Post by andy12345 on Sept 9, 2011 12:42:35 GMT
I'll be blunt about this:
I've had a rather disturbing experiencing with very large external hemmoroids aka perianal haematomas.
At hospital, I was prescribed 5% lidocaine ointment for dulling pain
Lidocaine doesn't seem to work for me.
Trouble is lidocaine is a calcium channel method mode of action and read below to understand why they may not be working...
Apparently, this can point towards a sign of being hypokalemic, something which I've only skimmed passed in the past.
symptoms of hypokalemia...
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The official link to the published document
jcn.sagepub.com/content/22/12/1408
Someone already grabbed the full report...
www.addforums.com/forums/showthread.php?t=70434
Interesting one below...from a person who was untreated then treated with drastic differences.
potsgrrl.blogspot.com/2011/07/my-lidocaine-mystery-solved-its.html
It all begs the question.....What happens if someone's medications/titration is affected by this (any medication that is calcium or potassium or sodium channel related? The failure of the drug will be incorrectly interpreted by those who are unaware, which no doubt, will be many.
calcium, sodium and potassium Ion channelopathies
www.jci.org/articles/view/26011/pdf
www.pprl.org/fileserv/Physiologic%20Principles%20Underlying%20Ion%20Channelopathies.pdf
There are examples of calcium, sodium and potassium channel blockers on wikipedia.
Well that's the end of my 2 hour research mission,zzzzzzzzzzzzzz
For those tempted to, I'll advise against reckless supplementation of potassium, sodium or calcium... I know of someone who tried the potassium and was suffering badly due to imbalances of his body etc..not good...
I've had a rather disturbing experiencing with very large external hemmoroids aka perianal haematomas.
At hospital, I was prescribed 5% lidocaine ointment for dulling pain
Lidocaine doesn't seem to work for me.
Trouble is lidocaine is a calcium channel method mode of action and read below to understand why they may not be working...
Apparently, this can point towards a sign of being hypokalemic, something which I've only skimmed passed in the past.
symptoms of hypokalemia...
Characterization of the disorder
The most prominent feature of hypokalemic sensory overstimulation is the feeling of sensory overstimulation that is characteristic of attention deficit disorder2. In hypokalemic sensory overstimulation, the sensory overstimulation goes away abruptly after taking potassium supplements; one person described the disappearance of the sensory overstimulation as being as if a shade had been pulled down 20 minutes after she took a dose of oral potassium.
3 The sensory overstimulation is triggered by large carbohydrate meals, sodium chloride intake, and the period following exercise1, the same factors known to trigger hypokalemic periodic paralysis
4. People with hypokalemic sensory overstimulation also have a reduced effectivenss of the local anesthetic lidocaine. This was first noted during minor surgery, in which one person was given lidocaine in repeated injections totaling 15 mL because the patient reported continued sensation but nevertheless he could document the inadequacy of anesthesia by reporting accurately the location of forceps touches to the toe under conditions in which he could not see his toe.1. Similar reduced effectiveness of lidocaine in dental work was noted in his mother1 and in another family.3
Molecular mechanism
Hypokalemic periodic paralysis results from mutations in subunits of sodium or calcium channels. Since hypokalemic sensory overstimulation and hypokalemic periodic paralysis have similar triggers and treatments, and since there is a relative ineffectiveness of the sodium-channel blocker lidocaine in hypokalemic sensory overstimulation, hypokalemic sensory overstimulation may be another disorder in the channelopathy group.1 Since the lidocaine effect occurs outside the brain, this suggests that in some patients with attention deficit disorder the underlying abnormality may be overstimulation from sensory pathways rather than a defect in the brain itself.1 The triggering effect of carbohydrates is believed to be due to digested carbohydrates causing release of insulin, which results in uptake of potassium into cells and the resulting hypokalemia.
The most prominent feature of hypokalemic sensory overstimulation is the feeling of sensory overstimulation that is characteristic of attention deficit disorder2. In hypokalemic sensory overstimulation, the sensory overstimulation goes away abruptly after taking potassium supplements; one person described the disappearance of the sensory overstimulation as being as if a shade had been pulled down 20 minutes after she took a dose of oral potassium.
