PAIN Flashcards
Pathophysiology of acute pain
acute pain usually occurs in response to tissue injury, results from activation of peripheral pain receptors and their specific A delta and C sensory nerve fibers (nociceptors).
Pathophysiology of chronic pain
Chronic pain related to ongoing tissue injury is presumably caused by persistent activation of A delta and C sensory nerve fibers (nociceptors).
However, the severity of tissue injury does not always predict the severity of chronic or acute pain. Chronic pain may also result from ongoing damage to or dysfunction of the peripheral or central nervous system (which causes neuropathic pain).
Consequences of poorly controlled pain
Inadequately managed pain can lead to adverse physical and psychological patient outcomes for individual patients and their families.
Continuous, unrelieved pain activates the pituitary-adrenal axis, which can suppress the immune system and result in postsurgical infection and poor wound healing.
Sympathetic activation can have negative effects on the cardiovascular, gastrointestinal, and renal systems, predisposing patients to adverse events such as cardiac ischemia and ileus.
Of particular importance to nursing care, unrelieved pain reduces patient mobility, resulting in complications such as deep vein thrombosis, pulmonary embolus, and pneumonia.
Postsurgical complications related to inadequate pain management negatively affect the patient’s welfare and the hospital performance because of extended lengths of stay and readmissions, both of which increase the cost of care
Evaluation of pain: assessment of severity of pain and monitoring responseto analgesia
Taking a pain history
Several tools provide a numeric rating of pain intensity (e.g., visual analogue scale, numeric rating scale (NRS)).
Simpler tools such as the verbal rating scale, which classifies pain as mild, moderate or severe, also are commonly used.
For patients with limited cognitive ability, scales with drawings or pictures are available
Outline approach to management of chronic non-cancer pain
MILD
first be treated with acetaminophen or a nonsteroidal antiinflammatory agent (NSAID).
This Step 1 of the ladder also states that this analgesic may be combined with an adjuvant drug that provides additional analgesia (ie, a so-called “adjuvant analgesic,” such as an analgesic antidepressant drug for neuropathic pain), treats a side effect, or manages a coexisting symptom
Outline approach to management of chronic non-cancer pain
Patients with moderate to severe pain
Step 2 drugs were previously designated with the misnomer “weak” opioids (with codeine as the prototype) and step 3 drugs were designated “strong” opioids (morphine as the prototype). On both steps 2 and 3, the approach indicates the potential for benefit with combination therapy that includes an NSAID or other drugs to enhance analgesia or treat side effects.
Pain management in elderly guidelines
The AGS guidelines recommend acetaminophen as the initial (first-step) and ongoing pharmacotherapy for pain management; opioids are recommended for the treatment of moderate-to-severe pain, and adjunctive analgesics are to be used for patients with specific pain types, such as neuropathic pain. The guidelines recommend that analgesics such as NSAIDs, corticosteroids, and TCAs be avoided due to their potential to cause AEs and worsen certain disease states.
Pain management in pregnancy
acetaminophen as a first line drug. Acetaminophen (category B) provides similar analgesia as nonsteroidal medications without the antiprostaglandin or platelet inhibition effects of NSAIDS. Antiprostaglandins, such as aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), are typically contraindicated throughout pregnancy
Opiods with conderation for withdrawal in newborn
pain management in children
Cognitive and behaviour interventions such as pain neuroscience education, activity pacing, relaxation, distraction, mindfulness, sleep hygiene o Psychological interventions such as cognitive-behavioural therapy, acceptance and commitment therapy o Physical treatments such as physiotherapy, occupational therapy, interventional procedures (e.g. nerve blocks) o Pharmacologic: acetaminophen (paracetamol), non-steroidal anti-inflammatory drugs, opioids, antidepressants, anti-epileptic drug
How to Manage Pain in Patients with Renal Insufficiency or End-Stage Renal Disease on Dialysis?
Safe nonopioid options for pain management in renally impaired and dialysis patients include acetaminophen and certain NSAIDs, such as ibuprofen.
Fentanyl, hydrocodone, and hydromorphone are the safest opioids to use in renally impaired and dialysis patients.
Tramadol in lower doses may also be safely used in renally impaired and dialysis patients.
