Physiology Flashcards
CONTROL MECHANISMS INVOLVED IN SALIVARY SECRETION CONTROL
PARASYMP & SYMP BOTH STIMULATORY
PARASYMP = FACIAL (VII) & GLOSSOPHARYNGEAL (IX) NERVES = THIN WATERY SECRETION
SYMP = THICK VISCOUS SECRETIONS & SMALL VOL.
ALPHA-ADRENORECEPTORS = INCREASES MUCUS BETA-ADRENORECEPTORS = INCREASES AMYLASE
ALSO ENETRIC REFLEXES = FOOD IN MOUTH IS DETECTED BY PRESSURE RECEPTORS/CHEMORECEPTORS OF ROOF OF MOUTH/TONGUE
EFFECTS OF PARASYMP. & SYMP. SYSTEM ON SECRETION & MOTILITY
PARASYMP. = STIMULATORY SYMP. = INHIBITORY (cept SALIVATION)
ARTERIAL SUPPLY & VENOUS DRAINAGE OF GIT
ARTERIAL SUPPLY:
COELIAC TRUNK (FOREGUT; DIVIDES INTO L GASTRIC ARTERY, SPLENIC ARTERY & HEPATIC ARTERY)
SUPERIOR MESENTERIC ARTERY (MIDGUT)
INFERIOR MESENTERIC ARTERY (HINDGUT)
VENOUS DRAINAGE:
SPLENIC VEIN & SUPERIOR MESENTERIC VEIN = HEPATIC PORTAL VEIN
ALSO INFERIOR MESENTERIC VEIN
ALSO SPLENIC VEIN (into IMA, for pancreas) & GASTRIC VEIN (into PORTAL VEIN, into stomach) & DUODENAL VEINS
PORTAL VENOUS SYTEM & ANASTOMOSIS WITH SYSTEM SUPPLY
PORTAL SYSTEM = STARTS & ENDS IN CAPILLARY BED, thru VEINS, w/o going thru HEART
PORTAL LIVER SYSTEM = RECEIVES BLOOD FROM GUT IN SERIES SO THAT LIVER CAN DETOXIFY/SCREEN BLOOD OF TOXINS
HEPATIC PORTAL VEIN GOES TO LIVER - HEPATIC VEIN TO IVC
PORTAL SYSTEM ALSO HAS ANASTOMOSES WITH SYSTEMIC SUPPLY = PORTOCAVAL ANASTOMOSES
IN ANAL CANAL
IN DISTAL OESOPHAGEAL
IN COLON
~UMBILICUS
IF PORTAL SYSTEM BLOCKED = AN CAUSES VARICES/ENLARGEMENTS
OESOPHAGEAL VARICES
CAPUT MEDUSAE
HAEMORRHOIDS/PILES
CAN TREAT USING PORTOCAVAL SHUNTS
GIT ANATOMY + GENERAL PHYSIOLOGICAL FUNCTIONS OF COMPONENTS
SAME STRUCTURE THROUGHOUT TUBE
4 LAYERS:
MUCOSA: EPITHELIUM, LAMINA PROPRIA (loose connective tissue, supports epithelium, muscularis mucosa = also support
EPITHELIUM: OESOPHAGUS & ANAL CANAL = STRATIFIED SQUAMOUS
IN BWTN = SIMPLE COLUMNAR
EPITHELIUM = SECRETES & CREATES MUCUS, HORMONES, ACID, DIGESTIVE ENZYMES + ABSORBS DIGESTIVE PRODUCTS
SUB-MUCOSA: provides services to other layers = blood vessels, lymph vessels, GLANDS IN OESOPHAGUS & DUODENUM; SUBMUCOSAL PLEXUS bwtn SUBMUCOSA & MUSCULARIS EXTERNA
MUSCULARIS EXTERNA: thick muscular layer, 2 layers: inner = circular, outer = longitudinal; constriction & shortens gut tube; MYENTERIC PLEXUS = bwtn muscular layers
SEROSA (inside peritoneum)/ADVENTITIA (outside peritoneum)
MOUTH = CHEWING, SPLITTING INTO SMALLER PARTICLES, AMYLASES IN SALIVA
OESOPHAGUS = MUSCULAR TUBE, TRANSPORTS FOOD
STOMACH = TEMPORARY FOOD STORAGE, STERILISES FOOD, PRODUCES INTRINSIC FACTOR, MIXES & GRINDS FOOD, CONTROLS DELIVERY TO S. INTESTINE
