MSK Flashcards
(252 cards)
polymyalgia reumatica and risk factors
A chronic systemic rheumatic inflammatory disease characterised by aching and morning stiffness in the neck, shoulder and pelvic girdle in people over age 50
PMR is the most common inflammatory rheumatic disease in older people
It is a syndrome associated with synovitis of proximal large joints, tenosynovitis and bursitis
The cause of PMR is unknown although thought to be both genetic and environmental factors contributing to susceptibility and severity
Risk factors:
Older age - highest incidence >65, peak between 70-80
Female (65% cases)
Northern european ancestry - uncommon in middle eastern, asian, african and hispanic descent
Infection - cyclic fluctuations and peak observed in winter and associated with epidemics of mycoplasma, chlamydia pneumoniae and parvovirus B19 infections
polymyalgia reumatica presentation
> 50 YO with at least 2 weeks of core symptoms (bilateral shoulder pain, pelvic pain and stiffness lasting >45 mins after rest)
Bilateral shoulder and/or pelvic girdle pain
Initially may be unilateral but quickly becomes bilateral
Worse with movement and interferes with sleep
Shoulder pain may radiate to elbow
Hip and neck pain is main presenting feature in 50-70% cases
Hip pain may radiate to knee
Stiffness lasting at least 48 minutes after waking or periods of rest that may cause them difficulty turning over , rising from bed/chair or raising their arms about their shoulders
Low grade fever, anorexia, weight loss, depression (systemic symptoms in around 50%)
Bilateral upper arm tenderness
Peripheral MSK signs like carpal tunnel syndromes, peripheral arthritis or swelling with pitting oedema of hands, feet, wrists, ankles
Muscles strength not usually impaired but pain may make movement too difficult to assess and can atrophy if prolonged enough without use
polymyalgia reumatica investigations
Clinical history and exam
Bloods: ESR; plasma viscosity; CRP usually raised.
Before starting corticosteroids must rule out other conditions with these tests:
FBC, U+Es, LFTs, calcium, alkaline phosphatase, protein electrophoresis, TSH, creatine kinase, rheumatoid factor
Dipstick urinalysis
Urine sample for Bence Jones protein, bloods for Antinuclear Antibody and anti-cyclic citrullinated peptide antibody and CXR
RULE OUT GCA!!
polymyalgia reumatica management, prognosis and complications
prednisolone 15mg daily follow up in 1 week to assess if effective
3-4 weeks recheck ESR/plasma viscosity/CRP to assess response and reduce/increase dose accordingly
give patient steroid card and advise on long term steroid complications
refer patients <60, red flags suggesting underlying conditions, no core PMR features or <70% response despite treatment
prognosis:
mostly good response, risk of relapse and long term steroid complications
complications:
GCA occurring spontaneously without warning
steroid complications
fibromyalgia
Chronic pain disorder characterised by widespread pain and tenderness
Cause unknown but evidence for genetic predisposition, abnormal stress response system or HP axis and possible triggering events
Thought to be caused by abnormal sensory processing in the CNS making them sensitive to pain and unpleasant sensations
Symptoms are chronic widespread pain associated with unrefreshing sleep and tiredness
Thought that it is more common than reported and underdiagnosed
Usual age of presentation is 20-50 but can be seen in any age
Classification:
Widespread pain involving both sides of body above and below waist as well as axial skeleton for at least three months and presence of 11 tender points among 9 pairs of specified sites (18 points around head, shoulders, elbows, hips and knees)
fibromyalgia risk factors and presentation
Risk factors: Not completing education Low socioeconomic status Female Divorced
Presentation: Widespread chronic pain: lower back, radiates to buttocks, legs, pain in neck, across shoulders are common Poor unrefreshing sleep and tiredness Usually 20-50 YO Morning stiffness Paraesthesia Feeling of joint swelling with no actual swelling Cognitive problems (memory, difficulty finding words) Headaches Light headed/dizziness Anxiety and depression Weight fluctuations
fibromyalgia investigations and management
