SECTION 1 principles of addiction medicine Flashcards
where are the changes in the brain associated with addiction?
addiction causes change in the orbital frontal lobes that are permanent and attics
what is the main reenforcer of addiction
–dopamine is the main reenforcer of addiction.
–There is increased concentration in the limbic system
–It does not cause addiction in itself
how does dopamine cause addiction
addictive drugs either cause reuptake inhibition of dopamine or increased sensitivity to dopamine
–Reduce 5-10 times greater effect
is addiction genetic?
40-60% of vulnerability to addiction is genetic
risk factors for addiction
–stress
–Low income status
–Drug availability
–Mental illness
defined prevalence
prevalence = number of cases/in total population
define incidence
incidence = number of new cases/number in total population
define relative risk
relative risk = number of people with disease plus special conditions/number with disease without special condition
prevalence of alcoholism
1980 prevalence of alcoholism was
–13% lifetime
–3% past month
relationship of age to alcoholism
–one third adolescent drinkers will develop dependence
–Alcoholism generally declines with age
prevalence of drug use
lifetime prevalence = 0.2%
–Males to ask more likely than females
–Half of adolescent users developed dependence
risk factors for drug use
risk factors for drug use
–Cohabitation
–Nontraditional jobs
–Childhood sexual abuse
peak hazard age for drug and alcohol abuse
19 years old
compare alcoholism by race
–whites (heavy drinking younger than blacks)
–Blacks have lower drinking rates than whites but are more likely to become chronic drinkers
–Heavy drinking among whites is declining
–Blacks have more problems with alcohol than whites
–Hispanic alcohol use is lower than whites
Hispanic alcohol use increases with acculturation
–Hispanic cirrhosis rates are higher than whites
what parts of the brain are involved in addiction and what are their function?
Limbic system is involved in addiction
–Subcallosal area
–Cingulate
–Parahippocampal gyri
These area are associated with motion, a density, and fight or flight
name opioid receptors
there are 3 opioid receptors
–mu
–kappa
–Delta
There are other opioid receptors throughout the brain, especially the limbic system
effects of MU agonist
selective MU agonist EG heroin, morphine –Analgesia –Euphoria –Respiratory depression –Emesis –Antidiuretic action
effects of opioid kappa Agonist
kappa Agonists produce –Dysphoria –Diuresis –Analgesia –impulse control disorders –NO respiratory depression
cannabinoid receptors
there are 2 cannabinoid receptors, CB 1, CB 2.
–There acted upon by exogenous or endogenous cannabinoids
–CB 1 is found in much of the brain
–CB 2 his founded lower levels of brain
what is physical dependence
physical dependence causes individual to become physically sick when drug administration ceases.
–Physical dependence is neither necessary nor sufficient to diagnosis addiction
list impulse control disorders
IMPULSE CONTROL DISORDERS –Explosive disorder –Kleptomania –Pathologic gambling –Pyromania –Trichotillomania –Excessive intranet use
criteria for pathologic gambling
–gambling with greater amounts of money to achieve same experience
–Unsuccessful attempts to quit or reduce
–Restless or irritable while trying to stop gambling (withdrawal)
–gambling to escape dysphoric state
–Gambling to regain gambling losses
–Lies in significant relationships about gambling
–Engages in illegal activity to Fund gambling
–Has risked or lost job or significant other because of gambling
paraphilia sexual behavior versus non-paraphilia sexual behavior
PARAPHILIA SEXUAL BEHAVIOR = uses abnormal selection EG animal, unwilling person, and object
NON-PARAPHILIA SEXUAL BEHAVIOR =engages in socially normative behavior In excessive, obsessive, or compulsive manner without that is Durbin 7 object twice
“involves recurrent and intense normophilic sexually arousing fantasies, sexual urges, and behaviors that cause clinically significant distress in social, occupational, or other important areas of functioning; and is not due simply to another medical condition, substance use disorder, or a developmental disorder
DSM-V definition of paraphilia
DSM-5 defines paraphilia as intense and persistent atypical preferences for sexual activities or targets like spanking, whipping, binding with erotic targets like children, animals, and/or rubber etc.
examples of Non- paraphilia sexual behavior
–compulsive multiple love relationships
–Compulsive sexuality interrelationship
–Compulsive autoerotism
–Compulsive use of Internet
–Compulsive fixation on unattainable partner
–Repetitive sexual fantasies causing distress or associated with loss of control
–Repeated sexual urges causing distress or associated with loss of control
–Repented engagements and sexual behavior causing distress or associated with loss of control
neurotransmitters that contributed to sexual behavior
–dopamine
–Serotonin
–Norepinephrine
–Opioid system
described problematic Internet use
PROBLEMATIC INTERNET USE
–Reduce face to face social activity
–Withdrawal, tolerance
–Preoccupation with Internet
–Longer than intended time on the Internet
–risks significant other relationships unemployment
–Lying about Internet use
–Repeat unsuccessful attempts to stop
–Associated with decreased social involvement and increased loneliness and depression
describe intermittent explosive disorder
INTERMITTENT EXPLOSIVE DISORDER
–Failure to inhibit aggressive impulses that are out of proportion to any precipitating stressor results and destruction of property or physical assault
–Stressors may be internal or external
–7% of Americans need lifetime criteria
–4% of Americans Meet twelve-month criteria
define pharmacokinetics
pharmacokinetics = movement of the drug within the body
–What the body does to the drug
define pharmacodynamics
pharmacodynamics = biologic and physiologic effects of the drug mechanism of action
–what the drug does to the body
define first pass metabolism
first-pass metabolism = metabolism before the drug reaches systemic circulation.
–Particularly important in oral and rectal routes.
–Usually occurs in the liver.