PANCREAS = PRODUCES DIGESTIVE ENZYMES FOR ALL MAJOR FOOD GROUPS
LIVER = BILES SALTS & DETOXIFIES BLOOD
GALL BLADDER = STORES & CONCENTRATES BILE
S. INTESTINE = FINAL STAGES OF CHEMICAL DIGESTION & FOOD IS ABSORBED
L. INTESTINE = H2O ABSORPTION, FAECAL AGGREGATION & BACTERIAL FORMATION
COMMON FEATURES OF ALIMENTARY CANAL WALL STRUCTURE
CONTINUOUS TUBE
SAME 4 LAYERS: MUCOSA, SUBMUCOSA, MUSCULARIS EXTERNA, SEROSA/ADVENTITIA
ORGANISATION OF ENTERIC NERVOUS SYSTEM
ENS = MYENTIC PLEXUS + SUBMUCOSAL PLEXUS
MYENTERIC PLEXUS = BWTN MUSCLE LAYERS OF MUSCULARIS EXTERNA
SUBMUCOSAL PLEXUS = BWTN SUBMUCOSA & MUSCULARIS EXTERNA
DIGESTIVE PROCESSS FOR CONVERSION OF COMPLEX CHOs TO MONOSACCHARIDES
MONOSACCHARIDES (GLUCOSE, GALACTOSE, FRUCTOSE)
DISACCHARIDES (LACTOSE - LACTASE = GLUCOSE + GALACTOSE; MALTOSE - MALTASE = 2 GLUCOSE; SUCROSE - SUCRASE = GLUCOSE + FRUCTOSE)
POLYSACCHARIDES ONLY BROKEN DOWN IF ALPHA-1,4 GLYCOSIDIC BONDS (STARCH = AMLYLOPECTIN & AMYLOSE) = BROKEN DOWN BY ALPHA-AMYLASES
MECHANISM OF MONOSACCHARIDE ABSORPTION BY INTESTINAL EPITHELIAL CELLS
GLUCOSE & GALACTOSE:
ABSORBED VIA NA-GLUCOSE SYMPORTER/SGLT1 (NEEDS NA & INDIRECTLY NEEDS ATP)
CONFORMATIONAL CHANGE DEPOSITS NA & GLUCOSE INSIDE INTESTINAL EPITHELIA
NA IMMEDIATELY PUMPED OUT BY NA-K PUMP (OSMOTIC EFFECT & DRAWS H2O PARACELLULARY/ACROSS TIGHT JUNCTIONS)
GLUCOSE TRANSPORTED INTO BLOOD VIA GLUT2 TRANSPORTERS (WHEN INTESTINAL CONC. > BLOOD CONC.)
FRUCTOSE = INTO CELLS VIA GLUT5 TRANSPORTERS & OUT OF CELLS VIA GLUT2 TRANSPORTERS (NO BLOOD CONC. SO IMMEDIATELY TRANSPORTED)
DIGESTIVE PROCESS FOR BREAKING DOWN PROTEINS INTO SMALLERS PEPTIDES/AMINO ACIDS
PROTEINS ~3-10 AMINO ACIDS = SMALLER PEPTIDES
PROTEINS BROKEN DOWN USING H2O HYDROLYSIS & PROTEASES/PEPTIDASES
ENDOPEPTIDASE = WORKS IN MIDDLE OF CHAIN EXOPEPTIDASE = WORKS AT END OF CHAIN
CARBOXYPEPTIDASE = WORKS AT CARBOXY END AMINOPEPTIDASE = WORKS AT AMINO END
MECHANISMS OF ABSORPTION FOR AMINO ACIDS & SMALL PEPTIDES
AMINO ACIDS:
AMINO ACID & NA TRANSPORTER = CONFORMATIONAL CHANGE = DEPOSITED INTO INTESTINAL CELLS
NA PUMPED OUT OF CELL VIA NA-K PUMP = DRAWS H2O
AMINO ACID TRANSPORTED INTO BLOOD
SMALLER PEPTIDES:
DEPENDANT ON BRUSH BORDER ACID MICROCLIMATE
PEPT1 = SMALLER PEPTIDE & H+ TRANSPORTED INTO CELL
SMALLER PEPTIDE TRANSPORTED OUT & H+ PUMPED BACK INTO CELL
H+ PUMPED BACK OUT WITH NA COMING INTO CELL (USING NHE3 = NA-H EXCHANGER)
NA PUMPED OUT OF CELL USING NA-K PUMP = DRAWS H2O
DIGESTIVE PROCESSES OF FATS TO TAG & MONOGLYCERIDES
MOST DIETARY FATS = TAG
TAG IS BROKEN DOWN BY H2O SOLUBLE LIPASE = 2FA & MONOGLYCERIDE
REQUIREMENT OF EMULSIFICATION OF INGESTED FATS
EMULSIFICATION REQ. AS FAT DROPLETS FAR TOO LARGE FOR H2O SOLUBLE LIPASE TO WORK QUICKLY AS CAN ONLY WORK ON OUTER SURFACE AREA
EMULSIFICATION NEEDS 2 THINGS:
MECHANICAL DISRUPTION (CHURNING MOTION OF MUSCULARIS EXTERNA = SPLITS LARGE DROPLETS INTO SMALLER DROPLETS)
EMULSIFYING AGENT (BILE SALTS + PHOPHOLIPIDS IN BILE = STOPS FAT DROPLETS FROM RE-AGGREGATING AS THEY ARE AMPHIPATHIC MOLECULES)
ROLE OF BILE SALTS IN PRODUCTION OF EMULSIFICATION DROPLETS + HOW ARE FATS TRANSPORTED INSIDE INTESTINAL CELLS & INTO BLOOD
BILE SALTS EMULSIFY SMALLER DROPLETS OF FAT
MICELLLES ARE FOR TRANSPORTING THE SMALL DROPLETS OF FAT TO INTESTINAL BRUSH BORDER (as unless fats come into contact with membrane it cannot diffuse across)
MICELLES = BILE SALTS + PHOSPHOLIPIDS + MONOGLYCERIDE + 2FA
FA BECOME PROTONATED IN ACID MICROCLIMATE OF BRUSH BORDER & SO MICELLE UNSTABLE & BREAKS DOWN & RELEASES MONOGLYCERIDE & FA
MICELLES REFORM ONCE AWAY ACID MICROCLIMATE
INSIDE CELL:
CYTOPLASM IS AQUEOUS SO MONOGLYCERIDE & 2FA GO TO SMOOTH ENDOPLASMIC RETICULUM
THERE GETS PACKAGED INTO TAG & FORMS VESICLES (FROM sER MEMBRANE)
VESICLES TRANSPORT TAG THRU GOLGI APPARTUS & RELEASED INTO ECF/BLOOD AT SEROSAL MEMBRANE BY FUSING AT BASOLATERAL MEMBRANE
OUTSIDE CELL:
RELEASED AS CHYLOMICRONS (PHOSPHOLIPIDS, CHOLESTEROL, FAT-SOLUBLE VITAMINS). WHICH ARE TOO BIG FOR CAPILLARY BM = PASSES THRU LACTEALS
In Tissue = broken down by lipoprotein lipase - absorbed by tissues/stored as TAG; transported by lipoprotein & serum albumin complex (free FA); VLDL, HDL, LDL
ABSORPTION OF FAT SOLUBLE & H2O SOLUBLE VITAMINS
VITAMINS ADEK = FAT SOLUBLE = FOLLOW SAME PATHWAY AS FATS
VITAMINS B GROUP, C & FOLIC ACID = FACILITATED TRANSPORT/PASSIVE DIFFUSION
VITAMIN B12 = LARGE & CHARGED = BINDS TO INTRINSIC FACTOR (of stomach) & FORMS COMPLEX = ABSORBED BY SPECIFIC TRANSPORT MECHANISM OF DISTAL ILEUM (intrinsic factor sent to be stored in liver)
IF B12 DEFICIENCY = PERNICIOUS ANAEMIA = RBCs DO NOT MATURE (takes ~3yrs to show up as liver has ~3yr supply of intrinsic factor)
ABSORPTION OF IMPORTANT DIETARY MINERALS
IRON:
INGESTED IRON ENTERS INTESTINAL CELLS VIA DMT1 (DIVALENT METAL TRANSPORTER) = H+ DEPENDANT
ONCE INSIDE CELL = BOUND TO FERRITIN = INTRACELLULAR STORE - INTESTINAL CELL EVENTUALLY SLOUGHS OFF AS ~5 DAY LIFE & TAKEN FERRITIN WITH IT
FERRITIN LVLS CHANGE ACCORDING TO BODY’S IRON STATUS
HYPERAEMIA = INCREASED FERRITIN EXPRESSION & MORE IRON STORED IN INTESTINAL ENTEROCYTES
