addiction Flashcards

1
Q

What is the epidemiology of alcohol addiction?

A
  • UK prevalence = 7% males, 2% females
  • 25% of emergency admissions are alcohol related
  • Females have a stronger genetic preposition so are more likely to suffer from the physical complications
  • Prevalence greater in deprived areas
  • Prevalence lower in east Asians - Asian flush, particular isoenzyme of alcohol dehydrogenase leads to accumulation of acetaldehyde
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2
Q

What are the genetic risk factors for alcohol addiction?

A

7x increased risk if first degree relative has alcohol misuse.
o The genetic influence is thought to exert itself through heritable personality traits or through single genes that modulate the body’s response to alcohol.

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3
Q

What are the neurochemical risk factors for alcohol addiction?

A

 Alcohol increases GABA, dopamine and serotonin
o Euphoric effects
 In alcohol dependence there is a compensatory upregulation of glutamate to compensate for the (GABA- ergic) CNS depressant effects of alcohol.
o Suddenly withdrawing alcohol therefore leads to symptoms of CNS hyperexcitability.

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4
Q

What are the psychological theories behind alcohol addiction?

A

 There is no such thing as an ‘alcoholic personality’, although anxiety disorders, borderline personality disorder, antisocial personality disorder, and a history of childhood conduct disorder are particularly associated with alcohol misuse.
 According to cognitive-behavioural theories, alcohol dependence may result from positive reinforcement (seeking out the pleasant effects of alcohol) and negative reinforcement (avoiding the negative effects of alcohol withdrawal), from a conditioned response to one or more circumstances (e.g. a pub or nightclub), or from modelling the drinking behaviour of relatives, peers, and ‘celebrities’.
 According to psychodynamic theories, alcohol dependence may result from maternal deprivation, childhood sexual abuse, or unconscious gains resulting from intoxication and personal damage caused.

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5
Q

What are the social risk factors for alcohol addiction?

A

 Life events: life events such as separation, bereavement, or loss of employment
 Occupation: certain occupational groups are at a higher risk of alcohol dependence
o E.g. publicans and bar staff, salesmen, entertainers, journalists, and doctors.
o Generally speaking, alcohol dependence is more prevalent in the unskilled manual social class and in the unemployed.
 Population levels of alcohol consumption:
o can be controlled through three factors: price, availability, and social attitudes to alcohol.

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6
Q

What comorbidities are common in alcohol addiction?

A

often occurs secondary to other psychiatric or medical disorders

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7
Q

What are the core features of alcohol dependence?

A
  1. Compulsion to drink
  2. Primacy of drinking over other activities
  3. Stereotyped pattern of drinking
    (e. g. narrowing of repertoire)
  4. Increased tolerance to alcohol
  5. Repeated withdrawal symptoms
  6. Relief drinking to avoid withdrawal symptoms
  7. Reinstatement after abstinence

DIAGNOSIS = 3/7 FEATURES OCCURRING ANYTIME DURING 12-MONTH PERIOD

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8
Q

What are alcohol withdrawal symptoms and when do they occur?

A

• Usually occur after several years of heavy drinking
• Range from mild anxiety and sleep disturbance to life threatening delirium tremens
• Occurs first thing in morning
• Common symptoms
o Agitation, tremor ‘the shakes’, nausea and retching

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9
Q

What is the acute management of alcohol withdrawal?

A

• Prevention and treatment involves:
o benzodiazepines (lorazepam)
o correction of fluid and electrolyte imbalances
o treatment of concurrent infections
o parenteral multivitamin injection (PABRINEX)
 THIAMINE – Pabrinex (water-soluble vitamins C (ascorbic acid), B1
(thiamine), B2 (riboflavin), B3 (nicotinamide) and B6 (pyridoxine).
• Prevent Wernicke’s encephalopathy
• Delerium Tremens often complicates other medical emergencies such as infection and injury, and
fever/signs of shock are poor prognostic signs.
• It’s untreated mortality rate is ~10%.

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10
Q

What is delerium tremens, when does it occur and what are the characteristics?

