Drugs- Basic High Yield Stuff for Boards > Neuro 2 > Flashcards

Neuro 2 Flashcards

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1
Q

Barbituates:

Name (4)

A
  1. phenobarbital
  2. pentobarbital
  3. thiopental (only one commonly used now)
  4. secobarbital
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2
Q

Barbituates:
MOA
Clinical Use (2)

A

“BarbiDURATes INCREASE DURATION”
-Facilitate GABA-A action by INCREASE DURATION of Cl- channel opening–>decrease neuron firing

  1. Sedative for anxiety/seizures/insomnia
  2. induction of anesthesia (THIOPENTAL)

“Barbie likes it to last longer, while Ben likes it more frequently” (yes, barbie dumped ken for ben)

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3
Q

Barbituates:
Adverse(4)
Contra(1)
Overdose treatment

A
  1. Respiratory & Cardiovascular depression (can be fatal)
  2. CNS depression (exacerbated by ETOH)
  3. Dependence
  4. P450 inducer
  • Contra: Porphyrias
  • Overdose tx: supportive (assist resp. and maintain BP)
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4
Q

Benzodiazepines:

Name 8

A
  1. Diazepam
  2. Lorazepam
  3. Triazolam
  4. Temazepam
  5. Oxazepam
  6. Midazolam
  7. Chlordiazepoxide
  8. Alprazolam
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5
Q

Benzodiazepines:
MOA
Which have short half-lives? Why does this matter?

A

“FREnzodiazepines INCREASE FREQUENCY”
-Facilitate GABA-A action by INCREASE FREQUENCY of Cl- channel opening

  • Most drugs have long half-lives and active metabolites except ‘ATOM’
    1. Alprazolam
    2. Triazolam
    3. Oxazepam
    4. Midazolam
  • these are short acting–>higher addiction potential
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6
Q

What 3 drugs all bind the GABA-A Receptor?

What type of receptor is it?

A
  1. Benzo
  2. Barbs
  3. Alcohol
    - Ligand-gated Cl- channel
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7
Q 
Benzodiazepines:
Clinical uses (8)
A
  1. Anxiety
  2. spasticity
  3. Status epilepticus (lorazepam/diazepam/midazolam)
  4. eclampsia
  5. detox (esp ETOH-withdrawal)
  6. Night terrors/ sleep walking (increase STAGE2/ decrease STAGE4&REM)
  7. General anesthetic (amnesia, muscle relaxation)
  8. hypnotic (insomnia)
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8
Q

What 3 benzo’s are used to treat status epileptics

A
  1. Diazepam
  2. lorazepam
  3. midazolam
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9
Q

Benzodiazepines:
Adverse
Comparison to Barbituates
Overdose treatment

A
  1. dependence
  2. CNS depression (exacerbated by ETOH)
  3. precipitate seizures w/ causing Acute Benzo if chronic Benzo use
  • Benzos safer than Barbs b/c less respiratory depression, coma, antidote available
  • Overdose tx: Flumazenil (competitive GABA:Benzo-R antagonist
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10
Q

Non-benzodiazepine Hypnotics:

Name 3

A

“all ZZZs put you to sleep”

  1. Zolipidem
  2. Zaleplon
  3. esZopiclone
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11
Q 
Non-benzodiazepine Hypnotics:
MOA
Effect on sleep cycle
Clinical Use (1)
Duration?
A
  • Bind BZI subtype of GABA-R
  • Sleep cycle less affected (no change in REM) as compared with Benzos
  1. insomnia
    - short duration b/c rapidly metabolized by liver
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12
Q

Non-benzodiazepine Hypnotics:
Adverse (2)
Antidote

A
  1. Ataxia
  2. HA/ confusion

-effects reversed by Flumazenil

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13
Q

Non-benzodiazepine Hypnotics:

Compare to older sedative hypnotics(4)

A
  1. Modest day-after psychomotor depression
  2. few amnestic effects
  3. less dependence risk than Benzos
  4. lower abuse potential (increase dose= increase GI upset)
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14
Q

2 ways for local anesthetic to cross BBB?

A
  1. lipid soluble

2. active transport

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15
Q

Drugs with decreased solubility in blood have what kind of onset/duration?
Example?

