Top Ten Topics Program

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GIT Physiology
Dr. Md Abdul Hamed Jasham
FCPS(Part I) (Internal Medicine)
MD(Phase-A) (Critical Care Medicine)
Banghabandhu Sheikh Mujib Medical University
 Top Ten Topics:চাঁদ রাতে ফরজ ইবদাত
Digestive end
Gastrin Secretin products and their
CCK absorption

Function of the liver

Gastric Cells

Gastric Secretion Liver Function test

Pancreatic Juice Jaundice

Bile Iron Metabolism

 Local Hormones
 
Local hormones of GIT:
These are the biologically active
polypeptides that are secreted by
nerve cells & gland cells in the
mucosa, act in the paracrine
fashion but they also enter the
circulation .
According to structural &
functional similarity, many of the
hormones fall into one of 2 families.
 Gut hormones and peptides
Hormone Origin Stimulus Action
Gastrin Stomach (G Products of protein i)Stimulates gastric acid secretion
cell) digestion, stomach ii)Stimulates growth of GIT mucosa
Antrum of distention iii)(+)Pepsin secretion
stomach Suppressed by acid iv) ↑Emptying of stomach
and v) Contract LOS
somatostatin vi) ↑Insulin secretion
Somatostatin Throughout GI Fat ingestion Inhibits gastrin and insulin secretion
tract (D cell) Decreases acid secretion
Decreases absorption
Inhibits pancreatic secretion
Cholecystoki Duodenum Products of protein Stimulates pancreatic enzyme
nin (CCK) and jejunum digestion secretion/Echbolic
(I cells); also Fat and fatty acids Gallbladder contraction
ileal and Suppressed by Sphincter of Oddi relaxation
colonic nerve trypsin Satiety
endings Decreases gastric acid secretion
Reduces gastric emptying
Regulates pancreatic growth
Secretin Duodenum and Duodenal acid Stimulates pancreatic fluid and
jejunum Fatty acids bicarbonate
(S cells) secretion
Decreases acid secretion
Reduces gastric emptying
Motilin Duodenum, Fasting Regulates peristaltic activity, including
small intestine Dietary fat migrating motor complexes (MMC)
and colon (Mo
cells)
Gastric Duodenum (K Glucose and fat Stimulates insulin release (also known as
inhibitory cells) and glucose-dependent insulinotrophic
polypeptide jejunum polypeptide)
(GIP) Inhibits acid secretion
Vasoactive Nerve fibres Unknown Vasodilator
intestinal throughout GI Smooth muscle relaxation
peptide (VIP) tract Water and electrolyte secretion
Ghrelin Stomach Fasting Stimulates appetite, acid secretion and
(parietal cell) Inhibited by gastric emptying ( ghre + gastrin)
eating
Peptide YY Ileum and colon Feeding Modulates satiety
Amylin Pancreatic islet Feeding Glycaemic control
β-cells
Factors regulating gastrin release
• Factor stimulates • Factor inhibits
• Luminal-
• Luminal- AA & peptides
• Acid
• Neural • Somatostatin
• Blood borne • Blood borne
• Calcium • Secretin, GIP, VIP,
• Epinephrine Glucagon,
Calcitonin
 Secretions from gastric glands

Glands Site Secretion (s)

Gastric Body and fundus except lesser Hydrochloric acid
or curvature Pepsinogens
oxyntic Intrinsic factor
Mucus

Pyloric Antrum of the stomach Gastrin

Mucus
Mucous Pyloric and cardiac region of the Mucus
stomach
 Cells present in gastric gland

Cells Secretion
1. Peptic (chief) cell Pepsinogen
2. Parietal (oxyntic) cell HCl, Intrinsic factor of Castle
3. Mucus neck cells Mucus, bicarbonate
4. Surface mucus cells
5. G cells Gastrin
6. Enterochromafin cells Histamine
 Parietal cell of stomach:
 
Synonym: Oxyntic cell

Location: Predominantly the upper half of gastric

glands in the fundus and body.

