7. psihopatologia Flashcards

(53 cards)

1
Q

what is comorbidity

A

the presence of 2 or more medical or psychiatric conditions occurring simultaneously in the same person

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2
Q

what is the relationship between substance use disroders SUD and other psychiatric conditions

A

there is comorbidity between SUD and other psychiatric conditions

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3
Q

what is the risk of psychiatric disorders in people with SUD

A

people with SUD are at a significantly higher risk of experiencing other psychiatric disorders comapred to the general population

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4
Q

why is there a higher risk in people with SUD

A

shared genetic vulenrabilities - genetic factors predisposing people to both conditions

alterations in brain chemistry caused by substance uce

substance use as a form of self-medication for underlying psychiatric symtpoms

life stressors that contribute to both conditions

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5
Q
  1. what are some psychiatric disorders associated with SUD
A

anxiety disorders - substances like alcohol may initially reduce anxiety, leading to misuse, but chronic use or withdrawal often worsens anxiety symptoms

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6
Q
  1. what are some psychiatric disorders associated with SUD
A

major depression

SUDs especially alcholo abuse, are closely linked to depressive episodes

substance use may worsen depression, and depression may increase the likelihood of substance use

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7
Q
  1. what are some psychiatric disorders associated with SUD
A

psychoses/ schizophrenia

psychotic disorders, including Sz show strong comorbidity with SUDs.

cannabis use is linked to an increased risk of psychotic episodes, epecially in vulnerable individuals

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8
Q
  1. what are some psychiatric disorders associated with SUD
A

SUDs are often seen in individuals with personality disorders such as borderline personality disorder and antisocial personality disorder

emotional dysregulation or impulsivity in these disorders can fuel substance abuse behaviours

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9
Q

what is the importance of early identification and treatment

A

recognitisng and treating comorbid SUDs and psychiatric disorders early is crucial because untreated comorbidities can lead to

worse heatlh outcomes
poor adherence to treatment
higher risk of relapse for both disorders

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10
Q

what is concurrent diagnoses

A

when an individual experiences both an SUD and another psychiatric disorder at the same time

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11
Q

what is lifetime risk

A

the person is at a higher overall likelihood of developing a psychiatric disroder or an SUD at any point in their life, not just simultaneously

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12
Q
  1. why are people who have psychiatric disroder more likely to develop an SUD
A

self medication

people may use substances to cope with the symtpoms of psychiatric disorders

e.g. someone with social anxiety might start misusing alcholo to feel more comfortable in social situations

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13
Q
  1. why are people who have psychiatric disroder more likely to develop an SUD
A

biological factors

underlying genetic of neurochemical vulnerabilities can predispose a person to both conditions

e.g. dysregulation in dopamine systems may contribute to both SUD and mood disorders

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14
Q
  1. why are people who have psychiatric disroder more likely to develop an SUD
A

environmental stressors

trauma or chronic stress can lead to both psychitric disorders and substance use as a maladaptive coping mechanism

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15
Q

what are the 12-month prevalance estimates of different disorders - based on 10 studies with same size of 47,000

A

Depression/mood disorders:
2.5 - 9.5%

Anxiety disorders: 5.0 - 18%

Personality disorders: 2.2 – 14.8%

SUDs: 3.4 – 8.9%

Alcohol Dependence: 0.7 – 4.7%

Drug Dependence: 0.3 – 1.5%

Nicotine Dependence: 10.5 – 32%

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16
Q

what might account for the observed co-morbidities

A

other disorders to SUD due to self-med

SUD to other disorders due to brain changes

shared vulnerability factors:
- intrapersonal risk factors (genes, personality, brain function)
- social/situational risk factors (family problems, stressors)

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17
Q

what was the use of stimulant use

A

stimulant medications such as AMPHETAMINES, were widely used for medical purposes, particularly in the uK and US after world war 2

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18
Q

what were amphetamines prescribed for

A

depression - due to their mood-elevating effects

weight loss - because they suppress appetite and boost energy levels

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19
Q

what was the scale of production of amphetamine

A

by 1962, an estimated 80,000 kg of amphetamine salt was being produced

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20
Q

what were the side effects of amphetamine

A

connell showed that amphetamine use is known to induce sympotms resembling psychosis e.g. paranoia, hallucinations, delusions

