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Unit 5 > Osteoarthiritis > Flashcards

Osteoarthiritis Flashcards

1
Q

Describe the structure of a synovial joint.

A

Hyaline Articular cartilage
Synovial membrane that produces synovial fluid
Outer fibrous capsule
The synovial membrane and outer fibrous capsule together form the joint capsule.

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2
Q

Describe the features of a healthy synovium

A

Connective tissue between the joint capsule and joint space, lines all surfaces expect from the articular cartilage
Inner layer is 1-2 cells thick and consists of type A synovial cells (behave like macrophages) and type B synovial cells (behave like fibroblasts)
Synovial sublining is loos connective tissue with lots of blood vessels, lymphatics and nerves.

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3
Q

What are the different layers of cartilage from the bone surface upwards?

A

Subchondral bone
Calcified layer
Tidemark - where growth occurs
Deep zone
Middle transitional zone
Superficial tangential zone.
Articular surface

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4
Q

What are some changes in the joint during osteoarthritis?

A

Subchondral joint cyst - fluid-filled space within a joint
Thickened joint capsule
Premature degeneration of articular cartilage
Synovitis - inflammation of synovial membrane
Fibrillated cartilage
Osteophytes - unusual growths of bone
Altered bone turnover

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5
Q

What is often the initial trigger to osteoarthritis?

A

Risk factors
Structural damage to cartilage *
Alters chondrocyte function
cytokine release
Results in synovial inflammation and bone remodelling.

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6
Q

What are some of the functions of chondrocytes?

A

Secrete collagenases
Secrete IL-1 and TNFa
Secrete nitrogen oxide
Secrete proteinases
Synthesises collagen

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7
Q

What is the function of proteinases?

A

Break down protein

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8
Q

What is the function of collagenase?

A

To degrade collagen and GAGs, hence degrades cartilage

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9
Q

What can activate a chondrocyte to secrete collagen?

A

Receptors activated by fragmented matrix molecules

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10
Q

What is the function of matrix metalloproteases in relationship to cartilage?
What is the consequence of this?

A

Degrade/cleeve aggrecan
Aggregan binds to GAGs to form ECM
Results in degradation of the cartilage ECM, looses its rigidity.
Cartilage is less able to withstand compression.

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11
Q

What are the tissue changes in cartilage in early OA?

A

Chondrocytes start to proliferate and form active clusters.
They produce proteinases such as MMPs.
There is a gradual loss of aggregan, then type 2 collagen fibres.
This causes cracks (or fibrilations) to appear in the cartilage.

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12
Q

What are some long term consequences of damage to cartilage?

A

Decreased swelling pressure of proteoglycans
Altered collagen synthesis
Decreased responsiveness of chondrocytes
Loss of shock absorbing properties

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13
Q

How can damage from cartilage cause inflammation?

A

Release DAMPs from ECM and chondrocytes

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14
Q

Give an overview of inflammation in osteoarthiritis

A

Synovitis - inflmmation of the synvoium
Identifiable by MRI not x-ray, predates radiological changes
Chronic and low grade
Includes DAMP, TRL signalling, Complement system, CPB, macrophages and mast cells.
Synovium damages create the pain

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15
Q

What are some molecular mediators of inflammation in OA?

A

Cytokines - TNFa, IL-6, IL-21
Chemokines
Growth Factors - TGFb
Adipokines - lectin, adiponectin, visfatin and resistin
Prostaglandins and Leukotrienes
Neuropeptides - bradykinin and substance P

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16
Q

How can osteoarthirits be classified using an ultrasound?

A

Ultrasound over affected joint
Use a colour doppler ultrasound signal
A positive doppler test can indicate inflammation of the synovium.
Oseteo is considered at grade 1 to 2 doppler signal
Rheumatoid arthritis is considered at the higher inflammatory score of grade 3 doppler signal.

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17
Q

What are some constitutional risk factors for osteoarthritis?

A

Ageing
Hereditary
Gender
Hormonal status (menopause)
Metabolic bone disease

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18
Q

What are some local risk factors for osteoarthritis?
Meaning for occurrence in a specific joint

A

Trauma
Knee - obesity, quadricpes weekness, joint laxity or malalignment
Hip - developmental dysplasia (flattened femur head or smaller acetabulum), occupation (farmer)

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19
Q

What are some of the links between ageing and osteoarthritis?

