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177 Cards in this Set
- Front
- Back
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GI anatomy (orthograde direction)
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mouth and tongue
pharynx esophagus stomach duodenum jejunum ileum colon rectum anus |
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Accessory digestive organs
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salivary glands
liver pancreas gallbladder |
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FX of Digestive System
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Ingestion
Motility Secretion Digestion Absorption Elimination |
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Ingestion
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taking in of solids and liquids into the stomach
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Motility
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mvmt of material in the GI tract
*propulsive movements move from one end toward the other (normally in an orthograde/ aboral direction, but may be retrograde) *mixing mvmt result in mixing of contents with digestive juices |
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Secretions
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Several types from a variety of cells and glands
serve various fxns: lubricate, liquefy, buffer, digest |
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Secretions: by type
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mucus: lubricate
water: liquefy bicarbonate: buffer enzymes: digest |
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Digestion
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breakdown of large substances into their constituents
*mechanical *chemical |
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Absorption
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mvmt of molecules out of digestive tract into circulation or lymphatic system
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Elimination
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removal of waste products from the digestive tract
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Structure of the GI tract
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Mucosa
Submucosa Muscularis externa Serosa |
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Mucosa
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Epithelium- single layer of specialized cells that line the lumen of the GI
Lamina Propria- layer of loose connective epithelium where the epithelia attach (also has blood vessel, lymph nodes and glands) Muscularis mucosae- thin layer of smooth muscle |
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Submucosa
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Loose connective tissue
also blood and lymphatic tissue, major nerve tracts and some glands |
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Muscularis externa
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Inner circular layer, outer longitudinal later
contraction mixes contents and moves it along the GI tract |
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Serosa
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outermost layer
consists of mainly connective tissue |
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Types of GI innervation
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Intrinsic (enteric nervous system, myenteric plexus, submucosal plexus)
Extrinsic/ Autonomic Nervous system (sympathetic, parasympathetic, afferent fibers) |
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Intrinsic Innervation (enteric nervous system)
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Myenteric plexus (Auerbach's Plexus)- larger of the two plexuses, located between circular and longitudinal muscles, concerned with control of motility
Submucosal Plexus (Meissner's)- lies within the submucosa, concerned with control of secretion through the glands |
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Extrinsic innervation (sympathetic)
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Postganglionics from cells in the paravertebral and prevertebral ganglia (most symp postganglionics end in the myenteric and submucosal plexuses to inhibit activity), some sympathetic fibers end on gland cells and blood vessels to inhibit secretion and produce vasoconstriction
activation of sympathetic system- inhibits contraction inmuscularis externa, stimulates contraction of the sphincters |
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Extrinsic Innervation (parasympathetic)
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supplied by preganglionic fibers from the vagus (GI to transverse colon) and pelvic nerves (desc colon to rectum), fibers terminate on ganglion cells in the myenteric and submucosal plexuses, their axons innervate smooth muscle and glands of the GI
Activation increases contracton and secretion |
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Extrinsic Innervation (afferent fibers)
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70% of vagal fibers, 50% of gut fibers
both intrinsic and extinsic afferent fibers receptors include chemoreceptors, mechanoreceptors, nociceptors (some of the ell bodie are in the plexuses and work on local reflex arcs, others are in the dorsal root ganglia or cranial ganglia (part of central reflex arcs) visceral nociceptive fibers oft he thorax and abdomen -> CNS via symp nerves, non-nociceptive sensory input from th region travels to CNS from PS nerves |
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Electrophys of GI
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single type unit
membrane potential (-40 to -80 mV) slow waves (basic electrical rhythm) can elicit contractile activity |
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Slow waves
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low freq fluctuations from stomach to colon
