NSAIDS Flashcards

1
Q

What are indications for NSAIDS?

A

Mild chronic pain: osteoarthritis, neoplasia, otitis

Anesthesia/surgery: acute peri-surgical pain in combo with opioids

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

What patients can you use NSAIDS in?

A

Well hydrated, normotensive, young-middle ages

Normal renal function

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

Which has a longer action, NSAIDS or opioids?

A

NSAIDS

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

T/F: Opioids have higher efficacy in inflmmatory conditions like dermatitis, polyarthtis, mastitis, or otitis than NSAIDS

A

False

NSAIDS greater for inflammation

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

What are the administration routes of NSAIDS?

A

Common: SQ and IM

Less: IV , oral, topical, suppositories

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

What is the MOA of NSAIDS

A

Inhibit COX (1 or 2)

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

NSAIDS have their anti-inflammatory effects by inhibiton of what mediators ?

A

Prostacyclin and prostaglandin

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

How do NSAIDS have an anti-pyretic effect?

A

Inhibit endotoxin or endogenous pyrogens (eg interleukin 1)

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

What is a water soluble tablet NASID registered for osteoarthritis in dogs?

A

Tepoxalin

Inhibits COX and lipooxygenase

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

Where do steroids exhibit their anti-inflammatory effects?

A

Inhibit phospholipase to prevent formation of arachadonic acid from cell membrane phospholipids

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

Where is COX1 found? And what are its functions ?

A

Constitutively expressed

Liver
Kidney
Platelet
Gastric mucosa

—> mucosal blood flow, mucous production, gastric se creations acidity, gastric epithelium cell turnover

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

Where is COX2 found and what are its actions?

A

Indictable in damaged or inflamed tissue —> monocytes, macrophages, or neutrophils

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

Why do we want high selectivity of COX2 inhibition

A

COX1 is good—> gastric mucosa

COX2 is bad—> inflammatory
Less adverse effects if you selectively inhibit COX2

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

What are the adverse effects on NSAIDS ?

A

GI- vomiting diarrhea and ulceration

Platelet aggregation —> impaired thromboxane

CV: prothrombotic state

Renal: block renal vasodilator COX2 induced PG —> not to be used in renal insufficiency

Liver: impaired hepatic blood flow

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

What can you give prophylactically to reduce GI ulcers caused by NSAIDS?

A

Sucralfate : salt binds mucosal defects

Misoprostal: synthetic PG analog

Ranitidine: H2antagonist block gastric secretions

Omeprazole: PPI blocking gastric secretions

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

What are contraindications for NSAIDS?

A

GIT disorder: GI ulcer/vomiting/diarrhea
Concurrent with steroids

Dehydration
Hypotension
Low circulating volume : CHF/acities/diuretics
Severe pulmonary dz

Shock or trauma
Acute renal insufficiency
Hepatic insufficiency

Thrombocytopenia
Pediatric/geriatric

17
Q

Should you give NSAIDS during pregnancy ?

A

No

COX2 expressed at ovulation, implantation, and Labour—> nessesary for nephrogenesis

Avoid during AI
Single use after C-section

18
Q

How many weeks after birth must you wait after birth before you can give NSAIDS to pediatric patients?

A

4weeks

Nephrogenesis is not compete until 3weeks after birth

19
Q

COX2 is essential for fracture healing, can NSAIDs be given to treat these animals?

A

Only at low dose for short period of time

20
Q

Why are cats predisposed to NSAID toxicity?

A

Deficient in glucuronidases —> slow clearance and longer halflife

21
Q

What are signs of NSAID toxicity in cats?

A

Fever, methemoglobinemia, hemorrhagic gastritis, kidney, and liver injury

Acetaminophen : methemoglobinemia and Heniz body anemia

22
Q

What precautionary measures can be taken to reduce the adverse effects of NSAIDS?

A

Food and water provision
CV load maintained
BP control inc ritical cases

Washout period 4-10days

23
Q

What selective COX2 inhibitor is approved for used in dogs and cats for up to 3days?

A

Robenacoxib (onsior)

Oral or SC

24
Q

What are the selective COX2 inhibitors?

A

Robenacoxib
Firocoxib
Deracoxib

25
Carprofen is a preferential COX2 inhibitor, what species can it be used in? How can it be administered?
Approved in dogs Off label - horse and ruminant SC, IV, oral
26
What species is meloxicam approved in and what are its admin routes?
Cat and dog SC and oral —few side effects, mostly GI
27
Is phenylbutazone, a selective or non-selective COX inhibitor? What species is it used in?
Non-selective Cattle and horse -prolonged halflife in cattle (causes residues, not used in cattle over 20months)
28
What are the adverse effects of phenylbutazone ?
GI ulcers and renal toxicity
29
What are the non-selective COX inhibitors?
``` Ketoprofen Phenylbutazone Flunixine meglumine Acetylsalicylic acid (Asprin) Acetaminophen (Tylenol) ```
30
What is the route of admin of ketoprofen and what species is it used in?
Ruminant and horse | Dog and cat (short term)
31
What adverse effect is of concern with ketoprofen
Hemorrhage GI effects
32
What is the main use of flunixine meglumine? How is it administered?
Colic pain in horses IV or IM
33
Asprin is not approved for vet use by USFDA but can be used at very low doses in cats and dogs. What are the most serious adverse effects?
Bleeding and GI effects —> dogs and cats often present for toxicity due to owner overdose
34
Acetaminophen is very toxic to cats. What are signs of toxicity? How can you treat?
Hemolytic anemia, cyanosis, fever, facial edema, and vomiting Treatment: N-acetylcystine (limits formation of liver and RBC toxic intermediates)