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Physiology > Unit 6 - Introduction to Gastrointestinal Physiology > Flashcards

Unit 6 - Introduction to Gastrointestinal Physiology Flashcards

1
Q

what are the major functional processes of the GI system? how are they initiated?

A
  • motility - movement of food through the system
  • secretion - coordinated delivery of appropriate fluids and enzymes
  • digestion - hydrolysis of macromolecules in food
  • absorption - transport of molecules into circulation
  • excretion - elimination of waste products

they are initiated by ingestion of food (sense, smell, sight) through integrated series of endocrine, paracrine, and neural responses

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2
Q

where do absorbed nutrients go before entering systemic circulation?

A

initially circulate through liver (via portal venous circulation) to be processed, filtered, and detoxified before entering systemic for general distribution to tissues

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3
Q

how many kcal/kg BW do sedentary humans need?

A

30 kcal/kg/day

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4
Q

how do GIT sphincters work?

A

respond to different stimuli and have different resting pressures

  • one-way valves with rings of circular muscle, functioning as barriers to flow to maintain positive resting pressures
  • activation of inhibitory motor neurons (like VIP) leads to transient relaxation and forward passage of material
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5
Q

upper esophageal sphincter

A

maintains highest resting pressure of all sphincters, preventing air from entering esophagus
-made of striated muscle, and under control of swallowing center in medulla, relaxing during swallowing to allow food to enter

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6
Q

lower esophageal sphincter

-what happens if it’s faulty?

A

separates esophagus from stomach

  • made of smooth muscle that relaxes during swallowing
  • coordinates passage of food into stomach after swallowing/deglutition
  • prevents reflux of gastric contents (acid) into esophagus
  • if incompetent, causes heartburn, acid indigestion
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7
Q

pyloric sphincter

-what happens if it’s faulty?

A

separates stomach from duodenum

  • its resting pressure contributes to regulation of gastric emptying to prevent duodenal-gastric reflux
  • reflux of bile acids and digestive enzymes can lead to gastritis, ulcers, and perforation
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8
Q

ileocecal sphincter

A

separates ileum and cecum, preventing back flux of colonic contents into ileum

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9
Q

what do some patients with irritable bowel syndrome have?

A

bloating and pain due to bacterial overgrowth in SI near ileocecal sphincter

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10
Q

what are the internal and external anal sphincters

A

internal = smooth muscle
external = skeletal muscle
control elimination of waste products

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11
Q

what is necessary to promote digestion, absorption, and detoxification of ingested materials?

A

substantial fluid shifts and pH changes

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12
Q

what is the comparison between ingested/secreted fluids and absorbed fluids?

A

both equal each other

  • ingested: 2 L, plus 8 L from GIT (SI, pancreas, stomach, saliva for buffers, acid, and enzymes)
  • absorbed: back into blood (mostly SI, also colon)
  • total excreted in feces = 100-200 mL of fluid
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13
Q

where are and what do parietal (oxyntic) cells do?

A

found in oxyntic glands of stomach

-acidify contents of stomach to promote digestion and breakdown of ingested bacteria and Ag

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14
Q

pH of stomach VS blood, and how it can be neutralized

A

highly acidic chyme around 1-2, so [H+] is 3 million times that of arterial blood
-HCO3- secretion from pancreas to duodenum neutralizes acid as it goes into duodenum

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15
Q

what is the enteric nervous system and what is it made of?

A

“minibrain” branch of ANS with ~100,000,000 neurons (similar to spinal cord)
-primary nerve nets (plexi) in ENS are myenteric (between longitudinal and circular muscle layers) and submucosal (between circular muscle and submjucosal layers)

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16
Q

what is the myenteric plexus?

A

Auerbach’s; between longitudinal and circular muscle layers of GIT, extending from proximal end of esophagus to rectum
-stimulation increases tone (tonic contraction), intensity of rhythmic/phasic contractions, and velocity of conduction of excitatory waves to enhance peristalsis (IOW: MOTILITY)

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17
Q

what is the submucosal plexus?

