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Neuro Exam 1 > Opioid Analgesics > Flashcards

Opioid Analgesics Flashcards

1
Q

Opioid Analgesics drug list

A
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2
Q

Definition . . .

  1. OPIATE
  2. OPIOID
  3. ANALGESIA
  4. HYPOALGESIA
  5. HYPERALGESIA
  6. ALLODYNIA
A
  1. OPIATE: compounds structurally related to products found in opium
  2. OPIOID: any agent that has the functional & pharmacological properties of an opiate
  3. ANALGESIA: without pain
  4. HYPOALGESIA: reduced pain perception induced by analgesics
  5. HYPERALGESIA: increased pain associated with mild noxious stimulus
  6. ALLODYNIA: pain evoked by non-noxious stimulus
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3
Q

Definition:

  1. NARCOTIC
  2. ENDORPHIN
  3. NOCICEPTIVE PAIN
  4. NEUROPATHIC PAIN
  5. CHRONIC PAIN
A

 NARCOTIC: agent that induces sleep (narcosis)
 ENDORPHIN: endogenous opioid peptide
 NOCICEPTIVE PAIN: involves pain receptors & transmission over intact nerves
 NEUROPATHIC PAIN: caused by damaged neural structures
 CHRONIC PAIN: pain that outlasts precipitating tissue injury

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4
Q

Endogenous opioid peptides (general)

A

Endogenous opioids have the same pharmacological properties as exogenous opioids: 1) analgesia 2) blocked by naloxone
.
Synthesized by 4 precursors:
› Preproenkephalin: met-enkephalin, leu-enkephalin
› Preproopiomelanocortin (POMC): β-endorphin, ACTH, α- MSH, β-LPH
› Preprodynorphin: dynorphin A, dynorphin B, neoendorphin
› Preorphanin FQ (N/OFQ): orphanin, nocistatin, orphanin-2, endomorphin-1, endomorphin-2
.
- Each of these precursors is produced in a variety of brain areas and goes through different proteolytic processing

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5
Q

pain or nociceptor

TWO COMPONENTS OF PAIN . . . and how

A
  1. Specific sensation: the perception, localization and discrimination of pain.
     Experimental pain is acute, of short duration, and non-inflammatory such
    as that associated with a surgical procedure.
     Pathological pain is chronic and inflammatory such as that associated with healing
    .
  2. Reaction to the sensation: the subjective & psychological aspect. This is
    related to the anxiety, fear, panic, and suffering associated with pain. This
    response depends on the individual’s personality, psychological profile, and
    previous experiences with pain.
    .
    Opioid analgesics OBTUND pain. Opioids raise the threshold for pain
    perception and alter the affective pain response. No other senses are
    affected
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6
Q

The Pain Pathway

A
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7
Q

Pain

  1. Integumental pain
  2. Visceral pain
A
  1. Integumental pain
    › Dermis, mucosa, skeletal muscle, joints, headache, dysmenorrhea
    › Controlled by NSAIDs which act locally at sites of inflammation to synthesis of prostaglandins and inhibit release of the algesic autacoid, bradykinin
    › May be combined with narcotics (two different mechanisms)
    .
  2. Visceral pain
    › Pain within body cavities (thorax and abdomen)
    › Diffuse, hard to localize and referred to other sites
    › Best treated with opioids with their main action on the spinal cord and upper CNS
    .
    NSAIDs are not as effective unless pain is associated with inflammation (concept is changing)
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8
Q

Pain - tissue injury and inflammation

A

-Components of tissue injury such as 5-HT, histamine, bradykinins, prostaglandins, K+, H+ lower the pain threshold. They produce inflammation, allodynia, and hyperalgesia.
.
- Nonsteroidal Antiinflammatory Drugs (NSAIDS) act to inhibit cyclooxygenases (COX) thereby preventing prostaglandin production. Prostaglandins sensitize
neurons to pain stimuli.This is a peripheral mechanism of action.
.
- Local anesthetics inhibit axonal action potential propagation. This is a peripheral mechanism of action.

