NSAIDS Flashcards

1
Q

3 effects of NSAIDS

A
  1. Antipyretic
  2. Anti-inflammatory
  3. Analgesic
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2
Q

Antipyretic effect

A

Fever-reducing

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3
Q

Analgesic effect

A

Painkiller / Pain reducing

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4
Q

Mechanism of action of NSAIDs

A

They block the formation of prostaglandins from arachidonic acid
(suppress the synthesis on cyclooxygenase level)
1. Impact other inflammation mediators
2. Depress neutrophil functions
3. Suppress immune response of organism

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5
Q

Functions of prostaglandins

A
  1. Regulation of function of
    reproductive organs
  2. Participation in blood coagulation
    process
  3. Inflammation mediators
  4. Occurrence of smooth muscle
    contractions
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6
Q

In particular what do prostaglandins do in regulation of the function of reproductive organs?

A

Contractions of uterus
Motility of ovarian tubes
Process of fertilisation

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7
Q

What is the role of prostaglandins in blood coagulation process

A

The formation of blood clots

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8
Q

What is PGE2

A

Prostaglandin E2
-Endogenous pyrogen leading to upward
resetting of temperature regulating
center in the hypothalamus
- Does not directly stimulate nociceptors,
but increases intensity and duration of
afferent discharge caused by histamine
and bradykinin

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9
Q

Allodynia

A

Allodynia is a condition in which pain is caused by a stimulus that does not normally elicit pain

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10
Q

Nociceptor

A

Sensory neuron that responds to damaging or potentially damaging stimuli by sending “possible threat” signals to the spinal cord and the brain

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11
Q

Arachidonic acid

A

Released in tissue damage following activation of phospholipase A2
-Serves as a substrate for prostaglandin synthase

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12
Q

Name 4 mediators of inflammation and pain

A
  1. Histamine
  2. Serotonin
  3. Bradykinin, leukotrienes
  4. Prostaglandins
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13
Q

Characteristics of histamine in inflammation and pain

A

Dilation of capillaries
Increase in permeability

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14
Q

Characteristics of serotonin in inflammation and pain

A

Increase in permeability of capillaries

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15
Q

Characteristics of Bradykinin, leukotrienes in inflammation and pain

A

Increases the permeability of small veins
Induces swelling and pain

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16
Q

Characteristics of prostaglandins in inflammation and pain

A

Dilation of blood vessels
Increase in permeability
Bronchoconstriction

17
Q

Functions of COX1

A

Mediates prostaglandin synthesis
Involved in maintaining tissue homeostasis,
Blood clotting,
Regulation of vascular homeostasis
Coordination of the actions of circulating hormones “housekeeper”

18
Q

COX2 functions

A
  1. Mediates synthesis of prostaglandins inducing inflammation
  2. Produces both pro- and anti-inflammatory PGs at the sites of inflammation
19
Q

COX2 inhibitors

A
  1. Firocoxib - eq + ca
  2. Robenacoxib - fe + ca
  3. Mavacoxib - ca
20
Q

General pharmacokinetics of NSAIDS

A
  1. Weak organic acids
  2. Absorb well per os
  3. Lipid-soluble, bind to serum albumins (free fraction is small)
  4. Metabolism occurs mainly in liver
    -> glucuronyl transferase essential
  5. Eliminated at slower rate from inflamed
    tissue
  6. Eliminated via kidneys
21
Q

Why are NSAIDS toxic to cats?

A

Because they lack the enzyme glucuronyl transferase which is essential for glucuronide conjugation

22
Q

Pharmacodynamics of NSAIDS

A
  1. Reduction of fever, inflammation and
    pain
  2. With inflammation; reduce
    exudation, swelling and phagocytosis
  3. Strength of effect depends on
    preparation and dose
  4. Suppress also coagulation of blood
    (esps aspirin) - antithrombotic effect
  5. Analgesic effect is best in case of
    somatic pains of endogenous origin
23
Q

Pathogenesis of fever

A

Endogenous pyrogens are released from leukocytes, acting specifically on the hypothalamic thermo-regulatory centre and raise the body temperature

24
Q

Where is the COX2 enzyme present?

A

In brain, kidney, ovary, uterus, ciliary body

25
Q

Side effects of complete long duration inhibition of COX2

A

Abortion
Fetal abnormalities
Delayed bone and soft tissue healing
Renotoxicity
Cardiovascular effects

26
Q

Toxicity and side effects of NSAIDS

A

Vomiting, diarrhea
Depression of CNS,
Ulcers in stomach & duodenum
-Cats: no glucuronyl transferase; duration
of action is long - risk of side effects is
very high

27
Q

Why can NSAIDS cause ulcers and bleeding in GI tract?

A

NSAIDs prevent the formation of COX1-mediated PGI2 and PGE2 in the epithelial layer of gastric mucous membrane
- necessary for the creation of new
epithelial cells of the mucous membrane
and for the production of mucus.
Therefore, the enzymes and gastric acid in the stomach make the protective mucous epithelium thinner and cause ulcers, which are also facilitated by the acidic pH of the drugs

28
Q

Mechanism of function of inhibition of blood coagulation in NSAIDS

A

NSAIDs inhibit the synthesis of prostaglandins - which are required for platelet aggregation.
Prostaglandin (thromboxane) synthesis is mediated by COX1

29
Q

Which NSAID is the most specific COX1

A

Aspirin. The acetyl group inhibits the cyco-oxygenase in platelets irreversibly - which may last for up to 1 week after administration

30
Q

What causes the renotoxicity of NSAIDS

A

PGs regulate glomerular filtration, renin release and tubular sodium reabsorption
- COX1 inhibitors can cause sodium
retention > edema, reduced glomerular
filtration and systemic hypertension
- Do not occur generally

31
Q

Hepatic toxicity of NSAIDS

A

Generally rare in animals
-Carprofen reported in dogs
-Paracetamol in dogs and cats: can cause
methemoglobinemia, hepatic necrosis
and stomach ulcers

32
Q

Other reactions to NSAIDS

A
  1. Allergy - mainly skin reactions
  2. Effects in reproductive system
    (abnormal cycle etc - inhibition of
    prostaglandins)
  3. CNS effects? PG-s modulate nerve
    transmission
33
Q

When can NSAIDS be used

A
  1. To relieve pain
    • Pre- and postoperative administration
    • Treatment of trauma
    • Musculoskeletal conditions
    • Colic in horses
    • Cancer
  2. To reduce body temperature
  3. Antihemostatic actions of aspirin
  4. Mastitis, metritis, endotoxemia
  5. Any inflammatory reaction +
    respiratory disease, infections and
    together with antibiotics