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Neuro Pharm Flashcards

1
Q

How do you treat essential tremor (postural tremor)?

A

Beta-blockers
Primidone (anti-convulsant)
ETOH (decreases tremor amplitude)

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2
Q

How do you precipitate Wernicke-Korsakoff syndrome?

A

Giving glucose without B1 to a B1 deficient patient

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3
Q

Treat subarachnoid hemorrhage?

A

Nimodipine (Ca channel blocker)

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4
Q

What is indicated in ischemic stroke?

A

tPA within 4.5 hours

as long as paint presents within 3 hours of onset & there is no major risk of hemorrhage

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5
Q

What are some ALS therapies?

A

Riluzole (decrease presynaptic glutamate release)

Baclofen (GABA-B agnoist to dec spasticity)

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6
Q

What is contraindicated in closed (narrow angle) glaucoma?

A

Epinephrine

bc causes mydriasis

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7
Q

How do you treat Dry ARMD (nonexudative age-related macular degeneration)?

A

prevent progression– multivitamins & antioxidants

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8
Q

How do you treat Wet ARMD (exudative age-related macular degeneration)?

A

anti-VEGF injections or laser

stops choroidal neovascularization

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9
Q

How do you treat MS?

A

Beta-interferon
Natalizumab (monoclonal AB against alpha-4 integrin for cell adhesion)
Glatiramer (immune modulator)
Symptomatic Tx: 1) Baclofen (GABA-B agonist– tx spasticity), 2) Muscarinic antagonist & catheterization (neurogenic bladder), 3) Opiods (pain)

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10
Q

How do you treat Guillain-Barre?

A

Respiratory ventilator support
Plasmapheresis
IV immune globulins

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11
Q

What is the DOC for partial (focal) seizures?

A

Carbemazepine

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12
Q

How do you treat cluster HA?

A

inhaled oxygen

sumatriptan

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13
Q

How do you treat migraine?

A

Abortive– triptans

Prophylacitc– propranolol, topiramate

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14
Q

What is the general mechanism of glaucoma drugs?

A

decrease amount of aqueous humor to decrease intraocular pressure

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15
Q

Which drug classes are used to treat glaucoma?

A 
alpha-agonists
beta-blockers
diuretics
cholinomimetics
prostaglandin
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16
Q

Which alpha-agonists are used to treat glaucoma?

A

Epinepherine

Brimonidine (alpha 2)

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17
Q

What is the MOA of alpha-agonists in glaucoma?

A

decrease aqueous humor synthesis

epi does so via vasoconstriction

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18
Q

Side effects of alpha-agonists in glaucoma?

A

Mydriasis– Epi is contraindicated in closed-angle glaucoma

blurry vision, ocular hyperemia, foreign body sensation, ocular allergic rxn, ocular pruritis

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19
Q

Which beta-blockers are used in glaucoma?

A

Timolol
Betaxolol
Carteolol

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20
Q

What is the MOA of beta-blockers in glaucoma treatment?

A

Dec aqueous humor synthesis

*no pupillary or vision change S/E

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21
Q

Which diuretic is used to treat glaucoma?

A

Acetazolamide

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22
Q

What is the MOA of acetazolamide?

A

dec aqueous humor synthesis via carbonic anhydrase inhibition
*no pupillary or vision change S/E

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23
Q

Which cholinomimetics are used to treat glaucoma?

A

Direct– Pilocarpine, Carbachol

Indirect– Physostigmine, Echothiphate

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24
Q

What is the MOA of cholinomimetics in glaucoma?

A

inc outflow of humor via contraction of ciliary muscle and opening of trabecular meshwork