A

A third of women and a quarter of men between 45 and 64 have been treated with OA, this rises to half of people aged 75yrs and over
Reduced muscle mass and increased fat mass alter joint loading.
Adipose tissue can increase the risk of inflammation
Increase ROS - oxidative damage and disruption of cell signalling
Chondrocytes have reduced levels of ECM genes expression and can undergo cellular senescence with age.

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20
Q

What statistics show the link between OA and hereditary factors?

A

Genetics acount for 60% of hand and hip OA, and 40% of knee OA.

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21
Q

What genes are mainly associated with OA in females?

A

IL 4 - hip OA in females
Oestrogen receptors - OA

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22
Q

What genes are mainly associated with OA in men?

A

Cartilage intermediate protein

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23
Q

What are some non-gender specific genes associated with OA?

A

Early OA - COL11A1/2 COL2A1 IL17
Knee - COL9A1, MMPs, cartilage intermediate protein (men)
Hip - Cartilage oligomeric matrix protein, IL 6,
General OA - Insulin like growth factor, transforming growth factor Beta, Vitamin D receptor.
Hand - aggrecan

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24
Q

What are Heberdens and Bouchards Node?

A

Heberdens nodes - distal pharangeal joint
Bouchards nodes - proximal pharangeal joint
Swelling of the joint due to inflammation in arthiritis

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25
Q

What genes are associated with hip osteoarthiritis?

A

GDF5 - bone morphogenetic protein, bone development
DIO2 - thyroid metabolism, hypothyroidism can increase risk of fluid build up is not cleared
SMAD3 - TGFbeta signalling, maintenance of articular cartilage.

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26
Q

What is the deal with women being more likely to suffer from OA?

A

Women have higher rates of OA in all age groups above 45yrs
Account for 60% of hip and knee replacements
Main burden in during menopause, oestrogen declines, less binding of oestrogen to oestrogen receptors
HRT improves symptoms
Precise mechanism is unclear.

27
Q

What is the deal with obesity increasing the risk of OA?

A

People who are overweight are 2.5 times more likely to develop knee OA
Average knee replacement BMI is 28.7 and hip 30.9
Exercise, weightloss and low fat diet reduce pain and improve joint function.
Obesity is associated with increased levels of CRP
Overweight people are also more likely to get hand OA?? - link not as straight forward.

28
Q

Why is adipose tissue linked to inflammation?

A

low grade inflammation
Endocrine - secretes adipokines and cytokines
Contains M1, dendtritic cells, lymphocytes and neutrophils
Secrete IL6, TNFa and VEGF
Inhibit the production of ECM compartments and upregulate MMPs and inflammation

29
Q

Give some examples of adipokines and how does their expression change with obesity?

A

Leptin - increases
Resistin - increases
Visfatin - increases
Adiponectin -decreases

30
Q

What is the role of leptin relating to OA?

A

Increases IL6 and CXCL8 in synovium
Cartilage destruction

31
Q

What is the role of resistin in OA?

A

Increases release of MMPs
Cartilage destruction and synovitis

32
Q

What is the role of visfatin in OA?

A

Increases MMPs and ADAMTS
synovitis and bone erosion

33
Q

What is the role of adiponectin in OA?

A

Cartilage destruction and synovial inflammation

34
Q

What occupations are the different types of OA most commonly associated with?

A

Knee - kneeling and squatting e.g tiler
Hip - prolonged lifting and standing
Hand - requiring manual dexterity.

35
Q

How does joint morphology relate to OA statistics?

A

Abnormal hip shape accounts for one in ten primary hip replacements in adults.
One in three hip replacements in under 60s

36
Q

What are the key characterisits of OA?

A

Progressive breakdown of the articular cartilage
Remodelling of the underlying bone
Formation of ectopic bone
Hypertrophy of joint capsule
Synovial inflammation (low grade and prolonged)

37
Q

What is meant by OA as a heterogenous disease?

A

Multiple different causes and presentations, diverse disease.

38
Q

What is arthiritis?

A

A term used to mean any disorder that affects the joints.
Symptoms generally include joint pain and stiffness

39
Q

What are the two different types of arthritis?

A

Inflammatory and non-inflammatory, note their is some overlap.
Osteoarthiritis is considered to be non-inflammatory.
Inflammatory is often autoimmune and at any age, an example os rheumatoid arthiritis.

40
Q

What is another term for non-inflammatory arthiritis?

A

Degenerative

41
Q

What is the most common form of arthritis?

A

Osteoarthiritis

42
Q

What are some clinical features of osteoarthiritis?

