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Pharmaco > Class 8-substances > Flashcards

Class 8-substances Flashcards

1
Q

Which substance is the less susceptible

to cause a toxic psychosis?

A

heroin

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2
Q

PATHOPHYSIOLOGY addiction

A

REINFORCING EFFECTS OF SUBSTANCE OF ABUSE
• Posited to be mediated through the mesolimbic reward pathway that involves DA transmission
• Reward pathway originates in the ventral tegmental area and projects to the nucleus accumbens

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3
Q

DEPRESSANTS

A 
↓ level of alertness and activity of the brain
(GABA, mu)
- Alcohol
- Benzodiazepines
- GHB
- Morphine and
derivates
- Methadone
- Heroin
- Solvents
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4
Q

STIMULANTS

A

↑ level of alertness and activity of the brain (DA / NA)

  • Cocaine
  • Amphetamines
  • Methamphetamines
  • Methylphenidate and other stimulants
  • Nicotine
  • Caffeine
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5
Q

DISRUPTIVE /

HALLUCINOGENS

A

Modify the brain, alter the senses (5-HT / glutamate)

  • Cannabis
  • Mushrooms
  • PCP / mescaline
  • Ketamine
  • Ecstasy
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6
Q

ALCOHOL PHARMACOKINETIC

A
  • Absorption : 80 % (rapid : 5 – 10 minutes)
  • Metabolic rate : 20 mg/dL/hour (i.e., one standard drink) and this rate is increased with chronic drinking
  • As the alcohol level rises in the body : process saturated and nicotinamide adenine dinucleotide (NAD+) is depleted
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7
Q

ALCOHOL DEHYDROGENASE

A
  • Located in the liver
  • Polymorphism (i.e., asian population)
  • Turns ethanol into acetadehyde
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8
Q

ALDEHYDE

DEHYDROGENASE

A

Turns acetadehyde into acetate

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9
Q

INTOXICATION sx roh

A
  • Slurred speed
  • Incoordination
  • Unsteady gait
  • Nystagmus
  • Inattention / memory impairment
  • Stupor / unconsciousness
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10
Q

Pathophysiology ROH

A

GABA / GLUTAMATE:
• Alcohol enhances the effect of GABA and inhibits glutamate receptors
• Chronic use : GABA receptors downregulate and glutamate receptors upregulate
• Abrupt cessation : hyper-excitability because of elevated glutamatergic effects
5-HT
• Chronic consumption
• Disrupt 5-HT transmission
• Obsessive behaviors concerning alcohol intake

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11
Q

WITHDRAWAL SYMPTOMS roh

A

LEVEL 1 (6 – 8 hours post abrupt cessation)
Hyperactivity of autonomic nervous system
LEVEL 2 (12 – 24 hours post abrupt cessation)
Hallucinations
LEVEL 3 (12 – 48 hours post abrupt cessation)
Seizure activity
LEVEL 4 (2 – 5 days post abrupt cessation)
Delirium tremens

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12
Q

PHARMACOLOGICAL TREATMENT WITHDRAWAL roh

A
  • Benzodiazepines ↑ GABA, ↓ withdrawal symptoms and prevent progression to severe symptoms, Anticonvulsant properties, Lorazépam, Diazépam, Chlordiazépoxide
  • Other options discussed :
  • Anticonvulsants:
  • Barbiturics
  • Antipsychotics
  • Betablockers / clonidine
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13
Q

LORAZEPAM +/-

A
  • Safer in elderly or hepatic failure
  • Predictable IM absorption
  • Intermediate onset of action
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14
Q

DIAZEPAM +/-

A
  • Faster onset of action
  • Longer half-life
  • Possible accumulation in elderly or hepatic failure
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15
Q

CHLORDIAZEPOXIDE +/-

A
  • Longer half-life
  • Possible accumulation in elderly or hepatic failure
  • Intermediate onset of action
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16
Q

SYMPTOM-TRIGGERED DOSING benzos

A
  • Requires that patients be monitored using the CIWA scale

* Benzodiazepines are administered based on CIWA score (>8)

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17
Q

FIXED DOSING benzos

A
  • Regularly schedule doses are gradually tapered over several days and include as needed doses
  • Risk of overmedicating
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18
Q

ANTICONVULSANTS roh withdrawal

A
  • Useful to treat seizures

* Do not prevent delirium trements

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19
Q

BARBITURICS roh withdrawal

A
  • For resistant withdrawals
  • Narrow therapeutic indexi
  • Risk of dependence, respiratory distress
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20
Q

