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Exam 3 Flashcards

1
Q

What are the three primary medical reasons that NSAIDs are used in animals

A

analgesia, anti-inflammatory, antipyretic

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2
Q

At what point in the nociceptive pathways do NSAIDs exert their predominant effect?

A

During the transduction phase, decreasing the sensitivity to nociception

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3
Q

What are the clinical advantages of using NSAIDs in our patients?

A

Readily available (not controlled)
Effective for acute and chronic pain
Oral forms (easy to administer)
Long duration of action
Relatively inexpensive
NO CNS side effects (rare)
Fewer side effects than steroids

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4
Q

What are risks of administering NSAIDS and glucocorticoids concurrently?

A

Increased likelihood of side effects
Increased chance of GI irritation (commonly dog)

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5
Q

The anesthesia section of the VTH delays administration of an NSAID in a brachycephalic dog or cat undergoing surgery for approx 15-30 min after the patient is extubated. What is the reasoning for administering the NSAIDs

A

If the patient has an upper airways obstruction, they will be administered a rapid acting corticosteorid to decrease airways swelling. That is why you want to wait to give the NSAID

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6
Q

What is the most common complication of NSAIDs in the dog?

A

GI side effects,
Anorexia, vomiting, diarrhea
gastritis, enteritis, gastric erosions/ulcers

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7
Q

Should dogs be administered GI protectants prophylactically to prevent GI irritation when administered a course of NSAIDs?

A

No evidence that this actually works, just more money and drugs to give the dog

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8
Q

What organ system is of most concern when giving an NSAID to the adult cat?

A

the kidney- tubular damage

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9
Q

What are the two types of liver toxicity caused by NSAIDs

A

Intrinsic-dose dependent (e.g dog eats whole bottom of Rimadyl)
Idiosyncratic- we do not know, can occur

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10
Q

Do dogs and cats need to have blood work before being administered an NSAID?

A

No easy answer, professional judgement is needed. No data, there is variation between every animal.

A complete physical exam and appropriate laboratory monitoring is needed (FDA)

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11
Q

What are the potential downsides of requiring bloo work prior to administering an NSAID to one of our patients?

A

Expense of blood work may prevent some animals from receiving NSAIDs following surgery/trauma

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12
Q

Is it appropriate to administer an NSAID to a dog or cat with mild elevations in liver enzymes?

A

it depends, up to your professional judgement

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13
Q

NSAIDs are commonly administered in the perioperative period in dogs, cats, and horses. In dogs and cats is it preferable to administer NSAID before, during, or after surgery. If there is a preference what is your rational?

A

Potential for better pain control if given before surgery (quick procedures)
Potential for more side effects if given before surgery (e.g hypertension seen during long surgeries cannot be fixed if prostaglandin is blocked)-

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14
Q

What are the pros and cons of using aspirin for chronic pain in dog?

A

Pros: inexpensive, readily available, effective
Cons: Higher risk of GI irritation/ulceration

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15
Q

Why do NSAIDs fail to control pain in some patients

A

the pain is too severe necessitating the use of more than one type of analgesic (e.g opioids)

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16
Q

What are commonly combined together to enhance postop analgesia?

A

opioid, NSAID, local anesthetic

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17
Q

Why choose an NSAID over a corticosteroid for post-op pain control

A

NSAIDs have fewer side effects and do not affect the immune system

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18
Q

How do NSAIDs work

A

inhibitors of cyclooxygenase (exception Galliprant)
Newer NSAIDs are COX-2 selective (COX-1 sparing)
*COX selectivity is dose dependent- all NSAIDs are non-selective COX inhibors at high doeses
Fixed doses (not a lot of dose manipulation)

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19
Q

What is Galliprant (Grapiprant) ?

A

an NSAID that was developed to control pain and inflammation associated with OA in dogs
Highly selective for the EP4 receptor
Prostaglandin E2 is a product of cyclooxygenase enzymes
PGE2 targets four types of eicosanoid receptors EPI 1-4.

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20
Q

How does grapiprant differ from a typical NSAID

A

it does not inhibit cyclooxygenase
It is an EP4 receptor antagonist

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21
Q

Why do we use opioids in animals

A

*analgesia- primary for acute pain
Sedation in some patients (not primary effect)

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22
Q

Why are clinically available opioids scheduled (controlled) by the DEA

A

Based on abuse potential
Acceptable medical use
Likelihood of causing dependence if abused
Politics of the times

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23
Q

What are the components of addiction?

A

Addiction is a chronic relapsing disorder characterized by compulsive drug seeking and use despite adverse consequences

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24
Q

How is the human opioid epidermic affecting veterinary medicine?

A

Vets are legally able to administer and prescribe opioids. Some states limit number of days they can be dispensed
Some states encourage or require use of PDMP
Some states are requiring vets to take CE on opioid use

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25
Q

According to the CDC, is the opioid epidermic control under control?

A

No

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26
Q

What guidance has the Colorado Board of Vet med provided vets regarding opioid epidemic

A

-Vet/Client Patient Relationship must be established, have to see the patient in person
-Verify and document need for opioids
-Dispense through an established pharmacy

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27
Q

How common is opioid addiction in veterinary patients?

A

It is not a problem

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28
Q

How does the development of tolerance affect the efficacy of the drug

A

Tolerance is biological phenomenon and is the most common response to the repetitive use of the same drug and can be defined as the decrease in effectiveness of a drug with its repeated administration

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29
Q

Can patients develop tolerance to the respiratory depressant effects of opioids? What about constipation?

A

Tolerance to respiratory depression (up to a point)
Tolerance to constipation: not typically- it can be managed

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30
Q

What is responsible for the development of tolerance to opioids

A

1) Pharmacokinetic tolerance - induced synthesis of hepatic microsomal enzymes
2) Pharmacodynamic tolerance- cellular adaptations such as changes in the number, affinity, and function of the receptors (activation of glutamate at NMDA receptor and stimulation of nitric oxide production)

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31
Q

Can animals become dependent on opioids?

A

Yes, physical dependence can occur with repeated use of opioids, as occurs with many medications

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32
Q

How can we avoid inducing withdrawl in a patient that has received opioids for several days?

A

Taper the opioid over time (1-2 days in most cases)

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33
Q

What are differences between general anesthesia and analgesia

A

Analgesia- loss of sensitivity to pain (it hurts less)
Anesthesia- total loss of sensation in: part of body (local or regional block) or in the whole body (general anesthesia)

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34
Q

What are the five components of general anesthesia?

A

Amnesia,
Hypnosis (loss of consciousness)
Hyporeflexia
Analgesia
Muscle relaxation

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35
Q

What are the two main opiate receptors that are targeted clinically?

A

Mu and Kappa receptors (g protein couple receptors part of the endogenous system of opiate receptors)

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36
Q

Endogenous opioid system

A

complex, anatomically widespread, and diverse system subserving multiple functions - including
sensory role (inhibiting responses to painful stimuli
Modulatory role in gastrointestinal, endocrine, and autonomic functions
Emotional role
Cognitive role in the modulation of learning and memory

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37
Q

What are endorphins

A

Endogenous opioid ligands (B-endorphins, enkephalins, dynoprhins, and nociceptin/orphanin FQ)
Definition: any chemical substances formed in the body (endogenous) that exhibits pharmacologically properties of morphine
Endorphins function at endogenous opiate receptors

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38
Q

What do endorphins do

A

Modulate numerous effects of the CNS
Stimulate mu receptors primarily and delta receptors to a lesser extent
Mediates analgesia (Beta endorphin is a potent analgesic)

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39
Q

What is the most potent endogenous opioid peptide mediating analgesia?

A

Beta endorphin, important role in injury and stress

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40
Q

What are enkephalins and dynorphin?

