Term
| what is the name for the smooth muscle of the GI treat, what makes it unique, where is it located |
|
Definition
it is everywher except the upper 1/3 of the esophagus and external anal sphinctor
connected via gap junctions, low resistance, coordinated
2 muscle components
circular: decreases diametes
longitudinal: shortens length |
|
|
Term
| what are the types of contraction for the smooth muscle of the GI tract: mechanism, location |
|
Definition
phasic: contraction followed by relaxation
in esophagus, gastric antrum, SI, and tissues with mixing and propulsion
tonic: constant level of contraction in orad, lower esophagus, ileocecal, intestinal sphinctor |
|
|
Term
| explain what a slow / myogenic wave is |
|
Definition
| not action potential, slow wave of oscillating depolarization and repolarization that does not cause contraction (EM below threashold) |
|
|
Term
| if slow waves dont cause contraction, how is there contraction in the smooth muscle of GI |
|
Definition
| parasympathetic innervation at the time of plateau of a slow wave gives it enough potential to pass threashold |
|
|
Term
| what is the range of frequencies for slow waves, in what areas is this the slowest and fastest |
|
Definition
| 3 in stomach to 12 in duodenum waves per minute |
|
|
Term
| how if the speed of the slow waves adjusted |
|
Definition
| it isnt, can only modulate product of AP (hormonal or neural) at platau and which adusts strength in contraction, not rate |
|
|
Term
| what is the origin of the slow wave, where is it located, why is it effective |
|
Definition
interstitial cells of cajal in myenteric plexus (between circular and longitudinal muscle)
effective because of spread of waves between low resistance gap junctions |
|
|
Term
| explain the cellular mechanism for slow waves |
|
Definition
depolarization: Ca channels open, Ca moves in
plaeau: membrane potential depolarized all the way until threashold (at this time parasympathetic innervation will do AP)
repolarization: K channels open, K moves out |
|
|
Term
| if there is no parasympathetic input what is the effect of slow waves? what about when there is sympathetic input |
|
Definition
| tonic (basal) contraction, sympathetic does nothing so it stays here |
|
|
Term
| when parasympathetic stimulates the slow wave plateau, explain the contraction |
|
Definition
| phasic, more AP stronger contraction |
|
|
Term
| what is the function of mastication (5) |
|
Definition
| mix food with saliva, reduce size of food particles, enable taste, swallowing, mixing with salivary amalyase to digest carbs |
|
|
Term
| what are the two ways to initiate mastication, how do they work |
|
Definition
• Involuntary: Mechanoreceptors connect to brainstem and make oscillatory pattern of muscle movement
• Voluntary: Can override involuntary chewing at any time |
|
|
Term
| what are the phases of deglutition, are the voluntary or involuntary |
|
Definition
oral: voluntary
pharyngeal: involuntary
esophageal: voluntary |
|
|
Term
| what are the 6 events in the oral phase |
|
Definition
o Tongue voluntarily forces bolus toward pharynx
o Bolus stimulates somatosensory receptors in pharynx
o Vagus and glossopharyngeal nerve send info to medullary swallowing center
o Efferent output to striated muscles of pharynx and upper esophagus stimulated
o Involuntary swallowing reflex initiated
o Lower esophageal sphincter relaxes |
|
|
Term
| what are the 6 events in the pharyngeal phase |
|
Definition
o Soft palate pulls up so food cannot get into nasopharynx (breathing inhibited)
o Epiglottis covers opening to larynx (Adam’s apple)
o larynx moves up against epiglottis to prevent entry into trachea
o Upper esophageal sphincter relaxes
o Peristalsis propels food through
Lower esophageal sphincter closes when peristalsis arrives |
|
|
Term
| in the esophageal phase, what events are under control of the swallowing reflex |
|
Definition
Upper esophageal sphincter closes to prevent reflux
Primary peristaltic wave travels down esophagus
receptive relaxation
sphinctor contracts to resting tone as soon as bolus enters |
|
|
Term
| in the esophageal phase, what events are under control of the enteric nervous system, explain it too |
|
Definition
| secondary peristaltic wave: clearns remaining food at begining point of distension (initiated by un-cleared food) |
|
|
Term
| what is receptive relaxation, how is it initiated |
|
Definition
• Food approaching opens the lower esophageal sphincter causes orad of stomach relaxation, decreasing the pressure to welcome bolus
• Vagus nerve releases VIP relaxing the areas |
|
|
Term
| explain how peristalsis works |
|
Definition
| • As an area closes it creates a high pressure that pushes the bolus |
|
|
Term
| explain the role of intra-thoracic pressure in deglutition, how is this regulated |
|
Definition
Intra-esophageal pressure is equal to intra-thoracic pressure which is lower than atmospheric and abdominal
Makes it hard to keep air out of the top and acid out of the bottom of the esophagus
Upper and lower esophageal sphincters have to take care of this so they are closed unless a bolus is passing |
|
|
Term
|
Definition
| difference between opening and closing of sphincters is a result of the delay of food passage down esophagus |
|
|
Term
| GERD: causes, symptoms, associations |
|
Definition
o Intra-abdominal pressure is increased
o Pregnancy, obesity
o Contents of stomach reflux into esophagus
o Esophageal mucosa damage |
|
|
Term
| what is dysphagia, what are the types |
|
Definition
| difficulty swallowing: oropharyngeal, esophageal |
|
|
Term
