Physio 2 - GI 2

drraythe's version from 2015-06-09 01:21

Cephalic and Gastric Phase CONTINUED

Question Answer
strongest stimulator of HCl release is?histamine
what is intrinsic factor? released from where? what does it do?(a glycoprotein) released from parietal cells (cosecreted with HCl), binds to VitB12 to protect it from being digested...both are then absorbed in the ileum
why is vit. B12 important?important cofactor for erythropoiesis
what secretes pepsinogen? what are they? how are they activated?secreted by chief cells, they are precursors of pepsins, and are activated by acid (HCl)
what kind of enzyme is pepsin? why is it unusual?proteolytic enzyme to initiate protein digestion via HYDROLYSIS. unusual b/c its optimum pH is between pH 1 and 3.
what is prochymosin? who secrets it? aka? what does it do?another proteolytic enzyme, secreted by nursing animals (aka rennin in calves) instead of pepsinogens, its specific to coagulation of casein (milk protein)
what are the three phases of the gastric control system? purpose of control systme?(1) cephalic phase, (2) gastric phase, (3) intestinal phase. To prepare stomach, match secretions+grinding with quality and amount of food, to not overload sm. int. with chyme, initiate stim of pancreas and bile
what is involved in the cephalic phase of the control system?anticipation of food, smell taste or touch stim CNX (vagus) to mildly stim gastric motility (prox relax and distal peristalsis) and secretions (musus, gastrin, histamine, HCl, pepsinogen)
what is involved in the gastric phase of the control system? initial stimulation?food arrives in stomach. stims mechano and chemo receptors to send strong stim of local(plexus) and central(vagal) reflexes.
effects of gastric phase of control system?relax mm in fundus (accomidation), vigorous mm contractions in distal portions,strong stim of all gastric secretions with massive HCl release
what is "self-limitation" of gastric phase of control system?when pH is <2, gastrin release becomes blocked and vagal/local reflexes are blocked to prevent excessive acidification
what is involved in the intestinal phase of the control system? stimuli for this response?chyme arrives in duo.-> inhibit gastric glands/motility via receptors in sm int= PREVENT OVERLOADING SM INT (negative feedback). stim are distension of sm. int, high acidity, high nutrient content, irritation of mucosa =enterogastric reflex
what is the enterogastric reflex? transmitted by what?reflex prevents overloading of sm ints, part of intestinal phase of control system. transmitted largely by endocrines (secretin and CCK)
what does Secretin do/stim by? what does CCK do?Secretin= stim by low pH, reduces gastric secretions. CCK= cholecystokinin, stim by fats and proteins, reduces gastric motility (why cheese sits in your belly!)
vomiting is a reflex under the control of? receives signals from? (4)vomiting center in brain gets afferent signals from...(1) GI mechano (**mucosa distention!) and chemo receptors and irritation, (2) viscera other than GI tract (3) extramedullary centers (psychogenic) (4) chemorecpetor trigger zone (stim by drugs, toxins, inflammation products)
Concequences of severe vomiting? (3)(1) loss of fluid (2) loss of K+ (3) loss of H+
what does loss of fluid in vomiting do?hypovolemia-> dec blood pressure-> circ. shock
what does loss of K+ in vomiting do?hypokalemia-> hyperpolarize membranes-> reduced excitability of nerve/mm cells -> weakness and hyporeflexia
what does loss of H+ in vomiting do?metabolic alkalosis-> hypoventilation
what animals cant vomit, why, and what happens?horses and some rodents cant because of the acute angle between the eso/stomach and clamp-like structure of diaphragm....stomach may rupture.
what are the components of the gastrointestinal barrier? (4) fxns of these?(1) mucus/bicarbonate(coat cells, neutralize acids,bind to bacteria) (2) Prostaglandin E2(inc mucus, *blood flow, and bicarb secretions. (3)epi. cells with tight junctions and stem cells (high regenerative capacity) (4) bactericidal peptides/immunoglobulins A
4 major causes of disruption of gastrointestinal barrier?(1) stress (symp stim+cortisol release->reduce blood flow, mucus, HCO3) (2) NSAIDs (inhibit prostaglandins) (3) ischemia (4) infections (*Helicobacter pylori)
consequences of disruption of gastrointestinal barrier?cell injury, gastritis, auto-digestion, erosion, ulceration
therapy for disruption of gastrointestinal barrier?stress relief, histamine blockers, proton pump blockers, antibiotics

