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Neuro Drugs > Week 2 - Neuro Drugs > Flashcards

Week 2 - Neuro Drugs Flashcards

1
Q

oral sumatriptan

A

peak plasma concentration 1-2 hours, half life 1-3 hours, dose may be repeated in 1-2 hours, headache relief take 1-3 hours, metabolized by monoamine oxidase in the liver - for migraine

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2
Q

injectable sumatriptan

A

peak plasma concentration 12-15 min, half life 1-3 hours, dose may be repeated in 1-2 hours, headache relief takes 30 min, metabolized by monoamine oxidase in the liver - for migraine

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3
Q

nasal sumatriptan

A

peak plasma concentration of minutes to 1-2 hours, half life 1-3 hours, dose may be repeated in 1-2 hours, headache relief takes 30 min, metabolized by monoamine oxidase in the liver - for migraine

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4
Q

triptan drugs for cluster headache

A

bind to 5HT1b serotonin receptors, vasoconstriction = less pain from cluster headache

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5
Q

triptan drugs for cluster headache

A

binding to 5HT1a receptors in naple nucleus inhibit serotonergic neurons

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6
Q

sumatriptan

A

5HT1d (serotonin) receptor agonist, autoreceptor, blocks release of more serotonin

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7
Q

ergots

A

5HT1d and 5HT1b serotonin receptors, cause vasoconstriction, St. Anthony’s Fire???

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8
Q

triptans

A

cause vasoconstriction of cerebral vessels

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9
Q

buspirone

A

5HT1a serotonin receptor agonist, Tx depression and anxiety

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10
Q

TCA amitriptyline

A

blocks 5HT serotonin reuptake transporter

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11
Q

fluoxeine

A

inhibits 5HT serotonin reuptake transporter, Tx depression, anxiety, OCD

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12
Q

ondanseron

A

5HT3 serotonin receptor antagonist on vagal nerve, decreases nausea

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13
Q

good CNS drugs

A

bactericidal, small, lipophilic, low plasma protein binding, not ligand of brain efflux pumps; ex: rifampin, fluoroquinolones, 3rd gen cephalosporins; increased CNS penetration in newborns and with CNS inflammation; beta-lactam antibiotics block GABA binding –> seizures

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14
Q

ceftriaxone (3rd gen cephalosporin)

A

binds penicillin binding proteins (transpeptidases), streptococci, gram -, crosses BBB, inactivated by beta-lactamases, rx with calcium containing meds making crystals in lungs and kidneys, associated with C. diff

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15
Q

amphotericin B and Nystatin

A

antifungal, polyenes, binds ergosterol in cell membrane making holes, broad - yeast and mold, small excretion, long half life, liposomal form can cross BBB, nystatin (topical) binds cholesterol / decreases renal blood flow / destroys basement membrane, resistance - decreased ergosterol in membrane

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16
Q

Fluconazole, Itraconazole, Voriconazole, Posaconazole

A

antifungal, azoles, fluconazole and voriconazole CNS, binds P450 blocking production of ergosterol -> accumulation of lanosterol, dimorphic and yeast, oral, brain efflux pump substrate, hepatotoxic, neurotoxic, alters hormones, avoid during pregnancy, resistance altered P450 or increase brain efflux pumps, triazole - slow metabolism (low enzyme affinity)

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17
Q

Terbinafine (Lamisil)

A

antifungal, allyamines, inhibits squalene epoxidase -> accumulation of squalene, dermatophytes (skin, hair), topical

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18
Q

Flucytosine

A

antifungal, nucleic acid synthesis inhibitor, converted to 5-fluorouracil in fungi, yeast, oral, CNS, bone marrow suppression (follow pt cell count), resistance loss of enzyme or transporter, combine with amphotericin B to increase uptake

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19
Q

caspofungin

A

antifungal, fungins, echinocandins, inhibits cell wall by blocking beta-d-glucan polysaccharide synthesis, systemic Candida Albicans, IV, large molecule = no CNS, fever, rash at injection

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20
Q

pain

A

sensory and emotional with actual or potential damage

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21
Q

four steps of pain

A

initiated by stimulus, transmitted to brain, perceived as pain, produces reaction

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22
Q

local anesthetics

A

prevent transmission by reversible blocking nerve impulse locally, blocks somatic sensory / somatic motor / autonomic transmission, function returns

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23
Q

local anesthetics chemistry

A

weak bases (pKa 8-9), less ionized form if pH is higher, more ionized form if pH is lower

