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Mental Health Nursing > Mental Health Conditions Overview > Flashcards

Mental Health Conditions Overview Flashcards

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1
Q

Depression

A
  • generally classified as mild-moderate condition
  • mild to moderate depression generally treated by a GP and psychologist, with anti-depressants and cognitive behavioural therapy (CBT)
  • often expressed as a mood state “I’m feeling depressed about…”
  • can be a major disorder, requiring extreme treatments such as electroconvulsive therapy (ECT)
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2
Q

Pathophysiology of depression

A

Several factors making people more susceptible

  • genetics
  • decreased functioning of seratonin and noradrenaline pathways
  • circadian rhythms
  • abuse and traumatic experiences
  • maladaptive coping strategies
  • cultural and socioeconomic factors
  • alcohol abuse
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3
Q

what is endogenous vs reactive depression?

A
  • endogenous depression - affective disorder with an internal cause, no external trigger. e.g. decreased functioning of seratonin and noradrenaline pathways
  • reactive depression is generally triggered by an external event, e.g. abuse or traumatic experience
  • symptoms and treatment of acute depression remain the same regardless of type
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4
Q

physical symptoms of depression

A
  • sleep disturbance and lack of energy
  • appetite loss or disturbance
  • exacerbation of other problems e.g. IBS, eczema, etc.
  • reduced activity of neurotransmitters
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5
Q

Emotional symptoms of depression

A
  • intense feelings of loss
  • guilt
  • shame
  • sadness
  • anxiety
  • self-loathing
  • anger and frustration
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6
Q

Cognitive symptoms of depression

A
  • negative thinking about themselves and their situation
  • intrusive, ruminative thoughts
  • thoughts of self-harm and in major depression, suicide
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7
Q

Behavioural symptoms of depression

A
  • withdrawal and isolation
  • avoidance
  • stopping pleasurable activities
  • lack of motivation
  • sometimes self-neglect
  • self-harm
  • maladaptive and unhelpful coping behaviours e.g. cutting, eating, drinking, unsafe sex
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8
Q

Treatment for depression

A
  • generally GP managed
  • anti-depressants
  • cognitive behavioural therapy (CBT) funded by Better Access and ATAPS federally funded therapy programs
  • if severe, inpatient admission
  • if severe/resistant/chronic and other strategies unsuccessful, electroconvulsive therapy
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9
Q

Anxiety

A
  • many types of anxiety disorders
  • all types incorporate intrusive cognitive features and intense feelings of emotional discomfort
  • low levels of occasional anxiety are normal. It becomes a mental health issue when anxiety gets out of control and becomes debilitating
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10
Q

Common anxiety disorders

A
  • obsessive compulsive disorder (OCD). Obsessive, irrational, intrusive and catastrophic thoughts neutralised or mitigated by compulsive behaviours
  • post traumatic stress disorder (PTSD) - heightened sense of responsibility for a traumatic event, characterised by flashbacks
  • panic disorder - triggering the sympathetic nervous system and causing intense and uncomfortable physical reactions
  • phobic conditions e.g. agoraphobia, social phobia, phobia of flying
  • generalised anxiety disorder (GAD) - intense and intrusive worry
  • health anxiety aka hypochondriacs
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11
Q

pathophysiology of anxiety disorders

A
  • no one single definitive cause

- all combine in a bio-psycho-social framework

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12
Q

how does anxiety impact the sympathetic nervous system?

A
  • all forms of anxiety can activate the sympathetic nervous system
  • when this occurs, the body goes into “protection mode” and blood is pushed away from our major organs and out into the muscles
  • this is sometimes referred to as ‘fight or flight’ response which can trigger a panic attack
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13
Q

sympathetic nervous system responses to ‘fight or flight’

A
  • pupils dilate
  • dry mouth
  • fast breathing
  • heart pounding
  • tense muscles
  • slow digestion
  • palms sweating
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14
Q

Hormonal responses to ‘fight or flight’

A

1 - amygdala reacts to threat
2- hypothalamus activates the sns, releasing adrenaline
3 - the adrenal cortex releases cortisol for continued alertness

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15
Q

Treatment for common anxiety disorders

A
  • CBT is first-line treatment
  • different cognitive models have been developed for all anxiety conditions
  • cognitive interventions range from basic psycho-educational techniques to full individualised formulations
  • eye movement desensitization and reprocessing (EMRD) for PTSD
  • occupational therapy - good for anxiety
  • mindfulness
  • physiotherapy and exercise
  • behavioural activation - activating positive behaviours e.g. going out and being social
  • changes in diet, sleep hygiene, smoking and alcohol reduction, relaxation
  • stress management
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16
Q

pharmacological treatment of anxiety disorders

A
  • benzodiazepines (not frequently used anymore as can make people more anxious in the long-term, and are addictive)
  • anti-psychotics
  • anti-depressants, e.g.
    • clomipramine for OCD
    • venlafaxine for anxiety/depression
    • escitalopram - SSRI for severe social anxiety
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17
Q

aetiology of personality disorders

A
  • goes across all tiers of MH care. Is very difficult to treat
    unknown but may be a combination of:
    • genetic factors
    • abuse or trauma
    • socioenvironmental factors and family dynamics
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18
Q

examples of cluster A (odd/eccentric) personality disorders

A
  • paranoid personality
  • schizoid personality
  • schizotypal personality
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19
Q

examples of cluster B (dramatic) personality disorders

A
  • antisocial personality disorder
  • emotionally unstable personality disorder “borderline”
  • histrionic personality disorder
  • narcissistic personality disorder
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20
Q

examples of cluster C (anxious/fearful) personality disorders

A
  • avoidant personality disorder
  • dependent personality disorder
  • obsessive-compulsive personality disorder
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21
Q

