MSK Flashcards
What is Osteoarthritis?
Loss of articular cartilage
Wear & tear of joints
MC type of arthritis
RF OA
Elderly
After 55 years, females (menopause increases risk)
Previous joint trauma
Genetics
Obesity
RA
Gout
Obesity - low-grade inflam state, not mechanical RF
Joint hypermobility
Occupation! - manual labour (small joints of hands), farming (hips), football (knees)
OSTEOPOROSIS = ↓OA RISK !
Signs / Symptoms OA
Typical Px : Elderly patient w/ hip or knee pain (weight-bearing joints) or carpometacarpal joint (base of thumb)
Asymmetrical!
LESS THAN 30 mins morning stiffness
↓Pain with rest
Pain at end of day
↑Pain with activity
Crepitus
Bony swellings - DIP (Heberden’s) and PIP (Bouchard’s)
Effusion
Synovitis
Functional impairment
Tenderness
Deformities
DDx OA
RA
Gout
Pseudogout
Causes OA
Most - 1º (idiopathic)
2º - caused by other diseases e.g. obesity, haemochromatosis,
??
Ix OA
XR - LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
CRP might be elevated
Rheum factor + ANA = NEG
MRI - shows early articular cartilage injury and subchondral BM changes
Aspiration of synovial fluid - if painful effusion, shows viscous fluid w few leucocytes
Main pathological features of OA
Loss of cartilage
Disordered bone repair
Tx OA
Conservative :
Px ed
Exercise
↓weight
Physio
Footwear
Occupational therapy
Walking aid
Medical
> Topical - NSAIDs, Capsaicin
> Oral - NSAIDs (caution!) w/ PPI if long term, paracetamol
Opioids - if above hasnt worked
not rlly gonna offer unless rllyyy bad and nothing else works ->
Intra-articular steroid injections (only short term relief - 2-10 weeks) - hyaluronic acid
Surgery
Remove osetophytes
Joint replacement - if VERY severe
Arthroscopy - ONLY if loose bodies (lasts only 10-15 years)
What is a loose body?
When small pieces of articular cartilage break off and “floats” in synovial fluid
Causes joints to lock
What are some indications of a loose body?
Uncontrollable pain (esp at night)
Significant limitations
What is Rheumatoid Arthritis?
A chronic, autoimmune, inflammatory symmetrical polyarthritis
RF RA
Female BEFORE menopause (After menopause, incidence is equal between M and F)
Family history
Smoking!!
Autoimmune conditions
Stress
Infection
Signs / Symptoms RA
Joint pain worse in mornings/with cold
Morning stiffness > 30 mins
Loss of function
Fatigue + malaise
Pain decreases with use
Warm, red, tender joints
Joints : SYMMETRICAL!
Small = MCP + PIP (not DIP usually)
Large (as disease progresses) = wrists, elbows, shoulders, knees, ankles
HAND DEFORMITIES : usually at IP joints
1. Ulnar deviation
2. Swan neck (or Z thumb)
3. Boutonniere deformity
Rheumatoid nodules at pressure points - elbow
Carpal tunnel syndrome
Popliteal cyst
What happens in a swan neck deformity?
PIP hyperextension
DIP flexion
What happens in a Boutonniere deformity?