A
  • medical emergency that occurs in about 5% of alcohol dependent people at 1-3 days after stopping alcohol.
    o It is relatively common - especially in hospital inpatients.
  • It is a delirious disorder characterised by:
    o Clouding of consciousness
    o Disorientation in time and place
    o Impairment of recent memory
    o Fear, agitation and restlessness.
    o Vivid hallucinations (most commonly visual) and delusions (most commonly paranoid).
    o Insomnia
    o Autonomic disturbances (tachycardia, hypertension, hyperthermia, sweating, dilated pupils).
    o Coarse tremor
    o N&V
    o Dehydration and electrolyte disturbances
    o Seizures.
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11
Q

What are the differentials for delerium tremens?

A

Hypoglycaemia, drug overdose and other causes of delirium (e.g. UTI).
DTs should be differentiated from alcohol hallucinations and Wernicke’s encephalopathy.

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12
Q

What is alcohol hallucinosis?

A

Auditory hallucinations – first fragmentary sounds then derogatory voices, usually 3rd person.

Can persist several months after abstinence and in some cases, leads to secondary delusions.

Notoriously unresponsive to antipsychotics.

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13
Q

What is wernickes encephalopathy and what is it caused by?

A

• Wernicke’s encephalopathy is a medical emergency.
• Results from thiamine (vit B1) deficiency
o Most commonly due to alcohol dependence but can be starvation, malabsorption, hyperemesis and CO poisoning

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14
Q

What are the symptoms of wernickes encephalopathy?

A

• Classic triad:
o Confusion
o Ataxia
o Ocular palsy

• Acute onset, other Sx include:
o impaired consciousness and confusion, episodic memory impairment, ataxia, nystagmus, abducens and conjugate gaze palsies, pupillary abnormalities, and peripheral neuropathy

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15
Q

What is the treatment for wernickes encephalopathy?

A
  • Treatment involves parenteral thiamine (pabrinex), but only 20% of suffers recover, and 10% die from haemorrhages in the brainstem and hypothalamus.
  • The remainder go on to develop Korsakov’s syndrome (amnestic syndrome)
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16
Q

What is korsakoffs syndrome and what symptoms do you get?

A

• An irreversible amnestic syndrome characterised by:
o Prominent impairment of recent memory
o A lesser extent remote memory

  • Resulting from neuronal loss, gliosis, hemorrhage in the mamilliray bodies and damage to the dorsomedial nucelus of the thalamus
  • Confabulation - falsification of memore in clear consciousness may be a marked feature but immediate recall, perception and other cognitive functions are usually intact
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17
Q

What is the cage questionnaire?

A

Rapid screening questionnaires such as the CAGE questionnaire may be useful in this context,
although they are not as sensitive as a comprehensive alcohol risk assessment.
 C Have you ever felt you should Cut down on your drinking?
 A Have people Annoyed you by criticising your drinking?
 G Have you ever felt bad or Guilty about drinking?
 E Have you ever taken a drink first thing in the morning (Eye opener)?
Two or more positive replies are said to identify alcohol misuse.

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18
Q

What should you do if patient drinking habits are difficult to assess?

A

take an informant history or ask the patient to keep an alcohol diary.

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19
Q

When might blood tests be useful in alcohol intake and which ones would you do?

A

helpful in augmenting the findings of screening questionnaires such as the CAGE questionnaire, and in monitoring progress.

• Blood tests may be useful in uncovering misuse and monitoring progress:
o GGT is raised in about 80% of heavy drinkers
o ALP in about 60%
o MCV in about 50%
 Of the three tests, MCV has the highest specificity for alcohol misuse but, due to the long half-life of red blood cells (120 days), may remain elevated for a long time after the patient has stopped drinking.

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20
Q

What is the very early intervention for alcohol misuse?

A

delivered in primary care and involves simple advice and support, and appraisal of current medical, psychological, and social problems.
o MOTIVATIONAL INTERVIEWING
 help to recognize problem; help to resolve ambivalence and encourage positive change and belief in ability to change; adopting a persuasive and supportive position rather than being argumentative
o For homeless patients consider offering residential rehabilitation for a maximum of 3 months. Then help the service user to find stable accommodation before discharge

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21
Q

What is the treatment for someone who is dependent on alcohol?

