STUDENTS' OF PHYSIOLOGICAL ASSOCIATION OF NIGERIA, UNIOSUN CHAPTER.

Dear Mr. President-Elect,
Please accept my warm congratulations on your victory and my best wishes for your success as you prepare to take up the responsibilities and challenges of your high office.
I’m extremely pleased to hear the good news. The Association need leaders like you to bring the members together and work for the betterment of the Association.
You do know that I am your staunchest and strongest supporter and you will always have my assistance in this regard.
I have every confidence in your ability to take the Association forward and make it a ’force’ among the Student Associations in Osun State University, Osogbo.
And I look forward enthusiastically to some great times ahead in the association. Please pass on my best wishes to other executives to be elected or appointed.
As you embark upon your new responsibilities, I wish to assure you that I will support you and your team as best I can as the Association is important to me and it would be pleasing to see it grow from strength to strength.
You have my support when needed, please do not hesitate to contact me.
Wish you and your executive committee a successful year ahead.
Once again, congratulations.
- Olaniyi Odunlami Salami, SPAN Ex-President

The Most Anticipated Ever!
It's happening tonight!!!

Students of Physiological Association of Nigeria {S.P.A.N}, Uniosun Chapter Dinner and Awards Nite!!!

Date: Friday, 1st July, 2016.
Venue: Values Events Hall.
Time: 7pm till dawn.
Gate Fee:
Regular Ticket ~ N500,
VIP Table for 4 ~ N6,000,
VIP Table for 6 ~ N8,000.
Free ticket for President of various departments.

Kindly contact the Social Director on 070-691-63457 for tickets and reservations.

Come One, Come All... Let's party together!

Don't afford to miss out!

Kindly Rebroadcast!

SPAN appreciates the efforts of workforce in making our country a better place to live in. Happy Workers Day! -Olaniyi Odunlami Salami, SPAN President

Belated: Yesterday 8th March was International Women's Day.
SPAN and it's male members thus celebrate every SPAN women but young and adult.
SPAN men recognise the beautiful contribution of you our women towards SPAN development.
We also join in standing against
Female ge***al mutilation,
Gender inequality,
Gender discrimination and every form of violence against women and children.
SPAN and it's men stand aloft for: Gender Balance,
Gender sensitivity and
Respect for women and children alike.
To all our beautiful and great women, we celebrate you today and always. Cheers! -Olaniyi Odunlami Salami, SPAN President.

Wishing you a fabulous 2016 with full of great achievements and experiences. A meaningful chapter waiting to be written.
Compliment of the Season from all of us at SPAN. -Olaniyi Odunlami Salami, SPAN President.

CALL FOR PAPERS: RESEARCH JOURNAL OF HEALTH SCIENCES

The Research Journal of Health Sciences is the bi-annual peer reviewed official publication of the College of Health Sciences, Osun State University. The Journal is dedicated to promoting high quality research work in the field of health and related biological sciences.

It acts as a medium of improving the quality of health care and medical education particularly in the context of developing countries with limited resources. RJHS is open access and available for free downloads.

We publish scientific reports on human and animal subjects in the form of original articles, reviews, brief reports, case reports, and letters. We also accept review articles, special communications and editorials. All submissions are subjected to peer review by the Editorial Board and by referees in appropriate specialties. We will consider for publication ma**scripts from any part of the world, but most particularly ma**scripts that would be of interest to readers in the third world and Africa in particular.

For details about the journal and submission of ma**scripts for publication, please download the files at www.uniosun.edu.ng

http://www.uniosun.edu/

We were here to wish our Muslim brothers and Sisters a wonderful end of Ramadan fast, thirty days ended; and now, we are more glad to congratulate you for a successful end. Wishes you Happy Eid-El-Fitr. Barka De Sallah!

Gastro Intestinal Tract (GIT)

Introduction:
GIT is formed of :
(1) The alimentary ca**l that extends from mouth to a**s.
(2) The accessory glands that include:
Salivary glands, liver, and exocrine part of pancreas.
Structure features of the wall of alimentary ca**l:
From esophagus to the a**l ca**l it is formed of 4 layers from in to outside, they are:
(1) Mucosa (2) Submucosa (3) Musculosa (4) Serosa

Function of GIT are:
(1) Digestion (2) Absorption (3) Secretion (4) Motility

[1] Digestion:
It is breakdown of large food molecules to small absorbable molecules. This is either physical or chemical.
(A) Physical digestion is mainly mechanical by:
a) Mastication b) Grinding by motility especially in stomach.
(B) Chemical digestion is by digestive enzymes and HCl of stomach.

