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Pharmacology test 2 > Psychopharmacological therapy > Flashcards

Psychopharmacological therapy Flashcards

1
Q

Agonist natural catecholamies

A
  • Epinephrine
  • Norepinephrine
  • Dopamine
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2
Q

Agonist Synthetic catecholamies

A
  • Isoproterenol

- Dobutamine

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3
Q

Alpha receptors

A

receptors that respond with the following order of potency NE>E>ISO
-theres alpha 1 and 2

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4
Q

Beta receptors

A

receptors that respond with the following order of potency: ISO>E>NE

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5
Q

Alpha 1

A

Postsynaptic

  • Vasculature, heart, glands, and gut
  • activation causes vasoCONstriction and relaxation of GI tract
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6
Q

Alpha 2

A

PREsynaptic
–peripheral vascular smooth muscle, coronaries, brain
–activation causes inhibition of NE release and inhibition of sympathetic outflow leading of decrease BP/HR, inhibition of CNA activity
POSTsynaptic
–Coronaries, CNS
–Activation causes constriction and sedation and analgesia

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7
Q

Beta 1

A

Found: 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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8
Q

Beta 2

A

Found: Vascular, brochial, and uterine smooth muscle, smooth muscle in the skin, myocardium, coronaries, kidneys, gi tract.
**Activation causes: vasodilation, brochodilation, uterine relaxation, gluconeogenesis, insulin release, potassium uptake by the cells

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9
Q

Dopamine receptor

A

receptor that interacts only with dopamine
D-1
*Postsynaptic. Found on: renal mesenteric, splenic, and coronary vessels. Renal tubules
-Activation causes: vasodilation.
D-2
*Presynaptic.
-Activation causes: inhibition of norepi release.
*Postsynaptic: May promote constriction

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10
Q

Serotonin

A

5-Hydroxytryptamine (5-HT)
-Neurotransmitter and local hormone
Highest concentration in 3 areas: -Wall of intestine -Blood -CNS

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11
Q

Antidepressants

A

Selective Serotonin Reuptake Inhibitors (SSRIs)
Tricyclic
Monoamine Oxidase Inhibitors

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12
Q

SSRI use

A

-mild to moderate depression
-panic disorder
-OCD
-PTSD
-social phobia
“POPS”

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13
Q

SSRI MOA

A
  • block repute of serotonin, NE, and/or dopamine

- some produce alpha 2 receptor blockade

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14
Q

SSRI drugs 5

A 
*serotonin
Fluoxetine (prozac)
Sertraline (zoloft)
Paroxatine (paxil)
Fluvoxamine (Luvox)
Escitalopram (Lexapro)
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15
Q

SSRI atypical 5

A 
*Serotonin and NE
Bupropion (wellbutrin)
Trazadone (desyrel)
Nefazodone (serzone)
Venlafaxine (effexor)
Duloxetine (cymbalta)
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16
Q

SSRI side effects

A

-different side effect profiles, higher index of safety that other classes of antidepres
*minimal effects of BP, Cardiac conduction, and changes in SZ threshold
Side effects:
-Insomnia/fatigue
-Agitation
-Orthostatic hypotension
-Headache
-Nausea/vomiting
-Sexual dysfunction
-Increased appetite

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17
Q

SSRI Anesthetic Consideration (AC)

A
  • INHIBITION of CP450 enzyme
  • -may increase plasma [ ] of certain drugs
  • Antiplatelet activity: increased risk of bleeding
  • Serotonin syndrome-medication induced:
  • –Confusion, fever, shivering, ataxia, diaphoresis, hyperreflexia, muscle rigidity
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18
Q

Tricyclics use

A

depression

  • chronic pain syndrom in lower doses
  • -chemical structure similar to LA and phenothiazines
  • -inhibits overactive inflamm responce system
  • can take 2-3 weeks to have clinical effects
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19
Q

