Musculoskeletal and Rheumatology Flashcards
What are the 2 types of bone at a macro level?
Cortical:
* Compact
* Dense, solid
* Only spaces are for cells and blood vessels
Trabecular:
* Cancellous (spongy)
* Network of bony struts (TRABECULAE)
* Looks like sponge, many holes filled with bone marrow
* Cells reside in trabeculae and blood vessels in holes
What are the different types of bone at a micro level?
Woven bone:
* Made quickly
* Disorganised
* No clear structure
Lamellar bone:
* Made slowly
* Organised
* Layered structure
What is the function of hollow long bones?
Keeps mass AWAY from the neutral axis and minimised deformation
What is the function of Trabecular bone?
Give structural support while minimising mass
What is the function of bone that has wide ends?
Spreads load over weak, low friction surface
What is the composition of bone in adults?
- 50-70% mineral:
- Hydroxyapatite - crystalline form of calcium phosphate
- 20-40% organic matrix:
- Type 1 Collagen - 90% of all protein
- Non-collagenous proteins - 10% of all protein
- 5-10% water
What do the minerals and collagen provide to bone respectively?
Minerals - Stiffness
Collagen - Elasticity
What is the function of a joint?
- Allow movement in 3 dimensions
- To bear weight
- To transfer the load evenly to the musculoskeletal system
Give some key joints and examples
- Fibrous - teeth sockets
- Cartilaginous - intervertebral discs
- Synovial - metacarpophalangeal and knee joint:
What are the main features of a synovial joint?
- Articular cartilage
- Joint capsule - the inner layer is the
synovial membrane - Joint (synovial) cavity - space filled with synovial fluid
- Synovial fluid
- Reinforcing ligaments
+Bursae and Menisci
What is the function of Synovial Fluid?
Lubrication
Shock absorption
Nutrient Distribution
What is ESR?
Erythrocyte Sedimentation
An Inflammatory marker That rises with inflammation and infection.
ESR rises and falls slowly
What is CRP?
C-Reactive Protein
Acute phase marker of inflammation and infection.
Produced by the liver in response to IL-6
Rises and falls rapidly (acute inflammation CRP rises but ESR takes longer)
Define Osteoarthritis
A non-inflammatory degenerative joint disorder characterised by joint pain and functional limitation.
Osteoarthritis is an age-related, dynamic reaction pattern of a joint in response to insult or injury (Wear and Tear)
All tissues of the joint are involved
Articular cartilage is the most affected – produced by chondrocytes
What is the pathophysiology of OA?
Imbalance in process of cartilage breakdown by wear and tear and by chondrocytes releasing cartilage breakdown Factors leading to erosion of the articular cartilage in synovial joints.
- Faulty cartilage undergoes erosion
- disordered repair
- fibrillations occur
- cartilage ulceration which exposes underlying bone to increased stress
- microfractures and cysts form as exposed bone attempts repair
- abnormal sclerotic subchondral bone and overgrowth at joint margins (osteophytes)
What are the main features in the pathology of OA?
Imbalance between
Loss of cartilage through wear and tear
Disordered cartilage repair by chondrocytes
What controls the development of OA?
Mediated by cytokines:
IL-1, TNFa, NO
Driven By mechanical Forces
What is the epidemiology of OA?
Most common type of arthritis
Especially in elderly and females
Most common condition affecting synovial joints
Most important condition relating to disability as a result of locomotor symptoms
8.75 million people in the UK seek treatment for OA
What are the non-modifiable risk factors for OA?
Genetics -COL2A1 has a role
Increasing Age - strongest RF
Female - Hip OA 2x more common
High bone density - protective against osteoporosis but RF for OA
What are the modifiable Risk factors for OA?
Obesity
Joint injury/damage
Exercise stress
What are the symptoms of OA?
Joint pain - exacerbated by movement and relieved by rest
Worse as the day goes on
Joint Stiffness
Crepitus
Swelling
Joint Locking - inability to straighten joints
What is the typical Presentation of OA?
Elderly Px with knee/hip pain.
