Week 30 anxiety and mental health Flashcards
1
Q
What are benzodiazepines?
A
GABA adrenergic medications.
Psychoactive effects; anxiolytic, sedative, muscle relaxant, anticonvulsant.
2
Q
Mechanism of Action of benzodiazepines?
A
Bind to GABA-A receptors -> increased propagation of ions through Cl- channels -> hyper polarizes neuron so it is less responsive to stimuli -> sedation, reduced anxiety, mm relaxation.
Prolonged use leads to down regulation of GABA-A receptors, disrupting the balance between excitatory and inhibitory neurotransmission.
3
Q
DSM-5 for Sedative, hypnotic, or anxiolytic use disorder
A
2 of the following within a 12 month period:
-Taken in larger amts or longer time than intended.
-Persistent desire or unsuccessful efforts to cut down.
-Time spent to obtain, use, or recover
-Craving
-Recurrent use resulting in failure to fulfil obligations
-Continued use despite problems from use
-Activities given up or reduced d/t use
-Use in situations that are physically hazardous
-Use continued despite knowing it causes probs.
-Tolerance
-Withdrawal
Mild 2-3, Moderate 4-5, Severe 6+
4
Q
Benzodiazapine toxicity
A
Sedation, confusion, stupor, coma
Lethargic, CNS depression
Hyporeflexia, mm weakness, ataxia
Pupils normal or slightly constricted
HR normal or slightly decreased
RR normal or decreased
Temp normal
No sweating, seizures
GI normal
5
Q
Benzodiazapine withdrawal
A
Anxiety, aggitation, panic, irritability
Tremors
Seizures in patients with complicated withdrawal
Pupils normal or dilated
Tachycardia
HTN
RR normal or increased
Temp elevated (fever in severe cases)
Diaphoresis
Nausea, vomitting, abdominal cramps
Hallucinations, delirium, paranoia
6
Q
Complications of benzodiazapine withdrawal
A
Tolerance: higher dose required to maintain depressant effect
Kindling Phenomenon: Increasing severity of withdrawal in an individual patient
7
Q
Benzo withdrawal timeline
A
6-8 hours - early; anxiety, increased HR, insomnia, restlessness, sweating
2 days (1-2 weeks long acting) - acute; more anxiety, sleep disturbances, tremors, nausea, weight loss, palpitations, irritability
1-3 weeks - full intensity; severe insomnia, depression, confusion, memory, stiffness, risk of seizure
3-8 weeks - diminishing symptoms; reduced but persistent anxiety, mood swings, mild tremors, episodic insomnia
8+ weeks - protracted withdrawal; ongoing anxiety, depression, sleep, cognitive disruptions
8
Q
Clinical features of benzodiazepine withdrawal syndrome
A
CNS hyperactivity (tachycardia, HTN)
Tremor
Diaphoresis
Insomnia, anxiety, anorexia, headache
Pupils dilated
9
Q
General principles of benzo withdrawal management
A
Detection and stratification
General supportive measures
Benzos
Other adjunctive medications
10
Q
Diagnosis of Benzo withdrawal
A
Consider in all patients with consistent clinical features
Consider in trauma and surgical patients with altered LOC
Consider prior history of severe withdrawal
Consider differences between alcohol use and benzos
11
Q
Assessment tools for benzo withdrawal
A
- CIWA-B: treat symptoms when present, requires frequent assessment for each med admin, less medication and shorter treatment periods.
- Fixed dose protocol: consider in patients at risk for more severe withdrawal, often used in conjuction with CIWA-B
12
Q
When should you use a longer acting benzo for withdrawal managment?
Shorter?
A
Longer: Diazepam, chlordiazepoxide; smoother course, less chance of recurrent AWS and seizure
Shorter: Lorazepam, oxazepam; use in elderly, or patients with liver disease.
13
Q
Adjunctive therapies to benzo withdrawal management
A
Gapapentin
Clonidine
Mirtazapine
other agents to support with sleep and mental health symptoms
14
Q
When to use barbituates in benzo withdrawal management
A
Acute benzo withdrawal in hospital.
Lots of potential harms, needs higher level monitoring - should begin with benzos before trying barpituates.
15
Q
Tapers
A
Long-term taper: typically 10-25% every 2-3 weeks.
