Prophylactically use H2 blockers, take with food
Assess support system
Monitor blood glucose level, adjust dose of hypoglycemic drugs
Baseline and follow up eye exams
Monitor wt, BP, lung sounds, edema
Monitor s/s bleeding buries, black emesis, stool, coffee ground emesis
Cardiac monitor, +/- supplements
Monitor s/s of infection, avoid crowds, hand washing
Monitor bone density and supplements
Monitor s/s, give NS, hydrocortisone IV, take steroids in AM, do NOT stop the meds suddenly
Two groups of COX inhibitors:
Nonselective COX inhibitors or 1st generation NSAIDs
aspirin (Aspirin, Ecotrin, Bayer), Ibuprofen (Advil, Motrin), Naproxen (Aleve, Anaprox, Naprosyn), Naproxen /lansoprazole (Prevacid Naprapac), Meloxicam (Mobic), Oxaprozin (Daypro), Diclofenac/misoprostol (Arthrotec), indomethacin (indocin),
Parenteral and oral: Ketorolac (Toradol)
Selective COX2 inhibitors or 2nd generation NSAIDs: celecoxib (Celebrex)
*Confusing drugs: Celebrex vs. Celexa
SE: GI upset (N/V/D/A, abd pain, heartburn), gastric bleeding/ulcers, fluid retention->wt gain, edema, and HTN, renal impairment (↓ renal blood flow)
ADE: Kidney failure, MI and stroke for nonaspirin NSAIDS, exacerbation of asthma ,
ASA only: Salicylism or ASA poisoning, Reye's syndrome, preg anemia, postpartum hemorrhage, may prolong labor
Seizure, restlessness, irritability, excessive and unorganized talking, fear or nervousness, dizziness, confusion, abnormally excited mood, hallucinations, drowsiness, loss of consciousness, double vision, tinnitus, uncontrollable shaking, increased HR and RR, burning throat pain, vomiting pain, decreased urination, fever, decreased Na and K, alkalosis, death MOA: Inhibit COX-2 receptors, reversible
Uses: arthritis, pain,
CI: not use celecoxib in pts w/ sulfa allergy, cautious use 2nd gen. NSAIDs in pts w/ CVD
SE: fewer than 1st generation drugs, but higher cardiovascular risks, last-choice drug for long-term management of pain, lower risk for GI side effects
ADEs: renal impairment, hypertension, and edema, increased risk for MI and stroke
Collect Hx of HTN, CHF, PUD, GERD
Monitor s/s of bruise and bleeding (black emesis, stool, Occult blood test), PTT, PT, INR
Monitor wt, VSs (T, HR, RR, BP), I &O, renal function (BUN, Cr)
Managing ASA poising or salicylism or ASA toxicity:
Give IV fluid and electrolytes
Activated charcoal and gastric lavage
Alkalization of urine to increase ASA elimination
Constipation (↓ GI motility), GI upset
drowsiness, sedation (mental clouding)
Dizziness (orthostatic hypotension)
Skin pruritus (itchiness), urticaria (hive)
Cough suppression -> mucus accumulation
respiratory depression (opioid blocker, Narcan)
Overdose triad: coma, resp. depression and pinpoint pupils
Addiction: psychological needs
Dependence: physical needs
Tolerance (Pharmacodynamics)<-receptor exhaustion
withdrawal : Nausea, vomiting, abdominal cramping, sweating, delirium, seizures
** withdrawal occurs when suddenly quitting the drug after long-term use
Concurrent use with opioids, NOT to use alone
Tricyclic antidepressants depression and neuropathic pain (cramping, aching, burning, darting, and lancinating pain)
Anticonvulsants CHRONIC neuropathic pain (DM, CA), migraines, fibromyalgia, and neuralgia
CNS stimulants enhance analgesia and reduce sedation.
Antihistamines relieve pain associated anxiety, prevent insomnia and relieve nausea.
Glucocorticoids pain induced by intracranial pressure and spinal cord compression.
Bisphosphonates manage hypercalcemia induced bone pain due to cancer
EE: enhance the effects of opioids, relieve depression, seizures and other symptoms aggravating pain, reduce opioid SE/ADE, reduce neuropathic and CA bone pain
other anticholinergic effects (10cants and 6 Ds)
Anticonvulsants: CNS depression, bone marrow suppression, GI distress
CNS stimulants: wt loss, insomnia,
Antihistamines: sedation, dry mouth
Steroids: adrenal insufficiency, Osteoporosis, hypokalemia, hypernatremia, hyperglycemia, peptic ulcer disease (PUD),
Bisphosphonate: transient flu-like s/s, irritation of injection site, renal failure/UTI
NSAIDs: bone marrow suppression, GI distress
Not for pts w/ recent MI and taking MAOI within 2week,
Cautious use in pts w/ seizure, urinary retention, BPH, close-angle glaucoma, hyperthyroidism, liver/renal disease
Not for pts w/ bone marrow suppression and taking MAOI within 2-wk,
Cautious use in pts w/ seizure
Not for pts w/ hyperthyroidism, HTN, taking MAOI within 2-wk,
Cautious use in pts w/ agitation or tics
Antihistamines: (1st generation)
Cautious use in elderly due to CNS sedation
Not for pts w/ fungal infection
Cautious use in pts w/ seizure disorder, peptic ulcer disease or PUD, hypertension, hypothyroidism, DM, or liver disease.
Bisphosphonate: Cautious use in pts w/ kidney disease
Not for pt w/ history of bronchospasm induced by NSAIDs
Cautious use in pts w/ PUD, hypertension, and liver/ kidney disease.
change position slowly, assist ambulation, monitor orthostatic BP
Avoid driving and operating heavy machinery
Other anticholinergic effects: increase fluid intake, chew gum/candy, physical active, laxative/stool softener, check bladder, vision, I/O
Not to use with other CNS depressants (alcohol)
Monitor CBC and platelets count, PT and INR when taking with warfarin
Instruct to watch bruising and bleeding, infection and anemic s/s
Take with food, but avoid grape fruit juice
Increase OC dose when taking together
monitor wt, VSs, drug and glucose level
take last dose no later than 4pm,
monitor Avoid caffeine, OTC sympathomimetic
Antihistamines: avoid driving and operating machine, increase fluid intake, suck on candy, chew gum, not to use with other CNS depressants (alcohol)
Monitor s/s adrenal insufficiency, cardiac rhythm, K+ , Na+, glucose levels, GI bleed
Take with food, use acid reduction meds
Increase hypoglycemic agents
take pill in AM
Bisphosphonate: Monitor fever, injection site, Cr, BUN, s/s UTI
NSAIDs: monitor bruise and bleeding.
Drug names: zolpidem (Ambien), eszopiclone (Lunesta), Zaleplon (Sonata), Trazodone (Desyrel)
Prolong sleep duration and reduce awakenings by ehancing the action of neurotransmitter gamma-aminobutyric acid (GABA-A) in the CNS.
Have NO antianxiety, muscle relaxant, antiepileptic effects
Low risk of tolerance, abuse and dependence.
insomnia, help improve both sleep maintenance and daytime alertness
short-acting, short-term use (7-10 days), < 4 weeks.
CI/Pr: Preg B. not for nursing mother, cautious use in elderly and pts w/ renal/liver/respiratory dysfunction.
Non-Benzodiazepines (Benzodiazepine receptor agonists )
SE/ADEs: lightheadedness, drowsiness, daytime sleepiness, dizziness, fatigue, headache, GI upset, sleep-related behavior (sleep-driving, phone calling, eating, sleepwalking)
DDI: additive CNS depression when concurrent use with other CNS depressants (alcohol)
Take zolpidem immediately before going to sleep
Take zolpidem only when able to get a full night' s sleep (7 - 8 hours)
Not drink alcohol the same evening
Drug names: "-pam" or "-lam"clonazepam (Klonopin), lorazepam (Ativan), alprazolam (Xanax), temazepam (Restoril), diazepam (Valium)
MOA: reduce anxiety and induce sleep by increasing action of GABA in CNS
Uses: anxiety, seizure, insomnia, muscle spasm, alcohol withdrawal, Panic disorder, induce anesthesia
Not for pts w/ sleep apnea, respiratory depression, organic brain disease or lactation
Cautious use in pts w/ hx of substance abuse, liver/renal failure
SE: CNS depression, respiratory depression, daytime sleepiness, anterograde amnesia, sleep-related behaviors, falls and urinary incontinence in elderly patients.
