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361 Cards in this Set
- Front
- Back
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List the nerves/hormones receptors of the GI
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Stretch Receptors
Chemoreceptors Osmoreceptors pH Receptors |
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What is are the components of saliva?
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Enzymes
Mucous Bicarb Antibacterial |
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What does the stomach secrete?
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Acid
Pepsin IF <-- MAIN SECRETION Mucous Hormones |
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What does the Pancreas secrete?
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Enzymes (many dif. ones responsible for digestion)
Bicarb (HC03-) |
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What does the Liver/Gallbladder secrete?
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Bile
Bicarb (HC03-) |
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What controls the extrinsic nervous system of the gut?
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Sympathetic and Parasympathetic
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What controls the Intrinsic Nervous system of the gut?
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Enteric AKA Intrinsic Nervous System (BUT modulated by Parasymp. and Symp.)
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What is the Enteric AKA Intrinsic Nervous System of the gut?
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Within gut wall. Completely independent = it functions on its own, but always modulated by Symp. and Parasymp.
Initiates motility patterns, can send out neural signals, can cause hormones to do what they do. |
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List the Phases of Digestion
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Cephalic
Gastric Intestinal |
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What are the functions of saliva?
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Lubricate
Protects Digests |
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What are the functions of the Orad (North) Stomach?
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Accomodates
Digests Delivers to the small intestine |
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What are the functions of the Caudad (South) Stomach?
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Mixes
Grinds Delivers to small intestines |
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Whats the primary site for digestion and absorption?
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Small Intestine
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Where is most water absorbed?
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Small Intestine
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What are the functions of the large intestine?
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Absorb water and electrolytes
Packs everything and gets it ready for evacuation (i.e. the shit) |
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In general, parasymps. ______ GI and symps. ______ GI, however this is opposite for the sphincters.
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parasymps stimulate, symps. inhibit
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Parasymps go to what cells in mucosa?
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MECS
Mechanoreceptors Endocrine Chemoreceptors Secretory Cells |
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Parasymps work via which Receptor/Neurotransmitter? Symps?
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Parasymps = M receptor with Ach
Symps = alpha 1, alpha 2, or Beta 2 with Epi |
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Where do parasymps and symps synapse, respectively?
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Parasymps synapse on organ
Symps go from paravertebral ganglia to synapse on: Celiac Ganglion, Superior Mesenteric ganglion, or Inferior Mesenteric Ganglion (=Prevertebral ganglia) |
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Smooth muscle can be found in what two places in GI?
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esophagus and external anal sphincter
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What modulates the activity of the intrinsic (enteric) nervous system?
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extrinsic nervous system
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Any nerves that are leaving the enteric nervous system are_____
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post-ganglionic (can be parasymp OR symp)
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Post-ganglionic nerves from enteric nervous system synapse on what?
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target cells and other enteric nerves
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List the layers of the GI from internal to external
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lumen - mucosa - muscularis mucosa - submucosa - inner circular - outer longitudinal - serosa
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Between what two layers can the submucosal and myenteric ganglion be located?
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Submucosal Ganglion= between submucosa and inner circular layer
Myenteric Ganglion = between inner circular and outer longitudinal |
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The enteric nervous system is excited by what hormones?
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Ach
Substance P |
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The enteric nervous system is inhibited by what hormones?
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VIP
NO |
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The distal rectum and anal canal are innervated by what?
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sympathetic fibers from hypogastric plexus
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If a vagal nerve stimulates an inhibitory neuron of a muscle, what is the result?
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muscle relaxation
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What are long reflexes?
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Afferent (sensory) to CNS, Efferent (motor) back to gut
ex. - vaso-vagal reflex |
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What are short reflexes?
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Entirely within gut wall, for ex. local or intramural reflexes...i.e. there is no traffic to and from the CNS.
One example would be a signal from a mechanoreceptor traveling down to a secretory cell to make it secrete |
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What are the different GI hormonal controls?
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Cell--> Cell
Autrocrine Paracrine Nervous Endocrine Neuroendocrine |
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What is over-secretion of Gastrin's effect on the stomach?
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the portion affected by Gastrin can atrophy (hyperplasia)
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What is Zollinger-Ellison disease?
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Gastrin over-secretion via a gastrinoma of the pancreas. Gastrin goes to stomach
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What are the symptoms of Zollinger-Ellison disease?
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diarhea, ulcers, steatorrhea (fat in stool)
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What releases Gastrin from G cells?
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GRP
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What nerves release GRP?
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post-enteric nerve - vagus nerve
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What are the two actions of Gastrin once it's released from the G cell?
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stimulate ECL cell or stimulate parietal cell
The ECL cell (which releases histamine) then goes on to stimulate the parietal cell which releases IF and H+ |
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Blocking any one of the 3 components of the Gastrin/ECL cell/Parietal cell does what?
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Decreases the effectiveness of the others.
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What are the actions of CCK after it is released from I cells in duodenum?
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Stimulates gallbladder to pump bile into duodenum (CCK is the most powerful gallbladder stimulator)
Inhibits gastric emptying/inhibits gastric acid Stimulates release of pancreatic digestive enzymes from pancreatic acinar cells (for ex., NZ) |
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What causes the release of CCK?
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Fat and Protein
CCK facilitates the absorption of these |
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CCK has a trophic effect on what organ?
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pancreas
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What is the function of the muscularis mucosa, made of the inner circular and outer longitundinal layer?
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gut motility
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What plexus controls gut motility and movement?
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myenteric (i.e. hourbach's plexus)
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What does the submucosal ganglion (i.e. meisner's plexus) control?
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crypts and villi of gut
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T/F: the enteric nervous system can function as an independent entity, but the extrinsic nervous system modulates much of its output
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TRUE
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T/F: Both afferent and efferent are carried in the vagus
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TRUE
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What are the five major GI hormones?
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Gastrin
CCK (cholecystokinin) Secretin GIP (Gastric Inhibitory Peptide) Motilin |
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Where is Gastrin located in the GI?
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Antrum --> Jejunum
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Where is CCK located in the GI?
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Duodenum --> Ileum
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Where is Secretin located in the GI?
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Duodenum --> Ileum
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Where is GIP located in the GI?
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Duodenum --> Jejunum
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Where is Motilin located in the GI?
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Duodenum --> Jejunum
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What triggers Gastrin?
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Protein and Distention (vagus nerve stimulates release)
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What triggers CCK?
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FAT is the number one trigger; Protein triggers it too
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What triggers Secretin?
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Acid (H+) and FA's
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what triggers GIP?
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Carbs (specifically glucose) and fat
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Wha triggers Motilin?
