FINAL: MSK Flashcards
What are two of the most common MSK disorders?
Osteoarthritis (less severe then RA) and rheumatoid arthritis
What is the most common form of arthritis and what is it caused by?
Osteoarthritis
> Caused by “wear and tear” on the body
that causes formation of bony buildup and
loss of articular cartilage in peripheral and
axial joints
○ Aging mechanical stress on the joints
Who is generally affected by OA?
people > 40 but most common over 60; found in men and women
What does OA affect?
Usually only affects the joints (not systemic)
Who is generally affected by RA?
more women then men b/w ages 20-50
What is occurring in patients experiencing RA?
The Immune system is attacking the body. It is an autoimmune disorder characterized by inflammation (therefore, symptoms can be felt throughout the entire body (systemic).
*** Genetic link (HLA DR alleles) that is specific to the X-chromosome which highlights the higher prevalence in females
What are some s/sx of OA?
○ Joint pain:
> Aching pain d/t synovial inflammation
and fibrosis of the joint
▪ Usually worsens with activity
□ Relieved by rest
○ Gelling
> Pt has difficulty initiating the joint
movement after a period of inactivity
▪ Stiffness of the joints (knees) when
initiating movement
□ “Getting joints warmed/oiled up…… “
○ Limitations in joint motion and stability
○ Crepitus
○ Joint locking upon movement
○ Joint enlargement
What joints are most affected by OA?
Hips, knees, lumbar & cervical vertebrae, PIP & DIP in hands, first carpometacarpal joint (base of thumb), and the first metatarsophalangeal joints of the feet (Great Toe)
Explain the development of the bouchard’s and hebreden’s nodes and why they occur
▪ Bouchard’s Nodules occur at the proximal IP joint
▪ Hebreden’s Nodules occur at the distal IP joint
- Occur d/t repeated trauma of the joint *
Explain the patho of OA:
Cartilage protects the bones from rubbing together
- OA results in injury to the chondrocytes and release of cytokines
(interleukin I, TNF) - Cytokines stim the release of Proteases (enzymes) that destroy the
joint structure - Chondrocytes are more susceptible to more injury and the cycle goes on and on
○ Inhibits their ability to repair itself - Chondrocytes become enlarged and disorganized
○ Trying to compensate for the quickly
deteriorating cartilage - Results in Inflammation of the cartilage and the cartilage loses its smooth/cushioning effect
○ Develops surface cracks and synovial
fluid seeps in the cracks
and causes widening of the cracks - Eventually completely wears through to the bone
○ Bone rubbing on bone
○ Fragments of cartilage and bone
become dislodged and float and causes
widening of the cracks
- Eventually completely wears through to the bone
○ Bone rubbing on bone
○ Fragments of cartilage and bone
become dislodged and float
in the joint cavity
- Synovial fluid leaks through these defects into the bone
○ Can lead to development of cysts inside the bone & osteophytes (bone spurs)
How is OA diagnosed and treated?
○ Pt Hx
○ XR, labs
○ Trying to exclude the presence of other diseases
○ There is no cure but symptomatic treatment is available. Oral medications can be taken and are aimed at reducing inflammation & pain relief (NSAIDs, ASA, Corticosteroids injection, Prednisone).
□ Have to take the meds frequently =
increases r/o GI bleeding w/ NSAIDS &
ASA
□ Corticosteroid injections are given
sparsely apart and w/ a small dose d/t
longterm effects (1x injection q3mos)
▪ Tylenol can help w/ pain but NOT
INFLAMMATION
What is the patho for RA?
○ Abnormal immune response = synovial inflammation and joint destruction
▪ Destruction of the joint (hypertrophy) is
irreversible (disease gets worse and is
very
debilitating)
▪ Disease can be launched w/ CD4 T-cell
mediated response d/t
immunologic triggers (infxn, stress,
bacterial, viral, etc.)
