Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Basic Pharmacology > Non-Steroidal Anti-Inflammatory Drugs > Flashcards

Non-Steroidal Anti-Inflammatory Drugs Flashcards

1
Q

non-steroidal anti-inflammatory drugs work primarily by inhibiting ______________________________________________

A

cyclooxygenase enzymes and reducing production of prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the effects of non-steroidal anti-inflammatory drugs?

A

antipyretic
anti-inflammatory
analgesic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the unifying mechanism of action of non-steroidal anti-inflammatories?

A

inhibit cyclooxygenases (COX) and decrease prostanoid (prostaglandin) concentrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the functions of COX and PGs in the kidneys?

A

PGs influence renal hemodynamics, body water and salt balance, and inflammatory processes
COX-1 and COX-2 contribute to normal function
both play a role in maintaining normal blood flow during low blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does cyclooxygenase-1 generally lead to?

A

production of prostaglandins that mediate homeostatic functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what do thromboxanes stimulate?

A

vasoconstriction and platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what do prostaglandins involved in the inflammatory response do?

A

vasodilation
pain
swelling
impaired cellular function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what cells produce PGE2?

A

inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what does PGE2 do?

A

dilates vascular smooth muscle
pyretic agent
sensitizes nociceptors
spinal cord transmission of pain signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

are prostaglandins involved in pain transmission?

A

yes- central transmission of pain
upregulate pain pathways- primarily mechanical pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what needs to happen for an NSAID to have a central effect?

A

NSAID must get into the CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

peripheral inflammation sensitizes the animal to __________________________

A

mechanical and other pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what helps mitigate central sensitization?

A

pre-emptive inhibition of peripheral inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what happens after bacterial products enter the systemic circulation (endotoxins)?

A

immunosuppression
vasodilation, increased vascular permeability, decreased perfusion
systemic effects (fever, decreased inotropy, metabolic abnormalities)
microvascular thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does septic shock ultimately lead to?

A

multi-organ failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

do non-steroidal anti-inflammatory drugs have additional effects above COX inhibition?

A

some may have: differences in response and profile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what do the primary clinical benefits and adverse effects of non-steroidal anti-inflammatory drugs result from?

A

reducing prostanoid production and thus their effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what drug is approved for dogs that you should not use due to toxicity?

A

phenylbutazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what drugs are approved in dogs in the COX-2 selective group?

A

deracoxib
firocoxib
meloxicam
robenacoxib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

are non-steroidal anti-inflammatory drugs protein-bound?

A

yes- highly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how are non-steroidal anti-inflammatory drugs metabolized?

A

cytochrome P450 and glucuronosyltransferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what should you keep in mind with non-steroidal anti-inflammatory drugs in cats?

A

lack certain UDP-GT enzymes
prolonged half life for aspirin
do not use acetominophen

23
Q

where do NSAIDs tend to stay?

A

in inflammatory exudate: anti-inflammatory effects may be longer than suggested by their half life

24
Q

when are NSAIDs most effective?

A

trauma
chemical
“infectious” inflammation

25
Q

what provides the pain relief associated with NSAIDs?

A

combination of anti-inflammatory effects and central analgesic effects

26
Q

are COX-2 selective NSAIDs more effective than non-selective NSAIDs as anti-inflammatory analgesics?

A

no, not as a class

27
Q

why do we use NSAIDs for their antipyretic effect?

A

reduce fever that is dangerously high (small animal primarily)
improve attitude and appetite (bovine and equine mostly)

28
Q

do some NSAIDs improve clinical parameters in patients with septic shock?

A

yes
may not be worth risk due to poor perfusion

29
Q

what drug is used to treat septic shock in cows and horses?

A

flunixin

30
Q

in which cancer are NSAIDs most commonly used?

A

transitional cell carcinoma in dogs

31
Q

what are the pharmacological toxicities of NSAIDs?

A

gastroenteropathies
renal toxicity
anti-platelet effects
reproductive effects (delay parturition)
delayed soft tissue healing (and bone healing if long-term)

32
Q

what is a host-dependent adverse effect we see with carprofen?

A

hepatitis

33
Q

current evidence suggests that inhibition of ___________________ required for ulceration

A

both COX1 and COX2

34
Q

what does COX-2 selectivity do with gastroduodenal irritation, ulceration, and gastric acid disturbances?

A

decreases it
not with small intestine ulcers

35
Q

which species is more susceptible to small intestine ulcers?

A

canines: enterohepatic recirculation likely role

36
Q

inhibition of ________ is most important in inflammation and associated pain

A

COX-2

37
Q

what can happen in the colon with NSAIDs?

A

colitis
especially right dorsal colitis in horses

38
Q

do corticosteroids interact with NSAIDs?

A

yes: marked increase in risk of adverse effects

39
Q

what are the risk factors of renal toxicity with NSAIDs?

A

high dose, prolonged duration
patients with prostaglandin-dependent glomerular blood flow: ischemic damage and decreased function
issues: surgery, compromised renal function
small animal probably more likely than equine

40
Q

in what does cyclooxygenase-1 play an important role in homeostatic functions?

A

gastric mucosa
kidneys
platelets
vascular endothelium

41
Q

what are the homeostatic functions of prostanoids?

A

inhibit acid secretion, stimulate mucous production, and enhance cell replication in GI tract
vasoconstriction or vasodilation
bronchoconstriction
stimulate smooth muscle contractions
lutolysis
aggregation (TXA2) or diaggregation of platelets
decrease intraocular pressure

42
Q

what cells produce prostacyclin (PGI2)?

A

endothelial cells and vascular smooth muscle cells

43
Q

what is pain caused by?

A

prostaglandins
nerve growth factor
leukotrienes
bradykinin
histamine
5-HT, substance P

44
Q

are most of the NSAIDs in small animal COX-2 selective?

A

yes
phenylbutazone is not- toxic

45
Q

how long are the half-lives of most NSAIDs?

A

relatively short

46
Q

what are the anti-inflammatory indications?

A

most effective in trauma, chemical, or infectious inflammation
limited in immune-mediated
osteoarthritis/musculoskeletal disease: inflammatory and mechanical pain
laminitis
uveitis/other inflammatory eye disease
pneumonia
coliform mastitis
post-operative inflammation

47
Q

are NSAIDs such as flunixin an effective analgesic in horses with colic?

A

yes

48
Q

who is flunixin used to treat septic shock in?

A

cows
horses

49
Q

what are some intrinsic toxicities with NSAIDs?

A

acid-base imbalance
direct gastrointestinal irritation
maybe hepatopathies and renal toxicity

50
Q

what are some preventative options for ulceration?

A

omeprazole
misoprostol
sucralfate

51
Q

do COX-2 selective agents display a decreased risk of renal toxicity?

A

no

52
Q

in whom do blood dyscrasias occur?

A

people: concern over food residues of phenylbutazone, dipyrone

53
Q

with what drug do we see idiosyncratic hepatitis?

A

carprofen
probably robenacoxib

54
Q

what are some drug interactions of NSAIDs?

A

corticosteroids
do not combine NSAIDs
furosemide
aminoglycosides

Basic Pharmacology (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions