Gastrointestinal tract Physiology Dr Suaad M Ghazi MBCh

Gastrointestinal tract Physiology Dr. Suaad M. Ghazi MBCh. B, MSc, Ph. D

Objectives of Lecture 10 1. Describe the regulation of defecation reflex. 2. Explain the main functions of liver.

Defecation reflexes ♦ The average transit time from caecum to pelvic colon is 12 hrs, but passage from the pelvic colon to the anus may take days. ♦ Mass movement forces feces into the rectum the desire (urge) for defecation is initiated reflex contraction of the rectum and relaxation of the anal sphincters.

Defecation is prevented by tonic constriction of 1. The internal anal sphincter ♦ Is a circular mass of smooth muscle that lies immediately inside the anus. ♦ Supplied by sympathetic nerve fiber which is excitatory and by parasympathetic fibers which is inhibitory.

2. The external anal sphincter ♦ Is compsed of striated voluntary muscle that surrounds the internal sphincter and also extends distal to it. ♦ The external sphincter is controlled by nerve fibers in the pudendal nerve, which is part of the somatic nervous system and therefore is under voluntary conscious control.

♦ Defecation reflex initiated parasympathetic nerve fibers: through 1. The sensory fibers pass through the pelvic nerves to the sacral segments of the spinal cord. 2. The spinal cord returns signals by way of the parasympathetic fibers in the pelvic nerves to the enteric nervous system and produces an effective and strong peristaltic wave in the sigmoid and rectum forcing feces toward anus.

3. Parasympathetic fibers relax the internal anal sphincter to allow the passage of feces. 4. Both the internal and external anal sphincters must relax for feces to be eliminated. However, these reflexes open the internal sphincter but close the external sphincter.

DEFECATION REFLEX

DEFECATION REFLEX Sensory neurone Parasympathetic neurone Somatic neurone Stretch receptors + - + Rectum Anal sphincters

The Defecation Reflex Figure 24. 25

♦ The actual release of feces requires a conscious effort to open the external sphincter. ♦ If circumstances are unfavorable for defecation, voluntary tightening of the external anal sphincter can prevent defecation despite the defecation reflex. ♦ If defecation is delayed, the distended rectal wall gradually relaxes, and the urge to defecate subsides.

♦ Next mass movement propels more feces into the rectum, once again distending the rectum and triggering the defecation reflex. ♦ If circumstances are favorable for defecation, voluntary relaxation of external anal sphincter can override the contraction directed by somatic motor neuron and consequently defecation occurs.

♦ When defecation does occur, assisted by voluntary straining movements Taking a deep breath Closure of the glottis Contraction muscles of the abdominal Pelvic floor to extend downward to pull outward on the anus to evacuate the feces.

♦ If the external sphincter is kept contracted, the defecation will not occur. ♦ Defecation reflexes die out after a few minutes, and they remain quiescent for several hours or until additional amounts of feces enter the rectum.

♦ Distention of the stomach by food initiates contraction of the rectum and frequently a desire to defecate, this response is called the gastrocolic reflex. ♦ It is mediated by parasympathetic fibers. ♦ There is some evidence due to CCK and gastrin actions on the colon and is not neurally mediated.

♦ Defecation after meals is the rule in children. In adults, habit and cultural factors. ♦ Emotional factors strongly influence large intestinal motility via the extrinsic autonomic nervous system. Irritable bowel syndrome may occur during periods of stress and may result in constipation (increased segmentation contraction) or diarrhea (decreased segmentation contractions).

Bacterial action in the colon ♦ Numerous bacteria especially colon bacilli, are present in the absorbing colon. ♦ The substances formed as a result of bacterial activity are vitamin K, vitamin B 12, thiamin, riboflavin, and various gases that contribute to flatus in the colon especially carbon dioxide, hydrogen gas, N 2, NH 4+ and methane.

♦ One of the actions of colonic bacteria is to convert NH 3 to NH 4+. ♦ Total colectomy blood ammonia levels, which would be exacerbated in a person with liver cirrhosis. ♦ Gas within the colon is primarily derived from Fermentation of undigested oligosaccharides by bacteria.

♦ Vitamin K is especially important, its insufficient in ingested food to maintain adequate blood coagulation. ♦ The colonic gas, or flatus, is produced in large intestine through the breakdown of undigested carbohydrates by intestinal bacteria.

♦ All gases except N 2 diffuse through the intestinal mucosa. ♦ Diffusion of gas from the blood to the intestinal lumen is responsible for the N 2 present in intestinal gas and is influenced by the atmospheric pressure.

♦ The feces are composed of: Ø Dead bacteria (such as Escherichia coli 1/3 of faecal weight). Ø Fat (derived from fat formed by bacteria and fat in the sloughed epithelial cell). Ø Inorganic matter. Ø Protein. Ø Undigested roughage of the food. Ø Dried constituents of digestive juices such as bile pigment. Ø Sloughed epithelial cells.

♦ The brown color of feces is caused by stercobilin and urobilin, which are derivatives of bilirubin. ♦ The odor is caused by the products of bacterial action which vary from one person to another depending on each person’s colonic bacterial flora and on the type of food eaten.

THE LIVER

Hepatic lobule

The liver ♦ The total blood flow through the liver is about 1450 ml/min. . ♦ It has double blood supply from hepatic artery (20%) and portal vein (80%). The portal vein drains the digestive tract, the spleen, pancreas and gallbladder. ♦ The liver lobule is constructed around a central vein that empties into the hepatic veins and into the vena cave.

The basic histological structure of a liver lobule.

