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c. pharm exam 3 (w13) > substance abuse 3/11 > Flashcards

substance abuse 3/11 Flashcards

1
Q

objectives:

  • identify possible symptoms of chemical abuse
  • compare implications of acute and chronic substance abuse
A
  • describe the pharmacological implications related to anesthesia for patients using
  • etoh –canabis-opiates –hallucinogens
  • stimulants –anabolic steroids
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2
Q

what are the biggest concerns of drug abuse regarding anesthesia?

A
  1. cardiac symptoms (tachycardia/ blood pressure)#1
  2. respiratory
  3. anesthetic need
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3
Q

chemical abuse needs to be addressed when?

A

during pre-op evaluation and preferably the day or more before the surgery

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4
Q

patients with known hx of drug abuse should be seen in pre op…

A

the day before surgery, to discuss withdrawl and plan of care.

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5
Q

alcohol:
1. what are they at risk for post op?
2. what comorbidities will you see?

A
  1. increased risk of infection & risk for withdrawl syndrome

2. Neuro, CV, resp, GI, endocrine, hematological

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7
Q

What are estimations on drug abuse?

A

• Estimated 30 million Americans (15%) have tried illegal drugs and 5 million admit to regular use

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8
Q

Drugs of Abuse by categories

CNS Depressants:

A

• CNS Depressants

– ETOH, benzodiazepines, barbiturates, others

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9
Q

Drugs of Abuse by categories

Opiates:

A

Opiates

– Heroin, morphine, codeine

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10
Q

Drugs of Abuse by categories

Cannabis:

A

• Cannabis

– Marijuana, hashish

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11
Q

Drugs of Abuse by categories

Stimulants:

A

Stimulants

– Cocaine/crack, amphetamines, methamphetamines, ecstasy

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12
Q
  1. symptoms of abuse ___ from drug to drug?
  2. what are some signs of abuse that you will see?
  3. what are the differences in pupil changes between opiates vs. cannibis or cocaine?
A
  1. Symptoms of Abuse VARY from drug to drug
  2. • Increased alertness, pupil contraction,
    - -• Mood swings exhaustion, sleeplessness, confusion
    - -• Hallucinations
    - -• Increased HR, BP
    - -• Confusion
    - -• Euphoria
    - -• Aggression
    - -• Needle tracks
    - -• Pupil changes
  3. Dilated in cocaine &cannabis (also benzos); constricted in opiate (benzos=benzodilation; norcos=narconstriction)
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13
Q

Factors to Consider with substance abuse:

regarding amount etc.

A 
Factors to Consider
• Type and amount of drug(s) taken
• Users experience (Chronic versus first time or infrequent user) 
• Route taken
• Other circumstances
– Where taken, with whom
– Psychological, emotional stability
– Simultaneous use or cross addiction-including ETOH
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14
Q

what drug abusing patient is not a cantidate for amublatory surgery?

A

• Not a candidate for ambulatory surgery if intoxicated or otherwise impaired due to risk of cardiovascular and autonomic response variability

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15
Q
  1. what are Main areas of concern with substance abuse patient?
  2. what should be considered regarding the whole surgical experience?
A
  • Main areas of concern are CV, respiratory depression, CNS (confusion, combativeness, lethargy, coma)
  • Consider means of postoperative analgesia – Local or regional may be desirable
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16
Q

Anesthetic implications of ETOH Abuse

  1. how does approach vary?
  2. what are some anesthetic issues they may have?
A

Anesthetic implications of ETOH Abuse
1• Vary based on clinical picture; acute, chronic, chronic with acute
2• Issues include;
–– enzyme induction
–– coexisting pathologies (i.e. hepatic, cardiovascular, esophageal, hematologic, CNS)
–– Increased risk of postop complications (impaired immune response- infection?)
–– Postoperative alcohol withdrawal syndrome (AWS)

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17
Q 
Coexisting Diseases in ETOH Abuse:
• Cardiovascular:
• CNS:
• GI/Endocrine:
• Hematologic:
A

Coexisting Diseases in ETOH Abuse
• Cardiovascular
– Cardiomyopathy, HTN, conduction defects
• CNS
– Agitation, aggression, depression, disorientation, cortex and cerebellar degeneration, encephalopathy
• GI/Endocrine
– Esophagitis/varices, gastritis ulcers, fatty liver, hepatitis, cirrhosis, hypoglycemia, Hypoalbuminemia
• Hematologic
– Anemia, thrombocytopenia, decreased prothrombin, –Decreased WBC chemotaxis

