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Exam 2 II Flashcards

1
Q

aspirin

A
  • cox inhibitor; more selective for cox 1

- anti-inflammatory

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2
Q

acetaminophen

A
  • cox 2 inhibitor
  • more of analgesic than anti-inflammatory
  • metabolized to cannabinoid
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3
Q

ibuprofen

A
  • non-specific cox inhibitor

- anti-inflammatory AND analgesic

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4
Q

naproxen

A
  • longer acting non-specific cox inhibitor

- anti-inflammatory

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5
Q

examples of NSAIDs / antipyretics

A
  • aspirin
  • acetaminophen
  • ibuprofen
  • naproxen
  • methyl salicylate
  • camphor
  • menthol
  • trolamine
  • capsacin
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6
Q

methyl salicylate

A
  • wintergreen oil
  • counter irritant; cause low level stimulation of pain receptors so that pain is transmitted less
  • metabolized to salicylic acid
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7
Q

camphor

A

counter irritant

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8
Q

menthol

A

counter irritant

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9
Q

trolamine

A

metabolized to salicylic acid

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10
Q

capsacin

A
  • TRPV1 channels mediates sensation and pain
  • TRPV1 agonist
  • you become tolerant to the heat effect
  • stimulating those channels keeps from pain mediation
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11
Q

examples of steroidal anti-inflammatory drugs

A
  • hydrocortisone
  • triamcinolone
  • beclomethasone
  • fluticasone
  • mometasone
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12
Q

hydrocortisone

A

same as cortisol

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13
Q

What are the synthetic analogues of hydrocortisone and what effect does it have on them?

A
  • triamcinolone
  • beclomethasone
  • fluticasone
  • mometasone
  • much more active
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14
Q

MOA of glucocorticoid /corticosteroid

A

decrease release and synthesis of cytokines and chemokines

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15
Q

examples of antihistamines

A
  • these are H1 blockers
  • diphenhydramine
  • doxylamime
  • cetirizine
  • loratadine
  • fexofenadine
  • ketotifen
  • pheniramine
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16
Q

With respect to antihistamines, what is the difference between sedating and non-sedating?

A
  • sedation happens when you block H1 in the brain

- if it’s peripherally restricted -> no sedation

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17
Q

Which one of the anti-histamines are (non-) sedating?

A
  • sedating: diphenhydramine and doxylamime
  • somewhat sedating: cetirizine
  • non-sedating: fexofenadine
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18
Q

example of mast cell stabilizer

A

cromolyn sodium

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19
Q

cromolyn sodium

A
  • has almost no side effects
  • stabilize mast cells that release inflammatory mediators
  • Rx ophthalmic drops
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20
Q

What antitussive is available OTC?

A

dextromethorphan

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21
Q

dextromethorphan

A
  • opioid structure

- MOA: blocks medullary cough center

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22
Q

levorphanol

A
  • L- isomer of dextromethorphan

- potent opioid

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23
Q

example of expectorant

A

guafenesin

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24
Q

guafenesin

A

increases volume and decreases viscosity of bronchial /tracheal secretions

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25
Q

MOA of decongestants

A

alpha-1 adrenoceptor agonists

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26
Q

examples of decongestants

A
  • phenylephrine
  • pseudoephedrine
  • naphazoline
  • oxymetazoline
  • tetrahydrozoline
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27
Q

What counseling point is important when dispensing nasal decongestants?

A
  • take it for a few days
  • if doesn’t work, then stop
  • if you don’t stop, you’ll get rebound congestion and it’ll get worst
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28
Q

examples of local anesthetics

A
  • lidocaine
  • xylocaine
  • benzocaine
  • dyclonine
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29
Q

MOA of local anesthetics

A
  • block pain neurotransmission through fast voltage-gated sodium channels
  • jams up sodium channel in skin; causes decrease in pain transmission
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30
Q

examples of topical anti-microbials

A
  • cetylpyridium
  • Neosporin
  • carbamide peroxide
  • phenol
  • terbenafine
  • clotrimazole
  • miconazole
  • zinc pyrithone
  • Permethrin
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31
Q

cetylpyridium

A

4° NH4 antiseptic

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32
Q

Neosporin

A
  • neomycin gram- (a little+)
  • polymyxin B gram-
  • bacitracin gram+
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33
Q

carbamide peroxide

A
  • broad spectrum antimicrobial

- oxidizing agen

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34
Q

phenol

A

local anesthetic and antimicrobial

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35
Q

terbenafine

A
  • tinea pedis (foot fungus)