16
Q
Psychosocial interventions for substance use disorder
A
Peer based support
Recovery based treatment programming
17
Q
Mental status headings
A
Appearance and behaviour
Speech and language
Affect and mood
Thought
Perceptions
Cognitive
Insight and judgement
18
Q
What is added to mental status exam for a more detailed neurocognitive examination?
A
Orientation
Concentration and attention
Language
Memory
Visuospatial function
Frontal function
Body image and left/right orientation
19
Q
Suicide screening questions
A
- Have you wished you were dead or wished you could go to sleep and not wake up? (Past month = yellow)
- Have you actually had any thoughts about killing yourself? (Past month = yellow)
If NO go to Q 6
If YES go to 3, 4, 5, 6. - Have you though about how you might do this? (Orange)
- Have you had any intention of acting on these thoughts of killing yourself, as opposed to you have the thoughts but definitely would not act on them? (Red = high risk)
- Have you started to work out or worked out the details of how to kill yourself? Did you intend to carry out this plan? (Red = high risk)
- Have you done anything, started to do anything, or prepared to do anything to end your life? (Lifetime = orange, Past 3 months = red = high risk)
20
Q
Anxiety
A
Response to FUTURE THREAT
Apprehension, WORRY, hypervigilance
Increased mm tension
Avoidance and escape behaviours
21
Q
Fear
A
Response to IMMEDIATE THREAT
Thoughts of imminent danger
Surges of autonomic arousal
Escape behaviours
22
Q
Stress reaction
A
Response to a RECENT OR ONGOING STRESSOR
Stressor = event or situation requiring adaptation or adjustment
Autonomic arousal, mm tension, agitation
Nervousness, IRRITABILITY
23
Q
DSM-5 Anxiety disorders
A
Separation anxiety disorder
Selective mutism
Specific phobia
Social anxiety disorder
Panic disorder
Agoraphobia
GAD
Other (unspecified)
24
Q
DSM-5 Obsessive-compulsive and related disorders
A
OCD
Body dysmorphic disorder
Hoarding disorder
Trichotillomania
Excoriation disorder
Other (unspecified)
25
DSM-5 Trauma and stressor related disorders
Reactive attachment disorder
Disinhibited social engagement disorder
PTSD
Acute stress disorder
Adjustment disorder
Prolonged grief disorder
Other (unspecified)
26
Significance of anxiety and related disorders
Among the most prevalent mental disorders
Considerable suffering and impairment
High costs
Tend to be chronic if untreated
Prevalence increasing?
27
Factors that can affect regional differences in anxiety prevalence
Reporting biases
Cultural factors
Mental health literacy
Social support and other stress buffering factors
Stressors endemic to a given culture
28
Pattern and pathways for onset of specific phobia
Trauma exposure
Observational learning
Unexpected panic attack
Failure of innate fears to extinguish
29
Pattern and pathways for onset of social anxiety disorder
Insidious: gradual emergence from a history of shyness
Abrupt: Following a stressful or humiliating experience
30
Pattern and pathways for onset of panic disorder
Onset with recurrent unexpected panic attacks
31
Pattern and pathways for onset of agoraphobia
Preceded by panic attacks or panic disorder in 30-50% of cases
32
Pattern and pathways for onset of GAD
Typically gradual onset
33
Pattern and pathways for onset of OCD
Typically gradual onset
34
Pattern and pathways for onset of PTSD
Onset usually within 3 months of trauma exposure
35
What is anxiety often comorbid with?
Other anxiety and mood disorders
Substance use disorders
Eating disorders
Personality disorders
36
Course of:
1. specific phobia
2. SAD
3. panic disorder, agoraphobia, GAD, OCD, PTSD
4. PTSD
1. Tends to be chronic in adults, transient in kids.
2. Tends to be chronic
3. Chronic, waxing, waning
4. Complete recovery within 3 months for 50% of adults. May be exacerbated by trauma reminders.
37
List the 6 neural circuits implicated in anxiety disorders
1. Acute threat responses
2. Responses to distant, potential, or uncertain threats
3. Responses to ongoing or sustained threats
4. Reward processing
5. Cognitive systems; cognitive control & working memory
6. Social processing
38
People prone to anxiety disorders tend to have high scores on:
Negative emotionality
Behavioural inhibition
Anxiety sensitivity
39
Define 'clinically significant' in terms of anxiety
Excessive in relation to threat.
Highly distressing and persistent.
Impairs social and occupational functioning.
