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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

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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

Study These Flashcards
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
Explain the dopamine theory of Schizophrenia + treatment and examples
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
First generation antipsychotic drugs block ______ transmission but cause ______ side effects
dopamine, extrapyramidal
27
Is schizophrenia associated with increased 5-HT function + examples
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
Is schizophrenia associated with decreased cortical glutamate function?
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
How is Schizophrenia diagnosed
30
Give 4 actions ALL antipsychotics will show + 2 long term s/e
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
Give an example of a typical antipsychotics + 4 facts about these
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
Give 4 side effects/toxicity problem a/w typical antipsychotics
1. Extrapyramidal side-effects 2. Neuroleptic malignant syndrome 3. Postural hypotension 4. Weight gain 5. Endocrine changes e.g. prolactinaemia 6. Pigmentation
33
Give an example of 2 extrapyramidal side-effects
Parkinsonism, acute dystonia, akathasia, tardive dyskinesia
34
What is Neuroleptic malignant syndrome?
Severe rigidity, hyperthermia, increased CPK, autonomic lability
35
Give 4 advantges of Atypical antipsychotics
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
What is the first line treatment in schizophrenia recommended by NICE
Atypical antipsychotics
37
Give 4 side effects of atypical antipsychotics
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
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
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
What are Anxiety disorders + examples
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
How do we treat anxiety?
Non pharmacological approaches first line - CBT Treat any co-morbid disorder Drugs- antidepressants and anxiolytics
41
Give 3 principle neurotransmitter systems involved in anxiety
GABA, serotonin (5-HT), Noradrenaline
42
Give 2 examples of Benzodiazepines + the 2 main BDZ receptors and how they differ
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
Give 4 pharmacokinetics of Benzodiazapines
1. Good oral bioavailability 2. Highly lipid soluble + rapid CNS diffusion 3. Renal excretion 4. Long half life
44
What is a risk of long term OR stopping of bezodiazapine treatment?
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
Give 3 common side effects of benzodiazepines + one occasional and one rare side effecr
1. drowsiness 2. dizziness 3. psychomotor impairment Occasional ➞ dry mouth, blurred vision, GI upset, ataxia, headache, reduced blood pressure Rare ➞ amnesia, restlessness, rash
46
Give 2 things which may occur if benzodiazepines are taken during pregnancy
Foetal cleft lip and palate Respiratory depression + feeding difficulties in baby If taken late in pregnancy
47
How do we treat a benzodiazepines overdose?
Flumazenil ➞ antagonist/partial inverse agonist at BDZ receptors may be useful in reversing effects
48
What is Bipolar Disorder + what is the main treatment
Episodes of Depression and hypomania/mania Treatment ➞ Lithium
49
Give 4 features of Mania
50
Give 4 examples of Mood stabilisers
1. Lithium 2. Sodium valproate 3. Carbamazepine 4. Lamotrigine 5. Antipsychotics
51
What is the Lithium theory
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
Give 3 pharamcokinetics of Litheium + the clinical implication of these
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
Give 4 common side effects of lithium + 4 other effects
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
Give 4 toxic effects of Lithium
1. vomiting 2. diarrhoea 3. coarse tremor 4. dysarthria 5. cognitive impairment 6. restlessness 7. agitation
55
How doe we treat Lithium toxicity
1. supportive measures 2. anticonvulsants 3. increase fluid intake / IV Fluids etc 4. haemodialysis may be necessary
56
Give 2 classes + drug examples for dementia medication What severity of dementia is each recommended for?
ACh Inhibitors (mild-moderate) ➞ donepezil, galantamine, rivastigmine NMDA antagonist (severe)➞ Memantine
57
Give 4 Important side effects of ACh Inhibitors
1. nausea, vomiting, anorexia, diarrhoea 2. fatigue insomnia, headache 3. bradycardia 4. worsening of COPD 5. gastric/duodenal ulcers
58
Give 4 common side effects of Memantine
1. Hypertension 2. dyspnoea 3. headache 4. dizziness 5. drowsiness
59
Why is Memantine useful in Alzheimer's Disease
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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