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185 Cards in this Set
- Front
- Back
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Varenicline has a high affinity for
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Alpha4beta2 nAChRs
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Varenicline-activates what?
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release of DA in NAcc
remove nicotine and DA levels drop acts as a partial agonist |
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Chantix was FDA approved for
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cessation of smoking
very effective in promoting absitnence decreased withdrawal symptoms completely absorbed after oral administration |
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Adverse effects of Chantix
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nausea, abnormal dreams, weigh gain
discontinuation due to adverse effects was less than Bupropion *risk of neuropsychiatric symptoms observed in pts who stopped or cont smoking changes in behavior should be used concurrently with bheavior modification and counseling support |
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what are the most abused CNS stimulants?
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Cocaine
Amphetamines |
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2 types of cocaine
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water soluble salt: IV or snorted
free base (crack): smoked |
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MOA of cocaine
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inhibits dopamine transmitter
at higher concentrations will also inhibit other biogenic receptors |
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effects of cocaine
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easily crosses BBB
euphoria and feeling of grandeur since it is well absorbed by most routes and it quickly metabolized by esterases the effects are shortlasting especially crack is extremely addicting |
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cocaine and amphetamines shares
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a unique effect with amphetamine of reverse tolerance
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withdrawal symptoms of cocaine -mild
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dysphoria
depression sleepiness fatigue bradycardia cocaine craving |
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perinatal toxicity of cocaine
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readily crosses the placenta and may accumulate in fetus
spontaneous abortions or premature labor cerebral infarct if used delivery concentrations in breast milk can be toxic abnormal development and growth of fetus higher % of SIDS |
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legitimate uses of cocaine
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local aneshetic
diagnosis and confirmation of Horner's never really used in practice |
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ex of amphetamines
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dextroamphetamine
methamphetamine club drugs: DOM, MDA, MDMA |
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amphetamine and methamphetamine MOA
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increase monoamine release
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effects of amphetamine
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feelings of euphoria, self-confience that contribute to rapid psychological dependence
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perinatal toxicity of cocaine
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readily crosses the placenta and may accumulate in fetus
spontaneous abortions or premature labor cerebral infarct if used delivery concentrations in breast milk can be toxic abnormal development and growth of fetus higher % of SIDS |
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legitimate uses of cocaine
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local aneshetic
diagnosis and confirmation of Horner's never really used in practice |
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ex of amphetamines
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dextroamphetamine
methamphetamine club drugs: DOM, MDA, MDMA |
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amphetamine and methamphetamine MOA
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increase monoamine release
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effects of amphetamine
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feelings of euphoria, self-confience that contribute to rapid psychological dependence
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perinatal toxicity of cocaine
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readily crosses the placenta and may accumulate in fetus
spontaneous abortions or premature labor cerebral infarct if used delivery concentrations in breast milk can be toxic abnormal development and growth of fetus higher % of SIDS |
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legitimate uses of cocaine
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local aneshetic
diagnosis and confirmation of Horner's never really used in practice |
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ex of amphetamines
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dextroamphetamine
methamphetamine club drugs: DOM, MDA, MDMA |
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amphetamine and methamphetamine MOA
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increase monoamine release
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effects of amphetamine
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feelings of euphoria, self-confience that contribute to rapid psychological dependence
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withdrawal symptoms of amphetamines
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increased appetite
sleepiness exhaustion mental depression |
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legitimate clinical uses of amphetamines
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hypotension
shock asthma epinephrine is still drug of choice for anaphylaxis for ADHD and Narcolepsy |
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ADHD
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Childhood psychiatric disorder characterized by attention-related difficulties & behavioral symptoms such as impulsivity & over activity
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drugs used for treatment of ADHD
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direct or indirect modulation of dopamine or NE levels in critical brain regions
amphetamine-like drugs non-stimulant drugs Atomoxetine -selective NE reuptake inhibitor not a stimulant under the CSA children, adolescents, and adults |
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exact mech of ADHD
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inhibits presynaptic NE reuptake
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narcolepsy
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abnormal balance between REM and NREM sleep
pathological sleepiness sleep paralysis hypnagogic hallucinations cataplexy |
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pathophysiology of narcolepsy
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heritable component
hypothalamic malfunction orexin and hypocretin peptides |
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mild tx of narcolepsy
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no meds
frequent naps - sleep scheduling avoid heavy meals and alcohol |
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TX narcolepsy-meds
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CNS stimulants: MODAFINIL
sodium oxybate tx of cataplexy and improves daytime sleepiness |
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MODAFINIL (Provigil)
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Psychostimulant
Long-lasting Less anxiety Locomotor activity & Less PNS stimulation Weak DA release in NA Inhibits norepi reuptake Decreases GABAergic NT on mesolimbic DA terminals by an increase in Glu NT Still has most of the adverse side effects observed with CNS stimulants HA (most common, nausea, dry mouth, diarrhea) |
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sodium oxybate
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CNS depressant via GABAB receptor agonist
Takes 4 weeks to take effect Tight restrictions due to high abuse liability Dangerous drug Seizures, coma, respiratory depression Safe if used as prescribed for cataplexy |
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drug of choice for alcohol cocaine and amphetamine toxicity
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IV benxodiazepines
eg lorazepam |
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treat symptoms of OD (CNS stimulants)
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hyperthermia
seizures (benzodiazepines eg Lorazepam) |
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Caffeine toxicity -symptoms
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tremor
insomnia nervousness arrhythmias convulsions |
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Tx for caffeine overdose
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evaluate
EKG monitor send home |
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cocaine addiction treatment (rehabilitation)
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not detox but prevention of relapse
competitive antagonists for DAT antibodies directed against cocaine best tx: therapy and surprise urine tests |
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toxicities of cocaine
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CV/vascular
neuro psychiatric renal probs pulmonary probs |
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long term probs with cocaine use
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sexual dysfunction
depression death from fatal heart attacks and strokes delayed cardiac death |
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to tx paranoia
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haloperidol
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to tx anxiety, agitation, seizures
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IV benzos
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tx hypertension
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esmolol
labetalol |
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tx tachyarrhythmia
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esmolol
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club drugs are variations of
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amphetamines
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A 19-year-old female presents to the ER at 4:00 a.m. complaining of
nausea. Her entire body shows visible tremor and her heart rate is elevated. She is extremely agitated and very worried because she has a major exam today. To remain awake and alert, she has consumed 12 NoDoz tablets in the past 12 hours with at least six Red Bull energy drinks. Activation of what CNS receptor by these substances is responsible for her symptoms? |
purinergic (adenosine receptors)
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absorption of alcohol occurs
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20-30 in stomach
the rest in the upper GI tract |
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max blood alcohol levels occurs at
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30-90 min
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where does ethanol go in our body
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distributes in total body water
crosses placenta to affect the fetus and will appear in breast milk |
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rate of absorption (etoh) is influenced by
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concentration ingested, type of beverage, blood flow to site of absorption, rate of ingestion, food and rate of gastric emptying
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is EtoH lipid soluble?
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no practically insoluble BUT readily crosses biological membranes
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how do we eliminate EtOH?
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first pass metabolism primarily in liver, some in stomach
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excretion of etoh in
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2-10% excreted unchanged through urine, saliva, sweat, and breath
equilibrates in breath at high BAL, EtOH is metabolized by P450-2E1 enzyme |
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etoh metabolism exhibits what kind of kinetics?
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(pseudo) zero order kinetics
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ALDH21 is responsible for
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metabolism of acetaldehyde by liver mitochondria
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genetically dominant yet inactive allele, ALDH22 gives natural protection from
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alcoholism
bc acetaldehyde is adversive |
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breakdown of ethanol can change metabolic status directly due to a change in the hepatic NADH/NAD ratio
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Hyperlacticacidemia
Hyperuricemia Hypoglycemia Hyperlipidemia Ketosis |
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ethanol is a CNS_____
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depressant
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pharmacological effects BAL 0.05-0.08
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euphoria minor motor disturbance
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acute tolerance (Mellanby effect)
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normally absent and measure nystagmus
at about 0.08-0.1 get nystagmus |
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pharmacological effects BAL 0.08-0.1
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nystagmus
impaired driving ability first EEG changes |
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pharmacological effects BAL 0.1-0.2
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emotional instability
gross motor incoordination |
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pharmacological effects BAL 0.2-0.3
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confusion
slurred speech amnesia to experiences |
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pharmacological effects BAL 0.3-0.5
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stupor or coma
occasional death |
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pharmacological effects BAL >0.5
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death
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pharmacological effects BAL 0.1-0.2
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emotional instability
gross motor incoordination |
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pharmacological effects BAL 0.2-0.3
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confusion
slurred speech amnesia to experiences |
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pharmacological effects BAL 0.3-0.5
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stupor or coma
occasional death |
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pharmacological effects BAL >0.5
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death
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alcohol - acute CNS effects
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anxiolytic
inhibits temperature regulation alters neuroendrocrine activity: diuresis and steroidogenesis |
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alcohol - chronic CNS effects
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neuroadaptive changes
alcohol consumption may benefit long-term cognition abilities neurotoxicity |
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alcoholic effects on CV system
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very little acute
moderate intake associated with reduced risk of coronary heart disease -heavy drinking associated with increased CV mortality |
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alcoholic effects on GI system
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low doses increase gastric secretion
high doses decrease gastric secretion and motility chronic alcohol use can lead to gastritis, diarrhea, esophageal dysfunctions, malabsorption syndromes |
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alcoholic effects on hepatic system
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acute alcohol has few direct pharm effect on hepatic functions
-fatty liver may occur with relatively small amounts of alcohol chronic intake causes persistent fatty liver that can eventually lead to cirrhosis and hepatic encephalopathy |
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mechanism of action: acute intoxication
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involve GABAa, NMDA-type glutamate receptors, PK
effects on different brain regions cause different symptoms of intoxication |
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mechanism of action: chronic CNS changes
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dopamine receptors
GABAa receptors mu opioid receptors involved in rewarding arg-vasopressin in maintenance of tolerance calcium channels-altered gene expression in physical dependence and withdrawal reaction neuroinflammation in brain damage |
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alcohol toxicity - acute
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causes stupor
seizures coma respiratory arrest |
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alcohol toxicity - chronic
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cirrhosis
brain damage teratogenesis in newborns (fetal alcohol syndrome) |
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excess drinking during pregnancy can cause
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fetal alcohol syndrome
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children with fetal alcohol spectrum disorder (FASD) or fetal alcohol effects (FAE)
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skin folds at corner of eye
low nasal bridge short nose indistinct philtrum small head circumference small eye opening small midface thin upper lip |
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alcohol interacts with many other drugs: list
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anesthetics
anxiolytics analgesics non-narcotic (tylenol) antihistamines antidepressants antipsychotic antiseizure CV drugs anticoagulants NSAIDS oral hypoglycemia antibiotics |
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what drug will suppress drinking?
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Disulfiram
acts by inhibition of ALDH |
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What drug will reduce relapse of drinking?
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Naltrexone
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What is the new drug for relapse in alcoholics?
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Acamposate
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accepted contraindications for alcohol ingestion
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hepatic disease
GI ulcers cardiac skeletal myopathy pregnancy |
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tx use of etoh
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Solvent for water-insoluble drugs (p.o. and topical)
Rubbing agent (50-70% v/v) to prevent bedsores Sponge baths for fever Skin disinfectant (70% v/v) |
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metabolism of methanol
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Catabolized by same enzymes as ethanol
Zero order kinetics also, but slower than ethanol ADH forms formaldehyde and ALDH forms formic acid |
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symptoms of methanol poisoning
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acidosis
partial or total blindness headache dizziness delirium nausea comiting |
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tx of methanol
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correct acidosis with bicarb
give ethanol to slow conversion of methanol to formaldehyde |
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isopropyl alcohol poisoning
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potent CNS and respiratory depressant
extreme abdominal pain, nausea, and vomiting giving ethanol will NOT HELP - dialysis only useful treatment for poisoning |
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ethylene glycol poisoning
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contained in antifreeze
metabolized by ADH, ALDH and eventually oxalic acid reacts with calcium and forms deposits in kidneys |
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metabolism of methanol
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Catabolized by same enzymes as ethanol
Zero order kinetics also, but slower than ethanol ADH forms formaldehyde and ALDH forms formic acid |
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symptoms of methanol poisoning
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acidosis
partial or total blindness headache dizziness delirium nausea comiting |
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tx of methanol
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correct acidosis with bicarb
give ethanol to slow conversion of methanol to formaldehyde |
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isopropyl alcohol poisoning
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potent CNS and respiratory depressant
extreme abdominal pain, nausea, and vomiting giving ethanol will NOT HELP - dialysis only useful treatment for poisoning |
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ethylene glycol poisoning
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contained in antifreeze
metabolized by ADH, ALDH and eventually oxalic acid reacts with calcium and forms deposits in kidneys |
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metabolism of methanol
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Catabolized by same enzymes as ethanol
Zero order kinetics also, but slower than ethanol ADH forms formaldehyde and ALDH forms formic acid |
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symptoms of methanol poisoning
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acidosis
partial or total blindness headache dizziness delirium nausea comiting |
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tx of methanol
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correct acidosis with bicarb
give ethanol to slow conversion of methanol to formaldehyde |
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isopropyl alcohol poisoning
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potent CNS and respiratory depressant
extreme abdominal pain, nausea, and vomiting giving ethanol will NOT HELP - dialysis only useful treatment for poisoning |
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ethylene glycol poisoning
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contained in antifreeze
metabolized by ADH, ALDH and eventually oxalic acid reacts with calcium and forms deposits in kidneys |
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tx for ethylene glycol poisoning
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gastric lavage
bicarbonate for acidosis methylene blue for methemoglobinemia and ethanol to decrease metabolism by ADH |
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ethanol is an antidote for what poisoning?
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methanol and ethylene glycol
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etoh is absorbed orally w/ peal blood levels ____min post-drink
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30-90
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ethanol is eliminated from body by what two enzymes?
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ADH
microsomal CYP2E1 |
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which has a higher Km? ADH of CYP2E1
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CYP2E1
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what is induced in the liver of chronic drinkers?
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microsomal CYP2E1
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hepatic clearance of alcohol increases what ratio?
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NADH/NAD
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NADH/NAD ratio causes what metabolic conditions?
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hyperlacticacidemia
hyperuricemia hypoglycemia hyperlipidemia ketosis |
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what gene is dominant negative for enzyme that gives natural protection from alcoholism?
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ALDH2 allel
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dominant negative ALDH2 -adversive to what?
|
acetaldehyde
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highest expression of ALDH2 allele in what population
causes what due to acetaldehyde buildup? |
asian-pacific population
facial flushing |
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what suppresses drinking by inhibiting ALDH?
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disulfiram --> acetaldehyde toxicity
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what is the Mellanby effect?
|
acute tolerance can modify acute intoxicating effects
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acute effects of etoh
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anxiolysis
loss of regulation of body temp altered neuroendocrine activities reduces steroidogenesis and diuresis |
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CNS receptors in acute intoxication
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ACTIVATE inhibitory GABAa receptors
INHIBIT excitatory NMDA glutaminergic receptors |
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chronic exposure to etoh
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neuroadaptive changes
changes in cognition neurotoxicity: neurophysiological deficits, signs of dementia when not intoxicated |
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mech of chronic intoxication
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dopamine, GABAa, mu-opiod receptors --> reward aspects of alcohol dependence
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what might be involved in maintenance of CNS tolerance?
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arg-vasopressin
|
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overdose sx
|
stupor
seizures coma respiratory arrest |
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chronic abuse sx
|
cirrhosis
neurotoxicity tetraogenesis in fetus (FAS) |
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effects of ethanol on CNS -CV
|
very little acute effects
peripheral vasodilation due to acetaldehyde sig interactions between gender, race, intake with BP changes and risk of stroke Moderate intake --> reduce CHD heavy drinking --> increase CV morality |
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effects of ethanol on GI system
|
low dose --> increase gastric secretion
high dose --> decrease gastric secretion and mortality chronic --> gastritis, diarrhea, esophageal dysfunction, malabsorption syndromes |
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ethanol effects on hepatic system
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reversible fatty liver w/ relatively small amounts of alcohol
chronic intake causes persistent fatty liver --> cirrhosis/hepatic encephalopathy |
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list drugs that interact with alcohol
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CNS depressants
psychoactive compounds CV drugs, anticoagulants, NSAIDS, non-narcotic analgesic Tylenol, oral hypoglycemic drugs, certain antibiotics |
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4 contraindications of alcohol ingestion
|
hepatic disease
gi ulcers pregnancy Cardiac/skeletal myipathy |
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therapeutic uses of etoh
|
• Solvent for water-insoluble medications using p.o. or topically
• 50-70% mixure w/ water → rubbing agent to help prevent bedsores • 70% etoh as skin disinfectant • sponge bath for pts with high fever • denatured alcohol is used by injection for relief of long-lasting pain of trigeminal neuralgia, inoperable carcinomas, related conditions • antidote for methanol and ethylene glycol poisoning |
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how is methanol metabolized?
