pharm_psych_seiz_dem

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pharm_psych_seiz_dem
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2012-01-26 00:13:02
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pharmacology psych seizure dementia drugs ms2
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pharm psych seizure dementia ms2
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  1. TCA DRUGS FOR DEPRESSION (3)
    DESIPRAMINE -- NE RI

    IMIPRAMINE -- NE/5-HT RI

    CLOMIPRAMINE -- NE/5-HT RI
  2. SSRI DRUGS FOR DEPRESSION (6)
    "SOME Pts CAN FEEL FINE EVENTUALLY"

    Sertraline

    Paroxetine

    Citalopram

    Fluoxetine

    Fluvoxamine

    Escitalopram
  3. NON TCA/SSRI (OTHER) DRUGS FOR DEPRESSION Tx
    mirtazapine --a2 rec antag

    duloxetine -- 5ht/ne reuptake inh

    venlafaxine -- low dose 5ht, high 5ht/ne ri

    bupropion -- inh da uptake
  4. MIRTAZAPINE
    NON TCA/SSRI (OTHER) DRUGS FOR DEPRESSION Tx

    alpha 2 receptor antagonist = inc NE release

    also blocks H1 and 5HT2 receptors = ↑weight
  5. VENLAFAXINE
    NON TCA/SSRI (OTHER) DRUGS FOR DEPRESSION Tx

    Low dose = 5HT reuptake inhibitor

    Higher dose = 5HT/NE reuptake inhibitor
  6. DULOXETINE
    NON TCA/SSRI (OTHER) DRUGS FOR DEPRESSION Tx

    5HT/NE reuptake inhibitor
  7. BUPROPRION
    NON TCA/SSRI (OTHER) DRUGS FOR DEPRESSION Tx

    affects DA uptake
  8. MAOI DRUG
    PHENELZINE

    irreversible inhibitor of MAO

    must inh monoamine oxidase A!!! B/c MAO-A in brain is what breaks down NE/5-HT.

    MAO-B breaks down DA.
  9. S/E OF TCAs
    (3 RECEPTORS AND 2 ORGANS)
    MUSCARINIC

    H1 HISTAMINE

    a1 ADRENERGIC

    CV

    CNS
  10. MUSCARINIC S/E OF TCA DRUGS (7)
    1. Dry mouth

    2. Urinary retention

    3. Constipation

    4. Blurred vision

    5. Memory impairment

    6. Sexual dysfunction

    7. (Tachycardia)
  11. H1 HISTAMINE S/E OF TCA DRUGS
    SEDATION

    WEIGHT GAIN
  12. a1 ADRENERGIC S/E OF TCA DRUGS
    ORTHOSTATIC HYPOTENSION

    SEXUAL DYSFUNCTION
  13. CV SIDE EFFECTS FOR TCA DRUGS
    1. Tachycardia (anticholinergic)

    2. Changes in cardiac conduction

    · Normal ♥ pts: not clin signf

    • · Most signf ECG changes:
    • ---- Inversion or flattening of T waves

    ---- Incr PR interval (b/c incr intraventr conductn time)

    · *Pts w/ pre-exist ♥ condtn: Incr risk of AV block

    · *Overdose: severe arrhythmias

    3. *Orthostatic hypotension
  14. CNS S/E OF TCA DRUGS
    1. Fine, rapid tremors of extremities or ataxia (esp in elderly on high doses)

    2. Manic episodes in bipolar pts

    3. Lower seizure threshold: incr risk of tonic-clonic seizures
  15. S/E OF MAOIs (4 MAIN)
    • HEPATIC TOX
    • CNS
    • CV
    • FOOD/DRUG INTERACTIONS
    • ---------------

    • CNS effects (~sx of excessive stim)
    • · Tremors
    • · Insomnia
    • · Agitation
    • · Poss hypomanic or manic rxn in bipolar pts
    • ----------------------

    • CV effects:
    • · Orthostatic hypotension b/c:
    • ----Incr stim of central α2, or
    • ----Accum of false transmitter “octopamine” in periph symp neurons
    • ------------------------

    • Food/Drug interxns: “Cheese Rxn”
    • · Ingest indirectly acting sympathomim amines (e.g. in OTC decongestants) → poss hypertensive crisis

    · e.g. Tyramine* not broken down by MAOA at GI → enters circ → release > nL amts of stored NE → incr BP)
  16. SSRI S/E (4)
    1. *N/V (5-HT3)

    2. *Sexual dysfunction (5-HT2): anorgasmia, ejac disturbance (b/c enhanced 5-HT transmission)

    3. Late-developing weight gain* (satiation/weight loss: 5-HT2C & 5-HT1B)

    4. Anxiety, insomnia, agitation (5-HT2)

    5. NO risk of HTN crisis b/c no inhb MAO

    6. *NO anticholinergic S/E

    7. NO effects on ♥ conduction system

    • 8. *NO orthostatic hypotension
    • --------------------

    SSRIs produce less serious S/Es than TCAs & MAOIs and are better tolerated.

