drugs - MH and overdose Flashcards

(98 cards)

1
Q

what is the monoamine theory in depression

A

depression results from functionally deficient monoaminergic (NA and/or 5HT) transmission in the CNS

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2
Q

what are the emotional symptoms of depression

A
  • misery, apathy, pessimism
  • low self esteem
  • indecisiveness
  • loss of motivation
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3
Q

what are the biological symptoms of depression

A
  • retardation of thought and action
  • loss of libido
  • sleep disturbance
  • change in weight and appetitie
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4
Q

how to tricyclic antidepressants work on 5HT and NA

A

inhibit the reuptake of 5HT and NA in the synaptic cleft - meaning there is more interaction with the receptors so increases the activity as there are more enzymes present to react

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5
Q

how do tricyclic antidepressants work on a1 and a2

A
  • they act to antagonise alpha-cholinergic
  • alpha 1 causes vasoconstriction which leads to orthostatic hypotension
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6
Q

how do tricyclic antidepressants work on muscarinic

A
  • they block the muscarinic receptors
  • causes mouth dryness and constipation
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7
Q

how do tricyclic antidepressants work on H1 receptors

A

they block the histamine receptors - causes sedation and weight gain

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8
Q

how do tricyclic antidepressants work on sodium chloride

A

block the sodium channels which causes ECG changes

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9
Q

what do TCAs work on

A
  • 5HT
  • NA
  • sodium channels
  • H1 receptors
  • alpha cholinergic receptors (a1,a2)
  • muscarinic receptors
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10
Q

examples of TCAs

A
  • imipramine
  • amitriptyline
  • desipramine
  • nortriptyline
  • clomipramine
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11
Q

what are TCAs also used to treat

A
  • neuropathic pain in adults
  • enuresis in children
  • insomina
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12
Q

why are TCAs not the first line of treatment

A
  • have a low threshold for overdose
  • less well tolerated than SSRIs
  • varying degrees of antimuscarinic and anticholinergic side effects
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13
Q

what are side effects of TCAs cause from muscarinic receptor blockages

A
  • dry mouth
  • urine retention
  • constipation
  • blurred vision
  • tachycardia
  • pupil dialtion
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14
Q

what are the side effects of TCAs caused from H1 receptor blockages

A
  • sedation
  • weight gaine
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15
Q

what are the side effects from TCA caused a1 receptor blockages

A

orthostatic hypotension

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16
Q

why are SSRIs used as a first line defence

A
  • they don’t target other receptors
  • so don’t cause as many side effects
  • they are relatively safe in an overdose
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17
Q

how do SSRIs work

A
  • decrease serotonin deficiency
  • inhibit reuptake of synaptic serotonin by the presynaptic neuron
  • serotonin can then stay in the synapse for linger
  • serotonin then repeatedly stimulated the postsynaptic receptors (increases activity)
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18
Q

what are examples of SSRIs

A
  • fluoxetine
  • fluvoxamine
  • paroxetine
  • sertraline
  • citalopram
  • escitalopram
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19
Q

what are the side effects of SSRIs

A
  • insomnia
  • sexual dysfunction
  • prominent GI disturbances
  • significant weight loss or anorexia
  • suicidal ideation
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20
Q

how do SNRIs work

A
  • same mechanism as TCAs
  • block the reuptake of 5HT and NA
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21
Q

what are examples of SNRIs

A
  • venlafaxine
  • duloxetine
  • reboxetine
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22
Q

what are side effects of SNRIs

A
  • insomnia
  • sexual dysfunction
  • nausea
  • dry mouth
  • hypertension
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23
Q

how do serotonin antagonist and reuptake inhibitor (SARI) work

A
  • inhibit the reuptake of 5HT - works as an agonist at 5HT1A and antagonist at 5HT3
  • blocking 5HT3 - post synaptic effect, needed for depression management
  • 5HT1a are pre-synaptic and are autoinhibitory, meaning thay block the slef release of serotonin. An agonistic affect, down regulates the receptor, if they are not present it mores that there is mrore serotonin to be released
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24
Q

what are the side effects of SARIs

A
  • nausea
  • diarrhoea
  • constipation
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25
how does noradrenergic and specific serotonergic antidepressants (NaSSA) work
- enhances 5HT and NA neurotransmission by blocking presynaptic alpah2 receptors - a2 works through inhibitions - blocking this inhibition enhances the release of NA - Block HT2 and 3 receptors on the post synaptic membrane meaning that there are more receptors such as 5HT1 which is presynaptic for an increase in reuptake - 5HT1 is activated by released serotonin - increase expression of post synaptic receptors
26
what are the side effects of NaSSA
- increased appetite - weight gain - NO antimuscarinic side effects or sexual function side effects
27
how to Monoamine oxidase inhibitors work
- inactivated monoamine oxidase (this is an enzyme that degrade NA and serotonin) - by stopping degradation of NA, dopamine and 5HT this allows for an accumulation of these in the presynaptic neurone and leak into the synaptic space
28
what are the 2 types of monoamine oxidase inhibitors
- irreversible, non-competitive, non-selective - reversible, selective MAO-A inhibitors
29
when are MAOIs indicated
unresponsive or allergic to other treatment options or experience strong anxiety
30
what is the cheese reaction in MAOIs
- tyramine is normally converted and degraded by MAO-A - when MAO-A is inhibited by drugs this causes tyramine not to be degraded - this causes there to then be an increase of norepinephrine in the body - this is a potent vasoconstrictor causing hypertensive crisis - tyramine rich foods then also increase the levels of norepinephrine
31
what is serotonin syndrome
- when there is too much serotonin in the synapses of the brain - happens from SSRI overdose or combination of meds that increase serotonin
32
what are mild symptoms of serotonin syndrome
- nervousness - nausea - diarrhoea - tremor - dilated pupils
33
what are moderate symptoms of serotonin syndrome
- increased reflexes - sweating - agitation - rhythmic muscle spasms - ocular clonus
34
what are severe symptoms of serotonin syndrome
- hyperthermia - delirium - rhabdomyolysis - sustained clonus or rigidity (bilaterally in the legs)
35
what are positive symptoms in schiziphrenia
- overt symptoms that shouldn't be present - hallucinations - delusions - disorganized thoughts
36
what are negative symptoms in schizophrenia
- lack of characteristics that should be present - reduced speech - lack of emotional and facial expression - diminished ability to begin and sustain activities - decreased ability to find pleasure in everyday - social withdrawal
37
what are cognitive deficits in schizophrenia
- difficulty in following aspects of cognition - memory - attention - planning - decision making
38
how to manage the first episode of psychosis
- can be treated using reassurance and de-escalation techniques - risk assess the situation for patient and your safety - make sure the patient is checked regularly and easily observable - remove dangerous objects and hazards - respect dignity - communicate calmly and respectfully - build a rapport - active listening and communication
39
what is the cause of positive symptoms
- overactivity in the mesolimbic dopaminergic pathway activating D2 receptors
40
what is the cause of negative symptoms
- decreased activity in the mesocortical dopaminergic pathway - D1 receptors
41
what are examples of first generation (typical) antipsychotics
- chlorpromazine - perphenazime - haloperidol - flupentixol
42
what do first gen antipsychotics act upon
high affinity to D2 receptors
43
what side effects do first gen antipsychotics have
- motor due to extrapyramidal effects: acute dystonia, akathisia, tardive dyskinesia
44
what to first generation antipsychotics aim to help
effect against positive symptoms
45
what are examples of second generations (atypical) antipsychotics
- clozapine - qutiapine - risperidone - aripiprazole - ziprasidone - olanzapine
46
what do second generation antipsychotics act upon
affinity to multiple receptors - 5HT, a, H1, M
47
what side effects do second generation antipsychotics have
- less incidence of extrapyramidal - higher indicines of weight gain and diabetes
48
what do second generation anti-psychotics aim to help
effective against both positive and negative symptoms
49
why is the depot used for antipsychotics
- used for second generation - it can be administered to enhance adherence due to its slow release
50
why is haloperidol used as first line treatment
- primarily blocks dopamine D2 receptors - leads to a reduction i the hyperactivity of dopamine neurotransmission (linked with psychosis) - it has a rapid onset of actions - efficacy in reducing agitation, hallucinations and delusion
51
what are extrapyramidal symptoms
- acute dystonia - akathisia - tardive dyskinesia - pseudoparkinsonism
52
what is acute dystonia
- facial grimacing - upward eye movement - muscle spasm of tounge, face, necks - laryngeal spasm
53
what is pseudoparkinsonism
- stooped posture - shuffling gait - rigidity - bradykinesia - tremors at rest
54
what is akathisia
- restlessness - trouble standing still - feet in constant motion
55
what is tardive dyskinesia
- late involuntary movements - protrusion and rolling of the tongue - choosing motions - facial dyskinesia - smacking/ sucking lip motions
56
what are the cardiovascular side effects of antipsychotics
- tachycardia - orthostatic hypotension - QT prolongation
57
what are the endocrine side effects of antipsychotics
- gynecomastia - menstrual irregulating - weight gain
58
what are antipsychotic med side effects from muscarinic receptor blockages
- dry mouth - urine retention - constipation - blurred vision - tachycardia
59
what are antipsychotic med side effects from H1 receptor blockages
- sedation - weight gain
60
what are antipsychotic med side effects from a1 receptor blockages
orthostatic hypotension
61
what is neuroleptic malignant syndrome
life threatening reaction as a side effect of antipsychotics (normally first gen)
62
what are symptoms of neuroleptic malignant syndrom
- mydriasis - hyperthermia - altered level of consciousness - hypertensive - tachycardia - tremor - clonus - hyperreflexia - increased bowel sounds - aggitation
63
when does neuroleptic malignant syndrome happen
- 24 hrs from initial treatment - fast progression reaching intensity within 72 hours - not usually from an overdose
64
what is the treatment for neuroleptic malignant syndrome
- immediate cessation of antipsychotics - most symptoms are self-limiting - fluid replacement, fever reduction, cardiac, respiratory and renal support - only when severe
65
what is GAD
unrealistic or excessive anxiety and worry about a number of events or activities
66
what is panic disorder
begins as a series of unexpected panic attacks involving an abrupt surge of intense fear or intense discomfort
67
what is obsessive compulsive disorder
where a person have obsessive thoughts and compulsive behaviours
68
what is PTSD
people who have experienced or witnessed and traumatic event or set of circumstances
69
pregabalin as an anxiolytic
- anticonvulsant - bins to voltage gated calcium channel to reduce the release of excitatory neurotransmitters (glutamate) - the reduction in postsynaptic neuron stimulation causes its anxiolytic anticonvulsant and analgesic effect
70
what are the side effects of pregabalin
- dizziness - drowsiness - weight gain - GI upset
71
how do benzodiazepines work as anxiloytics
- increase the activity of GABA, the primary inhibitory neurotransmitter in the CNS - this reduces the excitability of neurones and has a calming effect of the brain
72
classes of benzodiazepines
- short acting (midazolam) - intermediate acting (lorazepam, alprazolam ) - long acting (diazepam)
73
what class of benzodiazepines is used for anxiety
intermediate acting such as loazepam
74
what happens if benzos withdrawal symptoms
- confusion - anxiety - agitation - restlessness - insomnia - tension - tremor dizziness - loos of appetite - seizure
75
benzodiazepine overdose
can be lethal in patients taking alcohols or CNS depressants including opioids
76
what is the treatment for CNS and respiratory depression for benzodiazepines
flumazenil - a GABA-receptor antagonist - rapid onset and short duration of action
77
what are side effects of benzodiaepines
- drowsiness - incoordination - lethargy - slurred speech
78
how does buspirone work as anxiolytic
- it is a 5HT1A agonist (auto receptor that decreases release of 5HT) - has D2 receptor antagonist activity - slow onset of action
79
how does anxiolytic differ in action
- lack anticonvulsant, sedative and muscle relaxant activity - no risk of tolerance, physical dependence or withdrawal effects
80
what are the side effects of buspirone
- abdominal pain - paraesthesia - chest pain
81
what are b-blockers used for as anxiolytics
- do not affect psychological symptoms (anxiety, worry, fear) but reduce autonomic symptoms - palpitations and tremors
82
how do b-blockers work for anxiety
they cross the blood brain barrier so they affect the brain making them necessary for overactivity of the sympathetic neruvous system
83
example of b-blocker for anxiety
propranolol
84
what are the side effects of b-blockers
- insomnia - hypotension - nightmares - bradycardia
85
what benzodiazepines are uses as hypnotics
- triazolam - midazolam
86
examples of z drug
- zolpidem - zoplicone
87
what are z drugs for hypnotics
non-benzodiazepine hypnotics acting as benzodiazepine receptor agonists which then enhance GABA neuronal inhibition
88
what are the benefits of z drugs
- no anticonvulsant or muscle-relaxing properties - few withdrawal symptoms - show little or no tolerance
89
what are the side effects of z drugs
- drug mouth - bitter taste
90
examples of stimulant medication
amphetamines: methylphenidate, lisdexamfetamine, dexamfetamine
91
how do stimulants work
block dopamine and norepinephrine reuptake so increase their activity in certain brain regions
92
what are the side effects of stimulants
- dry mouth - tachycardia - hypertension - decrease in weight and height
93
what happens in an overdose of amphetamines
- wakefulness - excessive activity - paranoia - hallucinations - exhaustion - convulsion - hyperthermia - coma
94
what is the management for simulant overdose
- supportive - reduce core body temperature - rehydration - sedation - cardiac monitoring
95
what are non-stimulant medications used for ADHD
- SNRIs - atomoxetine - central a2-adrnergic agonist - guanfacine
96
what are the side effects of SNRIs (ADHD, non-stimulant)
- abdominal pain - nausea and vomiting - drowsiness - decreased appetite
97
what are the side effects of central a2-adrenergic agonist (nonstimulant, ADHD)
- abdominal pain - nausea and vomiting - drowsiness - decreased appetite - hypotension - bradycardia
98
how do central a2-adrenergic agonists work
presynaptic autoinhibitory - prevent the further stimulation of noradrenaline