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DIGESTIVE SYSTEM
FUNCTION??
MAKE FOOD SMALL ENOUGH TO BE
ABSORBED
 MONOMERS

DIGESTIVE SYSTEM
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DIGESTIVE SYSTEM
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DIGESTIVE SYSTEM
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MICROANATOMY OF THE
DIGESTIVE TUBE
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MUCOSA

SURFACE EPITHELIUM; CONNECTIVE
TISSUE; SMOOTH MUSCLE; SOME HAVE
FOLDINGS TO ?; TUBULAR GLANDS:
– MUCUS; DIGESTIVE ENZYMES
LUMEN
 PROTECTS LAYERS & BODY; SECRETION
AND ABSORPTION

SUBMUCOSA
LOOSE CONNECTIVE TISSUE; GLANDS;
BLOOD VESSELS; LYMPH VESSELS;
NERVES;
 TO NOURISH AND TRANSPORT MATERIAL
AWAY

MUSCULAR LAYER
INNER COAT: CIRCULAR SMOOTH
MUSCLE FIBERS: DIAMETER DECREASES
 OUTER COAT: LONGITUDINAL FIBERS:
TUBE SHORTENS
 FOR MOVEMENTS

SEROSA/SEROUS LAYER
OUTER COVERING: VISCERAL
PERITONEUM; CONNECTIVE TISSUE
WITH EPITHELIUM ON TOP (OUTSIDE);
 PROTECT TISSUES BELOW; SECRETE
SEROUS FLUID: MOISTENS AND
LUBRICATES SO ORGANS SLIDE FREELY

MUCOSAL EPITHELIUM
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MOVEMENTS

MIXING:
– MOVEMENT OF STOMACH, OR SEGMENTS
(SEGMENTATION); MIXES FOOD AND
DIGESTIVE ENZYMES

PROPELLING:
– PERISTALSIS: RING OF CONTRACTION &
CAUSES RECEPTIVE RELAXATION
SEGMENTATION
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PERISTALSIS
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PERISTALSIS
www.nlm.nih.gov
INNERVATION
USUALLY WHICH ONE ?
 PARASYMPATHETIC

– BY PLEXUSES ?
– INCREASE ACTIVITY; VAGUS NERVE &
SACRAL POTION OF S.C.

SYMPATHETIC
– DECREASE
– FIGHT OR FLIGHT
MOUTH
CHEEK & LIPS: SKELETAL MUSCLES
 TONGUE:

– LINGUAL FRENULUM: TO FLOOR
– PAPILLAE
 FRICTION, TASTE BUDS
– HYOID BONE
– LINGUAL TONSILS: OF ?

PALATE
– ANTERIOR: HARD
– POSTERIOR: SOFT
– UVULA
 SWALLOWING: CLOSE NASAL PASSAGES
– PALATINE TONSILS
– PHARYNGEAL TONSILS: ADENOIDS
TEETH
HARDEST STRUCTURES OF BODY
 NOT BONE ?
 PRIMARY: 10; 6 Mo TO 4y
 SECONDARY: 32; 6 y TO 22y
 FUNCTION: ? WHY?

– INCISORS: BITE
– CANINES: GRAB AND TEAR
– PREMOLARS, MOLARS: GRINDING
TEETH
en.wikipedia.org

CROWN
– ENAMEL: CALCIUM; HARDEST SUBSTANCE;
NOT REPLACED, WEARS DOWN
ROOT
 DENTIN: HARDER THAN BONE
 CENTRAL CAVITY: PULP

– BLOOD VESSELS, NERVES, CONNECTIVE
TISSUE
ROOT CANALS: CEMENTUM AROUND
ROOT
 PERIDONTAL LIGAMENT: COLLAGEN;
CEMENTUM TO JAW

SALIVARY GLANDS


PRODUCE ? FOR?
– MOISTENS, BINDS, STARTS CHEMICAL DIGESTINO
OF FOOD; SOLVENT: DISSOLVES FOOD = TASTE;
BICARBONATE IONS: BUFFER: BALANCE pH FOR
ENZYME ACTION; 3 PAIR AND MANY MINOR GLANDS
3 PAIR AND MANY MINOR GLANDS
– SEROUS GLANDS
 SALIVARY AMYLASE
– STARCH AND GLYCOGEN
– MUCOUS GLANDS
 BINDS; LUBRICATES
SALIVARY CONTROL

PARASYMPATHETIC
– LARGE AMOUNT OT WATERY SALIVA
– REFLEX: PAVLOV’S DOGS

SYMPATHETIC
– SMALL AMOUNT OF VISCOUS SALIVA
– UNPLEASANT LOOK, TASTE, SMELL
– LESS SALIVA= HARD TO SWALLOW
SALIVARY GLANDS
www.entassociates.com
MAJOR SALIVARY GLANDS

PAROTID
– LARGEST; CLEAR WATERY; LOTS OF
AMYLASE

SUBMANDIBULAR
– EQUALLY SEROUS AND MUCOUS

SUBLINGUAL
– SMALLEST OF 3
– MOSTLY MUCOUS
PHARYNX
CONNECT NASAL AND ORAL CAVITY TO
LARYNX AND ESOPHAGUS
 NASOPHARYNX
– BEHIND SOFT PALATE
– AIR PASSAGEWAY
– EUSTACHIAN CANAL OPENING
 OROPHARYNX
– END OF OUTH TO EPIGLOTTIS
 LARYNGOPHARYNX
– EPIGLOTTIS TO LARYNX

PHARYNX
1) Nasopharynx
2) Nasal Septum
3) Hard Palate
4) Tongue
5) Oropharynx
6) Laryngopharynx
anatomy.med.umich.edu

CIRCULAR MUSCLES= CONSTRICTOR
MUSCLES
– SUPERIOR; MIDDLE; INFERIOR
SOME OF INFERIOR CONSTRICTOR
MUSCLES ARE USUALLY CONTRACTED TO
KEEP AIR OUT OF ESOPHAGUS
 SKELETAL MUSCLES BUT MOSTLY A
REFLEX

SWALLOWING STEPS



1: VOLUNTARY; CHEWING AND TURNING FOOD INTO
BOLUS; TONGUE FORCES TO PHARYNX
2: SWALLOWING REFLEX STIMULATED
– SOFT PALATE RAISES ?
– EPIGLOTTIS BLOCKS TRACHEA ?
– TONGUE PRESSES ON SOFT PALATE ?
– LONGITUDINAL MUSCLES CONTSTRICT ?
– INFERIOR CONSTRICTOR MUSCLE RELAXES ?
– SUPERIOR CONSTRICTOR MUSCLE CONTRACTS
3: PERISTALSIS: FOOD THROUGH ESOPHAGUS TO
STOMACH

EPIGLOTTIS
– http://www.youtube.com/watch?v=aPMw7acr
Vro&feature=player_detailpage
SWALLOWING:
http://www.youtube.com/watch?v=wqMCzuIiPa
M
ESOPHAGUS
25 CM; COLLAPSIBLE ?;
 HOW DOES FOOD GET TO ABDOMEN ?

– HIATUS
– MUCOUS GLANDS ?
– LOWER ESOPHAGEAL SPHINCTER ?
– USUALLY CLOSED ?
– PERISTALSIS OPENS SPHINCTER ?
STOMACH





25-30 CM; CAVITY ~ 1L; RUGAE ?
JUST BELOW DIAPHRAGM
TYPE OF DIGESTION ?
– BOTH;
MIXES FOOD WITH GASTRIC JUICE; STARTS
PROTEIN DIGESTION; SOME ABSORPTION;
FOOD TO INTESTINES
REGULAR 2 SMOOTH MUSCLE LAYERS: PLUS
OBLIQUE MUSCLES (ESPECIALLY FUNDUS AND
BODY);
– STRONGER; MORE MIXING

http://gerd.emedtv.com/gerd-video/whathappens-when-you-have-gerd-video.html
PARTS






