musculoskeletal Flashcards
normal synovial (diarthrodial) joints
a synovial or diarthrodial joint is any joint that allows movement.
name the 4 major parts that the joint is made out of?
think A&P.
subchondral bone plate.
articular cartilage.
synovium.
joint capsule.
subchondral bone plate.
sub = under
chondral = cartilage
bone just underneath cartilage
articular cartilage.
covers bone of the joint. it provides a smooth slippery surface that allows free movement of joint.
synovium.
the space (synovial cavity) between 2 articulating bones.
there is a synovial membrane that is the inner lining of this cavity.
the synovial membrane secretes synovial fluid that lubricates joint surface and removes debris.
joint (articular) capsule.
surrounds joint.
unites articulating bones
3 phases of bone healing
- inflammatory
- reparative
- remodeling
what happens during the inflammatory phase
(1) hematoma forms at the fracture site (provides stability & aseptic inflammation occurs).
Duration: 1-3 days for hematoma; 3 days- 2 weeks for early repair
what happens during the reparative phase
fibrous cartilage (2)- formation of granular tissue containing blood vessels, fibroblasts, osteoblasts.
callous (3)- formation of callous. when granular tissue has matured.
ossification (4)- space in bone is bridged & fracture ends unite. callus replaced by trabecular bone.
duration: 6 weeks
what happens during the remodeling phase
remodeling (5): bone consolidation with final remodeling. Healing is complete.
when do women experience greater bone loss and at what rate does it continue?
women experience greater bone loss in early menopausal years & it continues at a gradual rate.
who has lower peak density, men or women?
women
who reaches “fracture threshold” earlier, men or women?
women
at around age 30: bone reabsorbed by osteoclast (< or >) bone formed by osteoblasts.
pick > or <.
>
factors that affect bone mass
age
gender
race
genetics
reproductive status
calcium levels
exercise
osteopenia
thinning of the trabecular matrix of the bone before osteoporosis.
t-score of -1 to -2.5
osteoporosis
bone mineral density 2.5 standard deviations below peak bone mass.
“porous bone”, common serious disease.
used when ACTUAL BREAKS in the trabecular matrix have occurred.
how is osteoporosis measured and how are results reported?
measured with DEXA scan.
reported in T-Score
osteoporosis is characterized by….
low density & structural deterioration of the bone
what bones do osteoporosis usually occur in?
the hips, vertebrae, & wrist (trabecular bones)
osteoporosis characteristics
low bone mass.
micro-architectural deterioration.
increase in bone fragility.
susceptibility to fracture is high.
MAJOR risk factors for osteoporosis
aging
female
Caucasian
hx of fracture as an adult
family hx/genetics
body wgt <127 lbs.
smoking
alcohol use
corticosteroid therapy & immunosuppressive drugs.
MINOR risk factors for osteoporosis
thin, small frame.
lack of wgt bearing exercise.
lack of calcium &/or vitamin D.
eating disorders
gastric bypass surgery.
lack of estrogen/testosterone
excessive caffeine consumption.
osteoporosis pathogenesis
increased bone resorption: osteoclast activity increased.
decreased bone formation: osteoblast activity decreased.
problems for osteoporosis can be….
failure to make new bone (osteoblasts).
too much bone resorption (osteoclasts).
both.
early clinical manifestations for osteoporosis
NONE
late clinical manifestations for osteoporosis
fractures
pain
loss of height
stooped posture (kyphosis)
complication of osteoporosis
hip fracture
True or false: osteoporotic hip fractures are linked to increased risk of morality
TRUE. death does not happen because of the fracture, death happens d/t complications & r/t immobility.
complications of a hip fracture
pneumonia, blood clots, sepsis, skin breakdown, immobility.
what age are hip fractures more common?
