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Revenged

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Everything posted by Revenged

  1. i think that it does sound like trochlear nerve damage... perhaps i should explain it a bit for the orginal poster as what they wanted to know is how can a virus cause double vision... ok, if the virus affects the trochlear nerve it may lead to the nerve becoming non-functional... the trochlear nerve runs from the stem of the brain and supplies the superior oblique muscle of the eye... this is the muscle that moves the eye downwards with the help of the inferior rectus muscle (another muslce of the eye)... if the superior oblique muscle does not work on one side, only the eye with a functional trochlear nerve will be able to use it's superior oblique muscle and so only in this eye will it be able to move the eye downwards... this causes the two eyes to be in different positions within the eye socket and this causes two separate images from different positions to be formed, which causes double vision... so in other words, your friend had a virus that affected a nerve that runs to the eye, which means a muscle that moves the eye can't function and this means that you get a double vision when that muscle of the eye is used (as the muscle only works on one side)... but as the neurologist said, the nerve would grow back and so the double vision shouldn't be permanent... i don't know how long this will take... i don't think the entire nerve needs to be regenrated... so i don't think you can do something like the trochlear nerve is X cm long and if it regenrates at a rate of 1 mm per day it'll take Y days to get better... it isn't like that...
  2. i know that my slagging off of psychology wasn't popular with you glider but bringing scientology into it ... that was a low blow... lol... I think you'll find that in the studies comparing "anti-depressant" to "congnitive behavioural therapy"... it's CBT that wins vertually every time...
  3. i'm glad you agree with my points glider... my experience of psychology was basically an exercise of blindly quoting what other people found in some studies - and much of these things i could tell you and i thought were obvious... and although some things i found interesting (i thought theory of mind and the sally-ann test for autism was quite impressive) it did seem a lot of copy and paste... btw, i'm not convinced by the idea that children with ADHD are bored and need to be stimulated by drugs to be treated... if that were true, most drug addicts would have ADHD... ok, point taking... i think what i have a real issue about is not psychology, it's the fact that medication is being given out like sweets... i would be interested to know why this happens... i don't know whether it's because people go to their doctors and pester them for medication or whether doctors try to medicate just about everyone they can...
  4. i don't think much of most psychology tbh... i think it's a very artificial way of studying behaviour and i don't believe most of it myself... i think what we have now is the medicalisation of what used to be normal behaviour and the view that quite a lot of GPs and psychiatrists is that people can best be treated by medication... i know enough pharmacology to realise that this is nonsense... but as you can see this by the epidemic of people who take anxiolytics and anti-depressants that i'm probably in a minority view there... for ADHD (in my world this is 'naughty children syndrome') amphetamines are given as a 'treatment'... go figure that one out...
  5. yes, i think they mean the same... http://en.wikipedia.org/wiki/Bronchoconstriction http://en.wikipedia.org/wiki/Bronchospasm
  6. what about 'anxiety' is that a compelling indication ... i've seen GPs give propranolol for daft reasons like stop getting stressed during a driving test and this made me think they were pretty harmless...
  7. i always thought diuretics were first line treatment for hypertention... and what was so bad about beta blockers that cause them to stop prescribing them for hypertention?...
  8. yep, ashtmatics shouldn't take beta blockers because blocking beta 2 adrenoreceptors causes bronchoconstriction... i can't really believe that there's any doctor that don't know that... then again asthmatics shouldn't take NSAIDs either because they cause bronchoconstriction but you don't see anything on over the counter medications containing aspirin or ibuprofen about this...
  9. I wouldn't think too much about it... In any case, the delta cells of the islets produce somatostatin that acts to decrease production of both insulin and glucagon...
  10. Revenged

