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Unit 1 Pharm III > MOAs > Flashcards

MOAs Flashcards

1
Q

Alcohol MOA

A

Binds GABAa receptor→ increased Cl- influx→ enhanced inhibitor GABA transmission

Synergistic with drugs that bind GABA at different sites: barbiturates, benzos

Increases dopamine in mesolimbic pathway (addiction)

Inhibits effect of glutamate on NMDA receptor

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2
Q

Naltrexone MOA for alcohol abuse

A

Blocks ability of alcohol to stimulate the reward pathway

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3
Q

Acamprosate MOA

A

Structural analogue of GABA→ restores disturbed GABA/glutamate balance (alcoholism) to normal

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4
Q

Disulfiram MOA

A

Inhibits aldehyde dehydrogenase→ aldehyde build up

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5
Q

Normal alcohol metabolism

A

Alcohol→ alcohol dehydrogenase (ADH)→ acetaldehyde→ aldehyde dehydrogenase (ALDH) oxidizes using NAD+→ acetate

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6
Q

Asians + Alcohol

A

lacking ALDH (aldehyde dehydrogenase)

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7
Q

Women + Alcohol

A

Lower levels of ADH (alcohol dehydrogenase)

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8
Q

Topiramate mechanism for alcoholism

A

Not understood, decreases craving and increases abstinence

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9
Q

Fomepizole MOA

A

alcohol dehydrogenase inhibitor

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10
Q

Barbiturates MOA

A

Bind GABA→ Cl- influx→ inhibitory

Produce inhibition independent of GABA: no ceiling effect

Hypnosis (CNS depressant)

Euphora→ abused

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11
Q

Benzodiazepines MOA

A

Specific site on GABAa receptor→ prolonged action

GABA dependent effects→ Ceiling effect

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12
Q

Flumazenil MOA

A

Benzodiazepine Antagonist→ competes for GABA receptor→ reverses effect of benzos and “z-drugs”

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13
Q

Z drugs MOA

A

Bind to BZ1 subtype of GABA receptor→ increased GABA-mediated inhibition

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14
Q

Suvorexant MOA

A

Antagonist at orexin receptors

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15
Q

Ramelteon MOA

A

Melatonin analogue

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16
Q

Chloral hydrate MOA

A

Converted to trichloroethanol→ similar effect as barbiturates on GABAa receptor→ sedation

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17
Q

Buspirone MOA

A

Partial agonist at postsynaptic 5-HT1a receptor (serotonin) → inhibition of cell signaling

Full agonist for presynaptic 5-HT1a receptor→ decreased release of 5-HT

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18
Q

Glutamate receptors are called

A

NMDA

also AMPA but never discussed

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19
Q

Glutamate causes seizures….

A

By activating NMDA receptors

Goal: decrease glutamate

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20
Q

GABA causes seizures

A

when GABA receptors are blocked

Goal: increase GABA

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21
Q

Phenytoin / Fosphenytoin MOA

A

Prolong inactivation of Na+ channels→ decreased glutamate activity

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22
Q

Carbamazepine MOA

A

Blocks Na+ channels→ decreased glutamate activity

Inhibits NE release + reuptake→ +/- potentiates GABA

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23
Q

Lamotrigine MOA

A

Inactivation of Na+ channels→ decreased glutamate activity

+/- inhibition of Ca++ channels

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24
Q

Topiramate MOA

A 
Blocks Na+ channels→ decreased glutamate activity
Some activity at Ca++ channels
Potentiates GABA receptors
Inhibits glutamate receptor (NMDA)
\+/- Inhibits spread of seizures
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25
Q

Levetiracetam MOA

A

Binds SV2A→ apparent decrease in glutamate and increase in GABA release

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26
Q

Gabapentin MOA

A 
GABA analog (but doesn’t act on receptor)
May augment GABA release
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27
Q

Pregabalin MOA

A

GABA analog→ binds to alpha-2-delta subunit of voltage-gated Ca++ channels inhibiting excitatory neurotransmitter release

