Unit 5: Pain and Inflammation Disorders and Medications

damage or trauma to tissue sets off

inflammatory response

To heal the area mediators are initiated that are

histamines and prostaglandins

histamines

natural chemicals made to protect the body

prostaglandins

hormones that manage healing

in a inflammatory response the kinin system is initiated this is a

a hormone regulator that when initiated causes an inflammatory response

inflammatory response activated the immune system that consists of

lymphocytes and myelocytes

Lymphocytes include

t cells, b cells, and NK cells

myelocytes include

neutrophils, basophils, eosinophils, monocytes/macrophages

symptoms of inflammation come from the release of

kinins and histamines

clinical manifestations of inflammatory response

pain, redness(erythema), swelling(edema), heat

osteoarthritis is known as

degenerative joint disease

osteoarthritis causes

deterioration of articulating cartilage and underlying bone, and inflames the joints

risk factors of osteoarthritis

age (older than 40), trauma to joints, occurs equally in men and women, obesity, heavy occupational work, and genetic predisposition

how to identify/clinical manifestations of osteoarthritis

heberdens nodes, bouchards nodes, joint pain/tenderness, joint swelling, joint stifness, altered gait, limited rom

rheumatoid arthritis is a

systemic autoimmune condition that damages many joints

rheumatoid arthritis primarily affects the

synovial membrane, but can also affect heart, skin, and eyes

rheumatoid arthritis are characterized by exacerbations and remissions meaning

there are times with no symptoms and others with acute painful swelling

rheumatoid arthritis causes

synovitis(synovial inflammation)

pannus formation(granulation tissue)

cartilage erosion

fibrous

ankylosis(joint fixation and deformity)

rheumatoid arthritis risk factors include

family history, advancing age, smoking, and female sex

clinical manifestation for rheumatoid arthritis

main symptoms grade fever, morning stiffness, swollen and boggy joints

other symptoms-fatigue/malaise, anorexia, lymphadenopathy, muscle spasms, stiff joints, bilateral joint pain, limited joint range, contractures and joint deformity,Unsteady gait

gout

recurrent joint inflammation caused by hyperuricemia

hyperuricemia

the overproduction of uric acid (created when the body breaks down substances)

increase uric acid in blood causes build up of

uric crystals in joints

Gout most likely affects what joint

first metatarsal

gout causes a defect in renal excretion causing most of it to be

uric acid (90%)

uric acid is a byproduct of

purine metabolism

gout risk factors

family history, african american males, women are affected until after menopause, high purine diet

gout clinical manifestations

tophi, joint pain, joint swelling, erythema

chronic-nepropathy, nephrolithasis, low grade fever

fibromyalgia

characterized by widespread muscular pains and fatigue

fibromyalgia affects

joints, muscles, tendons, and surrounding tissues

how many trigger points for fibromyalgia

18 throughout the body

no apparent inflammation or degeneration is noted in

fibromyalgia

why does fibromyalgia happen

uncertain of cause, could be an altered pattern of central neurotransmission that results in sensitivity to substance P(neurotransmitter responsible for pain sensation)

fibromyalgia causes decreased levels of inhibitory neurotransmitters like

serotonin and norepinephrine

fibromyalgia has an enhanced temporal summation of second pain meaning

the temporal lobe of the brain is delayed or enhanced, meaning longer lasting pain

fibromyalgia offers altered endogenous opioid analgesic activity meaning

if a medication opioid is taken it may alter it so it doesn’t give the pain relief needed

dopamine dysregulation and lowered pain threshold are what come with fibromyalgia this means

the rewarding neurotrasmitter is irregular and low pain tolerance

main clinical manifestation of fibromyalgia

widespread pain

salicytes common name

aspirin

how do salicytes work

inhibit synthesis of prostaglandin(stops the body from triggering pain and inflammation)

inhibit platelet aggregation(prevents clots)

pharmacokinetics of salicytes

peaks 5-30 min and metabolized in liver, excrete urine

adverse effects of salicylates

GI ulcers and bleeding

salicylates toxicity

main: ototoxicity(hearing doesn’t work)

nausea vomiting diarrhea, mental confusion

salicylates indications/ what it treats

mild to moderate pain, inflammatory conditions, reduce risk of CVA(stroke), reduce risk of MI(heart attack)

salicylates precautions

allergy to drug or NSAIDs, bleeding abnormalities, impaired renal function, chickenpox or flu, pregnancy/lactation, GI ulcers

salicylates nursing implications

evaluation, monitor pain and temp, CNS status, vital signs, monitor blood count, take with food

non-steroidal anti-inflammatory drugs(NSAIDs) main adverse effect

GI bleeding

nsaids adevrse effects

nausea, dyspepsia(heart burn), constipation, diarrhea, flatulence, Gi bleeding, headaxhe, dizziness, somnolence, fatigue, rash, anaphylaxis, and renal imparment

