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Psych Disorders > MCQs > Flashcards

MCQs Flashcards

1
Q

Which of these isn’t an advantage of classifying a mental disorder?

A. Helps determine the clinical features of a disorder
B. Systemises the diagnosis, meaning it can be applied universally
C. Simplifies the signs and symptoms into a single disease
D. Allows everyone to have a shared understanding of the disorder

A

C. The pigeon holing of a disorder can over-simplify the symptoms and signs. Comorbidities are common with mental disorders, and it is an oversimplification to classify it as just one disease.

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2
Q

Outline the disadvantages of a biological model

A

Passive patient

Situates the problem within the patient’s body

Biological treatment doesn’t necessarily mean there was a biological cause

Relapse is possible if take treatment away

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3
Q

How are things learnt in classical conditioning?

A

Through association

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4
Q

How are things learnt in operant conditioning?

A

Through consequences

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5
Q

How are things learnt by modelling?

A

Through copying

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6
Q

What is transference in the psychodynamic model?

A

The manifestation of the patient’s important feelings in emotional reactions to the therapist.
Acting towards a therapist how they did/do towards an important person in their life.

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7
Q

What does the social model believe triggers a mental disorder?

A

Life events

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8
Q

Which of these statements about the integrated model is incorrect?

A. The predominant level of dysfunction may change over the course of a disorder
B. Each level of functioning can be linked with multiple models
C. Successful treatment matches the main level of dysfunctioning with the appropriate model of treatment
D. The biological model is the most severe

A

B. Each level of functioning is matched with only one model

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9
Q

Outline the criteria used in the family resemblances approach to categorise a disorder.

A 
Statistical infrequency of characteristic
Unexpected response to certain stimuli
Norms violation
Personal distress
Disabling
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10
Q

Is abnormal behaviour always the result of a mental disorder?

A

No, needs to be understood in context

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11
Q 
Which of these are not a symptom of depression:
A. an absence of ability to feel
B. difficulty making decisions
C. Compulsive, ritualistic actions
D. Psychosis
A

C. Compulsive, ritualistic actions - these are experienced in OCD

Psychosis - nihilistic delusions and hallucinations of feeling dead can occur

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12
Q

What is the usual course of depression?

A

Chronic-recurrent

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13
Q

Are men or women more at risk of depression?

A

Women - twice more than men

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14
Q

Are older people more likely to get depression?

A

No - prevalence of MDD lower in older age

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15
Q

When there is perceived uncontrollability over an aversive stimuli, what can it lead to?

A

Learned helplessness - not trying to escape a situation due to unsuccessful attempts in the past

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16
Q

How did Mair & Seligman (1976) demonstrate learned helplessness?

A

In dogs - put them in cages where they got an electric shock, after a while they opened the cage, but the dogs didn’t try to get out due to previous unsuccessful attempts

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17
Q

Outline Lewinsohn’s cycle of reduced rewards

A

As depressed, feel less positive rewards (not motivated to do things etc.) –> feel more depressed due to lack of rewards

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18
Q

Name operant and classical conditioning treatment for depression

A

Operant - encourage testing out perceived uncontrollability
Classical - associate personal depressive stimuli with non-depressive things (e.g. associate getting out of bed with reward of breakfast)

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19
Q

What is the most depressing way to attribute things?

A

Internal, global, stable attribution

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20
Q

What did Beck believe depressive attributions were rooted in?

A

Schemata - assumptions/beliefs that shape how we understand the world, stem from childhood.

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21
Q

What do schemata lead to?

A

Cognitive biases, then leading to negative automatic thoughts

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22
Q

What are cognitive biases?

A

Errors in logic used when assessing a situation

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23
Q

What is cognitive rehearsal?

A

Depression treatment, where cognitive/behavioural coping strategies are developed, e.g. detecting automatic thoughts and identifying biases

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24
Q

What did Moore & Fresco (2012) find about people with depression?

A

That they had less illusion of control

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25
Q

What does the psychodynamic approach believe depression is due to?

A

A reaction to loss - can be real, symbolic or imagined

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26
Q

What psychosexual stage do we regress to after loss

A

Oral stage

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27
Q

What is diffuse anxiety?

A

No specific object or situation threatening an individual, causing their anxiety.

GAD and PD.

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28
Q

True/false: Women are more likely to get OCD

A

False - men and women are equally likely to have OCD.

But women are twice as likely to have anxiety.