CARDIA: NEAR ESOPHAGEAL OPENING
FUNDUS: BALLOON AREA AT START: STORAGE
BODY: DILATED AREA; MIDDLE;
PYLORIC ANTRUM: FUNNEL SHAPED; AT END
TO ?
PYLORIC CANAL: BEFORE SMALL INTESTINE
PYLORIC SPHNCTER: THICK CIRCULAR
MUSCLE; VALVE: CONTROLS EMPTYING
GASTRIC SECRETIONS



GASTRIC PITS: GASTRIC GLANDS: TUBULAR: OR 3
SECTRETORY CELL TYPES
– MUCOUS: NEAR OPEININGS OF PITS;
– CHIEF CELLS: DEEPER; DIGESTIVE ENZYMES
– PARIETAL CELLS: DEEPER; HCl
– ALL= GASTRIC JUICE
CHIEF CELLS RELEASE PEPSINOGEN: INACTIVE FORM
OF PEPSIN WHY INACTIVE?
– PEPSINOGEN AND HCl= PEPSIN
GASTRIC LIPASE: MOSTLY ON BUTTERFAT BECAUSE OF
LOW pH
MUCUS PROTECTS FROM PEPSIN
 PARIETAL CELLS ALSO SECRETE
INTRINSIC FACTOR: HELPS ABSORB
VITAMIN B12

CONTROL OF GASTRIC
SECRETIONS





PRODUCED CONTIUOUSLY BUT IN VARYING
AMOUNTS
CELLS OF GASTRIC GLANDS SECRETE
SOMATOSTATIN: INHIBITS ACID SECRETION
PARASYMPATHETIC: ACh SUPRESSES
SOMATOSTATIN AND MORE GASTRIC JUICE
PRODUCED
GASTRIN ALSO INCREASES SECRETION
CAUSE HISTAMINE TO BE RELEASED=
INCREASES GASTRIC SECRETION
http://highered.mcgrawhill.com/olcweb/cgi/pluginpop.cgi?it=swf::
535::535::/sites/dl/free/0072437316/1201
05/anim0037.swf::Three%20Phases%20of
%20Gastric%20Secretion
 http://highered.mcgrawhill.com/olcweb/cgi/pluginpop.cgi?it=swf::
535::535::/sites/dl/free/0072437316/1201
05/anim0037.swf::Three%20Phases%20of
%20Gastric%20Secretion

THREE STAGES


CEPHALIC PHASE:
– BEFORE FOOD ENTERS STOMACH: SMALL, TASTE,
LOOK, THOUGHT OF FOOD BY PARASYMPATHETIC
STIMULATION
– GREATER HUNGER = GREATER SECRETION
– 30-50% OF SECRETION
GASTRIC PHASE:
– 40-50%; WHEN FOOD ENTERS STOMACH
– DISTENSION OF STOMACH = RELEASE OF GASTRIN =
PRODUCTION OF MORE GASTRIC SECRETION
– pH AT 3.0 = GASTRIN INHIBITED; 1.5 = GASTRIC
SECRETION STOPS
– H FOR HCl COMES FROM BLOOD REPLACED BY
BICARBONATE ION

INTESTINAL PHASE:
– 5%; WHEN FOOD ENTERS SMALL
INTESTINES RELEASES INTESTINAL GASTRIN
FROM INTESTINES
– MORE FOOD ENTERS SMALL INTESTINES
AND SYMPATHETIC IMPULSES = INHIBITS
SECRETION
– PROTEIN AND FAT RELEASES
CHOLECYSTOKININ WHICH SLOWS MIXING
OF STOMACH
– FATS CAUSE RELEASE OF INTESTINAL
SOMATOSTATIN WHICH DECREASES
GASTRIC SECRETION
GASTRIC ABSORPTION

