Fundamental Of Nursing

Front 1

acute pain

Back 1

(PP def) has an identifiable cause, short duration, limited tissue damage & emotional response. can seriously threaten patient's recovery.

(Textb def) Pain directly related to tissue injury and resolves when tissue heals

Front 2

chronic pain

Back 2

(PP def.) Not considered protective. Pain last longer than anticipated. Major cause of psychological & physical disability. HCW usually less willing to tx. Pain specialists & pain centers often helpful(Textb def) Pain that persists 3-6 mos. 2° to chronic disorders or nerve malfunctions that produce ongoing pain after healing is complete

Front 3

nociceptors

Back 3

pain receptors

free nerve endings located throughout body

Front 4

Ao fibers

Back 4

sensory neuron wrapped in myelin

signals sharp, well defined pain

Front 5

C fibers

Back 5

unmyelinated sensory neuron

conducts dull, poorly localized pain signals

Front 6

substance P

Back 6

neurotransmitter responsible for continuing pain message to other neurons

controls whether or not pain signals will stop or continue to brain

Front 7

endogenous opioids

Back 7

chemicals produced naturally w/i body that decrease or eliminate pain

acts similar to morphine

group of neurotransmitters:
- endorphins
- dynorphins
- enkephalins

Front 8

analgesic

Back 8

drug used for pain relief

classifications:
*non-narcotic
*narcotic

Front 9

cyclooxygenase

Back 9

enzyme responsible for formation of prostaglandins

NSAIDS inhibit these

Front 10

NSAIDS

Back 10

drugs that inhibit cyclooxygenase

cyclooxygenase -> resonponsible for formation of prostaglandins -> prostaglandins activate peripheral nociceptors -> nociceptors produce pain

Front 11

bradykinin

Back 11

chemical mediator of pain

follows tissue damage

Front 12

prostaglandin

Back 12

chemical released after tissue damage

leads to pain, inflammation, etc.

Front 13

narcotic

Back 13

drug capable of producing numbness or stupor-like condition

includes opioids

Front 14

opiates

Back 14

natural narcotic extracted from poppy seeds

includes morphine & codeine

Front 15

opioid

Back 15

natural or synthetic morphine-like substance

Front 16

mu

Back 16

type of opioid receptor affecting:
- analgesia
- decreased GI motility
- respiratory depression
- sedation
- physical dependence

activated by:
- pure opioid agonist (morphine & codeine)

- mixed opioid agonist (buprenorphine)

Front 17

kappa

Back 17

type of opioid receptor affecting:
- analgesia
- decreased GI motility
- sedation

activated by:
- pure opioid agonist
(morphine & codeine)

- mixed opioid agonist
(pentazocine & butorphanol)

Front 18

antipyretic

Back 18

reduces fever

Front 19

tension headache

Back 19

muscles of head/neck area become tight

due to stress & tension

Front 20

Pain (whatever the client says it is, and is existing whenever the client says it does)

Back 20

-Unpleasant sensory/ emotional experience

-Can have destructive effects

-Can warn of potential injury

-A multidimensional experience:

Physical, psychological, emotional, social implications

" an unpleasant sensory/ emotional experience assoc. with actual or potential tissue damage, or described in terms of such damage" (Am. Pain Soc., 1992)

Front 21

Pain Threshold

Back 21

the least amount of stimuli that is needed for a person to label a sensation as pain

Front 22

Pain tolerance

Back 22

Maximum amount of painful stimuli that a person is willing to withstand w/o seeking avoidance of pain relief

Front 23

Neuropathic pain

Back 23

Assoc. w/ damaged or malfunctioning nerves due to illness (ex. post-herpatic neuralgia, diabetic peripheral neuropathy), injury (ex. phantom limb pain, spinal cord injury pain), or undetermined reasons

Front 24

Peripheral neuropathic pain

Back 24

follows damage or sensitization of peripheral nerves (ex. phantom limb pain, post-herpatic neuralgia, carpal tunnel syndrome)

Front 25

Central neuropathic pain

Back 25

results from malfunctioning nerves in the CNS

(ex. Spinal cord injury pain, poststroke pain, Multiple Sclerosis)

Front 26

Sympathetically maintained pain

Back 26

occurs occasionally when abnormal connections between pain fibers and the SNS perpetuate problems w/ both pain and the sympathetically controlled functions (ex. edema, temperature, and blood flow regulation)

Front 27

Hyperalgesia and Hyperpathia

Back 27

both terms used interchangeably to mean heightened responses to painful stimuli (ex. severe pain response to a paper cut)

Front 28

Allodynia

Back 28

non-painful stimuli (ex. light touch, contact with linen, water, or wind) that produces pain.

Front 29

Post-herpatic neuralgia

Back 29

Occurs when a case of herpes zoster (shingles) erupts decades after a primary infection (chickenpox) during a period of stress or compromised immune functioning.

Front 30

Headache

Back 30

40% of the worldwide population suffers 1 severe disabling HA per year. Caused by intracranial or extracranial problems, serious or benign conditions.

To establish plan of care, RN must assess Quality, location, onset, duration, and frequency of pain as well as s/sx that precede he headache.

*Migraine/ tension HA more common in Wom.

*Cluster HA more common in men

Front 31

Low back pain

Back 31

nearly everyone suffers from LBP @ some time during life. Most occurrences go away within a few days. Chronic LBP for more than 3 months, often progressive and cause is difficult to determine

Front 32

Fibromyalgia

Back 32

chronic disorder characterized by widespread musculoskeletal pain, pain, fatigueand mult. tender points (neck, spine, shoulders & hips); sufferers may also experience sleep disturbances, morning stiffness, IBS, anxiety, etc.

-It's considered to be a problem of abnormal CNS functioning, particularly as it relates to the way nerves process pain

Front 33

Dysesthesia

Back 33

an unpleasant abnormal sensation; it mimics the pathology of a central neuropathic pain disorder (ex post-stroke or spinal cord injury)

Front 34

Pain intensity (quality)

Back 34

Mild: 1-3

Moderate: 4-6

Severe: 7-10

Front 35

Intractable pain

Back 35

A pain state (gen. severe), no cure is possible even after accepted medical eval. and tx. have been implemented. *Focus of tx turns to pain reduction, functional improvement, and the enhancement of quality of life.

Front 36

Nociceptive pain

Back 36

Pain that is directly related to tissue damage. Somatic-damage to skin, muscle, bone

Visceral- damage to organs

Front 37

S/Sx of mild-severe Acute Pain:

Back 37

-SNS responses: ↑PR, ↑RR, ↑B/p, Diaphoresis, Dilated pupils. Related to tissue injury- resolves w/ healing., Pt. may be restless/ anxious. Pt. reports pain. Pt. exhibits indicative behavior of pain: crying, rubbing/ holding area

Front 38

S/Sx of mild-severe Chronic pain:

Back 38

-PNS responses: Vital Signs normal, dry/ warm skin, pupils normal or dilated. Pain cont. beyond healing. Pt. is usually depressed/ withdrawn. Pt. doesn't mention pain unless asked. Pain behavior is absent

Front 39

Nociception

Back 39

The physiological processes related to pain perception. 4 physiological processes that are involved: Transduction, Transmission, Perception, and Modulation

Front 40

Types of pain stimuli:

Mechanical

Back 40

1) Trauma to tissue ( surgery): direct irritation of pain receptors- inflammation

2) Alterations in body tissue (edema): pressure on pain receptor

3) Blockage of body duct: Distension of lumen of the duct

4) Tumor: Pressure on pain receptors; irritation of nerve endings

5) Muscle spasm: Stimulation of pain receptors

Front 41

Types of pain stimuli:

Thermal

Back 41

Extreme heat or cold (ex. burns): Tissue destruction; stimulation of thermosensitive pain receptors

Front 42

Types of pain stimuli:

Chemical

Back 42

1) Tissue ischemia (ex. blocked coronary artery): Stimulation of pain receptors b/c of accumulated lactic acid and other chemicals (bradykinin & enzymes) in tissues.

2) Muscle spasm: Tissue ischemia 2° to mechanical stimulation

Front 43

Transduction

Back 43

Nociceptors (pain receptors) excited by mechanical, thermal, and chemical stimuli. Harmful stimuli trigger the release of biochem mediators (prostaglandins, bradykinin, serotonin, histamine and sub. P). Pain stimulation causes movement of ions across cell membranes.

Front 44

Pain medications during transduction phase

Back 44

-Ibuprofen, aspirin (NSAID's) block the production of prostaglandin

-local anesthetic works by decreasing movement of ions across the cell membrane

-Topical analgesic (Zostrix) capsaicin, depletes the accumulation of substance P and blocks transduction

Front 45

Transmission: Conduction of pain message to spinal cord

Back 45

The nerve impulse travels along afferent peripheral nerve fibers until they end in dorsal horn of spinal cord (2 types of fibers: A-delta (fast), C-fibers (slow)) [Sub. P and other NT]. Continues via spinothalmic tracts, to thalamus, quickly transmitted to higher centers in brain

Rx: Opiods block Sub P from getting to spinal cord.

Front 46

Perception: recognizing and defining pain in cortex.

(Past experiences w/ pain shape the intensity of pain perception [men don't cry b/c of a booboo])

Back 46

the point at which a person is aware of pain. Occurs in cerebral cortex. A complex reaction unfolds. some take express" to thalamus, then relayed to cortex. Others "local" w/ many synapses in brain stem, hypothalamus & other limbic system structures before the thalmus.