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9
Q

Pain - nerve injury

A
  • Substance P, glutamate & calcitonin gene-related peptide (GCRP) are neurotransmitters in the C afferents
  • Neuropathic pain initiated by low-threshold sensory fibers (Aβ fibers, mechanoreceptors) i.e nerve trauma, chemotherapy, diabetes, post-herpetic neuralgia
  • Neuropathic pain is not as responsive to analgesics as nociceptive pain.
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10
Q

Pain and neurologic inflammation

A
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11
Q

Supraspinal actions - opioids

A
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12
Q

Spinal opiate action

A
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13
Q

Spinal cord site of action

A

Continue

  • Glutamate & Neuropeptides transmit pain signal in the dorsal horn of the spinal cord
  • Presynaptic opioid receptors on primary afferents decrease the action potential induced Ca2+ influx which decreases Substance P and CGRP release. › Axoaxonic mechanism
  • Postsynaptic opioid receptors increase K+ conductance which induces IPSP, hyperpolarization of the neuron and reduces pain neurotransmission
  • Intrathecal or epidural opioids. Produce analgesia. Such analgesia is rapid in onset, long lasting, has few side effects, and no physical dependence
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14
Q

Opioid peripheral action

A
  • Direct application of high [opiate] can produce local-anesthesia type response that is NOT reversed by naloxone
  • Peripheral sites under conditions of inflammation, where there is an increased terminal sensitivity leading to an exaggerated pain response, direct injection of opiate produces a localized “normalizing effect” on those exaggerated thresholds
  • Descending NE projections act on alpha-2 receptors on primary C-fiber terminals to decrease the opening of voltage-gated calcium channel -> reduce entry of Ca2+, reduce neurotransmitter release (Substance P, glutamate, CGRP)
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15
Q

Opioid Receptors . . . general

A
  • 3 classes: MOR, DOR, KOR (µ, δ, κ)
  • Virtually all clinically useful agonists target MOR
  • All opioid receptors have 7 TM regions are G-protein coupled
    .
  • Postsynaptic effects include
    › Decreased adenylyl cyclase production
    › Decreased neuronal inhibition by hyperpolarization (activation of receptor operated K+ channels)
    .
  • Presynaptic effects include
    › Inhibition of voltage sensitive Ca++ channels that decrease
    neurotransmitter release
    .
  • Ligands that bind specifically but have limited intrinsic activity are partial agonists (for MOR, i.e. buprenorphine)
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16
Q

Opioid Receptors classification

A
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17
Q

Opioid analgesics (general)

A
  • Considered to act by a central mechanism. Although opioid receptors are located peripherally and local injection of opioids in inflamed tissue is analgesic, such analgesia is not reversed by naloxone.
    .
  • Nociceptive Afferent Fibers
    › C-fibers: nonmyelinated & slow conduction speed (Mediates dull burning pain)
    › Aδ fibers: myelinated with rapid action potential conduction (High-threshold sensory afferents…Mediates sharp, well-localized pain)
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18
Q

Morphine . . . general/ stucture

A
  • Morphine is derived from opium, extract of the opium poppy papaver somniferum. Opium is a solid extract of the dried milky exudate of unripe seed capsules, contains 9-14% morphine
    › Raises pain threshold @ spinal cord level
    › Alters CNS perception of pain
    .
  • Morphine (µ) agonists act on secondary ascending neurons to activate K+ channels, inducing an IPSP, thus reducing the excitation of neurons
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19
Q

Tolerance and Cross tolerance . . . define all the diff type of tolerance

A

› Acute tolerance (desensitization): occurs within minutes of dose,
disappears parallel to metabolic clearance of drug
.
› Pharmacokinetic tolerance: less drug present at site of action
(hepatic enzyme induction will increase drug metabolism = metabolic tolerance)
.
› Pharmacodynamic tolerance: same amount of drug present at site of action, but response is reduced due to changes in receptors or mechanisms
.
› Cross tolerance: tolerance to most drugs within a class.
 May be partial or incomplete
 Opioid rotation
.
› Behavioral tolerance: individual compensates for decrease effect
.
› Innate tolerance: some individuals are less affected by the drug. G
 Genetically predetermined

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20
Q

Opioid dependence

  1. Physical dependence & cross-dependence
  2. Psychological dependence
A

1.) Physical dependence & cross-dependence
› Removal of drug from physically dependent person results in withdrawal/abstinence syndrome (Significant somatomotor & autonomic outflow (agitation, hyperalgesia, hypertension, diarrhea, mydriasis, dysphoria))
› Drugs that induce physical dependence are cross dependent to other drugs within the class
.
2.) Psychological dependence
› Patient feels effects of drug are necessary to maintain optimal state of well-being
› Does not imply pathology until drug use impairs functioning
› May occur without physical dependence or tolerance
› The basis for compulsive drug use and addiction

