1

The Digestive System-Chapters 62-66; 70; 78

Figure 62-1; Guyton & Hall

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Digestive Processes Ingestion Propulsion Digestion: Mechanical and

Chemical digestion Absorption- nutrients and

water Defecation

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Layers Alimentary Canal 1. Serosa 2. Longitudinal muscle

(muscularis externa) 3. Myenteric

(Auerbach’s) nerve plexus

4. Circular muscle 5. Submucosa 6. Submucosal

(Meissner’s) nerve plexus

7. Muscularis mucosae 8. Mucosa 9. Epithelial lining

4

Autonomic nerve fibers Both divisions found in myenteric

and submucosal nerve plexi—What do they do? Sensory neurons that monitor

tension, and efferent visceral motor fibers. OWN SYSTEM!

Myenteric-GI motility control- Stimulatory influences -

• tonic contraction (tone) • contraction frequency /

intensity ( propulsion)- Inhibitory influences

• Decreased Sphincter tone (relax) - pyloric sphincter, ileocecal sphincter, LES

Submucosal- Local control- Secretion- Absorption- Contraction of muscularis

mucosa

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Control of the digestive system Movement of

materials along the digestive tract is controlled by: Neural mechanisms

Parasympathetic (Ach) and local reflexes

Hormonal mechanisms Enhance or inhibit

smooth muscle contraction

Local mechanisms Coordinate response to

changes in pH or chemical stimuli and stretching

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Digestive Enzymes

Salivary glands-amylase

lingual lipase

Stomachpepsin

Intestinal Mucosa enterokinase sucrase maltase lactase amino-

oligopeptidase dipeptidase

Pancreas amylase trypsin chymotrypsincarboxypeptidaselipasecholesterolesterase

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The mouth opens into the oral or buccal cavity Its functions include:

Analysis of material before swallowing

Mechanical processing by the teeth, tongue, and palatal surfaces

Lubrication Limited digestion

Lingual lipase (negligible fat digestion)

Salivary amylase (limited carbohydrate digestion)

Antibodies and proteolytic enzymes

Primary SecretionAlpha-amylase

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Digestion and absorption in the stomach

Short-term storage reservoir

Secretion of intrinsic factor

Pepsinogen gastrin Chemical and enzymatic

digestion is initiated, particularly of proteins

Liquefaction of food Slowly released into the

small intestine for further processing

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Gastric glands Two types glands -

- Gastric - HCl

(oxyntic) pepsinogen intrinsic

factor mucus

- Pyloric - gastrin mucus

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Gastric glands- 3 types of cells Mucous Neck cell

(goblet)- release mucus to protect mucosa from acid and pepsin

Parietal cells- HCl and intrinsic factor (B12 absorption by small intestine).

Chief- numerous and release pepsinogen

80%

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K+K+K+

K+

Na+Na+

H+

Na+ Na+

Cl-Cl-

Cl-

Cl-

H2O

H2O

osmosis

H2O HO- + H+

HCO

3

HCO

3

CO2CO2

C.A. Final ResultsHCl - 155 mEq/LKCl - 15 mEq/LNaCl - 3 mEq.L

pH = 0.8

P

P

BLOOD LUMEN

P

P

Acid production and secretion

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2 cell types of Pyloric gland G-cells - release gastrin

Enteroendocrine cells -stimulates parietal cells to secrete acid and increases pyloric contraction; relaxes pyloric sphincter

Mucus neck cells - mucous

20%

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Gastric and Duodenal ulcers

Peptic ulcers occur when damaging effects of acid and pepsin overcome ability of mucosa to protect itself Gastric ulcers - main problem is decreased ability of

mucosa to protect itself

Duodenal ulcers - main problem is exposure to increased amounts of acid and pepsin

Strengthensmucus, HCO3

- secretion, gastrin, PGs, epidermal growth

factor

WeakensH. pylori, aspirin, ethanol,

NSAIDs, bile salts

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What is the Gastric Mucosal Barrier?

alkaline mucus resists the acid and enzymes Tight junctions-gastric juice can’t seep into

lamina propria Epithelial cell replacement- 3-6 day life span. Physiological - diffused H+ ions are transported back to

lumen

H+ back-leaks into mucosa in exchange for Na+. This is a forerunner to gastric ulcer - Decreased cell pH leads to cell death

Damaged mast cells (ECL cells) leak histamine

Viscous cycle - Histamine .. vascular damage .. local ischemia .. greater leakage of H+.. more cell death ...