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Its released in a cyclical pattern every 90 min. during FASTING (Vagus nerve stimulates release)
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What inhibits Motilin?
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a mixed meal of all dif. food groups.
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What inhibits the release of Gastrin?
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Acid (H+)
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Secretin is called "natures antacid" for what reason?
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It inhibits parietal cells, which produce Acid (H+)
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What are Secretin's actions once released?
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Stimulate bicarb (HCO3-) release from liver AND Pancreas which goes to duodenum. (Can also cause release of pepsin)
Inhibit Parietal cells (=no H+) and G cells (= no gastrin) |
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What are Somatostatin's effects once released from D cells all over GI tract?
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Basically inhibits everything
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What are GIP's affects (glucose-dependent insulinotropic peptide) once released?
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Stimulates pancreas to release insulin
Inhibits Pariental cells (=no H+) and G cells (no Gastrin) |
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List three GI neurocrines (=located in nerves, released into blood to affect distant target tissues) covered in lecture
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VIP
GRP Enkephalins; opiates |
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What are the actions of VIP once released?
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stimulates pancreas and intestinal secretions
Inhibits gastric secretions, causes relaxation of sm. m. in GI |
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What causes stimulation of VIP
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Vagus and Distention
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What are the actions of GRP?
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Releases Gastrin from G cells
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What causes stimulation of GRP?
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post-enteric nerve - Vagus nerve
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What are the actions of enkephalins; opiates?
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decrease motility and decrease intestinal secretion
GOOD FOR DIARRHEA |
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What are the actions of neurotensin?
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Inc. blood glucose by stimulating glycogenolysis and glucagon release.
Inhibits Insulin release (makes sense considering the above!) |
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What are the two paracine hormones we've talked about?
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Somatostatin
Histamine |
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What do most constituents of a meal release?
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pancreatic polypeptide
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What is the action of GLP-1?
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potent insulin releaser. Also plays a role in the ileal brake
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Motility is programmed by the _____ nervous system?
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enteric
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The fed (digestive) state in the small intestines is modulated by the ______ nervous system?
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extrinsic nerves/hormones
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The interdigestive state in the small intestines occurs how long after a meal?
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2-3 hrs.
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What are the actions that occur during the interdigestive state?
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Migrating Motor Complex (MMC) - "Housekeeper of the Gut"
Few or No contractions occur |
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What actions occur during the fed (digestive) state?
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propulsion of food bolus and mixing
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Define the MMC, or migrating motor complex
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Takes 90 min
Occurs during fasting Cycles every 90 min. Gets rid of bacteria and food Initiated by motilin Programmed in enteric nervous system |
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What controls intestinal motility?
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Small intestine contractions depend on:
1. slow waves and spike potentials (contractions require spike potentials on top of slow waves) |
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Gastrin, CCK, and Motilin do what to the contractility of the small intestines?
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Increase contractility
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List the small Intestine Reflexes
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Peristaltic
Intestino-Intestinal Power Propulsion Gastro-Ileal Ileal Brake |
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T/F: The Peristaltic reflex is not important in healthy people
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TRUE
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What does the peristaltic reflex depend on?
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enteric
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T/F: the peristaltic reflex can sweep the entire length of the small intestine
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TRUE
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If area of bowel is grossly distended, is contractile activity in the rest of the bowel inhibited?
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YES
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What does the intestino-intestinal reflex depend on?
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extrinsic
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Define Power Propulsion
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Long, Large, contractions in response to noxious stimuli
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Power Propulsion is responsible for what two reactions?
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vomiting in retrograde direction and diarrhea in orthograde direction
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What initiates the gastro-ileal reflex?
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Food in stomach
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What are the mediators of the gastro-ileal reflex?
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Opens ileal-cecal sphincter, causing food to move on down
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What are the mediators of the gastro-ileal reflex?
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CCK, Gastrin, Extrinsic
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Define Ileal Brake
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Inhibition of gastric and pancreatic secretion and motility that occurs when lipids/carbs infused into ileum in amts. sufficient to cause malabsorption
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During the Ileal Brake: The presence of what causes Neurohumoral signals from ileum to signal a delay in transit to the north and decreases in secretions?
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Fat and Calories
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What peptide mediates the Ileal Brake?
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GLP-1 (glucagon-like peptide)
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What keeps the sphincter mechanism at the ileocecal junction closed? What opens it?
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Colonic distention causes tone of sphincter to increase = closed = protects small intestine
Ileal distention = tone of sphincter relaxes = opens |
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What mechanism keeps food from entering back into the small intestine after it enters the large intestine (=colon)?
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Colonic distention = sphincter gets tight. Mediated by enteric nervous system
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What can modulate the pressure at the ileocecal sphincter?
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Vagus, Sympathetic, and Enteric Nervous system
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Define Haustration
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Lumpy areas of the colon. When food is in the colon, the colon will relax and then the huastrations will contract - its this returning haustral contraction that acts on the food = accomplishes most of the movement of food through colon
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Define the gastro-cholic reflex
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Food in stomach causes stretch = inc. motility and mass movements. Stmulus for this is efferent, CCK, gastrin, PNS
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Define the Recto-Sphincter (or recto-anal) reflex
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Motility in rectum or anal canal
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What normally causes the anal canal to be closed?
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contraction of internal anal sphincter
Contents distend rectum, pressure increases, active contraction increases pressure, relaxation of internal anal sphincter occurs, contraction of external anal sphincter, = contents dispelled. |
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How does one poop?
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Contents distend rectum, pressure increases, active contraction increases pressure, relaxation of internal anal sphincter occurs, contraction of external anal sphincter, = contents dispelled.
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Which takes longer to get through the stomach and duodenum; solid meal or liquid meal?
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solid meal
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Define Hirschsprung's disease (AKA Achalasia of the rectum)
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Congentital megacolon (=present at birth)
Colon is Without Ganglion (Aganglionic) No VIP or NO Always involves internal anal sphincter and most of the rectum |
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Most labeled feces is gone from the colon within what time frame?
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24 hrs.
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What is required for continence?
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SPAR (SPAR with your poop)
Sphincter Contraction Puborectalis contraction Anorectal angle (maintenance) Rectal Sensation |
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What is required for defecation?
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PAS (PAS your poop)
Puborectalis relaxation Anorectal Angle Straightening Sphincter Relaxation |
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Where can striated muscle be found in the GI?
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pharynx, upper esophagus and external anal sphincter.
Smooth m. makes up the rest of the GI |
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Define Phasic Muscle contraction vs. Tonic muscle contraction
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Phasic = rapid (seconds), contract/relax in "busy sections of gut = esophagus, antral stomach, small intestine
Tonic = Slow/Sustained (min-hrs), non-busy sections of GI = sphincters, orad stomach |
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All motility patterns for the Gi are programmed where?
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in the enteric nervous system, BUT can be influenced by nerves and hormones
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What is the action of peristalsis?
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Propulsion, which is accomplished by alternating contraction/relaxation of segments
Enteric program = peristalsis |
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The action of mixing is accomplished by what enteric "program"?
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Segmentation
(i.e. dif. segments of intestine either mix or propel food at dif. times) |
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T/F: There is no time when the GI is stationary, or parked.
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FALSE. The GI can be "parked" = no motility
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Define Physiologic Ileus
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Absence of motility = planned quiescence or quietude neurally programmed. Can be pathologic = not normal or physiologic = normal
With a block or pathological condition that blocks nerves, you can have disorganized, nonpropulsive contraction of GI that occurs continuously |
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Define Trituration
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Crushing and grinding of food in the stomach
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What do inhibitory motor neurons along the smooth muscle of the GI do in terms of contraction?
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If inhibitory neurons are Active, the smooth muscle is relaxed
If inhibitory neurons are Inactive, the smooth muscle is contracted |
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Inhibitory neurons must be A. turned off B. turned on For the circular muscle outside sphincters to contract
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TURNED OFF (A)
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Are inhibitory motor neurons to the lower esophageal sphincter normally turned on or off?
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OFF; they must be turned on for the sphincter to relax.
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What are the four phases of swallowing?
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OPEG
Oral Pharyngeal Esophageal Gastric |
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What propels the food bolus into the pharynx from the mouth?
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tongue, using the roof of the hard palate
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What accomplishes propulsion through the upper esophageal sphincter?
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Contraction of middle and lower constrictors of pharynx and relaxation of cricopharyngeal muscle
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What seals off the trachea during swallowing?
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upward glottis movement and downward epiglottis movement
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What propels the food to the stomach once it is in the esophagus?
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A peristaltic contraction
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______ Pressure is found from the esophagus to about halfway down the esophagus
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Subatmospheric
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______ Pressure is found from about half way down the esophagus to the stomach
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Intra-abdominal pressure
Pressure in body of esophagus reflects intrathroacic or intra-abdominal pressures |
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Manometric recordings are important for diagnosing what?
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dysphagia
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What pressures make up the pressure in the stomach?
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Intra-abdominal and pressure made by tonic contraction of fundus of stomach
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Between swallows, both the upper and lower sphincters of the esophagus are closed because of what reason?
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Pressure Greater than atmospheric pressure keeps them closed
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To allow passage of bolus into stomach, the lower sphincter and orad stomach A. Contract B. Relax
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They Relax, before the peristaltic contraction reaches them
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The Upper Esophageal Sphincter is innervated by what?
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Excitatory Somatic Nerves (travel in vagus)
Neurotransmitters = Ach and Substance P |
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The Lower Esophageal Sphincter is innervated by what?
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Parallel sets of parasympathetic excitatory and inhibitory pathways
Neurotransmitters (Excitatory nerves) = Ach and Substance P Neurotransmitters (inhibitory nerves) = VIP and NO |
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What keeps the Lower esophageal sphincter closed?
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Ach and Gastrin (gastrin has a contractile effect on LES)
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What occurs during a swallow in terms of the larynx and nerve impulses?
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Larynx displaced
Suppression of nerve impulses |
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Primary peristalsis follows what phase?
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The oral pharyngeal phase
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What opens the LES?
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Enteric inhibitory nerves, i.e.
Opens as a function of: Primary peristalisis, Secondary peristalsis, CCK, Belching Specifically: VIP and NO. Activated by vagus and distention. Vagus stimulates an inhibiroty neuron = net effect = relaxation |
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Motor activity in esophagus is accomplished by what nerve?
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vagus
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Muscles of the pharynx and striated areas of esophagus are activated by what?
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Nucleus ambiguous
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Areas of smooth muscle of the esophagus are activated by what?
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dorsal motor nucleus
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T/F: both central and peripheral nerves control swallowing
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TRUE
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A disease of the myoneural junction, disease of striated muscle OR CVA (vascular accident) causes what?
|
dysfunction in pharynx and upper esophagus
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Dysfunction of the enteric nerves and/or the smooth muscle causes what?
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Dysfunction with lower peristalsis or with tone or lower esophageal sphincter
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Define Achalasia and describe how to diagnose
|
Defective enteric inhibitory neurons
= loss of intramural neurons = LES has its myogenic tone unopposed = LES can't open = Can't pass food To Diagnose: give pt. barium. if we see "bird's beak" on x-ray = Achalasia |
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Is the myenteric or submucosal nervous system more prominent in the stomach?
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myenteric
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Receptive relaxation after low amplitude tone in the stomach is an example of what type of reflex?
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vagovasal
Efferents activate enteric inhibitory neurons In order to help the stomach relax |
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A truncal vagotomy does what to the size of a meal that a person can eat?
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decreases it (?)
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What triggers the adaptive reflex of the stomach?
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Distention of the stomach (stretch receptors)
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What triggers feedback relaxation in stomach?
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receptors in small intestine
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Motility patterns in the stomach and intestine depend on what?
|
Digestive phase
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Describe Gastric motility following a meal (Fed or Digestive state)
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Orad Stomach = receptive relaxation, gastric accomodation
Caudad Stomach = contractions are 3-5 cycles per minute |
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Define Retropulsion in terms of gastric motility in the fed state
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When only a small portion of food bolus goes through pyloric sphincter and the rest gets shoved back toward orad stomach
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During the fed or fasted state, what occurs in the stomach?
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MMC, migrating motor complex. = periodic bursts of high-amplitude contractions that sweep stomach clean
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Define the interstitial cells of Cajal
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Specialized smooth muscle cells called "the pacemakers of the gut"
Located mid-stomach through colon They set the cycle of contractions (for stomach:3-5 min) |
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What are slow waves?
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ALWAYS PRESENT whether or not there are contractions
FREQUENCY STABLE in each region of GI (for ex. stomach = 3-5/min) Spike potentials on top of slow waves initiate contractions Rhythmic oscillations of membrane potential (depol/repol) AKA BER (basic electrical rhythm) May cause contraction if they are large enough |
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T/F: Slow waves are action potentials
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FALSE. Slow waves may open as a result of Calcium-Activated K+ Channels
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T/F: Slow waves are minimally, if at all, affected by nerves or hormones
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TRUE (their frequency is NOT changed by these)
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What can increase slow wave frequency?
|
Temperature and Metabolic Activity
Nerves and hormones can affect the height of the plateau whether or not spike potentials occur |
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What increases contraction, overall, of the Stomach?