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21
Q

Classification of opioid compound

A
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22
Q

Pharmacological effects of opioids

A
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23
Q 
Pharmacological effects of opioids:
Mood changes (general)
A
  • Euphoria: sense of contentment and well-being
    › Especially apparent when relief of pain accompanies administration
    › µ agonists enhance DA release from neurons in Nucleus Accumbens to induce euphoria
    › Separate mechanism from analgesia
  • Mental Clouding
    › Drowsiness, lethargy, apathy (non-addictive type persons may experience
    mental clouding that can be reported as dysphoric)
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24
Q

Mood Alteration & euphoria

A
  • Neural systems that mediate opioid reinforcement overlap with those involved in physical dependence and analgesia. The mesocorticolimbic DA system that
    comes from the VTA & projects to the Nucleus Accumbens is pivotal in drug-induced reward and motivation.
  • Increased DA underlies a positive reward state
  • In the NAc, MOR’s exist on postsynaptic GABAergic neurons.
  • The reinforcing effects of opiates are mediated partly via inhibition of local GABAergic activity, which otherwise acts to inhibit DA outflow
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25
Q

Pharmacological effects of opioids

A
  • May occur @ therapeutic doses
    .
  • Most common cause of death
     Decreased response of brainstem respiratory neurons to CO2 (chemical drive)
     Hypoxic response of the carotid sinus and aortic arch chemoreceptors are only affected at high doses
     Hypoxic drive maintains respiration in opioid overdose; administration of O2 may further decrease respiration
    .
    › Bronchoconstriction can contribute to respiratory depression via histamine release
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26
Q

Pharmacological effects of opioids:

respiratory depression

A

 Administer with caution in cases of impaired pulmonary function
› Chronic bronchial asthma
› Chronic obstructive pulmonary disease (COPD)
› Other meds that cause respiratory depression
.
 Respiratory depression and increased pCO2 cause:
› Cerebrovascular vasodilation
› Secondary elevation of CSF pressure
.
 Can be exaggerated in the presence of head injury, other intracranial lesions or pre-existing increase in intracranial pressure. DO NOT USE.

27
Q

Pharmacological effects of opioids:
respiratory depression
.
Other factors that may increase the risk of opiate-related respiratory depression at therapeutic doses:

A

› CNS depressants: general anesthetics, ethanol, bzd’s, sedative- hypnotics, opioid combinations

› Sleep: decreases in sensitivity of medullary center to CO2 and depressant effects of morphine are at least additive. Sleep apnea is risk factor for fatal-respiratory depression

› AGE
 Newborns: if opioids are administered parenterally within 2-4 hours of
delivery, they are permeable to infant’s BBB
 Elderly: reduced lung elasticity, chest wall stiffening, decreased vital
capacity
.
› Relief of pain: pain stimulates respiration-removal of pain will reduce
ventilatory drive

› Organ dysfunction: renal &/or hepatic dysfunction

28
Q

Pharmacological effects of opioids:

nausea and vomiting

A

 Caused by direct stimulation of the CTZ for emesis in the area postrema of the medulla
 All clinically useful agonists produce some degree of N/V
 Nausea occurs in about 40% of ambulatory patients given analgesic doses
 Vomiting occurs in about 15%
 Opioid agonists produce an increase in vestibular sensitivity

29
Q

Pharmacological effects of opioids:

GI Effects

A

 Constipation and antidiarrheal effect
› Affects intestinal smooth muscle to relieve diarrhea by  Decreasing peristaltic gut motility  Increasing tone (persistent contraction)
› Acts through peripheral opioid receptors
.
 Constipation is resistant to tolerance and will delay passage of GI contents; may
also delay drug absorption

30
Q

Pharmacological effects of opioids:
GI Effects

Opioid-Induced constipation (OIC) in adults with chronic opioid use

A

Naloxegol (Movantik)
 Pegylated derivative of naloxone: doesn’t cross BBB and can reverse constipation produced by systemic opioid agonists
.
Relistor (Methylnaltrexone)
 Selective µ antagonist
 Quaternary amine: doesn’t cross BBB
 tx of OIC in patients with advanced illness who are receiving palliative care, when response to laxative therapy has not been sufficient

