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Psych pt ii Flashcards

(175 cards)

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
Alcohol withdrawal DSM 5
>/2 of: 1. ANS hyperactivity 2. Hand tremor 3. Insomnia 4. Nausea 5. Hallucinations/illusions 6. Psychomotor agitation 7. Anxiety 8. Generalized seizures
26
Substance Use Disorder (SUD)
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
27
Drug Dependence versus Abuse
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)
28
Schedule I - V drugs
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)
29
Sedatives
CNS depressants Alcohol, Benzodiazepines (diazepam, lorazepam), Barbiturates (phenobarbital, secobarbital) - barbitiruates have low safety margine and high abuse potential
30
Sedative intoxication
``` 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
31
Sedative Withrdawal
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.
32
Naltrexone (Revia)
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)
33
Acamprosate (Campral)
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.
34
Inhalants
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)
35
Amphetamines
Major stimulants, ie methamphetamine, MDMA, Adderall
36
Amphetamine-like drugs
Major CNS Stimulants. Ie methylphenidate (Ritalin)
37
Cocaine
CNS stimulant
38
Stimulant Intoxication
Psychological: euphoria and grandiosity, psychomotor acceleration and steroetypies, paranoia and hallucinations Physical: elevated HR and bp (life threatening), appetite loss and insomnia, mydriasis.
39
Meth versus cocaine
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)
40
Major Stimulant Withdrawal
Dysphoric mood (MUST BE SEEN) Fatigue and psychomotor slowing Hypersomnia with vivid and unpleasant dreams Increased appetite Symptoms non-life threatening and relatively mild
41
Ecstasy (methylene dioxymethamphetamine) MDMA
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.
42
BATH SALTS (ivory wave, purple wave, vanilla sky, bliss)
Designer drug containing, in part, amphetamine-like chemicals (MDPV) Acut toxicity includes: agitation, paranoia, hallucination, chest pian, tachycardia, HTN, suicidality
43
C Conditioning principles - Stimulus generalization
Responding to similar CSs with the same CR
44
C Conditioning principles - stimulus discrimination
Through trial and error, organism can learn to respond only to original CS
45
Classical extinction of a CR
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
46
Spontaneous recovery
Following extinctino, CR may 'spontaneously' reappear if CS is presented
47
Psychoneuroimmunology (classical cond. and medicine)
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
48
Bell and pad procedure
Classical cond - treatment of nocturnal enuresis CS (sensation of full bladder) - US (alarm), CR/UR awakening and tightening of muscles.
49
White coat hypertension
Classical conditioning - CS (docs office ) US (past anxiety provoking event in office) - CR/UR anxiety/elevated BP
50
Drug-like effects
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
51
Drug-opposite effects
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
52
Conditioned tolerance (Siegel)
Aspects of tolerance response via Classical Conditioning - become assoc with enviro stimuli prior to drug admin. Viewed as anticipatory, prepare body for arriveal.
53
Conditioned withdrawal
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
54
Classical conditioning basis for treating drug use
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
55
Classical Extinction
CS repeatedly presented (alleyway) but not followed by US (drug injection), diminished CR/UR
56
Conditioned avoidance examples
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.
57
Watson's Conditioned fear paradigm
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
58
Phobias
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
59
Treatment of phobias
Most do not seek. Anxiolytics limited, SSRIs OK CBT: exposure & systematic desensitization good Purely cognitive: less effective, pt usually realizes illogical.
60
Panic Attacks and agorophobia - conditioned fear and avoidacnce
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
61
Agoraphobica Conditioning
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.
