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Comprehensive flashcards covering pain definitions, classifications, pathophysiology, assessment tools, and pharmacological management based on the nursing transcript.
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Margo McCaffery's Landmark Definition (1968)
"Pain is whatever the experiencing person says it is, existing whenever he says it does."
IASP Definition of Pain
An unpleasant sensory and emotional experience associated with actual or potential tissue damage.
The 5th Vital Sign, which is routinely assessed alongside blood pressure, heart rate, respiratory rate, and temperature.
Pain
Acute Pain
Pain lasting < 3 months
Acute Pain
typically caused by tissue injury or surgery, characterized by elevated vitals (HR,BP,RR) and behaviors like grimacing and guarding
Chronic Pain
Pain lasting ≥3−6 months
Chronic (Non-Cancer) Pain
Often due to ongoing injury or nerve damage, characterized by normal vitals and effects such as withdrawal, depression, and fatigue.
Chronic (Cancer) Pain
Pain that is persistent or breakthrough due to tumor pressure, radiation or chemotherapy.
Nociceptive Pain
Normal processing of noxious stimuli, which can be further classified as somatic or visceral.
Somatic Pain
Nociceptive pain originating in bone, joint, muscle, skin, or connective tissue; described as aching, throbbing, and well-localized.
Visceral Pain
Nociceptive pain originating in internal organs; described as cramping, pressure, poorly localized, or referred.
Neuropathic Pain
Abnormal processing due to nervous system injury or dysfunction; described as burning, shooting, electric-shock-like, or "pins and needles."
Diabetic Neuropathy
Postherpetic Neuralgia
Phantom Limb
Examples of neuropathic pain
Allodynia
Pain caused by a normally non-painful stimulus, such as light touch.
Hyperalgesia
An exaggerated response to a normally painful stimulus.
Increase ACTH
Increase cortisol
Increase ADH
Increase epinephrine
Increase norepinephrine
Increase GH
Increase catecholamines
Increase renin
Increase angiotensin II
Increase aldosterone
Increase glucagon
Increase interleukin-1
decreased insulin
decrease testosterone
Endocrine Specific Responses to Pain (14)
Gluconeogenesis
Hepatic glycogenolysis
Hyperglycemia
Glucose intolerance
Insulin resistance
Muscle protein catabolism
Increase lipolysis
Metabolic Specific Responses to Pain (7)
Increase heart rate
Increase cardiac workload
Increase peripheral vascular resistance
Increase systemic vascular resistance
Increase myocardial oxygen consumption
Hypercoagulation
Deep vein thrombosis
Cardiovascular Specific Responses to Pain (7)
Decrease flows and volumes
Atelectasis
Shunting
Hypoxemia
Decrease cough, sputum retention
Infection
Respiratory Specific Responses to Pain (7)
Decrease urinary output
Urinary retention
Fluid overload
Hypokalemia
Genitourinary Specific Responses to Pain (4)
Decrease gastric and bowel motility
Gastrointestinal Specific Responses to Pain (1)
Muscle spasm
Impaired muscle function
Fatigue
Immobility
Musculoskeletal Specific Responses to Pain (4)
Reduction in cognitive function
Mental confusion
Cognitive Specific Responses to Pain (2)
Depression of immune response
Immune Specific Responses to Pain (1)
Increase behavioral and physiologic response to pain
Altered temperaments
Higher somatization
Possible altered development of the pain system
Increase vulnerability to stress disorders, addictive behavior and anxiety states
Developmental Specific Responses to Pain (5)
Debilitating chronic pain syndromes
postmastectomy pain
post thoracotomy pain
phantom pain
postherpetic neuralgia
Future Pain Specific Responses to Pain (5)
Sleeplessness
Anxiety
Fear
Hopelessness
Increase thoughts of suicide
Quality of Life Specific Responses to Pain (5)
Prostaglandins
Chemicals produced from arachidonic acid by the enzyme cyclo-oxygenase (COX) that contribute to pain and inflammation.
