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Flashcards in Common Mental Health Problems Deck (21)
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Describe the components of the mental state examination (7)

  1. appearance and behaviour
  2. speech
  3. mood
  4. thought content
  5. abnormal beliefs
  6. cognitive state
  7. insight
  1. What should be examined as part of appearance and behavior?
  2. What should be examined about speech?
  3. How should MOOD be assessed?
  4. what is affect? How may it be abnormal?
  5. how do we examine cognitive state (4)
  6. What is insight?
  1. GENERAL APPEARANCE - neglect, clothing (poorly fitting, inappropriate for weather)
  2. rate, quantity, volume,
    form - flight of ideas, neologisms, echolalia, thought blocking, Knight’s move thinking
  3. objectively - based on history, appearance, behaviour and posture
    subjectively - as described by patient
  4. expression of mood. May be inappropriate or flattened
  5. orientation
    attention and concentration
    general knowledge
  6. degree of insight of illness (i.e. does the person think they are ill?
  1. What are delusions?
  2. what is passivity phenomena?
  3. what is thought insertion?
  4. what is thought withdrawal?
  5. what is though broadcasting?
  6. what is delusional perception?
  1. fixed, false, personal beliefs based on incorrect inference about external reality
  2. belief that an external agency is controlling onself
  3. belief that thoughts are being put into someones head
  4. belief that thoughts are being taken away
  5. belief that thoughts are being read by others
  6. attachment of new and delusional significance to familiar, real perception without logical reason
  1. what are illusions?
  2. what are hallucinations?
  3. what is pareidolia?
  4. what is depersonalisation?
  5. what is derealisarion?
  1. false perceptions of real environmental stimulus
  2. false perceptions in the absence of real environmental stimulus
  3. phenomenon in which the mind responds to a stimulus, usually an image or a sound, by perceiving a familiar pattern where none exists.
  4. disturbance of awareness of self activity (feeling altered or not real)
  5. surroundings do not seem real
  1. What is the pharmacological action of anti-psychotic drugs?
  2. why are antipsychotics called “dirty drugs”
  3. Name an example of a first generation antipsychotic
  4. name an example of a second generation antipsychotic
  5. which antipsychotic is used as a drug of last resort? Name a serious side effect of this drug.
  6. Describe the side effects of antipsychotics (3)
  1. D2 antagonism in the mesolimbic system
  2. because they lack specificity for D2 receptors
  3. haloperidol
  4. olanzipine, risperidone
  5. clozapine. Agranulocytosis (bone marrow poisoning)
  6. effects on other dopamine pathways
    - extrapyramidal side effects due to inhibition of the nigrostriatal pathway
    - galactorrheal, amenorrhoea and fertilitiyy, linked to inhibition of the tubuloinfundibular pathway causing excess prolactin secretion

blocking other receptors

  • sedation due to H1 antagonism
  • muscarinic antagonism
  • alpha 1 antagonism - postural hypotension
  • hunger and weight gain due to 5-HT2c antagonism
  1. which DA pathway is associated with positive symptoms of schizophrenia? Which receptors dominate this pathway?
  2. which DA pathway is associated with negative symptoms of schizophrenia?
  3. How is glutamate and NDMA implicated in schizophrenia?
  4. Name 4 pieces of evidence that supports the dopamine hypothesis of schizophrenia
  5. name 3 pieces of evidence that rejects the dopamine hypothesis
  6. name 3 other hypotheses
  1. overactivity in the mesolimbic pathways. Excess D2 activation
  2. underactivity in mesocortical pathways, where D1 receptors dominate
  3. Glutamate and NMDA receptors are thought to control the activity of the mesolimbic and mesocortical pathways
    - NMDA hypofunction is thought to reduce the level of activity in the mesocortical pathway (giving rise to negative symptoms) and increase activity of the mesolimbic pathway (giving rise to positive symptoms)
  4. antipsychotics block DA receptors
    drugs that increase dopamine (cocaine, L-DOPA) cause psychosis
    resperine depletes DA transmission and has an antipsychotic effect
    PET scans show increased dopamine activity in people with schizophrenia
  5. neurotransmitter effects are immediate by drugs take 2+ weeks to wirk
    other transmitters involved
    cause of schizophrenia may be upstream, causing dopamine hyperactivity
  6. neurodevelopmental differences (enlargement of ventricles)
    damage from autoantibodies
  1. Name the 3 classes of antidepressants and how they work
  2. what are the side effects of the above antidepressants?
  3. which ones are referred to as dirty drugs?
    - block NA and 5-HT reuptake
    - e.g amitryptiline


  • selective serotonin reuptake inhibitors
  • e.g. fluoxetine, citalopram, sertraline