Tricyclics MOA

A

blocks repute of serotonin and/or NE at PREsynaptic terminals

  • *Tertiary amines-inhibit serotonin and NE reuptake
  • *Secondary amines-inhibit NE reuptake
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20
Q

Tertiary amines

A

Tricyclics

  • Amytriptyline (elavil),
  • imipramine (tofranil)
  • clomipramine (anafranil)
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21
Q

Secondary amines

A

Tricyclics

  • Desipramine (norpramin)
  • nortriptyline (pamelor)
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22
Q

Tricyclics Pharmacokinetics

A
  • highly lipid soluble
  • strongly protein bound
  • long elimination 1/2 time–10-80hrs
  • metabolized in liver
  • *have ACTIVE metabolites
  • elderly can take about 1 week to clear
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23
Q

Tricyclics side effects

A

Anticholinergic
–Dry mouth, tachy, urinary retention, ileum, slow gastric emptying
Cardiovascular
–Orthostatic hypotension, mild increased HR, depressed conduction through the atria and ventricles
CNS
–lower sz threshold (easier for sz), weakness, fatigue
These can be fatal with overdose

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24
Q

Tricyclics drug interaction

A
  • Monoamine oxidase inhibitors (MAOI): can cause CNS toxicity with tricyclics–hyperthermia, sz, coma
  • Sympathomimetics
  • Inhaled anesthetics
  • Anticholinergics
  • Antihypertensives
  • Opioids
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25
Q

Tricyclics AC sympathomimetics

A

Sympathomimetics

  • unpredictable
  • indirect acting–exaggerated responses due to larger ant of NE available to stimulate postsynaptic adrenergic receptors
  • Acute vs chronic (receptor becomes desensitized, with chronic) tx with tricyclics
  • -use lower dosages of sympathomimetics
  • Or may need potent direct acting drug
  • *basically do not use indirect acting!! ex ephedrine, USE phenylephrine, start slow on dose
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26
Q

Tricyclics AC

A

volatile anesthetic agents–may need higher mac

  • exogenous epinephrine
  • opioids–decreased dose
  • Barbs–decreased dose
  • Anticholinergics-more likely to have post op delirium and confusion
  • Anticholinergic Toxicity or Central Anticholinergic syndrome: flushing, dry mouth and skin, mydriasis
  • *atropine cross BBB
  • *glycopryate does not cross BBB
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27
Q

Tricyclics overdose

A

life threatening-intractable myocardial depression or ventricular dysrhythmias usual cause of death
-presenting features: agitation, excitement, delirium, sz, progresses to coma, resp depression and dysrhythmias and sudden death, hypotensive, anticholinergic effects

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28
Q

Tricyclic tx for overdose

A

vent support
manage CNS and cardiac toxicity
physostigmine for anticholinergic psychosis
acidosis may increased unbound drug—more dysrhythmias
**should be weaned to prevent withdraw syndrome

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29
Q

MAO enzyme system

A

found in outer mitochondrial membrane
function to inactivate the monoamines: do, serotonin, epi, NE
**this enzyme metabolizes the neurotransmitters

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30
Q

MAOI MOA

A
  • Block the enzyme that metabolizes biogenic amines–increasing availability of these neurotransmitters in the CNS and peripheral autonomic nervous system
  • Forms a stable irreversible complex with MAO enzyme
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31
Q

MAOI risk

A

Not often used- side effects, lethal in overdose, difficult dosing, tyramine free diet

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32
Q

MAOI drugs

A

Phenelzine (nardil)

  • Tranylcypromine (parnate)
  • Isocarboxazid (marplan)
  • Selegiline (eldepryl)
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33
Q

MAO A

A

serotonin
NE
Epi
dop

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34
Q

MAO B

A

Phenylethylamine

dop

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35
Q

MAOI side effect

A

most common is orthostatic hypotension: especially prominent in elderly

  • anticholinergic like effects
  • impotences/anorgasmy
  • weight gain
  • sedation or mild stimulant effects
  • *NO cardiac dysrhythmias and doesn’t change sz threshold
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36
Q