A

rapid induction & rapid recovery times

  • Nitrous Oxide (N2O) has low blood/low lipid solubility
  • -> fast induction & low potency
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16
Q

Describe MAC

A

Minimal Alveolar Concentration

=concentration required to prevent 50% of subjects from moving in response to noxious stimulus

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17
Q

what’s the relationship btw potency and MAC

A

inverse

potency= 1/MAC

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18
Q

What effect does increased drug solubility in lipids have on potency?
Example?

A

increase lipid solubility = increase potency

  • Halothane has high lipid/blood solubility–> slow induction and high potency
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19
Q

Inhaled anesthetics:

7

A

all end in “-ane” except N2O

  1. Desflurane
  2. Halothane
  3. Enflurane
  4. Isoflurane
  5. Sevoflrane
  6. Methoxyflurane
  7. N2O
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20
Q

What kind of effect does N2O as a inhaled anesthetic?

A

Not strong enough to suppress CNS alone but potentiates other drugs when used in combo

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21
Q

Inhaled anesthetics:
MOA
Effects (4)

A
  • Unknown MOA
  1. Myocardial depression
  2. respiratory depression
  3. increased cerebral blood flow (decrease cerebral metabolic demand)
  4. N/V (couple with anti-emetic post-surgery)
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22
Q 
Inhaled anesthetics:
Adverse
1. Halothane
2. Methoxyflurane
3. Enflurane
4. N2O
A
  1. ‘H’alothane–> ‘H’epatotox
  2. Methoxyflurane –>Nephrotox
  3. ‘E’nfluane–> ‘E’pileptic potential
  4. N2O–>expansion of trapped gases in body cavity
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23
Q

Describe Malignant Hyperthermia

Etiology

A

-rare, life-threatening condition in which inhaled anesthetics or succinylcholine induce F/Severe Muscle contractions

  • Autosomal Dominant with variable penetrance
  • Mutation in VSens RyR–>increase Ca+2 release from SR
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24
Q

