Early adolescence: Major depression and (social) anxiety Flashcards

1
Q

What are MDD diagnosis DSM-V?

A

5+ symptoms for 2+ weeks
* Depressed mood /anhedonia
* Weight and appetite fluctation
* Insomnia or hypersomnia
* Psychomotor agitation or retardation
* Fatigue or loss of energy
* Feeling worthless or guilty
* Difficulty to think, concentrate or indecisiveness
* recurring thoughts of death or suicidal ideation
* These symptoms should burden daily life- cause daily functioning impairment
* No other disorder or medical condition to explain the symptoms
* Never had a manic or hypomanic episode

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2
Q

What are some possible causes of MDD?

A
  • Gene-environment correlations: Certain genes can result in the individual being placed in certain environment which can influence the risk for depression ( for example if someone carries a gene which makes them shy, they’re more likely to avoid social interactions, and prone to experiencing social isolation and be at risk for depression.)
  • Gene-environment interactions: Certain environmental factors will have various affects on a person depending on their gene coding. For example, if someone experiences Adverse childhood experiences, and their genetic coding manifests as a less resilient to adversity, they’re more likely to develop MDD.
  • Epigenetics: It refers to changes in gene expression due to environmental factors. For example, environmental factors like trauma can cause high levels of stress, and chemical changes in their genetic expression, causing the person to be at risk for depression.
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3
Q

What are the impacts of prenatal maternal distress on later MDD in offspring?

A
  • It can result in higher cortisol levels and neuroinflammation in offspring.
  • HPA axis hyperactivity in the baby, higher cortisol levels and increased levels of cytokines
  • Negative impact at a cellular level
  • Reduced volume of hippocampus, and frontal areas
  • Influences functionality in brain networks
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4
Q

How is the Affective-Salience Network affected in MDD?

A

Affective-Salience Network:
* Key regions: Amygdala,Insula, Anterior cingulate cortex
* Responsible for: Detecting and prioritizing emotionally significant stimuli. / Regulating emotional response by focusing attention on important (salient) info.
* Dysregulation. Increased connectivity and activation; heightened focus mainly on negative information in MDD. Reduced activity in reward-related regions; anhedonia, persistent negative emotions.

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5
Q

How is the Cognitive Control Network affected in MDD?

A
  • Key Regions: DLPFC, PParietalC,ACC.
  • Responsible for: Managing attention, decision making, working memory, goal-directed behavior. Regulated emotional responses, adapts thinking based on task demands.
  • Hypoactivity: Reduced activity and connectivity, impairs attention, decision making, and cognitive flexibility./ Difficulty in regulating emotions, and switching beween networks. It contributes to negative thinking and reduced motivation
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6
Q

How is the Default Mode Network affected in MDD?

A
  • Key Regions: mPFC,PCC,MTemporal Lobe
  • Responsible for: Active during rest, mind wandering, self-referential thoughts. Reflecting on personal experiences, future planning and recalling memories.
  • Hyperactivity: Leads to excessive rumination, negative self-reflected thinking. Disruptive connectivity with other networks impair cognitive flexibility and increases depressive symptoms.
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7
Q

True or False? The risk of major depression disorder is the same in boys and girls

A

It depends. Until puberty, the risk levels are the same in boys and girls. After puberty, the girls are at a higher risk. Hormonal changes and the beginning of menstrual cycles can influence emotional regulation and mood. Girls often face peer pressure to maintain appearance and face higher societal expectations to be high functioning, this can lead to girls learning to mask their depressive symptoms and leave them more vulnerable. Girls are at higher risk for recurring periods of depression but. for a shorter period of time.

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8
Q

What are the brain regions implicated with anxiety disorder?

A

The anxious brain usually includes (Amygdala, Hippocampus, mPFC,Midbrain,Brainstem,Hypothalamus, HPA axis)
* Hyperactivity in Amygdala. Amygdala is responsible for the fear and stress responses to perceived threats.
* Impaired functioning in the prefrontal cortex. PFC, helps judge the situation and regulate amygdala responses.
* Impaired functioning of hippocampus. Hippocampus is our memory and learning center, in the anxious brain, the individual is unable to recall memories where they encountered the anxiety causing situation and survived.

