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Flashcards

GI

Stargazer English 148 cards

gastric structure

Cards in this deck (148)

  1. 1function of saliva− Cleanse and protect teeth
    − Digestion
    − Lubrication
    − Swallowing
    − Speech
    − Taste
    − Antimicrobial function
  2. 2salivary glands• Major gland
    − Parotid
    − Submandibular
    − Sublingual
    • Minor gland
    − Buccal Lingual palate
  3. 3what is saliva stimulated by?− Chemical stimuli
    − Physical stimuli
  4. 4stimulated saliva is released from the...?parotid and sub mandibular gland
  5. 5unstimulated saliva is released from the...?submandibular gland
  6. 6which protein protects the oral cavity from damage?enamel pelade
    - released in unstimulated saliva
  7. 7components of saliva• Water
    • Mucous → stops damaging tissues from what?
    • Enzymes
    − α amylase → from the parotid gland [initiates carbohydrate digestion]
    − lipase → within glands of the mucosa of the tongue (linguinal)
    • Proteins (100s)
    − Active research
  8. 8saliva Secretory structure- acini
    - ducts
  9. 9saliva acinus− 12 or more acinar cells; radially arranged around a central lumen
    − Zymogen granules; prevents auto-digestion
    − Mucus cells
    − Myoepithelial cells; contract to push saliva through duct to be excreted in the mouth
  10. 10saliva ducts− Intercalated duct
    − Striated duct
    − Excretory duct
  11. 11Process of saliva production• Produced and edited in 2 places
    − Acinar cells
    − Ductal cells
    1. Acinar cells produce primary saliva
    • Water
    • enzymes
    • Mucus
    • NaCl
    2. Passes through the intercalated duct and the striated duct
    3. Ductal cells modify saliva
    • NaCl reabsorption
    • HCO3 secretion
    4. Myoepithelial cells
    • stimulated by neural input → contract to eject saliva into mouth
  12. 12rate of flow of saliva. what is it affected by?• it is always hypotonic
    • flow is altered
    − ↑ flow; ↑ NaCl and HCO3 concentration why?
    → resembles plasma and primary saliva
    − ↓ flow; vice versa
    • saliva needs lots of contact time with the food
  13. 13define swallowing− process by which food passes from mouth to stomach
  14. 14mechanical digestion in the mouth− Chewing jaw opening and closing
    − movement of the tongue
  15. 15function of mechanical digestion in mouth− Breakdown of food into smaller particles and mixing with saliva for taste
    − Binding of particles into bolus for deglutition
  16. 16Mechanism of swallowing1. Oral phase
    2. Pharangeal phase
    3. Oesophageal phase
  17. 17Oral phase[voluntary]
    − Tongue moves upwards
    − Compression of bolus against hard palate
    − Respiration inhibited
    − Retraction of tongue forces bolus into pharynx
  18. 18Pharyngeal phase[involuntary]
    • process
    − Involuntary mechanism
    − Bolus pushed from pharynx into oesophagus
    − Soft palate reflected backward closing nasal pharynx
    − Epiglottis covers opening of larynx
  19. 19Oesophageal phaseo process
    − UOS relaxes → bolus moves into oesophagus
    − Stretch receptor activated
    − Start primary peristaltic wave (Vagal)
    − Secondary peristaltic wave (Enteric)
    − LOS relaxes → allows bolus to move into stomach
  20. 20Oesophageal manometry - purpose - how it works• Function
    − Esophageal manometry measures oesophageal motility
    − Diagnose abnormalities in;
    oesophageal contractions or
    strength of the muscle or
    LOS
    • How it works
    − Thin catheter with sensors is passed through the esophagus into the stomach
    − then patients swallows
  21. 21Lower esophageal sphincter - structure - function• Structure
    − 3-4cm long sphincter
    − Tonically contracted
    • Function
    1. Prevents reflux of material back into oesophagus
  22. 22Gastro-esophageal reflux disease• causes of retrograde flow of gastric contents into esophagus:
    − Abnormal peristalsis
    − Weak LOS contraction
    − Increase in thoraco-abdominal pressure
    • Effects
    − Pain/discomfort (heartburn)
    − Mucosal damage
    − Dysphagia [swallowing difficulties]
  23. 234 Cell types in gastric gland• mucus cell, parietal cell, chief cell and endocrine
  24. 24Gastric functions− Motility
    • Gastric accommodation- temporary storage reservoir
    • Trituration – Dissolve, mix and grind food particles
    • Gastric emptying - Control delivery to small intestine
    • Digestion – initiate digestive process (proteins) via gastric secretion
    − Protection
    • Foreign invasion (acid/proteases)
    • Mechanical abrasion (mucus)
    • Prevents autodigestion (mucus)
    − Absorption
    − Alcohol and fat soluble drugs (diffusion)
  25. 25causes of Gastric ulcers− ↓ mucus/HCO3 or ↑acid
    − NSIDs or H. Pylori
  26. 26'A window into digestion' - researcher - patient - discovery− William Beaumont (1822) and Alexis St Martin
    − Beaumont used the hole as a window- to ‘watch the process of digestion’
    − Discovered:
    − Digestion → chemical and mechanical process
    − Strong HCL secreted by the stomach to breakdown food
  27. 27Constituents of Gastric juice− Water and ions
    − HCl
    − Provides low pH (as low as 1 or 2!)
    − Prevents bacterial growth
    − Catalyses cleavage of pepsinogens to pepsin
    − Pepsinogens
    − proenzyme of pepsin
    − Pepsin breaks down proteins into peptides
    − Intrinsic factor
    • Glycoprotein
    • Binds to vitamin B12- allowing digestion in the ilium
    − Mucus
    • Protects gastric mucosa
    − Gastrin
    • From ‘G cells’
    • Regulates acid secretion
  28. 28gastric structuregastric structure
  29. 29Gastric GlandsGastric Glands
  30. 30cell types of the stomachcell types of the stomach
  31. 31Mucous neck Cell− Mucins
    − High molecular weight glycoproteins
    − Hydrophilic
    − Low solubility
    − High viscosity
    − High elasticity
    − Strong Adhesiveness
    − Bicarbonate ion secretion
    − Unstirred layer
  32. 32structure of mucus cellsstructure of mucus cells
  33. 33Gastric-mucosal barrier− gastric mucosal barrier structure
    − Mucus entraps alkali fluid
    − Disruptions to the barrier
    − Alcohol
    − vinegar
    − bile
  34. 34diagram of the gastro-mucosal barrierdiagram of the gastro-mucosal barrier
  35. 35chief cell− Zymogen granules
    • Inactive pepsinogen
    • Acid splits off part of molecule – active pepsin
    • Starts digestion of protein
    • 20% of the protein in a meal
  36. 36chief cell diagramchief cell diagram
  37. 37Endocrine cells consists of...?• G cells
    − - Secrete gastrin
    • D cells
    − - Secrete somatostatin which inhibits gastrin secretion
  38. 38Enterochromaffin-like (ECL) cells secrete− histamine → which stimulates gastric & acid secretion
  39. 39unstimulated Enterochromaffin-like (ECL) cellsunstimulated Enterochromaffin-like (ECL) cells
  40. 40How is gastric acid secreted?• H+/K+ ATPase
    − ‘Proton Pump’
    − Acid secretion against the concentration gradient
    ∴ process requires energy
    • Cl/HCO3- exchanger
    − When H+ is pumped out- excess of HCO3 left behind
    − Removed by HCO3- exchanger
    • Note: During acid secretion blood pH is high [aka Alkaline tide’]
  41. 41diagram of gastric secretiondiagram of gastric secretion
  42. 42control of acid secretion• Parietal cell
    • Receptors
    − Gastrin (from G cell)
    − ACh (from Vagus)
    − Histamine (from ECL cell)
    − Prostaglandins inhibit histamine stimulated secretion
    • These receptors act by
    − Increased intracellular calcium
    − Activation of proton pump
  43. 43diagram of gastric controldiagram of gastric control
  44. 44define Gastric /Peptic Ulcers• Break in mucosal barrier exposing underlying tissue to corrosive action (acid, proteases)
  45. 45Symptoms of ulcers− Abdominal pain
    − Bloating
    − Nausea/vomiting
    − Bleeding- haemorrhage and anaemia
  46. 46Ulcer Formation• Produced by imbalance:
    − ↓ mucus and/or HCO3
    − ↑ acid production
    • Endogenous Factors
    − Anxiety → Parasympathetic output (Ach, Gastrin) →↑acid
    − Stress → Sympathetic output (Ad) → ↓ HCO3/mucus
    • Exogenous Factors
    − Diet
    − Alcohol - damages cells, stimulates parietal cell
    − Coffee – stimulates parietal cell
    − Non-steroidal anti-inflammatory drugs (NSAIDs)
    •
    NB. prostaglandin production
    − inhibit acid production by histamine (aspirin, indomethecin)
    − ↑ bicarbonate and mucus secretion
    • bacterium
    − Helicobacter pylori and its role in gastritis and peptic ulcer disease”
  47. 47helobacter pylori effect• Releases [which breaks down tissues]
