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N550 Pharm > Psych Meds > Flashcards

Psych Meds Flashcards

0
Q

Where is alpha-1 found and what are the effects?

A

Postsynaptic
Found in vasculature, heart, glands, gut
Activation causes vasoconstriction and relaxation of the GI tract

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1
Q

What is the order of potency between norepi, epi, and isoproterenol for alpha and beta receptors?

A

Alpha: Norepi>epi>isoproterenol
Beta: Isoproterenol>epi>norepi
Note: a1/b1/dop1 are found post-synaptically, a2/b2/dop2 are found pre- and post-synaptically

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2
Q

Where is alpha-2 found and what are the effects?

A

Presynaptic found in peripheral vascular smooth muscle, coronaries, brain, CNS. Activation presynaptically causes inhibition of norepi release and inhibition of sympathetic outflow leading to decreased BP and decreased HR, inhibition of CNS activity
Postsynaptic found in coronaries, CNS. Activation causes constriction and sedation and analgesia

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3
Q

Where is beta-1 found and what are the effects?

A

(post synaptic??) Myocardium, SA node, ventricular conduction system, coronaries, kidney. Activation causes increase in inotropy, chronotropy, myocardial conduction velocity, coronary relaxation, and renin release

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4
Q

What are the beta-2 effects and where are they found?

A

(pre and post synaptic??) Found in vascular, bronchial, skin, and uterine smooth muscle, coronaries, kidneys, GI tract. Activation causes vasodilation, bronchodilation, uterine relaxation, gluconeogenesis, insulin release, potassium uptake by the cells

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5
Q

What catecholamines do dopamine receptors interact with?

A

Dopamine ONLY (no other catecholamines)

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6
Q

Where does dopaminergic-1 work and what are the effects?

A

Postsynaptic, found on renal mesenteric, splenic, and coronary vessels and renal tubules, causes vasodilation (increases urine output)

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7
Q

Where does dopaminergic-2 work and what effects?

A

Presynaptic causes inhibition of norepi release

Postsynaptic may promote constriction

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8
Q

What is serotonin and where is it concentrated?

A

Serotonin is 5-HT (hydroxytryptamine), a neurotransmitter and local hormone
Highest concentration in wall of intestine, blood, and CNS

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9
Q

SSRI uses?

A

Mild- moderate depression, panic disorder, OCD, PTSD, social phobia, bipolar

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10
Q

SSRI mechanism of action?

A

Block reuptake of serotonin
New SSRI’s act on serotonin, norepinephrine, and/or dopamine
Some produce alpha-2 receptor blockade

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11
Q

Which SSRI’s work only on serotonin?

A

Fluoxetine (prozac), sertraline (zoloft), paroxatine (paxil), fluvoxamine (luvox), escitalopram (lexapro)
Note: Prozac has the longest half-life

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12
Q

Which Atypical SSRIs work on serotonin and norepi?

A

Bupropion (wellbutrin), trazadone (desyrel), nefazodone (serzone), venlafaxine (effexor), duloxetine (cymbalta)

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13
Q

SSRI side effects?

A

Insomnia, fatigue, agitation, orthostatic hypotension, headache, N/V, sexual dysfunction, increased appetite
Note: SSRIs have a higher index of safety than other antidepressants (minimal BP effects, cardiac conduction, changes in seizure threshold)

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14
Q

Anesthetic Considerations: What do SSRIs do to CP-450 and platelet activity?

A

INHIBITS CP-450 enzymes which may increase plasma concentration of certain drugs
Antiplatelet activity, increased risk of bleeding

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15
Q

What is serotonin syndrome?

A

It can be medication induced for patients taking SSRIs

s/s: confusion, fever, shivering, ataxia, diaphoresis, hyperreflexia, muscle rigidity

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16
Q

What are uses and mechanism of action of TCAs (tricyclic antidepressants)?

A

Uses: depression and chronic pain in lower doses (TCAs have a similar chemical structure to LAs, inhibit overactive inflammatory response)
MOA: blocks reuptake of serotonin and/or NE at presynaptic terminals

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17
Q

What is the MOA of tertiary amines vs secondary amines and name specific drugs?

A

Tertiary amines- inhibit serotonin and NE reuptake. Amytriptyline (elavil), imipramine (tofranil), and clomipramine (anafranil)
Secondary amines- inhibit NE reuptake. Desipramine (norpramin), nortriptyline (pamelor)

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18
Q

TCA pharmacokinetics? (lipid/water soluble, protein bound or not, E1/2t, metabolize)

A

Highly lipid soluble, strongly protein bound
LONG e1/2t (10-80 hours).. especially elderly population
Metabolized in liver and has ACTIVE metabolites

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19
Q

TCA side effects?

