Non Opioids and Adjuvants (Exam 2) Flashcards

1
Q

Atypical pain Medications: tramadol

A

Centrally acting analgesic

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2
Q

tramadol: MOA

A

-Binds weakly to mu opioid receptors

-Inhibit reuptake of norepi and serotonin

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3
Q

tramadol: Indications

A

Treat moderate to serve pain

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4
Q

tramadol: Adverse effects

A
  • Seizures when combined with other CNS depressants (SSRI-MAOI)
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5
Q

Aptyipical pain Medication: Anti-convulsnats

A

Gabapentin and pregablin

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6
Q

Anti-convulsants: MOA

A

-Unknown, but thought to spontaneously suppress neuronal firing

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7
Q

Ant-convulsants: Indication

A

-To complement affects of opioids

-Used for neuropathic pain (chronic) (CNS)

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8
Q

Anti-convulsants: Adverse Effects

A

-Drowsy, dizzy, visual problems

-Can only be partially reversed with Naloxone (overdose reverse)

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9
Q

gabapentin has what effect?

A

Ceiling effect. 1800 mg per day.

taking more than that doesn’t give anymore benefit

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10
Q

Non-Opioid Analgesics

A

-NSAIDS
(Non-sterodial anti-inflammatory drugs)

-Acetaminophen
(Not an NSAID) (NO ANTI-INFLAMMATORY properties)

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11
Q

2 categories of NSAIDS

A

-Nonselective COX inhibitors

-Selective COX-2 inhibitors

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12
Q

NSAIDS: MOA

A

-Anti-prostaglandinds (Inhibit prostaglandin function)

-Decrease prostaglandins by blocking a key enzyme: cyclooxygenase (COX) that is crucial to the production of prostaglandins

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13
Q

2 types of cyclooxygenase (COX)

A

-COX 1: Enzyme that protect the gastric mucosa and needed for thomboxane synthesis (Synthesis of prostoglandins)

-COX-2 enzyme: Responsible for inflammation and fever and bone formation

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14
Q

Asprin special characteristic

A

-Being a irreversible inhibitor of COX 1 receptor in platelets itself

-Reduces the formation of thromboxan which reduces platelet aggravation. Patient is less likely to clot

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15
Q

Traditional (non specific NSAIDS)

A

-Blocking COX 1 and COX 2 action

-Stoping gastric protection, platelet function, pain, bone formation, and fever

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16
Q

Selective NSAIDS

A

-Blocks COX-2

-Only inhibits pain, bone formation, and fever

-Maintain Gastric Protection and platelet function

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17
Q

NSAIDS: Non-Selective COX inhibitors

A

asprin
ibuprofin
naproxen
ketorolac

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18
Q

NSAIDS: Selective COX-2

A

celecoxib

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19
Q

asprin

A

-non selective COX inhibitor

-Combined with caffeine is excedrin

20
Q

ibuprofen

A

-most common

-easiest on stomach

21
Q

naproxen

A

hard on kidney

last longer (once day)

22
Q

ketorolac

A

-IV NSAID

-Hard on kidneys

23
Q

celecoxib

A

COX-2 selective inhibitor

-decrease GI side effects

24
Q

NSAID indications

A

-Moderate pain
-Inflammation
-Fever
-Pain

25
NSAID: Non Selective: Side effects
-ASA, ibuprofen, naproxen, ketorolac -Both COX-1 and COX-2 inhibited------prostaglandins and thromboxan synthesis is blocked = analgesia, anti-pryetic and anti-thrombotic -GI upset, stomach ulcers, GI bleeding, rash, edema, kidney failure, increases BP, inhibits platelet aggregation, SOA in asthma patients
26
NSAID: Selective COX-2 Inhibitors: Side Effects
-GI mucosa still protected and platelet function not impacted -No impact/effect on platelets -More serious thrombotic events (More Heart attack and Stroke)
27
Aspirin in not a part of which black box warning list for all the NSAIDS
Cardiovascular Risk
28
Black Box Warnings with NSAIDS
Cardiovascular Risk Gastrointestinal Risk
29
asiprin specific side effect
-Salicylate poisoning/toxicity -Acute: N/V, seizures, cerebral edema -Chronic: N/V, tinnitus -Reyes Syndrome: NO ASPRIN FOR KIDS (rare life threatening illnnes of swelling of liver and brain)
30
Do you give aspirin to kids?
No Reyes Syndrome: -Rare-life threatening -Children <15 who have been given aspirin to treat a-viral infection -Swelling of brain and liver (High mortality rate)
31
ketorolac: Indication
-Most potent NSAID -Given IV or IM -Used to treat acute (short term) moderate to severe pain -Similar to morphine but without respiratory depression
32
ketorolac: Nursing consideration
-Used for 5 days or less -Has a very hard impact on the kidneys and GI tract
33
ketorolac: side effects
GI ulcers and high risk of renal dysfunction
34
acetaminophen: MOA
-Unknown -possible decrease prostaglandin synthesis in the CNS
35
acetaminophen: Indications
-Mild to moderate pain and fever (anti-pyretic) (Hypothalamus)
36
Acetaminophen: Limitations
-Ceiling effect -Non anti-inflammatory properties
37
Acetaminohphen: Side effects
-With normal doses (not really any) -Large amounts (hepatic necrosis = liver failure) -Nephropathy: Jaundice, elevated LFT's and creatinine levels
38
Acetaminophen: Adult dose restriction
4 gams/24 hours -Total of 4 grams per day. Must count normal Tylenol and other medications combinations with Tylenol (will see a question asking if the total Tylenol limit is safe)
39
acetaminophen toxicity and overdose management
-Potentially lethal drug when taken in overdose -Hepatotoxicity: One primary toxic metabolites is detoxifed in the liver by glutathione. Overdose depletes glutathione stores. So the toxic metabolite is able to accumulate in the liver resulting in necrosis
40
Acetaminophen acute ingestion antidote
acetylcysteine (Oral or IV) (Oral makes patients want to puke)
41
acetaminophen and alcohol
-Bad mixture -Chronic alcohol user should limit Tylenol use (Less than 2 grams / 24 hrs)
42
Who should avoid taking aceteminophen
Patients who have hepatitis or liver dysfunction
43
IV aceteminophen
Ofirmev Same MOA Advantage: manage pain with less opioid use with fewer side effects
44
Ofrimev: Indications
Acute pain/post opp Usually in combination with opioids somtimes first IV dose givin at time of incision or pre-opp STILL COUNTED TOWARD Tylenol total
45
Pearls for Practice: non-opioid analgesics
-Can alternate true NSAID's with acetaminophen -Good to give with conjuctnion with opioids for mediate to severe pain -Choose NSAID if inflammation is the causative factor (cut on hand that is inflamed)
46
What opioids do we not want to give with acetaminophen
PERCOCET
47
Liver Disease or a-lot of alcohol
-2 grams/24hrs