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ADDICITION > SECTION 1 principles of addiction medicine > Flashcards

SECTION 1 principles of addiction medicine Flashcards

1
Q

where are the changes in the brain associated with addiction?

A

addiction causes change in the orbital frontal lobes that are permanent and attics

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2
Q

what is the main reenforcer of addiction

A

–dopamine is the main reenforcer of addiction.
–There is increased concentration in the limbic system
–It does not cause addiction in itself

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3
Q

how does dopamine cause addiction

A

addictive drugs either cause reuptake inhibition of dopamine or increased sensitivity to dopamine
–Reduce 5-10 times greater effect

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4
Q

is addiction genetic?

A

40-60% of vulnerability to addiction is genetic

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5
Q

risk factors for addiction

A

–stress
–Low income status
–Drug availability
–Mental illness

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6
Q

defined prevalence

A

prevalence = number of cases/in total population

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7
Q

define incidence

A

incidence = number of new cases/number in total population

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8
Q

define relative risk

A

relative risk = number of people with disease plus special conditions/number with disease without special condition

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9
Q

prevalence of alcoholism

A

1980 prevalence of alcoholism was
–13% lifetime
–3% past month

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10
Q

relationship of age to alcoholism

A

–one third adolescent drinkers will develop dependence

–Alcoholism generally declines with age

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11
Q

prevalence of drug use

A

lifetime prevalence = 0.2%
–Males to ask more likely than females
–Half of adolescent users developed dependence

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12
Q

risk factors for drug use

A

risk factors for drug use
–Cohabitation
–Nontraditional jobs
–Childhood sexual abuse

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13
Q

peak hazard age for drug and alcohol abuse

A

19 years old

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14
Q

compare alcoholism by race

A

–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

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15
Q

what parts of the brain are involved in addiction and what are their function?

A

Limbic system is involved in addiction
–Subcallosal area
–Cingulate
–Parahippocampal gyri

These area are associated with motion, a density, and fight or flight

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16
Q

name opioid receptors

A

there are 3 opioid receptors
–mu
–kappa
–Delta

There are other opioid receptors throughout the brain, especially the limbic system

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17
Q

effects of MU agonist

A 
selective MU agonist EG heroin, morphine
–Analgesia
–Euphoria
–Respiratory depression
–Emesis
–Antidiuretic action
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18
Q

effects of opioid kappa Agonist

A 
kappa Agonists produce
–Dysphoria
–Diuresis
–Analgesia
–impulse control disorders
–NO respiratory depression
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19
Q

cannabinoid receptors

A

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

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20
Q

what is physical dependence

A

physical dependence causes individual to become physically sick when drug administration ceases.
–Physical dependence is neither necessary nor sufficient to diagnosis addiction

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21
Q

list impulse control disorders

A 
IMPULSE CONTROL DISORDERS
–Explosive disorder
–Kleptomania
–Pathologic gambling
–Pyromania
–Trichotillomania
–Excessive intranet use
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22
Q

criteria for pathologic gambling

A

–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

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23
Q

paraphilia sexual behavior versus non-paraphilia sexual behavior

A

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

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24
Q

DSM-V definition of paraphilia

A

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.

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25
Q

examples of Non- paraphilia sexual behavior

A

–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

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26
Q

neurotransmitters that contributed to sexual behavior

A

–dopamine
–Serotonin
–Norepinephrine
–Opioid system

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27
Q

described problematic Internet use

A

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

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28
Q

describe intermittent explosive disorder

A

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

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29
Q

define pharmacokinetics

A

pharmacokinetics = movement of the drug within the body

–What the body does to the drug

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30
Q

define pharmacodynamics

A

pharmacodynamics = biologic and physiologic effects of the drug mechanism of action
–what the drug does to the body

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31
Q

define first pass metabolism

A

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

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32
Q

defined volume of distribution

A

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

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33
Q

define 0 order elimination kinetics

A

ZERO ORDER ELIMINATION KINETICS = linear decay of concentration
–Fixed amount of drug eliminated per unit of time
–Only a few drugs in this category

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34
Q

first-order elimination kinetics

A

FIRST-ORDER ELIMINATION KINETICS = exponential decay cause by eliminating fixed percentage of the drug per time interval

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35
Q

examples of zero order elimination kinetic drugs

A 
examples of zero order elimination kinetic drugs
–Alcohol
–Phenytoin
–Omeprazole
–Fluoxetine

Very few drugs Eliminated this way

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36
Q

define pharmacokinetic tolerance

A

PHARMACOKINETIC TOLERANCE = increased metabolism resulting from repeated exposure

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37
Q

volume of distribution of alcohol is

A

volume distribution of alcohol is all tissues

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38
Q 
Metabolism of alcohol
–Where
–Excretion
–Enzyme affecting alcohol 
–type lamination kinetics
A

–most alcohol is metabolize rather than excreted
–alcohol is metabolize primarily by alcohol dehydrogenase
–zero order kinetics

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39
Q

rate of alcohol metabolism

A

adults can metabolize approximately 1 ounce of absolute alcohol every 3 hours = about 1 drink per hour

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40
Q

early effects of rising alcohol level in blood

A 
early effects of rising alcohol levels
–Relief of anxiety
–Increased talkativeness
–feelings of confidence in euphoria
–Increased assertiveness
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41
Q

effects of rising blood alcohol at moderate levels

A 
effects of moderate levels of rising blood alcohol =
–Impaired judgment
–Impaired reaction time
–Increased emotional outbursts
–Ataxia
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42
Q

effects of alcohol at higher-level

A

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

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43
Q

defined learned tolerance

A

LEARNED TOLERANCE = reduction of effects of drugs because of compensatory mechanisms that are alert
––EG roofers can walk a straight line despite alcohol intoxication