    − Proteases
    − Endotoxins
    • linked to
    − gastric cancer
  48. 48ulcer treatment• Aimed at
    − reducing acid environment to allow regeneration of cells
    − killing H.Pylori
    • ulcer treatment
    1. Diet
    − Avoid acid containing food and beverages
    Ex. Alcohol, coffee
    2. Antacids
    − Neutralise lumen acid
    3. Partial vagotomy (almost obsolete now)Reduce Ach is this a another treatment?
    4. Anti-bacterial drugs
    − Amoxicillin
    − Clarithromycin Bismuth
    5. H2 antagonists
    − Inhibition of parietal cell stimulation by histamine
    ex. cimetidine, ranitide
    6. Proton pump inhibitors
    − Inhibition of parietal cell activation
    Ex. omeprazole
  49. 49regions of the stomach• Anatomical and functional regions
  50. 50Functiona and Anatomical region of stomach• Anatomical regions
    − Cardia
    − Fundus
    − Corpus
    − Antrum
    − pylorus
    • Functional regions
    − Reservoir
    − Antral pump
  51. 51diagram of the stomach regiondiagram of the stomach region
  52. 52stomach motility after a meal• Fasting state- quiescent
    • Meal enters stomach
    − LOS relaxes- Receptive relaxation of fundus and body
    − Accommodation
    • Peristalsis begins
    1. Begin in the middle- push towards the pylorus
    2. Mixing occurs in antrum
    • Antral systole
    – Peristaltic wave pushes contents back into body- triturating partials
    – Some chyme into duodenum- pyloric sphincter contracts
  53. 53diagram of stomach motility after a mealdiagram of stomach motility after a meal
  54. 54Feedback Regulation of the stomach• Reason regulation of gastric emptying is highly controlled
    − Optimal digestion and absorption
    − Prevent overload of intestine
    − Controls delivery of calories and sugar
    • Gastric emptying influenced by
    − composition of chyme in stomach
    − duodenum
    − Ilium
    − Colon
    • Composition of chyme
    − Physical composition (particle size <1mm)
    − Chemical composition; Acid, Osmolality and Nutrients
  55. 55Rate of Gastric Emptying• Liquids
    − empty faster than solids – 2-3mins
    • Solids
    − lag due to time to reduce particle size (1 mm diam)
  56. 56Delivery of sugar to the intestineDelivery of sugar to the intestine
  57. 57Feedback regulation diagramFeedback regulation diagram
  58. 58what does the exocrine pancreas duct secrete?• Exocrine gland (85%) – Acinus
    [similar to salivary gland]
    − Water and ions
    − Bicarbonate
    − Enzymes –essential for normal digestion
    Note: water and bicarbonate neutralizes duodenal contents to prevent damage and pH for enzymes
  59. 59Pancreatic Enzymes• Responsible for digestive function of pancreas
    − proteins
    1. Trypsinogen - trypsin
    2. Chymotrypsinogen - chymotrypsin
    3. Proelastase - elastase
    4. Procarboxypeptidase – carboxypeptidase
    − Fats
    5. Lipase and phospholipase
    − Nucleic acids
    6. nucleases
    − Carbohydrates
    7. α-amylase
  60. 60Exocrine Pancreas• Acinar cells
    − produce a small amount of protein (enzyme rich) fluid
    − it passes through the intercalated duct- ductal cells and centroacrinar cells secret bicarbonate, water and ions
    • Note: A rise in [Ca] triggers acinar cell secretion
  61. 61diagram of acinar secretiondiagram of acinar secretion
  62. 62dual secretion diagramdual secretion diagram
  63. 63cystic fibrosis• Patients with cystic fibrosis had a defective
    − ductal secretion
    • effects of CF
    − Less negative in lumen
    − Less Na+ and water
    − Less secretion
    − Less enzyme action in gut (pH too low)
    − Malabsorption
  64. 64Duodenal feedbackDuodenal feedback
  65. 65Liver structureLiver structure
  66. 66function of liver• Metabolic power house of body, <500 vital functions
    1. Protein synthesis, particularly albumin and clotting factors (e.g. fibrinogen)
    2. Storage
    1. triglycerides
    2. glycogen
    3. some vitamins (e.g. vitamin A)
    3. Gluconeogenesis – conversion of lipids and amino acids to glucose
    4. Toxins
    1. Conjugation
    2. Breakdown
    3. Bile - Synthesis and secretion of bile acids and bilirubin
  67. 67liver lobulesliver lobules
  68. 68functional anatomyfunctional anatomy
  69. 69how much bile secretion?• 250ml-1000ml per day!