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24
Q

three segments of local anesthetics

A

hydrphobic lipophilic ring (potency, duration, toxicity), intermediate linkage (ester - allergic, amide, hydrophilic domain (amine - onset of action)

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25
Q

routes of local anesthetic administration

A

topical (hard to pass through skin), peripheral nerve endings, nerve trunks (blocks), spinal cord (epidural), intravenous regional (limb w/ tourniquet)

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26
Q

local anesthetics absorption

A

injected into area, if accidentally injected vascularly can be toxic, use vasoconstrictor (epinephrine) to decrease absorption = more at site / longer duration / higher doses / less toxicity; too much vasoconstrictor can delay healing with tissue edema or necrosis

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27
Q

local anesthetics distribution

A

non-ionized is lipid soluble can cross membrane, ionized charged form inside cell clogs Na channels inside neuron preventing action potential

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28
Q

infected tissue

A

lower pH = more drugs in ionized state that can’t enter cells and have effect, for infected tissue must increase dose 60x, for inflammed tissue must increase the dose 6x

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29
Q

local anesthetic metabolism

A

ester-type –> hydrolyzed in plasma, amide-type –> hydrolyzed by hepatic enzyme

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30
Q

local anesthetic mechanism of action

A

blocks neuronal sodium channels (on axons) that are open / inactivated from within cells, more frequent nerve stimulation makes anesthetic work faster because more channels are open / inactive, blocks signals before they go to brain

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31
Q

never sensitivity for local anesthetics

A

small fibers (fire more often) and myelinated fibers (smaller areas of impulse propagation) more sensitive, large fibers recover slower, effects pain / cold / warmth more then touch / deep pressure / motor

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32
Q

local anesthetics CNS adverse effects

A

tongue numbness, tinnitus, vertigo, slurred speech, muscle fasciculations, seizures

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33
Q

local anesthetics cardiovascular adverse effects

A

decreased myocardial excitability, conduction rate, and contraction force, arteriolar dilation, only if accidentally injected vascularly

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34
Q

local anesthetics hypersensitivity

A

rash to anaphylacsis, caused by ester-type

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35
Q

topical form of local anesthetic

A

EMLA (lidocaine +prilocane = lower melting point) to cross unbroken skin, eye / ear / nose / mouth, skin grafts, genital warts, venipuncture, lumbar puncture

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36
Q

regional anesthesia with local anesthetic

A

subcutaneous injection

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37
Q

intravenous block with local anesthetic

A

isolate extremity with tourniquet, inject local anesthetic IV, loss of sensory and motor

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38
Q

peripheral nerve block with local anesthetic

A

conduction block, injected into area of peripheral nerve of plexus

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39
Q

eipdural block with local anesthetic

A

injected into eipdural space at L3/4

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40
Q

spinal block with local anesthetic

A

injected into lumbar subarachnoid space

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41
Q

procaine (novocaine)

A

ester, short acting with vasoconstrictor, metabolized quickly in plasma, not good topical

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42
Q

lidocaine (xylocaine)

A

amide, widely used, metabolized in liver, OD can cause ventricular fibrillation / cardiac arrest, used for all types of local anesthesia

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43
Q

mepivacaine (carbocaine)

A

amide, like lidocaine, not good topically, little longer acting than lidocaine

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44
Q

bupivacaine (marcaine)

A

amide, long acting, potent, epidurals, surgery

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45
Q

ropivacaine (Naropin)

A

amide, long acting, less CNS / cardio toxicity than buoivacaine

46
Q

tetracaine (pontocaine)

A

ester, topical in eye, nose, throat, spinal

47
Q

cocaine

A

ester, penetrating, vasoconstrictor, used to be used for ENT - mucous membranes

48
Q

proparacaine (alcaine)

A

for cornea, antibacterial / antifungal properties

49
Q

dibucaine (nupercainal), benzocaine (americaine)

A

mucous membrane, skin

50
Q

opioids

A

affect the way pain is perceived, good for sharp pain, adverse effects –> respiratory depression / sedation / euphoria (abuse) / physcial depedence / tolerance, exogenous substance with morphine-like properties

51
Q

NSAIDs

A

good for inflammation

52
Q

opioid receptors

A

Mu, Kappa, Delta

53
Q

Mu opioid receptor

A

analgesia, resp. depression, sedation, decreased GI motility, physical dependence

54
Q

Kappa opioid receptor

A

analgesia, sedation, decreased GI motility

55
Q

Delta opioid receptor

A

modulates Mu receptor activity

56
Q

opiate

A

drug made from opium (poppy) - morphine

57
Q

opioids - morphine, methadone, oxycodone (oxycontin), heroin

A

Mu, Kappa, Delta receptor agonists

58
Q

Naloxone (narcan)