40
What is psychotherapy (5 points)
Interpersonal treatment
Involves a trained mental health professional
Patient has a problem to address
Based on psychological principles and intended to have a beneficial effect on the patient's disorder, problem, or complaint
Treatment is adaptable or individualized for the patient and their disorder, problem, or complaint
41
8 core elements of psychotherapy
Confiding relationship with a therapist.
Framework for understanding the patient's problem.
Therapeutic procedures/rituals for resolving problems.
Therapist expertise conveys rigor about the process.
Affective arousal.
Feeling understood by the therapist.
Hope/optimism for improvement.
Success experiences.
42
Discuss the professional relationship in therapy (4 points)
The therapy relationship is professional, with boundaries.
Power imbalance always exists.
Therapist expects nothing from patient except payment of fee.
Sexual relationships are unethical and strictly prohibited.
43
Discuss 3 points of confidentiality
Assurance of privacy and confidentiality is essential.
Strict rules and regulations about protection of patient information.
Confidentiality may only be broken under certain conditions.
44
Discuss 3 points of cultural sensitivity
Maintain openness toward patient's cultural experience.
Cultural norms or expectations may influence a patient's opinions about their problems and the help-seeking process.
Avoid making assumptions about or ignoring consideration of culture.
45
6 principles of CBT
Provide psychoeducation about the maintenance of depression via cognitive triangle.
Develop goals for treatment and maintain a structured agenda for therapy sessions.
Promote engagement in healthy behaviours to promote feelings of efficacy.
Examine thought patterns for negative cognitive bias.
Promote alternative, more balanced interpretation of the exprerience.
Homework to practice new behaviours and alternative cognitive interpretations.
46
What is the most robust predictor of treatment outcome?
The therapy relationship.
Relate to patients with empathy and acceptance.
Develop a collaborative agreement on where the therapy is going.
Respond differentially to each patient's unique characteristics.
47
Humanistic conditions as determined by Carl Rogers
Positive regard.
Unconditional acceptance.
Empathy.
Congruence.
48
Personality definition
Term used to describe the uniqueness of an individual, who the person really is and how they differ from other people.
49
Temperament
Basic biological disposition toward certain behaviours.
Genetically coded influences of nature.
50
Key dimensions of personality as reflected in the trait approach.
Affectionate
Aggressive
Ambitious
Bad-tempered
Courageous
Dependable
Egotistical
Impulsive
Intelligent
Introverted
Joyjul
Reliable
Sociable
Sympathetic
Talkative
51
5-Factor model of personality
O Openness to experience
C Conscientiousness
E Extraversion
A Agreeableness
N Neuroticism
52
Personality Disorder as per DSM-5
Enduring pattern of inner experience and behaviour that deviates markedly from expectations of person's culture.
Manifested in at least 2 areas: cognition, affect, interpersonal functioning, impulse control.
Pervasive, inflexible across time and situation.
Causes subjective distress or functional impairment.
Onset in late adolescence or young adulthood.
Not due to substance use or other medical condition.
53
Clusters of personality disorders
Cluster A: odd-eccentric
Cluster B: dramatic-emotional
Cluster C: anxious-fearful
54
One year prevalence of MDD
7.6%
55
Lifetime prevalence of MDD
15%
56
MDE vs MDD
MDE: 5 or more symptoms >= 2 weeks, can have other health concerns, or be part of another mental health issue.
MDD: 1 or more MDE with no other explanation for symptoms and NO mania/substance use. Recurrent requires >2 months remission.
MDE can occur within the context of different types of depressive disorders or bipolar disorder.
57
Of which 2 criteria does at least one have to be present for depression?
Depressed mood
Loss of interest/pleasure
Plus SIGECAPS
Total 5 symptoms.
58
MDD vs Persistent depressive disorder
MDD: one or more MDEs, no mania/hypomania/substance use.
Persistent depressive disorder: Depressed mood > 2years + 2 or more SIGECAPS.
59
PHQ-9 scoring
0-4: none or minimal
5-9: mild
10-14: moderate
15-19: moderately severe
20+: severe
(10 or higher indicates significant depression)
60
What to rule out as ddx for MDD
Bipolar disorders
Adjustment disorders
Substance induced
D/t another medical condition
Depression assessment must include assessment for rule out and comorbid conditions.
61
Often comorbid on ddx with MDD
Anxiety disorders
Personality disorders
Other medical conditions
Substance use
Depression assessment must include assessment for rule out and comorbid conditions.
62
Causes of depression
Multifactorial
Biopsychosocial model
63
Treatments for MDD
Medication
ECT
Transcranial magnetic stimulation
Light therapy
Counselling/psychotherapy
Self-management
Support groups
Exercise
64
Biological contributors to depression
Twin studies ~ 40%
First degree relative increases risk 2-3xs
No single gene; multiple genes of small effect
MOA receptors
Neurogenesis
Circadian rhythms
65
Monamine hypothesis of depression
Depression is caused by some deficiency in the transmission of monoamines in the brain.
Serotonin
Dopamine
Norepi
Supported by the efficacy of SSRI/SNRI meds, however an overly simplistic model b/c we know depression is multifactorial.
66
Psychosocial contributors to depression
ACEs are potent predictors of adult MDD.
Recent life stressor common precipitants of MDEs.
Personality trait of neuroticism linked to MDD.
Cognitive biases can increase vulnerability to MDEs.
67
Cognitive depression cycle
1. Negative stressful events
2. Negative explanatory style.
3. Hopeless depressed state.
4. These hamper the way the individual thinks and acts, further fueling the cycle.
68
CANMAT clinical guidelines for management of depression
Conduct thorough assessment
Obtain collateral information
Formulate ddx -> dx
Support education and self management
Establish therapeutic alliance
Construct a comprehensive safety & management plan
Deliver evidence based treatments
Use measurement based care to monitor outcomes
Back to assessment and start cycle again.
69
Selecting the initial treatment for MDE
Mild with low safety risks: Psychotherapy or pharmacotherapy. Psychotherapy preferred d/t fewer risks.
Moderate with low-moderate safety risks: Psychotherapy or pharmacotherapy - combination may be considered.
Severe w/out psychotic features: Combination psychotherapy & pharmacotherapy.
Severe with psychotic features: Combination antidepressant and antipsychotic medication.
Life-threatening conditions: Consider ECT
70
Major psychotherapies for MDD
Behavioural activation (BA): Depression is a consequence of compromised environmental sources of positive reinforcement -> Increase activity and access to rewarding experiences. Address inertia, avoidance, social withdrawal.
Cognitive therapy (CT)/(CBT): Distorted beliefs about the self, the world, and the future maintain depressive affect -> Recognize negative cognitions. Respond to negative thoughts and behaviours. Problem solve and test assumptions.
Interpersonal therapy (IP): Current interpersonal issues maintain depressive affect -> Identify issue (role transition, role dispute, grief, interpersonal deficits). Focus on social context.
71
Commonly used AD classes
SSRI
SNRI
NaSSA
NDRI
Multimodal
SARI
72
SSRIs
1. MOI
2. Representative meds
3. Possible symptom profiles
1. Blocks reuptake of 5-HT from synaptic cleft.
2. Citalopram, escitalopram, sertraline, fluoxetine, fluvoxamine, paroxetine.
3. Anxiety/agitation
73
SNRIs
1. MOI
2. Representative meds
3. Possible symptom profiles
1. Blocks reuptake of 5-HT and NE
2. Velafaxine, duloxetine, levomilnacipran, desvelafaxine
3. Low energy, comorbid pain (especially duloxetine), affective flattening, anxiety, menopausal vasomotor symptoms.
74
NaSSA
1. MOI
2. Representative meds
3. Possible symptom profiles
1. Blocks a2 autoreceptor and some 5-HT receptors
2. Mirtazapine
3. Insomnia, poor appetite
75
NDRIs
1. MOI
2. Representative meds
3. Possible symptom profiles
1. Blocks dopamine and Norepi reuptake
2. Bupropion
3. Low energy, low motivation, increased appetite, hypersomnia, comorbid ADHD
76
Multimodal ADs
1. MOI
2. Representative meds
3. Possible symptom profiles
1. Blocks 5-HT reputake and modulates multiple 5-HT receptors
2. Vortioxetine
3. Pronounced cognitive symptoms
77
SARIs
1. MOI
2. Representative meds
3. Possible symptom profiles
1. Blocks 5-HT reuptake and 5HT2A/2C receptors
2. Trazodone
3. Rarely used at antidepressant doses, usually a sleep aid at lower doses.
78
Factors to consider in selecting and antidepressant
Most modern classes are first line.
No robust evidence that on is better than another.
Symptom profiles based on clinical experience, not research.
Clinically choose based on: efficacy, tolerability, interactions, safety, simplicity, previous experiences, comorbidity, patient preference, cost.
79
Non pharmocologic first line treatment for mild-moderate MDD
Exercise
30 minutes 3x/week, moderate intensity for >9 weeks.
80
Non pharmacologic first line treatment for seasonal MDD.
Light therapy
2nd line for non seasonal MDD
81
Treatment for treatment resistant depression
Neurostimulation: ECT or rTMS
82
Bipolar 1 vs Bipolar 2
Bipolar I: One or more manic episodes
Bipolar 2: One or more hypomanic episode and 1 or more MDE.
83
DSM-5 manic episode (Bipolar 1)
7 days or more days of abnormally and persistently elevated, expansive, or irritable mood
AND
Abnormally and persistently increased goal-directed activity or energy lasting 1 week (any duration is needed to be hospitalized)
AND
3 or more:
Inflated self esteem
Decreased need for sleep
Pressured speech
Flight of ideas
Distractibility
Increase in goal-directed activity
Increased risky behaviour
(4 if the mood is only irritable)
May or may not have depressive episodes. Must include one full blown manic episode.
84
DSM-5 Hypomanic episode (Bipolar 2)
4 or more days of abnormally and persistently elevated, expansive, or irritable mood.
AND
Abnormally and persistently increased goal directed activity or energy
AND
3 or more:
Inflated self esteem
Decreased need for sleep
Pressured speech
Flight of ideas
Distractibility
Increase in goal-directed activity
Increased risky behaviour
(4 if the mood is only irritable)
Must include MDEs and mania is less severe than Bipolar 1.
85
LIfetime prevalence of bipolar 1/2
Bipolar 1: 1%
Bipolar 2: 1.1%
86
Etiology of bipolar
Likely genetic MZ: 80% risk, DZ: 20% risk but no single gene identified.
Dopaminergic dysfunction.
Chronobiological disturbance.
Neuroinflammation.
Neurocircuitry dysfunction.
Oxidative stress.
Mitochondrial dysfunction.
87
Medical management for bipolar 1 manic episode
Rule out substances/medical contributors.
Stop offending agents.
Decide appropriate treatment setting.
Initiate treatment w/1 or more first line agents:
Mood stabilizers: lithium, divalproex
Atypical antipsychotics: quetiapine, asenapine, aripiprazole, risperidone, paliperidone
May use monotherapy with mood stabilizer or APP or combination mood stabilizer + APP
Bipolar usually does not respond well to antidepressants.
88
Medical management for bipolar 1 depressive episode
Rule out substances/medical contributors.
Assess safety.
Stop offending agents.
Decide appropriate treatment setting.
Initiate treatment w/1 or more first line agents:
Mood stabilizers: lithium, divalproex, lamotrigine
Atypical antipsychotics: quetiapine, lurasidone
89
Diagnostic process in medicine vs phycology
Medicine: abnormal means morbid/diseased
Psychology: abnormal has a statistical meaning where it implies uncommon or rare.
In psychiatry, both frequency and severity may contribute to defining an experience as abnormal.
90
Steps to reaching a diagnosis in psychiatric disorders
1. Presenting problem
2. History - **Includes mental status exam.
3. Symptoms: signs & symptoms
4. Course
5. Risk and protective factors
6. ?Syndrome
7. Diagnosis
91
Symptoms vs syndrome
Symptoms can be distinguished from one another.
A cluster of symptoms with natural course of development and remission can be a syndrome.
92
SAFE approach for mood disorders
S Safety first
A Actively listen
F Find red Flags/other causes
E Empower recovery
93
Safety first 6 DO NOT MISS signs
1. Suicide
2. Violence
3. Self-medication
4. Weapons
5. Other cause
6. Do I need help
94
Actively listen Pearls
Risk: ALWAYS Ask and document
95
Mneumonic for serotonin syndrome
MAN
M - mental status changes
A - autonomic hyperactivity
N - neuromuscular abnormalities
96
Dx of serotonin syndrome
Hunter Criteria:
Has taken a serotonergic agent and has at least one one:
Spontaneous clonus
Inducible clonus + agitation or diaphoresis
Ocular clonus + agitation or diaphoresis
Tremor + hyperreflexia
Hypertonia + temp >38 + ocular clonus or inducible clonus
97
Treatment of serotonin syndrome
1. Stop serotonergic agent.
2. Sedation and supportive care.
3. Cyprohexadine if sedation and supportive care don't work.
98
Common SSRIs
Citalopram, escitalopram, sertraline, fluoxetine, fluvoxamine, paroxetine
99
Common side effects of SSRIs
Insomnia, anxiety, decreased libido, irritability d/t stimulation of brain 5-HT2 receptors.