Clinical diagnosis
Management:
Conservative: tailored exercise programmes, aquatic therapies, high intensity training, physio
Psychological therapies CBT, relaxation techniques
Acupuncture and massage can be helpful in conjunction
Analgesia: paracetamol, codeine, tramadol
TCA: amitriptyline, nortriptyline
SNRI: venlafaxine, duloxetine, milnacipran
Neuropathic drugs: pregabalin, gabapentin may help reduce pain and sleep problems
Referrals to rheumatology, physiotherapy, mental health, occupational therapy, pain clinic or chronic fatigue service
gout
Purine metabolism disorder characterised by raised uric acid in the blood (hyperuricemia) and deposition of monosodium urate crystals in other tissues like soft connective tissues of urinary tract or in joints
Uric acid if end product of purine breakdown and exists as sodium urate at physiological pH
70% urate excretion by kidneys and 30% by GIT
Normal serum uric acid levels are 2.4-6mg/dl (women) and 3.4-7mg/dl (men)
Hyperuricemia usually caused by issue with excretion, overproduction or both
Gout can present without hyperuricemia and vice versa
Gouty arthritis is arthritis due to urate crystals in joints
Gout tends to attack joints in extremities due to lower temperatures enough to precipitate urate from plasma. This tophi typically forms helix of the ear, fingertips, olecranon bursae and other colder sites in body
phases of gout pathology and risk factors
Long period of asymptomatic hyperuricemia
Period of acute gout attacks of gouty arthritis followed by arable intervals (months-years) with no symptoms
Chronic tophaceous gout where nodules are affecting joints
Risk factors:
Hyperuricemia: level of urate directly correlates with risk of disease, however gout can occur in people with normal plasma urate levels and many people with high urate never develop gout
Secondary causes of hyperuricemia: HTN, hyperparathyroidism, downs syndrome, lead neuropathy, sarcoidosis, medications, chronic renal disease, volume depletion, glycogen storage diseases, lymphoprliferative/myeloproliferative disorders, carcinomatosis, polycythaemia and severe psoriasis
High purine diet (meat/seafood) alcohol intake
Age
Male
Menopausal status
Obesity, metabolic syndrome, dyslipidemia
Diuretics
Trauma
Family history
presentation of gout
Acute pain in joint
Swelling
Erythema
Typically in MTP joints but can occur in knees, midtarsal joints, wrists, ankles, hands and elbows
Gout investigations
Joint fluid microscopy and culture - urate crystals or tophi, not usually indicated unless gout in doubt or septic arthritis suspected
The only way to differentiate from pseudogout is crystal analysis!! Gout = negatively birefringent (yellow and needle like). Pseudogout = weakly positively birefringent (blue and rhomboid shaped).
Serum uric acid 4-6 weeks after acute attack to confirm hyperuricemia (crystals form when persistently about 380micromol/L (DOES NOT EXCLUDE GOUT)
Joint XR often normal, nonspecific tissue swelling and cysts may be present
Screen for CVD risk factors and renal disease after diagnosis
Gout management
rest, elevate, ice packs, cool environment, avoid trauma
weight loss, avoid seafood, low fat/sugar, high fibre and veg, avoid alcohol, smoking cessation
GOOD = skimmed milk, low fat yogurt, soybeans and cherries. lots of water
vit C supplements
acute medications; NSAIDs (naproxen initially 750mg then 250mg every 8 hrs until attack passes) co-prescribe PPI AVOID aspirin as this INCREASES urate levels!
oral colchicine 500mcg 2-4x daily until symptom relief or nausea/vomiting do NOT exceed 6mg or repeat within 3 days!
short course oral steroids or single IM dose
prophylaxis: lifestyle advice; dietary changes, reducing alcohol and increasing water consumption. Medication is considered if there are >3 attacks/year, a family history or evidence of joint damage
urate lowering therapy first line allopurinol (low dose 50-100mg OD with food increase by 100mg increments every 4 weeks until serum uric acid below 300micromol/L. Max dose 900mg daily divided doses (lower in renal impairment). Risk of precipitating acute attacks
2nd line febuxostat: check LFTs before and after starting. 80mg OD is SUA level >300 after 4 weeks increase dose to 120mg daily aim for SUA <300.
