Anesthesiology Quiz 1 Drugs (AH) Flashcards

1
Q

When would you give pre-medication depending on the route of administration?

A

IV: 5-10mins, IM: 15-45mins, PO: 60min (rarely used)

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2
Q

What are the major classes of drugs used for pre-medication?

A

Phenothiazines, Butyrophenones, Alpha2-adrenoceptor agonists, Benzodiazepines, Opiods, Anticholinergics, Ketamine, Other (antibiotics)

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3
Q

What phenothiazine is most commonly used?

A

Acepromazine

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4
Q

What receptors does Acepromazine act on?

A

Blocks D (dopmamine) receptors, Blocks A1-adenoreceptors

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5
Q

Acepromazine blocking the D receptors leads to what desirable effects?

A

Sedation (variable), Is also an antipsychotic

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6
Q

What effects are the result of Acepromazine’s action on the A1-adrenoceptors?

A

Vasodilation and hypotension. –> HR may slightly increase with a drop in BP

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7
Q

How is Acepromazine administered?

A

IV - onset up to 20mins. IM, SC - up to 45 mins. Oral: dogs-> tablets, horses –> paste

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8
Q

When do the effects of acepromazine peak?

A

40 mins

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9
Q

How is Acepromazine metabolized?

A

By the liver, slowly –> 4-6 hour duration

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10
Q

What are the effects of Acepromazine on the CVS?

A

vasodilation, hypotension +/- slight increase in HR, ↓ PCV (sequestration in spleen), chatecholamine induced arrythmias ↓, inhibits platelet aggregation

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11
Q

How does acepromazine effect excited animals?

A

excited animal –> epi release –> paradoxical vasodilation

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12
Q

What breed shouldn’t be given Acepromazine and why?

A

Boxers (esp in europe and california). It can induce bradycardia and collapse

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13
Q

What are the clinical uses for Acepromazine?

A

Pre-med in SA and horses, Combine with opiods/ alpha2-agonists, horses - avoid ataxia (decreases mm movement), PO - long term sedation

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14
Q

What are the contraindications for Acepromazine?

A

Boxers (esp in europe and california)–> It can induce bradycardia and collapse. Breeding Stallions. Animals with hypotension, anemia, bleeding disorders. Animals prone to seizures –> it may lower the theshold but not enough data.

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15
Q

Does Acepromazine have analgesic effects?

A

No

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16
Q

Does acepromazine induce vomiting?

A

No, it is an anti-emetic

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17
Q

What can acepromazine cause in horses?

A

Piokilothermia, priapism

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18
Q

What effect does Acepromazine have of the resp system?

A

minimal effects

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19
Q

What are the two Butyrophenones?

A

Droperidol = innovar-vet, Azaperone = stresnil, suicalm

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20
Q

Which other class of pre-med drugs are Butyrophenones similar to?

A

Phenothiazines

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21
Q

How is Azaperone used clinically?

A

Used in combination with ketamine for anaesthesia in aggressive pigs.

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22
Q

What are the major A2-adrenoceptor agonisis used in vet met and in what species are they used?

A

Romifadine - horses, Detomidine - horse/cattle, Medetomidine & Dexmedetomidine - SA and can be used in others, Xylazine - all

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23
Q

Clinical uses of Alpha2-adrenoceptor agonists?

A

Protent sedative and analgesic

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24
Q

On what receptors do Alpha-2 adrenoceptor agonists act?

A

Post-synaptic A1 and A2, Pre-synaptic A2

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25
Q

What effects do a2-adrenoceptor agaonists produce when acting on post synaptic A1 and A2?

A

Vasocontriction, vagal tone increase –> relex bradycardia

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26
Q

What effects do a2-adrenoceptor agonists produce when acting on post synaptic A2?

A

Decrease NE release and sypathetic tone, prolong braycardia

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27
Q

Rank selectivity of A2-adrenoceptor agonists from least to most selective

A

Xylazine < Detomidine < Romifidine < Medetomidine < Dexmedetomidine

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28
Q

How does selectiviy alter A2-adrenoceptor agonists effects?