○ Rheumatoid Factors- (80% of people)
▪ RF reacts w/ IGG and forms immune
complexes
▪ High serum RF Titer = more severe sxs
& unremitting disease
○ INFLAMMATORY RESPONSE = Increased blood flow & capillary permeability
▪ Synovial cells and sub-synovial tissues
undergo reactive hyperplasia (abnormal
inc. of cell numbers)
▪ PANNUS: destructive vascular
granulation tissue forms b/w cartilage and
subchondral bone, limiting ROM and leads
to complete joint fusion; this only occurs in
RA
What are some articular manifestations for RA?
○ Joint involvement is symmetric and poly-articular = multiple joints involved
▪ Bilateral joints are effected at the same
time
▪ THIS IS DIFFERENT FROM OA (OA
depends on WHERE the wear/tear
occurred)
○ Pain and stiffness (lasting for 30 minutes – several hours)
○ Progresses to larger joints
▪ Ankles, knees, shoulders, etc.
▪ Spinal involvement is limited to the
cervical vertebrae
○ Progressive joint destruction leads to subluxation
▪ Subluxation = dislocation of the joint
and bone ends are misaligned
□ Leads to instability and limited ROM
of the joint / loss of fxn
○ Stretching of joint capsule and ligaments leading to joint deformities resulting in loss of function
This condition is hyperextension of PIP and partial flexion of DIP, is fairly common in long term RA pts and results in loss of fxn in hands
Swan Neck Deformity
What are some extra articular (systemic) manifestations for RA?
○ Fatigue / Weakness
▪ Fatigue related to systemic
inflammation (immune response)
○ Anorexia and weight loss (d/t inflammation like above)
○ Elevated ESR and CRP (inflammatory response)
▪ The more elevated, the higher the
severity of the RA
○ Rheumatic nodules
▪ Granulomatous lesion that can have a
central core filled w/ fibrin and proteins
▪ Usually occur on the bony surfaces
(edge of forearm)
▪ May or may not occur, and may be
tender… or not
▪ Vary in size
○ Dryness of the eyes, mouth and mucous membranes (more advanced sxs)
○ Episcleritis, scleritis, scleromalacia (eye issues)
○ Pulmonary fibrosis, pericarditis
○ Splenomegaly and lymph node enlargement
▪ D/t inflammatory process
○ Vasculitis (as in ischemic areas in the nail folds)
How is RA diagnosed?
○ Based on findings of patient history & physical examination
○ XR & blood tests
○ At least 4 criteria (from ARA) must be present for diagnosis
▪ Morning stiffness lasting x1 hr for 6 wks
▪ Simultaneous swelling of 3+ joints x6
wks
▪ Swelling of the wrist, PIP joints x6 wks
▪ Symmetric joint swelling x6 wks
▪ Presence of bone nodules
How is RA treated?
Goals: ▪ EDUCATE ▪ Reduce pain ▪ Minimize stiffness and swelling ▪ Maintain mobility
○ Physical rest
▪ Balance w/ mobility to prevent
permanent loss of ROM
▪ Reduces stress on the joints
○ Therapeutic exercises
▪ Help to maintain ROM of the joint and
improve muscle strength to prevent
atrophy
○ Safe use of heat and cold = nonpharm pain relief
○ Relaxation techniques
○ Medications:
▪ Salicylates (ASA) (can cause GI issues if overused)
▪ NSAIDs
▪ COX-2 inhibitors
□ Celebrex
□ Salicylates
□ Blocks prostaglandin synthesis which
decreases inflammatory response (less
tendency for GI bleeds than ASA)
▪ DMARDs
□ Disease Modifying Anti-Rheumatic
Drugs
□ Work to reduce the sxs of RA (prevent
permanent tissue damage of the joints)
□ Methotrexate (drug of choice)
□ DMARDs can be toxic and require close
monitoring for adverse effects (bone
marrow suppression)
▪ Corticosteroids
□ Help w/ pain, but don’t modify disease and don’t protect against joint destruction
□ Simply symptomatic treatment
▪ Biologic agents (Remicade, Enbrel, Humira, & drugs ending in “-umab”)
□ Block TNF (inflammatory mediator)
What can lead to gout?