62
Classical Extinction treatments
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*
63
Law of Effect
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)
64
Behavioural view of depression
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
65
Factors affecting effectiveness of reinforcement (operant)
Immediacy - reinforce most effective when presented immediately after the bhaviour Consistency - reinforcing every infstance of behaviour, most quick learning contingencies should be made clear
66
Continous Reinforcement
Every instance of behaviour is reinforced - quicker learning, but extinguished more quickly
67
Intermittent reinforcement
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
68
Shaping
Creating new behaviours through reinforcing successive approximations of the desired ehaviour
69
Supsersitious behavior
accidental conditioning | RAndom, non-continget reinforcement may lead humans to infer causality
70
Primary versus secondary reinforcers
Primary: naturally reinforcing, ie food, water, sex, some drugs, nurturance Secodnary: acquire reinforcing ability through learning, ie applause, grades, gold medals, money
71
Primary versus secondary punishers
Primary: naturally, ie shock, pain, nausea Secondary: learned ie ridicule, banishment, F grade
72
Negative reinforcement
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
Two factor theory
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
Reinforcemnt thory of drug dependence
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
Stimulus Control
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
Behavioural treatment for stress eating example of stimulus ctrl
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
Avoidance Conditioning
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
Prolonged exposure
Involves patient remaining in presence of feared stimulus until anxiety diminishes
79
OCD
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
Operant extinction
Reinforcement is consistently withheld following previously reinforced behaviour. Post-extinction burst - rapid burst of behaviour at beginning of extinction trials, followed by extinction
81
Extinctin versus punishment
Extinction: previously reinforced behav, NOTHING happens Punishment: behaviour, followed by consequence
82
Behavioural therapy
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
Contingency Managemnet
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
Shaping
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
Biofeedback
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
Time Out
OC | Contingent upon misbheavior child is removed from all sources or reinforcement (negative punishment)
87
Stimulus control
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
Differential reinforcement of other behaviours
reinforcement is delivered after a specified time period during which the undesirable behaviour is not performed TIME dependent rather than response
89
Premack Principle
Person wants to engage in some enjoyable behaviour - so that behaviour can be a reinforcer for some less enjoyable activity.
90
Contingency Contracts
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
Token Economies
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
ABAB experimental design
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
Rational Emotive Therapy (RET) (Ellis)
Primarily cognitive therapy. A (event) B (interpretation of event) C (emotion). C is caused by B, not A.
94
Cognitive Therapy (Beck)
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
Social Cognitive Thinking (bandura)
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
DialecticalBehvaiour Therapy (DBT)
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
Smoking facts
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
Stages of change model (prochaska and diclemente)
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
Zyban
Smoking cessation pdt. Sustained release buproprion - antidepressent with dopaminergic and noaradrenergic activity
100
Varenicline (Chantix)
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
NRTs not receommended if
Few withrawl sx relapse > 2weeks low FTND
102
NRTs recommended if
History of withrdrawl sx relapse < 1 wk high FTND
103
4 principles of motivational interviewing
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
Bath salts
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
Caffeine (stimulant)
Intoxication; typically after 250 mg - increased energy, insomnia, nervousness, rambling thoughts, tachycardia, diuresis, GI disturbance, muscle twitches Withdrawal: headache, dysphoria, fatigue, decreased concentration.
106
Hallucinogens and related substances
Classic hallucinogens: LSD, mescaline, psilocybin -- hallucinations Cannabis: marijuana, hashis -- distortions Dissociative anaesthetics: PCP, ketamine (animal tranquillisiez) -- depersonalization
107
Hallucinogèns effects
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
LSD
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
Cannabis
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
Dissociative anaesthetics
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
Opioids
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
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Naloxone (narcan)
Short acting opioid receptor antagonist used for acute OD (not used for addiction treatment)
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Opioid treatment
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.
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Opioid treatment - replacement therapy
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.
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yerkes dodson law
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
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Opposing effects of SNS and HPA in stress response
SNS - stimulates inflammation, suppressed by glucocorticoids resting HR increased by SNS, suppressed by glucocorticoids Basal metabolic energy expenditure accelerated by SNS, suppressed by HPA
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Suboptimal responders to stress
Glucocorticoid receptor response becomes impaired, resulting in a flood that - inhibits protein synthesis, - accelerates protein catabolism - increased lipolysis - decreases peripheral glucose utilisation
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Dysregulation of HPA - abnormal cortisol levels in...
