GI Mod 1 Flashcards
accessory organs of digestive system
liver, gallbladder, exocrine
4 layers of the GI tract
- mucosea
- submucosa
- muscularis
- adventitious (serosa)
3 parts of the mucosa layer of the GI tract
- mucosa epithelium
- lamina propria
- muscularis mucosae
what is the submucosa made up of in the GI tract
glands and associated ducts
what is the muscularis layer of the GI tract made up of
- circular layer
2. longitudinal layer
what is the adventitious (Serosa) layer of GI tract made up of
connective tissue
the enteric nervous system is considered part of which nervous system
ANS
the enteric nervous system functions ________ and influenced extrinsically via what nervous systems
- autonomously
- parasympathetic/sympathetic nervous systems
3 enteric plexuses
- submucosal plexus (Meissner plexus)
- located in submucosa - myenteric plexus (Auerbach plexus)
- located bw circular and longitudinal layers of muscularis - subserosal plexus
three general functional components of enteric plexuses
- sensory neurons monitor: distension and the chemical status of GI tract
- motor neurons control: motility of the gut wall, smooth muscle of GI vasculature, secretions of the mucosa/submucosa
- interneurons communication bw sensory and motor
definition of appetite
hunger
definition of satiety
sensation of fullness/satisfied
two centers that control appetite and satiety
lateral center and medial center
where are the two centers that control appetite and satiety located
hypothalamus
function of lateral center
(appetite center)
stimulate appetite
excitatory to hunger contractions in stomach
stimulus of lateral center
- smell (CN 1), visual, taste (CN 7&9), hearing (CN8)
- physiological depletion of nutrient/energy stores
- memory/fantasy - limbic/insular lobes
- gastric hormones
what gastric hormone stimulates appetite
ghrelin - hunger hormone - released from stomach
what is the function of the medial center
(satiety center)
suppress appetite
inhibitory to hunger contractions in stomach
stimuli of medial center
hormones:
- GI hormones - released during food ingestion (CCK,GLP) - short term
- Letpin - released by fat cells and chief cells
- PYY - released by SI after meal
- INsulin - released by pancreas after increase in blood glucose after meal
extrinsic regulation of the GI tract
sympathetic regulation and parasympathetic regulation
sympathetic regulation of the GI tract
- pathway
- function
pathway - nerves of sympathetic tract in thoracic and upper lumbar regions function - inhibitory to GI tract - decrease peristalsis and secretions, inhibit blood flow to GI tract
parasympathetic regulation of GI tract
pathway - vagus nerve (esophagus to transverse colon) and pelvic nerves of sacral plexus function - excitatory to GI tract - increase peristalsis and secretions, relax involuntary sphincters of GI tract, facilitate blood flow to GI tract
peristalsis require what two movements? how does the vagus nerve play into it?
requires contraction and relaxation
-vagus nerve has dual role on the smooth muscle of GI
structures of the GI tract
mouth, esophagus, stomach, SI, LI, rectum, anus
intrinsic regulation of the GI tract by?
enteric nervous system
how does the GI function autonomously
intrinsic system can feedback on itself - “brain in the gut”
two plexuses that are responsible for in the intrinsic regulation
- myenteric plexus (Auerbach’s) - controls motility
2. submucosal plexus (Meissner’s) - controls secretions and absorption
7 specific functions of the enteric nervous system
- controls motility - peristalsis/sphincter control
- regulation of fluid exchange and local GI blood flow
- regulation of gastric and pancreatic secretion
- regulations of gastrointestinal endocrine cells
- defense reactions
- entero-enteric reflexes
- ENS and CNS interaction
how does the enteric nervous system regulat fluid exchange and local GI blood flow
- regulates permeability to ions thus influencing fluid
- influences vasodilation of BC
- influences fluid secretion
how does the enteric nervous system regulate GI endocrine cells
