Preoperative medications Exam 1 Flashcards
1
Q
What cells release endogenous histamine?
A
Basophils & Mast cells
2
Q
What physiological mechanisms occur from general histamine release? (3)
A
- Bronchostriction
- Stomach acid secretion
- CNS neurotransmitter release (ACh, NE, 5HT)
3
Q
What drugs can induce histamine release? (4)
“MMAP”
A
Morphine
Mivacurium
Atracurium
Protamine
4
Q
Are anti-histamines competitive antagonists?
A
No, they are inverse agonists
they dont prevent the release of histamine, they block Histamine receptor sites
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. (4)
A
- Muscarinic
- Cholinergic
- 5HT3
- α-adrenergic
7
Q
Histamine-2 receptor activation can mimic these other receptor types? (2)
A
- 5-HT3
- β-1
8
Q
Histamine binding to H1 receptors generally elicits what effects? (3)
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 like stimulation)
10
Q
How prone are H1 antagonists to tachyphylaxis?
A
Very little tachyphylaxis development
11
Q
What signs/symptoms occur with excessive H1 & H2 activation?
A
- Hypotension (from NO) release
- ↑capillary permeability
- Flushing
- Prostacyclin release
12
Q
What are the side effects of H1 antagonists?
A
Drowsiness/sedation (1st Gen)
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 its 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, GERD
- ↓ Gastric volume, ↑ 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%
tubular secretion competition
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 strongly 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** >> H2 antagonists
38
For what four conditions are PPI’s indicated?
Esophagitis
Ulceration
GERD
**Zollinger-Ellison (excess acid)**
39
What five serious conditions have been associated with PPI’s?
Bone fractures
Lupus
Acute interstitial nephritis
C-diff
Deficient Vit B12 & Mg⁺⁺
40
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**.
41
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.
42
What are the most common side effects of omeprazole?
HA, agitation, & confusion **(crosses BBB)**
Bacterial overgrowth
N/V
Flatulence & abdominal pain
43
What are the benefits of pantoprazole over omeprazole?
**Better bioavailability** & **longer E½**
**Fast**: can be given **1 hour prior** to sx.
44
What is pantoprazole dosing?
40mg in 100mL over 2-15 minutes
45
In what situations is an **H2 blocker** preferred over a PPI?
**Aspiration Pneumonitis** possibility (H2 blocker works faster)
**Intermittent** symptoms
**Cost**
46
In what situations are **PPI’s** superior to H2 blockers?
Any **ulcerations**
**GERD**
Acute upper **GI hemorrhage**
47
Drug of choice for **NSAID ulcerations**
**Omeprazole** (+ D/C NSAID)
48
What types (and subtypes) of antacids exist?
**Particulate:**
* Aluminum & Magnesium
**Non-particulate:**
* Na⁺, carbonate, citrate, & HCO₃⁻ based
49
Why are **non-particulate** antacids superior to particulate antacids?
Non-particulates **neutralize acid** & **decrease gastric volume**.
Particulate aspiration just as bad as normal aspiration.
50
What is a general concern with long-term antacid use? (2)
Food breakdown inhibited
Acid rebound
51
What is a concern with long-term magnesium based antacids? (2)
Osmotic diarrhea
Neuromuscular impairment
52
What is a concern with long-term calcium based antacids?
Hypercalcemia
53
What is a concern with long-term sodium based antacids?
Hypertension
54
What is the mechanism of sodium citrate (Bicitra)?
Base + stomach acid = salt, CO₂, and H₂O
**neutralizes acid, increase intra-gastric volume**
55
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
56
What is sodium citrate used for and what are its downsides?
Protects against **aspiration pneumonia** (↑pH) (**not aspiration**)
**Increases gastric volume** & **increases aspiration risk**.
57
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**
58
What are the downsides of dopamine receptor blockers?
Extrapyramidal reactions (**crosses BBB**)
Orthostatic hypotension
**No change in gastric pH**
59
Name the three dopamine blockers discussed in lecture?
**Metoclopramide**
Domperidone
**Droperidol**
60
What drug is used for diabetic gastroparesis?
