Anxiety and mood disorders Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What are the key features of anxiety disorders?

A
Early onset (teen), 2:1 female predominance, symptoms wax and wane over lifetime
Functional impairment and decreased quality of life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the symptoms of anxiety disorders like?

A

Characteristically an ordinary physiological reaction to an actual threat, but in disorders they are serving no real purpose as no threat present - we say it is a maladaptive extension of natural body responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is pathological anxiety?

A

Anxiety that is excessive, impairs function, and cannot be controlled - MALADAPTIVE, UNREALISTIC, DISPROPORTIONAL, PERSISTENT, ANTICIPATORY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some of the physiological, emotional, cognitive and behavioural symptoms of anxiety?

A

Somatic - goosebumps, increased HR, dilated pupils
Emotional - Sense of dread, terror, irritability
Cognitive - Anticipation of harm, problems concentrating, hypervigilance etc.
Behavioural - Escape, avoidance, aggression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What other psychological disorders do anxiety symptoms play a role in?

A

Depression - anxiety as comorbidity
Schizophrenia - anxiety when believe slipping into new episode
Drug/alcohol abuse - try to dampen symptoms of anxiety
Many anxiety disorder sufferers have more than one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are early tendencies indicative of an anxiety disorder?

A

Neuroticism, negative affect, behavioural inhibition, easily anxious/depressed in presence of stressors
Interactions with parents are key e.g. if parents are anxious, or if they are pushy and the child has to try to meet their expectations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 2 major characteristics of generalised anxiety disorder?

A

General apprehensiveness not restricted to any particular circumstance
Worry about negative events occurring in several different aspects of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the symptoms of GAD like?

A

NOT transient - persist for several months, for more days than not during that time
This is a critical facet of diagnosis - many of the symptoms are non-specific and experienced by most people in response to stress so we need to differentiate what is a legitimate problem and what isn’t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What also needs to be clarified when diagnosing GAD?

A

Symptoms not being caused by a physiological condition e.g. hypothyroidism, effect of drugs on CNS, withdrawal or another mental disorder that could better account for symptoms
SYmptoms causing significant distress or significant functional impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is one of the most popular models of generalised anxiety disorder?

A

Cognitive-behavioural model of GAD - suggests that many different factors interact to continue the cycle of anxiety
Start with a situation, and this leads to “What if..” questions which then causes worry; worry leads to negative problem orientation, anxiety and cognitive avoidance
Mood state and life events interact within this, and the overall result is often exhaustion and demoralisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the key features of the biochemical basis of GAD?

A

In the DORSAL RAPHE NUCLEUS serotonin is produced, and this normally interacts with the BASAL GANGLIA, AMYGDALA and CORTEX, inhibiting their activity
In GAD there is serotonin hypofunction, so lack of usual inhibitory effect
Additionally, NA HYPERFUNCTION from the LOCUS COERULEUS –> excessive excitatory effect on hypothalamus (autonomic responses), thalamus and cortex
Also GABA hypofunction again reducing the inhibitory effect and producing further activation of cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is panic disorder characterised by?

A

Unexpected panic attacks not restricted to particular stimuli/situations - attacks are DISCRETE, RECURRENT and TRANSIENT episodes of intense fear along with rapid and concurrent onset of several other symptoms
Can be a disorder in own right or associated with other anxiety-related disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some of the associated symptoms in panic disorder?

A
Palpitations/raised HR
Sweating
Nausea
Shortness of breath
Parasthesia (tingling)
Depersonalisation
Fear of losing control/dying
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a key problem with the symptoms of panic disorder?

A

Easy to recognise, and fear about having attacks can actually lead to even more panic - patients need strong adaptive ways of dealing with the cognitive issue of over-perceiving the threat to themselves, to reduce the risk of attacks recurring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is “the panic circle”?

A
Trigger stimulus (internal or external)
Perception of threat --> apprehension/worry e.g. about panic attack or about any distressing situation --> body sensations e.g. tingling (can also be directly caused by a trigger stimulus e.g. exercise, excitement, anger, coffee etc) --> interpretation of sensations are catastrophic --> perception of threat --> apprehension or worry etc etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What follow panic attacks?

A

Persistent concerns/worries for weeks afterwards, e.g. worries of recurrence or perceived negative significance e.g. think chest pain is heart attack
Worries lead to behaviours to reduce risk of recurrence e.g. only leaving home with trusted companion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What must we make sure before diagnosing panic disorder?

