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Flashcards in Mental Health Deck (23)
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Identify the brain area associated with anxiety disorder.

  • Amygdala responsible for emotional processes and fear response.
  • Sensory stimuli passes along thalamo-cortical route to the cortex for “higher-level” processing; a second route, from the thalamus to amygdala facilitates faster response to danger based on previous learning
  • During stressful event, amygdala co-ordinates with brainstem nucleus (locus ceruleus) to activate physiological changes linked to sympathetic responses

Describe the mechanism of action for the 2 major drug groups used to treat anxiety disorders.

  • Neurotransmitter γ-Amino-Butyric Acid (GABA) is well distributed within amygdala with large number of neurones sensitive to inhibitory effects
  • Evidence of GABAergic involvement to modulate anxiety demonstrated by drugs such as benzodiazepines, barbiturates and alcohol which bind to GABA receptors to agonise post- synaptic inhibitory effects and reduce anxiety
  • Changes in composition of GABA receptor may be mechanism whereby neuronal inhibition is lost in pathological anxiety states

Discuss principle features of an individual who has obsessive-compulsive disorder.


Obsessive-compulsive disorder- intrusive thoughts that produce fear or worry (obsessions) and repetitive behaviors (compulsions) aimed at reduction of associated fear.

  • Theorise OCD is caused by chemical imbalance of neurotransmitter serotonin; vital chemical messages are lost (due to serotonin re-uptake) and OCD symptoms develop
  • Cortex becomes hyperactive, sends out equivalents of false alarms; when false signals reach basal ganglia they ‘lock’ into hyperactive transmission of distress signals back and forth to one another. Many view OCD as a “shake in the mind”, similar to tremors seen in Parkinson’s patients (both disorders based on irregularities of neuronal synapse in basal ganglia)

Describe the causes of PTSD and symptoms.

  • Post-traumatic stress disorder- symptoms (e.g. disturbing recurrent flashbacks, hyperarousal) that continue for more than a month after the occurrence of a traumatic event.
  • Post-traumatic stress disorder is the only major mental disorder with a known cause (an event that threatens one’s physical integrity or that of others and induces a response of intense fear, helplessness or horror)
  • Theorised that the ventromedial prefrontal cortex fails to inhibit the amygdala, whose hyperactivation leads to an increased fear response, impaired extinction of traumatic memories and deficits in emotion regulation

Describe the pathophysiology of a panic attack.


Panic attack- period of intense fear with sudden onset accompanied by at least four or more symptoms (e.g. palpitations, dizziness, shortness of breath) of variable duration.

  • Prevalence of people who experience at least one in lifetime = 28.3%
  • Fear response due to aroused sympathetic activity manifested in absence of actual danger
  • Theoretically, disruption in amygdala causes maladaptive and exaggerated fear responses

Identify the characteristics, classifications and biological basis of mood disorders.


• Depression
A sustained low mood over the entire day for at least 2 weeks.
-Loss of pleasure or enjoyment
-Feelings of hopelessness, helplessness, worthlessness, inappropriate guilt, poor concentration and lack of motivation
-Lack of energy, insomnia, reduced libido, motor slowing or agitation, loss of appetite and weight loss

• Major depressive disorder
Depressed mood or a loss of interest or pleasure in daily activities for more than two weeks
-Mood represents a change from the person’s baseline
-Impaired function: social, occupational, educational
-Specific symptoms( ≥5 ) present nearly every day:
– Depressed mood/irritable most of the day, nearly every day, indicated by subjective report or observation
– Decreased interest or pleasure in most activities, every day
– Significant weight change (5%)/ change in appetite
– Insomnia or hypersomnia
– Psychomotor agitation or retardation
– Fatigue/ loss of energy
– Feelings of worthlessness/ guilt
– Diminished ability to think/ indecisiveness
– Suicidality

• Dysthymia
A sustained low mood present most of the time for at least 2 years with at least 1 symptom of depression but without meeting criteria for major depressive disorder.

• Bipolar affective disorder
– Type I
Defined by manic episodes that last at least 7 days, or by manic symptoms that are so severe that the person needs immediate hospital care. Usually, depressive episodes occur as well, typically lasting at least 2 weeks. Episodes of depression with mixed features (having depression and manic symptoms at the same time) are also possible.
– Type II
Defined by a pattern of depressive episodes and hypomanic episodes, but not the full-blown manic episodes described above.
People with bipolar disorder experience periods of unusually intense emotion, changes in sleep patterns and activity levels, and unusual behaviors. These distinct periods are called “mood episodes.” Mood episodes are drastically different from the moods and behaviors that are typical for the person. Extreme changes in energy, activity, and sleep go along with mood episodes.


Tricyclic antidepressants (TCAs)

  • mechanism of action
  • adverse effects

Mechanism of action:
-NA, serotonin normally removed from synapse by reuptake sites; TCAs block neuronal reuptake of NA and/or serotonin
-Long half lives
-Amitryptiline (Endep)
-Doxepin (Deptran)
-Imipramine (Tofranil)
-Nortriptyline (Allegron)
-Clomipramine (Anafranil)
Adverse effects:
Block muscarinic, alpha 1 adrenergic and histamine H1 receptors. The blockade of these receptors results in:
• Anticholinergic effects: blurred vision, urinary retention, constipation and glaucoma.
• Sympatholytic effects (alpha 1 blockade): orthostatic hypotension, dizziness and tachycardia.
• Histamine (H1) antagonism: sedation.
More adverse effects:
-Cardiac toxicity (tachycardia, dysrhythmias)


Monoamine Oxidase Inhibitors (MAOIs)

  • mechanism of action
  • adverse effects

Mechanism of action:

  • MAO converts monoamine neurotransmitters (NA, serotonin and dopamine) into inactive products
  • MAOIs cause irreversible inhibition (lasts 2 weeks)

-Phenelzine (Nardil)
-Tranylcipromine (Parnate)
-Selegiline (Eldepryl)
All MAOIs administered orally

Adverse effects:
• CNS stimulation
• Orthostatic hypotension
• Hypertensive crisis from dietary tyramine


Selective Serotonin Reuptake Inhibitors (SSRIs)

  • mechanism of action
  • adverse effects

Mechanism of action:

  • Produce selective inhibition of serotonin reuptake
  • Produce CNS excitation
  • Fluoxetine (Prozac)
  • Sertraline (Zoloft)
  • Citalopram (Citalo)
  • Escitalopram (Lexapro)

Adverse effects:
• Serotonin syndrome (2–72 post treatment)
• Withdrawal syndrome
• Teratogenesis
• Extrapyramidal side effects
• Bruxism
• Bleeding disorders • Sexual dysfunction • Weight gain


Serotonin/Noradrenaline Reuptake Inhibitors (SNRIs)

  • mechanism of action
  • adverse effects

Mechanism of action:
• Blocks NA and serotonin uptake;
• Second generation antidepressant as improved tolerability and safety profile

  • Venlafaxine (Effexor)
  • Duloxetine (Cymbalta)
Adverse effects:
– Nausea                   – Somnolence
– Headache               – Diastolic hypertension
– Sexual dysfunction
– Hyponatremia (in older adult patients)
– Anorexia                 – Insomnia
– Nervousness          – Weight loss/anorexia
– Sweating                – Dry mouth

Identify the characteristics of and treatments for bipolar affective disorder.


Bipolar Affective Disorder- a mental disorder characterised by periods of elevated mood (mania) and periods of depression.
• Can be characterised solely by manic episodes (uncommon)
• Occurs in ~1% of the population
-BD associated with abnormal sleep/wake cycles, appetite, seasonal and social rhythms
-Genetic association studies demonstrate that variations in a core ‘clock gene’ may be linked to susceptibility to BD.
-Data suggest BD may be related to pro- inflammatory cytokine levels
Mood stabilisers (Lithium or valproate/carbamazepine)
-Relieve symptoms during manic/depressive episodes
-Prevent recurrence of manic/depressive episodes
-Do not worsen symptoms of mania or depression; do not accelerate the rate of cycling
• Given during severe manic episodes
• Given during depressive episodes
Lithium (e.g. Lithicarb, Quilonum)-
-Altered distribution of certain ions
-Altered synthesis and release of NA, serotonin and dopamine
-Increases volume of prefrontal cortex, hippocampus and amygdala, reflecting its neuroprotective effects
-Reduces excitatory (dopamine and glutamate) while increases inhibitory (GABA) neurotransmission


Describe the characteristics of schizophrenia and explain the role genetics is thought to play in development of schizophrenia.


Schizophrenia- a mental disorder characterised by abnormal social behavior and failure to recognise what is real.
-Affects ~1.4% of the population
-25% of people with psychotic symptoms recover; 25% will have episodic course with periods of relatively good mental health
-50% have continuous illness
– Paranoid, catatonic, disorganised and undifferentiated
– Subsyndromal forms include schizophreniform disorder and schizotypal personality

Positive symptoms: exaggerated function
– Delusions and illogical or incoherent thinking, hallucinations, disorganised speech and behaviour
Negative symptoms: diminished function
– Apathy, lack of motivation, inability to initiate action, poor concentration, emotional blunting, reduced thought and speech content, lack of pleasure, inability to maintain social relationships and sleep disturbance
-Hypothesis that critical metabolic changes occur during early neurodevelopment which contribute to schizophrenia (Maschietto et al., 2015)
-Suggested as syndrome of accelerated aging (Polho et al., 2015)
-Data suggest schizophrenia may be related to pro-inflammatory cytokine levels (Reus et al., 2015; Nakagawa & Chiba, 2014)


Contrast first generation antipsychotic drugs to second generation drugs in terms of mechanism of action and adverse effects.


First-generation antipsychotics-
• Block receptors for dopamine in CNS
• Cause serious movement disorders → extrapyramidal symptoms

Second-generation antipsychotics-
• Produce only moderate blockade of dopamine receptors; stronger blockade for serotonin
-Fewer extrapyramidal symptoms
-Risk of metabolic effects

Mechanism of action of antipsychotics-

  • Antagonise several receptor types within/outside CNS
  • Antagonise dopamine receptors in the mesolimbic area of the brain

Summarise the extrapyramidal side effects caused by antipsychotic drugs and therapeutic approaches to minimise them.

– Anticholinergic effects 
– Orthostatic hypotension 
– Galactorrhoea
– Sedation
– Neuroendocrine effects – Seizures
– Sexual dysfunction
– Dermatologic effects
– Agranulocytosis
– Severe dysrhythmias
Therapeutic approaches:
 -Establish a good therapeutic relationship with patient and family
-Promote treatment adherence
– Ensure that medication is taken
– Encourage family members to oversee medication for outpatients
– Provide patients with instructions/information on schedule and side effects
-Use IM depot preparation for long-term therapy

Describe the sleep process.


Stage 1:
We experience a light transitional sleep. This is where drowsiness and sleep begin.
Stage 2:
More stable sleep occurs. Chemicals produced in the brain block the senses making it difficult to be woken.
Stage 3:
Is deep sleep. Growth hormone is released during this stage. Most stage 3 sleep occurs in the first third of the night.
REM sleep revitalizes the memory. In this stage brain activity is very high and intense dreaming is likely to occur.


Summarise the main points of sleep fitness and approaches to sleep without medications.


Good sleep hygiene education
– regular bedtimes, no daytime nap, bedtime routine (hot drink, relaxation, bath, walk), no TV or computer before bedtime, milk (contains trypophan which induces sleep)


Explain the difference between anorexia nervosa and bulimia nervosa


Anorexia nervosa- a life-threatening mental illness associated with severe weight loss due to an eating disorder.
Characterised by:
-fear of becoming obese despite progressive weight loss
-distorted body image
-body weight 15% less than normal for age and height due to refusal to eat
-in females, absence of three consecutive menstrual periods

Bulimia nervosa- a mental illness in which an individual consumes large amounts of food followed by excessive fasting, exercise, vomiting or use of laxatives.
Characterised by:
-Recurrent bingeing (consumption of large amounts of food) with fear and lack of self control
-Self-induced vomiting, use of laxatives or fasting to oppose bingeing
-Two binge-eating episodes per week for at least 3 months


Discuss the issues of tolerance, physical dependence and abuse of amphetamines


– With regular use, develops to elevation of mood,
suppression of appetite and stimulation of the heart and blood vessels

Physical dependence
– Abstinence syndrome with abrupt withdrawal

– High potential for abuse due to euphoria


Describe the adverse and toxic effects of amphetamines


• CNS stimulation (convulsions, confusion, coma)
• Weight loss
• Cardiovascular effects (palpitations, hypertension,
cerebral hemorrhage, dysrhythmias)
• Psychosis (hallucinations, paranoid delusions)


Outline the mechanism of action for the CNS stimulants used in the treatment of ADHD.


Affect dopamine levels by blocking reuptake
Affect metabolic enzymes which absorb lose dopamine

ADHD is characterised by a hypofunction of dopaminergic neurons associated with executive brain tasks.


Identify the signs and symptoms of attention-deficit/hyperactivity disorder (ADHD).

Fails to give close attention to details
Difficulty sustaining attention in tasks
Does not seem to listen when spoken to directly
Does not follow through on instructions
Difficulty organizing tasks
Avoids, dislikes, or is reluctant to engage in tasks
Easily distracted by small stimuli

Define ADHD


A neurodevelopmental disorder characterised by persistent and age-inappropriate patterns of inattention, hyperactivity and impulsivity


Describe the important considerations involved when using sedative-hypnotic drugs.


Sedative-hypnotics are drugs that depress or slow down the body’s functions. Often these drugs are referred to as tranquilizers and sleeping pills or sometimes just as sedatives.

  • Regular use over a long period of time may result in tolerance
  • They can cause both physical and psychological dependence.
  • Small amounts produce calmness and relax muscles.
  • Larger doses can cause slurred speech, memory loss, irritability, changes in alertness, decreased interpersonal functioning, staggering gait, poor judgment, and slow, uncertain reflexes.
  • These effects make it dangerous to drive a car or operate machinery.
  • Large doses can cause unconsciousness and death.
  • Accidental deaths sometimes occur when a user takes one dose, becomes confused and unintentionally takes additional or larger doses.