A

they are widely distributed throughout the CNS and serve multiple opioid functions

Dynorphin stimualtes the kappa receptor to mediate spinal analgesia, possibly dysphoria

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41
Q

How do opioids work?

A

Stimualte cascade of intracellular events (hyper-polarization of cell membranes, decrease in nociceptive neurotransmitter release, and inhibition of nociceptive (pain) pathways.
*exert pre- and post-synaptic effects on sensory neurons
GTP-intraelluar functions (inhibition of adenylyl cyclase activity, inhibition of sodium channels, activation of post-synaptic receptor activated K+ channels, suppression on voltage gated Ca2+ channels)

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42
Q

Why is pro-opiomelanocortin so important following an inury?

A

it is a precursor for ACTH, a-MSH, and b-LPH. The close association between b-endorphin and ACTH indicates an important role of endorphins in stress response

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43
Q

In general, are opioids more effective for acute or chronic pain?

A

acute pain, but they do have important roles in management of some chronic debilitating pain and cancer pain

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44
Q

What is opioid-induced hyperalgesia

A

increased amount of pain following discontinuation of opioids
not fully understood
withdrawl of exogenously admin opioids can result in long term potentiation of synaptic transmission between primary afferent neurons in the dorsal root ganglion and second order neuron.

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45
Q

What is a full opioid agonist?

A

affinity and activity at all the opioid receptors
maximum amount of analgesia (dose dependent)
Characterized as mu agonists
Ex: fentanyl, hydromorphone, methadone, morphine, heroin

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46
Q

What is a partial mi-agonist?

A

affinity primarily for mu receptor
partially binds, provides less analgesia that the full mu agonist
Ex: buprenorphine

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47
Q

What is an opioid agonist-antagonist?

A

agonist at the kappa receptor
antagonist at the mu receptor
Less analgesia than full mu agonist
Ex: Butorphanol, nalbuphine

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48
Q

What is naloxone?

A

high affinity for mu and kappa opiate receptors
exerts no activity at normal dosages
competetive antagonist
used to reverse effects of opioids

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49
Q

Why is affinity of an opioid to the opiate receptor important to know?

A

a drug’s ability to bind to its receptor sites in the body affects the drug’s duration of action (buprenorphine) affects drug interaction when opioids of different classes used
Clinical examples: buprenorphine after hydromorphone

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50
Q

Which opioid is difficult to reverse due to high binding affinity?

A

buprenorphine

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51
Q

What is the difference between opioid analgesic potency and efficacy?

A

potency directly related to the affinity of the drug for opiate receptor sites. Clinically used to determine the dose of a given opioid but does not indicate the ability of the drug to provide analgesia.

efficacy relates to the maximal effect that a drug can induce (analgesia)

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52
Q

What is an equi-analgesic dose of hydromorphone (potency 5) to morphine given at a dose of 0.5mg/kg

A

morphine at 0.5mg/kg is same as hydromorphone at 0.1mg/kg.

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53
Q

Is butorphanol (potency =5) more or less effective than morphine for the treatment of severe, acute pain in the dog?

A

Butorphanol is less effective than morphine
Butorphanol works primarily throug hthe kappa receptor and has a ceiling effect on analgesia

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54
Q

What are two reasons why butorphanol is not a great choice to treat severe pain in a dog?

A

1) It is an opioid agonist-antagonist (less analgesia and ceiling effect)
2) It has a short duration of action (0.5 - 2 hours)

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55
Q

How can the usefulness of butorphanol be improved for the treatment of acute pain in the dog or cat?

A

1) Combine it with other analgesic drugs (NSAIDs, alpha-2 agonists, local anesthetics)
2) Administer butorphanol as a continuous rate infusion (0.1-0.4 mg/kg/hour)

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56
Q

What factors influence the degree of analgesia provided by an opioid?

A

Degree of tissue trauma/pain
Central and peripheral sensitization
Acute vs chronic pain
Degree of concurrent fear, anxiety, stress
Route of administration
Dose and dosing interval
Other pain treatments administered

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57
Q

Are opioids good sedatives in dogs and cats?

A

sometimes, depends on age, presence of pain, health status
usually not good sedatives by themselves in young, healthy dogs and cats

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58
Q

What is meant by euphoria in a dog or cat administered an opioid?

A

Pleasant feeling with freedom from anxiety, distress, and pain

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59
Q

What is meant by dysphoria in a dog or cat administered an opioid?

A

unpleasant feeling in response to opioid analgesic
disoriented or disturbed behavior
dogs/cats may be restless. may be afraid, attempt to hide or escape, vocalize
dysphoria and pain can coexist

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60
Q

What are effects of opioids on respiratory function?

A

Respiratory depression
Reduction in responsiveness of the brainstem respiratory centers to CO2 (more CO2 needed to trigger breathe)
May affect respiratory rate, tidal volume, or both
Depress pontine and medullary centers involved in regulating respiratory rhymicity

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61
Q

How does the respiratory depressant effect of butorphanol compare to that of morphine?

A

Butorphanol is less of a respiratory depressant than morphine
Respiratory depression is dose dependent and butorphanol has a ceiling effect on respiratory depression
In severely compromised animals, sedation from butorphanol may not be tolerated

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62
Q

What is the difference between low dose fentanyl (as used in CCU) and high dose fentanyl (used in anesthesia) on respiratory depression?

A

Low dose (1-4mc/kg/hour) is well tolerated and will keep breathing
High dose (5-40mcg/kg/hour) causes dose-dependent respiratory depression and apnea

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63
Q

Are opioids used for cough suppression?

A

yes, directly depress the cough center in the medulla
cough suppression and respiratory depression are not directly linked
Antitussive agents do not necessarily depress respiration (butorphanol, hydrocodone)

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64
Q

What effect, if any, do opioids have on the GI motility in the horse?

A

Can slow GI motility, excessive doses can lead to ileus and colic
Butorphanol is associated with less GI slowing than MU agonists

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65
Q

Do opioids cause constipation in species other than horses?

A

Yes, opioids can caused constipation in most species. The constipating effects is serious issue when on chronic opioids

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66
Q

What opioid is most likely to induce vomiting in the dog or cat?

A

Morphine
Hydromorphone to a lesser extent

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67
Q

Is opioid-induced vomiting an advantage or disadvantage in dogs and cats?

A

depends on the patient and circumstance: sometimes we want our patient to empty their stomach before being induced to anesthesia (decreased risk of aspiration)
Sometimes we do not want our patient to vomit (e.g patient with brain tumor)

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68
Q

How can you prevent opioid induced vomiting in a dog or cat?

A

Select an opioid that is unlikely to cause vomiting: methadone, fentanyl, butorphanol, buprenorphine
Administer an anti-emetic (maropitant)
Administer the opioid IV rather than IM or SQ

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69
Q

How do high doses of hydromorphone affect body temperature in cats

A

All opioids can increase body temperature in the cat
High doses of hydromorphone may be more likely to increase body temperature in cat
Uncommon clinical side effect

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70
Q

Mechanism responsible for analgesia from tramadol

A

a synthetically dervied analgesic that has weak mu-opioid activity (M1 metabolite), inhibition of norepinephrine and serotonin re-uptake
Metabolism of tramadol in dogs appears to be variable (some dogs have little detectable MI and limited analgesic effect)

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71
Q

What is the controversy regarding the use of tramadol to treat pain in dogs?

A

Study found it wasnt effective for treatment of OA pain in dogs but found it had beneficial effects in cats with OA

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72
Q

How do you treat fentanyl induced bradycardia in a cat?

A

Due to result of increased vagal tone
Treat heart rate with atropine or glycopyrrolate

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73
Q

How do you treat opioid-induced excitement in a dog?