PIP flexion
DIP hyperextension
Extra-Articular symptoms RA
Soft tissue :
Nodules! - usually at pressure points
Bursitis
Tenosynovitis
Muscle wasting
Haematological
Palpable lymph nodes
Splenomegaly
Anaemia
Felty’s triad (rare)
Eyes
Sicca
Sjogren’s
Episcleritis
Scleritis
Neuro
Mild sensory neuropathy (peripheral - legs>arms)
Cord compression
Myelopathy
Skin
Vasculitis
Lungs
Pleural effusion
Rheum nodules
Diffuse fibrosing alveolitis
Diagnostic criteria RA
Needs 4/7 of following
- Morning stiffness > 30 mins
- Arthritis of 3 or more joints
- Arthritis of hand joints
- Symmetrical
- Rheumatoid nodules
- Rheumatoid factor pos
- Radiographic changes - LESS
DDx RA
SLE
Psoriatic arthritis
Symmetrical seronegative spondyloarthropathies
Ix RA
XR - LESS
Loss of joint space
Erosions (peri-articular)
Soft tissue swelling
Soft bones (osteopenia)
Bloods
> Rheum factor = POS in 70% patients (but not specific)
> Anti-CCP = POS, vvv specific but not routinely done (If pos = worse prognosis)
> FBC - ↑ platelets, ↑ ESR, ↑ CRP, normochromic normocytic anaemia
MRI/US - erosions at joint margins and bones
If effusion present, then aspiration of joint = CLoudy bc ↑↑WBC
Tx RA
Upon diagnosis : 1st Line :
DMARDs - Methotrexate, Leflunomide
+
5-asa - Sulfasalazine
2nd Line:
Biologic - TNF-inhibitor
–
Symptom control - NSAID
–
If acute exacerbations, steroids (IM methyprednisolone)
MDT management - Rheum, OT, physio, GP
What is Osteoporosis?
Low bone mass
∴ bone fragility + ↑ fracture risk
What is osteopenia?
Precursor to osteoporosis
T score between -1 and -2.5
What is Osteomalacia?
Poor bone mineralisation
bc lack of calcium (adult form of rickets)
∴ soft bones
Causes Osteoporosis
1º - post-menopause & age
2º - ↑bone turnover, SHATTERED
Steroid use (prednisolone)
Hyperthyroidism/Hyperparathyroidism
Alcohol/smoking
Thin (low BMI)
Testosterone low
Early menopause
Renal or liver failure
Erosive/inflammatory bone disease e.g. RA, myeloma
Dietary calcium low
Why does early menopause/post-menopause cause Osteoporosis?
Oestrogen protects bones
RF Osteoporosis
Think : Patient, Disease, Medication
Also think : SHATTERED
Patient
Old age
Female
FHx
↓BMI
Alcohol & smoking
Diet - ↓Ca2+ (lactose intolerant)
Athletes
Disease
Joint disease (RA, SLE)
Hyperthyroidism, Hyperparathyroidism
↑Cortisol - Cushing’s
↓Oestrogen/Testosterone
Renal disease (↓Vit D)
Previous fractures
Anorexia
Medication
Corticosteroids
Hormonal
Pathophysiology Osteoporosis
Essentially : ↑Resorption by osteoclasts, ↓formation by osteoblasts
W/ age, trab architecture changes :
↓Trab thickness
↓Connections in horizontal trab
∴ ↓Trab strength and ↑ fracture risk
–
Oestrogen def causes remodelling imbalance
What is osteoporosis characterised by?
- ↑↑Bone turnover
- Mostly cancellous bone loss
- Microarchitectual disruption
∴ NET LOSS OF BONE
Why is horizontal trabeclae very important?
Eular-Buckling theory
What is Eular-Buckling theory?
Baso,
In a column, less likely to bend or snap if there are fixed points
don’t quote me on this but basically what it means i think
Signs / Symptoms Osteoporosis
ASYMPTOMATIC UNTIL FRACTURE
Hip - neck of femur (if elderly falls on side/back)
Wrist - Distal radius, Colle’s/Smith’s fracture (fall on outstretched arm)
Verterbra - shorter/stooping, sudden onset on pain in spine - often radiates to front
Fragility fractures
Ix Osteoporosis
DEXA BMD (Dual energy XR & absorptiometry bone mineral density) - T-score
< - 2.5 + fracture = severe OP
< -2.5 = OP
between -1 and -2.5 = osteopenia
> -1 = Normal
–
XR
FRAX - fracture risk assessment (age, sex BMI, prev. fractures, steroids)
FBC - normal Calcium phosphate and alklaine phosphate
Tx Osteoporosis
1st line - ORAL BISPHOSPHONATES
1- alendronate daily
2 - diff oral bis e.g. risendronate
3 - If CI to bis, then strontium ranelate (↓ fracture rate)
Denosumab - monoclonal Ab, inhibits RANK which would otherwise activate osteoclasts
–
HRT - in menopausal women
Raloxifene - SERM (selective oestrogen receptor modulator), similar to HRT
–
Testosterone for men
How should you tell patients to take bisphophonates?