A

Symptoms aren’t due to health condition e.g. pheochromocytoma (rare adrenal gland tumour)
Symptoms not due to meds affecting CNS
Symptoms not due to withdrawal effects
Another mental health condition doesn’t account for symptoms better e.g. OCD with panic attacks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does the Kindling model of panic disorders suggest?

A

Kindling is a term to describe a phenomenon wherein brain regions become primed for triggering conditions such as epilepsy but also mood disorders
Linked to neuroplasticity, where the brain learns and adapts responses to certain triggers - each bout of a mood disorder damages brain cells and nerve pathways and makes a person more susceptible to, for example, panic attacks, increasing sensitivity of hormonal response to stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What has been suggested regarding the kindling model?

A

Prevention is actually a better focus - neuroplasticity is undeniable, but we can help by educating young people to identify and cope with triggers to help avoid the development of chronic mental illnesses altogether

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the second key model for panic disorders?

A

The vulnerability stress-model - basic susceptibility to mental disorders, rooted in genetic makeup and early life experiences, combined with stress and life challenges, our coping skills and social support

(Biological vulnerability to hypersensitive fight/flight response) x (Tendency to engage in catastrophising cognitions about physical symptoms) –> panic attacks and hypervigilance

By addressing the factors that can be controlled e.g. coping skills and social support, we can reduce symptoms and relapses and improve the course of co-occurring disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the biological basis of the kindling model of panic

A

Panic attacks –> lower threshold for chronic anxiety in limbic system, leading to more panic attacks
This lower threshold –> chronic anxiety increases likelihood of dysregulation in locus coeruleus –>poor regulation in locus coeruleus –> more panic attacks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the cognitive model of panic disorders?

A

Pay close attention to bodily sensations and misinterpret them negatively - engage in snowball catastrophic thinking, exaggerating symptoms and their consequences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the underlying biology of panic disorder like?

A

Shares some similarities with GAD - poorly regulated norepinephrine in the locus coeruleus for example, producing an excessive excitatory response
Serotonin, GABA and CCK are also involved
The brain stem fires systemically to create autonomic symptoms, the amygdala and limb system generate anticipatory anxiety and the pre-frontal cortex generates phobic avoidance
Thought to be some genetic component too, with around 10% of first degree relatives of a patient also having the disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the metabolic models of panic disorders?

A

Metabolic studies focus on how we PROCESS particular substances - people with panic disorder have been found to be more sensitive to certain substances than “normal” people, further supporting the biological theory and demonstrating how those with panic disorder have a different makeup to those without

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is an example of a metabolic model of panic disorder?

A

Panic attacks can be triggered in those with disorder by injecting LACTIC ACID (naturally produced during muscular activity)
Breathing air with elevated CO2 can also trigger attacks, as can intake of caffeine, nicotine, and alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What do many panic disorder experts currently agree?

A

Disorder caused by a combination of factors, both chemical messengers and metabolic processes are likely involved, as are genetic and environmental factors
Biological - deficiency in serotonin and GABA receptors, amygdala and fear circuitry
Sociocultural - fewer among Asian and Hispanics, more in women
Social - anxiety-filled social environment, separation/loss
Psychological - catastrophic thoughts, conditioning etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is Agoraphobia?

A

A marked and intense fear in (or simply in anticipation of) situations in which escape is difficult or help may not be available
Individuals constantly fearful due to disproportionate sense of danger or fear if specific negative outcomes e.g. having a panic attack in public

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is a key feature of agoraphobia?

A

Situations that cause fear are ACTIVELY AVOIDED or only entered in specific circumstances e.g. when with someone
Home becomes a safe place and a destructive cycle forms in which avoidance of anxiety reinforces the avoidance behaviour because distress reduced (may also start to see generalisation of avoidance behaviours)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are 4 other examples of specific phobias?

A

Animal type - extreme fear of dogs, cats, spiders etc
Natural environment type - extreme fear of heights, storms etc
Situational type - scared of public transport, tunnels, elevators etc
Blood-injection type - person will panic when seeing a cut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How can general phobias be defined?

A

Marked and excessive fear or anxiety that CONSISTENLY occurs when exposed to one or more specific triggers, OUT OF PROPORTION to actual danger present
Phobic stimulus avoided or endured with intense fear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is social phobia?

A

Long-lasting and overwhelming fear of social situations - usually starts during teen years; more than shyness, more an intense fear that doesn’t go away and affects everyday activities and relationships
Feel worried about social situations before, during and after them

32
Q

What are some of the common symptoms of social phobia/social anxiety disorder?