diff freq in diff regions gen. by pacemaker cells (between longitudinal and circular smooth muscle of muscularis externa amplitude mediated by extrinsic and intrinsic innervation (symp decreases amplitude, parasymp increases amplitude) contractile activity *in stomach and small intestine if slow waves have large enough amplitude *in colon- not clear relation *stomach and small intestine- freq of slow wave is maximum frequency that contractions can occur |
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contractility of GI smooth muscle
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length tension curve- broader ength tension curve than skeletal muscle (dev. force over wider range of muscle lengths)
contaction time- 10x slower than skeletal muscle tone- resting tone from slightly elevated intracellular Ca++ levels |
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GI motility
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Mastication
Deglutition Esophagus |
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Mastication (fxn and control)
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Fxn: enjoyment, reduction of particle size, mixing food with saliva
control: involuntary and voluntary *coordination during chewing is result of actions between several motor and sensory nuclei in the brain stem *brain stem contains neural pattern generator (masticatory center) that is resp. for the oscillatory pattern of mvmts -cortical input fxn to initiate and modify masticatory mvmt -sensory input from the oral cavity terminates in the trigeminal sensory and mesenphalic nuclei act to modify chewing mvmt |
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Deglutition
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initiated voluntarily, then under reflex control of swallowing cetner (pons and medulla)
voluntary(oral) phase- tongue moves bolus of food up and back towards the pharynx involuntary/ relex (pharyngeal) phase- afferent input from pharyngeal mechanoreceptoros activates swallowing center, motor output from swallowing center produces orderly sequence of pharyngeal muscle contractions (mediated by cranial nerves 5,7,9, 12) |
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Esophagus (fxn)
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conduit for food from mouth to stomach
sphincters act as barriers *UES- keeps air out of GI tract *LES- keeps gastric reflux into the esophagus |
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Esophagus (anatomy)
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inner circular layer, outer longitudinal layer
*upper third is skeletal muscle *middle third is mixed *lower third is smoother muscle |
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Esophagus (peristalsis)
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Primary- wave beginning in the pharynx during swallowing continues through esophagus (~10 s)
*initiated and controlled by swallowing center (vagus) |
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Esophagus (peristalsis)
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Secondary- when primary fails to clear food.
Controlled by intrinsic nervous system |
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Esophageal Persitalsis (synonym)
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esophageal phase
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esophageal peristalsis (intensity)
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depends on the size and viscosity of the bolus
NOT REQUIRED FOR LIQUID BOLUS IN THE UPRIGHT POSITION |
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esophageal peristalsis (regulation of rate)
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if second wave is within 5 sec ofthe first, the first stop until the second catches up and they move together
series of rapid swallows inhibits peristalsis until the last swallow |
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LES tone
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*high during quiescent periods due to myogenic mechanisms, the rest of the esophagus is flaccid, can be increased by neural (ACh) or hormonal (gastrin) influences
*relaxation is mediated through the vagus, primarily NO and VIP |
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Disturbances of Esophageal Fxn
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Achalasia
GERD Diffuse esophageal Spasm |
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Acahalasia
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insufficient relaxation of LES to allow food into the stomach
attributed to abnormal inhibitory enteric nervous function |
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GERD
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normally LES transiently relaxes and closes, but with GERD is relaxes more frequently or it may be more prolonged, allowing gastric contents into the esophagus which may lead to ulceration
weak esophageal peristaltic contractions fail to push acid back into stomach 20% of pts have abnormally slow stomach emptying -> longer period for relux to happen hiatal hernia |
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Diffuse esophageal spasm
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prolonged painful contraction of esophagus after swallowing
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Stomach (fxn)
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reservoir for ingested food
digestive *acts as a homogenizer *mix food with gastric secretions to form chyme empty contents at a controlled rate so it doesnt overwhelm the small intestines digestive capabilities |
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Stomach (anatomy)
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3 layers of smooth muscle
outer- longitudinal middle- circular (most prominent) inner- oblique |
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Stomach (anatomy- innervation)
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extrinsic- PSymp inntervation from vagus stimulates motility and secretion
*Symp innervation from splanchnic inhibits secretion and motility intrinsic- through the plexuses afferent fiber responses |
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Stomach (anatomical division)
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cardia
fundus body antrum |
