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Case Pres > 3. Analgesics > Flashcards

3. Analgesics Flashcards

1
Q

Chronic pain is pain greater than how many months?

Exhibit reactive __ and increased/decreased function

A

3-6 months

Depression

Decreased

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2
Q

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

A
  1. Arachidonic acid

2. Inflammation, fever, pain

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3
Q

Why do we not give ASA to asthmatics?

A

Leukotriene will buildup in the lungs and trigger asthma

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4
Q

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

A
  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
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5
Q

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

A
  1. Promotes fever
  2. Promotes inflammation
  3. Promotes hyperalgesia
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6
Q

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
A
  1. Inhibits synthesis of prostaglandins
  2. Inhibits site on PGHS2 (prostaglandin H synthase 2)
  3. POX2 site
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7
Q

What is the secondary theory for acetaminophen’s MoA

A

Acetaminophen leads to increased levels of endogenous cannabinoids

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8
Q

Acetaminophen max dose for an adult >50 kg?

A

3000 mg/day

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9
Q

Acetaminophen is primarily metabolized where?

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

Liver

4000 mg acetaminophen

  • Acute hepatic failure in the US
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10
Q

Mechanism of acetaminophen toxicity? (Creation of what?)

A

Creation of a toxic metabolite (cytochrome P450 oxidation)

Overdose leads to creation of excess NAPQI which leads to toxicity

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11
Q

ASA - MoA (3)

A
  1. Inhibits enzyme cyclooxyrgenase active site (COX) irreversibly
  2. Prostaglandin-indepedent actions
  3. Inhibition of neutrophil activation and response
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12
Q

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

A
  1. Anti-inflammatory

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

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13
Q

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

A
  1. Dental: Treatment of post-op pain
  2. Medical: Treatment of pain/fever
  3. Prophylaxis of myocardial infarction and transient ischemic episodes
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14
Q

Side effects of ASA? (7)

A
  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
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15
Q

ASA interactions (3)

A

Hypotensive effect reduced

  • Beta blockers
  • ACE inhibitors
  • Diuretics

Increased INR (for anti-coagulants and thrombolytics)

Aspirin and alcohol leads to GI ulcers and bleeding

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16
Q

What is Cycloxygenase enzyme responsible for forming?

A
  1. Prostaglandins
  2. Prostacyclins
  3. Thromboxanes
17
Q

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

A

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

18
Q

COX-2 inhibitor - MoA

A

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

19
Q

Cox inhibitors - Adverse effects

  • Cardiovascular - increased risk of what three events?
  • May limit cardio-protective effects of aspirin by antagonizing aspirin’s what?
A
  1. Heart attack, stroke, thrombosis

2. Aspirin’s irreversible platelet inhibition

20
Q

Cox inhibitors reduce the efficacy of which hypertensive medications?

A

BAD (beta blockers, ace inhibitors, diuretics)

21
Q

Cox inhibitors increase the potency of coumadin due to what?

A

Protein bumping

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

22
Q

NSAIDs - Side effects

A
  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
23
Q

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
A
  1. Leukotrienes

2. Asthma

24
Q

Opioids: MoA

A

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

25
Q

What does binding to Mu receptor do? (Opioids)

A
  1. Analgesia, decreased GI motility, respiratory depression, sedation, physical dependence
26
Q

What does binding to Kappa receptor do?

A
  1. Analgesia, decreased GI motility, mitosis, sedation
27
Q

What are the major concerns with opioids? (2)

A
  1. CNS depression

2. Respiratory depression

28
Q

Common side effects of opioids (4)

A
  1. Constipation (due to decreased GI motility)
  2. Dizziness/nausea
  3. Loss of apatite
  4. Respiratory depression
29
Q

Tramadol (Ultra) - MoA

A

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

30
Q

Opioids - Interactions

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

A
  1. MAOI’s
  2. Matulane

(Especially meperidine)

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