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44
Q

define the class of alcohols

A

alcohol = a chemical name for a group of related compounds that contain a hydroxyl group bound to a carbon atom

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45
Q

list volume of standard drinks

A 
standard alcoholic drink =
–0.6 fluid ounces of absolute alcohol
–12 ounces of beer
–5 ounces of wine
–1.5 ounces of distilled spirits
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46
Q

percentage of 21–25-year-old using alcohol

A

25% of 21–25-year-old use alcohol

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47
Q

economic costs of alcoholism

A

loss of productivity and healthcare alcohol usage is estimated at $185 billion annually

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48
Q

define Wernicke psychosis

A 
WERNICKE PSYCHOSIS =
–Encephalopathy
–Ophthalmoplegia
–Ataxia
–Caused by vitamin B1 deficiency
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49
Q

define Korsakoff psychosis

A 
KORSAKOFF PSYCHOSIS =
–Extension of Wernicke psychosis
–Anterograde amnesia
–Retrograde amnesia
–Confabulation
–Meager content in conversation
–Lack of insight
–Apathy
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50
Q

mechanism of action of all addicting drugs

A

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

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51
Q

technical: Name for compulsive buying disorder

A

compulsive buying disorder = oniomania

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52
Q

discuss kleptomania

A

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

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53
Q

what disorders are associated with kleptomania

A 
kleptomania is associated with
–Mood disorders
–Obsessive-compulsive disorder
–Panic disorder
–Separation anxiety disorder
–Body dysmorphic.  Disorder
–Other impulse control disorders
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54
Q

treatment for kleptomania with drugs

A

kleptomania is treated with
–Fluoxetine 80 mg per day
–Naltrexone
–Topiramate

None work 100%

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55
Q

discussed trichotillomania

A 
TRICHOTILLOMANIA = pulling hair out
TRICHOPHAGIA= Hair eating
–Onset usually adolescence
–Often associated with other impulse control disorders or substance abuse
–OCD,
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56
Q

drug treatment for trichotillomania

A

Drug treatment trichotillomania = naltrexone

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57
Q

discussed skin picking

A

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

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58
Q

drug treatment for skin picking

A

skin picking is treated with SSRIs

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59
Q

define intermittent explosive disorder

A

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

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60
Q

define bioavailability

A

BIOAVAILABILITY = fraction of unchanged drug reaching systemic circulation

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61
Q

effects of Concurrent cocaine and alcohol use

A

Concurrent cocaine and alcohol use

–Enhances effect of cocaine and inhibits metabolism of cocaine

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62
Q

define potency

A

POTENCY = amount of drug necessary to induce a given effect

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63
Q

define tolerance

A

TOLERANCE = reduction in response to a drug after repeated exposure

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64
Q

define sensitization

A

SENSITIZATION = increase in drug response after repeated administration

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65
Q

define cross tolerance

A

CROSS TOLERANCE = tolerance to one drug generated by other drugs in the same category

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66
Q

at what rate will blood alcohol drop

A

blood alcohol level will drop about 20 mg/dL/h

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67
Q

define sedative

A 
SEDATIVE = a diverse group of chemical agents that suppress CNS activity
Includes
–Anxiolytics
–Hypnotics
–anticonvulsants
–Muscle relaxants
–Anesthesia induction agents
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68
Q

what are the classes of sedatives?

A 
CLASSES OF SEDATIVES
–Benzodiazepines
–Non-benzodiazepine hypnotics
––Zopiclone
––Eszopiclone
––Zaleplon
––zolpidem
–Barbiturates
–Miscellaneous compounds
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69
Q

what drug is used to treat sedative withdrawal?

A

phenobarbital is used to treat sedative withdrawal

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70
Q

which sedatives are most commonly abused?

A

Ambien is the most commonly abuse sedative

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71
Q

how many Americans use benzodiazepines?
–In one month?
–In one year?

A

past month use of benzodiazepines = 7%–17%

–1% of Americans use benzodiazepines for greater than 1 year

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72
Q

characteristics of long-term benzodiazepine users

A 
LONG-TERM USERS OF BENZODIAZEPINES
–Older women
–High anxiety persons
–Persons with chronic health problems
–Alcoholics = 20%
–Methadone users 70–90%
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73
Q

benzodiazepines and suicide

A

benzodiazepines very frequently involves in suicide

–Abuse of benzodiazepines as a solitary drug is rare

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74
Q

where our benzodiazepines metabolized?

A

benzodiazepines are metabolized in the liver by CPY enzymes systems

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75
Q

what drug characteristics affect euphoria?’s

A 
euphoria is affected by
–Drug
–Lipid solubility
–Protein binding
–Rate of entry into brain
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76
Q

what Neurotransmitter is affected by benzodiazepines?

A

benzodiazepines mediate GABA which is the main inhibitory transmitter of the brain

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77
Q

what drug gives the most serious sedation when taken with benzodiazepines?

A

alcohol gives the most serious sedation when combined with benzodiazepines

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78
Q

what drugs inhibit benzodiazepines?

A 
benzodiazepines are inhibited by
–ketoconazole
–Itraconazole
–Macrolide antibiotics
–Fluoxetine
–Nefazodone
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79
Q

what drugs enhance benzodiazepine effect?