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25
Which cholinomimetic is very effective in emergencies?
Pilocarpine (direct cholinomimetic) | acts quickly at opening trabecular meshwork into canal of schlemm
26
What are the side effects of cholinomimetics in glaucoma?
Miosis | Cyclospasm (contraction of ciliary muscle)
27
Which prostaglandin is used in glaucoma?
Latanoprost (PGF-2-alpha)
28
What is the MOA of prostaglandin used in glaucoma?
inc outflow of aqueous humor
29
What is the S/E of prostaglandin in glaucoma?
Darkening of the iris (browning)
30
What are the common opioid analgesics?
``` Morphine Fentanyl Codeine Heroin Methadone Meperidine Dextromethorphan Diphenoxylate ```
31
What is the MOA of opioid analgesics?
agonists at opioid receptors to modulate synaptic transmission opens K channels & closes Ca channels to decrease synaptic transmission. inhibits release of ACh, HE, 5-HT, glutamate, substance P
32
What are the opioid receptors?
``` Mu = morphine delta = enkephalin kappa = dynorphin ```
33
Clinical use of opioid analgesics?
``` pain cough suppression (dextromethorphan) diarrhea (loperamide & diphenoxylate) acute pulmonary edema maintenance for addicts (methadone) ```
34
Toxicity of opioid analgesics?
``` Addiction Respiratory depression constipation miosis (pinpoint pupils) additive CNS depression with other drugs (esp ETOH, BZD, Barbs) NO tolerance to miosis & constipation ```
35
What is the antidote to opioid OD?
Naloxone or Naltrexone | opioid receptor antagonists
36
What is the MOA of Butorphanol?
Mu-opioid receptor partial agonist | Kappa-opioid receptor agonist
37
Clinical use of Butorphanol?
Analgeisa for severe pain (migraine, labor, etc) | causes less respiratory depression than full opioid agonists.
38
What is the toxicity of Butorphanol?
opioid withdrawal symptoms if also taking full opioid agonist (competition for opioid receptors) OD not easily reversed with Naloxone
39
What is the MOA of Tramadol?
Very weak opioid agonist | inhibitis serotonin & NE reuptake
40
What is the clinical use of Tramadol?
chronic pain
41
What is the toxicity of Tramadol?
similar to opioids-- resp depression, miosis, constipation, etc. decreases seizure threshold
42
Anti-epileptic drugs
``` Phenytoin Carbamazepine Lamotrigine Gabapentin Topiramate Phenobarbital Valproic Acid Ethosuximide Benzodiazepines (Diazepam or Lorazepam) Tiagavine Vigabatrin Levetiraceteam ```
43
1st line for tonic-clonic?
Phenytoin Carbamazepine Valproic Acid
44
1st line for Complex partial?
Carbamazepine
45
1st line for simple partial?
carbamazepine
46
1st line for absence seizure?
ethosuximide
47
1st line for status epilepticus?
Acute tx-- loreazepam (or diazepam) | Prophylaxis-- phenytoin
48
MOA of Phenytoin?
inc Na channel inactivation (use-dependent blockade) | inhibits glutamate release from excitatory presynaptic neuron
49
Use of Phenytoin?
tonic-clonic (also simple partial, complex partial) status epilepticus prophylaxis *use Fosphenytoin if parenteral Class 1B antiarrhythmic
50
MOA of Carbamazepine?
Inc Na channel inactivation
51
Use of Carbamazepine?
1st line for simple partial, complex partial, tonic-clonic, and trigeminal neuralgia
52
MOA of Lamotrigine?
blocks voltage-gated NA channels
53
Use of Lamotrigine?
Simple partial, complex partial, tonic-clonic
54
MOA of Gabapentin?
GABA analog | inhibits high-voltage-activated Ca channels
55
Use of Gabapentin?
simple partial, complex partial, tonic-clonic | peripheral neuropathy, postherpetic neuralgia, migraine prophylaxis, bipolar disorder
56
MOA of Topiramate?
blocks Na channels | inc GABA action
57
Use of Topiramate?
simple partial, complex partial, tonic- clonic | migraine prevention
58
MOA of phenobarbital?
inc GABA-A Action
59
Use of Phenobarbital?
1st line in children w/ simple partial, complex partial, tonic-clonic
60
MOA of Valproic Acid?
inc Na channel inactivation | inc GABA concentration
61
Use of valproic acid?
