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Z Pharm II - Unit 1 > Pain Management-Intro through Non-opioids > Flashcards

Pain Management-Intro through Non-opioids Flashcards

1
Q

Indication for Acetaminophen

A

Tx of mild to moderate pain

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2
Q

Adverse effects of Acetaminophen

A

usually well tolerated; hepatotoxicity, analgesic neuropathy, anemia, blood dyscrasias, rare skin rxns.

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3
Q

Non-opioid analgesics

A

Acetaminophen, NSAIDS (Nonsalicylates and salicylates)

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4
Q

MOA for Acetaminophen

A

Analgesic; inhibits prostaglandin synthesis in CNS and peripherally blocks pain impulse generation

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5
Q

How does Acetaminophen Hepatotoxicity Occur

A

A small amount of APAP is metabolized via CYP450 to a hepatotoxic metabolite;
Usually glutathione binds to NAPQI to allow excretion of non conjugates, but when Acetaminophen is misused/OD it depletes glutathione and NAPQI isn’t detoxified

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6
Q

MOA for NSAIDS

A

Nonselective NSAIDS inhibit both COX 1 and COX 2
Partially selective NSAIDS inhibit COX 2 more than COX1
Selective COX 2 inhibitors only inhibit COX 2

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7
Q

NSAID adverse effects

A 
Cardiovascular
Hematologic Toxicity
CNS (high doses cause sedation/decreased cognition)
Hepatotoxicity
GI complications (mucosal damage)
(Renal) Nephrotroxicity
Skin (SJS/TEN)
Pneumonic = CH CH GRS
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8
Q

Indication for Acetylated Salicylates

A

Mild to moderate pain; prevention of MI, CVA

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9
Q

MOA for acetylated salicylates

A

Analgesic: Inhibit both COX 1 and COX 2
Antipyretic: Inhibition of hypothalamic heat-regulating center

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10
Q

Adverse Effects for acetylated salicylates

A

Reye’s syndrome
ASA sensitivity (asthma, bronchospasm, andioedema, urticaria)
platelet inhibition

PNEUMONIC = RAP

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11
Q

Adverse Effects for nonacetylated salicylates

A 
less GI toxicity than NSAIDS
no antiplatelet effects
same AE as N-NSAIDs
occasional cross reactivity in ASA sensitive pts
Reye's syndrome
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12
Q

What are nociceptors stimulated by?

A

Leukotrienes, prostaglandins, and histamine

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13
Q

What are the 3 endogenous endorphins used in the brain to modulate pain

A

Beta-endorphins, Enkephalins, Dynorphins

Think BED

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14
Q

4 types of pain

A

Nociceptive, inflammatory, neuropathic, functional

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15
Q

PQRST characteristics of pain

A 
Palliative/Provocative
Quality
Radiation
Severity
Temporal factors
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16
Q

WHO Step 1: levels of pain and treatment

A

Mild pain (1-3/10)
+ non-opioid
+/- adjuvents

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17
Q

WHO Step 2: levels of pain and treatment

A

Moderate pain (4-6/10)
weak opioid
+ non-opioid
+/- adjuvents

18
Q

WHO Step 3: levels of pain and treatment

A

Severe pain (7-10/10)
strong opioid
+ non-opioid
+/- adjuvent

19
Q

Difference in effects between Acetaminophen and NSAIDS

A

NSAIDS have anti-inflammatory effect and Acetaminophen do not

20
Q

Reason for NSAID mucosal damage

A

Due to direct or topical irritation of gastric epithelium OR systemic inhibition of endogenous GI mucosal prostaglandin synthesis

21
Q

High Risk Patients for NSAID caused ulcer

A 
Prior PUD or UGI bleed
Age >60
NSAID (high dose or more toxic )
concurrent corticosteroid, bisphosphonate, or SSRI use
anticoagulant use or coagulopathy
Chronic illness (ex. CV disease)
antiplatelet use (ex. ASA, clopidogrel)

PNEUMONIC: PANCACA

22
Q

Risk factors for Nephrotoxicity with NSAID use

A 
older age
HF
renal insufficiency
ascites
volume depletion 
diuretic therapy
23
Q

Reason for Nephrotoxicity with NSAID use

A

NSAID decrease renal prostaglandins that usually help increase renal blood flow and maintain renal function, but NSAIDs decreases it.

24
Q

How does ASA and non-selective NSAIDs differ in their hematologic effects.

A

ASA inhibits platelet aggregation for the lifetime of the platelet (7-10 days)
Other non-selective NSAIDs affect platelet aggregation to a lesser degree and only when the drug is on board

25
Q

Do COX2 and NAS affect platelet aggregation

A

No they have no affect on platelet aggregation

26
Q

How do NSAIDs affect the cardiovascular system

A

Selective inhibition of COX2 may decrease endothelial production of prostacyclin; this leaves platelet thromboxane A2 mediated by COX1 relatively unopposed which may lead to vasoconstriction, platelet aggregation, and thrombosis

27
Q

Which NSAID has the highest CV risk

A

Celecoxib

28
Q

Which NSAID has the lowest CV risk

A

Naproxen

29
Q

Why should you take ASA before ibuprofen or naproxen if you need to be on both

A

If you take ibuprofen or naproxen first, it will bind to the platelets and not allow ASA to bind and have a better antiplatelet affect

30
Q

Why do NSAIDs increase BP?

A

D/t sodium and water retention,there is an increase in plasma volume to the kidneys to keep them functioning. This leads to an increase in BP

31
Q

Dosing for ibuprofen

A

Pain= 200-400mg, max 2400/day

Inflamm=600-800, max 3200/day

32
Q

What is the max number of day you can be on Ketorolac

A

5 days

33
Q

What is nociceptive pain

A

transient pain in response to stimulus at nociceptors

34
Q

What is inflammatory pain

A

contributes to pain hypersensitivity

prevents contact or movement of injured part

35
Q

What is neuropathic pain

A

pain or hypersensitivity to damage or pathologic changes to peripheral nervous system

36
Q

What is Functional pain

A

pain from CNS response to normal stimuli

37
Q

What is acute pain

A

self-limited

subsides when injury heals

38
Q

What is chronic pain

A

pain after expected healing and serves no purpose

39
Q

What is chronic malignant pain

A

associated with progressive disease that is life threatening

40
Q

What is chronic nonmalignant pain

A

pain last > 6 months past healing period

non life theatening

41
Q

What pain is classified as neuropathic pain

A

chronic nonmalignant pain

disease of central and peripheral nervous systems

Z Pharm II - Unit 1 (9 decks)

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