Nsaids indication/when used to treat

mild to moderate pain, Rheumatoid arthritis, osteoarthritis, primary dysmenorrhea(cramps), fever reduction

Nsaids precautions

allergy to drug or salicyte, hypertension or CV dysfunction, pregnancy/lactation, GI ulcers

Nursing implications for NSAIds

evaluation, monitor pain and temperature, CNS status,vital signs, monitor blood count, take with food

acetaminophen coommon name is

tylenol

how does acetaminophen work

acts directly on the thermoregulatory cells in the hypothalamus to cause sweating and vasodilation

Acetaminophen is a pain reliever, but

it is not known how it is related to analgesic effects

pharmacokinetics of acetaminophen

peaks .5-2 hrs, metabolized in liver excrete in urine

acetaminophen main adverse effect

liver failure

acetaminophen adverse effects

headache, anemia, liver failure/dysfunction

acetaminophen toxicity

liver failure but it can stop with acetylcysteine

acetaminophen is used when

mild to severe pain, fever, cold and sinus

acetaminophen precautions

allergy to drug, hepatic disfunction, chronic alcoholism

nursing implications for acetaminophen

evaluation, monitor pain and temperature, monitor liver function

gold compound is also known as

chrysotherapy

gold compound is only used in clients that are

unresponsive to conventional therapy due to its risk of toxicity

how does gold compound work

inhibits phagocytosis, blocks the release of lysosomal enzymes(degradation of foreign particles)

gold compound has

varying absorption rates and is excreted in urine and feces

gold compound example

auranofin

adverse effects of gold compound

depends on where they accumulate can cause inflammation, allergic reaction, and bone marrow depression

gold compound is used for

rheumatoid arthritis if not responsive to NSAIDS

gold compound precautions

allergy to gold, pregnant(partner can pass it on during sex), severe diabtes mellitus, heart failure, renal or hepatic impairment, hypertension, bone marrow depression, radiation therapy

gold compound nursing implications

evaluation, monitor pain and function level

tumor necrosis factor(TNF) blockers are

usually first line of treatment for arthritis

TNF blockers how do they work

inhibit phagocytosis, block release of lysosomal enzymes

TNF pharmacokinetics

given SQ, slow onset with peak of 48-72 hrs, excrete tissues, very long half life 4 days to 2 weeks

TNF examples

etanercept, adalimumab, certolizumab

adverse effects of TNF

black box warning: fatal infections and lymphoma/leukemia development, MI, heart failure, hypotension, multiple sclerosis(MS)

TNF indications/taken for

rheumatoid arthritis, other arthritis, ankylosing spondylitis(spine arthritis) , plaque psoriasis

TNF precautions

acute infection, cancer, myelosuppresion(bone marrow suppression) , demyelinating MS(attacks the myelin sheath,slowing down electrical signals), allergy to chinese hamster ovary products, pregnancy/lactation

TNF nursing implications

evaluation, monitor function/mobility level, do not give live vaccines, monitor blood count, cancer screening

DMARDS stand for

disease modifying anti rheumatic drugs

Other DMARDs are used when

other conventional treatment doesnt work

How do DMARDs work

blocks the increased interleukin 1, which degrades cartilage in rheumatoid arthritis

pharmacokinetics for DMARDs

SQ daily injection, peak 3-7 hrs, metabolized in tissues, excreted in urine

DMARDs examples

anakinra

dmards adverse effects

increase risk of infection

Dmards indications/used for

rheumatoid arthritis

precautions for DMARDs

allergy to drug, pregnancy/lactation, acute infection

DMARDs nursing implications

evaluation, monitor function/mobility, monitor blood count, cancer screening

how do corticosteroids work

depresses inflammatory and infectious/immune response

pharmacokinetics of corticosteroids

SQ daily injection, peak 3-7 hrs, metabolized in liver, excreted in urine

corticosteroids examples

prednisone, prednisolone, methylprednisolone

corticosteroids precautions

allergy to steroid, have acute infection, caution in diabetes mellitus

corticosteroids nursing implications

evaluation, monitor blood sugar and blood count

How does antigout (colchicine) work

stops the inflammation process by interfering with interleukin production

pharmacokinetics of antigout(colcichine)

oral, takes effect 1-2 hrs, metabolized in liver, excreted in urine, narrow therapeutic range

antigout example

colchicine

antigout (colcichine) precautions

pregnancy and breastfeeding, severe renal and hepatic disease , fatal overdoses, cannot be dyalized

antigout (colchicine)nursing implications

evaluation

how does antigout (allopurinol) work

lowers blood levels of uric acid in symptomatic patients

Antigout(allopurinol) pharmacokinetics

oral, reaches peak 1,5 hrs, excreted renally and feces

antigout(allopurinol) precautions

allergy and avoid thiazide meds