Introduction
What is pathologic synovial disease?
- Inflammatory
- Infectious
- Degenerative
- Traumatic
- Haemorrhogic
- Neoplastic
=> Leading to irreversible joint destruction |
What are arthritides? Inflammation of joints due to infectious, metabolic, or constitutional causes |
Pathophysiology
⏺ Physiology/ function in abnormal states → specifically the functional changes that accompany a particular syndrome or disease |
⏺ It's about disordered function, i.e. there's function but it's abnormal |
⏺ When you wish to find/define the pathophysiology of a condition it's helpful to ask: What's not functioning well? |
Mechanisms
⏺ Determined by the pathophysiology, i.e. disordered function |
⏺ They're the defects in systems, organs, cellular & molecules that constitute the triggers of specific diseases |
⏺ They originate & explain the clinical signs & symptoms |
⏺ When you wish to find/define the mechanism of disease, it's helpful to ask: How is the specific pathophysiology leading to occurrence of these specific signs & symptoms? |
Gout
Signs & symptoms:
- Acute form: painful, warm & swollen joint
- Chronic tophaceous form: top in tendons, bursae & cartilages |
Pathophysiology:
- Hyperuricaemia & a ↓ in urinary excretion of uric acid → both lead to deposition & crystallisation of uric acid in joints → followed by an inflammatory response with release of enzymes in joint space |
Mechanism:
- Deposition & crystallisation occurs in previously traumatised or "cooler" joints. Neutrophil disruption leads to enzyme release & inflammatory cascade |
Does the pathophysiology explain/relate to the specific mechanisms of disease, how?
- Yes
- Hyperuricaemia leads to deposition of uric acid
- Previous trauma & location favours crystallisation
- Crystal deposition triggers immune response
- Damage to neutrophils produces the release of enzymes which irritate joints & cause an inflammation, i.e. arthritis |
Do the mechanism explain the clinical signs & symptoms, how?
- Yes
- Inflammation causes painful, warm, swollen joints in the acute form
- In chronic tophaceous form: long term deposition of uric acid crystals in avascular tissues cause tophi in tendons, bursae & cartilages |
Rheumatoid Arthritis
Signs & symptoms:
- Poly-articular joint pain, swelling & stiffness
- Most commonly affecting the small joints (wrists, metacarpal-phalangeals)
- Joint involvement is bilaterally symmetrical
- Extra-articular manifestations are often seen |
Pathophysiology:
- Autoimmune activation & proliferation of T-cells → leading to production of inflammatory cytokines & B-cells differentiation into plasma cells → there's an inflammatory response which is systemic & damage of cartilage tissue in joints |
Mechanism:
- The joint damage recruits more immune cells into joint spaces
- Immune cells infiltrate synovial membrane causing it to proliferate & forming new blood vessels
- Swollen & blood rich synovial (pannus) invades & enzymatically destroys joint tissue
- Severe RA will affect the entire body |
Does the pathophysiology explain/relate to the specific mechanisms of disease, how?
- Yes
- The autoimmune activation of T- & B- cells with consequent inflammation & cartilage damage stimulate nerve endings in subchondraln bone & synovial membrane
- Inflammation of synovial leads to its enlargement with formation of palpable lumps in the affected joints
- Neovascularisation & synovial enlargement cause physical narrowing of joint space & a decrease joint mobility
- Neovascularisation & synovial enlargement erode cartilage & subchondral bone which may cause joint mal-alignment, subluxation or collapse |
Does the mechanism explain the clinical signs & symptoms, how?
