parasympathetic (ACH, watery, more NaCl and HCO3, less K) and Sympathetic (NE, thick saliva, less Na)

Brainstem-> both symp and para triggered, salivation ↑.  parasympathetic > sumpathetic.

not: Enteric, Hormonal

In the GIT where are the

striated muscles

visceral smooth muscle

Striated Muscle:  pharynx, upper esophageal sphyncter, upper 1/3 esophageal body, and external anal sphyncter.  controlled by autonomic or somatic motor nerves

Smooth Muscle: everywhere else.  controlled by Sympathetic, parasympathetic, and enteric

Sphincters of GIT:

Upper Esophageal Sphincter

Lower Esophageal Sphincter

Pylorus

Ileocecal Sphincter

Internal Anal Sphincter

External Anal Sphyncter

UES: Skeletal Muscle, prevents food from entering esophagus when not swallowing, also prevents food from entering lungs

LES: Smooth Muscle, prevents food from stomach→Esophagus

Pylorus: Smooth Muscle, prevents Chyme from moving from Duodenum back to Stomach

Ileosesal Sphyncter: Smooth Muscle, prevents flow of fecal material from LI->SI

IAS: Smooth Muscle, prevents feces excretion

EAS: Skeletal Muscle, prevents involuntary excretion of feces.

Splanchnic Circulation

Parallel component

Series Component

Largest regional circulation in body, Largest Reservoir

Parallel: regulate BF to individual organs.  Celiac->Stomach, Superior Mesenteric->Jejunum, Inferior Mesenteric->Colon

Series: all venous blood enters liver first through portal vein.  good because pathogens/toxins filtered by kidney first.

postganglionic sympathetic nerves.

BF decreased by sympathetic control, but returns b/c acumulation of metabolic vasodilators

Salivary gland: increase secretion

Smooth Muscle: sphyncters constrict

Enteric Neurons: inhibit activity

Splanchnic arterioles: Constrict

Mucosa: inhibit electrolite/hormone secretion

Parasympathetic Nerves

Origination:

Termination:

Origination: Brainstem & sacral (pelvic) nerve

Termination:

Submandibular: more saliva secretion

abdominal accessory organs: increased

bile/digestive enzyme secretion

Enteric Ganglia: influences ENS activity

striated muscle: contraction during swallowing (innervated by vagus)

Enteric Neurons

Origination

Termination

Origination:

Myenteric plexus: mobility & tone

Submucosal Plexus: secretion/absorption, diameter, BF

Termination:

muscles: to contract/relax

Mucosal capillaries: regulate BF

Endocrine Cells: regulate secretion

1 bile acids made by hepatocytes from cholesterol

2 more bile acids returning by enterohepatic circulation, less bile made

3 fasting = low bile in portal blood, fed = high bile in portal blood

biliruben + albunin = unconjugated (OK)

biliruben + gluc = conjugated (bad)

• hemolitic anemia (RBC pop)
• low UGT1A1 activity (neonatal)

• plugged
• liver disorder

Esophagus

UES

Esphageal body

LES

UES: skeletal muscle.  constricts with ↑ ACH from Vagus.  relaxed from ↓ ACH

Body: skeletal top 1/3 smooth lower 2/3. no resting tone "flacid"

LES: Multy unit smooth, tone= ACH (from motor neurons) +NO (enteric inhib).  relax=more NO

Vagul Innervation of the Esophagus

Sriated muscle

Smooth Muscle

Striated:directly innervated by efferent Vagus (not post-ganglionic), motor end plate on muscle.

Smooth:Innervated indirectly by efferent vagus. vagus->myenteric motor neurons->smooth.

Deglutition (swallowing)

Oral

Pharyngeal

esophageal

1. Oral: voluntary.  food moved to oropharynx,

2. Pharyngeal: Involuntary.  starts when extrinsic nerves sense the food.  peristalsis moves food to esophageal body

3. esophageal: peristalsis moves food from esophageal body through LES to stomach.

Esophageal Peristalsis

Primary Peristalsis

Secondary Peristalsis

Primary Peristalsis: pushes food from esophageal body to stomach. Esophageal Peristalsis-> pharyngeal Peristalsis.  mediated by a long neural reflex

Secondary Peristalsis: clears esophagus of remaining or refluxed food.  (no pharyngeal peristalsis).  initiated by distension (stretch) of esophageal body.  short reflex.

