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Foundations 6 > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

Autacoids

A

Paracrine/autocrine hormones released in response to injury

Serotonin, histamine, kinins, lipid derivatives

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2
Q

Eicosanoids

A

20Carbon chains with short 1/2 lives - means it will act locally

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3
Q

Prostaglandin identification

A

Stimulated uterine contractions and lowered BP

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4
Q

PG made from, what do they bind, half lives, and what they do

A 
From AA
Bind surfac receptors 
Short T1/2 
Short duration of response need continuous synthesis
Local responses in tissues
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5
Q

Phospholipase A2

A

Rate limiting enzyme in PG production…liberates AA from the membrane

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6
Q

COX enzyme catalyzes formation of

A

Prostaglandins, prostacyclins, thromboxanes

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7
Q

Phospholipase C

A

Liberates IP3

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8
Q

COX reaction

A

Forms unstable intermediate from AA…then final product formed depending on the cell type

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9
Q

AA linear pathway

A

Creates Leukotrienes…not target for NSAIDs

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10
Q

What is NSAID disadvantage?

A

Bluntly inhibits synthesis of all prostaglandins…there are wide variety of effects

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11
Q

Prostaglandins mediate action of

A 
Inflammation
Smooth muscle
Thrombosis
Parturition
GI secretions 
Renal phys
Development
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12
Q

Glucocorticoids

A

Adrenal steroids with anti-inflam effects

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13
Q

Glucocorticoid systemic side effects

A

Immunosuppression

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14
Q

Steroid hormones come from

A

Cholesterol

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15
Q

Glucocorticoid action

A

Inhibits synthesis of COX at gene expression level
Upregulates Lipocortin Annexin 1 that inhibits phospholipase A2

Block RL step

This is longer lasting but longer onset to work

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16
Q

NSAID effects

A 
Antiinflam
Antipyretic (fever)
Analgesic (pain)
Platelet effects
Gastric
Renal
Cardiovascular
Gout
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17
Q

NSAID action

A

Competitive inhibitors of COX 1 and 2

Quicker acting than glucocorticoids

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18
Q

Aspirin is a

A

Salicylate

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19
Q

Salicylate (aspirin) uses

A

Prophylactic for thromboembolic (clotting) dz (cardiac and cerebral)

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20
Q

Pregancy and aspirin

A

Decrease birth weight and increase in mortality, anemia, and hemorrhage

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21
Q

Aspirin uses

A 
Analgesia
Antiinflam
Antipyretic
INhibit platelet aggregation
Prevent colorectal cancer
22
Q

Aspirin contraindiciation

A

Peptic ulcers
Pregnancy
Childrne with viral infections
Reye’s syndrome

23
Q

Aspirin mechanism

A

Irreversible inhibitor of COX…metabolite of salicylate is also an NSAID…acetal group covalently bound to serine hydroxyl group of COX

24
Q

Very low doses of aspirin

A

1mg/Kg…baby aspirin

Antiplatelet

25
Q

Low doses of aspirin

A

10mg/ky

Analgesic and antipyretic

26
Q

High doses of aspirin

A

100mg/kg
Antiinflam

Need high does because aspirin doesn’t work as well in acidic environment of macrophages

27
Q

Side effects of aspirin

A

Tinnitus
Deafness
Vertigo

28
Q

NSAIDs and gastric functions

A

AA normally produces PGI2 and PGF2 that works on parietal and epithelial cells…it decreases the proton pump and therefore increase secretion of mucouse…if this is inhibited, mucous decreases and pH decreases so more likely to cause ulcer

29
Q

Acetominophen is a

A

Analgesic and antipyretic but NOT antiinflammatory

30
Q

When is acetominophen used as aspirin alt

A

Peptic ulcer
Allergies
Viral infection
Hemophiliacs

31
Q

Contraindication of acetominophen

A

Post op

32
Q

Acetominophen main side effect

A

Fatal hepatic necrosis (liver death)…found in lots of other meds

33
Q

Acetominophen no effect on

A

Clotting and Gout

34
Q

Acetominophen liver toxicity with alcohol

A

Glutathione acetyltransferase typically neutralizes…in presence of alcohol CYP2E1 is increased and glutathione is lowered

35
Q

Tx of acetominophen OD

A

Activated charcoal to decrease abs in first 4 hours
N acetyl cysteine (PO or IV)
Supportive ABCD tx

If this doesn’t work, then liver transplant

36
Q

NAC

A

Precursor to glutathione

37
Q

COX 1 vs COX 2

A

COX 1 is constituitively active
COX 2 is inducible

COX1 - stomach, intestine, kidney, platelet
COX2 - macros and synoviocytes

38
Q

Glucocorticoids on COX

A

Block both

NSAIDS can be tailored

39
Q

Selectivity for 1 vs 2

A

Indomethacin and aspirin - COX 1
Naproxen and Ibuprofen - Both
Meloxicam, diclofenac, and celecoxib - COX2 more than 1

40
Q

Celecoxib is different because

A

Better for people at high risk for heart dz…5X more cost thoguh

41
Q

Prostaglandins in development

A

PGE2 helps patent ductus arteriosis/foramen ovale…NSAIDs can avoid need for surgery

42
Q

COX 1 knockouts

A

No ulcers, no renal dysfunction, majority died

43
Q

COX 2 knockouts

A

No inflam disruption
Females anovulatory
Serious renal deficiencies

44
Q

NSAIDS and cancer

A

Tumors express high levels of COX 2…both aspirin and COX 2 inhibitors have reduced size and number of colorectal polyps in animal models

45
Q

Piroxicam

A

Suppressed growth of human cancer cells

46
Q

Sulindac

A

Decreased incidence in animal models

47
Q

Cardiovascular risk of NSAIDS

A

Can increase risk of cardiovascular events
RIsk may increase with use
Possibly increase risk of CV dz
Contraindicated for coronary artery bypass grafts periop pain

48
Q

NSAID GI risk

A

Bleeding, etc.

May occur anytime, espcially in elderly patients

49
Q

NSAIDS with all 3 activities

A

Celecoxib, diclofenac, ibuprofen, indomethacin, meloxicam, naproxen

50
Q

NSAIDS with just analgesic and antipyretic

A

Acetominophen

Foundations 6 (17 decks)

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