1st line for tonic clonic | simple partial, complex partial, absence, and myoclonic seizures (can be used for all seizure types)
62
MOA of Ethosuximide?
blocks thalamic T-type Ca channels
63
Use of Ethosuximide?
absence seizures (1st line)
64
MOA of benzodiazepines in seizures?
inc GABA-A action
65
Use of Bezodiazepines in seizures?
1st line for acute status epilepticus | Use for eclampsia seizures (after 1st line MgSO4)
66
MOA of Tiagabine?
inhibits GABA reuptake
67
Use of Tiagabine?
simple & complex partial seizures
68
MOA of Vigabatrin?
irreversibly inhibits GABA transaminase to increase GABA
69
Use of Vigabatrin?
simple & complex partial seizures
70
MOA of Levetiracetam?
unknown | may modulate GABA and Glutamate release
71
Use of Levetiracetam?
simple & complex partial | tonic-clonic
72
Toxicity of benzodiazepines?
sedation tolerance dependence induction of cytochrome p450
73
Toxicity of Carbamazepine?
``` Blood Dyscrasias (agranulocytosis & aplastic anemia) Stevens-Johnson syndrome Diplopia, Ataxia liver toxicity teratogenesis induction of cytochrome p450 SIADH (dec Na) ```
74
Toxicity of Ethosuximide?
GI distress, fatigue, aggression HA, uritcaria Stevens-Johnson syndrome may worsen generalized tonic-clonic seizures
75
Toxicity of Phenobarbital?
sedation tolerance dependence induction of cytochrome p450
76
Toxicity of Phenytoin?
``` Gingival hyperplasia Hirsutism/ Hypertrichosis Teratogenesis (fetal hydantoin syndrome & inc risk of cleft palate) Nystagmus & Diplopia (will develop tolerance) megaloblastic anemia (dec folate absorption) SLE-like syndrome Ataxia Sedation induction of p450 lymphadenopathy peripheral neuropathy Stevens-Johnson syndrome ```
77
Toxicity of Valproic Acid?
Hepatotoxicty (rare but fatal-- measure LFTs) Neural tube defects (spina bifida)-- Contra in pregnancy GI distress tremor, weight gain
78
Toxicity of Lamotrigine?
Stevens-Johnson syndrome | increase dosage slowly
79
Toxicity of Gabapentin?
Sedation | Ataxia
80
Toxicity of Topiramate
Weight loss = decreases appetite Sedation Kidney stones Mental dulling
81
What are common barbiturates?
Phenobarbital Pentobarbital Thiopental Secobarbital
82
What is the MOA of barbiturates?
facilitate GABA-A action by increasing DURATION of Cl channel opening thus decreasing neuron firing) *BARBI (barbituates) likes it longer, BEN (benzodiazepines) wants it more often
83
What condition are barbiturates contraindicated in?
Porphyria
84
Clinical use of barbiturates?
sedative | anxiety, seizures, insomnia, induction of anaesthesia-- thiopental
85
Toxicity of Barbiturates?
Respiratory and cardiovascular depression (may be fatal) CNS depression (exacerbated with BZD & ETOH use) dependence drug interactions (induces p450)
86
Antidote for Barbiturate OD?
supportive-- respiratory assistance & BP maintenance
87
What are common Benzodiazepines?
``` Diazepam Lorazepam Triazolam Temazepam Oxazepam Midazolam Chlordiazepoxide Alprazolam ```
88
What is the MOA of Benzodiazepines?
facilitate GABA-A action by increasing the FREQUENCY of Cl channel opening dec REM sleep most have long-half lives *Barbi likes it longer, Ben wants it more frequently
89
Short-half life benzodiazepines?
Triazolam Oxazepam Midazolam *higher addictive potential
90
Clinical use of Benzodiazepines?
anxiety, spasticity, status epilepticus, detoxification (ETOH withdrawal/DT's), night terros, sleepwalking, general anethetic, hypnotic.
91
Toxicity of Benzodiazepines?
Dependence additive CNS depression effects w/ ETOH & Barbs Less coma & resp depression risk than Barbs
92
Antidone for OD?
Flumazenil | competitive antagonist at GABA benzodiazepine receptor
93
Nonbenzodiazepine Hypnotics
Zolpidem, Zaleplon, Eszopiclone
94
MOA of non-benzo hypnotics?
act via BZ-1 subtype of GABA receptor
95
clinical use of non-benzo hypnotics?
insomnia
96
Toxicity of non-benzo hyponotics?
ataxia, HA, confusion rapid metab by liver enzymes = short duration of action few amnestic events and modest day-after psychomotor depression lower dependence risk than BZDs