Slow waves

• in smooth muscle of antrum, SI & LI. oscilates between E_m -40 to -80
• occurs regardless of phasic contraction (exept colon)
• determines phasic contraction frequency

ACH: ↑amplitude of slow wave= more likely AP = more frequent phasic contraction.  doesn't change slow wave frequency.

NE: ↓ amplitude of slow wave= less likely AP= less frequent phasic contraction.  doesn't change slow wave frequency.

SI: slow wave decreases from duodenum to jejunum  to move chyme

LI: slow wave increases from ascending to descending to retain feces

Stomach

Orad

Caudad

Orad: acepts food, receptive relaxation, stores chyme.

Caudad: regulates rate of emptying of contents.  sieving and retropulsion.  emulsifys fats.

• The orad stomach is distended (filled)

• The strength of peristaltic contractions of the caudal stomach is increased
• The diamater of the pyloris is increased
• Segmenting contractions of the proximal duodenum are inhibited
• Parasympathetic nerves are increased
• Sympathetic nerves are decreased

Influencing gastric emptying

stomach

Duodenum

Stomach: small liquids faster than large fats,

Duodenum: substances in duodenum ↓ gastric emptying through short & long.  Acidic-> secretin.  fat-> CCk,

Segmentation: mixing, short distance, non propulsive

Peristalsis: propulsive movement.  relax circular muscle, contract longitudinal muscle behind the chyme. 

both SI and LI movement can be influenced by hormones, paracrines, NT released from autonomic nerves.

increasing intestinal motility

decreasing intestinal motility

increase:

Gastrin: hormones from G cells in gastric mucosa

Motilin: hormone from endocrine cells of SI mucosa interdigestive period only

ACH

Decrease:

EPP/NE: activates SNS

Opioids: cause constipation, lowers Seratonin release from neurons

Somatostatin: Paracrine released from endocrine cells of GIT

empty SI, fasting state

clears out the gastric antrum, and SI only

phase 1:no contraction (longest phase)

phase 2: irregular contractions

phase 3: 3-6 mins of intense phasic contractions.  emptys undigested particles

when fed, will switch back through long neural reflex.

Motilin

Tenia Coli: concentrated longitudinal smooth muscle cecum-> rectum.  at rectum the bands spread out

Haustra: bulges of tenia coli where longitudinal muscle is thin

IAS: thick smooth muscle

EAS: Skeletal Muscle

IAS: short & long reflex.  distensed rectum relaxes sphyncter recto-anal inhibitory reflex

EAS: conscious control.  regardless of distension of rectum.

rectum usually empty because of retropulsion

when rectum distensed, IAS relaxes Recto anal inhibitor reflex.

decreases transit time, so less constipation.

increased stool water content,

increased stool weight

stimulates motility by stretching colon wall

absorbs fats

pepsin digests duodenal protein -> peptides

exopeptidase turns proteins -> AA

high CCK causes

long chain FFA-> I cells

• pancreatic secretion
• raise gastric emptying
• bicard secretion
• open sphyncter of oddi
• contract galbladder/secrete bile
• release exoproteins/exopeptidase

↑ conjugated

↔ unconjugated

Chylomicrons

enterocyte-> lymphatic-> venous circulation

• tryglyceride+cholesterol
• beta lipoprotein coat before-> lacteals

micells

absord in lumen of GIT

• bile acid + LCFFA

Interdigestive period

MAX

• new bile

• somatostatin

Gastric Phase

Max

• Gastric acid
• plasma gastrin

Early intestinal phase

Max

• pancreatic bicarb
• contraction of gallbladder

• plasma CCK & secretin

Late intestinal phase

Max

• bile acids in portal blood
• secretion of bile acids by the liver
• absorption of water & electrolytes in colon

• Trypsin
• endopeptidase
• exopeptidase
• Brush border enzymes
• Cytoplasmic enzymes
• Enterokinase

Trypsin

Bile acids

pancreatic colipase

pancreatic lipase

Enterokinase

SGLUT1

SGLUT1: glucose or galactose. 

lumen-> enterocytes.

NA/K ATPase.

• ↑ Gastric mucous secretion
• ↑ Gastric mucosal bicarb secretion
• ↑ Gastric BF

• ↓ Gastric acid

SI secrete

SI Absorb

SI secrete: Electrogenic chloride secretion

SI Absorb: Na gradient.