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28
Q

Tiagabine MOA

A

Inhibits reuptake of GABA (GAT-1) → enhances GABA activity

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29
Q

Vigabatrin MOA

A

Irreversibly inhibits GABA transaminase (GABA-T) → decreased metabolism→ increased activity

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30
Q

Ethosuximide MOA

A

Inhibits low threshold (type T) Ca++ channels→ inhibits pacemaker for rhythmic cortical damage

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31
Q

Valproic acid MOA

A

Blocks Ca++ channels and Na+ channels

+/- Enhances GABA activity

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32
Q

Synaptic vesicular protein (SV2A)

A

Binding SV2A increases GABA and decreases excitatory glutamate activity

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33
Q

Some glutamate targets that can be blocked

A

SV2A
Voltage-gated Na+ channels
Thalamic voltage gated-Ca++ channels

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34
Q

Increase GABA by….

A

Block GABA reuptake (tiagabine)

Inhibit GABA metabolism (vigabatrin)

Stimulate GABAa receptors (benzos, barbs)

Bind synaptic vesicular protein SV2A (levetiracetam)

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35
Q

Drugs that block Na+ Channels

A

Phenytoin
Lamotrigine
Carbamazepine
Valproate

Can cause SJS/TENS, screen for HLAB1502

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36
Q

Local Anesthetics MOA

A

Block Na+ channels and inhibit neuronal firing
Increase threshold for excitation and impulse conduction slows.

Binding increases→ rate of action potential declines→ complete block

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37
Q

A faster local anesthetic is

A

Smaller, lipophilic

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38
Q

A longer acting local anesthetic….

A

Binds more extensively to proteins

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39
Q

Elevated Ca++ makes local anesthetics

A

Less effective

Elevated Ca++ → hyperpolarize membrane → channels in resting state

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40
Q

Elevated K+ make local anesthetics

A

More effective

Elevated K+ → depolarizes membrane→ more channels inactivated state

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41
Q

Local anesthetics have a high affinity for the Na+ channel in the _______ states

A

Activated/open state

Inactivated state

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42
Q

Local anesthetics have a low affinity for the Na+ channel in the _______ state

A

Resting/closed state

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43
Q

Esters cause allergic reactions by

A

the P-aminobenzoic acid (PABA) metabolite

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44
Q

A myelinated neuron is ______ to local anesthetics than an unmyelinated neuron

A

Less sensitive

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45
Q

A myelinated neuron is ______ to local anesthetics than an unmyelinated neuron

A

Less sensitive

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46
Q

Metabolism of ester local anesthetics

A

rapidly metabolized by plasma butyrylcholinesterase

Mutations affect metabolism

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47
Q

Metabolism of amide local anesthetics

A

CYP450s

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48
Q

Bupivacaine + Cardio MOA

A

more lipophilic: increased binding to cardiac Na+ channels, slower dissociative times
More toxic

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49
Q

Cardiac effects of local anesthetics

A

Inhibition of Na+ and Ca++ channels→ arrhythmias, vasodilation hypotension

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50
Q

Why won’t sulfas work if you’re taking procaine?

A

PABA metabolite inhibits sulfonamide action

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51
Q

Benzocaine MOA

A

Pka 3.5→ lipophilic, always non-ionized at physiological pH→ readily transported through membrane, minimal binding to Na+ channel
topical OTC only

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52
Q

Secondary mechanism of cocaine

A

Inhibits Na+ channels (local anesthetic)

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53
Q

Primary mechanism of cocaine

A

increasing dopamine in CNS and periphery

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54
Q

What does a lipid sink do?

A

IV lipids pull lipophilic local anesthetics out of cardiac tissue in toxicity

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55
Q

Ropivacaine is…

A

S-enantiomer of bupivacaine→ less lipid soluble and cleared more rapidly

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56
Q

Etidocaine effects

A

Inverse differential block→ causes motor block before or without sensory block

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57
Q

Articaine is….