    Stim of 5HT3 receptors by serotonin dec appetite & causes N/V

    --SSRIs --> ↑5HT in synapse --> dec weight, dec N/V

    --S/Es dissipate after several weeks
  17. BZs FOR ANTIANXIETY
    "BZs help you Calm Down A LOT"

    Alprazolam

    Clonazepam

    Diazepam

    Lorazepam

    Oxazepam

    • Triazolam
    • ---------------------

    INC Cl- CONDUCTANCE BY ALLOSTERIC ACTION ON GABA-A CHANNELS --> HYPERPOL NEURONS
  18. OXAZEPAM
    METABOLITE OF MOST BZs

    CONJUGATED w GLUCARONIC ACID TO EXCRETE

    NOT METABOLIZED BY OXIDATION

    USED IN ELDERLY AS OXIDATION IS SLOWED
  19. 5 USES FOR BZs
    • 1. Sedative-hypnotic:
    • -- Decr dur of stage 1, 3/4 & REM
    • -- Latency to persistent sleep
    • -- Incr stage 2 & total sleep time

    2. Anti-anxiety (inhb of suppressive effects of punishment)

    3. Anti-convulsant

    • 4. Muscle relaxant effects
    • (at spinal cord level)

    • 5. Anterograde amnesia
    • (surgery)
  20. MAIN S/E FROM BZs
    1. Sedation

    2. Dizziness

    3. Uncoordination

    4. Paradoxical agitation

    5. Impairment of cognitive func

    6. Minimal suicide potential. BUT combo w/ ETOH (or other CNS depressant) → incr suicide potential

    7. Little organ toxicity

    • 8. Minimal capacity to induce hepatic enz
    • --------------------------

    POTENTIAL FOR ABUSE, DEPENDENCE & WITHDRAWAL
  21. WITHDRAWAL FROM BZs
    • ***Withdrawal rxn
    • (esp w/ high doses of alprazolam)

    o Can occur even at clinical doses

    o Mostly in pts taking high doses or taking BZ for > 8 months

    “Flu-like” sx:

    1. Musc cramps

    2. Diarrhea

    3. Abdominal discomfort

    4. Seizures (rare) more freq in drugs w/ shorter t1/2 (esp w/ high doses of alprazolam)

    Prevent withdrawal → slowly taper dose
  22. TCA FOR ANXIETY
    CLOMIPRAMINE -- REUPTAKE INH

    5HT > NE
  23. "Z" DRUGS FOR ANXIETY
    ZOLPIDEM (ambien)

    ZALEPLON (sonata)

    • ESZOPICLONE (lunestra)
    • ----------------------

    ACT THROUGH GABA-A RECEPTOR (BZ1 RECEPTOR AGONIST)
  24. USES FOR "Z" DRUG COMPARED TO BZs
    Less abuse potential (not addicting) → No Withdrawal Symptoms

    • No ETOH potentiation of depression
    • (DO NOT take ETOH w/ BZ).

    NOT anxiolytic.

    NOT anticonvulsant.

    No skeletal relaxation.

    Soporific (induce sleep)

    Sedative - hypnotic

    • Cause AMNESIA. (Get up & drive in the
    • middle of the night)

    • For pt w/ a hx/fam hx of barbiturate abuse who cannot sleep.
    • -------------------------

    ZOLPIDEM (ambien)

    ZALEPLON (sonata)

    ESZOPICLONE (lunestra)
  25. RAMELTEON
    HELPS WITH ONSET OF SLEEP

    melatonin (MT) receptor agonist

    Soporific

    MT-1 & MT-2 RECEPTORS OF SUPRACHIASMATIC NUC OF HYPOTHALAMUS

    • SIDE EFFECTS
    • --HEADACHE
    • --DROWSINESS
    • --DIZZYNESS

    NO ABUSE POTENTIAL
  26. FLUMAZENIL
    BZ RECEPTOR ANTAGONIST

    • Rapidly reverses effects of BZ
    • (for BZ overdose or outpatient surgery)