[2] Absorption:
It is passage of the digested food to blood and lymph. This is mainly in small intestine, to lesser extent in large intestine, and very minimal in stomach for little amount of water.

[3] Secretion of:
a) Saliva and different GIT juices.
b) Mucus for lubrication and protection of GIT mucosa.
c) GIT hormones that control GIT function.
d) Some undesirable substances to be excreted with stool.

[4] Motility:
For: 1) Transport of food.
2) Digestion of food (Mechanical).

The control of GIT functions:
It is nervous and hormonal control.
Beside that the myogenic property of visceral smooth muscle play a role in controlling the motility.

[I] The nervous control:
(1) The intrinsic innervation: (the enteric nervous system).
- It depends upon nerves present in submucosa and musculosa.
- It affects both secretion and motility.
- It depends upon local reflexes that are stimulated by mechanical and chemical receptors. (Short intrinsic reflexes).
(2) The external innervation:
- Parasympathetic: it increases GIT activity.
- Sympathetic: it decreases GIT activity.

These modify the GIT activity by long reflexes which are:
a) Conditioned (Aquired reflexes).
b) Unconditioned (Inherent reflexes).

[II] Hormonal Control:
By varieties of hormones secreted from different parts of GIT.

Functions and Control of GIT
[1] Mouth
In mouth digestion is by mastication and salivation.
(1) Mastication (Chewing):
This breaks up large particles to smaller particles by the action of teeth. Also, helps mixing food with saliva. .

(2) Salivary Secretion:
Salivary glands are parotid, submaxillary & sublingual glands.

Composition of saliva:
- Amount 1500 ml/day.
- It is 99.5% & 0.2% inorganic materials & 0.3% organic materials.

(a) The inorganic materials are :
1) NaCl & KCl. Cl- ions are Catalyst for salivary amylase enzyme.
2) Buffering systems mainly bicarbonate & phosphate. This prevents loss of calcium from teeth.
(b) The organic materials are:
1) Salivary amylase (Ptylin):
It digests starch incompletely. It does not act for long time, as it is inhibited by the acidity of stomach.
2) Lingual Lipase: helps digestion of Fat in stomach.
3) Mucus for lubrication.
4) Lysozyme enzyme that have antibacterial action.

Function of saliva:
1) Digestion by amylase & lingual lipase.
2) Lubrication to mouth & pharynx to help deglutition.
3) Dissolve food particles. This helps stimulation of taste receptors.
4) Buffering action to protect teeth.
5) Anti-bacterial action.
6) Lubrication & moistening help articulation speech muscles.
7) Excretion visa saliva occurs for some substance like lead, mercury and arsenic & some others.

Control of salivary secretion:
It is pure nervous regulation by:
1) Unconditioned reflexes:
- It is inherent reflex occurs by direct contact of food.
- Receptors are: Taste receptors.
- Control of reflex is in medulla oblongata.

2) Conditioned reflexes:

- This is acquired reflex and related to the condition, hungry or not.
- It not by contact of food to any receptor in the mouth, it is by smelling, seeing, hearing about, and even by thinking in food.
- It needs training, experience, and depends on memory.
- The center of reflex is in the cerebral cortex.


Deglutition (Swallowing)
It is the process of passage of food from buccal cavity (mouth) to the stomach.
Deglutition is composed of [3] stages:

[A] Buccal stage:
- It is the only voluntary phase.
- The food is collected as a bolus and is pushed to the pharynx mainly by the tongue.

[B] Pharyngeal stage:
- It is a reflex stage pushing the food bolus to esophagus.
- Receptors are in wall of pharynx.
- Center: deglutition center is in medulla oblongata.
- Responses are:
1) Contraction of pharyngeal wall muscles to push food to the esophagus.
2) Elevation of soft palate & uvula to close the posterior nasal opening.
3) Elevation of larynx to be closed by epiglottis & closure of the vocal cords.
4) Stopping of respiration (Reflex apnea).

