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Advanced Pharmacology ANE 8433 (Spring 2023) > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

What is the definition of general anesthesia?

A

Induced loss of consciousness & not arousable, even by painful stimulation.

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2
Q

Describe minimal sedation?

A
  • Pt is still awake
  • Able to respond
  • No LOC change
  • Self sustained airway
  • Stable VS.
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3
Q

Describe Moderate sedation?

A
  • Easily arousable to verbal or touch
  • CV system unimpaired but a bit sleepy
  • Able to maintain own airway
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4
Q

Describe deep sedation?

A
  • Responsive to painful stimuli
  • Airway assistance may be required
  • CV usually maintained
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5
Q

What was the reversal for soporific sponges?

A

Vinegar

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6
Q

Why was Diethyl ether used recreational?

A

Due to whiskey tax

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7
Q

What did Sir Christopher Wren & Robert Boyle invent?

A

IV access

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8
Q

What did Joseph Priestly discover?

A

Oxygen & nitrous oxide, & photosynthesis

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9
Q

What did Humphry Davy discover & suggest?

A
  • Potassium, sodium, calcium, magnesium
  • Suggested nitrous oxide use for pain relief in surgery
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10
Q

What is Horace Wells known for?

A
  • Noticed no pain recall when using N2O.
  • Used N2On@ Mass General for amputation.
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11
Q

What is Hewitt known for?

A

Designing first anesthesia machine with nitrous & oxygen

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12
Q

What is Crawford Long known for?

A

Used ether for a Pt with 2 vascular neck tumors.

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13
Q

What is William Morton known for?

A
  • Needed anesthesia for denture fitting
  • Used ether
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14
Q

Why was the 1st public ether demonstration lucky?

A

Poor inhaler fit, no IV access, prolonged emergence.

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15
Q

What is Robinson Squibb known for?

A

Developed process for pure ether

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16
Q

What are disadvantages with ether?

A

Has a very slow onset & even slower offset, flammable, odor, high incidence of N/V

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17
Q

What is Sir James Simpson known for?

A

Defined pain: “actual or potential tissue damage”

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18
Q

What is Dr. John Snow known for?

A
  • Full time anesthesiologist for Queen Victoria
  • Discovered epidemiology
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19
Q

What is Guthrie known for?

A

Delayed chloroform hepatotoxicity in children

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20
Q

What is Dr. Koller known for?

A

Cocaine as an anesthetic for eye surgery.

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21
Q

What is Dr. Halsted known for?

A

1st regional (mandibular) nerve block using cocaine.

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22
Q

What is Dr. August Bier known for?

A
  • 1st spinal using cocaine
  • Developed Bier block
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23
Q

Who was the first nurse anesthetist?

A

Sister Mary Bernard

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24
Q

What is Agatha Hodgins known for?

A
  • Developed nitrous/oxygen techniques
  • Founded AANA
  • Opened one of the 1st CRNA schools
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25
Q

Why is cyclopropane not used anymore?

A

Violently explosive

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26
Q

Why is halothane not used anymore?

A

Slow onset & can cause Hepatitis

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27
Q

What is Isoflurane not used for & why?

A

Outpatient Sx due to slow offset

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28
Q

What is the most rapid onset & offset gas?

A

Desflurane

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29
Q

What is Edmund Egar known for?

A
  • Establishing MAC
  • Did lots of experiments & published info about desflurane (Suprane)
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30
Q

What is the best volatile gas for asthmatics & why?

A

Sevoflurane because it does not cause airway irritation.

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31
Q

What is the “triad” of anesthesia & what was added later?

A

Amnesia, analgesia, muscle relaxation & Homeostasis was added later

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32
Q

Why was analgesia not favorable initially?

A

It had a high death rate

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33
Q

What is Dr. Liston known for?

A

3 deaths from 1 operation

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34
Q

What is Dr. George Crile known for?

A
  • Local infiltration of procaine prior to Sx
  • Light use of nitrous/oxygen for anesthesia
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35
Q

What is Harvey Cushing known for?

A
  • Regional blocks
  • Anesthetic records
  • BP/HR measurements
  • Used ether
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36
Q

What was the issue with neurolept anesthesia?

A

High incidence of awareness, dysphoria, extrapyramidal movements.

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37
Q

When is stage 1 of anesthesia?

A

Beginning of induction of general anesthesia to loss of consciousness.

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38
Q

What are the 3 planes of stage 1 of anesthesia?

A

1= no amnesia or analgesia
2= amnestic but only partially analgesic
3= complete analgesia & amnesia

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39
Q

When is stage 2 of anesthesia?

A

Loss of consciousness to onset of automatic breathing.

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40
Q

What signs (can/could) be observed in stage 2 of anesthesia?

A
  • Eyelash reflex disappears
  • Coughing
  • Vomiting
  • Struggling may occur
  • Irregular respirations
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41
Q

When is stage 3 of anesthesia?

A

Onset of automatic breathing to respiratory paralysis

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42
Q

When is stage 4 of anesthesia?

A

Stoppage of respiration till death

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43
Q

What are the 4 planes of Stage 3 anesthesia?

A

1= automatic respiration to cessation of eye movement.
2= cessation of eye movement to beginning of intercostal muscle paralysis; secretion of tears increases.
3= beginning to completion of intercostal muscle paralysis, mydriasis, desired plane prior to muscle relaxants.
4= complete intercostal paralysis to diaphragmatic paralysis.

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44
Q

Competitive antagonism will do what to the dose response curve?

A

Shifts it to the right

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45
Q

Describe inverse agonism?

A

Competes for the same site as the agonist but produces the opposite effect

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46
Q

Continued albuterol treatment in asthma patients does what over time?

A

Downregulates receptors

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47
Q

Pheochromocytomas can cause?

A

Decreased beta receptors in response to release of catecholamines

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48
Q

What are examples (3) of drugs using intracellular proteins?

A

Insulin, steroids, milrinone

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49
Q

What drug class (covered in class) uses circulating proteins?

A

Anticoagulants

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50
Q

What are examples of drugs using lipid bilayer receptors?

A

Opioids, beta-blockers, catecholamines, NMB, benzos.

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51
Q

Acidic drugs primarily bind to___ & alkalotic drugs primarily bind to___?

A

Albumin & Alpha-1 glycoprotein

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52
Q

What determines concentration of a drug available to receptors?

A

Only free drug

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53
Q

What are examples of decreased plasma proteins?

A

Age, hepatic disease, renal failure, pregnancy

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54
Q

Poor protein binding & lipophilic leads to?

A

Big volume of distribution

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55
Q

Give some examples of drugs with active metabolites?

A
  • Midazolam
  • Diazepam
  • Propranolol
  • Morphine
  • Prodrugs
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56
Q

What is Phase 1 metabolism & examples?

A

Increase polarity & prepare for Phase 2 reactions. Oxidation, reduction, hydrolysis.

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57
Q

What is Phase 2 metabolism?

A

Covalently link with higher polarity molecule to become water soluble. Conjugation

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58
Q

What is the most common Phase 1 enzyme & examples it metabolizes?

A

CYP3A4. Opioids, benzos, antihistamines, immunosuppressants, LA

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59
Q

Chronic EtOH use results in___ anesthetic use & acute EtOH results in___anesthetic use?

A

Normal & less

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60
Q

Inhibition___ enzyme activity & induction___ enzyme activity?

A

Decreases & increases

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61
Q

What are examples that cause enzyme inhibition & induction?

A
  • Inhibition= grapefruit juice
  • Induction= phenobarbital
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62
Q

When does passive tubular reabsorption increase?

A

If drug is lipid soluble

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63
Q

What is elimination ½ time?

A

Time it takes to eliminate 50% of drug from plasma.

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64
Q

What drugs are weak acids?

A

Barbiturates

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65
Q

What drugs are weak bases?

A

Opioids, local anesthetics

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66
Q

Which drug molecule will cause a pharmacologic effect, ionized or non-ionized?

A

Non-ionized

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67
Q

Non-ionized drugs are___ soluble, & ionized drugs are___ soluble?

A

Lipid & water

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68
Q

Which drug form is hepatic metabolized?

A

Non-ionized

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69
Q

A barbiturate with a PK of 6.8 is put in a solution with pH of 7, is it ionized or not?

A
  • Barbiturates are acids (Pk after pH)
  • pH - pK
  • 7 - 6.8= 0.2 = ionized
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70
Q

An opioid with a PK of 7.9 is put in a solution with a pH of 7.3, is it ionized or not?

