NURS 116 - midterm (look at quiz 1+2) + this
Rheumatoid arthritis (RA)
Arthritis = joint inflammation
RA = chronic systemic rheumatic (inflammatory) disease, autoimmune (immune system attacks the body's own cells)
Risk factors: family hx, gender (female because of estrogen levels) , triggers, can also be triggered by antigens
Causes chronic inflammation of connective tissue
Affected tissue: joints, heart, lungs, kidneys, eyes
In joints:
Dysfunction of the synovial cavity ‘pannus’m
Destruction of surrounding tissue (bone, cartilage →articulating cartilage)
Deformity of the tissue
Loss of normal function
Pain
Progressive and autoimmune destruction of healthy endogenous tissue
S&S:
Synovial joint inflammation: hands, knees, cervical spine
Systemic symptoms (generalized fatugue, anorexia)
BW: will have high C-reactive protein (is a marker of inflammation)
Tx:
NSAIDs (nonsteroidal anti-inflammatory drugs - reduce pain, inflammation and fever) PO
Glucocorticoids (reduce inflammation and immune response) PO
Tx:
Drug class: BRMs (biologic response modifiers(
Biologics; IV, SC (not PO because they would be destroyed in the GI system)
Inhibits pro-inflammatory cytokines (ex. Interleukins, integrins) → decrease T and B cells response
Drugs: infliximab, Adalimumab, Ustekinumab
Drug class; DMARDs (disease modifying anti-rheumatic drugs)
Inhibits nucleotide synthesis (decrease replication)
Inhibits WBC synthesis and function
Used for chronic inflammatory disease
Drugs: methotrexate
Osteoarthritis (OA)
Degenerative disorder of articular cartilage
Risk factors: mechanical stress (too much stress on joints, think athletes), obesity (too much weight bearing on joints), age (anyone can get it), gender
Called wear and tear arthritis → few joints affected than in RA (not systemic)
Cartilage changes occur:
Repetitive pro/inflammatory mediator release (cytokines, prostaglandins) → chronic inflammation
Decreased proteoglycans (meshwork in joints)
Weakened collagen 2 network, and collagen 5 increases (chronic inflammation)
Cartilage tissue destruction → bone-bone in articulating surface
Tx:
NSAIDS, glucocorticoids
Local glucocorticoid administration useful
Glucocorticoid, intra-articular injection drug: betamethasone (celestone): made to stay low in bioavailability and systemic circulation, usually done under ultrasonic light
Inflammation 4
IBD - chronic inflammatory bowel disease: Crohn’s disease and Ulcerative Colitis (UC)
Risk factors: family hx and triggers (environmental, bacterial)
Autoimmune effect: GI cells targeted by an atypical immune response
Systemic S&S: fever, anemia (low oxygenation in the blood), fatigue (and malabsorption), weight loss, rash
Chron’s disease: anywhere within the GI tract (isnt intact so pathogens are able to enter)
UC: large intestine
Tx:
Drug classes
Glucocorticoids (good for flare ups, don't use long term)
Aminosalicylates
DMARDs (methotrexate) → decrease immune response, is potent, give in low doses
Stem cells research (mesenchymal stem cells)
**crohn's disease has patchy skip leisions
** sometimes with UC you can treat locally at the rectum because it usually starts there
Drug Class: aminosalicylates
Drug: sulfasalazine (azulfidine, salazopyrin)
PO administered, metabolized in the colon → active metabolites
5-ASA: salicylate (NSAID)
Sulfapyridine: immunomodulatory activity (DMARD)
Drug: 5-ASA (asacol, teva, mesalamine) → PO, rectal, is an NSAID
Asthma (aka bronchial asthma)
Chronic inflammatory airway disorder (not autoimmune)
Risk factors: family hx, atopy (presence of other associated allergies)
Etiology:
Noxious stimuli trigger that is present in the lungs (allergens, particles, infections, stress)
Reactivity of the airways to the stimulo leading to chronic hypersensitivity
Chronic inflammatory changes in the epithelial tissue of the lungs
High goblet cell activity (mucous)
Presentation:
Bronchial inflammation
Bronchoconstriction (narrows airway)
Mucous production (blocks airway)
Asthma challenges
Chronic bronchial inflammation
