| . |
L.A. Pain Clinic Sota Omoigui's Pain Drugs Handbook 2e 
Online Condensed Version
Alphabetical Listing To ORDER CONTACT: L.A. Pain Clinic Ph: 310 675-9121 or 800 9-MEDIC-9 Fax: 310 675-7989 e-mail: sota1@ aol.com ALL MATERIAL IS COPYRIGHTED. DO NOT COPY OR REPRINT WITHOUT PRIOR WRITTEN PERMISSION OF S.O.T.A. TECHNOLOGIES, INC. |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
Prior to purchase of compounded medications (e.g. Neurontin ointment)
that require a prescription, please fax or mail the prescription.
NOTICE: Every effort has been made to ensure that the drug dosage schedules herein are accurate and in accord with the standards accepted at the time of publication. As new research and experience broaden our knowledge, changes in treatment and drug therapy occur. The medications described do not necessarily have specific approval by the Food and Drug Administration for use in the situations and the dosages for which they are recommended. This information is advisory only. The package insert should be consulted for use and dosage as approved by the FDA, for any changes in indications and dosages and for added warnings and precautions. The ultimate responsibility lies with the prescribing physician. |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
A
B
C
D
E
F
G
H
I
J
K
L
M
N
O
P
Q
R
S
T
U
V
W
X
Y
Z
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . | ___________________________________ | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
ACETAMINOPHEN (Tylenol)
USE(S): symptomatic treatment of mild to moderate pain fever DOSING Pain and Fever: PO/rectal: 325 -650 mg (6-12 mg/kg) every four hours. Max. daily dose 4 grams. Max. dose for long term therapy 2.6 grams daily. Administer analgesic regularly (not prn). Addition of opioid analgesics antidepressant agents and use of non-drug therapies e.g. TENS may enhance analgesia (see front matter for drug combinations). In geriatric patients and patients with decreased renal or hepatic function decrease doses by one-third to one-half. Pharmacology A para-aminophenol derivative with analgesic and antipyretic properties similar to those of aspirin. Acetaminophen appears to be equipotent with aspirin in inhibiting central prostaglandin synthesis. However unlike aspirin acetaminophen does not inhibit peripheral prostaglandin synthesis. The antipyretic activity may be due to inhibition of the action of endogenous pyrogen on the heat regulating center in the hypothalamus and peripheral vasodilation. Acetaminophen is an effective analgesic when used for pain of non-inflammatory origin. Acetaminophen may have some weak anti-inflammatory action in some non-rheumatoid conditions e.g. in patients who have had oral surgery. In pain of inflammatory origin e.g. bone pain acetaminophen is not the drug of choice. The analgesic potency is identical to aspirin. Compared with aspirin acetaminophen produces relatively few side effects within the therapeutic dose range. Acetaminophen does not produce gastric irritation does not interfere with platelet function and has no uricosuric activity. Unlike aspirin acetaminophen is not well absorbed through the gastric mucosa but is rapidly absorbed through the small intestine and thus the rate of absorption is influenced by the gastric emptying time. Acetaminophen allergy is rare and there is no cross sensitivity between acetaminophen and aspirin. Chronic use or acute overdose of acetaminophen may result in hepatic toxicity due to depletion of glutathione stores and decrease in glutathione induced inactivation of a toxic metabolite of acetaminophen. Acetaminophen crosses the placenta but is safe for short term use during all stages of pregnancy. The drug is excreted in breast milk in low concentrations with no reported adverse effects in nursing infants. |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
Order Sota Omoigui's Pain Drugs Handbook, Magnets and Compounded Medications |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
ACYCLOVIR (Zovirax)
USE(S): treatment of initial and recurrent episodes of herpes zoster (shingles) genital herpes chickenpox (varicella) DOSING Initial genital herpes simplex: PO 200 mg every four hours for 10 days or Slow IV 5 mg/kg every eight hours for 5 days Topical: 5% ointment: apply every 6 hours. ( less effective than oral. Reduces the duration of viral shedding but has no significant effect on symptoms) Recurrent herpes simplex: Chronic Suppression: PO 400 mg two times daily for up to 12 months or Intermittent Suppression: PO 200 mg every four hours for 5 days at the earliest sign of recurrence. Short term treatment of recurrent episodes is more appropriate for patients with mild and infrequent disease. Herpes simplex encephalitis: Slow IV 10 mg/kg every eight hours for 10-14 days Neonatal herpes simplex: Slow IV 10 mg/kg every eight hours for 10-14 days Herpes zoster : Normal host: PO 800 mg every four hours for 7-10 days Compromised host: Slow IV 10 mg/kg every eight hours for 7-10 days Varicella (Chickenpox) Normal host : PO 20 mg/kg (Max. 800 mg) every six hours for 5 days Compromised host: Slow IV 10 mg/kg every eight hours for 7-10 days Intravenous administration should be reserved only for patients with severe local disease or systemic complication. Dose of acyclovir should be reduced in patients with impaired renal function. Creatinine clearance > 50 mls/min - 100 % of IV dose at eight hour intervals. Creatinine clearance 25-50 mls/min or 10-25 mls/min- 100 % of IV dose at twelve to twenty four hour intervals. Creatinine clearance < 10 mls/min - 100 % of PO dose at twelve hour intervals. Pharmacology Acyclovir is a synthetic purine nucleoside analogue with invitro and invivo inhibitory activity against human herpes viruses including herpes simplex types 1 (HSV-1) and 2 (HSV-2) varicella-zoster virus (VZV) Epstein Barr virus (EBV) and cytomegalovirus (CMV) - in decreasing order of potency. The inhibitory activity for these viruses is highly selective. Normal uninfected cells are not affected because they take up less acyclovir and activate it much less efficiently. Thymidine kinase encoded by HSV VZV and EBV viruses converts acyclovir into acyclovir monophosphate a nucleotide analogue. The monophosphate is further converted into diphosphate by cellular guanylate kinase and into triphosphate by a number of cellular enzymes. Acyclovir triphosphate interferes with herpes simplex virus DNA polymerase and inhibits viral DNA replication. Acyclovir triphosphate may to a lesser degree inhibit cellular alpha-DNA polymerase. The mode of acyclovir phosphorylation in CMV-infected cells may involve virally induced cell kinases or an unidentified viral enzyme. However acyclovir is not efficiently activated in CMV-infected cells which may account for the reduced potency of the drug. In patients with acute genital herpes herpes zoster and chicken pox infections acyclovir significantly reduces the duration of pain and incidence of new lesion formation. Patients with severe episodes may derive more benefit than those with mild disease. Acyclovir also decreases the frequency and/or severity of recurrences of genital herpes. Acyclovir crosses the placenta and may be excreted in breast milk. It should be used cautiously in pregnant and nursing mothers. |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
Order Sota Omoigui's Pain Drugs Handbook, Magnets and Compounded Medications |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
ALENDRONATE (Fosamax)
