+ 40 mv. Resting Membrane. Potential. Time (msec) Depolarization! Hyperpolarized. Na + equilibrium. Action. Potential. Threshold.
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1 Local Anesthetics
2 Local anesthetics Block nerve conduction of sensory impulses and, in higher concentrations, motor impulses from the periphery to the CNS. Na+ ion channels are blocked to prevent the transient increase in permeability of the nerve membrane to Na+ that is required for an action potential When propagation of action potentials is prevented, sensation cannot be transmitted from the source of stimulation to the brain. Delivery techniques include topical administration, infiltration, peripheral nerve blocks, and neuraxial (spinal, epidural, or caudal) blocks. Small, unmyelinated nerve fibers for pain, temperature, and autonomic activity are most sensitive. Structurally, local anesthetics all include a lipophilic group joined by an amide or ester linkage to a carbon chain, which, in turn, is joined to a hydrophilic group.
3 Depolarization! Action Potential Na + equilibrium mv 0-50 Na + influx K + efflux Threshold Potential -70 Hyperpolarized Resting Membrane Potential Time (msec)
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5 The most widely used local anesthetics are Bupivacaine [byoo-piv-uh-cane] Lidocaine [lye-doecane] Mepivacaine [muh-piv-uh-cane] Procaine [pro-cane], Ropivacaine [roe-piv-uh-cane], and Tetracaine [tet-truh-cane]. Bupivacaine is noted for cardiotoxicity if inadvertently injected IV. Bupivacaine liposome injectable suspension may provide postsurgical analgesia lasting 24 hours or longer after injection into the surgical site. [Note: Non-bupivacaine local anesthetics may cause an immediate release of bupivacaine from the liposomal suspension if administered together locally.] Mepivacaine should not be used in obstetric anesthesia due to its increased toxicity to the neonate.
6 Metabolism Biotransformation of amides occurs primarily in the liver. Prilocaine [PRY-low-cane], a dental anesthetic, is also metabolized in the plasma and kidney, and one of its metabolites may lead to methemoglobinemia. Esters are biotransformed by plasma cholinesterase (pseudocholinesterase). Patients with pseudocholinesterase deficiency may metabolize ester local anesthetics more slowly. At normal doses, this has little clinical effect. Reduced hepatic function predisposes patients to toxic effects, but should not significantly increase the duration of action of local anesthetics.
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8 Onset and duration of action The onset and duration of action of local anesthetics are influenced by several factors including tissue ph, nerve morphology, concentration, pka, and lipid solubility of the drug. Of these, the ph of the tissue and pka are most important. At physiologic ph, these compounds are charged. The ionized form interacts with the protein receptor of the Na+ channel to inhibit its function and achieve local anesthesia. The ph may drop in infected sites, causing onset to be delayed or even prevented. Within limits, higher concentration and greater lipid solubility improve onset somewhat. Duration of action depends on the length of time the drug can stay near the nerve to block sodium channels.
9 Actions Local anesthetics cause vasodilation, leading to rapid diffusion away from the site of action and shorter duration when these drugs are administered alone. By adding the vasoconstrictor epinephrine, the rate of local anesthetic absorption and diffusion is decreased. This minimizes systemic toxicity and increases the duration of action. Hepatic function does not affect the duration of action of local anesthesia, which is determined by redistribution and not biotransformation. Some local anesthetics have other therapeutic uses (for example, lidocaine is an IV antiarrhythmic).
10 Allergic reactions Patient reports of allergic reactions to local anesthetics are fairly common, but often times reported allergies are actually side effects from epinephrine added to the local anesthetic. Psychogenic reactions to injections may be misdiagnosed as allergic reactions and may also mimic them with signs such as urticaria, edema, and bronchospasm. True allergy to an amide local anesthetic is exceedingly rare, whereas the ester procaine is somewhat more allergenic. Allergy to one ester rules out use of another ester, because the allergenic component is the metabolite para-aminobenzoic acid, produced by all esters. In contrast, allergy to one amide does not rule out the use of another amide. A patient may be allergic to other compounds in the local anesthetic, such as preservatives in multidose vials.
11 Administration to children and the elderly Before administering local anesthetic to a child, the maximum dose based on weight should be calculated to prevent accidental overdose. There are no significant differences in response to local anesthetics between younger and older adults. It is prudent to stay well below maximum recommended doses in elderly patients who often have some compromise in liver function. Because some degree of cardiovascular compromise may be expected in elderly patients, reducing the dose of epinephrine may be prudent. Local anesthetics are safe for patients who are susceptible to malignant hyperthermia (MH).
12 Systemic local anesthetic toxicity Toxic blood levels of the drug may be due to repeated injections or could result from a single inadvertent IV injection. The signs, symptoms, and timing of local anesthetic systemic toxicity are unpredictable. One must consider the diagnosis in any patient with altered mental status or cardiovascular instability following injection of local anesthetic. CNS symptoms (either excitation or depression) may be apparent but may also be subtle, nonspecific, or absent. Treatment for systemic local anesthetic toxicity includes Airway Management. Support of breathing and circulation. Seizure suppression and, if needed. Cardiopulmonary resuscitation. Administering a 20% lipid emulsion infusion (lipid rescue therapy) is a valuable asset.
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14 Degenerative Diseases
15 Drugs Used In Alzheimer s Disease Current therapies aim to either: Improve cholinergic transmission within the CNS or Prevent excitotoxic actions resulting from overstimulation of NMDAglutamate receptors in selected areas of the brain. Pharmacologic intervention for Alzheimer s disease is only palliative and provides modest short-term benefit. None of the available therapeutic agents alter the underlying neurodegenerative process.
16 Acetylcholinesterase inhibitors Numerous studies have linked the progressive loss of cholinergic neurons and, presumably, cholinergic transmission within the cortex to the memory loss that is a hallmark symptom of Alzheimer s disease. It is postulated that inhibition of acetylcholinesterase (AChE) within the CNS will improve cholinergic transmission, at least at those neurons that are still functioning. The reversible AChE inhibitors approved for the treatment of mild to moderate Alzheimer s disease include Donepezil [doe-ne-peh-zil], Galantamine [Ga-lan-ta-meen], And Rivastigmine [ri-va-stig-meen]. All of them have some selectivity for AChE in the CNS, as compared to the periphery. Galantamine may also augment the action of acetylcholine at nicotinic receptors in the CNS.
17 At best, these compounds provide a modest reduction in the rate of loss of cognitive functioning in Alzheimer patients. Rivastigmine is the only agent approved for the management of dementia associated with Parkinson s disease and also the only AChE inhibitor available as a transdermal formulation. Rivastigmine is hydrolyzed by AChE to a carbamylate metabolite and has no interactions with drugs that alter the activity of CYP450 enzymes. The other agents are substrates for CYP450 and have a potential for such interactions. Common adverse effects include nausea, diarrhea, vomiting, anorexia, tremors, bradycardia, and muscle cramps
18 NMDA receptor antagonist Stimulation of glutamate receptors in the CNS appears to be critical for the formation of certain memories. However, overstimulation of glutamate receptors, particularly of the NMDA type, may result in excitotoxic effects on neurons and is suggested as a mechanism for neurodegenerative or apoptotic (programmed cell death) processes. Binding of glutamate to the NMDA receptor assists in the opening of an ion channel that allows Ca2+ to enter the neuron. Excess intracellular Ca2+ can activate a number of processes that ultimately damage neurons and lead to apoptosis.
19 Memantine [meh-man-teen] is an NMDA receptor antagonist indicated for moderate to severe Alzheimer s disease. It acts by blocking the NMDA receptor and limiting Ca2+ influx into the neuron, such that toxic intracellular levels are not achieved. Memantine is well tolerated, with few dose-dependent adverse events. Expected side effects, such as confusion, agitation, and restlessness, are indistinguishable from the symptoms of Alzheimer s disease. Given its different mechanism of action and possible neuroprotective effects, memantine is often given in combination with an AChE inhibitor.
20 Drugs Used In Multiple Sclerosis (MS) Multiple sclerosis is an autoimmune inflammatory demyelinating disease of the CNS. The course of MS is variable. For some, MS may consist of one or two acute neurologic episodes. In others, it is a chronic, relapsing, or progressive disease that may span 10 to 20 years. Historically, corticosteroids (for example, dexamethasone and prednisone) have been used to treat acute exacerbations of the disease. Chemotherapeutic agents, such as cyclophosphamide and azathioprine, have also been used.
21 A. Disease-modifying therapies Drugs currently approved for MS are indicated to decrease relapse rates or in some cases to prevent accumulation of disability. The major target of these medications is to modify the immune response through inhibition of white blood cell mediated inflammatory processes that eventually lead to myelin sheath damage and decreased or inappropriate axonal communication between cells. 1. Interferon β1a and interferon β1b: The immunomodulatory effects of interferon [in-ter-feer-on] help to diminish the inflammatory responses that lead to demyelination of the axon sheaths. Adverse effects of these medications may include depression, local injection site reactions, hepatic enzyme increases, and flulike symptoms.
22 2. Glatiramer: Glatiramer [gluh-teer-a-mur] is a synthetic polypeptide that resembles myelin protein and may act as a decoy to T-cell attack. Some patients experience a postinjection reaction that includes flushing, chest pain, anxiety, and itching. It is usually self-limiting. 3. Fingolimod: Fingolimod [fin-go-li-mod] is an oral drug that alters lymphocyte migration, resulting in fewer lymphocytes in the CNS. Fingolimod may cause first-dose bradycardia and is associated with an increased risk of infection and macular edema. 4. Teriflunomide: Teriflunomide [te-ree-floo-no-mide] is an oral pyrimidine synthesis inhibitor that leads to a lower concentration of active lymphocytes in the CNS. Teriflunomide may cause elevated liver enzymes. It should be avoided in pregnancy.
23 5. Dimethyl fumarate: Dimethyl fumarate [dye-meth-il FOO-marate] is an oral agent that may alter the cellular response to oxidative stress to reduce disease progression. Flushing and abdominal pain are the most common adverse events. 6. Natalizumab: Natalizumab [na-ta-liz-oo-mab] is a monoclonal antibody indicated for MS in patients who have failed first-line therapies. 7. Mitoxantrone: Mitoxantrone [my-toe-zan-trone] is a cytotoxic anthracycline analog that kills T cells and may also be used for MS.
24 B. Symptomatic treatment Many different classes of drugs are used to manage symptoms of MS such as spasticity, constipation, bladder dysfunction, and depression. Dalfampridine [DAL-fam-pre-deen], an oral potassium channel blocker, improves walking speeds in patients with MS. It is the first drug approved for this use.
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