Psychopharm Cases Flashcards
How far into the diagnosis process can you start treating psychosis?
Can start treating psychosis even before you have a diagnosis
- want to restores functioning
- relieve functioning
- make sure person has capacity to participate in future medical decisions
Drugs that can induce psychosis
- cocaine
- MJ
- PCP (NMDA blocker)
- K2
- amphetamines (due to surge of DA, NE)
Mechanism of cocaine activity
Cocaine = NE/DA/5HT2 reuptake inhibitor
=sympathomimetic
Mechanism of PCP activity
NMDA (glutamate) receptor blocker
Mechanism by which stimulants treat ADHD
D2 increase in the mesocortical tract
For agitation: use Haldol or Chlorpromazine
Asking high vs. low potency typical antipsychotic
-use Haldol (good for agitation)
Describe the mechanism by which congentin treats EPS
EPS can be seen as an imbalance btwn dopaminergic and cholinergic neurons
-decreasing cholinergic increases the dopaminergic => congentin increases the DA tone in the nigrostriatal pathway
Why is it so critical to monitor pts on antipsychotics for akithesia?
B/c big risk factor for suicide
Treatmetn for akithesia
- Beta-blocker (but watch out for bronchoconstriction)
- sometimes anticholinergisc or benzos
Mechanism of tardive dyskinesia
Due to upregulation of the DA receptors over time
What is the risk of depot antipsychotics?
If NMS is induced, you can’t stop the offending agent! So require long term very careful monitoring
Typical monitoring schedule for pt on clozapine
- every week for first 6 months
- every 2 weeks for next 6 mo
- then every month after that
Bromocriptine
(a) mechanism
(b) indications
Bromocriptine
(a) Dopamine agonist
(b) used in Parkinsons, also in hyperprolactinemia b/c DA and prolactin have reverse feedback mechanisms
Which antipsychotic causes the most hyperprolactinemia
Risperidone (even more than Haldol)
-not known why
How to keep someone on Risperidone despite hyperprolactinemia?
Add a bit of aripiprazole (has some partial D2 agonism) => aripiprazole will kick the Risperidol in the tuberoinfundibular tract off the receptor to decrease prolactin release => decrease sexual dysfuntion
Physostigmine
Physostigmine = cholinesterase inhibitor
-give for anti-cholinergic (ex: benadryl, TCA) overdose
Atropine
Anti-cholinergic
2 ways to judge a suicide attempt
(1) lethality of mechanism
ex: gun vs. cutting w/ plastic knife
(2) Intent to die
ex: at home alone or in public
Describe the cardiotoxicity of TCAs
Cardiotoxicity is due to the anticholinergic effect: increases AV node conduction => increases arrhythmia risk
-prolongs QTC => increased risk of Torsades (type of VT that => sudden cardiac death)
Biggest risk factors for SA
-previous attempts
Contraindication for antidepressants
Bipolar disorder!!!
Need to monitor carefully for subthreshold hypomanic symptoms
Describe the effects of 5HT on
(a) 5HT1A
(b) 5HT2A
(c) 5HT2C
5HT receptors
(a) More serotonin at 5HT1A is what creates the antidepressant/anxiolytic effects
(b) 5HT2 and 5HT2C => anxiety, agitation, akithesia, sexual side effects
How may SSRIs contribute to akithesia?
