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Neuro > Psych pt ii > Flashcards

Psych pt ii Flashcards

1
Q

ICD 10 Dependence Syndrome

A

Past year, 3 or more of the following present:
Strong DESIRE or compulsion to take, difficulties CONTROLLING in onset, termination, or levels of use .
Physiological WITHRDRAWAL
Evidence of TOLERANCe
Progress NEGLECT of alternative pleasures or interests
Persisting with substance use despite clear evidence of overtly harmful consequences.

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2
Q

Dependence syndrome - bio aspect of biopsychosocial model

A

Bio - Strong familial aggregation, ie seen in alcohol abuse (3-5x more frequent in 1st family). Evidence that alcohol and drug dependence share a genetic liability with each other.
Genes which confer risk: Proteins inv in alcohol metabolism, proteins in neurotransmission, GABAa receptor. Cholinergic system, endogenous opioid system, endogenous cannabinoid system.

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3
Q

Cloninger’s Tridimensinoal Personality theory

A

Personality comprises three genetically independent dimensions, extended to alcoholism (Bio part of dependence syndrome)
There are two types
Type 1: Novelty Seeking (NS) Low, Harm avoidance (HA) High, Reward dependence (RD) High.
Type 2; NS high, HA low, RD low

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4
Q

Addictive drugs that block DA transporters ( to increase dopamine)

A

Cocaine, amphetamines - block DA transporters to increase levels of dopamine

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5
Q

Drugs that enhance DA release to exert increase of DA effect

A

Nicotine

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6
Q

Addictive drugs that increase DA by inhibiting GABAergic suppression of VTA

A

heroin, morphine

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7
Q

Drugs that lead to physiological dependence

A

Sedatives and opiates, and nicotine
Sedatives incl - alcohol, barbiturates, benzodiazepines, cannabinoids
Opiates - heroin, morphine, methadone.

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8
Q

hallucinogenic drugs

A

Incl ketamine, LSD, phencyclidine, psilocybin, solvents

Psychological/psychic dépendance

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9
Q

Stimulant drugs

A

Incl amphetamines, cocaine, ecstasy

  • psychological/psychic dépendance - experience of impaired control over drug/substance use
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10
Q

Symptoms of alcohol withdrawal

A

Within 24 hours: tremor, hyperhydrosis, nausea/vomiting, insomnia
Post 24 hours: withdrawal seizures, ie generalised tonic-clonic
Post 48 hours to 72 hours: Delirium tremens, agitation, confusion, hallucinations, tachycardia, hypertension, hyperthermia

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11
Q

Neurotransmitter effects of alcohol withdrawal - noradrenaline DA and Glu

A

Alcohol decreases NE. Withdrawal effect is an increase in NE - hyperhydrosis, tachycardia, hypertension, tremor, nausea

Short term alcohol increase DA, but long term decreases. So withdrawal symptoms are an increase in DA - psychotic symptoms ie hallucinations

Alcohol decreases Glu. So withdrawal: have an increase, get epileptic seizures.

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12
Q

Symptoms of Opiate withdrawal

A

Severe flu-like syndrome
Rhinorrhoea, sneezing, abdominal cramping, leg cramping, piloerectino, nausea, vomiting, diarrhoea, dilated pupils.
NO hallucinations, seizures or altered mental status.

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13
Q

Treatment of alcohol withdrawal symptom of seizures

A

Diazepam - GABAa receptor modulator (promoting inhibitions, taking excess glutamate away)

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14
Q

Treatment of sympathetic side effects of alcohol withdrawal

A

Clonidine - partial alpha 2 agonist. Ie reuptake of norepinephrine, decreased effects

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15
Q

Treatment of psychotic symptom side effects of alcohol withdrawal

A

Haloperidol - high affinity D2 antagonist

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16
Q

‘Cold’ Detox - opiate withdrawal

A

Not life-threatening, provide symptomatic medication for nausea, diarrhoea, tachycardia./HTN
Symptômes peak at 2-3 days
Last no longer than 5-7 days, though hypersomnia can continue for weeks

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17
Q

‘Warm detox’ opiate withdrawal

A

Substitution of opiates with methadone
Réduction of methadone dose over ~ 3 weeks.
provide symptomatic meds for nausea, diarrhoea, tachycardia/HTN
Problem - long stay on closed ward, potential chance for relapse?

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18
Q

Etiology of drug use, 5 drug induced effects on brain function

A
  1. Stimulate reward circuitry. (Direct or indirect) - signal to repeat. Ie DA Mesolithic pathway - VTA to Nucleus accumbens.
  2. Reward path stimulation affects prefrontal cortex functioning, altering self-control.
  3. Can cause brain changes resulting in physical withdrawal symptoms. Discomfort drives relapse.
  4. Repeated use decrease availability of DA - prolonged anhedonia, triggers relapse (ie PROTRACTED ABSTINENCE SYNDROME)
  5. Drug use paired with environmental/internal cues - physiological changes trigger drug seeking. Ie conditioned stimuli.
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19
Q

Key assessment questions (alcohol screeing in primary care_

A

CAGE questions.- do you feel the need to CUT back, do you get ANNOYED with others for criticising your drinking, do you ever feel GUILTY about drinking, do you ever need an EYE opener (hare of the dog?) - Yes to >/2 highly suspicious of addiction.

FOY questions - has concern about your drinking been expressed by your family, others, or yourself? - yes to one highly suggestive of addiction.

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20
Q

Vaccination theory for drug addiction

A

Following vaccination, when substance used, antibodies bind to the drug, making it too large to enter the CNS. Thus, drug does not have reinforcing effects.