A

Anticholinergic- dry mouth, tachycardia, urinary retention, ileus
CV- orthostatic hypotension, tachycardia, depressed conduction
CNS- lower seizure threshold, weakness, fatigue
With overdose, cardiotoxicity, seizure, CNS depressant effects can be fatal

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20
Q

What can happen if someone is taking TCAs and MAOI’s?

A

CNS toxicity: hyperthermia, seizure, coma

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21
Q

What are drug interactions/considerations for people taking TCAs? (list the class of drugs)

A

Sympathomimetics, inhaled anesthetics, anticholinergics, antihypertensives, opioids

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22
Q

What is the anesthetic consideration with a patient taking TCAs and giving sympathomimetics?

A

Unpredictable because it is indirect acting, there will be exaggerated responses due to longer amounts of NE available to receptors
Use low dosages of sympathomimetics (ephedrine) OR use a potent direct acting drug (phenlyephrine will directly effect the receptor to increase BP)
Note: Someone just started TCA will react stronger than someone who has been on TCAs for a long time

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23
Q

What is the anesthetic consideration for patients on TCAs using… volatile anesthetics agents? Opioids? Barbiturates?

A

Higher mac of volatile anesthetic agents
Decrease dose of opioids
Decrease dose of barbiturates

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24
Q

What is the anesthetic consideration for patients on TCAs using anticholinergics?

A

More likely to have post op delirium and confusion (central anticholinergic syndrome)
s/s of anticholinergic toxicity or central anticholinergic syndrome- flushing, dry mouth and skin, mydriasis
Note: Use glycopyrrolate instead of atropine because atropine crosses BBB

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25
Q

What are s/s of TCA overdose? What will they die from?

A

s/s- agitation, excitement/delirium, progresses to coma, respiratory depression, and cardiac dysrhythmias and sudden death, hypotensive, anticholinergic effects
With TCA will die from myocardial depression or ventricular dysrhythmias

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26
Q

What inactivates MAO enzyme system?

A

Dopamine, epinephrine, norepinephrine, and serotonin inactivate MAOs
Note: MAOs found in the outer mitochondrial membranes

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27
Q

MAOI (monoamine oxidase inhibitors) mechanism of action?

A

Blocks the enzyme that metabolizes biogenic amines, forms a stable irreversible complex with MAO enzyme (breaks down amine) which increases amount of neurotransmitter available in the brain/CNS and peripheral nervous system

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28
Q

Why aren’t MAOIs used often?

A

Side effects
Lethal in overdose
Difficult dosing
Tyramine free diet

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29
Q

List MAOIs

A

Phenelzine (nardil)
Tranylcypromine (parnate)
Isocarboxaxid (marplan)
Selegiline (eldepryl) - also used for parkinson’s

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30
Q

What neurotransmitters do MAO A vs. MAO B work on?

A

MAO A: serotonin, norepinephrine, epinephrine (dopamine, tyramine too)
MAO B: phenylethylamine (also dopamine)

31
Q

MAOI side effects?

A 
Orthostatic hypotension (especially elderly)
Anticholinergic
Impotence/anorgasmy
Weight gain
Sedation or stimulant effects
32
Q

What dietary restrictions are there for MAOIs? Why?

A

Tyramine! Cheese, fava beans, wine, avocado, liver, cured meats
Dietary tyramine can cause a massive release of endogenous catecholamines leading to hypertensive crisis, hyperpyrexia, CVA (symptoms of headache, vomiting, or chest pain must be reported)
Note: MAO enzyme is present in the liver, GI tract, kidneys, lungs (MAO A in GI and liver)

33
Q

List of drug cautions with MAOIs

A

TCAs, opioid (NO meperidine!), cold/allergy drugs, sympathomimetics (NO ephedrine!), nasal decongestants, SSRIs
May need higher mac with volatile agents

34
Q

What is the MAOI interaction with demerol (meperidine)- an opioid?

A 
Excitatory response (type I) is agitation, skeletal muscle rigidity, hyperpyrexia
Depressive response (type II) is hypotension, respiratory depression, coma
35
Q

What is the interaction between MAOIs and sympathomimetics?

A

May get exaggerated response from indirect acting drugs (DONT give ephedrine), use direct acting agents if indicated, decrease dose by 1/3 and titrate to effect

36
Q

What are the s/s of MAOI overdose?

A

Excessive sympathetic discharge: tachycardia, hyperthermia, mydriasis, seizure to coma

37
Q

Why should Antidepressants be tapered when discontinued?

A

Discontinuation syndromes: dizziness, myalgia, paresthesia, irritability, insomnia, visual disturbances, tremors, lethargy, N/V/D

38
Q

Benzodiazepine mechanism of action?