A

birth control pills may enhance benzodiazepine effects

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80
Q

what drugs Will barbiturates decreasing activity of?

A 
Barbiturates will decrease the effects of
–Anticoagulants
–Birth control pills
–Steroids
–Various others
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81
Q

benzodiazepines and hedonic effects

A

benzodiazepines a rarely used alone for hedonic effects

–Usually Mixed with methadone

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82
Q

discussed tolerance to benzodiazepines

A

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

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83
Q

which benzodiazepines have the lowest risk of addiction?

A

benzodiazepines with the least RISK OF ADDICTION
–Clonazepam
–Chlordiazepoxide
–oxazepam

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84
Q

benzodiazepines with the highest risk of addiction

A

benzodiazepines with highest rate of addiction
–DIAZEPAM
–ALPRAZOLAM
–LORAZEPAM

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85
Q

benzodiazepine toxicity

A 
BENZODIAZEPINE TOXIC SYMPTOMS
–Sedation
–Anterograde amnesia 
–difficulty acquiring new learning
–Difficulty concentrating

Chronic heavy benzodiazepine use can resulting cognitive impairment which is often permanent

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86
Q

drug most associated with sleepwalking

A

zolpidem (Ambien) most associated with sleepwalking

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87
Q

using benzodiazepine during pregnancy may produce what syndromes

A

benzodiazepine Use during pregnancy
–CLEFT PALATE RISK
–FLOPPY BABY SYNDROME

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88
Q

what is GHB

A

GHB =gamma hydroxybutyrate
–Club drug
–Can induce absence seizures
–can treat catalepsy and narcolepsy

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89
Q

what of the effects of GHB

A 
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
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90
Q

treatment for GHB intoxication

A

GHB intoxication was treated with high-dose benzodiazepine followed by a taper

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91
Q

list endogenous opioid peptides

A

endogenous opioid peptides are
–Beta endorphin
–Enkephalins
–dynorphins

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92
Q

Decay products of heroin

A

decay products of heroin
–Morphine
–6 Mono acetyl morphine

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93
Q

list synthetic opioid agonist

A 
synthetic opioid agonists are
–Hydrocodone
–Oxycodone
–hydromorphone
–Heroin
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94
Q

synthetic opioid antagonists

A

synthetic opioid antagonists are
–naltrexone
–naloxone
–nalmefene

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95
Q

discuss oxycodone

A

oxycodone
–SEMI-SYNTHETIC Compound derived from thebaine
–STRUCTURALLY SIMILAR TO CODEINE,
–BUT PHARMACODYNAMICS SIMILAR TO MORPHINE

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96
Q

what is Talwin NX?

A

Talwin NX is pentazocine plus naloxone

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97
Q

what is LAAM

A

LAAM= levo alpha methanol
–Is congener of methadone
–Opioid agonist
–used for agonist therapy, a second line drug after methadone

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98
Q

described torsades de points

A

polymorphic ventricular tachycardia,
–Twisting effect around isoelectric axis
–can degenerate into ventricular fibrillation

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99
Q

side effects of LAAM

A

–prolonged QT intervals

–Torsade de points

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100
Q

how many people have used heroin?

A 
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
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101
Q

heroin pharmacokinetics

A

heroin pharmacokinetics
–Lipid solvable and water-soluble
–More potent than morphine
–Is prodrug, no intrinsic opioid activity

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102
Q

half-life of heroin and the blood?

A

heroin half-life and blood is about 3 minutes

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103
Q

why is heroin not used orally?

A

oral heroin is metabolized by first-pass metabolism to liver

–Has limited bioavailability when given orally

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104
Q

when do peak blood levels of heroin occur after using?

A

heroin peaks in the blood about 5 minutes after intranasal, intramuscular, or subcutaneous use

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105
Q

what is a half-life of Morphine?

A

the half life of morphine is 3 hours

–But analgesia lasts longer

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106
Q

how is morphine eliminated from the body?

A

90% of morphine is excreted in urine within 24 hours

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107
Q

what is a half-life for immediate release oxycodone?

A

Half-life of immediate release oxycodone is 3–4 hours

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108
Q

technical name for codeine

A

codeine is also known as methyl morphine

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109
Q

meperidine analgesia
–Onset
–Peaks
–Metabolize

A

–meperidine analgesia begins in 15 minutes
–peaks and 1–2 hours
–Metabolized and liver

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110
Q

pharmacokinetics of methadone

A 
methadone pharmacokinetics
–Is full mu opioid agonist
–Oral methadone is rapidly absorbed
––Has delayed onset of action
–Half life of methadone is 24 hours
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111
Q

name some drugs in the class of caffeine

A 
drugs in the same class as caffeine
–Caffeine = 1, 3, 7 tri-methyl–xanthine
–Dimethyl xanthene
–Theophylline
–Theobromine
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112
Q

therapeutic uses of caffeine?

A

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

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113
Q

when is peak level of caffeine?

A

caffeine reaches his peak level and 30–45 minutes after oral ingestion

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114
Q

volume of distribution of caffeine

A

caffeine is distributive all tissues equally

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115
Q

number of known metabolites of caffeine

A

–over 25 metabolites of caffeine have been identified
–Metabolic pathway involves cytochrome P450 liver enzymes
–produces para xanthine, theobromine ,and theophylline

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116
Q

what drugs and conditions alter caffeine metabolism?

A

Caffeine metabolism can be altered by any drug that involves cytochrome P450 liver enzymes

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117
Q

what are the effects of cigarette smoking on caffeine metabolism?