A

7.9 – 7.3= + 0.6= ionized

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71
Q

What is Ion trapping?

A

Drug crosses the lipid bilayer back cannot escape

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72
Q

What is pharmacodynamics?

A

What the drug does to the body

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73
Q

About what percentage of current drugs are racemic?

A

33%

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74
Q

R-Bupivicaine is ___ cardiac toxic than L-Bupivicaine?

A

More

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75
Q

Why is Cisatracurium, the isomer of atracurium, better?

A

Lacks histamine effects

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76
Q

Histamine causes vasodilation, and especially in someone that?

A

Is dehydrated or has inflammation

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77
Q

What percent of receptors must be bound for Vecuronium to have its greatest effect?

A

70%

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78
Q

Compare sedatives vs hypnotics?

A

Sedatives induce calm or sleep & hypnotics induce hypnosis or sleep.

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79
Q

Sedatives & hypnotics both inhibit?

A

Thalamic & mid-brain RAS

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80
Q

What is altered by anesthesia, seen on EEG’s?

A
  • Cerebral blood flow (CBF)
  • Cerebral metabolic rate of oxygen (CMRO2)
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81
Q

The lower the BIS level/number means?

A

The lower= less movement

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82
Q

What is a desired BIS level during anesthesia & why?

A

40-60 & it’s enough to have no recall or movement.

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83
Q

The BIS monitor works best with narcotics, hypnotics, or ketamine?

A

With hypnotics

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84
Q

A BIS monitor suppression ration of 55 means what?

A

The patient is almost brain dead. The higher the number the worse the Pt is.

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85
Q

What are the 5 effects of benzodiazepines?

A
  • Anxiolytic
  • sedation
  • anterograde amnesia
  • anticonvulsant
  • spinal-cord mediated skeletal muscle relaxation.
86
Q

What would cause retrograde amnesia?

A

ECT (electroconvulsive therapy)

87
Q

Why have benzos replaced barbiturates for pre-op sedation?

A
  • Less tolerance
  • less abuse potential
  • fewer & less serious side effects
  • do not induce CYP450 (CYP2A) enzymes.
88
Q

Which drug is most attractive for post-op sedation & why?

A

Midazolam & it has less ½ time than diazepam & lorazepam

89
Q

What is the MOA of benzos?

A

Attach to nearby receptor increasing affinity for GABA receptor leading to chloride hyperpolarization of the postsynaptic membrane

90
Q

The bzd receptor is located where on GABA receptor?

A

Between the alpha-1 & gamma-2 subunits

91
Q

What effects does a bzd binding the alpha-1 subunit of a GABA receptor have?

A

Sedation, amnesia, anticonvulsant

92
Q

What effects does a bzd binding to the gamma-2 subunit of a GABA receptor have?

A
  • Anxiolytic
  • Skeletal muscle relaxation
93
Q

The alpha-1 subunit of a GABA receptor affects which parts of the brain?

A
  • (C)erebral cortex
  • (C)erebellar cortex
  • (T)halamus
94
Q

The Gamma-2 subunit of a GABA receptor affects which parts of the brain?

A

Hippocampus, amygdala

95
Q

Besides benzos, what other drugs bind to GABA receptors?

A
  • Barbiturates,
  • Etomidate
  • Propofol
  • EtOH
96
Q

What are the general effects of benzos?

A
  • Decreased alpha activity
  • Antegrade amnesia
97
Q

Benzos have synergistic effects with these?

A
  • EtOH
  • Injected anesthetics
  • Opioids
  • Alpha-2 agonists
  • Inhaled anesthetics
98
Q

How do benzos affect platelets?

A

They inhibit plt aggregation by inhibiting conformational change

99
Q

What stabilizes & allows rapid metabolism of midazolam?

A

The Imidazole ring

100
Q

What lasts longer with versed, sedation or amnesia?

A

Amnesia

101
Q

When is versed water soluble & when is it lipid soluble?

A
  • Water soluble & pronated @ a pH <3.5
  • Lipid soluble & unprotonated @ a pH >4.0
102
Q

What are the pharmacokinetics of versed?

A
  • Onset 1-2mins,
  • highly plasma protein bound,
  • peak effect 5mins, does not stay on receptor very long,
  • rapid redistribution, Vd is 1-1.5L/kg (large)
  • E ½ time is 2hrs (double in elderly),
  • stays longer in obese & elderly.
103
Q

How is & into what is midazolam metabolized?

A
  • Hepatic & intestinal CYP3A4 into active & inactive metabolites.
  • Active metabolites cleared by kidneys
  • ½ inactive is 1-hydroxymidazolam.
104
Q

What drugs cause inhibition of P-450 enzymes?

A
  • (A)ntifungal
  • (F)entanyl
  • (E)rythromycin
  • (C)imetidine
  • (C)CB’s
105
Q

What are the CNS effects of midazolam?

A
  • Decreased CMRO2 & CBF,
  • No isoelectric,
  • Potent anticonvulsant,
  • Preserve vasomotor response,
  • No change in ICP (Good for neuro Pt’s)
106
Q

What are the pulmonary effects of midazolam?

A
  • Decreased hypoxic drive
  • Depressed swallow reflex
  • Decreased upper airway activity
  • Depression with COPD
  • Transient apnea (esp w/ opioids)
107
Q

What are the CV effects of midazolam?

A
  • Dose dependent increased HR & lowered BP
  • Decreased SVR
  • No Cardiac output change
  • Enhanced hypotension w/ hypovolemia
  • Does not inhibit BP/HR response to intubation
108
Q

What is the midazolam pre-op dose for children & peak effect?

A

0.25-0.5mg/kg PO & peak effect in 20-30mins

109
Q

What is the midazolam pre-op dose for adults & peak?

A

1-5mg IV & peak @ 5mins

110
Q

What is the induction dose for midazolam & its preceding medication & dose?

A
  • Give 50 - 100mcg fentanyl
  • Wait 1 - 3 mins
  • Versed dose: 0.1-0.2mg/kg IV over 30-60sec
111
Q

What are the N/V occurrences with midazolam?

A

Rare

112
Q

What is the post-op dosing for midazolam?

A

1-7mg/hr

113
Q

What are the IV infusion guidelines for midazolam?

A

2-3 days due to T-cell effect –> harder time fighting infection

114
Q

What is the preparation of diazepam?

A

Insoluble in water & mixed w/ propylene glycol, which can burn on injection

115
Q

What are the pharmacokinetics of diazepam?

A
  • Onset 1-5mins
  • E ½ time: 20-40hrs
  • Extensively protein bound
  • High Vd
  • Shorter duration of action than lorazepam but longer E ½ time.
116
Q

What is the metabolism of diazepam?

A
  • CYP3A pathway
  • Return of drowsiness in 6-8hrs
117
Q

What are the 2 active metabolites of diazepam?

A

Desmethyldiazepam (48-96hrs) & oxazepam

118
Q

What are the CNS effects of diazepam?

A
  • CAN produce isoelectric EEG
  • anticonvulsant
  • abolishes DT’s
119
Q

What is the diazepam dose for convulsions?

A

0.1mg/kg IV

120
Q

What are the pulmonary effects of diazepam?

A
  • Minimal decrease in Vt.
  • Reversed w/ surgical stimulation
121
Q

What are the CV effects of diazepam?

A
  • Minimal BP, CO & SVR decrease.
  • Decreased BP w/ opioids
122
Q

What happens when mixing diazepam & nitrous?

A

No BP change but prevents recall

123
Q

What are the neuromuscular effects of diazepam?

A
  • Decreased tonic effect on spinal neurons & muscle tone.
  • No action at NMJ
124
Q

What is the induction dose of diazepam & when is it decreased?

A
  • 0.5-1.0 mg/kg IV
  • decreased w/ elderly, hepatic disease & presence of opioids
125
Q

What is the difference between lorazepam & oxazepam?

A

Lorazepam has an extra chloride atom

126
Q

Compared to midazolam & diazepam, lorazepam is more potent in what?

A

Sedation & amnesia

127
Q

What is the preparation of lorazepam?

A

Requires polyethylene glycol d/t water insolubility

128
Q

What are the pharmacokinetics of lorazepam?

A
  • 1 - 4mg IV,
  • peak effect in 20-30mins,
  • E ½ is 14hrs (glucuronidation),
  • Less affected by blood flow
  • Less affected by hepatic function, age, drugs
129
Q

What is the metabolism of Romazicon?

A

Hepatic enzymes to inactive metabolites

130
Q

What is the consciousness dosing for Romazicon (IVP & infusion)?

A
  • Repeat 0.1 mg q1min to 1mg total
  • 0.2 mg IV & titrated to consciousness.
131
Q

What is the reversal (sedation & therapeutic dose) dosing for Romazicon?

A
  • 0.3 – 0.6 mg to reverse sedation
  • 0.5 – 1.0 mg to abolish therapeutic dose
132
Q

What is the duration of action of Romazicon?

A

30 – 60mins

133
Q

What is the infusion dose of Romazicon?

A

0.1 – 0.4 mg/hr

134
Q

What does using Romazicon as reversal not affect?

A
  • No acute anxiety
  • No HTN or tachycardia
  • No change in MAC of volatiles
  • No neuroendocrine evidence
135
Q

When is Romazicon contraindicated?

A
  • It reverses anticonvulsive effects &
  • Precipitates acute withdrawal seizures
136
Q

Which drugs (4) pre-op drugs induce histamine release & what kind (2)?

A
  • Morphine, mivacurium, protamine, atracurium
  • Basophils & mast cells
137
Q

Released histamines from pre-op drugs induce what unwanted effects?

A
  • Contraction of airway smooth muscles
  • Stomach acid secretion
  • Neurotransmitter release (ACh, NE, 5HT-3)
138
Q

Histamines binding to H1 receptor leads to what negative effects?

A
  • Hyperalgesia & inflammatory pain
  • allergic rhino-conjunctivitis symptoms
139
Q

Histamine on H2 receptor leads to?

A
  • Elevated CAMP (Beta-1)
  • increases acid/volume production
140
Q

Histamine receptor activation through an agonist causes what?

A
  • Hypotension (nitric oxide release)
  • Flushing
  • Prostacyclin release
  • Tachycardia
  • Increased capillary permeability
141
Q

What is the E ½ time for diphenhydramine & what is the IV dose?

A

7 – 12hrs & 25 – 50 mg

142
Q

Diphenhydramine may inhibit___ & stimulates___?

A
  • Afferent arc of oculo-emetic reflex (this reflex causes N/V)
  • ventilation
143
Q

How does Benadryl stimulate ventilation?

A

Augments relationship of hypoxic & hypercarbic drives if given solo

144
Q

What is the E ½ time , dose & onset for Phenergan?

A
  • E 1/2: 9 – 16hrs
  • Dose: 12.5 – 25 mg IV
  • Onset 5mins
145
Q

What is the dose for cimetidine (Tagament)?

A
  • 150 – 300 mg
  • ½ dose in renal impaired Pt’s
146
Q

What are the adverse effects of cimetidine (Tagamet)?

A
  • Bradycardia, hypotension (cardiac H2 receptors),
  • increased prolactin plasma levels
  • inhibits dihydrotestosterone binding to androgen receptors
147
Q

What does cimetidine (Tagamet) strongly inhibit & what is affected?

A

CYP450 & affects drug metabolism of warfarin, phenytoin, lidocaine, propranolol, nifedipine, meperidine, diazepam, tricyclics

148
Q

Where is cimetidine (Tagamet) metabolized & cleared?

A

CYP450 & cleared in urine

149
Q

What is the dose & administration for ranitidine (Zantac)?

A
  • 50 mg diluted to 20cc
  • Infused over 2mins
  • 1/2 dose for renal impaired
150
Q

Which H2 antagonist does not interfere with CYP450 & is the most potent, what is its E 1/2?

A
  • Famotidine (Pepcid)
  • E ½: 2.5 – 4hrs
151
Q

What is the dose for Pepcid (famotidine)?

A

20 mg IV & ½ dose for renal impaired

152
Q

What does famotidine (Pepcid) interfere with?

A

Phosphate absorption –> hypophosphatemia

153
Q

How do PPI’s work?

A

Irreversibly bind & inhibit proton movement across gastric parietal cells

154
Q

What are PPI’s most useful for?

A
  • Controlling gastric acidity
  • Decreasing gastric volume
155
Q

What are PPI’s more effective in, compared to H2 antagonists?

A
  • Healing esophagitis & ulcers
  • Relieving GERD
  • Treatment of Zollinger-Ellison syndrome
156
Q

What is Zollinger-Ellison syndrome?

A

Digestive disorder resulting in too much gastric acid

157
Q

What possible side effects do PPI’s have?