| what are the causes of oropharyngeal dysphagia |
|
Definition
| Neurological: bulbar palsy (paralysis), pseudo-bulbar palsy, myasthenia gravis (NMJ disorder, weakness) |
|
|
Term
| what are the causes of esophageal dysphagia |
|
Definition
| • benign (rings, polyps, peptic ulcer), malignant (carcinoma in esophagus, stomach, extrinsic compression), esophagitis (candidias, inflammation), achalasia (can’t relax) |
|
|
Term
| how can a dysphagia be diagnosed |
|
Definition
• endoscopy
• barium sulfate contrast radiology
• esophageal manometry: catheter into nose to stomach, withdrawal to detect pressure changes |
|
|
Term
| what are the 3 necessities for gastric motility |
|
Definition
o Relaxation of orad to receive bolus
o Contractions to reduce size and mix bolus with secretions to digest
o Gastric emptying and propulsion of chyme into SI |
|
|
Term
| what are the muscles of the stomach |
|
Definition
Outer longitudinal
Middle circular
Inner oblique |
|
|
Term
| what are the regions of the stomach, give their main functions |
|
Definition
Fundus
Body: stores food, weak contraction, many oxyntic glands
Antrum: thick muscle, peristalsis, retropulsion of bolus into antrum
Pylorus: regulates passage of chyme into duodenum to a small size |
|
|
Term
| what are the regions of the stomach based on motility. what traditional regions do they contain. what is another difference and function |
|
Definition
o Regions Based on motility
Orad: proximal thin walled. Contains fundus and proximal body
Caudad: distal thick walled. Strong contractions to mix food and propel it into SI. |
|
|
Term
| explain how receptive relaxation works in the stomach |
|
Definition
o Distension of the lower esophagus by food relaxes the lower esophageal sphincter
o Detected by mechanoreceptors
o Vasovagal reflex: afferent and efferent limbs on vagus nerve via VIP
o Reduces pressure and increases volume of orad of stomach |
|
|
Term
| vagotomy: purpose, procedure, results |
|
Definition
eliminates receptive relaxation
cutting of the vagus nerve
reduces stomach acid secretion |
|
|
Term
| how does mixing and digestion occur in stomach, in what direction |
|
Definition
o Waves of contraction begin at mid body and move distally along caudad increasing in strength and veolcity to pylorus
o Mix food and propel into duodenum |
|
|
Term
|
Definition
| Wave of contraction closes pylorus so much chyme is propelled back into the stomach for more mixing than into duodenum |
|
|
Term
| where do slow waves occur in stomach, how often |
|
Definition
| In caudad region at 3-5 per minute |
|
|
Term
| what does parasympathetic innervation do to stomach slow waves, what transmitters |
|
Definition
| • gastrin and motilin increase frequency of AP and force of wave / contraction |
|
|
Term
| what does sympathetic do to stomach slow waves, what transmitters |
|
Definition
| • GIP and secretin decrease frequency of AP and force of contraction |
|
|
Term
| migrating myoelectric complex: 2 functions, locations, regulators, definition, stimulated by, when it happens |
|
Definition
• Moltin causes contractions to occur in 90 minute intervals in fasting
• Regular cycle of waves every 5-10 min initiated by vagal stimulation
• Regulated by VIP, motilin, enkaphalin
• in small intestine and stomach
Functions
o Clear stomach and colon of residue and un-digestible things
o Inhibit colonization of bacteria in the small intestines |
|
|
Term
| gastric emptying: length, what empties faster, requirements for particles, stimulation to end |
|
Definition
o Takes approx. 3 hours
o Liquids and isotonic contents empty faster
o Particles must be 1mm3 or less, retropulsion continues until this is reached |
|
|
Term
| what regulates gastric emptying |
|
Definition
Fat in duodenum stimulates CCK which slows emptying so fat can digest
H+ stimulates mucosa of duodenum and enteric nervous system sends info to the stomach via myenteric plexus to slow emptying so there is more time for H+ to be neutralized by pancreas enzymes |
|
|
Term
| what isthe frequency of slow waves in the small intestine parts |
|
Definition
| 12 in duodenum, 8-9 in ileum |
|
|
Term
| what does parasympathetic and sympathet innervation do to the slow waves of the small intestines. what neurotransmitters |
|
Definition
| parasympathetic: increases contraction. cholinergic and some peptidergic fibers (VIP, encephalin, motilin) |
|
|
Term
| explain segmentation in the small intestines, what controls this movement, what is the function |
|
Definition
enteric NS
• mix cyme and expose it to pancreatic enymes
• bolus in intestinal lumen is split by contraction, the section relaxes and bolus comes back together
• produces no forward movement |
|
|
Term
| explain peristaltic contraction in the small intestines, what neurotransmitters are used |
|
Definition
• propel chyme toward large intestines
• contraction occurs behind bolus (orad) and a portion in front of bolus (caudad) relaxes
• neurotransmitters for contraction are Ach, substance P
• neurotransmitters for relaxation are VIP, NO |
|
|
Term
| what is the afferent portion of the vomitting reflex |
|
Definition
| back of throat and GI tract chemoreceptors carry information on vestibular system triggering zone in 4th ventricle (vomiting center in medulla) |
|
|
Term
| what is the efferent portion of the vomitting reflex |
|
Definition
Reverse peristalsis begins in small intestines
Stomach and pylorus relaxes
Forced inspiration to increase abdominal pressure
Relaxation of lower esophageal sphincter |
|
|
Term
| what movements produce reching |
|
Definition
vomitting reflex with...
