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Block 4 > Joints & Joint Disease > Flashcards

Joints & Joint Disease Flashcards

1
Q

What are the different components of connective tissue?

A
  1. Cells
  2. ECM:
    - Fibrous proteins (collagen and elastin)
    - Ground substance (proteoglycans, glycoproteins and water)
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2
Q

What determines a tissues physical properties?

A

ECM composition

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3
Q

What is collagen?

A

A fibre of connective tissue that is good at resisting tensile forces

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4
Q

What are the 3 types of collagen?

A
  1. Type I: bone, tendons, ligaments, dermis and organ capsules
  2. Type II: hyaline and elastic cartilage
  3. Type III (reticular fibres): structural framework of spleen, liver, lymph nodes, SM and adipose tissue
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5
Q

What is elastin?

A

The major component of elastic fibres that enables stretch and recoil of tissues found in a wide variety of structures e.g. walls of large arteries, lungs and skin (often mixed with collagen to prevent overstretch)

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6
Q

What are the 3 types of connective tissue?

A
  1. Loose irregular (areolar)
  2. Dense irregular
  3. Specialised
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7
Q

What is loose irregular connective tissue? Where is it found?

A

Contains lots of cells (fibroblasts, adipose cells, macrophages, mast cells + other cells responsible for immune/allergic reactions), loose arrangement of fibres (collagen, reticular + elastic), abundant ground substance and ECF - found below epithelial layer of resp. + GI tract (lamina propria - mucous membranes), below pleura, peritoneum + pericardium (serous membrane), below skin and associated with adventitia of blood vessels and glands

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8
Q

What is dense irregular connective tissue? Where is it found?

A

Contains lots of fibres, fewer cells, randomly arranged collagen (resists stress from all directions) and elastic fibres - forms the dermis of the skin, capsules of organs (kidneys, testes, ovaries, spleen + lymph nodes) and sheaths of nerves

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9
Q

What are the different types of specialised connective tissue?

A
  1. Dense regular connective tissue (tendons, ligaments and aponeuroses)
  2. Cartilage
  3. Adipose tissue
  4. Haemopoietic tissue (bone marrow + lymphoid tissue)
  5. Blood
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10
Q

What are the characteristics of cartilage?

A
  1. Strong, flexible and semi-rigid
  2. Withstands compression forces so can act as a shock absorber
  3. Smooth surface enables friction-free movement
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11
Q

What are the functions of cartilage?

A
  1. Forms articulating surface of bones
  2. Growth and development of bones (endochondral ossification)
  3. Supporting framework of some organs e.g. walls of airway
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12
Q

What are the features of cartilage extracellular matrix (ECM)?

A
  1. Contains aggrecan (proteoglycan) that has an osmotic effect thus, high water content and resists compressive forces
  2. Contains collagen and elastin fibres
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13
Q

What is the structure of the cartilage?

A

Cartilage in the centre ECM surrounded by perichondrium (outer fibrous and inner cellular layer) - avascular structure being supplied by diffusion

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14
Q

What are the different types of cartilage cells?

A

Mesenchymal stem cells produce chrondroblasts that are cartilage building cells sitting in the cellular layer. Chrondroblasts form chrondrocytes when they are trapped in ECM/lacuna.

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15
Q

How does cartilage grow in childhood and adolescence?

A
  1. Appositional growth: surface layers of matrix added by chrondroblasts in the perichondrium (inner cellular layer)
  2. Interstitial growth: chrondrocytes (now surrounded in ECM/lacuna) grow and divide laying down new matrix producing articular cartilage and endochondral ossification
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16
Q

How does cartilage repair?

A

Poor regeneration EXCEPT in children:

  • Small defects are dealt with by chrondrogenic cells from the perichondrium that form new cartilage
  • Large defects involve replacement with dense connective tissue
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17
Q

What are the 3 types of cartilage?

A
  1. Hyaline
  2. Fibrocartilage
  3. Elastic
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18
Q

What is hyaline cartilage?

A

The most common but weakest form of cartilage containing short and dispersed type II collagen fibres and large amounts of proteoglycans. It has a perichondrium layer (except on articular surfaces) and is found in articular joint surfaces, costal cartilages and epiphyseal growth plates.

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19
Q

What is fibrocartilage?

A

The strongest form of cartilage containing thick parallel bundles of type I collagen alternating with hyaline cartilage matrix and no perichondrium. It is found in places that need to resist significant force for example, insertion points of ligaments and tendons to bone, IV discs, joint capsules, knee menisci, pubic symphysis and TMJ.

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20
Q

What is elastic cartilage?

A

Strong, flexible and resilient cartilage containing elastic fibres and type II collagen fibres with a perichondrium. It is present in structures which require some degree of deformation but then rapidly regain their original shape for example, external ear, larynx and epiglottis.

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21
Q

What are joints?

A

Articulation of 2 or more bones

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22
Q

What are the 3 different joint types movement?

A
  1. Synarthrodial: fixed with no movement e.g. suture skull joints
  2. Amphiarthrodial: slightly moveable e.g. pubic symphysis
  3. Diarthrodial: freely moveable e.g. shoulder (glenohumeral)
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23
Q

What are the 3 different types of joints?

A
  1. Fibrous
  2. Cartilaginous
  3. Synovial
24
Q

What are fibrous joints? Give some examples.

A

Dense connective tissue (containing mainly collagen and no cartilage) that connects bones e.g:

  • Sutures between flat bones of skull (synarthrodial)
  • Syndesmoses: interosseous membrane connecting long bones (amphiarthrodial)
25
Q

What are cartilaginous joints? Give some example.

A

Cartilage (hyaline +/- fibrocartilage) connecting bones e.g:

  • Primary synchondroses (synathrodial) with hyaline cartilage only in epiphyseal growth plates and costal cartilages
  • Secondary symphysis (amphiarthrodial) that contain hyaline cartilage that lines bones with a pad of fibrocartilage in between in IV discs, pubic symphysis and manubriosternal joint
26
Q

What are synovial joints?

A

Hyaline cartilage based joint with the presence of a joint cavity between the bones containing synovial fluid and a joint capsule enclosing the joint with an outer fibrous and inner cellular/synovial membrane (synovium) - fibroelastic ligaments crossing the joint prevent excessive movement and provide additional reinforcement

27
Q

What is a bursa?

A

A sac made of synovial membrane containing synovial fluid reducing friction of one structure moving over another - can be extensions of synovial joints or not

28
Q

What are the 6 types of synovial joints, their movement and an example of each?

A
  1. Hinge: flexion/extension e.g. elbow
  2. Ball and socket: motion in multiple axes e.g. glenohumeral
  3. Plane: gliding/sliding e.g. acromioclavicular
  4. Saddle (concave/convex surfaces): flexion/extension, adduction/abduction and circumduction e.g. metatarsophalangeal
  5. Pivot: rotation e.g. atlantoaxial
  6. Condyloid/condylar: flexion/extension, adduction/abduction and circumduction e.g. metacarpophalangeal
29
Q

How can synovial joints be classified by their movement?

A
  1. Uniaxial: movement in 1 plane
  2. Biaxial: movement in 2 planes
  3. Multiaxial: movement in 3 or more planes
30
Q

What is osteoarthritis (OA)?

A

The most common joint disease resulting more a complex interaction between genetic, metabolic, biochemical and biomechanical factors leading to a loss of articular cartilage +/- bone leading to synovitis - inflammation can affect cartilage (reduces shock-absorbing ability), subchondral bone, ligaments, menisci, synovium and joint capsule

31
Q

What are the risk factors for osteoarthritis (OA)?

A 
Genetics
Increasing age
Sex (females)
Trauma
Mechanical stress on joints
Obesity

Bone density:

  • High bone density: increases risk of developing OA
  • Low bone density: increases risk of progression of knee/hip OA
32
Q

What are the different types of osteoarthritis (OA)?

A
  1. Primary: due to genetic factors and occurs in absence of a precipitating insult
  2. Secondary: occurs as a sequelae of joint pathology e.g. trauma, infection, joint defects or inflammatory conditions
33
Q

What types of joints does osteoarthritis (OA) commonly affect?

A

Unilaterally or bilaterally weight-bearing joints e.g:

  • Knees
  • Shoulders
  • Hips
  • Small joints of hands
  • Spine
34
Q

What is the pathophysiology of osteoarthritis (OA)?

A
  1. Mechanical injury causes chondrocyte response and release of cytokines (e.g. TNF, IL-1)
  2. Production and release of protease that degrade cartilage
  3. Loss of smooth cartilage and development of surface cracks = fibrillation of cartilage
  4. Synovial phagocytes release degradative enzymes in response to cartilage fragments causing chronic synovitis
  5. Destruction of subchondral bone
  6. Mechanical/chemical action triggers new bone growth producing sclerosis and osteophytes
  7. Destruction of joint structures continues the cycle by activating more chrondrocytes
35
Q

What are the characteristic features of the joints in osteoarthritis (OA)?

A
  • Change in cartilage composition reducing shock-absorbing ability
  • Erosion of cartilage = fibrillations
  • Ulceration of cartilage exposes underlying bone = microfractures + subchondral cysts
  • New bone growth = osteophytes + subchondral sclerosis
  • Synovium hyperplasia with inflammation
  • Thickening of joint capsule causing stiffness and restriction of movement
36
Q

What are the radiographic changes seen in osteoarthritis (OA)?

A
  • Joint space narrowing asymmetrically
  • Subchondral cysts and sclerosis
  • Osteophytes
  • Malalignment
37
Q

What are the characteristic nodes called in osteoarthritis (OA) due to osteophytes?

A

Distal interphalangeal joints of hands = Herberden’s nodes

Proximal interphalangeal joints at base of thumb = Bouchard’s nodes

38
Q

What are the symptoms of osteoarthritis (OA)?

