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neuro pharm Flashcards

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1
Q

mechanism of action of local anesthetics

A

blockage of voltage dependent sodium channels, reduces influx Na ions, prevents depolarization and conduction of action potential
-3 nodes of ranvier blocked for good effect

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2
Q

factors that affect the local anesthesia

A
  1. Ph/pKa: affects ionization of drug, which affects action of drug (eg. in infection, pH is lowered so there is more charged drug–which can’t cross into cells)
  2. lipid solubility–affects potency
  3. protein binding–affects duration of action (inc. protein binding inc. duration of action)
  4. vasoconstriction–affects duration and potency (slows blood flow and prevents removal of anesthetic from region)
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3
Q

factors that determine the susceptibility of nerve fibers to blockade of local anesthetics

A
  • smaller fibers are blocked more easily
  • myelinated nerves are blocked more easily (only have to block nodes of ranvier)
  • peripheral fibers blocked sooner than core (exposed to more drug
  • temporal progression: autonomic lost first, then sensory, then motor
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4
Q

major toxic effects of local anesthetics

A

Neuro/CNS:

  • mlid: excitability, slurred speech, face twitching, nystagmus, loss consciousness, disorientation
  • severe: tonic-clonic seizure, generalized CNS depression

Cardio:

  • mild: hypertension, tachycardia
  • severe: hypotension, bradycardia, bradypnea, cardiac arrest

Other: sweating, metallic taste, tinnitus

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5
Q

bupivicaine toxicity:

A 
severe cardiotoxicity (hypotension, arrhythmias)
no treatment of overdose
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6
Q

cocaine toxicity

A

severe HTN, cerebral hemorrhage, MI

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7
Q

amide local anesthetics

A 
used IV
bupivicaine, ropivicaine (long duration)
lidocaine (medium duration)
prilocaine, etidocaine
metabolized in liver (liver dyfx inc. half-life)
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8
Q

ester local anesthetics

A 
used topically
-long duration:  tetracaine
-medium duration:  cocaine
-short duration:  procaine
-surface active:  **benzocaine, cocaine
metabolized by psueocholinesterases in plasma
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9
Q

ester local anesthetic toxicities

A

allergic reaction

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10
Q

local anesthetics +/- vasoconstrictor (epineprhine)

A
  • *Cocaine does not require administration of vasoconstrictor since it has intrinsic sympathomimetic activity (all over LA are vasodilators)
  • when adding vasoconstriction to LA–>enhances duration of action (but does not make it work faster)
  • don’t use in end-organ surgery (tips of fingers, ears, nose) can cause ischemia
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11
Q

therapeutic uses of local anesthetics

A

-anesthesia of mucous membranes (optho-tetracaine (ester))
-topical application before needle stick (lidocaine, prilocaine)
-regional nerve block anesthesia (patient to sick for general anesthesia)
-spinal anesthesia (shorter acting)
-epidural anesthesia (longer acting)
benefts are no systemic effects!

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12
Q

half-life of anti-epileptic drugs

A
  • pts need 24hr coverage

- drugs with half life <6h but works with BID dosing

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13
Q

AED drug levels and toxicity

A
  • toxicity is always determined by patient symptoms not byt drug levels
  • phenytoin and valproate are highly protein bound
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14
Q

which AED are renally cleared?

A
  • gabapentin, pregabalin, levetiracetam and oxcarbazepine-active metabolite are excreted renally
  • dec. dose in renal failure
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15
Q

clearance of topiramate:

A

2/3 kidney and 1/3 liver

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16
Q

which AEDs induce CYP450 enzymes?

A

phenytoin, carbamazepine, barbituates are potent inducers

  • induce metabolism of other drugs–esp. oral contraceptive (dec. effectiveness)
  • carbamazepine auto-induces it’s own metabolism
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17
Q

which AEDs are inhibitors of CYP450 enzymes?

A

-valproate (raises levels of CYP450 metabolized drugs)

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18
Q

which AED has non-linear kinetics?

A

phenytoin

  • metabolizing enzymes saturate
  • raising dose higher can result in exponential increases in serum drug levels
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19
Q

Which AEDs can be given IV and used for status epilepticus?

A

o Fos-phenytoin (requires high loading dose in this setting)
o Barbiturates (requires high loading dose in this setting)
o Lacosamide
o Valproate
o Benzodiazepines
o Levetiracetam

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20
Q

treatment prognosis for patients with idiopathic generalized epilepsy

A

good, vast majority can be made seizure-free with drugs

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21
Q

treatment prognosis for patients with symptomatic generalized epilepsy

A

rarely controllable

goal is to reduce number of grand-mal seizures and atonic seizures

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22
Q

treatment prognosis for patients with focal epilepsy?

