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85 Cards in this Set
- Front
- Back
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Describe the cephalic phase of digestion.
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Site/smell/thought of food leads to vagus stimulation, causing gastrin releasing peptide (GRP) to act on antral G cells, releasing gastrin into circulation. Gastrin is sensed by ECL cells, which make histamine. Histamine has paracrine effects on parietal cells, which make HCl and intrinsic factor
Vagus also directly stimulates ECL cells to release histamine, parietal cells to make acid and chief cells to produce pepsinogen |
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Describe the gastric phase of digestion
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Initiated by gastric distention, via intramural and vagal stimulation, and via chemicals:
1) Gastrin from ECFs causes acid release from parietal cells 2) Vagus and Gastrin (weakly) stimulate pepsinogen from chief cells in fundus 3) Pepsin's action produces oligopeptides, which stimulate gastrin release |
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What is the role of pepsin?
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Digestion of complex proteins into oligopeptides
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What shuts off acid production in the stomach?
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D-cells in antrum sense pH <3, release somatostatin to shut off G cells.
D-cells in the fundus are stimulated by the vagus to produce somatostatin, shutting off histamine from ECL cells. |
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Describe the opposing effects of ACh on gastrin and somatostatin release in the stomach.
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ACh stimulates G cells to produce gastrin and acid, and inhibits D cells from producing somatostatin
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Describe the action of vasoactive intestinal polypeptide, and how it is released
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VIP causes D cells to produce more somatostatin, relaxes sphincter of Oddi, and enhances pancreatic acinar secretion.
Released through vagal afferent fibers in response to CCK release. |
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Describe the role of secretin, and how it is released
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Secretin stimulates H20 and bicarb release from pancreas and bile ducts by increasing intracellular cAMP. It also inhibits gastric emptying and acid secretion. Acts with the help of CCK.
Secretin is released by duodenal S cells when pH is below 4.5 |
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Describe the role of cholecystokinin, and how it is released
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Causes gallbladder to contract, relaction of spincter of Oddi, secretion of pancreatic enzymes.
Also synergistic with Secretin: causes release of water and CO3 from pancreas and bile ducts, inhibits gastrin and acid production. Released by duodenal I cells in response to fat, protein, AAs, Ca, and vagal tone. |
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What are the stimuli and actions of GRP?
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CCK and vagal tone cause release of GRP. GRP causes G cells to release gastrin, and enhances pancreatic secretion.
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What hormones are responsible for propagating peristalsis from the UES through the esophagus?
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NO and VIP
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Where is the gastric pacemaker located?
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Fundus
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What causes contraction of the gallbladder and relaxation of the sphincter of Oddi?
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CCK release from I cells in duodenal mucosa
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What do electro- or pharmaco-mechanical coupling induce in terms of peristalsis?
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Calcium influx, which binds to calmodulin, activating myosin LC kinase, which phosphorylates myosin light chain, causing attachment of myosin to actin, and generating sliding forces for contraction.
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What are the three levels of neural control of motility?
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Enteric plexi (Meissner's and Auerbach's)
Prevertebral ganglia (Celiac, SM, IM) CNS - parasympathetic/sympathetic innervation |
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The slow waves, which functions based on depolarization of myocytes via K/Ca channels, do not initiate contractions alone. What is needed in conjunction with slow waves to initiate enteric muscle contraction?
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Depolarization, which happens as a result of stretch, neural or humoral stimulation
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Contrast segmental and peristaltic contractions.
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Segmental occurs intestinally, and is the contraction of a section or ring of gut. Peristaltic contractions move
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Contrast primary vs. secondary peristalsis.
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Primary is initiated by a swallow, secondary is not.
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How is undigestible food moved through the stomach?
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After about 90 minutes, the pyloric sphincter and duodenum relax, and the MMC sweeps any remaining particles out of the stomach.
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What is the "fed" pattern of small intestine motility?
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Segmental contraction, which causes mixing and spreading of the chyme.
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Where are the most frequent contractions in the GI tract?
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Duodenum near SOD. Frequency decreases with distance from duodenum.