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21
Q

DSM 5 Substance Intoxication

A

Development of a reversible substance-specific syndrome due to recent ingestion of a drug. Syndrome due to drug effects on CNS and causes significant maladaptive behaviour or psychological changes

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22
Q

Alcohol Intoxication (DSM 5)

A

Significant Maladaptive psychological/behavioural change (ie impaired judgment PLUS >/1 of

  1. Slurred speech 2. Uncoordination 3. Unsteady gait 4. Nystagmus
  2. Impaired attention or memory 6. Stupor or coma
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23
Q

Substance intoxication varies within and between persons based on

A

Dose, chronicité of use, purity of drugs, polydrug use, tolerance, time since last use, environment drug consumed in, expectations of user

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24
Q

Substance withdrawal DSM 5

A

Substance specific syndrome following cessation of a substance after heavy/prolonged substance use
Syndrome causes significant distress or impairment of functioning

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25
Q

Alcohol withdrawal DSM 5

A

> /2 of:
1. ANS hyperactivity 2. Hand tremor 3. Insomnia 4. Nausea 5. Hallucinations/illusions 6. Psychomotor agitation 7. Anxiety 8. Generalized seizures

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26
Q

Substance Use Disorder (SUD)

A

Cluster o cognitive, behavioural, and physiological symptoms indicating that individual continues to use a substance despite significant substance related problems.
Maladaptive pattern as manifested by >/2 of the folllowing 11 over a 12 month period (1 year).
Impaired control ie 1. Larger amt than intended 2. Persistent unsuccessful cutting back 3. Time consuming 4. Cravings
Social impairment: 5. Fail to fulfill major role 6. Social.interpersonal problems 7. Reduction of important activities
Risky use: 8. Use in physically hazardous situations
9. Use despite having a problem
Pharmacological criteria: 10. Tolerance 11. Withdrawal syndrome upon cessation
– if tolerance and withdrawal are only two after appropriate use of prescribed drugs, DO NOT DIAGNOSE SUD.
Severity based on # of sxs

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27
Q

Drug Dependence versus Abuse

A

Now merged as USE disorder
Dependence (addiction) - pattern of drug use involving compulsive, drug seeking behaviour
Drug abuse: pattern of drug use with recurrent adversive consequences (ie role failure, risky situations, run-ins with law)

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28
Q

Schedule I - V drugs

A

I. NO safe accepted med use. Heroin, marijuana, LSD, ecstasy
II. High harm risk , but with safe accepted med use. Highly addictive ie opioids and stimulants, some barbiturates.
III, IV, V: harm risk less than schedule II with safe adn accepted uses
III: several barbiturates, anabolic steroids, codeine (tylenol III)
IV: Most benzodiazepines
V: liquid codeine preparations (eg robitussin)

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29
Q

Sedatives

A

CNS depressants
Alcohol,
Benzodiazepines (diazepam, lorazepam), Barbiturates (phenobarbital, secobarbital) - barbitiruates have low safety margine and high abuse potential

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30
Q

Sedative intoxication

A 
Sedation, sleepiness, decreased anxiety
Disinhibition, impaired judgment
Slurred speech, incoordination 
Stupor or coma
Respiratory depression ** OD on these drugs is potentially lethal

Other effects: anticonvulsant and anaesthetic, disrupted sleep architecture – unrefreshing sleep, alcohol related brain damage (korsakofs), cross tolerance to other sedatives

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31
Q

Sedative Withrdawal

A

Agitation, insomnia, anxiety. ANS hyperactivity**(can be fatal), nausea or vomiting — all are extreme “panic” reaction
Hand tremor, transient hallucinations, seizures
Hallucinations can occur in any sensory modality, incl tactile - formication (bugs Nader skin) - can occur as the main symptom of withdrawal without physical symptoms - ie alcohol hallucinoses.
Delirium Tremens (DTs) - a delirium (confusional state) may also occur: severe and uncommon, seen after chronic heavy use of a sedative (esp alcohol), associated with high mortality rate.

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32
Q

Naltrexone (Revia)

A

Opioid receptor blocker, reduces pleasurable effects of alcohol. This drug helps a person stop drinking after a few drinks when a ‘slip’ occurs. (Ie helps to avoid a full relapse)

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33
Q

Acamprosate (Campral)

A

An NMDA receptor antagonist that decreases craving for alcohol by reducing the discomfort of the protracted abstinence syndrome. Helps prevent the slip from occurring in the first place, because person feels euthymic and thus doesn’t crave alcohol.

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34
Q

Inhalants

A

CNS depressants - substances with psychoactive vapours (ie glues, paints). Similar to sedative intoxication. Teenage experimentation common.
Signs: rashly, red, runny nose, chemical smell, face discolouration
Associated with morbidity (organ failure)/mortality (sudden sniffing death)

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35
Q

Amphetamines

A

Major stimulants, ie methamphetamine, MDMA, Adderall

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36
Q

Amphetamine-like drugs

A

Major CNS Stimulants. Ie methylphenidate (Ritalin)

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37
Q

Cocaine

A

CNS stimulant

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38
Q

Stimulant Intoxication

A

Psychological: euphoria and grandiosity, psychomotor acceleration and steroetypies, paranoia and hallucinations

Physical: elevated HR and bp (life threatening), appetite loss and insomnia, mydriasis.

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39
Q

Meth versus cocaine

A

Both are major stimulants, especially addictive due to direct action on reward pathway, producing intense rush followed by euphoria.
Cocaine shorter lasting (hal life - 30 min versus 12 hours in meth)
Cocaine use is more frequent

Physical changes with meth (meth mouth and meth face)

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40
Q

Major Stimulant Withdrawal

A

Dysphoric mood (MUST BE SEEN)
Fatigue and psychomotor slowing
Hypersomnia with vivid and unpleasant dreams
Increased appetite
Symptoms non-life threatening and relatively mild

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41
Q

Ecstasy (methylene dioxymethamphetamine) MDMA

A

Stimulant effects PLUS mild hallucinogenic effects (perceptual alterations)
Common things look more interesting, empathogenesis, concern about neurotoxicity, other health consequences (ie hyperthermia), reputation as a safe drug despite schedule I status.

