Quiz 3 Flashcards
Pain Transduction (Phase 1)
- Begins when nociceptor nerve endings in the peripheral nervous system are stimulated
- Local tissue injury causes the release of chemical mediators of inflammation, including prostaglandins, leukotrienes, histamine, bradykin and substance P
- Substances sensitize peripheral nociceptors making them easy to activate
Pain Transmission (Phase 2)
Nerve impulse signalling pain travel from the nociceptor to the spinal cord along 2 sensory neurons:
- A-delta fibres = transmit SHARP pain
- C-fibres = transmit DULL ache (unmyelinated and slow)
- Nerve block involves the injection of alcohol or other neurotoxic substances into neurons for irreversible blockage of impulse transmissions along nerves
GLUTAMATE IS THE MAIN EXCITATORY NEUROTRANSMITTER**
Pain Perception (Phase 3)
Perception = conscious experience of pain, occurs in the brain
- Numerous cortical structures and pathways are involved, including the reticular activating system, somatosensory system and limbic system
- Brain maps it out and says that you are feeling pain and tells where the pain is
Pain Modulation (Phase 4)
- Modulation involves descending nervous impulses travelling down the spinal cord that inhibit afferent pain transmission
- Neurotransmitters (eg serotonin, norepinephrine, endogenous opioids) inhibit pain transmission
- GABA inhibits
PQRST Pain Assessment
Provocation = Relieving/aggravating factors
Quality = What’s it feel like?
Region = Where?
Severity = How intense?
Timing = When does it hurt?
Pain Management (NON-PHARMACOLOGICAL)
COGNITIVE-BEHAVIORAL INTERVENTIONS:
Typically more effective if taught before pain is present
- Relaxation (eg slow rhythmic breathing)
- Distraction (activities requiring concentration like counting)
- Imagery (developing a mental picture)
- Meditation
PHYSICAL AGENTS:
Heat = stimulates thermoreceptors in the skin, interfering w/ pain signal transmission to the brain, reducing the perception of pain
- Increases local blood flow helping to deliver more O2 and nutrients to injured tissues promoting healing and reduces inflammation
- Relaxes muscle tension, decreasing mechanical pressure on nociceptors
Cold = Numbs the area, slowing down nerve signal transmission which reduces pain perception
- Constricts blood vessels which helps reduce inflammation and swelling limiting further irritation of pain receptors
- No more than 10-20min at a time
Pain Management (PHARMACOLOGICAL TREATMENT)
At CNS Level:
- Non-opioid centrally acting agents (Eg Acetaminophen)
**NO Anti-inflammatory properties
- Opioids = From ‘opium’, Narcotics
At Peripheral Level:
- Non-steroidal anti-inflammatory drugs (NSAIDS)
**High efficacy if inflammation also present
Opioid Analgesics (Narcotics)
Narcotics = morphine-like drugs that produce analgesia and CNS depression
-Opioids DO NOT lower the threshold for pain at nociceptor level or slow/block the transmission of the pain impulse
-Opioids DO influence perception and emotional response to pain
2 Main Opioids Involved in Pain Management
Mu:
- produce analgesia, euphoria, RESPIRATORY DEPRESSION** (slow down breathing), physical dependence, sedation and GI MOTILITY** (slow down)
Kappa:
- Primarily associated w/ analgesia, sedation, MIOSIS and GI Motility
BOTH include = euphoria, Res Depression, Physical dependence, miosis
OPIOIDS = SLOW DOWN**
Opioid Agonists
Bind receptors and inhibit release of substance P (& Glutamate)
FULL AGONIST:
- Fully activate the mu and/or kappa receptors, leading to maximum effects (eg pain relief, euphoria etc)
Eg) Morphine, Fentanyl, Hydromorph, Oxy, Hydrocodone, Methadone
PARTIAL AGONIST:
- Have a ceiling so you can still give pain relief but it doesn’t feed addiction
- Partially activate the mu receptor and have a weaker effect even at higher doses
- May act as antagonists at other receptors (kappa)
Eg) Buprenorphine (partial mu agonist and kappa antagonist) produces less euphoria
ANTAGONIST:
- Block the effects of other opioids by binding to mu and/or kappa receptors without activating them
- Used to reverse opioid overdose or prevent opioid effects
Eg) Naloxone acts on all opioid receptors
Narcan only lasts 1-2hrs in blood stream so always continue monitoring because it can reactivate after the 2hrs. Multiple doses may be required***
Besides Analgesic Effects, Opiates Also…
- Cause sedation
- Suppress cough reflex
- Slow GI motility/emptying (useful in diarrhea)
- Cause Euphoria and intense relaxation
Can cause immunosuppression w/ long-term use (decrease in pro-inflammatory cytokines, suppression of macrophages activity, T-cells dysfunction etc) - Cause histamine release by stimulating mast cells (Lead to itching, rashes, low BP AND Morphine is the opioid most likely to cause this**)
Key Facts for Opioids
- Morphine crosses placenta and Breast Milk
- Hydromorphone (dilaudid) is prepared from morphine BUT is 5X MORE POTENT
- Routes of Opioid Administration = PO, SL, IM, IV, SC, Inhalation, Transdermal, Rectal, Epidural
Combination Opioids
- Can be combined w/ acetaminophen to enhance pain-relief and reduce the amount of opioid needed for effective pain management
- Minimizes adverse effects assoc, w/ higher opioid doses (Eg constipation, sedation, Res Depression)
Eg)
Percocet = Oxy + Acetaminophen (Ace.)
