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 THEDIGESTIVE 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

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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 WHICH SYSTEM?

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

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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

DIGESTION 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

WHY?

SALIVARY GLANDS

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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 MOUTH 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

ESOPHAGUS

25 CM; COLLAPSIBLE ?; WHICH STATE (COLLAPSED/UNCOLLAPSED) USUALLY? WHY?

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

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

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: BOLUSCHYME 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

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 2NUCLEASES: ?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

FUNCTIONS: 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

COMPOSITION: 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, KMOST 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-DENSITY-LIPOPROTEINS CARRY TRIGLYCERIDES TO ADIPOSE TISSUE

VLDL LDL (LOW-DENSITY-LIPOPROTEINS) 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