¡GoConqr estrena diseño! Cuéntanos qué te parece.

Regístrate gratis

Fichas

Alimentary 2

reynoldslaura Inglés 65 fichas

Fichas del conjunto (65)

  1. 1When do L cells in the distal ileum release enteroglucan?In response to glucose and fat. It should have been absorbed before this section therefore it acts to decrease motility
  2. 2When do the M cells in the duodenum release motilin?In response to acid and fat to stimulate gastric emptying
  3. 3When is neurotensin released and from what cells?It is a peptide released from N cells in the ileum in response to fats as they should have been absorbed before this section- acts to decrease motility
  4. 4How is glucose taken up by facilitated diffusion?It is taken up via GLUT 2 transporters in the small intestine
  5. 5How is glucose take up into the enterocytes via secondary active transport?Na⁺ is transported out of the enterocyte via active transport by the Na⁺/K⁺ pump. Na⁺ then moves into the enterocyte via diffusion and cotransports glucose with it
  6. 6What is creatorrhea and how is it caused?Creatorrhea is a form of smelly diahorrea and it can be caused by proteolytic enzymes not flowing into the duodenum therefore proteins are broken down by bacteria in L.I instead
  7. 7How are amino acids absorbed into the enterocytes?Via sodium dependent co-transport mechanisms (three main transporters depending the charge of the amino acid- neutral, basic or acidic)
  8. 8How do small peptides (di and tri) enter the enterocytes?They are linked to H⁺ co transport.(once the peptides enter the cell they are broken down to their constituent amino acids and leave via the amino acid carrier systems on the basolateral surface)
  9. 9What happens in cystic fibrosis?Duct cells have apical cAMP-activated Cl¯ channels which have a loss of function therefore reduced secretion of HCO₃¯ and H₂O lead to protein rich primary secretions in ducts
  10. 10What happens in acute pancreatitis?the exocrine cells of the pancreas—whose role is to manufacture enzymes that normally digest dietary proteins and fats, malfunction and digest themselves and surrounding tissues
  11. 11Where is CCK released and why?The release of CCK is stimulated by the products of digestion (particularly fat and protein) from the upper small intestine
  12. 12Pancreatic secretion is also controlled via the enteric nervous system. The release of which neurotransmitters causes an increase in PKA ?VIP and secretin
  13. 13What cellular mechanism underlies secretion from the acinar cells?An agonist e.g. CCK or ACh will bind to a receptor and activate Gq to increase PKC and consequently release intracellular calcium or Secretin or VIP will activate Gs and cause an increase in PKA
  14. 14What is the function of pancreatic secretions?In order to neutralise the acidic chyme produced by the stomach and to create a favourable pH for the functioning of pancreatic enzymes
  15. 15What are the two major components of pancreatic secretion?Bicarbonate fluid secreted from the pancreatic duct cells and enzymes stored as zymogen granules and released from pancreatic acinar cells
  16. 16Which of the following is NOT a proteolytic precursor? trypsinogen, chymotrypsinogen, ribonuclease and procarboxypeptidaseRibonuclease is not a protein precursor.
  17. 17How CCK, Ach increase Ca²⁺concentration?Stimulates exocytotic secretion of enzyme precursors and the production of an isosmotic NaCl secretion
  18. 18What substance stimulates secretion of isosmotic HCO₃¯ from the duct cells?Secretin via a cAMP mediated mechanism
  19. 19During which phase of GI control does pancreatic secretion occur most prominently?The intestinal phase (although it does occur a small amount in both cephalic and gastric phases)
  20. 20Where is secretin released from and why?It is released from the mucosa of the duodenum in response to acidic chyme during the intestinal phase of gastric secretion
  21. 21What cells produce gastrin?G- cells in the stomach and upper intestine
  22. 22Where is gastric juice secreted from and what is it composed of?Oxyntic glands in the proximal region of the stomach. It is composed mucus, pepsinogen, HCl and intrinsic factor
  23. 23What cells secrete pepsinogen?Chief cells
  24. 24What do the parietal cells secrete?HCl
  25. 25What two receptors are activated to switch off acid secretion by parietal cells?Somatostatin and prostaglandins receptors (thus ibuprofen can cause stomach ulcers etc as it suppresses production of prostaglandins)
  26. 26What is intrinsic factor needed for?The absorption of Vitamin B12
  27. 27Why is the intestinal phase of the GI tract mainly inhibitory for gastric secretion?Because it wants to neutralise the acidic chyme produced by the stomach by inhibiting the G cells and parietal cells to stop the production of H+
  28. 28What cell secretes histamine?ECL cells 'enterochromaffin like cells'
  29. 29What nerves control the upper esophageal sphincter?Cranial nerves V, IX, X and XII
  30. 30What nerve innervates the lower esophageal sphincter?Vagus
