Meds to control pain

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Author:
Prittyrick
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276683
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Meds to control pain
Updated:
2014-06-13 21:25:09
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pharm
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Fun stuff...no pain no gain
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  1. Assessment of Pain
    Pain is what the person says it is. 

    • Pain is subjective and personal
    • the most reliable method is to have the patient describe his/her pain experience
    • pain rating scale
    • PQRST
    • PAIND
  2. PQRST
    P- Provacation/Palliative (what makes it worst or better)

    Quality- how would u describe it

    • R- region where is the pain does it move
    • radiating


    A- severity

    T- timing
  3. Non Pharm
    • relaxation
    • changing position
    • distraction 
    • guided imaginery
    • massaging
  4. PAIND pain rating scale for patients
    • This is for confused
    • look at vital signs
    • restlessness
    • body language
    • show pain in other way
    • bp up HR up
  5. Analgesic Ladder
    • 1st for cancer management
    • mild to severe
    •  
    • Step 1- non opiods

    Step 2- less opiods

    Step 3- greater opiods

    broken down into levels used for all pain management
  6. Analgesic ladder levels
    • Level 1- mild to moderate pain
    • - 1-3
    • - non opiods, tylenol, mortrin, adjunct as well for anxiety

    • Level 2- moderate pain
    • - 4-6
    • - weaker opiods
    • - percocets- tylenol and codiene 
    • - lesser agent with a narcotic (lesser amounts)


    • Level 3- severe pain
    • - pain >7
    • - stronger opiods
    • -demorl, morphine


    • play by ear- stop and think what is going on
    • this gives u an idea
    • u will know where to start.
  7. Opiates agonist
    Treat: moderate- severe

    Ex: demorol, Morphine, dilaudid
  8. Opiates MOA
    • Stimulates opiate receptors in the CNS
    • Mu, Kappa, and delta- work on pain to reduce pain
    • Sigma- mood and anxiety- helps with this
    • (these are opiates receptors)
    • Increases the effect of the opiate (mimic action of opiate)

    • Binds the opiat receptors and mimics the action of endogeous opiate peptides
    • - decrease the release of Substance P (pain mediator)
    • - Decreses the transmission of pain
    • - changes the perception of pain (sigma- mood)
  9. Opiates agonist other actions, CI
    • Dilation of blood vessels in the head and neck
    • suppression of the cough center (codiene suppresses cough)
    • decreases the gi/gu muscle- increase constipation

    • CI- relieves moderate to severe pain, acute and chronic pain, decrease anxiety, augment sedation and anesthesia
    • decrease cardiac workload, treat pulmonary edema and CHF
    • Because it vasodilates and reduces the amount of blood that goes back to the heart.
  10. Opiates agonist SE
    • Respitory depression- most serious (higher doses- hod if rr less than 12)
    • Orthostatic hypotension- b/c drug vasodilates
    • cough supression- u want to cough to clear secretion- respiratory secretion (pneumonia)- cough and deep breath, incentive spirometor
    • constipation
    • urinary retention
    • emesis- stimulates the CTZ
    • Euphoria/sedation- b/c it stimulates the sigma
    • miosis- constictions
    • decrease renal blood flow
  11. Opiates agonist NI
    • assess for pain
    • assess RR and BP
    • assess for precautions to use- se hold med
    • pt teaching- increase fluids, encourage coughing, 
    • drug interaction- drugs causing CNS- sedation/depression
    • assess toxicity- overdoses LOC changes
    • Antidote- Narcan
  12. Opiod Analgesics
    • MS Contin
    • - controlled release
    • - CI for chronic
    • continuous release

    • Fentanyl
    • - Transdermal system (patch)
    • - chronic pain
    • - moderate to severe pain
    • - can use with another med
    • SE- CNS sedation, respiratory depression
    • - 24 hour for full effect to occur (pt may still need to take the short term agent)
    • - patch can stay on for 72 hours (q 3 days change patch
    • -wear gloves
    • - dispose needle box (controlled area)
    • - tell pt to properly throw away seperately
  13. Prostagladins Formation
    Fever pain and inflammation