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Vagus, Ach, Gastrin, CCK
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If fat slows gastric emptying, what hormone is involved?
|
CCK
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What contracts to squeeze salivary secretion through the ductal system?
|
Myoepithelial Cells
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What happens to Na+ and Cl- in the striated duct?
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Reabsorbed = Moved OUT of saliva
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What happens to K+ and HCO3- in the striated duct?
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Secreted = ion put INTO saliva
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What are examples of things that increase salivary secretions?
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taste, smell, pressure, nausea, conditioned reflexes
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What are examples of things that decrease salivary secretions?
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fatigue, sleep, fear, dehydration
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What are GI Hormone's effect on salivary secretions?
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no effect
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What is aldosterone's effect on salivary secretions?
|
Inc. resorption of sodium, K+ secretion, = Dec. Na+ content in saliva
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What happens to the saliva of someone with Addison's disease?
|
Addison's = Inc. in salivary Na+
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What is ADH's effect on saliva?
|
Sodium Reabsorption
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Hypoaldosteronism
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Inc. Na Absorption
Inc. K+ secretion =More Na+, Less K+ in saliva |
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How does the parasympathetic system increase salivary gland secretion?
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Via Ach through M3 receptors, then the IP3 pathway, increasing Ca2+ in salivary gland, Increasing secretion
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How does the sympathetic system increase salivary gland secretion
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Sympathetic nerves travel to Superior Cervical Ganglion, Use NE via a Beta receptor to activate cAMP pathway, increasing Ca2+ in salivary gland, increasing secretion
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T/F: Both parasympathetic and sympathetic are Stimulatory in the salivary glands
|
TRUE
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T/F: Both Cholinergic (Ach) and Adrenergic (NE) can act on salivary acinar cells to exocytose
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TRUE
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The two hormones that affect the ionic content of saliva are what?
|
Al and ADH
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What are the two ways the parasympathetic nervous system can increase blood flow to the salivary gland?
|
1. Stimulate VIP = inc. blood flow
2. Act via M3 receptor --> Kallikrien --> converts Kininogen to Lysyl-bradykin --> vasodilation and increased capillary permeability |
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How does the sympathetic nervous system increase blood flow to the salivary gland?
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Biphasic Effect
1. Acts on Alpha 1's to vasocontrict 2. This increases vasoDILATOR metabolites 3. Causing Vasodilation |
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Mucous cells in the Fundus of the stomach secrete what?
|
Mucous/HCO3-
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Oxyntic (parietal) cells in the stomach secrete what?
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HCL, IF
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Peptic (Chief) cells in the stomach secrete what?
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Pepsinogen and gastric lipase
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ECL cells in the stomach secrete what?
|
histamine
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Mucous cells in the body of the stomach secrete what?
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Mucous, HCO3-, pepsinogen
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G cells in the stomach secrete what?
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Gastrin
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D cells in the stomach secrete what?
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Somatostatin
|
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|
The superficial epithelial cells of the stomach secrete what?
|
HCO3-
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|
What are the mechanisms of HCL production in the parietal cell?
|
"Alkaline Tide"
H/K ATPase (Apical) AKA "proton pump" Omeprazole blocks this. Cl/HCO3- Exchanger (Basolateral) |
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|
What are the DIRECT mechanisms for increasing H+ secretion into the lumen?
|
Ach, Gastrin, Histamine stimulate parietal cell = H+ released into lumen
Pharmacologically, you can block this and block H+ secretion into lumen |
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|
What are the INDIRECT pathways for increasing H+ secretion into the lumen?
|
Ach and Gastrin Stimulate ECL cell = secretion of histamine = acts on parietal cell to increase H+ secretion
Pharmacologically, you can block this and block H+ secretion into lumen |
|
|
How can you treat someone with too much acid secretion into their lumen?
|
Vagotomy
H2 Histamine Blockers (ex. = tagamet, zantac) PPIs = Proton Pump Inhibitors |
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|
The cephalic phase accounts for what percent of acid secretion?
|
30%
Stimulated by vagus via taste, smell, chewing, swallowing etc. |
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|
What are the four main physiological events in the cephalic phase?
|
1. Vagus (Ach) stimulates parietal cells
2. Vagus (Ach) stimulates ECL cell (histamine from ECL cell goes to parietal cell) 3. Vagus (GRP) stimulates G Cell (gastrin goes to ECL cell and parietal cell) 4. Vagus (Ach) INHIBITS D Cell = Somatostatin inhibited |
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Gastrin is stimulated on the G cells basolateral side by what?
|
vagus nerve
|
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Gastrin is stimulated by what on the cell's luminal side
|
digested protein, AAs
|
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|
What does the Vagus stimulate in the Corpus of the stomach?
|
Parietal cells (via Ach)
ECL (inc. histamine) D Cells (dec. somatostatin = inc. gastric acid secretion) |
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|
What does the vagus do in the Antrum of the stomach?
|
G cells (via GRP = inc. gastrin release = gastric acid secretion via parietal cells and ECL cells)
D cells (via Ach = dec. somatostatin) |
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|
Luminal H+ secretion in the antrum of the stomach does what?
|
Stimulates D cells to release somatostatin = inhibits gastrin release = dec. H+ secretion
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|
Distention of the stomach by food causes what?
|
Local ENS relfex and Vaovasal reflex = Ach released and GRP released = Gastrin released = stimulates parietal cell (H+ released) and ECL cell (histamine released)
|
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|
What is a direct stimulator of the G Cells in the antrum of he stomach?
|
Digested Protein
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|
What percent of acid secretion does the Gastric phase account for?
|
50-60%
|
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|
Protein digestion during the intestinal phase stimulates what two things?
|
Intestinal G cells (=gastrin released = parietal cell releases H+)
Intestinal Endocrine Cell (= parietal cell releases H+) |
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What, besides Gastrin and Entero-oxyntin (i.e. intestinal endocrine cell) stimulates the parietal cell in the intestinal phase?
|
Absorbed AA's
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The intestinal phase accounts for what percent of gastric secretion?
|
5-10%
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|
What are the two "major player" hormones responsible for turning off acid secretion?
|
Somatostatin (inhibits G cell and parietal cell) and Secretin (inhibits G cell and parietal cell) in the duodenum
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|
Fatty Acids in the duodenum and Jejunum stimulate what?
|
GIP (which inhibits G cells and parietal cells)
CCK (inhibits parietal cell) FA's also work through a neural reflex to inhibit parietal cells |
|
|
What does PGE2 do?
|
Inhibit Parietal cells
|
|
|
In the stomach, what signals stimulate acid secretion?