> 65
are hip fractures more common in men or women?
women
most common location of a hip fracture?
proximal third of the femur
hip fracture: clinical presentation
sudden onset of hip pain before or after a fall.
inability to walk
severe groin pain
tenderness
affected leg is externally rotated and shortened
goal of osteoporosis pharm
reduce fractures
primary prevention of osteoporosis
calcium - diet+supplement (elemental calcium) = 1200 to 2000mg daily
vitamin D- diet+ supplement= 800 to 1,000 IU daily.
treatment of osteoporosis help ……. & ………..
promote bone formation (increase osteoblast) & decrease bone resorption (decrease osteoclasts)
aldendronate
class: biphosphates
MOA: binds permanently to surfaces of bones to INHIBIT OSTEOCLAST ACTIVITY
Indication: osteoporosis, reduces fractures by 50%
SE: GI (N/V/D), esophageal ulcerations
teaching: take with water, DO NOT lie down for 30 minutes after taking, DO NOT take with food, other drinks, calcium, or vitamins for 2hrs (very low bioavailability)
raloxifene
class: selective estrogen receptor modulators (SERMs)
MOA: mimics estrogen by increasing bone density; INHIBITS BONE RESORPTION
INDICATION: prevention & treatment of osteoporosis; reduces risk of spinal fractures by 50%
SE: hot flashes, leg cramping
Black box warning: stroke risk
NC: must take adequate calcium and vitamin D; DC @ least 72hrs before planned procedures (any prolonged immobilization period, high risk of blood clotting); DO NOT smoke, drink alcohol, or use if pregnant.
calcitonin- salmon
class: hormone therapy
MOA: inhibits bone removal by osteoclasts. slows down bone loss & increases spinal bone density.
INDICATION: treatment only
SE: nasal irritation d/t intranasal route.
NC: reduces spinal fractures by 30%, must take for @ least 5yrs to see long term benefits.
define fractures
any break in the continuity of bone that occurs when more stress is placed on the bone that it is able to absorb
causes of fractures
traumatic- fall
fatigue- repeated, prolonged stress
pathologic- weakened bone, possibly spontaneous (high risk in elderly)
open (compound) fracture
fractured bone penetrates skin
closed (simple) fracture
does not break through the skin
transverse fractures
straight line.
90 degree angle to the length of the bone.
most common in traumatic falls
spiral fracture
twisting fracture
comminuted fracture
more than one fracture line & more than 2 fragments
impacted fracture
bone moves into each other
(ex. people who fall and land on their feet)
greenstick fracture
common in children
incomplete break
(think of a bone getting sliced but piece does not detach)
stress fracture
from repeated use or fatigue
Clinical manifestations of fractures
the P.E.D
P = pain
E = edema (acts as natural splint)
D = deformity (loss of FUNCTION, abnormal MOBILITY).
why are the 3 phases of bone healing important?
because a lot of the complications r/t fractures are r/t the healing process.
name the 4 complications of fractures
delayed healing.
bone growth impairment
compartment syndrome
fat embolism syndrome
complication Delayed healing
3 month to 1yr after fracture.
1. delayed union = bone pain & tenderness increase; RF: tobacco use, old age, severe anemia, uncontrolled DM, decreased vitamin D, hypothyroid, poor nutrition, infection, complicated breaks.
2. malunion = improper alignment
3. nonunion = no healing 4-6 months post-fracture; causes: poor blood supply, repetitive stress
complication: impaired bone growth
pediatric consideration.
fracture through epiphyseal plate.
can delay future bone growth.
complication: compartment syndrome
seen with: crush injuries, cast
results from increased pressure within limited anatomic space.
“tourniquet effect”
manifestations: edema, loss/weakened pulse, PAIN
what is the “tourniquet effect” in relation to compartment syndrome?
edema at the fracture site puts intense pressure on soft tissues.
can lead to tissue hypoxia of muscles and nerves
complication: fat embolism syndrome: what is it?
fat molecules in lung following LONG BONE FRACTURE or major trauma
complication: fat embolism syndrome: how do they get there?
fat molecules from bone marrow or traumatized tissue release into the blood stream and go into the lungs.
complication: fat embolism syndrome
MANIFESTATIONS
hypoxemia, altered LOC or completely decreased LOC, petechial rash.
osteomyelitis: definition
an acute or chronic pyogenic infection of bone
osteomyelitis: cause
bacteria (staph aureus)
osteomyelitis: risk factors
recent trauma
DM
HD
IVDU
splenectomy
osteomyelitis: pathogenesis
pressure increases within the bone and causes local arteries to collapse.
decreases or eliminates supply of: oxygen, nutrition, immune cells, ANTIBIOTICS.
leads to impaired healing therefore difficult to treat.
osteomyelitis: clinical manifestations (local & systemic)
local: tender, warm, red, wound drainage, restricted movement, spontaneous fracture
systemic: fever, positive blood culture, leukocytosis.
osteomyelitis: pharm
obtain culture.
empiric abx therapy: nafcillin, cefazolin, vancomycin
bacteria specific therapy
which joint do most disorder affect?
synovial joints
Arthropathy
a joint disorder.
