Non opioid anagesics Flashcards
(101 cards)
1
Q
Non- opouids that can be effective for severe pain
A
IV tylenol and Ketoralac
2
Q
Ceiling effect of APAP and ASA is between _________. What might be more effecatious?
A
- 650 and 1300 mg.
- NSAIDS
3
Q
exceeding the ceiling dose results in________
A
More adverse side effects with no added efficacy
4
Q
Non- opioid analgesics have an andvantages as they do not develop_________.
A
Tolerance
5
Q
Does nothing for inflammmatory response
A
Tylenol
6
Q
What non opoid analgesics inhibit platelet functioning, and which ones do not?
A
- NSAIDs and ASA inhibit platelet functioning
- Tylenol does not - can use prior to surgery
7
Q
Central effect - MOA not entirely known….may:
- Cause NMDA activation in CNS
- Inhibit substance P in spinal cord
- Cause desensitization of TRIP A channel
A
8
Q
Good choice for:
- Peptic ulcer disease
- Pediatrics
- Parturients
- Patients who need well functioning platelets
A
Acetomenophen
9
Q
Tylenol PO dose
A
325-650mg q4-6 hours
10
Q
Tylenol IV dose
A
1gm over 15 minutes - q4-6 hours and NOT to exceed 4000mg in 24 hours
11
Q
APAP has similar potency to _______. Likewise, single anesthetic doses have the same _________ curve
A
- ASA
- Time - effect
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
13
Q
APAP is ______________ to an _____________ that is ______________. The name of this meotabolite is ______________.
A
- hydroxylated
- actve metambolite
- hepatotoxic
- N-acetyl- p- benzoquinone
14
Q
Maximum sage dose to APAP
A
4gm/day
15
Q
Doses of APAP should be lowered with _________ because they will produce _______ of the active metabolite.
A
- ETOH use
- more
16
Q
What breaks down the N-acetyl-p-benzoquinone? What is significant about it?
A
- The active metabolite for tylenol is broken down by glutathione
- when glutothione is outnumbered by the active metabolite ie overdose- it causes hepatic injury
17
Q
In acetomenophen overdose what can be substituted for glutathione?
A
- Acetylcystine - if given within 8 hours
- Activated charcole- only if it is given within 30 minutes of oral overdose
18
Q
APAP and Renal toxicity
A
Renal papillary accumulation of metabolites causes reanal cell necrosis with longterm use
19
Q
What has a higheer risk of renal injuty that APAP?
A
NSAIDs
20
Q
Arachadonic acid is released from___________ by the enzyme ___________. This pathway is upregualted by __________.
A
- Phosphalipids
- Phosphalipase II
- Inflammation
21
Q
Arachadonic acid is immediately metabolized by
- ________
- ________
- ________
The first tow are the ones we are mostly concerned with.
A
- Cyclooxygenase
- Lipoxygenase
- Epoxcygenase
22
Q
Metabolism of Arachadonic acid via Cyclooxygenase leads to the formation of:
- ____________
- ____________
- ____________
- ____________
A
- Prostaglandins
- Prostacycline
- Thromboxane A2
- Inflammatory pain responses
23
Q
for platelet aggreagation
A
Thromboxane A2
24
Q
causes pain, fever and inflammtion
A
prostaglandins produced from COX-2
25
COX-2 are called "\_\_\_\_\_\_\_\_"
Incucible
26
COX-1 are called "\_\_\_\_\_\_\_\_\_\_"
constrictive
27
Arachadonic acid metabolized by Liopoxygenase leads to the formation of:
1. \_\_\_\_\_\_\_\_
2. \_\_\_\_\_\_\_\_
1. Leukotrienes
2. Lipoxins
28
Arachadonic aced metabolized by epooxygenase lead to the formation of:
1. \_\_\_\_\_\_\_\_\_\_\_
Epoxygeicosatetraenoic Acid- which further **regulates infalmmation** and is being reserched
29
Asmatic patients can be __________ sensitive. We must ask thse patients if they have tolerated ______ or _______ in the past because of the risk of \_\_\_\_\_\_\_\_\_\_\_.