|
Distention
G cells (gastrin = works on parietal cells to secrete H+) |
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As the gastric phase continues, what two hormones/paracrines are stimulated that will help decrease acid?
|
D cells release somatostatin = inhibits gastrin release
|
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What does pepsin do?
|
Digests proteins. Formed from pepsinogen
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What controls the release of pepsinogen from chief cells?
|
vagus (via Ach)
ALSO: Vagus stimulates parietal cells = H+ released = works to 1. INC. secretion of pepsinogen from chief cells and 2. INC. Conversion of pepsinogen to pepsin |
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|
Define PUD, Peptic Ulcer Disease
|
A break in the normally protective gastric mucosal layer (NOTE- INCLUDES BOTH Gastric and Duodenal ulcers)
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|
What are the two ways the mucus layer secreted by the surface cells in the stomach work?
|
Diffusion barrier for H+ and pepsins
Traps HCO3- so it can titrate H+ |
|
|
What two things stimulate the mucous cells to release mucous?
|
Vagus
Chemical Irritation (like smoking?) |
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|
What are the functions of prostaglandins?
|
1. Regulate release of mucosal bicarb and mucous
2. Inhibit Parietal cell 3. Help maintain mucosal blood flow and epithelial restitution 4. Regulate epithelial regeneration |
|
|
What do NSAID drugs block?
|
Cox1 AND Cox2, even though we only want Cox 2
|
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|
What happens if H+ gets through the protective mucosal barrier?
|
Mast cell damage
=Histamine released =Vasodilation =Inc. blood flow (barrier maintained) HOWEVER, If damage is severe: Inflammatory cells released = platelet-activating factors, leukotrienes, endothelins, thromboxanes, oxidants released =Reduced blood flow =Tissue Ischemia/ Damage |
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|
What is H.Pylori?
|
A gram neg. bacteria that colonizes antrum stomach mucosa
Causes ulcers |
|
|
Why is H. Pylori so harmful?
|
Has Urease = converts Urea --> Ammonia (so it can tolerate the acidic environment of the stomach)
INHIBITS D CELLS = Somatostatin NOT secreted = gastrin levels increase = H+ increases = ULCERS |
|
|
What is the only essential secretion of the stomach?
|
IF (Intrinsic Factor) which is needed to absorb B12 (AKA Cobalamin)
|
|
|
What is the path of B12 Absorption?
|
B12+Food enter
Acid + pepsin release B12 from food B12 binds Haptocorrin (=glycoprotein) B12-Haptocorrin goes to Duodenum Pancreatic Protease in Duodenum splits B12-Haptocorrin IF + B12 link up = Imp. because Ileum has receptors for B12-IF complex =B12 Absorbed |
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|
What causes a B12 deficiency?
|
"PIB C"
Pernicious Anemia Ileal Resection Bacterial Overgrowth Chronic Pancreatitis (only in RARE cases) |
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T/F: The flux of water is generally passive in the GI
|
TRUE
It follows Startling forces = osmotic and hydrostatic pressure |
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T/F: Fluid flux in GI is dependent on the solute content of the GI (food and electryloyes) lumen
|
TRUE
Also dependent on osmotic pressures in blood |
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T/F: In general, GI luminal fluid is isotonic to plasma
|
TRUE
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|
In healthy individuals, there is a net absorption of what three things, while there is a net secretion of what two things?
|
Absorption of Na+, Cl- and Water
Secretion of K+ and CHO3- |
|
|
What are the mechanisms of Na+ Absorption?
|
Co-transport with either Sugars, AA's or Cl-
Na+ Channel Counter-transport with H+ Solvent Drag (i.e. Na+ will go where there's more water) |
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|
Which of the Na+ Absoprtion mechanisms dominate?
|
Counter-transport with H+ and co-transport with sugars and AAs
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T/F: Na+ co-transport with sugars and AAs is less in the ileum because most absorption has already occurred.
|
TRUE
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T/F: Cl-/HCO3- exhchange occurs in distal ileum and increases in the colon
|
TRUE
|
|
|
How is K+ Absorbed?
|
Passive Diffusion in small intestine via paracellular spaces
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There is a net ______ of K+ in Small Intestine, While there is a net _____ of K+ in Colon
|
net Absoprtion of K+ in small intestine
net secretion of K+ in colon |
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T/F: The basolateral membranes of the colon are permeable to K+
|
TRUE
(untrue for small intestines) |
|
|
What are the actions of Aldosterone?
|
Inc. Na+ absorption, Inc. K+ secretion
works via inc. activity of basolateral Na+/K+ pump |
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|
K+ secretion is dependent on what?
|
flow rate
Inc. flow rate (for ex. in diarrhea) = Inc. K+ secretion |
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|
What are three factors that inc. K+ secretion?
|
cAMP (ex. = cholera, E. Coli)
cGMP Ca2+ |
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|
Because of increased K+ secretion with high flows like with diarrhea, what do we need to be concerned with in such patients?
|
Hypokalemic metabolic acidosis
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|
|
What are things that could lead to an osmotic diarrhea?
|
Anything that leaves food particles in the digestive tract, for ex. Brush border enzyme deficiency (=inc. carbs in digestive tract)
Celiac Sprue Pancreatic Insufficiency Bacterial Infections (bacteria make sugar = draws water in) |
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|
What are three things that can open the Cl- channels on the apical membrane?
|
cAMP, cGMP, Ca2+
Water will follow this inc. NaCl secretion into lumen = loss of water SO, Oral rehydration thereapy |
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|
Define oral rehydration therapy
|
Increasing water absorption in small intestine by using co-transport of Na+ with sugars/AA's
Inc. conc. of sugars/AA's in lumen = Absorprtion Increases |
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|
What are the Endogenous Lipids?
|
CPD
Cholesterol Phospholipids Desquamated Intestinal Villus Epithelial Cells |
|
|
What are the Exogenous Lipids?
|
TCP
Triglycerides Cholesterol Phospholipids |
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|
Define emulsification
|
suspension of fat droplet held apart by lecitin, bile salts, fatty acids, or dietary protein (=a major emulsifying agent in stomach)
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|
What is the purpose of emsulsifying agents?
|
Inc. surface area of lipids = makes its easier for enzymes to attack
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T/F: gastric lipase is not important in most people
|
TRUE
Important in: newborns, patients with pancreatic lipase deficiency, Zollinger-Ellison (=Inc. gastrin) |
|
|
How is HCO3- concentration increased in the lumen?
|
HCO3- co-transports with Cl-.