Risk of acute attacks (sudden extreme inflammatory response)
Tx focus: stabilizing the bronchial inflammation and minimizing the number fo attacks
Avoidance of triggers
Daily maintenance drugs to decrease bronchial inflammation (controllers)
Correct administration technique (inhalation equipment: inhalers)
Immunizations to decrease respiratory infection risk
Recognize the S&S of an attack quickly
Asthma attack drugs: rescue drugs (relievers)
911 if attack persists
Tx; controllers
Anti-inflammatory drugs, inhaled:
1st line maintenance treatment daily
Prophylaxis against attacks
Drug class: glucocorticoids
Drug: pulmicorte (budenoside), qvar (beclomethasone), flovent (fluticasone)
Adjunct treatment
Mast cell stabilizers (ex. cromolyn)
Leukotriene modifiers (ex.singulair)
Long term maintenance: biologics (antibioties)
Xolair (omalizumab)
SC
High affinity for free IgE, decreases expression of mast cell bound IgE, reduction in allergic inflammation
Asthma attack
S&S:
Wheezing, shortness of breath, decreased/no air entry into lung lobes
Tachycardia (increase HR, increase BP)
Anxiety, panic
Fatigue
Patho:
Limited inspiration and longer expiration phase leads to air being trapped in the alveoli
Leads to hyper-inflated lungs with low gas exchange
Ventilation-perfusion mismatch
Hypoxemia and hypercarbia
High pulmonary pressure → increased RVED → low CO
Tx: rescue
Bronchodilator drugs, inhaled
Drug class: beta 2 adrenergic agonists
Potent, high receptor affinity
Stimulates SNS B2 receptors
Fast acting
Drugs: salbutamol (ventolin)
Drug class: anticholinergics
Less potent
Antagonize PNS
Slower onset of action
Synergy with beta2 adrenergic agonists
Drug: atrovent (ipratropium)
**typically will use BOTH albutamil and atrovent together
** BUT if airway is completely closed these wont work because they cannot reach the lungs
Severe attack, ER admission; S&S: life threatening
O2
Beta2 adrenergic agonists, inhalation (nebulizer), ventolin
Calcium channel blocker (smooth muscle) magnesium sulfate, IV
Anticholinergics, inhalation (nebulizer), synergy treatment
adrenergics/sympathomimetics, IV (epinephrine)
Glucoroticoids, IV
Magnesium sulfate, IV
Drug classes: electrolyte, enzymatic activator, calcium channel blockers
Inhibition of Ca channels in smooth muscle → reduces cellular excitability → bronchodilation
Stabilization of mast cells and t-cells → decreased pro/inflammatory ,ediators
Enhanced release of NO → vasodilation, pulmonary dilation = improved gas exchange
Titrate to effect for severe bronchoconstriction
Pain 1
Acute pain is normal physiology its a warning mechanism!!
Assess pain as symptom
LATERSNAPS: location, associated symptoms, timing (onset, duration)
Mechanism (with onset: ‘how did it start?’ → tells you how you should treat based on how it happened)
Severity: “how bad is your pain?” → scale of 0-10, pediatrics = face tool
Associated S&S (ex. fever)
Radiation anywhere? ‘Referred pain’
Assess pain when taking vital signs, we need to establish a baseline
** sensors in the epidermis, dermis, and visceral organs
Afferent pathways
Sensory information from PNS to CNS:
‘afferent’
starts at the sensory receptor/s in a specific body part
ends in the CNS’s Somatosensory Cortex
the sensory impulse needs to be strong enough to reach a threshold => action potential is initiated (if not strong enough, then no action = no pain message, -50mv is threshold)
nociceptor (in skin, bones, blood vessels, visceral organs) => 1st order neuron (PNS)
Sensitization → pain gets less worse over time
PNS → CNS
Nociceptors → A OR C NERVE fibers pf the PNS (1st order neuron) → spinal nerve → dorsal root and ganglion → posterior horn synapse (substance P neurotransmitter) → 2nd order neuron - decussate (cross over) → ascends spinal cord’s white matter column vis the ‘spinothalamic tract’ (lateral) → thalamus (relay station) → synapse with 3rd order neuron → somatosensory cortex in the brain ‘localization’: specific body part of the sensory homunculus → awareness!