ANAEMIA = DECREASED FERRITIN EXPRESSION & MORE IRON LEFT IN BLOOD
OTHER WISE, IRON TRANSPORTED SEROSAL MEMBRANE & BOUND TO TRANSFERRIN (eventually goes to liver & bound into Hb)
STOMACH & OESOPHAGUS - ANATOMY + GENERAL PHYSIOLOGICAL FUNCTIONS
OESOPHAGUS = MUCOSA(stratified squamous), SUBMUCOSA (glands); MUSCULARIS EXTERNA (upper 1/3 = skeletal; lower 2/3 = sm); SEROSA/ADVENTITIA
SPHINCTERS
DESCRIBE OESOPHAGUS
NORMAL 4 LAYERS
UPPER 1/3 = SKELETAL MUCLE, MUSCULARIS EXTERNA
LOWER 2/3 = SM, MUSCULARIS EXTERNA
GLANDS IN SUBMUCOSA
EPITHELIUM NOT KERATINISED
SPHINCTERS TO CONTROL GASTRIC REFLUX & PREVENT RESPIRATORY FAILURE
REFLEX CONTROL MECHANISM INVOLVED IN SWALLOWING
MOUTH:
CHEWING + SALIVA (H2O, MUCINS, AMYLASES, LYSOZOMES, ELECTROLYTES)
VOLUNTARY (SOMATIC NN. OF SKELETAL MUSCLES OF JAW & MOUTH) & REFLEXIVE CONTROL (PRESSURE OF FOOD DETECTED BY MECHANORECEPTORS & INHIBITS JAW CONTRACTION = SWALLOWING)
ORAL PHASE: BOLUS PUSHED TO BACK OF MOUTH & TONGUE PUSHES UP & BACK
PHARNGEAL PHASE: BOLUS PRE
REFLEX CONTROL MECHANISM INVOLVED IN SWALLOWING
MOUTH:
CHEWING + SALIVA (H2O, MUCINS, AMYLASES, LYSOZOMES, ELECTROLYTES)
VOLUNTARY (SOMATIC NN. OF SKELETAL MUSCLES OF JAW & MOUTH) & REFLEXIVE CONTROL (PRESSURE OF FOOD DETECTED BY MECHANORECEPTORS & INHIBITS JAW CONTRACTION = SWALLOWING)
ORAL PHASE: BOLUS PUSHED TO BACK OF MOUTH
PHARYNGEAL PHASE:
BOLUS PRESENCE = PHARYNGEAL MUSCLES CONTRACT (INVOLUNTARY) & SOFT PALATE REFLECTED UP & BACK (closes off nasopharynx)
WHEN FOOD REACHES OESOPHAGUS = UPPER OESOPHAGEAL SPHINCTER RELAXES & EPIGLOTTIS COVERS ENTRANCE TO LARYNX)
AFTER FOOD PASSES THEY RELAX
ALL CONTROLLED BY SWALLOWING CENTRE IN MEDULLA (close to respiratory centres & so swallowing & breathing do not occur at same time)
OESOPHAGEAL PHASE:
PASSES BOLUS TO STOMACH BY PERISTALTIC WAVE (wave of contraction & relaxation)
AS FOOD NEARS LOWER OESOPHAGEAL SPHINCTER = IT RELAXES & ALLOWS FOOD TO ENTER STOMACH
LOS RELAXATION ALSO CAUSES STOMACH RELAXATION (VIA VAGAL REFLEXES) = CAUSE THIN ELASTIC SM OF GASTRIC FUNDUS & BODY TO RELAX (vol. increase w/o change in pressure)
STOMACH STRUCTURE & FUNCTIONS
CARDIA = TRANSFERS FOOD INTO BODY
FUNDUS = THIN ELASTIC SM LAYER, MAINLY AIR-FILLED, EXTRA-STORAGE FOR FOOD
BODY: STORAGE OF FOOD, MUCUS, PEPSINOGEN, HCl, INTRINSIC FACTOR
ANTRUM = MIXES/GRINDS FOOD TO FORM CHYME & ALSO PRODUCES GASTRIN
SIMPLE COLUMNAR EPITHELIUM, MUCOSAL GLANDS INVAGINATE DOWNWARDS & DISTAL END OF STOMACH HAS 3RD INNERMOST OBLIQUE LAYER OF MUSCLE OF MUSCULARIS EXTERNA
ESSENTIAL ROLE OF INTRINSIC FACTOR IN VITAMIN B12 ABSORPTION