COX-1
COX enzyme that is constitutive and always present
COX-2
COX enzyme that is induced, present with tissue injury
GI protection
Platelet function
Manifestation of Prostaglandins made by COX-1
Pain
Inflammation
Manifestation of Prostaglandins made by COX-2
Transduction
The first step in the pain process where noxious stimuli excite peripheral nociceptors and release biochemical mediators like Bradykinin and Histamine.
Transmission
The process where pain signals move from peripheral nerves (A-Delta and C fibers) to the spinal cord and then to the brain via the spinothalamic tract.
A-Delta Fibers
Large, myelinated fibers that transmit "first pain," which is fast, sharp, and localized.
A-Delta Fibers
Fibers that are sensitive to mechanical and thermal perception.
C Fibers
Small, unmyelinated fibers that transmit "second pain," which is slow, dull, aching, and burning.
C Fibers
Fibers that are sensitive to chemical stimulus
A-Beta fibers
Non-pain fibers that relay vibration, massage and tension
Perception
The point where the cerebral cortex identifies pain location/intensity and the limbic system processes the emotional response.
Modulation
The descending control process where the brainstem releases endogenous opioids like endorphins and enkephalins to inhibit pain transmission.
Gate Control Theory (Melzack & Wall)
The theory that small fibers open the gate in the substantia gelatinosa (dorsal horn) to allow pain signals to the brain, while large A-beta fibers can close the gate.
PQRST
A core assessment tool for Provoking/Palliative factors, Quality, Region/Radiation, Severity (0−10), and Timing.
Numeric Rating Scale (NRS)
A standardized 0 to 10 scale for alert adults where 0 is no pain and 10 is the worst possible pain.
Comfort measures
Non-Opioids
Interpretation for NRS score of 0
Wong-Baker FACES Scale
A scale using 6 cartoon faces with scores ranging from 0 to 10 (0,2,4,6,8,10) for pain assessment.
FLACC Scale
An assessment tool for infants or non-verbal patients scoring Face, Legs, Activity, Cry, and Consolability.
PAINAD Scale
Pain Assessment in Advanced Dementia; evaluates breathing, vocalization, facial expression, body language, and consolability.
WHO Analgesic Ladder
A four-step framework for pharmacologic management ranging from non-opioids (Step 1) to invasive procedures like nerve blocks (Step 4).
Acetaminophen (Tylenol)
A non-opioid primarily for analgesia and fever with a maximum daily dose of 4,000mg/24hr for standard adults.
N-acetylcysteine (Mucomyst)
The antidote for acetaminophen toxicity or liver injury.
NSAIDs
Nonsteroidal anti-inflammatory drugs (e.g., Ibuprofen, Naproxen) that inhibit COX-1 and COX-2 enzymes; risks include GI ulceration and renal impairment.
Ketorolac (Toradol)
An NSAID that must be limited to ≤5 consecutive days due to severe renal and GI risk.
Meperidine (Demerol)
An opioid to avoid because its metabolite, normeperidine, causes CNS excitation, tremors, and seizures.
Pasero Opioid-Induced Sedation Scale (POSS)
A critical assessment scale where sedation level is monitored because it precedes respiratory depression in opioid use.
Naloxone (Narcan)
An opioid antagonist used for acute reversal; should be administered diluted and slowly unless in full arrest to prevent a withdrawal storm.
Adjuvant Analgesics (Co-analgesics)
Drugs like Gabapentin (anticonvulsant) or Amitriptyline (antidepressant) primarily indicated for other conditions but effective for neuropathic pain.
PCA by Proxy
A hazard where family members press the PCA button instead of the patient; nursing education must emphasize only the patient presses the button.
"Start Low and Go Slow"
A dosing strategy for gerontologic patients due to increased sensitivity to sedation and decreased renal/hepatic clearance.
Tolerance
A normal physiological response where an increased dose is needed over time to maintain the same analgesia.
Physical Dependence
A normal physiological response manifested by withdrawal symptoms if the drug is stopped abruptly.
Addiction (Substance Use Disorder)
A chronic, neurobiological disease characterized by impaired control, compulsive use, and continued use despite harm.
Central Sensitization
A "Wind-up" phenomenon involving NMDA receptor activation and increased neurotransmitter release, increasing chronic pain risk.