How would you counteract the effects on an antagonist on the post synaptic neuron?… by Lady
Specifically to combat strychnine? Would you use an agonist? Why and how would this work?
I'm looking for the pharmalogical approach to counteract the effects. Specifically at the synaptic level – would you introduce an agonist? A beta blocker?
Best Answer:
Sorry about this being so wordy, but it's tricky to follow without a thorough description.
From http://ccforum.com/content/6/5/456 “The mechanism of action causing strychnine toxicity is well understood. This poison is a competitive antagonist of the inhibitory neurotransmitter glycine at receptors in the spinal cord, brain stem and higher centres.”
This means that strychnine interferes with glycine, a neurotransmitter released from the presynaptic neurons of several parts of the nervous system into synapses to activate glycine receptors on the post synaptic neuron and in so doing, prevent those postsynaptic neurons from firing (inhibitory effect of glycine).
When strychnine is present, the glycine can't inhibit the post-synaptic neurons, which fire excessively, perhaps causing twitching, tremors and muscular contractions. Notice that strychnine is antagonizing an inhibitor (glycine), so it is facilitating the post-synaptic neuron, not inhibiting it.
Theoretically, you could antagonize this effect with something that competes with the strychnine for the post-synaptic receptors. If you could get hundreds of glycine molecules (or any other molecule capable of stimulating the glycine receptor, a so-called glycine receptor agonist) into the synapse for every strychnine molecule already there, you could antagonize the strychnine by diluting its presence and its effect. This is called competitive inhibition, and yes, it would be by using a glycine receptor AGONIST.
—THIS WOULD BE THE END OF THE ANSWER IF IT WAS POSSIBLE TO DO. MORE ON WHAT IS REALLY DONE FOLLOWS—
If it was possible to do, you could also antagonize the strychnine with any substance that chews it up or chemically alters it to reduce the amount of active strychnine in the synapses. No such chemical is known.
In practice, what is done is pancuronium is given, which is a competitive inhibitor not of the synapse between two neurons that we have been talking about, but of the synapse between the post-synaptic neuron and the muscle that it innervates preventing the muscle from contracting when the post-synaptic neuron overly stimulates it. This causes paralysis, which is what we want when the problem is excessive muscular contraction.
Of course, we need to breath for the patient with a mechanical ventilator after paralyzing him with pancuronium.
Notice that we have been talking about two synapses. One is between the first nerve and the second nerve. This is where the glycine and strychnine are able to work. We also have a second synapse between the second neuron and the muscle it stimulates. In reality, it is acetylcholine that is released here to stimulate the muscle, and it is acetylcholine that pancuronium competitively inhibits by getting onto the muscle receptor and blocking the acetylcholine from doing it's muscle stimulation thing without stimulating the blocked receptor. This makes pancuronium a competitive inhibitor of the acetylcholine like the glycine was to the strychnine, but instead of it being an agonist for the receptor like the glycine was (glycine stimulates the receptor and inhibits the next neuron), pancuronium is an acetylcholine antagonist.
From http://www.templejc.edu/dept/ems/drugs/pancuronium.html
“Pancuronium produces complete muscular relaxation by binding to the nicotinic M receptors for acetylcholine at the neuromuscular junctions, without initiating depolarization of the muscle membrane.”
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Have you experienced side effects from diabetes drug Januvia?… by thom
Do you research a drug in the internet before you begin taking it? There are some concerns with Januvia's side effects.
Best Answer:
I loved Januvia. But when the newer version of it “Janumet” came out my doctor put me on that. Janumet has metformin in it. It sort of made food taste differently for a few days, but after that I had no side effects and it worked great on lowering blood readings. I didn't have any side effects when I was on Januvia either. I no longer have to take it because I have been watching my diet and exercising better than I used to. The person above is correct. The pharmacist told me there are actually very few side effects of Januvia and they have to list every single thing that ever happened to anyone during the studies, even if it was a broken fingernail. I took both of these drugs with a long lasting insulin. I never had a bad drop in blood sugar. It was great to be on.