Pancreas and Liver

Question Answer
what is chyme a mixture of? what can be absorbed?mix of poly/oligopeptides, Lg emulsified fat globules, poly/oligosaccharides...NONE of them can be absorbed yet!
when chyme enters the sm int, two things must happen...(1) neutralize gastric acid (2) hydrolysis of macromolecules into micromolecules for absorption
exocrine fxns of pancreas?(1) BICARBONATE solution (2) DIGESTIVE ENZYMES
purpose of bicarbonate solution of pancreas?neutralize gastric acid, enable pancreatic enzymes to function (need pH >5)
3 major groups of pancreatic digestive enzymes?amylolytic, proteolytic, lipolytic
pancreatic alpha amylase digests what? how and where?digests most soluable (starch,glycogen) but not structural carbs (splits polysacc. into oligo and di). splits ONLY 1-4ALPHA glycosidic linkages. does NOT split end-standing molecules
what can panc. alpha amylase NOT digest?no disaccharides, no end standing molecules, no structural carbs
what are the proteolytic enzymes of the pancreas? why are there so many? what do they produce?**trypsinogen, chymotripsin, pro-elastase, pro-carboxypeptidases...there are so many because there are so many different amino acids. Produce OLIGOPEPTIDES
how are proteolytic enzymes secreted?as pro-enzymes to avoid auto-digestion in VESICLES which contain a trypsin-inhibitor
how are the pro-proteolytic enzymes of the pancrease activated?1st, trypsinogen is activated by mucosal enterokinase to trypsin, which activates all the other enzymes including its own precursor
how do pancreatic lipases work? their limit?attach to surface of fat globules, hydrolyze TGs into fatty acids and and monoglycerides. CAN ONLY DO SURFACE AREA so require BILE SALTS to furthur emulsify
how many absorbable products come from pancreatic enzymes?not many, but they are essential in the break-down process
the intestinal phase in the main phase of pancreatic stim via what 2 hormones? their fxn?(1) SECRETIN (released from duodenal endocrine cells when PH of chyme is TOO LOW and stim bicarb secretion.) (2) CCK (cholecystokinin- proteins and fats stim release from duo endocrine cells for panc to release enzymes)
cause of ACUTE pancreatitis? pathogenesis?cause (infections, trauma, neoplasms, toxoplasma, fatty/spicy foods). tissue damage->trypsin inhibitor is overwhelmed->enzymes activate->pancreatic autodigestion and enzymes leaking into circ.
cause of Exocrine Pancrease Insufficency (EPI)? pathogenesis?(heritable atropy(GSD), idiopathic, or result of chronic inflammation/acute pancreatitis.) lack of enzyme secretion-> maldigestion-> starvation (weight loss, steatorrhea)
two things the liver secretes and why?Bile acids (digest/absorb fats and lipophilic vitamins), bicarb (neutralize acidic chyme)
what do hepatocytes secrete?bile acids, lipophilic waste products(bile pigments, ie biliruben, chlosterol, etc)
what do liver duct cells secrete?bicarb, electrolytes and h2o
where is bile stored, what happens to it, who lacks this?gall bladder, absorbs all the electrolytes so conc organic compounds. No Gall in HORSE, birds, rodents...
what are bile acids derived from? how does it happen? what would you say this molecule is?Derived from chlosterol->cholic acid->conjugated with amino acids. its a DETERGENT
2 fxns of bile acids?(1) emulsification(inc surface area) (2) transport (aggregates of bile acids surround fatty acids/monoglycerides form MICELLES with hydophilic side out and lipophilic in.)
what do micelles do?Avoid re-condensation into triglycerides, keep lipid in solution to enable transport
most bile is released during intestinal phase via what two hormones?CCK (cholecystokinin) and secretin
how does CCK affect bile? what triggers its release?stimulates gall bladder contraction. stim by fats and proteins
how does secretin affect bile? what triggers its release?stim bicarb release into bile when pH is low.
what does she mean by recycling of bile?95% of bile reabsorbed in ileum reenter liver, and can be resecreted up to 20 times
what is the example of positive feedback with bile?the choleretic effect of bile acids...reuptake of bile acids into liver stims hepatocytes to secrete more bile juice
what is a sensitive diagnostic indicator of deficits in hepatic fxn?bile acids in PLASMA because damaged hepatocytes cant extract bile acids from portal blood

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