ANTIPSYCHOTICS roh withdrawal

A
  • Useful to treat psychiatric symptoms associated with delirium tremens
  • ↓ convulsion threshold
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21
Q

BETA BLOCKERS / CLONIDINE roh withdrawal

A
  • Useful to treat a few symptoms (tachycardia, hypertension, tremors)
  • Do not prevent delirium tremens and convulsions
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22
Q

THIAMINE

A

Commonly depleted in people with alcohol use disorders
because of altered GI absorption or a diet lacking sufficient thiamine
v Prevention and treatment of Wernicke’s encephalopathy
v Dosing : 100 mg PO, IM, IV daily for at least 1 – 4 weeks

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23
Q

ALCOHOL USE DISORDER

PHARMACOLOGICAL TREATMENT

A
  • Naltrexone
  • Disulfiram
  • Acamprosate
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24
Q

NALTREXONE

A

mu opioid receptor antagonist
Blocks the pleasurable effects of alcohol
CONTRAINDICATIONS : opioid use within the last 7 days, acute hepatitis, severe hepatic impairment
SIDE EFFECTS : nausea, headache, insomnia, nervousness

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25
Q

DISULFIRAM

A

Irreversible inhibitor of ALDH
Resulting in accumulation of acetaldehyde after alcohol
consumption
SYMPTOMS OF THE INTENDED DISULFIRAM-ALCOHOL REACTION:
warmness and flushing of skin, ↑heart rate, palpitations, ↓blood pressure, nausea, vomiting, shortness of breath, sweating, anxiety, dizziness, blurred vision, confusion
(goal is to increase motivation to avoid alcohol consumption)
CONTRAINDICATIONS : psychosis, use of ethanol/metronidazole, severe
myocardial disease
SIDE EFFECTS : fatigue, drowsiness, metallic taste, hepatotoxicity (rare)

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26
Q

ACAMPROSATE

A 
NMDA receptor antagonist
Enhances GABA receptor activation and restores the
GABA/glutamate balance
CONTRAINDICATIONS : renal failure
SIDE EFFECTS : diarrhea, insomnia
27
Q

GHB

A

DESIRED EFFECTS : euphoria, sedation, relaxation, sexual disinhibition
ONSET OF ACTION : 15 minutes
DURATION OF ACTION : approximately 3 hours
COMMENTS : use in gyms, use in replacement of alcohol (less caloric)

28
Q

OPIOIDS types

A

NATURALS
• Morphine (StatexMD, M-EslonMD, KadianMD)
• Codeine
SEMI-SYNTHETICS
• Hydromorphone (DilaudidMD, Hydromorph ContinMD)
• Oxycodone (SupeudolMD, OxycontinMD, OxyneeoMD)
• Buprenorphine
• Heroin
SYNTHETICS
• Methadone
• Mepiridine (DemerolMD)
• Fentanyl (DuragesicMD)
• Tramadol (UltramMD, ZytramMD, RaliviaMD, TriduralMD)

29
Q

MECHANISM OF ACTION OPIOIDS

A 
mu receptor: 
AGONISTS
• Methadone
• Heroin
• Morphine, oxycodone, hudromorhone, etc.
PARTIAL AGONIST
• Buprenorphine
ANTAGONISTS
• Naloxone (only absorbed IM/IN) Naltrexone: only PO
30
Q

mu receptor:

A
  • Analgesia
  • Euphoria
  • Reward system
  • Sedation
  • Respiratory distress
  • Myosis
  • ↓ gastrointestinal motility
31
Q

INTOXICATION OPIOIDS

A
  • Myosis
  • Slurred speech
  • Impaired attention / memory
  • Drowsiness / coma
  • Death
32
Q

WITHDRAWAL OPIOIDS

A
  • Dysphoria
  • Nausea / vomiting
  • Myalgias
  • Lacrimation / rhinorrhea
  • Mydriasis / piloerection / sweating
  • Diarrhea
  • Fever
  • Insomnia
33
Q

PHARMACOLOGICAL TREATMENT INTOXICATION OPIOIDS

A

NALOXONE
mu opioid receptor antagonist
Reversal of opioid activity
Onset of action : very rapid (< 5 min)
Duration of action : depending on the route of administration (often need to be repeated)
Side effects : abrupt reversal of opioid intoxication (tachycardia, hypertension, etc.)

