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EXAM 2 PHARM.NURSING STUDY GUIDE 2022

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AEMs, anti-depressants, anxiolytics, antipsychotics, Antibiotics, antivirals, antifungals, and anthelmintic meds **Know every drug– have a one-line mechanism of action on a table for each drug and understand it, as well as how and where it works All of the seizure meds have a level…so think what might differentiate them… Carbamazepine…we learned causes agranulocytosis…severe suppression of granulocytes (WBC) in the bone marrow …check CBC…concern about infection Antiepileptics block transmission, raise the seizure threshold, so that the patient will not peak over the seizure threshold and have a seizure. Anticonvulsants in terms of monitoring (most common side effects, most serious side effects) – know that they are all monitored with blood work for their levels so that is a similarity amongst them  Carbamazepine – CBC – Causes agranulocytosis so be watching the white count in particular although there is other bone marrow suppression as well  What do you monitor? – TSH because the med can affect the thyroid  Never want anyone to d/c suddenly, must be weaned off  Talk to patients about safety – driving limitations, may have to report patient to DMV if they are having active seizures  Oral health can be affected by anti-seizure meds and extra trips to the dentist may be required Neurotransmitters  GABA – calming  Acetylcholine – muscle action, thought and learning Seizure • Topiramate (Topamax) • Carbamazepine (Tegretol) • Valproate (Depakote) • Levetiracetam (Keppra) Antidepressant • SSRI • SNRI • TCAs (“amine”) • MAOIs (phenelzine (Nardil) Anxiolytics • Buspirone (Buspar) • Benzodiazepines (“pams”) Antipsychotics • Aripiprazole (Abilify) Insomnia • temazepam (Restoril), zolpidem (Ambien) ***If a specific drug is listed on the PowerPoint, know all about it.  All these drugs are listed on the PowerPoint  Seizure o Topiramate – topamax o Carbamazepine – Tegretol o Valproate – Depakote o Levetiracetam – Keppra  Antidepressants o SSRI o SNRI o TCAs (“amine” o MAOIs  Phenelzine – Nardil  Anxiolytics o Buspirone (Buspar) o Benzodiazepines (“pams”)  Antipsychotics o Aripiprazole (Abilify)  Insomnia o Temazepam (Restoril) o Zolpidem (Ambien) Antidepressants  SSRI blocks the reuptake of serotonin which keeps it present in the synapse for longer, so you get more effect from it  All of the antidepressants, whether a drug family or specific drug, you need to know and understand that drug and mechanism of action  Common side effects of SSRIs – weight gain, sometimes weight loss, anticholinergic effects like dry mouth and constipation, nausea, vomiting, sexual side effects – diminished, delayed or absent orgasm, premature ejaculation, decreased libido  SSRIs – serotonin syndrome – increased reflux, agitation, high body temperature, tremor, dilated pupils, diarrhea  Serotonin withdrawal – can see this in shorter acting SSRI’s when people forget to take them (paroxetine is the shortest acting), sertraline and citalopram can also happen but not as quickly as paroxetine.  Serotonin withdrawal syndrome – tremulous, paresthesia’s, nausea, vomiting, sweating SNRIs  Effect and block the reabsorption of norepinephrine – norepi effects specifically the sympathetic nervous system and also has serotonergic effects  Sevilla, Cymbalta, etc. names of drugs  Side effects – headaches, nausea, somnolence, dry mouth, anticholinergic things, palpitations, hypertension, and hyperhidrosis (excessive sweating). TCAs  Effect three brain chemicals o Serotonin – 5ht o Noradrenaline/norepinephrine o Acetylcholine –  This group of medications has the highest anticholinergic effects – the highest amount of dry mouth and constipation  People who have BPH, glaucoma, urinary problems should not take this medication due to the degree of anticholinergic effect  Side effects: anticholinergic, nausea, as well as cardiac conduction disorders including a prolonged QT interval with this drug – a baseline EKG is imperative before starting on this medication. Tardive dyskinesia (movement), neuroleptic malignant syndrome (  If you ever put someone on this for their depression, understand that in the first few weeks they can have increased suicidal ideation  An overdose of TCAs is fatal; whereas, with the SSRIs it isn’t. Buspirone (full agonist, serotonin) but can also be an antagonist  Full agonist for the presynaptic 5ht1 receptor… partial agonist at the postsynaptic 5ht1 receptor  If someone has too much serotonin, it will act as an antagonist  Or if they do not have enough serotonin, it will act as an agonist in the post synaptic  Structure similar to clozapine which is an atypical antipsychotic  Works well for anxiety and has a synergistic effect with SSRI for someone who has a resistant type of depression that needs an extra boost.  Non-benzodiazepine anxiolytic  Has similar structure to Haloperidol…was thought to be an antipsychotic at first as it is similar to clozapine in structure.  *agonist for the presynaptic and postsynaptic 5HT 1 a receptors…permits serotonin binding and blockage of neuron firing…when there is an excess of serotonin, buspirone acts as an antagonist, when deficit, it acts as an agonist (such as in depression or anxiety). Benzodiazepines – binds to receptors to inhibit the neurotransmitter release  Effect GABA receptors – which are very sedating.  Tend to be very habituating – be aware of this and limit prescribing  If you have to put a patient on a benzo, try to choose something that is longer acting so that patient does not need to redose constantly. Longer acting benzo example is klonopin  MOA – bind to GABA receptor – works at different allosteric sites to facilitate GABAs action  CNS depressant  Sedating esp when administered with ETOH or other CNS depressants.  *Increase the action of GABA (an inhibitory neurotransmitter), thereby decreasing neuronal excitement…high related to this drug…withdrawal symptoms do occur....must be weaned

