GI overview Flashcards
GI anatomy
Mouth
Salivary glands (submandibular and sublingual)
Esophagus (upper third-striated, lower 2/3 smooth)
Stomach
Pancrease (retroperitoneal)
Duodenum (5%)
Jejunum (45%)
Illeum (55%)
Ascending , transverse, descending, sigmoid, rectum
Large intestine ie colon
Right colon contains the cecum
Tenia coli is the longitudinal section of smooth muscle and haustra give the colon the segmented appearance
Sphincters and vlaves (tonic contraction)
Upper esophageal sphincter lower esophageal sphincter (acid reflux) Pylourus (passage from stomach to SI) Spincter of oddi( pancreatic and biliary juices into SI) ileocecal valve (SI to colon) internal anal sphincter External anal sphincteer
Organization of the GI tract
Mucosa (epithelium, lamina propria, muscalaris mucosa)
Submucosa (Meisseners/submucosal plexus)
Muscalaris propria (Circular muscle, auerbachs/myenteric plexus, and longitudinal muscle)
Serosa/Adventitia
Outer longitudinal smooth muscle and inner circular smooth muscle are located in the muscularis propria. The myenteric and submucosal plexus are enteric nervous system
Myenteric nerve plexus (auerbachs)- responsible for mixing and propagation functions. Located between longitudinal and circular muscle layers in muscularis propria
Submucosal nerve plexus (meissners plexus)- responsible for secretion and absorption at the mucosal level. Also responsible for blood flow at the mucosal and submucosal levels and has influence on neuro endocrine cells in the region
membrane potentials in the gi tract
baseline slow waves vary by location and dont cause contraction (except stomach)
slow waves are not action potentials
Things that depolarize the membrane potential (stretch, Ach, parasympathetics)
Things that hyperpolarize the membrane potential (sypathetics and norepinephrine)
Spikes occur on top of slow waves and are what cause the contractions (Phasic):
Occur only when threshold is reached, will continue as long as threshold is present, the more APs the stronger the contraction, due to influx of Ca NOT Na, longer lasting contractions compared to smooth muscle
GI muscle
functions as a syncytium
each region of the GI tract has underlying electrical activity that determines contraction rates (stomach =3, duodenum=12, ileum=8 per minute)
rate in each region dictated by interstitial cells of Cajal (pacemaker cells) which are located between the longitudinal and circular muscle layers
Nervous control of GI tract Parasym
Autonomic nervous system (parasympathetic (rest and digest)- increases GI activity and functions. Cranial division via vagus nuerve 10, and innervates until splenig flex. Sacral division via S234 to pelvic nerves and to distal colon to anus
postganglionic fibers end in enteric NS (myenteric and meisenners)
Nervous control of GI tract Sympathetic
When active inhibits GI functions
t5-L2, pre ganglionic fibers enter sypathetic chain. Post ganglionic fibers innervate the entire gut
Causes constriction of blood vessels to GI and divert blood
Reflexes in the GI tract
3 types of reflexes:
1) intragut reflexes (ENS): effect contraction and secretion, duodenal distention slows gastric emptying
2) gut to prevertebral sympathetic ganglia and back to gut (sympathetc). Duodenal distention inhibits gastric emptying via entero-gastric reflex. Cecal distension slows ileal emptying, colo-ileal relex
3. gut to CNS parasympathetic. Stomach to brain via vagus and back to stomach via vagus to allow for greater gastric accommodation, return to spinal cord and back to rectum defecation
Stimularoty substances made by myenteric: Ach, substance P
Inhibitory substances : VIP, NO (NO VIPs here)
Propulsive vs Mixing movements
propulsive-forward movement of contractile ring around gut wall (stimulus is distension of the wall (chemical, irritation), via ENS, ring forms and perastalsis starts. Intact, active myenteric plexus is mandatory, responses in retrograde direction normally die out very rapidly
Mixing movements: peristaltic against closed spincter. Constrictive: serves to shear and chop contents
GI hormones affecting motility and secretion
CCK (cholecystokinin)- released by duodenum and jejunum when fats are present. it slows gastric motility, causes gallbladder to contract to release bile to emulsify
Secretin: released by duodenum is response to acid present, slows gastric motility
GIP (gastric inhibitory peptide): Upper small intestine in response to presence of FAs, AA, and carbs to slow gastric motility
Villi structure and function
Villi are present in SI bc nutrients are absorbed there. The colon has large crypts but no villi bc nutrients are not absorbed in large intestine
The villus only gets 20% of the oxygen (80% goes to the viens and so its vulnerable to ischemia)
Splanchnic circulation
Liver has 2 blood supplies: 2/3 via portal vein, 1/3 via hepatic vein
GI blood flow
Neural Control: Parasympathetic NS increases flow. Sympathetics cause vasoconstriction
Local control: increased flow to intestinal wall and villi during absorption, increased flow factors (Dilators- CCK, VIP, gastrin and secretin). Release of kinins (kallidin and bradykinin) which as a whole induce vasodlation