–Not significant and intravenous, sublingual, transdermal, and injection routes
defined volume of distribution
VOLUME of DISTRIBUTION= amount of serum, plasma, blood required for culture all the drug of the body is uniformly dispersed
–Drugs with a small VD are confined to the intravascular space of approximately 5 L
–Drugs with large VD (up to 50,000 L) are tightly bound to tissue types or lipophilic
define 0 order elimination kinetics
ZERO ORDER ELIMINATION KINETICS = linear decay of concentration
–Fixed amount of drug eliminated per unit of time
–Only a few drugs in this category
first-order elimination kinetics
FIRST-ORDER ELIMINATION KINETICS = exponential decay cause by eliminating fixed percentage of the drug per time interval
examples of zero order elimination kinetic drugs
examples of zero order elimination kinetic drugs –Alcohol –Phenytoin –Omeprazole –Fluoxetine
Very few drugs Eliminated this way
define pharmacokinetic tolerance
PHARMACOKINETIC TOLERANCE = increased metabolism resulting from repeated exposure
volume of distribution of alcohol is
volume distribution of alcohol is all tissues
Metabolism of alcohol –Where –Excretion –Enzyme affecting alcohol –type lamination kinetics
–most alcohol is metabolize rather than excreted
–alcohol is metabolize primarily by alcohol dehydrogenase
–zero order kinetics
rate of alcohol metabolism
adults can metabolize approximately 1 ounce of absolute alcohol every 3 hours = about 1 drink per hour
early effects of rising alcohol level in blood
early effects of rising alcohol levels –Relief of anxiety –Increased talkativeness –feelings of confidence in euphoria –Increased assertiveness
effects of rising blood alcohol at moderate levels
effects of moderate levels of rising blood alcohol = –Impaired judgment –Impaired reaction time –Increased emotional outbursts –Ataxia
effects of alcohol at higher-level
at higher levels of alcohol
–Acts as sedative and hypnotic
–Reduces quality of sleep
–Increases frequency and severity of apneic episodes and OSA
–Potentiates other sedative hypnotic products
–May provoke violent behavior
defined learned tolerance
LEARNED TOLERANCE = reduction of effects of drugs because of compensatory mechanisms that are alert
––EG roofers can walk a straight line despite alcohol intoxication
define the class of alcohols
alcohol = a chemical name for a group of related compounds that contain a hydroxyl group bound to a carbon atom
list volume of standard drinks
standard alcoholic drink = –0.6 fluid ounces of absolute alcohol –12 ounces of beer –5 ounces of wine –1.5 ounces of distilled spirits
percentage of 21–25-year-old using alcohol
25% of 21–25-year-old use alcohol
economic costs of alcoholism
loss of productivity and healthcare alcohol usage is estimated at $185 billion annually
define Wernicke psychosis
WERNICKE PSYCHOSIS = –Encephalopathy –Ophthalmoplegia –Ataxia –Caused by vitamin B1 deficiency
define Korsakoff psychosis
KORSAKOFF PSYCHOSIS = –Extension of Wernicke psychosis –Anterograde amnesia –Retrograde amnesia –Confabulation –Meager content in conversation –Lack of insight –Apathy
mechanism of action of all addicting drugs
mechanism of action of all addicting drugs is to affect reward pathways by enhancing release of dopamine from midbrain dopaminergic projections that regulate excitatory good allergic neurotransmission in––and meso Cortical areas of the brain
technical: Name for compulsive buying disorder
compulsive buying disorder = oniomania
discuss kleptomania
KLEPTOMANIA =
–diminished ability to inhibit impulses to steal
–Has increased tension prior to theft
–Has subjective pleasure or relief associated with stealing
–Generally begins in adolescence or early childhood
–Incidence = 1%
–More common in women
what disorders are associated with kleptomania
kleptomania is associated with –Mood disorders –Obsessive-compulsive disorder –Panic disorder –Separation anxiety disorder –Body dysmorphic. Disorder –Other impulse control disorders
treatment for kleptomania with drugs
kleptomania is treated with
–Fluoxetine 80 mg per day
–Naltrexone
–Topiramate
None work 100%
discussed trichotillomania
TRICHOTILLOMANIA = pulling hair out TRICHOPHAGIA= Hair eating –Onset usually adolescence –Often associated with other impulse control disorders or substance abuse –OCD,
drug treatment for trichotillomania
Drug treatment trichotillomania = naltrexone
discussed skin picking
SKIN PICKING
Classified as stereotypic movement disorder
–25% of institutionalized retarded people have stereotypic behaviors
–Usually done in isolation
–Often comorbid with suicide ideation
–More common in females
–Occurs in 4% of college students
–2% of dermatology patient’s meet criteria for skin picking
drug treatment for skin picking
skin picking is treated with SSRIs
define intermittent explosive disorder
INTERMITTENT EXPLOSIVE DISORDER = failure to to inhibit aggressive impulses that are out of proportion to any precipitating stressor results in numbness destruction of property or physical assault
define bioavailability
BIOAVAILABILITY = fraction of unchanged drug reaching systemic circulation
effects of Concurrent cocaine and alcohol use
Concurrent cocaine and alcohol use
–Enhances effect of cocaine and inhibits metabolism of cocaine
define potency
POTENCY = amount of drug necessary to induce a given effect
define tolerance
TOLERANCE = reduction in response to a drug after repeated exposure
define sensitization
SENSITIZATION = increase in drug response after repeated administration
define cross tolerance
CROSS TOLERANCE = tolerance to one drug generated by other drugs in the same category
at what rate will blood alcohol drop
blood alcohol level will drop about 20 mg/dL/h
define sedative
SEDATIVE = a diverse group of chemical agents that suppress CNS activity Includes –Anxiolytics –Hypnotics –anticonvulsants –Muscle relaxants –Anesthesia induction agents
what are the classes of sedatives?
CLASSES OF SEDATIVES –Benzodiazepines –Non-benzodiazepine hypnotics ––Zopiclone ––Eszopiclone ––Zaleplon ––zolpidem –Barbiturates –Miscellaneous compounds
what drug is used to treat sedative withdrawal?
phenobarbital is used to treat sedative withdrawal
which sedatives are most commonly abused?
Ambien is the most commonly abuse sedative
how many Americans use benzodiazepines?
–In one month?
–In one year?
past month use of benzodiazepines = 7%–17%
–1% of Americans use benzodiazepines for greater than 1 year
characteristics of long-term benzodiazepine users
LONG-TERM USERS OF BENZODIAZEPINES –Older women –High anxiety persons –Persons with chronic health problems –Alcoholics = 20% –Methadone users 70–90%
benzodiazepines and suicide
benzodiazepines very frequently involves in suicide
–Abuse of benzodiazepines as a solitary drug is rare
where our benzodiazepines metabolized?
benzodiazepines are metabolized in the liver by CPY enzymes systems
what drug characteristics affect euphoria?’s
euphoria is affected by –Drug –Lipid solubility –Protein binding –Rate of entry into brain
what Neurotransmitter is affected by benzodiazepines?
benzodiazepines mediate GABA which is the main inhibitory transmitter of the brain
what drug gives the most serious sedation when taken with benzodiazepines?
alcohol gives the most serious sedation when combined with benzodiazepines
what drugs inhibit benzodiazepines?
benzodiazepines are inhibited by –ketoconazole –Itraconazole –Macrolide antibiotics –Fluoxetine –Nefazodone
what drugs enhance benzodiazepine effect?
birth control pills may enhance benzodiazepine effects
what drugs Will barbiturates decreasing activity of?