A
  • Bone fractures
  • SLE
  • Acute interstitial nephritis
  • C-diff
  • Vit B-12 & magnesium deficiency
158
Q

Which two important drugs do PPI’s affect & how?

A

Blocks warfarin metabolism & blocks Plavix activation enzyme

159
Q

What is the dose for pantoprazole (protonix)?

A

40 mg in 100mL over 2-15mins

160
Q

What can long term use of antacids lead to?

A

Increased stomach pH –> inhibit food breakdown by acid & acid rebound can occur

161
Q

What are long term side effects of magnesium-based antacids use?

A
  • Osmotic diarrhea
  • Neurologic & neuromuscular impairment
162
Q

What are side effects of long term use of calcium-based antacids?

A

Hypercalcemia

163
Q

What are side effects of long term use of sodium-based antacids?

A

Increased sodium load (hypertensive Pt’s)

164
Q

Activating H1 receptors can lead to activation of what other receptors?

A

Muscarinic, cholinergic, 5-HT3, alpha-adrenergic

165
Q

Activating H2 receptors can lead to activation of what other receptors?

A

5-HT3 & Beta-1

166
Q

What is Benadryl mostly used for?

A

Antipruritic (allergies, anaphylaxis)

167
Q

Histamine antagonists are technically what?

A

Inverse agonists, they don’t prevent histamine release but responses

168
Q

What are H1 antagonists effective for?

A
  • Motion sickness
  • Bronchospasms
  • Cardiac stability
  • Anaphylaxis
169
Q

What are the side effects of H1 antagonists?

A

Blurred vision, urinary retention, dry mouth, drowsiness (1st gen).

170
Q

H2 receptor antagonists work by?

A
  • Decreasing CAMP, hypersecretion of gastric protons & gastric volume
  • increasing pH
171
Q

What are the side effects of H2 antagonists?

A
  • Diarrhea
  • HA
  • skeletal muscle pain
  • weakened gastric mucosa
  • bradycardia
  • increased creatinine by 15%
172
Q

What is the dose for omeprazole (Prilosec)?

A

40 mg in 100cc NS over 30mins or PO >3hrs prior

173
Q

How does omeprazole work?

A
  • Protonates parietal cells to active form,
  • only inhibits present pumps up 66% inhibition
174
Q

What are Omeprazole’s side effects?

A
  • Crosses BBB –> HA, agitation, confusion,
  • abd pain, N/V, flatulence, bowel bacterial growth
175
Q

Aspirating which antacids is worse?

A

Particulate (aluminum or magnesium based ones)

176
Q

Which antacids should be given for a trauma surgery?

A

Non-particulate, they neutralize stomach acid making it more alkalotic

177
Q

What is the dose & half-life of Sodium citrate (Bicitra)?

A

15 – 30mL PO & works immediately for 30 – 60mins

178
Q

What do dopamine blockers do?

A
  • Increase lower esophageal sphincter tone
  • Stimulate peristalsis
  • Increase gastric emptying
179
Q

What are side effects of dopamine blockers?

A
  • Orthostatic hypotension
  • Extrapyramidal reactions (crosses BBB)
  • Dopamine inhibition/depletion
180
Q

What is the dose for Reglan & when is it given?

A
  • 10 – 20mg over 3 – 5mins
  • Given 15 – 30mins prior to induction
181
Q

What are side effects of Reglan?

A
  • (D)ecreased plasma cholinesterase levels
  • (A)bd cramping
  • (M)uscle spasms
  • (N)euroleptic malignant syndrome (temp, rigidity, tachycardia, confusion)
  • (H)ypotension
  • (I)ncreased prolactin
  • (S)edation
182
Q

What is the dose for Droperidol?

A

0.625 – 1.25mg IV

183
Q

What are the side effects of Droperidol & what other class of meds should be avoided?

A
  • Extrapyramidal symptoms (involuntary movements)
  • Neuroleptic malignant syndrome
  • Prolonged QT
  • Avoid CNS depressants
  • Volatile anesthetics
184
Q

How does serotonin cause vomiting?

A

Chromaffin cells of small intestine release serotonin, which stimulates vagal afferents thru 5HT-3 –> vomiting

185
Q

What are 5HT-3 antagonists not effective for?

A

Motion sickness/vestibular stimulation

186
Q

What are the side effects of ondansetron?

A
  • HA
  • Diarrhea
  • Slight QT prolongation
187
Q

What is the plasma ½ life of ondansetron?

A

4hrs

188
Q

What is the onset & half life of Decadron?

A

Onset is 2hrs & 24hrs half life

189
Q

What is the dose for Decadron?

A

4mg, 8mg, or higher if airway issues/trauma while intubating

190
Q

What are the side effects of Decadron?

A
  • Perineal burning/itching (if rapid IV),
  • Slight perioperative hyperglycemia for DM Pt’s
191
Q

How does a scopolamine patch work?

A
  • Priming dose of 140mcg
  • 1.5mg released over next 48 - 72hrs
192
Q

What are the side effects of scopolamine?

A

Mydriasis, photophobia, sedation

193
Q

What is the onset & peak concentration for a scopolamine patch?

A

Apply 4hrs pre-op & peak in 24hrs

194
Q

What is the MOA of a scopolamine patch?

A

Muscarinic antagonist, competitive antagonist of ACh

195
Q

Where should a scopolamine patch be placed?

A

On thin skin areas like postauricular

196
Q

What are the actions of bronchodilators?

A

Reduce inflammatory cell activation & directly reax smooth muscle

197
Q

Compare SABA delivery via inhalation & ET tube?

A
  • Inhalation delivers 12% of drug
  • ETT delivers 50 – 70%
198
Q

What are the side effects of bronchodilators?

A
  • Tremors
  • Tachycardia
  • Hyperglycemia
  • Transient decrease in O2 sats
199
Q

Name all people relating to Nitrous Oxide

A
  • Joseph Priestly (discovered N, O, photosynthesis)
  • Humphry Davy (discovered electrolytes, suggested N2O use)
  • Horace Wells (dentist, N2O= no recall)
  • Andrews (surgeon)
  • Hewitt (1st anesthesia machine)
  • George Crile (Light N2O/O2 & LA w/Procaine)
200
Q

Name all people relating to cocaine

A
  • Koller (Eye anesthetic)
  • Halsted (Head/Mandibular block)
  • Bier (spinal block/Bier block)
201
Q

Name all people related to Ether

A
  • Crawford Long (vascular neck tumors)
  • William Morton (Dental fittings)
  • Morton/Warren (Public demonstration in London “Letheon”)
  • Robinson Squibb (Purified ether)
  • Valerius Cordus (Tested diethyl ether on chickens)
  • Harvey Cushing (Regional block after ether; Anesthesia records, BP, HR; Cushing’s Triad)
202
Q

Name all people related to chloroform

A
  • Sir James Simpson (Defined pain)
  • John Snow (1st full time anesthetist for Queen, Father of Epidemiology)
  • Hyderbad Commission (safe practices, chloroform is not)
  • Guthrie (delayed chloroform hepatotoxicity in children)
  • Levy (light chloroform + Epi= V-fib)
203
Q

Compare onset, offset, side effects of inhaled volatile anesthetics.

A
  • Halothane: super slow onset & offset; Hepatitis.
  • Isoflurane: Slow onset & offset; Less N/V.
  • Desflurane: Rapid onset & offset, large quantities needed.
  • Sevoflurane: Intermediate onset & offset, toxic degradation concerns.
204
Q

What is neuropathic pain?

A

Pain caused by lesion or disease of somatosensory nervous system.

205
Q

What is neuralgia?

A

Pain in the distribution of a nerve or group of nerves.

206
Q

The dose required to produce a therapeutic response is called?

A

Potency

207
Q

Central volume refers to?

A

Intravascular

208
Q

What are the examples for H1 receptor antagonists?

A
  • Diphenhydramine (Benadryl)
  • Promethazine (Phenergan)
  • Cetrizine (Zyrtec)
  • Loratidine (Claritin)
209
Q

What are the drug examples for H2 receptor antagonists?

A
  • Cimetidine (Tagament)
  • Ranitidine (Zantac)
  • Famotidine (Pepcid)
210
Q

What are the drug examples for dopamine blockers?

A
  • Metoclopramide (Reglan)
  • Domperidone
  • Droperidol (Inapsine)
211
Q

What are the drug examples for anti-emetics?

A
  • Ondansetron (Zofran)
  • Granisetron (Kytril)
  • Dolasetron (Anzemet)

Advanced Pharmacology ANE 8433 (Spring 2023) (16 decks)

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