Cluster A

A
  • Characterised by enduring patterns of thinking and behaviour
  • Distress and impairment in important areas of functioning
  • The presentation is usually long term, and can be traced back to childhood.
  • The pattern cannot be better explained by another disorder
  • The pattern is not due to substance abuse or a medical condition
22
Q

Cluster B

A
  • Self-focus, prone to exaggerate importance of events
  • Emotional regulation
  • Difficulties in forming and maintaining relationships
23
Q

Cluster C

A
  • Often anxious, fearful and depressed
  • Obsessive compulsive personalities are generally not maintained by the fear of the obsessed belief, but by the reinforcement of behaviour.
  • Often undiagnosed and sub-clinical.
24
Q

Emotionally Unstable Personality Disorder

A
  • Emotionally unstable personality disorder is significant because of the number of admissions to secondary mental health care facilities
  • Formerly known as “borderline” personality disorder.
  • Evidence to support that in-patient treatment is ineffective, but patients often perceived as high risk when acutely unwell.
  • Treatment outcomes are generally poor
  • However, new evidence based psychological treatments and pathways of care are showing more positive outcomes.
25
Q

Emotionally unstable personality disorder common features

A
  • Instability in mood, self-image and interpersonal relationships
  • Frantic efforts to avoid real issues
  • Unrealistically positive or negative opinions about others
  • Threats and actions of self-harm
  • Pattern of unstable and intense relationship
  • Recurrent suicidal behaviour, gestures and threats
  • Overly expresses emotions and affective instability
26
Q

Treatment for emotionally unstable personality disorder

A
  • Most pharmacological treatments tend to be aimed at the management of behavioural aspects of the disorder: sedation, mood stabilization etc. However there is little evidence to support the long term use of the medication where there is no co-morbid condition.
  • Dialectical Behavioural Therapy (DBT). DBT was developed in the 70’s by Marsha Linehan to treat chronically suicidal and self-harming patients. It incorporated many aspects of CBT but the focus is on triggers (usually relationship based) that lead to the emotional states often seen in BPD. Key elements of DBT include
    • Mindfulness
    • Distress Tolerance
    • Emotional Regulation
    • Interpersonal Skills
  • Limited in-patient treatment and “alternative to hospital” programmes
  • Open borders
27
Q

Facts about schizophrenia

A
  • characterised by the presence of psychosis - disordered thinking and reasoning, loss of contact with reality, hallucinations.
  • NOT split personality
  • 1.4% of people worldwide have schizophrenia and ~1% in Australia
  • onset typically -16-35 years of age
28
Q

Pathophysiology of schizophrenia

A
  • likely a strong genetic influence, but not conclusively proven
  • possibly caused by multiple interacting genes
  • dysfunctional upbringing + trauma when coupled with genetics increases likelihood
  • substance abuse, especially hallucinogens and stimulants, may increase risk,
  • possibly links to in-utero infection
29
Q

what is the “dopamine hypothesis’?

A
  • suggested by Meltzer & stahl, 1976
  • suggests that the psychotic symptoms of schizophrenia are a result of excess dopamine activity in the synapse
  • dopamine effects outweigh acetylcholine effects during acute episodes of psychosis
  • increased dopamine results in ‘positive symptoms’ (eg hallucinations)
  • most anti-psychotics target dopamine
30
Q

Symptoms of schizophrenia

A
  • positive symptoms (exaggeration or distortion of normal function)
    • hallucinations (auditory, visual, tactile, olfactory)
    • illogical or incoherent thinking
    • disorganised speech and behaviour
  • negative symptoms (reduction in normal functioning)
    • apathy
    • lack of motivation
    • reduction in energy
    • low mood and depression
    • social inactivity
    • isolation
    • loss of pleasure
31
Q

Phases of schizophrenia

A
  • prodromal: begins usually in teenagers. loss of social, organisational and intellectual functioning
  • acute - distortion of perception and further loss of functioning. hallucinations and delusions, decreased self-care, isolation, acute distress and anxiety, sometimes paranoia
  • chronic: “burnout” of positive symptoms and increased negative symptoms
32
Q

pharmacology and treatment of schizophrenia

A
  • mainly pharmacological with anti-psychotic medicating targeting dopamine receptors
  • occupational therapy
  • physiotherapy
  • CBT
  • social and welfare needs
  • education and career support
  • ongoing support with physical health
33
Q

typical anti-psychotics

A

1st generation (50s)
- chlorpromazine
- haloperidol
- trifluoperazine
still used in severe psychosis when other medications unsuccessful.
High risk of extra pyramidal side-effects (ESPE)

34
Q

atypical antipsychotics

A 
2nd gen (90s)
- clozaril (clozapine)
- risperdal (risperidone)
- seroquel (quetiapine)
- zyprexa (olanzapine)
less sedating and lower risk of EPSE
35
Q

Extra Pyramidal Side Effects (EPSE)

A
  • dystonia: muscle spasms, mainly in the neck, jaw and back. Sometimes eyes
  • parkinsonism: tremor, bradykinesia (flat voice, facial expressions and movement), bradyphrenia (slowed thinking), salivation. may be mistaken for depression
  • akathisia: restlessness, pacing, fidgeting, rocking, foot-tapping
  • tardive dyskinesia: mainly orofacial - protruding tongue, lip-smacking, difficulty eating, speaking and breathing.

-commonly treated with anti-cholinergic drugs such as benzhexol (artane) and benztropine (congentin)

36
Q

monitoring of ESPEs

A
  • can be extremely uncomfortable and frightening, influencing compliance with medication and therapeutic outcome
  • MH nurses play a large role in monitoring patients taking anti-psychotics
  • no standardised assessment for ESPE.
  • Some tools include:
    • abnormal involuntary movement scale (AIMS)
    • extrapyramidal side effects scale
    • liverpool university neuroleptic side-effect rating scale
37
Q

other common side effects of antipsychotics

A
  • weight gain
  • insulin disregulation
  • loss of libido/sexual function
  • less likely in atypical antipsychotics
38
Q

Clozapine

A
  • first atypical anti-psychotic developed
  • can cause agranulocytosis, which can lead to immunocompression and death
  • patients on clozapine require regular monitoring of neutrophils and lymphocytes
  • often used when other atypicals have been ineffective
39
Q

Depot injection

A
  • long acting, deep intramuscular injection given fortnightly
  • depots allowed for the closure of many MH institutions and allowed for more community MH nursing and MH wards in general hospitals
40
Q

early interventions in psychosis

A
  • trusting, therapeutic relationship formed between key worker and patient
  • care primarily given in community settings, eg youth wellbeing services
  • key worker also assists with career support, education, individuality and self esteem, occupational and physio-therapy.
  • recovery-focused care
  • CBT focused on negative symptoms and voices
41
Q

Bi-Polar Affective Disorder

A
  • characterised by extreme cycles in mood.
  • previously referred to as manic-depression
  • often have long periods of stability without need of active psychiatric treatment.
42
Q

pathophysiology of bipolar

A
  • several causal factors including psychological, socio-environmental and biological
  • most likely primarily biological (genetic, hormonal and neurochemical)
    • neurotransmitter imbalance
    • HPA axis significance
    • neuroanatomical influences (differences in blood flow to areas of the brain)
  • circadian rhythms
43
Q

symptoms of bipolar

A
  • extreme “highs” and “lows” in a person’s mood
  • low periods present as major depressive phases
  • acute mania, or “manic” phases are often accompanied by psychotic symptoms/ delusional thinking
44
Q

symptoms of acute mania

A
  • Behavioural: distractive, impulsive, increased sexual desire, extravagant with money, disinhibited
  • communication: pressure of speech, talkative, loud and argumentative
  • mood: euphoric, irritable, over-optimistic and inflated self-esteem
  • physical: increased activity, no time for food or rest, decreased sleep, exhaustion
  • cognitive: grandoise delusions, flights of ideas, racing thoughts, inability to focus
45
Q

diagnostic criteria of acute mania

A
  • grandiosity
  • increased sexual desire
  • decreased need to sleep
  • more talkative than usual
  • flight of ideas, racing thoughts and irritability
  • distractibility and increased activity
  • extravagance with money
  • disinhibition
  • over- optimism, loss of critical judgement and foresight
  • excessive involvement in pleasurable activities
46
Q

depressive phase of bipolar

A
  • can be extremely debilitating with total loss of functioning
  • reduced energy and motivation
  • anhedonia
  • self-care deficit
  • hopelessness
  • poverty of thought and speech
  • severely impaired social interaction
  • disturbed sleep and appetite
  • suicide risk as energy increases
47
Q

treatment for bipolar

A
  • differs depending on the phase
  • for depressive phase: anti-depressants
  • for manic and psychotic symptoms: anti-psychotics, anxiolytics and mood stabilisers
  • aim is to stabilise the cyclic nature of BPAD using mood-stabilisers
48
Q

Mood stabilisers

A

lithium

  • naturally occurring salt
  • extremely effective in treating BPAD
  • very narrow therapeutic range. regular monitoring of serum levels required
  • toxicity can be life-threatening, affecting CN and renal systems
49
Q

anti-convulsants

A
  • high-dose anticonvulsants are affective in treating BPAD
  • sodium-valporate, carbamazapine and lamotrigine
  • less toxic than lithium, but regular serum level monitoring still required
50
Q

other treatments of BPAD

A
  • CBT - commonly used in depressive phase of BPAD
  • Occupational therapy
  • ECT - rarely used but effective in severe depressive states

Mental Health Nursing (9 decks)

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