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What is the "fasting" pattern of small bowel motility?
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MMC cycle every 90 minutes to sweep out undigestible components. MMC only functions when not digesting.
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What is the gastro-colic reflex?
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Increase in colonic activity within 30 minutes after a meal. Increased with fatty meals, so CCK may be involved.
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What is the frequency of colonic muscle contraction?
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Slow at ileocecal valve, increasing toward mid-colon, then slowing again.
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What is "passive" tension caused by?
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stretch
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What is another name for slow waves?
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Basal Electric Rhythm (BER)
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How does neural control in the mouth differ from the pharynx?
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Mouth = cortical (voluntary)
Pharynx = cortical / medulla |
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What causes contraction vs. relaxation of LES?
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Contraction - myogenic (normal state)
Relaxation - neurogenic via vagus (for allowing passage of food to stomach) |
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What blocks relaxation of the LES?
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Tetrodotoxin
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How is the size of the gastric reservoir controlled?
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Neurally (medulla) via vago-vagal response
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What inhibits gastric emptying?
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CCK and duodenal distension
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In segmental contraction, is the "propulsive" segment contracted at longitudinal or circular layer?
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Circular layer is contracted in propulsive segment, longitudinal is contracted in receiving segment
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What type of cells sense mucosal distortion and signal interneurons to initiate segmental contraction in small gut?
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Enterochromaffin cells, which release serotonin and cause segmental contraction.
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What type of receptors are key in causing the sensation of nausea?
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5-HT3 receptors in the chemoreceptor trigger zone of the medulla. When an irritant causes enterochromaffin cells to produce more serotonin than platelets can absorb, the CTZ senses and reacts by inducing vomiting.
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What are the phases of MMC activity?
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Phase I: physiologic ileus
Phase II: irregular contractions Phase III: Strong peristaltic contractions |
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What plasma hormone increases with MMC phase III?
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Motilin
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What is responsible for GERD?
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Low LES town, or frequent relaxations
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What is a patient with "bird's beak" appearance on barium swallow and dysphagia likely suffering from?
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Achalasia - high resting LES pressures that do not relax with swallowing
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What does a biopsy with absent intramural neurons in esophagus, and eosinophilic infiltrate suggest?
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Achalasia
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What part of the esophagus is controlled by the nucleus ambiguus of the brainstem?
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Upper (striated) esophagus
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Injecting the LES with botulinum toxin is indicated for which entity?
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achalasia - relaxes LES. Alternative to surgical myotomy or dilation
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What does uncontrolled achalasia progress to?
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megaesophagus, weight loss, aspiration/pneumonia
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What nucleus of the brain innervates the lower esophagus?
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Dorsal motor nucleus - both for contraction and relaxation
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What is Zenker's diverticulum?
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an outpouching of the esophagus in the middle of the UES (cricopharyngeus / posterior constrictors)
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At what point in respiration does the diaphragm pinch the LES?
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During inspiration, helps prevent reflux aspiration
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In patients with GERD, LES resting pressures are…
A. Increased B. Decreased C. Normal |
C: Normal in the vast majority of GERD
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What is the difference betwen normal LES relaxation and TLESR?
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TLESR last >10 seconds, allowing acid to bathe lower esophagus for too long
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When is pH testing indicated for GERD?
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When EGD is normal, but pat has persistent or pulm sx
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When is medical therapy indicated for ERD?
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If sx severe or esophagitis present
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How can you tell if there is a mechanical or motility issue causing dysphagia?
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Mechanical: difficulty with solids
Motility: difficulty with liquids |
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What causes achalasia?
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Degeneration of the ganglia that produce NO, allowing relaxation of LES
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Why are elderly likelier to be sensitive to NSAIDs?
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Gastroparesis, and reduction in protective prostaglandins
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Why is metoclopromide not indicated as a prokinetic agent for gastroparesis anymore?
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Because 30% get side effects, including 10% tardive dyskinesia which is irreversible
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What is the characteristic finding on manometry for scleroderma/sclerosis?
