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Author: John Williams, M.D., Ph.D., 2009

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M1 - GI Sequence



               Intestines
        John Williams, M.D., Ph.D.



Winter, 2009
THE SMALL INTESTINE



Human small intestine 6-7 m long
    Duodenum 20-30 cm
    Jejunum 2.5 m
    Ileum      3.5 m




     FUNCTIONS
      Digestion
      Absorption
      Secretion
      Motility

                                   Fig. 7-2 Granger, D, et al. Clinical Gastrointestinal
                                   Physiology. W.B. Saunders, Philadelphia, PA; 1985: 144.
Small Intestine Anatomy




   Sources Undetermined
Histologic organization of the small intestinal mucosa




         Trier, JS, Modara, JL. “Functional morphology of the mucosa of the small intestine”. In Johnson, LR.
         Physiology of the Gastrointestinal Tract. Vol. II. Raven Press, New York, NY, 1981: 926.
60%


30%
DIETARY CARBOHYDRATES (cont)

•  Normal American diet contains 200-300 g
     (50% of caloric intake)

•  Serves an energy and carbon source

•  Digestion includes a luminal phase and
      a brush border phase

•  Only monosaccharides are appreciably
     absorbed
Starch= Amylose & Amylopectin




          Source Undetermined



•  Amylase (pH optima 7) cleaves interior α1-4 linkages but not α1-6
•  Endproduct is a mixture of maltose, maltotriose and limit dextrans
•  Acarbose – Amylase inhibitor
Source Undetermined
MECHANISM OF MONOSACCHARIDE ABSORPTION




           2




 John Williams
Lactase is present in infancy
                                                                                      by disappears to a variable
                                                                                      extent during childhood in
                                                                                      most humans.

                                                                                      Exception is Northern
                                                                                      Europeans and European
                                                                                      Americans-commonly retain
                                                                                      lactase into adulthood.




Fig. 7-15 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 169.
DIETARY PROTEIN
•  Normal humans require about 0.75 g/kg body
   weight of high quality dietary protein daily

•  Nine essential amino acids are not synthesized and
   must be obtained from diet

•  Normal American diet contains 70-90 g/day

     Also endogenous protein in digestive secretions
     and shed epithelial cells
DIETARY PROTEIN (cont)

•  Digestion includes a luminal and brush
   border phase

•  Both amino acids and di- and tri-peptides
   absorbed

•  Digestion normally quite complete
Fig. 11-8 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 114.
Fig 7-18 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 174.
Peptidases ~20                                     Protein Digestion
 Including enterokinase                             1 luminal (stomach, pancreas)
 Endo-; amino; carboxly etc                         2 brush border (enterocyte)
                                                    3 intracellular (enterocyte)

Di & tri Peptides
H+ coupled                                                  Na+ coupled
PepT1




Small amounts of peptides enter blood intact- may       Carrier to exit cell
be important in immune response
      Source Undetermined
Apical transporter
PepT1




                 Source Undetermined
Defects in Absorption of Protein Digestion
Products due to Altered Transport Systems in
Gut and Kidney

 •  Cystinuria
      Autosomal Recessive
      Increased excretion in urine with renal stones

 •  Hartnup Disease
      Autosomal Recessive
      Impaired absorption of neutral amino acids
      Symptoms of Niacin deficiency (Pellagra)

 Patients normally don’t show protein malnutrition-
        di and tri peptides sufficient
DIETARY LIPID
•  Normal American diet about 100g/day primarily as
   triglyceride

•  Long chain “essential” polyunsaturated fatty acids,
   cholesterol, and fat soluble vitamins also present

•  Lipid digestion begins in stomach and is
   completed in upper intestine in the lumen

•  Multiple lipase enzymes have pH optima between
   6 and 7
STEPS IN LIPID DIGESTION
1. Emulsification
    physical process takes place in stomach
    phospholipids, proteins facilitate

2. Digestion
     stomach and duodenum

3. Solubilization
      requires bile salts
      role of mixed micelles

4. Absorption
    normally <5gm in stool- more is “steatorrhea”
• pH optimum 6-7
    • in presence of bile salts acid inactivates




Fig. 8 Johnson, L. Essential Medical Physiology New York Raven Press 1992: 515.
Mixed micelles solubilize the
   products of lipid digestion.




