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WEEK 32:
Introduction to rheumatoid arthritis (RA) and osteoarthritis (OA)...
| Question | Answer |
|---|---|
| Types of arthritis (5) | Gout, juvenile idiopathic arthritis, osteoarthritis (OA), rheumatoid arthritis (RA), and spondyloarthritis |
| Osteoarthritis (OA) | |
| Osteoarthritis prevalence by age | Highest is knee then hip in female and knee then hip in male |
| OA symptoms | Joints become painful and stiff (worsening in the morning) lasting no longer than 30 mins |
| diagnosis of OA | |
| what age do most people have OA | Most people over 50 have some form of OA |
| OA not associated with | Raised ESR (Erythrocyte Sedimentation Rate)/ CRP |
| ESR meaning | Erythrocyte Sedimentation Rate- blood test measuring how fast RBC fall to the bottom of the test tube |
| Hand OA | Nodal osteoarthritis that develop on DIP joint (Heberden’s node) |
| What % of people and what age has knee OA | 40% people over 75 have knee OA |
| Spondylosis | Very common spinal condition degeneration of interveterbal discs L5/S1, L4/L5 and neck (facet joint osteoarthritis- bad back) |
| Spondylolisthesis | Bone of vertebra moves forward or backwards cousin severe nerve pain (sciatica) |
| Which nerve roots does Spondylolisthesis occur | L5/S1 and C2/C3 |
| Spondylolisthesis cervical symptoms | Cervical presents with finger tingling and headaches |
| Treatment of Spondylolisthesis | NSAIDs and amitriptyline |
| Cauda equina syndrome | |
| Other characteristics of OA (s13) | |
| Management of OA includes (2) | Non pharmacological treatment, pharmalogical treatment, and surgery |
| Non pharmacological treatment includes (2) | |
| pharmacological treatment includes (3) | |
| s15 | |
| Last resort management of OA | surgery |
| Drugs that inhibit cyclooxygenase (COX) in inflammatory drugs (7) | |
| s18 mechanisms | |
| Non steroidal anti inflammatory drugs (NSAIDs) mechanism of action | |
| Non steroidal anti inflammatory drugs (NSAIDs) clinical use | |
| Non steroidal anti inflammatory drugs (NSAIDs) examples | |
| Main Non steroidal anti inflammatory drugs (NSAIDs) side effects | GI disturbances (dyspepsia, nausea, vomiting, damaged mucosa/ ulceration), and analgesic (nerve damage) associated neuropathy due to renal blood flow disturbances |
| Difference between COX1 and COX2 | COX 2 is Inducible (switched on during inflammation, pain and fever) whereas COX1 is constitutive (always on for sotmahc, kidney and blood vessels) |
| Other Non steroidal anti inflammatory drugs (NSAIDs) side effects | |
| Non steroidal anti inflammatory drugs (NSAIDs) side effects contraindications | Patient with asthma (aspirin induced asthma) as may cause constriction |
| Where do COX1 and COX2 come from | Arachidonic acid |
| Arachidonic acid comes from | Phospholipids using leukotrienes |
| [highly] selective COX2 inhibitors (COXIBS) | Originally developed to minimise the adverse effects of NSAIDS while maintaining the same analgesic and anti-inflammaotry properties |
| COXIBS mechanism of action | Inhibit prostaglandin/ thomboxane biosynthesis by a direct action on the COX 2 isoenzyme |
| COXIBS clinical use | Anti-inflammatory: symptomatic relief in the treatment of osteoarthritis and rheumatoid arthritis |
| COXIBS examples | Delecoxib and etoricoxib |
| Arthroplasty | Very effective surgery for bones |
| Rheumatoid arthritis (RA) | Autoimmune disease leading to irreversible joint destruction, not only affecting joints but also has systemic effects e.g. affects eyes, lungs, skin etc. It involves chronic inflammation of joint |
| Population of those with RA | 430,000 people in UK |
| Is RA related to any factors | |
| Prevalence of RA | Uncommon (relatively) overall prevalence of 0.8% and decreasing |
| RA links to inflammation | |
| RA main symptoms | |
| RA diagnosis | |
| Rheumatoid disease | Systemic disease involving emphasis on joint, eyes (50%), skin (nodules), vasculitis, lungs, salivary glands, and pericaridtic etc |
| RA referral | |
| When should RA be urgently referred | Refer urgently even if RF + anti CCP are negative but patients more than one small hand joints/feet affected with a delay of 3 months of longer between onset of symptoms and seeking medical advice |
| management of RA includes (4) | non -pharmacological treatment, treat to target, phamacological treatment, and surgery |
| Non pharmacological treatment of RA includes (2) | |
| Treat to target management of RA | |
| Pharmacological treatment of RA | |
| Combination therapy as a pharmacological treatment of RA includes | Rituximab and methotrexate for severe active RA |
| When is Rituximab and methotrexate used | For severe active RA |
| Methotrexate mechanism of action | (antimetabolite, folic acid anatagonist) Competitively inhibits dihydrofolate reductase which participates in the synthesis of tetrahydrofolate - where in RA it increases adenosine levels which significantly reduces inflammation |
| Examples of methotrexate | |
| Dosing of methotrexate | |
| Side effects of methotrexate | Anaemia, throat ulcer, fever, nausea, and GI disturbance |
| Prednisolone symptoms of efficacy | |
| Prednisolone toxicity | |
| Prednisolone can be given as | Intrathecal treatment |
| Sulfasalazine mode of action | |
| Leuflunodmie mode of action | Inhibitory effects on activated T-cells involved in inflammatory processes |
| Normal inflammatory process SL43 | |
| tumour necrosis factor | Cytokine produced by macrophage inr response to infection, involved in sepsis etc SLIDE 44 |
| Adalimumab and etanercept mode of action | |
| Rixumimab mode of action | Lysis of B cell, given every 2 weeks |
| Main side effects of biologicals |
Created by:
kablooey
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