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42
Q

BATH SALTS (ivory wave, purple wave, vanilla sky, bliss)

A

Designer drug containing, in part, amphetamine-like chemicals (MDPV)
Acut toxicity includes: agitation, paranoia, hallucination, chest pian, tachycardia, HTN, suicidality

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43
Q

C Conditioning principles - Stimulus generalization

A

Responding to similar CSs with the same CR

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44
Q

C Conditioning principles - stimulus discrimination

A

Through trial and error, organism can learn to respond only to original CS

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45
Q

Classical extinction of a CR

A

CS-CR bond will tend to decay if CS no longer followed by US - get a classical extinction curve as CR weakens and is eliminated

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46
Q

Spontaneous recovery

A

Following extinctino, CR may ‘spontaneously’ reappear if CS is presented

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47
Q

Psychoneuroimmunology (classical cond. and medicine)

A

Classical conditionig of an immune response. Rob Ader. Ie pair saccrin with immunosuppresant, start to see immunosuppression with only saccrin.
Hospital chemo: UR = immunosuppresion
CR= immunosuppression and anticipatory nausea

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48
Q

Bell and pad procedure

A

Classical cond - treatment of nocturnal enuresis CS (sensation of full bladder) - US (alarm), CR/UR awakening and tightening of muscles.

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49
Q

White coat hypertension

A

Classical conditioning - CS (docs office ) US (past anxiety provoking event in office) - CR/UR anxiety/elevated BP

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50
Q

Drug-like effects

A

Classical conditioning - CS sights sounds smells drug environ, US drug injected (receptors occupied), CR/UR - drug like physio changes/psych effects. CR mimics aspects of the UR

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51
Q

Drug-opposite effects

A

Compensatory response of body to drug effects - also subject to conditioning
US - morphine injection UR - homeostatis mechanisms to counter
CS - sights sounds etc CR - homeostatic responses

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52
Q

Conditioned tolerance (Siegel)

A

Aspects of tolerance response via Classical Conditioning - become assoc with enviro stimuli prior to drug admin. Viewed as anticipatory, prepare body for arriveal.

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53
Q

Conditioned withdrawal

A

Obrien. Ie physicially dependent methadone users in detox. Pair spearmint smell with withrdawal period
Classical cond, CS later produced a CR mimicking withrdawal symptoms.
Concusion - conditioned withrdawal symptoms increase likelihood of relapse

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54
Q

Classical conditioning basis for treating drug use

A

CS’s play a significant role in continued drug use, craving, and relapse
Treatments based on classical extinction - break the learned association between stimuli in drug-using enviro and drug use

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55
Q

Classical Extinction

A

CS repeatedly presented (alleyway) but not followed by US (drug injection), diminished CR/UR

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56
Q

Conditioned avoidance examples

A

Thru classical cond, anxiety associated with enviro objects, events and situations, and somatic sensations
ex - phobias (specific and SAD), PTSD and ASD, panic attack, panic disorder, agoraphobia.

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57
Q

Watson’s Conditioned fear paradigm

A

many phobias acquired through classical conditioning - CS previously neutralstimulus (heights), US (naturally fear-producing stim ie perceived threat of falling), CR/UR feat/anxiety/avoidance

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58
Q

Phobias

A

Fear prodocing US does not ALWAYS lead to a phobia
can also be acquired through vicarious learning or verbal report
Acquired through classical conditioning, maintained by operant conditioning

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59
Q

Treatment of phobias

A

Most do not seek.
Anxiolytics limited, SSRIs OK
CBT: exposure & systematic desensitization good
Purely cognitive: less effective, pt usually realizes illogical.

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60
Q

Panic Attacks and agorophobia - conditioned fear and avoidacnce

A

Classical: initial attack occur in enviro with external and intrnal stim
External (exterioceptive) ie shopping mall
Internal (interioceptive) ie somatic sensation incr HR
Stimuli become CSs that elicit anxiety
Spiraling anxiety and physical symptoms
Maintenance however is operant… see later

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61
Q

Agoraphobica Conditioning

A

Panic attacks and PD often develop agroraphobic avoidance of external and internal stimuli assoc
Learned avoidance - often involves external CSs
Can also avoid CSs producing internal stimuli - ie activities producing elevatd HR - exercise, sex.

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62
Q

Classical Extinction treatments

A

Exposure: Gradual exposure to fearful stimulus (NO RELAXN TRAINING)
Flooding: Abrupt, prolonged full intesnsity exposure to fearful stim (careful, can be counterproductive)
Exposure and response prevention: Exposure followed by prevention of rituatlistic avoidance behaviour - first line for OCD - BOTH CLASSICAL AND OPERANT*

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63
Q

Law of Effect

A

Behavior followed by a pleasant consequence is strengthened & tends to be repeated; that followed by an unpleasant consequence is weakened & less likely to be repeated
(operant)

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64
Q

Behavioural view of depression

A

Too littl positive reinforcement in life –> depression
Downward emotinoal spiral of increasing levels of depression
Less you do, worse you feel, worse you feel, less you do.
CBT gold standard

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65
Q

Factors affecting effectiveness of reinforcement (operant)

A

Immediacy - reinforce most effective when presented immediately after the bhaviour
Consistency - reinforcing every infstance of behaviour, most quick learning
contingencies should be made clear

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66
Q

Continous Reinforcement

A

Every instance of behaviour is reinforced - quicker learning, but extinguished more quickly

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67
Q

Intermittent reinforcement

A

Not every behavior reinforced , learned less quickly but more resistant to extinctino
intermittent reinforcement Delivered on a variable ratio schedule is the MOST resistant to extinction

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68
Q

Shaping

A

Creating new behaviours through reinforcing successive approximations of the desired ehaviour

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69
Q

Supsersitious behavior

A

accidental conditioning

RAndom, non-continget reinforcement may lead humans to infer causality

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70
Q

Primary versus secondary reinforcers

A

Primary: naturally reinforcing, ie food, water, sex, some drugs, nurturance
Secodnary: acquire reinforcing ability through learning, ie applause, grades, gold medals, money

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71
Q

Primary versus secondary punishers

A

Primary: naturally, ie shock, pain, nausea
Secondary: learned ie ridicule, banishment, F grade

72
Q

Negative reinforcement

A

OC. incl Avoidance behaviour: Behaviour allows subject to avoid an unpleasant stimulus. See in phobias, OCD, PTSD, panic attack, substance use
neg reinforcement:
Ie. seeking medical treatment, results in alleviation of discomfort, pain, anxiety. Negatiely reinforced

73
Q

Two factor theory

A

Two-factor theory posits that both classical & operant conditioning are operating in the case of phobias & a number of other psychological disorders.
Acquired through classical, maintained via operant

74
Q

Reinforcemnt thory of drug dependence

A

Incl
Positive reinforcement: psychoactive drugs are reinforcers and stregthn drug taking and seeking behaviours
Negative reinforcement: physically dependent ppl, drug terminates unpleasant withdrawal effects. strengthening behaviour

75
Q

Stimulus Control

A

Whether previously reinforced behaviour is actually performed, depends on presence of stimuli in enviro.
If previously associated with reinforcement - they are antecedent or discriminative stimuli (SDs)
make the behaviour more likely because they predict reinforcement
–> behaviour result of consequence AND antecedent environmental stimuli

76
Q

Behavioural treatment for stress eating example of stimulus ctrl

A

Eating associated with stimulus situatins and internal mood states. Presence of these discriminatory stimuli make behaviour of eating more likely.
Goal: bring eating behaviour under appropriat stimulus control ie only at meal time in dining room.