Colipase anchors lipase to the
fat droplet in the presence of
bile salts.




             Source Undetermined
Ways to alter fat digestion and absorption


  1.  Olestra - Fake fat, can’t be digested

  2.  Orlistat (Xenical) – Covalent Lipase inhibitor
                           Now available OTC as Alli




  Side effect of both is malabsorption and diarrhea
FABP




Source Undetermined
Short and medium
                                                                                chain fatty acids
                                                                                as well as glycerol




Fig. 11-14 Johnson, L. Gastrointestinal Physiology, 6th ed. Mosby Elsevier, St. Louis, MO; 2001: 136.
Medium Chain Triglycerides


1.  Fatty acids are 6-12 carbons in chain length

2.  Present in small amounts in normal diet

3.  Can be digested and absorbed without bile
     salts due to increased water solubility

4. Fatty acids not reesterified but taken up into
   the portal vein
Source Undetermined
Cholesterol Absorption

•  Luminal cholesterol comes largely from diet
   and bile; about 50% absorbed by intestine

•  Cholesterol absorbed selectively as
   compared to plant sterols

•  Absorbed cholesterol released in
   chylomicron and goes back to liver as
   chylomicron remnants

•  Ezetimibe (Zetia) is a new drug that blocks
   cholesterol entry into the enterocyte
CALCIUM ABSORPTION

1.  Dietary intake about 1000 mg/day with net
    absorption of about 100 mg/day

2.  Most active in duodenum and involves an energy
    dependent, transcellular pathway

3.  Regulated by active form of Vit D, 1,25(OH)2 Vit
    D, also known as 1,25(OH)2-cholecalciferol
Mechanism of Intestinal Calcium Absorption
                     Paracellular – Vit D-independent




Transcellular – Vit D-dependent

Fig. 9 Chang, E, Sitrin, M, Black, D. Gastrointestinal, Hepatobiliary, and Nutritional Physiology. Lippincott – Raven, Philadelphia, PA;
1996: 204.
MOLECULAR COMPONENTS
 OF INTESTINAL CALCIUM ABSORPTION

1.  Entry across the apical brush border is mediated
    by a specific Ca2+ entry channel known as CaT1

2.  Within the enterocyte a calcium binding protein,
    calbindin binds and transports Ca2+

3.  Ca2+ exit across the basolateral membrane is
    mediated by the plasma membrane
    Ca-2+ATPase, PMCA1
Synthesis and Action of Vitamin D




    Fig. 12-6 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 133.
Primary Sites of Nutrient Absorption
                        Stomach
                        Lipophillic molecules (ethanol)
                        Weak acids (aspirin)




      John Williams
INTESTINAL ELECTROLYTE ABSORBTION
           AND SECRETION
Volumes and ionic composition of fluid
         entering the human intestine




Source Undetermined
DUODENAL FLUID DYNAMICS

•  Mucosa is leaky allowing rapid osomotic
   equilibration of hypertonic and hypotonic
   meals

•  Duodenal secretion of HCO3- from Brunner’s
   glands

•  Absorption by small intestine is then isotonic
Cellular Models of Intestinal Sodium
                    Absorption




Figs. 7-7 and 7-8 from Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA;
1985.




                         Can be regulated by contents, neurotransmitterers,
                         inflammatory mediators and systemic hormones
                         particularly Angiotensin II
Fluid Absorption According to the Standing Osmotic Gradient Model




                                                                                Can account for isotonic movement
                                                                                Of fluid by use of localized
                                                                                hypertonicity




    Fig. 12-4 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007.
Absorption




                                   Secretory diarrhea of Cholera
                                   Is due to Cholera Toxin activating
Secretion                          cAMP and stimulating secretion
                                   To 15 –20 liters per day




             Source Undetermined
INTESTINAL MOTILITY
FUNCTIONS OF INTESTINAL MOTILITY


1.  Mixing of foodstuffs, digestive secretions and enzymes

2.  Facilitate contact of chyme with intestinal mucosa

3.  Net propulsion in an aboral direction
Intraluminal Pressure Changes in the Duodenum of
                 a Concious Man




       Fig. 5-1 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 42.