97
Anesthetic drugs with low solubility in blood
rapid induction and recovery times | lower potency
98
Anesthetic drugs with high solubility in lipids
high potency = 1/ MAC | MAC = minimal alveolar concentration at which 50% of the population is anesthetized. varies with age
99
Inhaled anesthetics
``` halothane enflurane isoflurane secoflurane methoxyflurane nitrous oxide ```
100
Effects of inhaled anesthetics?
unknown MOA | myocardial depression, respiratory depression, nausea/ emesis, inc cerebral blood flow (dec cerebral metabolic demand)
101
Toxicity of inhaled anesthetics?
Hepatotoxicity (halothane) nephrotoxicity (methoxyflurane) proconvulsant (enflurane) malignant hyperthermia (all but nitrous oxide-- rare & life-threatening, inherited susceptibility) expansion of trapped gas in body cavity (Nitrous oxide)
102
IV anesthetics?
``` Barbiturates (Thiopental) Benzodiazepines (Midazolam) Arylcyclohexylamines (ketamine-- PCP analogs) Opioids (morphine & fentayl) Propofol ```
103
Thiopental
barbiturate anesthetic high potency-- high lipid solubility & rapid entry into brain used for induction of anesthesia & short surgical procedures effects terminated by rapid redistribution into tissue & fat decreased cerebral blood flow
104
Midazolam
most common drug used in endoscopy used adjunctively with gas anesthetics & narcotics may cause severe post-op respiratory depression, dec BP (tx OD w/ Flumazenil) and amnesia
105
Ketamine/ PCP analogs
``` dissociative anesthetics block NMDA receptors Cardiovascular stimulants cause disorientation, hallucination, and bad dreams inc cerebral blood flow ```
106
Morphine & Fentanyl
used with other CNS depressants in general anesthesia
107
Propofol
``` sedation in ICU rapid induction of anesthesia short procedure anesthesia less post-op nausea than thiopental potentiates GABA-A ```
108
Local anesthetics
2 classes: 1) esters--- procaine, cocaine, tetracaine 2) amides--- lidocaine, mepivacaine, bupivacaine (all have 2 I's in name) *if ester allergy, give amide
109
MOA of local anesthetics
blocks Na channels by dividing into specific receptors on inner portion of channel preferentially bind to activated Na channels-- so most effective in rapidly firing neurons tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form
110
Order of nerve blockade in local anesthetics?
small-diameter fibers > large-diameter fibers myelinated fibers > nonmyelinated fibers *size predominates over myelination status sm myelinated > sm unmyelinated > lg myelinated > lg unmyelinated
111
Order of loss of sensations in local anesthetic?
1) pain 2) temperature 3) touch 4) pressure
112
What happens when you give local anesthetic at an infected tissue?
infected tissue is acidic anesthetic is alkaline and charged (therefore cannot penetrate membrane as effectively) *must give more anesthetic at infected tissues
113
What can you combine with local anesthetics to enhance local action?
vasoconstrictors (epinephrine) | decreases bleeding, increases anesthesia locally by decreasing systemic concentration
114
Clinical use of local anesthetics?
Minor surgical procedures | Spinal anesthesia
115
Toxicity of local anesthetics?
CNS excitation severe cardiovascular toxicity (bupivacaine) hypertension, hypotension & arrhythmias (cocaine)
116
What are neuromuscular blockade drugs used for?
muscle paralysis in surgery or mechanical ventilation | selective for motor nicotinic receptor (not autonomic)
117
What are the two types of neuromuscular blockade drugs?
Depolarizing (succinylcholine) | Nondepolarizing (Tubocurarine, etc)
118
What is the common depolarizing NM blocking drug?
Succinylcholine | strong Ach receptor agonist
119
What is the MOA of succinylcholine?
produces sustained depolarization and prevents muscle contraction
120
How does blockade reversal occur in succinylcholine?
