advance pharm exam 1

neuropathic pain

A type of chronic pain that results from damage to the nervous system, characterized by burning or shooting sensations. It's often challenging to treat and may require specific medications like anticonvulsants or antidepressants.

nociceptive pain

A type of pain that is caused by the activation of pain receptors in response to tissue injury or inflammation. physical pain

timeline of acute pain

less than 3 months

timeline of chronic pain

greater than 3 months

what type of pain do you feel throughout entire treatment course

cancer

patio: Afferent nerves

send signal to brain

patio: CNS

localizes pain

patho: efferent nerves

modulate responses from the brain to the body, transmitting signals that can affect pain perception and motor function.

transmission of pain step 1

step 1: afferent fibers synapse of spinal cords dorsal horn

transmission of pain step 2

neurotransmitters are released ( glutamate, substance p, calcitonin, K/H, etc)

transmission of pain step 3

pain impulses go through ascending pathways to the thalamus and brain stem

transmission of pain step 4

Descending pathways modulate pain perception.

NSAIDS

aspirin

naproxen

ibuprofen

celecoxib

ketorolac

topical diclofenac

lidocaine

mild pain 1-3

acetaminophen +- NSAID

moderate pain 4-6

NSAID+- Opiod +- adjunct

serve pain 7-10

opioid +- adjunct

acetaminophen MOA

inhibits synthesis of prostaglandins in the CNS wha

what are prostaglandins

Prostaglandins are lipid compounds derived from fatty acids that have various roles in the body, including mediating inflammation, pain, and fever. They are synthesized at sites of tissue damage or infection and play a crucial role in the body's healing process.

starting dose for acetaminophen

is typically 650 mg to 1000 mg every 4 to 6 hours for adults, not exceeding 4000 mg per day.

if a pt have liver disease what is their max dose

2000mg

risk for acetaminophen

liver damage

acetaminophen antidote

Acetadote

cox 1 pathway

protective pathway for GI, kidney lung, platelet aggration, and vasoconstriction

cox 2 pathway

pathway associated with inflammation, pain, and fever reduction.

aspirin MOA

irreversibly binds to cox 1 and cox 2 pathways

anti platelet is irreversible

characteristics of aspirin

analgesic, anti-inflammatory, antipyretic, and anticoagulant effects.

NSAID adverse effects

cardio: fluid retention, hypertension, edema

GI: ulcers, bleeding, perforation, irritation

resp: bronchospams

skin: rash

renal: insufficiency or failure

what pts should avoid NSAIDs

gi bleeds

CV

renal pts

asthma

PREGNANCY

allergies

renal pts on NSAIDS need to be sure not to mix with which drug classes

Diuretics and ACE inhibitors.

what is the purpose of ketorolac ( toreadol)

moderate to serve pain treatments ho

how long can a pt be on ketorolac

ONLY 5 DAYS

will increase risks of adverse effects

celecoxib MOA

inhibits cox 2 pathways

therefore protecting the GImucosa from damage and reducing inflammation.

increases risk of platelet aggregation (cox 1pathway)

what pt should avoid celecoxib use

SULFA ALLERGY

which NSAID increases risk of CV events

celecoxib

• cox 2 pathway inhibitor therefore it inhibits anti platelet characteristics and platelet aggregation from cox 1 pathway is unchanged

which NSAIDs has a decreased risk of CV events

naproxen and ibuprofen

• due to dual inhibition because they are non selective nsaids that affect both COX-1 and COX-2 pathways.

which NSAIDs increase the GI effects

nonselective NSAIDs

• aspirin

• ibuprofen

• naproxen

  • ketorolac

purpose of topical diclofenac ( Voltaren)

is to reduce localized pain and inflammation in conditions such as osteoarthritis and rheumatoid arthritis by inhibiting the COX enzymes locally.

max dose of topical diclofenac

32 g a day

purpose of lidocaine patch

is to provide localized analgesia by blocking sodium channels and inhibiting nerve conduction in painful areas.

dosing of lidocaine patches

1-3 patches

remove after 12 hours

purpose of capsaicin cream

not an NSAID

localized chronic pain and neuropathic pain relief.

capsaicin cream dosing

varies; typically applied 3-4 times daily, with initial use requiring consistent application for optimal effect/ slow onset. need 2-4 weeks of use

types of opioid receptors

mu

delta

kappa

what does a Mu receptor produce

it is the main analgesic receptor

it produces strong analgesia, euphoria, and sedation

what are adverse effects of mu

respiratory depression

constipation

physical dependence

what does delta produce

it produces analgesia and regulates mood, as well as affecting emotional responses and reward.

what does kappa produce

it produces analgesia, sedation, and dysphoria.