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9
Q

What are the risk factors for Anxiety Disorder?

A
  • Female sex (after puberty)
  • Family of history of enxiety (heritable)
  • Parental Depression
  • Negative parenting interactions
  • Adverse Childhood Events
  • Reduced Peer Relationships
  • Living in a high-income country (could be due to higher expectation, more social interactions, and more complex lifestyles burden the individuals with anxiety. It could also be that people in high-income countries are more diagnosed due to having more access to resources)

  • Anxiety in early life is a predictor for AD and MDD in later life at a higher severy and more treatment-resistant
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10
Q

Why would it be hard to diagnose anxiety in children?

A
  • In children, anxiety is often disregarded and not taken seriously by caregivers or mental health professionals.
  • The symptoms could be physical like stomach ache, so the anxiety isn’t thought to be the cause.
  • Parents are afraid of the stigma and social pressure it can bring.
  • Children might have a hard time expressing how they feel.
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11
Q

You are at a neurodevelopmental conference and attend a talk about increasing societal awareness of psychiatric illnesses. In the talk, the researchers discuss about different psychiatric illnesses, how prevalent they are, and the current state of research within this field. At the end of the talk, a discussion ensues among the audience about potential methods through which clinicians could potentially help prevent the onset of psychiatric illnesses in individuals.
* Provide and elaborate on one potential idea to help alleviate the onset of psychiatric illnesses, using a specific illness as an example. (6 points)

*	Related to your idea, are there any interventional strategies you think would or would not be appropriate for implementation? (4 points).
A
  • For example, for Anxiety disorders early intervention programs could help prevent the onset. Anxiety disorders manifest during childhood and if untreated, they can lead to recurring, more severe, and treatment resistent anxiety disorder or depression. Schools could implement classes about mindfulness and emotional expression. One reason why it’s hard to detect anxiety issues in children is that they have a hard time expressing their emotions. These classes could teach children to observe, understand, feel and express their emotions. These can also help them develop more sophisticated socio-emotional skills. Early detection can help with prevention and if the child has a better grasp at how they’re feeling and how to express it, we can detect the issue early, and treat it appropriately.
  • A guided class to understand emotions, how to feel and express them would be age appropriate. However, more advanced and focused interventions might not be suitable. For example, CBT is helpful at a personal level but it wouldn’t be appropriate at a class setting. It requires ta personal approach, and unique plans for the person’s needs. In this case, during these classes, when teachers observe or when children come forward with anxiety issues, they could be guided toward CBT sessions, by informing their parents and helping them pair with a therapist.
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12
Q

Kylian, a 14-year-old boy, is brought into your clinic by his parents. He mentions that he finds it challenging to learn certain new skills at school. Although he excels in language classes and tasks requiring verbal reasoning, he finds it more challenging to do tasks requiring quantitative reasoning. His teachers comment that although Kylian’s academic performance varies based on the subject, he is by no means under-performing compared to his peers. Kylian asks you if in the brain, the development of different cognitive abilities occur in a mutually exclusive manner.
* Provide and elaborate on two different views on the matter (4 points).

*	In your opinion, is there one view that you predominantly agree with? If so, why? (2 points).
*	By giving an example, consider what the consequence of focal brain injury might be, according to these different points of view? (4 points)
A
  • Two different views on this matter are: Domain-specific and domain-general ideas. Domain-specific idea refers to the idea that certain parts of the brain that are responsible for certain skills develop exclusively and independently. Domain-general view refers to the idea that while specific cognitive skills may have a focal region, skill development is dependent on a range of cognitive processes. There is an overlap in development process and skill areas.
  • I predominantly agree with the Domain-general hypothesis because multiple brain regions are usually activated/involved when individuals engage in certain cognitive skills (eg. When learning new information, attention and memory related brain regions are often engaged).
  • According to domain-general hypothesis, focal brain injury should impact multiple cognitive skills (1 point). For example, injuries to brain regions involved in attention could give problems with learning & memory in school across multiple areas (e.g. mathematics, language, science, etc.)(1 point).
    According to domain-specific hypothesis, focal brain injury should only impact cognitive skills dependent on the specific brain region affected (1 point). For example, injury to the language related regions of the brain would affect verbal reasoning but not necessarily quantitative reasoning (1 point).
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13
Q

