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Toxicology > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

M3 Agonists role in the eye

A 
o	accommodation (near vision)
o	miosis (pinpoint)

o	
increased drainage (conventional route) ->
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2
Q

M3 Antagonists role in the eye

A

o profound mydriasis (dilated)

o may precipitate acute pressure
o increase dry eyes and loss of accommodation

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3
Q

Beta Agonist Vs Antagonist role in the eye

A

beta agonist
o increase ocular fluid

beta antagonist
o decrease ocular fluid formation

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4
Q

Alpha Agonists role in the eye

A

relatively weak mydriasis (a1) (dilation)

decrease fluid formation
• a2 - direct

• a1 - indirect (vascular)

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5
Q

Drugs to decrease ocular fluid formation

A

o Adrenergic agonists / NET inhibitors
o Beta antagonists (Timolol)
o Carbonic Anhydrase inhibitors

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6
Q

Drugs to Increase drainage of the eye through trabecular meshwork

A

o Muscarinic agonists / AChE inhibitors
o ROCK inhibitors (Netarsudil)
o Nitric Oxide

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7
Q

Drugs to pull ocular fluid out & reduce fluid formation

A
  • Systemic Osmolites
  • Mannitol or glycerin
  • Reduces ultrafiltrate in ciliary blood vessels
  • Emergency cases only
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8
Q

Drugs to Increase ocular drainage through uveoscleral route

A

o PGF2 analogs
o Latanoprost
o only useful in dogs

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9
Q

Topical Muscarinic Blocker; use, drugs, side effects

A

used to dilate pupil

Tropicamide
• Short acting
• Good for eye exam

atropine
• long acting

adverse effects
• paralysis of ciliary muscle
• acute glaucoma
• decreased tears

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10
Q

Topic alpha-adrenergic agonist use & drug

A
  • used to dilate pupil
  • Phenylephrine
  • Not as effective as muscarinic blocker
  • Useful as vasoconstrictor
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11
Q

Keratoconjuctivitis sicca (dry eye); what is it? what drugs to use? side effects of drug

A

o May be immune mediated
o Dogs

Drug to use
• Topical cyclosporine

Side Effects of Drug
•	Suppresses immune system
•	Increases tears
•	Dry eye returns after stopping med
•	Rare systemic toxicities
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12
Q

Drugs to use in eye inflammation

A

Topical corticosteroids
• prednisolone or dexamethasone 
or NPDex
• used for conjunctiva, sclera, cornea, and anterior chamber 

• deeper structures require systemic drug 

• immunosuppressive and inhibit wound repair
• can worsen or cause corneal ulceration
• should not be used if viral infection present 


Topical NSAID

Muscarinic antagonists
• Atropine or tropicamide
• Treat uveitis & prevent synechia and ciliary spasm pain

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13
Q

Drugs to use in eye infection

A

Topical tetracyclines
• conjunctivitis in cats
• Works against chlamydia & mycoplasma

Triple antibiotic ointment
• Conjunctivitis in dogs
• Bacitracin + polymixin B + neomycin
• Systemic toxicity

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14
Q

Drugs to use for viruses like feline herpes virus

A 
Antivirals
•	Agent incorporated into viral DNA & breaks protein transcription
•	Nucleiside analogues = Trifluridine
•	Reduce signs but don’t sure virus
•	Need frequent dosing
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15
Q

Define Pain

A

o protective mechanism to make animal withdraw from damaging situation
o can have detrimental health impacts

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16
Q

Define Nociception & what are the fibers?

A

o Neural response to painful stimulus

A-delta fibers
• fast conducting
• sharp and acute pain
• easy to localize

C fibers
• slow conducting
• dull, aching, burning or throbbing pain
• hard to localize.

