Gastro Flashcards
Gastro-oesophageal junction 2 features
Epithelial transition: change in function
Gastric folds: allow stomach distention
Oesophagus motility measurement and regulation
Measured using manometry(peristaltic waves 40mmHg, resting LOS 20mmHg)
Mediated by inhibitory noncholinergic nonadrenergic neurons of myenteric plexus
Hypermotility(Achalasia) pathophysiology
Environmental trigger->inflammation
Fibrosis->neuron apoptosis
Loss of ganglion cells in LOS wall
Less NCNA activity->less inhibition so higher resting LOS pressure
Increased risk of oesophageal cancer
Achalasia causes
Chagas’ disease
Protozoa infection
Amyloid/sarcoma/eosinophilic oesophagitis
Achalasia treatment
Pneumatic dilation: circumferential stretching/tearing of muscle fibres
Heller’s myotomy:6cm oesophagus, 3cm stomach
Dor fundoplication: anterior fundus folded over oesophagis and sutured
Risks of surgery for achalasia
Perforation
Splenic injury
Division of vagus nerve
Hypomotility(scleroderma) pathophysiology
Autoimmune disease Neuronal defects->smooth muscle atrophy Distal peristalsis ceases Low resting LOS pressure CREST syndrome
Scleroderma treatment
Exclude organic obstruction
Improve peristaltic force with prokinetics
Corkscrew oesophagus pathophysiology and symptoms
Diffuse oesophageal spasm Disordered coordination Hypertrophy of circular muscle Dysphagia and chest pain 400-500mmHg
Corkscrew oesophagus treatment
Forceful pneumatic dilation of cardia
Oesophageal perforation symptoms
Pain
Fever
Dysphagia
Emphysema(uncommon)
Oesophageal perforation causes
Boerhaave’s(vomiting against a closed glottis)
Foreign body(batteries, sharp objects)
Trauma(neck, thorax)
3 protective mechanisms against GORD
Volume clearance by oesophageal peristalsis reflex
pH clearance by saliva
Oesophageal epithelium barrier properties
GORD risk factors
Smoking Chocolate Alcohol Sliding hiatus hernia Rolling hiatus hernia
GORD treatment
Lifestyle changes
PPIs
Dilation peptic strictures
Laparoscopic Nissen’s fundoplication
Stomach cells and secretions
Chief cell: pepsinogen
Parietal cell: acid
Gastritis causes
H. pylori Atrophic gastritis(autoimmune against parietal cell)->pernicious anaemia, G cell hyperplasia(carcinoma)
Gastric ulcer pathology
Lack of mucosal protection
Erosive haemorrhagic gastritis->acute ulcer->gastric bleed & perforation
H. Pylori secretions
VacA toxin: gastric mucosal injury
Urease: neutralise acid
Enzymes: mucinase, lipase, protease
Portal triad
Hepatic artery: O2 rich blood
Portal vein: process nutrients, detoxify blood
Bile duct: produce bile
Liver cells and function
Sinusoidal endothelial cells: fenestrated, movement of molecules
Kuppfer cells: macrophages
Hepatic stellate cells: damage->deposit collagen
Hepatocyte: metabolism and synthesis of albumin/clotting factors
Cholangiocyte: secrete HCO3 and H2O into bile duct
Enzyme for detoxification in liver
P450: modification followed by conjugation
Functions of bile
Cholesterol homeostasis
Lipid and soluble vitamin absorption
Excretion of waste
Pancreas exocrine cells
Acinar cells: low volume, enzyme rich, viscous
Ductal and centroacinar cells: high volume, bicarbonate rich, watery