- corporis (ring worm)

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36
Q

clotrimazole

A
  • tinea pedis (foot fungus)
  • corporis (ring worm)
  • anti-yeast
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37
Q

miconazole

A
  • tinea pedis (foot fungus)
  • corporis (ring worm)
  • vaginal yeast infections
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38
Q

zinc pyrithone

A
  • very weak

- used for dandruff

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39
Q

Permethrin

A
  • fairly broad spectrum and weak
  • insecticide from chrysanthemum
  • lice treatment
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40
Q

What are the types of GI drugs?

A
  • H2 blockers
  • PPI
  • Antacids
  • Anti-gas
  • Anti-diarrheals
  • Laxatives
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41
Q

H2 blockers MOA and examples

A
  • blocks H2 receptors in parietal cells -> decrease stomach acid
  • ranitidine
  • famotidine
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42
Q

PPI MOA

A

blocks H/K ATPase in parietal cells -> decrease stomach acid

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43
Q

Examples of antacids

A
  • calcium carbonate

- magnesium / aluminum hydroxide

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44
Q

Anti-gas MOA and examples

A
  • decrease surface tension on gas bubbles

- simethicone

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45
Q

examples of anti-diarrheals

A
  • loperamide: µ opioid agonist → ↓ GI motility; actus on gut and low CNS activity
  • bismuth subsalicylate: antibacterial / NSAID
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46
Q

examples of laxatives

A
  • fiber
  • PEG 3350
  • bisacodyl
  • senna
  • docusate
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47
Q

fiber

A

draws water/ add bulk into stool

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48
Q

PEG 3350

A

draws water into stool

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49
Q

bisacodyl

A

stimulant (local irritant)

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50
Q

senna

A

stimulant (local irritant)

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51
Q

docusate

A
  • stool softener

- surfactant - makes stool easier to pass

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52
Q

examples of acne drugs

A
  • benzoyl peroxide: peeling agent - ↑ skin turnover → ↓ bacterial count
  • salicylic acid: peeling agent, antibacterial, lyses pimples
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53
Q

Where are fast action potentials found?

A
  • atria
  • ventricles
  • Purkinje fibers
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54
Q

Where are slow action potentials found?

A
  • SA node

- AV node

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55
Q

What is responsible for automaticity of cardiac tissues?

A

pacemakers

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56
Q

Parasympathetic effect on SA and AV node

A
  • ↓Ca++ channels
  • ↑K+ channels
  • ↓I-f currents
  • ↓APs
  • ↓HR
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57
Q

Sympathetic effect on SA and AV node

A
  • ↑Ca++ currents

- ↑HR

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58
Q

What does after-depolarization lead to?

A
  • getting a second stimulation during refractory period

- ineffective pumping throughout the body

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59
Q

conduction block

A
  • abnormal conduction through AV node, bundle of His, bundle branch
  • leads to stimulation of the tissue itself
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60
Q

What are the reasons for which conduction block can occur?

A
  • Abnormal anatomy (Wolf-Parkinson White)

- Damaged cardiac tissue

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61
Q

What is the therapeutic class of Vaughn-Williams Classification?

A

anti-arrhythmic

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62
Q

What are the Vaughn-Williams Classification?