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18
Q

Postoperative AWS (alcohol withdrawl syndrome)

  1. what is severity based on?
  2. what are the s/s
  3. DTs are sometimes resistant to what med? what meds are used to help with this?
A

Postoperative AWS
1• Severity related to severity of abuse
2• broad array of s/s
–• May cause increased catecholamines (increased HR, vasoconstriction, O2 consumption)
–• Tachypnea, work of breathing is increased
–• Symptoms of NV, anxiety, clouded sensorium, HA can occur postop
–• Other symptoms include sweats, agitation, tactile, auditory or visual disturbances
–• Tremors which may progress to DTs
3. DTs are often resistant to benzodiazepines and other therapy (Clonadine po or intrathecal shows promise)

19
Q

what is the most abused opiate?

A

• Heroin remains the most abused opiate, but don’t forget prescription drugs

20
Q

Heroin:

  1. where does it come from? what else comes from that?
  2. how does it look? how is it taken?
  3. what is duration of action
  4. what is metabolism; what does that say about withdrawl?
  5. whithdrawl begins in how many hours post intake of heroin?
  6. technique (shooting up) of taking heroin leads to what?
  7. are there contraindications to any anesthetic?
  8. what are NOT DOING with these patients?
A

Heroin
1• Derived from the milk of the poppy (same as morphine and codeine)
2• Pure heroin is a white powder. In the past was an IV drug due to lower potency; Current purity/potency allows smoking
3• DOA is typically 3-5 hours therefore taken a few times a day
4• Metabolism is fairly quick so withdrawal symptoms, variability of receptors and therefore unpredictable responses
5• Withdrawal begins around 6-12 hours. Treated with long acting opiates
6• Nonsterile administration therefore potential bloodborne infections, endocarditis, sepsis, hepatitis
7• No specific contraindications to general or regional
8• Not the time to treat addiction

21
Q

Cocaine as a Drug of Abuse PART 1

  1. how is it absorbed?
  2. what is cocaine? how is it made into crack?
  3. what is the action on the brain? what are s/e?
  4. what is the cardiac action? what are s/e?
  5. what does chronic use lead to with regards to heart?
  6. what are other issues (localized) from sniffing or injecting it?
A

Cocaine as a Drug of Abuse
1• Absorbed through mucous membranes or or veins (IV–Nonsterile administration)
2• Alkaloid form heated with baking soda and water yields crack-can be heated and inhaled
3• CNS stimulant
–– Euphoria-paranoia
–– Insomnia, restlessness, hallucinations
4• Sympathomimetic effects
–– Tachycardia, HTN, hyperthermia, dysrythmias
–– CV Collapse with high levels
5• Chronic use has lead to cardiomyopathy possibly due to MI, neuronal affect, direct myocardial depression
6• Chronic complications associated with route
–– sinus and septal issues,
–– IV issues

22
Q

Cocaine as a Drug of Abuse PART 2:

  1. what are pulmonary issues (especially to crack)?
  2. issues with pregnancy?
  3. how is it metabolized?
  4. excreted where? how much unchanged (%)? how long are metabolites in urine?WOW!
  5. What are side effects of using it as a local anesthetic?
  6. what NTs does it block to cause cardiac effect? what ones are blocked to cause CNS effect?
A 
1• Pulmonary issues-asthma, cough, pneumonitis, pulmonary edema, pulmonary hemorrhage
2• OB-preterm labor, abruption,precipitate delivery, meconium stained still born, SIDS, low birth weight
3• Metabolized by plasma esterase (watch for deficient patients)
4• 5% unchanged in urine. Metabolites (some active) present for up to 60 hours
5• As a LA class can cause negative ino/chronotropic effects (increase HR, BP)
6• Effect on NE uptake predominates ( Also inhibits dopamine, serotonin and tryptophan uptake resulting in CNS effect)
23
Q

Anesthetic Priorities in Cocaine Abuse:

  1. should you reley on self reporting?
  2. what about CV effects: what pre op? what should be handy?
  3. what beta blocker may cause issues? what are they? what should you use instead?
  4. what should you look for on the monitor?
  5. what about crack smokers?
  6. remember CNS effects; what might be needed pre and post op?
  7. what should you watch for as far as our medications?
A