Treatment for Malignant Hyperthermia

MOA

A

Dantrolene, RyR antagonist

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25
IV anesthetics: | Name 5
"The Mighty King Proposes Foolishly to Oprah" 1. Thiopental (Barb) 2. Midazolam (Benzo) 3. Ketamine (Arylcyclohexylamines) 4. Propofol 5. Opioid (morphine/ fentanyl)
26
``` Thiopental: Potency Lipid Solubility Brain entry/ brain effect Use ```
- high potency - high lipid solubility - rapid entry into brain/ decrease cerebral blood flow Use: induction of anesthesia and Short surgical procedures
27
Thiopental: | elimination
rapid redistribution into tissue and fat
28
``` Midazolam: Use Admin w/... Adverse (3) Treatment of overdose ```
1. endoscopy (short procedure where you don't need to put patient completely under Admin with Gaseous Anesthetics and Narcotics Adverse: 1. severe post-op Respiratory depression 2. decrease BP 3. anterograde amnesia Overdose tx: Flumazenil
29
Ketamine ( a Arylcyclohexylamines) MOA Heart effects, CNS effects Adverse (2)
PCP analog-->block NMDA-R - cardiovascular stimulants/ increase cerebral blood flow 1. disorientation 2. hallucination/ bad dreams
30
``` Propofol: MOA induction Use(2) comparison to thiopental ```
- potentiates GABA-A and inhib NMDA-R ('pro' GABA-a, 'fool' NMDA-R) - rapid induction 1. Sedation in ICU 2. short procedures Less post-op Nausea than thiopental
31
Opioids: Name 2 IV MOA
1. Morphine 2. Fentanyl -bind mu-R and typically combined with other CNS depressants during general anesthesia
32
which IV anesthetic increases cerebral b.flow? | decreases?
``` increase = ketamine decrease= thiopental ```
33
Effect of COPD/atelectasis on induction time for inhaled anesthetics
increase Dead space-->increase time of anesthetic to become effective
34
Effect of increased HR on induction time
increase HR--> increase b.flow--> decrease partial pressure of drug (dilutes drug in blood) --> increase time of anesthetic to become effective
35
MAC not affected by:
1. Type of Noxious stimulus 2. Sex 3. Height 4. Weight 5. Duration of exposure
36
``` How is MAC affected by: Age Hyperthyroidism Sedative interaction Amphetamine interaction Red hair ```
- MAC is approximated for a 40yo, increase MAC in infancy and decrease MAC in old age - hyperthyroidism- increase MAC - Sedative- decrease MAC - Amphetamine- increase MAC - Red hair- increase MAC
37
``` Local Anesthetics: Name Esters (4) ```
1. Procaine 2. Cocaine 3. Tetracaine 4. Benzocaine
38
Local Anesthetics: | Amides (3)
"am'I'des have 2 I's in name" 1. Lidocaine 2. Mepivacaine 3. Bupivacaine
39
Local Anesthetics: | MOA
block Na+ channels by binding inner portion of receptor
40
Local Anesthetics: Order of Neuron affected Order of sensation loss
- most effective in rapidly firing neurons - small myelinated >small unmyelinated> large myelinated > large unmyelinated -pain > temp > touch > pressure
41
Local Anesthetics: Structure/charge Affect of Infection in area to drug effect
- tertiary --> penetrate membrane in uncharged form then binds to ion channel as charged form - In infected/acidic tissue, alkaline anesthetics are charged and can't penetrate membrane effectively ---> NEED MORE ANESTHETIC
42
Local Anesthetic: Use Allergy
1. Minor surgical procedures 2. spinal anesthesia * if allergic to esters, give amides
43
Local Anesthetics: | Adverse
1. CNS excitation 2. Severe cardiovascular tox (Bupivacaine) 3. HTN, Hypotension, Arrhythmia (cocaine) 4 Methemoglobinemia (Benzocaine)
44
Neuromuscular blocking drugs: | Clinical Uses
Muscle paralysis in surgery or Mechanical Ventilation | selective for motor nicotinic-R
45
``` Depolarizing Neuromuscular Blocking Drugs: Name Drug (1) ```
Succinylcholine
46
Succinylcholine: | MOA
Strong Ach-R agonist-->produces sustained depolarization and prevents muscle contraction
47
Succinylcholine: | Phase I vs Phase2 block
Phase I: prolonged depolarization-->Flaccid paralysis - No Antidote - Potentiated by AchEi Phase 2: repolarized but desensitized - Ach-R are available - reversed with AchEi
48
Succinylcholine: | Complications (3)
1. hypercalcemia 2. hyperkalemia 3. malignant hyperthermia
49
``` Nondepolarizing Neuromuscular Blocking Drugs: Name Drugs (6) ```
"containe -cur-" in them 1. Tubocurarine 2. atracurium 3. mivacurium 4. pancuronium 5. vecuronium 6. rocuronium
50
Nondepolarizing Neuromuscular Blocking Drugs: MOA Reversal(3)
- competitive antagonists- compete with Ach for receptor - Reversal: 1. Neostigmine (w/atropine to prevent bradycardia) 2. edrophonium 3. other cholinesterase inhibitors
51
Dantrolene: MOA Clinical Use(2)
- binds RyR to prevent Ca+2 release from SR 1. Malignant Hyperthermia 2. Neuroleptic Malignant Syndrome
52
Baclofen: MOA Clinical Use (3)