can signal release of GI hormones
ex. excessive serotonin released from GI walls = nausea/vomit
examples of defense reactions of the enteric nervous system
vomit, diarrhea, exaggerated propulsive motility reflexes
what are the entero-enteric reflexes of the enteric nervous system
signaling system bw regions of the GI tract
- ex. gastric activity stimulates SI motility and relaxation of ileocecal valve
- ex. small intestine activity signals release of enzymes from pancreas
how many neurotransmitters exist in intrinsic nervous system of GI
2 functions and examples of each
20+
- ex’s: excite smooth muscle (contract): ACh and substance P
- ex’s: inhibit smooth muscle: nitric oxide & VIP (vasoactive intestinal peptide)
general function of extrinsic GI regulation
directly influences intrinsic system (parasympathetic - excitatory to GI motility and secretions; sympathetic - inhibitory to GI motility and secretions)
general function of intrinsic nervous system of GI
- myenteric plexus - located in muscular layers = controls motility
- submucosal plexus - located within/beneath mucosal layers so controls secretions
function of mouth
salivation
3 salivary glands of the mouth
submandibular
sublingual
parotid
autonomic control of saliva
both parasympathetic and sympathetic systems stimulate salivary glands - secretion of saliva IS NOT controlled by hormones
what does saliva contain? (3)
- water - with mucus, sodium, bicarb, chloride, and potassium (bicarbs maintain pH in mouth to neutralize bacteria = tooth decay)
- salivary amylase - digestion initiated in mouth, begins first steps of break down of carbs
- immunoglobulin A - prevents infection (animals lick their wounds)
hormones in obseity
Leptin: increased (resistance) - effectiveness may be blunted
ghrelin: decreased - body trying to tell brain its not hungry
*role of each not fully understood in obesity - pharmaceutical target
role of hormones in hunger
ghrelin - fast acting
- levels rise just before meals
- most circulating levels produced by stomach
- other roles: memory & sleep
roles of leptin in satiety
- long term role in energy balance and suppressing food intake
- released from fat cells
role of PYY in satiety
fast acting, counteracting role to ghrelin post feeding
-released from SI
3 portions of the esophagus
- upper third - striated (voluntary)
- middle third - mixed muscle
- lower third - smooth (involuntary) muscle
location of UES
junction of lower pharynx and esophagus
approx at level of cricoid cartilage
function of UES
prevent air from entering esophagus during ventilation
location of LES
narrowing of the esophagus proximal to the junction of esophagus and stomach
function of LES
barrier to reflux of the acidic content of the stomach
LES is maintained by what
increased smooth muscle tone
what is resting tone of LES
- LES smooth muscle tone increased to 20 mmHg
- belching: air pressure in stomach exceeds LES pressure
how does swallowing tie in with LES
LES smooth muscle to tone is relaxed
peristaltic wave relaxes smooth muscle of LES
where are the control centers for swallowing
located in brainstem (reticular formation)
-complex function requiring coordination bw digestive tract and respiratory system
phases of swallowing
- voluntary (oropharyngeal) phase chewing and pushed past uvula; soft palatte contracts to close nasopharynx
- pharyngeal phase - epiglottis closes off larynx/trachea 1-2 seconds
- esophageal phase - bolus enters esophagus and ends as bolus enteres stomach - 5-10sec
how is the bolus of food moved
peristalsis
role of insulin in satiety
fast acting, post feeding
released from pancreas
how is peristalis coordinated
contraction/relaxation of longitudinal/crcular muscles
what is the esophageal muscular pressure range
35 to 80 mmHg
differences in esophageal pressures by the three portions
- upper portion & lower - tend to be higher (60-80)
2. middle portion - lower pressure (30-45 mmHg)
what happens if esophageal pressure is
may leave food residue within esophagus
what is the effect of tension on esophageal movement?
what happens with intense contractions?