Anesthetic Priorities in Cocaine Abuse
1• Self report is unreliable
2• Managing CV effects (preop EKG, alpha and beta blockers)
3• Beware of inderal due to unopposed Beta block (labetalol may be better)
4• Monitoring for MI, dysrythmias and other CV complications
5• Manage pulmonary effects
6• Pre and post op sedation, management of CNS effects
7• Watch for drug interactions

24
Q
  1. what is the increase in risk of MI one hour post cocaine abuse?
  2. what about cocaine causes cardiac risks?
A

1• Stats vary, may be up to 23 fold increased risk of MI within an hour after abuse
2• Multiple mechanisms including increased myocardial O2 demand, accelerated atherosclerosis and thrombus formation, coronary spasm, vasoconstriction and abnormal increased platelet aggregation

25
Q

Marijuana as a Drug of Abuse

  1. how common of an illegal drug?
  2. what does it come from? what amount of the drug is in the leaves and flower? what is the drug?
  3. what is plasma clearance (t-1/2 time) and how long do effects last?
  4. how long does it last in urine?
  5. route?
  6. what are effects of THC? Can it make you stupid?
  7. what are other effects?
  8. what happens with chronic use (especially with smoking)?
  9. what anesthesia drugs are potentiated by THC?
A

Marijuana as a Drug of Abuse
1• MOST common of the illegal drugs used
2• From the Cannabis Sativa: Approximately 5% of the dried leaves and flower contains the main psychoactive component-tetrahydrocannabinol (THC)
3• Plasma t-1/2 20-30 hours but effects last 2-3 hours.
4• Present in urine for days to months depending on extent of use
5• Most often smoked but can be taken PO (brownies)
6• Effects are dose dependent and mainly CNS:
—-– Altered mood, altered perceptions
—-– impaired coordination and learning (effects linger after high) wears off
7• Other effects can include;
—-– CV: Tachycardia, peripheral vasodilation
—-– resp: Bronchodilation acutely, irritated bronchial mucosa
—-– opthalmic: Decreased IOP, conjunctival vascular congestion (both from vasodilation)
——GI: dry mouth (and increased appetite)
8• Chronic use concerns
—-– Obstructive and restrictive disease
—-– Decreased diffusion capacity (of lungs)
9• Beware of potentiation of CNS depressant anesthetics and adjuncts

26
Q

Hallucinogens:

  1. what are they?
  2. where do they come from?
  3. what are examples?
  4. what are other effects?
  5. should you sedate? what type of anesthesia for this patient?
A

Hallucinogens
1• Defined as a drug that radically changes the users mental state by distorting the perception of reality to the point of hallucination
2• Can be manufactured or naturally occurring (i.e. mescaline can come from peyote cactus or it can be synthetic)
3• LSD, PCP, Mescaline, are examples
4• Can produce analgesia, amphetamine-like stimulation
5• Sedation is tough but a priority (regional may be problematic but not contraindicated

27
Q

Hallucinogenics: PCP (phencyclidine)

(iupac: PhenCyclohexylPiperidine)
1. what was it first developed for? why not use it?
2. what is its form? how is it administered?
3. what drug is it similar to (that we use)?
4. what are side effects?

A

1• First developed as an anesthetic but side effects were great
2• Crystalline powder- can be smoked with tobacco (“getting wet” “Sherm”, snorted or injected (“free base”).
3• Relative of ketamine
4• side effects: Unpredictable behavior, agitated, labile, disorientation also: Increased HR, BP and maybe respiratory rate

28
Q

Hallucinogenics: LSD (lysergic acid diethylamide)

  1. how is its potency?
  2. what are side effects?
  3. what anesthetic problems will the provider have?
A

LSD (Lysergic acid diethyamide)
1• Very potent -effects at low doses
2• Besides hallucination may cause pupil dilation, increased BP, HR, flushing (sympathimimetic), salivation, tearing (cholinergic), hyperreflexia
3• may have sedation issues with these patients

29
Q

CNS Stimulants:

  1. name common cns stimulants:
  2. where does it come from?
  3. route of administration?
  4. addictive properties?
  5. side effects?
A

CNS Stimulants
1• Amphetamine, methamphetamine (ice) and dextroamphetamine, Dextro (dexadrine is the only legal form)
2• Produced synthetically in labs
3• Can be injected (speed) snorted, inhaled or taken PO
4• Highly addictive
5• CNS and CV stimulation. Resembles epi/norepi effects (sympathimimetic)

