GASTROINTESTINAL

SYSTEM
 PHASES OF NUTRITION

R
 INTAKE E
G
 MECHANICAL PROCESSING U
 FORWARDING L
A
 DIGESTION T
I
 ABSORPTION O
 ELIMINATION OF USELESS COMPONENTS N
 NUTRIENTS
STRUCTURAL ELEMENTS – FUEL SOURCE

 Proteins  Lipids
 Built up of 20 amino acids  Glycerine + fatty acids
 Essential amino acids: (saturated, unsaturated)
• Arginine  Essential fatty acids
• Isoleucine • Linolic acid
• Histidine • Linolenic acid
• Leucine • Arachidonic acid
• Lisine  Use
• Methionine • Source of energy (neutral
• Phenylalanine lipids)
• Treonine • Membrane constituents
• Triptophan In childhood (phospholipids, cholesterine)
• Valine • Bile acids (digestion)
 Mostly structural • Synthesis of hormones
(cholesterine)
 Physiologic minimume: 40 g/d
• Vitamins, absorption of
 Optimal: 80 g/d vitamins
• Cerebrosides
 NUTRIENTS (CONT.)

 Carbohydrates  Vitamin
 Monosacharides  Inorganic components
• Hexose (glucose, fructose)
• Pentose (ribose, desoxyribose)  water
• Triose (gycerine aldechyde)  Other small organic
 Disacharides compounds (i.e.
• Lactose
• Maltose
alkaloids, etc.)
• Sacharose  Fibers
 Polysacharides
• Starch
• Glycogen
• Cellulose
• Dextrane
• Pectine
• Heparine
 Mostly source of energy
 GASTRO-
INTESTINAL EPIGLOTTIS

TONGUE

TRACT SALIVARY GLANDS

TEETH

ESOPHAGUS

PANCREAS

LIVER STOMACH

GALL BLADDER

LARGE INTESTINE SMALL INTESTINE

RECTUM

ANUS (R.M.Pool ed.. The Incredible Machine)

(W.F.Genong: Review of Medical Physiology.)
 INTAKE OF NOURISHMENT
 Appetite
 Voluntary food intake – cortical regulation
 Hypothalamic regulation:
• Feeding center (ventrolateral nucleus)
• Satiety center (ventromedial nucleus)
 Exogenous and endogenous stimuli - hunger
 Cephalic phase of regulation of digestion
• Saliva secretion 
• HCl secretion in the stomach 
• Stomach motility
• Pancreatic and bile secretion 
INTAKE AND FORWARDING OF NOURISHMENT
 Physical digestion
 Mastication
• Bite – voluntary
• Chewing – myotatic reflex
 Secretion (water, HCl, etc)
 Wall motility
 Chemical digestion – digestive enzymes (later)
 Taste receptors
 Formation of saliva
 Salivary glands
• Parotide glands (serous)
• Submandibular glands (mixed)
• Sublingual glands (mucous)
 Saliva (1.5 L/d)
• Mucine
• Lysozym
• Digestive enzymes
 Lingual lipase
 Salivary -amylase (ptyalin)
 Bolus
 Salivary gland

Serous
chambers

Mucous
chambers

Submandibular gland (Rölich: Szövettan, 1999.)

Fat degrading enzyme in the saliva
A. ptyalin
B. maltase
C. lactase
D. lingual lipase
___ E. Aminopeptidase
FORWARDING OF NOURISHMENT
 Swallowing (deglutition)
 Initiated by voluntary action
 Followed by reflex movements
 Complex process (involving the tongue, pharynx, epiglottis,
esophagus, etc)
 Receptors: mouth, pharynx
 Center: brainstem
 Nerves: afferent - trigeminal, glossopharingeal and vagus
efferent – facial, trigeminal and hypoglossal
 Esophagus
 Proximal third – striated muscle
 Distal two third – smooth muscle
 Peristalsis
 Active process
 Lower esophageal sphincter (LES) – tonic activity
 STOMACH Longitudinal
smooth
fundus muscles
cardia
esophagus
Circular
smooth
corpus muscles

curvatura minor (body)

pylorus
pylorus

curvatura
major

duodenum antrum Diagonal

smooth
muscles
 STOMACH
 Function
• Storage
• Mixing
• Secretion
 Gastric juice – approx. 2.5 L/d
 Hydrochloric acid – parietal cells
 Pepsinogen – (pepsin) – chief cells
 Gastrin – G cells
• Digestion Gastric tissues are
protected by mucosal barrier
• Forwarding to the duodenum (mucin + HCO3-

 Content: chyme
Molecular physiology of Gastric pits

the stomach
Neck
mucous
cells (mucin,)

Lumen

Parietal cells
(HCl)

(W.F.Genong: Review of Medical Physiology.)