A

Meissner’s; between circular muscle and submucosa in intestines only
-controls local intestinal secretions, absorption, and contraction of submucosal muscle, affecting local infolding of GI mucosa

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18
Q

layers of GIT, from mucosa to serosa

A

epithelium - lamina propria - muscularis mucosa - submucosa - submucosal plexus - circular muscle - myenteric plexus - longitudinal muscle - serosa

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19
Q

how does the ENS respond to input from local environment? how is it modulated?

A

mechanoreceptors, chemoreceptors, and osmoreceptors in epithelial lumen

  • can be done in absence of extrinsic innervation, via intrinsic ENS neural network
  • -sensory neurons, interneurons, and motor neurons intrinsic to ENS are connected synaptically via varicosities for efficient bidirectional flow of info
  • activity can be modulated extrinsically by both sympathetic and parasympathetic input from ANS
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20
Q

what can musculomotor and secretomotor neurons alter?

A

smooth muscle activity, secretion, and absorption of fluid or electrolytes by epithelium, activity of endocrine cells, submucosal blood vessels

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21
Q

what do mechanoreceptors sense?

A

stretch of smooth muscle; generated signal is transduced through myenteric plexus to stimulate contractions

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22
Q

what do chemoreceptors sense?

A

chemical composition of chyme and regulate motility and secretion of buffers to control luminal pH during influx of acidic chyme into duodenum

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23
Q

what do osmoreceptors sense? why is this very important? so what does this mean they control?

A

osmolarity of chyme in small intestine

  • important b/c one-cell barrier between chyme (in lumen) and capillaries
  • -hypertonic chyme exerts osmotic force, pulling fluid out of cells and plasma
  • thus they control amount of chyme entering SI and amount of secretions needed to buffer chyme
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24
Q

where do parasympathetic preganglionic fibers (from vagus and pelvic nerves) terminate?

A

postganglionic cholinergic or peptidergic neurons located in plexi
-PNS activation leads to increased motility in wall of gut, relaxation of sphincters, and enhanced secretions

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25
Q

what are vasovagal reflexes?

A

long reflexes in which both afferent and efferent impulses are carried by neurons in “mixed” vagus nerve
-prominent in coordinating GI function

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26
Q

how do afferent, interneurons and efferent neurons coordinate?

A

sensory (afferent) monitor changes in luminal activity, then activate interneurons, which relay signals to activate efferent secretomotor neurons, or neurons that control blood vessels, smooth muscle cells, epithelial cells, and enteric endocrine cells
-ANS can modify these responses

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27
Q

how does the PNS innervate the ENS?

A
  • vagus to proximal 2/3, from pharynx to beginning of distal colon
  • pelvic nerves to distal 1/3 of colon
  • ACh is major neurotransmitter for pre/post-ganglionic fibers of PNS, but some postganglionic fibers release peptides (substance P, VIP)
  • activation promotes digestion and absorption by increasing salivary, pancreatic, and gastric acid secretions; increasing contraction of smooth muscle wall; relaxing sphincters
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28
Q

how does the SNS innervate the ENS?

A

postganglionic fibers from celiac plexus, hypogastric, and superior/inferior mesenteric ganglia

  • NE is major transmitter released by postsynaptic neurons, exerting inhibitory effects on excitatory cholinergic neurons via presynaptic inhibition
  • activation will inhibit digestion/absorption by relaxing gut wall, reducing secretions, contracting sphincters, and diverting blood flow from GIT by contracting vasculature
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29
Q

what is the hierarchy of 5 levels for neural organization of digestive tract?

A

determines moment-to-moment motor behavior

  1. ENS - independent integrative nervous system
  2. prevertebral sympathetic ganglia
  3. central sympathetic fibers
  4. central parasympathetic centers
  5. higher brain centers
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30
Q

how is salivation initiated? during which phase by which nerves?

A

upon seeing, smelling, and tasting food during cephalic phase through VII and IX

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31
Q

how is acid production initiated? during which phase by which nerves?

A

when food is in the mouth during cephalic and gastric phases of gastric acid secretion through X

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32
Q

how is pancreatic enzyme secretion stimulated? during which phases?

A

during cephalic, gastric, and intestinal phases by X

-during intestinal phase, buffer is secreted too

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33
Q

how is primary peristalsis stimulated?

A

swallowing center of medulla and vagus

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34
Q

how is initial relaxation of the sphincter of Oddi done? during which phase by which nerves?

A

during cephalic and gastric phases by vagus

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35
Q

how is receptive relaxation of stomach and duodenum done, and why?

A

done by vagus to accommodate entry of food/chyme

36
Q

what simulates synthesis of bile by liver?

A

vagus

37
Q

what stimulates intestinal motility (ileal motility and colonic mass movements)

A

vagus to upper colon, pelvic nerves to lower colon

38
Q

what are the interstitial cells of Cajal?

A

ICCs; pacemakers in GIT (abundant in myenteric plexus) that generate electrical slow waves via gap functions to GI muscle, especially circular muscle
-ionic current flows across GJs to depolarize membrane potential of circular muscles to threshold for discharge of APs

39
Q

when does contraction of GI muscle wall occur?

A

only when APs are generated at peaks of slow waves (from mid-stomach thru rectum) when depolarized above -40 mV

40
Q

how is smooth muscle of GIT excited and what are the steps?

A

continual slow intrinsic elecctrical activity generated by ICCs; electrical activity and associated contractions spread in 3D from point of initiation

  1. slow waves; undulating changes in resting membrane potential (no APs) varying intensity from 5-15 mV
  2. spike potentials; APs made when threshold (40 mV) reached during plateau phase of slow wave, triggering phasic contractions
    - APs last 10-40 x longer than nerve AP, produced by Ca++ entry thru L-type VSCCs (with some Na+ influx)
41
Q

how can treating cardiovascular disease cause disordered GI motility?

A

treatment with L-type VSCC blockers will prevent spike potentials

42
Q

how does ENS control distance and direction of electrical activity?

A

excitatory (ACh, substance P) and inhibitory (VIP) motor neurons

43
Q

how are slow wave motor patterns influenced?

A

hormones, paracrine factors, ANS, and drugs

  • PNS, stretch, ACh will increase appearance/number of APs, thus increasing strength of phasic contractions
  • SNS, NE has opposite effects by hypoerpolarization
44
Q

where is slow wave frequency highest, intermediate, and lowest?

A

highest in SI (up to 12/minute; fastest right after meal), intermediate in colon, and lowest in stomach (3/minute)

45
Q

does the max contractile frequency in muscle exceed frequency of slow waves?

A

no, it doesn’t exceed the frequency of slow waves, but may be less if slow wave doesn’t make a spike (AP)
-neural and hormonal input modulate production of APs, thus strength of muscle contractions

46
Q

what can failure of ENS control lead to?

A

disordered motility, including spasm and abdominal cramping

47
Q

how is chyme moved?

A

by segmental (mixing, nonpropulsive) and peristaltic contractions

48
Q

segmental contractions

  • how are they determined?
  • what is important for excitation?
A

(mixing, non-propulsive)

  • chyme enters SI distending wall, eliciting local contractions and mixing chyme with intestinal secretions
  • local events and occur in different segments (2-3/minute, no more than 12/minute)
  • -determined by frequency of electrical slow wave
  • excitation from myenteric plexus is important, b/c only weak contractions are observed in presence of atropine (muscarinic cholinergic antagonist)
49
Q

peristaltic contractions

-how long does it take to move chyme?

A

move material from mouth to colon (aboral direction; orad to caudad)
-relatively weak and move material thru SI 1 cm/minute, so 3-5 hours are needed to move chyme from pylorus to ileocecal valve

50
Q

when is peristalsis intensified?

A

after a meal, by stretch of duodenal wall upon entry of chyme

51
Q

gastroenteric reflex

A

enhances peristaltic motility and secretions

52
Q

gastroileal reflex

A

triggers opening of ileocecal valve to allow movement of chyme from SI to LI
-distention of ileum causes relaxation of sphincter, while distention of ascending colon will contract it

53
Q

enterogastric reflex

A

decreases gastric motility and secretions, stimulating contraction of pyloric sphincter to inhibit chyme from entering duodenum (to optimize digestion and absorption)

54
Q

what is intestinal motility after ingestion of a meal characterized by?

A
  • mixing to optimize contact between ingested food and digestive secretions
  • circulation of intestinal contents to facilitate contact with mucosa
  • net propulsion of contents in aboral direction
55
Q

what is peristaltic rush?