Upper esophageal sphincter remains closed
Lower esophageal sphincter is opened and gastric contents return to stomach |
|
|
Term
| what are the contents of the large intestine called |
|
Definition
|
|
Term
| why is there less movement in the large intestines |
|
Definition
| • Less myenteric plexus development and vagus innervation t leads to slower movement |
|
|
Term
| what is the function of the bacteria in the large intestines |
|
Definition
| Bacteria: Make vitamin K and vitamin B complexes |
|
|
Term
| what is the function of mucous in the large intestines |
|
Definition
| • Mucous: holds feces together, alkinity prevents acid attacks to wall |
|
|
Term
| what prevents reflux into the ileum |
|
Definition
|
|
Term
| what types of movements occur in the large intestines |
|
Definition
| segmentation contection, mass movement |
|
|
Term
| where does most of the water absorption in the GI occur, what is the consequence of this |
|
Definition
| distal colon (can make contents difficult to move) |
|
|
Term
| where does large intestine segmentation occur, how |
|
Definition
o Occur in cecum and proximal colon
o Mix contents in haustra (segments) |
|
|
Term
| how often to mass movements occur, why is this diffiuclt, how does it work |
|
Definition
o Occur in colon 1-3 times per day
o Move contents to rectum where it is stored until defecation
o Water absorption occurs (makes contents more difficult to move)
o Longitudinal muscle layer is teniae coli which contract hastura |
|
|
Term
| what reflex controls defecation, what controls it, how does it work |
|
Definition
Rectum filles with feces and smooth muscle of rectum contracts, internal anal sphincter relaxes
External anal sphincter is voluntarily relaxed and smooth muscle of rectum contracts to make pressure (innervated by the pudendal nerve) |
|
|
Term
| what is valsalva, what is the function |
|
Definition
Expiring against closed glottis
Can increase intra-abdominal pressure for additional pressure |
|
|
Term
| what happens if there is an urge to defecate and it does not occur |
|
Definition
Rectum contracts and forces feces back into colon
Urge to defecate can be over ridden by contraction of the external anal sphinctor |
|
|
Term
| explain the ileocecal reflex |
|
Definition
| Distension of ileum causes ileocecal sphincter to relax. Distension of the colon causes ileocecal sphincter to contract |
|
|
Term
| explain the gastroileal reflex |
|
Definition
| produces mass movement shortly after a meal due to action of gastrin and extrinsic autonomic nerves |
|
|
Term
| hirschsprung disease: AKA, cause, effect |
|
Definition
o Chronically constricted colon blocks feces which accumulate and distend colon
o Loss of ganglion cells and low VIP
o bad neural crest migration to make auerbach's plexus in part of colon
o most of the time near the anus |
|
|
Term
|
Definition
o Alternating diarrhea and constipation
o Pain and discomfort with unknown etiology (diffuse or localized to the left iliac fossa)
o relieved by defication
o frequent small stools but patient feels emptying is incomplete
o abdomen distended
o painful spasms, constipation, dirrhea, mucous
o related to stress, sedentary
o relieved by exercise |
|
|
Term
| what are the functions of saliva (13) |
|
Definition
o Initial digestion of starch and lipid
o Dilution and buffering of ingested foods
o Lubrication with mucus to aid in movement
o Hydrating, cleansing, maintenance of mucus
o Antifungal, antibacterial
o Immunity mediator
o Enable swallowing, tasting, and speech articulation |
|
|
Term
| how much saliva is secreted per day |
|
Definition
|
|
Term
| where are glands with serous cells located, what do they secrete |
|
Definition
In Parotid and lingual gland
secrete water, ions and enzymes |
|
|
Term
| where are glands with mucous cells located, what do they secrete |
|
Definition
Secrete Glycoproteins, palatine
In pos-lingual and labial buccal gland |
|
|
Term
| where are glands with serous and mucous cells (mixed) located? which type of cells do these glands have more of? what is the mixed secretion called |
|
Definition
Submaxillary (more mucous) and submandibular glands (more serous)
secrete aqueous fluid and mucus (glycoproteins) |
|
|
Term
| list the branches of the gland in order begining with the most inner part. what cells are in each part |
|
Definition
acinus: acinar cells and myoepithelial cells
intercalated duct: myoepithelial cells
striated duct: ductal cells |
|
|
Term
| what do acinar cells do, what stimulates them |
|
Definition
• make initial saliva
• Innervation is parasympathetic (dominant) and sympathetic both stimulate secretion |
|
|
Term
| what do myoepithelial cells do what stimulates them |
|
Definition
| eject saliva via neural input |
|
|
Term
| what do ductal cells do, what stimulates them |
|
Definition
• modify initial saliva into final saliva by altering enzymes and electrolytes
• Innervation is sympathetic and parasympathetic (dominant) both stimulate secretion |
|
|
Term
| what substances does saliva have in it, what is the tonicity, what are the relative ion concentrations |
|
Definition
Water, lingual lipase, kallikerin, mucus, a-amalyase
Hypotonic to plasma
More K and bicarbonate, low Na and Cl |
|
|
Term
| what is in initial saliva, give a brief function of each |
|
Definition
o water, ions, enzymes, mucus
o a-amalyase: begins digestion of carbs
o lingual lipase: begins digestion of lipids
o mucin glycoproteins: lubricant
o IgA
o Kallikerin: cleaves kininogen to bradykinin which is a vasodilator helping the high salivary blood flow |