A LITTLE BIT
– WATER, SOME SALTS, SOME LIPID-SOLUBLE
DRUGS, ALCOHOL
MIXING/EMPTYING






STOMACHACHE FROM TOO MUCH FOOD
MIXING: BOLUSCHYME
PERISTALSIS SLOWLY MOVES CHYME INTO
SMALL INTESTINES
PASSING THROUGH DEPENDS ON TYPE OF
FOOD: FATS UP TO 6 HOURS
AS FOOD ENTERS SMALL INTESTINES THE
PRESSURE BUILDS UP AND ENTEROGASTRIC
REFLEX INHIBITS STOMACH PERISTALSIS AND
SLOWS INTESTINAL FILLING
CHOLECYSTOKININ RELEASED TO DECREASE
PERISTALSIS
Peristalsis

http://www.nature.com/gimo/contents/pt
1/fig_tab/gimo13_V1.html
http://www.youtube.com/watch?v=Ln09qi
hUi3g&feature=player_embedded

http://emedicine.medscape.com/article/19
48973-overview

VOMITTING: REVERSE PERISTALSIS BY
VOMITTING CENTER OF MEDULLA
CONTRACTS ON STOMACH TO EXPELL
STOMACH
PANCREAS
DUCT TO DUODENUM
 CELLS:

– PANCREATIC ACINAR CELLS
PANCREATIC JUICE

PANCREATIC ACINAR CELLS:
– PANCREATIC AMYLASE: ?
– PANCREATIC LIPASE: ?
– TRYPSIN, CHYMOTRYPSIN,
CARBOXYPEPTIDASE: SPECIFIC PEPTIDE
BONDS
 STORED AND RELEASED IN INACTIVE FORMS ?
 TRYPSINOGEN ACTIVATED BY ENTEROKINASE
THEN TRYPSIN ACTIVATES THE OTHER 2
NUCLEASES: ?
BICARBONATE:
ALKALINE; NEUTRALIZES HCl
CONTROL OF SECRETION
NERVOUS AND ENDOCRINE SYSTEMS
 DURING CEPHALIC AND GASTRIC PHASES
PARASYMPATHETIC STIMULATES
PANCREAS
 SECRETIN STIMULATES RELEASE WHEN
CHYME ENTERS DUODENUM: MOST;LY
BICARBONATE IONS
 PROTEIN & FAT STIMULATES RELEASE
OF CHOLECYSTOKININ STIMULATES
SECRETION

LIVER
FIBROUS CAPSULE; TWO MAJOR LOBES;
TWO MINOR LOBES
 HEPATIC LOBULES: FUNCTIONAL UNIT

– HEPATIC CELLS; HEPATIC SINUSOIDS;
– KUPFFER CELLS: REMOVE BACTERIA
– COMMON HEPATIC DUCT

CARBOHYDRATE METABOLISM,
GLYCOGEN; GLUCONEOGENESIS;
OXIDIZING FATTY ACIDS; SYNTHESIS OF
MOLECULES; DEAMINATION OF AMINO
ACIDS, FORMATION OF UREA AND
OTHER AMINO ACIDS; STORAGE:
GLYCOGEN, IRON, VITAMINS A, D, B12;
DESTROY DAMAGED RBCs; REMOVES
TOXIC MATERIAL; PHAGOCYTIZE
PATHOGENS; BLOOD RESERVOIR;
SECRETES BILE
BILE

WATER, BILE SALTS, BILE PIGMENTS,
CHOLESTEROL, ELECTROLYTES
GALL BLADDER
DEPRESSION IN LIVER
 STORES, CONCENTRATES AND RELEASES
BILE
 RELEASED WHEN STIMULATED BY
CHOLECYSTOKININ
 RELEASED THROUGH BILE DUCT TO
HEPATOPANCREATIC SPHINCTER
 CHOLESTEROL COULD FORM GALL
STONES

BILE SALT FUNCTION

EMULSIFICATION
– AIDS LIPASE

AIDS ABSORBTION
– FATTY ACIDS, GLYCEROL, & FAT SOLUBLE
VITAMINS: A, D, E, K
MOST OF BILE SALTS ARE REABSORBED IN
SMALL INTESTINES
SMALL INTESTINE
9-10 FT LONG
 RECEIVES DIGESTIVE ENZYMES FROM
LIVER AND PANCREAS; FINISHES
CHEMICAL DIGESTION; ABSORBTION;
MOVES MATERIAL TO LARGE INTESTINES

PARTS
DUODENUM:
– SHORTEST (25cm); MOST FIXED;
 JEJUNUM:
– PROXIMAL 2/5THS; MOBILE
 ILEUM:
– REST; MOBILE;
USUALLY NO DISTINCT BREAK BUT JEJUNUM HAS
LARGER DIAMETER; THICKER WALL, MORE ACTIVE,
MORE VASCULAR, MORE LYMPH MATERIAL
HELD BY MESENTERY

