Physio E3: GI

4 layers of the GI (inner to outer)

mucosa, submucosa, muscularis, serosa

Which layer is the most variable zone?

mucosa

Mucosa consists of

epithelium: fold to increase SA

Exocrine and endocrine functions of the mucosa

exo: secrete mucous, elites, water, digestive enzymes

endo: release GI hormones into blood in response to changes in environment

Which hormone does the mucosa secrete in response to fat and protein in the gut lumen? is this endocrine or exocrine?

Cholecystokinin (CCK); endocrine

Submucosa consists of

connective tissue with major blood and lymphatic vessels

-contains submucosal (meissner) nerve plexus

Muscularis externa layer contains

two major smooth muscle layers

-inner circular layer, outer longitudinal layer

-contains myenteric (Auerbach) nerve plexus

Serosa makes up the ___

thin connective tissue layer

Control of GI requires coordination of what mechanisms?

neural, hormonal, paracrine

Control of what underlies gut motility?

smooth muscle

Most GI smooth muscle cells have what type of waves

slow waves: facilitate rhythmic smooth contractions

Smooth muscle contraction occur via

voltage-gated Ca channels (Ca entry and contraction)

Paralytic ileus

temporary cessation of gut motility

Enteric Nervous system is also known as the ___ and is a division of

gut brain; ANS

what is the ENS responsible for

most of moment-to-moment control of gut motility and secretion

Fx of the submuscosal plexus

coordinates intestinal absorption and secretion via innervation of epithelium, endocrine cells, and submucosal blood vessels

Fx of the myenteric plexus

control of gut motility and innervated longitudinal and circular smooth layers

ENS neurotransmitters

Ach, ATP, NO, Gut-brain peptides

Ach role

primary neurotransmitter, involved in stimulation of secretion and motility

ATP & NO role

inhibitory neurotransmitters

Where are gut-brain peptides found and an example

in ENS and CNS; Vasoactive intestinal peptide (VIP)

VIP role

potent stimulator of intestinal fluid and elyte secretion BUT inhibits motility —> allows time for absorption

How is the ENS linked with the CNS?

PNS/SNS nerves → gut brain axis

-CNS may send command signals → link GI activity w/ behavior

-sensory input to brain, fullness, satiety, nausea, pain

PNS afferents and efferents

aff: nausea, distension, satiety

eff: stimulation- intestinal mobility, exocrine secretion

SNS afferents and efferents

aff: pain

eff: inhibition - intestinal mobility

PNS innervation

vagus (upper GI) and sacral (s2-4)

vasovagal reflex -signals confined to vagus nerve

SNS innervation

postganglionic fibers innervate smooth muscle → vasoconstriction

inhibitory responses

Mast cells release ___ in response to foreign antigens

histamine

Which cells ‘taste’ the gut lumen?

enteroendocrine

before entering systemic circulation GI hormones must go through

the liver : first pass metabolism

GI hormones

Gastrin, Secretin, Cholecystokinin (CCK), Glucose dependent insulinotropic peptide (GIP)

Gastrin: stimulus, secretion, action

Stimulus: stomach expansion, protein, caffeine

Secretion: stomach mucous

Action: stimulate gastric acid production

Secretin: stimulus, secretion, action

Stimulus: acidic chyme in duodenum

Secretion: duodenum mucosa

Action: pancreatic juice secretion (contains bicarb to neutralize acidity)

CCK: stimulus, secretion, action

Stimulus: triglycerides, fatty acids, amino acids

Secretion: duodenum mucosa

Action: bile release, relax pancreatic sphincter (Odi)

GIP: stimulus, secretion, action

Stimulus: glucose, fatty acid, amino acids in the duodenum

Secretion: duodenum mucosa

Action: produce insulin, inhibit gastric juices

Paracrine control

hormone diffuses locally to affect target cells

-serotonin, somatostatin, histamine

Serotonin

produced by enterochromaffin cells in intestinal mucosa in response to distention of gut wall

-excitatory → increase motility and secretion

Somatostatin

produced by D cells and is potent INHIBITOR in GI system

-inhibits pancreatic & gastric secretion, relaxes stomach and gb, decrease nutrient absorption

-potent vasoconstrictor

Histamine

enterochromaffin-like cells

-stimulatory effect on acid secretion in stomach

Cimetidine is a H2 receptor blocker → volume and acidity of gastric juices are reduced

What 2 reflexes are you born with?

chewing/sucking

grasping

Mastication glands

parotid, submandibular, sublingual, tiny buccal

Saliva contains what type of anitbodies

IgA

Deglutition

swallowing

3 phases of deglutition

-oral

-pharyngeal

-esophageal

Oral (buccal) phase

voluntary; tongue pressing upwards against palate

Pharyngeal phase

involuntary; initiated by swallowing receptors in posterior oral cavity and oropharynx