    • Concentrated in the gall bladder for storage ( 15-60ml volume)
  70. 70main functions of bile• Adequate pH
    • Facilitate fat digestion/ emulisification
    • Excretion of waste products (cholesterol)
  71. 71Bile composition• Depends on the meal
    • Contains
    • Water and ions- alkali
    • Bile acids- digestion and absorption of dietary fats (micelle formation) 70%
    • Proteins- protect against infection
    • Bile pigments- breakdown products of hemoglobin (bilirubin)
    • Organic molecules
    • Cholesterol (4%)
    • Phospholipid- Lecithin (20%)
  72. 72Bile acids contains...?• Hydroxyl and carboxyl groups
    • Alcohol group
  73. 73diagram bile acidsdiagram bile acids
  74. 74difference between bile acid and bile saltbile salt is a conjugated [taurine/glycine] bile acid
  75. 75micelle formationmicelle formation
  76. 76the gallbladder function• Absorption
    • Na+, Cl- and H2O- concentrates bile
    • Secretion
    • (H+, Mucin) -neutralise alkaline bile and protect epithelium of gall bladder
    • Motor
    • No digestion – relaxation and storage
    • Digestion- contraction and delivery of bile
  77. 77hormonal control in the small intestins• Secretin
    • Stimulates secretion of bile
    • CCK
    • -Relaxes the sphincter of Oddi
    • -Contracts the gall bladder
  78. 78Enterohepatic circulationrefers to the circulation of biliary acids, bilirubin, drugs, or other substances from the liver to the bile, followed by entry into the small intestine, absorption by the enterocyte and transport back to the liver.
  79. 79sphincter from the gall bladder to the small intestinesphincter of oddi
  80. 80diagram of the movement of chyme form the stomach to the duodenumdiagram of the movement of chyme form the stomach to the duodenum
  81. 81characteristic of villus• 1mm long, rich blood supply with central lacteal
  82. 82• Enterocytescontinuous mitosis at base of crypt
  83. 83small intestine secretion of fluid• Crypt cells- Na Cl
    • Paneth cells –defensins
    • Goblet cells- mucus
    • Endocrine cells- hormones
  84. 84micro-villli: brush border• Increase in surface area
    • Glycocalyx (unstirred layer)
    • Brush border enzymes
    • Additional surface for absorption
    • Maltase, lactase, sucrase, dipeptidases
    • Absorbed pancreatic enzymes
  85. 85advantages of brush border• Limits rise in luminal osmolality
    • Close proximity to site of absorption
  86. 86carbohydrate digestioncarbohydrate digestion
  87. 87carbohydrate transportcarbohydrate transport
  88. 88protein digestionprotein digestion
  89. 89protein transportprotein transport
  90. 90Lipid digestionLipid digestion
  91. 91Lipid absorptionLipid absorption
  92. 92Absorption key pointsAbsorption key points
  93. 93relationship between absorption and secretionrelationship between absorption and secretion
  94. 94Malabsorbtioncauses
    • Absent or defective digestive enzymes
    • Defects in transporter proteins
    • Diseases or infections of small intestine
    symptom
    steatorrhea (frothy greasy stools), diarrhoea, weight loss
  95. 95example of malabsorption• Lactase deficiency - lactose intolerance, local osmolality ↑
    • Coeliac disease – abnormal immune response to gluten – loss of mucosal epithelium
  96. 96large intestine structure• Tenia coli – 3 bands longitudinal muscle
    • Haustra – pockets undergoing segmentation
    • Slow movement of contents
    • No villi
    • High concentration of goblet cells- mucus secretion