    LIMITED USE DUE TO SHORT HALF LIFE
  27. BUSPIRONE
    NON BZ ANTI-ANXIETY AGENT

    SLOWER ONSET OF ACTION THAN BZ (4-8 WEEKS)

    MINIMAL WITHDRAWAL POTENTIAL

    • S/E
    • -- DIZZINESS & NAUSEA
    • -- NO ALC INTERACTION

    MOA -- DIRECT ACTIVATION OF 5-HT RECEPTORS (prob 5ht-1a)

    INC K+ CONDUCTION --> HYPERPOL NEURONS
  28. DRUGS FOR GAD Tx
    • BZ
    • SSRI
    • VENLAFAXINE
    • BUSPIRONE
  29. DRUGS FOR PANIC DISORDER (PD) Tx
    • SSRI
    • BZ
    • TCA
  30. DRUGS FOR OCD Tx
    • CLOMIPRAMINE
    • SSRI

    • NEED TO INC 5-HT
    • ----------------------

    • CLOMIPRAMINE
    • --DERIVATIVE OF IMIPRAMINE
    • --POTENT 5-HT REUPTAKE INH (UNLIKE OTHER TCAs)
    • --NE REUPTAKE INH
  31. DRUGS FOR PTSD Tx
    SSRI
  32. DRUGS FOR SOCIAL ANXIETY DISORDER (SAD) Tx
    SSRI
  33. DRUGS FOR ABSENCE Szs
    ETHOSUXIMIDE

    if can't tolerate -- LAMOTRIGINE
  34. BZ WORK WELL FOR ALL GENERALIZED Sz EXCEPT ____
    TONIC-CLONIC
  35. TWO DRUGS WITH BROADEST SPECTRUM ANTI-Sz ACTIVITY
    • VALPROATE
    • LAMOTIGINE
  36. DRUGS FOR Tx OF PARTIAL Szs
    • CARBAMAZEPINE
    • PHENYTOIN
  37. SIGNS & Sx OF ABSENCE Szs
    BRIEF LOSS OF AWARENESS

    EYE BLINKING

    LIP SMACKING

    • NO LOSS OF CONSCIOUSNESS OR
    • BODY TONE

    ALMOST ALWAYS SEEN IN YOUNG CHILDREN
  38. PHENYTOIN MOA
    PROLONG Na CHANNEL INACTIVATION

    (same as phenytoin, ethotoin, carbamazepine)
  39. PHENYTOIN S/E
    1. Gingival hyperplasia

    2. Hirsutism

    3. Osteomalacia (responds to Vit D)

    • 4. Megaloblastic anemia
    • (responds to folate)

    5 Blood dyscrasias
  40. FOSPHENYTOIN MOA
    PROLONG Na CHANNEL INACTIVATION

    WATER-SOLUBLE PRODRUG OF PHENYTOIN
  41. ETHOTOIN MOA
    PROLONGS Na CHANNEL INACTIVATION

    A HYDANTOIN RELATED TO PHENYTOIN

    (same as phenytoin, ethotoin, carbamazepine)
  42. VALPROATE MOA (4)
    PROLONGS Na CHANNEL INACTIVATION

    REDUCES LOW THRESHOLD Ca CURRENTS (T currents)

    INCREASES GABA LEVELS BY STIM SYNTHETIC ENZYME GLUTAMIC ACID DECARBOXYLASE

    INHIBITS DEGRADATION OF GABA
  43. VALPROATE S/E
    HEPATOTOXICITY

    (esp when combo w/ other anti-sz meds)
  44. CARBAMAZEPINE MOA
    PROLONGS Na CHANNEL INACTIVATION

    (same as phenytoin, ethotoin, carbamazepine)
  45. CARBAMAZEPINE S/E
    1. Bone marrow depression (leukopenia)*

    2. Aplastic anemia

    3. Agranuloctosis

    4. Hyponatremia

    • 5. H2O retention
    • (serious in elderly w/ ♥ disease)
  46. LAMOTRIGINE MOA
    Prolong state of Na+ channel inactivation

    → ↓decr freq of repetv action potential
  47. TOPIRAMATE MOA (3)
    1. Prolong state of Na+ channel inactivation

    2. Blocks excitatory (glutamate) receptors

    3. Promotes realease of GABA
  48. ETHOSUXIMIDE MOA
    • Reduce low threshold Ca++ currents
    • (T currents)
  49. PHENOBARBITAL MOA
    (sz)
    INC DURATION OF CHANNEL OPENING

    BARBITUATE

    Act at distinct allosteric binding sites on GABAA receptors

    • → enhance GABA-mediated incr in Cl-
    • conductance → hyperpolarization
  50. DIAZEPAM MOA
    (sz)
    INC FREQ OF CHANNEL OPENING

