Physio 2 - GI 1

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

Overview and General Principals

Question Answer
function of digestive system nutrients from enviro to circ system
3 fundamental processes used by GI to carry out its function? (1) motility(=mechanical digestion) (2) secretions (=chemical digestion) (3) absorption
names for size of protein portions (peptides) smallest to largest? monopeptide, dipeptide, tripeptide, oligopeptide (4-25 peptides), polypeptide (over 25)
word for the coordinated movement of the GI?syncytium
explain basic action potentials of GI muscle cells....SELF-EXCITATORY with undulating resting membrane potentials. have SLOW WAVES and SPIKE POTENTIALS
explain slow wave resting potential. (where is baseline? what is the slow wave generated by? name of it? how are the conducted along a GI section? frequency?)baseline= -50-60mV. Generated by special SM MM CELLS= CELLS OF CAJAL. waves conducted b/c of the GAP JUNCTIONS. Frequency= 3-12/min
critical threshold to induce a spike potential/contraction? Explain what happens after threshold reached? -40/-35mV= threshold. The voltage-gated Ca channels open, rapic Ca influx causes spike potentials, elicits mm contraction, which spread along the GI
two things that the amplitude of slow waves can be modulated by? (1) priming factors (2) hyperpolarizing factors
explain what priming factors do and howmodulate slow wave amplitude. Move threshold of membrane to higher negative amount (so, has to travel less, from -70 to -50 instead of from -70 to -40.) which means more slow waves reach threshold, which means GI motility is increased
examples of priming factors?Gut wall stretching, parasymp. stim, some GI hormones
explain what hyperpolarizing factors do and how?hyperpolarize membrane so threshold is a lower neg number (slow wave has to travel bigger distance, less reach threshold) so /////////GI motility decreases.//////////
examples of hyperpolarizing factors?symp. stim, some GI hormones
2 basic patterns of GI motility?(1) segmentation/mixing (localized contractions, mostly circular mm, short distance travel to chop food). (2) peristalsis/propulsion (circular contraction cr to bolus and relaxation ca to border..longer distances.
what is the strong local reflex (arc) associated with peristalsis?ADAPTIVE RELAXATION
secretory and motor fnxs of GI controlled by...(3 things? any subcategories?)(1) endocrine system. (2) nervous system [(a) enteric NS, (b) autonomic NS] (3) immune system in special circumstances
enteric endocrine system secretes what two things? how do they act?(1) endocrines[act via blood stream]. (2) paracrines [act via diffusion]
where are GI enteric endocrine cells located? how are they stimulated?located diffusely throughout mucosa. Stimulated by sampling gut contents OR via the enteric plexus
what do regulatory peptides (ca 35) affect? secretions of GI tract and accessory organs, and affect their motility functions.
The enteric (intrinsic) nervous system consists of what two branches?myenteric plexus and submucosal plexus
where does the enteric NS lie? regulates what? enables communication between what?lies in the gut wall, autonomously regulates GI sm mm, endocrine+secretory cells. enables communication amont adj. GI sections
what kinda neurotransmitters does the enteric NS use?*ACh, *Norepi(mostly inhibitory), *Serotonin, also dopamine,CCK,ATP,somatostatin,bembesin, etc. etc.
Myenteric plexus influences what? How? influences GI motility! (mechanoreceptors for degree of mm stretch-> afferent neurons-> cell body-> efferent neurons-> affect mm cells
submucosal plexus influences what? how?influences GI secretions! (chemoreceptors-> afferent-> cell body-> efferent-> affect the secretory, endocrine, and mucous cells
how are muscle and secretory activity coordinated?mult. interneurons between myenteric and submucosal plexuses
how is autonomic parasympathetic control exerted on the GI system? (supply, fibers, NT, stim causes what?)VAGUS N. and PELVIC nerves, contain sensory and motor fibers, NT is ACh. parasymp is MOSTLY STIMULATION of GI fxns. (inc motility, inc secretion, dec sphincter tone)
how is autonomic sympathetic control exerted on the GI system? (supply, fibers, NT, stim causes what?)nn. originate from T5 to L2, pass to MESENTERIC GANGLIA, has sensory and motor fibers. NT is NOREPI. Stim of symp. system= MOSTLY INHIBITS GI fnxs (dec motility, dec secretion, inc sphincter tone)
is there a difference in enteric (local reflexes) and autonomic (central reflexes) mechano and chemo receptors?NOPE. both use the same receptors in the GI wall
what is the main stim for GI mvt? DISTENSION of GI wall
pathway for stim of GI mvt?distension of GI wall-> stim both NSs via mechano receptors-> release PRIMING FACTORS-> open ligand-gated ion channels->depol sm mm membranes-> passing slow waves reach threshold-> spike potentials-> contractions-> mixing and peristalsis
enteric immune system consists of?mesenteric Lns, peyer patches, diffuse lymphoid tissue, intraepithelial leukocytes
if enteric immune system is challanged, what does it release? what do they act as?inflammatory mediators= prostaglandins, histamine, cytokines, etc....these act as PARACRINES(via diffusion)
inflammatory mediators of enteric immune system stimulate what, which leads to what?stim. secretory/motility fxns to lead to PERISTALTIC RUSH
what is peristaltic rush?powerful and rapid peristaltic mvt. of sm. int. caused by intense mucosal inflammation (protective, quickly push potentially harmful contaminants into Lg int.)
how is GI blood flow regulated? adjusts to what? how much can it change?it's AUTOREGULATED by level of local activity...can increase by a factor of 8 between inactivity and active digestion.
how is GI blood flow stimulated?pumping action of GI, several endocrines(bradykinin, kallidin), decreased O2 and increased CO2
what does nervous symp. stim of GI blood flow do? limits of this? how does it measure up to the autoregulatory blood flow?symp stim will constrict all the GI vessels....up to //1// hour without damage in an emergency. autoreg system will OVERRULE symp stim to protect mucosa