Arthritis
inflammation of one or more joints
route of contamination: direct
open wound: open fracture, gunshot, puncture (stabbing), surgery (sternotomy)
surgery/insertion of metal plates or screws
route of contamination: indirects
from bloodstream (most common)
bacteremia
osteoarthritis (OA): definition
degeneration of joints caused by aging & stress
osteoarthritis (OA): common joint affected
cervical spine
lumbosacral spine
hip
knee
hands
first metatarsal phalangeal joint (big toe)
osteoarthritis (OA): spared joints
wrists, elbow, ankles
osteoarthritis (OA): risk factors
aging >40
obesity
hx of participation in team sports (prolonged)
hx of trauma or overuse of joint
heavy occupational work
misalignment of pelvis, hip, knee, ankle, or foot
osteoarthritis (OA): etiology
stresses applied to joint (wgt bearing)
degeneration of cartilage (excessive loading of healthy joint, normal loading of previously injured joint)
chronic disease.
osteoarthritis (OA): pathophysiology
prolonged excess pressure on joint wears away cartilage & subchondral bone exposed that leads to cyst development.
cysts move through remaining cartilage & destroys the rest.
localized inflammation leads to more degradation.
chondrocytes synthesize fluid called proteoglycans to try & repair causing swelling.
osteoblast activation leads to bone spurs & synovial fluid thickening = less movement.
loss of cartilage narrows joints space.
osteoarthritis (OA): clinical manifestations
Deep, aching joint pain, especially with exertion & Relieved with rest.
Joint pain with cold weather
Stiffness in morning
Crepitus of joint during motion
Joint swelling
Altered gait
Limited ROM
osteoarthritis (OA): physical exam
joint tenderness
joint deformity
decreased ROM
fingers often involved: Herbeden’s nodes, Bouchard’s nodes
Herbeden’s nodes
distal interphalangeal joint
Bouchard’s nodes
proximal interphalangeal joint
treatment goals for OA
Manage pain
Maintain mobility
Minimize disability
goal of pharmacotherapy
manage pain and reduce swelling
mild to moderate treatment for OA
acetaminophen, topical capsaicin, NSAIDS (OTC)
moderate to severe treatment of OA
NSAIDS (Rx strength), NSAIDS + colchicine, acetaminophen + tramadol, opioids, steroid injections (into joint)
NSAIDS
Use lowest effective dose possible
Can affect kidney function
Risk for GI bleed: risk increases dramatically with aging, Contraindicated for patients with PUD, Use with caution in those with history of GI bleeds or on anticoagulation therapy
other treatments for OA
Dietary supplements: Chondroitin sulfate and glucosamine
Artificial joint fluid– contains hyaluronic acid
Joint replacement, arthroplasty
Degenerative Disc Disease (DDD)
common cause of pain, motor weakness, & neuropathy.
most often occurs in the lumbar or cervical spine.
specific to spinal cord
effects men & women equally
2nd most common reason people visit the drs.
Degenerative Disc
Intervertebral disc compression occurs with age.
Motor & sensory spinal nerves enter & exit from the spinal cord & travel through narrow openings of the vertebral bone.
With age, intervertebral discs dehydrate & vertebral bone become compressed & impinge on the entering & exiting nerves.
Dysfunction of motor & sensory spinal nerves impedes movement & sensation in the extremities.
May see weakness & paresthesia’s
S/S of DDD: lumbar & cervical
lumbar: pain- lower back that radiates down the back of the leg (sciatica), in the buttocks or thighs, worsens when sitting, bending, lifting, or twisting, minimized when walking, changing positions, or lying down. Numbness, tingling, or weakness in the legs, Foot drop.