Inc. Cl- in Lumen = More Cl- available to co-transport with HC)3- = more HCO3- secreted |
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|
What are some of the dominant house-keeping functions of the colon?
|
Absorption ob NaCl and water, and some absorption and secretion of KCL
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|
|
How does secretion of NaCl and KCL differ in secretory diarrheas vs the normal state?
|
Secretion of NaCl and KCL can exceed absorption in secretory diarrheas
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T/F: The colon is incapable of absorbing short chain fatty acids.
|
FALSE. The colon CAN absorb short chain FAs.
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|
|
T/F: The surface epithelium of the crypts can absorb, but not secrete.
|
FALSE. Surface epithelium at crypts can absorb and secrete.
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|
|
What cells secrete mucus in the gut?
|
goblet and crypt columnar epi cells
|
|
|
Aldosterone has what effect on K+?
|
Inc Al = Inc. K+ secretion (and Na+ absoprtion)
|
|
|
What things Inc. K+ Secretion?
|
Aldosterone, cAMP (VIP and Cholera Increases cAMP.), cGMP, Ca2+ (serotonin increases Ca2+)
Inc. K+ secretion = on apical side = with diarrhea we see Hypokalemia |
|
|
What accounts for the high HCO3- content and alkaline pH of stool water?
|
Exchange of Cl- for HCO3- in lumen = stool water basic (alkaline)
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|
|
What is the major source of water and electrolytes in diarretic stool?
|
small intestines
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|
|
How does an Epsom salt laxatine work?
|
Lumen is Hypertonic = water goes from blood to lumen and softens stool
|
|
|
What are some conditions that could lead to osmotic diarrhea?
|
Brush border enzyme deficiency (=less carbs absorbed = more carbs in lumen)
Celiac sprue Pancreatic Insufficiency Bacterial Infections (bacteria make sugar = lumen hypertonic = draws water in) |
|
|
Define Celiac Sprue
|
allergy to gluten, where there is an allergic reaction when gluten is eaten. Causes decreased absorption
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|
T/F: cAMP, cGMP and Ca2+ open the Cl- channels on the apical membrane
|
Can be increased in normal physiological functioning = these are normal secretogogues
|
|
|
What are some examples of abnormal secretogogues and what do they do?
|
Bacterial enterotoxins work by increasing Ach (Inc. Ca2+), Secretin and VIP (BOTH via Inc. cAMP) messengers
Examples of bacterial enterotoxins = cholera (Inc. cAMP) and E-Choli (Inc. cAMP) |
|
|
What type of diarrhea do enterotoxins form?
|
secretory diarrhea
increased volume of the diarrhea bc of more water entering lumen (also, absorptive capacity of colon overwhelmed) |
|
|
What organisms cause secretory and inflammatory diarrhea?
|
E.Coli, Shigella, Salmonella, Vibrio (note, only first part of bacterial name given here)
|
|
|
How do V. Cholera and Cholera work?
|
Produce another toxin called zonula occludens (ZOT) that increase tight junction permeability and stimulate Ca2+ dependent secretion
Cholera affects both large and small intestine Increases intracellular cAMP in crypt and villus epi cells = both compartments contribute to the secretory activity |
|
|
What increases Ca2+ absorption?
|
Vitamin D3 (via interacting with nuclear receptors to affect CaBP synthesis in brush border)
|
|
|
How does Ca2+ leave the cell?
|
CaBP stimulates Ca2+ ATPase
Binding proteins in golgi, ER, and mito prevent a rise in intracellular Ca2+ during absoprtive process |
|
|
Where do enterocytes absorb iron?
|
Duodenum
|
|
|
Iron must be in what form to be absorbed?
|
Ferrous (Fe2+)
|
|
|
What reduces Fe3+ to Fe2+
|
ferric reductase on enterocyte brush border
|
|
|
What transports iron across enterocyte membrane?
|
DMT-1 (divalent metal transporter)
|
|
|
What are the processes of Lipid Assimilation?
|
SEEST
Secretion of Bile and Lipases Emulsification Enzymatic Hydrolysis (of ester linakges) Solubilization (of lipolytic products within bile salt micelles) Transportation (into and out of enterocyte) |
|
|
What is an ex. of a food lipase that comes packaged with the food we eat?
|
Carboxyester Lipase (= a food lipase)
|
|
|
Out of the following, which are the most important in fat assimilation? Lingual lipase, food lipases, gastric lipase, emulsification, bile, pancreatic lipases?
|
Bile and pancreatic lipase (work together)
In some cases, bile can inhibit pancreatic lipase (over-come by co-lipase) In some cases, bile salts are required for lipase to work |
|
|
Bile salts stimulate what?
|
milk lipase activity (good for newborns)
|
|
|
What do pancreatic acinar cells release?
|
H2O and enzymes
|
|
|
Pancreatic acinar cells are stimulated by what?
|
Ach and CCK
|
|
|
Pancreatic centroacinar and ductal cells release what?
|
HCO3- and H20
|
|
|
Centroacinar and ductal cells are stimulated by what?
|
Secretin, an effect that is potentiated by Ach and CCK
|
|
|
Out of Triglycerides, Phospholipids and Cholesterol Ester, which need/work better with bile salts to function as Lipases?
|
Phospholipase (needs bile salts) and Cholesterol Ester (works better with bile salts)
|
|
|
What are the steps involved in Fatty Acid Transport by Micelles?
|
SER+RER --> Golgi --> Basolateral Membrane --> Interenedothelial channels of Lymphatic Capillaries --> Lymph --> Enterocyte --> Blood
1. LONG CHAIN FAs converted to TGs, Phospholipds and Esters (=Exogenous Lipids) = Fat Droplet formed in SER 2. AT SAME TIME Apoprotein Synthesized in RER, transferred to SER, associate with lipid droplet 3. Chylomicorns/VLDLs arrive at cis face of Golgi = apoproteins glycosylated 4. Vessicle with Chylomicron or VLDL bud off from Golgi, move to basolateral membrane in transport vessicle 5. Transport Vessicle fuses with basolateral membrane, releasing chylomicrons and VLDLs 6. Chylomicron/VLDL pass through interendothelial channel of lymphatic capillary, enter lymph 7. Glycerol, short/med. chain FAs pass through enterocyte and enter blood capillary |
|
|
What is the difference between endogenous and exogenous lipids
|
Endogenous = Originate IN Liver
|
|
|
What are the potential abnormalities that can occur in lipid assimilation?