Front 47

Modulation: Changing pain perception

Back 47

Inhibition of the pain impulse. Mechanisms that interfere w/ pain transmission in spinal cord. Release inhibitory NT( ex. endogenous opiods [endorphins & enkephalins])

Rx: Tricyclic Antidepressants- block reuptake of serotonin and NE, making them more avail. to fight pain. & NMDA antagonists (ex Ketamine) used to help diminish pain signals

Front 48

Neuroregulators

Back 48

Substance P- Pain neurotransmitter

Serotonin- released by descending pain suppressor fibers into dorsal horn neurons- activate enkephalin-releasing interneurons [decrease release of substance P]

Front 49

Neuromodulators

Back 49

Endorphin's and dynorphins: produced in brain, binds to receptor sites

Front 50

Gate-ControlTheory of Pain

Back 50

•Theory proposed 1st in 1965 – pain a physical sensation&obligatory emotional & cognitive components

•No specific pain center in brain•Gating mechanisms along the CNS

–Gate open = pain impulses pass through

–Gate closed = pain impulses regulated or blocked

•Pain relief measures to close the gate

Front 51

ClinicalApplication ofGate Control Theory

Back 51

•Stop nociceptor firing

•Apply topical therapies

•Address client’s mood

•Address client’s goals

Front 52

•Physiological responses – autonomic nervous system is stimulated

Back 52

–Sympathetic stimulation– low - moderate intensity & superficial pain - systB/P, HR, RR, alertness, dilated pupils, rapid speech

–Parasympathetic Stimulation– severe or deep pain or prolonged pain - systB/P, HR, variable resp. patterns, slow speech, constricted pupils

Front 53

Preemptive analgesic

Back 53

Administered pre-surgery to decrease or relieve pain after surgery

Front 54

World Health Organization 3 step analgesic ladder

Back 54

step 1: for mild pain (1 to 3 / 10) =non-opiod analgesic

step 2: for moderate pain: (4 to 6/10)=opiod (Tramadol, codeine) or a combo (oxycodone/ acetaminophen, etc.)

step 3: for severe pain: (7 to 10/ 10)= opiod (morphine, hydromophone, fentanyl)

Front 55

Nonopiod analgesics/NSAIDs for mild pain

Back 55

Acetominophen, Aspirin, Ibuprofen, Celebrex (Cox2 inhibitor), Naproxen, etc

Front 56

Opiod analgesics for moderate pain

Back 56

Hydrocodone (lortab, Vicodin)

Codeine (Tylenol 3)

Tramadol (Ultram, Ultracet)

Pentazocine (Talwin)

Front 57

Opiod analgesics for severe pain

Back 57

Fentanyl

Hydromorphone HCL (Dilaudid)

Oxycodone (OxyContin)

Morphine sulfate

Oxymorphone

Methadone

Front 58

Coanalgesics (fka: adjuvant)

Back 58

Tricyclic antidepressants

Anticonvulsants (gabapentin, pregabalin)

Topical local anesthetic (Lidoderm)

Front 59

Physical dependence

Back 59

NOT ADDICTION.

an expected physical response when a pt. is on long-term opiod therapy has the opiod significantly reduced or withdrawn.

Front 60

Addiction

Back 60

Chronic, relapsing, treatable disease influenced by genetic, psychosocial, and enviornmental factors 9a) craving for substance, (b)lack of control over substance (c) compulsive use (d) cont'd use despite harm

Front 61

Pseudoaddiction

Back 61

condition that results from the undertreatment of pain where the pt. becomes so focused on obtaining pain medications for relief they become angry, "clock watch", etc.

Front 62

3 primary types of opiods

Back 62

1) Full agonist analgesic- morphine, the gold standard. There is no ceiling for these Rx, unless combined with a non-opiod analgesic

2) Mixed agonists-antagonist: act like opiods and relieve pain (for pt. who hasn't taken opiods) But, can block/ inactivate other opiod analgesics (for a pt who has been taking opiods)

3) Partial agonists- have a ceiling effect in contrast to a full agonist

Front 63

Pasero Opiod-Induced Sedation Scale

Back 63

-S= Sleep, easy to arouse

-1= awake and alert

-2= Slightly drowsy, easily aroused

-3= Frequently drowsy, arousable, drifts to sleep during conversation

-4= somnolent, minimal or NO response to physical stimulation

NOXIOUS STIMULI- STERNAL RUB

Front 64

Nonpharmacologic Pain Management

Back 64

Physical: Cutaneous stimulation- massage, ice/ heat, immobilization or therapeutic exercises, TENS, and acupuncture

Mid/body (cog-behav): distracting activities, relaxation tech., imagery, meditation, biofeedback, hypnosis, cog. reframing, emotional counseling, stress management

Front 65

Effleurage

Back 65

Type of massage consisting of long, slow, gliding strokes

Front 66

Nerve Block

Back 66

chemical interruption of a nerve pathway caused by injecting a local anesthetic into the nerve