A

Sedate with acepromazine or dexmedetomidine
also could partially or completely reverse opioid (if not pain of procedure was performed yet_

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74
Q

What is a convenient and effective way for clients to administer buprenorphine to a cat

A

give it transmucosally- proved to be as effective as IV for bioavailability

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75
Q

Why is fentanyl administered as an IV infusion or transdermal patch

A

it has a short duration of action (approx 20 min into anesthesia)
IV infusion prolongs the effect
Transdermal patch- 3 days of analgesia

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76
Q

What are the potential consequences of morphine-induced histamine release?

A

Vasodilation and hypotension, especially under anesthesia- bronchoconstriction
if concerns use hydromorphone
If use morphine- SQ or IM
IV (low dose)

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77
Q

Heart rate in an anesthetized dog drops from 100 to 40bpm after IV administration of fentanyl. What can you do?

A

Administer atropine or glycopyrrolate
Dont give naloxone because dont want fully reversal

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78
Q

Are opioids used to treat pain in animals with a history of seizures. Why or why not

A

Yes, opioids do not lower the seizure threshold
exception overdoses

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79
Q

What are the effects of opioids on body temp?

A

Some patients can be hypothermic or hyperthermic

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80
Q

What are predominant cardiovascular effects of hydromorphone in the dog?

A

Bradycardia

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81
Q

Do opioids cause vasodilation

A

yes, under some circumstances histamine release
Morphine or meperidine
more likely in large IV doses
May be due to pain relieve and withdrawal of sympathetic tone

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82
Q

How could you completely reverse the effects of hydromorphone?

A

Naloxone

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83
Q

How could you completely reverse the effects of butorphanol

A

Naloxone (not complete reversal though
better at mu receptor) dose is not established
repeated doses or CRI may be needed

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84
Q

How can you partially reverse the effects of hydromorphone

A

Low dose of naloxone (102mcg/kg IV)
Buprenorphine
Butorphanol
Nalbuphine

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85
Q

What is the rationale for giving buprenorphine and meloicam to a cat following dental surgery?

A

Provide multi-modal analgesia
Buprenorphine and meloxicam have different mechanisms of actions

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86
Q

What is the mechanism of action of diazepam?

A

Enhance the effect of the inhibitory amino acid gamma-aminobutyric acid (GABA). The BZD receptor is a modulatory site of the GABAa receptor (regulates postsynaptic chloride channel gating, net result is an increase in the frequency of chloride ion channel opening)

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87
Q

How effective of a sedative in diazepam in young, healthy animals?

A

not effective in young, healthy, or excited animals
make animals harder to handle

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88
Q

Why is diazepam combined with xylazine and ketamine to induce anesthesia in the horse?

A

Diazepam and midazolam induce muscle relaxation. smooth induction (smoother transition to the ground, less rigidity of limbs, jaw, neck)
Prolong anesthesia (gives more time to finish procedure or transition to gas anesthesia)

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89
Q

Why is midazolam or diazepam used in anesthetic protocols in dogs and cats?

A

decrease dose of anesthetic induction drug
minimuze the effects on blood pressure
muscle relaxation (ketamine, etamidate)
frequently used in senior/geriatric patients

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90
Q

How do diazepam and midazolam differ? Is this clinically important

A

Midazolam is more potent than diazepam (does not appear to change the dose)
Midazolam is water soluble (diazepam is not) so it does not sting when administered IV and absorbed well from IM or SQ sites

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91
Q

Why do we administer flumazenil to a dog or cat?

A

If the patient had received midazolam or diazepam (Recovery is too slow), unsettled or strange behavior on recovery (disoriented, not able to focus, excited)
no down side to giving flumazenil

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92
Q

What is primary use of acepromazine

A

tranquilize and calm patients
tranquilizers act by depressing the hypothalmaus and the reticular activating system
tranquilized patients are calm/relaxed, awake and unconcerned with their surroundings, the patient can override drug effects with stimulation though

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93
Q

How are the effects of acepromazine antagonized?

A

there is no antagonist for acepromazine, just need to wait for it to go away, MoA involves multiple receptor sites, can last 4-6 hours, if you dont want to wait use dexmed and reverse with an a2 antagonist (atipamezole)

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94
Q

What effect does acepromazine have on clotting?

A

Decrease the number of platelets
Decrease release of ATP by platelets resulting in a decrease in aggregation
not a whole lot of literature about it but keep it in mind

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95
Q

What are the effects of acepromazine on the CV system?

A

alpha-adrenergic blocker
- vasodilation (hypotension, particularly under anesthesia, splenic enlargement and sequestrations of RBCs, Decrease packed cell volume)
-*Systemic hypotension (most important CV effect, dose dependent hypotension, treat with IV fluids)

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96
Q

Why does reflex tachycardia occur after administering acepromazine?

A

sympathetic response to decrease in blood pressure
mediated through the baroreceptors

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97
Q

How can you enhance the sedative effects of acepromazine in a dog or cat?

A

increase the dose of acepromazine
combine with an opioid
Combine with alpha-2 agonist like Dexmedetomidine
combine with an opioid and alpha-2 agonist (low dose of all)

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98
Q

Would you sedate an anxious dog with a history of seizures using acepromazine

A

acepromazine purported to decrease seizure threshold, but never documented
some data suggest that it does not lower the seizure threshold

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99
Q

What effect would high circulating concentrations of catecholamines have on acepromazine-induced hypotension?

A

acepromazine blocks a adrenergic receptors
epinephrine stimulates a-1, b1 and b2 adrenergic receptors so just b1 and b2 adrenergic receptors

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100
Q

What are the primary used of trazadone?

A

Anxiolytic- increasing the use of behavior issues (anxiety) in dogs
Decrease the dose of acepromazine and other premed drugs
used in human medicine as an anti-depressant and anxiolytic

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101
Q

How does trazadone work?

A

Serotonin receptor antagonist and reuptake inhibitor
Blocking the reuptake of serotonin increases the amount in the synpase leading to increase action of the post-synaptic 5HT1A receptors
also blocks post-synaptic 5HT2A and 5HT2C receptors (normally for insomnia, anxiety and sexual dysfunction)

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102
Q

What are two desirable effects of alpha-2 agonist?

A

1) Sedation- enhanced by concurrent opioid administeration, can be overridden with stimulation
2) Analgesia- different from acepromazine which has no analgesic effect

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103
Q

Does acepromazine have an analgesic effect?

A

NO

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104
Q

How do alpha-2 agonist exert their analgesic and sedative effects ?

A

Stimulation of pre and post synaptic a2 adrenoreceptors (G-protein linked receptors)
Stimulation of central alpha-2 adrenoreceptors decreases the release of norpinephrine-decreased sympathetic outflow
alpha-2 adrenoreceptor subtypes may play a role in specific effects observed with various alpha-2 agonists

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105
Q

What are the effects of alpha-2 agonists on the cardiovascular system?

A

Marked negative CV effects possible (dose and route dependent)
*Hypertension
*Bradycardia and bradyarrythmias
Xylazine sensitizes the myocardium to epinephrine-induced arrhythmias
*Decreased cardiac output
Hypotension (ony w general anesthesia)

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106
Q

What are the effects of alpha-2 agonists on the respiratory system?

A

Mild to moderate respiratory depression
depress respiratory center centrally- decrease sensitivity and increase threshold to CO2
May induce stridor and dyspnea in horses and brachycephalic dogs with upper airway obstruction
Sheep- Iv xylazine may induce pulmonary edema secondary to alterations in the alveolar capillary membrane

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107
Q

What are the advantages and disadvantages of giving atropine with an alpha-2 agonist

A

Advantages: Increase heart rate, blood pressure, cardiac output?

Disadvantage: Increased myocardial work, cardiac output may not increase

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108
Q

What is vatinoxan? How does it work?

