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Neuropsychiatry and Psychopharmacology > L10 - Alcohol > Flashcards

L10 - Alcohol Flashcards

1
Q

What is cross tolerance?

A

 Response to a novel drug is reduced because of tolerance developed in response to a related drug
 Suggests that the two drugs affect a common nervous system target
Example: Barbiturates and benzodiazepines affect the inhibitory neurotransmitter GABA

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2
Q

3 types of tolerance?

A

Metabolic Tolerance
 Number of enzymes needed to break down alcohol may
increase

Cellular Tolerance
 Activities of brain cells may adjust to minimize the effect of alcohol

Learned Tolerance
 People can learn to cope with effects of alcohol and therefore may not appear to be drunk

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3
Q

when do alcohol withdrawal symptoms usually start?

A

several hours after last dose, and intensify over several days before subsiding.

These are just symptoms that are a swingback furtherthan that normal… overcorrection

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4
Q

What is addiction caused by

A

 Largely caused by the pleasurable effects of the drug
 The ability of a drug to act as a positive reinforcer in animals sustains those behaviours and are also highly correlated with the abuse potential of the drug in humans
 Short-acting substances have much greater potential for development of abuse or dependence (e.g. amphetamine, cocaine, some anxiolytics)

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5
Q

What kind of drugs have the most potential for abuse/dependence?

A

short-acting drugs

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6
Q

DSM-5 Alcohol use disorder

A

impairment or distress, as manifested by at least two of the following, occurring within a 12 month period:
1. Alcohol is often taken in larger amounts or over a longer period than was intended.
2. There is persistent desire or unsuccessful efforts to cut down or control, alcohol use
3. A great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects.
4. Craving, or a strong desire or urged to use alcohol.
5. Recurrent alcohol use, resulting in a failure to fulfil major role obligations
at work, school or home
6. Continued alcohol use despite persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol
7. Important social, occupational, or recreational activities are given up or reduced because of alcohol use.
8.Recurrent alcohol use in situations in which it is physically hazardous
9. Alcohol use is continued despite knowledge of having persistent or recurrent physical or psychological problems that is likely to have been caused or exacerbated by alcohol.
10.Tolerance, as defined by either of the following:
a) A need for markedly increased amounts of alcohol to achieve intoxication or desired effect.
b) A markedly diminished effect with continued use of the same amount of alcohol
11.Withdrawal, as manifested by either of the following:
a) Characteristic withdrawal syndrome for alcohol.
b) Alcohol (or a closely rented substance, such as a benzodiazepine) is taken to relieve or avoid withdrawal symptoms

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7
Q

DSM-5 Smptoms of alcohol intoxication

A

One (or more) of the following signs or symptoms developing during, or shortly after, alcohol use:
Slurred speech
Incoordination
Unsteady gait
Nystagmus.
Impairment in attentional memory Stupor or coma

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8
Q

Mechanism of action for alcohol?

A

 Stimulate GABA receptors (reduces tension)
 Increases dopamine/serotonin levels (pleasurable
aspects of intoxication)
 Inhibits glutamate receptors (cognitive actions)

is absorbed from stomach into the blood

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9
Q

What does peak BAC depend on

A

 Peak blood alcohol concentration (BAC) depends on:
Amount and alcohol concentration of beverage
Rate of drinking
Food consumption and composition
Gastric emptying and gastric metabolism Hepatic first pass

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10
Q

What are the CNS effects of alcohol

A

Alcohol is a CNS depressant
But a transient stimulant at the lowest
doses

(1-2 drinks - stimulant, 6-7 drinks - depressant)

Apparent stimulatory effects result from depression of inhibitory control mechanisms in the brain
Characteristic response: euphoria, impaired thought processes, decreased mechanical efficiency

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11
Q

Which area of the brain does alcohol effect?

A

CEREBELLUM!!

anterior superior vermis.

anterior and superior cerebellum is affective, gives characteristic cerebellar signs of alcoholism, wide based high stepping gait.

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12
Q

What are some physical signs of alcohol abuse?

A
  • facial puffiness
  • dilated capillaries
  • facial flush
  • nail infection
  • easy brusing
  • sweating
  • tremors
  • rhinophyma (big nose?)
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13
Q

Some signs of alcohol withdrawal?

A

3-12 hours - tremors, shaking of body

3-12 hours - hallucinosis

12-48 hours - seizures

3-4 days - delirium tremens (confusion, agitation, sleep disorder).

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14
Q

what BAC is intoxication

A

0.08g/l

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15
Q

Concentration effect relo?

A

see slide

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16
Q

what is delirium tremens?

A

withdrawal delirium

 generally between 48-72 hours
 altered mental status, hallucinations, marked autonomic
instability
 life-threatening

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17
Q

What are the earliest signs of ETOH withdrawal

A

 anxiety, irritability, tremor, headache, insomnia, nausea,

tachycardia, hyperthermia, hyperactive reflexes

18
Q

What is cross tolerant with alcohol

A

BENZOS - gaba agonist

19
Q

What drugs are used to help with alcohol withdrawal?

A

Benzos - to reduce risk of seizures, and provide sedation and comfort.

Anticonvulsant - to reduce risk of seizures and kindling. helpful for protracted, longer, withdrawal

Thiamine supplementation - risk thiamine deficiency - wernicke/korsakoff.

20
Q

What is wernicke’s encephalopathy

A

 Severe deficiency of thiamine vitamin (B1)
 Characterised by the classic triad of symptoms:
 nystagmus, gaze palsies (96%)  ataxia of gait (87%)
 global confusional state (82%)  but also
peripheral neuropathy (82%)
malnutrition (84%)

21
Q

Neuropathology of WKS?

