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!!!!! Pharm Spring 16 Exam 2 !!!!! > Non opioid anagesics > Flashcards

Non opioid anagesics Flashcards

1
Q

Non- opouids that can be effective for severe pain

A

IV tylenol and Ketoralac

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2
Q

Ceiling effect of APAP and ASA is between _________. What might be more effecatious?

A
  1. 650 and 1300 mg.
  2. NSAIDS
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3
Q

exceeding the ceiling dose results in________

A

More adverse side effects with no added efficacy

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4
Q

Non- opioid analgesics have an andvantages as they do not develop_________.

A

Tolerance

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5
Q

Does nothing for inflammmatory response

A

Tylenol

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6
Q

What non opoid analgesics inhibit platelet functioning, and which ones do not?

A
  1. NSAIDs and ASA inhibit platelet functioning
  2. Tylenol does not - can use prior to surgery
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7
Q

Central effect - MOA not entirely known….may:

  1. Cause NMDA activation in CNS
  2. Inhibit substance P in spinal cord
  3. Cause desensitization of TRIP A channel
A
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8
Q

Good choice for:

  1. Peptic ulcer disease
  2. Pediatrics
  3. Parturients
  4. Patients who need well functioning platelets
A

Acetomenophen

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9
Q

Tylenol PO dose

A

325-650mg q4-6 hours

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10
Q

Tylenol IV dose

A

1gm over 15 minutes - q4-6 hours and NOT to exceed 4000mg in 24 hours

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11
Q

APAP has similar potency to _______. Likewise, single anesthetic doses have the same _________ curve

A
  1. ASA
  2. Time - effect
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12
Q

When does IV APAP peak, when should it be given

A

It peaks in 15 minutes, so the infusion shoulg be given 15 minutes prior to the patient waking up

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13
Q

APAP is ______________ to an _____________ that is ______________. The name of this meotabolite is ______________.

A
  1. hydroxylated
  2. actve metambolite
  3. hepatotoxic
  4. N-acetyl- p- benzoquinone
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14
Q

Maximum sage dose to APAP

A

4gm/day

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15
Q

Doses of APAP should be lowered with _________ because they will produce _______ of the active metabolite.

A
  1. ETOH use
  2. more
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16
Q

What breaks down the N-acetyl-p-benzoquinone? What is significant about it?

A
  1. The active metabolite for tylenol is broken down by glutathione
  2. when glutothione is outnumbered by the active metabolite ie overdose- it causes hepatic injury
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17
Q

In acetomenophen overdose what can be substituted for glutathione?

A
  1. Acetylcystine - if given within 8 hours
  2. Activated charcole- only if it is given within 30 minutes of oral overdose
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18
Q

APAP and Renal toxicity

A

Renal papillary accumulation of metabolites causes reanal cell necrosis with longterm use

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19
Q

What has a higheer risk of renal injuty that APAP?

A

NSAIDs

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20
Q

Arachadonic acid is released from___________ by the enzyme ___________. This pathway is upregualted by __________.

A
  1. Phosphalipids
  2. Phosphalipase II
  3. Inflammation
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21
Q

Arachadonic acid is immediately metabolized by

  1. ________
  2. ________
  3. ________

The first tow are the ones we are mostly concerned with.

A
  1. Cyclooxygenase
  2. Lipoxygenase
  3. Epoxcygenase
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22
Q

Metabolism of Arachadonic acid via Cyclooxygenase leads to the formation of:

  1. ____________
  2. ____________
  3. ____________
  4. ____________
A
  1. Prostaglandins
  2. Prostacycline
  3. Thromboxane A2
  4. Inflammatory pain responses
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23
Q

for platelet aggreagation

A

Thromboxane A2

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24
Q

causes pain, fever and inflammtion

A

prostaglandins produced from COX-2

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25
Q

COX-2 are called “________”

A

Incucible

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26
Q

COX-1 are called “__________”

A

constrictive

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27
Q

Arachadonic acid metabolized by Liopoxygenase leads to the formation of:

  1. ________
  2. ________
A
  1. Leukotrienes
  2. Lipoxins
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28
Q

Arachadonic aced metabolized by epooxygenase lead to the formation of:

  1. ___________
A

Epoxygeicosatetraenoic Acid- which further regulates infalmmation and is being reserched

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29
Q

Asmatic patients can be __________ sensitive. We must ask thse patients if they have tolerated ______ or _______ in the past because of the risk of ___________.

