Neuro Flashcards
(68 cards)
1
Q
Zolpidem
A
MOA:
- Bind to GABAa receptor and enhance inhibitory action of GABA on CNS
- Same MOA as benzo’s
Use:
- Short term Tx. of insomnia
- Rapid onset of action (15 mins after admin)
- Metabolized by P450 liver
Tox:
Less chance for tolerance and addiction
2
Q
Chlorpheniramine
Diphenhydramine (Benadryl)
Promethazine
Hydroxyzine
A
MOA:
-1st gen H1-histamine receptor antagonist
Use:
-To tx. and prevent allergic rxns, motion sickness, anti emetics
Tox:
-Especially sedating when used with Benzo’s (Diazepam)
3
Q
Diazepam
A
MOA:
- Long acting benzo
- Binds GABAa receptors
Use:
-Anxiolytic; Sedative hypnotic; Anticonvulsant; M. relaxant
Tox:
- Sedation
- Impaired coordination balance (avoid in elderly)
- Decreased memory and [ ]
- Confusion
- Should not be used in combo with other CNS depressants*
4
Q
Nimodipine
A
MOA:
-Ca2+ chan blocker
Use:
-Assist in prevention of cerebral vascular spasm following subarachnoid hemorrhage (SAH)… this is an alternative use to CCB’s
Tox:
5
Q
Methyldopa
Clonidine
A
MOA:
- Central sympatholytics
- Stim. alpha-2A receptors centrally which causes a decreased in generalized sympathetic flow
Use:
-To decrease BP
Tox:
HypoTN
6
Q
Valproic Acid
A
MOA:
-Suppresses abnormal electrical activity in the cortex by affecting GABA and NMDA receptors as well as Na+ and K+ channels
Use:
-Myoclonic seizures (a type of generalized seizure, except w/o loss of consciousness)
7
Q
Antipsychotics & their associations
Thioridazine Chlorpromazine Haloperidol Ziprazidone Olanzapine Clozapine
A
- ->Retinal deposits that resemble retinitis pigments
- ->Corneal deposits
- ->Extrapyramidal symoptoms
- ->Prolonged QT
- ->Wt. gain
- ->Agranulocytosis and seizures
8
Q
Important antipsychotic SE’s
A
Extrapyramidal SE’s –> acute dystonic rxn; akathisia; drug induced parkinsonism
Tardive dyskinesia
Neuroleptic malignant syndrome
9
Q
Modafinil
A
MOA:
- Enhance dopaminergic signaling
- Non-amphetamine stimulant
Use:
-Narcolepsy (low levels of stim NT, orexin (hypocretin), for maintaining wakefulness and suppressing REM sleep-related phenomena)
10
Q
Cocaine
A
MOA:
- Inhib’s presynaptic uptake of NE, DO, SE
- Short acting sympathomimetic
Tox:
- BP elevation
- Chest pain 2ndry to coronary a. vasoconstriction
- Agitation from CNS activation
- Mydriasis
11
Q
Buspirone
A
MOA:
- anxiolytic agent
- selective agonist of 5HT1a receptor
Use:
- Generalized anxiety disorder
- *clinical response is delayed up to 2wks of daily use**
Tox:
- Dependence does not occur with chronic use
- No m. relaxant or anticonvulsant properities
12
Q
Phenelzine
Tranylcypromine
A
MOA:
-Monoamine oxidase inhibitors
-
Use:
-Atypical depression characterized by mood reactivity (improvement in mood in response to something positive), leaden fatigue, rejection sensitivity, increased sleep/appetite
13
Q
What is the single most effective agent in treating TCA associated cardiac abnormalities?