Vicodin = Hydrocodone + Ace.
Tramacet = Tramadol + Ace.
Tylenol 3 = Ace. + Codeine + caffeine
Opioid Adverse Effects
CNS Depression:
- Sedation
- Decreased RR, HR & BP
- Pupillary constriction
Nausea
Pruritus
Constipation
Urinary Retention
Euphoria
**If RR is less than 12 = HOLD OPIOIDS
Check for allergies (don’t give if asthmatic*)
Caution w/ Pregnancy
Opioids: Nursing Assessments
Vitals = RR, BP etc
CNS = dizziness, decreased LOC, seizures
Orthostatic hypotension (Check BP 3x - laying, sitting and standing)
Itching = histamine release (need antihistamine)
Nausea & Vomiting = may need anti-emetics
Constipation = consider laxatives
Urinary Retention = Assess Ins/Out if on high or frequency dosing (what are they drinking and whats coming out)
should be peeing 30ml/hr
Opioid Overdose & Dependence
Toxicity resulting from overly aggressive pain therapy or substance abuse
Symptoms:
- Res Depression (EMERGENCY), pinpoint pupils (miosis), unconsciousness, low BP
Treatment = Naloxone (Narcan)
- Opioid receptor antagonist
- Administered when RR < 12
- Onset 2-4min
- Duration 30-120min
-Constant monitoring is required
- More than 1 dose may be needed (0.4-2mg IV/IM/SC/Intranasal Q2-3min. max 10mg)
Effects = Opposite effects of opioids (may cause agitation)
Physical Dependence of Opioids
Physiological adaptation to the drug, requiring continued use to function or avoid withdrawal
Physical Dependence and Addiction are DIFFERENT
Addiction
Chronic condition characterized by a strong, compulsive need to use opioid drugs DESPITE HARMFUL CONSEQUENCES
adjusting lifestyle
Characteristics:
- Cravings, Compulsive use, continued use despite negative consequences
Compulsive use + tolerance + dependence (physical & psych) + loss of control + change in lifestyle etc
Withdrawal
- Experienced when opioid use is reduced or stopped in dependent users
- Typically occurs 6-72hrs after last use (can last 1-2 weeks)
Physical Discomfort = aches and pain, chills, muscle spasms, sweating, diarrhea, nausea and vomiting, insomnia
Psychological Distress = anxiety, irritability, intense cravings
Autonomic Symptoms = increased HR, elevated BP and dilated pupils
**use “COWS” aka Clinical Opiate Withdrawal Scale every hour to monitor
Treating Dependence, Addiction and Withdrawal
METHADONE:
- No intense euphoria
- Effects plateau at higher doses (reducing risk of misuse & OD)
- Activates mu receptors like other opioids BUT more slowly and steadily for longer-lasting effect
- LONG HALF-LIFE helps prevent withdrawal symptoms by stabilizing cravings
- DOES NOT cure dependence b/c pt must keep taking the medication to avoid withdrawal
SUBOXONE (BUPRENORPHINE + NALOXONE):
Buprenorphine = (partial opioid agonist) helps reduce cravings and manage withdrawal symptoms by partially activating the opioid receptors, easing the transition for people
Naloxone = blocks effects of opioids and can trigger precipitated withdrawal (unpleasant feeling discourages abuse)
Naltreoxone in alcohol and opioid withdrawal (if you take this and then take drugs or alcohol, instead of feeling the high, you feel terrible)
Patient-Controlled Analgesic (PCA)
-Self-administration
-Allows pt to participate in care
-Frequent, small doses of analgesia gives more consistent serum drug level than larger doses 3-4x a day
Non-Opioid Analgesics - NSAIDS
-Modulate pain from effect at peripheral site
- Inhibit cyclooxyrgenase = inhibiting prostaglandin production = analgesic, anti-inflammatory, anti-pyretic and anti-platelet effects
COX 1 Enzyme:
- Continuous produced by the body at baseline
- Maintain protection of gastric mucosa, renal perfusion, stimulate platelet aggregation
