Preoperative Medications (Exam I) Flashcards
1
Q
What cells release endogenous histamine?
A
- Basophils & Mast cells
2
Q
What physiological mechanisms occur from
general histamine release?
A
- Bronchostriction
- Stomach acid secretion
- CNS neurotransmitter release (ACh, NE, 5HT)
3
Q
What drugs can induce histamine release?
A
- Morphine
- Protamine
- Mivacurium
- Atracurium
4
Q
Are anti-histamine’s competitive antagonists?
A
No, they are inverse agonists.
5
Q
What would be used to treat drug-induced histamine release?
A
- H1 & H2 antagonists
6
Q
Histamine-1 receptor activation can mimic these other receptor types.
A
- Muscarinic
- Cholinergic
- 5HT3
- α-adrenergic
7
Q
Histamine-2 receptor activation can mimic these other receptor types?
A
- 5-HT3
- β-1
8
Q
Histamine binding to H1 receptors generally elicits what effects?
A
- Hyperalgesia
- Inflammatory pain (insect stings)
- Allergic rhino-conjunctivitis s/s
9
Q
Histamine binding to H2 receptors generally elicits what effect?
A
- Stomach acid secretion
- ↑ cAMP (β-1 similar stimulation)
10
Q
How prone are H1 antagonists to tachyphylaxis?
A
- Very little tachyphylaxis development
11
Q
What signs/symptoms occur with excessive H-1 & H-2 activation?
A
- Hypotension (from NO) release
- ↑capillary permeability
- Flushing
- Prostacyclin release
- Tachycardia
12
Q
What are the side effects of H1 antagonists?
A
- Drowsiness/sedation
- Blurred vision
- Urinary retention
- Dry mouth
13
Q
What are four examples of H1 receptor antagonists?
A
- Diphenhydramine (Benadryl)
- Promethazine (Phenergan)
- Cetirizine (Zyrtec)
- Loratidine (Claritin)
14
Q
What is diphenhydramine’s primary use and secondary uses?
A
- Antipruritic
- Pre-treatment of known allergies (IV dye)
- Anaphylaxis
15
Q
What is the E ½ time of diphenhydramine?
A
7-12 hours
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.
17
Q
What H1 antagonist stimulates ventilation? Can this overcome narcotics?
A
- Diphenhydramine (Benadryl)
- No
18
Q
What is normal dosing of Benadryl?
A
- 25 - 50mg IV
19
Q
What is promethazine’s primary use?
What is it’s E ½ time?
A
- Rescue anti-emetic
- 9-16 hours
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
21
Q
What is the dosing of promethazine and when would one expect onset to occur?
A
- 12.5 - 25mg IV
- Onset: 5 minutes
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
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.
24
Q
What considerations should be given for renal patients when giving H2 receptor antagonists?
A
- Chronic H2 antagonist = creatinine ↑ by 15%
25
What is the overall side effect list for H2 antagonists?
- Diarrhea
- Headache
- Skeletal muscle pain
- ↑ stomach bacteria
- HA, & confusion
- Bradycardia
- ↑ serum creatinine
26
What CNS effects might be seen from H2 antagonist administration? When would this occur more often?
- Headache/confusion from CNS H2 receptors (occurs more in the elderly)
27
What examples of H2 antagonists were given in lecture?
- Cimetidine
- Ranitidine
- Famotidine
28
Which H2 antagonist strong inhibits CYP450's?
- Cimetidine
29
What can occur with rapid infusion of cimetidine?
How can this be avoided?
What other adverse effects does cimetidine have?
- Bradycardia & hypotension (from cardiac H2 receptors)
- Give over 30 min
- ↑ prolactin & impotence
30
What is the dose for cimetidine?
What is the renal dose?
- 150 - 300 mg IV
- 150 mg IV
31
Describe cimetidine, ranitidine, and famotidine's interactions with CYP450 enzymes.