Cephalic Phase and Gastric Phase

Question Answer
what is the cephalic phase? involves?aka pregastric digestion, first step in mechanical digestion.
how many/what salivary glands for avg animal?3 pairs (parotid, mandibular, sublingual) and buccal glands in ruminants/birds
4 main fnxs of saliva?(1) moisten/lubricate/bind food into bolus. (2) control bact. growth. (3) start carb digestion via salivary amylase in ONLY OMNIVORES. (4) cool body via evaporation
how is saliva produced in a gland? resulting properities of saliva?acini secrete mucous and plasma like fluid, which is altered during duct passage--- Na and Cl are exchanged against K and HCO3 (therefore K-rich and slightly alkaline saliva--also hypotonic)
how is salivation controlled by ANS? (2 ways)(1) parasympathetic reflex (chemo/mechano receptors->salivary center in brain->parasymp efferent via CN7 and 9->salivation) (2) conditioned reflex (anticipation and smell-> higher CNS->salivary center-> salivation)
stims that induce salivation also induce what, and how?stim "warming up" (mild stim of stomach, sm int, pancrease and bile) by the stimuli activiating CNX to initiate VAGAL REFLEXES
why is alkaline saliva esp. important in ruminants?to neutralize fermentation products (volatile fatty ACIDS) in rumen
chewing reflex of mastication mainly involves what nerve?CN V
path of chewing reflex?presence of bolus-> pressure against palate-> inhibition of cheek mm-> lower jaw drops-> stim stretch receptors in cheek mm-> contraction-> pressure against palate....etc.
jaw and chewing of carnivore vs herbivore?carni= equally wide jaws, vertical jaw mvt for cutting. herbi= narrower lower jaw, horizontal jaw mvt, for grinding
what are the two phases of swallowing? what happens during them?(1) voluntary phase ( tongue moves bolus to pharynx). (2) reflex phase (touch receptors stim swallowing center in medulla ob.via CN IX (gag reflex)-> initiates lifting of soft palate and closure of larynx-> peristaltic wave over pharynx-> upper eso. sphincter relaxes, bolus enters eso.
esophagal phase of of swallowing involves what?bolus propelled via peristalsis towards stomach, lower eso sphincter relaxes ahead of peristalsis to allow entery to stomach
names of eso. sphincters, and what are they doing during not swallowing?upper=cricopharyngeal mm and lower=cardia are tightly closed when not swallowing to prevent entry of air and reflux of gastric contents
disturbances of pregastric digestion are common in animals. examples?broken teeth, oral mucosal injuries, nerve or CNS damage (ecephalitis, tetanus, rabies, trigeminal paralysis) or megaesophagus
possible causes of megaesophagus?achalasia (lower sphincter cant relax due to malfxn of myenteric plexus- botox is a possible tx). PRAA (persistant right aortic arch), or myasthenia gravis (ACh malfxn-> in dog all eso. is skele mm), SPIROCERCA lupi (worm lives in eso, inflammation-> compression of eso) or idiopathic
4 fxns of the stomach? applicable locations of fxns?(1) temp. storage of food (fundus.) (2) mixing of food with gastric secretions and grinding/liquefaction of ingesta into chyme (corpus and antrum) (3) chemical and enzymatic digestion (esp. proteins). (4) controlled release of liquified chyme into sm. int.
what is absorbed in stomach? noteable about absorption in stomach?absorption is NOT a physiological fxn of stomach....alcohol, NSAIDS (lipophilic drugs) are absorbed in the stomach tho