Which neurodevelopmental process mainly occurs throughout adolescence

A

Synaptic pruning, continues throughout adolescence and is a second window of opportunity for brain development. Possible to program brain to keep certain neural connections & integrate new connections into sophisticated networks

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14
Q

In the adolescent brain, which brain regions are in conflict

A

PFC and amygdala. PFC is responsible for planning and regulation and other higher order executive functions ; amygdala is responsible fear and stress related emotions and responses. During adolescence, amygdala is hyperactive causing the teenager to act impulsively and more likely to be engaging in risk taking behaviors. PFC is underdeveloped so the teenager isn’t mature enough to assess the consequences of actions or what’s appropriate. (The imbalance Model)

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15
Q

True or False?Schizophrenia and psychosis are two different terms for the same disorder

A

False. They’re related but not the same. Psychosis is a mental state where the individual loses sense of reality for a period of time ; schizophrenia is a mental disorder that has psychosis as one of its symptoms.

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16
Q

True or false? Schizophrenia is only characterised by delusions and hallucinations

A

False. There are various other symptoms to consider in the diagnosis of schizophrenia and there are individuals with schizophrenia who don’t have delusions and hallucinations.These are positive symptoms. Other symptoms are categorized as negative symptoms (anhedonia, affective flattening) , cognitive symptoms (executive function impairment). Often need to exhibit 2+ symptoms for 1+month

17
Q

True or false? Schizophrenic patients are dangerous

A

This is a common misconception perpetuated mostly by media and literary arts. Some schizophrenic patients could be dangerous, but usually they’re more dangerous to themselves as the suicide rate is high among schizophrenic patients. There are also geographical differences in how the auditory and visual hallucinations are perceived (In US, it’s more associated with aggresion and violence ;In the East it’s more associated with being in touch with higher being and positivity)

18
Q

Define adolescence.

A

Adolescence is the period life that starts with biological, hormonal and physical changes of puberty and end at the age in which the individual has a stable, independent role in society. Usually between 10-19 years of age. Characterized by significant physical, emotional, and social changes.

19
Q

adolescent brain’s characteristics

A
  • PFC changes dramatically and is on its way of maturing (responsible for executive functions , can result in lack of self-control, impairment in regulation and impulsivity)
  • mPFC activity hypoactive
  • Synaptic pruning is happening at a high level (fine tuning neuroconnections used/unused)
  • Myelination continues throughout adolescence (controls processing speed)
  • Overactive lymbic system Amygdala matures before the PFC (imbalance model)
  • Dopamine surge ( makes them more sensitive to reward, risk taking behavior )
  • Gray matter volume increase (peak in adolescent)
  • High neuroplasticity
  • enhanced emotional processing and sensitivity
20
Q

MDD definition

A

depression, a very common psychological disorder characterized by persistent and intense feeling of sadness or lack of interest in previously enjoyed activities.

21
Q

MDD risk factors?

A
  • Having no partner
  • Negative life events
  • Childhood trauma
  • Genetic predisposition
22
Q

Characteristics of MDD course?

A
  • Varies in remission and chronicity
  • Risk factors for worse course: Comorbidity, childhood trauma, higher sensitivity
  • 80% recurrence
  • Better course in younger patients
23
Q

Comorbidities of MDD?

