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Pharmacology and Pathophysiology Own notes > Anti-inflammatory/Anti-gout drugs (week 3) > Flashcards

Anti-inflammatory/Anti-gout drugs (week 3) Flashcards

1
Q

What does NSAIDS stand for?

A

Non-sterodial anti-inflammatory drugs

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2
Q

What are NSAIDS?

A

They are a large and chemicals diverse group of drugs known to have the following affects:

  • analgesic
  • anti-inflammatory
  • antipyretic
  • platelet inhibition (ASA)
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3
Q

What is the action of NSAIDS?

A
  • inhibition of the leukotriene pathway, the prostaglandin pathway, or both
  • block the activity of the COX enzymes
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4
Q

What is the role of the COX-1?

A

COX-1 has the role of the gastrointestinal mucosa, so if this enzyme is blocked it increases G.I. side effects

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5
Q

What is the role of COX -2?

A

COX-2 promotes synthesis of prostaglandins involved in the inflammatory response

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6
Q

Why were COX-2 inhibitors developed?

A

To help decrease the risk for G.I. adverse reaction’s

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7
Q

briefly describe the arachidonic pathway.

A

Arachidonic acid is released from Phospholipid’s in cell membranes in response to a triggering event. It is metabolized by either prostaglandin pathway for the Leukotriene pathway, both of which cause inflammation, headache, edema, and other pain associated with inflammatory response.

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8
Q

Describe what happens in the prostaglandin pathway.

A
  1. arachidonic acid is converted by the enzyme cyclooxyrgenase into prostacyclin and thromboxane.
  2. prostaglandins mediate and perpetuate inflammation by inducing vasodilation and enhancing vasopermeability
  3. potentiate the action of pro inflammatory substances such as histamine and bradykinin, in the production of edema and pain
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9
Q

Why does edema and pain occur during the inflammatory process of the prostaglandin pathway?

A

edema and pain is caused by PG-induced hyperalgesia which is excessive motor sensitivity

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10
Q

What happens when PGE-2 is synthesized in the pre-optic hypothalamic region of the hypothalamus?

A

a fever results.

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11
Q

Describe what happens in the leukotriene pathway.

A
  1. arachidonic acid is metabolized by lipoxygenase and converted into leukotriene pathways
  2. mediation of inflammation, vasoconstriction, bronchospasm and permeability occur.
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12
Q

This unsaturated fatty acid is oxygenated and further transformed into a variety of products which mediate or modulate inflammatory reactions

A

Arachidonic acid

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13
Q

What does prostacyclin do?

A

prostacyclin inhibits platelet activation and is also an effective vasodilator

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14
Q

What does thromboxane do?

A

thromboxane induces platelet aggregation and arterial constriction

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15
Q

what is another term for aspirin?

A

acetylsalicylic acid (ASA)

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16
Q

What does aspirin do in the body?

A

reverses the inhibitor of COX-1 receptors within the platelets themselves.

-Reduced formation of thromboxane A2,

17
Q

What does thromboxane do in the body?

A

a substance that promotes platelet aggregation (also known as antiplatelet activity)

18
Q

What are some conditions that place the patient at risk for bleeding when taking NSAIDS?

A
  • rhinitis
  • vitamin k deficiency
  • peptic ulcer disease
19
Q

what is rhinitis (think autumn has it)

A

is irritation and inflammation of the mucous membrane inside the nose

20
Q

When NSAIDs are mixed with alcohol what can result?

A

GI bleeding

21
Q

What results when aspirin interacts with other NSAIDS?

A

Increased G.I. toxicity with no therapeutic advantage

22
Q

What would you monitor, as a nurse, in a patient who is taking NSAIDs?

A

decrease swelling, pain, stiffness, tenderness of a joint or muscle

23
Q

list properties that all NSAIDS share.

A

antipyretic
analgesic
anti-inflammatory

24
Q

What can NSAIDS treat?

A

gout and hyperuricemia

25
Q

What is hyperuricemia?

A

the overproduction or under secretion of uric acid.

26
Q

myalgia

A

muscle paoin

27
Q

neuralgia

A

sever pain due to nerve damage

28
Q

arthralgia

A

pain in a joint

29
Q

What are conditions that place the patient at risk for bleeding

A

rhinitis
vitamin k deficiency
peptic ulcer disease

30
Q

what are some adverse effects of NSAIDS?

A 
dyspepsia 
heartburn
GI bleeding
musical lesions
abdominal pain
31
Q

What are some symptoms of salicylate intoxication?

A

increased heart rate
tinnitus
naseau, vomiting, diarrhea
sweating, thirst, hyperventilation

Pharmacology and Pathophysiology Own notes (9 decks)

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