(distention of esophagus)
increases force of contractions
–intense contractions = substernal pain similar to angina/heartburn
control of peristalsis
requires complex coordinated signaling
- -parallel vagal inhibitory and excitatory pathways to coordinated
- -vagus nerve has both excitatory and inhibitory pathways to coordinate contraction/relaxation of esophageal peristalsis
what is primary peristalsis
normal peristaltic wave as bolus descends in esophagus
coordinated muscular activity of all phases of swallowing
-oral phase, pharyngeal peristalsis, UES relaxation, esophageal peristalsis, and LES relaxation
what is secondary peristalsis
food residue from ineffective primary peristalsis or a bolus that is stuck will cause addition or second peristaltic wave
-esophageal peristaltic wave only - DOES NOT incldue swallowing reflex
what does bolus/food residue distenetion cause
intrinsic feedback to:
- constrict esophagus above the distention
- relax esophagus below distention
- which pushes residue/bolus along
what happens when swallowing food
- a single swallow will initiate esophageal peristaltic contraction that lasts about 5-10 seconds short refractory period also follows peristaltic contraction (inhibits ability to swallow a second bite of food)
- in general: attempting to swallow food more frequently than 10-15 seconds is difficult because of inhibitory mechanisms
what happens when swallowing liquid
- normal drinking - swallow every 1-2 seconds
- the quick subsequent swallows create and inhibitory reflex that prevents the esophagus from ongoing contraction
- -this inhibitory reflex cause esophagus to stay relaxed to allow more liquid to descend - this will continue until the last swallow in a series of swallows - after which a full peristaltic contraction will occur
basal tone of LES is a net result of 3 factors
- myogenic tone that is independent of any neural input
- excitatory vagal tone (cholinergic)
- inhibitory vagal tone (nitrergic - NO)
what is deglutitive inhibition
inhibitory reflex triggered by quick subsequent swallows that prevent the esophagus from ongoing contraction
normal tone of UES
50 mmHg
factors that increase LES pressure
- vagus nerve influence - excitatory pathways of vagus nerve, cholinergic post gagnlionic neurons release ACh
- gastrin - in stomach promtoes acid secretion/motility so need to keepy LES closed
factors that decrease LES pressure
- vagus nerve influence
- hormones
- common foods/substances suggested to relax LES
how does vagus nerve decrease LES pressure
non cholinergic post gagnlionic neurons (stimulate NO and VIP release)
how do hormones decrease LES pressure
progesterone, secretin, glucagon
-progesterone levels elevated during pregnancy and second half of menstrual cycle - transient reflux may occur
what common foods decrease LES pressure
(relax LES)
-fried fatty foods, tomatoes, citrus, high protein diet, chocolate, peppermint, tobacco, alcohol, caffeine
what is GERD
gastroesophageal reflux dz
- decreased LES pressure and ineffective clearance mechanism of secondary peristaltic waves
- chronic acid reflux results in inflammation/pain and eventrual destruction of esophageal wall (esophagitis)
meds for GERD
- antacids - neutralize stomach acids
- histamine receptor blockers - decrease acid secretion histamine receptors
- proton pump inhibitors - stop acid secretion
- parasympathetic drugs - increase LES tone
what is Achalasia
(opposite of GERD)
- failure to relax = peristalsis of esophageal musculature + failure of LES to relax
- rare, causes pain with eating and drinking
- looks like cardiospasm, so rule out cardiac issues first
- unknown etiology thought to be defect of intrinsic esophagus plexus (loss of inhibitory neurons in esophageal layers)
treatment for achalasia
pneumatic dilation (stretch LES to relax) meds
what is esophageal varices
severely dilated sub mucosal veins in the esophagus
most often a consequence of portal HTN (common with cirrhosis)
pts have tendency to develop bleeding (chronic GI bleed can progress to severe systemic consequences)
what is barretts’s esophagus
where normal mature cells lining esophagus are replaced with abnormal cells due to exposure to stomach acids
-normal esophageal squamous epithelium is replaced by a spectrum of metaplastic columnar mucosa
what is metaplasia
one mature adult cell type is replaced by another type of mature cells
symptoms of barrett’s esophagus
metaplasia itself does not cause physical heartburn sytmpoms but is histological reflection of the chronic exposure to acid
–the stomach acid is the physical stimulus for heartburm symptoms
do all pts with GERD develop Barrett’s?
NO
what kind of cancer can develop with Barrett’s esophagus
adenocarcinoma
will all pts with Barrett’s esophagus develop cancer?
no
risk of cancer with Barrett’s esophagus
1:300
amunt of what in Barrett’s esophagus will increase risk of cancer
dysplasia
what is dysplasia
- abnormal development/matruation of cells
- delay/abnormal differentiation of cells results in number of immature cells
- often an indication of early neoplastic process
how does esophageal cancer rank among other cancers
8th most common
what % of esophageal cancers are adenocarcinmoa
50%
what population does adenocarcinoma affect
caucasian male
what % of population is afflicted with GERD
20% - in US and western Europe
what % of pts with Barrett’s esophagus deevlop adenocarcinoma each year
0.5-1%
pts with Barrett’s esophagus whould be monitored how often and with what procedure?
yearly with endoscopy and biopsy of the esophagus