A

“diarrhea” that is caused by irritation of intestinal mucosa by infectious agents

  • helps to clear intestine of irritant
  • 2 to 25 cm/sec
56
Q

what is the “law of the gut”?

A

myenteric reflex (peristalsis) when contractile ring forms on orad side, pushing contents toward anus

  • receptive relaxation downstream aids unidirectional
  • so excitation of circular muscle behind bolus, and inhibition ahead of it; opposite for longitudinal muscle
57
Q

what is longitudinal muscle mainly innervated by?

A

excitatory motoneurons (circular is both excitatory and inhibitory)

58
Q

how is peristalsis coordinated locally?

A
  • ascending path leads to excitatory motoneurons behind bolus (ACh, substance P) to depolarize slow waves, generate AP, and contract
  • descending path ends in inhibitory motoneurons (VIP), which hyperpolarize slow waves in muscle, relax front of bolus
59
Q

what is physiological ileus

A

absence of motility in SI and LI

  • output of specific motor program stored in ENS
  • normal state and remains in effect for different periods in different intestinal regions
  • subset of inhibitory neurons are active and suppress response of circular muscle to electrical slow waves
60
Q

what is pathological (paralytic) ileus? what are examples?

A

state where normal periods of quiet are longer

  • inhibitory neurons are abnormally active and continously suppress myogenic activity
  • passage of stool/gas impaired, causing cramping pain, nausea, and vomiting
  • altered motility and delayed transit common after abdominal surgery, anticholinergic, or opiate treatment
61
Q

what is the migrating motor complex?

A

MMC; the short rhythmic waves of strong propulsive contractions that pass down distal stomach and SI
-divided into 3 phases: quiescence (I), little activity (II), and strong activity (III)

62
Q

what are functions of MMC, and when is it observed?

A

“sweeps” stomach and SI of residue like undigested foods/fiber, bacteria (prevent overgrowth), desquamated cells

  • pyloric sphincter is inhibited, and particles larger than 2 mm can pass into duodenum (usually canot)
  • observed 3 hours after last meal, and happens at cyclic intervals of 90 minutes
  • starts in distal 1/3 of stomach and continues to terminal ileum, emptying material into colon
  • intrinsic property of GIT, but vagotomy reduces contractile activity
63
Q

what is motilin?

A

“hormone” made in duodenal Mo cells, and released into circulation and stimulates contractions (5-10 min) during active phase
-acts thru ENS and ANS to stimulate contractions

64
Q

what happens if MMC is faulty/absent?

A

indigestible “bezoars” accumulate and obstruct lumen of stomach especially

65
Q

what is deglutition?

A

swallowing; voluntary movement of food to pharynx activating swallowing reflex, including primary peristaltic wave in esophagus

66
Q

what is the voluntary stage of swallowing?

A
  1. shaping of food into bolus
  2. collection on tongue
  3. raising of tongue against hard palate to create pressure gradient that pushes bolus into pharynx
67
Q

what are the involuntary events of swallowing in the pharyngeal phase?

A

initiated when food enters pharynx

  1. activates sensory neurons from tonsillar pillars that project via X, IX, and V to swallowing center in medulla
  2. efferent impulses sent back to pharynx, esophagus, esophageal sphincters, and stomach to cause
    - soft palate to pull upward, preventing food reflux into nasopharynx
    - movement of epiglottis and pharynx to prevent food from entering trachea
    - relaxation of UES
68
Q

what are the involuntary events of swallowing in the esophageal phase?

A
  1. swallowing reflex initiates primary peristaltic wave that propels food thru open UES, then closes it to continue peristalsis that traverses length of esophagus, ending in opening of LES, and receptive relaxation of stomach
    - if primary wave fails to move all food into stomach, a secondary peristaltic wave comes from distention of esophagus
69
Q

how is the respiratory center inhibited during swallowing?

A

when CN V and IX send impulses to medulla swallowing center, it initiates sequence of motor impulses from medulla and lower pons via sequential activation of V, IX, X, and XII, taking about 6 seconds

70
Q

which parts of esophagus are striated and smooth muscle?