77
Q

Avoidance Conditioning

A

Reason Conditioned behaviours are not forgotten. Maintains conditioned fear for phobias etc. Patients avoidance of feared object is negatively reinforced - avoidance or alleviation of anxiety. Learned fear does not extinguish

78
Q

Prolonged exposure

A

Involves patient remaining in presence of feared stimulus until anxiety diminishes

79
Q

OCD

A

Involves avoidance conditioning. Obsessions & compulsions
Performance of compulsive behaviour reduces anxiety assoc with obsessive thought - performance of ritualistic behaviour serves as avoidance behaviour, and is thus negatively reinforced.
Treatment: Exposure&Ritual/Response Prevention (CC and OC)

80
Q

Operant extinction

A

Reinforcement is consistently withheld following previously reinforced behaviour.
Post-extinction burst - rapid burst of behaviour at beginning of extinction trials, followed by extinction

81
Q

Extinctin versus punishment

A

Extinction: previously reinforced behav, NOTHING happens
Punishment: behaviour, followed by consequence

82
Q

Behavioural therapy

A

Focus on behaviour itself and role of learning and environment in maintnance
Shift from psychoanalysis - concept behaviour as a symptom of underlying conscious conflic.

83
Q

Contingency Managemnet

A

OC Treatment
Using reinforcement to encourage desirable behaviours, and punishment or extinction to elminiate undesirable. - ie parents restrict teenagerscar if doesnt keep curfew, praise if someone adheres, encourageent if exercise

84
Q

Shaping

A

OC
Creating new desirable behaviour by reinforcing successive approximations of it - used with population of limited speech - ie young children, intllectual probs, autism specturm

85
Q

Biofeedback

A

OC
Providing auditory or visual feedback to pt contingent upon modifaction of physiological correlates of anxiety and pain
ie EMG feedback indicating level of tension in neck/back in treatment of tension headaches. - ie they have tried this meditation tchnique, real life proof that it is working. Reinforces their relaxation behvaiour.

86
Q

Time Out

A

OC

Contingent upon misbheavior child is removed from all sources or reinforcement (negative punishment)

87
Q

Stimulus control

A

OC
Pt learns behaviour only under certain stimulus condtions - ie commonly seen in CBT programs ainmed at weight reduction and insomnia treat, bring eating and sleeping behaviour under stim crl.

88
Q

Differential reinforcement of other behaviours

A

reinforcement is delivered after a specified time period during which the undesirable behaviour is not performed
TIME dependent rather than response

89
Q

Premack Principle

A

Person wants to engage in some enjoyable behaviour - so that behaviour can be a reinforcer for some less enjoyable activity.

90
Q

Contingency Contracts

A

OC Theraputic understanding, family or couple and therapist, pertainig to desirable and undesirable behaviours made explicit and agreed to by all parties.
If i do this then this

91
Q

Token Economies

A

Operant based system often employed in residential treatment facilities, prisons, and halfway houses. Secondary reinforcers (ie tokens) used to reinforce desirable behaviours - tokens redeemed for merchandise/privileges

92
Q

ABAB experimental design

A

To establish effectiveness of a single case behavioral intervention
A - inital baseline
B - treatment intervention stage - not whether A changed
Treat withdrawn - note if returns to baselin
Treatment reinstated - noted whether behaviour again imrpoves
Dtermine whether our cog behav intervention has been effective.

93
Q

Rational Emotive Therapy (RET) (Ellis)

A

Primarily cognitive therapy. A (event) B (interpretation of event) C (emotion). C is caused by B, not A.

94
Q

Cognitive Therapy (Beck)

A

Negative triad - depression is caused by negative interpretations of self, life events, and future
Negative thinking CAUSES depression.
Negative ‘self schema’ - negative filters through which we view the world distort the world and cause depression
Learned helplessness: avoidance behaviours are prevented - passivity and depression result

95
Q

Social Cognitive Thinking (bandura)

A

Emphasizes learning through observation (modeling and vicarious cond)
Reciprocal relationship between behavriour, cognition, and personal factors.
Person;s behavior both influenced by and influences personal factors (eg personality and thinking), and by the social environment

96
Q

DialecticalBehvaiour Therapy (DBT)

A

Empirically demonstrated success with difficult patient populations - ie borderline PD, suicidal self harm, depressed teens, chronic eating D, drug dependent, chronic pain.
Cog behav therapy - incl behavioral skills training, emotion regulation, and mindfulness
Emphasis on patient acceptance of themselves as they ARE, and their commitment to CHANGE destructive behaviours.
MINDFULNESS - aware moment by moment of emotions and thoughs that precede destructive behaviour. learn to experience emotions without acting

97
Q

Smoking facts

A

Just below 1/4 of americans smoke - most report they would like to quit
Leading preventable cause of death (1/5)
70% see a physician each year, advice to quit by MD significantly increasing cessation rate
Cessation has benefits even after age 65, or quitting after disease
Decrease risk of lung cancer etc.
10-15 yrs of abstience, mortality rates approach non-smokers
30% with state of art treatment not smoking 1 yr later, most resume after 3 months
Only 5% who self quit succeed for 1 year

98
Q

Stages of change model (prochaska and diclemente)

A

Behavioural change is a process occurring over time.
PRECONTEMPLATION - initial disinterest, patint doesnt see prob or has given up. listen educate and raise doubt
CONTEMPLATION - thinking of health risks and quitting - ambivalent, vacillation. Emphasize risks and benefits, self efficacy, past successes
PREPARATION - preparing to quit in near future - explor options, set quit date, realistic.
ACTION - taking steps to stop - identify risk situations, coping strat, reinforce self efficacy
MAINTENANCE - maintaining non-smoking

99
Q

Zyban

A

Smoking cessation pdt. Sustained release buproprion - antidepressent with dopaminergic and noaradrenergic activity

100
Q

Varenicline (Chantix)

A

Smoking cessation pdt. Partial agnoist - eases withdrawl by stimulating nicotine receptors, blocks them if patient takes up smoking again - associated with suicidal ideation - banned in 2008 by FAA for use amont pilots and air trafic ctrllers.

