Systemic Conditions Flashcards
Ankylosing spondylitis
Chronic inflammatory disorder of axial skeleton resulting in formation of new bone at attachments of ligaments and tendons
Caucasian, male, 15-35 yrs, HLA-B27
DX: inflammatory back pain + x-ray (SI joint fusion, sacroiliitis, bamboo spine, etc)
+Schober’s, increased ESR, CRP, alk phos
CRPS
pain syndrome d/t nerve disorder that occurs at site of injury where patient experiences intense, burning pain in one or more extremities; results in pain that is usually non-anatomic and disproportionate to initial event or expected healing response
Describe/define OA
Progressive degeneration, loss of articular cartilage, subchondral bone and joint capsule of synovial joints. Pain from effusion (stretching joint capsule), increased vascular pressure on subchondral bone, periarticular myospasm or bursa inflammation, or torn meniscus or fibrocartilage complexes. Can be d/t wear and tear or secondary to metabolic disturbances, genetic predisposition etc.
Osteoporosis definition/description
General decrease in bone density resutls in fragile bones and increased risk of fractures, even after minimal trauma. Axial skeleton most affected, as well as pelvis and proximal long bones (femur).
Gout
Group of metabolic conditions that manifest in acute arthritic events initiated by urate crystals in affected joints and soft tissues
Acidosis predisposes to crystal formation
HTN, obesity, diabetes, hyperlipidemia, renal insuff, genetics, high purine diet, dehydration, starvation, hypothyroidism…etc
Spontaneous onset painful, hot, erythematous, tender, swollen MTP joint
Early x-ray unremarkable; later can show bony erosion, joint space narrowing and joint destruction
Labs: hyperuricemia
Dx: joint aspiration during attack shows monosodium urate crystals in synovial fluid
What pain med can pts w/ gout NOT have?
aspirin - can alter uric acid levels and prolong attack
Can use NSAIDs. Indomethacin, COX-2 inhibitors, Colchicine (w/in first 24 hrs), allopurinol are options.
What is the goal of gout tx?
Keep serum uric acid levels to 6mg/dL or less
What is the pathophysiology of OA?
Early: mechanical lesion or stress leads to degenration. Mild subchondral reactive sclerosis. Synovial fluid loses viscosity and cartilage wears out. Chondrocyte metabolism increases production of cartilage matrix destroying enzymes
Middle: Irregular joint space due to loss of cartilage, cartilage fragmentation (joint mice), reactive sclerosis.
Late: osteophytes, periarticular fibrosis, cartilage calcification, subchondral cysts (geodes). Exposure of subchondral bone after loss of cartilage causes joint instability, compensatory bone overgrowth and remodeling (reactive sclerosis and osteophyte formation). Fibrous adhesions and bony ankylosis may occur. Breakdown products create chronic inflammatory repsonse in synovium
Risk factors for OA
female (more likely to develop OA in hands)
age, obesity, trauma, genetics, menopause, infection, crystal deposition, acromegaly, previous RA
Presentation of OA
gradual onset of deep, achy joint pain worse in morning, better with mild activity and worse with excessive activity
limited ROM, crepitus
pain at rest or at night indicates severe progression
affected by changes in barometric pressure
OA PE
Heberden’s nodes (DIP)
joint enlargement
limited ROM
crepitus and pain w/ passive motion
Ortho tests for OA
anything that compresses damaged cartilage can reproduce symptoms (Scour, Ellman’s, etc)
X-ray findings in OA
large weight bearing joints: non-uniform joint space loss, subchondral sclerosis and cysts, osteophyte formation, joint mice
spine: osteophytes, facet arthrosis, loss of disc height, curve changes
What is the pathophysiology of OA?
exact mechanism not well understood
bone loss occurs without symptoms, fracture is often first indication of problem
typical preceding events are menopause, advanced age
bone mass peaks in mid 20’s
women lose a greater percentage of cortical bone and trabecular bone over lifetime compared to men
What are the types of OA?
postmenopausal - thought to result from estrogen and testosterone deficiency
senile - d/t decreased formation of bone and decreased renal production of vitamin D3 occuring later in life
secondary - d/t medications (glucocorticoids) or other conditions
Risk factors for OA
female age genetics European or Asian descent Strenuous exercise resulting in amenorrhea Smoking, alcohol, low physical activity Low calcium, vitamin D intake Parathyroid abnormalities Low BMI
Presentation of OA
usually asymptomatic until fracture
gradual height loss, increased kyphosis
fracture may cause: severe back pain, loss of height, thoracic kyphosis, breathing difficulties if kyphosis and rib fractures, reduced mobility