  97. 97Anatomy of large intestineAnatomy of large intestine
  98. 98colon motilitycolon motility
  99. 99large intestine main function• High Mucus secretion- goblet cell
    • No carrier mediated transport of nutrients (absorption by diffusion)
    • Efficient water reabsorption
    • Follows Cl and Na movement
    • HCO3 buffers acid produced by bacterial fermentation
  100. 100Gastro-colic response• 2-3 times per day
    • Mass movement of material into aboral end of colon- ready for defecation
  101. 101Segmented contractions• 99% of the time
    • 1. Retain material in the proximal colon (water reabsorption and fermentation)
    • 2. Mixing contents
  102. 102diagram of gut celldiagram of gut cell
  103. 103Gut flora• Gut ‘microbiome’ forms hours after birth
    • Primes the guts immune system
    • Many functions
    • Symbiosis between host and bacteria
  104. 104how many micro organisms in the gut?• 1014 micro organisms (100 000 billion!!) >500 different species
  105. 105GI tract flora• Oral – Dental caries
    • Stomach – H pylori
    • Large Intestine
    • Bacterial fermentation
    • Short chain fatty acids,
    • Synthesise essential nutrients - folic acid, Vit K
    • Absorb B12
    • Probiotics? No clear evidence
  106. 106Dietary fibre: fermentation• Indigestible portion of plant foods - bulk
  107. 107purpose of bulk in the GI• Motility
    • Decrease gastric emptying-stomach
    • Increase motility of colon-intestine
    • Absorption
    1) Holds water
    2) Traps sugars, cholesterol and fats- slows absorption
    3) Slows absorption of enzymes and nutrients
    4) Colonic bacterial substrate
    • Prevention and treatment of constipation, hemorrhoids and diverticulosis
  108. 108Dietary fibre: fermentation diagramDietary fibre: fermentation diagram
  109. 109how many GI gas produced per day• 1-4 pints of gas produced per day!!
  110. 110sources of GI gas• Sources
    • Swallowed air
    • Result of neutralisation of acid or bacterial metabolism
    • Diffusion from blood (small)
  111. 111Bacterial fermentation- fibre• Non absorbable substrate -beans (stachyose), onions, cabbage,
    • prunes and nuts
  112. 112Component GI gases• Hydrogen, Methane (ammonia, hydrogen sulphide, indole, skatole, volatile amines)
  113. 113harmful effects of GI gases• Avoid by fasting, enemas, inert gas perfusions
  114. 114net absorption in the stomach• Alcohol absorption
  115. 115net absorption in the small intestine• 100% protein
    • 100% digestible carbohydrate
    • 95% fats
    • Water, electrolyte (eg Na+, Cl-, Ca2+, Fe2+) vitamins (eg B12)
  116. 116net absorption in the large intestine• Fermentation products, esp SCFA (eg butyrate)
    • Water and electrolytes
  117. 117Name the substances that are excretedindigestible fibre, bacteria, inorganic material, fat derivatives, desquamated cells, mucus
  118. 118causes of diarrhoea- osmotic
    - secretory
    - inflammation /infectious
    - deranged motility
  119. 119what happens with diarrhoea• Increase stool volume or increased frequency of defecation
    • Can be fatal- 2 million die per year (e.g. cholera)
  120. 120Osmotic causes of diarrhoea• Increased solutes in lumen causes less water reabsorption
    • Poorly absorbed substrate (i.e. sorbitol)
    • Malabsorption disorder (lactose intolerance)
  121. 121secretory causes of diarrhoea• Increased secretion of water into the lumen (when secretion exceeds absorption).