• salivate
• relax LES

entero-hepatic circulation of bile acids is interrupted

no ilium

disease: ↑ fasting bile acids

no ileum: make new bile

↑ jejunum phasic contraction

↑ duodenum motility

SGLUT2: glucose and galactose

enterocyte-> interstitial space

GLUT5: Fructose

lumen-> enterocyte-> interstitial space.

Saliva, and flow rates

slow

fast

Aldosterone

saliva is always hypotonic

slow: ductal reabsorb most NaCl, net low NaCl, high K HCO3

Fast: Higher NaCl and HCO3, lower K

Layers of the GIT

Circular Muscle Layer

Longitudinal Muscle Layer

Mucosa

Myenteric Plexus

Submucosal Plexus

Circular Muscle Layer: determines radius of tube.  (innermost) (circumference)

Longitudinal Muscle Layer: determines "anterior-posterior dimensions of the tube" (outside of circular muscle layer) (length)

Mucosa: has Mucosal Capillaries, Enterocytes, Endocrine Cells, Lymph Vessels

Myenteric Plexus: enteric neuron plexus, controls motility & tone of smooth muscle in GI sphincters (between circular & longitudinal)

Submucosal Plexus: enteric neuron plexus controls secretion/absorption of nutrients and electrolites and mucosal BF. (between ucosa & circular)

Sympathetic nerve innervation/origination at GIT

Esophagus:

Stomach:

Jejunum:

Colon

Esophagus: Superior Cervical Ganglia

Stomach: Celiac Ganglia

Jejunum: Superior Mesenteric Ganglia

Colon: Inferior Mesenteric Ganglia

primary bile acids

secondary bile acids

primary: made in hepatocytes.  changed by glycene/taurine.

secondary: made in lumen of colon by bacteria

bile acids from liver -> gallbladder -> duodenum -> ileum/colon-> portal vein-> liver.

pasive: lipophylic bile acids (secondary bile acids) absorbed from colon to enterocytes

Active: water soluble bile acids (primary)  ileum -> enterocyte by Na dependent. 

in liver portal blood-> hepatocyte by Na dependent.

hepatocytes-> canaliculi by ATP dependent protein.

Interstitial cells of Cajal

(ICC)

• at walls of GIT.  conected to each other, and smooth muscles by GAP junctions for electrical signals

• generates frequency of slow wave
• ICC not effected by external forces.

controled in brainstem. 

1. bulged stomach->Seratonin release from enterochromaffin cells.  afferent vagal nerves are activated

2. Emetic chemicals released->activates afferent chemoreceptors

3. chemicals trigger brain "chemoreceptor trigger zone.

4. tactile receptors in the pharynx

5. vestibular system

6. higher emotional brain centers

autonomic nerves

parasympathetic vagus nerve: innervate cecum, ascending colon, transverse colon

Pelvic nerve: parasympathetic efferent nerves innervate descending colon, sigmoid colon, rectum.

Sympathetic nerves: innervate entire colon

Enteric Neurons: myenteric innervates smooth muscle, submucosal innervates mucosa of entire colon

EAS: innervated by pudendal nerve (somatic control)

Haustral Shuttling: haustral appear/dissapear b/c contractions of tenia coli & circular muscle.  to mix contents.  no net movement, to absorb water and electrolites.(

Haustral Propulsion: adjacent haustral contract together, contents, move.  fast short movements.

multihaustral Propulsion: many haustra, net abnormal movement.  medium distance

Haustral retropulsion: moved orally.  med distance

Mass movement: strong contraction of circular muscle and tenia coli.  long distance.  fae occurence.

colon no MMC, no motility change during fasting

Cecum/ascending/transverse colon:

haustral shuttling, haustral propulsion, mass movement ascending and transverse only

Descending and sigmoid colon:

slower movement because dehydrated.  haustral shutling, haustral retropulsion, mass movement

Rectum: Haustral retropulsion pushes out, mass movement brings in

wanting to deficate 30 mins after eating

rapid: gastric distension activates long parasympathetic vagus (afferent) and pelvic (efferent).  more pelvic nerve activity increases colonic motility through enteric motor neurons

Slow Component: gastrin release (short) increases colonic motility

Short:

when IPANS activated by rectal distension, increase haustral propulsion in descending, sigmoid, and rectum

increased intraluminal pressure in descending, sigmoid, and rectum

relax the IAS

Long: same as short, triggered by parasympathetic pelvic afferents by rectal distension

Pudendal Nerve: EAS consciously relaxed.

