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PSYCHIATRY > PPT - DEPRESSION, BIPOLAR, MANIA, SCHIZO > Flashcards

PPT - DEPRESSION, BIPOLAR, MANIA, SCHIZO Flashcards

1
Q

What drug class is citalopram?

A

SSRI

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2
Q

What drug class is citalopram?

A

SSRI

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3
Q

What drug class is agomelatine?

A

Melatonin receptor agonist and serotonin receptor antagonist

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4
Q

What drug class is phenelzine?

A

Non-selective MAOI

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5
Q

What drug class is duloxetine?

A

SNRI

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6
Q

What drug class is mirtazapine?

A

Presynaptic alpha2 adrenoreceptor blocker

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7
Q

What drug class is fluoxetine?

A

SSRI

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8
Q

What drug class is reboxetine?

A

Selective noradrenaline reuptake inhibitor

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9
Q

What drug class is trazadone?

A

Serotonin receptor blocker

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10
Q

What drug class is imipramine?

A

TCA

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11
Q

What drug class is moclobemide?

A

Reversible inhibitor of MAO A

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12
Q

What drug class is trancyclopromine?

A

Non-selective MAOI

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13
Q

What drug class is paroxetine?

A

SSRI

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14
Q

What drug class is venlafaxine?

A

SNRI

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15
Q

What drug class is amitryptiline?

A

TCA

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16
Q

What drug class is lofepramine?

A

TCA

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17
Q

Why are TCAs not used as widely as they used to?

A

They are much more dangerous in overdose as they cause prolongation of QT, sinus tachycardia and widened QRS = arrythmia risk
Widening of QRS >100ms is associated with an increased risk of seizure
Widening of QRS >160ms is associated with ventricular arrhythmias

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18
Q

What is the monoamine theory of depression?

A

Depression is caused by a functional deficit in monoamine transmitters, noradrenaline and 5HT at certain sites in the brain whilst mania results from a functional excess

Evident by TCA, MAOIs increasing mood and methyldopa which inhibits noradrenaline synthesis decreases mood

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19
Q

Whats the moa of TCAs?

A

They block the reuptake of serotonin and norepinephrine in presynaptic terminals, which leads to increased concentration of these neurotransmitters in the synaptic cleft

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20
Q

What is the hypothalamic-pituitary-cortisol system in depression?

A

Chronic stress causes upregulation of Hypothalmopituitaryadrenal system = increases CRH so ACTH so cortisol secretion = inhibitory effect on hypothalamus and hippocampus

Injected into the brain of experimental animals, CRH mimics some aspects of depression in humans, such as diminished activity, loss of appetite and increased signs of anxiety. Furthermore, CRH concentrations in the brain and cerebrospinal fluid of depressed patients are increased.

Explains depression in those overweight, Cushings

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21
Q

Outline the role of brain-derived neurotrophic factor?

A

Lowered levels of BDNF or malfunction of its receptor is typically seen in depression and antidepressants tend to elevate BDNF levels

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22
Q

Outline the chronic adaptive changes seen in SSRI use?

A

when SSRIs are administered, they inhibit the reuptake of 5-HT into nerve terminals, which should increase the levels of 5-HT in the synapse. However, the increase is less than expected because 5-HT1A receptors on the soma and dendrites of 5-HT-containing raphe neurons are activated, which reduces 5-HT release. This partially cancels out the effect of inhibiting reuptake. But, with prolonged drug treatment, the increased level of 5-HT in the somatodendritic region desensitizes the 5-HT1A receptors, reducing their inhibitory effect on 5-HT release from nerve terminals. This explains the slow onset of antidepressant action of 5-HT uptake inhibitors because it takes time to desensitize the somatodendritic 5-HT1A receptors.

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23
Q

Why are SSRIs first line?

A

Safer in overdose
Less likely than TCAs to cause anticholinergic side effects
Dont cause ‘cheese reactions’
Better tolerated
Sertraline safe in unstable angina and recent MI
Not sedating like TCAs

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24
Q

What are the unwanted effects of SSRIs?

A

Nausea
Anorexia
Insomnia
Loss of libido
Failure of organism
SIADH - hyponatraemia
Anxiety and agitation
Increased risk of bleeding particularly if taking NSAIDs
Increased risk of suidicdal thoughts and behaviour particularly in young people
Serotonin syndrome

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25
Q

How soon do SSRIs work?

A

2 weeks but it often gets worse before it gets better - u

26
Q

What are the characteristic symptoms of serotonin syndrome?

A

Neuromuscular hyperactivity - tremor, hyperreflexia, clonus, myoclonus, rigidity
Autonomic dysfunction - tachycardia, blood pressure changes, hyperthermia, diaphoresis, shivering, diarrhoea
Altered mental state - agitated, confused, manic

27
Q

How often should you be monitoring on SSRIs?

A

Review every 1-2 weeks at start of treatment
Continue treatment for at least 4 weeks (6 weeks in elderly)
Following remission, continue treatment at same dose for at least 6 months (12 if GAD)

28
Q

Which SSRIs cause QT interval prolongation?

A

Citalopram and escitalopram

29
Q

What are the important interactions for SSRIs?

A

NSAIDS - if co-prescribing give PPI
Warfarina nd heparin - avoid
Aspirin
Triptans - avoid

30
Q

What should you give instead of SSRIs in a pt on warfarin or heparin?

