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Anesthesiology > Pre-Meds I > Flashcards

Pre-Meds I Flashcards

1
Q

What are the basic aims of premedication?

A
  • relieve anxiety/fever
  • facilitate handling
  • counteract side effects of anesthetics
  • reduce anesthetic dose
  • contribute to perioperative analgesia
  • contribute to smooth recovery
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2
Q

What are the 3 classes of sedatives and tranquilizers we use for pre-meds?

A
  • phenothiazines
  • benzodiazepines
  • alpha2 adrenergic agonists
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3
Q

What common analgesics are used as pre-meds?

A

opioids and NSAIDs

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4
Q

Which 6 classes of anti-emetics and GI protectants do we use as pre-meds?

A
  • NK-1 antagonists
  • D2 antagonists
  • 5-HT antagonists
  • PPIs
  • Anti-H2
  • Buffers
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5
Q

What are the 3 hypnotics we use as pre-meds?

A
  • Alfaxalone
  • Ketamine
  • Tiletamine
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6
Q

What is the MOA and effect of anticholinergics on each body system?

A

MOA: competitive antagonists MAchR (M1-M5)

  • CV: +/- paradoxical bradycardia (IV), incr HR
  • Lungs: bronchodilation, reduced secretions (incr viscosity)
  • Eye: mydriasis, +/- incr IOP
  • GI: antisialogue, decr motility/ileus
  • CNS: sedation/hallucinations (hum)
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7
Q

What type of drug is atropine?

A

an alkaloid anticholinergic

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8
Q

What type of drug is glycopyrorlate?

A

a quaternary ammonium anticholinergic; low lipid solubility and does not cross BBB + placenta

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9
Q

Does atropine cross the BBB?

A

Yes

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10
Q

How is atropine metabolized?

A
  • Dogs + humans = hydrolysis + excreted unchanged
  • Cat + small ruminants = hepatic and renal esterases
  • Atropinase = 30% of rabbits
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11
Q

How is glycopyrrolate metabolized?

A
  • no species variability
  • excreted unchanged in urine
  • effective in rabbits
  • slower onset/longer duration than atropine
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12
Q

Why use anticholinergics as premeds?

A
  • prevent bradycardia
  • reduce salivation
  • reduce bronchial secretions
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13
Q

What are the disadvantages to using anticholinergics as premeds?

A
  • thickening of saliva + bronchial secretions
  • decreased GI motility
  • incr myocardial O2 consumption/arrhythmias
  • no study to prove benefit
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14
Q

Given what we know about the disadvantages of using anticholingergics as premeds, should we use them to treat bradyarrhythmias and hypotension?

A

YES - these are life-saving drugs!

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15
Q

My anesthetized patient is bradycardic and hypotensive, what should I do?

A. Bradycardia and hypotension are not a problem

B. Anticholinergics can cause bradycardia, so I wouldn’t use them

C. Administer an anticholinergic

D. Tell the surgeon it is time to wake the patient up

A

C

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16
Q

What is the MOA and effect of phenothiazines on the various body systems?

A

MOA: D2, alpha1, H1, MAchR antagonists

  • CNS: tranquilization, + opioids = neuroleptoanalgesia, decr MAC, anxiolysis?
  • CV: vasodilation, +/- antiarrhythmic
  • T°: hypothermia
  • GI: antiemetic, relax LES, delay gastric emptying
  • Hematologic: decr HCT (20-30%), decr PLT aggregation?
  • Antihistamic
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17
Q

How is acepromazine metabolized?

A

hepatic metabolism, lasting up to 12 hours!

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18
Q

T or F: acepromazine can be antagonized

A

False

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19
Q

What types of patients should acepromazine be avoided for?

A

pediatric, geriatric, debilitated, hepatic dysfunction, or hypovolemic (causes low BP)

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20
Q

Why should you only use low doses of acepromazine?

A

the dose-response curve reaches a plateau with no increase in sedation, but it lasts longer

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21
Q

T or F: acepromazine is more reliable than alpha2 agonists and is a good choice for aggressive/excitable patients

A

False - poor choice and less reliable

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22
Q

Why should acepromazine be avoided in breeding stallions and bulls?

A

it causes priapism

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23
Q

What is one reason brachycephalic breeds might be at extreme risk when using acepromazine as a premed?

A

it may cause CV collapse (and potentially vasovagal syncope)

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24
Q

I gave my patient acepromazine, and now it is tachycardic and very hypotensive. What do I do?