alcohol and dieting
Describe the results of an acute gout attack
Acute attack is usually mono-articular
○ Most common joint = great toe
○ Attacks usually occur at night and
follow a pattern (activity during the day
and pain at night)
Explain the patho for Gout:
○ Elevation of serum uric acid
□ End product of PURINE metabolism
□ Can be from overproduction of Purines,
Uric Acid, or inadequate elimination of
uric
acid through urine
> Treat based on the underlying problem
○ Monosodium urate crystals precipitate in joints resulting in inflammation
○ Repeated attacks lead to chronic arthritis and tophi (large, hard nodules)
▪ Tophi don’t appear until after about 10
years w/ gouty flare-ups
What are the s/sx of gout?
○ Pain
▪ Onset of pain is abrupt
▪ Can be VVV severe (weight of
bedsheets on toes cause severe pain!)
○ Redness, swelling, may begin at night
○ Low grade fever, pruritis and renal calculi
How is gout diagnosed?
○ Synovial fluid analysis
▪ Look for monosodium urate crystals,
tophi, etc.
○ Serum uric acid levels
○ 24 hours urine sampleHow is gout treated?
○ Reduce inflammation
▪ Allopurinol (reduces uric acid levels)
▪ NSAIDs
▪ Colchicine
□ Anti-inflammatory
□ Given PO & IV (IV acts rapidly to
decrease acute attack
▪ Steroids
○ Nonpharm
▪ Alcohol cessation
▪ Maintain ideal body weight (obesity =
predisposing)
▪ Avoid foods high in purines
□ Red meat
□ Organ meat (liver, kidney)
□ Sardines, anchovies
This condition is a very common cause of complaints in the elderly and results in pain, weakness, and muscle stiffness; it can be very debilitating and lead to decreased QOL, life span and depression
rheumatic disease
What factors affect daily life, threaten independence, and quality of life?
Pain, Stiffness and Muscle Weakness
- Mobility: Weakness & pain = Gait Disturbance = increased r/o falls and fractures = decreased independence
How is rheumatic disease treated?
Non-Pharmacological Treatment:
○ Aimed at reducing load on joints & maintaining mobility
▪ Lose weight & use walking aids to
reduce load
▪ Muscle-building exercise
▪ Muscle-strength & stretch particularly
effective with early start
▪ Local heat
○ Caution: excess rest provides PAIN RELIEF BUT causes lost muscle strength & immobility
Drug Therapies:
○ NSAIDS & Analgesics
▪ NSAIDs not tolerated as well & side
effects more serious
○ Elderly have decreased renal and liver fxn = decreased drug metabolism
This condition is very hard to treat and can cause acute or chronic infection of the bone and marrow
Osteomyelitis
What is the most common source of infection that results in osteomyelitis?
the microorganism S. Aureus and MRSA
- these microorganisms can be introduced during injury, operative procedures, from the blood stream (systemic infxn that travels to the bone and cultures). acute osteomyelitis usually occurs from a foreign object being introduced into the bone *
What are some s/sx of osteomyelitis?
○ Severe Pain (exacerbated w/ movement)
○ Warmth, swelling, redness, etc.
○ Fever, chills, malaise
○ Nausea
○ Drainage of pus through the skin if infxn is severe enough
○ Post-Op Osteomyelitis sxs:
▪ Persistent and recurrent fever
▪ Severe pain at the operative
site/trauma site
▪ Poor incision healingHow is osteomyelitis treated?
○ Identification of causative organism (via blood, bone or wound culture and sensitivity)
▪ Have to treat w/ the right Abx since it is
so serious
○ Antimicrobials (Abx, antivirals, etc.)
