3. Analgesics

Question 1

Chronic pain is pain greater than how many months?

Exhibit reactive __ and increased/decreased function

Answer 1

3-6 months

Depression

Decreased

Question 2

Prostaglandins are lipid mediators derived from ___ that play roles in the pathogenesis of what three symptoms?

Answer 2

1. Arachidonic acid

2. Inflammation, fever, pain

Question 3

Why do we not give ASA to asthmatics?

Answer 3

Leukotriene will buildup in the lungs and trigger asthma

Question 4

Effects of COX-1 activated sites on PGHS-1/2 molecules (3)

Answer 4

1. Promotes platelet aggregation (through thrombin A2 production)
2. Promotes kidney blood flow in compromised kidney
3. Promotes protection of the stomach and intestine line

Question 5

Effects of COX-2 activated sites on PGHS-1/2 molecules

Answer 5

1. Promotes fever
2. Promotes inflammation
3. Promotes hyperalgesia

Question 6

Acetaminophen - MoA

• Acts primarily in CNS to inhibit synthesis of what?
• Inhibits this synthesis by inhibiting a specific site on what?
• It also acts as a reducing co-substrate at the ___ site

Answer 6

1. Inhibits synthesis of prostaglandins
2. Inhibits site on PGHS2 (prostaglandin H synthase 2)
3. POX2 site

Question 7

What is the secondary theory for acetaminophen’s MoA

Answer 7

Acetaminophen leads to increased levels of endogenous cannabinoids

Question 8

Acetaminophen max dose for an adult >50 kg?

Answer 8

3000 mg/day

Question 9

Acetaminophen is primarily metabolized where?

• At what dosage do you get cell necrosis?
• Acetaminophen toxicity is the most common cause of?

Answer 9

Liver

4000 mg acetaminophen

• Acute hepatic failure in the US

Question 10

Mechanism of acetaminophen toxicity? (Creation of what?)

Answer 10

Creation of a toxic metabolite (cytochrome P450 oxidation)

Overdose leads to creation of excess NAPQI which leads to toxicity

Question 11

ASA - MoA (3)

Answer 11

1. Inhibits enzyme cyclooxyrgenase active site (COX) irreversibly
2. Prostaglandin-indepedent actions
3. Inhibition of neutrophil activation and response

Question 12

A high dose of ASA (4-8g/day) has what two effects?

Answer 12

1. Anti-inflammatory

2. Limited due to toxicity, tinnitus, gastric issues (GI issues are a COX-1 side effect)

Question 13

Three use of ASA? (dental, medical, prophylaxis)

Answer 13

1. Dental: Treatment of post-op pain
2. Medical: Treatment of pain/fever
3. Prophylaxis of myocardial infarction and transient ischemic episodes

Question 14

Side effects of ASA? (7)

Answer 14

1. Increased bleeding time
2. GI issues (ulcers, bleeding)
3. Reye syndrome
4. Pregnancy (ductus arteriosus pre-mature closure)
5. Caution breast-feeding
6. Renal function
7. At high levels, tinnitus, confusion, N/V, thirst, headache, ab pain, diarrhea

Question 15

ASA interactions (3)

Answer 15

Hypotensive effect reduced

• Beta blockers
• ACE inhibitors
• Diuretics

Increased INR (for anti-coagulants and thrombolytics)

Aspirin and alcohol leads to GI ulcers and bleeding

Question 16

What is Cycloxygenase enzyme responsible for forming?

Answer 16

1. Prostaglandins
2. Prostacyclins
3. Thromboxanes

Question 17

NSAIDs (cox-1 and cox-2) moa?

Answer 17

Reversibly block COX enzyme and reduce prostaglandins throughout body (this affects the stomach)

Question 18

COX-2 inhibitor - MoA

Answer 18

Inhibit prostaglandin synthesis by decreasing activity of COX-2 enzyme (decreased formation of prostaglandin precursors)
- Anti-pyretic, analgesic, and anti-inflammatory properties

Question 19

Cox inhibitors - Adverse effects

• Cardiovascular - increased risk of what three events?
• May limit cardio-protective effects of aspirin by antagonizing aspirin’s what?

Answer 19

1. Heart attack, stroke, thrombosis

2. Aspirin’s irreversible platelet inhibition

Question 20

Cox inhibitors reduce the efficacy of which hypertensive medications?

Answer 20

BAD (beta blockers, ace inhibitors, diuretics)

Question 21

Cox inhibitors increase the potency of coumadin due to what?

Answer 21

Protein bumping

- Bind serum albumin and leads to free Coumadin. This leads to increased anti-coagulation effect

Question 22

NSAIDs - Side effects

Answer 22

1. Skin reactions
2. CV: Increased risk of thrombotic events
3. GI irritation and ulcers
4. CNS: Dizziness, drowsiness, blurred vision
5. Platelet adhesion/aggregation may be decreased

Question 23

NSAIDs - Respiratory system adverse effects

• Blocking cyclooxyrgenase can shunt arachidonic acid towards the formation of the bronchoconstricting ___
• Estimated that 10% of patients with ___ experience a decline in their respiratory function

Answer 23

1. Leukotrienes

2. Asthma

Question 24

Opioids: MoA

Answer 24

Raise pain threshold and alter brain’s perception of pain (bind to Mu and Kappa receptors) and emotional response to pain - Inhibits flow of pain sensations

Question 25

What does binding to Mu receptor do? (Opioids)

Answer 25

1. Analgesia, decreased GI motility, respiratory depression, sedation, physical dependence

Question 26

What does binding to Kappa receptor do?

Answer 26

1. Analgesia, decreased GI motility, mitosis, sedation

Question 27

What are the major concerns with opioids? (2)

Answer 27

1. CNS depression | 2. Respiratory depression

Question 28

Common side effects of opioids (4)

Answer 28

1. Constipation (due to decreased GI motility) 2. Dizziness/nausea 3. Loss of apatite 4. Respiratory depression

Question 29

Tramadol (Ultra) - MoA

Answer 29

Bind to opioid receptors to cause inhibition of pain pathways and block re-uptake of nor-epi. (More mu receptor selective)

Question 30

Opioids - Interactions | - Combining the follow drugs with opioids can result in marked toxicity (2) and especially one other drug

Answer 30

1. MAOI's 2. Matulane (Especially meperidine)