A

Cigarette smoking increases liver enzymes and therefore Decreases caffeine half-life by up to 50%

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118
Q

name some inhibitors of caffeine metabolism

A 
caffeine metabolism can be inhibited by
–High doses of caffeine
–Oral contraceptives
–Cimetidine
–Some quinolone antibiotics
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119
Q

what is primary site of action of caffeine?

A

the primary site of action of caffeine is the adenosine receptor

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120
Q

where is adenosine found?

How was informed?

A

adenosine is an endogenous nucleoside found throughout the brain–
–It is formed by the breakdown of adenosine triphosphate

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121
Q

how does adenosine react with caffeine?

A

–caffeine is structurally similar to adenosine and is therefore an antagonist
–Therefore caffeine produces the opposite effect of adenosine

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122
Q

how his caffeine affects sleep?

A

effects of caffeine on sleep are not dopamine dependent

–Caffeine antagonizes sleep promoting effects of adenosine

123
Q

what the cardio vascular effects of caffeine?

A

caffeine
–Increases blood pressure
–Decreases or no effect on heart rate

124
Q

what is the effect of caffeine on the gastrointestinal system?

A

–caffeine stimulates gastric acid secretion

–Caffeine as a colonic stimulant similar to a meal

125
Q

what is a caffeine effect on the respiratory system?

A

–caffeine as a respiratory stimulant

–Caffeine is a bronchodilator at high doses

126
Q

what are the renal effects of caffeine?

A

–caffeine acts as a diuretic
–Increase his urinary volume by 30% for several hours
–Increases detrussor pressure, therefore increasing urinary urgency and detrussor instability

127
Q

what are the effects of caffeine on the muscular system?

A

caffeine is ergogenic, therefore Increases performance, especially during prolonged exercise

128
Q

what our the adverse effects of caffeine on health?

A

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

129
Q

what are the positive effects of caffeine on health?

A

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

130
Q

what are the subjective effects of caffeine in low to moderate dose?

A

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

131
Q

what dose of caffeine is most likely to produce negative subjective effects?

A 
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

132
Q

to what effects will caffeine users develops tolerance?

A 
high-dose caffeine users developed tolerance to:
–Sleep effects
–Diuresis
–Salivation
–Metabolic rate changes
133
Q

symptoms of caffeine intoxication

A 
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
134
Q

what is a lethal dose of caffeine?

A

lethal dose of caffeine is 5-10 g

135
Q

caffeine withdrawal symptoms are

A 
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
136
Q

when will caffeine withdrawal occur?

A

–caffeine withdrawal usually begins 12-24 hours after last caffeine intake
–Peaks in 20-51 hours

137
Q

duration of caffeine withdrawal symptoms

A

caffeine withdrawal symptoms last 2–9 days

–But can last for 3 weeks

138
Q

how much caffeine is necessary to suppress withdrawal symptoms?

A

25 mg of caffeine will suppress caffeine withdrawal headache

139
Q

what is a relationship between caffeine use and nicotine use

A

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

140
Q

relationship between alcohol use and caffeine use

A

heavy alcohol use is associated with heavy caffeine use

141
Q

what percentage of patients admitted to the hospital have alcohol problems

A

about 10–20 percent of patients admitted to the hospital have alcohol problems

142
Q

what is the rate of substance abuse in primary care

A

illicit and prescription drug abuse varies from about 5%–10% in primary care

143
Q

what are considered safe drinking levels

A

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

144
Q

define “at risk drinking”

A

at risk drinking = safe limits of drinking are exceeded, but abuse or dependency criteria are not met

145
Q

what percentage of college students report binge drinking?

A

40% of college students report binge drinking in prior 2 weeks

–One third of college students meet criteria for alcohol abuse

146
Q

percentage of pregnant / nonpregnant women who engage in binge drinking

A

–2% of pregnant women engaged in binge drinking

–13% of non-pregnant women engaged in binge drinking

147
Q

first trimester drinking can produce…

A

drinking during first trimester can produce
–low birthweight
–Decreased birth length
–Decrease head circumference
–Physical abnormalities
–Alcohol-related neural developmental disorders

148
Q

second and third trimester drinking can produce

A

second and third trimester drinking can produce

–Developmental delay caused by drinking

149
Q

what of the medical complications of illicit drug use in pregnancy?

A 
illicit drug use during pregnancy can produce
–Placental abruption
–Placental insufficiency
–Chorioamnionitis
–Spontaneous abortion
–Postpartum hemorrhage
–Preeclampsia
150
Q

what percentage of life-threatening injuries involving alcohol?

A

70% of life-threatening injuries involve alcohol

151
Q

What is The chemical treatment of acute alcoholism?

A

Treatment of acute alcoholism:
–Thiamine 100 mg IM (to prevent Wernicke’s encephalopathy)
–Long-term benzodiazepines to prevent and treat alcohol withdrawal syndrome

152
Q

when does withdrawal from short acting benzodiazepines ?

A

Withdrawal from short acting benzodiazepines may occur within 24 hours and may last for several days

153
Q

What percentage of elderly have alcohol in Their systems when admitted to the hospital?

A

6%–11% of elderly have alcohol in them when admitted to the hospital

154
Q

How Does alcoholism rank as a psychiatric disorder among elderly?

A

Alcoholism is the third most common psychiatric disorder among elderly.

One third Of older alcoholics are late onset alcoholics

155
Q

Why is alcohol metabolized differently in the elderly?