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17
Q

Hyperalgesia & Allodynia

A

Hyperalgesia
o Exaggerated response to painful stimuli

Allodynia
o Pain due to stimuli which does not normally provoke pain

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18
Q

Opioid Receptors

A
  • 7 G-couple protein receptors
  • Mu, delta, & kappa
  • Mostly inhibitory
  • Most drugs use Mu receptor
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19
Q

Opioid Receptor Signaling Pathway

A
  • Activation of receptor ->
  • Inhibit cAMP production ->
  • Open K+ channels (hyperpolarization) ->
  • Close voltage gated Ca2+ channels
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20
Q

Analgesic Effect of Opioids & Location Targeted

A

o Decrease chronic dull pain better than acute sharp pain

CNS
• Decrease pain perception
• Increase descending inhibitory path

Spinal Cord
• Decrease activation of spinothalamic tract by incoming nociceptor afferents

Pre-synaptic
• Inhibits glutamate release from nociceptor neurons

Post-synaptic
• Directly inhibits ascending neurons

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21
Q

Sedative Effects of Opioids

A

o sedation greater in dogs than cats
o Excitement occurs in some animals: cats, horses, and huskies, sheep, cattle, swine
o Need to distinguish between agitation due to pain or drug!
o Can be used for chemical restraint

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22
Q

Calming/euphoria & antitussive Effects of Opioids

A

Calming/euphoria Effects
o activate the reward centers of the brain
o how much euphoria occurs is unclear and is probably species dependent.

Antitussive Effects & Depression of Laryngeal Reflex
o Inhibition of cough center of medulla oblongata
o Dextromethorphan, Morphine, codeine, butorphanol

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23
Q

GI effects of Opioids

A

o Contraindicated in pancreatitis or biliary dz

Acute:
• vomiting and defecation
• Initial stimulation of medullary chemoreceptor trigger zone (CTZ), & delayed suppression of inhibition of medullary vomiting center

later:
• cause constipation
• increase spontaneous GI smooth muscle contraction but decrease coordinated peristalsis

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24
Q

Loperamide

A

o opioid that doesn’t cross the BBB at therapeutic concentrations
o used to treat diarrhea
o removed from the CNS by the efflux transporter P-glycoprotein
o can cause neurological toxicity in dogs w/ MDR1 mutation

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25
Q

Respiratory & Cardiovascular Effects of Opioids

A

Respiratory Effects
o decrease sensitivity of respiratory center in medulla oblongata to CO2
o Normally the cause of death in an overdose
o Less of a problem given alone
o cross the placenta and depress fetus respiratory

Cardiovascular Effects
o bradycardia more likely in animal not in pain
o can increase cardiac output in horses.
o can also cause hypotension due to vasodilation, particularly during surgery

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26
Q

Temperature Effects & Panting w/ Opioid Use

A

Temp Effects
o Can interfere with thermoregulation
o Most animals get hypothermic
o Cats may get hyperthermic

Panting
o may occur in some dogs, particularly after oxymorphone.
o due to resetting the thermoregulatory center in thalamus

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27
Q

Effects of Opioids on Urinary Tract & pupils

A

Urinary Retention
o Increase detrusor muscle and sphincter tone
o Especially common after epidural morphine

Effects on pupils
o Miosis – dogs, humans
o Mydriasis – cats, sheep, horses

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28
Q

Neuroendocrine Effects of Opioids

A

o Increase vasopressin (ADH) release -> oliguria
o Decrease gonadotropin release
o Increase prolactin release

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29
Q

Histamine & Opioids

A

o histamine release W/ IV administration of morphine.

o cause vasodliation and hypotension

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30
Q

Acute Symptoms & Antidote for Opioid Overdose

A

Acute
• Miosis
• Respiratory depression
• Coma

Antidotal Therapy
• Opioid antagonists: Naloxone, Naltrexone, Diprenorphine
• Supportive respiration

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31
Q

Long Term Opioid Treatment Results

A

Tolerance:
• Tolerance to all effects except Miosis & Constipation
• Cross tolerance to other opioid analgesics