A

DETOXIFICATION is required.
o Over 15 units/day or >20 on AUDIT

o This involves a reducing course of a benzodiazepine in lieu of alcohol
 e.g. chlordiazepoxide 20 mg QDS reducing daily over 5–7 days and supplemented by thiamine 200 mg OD (often in the form of a multivitamin preparation).
• The starting dose of chlordiazepoxide is estimated by units of alcohol intake per day (or SADQ score) e.g. 30 U/day  30 mg QDS
 Lorazepam preferred over chlordiazepoxide in patients with hepatic failure to avoid the risk of increased sedation

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22
Q

When should hospitalisation be considered in detox?

A

o Detoxification can usually be carried out in the community either by the GP practice or the local substance misuse service, but hospital admission should be considered if the patient has a comorbid medical or psychiatric disorder (including drug misuse), a history of convulsions or delirium tremens, or a lack of social support.

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23
Q

How can you enhance abstention from alcohol in patients?

A

maintenance treatments such as the opiate antagonist naltrexone (not currently licensed in the UK), acamprosate (Campral), and disulfiram (Antabuse).

 Acamprosate is an ‘anticraving’ drug that enhances GABA neurotransmission and therefore mimics the CNS depressant effects of alcohol.

 Disulfiram on the other hand is an alcohol-sensitising deterrent drug that blocks the oxidation of alcohol by irreversibly inhibiting the enzyme aldehyde dehydrogenase, leading to an accumulation of acetaldehyde and associated symptoms of flushing, palpitations, headache, nausea, and a choking sensation (it can be thought of as a chemical form of aversion therapy). For this reason, it should not be started until the breath alcohol has returned to zero. It is contra- indicated in hypertension, coronary artery disease, and cardiac failure as it can cause cardiac arrhythmias; other side-effects include sedation, constipation, and halitosis (bad breath).

• Maintenance treatments require close supervision, often by a nominated ‘supervisor’ such as the patient’s spouse, and are not a substitute to psychosocial interventions.

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24
Q

What psychosocial interventions should be used for alcohol abusers?

A

community alcohol services, Alcoholics Anonymous, supportive psychotherapy (including supportive psychotherapy for carers), cognitive-behavioural therapy, and marital and family therapy.

• Social skills training is an effective component of substance misuse treatment programmes
o aims to impart the skills needed to function more effectively in social situations, and involves a variety of interventions such as role playing in groups (e.g. declining the offer of an alcoholic drink, or going to a bar and ordering a non-alcoholic drink), assertiveness training, and problem solving skills.

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25
Q

What is an opioid?

A

any agent that binds to opioid receptors, including endogenous opioid peptides, opium alkaloids such as morphine and codeine, semi-synthetic opioids such as heroin and oxycodone, and fully synthetic opioids such as pethidine and methadone.

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26
Q

What is an opiate?

A

natural opium alkaloids and the semi-synthetic opioids derived from them.

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27
Q

What are the possible routes of administration for opioids?

A

oral, intramuscular, intra-venous, subcutaneous (‘skin popping’), sniffed (‘snorted’). Heroin can also be inhaled (‘chasing the dragon’).

28
Q

What is the mechanism of action for opioids?

A

act at specific opioid receptors. Morphine and heroin are relatively selective for the μ- opioid receptor subtype. As heroin is only detectable in the urine for 1–2 days, taking heroin rather than cannabis gives patients and prisoners a better chance of evading random urine drug screens.

29
Q

What effects can opioids have?

A

euphoria, analgesia, respiratory depression, constipation, anorexia, loss of libido, pruritus, pinpoint pupils (miosis). Tolerance develops rapidly but diminishes as soon as the drug is stopped, leading to a potentially fatal accidental overdose if the drug is restarted at the previous dose, e.g. after the patient is discharged from hospital.

30
Q

What happens in opioid overdose?

A

respiratory depression and death

31
Q

What withdrawal symptoms do you get from opioids?

A

intense craving, restlessness, insomnia, muscle pains, tachycardia, dilated pupils, running nose and eyes, sweating, piloerection (hence the expression ‘going cold turkey’), abdominal cramps, vomiting, diarrhoea. These symptoms begin about 8–12 hours after the last dose, peak at 36–72 hours, and subside over 7–10 days.

32
Q

How do you manage opioid detoxification?

A

stop the drug and prescribe reducing doses of a substitute drug such as methadone or buprenorphine (first ensure that the person really is using opioids and not just angling for a substitute drug to misuse or sell off).

