pt19 Flashcards
(50 cards)
What prognostic factor most influences prostate cancer outcome?
Stage at diagnosis
How many layers does the GI tract wall have, and what are they?
Four layers—mucosa, submucosa, muscularis (inner circular & outer longitudinal), and serosa
What epithelium lines the oesophagus?
Non-keratinised stratified squamous epithelium
What is the “functional” lower oesophageal sphincter (LES)?
An acute musculomucosal angle plus mucosal folds at the gastro-oesophageal junction that prevent reflux
By what mechanism is a food bolus propelled down the oesophagus?
Coordinated peristalsis under control of the oesophageal (enteric) plexus
What is dysphagia and what are its main causes?
Difficulty swallowing; caused by obstructive rings/strictures (scar tissue), carcinoma (late stage), stroke, or neurological disease
Define oesophagitis and list its key causes.
Inflammation of oesophageal mucosa; from GORD (reflux HCl), CNS depressants, pregnancy, alcohol relaxing LES
What histological changes occur in acute reflux oesophagitis?
Neutrophil infiltration into squamous epithelium and mucosal hyperaemia
What is Barrett’s oesophagus and why is it important?
Replacement of squamous mucosa by metaplastic columnar epithelium in chronic GORD (10% cases), a precursor to carcinoma
How is oesophageal inflammation visualized endoscopically?
Gastroscopy shows erythematous, friable mucosal patches at the LES
What are the three main secretagogues for gastric acid?
Gastrin (endocrine), histamine (paracrine), and acetylcholine (neural)
What volume changes can the stomach undergo?
From an empty ~75 mL to a post-prandial capacity of ~2 L
Name the protective factors that guard the gastric mucosa.
Mucus layer, bicarbonate secretion, rich blood flow
Define gastritis and differentiate acute vs. chronic.
Gastric mucosal inflammation; acute shows neutrophils, chronic shows lymphocytes, atrophy, metaplasia
List the four principal aetiologies of gastritis.
NSAIDs (↓ mucus/HCO₃⁻), H. pylori infection, alcohol/tobacco (↑ acid, ↓ blood flow), autoimmune parietal-cell loss
How is H. pylori gastritis diagnosed?
Urea-breath test, stool antigen, or biopsy with rapid urease assay
What complications arise from untreated gastritis?
Mucosal erosion → ulceration/perforation (peritonitis), bleeding, strictures, cancer risk
Outline first-line pharmacological treatments for gastritis.
Antacids (Al/Mg hydroxide), H₂-blockers, proton-pump inhibitors; add antibiotics for H. pylori
What endoscopic finding confirms gastric perforation?
Visible hole in gastric wall with free air/fluid on CT or serosal inspection
What are the three main categories of malabsorption syndromes in the small intestine?
Defective intraluminal digestion, mucosal (absorptive) defects, and disorders reducing small-intestinal surface area
Give three causes of defective intraluminal digestion.
Pancreatic insufficiency (e.g., pancreatitis, cystic fibrosis), biliary insufficiency (no bile for fat emulsification), Small Intestinal Bacterial Overgrowth (SIBO)
What is Small Intestinal Bacterial Overgrowth (SIBO)?
Excessive colonic-type bacteria in the small intestine due to impaired peristalsis, loss of gastric acidity, ileocaecal valve failure, or immunodeficiency
Name four causes of mechanical small-intestinal obstruction.
Herniation (gut wall defect), surgical adhesions (post-peritonitis scars), intussusception (telescoping), volvulus (twisting from malrotation)
Which hernia type commonly causes small-bowel obstruction?
Loop of intestine protrudes through abdominal wall weakness, strangulates, and blocks lumen & blood supply