Morning stiffness lasting less that 30 mins
Pain increases with use (crepitus) and during the day
Asymmetrical joint involvement.
Bony swellings DIP/PIP
What are the clinical signs of OA?
Hands:
Bouchard’s Nodes (PIPJ)
Heberden’s Nodes (DIPJ)
Thenar Muscle wasting
First CMC Joint squaring at base of thumbf affected most
Knees:
Crepitus
Hips:
Antalgic gait
Restricted internal rotation
All affected Joints:
Joint tenderness
What is Heberden’s and Bouchard’s Nodes?
What condition are they seen in?
Seen in OA.
Bouchard’s - Bony swelling at PIP
Heberden’s - Bony swelling at the DIP
Remember B before H and proximal before distal
What is the most commonly affected joint in OA?
First Carpometacarpal joint of the thumb
What joints are the most commonly affected in OA?
Hips
Knees
Sacro-iliac joints
Distal-interphalangeal joints in the hands (DIPs)
The carpometacarpal joint at the base of the thumb (CMC)
Wrist
Cervical spine
What is Crepitus?
Crackling or grating sensation when moving a joint
What is a common differential diagnosis to OA?
Rheumatoid arthritis
Gout/Pseudogout
This differs from RA due to the absence of systemic features and the pattern of joint involvement.
What are the primary investigations to diagnose OA?
Joint X rays show OA hallmarks: LOSS:
Loss of Joint space (Joint space narrowing)
Osteophyte formation
Subarticular Sclerosis
Subchondral Cysts
(+ Abnormalities of Bone Contours)
What other investigations may be done in OA?
Diagnosis can be made if Px is over 45, has typical OA pain and this is not associated with early morning stiffness (like in RA)
XR
Bloods - normal in OA
ESR/CRP - inflammatory markers to distinguish between RA or Gout
Negative anti-nuclear and RF antibodies
What is the conservative management of OA?
Weight loss if overweight to reduce the load on the joint
Physiotherapy to improve strength and function
Occupational therapy to support activities and function
Orthotics to support activities and function (e.g., knee braces)
What medical treatments can be used in OA?
Analgesics to control pain and Sx:
1st. Oral paracetamol / topical NSAIDs
2nd. Add oral NSAIDs
3rd . Consider Opiates - Codeine
If these fail:
Inter-articular steroid injections
Surgical - Joint replacement/osteotomy/arthroplasty
When should oral NSAIDs be used with caution for OA?
In an older patient who may be on anticoagulants such as aspirin/DOACs
There may be some drug interactions/side effects using both Tx
Define Rheumatoid Arthritis (RA)
A chronic systemic autoimmune arthritis that progresses from a symmetrical deforming poly-arthropathy affecting the synovial joints to a multi-system disorder
Characterised by deposition of immune complexes in synovial joints
What is the pathophysiology of RA?
RA is primarily a synovial disease that spreads to extra articular areas.
Genetic predisposition and environmental event allows a triggering factor to cause Arginine - citrulline mutation in T2 collagen (citrullination) - anti-CCP Abs form.
T cells that entre the joints release chemoattractant (IFN and TNF-alpha) produced in the joint, this recruit circulating inflammatory cells
The Synovium is thickened by inflammatory cells and it proliferates to produce a “pannus”
The pannus DESTROYS the articular cartilage and subchondral bone resulting in bony erosions
What is the key chemoattractant involved in the progression of RA?
IFN and TNF-alpha
What is the epidemiology of RA?
Affects 1% of global population
More common in females than males
Linked to autoimmune conditions
Prevalence peaks at 30-50yrs
What are the genetic factors for RA?
HLA-DR1 and HLA-DR4 (crucial in activating T-cells)
PTPN22
What are the risk factors for RA?
Increasing age (but also middle aged women)
Genetics (HLA-DRB1, HLA-DR4)
Female - (pre-menopause)
FHx
Smoking
What is the role of the immune system in RA?
Triggering antigen is unknown but immune system has a role in synovial inflammation:
- T cells - interferon, IL-2 & -4
- Macrophages - IL-1 & -8 & TNF-alpha
- Mast cells - histamine & TNF-alpha
- Fibroblasts - IL-6
What are the symptoms of RA?