Provide psychological support, e.g. abstinence/rehabilitation programme and social support.

Clonidine and lofexidine are centrally acting α2 agonists that can also be used in detoxification.

Naltrexone, a long-acting opioid antagonist, can be used to help prevent relapses. However, it induces withdrawal if the patient is still dependent

Harm reduction and maintenance therapy: if abstinence is unrealistic, consider substitute prescribing of oral methadone or buprenorphine with the aim of reducing injecting, stabilising drug use and lifestyle, and reducing crime. Needle exchanges and drug education programmes are also good practice, and may lead the addict to consider detoxification

33
Q

How do you treat opioid overdose?

A

cardiorespiratory support, IV naloxone. Upon regaining consciousness the addict may not be pleased that you have ruined his or her hit, but the half-life of naloxone is shorter than that of heroin and, unless you bear this in mind and use a continuous infusion, he or she may soon collapse again.

34
Q

What are compounds related to cocaine?

A

crack or freebase cocaine, speed-ball (a mixture of cocaine and heroin). Crack cocaine, so named for the sound it makes upon burning, produces a short-lived high that especially encourages dependence.

35
Q

what are the possible routes of administration for cocaine?

A

inhaled (snorted), injected, smoked (crack cocaine). Inhalation can cause perforation of the nasal septum.

36
Q

What is the mechanism of action for cocaine?

A

blocks reuptake of serotonin and catecholamines, especially dopamine.

37
Q

What effects can cocaine have?

A

euphoria, increased confidence and energy, decreased inhibition, decreased need for food or sleep, dilated pupils, tachycardia, hypertension, hyperthermia. In higher doses, visual and auditory hallucina- tions, paranoid ideation, aggression – increased dopamine mimics schizophrenia. Formication (‘cocaine bugs’) describes the feeling of having insects crawling under the skin. Violence is common.

38
Q

What symptoms can cocaine overdose cause?

A

tremor, confusion, seizures, stroke, cardiac arrhythmias, myocardial infarction, myocarditis, car- diomyopathy, respiratory arrest.

39
Q

What are the withdrawal symptoms from cocaine?

A

generalised malaise, intense craving, dysphoria, anxiety, irritability, agitation, fatigue, hypersomnolence, vivid and unpleasant dreams, suicidal ideation.

40
Q

How do you manage cocaine abuse?

A

cognitive behavioural therapy and treatment of comorbid psychiatric illness. In acute intoxication consider benzodiazepines and antipsychotics to treat symptoms, and treat complications.

41
Q

What is the mechanism of action for amphetamines?

A

blocks reuptake of noradrenaline and dopamine. Note that amphetamines are used in the treatment of narcolepsy and hyperactivity disorders.

42
Q

What are the effects of amphetamines?

A

over-activity, talkativeness, insomnia, anorexia, dry lips, mouth, and nose (frequent lip licking), pupil dilatation (mydriasis), tachycardia, hypertension, hyperthermia. Adverse effects include dysphoria, anxiety, irritability, insomnia, and confusion. Prolonged use in high doses may lead to stereotyped repetitive behaviour and paranoid psychosis that is almost impossible to differentiate from schizophrenia.

43
Q

what does amphetamine overdose cause?

A

cardiac arrhythmias, severe hypertension, stroke, circulatory collapse, seizures, coma.

44
Q

What symptoms do you get in amphetamine withdrawal?

A

dysphoria and decreased energy, and sometimes depression, anxiety, fatigue, and nightmares. There may be intense craving and suicidal ideation.

45
Q

How do you manage amphetamine abuse?

A

cognitive-behavioural therapy, treat comorbid psychiatric illness. In acute intoxication con- sider benzodiazepines and antipsychotics to treat symptoms. Treat complications.

46
Q

How long do amphetamines remain in the urine for?

A

72 hrs

47
Q

How does Ecstasy work?

A

increases serotonergic, dopaminergic, and noradrenergic neurotransmission. High lasts 4–6 hours.

48
Q

What effects does ecstasy have?

A

euphoria, sociability, intimacy, heightened perceptions, loss of appetite, nausea, tachycardia, hyper- tension, hyperthermia, sweating, dehydration, teeth grinding (bruxism).

49
Q

What does ecstasy withdrawal cause?