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21
Q

what are some stats on amphetamine use

A

1969 - 2,500,000 defined doses

2005 - 1,500,000 defined doses

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22
Q

what is the relationship between stimulant use and psychosis

A

stimulants such as amphetamine can induce temporary Sz like symptoms

23
Q

what is an example on how stimulants can lead to sz like symptoms

A

Angriest et al (1970) have 9 healthy volunteers up to 50mg amphetamine, all became psychotic within 7-45 hours

they all recovered within 6 dahs of abstinence

40% of amphetamine dependent patients report Sz like symptoms at some point

24
Q

what is one subject’s experience

A

‘After 270 mg of d-amphetamine, he suddenly “realized” there was something “else” in the experiment that we would not tell him A pile of tables and chairs in the hall was suddenly perceived as an operating table. He felt that the doctors planned to subdue and drug him and then operate on him or kill him. He became alternately belligerent and hostile, panicky and tearful.’

25
what are the most commonly reported psychotic like symptoms induced by stimulants
paranoid delusions (25-75%) auditory hallucinations (50-85%) negative symptoms e.g. catatonia (c. 30%)
26
how many schizophrenics have history of use/ dependence on stimulants
up to 60%
27
what do stats show
that those who have used amphetamine are more likely to have psychosis
28
what is the relationship between cannabis use and psychosis
cannabis use causes psychotic disorder that would not have occurred in the absence of cannabis use cannabis use may precipitate Sz or exacerbate its symptoms cannabis use functions as self-medication for those with a psychotic disorder
29
what is evidence for the risk between cannabis use and psychotic disorder
studies show that heavy or frequent cannabis use is associated with an increased risk of psychosis early use: the risk appears higher when cannabis use begins in adolescence, a critical period for brain development
30
why is cannabis used as a self-medication for psychotic disorders
people with psychotic disorders or symptoms may use cannabis as a way to manage their symtpoms (anxiety) some studies suggest that individuals with psychosis report using cannabis to relieve distress or improve mood
31
what are transient symptoms
short-lived mental or psychological effects that occur after using cannabis, typically subsiding once the user abstains from further use these symptoms are not permanent and usually resolve within days or weeks
32
what are the transient symptoms induced by cannabis in experimental conditions
de-realisation - a feeling that the world around you isn't real depersonalisation - a sense of detachment from oneself , as if observing oneself from the outside paranoia irrational suspicion of being watched
33
what are the transient symptoms induced by cannabis in naturalistic settings
hallucinations delusions
34
what is one study that shows rship between cannabis use and Sz
Zammit studied 50,000 military conscripts over time examined rship between baseline cannabis use (recorded at the start) and the subsequent risk of devceloping Sz individuals who used marijuana at baseline had a 2.4 to 6.0 times higher risk of developing Sz compared to those who did not use cannabis dose-dependent effect = the risk of sz was greater among individuals who used cannabis more frequently HOWEVER cannabis might act as a trigger for sz in people who are already vulnerable due to genetics, developmental, or environmental factors
35
what is some other data
Di Forti et al (2015) more patients with first-epsiode psychosis use cannabis every day than controls more controls than patients with first episode psychosis use less than once per week
36
what did the dunedin longitudinal study find
examined measures of sz and depression at age 26 across 3 groups: controls, cannabis users at 18 and cannabis users at 15 early cannabis use (15) confers greater risk than later use (18) risk was specific to cannabis, as opposed to other drugs risk factor even when controlling for psychotic symptoms prior to onset of cannabis use difficult to know if this is the result of usage during a sensitive period or greater cumulative exposure
37
what did Caspi et al (2005) find
examined the moderating effect of the COMT gene, on the rship between cannabis use and the risk of psychosis in the Dunedin cohort the COMT gene is involved in the brakdown of dopamine, a NT crucial for mood regulation, cognition, and perception it has different genetic variants, one of which is VAL/VAL The VAL/VAL genotype was found to moderate the effect of cannabis use on psychosis risk individuals with this genotype were at a higher risk of developing psychosis if they used cannabis during adolsecence the adolescent-onset usesrs with the VAL/VAL genotype had a significantly higher risk of developing psychotic symptoms compared to those with adult-onset use = timing of cannabis use plays a critical role adolescence is a crucial period for brain development, for areas like prefrontal cortex
38
what is the bidirectional link between cannabis use and psychosis
Griffith-Lendering et al assessed 2120 adolescents at ages 13, 16, 19 cannabis use at age 16 predcted psychosis vulenrability at age 19 psychosis vulenrability at ages 13 and 16 preidcted cannabis use at, respectively ages 16 and 19
39