USE(S): treatment and prevention of osteoporosis in post menopausal women treatment of Paget's disease of the bone treatment of hypercalcemia reduction of the incidence of pathologic fractures slowing of bone disease progression and reduction of tumor associated metastatic bone pain treatment of reflex sympathetic dystrophy (RSD) associated osteoporosis and bone pain. DOSING Treatment of Osteoporosis/ Metastatic Bone Pain: PO: 10 mg once a day. Treatment of Paget's Disease of the Bone: PO: 40 mg once a day for six months. Prevention of Osteoporosis: PO 5 mg once a day Medication must be taken at least half an hour before the first food beverage or medication of the day with plain water only. Other beverages food and some medications are likely to reduce the absorption of Fosamax. To facilitate delivery to the stomach and reduce the potential for esophageal irritation Fosamax should only be swallowed upon arising for the day with a full glass of water (6-8 oz) and patients should not lie down for at least 30 mins AND until after their first food of the day. Fosamax should not be taken at bedtime or before arising for the day. Failure to follow these instructions may increase the risk of esophageal adverse experiences. Patients should receive supplemental calcium and vitamin D if dietary intake is inadequate. Pharmacology This aminobisphosphonate binds to bone hydroxyapatite and specifically inhibits the activity of osteoclasts the bone resorbing cells. Alendronate reduces bone resorption with no direct effect on bone formation although the latter process is ultimately reduced because bone resorption and formation are coupled during bone turnover. Alendronate thus reduces elevated rates of bone turnover. Alendronate shows preferential localization to sites of bone resorption specifically under osteoclasts. The drug inhibits osteoclast activity but does not interfere with osteoclast recruitment or attachment. The osteoclasts adhere normally to the bone surface but lack the ruffled border that is indicative of active resorption. Dose dependent inhibition of resorption is manifested by decreases in urinary calcium and urinary markers of bone collagen degradation (such as deoxypyridinoline and cross linked N-telopeptides of type I collagen). Within 6-49 days after administration normal bone is formed on top of the alendronate. When incorporated into bone matrix alendronate is no longer pharmacologically active. Thus alendronate must be continuously administered to suppress osteoclasts on newly formed resorption surfaces. In treatment of metastatic bone disease alendronate and other bisphosphonates e.g. pamidronate clodronate treat hypercalcemia reduce tumor associated pain reduce the incidence of pathologic fractures and also slow bone disease progression. Administration of bisphosphonates shortly after adjuvant chemotherapy can preserve bone density in female patients with chemotherapy induced menopause. A related bisphosphonate clodronate has been shown to reduce the incidence of bone metastasis in patients with early stage breast cancer. There was no difference in the incidence of non skeletal metastatic disease. Alendronate may reduce bone resorption and relieve bone pain in patients with RSD. Osteoporosis and bone resorption in RSD may be partly due to increased deep tissue blood flow secondary to surface or capillary vasoconstriction. |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
Order Sota Omoigui's Pain Drugs Handbook, Magnets and Compounded Medications |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
ALFENTANIL (Alfenta)
USE(S): treatment of acute pain DOSING Analgesia IV/IM 250-500 mcg (5-10 mcg/kg) Epidural: bolus: 500-1000 mcg (10-20 mcg/kg) infusion 100-250 mcg/hour (2-5 mcg/kg/hr) Pharmacology Alfentanil is a phenylpiperidine derivative and potent opioid analgesic with rapid onset and short duration of action. Alfentanil is associated with less sedation when used in patient controlled analgesia compared with meperidine or fentanyl. Repeated doses or continuous infusions do not result in a significant cumulation. Alfentanil crosses the placental barrier and may produce depression in the neonate. Significant amounts of the drug may appear in breast milk and it should be used with caution in nursing mothers. |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
Order Sota Omoigui's Pain Drugs Handbook, Magnets and Compounded Medications |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
AMITRIPTYLINE (Elavil)
USE(S): treatment of neurotic and endogenous depression migraine prophylaxis adjunct treatment of neuropathic pain syndromes including diabetic neuropathy post herpetic neuralgia; tic doloureux cancer pain anxiety disorders phobias panic disorders enuresis eating disorders. DOSING Pain Syndromes Initial PO 10 -25 mg (0.2-0.5 mg/kg) daily at bedtime. Titrate dose upward every three-four weeks by increments of 10-25 mg as necessary. Maintenance PO 10-150 mg (0.2-3 mg/kg) daily at bedtime. Doses should be decreased if unacceptable side effects occur. Serum levels should be determined if there are signs of toxicity. Doses of 150 mg/day may be required in the management of painful diabetic neuropathy. Migraine Prophylaxis/Tension Headache: PO 25-75 mg (0.5-1.5 mg/kg) daily Depression: Initial PO 75-100 mg (1.5-2 mg/kg) daily in one to four divided doses. Maintenance PO 25-150 mg (0.5-3 mg/kg) daily in one to four divided doses IM 20-30 mg four times daily. Replace with oral medication as soon as possible. Do not administer intravenously Doses for pain are generally smaller than those used for treatment of affective disorders. Medication should be administered on a fixed schedule and not p.r.n. Administration of the entire daily dose at bedtime may reduce daytime sedation. After symptoms are controlled dosage should be gradually reduced to the lowest level that will maintain relief of symptoms. When amitriptyline is used in conjunction with a phenothiazine dosages should first be adjusted by administering each drug separately. Commercial fixed-ratio combinations should be used only when the optimum maintenance dosage ratios have been determined and correspond to the ratios in the commercial preparation. Analgesia may be enhanced by addition of opioid analgesics (see front matter for drug combinations) non-steroidal anti-inflammatory agents (NSAIAs) and use of non-drug therapies e.g. TENS. In geriatric patients and patients with decreased renal or hepatic function decrease doses by one-third to one-half. The possibility for suicide is inherent in depression and may persist until significant remission occurs. The quantity of drug dispensed should reflect such consideration. Pharmacology A dibenzocycloheptene derivative and a tertiary amine tricyclic antidepressant. Amitriptyline is structurally related to the phenothiazine antipsychotic agents. Antidepressant activity may be partly due to inhibition of the amine-pump uptake of neurotransmitters e.g. norepinephrine and serotonin at the presynaptic neuron down regulation of beta receptor sensitivity sedation and peripheral/central anticholinergic effects. Although blockade of neurotransmitter uptake may occur immediately antidepressant response may take days to weeks. Patients with low serotonin levels may respond better to amitriptyline compared with norepinephrine deficient patients. Amitriptyline (and other tricyclics) does not inhibit the monoamine oxidase (MAO) system. Amitriptyline is demethylated in the liver to the active metabolite nortriptyline. The analgesic effects of amitriptyline (and other antidepressants) may occur partly through the alleviation of depression which may be responsible for increased pain suffering but also by mechanisms that are independent of mood effects. Serotonin and norepinephrine activity may be increased in descending pain inhibitory pathways. Activation of these pathways decreases the transmission of nociceptive impulses from primary afferent neurons to first order cells in laminae I and V of the spinal cord dorsal horn. Amitriptyline may also potentiate the analgesic effect of opioids by increasing their efficacy of binding to opioid receptors. Amitriptyline has varying degrees of efficacy in different pain syndromes and may be better at relieving the burning aching and dyesthetic component of neuropathic pain. The drug is seldom useful in the management of lancinating shooting paroxysmal pain. At full antidepressant dosages amitriptyline (and other tricyclic antidepressants) are especially effective in chronic low back pain with associated major depression. Patients with uncomplicated low back pain (i.e. without major depression) do not respond as well. The antimigraine activity of amitriptyline is relatively independent of its antidepressant effects. Low doses of amitriptyline (and other tricyclic antidepressants) are just as effective for chronic tension headache as the commonly used antianxiety drugs. Amitriptyline produces varying degrees of sedation blocks alpha-1 adrenergic H1 and H2 receptors. Amitriptyline may enhance ulcer healing and is a more potent invitro antagonist of H2 receptors than cimetidine. Abnormal EEG patterns may be produced with decrease in alpha activity and increase in theta activity. The seizure threshold may be lowered. Therapeutic doses do not affect respiration but toxic doses may lead to respiratory depression. The direct quinidine-like effects may manifest at toxic doses and produce cardiovascular disturbances e.g. conduction blockade. Amitriptyline does not have addiction liability and its use is not associated with drug seeking behavior. Withdrawal symptoms including sleep disruption with vivid dreams may be precipitated by acute withdrawal. Tolerance develops to the sedative and anticholinergic effects but there are no reports of tolerance to the analgesic effects. Amitriptyline crosses the placenta and use in pregnancy may be associated with fetal malformations. The drug is excreted in breast milk and has a potential for serious adverse effects in nursing infants. |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
L.A. PAIN CLINIC COMPOUNDED PREPARATION Amitriptyline Ointment
___________________________________ |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
BACLOFEN (Lioresal)
USE(S): relief of muscle spasticity and rigidity e.g. in multiple sclerosis Parkinson’s disease; adjunct treatment of trigeminal neuralgia pre-trigeminal neuralgia glossopharyngeal neuralgia vago-glossopharyngeal neuralgia organic (non traction) headache neuropathic pain post herpetic neuralgia DOSING Spasticity/Trigeminal neuralgia/Organic Headache/Neuropathic pain: Initial PO: 5 -10 mg three times daily. Maintenance: PO 5-25 mg three times daily and at night. Doses should be increased by 15 mg increments (smaller in geriatric patients) at three day intervals until the optimum effect is achieved. For increased muscle relaxation baclofen doses may be supplemented with Tizanidine (Zanaflex) Severe Spasticity of Spinal Cord Origin (spinal cord trauma multiple sclerosis) : Intrathecal Bolus - Screening Phase: 50-75 mcg (Dilute to a concentration of 50 mcg/ml. Administer into the intrathecal space by barbotage over a period of not less than one minute. Observe patient for 4-8 hours. If inadequate response Repeat dose of 75 mcg (in 1.5 mls) may be administered 24 hours later. If inadequate response another repeat dose of 100 mcg (in 2 mls) may be administered 24 hours later. Patients who do not respond to the 100 mcg dose should not be considered candidates for chronic infusion therapy with an implanted pump. Epidural Bolus: Initial 100-400 mcg. Dilute in 3 mls preservative free Normal Saline. Titrate dose cautiously and to effect. Use intrathecal preparation of baclofen. Maintenance: 100 mcg - 30 mg daily - twice weekly. Dilute in 3- 10 mls preservative free Normal Saline. Start with low dose and titrate cautiously to effect. May be administered via an implanted subcutaneous port. Intrathecal Infusion - Initial : 3-6 mcg/hr or administer 2x the effective bolus dose over 24 hours. If the bolus dose was effective for longer than 12 hours then administer 1 x bolus dose over 24 hours. No dose increases should be given in the first 24 hours. After the first 24 hours the daily dosage may be increased slowly by 10-30% increments and only once every 24 hours. Patients must be monitored closely in a fully equipped and staffed environment during the screening phase and infusion dose titration period immediately following an implant. Intrathecal Infusion -Long term Maintenance: 12-1500 mcg/day. Titrate to symptom control. During periodic refills of the infusion pump the daily dosage may be increased by 10-40%. The daily dose may be reduced by 10-20% if patients experience side effects. A sudden large requirement for dose escalation suggests a catheter complication (i.e. catheter kink or dislodgment). Oral baclofen should be used in combination with anticonvulsants e.g. carbamazepine antidepressants or phenytoin in the management of trigeminal neuralgia and organic headaches. Baclofen should be combined with antidepressant agents opioids and/or NSAIAs in the management of neuropathic pain. Pharmacology A p-chlorophenyl derivative of y-aminobutyric acid (GABA) and a skeletal muscle relaxant. Baclofen inhibits monosynaptic and polysynaptic reflexes at the spinal level possibly by acting as an inhibitory neurotransmitter and/or hyperpolarization at afferent terminals. Baclofen is the drug of choice for muscle spasm in patients with multiple sclerosis and other spinal cord lesions where it decreases the number and severity of muscle spasms (especially flexor spasms) alleviates associated pain clonus muscle rigidity and improves mobility. When introduced directly into the intrathecal space effective CSF concentrations of baclofen are achieved with resultant plasma concentrations 100 times less than those occurring with oral administration. Intrathecal baclofen is effective in the treatment of severe chronic spasticity in patients who do not respond adequately and/or do not tolerate high oral doses. Either baclofen or diazepam (the drug of second choice ) are preferable to intrathecal injections of sclerosing agents (e.g. phenol) rhizotomy or cordotomy. Intrathecal baclofen may suppress the allodynic dyesthetic pain from spinal lesions. Baclofen like carbamazepine and phenytoin depresses excitatory transmission and facilitates segmental inhibition in the trigeminal nucleus. Oral baclofen has been shown to be effective in the treatment of trigeminal neuralgia and nonvascular headache. Baclofen may relieve the episodic and allodynic pain in post herpetic neuralgia. The levo form of baclofen may be more effective than the readily available racemic d-l form. In large doses baclofen may produce generalized CNS depression including sedation ataxia respiratory and cardiovascular depression. |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
L.A. PAIN CLINIC COMPOUNDED PREPARATION Baclofen Ointment
___________________________________ |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
BOTULINUM TOXIN TYPE A (Botox)
USE(S): treatment of involuntary muscle spasm and tremors associated with dystonias e.g. spasmodic torticollis blepharospasm strabismus limb dystonia paraspinal muscle spasm DOSING: Strabismus/Blepharospasm/RSD: 1.25 - 2.5 Units/muscle. Volume of 0.05 - 0.15 mls/muscle Spasmodic Rotational Torticollis with or without Retrocollis: Contralateral Sternocleidomastoid/Ipsilateral and Contralateral Trapezius 50-100 Units/muscle. Inject 5 Units/0.2 mls per muscle site. Dilution: 25 Units/ml With presence of head tilt inject ipsilateral splenius capitis with 15-30 Units/muscle 5 Units/muscle site Dilution 25 Units/ml Scalene Compartment Block - Interscalene Brachial Plexus Approach 100 Units Botox in 10-20 mls Presv. Free Normal Saline Psoas/Quadratus Lumborum Compartment Block - Lumbar Plexus Block 100 -200 Units Botox in 10-20 mls Presv. Free Normal Saline. For bilateral blocks inject 50-100 Units each side. Paravertebral Nerve Block - Lumbar Plexus Block 100 Units Botox in 10 mls Presv. Free Normal Saline. For bilateral blocks inject 50 Units each side. Piriformis Compartment Block - Lumbar Plexus Block 100 -200 Units Botox in 2 mls Presv. Free Normal Saline. For bilateral blocks inject 50-100 Units each side. Trigger Point Injections e.g. Trapezius Muscle 100 -200 Units Botox in 4-10 mls Presv. Free Normal Saline. Inject 0.5-2 mls (5-25 Units) in each trigger point. each side. Treatment of Facial Lines: Corrugator Superciliaris/Frontalis/Orbicularis Oculi Muscle : 5-10 Units (0.2 - 0.8 mls) in each target muscle. Use Dilution of 25 units/ml Botulinum toxin should be infiltrated at various sites in muscle belly. Addition of local anesthetics may make injection more comfortable but effect on efficacy of Botox is undetermined. Electromyographic guidance is required for injection into the small extraocular muscles. Pharmacology Botulinum Toxin Type A blocks neuromuscular conduction by binding to receptor sites on motor nerve terminals entering the nerve terminals and inhibiting the release of acetylcholine. When injected intramuscularly at therapeutic doses BOTOX produces a localized chemical denervation muscular paralysis. When the muscle is chemically denervated it atrophies and may develop extrajunctional acetylcholine receptors. There is evidence that the nerve can sprout and reinnervate the muscle with the weakness thus being reversible. BOTOX may affect muscle pairs e.g. in strabismus by inducing an atrophic lengthening of the injected muscle and a corresponding shortening of the muscle's antagonist. The paralytic effect on muscles injected with BOTOX is useful in reducing excessive abnormal contractions associated with muscle spasm. Paralysis of injected muscles begins one to two days after injection and increasing in intensity for the first week. The paralysis lasts for 2-6 weeks and gradually resolves over a similar time period. Over corrections lasting over 6 months have been rare. About one-half of patients will require subsequent doses because of inadequate paralytic response of the muscle to the initial dose or because of mechanical factors such as large deviations or restrictions. |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
Order Sota Omoigui's Pain Drugs Handbook, Magnets and Compounded Medications
___________________________________ |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
BUPIVACAINE (Marcaine)
USE(S): regional anesthesia sympathetic blockade DOSING: Infiltration/Peripheral Nerve block : 1-20 mls (0.25-0.5% solution) Caudal: 37.5-150 mg (15-30 mls of 0.25 or 0.5% solution.) Children 0.4- 0.7-1.0 ml/kg (L2-T10 -T7 level of anesthesia) Brachial Plexus Block: 75-250 mg (30-50 mls of 0.375-0.5% solution) Children 0.5-0.75 mls/kg. With high doses (>2 mg/kg) add epinephrine 1:20000 to decrease systemic toxicity (in the absence of any contraindications) . Regional blockade may be potentiated by the addition of Tetracaine 0.5-1 mg/kg or Fentanyl (1-2 mcg/kg) or Morphine (0.05-0.1 mg/kg) Scalene Compartment Block - Interscalene Brachial Plexus Approach 20 mls of 0.25-0.5% solution with or without steroid e.g.40-80 mg Triamcinolone Stellate Ganglion Block: 10-20 mls of 0.25% solution (25-50 mg) with or without epinephrine 1:200000. Psoas/Quadratus Lumborum Compartment Block - Multiple Paravertebral Nerve Block - Lumbar Plexus Block 20 mls of 0.25-0.5% solution with or without steroid e.g.40-80 mg Triamcinolone. For bilateral blocks inject each side with 10-15 mls of 0.125% solution with steroid e.g. 20-40 mg of Triamcinolone. Paravertebral Nerve Block 3-4 mls per segment of 0.25-0.5% with or without epinephrine. Piriformis Compartment Block - Lumbar Plexus Block 10 - 20 mls of 0.25-0.5% solution with or without steroid e.g.40-80 mg Triamcinolone. For bilateral blocks inject each side with 5-10 mls of 0.125% solution with steroid e.g. 20-40 mg of Triamcinolone. Trigger Point Injections e.g. Trapezius Muscle 10 mls of 0.25-0.75% solution with or without steroid e.g.40-80 mg Triamcinolone. Lumbar Sympathetic Block: 10-15 mls of 0.25% solution (25-50 mg) with or without epinephrine 1:200000. Posterior Tibial Nerve Sympathetic Block: 2-2.5 mls of 1 % solution (20-25 mg) with or without epinephrine 1:200000 and with or without steroids (e.g. triamcinolone acetonide). Note: The posterior tibial sympathetics control 85% of the sympathetics to the foot including all four muscle layers and the vital structures of the sole of the foot. Such selective sympathectomy may be preferable to a lumbar paravertebral block for RSD of the foot. Celiac Plexus Block: 20-25 mls of 0.25% solution (25-50 mg) with or without epinephrine 1:200000. Epidural: bolus 50-150 mg (0.25-0.75% solution) Children 1.5-2.5 mg/kg (0.25-0.5% solution) Epidural infusion: 2-12 mls/hr (0.0625-0.125% solution with or without epidural narcotics. Children 0.04-0.35 mls/kg/hr. Epidural infusion (chronic malignant pain) 3-20 mg daily (0.00625-0.0625% solution). When used in combination with epidural morphine infusions dilute the daily amount of bupivacaine in the daily volume of the morphine infusion. Total Amount of Bupivacaine = Total Daily Amount of Bupivacaine x Total Vol.. of Infusion for Infusion Solution Total Daily Volume of MorphineSolution e.g. Patient is receiving Epidural Morphine diluted in a total volume of 250 mls presv. free NS at 1 mg/day and 2 mls per hour. If patient is to receive Bupivacaine at 10 mg/day then Total Amount of Bupivacaine to add to the Infusion will be: 10/48 x 250 = 52.08 mg. This is approx. equivalent to adding 6.9 mls of 0.75% Bupivacaine solution or 10.4 mls of Bupivacaine 0.5% solution to the Infusion solution. Final concentration of Bupivacaine in the Infusion solution is 0.02% or 0.2 mg/ml. Rate of onset and potency of local anesthetic action may be enhanced by carbonation. (Add 0.1 ml of 8.4% Sodium Bicarbonate with 20 mls of 0.25 Bupivacaine. Do not use if there is precipitation.) Intrathecal : bolus 7-15 mg (0.75% solution) [Children: 0.5 mg/kg with a minimum of 1 mg.] Intrathecal infusion (chronic malignant pain) 1-5 mg daily (0.1-0.75% solution) . When used in combination with intrathecal morphine infusions dilute the daily amount of bupivacaine in the daily volume of the morphine infusion (see Epidural infusion above). Interpleural: bolus 100 mg (20 mls of 0.25-0.5% solution. [0.4 mls/kg] infusion 5-7 mls/hr [0.125 mls/kg/hr] (0.125-0.25% solution) Intraarticular: <100 mg (20-40 mls of 0.25% solution). If desired add Morphine 0.5- 1 mg. Max. Safe Dose: 2 mg/kg without epinephrine 2-3 mg/kg with epinephrine. Solutions containing preservatives should not be used for epidural or caudal block. Except where contraindicated vasoconstrictor drugs (e.g. epinephrine phenylephrine) may be added to increase effect and prolong local or regional anesthesia For dosage/route guidelines see Epinephrine Dosing p.*** Do not use vasoconstrictor drugs for IV Regional Anesthesia or Local Anesthesia of end organs (digits penis ears). Pharmacology This amino amide local anesthetic stabilizes neuronal membranes by inhibiting ionic fluxes required for the initiation and conduction of impulses. The progression of anesthesia is related to the diameter myelination and conduction velocity of affected nerve fibers with order of loss of function being: (1) autonomic; (2) pain; (3) temperature; (4) touch; (5) proprioception; and (6) skeletal muscle tone. The onset of action is reasonably rapid and duration is significantly longer than with any other commonly used local anesthetic. Addition of epinephrine improves the quality of analgesia but only marginally increases duration of effect of bupivacaine concentrations ≥ 0.5%. Hypotension results from loss of sympathetic tone as in spinal or epidural anesthesia. Compared with other amides there is more cardiotoxicity with intravascular injection. Epidural bupivacaine provides long acting neural blockade. Impulse transmission is blocked at the nerve roots and dorsal root ganglia. When administered by infusion tachyphylaxis may occur possibly due to an increase in blood flow within the epidural space or an increase in size of the pain field at the spinal cord level. Tachyphylaxis may be circumvented by incremental dosing or addition of epidural/intrathecal narcotics. Systemic absorption of bupivacaine (and other long acting amides) is less than that of lidocaine (and other short acting amides) due to greater non specific binding in the fat of the epidural space. |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| . |
Order Sota Omoigui's Pain Drugs Handbook, Magnets and Compounded Medications
.
|
Book Price: $35.00
|
___________________________________
.
|
CELECOXIB (Celebrex)
|
USE(S): symptomatic treatment of osteoarthritis and rheumatoid arthritis DOSING: Osteoarthritis: PO 200 mg once daily or 100 mg twice daily Rheumatoid arthritis: PO 100 - 200 mg twice daily. Celecoxib capsules may be administered without regard to meals. Dose adjustment in the elderly is generally not necessary. However for patients less than 50 kg in body weight initiate therapy at the lowest recommended dose. Pharmacology This nonsteroidal anti-inflammatory agent (NSAIA) was designed using advance molecular technology. Celecoxib in clinical trials was as effective as naproxen in treating arthritis pain and inflammation. In osteoarthritis patients Celecoxib improved pain stiffness and patient functions such as walking and bending. The analgesic and anti-inflammatory activity of Celecoxib is partly due to the inhibition of prostaglandin synthesis and/or release secondary to the inhibition of cyclooxygenase-2 isoenzyme (COX-2). Cyclooxygenase enzyme (prostaglandin G/H synthetase) catalyzes the formation of prostaglandin precursors - endoperoxide intermediate prostaglandin G2 (PGG2) - from arachidonic acid. PGG2 is reduced by peroxidase activity to another endoperoxide intermediate prostaglandin H2 (PGH2). These endoperoxide intermediates are the common precursors for the synthesis of prostaglandins prostacyclins and thromboxanes. The inhibition of cyclooxygenase and thus prostanoid synthesis by classical NSAIAs is associated with side effects such as irritation and ulcer formation in the upper gastrointestinal tract and impairment of kidney function. It has been recognized recently that mammalian cells express two forms of cyclooxygenase (COX) activity. COX-1 isoenzyme is expressed in many normal tissues and is the major form present in platelets kidney and gastrointestinal tract. COX-2 isoenzyme is induced in response to pro-inflammatory cytokines lipopolysaccharide (LPS) and growth factors and subjected to repression by glucocorticosteroids. This second form is generally not detected in healthy tissues but is found in elevated levels in inflammatory exudates. This has led to the hypotheses that COX-1 is mainly associated with homeostasis (including cytoprotection in the stomach and regulation of kidney function) and COX-2 with the edematous nociceptive and pyretic effects of inflammation. Most classical NSAIAs including diclofenac naproxen and ibuprofen show little specificity of inhibition towards COX isoforms. Uniquely Celecoxib at therapeutic concentration does not inhibit the cyclooxygenase -1 isoenzyme (COX-1). Ulcerogenic-sparing COX-2 inhibition does not inhibit cytoprotective stomach PGE2 production in contrast to non-specific NSAIAs. Celecoxib is better tolerated than the classical NSAIAs and equipotent doses are associated with less gastric mucosal abnormalities. The antipyretic activity of Celecoxib may occur secondary to inhibition of pyrogen induced release of prostaglandins in the central nervous system (including the hypothalamus) and possibly to centrally mediated peripheral vasodilation. Celecoxib (like other NSAIAs) exhibits a ceiling effect for analgesia. Exceeding recommended doses results in increased toxicity without improvement in analgesia. Inhibition of prostaglandin synthesis may result in decreased uterine tone contractility and prolonged gestation in the parturient and premature closure of the ductus arteriosus in the fetus. Celecoxib has no effect on platelet aggregation or bleeding time and unlike aspirin cannot be used for cardiovascular prophylaxis.
.
|
| Click here to order CELEBREX and other Pain Medications Herbs and Magnetic Supplies. Additional information on Celebrex in Sota Omoigui's Pain Drugs Handbook 1999 Edition
.
|
Book Price: $35.00
|
___________________________________
.
|
CLONAZEPAM (Klonopine)
|
USE(S): anticonvulsant adjunct treatment of neuropathic pain e.g. phantom limb reflex sympathetic dystrophy (chronic regional pain syndrome) trigeminal and other cranial neuralgias migraine or cluster headache; treatment of panic disorder and restless leg syndrome; treatment of myoclonus. DOSING: Seizure Control: Initial PO 1.5 mg (0.01-0.03 mg/kg) daily in two or three divided doses. Maintenance: PO 1.5-20 mg daily in two or three divided doses. Doses should be titrated upwards in 0.5-1 mg increments every third day until seizure control is achieved with minimal adverse effects. Neuropathic Pain/Panic Disorder/Myoclonus: PO 0.25 mg twice daily increasing to 1 mg/day after 3 days in most patients. Doses should be titrated upwards in 0.5-1 mg increments every third day. Max daily dose: 4 mg. Do not use generic formulation due to unpredictable therapeutic efficacy. Pharmacology This benzodiazepine produces a dose related sedation relief of anxiety and skeletal muscle relaxation. Like other benzodiazepines the action of the drug is mediated in the brain through the inhibitory neurotransmitter gamma amino butyric acid. Clonazepam more than any other benzodiazepine is used alone or with other drugs as an anticonvulsant. In chronic pain syndromes the pain threshold may be increased by relief of anxiety and agitation. Clonazepam does not have intrinsic analgesic activity and should be used in combination with analgesics e.g. opioids NSAIAs antidepressant agents. As an adjunct clonazepam is effective in the relief of acute muscle spasm lancinating or burning neuropathic pain and concomitant chronic pain and anxiety. Clonazepam relieves myoclonic activity associated with high dose opioid therapy. Clonazepam alone or in combination with baclofen may relieve the syndrome of painful legs and involuntary movement of the toes that may result from ephatic transmission in damaged nerve roots scondary to spinal cord or cauda equina trauma lumbar radiculopathy injury to the feet peripheral neuropathy or drug therapy. Clonazepam produces minimal depressant effects on ventilation and circulation in the absence of other CNS depressant drugs. The drug is intermediate in speed of onset compared to other benzodiazepines.