1. Leukotrienes
2. ASA
3. NSAIDs
4. Bronchospasm
30
Normally provide gastric protection, hemostasis and platelet aggrigation and renal function
Prostaglandins produced by COX-1
31
If we block one pathway the prostaglandins will be shuttled down the other pathway. This resulted in what from VIOXX
It was a selective COX-2 inhibitor so it caused increased COX-1 action including increased platelet aggregation and caused thrombosis and MI
32
NSAIDs block __________ which sets up patients who are at risk for ESRD because all _________ are being inhibited including those for \_\_\_\_\_\_\_\_\_\_
1. COX-1 and COX-2
2. prostaglandins
3. renal protection (COX-1)
33
Inflammation
COX-2 inducible pathway that can be increased 20 fold
34
ASA is best at inhibiting platelt aggregation
at lower doses 81mg
35
Irreversible inhabition of COX
ASA
36
Reversible inhabition of COX-1
NSAIDs
37
why does ASA need to se d/c'd 1 week to 10 days pre-op
it irreversibley inhibits COX-1 and inhibits platelet function for the **lifetime** of the platelet
38
Large doses of ASA can decrease
Prothrombin
39
ESRD and ASA
ASRD **NOT** induced by ASA
40
A single dose of ASA can precipitate __________ there is also corss sensitiveity with \_\_\_\_\_\_\_\_
1. Asthma
2. other NSAIDs
41
Higher doses of ASA can cause \_\_\_\_\_\_\_\_\_\_\_. which my present as \_\_\_\_\_\_\_\_\_\_,
1. CNS stimulation
2. Ringing in the ears (tinnitus)
42
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 \_\_\_\_\_\_\_\_\_.
1. Acidotic
2. CNS toxicity
3. acid
4. non-ionized
5. BBB
6. **SEIZURES**
43
Can cause an increase in LFTs that is usually reversible
ASA
44
ASA analgesic/antipyretic dosing
325-650mg
45
ASA antiinflammatory dosing and consiterations
1. **1000mg** (3-5g/day)
2. increase dose gradually
3. follow **serum salicylate** levels
4. **rarely** used (GI side effects)
46
What is the preferred anti-inflammatory
NSAIDs over ASA
47
ASA clearance
1. **Hepatic**
2. With an E1/2t **15-20 minutes** for **ASA**
3. E1/2t **2-3 hours** for **salicylic acid**
48
**Acidosis, tinnitus**
Salicylate overdose
49
rye syndrome
ASA should **not** be used during **viral syndromes** in **children** and **teenagers**
50
1. do not interfere with platelet aggregation
2. rarely associated with GI bleeding
3. well tolerated by asthmatics
Non-acytylated salicylates
51
more effective than full doses of ASA or APAP but have a ceiling effect
NSAIDs
52
NSAIDs Mechanism of action
1. Non-selective COX inhibition
2. Block the **conversion** of arachadonic acid to to prostaglandins
3. Decreases **production** of prostaglandins
53
NSAIDs and Joints
1. NSAIDs are **acidic**
2. Joint pain with **lactic acidosis** will **trap** NSAIDs in joints
54
NSAIDs and protein binding
1. highly protein bound at \>95%
2. **Displaces/competes** other protein bound drugs
3. increases level of warfarin, phenytoin, sulfonulureas, sulfonamides, digoxin
55
Nsaids Vd
Small Vd
56
NSAIDs half life
1. varies depeding on drug **\<6 to \>12**
2. Ibuprofun vs naproxen
57
NSAIDS and asthma
can have an anaphylactoid reaction in ASA sensitive patients
58
NSaids and platelet inhabition
1. Blocks **COX-1** synthesis of **thromboxane A2** which **inhibits platelets**
2. It is reversible
3. stop **48-72 hours** before surgery
59
Hepatic injury and aseptic menningitis are rare side effects
NSAIDs
60
NSAIDS prefnancy class
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
Periop inhabition of COX-1 may result in
1. renal injury
2. gastric ulceration
3. excessive bleeding - back to OR
62
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 \_\_\_\_\_\_\_\_\_.