30
Q

Amphetamine (and related drugs):

  1. side effects:
  2. what happens with catecholamines?
  3. what can chronic use lead to?
  4. what drug are implications similar with?
A

Amphetamine (and related drugs)
1• Hyperactive behavior, euphoria, restlessness, anxiety, talkative etc (also cardiac stimulation)
2• Increases levels of epi, norepi and dopamine acutely, depleted catecholamines over time
3• Chronic use leads to stroke, cardiotoxicity, epilepsy, depression, brain damage similar to Alzheimer’s
4• Implications are similar to cocaine abuse

31
Q

Methamphetamine:

  1. what are they?
  2. how long can effects from smoked form last?
  3. addictive properties?
  4. what happens in CNS?
  5. cardiac effects (long term)
  6. what does overdose cause (cardiac/integument)?
A

Methamphetamine
1• Synthetic non-catecholamine derivative stimulates CNS and CVS (epi, norepi, dopa)
2• Effects vary by route, Smoked form can last 12 hours
3• High incidence of tolerance and therefore addiction (tachyphylaxis like tolerance)
4• Up-regulates CNS stimulates release and decreases reuptake
5• Long term cardio effects include cardiac fibrosis, LVH
6• Hyperthermia associated with OD

32
Q

Rave Drugs: Ecstasy, Eve, Rohypnol, Ketamine, Fry, Ecstasy:

  1. chemical name?
  2. what is the structure/class?
  3. where did they come from?
  4. route?
A

Rave Drugs: Ecstasy, Eve, Rohypnol, Ketamine, Fry Ecstasy
1• 3,4 methylenedioxymethamphetamine (MDMA)
2• Semisynthetic hallucinogenic amphetamine similar in structure to catecholamines
3• Designed in 1914 by Merck and sold as an appetite suppressant. Used in psycotherapy in the 1970s. Currently a schedule 1 drug
4• Taken PO or PR

33
Q

Ecstasy

  1. CNS side effects?
  2. what deadly condition can it cause?
  3. CV effects?
  4. hepatic/ renal effects?
A

Ecstasy
1–CNS effects: Increased temperature, profuse sweating and large water intake (subsequent hyponatremia) increased neuromuscular activity (including teeth grinding (bruxism), jaw clenching (trissmus), vigorous dancing) may cause seizures, sub arachnoid bleeding
2– Suggested that MDMA can cause MH in predisposed patients
3• Cardiopulmonary effects;
– Sympathomimetic effects, increased epi, norepi and dopamine release, increase MRO2, initial tachycardia and HTN followed by hypotension and low cardiac output, MI, arterial vasospasms, prolonged use can cause cardiomyopathy
– Pulmonary edema (may be secondary to water intoxication
4• Hepatic and renal effects;
– Hepatitis, hepatic fibrosis possible liver failure
– Acute renal failure due to rhabdomyolysis and DIC, sharp increase in creatinine levels

34
Q

ecstasy:

  1. peak?
  2. t-1/2?
  3. metabolized where?
A
  1. 2 hours
  2. 8 hours
  3. liver
35
Q

Rohypnol

  1. what class of drug?
  2. what was added to it to combat date rape?
  3. what schedule is it? what are penalties similar to in schedule? where is it smuggled from?
  4. acts like what common benzo?
  5. onset? peak? duration? half life?
A

Rohypnol (roofie)
1• Flunitrazepam, a benzodiazepine manufactured by a US company (Hoffman LaRoche) but sold in Europe and Latin America as a sleep aid
2• To combat date rape use it was reformulated to release a blue dye when added to liquid
3• Schedule IV but penalties are same as Schedule 1. Smuggled in via Mexico
4• Acts like diazepam only more so
5• PO- onset of effects in 30 minutes, peaks 1-2 hours lasts 8-10 hours (longer when combined with other CNS depressants). Half life 19-23 hours

36
Q

“FRY”

  1. what is it?
  2. what are effects?
  3. what are side effects?
A

Fry
1• PCP laced, formaldehyde soaked marijuana
2• Causes toxic psychosis, hallucinations, delusions, panic, paranoia, LOC changes
3• Can cause bronchitis, lung damage, body tissue destruction, loss of coordination, brain damage

37
Q

Anabolic Steroids

  1. what percent of amateur athletes and high school males are juicing?
  2. what drugs are used to mask effects?
A