  • monoamine oxidase inhibitors
  • prevents breakdown of monoamine neurotransmitters
  1. Tricyclic Antidepressants:
    - block Sodium Channels involved in cardiac action potential, so can cause arrythmia and can be toxic in overdose
    - Antagonise H1, muscarinic and alpha1 receptors


  • side effects linked to the other uses of serotonin
  • nausea and vomiting
  • sexual dysfunction
  • increase in suicidal ideation, particularly in under 18s
  • withdrawal reaction

- cheese effect (MAOA is found in intestine and involved in breakdown of tyramine). Excessive concentrations of tyramine in blood plasma can lead to hypertensive crisis as tyramine potentiates the release of noradrenaline.

  1. TCAs
  1. What is the monoamine theory of depression?
  2. name 3 pieces of evidence that:
    a) supports this hypothesis
    b) rejects this hypothesis
  3. Name 3 other theories of depression
  1. depression is a result of deficiency of brain monoamine neurotransmitters
    2a) antidepressants increase the availability of monoamines at the synapse
    resperine which depletes monoamine transmission causes depression
    people with depression have lower levels of monoamine precursors/metabolites in their CSF/blood

2b) neurotransmitter effects are immediate but antidepressants take 2+ weeks to work
cocaine and amphetamine mimick NA and 5-HT but do not act as antidepressants
Inputindole is an antidepressant which does not affect NA and 5-HT reuptake.

  1. behavioural, congnitive, psychological

Describe the theory that explains why antidepressants take a long time to work


initially, the increased 5-HT at the synapse is cancelled out by autoreceptors on the pre-synaptic terminal, which act to reduce the release and increase reuptake of extra 5-HT
Over time, these receptors become desensitised, thus the blocked reuptake transporters get internalised.

  1. Which drugs are primarily used to treat anxiety. How do they work?
  2. Name examples of these drugs
  3. name side effects of these drugs
  4. Name 4 other drugs used to treat anxiety
  1. Benzodiazapines
    - GABA agonists
    - bind to allosteric site on GABA receptor, which potentiates their Cl influx, thus neurons are hyperpolarised
  2. diazepam, lorazepam
    Gabapentin and Pregabalin are GABA agonists.
  3. drowsiness, confusion, forgetfulness, impaired motor control.
    tolerance and dependence
    respiratory depression
  4. SSRIs
    Z drugs
    short acting benzodiazapines such as temazepam
  1. what is addiction?
  2. What is ambivalence and how is it a hallmark of addiction?
  3. Describe the hallmarks of dependence syndrome (7)
  4. Name 4 things that makes a substance addivitve
  1. the continued, compulsive engagement in a behaviour, despite adverse consequences
  2. the state of having conflicting beliefs at one time. I.e. knowing that the addictive behaviour is damaging but doing it anyway
  3. salience - use of substance takes on higher priority than any other behaciour
    withdrawal symptoms
    relief of symptoms by further use
    compulsion to use substance
    narrowing of repertoire - addiction is satisfied in a very stereotyped way
    reinstatement after abstience
  4. pleasure producing potency
    rapid onset of action
    short duration of action
    tolerance and dependence

Describe the stages of change model


pre-contemplation (no intention of stopping)
contemplation (considering changing behaviour)
determination (wants to change behaviour)
action (actively changes behaviour)
maintenance (maintains behavioural change)

  1. How can positive reinforcement be used to explain addiction?
  2. How can negative reinforcement be used to explain addiction?
  3. What is a variable reinforcement schedule?
  1. performing addictive behaviour for positive effect
  2. performing addictive behaviour to remove withdrawal symptoms
  3. reinforcement following performing a desired behaviour a random number of times
  1. Describe the mesolimbic dopaminergic pathway
  2. How is the frontal cortex implicated in this pathway?
  3. what is the effect of drugs on this pathway?
  1. DA is produced in the ventral tegemental area. It is released into the nucleus accumbens and prefrontal cortex leading to feelings of pleasure
  2. involved in inhibition of this pathway to enable control over pleasurable activities
  3. drugs reduce the inhibitory effect of the frontal cortex, and as a consequence, there is a loss of control over pleasurable activities, leading to repeated behaviours and addiction
  1. What is end stage addiction?