A

Elderly have altered pharmacokinetics For alcohol because of:
–More body fat
–Less water than younger people
–Therefore higher alcohol concentrations with less alcohol ingestion

156
Q

What conditions are associated with alcoholism in the elderly

A 
conditions associated with alcoholism in the elderly include:
–Depression
–Delirium
–Chronic fatigue
–Seizures
–Repeated infections
–Hypertension
–Malnutrition 
–cardiomyopathy
–Peripheral neuropathy
–Sexual dysfunction
157
Q

What the limitations of urinalysis for drugs?

A

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

158
Q

What level of creatinine must be present in urine for a valid drug sample?

A

20 ng/mL creatinine must be present to be considered valid

159
Q

what are the temperature limits for a valid urine drug screen?

A

urine must be between 90° and 100°F within 4 minutes of collection

160
Q

define dilute urine

A

“Dilute urine” contains 02 20 mg/dL of creatinine
And
Specific gravity between 1.0010 and 1.0200

161
Q

defines substitute urine

A

“substituted urine” = creatinine <2 mg/Deciliter

And specific gravity not between 1.0010–1.0200

162
Q

what substances does DOT test for?

A 
DOT test for 5 substances
–Amphetamines
–Cannabinoids
–Cocaine
–Opioids
–PCP
163
Q

What are the best tests for chronic alcoholism?

A

The best test for chronic alcoholism are
–GGT
–AST
–MCV

164
Q

How much alcohol was Must one consume to elevated GGT?

A

5 drinks per day for 2 weeks will elevated GGT in most individuals

165
Q

how fast we’ll GGT decline with abstinence

A

–GGT will decline 50% in 2 weeks

–GGT will return to normal in 2 months

166
Q

What are some non-alcohol-related conditions that can increase the MCV?

A 
Nonalcoholic conditions that can raise MCV R:
–Chronic liver disease
–Hypothyroidism
–Folate deficiency
–Megaloblastic disorder
167
Q

What is NADH?

A

NADH is produced during oxidation of alcohol and can be a marker for alcohol abuse

168
Q

What alcohols can falsely elevate NADH

A 
NADH can be falsely elevated with the consumption of:
–Isopropyl alcohol
–Methanol
–Ethylene glycol
–Acetone
–diabetic ketoacidosis
–starvation acidosis
169
Q

What is the ratio of blood-alcohol to breath alcohol?

A

The ratio of alcohol in the breath to alcohol in the blood is approximately 2100:1

170
Q

How long after an alcoholic drink can breath analysis be done?

A

Should wait 15 minutes after the last drink before measuring blood alcohol in the breath

171
Q

what her instructions for breath alcohol analysis?

A

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

172
Q

Discuss urine tests for alcohol

A

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

173
Q

list most common amphetamines

A 
most common amphetamines are… 
–Amphetamine
–Methamphetamine
–MDMA = ecstasy
–MVA
–MDEA = Eve
174
Q

What is the following stand for

MDMA?

A

MDMA = ecstasy = 2, 3 methylene dioxy methamphetamine

175
Q

what’s is the following stand for?

MDA

A

MVA = 3 , 4 methylene dioxy amphetamine

176
Q

What this the following stand for?

MDEA

A

MDEA =Eve = 3,4 Methylene dioxy N ethylene amphetamine

177
Q

which isomer of amphetamine has stronger effects

A

the D isomer of amphetamines more active and has more abuse potential

178
Q

Vicks inhaler we’ll give a false positive test for?

A

Vicks nasal inhaler is the L isomer of methamphetamine and will test positive for that

179
Q

what are some of the sympathomimetic amines that cross-react with the urine test for amphetamines

A

the following will cross-react in the immunoassay for amphetamines
–Amphetamines
–Phenyl propyl amine
–Pseudoephedrine
–L methamphetamine (he Vicks)
–Appetite suppressants containing ephedrine
–Phentermine

180
Q

how long are amphetamines detectable in the urine?

A

amphetamines are usually detectable for 1–3 days

181
Q

what chemicals will reduce detection of amphetamines and urine?

A

A high pH will reduce excretion, therefore ingesting bicarbonate will reduce detection of amphetamines

182
Q

what is the urine test for amphetamines and methamphetamine actually tests for?

A

The urine immunoassay for amphetamines actually tests for amphetamines and methamphetamine

183
Q

what are the 3 classes of barbiturates based on duration of action:

A

the 3 classes of barbiturates based on duration of action are:

Ultrashort = thiopental
Short acting = pentobarbital, secobarbital, amobarbital
–––Most commonly abused
long-lasting =phenobarbital

184
Q

how long are short acting barbiturates detectable in the urine?

A

short-acting barbiturates are usually detectable for 1–4 days in urine

185
Q

what drugs metabolize to oxazepam

A 
the following drugs metabolize to oxazepam
–Clorazepate
–Chlordiazepoxide
–Diazepam
–Temazepam
186
Q

what benzodiazepines are likely to be missed in urine screenings for benzodiazepines?

A

urine tests for benzodiazepines target oxazepam

Therefore, can miss
–Clonazepam
–Lorazepam
–Triazolam

187
Q

what common drugs can give false positives for benzodiazepines?

