GI pathology 1 Flashcards

1
Q

Define gastritis

A

Gastritis is the inflammation of the stomach

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2
Q

Recall clinical consequences of gastric H pylori infection.

A
  • a minority of patients develop symptomatic gastritis.
  • a minority of patients develop a peptic ulcer.
  • a small minority of patients develop gastric carcinoma.
  • a very small minority of patients develop gastric lymphoma.
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3
Q

Define peptic ulcer

A

A peptic ulcer is a full thickness breach in the mucosa of the lower oesophagus, stomach or duodenum which fails to heal over a reasonable period of time

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4
Q

Describe how a chronic gastric ulcer is a good example of chronic inflammation and describe its complications.

A

Peptic ulcers are a good example of chronic inflammation in which there is simultaneous:
• persistent tissue injury and destruction at the surface.
• an on-going inflammatory response to limit the damage.
- the main inflammatory cells are macrophages, lymphocytes and plasma cells.
• attempts to organise and heal by fibrosis (scarring).

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5
Q

Describe the pathology of gastric cancer, in particular that the two most common types are intestinal-type adenocarcinoma and diffuse-type adenocarcinoma.

A

• intestinal-type adenocarcinomas - show gland formation, lined by mucus-secreting cells. Better prognosis than diffuse-type (but still a poor 5 year survival). Tend to occur in older individuals.
• diffuse-type adenocarcinomas - consist of ‘signet ring’ cells, with a diffuse pattern of infiltration. Very aggressive
→ very bad prognosis. Tends to occur in a younger age group

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6
Q

Describe the causes/ risk factors of GORD

A
  • smoking, alcohol and coffee consumption (lowers oesophageal sphincter tone).
  • hiatus hernia
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7
Q

Describe the complications of GORD

A

oesophagitis, Barrett’s oesophagus, stricture and bleeding

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8
Q

Define Barrett’s oesophagus

A

Metaplasia that occurs as an adaptive response to prolonged injury caused by GOR.

Barrett’s oesophagus is asymptomatic. Most cases are identified when patients undergo

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9
Q

Risk factors for oesophageal cancer

A

smoking

alcohol consumption

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10
Q

Explain the role of anti-TTG and anti-EMA antibodies in the pathogenesis and diagnosis of coeliac disease

A

Gluten is digested by luminal and brush-border enzymes in the small intestine into amino acids and peptides, including a 33-amino acid gliadin peptide. Gliadin is deamidated (deamidation = removal of an amide group from an organic compound) in the mucosa by tissue transglutaminases (tTG).

In addition to the cell mediated immune response, there is also a humoral immune response with generation of antigliadin, antiendomysial and antiTTG antibodies. These antibodies are useful diagnostically.

In individuals with the HLA-DQ2 and HLA-DQ8 haplotypes, the deamidated gliadin closely fits the MHC II grooves and is presented to T helper cells by antigen presenting cells.

This initiates a Th2- predominant immune response which generates cytotoxic T cells against gliadin.

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11
Q

Describe the changes seen in a duodenal biopsy from a patient with coeliac disease and explain the pathophysiology of the changes.

A

The biopsy should show villous atrophy, crypt hyperplasia and prominent intraepithelial lymphocytes

The T cells damage and destroy epithelial cells resulting in progressive villous atrophy.

As a result, the crypts become hyperplastic to compensate for the cell loss.

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12
Q

Describe the complications of coeliac disease.

A

malabsorption
osteopenia/osteoporosis
dermatitis herpetiformis
lymphoma

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13
Q

Describe the pathophysiology of gallstone formation

A

Normally cholesterol is solubilised in bile as a micelle with bile salts.
An imbalance between the proportions of cholesterol and bile salts leads to precipitation of the excess component as gallstones.

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14
Q

Describe and discuss some important complications of gallstones

A

biliary colic- obstruction of cystic duct
acute cholecystitis- result of ischaemia,
obstructive jaundice- obstruction of common bile duct (choledocolithiasis will cause jaundice)
ascending cholangitis- inflammation of CBD
acute pancreatitis- obstruction of the Ampulla of Vater
gallstone ileus- large stone causing small bowel obstruction- enters bowel via a fistula between gallbladder and small bowel loop

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15
Q

Most common type of pancreatic cancer

A

adenocarcinomas arising from the ductal epithelial cells.

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16
Q

Explain why cancer of the head of pancreas may present with obstructive jaundice and why the prognosis is generally poor.

A
  • they tend to present with obstructive jaundice. The tumour compresses the common bile duct as it passes through the head of the pancreas, so that bile is unable to drain into the duodenum.
  • other features include weight loss and mid-epigastric pain (often radiating to the back).

Usually diagnosed at a later stage so prognosis is poor.

17
Q

Px of gastric cancer

A
  • history of new-onset dyspepsia (especially in a patient >55yr).
  • unintended weight loss.
  • progressive dysphagia.
  • vomiting.
  • Virchow’s node in the lek supraclavicular fossa may be palpable (Troisier’s sign)
18
Q

RFs for gastric cancer

A
chronic H pylori infection
EBV infection
diet- nitrates/nitrites
cigarettes
alcohol
AI gastritis
inherited syndromes
19
Q

Pathogenesis of GORD

A

In GOR there is regurgitation of acidic gastric contents into the lower oesophagus. The acid injures the squamous epithelium lining the oesophagus and results in inflammation (reflux oesophagitis)

20
Q

Explain the place of Barrett’s oesophagus in the metaplasia-dysplasia-carcinoma sequence

A

squamous epithelium- oesophagitis- barrett oesophagus- dysplasia- adenocarcinoma

21
Q

Describe the two main types of oesophageal cancer

A

Adenocarcinoma and squamous cell carcinoma

22
Q

Recall the important risk factors for gallstones

A
female
obesity 
middle aged
Fhx 
Crohn's 
haemolytic anaemia