A

Joint pain that becomes worse with pain typically worse towards the evening and after rest
Morning stiffness lasting no longer than 30 mins
Functional limitations/reduced quality of life.

43
Q

What are the clinical features of osteoarthritis found on the joints?

A

Bony swelling
Muscle wasting
Deformity
Palpable crepitus of movement (funny sound)
Restricted painful movements
Bow legged is in knees
Hallux valgus or hernia on big toe
1st CMCJ squaring -makes holding difficult and painful

44
Q

What joints is ostearthiritis most common in?
How is this different to rheumatoid arthritis?

A

OA - larger joints, hip, knees, big toe, phalagneas
RA - smaller joints phalagnes and metacarpals

45
Q

What are some radiographic features of osteoarthiritis?

A

Joint space narrowing
Osteophyte (small outgrowth of bone)
Subchondral sclerosis
Subchondral cyst.

46
Q

What can x-rays exclude in a differential diagnosis from OA?

A

Fracture
Pagets disease
Pseudogout
Avascular necrosis

47
Q

What can x-rays not disclude in a differential diagnosis from OA?

A

Ligament/ meniscal problems
Inflammatory arthiritis - gout or rheumatoid
Tumour
Infection

48
Q

What is the professional clinical defintion of OA?

A

OA refers to a clinical syndrome of joint pain accompanied by varying degrees of functional limitation and reduced quality of life.

49
Q

When does NICE state that OA can be diagnosed without an x-ray?

A

Persistent joint pain with use
Age 45 yrs and over
Any morning stiffness lasting not more than half an hour

50
Q

What is the role of blood tests in OA diagnosis?

A

Usually normal
Investigates other diagnosis

51
Q

What are some impacts of OA on society?

A

8.75 million people aged 45yrs and over in the UK have OA
3/4 report constant pain
20% OA patients report depression and anxiety
One third retire early
2 million GP consultations per year.

52
Q

What is the burden of OA on surgery?

A

90% of primary hip replacements - 101,000
99% of primary knee replacements - 109,000
Over 1% of the NHS budget

53
Q

What is more accurate than describing OA as wear and tear?

A

Metabollically active condition
Homeostasis between cartilage degradation and repair is unbalanced, dynamic repair process is lost.
Repair process being unable to compensate results in more severe symptoms

54
Q

What makes up the tissue loss in OA?

A

Cartilage microfracture
Fragments break off
Pitting and abrasion of cartilage
Localised loss of articular hyaline cartilage

55
Q

What are some reactive changes in OA?

A

Remodelling of adjacent bone
New bone formation
Synovitis/effusion
Reabsorption of necrotic fractured subchondral bone

56
Q

What are the different outcomes of OA?

A

Outcome is variable
Radiographic improvement is rare
Symptoms are episodic not persistent
Varies according to site
In the hand improvement in pain/function is common
Knee rule of thress - 1/3 mild. 1/3 moderate, 1/3 severe

57
Q

Is exercise recommended for OA?

A

Yes - physiological loading helps maintain muscle mass and joint function
Recommend aerobic exercise and quadriceps strengthening - need a long time to take effect.
Disuses of muscles can result is muscle atrophy
Extreme loading results in tissue damage

58
Q

What makes up the core management of OA?

A

Education, advice and access to information
Strengthening exercise and aerobic fitness
Weight loss if overweight or obese

59
Q

What are some intermediate management strategies of OA?

A

Pain killers - anaglesic drugs
NSAIDs - topical
Paracetamol - low dose, can be given regular, first line of defences

60
Q

What anaglesic drugs does NICE not recommend for OA?

A

Chondoroitin and Glucosamine

61
Q

What are some final steps of management of OA?

A

Opiods
Local heat and cold applications
Assisstive devices
Surgery
Braces
Appropriate footwear

62
Q

What are intraarticular knee injections?

A

Used for OA, last resort to reduce pain if other non-surgical methods have failed
Inject corticosteroids, hyaluronic acid or drain fluid from the knee joint using a needle
Provides short term relief often lasting 6 weeks.

63
Q

What are the general outcomes of hip and knee replacement surgery?

A

8/10 knee surgeries have a good outcome
9/10 hip have a good outcome

64
Q

What do NICE guidelines suggest about OA in the knee treatment?

A

All patients must be offered atleast one core none surgical intervention.
Arthroscopic surgery is not recommended unless there is a clear history of mechanical locking.

Unit 5 (12 decks)

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