    • Cholera Toxin- opening of Cl- channel, increase secretion of water
    • Laxatives, Hormones, Drugs (antidepressants), Caffeine
  122. 122Inflammatory/infectious causes of diarrhoea• Pathogens breach and damage the absorptive epithelium
  123. 123deranged motility• Altered transit time hence less time for water reabsorption
  124. 124how is defecation controlled. Faeces moved into the rectum, leading to distension. This activates stretch receptors- afferent signals to the spinal cord [sensory]
    • 2. If it is convenient to defecate, voluntary motor nerves are inhibited allowing the external anal sphincter to relax [pudendal]
    • 3. Symp and Parasymp- Stimulate contraction of the rectum and relaxation of the internal anal sphincter
  125. 125diagram of defecation controldiagram of defecation control
  126. 126defecation- storage and emptyingthere is a switch between the two
  127. 127storage continence [ ability to control movement]- Continence[ ability to control movement]
    • Rectal accommodation
    • Sphincter closure
  128. 128storage incontinence• Pelvic floor damage
    • Pudendal nerve damage
  129. 129how does defecation occur?• Colorectal contraction
    • Raised abdominal pressure
    • Sphincter relaxation
    • Internal (autonomic)
    • External (somatic)
  130. 130what happens in defecation failure?• Spinal injury
    • Outlet obstruction
  131. 131difference between appropriate and inappropriate vomiting• Some may be appropriate – e.g. the need to expel ingested toxin. Others are inappropriate and have no useful purpose (pregnancy)
    • Food poisoning
    • Bowel obstruction
    • Bowel disease
    • Pregnancy
    • Motion sickness
    • Cancer therapy
  132. 132what is vomiting preceded by?-nausea
    − Pallor
    − Sweating
    − Salivation
    − Irregular breathing
    − Increased heart rate
    − Retching (several, increased force)
  133. 133GI motor correlates of nausea• Expulsion caused by contractions of the diaphragm and abdominal wall
    • The proximal stomach relaxes to accommodate returning intestinal contents
    • Antral motility inhibited to prevent gastric emptying
    • Retrograde Giant contractions return intestinal contents to the stomach
  134. 134diagram of GI motor correlates of nauseadiagram of GI motor correlates of nausea
  135. 135diagram of the act of vomitingdiagram of the act of vomiting
  136. 136the act of vomiting• GI smooth muscle
    • Relaxation of all areas from gastric body to upper oesophagus
    • Violent contractions of gastric antrum
    • Respiratory system
    • Slow deep inspirations to decrease oesophageal pressure
    1. Skeletal muscle
    • Contraction of abdominal muscle
    • Retching
    • Upper oesophageal sphincter remains closed
    • Vomiting
    • Upper oesophageal sphincter opened
  137. 137how are toxins detected?- pre-ingestion
    - pre-absorbtion
    - post-absorption
    Note: 1 and 2 are rapid detections before the toxins enter the blood stream
  138. 138pre-ingestion toxin detector• Smell, sight, taste
  139. 139pre-absorption toxin detector• Toxin detection in the lumen
    • Mechanoreceptors and chemoreceptors
    • Neutralisation/expulsion (vomiting)
  140. 140post-absorption toxin detector• Chemoreceptive trigger zone -area postrema
    • Outside of blood brain barrier- samples toxins in the blood
    • Induces nausea to prevent further ingestion and activates vomiting centres
    • Can be activated directly with drugs (emetics)
  141. 141Origin of sensory triggers• GI
    • Genitourinary system
    • Hypothalamus/cerebellum
    • Vestibular apparatus
    • Chemoreceptor trigger zone- 4th ventricle
  142. 142GI origin of sensory triggers• Distension (stomach and duodenum)
    • Irritation of back of throat
    • Chemical or toxin
  143. 143origin of sensory triggers; Genitourinary systeminjury/infection
  144. 144origin of sensory triggers; Hypothalamus/cerebellumo stimulation or injury
  145. 145origin of sensory triggers; Vestibular apparatuso Motion sickness
  146. 146origin of sensory triggers; Chemoreceptor trigger zone- 4th ventricleo Anaesthesia
    o Drugs
    o Radiation
    o Toxins
  147. 147Inputs to the vomiting centres− All go to the medulla oblongata
    − Higher centres
    − Vestibular systems
    − Cranial nerves [vagus]
    − Postrema
    − Stimulared by chemotherapy drug
  148. 148diagram GI origins of sensory triggersdiagram GI origins of sensory triggers

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Flashcards on GI, created by Stargazer on 04/06/2014.
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