-Activates GABA-b-R at spinal cord level-->skeletal muscle relaxation (PERIPHERAL) 1. Muscle spasms (acute low back pain) 2 Post-spinal injury 3. MS
53
``` Cyclobenzaprine: MOA Structurally similar to what? Clinical Use (1) Adverse ```
-CENTRALLY acting sk.muscle relaxant. Structurally similar to TCAs 1. Muscle spasms (not neuro-related) Adverse similar to anticholinergic drugs. 1. Drowsiness 2. Dry mouth 3. Dizzy 4. Blurred Vision
54
NT changes in Parkinson's disease
decrease DA | increase Ach
55
Parkinson's Disease drugs (5)
"BALSA" 1. Bromocriptine 2. Amantadine 3. Levodopa (w/ carbidopa) 4. Selegiline (and COMT inhibitors 5. Antimuscarinics (Benztropine)
56
Which parkinson's drug inhibits DOPA decarboxylase (DDC)? | Overall effect
Carbidopa | prevents peripheral L-DOPA --> dopamine conversion
57
Name the 2 COMT inhibitors. Overall effect Which crosses the BBB?
1. Entacapone ('can't get ENTA the brain') 2. Tolcapone ('can go TOLtally everywhere') prevents L-Dopa breakdown into 3-O-methyldopa (3-OMD)
58
Name the 2 MAO inhibitor used in Parkinson's. What specific MAOi do they inhibit Overall effect
1. Selegiline= enhances response to L-DOPA 2. Rasagiline - inhib MAO-Type B - prevent Dopamine --> DOPAC conversion
59
Name 3 Dopamine agonists in PD. | Which are ergots and which are non-ergots?
Ergot: 1. Bromocriptine Non-Ergot 2. Pramipexole 3. Ropinirole
60
Drug which increases dopamine availability in PD? | Adverse
Amantadine (increase DA release, decrease DA reuptake) Adverse: 1. Ataxia 2. Livedo reticularis (purple lacey skin- may want to google picture)
61
Agents which increase L-DOPA availability in Pd
Agents prevent PERIPHERAL L-DOPA degradation--> increase L-DOPA entering CNS to be converted to Dopamine centrally 1. Levodopa (w/ carbidopa)- blocks DDC, reduces Levodopa side effects of N/V 2. Entacapone & Tolcapone- block COMT
62
Agents which prevent DA breakdown in PD
Agents act CENTRALLY to inhib breakdown of dopamine 1. Selegiline- block MAO-B (adverse= orthostatic hypotension) 2. Tolcapone- block COMT centrally
63
Agents which curb excess cholinergic activity in PD
Benzotropine ("PARK your Mercedes-BENZ") -improves tremor and rigidity but has little effect on bradykinesia in Parkinsons
64
Levodopa/ carbidopa: MOA Adverse (2)
- L-DOPA can cross BBB --> converted by central -DDC to dopamine - peripheral DDC is inhibited by Carbadopa - this combo together increases the bioavailability of L-DOPA in brain with limited adverse 1. Arrhythmias (from peripheral formation of catecholamines) 2. Dyskinesia-Akinesia ('on-off') symptoms (long-term use)
65
Selegiline, Rasagiline: MOA Clinical Use Adverse (1)
-inhib MAO-B-->increase dopamine availability Use: adjunct agent to L-dopa in PD Adverse: enhance effects of L-dopa
66
Alzheimers drugs: | Name (5)
NMDA-R antagonist 1. Memantine AchEi 2. Donepezil 3. galantamine 4. rivastigmine 5. tacrine
67
Memantine: MOA Use Adverse (2)
- non-competitive NMDA-R antagonist--> prevent excitotox mediated by Ca+2 - Alzheimer drugs 1. Dizzy/confusion 2. Hallucinations
68
Donepezil, galantamine, rivastigmine, tacrine: MOA Use Adverse (3)
- AchEi--> increase Ach - Alzheimer treatment: don't change disease course but may slow progression 1. N 2. Dizzy 3. insomnia
69
Huntington Disease: | Name 3 drugs
1. Tetrabenazine 2. Reserpine 3. Haloperidol
70
Tetrabenazine, reserpine: MOA Use Adverse (2)
- inhib vesicular monoamine transporter (VMAT) --> decrease dopamine vesicle packaging and release -Huntington disease Adverse: monitor for hypotension and depression
71
Haloperidol: MOA Use
- D2-R antagonist 1. Huntington disease 2. Anti-psych drug
72
Riluzole: MOA Effect
- unknown MOA - decrease glutamate excitotoxicity --> increase survival "For LOU Gehrig disease, give riLOUzole"
73
Triptans: Name (1) MOA
Sumatriptan (nasal or pill) - 5-HT1b/1d agonists. 1. inhib CN V 2. prevent vasoactive peptide release 3. induce vasoconstriction
74
Triptans: Use (2) Adverse (2) Contra (2)
Use: 1. Acute migraine 2. cluster HA Adverse: 1. Coronary vasospasm 2. mild paresthesia Contra: 1. CAD(caution in elderly) 2. Pritzmetal angina
75
Drugs causing Cinchonism (2)
1. Quinidine | 2. Quinine
76
Drugs causing Parkinson-like syndromes (3)
"cogwheel rigidity of ARM" 1. Antipsychotics 2. Reserpine 3. Metoclopramide
77
Drugs causing Seizures(4)
"with seizures, I BItE my tongue" 1. Isoniazid (B6 def) 2. Buproprion 3. Imipenem/cilastatin 4. Enflurane
78
Drugs causing Tardive Dyskinesia (2)
1. Antipsychotics | 2. Metoclopramide
79
Drugs causing Nephrotoxicity/ Ototoxicity (4)
1. Aminoglycosides 2. Vancomycin 3. Loop diuretics 4. Cisplatin (may respond to amifostine)
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