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 SMALL INTESTINE AND LARGE INTESTINE-
DIGESTION AND ABSORPTION

SMALL INTESTINE
SECRETION
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 Mucus by Brunner’s glands in duodenum
 Stimuli: tactile, irritating, vagal, GI hormones
 Alkaline mucus: protection from gastric acid
 Inhibited by sympathetic stimulation…?duodenal
ulcers
 Intestinal digestive juices by Crypts of
Lieberkuhn:
 Goblet cells (mucus) & enterocytes (water &
electrolytes)
 1800mls/d; pH 7.5-8.0; creates watery vehicle
for absorption

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 Digestive
enzymes:
 Peptidases
 Dissacharidases
 Intestinal lipase
 Local regulation
 Intestinal
epithelium has a
life cycle of 5 days

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FUNCTION OF SMALL
INTESTINE
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 Secretion-
digestion,protection,activation,haemopeisis
 Hormonal
 Mechanical
 Absorption

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LARGE INTESTINE
SECRETION
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 Have crypts of Lieberkuhn that secrete only mucus and
a little HCO3
-
 Protects mucosa from: acids from bacterial activity and
physical excoriation.
 Mucus adheres feces together.
 Stimuli:
 Tactile by local reflexes
 Parasympathetic nervous system

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DIGESTION & ABSORPTION
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DIGESTION AND
ABSORPTION
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OBJECTIVES:
 To describe the site, digestive enzymes and
secretions involved in the digestion of:
 CHO’s, Proteins, Lipids
 To describe the absorbable units, transporters
involved and disorders in absorption of:
 CHO’s, Proteins, Lipids, Fluid & Electrolytes.

Introduction
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 Digestion and absorption is the ultimate
function of GIT.
 Digestion is the breakdown of ingested food
into absorbable particles.
 Absorption is movement of nutrients, water &
electrolytes from intestinal lumen into the
blood.
 Occurs through cellular or paracellular paths

The small intestine
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 Most of the absorption occurs here.
 The intestinal mucosa has longitudinal folds of
Kerckring, villi & microvilli.
 These increase absorptive surface area 600-1000
times.
 They contain epithelial cells interspersed with
goblet cells.
 Epithelial cells are shed every 3-6 days making
them vulnerable to irradiation and chemotherapy.

1. CARBOHYDRATES
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 Almost all ingested foods have >50% CHO’s
 Contains polysaccharides (starch),
disaccharides (trehalase, maltose, sucrose &
lactose) and monosaccharide (glucose &
fructose).
 Absorbed only as monosaccharide.
 Digestion begins in the mouth and is as
follows:

For starch
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The disaccharides
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Cho’s absorption
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 Absorbed as monosaccharides.
 Glucose and galactose: through Na-dependent 20 active
transport against the gradient on the apical membrane.
 Fructose: by GLUT 5(fructose specific transporter) by
facilitated diffusion hence none against gradient.
 Once in the cell all are absorbed across basolateral
membrane via GLUT 2 by facilitated diffusion.

Lumen blood
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Lactose intolerance
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 A condition where there is absence of lactase and
one fails to breakdown lactose into glucose and
galactose.
 As such lactose is not absorbed and remains in
the lumen
 Being osmotic it retains water in the lumen and
leads to Diarrhea.
 Treatment: avoid milk products or lactase
supplementation.

2. PROTEINS
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 Absorbable forms are amino acids, dipeptides and
tripeptides.
 This is facilitated by the proteases in stomach and
small intestine.
 In the stomach(pepsin), small intestines
(endopeptidases- trypsin, chymotrypsin, elastase
& exopeptidases- carboxypeptidase A&B)
 Pancreatic secretions which are mostly proteins
are also absorbed in the same manner.

Digestion
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 The pancreatic peptides are released in inactive
form.
 Trypsinogen is activated by enterokinase and the
resulting trypsin catalyzes the activation of the
other proteases including trypsinogen.
 Breakdown proteins to amino acids, dipeptides
and tripeptides.
 Finally the proteases digest themselves.

Activation of proteases
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Absorption
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 Absorbable in larger molecules than CHO’s
 Amino acids by the Na-aa co transporter each for
acidic, basic, neutral and imino amino acids.
 Most proteins are absorbed as di/tri peptides
through the H+ dependent transporter
 In the cells they are hydrolyzed by cytosolic
proteases to amino acids.
 On the basolateral membrane, there is facilitated
diffusion of aa’s and remaining di/tri peptides.

Figure 8-30
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Disorders of protein digestion &
absorption
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 Chronic pancreatitis
 Cystic fibrosis of the pancreas
 The two lead to failure in production of pancreatic
proteases and failed protein digestion.
 Cystinuria: involves absence of Na-aa co
transporter of basic aa’s in the kidney and GIT
 Leads to loss in urine and feces of cysteine,
lysine, arginine and ornithine.

3. LIPIDS
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In the stomach:
 Lingual and gastric lipases
 Mixing and churning breakdown lipids further
 Dietary proteins emulsify lipids for lipases to
act
 Accounts for about 10% of all lipids.
 Delayed gastric emptying by CCK allows time
for duodenal digestion.

Small intestine
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 Bile salts: emulsify fats and help in micelles
formation
 Pancreatic lipase and colipase: breakdown
triglycerides
 Cholesterol ester hydroxylase: cholesterol esters
and triglycerides (glycerol)
 Phospholipase A2 : breaks phospholipids into
lysolecithin and fatty acids.
 Procollipase and prophospholipase A2 are
activated by trypsin.

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Disorders
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1) Pancreatic insufficiency (pancreatitis, fibrosis)
2) Duodenal acidity e.g. in ZE syndrome
3) Bile salts deficiency: resection of ileum
4) Bacterial overgrowth
5) Decreased intestinal cells e.g. tropical sprue
6) abetalipoproteinemia

4.VITAMINS
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 Required in small quantities as cofactors or
coenzymes in metabolism.
 Not synthesized in the body hence gotten from
GIT
 Fat soluble vitamins:
 ADEK
 Absorbed as lipids.
 Incorporated into micelles….taken to
chylomicrons…to lymphatics…general
circulation

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 Water soluble vitamins:
 Vitamins C and B complex
 Absorbed through Na-dependent co transport
except vitamin B12.
 Vitamin B12 is absorbed in the terminal ileum with
the help of intrinsic factor and transcobalamine
transporters.
 Lack of intrinsic factor leads to????????
 Pernicious anemia.

5.CALCIUM
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 1,25 dihydroxy cholecalciferol induces
synthesis of vitamin D-dependent Ca2+ binding
protein (Calbindin D-28K) in intestinal
epithelial cells.
 This mediates absorption of calcium
 Vitamin D deficiency impairs calcium
absorption and leads to deficiency.
 Causes rickets in children and osteomalacia in
adults.

6.IRON
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 Absorbed into intestinal epithelial cells as free iron
or as heme (bound to Hb or myoglobin).
 The heme iron is converted to free iron.
 The free iron is then transported out of the
intestinal epithelial cells into blood by apoferritin
as ferritin.
 In the blood iron is transported by transferrin (a
βglobulin) to the liver storage sites.
 From the liver to the bone marrow to make
Hemoglobin.

INTESTINAL FLUID AND
ELECTROLYTE
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 9 Liters of fluid in GIT every day. (2L from diet
and 7L from GI secretions)
 Almost all reabsorbed with 100-200mls in
feces.
 Intestinal epithelial cells also secrete into the
GIT which also needs to be reabsorbed.
 Absorption is through cellular and paracellular
path
 Tight junctions are leaky in SI and tight in

Intestinal absorption
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 Isosmotic absorption like in the PCT of the
kidneys.
 Absorptive mechanisms vary in the jejunum,
ileum and colon.
 Jejunum: net absorption of NaHCO3
 Ileum: net absorption of NaCl
 Colon: net absorption of Na+ and K+

Jejunal absorption
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Ileum absorption
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Intestinal secretion
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 Cells lining the crypts secrete and those lining villi
absorb.
 The apical membrane has Cl- channels which are
closed but can be opened by hormones or NT’s.
 Ach & VIP activate adenyl cyclase>>>↑cAMP>
opening of Cl- channels
 Na+ follows Cl- and water follows them.
 If the secretion exceeds the absorption capacity
then a secretory diarrhea results as in Cholera.

DIARRHOEA
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 “TO RUN THROUGH”
 Fluid loss>> ↓ECF>> ↓intracellular volume>>
↓arterial pressure>> Baroreceptors and RAAS try
to compensate and if they fail>> circulatory
collapse.
 K+ loss: flow rate dependent and leads to
hypokalemia
 HCO3- loss: GI secretions have a high HCO3-
level

Causes of diarrhea
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 Decreased absorptive surface area: infection
or inflammation of small intestine, sprue
 Osmotic diarrhea : lactose intolerance.
Bacteria can compound this diarrhea by further
breaking lactose into more osmotic
compounds.
 Secretory diarrhea: in Cholera and Escherichia
coli infection.
 How does Cholera cause Diarrhea?

FECES FORMATION
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 Bacterial action in the colon:
 Cellulose digestion
 Vit K, B12, B1, B2
 Gasses (flatus): Carbon dioxide, hydrogen,
methane.
 Feces composition:
 ¾ water
 ¼ solid matter
 Brown colour: stercobilin, urobilin
 Odour: indole, skatole, mercaptans, hydrogen
sulphide

Thank you.
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