Conditions of Upper GIT Flashcards

1
Q

What is the definition of GORD, including pathophysiology, risk factors, and classic triad of symptoms?

A

Definition:
Gastro-oesophageal reflux disease (also called reflux oesophagitis or heartburn)

Pathophys:

  • Passage of gastric contents from the stomach through the lower oesophageal sphincter up into the lower oesophagus
  • exposure to low pH gastric juice causes inflammation and damage to oesophageal mucosa
  • metaplasia can occur (Barrett’s mucosa), where the normal stratified squamous epithelium in oesophagus is replaced by simple columnar (pre-malignant change)

Risk factors:

  • increased intra-abdominal pressure (obesity, pregnancy, lifting and bending)
  • impaired mucosal defence (tobacco, alcohol)
  • caffeine and fatty foods

Classic triad SSX:

  • heartburn (epigastric / retrosternal pain, agg. by eating, bending and lifting, lying down)
  • dyspepsia
  • dysphagia / odnyophagia
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2
Q

Which 3 medications are used in the management of GORD?

A
  1. Antacids (neutralize hydrochloric acid in oesophageal lumen)
  2. Proton pump inhibitors (PPIs) - inhibit proton pump (hydrogen-potassium-ATPase system) in stomach from producing gastric acid
  3. Histamine H2 receptor antagonists (inhibit histamine at H2 receptors on gastric parietal cells)
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3
Q

What is Barrett’s mucosa?

A

A pre-malignant metaplasia of oesophageal mucosa

  • mucosa changes from stratified squamous epithelium to simple columnar epithelium
  • changes occur because of chronic exposure to low pH gastric juice from stomach
  • pre-malignant change that must be monitored with regular endoscopies to monitor development into oesophageal cancer
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4
Q

Describe gastritis, including the common causes and SSX

A

Definition:

  • inflammation of the gastric lining
  • chronic: prolonged inflammation causes lymphocytic infiltration of mucosa and epithelial damage

Causes:

  1. acute:
    a. infective agents (salmonella, ecoli)
    b. damage (alcohol, NSAIDs)
    c. inhibited mucosal production (chemo/radiotherapy)
  2. chronic
    a. H.pylori 80% of cases

SSX:

  • epigastric pain / discomfort
  • nausea
  • anorexia
  • haematemesis (vomiting blood)
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5
Q

Describe the condition of pernicious anaemia associated with autoimmune gastritis, including pathophysiology and SSX

A

Autoimmune gastritis:
- antibodies attack parietal cells in the gastric pits of the stomach

Pernicious anaemia:

  • damage to parietal cells inhibits production of IF (intrinsic factor)
  • without IF, B12 can’t be absorbed by the small intestine
  • without adequate B12, body produces overlarge red blood cells (megaloblastic anaemia) which cannot transport iron properly

SSX:

  • all normal SSX of anaemia
  • also neuro deficits caused by demyelinating lesions
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6
Q

Describe the condition of peptic ulceration, including common sites, common causes, and classic SSX

A

Definition:
- ulceration in stomach or duodenum

Common sites:

  • usually duodenal (most common: D1)
  • sometimes gastric (most common: lesser curvature)

Causes:

  • H.pylori: most common cause
  • NSAIDs (reduce prostaglandin and therefore mucous secretion)
  • aspirin (damages cell membranes)
  • tobacco (damages mucosa and reduces healing rate)

SSX:
- epigastric pain (recurrent periods of several weeks)
- nausea, vomiting
- anorexia
- dyspepsia
(can be asymptomatic, especially in elderly)

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7
Q

What is the mechanism of peptic ulceration caused by H.pylori infection?

A

H.pylori responsible for the vast majority of peptic ulcers

  1. produces urease to survive in low pH
  2. burrow into mucosa (helical structure and flagella)
  3. release bacterial toxins that damage mucosa
  4. recruit immune cells that release inflammatory cytokines and cause further damage
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8
Q

What are the management strategies for peptic ulcers?

A

General:

  • stop smoking
  • monitor NSAID and aspirin use
  • endoscopic reviews

With H pylori:
- antibiotics

Without H pylori:
- H2 receptor antagonists or proton pump inhibitors (PPIs) both dramatically reduce secretion of gastric juice

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9
Q

Describe coeliac disease, including common sites, pathophysiology, sources of gluten, and SSX

A

Definition:
- genetic hypersensitivity to gluten or gliadin

Common sites:

  • proximal bowel
  • esp. duodenal-jujenal flexure

Pathophysiology:

  • cell mediated (type 4) hypersensitivity reaction
    1. immune cells infiltrate lamina propria
    2. T lymphocytes release inflammatory cytokines
    3. plasma cells produce IgA antibodies
    4. damage to mucosa and atrophy of villi occurs

Sources of gluten:

  • wheat
  • oats
  • barley
  • rye

SSX:

  • abdo discomfort
  • diarrhea
  • excessive flatus
  • weight loss
  • fatigue
  • amenorrhea
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10
Q

What are tests for coeliac disease?

A
  • blood test (elevated IgA)

- endoscopy

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11
Q

What are complications associated with coeliac disease?

A
  • malabsorption and nutritional deficiencies
  • ulcerative jujeno-ileitis can perforate, bleed and scar
  • increased risk of GIT cancers
  • skin disorders
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12
Q

Describe the condition of oesophageal cancer, including incidence and mortality, aetiology and risk factors, types, and classic triad of SSX

A

Incidence:
- very rare (1% of GIT cancers)

Mortality:
- usually fatal

Aetiology:

  • not well understood
  • smoking and Barrett’s mucosa risk factors

Types:

  • squamous cell carcinomas (middle 1/3)
  • adenocarcinoma (lower 1/3, usually from Barrett’s mucosa)

SSX Classic Triad:

  1. dysphagia
  2. odnyophagia
  3. weight loss

SSX other:

  • anaemia
  • blood in stool (melena) and vomit (haematemesis)
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13
Q

Describe the condition of stomach cancer including incidence, prognosis, aetiology, pathophysiology, and SSX

A

Incidence:
- rare in people under 50

Prognosis:
- good: 85% 5 year survival if detected before lymph spread

Aetiology:

  • high sodium diet a risk factor
  • GIT conditions (H pylori infections, chronic gastritis)

Pathophysiology:

  • adenocarcinomas 95% of all stomach cancers (usually in pylorus or antrum)
  • mucosal change earliest sign

SSX:

  • asymptomatic until late stage
  • can mimic gastric ulcers
  • dyspepsia
  • nausea
  • weight loss
  • anorexia

late SSX:
- blood in stool (melena) or vomit (haematemesis)

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