A

Urine immunoassays for benzodiazepines can give false positives with the following:
–Oxaprozin
–sertraline
–tolmetin

188
Q

discuss signs and symptoms of alcoholic fatty liver

A 
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
189
Q

discussed signs and symptoms of alcoholic cirrhosis

A 
ALCOHOLIC cirrhosis
–Nausea
–Weight loss
–Commonly portal hypertension
–Variceal bleeding
–Ascites
–Liver failure
–May progress to hepatocellular carcinoma
190
Q

treatment of ascites

A

–salt restriction to reduce fluid retention
Management portal hypertension with
–– beta blockers
––spironolactone
––Furosemide
–Transjugular intrahepatic portal–systemic shunting

191
Q

treatment of hepatic encephalopathy

A

–treat precipitating factors
–Decreased colonic production/absorption of ammonia with lactulose
–Treat H. pylori

192
Q

discuss hepatitis A

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

193
Q

discussed hepatitis B

A

hepatitis B
–Most prevalent chronic infectious viral disease in humans
–Readily transmitted among intravenous drug users

194
Q

risk groups for hepatitis B

A 
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
195
Q

hepatitis B prodrome symptoms

A 
HEPATITIS B PRODROME SYMPTOMS
–transient serum sickness prodrome
––Polyarthralgia
––Fever
––Malaise
––Proteinuria
196
Q

hepatitis B acute infection symptoms

A 
symptoms of acute hepatitis B infection
–Anorexia
–Nausea
–Plus or minus vomiting
–Jaundice
–Pale stools
–Dark urine
–Very often subclinical
197
Q

chronic stage of hepatitis B

A

5% of hepatitis B converts to chronic hepatitis B and adults

198
Q

making diagnosis of chronic hepatitis B

A

HBS AG for more than 6 months

199
Q

complications of chronic active hepatitis B

A

chronic active hepatitis B
–Chronic hepatitis
–Cirrhosis
–Hepatocellular carcinoma

200
Q

treatment of active chronic hepatitis B

A

only treated it active liver inflammation
–Pegylated interferon is 30% effective
–Used to more agents

201
Q

discuss hepatitis C

A 
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
202
Q

Hepatitis C risk factors

A

–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

203
Q

Hepatitis C primary infection

A

primary infection is usually subclinical

–Peak viremia usually in week 2–3

204
Q

Hepatitis C chronic infection

A

–chronic infection develops in three fourths of patient’s with acute infection
–Liver damage results from immune damage to infected cells

205
Q

Long-term damage with hepatitis C

A

–8% developed cirrhosis in 20 years

–20% developed cirrhosis after 40 years

206
Q

Symptoms of chronic hepatitis C

A 
–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
207
Q

Percentage of acute hepatitis C that developed persistent chronic infection

A

60% that 70% of acute hepatitis C patients Will develop chronic infection

208
Q

Mechanism of liver injury in hepatitis C

A

Hepatitis C causes liver damage predominantly by immune damage to affected liver cells

209
Q

Assessing severity of hepatitis C

A

–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

210
Q

Effects of alcohol on hepatitis C

A

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

211
Q

Goal of antiviral therapy in hepatitis C

A

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

212
Q

risk of cirrhosis during sustained viral response in hepatitis C

A

low risk of cirrhosis after 6 months of sustained virologic response and a normal PCR with normal ALT

213
Q

treatment of patients with hepatitis C and ongoing substance abuse

A

NIH recommends against treating rations with ongoing substance abuse (Excluding methadone and buprenorphine)

214
Q

Rate of progression of hepatitis C From cirrhosis to hepatocellular carcinoma

A

Approximately 5% of cirrhotic hepatitis C patient’s progress to hepato-cellular carcinoma

215
Q

treatment of small primary hepatocellular carcinomas

A

excision

216
Q

indications for liver Transplantation in the presence of hepatitis C

A

–major complications of cirrhosis

–Life Expectancy of 1–2 years without transplantation

217
Q

3 year posttransplantation survival rate with hepatitis C

A

similar to other transplantations of liver

–84% every 3 year survival rate

218
Q

What is cocaine hepatitis

A 
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
219
Q

mechanism of cocaine hepatitis injury

A

cocaine hepatitis injury most likely caused by ischemia from the vasoconstrictive effects of cocaine and possibly toxic metabolites

220
Q

where the effects of alcohol and cocaine taken together

A

ethyl cocaine (coca ethylene) is produced
–Has similar faxes cocaine
–Has slightly longer half-life therefore accumulates higher
–Has lower LD 50 rate

221
Q

hepatic injury from ecstasy

A

ecstasy and MDMA rarely cause hepatic injury

222
Q

most common toxic material designed for oral use but injection

A

Talcum powder

–Accumulation causes damage at several sites especially lung and liver

223
Q

Pathogenesis of injected talc

A

Talc is strongly fibrogenic in the lung and leads to pulmonary granulomatosis disease with progressive or fatal outcome
–Talc and liver is inconsequential

224
Q

effects of opiates on the liver

A

no hepatotoxicity from sure preparations of opiate agonists

–Opiate antagonists such as naltrexone can cause minor elevation of liver enzymes, but rarely serious

225
Q

lists toxic effects of anabolic steroids

A 
–cholestasis
–Toxic hepatitis
–Hepatic adenomas
–Hepatic carcinomas
Hepatotoxicity from contaminants
226
Q

list renal problems associated with opiate use

A 
–HIV nephropathy
–Hepatitis C associated glomerular nephropathy
–Bacterial endocarditis
–Acute glomerulonephritis
–Subcutaneous injection amyloidosis
–Nontraumatic rhabdomyolysis
–Acute renal failure
–Heroin nephropathy
227
Q