A
Sodium bicarbonate
14
Q
Carbamazepine
A
MOA:
-Blocks voltage gated Na+ chan’s in neuronal membranes
Use:
- Simple partial, complex partial, and generalized tonic-clonic seizures
- Mood stabilizer in bipolar disorder
- Tx. trigeminal neuralgia
- Diabetic neuropathy
Tox:
- Bone marrow suppression
- Hepatotoxic
- Increase in ADH secretion may cause SIADH
15
Q
Ethosuximibe
A
MOA:
-Blocks T-type Ca2+ chan’s and decreases Ca2+ current in thalamic neurons
Use:
-Absence seizures
16
Q
Acetylecholinesterase inhib’s
A
- Physostigmine (Tertiary amine–> works centrally & peripherally)
- Neostigmine & Edrophonium (Quaternary ammonium structures that limits CNS penetration)
17
Q
Phenytoin
A
MOA:
-Inhibits neuronal high-frequency firing of AP’s by blocking Na+ chain’s and prolonging their rate of recovery
Use:
- Tonic clonic seizures (grand mal)
- Status epilepticus
Tox:
- Gingival hyperplasia
- Hersuitism
- Coarsening of facial features
- Acneform skin rash
- Generalized lymphadenopathy (pseudolymphoma)
18
Q
Pentazocine
A
MOA:
- Opioid narcotic
- Partial agonist and weak antagonist activity at mu R’s
**b/c of its weak antagonistic affects, it can cause withdrawal symptoms in pt’s who are dependent or tolerant to morphine or other opioids
19
Q
Cyproheptadine
A
MOA:
-Antihistamine with anti-serotonergic properties
Use:
-Serotonin syndrome
20
Q
Lamotrigine
A
MOA:
-Anticonvulsant
Use:
- Management of generalized tonic-clonic seizures
- Bipolar disorder
Tox:
-Rash (discontinue drug immediately in children)
21
Q
Drugs used for refractory partial seizures
A
Tiagabine–> inhib of GABA uptake
Topiramate–> blocks Na chan and enhances effect of GABA
Vigabatrin–> inhib GABA-transaminase and increase GABA [ ]
Gabapentin–> increase brain GABA [ ]
22
Q
Methimazole
A
MOA:
-Inhib thyroid hormone synthesis by suppressing iodination and coupling of tyrosine
Use:
-Hyperthyroidsm
Tox:
- Edema
- Rash
- Agranulocytosis
23
Q
What is the main therapy for acute mania?
A
Mood stabilizers:
- Lithium
- Valoproic acid
- Carbamazepine
Atypical antipsychotic:
-Olanzapine
24
Q
Glaucoma drugs
A
↓ IOP via ↓ amt of aqueous humor (inhibit synthesis/ secretion or ↑ drainage)
25
Epinephrine
MOA:
- α-agonist
- ↓ aqeuous humor synthesis via vasoconstriction
Use:
-Glaucoma
Tox:
Mydriasis; do not use in closed-angle gluacoma
26
Brimonidine
MOA:
- α2-agonist
- ↓ aqeuous humor synthesis
Use:
-Glaucoma
Tox:
Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritus
27
Timolol
Betaxolol
Carteolol
MOA:
- β-blocker
- ↓ aqeuous humor synthesis
Use:
-Glaucoma
Tox:
-No pupillary or vision changes
28
Acetazolamide
MOA:
- Diuretic
- ↓ aqeuous humor synthesis via inhibition of carbonic anhydrase
Use:
-Glaucoma
Tox:
-No pupillary or vision changes
29
Glaucoma Cholinomimetics
Direct (pilocarpine, carbachol)
Indirect (physostigmine, echothiophate)
MOA:
- ↑ outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
- Use pilocarpine in emergencies---very effective at opening meshowrk into canal of Schlemm
Use:
-Glaucoma
Tox:
-Miosis and cyclospasm (contraction of ciliary muscle)
30
Latanoprost (PGF2α )
MOA:
- ↑ outflow of aqueous humor
Use:
-Glaucoma
Tox:
-Darkens color of iris (browning)
31
Opiod analgesics
```
Morphine
Fentanyl
Codeine
Loperamide
Methadone
Meeperidine
Dextromethorphan
Diphenoxylate
```
MOA:
- Acts as agonists at opioid receptor (mu = morphine, delta = enkephalin, kappa = dynorphin) to modulate synaptic transmission__ open K+ chan, close Ca2+ channel --> ↓ synaptic transmission
- Inhib rlease of ACh, norepi, 5-HT, glutamate, substance P
Use:
- Pain, cough suppression (dextromethorphan)
- Diarrhea (loperamide and diphenoxylate)
- Acute pulm edema, maintenance programs for heroin addicts (methodone)
Tox:
- Addiction, respiratory depression, constipation, miosis (pinpoint pupils), additive CNS depression with other drugs. Tolerance does not develop to miosis and constipation.