** typical cutaneous nerve: A alpha = fastest transmission. C= slowest transmission (gate control theory)
Somatosensory cortex: sensory homunculus
Maps the cortex region per anatomical body part (based on innervation #s) somatosensory association areas: link the sensation to previous experiences
More sensitive = more nociceptors
Large stimuli may trigger many or all receptors → high awareness of pain
Ex.trauma (tissue tearing): pressure receptors, free nerve endings = big inflammation to the point where tissue is ripping (the bigger the message the more ripping)
Ex. temperature (ex. Blood present)
Non-pharmacological techniques
Decrease inflammation and sensation: PNS
Ice ( ⬇perfusion to tissues, ⬇excitability of nociceptors, ⬇cellular function)
Pain is a warning mechanism, you cant just treat the pain you have to figure out what is causing it)
Alleviate the trigger (PNS):
massage - muscle spasm
Physiotherapy : jointm muscle, tendon
distraction/behaviour modulation: CNS
CBT- cognition behaviour therapy
Activities
Pain terminology
•Location:
Visceral pain – deep pain, organ related
Cutaneous pain – superficial, surface related
Referred pain – due to body surface innervated by the same spinal nerve/nerve plexus (divides into different nerve innervations)+ interneuron communication (radiating pain - nerves come from the same plexus)
Reflexes - e.g. withdrawal reflex
Chronic pain – persistent pain
Neuropathic pain – persistent nerve irritation, difficult to tx
e.g. allodynia (pain caused by a non-painful stimulus)
e.g. hyperalgesia (hypersensitivity to a painful stimulus)
e.g. paresthesias (‘pins & needles’)
can occur with decreased perfusion of a nerve, positional
Phantom pain – neuropathic pain post amputation
spinal cord neurons are still active despite the lack of stimulus (no nociceptor), interneurons are still communicating pain
often leads to chronic pain
Dermatomes - clinical application
Cutaneous segments serviced by the same spinal nerve, clinically assessed to determine sensory/motor pathways
Reflexes: flexor ‘withdrawal’ reflex
Stimulus (sharp pain) → reflex to withdraw without cerebral control: activation of a sensory neuron (afferent) – interneuron (at level of stimulus in CNS) - automatic activation of a motor neuron (efferent) - response by the effector; awareness
Acute vs chronic pain
Acute pain < 10 days
Self-limiting - modulator neurotransmitters are released to desensitize the pain
Endogenous modulators secreted
can persist but improving
SNS responses are active
Innate protective mechanism
Appropriate tx is effective
Persists but improves
Chronic pain > 6 months
Likely travels along C fibres
Neurogenic inflammation => pain
outcome of e.g. under-treated acute pain, chronic inflammatory disorders
Not self-limiting
Endogenous modulators are absent
SNS responses not active
Destructive mechanism, not beneficial to the host
yields other dysfunctions: insomnia, anxiety, anorexia, depression, …
Treatment requires many modalities e.g. CBT p.1269
Endogenous neurotransmitter modulator ‘neuromodulators’: efferent pathway
endogenous opioid peptides: endorphins, enkephalins, dynorphins
serotonin & norepinephrine
released from the CNS: hypothalamus, limbic system, reticular formation
DESCENDING (efferent) pathway
bind opioid receptors (mu, kappa, delta) => inhibit substance P
Substance P: excitatory CNS neurotransmitter
propagates pain input
Pain 2: pain management - opioids
Opioids
OPIUM- naturally occurring milky extract from the unripe seeds of the poppy plant. Contain morphine and codeine substance (and other 18 substances)
OPIATES- naturally occurring chemical compounds extracted from opium, natural
OPIOIDS- any drug that is derived from the opium formula, synthetic or natural
NARCOTICS- morphine like drugs that produce analgesia and CNS depression, terminology is associated with illegal use (hallucinogen, heroin, amphetamines, marijuana)
These terms opiates/opioids/narcotics analgesics are used unterchangeably
Opioids
Purpose:
Remain therapeutic mainstay for moderate to severe pain management
May be combined with other therapies to manage chronic or complicated pain
Titration purpose:
MOST opioids have No ceiling doses (titrate dose as high as you need but that leads to abuse)
Titrate upward as needed
All will cause dependance
Titrate downward as soon as patient can tolerate