31
Q

Pharmacological effects of opioids:
GI Effects
.
Eluxadoline (Viberzi)

A

› Indicated for tx of irritable bowel syndrome with diarrhea (IBS-D)
› µ agonist, κ agonist, δ antagonist
› Warnings:
 Spasms in muscle of digestive tract (sphincter of Oddi) which may cause new or worsening abdominal pain. Increased risk in patients w/o gallbladder
 Pancreatitis - increased risk in patients who drink >3 alcoholic drinks per day

32
Q

Pharmacological effects of opioids:

Urinary tract

A

 Inhibits urinary voiding reflex
.
 Increases tone of the external sphincter
.
 Water retention
› Increases ADH release by central mechanism
› Decreases bp (reduced glomerular filtration) results in water retention
› Catheterization may be required in severe cases, usually after spinal drug administration
.
 Effect is through peripheral opioid receptors and can be reversed by peripherally acting antagonists
.
 Tolerance develops

33
Q

Pharmacological effects of opioids:

Miosis

A

 Stimulation of µ and κ receptors located in the Edinger-Westphal nucleus of the oculomotor nerve III.
 Activates parasympathetic outflow – pupil constriction
.
 HIGH DOSES of opioid agonists produce marked pinpoint pupils.
› While some tolerance to the miotic effect may develop, addicts with high circulating concentrations of opioids will continue to experience miosis
› Marked mydriasis will occur with the onset of asphyxia
› Does NOT develop with meperidine; tends to be a narcotic of choice for abuse by health care professionals
› Blocked/reversed by opioid antagonists or atropine

34
Q

Pharmacological effects of opioids:

Histamine release

A

 Morphine causes mast cell degranulation with release of histamine causing urticaria, itching, diaphoresis and vasodilation.
 May precipitate bronchospasm in asthmatics
 Reversed by antihistamines but not naloxone
 Itching is readily seen with morphine and meperidine, but to a much lesser extent
with oxymorphone, methadone, fentanyl or sufentanil.

35
Q

Pharmacological effects of opioids:

neuroendocrine effect

A 
 Decreases LH and FSH release
.
 Decreased testosterone
› Decreased sexual drive
› Decreased sperm count
.
 Decreased estrogen
› Menstrual irregularities including amenorrhea
› Hot flashes
.
 Switch to non-opioid or use buprenorphine
36
Q

Pharmacological effects of opioids:

Cardiovascular system

A

 Opioid induced histamine release can lead to peripheral arteriolar and venous dilation => hypotension
 CNS depression of vasomotor and adrenergic tone
 May result in postural/orthostatic hypotension
.
 Morphine is used in patients with dyspnea from pulmonary edema associated with left ventricular heart failure
› Reduced cardiac preload (reduced venous tone) and afterload (decreased peripheral vascular resistance) leading to a decrease in myocardial oxygen consumption
› Dramatically relieves dyspnea associated with pulmonary edema due to LV heart failure

37
Q

Pharmacokinetic of morphine

A
  • Oral absorption undergoes significant first pass metabolism . Equianalgesic dose of morphine is 30mg PO vs. 10mg parenteral
    .
  • Low lipid solubilityonly 20% is unionized @ plasma pH.
    .
  • Morphine is metabolized by glucuronideconjunction by CYP2D6.
    › Morphine-6-glucuronide is a major active metabolite that is 2X potent as morphine
    › Conjugates excreted in urine
    › High levels of morphine-3-glucuronide can produce seizures
    › With renal impairment, morphine-6-glucuronide accumulates & overdose may result
38
Q

Comparison of opioid analgesics (4 main things to consider)

A
  1. Naturally occurring (morphine, codeine)
  2. Partial synthetic (heroin, naloxone)
  3. Synthethic (levorphanol, meperidine, methadone)
  4. Agonist/antagonist (pentazocine, butorphanol, nalbuphine)
39
Q

Natural and partially synthetic . . . list general

A
  • Codeine
  • Heroine
  • Oxycodone
  • Hydrocodone
  • Hydromorphone (dilaudid)
  • Apomorphine
  • Levorphanol
  • Dextromethorphan
40
Q