Barbiturates will decrease the effects of –Anticoagulants –Birth control pills –Steroids –Various others
benzodiazepines and hedonic effects
benzodiazepines a rarely used alone for hedonic effects
–Usually Mixed with methadone
discussed tolerance to benzodiazepines
TOLERANCE TO BENZODIAZEPINES
–Causes escalation of dose to get same effect
–Rapidly develops for sedative effect
–Does not occur for anxiolytic effect
––Therefore patient likely to reduce the dose over time
which benzodiazepines have the lowest risk of addiction?
benzodiazepines with the least RISK OF ADDICTION
–Clonazepam
–Chlordiazepoxide
–oxazepam
benzodiazepines with the highest risk of addiction
benzodiazepines with highest rate of addiction
–DIAZEPAM
–ALPRAZOLAM
–LORAZEPAM
benzodiazepine toxicity
BENZODIAZEPINE TOXIC SYMPTOMS –Sedation –Anterograde amnesia –difficulty acquiring new learning –Difficulty concentrating
Chronic heavy benzodiazepine use can resulting cognitive impairment which is often permanent
drug most associated with sleepwalking
zolpidem (Ambien) most associated with sleepwalking
using benzodiazepine during pregnancy may produce what syndromes
benzodiazepine Use during pregnancy
–CLEFT PALATE RISK
–FLOPPY BABY SYNDROME
what is GHB
GHB =gamma hydroxybutyrate
–Club drug
–Can induce absence seizures
–can treat catalepsy and narcolepsy
what of the effects of GHB
EFFECTS OF GHB –Slurred speech –Feelings of increased sexual intimacy –Drowsiness –Depression after use –Physical dependence and addiction –Withdrawal if use for > 1 week – Stimulates at lower doses, depresses at higher doses
treatment for GHB intoxication
GHB intoxication was treated with high-dose benzodiazepine followed by a taper
list endogenous opioid peptides
endogenous opioid peptides are
–Beta endorphin
–Enkephalins
–dynorphins
Decay products of heroin
decay products of heroin
–Morphine
–6 Mono acetyl morphine
list synthetic opioid agonist
synthetic opioid agonists are –Hydrocodone –Oxycodone –hydromorphone –Heroin
synthetic opioid antagonists
synthetic opioid antagonists are
–naltrexone
–naloxone
–nalmefene
discuss oxycodone
oxycodone
–SEMI-SYNTHETIC Compound derived from thebaine
–STRUCTURALLY SIMILAR TO CODEINE,
–BUT PHARMACODYNAMICS SIMILAR TO MORPHINE
what is Talwin NX?
Talwin NX is pentazocine plus naloxone
what is LAAM
LAAM= levo alpha methanol
–Is congener of methadone
–Opioid agonist
–used for agonist therapy, a second line drug after methadone
described torsades de points
polymorphic ventricular tachycardia,
–Twisting effect around isoelectric axis
–can degenerate into ventricular fibrillation
side effects of LAAM
–prolonged QT intervals
–Torsade de points
how many people have used heroin?
number of heroin users = –1 million in the United States –3.5 million worldwide –100,000 new users annually –15% of substance-abuse treatment is for heroin
heroin pharmacokinetics
heroin pharmacokinetics
–Lipid solvable and water-soluble
–More potent than morphine
–Is prodrug, no intrinsic opioid activity
half-life of heroin and the blood?
heroin half-life and blood is about 3 minutes
why is heroin not used orally?
oral heroin is metabolized by first-pass metabolism to liver
–Has limited bioavailability when given orally
when do peak blood levels of heroin occur after using?
heroin peaks in the blood about 5 minutes after intranasal, intramuscular, or subcutaneous use
what is a half-life of Morphine?
the half life of morphine is 3 hours
–But analgesia lasts longer
how is morphine eliminated from the body?
90% of morphine is excreted in urine within 24 hours
what is a half-life for immediate release oxycodone?
Half-life of immediate release oxycodone is 3–4 hours
technical name for codeine
codeine is also known as methyl morphine
meperidine analgesia
–Onset
–Peaks
–Metabolize
–meperidine analgesia begins in 15 minutes
–peaks and 1–2 hours
–Metabolized and liver
pharmacokinetics of methadone
methadone pharmacokinetics –Is full mu opioid agonist –Oral methadone is rapidly absorbed ––Has delayed onset of action –Half life of methadone is 24 hours
name some drugs in the class of caffeine
drugs in the same class as caffeine –Caffeine = 1, 3, 7 tri-methyl–xanthine –Dimethyl xanthene –Theophylline –Theobromine
therapeutic uses of caffeine?
Therapeutic uses of caffeine
–Mild central nervous stimulant
–Some analgesic effects
–Treat apnea In neonates
–Given before electroconvulsive therapy to lengthen seizure duration
–Lipophilic and thrombogenic effects, therefore use in weight loss preparations
when is peak level of caffeine?
caffeine reaches his peak level and 30–45 minutes after oral ingestion
volume of distribution of caffeine
caffeine is distributive all tissues equally
number of known metabolites of caffeine
–over 25 metabolites of caffeine have been identified
–Metabolic pathway involves cytochrome P450 liver enzymes
–produces para xanthine, theobromine ,and theophylline
what drugs and conditions alter caffeine metabolism?
Caffeine metabolism can be altered by any drug that involves cytochrome P450 liver enzymes
what are the effects of cigarette smoking on caffeine metabolism?
Cigarette smoking increases liver enzymes and therefore Decreases caffeine half-life by up to 50%
name some inhibitors of caffeine metabolism
caffeine metabolism can be inhibited by –High doses of caffeine –Oral contraceptives –Cimetidine –Some quinolone antibiotics
what is primary site of action of caffeine?
the primary site of action of caffeine is the adenosine receptor
where is adenosine found?
How was informed?
adenosine is an endogenous nucleoside found throughout the brain–
–It is formed by the breakdown of adenosine triphosphate
how does adenosine react with caffeine?