what are kappa adverse effects

It can lead to sedation, dysphoria, and hallucinations.

meds that are in the class os phenanthrenes

used for acute and chronic pain

morphine

codeine

hydromorphone

oxymorphone

hydrocodone

oxycodone

what are drugs that are in phenylpiperdines

used for sedation, serve pain, preoperative pain

fentanyl

merpiperidine
sufentanil

what drug is in the class of phenylheptanes

used for chronic pain or opioid use disorder

methadone

if someone is prescribed an opioid what other drugs should they combine them with

stool softener and stimulate laxative

mush with push!

what do pts who take opioids constantly not build a tolerance to

mitosis and constipation

morphine starting dose

po= 15-30 mg

iv= 2-4 mg

EVERY 4 HOURS

what are adverse effects of morphine

renal dysfunction bc it is renally eliminated

histamine release can cause itching/hypotension

• hard to tell if pt is actually allergic or simply experiencing SE

hydromorphone ( diluadid) dosing

po= 2-4 mg q4-6 hrs

iv= 0.2-1 mg q2-3 hrs

hydromorphone elimination

primarily non renally excreted so it preferred in renal patients over morphine due to reduced risk of accumulation and side effects.

oxycodone metabolism

has some renal elimination therefore used cautiously in patients with renal impairment.

methadone effects on cardiac

rhythm can cause QT interval prolongation, leading to a risk of torsades de pointes and other arrhythmias. It should be monitored in patients at risk.

methadone metabolism

cleared by the kidneys and liver, primarily through CYP450 enzymes. adjust dose in renal pts. methadone has a long half life

methadone serotoninergic effects

can include increased risk of serotonin syndrome, particularly when used with other serotonergic medications. use cautiously with pmh of seizures

meperidine pearls

• BLACK BOX

• renally eliminated and can accumulate active metabolite normeperidine warning for seizures, anxiety , and tremors

• serotonergic effects so be cautious with other serotonergic agents.

what king of drag is codeine

pro drug and a weak opioid

must be converted to morphine in the liver in order to be active by enzyme CYP2D6. if pt does not have this enzyme then analgesic property will not work

hydrocodone is available in what form only

po

what kind of drug is hydrocodone

pro drug that requires conversion to hydromorphone with enzyme cyp2d6 in liver

used for moderate to severe pain

what kind of drug is fentanyl

potent synthetic opioid making it very easy to make and bioavailabile

how is fentanyl metabolized

Fentanyl is primarily metabolized in the liver by the CYP3A4 enzyme, which converts it into inactive metabolites.

adverse effects of fentanyl

bradycardia

chest rigidity

serve respiratory depression nausea, vomiting, sedation

why does fentanyl work so quickly

it is highly lipophilic, allowing it to rapidly cross the blood-brain barrier.

starting dose for fentanyl

iv= 25-50 MICROGRAMS q2-3 hrs

tramadol MOA

Tramadol works by inhibiting the reuptake of serotonin and norepinephrine, and also binds to opioid receptors, providing analgesic effects.

metabolism of tramadol

liver

opioid considerations in older adults

start 25-50 % lower than adult doses

CNS effectsmay be amplified; monitor closely for sedation and respiratory depression.

what are preferred opioids in older adults

oxy and hydromorphone

what opioids to avoids in renal pts

morphine

codeine

meperidine

what opioids are preferred in renal pts

hydromorphone

hydrocodone

fentanyl

what opioid is preferred in advanced liver disease

fentanyl

buprenorphine moa

binds to mu receptors in cns and acts as a partial agonist, providing analgesia while also inhibiting opioid receptors.

what is buprenorphine mainly used for

moderate to serve pain and opioid use disorder

naloxone moa

Naloxone works by competitively binding to opioid receptors, effectively reversing the effects of opioid overdose.

why would naloxone may need to be repeated

because its duration of action is shorter than that of many opioids, leading to potential recurrence of respiratory depression or overdose effects.

naltrexone Moa

Naltrexone works by antagonizing opioid receptors, preventing the effects of opioids and reducing cravings in individuals with opioid use disorders.

naltrexone metabolism

Naltrexone is primarily metabolized in the liver and must be watched for liver toxicity due to its potential to cause hepatotoxicity, especially with higher doses or prolonged use.

PAMORAs MOA

PAMORAs (Peripherally Acting Mu-Opioid Receptor Antagonists) work by selectively blocking mu-opioid receptors in the gastrointestinal tract, thereby alleviating opioid-induced constipation without affecting central analgesia

DOES NOT CROSS BBB

names of PAMORAs

include methylnaltrexone, naloxegol, and naldemedine.