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

Neuro 2 Flashcards

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
Q

IV anesthetics:

Name 5

A

“The Mighty King Proposes Foolishly to Oprah”

  1. Thiopental (Barb)
  2. Midazolam (Benzo)
  3. Ketamine (Arylcyclohexylamines)
  4. Propofol
  5. Opioid (morphine/ fentanyl)
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26
Q 
Thiopental:
Potency
Lipid Solubility 
Brain entry/ brain effect
Use
A
  • high potency
  • high lipid solubility
  • rapid entry into brain/ decrease cerebral blood flow

Use: induction of anesthesia and Short surgical procedures

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27
Q

Thiopental:

elimination

A

rapid redistribution into tissue and fat

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28
Q 
Midazolam:
Use
Admin w/...
Adverse (3)
Treatment of overdose
A
  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

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29
Q

Ketamine ( a Arylcyclohexylamines)
MOA
Heart effects, CNS effects
Adverse (2)

A

PCP analog–>block NMDA-R
- cardiovascular stimulants/ increase cerebral blood flow

  1. disorientation
  2. hallucination/ bad dreams
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30
Q 
Propofol:
MOA
induction
Use(2)
comparison to thiopental
A
  • 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

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31
Q

Opioids:
Name 2 IV
MOA

A
  1. Morphine
  2. Fentanyl

-bind mu-R and typically combined with other CNS depressants during general anesthesia

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32
Q

which IV anesthetic increases cerebral b.flow?

decreases?

A 
increase = ketamine
decrease= thiopental
33
Q

Effect of COPD/atelectasis on induction time for inhaled anesthetics

A

increase Dead space–>increase time of anesthetic to become effective

34
Q

Effect of increased HR on induction time

A

increase HR–> increase b.flow–>
decrease partial pressure of drug (dilutes drug in blood)
–> increase time of anesthetic to become effective

35
Q

MAC not affected by:

A
  1. Type of Noxious stimulus
  2. Sex
  3. Height
  4. Weight
  5. Duration of exposure
36
Q 
How is MAC affected by: 
Age
Hyperthyroidism
Sedative interaction
Amphetamine interaction
Red hair
A
  • 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
Q 
Local Anesthetics: 
Name Esters (4)
A
  1. Procaine
  2. Cocaine
  3. Tetracaine
  4. Benzocaine
38
Q

Local Anesthetics:

Amides (3)

A

“am’I’des have 2 I’s in name”

  1. Lidocaine
  2. Mepivacaine
  3. Bupivacaine
39
Q

Local Anesthetics:

MOA

A

block Na+ channels by binding inner portion of receptor

40
Q

Local Anesthetics:
Order of Neuron affected

Order of sensation loss

A
  • most effective in rapidly firing neurons
  • small myelinated >small unmyelinated> large myelinated > large unmyelinated

-pain > temp > touch > pressure

41
Q

Local Anesthetics:
Structure/charge
Affect of Infection in area to drug effect

A
  • 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
Q

Local Anesthetic:
Use
Allergy

A
  1. Minor surgical procedures
  2. spinal anesthesia
  • if allergic to esters, give amides
43
Q

Local Anesthetics:

Adverse

A
  1. CNS excitation
  2. Severe cardiovascular tox (Bupivacaine)
  3. HTN, Hypotension, Arrhythmia (cocaine)
    4 Methemoglobinemia (Benzocaine)
44
Q

Neuromuscular blocking drugs:

Clinical Uses

A

Muscle paralysis in surgery or Mechanical Ventilation

selective for motor nicotinic-R

45
Q 
Depolarizing Neuromuscular Blocking Drugs:
Name Drug (1)
A

Succinylcholine

46
Q

Succinylcholine:

MOA

A

Strong Ach-R agonist–>produces sustained depolarization and prevents muscle contraction

47
Q

Succinylcholine:

Phase I vs Phase2 block

A

Phase I: prolonged depolarization–>Flaccid paralysis

  • No Antidote
  • Potentiated by AchEi

Phase 2: repolarized but desensitized

  • Ach-R are available
  • reversed with AchEi
48
Q

Succinylcholine:

Complications (3)

A
  1. hypercalcemia
  2. hyperkalemia
  3. malignant hyperthermia
49
Q 
Nondepolarizing Neuromuscular Blocking Drugs:
Name Drugs (6)
A

“containe -cur-“ in them

  1. Tubocurarine
  2. atracurium
  3. mivacurium
  4. pancuronium
  5. vecuronium
  6. rocuronium
50
Q

Nondepolarizing Neuromuscular Blocking Drugs:
MOA
Reversal(3)

A
  • competitive antagonists- compete with Ach for receptor
  • Reversal:
    1. Neostigmine (w/atropine to prevent bradycardia)
    2. edrophonium
    3. other cholinesterase inhibitors
51
Q

Dantrolene:
MOA
Clinical Use(2)

A
  • binds RyR to prevent Ca+2 release from SR
  1. Malignant Hyperthermia
  2. Neuroleptic Malignant Syndrome
52
Q

Baclofen:
MOA
Clinical Use (3)

A

-Activates GABA-b-R at spinal cord level–>skeletal muscle relaxation (PERIPHERAL)

  1. Muscle spasms (acute low back pain)
    2 Post-spinal injury
  2. MS
53
Q 
Cyclobenzaprine:
MOA
Structurally similar to what?
Clinical Use (1)
Adverse
A

-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
Q

NT changes in Parkinson’s disease

A

decrease DA

increase Ach

55
Q

Parkinson’s Disease drugs (5)

A

“BALSA”

  1. Bromocriptine
  2. Amantadine
  3. Levodopa (w/ carbidopa)
  4. Selegiline (and COMT inhibitors
  5. Antimuscarinics (Benztropine)
56
Q

Which parkinson’s drug inhibits DOPA decarboxylase (DDC)?