Both of these drugs are xanthine oxidase inhibitors which inhibit xanthine oxidase which prevents conversion of xanthine into uric acid
START URIC ACID THERAPY AFTER ATTACK HAS RESOLVED BUT DO NOT STOP DURING ATTACK IF ALREADY ON DRUGS
Oral colchicine: 500mcg O/TD following allopurinol/febuxostat treatment. Renal impairment doses: eGFR 30-60 500mcg OD; eGFR 10-30 500mcg once every 2-3 days
Gout complications
Tophi (firm white nodules under translucent skin) in 50% people with untreated gout after 10 years. Can become inflamed, develop infection, exude tophaceous material
Urinary stones
CKD, MI and CVD
Septic arthritis
osteoarthritis
Synovial joint disorder when damage triggers repair process leading to structural changes within the joint
Characterised by bone spurs (osteophytes), loss of cartilage and no major inflammation (mild synovitis)
Commonly due to increasing age but exact cause is unknown; complex multifactorial condition
Joint damage may occur through repeated excessive loading and stress over time or by injury
Any synovial joint can be affected but most commonly in knees, hips and small joints of hands
osteoarthritis risk factors
Family history Increasing age Female Obesity High bone density, low bone density (increased risk of rapid progression of knee and hip) Joint injury and damage Joint laxity and reduced muscle strength Joint malignancy; history of developmental dysplasia; femoroacetabular impingement; leg length discrepancy; varus and valgus knee deformities Exercise stresses Occupational stresses
osteoarthritis presentation
Bony swelling and joint deformity Joint effusions (uncommon except for in knee) Joint warmth or tenderness (synovitis) Muscle wasting and weakness Restricted and painful range of motion, crepitus (grating sound or friction sensation) Joint instability Heberden’s nodes (hands) other nodes specific to area
osteoarthritis investigations
Clinical presentation and history: activity related pain, no morning joint stiffness lasting >30 minutes, functional impairment in those >45 YO
XR for uncertainty, to exclude alternatives or if sudden deterioration: typical features show subchondral bone thickening and cysts; osteophyte formation; loss/narrowing of joint space from cartilage loss
Structural changes may not correlate with functional impairment
osteoarthritis management
Weight loss, strengthening exercises and aerobic fitness training. (hands - repetitive grasping, pinching motions etc), appropriate footwear, local heat/cold packs or transcutaneous electrical nerve stimulation (TENS)
ARTHRITIS UK, NHS, ARTHRITIS AND MUSCULOSKELETAL ALLIANCE (ARMA)
Psychological support
Carer assessment and referral PRN
Occupational health assessment
Simple analgesia (paracetamol and topical NSAIDs)
Oral NSAIDs, codeine (30-60mg QDS with paracetamol) or topical capsaicin for moderate-severe pain
Can be given Intra-articular corticosteroid injections to reduce pain and synovitis; not more than 4 injections/year
Hyaluronic acid can be used for intra-articular injection to increase synovial fluid integrity and delay time to surgery
Refer for MDT if symptoms cannot be controlled or have severe impact on quality of life
Eventually may need joint replacement
osteoporosis
Disease characterised by low bone mass and structural deterioration of bone tissue with consequent increase in bone fragility and susceptibility to fracture
End result of imbalance of bone remodelling and net turnover by osteoclasts and osteoblasts
During normal ageing, bone breakdown increases and is no longer balanced by osteoblast activity/formation resulting in combination of reduced bone mineral density (BMD) and changes to bone composition, architecture, size and geometry
BMD is the amount of mineral (calcium hydroxyapatite) per unit of bone
Very common in elderly men and postmenopausal women
Pathological fractures are common
Osteoporosis is a BMD of <2.5 standard deviations below mean peak mass (average of young healthy adults) however this does not take into account the bone deterioration so many women without osteoporosis may have fragility fractures
Osteoporosis is considered severe if the patient has experienced one or more fragility fractures
Osteopenia refers to decreased BMD. change can be general or regional. WHO define it as BMD score between -1 and -2.5 standard deviations
postmenopausal osteoporosis
After age 30 bone resorption will slightly exceed formation and bone will begin to diminish
In women this can be exacerbated by menopause onset where decline in oestrogen further decrease formation and increase absorption
RANK antigen promotes formation of bone but this is regulated by estrogen and decline results in increased reabsorption
Thickness of cortical and trabecular bone decrease overtime
Vertical fractures are much more common in women
Other factors that affect the rate of decline: lifestyle, medications etc.