A
  • 65% can be made seizure free with drugs
  • if focal epilepsy doesn’t respond to first 2-3 drugs tried it won’t respond at all
  • non-responsive may be candidates for resective epilepsy surgery (most commonly performed surgery is anterior temporal lobectomy for mesial temporal lobe epilepsy)
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23
Q

AEDs that work on GABAergic system

A

Benzodiazepines (midazolam, lorazepam, diazepam, clonazepam)

  • barbituates (phenobarbitol, pentobartbitol, primidone)
  • gabapentins (gabapentin, pregabalin)
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24
Q

AEDs that work as Na-channel blockers

A
  • Phenytoins (phenytoin, fos-phenytoin)
  • carbamazepine (carbamazepine, oxcarbazepine)
  • lamotrigine
  • lacosamide
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25
Q

AEDs that work as T-type Ca channel blockers

A

Ethosuximide

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26
Q

AEDs that work for every type of seizure

A

o Benzodiazepines
o Valproate
o Lamotrigine
o Zonisamide

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27
Q

AEDs that work on generalized tonic-clonic seizures

A

all except euthosixumide (absence seizures) and lacosamide (focal sz)

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28
Q

AEDs for focal seizures

A

o All except for ethosuximide (which only treats absence seizures)

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29
Q

AEDs for absence seizures

A

o Ethosuximide

o Benzodiazepines, Valproate, Lamotrigine, Zonisamide

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30
Q

AEDs for myoclonic sz

A

o Topiramate
o Levetiracetam
o Benzodiazepines, Valproate, Lamotrigine, Zonisamide

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31
Q

AEDs for atonic seizures

A

o Topiramate

o Benzodiazepines, Valproate, Lamotrigine, Zonisamide

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32
Q

benzodiazepines
MOA
specific drugs and indications

A

-MOA:Bind to an allosteric modulation site on the GABAA receptor, which is coupled to a Cl- channel → Cl- opens more frequently → hyperpolarization → inhibition

  • Midazolam: status epilepticus (IV)
  • lorazepam/diazepam: #1 for acute sz
  • clonazepam: myoclonic sz

Lose effect and have significant potential for addiction when given chronically

Flumazenil: competitive antagonist at benzodiazepine receptor (can cause sz in patients taking benzos)

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33
Q

barbituates
MOA
toxicities

A

MOA: Bind to an allosteric modulation site on the GABAA receptor (different from benzodiazepines) → Cl- remains open for longer → hyperpolarization → inhibition

toxicities: respiratory depression (when used IV), sedation, depression, cognitive impairment, hepatotoxicity and allergic rash; NOT first line drugs

  • phenobarbitol: acute or chronic sz
  • pentobarbital: refractory status epilepticus
  • primidone: GTC, focal sz, essential tremor
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34
Q

gabapentins
MOA:
specific agents

A

MOA: Binds to the α2δ subunit of presynaptic Ca2+ channel → leads to modest reduction in release of several neurotransmitters (including substance P)

gabapentin: focal sz *dose limited by gastric absorption; few side effects
pregabalin: neuropathic pain is main use; side effects are sedation and wt gain; more potent

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35
Q

Phenytoins
MOA
toxicities
specific agents

A

MOA: Voltage and frequency-dependent block of Na+ channels (if cell is depolarized and firing at high frequencies) → prevents high frequency firing, allows normal frequency firing

  • NOT useful for types of seizures other than generalized tonic-clonic (GTC) or focal seizures
  • Acute side effects include sedation, ataxia, dizziness and diplopia
  • Chronic side effects include gingival hyperplasia, hirsutism, acne, coarsening of facial features and osteomalacia (induces metabolism of vitamin D by CYP450)
  • Dangerous side effects include SLE-like syndrome, hepatotoxicity, myelosuppression
  • Many drug interactions (because of induction of CYP450 enzymes and high protein-bound state)

-phenytoin and fos-phenytoin: GTC and focal seizures

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36
Q

carbamazepine
MOA:
toxicities

A

MOA: Voltage and frequency-dependent block of Na+ channels (if cell is depolarized and firing at high frequencies) → prevents high frequency firing, allows normal frequency firing

toxicities:

  • Can worsen absence, atonic and myoclonic seizures
  • Acute side effects include ataxia, dizziness, diplopia, sedation, but NONE of the cosmetic effect associated with phenytoin (e.g. acne, hirsutism)
  • Chronic side effects include hyponatremia and leukopenia (not too big of a deal)
  • Serious side effects include rash and aplastic anemia
  • Many drug interactions (because of induction of CYP450 enzymes)

Uses: partial sz, GTC

  • carbamazepine: more toxicity; autoinduces it’s own metabolism
  • oxocarbazepine: hyponatremia is more common
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37
Q

lamotrigine
MOA:
toxicities
uses

A

MOA: Voltage and frequency-dependent block of Na+ channels (if cell is depolarized and firing at high frequencies) → prevents high frequency firing, allows normal frequency firing

Toxicities:

  • Very well tolerated
  • Most common side effects are insomnia and headaches
  • Dangerous side effects include Stevens Johnson syndrome and other rashes (prevented by titrating the drug extremely slowly)
  • Very few drug interactions and probably NOT teratogenic (so safe to give to pregnant epileptics)

Uses: all types of sz

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38
Q

lacosamide
MOA
toxicities
Uses

A

MOA: Enhances SLOW inactivation of Na+ channels, through a different molecular mechanism than lamotrigine, carbamazepine or phenytoin

  • Toxicities: dizziness when combined with other NA channel blockers
  • used for focal sz
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39
Q

ehthosuximide
MOA
Use
toxicities

A

MOA: Voltage-dependent block of “transient” T-type Ca2+ channels in the thalamus → blocks abnormal thalamic excitability → stops 3 Hz spike-and-wave activity in cortex

Use: only works on absence sz

Toxicities:

  • Mild side effects include sedation, dizziness, cognitive impairment, headache and behavioral changes
  • Severe side effects include Stevens Johnson syndrome and myelosuppression
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40
Q

valproate
MOA
Use
Toxicities

A

MOA: Has ethosuximide effects on T-type Ca2+ channels, increases brain GABA levels and may have phenytoin-like effects on Na+ channels

Uses: all types of sz

toxicities:

  • Contraindicated during pregnancy (neural tube defects)
  • Very bothersome triad of side effects includes weight gain, hair loss, tremor
  • Mild side effects include GI upset, sedation, cognitive problems
  • Severe side effects include hepatic failure (infants), pancreatitis, thrombocytopenia and hyperammonemia
  • Can rarely cause a reversible form of polycystic ovary syndrome
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41
Q

topiramate
MOA
Use
toxicity

A

MOA: Inhibits voltage-sensitive Ca2+ channels and Na+ channels, has benzodiazepine-like effects on GABA-induced Cl- currents, inhibits carbonic anhydrase and Glu-receptors

Use: all sz except absence

toxicities:

  • Very safe drug with few drug interactions
  • Milder side effects include sedation, paresthesias, cognitive impairment (especially aphasia), weight loss
  • More notable effect is kidney stones (1% of patients due to inhibition of carbonic anhydrase)
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42
Q

zonisamide
MOA
Use
toxicities

A

MOA; Phenytoin-like effect on Na+-channels, ethosuximide-like effect on T-type Ca2+ channels, inhibits carbonic anhydrase

Use: all sz types

toxicities:

  • NO drug interactions
  • Milder side effects include sedation, dizziness, cognitive impairment, decreased appetite, weight loss
  • More severe side effects include rashes, kidney stones (1% of patients due to inhibition of carbonic anhydrase)
  • Extremely rare side effects include agranulocytosis, oligohydrosis with hyperthermia
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43
Q

levetiracem
MOA
Use
Other

A

MOA: Binds very strongly and specifically to the synaptic vesicle protein SV2A (but the precise mechanism of action is not yet known)

Use: partial sz, myoclonic sz

Notes:

  • Faster onset then most antiepileptic drugs
  • Appears completely safe (so far)
  • Mild side effects include sedation, irritability and psychosis (1%)
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44
Q

Which drugs could I use to treat a productive cough? MOA? AE?

A

expectorant: guaifenesin

MOA-Increase secretion of mucus and thin out mucus→facilitates upward expulsion of sputum

AE-GI (N/V, irritation to gastric mucosa)

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45
Q

which drugs could I use to treat a nonproductive cough?

A

central acting-Codeine/hydrocone

central acting-dextromethorphan (promethazine)

peripheral acting-benzonatate

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46
Q

which drug could I use to treat a patient with thick bronchial secretions due to cystic fibrosis? MOA? AE?