    BENZODIAZEPINE

    Act at distinct allosteric binding sites on GABAA receptors

    • → enhance GABA-mediated incr in Cl-
    • conductance → hyperpolarization
  51. CLONAZEPAM MOA
    (sz)
    • INC FREQ OF CHANNEL OPENING
    • (same as diazepam)

    BENZODIAZEPINE

    Act at distinct allosteric binding sites on GABAA receptors

    • → enhance GABA-mediated incr in Cl-
    • conductance → hyperpolarization
  52. GABAPENTIN MOA
    (sz)
    PROMOTE RELEASE OF GABA

    MOA UNKNOWN
  53. STATUS EPILEPTICUS Tx
    IV LORAZEPAM or DIAZEPAM

    if not effective

    IV FOSPHENYTOIN
  54. BENZOTROPINE MOA
    (pd)
    Anticholinergic

    Muscarinic antagonist (-)

    • ↓Decr cholinergic dominance →
    • Balances dopaminergic-cholinergic systems
  55. DIPHENHYDRAMINE MOA
    (pd)
    Anticholinergic

    Antihistamine

    • Central muscarinic blockade
    • (→ anti-emetic & sedative)
  56. LEVODOPA MOA
    (pd)
    Dopaminergic Agents

    DA precursor
  57. CARBIDOPA MOA
    (pd)
    Dopaminergic Agents

    DA precursor

    ***Carbidopa is a peripheral DOPA decarboxylase inhibitor. Does NOT cross BBB.

    ALLOWS MORE L-DOPA TO ENTER BRAIN

    LEVODOPA + CARBIDOPA

    Combo benefits:

    1. Can decr dose of levodopa

    2. Effective dose of l-dopa can be reached more quickly in the initial therapy

    • 3. Avoids antagonism of therapeutic efficacy of l-dopa by pyridoxine (Vit B6).
    • --Pyridoxine (Vit B6) enhances decarboxylase.

    4. Elim n/v (a S/E of levodopa)

    5. Decr ♥ S/E (of levodopa. Cardiac arrhythmias & transient tachycardia).
  58. BROMOCRIPTINE MOA
    (pd)
    Dopaminergic Agents

    DA agonist (+)

    Directly stim DA receptors
  59. PRAMIPEXOLE MOA
    (pd)
    Dopaminergic Agents

    DA agonist (+)

    Directly stim DA receptors
  60. SELEGILINE MOA
    (pd)
    Dopaminergic Agents

    MAOB inhibitor (-)

    Elevates DA levels

    Also poss neuroprotective
  61. ENTACAPONE MOA
    (pd)
    Dopaminergic Agents

    • Catechol-O-methyltransferase inhibitor (-)
    • (comt)

    Elevates DA levels

    Also poss neuroprotective
  62. Tx OF TOURETTE'S SYNDROME
    • HALOPERIDOL -- USMLE DOC
    • --DA RECEPTOR ANTAGONIST
    • --S/E SEVERE TERDIVE DYSKINESIA

    • FOR PEDS:
    • --CLONIDINE OR GUANFACINE, a-ADREN RECEPTOR AGONIST
    • --RISPERIDONE, ATYP ANTIPSYCHOTIC
  63. CNS STIMULANTS
    • AMPHETAMINE
    • DEXTROAMPHETAMINE
    • PHENTERMINE
    • METHYLPHENIDATE
    • ATOMOXETINE
    • MODAFINIL
    • THEOPHYLLINE
    • CAFFEINE
  64. NARCOLEPSY Tx
    MODAFANIL

    RELEASES DA, NE, AND 5-HT

    NOT USED FOR ADD/ADHD
  65. DOC FOR NEONATAL APNEA
    CAFFEINE AND THEOPHYLLINE
  66. AMPHETAMINE MOA
    (cns stim)
    INDIRECT ACTING SYMPATHOMIMETICS

    RELEASE CATECHOLES FROM INTRANEURONAL STORES

    BLOCK CATECHOL REUPTAKE
  67. ACUTE TOXICITY OF AMPHETAMINES
    Esp with i.v. use

    1. Marked CNS stim

    2. Paranoid psychosis

    3. ♥ Hypertensive crisis

    4. ♥ Tachycardia

    5. ♥ Arrhythmias

    6. Hyperthermia

    7. Convulsions

    • 8. Coma
    • ---------------------------------

    CHRONIC

    Continued use → marked tolerance

    • → psych & physio dependence
    • (→ withdrawal syndrome)