1. what might explain the link between cannabis use and risk for psychosis
DISRUPTION OF DEVELOPMENT OF NT Cannabis (particularly THC) interacts with the brain's dopamine system excess dopamine activity in certain brain regions e.g. the mesolimbic pathway is strongly associated with psychotic symptoms such as hallucinations and delusions cannabis use during adolesecence may interfere with the development of GABAergic circuits, particularly in the prefrontal cortex, which regulates decision-making and inhibition THC disrupts normal endocannabinoid signaling, especially during adolescence when the brain is still developing endocannabinoid system is crucial for regulating mood, memory, and neural development
40
2. what might explain the link between cannabis use and risk for psychosis
genetic liability variations in the COMT gene e.g. VAL/VAL genotype increase susceptibility to cannabis induced psychosis due to its role in dopamine regulation individuals with a family history of SZ or other psychotic disorders are more likely to experience cannabis-induced psychosis, as they may already have a predisoposition gene-envo interaction: cannabis use acts as an environemntal trigger that interactd with genetic vulenrabilities to unmask latent psychotic disorders
41
3. what might explain the link between cannabis use and risk for psychosis
Adolescence is a time of significant brain development, including synaptic pruning and myelination (strengthening neural connections). Cannabis use may disrupt these processes, leading to structural changes in brain regions associated with psychosis. Findings in Imaging Studies: -Reduced gray matter volume in the prefrontal cortex and hippocampus (both involved in cognition and memory). -Abnormalities in white matter connectivity- affects communication between brain regions. -Changes in the amygdala, which plays a role in emotion regulation, may contribute to psychotic symptoms e.g. paranoia.
42
4. what might explain the link between cannabis use and risk for psychosis
age of onset adolescent cannabis use is more strongly linked to psychosis than adult-onset use, bc the brain is more vulenrable to disruption during this period
43
why is post-morbid cannabis use often associated with worse treatment outcomes
post-morbid cannabis use occurs after the onset of psychosis often as a form of self-mdeication to alleviate symtoms cannabis might worsen symptoms and reduce effectiveness of antipsychotic medication
44
what is the link between smoking and psychological disorders
nicotine has stimultant properties which are associated with arousing and alerting effects smokers reporting smoking to enhance their altertness/cognitive function, and there is evidnece that they do perform faster immediately after smoking than when acutely abstinent however, this may reflect their dependence rather than a normal benefit of smoking as there is very little evidence that non-smokers show performance imrpovements when given nicotine via routes such as patch or gum
45
what is the evidence that people with psychological disorders smoke more
Leon and Diaz meta-analysis showed that patients with mental illness are up to 5 times more likely to smoke Sz patients are particularly likley to smoke (70%-88%) comapred to patients with other forms of mental disorder (c. 50%) and the general population (c. 25%) patients extract more nitocotine from each cigarette and are less likely to succeed in attempts to quit
46
what is some more data showing the link between smoking and psychotic disorders
those with severe psychotic disorders smoke more than controls data on daily smoking
47
what are the beenfits of smoking on patients
smoking appears to enhance cognitive function or attenuate some specific deficits in patients suffering from various neurological and psychiatric disorders, including SZ with respect to SZ, nicotine has been reported to reduce impairments in: - visuospatial working memory - sensory gating and smooth pursuit eye movements - inhibitory control of antisaccadic eye movement
48
what is sensory gating
the brains ability to filter out irrelevant or repetitive sensory information, helping individuals focus on important stimuli
49
what is smooth pursuit eye movement
the ability to track a moving objects smoothly with the eyes
50
what is antisaccadic eye movement
intentional eye movements in the opposite direction of a visual stimulus, requiring inhibitory control and cognitive felxibility ppl with Sz often struggle with inhibitory control nicotine imrpoves inhibitory control in sz
51
1. how do rates of smoking differ depending on the medication type in szs
typical antipsychotic medications such as haloperidol block DA receptors which reduces the positive symptoms of sz such as delusions when dose of typical antipsychotics is increased, patients tend to smoke more patients smoke more to self-medicate and alleviate aversive side effects such as anhedonia (reduced ability to feel pleasure) and motor symptoms.
52
2. how do rates of smoking differ depending on the medication type in szs
atypical anitpsychotics such as clozapine or risperidone which do not block DA transmission to the same extent smoke less heavily
53
what was found about how szs patients and controls perceive smoking
Gurpegui et al (2007) asked 173 szs and 100 non-psychaitric smokers about benefits of smoking in terms of calmness, cheerfulness, alertness, concentration, agility and sociability, sz patients gave higher ratings