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    Paramedic student

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  1. This is perfect. I believe this is my exact form of thinking but put into words that I can digest and fully understand. Thanks so much! Hey Plain, You are right my friend I see not benefit it getting an "answer anyone can cut and paste but it doesn't help me to learn. Imagine showing upto treat a patient and being like huh? Where my cut and paste treatment haha. Stroke patient is definitely a candidate I think anyone that can be immobilized without help is something that is a potential candidate for crush syndrome. Thanks
  2. I put a question to all of you here. When speaking in regards to immobilized patients and the compression of muscle tissue in a specific area causing crush syndrome that will release toxic metabolites/enzymes. Would you consider the following as potential candidates for crush injuries. Obese patients who can't walk but and are alone in their homes? Chronically depressed patients who mentally cannot move and live independently? Please bear with me As I am still learning so if my answer are incorrect please just correct my constructively
  3. Hi. Just want to thank you for your answer. Crush injuries and their associated causes and effects on the body formed a portion of a test paper that I have already finished. What I found was that Mosbys Paramedic textbook didn't provide me with enough information to actually fully understand the effects behind crush injuries further than the aspect of natural disasters and obvious crush. What I want to know and understand is how can a crush injury be caused by a not so obvious MVA, Building collapse and so forth. I have read ncbi and found it to very useful in digging further into the whole "pre-cursor" for crush injuries. Especially in relation to crush caused by an excessively overweight patient who has suddenly become immobilized, this was a very interesting read. I do appreciate your help in pointing me in the direction of additional information. Hi Off Label. I agree with your reasoning. However would the end organ damage exist if the crush didn't occlude the anatomical process that would have taken place without the obstruction. From my understanding the end of organ damage is caused by the release of the crush object or by an occlusion met when the crush has occurred. So far I have found this topic very interesting. In Australia up until recently the ANZCOR actually advised against removal of crush objects, however have moved away from this and recommended where safe to do so that they are removed. Thanks again for your feedback. Hi Spock, Thank you for this, you are right in so far as the DKA from a diabetic patient, in fact this was a case scenario in my workbook. I found researching it interesting. What I was further trying to understand is not so much the "cut and dry" of crush injuries causing toxic releases but more the other side of the equation where a medical condition may promote a crush injuries (DKA diabetic who is immobilized).
  4. Hi Everyone, I am having a little trouble seeking an answer to this question. what type of medical conditions could result in a crush injury or crush syndrome. Would this be something along the lines of Diabetes? Thank you for your input.
  5. Thank you guys appreciate the information.
  6. Ha You are right, why do we need to know what cytochrome oxidase is, at a cellular level. We are there to treat it. But that is the question they wish to have an answer for. But to answer your question, Cytochrome oxidase is just part of the cellular reaction that cyanide has, the most important thing that we need to know at an EMT or above level is the shift in the oxyhaemoglobin dissociation curve and how our treatment can rectify this injury. The enzyme cytochrome c oxidase or Complex IV is a large transmembrane protein complex found in bacteria and the mitochondrion of eukaryotes. I believe that your cyanide poison kits that are present in some states in the Americas actually acts on this enzyme to promote a positive shift in the curve, however I have no researched this a lot. But hey I am just a training, I like this forum so far, very helpful people. I am sure I will have other questions. Thanks again all.
  7. Hi There, I don't judge people, no need to clarify. I appreciate any and all feedback required. Thank you very much for your time mate.
  8. Hi, I am currently studying paramedics within Australia. Could you find me the video? That would be appreciated, although I have actually watched a few videos regarding this. Thanks! Hi Off Label, In a perfect world I would say that I understand 85% of this, yes. I found the major cause of cyanide poisoning is the ability for the cellular damaged causes by the attachment to hemoglobin. Do you care to elaborate on this? I am very much happy for any kind of constructive feedback
  9. Hi Everyone, I have been working on the pathophysiology of Cyanide poisoning I believe that I have captured this correctly, but would love a second a opinion.. Pathophysiology: Cyanide exposure can be a result of inhalation, ingestion or absorption. Once this has entered the body it is rapidly spread to the organs of the body. Inside the cells of the body the cyanide binds to ubiquitous metalloenzymes, rendering them inactive for use. The primary reason toxicity causes by cyanide poisoning is a result of the inactivation of cytochrome oxidase at cytochrome A3. Intracellular, cyanide attaches itself to ubiquitous metalloenzymes, rendering them inactive. The toxicity results from inactivation of cytochrome oxidase and further uncouples mitochondrial oxidative phosphorylation and inhibiting cellular respiration even in the presence of excessive oxygen saturation during treatment. Because of this cellular respiration shifts from aerobic to anaerobic, causing a rise is lactic acid. Because of this process the brain and heart which are at the highest risk due to the additional oxygenation required for normal homeostatic purposes. One type of treatment (Antidote) of cyanide positioning can be to convert (oxidize) ferrous ions in hemoglobin to ferric ions. This forms methemoglobin, which is hemoglobin with ferrous ion in the oxidized state. Cyanide which has a greater attraction to these ferric states of the cells. Because of this the cyanide is released from the cytochrome oxidase and combines with the newly created methemoglobin. This process allows cytochrome oxidase to results its function in cellular respiration. Methemoglobin cannot transport oxygen, so without counter measures this will result in further tissue damage and necrosis. So this all forms part of a 3 phase treatment plan that is aimed at restoring the hemoglobin to its original state. Through the administration of amyl nitrate, sodium nitrate the conversion of ferrous hemoglobin to methemoglobin to capture the cyanide molecules, Further to this administration of hydroxocobalamin with or without sodium thiosulfate allows the detoxification to be completed and cellular respiration recommence. Please feel free to provide constructive feedback
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