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Cardia
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region surrounding the superior opening (cardiac sphincter)
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fundus
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superior portion, above cardia
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body (corpus)
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main portion of the stomach
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antrum (pyloric antrum)
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inferior region (2 parts)
*antrum- continuous with body of stomach *pyloric canal- leads to duodenum |
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responses to gastric filling (receptive relaxation)
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fundus and body of stomach relax
-initiated by swallowing as part of reflex relaxation of LES induced by primary esophageal peristalsis - relaxation also by filling stomach with gas or liquid (uses stretch receptors)- gastric accommodation reflexes dep. on intact vaus allows 1-2L w/o sig inc. in intragastric pressure |
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Mixing and emptying of gastric contents (body and fundus)
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Little mixing occurs here
*muscle layers are thin and contractions are weak *contents form layers based on density *fats are part of an upper oily layer, and are emptied last |
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Mixing and emptying of gastric contents (rate)
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depends on physical characteristics
*inert, isotonic leave rapidly *solutions with nutrients leave slower (feedback from sm. intestine) *solids are even slower (1 hr lag time for retropulsion and mixing through peristalsis) *Large particles remain in stomach until a period of fasting |
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Antrum (main fxns)
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most mixing occurs here
produces vigorous peristaltic contractions food broken down and mixed with gastric juices |
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Peristalic contractions during emptying
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contractions by gastric slow waves start in the middle of the body of the stomach ->plyorus
force and velocity increase *antrum and pylorus contract almost simultaneously *some food and chyme (<2mm2 pushed into duodenum- pyloric pump) *pyloric sphincter closes and forces antral contents back (retropulsion) frequency ~3/min, similar to slow waves duration: 2-20s |
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Duodenal factors that delay gastric emptying
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hypertonicity of durodenal contents
decrease in pH (normally at 5, less than 3.5 delays emptying) fatty acids, mono/diglycerides peptides and amino acids duodenal distension |
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Mechanisms for regulation of duodenal emptying
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receptors in duodenum and jejunum responsible for reflex control
control pathways are neural and hormonal -neural involve ENS and vagvagal reflex arcs -hormones released from duodenum and jejunum(secretin, CCK, gastrin,etc) |
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Hormonal Mediators and what they are released due to
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Secretin due to acid
CCK and GIP due to fats Gastrin due to amino acids Unknown hormone due to hypertonicity |
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Non- duodenal factors affecting gastric contraction
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ileal break (glucose or fats in ileum reduce emptying)
colonic distention causes gastric muscle to relax |
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Migrating Myoelectric Complex
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occurs during fasting
antrum quiescent for 1-2 hours (lag time) followed by intense 10-20 min of electrical and motor activity strong antral contractions, pylorus relaxed allows emptying of large chunks of food triggered by motolin (from enteroendocrine cells) |
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Vomiting
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ejection of gastric (sometimes duodenal and jejunal) contents through the esophagus and mouth (normally preceeded by retching)
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Retching
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contents forced into esophagus without reaching the pharynx
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Vomiting- reflex behavior
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controlled by medullary centers-
*vomiting center (vomiting with no retching) *retching with no vomiting *chemoreceptor trigger zone (in rostral medulla, outside of BBB -> chemical/ stimuli may reach through the blood) |
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Stimuli for vomiting
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distention of stomach and duodenum
tickling back of throat noxious stimuli to genitourinary system smells/ sight semicircular canal stimulation (motion sickness) emetic agents |
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Motion sickness
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Semicircular canal stimulation- impulses transmitted to a chemoreceptor
Antihistamines (H1 blockers) work at chemoreceptor trigger zone |
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Emetic agents
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Two types depending on site of action
*stimulate receptors in stomach or duodenum (ipecac) *at chemoreceptor trigger zone (morphine, hormones) |
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Antiemetic actions
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Anticholinergics: motion sickness (vestibular input)
antihistamines: motion/morning sickness (circulating hormones) DA antagonists: opioids, neoplastic disease, radiation sickness 5-HT anatagonists: post-op vomiting Cannabinoids: chemo |