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29
Q

How is avoidance-conditioning formulation learnt? And maintained?

A

Learnt through classical conditioning - associating object/situation with fear

Maintained through operant conditioning: avoid object/situation –> don’t learn that is harmless

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30
Q

Systemic desensitisation is:
A. Straight away confronting the most phobic situation
B. Watching someone else be in the phobic situation
C. Slowly, step by step becoming more comfortable with the phobic stimulus

A

C - step by step becoming more comfortable

A is flooding
B is modelling

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31
Q

What is the preparedness theory?

A

That we have an evolutionary predisposition to stay away from things that could be harmful to us

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32
Q

What is catastrophising?

A

The catastrophic misiniterpretation of bodily stimuli - occurs in panic disorder - think panic is actually you dying

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33
Q

Why can it be therapeutic to mimic the start of an attack in CBT for panic disorder?

A

Can make the cognitive link between the behaviour and the sensations

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34
Q

According to psychodynamic theory, what are obtrusive thoughts in OCD linked to?

A

Unconscious id wishes

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35
Q

What is the cognitive feature of the comorbidity of anxiety and depression?

A

Helpless and uncertain hopelessness

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36
Q

What are delusions?

A

Fixed and rigid beliefs that are culturally bizarre

37
Q

How do cognitive biases lead to a cycle of worsening hallucinations?

A

Experience mild hallucinations (hearing voices) –> cognitive bias causes exaggerated beliefs and explanations for these voices –> become more distressed –> hallucinations worsen when distressed –> more bizarre explanation for hallucinations

38
Q

In token economy programmes for schizophrenia, when is a reward given?

A

When the patient doesn’t express symptoms, or behaves in a socially acceptable way

39
Q

What is reattribution therapy for schizophrenia?

A

The questioning of where the voices are coming from, and exploring alternative beliefs about the origin of the hallucinations.

Can also test the reality of unusual beliefs

40
Q

What did Freud believe caused schizophrenia?

A

Regression to the pre-ego stage

41
Q

What did Fromm-Reichmann (1948) believe caused schizophrenia?

A

Schizophrenogenic mothers

42
Q

Outline the sociogenic hypothesis

A

Schizophrenics tend to be in the lowest socioeconomic class because poverty triggers psychosis

43
Q

Outline the social selection theory

A

Schizophrenia can happen to anyone, but because it causes an inability to economically support oneself, there is a fall in social classes

44
Q

What is the neuron hypothesis?

A

The nerve cell is the basic unit of structure and function in the nervous system

45
Q

Name the four functions of glial cells

A

Matrix to hold the neurons
Myelin sheath
Lymphocytes
Barrier

46
Q

How are signals transmitted between neurons?

A

Chemically - using neurotransmitters across the synapse

Electrically - directly via gap junctions

47
Q

What is the most important factor in maintaining the resting membrane potential?

A

Selectively permeable membrane

48
Q

Which of these statements are true?
A. There is a high concentration of K+ on the outside of the membrane.
B. There is a high concentration of Cl- on the inside of the membrane
C. There is a high concentration of Na+ on the outside of the membrane
D. K+, Cl- and Na+ are all in high concentrations on the inside of the membrane.

A

C. There is a high concentration of Na+ on the outside of the membrane, driven by the Na+/K+ pump

49
Q

When is the strength of the sodium-potassium pump at its maximum?

A

At the RMP

50
Q

What happens to the Na+/K+ pump if the membrane potential becomes less negative?

A

It breaks down

51
Q

What do the microtubules do?

A

Transport the vesicles from the cell body to the terminal

52
Q

Where are the synaptic vesicles manufactured?

A

In the cell body

53
Q

What occurs when the action potential reaches the terminal?

A

Calcium channels open

54
Q

What causes the vesicles to migrate to the synaptic membrane?

A

Influx of calcium ions

55
Q

Which of these statements is correct?
A. Excitatory neurotransmitters cause an Na+ efflux
B. Inhibitory neurotransmitters cause a Cl- efflux
C. Inhibitory neurotransmitters cause a K+ efflux
D. Excitatory neurotransmitters cause a Cl- influx

A

C. Inhibitory neurotransmitters cause a K+ efflux –> making it partially hyperpolarised

56
Q

What controls the opening of ionophores?

A

Neurotransmitters

57
Q

How is further release of neurotransmitters prevented from the pre-synaptic terminal?

A

Negative feedback on the inhibitory autoreceptors

58
Q

What is any substance that is recognised by a receptor called?

A

A ligand

59
Q

What was the antihypertensive drug involved in the origin of the monoamine theory for depression?

A

Reserpine

60
Q

What does decreased MHPG imply?

A

Depleted NA, as MHPG is a metabolite of NA

61
Q

What is the cheese effect?

A

There are pressure amines in cheese that lead to hypertension. These are normally broken down by MAO, so when MAOIs are prescribed, eating too much cheese can be dangerous

62
Q

Outline problems with the classical monoamine theory of depression

A

The therapeutic response delay, implies that it cannot just be due to depleted neurotransmitters.

Cocaine blocks reuptake of NA and 5-HT but it isn’t an effective antidepressant

Atypical antidepressants don’t affect reuptake but act directly at the receptors

63
Q

What is the role of 5-HT1A?

A

It is an inhibitory autoreceptor

64
Q

Why can patients on SSRIs sometimes get worse before they get better?

A

Increased levels of 5-HT acting on the hypersensitive inhibitory autoreceptor (5-HT1A) will initially further suppress 5-HT release.

65
Q

What is the NA equivalent of 5-HT1A?

A

alpha-2

66
Q

Where is ACTH released from?

A

Pituitary gland

67
Q

What occurs with the HPA in chronic stress?

A

Too much cortisol leads to desensitisation of GR receptors, reducing their negative feedback on the HPA

68
Q

Which form of the 5-HTT gene is thought to be linked to stress and depression?

A

Short allele

69
Q

Why do people receive ECT?

A

They fail to respond to antidepressants
They can’t tolerate drug side effects
They’re too ill that they can’t wait for drugs to take their full effect

70
Q

What is the maximum amount of times ECT can be administered a week?

A

3 times

71
Q

What is maladaptive anxiety?

A

When it is an exaggerated anxious response that is inappropriate to context

72
Q

Which anxiolytic does panic disorder respond best to?

A

Xanax is the only BDZ it responds to

Best to treat with SSRIs or other antidepressants

73
Q

Which receptor are benzodiazepines linked to?

A

GABA-A

74
Q

What ion channel do GABA-A receptors surround?

A

Choride

75
Q

What does the binding of BDZ to the GABA A receptor mean?

A

Means less GABA is required for the same amount of inhibition

76
Q

What is the mechanism of action of buspirone?

A

Has a high affinity for 5-HT1A receptors, so reduces 5-HT release in the forebrain

77
Q

Why is patient compliance low in buspirone?

A

Due to a therapeutic delay, unlike BDZs which work straight away. Patients have likely already experienced BDZ, therefore will think buspirone isn’t working

78
Q

Which subunit of GABA A may be responsible for side effects from BDZs?

A

Alpha1

79
Q

In mice, which subunit of GABA A did Mohler (2012) find had the anxiolytic effects?

A

Alpha 2

80
Q

Which dopamine pathway is thought to be involved in the pathology of schizophrenia?

A

Mesolimbic

81
Q

Which type of receptor is increased in schizophrenia?

A

D2-like

82
Q

What do amphetamine, cocaine and L-dopa all induce?

A

Psychosis

83
Q

Why do antipsychotics cause an increase in the firing of DA neurons?

A

They block D2 receptors, which are both pre-synaptic inhibitory and post-synaptic, therefore by blocking the inhibitory receptor, there is less DA release inhibition, so increased firing

84
Q

What are some of the pressures to develop new drugs for schizophrenia?

A 
Side effects (motor, weight gain etc.)
Delayed therapeutic response
30% patients don't respond to classical agents (particularly negative symptoms)
85
Q 
Which of these is incorrect about the receptor profile of clozapine?
A. High affinity for D4
B. High affinity for 5-HT2
C. High affinity for NMDA
D. High affinity for NA alpha-2
A

C. high affinity for NMDA - not involved with glutamate

86
Q

What is the pattern of dopamine receptors in type II schizophrenia?

A

Reduce D1 density in the prefrontal cortex

87
Q

What is pruning?

A

The elimination of redundant connections and synapses which occurs during adolescence

88
Q

How is maternal infection linked to schizophrenia?

A

Leads to infection stimulated neuroinflammation where pro-inflammatory cytokines are activated.
If cytokines are overactive they can lead to progressive neurodegeneration

89
Q

What gene is linked with excessive synaptic pruning?

A

C4A

Psych Disorders (1 decks)

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