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PathopharmA 2

neurolo chapter 20,24, 25

QuestionAnswer
chapter 20
Central Nervous System (CNS) Drugs Agents that act on the brain and spinal cord Medical uses Relief of pain Suppression of seizures Production of anesthesia Treatment of psychiatric disorders
DRUGS Nonmedical uses Stimulant, depressant, euphoriant, and other “mind-altering” abilities
Transmitters of the CNS Peripheral nervous system: Acetylcholine, norepinephrine, and epinephrine CNS: At least 21 compounds that serve as neurotransmitters PRESENCE OF neurotransmitter role for dopamine, norepinephrine, serotonin, and enkephalins , BUT LOT STILL UNKNOWN
The Blood-Brain Barrier Not fully developed at birth Impedes entry of drugs into the brain“Mixed Blessing”•Keeps out toxic substances•Can also be a barrier to therapeutic substancesPassage across the blood-brain barrier limited to lipid-soluble drugsProtein-bound or highly ionized drugs cannot cross
Adaptation of the CNS to Prolonged Drug Exposure Different effects possible when drug is taken chronically versus the initial use of the drug (d/t adaptive changes)  Increased therapeutic effects over time START WORKING IN 4-8 WEEKS DUE TO CNS ADAPTING TO DRUG
SEIZURE-WHEN DID THE AURA STARTED, WHAT TIME, HOW DID THEIR PRESENT DURING THE EPISODE-how often and what type od seizure Adaptation of the CNS to Prolonged Drug Exposure PROLONGED TREATMENT DECREASE SIDE EFFECTS,BUT THE THERAPEUTIC EFFECT REMAINS THE SAME COUD DEVEOP TOLERANCE PHYSICL DEPENDENCE : WITHDRAWING S/S; JITTERINESS, sweating, goosebumps, vomiting, anxiety, insomnia, and muscle pain.
Psychotherapeutic Drugs Difficult and Slow!  Complexity of mental health  Lack of adequate animal models of mental illness  Mentally healthy individuals cannot be used as subjects • No effect or paradoxical effects • Psychopharmacologic accidental discoveries
Difficult and Slow!  Complexity of mental health  Lack of adequate animal models of mental illness  Mentally healthy individuals cannot be used as subjects • No effect or paradoxical effects • Psychopharmacologic accidental discoveries There are numerous neurotransmitters  Their precise functional roles are not clear  Their complexity makes it difficult to know with certainty just how CNS drugs produce their effects
Chapter 24 AED-CAUSES -SUICIDAL THOUGHT-DEPRESSION(WORSEN WITH ALCOHOL, ANTIHISTAMINE, OR OPIODS}
Definition of Seizure Disorders May also cause problems with learning, memory, and mood FIRING OF SEIZURE -excessive excitability of neurons in the central nervous system -Seizures are initiated by discharge from a group of hyperexcitable neurons, called a focus(PLACE WHERE IT STARTS)
Focus may result from the following: Congenital defects  Hypoxia at birth  Head trauma  Brain infection  Stroke  Cancer  Genetic disorders
Partial (focal) seizures - excitation undergoes limited spread from the focus to adjacent cortical areas TYPES: Simple partial  Complex partial  Secondarily generalized
DRUGS- PHENYTOIN(OLDER AGENT) Traditional AEDs • Phenytoin, fosphenytoin, carbamazepine, valproic acid, ethosuximate, phenobarbital, and primidone Selective inhibition of Na channel  TE 10 to 20 mcg/mL( Narrow -SLOW liver’s capacity to metabolize phenytoin) ADR  Nystagmus, Sedation, Ataxia, Diplopia, Cognitive impairment  Gingival hyperplasia, Skin rash, Effects in pregnancy  Cv effects
OXCARBAMAZEPINE(NEWER AGENT-BETTER TOLERATED total of 14) Stevens-Johnson syndrome  Toxic epidermal necrolysis hyponatremia (<125 mmol/L) MONOTHERAPY AND ADJUNCTIVE THERAPY IN CHILDREN AND ADULTS BLOCK Electrical Na channel=suppress hyperexcitable neurons stabilized, and seizures ADR Dizziness, drowsiness, double vision, nystagmus, headache, nausea, vomiting, and ataxia-
LAMICTAL TE:  Broad spectrum of antiseizure activity  Bipolar disorder ADR Dizziness, diplopia, blurred vision, nausea, vomiting, and headache  Severe skin reactions  Aseptic meningitis  Risk for suicide GABAPENTIN TE: Adjunctive therapy of partial seizures Off-label use: Neuropathic pain, prophylaxis of migraine, treatment of fibromyalgia, and relief of postmenopausal hot flashes
GENERALIZED SEIZURE Tonic-clonic-JERK MUSCLE-INCONTINENCE-LOSS OF CONSCIOUNESS  Absence (petit mal)-FROM BODY 10-30sec  Atonic-LOSS MUSCLeTONE  Myoclonic-MUSCLE RIGIDITY  Status epilepticus-CONTINIOUS, IF DOESNT STOP=911  Febrile-RESPONSE TO FEVER IN YOUNG CHILDREN
PHENYTOIN Decreases the effects of oral contraceptives, warfarin, and glucocorticoids  Increases levels of diazepam, isoniazid, cimetidine, alcohol, and valproic acid  Dosing: Highly individualized Gingival hyperplasia: Swelling, tenderness, and bleeding of the gums  Gingivectomy  Folic acid (0.5 mg/day) may prevent gum overgrowth  Risk can be minimized by good oral hygiene, including dental flossing and gum massage