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Events during vomiting
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central coordination of contraction of thoracic, diaphragmatic and abdominal musculature
basic electrical rhythm suspended and replaced by bursts in the oral direction -> retrograde giant contractions (move contents orally) retrograde propulsion during emesis is driven only by ENS |
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Vomiting consequences
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metabolic alkalosis (HCl loss from stomach in excess)
dehydration hypokalemia ([K+] higher in gastric juices than blood) |
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Small intestine (characteristic)
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2 hours for chyme to go through
major portion of digestion and absorption (not alcohol or aspirin) intestinal motility mixes chyme and digestive enzymes, moving in an aboral direction |
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Small Intestine (histology)
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Large surface area (enhances digestion and absorption)
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Circular folds (plicae circulares)
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folds of the mucosal and submucosal layers that truples the surface area
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Villi
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finger-like projections of the mucosa
*covered with epithelial cells *each villus has a capillary and lacteal (lymphatic) *increase surface area 10 fold |
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Microvilli
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apical portions of the absorptive epithelial lining of the villi
*contain enzymes that hydrolze carbs and peptides *increase surface area 20 fold *microvilli across the entire epithelium is called BRUSH BORDER |
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Small Intestine (blood supply and lymphatics)
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AA, sugars, some water soluble lipids are taken up into the capillaries in the villi and emptied into the portal vein to the liver
lipids are re-synthesized in epi. cells triglycerides and coated, forming chylomicrons. chylomicrons are secreted into the villus and taken up into the lymphatic system by the lacteals. the lymph drains into the venous circulation at the left subclavian vein |
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electrical waves of the small intestine
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freq.- 3 per min in stomach, 12 per min in GI tract
(rate in the small intestine declines from 12 down to 8 or 9 per min in the ileum) slow wave freq determines the maximum contraction frequency |
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basic electrical rhythm of small intestine
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independent of extrinsic innervation
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Contractile behavior of small intestine
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Segmentation
*most common type in small intestine *contraction of circular muscle divide the sm intestine into small segments *11-12 per min in duodenum, 8-9 in ileum *sites of contraction alternate Peristalsis *less frequent than segmentation *travel less than 5 cm in small intestine *produce small net mvmt of chyme in aboral direction |
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MMC and bacteria
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MMC contractions are stronger than those occurring after a meal.
*cleans and empties small intestine *inhibits colonic bacteria in ileum |
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MMC
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disrupted by stress
ends with eating |
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ileocecal sphincter
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prevents retrograde flow of chyme from cecum to ileum
opened by peristalsis in distal ileum distention of distal ileum causes sphincter to relax distention of cecum causes spincter to constrict further |
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Colon
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most salts and water are absorbed (not excreted in feces)
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Colonic mvmt
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SLOW
majority of transit time is in the colon takes ~1-3 days |
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Colon structure
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cecum
ascending colon descending colon sigmoid colon rectum anal canal |
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Colon Innervation (extrinsic)
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PS- stimulates motility
*vagus innervates proximal colon (cecum ->transverse colon) *pelvic nerves innervate descending colon through anal canal SYMP- *postgangionics from mesenteric and hypogastric ganglia *sympathetic inhibits motility |
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Colon inntervation (intrinsic)
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plays role in propulsive and non-propulsive contractile activity in the absence of extrinsic innervation
Hirschsprung's disease- enteric nervous system doesnt develop properly, also by radiation damage *colon becomes constricted in region where the intramural plexus is absent |
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Colonic contractions
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NO MMC
haustral contractions- haustraul shuttling, back and forth mvmt of chyme in the haustra *mix chyme and expose it to gut epithelium mass movements- 1-3 times daily.haustra disappear and are replaced by waves resembline intense peristaltic waves *push contents long lengths of colon toward the rectum |
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intestinal reflexes
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gastroileal