34
Q

OPIOID WITHDRAWAL AND

DETOXIFICATION PHARMACOLOGICAL TREATMENT

A
  • Methadone

- Buprenorphine (+/- naloxone)

35
Q

METHADONE

A

mu opioid receptor agonist
• less « peaks » vs heroin
• ↓ or cancel effect of other opioids if consumed (because has better affinity)
• No euphoria if taken by oral route of administration
DURATION OF TREATMENT :
- Detoxification : few days to 6 months
- Maintenance treatment : can be continued indefinitely
PHARMACOKINETICS
- Good bioavailability
- Long half-life (die)
- Metabolism via numerous CYP : interactions ++
ORAL SOLUTION
- Mixed with orange juice to avoid injection (high risk of addiction if injected)
- Patient must take it in front of the pharmacist
Pharmacodynamics:
- CNS depressants
- Rx causing QTc prolongation
SIDE EFFECTS:
- Similar to other opioids
- Sedation
- Transpiration
- Weight gain
- QTc prolongation
Useful for severe withdrawal (patients on a high dose of opioids)

36
Q

BUPRENORPHINE

A

mu opioid receptor partial agonist
• Reduces craving and withdrawal symptoms
• Administering buprenorphine to patient who are currently taking full
agonists can precipitate withdrawal à induction after patient presents
withdrawal symptoms
DURATION OF TREATMENT :
- 7 – 10 days for acute withdrawal phase
- Maintenance treatment : years or lifelong

37
Q

BUPRENORPHINE + NALOXONE

A
  • Decreases abuse potential of buprenorphine if crushed and injected
  • There is no effect from oral or sublingual naloxone secondary to poor absorption
    PHARMACOKINETICS
  • Long half-life (die)
  • Metabolism via CYP3A4 (less interactions than methadone)
    SCHEDULE
  • Many possible schedules when patient is stabilized (die, q2 days)
    SIDE EFFECTS
  • Better tolerated than methadone (less sedation)
  • Headache
  • Constipation
  • Nausea / vomiting
  • Sweating
    INTERACTIONS
  • Few pharmacokinetics interactions
  • Pharmacodynamics
  • CNS depressants
    • Useful for less severe withdrawal (higher risk of withdrawal symptoms if patients on a high dose of opioids)
38
Q

GUIDELINES opioid use disorder

A
  • Buprenorphine + naloxone if possible, for a safer use
  • Methadone if buprenorphine + naloxone not effective enough
  • Methadone if treatment with buprenorphine is not the best choice
39
Q

NICOTINE

A

Binds to nicotinic acetylcholine receptors (nAchRs)
ABSORPTION : Readily absorbed throughout the pulmonary alveoli
and passes directly into the blood avoiding first-pass metabolism
DISTRIBUTION : < 10 seconds to reach the brain
METABOLISM : primarily hepatic
ELIMINATION : half-life 1 – 2 hours

40
Q

SYMPTOMS INTOXICATION NICOTINE

A
  • Nausea, vomiting
  • Diarrhea
  • Dry mouth
  • Palpitations
  • Headache
  • Insomnia
41
Q

SYMPTOMS WITHDRAWAL NICOTINE

A
  • Depressed mood
  • Insomnia
  • Anger, irritability
  • Anxiety
  • Trouble concentrating
  • Restlessness
  • ↑appetite
42
Q

NICOTINE AND SCHIZOPHRENIA

A
  • Patient more vulnerable to effects of nicotine (dependence +)
  • Effect of nicotine can modulate symptoms / response to treatment
  • Mesolimbic pathway : DA cells receive direct nicotine cholinergic input that is stimulated by cigarette smoking, which likely mediates the reward experience
  • Long-term disrupt of these neurotransmitters
43
Q

PHARMACOLOGICAL TREATMENT nicotine

A

To reduce motivation to smoke / withdrawal symptoms

  • Nicotine replacement therapy (NRT)
  • Bupropion
  • Varenicline
  • Others : tricyclic antidepressants, clonidine
44
Q

NRT

A

Nicotine substitution that alleviates withdrawal,
including long-term cravings
NICOTINE PATCH 1 cig= 1 mg
- Slow liberation (16 – 24 hours)
NICOTINE GUM, LOZENGE, ORAL INHALER, SPRAY
- Fast acting
- Often used in combination with the patch to reduce cravings
SIDE EFFECTS
- Insomnia / nightmares (take off the patch before bedtime)
- Nausea
- Cutaneous irritation with the patch (fluticasone before application)
Contraindications : pregnancy, cardiac arrhythmias (RELATIVE!!)