[C] Esophageal stage:
- It is reflex stage done by peristaltic movement to push the food to stomach.
- The center of deglutition is in medulla oblongata.
- This reflex stage depends on vagus nerve.
- The lower esophageal sphincter relaxes to allow passage of food to stomach.


II The Stomach

Functional Structure of the Stomach:
It is formed of:

1) Cardiac region which is guarded by cardiac sphincter.
2) Fundus
3) Body.
4) Pyloric antrum .
5) Pylorus which end by pyloric sphincter.

Functions of stomach:
1) Storage of food.
2) Digestion by:
a. Mechanical by the strong gastric motility, which also mixes food with gastric juice.
b. Chemical by gastric juice, especially by HCl & pepsinogen enzyme.
3) Secretion of:
a. Gastric juice (exocrine).
b. Some hormones, the most important is gastrin hormone.
4) Absorption of little water & alcohol.

Gastric juice (secretion):
Amount : 2500 ml/day.
PH: 1 – 2 (acidic due to HCl).
Composition: 99% water, 0.5% HCl, 0.5% gastric enzymes; the most important is pepsinogen.
- Mucus for lubrication & also protect the gastric mucosa from being digested by HCl & pepsinogen.
- Anions as Cl-, phosphate and sulfate & cations like Na+, K+, Mg+2, H+.
- Intrinsic factor for B12 absorption.

Functions of HCl of gastric juice:
1) It helps protein digestion by:
a. Causing denaturation of protein.
b. Activation of pepsinogen to the active form pepsin.
c. Giving suitable PH for pepsin.
2) Powerful antibacterial action.
3) Helps absorption of iron and Vit. B12 and Ca2+.

Enzymes of gastric juice:
1) Pepsinogen:
- It is activated by HCl to pepsin & also by auto activation.
- It digests proteins & polypeptides to small fragments & few amino acids.
2) Gastric Lipase:
- Together with lingual lipase digest fat, but do not work in low pH, but may act in young babies as their gastric acidity is low.
3) Lysozymes: for antibacterial action.
4) Gelatinase enzyme for liquefying gelatin.

Control of gastric juice secretion

It is both nervous and hormonal and passes in 3 phases:
I Cephalic Phase: (nervous):
- this phase stimulates gastric secretion before food arrival to stomach.
- It is by :
• Conditioned reflexes like saliva, before food enters the mouth.
• Unconditioned reflexes when food is in mouth, pharynx and esophagus.
- The parasympathetic vagus nerve is responsible for that.
- The cephalic phase account for 10% of gastric secretion.

II Gastric Phase: (For 70% of gastric secretion):
- Mainly hormonal by gastrin hormone secretion.
- Gastrin hormone is secreted by local reflexes. Both mechanical by stretch of stomach by food & chemical by composition of food stimulate gastric hormone secretion.

III Intestinal phase (For 20% of gastric secretion)
- It is hormonal also depends upon secretion of an intestinal gastrin hormone that circulate to stimulate the stomach.
- It is chemically stimulated when food arrives the duodenum especially by protein derivatives.

V. B: The food now is called acid chyme.
V. B: Presence of excess fat, carbohydrates & acidity in duodenum will stimulate.
• Reflex inhibition of stomach called entero gastric reflex.
• Secretion of the hormones secretin, CCK, GIP & VIP that inhibits gastric secretions & motility besides their other actions.

Gastrin hormones:
It is a peptide hormone
Sites of secretion:
a) Stomach : it is called Gastric Gastrin. It is secreted from certain cell in gastric mucosa called (G) cells.
b) Small intestine: it is called intestinal gastrin and is secreted by cells called (TG) cells.

Gastric motility:
There is continuous myogenic tonus basal rhythm. It is spontaneous slow and continuous contraction of gastric muscles.

Types of motility:
1) Receptive relaxation:
There is reflex inhibition of any gastric contraction and the wall stomach is relaxed for receiving the new food. This reflex is by vagus and is stimulated by presence of food in pharynx esophagus.
2) Peristaltic movement:
- It is in the form of aware of constriction followed by a wave of relaxation.
- It occurs by local reflex that is stimulated, mainly, mechanically.
- It is for pushing of food towards pylorus for emptying of stomach.
- It starts from mid-part of stomach to duodenum.