A

Increases sedation and analgesic effects

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29
Q

Which last longer with A2-adrenoceptor agonists, sedation or analgesia?

A

Sedation

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30
Q

Do A2-adeno agonisist cause emesis?

A

yes

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31
Q

Why shouldn’t you use an A2-adeno agonist in a blocked male cat?

A

They inhibit ADH production –> diuresis

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32
Q

What effect do A2-adeno agonists have on Resp system?

A

depresses resparatory system at high doses

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33
Q

What species is senstitive to Xyalazine?

A

Ruminants

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34
Q

What can you give to counteract bradycardia with A2-adeno agonisists?

A

Atropine (carefully), but only in healthy animals. Atropine increases HR which fights against increased pressure –> exploded heart in compromised patient.

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35
Q

If you were worried about ataxia in horses, which A2-adeno agonist would you use?

A

Romifidine –> less ataxia in horses

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36
Q

CV effects of A2-adeno agonists?

A

Bradycardia/arrythmia (1* and 2* AV blocks), vasoconstriction followed by BP decrease, Pale MM, CO decreased

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37
Q

Horses may develop colic from A2-adeno agonists, why?

A

Decreases GI motility

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38
Q

What SE of A2-adeno agonists?

A

Vomiting ( bad for GDV), Decreases GI motility (Colic in horses), sheep –>Hypoxemia and pulmonary edema, Pregenant cows –> uterine contractions, Increased intercranial pressure (bad for head trauma), Startle response, Inhibition of insuline release –>

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39
Q

What are the three A2-antagonists?

A

Atipamezole, Yohimbine, and Tolazoline (only effective for xylazine)

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40
Q

How much Atipamezole should be used when reversing Met or Dex?

A

equal volumes

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41
Q

Off lable use for Atipamezole?

A

Use in horses and wildlife

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42
Q

How should Atipamezole be administered?

A

IM 5-10min, or very slowly via IV

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43
Q

List the main Benzodiazepines

A

Diazepam, Midazolam, Zolazepam( +tiletamine)

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44
Q

What effects do Benzodiazepines have on the CNS?

A

Enhanced GABA binding –> open Cl- channels –> decrease in CNS APs.

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45
Q

what does the decreased CNS activity produced by Benzodiazepines produce?

A

Anti-anxiety effects, anti-convulsant, decreased ICP, Amnesia

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46
Q

Do Benzodiazepines produce analgesia?

A

no

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47
Q

what are the effects on CV and Resp for Benzodiazepines?

A

CV: no depression, Resp: mild dose related resp. depression

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48
Q

Clinical uses of Benzodiazepines?

A

Sedation of sick, pediatric, or geriatric patients (won’t produce enough sedation in healthy patients), Combo with other drugs to reduce amount of other drugs needed, Anti-convulsants

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49
Q

Which is the better drug, midazolam or diazepam and why?

A

Midazolam is better: Water soluble –> IM injection, no active metabolites –> less cummulative, shorter acting time but 2X as potent. Diazepam: reacts with light, not water soluble –> IV only (painful), 2 active metabolites, absorbs to plastic

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50
Q

Benzodiazepine antagonist?

A

Flumazenil

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51
Q

What type of antagonist is Flumazenil?

A

Competative antagonist –> reversal is reversable

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52
Q

Indications for Flumazenil?

A

Benzo overdose, prolonged sedation, equine recovery

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53
Q

Name a centrally acting mm relaxant used mostly in LA?

A

Guaifenesin

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54
Q

What are the CV/ Resp effects of Guaifenesin>

A

minimal depression for both. (mm without resp depression = good)

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55
Q

What other drugs are often combined with Guaifenesin when it is given in horses?

A

Thiopental or Ketamin

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56
Q

How is Guaifenesin administered?

A

IV only. Takes a large volume –> TIVA with Ketamine and Xylazine

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57
Q

SE of Guaifenesin?

A

Hemolysis and thrombophlebitis

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58
Q

What group of drugs are considered the “gold standard” for analgesia?

A

Opioids

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59
Q

What receptors do Opiods act on and what is the resulting effect?

A

μ (OP3) - analgesia, moisis, eupphoria, resp. depression, inhibition of gut motility. κ (OP2) - analgesia, sedation, miosis. Δ (OP1) - analgesia, resp. depression

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60
Q

Where are Opiod receptors found?

A

all over, increased in areas of injury

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61
Q

Opiod CNS effects?

A

Analgesia, Dogs - mild sedation, antitussive, Cats/Horses- excitement and increased locomotor activity, Cats - hyperthermia, Dogs/Cats - nausea/vomiting,

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62
Q

What do opioids depress?

A

respiration, GI motility, HR with high doses

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63
Q

Which opioids release histamine?

A

Morphine and Meperidine IV –> hypotension and reflex tachycardia

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64
Q

Which opioids cause emesis?

A

Morphine, hydromorphone, ocymorphone

65
Q

Which opiods are unlikely to cause emesis?

A

Butorphanol, buprenorphine, meperidine, methadone, fentanyl

66
Q

How is morphine used?

A

As a baseline analgesic for severe pain

67
Q

Morphine in cats?

A

Slow elimination and causes euphoria/disphoria in cats

68
Q

Methadone has what additional MOA?

A

NMDA antagonism –> additional analgesic mechanism

69
Q

What route of admin should you avoid with Meperidine and why?

A

No IV use - histamine release

70
Q

Is Meperidine short or long acting?

A

short

71
Q

Does Meperidine cause emesis?

A

unlikely

72
Q

Uses for Fentanyl?

A

CRI for surgery, intraoperative bolus, rapid onsetsetitive if IV or IM, rapid sequnce induction

73
Q

How long does a fentanyl patch last for?

A

72 hours about

74
Q

What can you do if a fentanyl patch isn’t providing enough analgesia?

A

Add another M agonist

75
Q

How do you prepare a patient for a fentanyl patch?

A

shave but don’t scrub - you need the oils in the skin for absorption.

76
Q

Why are fentanyl patches useful?

A

Long duration

77
Q

What are the drawbacks to using fentanyl patches?

A

variable time to onset, variable plasma conc., poor alternative to opioid CRI, potential for abuse (by owners)

78
Q

Remifentanil is indicated in what type of patient?

A

Patients with liver problems. Metabolized by plasma esterases instead of hepatic

79
Q

How long does Remifentanil last?

A

3-4mins, ultra short acting. Give something about 20mins before stopping so keep analgesia going

80
Q

Buprenorphine acts on what receptors as an agonist?

A

Partial M agonist

81
Q

Buprenorphine timing?

A

slow onset, long duration of action 4-6h

82
Q

SE of buprenorphine?

A

minimal

83
Q

Burorphanol receptors?

A

M antagonist, K agonist

84
Q

What is butorphanol good for?

A

Only a weak analgesic but good sedation and antitussive with minimal SE

85
Q

List 3 opioid antagonists

A

Naloxone and Naltrexone (complete), Butorphanol (partial)

86
Q

Which opiod is most commonly used in horses?

A

Butorphanol

87
Q

What behavioral modification can occure in unsedated horses as a result of IV administered opioids?

A

box walking

88
Q

What does Neuroleptoanalgesia mean?

A

Sedative + opioid

89
Q

What is neuroleptoanalagesia used for?

A

Preanesthetic medication (ace + morphine), restraint for minor procedures

90
Q

List 4 anticholinergic agents used in pre-med

A

Atropine, Glycopyrrolate, Scopolamine (Hyoscine)

91
Q

What is the main use for anticholinergic agents?

A

for treatment of bradycardia caused by vagal stimulation (brought on by opioids)

92
Q

Effects of Anticholinergics?

A

increased HR, Reduce salivation, Reduce gut motility (colic), Dilate pupils (–> panic in horse/cat), Relax bronchial smm.

93
Q

Which anticholinergic crosses the BBB?

A

Atropine

94
Q

Which anticholinergic is preffered for rabbits? Why?

A

Glycopyrrolate. Rabbits have atropine esterase –> very short acting.