Receptors present on the parictal cells:

1. M3 muscarinic receptor
2. Gastrin receptor
3. H2 receptor
Secretion:
1. HCI
2. Intrinsic factor of Castle
 
Functions of the secretion:
1. HCI: Activates pepsinogens & kills microorganisms in
the food
2. Intrinsic factor of Castle: It is essential for absorption
of vitamin B12.
 Gastric Juices
 Features of gastric juice
Daily secretions : 1500-2500 ml
Color : Clear, pale yellow fluid
PH : 0.9-1.45
Reaction : Highly acidic
Osmolarity : Isosmotic to plasma
Regulation of gastric juice secretion:
 
Gastric juice secretion occurs at cephalic phase,
gastric phase and intestinal phases. This secretion
is regulated by-
1. Neural mechanism &
2. Hormonal mechanism
 
Basic factors that stimulate gastric secretion are
1. Acetylcholine
2. Gastrin, and
3. Histamine
Functions of gastric HCl:
 
1. Converts inactive pepsinogen into active pepsin
2. Provides suitable environment for pepsin to start
protein digestion.
3. Kills many ingested bacteria
4. Stimulates the flow of bile and pancreatic juice
5. Keeps the iron in ferrous state for absorption
6. Hydrolyzes sucrose into glucose & fructose.
 Factors affecting gastric secretion:
1. Emotion
 Pleasant surroundings, clated mood increase gastric
secretion
 Unpleasant surroundings, fear, anger, hostility, worries,
grief, shock decrease gastric secretion.
2. Food: Palatable food stimulates gastric secretion, while
disagreeable food depresses it.
3. Drink: Pre-lunch-drinks (alcoholic) stimulate gastric
secretion.
4. Alkalies:
 In large doses – increases secretion
 In small doeses – decreases secretion due to release of
CO2 (rebound acidity)
5. Bitters: Unless the bitters contain alcohol, they have
hardly any effect on gastric secretion.
6. Acids: HCI (1%) decreases secretion when directly put
inside the stomach
7. Drugs: Drugs like histamine, histalog, caffeine, insulin
stimulate secretion.
8. Tobacco smoking: It stimulates gastric secretion.
9. Vitamins: Deficiency of vit-B12 & Vit-B1 respectively
cause achylia gastric and achlorhydria
10. Electrolytes: Changed blood calcium level depresses
gastric secretion.
11. Hormones:
 Parathormone, ACTH, steroids, insulin, and gastrin
stimulate gastric secretion
 Serotonin, enterogastrone decreas gastric secretion
 Substances affecting HCI secretion

HCI secretion HCI secretion inhibited

stimulated by by
Acetylcholine Somatostatin
Histamine Low PH
Gastrin GIP
Alcohol Drugs
Caffeine
Calcium
Amino acid
Hypoglycemia
 Pancreatic Juice
 
 Hydrolytic secretion: The copious, thin, watery
secretion rich in bicarbonate with almost no
enzymes is called hydrolytic type of secretion.
 
 Echbolic secretion: The thick, less copious juice
rich in enzymes, poor in HCO3- is called echbolic
type of secretion.
 Difference between hydrolytic & echbolic types of
secretion:
Hydrolytic type
1. It is rich in HCO3-, but poor
in enzyme
2. It is thin & watery
3. Its secretion is stimulated
by secretin
4. It is secreted in response
to acid chime in the
duodenum
5. It mainly neutralizes the
acidity of the chime
Echbolic type
1. It is rich in enzymes, poor in
HCO3-
2. It is thick
3. Its secretion is stimulated
by CCK & acetylcholine
4. It is secreted in response to
fatty food in the duodenum
5. It is digestive in function
 Features of pancreatic juice
 
Daily secretion : 1200-1500ml
PH : 8.0 (approximately)
Osmolarity : Isosmotic
Reaction : Alkaline
 
 Water Solid Organic Inorganic

Pancreatic 98.5% 1.5% 1. Carbohydrate splitting enzymes:  Cation: Na+, K+, Mg2+,
juice Pancreatic amylase H+3
2. Proteolytic enzymes: Trypsin,
 Anion: Cl-, HPO42-, PO-4
Chymotrypsin, Carboxypolypeptidase,
Elastase.
3. Lipolytic enzymes: Pancreatic lipase,
Cholesterol esterase, Phospholipase A2,
Colipase.
Bile:
 
Bile is the secretory product of liver made up of bile salts, bile pigments
and other substances dissolved in an alkaline solution that resembles
the pancreatic juice.
 
Criteria:
 
1. Yellowish-green fluid
2. Consistency: viscid mucoid liquid
3. Reaction; alkaline
4. Taste: bitter
5. Produced by hepatocytes
6. Stored in gall bladder
7. Secreted into the 2nd part of the duodenum along with the pancreatic
juice through the hepatopancreatic duct.