1. Dyspepsia , GI bleed, Pepetic ulcer disease
2. increase, decrease
3. low, ion trapped
63
Risk factors for NSAIDs and adverse GI effects
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
\_\_\_\_\_\_\_\_\_\_\_ can block the Arachadonic acid pathway higher up than NSAIDs and ASA and thus re helpful in Asthma
Corticosteroids
65
Low GI risk NSAIDS
1. Ibuprofun and Naproxen at **low doses**
2. Etodolac, sulindac
3. Celecoxib- selective COX-2
66
Moderate GI risk NSAIDS
1. Ibuprofen and Naproxen at **mod-high doses**
2. Dilofenac, oxaprozinm meloxicam, nabumetone
67
High GI risk NSAIDS
1. **Ketoralac** - this is why we limit the # of doses
2. Telmetin, piroxicam, indomethacin
3. **ASA**
68
Isoniazid
Used for TB- will increase the risk of **APAP toxicity**
69
NSAIDS and renal adverse effects
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
NSAIDS and rare renal adverse effects
interstitial nephritis
71
risk factors for NSAIDS and renal adverse effects
1. Age
2. CHF
3. DM
4. HTN
5. Renal insuffiency
6. Ascites
7. volume depletion
8. diuretic therapy
72
Drug qualities of NSAIDs that increase the renal risks
1. Longer half life
2. Higly potent COX inhibitors
3. Higher dose
73
Highly potent COX inhibitors
1. Ketoralac
2. Indomethicin
74
Renal sparing- COX-2 selective
1. Celecoxib
2. Sulindac, nabumetone
75
NSAIDS and antihypertensives
1. not recommended
2. Bringing PGs down will offest the decrease in PGs by antihypertensive drugs (ACEIs, B-Blockers)
76
NSAIDS and Diuretics
Reduces the effect
77
NSAIDS and lithium
Increases litium levels- compeditive protein binding
78
NSAIDs and anticoagulats
increases risk of GI bleed
79
NSAIDS and probenecid
1. (Gout) increases levels of most NSAIDs
2. **AVOID with Ketoralac**
80
Only IV NSAID available in US
Ketorolac
81
1. can be comparable to opioids
2. Similar efficacy to morphine
3. No ventilatory of cardiac depression
Ketoralac
82
GI risks the same as NSAIDs
Ketoralac
83
Can produce life threatening bronchospasm
Ketoralac
84
Avoid in elderly due to renal toxicity
Ketoralac
85
Length of Tx with Ketoralac
Max 5 days
86
Ketoralac IV onset
10 minutes- give when waking up
87
Ketoralac E1/2t and dosing schedule
1. 5 hours (prolonged in elderly 30-50%)
2. Dose q6-8 hours (elderly q8-12 hours)
88
Ketoralac and protein binding
99% protein bound and conjugated in the liver
89
Ketoralac dose
1. **30mg** IV x 1 q6 hours
2. 120mg daily **max**
90
Ketoralac elderly dosing
If used at all with elderly cut the dose in half
91
Selective COX-2 inhibitor
Celacoxib (Celebrex)
92
celacoxib and renal effects
same as all NSAIDs
93
inhibits the production of prostacyclin
1. Celecoxib (COX-2 inhibitor)
2. prastacyline is a vasodialtor and platelet inhibitor
94
Celecoxib dosing
1. Use the lowest dose
2. \<200mg/day
3. 200mg/day = Naproxin 500mg BID
95
should avoid in patiets with sulfonomide allergy
Celacoxib
96
Blackbox warning
Celacoxib
1. CV - thrombotic events, MI, Stroke
2. GI - bleeding
97
Drug of choice for neuropatheic pain syndromes
Tricyclic antidepressants and Anticonvulsants
98
anticonvulsnt meds for pain
1. Gabapentin
2. Pregabalin
3. Carbamazepine
4. Phenytoin- induces CYP 450
5. Clonazapam
6. Lamitrogen
99
Used in short bursts for pain
corticosteroids
100
topical causing desensitization of TRIP1
Capsaicin
101
1. alpha 2 agonist for sympathetically maintained pain
2. centrally modulates analgesia and decreases sympathetic NS outflow
Transdermal clonondine