Chief cells
(pepsinogen

Tunica mucosa with fundus glands (Rölich: Szövettan, 1999.)

REGULATION OF STOMACH FUNCTION
 Cephalic phase
• Sympathetic 
• Parasimpathetic 
 Gastric phase
• Afferents: baro and chemoreceptors
• Local reflexes (submucous [Meissner’s] plexus)
• Efferents
• Parietal cell G-cell Chief cell

HCl gastrin pepsinogen

 Intestinal phase
• Feed back
• CCK-stimulates, secretin, GIP, VIP inhibits acid secretion
One or more than one of the answers may be correct Select
A if 1,2 and 3 are correct
B if 1 and 3 are correct
C if 2 and 4 are correct
D if only 4 is correct
E if all are correct

Secreted by stomach wall cells

1. HCl
2. gastrin
3. pepsinogen
____ 4. bile

Select the single incorrect answer

Stomach functions
A. mixing
B. production of pepsinogen
C. production of bile
D. storage
___ E. production of HCl
Damaging and protective agents at
the mucous membrane of stomach
 Damaging  Protective
 HCl  Mucus secretion
 Pepsins  Normal stomach motility
 Decreased mucus  Intact mucous barrier
secretion  Inhibition of HCl secretion
 Disturbances of emptying (secretin, GIP,
 Bile reflux somatostatine)
 Decreased mucous barrier
(H. pylorí, drugs)
 Decreased perfusion
 Mental effects
 Increased gastrine
production
GASTROINTESTINAL HORMONES
 Gastrin
 Cholecystokinin-pancreozymine (CCK-PZ)
 Secretin
 GIP (glucose-dependent insulinotropic polypeptide)
 VIP (vasoactive intestinal polypeptide)
 Motilin
 Neurotensin
 Substance P (SP)
 Neuropeptid Y (NPY)
 Somatostatin (SST)
 Ghrelin
 Bombesin
 GASTROINTESTINAL HORMONES
Peptide Secretion Effect
Gastrin G-cells, antrum HCl, pepsin 
CCK-PZ Duodenum Gall bladder contraction, bile, HCl , pancreatic
(cholecystokinine-
pancreozimine) secretion 
Secretin Duodenum Pancreatic bnicarbonate secretion 
GIP (glucose- Duodenum Stomach secretion and motility , pancreatic
dependent insulinotropic
polypeptide) secretion 
VIP (vasoactive Duodenum Vasodilation , stomach secretion , absorbtion
intestinal polypeptide) of water and electrolites 
Motilin GI tract Contraction of smooth muscle
Glucagon Pancreas, small intestine Blood glucose 
SP (Substance P) Small intestine Motility of small intestine 
NPY (neuropeptide Y) Small intestine Food intake 
SST (somatostatine) Small intestine Secretion 
Ghrelin Stomach Food intake, growth hormone secretion 
GRP (Bombesin) Vagal nerve endings Gastrin
 SMALL INTESTINE
 Duodenum (30 cm)
 Jejunum (120 cm)
 Ileum (180 cm)
 Intestinal content:
• Chyme from stomach
• Bile
• Pancreatic juice
• IgA
• Epithelial cells
• Secretion (Brunner glands)
 Mucous membrane (increased
surface for absorption)
 Cicular folds
 Villi
 Brush border (microvilli on the apical
surface)
 Mucosal cells: enterocytes
 Intestinal juice
• 10-20 L/d
• pH7,2-7,6 Villi of the small intestine
(R.M.Pool ed.. The Incredible Machine)
SMALL INTESTINE-ABSORPTION
 Carbohydrates  Water
 Hexose and pentose  Small intestine: 9-10 L
 Na+/glucose transporters  Large intestine: 0,5 L
 Proteins  Electrolytes:
 Amino acid transportes  Transportes and diffusion
 at least 7 different for
 5 Na+ cotransporter • Na+
 Max. di and tripeptides • Cl-
 Endocytosis of maternal • Ca++
antibodies
 Vitamins
 Lipids
 10-12 C  Free fatty acids to
the blood
 Larger C  triglycerides +
protein + cholesterol
chylomicrons to lymph
 DIGESTIVE ENZYMES IN THE GI SYSTEM
SOURCE ENZYME ACTIVATION SUBSTRATE PRODUCT
SALIVARY GLANDS Salivary -amylase Cl- Starch Dextrin, maltose
LINGUAL GLANDS Lingual lipase Triglycerides Di- and monoglycerides
+ fatty acid
STOMACH Pepsins (pepsinogens) HCl Protein Pepton
Trypsin (trypsinogen) Enteropeptidase Protein Pepton
Chymotrypsins Trypsyn Protein Pepton
(chymotrypsinogens)
Carboxypeptidase A and B Peptone Amino acid (from C-
(procarboxypeptidase A and Trypsin terminal)
B)
EXOCRINE
PANCREAS Pancreatic -amylase Cl- Starch, glycogen Dextrin, maltose
Lipase/colipase (procolipase) Bile acid/- Triglycerides Di- and monoglycerides
+ fatty acid
Elastase (proelastase) Trypsin Elastin Amino acids
Cholesteryl ester hydrolase Cholesteryl esters Cholesterol
Ribonuclease/deoxyribonucl DNS, RNS Nucleotides
ease
Phospholipase A2 (pro- Trypsin Phospholipids Fatty acids
phospholipase A2