101
Q

NRTs not receommended if

A

Few withrawl sx
relapse > 2weeks
low FTND

102
Q

NRTs recommended if

A

History of withrdrawl sx
relapse < 1 wk
high FTND

103
Q

4 principles of motivational interviewing

A
  1. Roll with resistance - don’t fight, avoid righting reflex, dont directly persuade
  2. Develop discrepancy - pt is stuck and needs hlep, help patint see discrepancy btwn where they want to be and where they are now, if accept your invitation will be for their own reasons
  3. Express empathy - accepting patient frees them to change, judging blaming is counterproductive, accepting does nt necessarly mean you agree
  4. Enhance self-efficacy - critical, have to believe they can do it, be supportive, creative
104
Q

Bath salts

A

Major stimulant. Ivory wave, purple wave, vanilla sky, bliss. Designer drug, containing, in part, amphetamine like chemicals (MDPV)
Acute toxicity incl: agitation, paranoia, hallucinations, chest pain, tachycardia HTN, suicidality.

105
Q

Caffeine (stimulant)

A

Intoxication; typically after 250 mg - increased energy, insomnia, nervousness, rambling thoughts, tachycardia, diuresis, GI disturbance, muscle twitches
Withdrawal: headache, dysphoria, fatigue, decreased concentration.

106
Q

Hallucinogens and related substances

A

Classic hallucinogens: LSD, mescaline, psilocybin – hallucinations
Cannabis: marijuana, hashis – distortions
Dissociative anaesthetics: PCP, ketamine (animal tranquillisiez) – depersonalization

107
Q

Hallucinogèns effects

A
  1. Perceptual altering ie hallucinations (classic), distortions (cannabis), depersonalitatino (disscoiateive anaesthetics)
  2. Mind calming effects - despite sympathomimétique effects - sometimes associated with agitation/paranoia (bad trip)
  3. Concerns exist that they cause persisting psychosis (ie marijuana causing schizophrenia, largely unproven)
108
Q

LSD

A

V potent hallucinogen, long lasting (8-12 hours)
Visual, poorly formed hallucinations (unlike those in schizophrenia).
Myrdriasis
NO withrdawal syndrome recognised.

Associated with “flashback” perceptual experiences long after LSD is metabolized - “hallucinogen persisting perception disorder”
Ie; false perceptions of movement, intensifications of colour. Generally not pleasant.

109
Q

Cannabis

A

Gateway drug along Rx opioids
Rarely causes hallucinations unless ingested
shorter acting than LSD (2-4 hours) unless ingested
Associated with amotivational syndrome

INTOXICATION: perceptual distortions, intensification of senses, perception of slowed time
Pyshical: conjunctival injection, increased appetite, dry mouth

WITHRDAWAL: psychological: irritability and nervousness (agitation), dysphoric mood, sleep disturbance (insomnia, vivid dreams), decreasd appetite
Physical: headaches, night sweats, stomach cramping, shakiness

Currently schedule I

110
Q

Dissociative anaesthetics

A

Ie PCP
Intoxication: depersonalization, agitation, belligérance and confusion, impulsivity and unpredictability, nystagmus, hyperacusis, decreased responsiveness to pain, ataxia, muscle rigidity, seizures, coma.

Intox is a psych emergency because of violent and unpredictable behaviours
Treatment: benzos, antipsychotics, reduced environmental stimulation, restraints might be needed.

No withrdawal syndrome recognised.

111
Q

Opioids

A

Main medical use of opioids (narcotics) - analgesia.
Additional effects: euphoria in varying intensities
Incl heroin - intense euphoria, highly addictive, can be smoked/snorted (not always needle tracks)
INTOXICATION: initial intense rush followed by euphoria and drowsiness, dysphoria (as high dissipates), MIOSIS, unconscious, respiratory depression

WIthrdawal: dysphoria, nausea, vomiting, diarrhoea, muscle aches, lacrimation and rhinorrhea, piloerecetino, sweating, fever, yawning, pupillary dilation. Sever “flu like symptoms”

Withdrawal usually non-life threatening, opioid use deadly by OD and health hazards associated with addiction

112
Q

Naloxone (narcan)

A

Short acting opioid receptor antagonist used for acute OD (not used for addiction treatment)

113
Q

Opioid treatment

A

Abstinence based therapy - patient to be completely abstinent, often involves use of naltrexone (long acting opioid receptor blocker) to block opioid effects if relapse occurs. Tends to be unsuccessful (compliance)

Replacement Therapy (RT) - giving patient a safer opioid drug (methadone, buprenorphine) - regulated, still get a high just not like heroin
Tends to be more successful than abstinence-based therapies.

Chronic, heavy opioid use resultsin anhedonia (reduced dopamine), physical discomfort (reduced avail of endogenous opioids).- make abstinence difficult
RT choices - methadone (schedule II) - only available at OTP, canno be prescribed.
Buprenoprhine (schedule III) - is available from a doctors office after approval by DEA when used for addiction, can be prescribed administered or dispensed.
Subodore -= buprenorphine +naloxone - naloxone only released when patient abuses medication, get negative effects overpowering.

114
Q

Opioid treatment - replacement therapy

A

Methadone (schedule II) cannot be prescribed, only in opioid treatment program - dispensed/administered
Buprenorphine (schedule III) - available from doctor after DEA approval. Prescribed dispensed or administered.