Cervical: Chronic neck pain can radiate to the shoulders & down the arms; Numbness or tingling in the arm or hand; Weakness of the arm or hand
Rheumatoid arthritis (RA): definition
Systemic, autoimmune disease
Type III hypersensitivity
Inflammatory disease of synovium
Rheumatoid arthritis (RA): etiology/ risk factors
Not well understood
Environmental and genetic factor: Genetic link + triggering event; Inappropriate immune response to joint injury.
Age: 40’s-60’s
Women
Tobacco use
Family history (genetic link)
Rheumatoid arthritis (RA): pathogenesis
Immune cells attack synovial tissue
Immune cells: lymphocytes and macrophages
Produce rheumatoid factor (RF): Antibody against the body’s own antibodies (IgG), Formation of immune complex.
Rheumatoid arthritis (RA): a progressive disease
Intensifying inflammatory response
Cartilage destroyed by osteoclasts
Pannus develops: inflammation and exuberant proliferation of synovium (hypertrophied synovium)
Pannus leads to: Bone erosion, Bone cysts, Fissure development.
Rheumatoid arthritis (RA): clinical manifestations
EARLY: very little, maybe joint pain/discomfort, siffness.
EVENTUAL joint manifestations: Symmetrical, Pain, stiffness, motion limitation; Inflammation: heat, swelling tenderness; swelling in soft spongey and warm.
ADVANCED disease: deformity and disability, joint subluxation.
Rheumatoid arthritis (RA): systemic involvement
Fatigue and malaise.
Potentially affects any and all body systems (Depending on severity).
IMPORTANT TO ASSESS THE HEART: can develop pericarditis, myocarditis.
Most common: Sjorgren’s Syndrome, Rheumatoid nodule
Sjorgren’s Syndrome
destruction of moisture-producing gland (salivary and lacrimal)
Rheumatoid nodules
immune mediated granulomas; develop around inflamed joints, subcutaneous and firm, sometimes painful
Goals of Pharm for RA
Relieve pain and swelling
Slow or stop progression of disease
Long term drug therapy requires patient adherence
long term drug therapy for RA
NSAIDS
Glucocorticoids (short-term)
Disease-modifying anti-rheumatic drugs (DMARDS): slow/stop progression.
Corticosteroids in RA
Rapid suppression of inflammation
Use only when symptoms NOT controlled with NSAIDS
Not best choice for long term therapy
Usually small doses <10mg/day (seen as small as 2.5mg)
Methotrexate
CLASS: antineoplastic, anti-rheumatic, DMARD
MOA: : immunosuppressive
INDICATION: first line therapy
SE: GI, Bone marrow suppression, Shortened life expectancy.
NC: 11 black box warnings, need folic acid supplementation, NO alcohol (liver involvement), Teratogenic– NEVER for pregnant female, Higher risk of infection: contact HCP if there are signs of infection-Pneumocystis carinii, Caution with liver and kidney disease, Aplastic anemia risk when using with NSAIDs. MONITOR LIVER ENZYMES.
hydroxychloroquine
CLASS: antimalarial, anti-rheumatic, DMARD
MOA: Unknown, anti-inflammatory processes; Slow progression of RA when used in combination with other DMARDs
INDICATION: Used alone or in combination with methotrexate for early/mild RA.
SE: retinopathy (rare)
NC: Very expensive, Can increase risk of severe skin or lung infections, skin cancers, serious allergic reactions, Biologic response modifiers, Target parts of the immune system that trigger inflammation that cause joint and tissue damage.
Gout: definition
INFLAMMATORY disease resulting form deposits of uric acid crystals in tissues and fluids within the body.
Gout: pathogenesis
Key Concept: URIC ACID CRYSTAL deposits in tissues
Gout: etiology
HYPERURICEMIA
Overproduction & Under excretion of uric acid
Gout: risk factors
Obesity
Preexisting diseases: HTN, DM, Renal disease, sickle cell anemia
Consuming ETOH (beer and spirits)
Diet rich in meat and seafood
Use of diuretics
Most common in males
African Americans
phases of gout
Phase 1: ASYMPTOMATIC but with elevated serum uric acid levels & deposits in tissues, Crystals accumulate & tissue is damaged, Tissue damage triggers ACUTE INFLAMMATION
Phase 2: ACUTE FLARES or attacks occur- hyperuricemia.
