Digestive System - Paper 2000

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2000_2^nd semester_Q6_PartB  

The three regulatory phases of gastric secretion are the cephalic phase, gastric phase and the intestinal phase. During each of these phases, excitatory and inhibitory influences occurs which regulate gastric secretion.  

The mechanisms involved in the control can be neural and hormonal. The neural controls can be either through long reflexes or short reflexes. Long reflexes represent an afferent limb, which proceeds to an integration center which is normally the CNS and an efferent limb. For example: the afferent limb may detect the distension of the smooth muscle of the gastric wall and the efferent limb may involve the vagus nerve having a stimulatory effect on gastric motility. Short reflexes are when the neurons within the digestive system synapse with one another and produce a reflex. There is no involvement of the ANS.

During the cephalic phase, the sight, thought, taste and smell of food prepares the stomach for gastric secretion. During this phase, the neural mechanism is involved in preparing the stimulatory reflex. The gastric phase begins as soon as food enters the stomach. A reflex caused by the distension of the smooth muscles of the gastric wall is mediated by neural control. Also the chemical nature of the food that enters sparks G cells (enteroendocrine cells) to produce a hormone known as gastrin which has a stimulatory influence on gastric secretion and motility. The intestinal phase is largely inhibitory towards gastric secretion. This phase begins as soon as chyme is ejected into the small intestine. This phase results in the release of intestinal hormone which for a while has an excitatory response to gastric secretion, but later the enterogastric reflex takes over and begins the inhibitory influence. This tightens the pyloric sphincter preventing further entry of chyme into the small intestine and also produces more hormones (such as CCK, secretin) that have an inhibitory influence on gastric secretion and motility.

Major Points: Cephalic Phase --> Gastric Phase --> Intestinal Phase --> explain the neural controls involved --> explain what happens during cephalic phase --> explain what happens during gastric phase --> what happens during intestinal phase.

2000_2^nd semester_Q6_PartA  

The mucosal lining of the stomach is of a simple columnar nature with many goblet cells. Apart from this, the surface is studded with many gastric pits, which are lined by the same epithelium. These pits forms deep glands on the surface of the gastric wall. There are a variety of cells found on the mucosal surface of the stomach. These are parietal cells, mucous neck cells, chief cells, and enterendocrine cells.  

Parietal cells are found dispersed between the chief cells within the gastric glands, and they secrete hydrochloric acid and also intrinsic factor. Hydrochloric acid is responsible for the activation of pepsin which is secreted by chief cells. Intrinsic factor is important for the absorption of vitamin B12 by the small intestine.  

Chief cells are found predominantly at the bottom of the gastric glands and these secrete pepsinogen, the inactive form of pepsin. Pepsinogen is converted to pepsin by contact with hydrochloric acid and then pepsin converts from then on. The mucous neck cells are epithelial cells found at the start of the pits, and no function has been determined as of yet for these cells. The enterendocrine cells are deep within the glands and these secrete important gastric hormones, include CCK, secretin and gastrin which all regulate gastric secretion and motility during the phases. These hormones are secreted into the underlying connective tissue and are carried away by capillary blood.  

The gastric juice produced by the stomach is very acidic. There are four protective barriers the stomach has in order to protect itself from this acidic substance. These are, the high mitotic rate of the epithelial cells, therefore any damage caused is quickly repaired. The impermeability to HCL of the cells below the epithelium, therefore no tissue damage can be caused. The mucosal covering of the epithelial surface protects the underlying tissues and lastly the epithelial cells are connected together by tight junctions, preventing entry of acidic substance into underlying tissues.  

Major Points: What type of epithelium? --> goblet cells --> cells present, where --> what do they secrete --> four protective barriers --> high mitotic rate, mucous layer present, tight junctions between cells, impermeability of underlying tissue cells to HCL.

Summary (Stomach):  

• Major functions of the stomach

• Phases of Gastric Motility

• Composition of Gastric Juice, cells involved and also the protective barriers of the mucosal lining

• Regulation of Gastric Juice, Phases

• Mechanisms of this regulation

2000_2^nd semester_Q7_PartA  

Part I)  

Bile is produced by the liver. It is produced by the liver cells, hepatocytes. Between cords of hepatocytes, there is wide network of leaky capillaries known as sinusoide, which contain special macrophages called Kuffer Cells. Between the tightly packed hepatocytes, there is small channel called the bile canaliculli. This is where the bile is secreted into. The bile canaliculli connect to each other and go towards the hepatic portal areas, which contain the blood vessels, and bile ductules. These ductules eventually combine and form the hepatic common duct which is then connected by the duct from the gall bladder called the cystic duct. The common bile duct, which is the continuation of the hepatic duct then empties into the small intestine and this is where bile eventually ends up. The gall bladder acts as a storage device for bile, and secretes bile when required.  

DIAGRAM --> showing the lobulated structure of the liver bile canaliculli, and also ductules and also the common hepatic duct.  

Part ii)  

The composition of bile is largely bicarbonate ions and bile salts. Bile salts are derived from cholesterol and when released into the small intestine they help emulsify lipids present as part of the chyme. This way, these fat droplets are broken down into smaller droplets and as a result, the surface area of these droplets has tremendously increased therefore allowing for the pancreatic enzymes to hydrolyze these lipid droplets much faster and easily.  

The bile salts also have a function as to make the lipid droplets more soluble therefore they pancreatic enzymes further can hydrolyze these products.