A

Mucolytic: N-acteylcysteine (delivered by nebulizer or directly w/ bronchoscope)

Breakdown of mucopolysaccharides in bronchial secretions to smaller components

smells and tastes bad

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47
Q

what demulcents?

A

Sticky substances that protect lining of respiratory tract from irritation

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48
Q

Codeine–MOA, Uses, AE

A

-MOA: reduce excitability of the cough center in the medulla

AE: respiratory depression (worse in small kids, pts w/ COPD, head injury, inc. intracranial pressure), constipation, miosis, sedation/drowsiness, addiction potential

-used in non-productive cough

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49
Q

dextromethorphan (promethazine)–MOA, Uses, AE

A
  • MOA: : reduce excitability of the cough center in the medulla
  • Uses: non-productive cough
  • AE: fewer side effects than codeine! (At high doses—confusion, excitation, nervousness, irritability, nausea, dizziness, cardiac arrhythmias, respiratory depression)
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50
Q

benzonatate–MOA, uses, AE

A
  • MOA: local anesthetic affect on stretch receptors in respiratory passages→reduces afferet input to cough center
  • Uses: non-productive cough
  • AE: hypersensitivity (bronchospasm, laryngospasm, CV collapse; contraindicated in allergic to procaine/tetracaine
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51
Q

Which drugs can be used to treat cytotoxic drug induced emesis? Which ones are most effective?

A

most effective: 5-HT3 receptor antagonists (odansetron), centrally acting dopamine receptor antagonists (metoclopramide)

  • neurokinin receptor antagonist (aprepitant): delayed vomiting
  • also cannabinoid receptor antagonist (dronabinol)
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52
Q

Which drugs can be used to treat motion sickness?

A

muscarinic receptor antagonists (scopolamine)

histamine-1 receptor antagonist (meclizine)

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53
Q

Which anti-emetics are dopamine antagonists? What is the MOA? What are the AEs?

A
  • chlorpromazine
  • prochlorperazine
  • thiethylperazine
  • droperidol

MOA: Depress excitability of CTZ by blocking dopamine (D2) receptors and transmission

AE:

  • Sedation
  • Extrapyramidal sx: dystonia, torticollis, oculogyric crises, akathisia, gait disturbances
  • allergic
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54
Q

trimethobenzamide–MOA, Uses, AEs?

A

MOA: anti-emetic (depress CTZ by blocking dopamine D2-R); antitussive (suppress laryngeal and pharyngeal reflexes to cough center in medulla)

Use: post-op n/v; post-op coughing

AE: CNS depression, extrapyramidal, Reye’s syndrome in children

55
Q

metoclopramide–MOA, uses, AEs?

A

MOA: prokinetic (stimulates motility of upper GI tract) and anti-emetic (antagonist at D2-R in CTZ and GI tract)

Uses: symptomatic GERD, diabetic gastric stasis, radiologic exam of GI tract, n/v assoc. chemo/radiation therapy

AE: CNS depression, extrapyramidal

56
Q

scopolamine–MOA, uses, AEs?

A

MOA: Blocks Ach (M) receptors in CTZ, vestibular nuclei, and GI tract

Uses: motion sickness

AE: Sedation, blurred vision (crosses BBB), reduced GI and bladder tone

57
Q

dimenhydrinate–MOA, uses, AEs?

A

MOA: antihistamine–Block Ach (M) receptors in CTZ and vestibular nuclei

Uses: Motion sickness, mild n/v

AE: sedation, blurred vision, dry mouth

58
Q

hydroxyzine/meclizine–MOA, use, AE?

A

MOA: Block Ach (M) receptors in CTZ and vestibular nuclei

Use: vertigo, motion sickness

AE: controversial in pregnancy

59
Q

odanestron

A

MOA: Blocks serotonin receptor 5-HT3 in GI tract and CTZ

Use: cytotoxic drug induced emesis

AE:

  • metabolized by P450 enzymes but do not induce or inhibit
  • headache, diarrhea, constipation, asthenia, phlebitis
60
Q

Which anti-emetic is a potent CYP3A4 inhibitor?