 In duodenum contractions occur at intervals of 5 sec or multiples of 5
Electrical Threshold for Generation of Action
                     Potentials




        Source Undetermined




Frequency of slow waves is 12/min in duodenum and decreases to 9/min in
The ileum. (Another site of pacemaker activity)
ICC Cells
Interstitial Cells of
Cahal




              Source Undetermined
Fed pattern initiated by the
                      Presence of chyme in the
                      intestine




Source Undetermined
Villus contraction which
                                                                                         increases after a meal
                                                                                         also helps mix unstirred
                                                                                         layer and compress the
                                                                                         lacteal




                                                                                         Only very short peristaltic
                                                                                         movements occur in the
                                                                                         fed state




Fig. 5-3 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 44.
Jim Sherman
Migrating Motility Complex




    Jim Sherman
Relationship between Plasma Motilin and the MMC




Source Undetermined
MINERAL ABSORPTION
ESSENTIAL MINERAL ELEMENTS

1.  Required to maintain normal physiology and
    health

2. Occur in diet, sometimes as trace elements

3. Variable absorptions may be regulated

4. In steady state intestinal absorption equals
   body losses
Additional Source Information
                   for more information see: http://open.umich.edu/wiki/CitationPolicy

Slide 4 – Fig. 7-2 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 144.
Slide 5 – Source Undetermined
Slide 6 – Trier, JS, Modara, JL. “Functional morphology of the mucosa of the small intestine”. In Johnson, LR. Physiology of
          the Gastrointestinal Tract. Vol. II. Raven Press, New York, NY, 1981: 926.
Slide 9 – Source Undetermined
Slide 10 – Source Undetermined
Slide 11 – John Williams
Slide 12 – Fig. 7-15 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 169.
Slide 15 – Fig. 11-8 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 114.
Slide 16 – Fig 7-18 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 174.
Slide 17 – Source Undetermined
Slide 18 – Source Undetermined
Slide 22 – Fig. 8 Johnson, L. Essential Medical Physiology New York Raven Press 1992: 515.
Slide 23 – Source Undetermined
Slide 25 - Source Undetermined
Slide 26 – Fig. 11-14 Johnson, L. Gastrointestinal Physiology, 6th ed. Mosby Elsevier, St. Louis, MO; 2001: 136.
Slide 28 – Source Undetermined
Additional Source Information
                    for more information see: http://open.umich.edu/wiki/CitationPolicy

Slide 31 – Fig. 9 Chang, E, Sitrin, M, Black, D. Gastrointestinal, Hepatobiliary, and Nutritional Physiology. Lippincott –
           Raven, Philadelphia, PA; 1996: 204.
Slide 33 – Fig. 12-6 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 133.
Slide 34 – John Williams
Slide 36 – Source Undetermined
Slide 38 – Figs. 7-7 and 7-8 from Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985.
Slide 39 – Fig. 12-4 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007.
Slide 40 – Source Undetermined
Slide 44 – Fig. 5-1 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 42.
Slide 45 – Source Undetermined
Slide 46 – Source Undetermined
Slide 47 – Source Undetermined
Slide 48 – Fig. 5-3 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 44.
Slide 49 – Jim Sherman
Slide 50 – Jim Sherman
Slide 51 – Source Undetermined