Drug schedule:
Regulated
Most are schedule 1 while some are schedule 2
Opioids
Opioids are agonists for receptors mu (1 and 2), kappa, delta, sigma, and epsilon (opiate)
When the synaptic knob at the primary or secondary synapse is activated by an opioid agonist, it will inhibit release of pain neurotransmitters such as substance P and glutamate
SUBSTANCE P:
involved in acute pain transmission (focus)
opioids act at the mu or kappa receptors which inhibit the release of substance P
this inhibition reduces depolarization of ascending pain neurons, thereby blocking pain transmission
OPIOIDS AND DOPAMINE :
Dopamine release in the mesolimbic reward pathway (ventral tegmental area → nucleus accumbens prefrontal cortex) contributes to the rewarding and reinforcing effects of opioids
This results in a calming or pleasurable sensation
However, dopamine is nor directly responsible for analgesia but plays a role in addiction and reinforcement
Opioids
ADME
ABSORPTION - variable depending on the route of administration (PO, IV, TD)
DISTRIBUTION - distributes to skeletal muscle, liver, kidneys, lungs, intestinal tract, spleen, brain. Adults: 20% to 35% protein binding (not heavily PPB). peak plasma concentration ( oral → 1h, IV → 20mins)
METABOLISM - Hepatic vis conjugation
ELIMINATION - via urine and feces, metabolites might cause toxicity with renal insufficiency
Opioids
Opioids
Opioids based on efficacy:
-high efficacy ex
Fentanyl (80-100 times more potent than morphine) → TD, IV, highly potent (dont give out as easy), used in post op pain
Hydromorphone (dilaudid) - 5x stronger than morphine →post-op, cancer treatment, less histamine release (less itching)
Meperidine (demerol) → seizures
Morphine → more histamine (itching)
Methadone (metadol) → opioid addiction and chronic pain
-moderate efficacy ex
Hydrocodone, oxycodone (oxyneo), oxycontin, tramadol (ultram)
Combo drugs: percocet, percodan, vicodin, tramacet
Codeine (no to kids- codeine is pro drug, that get changed to morphine when being metabolized, kids metabolism is not reliable)
⭐️high benefit = high risk
Opioids
Combination drugs:
Opioid + non narcotic analgesic (synergistic effect: Drug A + Drug B = synergistic effect)
Benefit - dependance on opioid can be reduced
Ex.
Percocet (oxycodone + acetaminophen)
Percodan (oxycodone + ASA)
Vicodin ( hydrocodone + acetaminophen)
Tramacet (tramadol + acetaminophen)
Atasol (acetaminophen + caffeine + codeine)
Tylenol #1 - #4 (amount of codeine present)
Opioids
Side effects:
Central nervous system (CNS)
CNS-depression -drowsiness, dizziness, confusion, or menta; clouding
Excessive sedation or unresponsiveness in high doses
Respiratory system
Respiratory distress (slow, shallow breathing)
Apnea in severe cases
Cardiovascular system
brady cardia in most cases, tachycardia during compensation (when body is trying to deal with the decrease in CO and the side effects)
Hypotensio or palpitations
Gastrointestinal system
Constipation due to slower intestinal mobility
Nausea, vomiting, or reduced appetite
Genitourinary system
Urinary retention
Integumentary system
Pruritus bc of histamine
Opioids
Side effects
Nausea and vomiting: usually resolves in a few days; antiemetics, switch opioids
Sedation: mostly during unutation or change in dose, decrease dose
Constipation: most common and should be anticipated, stool softeners, osmotic stimulants, peripherally-acting mu-opioid antagonists, switch opioids; avoid bulking agents
Pruritus: switch opioids, antihistamines
Urinary retention: switch opioid
Morphine
Class; opioid analgestic/ opiate receptor agonist
Dose form: tablets; parenteral
MOA: opioids bind to opiate receptors (mu, Kappa, delta) in the CNS, where they act as agonists of endogenously occurring opioids (enkephalins, endorphins, and dynorohins), reducing perception of and response to pain
naloxone/narcan
Respiratory depression is seen in less than 10% of opioid users, almost always in those who are naive to opioid therapy (have not been giev opioids for more than 7 days in a row)
Indication- when the respiratory rate falls below 8-10 and teh client has altered mental status, nalozone will be given to reverse the opioids effect
MOA- narcan blocks mu and kappa receptors
Administration - it should be given carefully, and administered slowly just until the client starts ti respond with increased respiratory rate and a clearing mental status