A

AD, Substance Abuse, PTSD, Bipolar, Personality Disorders, Medical issues (chronic pain, diabetes, cardiovascular diseases, obesity), Eating disorders, cognitive impairments

24
Q

Mechanism of developing MDD

A
  • Genetics and environmental factors work together:
  • Genes affect the environment you’re in: if you have introverted genes, you’re less likely to involve in social activies, less friendships built, can lead to social isolation and be a risk factor.
  • Gene and Environment interaction:
    If you experience childhood traume and have less resilient genes, increased risk factor for developing MDD.
    -Epigenetics:
    The environment can affect the expression of certain genes. Dysregulated HPA axis is common. Example: In stressful environment, High cortisol level can affect certain genes’ expression causing less effective regulation and increase risk for MDD.
25
Q

Neuroendocrinology in MDD

A
  • Glucocorticoid resistance
  • Hyperactive HPA Axis
  • Higher cortisol levels
  • Altered immune response
26
Q

Neuroplasticity in MDD

A

Changes in cortisol levels and inflammatory mechanisms affects brain at a cellular level. Reduced neuroplasticity.

27
Q

What neurotransmitters are involved in MDD? How do they work in a depressed brain?

A

Monoamins: Serotonin, dopamine,noradrenaline. They work inefficiently.

28
Q

Compare depressed and normal brain

A

Depressed:
* PFC activity reduced
* Reduced Gray matter volume : cognitive/emotional issues
* Weakened neuroconnectivity especially between PFC and lymbic system :causes poor emotional regulation
* Neurochemical imbalance : Imbalanced neurotransmitter activity, mood disturbances, low mood, lack of motivation
* Reduced hippocampus size
* Lack of serotonin

29
Q

Describe types of prevention methods for MDD. Give one example each.

A
  • Universal: Entire population, public health campaigns.
  • **Selective ** : At risk groups,support programs for at risk children
  • Indicated: Personal level , individuals who show early signs,CBT.
30
Q

Specifiers of MDD?

A

Severity (Mild, moderate, severe)
MDD w/mixed features (anxious,mixed,melancholic,atypical,psychotic,catatonic)
MDD w/anxious distress

31
Q

Treatment levels for MDD?

A

1: assessment, support, psychoeducation
2: Low-intensity psychosocial interventions, medications
3:medication, high-intensity psychosocial intervention, combined treatment
4: medication, high intensity psychosocial intervention, ECT, TMS, crisis service, in patient care

32
Q

describe the 2 models of efficacy of psychotherapy

A

1) Non specific factors: Refers to the hypothesis that the effectiveness of different psychotherapies is due to their common factors. (theurapetic alliance, client expectation, empathy and support, instilling hope)
2) Specific factors: Refers to the hypothesis that specific types of psychotherapies is due to their unique set of approach adn techniques.

33
Q

Pharmacotherapy efficiency for MDD?

A

Mostly useful but takes a while to see effects. Relieves symptoms, accessible, side effects, risk of dependency.
combination therapy is best.

34
Q

How do the SSRIs work?

A

Mechanism: In depressed brain there’s kack of serotonin between synapses. Serotonin is a neurotransmitter that regulates mood, emotion and anxiety. SSRIs block the reabsorption of serotonin into neurons, making more serotonin available.

Neuron is activated, serotonin released, serotonin binds receptors, transmits signal, when done transmitting serotonin is reabsorbed or broken down to MAO.

35
Q

How do to TCAs(SNRIs) work?

A

Mechanism: inhibits the reuptake of serotonin and norepinephrine. Increases level of serotonin and norephineprhine and alleviates depression symptoms.

36
Q

How do MAOIs work?

A

Mechanisms: When a neurotransmitter is done transmitting a signal, they’re either reabsorbed or broken down to enzymes, MAOs which helps with mood regulation and emotional responses. Monoamine oxidase inhibitors, inhibits the breaking down of neurotransmitters. More neurotransmitter available, better regulation.

37
Q

How to approach Treatment Resistant Depression?

A

TRD is the type of depression where the patient doesn’t adequately respond to treatment.
- Diagnosis reassessment
- Switch medication
- Combination therapy
- Increase dosage of medication
- ECT
-Emerging treatments : TMS,Ketamine

38
Q

Types of ADs?

A

separation anxiety
selective mutism
generalized anxiety disorder
phobias
social anxiety disorder
agoraphobia
panic disorder