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01.13.09: Intestines

  • 1. Author: John Williams, M.D., Ph.D., 2009 License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution–Non-commercial–Share Alike 3.0 License: http://creativecommons.org/licenses/by-nc-sa/3.0/ We have reviewed this material in accordance with U.S. Copyright Law and have tried to maximize your ability to use, share, and adapt it. The citation key on the following slide provides information about how you may share and adapt this material. Copyright holders of content included in this material should contact open.michigan@umich.edu with any questions, corrections, or clarification regarding the use of content. For more information about how to cite these materials visit http://open.umich.edu/education/about/terms-of-use. Any medical information in this material is intended to inform and educate and is not a tool for self-diagnosis or a replacement for medical evaluation, advice, diagnosis or treatment by a healthcare professional. Please speak to your physician if you have questions about your medical condition. Viewer discretion is advised: Some medical content is graphic and may not be suitable for all viewers.
  • 2. Citation Key for more information see: http://open.umich.edu/wiki/CitationPolicy Use + Share + Adapt { Content the copyright holder, author, or law permits you to use, share and adapt. } Public Domain – Government: Works that are produced by the U.S. Government. (USC 17 § 105) Public Domain – Expired: Works that are no longer protected due to an expired copyright term. Public Domain – Self Dedicated: Works that a copyright holder has dedicated to the public domain. Creative Commons – Zero Waiver Creative Commons – Attribution License Creative Commons – Attribution Share Alike License Creative Commons – Attribution Noncommercial License Creative Commons – Attribution Noncommercial Share Alike License GNU – Free Documentation License Make Your Own Assessment { Content Open.Michigan believes can be used, shared, and adapted because it is ineligible for copyright. } Public Domain – Ineligible: Works that are ineligible for copyright protection in the U.S. (USC 17 § 102(b)) *laws in your jurisdiction may differ { Content Open.Michigan has used under a Fair Use determination. } Fair Use: Use of works that is determined to be Fair consistent with the U.S. Copyright Act. (USC 17 § 107) *laws in your jurisdiction may differ Our determination DOES NOT mean that all uses of this 3rd-party content are Fair Uses and we DO NOT guarantee that your use of the content is Fair. To use this content you should do your own independent analysis to determine whether or not your use will be Fair.
  • 3. M1 - GI Sequence Intestines John Williams, M.D., Ph.D. Winter, 2009
  • 4. THE SMALL INTESTINE Human small intestine 6-7 m long Duodenum 20-30 cm Jejunum 2.5 m Ileum 3.5 m FUNCTIONS Digestion Absorption Secretion Motility Fig. 7-2 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 144.
  • 5. Small Intestine Anatomy Sources Undetermined
  • 6. Histologic organization of the small intestinal mucosa Trier, JS, Modara, JL. “Functional morphology of the mucosa of the small intestine”. In Johnson, LR. Physiology of the Gastrointestinal Tract. Vol. II. Raven Press, New York, NY, 1981: 926.
  • 8. DIETARY CARBOHYDRATES (cont) •  Normal American diet contains 200-300 g (50% of caloric intake) •  Serves an energy and carbon source •  Digestion includes a luminal phase and a brush border phase •  Only monosaccharides are appreciably absorbed
  • 9. Starch= Amylose & Amylopectin Source Undetermined •  Amylase (pH optima 7) cleaves interior α1-4 linkages but not α1-6 •  Endproduct is a mixture of maltose, maltotriose and limit dextrans •  Acarbose – Amylase inhibitor
  • 11. MECHANISM OF MONOSACCHARIDE ABSORPTION 2 John Williams
  • 12. Lactase is present in infancy by disappears to a variable extent during childhood in most humans. Exception is Northern Europeans and European Americans-commonly retain lactase into adulthood. Fig. 7-15 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 169.
  • 13. DIETARY PROTEIN •  Normal humans require about 0.75 g/kg body weight of high quality dietary protein daily •  Nine essential amino acids are not synthesized and must be obtained from diet •  Normal American diet contains 70-90 g/day Also endogenous protein in digestive secretions and shed epithelial cells
