Psych (Antidepressants/Antiepileptic/Etc) SG Flashcards
Get inside yo head!
MOA of SSRIs
Block nerve terminal uptake of serotonin
Produce therapeutic action through an ability to increase 5-HT concentration
Clinical uses of SSRIs
effective in treating major depressive disorder
Metabolism of SSRIs
Oxidized by liver microsomal enzymes
(can inhibit hepatic microsomal oxidases)
Medication interactions with SSRIs
Caution in combination with other antidepressants, benzodiazepines, neuroleptics, carbamepazine, as blood levels can increase
Side effects of SSRIs
GI effects – nausea and diarrhea
CNS stimulation – insomnia and anxiety
Sexual dysfunction – aorgasmia and delayed ejaculation
Weight loss
Anesthesia effects of SSRIs
The anticholinergic and cardiovascular side effects (seen in the TCAs) were not present in the SSRI group
Examples of SSRIs
Escitalopram (lexapro)
Fluoxetine (Prozac)
Paroxetine (Paxil)
Sertraline (Zoloft)
citalopram
fluvoxamine
MOA of Tricyclic Antidepressants (TCAs)
Inhibition of norepinephrine neuronal reuptake
Mild effect on 5-HT serotonin concentration
All are weak alpha adrenergic antagonists
Potentiate effects of directly acting sympathomimetics
TCAs and heterocyclics block effects of indirectly acting sympathomimetics
Clinical uses of TCAs
Effective in treating major depressive disorder
(Benefit p 2-3 wks; Ineffective in treating schizophrenia)
Metabolism of TCAs
Oxidized by microsomal liver enzymes
Anesthetic/Medication interactions of TCAs
Anesthetics: poss. ↑ incidence of cardiac dysrhythmias on induction
Sympathomimetics: exaggerated response to these meds, use small titrations
Anticholinergics: ↑ risk of central antichol syndrome, less likely with Glycopyrrolate
AntiHTNs: rebound HTN p D/C clonidine
Opioids: ↑ analgesia and ventilatory depressant effects
Side effects of TCAs
Antimuscarinic effects
Tachycardia, blurred vision, constipation, dry mouth
Sedation
Toxic delirium
Seizures
Weight gain
Involuntary movements
Neuroleptic malignant syndrome
Anesthetic-specific effects with TCAs
Most antidepressants will lower the seizure threshold
CNS toxicity presents as a delirium with affective, cognitive, motor, and psychotic symptoms
Overdose is frequently fatal with unresolvable arrhythmias
Examples of TCAs
Amitriptyline (Elavil)
clomipramine
desipramine
imipramine
nortriptyline
MOA of MAOis
Monoamine Oxidase exists on the body as type A and type B
Transmitter amines, such as norepinephrine, are preferentially metabolized by MAO-A in brain tissue
MAO-B is involved in the catabolism of dopamine
Drugs inhibit both A and B, but A is where the therapeutic effect occurs
Clinical uses of MAOis
Reserved for atypical depression
Depression unresponsive to TCAs or SSRIs
Depression resistant to ECT
Metabolism of MAOis
oxidation and acetylation by MAO
Medication interactions with MAOis
Cyclic antidepressants
Fluoxetine
Cold or allergy medications
Nasal decongestants
Sympathomimetic drugs
Opioids (esp. meperidine)
Side effects with MAOis
- Hepatotoxicity (explored on next card)
- Cardiovascular effects (explored on next card)
- Tremors
- Ejaculatory delay
- Orthostatic hypotension
- Hyperpyrexia with meperidine, dextromethorphan, TCAs
Hepatotoxicity and CV effects with MAOis
- Hepatotoxicity
- Occasionally seen with long term therapy
- Particularly for those identified as slow acetylators
- Nonhydrazine derivatives (those used clinically now) have a lower hepatotoxicity risk
- Cardiovascular effects
- Can occur with ingestion of certain foods
- Low tyrosine diet needed
- Cheese, beer, wine (no wonder they’re depressed!)
Anesthesia effects with MAOis
minimize SNS stimulation and drug-induced hypotension
regional is good, but avoid epi
minimize opioids
Exemplars of MAOis
Phenelzine (Nardil)
Tranylcypromine (Parnate)
Which SSRI is most associated with cardiac dysrhythmias?
Trazadone (S&H, p. 407)
Treatment of TCA overdose
Management of CNS and cardiovascular toxicity (seizures: diazepam, NaHCO3, phenytoin; Vent. Dysrhythmias: NaHCO3, lidocaine, phenytoin; Heart block: isoproterenol; Hypotension: Crystalloid/colloid, NaHCO3, sympathomimetics, inotropics)
Gastric lavage may be useful p cuffed tube in place (Stoelting & Hillier, p. 414)
WHAT TYPES OF FOODS OR THE COMPOUND IN THE FOODS ARE NOT TOLERATED BY PATIENTS TAKING MAO INHIBITORS AND WHY?
Cheese, beer, Chianti wine, avocados, fava beans, liver (Dr. Lector would not have done well on an MAOi); Dietary tyramine intake may interact with MAOIs resulting in systemic hypertension (Stoelting & Hillier, p. 414)
MOA for Lithium
Lithium alters Na+ transport in nerve and muscle cells and results in a shift towards intraneuronal metabolism of catecholamines.
The exact MOA in the treatment of mania in unknown.
Side effects with Lithium
Polydipsia & polyuria
Benign T-wave flattening
Hypothyroidism
Dermatological toxicities
Sedation
Possible prolongation of NMBAs’ effects
Let’s discuss on the next few cards the toxicities seen with Lithium.