A
  1. Leukotrienes
  2. ASA
  3. NSAIDs
  4. Bronchospasm
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30
Q

Normally provide gastric protection, hemostasis and platelet aggrigation and renal function

A

Prostaglandins produced by COX-1

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31
Q

If we block one pathway the prostaglandins will be shuttled down the other pathway. This resulted in what from VIOXX

A

It was a selective COX-2 inhibitor so it caused increased COX-1 action including increased platelet aggregation and caused thrombosis and MI

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32
Q

NSAIDs block __________ which sets up patients who are at risk for ESRD because all _________ are being inhibited including those for __________

A
  1. COX-1 and COX-2
  2. prostaglandins
  3. renal protection (COX-1)
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33
Q

Inflammation

A

COX-2 inducible pathway that can be increased 20 fold

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34
Q

ASA is best at inhibiting platelt aggregation

A

at lower doses 81mg

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35
Q

Irreversible inhabition of COX

A

ASA

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36
Q

Reversible inhabition of COX-1

A

NSAIDs

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37
Q

why does ASA need to se d/c’d 1 week to 10 days pre-op

A

it irreversibley inhibits COX-1 and inhibits platelet function for the lifetime of the platelet

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38
Q

Large doses of ASA can decrease

A

Prothrombin

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39
Q

ESRD and ASA

A

ASRD NOT induced by ASA

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40
Q

A single dose of ASA can precipitate __________ there is also corss sensitiveity with ________

A
  1. Asthma
  2. other NSAIDs
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41
Q

Higher doses of ASA can cause ___________. which my present as __________,

A
  1. CNS stimulation
  2. Ringing in the ears (tinnitus)
42
Q

With really high doses of ASA a patient can become _________, with CNS symptoms. There is an increased risk for __________ because ASA is an __________ and becomes ________ in the blood and can cross the __________. This will lead to _________.

A
  1. Acidotic
  2. CNS toxicity
  3. acid
  4. non-ionized
  5. BBB
  6. SEIZURES
43
Q

Can cause an increase in LFTs that is usually reversible

A

ASA

44
Q

ASA analgesic/antipyretic dosing

A

325-650mg

45
Q

ASA antiinflammatory dosing and consiterations

A
  1. 1000mg (3-5g/day)
  2. increase dose gradually
  3. follow serum salicylate levels
  4. rarely used (GI side effects)
46
Q

What is the preferred anti-inflammatory

A

NSAIDs over ASA

47
Q

ASA clearance

A
  1. Hepatic
  2. With an E1/2t 15-20 minutes for ASA
  3. E1/2t 2-3 hours for salicylic acid
48
Q

Acidosis, tinnitus

A

Salicylate overdose

49
Q

rye syndrome

A

ASA should not be used during viral syndromes in children and teenagers

50
Q
  1. do not interfere with platelet aggregation
  2. rarely associated with GI bleeding
  3. well tolerated by asthmatics
A

Non-acytylated salicylates

51
Q

more effective than full doses of ASA or APAP but have a ceiling effect

A

NSAIDs

52
Q

NSAIDs Mechanism of action

A
  1. Non-selective COX inhibition
  2. Block the conversion of arachadonic acid to to prostaglandins
  3. Decreases production of prostaglandins
53
Q

NSAIDs and Joints

A
  1. NSAIDs are acidic
  2. Joint pain with lactic acidosis will trap NSAIDs in joints
54
Q

NSAIDs and protein binding

A
  1. highly protein bound at >95%
  2. Displaces/competes other protein bound drugs
  3. increases level of warfarin, phenytoin, sulfonulureas, sulfonamides, digoxin
55
Q

Nsaids Vd

A

Small Vd

56
Q

NSAIDs half life

A
  1. varies depeding on drug <6 to >12
  2. Ibuprofun vs naproxen
57
Q

NSAIDS and asthma

A

can have an anaphylactoid reaction in ASA sensitive patients

58
Q

NSaids and platelet inhabition

A
  1. Blocks COX-1 synthesis of thromboxane A2 which inhibits platelets
  2. It is reversible
  3. stop 48-72 hours before surgery
59
Q

Hepatic injury and aseptic menningitis are rare side effects

A

NSAIDs

60
Q

NSAIDS prefnancy class

A
  1. 1st and 2nd trimester class B- ok to use if necessary
  2. 3rd trimester - Class D- Causes premature closure of DA which is under the influence of prostaglandins- if we inhibit them it closes
61
Q

Periop inhabition of COX-1 may result in

A
  1. renal injury
  2. gastric ulceration
  3. excessive bleeding - back to OR
62
Q
  1. NSAIDS may cause GI effects including ___________, _________, and __________.
  2. The inhibiton of PGs will _______acid production and _______ mucous production.
  3. The local irritaion is caused by NSAIDS being lipid souable at a ________, entering gastric mucosal cells becoming _________.
A
  1. Dyspepsia , GI bleed, Pepetic ulcer disease
  2. increase, decrease
  3. low, ion trapped
63
Q

Risk factors for NSAIDs and adverse GI effects

A
  1. High doses
  2. Prolonged use
  3. Previous GI ulcer/bleed
  4. Excessive ETOH- higher risk for GI bleed
  5. elderly
  6. corticosteroid use
64
Q