|
|
Term
| what anatomical feature allows for an increase in saliva production |
|
Definition
|
|
Term
| what pumps and channels do ductal cells use to modify saliva. what is the overall movement |
|
Definition
• Luminal side: Na/H exchanger, Cl/bicarb exchanger, H/K exchanger
• Blood side: Na/K ATPase pump, Cl channel into blood
• Overall secretion of K and bicarbonate and absorption of Na and Cl
• Net is absorption |
|
|
Term
| how do the ductal cells make saliva hypotonic to plasma |
|
Definition
| they are not permeable to water so pumps are able to create this |
|
|
Term
| where is the highest and lowest flow rate of saliva, what is the rate, what conditions are needed to make these rates |
|
Definition
o Highest rate: 4 mL/min. Final saliva closely resembles plasma, there was less time to modify saliva
o Lowest rate: < 1mL/min. Final saliva is not like plasma, it has lower NaCl and higher K |
|
|
Term
| what is the main determinant of salivary flow rate |
|
Definition
| changes in ionic composition |
|
|
Term
| explain the changes of the flow rate of bicarbonate in saliva, what makes it change |
|
Definition
| o Bicarbonate is lowest at high flow rates and highest at high because it is selectively secreted when saliva production is stimulated by the autonomic nervous system |
|
|
Term
| how does the parasmpathetic nervous system control the secretion of saliva: CN, neurotransmitter, where are receptors, what mechanism causes increased secretion |
|
Definition
| CN VII and IX release ACh which acts on muscarinic receptors of acinar and ductal cells to produce IP3 which increases Ca and causes saliva secretion |
|
|
Term
| how does the sympathetic nervous system regulate secretion of saliva: neurotransmitters, receptors, on what cells, what mechanism |
|
Definition
T1-T3 preganglionics synapse at the superior cervical ganglion
Postganglionics release norepinephrine which acts on B-adrenergic receptors on acinar and ductal cells signaling adenylyl cyclase and cAMP to increase IP3 and Ca |
|
|
Term
| what are the components of gastric juice |
|
Definition
HCl and pepsinogen: initiate protein digestion
Intrinsic factor: a mucoprotein required to absorption of B12 in ileum (only essential component)
Mucus: prevents mucosa from being corroded by HCl and lubricates |
|
|
Term
| what are the types of glands in the body of the stomach, what types of cells are they in, anatomically where are these glands in the mucosa |
|
Definition
oxyntic glands in cheif and parietal cells
secrete contents into openings, or pits, lined with epithelial cells then mucous neck cells, parietial (oxyntic cells), and chief (peptic) cells on the bottom |
|
|
Term
| what do chief cells secrete, what are they controlled by, what is the fate of the secretion |
|
Definition
• Secreted pepsinogen which is converted to pepsin via HCl secreted by parietal cells
• Pepsin breaks down proteins
• Controlled by vagal stimulation so it only releases pepsinogen when pH is low enough to convert it to pepsin |
|
|
Term
| what are parietal cells stimulated by, what precursor or pre-step do they need to function |
|
Definition
• Stimulated by vagus and secrete ACh
o CO2 from aerobic respiration and H2O join via carbonic anhydrase to make H2CO3 which breaks into H+ and HCO3- |
|
|
Term
| what transporters and channels are in a parietal cell |
|
Definition
• Luminal side
o H+/K+ ATPase: secreted H into the lumen
o Cl channel allows Cl into lumen
• Blood side
o Na/K ATPase reabsorbs Na into blood
o HCO3- /K exchanger reabsorbs HCO3- into blood |
|
|
Term
|
Definition
| inhibits H/K ATPase in luminal side of parietal cells to treat ulcers by reducing H |
|
|
Term
|
Definition
| high pH in gastric venous blood after a meal caused by bicarbonate via bicarbonate/K exchanger that reabsorbs bicarbonate into the blood on the blood side of parietal cells |
|
|
Term
| what secretes intrinsic factor, what does a decrease in this cause |
|
Definition
| parietal cells secrete, decrease causes pernnicious anemia |
|
|
Term
| how does ACh regulate gastric secretion: receptor, mechanism in cell |
|
Definition
Released via vagus to M3 receptors in parietal cells
Secondary messenger activating phospholipase C liberating DAG and IP3/Ca, Ca and DAG activate protein kinase, Cells secrete H |
|
|
Term
|
Definition
| block M3 receptors in parietal cells from ACh stimulation |
|
|
Term
| how does histamine regulate gastric secretion: where is it released from, what repceptors, what mechanism in the cell |
|
Definition
Released from enterochromaggin like cells (ECL) via paracrine to parietal cells
H2 receptors stimulate cAMP, adenylyl cyclase, PKA
Secretion of H by parietal cell |
|
|
Term
|
Definition
| blocks H2 receptors stopping histamine stimulation of gastric secretion |
|
|
Term
| how is the rate of gastric secretion regulated |
|
Definition
| Regulated by ACh, histamine, and gastrin independent and together (potentiation: combined response greater) |
|
|
Term
| what is potentiation, what challenges does this create, give an example |
|
Definition
potentiation: combined response greater)
Potentiation makes it difficult for drugs to control H secretion
• Example: Cimetidine blocks histamine and histamine potentiated effects of ACh and gastrin causing greater effect |
|
|
Term
| what glands are in the antrum of the stomach, in what cells, what do they secrete |
|
Definition
Pyloric glands:
: Smaller than oxyntic but with deeper pits
G cells: secrete gastrin into circulation
Mucous cells: secrete bicarb, mucous, and pepsinogen |
|
|
Term
| what are the stages of secretion in stomach |
|
Definition
| cephalic, gastric, intestinal, inhibition |
|
|
Term
| what occurs in the cephalic phase of stomach secretion |
|
Definition
Smell, tasting, chewing, swallowing, and conditioned reflexes in anticipation stimulate
30% of HCl secretion in response to a meal |
|
|
Term
| how is the cephalic stage of secretion initiated / stimulated |
|
Definition
Direct stimulation of parietal cell by vagus nerve which releases ACh
Indirect stimulation of parietal cell by gastrin via GRP released by vagus nerve onto G cells
Local reflexes and vagal stimulation stimulate for chielf cells to secrete pepsinogen |
|
|
Term
| gastric stage of stomach secretion: what is secreted, what stimulates it |
|
Definition
60% of HCl secretion in response to a meal
Distension of the stomach causes vagus to stimulate directly and indirectly
Distension of the stomach antrum initiates local reflexes to stimulate gastrin release
AA and peptides act on G cells to cause gastrin release |
|
|
Term
| what is secreted in the intestinal stage of gastric secretion, what is it mediated by |
|
Definition
10% of HCl secretion
Mediated by protein products of digestion |
|
|
Term
| how is secretion in the stomach inhibited |
|
Definition
HCl is no longer needed to activate pepsinogen so decreased pH stimulates. Food was buffering H but not its done and it becomes acidic
Somatostatin: Direct pathway: binds to parietal cells via G protein stopping adenylyl cyclase antagonizing histamine. Indirect pathway: inhibit histamine and gastrin release
Prostaglandins: Antagonize histamine actions on parietal cells |
|
|
Term
| describe the location of the pancreas |
|
Definition
| LUQ, retroperitoneal, tail touches spleen, sits in curve of duodenum |
|
|
Term
| what are the endocrine cells of the pancreas, also tell each type and what they secrete |
|
Definition
Islets of langerhan cells:
Beta cells: secrete insulin to decrease blood sugar
Alpha cells: secrete glucagon to increase blood sugar
Delta cells: secrete somatostatin
F/PP cells: secrete polypeptides |
|
|
Term
| how much fluid does the axocrine part of the pancreas secrete, what are the two components and their general functions |
|
Definition
o Secrete 1 L / day into the duodenum
o Aqueous component: Bicarbonate neutralizes H from stomach
o Enzymatic component digests carbs, proteins, lipids |
|
|
Term
| what cells does the acinus of the pancreas have, what do they secrete |
|
Definition
| acinar cells, secrete digestive enzymes stored in zymogen granules |
|
|
Term
| what cells are in the ducts of the pancreas, what do they do |
|
Definition
Ductal cells: extend into centroacinar cells into acinus. modify secretions of aqueous component
Centroacinar cells: Secrete bicarbonate, extend into the central acinar portion of the duct |
|
|
Term
| explain the parasympathetic and sympathetic innervation of the pancreas |
|
Definition
o Sympathetic: Postganglionic cells come from superior mesenteric and celiac plexuses. Inhibits secretion
o Parasympathetic: Synapse in enteric nervous system. Stimulates secretion |
|
|
Term
| enzymes of the pancreas: which ones are secreted active, what ones are secreted inactibe, where are they made |
|
Definition
Pancreatic amalyase and lipases are secreted as active enzymes
Pancreatic proteases are secreted as inactive. Pancreas also secretes trypsinogen which turns into trypsin to activate
Made in RER of acinar cells, golgi put them into vacuoles, concentrated into zymogen granules, stored until stimulated |
|
|
Term
| what are the contents of pancreatic juice |
|
Definition
• Isotonic, Na, K, Cl, bicarb
• Cl and bicarbonate concentrations vary with pancreatic flow |
|
|
Term
| how is pancreatic juice formed in general |
|
Definition
Centroacinar and ductal cells make isotonic secretion
Ductal cells modify aqueous component |
|
|
Term
| how do pancreatic ductal cells modify pancreatic juice: transporters on each side, net change |
|
Definition
• Apical side: Cl/bicarbonate exchanger puts Cl into cell
• Basal side: Na/H exchanger puts H into blood, Na/K ATPase puts Na into blood
• CO2 + H2O H2CO3H+ + HCO3-
o overall: Secretion of bicarbonate into pancreatic duct and absorption of H acidifying pancreatic blood |
|
|
Term
| how is the rate of pancreatic secretions regulated: when is it the highest, lowest, what is affected by the change in rate |
|
Definition
o Change in rate only affects Cl/bicarbonate
o High rate: Bicarbonate is high in pancreatic juice. Cl is low
o Low rate: Bicarbonate is low in pancreatic juice |
|
|
Term
| what are the phases of secretion in the pancreas |
|
Definition
| cephalic, gastric, intestinal |
|
|
Term
| cephalic phase of secretion in the pancreas: initiated by, nerves, secreted |
|
Definition
Initiated by smell, taste, and conditioning
Mediated by vagus nerve
Produces mostly enzymes |
|
|
Term
| gastric phase of secretion in the pancreas: initiated by, nerve, produces |
|
Definition
Initiated by smell, taste, and conditioning
Mediated by vagus nerve
Produces mostly enzymes |
|
|
Term
| intestinal phase of secretion in pancreas: stimulation, what cels stimulated |
|
Definition
| enzymes and pancreatic secretion stimulate acinar cells and ductal cells |
|
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Term
| what do acinar cells do when stimulated in pancreatic secretion: what stimulates them, nerves, secretions |
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Definition