MAOI diet

A

MAO enzyme present in liver GI tact, kidneys, lungs
**MAO A in GI and liver: metabolizes tyramine
So eat tyramine: massive release of endogenous catecholamines–hypertensive crisis, hyperpyrexia, CVA
**Dietary Restrictions:
-cheese -fava beans -wine -avocado -liver -cured meat

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37
Q

MAOI symptoms to report

A

serious HA
Vomiting
Chest pain

38
Q

MAOI drug interactions (which drugs)

A 
DRUG Caution: 
Tricyclic antidepress
-Opioids
-NO Meperidine
-Cold/allergy drugs
-Sympathomimetics
-Nasal decongestants
-SSRIs
Demerol

*HTN, CNA excitation, delirium, sz, death

39
Q

MAOIs interaction with Demerol

A
  • type1 excitatory responce
  • agitation
  • Skeletal muscle rigidity
  • hyperpyrexia
  • type 2 depressive response
  • Hypotension
  • resp depression
  • coma
40
Q

MAOIs interaction with sympathomimetics

A

may get exaggerated response from indirect acting drugs **NO EPHEDRINE

  • *use direct acting agents
  • decrease does by 1/3 and titrate to effect
41
Q

MAOI AC

A

Minimize possibility of sympathetic nervous stimulation or drug induced hypotension.

  • Caution with sympathomimetics
  • Caution with opioids - NO demerol
  • May need higher MAC with volatile agents
42
Q

MAOIs overdose

A 
excessive sympathetic discharge *think increased fight/flight
-tachy
-hyperthermia
-mydriasis
-Sz-coma
Tx: supportive
43
Q

Antidepressant discontinuation

A

All should be tapered

  • Can get dizziness
  • Myalgias
  • Parasthesia
  • Irritability
  • Insomnia
  • Visual disturbances
  • Tremors
  • Lethargy
  • N/V/D
44
Q

Anxiolytics

A
  • Benzodiazepines: for anxiety and insomnia

- Buspirone: non-benzo, used form anxiety but not panic disorder (no effect on GABA)

45
Q

Benzo MOA

A

Facilitates the action of GABA
(increases GABAs potencyX3
Causes greater frequency of channels to open:
-Increases chloride influx
-Hyperpolarization
-Decreased neuronal excitability)
-GABA- Major inhibitory neurotransmitter in the CNS

46
Q

Benzo 5 effects

A
  • Anxiolysis
  • Sedation
  • Anterograde Amnesia
  • Anticonvulsant Actions
  • Muscle Relaxation (Spinal Level)
47
Q

Benzo pharmacokinetics

A
  • highly protein bound
  • high lipid solubility
  • hepatic metabolism by CP450
  • eliminated via kidneys
48
Q

Benzo pharmacodynamics

CNS effects

A

Decreases CBF and CMRO2

  • Does NOT produce isoelectric EEG
  • Preserves cerebrovascular response to CO2
  • Does not attenuate ICP response to laryngoscopy
  • Potent anticonvulsant and amnestic
  • Paradoxical Excitement- RARE
49
Q

Benzo resp effects

A 
Dose dependent decrease in ventilation
-Hypoxemia and hypoventilation
enhanced in presence of opioid
-Depress (swallowing) reflex deglutition
-CO2 Response curve flattens- does not shift
50
Q

Benzo cardiovascular effects

A

Decreases SVR at induction dosage

  • BP consequently decreases
  • C.O. unchanged
51
Q

Benzos

A

Midazolam/Versed

Diazapam/Valium

52
Q

Midazolam

A

Water soluble preparation

  • Imidazole ring
  • 2-3* x potency of Diazepam
  • 90-98% Protein bound
  • Rapid redistribution → short duration
53
Q

Midazolam uses and dosages

A

Premedication/Pediatrics: 0.5 mg/kg po.
-IV sedation/Adults 1- 2.5 mg IV can give
as high as 5mg, as needed.
-Induction: 0.1 – 0.2 mg/kg over 30-60 sec
-Maintenance: Incremental or Infusion
**?? 1/2 life 2-3hrs?