w LOTS of water and sitting upright for > 30 mins
Wait at least 30 mins before eating
Mechanism of Bisphosphonates for Osteoporosis
Inhibits bone resorption by inhibiting enzyme Farnesyl Pyrophosphate synthase by removing ruffled border
∴ ↓osteoclast activity
Prevention Osteoporosis
Adcal D3 - VitD & Ca2+
Ca2+ rich diet
HRT - for postmenopausal women
Corticosteroids - consider prophylactic bis
Regular weight bearing exercise
Stop smoking and alcohol
DEXA scans
S/E Bisphosphonates
Osteonecrosis of jaw
GI distress
↓ Ca2+
Renal toxicity
Oesophageal ulcers
What is Systemic Lupis Erythematosus?
Inflammatory, multisystem, autoimmune condition
What is SLE assoc w?
Raynaud’s
Anti-Phospholipid syndrome
Typical Patient of SLE
Female
20 - 40 years old
More common in Afro-Caribbean and Asian population
RF SLE
Pre-menopausal women
Afro-Caribbean/Asian
Genetics - HLA: DR2, DR3, C4, A, Null Allele
Drugs - Hydralazine, Isoniazide, procainamide, penillamine !
UV light
Smoking
EBV
What type of hypersensitivity reaction is SLE?
TYPE 3
Pathophysiology of SLE
Autoantibodies are produced by B cells
These target autoantigens
∴ form IMMUNE COMPLEXES (T3) at a variety of sites
∴ complement system activated
∴ neutrophil influx
∴ INFLAMMATION
Signs / Symptoms SLE
Remitting and relapsing
V non-specific symptoms : Malaise, fatigue, myalgia, rash, weight loss, skin problems, fever
Correctable ulnar deviation
Haematologically :
Anaemia
Thrombocytopenia
Neutropenia
Lymphopenia
Raynaud’s
Ix SLE
MUST HAVE 4/11 OF FOLLOWING FOR DIAGNOSIS !!!!!!!!
MD SOAP BRAIN
Malar rush - butterfly rash on face
Discoid rash
Serositis - pleuritis, pericarditis
Oral ulcers
Arthritis (non-erosive - similar to RA)
Photosensitivity - rashes on sun exposed areas
Blood disorder - ALL LOW
Renal disease - proteinuria
Anti-nuclear antibody POSITIVE
Immunological disorder - anti ds-DNA
Neuro disorder - seizures, myasthenia gravis etc
∴ INVESTIGATIONS WILL INCLUDE :
> Anti-nuclear antibody test (sens but not spec)
> Double stranded DNA antibody (spec but not sens)
> Other Abs - RF, anti-cardiolipin, Anti-RO, Lupus antibodies
↑ ESR (CRP might be normal)
↓C3 + C4
MRI/CT brain
POP QUIZ!
Patient comes in with multi-systemic disorder, ↑ ESR but normal CRP
What do you think of?
SYSTEMIC LUPUS ERYTHEMATOSUS
Tx SLE
Avoid triggers - UV protections
Lifestyle - stop smoking, weight loss
Topical - suncream etc
–
If ACUTE - IV Cyclophosphamide + high dose prednisolone
If NOT severe - Anti-malarial e.g. hydroxychloroquine and/or steroids e.g. prednisolone
IF severe - Immunouppressives e.g. Cyclophosphamide, methotrexate, ciclosporin, azathioprine
NSAIDs
Anti-coagulants
Plasmapheresis
Monitoring SLE
Kidney function should be monitored!
What is Gout?
Inflammatory arthritis assoc w/ hyperuricaemia
Negatively bifringent needle-shaped monosodium urate crystals
Typical patient of Gout
Men > 40 years !
