Medications used for Management of Pain and Inflammation Flashcards
1
Q
NSAIDs effects
- safeness
- examples
- commonly used for?
A
- generally safe for long-term used; fewer, less severe side effects compared to opioids or steroid
- includes aspirin, ibuprofen (Motrin, Advil), celecoxib (Celebrex), naproxen sodium (nasprosyn), many others
- most commonly used to treat pain
2
Q
how did NSAIDs work generally
A
- Arachidonic acid triggers the release of cyclooxyrgenase which trigger prostaglandins, thromboxane, and prostacyclin
- NSAIDs block the cyclooxyrgenase which decreases some pain and inflammation
3
Q
What two types of substances do NSAIDs work to inhibit
A
- prostaglandins and thromboxane
- both of these substances are produced using cycloxygenase enzyme
- NSAIDs block COX-1 and COX-2 enzymes
4
Q
COX-1 and COX 2
A
- COX-1:
- functions to maintain homeostasis in the cell
- helps maintain GI mucosa, prevents ulcers - COX-2:
- primarily activated during injury;
- also plays an important role in maintain renal function
5
Q
Prostaglandins
A
- activated when cell is injured
- lipid compound
- can be produced by every cell, except RBCs
- most promote inflammation
- a few inhibit inflammation
- means a drug that blocks all prostaglandins production (or inhibits COX) can have variable effects
6
Q
Prostaglandins and injury
A
- prostaglandins seem to mediate the pain response
- increase in prostaglandins associated with increase in pain (esp. PGF2 alpha)
- prostaglandins are pyretogenic - increase fever with system infection/increase body temp
- less frequent with peripheral injury
7
Q
Thromboxanes
A
- also activated when cells are injured
- promote platelet aggregation and clot formation (limit bleeding)
- inhibiting thromboxane (or COX-1) = reduce platelet aggregation and reduced clot formation
8
Q
Asprins and NSAIDs - pharmcokinetics
A
- mostly taken orally
- absorbed in the stomach and small intestine
- biotransformation in the blood (works quickly)
- metabolism: liver
- excretion: kidneys
9
Q
What is aspirin effective at
A
- effective at reducing inflammation, pain, fever, platelet aggregation
10
Q
Describe aspirin’s dose-dependance
A
- the effects of aspirin are dose dependent
- low dose: anti thrombotic
- medium dose: anti-pyretic, analgesic (reduce fever and pain)
- higher dose: anti-inflammatory
11
Q
How does aspirin work as a prolonged anti-platelet action
A
- irreversibly binds to COX-1 in platelets (the more you take the less likely you will clot)
- prevents formation of thromboxane; limits platelet aggregation
- less effective if taken with other NSAIDs
12
Q
What are some other non-selective NSAIDs
A
- they bind to both COX-1 COX-2
- ibuprofen (Motrin)
- Naproxen sodium (Nasprosyn) – takes longer to each therapeutic level, but has longer half-life
- indomethacin – used for anti-inflammatory effect
- Ketorolac (toradol) – used for pain
- Meloxicam (Mobic) – long half-life, taken once per day
13
Q
Aspirin & NSAIDs - side effects
A
- GI upset: gets absorbed/COX-1 helps w/ gastric secretion
~ risk of gastric hemorrhage or ulcer
~ less with use of COX-2 selective drugs - Risk of hypertension with chronic use
~risk higher if pt. already has HTN - Increased risk of liver and kidney damage eps. in pts who already have impaired live or kidney function
~related to inhibition of prostaglandins - may impair healing, esp. of bone and cartilage (due to inhibition or prostaglandins)
14
Q
COX-2 selective NSAIDs
A
- Should better target pain and inflammation, reduce GI upset
- but: all have risk of adverse events, esp. heart attack or stroke, renal dysfunction – because it affects kidney
- celecoxib (Celebrex)
~ others taken off market
~ includes black box warning
15
Q
Acetaminophen (Tylenol)
- general effects and side effects
A
- as effective as NSAIDs of reducing pain and fever is non-steroidal
- no or little anti-flammatory properties
- less gastric upset
- can damage liver (metabolism almost completely) with prolonged use and/or high doses
- most common cause of acute liver failure in US
16
Q
Synthetic corticosteroids: effects/how it works/examples
A
- potent anti-inflammatory properties
- block production of arachidonic acid metabolites (prostaglandins, leukotrienes, Thromboxanes)
- Block COX-2
- reduces inflammation and pain
- example: dexamethasone, betamethasone, hydrocortisone, fluticasone, prednisone
17
Q
Side effects of corticosteroids/Glucocorticoids side effects
A
- osteoporosis
- hyperglycemia: working on liver
- weakness
- atherosclerosis due to increase plaque
- impaired skin integrity (dry and thin)
- hypertension
- glaucoma
- like having a stress response
18
Q
How do opioids reduce pain and when should they be used?
