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Pharmacology II > LEC 6 - Nonopioid Analgesics > Flashcards

LEC 6 - Nonopioid Analgesics Flashcards

1
Q

What are the four signs of inflammation?

A

Erythema + Edema + Tenderness + Pain

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2
Q

What are the three phases of inflammation?

A

Acute inflammation

Immune response

Chronic inflammation

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3
Q

What are the five mediators of acute inflammation?

A

Histamine

Serotonin

Bradykinin

Prostaglandin

Leukotrine

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4
Q

What are the four effects of the acute inflammatory mediators?

A

Vasodilation

Vascular permeability

Chemotaxis

Pain

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5
Q

Effects: Histamine

A

Vasodilation ++

Vascular Permeability +++

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6
Q

Effects: Serotonin

A

Vasodilation +/-

Vascular permeability +

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7
Q

Effects: Bradykinin

A

Vasodilation +++

Vascular permeability +

Pain +++

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8
Q

Effects Prostaglandin

A

Vasodilation +++

Vascular Permeabiltiy +

Chemotaxis +++

Pain +

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9
Q

Effects: Leukotrines

A

Vascular permeability +++

Chemotaxis +++

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10
Q

What is the precursor to LT’s + PG’s?

A

Arachodonic Acid

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11
Q

What makes LTs?

A

Lipoxygenases

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12
Q

What makes prostaglandins?

A

COX 1/2

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13
Q

What is the structure of prostaglandins?

A

Oxygenation products of polyunsaturated long chain FA’s

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14
Q

How does arachodonic acid leave the membrane?

A

Via phospholipase A2

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15
Q

Characteristic: COX-1

A

Constitutively expressed

Housekeeping functions

Widely distributed

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16
Q

Characteristics: COX-2

A

Inducible

Depends on stimulus

Immediate early response gene

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17
Q

What are the main functions of the products made by COX-2?

A

Stimulate growth factors

Tumor promoters

Cytokines

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18
Q

What is COX-2 mainly responsible for?

A

Prostacylcin in endothelial cells

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19
Q

Describe the mechanism by which Asprin Asthma occurs?

A

NSAID blocks COX enxymes = decrease in PG’s

Increase A. Acid that gets shuttled to Lipoxygenase path

Increased production of Leukotrines

= Increase broncoconstirction + congestion + mucous plugging

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20
Q

Mechanism: Asprin/ASA/Acetylsalicyclic acid

A

Nonselective, irreversible inhibitor of COX-1/2

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21
Q

Asprin - Effects

A

Analgesic

Antipyretic

Anti-inflammatory

Platelet

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22
Q

Describe: Asprin’s analgesic effects

A

Low intensity pain

Pain from integumental structures

Due to peripherial + CNS effects

Prevents sensitization of pain receptros to stimuli

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23
Q

How does asprin act locally?

A

Hypothalmic area to reduce fevers

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24
Q

When does asprin not work?

A

As an analgesic in non-inflammed painful conditions

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25
Q

When is aspirin successful at lowering temperature?

A

Febrile patients

Fever due to inflammation + infection + tissue damage

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26
Q

By what mechanism does aspirin reduce fever?

A

Resetting the thermostat to normal body temp

Therefore problem needs to be within the hypothalamus

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27
Q

Aspirin - Distribution

A

Throughout body tissues + ETC compartments

Crosses placenta

Slowly crosses BBB

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28
Q

Aspirin - Metabolism

A

Hydrolyzed = Plasma + Liver + Erythrocytes

Salicylic acid - Glucuronidated in liver

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29
Q

Aspirin - Elimination

A

Kidney

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30
Q

Aspirin - Half lives

Dog

Cat

Horse

A

8 hours - dog

38 hours - cat

30 min - horse

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31
Q

Aspirin - Protein Binding

A

Plasma protein - 50 ot 90%

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32
Q

Aspirin - Adverse Effects

A

GI upset

Paradoxical hyperpyrexia

Dehydration

Pulmonary edema in sheep

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33
Q

What happens in canines with chronic asprin use?

A

Canine chondrocytes are sensitive to COX-1 inhibition

Aggrevation of canine joint disease

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34
Q

How long before surgery must asprin be discontinuesd?

A

7 days

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35
Q

How does aspirin cause hyperpyrexia?

A

uncoupling of oxidative phosphorylation

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36
Q

How does asprin cause acid-base disturbances?

A

1- Alkalosis via stimulation of medullary respiratory center = hyperventilation

2 - Acidosis due to CNS depression

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37
Q

How does aspirin cause pulmonary edema in sheep?

A

Imbalance of vasodilatory PG’s + Vasocontrictive PG’s

Increased vascular permeability

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38
Q

Aspirin - Administration

A

Oral

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39
Q

Aspirin - Uses

A

Adjunct therapy for septic + endotoxic shock

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40
Q

Aspirin - Contraindicated treatment

A

OA

Colic

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41
Q

Aspirin - Drug interactions

A

Due to salicylate-mediated displacement of other drugs that compete for same albulmin binding site

Warfarin

Throxin T3

Penicillin

Thiopental

Bilirubin

Phenytonin

Naproxen

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42
Q

How do you treat aspirin toxicity?

A

Induce vomiting

Increase removal of drug - gastric lavage + activated charcoal

Increase urinary excretion - alkalinizing agent

IV fluids

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43
Q

NSAID’s pharmodynamics (effects)

A

Anti-inflammatory

Analgesic

Antipyretic

Platelet effects

44
Q

Describe the effects NSAID’s have on platelets

A

Irreversible inhibition of platelet COX enzymes

Cannot synthesize new ones

45
Q

How long do platelet effects from NSAID’s last?

A

8 to 10 days

46
Q

Describe NSAID Toxicity

A

GI - pain + bleeding + pancreatitis

CNS - confusion + depression + dizzy

Lung - bronchoconstriction

Bone marrow - argranulocytosis + aplastic anemia

Nephrotoxicity - renal failure + intersitial nephritis + nephrotic syndrome

Heptaotoxicity

Hypersensitivity

47
Q

Phenylbutazone - Mechanism of Action

A

Preferential COX-2 inhibitor

Horses + Dogs

48
Q

Phenylbutazone - Admin

49
Q

Phenylbutazone - use

A

Lameness + OA

Soft tissue pain

Nonarticular rheumatism

50
Q

Phenylbutazone - Duration of action

A

24 to 72 hours

51
Q

Why is phenylbutazone so long action?

A

Irreversible binding

52
Q

Phenylbutazone - Protein binding

A

99%

High plasma protein bdingin

53
Q

Phenylbutazone - Metabolism

A

Almost complete in Horse

54
Q

Phenylbutazone - Elimination

A

25% via renal over 24 hours

55
Q

What effect does phenylbutazone have on microsomal enzymes?

A

Induces the production of = lower plasma levels of drug with chronic administation

also leads to drug interactions

56
Q

Phenylbutazone - Adverse effects

A

Renal papillary necrosis

Petechial hemorrhages

Ulcers

Hypoproteinemia

57
Q

Phenylbutazone - Food animals

A

not to be given to dairy cattel > 20m of age

NO USE IN FOOD ANIMALS

58
Q

Phenylbutazone - Cause of Death

A

Protein losing enteropathy

= Decrease in blood volume + hemoconcentration + hypovolemic shock + circulatory collapse

59
Q

Phenylbutazone - Contraindications

A

Not to be given to patients with:

Cardiac/renal/hepatic disease

Hematocytologic disorder

60
Q

Flunixin meglumine - Indicated treatment

A

Acute + VISCERAL + Surgical pain

61
Q

Flunixin meglumine - Mechanism of action

A

COX-2 > COX-1 in horse

COX - 1 > COX-2 in dogs

62
Q

Flunixin meglumine - Contraindications

A

EGGUS - horses

63
Q

Flunixin meglumine - ADMIN

64
Q

Flunixin meglumine - Withdrawl times

A

4 days pre-slaughter

36 hours milk

65
Q

Flunixin meglumine - Adverse effects

A

Hypersensitivity in cattle

66
Q

Flunixin meglumine - BA

A

80% with PO admin

67
Q

Flunixin meglumine - Plasma protein binding

Cows

Dogs

Horses

A

Cows - 99%

Dogs - 92%

Horses - 87%

68
Q

Flunixin meglumine - 1/2 life

Horse

Cattle

Dog

Cats

A

Horse - 2 to 4 hours

Cattle - 3 to 8 hours

Dogs - 4 hours

Cats - 1 to 1.5 hours

69
Q

Flunixin meglumine - Excretion

70
Q

Naproxen - Use

A

Horses with soft tissue pain

Inflammatory swelling with lameness

71
Q

Naproxen - 1/2 life

A

4 hours = horses

72
Q

Naproxen - Time to see effect

A

5 to 7 days

73
Q

Naproxen - metabolism

A

Glucoronidation - liver

74
Q

Naproxen - Excretion

A

Urine

> 48 hours

75
Q

Naproxen - Mechanism

A

Non-selective COX inhibitor

76
Q

Ketoprofen - Mechanism

A

Non-selective inhibitor of COX

Blocks LTB4 synthessis

77
Q

Ketoprofen - Target

A

Sequestered at site of inflammation

(inflamed synovial joint)

78
Q

Ketoprofen - Admin

A

IV + IM + SC + PO

79
Q

Ketoprofen - BA

Horses

Dogs/Cats

A

Horses = ~ 1 hour

Dogs/Cats = 1.5 hours

80
Q

Ketoprofen - Eliminated

81
Q

Ketoprofen - Adverse effects

A

Safer then phenylbutazone + flunixin

82
Q

Ketoprofen - use

A

Horses

alleviation of inflammation + pain for acute/chronic musculoskeletal disorders

83
Q

Ketoprofen - Food animals

A

NOT ALLOWED

84
Q

Carprofen - Mechanism

A

Preferential COX-2 inhibitor

85
Q

Carprofen - Admin

A

PO + IV + CS

86
Q

Carprofen - Use

A

Analgesic + Anti-inflammatory in dogs

87
Q

Carprofen - 1/2 life

A

5 to 9 hours

88
Q

Carprofen - BA

A

90% with PO dose

89
Q

Carprofen - Protein binding

A

Bound to albulmin 99%

90
Q

Carprofen - Metabolism

A

Liver via

Oxidation then glucoronidation

91
Q

Carprofen - Elimination

A

Feces (70 to 80%)

Urine

92
Q

Carprofen - Adverse effects

A

Lower GI problems due to COX-2 target

93
Q

Carprofen - Contraindication in Cats

A

Increased risk of renal disease

94
Q

What are the COX-2 inhibitors?

A

Deracoxib

Robencoxib

Firocoxib

95
Q

Deracoxib - Indications

A

Pain + Inflammation in OA = Dogs

96
Q

Robenacoxib - Indications

A

Musculoskeletal disorders + soft-tissue surgeries in cats

97
Q

Firocoxib - Indications

A

Pain + Inflammation - OA

Postoperative pain

98
Q

Firocoxib - Admin

A

Oral paste - Horses

Tablets - Dogs

99
Q

Meloxicam - Mechanism

A

preferential COX-2 inhibitor

100
Q

Meloxicam - use

A

Chronic pain + inflammation with OA = dogs/cats

101
Q

Meloxicam - Absorption

A

Well absorbed

Food does not altered

102
Q

Meloxicam - Protein binding

A

97% boudn to albulmin

103
Q

Meloxicam - Metabolism

A

Liver - glucuronide conjugates

104
Q

Meloxicam - 1/2 life

Dogs

Cats

A

Dogs = 12 to 24 hours

Cats = 15 hours

105
Q

Meloxicam - Elimination

A

Feces via enteroheptatic recirculation

106
Q

Meloxicam - Adverse effects in cats

A

Repeated use = AKI + Death

107
Q

Acetaminophen - Cats contraindication

A

Deficiency in glucuronyl transferase

Makes them susceptible to metHg + centrilobular hepatic necrosis

Pharmacology II (20 decks)

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