``` Anxiety disorders (high cortisol) Depression (high cortisol) PTSD (high and low cortisol) History of child abuse (high cortisol) Professional burnout (high cortisol) ```
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Genetic differences in stress response
- 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.
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Stress responses - early life experiences (nurture)
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)
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Stages of stress adaptation
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.
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Chronic stress and immune response
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
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Stress and metabolic disorders
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.
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Stres and CVD
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).
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Exercise as a de-stressor
Reduces adrenaline and cortisol, stimulates endorphin release. Provides an acute physical stress to "reset" the stress response
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Psychological Approaches to behaviour
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
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Behavioural Psychology
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
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Psychoneuroimmunology
Classical conditioning of an immune response - Robert Ader's research
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Siegel's Conditioned Tolerance
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.
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O'brien's conditioned withdrawal
``` 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) ```
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Schedule of reinforcement most resistant to extinction
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)
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Psychic Determinism
Nothing in mental life occurs solely by chance (freudian slip) Basis for free association - défenses relax and repressed material can emerge.
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Dysregulation of HPA in disorders
Abnormal cortisol levels - anxiety disorders HIGH, depression HIGH, PTSD high and low history of child abuse HIGH, professional burnout HIGH.
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Stress and immune system
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)
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Reliability
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
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Validity
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
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Aptitude Tests
Measure specific abilities relevatnt to performance in academic or vocational settings ie MCAT GRE SAT US civil srvice exams
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Achievement Tests
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
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Neuropsychological Batteries
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.
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IQ
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.
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IQ with age, results of longitudinal studies
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
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WAIS IV IQ Classifications
``` <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% ```
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WISV V IQ
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
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WISC V IQ Verbal comprehension subtests
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
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Block design subtest
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.
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Digit Span subtest
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.
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Coding subtest
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.
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personality test types
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
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MMPI-2
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.
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Empirical criterion keying
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.
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HAM-D
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.
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Beck Depression Inventory II (BDII)
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
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Commonly used screening instruments in primary health care - to assess for depression in at risk patints
BDI II and patient health questionnaires (PHQ2 and PHQ9)
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Projective personality tests
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
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Projective hypothesis
Stimuli from the envoronment (incl test stimuli) are interpreted according to the pts needs, motive, and unconscious conflicts.
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Rorschach
10 bisymmetrical inkblots. B&w and colour. Several scoring systmes. Response features indicate personality traits
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TAT (thematic apperception test)
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.
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Delirium
AKA Acute confusional state, acute brain syndrome, encephalopathy, ICU syndrome 1. Disturbance in awareness and attention 2. + 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).
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Pathology of delirium
Multiple étiologies (fever, dehydration) Widespread brain regions affected Core deficit is in central cholinergic functioning, deficits in ARAS
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Risk and Course of delirium
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
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Treatment for delirium
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.
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Amnesia
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.
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Dementia
Refers to multiple and sever cognitive impairment WITHOUT impaired consciousness. Usually progressive and irreversible Most commonly in elderlyly
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Mild cognitive impairment
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
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Alzheimer's Dementia
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
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Alzheimer';s treatment
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)
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Vascular Dementia
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
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Frontotemporal dementia (FTD)
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)
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Lewy Body Dementia (LBD)
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.
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Parkinson's Disease Dementia (PDD)
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.
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Prion Disease
Dementia progresses rapidly over a few months, with death under a year.
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Pseudodementia
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.
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Benign Senescent Forgetfulness
Cognitive decline associated with normal ageing - neuropsych testing helps determine whether current cognition reflects a pathological process
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DSM 5 Neurocognitive Disorders Diagnoses
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
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Neuropsych evaluation
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 fluency Visuospatiel (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)