Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Anesthesia > Test 1- Pre-meds > Flashcards

Test 1- Pre-meds Flashcards

1
Q

Purposes of premedication

A

Sedation, analgesia
Anesthetic sparing effect
Reduction of stress and catecholamine release Reduction of O2 demand
Increased safety for animals and humans!
Decreasing parasympathetic tone
Others: antibiotics, antihistamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Anticholinergics

A

Atropine and Glycopyrrolate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Atropine

A

Lipid soluble
Absorbs well IM, SC, PO
Crosses the BBB and placental barrier Dose: 0.01 – 0.04 mg/kg iv

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Glycopyrrolate

A

Water soluble
Absorbs slowly IM, SC, PO
Onset of effect is slower than atropine even IV Doesn’t cross the BBB and placental barrier
Dose: half of that of atropine
Advantage over atropine is debated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are indications of anticholinergics?

A

Increasing heart rate
o Treatment of opioid induced bradycardia

o Prevention/treatment of reflex bradycardia

o Young animals and brachycephalic breeds

o Routine use is not recommended!

Decreasing salivation and bronchial secretion o Smaller amount but thicker mucus is not better

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the contraindications of anticholergenics?

A

Tachycardia

Hyperthyroidism

Most heart diseases
o Except when needed for treatment of bradycardia

Narrow angle glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

CV S/E of Anticholingerics

A

IT’S ALL ABOUT THE AV NODE!

2o AV block, bradycardia, cardiac arrest Tachycardia, hypertension

SA node: atrial conduction (p wave)

AV node: ventricular conduction (QRS)

Anticholinergics easily affect on the SA node o Lot’s of P waves

Effect on AV node is weaker and comes later o AV blocks, bradycardia (vagal tone increased?)

When the AV node finally conducts o Excessive tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What can you not use with atropine?

A

alpha 2 agonist

though you can use medetomidine +atropine— but measure the bp before giving atropine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are anticholergics used for?

A

Treatment of bradycardia

Be careful and think before you act!

Is there a problem? Yes or no?

o Consider species, age and disease of the patient.

o Is the patient hypotensive?

o Is the ET CO2 adequate (assuming constant ventilation)?

Treatment plan:
o Drugs: atropine, naloxone, othersH o Dose? Monitoring? Plan B?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Alpha 2 agonists

A

Strongest available sedatives (except pigs)

Have important cardiovascular side effects

Myriad of other effects
Have specific antagonists

Appropriate use is debated (crashing opinions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MOA of alpha 2 agonist

A

Competitive agonist of α2 adrenergic receptors

Location
o CNS: presynaptic membrane (autoreceptor)

o Post-synaptic membrane (vascular smooth muscle) o Extra-synaptic sites (e.g. pancreas, lipocytes etc.)

sedation, vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the CNS effects of alpha agonist

A

Sedative effect is species specific

o Strong: dogs, cats, horses, ruminants o Weak: pigs

Some analgesic effect o Synergistic with opioids

Muscle relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CV effects of alpha 2 agonist

A

Strong vasoconstriction
Leads to high SVR and BP
Reflex bradycardia develops
Result: low CO and tissue perfusion
BP may decrease later on (hypotension)

Common recommendation
o Don’t use atropine
o If necessary, give specific antidote (e.g. atipamezole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Respiratory effects of alpha 2 agonists

A

Mild respiratory depression

RR decreases but tidal volume increases

Upper airway resistance increases
o Relaxation of larynx, pharynx and nares o Head dropping in horses: nasal edema

V/Q mismatch in horses
o Low V/Q resulting in decreased PaO2

Mostly with xylazine in sheep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

α2 agonists: indications

A

Sedation of aggressive animals

Sedation in the ICU

Sedation to manage post operative airway

obstruction (e.g. after brachycephalic surgery) Prevention/treatment of seizures (epilepsy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

α2 agonists: contraindications

A

Too young or too old
Hemodynamic instability
Severely debilitated patient
Not suitable for most risk patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Available α2 adrenergic agents

A

Agonists

Xylazine

Medetomidine

Dexmedetomidine

Detomidine

Romifidin

Antagonist

Atipamezole Yohimbine Tolazoline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

α2 agonists

A

Specificity to α2/α1 receptor differ
Medetomidine >>> detomidine > xylazine
Most effects are mediated by α2 receptors
The main effects are very similar
Pharmacokinetics and purchase price may differ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Xylazine

A

Dog: 0.25 – 2 mg/kg
Horse: 0.5 – 1 mg/kg
Cattle: 10% of the horse’s dose
Small ruminants: between dogs and horses The dose of medetomidine does not differ Duration: 20-40 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Detomidine

A

Used for large animals
Dose: 0.01-0.02 mg/kg

Route: IM, IV, sublinqual

Duration: 90-120 min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the main indication to use an anticholergic during anesthesia?