- Toxicity tx'ed w/ naloxone or naltrexone (opiod receptor antagonist)
32
Butorphanol
MOA:
- Mu-opioid receptor partial agonist and kappa-opioid receptor agonist; produces analgesia
Use:
- Severe pain (migraine, labor, etc)
- Causes less resp depression than full opioid agonists
Tox:
- Can cause opioid withdrawal symptoms if patient is also taking full opioid agonist (competition for opioid)
- Overdose not easily reversed with naloxone
33
Tramadol
MOA:
-Very weak opioid; also inhibits serotonin and norepinephrine reuptake (works on multiple neurotransmitters__ "tram it all" in with tramadol).
Use:
-Chronic pain
Tox:
- Similar to opioids
- Decreases seizure threshold
- Serotonin syndrome
34
Ethosuximide
MOA: Blocks thalamic T-type Ca2+ channels
Use: 1st line for Generalized (Absence) seizure.
Side effects: GI, fatigue, headache, urticaria, Steven-Johnson syndrome.
EFGHIJ= Ethosuximide, GI distress, headache, Itching, and steven-Johnson syndrom.
Notes: Sucks to have Silent (absence) Seizures
35
Benzodiapzines (diazepam, lorazepam)
MOA: increase GABAa action
Use: 1st line prophylaxis for status epilepticus
Side Effects: sedation, tolerance dependence, respiratory depression
Notes: Also for eclampsi seizures (1st line if MgSO4)
36
Valproic Acid
MOA: increase Na+ channel inactivation
Use: simple, complex (partial)seizures. 1st line for tonic clonic seizures, and absence
Side Effects: GI distress, rare but fatal hepatoxicity (measure LFTs), neural
Notes: Also used for myoclonic seizures, bipolar disorder
37
Phenobarbital
MOA: incease GABAa action
Use: simple, complex, tonic-clonic seizures
Side Effects: sedation, tolerance, dependence, induction of cyt P-450, cardiorespiratory depression
Notes: 1st line in neonates
38
Topiramate
MOA: Blocks Na+ channels, increases GABA action
Use: simple, complex, tonic-clonic seizures
Side Effects: sedation, mental dulling, kidney stones, weight loss.
Notes: Also used for migraine prevention
39
Levetiracetam
MOA: Unknown; may modulate GABA and glutamate
Use: simple, complex, tonic-clonic seizures
40
Tiagbine
MOA: Increase GABA by inhibiting re-uptake
Use: simple, complex seizures
41
Vigabatrin
MOA: Increase GABA irreversibly inhibiting GABA transaminase
Use: simple, complex seizures
42
Steven-Johnson syndrome
- Prodrome of malaise and fever
- Followed by rapid onset of erythematous/purpuric macules (oral, ocular, genital).
- Skin lesions progress to epidermal necrosis and sloughing
43
Barbituates (Phenobarbital, pentobarbital, thiopental, secobarbital)
MOA: Facilitate GABAa action by increasing duratioin of Chloride channel opening, thus decreasing neuron firing. Contraindicated in porphyria.