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EXAM 2 PHARM
AEMs, anti-depressants, anxiolytics, antipsychotics, Antibiotics, antivirals, antifungals, and
anthelmintic meds
**Know every drug– have a one-line mechanism of action on a table for each drug and
understand it, as well as how and where it works
Seizure Antidepressant Anxiolytics Antipsychotics Insomnia

• Topiramate • SSRI • Buspirone • Aripiprazole • temazepam
(Topamax) • SNRI (Buspar) (Abilify) (Restoril),
• Carbamazepine • TCAs (“amine”) • Benzodiazepines zolpidem
(Tegretol) • MAOIs (“pams”) (Ambien)
• Valproate (phenelzine
(Depakote) (Nardil)
• Levetiracetam
(Keppra)

All of the seizure meds have a level…so think what might differentiate them…
Carbamazepine…we learned causes agranulocytosis…severe suppression of granulocytes (WBC)
in the bone marrow …check CBC…concern about infection

Antiepileptics block transmission, raise the seizure threshold, so that the patient will not peak
over the seizure threshold and have a seizure.
Anticonvulsants in terms of monitoring (most common side effects, most serious side effects) –
know that they are all monitored with blood work for their levels so that is a similarity amongst
them
 Carbamazepine – CBC – Causes agranulocytosis so be watching the white count
in particular although there is other bone marrow suppression as well
 What do you monitor? – TSH because the med can affect the thyroid
 Never want anyone to d/c suddenly, must be weaned off
 Talk to patients about safety – driving limitations, may have to report patient to
DMV if they are having active seizures
 Oral health can be affected by anti-seizure meds and extra trips to the dentist
may be required
Neurotransmitters
 GABA – calming
 Acetylcholine – muscle action, thought and learning

,***If a specific drug is listed on the PowerPoint, know all about it.
 All these drugs are listed on the PowerPoint
 Seizure
o Topiramate – topamax
o Carbamazepine – Tegretol
o Valproate – Depakote
o Levetiracetam – Keppra
 Antidepressants
o SSRI
o SNRI
o TCAs (“amine”
o MAOIs
 Phenelzine – Nardil
 Anxiolytics
o Buspirone (Buspar)
o Benzodiazepines (“pams”)
 Antipsychotics
o Aripiprazole (Abilify)
 Insomnia
o Temazepam (Restoril)
o Zolpidem (Ambien)