Daily secretion: 1000ml/day

Composition Liver bile Gall bladder bile
 Concentration It is dilute It is concentrated
 Specific gravity 1.01 1.04
 Water 97.5 g/dl 92.0 g/dl
 Solid 2-4% 10-12%
 PH 7.8-8.6 7.0-7.4
 Organic (g/dl) Bile salt 1.1 6
Bilirubin 0.04 0.3
Cholesterol 0.1 0.3-0.9
Fatty acid 0.12 0.3-1.2
Lectithin 0.04 0.3
Mucin 0.4% 0.3%
 Inorganic (mEq/L) Na+ 145 130
K+ 5 12
Ca2+ 5 23
Cl- 100 25
HCO3- 28 10
Justification of bile as a digestive juice:
 
Though bile has no enzymes, bile is a digestive juice
because-
1. It helps in the digestion & absorption of fat by-
 Emulsifying fat
 Activating pancreatic lipase
 Forming micelles
2. It also helps in the absorption of fat soluble
vitamins like A, D, E, & k.
 Functions of bile:
 
1. Digestive function:
Bile helps in the digestion of fat with the help of bile salt
which acts:
 By reducing surface tension
 By activating the lipase
 By solvent action & dissolve fat and lipases.
 
2. Absorptive function: With the help of bile salts, bile
helps in absorption of fat and fat soluble vitamins, iron,
calcium etc.
3. Choleratic: The secretion of bile from liver
4. Laxative function:  peristalsis and thereby helps in
defecation
5. Excretory function: Certain substances are excreted
through bile:
 Heavy metals, Cu, Hg, Zn.
 Certain drugs,
 Bile pigments-bilirubin etc.
 Cholesterol
 Toxin, bacteria.
 6. Mucin of bile acts as buffer and lubricant
 7. Neutralizing action: Maintains alkaline medium in
the intestine by neurtralizing gastric HCI by its HCO3-
Pathways of bile

Bile starts its journey from hepatocytes through bile

canaliculi to bile ducts. Thus the flow of bile can be
represented as follows:

Hepatocytes  bile canaliculi  intralobulr bile ducts

 interlobular bile duct  right and left hepatic ducts 
common hepatic ducts  gallbladder through cystic
duct Common bile duct  second part of the
duodenum at major duodenal papillae (an sphincter
named by sphincter of Oddi regulates the flow of bile to
the duodenum)
 
End products of carbohydrate, protein & fat
digestion
End products
Carbohydrate starch  Glucose (80%)
 Galactose
 Fructose
Protein  Amino acids
Fat/Triacylglycerol  Fatty acid
 Glycerol
 2-Monoacylglycerol
 1-Monoacylglycerol
 Functions of liver
 
1. Metabolic function: Liver is
the main organ for
metabolism of carbohydrate,
protein and fat. It is the
main site for alcohol
metabolism.
a. Carbohydrate metabolism:
Liver causes-
 Storage of large amount of glycogen
 Conversion of galactose & fructose to glucose
 Gluconeogenesis
 Formation of many chemical compounds from
intermediate products of carbohydrate metabolism.
 
b. Fat metabolism:
Liver causes-
 Oxidation of fatty acids to supply energy for other
body functions
 Synthesis of large quantities of cholesterol,
phospholipid and most lipoproteins
 Synthesis of fat from proteins and carbohydrate
 
 
c. Protein metabolism:
Liver causes-
 Deamination of amino acids
 Formation of urea for removal of NH3 from the body
 Formation of plasma proteins
 Interconversion of various amino acids & synthesis of
other compounds from amino acids
2. Storage function:
Liver is the storage site for-
Carbohydrate, in the form of glycogen
Vitamin-A, D, B12 in large amount
Vitamin-K, Folate in small amount
Iron as Ferritin Hemosiderin
Copper
 
3. Synthetic function:
• Plasma proteins except immunoglobulin
• Clotting factors: All except Factor III, IV, VI
 II, VII, IX, and X are K-dependent
 Natural anticoagulants Protein C, Protein S
 25-Hydroxycholecalciferol
 
4. Secretory function: Liver secretes mainly bile.
5. Excretory function: Heavy metals (Bi, As, Pb),
cholesterol, bile pigment, calcium are excreted
through liver
6. Detoxification function: Liver is the main site of
detoxification of NH3 and drugs such as penicillin,
ampicillin etc.
7. Haemopoietic function: In intra-uterine life, liver
is the main organ for the production of RBC. But in
adult, liver is an organ for the destruction of RBC.
8. Liver acts as a blood reservoir.
 Liver function tests
 
A. Tests for synthetic function:
1. Total protein conc. (Normal : 6-8 gm/dl)
2. Serum albumin level (Normal: 3-4 gm/dl)
3. Serum albumin /globulin ratio (Normal: 2:1)
4. Prothrombin time (Normal: 11-16 sec) It assays
the production factors II, VII, IX, and X by the liver.
If Prothrombin time remains increased even after
administration of vitamin K then liver disease is
confirm.
 