A

parenteral only, Mu, Kappa, Delta receptor antagonist

59
Q

Naltrexone (trexan, ReVia)

A

oral, longer lasting, given once ER patient wakes up, prevents alcoholic relapse, Mu, Kappa, Delta receptor antagonist

60
Q

Nalorphine (mixed agonist-antagonist)

A

opioid, alone morphine-like (K receptor agonist), with morphine reversed effect (Mu receptor antagonist), in dependent pts precipitates withdrawal (Mu receptor agonist), once pt is on Mu receptor agonist can only tapper that drug - can’t switch to weaker K receptor agonist (can only use K receptor agonist to start with)

61
Q

buprenorphine (subutex), naloxone (suboxone) - partial agonists

A

less efficacy than full agonist, used to prevent relapse in opioid addicts and for mild to moderate pain

62
Q

endogenous opioids

A

normally binds Mu, Kappa, Delta receptors, endorphins (Mu), enkephalins (pain modulation in brain), dynorphins (Kappa)

63
Q

oral opioids

A

first pass metabolism high, slower onset / action, delayed peak, longer duration, rapidly metab in liver (must elevate oral dose of morphine 6:1 parenteral), methadone only slowly metab oral

64
Q

IV opioids

A

precise, accurate dose, rapid onset, risk of adverse effects, bolus vs continuous, patient controlled

65
Q

intermuscular or subcutaneous opioids

A

relatively rapid onset and action, medium duration, subcutaneous pumps can go home with patients

66
Q

spinal opioids

A

longer duration with lower dose, acts at spinal site, no adverse reaction in brain

67
Q

rectal opioids

A

easy administration if vomiting

68
Q

buccal/subligual opioids

A

faster onset and action, avoids first pass metabolism / injection, ex: buprenorphine (subutex, suboxone) and fentanyl lollipop

69
Q

transdermal opioids

A

fentanyl (duragesic), buprenorphine (transtec_

70
Q

fentanyl deliveries

A

IV (sublimaze), transdermal (duragesic), buccal (actiq), nasal (instanyl), is 50x more potent than morphine

71
Q

lipid solubility and opioids

A

more lipid soluble = cross BBB better, creates sense of euphoria, ex: heroin

72
Q

opioid metabolites

A

longer action with impaired renal function because morphine 6-glucuronide still active, normeperidine has toxic metabolite meperidine (excitotoxic = tremor, twitch, agitation)

73
Q

ascending pain pathway

A

spinothalamic tract gray in midbrain and VML in thalamus, C or Asigma primary afferent synapses with 2nd order spinothalamic tract neuron in dorsal horn by releasing glutamate and substance P at, opioids do act directly at this synapse

74
Q

descending pain pathway

A

pain inhibiting from VML and midbrain to synapse in dorsal horn, releases ext serotonin onto inhibitory interneuron that releases inhibitory enkaphalin at original synapse, also releases inhibitory serotonin and norepinephrine at oringial synapse

75
Q

opioid action in cortex

A

decreased pain perception, altered reaction, euphoria / dysphoris, sedation

76
Q

opioid action in medulla

A

respiratory depression, coughing, nausea, vomitting

77
Q

opioid action in spinal cord

A

stimulates reflexes and spinal function

78
Q

opioid action at oculomotor nuclei

A

pinpoint pupils (slow tolerance)

79
Q

opioid action at vagus nerve

A

bradycardia, increased GI tone

80
Q

opioid action at GI tract

A

constipating, spasmogenic, increased segmental contractions without propulsion, decreases defication reflex (slow tolerance) - need bowel progam

81
Q

opioid uses

A

pre/post anesthetic med, anesthesia, post traumatic pain, cough, labor, terminal illness, diarrhea

82
Q

Naloxone (narcan)

A

opioid receptor antagonist, injection, reverses opioid OD, prevents alcohol relapse

83
Q

Naltrexone (ReVia)

A

opioid receptor antagonist, oral effective, longer acting, prevents opioid and alcohol relapse

84
Q

Alvimopan (entereq) and methylnaltrexone (relistor)

A

preipheral opioid receptor antagonist, relieves constipation from opioids, does not cause withdrawal

85
Q

opioid withdrawal

A

not life-threatening, matches degree of dependence, rhinorrhea, lacrimation, yawning, chills, gossbumps, hyperventiliation, hyperthermia, aches, vomiting, diarrhea, anxiety, hostility