A
  • Joint stiffness (for 20-30 minutes in the morning and post-inactivity)
  • Joint pain worst on movement
  • Functional limitation
  • Rest/night pain
39
Q

What are the examination findings (signs) of osteoarthritis (OA)?

A
  • Restricted movement
  • Crepitus
  • Bony swelling
  • Joint effusion
  • Joint instability, deformity and muscle wasting
  • Inflammatory signs LESS commonly
40
Q

What is the management of osteoarthritis (OA)?

A
  1. Education: advice and info
  2. Non-pharmacological: exercise to build muscle strength and lose weight, physiotherapy and aids/devices
  3. Pharmacology: topical/oral pain management
  4. Surgical: joint replacement (arthroplasty) joint fusion, joint excision and realignment surgery
41
Q

What are the 3 types of inflammatory arthritis?

A
  1. Rheumatoid arthritis (RA)
  2. Spondyloarthritis (inc. psoriatic arthritis, ankylosing spondylitis, enteropathy arthritis assoc. with IBD etc.)
  3. Crystal arthritis e.g. gout
42
Q

What is the predominant feature in inflammatory arthritis?

A

Synovial inflammation

43
Q

What is rheumatoid arthritis (RA)?

A

Multi-system inflammatory autoimmune disease primarily affecting the joints causing inflammation of synovial membrane and articular surfaces leading to joint destruction usually associated with +ve rheumatoid factor and raised inflammatory markers

44
Q

What are the symptoms of rheumatoid arthritis (RA)?

A
  • Warm, tender and swollen joints
  • Morning stiffness lasting > 1 hour
  • Joint deformities
  • Extra-articular features affecting eyes, skin, respiratory system and cardiovascular system
  • Generalized feelings e.g. fatigue, weight loss and anaemia
45
Q

What type of joints does rheumatoid arthritis (RA)?

A

Symmetrically:

  • Small joints
  • Large joints e.g. elbow
46
Q

What is the difference between the onset of osteoarthritis (OA) and rheumatoid arthritis (RA)?

A

OA: begins after age 40 usually developing slowly over many years (males/females)

RA: usually begins between 25-50 years developing within weeks or months (mostly females)

47
Q

What is gout?

A

A type of crystal arthritis caused by inflammatory response to urate crystals deposited in and around the joint and synovial fluid in peripheral area as they form better at lower temperatures (e.g. metatarsal-phalangeal joints esp. big toe) due to hyperuricaemia leading to synovitis, cartilage destruction and joint generation - can occur in acute and chronic (tophaceous) forms

48
Q

What are the 2 different types of gout?

A
  1. Primary (95%): inherited disorder that causes an overproduction or underexcretion of uric acid in the urine
  2. Secondary (5%); other factors cause overproduction of uric acid (e.g. high dietary purine, drugs, or conditions resulting in increased nucleic acid turnover like lymphoma, psoriasis or haemolysis etc.) or under-excretion in the urine (e.g. chronic renal failure, alcohol, drugs etc.)
49
Q

What complications can result from gout?

A

Urate crystals can be deposited in the renal parenchyma resulting in renal failure and urate calculi (kidney stones) can be formed in the urine

50
Q

What are the risk factors for gout?

A 
High serum urate
Family history
Excess alcohol
Renal disease
Chemotherapy for malignancy
51
Q

What are the signs and symptoms of acute gout?

A
  • Sudden onset
  • Precipitated by excess food or alcohol, dehydration or diuretics
  • Joint inflammation
  • Tender, swollen, hot and red joints
  • Affects often the 1st metatarsophalangeal joint
52
Q

What are the signs and symptoms of chronic topaceous gout?

A
  • Often associated with renal impairment and long-term diuretic use
  • Tophi: deposits of monosodium urate crystals in bursae, tendons, cartilage or periarticular bone (may ulcerate and discharge)
  • Chronic joint pain
  • May have superimposed acute gout attacks
53
Q

What are the radiographic changes in chronic gout?

A
  • Joint effusion
  • ‘Punched out’ bony erosions with sclerotic margins and over-hanging edges
  • Opacities (tophi) in soft tissue
  • Soft tissue swelling
  • Narrowing of joint space in late stage disease
54
Q

How do you manage gout?

A
  1. Generally: reduce alcohol intake, avoid purine-rich foods (e.g. offal, red meat, shellfish and spinach), lose weight + review medications inc. diuretics
  2. Acute attack: NSAIDs or colchicine
  3. Chronic gout: allopurinal (xanthine oxidase inhibitor that reduces uric acid synthesis) and uricosuric drugs (increases urinary excretion of uric acid BUT can cause kidney stones)
55
Q

What is the uric acid pathway? What happens when its in excess?

A
  1. Purine nucleotide metabolism produces xanthine
  2. Xanthine oxidase converts it to uric acid
  3. Uric acid is renally excreted and excreted through the GI tract
  4. If circulating in excess, there will be urate deposition in the peripheries called tophi

Block 4 (33 decks)

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