|
BELEAP
Bile Salt Micelles (Prob. w/ synthesis, obstruction = can't get to sm. intestine, bacterial over-growth = can't be reabsorbed) Emulsification (Fat gastric emptying = emuslification doesn't work properly) Lymphatic Transport (Ex. = Whipple's Disease) Enterocyte (within it..for ex. Abetalipoproteinemia = Not normal Apoprotein B = actually a efect in MTP which brings fat droplets together w/ Apoprotein to form chylomicron) Absorptive Surface Inadequate Pancreatic Lipase (prob. with quality OR quantity...Gastrinoma in ZE = Inc. Gastrin = Inc. H+ = Quality issue....Obstruction = quantity issue....CF=quality AND quantity issue...Chronic Pancreatitis etc) |
|
|
What pancreatic cells secrete the digestive enzymes?
|
Acinar cells
|
|
|
What do ductal and centro-acinar cells secrete?
|
Watery juice with Na+ and HCO3- (HCO3- neutralizes acid from stomach so pancreatic enzymes don't become denatured)
|
|
|
What are the general classes of enzymes?
|
ALP-N
Amylase Lipase Protease Nuclease |
|
|
List the steps in the secretory pathway of pancreatic enzymes
|
Rough ER
Golgi Condensing Vacuoles (maturation) Zymogen Granules (wait for secretory stimulus, not necessary in glands that have a high secretion rate) |
|
|
Whats the mechanism of HCO3- secretion in pancreatic ductal cells?
|
1. Na+/Bicarb co-transport on Basolateral
2. Cl- Channel (=CFTR Channel) on Apical gets Cl- into lumen for... 3. HCO3- and Cl- Counter-Transport on Apical = gets HCO3- into lumen to be secreted |
|
|
How can you increase HCO3- secretion in Pancreatic Ductal cells? What is the controller of this channel?
|
Inc. Cl- into lumen by stimulating CFTR channel = the Negative Lumen attracts Sodium Bicarb into it from ductal cells
Secretin controls CFTR Channel |
|
|
What potentiates Cl- Channel (CFTR Channel?
|
Ach
|
|
|
Whats the difference between the parietal cell and the Pancreatic ductal cell in terms of Bicarb and H+?
|
Parietal Cell = HCO3- to Blood, H+ to Lumen (= ALKALINE Tide)
Pancreatic Ductal Cell = opposite, Bicarb to Lumen, H+ to blood (=ACID Tide) |
|
|
Over 90% of HCO3- in pancreatic juice is derived from where?
|
Plasma
|
|
|
The RATE of HCO3- Secretion depends on what?
|
Availability of Luminal Cl-
|
|
|
T/F: Substance P inhibits HCO3- secretion
|
TRUE
|
|
|
Describe the pathophysiology behind CF
|
CF = Dec. in Secretion of HCO3- and water
=Thickened Secretions =Obstructed Duct Lumen = Ducts fill with fibrotic tissue =Ultimately tissue destruction |
|
|
Pancreatic Secretion is ______ rich and the osmolality is like that of ______
|
Pancreatic secretion is bicarbonate rich and the osmolality is like that of plasma
|
|
|
What are the three controllers of Pancreatic Secretion?
|
Vagovagal reflex
Secretin CCK |
|
|
What is the Symapthetic Nervous system's action on pancreatic secretion?
|
none or inhibitory
|
|
|
What are two things happen during Cephalic phase?
|
1. Ach released from Pancreatic Acinar cells = H2O and Enzymes released
2. HCO3- released from ductal cells |
|
|
What is one thing that occurs during Gastric Phase?
|
HCO3- released from pancreatic ductal cells
|
|
|
What are the roles of Vagus, Secretin and CCK in Intestinal Phase?
|
Vagus = Prootein + Lipid Breakdown Products stimulate it --> Vagus stimulates Ach at Acinar cells = H20 and Enzymes released
Secretin = H+ Stimulates S Cells in Duodenum to secrete Secretin = Pancreatic ductal cells release HCO3- Protein and Lipid Breakdown products stimulate I cells = secrete CCK = work on Acinar Cell receptors to stimulate enzyme secretion |
|
|
How does CCK Work in the Pancreas that is different than in the GI?
|
It works *Like* a neurotransmitter would, eliciting a vago-vagal reflex
|
|
|
What are the ways to turn off Pancreatic Secretions?
|
Time (secretions decrease after several hrs.)
Pancreatic Polypeptide Peptide YY (stim. by fat in distal sm. intestine...decreases blood flow to pancreas) Somatostatin Glucagon (from pancreatic Alpha cells) |
|
|
If you don't have HCO3- secretion, what processes are affected?
|
Digestion/Absorption of Food
Can't Neutralize Acid |
|
|
If you don't have Pancreatic enzymes, what processes are affected?
|
Can't digest things. you can lose 80-90% of pancreas and still absorb food. Liapses will be MOST affected = we'll see fat in stool FIRST b/c lipases affected first
|
|
|
The absence of apical Cl- channels in ductal cells means what in terms of processes?
|
Decreased Bicarb secretion
Denatured Enzymes |
|
|
Define Acute Pancreatitis (Autodigestion)
|
Inflammation and auto-digestion of pancreas. Pancreas starts digesting itself because proteolytic enzymes prematurely activated = eat pancreas
|
|
|
What causes acute pancreatitis?
|
Alcohol, toxins, trauma, gallstones, viral
|
|
|
What are the functions of the liver?
|
Bile Production
Carb/Protein/Lipid Metabolism Synthesis of Non-essential AAs and Plasma Proteins (albumin, globulins, fibrinogens, lipoproteins) Degrades drugs/toxins Bilirubin Excretion Iron, B12, A, D Storage |
|
|
What are the contents of bile?
|
PIC - BBB
Phospholipids Inorganics (=ions) Cholesterol Bile Salts Bicarb and Water Bile Pigments (bilirubin) |
|
|
By what portion of the GI are almost all bile salts reabsorbed via portal system back to liver?
|
Terminal Ileum (=conservation of bile acids)
|
|
|
What are the steps in the formation of bile?
|
Cholesterol (in Liver)
Primary Bile Acids (=Cholic and Chenodeoxycholic) (In Intestinal Bacteria) Secondary Bile Acids (=Deoxycholic and Lithocholic Acid) |
|
|
T/F: Primary and secondary bile acids can be conjugated with taurine or glycine to make them more soluble at intestinal pH
|
TRUE
|
|
|
How is most cholesterol eliminated in the body?
|
Bile Salt Formation = uses cholesterol
|
|
|
Secondary bile acids are formed where?
|
intestine, which dehydroxylates them (Primary's formed in liver)
|
|
|
Define conjugated in terms of bile acids
|
conjugated = paired with taurine or glycine to be more soluble
|
|
|
Bile salts arrange themselves as Micelles in what way to surround long chain FAs?