gastrocolic |
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defecation
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involves sphincters
internal anal sphincter- thickening of intestinal smooth muscle, under control of enteric and PSNS external anal sphincter- composed of striated voluntary muscle. innervated by somatic motor nerves *under voluntary and reflex control |
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defecation sequence of events
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rectum is normally empty
mass mvmt forces feces into rectum distension of rectum *initiates urge to defecate *initiates intinsic and extrinsic (only parasympathetic) reflexes *stool moves into anal canal *relaxation of external sphincter |
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diarrhea
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Osmotic
Secretory |
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Osmotic diarrhea
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poorly absorbable solute in the GI
*lactose deficiency *osmotically active solute draws water into intestine |
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Secretory diarrhea
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elevation in endogenous fluid and electrolye secretion
*bacterial enterotoxins increase fluid secretion via second messenger systems *some e.coli increase cAMP, other cGMP (resulting in high volume water diarrhea) *enteritis (low volume blood diarrhea) *ulcerative colitis- unknown or allergic effect. low volume, bloody diarrhea |
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constipation
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feces remaining prolonged periods in the colon
Irregular bowel habits overuse of laxatives opioids |
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aspirin absorption
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optimal pH 2-4
food slows the rate abs by pass diffusion also abs from proximal small intestine faster than the stomach *enteric coating- delays abs and reduces effectiveness of platelet aggregation |
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Exocrine secretion
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gland cells that release their products into ducts
ducts open onto epitheleal surface of the body |
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endocrine secretion
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HORMONE elaborated ian endocrine cell is released intthe blood and acts at a distant target
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paracrine secretion
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substance released from a cell and diffuses throug intrstitial fluid to act on a nearby target of different type
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neurotransmitter secretion
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substance released into a synaptic cleft to act on nearby cell
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secretagogue
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substance that stimulates secretion from the cell
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types of salivary glands
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parotid
submandibular sublingual |
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parotid gland
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largest of the salivary glands
entirely serous watery secretion with amylase, but not mucins |
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submandibular and sublingual
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mixed glands with acinar and mucus cell
sublingual secrete viscous saliva (mainly mucus) saubmandibular are mixed serous and mucus secretion |
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structure of salivary glands
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acinar cells (serous and mucus cells)secrete their products into the lumen of the acini
intercalated ducts drain the acini into larger striated ducts striated ducts drain into larger excretory ducts single duct takes secretions to each gland of the mouth |
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saliva (fxn)
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mucins lubricate food for easy swallowing
amylase begins digestion solubilizes material for taste cleans mouth and teeth (lysozyme and sIgA) facilitaes speakin helps clear esophagus of reflux |
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xerostomia
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Dry mouth
in people with decreased or no salivary gland function results in dental carries and mouth infections |
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organic components of saliva
(proteins from acinar cells) |
amylase
lipase mucus glycoproteins proline rich glycoproteins tyrosine/ histidine rich proteins peroxidase |
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organic components of saliva (proteins from non acinar cells)
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lysozyme
sIgA growth factors regulatory peptides circulating hormones |
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ionic concentration varies rate of salivary secretion
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with increased flow rate:
[K+] decreases slightly Na+, HCO3-, Cl- increase pH increase saliva becomes less hypotonic |
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salivary two stage model
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primary secretion is isotonic, execretory ducts modify secretion
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Nervous control of salivation (parasympathetic)
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Primary control
activates M2 receptors *copious, watery secretion (amylase containing) *vasodilation -> inc blood flow to glands *from cranial nerves 7 and 9 |
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Nervous control of salivation (sympathetic)
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Activates beta receptor