Esophageal phase

controlled by swallowing center of brain, peristalsis via CNX

-primary peristalsis

-secondary peristalsis: residual food

Esophageal secretions

mucous glans to aid food passage

5 main areas of stomach

cardia, fundus, body, gastric antrum, pyloric sphincter

What make up the oxyntic (parietal) gland area

cardia, fundus, body

-MAJOR exocrine secretions derived from this area

Pyloric gland

distal 20% of stomach

-major source of Gastric hormones

Parietal (oxyntic) cells secrete

HCl and intrinsic factor (important for vit b12 absorption)

Peptic (chief) cells

Pepsinogen (inactive)

D Cells

somatostatin

G Cells (antrum)

gastrin

Gastric motor functions

reservoir for ingested food, followed by mixing/grinding of food prior to deliver to SI

Gastric exocrine Fx

Water: dissolve and dilute food

Acid (HCl): denature dietary PTN and kill ingested microorganisms

Enzymes (pepsin and gastric lipase): PTN and fat digestion

Intrinsic Factor: glycoprotein for Vit B12 absorption in ileum

Mucus-Bicarb Barrier: mucosal surface, protects against gastric juices

Gastric Endocrine Fx

gastrin, somatostatin, ghrelin

What causing the growling in your stomach when you’re hungry?

migrating motor complex

Antral systole

food mixed with gastric juice to reduce particle size

What is secreted in exchange for HCO3-

Cl

H+ is produced via

carbonic anhydrase

Stimulation of gastric acid production

neural stimulation via Vagus → Ach

Endocrine stimulation from Gastrin

Paracrine stimulation from Histamine

Prostaglandin E2: produced in stomach, antagonist of histamine by inhibiting production of cAMP

How do NSAIDS lead to stomach ulcers?

inhibit prostaglandin formation → increase gastric acid secretion

3 phases of regulation

Cephalic, Gastric, Intestinal

Pepsins

proteolytic enzymes that attack internal peptic bonds in proteins

conversion of pepsinogen to pepsin occurs when pH <5

-stimulated by Ach from vagal and ENS efferent neurons

Type 1 pepsinogen

oxyntic gland area

Type 2 pepsinogen

pyloric gland area

Gastric mucosal protection

prevents acid erosion of mucosa, neutralizes acid because HCO3- secreted from surface cell is trapped in mucous

In a crypt villus unit the oldest cells are found where?

Brush border; slough off after 3-4 days

cells are gradually forced upward

What increases the SA of the small intestine

Villi

-enterocytes, goblet cells, endocrine cells

How much fluid does the SI reabsorb every day

6-8 L

If food has a high water content and hypotonic to plasma

rapid water uptake

meal is hypertonic

water initially enters SI from ECF

Colon absorbs ___/2 L of fluid delivered to it

1.9

Secretions of the SI

Brunners glands

Crypts of Lieberkuhn

Brunner’s glands

duodenum; secrete alkaline mucous

+Ach, secretin, duodenal irritation

Crypts of Lieberkuhn

entire small intestine

-Goblet Cells

-Enterocytes

Goblet cells action

secrete mucous

Enterocytes action

secrete water and electrolytes

-reabsorbed over surfaces of adjacent villi

-continually undergo mitosis

-new cells migrate towards tip of villi

fluid secretion is needed for

lubrication, provide source of Na for coupling when intake is insufficient

Water secretion occurs via

osmosis

Key step of fluid secretion

opening Cl channels in luminal cell membrane

cAMP activated Cl channels → ENS VIP is important

Ca activated Cl channels → Ach from ENS and serotonin from EC cells

steatorrhea

fat in fecal matter

Digestion and absorption relation

digestion breaks down polymers (CHO, FAT, PTN) into monomers (nutrients) via hydrolysis rxns

Absorption: takes these nutrients into bloodstream to be used by cells

Vitamin absorption

cannot be synthesized

required for metabolism

Large intestine fxn

absorption of H2O, electrolytes, vit K, and some B vitamins

storage of feces

How are vitamin K and some B vitamins produced in the body?

via microbial organisms; body can’t make

Gut bacteria types

mostly anaerobic

-commensal: they benefit, neither harm nor benefit us

-mutualistic: both us and bacteria benefit

Microbe roles in LI

make vitamins, cellulose → fatty acids

outcompete harmful species of bacteria

Disruption of microflora can lead to

inflammatory bowel disease

What protect the LI from bacteria?

mucous from goblet cells

secretion of IgA antibodies by plasma cells

In the LI, Aldosterone stimulates

greater Na+, Cl-, H2O absorption

The need to defecate rises when

pressure increases → internal sphincter relaxes

What type of control is the external anal sphincter under

voluntary

feces composition

75% H2O; 25% solid matter