A
  • Type I: sodium blockers
  • Type II: beta blockers
  • Type III: potassium channel blockers
  • Type IV: calcium channel blockers
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63
Q

Type I VWC

A
  • affect conductive tissue

- there are three types: IA, IB, IC

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64
Q

Type IA VWC

A
  • medium affinity for Na+ channels
  • bind inactivated version of sodium channels and keep them in their inactivated form
  • ↓ conduction velocity
  • ↑ refractoriness (will take longer for cell to recover)
  • ↓ automaticity through sodium channels
  • also blocks potassium channels -> increase repolarization time -> arrhythmia
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65
Q

examples of drugs for Type IA VWC

A
  • procainamide
  • disopyramide
  • quinidine
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66
Q

Type IB VWC

A
  • binds loosely to sodium channels
  • inhibits over-stimulation to heart
  • selective for depolarized tissue
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67
Q

examples of drugs for Type IB VWC

A

lidocaine

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68
Q

Type IC VWC

A
  • high affinity for Na channel
  • slows conduction of heart
  • also blocks potassium channels
  • arrhythmogenic
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69
Q

Torsades de Pointes

A

QT interval prolongation

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70
Q

examples of drugs for Type IC VWC

A
  • propafenone

- flecainide

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71
Q

Type II VWC

A
  • block beta receptors
  • affect mostly SA node
  • indirectly affect Ca channels; ↓sympathetic effects on Ca channels
  • slows ventricular response to AFIB via AV node
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72
Q

Type III VWC

A
  • block K channels but not completely
  • leads to delayed repolarization
  • lengthen refractory period
  • also affect slow potassium channels in pacemakers
  • increased QT prolongation
  • can be arrhythmogenic - not for chronic use
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73
Q

examples of drugs for Type III VWC

A

in order of decreasing activity:

  • ibutilide
  • dofetilide
  • sotalol
  • amiodarone
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74
Q

pacemaker conduction

A

SA -> AV -> bundle of His -> Perkinje

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75
Q

Type IV VWC

A
  • block Ca channels in SA and AV nodes
  • slows conduction
  • prolonged refractory
  • slows ventricular response to AFIB
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76
Q

adenosine

A
  • ↑K+ channels in atria and SA/AV nodes

- ↓automaticity

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77
Q

digoxin

A
  • affects nodes
  • ↓Ca channels
  • ↑K+ channels
  • parasymp. effects
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78
Q

angina definition and goals

A
  • cardiac ischemia = decreased O2 to the heart

- increase O2 to heart or decrease O2 demand

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79
Q

Define demand (equation) with respect to cardiac output

A

CO = HR x PVR

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80
Q

What are the consequences of cardiac ischemia?

A
  • thickening or tinning of heart muscle
  • systolic hypotension
  • contractility decrease
  • myocardial damage
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81
Q

What are the factors that determine myocardial oxygen demand?

A
  • heart rate
  • preload
  • after load
  • contractility
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82
Q

What are the three major types of angina?

A
  • fixed stenosis - stable occlusion
  • coronary artery spasm
  • unstable angina - dislodging -> thrombosis
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83
Q

MOA of nitrates

A

MOA cleaves nitrate → NO → ↑guanylate cyclase →↑ cGMP → vasorelaxation

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84
Q

In nitrates, what happens with quantity of dose?

A
  • low doses: favor venous dilation; decrease preload, decrease O2 consumption -> less stress on the heart
  • high doses: arterial AND venous dilation -> decrease both pre and after load
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85
Q

An example of drug-drug interaction with nitrate (that we discussed in class)

A

PDE5 inhibitor (denafils) -> both increase cGMP which would decrease the blood pressure way too much

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86
Q

coronary steal

A
  • dilating vessels that are already dilated

- these vessels are small and they don’t really contribute to helping the heart itself

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87
Q

MOA of beta blockers

A
  • ↓β1-adrenoceptors
  • ↓HR & contractility
  • ↓myocardial oxygen consumption
88
Q

examples of Ca blockers

A
  • verapamil
  • amlodipine
  • nifedipine
  • nicardipine
  • diltiazem
89
Q

MOA of Ca blockers

A
  • ↓ voltage-gated Ca++ channels
  • ↓contractility
  • ↓HR (slight)
  • ↓myocardial oxygen consumption
  • will also decrease preload
90
Q