A

Increase HR and inhibit PSNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the main indications to give an alpha 2 agonist?

A

SEDATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the biggest SE of alpha 2 agonists?

A
  1. reflex bradycardia
  2. vasoconstriction—> decreased CO, decreased tissue perfussion
  3. increased bp, increased vascular resisitance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which is more potent dexmedetomine or Medetomidine?

A

Dexmedetomidine is about twice as potent as medetomidine, but they act the same

25
Phenothiazines
Acepromazine, (chlorpromazine, etc.) Acting as antagonist on multiple receptors o Dopamine o Serotonine o α1 o Histamine
26
Acepromazine
Long acting drug (depending on dose) o 4–8hours o 48 hours for liver patients o Shorter if given in low doses (e.g. 10 μg/kg)
27
Phenothiazines: CNS effects
Actions on dopamine and serotonine receptors Weaker sedative effects compared to α2 agonists **No analgesic effect** Antiemetic effect Mild respiratory depression
28
Phenothiazines: CV effects
Actions on α1 receptors **Vasodilation** and hypotension Especially in hypovolemic animals **May cause death of hypovolemic patients** Measure blood pressure, give fluids!
29
Phenothiazines: indications
Mild sedation for premedication or post OP Prevention / treatment of opioid dysphoria Prevention of emesis caused by morphine Sedation for dogs with laryngeal paralysis Enhance the sedative effect of xylazine in horses
30
Phenothiazines: contraindications
**Hypovolemia, hemodynamic instability** Very young or very old patient Von-Willebrand disease (Doberman) Boxers may be sensitive (bradycardia) Breeding stallions
31
Butyrophenones
Similar drug family to phenothiazines Drugs: droperidol and azaperone (Stresnil) Sedative effect is similar to acepromazine More likely to cause behavioral side effects Less hypotensive and stronger antiemetic then acepromazine Less effect on platelets Anti arrhythmogenic, not seizurogenic
32
Benzodiazepines
GABA receptor agonists Sedative, anticonvulsant, muscle relaxant effects Minimal CV and respiratory effects No analgesia Sedative is species specific
33
Benzodiazepines
Agonists o Diazepam ``` o Midazolam o Zolazepam (Zoletil or Telazol) ``` Agonists o Diazepam ``` o Midazolam o Zolazepam (Zoletil or Telazol) ```
34
Benzodiazepines: sedation
Species specific effect Dogs, cats horses: disorientation, excitation may occur when used alone Better sedative effects in ruminants, camelids, pigs, birds, and ferrets Rarely used alone
35
Benzodiazepines: indications
_Premedication: combine with_ o Opioids o α2 agonist o Or both _Induction: combine with_ o Dissociative anesthetics (ketamine) o Barbiturates or propofol _Treatment of seizures (status epilepticus)_
36
Diazepam
Lipid soluble Formulated in propylene glycol or lipid emulsion Chemical compatibility is limited Give slowly IV Poor absorption and pain on IM injection Metabolized in liver and duration of action is 1 to 4 hours
37
Midazolam
Water soluble (no propylene glycol) Good chemical compatibility More potent than diazepam Shorter acting than diazepam Metabolized in liver, but metabolites are inactive (unlike diazepam). Can be given IM, IV or via mucus membranes Better choice than diazepam
38
Opioids
Exogenous substances that bind to opioid receptors and activate them Strongest available systemic analgesics Best choice for treatment of acute pain (e.g. surgery!) Decreases the doses of anesthetics Minimal CV side effects Suitable for most risk patients
39
Opioid receptors
μ: strong analgesia, resp. depression, dependency κ: weaker analgesia δ: weaker analgesia (human relevance) Location o Brain o Spinal cord (dorsal horn) o Peripheral nerves o Inflamed organs (e.g. arthritis)
40
Classification of opioids
Full agonists: activate receptors and trigger full tissue response Partial agonists: activate receptors but do not trigger full tissue response even at high doses Antagonists: bind to receptors but do not activate them These drugs concentration dependently compete for receptor binding
