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Pepsinogen
Pepsinogen release is dependent on the acetylcholine stimulation of the peptic cells, and the presence of hydrochloric acid in the stomach. Pepsinogen per se has no digestive function. When it comes in contact with previously formed pepsin and hydrochloric acid, it is activated as pepsin. Pepsin is as necessary as hydrochloric acid for protein digestion in the stomach.
The proteolytic activity of pepsin takes place in an acidic setting (optimum pH of 1.8 to 3.5). Above 5, pepsin has almost no activity.
Acid-Peptic Disorder
The pathology of acid-peptic disorder lies behind the imbalance between the rate of secretion of gastric juice and the degree of protection provided by the mucosal barrier and neutralization of gastric juice by pancreatic secretions. The scenario can be caused by Helicobacter pylori infecting the gastrointestinal tract and hypersecretion of acid-peptic complex. Smoking can also increase nervous stimulation of the stomach secretory glands. Alcohol and aspirin in turn breaks the mucosal barrier. Caffeine also increases gastric acidity.
Caffeine inhibits phosphodiesterase thus increasing cAMP within cells. In the parietal cells, this will mean a stimulation of gastric juice secretion. Aspirin and other non-selective anti-inflammatory drugs inhibt COX1, which generates prostanoid for epithelial cytoprotection.
Phases of Gastric Secretion
Gastric secretion involves three phases: cephalic, gastric, and intestinal phase. Cephalic phase occurs even before food enters the stomach. It results from the sight, smell, thought, or taste of food. Neurogenic signals that cause the cephalic phase of gastric secretion can originate in the cerebral cortex or in the appetite centers of the amygdala or hypothalamus. They are transmitted through the dorsal motor nuclei of the vagi and then through the vagus nerves to the stomach (Guyton and Hall, 2000). The cephalic phase accounts to 20 percent of gastric secretion.
The gastric phase accounts for 70 percent of gastric secretion. Once food enters the stomach, it excites the vagovagal reflexes, the local enteric reflexes, and the gastrin mechanism.
The presence of food in the upper part of the small intestine can cause the stomach to further release gastric juice. This is caused by small amount of gastrin secreted in the mentioned site of the small intestine.
Regulation of Gastric Secretion by Nervous and Hormonal Mechanism
The basic factors that stimulate gastric secretion are acetylcholine (involved via vagal/parasympathetic stimulation), gastrin, and histamine. These substances function by attaching to specific receptors, leading to the secretion of the gastric glands. Acetylcholine excites all glands involved in the secretion of hydrochloric acid, pepsinogen, and mucus. Histamine and gastrin, on the other hand, strongly stimulate the secretion of hydrochloric acid by the parietal cells but have little effect in stimulating other gastric secretory cells.
The enteric nervous system can stimulate release of H (to form HCl), either directly or indirectly. The nerve endings of fibers innervating the parietal cells secrete acetylcholie at the neuroeffector junction. The corresponding receptor is M3. Succeeding events include the increase in cytosolic calcium, stimulation of protein kinases, and activation of H /K ATPase. The end result is increased hydrochloric acid secretion.
The indirect stimulation of the parietal cells by the nervous system occurs as acetylcholine attaches to M1 receptor of enterochromaffin-like cells. This gives way to the release of histamine. Histamine in turn binds to H2 receptors found in the parietal cells. Afterwards adenylyl cyclase gets activated. This increases intracellular cAMP, activating protein kinase. Eventually this will stmulate H /K ATPase.
The same direct and indirect mechanisms can be onserved in parietal stimulation by gastrin-secreting cells.
The Stomach
The main site of pathology in acid-peptic diseases is the stomach. It is therefore the site of action of the antacids used in treating these disorders. It is indeed important to know how stomach contributes in the chemical digestion of food. What are the glands in the stomach involved in the process? What specific substances are they secreting? What are the stimuli and the mechanisms involved in the release and regulation of these secretions? How does an excess of these secretions contribute to the development of acid-peptic disorders?
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The Gastrointestinal Tract and the Accessory Organs for Digestion
The gastrointestinal tract or the alimentary tract is divided into two main parts: the upper and the lower. The upper part includes the mouth, the pharynx, the esophagus, and the stomach. The lower part is composed of the small and the large intestine, together with the anus.
Throughout the tract, we see many specialized glands. The functions of these secretory glands are: (1) for digestion of food through enzymes secreted anywhere from the mouth down to the distal end of the ileum; and (2) for lubrication and protection of the tract as being carried out by mucus secreted from mouth to anus.
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Antacids are drugs used to reduce intra-gastric acidity. They are mostly indicated in addressing stomach conditions that are characterized by an increase in the stomach acidity, like gastro-esophageal reflux and peptic ulcer. Collectively these conditions are termed as acid-peptic diseases.
In these disorders, the excessively low pH of the gastric content-major contributor is the hydrochloric acid and pepsin- erodes mainly the mucosal barrier of the gastric epithelium, leading to inflammation and ulceration. Epithelial injuries to nearby structures like in the esophagus are possible though, since gastric contents can spill out to the said area (as in gastro-esophageal reflux).
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In PD the patient's brain has neurotransmitter imbalance. Neurotransmitter are substances which signal specific instructions for proper functioning of our nervous system.
In this case the neurotransmitter imbalance is between dopamine and acetylcholine. dopamine becomes less, and because of this nothing restricts the excitatory functions of acetylcholine. And so the muscles are always contracted (excited), even in an individual's resting state.
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Lately an NBA forward, Brian Grant was reported to have Parkinson's disease. At 37 years old, such news is very unusual coz the condition usually affects old people.
Other known personalities diagnosed to have Parkinson's are Michael J. Fox and Muhammad Ali.
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Emphysema belongs to a group of diseases known as Chronic Obstructive Pulmonary Diseases. Such condition may be genetically predisposed due to a defect or lack in alpha1 anti-trypsin, which (simple and plain) protects the pulmonary system from damage caused by exttrinsic or intrinsic factors.
Nevertheless, more commonly affected by the disease are adults, due to long term smoking or environmental pollution
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Patient was given Phentolamine. How does it act? Why was it useful in this case? Phentolamine is a non-selective alpha-adrenoceptor antagonist. It inhibits alpha 1 receptors usually found in the smooth muscles of blood vessels, allowing the walls to relax and the lumen to dilate. This will decrease vascular resistance and blood pressure. However it inhibits presynaptic alpha 2 receptors as well. Alpha 2 modulates release of catecholamines in the presynaptic terminals. Phentolamine, therefore, will inhibit such modulation. Its potential effect is usually seen in the heart as tachycardia.
The use of phentolamine for hypertensive emergencies is justified with the rationale that we would want to counteract overexpression of sympathomimetic effect, as occurring with the presence of tyramine. According to Hoffman (2007) phentolamine and other alpha blockers theoretically bring about such effect.
In the management of emergency hypertension, we would not want to abruptly decrease the pressure for this may cause hypoperfusion. A 25% initial decrease in blood pressure is ideal. Phentolamine being a non-selective drug should help in acquiring this effect. Because of phentolamine, peripheral resistance decreases (alpha 1 antagonism), but cardiac output potentially increases (alpha 2 antagonism). The decrease of pressure is due to decreased vascular resistance. But such decrease is only gradual for blood flow and cardiac output will increase
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