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What are some home remedies for shingles pain?… by kathy
I came down with shingles and the meds are helping with the pain but not a whole lot. Is there any home remedies I should try?
Best Answer:
Axsain cream (made from chilli peppers or
What could happen if you take Premarin for longer than 5 years?… by serialmom
My girlfriend went to the ob/gyn today and the Dr was very upset that she's been on Premarin for over 8 years now (prescribed by her primary care doctor for hot flashes.) She's scheduled her for a sonogram to check her uterus to make sure it's ok.
What can happen if you're on this medication for longer than 5 years?
Best Answer:
nothing much other than increased risk to develop cancer of the breasts, and the hot flushes will come back when she stops premarin as it has only postponed the symptoms of menopause.
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How a mechanism methylprednisolone acts on spinal injury patients?… by J
I checked on the net, we need to consume about 30mg/kg. How about high dose of MP?
Best Answer:
Dosage and duration of treatment are based on your medical condition and response to therapy. … or stroke prevention (usually at dosages of 81-325 mg per day) …
http://msj.sagepub.com/cgi/content/abstract/11/4/425
http://www.spineuniverse.com/pdf/traumaguide/9.pdf
http://www.nature.com/ncpneuro/journal/v2/n8/full/ncpneuro0221.html
http://www.webmd.com/drugs/drug-6470-Methylprednisolone+Oral.aspx?drugid=6470&drugname=Methylprednisolone+Oral
Check out these links
Sorry, I couldn't be more helpful.
For the best advise you should ask your physician not a bunch of layman on Yahoo.
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Fentanyl is one of the strongest painkiller known. Do they make a pill form?… by ANTHONY
They have the patches, but have they produced a pill for this yet?
Pangolin mentioned Fentora. I was on the trial drug study for Fentora. In fact , they didn't have a name for it when I was on it. I was on the trial for 1 year along with other people for my back pain and they abruptly cut us off. When I called to see the cost they quoted me 6k per month! Unbelievable. Who can afford that? The withdrawal was horrific, and the drug company should be sued.
Best Answer:
There is an orally dissolving tablet:
http://www.fentora.com/home.aspx?f=1
It's designed for breakthrough pain – fast acting but it doesn't last too long. It's also quite dangerous, as the letter to doctors on the website indicates.
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How can I tell if I gave my cats ringworm?… by AlleyC
I may, or may not have ringworm on my hand. I have both outside and inside cats. I suspect, if I do have ringworm, that I got it from one of my outside cats. My question is….how can I tell if I have passed this on to my inside cats. They all look normal. I don't see any patches of hair falling out or anything. BTW I have had this spot on my hand for about 3 weeks. It is scaly and round. I just thought it was really dry skin.
Best Answer:
Ringworm, contrary to popular belief is not “worms”. Ringworm is a fungal infection. You can treat it at home with nothing more than the cream that you use on jock itch or athlete's foot.
The term “ringworm” or “ringworms” refers to fungal infections that are on the surface of the skin. The early belief was that the infection was due to a worm, which it is not. It is a result of a fungus infection. Nevertheless, the name “ringworm” has stuck.
While you may have picked up the infection from your cat, it is just as likely you picked it up from a swimming pool,shower, locker room, and it is hard to identify the cause of a fungi
Examples of such preparations to treat ringworm include those that contain clotrimazole (Cruex cream, Desenex cream, Lotrimin cream, lotion, and solution), miconazole (Monistat-Derm cream), ketoconazole (Nizoral cream); and terbinafine (Lamisil cream and solution). All of these are available over the counter.
While both humans and cats can get ringworm, passing it between species is very unlikely,(less than 3%) although not impossible.