A

an Amide with an additional ester→ metabolism by plasma esterases→ decreases half life and systemic toxicity

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58
Q

Baclofen MOA

A

Agonist at GABAb receptors (Gi/o protein coupled, metabotropic)

  1. Open K+ channels→ hyper-polarization
  2. Presynaptic inhibition of Ca++ influx→ decreased transmitter release
  3. Inhibits adenylyl cyclase→ decrease cAMP→ decreased release of excitatory transmitters in brain and spinal cord
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59
Q

Tizanidine MOA

A

Alpha2 receptor agonist:
Pre and post-synaptic inhibition of spinal cord synaptic activity→ decreased glutamate→ decreased muscle spasticity

Inhibits pain transmission in dorsal horn

60
Q

Dantrolene MOA

A

Blocking ryanodine receptor 1 (RyR1) channel→ inhibits Ca++ release from sarcoplasmic reticulum→ interferes with excitation-contraction coupling of actin and myosin in skeletal muscle fiber

61
Q

Botulinum Toxin MOA

A

Inhibits SNAP-25 protein→ inhibition of ACh release from nerve at neuromuscular junction

62
Q

What is the long term effect of reuptake inhibitors that has an effect on depression

A

Antidepressants down-regulate auto-receptors; increasing firing rate of 5-HT neurons

63
Q

Initially when taking a reuptake inhibitor

A

5-HT levels in synapse will increase but so does feedback inhibition, thus balancing synaptic amine levels

64
Q

TCA MOA

A

Inhibit reuptake of NE and 5-HT

Also block alpha-adrenergic, histamine, and muscarinic receptors

65
Q

Tertiary amine TCAs….

A

primarily block 5-HT reuptake

66
Q

Secondary amine TCAs….

A

primarily block NE reuptake

67
Q

Side effects of TCAs are due to

A

Cholinergic blockade
Alpha 1 receptor blockade
Histamine receptor blockage

68
Q

Analgesic effect of TCAs is due to

A

activation of descending NE pathways in spinal cord→ increase alpha 2 autoreceptor activation→ decreased glutamate input into pain pathway to brain

69
Q

SSRIs MOA

A

Selectively inhibit 5-HT reuptake

70
Q

SNRIs MOA

A

Inhibit NE and 5-HT reuptake

71
Q

MAO-A

A

Metabolizes NE, DA, 5-HT in both CNS and periphery (GI tract, liver)

72
Q

MAO-B

A

selectively metabolizes DA in CNS only

73
Q

Phenelzine MOA

A

Inhibits MOA-A and B → increased NE, 5-HT, DA.

Also a substrate for MAO.

74
Q

Selegiline MOA

A

selectively inhibits MAO-B→ increased DA

75
Q

Tyramine

A

Accumulates if MAO-A is inhibited

Tyramine causes release of catecholamines, causing severe hypertensive crisis +/- intracranial bleeding

should be avoided while taking MAOIs

76
Q

Bupropion MOA

A

Inhibits reuptake: DA, minimal of NE and 5 H-T

77
Q

Mirtazapine MOA

A

Blocks presynaptic alpha 2 receptors→ decreased inhibition of NE and 5-HT release→ increased NE and 5-HT

78
Q

Atomoxetine MOA

A

Selective inhibitor of norepinephrine reuptake

79
Q

Trazodone MOA

A

5-HT2A receptor antagonist

80
Q

Classical antipsychotics MOA

A

Block DA D2 receptor

Target mesolimbic system

Alleviate positive symptoms

81
Q

Atypical antipsychotics MOA

A

Block 5-HT2A and DA receptors

Target mesocortical and mesolimbic system

Alleviate both negative and positive symptoms

82
Q

All the receptors antipsychotics might act on

A 
*D2* (higher affinity for D2=more potent)
alpha 1
D4
5-HT2A
D1
H1
83
Q

Chlorpromazine MOA

A

Blocks DA D2 receptors + alpha adrenergic actions

84
Q

Haloperidol MOA

A

Potent blocker of DA D2 receptors

Affinity for DA D1, 5-HT2, and H1 receptors

85
Q

Clozapine MOA

A

Blocks 5-HT2A and DA D4 receptors

some DA D2 (least potent of all the antipsychotics)