Use: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)
Tox: Respiratory and cardiovascular depression (can be fatal); CNS depression ( can be exacerbated by alcohol use); dependence, drug interactions (induces cyt P-450).
Overdose tx is supportive (assist resp. and maintain BP).
44
Benzodiazepines (diazepam, lorazepam, triazolam, temazepam, oxzepam, midazolam, chlordiazepoxide, alprazolam)
MOA: Facilitate GABAa action by increasing frequency of chloride channel opening. -decreases REM sleep.
-Most have long half-lives and active metabolites (exceptions: triazolam, oxazepam, and midazolam are short acting --> higher addictive potential.
Use: Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxifcation (esp. alcohol withdrawal -- DTs), night terrors, sleepwalking, general anesthetic (amnesia, muscle relaxation), hypnotic (insomnia).
Tox: dependence, additive CNS depression effects with alcohol. Less risk of respiratory depression and coma than with barbituates.
Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor).
45
Nonbenzodiazepine hypnotics (Zolpdem (ambien), Zaleplon, esZopiclone. "All ZZZz put you to sleep."
MOA: Act via the BZI subtype of the GABA receptor. Effects reversed by flumazenil
Use: Insomnia
Tox: Ataxia, headaches, confusion. Short duration because of rapid metabolism by liver enzymes. Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects. Less dependence risk than benzo.
46
Anesthetics-general principles
- CNS drugs must be lipis soluble (cross the blood-brain barrier) or to be actively transported.
- Drugs with less solubility in blood = rapid induction and recovery times.
- Drugs with more solubility in lipids = more potency =1/MAC
MAC = Minimal Alveolar Concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (e.g. skin incision).
47
Inhaled anesthetics
MOA: Mechanism unknown
Use: Myocardial depression respiratory depression, N/V, increase cerebral blood flow (decreased cerebral metabolic demand).
Tox: Hepattoxicity (haothan(, nephrotoxicity (methoxyflurane), proconvulsant( enflurane), expansion of trapped gas in a body cavity (NO). Can cause malignanat hypernatremia -rare, life-threatening hereditary condition in which inhaled anesthetics (except NP0) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene.
48
Intravenous anesthetics, Barbituates
Theopental - high potency, high lipid solubility, rapid entry into brain.
Use: for induction of anesthesia and short surgical procedures.
Effect terminated by rapid redistribution into tissue (i.e., skeletal muscle) and fat decreases cerebral blood flow
49
Intravenous anesthetics, Benzodiazepines
Most common drug used for endoscopy; used adjunctively with gaseous anesthetics and narcotics.
Tox: May cause severe postoperative respiratory depression, low BP (treat overdose with flumazenil), and anterograde amnesia.
50
Intravenous anesthetics, Arylcylohexylamines (Ketamine)
PCP analogs that act as dissociative anesthetics.
MOA: Block NMDA receptors. Cardiovascular stimulants.
Side effects: Cause disorientation, hallucination, and bad dreams. Increases cerebral blood flow.
51
Intravenous anesthetics, Opiods
Types: Morphine and Fentanyl
Use: Used with other CNS depressants during gen. anesthesia
52
Intravenous anesthetics, Propofol:
MOA: Potentiates GABAa.
Use: Sedation in ICU, rapid anesthesia induction, and short procedures. less postoperative nausea than thiopental.
53
Local Anesthetics
(Esters- procaine, cocaine, tetracaine).
(Amides- lIdocaiI, mepIvacaIne, bupIvacaIne ( amIdes have 2 I's)
MOA: Block Na2+ channls by binding to specific receptors on inner portion of channel. Preferntially bind to activated Na+ channels, so most effective in rapidly firing neurons. 3^o amine local aneshetics penetrate membrane in uncharged form, then bind to ion channels as charged form
Use: Can be given with vasoconstrictors (usually epinephrine) t enhance local action -- decrease bleeding, increase ansesthesia by decreasing systemic concentration.
Used for minor surgerical procedures, spinal anesthesia. If allergic to esters, give amides.
