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Medicine year 1 semester 2 > Case 9- symptoms and treatment of mood disorders > Flashcards

Case 9- symptoms and treatment of mood disorders Flashcards

1
Q

Symptoms of depression

A
  • Emotional symptoms- sadness, lack of interest, feeling of guilt and suicidal thoughts.
  • Physical symptoms- lack of energy, decreased concentration, change in appetite, change in sleep and change in psychomotor skills. Mostly psychomotor retardation
  • Associated symptoms- excessive worry over physical health, pain (chronic pain), anxiety or phobias, brooding, obsessive rumination (worrying if you have turned off the stove or contamination) and irritability
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2
Q

DSM

A

Produced by the American psychiatric association. Is used most commonly in research. NICE advices DSM-5 for diagnosis. Objective with symptom count

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3
Q

ICD

A

Produced by WHO is used more commonly in diagnosis. Is based on description of symptoms without symptom count, depression is an exception,

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4
Q

Criteria for an episode of depression DSM-5

A

5 or more of the following symptoms over a two week period, must have one of the first two symptoms

  1. Depressed mood
  2. Reduced interest or pleasure in all activities
  3. Weight loss, decreased or increased appetite.
  4. Insomnia or hypersomnia
  5. Psychomotor agitation or retardation
  6. Fatigue or loss of energy
  7. Feelings of worthlessness or inappropriate guilt
  8. Diminished ability to think or concentrate
  9. Recurrent thoughts of death or suicide
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5
Q

icd-11 criteria for an episode of depression

A

ICD-11 is the same as DSM-5 but adds another symptom, feelings of hopelessness. In ICD-10 depression was defined as mild if you had just 4 of the symptoms, moderate with 5 or 6 and severe with over 7. You therefore need less symptoms in ICD-10 to be diagnosed with depression compared to the DSM-5. Using this criteria there are 4-5 times the number of people with depression.

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6
Q

Side effects for antidepressants

A

Hyponatraemia, Suicidal behaviour, Serotonin syndrome.

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7
Q

Side effects for antidepressants- Hyponatraemia

A

Usually in the elderly, more frequent in SSRI’s. The patient will appear drowsy and confused with convulsions.

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8
Q

Side effects for antidepressants- suicidal behaviour

A

Children, young adults and people with a history of suicidal behaviour are most at risk. Patients should be monitored especially at the start of treatment and if the dose changes

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9
Q

Side effects- Serotonin syndrome

A

Uncommon drug reaction caused by excessive central and peripheral serotonergic activity. Severe toxicity usually occurs with a combination of serotonergic drugs, one of which is generally an MAOI. Symptoms:
• Neuromuscular hyperactivity- tremors, hyperreflexia, rigidity
• Autonomic dysfunction- tachycardia, blood pressure change, shivering, hyperthermia, diarrhoea
• Altered mental state

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10
Q

How to treat Serotonin syndrome

A

Supportive care and remove the serotonergic medication

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11
Q

Examples of Tricyclic antidepressants

A

Imipramine, amitriptyline and clomipramine

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12
Q

Mechanism of action of TCA’s

A

They block the uptake of amines by nerve terminals. They do this by competing for the binding site of the amine transporter, this inhibits noradrenaline and 5-HT uptake.

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13
Q

Two types of TCA’s

A

TCA’s can have sedating properties or not. Agitated and anxious patients respond best to the sedative compounds. Withdrawn and apathetic patients benefit from the less sedating drugs. TCA’s are widely used despite the risk.

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14
Q

Pharmacokinetics of TCA’s

A

Once daily administration usually at night. They have a long half-life and are orally rapidly absorbed. They have a very large volume of distribution and low rates of elimination due to plasma protein and tissue binding.

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15
Q

Response to TCA’s

A

10-20% of patients don’t respond to drug treatment but could be due to inadequate dosage. They have a high risk of toxic effects, Haemodialysis is ineffective at increasing drug elimination if there is an overdose

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16
Q

TCA metabolism

A

TCA’s undergo Liver metabolism via N-demethylation and hydroxylation producing active metabolites and the plasma concentration of metabolites is comparable to parent drug. There is wide variation in metabolism between individuals. Inactivation is by glucuronide conjugation of the hydroxylated metabolites and is excreted in the urine.

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17
Q

Risks of TCA’s

A

Half life is longer in elderly patients so low doses should be used initially.
TCA’s have a narrow therapeutic window.
TCA’s are more likely to be discontinued because of side-effects. There is a significant risk of toxicity in over dosage (cardiotoxicity).

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18
Q

TCA side effects

A

Sedation (acts as a Histamine H1 antagonist), postural hypotension (it is an Alpha 1 antagonist), dry mouth, blurred vision and constipation (muscarinic block).