A

pharynx and upper 1/3 of esophagus are striated controlled by IX and X; the rest is smooth

71
Q

how can there be partial/total paralysis of swallowing mechanisms?

A
  • damage to CN V, IX, or X
  • diseases that damage swallowing center (poliomyelitis, encephalitis)
  • paralysis of swallowing muscles (muscular dystrophy, myasthenia gravis)
  • deep anesthesia (if vomit, will suck into trachea via aspiration and choke to death)
72
Q

what is receptive relaxation?

A

transient relaxation of proximal stomach with each bolus of food during ingestion of a meal

  • in LES and fundus, regulated by vasovagal reflex after swallowing (using VIP)
  • if primary doesn’t clear, need secondary beginning at point of distension
73
Q

how does receptive relaxation affect intragastric volume and pressure?

A

increased volume, but not pressure

74
Q

what is accommodation of stomach?

A

as food accumulates in stomach, there is gradual relaxation of entire stomach, allowing storage of food w/o increase in intragastric pressure
-mediated by vasovagal reflex

75
Q

how is gastric emptying affected by contents of a meal?

A

high fat meal will have slower emptying than acidic meal will have slower emptying than saline meal
-receptors in small intestine sense contents of chyme and regulate emtpying to optimize aborption (feedback arises from duodenum)

76
Q

what types of neural and hormonal signals can decrease rate of gastric emptying?

A

vagus, secretin, CCK, GIP from duodenal mucosa

77
Q

what does delayed gastric emptying represent?

A
  • coordinated function of fundic relaxation
  • inhibition of antral motor activity
  • stimulation of isolated, phasic contractions of pyloric sphincter
  • altered intestinal motor activity
78
Q

what is achalasia? how is it treated?

A

absence of relaxation of LES (cannot relax during swallowing); uncommon

  • caused by damage to myenteric plexus in lower 2/3 of esophagus (lack of inhibitory motoneuron activity), cannot transmit signal for receptive relaxation to LES as food approaches
  • esophagus gets enlarged over years, infected, ulcerated, necrosing, and rupture to death
  • treated with antispasmotic drugs and/or balloon inflation of lower esophagus
79
Q

lower esophageal sphincter into

A

maintains high pressure in distal 3-5 cm of esophagus to rpevent reflux of stomach contents
-during swallowing, sphincter tone relaxes (via VIP and NO) to allow food to enter stomach

80
Q

what is GERD?

A

when LES tone not properly maintained

-refluxed contents of stomach damage esophageal epithelium; very common

81
Q

how is stomach divided functionally?

A

proximal gastric reservoir (fundus and 1/3 of body)

distal antral pump (caudal 2/3 of body, antrum, and pylorus)

82
Q

what do muscles in gastric reservoir do? what happens if it fails? what would agents that relax musculature do?

A

maintain continuous contractile tone, and don’t contract phasically

  • accommodates arrival of meal w/o significant increase in intragastric pressure
  • -failure of mechanism causes bloating, epigastric pain, and nausea/dyspepsia
  • maintains constant compressive forces on contents of reservoir, pushing contents into antral pump region
  • if relax musculature (w/ insulin) would suppress gastric emptying
83
Q

what do muscles in the antral pump do?

A

contract phasically, propelling chyming towards gastroduodenal junction

  • strong waves generated 3/minute (set by ICC pacemaker)
  • propulsive and retropulsive forces grind/triturate stomach contents to reduce particle size
  • APs in antral pump are myogenic
  • nt released by musculomotor neurons change amplitude of platea phase of AP, thus strength of muscle contractions (ACh from PNS increase, NE from SNS decrease)
84
Q

what are the layers of muscle in stomach?

A

outer longitudinal, middle circular, and inner oblique muscle layers

85
Q

what is propulsion, grinding, and retropulsion of stomach?

A
  1. bolus pushed toward closed pylorus
    - contractions initiated by gastric pacemaker
    - increased pyloric resistance represents coordinated response of antral, pyloric, and duodenal motor activity
  2. churned to reduce size of particles, once a bolus is trapped near the antrum
  3. gastric contents returned to body for pulverization and shearing of solid particles
    - only a small portion of material less than 2 mm gets thru pyloric sphincter

Physiology (60 decks)

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