VITAMIN B12 = LARGE & CHARGED = CANNOT BE ABSORBED/TRANSPORTED THRU BODY W/O INTRINSIC FACTOR
IF VITAMIN B12 DEFICIENCY = PERNICIOUS ANAEMIA
FUNCTIONS OF GASTRIC MUCUS
CYTOPROTECTIVE (from stomach:
PREVENTS AGAINST HCL CORROSION & PEPSIN DIGESTION
LUBRICATES & PROTECTS MUCOSA AGAINST MECHANICAL INJURY
BASIC PHYSIOLOGY OF GASTRIC ACID SECRETION
BACKGROUND:
LOTS OF CO2 IN BLOOD = DIFFUSE INTO PARIETAL CELL, WHERE IT COMBINE WITH H2O (USING CARBONIC ANHYDRASE) = BECOMES CARBONIC ACID
CARBONIC ACID DISSOCIATES = H+ & BICARBONATE ION
BICARBONATE-CL EXCHANGER (BICARB INTO BLOOD & CL INTO CELL & THEN LUMEN)
PROTON PUMP = PUMPS H+ INTO LUMEN & K+ INTO CELL - REQUIRES LOTS OF ATP (LOTS OF MITOCHONDRIA NEAR FOR THAT)
ION TRANSPORT ALSO DRAWS H2O INTO LUMEN
H2O + CL + H = HCL ACID
POST-PRANDIAL ALKANISATION = AFTER MEAL = EXCESS BICARBONATE IN BLOOD
CAN BE STIMULATED:
GASTRIN & ACh = INCREASE INTRACELLULAR Ca & ACTIVATE PROTEIN KINASES = ACTIVATE PROTON PUMP
HISTAMINE (gut receptors diff. to other bodily receptors) = ATTACHED TO G STIMULATORY PROTEIN = ACTIVATES ADENYLYL CYCLASE & PROTEIN KINASE = ACTIVATES PROTON PUMP
CEPHALIC PHASE:
ANY FOOD STIMULI = STIMULATES VAGAL REFLEXES
VAGAL NN. RELEASES ACh = STIMULATES PARIETAL CELLS
ALSO INNERVATES G CELLS = RELEASES GASTRIN = STIMULATES PARIETAL CELLS
ACh/GASTRIN ACT ON ECL CELLS = RELEASE HISTAMINE = STIMULATE PARIETAL CELLS
GASTRIC PHASE:
STOMACH DISTENSION = VAGAL REFLEX = STIMULATES PARIETAL CELLS
SMALLER PEPTIDES PRESENT = STIMULATES G CELLS & GASTRIN RELEASE = STIMULATES PARIETAL CELLS
ACh/GASTRIN = STIMULAET ECL CELLS = RELEASE HISTAMINE & STIMULATES PARIETAL CELLS
CAN BE INHIBITED:
PROSTAGLANDINS ATTACHED TO G INHIBITORY PROTEIN - SWITCHES OF ADENYLYL CYCLASE
CEPHALIC:
STOP FOOD STIMULI = REDUCE VAGAL ACTIVITY
GASTRIC PHASE = INCREASED pH = REDUCE GASTRIN PRODUCTION (-ve feedback loop)
INTESTINAL:
ACID IN DUODENUM (expresses SECRETIN & ENTEROGASTRIC REFLEX = REDUCES GASTRIN RELEASE & EFFECTIVITY OF GASTRIN AT PARIETAL CELLS)
FAT IN DUODENUM (GIP RELEASED = GASTRIN REDUCED & HCL REDUCED)
ENTEROGASTRONES = HORMONES RELEASED BY DUODENAL MUCOSAL GLANDS WHEN HYPERTONIC SOLNS./FAT/ACID PRESENT IN DUODENUM (tells stomach to calm down)
WORKS BY:
INHIBITING GASTRIC SECRETIONS & PREVENTING MOTILITY/GASTRIC EMPTYING
IMPORTANCE OF GASTRIC ACID & PEPSIN SECRETION
NEURAL & HORMONAL MECHANISMS OF CONTROL
GASTRIC ACID = STERILISES FOOD = PROTECTIVE
PEPSINOGEN (ZYMOGEM = INACTIVE PRECURSOR) = PEPSIN PRECURSOR = PROTEIN BREAKDOWN; inactivated by neutral pH
NEUROCRINE = ACh ENDOCRINE = GASTRIN PARACRINE = HISTAMINE