♦ The venous sinusoids are lined by two types of cells [1] typical endothelial cells. [2] large Kupffer cells which are tissue macrophages (which is a part of RES) capable of phagocytizing bacteria and other foreign matter in the blood. These cells can remove 99% of bacteria in the portal venous blood before they can pass all the way through the liver sinusoids.

♦ The endothelial lining of the venous sinusoids has extremely large pores, therefore, the plasma substances and even the proteins can move freely from the blood through the endothelium to the space below it and become in direct contact with hepatic cells. ♦ Because of the pores in the endothelium of the hepatic sinusoids, the plasma proteins can pass to the interstitial spaces.

♦ Therefore the lymph draining from the liver usually has a protein concentration of about 6 gm/dl, which is only slightly less than the protein concentration of plasma. ♦ Also, the extreme permeability of the liver sinusoids allows large quantities of lymph to form. Therefore, about one half of all the lymph formed in the body under resting conditions arises in the liver.

Pressure and resistance in hepatic vessels ♦ The pressure in the hepatic vein leading from the liver into the vena cava is about 0 mm Hg. ♦ Whereas the pressure in the portal vein leading into the liver is about 9 mm Hg. ♦ This means that the resistance to blood flow through the liver sinusoids is normally low.

♦ However, in some pathological conditions such as liver cirrhosis, the hepatic vascular resistance may increase markedly because many vascular channels through the liver are severely restricted by fibrotic constriction of the sinusoids or even complete blockage or destruction. ♦ An increase in pressure in the veins draining the liver dams blood in the liver sinusoids and thereby causes the entire liver to swell markedly and congested.

♦ The most, common cause of hepatic congestion is cardiac failure. ♦ When the hepatic venous pressure rises only 3 -7 mm Hg above normal, excessive amounts of fluid begin to transudate into the lymph and also to leak through the outer surface of the liver capsule directly into the abdominal cavity.

♦ This fluid is almost pure plasma, containing 80 - 90% as much protein as normal plasma which may be so large that lead to ascitis (free fluid in the abdominal cavity) especially when the hepatic venous pressure is between 10 -15 mm Hg.

Blood flow into the liver comes from tow sources: ♦ Oxygenating blood containingmetabolites from peripheral tissues reaches the liver via the hepatic artery. ♦ Blood coming to the liver through the hepatic portal vein is rich in absorbed nutrients from the GIT, and contains haemoglobinbreakdown products from the spleen. ♦ Blood leaves liver in the hepatic vein.

♦ Bile synthesised in the liver is secreted into the common hepatic duct for storage in the gallbladder. From there, its secreted into the lumen of the intestine through the common bile duct.

Metabolic functions of the liver [1] Carbohydrate metabolism ♦ Storage of glycogen: The liver is important for maintaining a normal blood glucose concentration. Storage of glycogen allows the liver to remove excess glucose from the blood, store it, and then return it to the blood when the blood glucose concentration begins to fall too low. This is called the glucose buffer function of the liver. Circulating adrenaline and glucagon mobilize this liver glycogen and convert it to blood glucose. Only liver has the glucose-6 phosphatase necessary for this breakdown.

♦ Conversion of galactose and fructose to glucose. ♦ Gluconeogenesis : When the glucose concentration begins to fall below normal, large amounts of amino acids are converted into glucose, for maintaining a relatively normal blood glucose. ♦ Formation of many important chemical compounds from the intermediate products of carbohydrate metabolism.

[2] Fat metabolism ♦ Bile salts produced by the liver are essential for the digestion and absorption of fat. ♦ The fat-soluble vitamins (A and D) & watersoluble vitamins (B 12 ) are stored in the liver. ♦ The liver is the site for the synthesis of large quantities of cholesterol and phospholipids. ♦ The liver is the site for conversion of large quantities of carbohydrates and proteins to fat.

♦ The depot fat is converted to the ketone bodies (acetoacetic acid, βhydroxybutyric acid and acetone) by the liver. These ketone bodies are metabolized by other tissues with production of heat and energy. Ketosis is an excess of ketone bodies in the blood, does not occur in liver failure.

[3] Protein metabolism ♦ The liver is the main organ for deamination of surplus amino acids with the production of ammonia. In liver failure, the amino acids in the blood are increased and they appear in the urine.

♦ The liver is the only organ that can convert ammonia to urea. In the absence of this function of the liver to form urea, the plasma ammonia concentration rises rapidly and results in hepatic coma and death. ♦ Ability to synthesize certain amino acids and other important chemical compounds from amino acids. The non-essential amino acids can all be synthesized in the liver.

[4] Blood ♦ The liver plays an important role in the formation and destruction of RBC. ♦ The liver is a site of formation of RBC in fetal life. ♦ It stores the factors principal for the normal maturation of RBC such as iron and B 12. ♦ It removes from the blood the bilirubin formed when the RBC are broken down and excretes this bilirubin down the bile duct into the duodenum, as a bile pigments.

♦ The liver manufactures the plasma proteins. The plasma albumin exceeds the plasma globulin and the normal albumin/globulin ratio is 1. 7/1. In liver failure the plasma protein pattern is altered and the globulin fraction may exceed the albumin fraction. ♦ The blood clotting factors such as prothrombin and fibrinogen are made in the liver. In liver diseases, blood clotting may be impaired leading to bleeding from the skin and mucous membranes.

[5] Vitamin Mineral storage ♦ Vitamin A, Vitamin D, Vitamin E, Vitamin K, vitamin B 12, and Iron. [6] Poisons ♦ Many normal physiological substances as well as drugs are modified by the liver in some way before being excreted by the kidneys. This is called detoxication.

♦ Some substances, such as the short-acting barbiturates, are completely destroyed by the liver. ♦ Other, substances are conjugated with glucuronic acid, glycine, sulphate or acetate.