  • 14. DIETARY PROTEIN (cont) •  Digestion includes a luminal and brush border phase •  Both amino acids and di- and tri-peptides absorbed •  Digestion normally quite complete
  • 15. Fig. 11-8 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 114.
  • 16. Fig 7-18 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 174.
  • 17. Peptidases ~20 Protein Digestion Including enterokinase 1 luminal (stomach, pancreas) Endo-; amino; carboxly etc 2 brush border (enterocyte) 3 intracellular (enterocyte) Di & tri Peptides H+ coupled Na+ coupled PepT1 Small amounts of peptides enter blood intact- may Carrier to exit cell be important in immune response Source Undetermined
  • 18. Apical transporter PepT1 Source Undetermined
  • 19. Defects in Absorption of Protein Digestion Products due to Altered Transport Systems in Gut and Kidney •  Cystinuria Autosomal Recessive Increased excretion in urine with renal stones •  Hartnup Disease Autosomal Recessive Impaired absorption of neutral amino acids Symptoms of Niacin deficiency (Pellagra) Patients normally don’t show protein malnutrition- di and tri peptides sufficient
  • 20. DIETARY LIPID •  Normal American diet about 100g/day primarily as triglyceride •  Long chain “essential” polyunsaturated fatty acids, cholesterol, and fat soluble vitamins also present •  Lipid digestion begins in stomach and is completed in upper intestine in the lumen •  Multiple lipase enzymes have pH optima between 6 and 7
  • 21. STEPS IN LIPID DIGESTION 1. Emulsification physical process takes place in stomach phospholipids, proteins facilitate 2. Digestion stomach and duodenum 3. Solubilization requires bile salts role of mixed micelles 4. Absorption normally <5gm in stool- more is “steatorrhea”
  • 22. • pH optimum 6-7 • in presence of bile salts acid inactivates Fig. 8 Johnson, L. Essential Medical Physiology New York Raven Press 1992: 515.
  • 23. Mixed micelles solubilize the products of lipid digestion. Colipase anchors lipase to the fat droplet in the presence of bile salts. Source Undetermined
  • 24. Ways to alter fat digestion and absorption 1.  Olestra - Fake fat, can’t be digested 2.  Orlistat (Xenical) – Covalent Lipase inhibitor Now available OTC as Alli Side effect of both is malabsorption and diarrhea
  • 26. Short and medium chain fatty acids as well as glycerol Fig. 11-14 Johnson, L. Gastrointestinal Physiology, 6th ed. Mosby Elsevier, St. Louis, MO; 2001: 136.
  • 27. Medium Chain Triglycerides 1.  Fatty acids are 6-12 carbons in chain length 2.  Present in small amounts in normal diet 3.  Can be digested and absorbed without bile salts due to increased water solubility 4. Fatty acids not reesterified but taken up into the portal vein
  • 29. Cholesterol Absorption •  Luminal cholesterol comes largely from diet and bile; about 50% absorbed by intestine •  Cholesterol absorbed selectively as compared to plant sterols •  Absorbed cholesterol released in chylomicron and goes back to liver as chylomicron remnants •  Ezetimibe (Zetia) is a new drug that blocks cholesterol entry into the enterocyte
  • 30. CALCIUM ABSORPTION 1.  Dietary intake about 1000 mg/day with net absorption of about 100 mg/day 2.  Most active in duodenum and involves an energy dependent, transcellular pathway 3.  Regulated by active form of Vit D, 1,25(OH)2 Vit D, also known as 1,25(OH)2-cholecalciferol
  • 31. Mechanism of Intestinal Calcium Absorption Paracellular – Vit D-independent Transcellular – Vit D-dependent Fig. 9 Chang, E, Sitrin, M, Black, D. Gastrointestinal, Hepatobiliary, and Nutritional Physiology. Lippincott – Raven, Philadelphia, PA; 1996: 204.
  • 32. MOLECULAR COMPONENTS OF INTESTINAL CALCIUM ABSORPTION 1.  Entry across the apical brush border is mediated by a specific Ca2+ entry channel known as CaT1 2.  Within the enterocyte a calcium binding protein, calbindin binds and transports Ca2+ 3.  Ca2+ exit across the basolateral membrane is mediated by the plasma membrane Ca-2+ATPase, PMCA1
  • 33. Synthesis and Action of Vitamin D Fig. 12-6 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 133.
  • 34. Primary Sites of Nutrient Absorption Stomach Lipophillic molecules (ethanol) Weak acids (aspirin) John Williams