    Produced from phospholipids and are release when cell has trauma
  14. Prostagladins Production
    • Cell
    • phosopholipids get release- released, phospholipase (enzyme converts P to arachidonic acid)
    • than it converts to Arachidonic Acid- 
    • cyclooxygenase (this enzyme helps to convert into prostagladins)

    arachidonic acid- can turn into prostagladin or Thromboxone A- causes platelets to aggregate (cluster together)

    • Cox 1- found in all tissue, protects the GI mucosa, decrease acid, increases cyprotective membrane, Vasodilation, increase blood flow, helps to promote platelet aggregation (increase the risk of forming a clot), supports renal function
    • Cox 2- works on pain

    Cox- is an enzyme that needed to convert an non active substance to prostagladins
  15. Salicylates 1st generation NSAIDS
    • Non selective
    • - blocks Cox 1 &2 (cox 1 cox 2 inhibitor)
    • - Aspirin 
    • GI upset- bleeding, gi upset bc
    • when we block Cox 1 we block prostagladins. 

    • Cox 1 plays a role with Throm A- if u block cox 1 u will bleed because ur blood is not clotting
    • bc of this we get PUD and gastric ulcer
    • Works on cox 2- decrease pain

    MOA: Blocks Cox. and Throm A in the CNS and PNS

    results- decrease inflammation, pain, fever, and suppress platelet aggregation bc if blocks Throm A

    MOA:
  16. Salicylates NSAIDS CI
    • to reduce inflammation- decrease prosta.
    • mild to moderate pain- de prosta
    • decrease fever- blocks Cox 2 de prosta
    • suppresion of platelet aggregation (TIA ischemia attack, CVA, MI)- blocks Throm A (low dose aspirin helps to keep platelets from clustering and blood flows easily)

    • SE: GI (block COX 1 loss protetive function), bleeding, renal insufficiency, 
    • salicylism- overdose/toxicity 1st s/s tinnitus (reversible)
    • Reyes Syndrome- we dont see much, viral infection- tends to be in children and it caused brain damage. we dont see this often because we don't give to children anymore
  17. Salicylates NSAIDS NI
    • Accurate pain assessment
    • assess allergy 
    • Drug interaction- OTC becareful of other drugs that can cause bleeding
    • 1 week prior to surgery tell pt to stop aspirin bc bleeding
    • take with food to decrease GI upset.
  18. NSAIDS (non steriodal inflammatory drug)
    Non Selective Inhibitors
    Ex: Motrin (ibuprofen), Naxproxen

    • MOA: The inhibit prostagladins synthesis
    • Differetn NSAIDS disrupt the synthesis at different stages
  19. NSAIDS CI SE NI
    CI: antiflammatory, analgesic (mild to moderate pain, antipyretic

    SE: GI upset, increase risk for PUD, GI bleed, renal insufficiency, hypersensitivity 

    • NI: accurate pain assessment
    • increased risk of SE with elderly
    • drug interaction- other drugs that can increase bleeding
    • GI upset take with meals
  20. NSAIDS (naproxen, toradol (ketoroiac Tromethamine))
    • naproxen- pain related to joint disease (ortho)
    • high risk GI upset- nausea, PUD (u can take a PPI, H2), multiple drug interactions

    • Toradol (ketoroiac tromethamine)
    • short term pain relief (post op)
    • administer IV, IM
    • equal to demorol with fewer SE
    • SE: GI
    • Administer no more than 5 days after 5 days increase the risk of renal disease. 
    • starts to work with in ten minutes
  21. Cyclooxgenase 2 inhibitors
    selective inhibitor
    they keep the protective GI, and does not aggregate the platelets

    • Selective anti-inflammatory
    • reduce pain, inflammation, keep protective membrane
    • less GI bleeding and SE