Tox: CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine).
54
Neuromuscular blocking drugs(Depolarizing)
succinlyncholine
Use: for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
MOA: Succinlycholine- strong ACh recepto agonist; produces sustained depolarization and prevents muscle contraction.
Reversal blockade:
-Phase I (prolonged depolarization) - no antidote!!. Block potentiated by cholinesterase inhibitors.
-Phase II (repolarized but blocked; ACh receptors are available, but desensitized) - antidote consists of cholinesterase
Complications include hypercalcemia, hyperkalemia, and malignant hyperthermia
55
Neuromuscular blocking drugs (Polarizing)
-Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium
Use: for muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor.
MOA: competitive antagonsits - compete with ACh receptors.
Reversal of blockade - neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors.
56
Dantrolene
MOA: Prevents the relase of Ca2+ from the sarcoplasmic reticulum of skeletal muscle
Use: treat maligant hyperthermia and neuroleptic malignant syndrome( a toxicity of antipsychotic drugs).
57
Parkinson disease drugs
- Parkinsonism is due to loss of dopaminergic neurons and excess cholinergic activity
```
BALSA:
Bromocriptine
Amantadine
Levopdopa (with carbidopa)
Selegiline (and COM inhibitors)
Antimuscarinics
```
for essential or familial tremors, use a β-blocker (e.g., propranolol).
58
Bromocriptine (ergot), pramipexole, ropinirole (non-ergot)
MOA: dopamine agonists
non-ergots are preferred
59
Amantadine
MOA: increase dopamine release
Use: antiviral against influenza A and rubella
Tox: ataxia
L-dopa/carbidopa is converted to dopamine in CNS
60
Selegiline
MOA:
-Selegiline- selective MAO type B inhibitor, preferentially metabolizes dopamine over norpeinephrine and 5-HT, thereby increasing the availability of doapmine.
Use: adjunctive agent to L-dopa in treatment of Parkinson disease
Tox: May enhance effects of L-dopa
61
Entacapone
MOA: COMT inhibitors, prevent L-dopa degradation --> increase dopamine availability.
Use: Parkinson Disease
62
Tolcapone
MOA: COMT inhibitors, prevent L-dopa degradation --> increase dopamine availability.
Prevent dopamine breakdown
Use: Parkinson Disease
63
L dopa (leveodopa)/ carbidopa
MOA: Increase dopamine in brain. Can cross blood-brain barrier, converted by dopa decarboxylase in CNS to dopamine.
-Carbidopa, a peripheral decarboxylase inhibitor, given with L-dopa to increase bioavailibility of L-dopa in brain and limit peripheral side effects.
Use: Parkinson Disease
Tox: Arrhythmias from increased peripheral formation of catecholamines. Long-term use can lead to dyskinesia between doses.
64
Benztropine
MOA: Antimuscarinic, curb excess cholinergic activity
Use: Parkinson disease, improves tremor and rigidity but has little effect on bradykinesia
**Park your mercedes- Benz."
65
Memantine
MOA: NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+).
Use: Alzheimer treatment
Tox: dizziness, confusion, hallucinations
66
Donepezil, galantamine,rivastigmine
MOA: AChE inhibitors.
Use: Alzheimer treatment
Tox" Nausea, dizziness, insomnia
67
Huntington drugs
Neurotransmitter changes in Huntington disease: low GABA, low ACh, high dopamine,
Treatments:
Tetrabenazine and reserpine -inhibit vesicular monoamine transport (VMAT); limit doapmine vesicle packaging release
Haloperidol- dopamine receptor antagonist
68
Sumatriptan
MOA: 5-HT IB/ID agonist. Inhibits trigeminal nerve activation; prevents vasoactive peptide release; induces vasoconstriction. Half life <2 hours.
Use: Acute migraine, cluster headache attacks.
Tox: Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal angina), mild tingling.
