GI Smll Intest Colon Phases MCQ's

Fat in the duodenum causes the most pronounced slowing of gastric emptying. This is because fat takes longer to digest compared to other nutrients such as starch or protein. When fat enters the duodenum, it triggers the release of hormones that signal the stomach to slow down its emptying process. This allows for more time for the fat to be broken down and absorbed by the small intestine. Therefore, the presence of fat in the duodenum has a significant impact on the rate at which the stomach empties its contents.

Iron typically requires a change in valence (charge) for optimal absorption at the intestinal epithelium. This is because iron exists in two different forms in the body: ferrous iron (Fe2+) and ferric iron (Fe3+). Ferrous iron is the form that can be easily absorbed by the body, while ferric iron needs to be reduced to ferrous iron before absorption can occur. Therefore, a change in valence is necessary for iron to be optimally absorbed at the intestinal epithelium.

Release of CCK: I cells release CCK when specific food components are present in the lumen, particularly free fatty acids (FFAs) and certain amino acids. It is not clear whether these nutrients are able to stimulate the I cell directly to release CCK. The presence of FFAs cause other paracrine enterocytes to release a CCK releasing factor – CCK-releasing peptide (CCK-RP) that binds to receptors on the luminal membrane of I cells and stimulates them to release CCK. The second releasing factor, is called monitor peptide. which is secreted by pancreatic acinar cells and enters the duodenum whereupon it also binds to receptors on the I cell luminal membrane to stimulate CCK release. Both of these releasing factors are polypeptides and so, they are subject to proteolytic degradation by pancreatic trypsin in exactly the same way as dietary protein. As the concentration of nutrients and both peptides are decreased as the they are digested and absorbed, the releasing factors are also degraded and the signal for release of CCK is shut off. (slide 9 smll int&colon-White)

The pancreatic peptidases: Pancreatic enzymes are secreted in inactive forms. Activation of proteases is delayed until these enzymes are in the lumen by virtue of the localized presence of an activating enzyme, enterokinase, on the brush border of small intestinal epithelial cells. Enterokinase cleaves trypsinogen to yield active trypsin. Trypsin, in turn, is capable of cleaving all the other protease precursors secreted by the pancreas, thereby resulting in a mixture of enzymes that can almost completely digest the vast majority of dietary proteins (See Buxbaum lectures). Clearly, it is important for these enzymes not to become active in the pancreas itself – which would result in “autodigestion” of the pancreatic tissue as can occur in pancreatitis (very painful). Retention of pancreatic enzymes and consequent pancreatitis can occur due to obstruction (e.g. gallstones or a malignancy); cystic fibrosis and inflammation e.g. alcohol abuse. Besides storing enzymes in an inactive form, the pancreas also secretes a variety of trypsin inhibitors. (slide 23 smll int&colon-White)

The patient has a genetic defect that causes intestinal epithelial cells to produce disaccharidases of much lower activity than normal. Disaccharidases are enzymes that break down complex sugars into simpler sugars. Since the patient's disaccharidases have lower activity, they would not be able to effectively break down maltose, sucrose, and lactose in the small intestine. As a result, these complex sugars would pass through the digestive system undigested and end up in the stool. Therefore, the patient would exhibit higher levels of maltose, sucrose, and lactose in the stool compared to a normal person.

The correct answer is stomach. When we eat a meal, the stomach begins to stretch and distend as it fills with food. This stretching of the stomach walls sends signals to the brain, specifically to the hypothalamus, which is responsible for regulating bodily functions. In response to these signals, the brain initiates a reflex arc that promotes the need to use the restroom, as the body needs to eliminate waste products from the digestive process. Therefore, the proximal signal that triggers the impulse to use the restroom originates in the stomach.

Surgical removal of the distal ileum can lead to the development of anemia within the next twelve months. The distal ileum is responsible for the absorption of vitamin B12, which is necessary for the production of red blood cells. Without the distal ileum, the patient may not be able to absorb enough vitamin B12, leading to a deficiency and subsequently anemia.

The space of Disse is the correct answer because it is the area between the hepatocyte and the sinusoids. It is a narrow space where blood plasma can flow, allowing for the exchange of nutrients and waste products between the hepatocytes and the blood. The other options, such as the bile canaliculus, portal triad, hepatic sinusoids, and central vein, do not directly abut the hepatocyte in the same way as the space of Disse.