• I cells stimulated by AA, peptides, and FA release of CCK, phenylalanine, methionine, and tryptophan. CCK stimulates CCKA receptors
• ACh stimulates muscarinic receptors and stimulates CCK via vasovagal reflexes |
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Term
| ductal cells in pancreatic secretion: what stimulats them, what do they release |
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Definition
o Release by S cells in duodenum in response to H in lumen
o Stimulates bicarbonate secretion to neutralize to pancreatic lipases can work
o Potentiated by CCK and ACh |
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Term
| what are the parts of bile and general function |
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Definition
o Emulsify lipids and put into a micelle
o Bile salts, bile pigments, lipids, ions, water |
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Term
| what is the anatomical transition from the foregut to the midgut, where is it located |
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Definition
| o Amoulla of vatar (hepatopancreatic ampulla) at pancreatic and common bile duct junction |
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Term
| what are bile salts made of |
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Definition
| bile acids, glycine, taurine, cholesterol, phospholipids, bile pigments, electrolytes, water |
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Term
| what are bile acids made of, how is it made |
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Definition
• Primary bile acids (cholic and cheodeoxycholic acid) are dehydroxylated by intestinal bacteria in intestine to make secondary bile acids (deoxycholic and lighocholic acid)
• Cholic > chenodeoxycholic > deoxycholic > lithocolic |
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Term
| what is conjugation, where does it occur, what is the function |
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Definition
• Occurs in the liver
• Different acid and glycine or taurine combination allows for 3 different bile salts (glycoholic or taurocholic acid)
o function: To more bile acids more water soluble. pK of 1-4 so they deionize and are soluble |
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Term
| bile salts are conjugated to be amphipathic, what does this allow them do to, how does this contribute to the functions of the GI tract |
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Definition
o at oil-water interface hydrophilic part dissolves in aqueous phase and hydrophobic part dissolves in oil phase
o allows lipids to be soluble (emulsify) because negative charges surround lipid increasing SA for digestion
o forms micelles around product of lipid digestion |
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Term
| bile pigments / bilirubin: how does this contribute to colors of thigns in the GI system, what is the process of coversion of molecules to create these colors |
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Definition
yellow color pigment of Hb degradation by reticuloendothelial system
carried in blood on albumin
conjugates with glucronic acid in liver making bilirubin glucuronide
converted to bilirubin and to urobilinogen by intestinal bacteria
some is circulated back into liver, some is oxidized to urobilin and stercobilin (makes poo dark) |
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Term
| how does cholesterol and phospholipids get into bile, what happens to it once secreted |
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Definition
secreted into bile by hepatocytes
inside micelles with products of lipid digestion
phospholipids are amphipathic aiding in micelle formation |
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Term
| what happens to the electrohytes and water in the bile ducts |
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Definition
| secretin stimulates ion and water secretion in bile ducts |
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Term
| what do hepatocytes secrete |
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Definition
| bile salts, cholesterol, phospholipids, bile pigments, ions, and water |
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Term
| what are the functions of the gallbladder |
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Definition
• Stores bile
• concentrates bile salts: absorbing water and ions by epithelial cells in isosmotic fashion. organic components become concentrated
• ejects bile into duodenum: within 30 min of meal. I cell sense Fa, AA, and peptides and release CCK. CCK contracts gallbladder and relaxes sphincter of Oddi. Bile is ejected in spurts |
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Term
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Definition
| o Enterohepatic circulation: In terminal part of ileum bile (max digestion) salts are transported to portal blood via Na/bile co-transporter. Portal blood carries bile back to liver. Liver extracts bile salts and adds them to hepatic bile pool |
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Term
| how much bile is lost, where |
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Definition
| In feces about 600 mg/day |
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Term
| how is bile secretion regulated |
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Definition
o Bile salts recirculating to the liver stop the rate limiting step in their production, cholesterol 7a-hydroxylase via negative feedback
