squamous mucosa to columnar epithelium (with goblet cells) following chronic GORD. -> upwards migration of the SCJ

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7
Q

What percentage of people with symptomatic GORD develop Barrett’s oesophagus?

A

10%

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8
Q

What can Barrett’s oesophagus lead to?

A

Adenocarcinoma: metaplasia → dysplasia → cancer.

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9
Q

Presence of what feature confers a higher risk of development into cancer

A

NB Presence of goblet cells is intestinal metaplasia – confers even higher
risk of development into Ca .

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10
Q

Which part of the oesophagus does oesophageal adenocarcinoma usually affect?

A

the distal 1/3 of the oesophagus. (Associated with Barrett’s oesophagus)

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11
Q

What are the risk factors for oesophageal adenocarcinoma?

A

Barrett’s oesophagus, smoking, obesity, prior radiation therapy.

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12
Q

Which population is most commonly affected by oesophageal adenocarcinoma?

A

Caucasians, M»F.

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13
Q

What are the risk factors for squamous cell oesophageal carcinoma?

A

Alcohol and smoking (most common), achalasia of cardia, Plummer-Vinson syndrome, nutritional deficiencies, nitrosamines, HPV (in high prevalence areas).

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14
Q

Which population is most commonly affected by squamous cell oesophageal carcinoma?

A

Afro-Caribbeans, M>F.

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15
Q

Epidemiology of squamous cell oesophageal carcinoma

A

6x more common in Afro-Caribbeans, M>F

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16
Q

Where is squamous cell oesophageal carcinoma usually found?

A

Middle 1/3 (50%), Upper 1/3 (20%), Lower 1/3 (30%).

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17
Q

What are the common presentations of squamous cell oesophageal carcinoma?

A

Progressive dysphagia (solids then fluids), odynophagia (pain), anorexia, severe weight loss.

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18
Q

Prognosis of squamous cell oesophageal carcinoma

A

Rapid growth and early spread (to LNs, liver and directly to proximal
structures) —> palliative care

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19
Q

What causes oesophageal varices and how do they present?

A

Engorged dilated veins, Usually due to portal hypertension (back pressure). Patient vomits large volumes of blood.

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20
Q

How are oesophageal varices managed in an emergency?

A

Emergency endoscopy followed by sclerotherapy/banding.

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21
Q

What type of epithelium lines the stomach?

A

Gastric mucosa ((NO GOBLET CELLS), with columnar epithelium (mucin secreting) and glands.

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22
Q

What do parietal cells in the stomach secrete?

A

HCl and intrinsic factor (IF).

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23
Q

What do chief cells in the stomach secrete?

A

Pepsinogen.

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24
Q

What are the characteristics of acute gastritis?

A

Presence of neutrophils due to insults such as aspirin, NSAIDs, corrosives (bleach), acute H. pylori infection, severe stress (burns).

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25
Q

What are the characteristics of chronic gastritis?

A

Presence of lymphocytes and plasma cells due to insults such as H. pylori (tends to be antral), autoimmune conditions (e.g., pernicious anaemia), alcohol, smoking.

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26
Q

What are the complications of chronic gastritis?

A

May lead to gastric ulcer formation, induce lymphoid tissue in stomach increasing future risk of MALT lymphoma due to H.pylori, and result in intestinal metaplasia → dysplasia → cancer.

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27
Q

What defines a gastric ulcer?

A

A breach through the muscularis mucosa into the submucosa (otherwise it’s an erosion, not an ulcer).

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28
Q

What are the symptoms of a gastric ulcer?

A

Epigastric pain, possibly with weight loss. Pain is worse with food and relieved by antacids.

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29
Q

What are the risk factors for gastric ulcer?

A

H. pylori infection, smoking, NSAIDs, stress, delayed gastric emptying. Occurs mainly in elderly.

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30
Q

How is a gastric ulcer diagnosed?

A

Biopsy for H. pylori histology status. Punched out lesion with rolled margins.

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31
Q

What are the complications of a gastric ulcer?

A

Anaemia (IDA), perforation (seen on erect CXR), and malignancy.

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32
Q

Where is the incidence of gastric cancer higher and what is the primary type of tumour?

A

Higher incidence in Japan, China where more fermented/pickled food is eaten. >95% of tumours in the stomach are adenocarcinomas.

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33
Q

What are the types of gastric adenocarcinoma?

A

Intestinal type (well differentiated, goblet cells present following intestinal metaplasia) and diffuse type (poorly differentiated, no gland formation – includes signet ring cell carcinoma).

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34
Q

What causes gastric (MALT) lymphoma and how is it managed?

A

Caused by H. pylori – chronic antigen stimulation. Managed by removing the cause (H. pylori) using triple therapy: PPI, Clarithromycin, and Amoxicillin.

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35
Q

How common are duodenal ulcers compared to gastric ulcers?

A

Duodenal ulcers are 4 times more common than gastric ulcers.

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36
Q

What are the symptoms of a duodenal ulcer?

A

Epigastric pain, worse at night, relieved by food and milk.

