The primary function of gastrin is the stimulation of gastric acid secretion. It does not have a direct effect on exocrine or endocrine pancreatic function, and it does not participate actively in the digestion of starches.
Stimulation of pancreatic enzyme secretions
Release of insulin in response to glucose load
Conversion of polysaccharides to monosaccharides
Stimulation of HCl secretions by parietal cells
Ghrelin hormone has an important role in regulation of growth hormone secretion and energy balance. Gastric acid secretion is regulated by gastrin (in the stomach) and secretin (in the intestine). Pancreatic enzyme, bicarbonate, and biliary fluid secretion are functions of cholecystokinin in the intestine.
Gastric acid fluid
Absorption is accomplished by active transport and diffusion. A number of substances require a specific carrier or transport system. For example, transport of amino acids and glucose occurs mainly in the presence of sodium. The other electrolytes are not required for this specific process.
Brush border enzymes aid in the digestion of carbohydrates and proteins. The only food listed that is strictly carbohydrates is the garlic toast.
Green, leafy vegetables
Water absorption from the intestine is linked to absorption of osmotically active particles, such as glucose and sodium. It follows that an important consideration in facilitating the transport of water across the intestine (and decreasing diarrhea) after temporary disruption in bowel function is to include sodium and glucose in the fluids that are consumed. None of the other distractors addresses this principle. Activating the pancreatic enzymes of trypsin and elastase is needed for protein digestion and absorption. Emulsification of fats begins in the stomach and continues in the duodenum under the influence of bile from the liver.
Activating the pancreatic enzymes of trypsin and elastase
Activation of the ATP channels
Emulsification of fats
Facilitating the absorption of osmotically active particles
As with glucose, many amino acids are transported across the mucosal membrane in a sodium-linked transport system (for absorption) that utilizes APT as an energy source. Fat uses bile salts that form micelles for transport to the intestinal villi. Fat emulsification is a digestive process. Brush border enzymes break down carbohydrates for transport.
Bile salt micelles
Brush border enzyme
Bile performs a central role in fat metabolism. Gallbladder disease and the accompanying disruption of normal bile release do not result in impaired digestion of carbohydrates, impaired glucose metabolism, or inadequate gastric acid synthesis.
Impaired glucose metabolism
Impaired digestion of fats
Incomplete digestion of starches
Inadequate gastric acid production
Vitamin K is synthesized by colonic flora, and long-term antibiotic use can result in vitamin K deficiency. Antibiotic use does not curtail mucus production or protein metabolism, and it does not precipitate excessive release of pepsin.
Vitamin K deficiency
Impaired mucus production
Excessive release of pepsin
Impaired protein metabolism
The act of vomiting is integrated in the vomiting center, which is located in the dorsal portion of the reticular formation of the medulla near the sensory nuclei of the vagus. The vomiting center can be activated directly by irritants or indirectly following input from four different sources, one of which is the chemoreceptor trigger zone (which is activated by chemical agents such as drugs and toxins).
Chemoreceptor trigger zone
The recently developed Neurokinin-1 (NK-1) receptor antagonists are used for the treatment of acute and delayed chemotherapy-induced nausea and vomiting. These drugs act centrally to block the activation of the NK-1 receptors in the vomiting center. Serotonin (5-hydroxytryamine) antagonists are involved in the nausea and emesis associated with cancer chemotherapy and radiation. Promethazine is a neuroleptic medication. Compazine, a dopamine (D2) receptor antagonist, depresses vomiting caused by stimulation of the chemoreceptor trigger zone.
Serotonin (5-hydroxytryamine) antagonists
Neurokinin-1 receptor antagonists
Compazine, a dopamine (D2) receptor antagonist
Promethazine, a neuroleptic medication
Achalasia produces functional obstruction of the esophagus so that food has difficulty passing into the stomach, and the esophagus above the lower esophageal sphincter becomes distended. Symptoms following high-fat intake is usually associated with gallbladder disease. Projectile vomiting is usually related to increased intracranial pressure. Vomiting blood can be associated with esophagitis, erosion of the esophagus, bleeding esophageal varices, or esophageal cancer.
Projectile vomiting across the room unrelated to meals
Feeling like there is food stuck in the back of the throat
Excessive heartburn following a high-fat meal of French fries
Vomiting large amounts of bright red emesis
Complications can result from persistent reflux, which produces a cycle of mucosal damage that causes hyperemia, edema, and erosion of the luminal surface. Strictures are caused by a combination of scar tissue, spasm, and edema, which narrow the esophagus. The most frequent symptom of gastroesophageal reflux is heartburn. Other symptoms include belching, wheezing, chronic cough, hoarseness, and epigastric or retrosternal area chest pain, radiating to the throat, shoulder, or back. Because of its location, the pain may be confused with angina.
Difficulty in swallowing with feelings that food is “stuck” in the throat
Burning sensation a half-hour after a meal
“Hoarseness” unrelieved by coughing or taking a drink of water
Substernal chest pain that radiates to the shoulder and arm
Dysphagia is by far the most frequent complaint of persons with esophageal cancer. It is apparent first with ingestion of bulky food, later with soft food, and finally with liquids. Heartburn, reflux, and gastritis are not health problems that are closely associated with the development of esophageal cancer.
A new onset of gastroesophageal reflux in a previously healthy individual
Dysphagia in an individual with no history of neurologic disease
Recurrent episodes of gastritis that do not respond to changes in diet
Heartburn after an individual consumes high-fat meals
Acute gastritis refers to a transient inflammation of the gastric mucosa that is most commonly associated with local irritants such as bacterial endotoxins, alcohol, or aspirin. Gastritis associated with excessive alcohol consumption often causes transient gastric distress, which may lead to vomiting, bleeding, and hematemesis. Allergic response to ingested substances may cause acute itching, rash, vomiting, or diarrhea. Gastric reflux causes esophageal inflammation rather than gastritis.
Most cases of peptic ulcer are caused by H. pylori, which are a small, curved, gram-negative rods that can colonize the mucus-secreting epithelial cells of the stomach; these bacteria secrete urease, which enables them to produce ammonia to buffer the acidity of their immediate environment. H. pylori is nonerosive and produces enzymes and toxins that have the capacity to interfere with mucosal protection against gastric acid, produce intense inflammation, and elicit an immune response. Chronic infection with H. pylori can lead to gastric atrophy and peptic ulcer and is associated with increased risk of gastric adenocarcinoma and low-grade B-cell gastric lymphoma. The characteristic pain is relieved by food or antacids. Ischemia is a cause of stress ulcers, which is manifested by painless upper gastrointestinal tract bleeding.
Gastric cancer due to metaplasia changes in the cells
Failure to thrive due to malabsorption
GI bleeding due to peptic ulcer formation
Pyloric stenosis due to inability to empty the stomach
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