PBL 2 Flashcards
what are the signs and symptoms of rheumatoid arthritis?
insidious onset throbbing/aching pain in joints symmetrical early morning stiffness >30 mins normally >5 joints affected warmth, redness, swelling in joints fever malaise muscle weakness low appetite nodules, particularly around pressure points anaemia progressive SOB ulnar deviation boutonniere deformity swab bec deformity baker cyst
what joints are typically affected in rheumatoid arthritis?
smaller joints- metacaprle phalangeal, metatarsophalangial, proximal interphalangeal
wrists
can affect shoulders, elbows, knees and ankles
which arthritis responds bet to NSAIDs
rheumatoid
what is ulnar deviation?
when your metacarpophalangeal joints, become swollen and cause your fingers to bend abnormally toward your little finger
what is boutonniere deformity?
injury to the tendons that straightens the middle joint of your finger so the middle joint of the injured finger will not straighten, while the fingertip bends back.
what is swan neck deformity?
a flexion of the base of the finger, an extension of the middle joint, and a flexion of the outermost joint.
what is a baker cyst?
fluid-filled swelling that develops at the back of the knee
aka popliteal fossa
whats the cause of rheumatoid arthritis?
a combination of genetic predisposition and environmental factors causing modification of our own antigens/type2 collagen/vimentin through citrullination. the body recognises the mutated proteins as foreign = dysregulated inflammation = damage to bones and cartilage
what are 2 examples of genes that predispse us to rheumatoid arthritis?
HLA-DRB1 and HLA-DR4
what are some environmental factors that predispose us to rheumatoid arthritis?
cigarette smoke, infections
what cytokine is released by T helper cells to cause helper cell proliferation?
IL-2
what happens when T helper cells activate B cells in rheumatoid arthritis?
they produce antibodies which attack cyclic citrullinated peptides and those that attack our own IgG antibodies known as rheumatoid factor
what are rheumatoid factors?
IgM antiboides that attack our own, modified IgG antibodies
what are anti-CCP?
a type of autoantiodies that can attack cyclic citrullinated peptides
how do anti-CCP and rheumatoid factor cause joint injury?
antibodies enter the joint space and form immune complexes which activate the complement system and cause joint inflammation and injury
what inflammatory cytokines are released by phagocytes in rheumatoid arthritis?
TNF-alpha, IL-1, IL-6
what cytokine do T helper cells release in rheumatoid arthritis?
IL-17
why do we get pannus formation in rheumatoid arthritis?
white blood cells attack the synovium, releasing proteins that cause angiogenesis. This increased blood flow encourages tissue growth at an accelerated rate.
cytokines also stimulate fibroblast-like synoviocytes which cause synovial membrane proliferation
what is a pannus?
abnormal layer of fibrovascular tissue or granulation tissue over the joint surface
why is the risk of osteoporosis higher in RA patients?
as the inflammation causes increased expression of RANKL which activates more osteoclasts
why do we get cartilage breakdown in rheumatoid arthritis?
fibroblast-like synoviocytes secrete proteases which break down proteins in articular cartilage, leaving exposed unprotected bone which can rub together
why do we experience fever in rheumatoid arthritis?
IL-1 can escape into the bloodtsream and act as a pyrogen in the brain
why is cardiovascular disease 2x more likely in rheumatoid arthritis patients?
the inflammatory cytokines can escape into the blood stream, damage vessels and cause vasculitis = increased risk of atherosclerosis
why can rheumatoid arthritis cause anaemia?
inflammatory cytokines can escape into the blood stream and cause the live to produce high levels of hepcidin which causes decreased iron by inhibiting absorption and trapping it within macrophages
what lung conditions are linked to rheumatoid arthritis?
why?
The walls of the lungs’ small airways can become thickened because of chronic inflammation and infection (bronchiectasis) or inflamed or injured (bronchiolitis).
why is rheumatoid arthritis symmetrical?
fibroblast-like synoviocytes can actually migrate from joint to joint
how do we diagnose rheumatoid arthritis?
blood tests- erythrocyte sedimentation rate, C-reactive protein, rheumatoid factors, anti-CCP antibodies
joint scans - x-ray
assessing physical ability via health assessment questionnaires before and after treatment
what do you look for on an x-ray for rheumatoid arthritis?
decreased bone density
bony erosions
soft tissue swelling
narrowing of joint space
what are some consequences of untreated rheumatoid arthritis/chronic systemic inflammation?
early atherosclerosis/CVD insulin resistance Felty syndrome osteoporosis pain sensitisation dementia risk hypercholesterolaemia sarcopenia
what are the 4 types of medications for rheumatoid arthritis?