Dependence:
• Psychological dependence
• Physiological dependence

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32
Q

Withdrawal or Abstinence Syndrome

A

o opioid is stopped precipitously following chronic treatment (5-7 days)
o restlessness (thought to be craving for drug)
o vocalization, hyperactivity and aggression
o Hyperthermia,
o tremors,
o salivation
o Retching,
o Vomiting & diarrhea

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33
Q

Absorption, Distribution, & Metabolism of Opioids

A

Absorption
• Well absorbed
• substantial 1st pass metabolism orally

Distribution
• Lipophilic
• Well distributed
• Can accumulate in fat

Metabolism
• Many opioids metabolized via hepatic cyp/p520 enzymes and conjugated via glucoronidation
• filtered and eliminated via the kidney
• cats have low glucoronidation -> longer effects of drug

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34
Q

2 Types of Opium Alkaloids

A 
Morphine: 
•	standard narcotic analgesic 

•	used for severe pain 

•	Fairly well tolerated in most species 

•	can stimulate histamine release 

•	Can stimulate emesis 

•	lasts up to 4 hours 
•	useful for traumas and surgeries 


Codeine:
• Antitussive
• Weak analgesic

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35
Q

Hydromorphone

A
  • 5-7X more potent than morphine
  • greater lipophilicity = faster onset time
  • used for mild to severe pain
  • Less histamine release
  • Reduced emesis and nausea
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36
Q

Fentanyl

A
  • 100X potency of morphine
  • well tolerated in dogs and cats 

  • can cause excitation in horses 

  • no histamine release 

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37
Q

Etorphine

A
  • 1000X potency of morphine
  • tranquilizer
  • Mainly in zoo/wildlife vet med
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38
Q

Oxymorphone

A
  • 10X potency of morphine

* Less emesis, nausea, sedation and histamine release

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39
Q

Methadone

A
  • Ocationally used in vetmed

* treatment programs for heroin

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40
Q

Meperidine

A

• 1/8 potency of morphine

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41
Q

Sufentanil

A

• 5-10X potency of fentanyl

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42
Q

Carfentanil

A
  • 8000X potency of morphine

* Zoo tranquilizer

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43
Q

Buprenorphine

A
  • Much safer than morphine
  • partial agonist at mu receptors (ceiling effect)
  • antagonist at k receptors 

  • high affinity but low efficacy 

  • longer duration of action than morphine 

  • used in mild to moderate pain 

  • can precipitate withdrawal if following long-term full agonist 

  • less highly scheduled (III) than morphine (II) 

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44
Q

Butorphenol

A
  • Antagonist at mu receptor,
  • agonist at k receptor
  • limited degree of analgesia
  • mild to moderate pain only
  • reduced side effects,
  • less highly scheduled (IV),
  • can precipitate withdrawal
  • especially noted as better tolerated in horses (less excitement)
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45
Q

Tramadol

A
  • Derivative of codeine
  • 1/6000 the affinity of morphine for mu receptors
  • Multimodal analgesia
  • thought to inhibit NE and 5HT reuptake
  • binds a2-adrenergic receptors
  • has an active metabolite (M1) that has more potent opiate receptor binding, 200X more affinity, 6X more potent analgesia than tramadol (hepatic metabolism CYP2D6 (P450))
  • better oral bioavailability than morphine
  • controversial about how much pain relief it actually provides
46
Q

Tapentadol

A
  • mu opioid receptor agonist
  • inhibits 
NE reuptake 

  • In humans thought to produce less GI side effects 

  • Most concerned about respiratory depression
47
Q

Delta Opioids

A

o Analgesia generally equal to morphine 

o may be more effective than morphine in relief of neuropathic pain 

o less addiction liability than morphine 

o less respiratory depression than morphine 

o less gastrointestinal side effect than morphine

48
Q

Local Anesthetics: Mechanism of Action & Order of Sensation Loss

A

Mechanism of action
o Reversible block of voltage-dependent Na channels that are required for action potentials

Order of loss
o	Small unmyelinated fibers are most sensitive
o	Pain ->
o	Temp ->
o	Touch ->
o	Joint ->
o	Deep pressure
49
Q

