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GI Physiology

Lareyna Mcmenemy MD3002 Inglés 70 fichas

Fichas del conjunto (70)

  1. 1State the requirements of the GI tract- Movement of food
    - Secretion of digestive juices
    - Absorption of water, electrolytes, vitamins & digestive products
    - Circulation of blood
    - Functional control via local, nervous & hormonal systems
  2. 2Key physiological processes of the GI tract1. Motility
    --> propulsion of digested food
    --> mixing & decreasing particle size
    2. Digestion into absorbable molecules
    3. Absorption from intestinal lumen to blood stream
    --> water, electrolytes, vitamins & digestive products
    4. Secretion
    --> salivary glands, stomach, intestine, pancreas & liver
    5. Excretion
    --> indigestible particles are condensed & expelled
  3. 3What are the major defence mechanisms of the GI tract?Immunological: Mucosal immune system (GALT)
    - Peyers patches & diffuse immune cells (lymphocytes & mast cells)
    Non-immunological: gastric acid, mucin, peristalsis & epithelial barrier
  4. 4Layers of the GI wall1. Mucosa - Epithelia + Lamina propria + Muscularis mucosa
    2. Submucosa - connective tissue layer with larger blood vessels, lymphatics, secretory glands * submucosal plexus
    3. Muscularis externa - circular & longitudinal smooth muscle + myenteric plexus
    4. Serosa - connective tissue covered with epithelia
  5. 5Submucosal plexusMeissner's Plexus
    - throughout the intestine only
    - local effects on glandular, epithelial & endocrine secretion
    - local blood flow & absorptive effects
  6. 6Myenteric plexusAuerbach's Plexus
    - throughout the length of GI tract
    - controls peristaltic movement
    - when stimulated it:
    increases tonic contraction
    increases rate of contraction
    increases intensity of contractions
    increases velocity of conduction
  7. 7Describe smooth muscle contraction1. Ca2+ from SR binds to calmodulin
    2. Activates myosin light chain kinase
    3. Phosphorylation of myosin head
    3. Myosin actin binding
  8. 8What is the latch state? & what does it mean?Phase of decreased detachment of myosin head causing the cross-bridge binding to be maintained & therefore reducing ATP consumption
    --> allows stronger contraction with less energy expenditure
  9. 9Define slow wave potentialConstant rhythmic increase & decrease of membrane potential
    Rate of contraction is SET, but the intensity is EXTRINSICALLY controlled
  10. 10Describe the chain of events which occur during slow wave potentials1. Voltage gated Ca2+ channels open
    2. AP spike
    3. Increased [Ca2+]i
    4. Ca2+ dependent K+ channels open
    5. Increased K+g --> slow depolarisation
    6. Voltage gated Ca2+ channels close --> decreased [Ca+]i
    7. Ca2+ dependent K+ channels close
  11. 11What stimulates Depolarisation & Hyperpolarisation in Interstitial Cajal cellsDepolarisation - Stretch, ACh & Parasympathetics