A

Peripheral alpha-2 adrenoreceptor antagonist
helps to maintain CO by preventing a-2 induced arterial vasoconstriction (medetomidine, dexmedetomidine)
Intensity and duration of alpha-2 agonist induced cardiovascular effects reduced by vatinoxan

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109
Q

What is Zenalpha

A

a combination of medetomidine and vatinoxan. Used for its sedative and analgesic effects while helping to maintain CO by preventing a-2 induced arterial vasoconstriction

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110
Q

How can you antagonize the effects of dexmedetomidine?

A

Atipamezole (alpha-2 antagonist)

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111
Q

What are the potential adverse effects of atipamezole

A

rapid awakening (poor recovery)
anxiety
pain
vasodilation with hypotension
Arrhythmias
CV collapse

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112
Q

What fold difference of atipamezole do you need to administer in order to get reversal of dexmedetomidine induced sedation

A

10 fold difference higher

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113
Q

What characterizations do the anesthetic induction drugs (thiopental, propofol, alfaxalone, ketamine, etomidate) have in common?

A

they are designed to induce unconsciousness rapidly (within 1 to 2 minute) induction should be free from excitement or struggling recovery should be smooth
adverse effects of the anesthetic induction drugs are dose-dependent

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114
Q

How is ketamine fundamentally different from thiopental, alfaxalone, or propofol in the induction of anesthesia?

A

Does not unifromly depress the CNS like the other drugs
does selective depression of regions of the CNS (particularly the medial thalamic nuclei and neocortex)
stimulation of the limbic system
stimulation of the sympathetic nervous system
Decrease in CNS neurotransmission

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115
Q

Why is it desirable to induce general anesthesia quickly with a drug like thiopental?

A

Thiopental is a prototypical anesthetic induction drug, still used in many countries
administered as a rapid IV bolus in young, healthy, or poorly sedated animals
Slow administration can lead to excitement and struggling
Administer slowly IV to sick or debilitated patients

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116
Q

What accounts for the end of unconsciousness with thiopental?

A

Dog: half-life is about 7 hours but anesthesia is maintained for approximately 15 minute after a single IV dose.
short duration of anesthesia is due to redistribution of the drug away from the CNS
Long half-life results in a residual or “hangover effect”

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117
Q

What is the effect of peri-vascular injection of thiopental?

A

tissue irritation or necrosis (ph: 11)
effect dependent on the volume of thiopental injected perivascular and concentration
tissue irritation due to alkaline pH of thiopental

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118
Q

What effect does alfazalone have on respiratory system?

A

Depression, decreased tidal volume, RR
apnea is possible
effects are dose dependent

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119
Q

What are the respiratory effects of propofol?

A

similar to the respiratory effects of thiopental and alfaxalone
Decreased RR, Vt, MV
apnea
effects are dose-dependent

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120
Q

What are the respiratory effects of ketamine?

A

less respiratory depression than thiopental, alfaxalone, or propofol
patient is likely to keep breathing IVt and RR decreased but less chance of apnea)

121
Q

What are the respiratory effects of etomidate

A

mild depression of ventilation, possible short perioid of apnea but less than thiopental, alfaxalone, or propofol

122
Q

What are the effects of ketamine on cardiovascular function?

A

generally stimulates the CV system
Increases heart rate
blood pressure maintained or moderately decreased
cardiac output may be maintained
but Stim effects dampened by other drugs
Ketamine may depress cardiovascular function in compromised patients

123
Q

How does Ketamine increase heart rate and blood pressure?

A

Increases sympathetic output
Increases HR and BP an indirect effect
Compromised animals may have decreased HR and BP

124
Q

What are the effects of propofol on cardiovascular function?

A

Hypotension- dependent on the dose and speed of injection, primarily due to vasodilation, may last longer than expected, can be treated with IV fluids
Not arrhthmogenic

125
Q

What are the cardiovascular effects of alfaxalone?

A

Decreased cardiac output
Vasodilation and hypotension
Reflex tachycardia
Degree of vasodilation < propofol? (maybe)

126
Q

What are the cardiovascular effcts of etomidate?

A

minimal depression of cardiovascular function, mild bradycardia in some patients, small to no drop in blood pressure, most sparing anesthetic induction drug on cardiovascular function

127
Q

What are the differences between propofol and ketamine on the CNS function?

A

Propofol uniformly depresses CNS function- partially mediated through the GABAchannel

Ketamine depresses some parts of the brain and stimulates other parts

Induction is faster with propofol than ketamine
patients look awake during ketamine induction- tighter jaw tone, more active eye

128
Q

Why is recovery from anesthesia in dogs so rapid with propofol

A

Propofol is quickly cleared by the liver as well as by extra-hepatic sites
In the liver: glucuronidation and sulfation inactivates it
metabolites primarily excreted in the urine
clearance is 10 times that of thiopental

129
Q

Why is ketamine a poor choice to induce anesthesia in an animal with head trauma?

A

May increase cerebral blood flow and intracranial pressure
Ketamine stimulates parts of the brain (limbic system, SNS)
stimulation leads to increased CBF to meet metabolic demand
not a concern with normal patients

130
Q

What is the effect of liver disease on the recovery from propofol?

A

Recovery may be slowed a little by liver disease
essentially propofol will still clear via extra-hepatic metabolism

131
Q

What is the effect of a prolonged infusion of propofol on recovery in cats?

A

Prolonged recovery
Propofol metabolized by glucuronidation
Cats cant do this very well
Infusions <1 hour are recommended

132
Q

What are the primary advantages of alfaxalone compared to other anesthetic induction drugs in dog and cat?

A

Alfaxalone induction is similar to propofol
Advantages:
IM or SQ
Vasodilation/hypotension may be < propofol
used in many small exotic species
Does not have the precautions of ketamine
Ex: spicy cat

133
Q

What temporary endocrine abnormality is induced by etomidate?

A

can suppress the stress response
inhibits adrenocorticoid function for 2-3 hours in the dog
may require supplemental corticosteroid

134
Q

When is etomidate used to induce general anesthesia in animals?

A

patients with heart failure

135
Q

Which anesthetic induction drug should be used cautiously in a patient with glaucoma?

A

Ketamine - it increases the tone of extra-ocular muscles and increases intra-ocular pressure

136
Q

What are analgesic properties of ketamine

A

induction of general anesthesia (analgesia)
suppression of activity in dorsal horn of spinal cord
inhibition of glutamate neurotransmission at the NMDA receptor
*Not adequate at analgesia

137
Q

How can rough and prolonged recoveries from ketamine be avoided?

A

Keep the dose of ketamine be low
Large dose range clinically
combine with sedative/tranquilizing drugs (acepromazine, dexmedetomidine)

138
Q

Which anesthetics are vapors?

A

Methoxyflurane, halothane, isoflurane, sevofurane
(Liquid at ambient temperature and pressure while gas exist in gaseous form at room temp and sea level

139
Q

What is the relationship between anesthetic potency and lipid solubility?

A

Meyer-Overton Rule:
anesthetic potency is correlated with lipid solubility (the more lipid soluble the agent, the more potent the anesthetic)- brain is full of lipids

140
Q

What are the mechanisms of action of inhalant anesthetics

A

Alter intracellular functions of signaling proteins (including protein kinase C)
most likely target of volatile agents is the ion channel
Exert effects pre- and post- synaptic
inhibit neurotransmitter release and act post-synaptic to alter the response to neurotransmitters
Dampen all neuronal activity of brain via ion channels

141
Q

MAC

A

minimum alveolar concentration (MAC) of anesthetic is a measure of potency
experimentally derived value and is the minimum alveolar concentration at 1 atmosphere that produces immobility in 50% of those patients or animals exposed to noxious stimuli
exhaled what measured- gives indication

142
Q

What is saturated vapor pressure?

