Stress, Anxiety and Depression Flashcards

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1
Q

What is the mnemonic for the symptoms of depression?

A
SIG-E-CAPS
Sleep disturbances
Interest loss (anhedonia)
Guilt (self blame)
Energy loss
Cognitive/concentration difficulties
Appetite changes
Psychomotor retardation
Suicidal thoughts
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2
Q

How was the Office of National Statistics study on the prevalence of psychiatric morbidity among adults designed?

A

Two stages - screening interview and more detailed interview involving clinical tests
Large sample size achieved
Symptom questionnaire filled in by patients (potential for bias, but negligible due to large sample size)

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3
Q

What were the major findings of the Office of National Statistics study on the prevalence of psychiatric morbidity among adults?

A

The people most likely to have a neurotic disorder are women, middle aged, separated or divorced, living alone or a single parent.
People are more likely to have a psychotic disorder if they are separated or divorced, live alone, have low educational qualifications, are of a lower social class.
Most common neurotic symptoms are sleep problems, fatigue, irritability, worry.

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4
Q

Define stress.

A

Any condition that actually or potentially poses a challenge to the body’s ability to maintain homeostasis.

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5
Q

What are the two types of stress?

A

Eustress - helpful in preparing to meet challenges, and improves performance
Distress - more chronic, impairs performance

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6
Q

What is a stressor?

A

Any stimulus that produces a stress response.

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7
Q

What are the two types of stressor?

A

External - stressors from the physical environment

Internal - self-imposed stressors

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8
Q

What is the graph called that is a physiological response to stressors in an attempt to regain homeostasis?

A

General adaptation syndrome

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9
Q

What are the 3 phases of stress response?

A

1) Alarm phase - short term, initial flight or fight response
2) Resistance/adaptation phase - body attempts to cope with long term stress
3) Exhaustion phase - resources are depleted so the body is unable to maintain function and may die

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10
Q

What happens in the alarm phase of stress?

A

The stressor activates the cerebral cortex which activates the hypothalamus. The hypothalamus activates the sympathetic nervous system which causes the adrenal medulla to release catecholamines (noradrenaline and adrenaline). The catecholamines cause glycogenolysis and vasoconstriction and increased inotropy.

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11
Q

What happens in the resistance/adaptation phase?

A

There is activation of the HPA axis. The hypothalamus releases corticotropin releasing hormone (CRH) which causes the anterior pituitary gland to release adrenal corticotropic hormone (ACTH) which causes the adrenal cortex to release cortisol.

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12
Q

What are the effects of cortisol release in the resistance/adaptation phase?

A

Lipolysis and gluconeogenesis from protein (muscle) and glycerol due to depleted glycogen stores.
Immune cells are suppressed.
Aldosterone is released from the adrenal cortex, and increases Na+ reabsorption so that water resorption increases as blood volume and pressure is increased.

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13
Q

What re some of the negative effects of chronic stress?

A

Can lead to anxiety disorders and depression.
Can lead to hypertension.
Increased gastric acid production can lead to reflux and peptic ulcers.
Immunosuppression can lead to recurrent infections an increased risk of cancer.
Can lead to migraine headaches, asthma attacks, blood glucose fluctuations in diabetics.
Suppression of sex steroid secretion.

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14
Q

When is exhaustion phase entered?

A

When the body’s resources become so depleted that they can’t sustain the resistance phase. The likely outcome is death.

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15
Q

Name 6 effects of long term exposure to high cortisol levels that may be seen in the exhaustion phase.

A
Muscle wasting (as protein is broken down for gluconeogenesis)
Immunosuppression
Peptic ulcers
Depression/psychosis
Failure of pancreatic beta cells
Ageing
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16
Q

How do the hippocampus and amygdala affect the HPA axis?

A

The hippocampus provides a feedback loop for cortisol levels, if cortisol levels are too high the hippocampus inhibits the hypothalamus so less CRH is produced and less cortisol released.
The amygdala is activates by fear, and when the central nucleus of the amygdala is activated it activates the hypothalamus to increase the HPA axis and SAM system.

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17
Q

What three things does activation of the central nucleus of the amygdala cause?