A

Dread about everyday activities e.g. meeting new people, starting conversations, speaking on phone
Avoiding/worrying a lot about social situations
Worrying about doing something embarrassing
Struggling to perform with people watching - feel judged
Fear of criticism, avoiding eye contact
Physical symptoms such as sweating and nausea

33
Q

What is thought about the cause of social anxiety disorder?

A

Exact cause is not known - thought to be a combination of environmental and genetic factors
Childhood maltreatment or other early-onset psych adversity are risk factors
Individuals prone to behavioural inhibition and fear of judgement are also predisposed

34
Q

How can social anxiety disorder be treated?

A

Using anti-anxiety meds such as benzodiazepines and certain SSRIs, in conjunction with CBT is most effective
Only CBT can permanently change the neural pathway associations in the brain and so meds alone have no long-term benefit (CBT can be a challenge, however, as the therapist is initially a stranger)

35
Q

What is separation anxiety disorder?

A

A marked and excessive fear of separation from those individuals to whom a person is attached - in childhood particularly the bond is with parents/caregivers (it was initially thought to be a developmental disorder)
In adults it can be a romantic partner, spouse or child

36
Q

What are some of the manifestations of the fear of separation?

A

Persistent fear that harm/an untoward event e.g. kidnapping will lead to separation
Reluctance to go to school/work
Recurrent excessive distress related to separation
Reluctance to sleep without being near attachment figure
Physical symptoms such as nausea, stomach aches, headaches when separated

37
Q

What is selective mutism?

A

Consistent selectivity in speaking - a child can show adequate language competence in specific social situations e.g. at home but consistently fails to speak in others e.g. at school

38
Q

How can selective mutism be diagnosed?

A

Disturbance needs to have occurred for at least a month (not limited to first month of school)
Needs to be clarified that the disturbance isn’t due to lack of knowledge/comfort with the spoken language

39
Q

What other neurodevelopment disorders could account for symptoms of selective mutism?

A

Autism spectrum disorder or developmental language disorder, or even a psychotic disorder

40
Q

What are the two components of Obsessive Compulsive Disorder?

A

Obsessions - unwelcome thoughts/images/urges/worries that repeatedly appear, triggering anxiety/mental discomfort
Compulsions - repetitive activities to reduce the anxiety caused by the obsessions e.g. repeatedly checking that a door is locked; may go to great lengths to meet the compulsion
Individual will experience relief from their anxiety but the obsessive response will have been strengthened and reinforced for the future

41
Q

What are the 4 criteria for a clinical diagnosis of OCD?

A

Disruption of everyday life - might avoid situations that trigger OCD, so some people may stop going into work, or even go outside; obsessive thoughts make it hard to concentrate and are exhausting
Impact on relationships - feeling that have to hide the OCD, or the doubts an obsessions may be about the relationship making it hard to continue it
Feeling ashamed or lonely - feeling that the obsessive thoughts cannot be treated, can’t talk with others, feel very isolated
Impact on physical health due to chronic anxiety

42
Q

What do models of OCD involve?

A

Integration of genetic, environmental and neurobiological factors:
Environmental (triggers) - perinatal events, stress, trauma, neuroinflammation
Genetic (vulnerability) - Gene variants and gene expression; genetic vulnerability to impact of environmental factors that might modify expression of glutamate-, serotonin- and dopamine-system-related genes through epigenetic mechanisms

43
Q

What are the 5 main categories of OCD subtypes?

A

Checking - the need to check is the compulsion, but the obsessive fear might be to prevent damage, fire, leaks or harm; Checking is often carried out multiple times, and might last for an hour or even longer causing significant impact on the person’s life, being late for school, work, social occasions and other appointments.
Compulsions can also often damage objects that are constantly being pulled and prodded or over tightened
Contamination - The fear of being dirty and contamination is the obsessional worry, often fear is that contamination might cause harm to ones self or a loved one. The common compulsions might be to wash or clean or avoid, washing until FEEL something is clean, sometimes washing hands until they bleed
Symmetry/ordering - The need to have everything lined up symmetrically just ‘right’ is the compulsion, the obsessive fear might be to ensure everything feels ‘just right’ to prevent discomfort or sometimes to prevent harm occurring
Ruminations/intrusive thoughts - rumination is a train of prolonged thinking about a question or theme that is undirected and unproductive. Unlike obsessional thoughts, ruminations are not objectionable and are indulged rather than resisted. Many ruminations dwell on religious, philosophical, or metaphysical topics, such as the origins of the universe, life after death, the nature of morality, and so on. The intrusive thoughts are repetitive and not voluntarily produced, they cause the sufferer extreme distress – the very idea that they are capable of having such thoughts in the first place can be horrifying. However, what we do know is that people with Obsessive-Compulsive Disorder are the least likely people to actually act on the thoughts, partly because they find them so repugnant and go to great lengths to avoid them and prevent them happening.
Hoarding

44
Q

What is thought to be the underlying biochemical problem in OCD?