    Hyperpolarisation - NA & Sympathetics
  12. 123 types of GI reflexes1. Within the enteric NS
    - Secretion, peristalsis, mixing & local inhibition
    2. GI -> Pre-ganglionic sympathetic ganglia -> GI
    - Gastrocolic, Enterogastric & Coloileal
    3. GI -> Brain / Spinal cord -> GI
    - Pain reflexes
    - Defecation reflex
    - Control of gastric motility & secretory activity
  13. 13State 3 ways of increases splanchnic blood flow1. Decreased O2
    2. Adenosine release
    3. Vasodilator release (bradykinin, VIP, CCK etc.)
  14. 14Describe mastication- Mixes food with saliva for lubrication (mucin)
    - Decreases food particle size
    - Mixes food with digestive enzymes
  15. 15Where is mastication controlled?Brain stem nuclei - Reticular areas for rhythmic control
    Also in the hypothalamus, amygdala & cerebral cortex
    Nerve = trigeminal
  16. 16Describe the process of swallowing3 phases: Voluntary, Pharyngeal & Oesophageal
    1. Voluntary passage of food to the pharynx
    2. Trachea closes & oesophagus opens
    (Upper oesophageal sphincter) then closes
    3. Primary peristaltic wave is initiated by the deglutination centre --> sends signal via cranial nerves (5th, 9th, 10th & 12th) to produce a series of coordinated contractions creating an area of high pressure behind the bolus
    4. Lower oesophageal sphincter opens mediated by the vagus nerve (VIP release)
    5. Receptive relaxation
    6. Lower oesophageal sphincter closes
  17. 17Receptive relaxationDistension of the lower oesophagus stimulates the relaxation of the lower oesophageal sphincter & orad region of the stomach prior to the peristaltic wave
  18. 18Describe the innervation of gastric motilityENS
    Myenteric plexus-
    - Parasympathetic via vagus:
    stimulate gastric smooth muscle motility & secretions
    - Sympathetic via coeliac ganglion:
    inhibit motility & secretions
  19. 19Describe the motor functions of the stomach1. Storage - food forms concentric circles --> food stretches the stomach wall --> initiates the vagovagal reflex to decrease tone & increase capacity
    2. Mixing - weak peristaltic constrictor waves become more intense towards the antrum --> forces antral contents under increasing pressure --> repropulsion of food towards the body
    3. Emptying - promoted by the peristaltic waves but opposed by the pylorus
  20. 20Vagovagal reflex- Afferent vagus:
    Mechanoreceptors relay information to CNS via sensory neurones
    - Efferent vagus (info from the CNS):
    VIP released from post-ganglionic peptidergic vagal neurones causes relaxation
  21. 21Define retropulsionPropulsion of food material and gastric contents back into body of stomach for further mixing and churning before being passed into small intestine
  22. 22Explain Migrating Myoelectric complexesPeriodic gastric contraction occuring during fasting
    Occur in 90min intervals
    - mediated by MOTILIN
    - clear stomach of residue from previous meal
  23. 23Enterogastric inhibitory reflexes1. Distension of the duodenum
    2. Irritation of the duodenal mucosa
    3. Acidity / Osmolality of the chyme
    4. Presence of fat or protein in chyme
  24. 24What movement occurs in the small intestine?Segmentation contractions - chyme induced distension --> stretch --> local constrictive contractions --> segmentation)
    Peristalsis
  25. 25How is peristalsis in the small intestine controlled?Gastroenteric reflex via the enteric NS
  26. 26Peristaltic rushPowerful, rapid peristalsis
    - Due to mucosal irritation with infectious diarrhoea
  27. 27What causes a delay in the caecum emptying?Irritation or distension of the caecum due to the contraction of the sphincter
  28. 28What movements occur in the colon?Mass movement - constrictive ring forms, haustra lost, faeces moves en mass, increased contractions followed by relaxation
    Haustruations - mixing movements
  29. 29What reflexes occur in the colon?Gastrocolic & duodenocolic --> signals via ANS
    Defecation reflex - intrinsic or parasympathetic
  30. 30What controls the: 1. Intrinsic defecation reflex 2. Parasympathetic defecation reflex?1. Rectal enteric NS
    2. Sacral spinal segments
  31. 31What are the phases of GI function?1. Cephalic - initiated by the thought, smell or taste of food
    2. Gastric - initiated by the presence of food in the stomach causing distension & gastrin release
    3. Intestinal - initiated by the presence of food in the duodenum
