Non-opioid Analgesics

Question 1

Non-opioid

Answer 1

Salicylate (aspirin and non-aspirin)
NSAIDs
Acetaminophen

Question 2

Site of action non-opioid

Answer 2

Peripheral nerve endings

Antipyretic effect is mediated centrally

Question 3

Site of action opioids

Answer 3

CNS

Question 4

Non-opioid mechanism of action

Answer 4

Inhibit prostaglandin synthesis

Question 5

Opioid mechanism of action

Answer 5

Depresses cns

Question 6

Non-opioid adverse effects

Answer 6

No cns depression or addiction

Question 7

Opioid adverse effects

Answer 7

Respiratory and cns depression

Physical dependence

Question 8

COX (cyclooxygenase)

Answer 8

Acts on arachidonic acid
Synthesis of pro inflammatory prostaglandins
2 iso forms COX 1 CoX 2

Question 9

Cox 1

Answer 9

Expressed in most tissues (GI, kidneys, platelets)
Protect gastric mucosa, maintain kidney function
Inhibition cox 1=stomach pain, bleeding, ulcers

Question 10

Cox 2

Answer 10

Expressed in various tissues (kidney and Cns)
Induced in peripheral tissues (cause inflammation and pain)
Inhibition is responsible for anti inflammatory therapeutic effect

Question 11

Non-opioid cox mechanism of action

Answer 11

Inhibit production of prostaglandins by inhibiting cox enzyme
Compete with arachidonic acid for biding to cyclooxygenase enzyme

Question 12

ASA and cox

NSAIDs and cox

Answer 12

ASA=irreversible cox enzyme block

NSAIDs=reversible cox enzyme block

Question 13

Adverse effects (mainly salicylates and NSAIDs)

Answer 13

GI (pain, vomiting)
Platelet dysfunction (prolonged bleeding)
Renal dysfunction (edema, deterioration of kidney)
Cardiovascular (hypertension, MI)
Cns (anxiety, depression, headache)
Hypersensitivity (rashes, rhinitis, flushing, asthma)

Question 14

Adverse oral effects

Answer 14

Ulcerative stomatitis
Gingival ulcerations
Dry mouth

Question 15

ASA

Answer 15

Mild to moderate pain
Low dose=platelet aggregation inhibitor (irreversible)
Prophylaxis fo decrease heart attacks and thrombotic strokes
More potent against cox 1 than cox 2
Cause GI ulceration
Should not be used in children and teenagers (Reyes syndrome)
Avoid with warfarin, probenecid, methotrexate, sulfonylureas, antihypertensives

Question 16

Reye’s syndrome

Answer 16

Effects organs, hypoglycemia, fatality

Rash vomiting liver damage

Question 17

ASA dosage

Answer 17

Fever pain 325-650mg
Inflammation 3 g
MI 73-325 mg

Question 18

NSAIDs dental use

Answer 18

Pain (equivalent in analgesic efficacy to opioids)

Anti inflammatory

Question 19

Ibuprofen (NSAIDs)

Answer 19

Used in children
Rapidly absorbed orally
Food decreases rate but not extent of absorption

Question 20

Naproxen

Answer 20

Oral tablet
Longer half life than IB
More potent and tolerable than Asa
Efficacy for tMj pain

Question 21

Flurbiprofen

Answer 21

Long term basis has shown to slow progression of bone resorption

Question 22

Ketoralac

Answer 22

Postoperative pain
Initial dose MI/IV injection then oral tablets
Higher rate of GI ulceration and bleeding

Question 23

Celecoxib

Answer 23

Only selective cox 2 inhibitor for use in Canada

Question 24

Acetaminophen

Answer 24

Alternative for Asa allergies and children

Usually prescribed with an opioid (T3)

Question 25

Acetaminophen pharmacological effects

Answer 25

Pain relief
Reduction of fever
No anti inflammatory effects
No gastric bleeding, platelet adhesion, or Utica acid secretion

Question 26

Acetaminophen uses

Answer 26

Analgesic

Antipyretic

Question 27

Acetaminophen adverse reactions

Answer 27

Hepatic necrosis (3+ alcoholic beverages) 
Nephrotoxicity (avoid combo with aspirin/NSAIDs)

Question 28

Acetaminophen drug interactions

Answer 28

Barbiturates 
Carbamazepine
Phenytoin
Rifampin
Chronic doses of alcohol