|
catabolized by same enzymes as ethanol
ADH produces formaldehyfe ALDH produces formic acid rate of metabolism is SLOWER then ethanol |
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symptoms of methanol poisoning
|
acidosis
partial/complete blindness headache dizziness delirium nausea vomiting |
|
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tx for methanol poisoning
|
correct acidosis with bicarbonate
administer etoh to slow conversion of methanol to formaldehyde force fluids to increase elimination into urine |
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ethylene glycol metabolism
|
antifreeze
metabolized by ADH, ALDH --> oxalic acid oxalic acid + calcium/insoluble deposits in kidney --> kidney failure |
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tx for ethylene glycol
|
gastric lavage
bicarbonate to tx acidosis methylene blue to tx methemoglobinemia etoh to decrease metabolism by ADH |
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isopropryl alcohol poisoning symptoms
|
potent CNS and respiratory depressant
cause extreme abdominal pain, nausea, vomiting |
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tx of isopropyl alcohol poisoning
|
administration of EtOH will not help
BLOOD DIALYSIS is the only useful treatment |
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what is the leading preventable cause of death?
|
nicotine
70-85% that quit relapse within 6 months |
|
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what are the sx of nicotine withdrawal?
|
dysphoria/depressed mood
insomnia irritability frustration, anger anxiety difficult concentrating restlessness decreased heart rate increased appetite/weight gain |
|
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tx for nicotine
|
assess
behavioral/psychoeducational intervention nicotine replacement Pharmacological: bupropion (Zyban) or Varencline tartrate Chantix) |
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alcohol w/d
|
ANS hyperactivity: sweating/pulse rate increases
increased hand tremor insomnia nausea/vomiting transient visual, tactile, auditory hallucination, illusions psychomotor agitation anxiety grand mal seizures |
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tx for alcohol
|
neltrexone: blocks opiod receptors involved in craving
acamprosate: acts on GABA and glutamate NT systems to reduce sx of protracted abstinence disulfiram: interfers w/ degradation of alcohol, accumulation of acetaldehyde |
|
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cocaine + alcohol -->
|
cocaethylene, intensifies cocaine's euphoric effects --> may cause sudden death
|
|
|
cessation of cocaine:
|
prolonged and heavy
dysphoric mood and 2 or more of following: fatigue vivid, unpleasant dreams insomnia hypersomnia increased appetite psychomotor agitation of retardation |
|
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tx of cocaine
|
NO DRUG
behavioral and psychotherapy contingency management |
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what is the active ingredient in cannabis?
|
active chemical is THC
|
|
|
effects of cannabis
|
conjunctival injection
increase appetite dry mouth tachycardia |
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w/d from cannabis
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evidence of irritability
sleeplessness anxiety |
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tx of cannabis
|
behavioral and psychotherapy tx
contingency management no pharm tx for cannabis dependence of abuse |
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amphetamines - MOA
|
causes NTs to be released from their storage sites in neurons
|
|
|
effects of amphtamines
|
euphoria
affective blunting changes in socibality hypervigilance interpersonal sensitivity anxiety tension anger stereotyped behaviors impaired judgement impaired social and occupational functioning |
|
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w/d from amphetamines
|
fatigue
vivid, unpleasant dreams insomnia, hypersomnia increased appetite psychomotor retardation or agitation |
|
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tx for amphetamines
|
behavioral and psychotherapy tx
no pharm tx for amphetamine dependence or abuse |
|
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w/d from cannabis
|
evidence of irritability
sleeplessness anxiety |
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inhalant intoxication sx
|
dizziness
nystagmus incoordination slurred speech unsteady gait lethargy depressed reflexes psychomotor retardation tremor generalized muscle weakness blurred vision or diplopia stupor or coma euphoria |
|
|
tx of cannabis
|
behavioral and psychotherapy tx
contingency management no pharm tx for cannabis dependence of abuse |
|
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tx inhalant
|
behavioral psychotherapy tx
contingency management VERY POOR PROGNOSIS due to multiple comorbidities, psychitratic issues and high prob of cognitive impairment and brain pathology |
|
|
amphetamines - MOA
|
causes NTs to be released from their storage sites in neurons
|
|
|
what is the most abused opioid?