2. How are neuronal pathways different in end stage addiction?

  1. overwhelming desire to take the drug, diminished ability to control drug seeking and reduced pleasure from normal biological rewards. Drug use becomes very automatic/stereotypical
    - changes in the prefrontal-accumbens glutamatergic pathway
    - increase in excitability of neurons projecting to accumbens
    - alterations in post-synaptic proteins result in rigid dendritic morphology and signalling.
    - The increased prefrontal drive contributes overwhelming motivational salience to drug associated stimuli and mediates craving and drug seeking.
    - These pathways are maintained during abstinence.
  1. What is classical conditioning?
  2. how is classical conditioning related to phobias?
  3. What is operant conditioning?
  4. Describe the 4 dimensions of operant conditioning
  5. How is operant conditioning related to phobias?
  1. a learning process where a previously neutral stimulus becomes associated with another stimulus by repeated pairing (e.g. Pavlov’s dogs)
  2. can be used to explain the origin of phobias (e.g. Little Albert)
  3. the alteration of behaviour by reward or punishment
  4. POSITIVE REINFORCEMENT - presenting a pleasant stimulus after a desired behaviour has occurred
    Reinforcement can be continuous or partial.
    NEGATIVE REINFORCEMENT - removal of unpleasant stimulus after a desired behaviour has occured
    PUNISHMENT - presenting an unpleasant stimulus after a negative behaviour occurs
    EXTINCTION - removing a pleasant reinforcing stimulus upon negative behaviour
  5. negative reinforcement/escape avoidance learning - escape from phobic situation removes anxiety
  1. Name the 10 symptoms of depression
  2. What is required for a diagnosis of depression
    a) mild
    b) moderate
    c) severe
  3. How does extinction (operant conditioning) link to depression?
  4. What can be used to challenge this?
1. D- depressed mood
E - energy loss/fatigue
P - Pleasure loss (anhedonia)
R - retardation or aggitation
E - eating change
S - sleep change
S - suicidal thoughts/bleak future
I - "I'm a failure" - loss of confidence/self esteem
O - "Only me to blame" (guilt)
N - no concentration
  1. minimum of 2 weeks; must also take into account social context
    a) 4 symptoms
    b) 5-6 symptoms
    c) 7+ symptoms
  2. lack of pleasure therefore stop doing things. Worsening mood, vicious circle
  3. CBT - challenge unhelpful thinking. Behavioural activation
  1. what are the characteristics of schizophrenia?
  2. What are the 4 diagnostic criteria for schizophrenia
  3. Describe 4 positive symptoms
  4. Describe 8 negative symptoms
  5. What is Liddle’s 3 Syndrome Model?
  6. Name 3 associated findings in the brains of patients with schizophrenia
  1. fundamental and characteristic distortions in thinking and perception, and by inappropriate or blunted affect
  2. 1 syndrome or 2 symptoms for most of the time for at least one month
    no manic or depressive episode or at least present before the onset of symptoms
    not attributable to organic brain disease
    not attributable to alcohol or drug related intoxication, dependence or withdrawal
  3. delusions, including thought echo/insertion/withdrawal. delusions of control, persecutory delusions or delusions of reference
    thought disorder
    catatonic symptoms (movements)
4. Apathy
avolition (lack of movement)
anergia (lack of energy)
alogia (lack of words and thoughts)
affective flattening
impaired attention
  1. people with psychosis tend to fall into one of 3 symptom clusters
    - reality distortion - hallucinations and delusions (AKA paranoid schizophrenia)
    - disorganisation - thought disorder and inappropriate affect
    - psychomotor poverty - poverty of speech. Blunted affect
  2. Increased ventricular volume/decreased cortical volume
    more neurons with less connections
    patterns of activity that reflect symptoms
  1. is there any difference in the incidence of schizophrenia between males and females?
  2. What percentage of the population are affected by schizophrenia?
  3. in what populations (2) is scizophrenia more common?
  1. equal incidence, however earlier peak onset in males
  2. 1%
  3. urban communities. Socioeconomic class IV and V


  1. Name 6 prenatal risk factor
  2. Name 3 obstetric and neonatal factors
  3. name 3 early childhood factors
  4. Name 4 adult factors
  5. Name 2 precipitating factors
  6. What is the model of cumulative risk factors?
  1. premature birth; inwanted pregnancy; maternal infuenza or rubella; intrauterine growth restriction or malnutrition. Associated medical problems
  2. obstetric complications; low birth weight; hypoxia
  3. mixed handedness, mixed hand and eye dominace, late milestones
  4. age, gender effects, urban rearing, migrants
  5. stressful life events. Substance abuse - particularly dopamine agonists and cannabis
  6. factors during gestation/obstetric comploications may increase the risk of schizophrenia through an effect on intrauterine brain development/brain damage. These factors cumulate with other risk factors and can be precipitated by stressful life events or substance abuse.

Name the 5 treatment approaches for Schizophrenia

  1. antipsychotics
  2. psychological - pCBT, family therapy
  3. Social - housing, employment/educational support, community engagement
  4. treatment for substance abuse/co-morbid problems
  5. Hope