*low volume, short duration viscous saliva *initial vasoconstriction *removal of symp causes no alteration in saliva *symp input from postganglionics of superior cervical ganglia |
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gastric secretion (histology)
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columnar elithelial cells (secretes mucus and HCO3 and protects surface from mechanical and chemical injury
gastric pits are throughout the surface *opening for gastric gland |
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gastric juice (composition)
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HCl
Instrinsic factor pepsinogen gastrin mucus and bicarb salts and water |
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HCl
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secreted from parietal cells
kills bacteria activates pepsinogens enhances iron absorption releases free cobalamins (form of B12) |
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intrinsic factor
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secreted by parietal cells (different mechanism than HCl)
binds B12, alows its absorption from the ileum ONLY GASTRIC SECRETION NEEDED TO MAINTAIN LIFE |
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pepsinogen
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inactive form of pepsin, secreted by chief cells
cleaved to pepsin in the presence of acid |
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gastrin
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secreted by G cells
stimulates gastric acid secretion |
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mucus and bicarb
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secreted by columnar epithelial cell
protects stomach from mechanical and chemical destruction |
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salts and water
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at low secretion [Na] < [H]
[K]> that plasma conc at all rates at high rtes: gastric juices of the stomach approaches isotonic HCl venous blood from stomach becomes alkaline tide |
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stomach divisions
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cardiac (glandular) region
oxyntic (acid secreting) region pyloric (glandular) region |
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cardiac region
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glandular
narrow region in cardiac portion contains primarily mucus secreting cells |
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oxyntic region
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acid secreting, glandular region
primarily in the body and corpus mucus secreting cells pariental cells secrete HCl and intrinsic factor chief cells secrete pepsinogens |
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pyloric region
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glandular
few, if any, parietal or peptic cells predominantly mucus cells G cells secrete gastrin D cells secrete somatostatin |
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gastric acid secretion by parietal cells(mediation)
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by H,K ATPase
H-K in the apical membrane of the parietal cell pump extrudes H+ into gastric lumen and takes in K (Cl passively moves into gastric lumen -> net secretion of HCl) H+ from pump comes from CO2 and H2O uptake in the blood *CAH produces carbonic acid (goes toH and HCO3) *PPI blocks acid secretion by using H-K pump |
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Control of gastric acid secretion
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parietal cell level
acid secretion inhibitors |
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Acid secretion control (parietal level)
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Secretagogues
ACh Histamine Gastrin (potentiate effects of each other) |
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ACh gastric acid secretion regulation
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neurotransmitter regulation
from PSymp and intrinsic innervation increase acid secretion through M3 receptors blocked by atropine |
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histamine gastric acid secretion regulation
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paracrine regulator
from ECL cells in gastric mucosa, near parietal cells stimulates through H2 receptors blocked by cimetidine |
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Gsatrin gastric acid secretion regulation
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from G cells in the antrum and duodenum
hormonal regulation acts indirectly by releacing histimine from ECL cells role as trophic factor in growth and maintenance of the oxyntc region of the stomch |
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inhibitors of acid secretion
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somatostatin (in body and antrum)
prostaglandins epidermal growth factor |
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3 phases of increased acid secretion in response to food
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cephalic
gastric intestinal |
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Cephalic phase
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stim. by sight/ smell
reflex ONLY mediated by vagus and intramural plexuses Ach directly stimulates parietal cells, indirectly stimulates acid secretion by releasing gastrin from G cells and histamine from the ECL cells secretion decreased when pH <3 in the antrum (low pH -> release of somatostatin) |
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Gastric phase
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starts b/c of food in the stomach
stimuli are: distentsion of stomach presence of amino acids (bind to G cells and stim. release of gastrin) where greatest amount of acid secretion occurs (postprandial alkaline tide) decrease in pH to less than 2 increases gastric acid secretion other secretagogues of gastric HCl *Ca++ *caffeine *coffee *alcohol in high oncentration |
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Intestinal Phase
