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Pharmacology (Semester 6) > Psychiatric disease drugs 12.1 and 12.2 > Flashcards

Psychiatric disease drugs 12.1 and 12.2 Flashcards

1
Q

Give the 2 main ways CNS drugs work

A

1) Agonists or Antagonists of NT receptors ➞ compete with NT for binding site, mimic NT or block NT
2) Inhibitors of regulatory enzymes

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2
Q

Give an example for each catagory

A
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3
Q

Give 3 core symptoms of depression

A

Show 2 of 3:

  • Low mood
  • Anhedonia
  • Decreased energy
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4
Q

Give 2 secondary symptoms of depression

A
  • decreased appetite
  • sleep disturbance
  • reduced concentration
  • Irritability
  • reduced libido
  • self harm or suicidal ideas or acts
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5
Q

Brifly explain the Monoamine Hypothesis of depression + a drug treatment and why

A

Depression due to deficiency of monoamine NTs ➞ NA and serotonin

Certain drugs that depleted these could induce depression e.g. Reserpine

Treatment: MAOIs, block enzyme monoamine oxidase from destroying NTs

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6
Q

Brifly explain the Neurotransmitter Receptor Hypothesis of depression

A

Abnormality in the receptors for monoamine transmission leads to depletion of NT ➞ causes compensatory up regulation of post synaptic receptors leading to depression

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7
Q

Brifly explain the Monoamine Hypothesis of Gene Expression

A

Deficiency in molecular functioning ➞ hypothesised problem within the molecular events distal to the receptor

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8
Q

What severity of depression are SSRIs used to treat?

Give 2 examples

A

Moderate - severe depression (with CBT) ➞ first line medication

  • paroxetine most potent reuptake inhibitor
  • citalopram most selective
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9
Q

Give 3 pharmacokinetics of SSRIs

A
  1. almost completely absorbed from gut
  2. long elimination half lives (once daily dosage)
  3. metabolised in liver
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10
Q

Give 3 common side effects of SSRIs + 2 rare

A

Common:

  • anorexia
  • nausea
  • diarrhoea

Rare: precipitation of mania and increased suicidal ideation

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11
Q

Give 2 examples of Tricyclic antidepressants (TCAs)

Are these first line?

A

TCAs are first generation antidepressants

They are still used but less often and not first line

Eg. Amitryptiline, imipramine, clomipramine, lofepramine

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12
Q

Give 3 actions of TCAs

A

1) Inhibition of NA uptake ➞ sympathomimetic effect
2) Blocks Muscarinic cholinoceptors ➞ anticholinergic effect
3) Blocks α1-adrenoceptors ➞ sympatholytic effect

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13
Q

Give the pharmacokinetics of TCAs

A
  1. lipid soluble
  2. absorbed from gut
  3. long half lives
  4. metabolised in liver
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14
Q

Give 4 side effects/toxicity problems with TCAs

A

CNS: sedation + impaired psychomotor performance, lowering of seizure threshold

Autonomic: reduction in glandular secretions, block of eye accommodation

CVS: tachycardia, postural hypotension, impaired myocardial contractility

GI: constipation

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15
Q

What are Serotonin-noradrenalin reuptake inhibitors (SNRIs) + 2 examples

What “line” drugs are these?

A

‘Pure’ non-selective monoamine uptake inhibitors ➞ SSRIs with property of NA uptake inhibition

Eg. Duloxetine and Venlafaxine

Second/third line drugs

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16
Q

SNRIs are dose dependant, compare effect of lower vs higher doses?

A

Lower doses serotonin action

Higher doses noradrenaline action

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17
Q

Give 4 side effects/toxicity problems with SNRIs

A

SAME as SSRIs + sleep disturbance, increased BP, dry mouth, hyponatraemia

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18
Q

What is the implication of the half life and stopping treatment of SNRIs

A

Relatively short half-life therefore may be a withdrawal syndrome on discontinuation

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19
Q

Schizophrenia is an examples of a mental illness with ______ symptoms

Give 2 other conditons that also display these symtpoms

A

psychotic

Other examples: mania, severe depression, delusional disorder

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20
Q

What is psychosis?

A

Psychosis causes people to perceive or interpret things differently from those around them, they will have a different perspective on reality

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21
Q

Give 2 KEY symptoms of schizophrenia and explain each

A

1) Hallucination- a perception in the absence of an external stimulus (auditory, olfactory, visual, gustatory, tactile)
2) Delusion- a fixed false belief, not shaken by reasoning to the contrary, that is out of keeping with someone’s culture or religious beliefs

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22
Q

How is Schizophrenia diagnosed?