45
Q

BUPROPION (ZYBAN)

A

Inhibits the recapture of NA/DA

  • Can be combined with NRT
  • Start approximately a week before smoking cessation
46
Q

VARENICLINE (CHAMPIX)

A 
Nicotinic receptors partial agonist 
- Partial stimulation prevent withdrawal symptoms /prevents nicotine to bind and reduce pleasure (or reward effect) associated with smoking
- Can be combined with NRT
SIDE EFFECTS
- Nausea
- Insomnia
- Neuropsychiatric effects? not really
47
Q

SMOKING CESSATION AND

SCHIZOPHRENIA

A

• More complex
• Auto-medication ?
• Cardiovascular and metabolic side effects of tobacco
• Risk of relapse
NICOTINE REPLACEMENT DURING HOSPITALIZATION
- Be aware of interactions : no more induction of CYP1A2

48
Q

E-CIGARETTE

A
  • Less nicotine than a traditional cigarette
  • Important variability between the products
  • Few clinical studies on effectiveness and long-term safety
  • Not recommended except if failure to other treatments
49
Q

MECHANISM OF ACTION cocaine

A

↑ monoamines (DA, NE)

50
Q

Clinical differences between amphetamine and cocaine

A
  • Speed of onset of effects is generally quicker with injected or smoke cocaine
  • Duration of effect longer with amphetamine
  • Cocaine = DA transporter blocker, whereas amphetamines also increase release of DA
51
Q

METHAMPHETAMINES

A
  • More powerful than amphetamines
  • Often found in synthetic drugs
  • Dependence ++ (if inhaled or injected)
  • Risk of psychosis
  • Consequences : cardiac, pulmonary, psychiatric, neurologic
52
Q

INTOXICATION stimulants

A 
• Nausea, vomiting, weight loss
• Tachycardia or bradycardia ↑ or ↓ BP
• Mydriasis
• Chills or diaphoresis
• Myalgia, hyperventilation, chest pain,
or arrhythmias
• Seizures, confusion, coma
• Psychomotor agitation/retardation
53
Q

WITHDRAWAL stimulants

A
  • Fatigue
  • Vivid, unpleasant dreams
  • Insomnia or hypersomnia
  • ↑ desire to eat
  • Psychomotor agitation/retardation
54
Q

PHARMACOLOGIC TREATMENT intoxication stimulants/

A
  • Symptomatic management (VS, hydration, calm environment)
  • Benzodiazepines : for agitation, anxiety, seizures, hypertension
  • Antipsychotics : if psychosis do not recover spontaneously
55
Q

INTOXICATION sx cannabis

A
  • Impaired motor coordination
  • Euphoria
  • Anxiety / social withdrawal
  • Sensation of slowed time
  • Impaired judgment
  • Xerostomia
  • Tachycardia
  • ↑ appetite
56
Q

sx cannabis withdrawal

A 
• Irritability, anger, aggression
• Nervousness
• Insomnia
• Anorexia or weight loss
• Restlessness
• Depressed mood
• Physical symptoms : fever, chills, headache,
tremors, diaphoresis, abdominal pain
57
Q

PHARMACOLOGIC TREATMENT INTOXICATION cannabis

A
  • Supportive care
  • Benzodiazepines : for anxiety
  • Antipsychotics : for psychosis
58
Q

PHARMACOLOGIC TREATMENT cannabis withdrawal

A
  • Topiramate ?

* Pregabaline ?

59
Q

Ecstasy MECHANISM OF ACTION

A

↑ 5-HT
Part of the disruptive drugs even if it has a stimulant effect
- Also stimulates the reward center : ↑ DA
A few hours after :
- ↓ 5-HT : withdrawal and depressive symptoms
Less addictive than other drugs

60
Q

SYNTHETIC DRUGS

A
  • Modification of the chemical formula of a drug to obtain a new molecule
  • Danger :
  • Attractive tablets / low price
  • We don’t know which substance is contained in the tablet
  • Variability between tablets
  • Consequence : unpredictable effects
61
Q

SYNTHETIC CANNABIS

A
  • Sold as incense « Not for human consumption »
  • Variety of spices, herbs or vegetal material
  • Unpredictable and powerful effect
62
Q

QUETIAPINE

A

MIXED WITH COCAINE : Q-Ball
To replace heroin in the combination Speedball
Maximise effect of cocaine and prevent dysphoria at the end of the dose
** More accessible than benzodiazepines, often prescribed as PRN, no legal control

63
Q

OVER-THE-COUNTER

A
  • Codein (cocktails : Purple Drank)
  • 1st generation antihistamines
  • Dextrometorphan
  • Decongestives (e.g. pseudoephedrine)
  • Laxatives
  • Ipeca
  • Caffeine

Pharmaco (11 decks)

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