Chemical Structure of Local Anesthetics

A

o Weak bases
o Lipohilic group +
o Intermediate chain w/ ester or amide link +
o Hydrophilic group capable of ionization

50
Q

Amino Esters; basics, example drugs

A

o local anesthetic
o Hydrolyzed by plasma esterase
o Can form PABA
o Potential allergen

Drugs
• Benzocaine
• Procaine
• Proparacaine

51
Q

Amino Amides; basics, example drugs

A 
o	local anesthetic
o	Biotransformedd by liver enzymes
o	Rarely allergen
o	Liver issues affect metabolism
o	Longer T1/2 than esters

Drugs
• Lidocaine
• Mepivacaine
• Bupivacaine

52
Q

Bioavailability of Local Anesthetics

A

o Must be uncharged to cross cell membrane & get inside cell
o BUT must be charged to block Na channel
o Inflamed tissue is acid so local anesthetics less effective

53
Q

Routes of Administration for Local Anesthetics

A

Surface
• Oral spray
• Eye drops
• Patches

Conduction
• Nerve block

Spinal
• Injection into subarachnoid space
• Epidural

54
Q

Dose Related Drug Toxicity of Local Anesthetics

A

CNS
• Seizures, twitching, very high CNS depression

Cardiovascular
• Dysrhythmias
• Hypotension

Methoglobinemia
• High levels of hemoglobin that doesn’t bind O2

Respiratory
• Depression if drug affects C5-C7 or CNS

55
Q

Order of Adverse Effects of Local Anesthetics

A
  • Analgesia
  • Altered consciousness
  • Muscle twitching & hypotension
  • Myocardial depression & seizures
  • Unconsciousness & apnea
  • Cardiovascular collapse & death
56
Q

Unusual Effects of Local Anesthetics

A
  • Hypersensitivity or allergic reaction

* Drug idiosyncrasy

57
Q

Local Anesthetics Interactions w/ Vasoconstrictors

A

o Use w/ epinephrine, norepinephrine & phenylephrine
o Increase duration of anesthesia
o Decrease systemic toxicity
o Can cause problem w/ circulation
o Can increase risk of arrhythmias & V fib

58
Q

Lidocaine

A 
o	Very versatile & widely used in vet medi 
o	pKa = 7.9 
o	rapid onset of action(1-5minutes)
o	short duration(60- 120 minutes) 

o	metabolized by the liver 
o	also used IV as anti-arrhythmia
59
Q

Bupivicaine

A 
o	Long acting (5-8 hrs)
o	Slow onset (up to 20-30 mins)
o	Risk of cardiac toxicity
o	Metabolized by liver
o	Not used IV or topical
60
Q

Ropivicaine

A

o 5-10 min onset
o lasts 5-8 hrs
o lesk cardio & CNS risk than bupivacaine

61
Q

Mepivicaine

A

o Structure similar to lidocaine
o pKa = 7.6
o onset 2-5 mins
o lasts 2-3 hrs

62
Q

Procaine

A

o Non irritating
o Quick
o Lasts 45-60 mins
o Commonly used to reduce pain for IM injections

63
Q

Proparacaine

A

o Used in eye

o Fast onset & short lasting

64
Q

NSAIDs & Analgesia

A
  • PGs sensitize pain fibers to other chemical mediators
  • NSAIDs inhibit PGs -> reduce activation of pain fibers skeletomuscular and vascular pain responds better than visceral pain
65
Q

NSAIDs & Inflammation

A
  • COX-2 induced at sites of inflammation
  • PGs increase vascular permeability & vasodilation
  • NSAIDs inhibit PGs -> decrease inflammation
66
Q

NSAIDs & Fever

A
  • stimulated neutrophils release ‘endogenous pyrogens’ (IL-1 and TNF-a)
  • endogenous pyrogens generate PGs in hypothalamus