A
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23
Q

Give 2 environment interactions that are a/w Schizophrenia

A

Cannabis and Trauma

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24
Q

Give the 4 main dopamine pathways and the function of each

A

Mesolimbic- emotional response and behaviour

Mesocortical- important in arousal and mood

Nigrostriatal- key pathway damaged in Parkinson’s disease

Tuberoinfundibular - in hypothalamus and pituitary gland

25
Q

Explain the dopamine theory of Schizophrenia + treatment and examples

A

Excessive dopamine transmission in the mesolimbic pathway

Theoried because amphetamine increases dopamine release and causes symptoms very similar to positive symptoms of schizophrenia

Could treat with dopamine antagonists BUT these do not treat negative symptoms

26
Q

First generation antipsychotic drugs block ______ transmission but cause ______ side effects

A

dopamine, extrapyramidal

27
Q

Is schizophrenia associated with increased 5-HT function

+ examples

A

5-HT has been implicated in a number of behaviours which are disturbed in schizophrenia (e.g. perception, attention, mood, aggression, sexual drive, appetite, motor behaviour, sleep)

Many effective antipsychotic drugs = antagonists at 5-HT-2A receptors eg Clozapine

Precursors of 5-HT (e.g. tryptophan) exacerbate schizophrenia

28
Q

Is schizophrenia associated with decreased cortical glutamate function?

A

Glutamate is the predominant excitatory NT

Post-mortem studies have shown increased cortical glutamate receptors and increased binding of glutamate receptor ligands in cortex, basal ganglia and hippocampal formation.

BUT no current treatment

29
Q

How is Schizophrenia diagnosed

A
30
Q

Give 4 actions ALL antipsychotics will show + 2 long term s/e

A
  1. Sedation within hours
  2. Tranquilisation within hours
  3. Antipsychotic several days or weeks
  4. Extrapyramidal side effects hours or days

Longer term side effects ➞ tardive dyskinesia and metabolic syndrome

31
Q

Give an example of a typical antipsychotics + 4 facts about these

A

Typical ➞ eg Haloperidol

  • safe in emergencies
  • more sedating
  • well known side effects
  • wide range of action: blocks dopamine and α adrenergic receptors + anticholinergic and antihistamine effects
32
Q

Give 4 side effects/toxicity problem a/w typical antipsychotics

A
  1. Extrapyramidal side-effects
  2. Neuroleptic malignant syndrome
  3. Postural hypotension
  4. Weight gain
  5. Endocrine changes e.g. prolactinaemia
  6. Pigmentation
33
Q

Give an example of 2 extrapyramidal side-effects

A

Parkinsonism, acute dystonia, akathasia, tardive dyskinesia

34
Q

What is Neuroleptic malignant syndrome?

A

Severe rigidity, hyperthermia, increased CPK, autonomic lability

35
Q

Give 4 advantges of Atypical antipsychotics

A
  1. Less EPSE
  2. different preparations e.g. dissolvable
  3. some once daily dosage
  4. differing side effect profiles can be matched to patient characteristics
36
Q

What is the first line treatment in schizophrenia recommended by NICE

A

Atypical antipsychotics

37
Q

Give 4 side effects of atypical antipsychotics

A
  1. extrapyramidal side effects at HIGH doses
  2. weight gain- e.g. olanzapine
  3. increased prolactin e.g. risperidone
  4. sedation

Vary between drugs

38
Q

Which antipsychotic is used for treatment-resistant schizophrenia and the only one proven to reduce negative symptoms and aggression?

Give 2 disadvantges of this drug

A

Clozapine

1) Effective but many side effects ➞ CNS depression, cardiac toxicity, risk of sudden death with high dose
2) Requires regular blood tests due to risk of agranulocytosis

39
Q

What are Anxiety disorders + examples

A

Fear out of proportion to situation resulting in avoidance

  • Eg. Fear of dying, going crazy

Can also present with physical symptoms

  • Eg. light headedness, SoB, hot/cold flushes, nausea, palpitations, numbness, pins and needles
40
Q

How do we treat anxiety?