  32. 32State the sympathetic & parasympathetic changes which occur during the cephalic phase in: 1. The mouth 2. The stomach 3. Other regions1. S - Increased blood flow to salivary glands --> increased volume of saliva
    P - Increased salivary secretion
    2. S - increased blood flow to the stomach
    P - increased gastrin, mucus, pepsin & HCL secretion
    3. P - stimulation of bile ducts, hepatocytes & pancreatic acinar cells
  33. 333 types of salivary glands1. Parotid (mostly serous)
    2. Submandibular (mixed)
    3. Sublingual (mostly mucoid)
  34. 34What is the basic secretory unit of the salivary gland?Acinar cells
  35. 353 stages of salvation1. Acini cells
    - primary isotonic saliva (alpha amylase, serine protease, lingual lipases & mucin)
    2. Myoepithelial cells
    - under neural control to contract & expel exocrine cell contents
    3. Ductal cells
    - modify saliv a
    - absorb Na+ & Cl-
    - secrete K+ & HCO3-
  36. 36Neural regulation of salivary secretionsANS
    - increased by PSNS & SNS
    Results in:
    - increased saliva
    - increased HCO3- secretion
    - increased enzyme secretion
    - increased myoepithelial cell contraction
  37. 37State the gastric secretions & their cells of originHCl & Intrinsic factor via parietal cells
    Pepsinogen via chief cells
    Mucous via mucous neck cells
  38. 38What factors stimulate / inhibit gastric secretions?Stimulate: ACh, Gastrin, Histamine & Parasympathetics
    Inhibit: Enterogastric reflex
  39. 39Action of pepsinogenLocal reflexes by vagus & H+ trigger secretion
    Converted to active pepsin at pH <3.5
  40. 40Action of intrinsic factorEnables the absorption of Vit. b12 in the terminal ileum
    Absence or deficiency leads to pernicious anaemia
  41. 41Describe HCl secretionApical surface - H+ released via H+/K+ ATPase & Cl- follows by diffusion
    Basolateral surface - HCO3- exchanged for Cl- via exchanger
  42. 42Describe the inhibition of HCl secretionInhibited when it is no longer required for pepsinogen conversion to pepsin
    Somatostatin:
    - Directly binds to parietal cells & inhibits adenylate cyclase
    - Indirectly inhibits histamine & gastrin release
  43. 43Describe the pancreatic secretionsAqueous solution of HCO3- & enzymes
    Aqueous components secreted by centro-acinar cells - isotonic (Na+, K+, Cl- & HCO3-)
    Modification by ductal cells to make a HCO3- rich fluid
  44. 44What factors increase pancreatic secretions?CCK
    Secretin from S cells
    Parasympathetic supply via Vagus
  45. 45Pancreatic enzymesAmylase & lipase - secreted in active form
    Proteases - secreted in inactive form & activated y enterokinase in the duodenum
  46. 46What factors increase & decrease bile secretion?Increase - VIP & ACh
    Decrease - Adrenaline & Somatostatin
  47. 47Describe the regulation of secretion in the cephalic phase30% of gastric secretions
    1. Direct stimulation of parietal cells by the vagus
    2. Indirect stimulation of parietal cells by gastrin released from G-cells stimulated by vagal gastrin-releasing peptide
  48. 48Describe the regulation of secretion in the gastric phase60% of gastric secretions
    1. Direct stimulation of parietal cells by the vagus
    2. Indirect stimulation of parietal cells by gastrin released from G-cells stimulated by vagal gastrin-releasing peptide
    3. Local reflexes in antrum stimulated by gastrin
    4. Direct effects of amnio acids & small peptides on G-cells to secrete Gastrin
  49. 49Describe the regulation of secretion in the intestinal phase10% of gastric secretions
    - at pH >3 gastrin is released
    - at pH <2 buffering occurs via HCO3- & gastric inhibition occurs w/ intestinal stimulation
    - CCK is released due to presence of fat & breakdown products in duodenum
    - Secretin is released in response to acid
  50. 50State the main pancreatic secretion in each of the phases of GI secretionCephalic - Mostly enzymatic
    Gastric - Mostly enzymatic
    Intestinal - Enzymatic & aqueous (80% of total pancreatic secretions)
  51. 51State the exocrine secretions & their function of the Mouth, pharynx & salivary glands + of the oesophagusMouth, pharynx & salivary glands:
    Salt & water - moisten food
    Mucus - lubrication
    Amylase - polysaccharide digestion
    Oesophagus:
    Mucus - lubrication
  52. 52State the exocrine secretions & their function of the stomachHCL
    - solubilisation of food particles
    - kill microbes
    Pepsin
    - protein digestion
    Mucus
    - lubrication
    - protection of the epithelia