Onset - 2-4 minute (secure ABC’s)
Duration of action - 45 min
NOTE: if thus drug is given to chronic opioid user, the client will also wake up i aggressive behaviour (euphoria). Because they were on drugs to get rid of pain and you stopped it
Naloxone
Brand name - narcan
Class - opioid antidote (antagonist)
Dose forms - parenteral; intranasal
MOA - competitively blocks the effects of opioids, including CNS and respiratory depression, without producing any agonist (opioid-like) effects
Nursing considerations
Adequately assess pain
Treat pain holistically
Treat all patients adequately
Base the treatment plan on the patients stated goal
Use pharmacological and non-pharmacological pain strategies
Use a multimodal approach to pain management
Regularly monitor pain management strategies to ensure patients goals are being met
Continually educate and inform patients about the medications
Pain management
<4/10
Non opioid medications
Less invasive route, ex. PO
NSAIDs, Tylenol (or both →to get a synergyst effect)
4-6/10
Opioids
Less invasive route, ex. PO
Synergy, combination drugs, morphine
>6/10
Higher potency opioids
Consider IV route
Consider PCA (patient control anergisia)
Pain management
The PCA (patient controlled analgesia) device is a programmable syringe pump, which delivers the opioid infusions according to individualised settings: bolus dose, lockout time, dose duration, background infusion
Only if ABC’s are intact can the patient be in controll
Nurses and pain management
Each of us filter our understanding of pain through our own experiences
Personal use of medications or non-pharmacologic methods to manage pain
Family or significant others’ history or experience with substances for pain control or mood altering effect
Remember that pain is an individual subjective experience, and “is what the patient says it is”
Pain 3
Preparations for each administration is called a formulation
Advocate for your patient - best route available
PCA is a delivery method NOT route
PCA - patient has control over giving themselves a little boost
Pain and pain treatment
Cause?
Tx: risk vs benefit, consider synergy
monitor : efficacy of pain tx, side effects, adjunct tx (other therapy for a better job)
To alleviate anxiety around pain, treat the underlying cause/find
Synergy - using 1+ drug for the effect of them together additional effect
Higher potency = high affinity to drugs = ⬆side effects
Pain tx : analgesia (umbrella term)
synergy tx is common:
the interaction of 2 or more drugs when their combined effect is greater than the sum of the effects seen when each drug is given alone (adaptive effect)
lower doses/drug to create an effect (good! ⬇likelyhood of negative side effects)
tx at peripheral (PNS) level: high efficacy if inflammation is present (NSAIDS (anti inflammatory), glucocorticoids (COX inhibitory))
tx at CNS level: Opioids: potency (mg or mcg!!!), Tylenol (acetaminophen)
Acetaminophen (tylenol)
Centrally acting analgesic
Not anti-inflammatory
Synergy
Combined into >600 combination medications (ex.opioid Tramacet)
MOA as analgesic: many theories ex.
Interferes with PGs but not at peripheral level = not anti-inflammatory
Agonizes cannabinoid receptors (inhibitory effect on brain)
Antipyretics #1!!
fever : pyrexia
A nonspecific response to a threat
hypothalamic response to pyrogens: exogenous &/or endogenous
exogenous: bacteria-produced, e.g. endotoxins
endogenous: inflammatory mediators e.g. cytokine → body can produce
aim: destruction of pathogen by high temperature → ⬆basal metabolic rate (BMR)
high temperature: increases BMR, decreases cellular fx (proteins and enzymes may not like increase in temp), uncomfortable
symptom only: non-specific; what is the cause/the diagnosis?
Tx: antipyretics
Goal: patient comfort, decrease BMR, optimize cellular function
•Acetaminophen (Tylenol)
1st choice, best efficacy
MOA: induces hypothalamic-peripheral vasodilation (inhibits ProstiglandinE2)=> heat loss
safe in pediatrics (mg/kg, kid measurements) & in pregnancy
Liver issues don't mix with tylenol
NSAIDS (Ibuprofen, ASA)
anti-inflammatories reduce cytokines => decreased pyrogenic stimuli
no ASA in pediatrics
other tx:
Tx of the cause (e.g. infection)
hydration
congestion, cough, rhinitis, diaphoresis (sweating)….