Suboxone - buprenorphine and naloxone - naloxone only released if patient abuses drug.

Duration: 1-2 years,
Benefits of RT: oral admin, stable drug levels, less euphoria and less drowsiness.
RT plus other interventions – healthier, productive, and less crime-causing heroin addicts.

115
Q

yerkes dodson law

A

Performance and adaptive learning are optimal under moderate levels of stress
Corollary 1: learning new or difficult tasks is optimal with low/moderate arousal levels
Corollary 2: performance of well-learned tasks is optimal with moderate/high arousal levels

116
Q

Opposing effects of SNS and HPA in stress response

A

SNS - stimulates inflammation, suppressed by glucocorticoids
resting HR increased by SNS, suppressed by glucocorticoids
Basal metabolic energy expenditure accelerated by SNS, suppressed by HPA

117
Q

Suboptimal responders to stress

A

Glucocorticoid receptor response becomes impaired, resulting in a flood that

  • inhibits protein synthesis,
  • accelerates protein catabolism
  • increased lipolysis
  • decreases peripheral glucose utilisation
118
Q

Dysregulation of HPA - abnormal cortisol levels in…

A 
Anxiety disorders (high cortisol)
Depression (high cortisol)
PTSD (high and low cortisol)
History of child abuse (high cortisol)
Professional burnout (high cortisol)
119
Q

Genetic differences in stress response

A
  • Variations in HPA afferents - personality types and HPA response
  • Shorter form of serotonin transporter - assoc with increased stress response and vulnerability to depression and alcoholism
  • Val 66Met allele of the brain-derived neurotrophic factor (BDNF) gene leads to reduced hippocampal plasticity and increased anxiety.
120
Q

Stress responses - early life experiences (nurture)

A

Early experiences can hard wire stress response (modelling, secure attachement)
Greatest learning occurs in first 9 months
Early trauma/abuse
Uncertainty in food supply
Novelty/enriched environment (protective factor)

121
Q

Stages of stress adaptation

A
  1. Alarm stage - Adaptive responses are mobilised
  2. Resistance stage - organism attempts to cope by utilising available resources - in state of immunocompromise.
  3. Exhaustion stage - demands exceed available resources and defensive efforts fail, and individual becomes increasingly susceptible to disease.
122
Q

Chronic stress and immune response

A

Acute stress activates immune system
Chronic stress suppresses it. - excess glucocorticoids in blood impairs production of natural killer T cells and B cells. Reduced antibodies - chronic stress can also lead to heightened autoimmune response - attacks itself - get MS, RA, juvenile diabetes, allergies

123
Q

Stress and metabolic disorders

A

Excess glucocorticoids from chronic stress are diabetogenic - impair cell response to insuline
Increased glucose and fat in blood stream, decreased O2 flow and organ efficiency.
Chronic stress induced hyperinsulinemia is associated with Type II diabetes, CAD, metabolic syndrome.

124
Q

Stres and CVD

A

Stress induced SNS can lead to : spasms of arterial vasculature (migraines), broken heart syndrome (takotsubo cardiomyopathy)
Chronic stress-induced arterial constriction can result in:
Atherosclerosis, impeded blood oxygen flow (myocardial ischemia), chest pain (angina), cell death (infarct) , heart muscle lapse (arrhythmia or fibrillation).

125
Q

Exercise as a de-stressor

A

Reduces adrenaline and cortisol, stimulates endorphin release. Provides an acute physical stress to “reset” the stress response

126
Q

Psychological Approaches to behaviour

A

Psychodynamic: behaviour determined by unconscious processes
Behaviourism: focuses on learning and environment
Cognitive: learning based, but emphasises role of thoughts and beliefs in behaviour
Humanistic: human behaviour reflects a self-actualising principle

127
Q

Behavioural Psychology

A

Posits that most human behaviour is learned through associative le earning. Learned association made between two different stimuli, or events. - Two types of associative learning are classical and operant conditioning

128
Q

Psychoneuroimmunology

A

Classical conditioning of an immune response - Robert Ader’s research

129
Q

Siegel’s Conditioned Tolerance

A

Anticipatory response, homeostatic responses to counter direct drug effects (compensatory) are the UR, become CR to CS of environmental cues
CRs viewed as anticipatory, and prepare body for arrival of drug. Animals that dont have conditioned tolerance higher mortality rate.

130
Q

O’brien’s conditioned withdrawal

A 
Spearmint smell (CS) paired with withrdawal period
Through classical conditioning, the CS later elicited a CR mimicking aspects of withdrawal syndrome.
Conditioned withrdawal symptoms increase likelihood of relapse (use of drug quells such aversive withrdawl-like symptoms)
131
Q

Schedule of reinforcement most resistant to extinction

A

Intermittent reinforcement (not every instance of behaviour reinforced, learned more slowly) delivered on a variable ratio schedule (ie slot machine pay off on average every 10x)

132
Q

Psychic Determinism

A

Nothing in mental life occurs solely by chance (freudian slip)
Basis for free association - défenses relax and repressed material can emerge.

133
Q

Dysregulation of HPA in disorders

A

Abnormal cortisol levels - anxiety disorders HIGH, depression HIGH, PTSD high and low history of child abuse HIGH, professional burnout HIGH.

134
Q

Stress and immune system

A

Acute stress activates immune system
Chronic stress associated with immunosuppression - excess glucocorticoids in blood impairs production of natural killer T cells and B cells, reduced antibodies
Paradoxically, chronic stress can also lead to heightened autoimmune response (MS, RA, juvenile diabetes, allergies)

135
Q

Reliability

A
  1. Test-retest (administer same test again)
  2. Alternate form method (different form)
  3. Internal consistency - establish correlation between different parts of the exam
  4. Inter-scorer (or inter-rater) method: correlation between scores by different clinicians - not an issue with objective-forat tests, more important with subjective tsts ie ROrschach and TAT
136
Q

Validity

A
  1. Content validity - are the test items representative of the domain, commonly used to validate teacher-made tests
  2. Criterion-referenced validity - how well do test results correlate with a direct and independent measure (ie criterion) of what it is designed to measure. - used for aptitude and clinical/diagnosit tests ie MCAT, HAM-D
    - two types of criterion referenced - predictive ie correlation between tst and future GPA
    - concurrent -HAM D and current clinicians rating
137
Q

Aptitude Tests

A

Measure specific abilities relevatnt to performance in academic or vocational settings ie MCAT GRE SAT US civil srvice exams

138
Q

Achievement Tests

A

How much a person has learned in a specificed educational domain - in the US, tests given in primary school such as the iowa and stanford achievment tests

139
Q

Neuropsychological Batteries

A

Assess behavioural, cognitive, and personality deficits following head trauma or neurological disease - based on behavioural deficits, inferences made re location of damage. Complement neuroimaging - incl Halstead Reitan Battry, Luria nebraska , bender visual motor gestalt.