STRUCTURE

INTESTINAL VILLI ?
– ESPECIALLY DUODENUM AND PROXIMAL
JEJUNUM
– SIMPLE COLUMNAR EPITHELIUM; LACTEAL;
MICROVILLI ?
– INTESTINAL GLANDS/CRYPTS OF
LIEBERKUHN
– PLICAE CIRCULARES ?
SECRETIONS
GOBLET CELL: ?
 BRUNNER’S GLANDS
– SUBMUCOSA OF PROXIMAL DUODENUM
– THICK, ALKALINE MUCUS
 INTESTINAL GLANDS
– BASE OF VILLIE
– A LOT OF WATERY FLUID; NO ENZYMES ?
– ENZYMES IN MEMBRANE OF MICROVILLI CELLS
 PEPTIDASES
 SUCRASE, MALTASE, LACTASE
 INTESTINAL LIPASE

REGULATION OF SECRETION
MUCUS SECRETION INCREASES IN
RESPONSE TO MECHANICAL STIMULUS
AND IRRITANTS (GASTRIC JUICE)
 CHYME STIMULATES GOBLET AND
INTESTINAL CELLS TO SECRETE
 DISTENSION: PARASYMPATHETIC
STIMULATION TO INCREASE SECRETION

ABSORPTION




MOST ABSORBABLE MATERIAL IS ABSORBED
MONOSACCHARIDES
– FACILLITATED DIFFUSION
PROTEINS
– ACTIVE TRANSPORT
LIPIDS
– FATTY ACIDS:
 DIFFUSE
 RESYNTHESIZED BY ER
 CLUSTERS ENCASED IN PROTEIN: CHYLOMICRONS TO
LACTEALS
 CONTRACTIONS MOVE CHYLOMICRONS THROUGH LYMPH
 TO BLOOD TO MUSCLE AND ADIPOSE TISSUE
VLDL: VERY-LOW-DENSITYLIPOPROTEINS CARRY TRIGLYCERIDES
TO ADIPOSE TISSUE
 VLDL  LDL (LOW-DENSITYLIPOPROTEINS) HIGH CHOLESTEROL 
REMOVED BY CELLS
 HDL (HIGH-DENSITY-LIPOPROTEINS)
REMOVE CHOLESTEROL FROM CELLS TO
LIVER ENTER BY RECEPTORMEDIATED
ENDOCYTOSIS
 CHOLESTEROL BECOMES BILE OR BILE
SALTS MOST IS REABSORBED


ALSO REABSORBS
– WATER
– ELECTROLYTES
PROTEINS
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LIFE SPAN CHANGES
OVERALL: SLOW, LITTLE
 TOOTH CARE VITAL

– LOSS OF ENAMEL; WEAR; CEMENTUM AND
DENTUM THICKEN, PULP LESSENS; NEURON
LOSS; GUMS RECEDE; LOOSE TEETH;

XEROSTOMIA: DRY MOUTH
– MOST OFTEN DUE TO MEDICATIONS

PERISTALSIS SLOWS= HEARTBURN;
STOMACH LINING THINS; GASTRIC
SECRETIONS DIMININSH = TAKES LONGER
FOR DIGESTION

SMALL INTESTINE ABSORBS LESS: A,D,K,
AND ZINC
– A: SKIN AND VISION PROBLEMS
– D: WEAK BONES
– K: LESS CLOTTING
– ZINC: LOWERED HEALING AND IMMUNITY,
ALTERED TASTE
LACTOSE INTOLERANCE
 LESS INTRINSIC FACTOR: ANEMIA
 LOSS OF MUSCLE AND ELASTICITY: LESS
PERISTALSIS OF LARGE INTESTINE:
CONSTIPATION

PANCREAS AND LIVER DON’T CHANGE
MUCH
 LIVER MAY NOT DETOXIFY AS WELL
 GALLBLADDER LESS SENSITIVE BUT
COMPENSATES