    • Amphetamine psychosis
    • o Hallucination
    • o Delusions of persecution
    • o Feelings of omnipotence
  68. CHRONIC TOXICITY OF AMPHETAMINES
    Continued use → marked tolerance

    → psych & physio dependence

    (→ withdrawal syndrome)

    • Amphetamine psychosis
    • o Hallucination
    • o Delusions of persecution
    • o Feelings of omnipotence
    • ---------------------------------

    ACUTE

    • Esp with i.v. use
    • 1. Marked CNS stim
    • 2. Paranoid psychosis
    • 3. ♥ Hypertensive crisis
    • 4. ♥ Tachycardia
    • 5. ♥ Arrhythmias
    • 6. Hyperthermia
    • 7. Convulsions
    • 8. Coma
  69. PHENTERMINE
    • AMPHETAMINE DERIVATIVE
    • (cns stim)

    ANOREXIANT

    LOWER ABUSE POTENTIAL

    SCHEDULE 4

    SAME MOA AS AMPHs

    FDA --> SHORT-TERM Tx OBESITY
  70. DEXTROAMPHETAMINE
    ADHD Tx (cns stim, methylphenidate)

    RELEASE NE AND DA FROM NEURONS AND BLOCK REUPTAKE

    SCHEDULE II -- HIGH ABUSE POTENTIAL
  71. METHYLPHENIDATE
    ADHD Tx (cns stim, dextroamphetamine)

    RELEASE NE AND DA FROM NEURONS AND BLOCK REUPTAKE

    RITALIN

    SCHEDULE II -- HIGH ABUSE POTENTIAL
  72. ATOMOXETINE
    ADHD Tx (cns stim)

    SELECTIVE NE REUPTAKE INH

    DON'T GIVE WITH MOAI

    • ADVERSE
    • --HEADACHE, AGGRESSION & IRRIT IN KIDS
    • --PALPITATIONS, INSOMNIA, URINARY RET IN ADULTS

    • BLACK BOX WARNING
    • --INC RISK SUICIDAL THOUGHTS IN KIDS/ADOLESCENTS
  73. METABOLISM OF ETHANOL
    90% COMPLETELY OXIDIZED TO CO2 AND H2O BY GASTRIC AND HEPATIC ENZYMES

    • GASTRIC ADH METs 20%
    • --ADH PRODUCES ALDEHYDE WHICH IS THEN CONVERTED BY AlDH TO CO2/H2O

    HEPATIC ADH AND AlDH

    AVAILABILITY NAD+ RATE-LIMITING STEP

    • MICROSOMAL ENZYME OXIDIZING SYSTEM (MEOS)
    • --DOESN'T NEED NAD+
    • --INDUCED BY CHRONIC HIGH ETHANOL

    ZERO-ORDER KINETICS
  74. MOA OF ETHANOL
    EFFECTS OF ETHANOL ON MEMBRANES

    • ENZYMES (nonspecific)
    • --NA/K ATPase, ADENYL CYCLASE, PROT KINASE C
    • --VOLTAGE-GATED ION CHANNELS: Ca & Na

    • NEUROTRANSMITTER EFFECTS (specific)
    • --INC STIM EFFECTS AT LOW DOSES. DEC GABA AND INC DA IN NEC ACCUMBENS
    • --DEC STIM AT HIGHER DOSES. INC GABA AND INH GLUT AT NMDA RECs
  75. ACUTE AND CHRONIC ETHANOL EFFECTS ON HEPATIC SYSTEM
    ACUTE

    • PRODUCT OF ADH ENZ IS EXCESS H+
    • --TRANSIENT HYPERGLYCEMIA IF GLYC STORES, HYPOGLYCEMIA w DEC GLUCONEOGEN
    • --HYPERLACTIC ACIDEMIA
    • --HYPERURICEMIA
    • --HYPERLIPIDEMIA AND KETOACIDOSIS

    INC NADH/NAD+ RATIO

    CHRONIC

    --NADH INDUCED INH OF GLYCEROPHOS DEHYD LEADS TO INC GLYCEROPHOS AND ESTER OF FATTY ACIDS (triglycerides)

    --DEC OXIDATION OF FATTY ACIDS

    --HEPATIC ACCUM OF NEUTRAL FAT (fatty liver)
  76. PHYSIOLOGIC DEPENDENCE AND ADAPTATION TO ETHANOL
    DOWNREG OF GABA RECs