2 phases: Phase I-- prolonged deloparization. no antidone. block potentiated by cholinesterase inhibitors. Phase II-- repolarized but blocked (ACh receptors are available but desensitized) antidote = neostigmine (cholinesterase inhibitors)
121
Complication of succinylcholine?
hypercalcemia hyperkalemia malignant hyperthermia
122
Common Non-depolarizing NM blocking drugs?
``` Tubocurarine Atracurium Mivacurium Pancuronium Vecuronium Rocuronium ```
123
MOA of non-depolarizing NM blocking drugs?
competitive antagonists-- compete with ACh for receptors
124
Reversal of blockade by non-depolarizing NM blocking drugs?
neostigmine & edrophonium | cholinesterase inhibitors
125
MOA of Dantrolene?
prevents Ca release from sarcoplasmic reticulum of skeletal muscle
126
Clinical use of Dantrolene?
Treats malignant hyperthermia (rare, but life-threatening S/E of succinylcholine & inhalation anesthetics-- except N2O. Neuroleptic Malignant Syndrome (toxicity of antipsychotic drugs)
127
General Parkinson's Disease Drug strategies:
dopamine agonists increase dopamine release prevent dopamine breakdown curb excess cholinergic activity
128
Dopamine agonists used in Parkinsons?
Bromocriptine* (ergot) pramipexole ropinirole (non-ergot) (non-ergots are preferred)
129
Agents that Increase Dopamine release in Parkinsons?
Amantadine* (inc dopa release & also antiviral against influenza A & rubella) L-dopa/Carbidopa* (converted to dopamine in CNS)
130
Agents that prevent Dopa breakdown in parkinsons?
Selegiline* (selective MAO-B inhibitor) | Entacapone, Tolcapone (COMT inhibitors-- prevent L-Dopa degradation = inc dopamine availability)
131
Agents that curb excess cholinergic activity in Parkinsons?
Benzotropine (antimuscarininc that improves tremor & rigidity but has little effect on bradykinesia) *PARK your mercedes-BENZ here.
132
Typical regimen in Parkinson's Disease?
``` Bromocriptine Amantadine Levodopa (+ Carbidopa) Selegiline Antimuscarinics ``` *BALSA
133
Toxicity associated with Amantadine?
ataxia
134
MOA of Levodopa/Carbidopa?
increases level of dopamine in the brain unlike dopa, L-dopa can cross BBB and is converted by dopa decarboxylase in CNS to dopamine. Carbidopa = peripheral decarboxylase inhibitor given with L-dopa to increase brain bioavailability and limit peripheral side effects
135
Toxicity of Levodopa/Carbidopa?
Arrhythmias-- bc inc peripheral formation of catecholamines | Long term use = dyskinesia following administration & akinesia between doses
136
MOA of selegiline?
Selective inhibits MAO-B (which preferentially metabolizes dopamine over NE & 5-HT) = increase availability of dopamine
137
Toxicity of selegiline?
may enhance adverse effects of L-dopa (arrhythmia & dyskinesia with long term use)
138
Alzheimer's Drugs
Memantine | Donepezil, Galantamine, Rivastigmine
139
MOA of Memantine?
un-competitive NMDA receptor antagonist | helps prevent excitotoxicity (mediated by Ca & glutamate)
140
Toxicity of Memantine?
Dizzyness Confusion Hallucination
141
MOA of Dopepezil, Galantamine & Rivastigmine?
Acetylcholinesterase inhibitors = keep ACh levels up
142
Toxicity of Acetylcholinesterase inhibitors in Alzheimer's dz?
Nausea, diarrhea | dizziness, insomnia, urinary incontinence
143
Huntington's Treatment?
Tetrabenazine & Reserpine = inhibit VMAT (limit dopamine vesicle packaging & release) Haloperidol- dopamine receptor antagonist
144
Sumatripin MOA
``` 5-HT (1B/1D) agonist inhibits trigeminal nerve activation prevents vasoactive peptide release induces vasoconstriction half-life < 2 hrs ```
145
Clinical use of Sumatriptin?
Cluster HA attack | Acute Migraine
146
Toxicity of Sumatripin?
``` coronary vasospasm (CONTRA in CAD or Prinzmetal's Angina) mild tingling ```
147
What is the MOA of alpha methyl tyrosine?
Inhibits tyrosine hydroxylase decreasing conversion of tyrosine to DOPA thereby inhibiting the rate-limiting step in catecholamine synthesis

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