3) Antiperistaltic movement:
- It is in the opposite direction of peristaltic movement when there is undigested food particles in the pylons.
- It is by local reflex & end in mid potion of stomach.

4) Mixing movement (Segmentation movement):
- It is myogenic movement due to stretch of stomach.
- The strong gastric muscles contract to grind the food.
- To mix it with gastric juice. The contraction occurs in segments.

5) Hunger contraction (Hunger pain):
- These are strong rhythmic contractions occurs at time of meals. They increase in 15 minutes & inhibited after 45 minutes to reappear at time of next meal.
- It is reflex by vagus nerve due to stimulation of hypothalamus by hypoglycemia.


(III) Exocrine part of pancreas

Pancreatic contains Juice enzymes for digestion of all stuff also, it contains large amount of the alkali NaHCO3.
Composition:
Amount : 1500 ml/day PH: 8 (alkaline).
The digestive enzymes are:
[A] Proteolytic enzymes (digest protein):
a) Trypsinogen that is activated to trypsin by enterokinase enzyeme secreted by duodenal mucosa.
b) Chymotrypsinogen which is activated by trypsin to chymotrypsin.
c) Some other enzymes like carboxypeptidases, ribonuclease & deoxy-ribonuclease.

[B] Lipolytic enzymes: (For lipids)
a) As pancreatic lipase which is activated by bile salts.
b) Phospho lipase (for phospholipids) & is activated by trypsin.
c) Pancreatic esterase for cholesterol esters.

[C] Panceratic amylase (For starch, glycogen & other carbohydrates)
N.B: Pancreatic enzymes need alkali pH to act.
NaHCO3 which is alkaline, is secreted by pancreatic juice, bile & intestinal juice for alkalinization of the acid chyme coming from stomach.
Control of pancreatic secretion:
[A] Nervous (20%) by vagus nerve
- It occurs by conditioned & unconditioned reflexes.
- This secretion is little in amount, rich in enzymes & poor in alkali.

[B] Hormonal (more important)
It is by: secretion & CCK hormones.
1) Secretin hormone:
- It is secreted by duodenal mucosa in response to arrival of acid chyme.
- It stimulates alkaline pancreatic secretion rich in bicarbonate and poor in enzymes.
2) CCK (CCK-PZ – cholecystokinin – pancreozymin)
- It is secreted by duodenal mucosa in response to digested protein products & fatty acids.
- It stimulates pancreatic juice rich in enzymes and poor in alkali.

N.B.: Usually secretin hormone is secreted before CCK hormone.

IV. Liver and biliary system:

The liver is the largest gland in the body, with many complex functions. The digestive function of liver is formation and secretion of bile.

Bile
Bile, is the yellowish green alkaline fluid secreted by the cells of liver into the bile duct which drains into the duodenum between meals, the duodenal or***ce of this duct is closed and bile is stored in gallbladder. When food enters the mouth, the sphincter around the or***ce is relaxed and when gastric contents enter the duodenum, CCK hormone from intestine Causes contraction and evacuation of gallbladder. N.B. secretion hormone stimulate formation of bile by liver cells.

Composition of bile:
Amount: 500 ml/day.
pH: 8.5 (alkaline).
But in gallbladder, it is less (slightly acidic) due to absorption of NaHCO3.

Composition:
97% water
0.7% bile salts.
0.2% bile pigments.

Also, it contains cholesterol, fatty acids, lithium, fat, alkaline phosphates Z. and NaHCO3, and other inorganic substances.

Bile salts:
These are Na+, K+ salts of bile acids conjugated with glycine and taurine.
The major are Na+, K+ glyco-cholate and taurocholate.
They are formed in liver and pass to duodenum to function in small intestine. 90% or more are reabsorbed through portal circulation of liver again, this is called enterohepatic circulation of bile salts.
They are reabsorbed in ileum by active transport.