A
- affect pain perception not the cause
- alter nervous system transmission of pain information
- should be used for moderate to severe pain that is daily constance
- post surgical traumatic or sometimes for chronic pain and cancer
19
Q
Other uses of opioids
A
- prior to general anesthesia
- control cough
- control severe diarrhea –GI is active but opioids slow it down
20
Q
Opioids of pharmacokinetics: administration, distribution, metabolism, excretion
A
administration
- enteral (usually oral; can be rectal)
- IV or IM
- transdermal eg patch (fentanyl)
- iontophoresis, lozenges
- pumps, infusions
- patients controlled analgesia = when you feel pain they can click it to admin limited with clicks
- distribution: amount all tissues
- metabolism: mainly in liver (also in kidney, lungs, CNS)
- excretion via kidney
21
Q
Effects of opioids on pain/pain transmission
A
- affect neurotransmitter release presynaptically how many NT released
- postsynaptically, hyperpolarize neuron –harder to fire
- harder to elicit action potential
- nerves don’t respond to pain as easily
22
Q
Strong opioid agonist
A
- use to treat severe pain
- strong affinity for u receptor in CNS (Spinal cord, brain)
that modulate pain and function in CNS - includes morphine, fentanyl
23
Q
mild to moderate opioid agonist
A
- lower affinity to pain receptors
- effective for treating moderate pain
- induces codeine, hydrocodone, oxycodone
24
Q
Mix Agonist-antagonists
A
- agonist for some pain receptors (kappa), antagonists for others a strong CNS receptor
- fewer side effects
- decreased risk for addiction and fatal overdose
- may produce more psychotropic side effects
- hallucinations, vivid dreams
- includes buprenophrine, pentazocine
- not used as commonly used during known addiction
25
Q
Side effects of opioid medications
A
- in general, opioids slow down processes
- sedation
- respiratory depression
- orthostatic hypotension
- constipation
26
Q
Considerations when using an opioid
A
- start with mild-to-moderate agonist
- use strong agonist only as needed
- for chronic pain, must weight risks vs benefits
- consider quality of life esp. severe disease
- patients may due better if they follow a dosing schedule vs waiting until they have pain
27
Q
Addiction
A
- personal takes medication to receive “high” euphoric feeling from taking drug – sedation
- high may not correlated with physiology responses e.g. pain reduction
28
Q
tolerance: body
A
body uses drug more quickly
29
Q
opioid antagonist
A
- blocks opioid receptors
- used to treat opioids addiction and overdose
- naloxone used to treat overdose (IM or nasal)
- naltrexone used to help with addiction treatment (not a strong but will block receptor)
~creates opioid-free state
~ other meds: methadone, buprenorphine
30
Q
Neonatal abstinence syndrome
A
- infants born to mother who are addicied to opioids
- experience withdrawal symptoms
- often require medication to manage symptoms
- may affect development
- associated with later behavior problems
31
Q
opioid-induced hyperalgesia
A
- income patients, pain is increased once pt. stops taking opioid
- in some patients, pain is increased when pt. takes opioid
- importance of monitoring pain levels
- consider alternatives (exercise hypoalgesia)