95
Q

Dosages for atropine differ in what spp?

A

Ruminants need a very high dose

96
Q

Which anticholinergic produces and initial drop in HR when given IV?

A

Atropine

97
Q

Indications for injectable anaesthetics?

A

Induction of general anesthesia, maintenance of anesthesia (CRI/Bolus), Balanced anesthesia, TIVA, to provide sedation (sm amount of propofol)

98
Q

What are some of the most important characteristics of an ideal inj. anesthetic?

A

Rapid onset, high lipid solubility –> crosses BBB, no accumulation –> rapid recovery, high therapeutic index, no active metabolites, no endocrinologic effect, min CV/resp depression, no pain on injection.

99
Q

How do you calculate a dose for an obese patient?

A

Use ideal weight

100
Q

List 3 barbituates and what they are used for

A

Thiopental - induction in SA (short acting), Pentobarbital - euthanasia, Phenobarbital - long acting, anticonvulsant

101
Q

How do you reconstitute thiopental

A

with sterile water. Forms a very alkaline solution and can be extremely irritating to tissues.

102
Q

What is the only way to admin thiopental?

A

via IV cath. Necrosis if perivascular

103
Q

What must you do before admin or thiopental?

A

remove LRS and flush. LRS + thiopental –> precipitate.

104
Q

Main indications for Thiopental?

A

Anesthesia in SA, induction in horses when combined with guaifenesin –> reduced ataxia, bolus during maintenance in horses (emergency for when horse is waking up)

105
Q

contraindications for Thiopental?

A

Patients with hepatic Dz, Greyhouds (can’t metabolize), neontal/ pregnant animals, cachexic animals, spenectomy. Not used for maintenance due to accumulation.

106
Q

Which inj. Anesthetic is most commonly used?

A

Propofol

107
Q

What about the way propofol is prepared makes it less economical?

A

Propofol is prepared with soy and egg products –> bact growth –> discard after 24 hours (new formula lasts 28 days)

108
Q

Is propofol a tissue irritant?

A

no

109
Q

Clinical uses for propofol?

A

Induction (short acting) in dogs and cats, can be used in sm. Ruminants but usually not approved.

110
Q

When using propofol, what do you need to be ready to do?

A

be ready to intubate and ventilate.

111
Q

Propofol CVS/Resp

A

CVS - hypotension Resp - depression, apnea.

112
Q

Does propofol provide analgesia?

A

no

113
Q

Effects on CNS?

A

anticonvulsant and neuroprotectant

114
Q

Propofol and cats?

A

Not a good idea. Reduced capacity for glucuronidation –> prolonged recovery. Toxic injury to feline HB –> blood issues

115
Q

contraindications for Propofol?

A

hypovolemic patients, HF, hyperlibidemia and pancreatitis, cats (avoid repeated)

116
Q

Can you use propofol for CRI or TIVA?

A

Yes, minimal accumulation. Suppliment with O2 during repeated doses or TIVA

117
Q

SE during induction for propofol?

A

excitatory signs

118
Q

What is the main drawback to the classic prep of etomidate?

A

Perivascular injection causes necrosis and phlebitis

119
Q

What are the drawbacks to lipid emulsion prep of Etomidate?

A

promotes bact. Growth–> discard w/I 24 hrs

120
Q

Etomidate CNS stuff?

A

Quickly penetrates BBB, max CNS conc. within 1min

121
Q

Clinical use of Etomidate?

A

Anesthesia induction in high risk patients. Ideal induction agent for compromised patients (shock patients)

122
Q

What animals should not receive Etomidate?

A

animals with adrenal issues. Horses and Cattle

123
Q

How should etomidate be administered?

A

Pain on injection. Use combo of fentanyl, diazepan, etomidate via IV cath.

124
Q

Why isn’t etomidate used often in vet med?

A

expensive, rough indcution, inhibits adrenocortical fnx, hemolysis and hematuria reported, painful upon injection

125
Q

What is Alfaxalone?

A

It is a neuroactive steroid

126
Q

MOA of alfaxalone?