Drugs for angina

A
  • beta blocker
  • Ca blocker
  • ranolazine
  • ivabradine
91
Q

ranolazine

A
  • ↓ intracellular sodium level
  • ↓ sodiumdependent calcium channels
  • ↓myocardial contractility
  • ↓myocardial oxygen demand
92
Q

ivabradine

A
  • ↓ If sodium current in the SA node
  • ↓myocardial APs in SA node
  • ↓HR
  • ↓myocardial oxygen demand
  • Little to no effect on BP, contractility and conductance
93
Q

examples of inotropes

A
  • Cardiac Glycosides
  • Beta agonists
  • Phosphodiesterase (PDE) inhibitors
94
Q

Cardiac Glycosides

A
  • digoxin
  • blocks Na/K ATPase
  • increases intracell. Ca and Na
  • increase contractility and decreased heart rate
  • parasymp. stimulation
  • can lead to arrhythmias
95
Q

What happens to digoxin in hypokalemia?

A

higher affinity for Na/K ATPase

96
Q

examples of beta agonists

A
  • dopamine
  • dobutamine
  • isoproterenol
97
Q

dopamine

A
  • dose dependent
  • low dose: inotrophic effect, ↑ contractility
  • high doses: ↑ contractility AND α adrenoceptor stimulation → vasoconstriction
  • cut off is at 10 µg/kg/min
98
Q

dobutamine

A
  • favors β1 but also stimulates β2

- ↑ inotropy

99
Q

isoproterenol

A
  • nonselective β agonist
  • ↑ inotropy /chronotropy
  • ↓ PVR, ↑HR
100
Q

examples of PDE3 inhibitors

A
  • inamrinone

- milrinone

101
Q

effect of PDE3 inhibitors

A
  • ↑ cAMP
  • ↑ myocardial contractility
  • ↑ CO
  • ↑ myocardial relaxation
  • ↑ arteriole>venous dilation
  • ↓ afterload> preload
102
Q

lusitropy

A
  • myocardial relaxation

- how well the heart is going back to its resting state between beats

103
Q

chronotropy

A
  • heart rate

- due to conduction system of heart

104
Q

inotropy

A
  • contractility of heart

- due to contract of heart muscle

105
Q

What innervates 60-80% of neurons?

A
  • glutamate
  • major excitatory neurotransmitter in the
    CNS
106
Q

What are the receptors for glutamate?

A
  • NMDA
  • AMPA
  • they are ion channels
  • when they are bound -> neurotransmission
107
Q

What are the inhibitory neurotransmitters?

A
  • GABA - released via CNS
  • glycine - released via brainstem and spinal cord
  • hyperpolarize neuron
108
Q

What is responsible for the fine tuning of the brain?

A

Monoamine neurotransmitters:

  • DA
  • NE
  • 5-HT (serotonin)
109
Q

What does fine tuning mean?

A

can tweak considerably and still be alive

110
Q

What are drugs that are not a benzodiazepine but have the same effects?

A
  • zolpidem

- zaleplan

111
Q

MOA of GABA(a) agonists

A
  • Cl channel
  • Cl goes into cell
  • hyperpolarize cell
112
Q

Effects of benzo’s and GABA(a) agonists

A
  • muscle relaxation
  • sedation
  • anti-anxiety
  • hyponosis
113
Q

ADR of benzo’s / GABA(a) agonists

A
  • sedation
  • muscle relaxation
  • stimulatory effects
  • anterograde amnesia
  • psychological dependence
114
Q

melatonin

A

involved in circadian clock

115
Q

suvorexant

A
  • orexin antagonist

- associated with “wake” part in the sleep/wake cycle

116
Q

disease states of spasticity of muscle

A
  • CP
  • MS
  • MG
  • sroke
  • spinal injury
117
Q

mechanisms against spasticity

A
  • ↓ activity of nerve fibers that excite motor neurons

- ↑ activity of inhibitory interneurons (i.e., GABA)

118
Q

baclofen

A
  • GABA(b) agonist
  • skeletal muscle relaxant
  • mostly used for milder spasticity diseases
119
Q

tizanidine

A
  • central alpha-2 agonist
  • skeletal muscle relaxant
  • decrease NE
120
Q

dantrolene

A
  • calcium blockers via ryanodrine receptor

- skeletal muscle relaxant

121
Q

misc. skeletal muscle relaxants

A
  • carisoprodol
  • cyclobenzaprine
  • chlorzoxazone
122
Q

define depression

A

decreased of synaptic transmission of 5-HT, NE, and DA in brain

123
Q

How can you treat depression to get clinical results quicker?

