Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
98 Cards in this Set
- Front
- Back
What is the indication for psychopharmacology?
|
establish a diagnosis and identify the the target symptoms that will be used to monitor therpay response
|
|
What is the appropriate strategy for choosing an agent and dosage?
|
select an agent with acceptable side effect profile and use the lowest effective dose
remember the delayed response for many psych meds and drug-drug interactions |
|
What are some general principles in general pharmacology Rx?
|
Indication
Choice of agent and dosage Establish informed consent Implement a monitoring program |
|
What does 'informed consent' consist of?
|
the patient should understand the benefits and risks of the medication
make sure to document this discussion including pt understanding and agreement in fertile women make sure to document teratogenicity discussion |
|
What should a monitoring program in psychopharmacology consist of?
|
track and monitor complaince, side effects, target symptoms response, blood levels and blood tests as appropriate
|
|
What are some indications for antidepressants?
|
unipolar and bipolar depression
organic mood disorder schizoaffective disorder anxiety disorders, including OCD, panic, social phobia, PTSD Premenstrual dysphoric disorder Impulsivity associated with PD |
|
What is selection of antidepressants based on?
|
efficacy is similar in each selection
past history of response side effect profile coexisting medical conditions |
|
There is a delay typically of __ - ___ weeks after therapeutic dose is achieved before symptoms improve with antidepressants.
|
3 to 6 weeks
|
|
If no improvement is seen after a trail of adequate length (at least __ months) and adequate dose, what do you do?
|
2 months
switch to another antidepressant or augment with another agent |
|
What are the worries about TCAs?
|
have potentially unacceptable side effect profile i.e. antihistaminic, anticholenergic, antiadrenergic
lethal in overdose (even with 1 week supply) can cause QT lengthening even at a therapeutic serum level |
|
What is the structure of a tertiary TCA?
|
amine side chain
|
|
What causes tertiary TCA's to have more side effects?
|
amine side chains are prone to cross react wit hother types of receptors which leads to more side effects including antihistaminic (sedation and weight gain), anticholinergic (dry mouth, dry eyes, constipation, memory deficits, and ptentially delirium), antiadrenergic (orthostatic hypotension, sedation, sexual dysfunction)
|
|
Where to tertiary TCA's primary act?
|
serotonin receptors
|
|
What drugs are in the tertiary TCA category?
|
imipramine
amitriptyline doxepin clomipramine |
|
What is unique about secondary TCA structure?
|
often metabolites of tertiary amines
|
|
What do secondary TCA's block?
|
norepinephrine
|
|
Which have more side effects: tertiary or secondary amines?
|
tertiary
|
|
What are examples of secondary TCAs?
|
desipramine
notritriptyline |
|
What is the mechanism of action of monoamine oxidase inhibitors?
|
bind irreversibly to monoamine oxidase thereby preventing inactivation of biogenic amines such as norepinephrine, dopamine, and serotonin leading to increased synaptic levels
|
|
What are some typical side effects of monoamine oxidase inhibitors?
|
orthostatic hypotension
weight gain dry mouth sedation sexual dysfunction sleep disturbance hypertensive crisis with tyramine rich foods or sympathomimetics |
|
What are the s/s of serotonin syndrome?
|
abdominal pain
diarrhea sweats tachycardia HTN myoclonus irritability delirium can lead to: hyperpyrexia, CV shock and death |
|
How long should you wait to switch from and SSRI to a MAOI to twart serotonin syndrome?
|
2 weeks
5 weeks with floxetine due to long half-life |
|
What is the mechanism of action of selective serotonin reuptake inhibitors?
|
block presynaptic serotonin reuptake
|
|
What are SSRIs used to treat?
|
depression and anxiety symptoms
|
|
What are the most common SE of SSRIs?
|
GI upset
sexual dysfunction (30%+) anxiety restlessness nervousness insomnia fatigue or sedation dizziness |
|
What does a SSRI discontinuation syndrome look like?
