systematic and cellular pathology

• What are the main topics covered in the study material regarding upper gastrointestinal tract disorders?


  Oesophagus, stomach, liver, and gallbladder
• What is the primary focus of the study material?

  Disorders of the upper gastrointestinal tract and hepatic & biliary pathology
• What is the definition of epithelial erosions?


  Superficial breaches of the mucosa
• What are the pathological changes associated with GORD?


  Hyperemia, granular mucosa, mucosal damage, erosions, and ulcers
• What are common causes of GORD?


  Obesity, fatty food consumption, smoking, alcohol, coffee, chocolate, pregnancy, hiatal hernia, NSAIDs
• What symptoms are associated with GORD?


  Burning pain after eating, regurgitation, dysphagia, intolerance to certain foods
• How is GORD diagnosed?


  Through endoscopy and biopsy of tissues
• What does the Los Angeles Grading classify?


  It classifies the severity of GORD based on endoscopic findings
• What does the Lyon Consensus consider in GORD diagnosis?


  Acid reflux, acid exposure time, and motor function of the oesophageal gastric junction
• What is the treatment for GORD?


  Antacids, H2 receptor antagonists, proton pump inhibitors, lifestyle changes, and surgery
• What lifestyle changes can help manage GORD?


  Avoiding certain foods, elevating the head while sleeping, and not eating before bedtime
• What are potential complications of GORD?


  Haemorrhage, fibrosis, stricture, metaplasia, Barrett’s oesophagus
• What is acute gastritis characterized by?


  Inflammation of gastric mucosa without damage to deeper layers
• What are the clinical signs of acute gastritis?


  Vague abdominal discomfort, epigastric tenderness, and possible bleeding
• What distinguishes chronic gastritis from acute gastritis?


  Chronic gastritis may be asymptomatic and involves lymphocytes and plasma cells
• What is the role of Helicobacter pylori in gastritis?


  It is associated with multifocal atrophic gastritis and can lead to chronic inflammation
• What is autoimmune atrophic gastritis characterized by?


  Destruction of parietal cells leading to reduced acid and intrinsic factor production
• What is the treatment for H. pylori infection?


  Triple-therapy regimen including a proton pump inhibitor and antibiotics
• What are the symptoms of H. pylori infection?


  Anorexia, nausea, vomiting, food intolerance, epigastric pain, gastric bleeding
• How does NSAID use lead to gastritis?


  By inhibiting prostaglandin synthesis, which protects the gastric mucosa
• What are the histological features of acute gastritis?


  • Hyperemia
  • Presence of neutrophils
  • Superficial mucosal damage
  • Possible ulcers and erosions
• What are the histological features of chronic gastritis?


  • Absence of neutrophils
  • Presence of lymphocytes and plasma cells
  • Patchy mucosal necrosis
  • Possible intestinal metaplasia
• Compare and contrast acute and chronic gastritis.

  Acute Gastritis:

  • Rapid onset
  • Neutrophils present
  • Often heals spontaneously

  
  

  Chronic Gastritis:

  • Long-term condition
  • Lymphocytes and plasma cells present
  • Can be asymptomatic
• What is the immune response to H. pylori infection?


  • Activation of immune cells
  • Production of antibodies
  • Inflammation in the gastric mucosa
  • Potential for chronic gastritis
• What mechanisms does H. pylori use to survive in the stomach?


  • Produces urease to neutralize stomach acid
  • Adheres to gastric epithelium
  • Evades immune response
• How is H. pylori diagnosed?


  • Endoscopy with biopsy
  • Breath tests
  • Blood tests for antibodies
• What are the treatment options for H. pylori infection?


  • Triple therapy: PPI + amoxicillin + clarithromycin/metronidazole
  • Antacids and cytoprotectants
  • Dietary modifications
• What is the role of prostaglandins in gastric health?


  • Stimulate mucus and bicarbonate secretion
  • Protect gastric mucosa
  • Regulate acid secretion
• What are the four major changes in renal function due to renal disease?

  Impaired blood flow, Uraemia, Nephrotic Syndrome, Nephritic Syndrome
• What causes most types of Glomerulonephritis (GN)?

  Injury from antigen-antibody complexes
• What is the result of increased glomerular capillary permeability in GN?

  Increased protein in urine
• What are podocytes?

  • Visceral epithelial cells
  • Form inner wall of Bowman’s capsule
  • Wrap around capillary blood vessels
  • Create filtration slits
• What are mesangial cells responsible for?

  • Specialized smooth muscle cells
  • Regulate blood flow through glomerular capillaries
• What is the staining pattern in post-infectious GN?

  Granular staining pattern of IgG deposits
• What does the linear staining pattern in Goodpasture syndrome indicate?

  Deposits of IgG along the basement membrane
• What are the "spikes" seen in membranous glomerulonephritis?

  Intervening matrix of basement membrane
• How can allergic reactions to streptococci bacteria affect the kidneys?

  They may cause glomerular damage
• What are common symptoms of Glomerulonephritis?

  Proteinuria and haematuria
• What is the significance of proteinuria greater than 3.5g/24h?

  Indicates nephrotic syndrome
• What can cause pre-renal acute renal failure?

  Reduced circulating volume