|
heroin
|
|
|
effects of amphtamines
|
euphoria
affective blunting changes in socibality hypervigilance interpersonal sensitivity anxiety tension anger stereotyped behaviors impaired judgement impaired social and occupational functioning |
|
|
what are some irreversible effects of inhalants?
|
hearling loss
peripheral neuropathies and limb spasm CNS or brain damage bone marrow damage |
|
|
w/d from cannabis
|
evidence of irritability
sleeplessness anxiety |
|
|
w/d from amphetamines
|
fatigue
vivid, unpleasant dreams insomnia, hypersomnia increased appetite psychomotor retardation or agitation |
|
|
tx of cannabis
|
behavioral and psychotherapy tx
contingency management no pharm tx for cannabis dependence of abuse |
|
|
tx for amphetamines
|
behavioral and psychotherapy tx
no pharm tx for amphetamine dependence or abuse |
|
|
amphetamines - MOA
|
causes NTs to be released from their storage sites in neurons
|
|
|
inhalant intoxication sx
|
dizziness
nystagmus incoordination slurred speech unsteady gait lethargy depressed reflexes psychomotor retardation tremor generalized muscle weakness blurred vision or diplopia stupor or coma euphoria |
|
|
effects of amphtamines
|
euphoria
affective blunting changes in socibality hypervigilance interpersonal sensitivity anxiety tension anger stereotyped behaviors impaired judgement impaired social and occupational functioning |
|
|
tx inhalant
|
behavioral psychotherapy tx
contingency management VERY POOR PROGNOSIS due to multiple comorbidities, psychitratic issues and high prob of cognitive impairment and brain pathology |
|
|
w/d from amphetamines
|
fatigue
vivid, unpleasant dreams insomnia, hypersomnia increased appetite psychomotor retardation or agitation |
|
|
what is the most abused opioid?
|
heroin
|
|
|
tx for amphetamines
|
behavioral and psychotherapy tx
no pharm tx for amphetamine dependence or abuse |
|
|
what are some irreversible effects of inhalants?
|
hearling loss
peripheral neuropathies and limb spasm CNS or brain damage bone marrow damage |
|
|
inhalant intoxication sx
|
dizziness
nystagmus incoordination slurred speech unsteady gait lethargy depressed reflexes psychomotor retardation tremor generalized muscle weakness blurred vision or diplopia stupor or coma euphoria |
|
|
tx inhalant
|
behavioral psychotherapy tx
contingency management VERY POOR PROGNOSIS due to multiple comorbidities, psychitratic issues and high prob of cognitive impairment and brain pathology |
|
|
what is the most abused opioid?
|
heroin
|
|
|
what are some irreversible effects of inhalants?
|
hearling loss
peripheral neuropathies and limb spasm CNS or brain damage bone marrow damage |
|
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opiod tx
|
methadone
buprenorphine naltrexone behavioral and psychotherapy tx contingency managements |
|
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sedative, hypnotic, anxiolytics sx
|
FOR anxiety and insomnia
inappropriate sexual aggressive behavior mood lability impaired judgement impaired social and occupational functioning |
|
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w/d from sedatives
|
increased hand tremor
insomnia nausea and vomiting transient visual, tactile auditory hallucinations psychomotor agitation anxiety grand mal seizures |
|
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hallucinogen and dissociatives sx
|
profound distortions in persons' perceptions of reality
dissociative distort perception of sight and sound produce feeling of detachment-dissociation from environment and self act on NMDA systems |
|
|
hallucinogen and dissociatives sx of intoxication
|
marked anxiety
depression idea of reference fear of losing one's mine paranoid ideation impaired judgement, social and occupational functioning |
|
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ex of hallucinogens
|
profound distortions in person's perception of reality: LSD, psilocybin, peyote, mescaline
dissociative: PCP, ketamine, dextromorphan |
|
|
tx of hallucinogen
|
behavioral and psychotherapy tx
no pharmacoogical tx |
|
|
what are episodes of spontaneous repeated continuous recurrences of some sensory distortions originally produced by LSD
may include hallucinations but it most commonly consists of visual perceptual disturbances often persistent remains unchanged for yrs after last drug use |
Hallucinogen Persisting Perception Disorder (flashback)
|