Anabolic Steroids
1• Estimated up to 40% of amateur athletes/gym users; Estimated 7% of high school senior males
2• Beware of commonly abused drugs in combination
– Diuretics (masking agent, reduce edema)
– Tamoxifen (prevents gynecomastia)
– HGH (anabolic effects)
– Beta blockers (decrease tremors)
– Stimulants (ephedrine, amphetamines)
– Opiates (analgesia)-alot of joint pain
– Creatine

38
Q 
Anabolic Steroid Side Effects
1. vascular?
2. hepatic?
3. neuro/psych?
4. reproductive (male/female)?
5. dermatologic?
6. musculoskeletal?
7. cholesterol?
long term risks:
8. cardiovascular 
9. mental?
10. cancer?
A

Anabolic Steroid Side Effects
1• Vascular thrombosis
– hypercoagulability.-MI, CVA)
2• Hepatotoxicity
3• Neuro psych
– increased energy and enthusiasm, dis-inhibition, mood swings, (“roid rage”)
4• Reproductive system changes
– male: decreased testicular size, decreased sperm production, gynecomastia
– female: breast atrophy, menstrual changes, clitoral enlargement, hirsutism
5• Dermatologic Changes
– acne, male pattern baldness, alopecia, hirsutism, granulomas at injection sites
6• Tendon injury
– increase muscle strength, altered collagen
7• Abnormal lipid levels
– decrease HDL, increase LDL
—Longterm effects- increased risk—
8• Cardiovascular-LVH, vascular thrombosis, coronary spasm, increased platelet aggregation
9– Mental health issues-aggression, depression
10– Neoplasms (renal, hepatic, testicular)

39
Q

Anabolic Steroid Anesthetic Implications:

  1. o2 consupmtion, co2 production? why?
  2. dvt prophylaxis?
  3. NDMR effects? why?
  4. fasciculations?
  5. what 2 organs will cause issues?
  6. cardiac -what should you be watching? why?
  7. what induction agent should you avoid?
  8. what “enzyme” issue will they have? what about MAC?
A

Anabolic Steroid Anesthetic Implications
1• Large muscle mass and high caloric intake can lead to increased O2 consumption and CO2 production
2• May need prophylaxis against thrombosis, DVT
3• Resistance to NDMR has been reported (possibly due to increased volume of distribution from H2O retention or increased Ach receptors
4• May have excessive fasciculations
5• System physiologic changes (CV and hepatic)
6• In general- watch the heart
––Steroids=erythropoeitic stimulation-polycythemia-increased work of heart and O2 requirement, Myocardial fibrosis, LVH, etc.
7• ? Avoid etomidate due to adrenal cortical suppression
8• possible enzyme induction, increased MAC

40
Q

Drugs of Abuse by categories

Hallucinogens:

A

• Hallucinogens

– LSD, PCP

41
Q
  1. what part of the brain is involved with addiction?

2. what “cascade” may be stimulated by drugs?

A
  1. mesocorticolimbic-dopamine system

2. reward/stimulation cascade

42
Q
  1. what does undertreatment of pain in addicts lead to?

2. what is it sometimes unfairly called?

A
  1. drug ideation (cant stop thinking about pain relief)

2. drug seeking

43
Q

indications (why they are used) and side effects of these herbs:

  1. mau-huang
  2. ginko-biloba
  3. kava kava
  4. st. johns wart
  5. garlic
  6. black licorice
A
  1. Mau-huang: aka ephedra: used for diet, fatigue; contains ephedrine and pseuroephedrine alkyloids; simpathomimetic that stimulates alpha and beta- leads to tachyphylaxis
  2. ginko-biloba: used for memory, organic brain disease, claudication; causes vasodilation (central/peripheral) increases ICp, increases bleeding times (especially with nsaids)
  3. kava kava: cns depressant, anxiolytic: works on gaba; cases ataxia, weakness
  4. st. johns wart: inhibits serotonin; use direct acting sympathomimetic on these patients; they may have decreased plasmacholinesterase
  5. garlic; antibacterial, antilipid; inhibits platelet agg and enhances fibrinolysis
  6. licorice; cough suppressant, anti ulcer; causes high glucocorticoids leading to pseudoaldosteronism=increased sodium and h20=hypokalemia which potentiates digoxin

c. pharm exam 3 (w13) (6 decks)

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