    Ex: Celebrex

    MOA: inhibits Cox 2 enzyme blocker, decrease prostagladin synthesis

    • CI: mild, moderate pain, anti inflammatory
    • leep proctective effect in the GI
    • no platelet aggregation
  22. Cox 2 inhibitor Cerebrex SE, NI
    • SE: less GI upset and bleeding s/e than NSAIDS
    • headache, dizziness

    • NI: accurate pain assessment
    • allergy to Sulfa or aspirin bc it will increase the risk hypersensitivity
    • admin with food
    • drug interaction
    • more expensive
  23. Para Aminophenol Derivatives
    ex: acetaminophin (tylenol)

    MOA: selective prostaglandins inhibition in the CNS

    CI: analgesia (mild-moderate pain), antipyretic
  24. Para Aminophenol Derivatives SE NI
    • SE: rare at therapeutic- large dosage can cause liver damage
    • Usually less than 4g in 24 hours

    • NI: accurate assessment of pain
    • pain teaching
    • antidote: mucomyst (tylenol toxicity) helps to prevent liver damage (helps with not metabolizing the drug in the liver)
    • becareful of other agents that have tylenol
  25. Adjunct pain relief
    • neurontin- (Gabapentin)
    • use of chronic pain, neuropathic pain
    • MOA: not fully understood
    • SE: CNS
    • PTSD, Bipolar
    • well tolerated

    Tricyclic antidepressants, anticonvulsants- neuropathic pain- help decrease nerve transmission


    Glucocorticoids- decrease inflammation, decrease intracranial and intraspinal pressure- decrease pain
  26. Drugs affecting muscle spasms and spasticity
    • Muscle spasm: sudden involuntary contraction of a muscle or group of muscles
    • - work varies points either on the muscle or the CNS to decrease pain and spasm
    • - acute trauma, skeletal muscle imjury, electrolyte imbalance
    • - treated with centrally acting muscle relaxants, anti inflammatory agents, PT

    • Spasticity certain muscles are continously contracted
    • - damaged to the brain, SC
    • - treated with Spasmolytics
  27. Centrally Acting Muscle Relaxants
    Ex: Flexeril (cyclobenzapine)

    MOA: centrally acting- works in the CNS causes CNS depression, decreases nerve transmission at the spinal cord

    SE: CNS

    • NI: accurate assessment
    • assess safety
    • assess for CNS depression
    • drug interaction with other CNS depression
    • optimal effects in 1-2 weeks (not immediate)
    • short term- do not use longer than 3-4 weeks
  28. Centrally Acting muscle relaxants

    baclofen
    ex: Baclofen 

    • MOA: precise mechanism is unknown
    • works on GABA increase at the motor neurons to decrease impulses

    • CI: Skeletal muscle relaxant, muscle spasms, spinal spasticity 
    • Drug of choice for spasticity
    • baclofen pump- pt with spinal cord injury. inserted pump under the skin
  29. Centrall acting muscle relaxants SE NI
    • Se: CNS- drowiness, headache dizziness
    • other- gi, myalgias, tremors, ataxia, visual disturbances, hyperglycemia

    • NI: accurate assessment
    • titrate dose to control SE
    • assess safety needs
    • can increase the risk of seizures- reduced the seizure threshold
    • abrupt withdrawl: hallucinations, seizures, drug interactions CNS
  30. Direct acting Muscle relaxants
    Ex: dantrolene (dantrium)

    MOA: direct affect on skeletal muscle fibers. it interfers with the amount of ca released from the sacroplasmic reticulum

    CI; relief of muscle spasms, spasticity
  31. Directing acting muscle relaxants SE NI
    • SE: most common is muscle weakness
    • other Gi upset
    • drowiness, dizziness (low) bc doesnt work on CNS 
    • hepatoxicity

    • NI:
    • accurate assessment
    • low doses and titrate up to reduce se
    • safety concerns- risk for falls
    • drug interaction 
    • drug effects usually seen 1-2 weeks
    • administer with food to decrease gi upset

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