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37
Q

What age group is most commonly affected by duodenal ulcers?

A

Younger adults.

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38
Q

What are the risk factors for duodenal ulcers?

A

H. pylori, drugs, aspirin, NSAIDs, steroids, smoking, increased acid secretion.

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39
Q

What are the complications of duodenal ulcers?

A

Anaemia (IDA) and perforation (seen on erect CXR).

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40
Q

What is coeliac disease and what are its genetic associations?

A

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

41
Q

In which populations is coeliac disease commonly seen?

A

Young children and Irish women.

42
Q

What are the symptoms of coeliac disease?

A

Symptoms of malabsorption: Steatorrhoea, abdominal pain, bloating, nausea and vomiting, weight loss, fatigue, iron deficiency anaemia, failure to thrive, rash - dermatitis herpetiformis.

43
Q

What condition is coeliac disease associated with that may require extra vaccines?

A

Hyposplenism.

44
Q

What is the differential diagnosis for coeliac disease?

A

Tropical sprue.

45
Q

What serological tests are used for diagnosing coeliac disease?

A

Anti-endomysial antibody (best sensitivity and specificity), anti-tissue transglutaminase (IgA), anti-gliadin (poor marker of disease control).

46
Q

What is the gold standard investigation for diagnosing coeliac disease?

A

Upper GI endoscopy and duodenal biopsy showing villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes while eating gluten. Normal villous:crypt ratio is ~ 2:1.

47
Q

What is the management for coeliac disease?

A

Gluten-free diet.

48
Q

What percentage of untreated coeliac disease patients progress to Duodenal T-cell lymphoma (EATL)?

A

Around 10%.

49
Q

What are common congenital diseases of the duodenum in paediatric patients?

A

Atresia, stenosis, duplication, imperforate anus.

50
Q

What is Hirschsprung’s disease and what is its prevalence in males?

A

Absence of ganglion cells in myenteric plexus. It affects 80% males.

51
Q

What are the symptoms and signs of Hirschsprung’s disease in newborns?

A

Symptoms and signs of obstruction, failure to pass meconium within first 48 hours.

52
Q

What syndrome is Hirschsprung’s disease associated with?

A

Down’s syndrome (2%).

53
Q

What is the genetic association with Hirschsprung’s disease?

A

RET proto-oncogene on chromosome 10+.

54
Q

What is the gold standard investigation for Hirschsprung’s disease?

A

Full thickness biopsy showing hypertrophied nerve fibres and no ganglia.

55
Q

What is the treatment for Hirschsprung’s disease?

A

Resection of affected (constricted) segment and pull-through of normal functioning bowel.

56
Q

What are common causes of mechanical bowel obstruction?

A

Constipation, diverticular disease (v.common), adhesions, herniation, external mass (e.g. fetus, tumour, aneurysm, foreign body), volvulus, intussusception.

57
Q

What is volvulus and which areas are commonly affected?

A

Complete twisting of bowel loop at mesenteric base around vascular pedicle. Commonly affects small bowel (infants), sigmoid > caecal (elderly).

58
Q

What are common causes of acute colitis?

A

Infection (bacterial, viral, protozoal etc.), drug/toxin (especially antibiotics), chemo/radiotherapy.

59
Q

What are common causes of chronic colitis?

A

IBD: Crohn’s disease and ulcerative colitis, TB.

60
Q

What causes ischaemic colitis?

A

Arterial or venous occlusion, small vessel disease, low flow states (e.g. due to hypovolaemic shock), obstruction.

61
Q

What are common ‘Watershed areas’ affected by ischaemic colitis?

A

Splenic flexure (SMA transition to IMA), rectosigmoid (IMA transition to internal iliac).

62
Q

What are the epidemiological features of Crohn’s Disease?

A

Western populations, peak onset in 20’s, more common in females, white individuals 2-5x more than non-white individuals, smoking worsens symptoms.

63
Q

What are the epidemiological features of Ulcerative Colitis?

A

Slightly more common than Crohn’s, more common in white individuals, peak age is 20-25 years, smoking improves symptoms and is protective.

64
Q

What is the aetiology of Crohn’s Disease?

A

Unknown. MZ twin concordance 50%. ‘Hygiene hypothesis’ suggests less food contamination leads to less enteric infection, inadequate development of mucosal immune response, and exaggerated immune response to pathogens that would cause self-limiting disease.

65
Q

What is the aetiology of Ulcerative Colitis?

A

Unknown. MZ twin concordance 15%.

66
Q

What is the distribution and nature of lesions in Crohn’s Disease?

A

Affects the whole GI tract (mouth to anus), most common in terminal ileum and caecum. Patchy distribution leading to ‘skip lesions’. Areas of healthy mucosa lie above diseased mucosa creating a ‘cobblestone appearance’. Transmural inflammation, non-caseating granulomas, fistula/fissure formation common. First lesion is an ‘aphthous ulcer’, which are deep ‘rosethorn ulcers’ that can join to form serpentine ulcers.

67
Q

What is the distribution and nature of lesions in Ulcerative Colitis?