  53. 53State the exocrine secretions & their function of the small & large intestineSmall intestine:
    Enzymes - food digestion
    Salt & water - maintain fluidity
    Mucus - lubrication
    Large intestine:
    Mucus - lubrication
  54. 54State the exocrine secretions & their function of the pancreasEnzymes
    - digestion of carbohydrates, fats, proteins & nucleic acids
    Bicarbonate
    - neutralise HCl entering small intestine from the stomach
  55. 55State the exocrine secretions & their function of the liverBile salts
    - solubilise water-insoluble fats
    Bicarbonate
    - neutralise HCl entering the small intestine from the stomach
    Organ waste products & trace metals
    - elimination in faeces
  56. 56What are our main sources of nutrition?Carbohydrates
    Lipids - mainly triglycerides
    Proteins - exogenous or endogenous
  57. 57Define “digestion” in the context of human nutrition and physiologyThe breakdown of nutrients into absorbable molecules
  58. 58Define “absorption” in the context of human nutrition and physiologyThe movement of nutrients, water, and electrolytes from the gut lumen into the internal environment
  59. 59How is the small intestine adapted for efficient absorption?Intestinal mucosa is arranged in circular folds of Keckring from which villi project
    Villi are covered with enterocytes w/ goblet cell & in microvilli
  60. 60Describe carbohydrate digestionDigestion begins in the mouth with salivary amylase, it continues into the stomach where the amylase is denatured by the pH. Then pancreatic amaylases secreted into the duodenum digest it further into maltriose, maltose & alpha-limit dextrin. Brush border enzymes also act on the disaccharides to produce glucose, galactose & fructose
  61. 61Describe carbohydrate absorptionSecondary active transport
    - Glucose & Galactose
    - Sodium-dependent Glucose Transporter (SGLT1)
    Facilitated diffusion
    - Fructose
    - Glucose Transporter 5 (GLUT5)
  62. 62Describe protein digestionBegins in the stomach w/ pepsin & is completed by pancreatic & brush border proteases
  63. 63ProteasesActivated by trypsin (converted by enterokinase from trypsinogen)
    Endopeptidases:
    - Chymotrypsin
    - Elastase
    - Trypsin
    - Pepsin
    Exopeptidases:
    - A & B Carboxypeptidase
    - Amino peptidase
  64. 64Endopeptidases & ExopepidasesEndopeptidases - cleaves large polypeptides in the midd of the chain to oligopeptides
    Exopeptidases - cleaves amino acids 1 at a time from either end of a protein
  65. 65Describe protein absorptionAmino acids - Na+-dependent co-transport
    Dipeptides - H+-dependent co-transport
    Tripeptides - H+-dependent co-transport
  66. 66Describe lipid digestion & absorptionBegins in the stomach w/ lingual & gastric lipase --> Bile salts emulsify the fat producing lipid droplet --> Pancreatic enzymes (lipase, cholesterol ester hydrolase & phospholipase A2) are secreted & break lipids down to monoglycerides & fatty acids stored in micelles --> Monoglycerides & fatty acids move out of micelles into the interstitial cells via diffusion --> Cholesterol moves in via membrane transporter --> Emulsified fats (re-esterified triglycerides) combine with cholesterol & proteins to form chylomicrons --> Chylomicrons are released into the lymphatic system to travel to the thoracic duct & enter the blood stream
  67. 67Describe the structure of a chylomicronCore of triglyceride & cholesterol ester with a phospholipid & apoprotein coat
  68. 68Describe the structure of a mixed micelleCore of products of lipid digestion i.e. cholesterol, monoglycerides, lysolecithin & free fatty acids) with a surface of bile salts
  69. 69Describe the ejection of bile saltsRelease is stimulated by CCK
    Bile is synthesised & secreted by hepatocytes --> stored & concentrated in the gallbladder --> Chyme in the S.I. stimulated CCK release --> On completion of lipid absorption approx. 5% of bile salts are recirculated via the enterohepatic portal circulation
  70. 70Describe the absorption of water in the large intestineControlled by the enteric nerve plexi & hormones (particularly aldosterone increases water reabsorption)
    The process consist of ion exchange followed by osmotic absorption of water
    - Na+ reabsorbed for K+
    - K+ for H+
    - Cl- for HCO3-

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(Gastrointestinal System) MD3002 Fichas sobre GI Physiology, creado por Lareyna Mcmenemy el 30/04/2019.
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