Ch.18: Injectable Anesthesia Pharm (Shih) Flashcards

1
Q

therapeutic index

A

lethal dose50/effective dose50. High therapeutic index is better

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2
Q

rank therapeutic indices of propofol, ketamine, thiopental, etomidate, alfaxalone**

A

ketamine > alfaxalone (>20) > etomidate (16)&raquo_space; thiopental (5)> propofol (3)

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3
Q

Compartment theory

A

drugs have 3 main compartments that they go into: blood, high blood-flow organs (brain), and low-flow organs (fat, muscle, tendon, skin).
-Drug gets quickly redistributed from brain into GI, where it is eliminated slowly

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4
Q

elimination half-life

A

time for plasma conc. of drug to drop by 50%

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5
Q

elimination half-time

A

time for plasma conc. of drug to drop by 50% during elimination phase

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6
Q

time of awakening is dependent on:**

A

redistribution rate, NOT elimination rate. If 2 drugs causing sedation are elimated at different rates, time of awakening will still be the same because they are being redistributed at the same rate

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7
Q

how many half-times before drug can be considered effectively cleared from system?*

A

4

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8
Q

loading dose =

A

vol of distribution X target plasma conc.

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9
Q

vol of distribution =

A

total dose/drug plasma conc.

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10
Q

continuous infusion

A
  • a repeated bolus
  • “little sips throughout the night”
  • can lead to drug accumulation
  • rate of decay depends on elim. rate
  • CRI
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11
Q

CRI =

A

continuous rate infusion

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12
Q

context sensitive half life**

A

time necessary for the plasma drug conc. to decrease by 50% after discontinuing a CRI of a specific duration

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13
Q

barbiturates in general have low/high therapeutic index

A

low

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14
Q

barbiturates mech. of action**

A

interact with GABA receptor to open Cl channels and promote CNS depression

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15
Q

Can Cl channel be opened without GABA?*

A

yes (explains why some animals will sleep if given thiopentane)

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16
Q

thiopental fx

A
  • shuts down brain and lowers O2 requirement of the brain

- prevents ICP buildup

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17
Q

thiopental chars.

A
  • short lasting barbituric
  • awakening due to redistr.
  • long half life
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18
Q

thiopental metabolism

A

liver. Don’t use in patients with low hepatic fx (i.e. portal shunt!)

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19
Q

thiopental disadvantages**

A
  • expensive
  • skin irritant (it is very basic)
  • sight hounds have prolonged and agitated recovery. (drug can build up in blood instead of fat since they have low fat)**
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20
Q

propofol has low/high therapeutic index**

A

low

21
Q

propofol chars/advantages**

A
  • short acting/fast clearance
  • recovery due to redistr.
  • smooth induction/recovery
  • short half life
  • extra hepatic metabolism, so good for patients with liver problems such as PSS
  • vasodilator
22
Q

propofol disadvantages**

A
  • resp/CV depression (usually short-lived)
  • drops BP
  • oily vehicle can induce bacterial growth, fat embolism, high plasma triglyceride**
  • long-term use can result in oxidative injury, Heinz body form, MetHb, diarrhea/anorexia/malaise in cats
23
Q

indications for propofol

A

C-sections

24
Q

etomidate has low/high therapeutic index**

A

high

25
Q

Etomidate chars/desired effects**

A
  • doesn’t adversely affect CV stability
  • minimal resp. depression
  • dec. intracranial P
  • dec. cerebral oxygen consumption
  • poorly lipid soluble
26
Q

vehicle of etomidate

A

propylene glycol

27
Q

problems with propylene glycol

A
  • pain on inject
  • hemolysis
  • can cause hyperosmolar state
28
Q

adverse effects of etomidate**

A
  • ADRENAL SUPPRESSION: inhibits 11-beta-hydroxylase, which converts cholesterol to glucocorticoids and mineralocorticoids. results in decreased cortisol, corticosterone, aldosterone.
  • Do NOT give if animal is sick or stressed
29
Q

Is ketamine controlled drug?

A

YES

30
Q

Ketamine is classified as:

A
  • dissociative anesthetic (awareness altered)

- non-competitive NMDA receptor antagonist

31
Q

Which is more potent: ketamine-S or R in racemic mixture?**

A

S

32
Q

Is ketamine lipid soluble? Protein bound?

A

Yes very much so for both

33
Q

Ketamine absorption

A
  • good IV or IM absorption

- transmucosal

34
Q

ketamine metabolism

A
  • hepatic

- norketamine active metabolite

35
Q

ketamine mech. of action**

A
  • non-competitive NMDA receptor antagonist
  • prevents glutamate from binding NMDA
  • depresses activity in thalamocortical, limbic, and reticular activating system
  • also acts at opioid and muscarinic receptors
  • can be used as infusion
36
Q

ketamine effects

A
  • myocardial depressant (??)

- inc. sympathetic tone (inc. cardiac output/BP/HR/muscle tone)

37
Q

why is ketamine used with diazepam?

A

to counteract muscle rigidity caused by ketamine

38
Q

How is ketamine unique among injectable agents?**

A

provides some analgesia, even at low doses

39
Q

can give telazol IV?

A

yes

40
Q

telazol = combo of:

A

tiletamine + zolazepam

41
Q

Alfaxalone chars.

A
  • not yet available in US
  • water soluble
  • IV or IM
  • doesn’t cause histamine release
  • high therapeutic index
  • can be used as an infusion
42
Q

Alfaxalone controlled?

A

NO

43
Q

vehicle for alfaxalone**

A

cyclodextrin encapsulation (a protein)

44
Q

alfaxalone mech. of action

A

enhances GABA

45
Q

alfaxalone effects

A
  • dec. BP
  • inc. HR
  • depressed resp.
  • muscle relaxation
46
Q

alfaxalone provide analgesia?

A

no

47
Q

alfaxalone metabolism

A

-hepatic via glucuronidation

48
Q

see table from whiteboard

A

:)