Antidepressants
 SSRI blocks the reuptake of serotonin which keeps it present in the synapse for longer, so
you get more effect from it
 All of the antidepressants, whether a drug family or specific drug, you need to know and
understand that drug and mechanism of action
 Common side effects of SSRIs – weight gain, sometimes weight loss, anticholinergic
effects like dry mouth and constipation, nausea, vomiting, sexual side effects –
diminished, delayed or absent orgasm, premature ejaculation, decreased libido
 SSRIs – serotonin syndrome – increased reflux, agitation, high body temperature, tremor,
dilated pupils, diarrhea

,  Serotonin withdrawal – can see this in shorter acting SSRI’s when people forget to take
them (paroxetine is the shortest acting), sertraline and citalopram can also happen but
not as quickly as paroxetine.
 Serotonin withdrawal syndrome – tremulous, paresthesia’s, nausea, vomiting, sweating

SNRIs
 Effect and block the reabsorption of norepinephrine – norepi effects specifically the
sympathetic nervous system and also has serotonergic effects
 Sevilla, Cymbalta, etc. names of drugs
 Side effects – headaches, nausea, somnolence, dry mouth, anticholinergic things,
palpitations, hypertension, and hyperhidrosis (excessive sweating).
TCAs
 Effect three brain chemicals
o Serotonin – 5ht
o Noradrenaline/norepinephrine
o Acetylcholine –
 This group of medications has the highest anticholinergic effects – the highest amount of
dry mouth and constipation
 People who have BPH, glaucoma, urinary problems should not take this medication due
to the degree of anticholinergic effect
 Side effects: anticholinergic, nausea, as well as cardiac conduction disorders including a
prolonged QT interval with this drug – a baseline EKG is imperative before starting on
this medication. Tardive dyskinesia (movement), neuroleptic malignant syndrome (
 If you ever put someone on this for their depression, understand that in the first few
weeks they can have increased suicidal ideation
 An overdose of TCAs is fatal; whereas, with the SSRIs it isn’t.

Buspirone (full agonist, serotonin) but can also be an antagonist
 Full agonist for the presynaptic 5ht1 receptor… partial agonist at the postsynaptic 5ht1
receptor
 If someone has too much serotonin, it will act as an antagonist
 Or if they do not have enough serotonin, it will act as an agonist in the post synaptic
 Structure similar to clozapine which is an atypical antipsychotic
 Works well for anxiety and has a synergistic effect with SSRI for someone who has a
resistant type of depression that needs an extra boost.
 Non-benzodiazepine anxiolytic
 Has similar structure to Haloperidol…was thought to be an antipsychotic at first as it is
similar to clozapine in structure.
 *agonist for the presynaptic and postsynaptic 5HT 1 a receptors…permits serotonin
binding and blockage of neuron firing…when there is an excess of serotonin, buspirone
acts as an antagonist, when deficit, it acts as an agonist (such as in depression or
anxiety).


Benzodiazepines – binds to receptors to inhibit the neurotransmitter release
 Effect GABA receptors – which are very sedating.
 Tend to be very habituating – be aware of this and limit prescribing

,  If you have to put a patient on a benzo, try to choose something that is longer acting so
that patient does not need to redose constantly. Longer acting benzo example is
klonopin
 MOA – bind to GABA receptor – works at different allosteric sites to facilitate GABAs
action
 CNS depressant
 Sedating esp when administered with ETOH or other CNS depressants.
 *Increase the action of GABA (an inhibitory neurotransmitter), thereby decreasing
neuronal excitement…high related to this drug…withdrawal symptoms do occur....must
be weaned.
 CAUTION IN PRESCRIBING




MAOI Inhibitors
 Nardil, Parmate, Marplan
 Not used often and are not popular due to the amount of adverse effects
 Adverse effects: tardive dyskinesia
 Do not mix with other substances
 Do not eat anything pickled or aged because these things contain tyramine and interact
to cause severely increased bp, tachycardia, dizziness, sweating, tremors, etc.
 Do not mix well with other things so they need to be two weeks separated from
anything else (assuming this is specifically referring to other antidepressants)
 When starting new antidepressant, wean patient off this medication. Pt. must be off of
this medication at least two weeks before starting another antidepressant
 MAO – destroys norepi and serotonin in the synapse and the MAOIs basically inhibit it so
you have the neurotransmitters hanging around longer (so you get a longer serotonin,
norepi effect such as more energy as well as a better mood).

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