Metoclopramide (Reglan) **10-20 mg IV**
**15-30 mins** before induction
61
What drugs can potentially cause **neuroleptic malignant syndrome**? What are the symptoms of this syndrome?
**Metoclopramide** & **Droperidol**
↑temp, muscle rigidity, ↑HR, & confusion
62
Which dopamine blocker can **decrease plasma cholinesterase** levels? What is the consequence of this?
**Metoclopramide**
↓ metabolism of **succinylcholine**, mivacurium, & ester local anesthetics (**increased drug effect**)
63
What is the dosing for metoclopramide? When should it be given?
**10-20 mg** IV over **3-5min**
**15-30 min** prior to induction
64
Which dopamine blockers can potentially **increase** **prolactin** secretion? Where is prolactin secreted from?
Metoclopramide **< Domperidone**
Pituitary gland
65
In which three ways is Domperidone unlike other dopamine blockers?
**No anticholinergic activity**
**No BBB crossing**
**Unavailable in USA**
66
What was droperidol originally developed for?
Schizophrenia/Psychosis
67
What blackbox warning is associated with **droperidol**?
↑↑↑ doses cause **prolonged QT & torsades**
+ drug interactions
68
What is the dose of Droperidol?
0.625 - 1.25 mg IV
69
What dopamine blocker is **more effective than Reglan** and equally as effective as Zofran?
Droperidol
70
Where is serotonin released from and how does it cause emesis?
Released via **chromaffin cells of small intestine** → **vagal stimulation** via 5HT3 receptors
71
Where are the highest concentration of serotonin receptors found? Where else are they commonly found?
**Brain & GI tract**
Kidney, liver, lung, stomach
72
What is the greatest general benefit of 5HT3 antagonists? What are they not useful for?
Very few side effect, great for PONV
Not useful for **motion sickness**
**ondansetron 1st drug**
73
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.
74
What is the normal dose of Ondansetron?
4 - 8 mg IV
75
what kind of antagonist is ondansetron?
**competitive antagonist** to serotonin on 5HT3 receptors
76
If side effects are seen with ondansetron, what might be seen?
Slight **QT prolongation**, headache, diarrhea
77
What are the three prevailing theories for **corticosteroid**’s mechanism in treatment of PONV?
1. CNS **prostaglandin inhibition** suppressing **endorphin** release
2. ↑ effectiveness of **5HT3 antagonists & droperidol**
3. Anti-inflammatory = **less opioid usage**.
78
A patient is on 100mg hydrocortisone Q8 for 24 hours post-operatively, what dose of dexamethasone would you give?
No Dexamethasone
79
What is the time till onset of Dexamethasone? How long does efficacy persist?
Onset: **2 hours** (time accordingly)
24 hours of efficacy
80
What is the primary adverse effect of dexamethasone?
Perineal burning/itching
81
What is the normal dosing for dexamethasone? When would one consider giving more?
**4 - 8 mg**
Consider >12mg if **difficult airway** or **swelling** exists.
82
How does scopolamine work?
**Muscarinic Antagonist** with central & peripheral effects.
83
When do scopolamine patches need to be applied? When does concentration peak?
Onset: **4 hours** (pre-op, posterior-auricular)
Peak concentration: **8-24 hours**
84
What is scopolamine dosing and where do the patches need to be applied?
**140mcg** priming & **1.5mg/72 hours.**
Apply to **post-auricularly** or on the back
85
What is scopolamine’s best indication? What three adverse effects are most prevalent?
**Motion-sickness**
**Mydriasis**, **sedation**, & photophobia
86
How much of a benefit does a preoperative bronchodilator give?
**15% increase in FEV 6 minutes** after **2 puffs**.
(Not a lot)
87
Beta agonists MOA
* **Gs protein stimulation**
* activate cAMP
* decrease calcium entry
* decrease contratility
88
How many seconds should one take a deep breath when being administered a β2 agonist?
**5-6 seconds** + hold breath
89
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
90
What are the side effects of β2 agonists?
Tremor
Tachycardia
Hyperglycemia
Temporary decrease in PaO₂