Morning stiffness/pain - >30 mins and improves throughout the day
Joint pain worse in cold environments but eases with use.
Loss of function of joints
Constitutional Sx - malaise, myalgia, fever
Extra Articular involvement - pulmonary fibrosis, pericarditis
sleep disturbances
Felty’s Syndrome:
RA, Neutropenia, Splenomegaly
What are the clinical signs of RA?
Hand:
Symmetrical polyarthritis
Boutonniere Deformity
Swan neck deformity
Z thumb deformity
Ulnar deviation
Symmetrical
Hot/warm inflamed joints
Extra articular complications
What joints does RA most commonly affect?
Early disease:
Symmetrically affects Joints of the hands and feet (MCP, PIP, MTP)
Progressed Disease:
Wrists
Elbows
Shoulders
Knees
Ankles
What is Boutonniere deformity?
PIP flexion and DIP hyperextension seen in RA
What is Swan neck deformity?
PIP hyperextension and DIP flexion seen in RA
What are some extra articular complications seen in RA?
Scleritis
rheumatoid skin nodules
Pleural Effusions
Interstitial Lung Disease
Pericarditis
Coronary Artery Disease
Glomerulonephritis
Neuropathy
What is the Diagnostic Criteria for RA?
Need 4/7
1. Morning stiffness
2. Arthritis of 3 or more joints
3. Arthritis of hand joints
4. Symmetrical
5. Rheumatoid nodules
6. Rheumatoid factor positive
7. Radiographic changes – LESS
What are the primary investigations in RA?
Bloods:
ESR/CRP raised - inflammation
NORMOCYTIC, NORMOCHROMATIC anaemia
Serology:
Positive rheumatoid factor - 80% (not specific)
Positive anti-CCP Abs - 30% (very specific for RA)
XR = LESS
What is the X-ray like in RA?
LESS:
Loss of joint space
Eroded Bone
Soft tissue Swelling
Soft Bones (Periarticular osteopenia)
What Antibodies are present in RA?
Positive Rheumatoid Factor Abs - Not specific
Positive Anti-CCP Abs (Anti - Cyclic Citrullinated Peptide) - Very specific
What is the treatment of RA?
No cure - Sx management:
Initially NSAIDs analgesia - Often co prescribed with PPI (gastric protection)
Induce remission
DMARDs:
eg. methotrexate - GS treatment (others such as sulfasalazine (causes haemolytic anaemia)/hydroxychloroquine)
If unsuccessful then
2’ = Methotrexate + sulfasalazine/hydroxychloroquine
3’ Methotrexate + TNFi (infliximab)
4’ Methotrexate + Rituximab
If severe pain/flare ups - Intraarticular steroid injection (prednisolone)
What are DMARDS?
Disease Modifying anti Rheumatic Drugs:
Methotrexate is given as monotherapy or alongside biologics (but these are very expensive)
Also Hydroxychloroquine and Sulfasalazine
When is methotrexate Contraindicated?
Pregnancy as it is a folate inhibitor and therefore DNA synthesis is affected
What is the mechanism of action of methotrexate?
What must always be co-prescribed with methotrexate?
Folate acid synthesis inhibitor (inhibits dihydrofolate reductase)
Therefore must co-prescribe Folic Acid
What biologics are used in combination with DMARDs in RA?
1st - TNF-a inhibitor - INFLIXIMAB
2nd- B cell inhibitor (CD20 target) - RITUXIMAB
ADALIMUMAB - Monoclonal Ab
TOCOLIZUMAB - Il-6 antagonist
ABATERCEPT - Blocks T cell activation
BARACITINIB
What are the types of crystal arthritis?
Gout
PseudoGout
What type of crystals are formed in crystal arthritis?
Gout:
Needle Shaped monosodium Urate Crystals
Negatively Birefringent in polarised light
Pseudogout:
Rhomboid Brick shaped Pyrophosphate crystals
Positively Birefringent in Polarised Light
Define Gout?