Functions of bile salts:
1) Digestion of fat by:
a. Emulsification of fat. This increase the surface area of fat exposure to lipase.
b. Activation of pancreatic lipase.
2) Absorptive function:
a. For fat: by dissolving and digestion of fat.
b. Helps absorption of fat soluble vitamins ( A, D, E, K).
3) Helps intestinal motility and movement of the villi. This helps absorption in small intestine.
4) Auto choleretic action: bile salts after are reabsorbed from small intestine it stimulates liver cells production of bile salts, so, it autostimulate its secretion and choleretic action means action stimulate bile, secretion.
5) Antibacterial action.
6) Solvent for cholesterol.

Bile pigment:
Bile pigments are mainly bilirubin and very less amount of biliverdin.

Mechanism of formulation:
1) in Reticuloendothelial cells:
Hb of old RBCs is changed to bilirubin and small amount of biliverdin.
2) In blood:
Bilirubin combines with plasma protein (albumen and globulin) it is called hemobilirubin.
3) In liver:
Bilirubin enters the liver cells after leaving the protein and by reaction is changed to cholibilrubin. Cholibilirubin is secreted with bile into small intestine.
4) In intestine :

Cholibilirubin is changed by bacterial enzymes to bilinogen (sterchobilinogen and urobilinogen).

Fate of bilinogen:

a) Sterchobilin that gives brown color of feaces after being oxidized to strechobilin that gives brown color of feaces.
b) A part passes again to liver by the entero-hepatic portal circulation to be excreted again to bile ducts.
c) Small part is absorbed to systemic circulation (urobilinogen). This is excreted in urine as urobilinogen and on exposure to air its is oxidized to urobilin.

Van Den Bergh reaction:
It is test to detect the type of bile pigments in the serum by adding it to diazo reagent.
1) Direct reaction: (with cholibilirubin):
It is direct appearance of violet color. It occurs with cholibilirubin.
Indirect reaction : (with heamobilirubin):
The violet color appears only after adding methyl alcohol that separates the protein from hemobilirubin.
2) Biphasic reaction:
The violet color appears directly and increase by addition of methyl alcohol. This means presence of both hemo & cholibilirubin.

[N.B]: Cholibilirubin passes through kidney with urine while hemobilirubin cannot become it is because it is attached to protein.

Jaundice
It is yellowish coloration of skin sclera and mucous membrane due to high blood bilirubin.
Normally serum bilirubin is 0.5 – 1 mg/100cc. Jaundice occurs when it is above 2mg/100 cc.
Types of Jaundice
1) Obstructive Jaundice: (post hepatic)
Due to obstruction of bile duct. There is increase cholibilirubin in blood.

Manifestation:
- Stool:
• Color is pale due to absence of sterchobilin.
• Odour : offensive due to undigested fat the undergoes rancidity.
• Amount: large, stool is bulky greasy and offensive. This is called fatty diarrhea.
- Urine : deep brown due to excess bilirubin.
- VDB reaction direct.
- Itching: due to increase bile salts in blood.
- Bleeding tendency : due to decrease absorption of Vit K.
- Manifestation of fat soluble vitamins (A, D, E, K) deficiency .

2) Hemolytic Jaundice:
Due to excess production of bilirubin due to excessive RBX destruction as in hemolytic anemias.
The liver will excrete large amounts of cholibilrubin, but cannot change all hemobilirubin to cholibilirubin. Hemobilirubin is increased & causes jaundice.

Manifestation:
Stool: very deep brown.
Urine: normal but is changed to deep brown color after sometimes.
VDB : reaction is indirect.
Hemolytic anemia.

3) Hepato cellular (hepatic) Jaundice:
It is due to damage of liver cells. The affected cells will be unable to change all hemobilrubin to choliblirubin.
The damaged cells also causes some sort of intrahepatic obstruction. So, not all cholibilirubin pass to intestine and also there is decreased bile.
The increased in blood is both choli & hemobilirubin.

Manifestation:
- Stool: pale, bulky and greezy with offensive odour (fatty diarrhea).
- Urine: is dark.
- VDB reaction is biphasic.
- Liver is enlarged and render.
- There is itching and bleeding tendency.

There are some manifestation of obstructive Jaundice but less sever plus decreased liver function.