–caffeine is structurally similar to adenosine and is therefore an antagonist
–Therefore caffeine produces the opposite effect of adenosine
how his caffeine affects sleep?
effects of caffeine on sleep are not dopamine dependent
–Caffeine antagonizes sleep promoting effects of adenosine
what the cardio vascular effects of caffeine?
caffeine
–Increases blood pressure
–Decreases or no effect on heart rate
what is the effect of caffeine on the gastrointestinal system?
–caffeine stimulates gastric acid secretion
–Caffeine as a colonic stimulant similar to a meal
what is a caffeine effect on the respiratory system?
–caffeine as a respiratory stimulant
–Caffeine is a bronchodilator at high doses
what are the renal effects of caffeine?
–caffeine acts as a diuretic
–Increase his urinary volume by 30% for several hours
–Increases detrussor pressure, therefore increasing urinary urgency and detrussor instability
what are the effects of caffeine on the muscular system?
caffeine is ergogenic, therefore Increases performance, especially during prolonged exercise
what our the adverse effects of caffeine on health?
the negative effects of caffeine are:
–Increased systolic pressure by 5–15 millimeters
–Increase his diastolic pressure by 5–10 millimeters
–Both caffeinated and decaffeinated coffee raises total and LDL cholesterol
–Exacerbates GERD
–Risk factor for urinary incontinence
–Causes calcium excretion in the urine
what are the positive effects of caffeine on health?
positive effects of caffeine on health are:
–May reduce risk of Parkinson disease
–Reduce his incidence of chronic liver disease
–Some protective effect against type 2 diabetes
what are the subjective effects of caffeine in low to moderate dose?
low to moderate dose of caffeine:
–Improved task performance which has been inhibited by sleep deprivation, fatigue, or prolonged vigilance.
–Gives feelings of happiness, energy, arousal and sociability
what dose of caffeine is most likely to produce negative subjective effects?
negative subjective effects of caffeine produced by: –>200 mg caffeine –Anxiety –Nervous system –Jitteriness –Negative mood –Upset stomach
–Long-term high-dose caffeine can produce psychopathology
to what effects will caffeine users develops tolerance?
high-dose caffeine users developed tolerance to: –Sleep effects –Diuresis –Salivation –Metabolic rate changes
symptoms of caffeine intoxication
caffeine intoxication produces –Restlessness –Nervousness –Excitement –Insomnia –Flushed face –Diuresis –Gastrointestinal disturbances –Muscle twitching –Rambling flow of thought speech –Tachycardia or cardiac arrhythmias –Periods of inexhaustibility –Agitation
what is a lethal dose of caffeine?
lethal dose of caffeine is 5-10 g
caffeine withdrawal symptoms are
caffeine withdrawal symptoms are –Headache –Tired, fatigue –Drowsiness –Sleepiness –Decreased energy –Decreased alertness inattentiveness –Decreased sense of well-being –Decreased mood –Difficulty concentrating, not clearheaded –Flulike symptoms, nausea, vomiting –Muscle pain and stiffness
when will caffeine withdrawal occur?
–caffeine withdrawal usually begins 12-24 hours after last caffeine intake
–Peaks in 20-51 hours
duration of caffeine withdrawal symptoms
caffeine withdrawal symptoms last 2–9 days
–But can last for 3 weeks
how much caffeine is necessary to suppress withdrawal symptoms?
25 mg of caffeine will suppress caffeine withdrawal headache
what is a relationship between caffeine use and nicotine use
cigarette smokers consume more caffeine than nonsmokers
–Pregnant women with caffeine dependence Are 9 times more likely to smoke cigarettes daily
–Caffeine does not increase nicotine administration
relationship between alcohol use and caffeine use
heavy alcohol use is associated with heavy caffeine use
what percentage of patients admitted to the hospital have alcohol problems
about 10–20 percent of patients admitted to the hospital have alcohol problems
what is the rate of substance abuse in primary care
illicit and prescription drug abuse varies from about 5%–10% in primary care
what are considered safe drinking levels
male under 65 years old
–5 drinks per day
–14 drinks per week
Female or over 65 years old
–4 drinks per day
–7 drinks per week
define “at risk drinking”
at risk drinking = safe limits of drinking are exceeded, but abuse or dependency criteria are not met
what percentage of college students report binge drinking?
40% of college students report binge drinking in prior 2 weeks
–One third of college students meet criteria for alcohol abuse
percentage of pregnant / nonpregnant women who engage in binge drinking
–2% of pregnant women engaged in binge drinking
–13% of non-pregnant women engaged in binge drinking
first trimester drinking can produce…
drinking during first trimester can produce
–low birthweight
–Decreased birth length
–Decrease head circumference
–Physical abnormalities
–Alcohol-related neural developmental disorders
second and third trimester drinking can produce
second and third trimester drinking can produce
–Developmental delay caused by drinking
what of the medical complications of illicit drug use in pregnancy?
illicit drug use during pregnancy can produce –Placental abruption –Placental insufficiency –Chorioamnionitis –Spontaneous abortion –Postpartum hemorrhage –Preeclampsia
what percentage of life-threatening injuries involving alcohol?
70% of life-threatening injuries involve alcohol
What is The chemical treatment of acute alcoholism?
Treatment of acute alcoholism:
–Thiamine 100 mg IM (to prevent Wernicke’s encephalopathy)
–Long-term benzodiazepines to prevent and treat alcohol withdrawal syndrome
when does withdrawal from short acting benzodiazepines ?
Withdrawal from short acting benzodiazepines may occur within 24 hours and may last for several days
What percentage of elderly have alcohol in Their systems when admitted to the hospital?
6%–11% of elderly have alcohol in them when admitted to the hospital
How Does alcoholism rank as a psychiatric disorder among elderly?
Alcoholism is the third most common psychiatric disorder among elderly.
One third Of older alcoholics are late onset alcoholics
Why is alcohol metabolized differently in the elderly?
Elderly have altered pharmacokinetics For alcohol because of:
–More body fat
–Less water than younger people
–Therefore higher alcohol concentrations with less alcohol ingestion
What conditions are associated with alcoholism in the elderly
conditions associated with alcoholism in the elderly include: –Depression –Delirium –Chronic fatigue –Seizures –Repeated infections –Hypertension –Malnutrition –cardiomyopathy –Peripheral neuropathy –Sexual dysfunction
What the limitations of urinalysis for drugs?
Limitations of hair analysis for drug screening include:–More useful for forensic than clinical work
–Can be Corrupted from external environment
–Is present In higher concentration In pigmented hair than In nonpigmented hair
–Cosmetic treatments and ultraviolet exposure decreased concentrations of drugs
What level of creatinine must be present in urine for a valid drug sample?