A

Hypnosis and mm relax via GABAa

127
Q

Admin of Alfaxalone?

A

Perivascular injection not painful, no necrosis (pH=7), IV or IM via slow injection. Use premed and analgesic

128
Q

Uses for Alfaxalone?

A

Indcution and TIVA for dogs and cats.

129
Q

Does Alfaxalone provide analgesia?

A

no

130
Q

CVS/Resp for alfaxalone?

A

Hypotension (not as bad as propofol), relex tachycardia. Min resp depression.

131
Q

Alfaxalone SE in cats?

A

Myoclonus and poisthotonus during recovery

132
Q

Admin of Ketamine

A

IV, IM, SQ, Rectal, Epidural. Never given alone.

133
Q

What happens if you inject Ketamine perivascularly?

A

Pain! (pH 2-3) But no necrosis

134
Q

Clinical Uses for Ketamine?

A

Indcution in many spp. especially in zoo animals, short maintencance, CRI in subanesthetic doses for analgesia, Never use alone.

135
Q

Pros of Ketamine?

A

Analgesia, amnesia, hypnosis. Different routes of admin. Sympathetic stimulation, Min resp depression, bronchodilation

136
Q

Cons of Ketamine?

A

Muscle rigidity, Pain on injection, Emergence psychomimetic reactions

137
Q

How should you store Ketamine?

A

Away from light and heat. Otherwise it is stable

138
Q

Onset of action for Ketamine?

A

IV- 30-90sec, IM - 10-15min

139
Q

MOA of Ketamine?

A

NMDA = most improtant receptor –> antagonism in brain and spinal cord. Other receptor sites: opioid, cholinergic, adrenergic, GABAa

140
Q

What is the active metabolit of Ketamine?

A

Norketamine

141
Q

Does Ketamine accumulate?

A

Yes

142
Q

Ketamine CVS?

A

Unique! Increases in HR BP and CO. Also direct myocardial depression, but stimulatory effects normally predominate.

143
Q

Ketamine CNS

A

increases ICP, may elicit seizures, swallow and cough reflexes are retained, increases IOP, no eye rotaion –> use eye ointment

144
Q

Does Ketamine have analgesic properties/?

A

Yes, profound somatic analgesia –> orthopedic pain

145
Q

Besides the BBB, what other barrier does Ketamine cross and what effect does it have when it does?

A

Placental barier –> decrease in puppy vigor

146
Q

Contraindications for Ketamine?

A

CV Dz patients, heptic/renal insufficiency, hyperhyerosis (high BP Dz), Neuro problems & head trauma, Caesarean section, increased IOP.

147
Q

Pros of S(+) Ketamine?

A

Only need 1/2 dose, longer and stronger analgesia, decreased agitation, disorientation and anxiety, faster recover, suggestive of myocardial and neuronal protection

148
Q

How is Tiletamine sold?

A

As a combo with Zolazepam

149
Q

What is the main difference between ketamine/BZD and Tiletamine?

A

Tiletamine is longer acting

150
Q

What is recovery like with Tiletamine?

A

Rough and long. Zolazepam wears off first –> mm rigidity, excitations and seizures

151
Q

Tiletamine clinical use?

A

Indcution for many species.

152
Q

Admin of Tiletamine?

A

IV/IM (painful)

153
Q

Which pre-med drugs provide analgesia?

A

A2-agonists, opioids

154
Q

Which pre-med drugs do not provide analgesia?

A

Acepromazine, Benzodiazepines, Guaifenesin

155
Q

Which inj. anesthetics do not provide analgesia?

A

Propofol, Etomidate, Alfaxalone?

156
Q

Which drugs have minimal CV/Resp effects?

A

Resp only: Alfacalone, Ketamine. Both: Acepromazine,BDZ (@ clinical dose), Guaifenesin, Opiods (dose dep), Etomidate (dose dep).

157
Q

Which drugs are anti-convulstant

A

Benzodiazepines, Phenobarbital, Thiopental

158
Q

Which drugs decrease GI motility?

A

A2-agonists, Opioids