Pain and inflammation Flashcards

1
Q

NSAIDS

Cox 1 inhibitors

A

Stimulates release of protective prostaglandins (protect gastric mucosa, enhances platelet aggregation, maintain kidney function)
o When you block cox 1, these protective effects don’t take place, at risk for renal dysfunction, GI ulcers, bleeding

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2
Q

NSAIDS

Cox 2 inhibitors

A

Stimulates release of prostaglandins related to injury and causes inflammation, pain, fever
o Cox 2 blocked, analgesia, anti-inflammatory, antipyretic, pTT aggregation, and vasoconstriction.
 LOX- stimulate leukotriene release

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3
Q

 aspirin (ASA- acetylsalicylic acid); ibuprofen (Motrin); naproxen (Aleve), indomethacin (Indocin); ketorolac (Toradol)

Cox 1 inhibitors

A

 recognize that ASA is in a class of its own. As a salicylate, it has effects of decreasing platelet aggregation unlike the rest. It is generally no longer given for the treatment of pain, but instead for its antiplatelet properties.

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4
Q

Which NSAID is the only one considered cardioprotective?

A

aspirin

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5
Q

NSAID

NC

A

• Adverse Effects are all related to the inhibition of Cox 1 and 2.
 GI upset and or ulceration:
o Most of the tablets will come EC or SR – do not chew or crush
o Consider PPI—Proton pump inhibitor. Anything that ends in -prazole
 Asthma Exacerbation:
o Blocking Cox 1 and 2, body makes excess LOX which causes release of leukotrienes. Increases asthma exacerbation.

 Bleeding: ibuprofen doesn’t cause too much ptt aggregation at lower doses. Does cause issues at higher doses. Coffee ground emesis, black stools

 Reye’s syndrome: Give Tylenol for children w/ viral infections to avoid risk of Reyes syndrome. Causes liver and brain swelling. More risk if viral and not bacterial

 Renal: BUN, Cr baseline levels, watch trends. Not recommended for pts with renal insufficiency.

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6
Q

• Salicylism (Aspirin Overdose):

A

 Initially respiratory alkalosis leading to respiratory depression and acidosis. Hyperthermia, sweating, dehydration, electrolyte imbalance. Will eventually lead to coma and ultimately death from resp failure., tinnitus, loss of hearing, sweating***
 Lethal dose for adults is 20-25 gm
 Lethal dose for children can be as little as 4 gm

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7
Q

• Salicylism (Aspirin Overdose): treatment

A

 Focuses on respiratory support, cooling (for hyperthermia), fluid replacement, hemodialysis if needed.
 Bicarbonate can be given to correct resp acidosis.
 Activated charcoal may be given to decrease absorption.
 Perform gastric lavage within 1 hr. of ingestion

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8
Q

Cox 2 inhibitor

Celecoxib

A
Platelet aggregation
Increases risk of stroke and MI
Only one on the market
increases bleeding w patients on warfarin, steroids, ETOH
Cross allergy to sulfa
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9
Q

Acetaminophen overdose

A

o Based on body weight, will vary based on amount of Tylenol they took.
o Will give predetermined amounts in 3 stages.
 150mg/kg over first hour
 50 mg/kg over next 4 hours.
 100mg/kg over next 16 hours.

Acetylcysteine

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10
Q

Acetylcysteine other uses

A

Mucomist-decreases mucus
Prevention of further kidney complications in patient receiving dye.
Tylenol overdose

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11
Q

Centrally acting nonopioids

A

Tramadol

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12
Q

Tramadol

NC

A

• Avoid concurrent use w/ antidepressants and patient will have increased risk for serotonin syndrome (increases serotonin reuptake)

sedation, dizziness, urinary retention, seizures w/ known seizure disorders (decreases seizure threshold)

Oral med, should give 1 hr before treatment.

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13
Q

Opioid receptor locations

A

Head, GI tract, Heart

give morphine to decrease myocardial 02 demand.

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14
Q

opioid overdose

A

Naloxone-
 Initially 0.1-0.2 mg IV repeated every 2-3 mins until adequate response
 Give slowly over 30 sec- can cause cardiac arrhythmias if given too quickly, also withdrawal, cardiopulmonary edema

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15
Q

What could happen if you give naloxone or naltrexone to a chronic opioid user?