    UPREG OF GLUT NMDA RECs

    INC CENTRAL NOREPINEPHRINE ACTIVITY
  77. DRUG FOR ALCOHOL DETERENCE
    DISULFIRAM

    INH AlDH CAUSING BUILDUP OF ALDEHYDE IN BODY -->

    • ALDEHYDE SYND
    • --CUTANEOUS VASODILATION
    • --THROB HEADACHE
    • --RESP DIFFICULTIES
    • --NAUSEA
    • --COPIOUS VOM
    • --SWEATING
    • --CHEST PAIN
    • --BLURRED VISION
    • --HYPOTENSION
    • --ORTHOSTATIC SYNCOPE
    • --CONFUSION
  78. METHANOL
    WOOD ALCOHOL

    ADH --> FORMALDEHYDE + AlDH --> FORMIC ADIC

    HEADACHE, VERTIGO, VOM, DYSPNEA, BLURRED VISION

    METABOLIC ACIDOSIS

    FORMIC ACID --> DESTRUCTIVE INFLAM OF RETINAL GANGLION

    • Tx
    • --SUPPORTIVE
    • --CORRECT ACIDOSIS
    • --ETHANOL TIES UP ADH
  79. ETHYLENE GLYCOL
    ANTIFREEZE

    ADH --> GLYCOALDEHYDE + AlDH --> GLYCOLIC ACID --> --> OXALIC ACID

    CNS DEPRESSION FOLLOWED BY METABOLIC ACIDOSIS

    NEPHROTOX DUE TO OXALIC ACID CRYSTAL DEPOT IN RENAL TUBULES (crystals of ca+ oxalate found in urine)

    • Tx
    • --SUPPORTIVE
    • --CORRECT ACIDOSIS
    • --ETHANOL TIES UP ADH
  80. MUSCLE RELAXANTS THAT WORK ON NMJ
    • BOTULINUM TOX
    • CISATRACURIUM
    • VECURONIUM
    • SUCCINYLCHOLINE
  81. BOTULINUM TOXIN AS MUSCLE RELAXANT
    NMJ -- PRESYNAPTIC

    BLOCKS VESICULAR ACh RELEASE (snap prots)

    -facilitate endotracheal intubation

    -adjunct to anesthesia to dec reflex movement & relax sk muscle to get to operative site

    -facilitate mechanical ventilation
  82. CISATRACURIUM & VECURONIUM
    MUSCLE RELAXANT

    ACTS ON NMJ *postsynaptic

    COMPETITIVE NON-DEPOL BLOCKADE

    NON-HEPATIC METABOLISM

    *onset 4-6 min & duration 45-60 min

    • *contain at least 1 pos charged quaternary
    • ammonium group permitting electrostatic attraction & binding to neg charged
    • alpha subunit of ACh receptor

    • large bulky molecules bind receptor & competitively block access of ACh to
    • postjunctional receptor

    affinity for receptor but no intrinsic activity

    muscle will still respond to direct electrical stim

    may also block prejunc Na channels

    blockade can be overcome by inc ACh in synapse thru acetylcholinesterase inhibitors
  83. SUCCINYLCHOLINE
    MUSCLE RELAXANT

    NMJ -- POSTSYNAPTIC

    NON-COMPETITIVE DEPOL BLOCKADE

    *onset 1-1.5 min & duration 6-10 min

    binds to alpha subunit of ACh receptor --> transient disorganized muscle contraction

    also enters motor end plate Na channels --> flickering of ion conductance, fasiculations

    Not degraded by esterases as quickly as ACh so rec stays depol

    Phase 1 = initial blockade w/ depol. ACh inc blockade

    desensitization & membrane repol BUT as long as S occupies receptor, membrane can’t be depol again

    • Phase 2 = now competitive block that can be
    • reversed by acetylcholinesterase
    • inhibitors

    Used for brief surgical procedures

    • rapidly hydrolyzed by plasma cholinesterases
    • --> only small amt reaches NMJ

    *diffusion away from motor end plate accounts for its brief duration of action
  84. Pts WITH ATYPICAL REACTION TO SUCCINYLCHOLINE AND DRUG INTERACTIONS
    • *pts w/ atypical cholinesterases or low
    • cholinesterase exhibit a prolonged
    • blockade

    • *adverse reactions:
    • -bradycardia
    • -cardiac dysrhythmias
    • -inc intraocular, intragastric & intracranial
    • pressure
    • -myalgia & myoglobinuria

    • *should be used w/ caution in pts w/ ocular
    • disorders

    *pts w/ myasthenia gravis are resistant to effects

    *pts w/ burn injuries or trauma (esp CNS) respond w/ marked hyperkalemia (due to inc in receptors over injured site)