○ Debridement and/or surgical intervention may be used
** MUST TREAT OSTEOMYELITIS w/ LONG TERM IV Abx THERAPY **
Explain some facts about hematogenous osteomyelitis:
○ Comes from bacterial source in blood
stream
○ Rapid onset (few days) after primary infxn
▪ Resolves in 6-8 wks
Explain some facts about hematogenous osteomyelitis in children:
○ More common d/t immature bone tissue / rapidly dividing cells / high vascularity
▪ Affects long bones near the growth plates (terminal ends of arteries allow bacteria to
sequester
▪ Purulent exudate collects inside the bone
□ Not much room for expansion/swelling
□ Exudate has to escape the bone and
begins to seep out behind the periosteum
which damages the arteries that feed the
bone
- Results in necrosis
▪ May penetrate skin and involve joints
Explain some facts about hematogenous osteomyelitis in adults:
▪ More common in males > females (males = increased risky behavior = increased r/o trauma)
▪ Seen in debilitated pts-
□ Chronic UTI's
□ Chronic/recurring Skin Infections
□ Diabetes Mellitus
□ IV DRUG USERS (S. aureus &
pseudomonas)
□ Immunosuppressed
▪ In vertebrae, sternoclavicular, & sacroiliac joints/pubic symphysis
▪ Tends to affect joint spaceExplain some facts about chronic osteomyelitis:
○ More common in adults
○ Infxn continues past expected course (6-8 wks) and can last for years
▪ Usually results from inadequate or
delayed treatment of Acute
Hematogenous Osteomyelitis
What is the hallmark s/sx of chronic osteomyelitis?
Sequestrum
▪ Areas of dead bone separated from
healthy bone
How is chronic osteomyelitis treated?
Treat w/ IV Abx and surgery to remove necrotic bone & surgical devices that may have caused the infxn
This condition results in demineralization of bone leading to fragile bone and subsequent fractures
Osteoporosis
What is the patho for osteoporosis?
○ Unclear; imbalance between bone resorption and formation in which resorption exceeds formation
○ Bone loss varies depending on age, gender, genetics, activity
○ Bone mass density (BMD)-determinant of the subsequent risk for osteoporosis
> Race is key determinant of BMD and
the risk of fractures
> Women have higher fracture rates
> White and Asian women have higher
rates for all age groups over 50 years of
age
> Body size
> Hormonal factors
What are the 2 disease processes for osteoporosis?
- Postmenopausal
- Senile
What are some s/sx of osteoporosis?
- Back pain
- Pelvic or hip pain
- Problems with balance
- Decline in height
- Kyphosis of dorsal spine
- Pathological fractures
How is osteoporosis diagnosed?
- WHO Osteoporosis Screening Tool, Fracture Risk Assessment Algorithm
- Dual-energy x-ray absorptiometry (DXA) of the spine and hip
- Measurement of serial heights in older adults
- Refinement of risk factors
How is osteoporosis treated?
- Prevention and early detection
- Regular exercise to strengthen muscles
- Adequate calcium intake
- Instruct about diet and medications to promote bone strength and inhibit bone loss
- Estrogens, SERMs, biphosphates, and calcitonin
This is a major chronic inflammatory rheumatic disease that affects any organ system
Systemic Lupus Erythematosus
Who is more affected by SLE?
females (85%) more than makes and more common in AA, hispanics and asians
What are the 4 types of lupus?
- SLE
- Cutaneous lupus erythematosus
- Drug-induced
- Neonatal lupus
What is the patho for SLE?
- Cause unknown
- Formation of autoantibodies and immune complexes
- B-cell hyperactivity and increased production of antibodies against self and non-self antigens
What are some major triggers for SLE?
- sunlight
- infectious agents
- stress
- drugs
- pregnancy
What are some clinical manifestations for SLE?
- joint pain
- fever
- butterfly rash
- nephritis
- pleuritis
- pericarditis
How is SLE diagnosed and treated?
Dx:
- Complete history, physical exam, blood work analysis
- Immunofluorescence test for ANA
Tx:
- Management of the acute and chronic symptoms
- NSAIDS, antimalarials, corticosteroids, immunosuppressives
What education should be provided to a pt with SLE?
- Pain management and conservation of energy
- Avoid exposure to ultraviolet rays and reduce stress
- Use mild soaps, creams for skin care.
- Therapeutic exercise and heat therapy
- Pregnancy counseling