ADEs: Often occur with abrupt discontinuation
Physical dependence withdrawal Symptoms
Short-term therapy: GI distress, sweating, dysrhythmia, anxiety, insomnia, tremor and dizziness
Long-term therapy: delirium, paranoia, panic, HTN, seizures,
paradoxical response (rebound insomnia, excitation, euphoria, anxiety and rage)
Oral toxicity: drowsiness, lethargy, confusion
IV toxicity: respiratory depression
DDI: additive sedation with concurrent use with other CNS depressants (alcohol)
The second most common neurodegenerative disorder after Alzheimer's disease
Slow, progressive, degenerative CNS disorder, and unknown cause
Death of dopamine-containing cells in the substantia nigra (midbrain)
Decreased dopamine level in CNS
Imbalance between dopamine and acetylcholine (ACh)
Begins subtly; progresses gradually Symptoms:
Motor -related, including resting tremor, rigidity, bradykinesia (slow movement), postural instability and rapid shuffling gait
Non-motor: cognitive and behavioral, dementia
neuropsychiatric problems , dementia
mood, depression, behavior or thought alterations
sensory and sleep difficulties
Risk factors - age (> 50), genetics, environment
Reduced risk in tobacco smokers.
GI upset, Cardiovascular effects, OH, Psychosis, discolorate sweat and urine,
Activate malignant melanoma
depression with suicidal tendencies
neuroleptic malignant syndrome.
dopamine dysregulation syndrome due to compulsive drug overuse , manifested as "punding"
not for pt w/ maligant melanoma,
not use within 2 weeks of MAOI use,
Cautious in pt w/ heart disease, psychiatric disorders, and elderly
SE: day-time sleepiness and drowsiness, nausea and constipation, water retention, Orthostatic HYPOTENSION,
ADE: impulse control disorders (such as compulsive sexual activity and eating, and pathological gambling and shopping, stronger than levodopa), psychosis (visual hallucinations, nightmares), and dyskinesias
Cautious in pts w/ liver and kidney impairment.
DDI: concurrent use with levodopa OH, dyskinesias (monitor closely)
Centrally acting anticholinergics
Drug name: Benzatropine (Cogentin), trihexyphenidyl (Artane)
MOA: Block acetylcholine at muscarinic receptors -> keep balance between dopamine and acetylcholine in the brain.
SE/ADEs: N/V, anticholinergic SEs (10cants and 6Ds), antihistamine SE (sedation and drowsiness)
CI: narrow-angle glaucoma, elderly (BPH and urinary retention)
Drug name: amantadine (Symmetrel)
MOA: stimulate DA release, prevent dopamine reuptake, and block cholinergic and glutamate receptors
SE/ADEs: CNS effects (confusion, dizziness, restlessness), anticholinergic SE , and discoloration of skin
90% of patients develop non-motor symptoms (autonomic disturbances, depression, dementia, and psychosis)
Anticholinergic (Cogentin, Artane) exacerbates dementia
Antidepressants: Amitriptyline (TCA), only effective drug
Cholinesterase inhibitors: dementia,
Psychosis: Clozapine (Clozaril), only use antipycal antipsychotic drug
Modafinil (Provigil ): daytime sleepiness
Fetal Tissue Transplantation
The symptoms are often described as a clinical triad of abnormalities:
Cognitive effects: mental confusion, hypomania, hallucinations, agitation, headache, coma.
Autonomic effects: shivering, sweating, fever, hypertension, tachycardia, nausea, diarrhea.
Somatic effects: myoclonus/clonus (muscle twitching), hyperreflexia, tremor.
Have to have all 3
Herbs: St John's Wort, Yohimbe
Antidepressants: Monoamine oxidase inhibitors (MAOs), TCAs, SSRIs, SNRIs, mirtazapine, venlafaxine
Opioids: tramadol, pethidine, oxycodone, morphine, meperidine
CNS stimulants: phentermine, diethylpropion, amphetamines, sibutramine, methylphenidate
Illicit drugs: methylenedioxymethamphetamine (MDMA or ecstasy), lysergic acid diethylamide (LSD), cocaine, PMA
Others: selegiline, tryptophan, buspirone, kanna, lithium, linezolid, dextromethorphan (DXM), 5-Hydroxytryptophan, chlorpheniramine, bupropion, risperidone
Side effects of BZs are common, dose related, usually short term and harmless
Drowsiness, sedation, ataxia, dizziness
Feelings of detachment, irritability or hostility
Cognitive effects with long-term use
Tolerance, dependency, rebound insomnia/anxiety
Rarely nausea, headache, confusion, depression
Agitation, Anorexia, Hyperactivity, Insomnia, Irritability, Nausea, vomiting, Sensitivity to light, sounds, Tinnitus, Tremulousness, Anxiety, Autonomic arousal, Dizziness, Generalized seizures, Hallucinations, Headache MOA:
In low doses nicotine activates nicotinic receptors. Most effects occur from activated receptors in autonomic ganglia and the adrenal medulla. In the CNS, nicotine rapidly acts on the mesolimbic reward system of the brain, promoting the release of dopamine and mimicking the effects of cocaine and other highly addictive substances
Cardiovascular stimulation, increased myocardial oxygen consumption, CNS stimulation, increased RR and tremors, increased alertness and arousal, increased GI secretions and smooth-muscle tone, relaxation/relief of anxiety.
Abstinence syndrome is evidenced by irritability, nervousness, restlessness, insomnia, and difficulty concentrating.
Very strong psychological dependence.
nicotine replacement therapy (NRT)
nicotine patch, lozenges, nasal spray, and inhalers.
Bupropion (Zyban) - can cause dry mouth
Nortriptyline (Aventyl, Pamelor)
For Nicotine gum, use of chewing gum is not recommended for longer than 6 months, advise clients to chew gum slowly and intermittently over 30 min. Advise clients to avoid eating or drinking 15 minutes prior to and while chewing the gum. For Nicotine patch, clients should apply a nicotine patch to an area of clean, dry skin each day. Advise clients to avoid using any nicotine products while the patch is on. Patch should be removed prior to MRI scan and replaced when the scan is completed
Cocaine is the most potent of the abused stimulants.
Cocaine inhibits the neuronal uptake of dopamine in the brain and increases the activation of dopamine receptors in the brain reward system. This action magnifies pleasures and leads to rapid dependence. Cocaine also increases norepinephrine at postsynaptic receptor sites, producing intense vasoconstriction and cardiovascular stimulation.
stimulation of CNS, increased energy/alertness, impairment of concentration and memory, irritability and mood swings, paranoia, and depression.
paranoid delusions to visual hallucinations, tactile hallucinations, skin excoriations from scratching, needle marks, and increased BP, HR, and temp.
Acute cocaine toxicity may be manifested by cardiac palpitations, tachycardia, increased respiratory rate, and fever. At high levels of overdose, grand mal seizures, hypertension, and dysrhythmias or myocardial ischemia can occur. The client experiences restlessness, paranoia, agitated delirium, and confusion. Bizarre, erratic, and violent behavior may occur. Death is often related to a cerebrovascular accident, fatal dysrhythmias, or myocardial infarction
Amphetamines act similarly to cocaine, stimulating the release of dopamine and norepinephrine in the brain and the sympathetic nervous system. The dopamine release in the brain reward system produces euphoria and an increase in self-confidence.
increased alertness, improved performance, relief of fatigue, and anorexia, cardiovascular stimulation with increased HR and BP, irritability, anxiety, paranoia, and hostile and violent behaviors,
in tooth decay and dermatologic deterioration.
"overamping," may result in amphetamine psychosis, paranoia, seizures, and death.
Withdrawal symptoms of amphetamines are similar to those of cocaine use.
Patients often seek treatment for complications of amphetamine abuse such as panic reactions, psychosis, or depression. Emergency management of amphetamine toxicity is the same as that for cocaine. Elevated blood pressure and tachycardia can be controlled with vasodilators and adrenergic β-blockers. Drug elimination can be enhanced by administering agents such as ammonium chloride that acidify the urine. Cessation and maintenance of abstinence are difficult in amphetamine abuse. Depression can last for months.
Caffeine is a methylxanthine that stimulates the CNS, especially the medullary respiratory center. It also is a diuretic and myocardial stimulant. Caffeine relaxes smooth muscle and promotes peripheral vasodilation and cerebral vasoconstriction.
Oral doses of 200 mg (two cups of coffee) can elevate mood, produce insomnia, increase irritability, cause anxiety, and offset fatigue. Heavy intake of 500 mg or more per day is known to cause intoxication with symptoms of nervousness, insomnia, gastric hyperacidity, muscle twitching, confusion, chest pain, tachycardia, and cardiac dysrhythmias. In toxic doses, caffeine influences behavior patterns and may precipitate states of panic. Until the advent of caffeine pills and highly caffeinated energy drinks, caffeine overdoses were very rare because people developed undesirable symptoms before they could ingest enough.
Physical and psychological dependence on caffeine have been found with chronic use of more than 500 mg/day.
withdrawal symptoms are headache, irritability, drowsiness, and fatigue occurring within 12 to 24 hours.
Attention is given to controlling hypertension, dysrhythmias, and seizures as with other CNS stimulants. Gradually reduce daily intake.
Alcohol affects almost all cells of the body and has complex effects on the neurons in the CNS. Alcohol is a general CNS depressant. Additionally, alcohol binds with receptors in the brain reward system resulting in the release of dopamine and promoting the addictive process.
The symptoms of alcohol use include nausea; vomiting; tremors; restlessness and inability to sleep; depressed mood or irritability; increased heart rate, blood pressure, respiratory rate, and temperature; and tonic-clonic seizures. Illusions are also common. Acute overdose produces vomiting, coma, and respiratory depression. Alcohol-induced hypotension may lead to renal failure and cardiogenic shock, common causes of alcohol-related death.
hangovers manifested by malaise, nausea, headache, thirst, and a general feeling of fatigue. In alcoholics, sudden withdrawal may have life-threatening effects such as severe disorientation, psychotic symptoms (hallucinations), severe hypertension, and cardiac dysrhythmias that may progress to death.
Initial treatment of acute alcohol intoxication or overdose requires implementation of the basic principles of airway, breathing, and circulation (ABCs). No antidote for alcohol is available, and stimulants should not be given.
thiamine should be started before treatment with IV glucose solution in all patients with alcoholism and continued until the client resumes a normal diet.
Abstinence Maintenance Phase—Following Detoxification
These include disulfiram (Antabuse), a daily oral medication that is a type of aversion (behavioral) therapy and prevents drinking by causing an unpleasant reaction if alcohol is consumed, and naltrexone, which blocks the desired effects of alcohol
Naltrexone (ReVia, Depade) is a pure opioid antagonist that decreases craving and pleasurable effects of alcohol and blocks the "high" of alcohol use.
Acamprosate (Campral) is used to decrease unpleasant feelings such as tension, dysphoria, anxiety, restlessness and cravings brought about by abstinence from alcohol
Ondansetron (Zofran), an antagonist of receptors in the brain reward system, decreases motivation for drinking in early onset alcoholism; and topiramate (Topamax), an anticonvulsant, may be helpful in decreasing craving for alcohol as well as cocaine.
Sedative-hypnotic drugs act primarily on the CNS. Benzodiazepines enhance the effects of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter in the brain. Barbiturates not only enhance the inhibitory effect of GABA, but they can directly mimic the actions of GABA. Barbiturates are powerful respiratory depressants and can readily cause death by overdose.
initial euphoria and intoxication similar to that of alcohol.
Withdrawal from sedative-hypnotics can be very serious. In the first 12 to 16 hours following the last dose, the client may develop anxiety, tremors, weakness, nausea, vomiting, muscle cramps, and increased reflexes. After 24 hours, the client craves the drug and may experience delirium, grand mal seizures, and respiratory and cardiac arrest. Symptoms of withdrawal peak on the second or third day for short-acting (shorter half-life) drugs (e.g., alprazolam, secobarbital, pentobarbital) and on the seventh or eighth day for long-acting (longer half-life) drugs (e.g., diazepam, chlordiazepoxide, phenobarbital).
Overdoses of benzodiazepines are treated with flumazenil (Romazicon), a specific benzodiazepine antagonist
Gastric lavage may be used if the drug was taken orally within 4 to 6 hours. Dialysis may be required to decrease the drug level. Gradual withdrawal of the drug is required during withdrawal syndrome. Phenobarbital, a long-acting barbiturate, may be used to control withdrawal symptoms in a client dependent on barbiturates. Phenobarbital is then gradually withdrawn when the client is stable. To manage their symptoms safely, hospitalization is recommended during drug withdrawal for individuals who have been abusing large amounts of barbiturates.
Important to the abuse potential of opioids is their ability to activate the brain reward system, reinforcing their addictive effect
The primary effects of opioids include analgesia, drowsiness, slurred speech, and detachment from the environment. IV use usually causes a "rush" of feelings in the lower abdomen, along with warm skin flushing and a strong sense of euphoria. Cross-tolerance among the opioids is common, but cross-tolerance to other CNS depressants does not occur. However, additive effects of other CNS depressants may lead to increased CNS depression.
Although opioid withdrawal is acutely uncomfortable, it is not usually life threatening, as is withdrawal from other CNS depressants. However, suicidal ideation may occur.
A narcotic antagonist such as naloxone (Narcan) should be used to reverse respiratory depression and coma induce by opioids overdose. Treatment of withdrawal syndrome is symptom-based and does not always require the use of medication. Methadone (Dolophine) in decreasing doses over 10 to 14 days is the drug most often used to decrease symptoms during opioid detoxification. Methadone is an oral opioid agonist that replaces the opioid to which the patient is addicted. Some patients obtain relief from withdrawal symptoms with the use of clonidine (Catapres), a centrally acting alpha2-adrenergic agonist that may also be used for nicotine addiction. It is most effective against autonomic GI hyperactivity (diarrhea, nausea, vomiting), but it does not decrease craving. The action of clonidine in nicotine and opioid addiction is not fully understood. Buprenorphine (Subutex) is an agonist-antagonist opioid that may be used for detoxification and maintenance therapy. Because of its action on specific opiate receptors, it can decrease the symptoms of withdrawal and suppress drug craving, yet it has a low potential for abuse.
Naltrexone (oral ReVia, injectable Vivitrol) is an opioid antagonist that blocks euphoria and all other opioid effects. It is used for abstinence maintenance therapy. Like naloxone, it will precipitate withdrawal symptoms when administered to opioid-dependent individuals.
THC affects cannabinoid receptors in the brain and may act in part through the same reward system as opioids and cocaine.
euphoria, sedation, and hallucinations, relaxation, enhanced sensory perception, and distortion of time perception, short-term memory loss, decreased ability to perform multistep tasks, and temporal disintegration, Intense anxiety, delusions, paranoia, and a state of toxic psychosis can occur. Decreased sperm production and decreased reproductive hormones in both men and women. Decreased motor coordination, tremors, and increased heart and respiratory rates. A condition known as amotivational syndrome, characterized by apathy, dullness, and disinterest, may also occur.
Treatment is directed toward relief of symptoms
Interferon beta is a naturally occurring glycoprotein with antiviral, antiproliferative, and immunomodulatory actions. Natural interferon beta is produced in response to viral invasion and other biologic inducers. In patients with MS, benefits are thought to derive primarily from inhibiting the migration of proinflammatory leukocytes across the blood-brain barrier, thereby preventing these cells from reaching neurons of the CNS.
flu-like reactions, hepatotoxicity, myelosuppression or bone marrow suppression, injection-site reactions, depression, neutralizing antibodies, and drug interactions (Exercise caution when combining interferon beta with other drugs that can suppress the bone marrow or cause liver injury.)
In patients with MS, the drug promotes a "T-cell shift." That is, it decreases production of proinflammatory TH1 cells and increases production of anti-inflammatory TH2 cells. The anti-inflammatory cells migrate across the blood-brain barrier at sites of inflammation, and then suppress the inflammatory attack on myelin
Injection-site reactions—pain, erythema, pruritus (itching), induration (pitting)—are most common.
About 10% of patients experience a self-limited postinjection reaction—characterized by flushing, palpitations, severe chest pain, anxiety, laryngeal constriction, and urticaria—that typically lasts 15 to 20 minutes.
In patients with MS and Crohn's disease, natalizumab prevents circulating leukocytes (T cells and monocytes) from leaving the vasculature, and thereby prevents these cells from migrating to sites where they can do harm. In order to exit the vasculature, activated leukocytes must first adhere to the vascular endothelium, a process that requires the interaction of two types of molecules: (1) integrins (adhesion molecules) expressed on the surface of leukocytes and (2) integrin receptors expressed on cells of the vascular epithelium. Natalizumab binds with integrin molecules on leukocytes, and thereby renders these cells unable to bind with integrin receptors on the capillary wall. As a result, the leukocytes cannot cross the capillary wall, and hence are unable to exit the vasculature to reach their sites of inflammatory action. In patients with MS, natalizumab prevents activated leukocytes from crossing the blood-brain barrier. In patients with Crohn's disease, the drug prevents leukocytes from crossing capillaries that deliver blood to the GI tract.
headache, fatigue, abdominal discomfort, arthralgia, depression, diarrhea, gastroenteritis, UTI, and lower respiratory tract infections. The most serious effects are PML, liver injury, and hypersensitivity reactions.
). In patients with MS, mitoxantrone suppresses production of immune system cells (B lymphocytes, T lymphocytes, and macrophages), and thereby decreases autoimmune destruction of myelin. Additional protection may derive from reducing antigen presentation and reducing production of cytokines (eg, interleukin-2, TNF-alpha, interferon gamma) that participate in the immune response.
Mitoxantrone can cause a variety of adverse effects. Myelosuppression, cardiotoxicity, and fetal injury are the greatest concerns. Hepatotoxicity, hair loss and injury to the GI mucosa, resulting in stomatitis and GI distress.nausea, vomiting, menstrual irregularities (eg, amenorrhea), and symptoms of allergy (itching, rash, hypotension, shortness of breath). blue-green tint to the urine, skin, and sclera.
Carisoprodol (Soma), Cyclobenzaprine (Flexeril), Metaxalone (Skelaxin), Tizanidine (Zanaflex)
relax muscle spasm and dpress muscle spasticity by enhancing GABA and primarily causing CNS sedation. It has NOT direct effects on skeletal muscle
CNS depression (drowsiness, dizziness, lightheadedness, sleepiness, fatigue). dry mouth, blurred vision, photophobia, urinary retention, and constipation.
Hepatic toxicity (anorexia, nausea, vomiting, abdominal pain, jaundice) and physical dependence, life threatening abstinence syndrome if abruptly withdrawn.
Suppress hyperactive reflexes by mimicking the inhibitory neurotransmitter, GABA, on spinal neurons (CNS). It is centrally acting drug, having no direct effects on skeletal muscle
GI discomfort(Nausea, constipation), urinary retention, CNS depression (drowsiness, dizziness, lightheadedness, sleepiness, fatigue), weakness.
Abrupt stop can cause withdrawal symptoms: visual hallucinations, paranoid ideation, and seizures.
Diazepam (Valium), benzodiazepine
Acts in the CNS to suppress spasticity by mimicking GABA at receptors in the spinal cord and brain to produce sedation. Does not affect skeletal muscle directly.
CNS depression (drowsiness, dizziness, lightheadedness, sleepiness, fatigue). GI discomfort
Acts directly on spastic muscles and inhibits muscle contraction by suppressing release of calcium in skeletal muscles.
GI discomfort, muscle weakness, CNS depression (drowsiness, dizziness, lightheadedness, sleepiness, fatigue).
Hepatic toxicity (anorexia, nausea, vomiting, abdominal pain, jaundice)
succinylcholine (Anectine), pancuronium (Pavulon), atracurium (Tracrium), vecuronium (Norcuron)
Block acetylcholine (ACh) at the neuromuscular junction or NMJ to promote muscle relaxation and paralysis.
relaxed muscle during surgery and ventilation and intubation, no seizure during ECT
muscle ache, apnea, hypotension, hyperkalemia, malignant hyperthermia
pts with myasthenia gravis (MG), respiratory dysfunctions, fluid and electrolyte imbalance
general anesthetics, antibiotics, cholinesterase inhibitors for succinylcholine
pseudocholinesterase for succinylcholine, electrolytes like potassium
report family and history of malignant hyperthermia, using antibiotics, low level of pseudocholinesterase if applicable
Drug names: -caine or -cain
MOA: ↓pain by blocking conduction of pain impulses in local area, no loss of consciousness.
Uses: dental, minor surgical/procedures, diagnostics, L/D
SE/ADE: CNS excitations (seizures), hypotension, cardio-suppression (e.g., bradycardia/heart block, cardiac arrest), prolonged labor, fetal CNS and cardio-suppression, spinal HA due to hypotension, urinary retention
Nursing implications and patient educations
Vasoconstrictors, epi to keep and prolong local anesthetic effects and decreases the risk of systemic toxicity.
Protect numb area from injury
Resuscitation kits available
Instruct patient monitoring and reporting complications.
Locoreginal: Epidural, spinal, and combined spinal-epidurals
The only consistently effective means of relieving the pain of labor and delivery
Drug of choices: bupivacaine, ropivacaine, fentanyl and morphine
Uses: anticipated difficulty with intubation, hx of malignant hyperthermia, cardiopulmonary disorders, high spinal cord lesion, preeclampsia
Contraindications: patient refusal, risk for bleeding, lower back infection, unstable hypovolemia, increased intracranial pressure,
Systemic Drugs: IV, PCA , IM, and inhalation routes
prefers less invasive techniques
Regional techniques are contraindicated
Lack of availability of skilled providers
DOC: morphine, fentanyl, Remifentanil, Meperidine (Demerol), opioid agonists-antagonists (Nalbuphine [Nubain] and butorphanol [Stadol])
Not as effective as regional analgesia, more for sedation less analgesic
CI: delivery within 4 hrs of administration
SE/ADE: GI upset, sedation, maternal aspiration, maternal and neonatal respiratory depression, reduce fetal heart rate variability
Mild analgesics: aspirin or ASA, NSAIDs, acetaminophen (Tylenol)
serotonin agonists for acute migraine,
MOA: reduce pain by inhibiting vasoactive peptides release vasoconstriction, blocking pain pathways
Oral preparations are available
NOT concurrent use of Ergots
Ergots or ergotamine (DHE or dihydroergotamine)
Poor oral and rectal absorptions
SE/ADE: N/V, rebound headaches, cardiovascular complications, Ergotism , physical dependence, and abortion
Antiemetics: metoclopramide (Reglan), chlorpromazine (Thorazine) and prochlorperazine (Compazine)
Adjunct therapy for acute migraine headache
IV and IM preferred
Benzodiazepines, anticonvulsants, TCA, CCB, opioids and barbiturates
ONLY used for intractable migraine HA, NEVER for chronic management or FIRST line treatment
Staged approach per setting:
Outpatient setting: triptans for moderate to severe migraine
Severe migraine with severe N/V:
IV antiemetic + diphenhydramine or DHE + corticosteroid (dexamethasone)
Early treat and large single dose preferred.
Prophylactic therapy for migraine: propranolol (Inderal)