Hemolytic Hepatic Obstructive
the increased bilepigments Hemobilirubin Both cholibilirubin
Degree of Jaundice Mild Moderate Sever
VDBR Indirect Biphasic Direct
bile salts in plasma Absent Present Present
Itching No “ “
hemolytic anemia Present “ “
Urine Normal, dark by time Dark More dark
Stool Normal Fatty diarrhea Fatty diarrhea




Gall bladder
Functions:
1) Storage of bile.
2) Concentration of bile by H2O reabsorption.
3) Acidification of bile by NaHCO3 reabsorption.
4) Secretion of mucus.
5) Evacuation of bile by its wall contraction.

Emptying of gall bladder:
It is by contraction of its wall and relaxation of sphincter in end of common bile duct called sphincter of Oddi.

Mechanism:
A) Nervous:
1- Vagal stimulation by conditioned and unconditioned reflexes.
2- Also, distention of the wall of gall bladder is found to cause reflex evacuation.

B) Hormonal:
CCK-PZ hormone is released in response to presence of fatty acids in duodenum and causes it’s evacuation.
- When food reaches duodenum hepatic bile is secreted first by the effect of secret hormone in response to acidity to neutralize the acid chyme.
- Then CCK-PZ is secreted for the gall bladder bile (cystic bile) which is concentrated and poor in alkali.

Choleretics:
Are substances that increase formation and secretion of bile in liver e.g. bile salts and secretin hormone.

Cholagouge:
Are substances that cause gall bladder evacuation like CCK-PZ hormone.
Some hormones related to pancreas, liver, gall bladder:
(1) Secretin hormone:
Site of secretion: upper intestinal mucosa (mainly duodenal ).

Functions:
- Stimulate pancreatic secretion rich in bicarbonate
- It has cholagouge action.
- It decrease gastric secretion and inhibits gastrin hormone.

Stimulus for release:
Arrived acid chyme to duodenum.

(2) Cholecystokinin- pancreozymine (CCK-PZ) or (CCK)
Sites of secretion: like secretin.

Functions:
- Stimulate pancreatic secretion rich in enzymes.
- Cholagouge action.
- Inhibits gastric emptying.

Stimulus for CCK secretion:
- products of protein digestion.
- Fatty acids.

N. B.: Secretin is secreted before CCK to give alkaline hepatic bile and alkaline pancreatic juice to neutralize acid chyme. Then CCK stimulate pancreatic juice rich in enzymes and evacuates the gall bladder to give concentrated bile with excess bile salts.


(V) Small intestine

The main functions of small intestine are:
a) Completing digestion.
b) Absorption.
c) Secretion.
d) Motility.

Digestion in small intestine is by pancreatic juice and intestinal juice.

The intestinal juice:
It includes mucus, digestive enzymes and bicarbonate.

The intestinal enzymes are for completing digestion to the simplest form, they are:
a) On CHO:
The disaccharidases : maltase, sucrase, lactase, to give monosaccharides.
On protein

b) Proteolytic Zs. To give a. as :
c) Intestinal lipase for lipid.

Control of secretion:
1) Nervous:
a. Local enteric reflex: the main mechanism.
b. Vagal increases while sympathetic decreases especially mucus secretion.
2) Hormonal:
VIP hormone CCK and some other hormone, increase the secretion.

1) Absorption in small intestine:
It occurs either passive or active.
a. Absorption of CHO:
Almostly all hexoses are absorbed before reaching of food to terminal part of ileum.
b. Pentoses are absorbed by simple diffusion.
c. Fructose is absorbed by facilitated diffusion.

- Glucose and galactose are absoroped by 2ry active transport with Na+.
- Insulin has no role in glucose absorption in intestine.
- Some fructose is converted to glucose in the cells. All monosaccharides are absorbed to blood, then pass to liver and converted to glucose.

2) Absorption of proteins:
- The absorption is to blood.
- Most of amino acids are absorbed by 2ry active transport with Na+ like glucose.
- Absorption of amino acids is rapid in duodenum & jejunum.

3) Absorption of lipids:
- It is by passive diffusion.
- Short chain fatty acids are absorbed to blood.
- Long chain fatty acids are absorbed to the lymph .
- Defective fat digestion and absorption may be due to decrease bile salts or pancreatic secretion: this will be fatty diarrhea.
4) Absorption of water and electrolytes:
a. Water absorption:
Daily sources of water in CIT.
• Ingested water 2000/day.
• Endogenous water from digestive juice is 7000 cc/day, (salivary 1500, gastric 2500, bile 500, pancreatic 1500, intestinal 1000).