20 ng/mL creatinine must be present to be considered valid
what are the temperature limits for a valid urine drug screen?
urine must be between 90° and 100°F within 4 minutes of collection
define dilute urine
“Dilute urine” contains 02 20 mg/dL of creatinine
And
Specific gravity between 1.0010 and 1.0200
defines substitute urine
“substituted urine” = creatinine <2 mg/Deciliter
And specific gravity not between 1.0010–1.0200
what substances does DOT test for?
DOT test for 5 substances –Amphetamines –Cannabinoids –Cocaine –Opioids –PCP
What are the best tests for chronic alcoholism?
The best test for chronic alcoholism are
–GGT
–AST
–MCV
How much alcohol was Must one consume to elevated GGT?
5 drinks per day for 2 weeks will elevated GGT in most individuals
how fast we’ll GGT decline with abstinence
–GGT will decline 50% in 2 weeks
–GGT will return to normal in 2 months
What are some non-alcohol-related conditions that can increase the MCV?
Nonalcoholic conditions that can raise MCV R: –Chronic liver disease –Hypothyroidism –Folate deficiency –Megaloblastic disorder
What is NADH?
NADH is produced during oxidation of alcohol and can be a marker for alcohol abuse
What alcohols can falsely elevate NADH
NADH can be falsely elevated with the consumption of: –Isopropyl alcohol –Methanol –Ethylene glycol –Acetone –diabetic ketoacidosis –starvation acidosis
What is the ratio of blood-alcohol to breath alcohol?
The ratio of alcohol in the breath to alcohol in the blood is approximately 2100:1
How long after an alcoholic drink can breath analysis be done?
Should wait 15 minutes after the last drink before measuring blood alcohol in the breath
what her instructions for breath alcohol analysis?
Breath analysis for alcohol:
–Wait 15 minutes after last drink
–Take deep breaths in
–Measurement taken in the last third of the exhaled breath
–Shallow breath usually underestimates blood level
Discuss urine tests for alcohol
Urine testing for alcohol…
–Is qualitative, not quantitative
–Positive test indicates alcohol within preceding 8 hours
–ethanol glucuronide is a metabolite of alcohol in urine
–Highly sensitive, but mouthwash etc. will give false values
list most common amphetamines
most common amphetamines are… –Amphetamine –Methamphetamine –MDMA = ecstasy –MVA –MDEA = Eve
What is the following stand for
MDMA?
MDMA = ecstasy = 2, 3 methylene dioxy methamphetamine
what’s is the following stand for?
MDA
MVA = 3 , 4 methylene dioxy amphetamine
What this the following stand for?
MDEA
MDEA =Eve = 3,4 Methylene dioxy N ethylene amphetamine
which isomer of amphetamine has stronger effects
the D isomer of amphetamines more active and has more abuse potential
Vicks inhaler we’ll give a false positive test for?
Vicks nasal inhaler is the L isomer of methamphetamine and will test positive for that
what are some of the sympathomimetic amines that cross-react with the urine test for amphetamines
the following will cross-react in the immunoassay for amphetamines
–Amphetamines
–Phenyl propyl amine
–Pseudoephedrine
–L methamphetamine (he Vicks)
–Appetite suppressants containing ephedrine
–Phentermine
how long are amphetamines detectable in the urine?
amphetamines are usually detectable for 1–3 days
what chemicals will reduce detection of amphetamines and urine?
A high pH will reduce excretion, therefore ingesting bicarbonate will reduce detection of amphetamines
what is the urine test for amphetamines and methamphetamine actually tests for?
The urine immunoassay for amphetamines actually tests for amphetamines and methamphetamine
what are the 3 classes of barbiturates based on duration of action:
the 3 classes of barbiturates based on duration of action are:
Ultrashort = thiopental
Short acting = pentobarbital, secobarbital, amobarbital
–––Most commonly abused
long-lasting =phenobarbital
how long are short acting barbiturates detectable in the urine?
short-acting barbiturates are usually detectable for 1–4 days in urine
what drugs metabolize to oxazepam
the following drugs metabolize to oxazepam –Clorazepate –Chlordiazepoxide –Diazepam –Temazepam
what benzodiazepines are likely to be missed in urine screenings for benzodiazepines?
urine tests for benzodiazepines target oxazepam
Therefore, can miss
–Clonazepam
–Lorazepam
–Triazolam
what common drugs can give false positives for benzodiazepines?
Urine immunoassays for benzodiazepines can give false positives with the following:
–Oxaprozin
–sertraline
–tolmetin
discuss signs and symptoms of alcoholic fatty liver
alcoholic fatty liver –History of several days of heavy drinking and/or long-term drinking –Anorexia –Nausea –Right upper quadrant discomfort –Hepatomegaly –May have tender liver
discussed signs and symptoms of alcoholic cirrhosis
ALCOHOLIC cirrhosis –Nausea –Weight loss –Commonly portal hypertension –Variceal bleeding –Ascites –Liver failure –May progress to hepatocellular carcinoma
treatment of ascites
–salt restriction to reduce fluid retention
Management portal hypertension with
–– beta blockers
––spironolactone
––Furosemide
–Transjugular intrahepatic portal–systemic shunting
treatment of hepatic encephalopathy
–treat precipitating factors
–Decreased colonic production/absorption of ammonia with lactulose
–Treat H. pylori
discuss hepatitis A
HEPATITIS A
–RNA virus
–Fecal oral contamination
–Almost universal in underdeveloped countries
–More severe with advancing age
–Does not persist as chronic infection
–More associated with poverty and crowding then injection
High risk occupation
–Travelers
–Homosexual men
–Patient’s with chronic liver disease
discussed hepatitis B
hepatitis B
–Most prevalent chronic infectious viral disease in humans
–Readily transmitted among intravenous drug users
risk groups for hepatitis B
risk group for hepatitis B –Multiple sexual partners –Homosexual man –Asians, 7 Europeans, Mediterranean's –Indigenous peoples –Healthcare workers –Children with infected parents –IV drug use
hepatitis B prodrome symptoms
HEPATITIS B PRODROME SYMPTOMS –transient serum sickness prodrome ––Polyarthralgia ––Fever ––Malaise ––Proteinuria
hepatitis B acute infection symptoms
symptoms of acute hepatitis B infection –Anorexia –Nausea –Plus or minus vomiting –Jaundice –Pale stools –Dark urine –Very often subclinical
chronic stage of hepatitis B
5% of hepatitis B converts to chronic hepatitis B and adults
