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Gastric Acid Secretion

Hannah Tribe Alim 1 Degree English 53 cards

Cards in this deck (53)

  1. 1What are the contents of normal gastric juice in the fasting state? (6)1. Cations (Na+, K+, Mg++, H+)
    2. Anions (Cl-, HPO4 2-, SO4 2-)
    3. Pepsins
    4. Lipase
    5. Mucus
    6. Intrinsic factor
  2. 2What is secreted from the body and fundus of the stomach? (3)1. Mucus
    2. Pepsinogen
    3. HCl
  3. 3What is secreted from the antrum? (3)1. Mucus
    2. Pepsinogen
    3. Gastrin
  4. 4What is it that secretes HCl, along with intrinsic factor, from the body of the stomach?Parietal cells lining the tubular glands within the epithelial cells.
  5. 5What cells secrete paracrine agents? What is an example of such an agent?E.g. histamine, secreted from Enterochromaffin-like cells (ECL)
  6. 6How is gastric acid made? (HCl)On the basolateral membrane of the parietal cells, HCO3- is transported out of the cell into the blood (raising its pH) in exchange for Cl- entering the cell. This Cl- diffuses into the stomach through a Cl- channel on the apical surface. H+ is also pumped into the stomach via K+/H+ ATPase pumps, and the H+ and Cl- form the gastric acid.
  7. 7What is the composition of resting gastric juice?Same as plasma, but more alkaline as there is more HCO3- present.
  8. 8What is the composition of mucus and what is its purpose in the stomach?A thick, sticky, alkaline substance (due to high HCO3-) that forms a water-insoluble gel on epithelial surface to protect cells from H+
  9. 9What do lipases do?Break down triglycerides into fatty acids and glycerol
  10. 10What does intrinsic factor do?Facilitates absorption of vitamin B12, needed to make RBCs
  11. 11What is the function of the HCl in the stomach?1. Kills bacteria
    2. Acid denaturation of digested food
    3. Activates pepsinogen which digests proteins
  12. 12What are the 3 phases of gastric acid secretion?1. Cephalic
    2. Gastric
    3. Intestinal
  13. 13What's happening in the cephalic phase?Vagal afferents detect food is in the mouth, the smell, sight, taste, chewing motion etc. This stimulates ACh release from vagal efferents. ACh stimulates parietal cells directly to cause HCl secretion, but also indirectly by causing release of histamine, which stimulates release of HCl from ECL cells.
  14. 14What's happening in the gastric phase?When the stomach is distended, or the concentration of proteins is high, acid secretion is stimulated. Secretion decreases as the stomach becomes more acidic.
  15. 15What is the effect of a high protein meal?Increased gastric acid secretion due to detecting of high levels of protein in the stomach
  16. 16How do high levels of protein help acid secretion?Proteins act as buffers so remove H+ from the system by forming H+ + protein complexes. This removes the inhibitory effect of HCl on secretion of gastrin.
  17. 17What does the intestinal phase try to do?Balance the secretions from stomach with absorptive and digestive capacity of intestine
  18. 18When the chyme enters the duodenum, what properties of it cause reflex inhibition of gastric acid secretion? (6)1. Low pH, because high acidity will inhibit digestive enzyme activity, HCO3- and bile salts
    2. High volume (causing duodenal distension)
    3. Hypertonic solution
    4. Amino acids
    5. Fatty acids
    6. Monosaccharides
  19. 19Which hormones inhibit acid secretion from parietal cells or gastrin secretion from G cells? (3)1. Secretin
    2. CCK
    3. Somatostatin
  20. 20What are the symptoms of HCl deficency? (3)1. Undigested food in the stools
    2. Flatulence and bloating
    3. White spots on fingernails?
  21. 21What are you at increased risk of if you have HCl deficiency?Infection with H. pylori
  22. 22What are possible treatments for HCl deficiency? (3)1. Bitter herbs may stimulate HCl secretion
    2. Lemon juice and vinegar
    3. Vitamin B1
  23. 23What external substances can increase HCl secretion?1. Caffeine
    2. NSAIDs
    3. Alcohol
    4. Nicotine
  24. 24What is the overall effect of somatostatin?Inhibits secretion of H+, histamine and gastrin
  25. 25How is pepsin secreted?Secreted from chief cells as pepsinogen (an inactive form)
  26. 26How is it activated?High [H+] causes a change in its shape so binding site becomes exposed.
  27. 27Where does it become inactive again?In the small intestine, as acid has been neutralised by bile salts and HCO3-.