A 
Facilitates GABA (the major inhibitory neurotransmitter of the CNS)
Binds to GABA receptors in the brain and potentiates GABA mediated neuronal inhibition by increasing chloride permeability, cellular hyperpolarization, and inhibition of neuronal firing
39
Q

Benzodiazepine 5 pharmacological effects?

A 
Sedation
Anxiolysis
Anticonvulsant actions
Anterograde amnesia
Muscle relaxation (at spinal level, NOT neuromuscular junction)
40
Q

Benzodiazepine pharmacokinetics? (protein bound, lipid/water soluble, metabolism, elimination?)

A

Highly protein bound
High lipid solubility
Hepatic metabolism by CP-450 system
Eliminated by the kidneys

41
Q

How do benzodiazepines effect the CNS?

A

Decrease CBF and CMRO2
Preserves cerebrovascular response to CO2
Does NOT attenuate ICP response to laryngoscopy
Anticonvulsant, amnestic
Paradoxical excitement is rare

42
Q

What is the respiratory effect of benzodiazepines?

A

Dose dependent decrease in ventilation
Hypoxemia and hypoventilation enhanced in presence of opioid!!
Depress reflex deglutition (decreased esophageal motility)
CO2 response curve flattens (does not shift)

43
Q

Benzodiazepine effect on CV?

A

Decreases SVR at induction dosage (rarely used for induction)
BP consequently decreases
CO unchanged

44
Q

How does Midazolam (versed) compare to diazepam (which is more potent, which has a longer duration of time)?

A

Versed is 2-3 x more potent than diazepam
Both are highly protein bound
Versed has a rapid redistribution and short duration of action, prepared in water soluble mix
Diazepam (valium) is highly lipid soluble with prolonged duration of action, prepared in propylene glycol/ benzyl alcohol, low pH (Painful IV/IM injection!!), rapidly absorbed form GI

45
Q

What are the usages and dosages of versed?

Pediatrics vs. adults vs. induction dosages

A

Premedication/pediatrics: 0.5 mg/kg po
IV sedation/adults: 1-2.5 mg IV up to 5 mg as needed
Induction: 0.1-0.2 mg/kg over 30-60 sec

46
Q

What is diazepam’s E1/2t compared to desmethyldiazepam?

A

Diazepam: 21-37 hours
Desmethyldiazepam: 48-96 hours
**Desmethyldiazepam is diazepam’s active metabolite. So this is unique to have the active metabolite last so much longer than the drug

47
Q

What are uses and dosages of diazepam?

A

Premedication/oral: 10-15 mg
Premedication/IV: 0.2 mg/kg (reduces mac)
Induction: 0.5-1 mg/kg IV
Anticonvulsant: 0.1 mg/kg IV

48
Q

What are the classes of antipsychotic/ neuroleptic drugs?

A

Phenothiazines, thioxantheses, butyrophenones

49
Q

List phenothiazines and thioxanthenes

A 
Chlorpromazine (thorazine)
Thioridazine (mellaril)
Pherphenazine (trilafon)
Trifluoperazine (stelazine)
Thiothixene (navane)
50
Q

Phenothiazine and thioxanthene mechanism of action?

A

Blockade of dopamine receptors in the basal ganglia and limbic portions of the brain
Interfering with dopamine will cause extrapyramidal side effects
Blocking dopamine receptors in chemoreceptor trigger zone of the medulla will cause antiemetic effects

51
Q

What is absorption and E1/2t of phenothiazines and thioxanthenes?

A

Although highly lipid soluble and protein bound, erratic patterns of absorption from po administration
E1/2t 10-20 hours

52
Q

Side effects of phenothiazines and thioxanthenes?

A

Extrapyramidal effects: tardive dyskinesia (permanent, in the first year in 20% of patients)
Acute dystonic reactions (in the first few weeks of therapy), rigidity, respiratory distress (treat with diphenhydramine 25-50mg IV)
CV: decreases BP (depresses vasomotor alphas, relaxes smooth muscle), prolong QT
CNS: sedation (tolerance develops with chronic therapy) due to tolerance of alpha1/muscarinic/histamine receptors, seizure threshold is decreased, skeletal muscle relaxation of CNS
Antiemetic (effective against opioid N/V)
Neuroleptic malignant syndrome
Note: overdose is rarely fatal

53
Q

What is neuroleptic malignant syndrome?

A

Side effect of phenothiazine and thioxanthenes
Develops over 24-72 hours usually in young men
Hyperthermia, hypertonicity of skeletal muscles, instability of autonomic NS, fluctuating LOC

54
Q

What anesthetic considerations are there for phenothiazines and thioxanthenes?

