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).
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).