o When less is recirculated, more bile salts are made
o Choleretic effect: recirculation of bile salts stimulates biliary secretion |
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Term
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Definition
| fungal infection in the mouth |
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Term
| what is orallichen planus |
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Definition
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Term
| what is burning mouth syndrome |
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Definition
| glossodyna: normal appearing mucosa with burning sensation |
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Term
| what is an aphthous ulcer |
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Definition
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Term
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Definition
| tooth decay due to bacterial infection |
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Term
| what normally protects the lumen of the stomach |
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Definition
Mucous neck glands secrete mucous
Gastric epithelial cells secrete bicarbonate which traps in mucous and neutralizes
Prostaglandins, mucosal blood flow, growth factors |
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Term
| what are the causes of peptic ulcer disease |
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Definition
Lesion of gastric or duodenal mucosa cause by erosion via H and pepsin or H. pylori, NSAIDS, stress, smoking, and alcohol, hyperthyroidism (high Ca stimulates secretion), sollinger ellisons syndrome, ASA, caffiene stimulates gastric acid secretion
Loss of mucous , excessive H or pepsin secretion, or both |
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Term
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Definition
Usually due to mucous barrier issue
Major cause is H. plyori often in antrum releasing cytotoxins (cagA toxin) breaking down barrier and colonizing with the urease (converts urea to NH3 making it alkaline) |
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Term
| gastric ulcer disease, how do diagnose |
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Definition
| Diagnosis: drink 13C-urea which is converted to 13CO2 and NH3 in stomach. 13CO2 is absorbed into blood, expired by lungs, and measured in breath test. Secretion of H+ is low because some is secreting into mucosa |
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Term
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Definition
More common because H+ secretion is higher and can overwhelm bicarbonate
Can also be caused by H.pylori indirectly because. they inhibit somatostatin secretion from D cells in antrum increasing gastrin secretion and H+. they infect duodenum and inhibit bicarbonate secretion
gastrin levels may be normal but release in response to a meal is increased
genetic: no secretion of O blood group antigens into saliva and gastric juice have increased risk |
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Term
| zollinger ellison syndrome (gastrinoma): causes, effect, symptoms, treatment |
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Definition
highest H+ levels
tumor, usually in pancreas, secretes lots of gastrin
increased H+ secretion in parietal cells and increased parietal cell mass
overpowers bicarbonate and erodes
steatirrhea because pH deactivates pancreatic lipases
not feedback inhibited by H+
treatment: inhibit H+ secretion (cimetidine, omeptrazole), surgical tumor removal |
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Term
| how can you diagnose a peptic ulcer |
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Definition
urease breath test: drink 13C urea. converted to 13CO2 and NH3 in stomach. 13CO2 is absorbed into the blood and expired into the lungs and measured. Gastric ulcers give lower H than normal because H secreted leaks into damaged mucosa
Endoscopy: Barium meal with contrast x-ray biopsy to show bacterial or malignancy |
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Term
| what medications are used for peptic ulcers |
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Definition
H. pylori cause: proton pump inhibitor like omeprazole (Prilosec)
Non H. pylori cause: proton pump inhibitors
Cimetidine (tagmet), famotidine (Pepcid), ranitidine(zantac), antacid
histamine H2 antagonist like cimetidien, ranitidine, famotidine, nizatitine inhibit parietal cells
prostaglandin E analouge (misprostol) inhibits gastric acid secretion by inhibiting cAMP in parietal cells
surgery if there are lots of complications |
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Term
| decreased intrinsic factor: cause, why its bad |
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Definition
o Caused by decreased RBC, removal of stomach
o The only essential secretion |
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Term
| ileal resection: cause, symptoms |
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Definition
o Removal of ileum
o Recirculation of bile salt is interrupted and much is excreted
o Synthesis of new bile salts is very stimulated but cannot keep up
o Impaired lipid absorption
o Steatorrhea: increased fat in stool |
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Term
| what is bile acid diarrhea, what treats it |
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Definition
