IB BIO HL Option H; H2: Digestion

H.2.4: Outline the control of digestive juice secretion by nerves and hormones, using the example of secretion of gastric juice

Before food reaches the stomach, gastric juice is already being secreted, as a result of a reflex action. The sight or smell of food stimulates the brain to send nerve impulses to exocrine gland cells in the wall of the stomach. The gland cells start to secrete gastric juice in response. The food is detected by chemoreceptors. Impulses are sent from these receptors to the brain, which sends more nerve impulses to the exocrine gland cells. When food is in the stomach, impulses are also sent to endocrine gland cells in the stomach lining that secrete a hormone called gastrin. Gastrin is carried to the exocrine gland cells in the stomach wall, where it stimulates them to increase the secretion of hydrochloric acid. This causes the pH of the food that has entered the stomach to fall to about pH 3. or the initial release of gastric juice under nerve stimulation after sight or smell of food, and sustained release under the influence of gastrin secreted when food is in the stomach

H.2.6: Outline the reasons for cellulose not being digested in the alimentary canal

Cellulose cannot be digested in the alimentary canal because humans lack the gene that codes for the enzyme cellulase and so cannot make it. However, undigested cellulose is an important part of dietary fibre, which has beneficial effects on the digestive system.

H.2.1: State that digestive juices are secreted into the alimentary canal by glands, including salivary glands, gastric glands in the stomach wall, the pancreas and the wall of the small intestine.

Digestive juices are secreted into the alimentary canal by glands, including salivary glands, gastric glands in the stomach wall, the pancreas and the wall of the small intestine.

H.2.5: Outline the role of membrane-bound enzymes on the surface of epithelial cells in the small intestine in digestion

Enzymes secreted by exocrine gland cells become mixed with the food in the alimentary canal and carry out all the initial stages of digestion. However, some of the enzymes that complete the process of digestion work in a different way. They are produced by the wall of the small intestine, but are not secreted. Instead, these enzymes remain in the plasma membranes of cells on the surface of the villi. The active sites of the enzymes are exposed to the food in the small intestine. They can digest their substrates and the products of digestion can then immediately be absorbed. Epithelium cells tend to be lost from the tips of villi by abrasion, but the membrane-bound enzymes continue to work as they become mixed into the food in the small intestine. - some digestive enzymes (f.x. maltase) are immobilised in the exposed plasma membranes of epithelial cells in intestinal villi

H.2.2: Explain the structural features of exocrine gland cells

Exocrine gland cells: - one or two prominent nucleoli inside the nucleus, for production of ribosome subunits - an extensive area of rough endoplasmatic reticulum, for protein synthesis - golgi apparatuses for processing proteins - many large vesicles (secretory granules) for storage of the substance being secreted and transport of them to the plasma membrane - mitochondria to provide ATP for protein synthesis - secretory cells grouped into acini and ducts Exocrine glands: The secretory cells in an exocrine gland are in a layer that is only one cell thick. The total area of the layer of secretory cells can be very large because of invagination and branching. The digestive juice is released from the cells by exocytosis. It is then discharged from the gland by travelling along ducts. One group of secretory cells, clustered around the end of a duct, is called an acinus. (pl. acini)

H.2.8: Discuss the roles of gastric acid and Helicobactor pylori in the development of stomach ulcers and stomach cancers

Helicobactor pylori is an acid-tolerant bacterium that infects the lining of the stomach. 1. Stomach ulcers (areas of damage to stomach lining): - antacid treatments may relieve the symptoms of ulcers for a while - antimicrobial treatments that eliminate H. pylori infection cure ulcers on a long-term basis - H. pylori infection is strongly associated with the presence of ulcers - voluntary infection with the bacterium has shown that it can cause gastritis, which often leads to ulceration - about half of the H. pylori strains isolated from patients with stomach disease produce toxins that cause inflammation - and patients infected with these strains tend to have the most severe ulceration - proteases and other enzymes that are released by H. pylori damage the stomach lining 2. Stomach cancer (growth of tumours in the stomach wall) - a far high percentage of patients with stomach cancer are infected with H. pylori than the general population - H. pylori infection is associated with reduced Vitamin C concentration in gastric juice, which eill increase the chance of a tumour forming - however more evidence is needed to prove a causal link

H.2.9: Explain the problem of lipid digestion in a hydrophilic medium and the role of bile in overcoming this

Lipid molecules tend to coalesce and are only accessible to lipase at the lipid-water interface. Bile molecules have a hydrophilic end and a hydrophobic end, and thus prevent lipid droplets coalescing. The maximum surface is exposed to lipase. The lipase needs to be water-soluble and to have an active site to which a hydrophobic substrate can bind.

H.2.7: Explain why pepsin and trypsin are initially synthesised as inactive precursors and how they are subsequently activated

Pepsin and trypsin are potentially very harmful to the exocrine gland cells that secrete them. They are therefore secreted as inactive precursors, called pepsinogen and trypsinogen. Pepsinogen is activated by hydrochloric acid, which converts it into pepsin. Different cells in the stomach wall secrete pepsinogen and HCl. Activation therefore only happens after secretion. Trypsinogen is activated by the enzyme enterokinase, which is secreted by the lining of the small intestine. Activation therefore only happens when entering the small intestine.