Duct bicarbonate secretion: The secretion of bicarbonate by duct cells is critically dependent on a network of ion channels and transporters. The sodium pump actively extrudes sodium ions from the cell in exchange for potassium ions at the basolateral membrane. This process is known as “pump-leak coupling” : the activity of the pump is coupled to the exit of potassium ions through leak pathways – which are usually channels. • Pump-leak coupling underlies solute and water movement across epithelia everywhere in the body. Pump-leak coupling preserves a low concentration of sodium within the cell and a membrane potential that is negative with respect to the outside. The sodium ions that are pumped out of the cell are able to reenter by two pathways – the first in exchange (by a transporter called NHE1) for intracellular hydrogen ions. The hydrogen ions are generated from the hydration of carbon dioxide and water within the cell (catalyzed by carbonic anhydrase) which forms carbonic acid. Each molecule of carbonic acid dissociates into a bicarbonate and a hydrogen ion. The hydrogen ions formed by this process and transported out of the cell, then combine with extracellular bicarbonate to form carbonic acid, which in turn dissociates into carbon dioxide and water. Carbon dioxide enters the cell and combines with water and the cycle repeats continuously. • Thus there is a continuous cycle of formation and breakdown so that for every hydrogen ion formed and exchanged for a sodium ions, one bicarbonate ion leaves the cell. An additional supply of bicarbonate for secretion comes from cotransport (NBC transporter) across the basolateral membrane with sodium – which is then pumped out again! So both of these cyclical pathways supply bicarbonate for secretion. The secretion of anions (bicarbonate and chloride) into the duct generates an electrical potential difference so that the lumen becomes negative with respect to the serosal side. The tight junctions of the ducts are permeable to sodium ions which enter the lumen through this pathway. The net accumulation of sodium, chloride and bicarbonate generate an osmotic driving force for water entry through the paracellular pathway. The bicarbonate ions leave the cell across the luminal membrane in exchange for chloride ions which have been secreted from the cell into the lumen through CFTR channels. Bicarbonate secretion is therefore heavily dependent on the activity of CFTR. Loss of CFTR function (in cystic fibrosis) results in a severe reduction of ductular fluid and bicarbonate secretion. Secretion is not abolished completely, because chloride is present in the acinar fluid. However, this supply is tiny in comparison to that supplied via CFTR. Thus pancreatic juice becomes very viscous and sticky in cystic fibrosis. (slide 6 smll int&colon-White)

As a result of a 90% reduction in pancreatic function, the pancreas is unable to produce enough secretin, a hormone that stimulates the release of bicarbonate from the pancreas. Therefore, the levels of serum secretin would be increased in this case as the body tries to compensate for the reduced pancreatic function.

Digestion & Absorption of Lipids: Dietary fat consists mainly of triglycerides with some cholesterol and fat-soluble vitamins. Fat is emulsified by mechanical action in the stomach. Bile containing the amphipathic detergents - bile acids and phospholipids enters the duodenum following gall bladder contraction. They act to solubilize fat and promote hydrolysis of triglycerides in the duodenum by pancreatic lipase to yield fatty acids and monoglycerides. At the cell membrane the lipid contents of the micelles are absorbed, while the bile salts remain in the lumen. Inside the cell the monoglycerides and fatty acids are re-esterified to triglycerides. The triglycerides and other fat soluble molecules (e.g. cholesterol, phospholipids) are then incorporated into chylomicrons to be transported into the lymph. (slide 29 smll int&colon-White)

Segmentation is a process in the small intestine where the smooth muscles contract and relax in a coordinated manner, mixing and propelling the contents. This process is initiated as a response to bowel wall distention. When the intestine becomes distended due to the presence of food or other substances, the sensory receptors in the intestinal wall detect this and send signals to the smooth muscles to contract and relax, leading to segmentation. This helps in breaking down the food further and promoting absorption of nutrients.

The largest quantity of dietary starch is digested into smaller molecules in the lumen of the duodenum. The duodenum is the first part of the small intestine where the majority of chemical digestion takes place. Here, pancreatic amylase is secreted into the lumen and breaks down starch into maltose, a smaller carbohydrate molecule. This process is essential for the absorption and utilization of carbohydrates in the body.

The sucrase-isomaltase complex is mostly responsible for cleaving a-1,4 dextrins in the small intestine. This complex is made up of two enzymes, sucrase and isomaltase, which work together to break down complex sugars into simpler forms that can be absorbed by the body. Sucrase specifically breaks down sucrose into glucose and fructose, while isomaltase breaks down isomaltose and other a-1,4 dextrins into glucose molecules. Therefore, the sucrase-isomaltase complex plays a crucial role in carbohydrate digestion in the small intestine.

The majority of water reabsorption occurs in the duodenum and jejunum of the gastrointestinal tract following ingestion of a hypotonic meal. This is because these sections of the small intestine have a large surface area and are responsible for the absorption of nutrients and water. The duodenum and jejunum have specialized cells called enterocytes that actively transport water and nutrients from the intestinal lumen into the bloodstream. This process helps to maintain the body's water balance and prevent excessive loss of water in the feces.

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