Chinese, Polynesian, Filipino IF westernised diet (not in native county!)
Causes Gout
1. Under-excretion of Uric Acid
Hyperuricaemia
Alcohol
Obesity
DM (insulin resistance = ↑insulin)
HTN
Hypothyroidism, Hyperparathyroidism
Drugs - low dose aspirin, diuretics, lead poisoning, ethambutol, pyrazinamide, cyclosporine, tacrolimus
Renal - defect in URAT1 transported in kidney, seen in kidney disease
2. XS purines TOO MUCH RED MEAT, ORGAN MEAT, SHELLFISH, ANCHOVIES, ALCOHOL
Also : Metabolic syndrome - hyperlipidaemia
Lesch-Nyhan syndrome
3. ↑Production of uric acid
Chemo/Radiotherapy
Surgery - cell death
Carcinoma
Psoriasis
Myeloproliferative diseases - polycythaemia vera
Causes of Gouty attack
Anything that causes sudden alteration in uric acid conc
Aggressive intro/Sudden stop of hypo-uricaemic therapy
Alcohol/Shellfish binges
Sepsis, MI, acute severe illness
Trauma, surgery, dehydration
RF Gout
↑ Alcohol
Purine rich foods - shellfish, organ meat etc
High fructose intake - sugar
FHx
Age
Obesity
DM
IHD
HTN
Pathophysiology Gout
Purine from diet
Gets converted -> Hypoxanthine -> Xanthine
Then, Xanthine -> Uric acid
Catalysed by xanthine oxidase
Excreted in kidneys
–
If ↑↑Uric acid, XS is converted to monosodium urate crystals and deposited in tissues - TOPHI
Monosodium urate crystals can cause inflammation - ∴ more pain
Tends to form in peripheral joints (big toe) bc temperature is cooler and/or if previous trauma in joint
Signs / Symptoms Gout
Sudden onset of agonising pain, swelling and tenderness and redness - “toe on fire”
Pain precipitated by excess food, alcohol, dehydration, diuretic therapy
Recurrent episodes
Red, shiny, warm, PAINFUL joint w white deposits (tophi) on skin
Skin over joint has peeled off
DDx Gout
Septic Arthritis
Tophaceous gout
Ix Gout
JOINT ASPIRATION!! - to rule out septic arthritis, ALWAYS RULE OUT A RED, HOT JOINT
X-Ray ! - punched out erosions near joint
GS!! Polarised light microscopy - neg bifringent needle shaped monosodium crystals
Bloods - raised serum urate (can be normal)
POP QUIZ
A patient comes in with a hot, red joint. What do you do?
ASPIRATE ASPIRATE ASPIRATE!!!
ALWAYS RULE OUT A RED, HOT JOINT
to rule out septic arthritis
Tx Gout
Lifestyle - kcal restriction, modify diet, weight loss, ↓alcohol
DAIRY - protective! & cherries, vitamin C
–
1st line - NSAIDs e.g. ibuprofen
2nd line - Colchicine (If NSAIDs CI)
Prophylaxis - Xanthine oxidase inhibitors e.g. Allopurinol ! (rapidly reduces serum urate levels)
DO NOT use Allopurinol during acute attack!! Wait 3 weeks after attack to give
& ALSO give Colchicine for 6 months OR NSAID for 6 weeks otherwise will induce a gouty flare
Febuxostat if Allopurinol CI
What is Pseudogout?
Deposition of calcium pyrophosphate crystals in joints
Usually larger joints!
Knee > Wrist > Shoulder > Ankle > Elbow
Typical patient of Psuedogout
Female > 70 years
RF Pseudogout
Old age
OA
Hyperparathyroidism
Haemochromatosis
Hypophosphataemia
DM
Pathophysiology of Pseudogout
Deposition of calcium pyrophosphate in articular cartilage and periarticular tissue
Chondrocalcinosis = radiological appearance
What is chondrocalcinosis?