54
Q

Diazepam

A

Highly lipid soluble with prolonged duration of action

  • Commercially prepared in organic solvents including propylene glycol and benzyl alcohol
  • Viscous, pH 6.6 - 6.9
  • PAINFUL IV and IM injection (z-tract)
  • Rapidly absorbed from GI tract
  • Highly protein bound
55
Q

Diazepam T 1/2 elimination

A

21 - 37 hours in healthy volunteers, increases with age

to active metabolite: Desmethyldiazepam: 48 – 96 hours

56
Q

Diazepam uses and doses

A

Premedication/Oral: 10-15 mg

  • Premedication/IV: 0.2 mg/kg (reduces MAC)
  • Induction: 0.5 – 1.0 mg/kg IV
  • Anticonvulsant: 0.1 mg/kg IV
57
Q

Antipsychotics (neuroleptic) drugs

A
  • Phenothiazines
  • Thioxanthenes
  • Butyrophenones
58
Q

Phenothiazines

and Thioxanthenes

A
  • Chlorpromazine (thorazine)
  • Thioridazine (Mellaril)
  • Pherphenazine (trilafon)
  • Trifluoperazine (Stelazine)
  • Thiothizene (naval)
59
Q

Phenothiazines

and Thioxanthenes

A

Blockade of dopamine receptors in the basal ganglia and limbic portions of the forebrain

  • -Interference with dopamine leads to extrapyramidal side effects
  • Blockade of dopamine receptors in chemorecptor trigger zone of medulla: antiemetic effects
60
Q

Phenothiazines

and Thioxanthenes pharmacokinetics

A
  • Erratic patterns of absorption after po administration
  • Highly lipid soluble
  • Highly protein bound
61
Q

Phenothiazines

and Thioxanthenes metabolism

A
  • Oxidation in liver with conjugation
  • Most have inactive metabolites
  • T1/2 10-20 hours
  • Prolonged in the elderly or those with decreased capacity to metabolize drugs
62
Q

Phenothiazines

and Thioxanthenes side effects

A
  • Due to blockade of dopamine receptors in forebrain

- Large margin of safety and overdoses rarely fatal

63
Q

Phenothiazines
and Thioxanthenes side effects:
extrapyramidal

A

**Extrapyramidal effects
-Tardive dyskinesia: Abnormal involuntary movements involving the tongue, facial/neck muscles, extremeties, and occasionally skeletal muscle groups used in breathing/swallowing
-Occurs in 20% of patients receiving therapy for > 1 year
-Elderly and women more susceptible
**Usually permanent—no treatment
ACUTE dystonic reaction
-Usually occur in first few weeks of therapy
-Acute skeletal muscle rigidity & cramping in neck, tongue, face or back
-Respiratory distress from laryngeal dyskinesia (laryngospasm)
-Responds well to diphenhydramine 25-50 mg. IV

64
Q

Phenothiazines
and Thioxanthenes
Cardio side effects

A

Cardiovascular effects

  • Decreases in B/P
  • Due to depression of vasomotor reflexes/peripheral alpha adrenergic blockade
  • Relaxant effects on vascular smooth muscle
  • Direct cardiac depression
  • No cardiac dysrhythmic effects
  • Prolonged QT interval on ECG
65
Q

Phenothiazines
and Thioxanthenes
CNS side effects

A

*Sedation
–Due to antagonism of alpha 1, muscarinic, and
histamine receptors
–Tolerance to sedation develops with chronic therapy
*Seizure threshold is decreased-similar EEG pattern as seen with seizure disorders, and sensory evoked potentials often decreased in amplitude
*Skeletal muscle relaxation: By CNS action not neuromuscular junction