A

Mirtazepine

31
Q

What are the SSRI discontinuation symptoms?

A

Flu-like symptoms
Insomnia
Nausea and vomiting
Increased mood changes and imbalance (unsteady)
Sensory disturbances (paraesthesia, electric shock)
Hyperarousal

32
Q

Whats the goal for treatment of mania?

A

Remission - resolve mood symptoms or improvement to the point that only 1 or 2 of symptoms of mild intensity persist
If there are psychotic symptoms, resolution of psychosis is required for remission

33
Q

What are mood-stabilising drugs?

A

Lithium

anti-convulsants:
- sodium valproate
- carbamazepine
- lamotrigine

Antipsychotics for psychotic symptms or mania

34
Q

Whats the theory of how lithium therapy works?

A

Either:
Inhibition of inositol monophosphate or inhibitor of glycogen synthase kinase 3

35
Q

Why is lithium a dangerous drug?

A

Narrow therapeutic range of 0.4-1 and above 1.5 it produces its toxic effects

36
Q

What are the adverse effects of lithium?

A

nausea/vomiting, diarrhoea
fine tremor
nephrotoxicity: polyuria, secondary to nephrogenic diabetes insipidus
thyroid enlargement, may lead to hypothyroidism
ECG: T wave flattening/inversion
weight gain
idiopathic intracranial hypertension
leucocytosis
hyperparathyroidism and resultant hypercalcaemia

37
Q

How should lithium be monitored?

A

when checking lithium levels, the sample should be taken 12 hours post-dose
after starting lithium levels should be performed weekly and after each dose change until concentrations are stable
once established, lithium blood level should ‘normally’ be checked every 3 months
after a change in dose, lithium levels should be taken a week later and weekly until the levels are stable.

BMI, thyroid and renal function should be checked every 6 months
patients should be issued with an information booklet, alert card and record book

38
Q

What are contraindications?

A

Dehydration - more likely for toxicity
Renal impairment
Hyponatraemia e.g. addisons disease or low dosing diets
CVD

39
Q

How can lithium affect thyroid?

A

It can cause hypothyroidism

40
Q

How does lithium affect the kdineys?

A

It can cause renal diasbetes insipidus
Renal tubular damage after prolonged treatment
Na+ retention due to increased aldosterone secretion

41
Q

What is the patient and carer advice for lithium?

A

Advise them to report signs and symptoms of toxicity, hypothyroidism, renal dysfunction (polyuria and polydypsia), benign intracranial hypertension (persistent headache and visual disturbance)
Maintain adequate fluid intake and dont make dietary changes which change sodium intake

42
Q

What is in a lithium treatment pack?

A

Pt information booklet
Lithium alert card
Record book for tracking serum-lithium concentration

43
Q

Whats the key thing about the bioavailability of lithium?

A

Different brands or types have different concentrations so be careful with switching between

44
Q

What are drug interactions with lithium?

A

Thiazide diuretics (and other diretics to a lesser extent) - as hyponatraemia worsens lithium toxicity
ACEi/ARBs
NSAIDs
(I.e. any drug that can cause AKI because it’s really excreted so higher likelihood of toxicity)

45
Q

What can severe lithium toxicity cause?

A

Coma
Convulsions
Profound hypotension with oliguria

46
Q

What type of drug is chlorpromazine?

A

Typical antipsychotic

47
Q

What type of drug is aripiprazole?

A

Atypical antipsychotic

48
Q

What type of drug is clozapine?

A

Atypical antipsychotic

49
Q

What type of drug is flupentixol?

A

Typical antipsychotic

50
Q

What type of drug is Lurasidone?

A

Atypical antipsychotic

51
Q

What type of drug is fluphenazine?

A

Typical antipsychotic

52
Q

What type of drug is haloperidol?

A

Typical antipsychotic

53
Q

What type of drug is olanzapine?

A

Atypical antipsychotic

54
Q

What type of drug is pimozide?

A

Typical antipsychotic

55
Q

What type of drug is quetiapine?

A

Atypical antipsychotic

56
Q

What type of drug is risperidone?

A

Atypical antipsychotic

57
Q

What type of drug is sulpiride?

A

Typical antipsychotic

58
Q

What are antimuscarinic effects?

A

Drowsiness
Dry mouth
Constipation
Blurred vision
Urinary retention

59
Q

What causes the SE in antipsychotic therapy?

A

The drugs can’t discriminate between D2 receptors so other brain pathways other than mesolimbic pathway are affected:
Nigrostriatal - EPS and TD
Tuberoinfundibular - enhances prolactin secretion
Mesolimbic reward component - reduce pleasure
Prefrontal cortex - worsens negative sympotms

60
Q

How are the new drugs able to produce less EPS?

A

They have 5HT2A antagonist properties which enhance dopamine release in the striatum whic can reduce EPS

61
Q

What are acute dystonia?

A

Involuntary movements often accompanied by symptoms of parkinsons
Occur commonly in the first few weeks, decline in time and are reversible

62
Q

What is tardive dyskinesia?

A

Developers after months or years of typical antipsychotics
Disabling and often irreversible and often worsens when antipsychotics are stopped
Resistanc to treatment
Involuntary movements often face and tongue trunk and limbs

PSYCHIATRY (20 decks)

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