  28. 28What is the point of pepsin secretion?Pepsin degrades food proteins into peptides and so initiates the digestion process.
  29. 29How do NSAIDs play a role in gastric acid secretion disorders?NSAIDs can impair the barrier properties of the mucosa, and suppress prostaglandin synthesis (PGE2 usually stimulates acid secretion). They also decrease mucosal blood flow and platelet aggregation so impair the repair of superficial injury.
  30. 30What causes peptic ulcer formation?A breakage in the mucosal barrier so there is an imbalance between protective and damaging factors
  31. 31What is the consequence of the breakage of the mucosal barrier?Epithelium is exposed to the erosive effects of HCl and pepsin
  32. 32Which 3 sites can be affected by peptic ulcers?1. Oesophagus
    2. Stomach
    3. Duodenum
  33. 33Name 3 intrinsic substances that cause acid secretion so can potentially be damaging factors.1. Histamine
    2. ACh
    3. Gastrin
  34. 34Name 4 extrinsic substances that can be damaging factors too.1. Alcohol
    2. Caffeine
    3. Smoking
    4. NSAIDs
  35. 35Name 2 pathologies which can cause increased acid secretion.1. Hyperparathyroidism
    2. Infection with H. pylori
  36. 36Besides HCl and pepsin, what other mechanisms prevent infection of the gastric mucosa? (5)1. Peristalsis (constant motion)
    2. Mucus secretion
    3. Tight junctions between epithelial cells
    4. IgA on mucosal surfaces
    5. Fast cell turnover
  37. 37What does H. pylori do?Penetrates the gastric mucosa and releases virulence factors and urease.
  38. 38What does urease do?Breaks down urea to form ammonia and CO2. The ammonia acts as a buffer so raises the pH of the stomach
  39. 39What is the effect of H. pylori infection?Mucosal damage exposing the epithelium underneath, which can also be damaged by HCl and pepsin, causing an inflammatory response, with release of factors such as IL 8 which recruit neutrophils and macrophages.
  40. 40What diagnostic tests may be carried out to determine if an ulcer is present? (3)1. Endoscopy
    2. Biopsy
    3. Test for H. pylori (stool antigen, urease activity test or 13C urea breath test)
  41. 41What are symptoms of a peptic ulcer? (9)1. Anaemia
    2. Black, tarry stools
    3. Dyspepsia
    4. Vomiting (blood)
    5. Nausea
    6. Anorexia
    7. Epigastric pain
    8. Chest discomfort
    9. Weight loss
  42. 42What is the most common type of peptic ulcer?chronic peptic ulcer
  43. 43What causes acute peptic ulcer?Corrosive gastritis (inflammation of stomach), severe stress or shock (trauma), or acute hypoxia of surface epithelium.
  44. 44What are the differences in outcome between chronic and acute peptic ulcers?1. Chronic ulcers usually heal with replacement tissue and some scarring
    2. Acute ulcers result in severe bleeding, yet do not leave a scar when healed. Acute ulcers can lead on to chronic ulcers.
  45. 45What are 4 complications of peptic ulcers?1. Haemorrhage
    2. Perforation (peritonitis) and penetration resulting in leakage of contents
    3. Stricures of pyloric canal or oesophagus
    4. Malignancy
  46. 46What are the 2 types of drug that can be given to reduce acid secretions?1. Proton pump inhibitors (PPIs)
    2. H2 receptor antagonists (H2RAs)
  47. 47Give an example of each.PPI - Omeprazole
    H2RA - Ranitidine (Zantac)
  48. 48What is the mechanism of action of H2RAs?Block the histamine on H2 receptors on parietal cells in stomach to prevent acid secretion. As a result, pepsin secretion also decreases.
  49. 49What is Zollinger-Ellison syndrome?A disease characterised by gastrin-secreting tumours, often causing multiple ulcers, especially in the duodenum.
  50. 50What is the mechanism of action of PPIs?Irreversibly inhibit H+/K+ ATPase pumps on the secretory surface of gastric epithelial cells, so that basal and food-stimulated acid secretion is inhibited.
  51. 51What is gynaecomastia?Decreased sexual function in men, perhaps with growth of glandular breast tissue.
  52. 52What effect do prostaglandins have on the gastric mucosa?They are protective, as they inhibit acid secretion (basal, food-induced and histamine-induced), as well as increasing blood flow to the mucosa and the secretion of HCO3- and mucus.
  53. 53What drug can be given to produce these effects as it is a stable analogue of PGE2?Misoprostol

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Degree Alim 1 Flashcards on Gastric Acid Secretion, created by Hannah Tribe on 10/06/2014.
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