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19
Q

TCA drug interaction

A

Alcohol, anaesthetics, hypotensive drugs and NSAIDS. Should not be given with monoamine oxidase inhibitors

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20
Q

Examples of Monoamine-oxidase inhibitors

A

Phenelzine, tranylcypromine, isocarboxazid, moclobemide

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21
Q

Pharmacokinetics of Monoamine-oxidase inhibitors

A

Blocks the action of monoamine oxidase enzymes which break down neurotransmitters

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22
Q

When to prescribe MAOI

A

They are used less frequently due to adverse effects and interactions but may be prescribed when TCA’S are unsuccesful. Phobic patients and depressed patients with atypical hypochondriacal disorder may respond better to MAOI’s. Moclobemide may used for major depression and social phobia. Used in patents who don’t respond to other antidepressants

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23
Q

Risks of MAOI

A

If stopping a MAOI other antidepressant treatment should not be started for 2 weeks due to lag effect of the drug (washout period)

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24
Q

MAOI’s side effects

A

1) Postural hypotension as amines accumulate within the peripheral sympathetic nerve terminals, this displaces Noradrenaline from the storage vesicles reducing NA release and vasoconstriction (the baroreceptor response)
2) Excessive central stimulation causing tremors, excitement, insomnia, convulsions (overdose).
Increased appetite leading to weight gain.
3) Anticholinergic effects causing dry mouth, blurred vision, urinary retention.

25
Q

MAOI’s cheese reaction

A

You shouldn’t eat ripe cheeses or concentrated yeast products that contain tyramine (amino acid). As the tyramine is normally metabolised by the enzymes to stop it reaching the systemic circulation. Without the enzymes the Tyramine will enhance the sympathomimetic effect leading to severe acute hypertension, severe throbbing headache and intercranial haemorrhages.

26
Q

Contraindications of MAOI’s

A

Indirectly acting sympathomimetic amines also increase the sympathomimetic effect, for example in ephedrine nasal decongestants. Amphetamines can also cause severe hypertension in patient on MAOIs.

27
Q

Examples of SSRI’s

A

Paroxetine and Fluoxetine

28
Q

Contraindications of SSRI’s

A

1) Paroxetine and fluoxetine inhibit hepatic metabolism by CYP2D6 so should not be used in combination with TCAs as there is an increase risk of TCA toxicity.
2) There is an increased risk of bleeding in older patients so they should take a gastroprotective drug whilst taking NSAIDs/aspirin.

29
Q

Side effects of SSRI’s

A

Nausea, anorexia, insomnia, loss of libido and organ failure

30
Q

Mechanism of action of SSRI’s

A

Selective inhibition of re-uptake of Serotonin

31
Q

Prescribing SSRI’s

A

Most commonly prescribed antidepressants but can treat anxiety disorders as well. They are less likely than TCA’s to cause anticholinergic side effects. Not recommended for under 18’s as its not very effective and there are bad side effects. Less likely to overdose then with TCA’s but can cause ventricular arrhythmias and sudden death.

32
Q

Mechanism of action SSRI’s lots of info

A

Initially SSRI’s inhibit 5-HT uptake increasing stimulation of the post synaptic 5-HT1a receptors. Within the brainstem increased 5-HT in the raphe stimulates somatodendritic 5-HT1A receptors. This leads to a decreased firing rate within the raphe and lowered 5-HT available to activate 5-HT1a receptors. So initially SSRI’s will have little effect because they downregulate 5-HT receptor activity even through they increase the amount of 5-HT. However, after a long time SSRI’s downregulate 5-Ht auto receptors so stimulation of 5-HT1A receptors increase

33
Q

NARI’s antidepressant

A

They downregulate alpha2 receptors which increase the raphe firing rate and decreases inhibition of 5-HT release. Leading to postsynaptic 5-HT1A receptor stimulation

34
Q

NaSSA antidepressant

A

Blockage of alpha2 receptors increase both NA and 5-HT release.

35
Q

Non-pathological anxiety

A

A feeling of worry, nervousness or unease about something with an uncertain outcome. Anxiety and stress can improve performance up to a certain point, but too much can be detrimental

36
Q

Pathological anxiety

A

Anxiety in the absence of a threat or disproportionate to the threat

37
Q

Innate or learned anxiety

A

Fear can be innate i.e. of death or learned, electric fences cause fear in animals. Anxiety can be regulated by experience, a pilot may no longer fear height. The Amygdala and Hippocampus are important in anxiety disorder

38
Q

Conditions/Substances that can cause anxiety

A

Anxiety can be caused by systemic organ disorders i.e. hyperthyroidism. Can be caused by excess caffeine consumption and substance of abuse i.e. caffeine, cocaine. Anxiety is the side effect of a lot of medication i.e. steroids, asthma medication and OTC medication containing stimulants.