COX 2 Enzyme:
- Induced by tissue damage
- Responsible for inflammation, nociception, fever, inhibits platelet aggregation
Non-Opioid Medications
COX 1 INHIBITION:
Salicylate (aspirin) inhibits COX 1&2 (but 1 inhibition > 2)
- Side Effects = peptic ulcer, acid reflux, nephrotoxicity/renal failure, bleeding
COX 1 & 2 INHIBITION:
Ibuprofen, Naproxen, Ketorolac, Diclofenac, Indomethacin
- Little or no anti-platelet effects
COX 2 INHIBITION:
Celecoxib
- Effective for inflammation, pain, fever reduction
- Side Effects = increased risk for clotting (and cardiovascular events)
Nursing Considerations for Non-Opioid Analgesics
- Gastric upset is common = DO NOT TAKE ON EMPTY STOMACH
- NSAIDS may cause or worsen peptic ulcers or GI bleed (contraindicated in pts w/ peptic ulcers or GI bleed)
(Symptoms of GI Bleed = Bloody/coffee-ground emesis, black/tarry stool, abdominal cramps)
-Monitor Kidney Function: Creatinine (40-120umol/L) & Blood Urea Nitrogen (BUN) 3.0-9.0mmol/L
- Monitor Urine output
- Antacids may interfere w/ absorption (NSAIDS = weak acids = need acidic environment to dissolve aka don’t take with milk)
- Avoid or use NSAIDS cautiously in asthma pts (shift of arachidonic acid pathway towards leukotrienes which increase bronchoconstriction)
DO NOT TAKE 2 NSAIDS AT THE SAME TIME
- No ASA in kids** especially from viral infection (use tylenol NOT ibuprofen or aspirin)
ASA may cause Tinnitus
Acetaminophen
- Primarily inhibits COX-2 activity in CNS
- Reduces production of prostaglandins
- UNLIKE NSAIDS, has minimal peripheral COX-1 and COX-2 inhibition = has analgesic and anti-pyretic effects but NO ANTI-INFLAMMATORY properties
- Reduced risk of GI and platelet-related side effects
- Can cause hepatotoxicity at high doses
(<4g/day, monitor liver lab results, Avoid ETOH)
Antidote for OD = Acetylcysteine
DO NOT TAKE TYLENOL FOR A HANGOVER, USE IBUPROFEN**
Tension Headache
Occurs when muscles of the head and neck become very tight due to stress, causing steady and lingering pain
- Mild to moderate pain which can be utilized in one area of the head and generalized
- Can be effectively treated w/ OTC non-opioid analgesia
Migraine
- Headache w/ severe, recurrent pain
- Characterized by throbbing or pulsating pain on one side (but can be both sides)
- Often accompanied by nausea, vomiting, and sensitivity to light and sound
- May or may not be preceded by Aura
Aura = sensory cue that tells one a migraine is coming (eg flashing lights, special smell, taste etc)
Acute Migraine Treatment = OTC Non-opioid = Triptans (eg. Sumatriptan) which cause vasoconstriction (serotonin agonists)
Migraine Prophylaxis = Beta-Blockers (eg. Propranolol), Anti-epileptics, anti-depressants etc
Core Body Temp
Reflection of the balance between heat gain and heat loss by the body (36.0-37.5 degree C)
- Metabolic processes speed up or slow down depending on body temp
ACTUAL Core Temp
Rectal = most accurate
Esophagus
Pulmonary Artery
Urinary Cath
ESTIMATES of Core Temp
Oral = (0.2 lower than core)
Temporal
Axillary
Tympanic
Thermoregulation
Hypothalamus is the thermal control centre for the body
Receives info from the peripheral and central thermoreceptors, in the skin and other organs, and compares info w/ its temp set point (37 = ideal core temp)
- When temp falls under set point, hypothalamus signals for heat conservation (vasoconstriction and shivering = increase core temp)
- When core temp is higher than set point, hypothalamus signals for heat dissipation = vasodilation and sweating decreasing core temp
2 Adaptations of Temperature
Heat Production