A

They can go straight to withdrawals.

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16
Q

opioid agonist-antagonist

A

buprenorphine, nalbuphine

17
Q

bupenorphine

nalbuphine

A

B: treatment of opioid dependence, can cause withdrawal
N:treatment of itching symptoms of opioids.

18
Q

Opiate withdrawal symptoms

A
Early: 
anxiety, muscle aches, agitation, insomnia, sweating
Late:
Abdominal cramping
diarrhea
dilated pupils
nausea and vomiting
19
Q

opioid AE

A

• Depressed respiration, hypotension, bradycardia, constipation, urinary retention, N/V, pupils should constrict, if they are dilated, they are close to dying.

• Interact w/ all other CNS type depressants—increase all effects
• Pregnancy Risk Category D in (long term or high dose use, or 3rd trimester)
• Interventions include: Monitor vitals, bp, hr, rr,
o RR below 12 stop administering them and stimulate
 Depends on situation but may give Narcan
o Give something for nausea, constipation
o Do not chew or crush unless immediate release, usually controlled release.

20
Q

Steroids

A

prednisone, hydrocortisone, methyprednisolone

-sone, -lone

21
Q

Steroid theraputic use

A
  • Inflammatory disorders (arthritis, COPD, etc.)
  • Autoimmune disorders (RA, SLE, etc.)
  • Allergic reactions
  • Immunosuppression for organ rejection
22
Q

Steroid

NC

A

• Adrenal insufficiency & Myopathy: may have muscle aches. Sign that adrenal insufficiency is starting. May need to adjust dose.

• Infection: Immunosuppressants
• Hyperglycemia: Impaired glucose metabolism, insulin resistance.
• Fluid and Electrolyte disturbance: Hypernatremia & Hypokalemia: more often with drugs considered mineral corticoids. May see it with glucocorticoids too.
• Psychologic disturbances
a. From stopping too fast (hpa access)
b. Super high doses.
• Cataracts and glaucoma increased risk
• Ulcers: May give with food, give PPI
• Teach on taper/dose regimen
• High WBC—can’t lay down when on steroids so they are just floating around.
• Dose and length of therapy dependent.
• Thin skin: bruise easily, rip skin
• Too little: addison’s disease, too much cushings disease.

23
Q

steroid (cushing syndrome)

A

• Cushing’s Syndrome: Weight gain (trunk/face, but not limbs), “moon” face, “buffalo hump”, thinning of skin, bone loss (osteoporosis)—bones can’t lay down new cells.

24
Q

Steroid stress dosing

A

a. Acute event happening, body’s natural response is asleep, have to increase dose during these times.

25
Q

Allopurinol Probenecid, colchicine

A

Treats hyperuricemia

26
Q

Allopurinol Probenecid, colchicine

A

• AE: agranulocytosis and skin disorders such as SJS (steven Johnson syndrome)
• Teach about Purine diets and limiting intake to improve possible
• Monitor for hypersensitivity syndrome (fever, rash, liver & kidney dysfunction)
• Monitor CBC, BUN/Cr, Uric acid levels
• Encourage 3L/day fluid intake
Take with food, lots of nausea,
can cause kidney failure
lots of nausea

27
Q

colchicine

A

• Colchicine increases risk of rhabdo, don’t give with statins.
• Colchicine-GI and myopathy, first stages of toxicity
a. 2nd stage-bone marrow suppression, with that comes multiple organ failure.
b. 3rd stage-renal and hepatic failure.

28
Q

Migraine meds

A

Sumatriptan, ergotamine

HTN, cardiac events, chestpain

29
Q

Sumatriptin

A

 Activates 5HT causing vasoconstriction and therefore suppresses inflammatory response
 Not used for prevention, except for before menses
 SL, SQ, PO, or nasal; each route has different max doses. Typically take initial dose and then repeat if needed. Schedule and dosing limits vary based on route
 Can cause chest pressure d/t coronary vasospasm- watch if cardiac hx

30
Q

ergotamine

A

 Can alter transmission at sertonergic, dopaminergic and alpha-adrenergic junctions.
 Considered 2nd line treatment after SSRA
 Generally well tolerated w/ some nausea possible