    *depolarizing agents drug/drug interactions:

    -any agent that lowers serum K should be used w/ caution since dosage requirements may increase
  85. DIAZEPAM AS MUSCLE RELAXANT
    ACTION IN CNS

    *interneuron (polysynaptic reflexes)

    *inc GABA mediated inh synaptic transmission to dec spinal interneuronal signaling (BZ)

    • *dec motor reflexes (spasticity)- sprains,
    • arthritis, myositis, fibrositis

    *dec muscle hypertonicity & rigidity

    • *palliative & do not alter course of
    • primary lesion

    ADVERSE

    • *sedation
    • *w/ continued use- tolerance & dependence
  86. BACLOFEN
    MUSCLE RELAXANT w ACTION IN CNS

    · Interacts w/ GABA-B receptors linked to K channels → hyperpol cells of presynaptic membrane of Glut neurons in Spinal Cord → prevent release of glut onto alpha motor neurons

    → dec efferent excitation of spastic skeletal muscle

    used for flexor spasms & sk muscle rigidity assoc w/ MS & spinal cord injury

    • ADVERSE
    • *sedation
    • *mental confusion
    • *weakness
    • *sudden withdrawal --> auditory & visual hallucinations
  87. DANTROLENE Na
    MUSCLE RELAXANT: ACTS ON SKEL MUSC (not nmj)

    INH RYANODINE REC Ca+ CHANNEL FUNCTION IN SARCO RET --> INH RELEASE OF Ca DURING EXCITATION

    • Therapeutic Uses:
    • * strokes, ms,
    • * postencephalitic athetosis, dystonia
    • · Spasticity from SC injury
    • · Malignant Hyperthermia
    • · Neuroleptic Malignant Syndrome

    • ADVERSE
    • --MUSCLE WEAKNESS & FATIGUE
  88. ATYPICAL ANTIPSYCHOTIC DRUGS
    "Atypical Compounds Quickly Restore One's Zest"

    • Aripiprazole
    • Clozapine
    • Quetiapine
    • Risperidone
    • Olanzepine
    • Ziprasidone
  89. MOA FOR ATYPICAL ANTIPSYCHOTIC DRUGS
    nigrostriatal = no effect = no EPS

    mesolimbic = block of D2-receptors = no positive symptoms

    mesocortical = enhanced D2-receptor stim = improved negative symps

    tubuloinfundibular = no effect = no hyperprolactinemia
  90. MOA FOR TYPICAL ANTIPSYCHOTIC DRUGS
    nigrostriatal tract = BLOCK DA = EPS = BAD, schlimm, malo

    mesolimbic tract = BLOCK DA to prevent positive symptoms = GOOD, gut, bueno

    mesocortical = does not help neg sympts and may even make them worse because neg sympts appear to result from a lack of D2-receptor stim = BAD

    TI = BLOCK D2 = hyperprolactinemia = gynecomastia, amenorrhea = BAD
  91. TYPICAL ANTIPSYCHOTIC DRUGS
    • CHLORPROMAZINE
    • (equal d2/5-ht block)

    • HALOPERIDOL
    • (mostly d2)
    • D2 ANTAGONISTS
  92. ARIPIPRAZOLE MOA
    ATYP ANTI-PSY

    partial agonist at D2-receptors. agonist when little DA is being released, but antagonist when excessive DA is released
  93. AUTONOMIC SIDE EFFECTS FOR TYPICAL AND ATYPICAL ANTIPSYCHOTIC DRUGS
    SAME S/E FOR BOTH

    • 1. Anti-adrenergic (mostly α1 & α2):
    • o Sedation
    • o Orthostatic hypotension

    • 2. Anti-cholinergic:
    • o Dry mouth
    • o Blurred vision
    • o Urinary retention
    • o Sinus tachycardia
    • o Constipation

    • 3. Anti-histamine (H1):
    • o Sedation
    • o Weight gain


    • Exceptions:
    • -- Risperidone & Quetiapine are NOT
    • anticholinergic
    • -- Olanzopine VERY antihistaminic
  94. GENERAL TOXICITY OF TYPICAL ANTIPSYCHOTIC DRUGS
    • 1.
    • Skin rxns
    • (photosensitivity)

    • 2.
    • Jaundice

    • 3.
    • Ventricular arrhythmias

    • 4.
    • Agranulocytosis (<0.01%)
  95. EPS FOR TYPICAL AND ATYPICAL ANTIPSYCHOTIC DRUGS
    • TYPICALS:
    • 1. Pseudoparkinsonism: rigidity, tremor, shuffling gait