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begins with chyme in the duodenum
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Pepsinogen secretion
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secreted from chief cells
pepsinogen is proenzyme stimulated by vagal cholinergic activation. Also stim by: *low gastric pH *secretin stim chief cells *gastrin stimulation |
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Zollinger-Ellison Syndrome
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tumors in duodenum, produce high circulating levels of gastrin
*results in: -increased number of ECL and parietal cell - constant stim of acid secretion -> peptic ulcers, diarrhea, steatorrhea, hypokalemia, eventual erosion of the bowel |
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intestinal secretions
(small intestine) |
goblet cell
epithelial cells |
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goblet cells
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intermixed with columnar epithelial cells
mucus secreting |
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goblet cells
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intermixed with columar epithelial cells
secrete mucu |
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epithelial cells
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elaborate and secrete a watery, electrolyte secretion
rate of secretion is less than rate of fluid absorption |
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intestinal secretions
(colon) |
numberous goblet cells (mucus)
lower volume of secretion than small intestine, but more mucus aqueous portion is alkaline stimuli *irritation of mucosa *activation of PSymp pathways |
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pancreatic secretion (fxn)
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hydrolsis of protein, starch, triglycerides
neutralize gastric acid in duodenum maintain proper pH |
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Exocrine pancreas structure
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similar to salivary gland
lobules -> intercalalted ducts -> larger ducts -> main collecting duct drains pancreas and empties into duodenum with common bile duct through sphincter of Oddi |
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Innervation of exocrine pancreas
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PSymp
*preganglionic in vagus *postganglionic within pancrea Symp innervation *postganglionics of paravertebral ganglia *activation inhibits secretion |
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Pancreatic juice
(aqueous component) |
HCO3 (neutralize duodenal contents, conc depends on rate)
Cl (conc varies inversely with HCO3) Na and K (at plasm conc) produced at rest by intercalated and intralobular ducts secretin increase volume and HCO3 conc |
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Pancreatic juice
(enzymatic component) |
elaborated and secreted from acinar cells
necessary enzymes to prevent malaborption of lipid, protein, carbs amylase (starch) lipase (fats) protease (protein) *secreted as inactive proenzyme *activated by hydrolysis of lumen in intestine *trypsin *chymotripsin *carboxypeptidase nuclease (DNAase and RNAase) |
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regulation of pancreatic secretion
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acinar cells and ducts regulated by hormonal and nervous influences
electrolytica nd enzyme secretion controlled separately cephalic phase gastric phase intestinal phase CCK and secretin |
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cephalic phase regulation (pancreas)
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sham feeding
*vagal stim through ACh of ductal and acinar cells *low volume, high enzyme secretion, because ACh has greater effect on enzymes than fluid |
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gastric phase regulation (pancreas)
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distension of stomach and amino acids and peptides
*vagus stimulation *low volume, high enzyme |
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intestinal phase regulation (pancreas)
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presence of acids, peptides, fatty acids
*acid -secretin release from S cell -copious secretion of HCOS rich, low enzyme *fatty acids and amino acids - CCK release by I cells of small intesstin -secretion high in enzymes |
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CCK and secretin
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CCK is potent secretagogue of enzyme secretion (little effect on aqueous secretion)
secretin stim aqueous production (little effect on enzymes) CCK MARKEDLY POTENTIATES effect of secretin |
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Liver (fxn)
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metabolize, detox, and inactivate endogenous compound (steroid and hormones) and exogenous substances (drugs and toxins)
Digestive fxn is secretion of bile regulation of metabolism protein synthesis stores vitamins degrades and secretes hormones metabolism and excretion of drugs and toxins *bilirubin *heavy metals *steroids *fat soluble vitamins |
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Bile (fxn)
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required for fat digestion and absorption
SOLE EXCRETORY ROUTE for many substance, especially cholesterol |
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Bile
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elaborated in hepatocytes
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Bile contents
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bile acids
cholesterol lecithin bile pigments |
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Bile fxn in regards to lipids
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Emulsifies lipids (allows for easier digestion and absorption)
form micelles (then absorbed by intestinal epithelium) |
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Secretion of bile
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secreted into bile canaliculi
