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DT 53

1. MUCOSA:epithelium lamina propria: muscularis mucosae exocrine cells endocrine/paracrine cells

2.SUBMUCOSA connective tissue,

blood vessels, glands submucosal plexus(Meissners plexus)

SUBMUCOSAL PLEXUS

(MEISSNERS PLEXUS)

MYENTERIC PLEXUS

(AUERBACHS PLEXUS)

CIRCULAR MUSCLE

LONGITUDINAL MUSCLE

3.MUSCULARIS EXTERNA smooth muscle cell layer

inner circular layerouter longitudinal layer

myenteric nerve plexus (Auerbachs plexus)

4. SEROSA(adventitia)

Movement of materials along the digestive tract is

controlled by:

Hormonal mechanisms

Enhance or inhibit smooth muscle contraction

Neural mechanisms

ANS- Parasympathetic nerves(Vagus nerve,

Pelvic n.) - Sympathetic nerves (T6-12)

Enteric nervous system

- Submucosal plexus

- Myenteric plexus, receptors

Local mechanisms

Coordinate response to changes in pH or

chemical stimuli

Control of the digestive system

Intrinsic Nervous System

(gut brain)

Nerves that interconnect within GI organs and

plexuses, independent of the autonomic system.

Auerbachs, Meissners plexus contribute!

Receptor neurons are sensory (detect stretch,

damage), effector neurons are motor (cause SM

contraction)

Excitatory NTs- Ach, Subs.P ( contraction )

Inhibitory NTs- VIP , NO (relaxation of smooth

muscle)

The rate of basal electric rhyth (BER) is about

4/min in the stomach.It is about 12/min in the

duodenum and falls to about 8/min in the distal

ileum.

After vagotomy of the stomach wall, peristalsis in

the stomach becomes irregular .

MMC (migrating motor complex or interdigestive

myoelectric motor complex ) : !"#$%&"antrum '()

# 2 2 2

Deglutition (swallowing) begins as voluntary

activity

Oral phase is voluntary & forms a food bolus

Pharyngeal & esophageal phases are involuntary

cannot be stopped

continued

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swallowing (not after

vagotomy)

2 o Peristalsis:

Caused by residual

food in esophagus

Vagal nuclei run the

show (ambiguus,

DMN)

decreased salivation

Digitalis increased concentration of calcium &

potassium in saliva

Addisons disease- increased salivary sodium

Cushings syndrome, aldosteronism, pregnancy -

decreased salivary sodium

Tumors of mouth or esophagus, Parkinsons disease

- excessive salivation

Peristalsis propels

food thru GI tract

= wave-like muscularcontractions

After food passesinto stomach, thegastroesophageal

sphincter constricts,preventing reflux

continued

Fig 18.4

18-23

ORAL CAVITY

NEUROLOGICAL CONTROL

Hormonal Control

- Gastrin 01 9! : $ 0% 15 (& ;

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++

++

E

pH

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Ileogastric reflex decreases gastric motility inresponse to distension of ileum

Intestino-intestinal reflex causes relaxation ofrest of intestine when any part is overdistended

PANCREATIC AND BILLIARY SECRETIONS

Acinar cell +&A CCK

HCO3- + H+ = H20 + CO2

CCK

SecretinHCO

3

Fluid sec

gallbladder

bile

digestiveenzyme s

Pancrea

emptying

bile volume

Fat induodenum

Low pHin

duodenum

weak effect

Major digestive enzymes: acinar cells

- amylase

- lipase, colipase

- prophospholipase

- trypsinogen (autocatalytic)

- trypsin inhibitors

- chymotrypsinogen

- proelastase

- procarboxypeptidase

- RNAase, DNAase

Cleave peptide bonds

Categories of Pancreatic Enzymes

Proteases

Bile production

Salts emulsify fats, contain pigments asbilirubin

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y ro yze

Collagen digestion

Phospholipids to fatty acids

Triglycerides to fatty acids+

glycerol

Starch to maltose + glucose

Elastases

Phospholipases

Lipases

Amylase

Glycogen, fat, vitamins, copper and iron

Nutrient interconversion

Detoxification

Hepatocytes remove ammonia and convert tourea

Phagocytosis

Kupffer cells phagocytize worn-out and dyingred and white blood cells, some bacteria

Synthesis

Albumins, fibrinogen, globulins, heparin,clotting factors

Bile acids are derivatives of cholesterol.

Primary bile acids made in liver, converted to

secondary bile acids by enteric bacteria

95% of bile acids are absorbed by ileum.

Principal bile acids are:

Cholic acid.

Chenodeoxycholic acid.

Combine with glycine or taurine to form bile salts.

Bile salts aggregate as micelles.

Bile pigment

Free bilirubin combines with glucuronic acid and

forms conjugated bilirubin.

Secreted into bile.

Converted by bacteria in intestine to urobilinogen.

Urobilinogen is absorbed by intestine and enters

the hepatic vein.

Recycled, or filtered by kidneys and excreted in

urine. ( forms urobilin by oxidation on exposure

to air )

Urobilinogen enter the faeces darkening them

( refered to as stercobilinogen, which is oxidized to

stercobilin on exposure to air).

Absorption mechanism of monosaccharides

Digestion by brush border enzymes occurs in close vicinity

to monosaccharide transporters.

Glucose and galactose: SGLT1absorption via a secondary active (uphill), Na-dependent transport

Fructose: GLUT5absorption by facilitated (carrier mediated), Na-independent mechanism

ATP

Na +

Galactose

Glucose

Fructose

Brush

border

K +

2GLUT5

mu

cap

GItract

lumen

SGLT1 sodium-glucose transport protein1 for glucose and galactose

(secondary active transport)

GLUT5 transportprotein ratherspecific forfructose (facilitated transport)

GLUT2 t ranspor tp rote in fo rg lucose, f ruc tose and galactose across

b as ol at er al m em br an e ( fa ci li ta te d t ra ns po rt )

Galactose

Glucose

Na +

Fructose

GLUT2

SGLT1

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Lactose intolerance

(hypolactasia)

Decline lactase with age

Lactose fermented in colon

Gas and volatile FA

Water retention

diarrhea

Not all populations

Northern European low

incidence

Asian/African Americans

High

b 1-4 linkage

Proteins

Digestion and AbsorptionDigestion

Stomach

peptidases denature in stomach.

Pancreas and small intestine

hydrolyze with brush border enzymes

cleave between different amino acids

Endopeptidases ( trypsin, chymotrypsin, elastase ) break bonds

in middle of protein

Exopeptidases ( carboxypeptidase, aminopeptidase ) cleave

peptide bonds from ends of polypeptides

Carboxypeptidase - breaks apart carboxyl end of protein

Brush border enzymes aminopeptidases,

carboxypeptidases, and dipeptidases

Proteins Absorption

- small intestine, into blood capillaries

- amino acids by Na+ linked cotransport, di- & tri-peptides by H+

linked cotransport at luminal border

- peptides hydrolyzed in intestinal cell

- amino acids by facilitated diffusion at basolateral membrane

* secreted as inactive precursor moving down concentration gradient

into capillaries then onto the liver

Fats

monoglycerides diffuse into

cells

leave micelles behind

micelles are recycled

until run out of fats

Cholymicrons

coated with protein to

prevent sticking together

combine with apoproteins

- proteins carriers to become

soluble

lipoproteins are made in the

liver = HDL's, LDL's,

VLDL's

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