|
Hydrophilic head OUT
Hydrophobic Tails IN = they carry fat across water layer at epi cell to be absorbed |
|
|
Define critical micellar concentration
|
Conc. at which they agragate into micelles
|
|
|
Which have a LOWER crotical micellar concentration; conjugated or unconjugated bole acids?
|
Conjugated
|
|
|
T/F: The conc. of bile salts in Lumen usually has to reach a certain point before micelle's agragate
|
FALSE. Micelle conc. is usually well above critical micellar conc.
|
|
|
What is a simple micelle vs. a mixed micelle?
|
Simple = no fat inside
Mixed = fat inside |
|
|
T/F: Bile acids are continuously secreted by liver
|
TRUE
|
|
|
T/F: Deconjugated and Dehydroxylated bile acids can be passively absorbed all along intestine
|
TRUE
|
|
|
Which bile acids are absorbed via active transport at terminal ileum?
|
More hydrophilic (=mostly conjugated)
|
|
|
What are the two mecahnisms of bile reabsorption and where are thy located?
|
passive (in jejunum-ileum = conjugated taken up) and active (via portal blood in ileum = where conjugated AND UNconjugated taken up)
|
|
|
If you have bacteria in jejunum-ileum area, what happens to fat/bile reabsorption?
|
OVERALL: Decreases Fat Absorption
Inc. Bacteria in Jejunum-Iluem =Bacteria Dehydroxylate forming secondary bile acids = makes them more LIPID soluble = More subject to UPTAKE in jejunum/ileum = Fats don't travel down GI and get digested/absorbed by body =Poor Assimilation of fats |
|
|
The rate of synthesis of new bile acids is inversely proportional to what?
|
The RETURN of bile acids by PORTAL (not Passive) Circulation
|
|
|
The rate of secretion of of bile acids is proportional to what?
|
Rate of secretion is directly related to RETURN of bile acids by PORTAL (not passive) circulation
Inc. Return = Inc. Secretion (positive feedback) |
|
|
What percent of bile acids are returned to the liver via PORTAL circulation?
|
90%
|
|
|
What is the effect of ileal resection on bile acid reabsoprtion?
|
Ileum = where a lot of bile acids reabsorbed
Ileal resection = removal of ileum = bile acids NOT reabsorbed = bile acids dumped into colon = lost. |
|
|
What takes place in the ducts connecting the liver to the gallbladder etc? What hormone is important in this process?
|
Secretion and Absorption of electorlytes, Secretion dominates. Done by Secretin Hormone (VIP and Glucagons also stimulate. Somatostatin Inhibits)
HCO3- secreted... Na+, Cl- and H2O cna be absorbed OR secreted |
|
|
During the Interdigestive period (=between meals) what is happening to bile?
|
sent to gallbladder to be concentrated
Motility pattern during interdigestive period = MMC |
|
|
During the Digestive period, what is happening to bile? What hormone is important here?
|
Secreted into ducts, through sphincter, and into Duodenum
CCK important |
|
|
Parasymps do what to bile ?
|
Inc. Bile flow (= gallbladder contraction)
= Opening of sphincter |
|
|
How does the gallbladder concentrate bile?
|
Increasing HCO3- conc. in bile.
Does this via: Twin exchanger (Na+/H+ exchanger) |
|
|
What is bilirubin?
|
A breakdown product of hemoglobin
|
|
|
What does the liver do to bilirubin?
|
Uptakes it and Conjugates it so it can be excreted (Conjugated = Direct bilirubin)
|
|
|
Define Jaundice, and what it means clinically
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Jaundice = Bilirubin Buildup
Means there is a problem with pathway of bilirubin excretion = hemolytic disease (HB) or Liver disease |
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Increased Uncojugated (=Indirect) Bili can occur bc?
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over-production, for ex. Inc. hemolysis, Impaired uptake into liver, Impaired Conjugation
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Increased Conjugated (=Direct) bilirubin can occur bc?
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Decreased excretion, for ex. Bile duct obstruction, gallstones, tumors, scarring, inflammation
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Glucoamylase Turns _____ into _____
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maltose and maltotriose into glucose
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Lactase turn ___ into _____
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lactose into glucose, galactose
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Sucrase-isomaltase turns ____ into _____
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sucrose, maltose, maltotriose, alpha 1-6 limit dextrins into glucose and fructose
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Whats the rate limiting step for carb absorption?
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uptake, (NOT the digestion)
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Products of amylase digestion?
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Maltose, maltotriose, alpha-limit dextrans
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monosaccharide products that are absorbed?
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glucose, galactose, fructose
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Glucose, galactose transported via?
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SGLT (apical) with Na+ THEN GLUT 2 (basolateral)
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Fructose transported via?
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GLUT 5 (apical) THEN GLUT 2 (basolateral)
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If we can't digest stuff we get what?
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osmotic diarrhea
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protein digestion begins in stomach with?
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pepsin then pancreatic peptidases in duodenum
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pepsin (from pepsinogen) requires what pH?
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Acidic
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Pepsin formation?
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Vagus stimualtes Chief cells to secrete pepsinogen --> pepsin
AND Vagus works of Parietal cells to secrete H+ = stimulates Cheif cells and conversion of pepsinogen to pepsin |
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Define Endopeptidase
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break peptide bonds of Nonterminal AAs
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Define Exopeptidase
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Break peptide bond of Terminal AAs
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Examples of Endopeptidases? Exopeptidases
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Exopeptidases: All begin with letters OTHER THAN "Ca":
Trypsin, Chymotrypsin, Elastase Edopeptidases? Carboxypeptidase A Carboxypeptidase B |
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What does Trypsin do?
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Activates precursors = they become active proteases
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Pancreatic Proteases Are:
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Activated by Trypsin
Secreted as inactive precursors Activated after trypsinogen |
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Trysinogen is activated by?
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Enterokinase (= bile salts cause this to be released from brush border)
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Premature activation of pepsinogen in pancreas?
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cascade of other proteases and pancreas autodigestion
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Protein absorption accomplished by what transporter?
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PepT1
H+/Oligopeptide co-transporter = co-transports larger peptides with H+ |
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Large peptides turned into what via peptidases to then enter cell?
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Di- and Tri- Ppetides and Free AAs
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T/F: Dipeptides, Tripeptides and AAs can all cross cell membrane
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TRUE (Di and Tri peptides in small amount only, though)
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You can feed a pt. what types of peptides to ensure they get into blood?
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Di and Tri peptides = go into blood faster, more efficiently = better absoprtion
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CF leads to poor protein assimilation how?
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CF = inc. mucus thickness = dec. ability to absorb shit. BOOM
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Clinical disorders of peptide absorption?
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Apical/Basolateral transporter fuck up.
Deficiency of pancreatic or brush border peptidase fuck up |