VALPROIC not o be used during pregnancy, unless it is the only AED that works 80-100mcg a broad-spectrum AED FOR partial seizures , tonic-clonic, absence, atonic, and myoclonic ADR FATAL LIVER FAILURE IN <2YRS OLD TAKING OTHER AED fatal pancreatitis. teratogenic- reduce the IQ of children exposed to it in utero
CARBAMAZEPINE decrease oral contraceptives PREFERRED B/C BETTER TOLERATED ADR leukopenia, anemia, and thrombocytopenia—and, very rarely, fatal aplastic anemia. SJS/TEN. Risk is clearly increased by the HLA-B*1502 gene variation DECREASE RISK OF TOXICITY - CBC at baseline and thereafter
TARGET OF AED gamma-aminobutyric acid (GABA) EFFECT  Suppress discharge of neurons within a seizure focus  Suppress propagation of seizure activity from the focus to other areas of the brain MOA Suppression of Na-Ca influx  Antagonism of glutamate  Potentiation (GABA)
Goals of Treatment Reduce seizures to a level that allows the patient to live as normal a life as possible  Balance the desire for complete seizure control with acceptable side effects -DUE TO SEDATION PATIENT FEAR HAVING ANOTHER SEIZURE-COULD BE TEENS OR ADULT
Epilepsy: Therapeutic Considerations Treatment options  Neurosurgery  Vagal nerve stimulation  Ketogenic diet-makes it difficult for teens to adhere  Medication  Diagnosis  Physical, neurologic, and laboratory evaluations along with a thorough history  Electroencephalogram-
Epilepsy: Therapeutic Considerations Drug evaluation  Antiepileptic drug (AED) trial period- • Precautions?  Dosage adjustment  Seizure frequency chart-NEED TO KNOW WHEN, HOW LONG IS IT LASTING-FOLLOW UP S/S
Epilepsy: Therapeutic Considerations  Monitoring plasma drug levels  Promoting patient adherence  Withdrawing antiepileptic drugs  SLOW! 6 weeks - months-TO PREVENT SE  Suicide risk: Antiepileptic drugs  Topirimate and Lamotrigine as AED
FACTS Rarely, phenytoin causes severe skin reactions: StevensJohnson syndrome (SJS) or toxic epidermal necrolysis (TEN) . Risk may be increased by the HLA-B*1502 gene variation, seen almost exclusively in patients of Asian descent.
FACTS Fetal risk can be minimized by avoiding valproic acid and by using just one AED (if possible) in the lowest effective dosage. All traditional AEDs (and some newer AEDs) can harm the developing fetus(1st trim.) However, women with major seizure disorders should continue taking AEDs throughout pregnancy TO MINIMIZE RISK
IMPORTANT Initial control of generalized convulsive SE is accomplished with an IV benzodiazepine—either diazepam or lorazepam. When diazepam is used, follow-up treatment with phenytoin or fosphenytoin is essential for prolonged seizure suppression.
CHAPTER 25
Drugs for Muscle Spasm and Spasticity - skeletal muscle relaxation  One group for localized muscle spasm  One group for spasticity  Most drugs (except dantrolene) produce their effects through actions in the central nervous system (CNS)  Groups are not interchangeable
Muscle spasm-RELAXE-TIGHTEN UP-RELAX Involuntary contraction of muscle or muscle group Causes  Epilepsy  Hypocalcemia  Pain syndromes: Acute and chronic  Trauma: Localized skeletal muscle injury-I.E CAR ACCIDENT
Treatment of spasm Pharmacologic therapy Analgesics  Acetaminophen  NSAIDs • Centrally acting muscle relaxants  Cyclobenzaprine  Physical measures • Warm compresses • Whirlpool baths • Physical therapy
Centrally Acting Muscle Relaxants Cyclobenzaprine  first line drug  Not for spacticity ADR Generalized CNS depression  Anticholinergic effects  Cardiac rhythm disturbances  Interactions • Serotonin syndrome with some antidepressants • Alcohol and other CNS depressants
Spasticity-CONTINUOUS CONTRACTION-INCREASED MUSCLE TONE Movement disorders of CNS origin  common causes: Multiple sclerosis, cerebral palsy, and spinal cord injury  Characteristics include the following: • Heightened muscle tone • Spasm • Loss of dexterity
Baclofen [Lioresal]  NOT used with stroke ■ relieves spasticity by mimicking the inhibitory actions of GABA in the CNS TE Multiple sclerosis, spinal cord injury, and cerebral palsy  Decreases flexor and extensor spasms  Suppresses resistance to passive movement  No direct effect on skeletal muscle so doesn’t cause muscle weakness-ACT ON CNS
Baclofen [Lioresal] ADR  No antidote for overdose  withdrawal over 1 to 2 weeks • Abrupt intrathecal withdrawal: Risk for rhabdomyolysis-break down of muscle=clog kidneys  CNS depressant  Gastrointestinal symptoms (eg, nausea, constipation)  Urinary retention
Dantrolene MOA  Acts directly on skeletal muscle  Suppresses the release of calcium from the sarcoplasmic reticulum  TE  Spasticity associated with multiple sclerosis, cerebral palsy, and spinal cord injury  Malignant hyperthermia - succinylcholine
Dantrolene Adverse effects  Hepatic toxicity  Muscle weakness  Drowsiness  Diarrhea  Acne-like rash
FACTS ■ Spasticity is treated with four drugs: baclofen, diazepam, dantrolene, and tizanidine
FACTS AVOID ALL CNS DEPRESSANTS Abrupt discontinuation of intrathecal baclofen can lead to rhabdomyolysis, multiple organ system failure, and death.
Created by: Seka_nurse
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