Gout is an inflammatory arthritis caused by deposition of monosodium urate crystals within joints due to hyperuric acid levels
What is the most common inflammatory arthritis in the UK?
Gout
Who does Gout affect?
More common in males than females (2-7:1)
Typically in adulthood >40 years
Rises in postmenopausal women - due to oestrogen protection prior to menopause
What are the risk factors for gout?
Male
Obesity - high fructose intake
High purine diet (e.g. meat and seafood)
Alcohol (beer/larger)
Diuretics
Existing cardiovascular or kidney disease
Family history
What factors can increase uric acid production?
Malignancy - increased cell turnover
Cytotoxic drugs
Purine rich diet
Obesity
Alcohol
Surgery
Psoriasis
What factors can impair the excretion/removal of uric acid?
CKD
Diuretics
Pyrazinamide
Lead Toxicity
What are the causes of Gout?
Under excretion of uric acid:
Hyperuricaemia
Drugs
Alcohol/obesity
CDK
Overproduction of purines:
High purine Diet (meat, beer, seafood)
Psoriasis
Malignancy
Methotrexate
Renal Causes
What is the pathogenesis of Gout?
High purine intake (food/alcohol)
Is oxidised to Uric acid by Xanthine oxidase.
Normally uric acid is then excreted by the kidneys
But in hyperuricaemia this cannot occur fast enough and this can lead to kidney damage
The Uric acid is converted to monosodium urate crystals that trigger intracellular inflammation.
These deposit in joints and cause an inflammatory arthritis
What are common causes of a gout attack?
Anything that causes sudden alteration in uric acid concentration
Alcohol
Diet
MI
Trauma
What food substances can be anti-gout?
Dairy
What are the symptoms of gout?
Often ASx hyperuricaemia but attacks come on in episodes.
Rapid onset severe joint pain
Joint stiffness
Commonly swollen red big toe which is painful you cannot put weight on it (TOE ON FIRE)
What are the clinical signs of gout?
Monoarticular/oligoarticular - 1-4 joints affected
1st joint = MTP of big toe
Ankle and wrist also affected
Gouty Tophi - nodular masses of urate acid crystals
Precipitated by purine triggers. Often have recurrent episodes.
What are the primary investigations for Gout?
Joint aspirate and POLARISED:
Negatively BIREFRINGENT needle shaped crystals
Serum Urate - may give an indication if hyperuricaemia (but may be normal)
Why may there be low serum uric acid levels in a Px who is having a gout attack?
Due to all the uric acid forming crystals that has collected in the joints and therefore is not present in the blood.
What result do gout crystals give when undergoing polarised microscopy?
Negatively Birefringent needle shaped crystals
Why must you always aspirate a red hot joint?
To rule out septic arthritis
What is the management of Gout?
Low uric acid level:
Lifestyle Mx
Diety - decrease purines and increase dairy
Weight loss
Reduce alcohol.
Prophylaxis - Allopurinol
Pain Mx:
1st - High dose NSAIDs
2nd Colchicine (if NSAIDs CI)
3rd - Steroid injection -
What is given to prevent gout (prophylaxis)?
Allopurinol -Xanthine oxidase inhibitor to reduce uric acid production.
Given after resolution of the first attack of gout.
Why must you be careful when prescribing Allopurinol?
Shouldn’t be used during a gout attack.
Cover with Colchicine or NSAIDs to prevent a Gout Flare
What is Pseudogout?
Pseudogout is a form of inflammatory arthritis caused by deposition of calcium pyrophosphate crystals (chondrocalcinosis) in the synovium and joint capsule
Who is affected by pseudogout?
Typically elderly women >70 yrs
What are the risk factors for pseudogout?
Elderly Female
Diabetes
Metabolic diseases - Hyperparathyroidism, HH
Hypophosphataemia
OA - High overlap with OA and pseudogout
What can cause an acute pseudogout attack?
Direct trauma to the joint
Intercurrent illness
Surgery – especially parathyroidectomy
Blood transfusion, IV fluid
T4 replacement
Joint lavage
What is the pathophysiology of Pseudogout?
Deposition of calcium pyrophosphate in articular cartilage and periarticular tissue producing the radiological appearance of chondrocalcinosis
Typical distribution – usually affects larger joints
Knee > wrist > shoulder > ankle > elbow
What is the clinical presentation of pseudogout?
Resembles gout however the most commonly affected joints are Knee, shoulder and wrist
(MTP joint is primary affected joint in gout)
What are the common clinical features of Pseudogout?
Asymptomatic
Severe joint pain
Acute synovitis – due to shedding of crystals into joint
Acute hot and swollen joint or OA joint
Fever
Stiffness
What is the primary investigation for pseudogout?
Joint aspiration + polarised microscopy:
Weakly - Positively BIREFRINGENT rhomboid shaped crystals
XR - Evidence of chondrocalcinosis - Pathognomonic
FBC - Raised WCC
What is the management of Pseudogout?
Only acute management:
1st - NSAIDs
2nd - Colchicine
3rd Steroid injection - IM Prednisolone
+ physiotherapy and rest/icepacks
Long term Tx with DMARDs may be considered if poor inflammatory change
How can you distinguish Osteoarthritis from Pyrophosphate arthropathy?
- Pattern of involvement – knee, wrists, shoulders, ankles, elbows
- Marked inflammatory component
- Superimposition of acute attacks
What is Osteoporosis?
Osteoporosis is the reduction in trabecular bone mass/density and disruption of bone microarchitecture, resulting in porous bone with increased fragility and fracture risk
Define Osteoporosis?
Defined as bone mineral density (BMD) MORE than 2.5 standard deviations
BELOW the young adult mean value (T score < -2.5)
What is Osteopenia?
Pre-cursor to osteoporosis characterised by low bone density
Define Osteopenia?
Defined as BMD between 1-2.5 standard deviations BELOW the young adult
mean value (-1< T score > -2.5)
What is Osteomalacia?
Poor bone mineralisation leading to soft bone due to lack of Ca2+ (adults form of Ricket’s)
Rickets is poor bone mineralisation in children
What is the key difference between osteoporosis and osteomalacia?
Osteoporosis is poor bone density
Osteomalacia is poor bone mineralisation
Who does osteoporosis typically affect?
Typically 50yrs + post menopausal Caucasian women
1/2 of Women and 1/5th of men over 50
230, 000 osteoporotic fractures each year
What are the risk factors for osteoporosis?
SHATTERED
Steroids
Hyperthyroidism, hyperparathyroidism, hypercalciuria
Alcohol + Smoking
Thin (Low BMI)
Testosterone (Low)
Early Menopause
Renal / Liver Failure
Erosive Disease
Diabetes Type 1 / Diet
What are the causes of Osteoporosis?
Primary: Post Menopausal
Secondary (SHATTERED):
Steroids
Hyperthyroid/Hyperparathyroid
Alcohol/Smoking
Thin (low BMI)
Testosterone (low)
Early menopause (low estrogen)
Renal/liver failure
Erosive + inflammatory disease
Diabetes Mellitus - Type 1
What is the T score?
Young adult bone Density
What is the pathogenesis of Osteoporosis?
Increased resorption by osteoclasts
Decreased bone formation by osteoblasts
Inadequate peak bone mass
Changes in trabecular architecture with ageing
How does oestrogen affect bone remodelling in osteoporosis?
Post menopausal women
Oestrogen deficiency
Remodelling imbalance - net loss of bone
(preventable by oestrogen replacement)
What are the symptoms of Osteoporosis
ASx until fracture.
HIP - Neck of Femur if elderly falls on side or back
Wrist - Distal radius if fall on outstretched arm
May have evidence of acute fractures (vertebrae, fragility fractures)
What are the clinical signs of Osteoporosis?
Fractures of:
Proximal femur
Colles’ Fracture (forked wrist)
Compression of vertebral column - Kyphosis
What are the primary investigations of Osteoporosis?
DEXA Scan (Dual Energy X-ray Absorptiometry)
Yields T score - compares Px BMD to reference
FRAX Score - Fracture risk assessment
What result on the DEXA score indicates osteopenia/ osteoporosis?