  • PGs in hypothalamus increase temperature ‘set point’,
  • fever is induced
  • NSAIDs inhibit PGs -> decrease fever
67
Q

NSAIDs & Platelets

A
  • NSAID targets COX-1 -> inhibits platelet aggregation
  • NSAID targets COX2 -> platelets aggregate
  • TXA generated by platelets causes aggregation
  • PGI generated by endothelial cells inhibits aggregation
  • aspirin has an irreversible action
68
Q

NSAIDs & Gastric Ulcers

A
  • Most common side effect of these drugs 

  • PGI and PGE inhibit acid secretion and stimulate cytoprotective mucous secretion 

  • can cause secondary anemia due to gastric bleeding
  • not as much an issue with COX-2 selective agents
69
Q

NSAIDs & Renal Blood Flow

A
  • COX-1 maintains GFR
  • COX-2 regulates Na+ reabsorption
  • inhibition causes salt and water retention 
(reduced renal blood flow)
  • prolonged use can lead to papillary necrosis and nephritis
70
Q

NSAIDs & the Heart

A
  • concern for all COX2 selective agents 


* COX2 inhibition encourages thrombic events

71
Q

Salicylates (Aspirin); basics, signs of acute overdose

A

o used in all species, but high tendency towards gastric ulceration
o can induce hepatic damage,
o detrimental to cartilage
o has been replaced by newer and safer NSAIDs
o irreversible inhibition of cyclooxygenase = anti-platelet compound
o metabolized via glucuronidation (slow in cats!)

acute overdose
• respiratory actions via CNS
• acid/base problems

72
Q

Pyrazolone Derivatives (Phenylbutazone)

A

o very popular in equine
o used for bone, joint, & soft tissue pain
o problems associated with blood disorders
o certain pony breeds very sensitive to GI effects
o classic microsomal enzyme inducer (many drug interactions!)
o T1/2 cattle = 40 hr
o T1/2 horse = 6hr
o drug has tendency to accumulate

73
Q

Proprionic Acid Derivatives

A

o Reversible inhibition of cyclooxygenases

Carprofen
•	approved in dogs for osteoarthritis 
•	high selectivity for canine COX2 
•	high safety level in dogs 
•	thought to inhibit PLA2 
•	liver metabolism 
•	rare hepatotoxicity ( reversible if caught early)

Naproxen
• Use in horses
• Many adverse reactions in dogs

Ibuprofen
• Serious GI erosion in dogs

74
Q

Nicotinc Acid Derivatives (Flunixin meglumine)

A

o Horses IV or IM to treat visceral pain (colic)
o Cows IV for pyrexia, endotoxemia, inflammation
o Dogs in septic shock
o Causes GI upset in dogs
o Use for only short duration

75
Q

Oxicams (Meloxicam)

A
  • COX2 selective
  • in dogs osteoarthritis & post op pain
  • in cats post-operative pain – one dose only (fatal kidney damage)
76
Q

Coxibs (Robenacoxib)

A

o Highly COX2 selective

o One of few NSAIDs for cats

77
Q

Piprants (Grapiprant)

A

o PG receptor antagonist
o recently approved for use in dogs (2016) 

o Targets EP4 receptor
o Helps with pain and inflammation associated with osteoarthritis
o preserves PGE2 action at other EP receptors (e.g., GI tract) 

o so far relatively mild toxicities have been seen

78
Q

Aceteminophen (Tylenol)

A 
o	analgesic and antipyretic 
o	only weakly anti- inflammatory 
o	COX3 inhibitor 
o	not effective on platelets

o	low incidence of GI side-effects
o	hepatic damage
o	not used in veterinary medicine 
o	generation of toxic metabolite prevented by glucuronidation 
o	TOXIC to CATS
79
Q

elete

A

Delete

80
Q

Control of Release of cortisol & ACTH

A
  • ACTH released by stress & diurnal rhythm ->
  • ACTH acts on fasiculata/reticularis to release cortisol ->
  • cortisol feeds back to reduce ACTH release
81
Q

Receptors for Glucocorticoids

A
  • found on almost every cell in body
  • Mostly glucocorticoid (GC) receptors
  • Some mineralocorticoid (MC) receptors
82
Q

Metabolic Effects of Glucocorticoids

A

o Decrease insulin sensitivity
o Release protein from muscle & lymph for glucose production
o Release fat from adipocytes & redistribute to central compartment
o Increase gluconeogenesis & glycogen storage in liver

83
Q

Actions of Glucocorticoids on CNS

A

o sense of well being
o decrease sensory acuity
o other behavioral effects

84
Q

Actions of Glucocorticoids on Cardiovascular

A

o decreases vascular permeability

o Maintain catecholamine effects on vasoconstriction
o Maintain cardiac contractility
o Excess can lead to hypertension

85
Q

Actions of Glucocorticoids on Kidneys

A

o needed to concentrate or dilute urine
o excess interferes with ADH action
o excessive drinking/urination = early sign of overdose

86
Q

Actions of Glucocorticoids on GI

A

o Increases gastric acid secretion (via decrease PGs)

o inhibits Ca2+ and PO4 absorption

87
Q

Actions of Glucocorticoids on Bone

A

o decrease turnover

o increases reabsorption
via indirect decreased absorption of Ca2+ from GI tract

88
Q

Actions of Glucocorticoids on Connective Tissue

A

o excess causes decrease in collagen synthesis

89
Q

Actions of Glucocorticoids on Hematopoietic System

A

o pharmacological doses decrease proliferation of B and T lymphocytes
o high doses kill lymphocytes
o reduced size of thymus, spleen, and lymph nodes
o increased neutrophils, platelets, & rbc’s
o decreased eosinophils

90
Q

Anti-Inflammatory Actions of Glucocorticoids

A

o Decrease proliferation, differentiation, and survival of inflammatory cells (T lymphocytes and macrophages) 

o Prevent release of histamine, serotonin, and lyzosomal enzymes
o Decrease generation of arachidonic acid metabolites (prostaglandins and leukotrienes) 

o Prevent release and actions of IL-1, IL-2, TNF-a 

o Inhibit release of cell adhesion molecules reducing recruitment of inflammatory cells 


91
Q

Uses for Glucocorticoids in Musculoskeletal, skin, renal, GI, Lungs

A

Musculoskeletal

• arthritis, bursitis, tendenitis, myositis

Skin

• allergic dermatitis, otitis externa

Renal
• glomerulonephritis

GI tract

• colitis, gastroenteritis

Lungs
• asthma

92
Q

Adverse Reactions of Glucocorticoids

A 
o	PU/PD
o	Polyphagia
o	Muscle weakness
o	Osteoporosis
o	Fat mobilization
o	Pancreatitis
o	GI ulcers
o	Seizures
o	Diabetes
o	K+ loss & Na+ retention
o	Prone to infection
o	Slow wound healing
o	Corneal ulcers
o	Hypogonadism
o	Lethargy, depression, behavioral change
o	Hepatomegaly
o	Blunted HPA axis
o	GI issues
o	Laminitis
o	Drug interactions
93
Q

Strategies to Reduce Side Effects of Glucocorticoids

A

o Use minimal dose for shortest time
o Intermittent dosing
o Supplementing protein, Vit D & A, & K+

94
Q

T1/2 in Plasma & Time till Tissue Effect of Cortisol, Cortisone, Prednisone, Prednisolone, Fludrocortisone, & Dexmethasone

A

JUST REMEMBER WHICH DRUGS ACT LONGER THAN OTHER

Cortisol
• T1/2 Plasma = 90 min
• Tissue = 8-12 hr

Cortisone
• T1/2 Plasma = 30 min
• Tissue = 8-12hr

Prednisone
• T1/2 Plasma = 60 min
• Tissue = 12-36hr

Prednisolone
• T1/2 Plasma = 200 min
• Tissue = 12-36 hr

Fludrocortisone
• T1/2 Plasma = 200 min
• Tissue = 8-12hr

Dexmethasone
• T1/2 Plasma = 200 min
• Tissue = 36-54 (too long for alternate day therapy)

95
Q

Relative GC & MC (kidney) Potency of Cortisol, Cortisone, Prednisone, Prednisolone, Fludrocortisone, & Dexmethasone

A

s AREN’T IMPORTANT JUST REMEMBER WHICH DRUGS HAVE MORE GC OR MC

Cortisol
• GC & MC = 1

Cortisone
• GC & MC = 0.8

Prednisone & Prednisolone
• GC = 4
• MC = 0.8

Fludrocortisone
• GC = 10
• MC = 125

Dexmethasone
• GC = 25
• MC = 0

96
Q

Cortisol & Cortisone

A
  • Cortisol is natural GC.

* Cortisone needs to be converted to cortisol

97
Q

Prednisone & Prednisolone

A
  • Widely used GC
  • Prednisone is converted to prednisolone (active) in the liver
  • If liver disease may not convert
  • Cats have a limited ability to convert, therefore prefer prednisolone (& horses)
  • Clinician preference
98
Q

Dexmethasone

A
  • Extremely strong GC
  • very powerful to treat signs initially
  • Longer term use = more side effects
  • not useful for alternate day dosing
99
Q

Fludrocortisone

A
  • Used to treat hypoadrenocorticism in dogs and cats
  • Has both MC and GC
  • While GC is lower it is sufficient to restore GC activity
100
Q

Nutraceuticals

A

o Symptomatic Slow-Acting Drug for Osteoarthritis
o oral
o effectiveness questionable
o sold as supplements

101
Q

Hyaluronate

A

o Symptomatic Slow-Acting Drug for Osteoarthritis
o Restores synovial fluid viscocity
o Given intra-articular
o Works best when degeneration isn’t severe

102
Q

Polysulfated Glycosaminoglycans

A

o Symptomatic Slow-Acting Drug for Osteoarthritis
o Isolated from bovine cartilage
o Use in horses & dogs
o inhibits proteolytic enzymes that degrade proteoglycans
o precursor for proteoglycan synthesis
o decreases PGE2 levels
o increases hyaluronic acid concentration in synovial fluid
o actions are slow
o prolonged use can help maintain joint cartilage
o intra-articular or IM
o interfere w/ platelet aggregation

103
Q

Glucocorticoids for Osteoarthritis

A

o intra-articular injection
o long acting (3-4 weeks)

positive effects

• decreases release of lyzosomal enzymes
• inhibits PG synthesis
• relieves pain and inflammation

negative effects

• catabolic - will inhibit repair process
• decrease hyaluronate synthesis

• may obscure true degenerative process

104
Q

NSAIDs used for Osteoarthritis

A

Carprofen
o Kidney & liver issues prevalent in older animals

Gapiprant
o EP4 receptor antagonist 

o PGE2 interacts with EP1, EP2, EP3, and EP4 

o EP4 receptors mediates PGE2 effects to cause pain and swelling 

o preserves PGE2 functions at other sites
o newer agent with limited experience

105
Q

Dimethylsulfoxide

A

o Free radical scavenger
o vasodilator
o analgesic action (inhibits PGs generation)
o Topical
o Rapidly absorbed
o Labeled for reduction of acute swelling and trauma

106
Q

Timolol

A

o beta antagonist
o lower occular pressure
o decrease occular fluid
o use carefully w/ respiratory or heart dz

107
Q

Demecarium

A

o Acetylcholinesterase inhibitor.

o Improves fluid drainage

108
Q

Pilocarpine

A

o muscarinic agonist
o lowers intra ocular pressure
o improve fluid drainage

109
Q

Epinephrine

A

o mixed α−β-adrenergic receptor agonist

o decrease occular pressure & fluid formation

110
Q

Dorzolamide

A

o carbonic anhydrase inhibitor

o reduces occular fluid formation

Toxicology (6 decks)

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