Digestion

You might also like

Download as pdf or txt
Download as pdf or txt
You are on page 1of 7

NOTES

NOTES
DIGESTION & ABSORPTION
DIGESTION & ABSORPTION ▫ Cranial nerves (mainly Vagus) activate
▪ Digestion: breakdown of large food muscles of pharynx, esophagus
molecules into monomers for absorption in ▫ Soft palate rises, closes nasopharynx,
gastrointestinal (GI) tract epiglottis covers larynx, upper
▪ Chemical digestion accomplished by esophageal sphincter relaxes →
enzymes secreted into alimentary canal by peristalsis moves food through pharynx,
glands esophagus → gastroesophageal
sphincter relaxes allowing food to enter
Mechanical digestion
▪ Mastication Two absorption pathways
▫ Mouth ingests food, begins mechanical, ▪ Cellular pathway: substance crosses apical/
chemical digestion (mastication, luminal membrane to enter intestinal
salivation), initiates propulsion by epithelial cell, then crosses basolateral
swallowing membrane to enter into blood
▫ Partly voluntary, partly reflexive (e.g. ▪ Paracellular pathway: move across tight
stretch reflexes, pressure inputs) junctions between intestinal epithelial cells
to enter blood
Deglutition (swallowing) ▪ Absorptive surface maximized by villi,
▪ Movement of food from mouth to stomach microvilli, folds (folds of Kerckring) in small
▪ Buccal phase: voluntary intestine
▫ Occurs in mouth ▫ Most digestion occurs in duodenum,
▫ Tongue pushes against hard palate least amount of digestion occurs in
forcing food bolus into oropharynx ileum (as reflected by length of villi -
longest villi in duodenum, shortest in
▪ Pharyngeal-esophageal phase: involuntary
ileum)
▫ Controlled by brainstem swallowing
▫ Brush border: surface of microvilli
center
containing digestive enzymes

OSMOSIS.ORG 325
HYDRATION
osms.it/hydration
▪ Total body water DEHYDRATION
▫ Intracellular fluid (inside cells) + ▪ Occurs when water loss > water intake
extracellular fluid (outside cells—e.g. ▪ Causes
blood, interstitium) ▫ Vigorous exercise, decreased oral intake,
▪ Water functions dry air, vomiting, diarrhea, excessive
▫ Bodily secretions, digestion, sweating, inability to swallow, diuretics
detoxification (urination), ▪ Symptoms
thermoregulation (sweating) ▫ Thirst, dry mouth/lips, nausea, fatigue,
▪ Total body water balanced by intake, lightheadedness, darkened/decreased
elimination urine
▪ High risk groups
Water intake
▫ Children: lower stores of water, ↑
▪ Water ingested in fluid/food form
surface area to body mass, thirst
▫ 80% → fluid; 20% → food sensors not fully developed, depend on
▪ Bloodstream absorption in small, large caregivers
intestines ▫ Elderly: decreased thirst sensation,
Water loss medication, chronic diseases affecting
kidneys
▪ Breathing; sweating; urinating, defecating

CARBOHYDRATES & SUGARS


osms.it/carbohydrates-and-sugars
DIGESTION 1,4-glycosidic bonds in starch yielding
disaccharides
Mouth
▫ Intestinal brush border enzymes: digest
▪ Begins carbohydrate digestion oligosaccharides, disaccharides →
▪ Enzyme: salivary alpha amylase lactose, maltose, sucrose → galactose,
▫ Starts starch digestion → dextrins, glucose, fructose; e.g. dextrinase,
maltose, maltotriose maltase, glucoamylase, lactase, sucrase

Stomach
▪ Salivary amylase inactivated
ABSORPTION
▪ Primary site of absorption: small intestine
▪ Relatively no breakdown of starch
Pathway of absorption
Small intestine
▪ Glucose, galactose: absorbed into
▪ Majority of carbohydrate digestion
enterocytes via sodium ion cotransport
▪ Enzymes include (secondary active transport) → GLUT2
▫ Pancreatic amylase: digests starch transporter extrudes glucose, galactose
→ disaccharides; hydrolyzes interior across basolateral membrane into blood