Linear calcification parallel to articular surfaces
Causes of acute Pseudogout attack
Direct trauma to joint
Intercurrent illness
Surgery - esp parathyroidectomy
Blood transfusion, IV fluids
T4 replacement
Joint lavage
Signs / Symptoms Pseudogout
Severe jont pain
Acute synovitis
Acute hot, swollen joint
Fever
Stiffness
What are Tophi?
Onion-like aggregates of monosodium urate crystals with inflammatory cells
What is Tophaceous Gout?
Appears in people w/ persistently high levels of uric acid
Tophi form in skin around joints - ear, fingers, Achilles tendon
Tophi release proteolytic enzymes ∴ erosions to bone
Assoc w/ renal impairment and/or long-term use of diuretics
S/E Colchicine
Diarrhoea
Abdo pain
S/E Allopurinol
Rash
Fever
Low WBC
How to distinguish OA and Pseudogout
- Pattern on involvement - which joint?
- Marked inflam component
- Superimposition of acute attack
What is Pseudogout also known as?
Pyrophosphate arthropathy
Ix PseudoGout
XRAY - evidence of chondrocalcinosis
JOINT ASPIRATION - ALWAYS ASPIRATE A RED HOT JOINT
GS Polarised light microscopy - positively bifringent rhomboid shaped calcium pyrophosphate crystals
FBC - ↑ WBC
Tx Pseudogout
1st line - NSAIDs
2nd line - Colchicine
Analgesia
Physio
Rest and icepacks
–
Long term Tx :
Try anti-rheum treatment e.g. methotrexate, hydroxychloroquine
Synovectomy if bad
Surgery
Name the 5 most common tumours that spread to bone
LEAD KETTLE - PB KTL
Prostate
Breast
Kidney
Thyroid
Lung
Typical patient of 1º Bone tumours
Rare
Usually only seen in YA and children
RF 1º Bone tumours
Radiation - XR, CT
Padget’s disease
MC : 1º or 2º bone tumours?
2º
Name the types of Benign 1º bone tumours
- Osteochondroma
- Giant cell tumour
- Osteoblastoma & osteoid osteomas
Name the types of Benign 1º bone tumours
AND state who they affect and where on the body if you can
OGO
1. Osteochondroma
Males < 25 years old
Develop in metaphysis of long bones (distal femur, distal tibia, ilium, scapula)
2. Giant cell tumour
Develop in epiphysis of long bones (distal femur, proximal tibia)
3. Osteoblastoma & osteoid osteomas
From osteoblasts, forms nidus
Name the types of Malignant 1º bone tumours
OEC
- Osteosarcomas
- Ewing’s sarcomas
- Chondrosarcoma
What is Osteosarcoma strongly associated with?
Padget’s
What age does Osteosarcoma usually affect?
15-19
Where does Osteosarcoma usually affect?
Knees or proximal humerus
Destroys bones, spreads to tissues
RAPIDLY METASTASISES TO LUNGS
Which 1º rapidly metastasises to the lungs?
Osteosarcoma!
What age range does Ewing’s sarcoma usually affect?
Is it a common disease?
RARE
< 25 years old
15 years old = peak incidence
What areas does Ewing’s sarcoma usually affect?
Hips + long bones
How does Ewing’s sarcoma specifically tend to present?
Painful swelling/redness in long bones of arms, legs, chest, pelvis
Sometimes skull, flat bones of trunk
Can cause paralysis +/- incontinence if affects spine
What region does chondrosarcoma usually affect?
Pelvis MC
Also : femur, humerus, scapula, ribs
How does chondrosarcoma specifically tend to present?
Deep, dull pain
Affected area is swollen and tender
How does an osteoid osteoma specifically tend to present?
Pain worsens at night
Osteochondroma and Osteoblastoma can both press on ______
spinal cord
∴ numbness, limb weakness, avascular necrosis
Chondrosarcoma forms from?
Chrondrocytes
What is Enteric Arthritis?