.
|
| Order Sota Omoigui's Pain Drugs Handbook and Compounded Medications
.
|
Book Price: $35.00
|
___________________________________
.
|
CLONIDINE (Catapres)
|
USE(S): supplemental relief (in combination with opioids) of pain and muscle spasm in fibromyalgia back chronic cancer and neuropathic pain; treatment of hypertension migraine prophylaxis treatment of opioid/alcohol withdrawal states; epidural/spinal analgesia; prolongation of duration of action of local anesthetics. DOSING: Premedication: PO 0.1-0.3 mg (3-5 mcg/kg) Antihypertensive: Initial PO 0.05-0.1 mg twice daily (morning and bedtime). Maintenance PO 0.05-0.2 mg two to four times daily. Use lower doses in geriatric patients. Migraine Prophylaxis PO 0.025-0.1 mg 2 or 3 times daily (Children 0.5-2 mcg/kg/day) Detoxification PO 0.1-0.3 mg 3 or 4 times daily. Titrate to patient response and tolerance. Hypertensive crisis: IV 0.15-0.3 mg over 5 minutes Supplementation of Analgesia PO 0.025-0.1 mg two to four times daily (0.05-0.4 mg/day) Transdermal 0.1-0.3 mg/24hr. Replace systems every 7 days. Dosage adjustments may be made at weekly intervals. The transdermal system provides reliable delivery of clonidine for 7 days. Therapeutic plasma levels are achieved after 2-3 days. Therapeutic levels persist for about 8 hours following removal of the systems then decline over several days. IV bolus 0.1-0.2 mg (2-4 mcg/kg) over 5 minutes infusion 0.05-0.1 mg/hr (1-2 mcg/kg/hr) Epidural Analgesia: bolus: 100 -200 mcg [2-4 mcg/kg] Dilute in 10 mls (preservative free) NS. or Local Anesthetic infusion: 10-40 mcg/hr (0.2-0.8 mcg/kg/hr) Start infusion (conc. 2 mcg/ml) at 5 mls/hour and titrate to effect. Epidural Anesthesia: bolus: 200 -500 mcg [4-10 mcg/kg] Dilute in 10 mls (preservative free) NS. or Local Anesthetic Spinal Analgesia: bolus 15-100 mcg (0.3-2 mcg/kg) infusion: 2-8 mcg/hr (0.04-0.16 mcg/kg/hr) or 3 X bolus dose/24 hours Brachial Plexus Block: Add 25-150 mcg (0.5-3 mcg/kg) clonidine to 40 mls Local Anesthetic. Peripheral Nerve Block: Dilute clonidine in Local Anesthetic to concentration of 5 mcg/ml. Max dose of 100-150 mcg clonidine. Caution: Significant hypotension and sedation may occur at the high dose ranges of clonidine (100-150 mcg). Treat with intravenous fluids. Pharmacology Clonidine is a selective agonist at the alpha-2 adrenoceptor with a ratio of 200:1 (alpha-2 : alpha-1). It inhibits central sympathetic outflow through activation of alpha-2 adrenergic receptors in the medullary vasomotor center. Clonidine decreases blood pressure heart rate cardiac output. and produces a dose dependent sedation. Unlike opioids it produces minor respiratory depression with a ceiling effect and unlike benzodiazepines does not enhance opioid-induced respiratory depression. Direct stimulation of peripheral alpha-1 adrenergic receptors results in transient vasoconstriction. Rebound hypertension occurs when therapy is discontinued abruptly. Clonidine suppresses signs and symptoms of opioid withdrawal by replacing opioid mediated inhibition with alpha-2 mediated inhibition of central nervous system sympathetic activity. Analgesic activity of clonidine may be mediated by attenuation noxious stimulus-evoked and alpha-2 mediated neuronal firing. Epidural / intrathecal clonidine produces analgesia by acting on alpha-2 adrenoceptors located in the dorsal horn neurons of the spinal cord. Local effects may include inhibition of the release of nociceptive neurotransmitters such as substance P (presynaptic first-order neurons) and decrease in the rate of depolarization (postsynaptic second order neurons). These effects which are separate from opiate-mediated analgesia are not inhibited by opiate antagonists e.g. naloxone but are blocked by alpha-2 antagonist drugs e.g. phentolamine. Epidural/spinal analgesia with clonidine may be accompanied by sensory and motor blockade. This may be due to membrane stabilizing effects on neurons similar to that of local anesthetics. Compared with opioids epidural clonidine is more effective in patients with neuropathic pain. As an analgesic adjunct clonidine reduces requirements for opioids prolongs regional block and enhances postoperative analgesia. Clonidine (oral transdermal intrathecal) may be effective in the treatment of fibromyalgia and spasticity (alone or combined with baclofen) presumably by alpha2-adrenergic mediated presynaptic inhibition of spinal motor neurons.
.
|
L.A. PAIN CLINIC COMPOUNDED PREPARATION Clonidine Ointment
|
___________________________________
.
|
COSYNTROPIN (Cortrosyn)
|
USE(S): treatment of post dural puncture headache diagnostic agent for adrenocortical insufficiency. DOSING: Post Dural Puncture Headache IM/SC 0.5-1 mg. May repeat in 24 hours Screening test for Adrenal Function: IM/IV 0.25-0.75 mg Reconstitute 0.25 mg Cosyntropin in 1 ml of Normal Saline Pharmacology A synthetic subunit of ACTH (adreno-corticotrophic hormone) Cosyntropin is alpha-1-24 corticotropin. Cosyntropin exhibits the full corticosteroidogenic activity of ACTH. 0.25 mg of Cosyntropin will stimulate the adrenal cortex maximally and to the same extent as 25 units of natural ACTH In contrast to human and synthetic ACTH which all contain 39 amino-acids and exhibit similar immunologic activity Cosyntropin contains 24 amino acids and has very little immunologic activity yet retaining full biologic activity. This property of Cosyntropin assumes added importance in view of the known antigenicity of natural ACTH. Case reports have documented complete and permanent relief from postdural puncture headache after intravenous infusion of of ACTH or IM/IV administration of Cosyntropin.
.
|
|
Order Sota Omoigui's Pain Drugs Handbook, Magnets and Compounded Medications
.
|
GABAPENTIN (Neurontin)
| USE(S):adjunct treatment of partial seizures with or without secondary generalization treatment of sympathetic mediated pain neuropathic pain. DOSING: Anticonvulsant / Sympathetic Mediated Pain / Neuropathic Pain Initial PO Day 1 - 300 mg once a day Day 2 - 300 mg twice a day. Day 3 - 300 mg three times a day Maintenance PO 300-600 mg three times a day. Dose may be titrated upwards in increments of 300 mg daily every 5-7 days. Doses of up to 2400 mg daily have been used. It is not necessary to monitor serum levels to optimize therapy. Dosage should be decreased (by 50-75%) in patients with compromised renal function or undergoing hemodialysis. Pharmacology A structural analog of the neurotransmitter GABA gabapentin has an unknown mechanism for its anticonvulsant activity. Binding of the drug occurs in the outer layers of the isocortex and the hippocampus. The drug does not bind to GABA benzodiazepine glutamate glycine opiate or N-methyl-d-aspartate receptors and may have an uncommon binding site in the CNS. Gabapentin has a unique pharmacokinetic profile for an anti convulsant drug including no binding to plasma proteins primary elimination by the kidney and dose dependent oral absorption at high dosages. No drug interactions occur with other anti convulsants. Beneficial effects of gabapentin in alleviating the peripheral manifestations of sympathetic mediated pain (hyperpathia allodynia edema stiffness discoloration vasomotor and sudomotor changes) may be due to inhibitory action at its receptor sites increase in the bioavailability of serotonin consequent decrease in catecholamine outflow and antidepressant effects. Gabapentin crosses the blood-brain barrier and may produce CNS side-effects. e.g. somnolence
.