disease-modifying anti-rheumatic drugs
biological treatments
JAK inhibitors
NSAIDs/painkillers/steroids
what do disease-modifying anti-rheumatic drugs do?
ease the symptoms of the condition and slow down progression by blocking the effects of cytokines and suppressing the body’s immune and inflammatory response
what are examples of disease-modifying anti-rheumatic drugs?
methotrexate
leflunomide
hydroxychloroquine
sulfasalazine
what are common side effects of methotrexate?
nausea loss of appetite sire mouth diarrhoea headaches hair loss
why do you need regular blood tests whilst taking methotrexate?
as it can affect blood cells and the liver
why might you have a chest x-ray and breathing test when you start taking methotrexate?
because it can affect the lungs uncommonly - these scans and tests provide a comparison for if you develop SOB or perisstant dry cough
when are biological treatments taken in rheumatoid arthritis?
if DMARDs are not effective on their own then biologicals will be taken with DMARDs
what are examples of biologicals and how do each work?
abatacept - suppresses T cells rituximab - suppresses B cells asalimumab, etancercept and infliximab block chemokines anakinra - blocks IL1 toxilizumab - blocks IL-6
how are biologicals given?
by injection
what are the side efefcts of biologicals?
skin reactions at injection site infections nausea fever hedaches
when are JAK inhibitors offered in rheumatoid arthritis?
to those who cannot take DMARDs or biologicals or those who tried them but did not find them effective
what are JAK inhibitors usually taken in combination with?
methotrexate
what are the 3 examples of JAK inhibitors given in rheumatoid arthritis?
baricitinib, tofacitinib, upadacitinib
what are some side effects of steroids?
weight gain osteoporosis easy bruising muscle weakness thinning of skin
what are some supportive treatment options for rheumatoid arthritis?
physiotherapy to improve fitness and muscle strength occupational therapy (strains, splints, gadgets) podiatry
what types of surgery can you have in rheumatoid arthritis?
joint replacement, arthrodesis and synovectomy.
what is an arthrodesis?
the fusion of two or more bones in a joint.
wht is a synovectomy?
the destruction or surgical removal of the synovium
what are the 3 questiosn to as when appraising systematic reviews?
are the results valid?
what are the results?
will the results help me care for my patients?
what 4 questions do we ask when appraising RCTs?
is the basic study design valid?
was the study methodologically sound?
what are the results?
will the results help locally?
what are the 10 questions on a CASP checklist for systematic reviews?
- didthe review address a clearly focussed question?
- did the authors looj for the right type of papers?
- do you think all important, relevant studies were included?
- did the reviews authoers do enough to assess quality of included studies?
- if the results of the review have been combines, was it reasonable to do so?
- what are the overall results of the review?
- how precise are the results?
- can the results be applied to the local population?
- were all important outcomes considered?
- are the benefits worth the harms and costs?
what are thw 11 questions asked in a CASP checklist for RCTs?
- did the study adress a clearly focused research question?
- was the assignement of participants to interventions randomised?
- were all participants who entered the study accounted for at its conclusion
- were participants blind? were investigators blind? were those assessing blinded?
- were the study groups similar at the start of the RCT?
- apart from the experimentally intervention, did each study group receieve the same level of care?
- were the effects of intervention reported comprehensively?
- was the precision of the estinate of the intervention or treatment effect reported? (confidence intervals)
- do the benefits of the experiemental intervention outweight harms and costs?
- can the results be applied to your local population?
11, would the experimental intervention provide greater value to the people in your care than any of the existing interventions?
when is etics approval needed from supervisors?
- Research involves access to records of personal or sensitive confidential information
- Research involves the use of administrative or controlled data
- Research involves linking or sharing of personal data or confidential information
- Research involves participants over 18 years old than are not considered ‘vulnerable adults’
when is ethics approval needed from the research cmitte, HSS research ethics comitee and any other relevant external ethics comittees?
- research involves participants under 18 years old
• Research involves participants over 18 years old that are considered ‘vulnerable
adults’
• Research involves human biological materials, as well as human embryos, foetuses, foetal tissue, reproductive material and stem cells
when does research not need ethical approval?
if it doesnt involve participants or personal data
how can evidence based practice be carried out in the clinical environments?
assess need for change
construct a clinical question
acquire best, rleevant evidence
appraise literature for validity and usefulness
apply findings to clinical decision making by integrating with clinical expertise, patient preferences and values
evaluate outcomes
disseminate information
how does anxiety affect pain?
anxiety makes sufferers hypersensitive to pain which makes them focus on pain more = pain feels worse
how does mood affect pain tolerance?
low mood lowers pain tolerance and happy mood causes greater pain tolerance