Arthritis 2ºto IBD
Cause Enteric Arthritis
Bacteria
RF Enteric Arthritis
MALE»_space; Female
Signs / Symptoms Enteric Arthritis
Asymmetrical joints
Synovitis affecting PERIPHERAL JOINTS
Monoarticular OR polyarticular
Large joints - knees, ankles, feet
Sacroilitis
Tx Enteric Arthritis
Will subside with remission of IBD
What is Vasculitis?
Inflam of blood vessels
Conditions assoc w Vasculitis
Infective - subacute IE
Non infective - SLE, Scleroderma, Polymyositis, Dermatomyositis, Goodpasture’s
What does Giant Cell Arteritis affect?
Affects aorta +/- its major branches - carotid, vertebral arteries
TEMPORAL ARTERY
RF Giant Cell Arteritis
> 50 !!
Atherosclerosis
Females»_space;>
Smoking
Hx of polymalgia rhematica
Signs / Symptoms Giant Cell Arteritis
HEADACHE - New onset, unilateral over temporal area
Scalp tenderness - hurts to brush hair
Jaw claudication
Visual disturbances - blurred vision, diplopia, amaurosis fugax, blindness
Ix Giant Cell Arteritis
↑ESR +/- ↑CRP , (ESR > 50mm/hour)
GS!!!* TEMPORAL ARTERY BIOPSY
Giant cells, granulomatous inflam
–
On examination, temporal arteries might be tender + thickened on palpation
Pulse might be diminished
US - Halo sign of temporal and axillary artery
Tx Giant Cell Arteritis
High dose glucocorticoid ASAP
Usually Prednisolone 40-60mg
Comps Giant Cell Arteritis
Blindness
Irreversible neuropathy
Big vessels - Vasculitis
What is it?
Giant cell arteritis
Medium vessels - Vasculitis
What is it?
Polyarteritis Nodosa
Small vessels - Vasculitis
What is it?
Granulomatosis w Polyangiitis
Where does Polyarteritis Nodosa affect?
Mid-sized vessels in locations like :
Skin
GI tract
Kidneys
Heart
RF Polyarteritis Nodosa
HEP B
Hep C
HIV
MC in developing countries
Ix Polyarteritis Nodosa
↑ESR +/- CRP
HBsAg
BIOPSY - transmural fibrinoid necrosis
Signs / Symptoms Polyarteritis Nodosa
Peripheral neuropathy - mononeuritis multiplex
Cutaneous/Subcutaneous nodules !!!
Unilateral orchitis!!!
Abdo pain
Livedo reticularis
HTN
What is Livedo reticularis?
Mottled, purplish, lace-like rash
Tx Polyarteritis Nodosa
If Hep B pos - antiviral agents, plasma exchange and corticosteroids
If Hep B neg - corticosteroids + cyclophosphamide
Where does Granulomatosis w Polyangiitis affect?
Small vessels
Resp tract + Kidneys
What age group does Granulomatosis w Polyangiitis affect?
Late teens
Early adulthood
Signs / Symptoms Granulomatosis w Polyangiitis
CLASSIC SIGN = Saddle shaped nose!!
bc perforated nasal septum
Epistaxis
Crusty nasal/ear secretions - hearing loss
Sinusitis
Might be mistaken for pneumonia - cough, wheeze, haemoptysis
Ix Granulomatosis w Polyangiitis
FBC - ↑Eosinophils
Histology - granulomas
c-ANCA !!!
NOT p-ANCA
what does ANCA stand for?
Anti-Neutrophil Cytoplasmic Abs
Tx Granulomatosis w Polyangiitis
Nasal corticosteroids
Cyclophosphamide
When is Septic Arthritis MC?
< 4 years
or Older adults
Pathophysiology Septic Arthritis
Infection of at least 1 joint by pathogenic inoculation by microbes
Either directly or haematogenously
Causes Septic Arthritis
Staph. Aureus - MC!!
Group A Strep - Strep Pyogens
E. Coli
Neisseria gonorrhoea
Haem. Influenzae
Can be a comp of joint replacement
RF
Pre-Existing joint disease (OA or RA)
Prosthetic joint
IVDU
Immunosuppression
Alcohol
DM
Intra-articular corticosteroid injection
Signs / Symptoms Septic Arthritis
HOT RED SWOLLEN JOINT
Refusing to weight bear (kids usually), stiffness, reduced range of motion
Knee or hip usually! Usually only one knee
CONSIDER IN EVERY CHILD W A JOINT PROBLEM !!!!!!
Fever
Lethargy
Sepsis
Onset of Septic Arthritis
< 2 weeks
DDx Septic Arthritis
Transient sinovitis
Perthes disease
Slipper upper femoral epiphysis
Juvenile idiopathic arthritis
Ix Septic Arthritis
ASPIRATE !!!! - gram stain, crystal microscopy, MC+S
Blood culture
WBC - might be raised
ESR/CRP ↑
Tx Septic Arthritis
Aspirate + Surgical drainage + washout of joint to clear infection if severe !
Empirical Abx e.g. flucloxacillin
Spec Abx - after results (cont for 3-6 weeks)
Analgesia
Be esp cautious w immunosupp patients
Consult orthopedic team!
What is Osteomyelitis?
Inflam of BONE
Cause Osteomyelitis
Staph. Aureus - If haematogenous
Staph. Epidermidis - Exogenous/Local
MC mode of infection Osteomyelitis
Haematogenous!
But also through surgery
RF Osteomyelitis
Open fracture
Orthopaedic ops
DM - esp foot ulcers
Periph arterial disease
IVDU
Immunosuppresion
Children - URTI or varicella infection
Signs / Symptoms Osteomyelitis
Limp/Reluctance to weight beat (children)
Non-Spec pain and tenderness at site of infection
Fever
Erythema
Swelling
Ix Osteomyelitis
FBC - ↑WBC
↑ ESR/CRP
X-Ray - can see periosteal reaction
If neg, doesn’t discount!
GS MRI
Blood cultures, bone cultures
Tx Osteomyelitis
Abs - 6 weeks flucloxacillin (+rifampicin for first 2 weeks)
Clindamycin if penicillin allergy!
Vancomycin - MRSA
Surgery - debridement of infected bone and tissue
Advice for taking bisphophonates
First thing in morning
Empty stomach
Remain upright for 30 mins after taking
What is a classic patient of Fibromyalgia?
20 - 50 year old woman with poor socioeconomic status
Signs / Symptoms Fibromyalgia
↑Sensitivity to pain
Fatigue
Fibro-fob - problems with memory and conc
Morning stiffness
Headaches
IBS
Ix Fibromyalgia
11 tender points in 9 pairs of sites, for at least 3 months
http://www.fibromyalgiaawareness.com/2012/04/fibromyalgia-tender-points-poster.html
^^^^^ NOT RECOMMENDED AS DIAGNOSIS NOW BUT KEEP IN MIND
Now - widespread pain in combo w fatigue, sleep difficulties, memory issues
Tx Fibromyalgia
Education
Exercise + Relaxation
Analgesia
CBT
What is Sjogren’s?
Autoimmune condition that affects exocrine glands
∴ Dry mucous membranes
RF Sjogren’s
1º - just happens
FHx - 1st degree relative = 7x risk!!
Female
40+
Signs / Symptoms Sjogren’s
Dry mouth
Dry eyes
Dry vagina
Ix Sjogren’s
Anti-Ro and Anti-La antibodies
POS Schirmer test
Describe the Schirmir test
Insert folded filter paper under lower eyelid with strip hanging out over eyelif
Tear travelling < 10mm is POS test!!
Healthy adults = tear travels > 15mm
Tx Sjogren’s
Artificial tears, artificial saliva, vaginal lubricants
Hydroxychloroquine used to halt progression
Comps Sjogren’s
Eye infection - conjugutivitis
Oral problems - dental cavity
Vaginal problems - candidiasis, sexual dysfunction