Phase 3: CLINICALLY INACTIVE until the next flare – continued hyperuricemia. May be months or years before the next flare. Later, reoccurring attacks get closer and closer together
Phase 4: CHRONIC ARTHRITIS – joint pain and other sx present most of the time
What causes uric acid crystals to form?
From the breakdown of PURINES
Body makes purine
Found in food: organ meats, shellfish, anchovies, herring, asparagus, mushrooms
Normally, uric acid dissolves in the blood and excreted by the kidneys.
Gout: Clinical Manifestations
PAIN: may be mild or excruciating, usually the lower extremities.
Burning
Redness
Swelling and warmth
Fever
Symptoms present for days to weeks
Metatarsophalangeal joint of the big toe is the presenting joint for 50% of people with gout.
Gout complications
Tophi.
renal calculi.
Tophi
large HARD NODULES composed of uric acid crystals deposited in soft tissues.
May form below the skin around the joints
Can cause a local inflammatory response
May drain CHALKY MATERIAL
Goal of Gout Pharm
Decrease symptoms of an acute attack AND prevent recurrent attacks
what is usually the first line therapy for gout?
NSAIDS
allopurinol
CLASS: Xanthine oxidase enzyme inhibitors
MOA: inhibits the xanthine oxidase enzyme, which PREVENTS uric acid production
INDICATION: pts whose gout is r/t EXCESS uric acid production (as seen by hyperuricemia); PREVENTION MEDICATION.
SE: : agranulocytosis, aplastic anemia, known to cause fatal skin reactions (SJS/TENS)
NC: interactions: anti-diabetic meds & warfarin. monitor WBC/RBC
colchicine
CLASS
MOA: reduces inflammatory response to the deposits or urate crystals in joint tissues.
INDICATION: gout flares and prophylaxis
SE:GI & urinary bleeding.
contraindicated: : any person with severe renal, GI, hepatic or cardiac disorders, or bleeding disorders
NC: second line therapy, PO only. Powerful inhibitor of cell mitosis and can cause short-term leukopenia: Bone marrow suppression.
Probenecid
CLASS: Uricosuric Agent
MOA: Inhibits reabsorption of uric acid in kidney, promoting excretion.
INDICATION: Treats hyperuricemia with gout
SE: GI upset, Dizziness or headache, Kidney/Liver impairment, Lots of drug interactions
NC: Used alone or in combination with allopurinol when not effective alone
Lupus: Pathogenesis
B-lymphocytes are hyperactive and produce autoantibodies
MAJOR antibody produced: ANA: antinuclear antibody.
Activated against DNA
Formation of: Immune complexes
Can impact all major organ systems!
Inflammatory response destroys tissue
Lupus: Predisposing Factors
Genetic factors
Gender: females
Age: 20-40
Race: Black/African Americans Higher likelihood
Environmental Triggers (EX. sun exposure)
Allergy to antibiotics
Hormonal factors (EX. birth control that contains estrogen, or women who start menstruation before 10)
Tobacco use
Lupus: Manifestations
Extreme fatigue
Photosensitivity
Butterfly rash*
Fever
Weight changes
Unusual hair loss
Edema
Raynaud’s Phenomena*
Lupus: Manifestations (think organs)
CNS: HA, dizziness, seizures, stroke
Lungs - Pleuritis, pleural effusions
Heart - Myocarditis & endocarditis
Kidneys - Nephritis**
Blood vessels - Vasculitis
Blood - Anemia, leukopenia, thrombocytopenia, blood clots
Joints - Arthritis
SLE: Flares
Clinical course: exacerbations & remissions
A flare is: acute exacerbation of symptoms
Warning signs of a flare: Fatigue, Pain, Headache.
Prevention: recognize warning signs and avoid triggers- Sunlight exposure, Infection, Abruptly stopping a medication, Stress
SLE: Pharmacotherapy
GOAL: to control symptoms
NSAIDS
high dose corticosteroids
low dose corticosteroids
antimalarials (hydroxychloroquine)
immunosuppressives (methotrexate)