|
agitation
nausea disequilibrium dysphoria |
|
What are the pros and cons of Paroxetine?
|
pro: short half life with no active metabolites means no build-up and sedating properities offers good inital relief of anxiety and insomnia
cons: significant CYP2D6 inhibition; sedating, wt gain, more anticholinergic effects, most likely to cause discontinuation syndrome |
|
What are the pros and cons of Sertraline?
|
Pros: very weak P450 interaction (only slight CYP2D6); short half life with lower build-up of metabolites; less sedating comparied to paroxetine
Cons: Max absorption requires a full stomach; increased number of GI adverse drug reactions |
|
What are some of the pros of Fluoxetine?
|
long half life so decreased incidence of discontinuation syndromes
Initally activating so can provide increased energy secondary to long half life, can give one 20 mg to taper someone of SSRI when trying to prevent SSRI discontinuation syndrome |
|
What are some of the cons of Fluoxetine?
|
long half life and active metabolite may build up
significant P450 interactions so this may not be a good choice in patients already on a number of meds initial activation may increase anxiety and insomnia more likely to induce mania than some other SSRIs |
|
What is the mechanism of action of SNRIs?
|
inhibit both serotonin and noradrenergic reuptake like the TCAs but without the antihistamine, antiadrenergic or anticholinergic side effects
|
|
What are SNRIs used to treat?
|
depression
anxiety and possibly neuropathic pain |
|
What are the pros in using venlafaxine?
|
minimal drug interactions and almost no P450 activity
short half-life and fast renal clearance avoids build-up (good for geriatric populations) |
|
What are the cons for using venlafaxine?
|
can cause a 10-15 mmHg dose dependent increase in diastolic BP
may cause signficant nausea, primarly with immediate-release (IR) tabs can cause a bad discontinuation syndrome, and taper recommended after 2 weeks of administration noted to cause QT prolongation sexual side effects in >30% |
|
What are the pros and cons for using duloxetine?
|
pros: some date to suggest efficacy for the physical symptoms of depression; thus far less BP increase as compared to venlafaxine, however this may change in time
cons: CYP2D6 and CYP1A2 inhibitor; cannot break capsule, as active ingredient not stable within the stomach |
|
What are two novel antidepressants?
|
mirtazapine
buproprion |
|
What are the pros and cons of mirtazapine?
|
pros: different mechanism of action may provide a good augmentation strategy to SSRs; can be used as a hypnotic at lower doses secondary to antihistamine effects
cons: increases serum cholesterol by 20% in 15% of patients and triglycerdies in 6% of patients; very sedating at lower doses. At doses 30 mg and above it can become very activating and require change of administration time to the morning; associated with weight gain (particularly at doses below 45 mg) |
|
What is the mechanism of action of mirtazapine?
|
5HT2 and 5HT3 receptor antagonist
|
|
What are the pros of buproprion?
|
good for use as an augmentation agent
no weight gain, sexual side effects, sedation or cardiac interactions low induction of mania is second line ADHD agent to consider if patient has co-occuring diagnosis |
|
What is the mechanism of action of buproprion?
|
mechanism of action likely reuptake inhibition of dopamine and norepinephrine
|
|
What are the cons of buproprion?
|
may increase seizure risk at high doses (450 mg+) and should be avoid in patients with TBI, bulemia, anorexia
Does not treat anxiety unlike many other antidepressants and can actually cause anxiety, agitation and insomnia has abuse potential because can induce psychotic sx at high doses |
|
What are the indications for mood stabilizers?
|
bipolar
cyclothymia schizoaffective impulse control intermittent explosive disorders |
|
What are the two classes of mood stabilizers?
|
lithium
anticonvulsants |
|
The only medication to reduce suicide rate is?
|
lithium
|
|
What is lithium used for?
|
long-term prophylaxis of both mania and depressive episodes in 70+% of BAD I patients
|
|
What factors predict positive responses to lithium?