326 OSMOSIS.ORG
Chapter 39 Gastrointestinal Physiology: Digestion & Absorption

▫ Sodium-glucose cotransporter (SGLT1): in apical membrane → GLUT2 transporter


moves glucose inside enterocytes extrudes fructose across basolateral
against electrochemical gradient using membrane into blood; fructose absorption
ATP created from sodium gradient cannot occur against electrochemical
created by sodium-potassium ATPase gradient
on the basolateral membrane ▪ Monosaccharides leave epithelial cells via
▪ Fructose: absorbed into enterocytes via facilitated diffusion → enter villi capillaries
facilitated diffusion by GLUT5 transporter → hepatic portal vein → liver

Figure 39.1 Overview of the actions of some of the enzymes involved in carbohydrate digestion.

PROTEINS
osms.it/proteins
▪ Proteins can be absorbed in the form of (pepsin, trypsin, chymotrypsin)
amino acids, dipeptides, or tripeptides (as ▫ Exopeptidases: hydrolyze individual
opposed to carbohydrates) individual amino acids from carboxyl
end (carboxypeptidases A, B)
DIGESTION Small intestine
▪ Proteins → large polypeptides → smaller ▪ Pancreatic, intestinal brush border enzymes
polypeptides/peptides → individual amino continue digestion
acids/dipeptides/tripeptides
▪ Pancreatic enzymes
Stomach ▫ Zymogens: trypsinogen,
▪ Gastric pepsin (with HCl): digests proteins chymotrypsinogen,
→ large polypeptides procarboxypeptidase A, B
▫ Protein digestion starts with gastric ▫ Active forms: trypsin, chymotrypsin,
pepsin carboxypeptidase
▫ Secreted by chief cells, activated by low ▫ Enterokinase activates trypsinogen
pH → trypsin → trypsin autocatalyzes
▪ Proteases (endopeptidases, exopeptidases) itself, activates additional pancreatic
zymogens
▫ Endopeptidases: trypsin, chymotrypsin,
pepsin; hydrolyze interior peptide bonds

OSMOSIS.ORG 327
▫ Digest large polypeptides → small ▪ Dipeptides, tripeptides: absorbed into
polypeptides/peptides enterocytes via cotransport with protons →
▪ Intestinal brush border enzymes broken down into amino acids/transcytosis
▫ Dipeptidase, aminopeptidase,
carboxypeptidase NUCLEIC ACID DIGESTION &
▫ Digest small polypeptides/peptides → ABSORPTION
amino acids/dipeptides/tripeptides ▪ Nucleic acids → pentose sugars, nitrogen-
containing bases, phosphate ions
ABSORPTION ▪ Site of digestion: small intestine only
▪ Site of absorption: small intestine ▪ Enzymes
▫ Pancreatic ribonuclease,
Pathway of absorption deoxyribonucleases
▪ Amino acids: absorbed via cotransport with ▫ Intestinal brush border enzymes
sodium ions or facilitated diffusion out of (nucleosidases, phosphatases)
epithelial cells → enter villi capillaries → ▪ Site of absorption: small intestine
hepatic portal vein → liver
▪ Absorption pathway: active transport into
▫ Four separate transporters one each for enterocytes by membrane carriers → villi
neutral, acidic, basic amino acid capillaries → hepatic portal vein → liver

FATS
osms.it/fats
▪ Unemulsified triglycerides →
monoglycerides/diglycerides, fatty acids
▪ Site of digestion: mouth, stomach, small
intestine
▪ Lipid digestion begins with lingual, gastric
lipases hydrolyzing triglycerides → glycerol,
fatty acids
▫ CCK slows gastric emptying, allowing
adequate time for pancreatic enzymes
to work
▪ Pancreatic enzymes (pancreatic lipase,
cholesterol ester hydrolase, phospholipase
A2), colipase finish digestion in small
intestine
▫ Bile salts, lysolecithin surround, emulsify
dietary lipids to create large surface area
for pancreatic enzymes
▫ Pancreatic lipase secreted as active
enzyme, hydrolyzes triglyceride →
monoglyceride + 2 fatty acids
▫ Colipase (secreted as inactive
procolipase, activated by trypsin) binds Figure 39.2 Fats are comprised of glycerol
to pancreatic lipase protecting it from backbone and one or more fatty acid chains.
being inactivated by bile salts A few examples of fats shown above.