Overall effect

A

Carbidopa

prevents peripheral L-DOPA –> dopamine conversion

57
Q

Name the 2 COMT inhibitors.
Overall effect
Which crosses the BBB?

A
  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
Q

Name the 2 MAO inhibitor used in Parkinson’s.
What specific MAOi do they inhibit
Overall effect

A
  1. Selegiline= enhances response to L-DOPA
  2. Rasagiline
  • inhib MAO-Type B
  • prevent Dopamine –> DOPAC conversion
59
Q

Name 3 Dopamine agonists in PD.

Which are ergots and which are non-ergots?

A

Ergot:
1. Bromocriptine

Non-Ergot

  1. Pramipexole
  2. Ropinirole
60
Q

Drug which increases dopamine availability in PD?

Adverse

A

Amantadine (increase DA release, decrease DA reuptake)

Adverse:

  1. Ataxia
  2. Livedo reticularis (purple lacey skin- may want to google picture)
61
Q

Agents which increase L-DOPA availability in Pd

A

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
Q

Agents which prevent DA breakdown in PD

A

Agents act CENTRALLY to inhib breakdown of dopamine

  1. Selegiline- block MAO-B (adverse= orthostatic hypotension)
  2. Tolcapone- block COMT centrally
63
Q

Agents which curb excess cholinergic activity in PD

A

Benzotropine (“PARK your Mercedes-BENZ”)

-improves tremor and rigidity but has little effect on bradykinesia in Parkinsons

64
Q

Levodopa/ carbidopa:
MOA
Adverse (2)

A
  • 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
Q

Selegiline, Rasagiline:
MOA
Clinical Use
Adverse (1)

A

-inhib MAO-B–>increase dopamine availability
Use: adjunct agent to L-dopa in PD
Adverse: enhance effects of L-dopa

66
Q

Alzheimers drugs:

Name (5)

A

NMDA-R antagonist
1. Memantine

AchEi

  1. Donepezil
  2. galantamine
  3. rivastigmine
  4. tacrine
67
Q

Memantine:
MOA
Use
Adverse (2)

A
  • non-competitive NMDA-R antagonist–> prevent excitotox mediated by Ca+2
  • Alzheimer drugs
  1. Dizzy/confusion
  2. Hallucinations
68
Q

Donepezil, galantamine, rivastigmine, tacrine:
MOA
Use
Adverse (3)

A
  • AchEi–> increase Ach
  • Alzheimer treatment: don’t change disease course but may slow progression
  1. N
  2. Dizzy
  3. insomnia
69
Q

Huntington Disease:

Name 3 drugs

A
  1. Tetrabenazine
  2. Reserpine
  3. Haloperidol
70
Q

Tetrabenazine, reserpine:
MOA
Use
Adverse (2)

A
  • inhib vesicular monoamine transporter (VMAT) –> decrease dopamine vesicle packaging and release
    -Huntington disease
    Adverse: monitor for hypotension and depression
71
Q

Haloperidol:
MOA
Use

A
  • D2-R antagonist
    1. Huntington disease
    2. Anti-psych drug
72
Q

Riluzole:
MOA
Effect

A
  • unknown MOA
  • decrease glutamate excitotoxicity –> increase survival

“For LOU Gehrig disease, give riLOUzole”

73
Q

Triptans:
Name (1)
MOA

A

Sumatriptan (nasal or pill)

  • 5-HT1b/1d agonists.
    1. inhib CN V
    2. prevent vasoactive peptide release
    3. induce vasoconstriction
74
Q

Triptans:
Use (2)
Adverse (2)
Contra (2)

A

Use: 1. Acute migraine 2. cluster HA
Adverse: 1. Coronary vasospasm 2. mild paresthesia
Contra: 1. CAD(caution in elderly) 2. Pritzmetal angina

75
Q

Drugs causing Cinchonism (2)

A
  1. Quinidine

2. Quinine

76
Q

Drugs causing Parkinson-like syndromes (3)

A

“cogwheel rigidity of ARM”

  1. Antipsychotics
  2. Reserpine
  3. Metoclopramide
77
Q

Drugs causing Seizures(4)

A

“with seizures, I BItE my tongue”

  1. Isoniazid (B6 def)
  2. Buproprion
  3. Imipenem/cilastatin
  4. Enflurane
78
Q

Drugs causing Tardive Dyskinesia (2)

A
  1. Antipsychotics

2. Metoclopramide

79
Q

Drugs causing Nephrotoxicity/ Ototoxicity (4)

A
  1. Aminoglycosides
  2. Vancomycin
  3. Loop diuretics
  4. Cisplatin (may respond to amifostine)

Drugs- Basic High Yield Stuff for Boards (20 decks)

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