DEXA score is normal distribution of BMD
-1 to -2.5 SD below mean is osteopenia
> -2.5 SD below mean is osteoporosis
> 3 SD below mean is severe osteoporosis
What is the FRAX score?
Fracture risk assessment tool:
Age
Sex
BMI
Previous Fractures
Steroids
What is the management of Osteoporosis?
Conservative:
Lifestyle changes - reduce RFs
Vit D and Calcium supplements
Medical:
1st Line - Bisphosphonates - Alendronate, Risedronate
2ndLine - Different Bisphosphonate (risedronate)
3rd Line - mAB Denosumab or HRT
What is the first line treatment of osteoporosis and what is the mechanism of action?
Bisphosphonates:
Interfere with osteoclasts by inhibiting RANK-L signalling to reduce the amount of bone resorption
Give some examples of bisphosphonates?
Alendronate
Risedronate
Zoledronic Acid
What are some key side effects of Bisphosphonates?
Reflux and Oesophageal Erosions
Atypical Fractures
Osteonecrosis of the jaw
Osteonecrosis of external auditory canal
How would you advise bisphosphonates to be taken?
Once a Week
On an Empty Stomach
Patient should remain upright for 30 mins after taking
What are some third line treatments for osteoporosis?
Denosumab - monoclonal Ab against RANK-L
Raloxifene - used as secondary prevention as an oestrogen receptor modulator
HRT - Oestrogen inhibits bone resorption of osteoclasts by promoting osteoclast apoptosis
What is the Primary Prevention of Osteoporosis?
o Adcal D3 – Vitamin D + calcium
o Calcium-rich diet e.g. dairy or sardines, white beans
o HRT – menopausal women
o Corticosteroids – consider prophylactic bisphosphonates
o Regular weight bearing exercise
o Smoking and alcohol cessation
o DEXA scans
What is Fibromyalgia?
A syndrome characterised by widespread pain and tender points at specific anatomical sites.
No signs of inflammation - Non-specific muscular disorder
It is often accompanied by depression, fatigue and sleep disturbance
Define Fibromyalgia?
Fibro - Soft tissue
Myalgia - Muscle Pain
What is Fibromyalgia equivalent to?
Equivalent to IBS:
Chronic widespread MSK pain for 3+ months when all other causes have been ruled out
What is the definition of Fibromyalgia?
- Widespread musculoskeletal pain for at least 3 months AFTER other diseases have been excluded
- Pain at 11 of 18 tender point sites on digital palpation (with enough pressure so that the thumb blanches)
What are the risk factors for fibromyalgia?
Females: Middle aged 30-60 yrs
Depression
Stress
Poverty
IBS
What are the symptoms of fibromyalgia?
Chronic Muscle pain > 3 months
Pain worse with stress and cold weather
Morning stiffness <1hr
non-restorative sleep
Fatigue
Mood disorder
Sleep Disturbances
Headaches and difficulty concentrating
What are the clinical signs of fibromyalgia?
Specific tender points throughout body: (9 pairs)
Occiput
Low cervical region
Trapezius
Supraspinatus
Second rib
Lateral epicondyle
Gluteal region
Greater trochanter
Knees
What pain pathway is affected in fibromyalgia
Non-nociceptive (neuropathic) pain pathway
Low serotonin - lack of pain signal inhibition
Raised Substance P - Increased pain signals
What is the diagnosis of fibromyalgia?
Diagnosis of exclusion:
No serological markers - rule out SLE
No ESR/CRP raised - rule out inflammatory arthritis
TFTs - rule out hypothyroidism
Pain in 11+ of 18 tender regions palpated
Clinically made diagnoses
What primary investigations are made to rule out other conditions in fibromyalgia?
TFTs - exclude hypothyroidism
ESR/CRP - exclude inflammatory arthropathy
Creatine kinase
Bone profile and LFTs - Exclude hyperparathyroidism and osteomalacia
What is the management of fibromyalgia?
1st line: HOLLISTIC APPROACH
Patient education of condition
Physical Therapy
Exercise
Analgesia
2nd Line:
Antidepressants and CBT for severe neuropathic pain.