A

 WKS produces lesions in:
 the walls of the third ventricle and periaqueductal region the floor of the fourth ventricle
certain thalamic nuclei
the mamillary bodies
the terminal portion of the fornices
anterior superior vermis of the cerebellum
 Lesions rarely seen in:
 the cerebral cortex, corpus striatum, subthalamic and septal regions, cingulate gyri or hippocampi

22
Q

avitaminosis?

A

A result of alcoholism - when food is replaced by drink.

decreased absorption of thiamine and decreased storage and use of thiamine by liver.

23
Q

Different types or ARBI’s?

A
  • wernicke’s encephalopathy (b1 deficiency)

- wernicke-s korsakoff syndrome (aka korsakoff psychosis)

24
Q

What is wernicke’s encephalopathy?

A

arbi
b1 deficiency

Characterized by nystagmus, abducens and conjugate gaze palsies, ataxia, and mental disturbance (confusional state)

25
Q

What is wernicke-korsakoff syndrome

A

(aka Korsakoff Psychosis or Korsakoff’s amnesia)
Retentive memory impaired out of proportion to other cognitive functions (chronic manifestation of Wernicke disease)
 With treatment, recovery occurs in less than 20% of patients

26
Q

What are thought to be the three predominant consequences of alcoholism on the brain?

A
  1. Premature aging/whole brain
  2. Right brain
  3. Frontal lobes
27
Q

Which hemisphere of the brain is more vulnerable to alcoholism?

A

Right hemisphere is more vulnerable to the effects of alcoholism than the left hemisphere
 Impairments in visuospatial functioning and
emotional processing
 Emotional processing deficits also may be due to abnormalities in other brain regions (e.g., limbic system, frontal lobes)

28
Q

What happens to the frontal lobes in alcoholism

A

 Frontal lobes show increased susceptibility to alcoholism-related damage
Evidence from post-mortem neuropathological studies (Harper, 1998) and neuroimaging of living patients (Sullivan, 2000)
Also behavioural and neuropsychological deficits in executive functioning seem to be prominent in both currently-drinking and recently-detoxified alcoholics (e.g., Bechara et al., 2001)

29
Q

What neurocognitive disorders are associated with ETOH

A
  • alcohol (major nCD) non-amnestic-confabulatory type i.e. well-fed alcohol
  • alcohol (major nCD) amnestic-confabulatory type i.e. wernicke-korsakoff
30
Q

What are neurotoxic changes from ETOH from

A

cell loss
volume loss
synaptic plastic changes

association between alcohol use and dementia

31
Q

Alcohol-induced brain injury ?

A

 Localized loss of neurons and their axons, superior frontal cortex (= gray matter, GM)
 Widespread shrinkage of neuronal cell bodies, in frontal, cingulate, and motor cortices
 Reduced synaptic branching and dendritic pruning
 Loss of white matter, demyelination (Harper, Kril et al. 1992-2001)

 Enlarged ventricles and sulci
 Brain tissue loss, especially frontal
 Smaller size and other abnormalities of
subcortical structures, pons, hippocampus, and cerebellum
 Dose-response relationship
 Unclear if magnitude of injury similar in men
and women
 Smaller tissue volumes in older alcoholics

32
Q

reversibility of neuropsychological and radiological impairments?

A
  • recovery is likely, some repor only partial
  • cognition gets better with extended abstinence

this is through glial regeneration, synaptic plasticity.

33
Q

What does the amnestic syndrome look like

A

 an inability to learn new material
 a normal STM
 retrograde amnesia with a temporal gradient
improved by direct questioning
 worse as move closer to the present in time
no time tags to events
 preservation of skills and habits, and procedural memory
 confabulation
 decreased initiative and spontaneity, together with blunting of affect

34
Q

areas of cog impairment for alcoholics?

A

 Problem solving
 Short term memory
- anterograte worse than retrograde, visual worse than verbal
 Visuospatial ability
 Balance and postural stability
 Similar impairments for alcoholic men and women

35
Q

medications for alcohol treatment?

A

disulfiram
naltrexone
acamprosate

36
Q

disulfiram

A

a medication for alcohol treatment - aka antabuse

 Inhibits aldehyde dehydrogenase and dopamine beta
hydroxylase
 Aversive reaction when alcohol ingested- vasodilatation, flushing, N/V, hypotenstion/ hypertension, coma / death
 Hepatotoxicity - check LFT’s and hep C
 Neurologic with polyneuropathy / paraesthesias that slowly
increase over time and increased risk with higher doses
 Psychiatric side effects - psychosis, depression, confusion, anxiety
 Dermatologic rashes and itching
 Watch out for disguised forms of alcohol - cologne, sauces, mouth wash, OTC cough meds, alcohol based hand sanitizers, etc

37
Q

Naltrexone?

A

medication for alcohol treatment

 Opioid antagonist thought to block mu receptors reducing
intoxication euphoria and cravings
 Hepatotoxicity at high doses so check LFT’s

38
Q

Acamprosate

A

aka campral

 Unknown MOA but thought to stabilize neuron excitation and inhibition - may interact with GABA and Glutamate receptor - cleared renally (check kidney function)

39
Q

What are treatment options for alcohol use disorder?

A 
Medications
 support, education, skills training, psychiatric and
psychological treatment, AA
CBT - Contingency-Management therapy
- relapse prevention
- motivational interventions
40
Q

What is Contingency-Management Therapy?

A

CBT for alcohol use disorder
 Patient and family reinforce behaviours inconsistent with drinking
 e.g., avoiding places associated with drinking
 Teach problem drinker how to deal with uncomfortable situations
 e.g., refusing the offer of a drink

Neuropsychiatry and Psychopharmacology (12 decks)

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