Natural and partially synthetic

  1. Codeine
  2. Heroine
A
  1. CODEINE
    › Orally active @ 1/10th potency of morphine.
    › 10% of codeine metabolized to morphine by CYP2D6
    › Anti-tussive at sub-analgesic doses
    › Mild analgesic used in combination with ASA or APAP
    .
  2. Heroine (diacetylmorphine))
    › Crosses BBB rapidly due to high lipid solubility
    › Metabolized to monoacetylmorphine and morphine which are responsible for
    effects of heroin
41
Q

Natural and partially synthetic

  1. Oxycodone
  2. Hydrocodone
  3. Hydromorphone (dilaudid)
A
  1. Oxycodone- Same effects and potency as morphine but has a higher oral activity
  2. Hydrocodone - usually formulated with acetaminophen; same effects as morphine, orally active
  3. Hydromorphone (dilaudid) - same effects as morphine but with higher oral activity
    › 10x more potent than morphine, › Greater respiratory depression
42
Q

Natural and partially synthetic

  1. Apomorphine
  2. Levorphanol
  3. Dextromethorphan
A
  1. Apomorphine- › Has little analgesic activity, does cause respiratory depression, DA agonist activity used to induce vomiting by its direct action @ CTZ
    .
  2. Levorphanol- › Good oral activity with longer duration of action than morphine with less N/V, Incomplete cross-tolerance with morphine
    .
  3. Dextromethorphan- D-isomer of codeine analog “methorphan” that has very little
    analgesic activity, Antitussive, Less drowsiness or GI disturbances, NMDA antagonist activity may contribute to abuse potential
43
Q

Synthetics opioid . . . general ( 9 in all)

A
  1. Meperidine (Demerol)
  2. Propoxyphene
  3. Diphenoxylate (Lomotil)
  4. Fentanyl
  5. Sufentanil (Sufenta)
  6. Remifentanil (Ultiva)
  7. Tapentadol (Nucynta)
  8. Tramadol (Ultram, Ultracet)
  9. methadone (Dolophine)
44
Q

Synthetics opioid

1.Meperidine (Demerol)

A
45
Q

Synthetics opioid

  1. Propoxyphene
  2. Diphenoxylate (Lomotil)
A
  1. Propoxyphene- Same indications and spectrum of activity as codeine.
    › d/c in United States in 2011
    .
  2. Diphenoxylate (Lomotil) - › Formulation contains atropine that can produce
    undesirable anticholinergic side effects at supratherapeutic doses
    › Only available for PO administration for tx of diarrhea
    › Difenoxin (Motofen) is metabolite with similar properties to diphenoxylate
46
Q

Synthetics opioid

4. Fentanyl (Sublimaze, Actiq, Duragesic)

A
47
Q

Synthetics opioid

  1. Sufentanil (Sufenta)
  2. Remifentanil (Ultiva)
  3. Tapentadol (Nucynta)
A
  1. Sufentanil (Sufenta) -Similar to fentanyl in action & use
    .
  2. Remifentanil (Ultiva)- › metabolized by plasma esterases with an elimination t1/2 of 8-20 minutes. › After 5 hour infusions, full recovery seen in 15 minutes, › Allows for minute by minute control of analgesia
    .
  3. Tapentadol (Nucynta)- Similar in mechanism of action, efficacy, side effect profile as tramadol
48
Q

Synthetics opioid

8. Tramadol (Ultram, Ultracet)

A
49
Q

Synthetics opioid

9. methadone (Dolophine)

A
50
Q

Methadone maintenance

A
51
Q

Opioid Antagonist. . . Pure antagonist (drug example)

A

Naloxone (Narcan)
Naltrexone (Trexan)
Methylnaltrexone (Relistor)
Vivitrol (XR injectable naltrexone)

52
Q

Pure antagonist part 1

1. Naloxone (Narcan)

A

› Naloxone (Narcan): pure competitive antagonist at all opioid receptors with no opioid agonist activity
› No apparent activity of it’s own at therapeutic doses, but will enhance pain in someone who is already in pain
› Short duration of action-approx 1 hour
› Rapid hepatic metabolism (little or no oral activity, must be given parenterally)
› Drug of choice for opioid overdose: 0.4 – 0.8 mg IM or IV for µ agonists, 10-15mg for κ agonist