    MCAT

    In the UK there are two exams for undergraduate medicine - UKCAT and BMAT... Some universities want UKCAT and some want the BMAT...
  11. Picking out one very rare side effect is not a good reason not to favour a drug. In any case, all the asthma medication have side effects and none of them are perfect but it is much better that than being unable to breath and dying of an asthma attack.
  12. 1) Asthma is charaterised by bronchoconstriction and inflammation. 2) Typical treatment for asthma is a bronchodilator (beta 2 adrenoreceptor agonist) taken when you have symptoms of asthma. This causes bronochodilation. A steroid inhaler is taken regularly and has an anti-inflammatory effect to prevent inflammtion. These drugs are very good, which is why they are given to vertually everyone with asthma. 3) Sodium cromoglycate (which you are calling 'cromolyn sodium') is an anti-allergy drug and it is rarely prescribed. I have only ever seen it being prescribed to young children. 4) Anti-histamines are NOT used to treat asthma. Anti-histamines do not work for asthma but they are used to treat other allergies such as hayfever and anaphylatic shock. 5) Newer drugs such as Leukotriene receptor antagonists are being produced to treat asthma. Hope that helps.
  13. The three most common treatments for high blood pressure are the thiazide diuretics (e.g. bendroflurazide), beta blockers (e.g. atenolol) and ACE inhibitors (e.g. enalapril). The drugs can be taken together as they work by different mechanisms. I'm guessing 'beta blasters' you mean beta blockers and that by 'alpha blasters' you mean anti-hypertensitves that target alpha adrenoreceptors. Alpha blockers include alpha 1 adrenoreceptor antagonists (e.g. prazosin) but they are old drugs that are very rarely prescribed now and I doubt that you'd be able to take alpha and beta blockers simultaneously. Hypertension can have hereditary causes such as familal hypercholesterolaemia but it is lifestyle factors that are most important. I doubt you can say that having hypertention doesn't cause you to become angry or stressed. I personally would argue that people that are more 'stressed' are more likely to smoke, drink excessive cups of coffee and do more negative things that may cause hypertention but I don't believe that there is a causal link between stress/anger and hypertention. Hypertention is linked with a lot of diseases such as probably stroke, heart attack but chronic hypertention can also lead to renal failure.
  14. all i could remember from immunology is that MHC class I on is where foreign peptides inside the cell are produced to the surface of virus infected cells and stimulates phagocytosis/atoptosis of the cell... and that MHC class II is where bacterial proteins get placed on the end of antigen presenting cells and stimulates the antibody responce... wasn't sure how cancer fits into all this... is it MHC class I pathway that is involved as it involves processing endogenous material?
  15. i don't think cancer cells do not become immune to treatment... i think it is that the treatment doesn't work on all the cancerous cells in the first place... most traditional chemotherapy simply works by stopping cell devision... this is why cancers that are very rapidly growing respond best to this kind of treatment... but a lot of these traditional chemos target all dividing cells in the body, which is why they are so toxic and this is why cancer therapy is traditionally such an ordeal to go through...the perfect example of chemotherapy working at its best is testicular cancer, which is now very easily treatable with combination chemotherapy (bleomycin-etoposide-cisplatin)... but this is only one example... if we had a slow growing benign cancer - such traditional chemotherapy would be next to usless and wouldn't work... alteratively, if we used Avastin - monoclonal antibody that targets angiogenesis (production of blood vessels) - it would be useless are targeting hypoxic areas of tumours... or if we used surgery to remove a breast tumour -the tumour may have already metastasised to the axillary lymph nodes... or we could have pancreatic cancer and by the time the doctors find out you will be dead within the year and the treatment is next to useless... as you can see, cancer is a complicated subject and it's treatments are very different so it's hard to answer such generalised questions... often surgery, chemotherapy and radiotherapy are all used together to try and destroy as much tumours cells as possible... and i don't really understand immunology but somehow the body can destroy cancerous cells and so often if you get get a tumour small enough, the immune system can deal with it and you can be cured/permanent remission... so it doesn't necessarily matter if the cancer treatment doesn't target all the cells - it doesn't necessarily mean that you'd get the cancer back... you'd have to ask someone else if you want to know how the immune system targets cancerous cells because i don't know...
  16. Revenged

    Question

    it would form phospholipid bilayer... like a membrane...
  17. i don't think this has been mentioned but i think the pleasure-pain responce can be partially explaned by the production of endogenous opioids... endogenous opioids, e.g. endophins, stop the activation of second order neurones in the spinothalamic pathway (the 'pain pathway') and can also affect mood... so if you are given a continuous painful stimulus... you'll find that after a while the pain will reduce... this can be explained by production of endogenous opioid decreasing the activation of the pain pathway... i think that adreanline can affect pain sensation but i can't remember how... for example, you here of people who suffer very painful injuries in wars and do not complain of feeling any pain until several hours afterwards... but i'd be careful when saying things like 'some people find pleasure with pain'... people who do things like slitting their wrists tend to have real issues... they often do it as a way of escape or as a cry of help and it doesn't necessarily mean they are getting any pleasure out of it...
  18. And I actually got the statistic wrong... It's 1 in ~3 get cancer... 1 in ~4 die from cancer... and i agree that no 1 in 3 isn't 'everyone' but it is quite a lot...
  19. Ok, no worries... I will refrain from using the ":doh:" smiley in future as it clearly is not popular ...
  20. no, it has not been done... methadone isn't used as an anti-depressant... what are you talking about!... that is like saying heroin is an anti-depressant... it is absolute madness... the smiley was because after all that everyone said about the differences of opioids and anti-depressants you both seem to think that opioids are used as anti-depressant when they are not... I was simply losing patience... i wasn't at all 'confused' as geoguy put... In fact it seems the other way around... I also do not take kindly to a geologist patronising me when he clearly is his own subject... and notice how glider agreed with me...
  21. the problem was caused because the newer atypical neuroleptics that target both the positive and negative symptoms of schizophrenia work by antagnosing serotonin receptors... they do not block dopamine D2 receptors like the older typical neuroleptics... this questions the dopamine theory of schizophrenia...
  22. Opioids are NOT used as anti-depressants...
  23. when you are looking into how anti-depressants work you should be aware that it is far from simple... the story many people are told is that depression is due to low levels of neurotransmitters in the brain... however, there are many problems with this theory... Problems with this theory: 1) anti-depressants take about 3 weeks to work and no one really knows why 2) cocaine is a reuptake inhibitor - and so it should be an anti-depressant... but the only problem is that it isn't 3) 'atypical' anti-depressants (e.g. mianserin) do not affect amine levels but are anti-depressants 4) afaik, there has been little evidence to suggest that there are low levels of neurotransmitters in the brains of people with depression Opiates have a completely different mechanism of action and work fairly quickly... as it has been pointed out, they are taken medically for pain relief... You give someone morphine and the drug will very quickly pass through the blood brain barrier and will bind to opioid receptors in the central nervous system... The reason that they cause addiction and as you put it 'brighten the day' is because they cause activation of the reward centres in the brain... and as glider pointed out, this is because of the activation of opioid receptors by opioids cause the disinhibition of GABA, which increases dopamine levels in the reward centres of the brain... but you only get such effects if you abuse opioids as it is very uncommon to get addicted to opioids if you are taken them for pain... this is where the idea comes from that pain inhibits the reward centre activation of the brain... Btw, anti-depressants can also be given for chronic pain... e.g. low dose amitriptyline may be given...
  24. ok, no worries... i thought you were suggesting that the brain has no influence on reflex responce that's all... but i agree with what you are saying anyway...
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