86
Q

Olanzapine MOA

A

Blocks
5-HT2A
DA D4
DA D2

“similar to clozapine”

87
Q

Ziprasidone MOA

A

Blocks 5-HT2A, DA D2 receptors

Some antidepressant: 5-HT1a receptor agonist, inhibition of 5-HT reuptake

88
Q

Risperidone

A

Blocks 5-HT2A, DA D2 receptors

No effect on DA in nigrostriatal pathway (EPS, TD rare)

89
Q

Extrapyramidal symptoms from antipsychotics are due to

A

DA receptor antagonists block DA receptors in the nigrostriatal pathway

90
Q

Quetiapine MOA

A

Blocks 5-HT2A, DA D2 receptors

“Similar to clozapine”

91
Q

Aripiprazole MOA

A

“Dopamine system stabilizer”
Partial agonist for DA, 5-HT
Antagonist 5-HT2a, alpha 1, histamine receptors

92
Q

Lurasidone MOA

A

Blocks D2, 5-HT2a receptors
Partial agonist 5-HT1a
No antihistamine or antimuscarinic

93
Q

Lithium MOA

A

Suppress second messengers: IP3

+/- increase ACh, NE, DA

94
Q

Lithium in the kidney

A

Reabsorbed by proximal tubule of kidney

Competes with Na+ for reabsorption

Na+ decreases–>Li absorption increases→ Toxicity
Na+ increases→ Li absorption decreases and excretion increases

Li increases→ Na+ absorption decreases→ hyponatremia

95
Q

Valproic acid MOA for bipolar

A

Mechanism unknown

96
Q

Beta-endorphins

A

decrease pain transmission in spinal cord, facilitate dopamine in reward system→ euphoria

97
Q

Enkephalins

A

decrease pain transmission in the spinal cord

98
Q

Dynorphins

A

bind to kappa receptors→ analgesia and dysphoria

99
Q

Mu receptor (MOR)

A

analgesia, euphoria, sedation, side effects

100
Q

Kappa receptor

A

Analgesia or dysphoria

101
Q

Delta receptor

A

Dysphoria

102
Q

Opioids + GABA

A

GABA→ inhibits descending neuronal pain modulation pathways

Opioids→ decreased GABA release→ allow pathways to be activated→ decreased pain transmission in dorsal horn of spinal cord

103
Q

Opioids + Glutamate

A

Decreasing glutamate release in the dorsal

horn reduces activation of the ascending pathway.

104
Q

Opioids MOA

A

Coupled to Gi/o → decrease cAMP

Close voltage gated Calcium channels on presynaptic nerve terminals→ decreased neurotransmitter release, decreased neuronal activity

Mu receptors open K+ channels→ hyperpolarization→ inhibition of nerve transmission→ difficult to respond to pain signals

105
Q

3 opioids that paradoxically cause CNS excitement in overdose

A

Codeine
Meperidine
Proxyphene

106
Q

Opioids and respiratory depression mechanism

A

Decreased response of brainstem to elevated CO2 +/- bronchoconstriction

107
Q

Opioids and ICP mechanism

A

Increased CO2→ vasodilation→ increased cerebral blood flow→ increased intracranial pressure

108
Q

Opioids and body temperature mechanism

A

Hypothermia, dysregulation in hypothalamus

109
Q

Atropine

A

blocks parasympathomimetic effects

Reverses opioid miosis

110
Q

Opioid CV effects mechanism

A

CNS vasomotor depression and/or vasodilation via histamine release

111
Q

Opioid GI effects mechanism

A

Decreased gastric activity: CNS and local effect inhibition of transmitter release

112
Q

Opioids cause itching because

A

they cause histamine release

not an allergy

113
Q

Opioid tolerance mechanism

A

Due to receptor desensitization, down regulation and uncoupling from G- proteins in thalamus and spinal cord