A

the maximum concentration of molecules in in the vapor state that can exsist for a given liquid at each temperature, unique for each volatile anesthetic

143
Q

Why is the vapor pressure of inhalant anesthetic important?

A

it determines the type of vaporizer that is required to safety deliver the inhalant
Ex:
Isoflurane: Vapor pressure 252mmHg vaporize at sea level 33% while 39% at Colorado altitude. vaporizer needs to dilute out vapor so patient not given vapor dose of inhalant

144
Q

How does the blood:gas solubility of an inhalant affect the rate of change of anesthesia?

A

determines how rapidly anesthetic saturates he blood and induces general anesthesia
Less soluble the anesthetic, the more rapid the partial pressure of anesthetic vapor reaches within the lungs and the more rapid anesthetic concentrations increase in the brain
Ex: methoxyflurane (slow), halothane, isoflurane, sevoflurane, desflurane (fast)

145
Q

How is MAC used clinically

A

to compare different inhalant anesthetics
provide a general guide to vaporizer settings
*anesthetic potency increases as MAC decrease (lower the MAC, the greater the anesthetic potency)

146
Q

What decreases MAC?

A

1) Other anesthetic/analgesic drugs used for premedicaton or induction: opioids, alpha-2 agonists, acepromazine, benzodiazepine
2) Decreased body temperature
3) Sick and/or debilitated

147
Q

Why would you want a MAC reduction during general anesthesia?

A

A MAC reduction allows us to use a lower concentration of inhalant and maintain appropriate anesthetic depth
important approach to prevent induced hypotension

148
Q

What are the effects of inhalants on cardiovascular function?

A

Dose dependent CV effects: depressed cardiac contractility
Decreased cardiac output
Vasodilation
May affect heart rate and rhythm
Hypotension
Depressed sympathetic outflow and obtunded cardiovascular reflexes

149
Q

How do inhalant anesthetics affect heart function

A

Inhibit K+ and Ca2+ channels in the heart
Clinical result= dose dependent negative chronotropic and inotropic effects and arrhythmogenic effects

150
Q

What are the effects of inhalants on respiratory function?

A

Depressed
Responsed to CO2 are blunted
Tidal volume and alveolar ventilation is decreased, minute ventilation is decreased, respiratory rate may increase or decrease
responses to increased CO2 are lost at deeper planes of anesthesia

overall: PaCO2 increased, PaO2 generally increased (delivered in 100% oxygen)

151
Q

How are inhalants eliminated from the body?

A

primarily through respiration
all inhalants undergo metabolism to some extent ex: Methoxyflurane- 50% metabolite, isoflurane - 0.17%

152
Q

What is the mechanism by which inhalant anesthetics can induce toxicity?

A

Metabolic byproducts: fluoride ions
Toxic byproducts: Compound A from sevoflurane and CO2 absorbents
Most common: decreased renal or hepatic blood flow during anesthesia

153
Q

What are the differences between isoflurane and sevoflurane?

A

Very simular anesthetics

Sevoflurane has a lower vapor pressure (different vaporizer), Lower blood:gas solubility (faster), higher MAC (less potent- needs to run vaporizer higher), more metabolites, similar CV and resp effects

154
Q

Which inhalant is the safest

A

no significant differences between isolfurane and sevoflurane
Some species/case advantages (ex: mice-sevoflurane)

155
Q

Why do we use local anesthetics

A

facilitate performing a wide variety of minor and major surgeries (sedated animals)
Provide analgesia for invasive diagnostic procedures
Decrease the requirement for intraop opioids and lower inhalant doses
Provide analgesia in the immediate postop period
Provide multi-day analgesia

156
Q

What are the advantages of local anesthetics

A

Advantages: Local anesthetics readily available
relatively safe drugs (dose-dependent)
Very effective at reducing or eliminating pain
many local blocks are relatively easy to do
Local anesthetics are affordable

157
Q

What are the disadvantages of local anesthetics

A

Disadvantages:
Local/regional blocks dont always work
Some blocks are time consuming to perform
Toxicity if over-dose
Motor block may complicate patient care
Local anesthetic may not last long enough (lidocaine)
Local anesthetics vasodilate
Possible CV effects with IV injection

158
Q

What is the mechanism of action of local anesthetics

A

stabilize the membranes of excitable tissues (inhibit the transmission (conduction) of nerve pulses, selectivity to bind Na+ channels in the nerve membrane, Na+ channel blockers making the action potential not conducted)

159
Q

What is the effect on inflammation on the efficacy of lidocaine

A

inflammation decreases efficacy of local anesthetics because inflammed tissues have a lower pH (more H+) prevents the local anesthetic from dissociating into the unionized form

160
Q

How does the addition of epipinephrine affect the action of lidocaine

A

it will prolong the duration of action. Dilute concentration
decreases rate of absorption of lidocaine (because epi vasoconstricts)

161
Q

What type of nerve fiber is likely to be affected first with a local anesthetic

A

Unmyelinated small fibers first
Sympathetic post-ganglionic, C fibers, pre-ganglionic autonomic
Delta fibers (pain)
Gamma fibers (muscle),
beta fibers (touch/pressure)
Alpha fibers (proprioception, somatic motor)

162
Q

What local anesthetic does no vasodilate?

A

cocaine

163
Q

How do local anesthetics exert an analgesic effect

A

Primarily block depolarization of A-Delta and C-fibers
nerves that are repetitively stimulated are more sensitive to local anesthetics than resting nerves

Also: bind Na+ and K+ channels in the SC
Binding of Ca2+ channels
Inhibitition of Substance P
Inhibit GABA uptake-potentiating Cl- channels

164
Q

How are amide local anesthetics metabolized

A

Amide local anesthetics (lidocaine, bupivacaine, mepivacaine, and ropivacaine) are metabolized in the liver (microsomal enzymes)
Liver metabolism and hepatic blood flow affect the rate of metabolism
prolonged in patients with liver failure

165
Q

Is bupivacaine or lidocaine a more toxic drug?

A

Bupivacaine is more toxic,
dissociates slowly from Na+ channels (longer lasting)
Difficult to resuscitate a patient with CV collapse from bupivacaine overdose because of tight binding, be careful calculating dose

166
Q

What are the clinical signs of lidocaine toxicity?

A

1) CNS effects: Muscle twitching, seizures, depression, unconsciousness, coma, respiratory arrest
2) CV signs of toxicity: hypotension, decreased cardiac output, arrhythmias, CV collapse and cardiac arrest

167
Q

How do you treat lidocaine toxicity?

A

Symptomatic treatment (IV fluids, O2 supp, intubate if needed and IPPV, Diazepam or midazolam for seizures, monitor closely)

168
Q

How does systemic admin of lidocaine produce analgesia (IV)?

A

Several mechanisms
inhibition of spinal Na+ and K+ channels
Inhibition of NMDA receptors
Inhibition of glycine reuptake (inhibitory neurotransmitter)

169
Q

What is Nocita and how does it differ from bupivacaine

A

Liposome encapsulated bupivacaine
Dosed at 5.3mg/kg Bupivacaine effect is approx 72 hours
Infiltrated at surgery site at the time of closure

170
Q

What are the advantages of Nocita?

A

up to 3 days of analgesia
avoid the need to readminister local anesthetic
Decreases the need for postop opioids

171
Q

What are the disadvantages of Nocita

A

infiltrated in the latter half of surgery, used in combination of other blocks (stays where you put it, wont diffuse)
Expensive

172
Q

What is unique about grapiprant?

A

an NSAID that does not inhibit COX, EP4 antagonist, specific receptor for prostaglandins

173
Q

What is the mechanism of action of diazepam?

