MSK/rheumatology Flashcards
What is the most common arthritis?
Osteoarthritis.
What is osteoarthritis?
Non-inflammatory degenerative mechanical shearing - wear and tear.
What are the most commonly affected joints in osteoarthritis?
Hips, knees, sacro-iliac, wrists, cervical spine, thumbs.
What are seven risk factors for osteoarthritis?
Higher age, female, obesity, family history, occupation, sports, trauma.
Describe the pathophysiology of osteoarthritis.
Imbalanced cartilage breakdown and repair which leads to cartilage loss.
-Chondrocytes repair this which leads to structural issues.
How does osteoarthritis present?
Joint pain and stiffness with little morning pain but worsened as the day goes on and with exercise.
What are two signs of osteoarthritis? Where is affected?
Heberden’s (DIP) and Bouchard’s nodes (PIP) - asymmetrical, hard, non-inflamed joint.
-Affects big toe, hips and knees.
How is osteoarthritis diagnosed?
Over 45 with activity pain and no morning stiffness.
-Normal bloods.
-XRAY (LOSS).
What are the XRAY findings in osteoarthritis?
LOSS:
-Loss of joint space.
-Osteophytes.
-Subchondral sclerosis.
-Subchondral cysts.
What is the management of osteoarthritis?
-Lifestyle changes - weight loss and physio.
-NSAIDs for pain relief.
-Steroid injections.
-Last resort - Joint replacement.
What is rheumatoid arthritis?
Chronic inflammatory autoimmune polyarthritis which is symmetrical.
Where does RA usually affect?
Multiple joints - wrist, hand, feet.
What are the three risk factors for RA?
Women aged 30-50. Smoking. Family history - HLA-DR4, HLA-DR1.
Describe the pathophysiology of RA.
Autoantibodies:
-Rheumatoid factor (RF) autoantibody is present in 70%.
-Anti-CCP autoantibodies more sensitive and specific than RF.
How does someone with RA present?
Symmetrical distal polyarthritis (pain, swelling, hot, stiffness) that is worse on a morning and eases as the day goes on and with activity.
What are the signs of RA?
Hands - Boutonnieres deformity (flexed), swan neck deformity, Z thumb, ulnar deviation.
Extra-articular - Pulmonary fibrosis/bronchiolitis, CVD, CKD, elbow skin nodules.
How is RA investigated?
Bloods, serology, XRAY.
What are the blood and serology results of RA?
Raised ESR and CRP, normocytic normochromic anaemia.
-Positive anti-CCP and RF serology.
What are the XRAY findings on RA?
LESS:
-Loss of joint space.
-Eroded bone.
-Soft tissue swelling.
-Soft bones.
What are the first and second line medication treatments for RA?
DMARDs - methotrexate and leflunomide.
What are the 3rd and 4th line medication treatments for RA?
-Methotrexate and infliximab (anti-TNF).
-Methotrexate and rituximab (anti-CD20).
What is gout?
A crystal arthropathy associated with high blood uric acid levels.
What is the most common inflammatory arthritis in the UK?
Gout
What is the typical patient with gout?
Middle aged overweight men.
Describe the pathophysiology of gout.
Sodium urate crystal are deposited into the joint causing it to become hot, swollen and painful.
What is gouty tophi?
Subcutaneous deposits of uric acid typically affecting the small joints and connective tissues of the hands, elbows and ears.
What are the three joints most affected by gout?
-Metatarsophalangeal joints (base of big toes).
-Wrists.
-Carpometacarpal joints (base of thumbs).
What are seven risk factors of gout?
Male, obesity, family history, diuretics, alcohol, CVD/CKD, purine rich foods (meat, seafood).
What is a key differential diagnosis of gout?
Septic arthritis.
How does gout present?
Monoarticular sudden onset, severely swollen red toe that you can’t put weight on.
How is gout diagnosed?
Aspiration of fluid from the joint.
What are the results of joint aspiration in gout?
-Needle shaped crystals.
-Monosodium urate crystals.
-Negatively befringement of polarised light.
-No bacterial growth.
What is the acute treatment for gout?
1st line - NSAIDs.
2nd - Colchicine.
3rd - Steroids.
What is the prophylaxis for gout?
Allopurinol and lifestyle changes (less purines and more dairy).
What is pseudogout?
Crystal arthropathy caused by calcium pyrophosphate deposits.
What is another name for pseudogout?
Chondrocalcinosis.
Who does pseudogout usually affect?
Elderly females.
What are three risk factors for pseudogout?
Diabetes, metabolic disease, osteoarthritis.
What is the presentation of pseudogout?
Polyarticular with knee commonly affected (also hips, shoulders and wrists).
Swollen, hot and red joint.
How is pseudogout diagnosed?
Joint aspiration.
What does aspiration fluid show in pseudogout?
-Calcium pyrophosphate crystals.
-Rhomboid shaped crystals.
-Positive befringement in polarised light.
-No bacterial growth.
What does an XRAY show in pseudogout?
Same as OA - LOSS.
What is the management for pseudogout?
-Chronic changes require no management.
-Acutely: NSAIDs, colchicine, steroids.
-Severe: Joint washout.
What is osteoporosis? What is a complication?
A condition characterised by a reduction in bone density. This makes bones more weak and prone to fractures.
What is osteopenia?
A less severe reduction in bone density than osteoporosis.
Who does osteoporosis usually affect?
Post-menopausal white woman above 50y.
What are the risk factors for osteoporosis?
SHATTERED:
-Steroids, hyperthyroid/para, alcohol/smoking, thin, testosterone low, early menopause, renal/liver failure, erosive + inflammatory disease, DMT1/malabsporption.
What are the four main causes of osteoporosis?
Endocrine (Cushing’s, parathyroid).
Haematology (myeloma).
GI (malabsorption).
Iatrogenic (steroids).
What is a T score?
Young adult bone density.
0 < T < 1 is normal.
1 < T < 2.5 - Osteopenia.
T > 2.5 - Osteoporosis.
How does osteoporosis present?
With fractures:
-Femur, Colle’s (wrist), compression vertebral crush.
What is the gold standard investigation for osteoporosis?
DEXA scan - yields a T score.
After a diagnosis of osteoporosis, which score is performed?
FRAX score - fracture risk assessment tool.
What is the 1st line treatment for osteoporosis?
Bisphosphonates (alendronate) which reduce osteoclast activity.
Which supplements are given to someone with osteoporosis?
Calcium and vitamin D.
What are other treatment options for osteoporosis?
Denosumab, HRT and raloxifene.
What is septic arthritis?
A bacterial infection within a joint (native or replacement).
What is the mortality of septic arthritis?
10%.
What are the organisms that can cause septic arthritis?
S. aureus (mc).
H. influenzae (children).
Gonorrhoea (sexually active).
E. coli and pseudomonas (IVDU).
What are six risk factors for septic arthritis?
IVDU, immunosuppression, surgery, trauma, prosthetic joints, RA.
How does septic arthritis present?
Acutely inflamed, hot, red joint with fever usually at the knee.
-Extremely painful with stiffness and reduced motion.
-Fever and systemic illness.
How is septic arthritis diagnosed?
Joint aspiration then mc + s - shows bacteria.
Bloods - Raised ESR and CRP.
What are four differential diagnoses of septic arthritis?
Gout, pseudogout, reactive arthritis and haemarthrosis.
What is the management of septic arthritis?
Joint aspiration and empirical antibiotics.
NSAIDs for pain.
Describe the antibiotic management of septic arthritis.
3-6 week antibiotics:
-1st line - Flucloxacillin and rifampicin.
-MRSA, prosthetic joint, penicillin allergy - Vancomycin and rifampicin.
What is osteomyelitis?
Infection of the bone or bone marrow.
How does osteomyelitis occur?
Local - Directly to the bone due to fracture.
Haematogenous - To bone through blood after entering body from another route.
What are the organisms responsible for osteomyelitis?
S. aureus (mc - 90%).
Who is osteomyelitis most common in?
Young boys under 10y.
What are seven risk factors for osteomyelitis?
Open bone fracture, bone surgery, immunocompromised, IVDU, sickle cell anaemia, HIV, TB.
How does osteomyelitis present?
Acutely and chronic:
Pain with swelling, tenderness and refusing to bear weight.
May have fever.
What are the investigations for osteomyelitis and what their findings?
XRAY/MRI.
Bloods - Raised ESR and CRP.
BM biopsy - mc + s to ID causative organism.
What is the management of osteomyelitis?
Immbolisation and antibiotics (vancomycin).
May need surgery/drainage.
What are spondyloarthropathies?
Inflammatory seronegative (RF) arthritis associated with HLAB27.
What are the general features of spondyloarthropathies?
SPINEACHE:
-Sausage fingers, psoriasis, inflammatory back pain, NSAIDs good, enthesitis, arthritis, Crohn’s/colitis, HLAB27, eyes (uveitis).
What is ankylosing spondylitis?
Inflammatory spondyloarthropathy mainly affecting the spine with abnormal stiffening and pain.
Which joints does ankylosing spondylitis mostly affect?
Sacro-iliac joints and the vertebral column.
Describe the genetic link to ankylosing spondylitis.
Associated with HLAB27:
-90% with AS have HLAB27.
-2% with HLAB27 develop AS.
What is a complication of ankylosing spondylitis?
Vertebral fractures.
What is the typical presentation of AS?
Young male (teens/20s) with progressively worsening back stiffness. Develops over a few months and can have flare ups.
-Worse in the morning and night, improves with exercise.
What are four signs of ankylosing spondylitis?
Anterior uveitis, enthesitis, dactylitis, lumbar pathology (decreased lordosis and flexion).
What is Schober’s test?
A test to assess the mobility of the spine.
-Making marks above and below L5 vertebrae and seeing if the distance increases, if movement is restricted - AS.
What are the investigations of AS?
-Raised ESR and CRP, RF negative.
-XRAY - Bamboo spine with squared vertebral bodies and syndesmophytes.
-HLAB27 positive.
What is the management of AS?
NSAIDs and exercise for pain.
Steroids during flare ups.
Anti-TNF medications - infliximab.
What is psoriatic arthritis?
Inflammatory arthritis associated with psoriasis.
How strong is the link between psoriasis and psoriatic arthritis?
20% of those with psoriasis develop it arthritis within 10y.
When does psoriatic arthritis usually occur?
Middle age but can occur at any age.
How severe is psoriatic arthritis?
Can range from mild stiffening to arthritis mutilans.
How common is arthritis mutilans in psoriatic arthritis?
5% develop arthritis mutilans.
What is the screening tool for psoriatic arthritis?
PEST - asks about joint pain, swelling, arthritis history and nail pitting.
What is arthritis mutilans?
Severe arthritis in the fingers and toes that presents in psoriatic arthritis.
-There is osteolysis which leads to progressive shortening of the finger and skin folding leading to ‘telescope finger’.
What are the patterns of psoriatic arthritis?
-Symmetrical polyarthritis - Presents similar to RA, more common in women. Affects hands, wrists, ankles and DIP joints.
-Asymmetrical polyarthritis - Mainly affects digits and feet.
-Spondylitic - Back stiffness, sacroiliitis.
What are five signs of psoriatic arthritis?
Psoriasis plaques, nail pitting, onycholysis, dactylitis, enthesitis.
What are three associations of psoriatic arthritis?
Eye disease (conjunctivitis/uveitis).
Aortitis.
Amyloidosis.
How is psoriatic arthritis diagnosed?
XRAY.
What are the XRAY changes in someone with psoriatic arthritis?
Ankylosis, dactylitis, osteolysis, pencil-in-cup deformity.
What is the management for psoriatic arthritis?
DMARD - Methotrexate.
Anti-TNF - Infliximab.
Last line - Ustekinumab.
NSAIDs for analgesia.
What is reactive arthritis?
Inflammation of the synovial membranes due to recent infective trigger.
What is the difference between septic and reactive arthritis?
In reactive arthritis there is no infection in the joint.
What are the triggers of reactive arthritis?
Gastroenteritis or STI (chlamydia).
What is the presentation of reactive arthritis?
Reiter’s triad - can’t pee, can’t see, can’t climb a tree.
-Uveitis, urethritis, arthritis.
How is reactive arthritis diagnosed?
Joint aspiration and mc + s - No organism and negative for crystalarthropathy.
-Raised ESR and CRP, HLAB27.
What is the management of reactive arthritis?
NSAIDs, steroid injections.
-If recurrent - DMARD (methotrexate) and infliximab.
What is systemic lupus erythematous (SLE)?
An inflammatory autoimmune connective tissue disorder -Systemic and involves multiple organs.
What is the pattern of disease in SLE?
Usually relapse-remitting with flare ups.
What type of reaction is SLE?
T3 hypersensitivity (Ab-Ag complex deposition).
What is the typical patient affected by SLE?
Afro-Caribbean females aged 20-40.
What are five risk factors for SLE?
Female, HLAB8, HLADR2, HLADR3 and drugs.
What is the pathophysiology of SLE?
Anti-nuclear autoantibodies (ANA), these attack proteins in the cell nucleus. The immune system attacks these and an inflammatory response is generated.
How does SLE present?
Photosensitive malar rash (butterfly shaped).
-Fatigue, fever, weight loss, myalgia, arthralgia.
-SOB, chest pain, hepatosplenomegaly.
-Hair loss, mouth ulcers, Raynaud’s.
What are the investigations in SLE and what are their findings?
Bloods - Anaemia, raised ESR and CRP. Decreased C3 and C4.
Urinalysis and renal biopsy - Lupus nephritis.
Serology:
-ANA and anti-dsDNA are common.
-Types of ANA:
Anti-RO, anti-SM, anti-LA.
What is the management of SLE? Severe?
Lifestyle - less sunlight and suncream.
Prednisolone, hydroxychloroquine and NSAIDs.
-Severe - Methotrexate and rituximab.
What are five severe complications of SLE?
CVD, infection, anaemia, nephritis, antiphospholipid syndrome.
What is vasculitis?
Inflammation of the blood vessels.
What are the types of vasculitis?
Affecting:-Large vessels, medium vessels and small vessels.
What are the two types of vasculitis affecting large vessels?
Giant cell arteritis, Takayasu’s arteritis.
What are the three types of vasculitis affecting medium vessels?
Polyarteritis nodosa, Kawasaki’s disease and Buerger’s disease.
What are two types of vasculitis affecting small vessels?
Granulomatosis with polyangitis, Henoch-Schoenlein purpura.
What is the general treatment for vasclitis?
Corticosteroids.
-If long term consider gastric and bone protection.
What is giant cell arteritis?
Systemic vasculitis of the medium and large arteries, typically presents affecting the temporal artery.
What is a severe complication of giant cell arteritis?
Sudden painless vision loss in one eye.
What are the typical patients affected by giant cell arteritis?
White females 50 and above.
How does giant cell arteritis present?
Severe unilateral headache around temple and forehead with scalp tenderness, jaw claudication and double/blurred vision.
How is giant cell arteritis diagnosed?
-Temporal artery biopsy - granulomatous inflammation and multinucleated giant cells.
-Raised ESR and CRP.
What is the management of giant cell arteritis?
Prednisolone, aspirin and PPI for gastric protection.
What are three complications of giant cell arteritis?
Vision loss, stroke, aortitis (aneurysm/dissection).
What is polyarteritis nodosa?
Medium vessel arteritis associated with hepatitis B and C and HIV.
What does polyarteritis nodosa affect?
The skin, GI tract, kidneys and the heart - causes CKD/AKI, strokes, MI and skin nodules.
What does polyarteritis nodosa cause?
Livedo reticularis - mottled purple rash.
What is granulomatosis with polyangitis?
Small vessel arteritis that affects the respiratory tract and kidneys.
What does granulomatosis with polyangitis cause?
Nose bleeds, crusty nasal secretions, hearing loss and sinusitis.
What can granulomatosis with polyangitis progress to?
Glomerulonephritis.
What is fibromyalgia?
Chronic widespread pain for 3+ months with all the other causes ruled out.
What are the five risk factors for fibromyalgia?
60+, females, depression, stress, poor.
How does fibromyalgia present?
Stressed, depressed 60y woman with fatigue and pain.
Sleep disturbance, morning stiffness.
How is fibromyalgia diagnosed?
Diagnosis of exclusion and clinically made.
-No serological markers, normal ESR and CRP.
-Pain in 11 out of 18 regions.
What is the treatment for fibromyalgia?
Educating patients, physiotherapy.
Antidepressants and CBT.
What is the key differential diagnosis of fibromyalgia?
Polymyalgia rheumatica.
What is Sjogren’s syndrome?
Chronic inflammatory autoimmune condition affecting exocrine glands.
What are the types of Sjogren’s syndrome?
Primary - in isolation.
Secondary - in relation to SLE or RA.
What are the four risk factors for Sjogren’s syndrome?
Females, middle aged, family history, HLAB8/DR3.
How does Sjogren’s syndrome present?
Dry mucous membranes:
-Dry eyes, dry mouth and dry vagina.
What are the investigations for Sjogren’s syndrome?
Serology - Anti-Ro, anti-La antibodies.
Schirmer tear test - Induce tears and place paper filter under eyes. Tears should travel 20mm, significant is <10mm.
What is the management for Sjogren’s syndrome?
Artificial tears, saliva and lubricant for sex.
Hydroxychloroquine - slows progression.
What are four complications of Sjogren’s syndrome?
Eye infections, dental/oral problems, vaginal problems, sexual dysfunction.
How common are primary bone tumours?
Rare, seen mostly in children.
-Secondary bone tumours are more common.
What are the four primary bone tumours?
Osteosarcoma, Ewing sarcoma, chondrosarcoma, fibrosarcoma.
What are the cancers that metastasise to bone?
BLTKP:
-Breast, lung, thyroid, kidney, prostate.
What is osteosarcoma?
Most common primary bone cancer, associated with Paget’s.
What is Ewing sarcoma?
Very rare bone cancer from mesenchymal stem cell.
What is chondrosarcoma?
Cancer of the cartilage.
What is the general presentation of bone cancer?
Severe pain worse at night with weight loss, fatigue, fever and malaise.
How is bone cancer diagnosed and treated?
XRAY.
Chemo, radio, bisphosphonates and surgery.
What is systemic sclerosis?
An autoimmune inflammatory and fibrotic connective tissue disorder with unclear cause.
What is the most common type of systemic sclerosis?
Limited cutaneous scleroderma.
What does systemic sclerosis put you at risk for?
Pulmonary hypertension and fibrosis.
What are the features of systemic sclerosis?
CREST:
-Calcinosis - calcium deposits under the skin at fingertips.
-Raynaud’s phenomenon - blue fingers when cold.
-oEsophageal dysmotility - swallowing difficulties.
-Sclerodactyly/scleroderma - skin hardening, thickening and tightening on hands which restricts mobility.
-Telangiectasia - spider veins on face.
How is systemic sclerosis diagnosed?
ACA antibodies seen in 70%, ANA also positive.
What is the management of systemic sclerosis?
No cure, treat symptoms and complications.
-Steroids and immunosuppressants.
-Treat complications: GI symptoms (PPI), Raynaud’s (hand warmers).
What is polymyositis?
An autoimmune disorder where there is chronic inflammation of the muscles.
What is dermatomyositis?
Autoimmune connective tissue disorder where there is chronic inflammation of the muscles and skin.
What can cause dermatomyositis and polymyositis? What does this make them?
Underlying malignancy - paraneoplastic syndromes.
Which cancers are most commonly associated with dermatomyositis and polymyositis?
Lung, breast, ovarian and gastric.
How does polymyositis present?
Symmetrical wasting of muscles mostly the shoulder and pelvic girdle.
-With muscle pain, fatigue and weakness.
What is the difference between polymyositis and dermatomyositis?
Dermatomyositis have skin changes involved.
What are four features of dermatomyositis?
Gottron lesions - scaly knuckles.
Photosensitive erythematous rash.
Purple rash on face and eyelids.
Periorbital swelling.
Which investigations are used for polymyositis and dermatomyositis?
Muscle biopsy for definitive diagnosis.
-Raised creatine kinase.
-Autoantibodies:
Anti-Jo1 for polymyositis.
Anti-Mi2 and ANA for dermatomyositis.
What is the management of polymyositis and dermatomyositis?
1st line - Corticosteroids (prednisolone).
-Others: Immunosuppressants, IV Ig, biological therapy (infliximab).
What is antiphospholipid syndrome?
Disorder associated with antiphospholipid antibodies where the blood is prone to clotting - hypercoagulable state.
What is antiphospholipid syndrome associated with?
Thrombosis (stroke, MI, DVT, PE) and recurrent miscarriages.
What are the types of antiphospholipid syndrome?
Primary (idiopathic) and secondary to other diseases (e.g. SLE).
How does antiphospholipid syndrome present?
Clots and pregnancy complications:
-DVT, PE, MI, stroke.
-Recurrent miscarriage, preeclampsia, stillbirth.
Others:
-Livedo reticularis (purple rash).
-Thrombocytopenia.
How is antiphospholipid diagnosed?
History of thrombus and pregnancy complications with autoantibodies:
-Lupus anticoagulant.
-Anticardiolipin antibodies.
-Anti-beta-2 glycoprotein I antibodies.
How is antiphospholipid syndrome managed?
Long term warfarin to prevent thrombi.
-If pregnant - LMWH and aspirin.
What is mechanical lower back pain?
Lower back pain often due to trauma or work.
-Normal in 20-55, very common and self-limiting.
What are the signs for serious pathology in back pain?
Elderly (myeloma), neuropathic pain (spinal cord compression).
What is lumbar spondylosis?
Degeneration of intervertebral discs, loses its compliance and thins over time.
What is osteomalacia?
Defective bone mineralisation causing soft bones.
How does osteomalacia occur?
Due to vitamin D deficiency.
What is the difference between Ricket’s and osteomalacia?
Ricket’s is in children before epiphyseal fusion whereas osteomalacia is in adults after epiphyseal fusion.
Describe the pathophysiology of osteomalacia.
Vitamin D is essential for the absorption of calcium and phosphate from the intestine. If deficient, there is a lack of calcium and phosphate which leads to defective bone minerlisation.
-Low calcium causes secondary hyperparathyroidism as there is increased PTH to increase the calcium level, stimulating bone resorption which causes further problems with bone mineralisation.
What are three causes of osteomalacia?
-Malabsorption/less intake/poor sunlight - No vitD.
-CKD/renal failure - Less active vitD formation.
-Liver failure.
How does osteomalacia and Ricket’s present?
May be asymptomatic.
-Fatigue, bone pain, muscle weakness and aches.
-Fractures and difficulty weight bearing.
Rickets:-Skeletal deformities (knocked knees, bowed legs).
What are the investigations for osteomalacia?
Bloods - Low vitD (serum 25-hydroxyvitamin D), low calcium, low phosphate.
XRAY - Osteopenia.
BM biopsy - Incomplete minerlisation.
DEXA scan - Low bone mineral density.
What is the treatment for osteomalacia?
Supplementary vitamin D and increased dietary intake.
What is Paget’s disease?
Disorder of bone remodelling due to excessive activity of osteoclasts and osteoblasts.
-Leading to patchy areas of high and low density (sclerosis and lysis).
-Results in enlarged and misshaped bones with structural problems.
What causes Paget’s disease?
Idiopathic.
How does Paget’s disease present?
Older patients with: Bone pain, bone deformities, fractures and hearing loss (damaged inner ear bones).
What are the investigations in Paget’s disease?
XRAY and bloods.
What are the blood results in someone with Paget’s disease?
Raised ALP, normal calcium and normal phosphate.
What are the XRAY findings in Paget’s disease?
Osteoporosis circumscripta - osteolytic lesions.
Cotton wool appearance - areas of sclerosis and lysis in skull.
V-shaped defects - in long bones, V shaped osteolytic lesions.
What is the management of Paget’s disease?
Bisphosphonates and analgesia for pain.
What are two major complications of Paget’s disease?
Osteosarcoma and spinal cord compression.
What is polymyalgia rheumatica?
Inflammatory condition that causes pain and stiffness in the shoulders, neck and pelvic girdle.
Which condition is PR strongly linked to?
Giant cell arteritis.
What is the typical patient with polymyalgia rheumatica?
White women over 50y.
How does polymyalgia rheumatica present?
Bilateral shoulder and pelvic girdle pain which is worse with movement and interferes with sleep.
-Stiffness for at least 45m in the morning.
-Systemic symptoms - weight loss, fatigue, low mood.
How is PR diagnosed?
With clinical presentation and response to steroid treatment.
What are the investigations for PR?
Bloods to exclude other things - Raised ESR and CRP, FBC, U+E, LFTs, TFTs, CK, RF, calcium, urine dipstick and Bence-Jones protein.
What are seven differential diagnoses of PR?
OA, RA, SLE, myositis, osteomalacia, fibromyalgia, thyroid pathology.
How is PR treated? How do you know that is it PR?
With prednisolone - poor response probably isn’t PR.
-If they work start a reducing regime.
What are the long term steroids precautions?
DONT STOP:
DON’T - Steroid dependent, Adrenal crisis.
S - Sick day rules.
T - Treatment card.
O - Osteoporosis prevention.
P - PPI for gastric protection.
What do connective tissue disorders lead to?
Weak valves and weak vessels - regurgitation murmurs and aortic aneurysm rupture.
What are two connective tissue disorders?
Marfan’s and Ehlers-Danlos syndrome.
What is Marfan’s syndrome?
Autosomal dominant FB1 mutation resulting in decreased connective tissue strength.
How does Marfan’s syndrome present?
Tall and thin patients with long fingers and pectus excavatum.
-Aortic complications - Regurgitation murmur, AAA and aortic aneurysm.
What is Ehlers-Danlos syndrome?
Autosomal dominant mutations affecting collagen proteins.
How does ED syndrome present?
Joint hypermobility and CV complications (mitral regurgitation, AAA, AD).
How should bisphosphonates be taken?
First thing on morning on an empty stomach with plenty of water, staying upright for 30mins and no eating.
What are four side effects of bisphosphonates?
Oesophageal ulcers, GI distress, renal toxicity, hypocalcaemia.
Which biochemical findings would be specific and which would be sensitive for RA?
Sensitive - RF.
Specific - Anti-CCP.