A

Imbalance between direct and indirect loops of the CORTCIO-STRIATAL-THALAMO-CORTICAL CIRCUIT

45
Q

What does the direct loop of the CSTC circuit involve?

A

Increased glutamatergic signals from frontal cortex –> increase excitation in striatum –> increases inhibitory GABA signals to internal globus pallidus and substantia nigra
This decreases inhibitory output via GABA to thalamus –> thalamic excitatory glutamatergic output to frontal cortex –> positive feedback loop leading to repetitive thoughts and behaviour

46
Q

What is the structure of the indirect loop?

A

Composed of external globus pallidus and subthalmic nucleus, contributing to a steady state of excitation/inhibition
Or there is an unknown dysfunction at the striatum and external GP –> decreased inhibition on GPe leads to increased inhibition of STN, which decreases its activation of GPi/SNr –> GPi/SNr decreases its inhibitory output on the thalamus, resulting in excitatory output to frontal cortex

47
Q

What are the 3 universal characteristics of OCD?

A

Obsessive concern about danger and subsequent engagement in rituals to neutralise the threat
Distress accompanying obsessions
Negative reinforcement cycle - perpetuate psychopathology

48
Q

What has the APA now classified OCD as?

A

Own category of disorders rather than just being one of the anxiety disorders - other disorders in the category include body dysmorphic disorder, trichotillomania, and hoarding disorder

49
Q

What are the classes of medications used to treat anxiety disorders?

A

SSRIs (all anxiety disorders), SNRIs (serotonin-noradrenaline-reuptake inhibitor - all anxiety disorders except OCD), tricyclic antidepressants, benzodiazepine (mainly GAD but also panic/agoraphobia), monoamine oxidase inhibitors and antipsychotics

50
Q

How do SSRIs work?

A

At the synaptic cleft, increasing serotonin available thus increased serotonergic signalling (help GAD, panic disorder and OCD)

51
Q

What is one of the main benzodiazepines, and how do they work?

A

Diazepam

Involve GABA and calm down hyperactivity via hyperpolarisation (increase permeability of cell to Cl-)
Also influence serotonin and noradrenaline neurotransmitter systems

52
Q

What is an example of a barbiturate and how do they work?

A

Phenobarbitol
Similar to benzodiazepines but have stronger binding effect, thus stronger release of Cl- into the cell –> stronger hyperpolarisation (this creates a smaller window for what is considered a toxic dose)

53
Q

How do tricyclic antidepressants work?

A

Assist in increasing levels of noradrenaline, serotonin, and dopamine to a small extent (useful for panic and GAD)

54
Q

What is the cognitive triangle?

A

The system targeted by CBT - thoughts e.g. “I can’t do this”, feelings e.g. inadequacy, and behaviours e.g. acting out to avoid work because feel inadequate

55
Q

What are some of the most common symptoms of depression

A

Sadness and anhedonia (loss of interest in activities)
Physiological/behavioural - sleep disturbance, agitation, fatigue, catatonia
Cognitive - poor concentration, indecisiveness, worthlessness, suicidal thoughts, depressing delusions

56
Q

What is the relationship between anxiety and depression?

A

Most depressed people are anxious, but not all anxious people are depressed

57
Q

How can UNIPOLAR depression be categorised?

A

Major depression - depressed mood plus at least 4 of other symptoms, chronic and causes significant impairment
Dysthymic disorder - less severe but more chronic, depressed mood plus at least 2 symptoms, harder to treat as symptoms wax and wane

58
Q

What is double depression?

A

Suffering from both categories of unipolar depression - most severe form, constant low mood with intermittently even more severe bouts

59
Q

What is the underlying brain chemistry of depression?

A

A number of brain areas involved, hence why it can be so debilitating - most effects likely due to impaired serotonergic function
The insular cortex (processes convergent info to produce emotionally relevant context for sensory experience) is often overactive
Activity of the striatum slows down (responsible for movement and reward)
Underactivity of medial part of PFC, area for processing meaningful events (explains loss of interest in things)

60
Q

What are the 3 components of Beck’s cognitive explanation of depression?