Toxicities closely correlate with plasma levels.
Mild: 1.0-1.5 mEq/L
(Therapeutic index 1.0-1.2 mEq/L)
Moderate: 1.6-2.5 mEq/L
Severe: >2.5 mEq/L
So what is normally seen with mild lithium toxicity (1.0-1.5)?
Lethargy
irritability
skeletal muscle weakness
tremor
slurred speech
nausea
Ok then, what are you going to see with moderate lithium toxicity (1.6-2.5) mEq/L)?
Confusion
Drowsiness
Restlessness
Unsteady gait
Coarse tremor
Skeletal muscle fasciculations
Vomiting
Well then smarty-britches, what are you going to see with severe (I always want to say EXTREME!!) lithium toxicity (>2.5 mEq/L)?
Impaired consciousness (coma)
delirium
ataxia
EPS
seizures
impaired renal function
What are the side effects of antipsychotic (neuroleptic) drugs?
(This is a booger of a card, so just read it for information)
Tardive dyskinesia
laryngeal dyskinesia (laryngospasm → sudden respiratory distress)
opisthonosis and oculogyric crises may occur (we’ll discuss this momentarily)
acute dystonia (responds to diphenhydramine)
hypotension (a-adrenergic blockade, direct vasodilation, and direct cardiac depression)
neuroleptic malignant syndrome (NMS)
↑ prolactin levels (Gynecomastia, galactorrhea)
sedation
antiemetic effects
obstructive jaundice (an allergic reaction 2-4 wks p administration)
hypothermia (with chlorpromazine)
↓ seizure threshold
skeletal muscle relaxation
So, what is this opisthonosis junk? (For KNOWLEDGE!!!)
Opisthotonos [ō′pisthot′ənəs]: a prolonged severe spasm of the muscles causing the back to arch acutely, the head to bend back on the neck, the heels to bend back on the legs, and the arms and hands to flex rigidly at the joints. It is related to meningitis.
Alright, then what is that oculogyric crisis business? (For MORE KNOWLEDGE!!!)
Oculogyric crisis [ok′yəlōjī′rik]: a paroxysm in which the eyes are held in a fixed position, usually up and sideways, for minutes or several hours, often occurring in postencephalitic patients with signs of parkinsonism. In some cases, the eyes are held down or sideways, and there may be spasm or closing of the lids. Oculogyric crises may be precipitated by emotional stress and neuroleptic overdose, and patients with the disorder frequently show psychiatric symptoms.
What is this Neuroleptic Malignant Syndrome all the hip kids are talking about nowadays?
Hyperthermia
hypertonicity of skeletal muscles
ANS instability (alterations in systemic BP, tachycardia, cardiac dysrhythmias)
fluctuating levels of consciousness
Likely R/T dehydration and intercurrent illness in pts treated with antipsychotic drugs.
Hmm… So what is the treatment for NMS?
Treatment is empirical and supportive: Dantrolene (direct-acting muscle relaxant) and bromocriptine or amantadine (dopamine agonists)
Malignant hyperthermia and central anticholinergic syndrome may mimic NMS (NDNMBDs produce flaccid paralysis in NMS pts but NOT in MH pts!)
(S&H p. 424-425)
WHAT IS THE MECHANISM OF ACTION OF DROPERIDOL AND HALOPERIDOL?
MOA thought to be due to the blockade of DA receptors (DA2) in the basal ganglia and limbic portions of the forebrain (blockade of DA receptors in the chemoreceptor trigger zone of the medulla is responsible for the antiemetic effects)
To which class of drugs does DROPERIDOL belong?
Why, butyrophenones (antipsychotics/neuroleptics), of course!
WHAT ARE CLINICAL USES OF DROPERIDOL?
FDA labeled: acute or prophylactic treatment of N/V with surg/diag procedures
Non-FDA labeled: Agitation-psychotic disorder, chemo-induced N/V, benign HA, migraine
WHAT DISEASE IS DROPERIDOL CONTRAINDICATED? WHY? (These all-caps questions were just copied and pasted here. Ask Shores about his syntax and desire to yell at the students…)
Heart block?
Prolongation of QT interval (this is the best answer I could find within the book)
Also: “Of note, since droperidol was approved in 1970, not a single case report has surfaced in which droperidol in doses used for the management of port-operative N/V has been associated with QTc prolongation, cardiac dysrhythmias, or cardiac arrest.” (S&H)
I like this quote because I love this drug. And now you know.
Define epilepsy, please. Thank you.
Recurring disturbance in the normal pattern of neuronal activity.
Must occur more than once to be considered epilepsy, as opposed to a single episodic seizure (e.g., febrile)
FYI: not a mental illness, not a sign of low intelligence, and not contagious.
WHAT ARE THE DRUG INTERACTIONS OF COMMON ANTIEPILEPTIC DRUGS?
Opioids
(ventilatory depressant, miotic, sedative, and analgesic effects likely exaggerated)
How does levodopa work?
Crosses BBB and converted to DA by aromatic-L-amino-acid decarboxylase; this acts to replenish DA stores in the basal ganglia
What are these Peripheral Decarboxylase Inhibitors?
Carbadopa or benserazide
Administered with levodopa to increase the CNS action of levodopa; think of it as a “fall guy” that takes the metabolic hit while allowing levodopa to escape across the BBB to act on the CNS.
MOA of Selegiline?
MAO-B inhibitor; ↓ catabolism of endogenous DA