A

it binds to specific site on GABA a receptors and increasing efficacy of GABA, increasing chloride ion conductance and hyperpolarizes the membranes

174
Q

How can we avoid inducing withdrawal in a patient receiving opioids for several days

A

taper the opioids

175
Q

What organ system is most concerning when giving an NSAID to an adult cat?

A

Kidneys

176
Q

What is a partial mu agonist and what is the clinically used drug?

A

buprenorphine, only partial activation of the mu receptor

177
Q

When should you give flumazenil to animal

A

if you want to reverse a benzodiazepam

178
Q

How can you enhance the sedative effects of acepromazine in a dog or cat?

A

1) Add Alpha-2 agonist
2) Add opioid
3) Increase dose

179
Q

Why are NSAIDs used in animals

A

1) analgesia
2) anti-inflammatory
3) antipyretic

180
Q

Which opioid is difficult to reverse due to high binding affinity

A

buprenorphine

181
Q

What is the most common complication of NSAIDs in dogs

A

GI issues: nausea, vomitting, diarrhea, erosion, ulceration

182
Q

How can you treat opioid-induced excitement in a dog

A

1) Alpha-2 agonist
2) Reverse opioid

183
Q

How does ketamine increase heart rate and blood pressure

A

increases sympathetic tone (indirect effect)

184
Q

How can you partially reverse the effects of hydromorphone

A

Low dose of naloxone (102mcg/kg IV)
Buprenorphine
Butorphanol
Nalbuphine

185
Q

What is a clinically convenient way to administer buprenorphine to a cat

A

transmucosal

186
Q

How do diazepam and midazolam differ?

A

midazolam is water soluble and can be given IM

187
Q

What is primary use for acepromazine

A

sedation and tranquilization

188
Q

How are the effects of acepromazine antagonized

A

they are not, no antagonist available

189
Q

What are two desirable effects of alpha-2 agonist

A

sedation and analgesia

190
Q

How can you completely reverse effects of buprenorphine

A

naloxone (high dose because it binds really tightly to mu receptor)

191
Q

What are the main effects of acepromazine on the cardiovascular system

A

vasodilation leading to hypotension

192
Q

What are some uses of NMJ blockers?

A

1) tracheal intubation
2) orthopedic manipulations (fractures)
3) Balanced anesthesia
4) Anytime that skeletal muscle paralysis is desired

193
Q

Competetitive NMJ blockers

A

prevent motor end plate depolarization
initial muscle weakness followed by flaccid paralysis

194
Q

What is Pancuronium used for?

A

it is a NMJ blocker
useful with tachycardia
long duration of 2-3 hours

195
Q

How does renal disease influence pancuronium?

A

it increases the half life of its NMJ blocking

196
Q

What NMJ blocker has a long duration of action

A

Pancuronium (2-3 hours)

197
Q

What NMJ blocker has a short duration of action

A

Miracurium (15 minutes)

198
Q

Rank the NMJ blockers on their duration of action

A

Pancuronium, Atracurium, Miracurium (shortest)

199
Q

What NMJ blockers promote histamine release?

A

Succinylcholine, Atracurium and Miracurium

200
Q

What NMJ blockers would you recommend for a patient with renal disease

A

Atracurium and Miraciurium (pancuronium’s half life is increased with renal disease)

201
Q

What increases the half life of Atracurium?

A

Hypothermia and acidosis because it is degraded spontaneously and hydrolysis by plasma esterases and renal elimination

202
Q

How do you reverse NMJ blockers

A

acetylcholinesterase inhibitors (like physostigmine or neostigmine)

203
Q

Name a depolarizing NMJ blocker

A

Succinylcholine

204
Q

What are the competetive NMJ blockers?

A

Pancuronium, Atracurium, Miracurium

205
Q

Succinylcholine

A

a depolarized NMJ blocker used clinically, essentially mimics ACh at the NMJ, rapid onset, some histamine release

206
Q

How do you reverse succinylcholine

A

you cant

207
Q

What is a side effect from succinylcholine

A

hyperkalemia from the release of intracellular potassium from skeletal muscles, avoid in presence of extensive soft tissue damage or burns

208
Q

When should you use succinylcholine

A

short lived MNJ blockade (via depolarizing) such as facilitating tracheal intubation or wildlife immobilization
(immobilization without the CNS effect- not analgesic, and not dissociative)

209
Q

Do you get CNS effects with succinylcholine

A

No

210
Q

Potential problems with NMJ blockers

A

1) Unable to monitor the depth of anesthesia using muscular signs (ex: general and jaw tone)
2) Respiratory distress- make sure to monitor oxygenation and carbon dioxide levels
3) Toxicities via ganglionic blockade and histamine release leading to bronchospam, hypotension, bronchial and salviary secretion
4) Malignant hyperthemia: life threatening from excessive contracture and heat production from skeletal muscle initiated by release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

211
Q

How might you limit the histamine release from the NMJ blockers that release histamine ( succinylcholine, miracurium, atracurium)

A

Minimize with antihistamine treatment of diphenhydramine (Benedryl)

212
Q

What NMJ blocker does not release histamine

A

Pancuronium

213
Q

How can you treat malignant hyperthermia caused by NMJ blockade?

A

Dantrolene- a drug that limits SR Ca2+ release
also so supportive measures like rapid cooling and oxygen

214
Q

What happens when you give a NMJ blocker IV?

A

paralysis to all skeletal muscles

215
Q

Diuretic

A

agent that produces diuresis (Increased urine flow rate)

216
Q

What are the major osmolytes being reabsorbed/secreted when making urine?

A

Reabsorbed: NaCl, Bicarbonate (HCO3-), Calcium (Ca2+)

Secreted: Hydrogen and Potassium

217
Q

Why might you give a diuretic?

A

1) reduce extracellular fluid volume (Pulmonary congestion- CHF, fluid overload or ascites- CHF, liver disease)
2) Oliguric renal failure- pathogen: vasoconstriction leading to decreased blood flow and cellular ischemia/necrosis
3) Hypertension (systemic or excerise induced pulmonary hemorrhage)
4) Promote urinary excretion of selected agents/electrolytes (hypercalcemia)

218
Q

Osmotic Diuretics

A

inhibits water reabsorption in the proximal tubule and thin loop by increasing the osmotic gradient in the lumen
Includes: Mannitol

219
Q

Mannitol

A

an osmotic diuretic that functions to inhibit water reabsorption in the proximal tubule and thin loop by increasing the osmotic gradient in the lumen

Uses: Oliguric renal failure, cerebral edema, acute glaucoma

Dont use: if cant establish urine flow, or if there is intracranial bleeding

220
Q

How does DM act as an osmotic diuretic

A

too much glucose infiltrate leads to water retained in the urine leading the clinical signs of PU/PD and causing dehydration

221
Q

Carbonic Anhydrase inhibitors

A

promote reabsorption in the proximal tubule by increasing the retentions of bicarbonate reabsorption leading to increased retention of bicarb in urine (alkanization, blood acidifcation, and increasing H20 excretion)

ex: Acetazolamide

222
Q

Acetazolamide

A

an CA inhibitor that inhibits bicarbo resportion leading to increased retention of bicarb in the urine, blood acidification, and increased H20 ecretion
Weak diuretic effect
Uses: treat metabolic alkalosis, glaucoma, altitude sickness
Side effects: may cause systemic acidosis through bicarb loss in urine. also hypokalemia due to H+/K+ exchange

223
Q

What are some side effects of acetazolamide

A

may cause systemic acidosis and hypokalemia

224
Q

Loop diuretics

A

inhibit NaCl resorption in the thick ascending limb of the loop of henle
induces urinary loss of NaCl and water, most commonly used
ex: Furosemide

225
Q

Furosemide

A

most effective diuretic, most widely use in vet med
functions to inhibit NaCl resportion in the think ascending limb of loop of henle inducing urinary loss of NaCl and water
-also may cause hypokalemia and hypocalcemia

uses: oliguric renal, CHF, acute pulmonary hypertension, EIPH

226
Q

Why is furosemide banned on the day of the race

A

because its diuretic effect can mask the presence of other drugs in urine

227
Q

What can you use for EIPH in horses, commonly racehorses

A

Horses with EIPH commonly get epistaxis associated with impaired function from repeated capillary rupture and healing leads to scarring, decreased lung capacity

Treat with Furosemide: fluid loss- reduced blood pressure in the pulmonary circulation, bronchodilator effecr

228
Q

Thiazide diuretics

A

act on the distal convoluted tubule to prevent the resorption of Na and Cl in the dital tibule by blocking the symporter leading to Na and Cl being retained in the filtrate
ex: chlorothiazide

229
Q

Chlorothiazide

A

not as effective as loop diuretics but lead to Na, Cl being retained in the filtrate by blocking symporter in the distal tubule
use: treat nephrogenic diabetes inspidus, udder edema (cattle), and Ca2+ containing uroliths

230
Q

What is furosemide used to treat?