Damaged Gastric Mucosal Barrier

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Helicobacter pylori H. pylori found in 95% patients with DU

and 100% patients with GU (when alcohol, aspirin, NSAIDS are eliminated)

Gram negative bacterium

High urease activity - high NH4+ activity

- can withstand acid environment- NH4

+ damages epithelial cells (GU)- Increases acid secretion (DU)

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Treatment of Peptic Ulcers Antacids H2 receptor blockers - Rantidine (Zantac)

- Cimetidine (Tagamet)

Proton pump inhibitors - Omeparazole (Prilosec)

Antibiotics

Surgical (rare) - vagotomy- antrectomy

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Stimulation of acid secretion Gastric secretion is

stimulated by local (distention), neural, and endocrine mechanisms Acetylcholine - HCl

secretion - mucus, pepsinogen, and

gastrin Histamine - HCl

secretion Gastrin - HCl

secretion (1500x more powerful compared to histamine)

Seeing, smelling and anticipating food is perceived in brain. Brain tells stomach to prepare for receipt of mealAccounts for 30% of acid response to meal

60%

10%

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Small intestine Important digestive

and absorptive functions Secretions and buffers

provided by pancreas, liver, gall bladder

Three subdivisions: Duodenum Jejunum Ileum

Ileocecal sphincter Transition between small

and large intestine

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Histology of the small intestine Plicae

Transverse folds of the intestinal lining Villi

Fingerlike projections of the mucosa Lacteals

Terminal lymphatic in villus Microvilli

Brush border: increases surface area 20-fold

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Intestinal glands secretin to stimulate

pancreas to release bicarbonate mucus

cholecystokinin to stimulate pancreas and gallbladder

Gastric Inhibitory peptide (GIP)- inhibits gastrin secretion and decreases stomach emptying

Duodenal glands- bicarbonate mucus.

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The Activities of Major Digestive Tract Hormones

Figure 24.22

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Small Intestine- digestive enzymes Maltase- splits maltose into 2

glucose units Lactase- splits lactose into glucose

and galactose Sucrase- splits sucrose into glucose

and fructose Peptidase- breaks down small

peptides into amino acids Intestinal lipase- breaks down

triglycerides into free fatty acids and monoglycerides

Enterokinase- Activates trypsinogen to trypsin (trypsin then activates chymotrypsinogen and procarboxypeptidase)

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Pancreas As chyme floods into small intestine two

things must happen:

Acid must be neutralized to prevent damage to duodenal mucosa

Macromolecular nutrients - proteins, fats and starch must be broken down much further so their constituents can be absorbed

Pancreas plays vital role in accomplishing both objectives

Digestive enzymes for all food types

Bicarbonate solution to neutralize acid chyme

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Regulation of Pancreatic Secretion Secretin and CCK are

released when fatty or acidic chyme enters the duodenum

CCK and secretin enter the bloodstream

Upon reaching the pancreas: CCK induces the secretion of

enzyme-rich pancreatic juice Secretin causes secretion of

bicarbonate-rich pancreatic juice

Vagal stimulation also causes release of pancreatic juice

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The Pancreas

Exocrine function (98%) Acinar cells make,

store, and secrete pancreatic enzymes

Endocrine function – ( cells) release

somatostatin (inhibitory to gastrin and insulin and glucagon)

β-cells –release insulin α-cells-Release glucagon

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The Pancreas as an Endocrine Gland Insulin

Beta cells Skeletal muscle and

adipose tissue need it to make glucose receptors

Promotes glucose uptake Prevents fat and glycogen

breakdown and inhibits gluconeogenesis

Increases protein synthesis

Promotes fat storage

Picture from:http://www.dkimages.com/discover/Home/Health-and-Beauty/Human-Body/Endocrine-System/Pancreas/Pancreas-1.html

Epi/Norepi inhibit insulin!Help maintain glucose levels during times of stress and increase lipase activity in order to conserve glucose levels

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The Pancreas as an Endocrine Gland Glucagon

Maintains blood glucose between meals and during periods of fasting.

Nervous tissue (brain) do not need insulin; but are heavily dependent on glucose levels!

Increases blood glucose levels.

Initiates glycogenolysis in liver (within minutes)

Stimulates amino acid transport to liver to stimulate gluconeogenesis

Image from: http://www.dkimages.com/discover/previews/768/74261.JPG

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Disorders of the Pancreas: Diabetes Mellitus Gestational Diabetes Type I diabetes – develops

suddenly, usually before age 15 Destruction of the beta cells Skeletal tissue and adipose

cells must use alternative fuel and this leads to ketoacidosis

Hyperglycemia results in diabetic coma

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Disorders of the Pancreas: Diabetes Mellitus Type II diabetes and

metabolic syndrome– adult onset Usually occurs after age

40 Cells have lowered

sensitivity to insulin Controlled by dietary

changes and regular exercise

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Pancreatic Failure

Digestion is abnormal when pancreas fails to secrete normal amounts of enzymes. Pancreatitis Removal of pancreatic head - malignancy

Without pancreatic enzymes - 60% fat not absorbed (steatorrhea) 30-40% protein and carbohydrates not absorbed

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Pancreatitis Pancreatitis means inflammation of pancreas.

Autodigestion theory can explain condition.

Chronic pancreatitis - (multiple shared causes) alcohol - most common cause in adults cystic fibrosis - most common cause in childre

CF patients lack chloride transporter at apical membrane. Watery ductal secretion decreases which concentrates acinar secretions in

ducts. Precipitation of proteinaceous secretions block ducts and can destroy

gland by autodigestion.