making diagnosis of chronic hepatitis B
HBS AG for more than 6 months
complications of chronic active hepatitis B
chronic active hepatitis B
–Chronic hepatitis
–Cirrhosis
–Hepatocellular carcinoma
treatment of active chronic hepatitis B
only treated it active liver inflammation
–Pegylated interferon is 30% effective
–Used to more agents
discuss hepatitis C
hepatitis C –Strongly associated with IV drugs –Approximately 20% per year of IV drug users will become infected –Most IV drug users are infected –Low sexual transmission
Hepatitis C risk factors
–Bloods transfusions prior to 1990
–Body piercings and tattoos
–Incarceration
–10% transferred from mother to baby
Low risk activities –Sharing toothbrushes, razors etc. –Healthcare workers, needlesticks –Bruits or medical procedures –Sexual activities
No known transmission through breast milk
Hepatitis C primary infection
primary infection is usually subclinical
–Peak viremia usually in week 2–3
Hepatitis C chronic infection
–chronic infection develops in three fourths of patient’s with acute infection
–Liver damage results from immune damage to infected cells
Long-term damage with hepatitis C
–8% developed cirrhosis in 20 years
–20% developed cirrhosis after 40 years
Symptoms of chronic hepatitis C
–Severity does not correlate with disease activity well –Usually nonspecific, mild, intermittent symptoms –Most common symptoms are –Fatigue –Nausea –Muscle aches –Right upper quadrant pain –Weight loss
Percentage of acute hepatitis C that developed persistent chronic infection
60% that 70% of acute hepatitis C patients Will develop chronic infection
Mechanism of liver injury in hepatitis C
Hepatitis C causes liver damage predominantly by immune damage to affected liver cells
Assessing severity of hepatitis C
–symptoms do not correlate with severity of liver disease
–Spider nevi common, but nonspecific
–ALT is best indicator of active viral hepatitis but does not indicate severity
Effects of alcohol on hepatitis C
Alcohol consumption in the presence of chronic hepatitis C as an additive effect on liver inflammation and accelerates hepatic Fibrosis
Heavy alcohol use increase his viral load and risk of progression to hepatocellular carcinoma
Goal of antiviral therapy in hepatitis C
the goal of antiviral therapy in hepatitis C is a sustained virologic response evidenced by normal ALT and negative hepatitis C PCR at least 6 months after treatment
risk of cirrhosis during sustained viral response in hepatitis C
low risk of cirrhosis after 6 months of sustained virologic response and a normal PCR with normal ALT
treatment of patients with hepatitis C and ongoing substance abuse
NIH recommends against treating rations with ongoing substance abuse (Excluding methadone and buprenorphine)
Rate of progression of hepatitis C From cirrhosis to hepatocellular carcinoma
Approximately 5% of cirrhotic hepatitis C patient’s progress to hepato-cellular carcinoma
treatment of small primary hepatocellular carcinomas
excision
indications for liver Transplantation in the presence of hepatitis C
–major complications of cirrhosis
–Life Expectancy of 1–2 years without transplantation
3 year posttransplantation survival rate with hepatitis C
similar to other transplantations of liver
–84% every 3 year survival rate
What is cocaine hepatitis
Cocaine hepatitis –Uncommon condition –About 1% of hepatic failures –Probably as a result of heat shocklike features of cocaine toxicity –Is both dose and time-dependent
mechanism of cocaine hepatitis injury
cocaine hepatitis injury most likely caused by ischemia from the vasoconstrictive effects of cocaine and possibly toxic metabolites
where the effects of alcohol and cocaine taken together
ethyl cocaine (coca ethylene) is produced
–Has similar faxes cocaine
–Has slightly longer half-life therefore accumulates higher
–Has lower LD 50 rate
hepatic injury from ecstasy
ecstasy and MDMA rarely cause hepatic injury
most common toxic material designed for oral use but injection
Talcum powder
–Accumulation causes damage at several sites especially lung and liver
Pathogenesis of injected talc
Talc is strongly fibrogenic in the lung and leads to pulmonary granulomatosis disease with progressive or fatal outcome
–Talc and liver is inconsequential
effects of opiates on the liver
no hepatotoxicity from sure preparations of opiate agonists
–Opiate antagonists such as naltrexone can cause minor elevation of liver enzymes, but rarely serious
lists toxic effects of anabolic steroids
–cholestasis –Toxic hepatitis –Hepatic adenomas –Hepatic carcinomas Hepatotoxicity from contaminants
list renal problems associated with opiate use
–HIV nephropathy –Hepatitis C associated glomerular nephropathy –Bacterial endocarditis –Acute glomerulonephritis –Subcutaneous injection amyloidosis –Nontraumatic rhabdomyolysis –Acute renal failure –Heroin nephropathy
List renal problems associated with cocaine usage
cocaine usage can cause –Rhabdomyolysis –Acute renal failure –Accelerated hypertension and renal failure –HIV nephropathy –Hypertensive Nephrosclerosis –Renal infarction –Thrombotic microangiopathy and renal failure
llist renal problems associated with alcohol consumption
alcohol consumption is associated with –Hepatorenal syndrome –Rhabdomyolysis and acute renal failure –Increase Incidents and severity of postinfectious glomerulonephritis –Electrolyte disorders
define nephrotic syndrome
nephrotic syndrome characterized by: –Heavy proteinuria (>3.5 g per day) –Hypoalbuminemia –Hyperlipidemia –Lymphedema –Edema
Not all must be present to diagnose
differences between nephritic and nephrotic syndrome
Both have –Proteinuria greater than 3.5 g per day –Hypo-albuminuria –Hyperlipidemia –Edema –Hypertension –Renal insufficiency
Nephritic syndrome also has hematuria to the larger pore size
Most common presentation of renal disease with hepatitis C
renal disease in the presence of hepatitis C most often presents with
–Nephritic and/or nephrotic syndromes
–Urine containing large amounts of protein, red blood cells, red blood Cell cast
Discuss heroin nephropathy
heroin nephropathy
–Secondary cause of focal and segmental glomerulonephritis
–Often associated with hypertension
–Often associated with slow progression ESRD
–Not common
Frequency of hep C in HIV drug users?