86
Q

methadone (dolophine)

A

opioid receptor agonist, longer acting, may act on other pain related receptors (neuropathic), addict maintenance programs and pain treatment

87
Q

buprenorphine (naloxone = subaxone)

A

partial opioid agonist, lower abuse, must be off opioids before starting Tx or will cause withdrawal

88
Q

non-steroidal anti-inflammatory drugs

A

analgesic, antipyretic, anti-inflammatory - not a steroid

89
Q

NSAIDs action

A

inhibit COX1 (homeostatic) and COX2 (inflammatory), COX -> prostaglandins -> inflammatory prostaglandins + thromboxane (platelet aggregation) + prostacyclin (decreased platelet aggregation), aspirin irreversibly inhibits, other NSAIDs reversibly inhibit

90
Q

peripheral effects of prostaglandins

A

reduces stimulation threshold of nociceptors (sensitization)

91
Q

central effects of prostaglandins

A

basal COX-2 in neurons and glia cause early sensitization to peripheral inflammation

92
Q

NSAIDs - antipyretic

A

cytokines cause fever in hypothalamus, mediated by prostaglandins from elsewhere

93
Q

NSAIDs pharm effects (salicylates)

A

respiratory stimulation (medulla), uncouple oxidative phosphorylation, increased O2 / CO2 / metab rate (metabolic acidosis / electrolyte imbalance) –> hyperventilation –> respiratory alkalosis

94
Q

NSAIDs GI effects (salicylates)

A

epigastric distress (CTZ in medulla), bleeding –> iron def anemia, prostacyclin inhibition of gastric acid secretion gone

95
Q

NSAIDs antithrombic effects (salicyclates)

A

decreased clotting time, aspirin irreversibly inhibits thromboxane in platelets for aggregation, caution with anticoagulants, stop taking 1 week prior to surgery

96
Q

salcylate toxicity

A

tinnitus, headache, nausea / vomiting (CNS effect), sweating, thirst, hyperventilation, epigastric distress, repsiratory alkalosis followed by metabolic acidosis, fever

97
Q

Tx aspirin OD

A

reduce absorption (emesis, gastric lavage, charcoal), correct acid / base and electrolytes

98
Q

aspirin hypersensitivity

A

middle aged, hx urticaria / asthma, rhinitis / secretions / bronchoconstriction / hypotension, not IgE immune response, from accumulation of leukotrienes in lipoxygenase AA pathway, Tx epinephrine

99
Q

Reye’s syndrome

A

aspirin given during varicella infection, often fatal

100
Q

acetaminophen

A

not NSAID, analgesic and antipyretic, not anti-inflammator, most actinve in hypothalamus with no peroxidases, does not effect bleeding time / respiration / GI, increased hepatoxicity with ethanol or fasting

101
Q

Tx acetaminophen OD

A

N-acetylcysteine scavenger drug (like glutathione)

102
Q

Ibuprofen

A

NSAID, less GI prob, reversible blocks COX, increases bleeding time, good for dysmenorrhea, naproxen - long acting, oxaprozin - long half life

103
Q

Indomethacin

A

NSAID, most potent COX blocker, high toxicity, high GI prob, headache, ulcers - not used during pregnancy or with psychiatric disorders or ulcers, used for fever / OR / RA / gout

104
Q

Ketorolac

A

NSAID, IM injection or IV, strong as morphine, combined with morphine to reduce amount of morphine needed, use with suspected drug seekers

105
Q

selective COX2 inhibitors (celexicob)

A

reduces inflammation, celexicob, lumiracoxib

106
Q

meperidine

A

opioid, has exotoxic metabolite that can cause agitation and tremors, especially in people with poor kidney function

107
Q

Tx for insomnia and migraines

A

amitriptyline preferable to sumatripan due to its affinity for H1 histamine receptors and muscarinic receptors

108
Q

prophylactic Tx for N. meningitides

A

ceftriaxone

109
Q

action of acyclovir

A

turned into monophosphate by thymadine kinase, converts virus into monophosphate, stops DNA replication by replacing sugar normally bound to guanine

110
Q

triptan-mediated agonism for migraines

A

agonism of 1b serotonin receptors causes vasoconstriction, agonism of 1d serotonin receptors decreases serotonergic tone

111
Q

agonism of 1b serotonin receptors

A

cerebral vasoconstriction, for migraines

112
Q

agonism of 1d serotonin receptors

A

decreases serotonergic tone, for migraines

Neuro Drugs (4 decks)

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