o High bile acids in the intestinal lumen stimulates cAMP dependent Cl secretion in colon epithelial cells. Na and water follow Cl into lumen causing secretory diarrhea
o Cholestyramine treats |
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Term
| how does cholestyramine work |
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Definition
Treatment bunds bile acids in the colon so they do not stimulate Cl secretion
Does not prevent steatorrhea
Plasma cholesterol is converted to bile acids lowering plasma cholesterol
• Also used for hypercholesterolemia |
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Term
| what are the diseases of the exocrine pancreas |
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Definition
| cystic fibrosis, acute pancreatitis, chronic pancreatitis, carcinoma of the pancreas |
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Term
| cystic fibrosis: cause, effect, symptoms |
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Definition
Most common lethal genetic disease
Mucosa secretions are thick and block airway and pancreatic duct
Recurrent pulmonary infection, pancreatic insufficiency, high NaCl in sweat, transmembrane regulator (CFTR) defective, pancreatic duct may have cyst, malabsorption, duct dilation
CF gene on chromome 7 mutated |
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Term
| acute pancreatitis causes |
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Definition
Inflammation of the pancreas, almost always associated with acinar cell injury
• Metabolic: alcohol, hyperlipoproteinemia, hyperclacemia, drugs
• Mechanical: gall stones, traumatic periperative injury
• Vascular: shock, atherombolism |
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Term
| acute pancreatitis pathology / issues associated |
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Definition
• Protrolytic destruction of pancreatic substance
• Necrosis of vessels and interstitial hemorrhage
• Fat necrosis by lipolytic enzymes
• Associated acute inflammatory reaction |
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Term
| chronic pancreattis: cause, effects |
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Definition
Protein hyper secretion (acinar cells)
Protein precipitation forming ductal plugs enlarge to form aggregates |
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Term
| carcinoma of the pancreas: cause, definition, diagnosis, prognosis |
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Definition
Malignant epithelial neoplasm of exocrine pancreas
Causes: unknown, frequent in smokers
Usually silent until first symptom, obstructive jaundice
1 year survival |
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Term
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Definition
| a fodm of hirschspring disease that affects people with parkinsonism diabetic neuropathy |
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Term
| constipation: causes, symptoms, treatment |
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Definition
low fiber in sedentary persons
irregulat defecation
irrational use of laxatives supressing natural reflexes
treatment: increase fiber, walking, suppositories |
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Term
| chagas: how is it aquired |
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Definition
cause vby trypanosome cruzi a parasite that causes african sleeping sickness
spread by bite from reduvid bugs |
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Term
| how is the lumen protected |
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Definition
mucous neck glands
gastric epithelial cells secrete bicarbonate trapped in mucous
prostaglandins, mucosal blood flow, growth factors |
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Term
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Definition
| pain after a meal, worken up with epigastric pain, bleeding from ulcers, uper GI bleeding, hematemesis (vomitting blood or clots), melena (dark, tarry stool, shiny, sticky, foul smelling) |
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Term
| gastritis: definition, classifications, symptoms |
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Definition
lining of stomach becomes inflammed or swollen
acute, erosive, chronic, non-erosive
symptoms: loss of appetite, nausea, vomiting, pain in upper abdomen, pernicioous anemia |
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Term
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Definition
alcohol, drugs, (corticosteroids, NSAIDS, ASA)
main cause in antrum: H. pylori leading to loss of parietal cells (achlorhydria), decreased HCl and intrinsic factor |
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Term
| autoimmine / pan gastritis: cause, risks |
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Definition
autoantibodies to parietal cells
vitamin b12 not absorbed in ileum due to lack of intrinsic factor, pernicious anemia |
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Term
| what is a risk of long term treatment with acid supression drugs |
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Definition
| mucosal hypertrophy and further rise in acid production with a higher ulcer recurrance rate |
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Term
| what protects the esophagus from the GI mucosa |
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Definition
clearance mechanisms (UES, LES)
mucosal integrity
LES compliance
gastric emptying |
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