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SSRI's theoretically increase Serotonin levels. Serotonin is an agonist to the 5HT-3 receptors. The 5HT-3a primarily associated with the upper gut and the 5HT-3b with the lower gut. I would guess that theoretically again, SSRI's would tend to increase nausea, emesis, and diarrhea. There may be other effects, but these are the ones I have researched. The ...


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It's all about the synapses, the places where separate neurons connect to one another. All psychoactive drugs act in some way so as to modulate the signals that are passed from one neuron to another. Nicotine acts by increasing the effect of signals that pass through a particular type of synaptic receptor called nicotinic acetylcholine receptors (they're ...


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If you look at the very beginning of the Wikipedia page, you'll see that azacitidine is an analog of cytidine, the C letter of both DNA and RNA fame. Decitabine is a deoxy derivative, and hence would only be incorporated into deoxyribonucleic acid, or DNA. Reading further, by structure azacitidine is ribonucleoside derivative, and is preferentially ...


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Let's figure it out. Suppose an adult with an average blood volume of 5 L (5000 mL) drinks a cup of strong coffee with 100 mg of caffeine in it. Given caffeine's formula weight of 194.19 g/mol, and assuming 100% of the caffeine is in the blood stream, its concentration (from this awesome calculator page from Graphpad, the makers of Prism) would be ...


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From a pharmacology point of view, there is no difference between caffeine in caffeine pills and in a cup of coffee. It doesn't matter, how a chemical substance (in this case caffeine) is made, the effect of the substance is the same. What can make a difference is the presence of secondary plant ingredients. For pure caffeine there are two possible sources: ...


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One possibility is that these antibiotics could disrupt your normal gut bacteria. Given that your gut has the surface area of a tennis court and is typically coated with symbiotic microbes, antimicrobial therapies could dramatically change the population dynamics of your gut ecosystem. One might imagine that the immune system of the gut is in homeostasis ...


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This is a draft. How do the pharmacodynamics of the NSAIDs differ - -? Merck's manual ch. 36 to start little bit at an introductory level: The anti-inflammatory activity of the NSAIDs is mediated chiefly through inhibition of biosynthesis of prostaglandins (Figure 36–2). Various NSAIDs have additional possible mechanisms of action, including ...


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Short answer: different people have different amount of active receptors. In treatment, combination scores of Pharmacodynamics and Pharmacokinetics determine the final effect of the drug. Receptors determine many effects of the drug in many pathways. Different people also sense pains differently (Psychology). Review answer The purpose of treatment is ...


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Check out this consensus statement (PMID 17552466): J Vet Intern Med. 2007 May-Jun;21(3):542-58. Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. Brown S1, Atkins C, Bagley R, Carr A, Cowgill L, Davidson M, Egner B, Elliott J, Henik R, Labato M, Littman M, Polzin D, Ross L, Snyder P, Stepien R; ...


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I don't know of any interesting mechanism that is specific to pain killers, so I will instead answer for drugs in general. Drug action is a complex process consisting of many steps. Let's take a simple example: A systemic direct inhibitor of a kinase. This drug would need to*: Be absorbed into your bloodstream Remain in your bloodstream for sufficient ...


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Your cells produce thymidine by converting uridine using an enzyme called Thymidylate Synthase. 5-Fluorouracil irreversibly inhibits this enzyme. Here is the structure of 5-Fluorouracil: Here is the mechanism the enzyme uses to make thymidine: It looks like the enzyme forms a bond to the uridine ring through a sulfur. 5-Fluorouracil probably inhibits ...



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