78% of HIV drug users have hepatitis C
treatment of acute hypertension connection with cocaine use
Steroids are the treatment for Acute hypertension Associated with cocaine use
Drugs of abuse associated with rhabdomyolysis
–Phencyclidine –Methamphetamine –MDMA –Cocaine –Heroin –Alcohol
Discuss hepatorenal syndrome
Hepatorenal syndrome
–Results from chronic alcohol ingestion producing liver damage
–Is state of profound renal vascular constriction and splenic basal dilatation associated with severe liver function impairment
–Often with hypertension and ascites
–Kidney damage as a result of decreased blood flow rather than direct action
–Often treated with dialysis or liver transplantation
–Usually fatal without transplant
Diagnoses of Hepatorenal syndrome
Hepatorenal syndrome is a diagnosis of exclusion
–Must have trial of volume replacement with salt poor albumin
–Must remove any potential nephro toxic agents
–No improvement of Oliguric acute renal failure
Above makes hepatorenal syndrome probable
Other name for ecstasy
Ecstasy= MDMA
= methylene dioxy methamphetamine
Effects of MDMA at rave party
MDMA can lead to –Agitation –High fever –Hyperventilation –Impaired sensorium
–Increased insensible fluid losses leading to dehydration, hypernatremia, fluid depletion
Results in hypotension, shock, brain damage, rhabdomyolysis, renal failure
Major target of alcohol in other drug toxicities
Liver is major target for all alcohol And drug toxicities
Hepatic cirrhosis is__leading cause of death and USA
Hepatic cirrhosis is__most common cause of death in middle-age American man
12th
Fifth
Number of deaths per year from hepatic cirrhosis
28,000 US deaths per year from hepatic cirrhosis
Most common causes of liver transplantation
Most common causes of liver transplantation are:
–Hepatitis C
–Alcoholic cirrhosis
Amount of alcohol needed to produce fatty liver
fatty liver can occur after a single heavy drinking episode
–Usually needs 10 years of alcohol consumption at 100 g per day to develop alcoholic liver disease
Amount of alcohol in standard drink
Standard drink contains 14 g of alcohol
How much alcohol is needed to develop hepatic cirrhosis
Hepatic cirrhosis usually requires long-term alcohol consumption
–40 g per day for men
–20 mg per day for women
Very heavy drinkers only have 50% chance of developing cirrhosis
Risk factors for alcoholic liver disease
–Women require only half the alcohol as mentioned to develop alcoholic liver disease
–Genetics produced Threefold susceptibility
–Nonalcoholic fatty liver disease progresses more common with obesity
–Obesity increased risk of alcoholic liver disease
What classes of drugs have increased hepatotoxicity with alcohol consumption?
Chronic alcohol consumption increases hepatotoxicity of colon –Acetaminophen –Industrial solvents –Anesthetic gases –Illicit drugs
what is the cause of alcohol liver damage?
Alcoholic liver damage was previously thought to be due to poor nutrition. Today it is thought to be a direct results of the alcohol on the liver in spite of adequate nutrition
How do his chronic alcohol consumption increased hepatotoxicity
via CPY 2 E1 & Which metabolizes many other things
alcoholic fatty liver history, signs, symptoms
Alcoholic fatty liver occurs after heavy or long-term drinking, even for a few days –Anorexia –Nausea –Right upper quadrant discomfort –Enlarged liver –Plus minus liver tenderness
Alcoholic hepatitis signs and symptoms
Alcoholic hepatitis signs and symptoms –Anorexia –Nausea –Abdominal pain –Impaired liver function –Jaundice –Bruising –Encephalopathy –Fever and/or leukocytosis
Significance of AST/ALT ratio
ALT >AST
–Suspect chronic hepatitis C
–Acetaminophen ingestion
–Other liver injury
AST greater than ALT
–Suspect alcoholic liver disease
Pathogenesis of alcoholic hepatitis
pathogenesis of alcoholic hepatitis
–Neither detectable nor preventable
–Multifactorial including post, toxin, etc.
–Ethanol metabolizes to acetyl aldehyde via ADH and other enzymes
alcoholic liver disease treatment
avoid alcohol!
–If 6 weeks abstinence resolves elevated liver function tests, may return to drinking at low level if able to control
apparent half-life of gamma GT in alcoholic liver disease
gamma GT has an apparent half-life 26 days
–Failure to drop suggests coexistent disease
Metabolites of alcohol and pharmacologic effects
metabolites of alcohol are
–Acetyl aldehyde
–Acetate
Acetyl aldehyde and acetate her adrenergic and Vasodilators
Wide does cardiac output increased with alcohol in healthy patient’s
alcohol increase his heart rate and reduce his peripheral resistance.
However
–Left ventricular ejection fraction is reduced
–Alcohol increase his skin and splanchnic blood flow
–But reduce his pancreatic bloodflow
List heart disease they can result from alcohol
Excessive alcohol consumption can produce: –Hypocontractile heart –Reduced cardiac output –Increased systemic vascular resistance and alcoholic cardiomyopathy –Hyperdynamic heart –Four-chamber dilatation –Cardiomegaly –Interstitial and perivascular fibrosis
Defined holiday heart
Holiday heart
–Excessive alcohol consumption especially binge drinking producing
––Cardiac arrhythmias
–––Especially atrial fibrillation
Always look for alcohol in the presence of cardiac arrhythmias
probable cause of sudden cardiac death in alcoholics
sudden cardiac death in alcoholics is thought to be due to arrhythmias, most likely produced by alcohol withdrawal symptoms
Nicotine effects on
the heart rate
blood pressure
on skin
Nicotine increases heart rate and blood pressure for at least 30 minutes
–Reduce his blood flow to scan
Nicotine effects on: –Hemoglobin –Platelet aggregation –Blood this capacity –HDL –Oral contraceptives
Nicotine effects are:
Coronary artery spasm
–Increased carboxyhemoglobin and decreased oxygen delivery
–Induces platelet aggregation and blood viscosity
–Lowers HDL
coronary risk reduction by stopping smoking
–Nicotine replacement does not cause heart disease
–2 years of nicotine abstinence Reduces coronary risk by 50%
–20 years of nicotine abstinence Reduces coronary Risk to that of nonsmokers
Cannabis effects on circulatory system and heart
Cannabis, regardless of method of the abuse,
–Increase his heart rate up to 50%
–The increase, decrease or have no effect on blood pressure
–Causes Vasodilatation
–Cardiac output increases because of increased heart rate and vasodilatation
Increases carboxyhemoglobin
–5 times more likely to have an acute MI within 1 hour smoking cannabis
Effexor opioids on cardiovascular system
opioids:
–Lower blood pressure
–Reduce heart rate
–Have a favorable effect on cardiac ischemia
Name the for neurotransmitters Systems within the brain stem reticular formation
–Serotonin
–Acetylcholine
–Dopamine
–Noradrenaline
treatment of cocaine-induced vasoconstriction
–what not to use!
Cocaine-induced vasoconstriction of coronary arteries is enhanced by a beta adrenergic blocker Such as propranolol
Treatment of cocaine-induced vasoconstriction
–What to use
Treatment of coronary vasoconstriction from cocaine:
–Benzodiazepines
–Nitrates
–Calcium channel blockers
Acute coronary artery syndrome and cocaine
Acute coronary artery syndrome with cocaine:
–Occurs in adolescence and young people
–Occurs in both occasional individual cocaine users
–First hour after cocaine use is greatest risk
–Coronary thrombosis as usual cause
Treatment of cocaine induced coronary artery syndrome
treatment of acute coronary syndrome produced by cocaine
–Nitroglycerin, sublingual and IV
–Prevent seizures with benzodiazepines
–May need angiography and thrombolysis
–Morphine can attenuate cocaine-induced vasospasm therefore useful for continuing chest pains
Do not use beta blockers until coronary patency established
Effects of chronic cocaine use on heart
chronic cocaine usage:
–Increase his atherosclerosis
–Increase his myocardial injury
–Increases vascular complications related to hypertension
–Part of damage is from repeated elevations of blood pressure
–Can cause sudden cardiac death by producing arrhythmias
List significant amphetamines of abuse
Abused amphetamines include: –Amphetamine –Methamphetamine –Methylphenidate –MDMA
Effects of amphetamines on cardiovascular system
amphetamine effect on cardiovascular system
–Dose-dependent elevation of blood pressure and heart rate
Effects of phencyclidine and lysergic acid diethylamide on cardiovascular system
PCP and LST increase heart rate
side effects of anabolic steroids
anabolic steroids (mainly testosterone and is congeners) when use in 100 X–1000 X therapeutic doses can produce:
–Marked cardiac hypertrophy
–Acute myocardial infarction even with patent coronary arteries
–Stroke
–Physical signs of addiction
Best labs Test nutritional status
Serum Pre-albumin
Treatment of heroin addict and hospital
10–20 milligrams of methadone every 2 hours as needed
If history of prior withdrawal, give diazepam 10–20 milligrams orally
Treatment of pain in opioid addiction
Need much higher dose to control pain
–Do not use when necessary schedule for dosing
How long after last drink will DTs start?
Delirium tremens will begin in 6–48 hours after the last drink
What are the sympathetic splanchnic nerves to the GI tract
Thoracic, lumbar
What of the symptoms of delirium tremens?
Delirium tremens symptoms are:
–Tremor
Moist warm skin
–Hypertension (treat with clonidine)
–Agitation( Treat with Haldol)
–Tachycardia (treat with benzodiazepines and maybe beta blockers
–Seizures (treat with benzodiazepines NOT WITH DILANTIN
What structures are suspended by the mesentery?
Jejunum and ileum
Cause and treatment of Wernicke-Korsakoff syndrome
Main cause is thiamine deficiency
Give 100 mg thiamine IM before giving glucose
Symptoms of alcoholic cerebellar dysfunction
Symptoms of alcoholic cerebellar dysfunction
–Ataxia and incoordination
Often irreversible
symptoms of Korsakoff syndrome
main symptom of Korsakoff’s syndrome is confabulation
Symptoms of alcoholic peripheral neuropathy
Symptoms of alcoholic peripheral neuropathy:
–Burning pain
–Numbness in stocking–glove distribution
Symptoms of alcoholic hepatitis
Alcoholic hepatitis symptoms: –Fever –Leukocytosis –Right upper quadrant pain and tenderness Elevation of AST greater than ALT
Complications of hepatic cirrhosis
complications of hepatic cirrhosis are: –Hypoalbuminemia –Coagulopathy –Hyperbilirubinemia –Hepatic encephalopathy –Esophageal or gastric variceal bleeding –Ascites –Spontaneous bacterial peritonitis –Volume overload and edema –Hepatorenal syndrome
Five-year prognosis for cirrhosis
if alcohol continues 50 Percent
Hematologic consequences of alcoholism
Hematologic consequences of alcoholism:
–Iron deficiency from gastrointestinal hemorrhage
–Mallory-Weiss tears
–Pancytopenia
–Megaloblastic anemia from folate deficiency
Cardiovascular consequences of alcoholism
Cardiovascular consequences of alcoholism:
–Hypertension, especially during withdrawal
–Alcoholic cardiomyopathy
–Congestive heart failure
effects of alcoholism on EKG
EKG shows diffuse hypokinesis and four-chamber dilatation
–Tachycardia and T-wave changes
effects of alcohol on esophagus
alcoholism promotes blurred
predisposing factors for pancreatitis
75% of pancreatitis has following predisposing factors:
–Heavy alcohol consumption
–Gallstones
frequency of pancreatitis and heavy drinkers
5% of heavy drinkers developed pancreatitis
how does alcoholism cause pancreatitis
–alcohol contracts the sphincter of Oddi
–Inhibits pancreatic secretion
––Results and cascade about a digestion
treatment of pancreatitis
pancreatitis is treated by –Bedrest –Analgesics –Intravenous fluids –Fasting
causes and clinical features of chronic pancreatitis
principal cause of chronic pancreatitis is excessive alcohol consumption. (75%)
Clinical features: –Pain is main problem –Upper abdominal pain that may radiate to the back –Pain increases with meals –Anorexia and weight loss –Can lead to diabetes and steatorrhea
most common cause of pancreatitis in children is
cystic fibrosis
mechanism of diarrhea in acute and chronic alcoholism
diarrhea and alcoholics occur from: –Altered motility –Altered permeability –Nutritional disorders –Small intestinal mucosa injury
treatment of opioid-induced constipation
treat opioid-induced constipation with:
–Increase fluid intake
–Fiber supplementation
–Lactulose
what his body packing?
Body packing =
–ingestion of condoms or other bags fill the cocaine or other drugs
–Absorption can occur without rupture of bag
–Takes 3–6 days to clear GI tract
–Give dilute contrast media to assist visualization
effects of cocaine and amphetamines on gut
cocaine mainly causes ischemic injury of the gut producing
–Intestinal perforation
–Infarction
–Ischemic colitis