A. Administer an anticholinergic

B. Reverse acepromazine

C. Administer a fluid bolus

D. Turn off all monitors

A

C; cannot reverse and anticholinergics cause tachycardia

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25
Q

What is the MOA and effect of benzodiazepenes on various body systems?

A

MOA: allosteric modulator of GABA @ GABAA rec

  • No direct action
  • Incr susceptibility to GABA –> incr Cl- conduction –> decr excitability
  • Effects: sedation, anxiolysis, anticonvulsants, MM relaxants
    • Minimal CV effects
    • mild dose-dependent resp depressant
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26
Q

T or F: Benzos may cause excitement in healthy dogs and cats

A

True, potentially due to a decreased learned inhibition

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27
Q

Benzodiazepines are reliable sedatives in what types of animals?

A
  • very young
  • very old
  • very sick
  • small ruminants
  • pigs
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28
Q

What type of metabolism do benzos undergo?

A

hepatic

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29
Q

What are 2 benefits of using benzos as a premed?

A

they reduce your anesthetic requirement and can be antagonized

30
Q

What do benzos need to be paired with for a reliable effect?

A

opioids or hypnotics

31
Q

What type of drug is diazepam and what are some features of it?

A
  • benzodiazepine
  • insoluble in water
  • 35% propylene glycol (–> pain, hemolysis, erractic IM SQ absorption)
  • light sensitive
  • absorbed in PVC (in syringes)
32
Q

What type of drug is midazolam and what are some basic features of it?

A

benzodiazepine

  • no propylene glycol
  • in vial pH (3.5) = water soluble
  • at physiologic pH = liquid soluble (reaches brain and has an effect)
33
Q

What type of drug is zolazepam and what are some basic features of it?

A

benzodiazepine

    • tiletamine = Telazol (trade name)
  • excellent immobilization
  • powder = can be reconstituted with small volumes
  • metabolism:
    • cats, pigs - tiletamine > zolazepam (smooth recovery)
    • dogs, horses - zolazepamn > tiletamine (rough recovery)
34
Q

What is flumazenil and what is a potential side effect of it?

A

a competitive antagonist for benzodiazepines; can cause seizures!

35
Q

I was not paying attention in class, so I gave midazolam IV to a young, healthy dog as a pre-medication. The dog is now climbing the wall. What do I do?

A. Administer more midazolam to achieve sedation

B. Administer an anticholinergic

C. Give a hypnotic or an opioid

D. Leave the room

A

C

36
Q

What are the effects of alpha2 adrenergic agonists on various body systems?

A
  • CNS: sedation - ruminants alpha2D, touch/sound sensitive, MAC reduction, analgesia
  • GI: vomit, decr motility
  • CV: biphasic- incr BP, decr HR; decr BP, decr HR; CO reduction (50-66%)
  • T°: decr ability to thermoregulate
  • Resp: mild depressant, cyanosis, pulm edema in small ruminants
  • M/S: central mm relaxant
  • Uterus: ecbolic effect
  • Renal: incr urine production
  • Endocrine: suppression of stress response, insulin (hyperglycemia)
  • IOP/ICP: no change, vomit may increase!
37
Q

Describe MOA of alpha2 adrenergic agonists?

A

mimics NE at pre-synaptic alpha2 receptors, causing negative feedback and decreased NE release + decr Ca2+ conductance on post-synaptic cells

38
Q

Where are alpha2A receptors located and what is their effect?

A

cortex and brainstem; sedation, supraspinal analgesia, central bradycardia, hypotension

39
Q

Where are alpha2B receptors located and what is their effect?

A

spinal cord and vascular endothelium; increased SVR = reflex bradycardia

40
Q

Where are alpha2C receptors located and what is their effect?

A

spinal cord; impaired thermoregulation

41
Q

Where are alpha2D receptors located and what is their effect?

A

2A; ruminants only

42
Q

Of these alpha2 agonists, which has the greatest alpha2:alpha1 selectivity? The least?

detomidine, romifidine, medetomidine, dexmedetomidine, xylazine

A

Medetomidine, dexmedetomidine = greatest

Xylazine = least

43
Q

What are the side effects of alpha2 agonists?

A
  • profound CV effects - transient hypertension, persistent bradycardia, hypotension, decr CO, do NOT give to neonates (relie heavily on HR for CO)
  • decr ability to thermoregulate
  • emesis
  • decr GI motility
  • hyperglycemia
  • incr urine production
44
Q

What is the proposed mechanism of alpha2 agonists causing pulmonary edema in small ruminants?

A
  • mediated by macrophages -> reversal of alpha2 agonists does NOT improve edema, ONLY reverses sedation
45
Q

What problematic condition do alpha2 agonists cause in large felids and what is the proposed mechanism behind it?

A

hyperkalemia (lethal if not promptly treated); postulated mechanism = anti-insulinic effect leads to translocation of K+ to ECF

46
Q

T or F: xylazine is commonly used as a pre-med drug in small animals

A

false; used as a pro-emetic in cats

47
Q

Name one significant adverse effect of xylazine in horses?

A

seizures following intra-carotid injections

48
Q

In what animals is Detomidine used most commonly as a pre-med for and in what form?

A

horses and pigs; oral gel

49
Q

Detomidine is ______ (more/less) potent and ______ (shorter/longer lasting) than xylazine

A

more; longer lasting

50
Q

In what animal is romifidine licensed to be used as a pre-med for? Is it shorter or longer lasting than xylazine?

A

horses; longer lasting

51
Q

Medetomidine is most commonly used for what purpose?

A

capture (with ketamine); no longer used for domestic species

52
Q

What are common uses of dexmedetomidine?

A

analgesia and sedation in ICU (as a CRI); in theory 2x as potent as medetomidine

53
Q

What are the uses of alpha2 antagonists?

A
  • to terminate sedation
  • to treat overdoses
  • after capture of wild animals
54
Q

What are some considerations you should have when using alpha2 antagonists?

A
  • analgesia will be reversed too
  • alpha2 adrenergic + ketamine = ketamine convulsive action may be revealed
  • these may have profound CV side effects
  • if used to treat alpha2 agonist-induced bradycardia, HR doesn’t change much but systemic vascular resistance will decrease! (low BP)
55
Q

What are 3 examples of alpha2 adrenergic antagonists?

A

Tolazoline, yohimbine, and atipamezole

56
Q

What are the effects of tolazoline? Side effects?

A
  • Effects: vasodilation, cholinergic, H release
  • SE: fasciculations, hypotension, ventricular arrhythmias, death
57
Q

Rank these 3 drugs from greatest to lowest alpha2:alpha1 receptor selectivity:

tolazoline, yohimbine, atipamezole

A

Atipamezole >>>> Yohimbine > Tolazoline

58
Q

Atipamezole has been licensed to only be given by what adminstration method?

A

IM

59
Q

I gave my patient dexmedetomidine, and now it is bradycardic. What do I do?

A
  • If patient’s hypertensive,
    • nothing
    • increase halogenate
    • reverse
  • If normotensive,
    • nothing
    • atropine?
    • glycopyrrolate?
  • If hypertensive,
    • Atropine
    • Glycopyrrolate
60
Q

What are the centers of the brain anti-emetics work on?

A

Chemoreceptor trigger zone (opioids), cortex/thalamus (pain, anxiety) and vestibular system (motion)

61
Q

Why should you use anti-emetics and/or antacids for pre-meds?

A
  • peri-operative nausea and vomiting (PONV) is frequent in small animal patients
    • ​factors: anesthesia-related, surgery-related
  • Gastroesophageal reflux has high incidence in SA patients –> esophageal stricture, aspiration of gastric content (potential sequelae)
62
Q

What are three commonly-used antiemetics?

A

maropitant, metoclopramide, ondansetron

63
Q

What is the MOA of maropitant?

A

MOA: NK1 antagonist

*PO admin prior to pre-med reduces incidence of alpha2 agonist-induced vomit

(painful given SQ!)

64
Q

What is the MOA of metoclopramide and what is it commonly used for?

A

MOA: 5H3 antagonist, D2 antagonist

Used as a pro-emetic and antiemetic (often CRI)

65
Q

What is the MOA of ondansetron?

A

MOA: 5H3 antagonist

66
Q

Name three common antiacids used as pre-meds

A

Famotidine, omeprazole, Na citrate

67
Q

What is the MOA of famotidine?

A

MOA: H2 antagonist

68
Q

What is the MOA of omeprazole and what is it more effective at doing than famotidine?

A

MOA: proton pump inhibitor

More effective at incresing pH that famotidine

69
Q

What is the MOA of Na citrate and how must it be given? What patients should you be careful using it in?

A

MOA: buffer (converted to NaHCO3)

Must be given orally

Be careful in patients with CKD (metabolic alkalosis) or cardiac disease (risk of CHF due to Na overload)

70
Q

Which of the following patients is most likely to benefit from an administration of a gastro protectant and an antiemetic?

A. GI foreign body

B. C-section

C. Chronic kidney disease

D. Severely painful dog that has been on opioids and NSAIDs for a week

E. All the above

A

E

Anesthesiology (12 decks)

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