Conditions of Upper GIT Flashcards
What is the definition of GORD, including pathophysiology, risk factors, and classic triad of symptoms?
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
Which 3 medications are used in the management of GORD?
- Antacids (neutralize hydrochloric acid in oesophageal lumen)
- Proton pump inhibitors (PPIs) - inhibit proton pump (hydrogen-potassium-ATPase system) in stomach from producing gastric acid
- Histamine H2 receptor antagonists (inhibit histamine at H2 receptors on gastric parietal cells)
What is Barrett’s mucosa?
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
Describe gastritis, including the common causes and SSX
Definition:
- inflammation of the gastric lining
- chronic: prolonged inflammation causes lymphocytic infiltration of mucosa and epithelial damage
Causes:
- acute:
a. infective agents (salmonella, ecoli)
b. damage (alcohol, NSAIDs)
c. inhibited mucosal production (chemo/radiotherapy) - chronic
a. H.pylori 80% of cases
SSX:
- epigastric pain / discomfort
- nausea
- anorexia
- haematemesis (vomiting blood)
Describe the condition of pernicious anaemia associated with autoimmune gastritis, including pathophysiology and SSX
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
Describe the condition of peptic ulceration, including common sites, common causes, and classic SSX
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)
What is the mechanism of peptic ulceration caused by H.pylori infection?
H.pylori responsible for the vast majority of peptic ulcers
- produces urease to survive in low pH
- burrow into mucosa (helical structure and flagella)
- release bacterial toxins that damage mucosa
- recruit immune cells that release inflammatory cytokines and cause further damage
What are the management strategies for peptic ulcers?
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
Describe coeliac disease, including common sites, pathophysiology, sources of gluten, and SSX
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
What are tests for coeliac disease?
- blood test (elevated IgA)
- endoscopy
What are complications associated with coeliac disease?
- malabsorption and nutritional deficiencies
- ulcerative jujeno-ileitis can perforate, bleed and scar
- increased risk of GIT cancers
- skin disorders
Describe the condition of oesophageal cancer, including incidence and mortality, aetiology and risk factors, types, and classic triad of SSX
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:
- dysphagia
- odnyophagia
- weight loss
SSX other:
- anaemia
- blood in stool (melena) and vomit (haematemesis)
Describe the condition of stomach cancer including incidence, prognosis, aetiology, pathophysiology, and SSX
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)