A

Non pharmacological approaches first line - CBT

Treat any co-morbid disorder

Drugs- antidepressants and anxiolytics

41
Q

Give 3 principle neurotransmitter systems involved in anxiety

A

GABA, serotonin (5-HT), Noradrenaline

42
Q

Give 2 examples of Benzodiazepines

+ the 2 main BDZ receptors and how they differ

A

Diazepam and lorazepam

Exerts effects through structure known as GABABDZ receptor complex ➞ 2 main groups high and low affinity (high responsible for anticonvulsant effects of BDZs)

BDZ act as full agonists at these receptor sites which lead to enhancement of GABA

43
Q

Give 4 pharmacokinetics of Benzodiazapines

A
  1. Good oral bioavailability
  2. Highly lipid soluble + rapid CNS diffusion
  3. Renal excretion
  4. Long half life
44
Q

What is a risk of long term OR stopping of bezodiazapine treatment?

A

Tolerance and Dependence

Tolerance ➞ need to increase the dose to achieve the same effect.

Dependence on discontinuation of treatment ➞ withdrawal effects such as insomnia, agitation, anxiety

45
Q

Give 3 common side effects of benzodiazepines

+ one occasional and one rare side effecr

A
  1. drowsiness
  2. dizziness
  3. psychomotor impairment

Occasional ➞ dry mouth, blurred vision, GI upset, ataxia, headache, reduced blood pressure

Rare ➞ amnesia, restlessness, rash

46
Q

Give 2 things which may occur if benzodiazepines are taken during pregnancy

A

Foetal cleft lip and palate

Respiratory depression + feeding difficulties in baby If taken late in pregnancy

47
Q

How do we treat a benzodiazepines overdose?

A

Flumazenil ➞ antagonist/partial inverse agonist at BDZ receptors may be useful in reversing effects

48
Q

What is Bipolar Disorder + what is the main treatment

A

Episodes of Depression and hypomania/mania

Treatment ➞ Lithium

49
Q

Give 4 features of Mania

A
50
Q

Give 4 examples of Mood stabilisers

A
  1. Lithium
  2. Sodium valproate
  3. Carbamazepine
  4. Lamotrigine
  5. Antipsychotics
51
Q

What is the Lithium theory

A

1) Electrolytes and channels may compete with Mg and Ca2+ ions
2) NT-Li increases 5-HT ➞ chronic Li may reduce 5-HT receptor sites
3) Second messenger systems ➞ lithium attenuates the effects of certain NTs on their receptors without altering receptor density

52
Q

Give 3 pharamcokinetics of Litheium + the clinical implication of these

A

1) renal excretion ➞ check renal function before starting + every 6 months (and thyroid b/c risk of hypothyroidism)
2) slow release preparations can be given once daily
3) narrow therapeutic window ➞ must be taken within 12 hours of last oral dose and requires monitoring (at least 3/month)

53
Q

Give 4 common side effects of lithium + 4 other effects

A
  1. Memory problems
  2. Thirst
  3. Polyuria
  4. Tremor
  5. Drowsiness
  6. Weight gain

Other effects ➞ effect on kidneys, endocrine changes, hair loss and ashes

54
Q

Give 4 toxic effects of Lithium

A
  1. vomiting
  2. diarrhoea
  3. coarse tremor
  4. dysarthria
  5. cognitive impairment
  6. restlessness
  7. agitation
55
Q

How doe we treat Lithium toxicity

A
  1. supportive measures
  2. anticonvulsants
  3. increase fluid intake / IV Fluids etc
  4. haemodialysis may be necessary
56
Q

Give 2 classes + drug examples for dementia medication

What severity of dementia is each recommended for?

A

ACh Inhibitors (mild-moderate) ➞ donepezil, galantamine, rivastigmine

NMDA antagonist (severe)➞ Memantine

57
Q

Give 4 Important side effects of ACh Inhibitors

A
  1. nausea, vomiting, anorexia, diarrhoea
  2. fatigue insomnia, headache
  3. bradycardia
  4. worsening of COPD
  5. gastric/duodenal ulcers
58
Q

Give 4 common side effects of Memantine

A
  1. Hypertension
  2. dyspnoea
  3. headache
  4. dizziness
  5. drowsiness
59
Q

Why is Memantine useful in Alzheimer’s Disease

A

Blocks the NMDA receptor (glutamate receptor)

It is thought that excess glutamate leads to neuronal excitability and excessive stimulation in Alzheimer’s Disease

Pharmacology (Semester 6) (17 decks)

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