where does storage of the stomach take place, what facilitates it?in proximal stomach (fundus), facilitated by the ACCOMMODATION REFLEX
why is the accommodation reflex special?unusual vagal reflex leads to RELAXATION of GI, and NT is either nitric oxide or VIP
pathway of accommodation reflex?food enters stomach-> stim mechanoreceptors-> vagal reflex-> reduction in mm tone in proximal parts-> relaxation->expansion of stomach WITHOUT pressure inc.
how does stress make you feel full?suppression of vagus or stim of symp system reduces accommodation reflex -> inc gastric pressure after food intake-> feel full
pathway of how food is ground up in distal stomach?food stim local and central reflexes-> enhance peristalsis in pacemaker area-> travel toward antrum-> sm amount of fluid gets through before pylorus contracts ahead of peristaltic wave-> content is kneaded and squirted back(=retropulsion)-> mixing continued with next peristaltic wave
gastric retention time? (liquid vs solid) exceptions?30min fluid. 2-4hr for solid food. SMALL animals have a faster passage time (ex: ferrets 4hrs for whole GI passage)
what can happen when stomach is empty? possible problem with it?A MIGRATING MOTILITY COMPLEX (MMC)...occasional strong peristaltic wave between stom and ileum when pylorus relaxed. Clear stom/sm. int of undigested particles. Problem bc THIS is when a foreign body will get out of stom into ints. need to make vomit before MMC!
two types of mucosa in the stomach?glandular and non-glandular
fxn of nonglandular mucosa of stomach?storage, fermentation(?)
glandular mucosa has what three regions, and what 5 secretory cells and their products?regions= cardiac, parietal, and pyloric regions. cells= (1)mucus cells, (2)parietal cells(HCl and intrinsic factor-which is to absorb vit. B12), (3) enterochromaffin-like cells (histamine), (4) Cheif cells (pepsiongen or prochymosin) (5) G (endocrine) cells (gastrin, pyloric region only)
what is numerous in mucosa but isnt a secretory cell? what is its fxn?stem cells! enable replenishment of all GI cells, so mucosa has high regenerative ability
what does the mucus layer protect the gastric mucosa against?mechanical stress, acids, and digestive enzymes
what is mucus produced by? what does it contain?made by goblet cells, has nearly insoluable mucins, is alkaline (containing bicarbonate= protection against protons)
pathway for creation of mucus?local reflexes(enteric NS) and central reflexes(vagus) lead to synth of prostaglandin E2 in goblet cells-> increase mucus and bicarbonate release
why do NSAIDs affect mucous production?NSAIDs interfere with prostaglandin production, which interferes with mucus production
when parietal cells secrete HCl into the stomach, what is it's pH? species diffs? how does the HCl get into the stomach?secrete isotonic HCl solution with a pH of <1 into stomach. (carnivore pH 1, most others 3-4). HCl pumped via a H+/K+ exchanger pump
5 fxns of HCl?(1) macerate ingesta into fluid (2) denature proteins (3) begin to emulsify fats (4) activate proteolytic enzymes pepsinogen or prochymosin (5) be bacterialcidal
3 ways to stim parietal cells to release HCl? from where did they originate?(1) *ACh release via local / central reflexes (2) *gastrin released from G cells into blood in response to peptides (so, a mild direct stim here) (3) *histamines- gastrin stim enterochromaffin cells to release histamine, histamine acts as paracrine and is strongest stim of HCl release

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