A

Cognitive bias
Negative self-schemas
Negative triad

61
Q

What is meant by cognitive bias?

A

More likely to focus on negative aspects if a situation, prone to misinterpreting/distorting info
Two such biases are OVER-GENERALISATIONS and CATASTROPHISING - e.g. if fail one test, make sweeping conclusion that will fail all tests; or exaggerate a minor setback and believe it to be a complete disaster e.g. fail one exam means never get a good job

62
Q

What are negative self-schemas?

A

May come from negative experiences, such as criticism from parents
Make someone more likely to interpret info about themselves in a negative way, which could then lead to cognitive biases

63
Q

What is the negative triad?

A

Cognitive biases and negative self-schemas maintain the negative triad, a negative and irrational view of ourselves, our future and the world around us - such thoughts are automatic

64
Q

What are the 2 types of bipolar disorder?

A

TYPE 1 - alternate between full manic and depressive episodes, chronic and usually begins in late teens, suicide as common consequence
TYPE 2 - Alternate between MAJOR depressive episodes and HYPOMANIC (not fully manic) episodes, only around 10% progress to full type 1 disorder

65
Q

What are some symptoms of the manic phase of bipolar?

A

Extreme pleasure and joy from everyday activities
Extraordinarily active
Sleep very little without tiredness
Grandiose plans leading to reckless behaviour
Racing thoughts
Talk very fast

66
Q

What are some symptoms of the depressive phase of bipolar?

A
Tired all the time
Worthless and hopeless
Trouble concentrating
Lose all interest in activities
Physical aches and pains with no physical cause
67
Q

What is the integrated model of bipolar disorder?

A

Biological vulnerability (particularly strong genetic influence)–> Psychological vulnerability –> stressful life events –> Activation of stress hormones with wide-ranging effects on NTs, negative attributions + sense of hopelessness + dysfunctional attitudes and negative schema, and problems in interpersonal relationships with lack of social support –> mood disorder

68
Q

What are the neurobiological influences on mood disorders?

A

Commonly related to low levels of serotonin
Elevated cortisol and problems with HPA axis also possibly involved
Disturbed sleep and circadian rhythms are a hallmark of mood disorders

69
Q

What is the learned helplessness theory of depression and what does learned helplessness and depressive attributional style involve?

A

Related to lack of perceived control over life events
Internal attributions - belief that negative outcomes are own fault
Stable attributions - believing future negative outcomes will be ones own fault
Global attributions - believe negative events will disrupt many life activities
All 3 of these contribute to sense of hopelessness

70
Q

What cognitive errors do depressed people engage in?

A

Arbitrary inference - overemphasising negatives

Overgeneralisation - generalise single negative aspects to whole situations

71
Q

What are the psychological dimensions of mood disorders?

A

Stress is strongly related and produces poorer response to treatment
Bipolar individuals engage in negative coping styles and tendencies to interpret life events negatively

72
Q

What are the most common antidepressants?

A

Tricyclic, monoamine oxidase inhibitors (severe side effects esp when combined with certain foods or over-counter meds), SSRIs e.g. Prozac, fewer side effects

73
Q

What is the aim of CBT?

A

Help people learn to replace negative depressive thoughts and attributions with more positive ones, developing more effective coping behaviours

74
Q

What are 3 alternative options for treatment of mood disorders?

A

Interpersonal psychotherapy - helps focus on social and interpersonal triggers e.g. loss of loved one, developing skills to resolve interpersonal conflicts and build new relationships
Light therapy - for SAD
ECT - for severe depression when other treatments are ineffective

75
Q

What are some of the side effects of Tricyclic antidepressants?

A

Affect levels of ACh:
Sedation - histamine H1 receptors blocked
Postural hypotension - adrenoreceptor blockage
Blurred vision and dry mouth - muscarinic ACh receptor blockage

76
Q

How do MOIs work?

A

Elevate levels of NA, 5HT and DA by inhibiting monoamine oxidase which usually breaks these down

77
Q

What is lithium?

A

Most common treatment for bipolar, stabilising a number of NT systems including glutamate, serotonin and dopamine
More effective for manic rather than depressive episodes
(Bipolar is one of the only disorders where SSRIs are ineffective - because of both manic and depressive ends of spectrum, requires broader spectrum of treatment)