66
Q

Phenothiazines
and Thioxanthenes
yup more side effects

A

Antiemetic properties
-Interacts with dopaminergic receptors in
chemoreceptor trigger zone
-Effective in preventing opoid induced N/V
-No sedation or hypotensive effects and rarely cause extrapyramidal symptoms
*Neuroleptic malignant syndrome
-Develops over 24-72 hrs usually in young men
-Hyperthermia
-Hypertonicity of skeletal muscles
-Instability of autonomic N.S.
-Fluctuating LOC

67
Q

Phenothiazines

and Thioxanthenes drug interaction

A

Potentiation of opioids: Sedative effects, Ventilatory depression, Analgesic properties

68
Q

Butyrophenones

A
  • Droperidol (inapsine)
  • Haloperidol (haldol)
  • *Structurally resemble phenothiazines
  • Side effects similar to phenothiazines
69
Q

Butyrophenones: Droperidol Pharmacokinetics

A
  • Clearance is perfusion dependent-Hepatic metabolism opposed to hepatic enzyme activity
  • accumulation of drug with decreased hepatic blood flow
  • max excretion of metabolites in first 24 hrs
70
Q

Butyrophenones: Droperidol side effects

A

CNS: extrapyramidal reactions, cerebral vasoconstrictor (decreased CBF), dysphoria
CV
-Decrease in systemic BP from alpha
blockade-usually minimal
-Antidysrhythmic, protects against epinephrine induced dysrhythmia
-Large doses decrease conduction along accessory pathways responsible for tachy dysrhythmias WPW syndrome
-Prolonged QT
-Torsades: have occurred at low doses, pt with no risk factors, no precise cause, some fatal

71
Q

Droperidol Black box warning

A

all pts get 12 lead prior to administration

  • must be monitored prior to and continues for 2-3 hrs
  • caution with pts at rick for developing QT syndrome
72
Q

Droperidol uses

A
  • neurolept analgesia: combines with fentanyl (innovate), prolonged action of fentanyl, intense analgesia
  • antiemetic: simmilar to zofran
  • does not help motion sickness
73
Q

Mood stabilizer

A

Lithium

74
Q

Lithium

A
  • tx of bipolar
  • Neurobiogenic effects not well understood how it works or which effects are necessary for mood stabilization
  • Competes with Na+, Ca+, and Mg+ affecting cell membranes, H2O, and neurotransmitters
75
Q

Lithium pharmacokinetics

A
  • Distributed throughout total body H2O and excreted by the kidneys
  • Filtered by glomerulus and reabsorbed by the proximal renal tubules
  • Proximal reabsorption of lithium and Na+ is competitive (so low Na and more lithium is absorbed)
  • Elimination 1⁄2 time is 24 hrs.
  • Steady state is 4-5 elimination 1⁄2 times
76
Q

Lithium side effects

A

kidneys-evaluate renal function every 6 months

  • Polydipsia and polyuria: > 3 liters/day
  • Impaired renal concentrating ability
  • Decrease in sensitivity to ADH
  • EKG—T wave changes, flattening or inversion: No related clinical effects
  • Hypothyroidism can develop– more common in females
  • New onset psoriasis/acne
  • Hand tremor
  • Sedation
  • Memory disturbances/cognitive slowing
77
Q

Lithium Toxicity

A

*Mild: Sedation, nausea, skeletal muscle weakness, wide QRS complex, AV heart block, hypotension, dysrhythmia, seizure
**Significant toxicity
Medical emergency
Aggressive RX
Hemodialysis
Osmotic diuresis and IV bicarbonate

