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TxWes Spring '25: Anesthesia Pharm > Preoperative medications Exam 1 > Flashcards

Preoperative medications Exam 1 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-histamines 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 its 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 strongly 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

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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

Better bioavailability & longer E½
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 hemorrhage

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 its 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⁺⁺

88
Q

When was thiopental introduced?

A

1934

TxWes Spring '25: Anesthesia Pharm (8 decks)

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