A
  • NMDA receptor antagonist (ex. ketamine)
  • stimulation of dopaminergic pathway
  • keeping BDNF in the brain
124
Q

iproniazid

A
  • MAO inhibitor

- used for depression

125
Q

reserpine

A

used for BP but also depletes stores of NT -> depression

126
Q

examples of tricyclic antidepressants

A
  • amitripyline

- imipramine

127
Q

MOA of tricyclic antidepressants

A
  • inhibit reuptake of NT

- block specific 5-HT receptors

128
Q

ADR of tricyclic antidepressants

A
  • drowsiness
  • CNS stimulation
  • hypotension
  • dry mouth, blurred vision
  • increased suicide risk
129
Q

examples of SSRI

A
  • fluoxetine
  • paroxetine
  • citalopram
  • escitalopram
  • sertraline
130
Q

MOA of SSRI

A

inhibit reuptake of 5-HT

131
Q

ADR of SSRI

A
  • decreased libido
  • drowsiness
  • insomnia
  • dry mouth
  • increase suicide risk
132
Q

MOA of SNRI

A
  • inhibit reuptake of 5-HT and NE
133
Q

examples of SNRI

A

venlafaxine

134
Q

ADR of SNRI

A
  • drowsiness
  • insomnia
  • increased suicide risk
  • FYI may work better than anxiety patients
135
Q

examples of DNRI

136
Q

MOA of DNRI

A

inhibit reuptake of NE and DA

137
Q

ADR of DNRI

A
  • less change of weight gain
  • decreased libido
  • should not be used on patients with insomnia
138
Q

lithium

A
  • drug of choice for manic phase of bipolar disorder
139
Q

MOA of lithium

A

decreases neuronal signaling proteins

140
Q

ADR of lithium

A
  • metallic taste
  • lethargy
  • cognition problems
  • muscle spasms
  • cleared by kidneys; if pt on diuretic, will decrease levels of this
141
Q

MOA of anti-epileptics

A
  • Na channel blocker/ inactivator
  • Ca channel blocker/ inactivator
  • Cl channel enhancers (via GABA)
  • down-regulation of neuronal firing
  • Glutamate antagonism
  • K enchancement
142
Q

anti-epileptics and metabolism

A
  • highly lipophilic -> high protein binding

- CYP450 inducer

143
Q

phenytoin

A
  • antiepileptic
  • Na channel blocker
  • Michaelis Menten metabolism
144
Q

carbamazepine

A
  • antiepileptic

- Na blocker

145
Q

ethosuximide

A
  • antiepileptic
  • Ca blocker
  • drug of choice for absence seizures
  • ADR: can make other types of seizures worst
146
Q

gabapentin

A
  • antiepileptic
  • can also be used for: fibromyalgia, headache
  • Ca blocker
147
Q

lamotrigine

A
  • antiepileptic
  • Na and glutamate blockers
  • also used for bipolar
148
Q

valproate

A
  • antiepileptic
  • broad: affects Na, Ca, GABA, etc
  • also used for: pain, bipoar
149
Q

dopamine pathway: mesocortical

A

affect thoughts; cognition and processing information

150
Q

dopamine pathway: nigrostriatal

A

affect movement

151
Q

dopamine pathway: tuberoinfundibular

A

regulate prolactin level

152
Q

L-DOPA

A
  • enters CNS but broken down by DOPA decarboxylase, COMT, and MAO
153
Q

carbidopa

A
  • peripheral DOPA decarboxylase inhibitor

- given with L-DOPA to increase DA in CNS

154
Q

tolcapone

A

COMT inhibitor

155
Q

selegeline

A

MAO inhibitor

156
Q

schizophrenia

A
  • increased DA in CNS

- psychosis

157
Q

chlorpromazine

A
  • class: phenothiazines
  • used for psychosis
  • non-specific D2 receptor blockers
  • ADR: can also block ACh, H, NE; can cause pseudo-Parkinson
158
Q

haloperidol

A
  • used for psychosis
  • increased D2 blocking activity
  • ADR: non-selective so also blocks nigrostriatal
159
Q

serotonin receptor antagonist

A
  • used for psychosis
  • clozapine
  • risperidone
  • aripiprazole
160
Q

aripiprazole

A
  • serotonin receptor antagonist

- has dopaminergic activity and can help with Parkinsons

161
Q

clozapine

A
  • serotonin receptor antagonist

- best agent but causes severe blood effects

162
Q

What is the site of action of local anesthetics?