Aminopeptidase pepton Amino acid (from N-

terminal)
Dipeptidase dipeptides Amino acids
INTESTINAL
Lipase Bile acid Triglycerides Di- and monoglycerides
MUCOSA + fatty acid
Dextrinase Dextrine Gucose+maltose
Maltase Maltose Glucose
Lactase Lactose Glucose+galactose
Sacharase sacharose Glucose+fructose
 Large intestine (colon)

 Length: ~1.5 m
 Cecum, appendix, colon, rectum, anus
 No villi in the mucosa
 No digestive function
 Secretion: mucus
 Intestinal bacteria (cellulose degradation, synthesis of
Vitamins K, B12 and other B)
 Water reabsorption: 300-1000 mL
 Peristaltic movement
 Defecation (voluntary, internal and external anal sphincters)
 GI PATHOPHYSIOLOGY
 Expulsion from the GI tract
 Vomiting
• Vomitus
• Vomiting center (medula oblongata)
• Nausea
• Chemoreceptor trigger zone – drugs, neurologic conditions ie
meningitis, etc.), input from inner ear (motion sickness)
• Mallory-Weis syndrome (alcohol abuse, general anesthesia)

 Diarrhea
• Increased fecal fluidity, or fecal volume or frequency of defecation
• Secretion of water (due to irritation)
• Osmosis (faulty digestion, impaired absorption)
• Impaired water absorption
• Laxatives (to counter constipation)
 GI PATHOPHYSIOLOGY
 GI inflammations
 Esophagitis (reflux esophagitis)
 Appendicitis
 Peritonitis
• Fistula
 Diverticulitis
 Inflammatory bowel disease
• Chron’s disease
• Ulcerative colitis
 Ulceration
 Peptic ulcers
 Stress ulcers
 GI tumors
 Malabsorption syndrome
 MALABSORPTION SYNDROME
 Reduced absorption – general symptoms
 Weight loss
 Fatigue
 Diarrhea
 Carbohydrate absorption 
Reasons: 1.digestion disturbances
 Energy deficiency Hypoacidity
 Protein absorption  Pancreatic enzyme synthesis 
 Hypoproteinemia Bile production 
 Odema Intestinal enzymes 
 Lipid absorption  2. Transport (absorption )disturbances
Intestinal inflammation
 Steathorrhea
Autoimmune – Chrone dis.
 Osteoporosis (Vit D def.) Allergic
 Coagulopathy (Vit K def.) Irradiation
 Fe, B12 absorption  Bacterial
Parasite
Enzymopathies
 Diseases of the colon
 Obstipation  Diarrhea
 Feeding  Infection
 Lifestyle  Allergy
 Abdominal pressure  Neural
 Muscular hypofunction  Venous stagnation
 Muscle dystonia
 Hyperpepsia
 LIVER