- Yes
- Stimulation of nerve endings in subchondraln bone & synovial membrane, causes joint pain
- Inflammation of synovial leads to its enlargement with formation of palpable lumps in the affected joints
- Physical narrowing of joint space & ↓ in joint mobility causes joint stiffness & a ↓ in the range of movement
- Cartilage & subchondraln bone erosion causes joint mal-alignment, subluxation or collapse, explaining the various types of joint deformities
- The systemic inflammation explains the various extra-articular signs of the disease |
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Ankylosing Spondylitis
Signs & symptoms:
- Pain in Lx & gluteal regions
- ↓ in Lx spine flexion
- ↓ in Lx lordosis
- ↑ in Tx kyphosis
- Asymmetric arthritis & enthesitis |
Pathophysiology & mechanism:
- Autoimmunity causes inflammation of axial joints, peripheral joints & entheses |
Does the pathophysiology explain/relate to the specific mechanisms of disease, how?
- Yes
- Axial joint arthritis (sacroiliac & vertebral column) causes release of inflammatory substances that stimulate nociceptors
- Inflammation leads to osteoclast activation & erosion of bone, which in turn causes osteoblast activation with new bone formation
- Leads to an ↑ in spinal rigidity
- In peripheral joints, the arthritis causes release of inflammatory substances that stimulate nociceptors
- There's infiltration of the synovium by inflammatory cells & inflammation of the entheses (places of tendon insertions in bone) |
Do the mechanism explain the clinical signs & symptoms, how?
- Yes
- Stimulation of nociceptors causes pain in axial & peripheral joints
- ↑ in spinal rigidity causes a ↓ in Lx spine flexion, ↓ in Lx lordosis & ↑ in Tx kyphosis
- Late complications include spinal ankylosis & fractures
- In peripheral joints, stimulation of nociceptors causes pain of lower limb joints & knees
- Enthesitis causes pain in achilles tendon, plantar fascia & tibial tuberosity* |
Osteoarthritis
Signs & symptoms:
- Joint pain with loading & motion
- Palpable bone hypertrophy
- ↓ in ROM
- Crepitus (popping/crackling sound)
- Joint effusion |
Pathophysiology & mechanism:
- Joint cartilage destruction with inflammation |
Does the pathophysiology explain/relate to the specific mechanisms of disease, how?
- Yes
- Cartilage inflammation in weight bearing joints (knee,hip) & smaller joints stimulates nociceptors
- Joint cartilage loss causes wear of exposed subchondral bone, which induces defective new bone formation leading to the appearance of osteophytes & subchondral bone sclerosis leading to changes in joint architecture
- During movement osteophytes & subchondral sclerosis are firmly pressed against normal joint structures
- Cartilage loss brings joint bones into direct contact between themselves with reduction in joint movement & stimulation of nociceptors
- Joint inflammation leads to chemical changes within the joint causing a ↓ in synovial fluid viscosity & an ↑ in joint fluid production |
Do the mechanism explain the clinical signs & symptoms, how?
- Yes
- Stimulation of joint nociceptors causes joint pain whether upon loading or during motion
- Change in joint architecture consists of the appearance of palpable bone hypertrophy, i.e. Bouchard's nodes
- Osteophytic & subchondral sclerosis impaction against normal joint structures causes pain & ↓ joint ROM
- Joint bones into direct contact causes friction & crepitus, pain & further ↓ in ROM
- ↓ in synovial fluid viscosity & an ↑ in joint production produce joint effusions |
Polymyalgia Rheumatica
Signs & symptoms:
- Morning stiffness
- Aching of pectoral & pelvic girdle muscle structures
- Malaise
- Weight loss |
Pathophysiology & mechanism:
- Aging combined with systemic (auto) immunologic/inflammatory process targeting structures in the walls of arteries with activation of macrophages |
Does the pathophysiology explain/relate to the specific mechanisms of disease, how?
- More challenging to connect pathophysiology & mechanism
- The inflammation of arteries may lead to their obstruction potentially causing hypoxia, ischemia & necrosis of affected tissues
- This include muscles in the shoulder girdle & pelvic girdle |
Do the mechanism explain the clinical signs & symptoms, how?
- Yes but challenging
- It's plausible that the arteritis & consequent hypoxia & ischemia of affected muscles together with the systemic inflammation lead to stiffness, aching, malaise & weight loss* |
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