A

oliguric renal, CHF, acute pulmonary hypertension, EIPH

231
Q

What is used to treat nephrogenic diabetes insipidus

A

Chlorothiazide

232
Q

What are the two K+ sparing diuretics

A

Spironolactone and Amiloride

233
Q

What drug is a competitive aldosterone antagonist?

A

Spironolactone

234
Q

What drug is a principal cell Na+ channel blockers

A

Amiloride

235
Q

K+ sparing diuretics

A

help maintain electrolyte balance (K+) , unlike other diuretics by influencing aldosterone either by antagonism (Spironolactone) or blocking sodium channels of distal tubules (Amiloride) which aldosterone normally acts on to increase sodium, potassium channels, urine retention, and increased blood pressure, K+ excretion

236
Q

What drug interaction can be prevented by giving K+ sparing diuretics like spironolactone and amiloride?

A

Digoxin is enhanced with hypokalemia and can lead to arrhythmias. patients on digoxin shouldnt be given diuretics

237
Q

Spironolactone

A

Blocks aldosterone induced expression of multiple genes leading to mild diuresis with reduced potential for K+ loss
used in combination with loop diuretic to prevent hypokalemia, hypertension, treat hormonal acne in women
delayed onset of action and prolonged effect

238
Q

Amiloride

A

an epithelial sodium channel blocker leading to an immediate but mild diuretic effect. used in combination with loop diuretics

239
Q

Diabetes inspidus

A

lack of ADH leading to severe diuresis

240
Q

Aquaretics

A

a class of diuretics that antagonize ADH/vasopressin V2 receptors in the kidney promoting solute free water clearance (no loss of Na+)
includes: Demeclocycline

241
Q

Demeclocycline

A

an antibioitic that also antagonized the v2 receptor in the kidney leading to diuresis by diminishing responsiveness to ADH
Used to tx syndrome of inappropiate ADH production
effective in heart failure but not et approved

242
Q

What dietary change can often increase the effectiveness of diuretics?

A

Restricting dietary NaCl
or add K+ to diet to decrease induced hypokalemia

243
Q

What is an autacoid

A

a biological factor which act near the site of synthesis and have brief duration of action, act as local hormones essentially for diverse functions like modulating blood flow, regulating secretions, altering smooth muscle function, and participating in allergy, inflammation, and pain related processes

244
Q

Derived from aa histidine, mast cells and basophils contain it and is released by exocytotic extrusion via IgE

A

Histamine

245
Q

Mast cell degranulation results in

A

histamine to be released with other biologically active compounds like proteases, serotonin, phospholipid derivatives (prostaglandins and leukotrienes)

246
Q

What histamine receptors are the most clinically relevant

A

H1: modulates smooth muscle function (vasodilation and bronchail contraction) and increase capillary permeability

H2: Stimulate gastric acid secretion

247
Q

H1 antangonist

A

antihistamines that are specific to H1 receptors, function in varous allergic, anaphylactic, and other histamine related reactions, relax constricted bronchial smooth muscle, inhibit histamine vasodilation, decrease swelling and redness by decreasing capillary permeability, decrease itching

1st gen: Diphenhydramine, Chlorpheniramine, Dimenhydrinate, Promethazine

2nd gen: Loratadine

248
Q

What does the swelling and redness of allergies come from

A

The H1 receptor increasing capillary permeability

249
Q

How do 1st gen and 2nd gen H1 antagonist antihistamines differ

A

1st gen: unionized at physiological pH- able to enter the CNS often sedating

2nd gen: ionized at physiological pH, less enters the CNS and is less sedating

250
Q

List the 4 1st generation H1 antagonists

A

1) Diphenhydramine (Benadryl)
2) Chlorpheniramine (Chlor-Trimeton)
3) Dimenhydrinate (Dramamine)
4) Promethazine (Phenergan)

251
Q

What 1st generation H1 antagonist is not anti-muscarinic

A

chlorpheniramine

252
Q

What is a 2nd generation H1 antagonist

A

Loratadine (Claratin)

253
Q

What are the adverse effects of H1 antagonists?

A

1) CNS depression (lethargy, ataxia, sedation)
2) Antimuscarinic effects (dry mouth, urine retention, anti-sludge) - contraindicated in glaucoma
3) CNS stimulation- paradoxial or with high doses

254
Q

Name an H2 antagonist

A

Famotidine (Pepcid)

255
Q

What is the function of H2 antagonist like Famotidine?

A

Inhibiting gastric acid secretion by blocking H2 receptors on parietal cells in the gastric mucosa

Used in gastric, abomasal, and duodenal ulcers, drug-induced gastritis, reflux

256
Q

Why might you use Famotidine?

A

reduce gastric acid secretion for gastric, abomasal, and duodenal ulcers, drug-induced gastritis, reflux

257
Q

Derived from the amino acid tryptophan, found in platelets, neurons, and mostly in the GI tract
function to regulate gut motility, body temperature, sleep, mood, behavior, and pain

A

Serotonin

258
Q

Ergot alkaloids

A

serotonin agonists from fungus on seeds, lead to cattle losses

259
Q

Why might you use an SSRI

A

to increase serotonin levels leading to behavioral changes
Dogs: separation anxiety, compulsive behaviors, aggression
Cats: spraying, compulsive behaviors, aggression, psychogenic aopecia

260
Q

What does angiotensin result in

A

Vasoconstriction and increase in blood pressure

261
Q

What does bradykinin result in

A

vasodilation

262
Q

Non-steroidal immunomodulators

A

drugs that suppress immune function via mechanisms distinct from corticosteroids
inhibit T cell activation, B cell activation, or both
often used when NSAIDs or corticosteroids fail
-Systemic disease (IMHA, IMTP, SLE)
-Dermatological Diseases (Pemphigus, Discoid Lupus)

263
Q

Consequences of NSIMs

A

inappropiate autoimmune responses are blunted (good), normal immune responses are blunted (bad)

264
Q

Calcineurin inhibitors

A

inhibits calcineurin an enzyme that activates T cells, leading to blockade of T cell proliferation and cell-mediated immunity
Cyclosporine and Tacrolimus

265
Q

Cyclosporine

A

a calcineurin inhibitor that binds to cyclophilin leading to dephosphorylation of NFAT leading to decreased T cell activation and cell mediated immunity
Uses: IMHA, IBD, Immune mediated polyarthritis, atopic dermatitis, perianal fistulas (dogs), organ transplant regiments , keratoconjunctivitis sicca (KCS)

266
Q

Tacrolimus

A

a calcineurin inhibotr that binds FKBPI2, an immunophilin involved with calcineuron function
Prevents dephosphorylation of NFAT leading to a decrease in T cell activation and cell mediated immunity
Minimal use in vet med
Topic administration for dermatoses in dogs

267
Q

What drug is a Janus Kinase Inhibitor (JaK-1 and 3)

A

Oclacitinib (Apoquel)

268
Q

Oclacitinib (Apoquel)

A

a JAK 1 and 3 inhibitor that decrease the effects of inflammatory cytokines made by lymphocytes as well as decreasing IL-31- directly involved in itch sensation
Use: manage chronic itching
side effects: Bone marrow suppression (increased risk of infection)

269
Q

What drug is a monoclonal antibody against IL-31

A

Cytopoint

270
Q

Cytopoint

A

a monoclonal antibody against IL-31, eliminating the itch sensation cytokine
SQ injection that last 4-6 weeks
minimal immunosuppression
used for atopic dermatitis in dogs

271
Q

What are the cytotoxic alkylating agents?