___________ can block the Arachadonic acid pathway higher up than NSAIDs and ASA and thus re helpful in Asthma

A

Corticosteroids

65
Q

Low GI risk NSAIDS

A
  1. Ibuprofun and Naproxen at low doses
  2. Etodolac, sulindac
  3. Celecoxib- selective COX-2
66
Q

Moderate GI risk NSAIDS

A
  1. Ibuprofen and Naproxen at mod-high doses
  2. Dilofenac, oxaprozinm meloxicam, nabumetone
67
Q

High GI risk NSAIDS

A
  1. Ketoralac - this is why we limit the # of doses
  2. Telmetin, piroxicam, indomethacin
  3. ASA
68
Q

Isoniazid

A

Used for TB- will increase the risk of APAP toxicity

69
Q

NSAIDS and renal adverse effects

A
  1. Decreased synthesis of renal vasodialator PGs (PGE2)
  2. Those dependant on them can go int renal failure
  3. Epinepherine release due to stress respone decreases renal profusion
  4. Fluid and sodium retenton - HTN/Renal failure
70
Q

NSAIDS and rare renal adverse effects

A

interstitial nephritis

71
Q

risk factors for NSAIDS and renal adverse effects

A
  1. Age
  2. CHF
  3. DM
  4. HTN
  5. Renal insuffiency
  6. Ascites
  7. volume depletion
  8. diuretic therapy
72
Q

Drug qualities of NSAIDs that increase the renal risks

A
  1. Longer half life
  2. Higly potent COX inhibitors
  3. Higher dose
73
Q

Highly potent COX inhibitors

A
  1. Ketoralac
  2. Indomethicin
74
Q

Renal sparing- COX-2 selective

A
  1. Celecoxib
  2. Sulindac, nabumetone
75
Q

NSAIDS and antihypertensives

A
  1. not recommended
  2. Bringing PGs down will offest the decrease in PGs by antihypertensive drugs (ACEIs, B-Blockers)
76
Q

NSAIDS and Diuretics

A

Reduces the effect

77
Q

NSAIDS and lithium

A

Increases litium levels- compeditive protein binding

78
Q

NSAIDs and anticoagulats

A

increases risk of GI bleed

79
Q

NSAIDS and probenecid

A
  1. (Gout) increases levels of most NSAIDs
  2. AVOID with Ketoralac
80
Q

Only IV NSAID available in US

A

Ketorolac

81
Q
  1. can be comparable to opioids
  2. Similar efficacy to morphine
  3. No ventilatory of cardiac depression
A

Ketoralac

82
Q

GI risks the same as NSAIDs

A

Ketoralac

83
Q

Can produce life threatening bronchospasm

A

Ketoralac

84
Q

Avoid in elderly due to renal toxicity

A

Ketoralac

85
Q

Length of Tx with Ketoralac

A

Max 5 days

86
Q

Ketoralac IV onset

A

10 minutes- give when waking up

87
Q

Ketoralac E1/2t and dosing schedule

A
  1. 5 hours (prolonged in elderly 30-50%)
  2. Dose q6-8 hours (elderly q8-12 hours)
88
Q

Ketoralac and protein binding

A

99% protein bound and conjugated in the liver

89
Q

Ketoralac dose

A
  1. 30mg IV x 1 q6 hours
  2. 120mg daily max
90
Q

Ketoralac elderly dosing

A

If used at all with elderly cut the dose in half

91
Q

Selective COX-2 inhibitor

A

Celacoxib (Celebrex)

92
Q

celacoxib and renal effects

A

same as all NSAIDs

93
Q

inhibits the production of prostacyclin

A
  1. Celecoxib (COX-2 inhibitor)
  2. prastacyline is a vasodialtor and platelet inhibitor
94
Q

Celecoxib dosing

A
  1. Use the lowest dose
  2. <200mg/day
  3. 200mg/day = Naproxin 500mg BID
95
Q

should avoid in patiets with sulfonomide allergy

A

Celacoxib

96
Q

Blackbox warning

A

Celacoxib

  1. CV - thrombotic events, MI, Stroke
  2. GI - bleeding
97
Q

Drug of choice for neuropatheic pain syndromes

A

Tricyclic antidepressants and Anticonvulsants

98
Q

anticonvulsnt meds for pain

A
  1. Gabapentin
  2. Pregabalin
  3. Carbamazepine
  4. Phenytoin- induces CYP 450
  5. Clonazapam
  6. Lamitrogen
99
Q

Used in short bursts for pain

A

corticosteroids

100
Q

topical causing desensitization of TRIP1

A

Capsaicin

101
Q
  1. alpha 2 agonist for sympathetically maintained pain
  2. centrally modulates analgesia and decreases sympathetic NS outflow
A

Transdermal clonondine

!!!!! Pharm Spring 16 Exam 2 !!!!! (11 decks)

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