List renal problems associated with cocaine usage

A 
cocaine usage can cause
–Rhabdomyolysis
–Acute renal failure
–Accelerated hypertension and renal failure
–HIV nephropathy
–Hypertensive Nephrosclerosis
–Renal infarction
–Thrombotic microangiopathy and renal failure
228
Q

llist renal problems associated with alcohol consumption

A 
alcohol consumption is associated with
–Hepatorenal syndrome
–Rhabdomyolysis and acute renal failure
–Increase Incidents and severity of postinfectious glomerulonephritis
–Electrolyte disorders
229
Q

define nephrotic syndrome

A 
nephrotic syndrome characterized by:
–Heavy proteinuria (>3.5 g per day)
–Hypoalbuminemia
–Hyperlipidemia
–Lymphedema
–Edema

Not all must be present to diagnose

230
Q

differences between nephritic and nephrotic syndrome

A 
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

231
Q

Most common presentation of renal disease with hepatitis C

A

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

232
Q

Discuss heroin nephropathy

A

heroin nephropathy
–Secondary cause of focal and segmental glomerulonephritis
–Often associated with hypertension
–Often associated with slow progression ESRD
–Not common

233
Q

Frequency of hep C in HIV drug users?

A

78% of HIV drug users have hepatitis C

234
Q

treatment of acute hypertension connection with cocaine use

A

Steroids are the treatment for Acute hypertension Associated with cocaine use

235
Q

Drugs of abuse associated with rhabdomyolysis

A 
–Phencyclidine
–Methamphetamine
–MDMA
–Cocaine
–Heroin
–Alcohol
236
Q

Discuss hepatorenal syndrome

A

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

237
Q

Diagnoses of Hepatorenal syndrome

A

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

238
Q

Other name for ecstasy

A

Ecstasy= MDMA

= methylene dioxy methamphetamine

239
Q

Effects of MDMA at rave party

A 
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

240
Q

Major target of alcohol in other drug toxicities

A

Liver is major target for all alcohol And drug toxicities

241
Q

Hepatic cirrhosis is__leading cause of death and USA

Hepatic cirrhosis is__most common cause of death in middle-age American man

A

12th

Fifth

242
Q

Number of deaths per year from hepatic cirrhosis

A

28,000 US deaths per year from hepatic cirrhosis

243
Q

Most common causes of liver transplantation

A

Most common causes of liver transplantation are:
–Hepatitis C
–Alcoholic cirrhosis

244
Q

Amount of alcohol needed to produce fatty liver

A

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

245
Q

Amount of alcohol in standard drink

A

Standard drink contains 14 g of alcohol

246
Q

How much alcohol is needed to develop hepatic cirrhosis

A

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

247
Q

Risk factors for alcoholic liver disease

A

–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

248
Q

What classes of drugs have increased hepatotoxicity with alcohol consumption?

A 
Chronic alcohol consumption increases hepatotoxicity of colon
–Acetaminophen
–Industrial solvents
–Anesthetic gases
–Illicit drugs
249
Q

what is the cause of alcohol liver damage?

A

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

250
Q

How do his chronic alcohol consumption increased hepatotoxicity

A

via CPY 2 E1 & Which metabolizes many other things

251
Q

alcoholic fatty liver history, signs, symptoms

A 
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
252
Q

Alcoholic hepatitis signs and symptoms

A 
Alcoholic hepatitis signs and symptoms
–Anorexia
–Nausea
–Abdominal pain
–Impaired liver function
–Jaundice
–Bruising
–Encephalopathy
–Fever and/or leukocytosis
253
Q

Significance of AST/ALT ratio

A

ALT >AST
–Suspect chronic hepatitis C
–Acetaminophen ingestion
–Other liver injury

AST greater than ALT
–Suspect alcoholic liver disease

254
Q

Pathogenesis of alcoholic hepatitis

A

pathogenesis of alcoholic hepatitis
–Neither detectable nor preventable
–Multifactorial including post, toxin, etc.
–Ethanol metabolizes to acetyl aldehyde via ADH and other enzymes

255
Q

alcoholic liver disease treatment

A

avoid alcohol!

–If 6 weeks abstinence resolves elevated liver function tests, may return to drinking at low level if able to control

256
Q

apparent half-life of gamma GT in alcoholic liver disease

A

gamma GT has an apparent half-life 26 days

–Failure to drop suggests coexistent disease

257
Q

Metabolites of alcohol and pharmacologic effects

A

metabolites of alcohol are
–Acetyl aldehyde
–Acetate

Acetyl aldehyde and acetate her adrenergic and Vasodilators

258
Q

Wide does cardiac output increased with alcohol in healthy patient’s

A

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

259
Q

List heart disease they can result from alcohol

A 
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
260
Q

Defined holiday heart

A

Holiday heart
–Excessive alcohol consumption especially binge drinking producing
––Cardiac arrhythmias
–––Especially atrial fibrillation

Always look for alcohol in the presence of cardiac arrhythmias

261
Q

probable cause of sudden cardiac death in alcoholics

A

sudden cardiac death in alcoholics is thought to be due to arrhythmias, most likely produced by alcohol withdrawal symptoms

262
Q

Nicotine effects on
the heart rate
blood pressure
on skin

A

Nicotine increases heart rate and blood pressure for at least 30 minutes
–Reduce his blood flow to scan

263
Q 
Nicotine effects on:
–Hemoglobin
–Platelet aggregation
–Blood this capacity
–HDL
–Oral contraceptives
A

Nicotine effects are:
Coronary artery spasm
–Increased carboxyhemoglobin and decreased oxygen delivery
–Induces platelet aggregation and blood viscosity
–Lowers HDL

264
Q

coronary risk reduction by stopping smoking

A

–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

265
Q

Cannabis effects on circulatory system and heart

A

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

266
Q

Effexor opioids on cardiovascular system

A

opioids:
–Lower blood pressure
–Reduce heart rate
–Have a favorable effect on cardiac ischemia

267
Q

Name the for neurotransmitters Systems within the brain stem reticular formation

A

–Serotonin
–Acetylcholine
–Dopamine
–Noradrenaline

268
Q

treatment of cocaine-induced vasoconstriction

–what not to use!