 
B. Tests for excretory function:
1. Serum bilirubin level, by van den Bergh reaction
2. In urine –Urine urobilinogen, bilirubin
3. In stool-Sterocobilinogen
D. Tests for hepatocellular damage: Done by
measurement of the following serum enzymes-
1. Alamine aminotransferase (ALT)/ serum glutamate
pyruvate transaminase (SGPT) (in hepatocellular
damage)
2. Aspartate aminotransferase (AST) / Serum glutamate
oxaloacetate transminase (SGOT) (In hepatocellular
damage)
3. -glutamyl transferees . ( in alcoholic liver diseases)
4. Lactate dehydrogenase
 
E. Tests for cholestasis (biliary tract obstruction):
Done by measurement of the following serum
enzymes-
1. Alkaline phosphatase (ALP). ( in biliary obstruction,
cirrhosis of liver)
2. -glutamyl transferees
3. 5’-NT (5’-Nucleotide)
 
F. Test for detoxification functions:
1. NH3 conc. in the blood: In liver disease, NH3 can’t be
converted to urea. So, blood NH3 level increases.
2. Hippuric acid tests
 
G. Other determinations:
1. Serum ferritin ( in liver diseases)
2. Iron binding capacity saturation
3. Alpha 1-antitrypsin
4. -fetoprotein (normally produced by fetal liver. If it is
found in adult, it indicates hepatocellular carcinoma)
5. Ceruloplasmin ( in Wilson’s disease)
6. Copper.
 
 Difference between different types of jaundice
Haemolytic jaundice Hepatocellular Obstructive
jaundice jaundice
A. Blood Biochemistry
1. Serum bilirubin Raised, mostly Raised, both Raised,
unconjugated conjugated and conjugated.
unconjugated
2. Alkaline phosphatase Normal Small rise High
3. AST (SGOT) Normal High rise Small rise
4. ALT (SGPT0 Normal High rise Small rise
5. Prothrombin time Normal Prolonged Prolonged
6. Serum albumin Normal Low Normal
B. Haematological test Findings of haemolytic Leucopenia in viral hepatitis
anaemia
C. Urine
1. Bilirubin Absent Variable Present
2. Urobilinogen Increased Normal or increased Decreased
3. Bile salts Absent Absent Present
D. Stool
1. Naked eye Dark Normal colour or pale Pale or normal colour,
Bulky, frothy due to high
fat content
2. Stercobilinogen Increased Decreased Decreased
E. Special blood test
1. Viral markers (HBsAg, Not found Found in viral hepatitis Not found
HBeAg etc).
Others Anaemia,Feature of Fever,Hepatomegaly Pruritus,Scratch mark
hemolysis
 Factors favouring absorption Factors reducing absorption
Haem iron Inorganic iron
Ferrous form ( Fe2) Ferric form ( Fe3+)
Acids ( HCl, vitamin C) Alkalis-antacids, pancreatic secretions
Solubilizing agents ( e.g. sugars, amino acids) Precipitating agents – phytates, phosphates, tea
Reduced serum hepcidin, e.g. iron deficiency Increased serum hepcidin, e.g. iron excess
Ineffective erythropoiesis Decreased erythropoiesis
Pregnancy Inflammation
Hereditary haemochromatosis Decreased expression of DMT-1 in duodenal
Increased expression of DMT-1 in duodenal enterocytes
enterocytes
Factors enhance Fe absorption Factors inhibit Fe absorption
Amino Acid Phytates
Vitamin C Tannins
Phosphates
↓ Plasma ferritin ↑ Plasma ferritin
Fe deficiency Liver disease
Hypothyroidism Acute phase response
Vit-C deficiency
Low plasma ferritin is best single test to confirm Iron deficiency anaemia (IDA).
↓ Plasma Iron ↑ Plasma Iron
Acute phase response Liver disease
Hemolysis
↓ Transferin ↑ Transferin
Malnutrition Pregnancy
Liver disease OCP
Acute phase response
Nephrotic syndrome
 Topics tobe covered
Major Salivary glands and their
Secretions
Local Hormones of GIT
Gastrin: Factors affecting gastrin
secretion, Function
Secretin: Stimulus, Function &
Effect
Cholecystokinin: Stimulus,
Function & Effect
Factors affecting gastric emptying
HCL: Factors affecting and
mechanism of secretion
Cells of the stomach with their
functions
Parietal Cell
Bile: Constituent and function
Digestive end products and their
absorption
 Topics tobe covered
Glucose Transporters Jaundice
Absorption of vitamin and Trace Element: Zinc deficiency
minerals Iron Metabolism
Hormone regulating food Vitamin A,C,D,B-12
intake Antioxidants
Action potential in GUT Rickets
Function of the liver
Liver Function test

Viral Markers