78
Q

Lithium AC

A
  • Pre operative labs and ECG
  • Many drug interactions
  • Anesthetic requirements may be decreased
  • Action of neuromuscular blocking agents may be prolonged
79
Q

epilepsy

A

Designates a group of chronic central nervous system disorders characterized by sudden onset of sensory, motor, autonomic, psychic disturbances

  • usually transient and associated with rapid, synchronous uncontrolled spread of eletrical activity in the brain.
  • May be associated with an identifiable neurologic/systemic disorder or may be idiopathic
80
Q

Antiepileptics

A

Goal of therapy is to control seizures without medication related side effects

  • 70% of patients can achieve this using a single anti epileptic drug
  • Drug selected to treat is influenced by the type of seizure experienced
81
Q

Antiepileptics MOA

A

Decrease neuronal excitability or enhance
inhibition of neurotransmission
-Achieve by altering intrinsic membrane ion currents (sodium, potassium, and calcium conductance)
-Enhancement of GABA action

82
Q

Antiepileptics Pharmacokinetics

A

Slow absorption from GI tract

  • Protein binding varies 0%->90%
  • Most are metabolized by the liver and excreted by the kidneys
  • Elimination 1⁄2 times range from hours to days
  • Most all associated with drug interactions in which effects of concomitantly administered drugs may be altered
83
Q

Antiepileptics lab testing

A

Routine monitoring of plasma concentration
guide dosing adjustments
-“Therapeutic ranges” often do not correspond to individual responses
-Titrate to clinical efficacy: Check plasma levels to determine compliance with RX and pharmacokinetic interactions
-Many antiepileptics associated with life threatening bone marrow suppression and hepatotoxicity: Liver function tests and Hematologic studies

84
Q

Antiepileptics

A 
Phenobarbital
Phenytoin (dilantin)
Fosphenytoin (cerebyx)
Primidone (mysoline)
Carbamazepine (tegretol)
Valproate (depakote)
Levetiracetam (Keppra)
85
Q

Phenytoin MOA

A

-Effective for Rx of partial and generalized
seizures, can be given po or IV
-Regulates neuronal excitability and thereby the spread of seizure activity from a seizure focus by regulating Na+ and Ca++ ion transport across neuronal membranes

86
Q

Phenytoin

Pharmacokinetics

A

Pharmacokinetics
-pH of 12 and precipitates in solutions with pH
of < 7.8
-Not recommended for IM injection- precipitates at site and poorly absorbed
-Infusion no faster than 50 mg./min in adults; 1-3mg/kg/min in peds or 50mg/min whichever is slower.
-Poorly H2O soluable-variable absorption from GI tract
-Highly protein bound-90% to plasma albumin

87
Q

Phenytoin metabolism

A
  • By hepatic microsomal enzymes CP450
  • Inactive metabolites
  • Plasma concentration 10mcg/ml zero order kinetics
88
Q

Phenytoin Side effects

A 
CNS toxicity-nystagmus, ataxia, diplopia,
vertigo, peripheral neuropathy
-Acne
-Facial coarsening
-Allergic rash→Stevens Johnson Syndrome
-GI irritation
-Hepatotoxicity
-Induces hepatic enzyme system
89
Q

Fosphenytoin

A 
-Slightly safer than dilantin
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/treat seizures
-10-20 mg/kg IV loading dose
90
Q

Phenobarbital

A

-Long acting barbiturate
-Cognitive and behavioral side effects limit
usefulness-2nd line drug
-Sedation in adults; hyperactivity in children
-Depression
-Confusion in elderly

91
Q

Phenobarbital MOA

A

Mechanism of action
-Modulation of post synaptic actions of GABA
and glutamate
-Enhances cytochrome P450 system in liver

92
Q

Benzodiazepines: as antiepileptics

A

Binds to GABA receptors in brain and potentiate GABA mediated neuronal inhibition by increasing chloride permeability, cellular hyperpolarization,and inhibition of neuronal firing

Pharmacology test 2 (6 decks)

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