- Cimetidine: strong CYP450 inhibition
- Ranitidine: weak/no CYP450 inhibition
- Famotidine: no CYP450 inhibition
32
What is normal ranitidine dosing?
What is the renal dosing?
- 50 mg diluted in 20cc's over 2 minutes
- 25 mg diluted in 20cc's over 2 minutes
33
Which H2 antagonist is most potent and has the longest E ½ time? What is this E ½ time?
- Famotidine: E½ = 2.5 - 4 hours
34
What adverse effect can occur with famotidine?
- Hypophosphatemia (look for fractures)
35
What is the dose of famotidine?
What is the renal dose?
- 20mg IV
- 10mg IV
36
How do proton pump inhibitors work?
What is the onset of action for proton pump inhibitors?
- **Irreversible** binding to H⁺ pumps preventing acid creation.
- 3-5 days for full result.
37
What is the most effective drug for controlling gastric acidity and volume?
- PPI's
38
For what four conditions are PPI's indicated?
- Esophagitis
- Ulceration
- GERD
- Zollinger-Ellison (excess acid)
39
What coagulation considerations have to be made with PPI's?
- PPI's **inhibit warfarin metabolism** = warfarin overdose
- PPI's **block clopidogrel** = plavix won't work.
40
What is the maximum acid inhibition that can be achieved by omeprazole?
What is omeprazole's dosing?
- 66%
- 40mg/100cc over 30min or PO >3hours prior to sx.
41
What are the most common side effects of omeprazole?
- HA, agitation, & confusion (crosses BBB)
- Bacterial overgrowth
- N/V
- Flatulence & abdominal pain
42
What are the benefits of pantoprazole over omeprazole?
1. Better bioavailability & longer E½
2. Fast: can be given 1 hour prior to sx.
43
What is pantoprazole dosing?
- 40mg in 100mL over 2-15 minutes
44
In what situations is an H2 blocker preferred over a PPI?
- Aspiration Pneumonitis possibility (H2 blocker works faster)
- Intermittent symptoms
- Cost
45
In what situations are PPI's superior to H2 blockers?
- Any ulcerations
- GERD
- Acute upper GI hemmorhage
46
What types (and subtypes) of antacids exist?
Particulate:
- Aluminum & Magnesium
Non-particulate:
- Na⁺, carbonate, citrate, & HCO₃⁻ based
47
Why are non-particulate antacids superior to particulate antacids?
- **Non-particulates neutralize acid & decrease gastric volume.**
- Particulate aspiration just as bad as normal aspiration.
48
What is a general concern with long-term antacid use?
- Food breakdown inhibited
- Acid rebound
49
What is a concern with long-term magnesium based antacids?
- Osmotic diarrhea
- Neuromuscular impairment
50
What is a concern with long-term calcium based antacids?
- Hypercalcemia
51
What is a concern with long-term sodium based antacids?
- Hypertension
52
What is the mechanism of sodium citrate (Bicitra) ?
- Base + stomach acid = salt, CO₂, and H₂O
53
What is the time of onset for sodium citrate?
How long does it last?
What is the dose?
- Immediate onset
- Loses effectiveness in 30-60min
- 15 - 30 mL PO
54
What is sodium citrate used for and what are it's downsides?
- Protects against aspiration pneumonia (↑pH)
- Increases gastric volume & increases aspiration risk.
55
What are dopamine blockers used for in the preoperative setting? What is the mechanism of action?
Stimulation of gastric motility:
- increases lower esophageal sphincter tone
- stimulates peristalsis
- relaxes pylorus & duodenum
56
What are the downsides of dopamine receptor blockers?
- Extrapyramidal reactions (crosses BBB)
- Orthostatic hypotension
- No change in gastric pH
57
Name the three dopamine blockers discussed in lecture?
- Metoclopramide
- Domperidone
- Droperidol
58
What drug is used for diabetic gastroparesis?
- Metoclopramide (Reglan)
59
What drugs can potentially cause neuroleptic malignant syndrome?
What are the symptoms of this syndrome?