53
Q

Pure Antagonist part 2

  1. Naltrexone (Trexan)
  2. Methylnaltrexone (Relistor)
  3. Vivitrol (XR injectable naltrexone)
A

 Naltrexone (Trexan): pure competitive opioid antagonist with a 24-hour duration of action.
› Available only in oral formulation
› More potent than naloxone with t1/2 = 3 hours
› Active metabolite 6-naltrexol has t1/2 = 13 hours
.
 Methylnaltrexone (Relistor)
› Peripheral action only
› Used to manage constipation in long-term opioid pain treatments
.
 Vivitrol (XR injectable naltrexone)
› Treats alcohol and opioid dependence
› 380mg Q4w IM

54
Q

Uses of pure antagonists

A 
 Treatment of acute opioid overdose
 Diagnosis of addiction
 Treatment of compulsive opioid use
 Treatment of alcoholism (naltrexone)
 Treatment of consitpation secondary to long-term opioid treatment (methylnaltrexone)
55
Q

Agonist-Antagonist

Pentazocine (Talwin)

A

› Analgesic for moderate/severe pain
› Oral and parenterally active
› Weak µ antagonist or partial agonist
 Blocks morphine analgesia and induces opioid (mu) withdrawal in physically
dependent patients
 Does NOT block morphine respiratory depression

56
Q

Agonist-Antagonist

Talwin at Agonist @ κ receptors

A

› Spinal analgesia that is as effective as morphine supraspinal analgesia
› Limited respiratory depression; not as severe as morphine
› Dysphoria, uncontrolled “weird” thoughts & hallucinations esp. with higher doses
› Withdrawal from the physical dependence of pentazocine results in mild morphine-like withdrawal syndrome
› All κ agonist effects are blocked by naloxone
› Talwin NX = combination of pentazocine & naloxone

57
Q

Agonist-Antagonist

Nalbuphine (Nubain) & Butorphanol (Stadol)

A

› Analgesic for moderate/severe pain
› Available for injection, butorphanol available as nasal spray
› µ antagonists: antagonize morphine analgesia & will induce abstinence
syndrome in those physically dependent to morphine

58
Q

Agonist-Antagonist

Nalbuphine (Nubain) & Butorphanol (Stadol) . . . k agonist?

A 
 κ agonists:
› Produce effective analgesia with limited respiratory depression
› Low incidence of psychomimetic effects
› Mild abstinence syndrome
› Antagonized by naloxone
59
Q

Agonist-antagonist . . .

Buprenorphine (Buprenex)

A

› Analgesic for moderate/severe pain
.
› Partial agonist @ µ receptors
 High affinity for and slow dissociation from µ receptors – slow onset & long lasting effects
 Potentially useful replacement for methadone as maintenance drug for opioid abusers.
 Induces tolerance to euphoric effects
 Partial agonist activity may antagonize the euphoria of street drugs as well as reduce cravings in recovering addicts
.
› Initiate therapy with buprenorphine alone & then maintain with buprenorphine + naloxone (Suboxone)

60
Q

Agonist-antagonist

Effects of buprenorphine include

A 
› Analgesia
› Respiratory depression (different from other µ receptor agonists): as a partial µ agonist, induces only part of the full agonist response. May be a ceiling effect.
› Euphoria
› Mild morphine abstinence syndrome
› κ agonist: clinical use unknown
61
Q

Opioid abstinence/ withdrawal

A

 All tolerance to opioids is pharmacodynamic
 There is little/no metabolic tolerance
 NOT life threatening….Morphine: first sx occur 8-12 h after last dose, peak effects occur @ 36-72 h….Long lasting opioids: symptoms will come & go later; will be less severe
 Symptoms similar to severe influenza:
› Diarrhea/vomiting
› Chills/fever/sweating
› Piloerection
› Lacrimation, rhinorrhea
› Yawning, insomnia
.
 Protracted withdrawal: anxiety, insomnia & drug cravings can continue for up to 6 months

62
Q

Opioid overdose . . . classic triad of symptoms

A
  1. Depressed respiration
  2. Pinpoint pupils
  3. Coma
63
Q

Opioid overdose . . .

Opioid interactions worsen symptoms

A 
› Additive or synergistic effects to produce CNS &/or respiratory depression can occur with:
 Sedative-hypnotics
 Ethanol
 MAOI’s
 Antihistamines
 Tricyclic antidepressants
 Antipsychotics

Neuro Exam 1 (7 decks)

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