A

Activation of the hypothalamus.
Activation of the periaqueductal grey matter (which causes avoidance behaviour).
Activation of the reticular activating system (diffuse modulatory systems) which increases alertness and vigilance.

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18
Q

How do the stress hormones affect memory?

A

Emotionally salient events are remembered better, and injecting cortisol improves memory. Lesions in the amygdala reduce memory.

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19
Q

What happens to the immune system during the alarm phase and during the resistance phase?

A

During the alarm phase the immune system is initially upregulated, but during the resistance phase it is suppressed due to cortisol decreasing the numbers of B and T cells.

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20
Q

What is the difference between normal fear response and an anxiety disorder?

A

A normal fear response is a realistic response to a known threatening stimulus, which is normally short term.
An anxiety disorder is when the fear response occurs in an anticipatory manner and is an unfounded fear, leading to the inappropriate expression of fear which interferes with normal daily activities.

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21
Q

What are 5 types of anxiety disorder?

A
Generalised anxiety disorder 
Panic disorder
Phobias
Obsessive compulsive disorder
Post-traumatic stress disorder
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22
Q

What are the symptoms of a panic attack?

A

Dyspnoea, hyperventilating, palpitations, chest pain, trembling, tingling, can often be mistaken for a heart attack.

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23
Q

What is obsessive compulsive disorder?

A

Intrusive thoughts (obsessions) which cause anxiety and compulsions (repetitive behaviours) to neutralise the anxiety.

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24
Q

What are the symptoms of PTSD?

A

Nightmares and flashbacks, difficulty sleeping, detachment, increased arousal, and avoidance of the stimuli associated to the trauma. Hippocampus is reduced in size and amygdala uncontrollably activated.

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25
Q

What is the mechanism of action of benzodiazepines?

A

Bind to an allosteari cistern on the GABAa receptor to increase affinity of GABA so the effect of GABA is enhanced. This means there is a greater influx of chloride ions and greater hyperpolarisation of the membrane, so action potentials are inhibited.

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26
Q

Which anxiolytic does ethanol have a similar mechanism of action to?

A

Benzodiazepines

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27
Q

What is schizophrenia?

A

A relapsing and remitting illness with typical onset on young adulthood.

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28
Q

What is the difference between the positive and negative symptoms of schizophrenia?

A

Positive symptoms = symptoms that occur during episodes e.g hallucinations, delusions, thought disorder
Negative symptoms = an accumulation of symptoms over time e.g lack of motivation, reduced speech, reduced emotion, social withdrawal

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29
Q

What are some symptoms of depression?

A

Persistent low mood, loss of enjoyment and interest (anhedonia), fatigue, changes in sleep and appetite and weight and concentration, loss of confidence, suicidal thoughts, feelings of guilt and helplessness

30
Q

What is bipolar disorder?

A

Episodes of depression and episodes of mania.

The mania is characterised by elation, increased energy, overactivity, disinhibition, reduced sleep, rapid speech.

31
Q

What are the 4 main dopamine pathways?

A

Mesolimbic - from ventral tegmental nuclei to limbic system (involved in reward)
Mesocortical - from central tegmental nuclei to cortex (involved in planning)
Nigrostriatal - increase inhibition of gloves pallidus pars internal, and decrease inhibition of pars external (involved in control of movement)
Tubero-infundibular - hypothalamus to pituitary to inhibit prolactin release (prolactin causes galactorrhea and amenorrhea)

32
Q

How is noradrenaline inactivated after it has been released into the synaptic cleft?

A

It is taken back up by reuptake 1 then oxidised by MAO.

33
Q

Where is serotonin released in the brain, and what are 3 things it is involved in?

A
Raphe nucleus (midline of midbrain, pons, and medulla).
Serotonin influences mood, sleep and emotional behaviour.
34
Q

Which neurotransmitter hyperpolarises the membrane of neurones in the CNS by opening chloride ion channels?

A

GABA (gamma aminobutyric acid)

35
Q

What is the mechanism of action of antipsychotics?

A

Antagonise D2 receptors in the mesolimbic and mesocortical pathways. These treat particularly the positive symptoms of schizophrenia.

36
Q

What are olazapine, risperidone, haloperidol examples of?

A

Antipsychotics (D2 receptor antagonists)

37
Q

What are the two types of side effects of antipsychotics that are caused by their action on dopamine receptors?

A

1) Extrapyramidal side effects caused by antagonism of D2 receptors in the nigeostriatal pathway - Parkinsonism, akathesia, acute dystonias, tardive dyskinesia
2) Tuberoinfundibular side effects caused by excess prolactin - galactorrhea, amenorrhea, infertility

38
Q

What are the side effects of antipsychotics and tricyclics antidepressants caused by their activity on non-target receptors?

A

Drowsiness caused by histamine H1 receptor antagonism.
Orthostatic hypotension caused by antagonism of alpha adrenoceptors.
Dry mouth, blurred vision and constipation and urinary retention caused by antagonism of muscarinic receptors.
Weight gain caused by antagonism of serotonin receptors.

39
Q

What are the metabolic side effects caused by antipsychotics

A

Weight gain, diabetes, raised cholesterol. Particularly common with second generation antipsychotics.
Rarely - idiosyncratic neuroleptic malignant syndrome (rigid muscles and increased temperature).

40
Q

What are the two types of antipsychotics, and which type of side effects does each cause?

A
First generation (e.g haloperidol) - cause more extrapyramidal side effects 
Second generation (e.g olazapine, risperidone) - cause more metabolic and cardiovascular side effects
41
Q

What is the mechanism of action of tricyclics antidepressants?

A

They block the reuptake of noradrenaline and serotonin from the synaptic cleft, so the effect is prolonged.

42
Q

What are the side effects of tricyclic antidepressants?

A

The same as the side effects of antipsychotics which are caused by activity on non-target receptors:
Drowsiness due to H1 antagonism.
Dry mouth, blurred vision, constipation, urinary retention due to muscarinic antagonism.
Orthostatic hypotension due to alpha adrenoceptor antagonism.

43
Q

What are fluoxetine and citalopram examples of, and what is their mechanism of action?

A

SSRIs which block the reuptake of serotonin from the synaptic cleft.

44
Q

What are the side effects of SSRIs (which are due to increased 5-HT action)?

A

Nausea and vomiting, sexual dysfunction, increase in suicidal ideation in children.

45
Q

What are phenelzine and moclobemide examples of, and what is their mechanism of action?

A

Monoamine oxidase inhibitors - inhibit monoamine oxidase in the synaptic terminals so there is increased availability of the monoamines dopamine, serotonin, noradrenaline.

46
Q

What is the danger if people taking monoamines oxidase inhibitors eat mature cheese, Chianti, bovril?

A

A hypertensive crisis can be produced because these foods contain tyramine, and tyramine precipitates noradrenaline release from synaptic vesicles. The hypertensive crisis can lead to a stroke.

47
Q

What is lithium used for?

A

It is a mood-stabilising drug which prevents further episodes of depression and mania in people with bipolar disorder.

48
Q

What is the danger of giving lithium?

A

It has a very narrow therapeutic window so is easy to overdose.

49
Q

Why is lithium a problem for people taking NSAIDs or diuretics?

A

They interfere with the excretion so the lithium will be easy to overdose.

50
Q

What are the side effects of lithium?

A

Weight gain
Fine tremor
Polyuria (because kidneys can’t concentrate urine)
Under active thyroid gland

51
Q

What are diazepam, lorazepam, temazepam examples of?

A

Benzodiazepines (have sedative and muscle relaxant effects, and are hypnotics [treat insomnia])

52
Q

What are the side effects of benzodiazepines?

A
Sedation
Drowsiness
Confusion
Forgetfulness
Impaired motor control
Tolerance and dependence
Respiratory depression
53
Q

What is the dopamine hypothesis for schizophrenia, and what evidence is there?

A

Schizophrenia is a result of dopamine hyperactivity in the mesolimbic pathway.
Arguments for = antipsychotics antagonise D2 receptors, drugs that increase dopamine (e.g levodopa, amphetamine, cocaine) cause psychosis, reserpine depletes dopamine and have antipsychotic effects, PET and SPECT scans show increased brain dopamine activity in patients with schizophrenia.
Argument against = drugs block D2 receptors immediately, but therapeutic effect doesn’t start for a few weeks.