Gastrin

Type

From

Stimulus

Action

Type: Hormone

From: G cells of gastric mucosa

Stimulus: GRP & ACE from enteric neurons, protein digested products , gasric distension

Action: ↑ HCl, intrinsic factor, histamine, motility, starts gastrocolonic reflex,

Histamine

Type

From

Stimulus

Action

Type: Paracrine

From: ECL cells from gastric mucosa

Stimulus: Gastrin

Action: ↑ HCl and Intrinsic factor, inhibit somatostatin secretion

Somatostatin

Type

From

Stimulus

Action

Type: Paracrine

From: D cells of Gastric Mucosa

Stimulus: PH <3 in gastric lumen

Action: inhibit HCl, intrinsic factor, histamine & gastrins

Motilin

Type

From

Stimulus

Action

Type: Hormone

From: Endocrine cells of SI mucosa

Stimulus: unknown

Action: increase % of slow waves with AP during MMC

Secretin

Type

From

Stimulus

Action

Type: Hormone

From: S cells of SI mucosa

Stimulus: H in  SI

Action: ↑↑ bicarb from pancreas, ↑ pancreatic enzyme secretion, hepatic bicarb secretion, cAMP.  ↓  HCl secretion, gastric emptying.

rectoanal reflex

rapid

slow

inhibitory

Rapid: gastric distension -> long neural reflex -> (parasympathetic vagus afferent) (pelvic efferent activats motor neurons)

Slow: gastric distension -> short to release gastrin -> gastric motility

Inhibitory: feces enters rectum -> rectum increased pressure -> relax internal anal sphyncter (NO)as rectal P ↓, IAS P ↑

Amylase

Lipase

Proteolytic

Enterokinase

Parasympathetic

Sympathetic

CCK

Amylase: digest carbs (Active)

Lipase: digest fats (Active)

Proteolytic: digest proteins (inactive)

Enterokinase: Trypsinogen -> Trypsin

Parasympathetic: vaguc nerve, ↑ secretion

Sympathetic: ↓ secretion b/c ↓ BF

CCK: CCK (↑ Ca) + Secretin (↑ cAMP) = synergistically ↑ pancreatic exocrine secretion

CCK

Type

From

Stimulus

Action

Type: Hormone

From: I cells of SI mucosa

Stimulus: Fats in SI

Action: contracts gallbladder, relaxes sphincter of oddi, ↑↑ pancreatic enzymes, ↑ pancreatic  bicarb, Ca.  ↓ gastric emptying

Vasoactive Intestinal Peptide (VIP)

Type

From

Stimulus

Action

Type: Neurocrine

From: Enteric Neurons

Stimulus: Short Neural Reflexes

Action: ↑ electrogenic chloride secretion by SI enterocytes.

UES

Type of muscle

Innervated by

Constriction

Relaxation

Swallowing

Type: Skeletal Muscle

Innervated by: Vagus Nerve directly

Constriction: ACH

Relaxation: less ACH

Swalowing: oropharynx sensory nerves -> Cranial nerve -> brain -> Vagus -> ↓ ACH to open sphyncter -> ↑ ACH for paristalsis

LES

Muscle type

Innervated by

Constriction

Relaxation

Swallowing

Type: smooth muscle

Innervated by: tonic input from motor neurons indirect

Constriction: ACH

Relaxation: NO

Swalowing: dorsal motor neucleus -> myenteric plexus -> ↑ ACH for paristalsis -> ↑ NO to open Sphyncter, receptive relaxation

Effects on phasic contraction

Gastrin

ACE

Motilin

ACE Inhib

EP/NE

Opioids

Somatostatin

Gastrin: increase

ACE: increase

Motilin: increase (MMC ONLY!)

ACE Inhib: Decrease

EP/NE: Decrease

Opioids: Decrease

Somatostatin: Decrease

Salivary secretion

Parasympathetic

Sympathetic

fast

slow

Aldosterone

sense -> brain -> Nicotinic -> muscarinic

Parasympathetic: ACH.  watery

Sympathetic: NE. thick

fast: (P) More NaCl and Bicarb, less K

Slow: (S) Less NaCl, more Bicarb and K

Aldosterone: ductal absorbs more Na, release more K, flow not changed

Gastric acid secretion

1

2

3

4

5

1. Apical of parietal cells has a H/K ATPase to bring K in, H out

2. H for the pump is from carbonic anhydrase (bicarb traded for Cl)

3. basolateral membrane cl exchanged for bicarb

4. HCl secretion followed by diffusion

5. rate limiting is HCl