Extra 5HT causes decreased DA release => akithesia
Why side effects of SSRIs may decrease after the first few weeks
5HT2A receptors downregulate more than 5HT1A receptors
Dose dependent effects of SNRIs
- Venlafaxine doesn’t becoming N until decently high dose
- Desvenlafaxine becomes SN at low doses
What may you add as as adjunct to SNRI/SSRIs for depression
Mertazapine b/c it has a different mechanism => can be added w/ synergistic effect
Effect of SSRIs on hemoregulation
Platelets also have 5HTT => SSRIs cause platelets to be less active => increased risk for GI, surgical etc bleeding
Explain basic approach to antidepressant therapy for basic depression
Start on SSRI
(a) if partial response- increase dose
(b) if at max dose- stick w/ it (max effect at 1-2 mo) and add
- psychotherapy
- buproprion
- mirtazapine if having trouble sleeping
- thyroid hormone
3 things proven to decrease suicidality
- lithium
- clozapine
- ECT
Miosis vs. mydriasis
Miosis = pinpoint pupils
Mydriasis = huge pupils
Miosis vs. mydriasis
(a) trazodone
(b) opioid overdose
(c) stimulants
(d) SSRI/SNRI
(e) Mirtazapine
(f) opiate withdrawal
(g) antipsychotics
(h) anticholinergics
(i) cocaine intoxication
Miosis (pinpoint pupils) vs. mydriasis (dilated pupils)
(a) trazodone => miosis
(b) opioid overdose => pinpoint pupils
(c) stimulants => mydriasis
(d) SSRI/SNRI => mydriasis
(e) Mirtazapine => miosis
(f) opiate withdrawal => mydriasis
(g) antipsychotics => miosis
(h) anticholinergics => mydriasis
(i) cocaine (sympathomimetic => mydriasis
Mechanism by which opiate OD => pupil change
Opiate OD => miosis (pinpoint pupils)
due to loss of sympathetic activity to the ciliary ganglion => parasympathetics work uninhibited
3 main clinical signs of serotonin syndrome
clonus, tremor, diarrhea
Pharmacologic treatment for
(a) serotonin syndrome
(b) NMS
pharmacologic tx for
(a) serotonin syndrome = benzos
(b) NMS
- benzos
- bromocriptine (DA agonist)
- dantriline (CCB) for rigidity
Clinical signs of alcohol withdrawal
-hypertension, tachycardia, tremor
Differentiate the 3 benzos used in alcohol withdrawal
(1) Lorazepam
- safest if there’s liver dysfxn, but not long acting
(2) Chlordiazeproxide (librium)
(3) Diazepam (valium)
- advantage that they’re longer acting
- but be careful b/c they have active metabolites
Goal of benzo use during alcohol withdrawal
- keep vitals stable
- keep pt resting but arousable
Medication to treat opiate withdrawal
Clonidine (alpha agonist) directly targets the withdrawal
-opiates (sympathomimetic) => alpha receptors downregulate
Signs of MJ overdose
- can cause psychosis
- hyperphagia
- conjunctiva injection
Signs of MJ withdrawal
No such thing…MJ doesn’t cause withdrawal
CV risks of cocaine overdose
Cocaine-induced MI
-increased inotropy increases myocyte oxygen demand
Psychiatric risks of cocaine overdose
-mood and psychotic symptoms
Best way to treat bipolar manic episode
- Can use Depakote alone (good for mania and works quickly)
- Can’t use lithium in isolation for acute mania (takes 1-2 weeks to have effect) => use Li + benzo or atypical
distant 3rd choice = carbamazepine
Drugs for bipolar maintenance
Aka how to avoid mania btwn episodes
- lithium: slower acting tho so if used acutely add another
- depakote: faster acting than lithium, good for manic (but not depressive) bipolar
adjuncts: atypicals, carbamazepine
Drugs for bipolar depressive episode
-NOT depakote- does little for depression
(1) Lithium + lamotrigine
- atypicals
- carbamazepine
What to look for on ECG of pt on lithium
Bradycardia
-T wave flattening (which is benign)
What to look for on CBC of pt on lithium
Benign leukocytosis
-b/c of margination: WBCs acucmulate to the edge of the vessel => get higher white count when take blood from edge of vessel
Clinical signs of lithium toxicity
- tremors
- renal failure
Major classes of drug interactions w/ lithium
- thiazide diuretics
- ACEi
- NSAIDs
What to look for on CBC of pt on valproic acid
- thrombocytopenia
- aplastic anemia (pancytopenia)
What to monitor on BMP for pt on valproic acid
Ammonia level
-valproic acid can cause hyperammonium => delirium
Ideal lithium serum level in
(a) acute mania
(b) bipolar maintenance
Ideal serum lithium level
(a) acute mania: .8-1.2
(b) bipolar maintenance .5-1.0
-and for some ppl even w/in that range might be too high, so close monitoring required
Common side effects of lithium
- GI irritation
- cognitive blurring
- weight gain
- polyuria, polydipsia
When can benzo intoxication be lethal?
When combined w/ EtOH or opiates
What determines the
(a) half life of a benzo
(b) time to onset of a benzo
Benzo
(a) half life (duration of action) depends on active metabolites
(b) time to onset depends on its lipid solubility
Name 4 short acting benzos
Short acting benzos:
- aprazolam (Xanax)
- lorazepam (Ativan)
- oxtazepam (Serax)
- temazepam (restoril)
Name 3 long acting benzos
Long acting benzos:
- clonazepam (klonopin)
- diazepam (valium)
- chlordiazepoxide (librium)
California rocket fuel
Velafaxine (SNRI) + Mirtazapine (NaSSA)