41
Potency
Potency: tells you the dose
42
Efficacy:
Efficacy: tells you the strength of the effect
43
Pharmacokinetics:
Pharmacokinetics: onset, duration of effect, administration strategy etc.
44
Opioids: CNS effects
Analgesia o Excellent for acute pain o Less good for chronic pain Decreasing the MAC of inhalants o Species dependent o Primates \> dogs \> cats \> pigs \> horses o May increase the MAC in horses Sedation depends on o Species: primates and dogs sedate better o Pain level: stronger if there was pain Excitation, dysphoria o Cats may become excited o Horses after high doses Tolerance Dependence
45
Opoids cause what clinic sign?
Opioids may trigger or may inhibit vomiting They stimulate the chemoreceptor trigger zone outside of the BBB and may trigger vomiting After entering the brain they inhibit the vomiting center Water soluble opioids (morphine) enter the brain slowly: cause more vomiting Lipid soluble opioids (e.g. fentanyl) enter the brain fast, vomiting does not occur.
46
Opioids: CV effects
No direct negative inotropy or vasodilation Indirectly may reduce sympathetic outflow from the brain and reduce Bp that way Increase parasympathetic tone and may cause bradycardia, this is treatable with atropine **Suitable for most risk patients** Improves CV function by allowing to reduce the doses of anesthetics
47
Opioids: respiratory effects
May depress respiration but not as strongly as in humans and primates Healthy small animals tolerate high doses well Be careful with combinations and sick patients Opioids have antitussive effect: therapy May inhibit airway protective reflexes (e.g. coughing)
48
Opioids: GI effects
Nausea, vomiting Defecation Obstipation Spasm of the sphincter of Oddi (hepatopancreatic sphincter)
49
Opioids: other effects
Hypothermia Post OP hyperthermia (in cats) Myosis (dogs), mydriasis (cats) Inhibition of urination Noise sensitivity
50
Morphine
Cheap and strong analgesic, water soluble Slow onset (30-45 min) long duration (4-6 hours) High individual variability in elimination Metabolized in the liver to an active metabolite Elimination is slow in liver and renal patients May cause histamine release, especially after high iv doses Duration of epidural analgesia is 12-24 hours
51
Hydromorphone, oxymorphone
Strong analgesics (full μ agonists) Duration is about 4 hours Reliable metabolism No histamine release Better choices than morphine
52
Fentanyl
Strong analgesic (full μ agonist) Fast onset short duration (15-20 min) No histamine release May accumulate after long infusions
53
Remifentanil
Similarly potent to fentanyl Very short acting (5 min) and does not cumulate, ideal for CRI Metabolized by non-specific esterases in muscles and intestines Caution: accidental disruption of administration may trigger strong pain Boluses may cause sudden bradycardia
54
Butorphanol
Butorphanol is a mu ANTAGONIST and kappa agonist Weak and short acting analgesic It may worsen pain sensation in case of strong pain May be used for premedication in combination with benzodiazepines or α2 agonists if there is no ``` strong pain (e.g. radiology) May partially antagonize full μ agonists ```
55
Buprenorphine
Partial μ agonist Stronger analgesic than butorphanol Relatively long acting: 6-8 hours Onset is slow (20-40 min iv) Often given to cats because may cause less excitation than full μ agonists The owner of cats may continue giving is via the oral mucosa
56
Tramadol
Weak analgesic Metabolizes in the liver and its metabolite is μ opioid agonist Inhibits Tramadol itself inhibits NE and serotonin reuptake (analgesia) Not scheduled drug Can be given PO
57
Opioid antagonists
Naloxone: 30 min duration o May be used in small animals to reverse respiratory depression o Routine use is not recommended (reverses analgesia) Naltrexone: long acting (~10 hours). Used to antagonize wild animals after long acting opioids e.g. carfentanyl or etorphine
58

Anesthesia (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions