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