A

aprepitant (neurokinin-1 receptor antagonist)

61
Q

competitively inhibits tyrosine hydroxylase (the enzyme that converts tyrosine to L-DOPA)

A

competitively inhibits tyrosine hydroxylase (the enzyme that converts tyrosine to L-DOPA)

62
Q

carbidopa

A

inhibits peripheral DOPA decarboxylase (increasing the bioavailability and reducing peripheral side effects of dopamine

63
Q

reserpine and tetrabenazine

A

deplete brain dopamine by inhibiting vesicular storage → accelerates presynaptic degradation

64
Q

amphetamine and cocaine

A

inhibit reuptake of dopamine and norepinephrine by dopamine transporter (DAT)

65
Q

selegiline and rasagline

A

inhibit monoamine oxidase (MOA) which converts DA to homovanillic acid

66
Q

tolcapone and entacapone

A

inhibit peripheral and CNS catechol-O-methyltransferase (COMT) which converts DA–>HVA

67
Q

What is the name of the major motor pathway of dopamine?

A

nigrostriatal pathway

68
Q

What is the major inhibitor NT of the basal ganglia

A

GABA

69
Q

what is the major excitatory NT in the CNS

A

glutamate

70
Q

direct pathway of basal ganglia

A
  • mediated by dopamine receptor D1

- “accelerator” overactivity of direct pathway leads to hyperkinetic movment d/o

71
Q

indirect pathway of basal ganglia

A
  • mediated by dopamine receptor D2

- “brake” overactivity of indirect pathway leads to hypokinetic movement d/o

72
Q

how does dopamine released from the substantia nigra pars compacta mediate movement

A
  • Dopamine activates D1 receptors in the striatum, thereby activating the direct pathway
  • Dopamine inhibits D2 receptors in the striatum, thereby inhibiting the indirect pathway
73
Q

what is the basis of huntington’s disease

A

• Huntington’s disease results in the loss of GABAergic neurons in the INDIRECT pathway of the striatum
o Balance shifts→overactivity of direct pathway→hyperkinetic movements

74
Q

what is the basis of hemiballismus?

A

• Hemiballismus is a dramatic flailing movement of one arm and/or leg caused by lesions of the contralateral subthalamic nucleus
o Balance shifts→overactivity of direct pathway→hyperkinetic movements

75
Q

what is the basis of Parkinson’s disease?

A

• Parkinson’s disease is caused by the progressive loss of dopaminergic neurons in the Substantia nigra pars compacta (SNpc)
o Relative overactivity of indirect pathway→hypokinetic movment d/o

76
Q

levo-dopa + carbidopa

A

MOA: replaces dopamine

  • very effective
  • target sx: tremor, rigidity, bradykinesea
  • side effects: nausea, orthostatic HTN, hallucinations
  • carbidopa reduces peripheral effects/side effects
77
Q

Anticholinergics: Trihexyphenidyl and

Benztropine in the treatment of PD

A
  • MOA: block central muscarinic receptors
  • mild efficacy
  • side effects: dry mouth, blurry vision, urinary retention, confusion, sedation
  • use imited by mental side effects in the elderly
78
Q

Ergot D3 DA Agonists: Bromocriptine and Pergolide in treatment of PD

A
  • MOA: directly stimulate dopamine receptors
  • moderate efficacy
  • side effects: peptic ulcer disease, vasoconstriciton, pulmonary fibrosis, valve disease
79
Q

Non-Ergot DA Agonists: Pramipexole and Ropinirole in the treatment of PD

A
  • moderate efficacy
  • MOA: directly stimulate dopamine receptors
  • side effects: compulsive behaviors, somnolence, hallucinations, leg edema
80
Q

COMT Inhibitors: Entacapone and Tolcapone in the treatment of PD

A
  • inhibit dopamine breakdown by COMT
  • used as adjunct only to improve levodopa bioavailability
  • side effects: orange urine, diarrhea, hepatitis
  • tolcapone assoc/ w/ fatal hepatitis
81
Q

MAO-B Inhibitors: Selegiline and Rasagiline in the treatment of PD

A

MOA: inhibit breakdown of dopamine by MAO

  • mild effecacy
  • side effects: tyramine effect, serotonin syndrome, hypertensive crisis
82
Q

amantadine in the treatment of PD

A
  • antiviral
  • mild efficacy
  • MOA: dopaminergic, anticholinergic, NMDA-antagonist
  • side effects: peripheral edema, hallucinations
83
Q

motor complications of levodopa treatment

A
  1. Wearing-off of the medication effect over several hours
  2. Delayed onset of the medication effect
  3. Random dose failures may occur
  4. Sudden ON-OFF, when medications stop working or kick-in abruptly
  5. Levodopa-induced dyskinesia, the overexpression of movement due to excess dopamine and receptor hypersensitvity.
84
Q