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Nothing happens after the swallow - all low pressure.
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What disorder is associated with megacolon?
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Hirschprung's disease - failure of enteric neurons to migrate into bowel. Characteristic finding is that Internal anal sphincter does not relax with distension.
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What is the fxn of the Interstitial Cells of Cajal?
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gastric pacemaker cells
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What is the gold standard for identifying gastroparesis?
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Radiographic scintigraphic with a solid phase, physiologic and caloric meal.
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How is gastroparesis managed non-medically?
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Small, frequent carb rich meals, liquids.
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Cisapride, a 5-HT4 agonist, was pulled from the market for cardiac arrhythmias, even though it was very effective for what?
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Gastroparesis - prokinetic.
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What are tx options for pharmacologic refractory gastroparesis?
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Gastrostomy with suctioning
Gastric pacemaker - alleviates nausea and vomiting. |
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What are the two most affected GI areas in systemic scleroderma?
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Esophagus, anorectum
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What antibiotic is used as a prokinetic in GI dysmotility?
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Erythromycin, DO NOT combine with cisapride due to cardiac tox
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What type of dysmotility is octreotide (somatostatin) effective in treating?
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Small bowel dysmotility
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How will a biopsy of megacolon appear histologically?
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Normal - lack of ENS cells is more distal to the distended region, and is typically contracted and devoid of content.
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When might you suspect Hirschprung's disease?
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In a newborn that does not pass meconium within 48 hours, or a child with chronic constipation
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How is Hirschprung's treated?
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Surgically - remove colon without ganglia.
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Which pepsinogens are particularly effective for digesting collagen?
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Pepsinogens 1-5 (out of 7)
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What stimulates the release of pepsinogen from chief cells?
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ACh from vagus stimulation (weakly by gastrin, secretin and CCK)
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What stimulates IF secretion?
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histamine, gastrin, ACh.
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When does IF bind B12?
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In the duodenum. R binding proteins bind B12 in the acid stomach, but Rs are cleaved by trypsin in duodenum.
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Where is B12 absorbed?
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In the distal ileum
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What are trefoil peptides
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Play a role in rebuilding local damage in GI lining
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What type of bacteria is H pylori?
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GN spirochete
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What is the enzyme that H pylori produces to prevent its digestion?
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Urease - splits urea into ammonia and CO2
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What are BabA and SabA?
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The adhesin proteins that H pylori uses to attach specifically to gastric mucosal cells.
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What is the toxin that H pylori secretes that damages epithelium?
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Vac A. Particularly active Vac A is likelier to cause an ulcer.
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What is the importance of cag in H pylori?
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codes for syringe which injects genes into epithelial cells. Causes release of IL-8 which breaks up tight jxns, bringing inflammatory response and allowing other H pylori to bind.
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What is the most important NSAID cause of gastritis?
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Blocks COX1 production of prostaglandin
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What is the triple therapy for H pylori?
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PPI, metronidazole, clarithromycin BID for 10-14 days
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How can you tell if high gastrin is related to achlorhydria or not?
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Gastrin >1000 pg/mL with pH >2 is due to achlorhydria
ph<2 is likely due to gastrinoma* *To test, stop PPIs for 1 week and H2 for 2 days. |
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What syndrome do 40% of gastrinoma patients have?
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MEN-1 = multiple endocrine neoplasia syndrome 1
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Contrast acid levels in gastric vs. duodenal ulcers
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gastric ulcer = low acid (H pylori)
duodenal ulcers = high pH. |
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What cytokines are Corpus-predominant H pylori strains likelier to elicit?
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IL-1beta and TNF-alpha. These are likelier to produce cancer than mixed or antral-predominant strains.
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What are non-invasive options for dxing H pylori?
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stool antigen and urea breath test.
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How is breath tested for H pylori?
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Drink radiolabeled Urea with C13. H pylori (if present) splits urea into ammonia and CO2. CO2 radiolabeled will be exhaled.
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When would you suspect Zollinger-Ellison/gastrinoma?
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multiple ulcers, in odd places and refractory to tx.
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