A
  • bind to Na channels to block nerve conduction

- decrease membrane permeability of Na

163
Q

What happens with the administration of local anesthetics?

A
  • nerve excitation threshold increases
  • impulse conduction slows
  • action potential declines
164
Q

What are factors that affect a nerve’s susceptibility to blockade by local anesthetics?

A
  • myelination
  • pH
  • location of administration
  • plasma protein binding
  • metabolism
165
Q

susceptibility to nerve blockade by LA: myelination

A

myelinated fibers more sensitive because they interact with nodes of ranvier

166
Q

susceptibility to nerve blockade by LA: diameter

A
  • smaller is more sensitive

- 3 nodes must be exposed –> smaller diameter = more nodes exposed

167
Q

loss of sensation in decreasing order

A

pain > cold > warmth > touch > deep pressure > motor

168
Q

How can you create intracellular acidosis when administering LA?

A

administer solutions saturated with CO2

169
Q

Why would you need to create intracellular acidosis with respect to LA?

A
  • to make the drug into the cationic form

- the cation form binds to Na channel

170
Q

Onset of blockade is increased with addition of bicarbonate. Why is this?

A
  • increases concentration of uncharged form of drug

- more can pass through membrane

171
Q

Percent of protein bound drug with respect to pH

A

decrease pH = decrease binding

172
Q

What are the classes of anesthetics?

A
  • esters

- amide

173
Q

What happens to esters in circulation?

A
  • inactivated by hydrolysis

- spinal fluid doesn’t contain much esterases

174
Q

How does amides get inactivated?

A
  • metabolism by liver enzymes

- but some metabolites are more active than their parent compound

175
Q

What rx is a mixed structure between the two groups of LA?

A
  • articaine
  • classified as amide but ester required for binding
  • hydrolysis of ester terminates action
  • used for dental procedures
176
Q

How does age affect plasma binding of LA?

A
  • neonates and elders have fewer plasma binding proteins

- elder have lower CO -> slow delivery to liver

177
Q

How does lipid solubility affect LA rx?

A
  • improve diffusion through neuronal membrane

- reduce diffusion through extracellular fluids

178
Q

What are examples of drugs with contain the vasoconstrictor enhancement effects?

A
  • epi
  • levonordefrin
  • oxymetazoline
179
Q

ADR of LA

A
  • drowsiness
  • CNS stimulation
  • tongue numbness, metallic taste
  • nystagmus / muscle twitching
  • convulsions
180
Q

What are the LA effects to the cardiovascular system?

A
  • decrease pacemaker activity

- hypotension

181
Q

Which LA are antiarrythmic drugs?

A
  • lidocaine

- procainamide

182
Q

Which LA is cardiotoxic?

A

bupivacaine

183
Q

What are LA formulated with that can provoke allergic reactions?

A
  • preservatives

- anti-oxidants

184
Q

methemoglobinemia

A

accumulation of hydrolytic metabolites

185
Q

How can methemoglobinemia occur?

A
  • administering > 400mg of prilocaine in adults

- administering benzocaine to gums / mouth in children < 2 years

186
Q

What symptoms does methemoglobinemia produce?

A
  • cyanosis
  • SOB
  • faituge
  • increased heart rate
  • headache, lightheadedness, confusion
187
Q

ADR of EPI

A
  • decrease peripheral resistance
  • increase heart rate
  • increase stroke volume
  • in higher doses: heart palpitations, increase BP, CP
188
Q

ADR of phenylephrine

A
  • increase BP

- increase HR

189
Q

ADR of nordefrin

A
  • increase BP

- increase HR

190
Q

properties of lidocaine

A
  • amide
  • potent
  • rapid onset
  • ADR: drowziness, heart block, arrythmia, hypotension
191
Q

properties of mepivacaine

A

3% solution has its own vasoconstriction and doesn’t need to be formulated with EPI

192
Q

Which LA will give paresthesia (numbness / tingling) with a 4% solution?