114
Q

Opioid physical dependence mechanism

A

Results from desensitization of mu receptors, or receptor uncoupling

115
Q

Opioid hyperalgesia mechanism

A

Mediated by increases in spinal cord dynorphin→ more effective pain transmission

116
Q

NMDA receptor antagonists + opioids

A

Decrease tolerance and hyperalgesia

117
Q

Changes in the brain from addiction

A

Addictive drugs→ more dopamine release than normal rewards→ down regulation of dopamine receptors→ substance provides less pleasure but more craving

118
Q

Morphine MOA

A

stimulates all opioid receptors, potent, produces all effects

119
Q

Methadone MOA

A

Stimulates mu receptors
+/- block NMDA receptors
+/- inhibit NE/5-HT reuptake

120
Q

Meperidine MOA

A

Mu agonist

121
Q

Pentazocine MOA

A

Kappa receptor agonist

Mu receptor partial agonist

122
Q

Buprenorphine MOA

A

Partial agonist on mu +/- kappa

123
Q

Tramadol MOA

A

Weak mu agonist

Inhibits NE/5-HT→ contributes to analgesia

124
Q

Dextrometorphan MOA

A

Blocks NMDA receptors→ abuse potential

125
Q

L-dopa MOA

A

Dopamine does not cross blood brain barrier, but L-Dopa does→ converted into dopamine in neuron

126
Q

Carbidopa MOA

A

inhibits dopa-decarboxylase in the periphery (doesn’t cross blood brain barrier) → Decreases the dose of l-dopa needed

127
Q

Inhibition of MAO-B in the CNS

A

reduces striatal metabolism of DA

MAO inhibitors used for parkinsons

128
Q

COMT…

A

Catechol-O-methyltransferase (COMT) metabolizes DA and l-dopa
COMT-I → Inhibit DA and l-dopa metabolism

129
Q

Tocalpone MOA

A

COMT inhibitor in CNS and periphery

130
Q

Entacopone MOA

A

COMT inhibitor in periphery only, inceases pool of l-dopa for transport into brain

131
Q

Dopamine receptor antagonists primarily target

A

DA D2

132
Q

Amantidine MOA

A

Increased dopamine neurotransmission
+/- increased release of dopamine
+/- inhibition of dopamine reuptake

133
Q

Anticholinergics MOA

A

Muscarinic receptor antagonists→ restores DA/ACh balance in striatum

134
Q

Galantamine MOA

A

inhibit metabolism of ACh by acetylcholinesterase
Increases the amount of ACh in the nerve terminal
AND
blocks presynaptic acetylcholine autoreceptor

135
Q

Donepezil and rivastigmine MOA

A

Inhibit metabolism of AC by acetylcholinesterase Increase the amount of ACh in the nerve terminal

136
Q

Memantine MOA

A

NMDA receptor antagonist (channel blocker)
Blocks pathological activation of NMDA receptors
Reduces excitotoxic effect of glutamate and slows degeneration

137
Q

(meth)amphetamine MOA

A

Reverses dopamine transport through DAT (reuptake) → increased release of dopamine

138
Q

Cocaine MOA

A

inhibits DA reuptake

139
Q

Crack cocaine aka freebase cocaine

A

No HCl group on cocaine, can be inhaled for more rapid onset

140
Q

Nicotine MOA

A

Activates nicotinic receptors in the CNS and periphery→ increases 5-HT and DA release

141
Q

MDMA MOA

A

Increases 5-HT activity by blocking

reuptake and stimulating 5-HT receptors

142
Q

Marijuana (THC) MOA

A

Stimulates presynaptic CB1

receptors to inhibit transmitter (ACh) release

143
Q

LSD, Mescaline, Psilocybin MOA

A

Act on 5-HT receptors in the brain

144
Q

PCP and Ketamine MOA

A

NMDA receptor antagonists

145
Q

GHB MOA

A

GABA receptor weak agonist

146
Q

MOA of inhalants

A

Mechanism unknown→ +/- alter

ionotropic receptors and increase DA

147
Q

Amyl and Butyl nitrite (poppers or snappers) MOA

A

Smooth muscle relaxants

Unit 1 Pharm III (4 decks)

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