  • 36. Volumes and ionic composition of fluid entering the human intestine Source Undetermined
  • 37. DUODENAL FLUID DYNAMICS •  Mucosa is leaky allowing rapid osomotic equilibration of hypertonic and hypotonic meals •  Duodenal secretion of HCO3- from Brunner’s glands •  Absorption by small intestine is then isotonic
  • 38. Cellular Models of Intestinal Sodium Absorption Figs. 7-7 and 7-8 from Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985. Can be regulated by contents, neurotransmitterers, inflammatory mediators and systemic hormones particularly Angiotensin II
  • 39. Fluid Absorption According to the Standing Osmotic Gradient Model Can account for isotonic movement Of fluid by use of localized hypertonicity Fig. 12-4 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007.
  • 40. Absorption Secretory diarrhea of Cholera Is due to Cholera Toxin activating Secretion cAMP and stimulating secretion To 15 –20 liters per day Source Undetermined
  • 41.
  • 43. FUNCTIONS OF INTESTINAL MOTILITY 1.  Mixing of foodstuffs, digestive secretions and enzymes 2.  Facilitate contact of chyme with intestinal mucosa 3.  Net propulsion in an aboral direction
  • 44. Intraluminal Pressure Changes in the Duodenum of a Concious Man Fig. 5-1 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 42. In duodenum contractions occur at intervals of 5 sec or multiples of 5
  • 45. Electrical Threshold for Generation of Action Potentials Source Undetermined Frequency of slow waves is 12/min in duodenum and decreases to 9/min in The ileum. (Another site of pacemaker activity)
  • 46. ICC Cells Interstitial Cells of Cahal Source Undetermined
  • 47. Fed pattern initiated by the Presence of chyme in the intestine Source Undetermined
  • 48. Villus contraction which increases after a meal also helps mix unstirred layer and compress the lacteal Only very short peristaltic movements occur in the fed state Fig. 5-3 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 44.
  • 51. Relationship between Plasma Motilin and the MMC Source Undetermined
  • 53. ESSENTIAL MINERAL ELEMENTS 1.  Required to maintain normal physiology and health 2. Occur in diet, sometimes as trace elements 3. Variable absorptions may be regulated 4. In steady state intestinal absorption equals body losses
  • 54. Additional Source Information for more information see: http://open.umich.edu/wiki/CitationPolicy Slide 4 – Fig. 7-2 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 144. Slide 5 – Source Undetermined Slide 6 – Trier, JS, Modara, JL. “Functional morphology of the mucosa of the small intestine”. In Johnson, LR. Physiology of the Gastrointestinal Tract. Vol. II. Raven Press, New York, NY, 1981: 926. Slide 9 – Source Undetermined Slide 10 – Source Undetermined Slide 11 – John Williams Slide 12 – Fig. 7-15 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 169. Slide 15 – Fig. 11-8 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 114. Slide 16 – Fig 7-18 Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985: 174. Slide 17 – Source Undetermined Slide 18 – Source Undetermined Slide 22 – Fig. 8 Johnson, L. Essential Medical Physiology New York Raven Press 1992: 515. Slide 23 – Source Undetermined Slide 25 - Source Undetermined Slide 26 – Fig. 11-14 Johnson, L. Gastrointestinal Physiology, 6th ed. Mosby Elsevier, St. Louis, MO; 2001: 136. Slide 28 – Source Undetermined
  • 55. Additional Source Information for more information see: http://open.umich.edu/wiki/CitationPolicy Slide 31 – Fig. 9 Chang, E, Sitrin, M, Black, D. Gastrointestinal, Hepatobiliary, and Nutritional Physiology. Lippincott – Raven, Philadelphia, PA; 1996: 204. Slide 33 – Fig. 12-6 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 133. Slide 34 – John Williams Slide 36 – Source Undetermined Slide 38 – Figs. 7-7 and 7-8 from Granger, D, et al. Clinical Gastrointestinal Physiology. W.B. Saunders, Philadelphia, PA; 1985. Slide 39 – Fig. 12-4 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007. Slide 40 – Source Undetermined Slide 44 – Fig. 5-1 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 42. Slide 45 – Source Undetermined Slide 46 – Source Undetermined Slide 47 – Source Undetermined Slide 48 – Fig. 5-3 Johnson, L. Gastrointestinal Physiology, 7th ed. Mosby Elsevier, Philadelphia, PA; 2007: 44. Slide 49 – Jim Sherman Slide 50 – Jim Sherman Slide 51 – Source Undetermined