54
Q

What is the neuro-developmental hypothesis for schizophrenia?

A

Schizophrenia is caused by a problem in brain development during childhood and adolescence which means the ventricles are too large.

55
Q

What is the monoamines theory of depression, and what evidence is there?

A

Depression results from a deficiency of monoamine neurotransmitters in the brain (dopamine, noradrenaline, serotonin).
Arguments for = antidepressants work by increasing the availability of monoamines at the synapses, reserpine depletes monoamine transmission and can cause depression, people with depression have lower levels of monoamines precursors/metabolites in their blood and CSF.
Arguments against = antidepressants immediately increase monoamine availability but take a few weeks to have a therapeutic effect, cocaine and amphetamines mimic noradrenaline and serotonin but don’t have antidepressant effect, some effective antidepressants don’t actually affect noradrenaline or 5-HT reuptake.

56
Q

What is the mechanism of action of resperpine?

A

It stops monoamines getting into the synaptic vesicles.

57
Q

What is the difference between a neurotransmitter and a neuropeptide?

A

Neurotransmitters are small molecules, neuropeptides are large molecules e.g opioids.

58
Q

Where is the neurone are neurotransmitters synthesised?

A

In the cytosol of the presynaptic terminal.

59
Q

What is the difference between an ionotropic and metabotropic receptor?

A

An ionotropic receptor is an ion channel which is regulated by neurotransmitters at an allostearic site and produces a fast response.
A metabotropic receptor is a GPCR so works via intracellular signalling and produces a much slower response.

60
Q

What is buspirone?

A

A serotonin receptor agonist that can be used as an anxiolytic.

61
Q

Why is tingling fingers and toes a symptom of anxiety?

A

Hyperventilation cause the pCO2 in the blood to drop (respiratory alkalosis) which causes muscle spasm and vasoconstriction.

62
Q

Which of the catecholamines noradrenaline and adrenaline acts on both alpha and beta adrenoceptors, and which acts on only alpha adrenoceptors?

A

Adrenaline - activates alpha and beta adrenoceptors

Noradrenaline - activates alpha adrenoceptors

63
Q

Which stress-related hormone is secreted by the anterior pituitary gland, and which is secreted by the posterior pituitary gland?

A
Adrenocorticotropic hormone (ACTH) secreted by anterior pituitary as part of HPA axis.
Vassopressin (ADH) secreted by posterior pituitary in response to stress.
64
Q

The release of which hormone from the hypothalamus is controlled by the circulating levels of cortisol (negative feedback)?

A

Corticotropin releasing hormone (CRH)

65
Q

Which cells secrete renin?

A

Juxtaglomerular cells secrete renin in response to a decrease in blood pressure and volume, renin acts on angiotensinogen produced by the liver.

66
Q

What is an affective disorder?

A

A disorder where the central and common feature is an abnormality of mood

67
Q

What is dysthymia?

A

A mild depressive illness lasting for 2 or more years.

68
Q

What is the main action of tricyclic antidepressants?

A

Inhibit reuptake of noradrenaline and 5-HT, so there is greater activity on postsynaptic receptors.

69
Q

What are common side effects of tricyclic antidepressants?

A
Sedation
Dry mouth
Difficulty with micturition
Constipation
Tachycardia
Hypotension
70
Q

How can you define whether or not an event is stressful?

A

The key issue is how you appraise the event, so an event is stressful if you perceive you can’t cope with the demands it places on you.

71
Q

What are the dimensions of illness cognition suggested by Leventhal?

A

Identity - signs symptoms and illness label
Timeline - perceived time for development and duration of illness threat
Consequences - perceived physical, social, economic and felt emotional consequences
Causes - perceived cause of disease
Cure - extent to which illness is responsive to medical treatment

72
Q

Which stage of adjustment to illness is someone at if they are making lifestyle changes in an attempt to improve their recovery?

A

Search for mastery - taking control of the situation and their perceptions of the possible causes of the illness.