Dopa responsive dystonia

A
  • rare, childhood disease
  • Caused by mutations in the GTP cyclohydrolase gene (GCH1) on chromosome 14
  • Results in lack of cofactor necessary for tyrosine hydroxylase synthesis
  • clinical: Dystonia of the lower limbs, Diurnal variation, Parkinsonism, Hyperreflexia
    tx: levodopa (excellent response; no dyskinesias)
85
Q

which antipsychotic is least likely to cause extrapyramidal syndromes

A

clozapine

86
Q

acute dystonia

A

hypokinetic extrapyramidal sx
• Presents with sustained abnormal posture, whole body arching, oculogyric crisis, sudden tongue protrusion, jaw clenching
• Occurs within hours to days of using an antipsychotic medication (dopamine receptor blockers)
• More common in young males and after parenteral administration of high dose dopamine receptor blockers
• Treatment: diphenhydramine (antihistamine) or benztropine (anticholinergic)

87
Q

drug-induced parkinsonism

A

-hypokinetic extrapyramidal syndrome
-• Presents with features almost indistinguishable from Parkinson’s disease (tremor, rigidity, akinesia, postural instability)
• Occurs within first several months of treatment
• More common in elderly female patients
• Treatment: stop the typical antipsychotic and switch to an atypical antipsychotic (+/- anticholinergics)

88
Q

tardive dyskinesia

A

-hyperkinetic extrapyramidal syndrome
-• Presents with choreiform movements of the lower face including grimacing, tongue protrusion, lip smacking
• Occurs in 15% of patients chronic treatment with dopamine receptor blockers (longer use correlates with higher risk)
• May also occur with abrupt reduction or withdrawal of dopamine receptor blockers (withdrawal-emergent syndrome)
• Treatment: stop the typical antipsychotic and switch to clozapine (an atypical that does not cause extrapyramidal syndromes

89
Q

neuroleptic malignant syndrome

A

extrapyramidal syndrome

  • Triad: mental status change, muscle rigidity, autonomic dysfx
  • risk factors: Dehydration; Young males; Sudden increase in antipsychotic dose; Previous reaction to an antipsychotic
Treatment:
•	Discontinue antipsychotic drug
•	Dantrolene (for muscle rigidity, hyperthermia, rhabdomyolysis)
•	Bromocriptine (dopamine agonist)
•	Hydration
•	Benzodiazepines to reverse catatonia
90
Q

dystonia

A

: Condition of involuntary sustained muscle contractions that produces twisting or “torsion” across a joint

  • general treat w/ anticholinergics
  • focal treat with botox
91
Q

botulinum toxin

A

• MOA: inhibits release of acetylcholine at the neuromuscular junction
o Binds to the presynaptic terminal via the heavy chain
o The light chain then disrupts acetylcholine release by interfering with vesicular membrane potentials
• Efficacy: selective weakening of muscles allows improved posture and function of the dystonic muscle(s)
• FDA indications
o Cervical dystonia
o Blepharospasm
o Hemifacial spasm (and other facial dyskinesias)

92
Q

principle of acute treatment of migraine

A

o Treat early in attack
o Use correct dose and formulation
o Use a maximum of 2-3 days per week

93
Q

what is a rebound headache?

A

refractory chronic daily headache due to overuse of acute migraine meds

94
Q

What is the MOA and physiologic effects of ergotamines and triptans?

A

• MOA: 5-HT1B/D receptor agonists

• Physiologic Effects
o Constrict cerebral vessels
o Block neurogenic inflammation
o Block pain transmission in the trigeminal nerve

95
Q

Dihydroergotamine

A

-used for acute treatment of migraine
• Non-selective 5-HT1 agonist
• Fewer side effects than ergotamine (less nausea, vomiting, leg cramps)
• Low rate of headache recurrence
• Rarely associated with rebound headaches
• Disadvantage is that the delivery methods are via injection (IV, IM, SC) or nasal spray (lower efficacy)

96
Q

sumatriptan

A

-used for acute treatment of migraine
• Effective in migraine with and without aura and
• Work well early and late in the attack
• Synergistic with NSAIDs

• Second dose is NOT effective in the same attack if the initial dose failed
• NOT indicated for basilar or hemiplegic migraine
• Minor adverse effects are common
(Chest tightness, Paresthesias and atypical sensations)
• Severe adverse effects are rare
• Triptans are more likely than other drugs to increase migraine frequency

97
Q

principles of preventive migrain therapy

A

o Start with low dose and increase slowly
o Need adequate trial (1-2 months)
o Evaluate therapy (use calendar, taper or even discontinue if headaches are well controlled)
o Avoid pregnancy (ascertain birth control use, since some of these drugs are teratogens)

98
Q

goals of preventive migraine therapy

A

o Reduce attack frequency, severity and duration
o Improve responsiveness to acute medications
o Reduce costs
o Prevent disease progression (perhaps)

99
Q

1st line drugs for preventive migraine therapy

A
  • Amitriptyline (tricyclic antidepressant)
  • Divalproex or topiramate (anticonvulsant)
  • Propranolol, timolol (beta-blocker)
100
Q

which migraine drug is ideal for pregnant women

A

acetominophen

101
Q

mu-opioid receptor agonists and antagnoists?