|
prior long-term response or family member with good response
classic pure mania mania is followed by depression |
|
Before starting lithium, what baseline tests should you get?
|
creatinine
TSH CBC Pregnancy test |
|
Why do we check a pregnancy test in women beginning lithium?
|
lithium in the first trimester is associated with Ebstein's anomaly 1/1000 (20x the risk in general population)
|
|
When is a steady state of lithium achieved?
|
5 days
|
|
What should we check lithium levels?
|
12 hours after last dose
once stable check q 3 months |
|
How often should we check TSH and creatinine in patients on lithium?
|
q 6 months
|
|
What is the effective blood level of lithium?
|
0.6-1.2
|
|
What are some of the side effects of lithium?
|
most common are GI distress including reduced appetite, nausea/vomiting, diarrhea
thyroid abnormalities nonsignificant leukocytosis polyuria/polydypsia secondary to ADH antagonism; in a small number of patient can cause intersitial renal fibrosis hair loss, acne reduces seizure threshold, cognitive slowing, intention tremor |
|
At what level do you see mild levels of lithium toxicity? What are the symptoms?
|
1.5 to 2.0
vomiting diarrhea ataxia dizziness slurred speech nystagmus |
|
At what level do you see moderate levels of lithium toxicity? What are the symptoms?
|
2.0 to 2.5
nausea vomiting anorexia blurred vision clonic limb movements convlusions delirium syncope |
|
At what levels do you see severe lithium toxicity? What are the symptoms?
|
> 2.5
generalized convulsions oliguria renal failure |
|
Is valproic acid as effective as lithium in mania prophylaxis? What about depression prophylaxis?
|
as effective in mania
not as effective in depression |
|
What factors predict a postive response to valproic acid?
|
rapid cycling patients (females>males)
comorbid substance issues mixed patients patients with comorbid anxiety disorders |
|
Which is better tolerated: lithium or valproic acid?
|
valproic acid
|
|
What tests should you get before starting valproic acid?
|
baseline liver funciton tests
pregnancy test and CBC |
|
When starting valproic acid in women, you should supplement with?
|
folic acid
|
|
How should you monitor a patient on valproic acid?
|
steady state is achieved after 4-5 days
check 12 hours after last dose repeat CBC and LFTs |
|
What is the target level for valproic acid?
|
50-125
|
|
What are some side effects of valproic acid?
|
thrombocytopenia and platelet dysfunction
nausea, vomiting, weight gain transaminitis sedation, tremor high risk of neural tube defects hair loss |
|
What is the risk of neural tube defect with valproic acid? general population?
|
valproic acid 1-2%
general population 0.14-0.2% |
|
What is first line for actue mania and mania prophylaxis?
|
carbamazepine
|
|
When is carbamazepine indicated?
|
rapid cyclers and mixed patients
|
|
What tests should you order before startin carbamazepine?
|
baseline liver function tests
CBC EKG |
|
How should you monitor carbamazepine?
|
steady state achieved after 5 days
check 12 hours afte rlast dose repeat CBC and LFTs |
|
What is the target level of carbamazepine?
|
4-12 mcg/ml
|
|
When should you recheck carbamazepine levels? Why?
|
around 1 month after starting because induces own metabolism
|
|
What are some side effects of carbamazepine?
|
rash- most common side effect seen
nausea, vomiting, diarrhea, transaminitis sedation, dizziness, ataxia, confusion AV conduction delays aplastic anemia and agranulocytosis (<0.002%) Water retention due to vasopressin-like effect which can result in hyponatremia drug-drug interaction |
|
What are the indications for lamotrigine?
|
similar to anticonvulsants
has specific efficacy for bipolar depression also used for neuropathic/chronic pain |
|
What tests should you conduct prior to starting lamotrigine?
|
baseline liver function tests
|
|
What is the procedure for starting lamotrigine?