Absorption occurs for 8800 cc and only 200 cc are in stool.
Little water is reabsorbed in stomach. Most of it in small intestine and to less extent in large intestine.
It is passive absorption.
b. Na+ absorption:
• It is active from intestinal cells to blood.
• Aldosterone hormone facilitates it.

c. K+ absorption:
• manly in ileum and colon. It is active.
d. Cl- & bicarbonate:
• Are actively changed with each other.
e. Absorption of vitamins and mineral:
• Absorption of water soluble vitamins is rapid.
• Fat soluble vitamins (A, D, E, K) needs bile salts and pancreatic enzymes.
• Most vitamins are absorbed in upper intestinal mucosa, but vit. B12 is in ileum.
f. Calcium absorption:
• It is active and is facilitated by active Vit D3.
• HCl helps its absorption.
g. Irone:
• It needs HCl and Vit. C.

Factors affecting absorption in small intestine:
1. Complete digestion of food.
2. Vitality of epithelium.
3. Lymph supply.
4. Surface area of intestinal mucosa.
5. Time of contact of food with villi. In diarrhea, it is decreased.
6. Intestinal movement as many substance have special site for absorption.
7. Movement of villi that increase surface area. N.B: VilliKinin hormone is an intestinal hormone that stimulate movement of villi and so, helps absorption.
8. Bile salts for fact and fat soluble vitamins.
9. Thyroxin increase absorption generally and especially glucose.
10. Vit. D and parathyroid hormone increase the absorption of Ca2 and phosphate .

Movement of Intestine:
1) Tonus Rhythm:
It is slow myogenic spontaneous movement

2) Mixing movement:
It is myogenic due to stretch of wall and help mixing of food with juice.

3) Peristaltic movement:
It is by local reflex and pushes food towards colon, it helps absorption and evacuation of small intestine.

4) Anti peristaltic movement:
It is by local reflex and occurs when there is unabsorbed food at the end of small intestine.
N.B. movement and villi is by local reflex and facilitated by villikinin Hormone.

VI Colon (Large intestine)

Functions of large intestine:
1) Absorption: (It is mainly in the ascending color)
- mainly for Na+ and H2O and Cl- ions.
- Also for the vitamins formed by intestinal bacteria.

2) Secretion of K+ ,HCO3 and Mucus:
3) Excretion of some substances like heavy metals, e.g. mercury.
4) Storage of f***s till defecation.
5) Putrefactions:
It is the action of intestinal bacteria. This is result in formation of (a) beneficial materials like some vitamins especially vit. K and members of B complex. (b) Toxic material to be excreted

F***s: (200 ml/day)
pH: (5.0 – 7)
water: 75% , solids 25%

The solids include 30% bacteria, 15% inorganic materials mostly calcium and phosphate, 5% fat and fat derivative, also there are desquamated cells, mucus and small amount of digestive enzymes.
There are also variable amounts of glucose and other indigestive fibers.

Movement of the Large intestine:
(1) Toxic Rhythm (Myogenic )
(2) Segmentation movement: Myogenic that helps absorption.
(3) Peristaltic movement: by local reflex.
(4) Anti peristaltic movement: by local reflex, mainly at end of ascending color if there is non absorbed water and food.
(5) Mass peristaltic:
- It is long reflex due to arrival of food to stomach and is called gastro-colic reflex. The same occurs in small intestine and the reflex is called gastro-ileal reflex.
- These results in rapid pushing of the colonic contents to re**um. Distension of re**um will result in sense of defecation and may initiate defecation reflex.

Defecation
Mechanism of defecation:
It is spinal reflex under high control.

The spinal reflex:
Stretching the re**al wall send impulses to the spinal cord to stimulate the pelvic nerve. Pelvic nerve is the parasympathetic supply that stimulate wall contraction and open the internal a**l sphincter.
The external sphincter is skeletal muscle under voluntary control.

Higher control is:
a) Inhibition of the reflex if the condition is unfavorable for defection.
b) Stimulation of the reflex if the conditions are favorable conditions