Low-dose gabapentin and lidocaine patches can be safely used as adjunctive therapy in renally impaired and dialysis patients; TCAs may also be used in lower doses in renally impaired patients
Pain management in hepatic disease
Paracetamol is safe in patients with chronic liver disease but a reduced dose of 2-3 g/d is recommended for long-term use. Non-steroidal anti-inflammatory drugs (NSAIDs) are best avoided because of risk of renal impairment, hepatorenal syndrome, and gastrointestinal hemorrhage. Most opioids can have deleterious effects in patients with cirrhosis. They have an increased risk of toxicity and hepatic encephalopath
pain management in pulmonary disease
NSAIDs — including Motrin, Naproxen, and aspirin
Opioids — including morphine, codeine, and topical analgesics like Capsicum.
Pain mx. in trauma
Include acetaminophen (APAP) and nonsteroidal anti-inflammatory drugs (NSAIDs) in pain management unless contraindicated. z Opioids are the standard comparison for effectiveness of pharmacologic analgesics to treat acute, severe nociceptive pain; however, their use may be limited by central nervous system and respiratory depression, as well as ileus and tolerance. z Overreliance on opioids, specifically as monotherapy for analgesia, may contribute to opioid dependence
Pain in burns
Ketamine has special place for procedural pain in children but requires monitoring
Opiod MOA
There are three major classes of opioid receptors being δ-opioid, κ-opioid and μ-opioid. Opium will generate an agonist activity which will later open the potassium channels and prevent the opening of voltage-gated calcium channels. This activity causes a reduction in neuronal excitability and inhibits the release of pain neurotransmitters
Pharmacokinetic and pharmacodynamic principles, of opioids
Morphine has a considerably slower transfer between plasma and effect site. It appears therefore to be quite unsuitable for short-term interventions. The time to build up the effects is longer and, more importantly, the effects persist for a longer time than those of alfentanil or fentanyl. On the other hand, when longer effects are desired, morphine will require less attention to short-interval or continuous dosing, and for long-term therapy, the slower equilibration-time is no problem.
Opioid SEs
Sleepiness
Constipation
Nausea
Shallow breathing
Slowed heart rate
Loss of consciousness
Paracetamol MOA
inhibiting two isoforms of cyclooxygenase, COX-1 and COX-2, which are involved in prostaglandin (PG) synthesis. Prostaglandins are responsible for eliciting pain sensations.13 Acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, therefore, has no peripheral anti-inflammatory effects
Paracetamol pharmacodynamics
Antipyretic and analgesic effects
SEs of paracetamol
nausea, vomiting, constipation
NSAIDS MOA
inhibition of the enzyme cyclooxygenase (COX). Cyclooxygenase is required to convert arachidonic acid into thromboxanes, prostaglandins, and prostacyclins
NSAID adverse effects
indigestion – including stomach aches, feeling sick and diarrhoea.
stomach ulcers – these can cause internal bleeding and anaemia; extra medicine to protect your stomach may be prescribed to help reduce this risk.
headaches.
drowsiness.
dizziness.
allergic reactions
Drug interactions with NSAIDS
reduce the efficacy of antihypertensives, with a poor control of blood pressure
interfere with the angiotensine converting enzyme (ACE) inhibitors directly and indirectly by decreasing renal prostaglandin synthesis and by reducing ACE inhibitors‐induced prostaglandin synthesis.
Also, NSAIDs decrease the efficacy of diuretics by reducing their natriuretic effect
NSAIDs inhibits the clinical benefits of aspirin
Several NSAIDs have been found to reduce renal clearance of methotrexate, which could generate toxic events (renal failure, pancytopenia
Opioid tolerance
In response to long-term exposure to relatively high doses of exogenous opioids, cells internalize their mu and delta opioid receptors. Therefore, increased opioid levels and/or increased opioid potency are necessary to generate the same effect on fewer receptors
Opioid withdrawal
Similarly, once the exogenous opioids are removed from the system (tolerance), the remaining endogenous opioids are unable to sufficiently activate the small number of remaining receptors
Who should not take a Non-Steroidal Anti-Inflammatory Drug (NSAID)?
if you had an asthma attack, hives, or other allergic reaction with aspirin or any other NSAID medicine • for pain right before or after heart bypass surgery
NSAID Gastro Intestinal Tract effects
PGs inhibit H+ secretion and promote mucous production. NSAIDs block this promoting gastric erosion, ulceration and bleeding.
Mechnism of Cardiovascular NSAID Effects
COX-2 inhibition causes suppression of prostacyclin (PCI2), which is a potent vasodilator and prevents platelet aggregation helping protect endothelial cells during shear stress and inhibiting smooth muscle cell proliferation
Discuss the role of COX-2 specific NSAIDs in pain management
inhibition of COX-2 is more directly implicated in ameliorating inflammation
Discuss the risks of COX-2 specific NSAIDs in pain management
higher potential for causing acute myocardial infarction (AMI