What are the effects of activating the mu-opioid receptor?

A

agonists: b-endorphin, morphine
antagonist: naloxone

Effects:
•	Supraspinal analgesia
•	Sedation
•	Euphoria
•	Nausea-vomiting
•	Miosis
•	Respiratory depression
•	Tolerance
•	Physical dependence
•	Decreased GI motility and constipation
102
Q

k-opioid receptor agonists and antagonists? What are the effects of activating this receptor?

A

agonists: dynorphin, pentazocine
antagonist: naloxone (high dose)

effects:
•	Visceral analgesia (peripheral effect)
•	Dysphoria (central effect)
•	Spinal analgesia
•	Sedation
•	Diuresis
•	Psychomimetic effects
•	Hallucinations
103
Q

delta-opioid receptor agonist and antagonist?

what are the effects of activating this receptor?

A

agonist: enkephalin
antagonist: naloxone (high dose)

Effects:
• Spinal analgesia
• Supraspinal analgesia

104
Q

What are the side effects of opioids?

A
  • RESPIRATORY DEPRESSION (most dangerous, dec. sensitivity of central CO2 sensing receptors)
  • CONSTIPATION (dose-limiting, tolerance does not develop over time, give stool softener)
  • seizures (meperidine)
  • miosis (common sign of overdose)
  • bradycardia
  • antitussive (cough suppressant)
  • pruritis
105
Q

metabolism and excretion of opioids

A

metabolism is primarily hepatic

excretion is primarily renal

106
Q

opoid hyperalgesia

A

• Opioid exposure may produce progressive and lasting reductions of pain thresholds, resulting in paradoxical pain with opioids

107
Q

paregoric

A

opioid agonist used for intestinal colic

108
Q

morphine

A

opioid agonist used for moderate-severe pain

109
Q

codeine

A

opioid agonist used as 1) antitussive for cough or 2) analgesic for mild-to-moderate pain

toxicity: seizures

110
Q

hydromorphone

A

opioid agonist used as analgesic for moderate-to-severe pain

111
Q

apomorphine

A

opioid agonist used for induction of emesis

potent stimulator of CTZ and dopamine agonist also

112
Q

oxycodone

A

opioid agonist used as analgesic for moderate to severe pain

commonly combined with aspirin or acetominophen

113
Q

merperidine

A

opioid agnoist with limited clinical use

toxicity: seizures (interact with MAOIs)
contraindications: renal impairment or seizure d/o

114
Q

fentanyl patch

A

opioid agonist used to treat chronic pain in patients already on opioids
-contraindicated in opioid naive patients

115
Q

loperamide

A

opioid agonist used to treat diarrhea

only acts peripherally, has no action in CNS

116
Q

methadone

A

opioid agonist used for analgesia, opioid dependance (cure and maintenance)

117
Q

mixed agonist-antagonist opioids

A
  • Pentazocine
  • Nalbuphine
  • Butorphanol

used to treat mu-opioid side effects (itching, nausea)

pharm:
• Alone, they are partial agonists at µ-receptors (with limited capacity for activation – ceiling effect)
• In the presence of full agonists, they act as antagonists at µ-receptors
• At peripheral κ-receptors, they relieve visceral pain
• At central κ-receptors, they cause dysphoria
• NOT generally used for chronic pain
• Can precipitate withdrawal in physically-dependent patients

118
Q

antagonist opioids

A
  • Naloxone (IV, short acting)
  • Naltrexone (oral, long acting)

o Indications: Reversal of µ-opioid side effects

o Cautions
• Titrate slowly in order to prevent acute reversal of analgesia
• Acute reversal of opioid analgesia can precipitate acute withdrawal or other things (e.g. hypertension, pulmonary edema, MI)

119
Q

opioid partial agonists

A
  • Buprenorphine
  • Suboxone (buprenorphine + naloxone)

o Indications
• Prevention of withdrawal in opioid-dependent patients
• Treatment of opioid addiction and dependence

o Pharmacology
• Highest binding affinity for µ-receptor of any known opioid, so it will displace any other opioid
• Only partial stimulation of µ-receptor (enough to relieve the craving, but does not give opioid “benefit”)
• Long half-life
• Limited analgesic use

o Cautions
• Opioids will not relieve pain while this drug is in the system, so discontinue it prior to any surgery or pain-causing procedure

120
Q

selective peripheral mu-opiod receptor antagonists

A

o Agents
• Methylnaltrexone
• Alvimopan

o Indications
• Opioid-induce constipation
• Bowel dysfunction following surgery (ileus)

o Pharmacology
• Selectively antagonize peripheral µ-opioid receptors

121
Q

when using inhaled anesthetic agents, minimum alveolar concentration measures what?

A
  • Measures potency

* Steady state alveolar concentration necessary for 50% of the population to not react to a surgical stimulus

122
Q

which factors can affect the uptake of an inhaled agent?

A
  • Inspired concentration: higher concentration=more rapid uptake
  • Alveolar ventilation: greater ventilation=more rapid uptake
  • Solubility of agent: greater solubility=slower uptake
  • Cardiac output: greater cardiac output=slower uptake
  • Alveolar to venous anesthetic concentration gradient
123
Q

halothane

A

o 20% metabolized (rest is exhaled)
o massive hepatic necrosis (halothane hepatitis)—unlikely to occur in kids
o agent of choice in children

124
Q

enflurane

A

o Metabolized less than halothane

o Free F- is released, can cause renal failure at high levels (but only if patient has preexisting renal disease)

125
Q

sevoflurane

A

o Same as enflurane

o Can degrade in anesthesia machine’s soda lime

126
Q

desflurane

A

o Minimal biotransformation in the liver

127
Q

cardiovascular effects of halogenated hydrocarbons

A

All volatile anesthetics depress myocardial contractility
o All increase HR except halothane (dec. HR) and sevoflurane (no effect on HR)
o All decrease mean arterial pressure
o All reduce cardiac output except: isoflurane (no effect) and sevoflurane (no effect)
o Halthonae sensitizes the myocardium to exogenous catecholamines

128
Q

respiratory effects of halogenated hydrocarbons

A

o Decrease bronchial smooth muscle tone (good in asthmatic patients)
o Decrease pulmonary vascular resistance
o Inhibit hypoxic vasoconstriction
o Depress mucociliary function
o Reduce tidal volume and increase respiratory frequency
o Block ventilatory response to hypoxia
o Decrease response of CO2 and reduce slope of CO2 response curve

129
Q

nitrous oxide as a general anesthetic

A

o not very potent so can’t be used as a general anesthetic by itself, so usually used in combination with IV narcotics, barbituates, and muscle relaxant to produce general anesthesia
o not metabolized so termination of action is entirely through respiratory system
o irreversibly oxidizes B12 so if given in high concentration for long enough, can cause bone marrow depression, neuropathy
o minimal CV side effects
o should not be used when there are closed air cavities (pneumothorax)

130
Q

ketamine

A

o Given IV general anesthetic

o Metabolism by oxidation and demethylation

o CNS effects:
• Muscarinic antagonist
• Opiate agonist
• Blocks NMDA receptors (assoc. w/ pain “windup”)
• “dissociation anesthesia”: patients are pain free and unconscious but may have random movements and nystagmus
• increases intracranial pressure
• produces emergence rxns and hallucinations

o CV effects:
• Direct myocardial depressant
• In patients with normal sympathetic NS, it causes inc. blood pressure and HR

o Respiratory effects:
• Normal response to CO2 (unlike halogenated hydrocarbons)
• Bronchial smooth muscle relaxant
• Pharyngeal and laryngeal reflex pressure and may be hyperactive

131
Q

propofol

A 
IV general anesthetic
o	Depresses BP and respiration
o	More rapid and “clear” (no hangover) recovery than barbituates
o	Less N/V than barbituates
o	Given as continuous infusion
132
Q

etomidate

A

o Non-barbituate hypnotic
o Minimal CV effects
o Causes reversible adrenocortical suppression after single bolus dose

133
Q

malignant hyperthermia

A

Mutation in calcium channel receptor, ryanidine receptor 1 (RyR1)
•Tachycardia, hyperthermia, hypercarbia, muscle rigidity, severe metabolic acidosis, death
•Treatment: dantrolene sodium (muscle relaxant)

neuro.psych.optho (8 decks)

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