39
Q

Psychological theories of anxiety

A
  • Childhood trauma
  • Psychodynamic theories of intrapsychic conflict
  • Pavlonian conditions
  • Operant conditioning theories
  • Cognitive theories
40
Q

Pavlonian conditions

A

When you begin to associate an object with fear i.e the hoover makes a loud noise so you fear it

41
Q

Operant conditioning theories

A

An association is made between a behaviour and a consequence (negative or positive) for that behaviour. By avoiding an anxiety provoking situation you are rewarded by a decrease in anxiety. So avoidance behaviour increases.

42
Q

Cognitive theories

A

Patients with anxiety disorders tend to overestimate dangers which can lead to avoidance

43
Q

Biological mechanisms of anxiety

A

Anxiety is mediated by the sympathetic component of the autonomic nervous system, in extreme situation it can lead to ‘fight or flight syndrome.’ In anxiety the stressor causes sympathetic activation and cortisol is released from the adrenal glands.

44
Q

Types of phobic anxiety disorders

A

Agoraphobia, social phobia, specific phobia

45
Q

Phobias

A

Have the same core symptoms of anxiety. The symptoms are brief and due to specific situations/objects/living things. It is out of proportion and normally results in avoidance. May get anticipatory anxiety, where you have anxiety before the event.

46
Q

Specific phobias

A

Will be of an object or event like spiders, has childhood onset. Leads to avoidance. For diagnosis the symptoms should be present for more then 6 months.

47
Q

Social phobias

A

Emerges in teens, slightly higher percentage of females get it. Its fear of social situations or being the centre of attention (public speaking, parties, meetings). It is a fear of behaving in an embarrassing way and humiliating yourself. Leads to avoidance and blushing. Symptoms should be present for more then 6 months.

48
Q

Agoraphobia

A

More common in females, onset is mid-twenties to mid-thirties. This is a fear of leaving the home, travelling alone and crowds and public places. Very debilitating, causes avoidance. Symptoms should be present for more than 6 months.

49
Q

Panic disorders

A

They start abruptly and are discrete episodes of intense fear. They last some minutes and it is a fear of catastrophic outcomes. It is random, not situational. Lasts for 20 minutes. They have the 4 symptoms of anxiety, the patient tends to think that they are going to die and lose control

50
Q

Diagnosing anxiety disorders

A

When the anxiety is not caused by substances/medication or another medical condition. It is not better explained by another medical disorder

51
Q

Symptoms of anxiety disorders

A
  • Cardiovascular (palpitations/rapid chest beat)
  • Chest pain and sweating
  • Trembling, shaking, feeling of choking
  • Nausea/abdominal distress
  • Fear of dying or loosing control ‘going mad’
  • Depersonalisation/derealisation
  • Chills/ heat sensations
  • Paraesthesia- pins and needles
52
Q

Diagnosing generalised anxiety disorders

A

It is diagnosed when they have four or more of: restlessness/feeling on edge, fatigue, difficulty concentrating, irritability, muscle tension and sleep disturbances.

53
Q

Generalised anxiety disorders

A

A period of at lest 6 months with prominent tension, worry and feelings of apprehension about everyday events and problems. They have difficulty controlling their worry. It is chronic but fluctuating. Not situational. Fairly constant anxiety

54
Q

Obsessive compulsive disorders

A

Either obsessions or compulsions that present on most days for a period of at least two weeks. The obsessions or compulsions cause distress and interfere with the subjects social or individual functioning, usually by wasting time. Might be they have to check the cooker nine times before they leave, because they are scared the house will burn down.

55
Q

What are obsession and compulsions

A

Obsessions- thoughts, ideas or images

Compulsions- acts

56
Q

What features must obsessions and compulsions have

A

All features must be present:
• Originate in the mind of the patient
• They are repetitive and unpleasant
• The individual tries to resist them unsuccessfully
• Carrying out the obsessive thoughts or compulsive act is not pleasurable

57
Q

PTSD (post traumatic stress disorder)

A

Exposure to a stressful event or situation which is highly traumatic. You then have persistent remembering or reliving of the stressor by intrusive flash backs, vivid memories or recurring dreams. You may also experience distress when exposed to a situation resembling or associated with the stressor

58
Q

Behaviour PTSD can lead to

A

Avoidance behaviour, may not want to go in a car after a car accident. Might forget parts of the incidence. May result in difficulty falling or staying asleep, irritability or outbursts of anger, difficulty in concentration, hyper-vigilance and an exaggerated startle response.

Medicine year 1 semester 2 (61 decks)

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