DIGESTIVE SYSTEM. FUNCTION?? MAKE FOOD SMALL ENOUGH TO BE ABSORBED MAKE FOOD SMALL ENOUGH TO BE...
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Transcript of DIGESTIVE SYSTEM. FUNCTION?? MAKE FOOD SMALL ENOUGH TO BE ABSORBED MAKE FOOD SMALL ENOUGH TO BE...
DIGESTIVE SYSTEM
FUNCTION??
MAKE FOOD SMALL ENOUGH TO BE ABSORBED
MONOMERS
DIGESTIVE SYSTEM
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DIGESTIVE SYSTEM
www.nlm.nih.gov
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
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 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
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