328 OSMOSIS.ORG
Chapter 39 Gastrointestinal Physiology: Digestion & Absorption

▫ Cholesterol ester hydrolase (secreted as Pathway of absorption


active enzyme) hydrolyzes cholesterol ▪ Fatty acids, monoglycerides absorbed via
ester → free cholesterol, fatty acids; ▫ Diffusion
hydrolyzes triglycerides → glycerol
▫ Fatty acids, monoglycerides leave
▫ Phospholipase A2 (secreted as micelles → enter epithelial cells →
proenzyme, activated by trypsin) triglyceride formation → chylomicrons
hydrolyzes phospholipids → lysolecithin, formation (fat globules plus surface
fatty acids apoproteins) → chylomicrons enter
▪ Final products of lipid digestion: lacteals → lymph in lacteal transports
monoglycerides, cholesterol, glycerol, fatty chylomicrons into systemic circulation
acids, lysolecithin ▪ Apoproteins are essential for absorption of
▫ Since products are hydrophobic (except chylomicrons (specifically Apo B)
glycerol),must be solubilized in micelles ▪ Short chain fatty acids diffuse into villi
before transport to enterocyte apical capillaries → hepatic portal vein → liver
membrane for absorption
▫ Micelles: products of lipid digestion
surrounded by bile salts
▪ Site of absorption: small intestine

Figure 39.3 Overview of the fat absorption pathway.


1. Fatty acids and monoglycerides leave micelles and
2. enter epithelial cells.
3. They form triglycerides.
4. Chylomicrons containing the fats are then formed.
5. The chylomicrons enter lacteals, and
6. are transported into systemic circulation.

OSMOSIS.ORG 329
VITAMINS
osms.it/vitamins
▪ With the exception of vitamin K, which is calcium binding protein → promotes
produced by intestinal bacteria, vitamins calcium absorption from small intestine
are not synthesized in body therefore must ▪ Decreased by: oxalic acid, tannins,
be attained by diet magnesium, phosphorus, phytates
▪ Increased by: acidic conditions in intestine,
Fat soluble (Vitamins A, D, E, K)
vitamin D, estrogen, lactose
▪ Location: small intestine
▪ Location: small intestine (primarily
▪ Mechanism: incorporated into micelles duodenum)
along with products of lipid digestion,
▪ Mechanism: vitamin D-dependent calcium
absorbed into enterocytes
binding protein
Water-soluble (B vitamins, vitamin C,
Absorption of iron
biotin, folic acid, nicotinic acid, pantothenic
acid) ▪ Location: small intestine
▪ Location: ileum ▪ Mechanism: ferric state (Fe3+) reduced
▪ Mechanism: cotransport with sodium → to ferrous state (Fe2+) → binds
(need intrinsic factor) except vitamin B12 apoferritin in enterocytes → transported
(cobalamin) across basolateral membrane → binds to
transferrin in blood → transferrin carries to
▪ Vitamin B12
liver
▫ Requires intrinsic factor
▫ Pathway: ingestion → stomach acidity The absorptive state: hormones
releases B12 from its food carrier ▪ Digested nutrients enter blood stream
proteins → free vitamin B12 binds to from intestines → blood glucose rises →
haptocorrin (R proteins) secreted by stimulation of pancreatic insulin release →
salivary glands (protects B12 from acid body cells increase glucose uptake reducing
degradation) → pancreatic proteases blood glucose concentration back to normal
degrade R proteins in duodenum → ▪ Hepatocytes
B12 binds to intrinsic factors (secreted ▫ Excess glucose → glycogen for storage
by gastric parietal cells) to protect it via glucose-6-phosphate intermediate
from pancreatic enzymes → intrinsic
▫ Amino acids → ketone bodies
factor-B12 complex resistant to
(converted to acetyl CoA if needed later)
degradation from pancreatic enzymes
→ absorbed in ileum ▪ Myocytes
▫ Excess glucose → glycogen for storage
Absorption of calcium via glucose-6-phosphate intermediate
▪ Active form of vitamin D, ▫ Amino acids → actin, myosin → muscle
1,25-dihydroxycholecalciferol, required for fibers
calcium absorption ▪ Adipocytes store excess lipids increasing
▪ Dietary vitamin D3 (cholecalciferol) is fat reserves
inactive
▪ Cholecalciferol → 25-hydroxycholecalciferol
(inactive) in liver →
1,25-dihydroxycholecalciferol in kidney
by 1alpha-hydroxylase → synthesizes
calbindin D-28K (vitamin D-dependent