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What exactly will consuming 25 advil at once do to your body?… by christian
My friend tried to OD last night and we cant get ahold of her or her family… so yea
25 advil?
what will that do
normal strength
Best Answer:
Mainly, ulcerations, hepatotoxicity and renal damage. There's also risk of some cardiovascular damage.
Advil is a popular brand of ibuprofen, an NSAID (non-steroidal anti-inflammatory drug)
The widespread use of NSAIDs has meant that the adverse effects of these relatively safe drugs have become increasingly prevalent. The two main adverse drug reactions (ADRs) associated with NSAIDs relate to gastrointestinal (GI) effects and renal effects of the agents.
These effects are dose-dependent, and in many cases severe enough to pose the risk of ulcer perforation, upper gastrointestinal bleeding, and death, limiting the use of NSAID therapy. An estimated 10-20% of NSAID patients experience dyspepsia, and NSAID-associated upper gastrointestinal adverse events are estimated to result in 103,000 hospitalizations and 16,500 deaths per year in the United States, and represent 43% of drug-related emergency visits. Many of these events are avoidable; a review of physician visits and prescriptions estimated that unnecessary prescriptions for NSAIDs were written in 42% of visits
Combinational risk
If a COX-2 inhibitor is taken, one should not use a traditional NSAID (prescription or over-the-counter) concomitantly.[1] In addition, patients on daily aspirin therapy (as for reducing cardiovascular risk or colon cancer risk) need to be careful if they also use other NSAIDs, as the latter may block the cardioprotective effects of aspirin.
Cardiovascular risk
A recent meta-analysis of all trials comparing NSAIDs found an 80% increase in the risk of myocardial infarction with both newer COX-2 antagonists and high dose traditional anti-inflammatories compared with placebo.
NSAIDs double the risk of development of symptomatic heart failure in patients without a history of cardiac disease. In patients with such a history, however, use of NSAIDs may lead to a more than 10-fold increase in heart failure
Overall, NSAIDs are estimated to be responsible for up to 20 percent of hospital admissions for congestive heart failure
Gastrointestinal ADRs
The main ADRs (adverse drug reactions) associated with use of NSAIDs relate to direct and indirect irritation of the gastrointestinal tract (GIT). NSAIDs cause a dual insult on the GIT – the acidic molecules directly irritate the gastric mucosa; and inhibition of COX-1 reduces the levels of protective prostaglandins.
Common gastrointestinal ADRs include:
* Nausea/Vomiting
* Dyspepsia
* Gastric ulceration/bleeding
* Diarrhea
Risk of ulceration increases with duration of therapy, and with higher doses. In attempting to minimise GI ADRs, it is prudent to use the lowest effective dose for the shortest period of time, a practice which studies show is not often followed.
There are also some differences in the propensity of individual agents to cause gastrointestinal ADRs. Indomethacin, ketoprofen and piroxicam appear to have the highest prevalence of gastric ADRs, while ibuprofen (lower doses) and diclofenac appear to have lower rates
Certain NSAIDs, such as aspirin, have been marketed in enteric-coated formulations which are claimed to reduce the incidence of gastrointestinal ADRs. Similarly, there is a belief that rectal formulations may reduce gastrointestinal ADRs. However, in consideration of the mechanism of such ADRs and indeed in clinical practice, these formulations have not been shown to have a reduced risk of GI ulceration.
Commonly, gastrointestinal adverse effects can be reduced through suppressing acid production, by concomitant use of a proton pump inhibitor, e.g. omeprazole; or the prostaglandin analogue misoprostol. Misoprostol is itself associated with a high incidence of gastrointestinal ADRs (diarrhoea). While these techniques may be effective, they prove to be expensive for maintenance therapy.
Renal ADRs
NSAIDs are also associated with a relatively high incidence of renal ADRs. The mechanism of these renal ADRs is due to changes in renal haemodynamics (blood flow), ordinarily mediated by prostaglandins, which are affected by NSAIDs. Prostaglandins normally cause vasodilation of the afferent arterioles of the glomeruli. This helps maintain normal glomerular perfusion and glomerular filtration rate (GFR), an indicator of renal function. By blocking this prostaglandin-mediated effect, NSAIDs ultimately may cause renal impairment. Horses are particularly prone to these adverse affects compared to other domestic animal species.