A

Cyclophopshamide
Chlorambucil

272
Q

What is the mechanism of action of cyclophosphamide and Chlorambucil

A

Nitrogen mustard that adds alkyl groups to damage DNA of T, B, and other rapidly dividing cells of the bone marrow

273
Q

What cells are cyclophosphamide and Chlorambucil toxic to?

A

T and B cells

274
Q

Cyclophosphamide

A

a cytotoxic alkylating agent that is potent to T, B, and other rapdily dividing cells in the bone marrow

Uses: anti-neoplastic and immunosuppression (IMT, SLE, rheumatoid arthritis, pemphigus, IMHA)

Toxicity: Bone marrow suppression, nausea, vomiting, diarrhea, alopecia, Sterile hemorrhagic cystitis

275
Q

Sterile hemorrhagic cystitis

A

seen in cyclophosphamide toxicity primarily in dogs
due to accumulation of acrolein that damages bladder epithelium. Minimize with glucocorticouds/diuretics and MESNA to bind the toxin

276
Q

Chlorambucil

A

a cytotoxic alkylating agent that is potent to T, B, and other rapdily dividing cells in the bone marrow

Uses: substrate for cyclophosphamide and often immune mediated skin diseases in cats like pemphigus

Toxicity: less toxic than cyclophosphamide but not as effective

277
Q

What are the cytotoxic inhibitors of purine synthesis

A

Azathioprine and Mycophenolate mofetil

278
Q

Azathioprine

A

a cytotoxic inhibitor of purine synthesis disrupting T and B cell proliferation
primarily in dogs for immunosuppression, IBD, immune mediated skin disease, IMHA

Uses: often with corticosteroids so both can be given at lower doses and limits the adverse effects

Toxicity: Major- immunosuppression and bone marrow supression (especially in cats)
Minor: GI distress, anorexia, pancreatitis, hepatotoxicity

279
Q

Mycophenolate mofetil

A

a cytotoxic inhibitor of purine synthesis disrupting T and B cell proliferation, used as an alternative to azathioprine

Uses: similar to azathioprine- IBD in dogs, organ transplant regiments, immuosuppression, IMHA, immune mediated skin diseases
Potentially useful in cats but still use with caution
Limited Vet med use

280
Q

What results in increased pain?

A

Peripherally: activation of nociceptors via TRPV1 (heat), TRPA1 (pressure), and TRPM8 (cold) via inflammaion (prostaglandins, bradykinin, cytokines, and lipids

Centrally: Increased action potentials through pain pathways to the brain (modification of synapses in dorsal horn- windup leading to increased pain perception, decreased activity of descending inhibition)

281
Q

Where is aldosterone produced

A

zona glomerulosa under ACTH, angiotensin II, and increased extracellular K+

282
Q

Why is aldosterone produced

A

to increase salt and water retention

283
Q

Where is glucocorticoid produced

A

in the zona fasciculata of the adrenal cortex under CRH from hypothalmus and ACTH from anterior pituitary

284
Q

What are the 8 effects of glucocorticoids

A

1) Metabolism (increased gluconeogensis, increased insulin secretion, increased protein breakdown, increase lypolysis)
2) Cardiovascular (increased adrenergic and angiotensin signaling, increased vasoconstriction and cardiac contraction, CV effects associated with hypertension and CHF)
3) Respiratory effects Bronchodilation and B2 receptor expression, decreases histamine release
4) Skeletal muscle effects: maintains muscles but can waste at high amounts
5) Integumentary skin effects: epidermal and dermal thinning, easily bruiing, poor wound healing, poor quality hair, alopecia
6) Immunological skin effects: easy bruising, poor wound healing, epidermal and dermal thinning, alopecia
7) Water and Electrolyte balance: Polyuria and Polydypsia from inhibiting ADH
8) Gastrointestinal effects: possible ulceration from increased HCl and pepsin
9) Anti-inflammatory at pharmacologically high doses- primarily cell mediated immunity more than humoral immunity

285
Q

What 3 ways do different glucocorticoids differ?

A

1) Ant-inflammatory potency
2) Duration of action
3) Mineralocorticoid activity

286
Q

Hydrocortisone (cortisol)

A

Short duration (<12 hours)
Anti-inflammatory and mineralocorticoid potency=1
Uses: topically for pruritus and inflammation associated with allergy

287
Q

Fludrocortisone

A

Short duration of <12 hours
Anti-inflammatory potency of 10
Mineralcorticoid potency of 125
Uses: Systemically for cortisol and aldosterone replacement during adrenal insufficiency (Hypoadrenocorticism- Addisons)

288
Q

inactive pro-drug that gets metabolized to prednisolone
intermediate duration (12-36 hours)
Anti-iflammatory potency of 4
Mineralocorticoid potency of 0.8
Used for long term allergy management, chronic inflammation like arthritis, immunosuppression (autoimmune)

A

Prednisone

289
Q

Give for Cats/horses or hepatic failure as they have less prednisolone conversion
intermediate duration (12-36 hours)
Anti-iflammatory potency of 4
Mineralocorticoid potency of 0.8
Used for long term allergy management, chronic inflammation like arthritis, immunosuppression (autoimmune)

A

Methylprednisolone

290
Q

long duration (36-72 hours)
Anti-inflammatory potency of 25
A mineralocorticoid Potency of 0
Used systemically for immediate relief of hypersensitivity and septic shock, long term control of allergy, and immunosuppression

A

Dexamethasone

291
Q

What is mitotane used for

A

it eliminates of decreases the availability of adrenal steroids
cytotoxic to the zonae fasciculata and reticularis
reduces all adrenal steroids except for aldosterone
Used for Hyperadrenocorticism or steroid-secreting adrenal tumors

292
Q

How can you get iatrogenic hypoadrenocorticism

A

adrenocortical suppression can occur a few weeks of glucocorticoid therapy
Additional supplementation may be necessary during periods of stress,
tapering to wean animal off of the steroid, based on GC involved, dose, duration of therapy, stress level, etc.

293
Q

what does COX 1 produce?

A

PGE2 (Vasodilation, sensitization of nociceptors, GI protection via mucous production)

Thromboxane A2 (Platelet aggregation and vasoconstriction resulting in enhanced coagulation and clot formation

294
Q

Does COX 1 have constitutive or inducble expression?

A

constitutive

295
Q

What does COX 2 produce?

A

1) PGE2 (Vasodilation, sensitization of nociceptors, GI protection via mucous production)

2) PGI2: produced in endothelial cells, causes vasodilation, inhibits platelet aggregation

296
Q

How do NSAIDs produce an analgesic effect?

A

by inhibiting prostaglandin synthesis and decreasing nociceptor activity

297
Q

COX-2 selective drugs

A

fewer GI effects than non-selective NSAIDs but not safer for kidneys.
have a procoagulant effect through losing PGI2

298
Q
A

Pharm (4 decks)

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