risk factors for osteoporosis
Old age Female white/asian Small body frame Genetics Hormone imbalances Low calcium diet, vitamin D or proteins Sedentary lifestyles/immobility Diabetes, hyperthyroidism, hyperparathyroidism GI conditions: crohn's disease, ulcerative colitis, coeliac disease and pancreatitis CKD, chronic liver disease BMI <18.5 Oral steroids (depending on duration and dose) Smoking Alcohol >3 units daily Previous fragility fracture (highest for hip fracture lowest for lower vertebral fracture) Rheumatological conditions
osteoporosis presentation
Asymptomatic and often remains undiagnosed until fragility fracture occurs
An osteoporotic fragility fracture is a fracture occurring as a consequence of osteoporosis.
Fractures often occur at the wrist, spine, hip but can occur at arm, pelvis, ribs and other bones
Fragility fracture is defined as a fracture following a fall from standing height or less although vertebral fractures may occur spontaneously or as result of routine activity like bending or lifting
osteoporosis investigations
DEXA scan for BMD: osteoporosis is a BMD of <2.5 standard deviations below mean peak mass (average of young healthy adults)
T score to calculate fragility fracture risk: QFracture score: >10% high risk; close to but <10% intermediate and low risk is <10% (FRAX score red high risk, orange mod and green low risk)
Clinical history or diet; Identify risk factors for falls: imapaired vision, neuromuscular weakness/incoordination, cognitive impairment, use of alcohol and sedative drugs
Bloods: vitamin D deficiency
osteoporosis management and complications
All patients should be encouraged to increase dietary intake of Ca and vitamin D
Bisphosphonates for high/intermediate risk of fragility fractures. Alendronate 10mg OD or 70mf once weekly or risedronate 5mg OD or 35mg once weekly if not CI. MUST TAKE AT LEAST 30MINS BEFORE BREAKFAST ON EMPTY STOMACH. TAKE RISEDRONATE AT LEAST 2 HOURS EITHER SIDE OF FOOD. MUST SWALLOW WHOLE WITH AT LEAST 200ML WATER. DO NOT SUCK OR CHEW (oropharyngeal ulceration). SIT UPRIGHT AND DONT LIE DOWN FOR 30 MINS. DO NOT TAKE AT BEDTIME/BEFORE GETTING UP. TAKE WEEKLY PREP SAME TIME EACH WEEK. MINIMUM OF 30 MINS BETWEEN TAKING CALCIUM SUPPLEMENT OR ANTACID (changes absorption)
side effects include nausea, vomiting, mild gastritis, abdo pain in first month, bone, joint or muscle pain, oesophagitis
Assess for vitamin D deficiency and inadequate calcium intake and prescribe cholecalciferol (Calcichew D3 forte tablets) 1250mg Ca carbonate (500mg Ca) and 400 units of vitamin D3 for supplementation if needed
Identify risk factors for falls: impaired vision, neuromuscular weakness/incoordination, cognitive impairment, use of alcohol and sedative drugs
For those who do not qualify for medication, give lifestyle advice and review in 5 years time
Complications: Hip fracture Vertebral fracture Severe kyphosis causing breathing difficulty Reduced quality of life