Esophagus and Stomach Physiology Flashcards
Esophagus Outline
Muscular tube connecting mouth to stomach. Separated from pharynx by upper esophageal sphincter and from stomach by lower esophageal sphincter. 4 layers: mucosa, submucosa, lamia propria and serosa. Muscularis is thicker the normal for peristalisi
3 phases of swallowing
mouth (voluntary), pharyngeal (involuntary) and esophagus (involuntary)
Oral Phase Outline
Voluntary. Stimulated by force applied to roof of mouth by bolus being pushed by tongue
Pharyngeal Phase Outline
Involuntary. Pressure in pharynx triggers receptor firing to swallowing center in brain (medulla and pons)
Pharyngeal Phase steps
closing of nasopharynx, closing of vocal cords, closing of UES, stopping of breathing, contracts pharyngeal constrictor (generates peristaltic wave) and food passes through esophagus to lower esophageal sphincter. Lower esophageal sphincter relaxes allowing bolus into stomach
Dysphagia Outline
Difficulty swallowing. Neurological (eg Parkinson’s), developmental (Downe’s syndrome) ,structural ( tumors) and psychological (phagophobia) disorders.
Dysphagia Complications
Malnutrition (nutrients can’t reach stomach) and respiratory problems (food enters trachea)
Dysphagia Outline
X-ray: barium solution coats esophagus, shows on x-ray. Endoscopy: put in esophagus to observe tissue
Dysphagia Treatment
Swallowing exercises, dietary changes (soft foods and liquids), feeding tubes (bypass swallowing), manometry (synthetically expanding throat by balloon expansion) and surgery
Achalasia Outline
Degeneration of esophageal muscle and the nerves that supply them, results in difficulty for LES to relax. Results in difficulty swallowing and regurgitation of food (food never reaches stomach)
Achalasia Treatment
oral medication (eg Ca channel blockers), muscle relaxants (direct injection), manometry at LES and surgery
Heartburn Outline
Acute backflow of stomach contents into esophagus due to LES inability to fully contract. Common occurs in everyone. Symptoms: burning in chest, cough and hoarsness
Gastroesophageal Reflux Disease (GERD/GORD) Outline
Chronic backflow of stomach’s contents into esophagus. Results in esophagitis and ulcers (progresses to Barett’s Esophagitis, and esophageal cancer)
GORD Diagnosis
Barium x-ray, ambulatory acid (pH) probe and upper endoscopy
Gord Treatment
Medication: antacids, H2 antagonists, PPI (step up). Surgery: lix ring (exerts enough pressure to help LES close)
4 anatomical regions of stomach
Cardia, Fundus, Body and Pylorus (antrum and pyloric canal)
Cardia Function
Receives food from esophagus. Contains mucosal glands that secrete mucus
Fundus Function
Stores undigested food
Body Function
Where bulk of gastric digestion occurs. Biggest region
Pylorus Function
2 parts: antrum and the pyloric canal. Antrum opening of pyloric canal to the stomach’s body. Pyloric canal channels food to duodenum
3 muscle layers in stomach (1 extra then esophagus)
Circular (innermost), oblique, longitudinal (outermost)
Gastric Mucosa Cells
Surface mucus secreting, parietal cells, chief cells, enteroendocrine cells, enterochromaffin-like cells and nerve
Surface secreting mucus cells
Secrete mucus and HCO3^-. Protects stomach lining from abrasion and intense acid
Parietal Cells Outline
Produces HCl and intrinsic factor
Chief cells function
secrete pepsinogen and lipase
Enteroendocrine Cells
Secrete gastrin and somatostatin. Found mainly in antrum
Enterochromaffin-Like cells
Secrete histamine in response to gastrin. Found in lamina propria
Nerves in GIT Function
Effector and sensory nerves
Response to food entering and distending stomach (baroreceptors)
Acetylcholine release from enteric nervous system
Response to stomach registering food particles (chemoreceptors)
Gastrin release from G cells in body and antrum
Action of acetylcholine and gastrin
Either works directly on enteric cells (M3-Ach and CCKB-Gastrin receptors) or stimulates release of histamine from heterocroffin-like cells (M1-Ach and CCKB-Gastrin)
What happens with increased HCl concentration
D cells begin to produce somatostatin inhibiting G and parietal cells (forms negative feedback)
Response of Histamine, Ach and gastrin binding to receptors on parietal cells
Increase in cAMP and Ca^2+ production. Act as intracellular signalers. K+ and Cl- secretion begins
Response to K+ leaving cell
K+ binds to cell membrane receptor of K+-H+ ATPase pump activating transporter. K+ is pumped into cell and H+ is pumped out into lumen. H+ and Cl- combine outside of cell forming HCl which is released into stomach
Response to pH dropping (HCl conc increasing) in stomach
D cells produce somatostatin which inhibits cAMP aresponse to histamine
Intrinsic Factor Outline
Binds to Vitamin B12 in duodenum (after transcobalamin1 is degraded by pancreatic enzymes). This forms a complex that allows absorption through the epithelium (tubulin facilitated transporters). IF dissociates and trancobalamin 2 carries vitamin B to liver
Vitamin B12 Function in Body
DNA synthesis, red blood cell development, metabolism, neurotransmitter synthesis
B12 Deficency Symptoms
Anaemia, fatigue and lack of balance
Chief Cells Function
Secrete pepsinogen in response to Ach and gastrin levels
Pepsinogen as a zymogen
Not secreted in active form. It unfolds and undergoes autoclayses
3 protein digesting enzymes in GIT
pepsin (stomach), chymotrypsin (pancreas) and trypsin (pancreas)
2 main types of Gastric motility
Receptive relaxation and gastric contraction
Receptive Relaxation Outline
Vagally mediated reflex in fundus and body stimulated when bolus passes through esophagus (same time as LES relaxation), stomach wall relaxation. Stomach expands without significant pressure increase. Mediated as well by vasoactive intestinal peptide (VIP) and NO
Gastric Motility Outline
Driven by circular, oblique and longitudinal muscles. Maintained by basal electric rhythms generated by interstitial cells of Cajal (pacemakers). BER stimulates electrical depolarisation but can’t induce contraction independent of hormones (Ach and Gastrin)
Gastric Motility Steps
Peristaltic contraction moves from fundus to pyloric sphincter (contraction becomes stronger as it approaches antrum). Chyme is pushed through LES (stronger contraction = more chyme). When peristaltic contraction reaches pyloric sphincter, sphincter closes (no further emptying). Chyme is pushed back into antrum and then propelled forward again by peristaltic wave (mixing)
Chyme movement in duodenum
~ 40 mins - few hours. Influencing factors: meal size, content (eg lipid, carbohydrate) and viscosity
Duodenum signaling for controlling gastric emptying
Duodenal distension (stretch receptors - enterogastric reflex), cholecytokinin and gastric inhibitory peptide responding to digestion products and secretin released in reponse to acid in duodenum (inhibits gastrin). These all inhibit/reduce gastric emptying. Allows duodenum to better process food
Gastroparesis Def
Stomach motility loss leading to blockages and stagnation. Treatment: change of diet/medication
Gastritis/ Peptic Ulcer Disease Def
Inflammation/ulceration of stomach wall due to loss of barrier function and mucosal exposure to acid. Treatment: acid inhibitors or antibiotics
Advantages of drug absorption in stomach
Cheapest, most convenient dosing method. Deviation between and within patients (food intake on the day and different rates of gastric emptying)
What substances can pass through lipid cell membrane
Lipophilic (non-ionised) drugs. Acidic