A

Cocaine-induced vasoconstriction of coronary arteries is enhanced by a beta adrenergic blocker Such as propranolol

269
Q

Treatment of cocaine-induced vasoconstriction

–What to use

A

Treatment of coronary vasoconstriction from cocaine:
–Benzodiazepines
–Nitrates
–Calcium channel blockers

270
Q

Acute coronary artery syndrome and cocaine

A

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

271
Q

Treatment of cocaine induced coronary artery syndrome

A

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

272
Q

Effects of chronic cocaine use on heart

A

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

273
Q

List significant amphetamines of abuse

A 
Abused amphetamines include: 
–Amphetamine
–Methamphetamine
–Methylphenidate
–MDMA
274
Q

Effects of amphetamines on cardiovascular system

A

amphetamine effect on cardiovascular system

–Dose-dependent elevation of blood pressure and heart rate

275
Q

Effects of phencyclidine and lysergic acid diethylamide on cardiovascular system

A

PCP and LST increase heart rate

276
Q

side effects of anabolic steroids

A

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

277
Q

Best labs Test nutritional status

A

Serum Pre-albumin

278
Q

Treatment of heroin addict and hospital

A

10–20 milligrams of methadone every 2 hours as needed

If history of prior withdrawal, give diazepam 10–20 milligrams orally

279
Q

Treatment of pain in opioid addiction

A

Need much higher dose to control pain

–Do not use when necessary schedule for dosing

280
Q

How long after last drink will DTs start?

A

Delirium tremens will begin in 6–48 hours after the last drink

281
Q

What are the sympathetic splanchnic nerves to the GI tract

A

Thoracic, lumbar

282
Q

What of the symptoms of delirium tremens?

A

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

283
Q

What structures are suspended by the mesentery?

A

Jejunum and ileum

284
Q

Cause and treatment of Wernicke-Korsakoff syndrome

A

Main cause is thiamine deficiency

Give 100 mg thiamine IM before giving glucose

285
Q

Symptoms of alcoholic cerebellar dysfunction

A

Symptoms of alcoholic cerebellar dysfunction
–Ataxia and incoordination

Often irreversible

286
Q

symptoms of Korsakoff syndrome

A

main symptom of Korsakoff’s syndrome is confabulation

287
Q

Symptoms of alcoholic peripheral neuropathy

A

Symptoms of alcoholic peripheral neuropathy:
–Burning pain
–Numbness in stocking–glove distribution

288
Q

Symptoms of alcoholic hepatitis

A 
Alcoholic hepatitis symptoms:
–Fever
–Leukocytosis
–Right upper quadrant pain and tenderness
Elevation of AST greater than ALT
289
Q

Complications of hepatic cirrhosis

A 
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
290
Q

Five-year prognosis for cirrhosis

A

if alcohol continues 50 Percent

291
Q

Hematologic consequences of alcoholism

A

Hematologic consequences of alcoholism:
–Iron deficiency from gastrointestinal hemorrhage
–Mallory-Weiss tears
–Pancytopenia
–Megaloblastic anemia from folate deficiency

292
Q

Cardiovascular consequences of alcoholism

A

Cardiovascular consequences of alcoholism:
–Hypertension, especially during withdrawal
–Alcoholic cardiomyopathy
–Congestive heart failure

293
Q

effects of alcoholism on EKG

A

EKG shows diffuse hypokinesis and four-chamber dilatation

–Tachycardia and T-wave changes

294
Q

effects of alcohol on esophagus

A

alcoholism promotes blurred

295
Q

predisposing factors for pancreatitis

A

75% of pancreatitis has following predisposing factors:
–Heavy alcohol consumption
–Gallstones

296
Q

frequency of pancreatitis and heavy drinkers

A

5% of heavy drinkers developed pancreatitis

297
Q

how does alcoholism cause pancreatitis

A

–alcohol contracts the sphincter of Oddi
–Inhibits pancreatic secretion
––Results and cascade about a digestion

298
Q

treatment of pancreatitis

A 
pancreatitis is treated by
–Bedrest
–Analgesics
–Intravenous fluids
–Fasting
299
Q

causes and clinical features of chronic pancreatitis

A

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
300
Q

most common cause of pancreatitis in children is

A

cystic fibrosis

301
Q

mechanism of diarrhea in acute and chronic alcoholism

A 
diarrhea and alcoholics occur from:
–Altered motility
–Altered permeability
–Nutritional disorders
–Small intestinal mucosa injury
302
Q

treatment of opioid-induced constipation

A

treat opioid-induced constipation with:
–Increase fluid intake
–Fiber supplementation
–Lactulose

303
Q

what his body packing?

A

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

304
Q

effects of cocaine and amphetamines on gut

A

cocaine mainly causes ischemic injury of the gut producing
–Intestinal perforation
–Infarction
–Ischemic colitis

ADDICITION (5 decks)

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