A

dysphoria and fatigue (‘coming down’), which limits abuse potential

50
Q

how do you manage ecstasy abuse?

A

education to avoid hyperthermia by replacing fluids and taking breaks from dancing (ecstasy is typically used in nightclubs or at rave parties).

51
Q

What are related compounds to LSD?

A

other synthetic hallucinogens include dimethyltryptamine and ecstasy. Naturally occurring hallucinogens include psilocybin (magic or psychedelic mushrooms) and mescaline (peyote cactus). In the UK the Drugs Bill 2005 made psychedelic mushrooms a class A drug.

52
Q

How does LSD work?

A

partial agonism at serotonin 5-HT2A receptors

53
Q

What effects does LSD have?

A

pupil dilatation, tachycardia, hypertension, mood changes (euphoria, distress, or anxiety), distortion or intensification of sensory experience, synaesthesia (cross-referencing of the senses, e.g. seeing sounds, hearing colours), and in some cases distortion of body image. Psychological effects last from 8 to 14 hours. ‘Bad trips’ occur if the user is not relaxed, e.g. if he or she has had a recent argument or is feeling resentful, or if the setting is overly stimulating.

54
Q

What does LSD overdose cause?

A

overdose is rare but may result in nausea and vomiting, autonomic overactivity, hyperthermia, coma, and respiratory arrest.

55
Q

What symptoms do you get in LSD withdrawal?

A

a withdrawal syndrome has not been described, although a minority of users experience disturbing flashbacks. Tolerance can occur but dependence is rare.

56
Q

What is the mechanism of action for cannabis?

A

acts on a specific cannabinoid receptor in the CNS. The endogenous ligand for this receptor is anandamide.

57
Q

What are the effects of cannabis?

A

variable according to dose and circumstances; the pre-existing mood tends to be exaggerated
o include heightened aesthetic experiences, altered perception of time and space, impaired short-term memory, attention, and motor skills, reddening of the eyes, irritation of the respiratory tract, dry mouth, and tachycardia
o Adverse effects include anxiety, paranoid ideation, gynaecomastia, reduced spermatogenesis, and carcinoma of the bronchus.
o Cannabis use has been linked with an increased risk of psychotic disorders, conferring an approximate two-fold increase in an individual’s relative risk of subsequently developing schizophrenia. No direct mechanism for this link has been identified.

58
Q

What symptoms do you get in cannabis withdrawal?

A

mild and short-lived symptoms of restlessness, irritability, nausea, anorexia, and insomnia. Tolerance and dependence can occur but are both uncommon.

59
Q

What is the mechanism of action for benzodiazepines?

A

benzodiazepines act at the GABAA–BDZ receptor complex to enhance the inhibitory action of GABA.

60
Q

What are the effects of benzos?

A

anxiolytic, hypnotic, anticonvulsant, muscle relaxant, and amnesic properties. Tolerance develops rapidly. Dependence is common: about one-third of patients taking benzodiazepines for more than six months develop dependence.

61
Q

What symptoms do you get in benzo overdose?

A

oversedation, coma, death. Additive effects with other drugs, including opiates and alcohol

62
Q

What symptoms do you get in benzo withdrawal?

A

anxiety, irritability, tremor, disturbed sleep, altered perception and, rarely, depression, psychosis, seizures, and delirium tremens. In some cases the withdrawal syndrome may be prolonged for several months.

63
Q

How do you manage benzo overdose?

A

flumazenil

64
Q

How do you manage benzo detox?

A

switch from benzodiazepines with a short half-life to benzodiazepines with a long half- life (e.g. diazepam) and taper off over a period of several weeks or months.
 Prevention: iatrogenic dependence is the commonest form of benzodiazepine dependence, so restrict the use of these drugs and prescribe them for short- term use only

65
Q

What are the effects of sniffing volatile substances?

A

similar to those of alcohol, but more rapid onset. Euphoria, disorientation, nausea, vomiting, blurring of vision, slurring of speech, incoordination, staggering gait, hallucinations. Adverse effects include cardiac arrhythmias and respiratory depression leading to sudden death. There is a high risk of trauma, asphyxia, and aspiration pneumonia. Chronic misuse may lead to organ damage, peripheral neuropathy, and CNS neurotoxicity.