Amitriptyline for sleep
What is an important differential diagnosis of fibromyalgia?
Polymyalgia Rheumatica (PMR)
Hypothyroidism
SLE
Inflammatory Arthritis
What is Polymyalgia Rheumatica?
Chronic inflammatory rheumatic condition causing chronic pain in the shoulders, pelvic girdle and neck.
This condition affects both muscles and joints
What is polymyalgia rheumatica associated with?
Giant cell Arteritis (a form of large cell vasculitis).
These conditions often occur together
What is the epidemiology for polymyalgia rheumatica
ALWAYS over 50 +yrs
Females
Caucasian
Giant Cell Arteritis
What are the risk factors for Polymyalgia Rheumatica?
Over 50
Females
SLE
Polymyositis/Dermatomyositis
What is the pathology of PMR?
Inflammatory disorder causing pain or stiffness in shoulders and hips
Muscles are actually spared
Pain comes from bursae and tendons 🡪 referred pain
What is the presentation of polymyalgia rheumatica?
Bilateral shoulder/pelvic girdle pain that presents for more than 2 weeks
Morning stiffness (>30 mins) typically in shoulders and proximal limb muscles
Pain more severe in morning and evening
Improves with activity
Symmetrical aching
50% of Px have Systemic Sx:
Fever
Weight loss
Fatigue
What are the primary investigations for polymyalgia rheumatica?
CLINICAL DIAGNOSIS BASED ON PRESENTATION AND RESPONSE TO STEROIDS
ESR/CRP raised
Other Ix are typically normal
Temporal artery biopsy - may show GCA
What is the treatment for polymyalgia rheumatica?
Oral 15mg Prednisolone
if used long term give GI and bone protection:
Lanzoprazole + alendronate
Exercise and healthy diet
What are some important differential Diagnoses that should be ruled out in Polymyalgia Rheumatica?
Osteoarthritis
Rheumatoid arhtirits
Systemic lupus erythematosus
Myositis (from conditions like polymyositis or medications like statins)
Cervical spondylosis
Adhesive capsulitis of both shoulders
Hyper or hypothyroidism
Osteomalacia
Fibromyalgia
What is Sjogren’s Syndrome?
Chronic inflammatory autoimmune disorder that is characterised by the destruction of epithelial exocrine glands:
Specifically the lacrimal and salivary glands.
What is the difference between primary and secondary Sjogren’s Syndrome?
1’: (Sicca Syndrome ONLY)
Syndrome of dry eyes in the absence of RA due to genetic factors
2’:
Sjogren’s Syndrome associated with other Connective tissue disease; RA, SLE
What are the risk factors for Sjogren’s Syndrome?
Females
FHx
Age 40-50
Genetics
Other Autoimmune disorders (SLE, RA, PBC)
What are the genetic associations of Sjogren’s Syndrome?
HLA-D8 and HLA-DR3
What is the pathophysiology of Sjogren’s Syndrome?
Autoimmune, Lymphocytic infiltration and fibrosis of exocrine glands, especially the lacrimal and salivary glands leading to dry mucous membranes
What are the symptoms of Sjogren’s Syndrome?
Dry Eyes (keratoconjuctivitis Sicca)
Dry Mouth (xerostomia)
Dry Vagina
Fatigue and Joint pain
What are the Primary investigations of Sjogren’s Syndrome?
Saliometry - Low Saliva Flow
Serology:
Anti-Ro - most common
Anti-LA antibodies - most specific
ANA often positive
Presence of Anti-SS-A and Anti-SS-B Abs
Schirmer Test - Conjunctival Dryness
What is the Schirmer test and what condition is it used to diagnose?
Diagnose - Sjogren’s Syndrome
Filter paper on inside of lower eyelid - tears travel along strip - a result of <10mm travel is significant
15mm = normal young adult
What is the treatment for Sjogren’s Syndrome?
Artificial Tears and Saliva replacement
Vaginal Lubricants
NSAIDs and Sometimes Hydroxychloroquine - halts progression
What can be used to halt progression of Sjogren’s Syndrome?
Hydroxychloroquine