A

Potentiation of opioids: sedative effects, ventilatory depression, analgesic properties

55
Q

List 2 butyrophenones

A

Droperidol (inapsine): used for neurolept analgesia with fentanyl, also used as antiemetic
Haloperidol (haldol): similar to structure and side effects of phenothiazines

56
Q

Is Droperidol’s clearance perfusion dependent?

A

Clearance is perfusion dependent, hepatic metabolism opposed to hepatic enzyme activity, so accumulation will occur with decreased hepatic flow

57
Q

Droperidol side effects?

Note: Haldol’s side effects are similar to phenothyazine side effects

A

CNS: extrapyramidal, cerebral vasoconstriction (decreased flow but not consumption), dysphoria
CV: decrease BP from alpha blockade (minimal), protects against epi-inducced dysrhythmias (large doses will decrease conduction for tachy-dysrhythmias/ WPW syndrome), prolonged QT, Torsades de pointes (Block Box Warning!)

58
Q

Due to the black box warning on Droperidol, what is required?

A

12-lead EKG prior to administration, monitor 2-3 hours after administration
This is why it isn’t used as a common antiemetic used for surgery anymore

59
Q

What is lithium used for? How does it work?

A

Mood stabilizer, treatment of bipolar (gold standard),
Competes with Na, Ca, and Mg affecting cell membranes, H2O, and neurotransmitters (but not well enough understood to know exactly how it works)

60
Q

What are lithium’s pharmacokinetics?

A patient with low levels of ______ will absorb MORE lithium

A

Filtered by glomerulus and reabsorbed by proximal tubules
Proximal reabsorption of lithium and Na is competitive, so a pt with low sodium will absorb more lithium
E1/2t is 24 hours
Steady state is 4-5 E1/2t (blood draw is important to monitor)

61
Q

Lithium side effects?

A

Kidneys- evaluate renal function every 6 months for polyuria/polydipsia
EKG- T wave changes, flattening or inversion
(for OR pt we need baseline EKG and electrolytes)
Other- hypothyroidism, psoriasis, acne, tremor, sedation, memory disturbances/cognitive slowing

62
Q

What are s/s of lithium toxicity?

A

Mild- sedation, nausea, weakness, wide QRS, AV block, hypotension, dysrhythmia, seizure
Significant toxicity- emergency! hemodialysis, osmotic diuresis and IV bicarb

63
Q

Lithium anesthetic considerations

A

Prolonged neuromuscular blocking agents, anesthetic requirements may be decreased
Get EKG and labs (electrolytes)

64
Q

Antiepileptic mechanism of action?

A

Decrease neuronal excitability or enhance inhibition of neurotransmission by altering intrinsic membrane ion currents (sodium, potassium, and calcium) or enhancing GABA

65
Q

Antiepileptic pharmacokinetics

A

Slow absorption from GI tract, protein binding varies
Most are metabolized by liver and excreted by kidneys
E1/t from hours to days
Monitor plasma concentration to determine compliance with drug and pharmacokinetic interactions

66
Q

Dangerous side effects of antiepileptics?

A

Life threatening bone marrow suppression and hepatoxicity

This is why labs (liver function tests and hematologic studies) are done to monitor.

67
Q

List antiepileptics

A

Phenobarbital, phenytoid (dilantin), fosphenytoin (cerebyx), primidone (mysoline), carbamazepine (tegretol), valproate (depakote), levetiracetam (keppra)

68
Q

Phenytoin uses and mechanism of action?

A

Effective for partial and generalized seizures
MOA: regulates neuronal excitability and spread of seizure activity from a seizure focus by regulating Na and Ca transport across neuronal membranes

69
Q

Phenytoin pharmacokinetics

A

pH of 12, precipitates in solutions with pH 10 mcg/ml for zero order

70
Q

Phenytoin side effects?

A

CNS toxicity- nystagmus, ataxia, diplopia, vertigo, peripheral neuropathy
Acne, facial coarsening
Allergic rash ( SJS)
GI irritation
Hepatotoxicity, induces hepatic enzyme system

71
Q

Fosphenytoin: how does it work? Pharmakodynamics?

A

Acts on Na ion channel blockade
Highly protein bound, water soluble phenytoin pro drug
Used in hospitals for status epilepticus and in neurosurgery to prevent seizures

72
Q

What is the dose of fosphenytoin when used for status epilepticus or in surgery to prevent seizures?

A

10-20 mg/kg IV loading dose

73
Q

What is the mechanism of action of phenobarbital? Pharmacokinetics?

A 
Modulates post synaptic actions of GABA and glutamate
Enhances CP450 (dilantin and phenobarbital both do this, meaning you need to give more doses)
74
Q

Phenobarbital side effects?

A

Long acting, cognitive and behavior side effects limit its usefulness
Sedation in adults, hyperactivity in children
Depression
Confusion in elderly

N550 Pharm (14 decks)

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