Osteoarthritis & Chronic Inflammatory Arthritis Flashcards
1
Q
Impact of Arthritis
A
- 1 out of 5 US adults carries diagnosis of arthritis (52 million)
- Most common is osteoarthritis (degenerative)
- Other forms : RA, lupus, gout
- 2/3 individuals with arthritis are <65 yo
- More common among women (26%) vs men (19%)
- $128 billion in medical expenditures/lost earnings in 2003
2
Q
Osteoarthritis (OA)-aka Degenerative Arthritis-General (1/2)
A
- Characterized by DEGENERATION (wear and tear) of articular cartilage
- **Distinct from an inflammatory arthritis
- Chondrocytes of articular cartilage respond to biomechanical and biologic stresses in way that results in breakdown of matrix
- Most common type of arthritis
- Classified as primary or secondary
- Primary most common
- secondary-see with trauma (knee or shoulder)
3
Q
Secondary OA
A
- several ways to develop
- **trauma
- inflammatory arthritis
- dysplastic and hereditary conditions
- Kashin-Bek dz
- bone disorders
- metabolic and endocrine disorders
4
Q
Osteoarthritis (OA)-aka Degenerative Arthritis-General (2/2)
A
- Seen most commonly in persons >65 yo
-
Radiographic changes
- >45 yo: knee 37%, hip 27%, hands >90%
- Most with radiographic changes have few sx
-
**Symptomatic OA (lower #s)
- >45 yo: 17% knee, 9% hip
- Lifetime risk of symptomatic OA of knee: 66%
- Higher with obesity and risk factors
5
Q
OA/DA: Pathogenesis-RF
A
- *Age=strongest RF*
-
Obesity most associated with OA of the knee but may contribute to hip & hand
- Leptin may have influence on chondrocytes
- Chronic repetitive impact loading
- Long term weight bearing sports
-
Genetic factors (if gma has bony nodules)
- Many have family history, especially finger involvement in women
- Jt dysplasia increases risk for hip OA
6
Q
Nml Morphology (3+1 main players)
A
- Specialized connective tissue
- Collagen, proteoglycans, water, chondrocytes
-
Collagen: Mostly type II collagen
- Distributes compressive forces
- Tethers cartilage to subchondral bone
- Dissipates weight bearing force, protecting soft tissue & subchondral bone
-
Proteoglycans=cushion
- Aggrecan: high fixed negative charge allows for retention of water
-
Chondrocytes mediate turnover of matrix components
- Sparsely scattered
- Chondrocytes influenced by factors ie) GF, cytokines, physical stimuli
7
Q
OA/DA Morphology
A
- Articular cartilage
- Loss of homogeneity, disruption & fragmentation of surface
- Deeper layers of cartilage invaded by capillaries from calcified cartilage
- Chondrocytes which are normally isolated cells now proliferate & cluster
- Osteophytes form (bone spurs)
- **Early OA: WATER content of diseased cartilage INCREASES & cartilage swells
- Increase in both anabolic (build up) & catabolic (break down) activity
- Eventually, anabolic cannot keep up with catabolic activity
- Degradative enzymes released by chondrocytes
- Matrix less structurally sound & less organized; cannot withstand forces
- Causes for biochemical & metabolic changes not fully understood
8
Q
OA/DA Clinical Characteristics
A
- Localized joint pain
- Stiffness
- Worse with weight bearing-after activity or at the end of the day
- Better with rest
- Very little morning stiffness (diff from other)
-
Distal & Proximal interphalangeal joints
- Heberdens & Bouchards nodes
- Knees, Hips, Cervical & lumbar spine
- Joint crepitus-crunching
- Swelling not common
- Bony enlargement
9
Q
OA: Xrays and Labs
A
- Xrays
- Decreased joint space
- Subchondral sclerosis (bones start touching) & cysts
- Osteophytes (spurs)
- ***xray findings may not always be proportionate to pain
- Labs
- No useful tests
- Not inflammatory
10
Q
OA/DA: Early and Late Stages
A
- losing the dark line (joint space) and joint connections starting to get misaligned
11
Q
OA/DA Management
A
- No cure
- Manage risk factors: physical therapy, exercise, weight loss, dietary measures
- Quadriceps strengthening in knee OA
- Pharmacologic (pain control)
- Acetaminophen, Nonsteroidal anti-inflammatory drugs & other analgesics
- Intra-articular steroid injections in selected cases
- Sx: Jt replacement (especially knees, hips-large jts)
12
Q
RA General
A
- Systemic
- Chronic (>6wks, some infections can mimic-Parvovirus B19)
- Inflammatory
- Autoimmune-WBC attacks jts
- Primarily involves jts but can affect extra-articular organs
- Lungs (interstitial lung disease, pleural effusion)
- Anemia of chronic disease
- Eyes (episcleritis, scleritis)
- Skin (vasculitis), soft tissue (rheumatoid nodules)
- Heart (pericarditis)
- CNS v. rarely (pachymeningitis), peripheral neuropathy (v. severe)
13
Q
RA-Epidemiology and RF
A
- Prevalence: 1%
- 5 times more common in women vs men (duh, a.i. dz)
- Peak incidence 2nd-5th decade of life
- Genetic risk factors: HLA-DRB1 locus (MHC-Class 2)
- Genetic susceptibility
- Environmental risk factors
- Potential triggers: infectious (P gingivalis and others)
- Prevalence of periodontal disease 2 fold amongst RA
-
Smoking: anti-CCP Ab (cyclic citrullinated peptide)-MAKE MORE!
- Relative risk 1.4 for developing RA compared to nonsmokers
- Potential triggers: infectious (P gingivalis and others)
14
Q
**RA vs. OA/DA**
A
- Inflammatory (swelling) VS. OA/DA-no swelling
- Prolonged morning stiffness VS. OA/DA: limited morning stiffness
- Systemic manifestations VS. OA/DA: localized symptoms
- Joints involved:
- PIPs, MCPs, wrists VS OA/DA: PIPs, DIPs, CMCs
- Lumbar spine not involved VS. DA lumbar spine commonly involved
15
Q
Morphology: RA vs. OA
A
- sides, where synovium joins up with bone-inflamm is fom jt space lining
- RA:**eroding cartilage
- OA/DA: **bony spur; more evenly thoughout