water and plasma electrolytes are osmotically drawn into canaliculi glucose and other plasma constiuents can also enter bile |
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sequence of bile secretion
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canaliculi ->small bile ducts ->enterohepatic circulation
stored in gallbladder between meals |
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bile in small ducts
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lined with cholangiocytes
*secrete HCO3 rich soln (stim by secretin) *inhibited by somatostatin cholangiocytes reabsorb fluid and solutes from bile *glucose and AA acids leaked into bile are actively removed *cholangiocytes concentrate bile after gallbladder removal |
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Bile storages between meals
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In gallbladder
*during ingestion sphincter of Oddi constricts and forces bile into gallbladder *half of bile is store in gallbladder, other half is in the bile duct (hepatic bile) *gallbladder conc's bile -absorbs Na, Cl, HCO3 |
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bile retrieval
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through enterohepatic system
*small amt of bile acids are abs passively through intestines, but the bulk of acids are taken up by Na driven secondary active transport in the terminal ileum -abs bile enters portal circulation -hepatocytes take up bile and resecrete into bile canaliculi non-absorbed bile acids are secreted in the feces bile pool is circulated twice during meals |
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control of gallbladder emptying
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during cephalic and gastric phases
-intermittent contractions force bile through partially relaxed sphinter of Oddi -contraction of gallbladder and relaxation of sphincter are mediated by cholinergic fibers during intestinal phase -highest rate of gallbladder emptying -strongest stimulus is CCK (CCK is released in response to fat, reaches gallbladdr via circulation, causes strong contraction of gallbladder and relaxation of sphincter) |
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control of bile acid secretion and synthesis
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conc of bile acids in hepatic portal blood is major influence
*presence of bile acids (choleretic effect), *low conc of bile acids -inc synthesis of bile acids -decreased secretion of bile acids |
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secretin in response to gallbladder emptying
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released from duodenum in response to acid
stimulates epithelia to release greater volume of HCO3 |
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CCK in bile secretion from hepatocytes
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CCK DOES NOT PLAY A ROLE
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pathology of GI tract
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PUD
gastric carcinoma acute and chronic carcinoma |
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acute gastritis
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inflammation of gastric mucosa
predominant neutrophilic infiltrate usually transient |
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acute gastritis pathology
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intact epithelium
neutrophils superficial erosion (severe) |
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acute and chronic gastritis damaging factors
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acute
*Heavy NSAID use *high alcohol consumption severe stress *uremia *heavy smoking Chronic *H. pylori *gastric hyperacidity *autoimmune *alcohol |
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chronic gastritis
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chronic mucosal inflammatory changes (mononuclear cell infiltrate, plasma cells and lymphocytes)
*mucosal atrophy *absence of erosions |
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chronic gastritis
(H pylori) |
causes:
inflammation mucosal changes metaplasia regeneration dysplasia |
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Peptic Ulcer Disease
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breach in the mucosa of the alimentary tract
extends through the muscularis mucosa into submucosa or below |
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Peptic ulcer disease (imbalance)
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between gastroduodenal mucosal defense and damaging forces
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PUD biology
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>30 yrs
higher in blood group O higher in alcoholic cirrhosis men get them more than women |
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PUD frequency
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Duoudenum
Stomach GE junction ZE syndrome |
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H pylori in PrUD
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most common cause of chronic gastritis
almost always present with DU 90% in chromic gastritis of the antrum |
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H pylori
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G neg rod
Motile Urease Superficial colonization No invasion Virulence factors *protease *phospholipase (neutrophil sequestration, mucosal damage) |
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PUD morphology
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DU- near pyloric ring
GU- lesser curvature Ulcer size *benign/ malignant Mucosal puckering around the ulcer |
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Gastric Ulcers
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lesser curvature
body/ antrum factors: H. pylori, NSAID, tobaccos, alcohol, steroids |
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Duodenal ulcers
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factors: H. pylori, acid hypersecretion, rapid gastric emptying
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