193
Q

Which LA is metabolized into PABA?

A
  • Procaine
  • Tetracaine
  • PABA inhibits sulfonamide drugs
194
Q

What is the LA that can be used intra-nasally?

A

Tetracaine + Oxymetazoline

195
Q

With respect to the physical state of the skin, when is the potential for toxicity greater than normal?

A

when skin or mucous membrane is abraded and/or if applied to large surface area

196
Q

Characteristics of ideal anesthetic

A
  • rapid onset of action
  • wide safety margin
  • permit rapid recovery
  • devoid adverse effects
197
Q

Examples of inhaled anesthetics

A
  • fluranes: volatile liquids

- NO

198
Q

If we can’t measure how much drug gets into the brain, how do we measure how much medication reach CNS via inhalation route?

A
  • assume equilibrium and measure how much gets into the lung
  • Palv is used for substitute for Pcns
199
Q

How do you compare potencies of gases?

A
  • MAC: median alveolar concentration

- concentration that produces immobility of 50% of patients

200
Q

Factors that affect potency of therapeutic gas

A
  • lipid solubility
  • age
  • body temp
  • hematocrit
  • PaO2, PaCO2
  • current CNS being used
201
Q

Factors that affect rate of induction of general anesthesia

A
  • solubility (in different compartments)
  • pulmonary ventilation
  • pulmonary blood flow
202
Q

Rate of induction consequences

A
  • ↑ delivery of gas by ↑ ventilation
    → ↑ Palv
  • ↑ Rate of uptake into blood by ↓ cardiac output (↓ pulmonary blood flow)
203
Q

respiratory anesthetics

A
  • resp. depressant
  • ↓ response to CO2
  • ↑ resp. rate
  • ↓ tidal volume
  • ↓ musociliary function
204
Q

propofol

A
  • GABAa and Glycine-R activator
  • rapid recovery
  • less N/V
  • no histamine release
  • no analgesic properties
205
Q

etomidate

A
  • enhance GABA but not glycine
  • maintain CV stability
  • induce nausea and vomiting
206
Q

ketamine

A
  • analgesia, amnesia, catalepsy
  • NMDA agonist
  • ADR: floating sensation, hallucinations, HTN, ↑ CO, tremor
207
Q

dexmedetomidine MOA

A

α2A-AR agonist approved for sedation in intubated and pre- and perioperative nonintubated patients

208
Q

dexmedetomidine advantages

A
  • Analgesic and anxiolytic w/no respiratory
  • ↓ MAC of inhaled anesthetics
  • Sedation is short acting; pts easily aroused
  • Shorter half-life than clonidine
209
Q

dexmedetomidine disadvantages

A

no reversal agent yet

210
Q

dexmedetomidine ADR

A
  • hypotension
  • bradycardia
  • xerostomia
  • large doses: OD, vasoconstriction, bradycardia, ↓ CO
211
Q

For anesthesia, what would barbiturates be used for?

A

induce / maintain anesthesia

212
Q

How does barbiturates help in anesthesia?

A
  • increase duration of GABAa-receptor mediated Cl channel opening
  • not GABA dependent
  • inhibits excitatory AMPA/kainate receptors
  • increases capacity of glycine receptor activation
213
Q

For anesthesia, what would benzodiazepines be used for?

A

sedate and reduce anxiety

214
Q

examples of benzodiazepines

A
  • midazolam

- versed

215
Q

benzodiazepines MOA

A
  • promote binding of GABA to its receptor

- requires GABA for activity

216
Q

What is the difference between benzodiazepines and barbiturates?

A
  • benzodiazepines: do not produce true general anesthesia; antidote is flumazenil
  • barbiturates: do produce true general anesthesia; no antidote

OU PDA (8 decks)

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