Acute pancreatitis - (multiple shared causes) Gallstones - most common cause

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Absorption of digested polymers is linked to Salt Absorption in Small Intestine

• Sodium is absorbed across apical cell membrane by 4 mechanisms - 1. Diffusion - through water-filled channels 2. Co-transport - with AA and glucose 3. Co-transport - with chloride 4. Counter-transport - in exchange for H+

• Chloride follows electrical gradient created by absorption of sodium

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Sodium Absorption in Small Intestine

Na+Na+

Na+

S

S

Na+

Na+Cl-Na+ Cl-

Na+

H+

Na+

H+

PNa+ Na+

K+ K+

Cl-Cl-

1

2

3

4

Aldosterone increasesNa+ reabsorption and K+ secretion in S.I. and colon.

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Chemical Digestion: Carbohydrates Begins in the mouth (minimal) and

mostly occurs in small intestine when pancreatic enzymes are released

Absorption of monosaccharides occurs across the intestinal epithelia Absorption: via cotransport with Na+, and facilitated diffusion Enter the capillary bed in the villi Transported to the liver via the hepatic

portal vein Enzymes used: salivary amylase,

pancreatic amylase, and brush border enzymes (maltase, lactase, and sucrase)

lumen

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Chemical Digestion: Proteins Absorption: similar to

carbohydrates (sodium co-transport)

Enzymes used: pepsin in the stomach

Enzymes acting in the small intestine Pancreatic enzymes –

trypsin, chymotrypsin, and carboxypolypeptidase (these must be activated!)

Brush border enzymes – peptidases

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Lipid digestion and absorption Lipid digestion utilizes

lingual and pancreatic lipases, cholesterol esterase (cleaves ester bond to release cholesterol) and phospholipases release fatty acids and monoglycerides. Bile salts improve chemical

digestion by emulsifying lipid drops

Lipid-bile salt complexes called micelles are formed

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Fatty Acid Absorption Fatty acids and

monoglycerides enter intestinal cells via diffusion; bile salts can be reused to ferry more monoglycerides

They are combined with proteins within the cells

Resulting chylomicrons are extruded

They enter lacteals and are transported to the circulation via lymph

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Sprue• Diseases that result in decreased

absorption even when food is well digested are often classified as “sprue” - - Nontropical sprue - also called celiac disease

- allergic to gluten (wheat, rye)- destroys microvilli and sometimes

villi- Tropical sprue - bacterium (?)

- treated with antibacterial agents

• Steatorrhea - if stool fat is in the form of FFA - digestion has occurred

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Stomach(2)

Fluid Entering and Exiting the Gut

Bile (1)

0

2

4

6

8

10

Vol

ume

(L/d

ay)

Diet (2)

Pancreas (1)

Saliva (1)

S.I. (2)

Duodenum and

Jejunum (4)

Colon (1.4)

Ileum(3.5)

Volumeentering

Volume absorbed

Volume Excreted

100-200 ml

•95% of water is absorbed in the small intestines by osmosis•Water moves in both directions across intestinal mucosa•Net osmosis occurs whenever a concentration gradient is established by active transport of solutes into the mucosal cells

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The Liver Digestive function – bile

production; emulsifies fats Bilirubin- decomposed

hemoglobin Urobilinogen- by-

product of bilirubin metabolism

bile salts- keep cholesterol dissolved in bile

Performs many metabolic functions- stores vitamins, processes fats, detoxifies,

makes blood proteins

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Physiology of the large intestine

Reabsorption in the large intestine includes: Water and electrolets Bacteria make: Vitamins –

K, biotin, and B5

Organic wastes – urobilinogens and sterobilinogens

Bile salts Toxins

Mass movements of material through colon and rectum Defecation reflex triggered

by distention of rectal walls

Figure 8-18 Agents that stimulate and inhibit H+ secretion by gastric parietal cells. ACh, Acetylcholine; cAMP, cyclic adenosine monophosphate; CCK, cholecystokinin; ECL, enterochromaffin-like; IP3, inositol 1,4,5-triphosphate; M, muscarinic.

Downloaded from: StudentConsult (on 23 April 2010 06:51 PM)© 2005 Elsevier

Figure 8-19 Regulation of HCl secretion during cephalic and gastric phases. ACh, Acetylcholine; GRP, gastrin-releasing peptide (bombesin).

Downloaded from: StudentConsult (on 23 April 2010 06:51 PM)© 2005 Elsevier

Figure 8-20 Balance of protective and damaging factors on gastroduodenal mucosa. H. pylori, Helicobacter pylori; NSAIDs, nonsteroidal anti-inflammatory drugs.

Downloaded from: StudentConsult (on 23 April 2010 06:51 PM)© 2005 Elsevier

Figure 8-15 Secretory products of various gastric cells.

Downloaded from: StudentConsult (on 23 April 2010 06:51 PM)© 2005 Elsevier