- Metoclopramide & Droperidol
- ↑temp, muscle rigidity, ↑HR, & confusion
60
Which dopamine blocker can decrease plasma cholinesterase levels?
What is the consequence of this?
- Metoclopramide
- ↓ metabolism of succinylcholine, mivacurium, & ester local anesthetics.
61
What is the dosing for metoclopramide?
When should it be given?
- 10-20 mg IV over 3-5min
- 15-30 min prior to induction
62
Which dopamine blockers can potentially increase prolactin secretion?
Where is prolactin secreted from?
- Metoclopramide & Domperidone
- Pituitary gland
63
In which three ways is Domperidone unlike other dopamine blockers?
- No anticholinergic activity
- No BBB crossing
- Unavailable in USA
64
What was droperidol originally developed for?
- Schizophrenia/Psychosis
65
What blackbox warning is associated with droperidol?
- ↑↑↑ doses cause prolonged QT & torsades.
- Lots of drug interactions
66
What is the dose of Droperidol?
0.625 - 1.25 mg IV
67
What dopamine blocker is more effective than Reglan and equally as effective as Zofran?
- Droperidol
68
Where is serotonin released from and how does it cause emesis?
- Released via chromaffin cells of small intestine → vagal stimulation via 5HT3 receptors
69
Where are the highest concentration of serotonin receptors found?
Where else are they commonly found?
- Brain & GI tract
- Kidney, liver, lung, stomach
70
What is the greatest general benefit of 5HT3 antagonists?
What are they **not** useful for?
- Very few side effects
- Not useful for motion sickness
71
What is the E ½ time of Ondansetron? Why is this relevant?
- 4 hours: dose must be given so that effect peaks towards end of the case.
72
What is the normal dose of Ondansetron?
- 4 - 8 mg IV
73
If side effects are seen with ondansetron, what might be seen?
- Slight QT prolongation, headache, diarrhea
74
What are the three prevailing theories for corticosteroid's mechanism in treatment of PONV?
- CNS prostaglandin inhibition suppressing endorphin release
- ↑ effectiveness of 5HT3 antagonists & droperidol
- Anti-inflammatory = less opioid usage.
75
A patient is on 100mg hydrocortisone Q8 for 24 hours post-operatively, what dose of dexamethasone would you give?
- No Dexamethasone
76
What is the time till onset of Dexamethasone?
How long does efficacy persist?
- Onset: 2 hours
- 24 hours of efficacy
77
What is the primary adverse effect of dexamethasone?
- Perineal burning/itching
78
What is the normal dosing for dexamethasone? When would one consider giving more?
- 4 - 8 mg
- Consider 12mg if difficult airway or swelling exists.
79
How does scopolamine work?
- Muscarinic Antagonist with central & peripheral effects.
80
When do scopolamine patches need to be applied? When does concentration peak?
- Onset: 4 hours
- Peak concentration: 8-24 hours
81
What is scopolamine dosing and where do the patches need to be applied?
- 140mcg priming & 1.5mg over the next 72 hours.
- Apply to post-auricularly or on the back
82
What is scopolamine's best indication?
What three adverse effects are most prevalent?
- Motion-sickness
- Mydriasis, sedation, & photophobia
83
How much of a benefit does a preoperative bronchodilator give?
- 15% increase in FEV 6 minutes after administering.
84
How many seconds should one take a deep breath when being administered a β2 agonist?
- 5-6 seconds
85
How much of a bronchodilator reaches the lungs with an inhaler method of delivery?
How much does this decrease/increase with an ETT?
- Inhaler: 12% of drug reaches lungs
- ETT: 30-50% of drug reaches lungs
86
What are the side effects of β2 agonists?
- Tremor
- Tachycardia
- Hyperglycemia
- Temporary decrease in PaO₂
87
What five serious conditions have been associated with PPI's?
- Bone fractures
- Lupus
- Acute interstitial nephritis
- C-diff
- Deficient Vit B12 & Mg⁺⁺