330 OSMOSIS.ORG
Chapter 39 Gastrointestinal Physiology: Digestion & Absorption

INTESTINAL FLUID BALANCE


osms.it/intestinal-fluid-balance
▪ Along with nutrient digestion, GI tract re- ▪ H+ secreted into lumen + HCO3- secreted
absorbs large amounts of fluid, electrolytes into lumen (via Cl--HCO3- exchanger;
(Na+, Cl-, HCO3-, K+) not absorbed into blood) → Cl--HCO3-
▪ Small, large intestine together absorb exchanger, Na+-H+ exchanger → net NaCl
approximately 9L/2.38 gallons daily movement into cell → net NaCl absorption
▫ Diet → 2L/0.44 gallons; pancreatic, Colon
biliary, intestinal secretions → 7L/1.85
▪ Apical membrane contains Na+, K+ channels
gallons
▫ Approximately 100–200mL /0.03–0.06 ▪ Net Na+ absorption + K+ secretion
gallons) excreted in feces ▪ Aldosterone induces Na+ channel synthesis
▫ Absorptive mechanisms disrupted → → ↑ Na+ absorption, secondary to K+
diarrhea (enormous potential body- secretion
water, electrolyte loss ) Fluid, electrolyte secretion
Villi ▪ Epithelial cells lining crypts of small
▪ Line intestinal epithelial cells intestine → secrete fluid, electrolytes
(mucus, lubricating fluids assisting in
▫ First step: solute absorbed; second step:
mixing, digestion) → must also be absorbed
water follows
more distally
▫ Fluid absorbed = isosmotic (water,
▪ Electrolyte, fluid secretion route
solute absorption: parallel proportions)
▫ Small intestine: paracellular route →
▫ Similar to renal proximal tubule
“leaky” tight junctions (↓ resistance)
▫ Absorptive mechanisms vary by
▫ Colon: cellular route → “tight” tight
intestinal part
junctions (↑ resistance)
Jejunum ▪ Electrolyte, fluid secretion mechanism
▪ Major site of Na+ absorption ▫ Apical membrane: Cl- channel
▫ Enters epithelial cell → Na+-dependent ▫ Basolateral membrane: Na+-K+-2Cl-
coupled transporters on apical cotransporter (similar to thick ascending
membrane (Na+-monosaccharide loop of Henle)
cotransporters (Na+-glucose/ ▫ Na+, K+, Cl- ions move into cells from
Na+-galactose), Na+-amino acid blood → Cl- diffuses into lumen via
cotransporters, Na+-H+ exchanger) Cl- channel on apical membrane → Na+
▫ Translocates across basolateral follows Cl- passively, paracellularly →
membrane via Na+-K+ ATPase H2O secretion follows NaCl secretion
▫ H+ source (for Na+-H+ exchanger) = ▫ Apical Cl- channels closed in resting
intracellular CO2 + H2O → carbonic state → opens after various hormones/
anhydrase converts to H+, HCO3- → H+ neurotransmitters (ACh, VIP) bind
secreted into lumen → blood absorbs ▫ Bind to basolateral receptor → activate
HCO3- (“alkaline tide”) adenylyl cyclase → ↑ cAMP in crypt cells
→ cAMP opens Cl- channels
Ileum
▫ Adenylyl cyclase can be maximally
▪ Same transporters as jejunum + Cl--HCO3- activated in cholera → severe, life-
exchanger on apical membrane threatening diarrhea
▪ Cl- transporter in basolateral membrane

OSMOSIS.ORG 331

You might also like