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Spr24 Pharm II > Preoperative Medications (Exam I) > Flashcards

Preoperative Medications (Exam I) Flashcards

1
Q

What cells release endogenous histamine?

A
  • Basophils & Mast cells
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2
Q

What physiological mechanisms occur from
general histamine release?

A
  • Bronchostriction
  • Stomach acid secretion
  • CNS neurotransmitter release (ACh, NE, 5HT)
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3
Q

What drugs can induce histamine release?

A
  • Morphine
  • Protamine
  • Mivacurium
  • Atracurium
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4
Q

Are anti-histamine’s competitive antagonists?

A

No, they are inverse agonists.

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5
Q

What would be used to treat drug-induced histamine release?

A
  • H1 & H2 antagonists
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6
Q

Histamine-1 receptor activation can mimic these other receptor types.

A
  • Muscarinic
  • Cholinergic
  • 5HT3
  • α-adrenergic
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7
Q

Histamine-2 receptor activation can mimic these other receptor types?

A
  • 5-HT3
  • β-1
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8
Q

Histamine binding to H1 receptors generally elicits what effects?

A
  • Hyperalgesia
  • Inflammatory pain (insect stings)
  • Allergic rhino-conjunctivitis s/s
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9
Q

Histamine binding to H2 receptors generally elicits what effect?

A
  • Stomach acid secretion
  • ↑ cAMP (β-1 similar stimulation)
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10
Q

How prone are H1 antagonists to tachyphylaxis?

A
  • Very little tachyphylaxis development
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11
Q

What signs/symptoms occur with excessive H-1 & H-2 activation?

A
  • Hypotension (from NO) release
  • ↑capillary permeability
  • Flushing
  • Prostacyclin release
  • Tachycardia
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12
Q

What are the side effects of H1 antagonists?

A
  • Drowsiness/sedation
  • Blurred vision
  • Urinary retention
  • Dry mouth
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13
Q

What are four examples of H1 receptor antagonists?

A
  • Diphenhydramine (Benadryl)
  • Promethazine (Phenergan)
  • Cetirizine (Zyrtec)
  • Loratidine (Claritin)
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14
Q

What is diphenhydramine’s primary use and secondary uses?

A
  • Antipruritic
  • Pre-treatment of known allergies (IV dye)
  • Anaphylaxis
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15
Q

What is the E ½ time of diphenhydramine?

A

7-12 hours

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16
Q

What salt of diphenhydramine is useful for motion sickness and why?

A
  • Dimenhydrinate (dramamine) is thought to inhibit the afferent arc of the oculo-emetic reflex.
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17
Q

What H1 antagonist stimulates ventilation? Can this overcome narcotics?

A
  • Diphenhydramine (Benadryl)
  • No
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18
Q

What is normal dosing of Benadryl?

A
  • 25 - 50mg IV
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19
Q

What is promethazine’s primary use?
What is it’s E ½ time?

A
  • Rescue anti-emetic
  • 9-16 hours
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20
Q

What are the black box warnings associated with promethazine?

A
  • 2005: children under 2 shouldn’t take (resp depression)
  • 2009 - Tissue extravasation injuries
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21
Q

What is the dosing of promethazine and when would one expect onset to occur?

A
  • 12.5 - 25mg IV
  • Onset: 5 minutes
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22
Q

When are H2 antagonists most often utilized and what is their mechanism of action?

A
  • Duodenal ulcer disease and GERD
  • ↓ Gastric volume and ↑ gastric pH
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23
Q

What side effect(s) is/are especially pertinent with long term H2 antagonist administration? Why does this occur?

A
  • Bacterial overgrowth → pulmonary infections, weakened mucosa, and candida albicans.
  • This bacterial overgrowth occurs from chronically alkalotic stomach fluid.
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24
Q

What considerations should be given for renal patients when giving H2 receptor antagonists?

A
  • Chronic H2 antagonist = creatinine ↑ by 15%
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25
Q

What is the overall side effect list for H2 antagonists?

A
  • Diarrhea
  • Headache
  • Skeletal muscle pain
  • ↑ stomach bacteria
  • HA, & confusion
  • Bradycardia
  • ↑ serum creatinine
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26
Q

What CNS effects might be seen from H2 antagonist administration? When would this occur more often?

A
  • Headache/confusion from CNS H2 receptors (occurs more in the elderly)
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27
Q

What examples of H2 antagonists were given in lecture?

A
  • Cimetidine
  • Ranitidine
  • Famotidine
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28
Q

Which H2 antagonist strong inhibits CYP450’s?

A
  • Cimetidine
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29
Q

What can occur with rapid infusion of cimetidine?
How can this be avoided?
What other adverse effects does cimetidine have?

A
  • Bradycardia & hypotension (from cardiac H2 receptors)
  • Give over 30 min
  • ↑ prolactin & impotence
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30
Q

What is the dose for cimetidine?
What is the renal dose?

A
  • 150 - 300 mg IV
  • 150 mg IV
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31
Q

Describe cimetidine, ranitidine, and famotidine’s interactions with CYP450 enzymes.

A
  • Cimetidine: strong CYP450 inhibition
  • Ranitidine: weak/no CYP450 inhibition
  • Famotidine: no CYP450 inhibition
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32
Q

What is normal ranitidine dosing?
What is the renal dosing?

A
  • 50 mg diluted in 20cc’s over 2 minutes
  • 25 mg diluted in 20cc’s over 2 minutes
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33
Q

Which H2 antagonist is most potent and has the longest E ½ time? What is this E ½ time?

A
  • Famotidine: E½ = 2.5 - 4 hours
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34
Q

What adverse effect can occur with famotidine?

A
  • Hypophosphatemia (look for fractures)
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35
Q

What is the dose of famotidine?
What is the renal dose?

A
  • 20mg IV
  • 10mg IV
36
Q

How do proton pump inhibitors work?
What is the onset of action for proton pump inhibitors?

A
  • Irreversible binding to H⁺ pumps preventing acid creation.
  • 3-5 days for full result.
37
Q

What is the most effective drug for controlling gastric acidity and volume?

A
  • PPI’s
38
Q

For what four conditions are PPI’s indicated?

A
  • Esophagitis
  • Ulceration
  • GERD
  • Zollinger-Ellison (excess acid)
39
Q

What coagulation considerations have to be made with PPI’s?

A
  • PPI’s inhibit warfarin metabolism = warfarin overdose
  • PPI’s block clopidogrel = plavix won’t work.
40
Q

What is the maximum acid inhibition that can be achieved by omeprazole?
What is omeprazole’s dosing?

A
  • 66%
  • 40mg/100cc over 30min or PO >3hours prior to sx.
41
Q

What are the most common side effects of omeprazole?

A
  • HA, agitation, & confusion (crosses BBB)
  • Bacterial overgrowth
  • N/V
  • Flatulence & abdominal pain
42
Q

What are the benefits of pantoprazole over omeprazole?

A
  1. Better bioavailability & longer E½
  2. Fast: can be given 1 hour prior to sx.
43
Q

What is pantoprazole dosing?

A
  • 40mg in 100mL over 2-15 minutes
44
Q

In what situations is an H2 blocker preferred over a PPI?

A
  • Aspiration Pneumonitis possibility (H2 blocker works faster)
  • Intermittent symptoms
  • Cost
45
Q

In what situations are PPI’s superior to H2 blockers?

A
  • Any ulcerations
  • GERD
  • Acute upper GI hemmorhage
46
Q

What types (and subtypes) of antacids exist?

A

Particulate:
- Aluminum & Magnesium
Non-particulate:
- Na⁺, carbonate, citrate, & HCO₃⁻ based

47
Q

Why are non-particulate antacids superior to particulate antacids?

A
  • Non-particulates neutralize acid & decrease gastric volume.
  • Particulate aspiration just as bad as normal aspiration.
48
Q

What is a general concern with long-term antacid use?

A
  • Food breakdown inhibited
  • Acid rebound
49
Q

What is a concern with long-term magnesium based antacids?

A
  • Osmotic diarrhea
  • Neuromuscular impairment
50
Q

What is a concern with long-term calcium based antacids?

A
  • Hypercalcemia
51
Q

What is a concern with long-term sodium based antacids?

A
  • Hypertension
52
Q

What is the mechanism of sodium citrate (Bicitra) ?

A
  • Base + stomach acid = salt, CO₂, and H₂O
53
Q

What is the time of onset for sodium citrate?
How long does it last?
What is the dose?

A
  • Immediate onset
  • Loses effectiveness in 30-60min
  • 15 - 30 mL PO
54
Q

What is sodium citrate used for and what are it’s downsides?

A
  • Protects against aspiration pneumonia (↑pH)
  • Increases gastric volume & increases aspiration risk.
55
Q

What are dopamine blockers used for in the preoperative setting? What is the mechanism of action?

A

Stimulation of gastric motility:
- increases lower esophageal sphincter tone
- stimulates peristalsis
- relaxes pylorus & duodenum

56
Q

What are the downsides of dopamine receptor blockers?

A
  • Extrapyramidal reactions (crosses BBB)
  • Orthostatic hypotension
  • No change in gastric pH
57
Q

Name the three dopamine blockers discussed in lecture?

A
  • Metoclopramide
  • Domperidone
  • Droperidol
58
Q

What drug is used for diabetic gastroparesis?

A
  • Metoclopramide (Reglan)
59
Q

What drugs can potentially cause neuroleptic malignant syndrome?
What are the symptoms of this syndrome?

A
  • Metoclopramide & Droperidol
  • ↑temp, muscle rigidity, ↑HR, & confusion
60
Q

Which dopamine blocker can decrease plasma cholinesterase levels?
What is the consequence of this?

A
  • Metoclopramide
  • ↓ metabolism of succinylcholine, mivacurium, & ester local anesthetics.
61
Q

What is the dosing for metoclopramide?
When should it be given?

A
  • 10-20 mg IV over 3-5min
  • 15-30 min prior to induction
62
Q

Which dopamine blockers can potentially increase prolactin secretion?
Where is prolactin secreted from?

A
  • Metoclopramide & Domperidone
  • Pituitary gland
63
Q

In which three ways is Domperidone unlike other dopamine blockers?

A
  • No anticholinergic activity
  • No BBB crossing
  • Unavailable in USA
64
Q

What was droperidol originally developed for?

A
  • Schizophrenia/Psychosis
65
Q

What blackbox warning is associated with droperidol?

A
  • ↑↑↑ doses cause prolonged QT & torsades.
  • Lots of drug interactions
66
Q

What is the dose of Droperidol?

A

0.625 - 1.25 mg IV

67
Q

What dopamine blocker is more effective than Reglan and equally as effective as Zofran?

A
  • Droperidol
68
Q

Where is serotonin released from and how does it cause emesis?

A
  • Released via chromaffin cells of small intestine → vagal stimulation via 5HT3 receptors
69
Q

Where are the highest concentration of serotonin receptors found?

Where else are they commonly found?

A
  • Brain & GI tract
  • Kidney, liver, lung, stomach
70
Q

What is the greatest general benefit of 5HT3 antagonists?
What are they not useful for?

A
  • Very few side effects
  • Not useful for motion sickness
71
Q

What is the E ½ time of Ondansetron? Why is this relevant?

A
  • 4 hours: dose must be given so that effect peaks towards end of the case.
72
Q

What is the normal dose of Ondansetron?

A
  • 4 - 8 mg IV
73
Q

If side effects are seen with ondansetron, what might be seen?

A
  • Slight QT prolongation, headache, diarrhea
74
Q

What are the three prevailing theories for corticosteroid’s mechanism in treatment of PONV?

A
  • CNS prostaglandin inhibition suppressing endorphin release
  • ↑ effectiveness of 5HT3 antagonists & droperidol
  • Anti-inflammatory = less opioid usage.
75
Q

A patient is on 100mg hydrocortisone Q8 for 24 hours post-operatively, what dose of dexamethasone would you give?

A
  • No Dexamethasone
76
Q

What is the time till onset of Dexamethasone?
How long does efficacy persist?

A
  • Onset: 2 hours
  • 24 hours of efficacy
77
Q

What is the primary adverse effect of dexamethasone?

A
  • Perineal burning/itching
78
Q

What is the normal dosing for dexamethasone? When would one consider giving more?

A
  • 4 - 8 mg
  • Consider 12mg if difficult airway or swelling exists.
79
Q

How does scopolamine work?

A
  • Muscarinic Antagonist with central & peripheral effects.
80
Q

When do scopolamine patches need to be applied? When does concentration peak?

A
  • Onset: 4 hours
  • Peak concentration: 8-24 hours
81
Q

What is scopolamine dosing and where do the patches need to be applied?

A
  • 140mcg priming & 1.5mg over the next 72 hours.
  • Apply to post-auricularly or on the back
82
Q

What is scopolamine’s best indication?
What three adverse effects are most prevalent?

A
  • Motion-sickness
  • Mydriasis, sedation, & photophobia
83
Q

How much of a benefit does a preoperative bronchodilator give?

A
  • 15% increase in FEV 6 minutes after administering.
84
Q

How many seconds should one take a deep breath when being administered a β2 agonist?

A
  • 5-6 seconds
85
Q

How much of a bronchodilator reaches the lungs with an inhaler method of delivery?
How much does this decrease/increase with an ETT?

A
  • Inhaler: 12% of drug reaches lungs
  • ETT: 30-50% of drug reaches lungs
86
Q

What are the side effects of β2 agonists?

A
  • Tremor
  • Tachycardia
  • Hyperglycemia
  • Temporary decrease in PaO₂
87
Q

What five serious conditions have been associated with PPI’s?

A
  • Bone fractures
  • Lupus
  • Acute interstitial nephritis
  • C-diff
  • Deficient Vit B12 & Mg⁺⁺

Spr24 Pharm II (32 decks)

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