Pharmacology Flashcards

1
Q

What does Monoamine Oxidase do?

A

Breaks 5-HT down into its inactive products, once it has re entered the pre synaptic bulb.

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2
Q

What do most Anti Depressants do?

A

Increase the concentration of serotonin in the synaptic cleft.

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3
Q

What is the precursor for 5HT?

A

Trytophan

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4
Q

Examples of Monoamine Oxidase inhibitors

A

Phenelzine

Moclobemide

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5
Q

Examples of monoamine neurotransmitters

A

Dopamine
Noradrenaline
5HT

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6
Q

Irreversible Monoamine Oxidase Inhibitors

A

Phenelzine

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7
Q

Reversible Monoamine Oxidase Inhibitors

A

Moclobemide

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8
Q

What severe side effect is linked to Monoamine Oxidase Inhibitors?

A

Cheese reaction

Dietary tyramine is not broken down leading to a hypertensive crisis.

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9
Q

What common side effect are linked to Monoamine Oxidase Inhibitors?

A

Insomnia
Postural hypertension
Peripheral oedema

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10
Q

How do Tricyclics work?

A

Block reuptake channels for 5-HT and Noradrenaline

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11
Q

Examples of Tricyclic antidepressants.

A

Imipramine

Amitriptyline

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12
Q

Tricyclic antidepressants have no Anticholinergic effects.

T/F

A

False they have a strong anticholinergic effect

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13
Q

What are some of the anticholinergic side effects of Tricyclic drugs?

A

Blurred Vision
Dry mouth
Constipation
Urinary retention

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14
Q

List some common side effects of Tricyclic antidepressants.

A
Sedation 
Weight gain
postural hypertension
tachycardia
Arrhythmias
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15
Q

Why should Tricyclics never be prescribed for anyone with arrhythmias?

A

They are Cardiotoxic

Prolong QT

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16
Q

How do SSRIs work?

A

Selective Seretonin Reuptake Inhibitors

Block serotonin channels

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17
Q

Examples of SSRIs

A

Fluoxetine
Citalopram
Setraline

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18
Q

Give some common side effects of SSRIs

A
Nausea
Headache 
Worsened anxiety
Sweating
Sexual dysfunction
Hyponatraemia - elderly
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19
Q

SSRIs should be used in patients with a history of self harm. T/F

A

False

Be careful as SSRIs linked to transient increase in Self Harm

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20
Q

Side effects of SSRIs discontinuation

A

Flu like symptoms
Insomnia
N+V

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21
Q

How do SNRIs work?

A

Seretonin Norepinephrine re-uptake inhibotors

Noradrenaline and 5HT channels are blocked

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22
Q

Examples of SNRIs

A

Venlafaxine

Dulaxetine

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23
Q

Side effects of SNRIs

A

Similar to SSRIs

Less Anticholinergic side effects

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24
Q

A Tetracyclic Antidepressant selective for α2 5-HT2 and 5-HT3 reuptake channels.

A

Mirtazapine

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25
Q

Which side effects of Mirtazapine is actually a desirable one which advocates for its use?

A

Sedative
Use in patients who are suffering from insomnia or poor sleep.
Weight gain
Use in patients who are underweight

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26
Q

Some side effect so Mirtazapine.

A

Dry mouth

Increased appetite

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27
Q

List of Antidepressant Drugs

A
TCA
MAOI
SSRIs
SNRIs
Mirtazapine
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28
Q

What is the most common mood stabilising drug?

A

Lithium Carbonate

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29
Q

Side effects of Lithium

A
Dry mouth 
Polyuria
Tremor
Hypothyroidism
Nephrogenic Diabetes Insipidus
Weight gain
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30
Q

What are some signs a patient has toxic Lithium poisoning?

A
Diarrhoea 
Vomiting
Ataxia
Drowsiness
Convulsiona
Coma
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31
Q

List some common Anticonvulsants

A

Valproic acid
Lamotrigine
Carbamazepine

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32
Q

List some Antipsychotic drugs

A

Olanzapine
Aripiprazole
Quetiapine

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33
Q

What is the mode of action in Antipsychotic drugs?

A

Dopamine and 5 HT2 seretonin receptor antagonists

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34
Q

Some common side effects of Antipsychotic drugs.

A

Sedation
Weight gain
Metabolic syndrome
Extra pyramidal effects

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35
Q

What are the dopamine pathways within the Brain?

A
Mesolimbic
Mesocortical
Nigrostriatal
Tuberoinfundibular
Hypothalamospinal
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36
Q

Where does the mesolimbic pathway originate and terminate?

A

Ventral Tagmatic area to the limbic region

37
Q

What does the mesolimbic pathway control?

A

Memory
Emotional control
Personality

38
Q

Damage or dysfunction in the mesolimbic pathway results in what?

A

Delusions
Hallucinations
Thought insertion

39
Q

What does the mesocortical pathway control?

A

Higher brain function

40
Q

What does the Nigrostriatal pathway control?

A

Voluntary movement

41
Q

Damage of dysfunction in the nigrostriatal pathway results in what?

A

Parkinsonism - tremor bradykinesia rigidity

42
Q

Where is the tuberoinfundibulnar pathway found?

A

Around the pituitary gland

43
Q

What are the main dopamine receptors?

A

D1-D5

44
Q

Where would you find D1-D2 receptors?

A

Limbic and striatal areas

45
Q

Which receptor is found most commonly in the mesolimbic pathway?

A

D2

46
Q

List some D2 receptor antagonists

A

Raclopride

Haloperidol

47
Q

Give an example of D4 receptor agonists

A

Clozapine

48
Q

What do D2 receptors do when activated ?

A

Inhibit adenyl cyclase
Inhibit voltage gated Ca2+ channels
Open K+ channels
Hyperpolarise

49
Q

What do D1 receptors do when activated ?

A

Stimulate cAMP

50
Q

How does GABA affect the post synaptic membrane?

A

Inhibits neuronal activity by activating Cl- channels causing hyperpolarisation.

51
Q

How do Benzodiazepines work?

A

Enhance the affect if GABA increasing the inhibition of postsynaptic potential

52
Q

Describe the efficacy of Benzodiazepines?

A

Rapid action

Well tolerated for less than two weeks

53
Q

What are the issues of Benzodiazepines?

A
Sedation Psychomotor impairment
Withdrawal issues
Dependancy and abuse
Alcohol interactions- both act on same receptor
Can worsen co-morbid depressions
54
Q

What drugs are used in the treatment of anxiety?

A
Benzodiazepines 
Antidepressant drugs 
Buspirone
Pregablin
Beta Blockers Propanolol
55
Q

What pathway is involved in anxiety?

A

Corticostriatal thalamic cortical circuit

56
Q

What are the main neurotransmitters in the amygdala centred circuit?

A
5 HT
GABA
Glutamate
CRF - Corticotrophin releasing factor 
Norepinephrine
57
Q

What is the affect of GABA on anxiety?

A

Reduces affect of neurones in Amygdala and Corticostriatal thalamic cortical circuit
reduces anxiety

58
Q

How do BDZ work to reduce anxiety?

A

BDZ enhance the action of GABA hence increasing suppression of amygdala and CTCC

59
Q

How many types of GABA receptors are there?

A

A
B
C

60
Q

GABA A is bound by what?

A

BDZ
Barbiturates
Alcohol

61
Q

Activation of GABA A receptors does what?

A

Hyperpolarises the membrane by opening Cl- channels alowing influx of Cl- ions.

62
Q

What properties do Ethanol, Neurosteroids and Barbiturates display?

A

Anxiolytic - reduce anxiety

63
Q

Give a example of an Inverse BD2 agonist

A

B-Carboline

64
Q

What properties do Inverse BD2 agonists displays i.e B-Carboline

A

Anxiogenic - Increase anxiety

65
Q

What GABA antagonists are used in the treatment of BDZ overdose?

A

Flumazenil - Bind and block GABA A receptors

66
Q

Give examples of Benzodiazepines.

A

Lorazepam
Diazepam
Chlordiazepam

67
Q

What is Xanax?

A

Alprazolam - form of BDZ

68
Q

What effect do BDZ have?

A

Reduce anxiety and aggression
Hypnosis and sedation
Muscle relaxent
Anticonvulsant effect

69
Q

What are some clinical uses of BDZ?

A
Acute anxiety
Hypnosis
Alcohol withdrawal
Mania
Delirium 
Rapid tranquillisation
Status Epilepticus
70
Q

Why is a BDZ “fairly safe”?

A

As it is unlikely to cause respiratory depression

71
Q

What are some issues surrounding the use of BDZ?

A

Some have paradoxical aggression
Anterograde amnesia
Impaired coordinations
Tolerance and dependance are risks

72
Q

What some side effects of BDZ withdrawal?

A

Abdo cramps, Increased anxiety and panic attacks, Blurredvision
Muscle tension, chest pain, palpitation, sweating
Depression insomnia nightmares dizziness
N+V restlessness

73
Q

What causes the withdrawal symptoms from BDZ?

A

Chronic BDZ used reduces GABA receptors response to GABA.

Less inhibitory input, as less GABA and less receptive to its presence.

74
Q

What are some signs of rapid BDZ withdrawal?

A
Confusion
Psychosis
Convulsions
Tachychardia
Hypertension
Agitation
Tremor
75
Q

How do you withdraw somoene from BDZ?

A

Transfer over to Diazepam or Chlordiazepam - taken at night
Reduce dose every 2-3 weeks - 2- 2.5 mg
Time needed varies from around 4 weeks to 1 year

76
Q

If whilst withdrawing your patient from BDZ they start to develop symptoms what do you do?

A

Maintain dosage

77
Q

What does seretonin do within the amygdala?

A

Innervates it

78
Q

How do SSRIs and SRNIs increase extracellular seretonin?

A

Blockage of the Serotonin reuptake transporters

79
Q

How does SSRI and SRNI usage help to reduce anxiety

A

After chronic usage due to increased extracellular Serotonin expression of serotonin and glucocorticoid receptors is decreased - less stimulation

80
Q

What can SSRIs be used for, anxiety and fear?

A

Panic disorders OCD PTSD Phobias GAD

81
Q

What SSRIs can be used, Anxiety?

A

Escitalopram
Paroxetine
Fluoxetine

82
Q

What can Tricyclics be used for, anxiety and fear?

A

OCD

Panic disorder 2nd line

83
Q

What Tricyclic are used, anxiety.

A

Clomipramine

Imipramine

84
Q

What are SNRIs used for? Anxiety disorders.

A

GAD

85
Q

What SRNI is sued in GAD?

A

Venlafaxine

86
Q

What are MAOI used for? Anxiety disorder.

A

Social Anxiety disorders

87
Q

What MAOI is use for social anxiety disorders?

A

Moclobemide

88
Q

What is Pregablins mode of action?

A

GABA enhancer and Ca2+ channel blocker

89
Q

When is Pregablin used in anxiety?

A

Only for unresponsive disease