140
Q

IQ

A

Standard score, mean = 100, SD = 15
Not an absolute score, is a COMPARISON among people
Tends to be stable throughout adulthood, fluctuate in teens
In mental disorders: varies, symptoms can interfere with IQ assessment, IQ is NOT related to suicide risk.

141
Q

IQ with age, results of longitudinal studies

A

Very little decline in elderly, VERBAL ability holds up best, perceptual and motor abilities show some decline, increased exposure to verbal behaviour EARLY in life leads to HIGHER IQ

142
Q

WAIS IV IQ Classifications

A 
<69: Very low, approx 2.5% of population
70-79 low
80-89 low average
90-109 average (~50% of the population)
110-119 high average 
120-129 superior
>130 very superior, approx 2.5%
143
Q

WISV V IQ

A

For children ages 6-16
Measures of general intelligence along with specific indices incl. 1. verbal comprehension, 2. fluid reasoning 3.working memory, 4. processing speed 5. visual spatial. 45-65 minutes

144
Q

WISC V IQ Verbal comprehension subtests

A

Similiarities subtest - two words of everyday objects, describ how the objects are similar - ie shoe and shirt
Comprehension subtest - asked questions that have to do with appropriate behaviour - why do people was their hands?
Information subtest: Questions that sample a braod range of areas inv. general knowledge- wheels on a bicycle, who is einstein, where do raisins come from

145
Q

Block design subtest

A

Subtest of visual spatial category of WISC V. Red and white blocks, child asked to recreate an increasingly more complex stimulus design within a specified TIME LIMIT.

146
Q

Digit Span subtest

A

Subtest of working memory for WISC V. Child presented with sequence of numbers, asked to repeat them either forwards or backwards. Number of digits presented (2-9) increases based upon child’s performance.

147
Q

Coding subtest

A

Subtest for processing speed of WISC V
Asked to copy symbols that are paired with geometric shapes into the row of shapes that lack symbols. is a timed exercise.

148
Q

personality test types

A

Asses enduring and stable beliefs values attitudes and traits characterizing behaviour across situations and over time

  1. objective ie MMPI 2
  2. projective - subjective format and scoring ie Rorschach
149
Q

MMPI-2

A

Objective personality test. Global.
Most commonly used, objective format & scoring - 567 T/F questions yields scores on 10 personality dimensions.
Computer scoring yields a narrative report. Often finds its way into patients chart, but should only be used in conjuction with interview data.
0 - social introversion
1. hypochondriasis 2. depression 3. hysteria 4. psychopathic deviancy 5. masculinityfeminiity 6. paranoia 7. psychasthenia - worry anxiet doubts=obsessiveness 8. schizophrenia - odd thinking and social isolation 9. hypomania - excitablity
Often used in inpatient psych eval for differential dx and expert witness forensics.
And in medical cases with physical symptoms with no apparent organic basis.

150
Q

Empirical criterion keying

A

Used in development of MMPI - itms chosen from a pool, choose the ones that discriminate betwen “sick” and “healthy” people - basis on whether they discriminate between depressed and normal test takers for whatever reason.

151
Q

HAM-D

A

Objective personality/clinical test. Clinician rated. One of most widely used depression scales. GOOD reliablitiy and validity - becoming gold standard in psychopharm antideps clinical trials
Rates patint on 21 items assessing: somatic symptoms, insomnia, working capcity & interest, mood, guilt, psychomotor retard, agitation, anxiety, insight.

152
Q

Beck Depression Inventory II (BDII)

A

Assesses cognitions (feelings, guilt), physical symptoms (fatigue, weight loss, libido) - based on beck’s negative triad - negative views of self, world, and future.
Hopelessness - despair, resignation. Assumes negative cognitions are cause of depression - due to negative schema developed early in life. World viewed negative and hopeless. Itms are weighted and inventory can be self scored
1 - i feel discouraged about the future etc

153
Q

Commonly used screening instruments in primary health care - to assess for depression in at risk patints

A

BDI II and patient health questionnaires (PHQ2 and PHQ9)

154
Q

Projective personality tests

A

Ambiguous tst stimuli - purposeful, pt project own meaning and order
subjective scoring - different systems, empirical support difficult
lower reliability - partic low inter-rater
validityl difficult to demonstrate due to subjectivity and psychodynamic concepts

155
Q

Projective hypothesis

A

Stimuli from the envoronment (incl test stimuli) are interpreted according to the pts needs, motive, and unconscious conflicts.

156
Q

Rorschach

A

10 bisymmetrical inkblots. B&w and colour. Several scoring systmes. Response features indicate personality traits

157
Q

TAT (thematic apperception test)

A

provide narrative story of ambiguous scenes of human interaction, subjective scoring looking for common thmes. Characteristic ways of addressing conflict, authority, sexuality lead to hypotheses re underlying MOTIVES, CONCERNS, and how pt VIEWS SOCIAL WORLD.