  31. 31How are parietal cells regulated to prevent constant acid secretion and therefore prevent peptic ulcers?When the parietal cells aren't stimulated the tubulovesicles seperate from the caniculi therefore the 'proton pump' goes back into the tubovesicles inside parietal cell
  32. 32Is the pyloric sphincter normally relaxed or contracted?It is normally relaxed, however it closes upon arrival of the peristaltic wave
  33. 33What are the three activities of the pyloric antrum of the stomach?propulsion, grinding and retropulsion
  34. 34What does the term 'alkaline tide' mean?OH- is produced via the ionisation of water and carbonic anhydrase catalyses CO2 and OH- to produce HCO3-. This enters venous circulation around stomach via a Cl-/HCO3- exchanger
  35. 35What are the four basic types of movement in the small intestine?Individual villi, mixing (perpendular and segmentation), peristaltic waves and the migrating motility complex during fasting
  36. 36How can helicobacter pylori contribute to production of peptic ulcers?It uses urease to produce bicarbonate and ammonia from urea which allows it to produce a neutralised area around it. It then attracts Tcells which release superoxides which lead to ulceration
  37. 37Name the four receptors identified on the parietal cell membrane.Cholinergic receptors, gastrin receptors, histamine receptors and prostaglandins receptors
  38. 38Name two drugs which can be used to control gastric secretionsAny two from:
    Atropine, aluminium hydroxide, ranitidine and omeprazole
  39. 39What cells produce saliva?Acinar cells
  40. 40Salivary secretion is under what nervous control?The autonomic nervous system- in particular the parasympathetic division
  41. 41How does atropine work in controlling gastric secretions?It is a competitive antagonist of muscarinic acetylcholine receptors therefore it can target the M3 receptors on the parietal cells and prevent acid secretion
  42. 42What receptor does gastrin act on?CCK2 receptors
  43. 43What is produced by D cells?Somatostatin
  44. 44What does fat do to the rate of acid secretion?It tends to slow it down- the intestinal phase releases enterogastrones e.g. Gastric inhibitory peptide in response to fatty acids
  45. 45What effect will disruption to the parasympathetic and sympathetic innervation to the gut have on the enteric nervous system?None, as it acts independently from them and it will continue its role as the main regulator of gut activity
  46. 46What are hormone secreting cells in the mucosa called?APUD cells (amine precursor uptake and decarboxylation)
  47. 47Name the three hormones released into the circulation from the duodenum?Cholecystokinin (CCK), secretin and motilin
  48. 48Roughly how many regulatory peptides are used by the GI tract, and how many of these act as endocrine hormones?There are more than 20 regulatory proteins and out of these 8 are released into the circulation as hormones
  49. 49What is the cephalic phase of GI control?This phase occurs even before any food is eaten. It produces gastric secretions on the sight, smell and thought of food and the greater the appetite, the more intense the stimulation
  50. 50How is water absorbed in the small intestine and the colon?Via passive osmosis
  51. 51How much fluid do we absorb per day?9L
  52. 52What is the pH of the stomach?1.5-3
  53. 53Where is the strongest alkaline secretion in the body?Pancreas (pH of 8.0-8.4)
  54. 54How much fluid does the average person excrete per day?0.1L per day
  55. 55Where does the majority of absorption of Calcium and iron occur?In the duodenum
  56. 56What type of molecule act as neurotransmitters in the enteric nervous system?Peptides
  57. 57How is the GI tract controlled intrinsically?Via the enteric nervous system
  58. 58How is the GI tract controlled extriniscally?Via the parasympathetic and sympathetic parts of autonomic nervous system
  59. 59What are the two plexus's of the enteric nervous system?The myenteric plexus- largely motor in function and the submucosal plexus- mainly sensory in function
  60. 60What effect does the parasympathetic nervous system have on the GI tract?It increases motility. 'rest and digest'
  61. 61What effect does the sympathetic nervous system have on the GI tract?Generally decreases motility (fight or flight- don't want to waste energy that could be given to muscles to run away by digestion)
  62. 62Does the enteric nervous system involve the CNS?No , however the neural activity of one plexus will affect the other (myenteric and submucosal plexuses)
  63. 63What do mechanoreceptors respond to?respond to distension or irritation of the gut wall
  64. 64What do chemoreceptors respond to?substances present in food or by products of digestion
  65. 65What are the four sympathetic plexuses of the GI tract?Coeliac, superior messenteric, inferior messenteric and the hypogastric plexuses

Información

Descripción
Fichas sobre Alimentary 2, creado por reynoldslaura el 03/05/2013.
Creado por
reynoldslaura
Visitas
89
Valoración

Escríbenos

¿Sobre qué es tu mensaje?

¿Qué te parece el nuevo diseño?

¿Te gusta?