Heat Loss
Heat Production
VASOCONSTRICTION = confines blood to inner core of body
SHIVERING = increases heat production by the muscles
PILOERECTIONS = contraction of pilomotor muscles of the skin raises skin hairs (goosebumps), reducing heat loss surface
INCREASED EPINEPHRINE PRODUCTION = shift body metabolism to heat production instead of energy production (might explain weakness/fatigue in fever)
INCREASE IN THYROID HORMONE = long-term mechanism to increase metabolism and heat production
Heat Loss
Most of the body’s heat losses occur at the skin surface as heat from the blood moves through the skin, then into the surrounding environment
VASODILATION = delivers blood to the periphery where heat is dissipated through radiation, conduction and convection
SWEATING = increases heat loss through evaporation (evaporation uses body heat to convert water on the skin to water vapor in cooling)
2 Types of Increased Body Temp
Fever
Hyperthermia
Fever aka Pyrexia
Change in Set point
Results from a cytokine induced increase in the temp set point in hypothalamus
- Phagocytotic cells digest bacteria, release cytokines (these induce prostaglandin production)
PGE-2 binds to receptors in the hypothalamus to induce increases in the thermostatic set point
Clinical manifestation:
Prodromal period = fatigue, malaise, aches & pains
Chills = result from body temp trying to catch up to the new set point. Causes shivering to generate heat and raise temp
Flush = vasodilation causing skin to become warm & flushed
Defervescence = reduction in temp, marked by sweating
TREATMENT:
-Increasing heat transfer from internal to external environment Eg) sponge bath w/ cool water, cold cloth
- Supporting hypermetabolic state that accompanies fever = adequate fluids and sufficient amount of simple carbs
- Protections of vulnerable organs & systems = treatment w/ anti-pyretic (re-set set point by blocking PGE-2 production)
- Treatment of original causes of fever (eg. infection)
Rigors
More intense chills that cause the muscles to shake uncontrollably when the body’s temp rises rapidly to a new set point (eg during a serious infection)
Hyperthermia
Increase in body temp WITHOUT A CHANGE IN HYPOTHALAMIC SET POINT
- Thermoregulatory centre struggles to control temp
- Related to overproduction of heat, excessive environmental heat or impaired heat dissipation
3 Types of Hyperthermia
Heat Exhaustion
Heat Stroke
Malignant Hyperthermia
Heat Exhaustion
-Related to loss of salt and water after prolonged exertion in hot environment
- Temp >37.8 >40, tachy, thirst, fatigue, nausea, oliguria (low urine output), delirium
Heat Stroke
Core Temp >40
Severe, life-threatening**
Symptoms:
- Hot & dry skin
- Tachy
- Hyperventilation
- Weakness
- Delirium
- Blurred vision
- Convulsions
- Collapse
- Coma
Malignant Hyperthermia
- A genetic disorder where heat is generated from uncontrolled skeletal muscle contraction, resulting in severe and potentially fatal hyperthermia
- Typically triggered by GA agents and muscle relaxant used in surgery
- Mechanism r/t abnormally high release of calcium
- Treated w/ Dantrolene (muscle relaxant that blocks calcium release)
Hypothermia
Occurs when the body temp drops below 35 degrees, impairing normal physiological function
- Typically due to exposure to cold environments or immersion in cold water
Considerations:
- Malnutrition decreases fuel available for heat generation
- Loss of body fat decreases tissue insulation
- Alcohol and sedative drugs dull mental awareness to cold temps
- Certain diseases predispose pts to hypothermia (Eg diabetes, hypothyroidism, spinal cord injury)