Acetaminophen in combination drugs:
Always check label for active drug ingredients
Allergy-related symptom tx: antihistamines
drugs: diphenhydramine, chlorpheniramine
Cough tx: antitussives
Coughing is a protective innate response, sometimes it is good
CNS depression of cough reflex
Caution – not always desirable
drugs: Codeine (opioid, CNS sedation, ⬇coughing reflex); Dextromethorphan (robitussan)
Congestion tx: adrenergic agonist (sympathomimetic)
SNS stimulation decreases nasal secretions
Drugs: Ephedrine, Pseudoephedrine
More selective in binding
Menthol as an analgesic
activates cold-sensing receptors
MPA - topical
not actually cold but cooling effect
Gate Control theory (works on pain receptors) → inhibitory interneuron: reduction of the sensation of pain through the inhibitory interneuron being activated within the spinal cord
Inhibitory interneurons signalling back and override that sensation of pain
Buckleys medicine “it tastes bad but it works”
Drug combo:
Robaxacet
‘Robax’: muscle relaxant (methocarbamol) →MOA is unknown
‘Axet’: acetaminophen (analgesic)
Helps with back pain (tylenol), muscle spasms + tense neck muscles + strains and sprains →relaxing piece
Is a CNS depressant → of SNS therefore allowing for muscle relaxant (drowsiness, no heavy machinery, do not mix with other CNS depressants
Robaxisal
‘Robax’: muscle relaxant (methocarbamol) →MOA is unknown
‘isal’ : Acetylsalicylic acid → pain relief
Barriers to pain relief: be aware of them
Healthcare professionals: acute pain <10 days, acuity of pain will decrease over time if you are treating the cause of the pain
Patients: denial, not voicing pain (culture), dont want to get addicted/ past of addiction
Healthcare system: portects patients, tracks patient history (see patterns), hinder acute pain (who provides drugs, credentials, ect)
Fear of creating addiction
Euphoria: psychological addiction + physical addiction
Physical addiction: happens at the receptor level. A substance is causing a receptor response, because of that receptor responds it is triggering a series of events to take place within the body but the patient is not actively seeking that drug for a high. Treat with weaning protocol
4 C’s of psychological addiction
Cravings
Compulsion to use
Loss of Control over use
Use despite harmful Consequences
Is a change in behaviour to have that substance as much as possible
Acute vs chronic pain
Acute pain < 10 days
Self-limiting - modulator neurotransmitters are released to desensitize the pain
Endogenous modulators secreted
can persist but improving
SNS responses are active
Innate protective mechanism
Appropriate tx is effective
Persists but improves
Chronic pain > 6 months
Likely travels along C fibres
Neurogenic inflammation => pain
outcome of e.g. under-treated acute pain, chronic inflammatory disorders
Not self-limiting
Endogenous modulators are absent
SNS responses not active
Destructive mechanism, not beneficial to the host
yields other dysfunctions: insomnia, anxiety, anorexia, depression, …
Treatment requires many modalities e.g. CBT p.1269
Chronic pain
Repetitive and altered SNS initiation of responses → chronic inflammation + chronic pain cycle
How to assess chronic pain? Length of time, location/site that is stimulating the pain, always try to reassess the pain and see if you missed something
Ex. CRPS
CRPS: complex regional pain syndrome
Allodynia
Skin changes to the injured area: hair loss, temperature changes, color changes
Muscle and joint stiffness
Treatment of Chronic Pain
•What is the underlying dx? appropriate tx?
Chronic pain clinics
counselling: CBT
physiotherapy
CNS drugs
•! Opioids: not 1st line in chronic pain (too addictive)
Decrease excitatory neurotransmitters
drug: Gabapentin (Gabarone)
NMDA antagonists: NMDA receptor binds glutamate (excitatory neurotr.)
Enhance serotonin
Certain antidepressants which increase serotonin (serotonin modulates pain)
Efficacy overview
Treatment of inflammation: allergy, antihistamine
Tissue injury: NSAIDS, glucocorticoids, disease specifics (DMARDS
Bronchoconstriction: beta 2 adrenergic agonists
Treatment of pain: acetaminophen, NSAIDS, glucocorticoids, opioids
Treatment of fever: acetaminophen, NSAIDS