|
start with 25 mg daily x 2 weeks
then increase to 50 mg x 2 weeks then increase to 100 mg faster titration has a higher incidence of serious rash |
|
If the patient stops lamotrigine for __ days or more have to start at ___ mg again!
|
5 days
25 mg |
|
What are some side effects of lamotrigine?
|
nausea/vomiting
sedation, dizziness, ataxia and confusion Steven Johnson's Sndrome blood dyscrasias is rare |
|
What drugs increase lamotrigine levels?
|
VPA (doubles concentration, so use slower dose titration)
sertraline |
|
What are some indications for antipsychotics?
|
chizophrenia
chizoaffective disorder bipolar disorder for mood stabilization or when psychotic features are present: delirium psychotic depression dementia trichotillomania augmenting agent in treatment resistant anxiety disorders |
|
What four pathways are key pathways affected by dopamine in the brain?
|
mesocortical
mesolimbic nigrostriatal tuberoinfundibular |
|
Where does the mesocortical pathway project? What is it thought to contain? How is this thought to relate to psychotic patients?
|
projects from the ventral tegmentum (brain stem) to the cerebral cortex. This pathway is felt to be where the negative symptoms and cognitive disorders (lack of executive function) arise. too little dopamine
|
|
Where does the mesolimbic pathway project? What is it thought to contain? How is this thought to relate to psychotic patients?
|
projects from the dopaminergic cell bodies in the vental tegmentum to the limbic system. This pathway is where the positive symptoms come from (hallucinations, delusions, and thought disorders). too much dopamine
|
|
Where does the nigrostriatal pathway project? What is it thought to contain? How is this thought to relate to psychotic patients?
|
projects from the dopaminergic bodies in the substantia to the basal ganglia. This pathway is involved in movement regulation.
|
|
What can dopamine hypoactivity cause? Why?
|
Parkinsonian movements, akathesia and dystonia because dopamine suppresses acetylcholine activity
|
|
Where does the tuberoinfundibular pathway project? What is it thought to contain? How is this thought to relate to psychotic patients?
|
projects from the hypothalamus to the anterior pituitary.
|
|
What is the mechanism of action of typical antipsychotics?
|
are D2 dopamine receptor antagonist
|
|
Why do high potency typical antipsychotics have a higher risk of extrapyramidal side effects?
|
igh potency typical antipsychotics bind to the D2 receptor with high affinity
as a result they have a higher risk |
|
What are some examples of high potency typical antipsychotics?
|
fluphenazine
haloperidol pimozide |
|
What side effects are low potency typical side effects known for? Why do these occur?
|
cardiotoxic and anticholinergic adverse effects including sedation, hypotension
because have less affinity for D2 receptors |
|
What are some examples of low potency typical anitpsychotics?
|
chlorpromazine
thioridazine |
|
What is the mechanism of action of atypical antipsychotics?
|
serotonin-dopamine 2 antagonists
|
|
What forms of risperidone are available?
|
regular tabs, IM depot form and rapidly dissolving tablets
|
|
Risperidone functions more like a typical antipsychotic at doses greater than __ mg.
|
6
|
|
What are some unfortunate SE of risperidone?
|
increased extrapyramidal SE (dose dependent)
most likely atypical to induce hyperprolactinemia weight gain and sedation (dose dependent) |
|
What are the indications for anxiolytics?
|
panic disorder
generalized anxiety disorder substance-related disorders and their withdrawal insomnia and parasomnias |
|
What are the pros and cons of buspirone?
|
pros: good augmentation strategy, no sedation
cons: takes around 2 weeks before patients take notice; will not reduce anxiety in patients that are used to taking BZDs because there is no sedation effect to 'take the edge off' |
|
What are benzodiazapines used to treat?
|
insomnia
parasomnias anxiety disorders CNS depressant withdrawal (ex. EtOH withdrawal) |
|
What are some of the SE of benzodiazapines?
|
somnolence
cognitive deficits amnesia disinhibition tolerance dependance |