    2. Acute dystonia: muscle spasms

    3. Akathisia: motor restlessness

    4. Tardive dyskinesias (TD): oral-facial dyskinesias. Late onset. Poss IRREV.

    • ATYPICALS:
    • (less incidence of eps)

    • 1. NO dystonia
    • 2. Some akathesia
    • 3. Risperidone: dose-related EPS
    • 4. NO tardive dyskinesia

    • Clozapine:
    • --DECR TD in pts on typical neuroleptics
    • --Granulocytopenia (Agranulocytosis)
  96. ATYPICAL ANTIPSYCHOTIC THAT INCREASES PROLACTIN
    RISPERIDONE
  97. KNOW GREATER WEIGHT GAIN WITH MANY OF THE ATYPICAL ANTIPSYCHOTIC DRUGS
    ESP CLOZAPINE AND OLANZAPINE

    INH 5-HT2 AND H1 --> WEIGHT GAIN

    CAN LEAD TO TYPE II DIABETES AND HYPERLIPIDEMIA
  98. ATYPICAL ANTIPSYCHOTIC DRUG THAT CAUSES AGRANULOCYTOSIS
    CLOZAPINE
  99. IF SCHIZO Pt HAS ONLY (+) Sx, Tx WITH ____. IF Pt ONLY HAS (-) Sx, Tx WITH ____. IF MIXED, Tx WITH _______.
    TYPICAL

    ATYPICAL

    ATYPICAL
  100. WHAT ARE THE (+) AND (-) Sx OF SCHIZOPHRENIA
    • (+) Symptoms:
    • Excessive ↑↑↑ dopaminergic actvy in limbic system

    • 1. Hallucinations
    • 2. Delusions
    • 3. Conceptual disorg in speech & beh
    • 4. Agitation



    • (-) Symptoms:
    • Reduced ↓↓↓ dopaminergic actvy in prefrontal cortex

    • 1. Social & emotional withdrawal
    • 2. Blunted affect
    • 3. Poverty of speech
    • 4. Anhedonia (lack of pleasure)
    • 5. Avolition (lack of initiating goal directed behavior)
  101. ADVERSE S/E OF LITHIUM
    • -diabetes insipidus
    • -hypothyroidism
    • -dysrhythmias
    • CNS:
    • FINE HAND TREMOR

    • GI:
    • N/V

    • KIDNEY:
    • TUBULAR FUNC IMPAIRMENT
    • --POLYURIA IN 50%
    • --DEC CONC ABILITY

    • DERM:
    • --PSORIASIS
    • --MACULOPAP AND ACNE

    • WEIGHT GAIN --> NONCOMPLIANCE
  102. Tx OF BIPOLAR DISEASE
    Prophylactic "sandwich" therapy is designed to eliminate both highs (mania) and lows (depression)

    valproate (for mania) + lamotrigine (for depression)

    atypical antipsychotic drug (for mania) + lamotrigine (for depression)

    aripiperazole (for mania and depression)
  103. PROCAINE
    LOCAL ANESTHETIC

    Ester- hydrolyzed by plasma cholinesterase to water soluble metabolites which are elim by kidney

    short duration of action
  104. LIDOCAINE
    LOCAL ANESTHETIC

    Amide- metabolized largely by liver to metabolites that are excreted by kidney

    Intrinsic vasodilator properties

    • Effective topically & also orally as an
    • antiarrhythmic agent

    • Hepatic dz or dec hepatic blood flow dec
    • metabolism
  105. TETRACAINE
    LOCAL ANESTHETIC

    • Ester w/ sig greater potency (16X greater)
    • compared to procaine

    Prolonged duration of action due to slow ester hydrolysis

    • NOT used in peripheral nerve blocks due to
    • prolonged duration of action & potential for toxicity
  106. MOA FOR LOCAL ANESTHETICS
    Blocking voltage-gated Na channels

    Selectively bind to channels in inactivated –closed state to prevent their change to activated-open

    Effect is greater in rapidly firing axons

    Inc in threshold for elec excitability

    Dec rate of rise of depol phase of AP

    Lengthened refractory period

    Resting membrane potential not sig affected

    Elec changes are progressive w/ an inc number of Na channels blocked due to absorption of local anesthetic

    Nerve fibers differ in susceptibility based on size & myelination --> A delta, B & C fibers are smallest & least myelinated so are blocked first --> PN sensation reduced before motor is blocked

    *preferentially block small fibers b/c distance over which fibers can passively propagate an impulse is shorter

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