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49 Cards in this Set
- Front
- Back
What type of Collagen is in Hyaline cartilage |
Type II |
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What type of cells are responsible for maintenance and synthesis of the extracellular matrix of the hyalin cartilage? |
Chondrocytes |
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What are the 5 layers of the articular cartilage? |
Tangential (superficial zone) Transitional (middle zone) radial (deep zone) calcified bone |
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How does chondrocyte shape change according to position? |
Superficial zone - flatter smaller intermediate - rounder and large deep - stacked on top of one another. |
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Where do chondrocytes sit? |
in lacuna in the cartilage |
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How are deep chondrocytes adapted from more superficial chondrocytes? |
more prominent golgi apparatus and endoplasmic reticulum for protein synthesis |
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Describe the collagen composition of the extracellular matrix from the superficial zone |
Superficial is mostly Type II, slowly changes to Type X as it gets deeper |
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What gene is associated with OA? |
HMGB2 - High mobility group B2 protein. Supports chondrocytes in superficial zone. Loss of HMGB2 increases likelihood of DNA damage and fewer progenitor cells and chondrocytes, reducing ECM. |
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What type of cells form the Synovial Membrane? |
Synoviocytes: Type A - macrophage like cells involved in the immune response Type B - Fibroblast-like cells that produce hyluronic acid. |
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How is Synovial Fluid produced? |
Ultrafiltrate of blood plasma. Synovium is highly vascularised with fenestrated capillaries that leak plasma. Synovium has no basement membrance between the synoviocytes and subintima making movement of plasma easier. Type V synoviocytes add hyluronic acid to plasma (Note: due to the above adaptations the synovium is easily damaged and has lower immune surveillance) |
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What is the function of synovial fluid? |
Slippery weight bearing, to reduce friction Nourish articular cartilage forms a reserve volume |
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What does antictrulinated protein do? |
stimulate osteoclast differentiation and proliferation in RA, leading to bone erosion
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define osteoporosis |
A skeletal disorder characterised by comprimised bone strength, increasing a persons risk of fracture |
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What is a Z- score? |
A bone mineral density test that compares the bone density of the patient to someone of their own age. The number is measured in standard deviations from the normal |
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What is a T - Score |
A bone mineral density test that compares thebone density of the patient to that of an average 30-year old women. |
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What are some causes of secondary Osteoporosis |
Cushing syndrome, malabsorption, thyrotoxicosis |
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What are some pharmocological treatment for Osteoporosis |
Raloxifene (selective oestrogen receptor modulator) Vit D and Calcium Denosumab (inhibits RANKL, therefore inhibiting osteoclast activity); |
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What is the crystal present in gout? |
monosodium urate |
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What are risk factors for Gout? |
being male (higher uric acid levels than women) Diet (more purines in diet = more uric acid, meat, seafood, alcohol) |
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describe the pathophsyiology of gout |
high levels of uric acid caused by either: 1. insufficient protein to keep them inert 2. too much uric acid increased uric acid causes urate crystals to precipitate This attracts neutrophils. However the shape of the urate crystals causes them to burst, releasing inflammatory agents and lysosomes. This lowers pH and causes more urate crystals to precipitate. |
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What are Tophi? |
A symptom of gout where macrophages surround urate crystals which have been deposited in soft tissue such as ears or the elbow. |
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What is uric acid? |
The end stage product or purine metabolism |
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What is unique about the synovial fluid found in gout? |
It has many polymorphonuclear neutrophils |
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What is are the pharmocological treatments for gout? |
NSAIDS for pain Colchicine Corticosteroids Rilonacept Allopurinol Probenecid - increases uric acid excretion. |
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What is the mechanism of action of allopurinol? |
Xanthase oxidase inhibitorXanthase oxidaseis responsible for the conversion of xanthase to uric acid |
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how is gout different from pseudogout? |
Gout - primarily the first MCP joint, monosodium urate crystals (sharp, needle-like) pseudo-gout - happens at soft tissue (shoulder, wrist), calcium pyrophosphate crystals (rhomboid), associated with osteoarthritis |
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Where are the common sites of tendonitis? |
lateral epicondlitis (Tennis elbow) Achilles tendonitis Suprasinatus Tendonitis |
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What are the common causes of tendonitis? |
Overuse of tendon Collagen Type I disorders (Vit C deficiency, Osteogenesis imperfecta) Renal Dialysis - Causes dissarangement of collagen production and excretion (unclear what this means) |
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What is RICE? |
Rest Ice Compression Elevation |
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What is a common complication of achilles tendonitis? |
heterotopic ossification calcification of the tendon |
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What are the two types of Entheses? |
Fibrous Fibrocartilage |
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What conditions are assoiated with enthesitis |
Inflammatory Bowel Disease Ankolysing spondylitis (targets anterior longitudinal ligament) Psoriatic Arthritis |
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What is the difference between an enthesophyte and an osteophyte? |
Enthesophytes originate from the insertion point of the tendon/ligament. No articular border involvement Osteophytes originate from the border of the articular cartilage Both are bony spurs |
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What is the treatment for enthesitis? |
RICE NSAIDS DMARDS - Methotrexate, Sulfasalazine Anti-TNF alpha - Infliximab |
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What is the purpose of the tendon sheath? |
Cushions tendon Guides Tendon Nourishes Tendon: Synovial fluid produced by it + vincula blood supply |
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What is the pathophsyiology of systemic lupus erythematosus? |
Antibodies against a wide number of self antigens (e.g. intranuclear proteins, DNA, ribonucleic acids) are produced by b-cells The autoantobody immune complexes can cause clots in smaller blood vessels such as thoe in the renal system, causing renal failure. |
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What is Malar rash a sign of ? |
Also known as "butterfly sign" it is caused by SLE (systemic lupus erythematous |
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Why does SLE lead to tendonitis/tendosynovitis? |
Autoantibody immune complexes clump together in smaller blood vessels such as those present in the tendon and tendon sheath. This damage to these blood vessels and can lead to tendon and tendon sheath damage that can cause deformities that resemble arthropies. |
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What is the treatment for NSAIDS? |
DMARDS - methotrexate NSAIDS Abatabacept - prevents APC from signalling T-cells. Preventing T-Cell activation Infliximab - TNF alpha monoclonal antibody |
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Describe Heterotopic Ossification |
COX-2 acts on mesenchymal stem cells to chondrocyte, then it acts again with prostaglandins to cause chondrocyte hypertrophy. Then a variety of factors such as RANKL act on hypertrophic chondrocytes to cause ossifcation. |
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Describe Polymyositis and Dermatomyositis |
CD8+ Tcells invade muscle fibres primarily around the fascicles of the muscles and cause inflammation and damage. Macrophages then absorb the necrotic fibres They are very hard to differentiate without very specialised antibody tests. |
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What is the most noticable difference between dermatomemyositis and polymyositis? |
Dermatomemyositis sometimes has a rash that appears on the back, eyes and cheeks. |
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What is a common complication of dermatomyositis? |
subcutaneous calcification calcification at junction between dermis and epidermis (skin). |
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What is subcutaneous calcification |
An autoimmune connective tissue disease. Caused by anti-nuclear antibodies. (anti-jo1 found in 20%-40% of cases. Calcification in skin and muscle |
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What is the treatment for subcutaneous calcification? |
High dose Prednisolone - maintained 2 weeks after symptoms stop, as if it is stopped early there is a more significant rebound flare Methotrexate Azathioprine |
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What is inclusion body myositis |
Muscle disease of the elderly More likely to effect certain muscle (e.g. knee extensors, muscles of swallowing) vacuoles where they shouldn't, or amyloid like material appear in muscle fibres. |
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What is the inheritance pattern of duchenne and becker muscular dystropy |
x-linked recessive |
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What is the pathophysiology of duchenne and becker muscular dystrophy |
Loss of dystrophin means that the muscle is damaged everytime it is contracted. This leads to a slow decline by 7-12 years old. |
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What muscles are affected by duchenne becker muscular dystrophies |
shoulders, elbow flexors and extensors Hips, foot dorsiflexors, knee extenders |