A

Extends proximally from rectum with continuous involvement of mucosa. Small bowel not affected unless very severe pancolitis causes ‘backwash ileitis’. Inflammation is superficial and confined to mucosa. No granulomas, fissures, fistulae, or strictures. Islands of regenerating mucosa bulge into lumen creating pseudopolyps, which can fuse to form mucosal bridges.

68
Q

What are the clinical features of Crohn’s Disease?

A

Usually presents with intermittent diarrhoea, pain, and fever.

69
Q

What are the clinical features of Ulcerative Colitis?

A

Associated more with bloody diarrhoea and mucus. Crampy abdominal pain relieved by defecation.

70
Q

What are the extra-GI manifestations common to both Crohn’s Disease and Ulcerative Colitis?

A

Malabsorption & iron deficiency anaemia leading to angular stomatitis. Eyes: Anterior uveitis, conjunctivitis. Skin: Erythema nodosum, pyoderma gangrenosum, erythema multiforme, digital clubbing. Joints: Migratory asymmetrical polyarthropathy of large joints, sacroiliitis, myositis, ankylosing spondylitis. Liver: Pericholangitis, primary sclerosing cholangitis (more common in UC than CD), steatosis.

71
Q

What are the complications of Crohn’s Disease?

A

Strictures requiring bowel resection (often recurrent), fistulae, abscess formation, perforation

72
Q

What are the complications of Ulcerative Colitis?

A

severe haemorrhage, Toxic megacolon leading to perforation (damage to muscularis propria with disruption of neuromuscular function leading to colonic dilatation), 30% require colectomy within 3 years for uncontrollable symptoms, adenocarcinoma (20-30x increased risk).

73
Q

What investigations are used for Crohn’s Disease?

A

Systemic markers of inflammation such as ESR, CRP, barium contrast, endoscopy.

74
Q

What investigations are used for Ulcerative Colitis?

A

Rectal biopsy, flexible sigmoidoscopy or colonoscopy, AXR, stool culture.

75
Q

What is the management for Crohn’s disease?

A

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

76
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)

77
Q

What antibiotics are associated with Clostridium difficile infections?

A

The 4 Cs of C. diff: Ciprofloxacin, Cephalosporins, Co-amoxiclav, and Clindamycin.

78
Q

How do Clostridium difficile infections occur?

A

Antibiotics kill off commensals allowing C. diff to flourish. Its exotoxins cause pseudomembranous colitis.

79
Q

How are Clostridium difficile infections investigated?

A

Stool culture/toxin assay.

80
Q

What is the management for Clostridium difficile infections?

A

Vancomycin PO (not absorbed well so accumulates in gut), isolation in a side room, and use of Metronidazole.

81
Q

What are other common bacteria causing GI infections?

A

Campylobacter, Salmonella, Shigella spp.

82
Q

What is the incidence and main cause of diverticular disease in the West?

A

High incidence in the West likely due to low fiber diet.

83
Q

What causes the outpouchings in diverticular disease?

A

High intraluminal pressure results in outpouchings at ‘weak points’ in the wall of the bowel (seen on barium enema CT or endoscopy).

84
Q

Where do 90% of diverticula occur?

A

90% occur in the left colon.

85
Q

What is the difference between diverticulosis and diverticulitis?

A

Presence of diverticula is diverticulosis (not diverticulitis).

86
Q

What are the symptoms of diverticulosis?

A

Often asymptomatic, sometimes PR bleed.

87
Q

What is the management for mild diverticular attacks?

A

Prednisolone.

88
Q

What is the management for severe diverticular attacks?

A

IV hydrocortisone, metronidazole.

89
Q

What additional therapies are available for diverticular disease?

A

Azathioprine, methotrexate, infliximab.

90
Q

What is the management for mild diverticulitis?

A

Prednisolone + mesalazine (5 ASA).

91
Q

What is the management for moderate diverticulitis?

A

Prednisolone + 5-ASA + steroid enema twice daily.

92
Q

What is the management for severe diverticulitis?

A

Admit, NBM, IV fluids and IV hydrocortisone, rectal steroids.

93
Q

What is the management for remission of diverticular disease?

A

All 5-ASA (1st line), azathioprine (2nd line).

94
Q

What are the complications of diverticulitis?

A

Fever and peritonism, gross perforation, fistula, obstruction (due to fibrosis).

95
Q

What are carcinoid tumors and where are they commonly found?

A

Diverse group of tumors of enterochromaffin cell origin that produce 5-HT (serotonin). Commonly found in the bowel, but also in the lung, ovaries, and testes.

96
Q

What are the symptoms of carcinoid syndrome?

A

Bronchoconstriction, flushing, diarrhea.

97
Q

What are the symptoms of a carcinoid crisis?

A

Life-threatening vasodilatation, hypotension, tachycardia, bronchoconstriction, hyperglycemia.

98
Q

What investigation is used for carcinoid syndrome?

A

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

99
Q

What is the management for carcinoid syndrome?

A

Octreotide (somatostatin analogue).

HISTOPATHOLOGY PATH GUIDE (1 decks)

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