KCP Osteoarthritis Past Paper PDF

Osteoarthritis Osteoarthritis Year 1 KCP Learning outcomes 1. Describe the pathophysiology of osteoarthritis 2. List risk factors for osteoarthritis 3. Describe common microscopic changes in osteoarthritic joints 4. Recognise common fe...

Osteoarthritis Osteoarthritis Year 1 KCP Learning outcomes 1. Describe the pathophysiology of osteoarthritis 2. List risk factors for osteoarthritis 3. Describe common microscopic changes in osteoarthritic joints 4. Recognise common features of presentation of osteoarthritis 5. Describe joint distribution of osteoarthritis 6. Outline findings of osteoarthritis on clinical examination 7. Understand the term clinical diagnosis 8. List common differential diagnoses for presentations of osteoarthritis 9. Understand the terms relating to disability 10. Describe the components of a biopsychosocial model in healthcare 11. Describe the role of investigations in diagnosis of osteoarthritis 12. Outline the principles of management of osteoarthritis 13. Describe common analgesics and their mechanism of action in treatment of osteoarthritis 14. Outline the principles of the role of joint replacement Preparation Video 1: Drugs likely to have been received aspirin Reading Osteoarthritis is the most common form of arthritis Osteoarthritis 1  Characterised by focal loss of articular cartilage, subchondral osteosclerosis, osteophyte formation at the joint margin and remodelling of joint contour with enlargement of affected joints Some will be asymptomatic Both genetic and environmental components in most cases, the inheritance is polygenic and mediated by several genetic variants of small effect. OA can be a component of multiple epiphyseal dysplasias, which are caused by single gene mutations affecting components of cartilage matrix Structural abnormalities, such as slipped femoral epiphysis and developmental dysplasia of the hip, are also associated with a high risk of OA, presumably due to abnormal load distribution across the joint Similar mechanisms probably explain the increased risk of OA in patients with limb deformity secondary to Paget’s disease of bone Biomechanical factors play an important role in OA related to certain occupations, such as farmers (hip OA), miners (knee OA) and elite or professional athletes (knee and ankle OA). It has been speculated that the higher prevalence of knee OA in South and East Asia might be accounted for by squatting There is also a high risk of knee OA in people who have had destabilising injuries, such as cruciate ligament rupture, and those who have had meniscectomy There is a strong association between obesity and OA, particularly of the hip knee. This is thought to be due partly to biomechanical factors, but it has also been speculated that cytokines released from adipose tissue may play a role Oestrogen appears important; lower rates of OA have been observed in women who use hormone replacement therapy (HRT), while women who receive aromatase inhibitor therapy for breast cancer often experience a flare in symptoms of OA. Risk factors for osteoarthritis: Osteoarthritis 2  Genetics Skeletal dysplasias Polygenic inheritance Developmental abnormalities Developmental dysplasia of the hip Slipped femoral epiphysis Repetitive loading Farmers Miners Elite athletes Adverse biomechanics Meniscectomy Ligament rupture Paget’s disease Obesity Trauma Hormonal Oestrogen deficiency Aromatase inhibitors Degeneration of articular cartilage is the defining feature of OA: Usually chondrocytes are terminally differentiated cells. However, in OA they start dividing to produce nests of metabolically active cells. Initially, matrix components are produced by these cells at an increased rate, but at the same time there is accelerated degradation of the major structural components of cartilage matrix, including aggrecan and type II collagen. Osteoarthritis 3  Eventually, the concentration of aggrecan in cartilage matrix falls and makes the cartilage vulnerable to load-bearing injury. Fissuring of the cartilage surface then occurs, leading to the development of deep vertical clefts, localised chondrocyte death and decreased cartilage thickness. Initially focal, mainly targeting the maximum load-bearing part of the joint, but eventually large parts of the cartilage surface are damaged. CPP and basic calcium phosphate crystals often become deposited in the abnormal cartilage. Osteoarthritis 4  Pathological changes in osteoarthritis. A Abnormal nests of proliferating chondrocytes (arrows) interspersed with matrix devoid of normal chondrocytes. B Fibrillation of cartilage in osteoarthritis (OA). C X-ray of knee joint affected by OA, showing osteophytes at joint margin (white arrows), subchondral sclerosis (black arrows) and a subchondral cyst (open arrow). OA is also accompanies by abnormalities in subchondral bone, which becomes sclerotic and the site of subchondral cysts Fibrocartilage is produced at the joint margin, which undergoes endochondral ossification to form osteophytes. Bone remodelling and cartilage thinning slowly alter the shape of the OA joint, increasing its surface area. Osteoarthritis 5  It is almost as though there is a homeostatic mechanism operative in OA that causes enlargement of the failing joint to spread the mechanical load over a greater surface area. Clinical features Characteristic distribution, mainly targeting hips, knees, PIP and DIP joints of the hands, neck and lumbar spine Main presenting symptoms are pain and functional restriction Pain may relate to increased pressure in subchondral bone, trabecular microfractures, capsular distension and low-grade synovitis also result from bursitis and enthesopathy secondary to altered joint mechanics Symptoms and signs of osteoarthritis Pain Insidious onset over months or years Variable or intermittent nature over time (‘good days, bad days’) Mainly related to movement and weight-bearing, relieved by rest Mild morning stiffness (