Common ADRs associated with altered renal function include:
* Salt and fluid retention
* Hypertension
These agents may also cause renal impairment, especially in combination with other nephrotoxic agents. Renal failure is especially a risk if the patient is also concomitantly taking an ACE inhibitor and a diuretic – the so-called “triple whammy” effect.
In rarer instances NSAIDs may also cause more severe renal conditions:
* Interstitial nephritis
* Nephrotic syndrome
* Acute renal failure
* Acute tubular necrosis
Photosensitivity
Photosensitivity is a commonly overlooked adverse effect of many of the NSAIDs. It is somewhat ironic that these anti-inflammatory agents may themselves produce inflammation in combination with exposure to sunlight. The 2-arylpropionic acids have proven to be the most likely to produce photosensitivity reactions, but other NSAIDs have also been implicated including piroxicam, diclofenac and benzydamine.
Benoxaprofen, since withdrawn due to its hepatotoxicity, was the most photoactive NSAID observed. The mechanism of photosensitivity, responsible for the high photoactivity of the 2-arylpropionic acids, is the ready decarboxylation of the carboxylic acid moiety. The specific absorbance characteristics of the different chromophoric 2-aryl substituents, affects the decarboxylation mechanism. While ibuprofen is somewhat of an exception, having weak absorption, it has been reported to be a weak photosensitising agent.
During pregnancy
NSAIDs are not recommended during pregnancy, particularly during the third trimester. While NSAIDs as a class are not direct teratogens, they may cause premature closure of the fetal ductus arteriosus and renal ADRs in the fetus. Additionally, they are linked with premature birth (Ostensen & Skomsvoll, 2004). Aspirin, however, is used together with heparin in pregnant women with antiphospholipid antibodies
In contrast, paracetamol (acetaminophen) is regarded as being safe and well-tolerated during pregnancy. Doses should be taken as prescribed, due to risk of hepatotoxicity with overdoses
Other ADRs
Common ADRs, other than listed above, include: raised liver enzymes, headache, dizziness
Uncommon ADRs include: hyperkalaemia, confusion, bronchospasm, rash. Ibuprofen may also rarely cause irritable bowel syndrome symptoms.
Most NSAIDs penetrate poorly into the central nervous system (CNS). However, the COX enzymes are expressed constitutively in some areas of the CNS, meaning that even limited penetration may cause adverse effects such as somnolence and dizziness.
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I think I have a yeast infection, what do I do?… by karolee.chambe
I have the white, clumpy cottage-cheese like discharge.. It doesn't smell though. But I have been itchy down there..
I am not sexually active.
I am only 14, I don't have a gynea and I really DON'T want to ask my mum to take me to one..!!!
“Mummy.. I have a yeast infection..” – It wouldn't be a fun conversation..!
Help!
How can i get rid of it?
Best Answer:
yeast infection are common. there are many over the counter vaginal medications for it. Ask your local pharmacist to recommend one.
Mycelex 7, gynazole 1, etc
I highly suggest for your first yeast infection to see your primary MD.. you dint need to see a gynecologist. and mom may be more sympathetic than you think
good luck
good luck
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The tips of my fingers are peeling, dry and scaling. What should I do?… by Alice Lockwo
Oddly, it's only my thumbs and pointer fingers.
Best Answer:
I have this same problem on my right pointer finger. I have a Rx for Diprolene for eczema, and I used it for awhile on the finger and it cleared up. I'm kind of a germaphobe and I've been washing my hands a lot lately because it's cold/flu season, and the peeling fingertip came back again. You may want to go to the doc and get an ointment, especially if your fingers hurt.
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