 Exocrine function (bile production)

 Synthesis (proteins, glycogen, purins, pirimidins,
porphirine, amino acids, lipids – cholesterine, etc.)
 Storage (carbohydrates)
 Intermedier metabolism
 Detoxication
• Oxidation-reduction
• Conjugation
• Enzymatic transformations
• Catabolic reactions
 STUCTURE OF LOBULUS
LOBULUS

CENTAL VEIN

BILE CAPILLARY
BILE DUCT

CENTRAL VEIN PORTAL VEIN

HEPATIC ARTERY
HEPATOCYTES

SINUSOIDE

KUPFFER- CELL

PHENESTRATED EPITHELIUM

(R.M.Pool ed.. The Incredible Machine)

 BILE
 Composition  Storage: gall bladder
 Water 97.5 %  Emptying: CCK
 Bile salts 0.7 %  Absence:
 Bilirubin 0.04%  Occlusion
 Cholesterine 0.06% • Gallstone
 Fatty acids 0.12% • Tumor
 Protein 0.6% • Hepatitis
 Inorg. salts 0.8%  Seizures
 Lecitine 0.1% • Sphincter Oddi
 Function  Inflammation
 Surface tension lowering • Cholecistitis
• Hepatitis
 Emulsification
 Stimulation of pancreatic  Jaundice
secretion  Hepatocellular
 Haemolyitic
 Occlusion
 PANCREAS

 Exocrine function (production of digestive pancreatic juice)

• Alkaline pH=~8.0 (HCO3-)
 -amylase
• Procarboxypeptidase A and B
• Trypsinogen
• Chymotrypsinogen
• Lipase (pancreatic)
• Ribonuclease, deoxyribonuclease
• Cholesteryl ester hydrolase
 Endocrine function
• Islets of Langerhans
 A () cells - glucagon
 B () cells - insuline
 TOXIC LIVER DISEASES

 Necrosis CCl4, phalloidin (mushrome toxin), acetaminophen

 Hepatitis halothan, isoniacide, chlorotiazide

 Cholestasis oestrogens, erythromycin

 Cirrhosis ethanol, tetracyclines

 Tumor vynil-chloride

 Granuloma phenylbuthasone
 ETHANOL ABUSE
ETHANOL

STEATOSIS
(FATTY LIVER)

ACUTE SUBACUTE INACTIVE

HEPATITIS HEPATITIS CIRRHOSIS

RECOVERY
ACTIVE
CIRRHOSIS

Further ethanol consumption

DEATH
Total abstinence
 Cirrhosis of the liver
Loss of hepatocytes + Increase in connective tissue

Decreased liver function Portal hypertension

1. GOT, GPT GT ,
2. Protein synthesis  collateral circulation
Hypalbuminemia
Plasma osmotic pressure  ASCITES osephagus varix
Coagulation factors  COAGULOPATHY
3. Bile production  osephagus ruptura
Disturbances of fat absorbtion
4. Intermedier metabolism  DEATH
5. Detoxication 
Direct bilirubin in blood  ICTERUS
Ure cycle  NH3 
Toxic metabolites 

DEATH
 Viral hepatitis
Characteristic Hepatitis A Hepatitis B Hepatitis C Hepatitis E

Type of virus RNA DNA RNA RNA

Incubation 15-45 d 30-180 d 15-160 d 14-60

period
Age Children, All age groups More frequent Young adults
young adults in adults
Route of Enteral parenteral parenteral Other enteral
infection
Course mild Frequently Moderetly Mild
grave grave
Prognosis Usually good Frequently Moderetly Good
oppressive oppressive
Chronic No 5-10 % 10-50 % No

Virus carrier No 0.1-30% 1% No