3 The sensory overstimulation is triggered by large carbohydrate meals, sodium chloride intake, and the period following exercise1, the same factors known to trigger hypokalemic periodic paralysis
4. People with hypokalemic sensory overstimulation also have a reduced effectivenss of the local anesthetic lidocaine. This was first noted during minor surgery, in which one person was given lidocaine in repeated injections totaling 15 mL because the patient reported continued sensation but nevertheless he could document the inadequacy of anesthesia by reporting accurately the location of forceps touches to the toe under conditions in which he could not see his toe.1. Similar reduced effectiveness of lidocaine in dental work was noted in his mother1 and in another family.3
Molecular mechanism
Hypokalemic periodic paralysis results from mutations in subunits of sodium or calcium channels. Since hypokalemic sensory overstimulation and hypokalemic periodic paralysis have similar triggers and treatments, and since there is a relative ineffectiveness of the sodium-channel blocker lidocaine in hypokalemic sensory overstimulation, hypokalemic sensory overstimulation may be another disorder in the channelopathy group.1 Since the lidocaine effect occurs outside the brain, this suggests that in some patients with attention deficit disorder the underlying abnormality may be overstimulation from sensory pathways rather than a defect in the brain itself.1 The triggering effect of carbohydrates is believed to be due to digested carbohydrates causing release of insulin, which results in uptake of potassium into cells and the resulting hypokalemia.
The official link to the published document
jcn.sagepub.com/content/22/12/1408
Someone already grabbed the full report...
www.addforums.com/forums/showthread.php?t=70434
Interesting one below...from a person who was untreated then treated with drastic differences.
potsgrrl.blogspot.com/2011/07/my-lidocaine-mystery-solved-its.html
It all begs the question.....What happens if someone's medications/titration is affected by this (any medication that is calcium or potassium or sodium channel related? The failure of the drug will be incorrectly interpreted by those who are unaware, which no doubt, will be many.
calcium, sodium and potassium Ion channelopathies
www.jci.org/articles/view/26011/pdf
www.pprl.org/fileserv/Physiologic%20Principles%20Underlying%20Ion%20Channelopathies.pdf
The activity of ion channels has been recognized as an
important contributor to cellular homeostasis and main-
tenance of health for more than half a century. Channels
have a vital role in epithelial transport (gut, kidney,
lung), endocrine function (adrenals, gonads, pituitary,
pancreas), contractility (heart, skeletal muscle, smooth
muscle), and neuronal excitability. Modulation of chan-
nel activity by drugs is widely used for therapeutic in-
tervention in diseases affecting these tissues. Ion chan-
nels are the primary site of action for many antiepileptic
drugs, local anesthetics, migraine treatments, antipsy-
chotics and mood stabilizers, antiarrhythmics, antihyper-
tensives, and oral hypoglycemic agents.
A more recent concept is that ion channel dysfunction
may itself be a cause of human disease.
important contributor to cellular homeostasis and main-
tenance of health for more than half a century. Channels
have a vital role in epithelial transport (gut, kidney,
lung), endocrine function (adrenals, gonads, pituitary,
pancreas), contractility (heart, skeletal muscle, smooth
muscle), and neuronal excitability. Modulation of chan-
nel activity by drugs is widely used for therapeutic in-
tervention in diseases affecting these tissues. Ion chan-
nels are the primary site of action for many antiepileptic
drugs, local anesthetics, migraine treatments, antipsy-
chotics and mood stabilizers, antiarrhythmics, antihyper-
tensives, and oral hypoglycemic agents.
A more recent concept is that ion channel dysfunction
may itself be a cause of human disease.
There are examples of calcium, sodium and potassium channel blockers on wikipedia.
Well that's the end of my 2 hour research mission,zzzzzzzzzzzzzz
For those tempted to, I'll advise against reckless supplementation of potassium, sodium or calcium... I know of someone who tried the potassium and was suffering badly due to imbalances of his body etc..not good...