ED, anorgasmia, ejaculatory delay d/t stimulation of spinal 5-HT2 receptors.
Nausea, diarrhea, vomiting d/t stimulation of 5-HT3 receptors in GI
100
Metabolism and elimination of SSRIs
Mostly metabolized in liver by CYP enzymes.
1/2 life long enough for 1/daily dosing
101
Common SNRIs
Venlaxafine, duloxetine
102
MOI of SNRIs
Block reuptake of NE and serontonin.
Noradrenergic effect stimulates gene expression affecting BDNF.
103
Adverse effects of SNRIs
Nausea, headache, sexual dysfunction, constipation.
HTN
Sweating
Wt loss
Insomnia
104
Metabolism and elimination of SNRIs
Metabolized by liver and excreted by kidneys.
1/2 life long enough for 1/day dosing.
105
Common NDRIs
Buproprion
106
MOI of NDRIs
NE and dopamine reuptake inhibitor
107
Adverse effects of NDRIs
Anxiety
Tachycardia
HTN
Tremor
Insomnia
Irritability.
Can increase risk of seizures.
108
Common NaSSAs
Mirtazapine
109
MOI of NaSSas
Complex action on serotonergic & alpha receptors.
110
Adverse effects of NaSSAs
Somnelence
Sedation
Increased appetite
Wt gain
Agranulocytosis
111
Vortioxetine method of action and adverse effects
Serontonin modulator and stimulator.
Same effects as SSRIs plus nausea and dizziness.
Less incidence of sexual dysfunction.
112
Trazodone method of action and adverse effects
5-HT2a antagonist and reuptake inhibitor.
Limited efficacy. Low doses used to treat insomnia.
Adverse effects: Sedation, orthostatic hypotension, priapism.
113
Moclobemid method of action and adverse effects
Reversible inhibitor of MAO-A, increases levels of NE, 5-HT, Dopamine.
Adverse effects: Insomnia, hypomania, headache, tremor, orthostatic hypotension, palpitations, dry mouth, blurred vision, constipation.
**Needs a washout period when switching to other drugs to avoid serotonin syndrome.
114
TCA method of action
Block reuptake of serotonin and NE.
115
Common TCAs
Amitryptyline, nortriptyline, desipramine, clomipramine, imipramine.
116
TCA side effects
Sedation d/t antagonism of brain H1 receptors.
Cognitive dullness d/t antagonism of central muscarinic receptors.
Blurred vision, dry mouth, tachycardia, constipation, urinary retention d/t antagonims of peripheral muscarinic receptors.
Orthostatic hypotension d/t antagonism of A1 receptors.
117
MAOi method of action
Block enzymes responsible for metabolism of monoamines.
Irreversible inhibitors.
118
Common MAOis
Phenylzine
Tranylcypromine
Isocarboxazid
119
Adverse effects of MAOis
Toxicity and major drug and food interactions.
120
Brain structures involved in Fight-Flight-Freeze response
Hypothalamus:
Endocrine and neural responses.
Increase heartbeat.
Increase respt.
Increase glucose release.
Locus Ceruleus:
Norepinephrine
Striatum (nucleus accumbens):
Complex motor responses.
Anterior cingulate cortex:
Interprets signal, resolving conflicting info.
Ventromedial prefrontal cortex:
Brakes for the amygdala.
Insula:
Decoding internal representations.
Hippocampus:
Contextual control of reactions based on memory.
Higher cortical regions are part of the cognitive loop, giving rise to conscious feelings of fear/anxiety.
121
Discuss the neural circuitry associated with MDD
Default Mode: Rumination
Salience: Anxious avoidance
Positive affect: anhedonia
Cognitive Control: cognitive flexibility
Reflect different signalling pathways involved in MDD.
122
Which physiological axis has been implicated in anxiety and depression?
HPA axis.
Depression: hypersecretion of CRF -> hypercortisolemia -> decreased suppression of cortisol/impaired negative feedback.
Anxiety: dysregulated HPA as well.
123
Immune system and depression
Symptoms of sickness behaviour are similar to MDD.
Rates of MDD higher in patients with AI disorders.
Depression a common side effect of immune therapies.
Patients with MDD have increased serum cytokines.
124