158
Q

Delirium

A

AKA Acute confusional state, acute brain syndrome, encephalopathy, ICU syndrome

  1. Disturbance in awareness and attention
    • at least one additional disturbance in a cognitive domain (memory, language, thoughts (delusions) and perceptions (hallucinations)
  3. Sudden onset of symptoms, and fluctuating during the day
  4. Evidence for a direct PHYSIOLOGICAL CAUSE (medical condition, drug intox, withrdawal).
159
Q

Pathology of delirium

A

Multiple étiologies (fever, dehydration)
Widespread brain regions affected
Core deficit is in central cholinergic functioning, deficits in ARAS

160
Q

Risk and Course of delirium

A

Risk: health, old age, male gender.
SLeep, immobilisation, benzo use in ICU

Course: until cause is reversed, resolution typically within 3-7 days
Amnesia for events during delirium is common
Poor prognostic sign for longer ICU stays

161
Q

Treatment for delirium

A

Treat underlying medical condition, and manage associated symptoms (ie agitation, psychosis).
Antipsychotics - agitation, psychosis of most delirium
Benzodiazepines - to treat delirium caused by alcohol withrdawal

Environmental supportive meausres: regulate amount of environmental stimulation, provide orienting stimuli, and provide for safety needs.

162
Q

Amnesia

A

Significant acquired memory deficit caused by a medical condition or effect of a substance (NOT dissociative)
NOT diagnosed if with general cog decline (ie dementia)
Typically from damage to HIPPOCAMPUS

Intact STM (Working), short duration retrograde (if longer, have a gradient loss), prominent anterograde

Treat: underlying cause ie korsakoffs
Cog rehab: restoration of function (memory exercises), and compensation (external strategies ie lists calendars) and internal strategies ie acromynms.

163
Q

Dementia

A

Refers to multiple and sever cognitive impairment WITHOUT impaired consciousness.
Usually progressive and irreversible
Most commonly in elderlyly

164
Q

Mild cognitive impairment

A

Refers to cognitive decline that DOESNT impair activities of daily living - ie maybe cant multitask so well, a bit forgetful, but doesnt significantly impair functioning. But get a baselin, do a neuropsych battery for future comparison.
MCI - higher risk fo developing dementia

165
Q

Alzheimer’s Dementia

A

Significant memory impairment plus impairment in at least one other cognitive domain.
Gradual onset, progressive decline
Early stages: rapid forgetting, anomia
middle: decreased memory and language, visuospatial problems, agnosias, mood, personality changes, psychosis
Late: global aphasia, motor dysfunction, death.

Neuroanatomical: cortical atrophy, hippocampal atrophy, enlarged ventricles
neurochemical: multiple NT deficiency, loss of ACh in nucleus of meynrt.
Neurofunctional: POSTERIOR hyPOmetabolism (ie parietal/temporal)
Histo: B amyloid plaques and neurofibrillary tangles - in vivo CSF and amyloid tau , PET imaging of amyloid plaques.

Definitive diag on post-mortem

166
Q

Alzheimer’;s treatment

A

3 cholinesterase inhibitors: donepezil, galantamine, rivastigmine (mild-moderate)

1 NMDA receptor blocker - memantine (for moderate-severe AD)

Generally considered ineffective, with side effects of hypotension, GI problems,

Research on decreased production and increased clearance of B amyloid plaques through antibody drugs.

Other: treat neuropsychiatric symptoms ie aggression and agitation
Music therapy,
Antipsychotics (off label, black box increased mortality), anticonvulsants and anti-depressants (select)

167
Q

Vascular Dementia

A

Dementia from multiple infarcts caused by CVD
Sudden onset, stepwise progression
Focal neurological signs
Headache and seizure onset more common than in AD

Treatment: treat underlying CVD, and alzheimer’s drugs for cognitive problems

168
Q

Frontotemporal dementia (FTD)

A

Ie Pick’s disease
Earlier age of onset (40s-50s) than AD
Similar to AD but “frontal” signs are prominent early in the dementia (ie disinhibition and personality change)
Frontal lobe atrophy and hypometabolism
Histopathological changes (ie pick bodies)

169
Q

Lewy Body Dementia (LBD)

A

Fluctuating cognition/alertness, visual hallucinations, mild parkinsonism (but usually not tremors)
Histo changes: lewy bodies
REM sleep behaviour disorder often precedes onset by many years

Treatment:
hallucinations - have severe neuroleptic sensitivity (EPS, NMS so cant give antipsychotics) , instead treat hallucinations with “benign neglect”
Parkinson’s drugs are relatively ineffective in LBD and worsen psychosis.

170
Q

Parkinson’s Disease Dementia (PDD)

A

Up to 50% of PD patients develop dementia, similar pathology to LBD
1 year rule:
If dementia develops >12 months after well established PD –> PDD

If develops first or within first 12 months of motor signs –> LBD.

171
Q

Prion Disease

A

Dementia progresses rapidly over a few months, with death under a year.

172
Q

Pseudodementia

A

AKA dementia syndrome of depression
Depressed elderly patients often show memory and other cognitive disturbances that resemble a dementia.
Defferential:
This is more pinpointable, shorter, inconsistent impairment, highlight their impairment, they answer with “dont know” instead of confabulation, and they have RETRIEVAL problems versus encoding problems - ie cues given help remember.

173
Q

Benign Senescent Forgetfulness

A

Cognitive decline associated with normal ageing - neuropsych testing helps determine whether current cognition reflects a pathological process

174
Q

DSM 5 Neurocognitive Disorders Diagnoses

A
  1. Delirium - awareness and attention disturbance _+additional cognitive disturbance, sudden onset fluctuates during day, and evidence of direct physio cause
  2. Major NCD: “Significant”: decline in AT LEAST ONE cognitive domain - interferes with independence in daily activities
  3. Mild NCD: “modest” decline in at least one cognitive domain, does NOT interfere with capacity for independence in daily activities
175
Q

Neuropsych evaluation

A

Intellligence: Weschler (verbal comp, perceptual reasoning, hemispheric lateralisation and localisation signs)
Attention: visual (cancellation test), verbal (serial addition test)
Memory: World lists/paragraphs (left hemi), spatial designs (right hemi). Immediate recal versus delayed recall - rate of forgetting encoded info . Free recall (uncued) versus recognition (cued) - cues determines econdign versus retrieval based.
Retrieval based(PFC), encoding based (Mesial temporal)

Language: naming and verbal fluencyVisuospatiel (right parietal) - copying and drawing tests
: executive functions (PFC) - abstraction, and concept formation./mental flexibility , inhibiting responses (strop test)
motor functions: dexterity and speed (finger tapping, pegboard test)

Neuro (6 decks)

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