|
L.A. PAIN CLINIC COMPOUNDED PREPARATION Gabapentin Ointment
|
___________________________________
.
|
LEFLUNOMIDE (Arava)
|
USE(S): treatment of rheumatoid arthritis DOSING Rheumatoid arthritis: Initial Loading: PO 100 mg once daily for 3 days Maintenance: PO 20 mg once daily. If not well tolerated, dose may be decreased to 10 mg once daily. Maintenance doses higher than 20 mg once daily are not recommended due to greater incidence of side effects. Dosage recommendations are not available for children at this time. The use of leflunomide in patients less than 18 years of age is not recommended. Exclude pregnancy prior to administration to women of child bearing potential. Liver enzymes should be monitored prior to the initiation of treatment and monthly thereafter. Patients with hepatic impairment: Leflunomide is not recommended in patients with pre-existing hepatic impairment. If ALT elevations greater than 2-fold of the upper limits of normal (ULN), occur while on leflunomide treatment, a dose reduction to 10 mg PO once daily may allow continued administration of the drug. Patients should continue to be monitored clinically and with frequent, repeated serum Liver Function Test (LFT) measurements. Patients who have persistence of elevations > 2-fold but <= 3-fold ULN despite dose reduction are recommended to have a liver biopsy before deciding to continue treatment. Patients with ALT elevations > 3-fold ULN are recommended to have dose reduction or discontinuation of the treatment. Treatment may require the use of the drug elimination protocol with cholestyramine (see below). If elevations of hepatic enzymes persist, leflunomide should be discontinued, cholestyramine should be readministered and close clinical monitoring should continue. Retreatment with cholestyramine may be needed to lower Leflunomide M1 levels to less than 0.02 mg/L. Patients with renal impairment: There are no specific dosing guidelines. Leflunomide M1 serum levels may be doubled in dialysis patients. Use with caution. Dose adjustments may be necessary during treatment with Leflunomide. Due to the prolonged half life of the active metabolite of leflunomide, observe patients carefully after dose reduction since it may take several weeks for metabolite level to decline. After stopping treatment with leflunomide, and if it is desirable to rapidly obtain plasma levels less than 0.02 mg/L, a drug elimination procedure with cholestyramine is recommended, (see below). The procedure can achieve a 40% lowering of serum leflunomide (M1) concentrations within 24 hours. Without the procedure, it may take 2 years for concentrations to decrease to this level. Drug Elimination Procedure - Cases of pregnancy, significant overdose or toxicity, or other circumstances that require rapid lowering of leflunomide M1 plasma levels. 1. Stop Leflunomide 2. Administer cholestyramine PO 8 grams three times daily for 11 days 3. Verify plasma levels of the leflunomide M1 metabolite are less than 0.02 mg/L by 2 separate tests at least 14 days apart. If plasma M1 levels are higher than 0.02 mg/L, additional cholestyramine treatment should be considered. 4. Alternatively, administer activated charcoal suspensions PO or via a nasogastric tube: 50 grams every 6 hours for 24 hours. Plasma concentrations of M1 have been reduced by 48% within 48 hours. Repeat administration may be necessary. Pharmacology An isoxazol derivative and pyrimidine synthesis inhibitor, Leflunomide is the first agent for rheumatoid arthritis that is indicated for both symptomatic improvement and retardation of structural joint damage based on radiographic evidence of its disease modifying activity. Leflunomide exhibits essentially all its pharmacologic activity via its active primary metabolite M1. M1 inhibits Dihydroorotate dehydrogenase (DHODH), an enzyme involved in de novo pyrimidine synthesis. Suppression of pyrimidine synthesis in T and B lymphocytes interferes with RNA and protein synthesis within the cells. T and B cell collaborative actions are interrupted and immunoglobulin production is suppressed. The effect appears to be cytostatic and not cytotoxic. Leflunomide M1 may also have anti-inflammatory properties secondary to reduction of histamine release, and inhibition of induction of cyclooxygenase-2 enzyme (COX-2). Leflunomide may decrease proliferation, aggregation and adhesion of peripheral and synovial fluid mononuclear cells. Decrease in the activity of lymphocytes leads to reduced cytokine and antibody mediated destruction of the synovial joints and attenuation of the inflammatory process. After 52 weeks of treatment in clinical trials, leflunomide showed similar improvements in tender and swollen joint counts, pain and other symptoms when compared to methotrexate and sulfasalazine. Leflunomide was significantly superior to placebo in time to progression of structural disease as evidenced by Sharp X-ray scores. Sharp scores were not consistently different between leflunomide and methotrexate. Leflunomide has a fast onset of action (4 weeks) relative to other disease-modifying agents. The drug has a uricosuric effect and may produce hypophosphaturia in some individuals.
.
|
|
Order Sota Omoigui's Pain Drugs Handbook, Magnets and Compounded Medications
.
|
ONDANSETRON (Zofran)
|
USE(S): prevention and treatment of chemotherapy-induced and postoperative nausea and vomiting DOSING Chemo/Radiotherapy induced Nausea : Adults PO 8 mg two or three times daily Children: PO 4 mg three times daily Administer first dose 30 mins-2 hours before start of Chemo or Radiotherapy and for 1-2 days after Chemo or Radiotherapy. IV: 32 mg in one dose. Dilute in 50 mls D5W and infuse over 15 minutes beginning a half hour before the start of chemotherapy; or IV : 0.15 mg/kg - three doses. Dilute each dose in 50 mls D5W and infuse over 15 minutes. Give dose a half hour before the start of chemotherapy and repeat dose 4 hours and 8 hours after. Dosage should be reduced (max. daily dose of 8 mg) in patients with hepatic impairment. Postoperative Nausea : PO 8-16 mg (administer as premedication) 1 hour before induction of anesthesia. Slow IV 4 mg. Give undiluted over 1-5 minutes immediately before induction of anesthesia or postoperatively. Dose may be repeated if necessary. Pharmacology Ondansetron is a selective serotonin 5-HT3 receptor antagonist. 5-HT3 receptors are present both peripherally on vagal nerve terminals and centrally in the chemoreceptor trigger zone of the area postrema. Ondansetron may antagonize the emetic effects of serotonin at either or both receptor sites. Ondansetron does not antagonize dopamine receptors. Transient increases in hepatic transaminase levels may occur following therapy. The drug may cross the placenta and may be excreted in breast milk. It should be used with caution in pregnant and nursing mothers. .
.
|
|
Order Sota Omoigui's Pain Drugs Handbook, Magnets and Compounded Medications
.
|
OXYCODONE HCL (OxyContin OxyIR)
|
USE(S): treatment of acute chronic and cancer pain treatment of severe refractory headache and migraine DOSING Analgesia: PO immediate-release 5-10 mg every 4-6 hours PO sustained release (OxyContin): 10-80 mg every 12 hours. Titrate dose to maintain adequate analgesia with acceptable side effects. Opioid tolerant patients with severe pain may require up to 240 mg every 12 hours. Combinations with adjuvant drugs e.g. NSAIDs, antidepressant agents and use of non-drug therapies enhance analgesia and reduce opioid requirements. Max Daily Dose of Non Opioid Ingredient in Fixed-Combination Preparations (e.g. Percocet): Acetaminophen - 4 Grams, Aspirin - 6 Grams Administer sustained release preparation regularly (i.e. around-the-clock). Administer immediate-release preparation prn for breakthrough pain. Due to impaired elimination, dose should be modified depending on clinical response in patients with renal or hepatic dysfunction. Pharmacology A synthetic phenanthrene derivative opiate agonist. Oxycodone differs from hydrocodone by the attachment of a hydroxyl group on the phenanthrene nucleus. Oxycodone exerts its primary effects on the central nervous system and organs containing smooth muscle. Excitatory synaptic pain transmission is decreased by opioid-receptor mediated inhibition of neurotransmitter release e.g. bradykinin at site of tissue injury, substance P in the dorsal horn and dopamine in the basal ganglia. In addition, oxycodone (and other opioids) may alter cognitive and emotional processing of painful input by acting on limbic and cortical opioid receptors. Oxycodone is a potent analgesic and has no ceiling effect for analgesia. Drowsiness, euphoria, depression of the cough reflex and dose dependent respiratory depression may occur. Clinically important respiratory depression is rarely seen in patients with severe pain due to malignant disease even with large doses, because pain and emotional stress are powerful antagonists to narcotic induced respiratory depression. Constipating effects of oxycodone result from induction of non-propulsive contractions through the GI tract. Emetic effects are due to opioid-induced stimulation of the chemo-receptor trigger zone in the floor of the fourth ventricle. Adverse effects are generally milder than those of morphine.10 mg of orally administered oxycodone is equivalent in analgesic efficacy to 20 mg of oral morphine sulfate, 70 mg of oral codeine, 5 mg of intramuscular oxycodone, and 3.3 mg of intramuscular morphine sulfate. Antitussive effects may occur with doses lower than those usually required for analgesia. The drug has no antipyretic effects. Physical dependence and tolerance may develop with repeated administration. Abuse liability is similar to that of codeine. Oxycodone will only partially suppress the withdrawal syndrome in patients physically dependent on other narcotics. Oxycodone crosses the placenta and low levels may be detected in breast milk. However no adverse effects have been noted in nursing infants.
.
|
L.A. PAIN CLINIC COMPOUNDED PREPARATION Oxycodone Sustained Release
| ___________________________________
.
|
SUMATRIPTAN (Imitrex)
|
USE(S): acute treatment of migraine attacks with or without auras DOSING: SC: 3-6 mg. Dose may be repeated after one hour if needed or PO medication may be utilized. Max. SC daily dose 12 mg. PO 25-100 mg. Dose may be repeated every two hours. Max. 24-hour PO dosage: 300 mg Max. 24-hour PO dosage after initial SC dose : 200 mg Intranasal: 20 mg per 0.1 ml insufflation. Administer two insufflations of 20 mg fifteen minutes apart Slow IV: 1-2 mg (20-30 mcg/kg) Dilute in NS and infuse over 10 mins Sumatriptan is approved for subcutaneous intranasal and oral administration only in the United States. Intravenous administration may be associated with coronary vasospasm. Pharmacology Sumatriptan is a selective serotonin 5-hydroxytryptamine (5-HT1) receptor agonist. It produces brief and selective vasoconstriction of the arteriovenous anastomosis of the carotid distribution and prevents neurogenic dural plasma extravasation. Sumatriptan is a stronger vasoconstrictor of the dural arteries than cerebral and temporal arteries. The drug has no effect on alpha beta dopamine and other serotonin (5-HT2 5-HT3) receptors. There is no effect on cerebral blood flow peripheral arteries or perfusion of peripheral organs. Sumatriptan reduces the incidence of nausea vomiting photophobia and phonophobia. It appears to be more effective than Cafergot (ergotamine and caffeine) in the acute treatment of migraine. The efficacy of sumatriptan is unaffected whether or not migraine is associated with aura duration of attack gender of the patient or concomitant use of common migraine prophylactic drugs (e.g. beta blockers).
.
|
|
Order Sota Omoigui's Pain Drugs Handbook, Magnets and Compounded Medications
.
|
TIZANIDINE (Zanaflex)
|
USE(S): Acute and intermittent management of increased muscle tone associated with spasticity; adjunct treatment of acute compression radiculopathy reflex sympathetic dystrophy multiple sclerosis trigeminal neuralgia pre-trigeminal neuralgia glossopharyngeal neuralgia vago-glossopharyngeal ; neuralgia organic (non traction) headache neuropathic pain post herpetic neuralgia fibromyalgia; perioperative sedation DOSING Spasticity/Trigeminal neuralgia/RSD/Organic Headache/Neuropathic pain: Initial PO: 2 mg (half tablet) in the morning and afternoon 4 mg (one tablet) at bedtime. Maintenance: PO 4-12 mg three times daily For increased muscle relaxation Tizanidine doses may be supplemented with Baclofen. Pharmacology A short acting alpha2-adrenergic receptor blocker Tizanidine appears to reduce spasticity by increasing presynaptic inhibition of motor neurons. Its effects are greatest on polysynaptic pathways and the overall result is both direct impairment of the release from spinal neurons of excitatory neurotransmitters (such as glutamic acid) and the concurrent inhibition of 'facilitatory' spinal pathways (those that enhance muscle movement). Although it is chemically related to clonidine and other alpha2-adrenergic agonists it has one-tenth to one-fiftieth the antihypertensive potency of these drugs.12 mg of Tizanidine is equipotent in sedative and sympatholytic activity with 150 mcg of Clonidine. Tizanidine and baclofen are equally effective in anti-spastic activity. However Tizanidine may be associated with fewer side effects such as severe muscle weakness. Tizanidine or baclofen are the drugs of choice for muscle spasm in patients with multiple sclerosis and other spinal cord lesions where the decrease in the number and severity of muscle spasms (especially flexor spasms) alleviates associated pain clonus muscle rigidity and improves mobility. Either tizanidine or intrathecal baclofen are preferable to intrathecal injections of sclerosing agents (e.g. phenol) rhizotomy or cordotomy. Tizanidine (like clonidine) mediates gastric mucosal protection and may reduce the incidence of NSAID induced gastric irritation. Tizanidine may have anti-nociceptive properties. It has been reported to relieve neuropathic (lancinating shooting) and causalgic (hot burning cramping) components of phantom limb pain. Oral tizanidine may be effective in the adjunctive treatment of reflex sympathetic dystrophy trigeminal neuralgia fibromyalgia and nonvascular headache. Tizanidine may relieve the episodic and allodynic pain in post herpetic neuralgia. In large doses tizanidine may produce excess sedation and hypotension.
.
|
|
Order Sota Omoigui's Pain Drugs Handbook and Compounded Medications | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| copyright Sota Omoigui M.D. - 1999 | |||
|
|||
|
Home Page | Ordering Infor- mation |
Pain Relief Guide |
Androstene Love Pill |
Herbal Supplements for Weight Loss |
Anesthesia Drugs Handbook |
Pain Drugs Handbook |
Magnetic Therapy |
Herbs
& Supple- ments |