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2A > MUSCULOSKELETAL & RHEUMATOLOGY > Flashcards

MUSCULOSKELETAL & RHEUMATOLOGY Flashcards

1
Q

what is Systemic Lupus Erythematosus (SLE)?

A

chronic autoimmune disease that can affect any part of the body, including the skin, joints, kidneys, brain, and other organs

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2
Q

what is the clinical criteria of SLE?

A
  • malar (butterfly)rash, discoid rash, photosensitivity rash
  • oral ulcers, alopecia
  • arthritis (symmetrical)
  • kidney disorder (proteinuria/cellular casts/high BP),
  • neurological disorder (seizures or psychosis),
  • hematologic disorder (hemolytic anemia (Coombs positive), lymphopenia, or thrombocytopenia)
  • other organ involvement
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3
Q

what are tests done for SLE?

A
  • Anti-dsDNA and Anti-Smith (Anti-Sm) Antibodies - specific
  • Antinuclear Antibody (ANA) Test - positive, less specific
  • complement factors, C3, C4 - low is LSE
  • FBC, CRP, ESR - indicate inflammation and anaemia
  • urinanalyis - kindey involvement
  • imaging eg xray for other organ involvement
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4
Q

what is the treatment/management of SLE?

A
  • (NSAIDs): For joint pain and stiffness.
  • Antimalarial Drugs (Hydroxychloroquine): skin and joint symptoms.
  • Corticosteroids and Immunosuppressive Agents: For more severe disease manifestations
  • cytotoxic drugs
  • Biologics: belimumab
  • Lifestyle Modifications: sun protection, exercise, healthy diet.
  • stem cell transplant
  • Identify patients with phospholipid antibodies
  • assess atherosclerosis/major organs
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5
Q

what is Raynaud’s phenomenon?

A

blood stops flowing properly to your fingers and toes

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6
Q

what causes primary vs secondary Raynaud’s phenomenon?

A

primary - unknown, absence of another underlying disease
secondary - autoimmune diseases (e.g. SLE, scleroderma, rheumatoid arthritis), injuries, drugs, vascular damage

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7
Q

what kind of vascular damage can cause Raynaud’s phenomenon?

A

Atherosclerosis
Frost bite
Vibrating tools

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8
Q

what are the 2 subtypes of systemic slerosis/scleroderma?

A
  • Limited cutaneous systemic sclerosis (lcSSc) (AKA CREST)
  • Diffuse cutaneous systemic sclerosis (dcSSc)
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9
Q

what are the main features of systemic sclerosis?

A

Vasculopathy
Excessive collagen deposition
Inflammation
Auto-antibody production

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10
Q

what is the diffrence between limited and diffuse systemic sclerosis?

A

limited:
- Long history of Raynaud’s phenomenon
- skin thickening at hands, arms, and face
- slow progressing
Diffuse:
- Short History of Raynaud’s phenomenon
- thickening extends to trunk and proximal limbs
- increased risk of organ involvement - renal, lung, cardiac

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11
Q

what investigations/tests are required for systemic sclerosis?

A
  • blood tests - anti-Scl-70 & ANA = diffuse, anti-centromere = limited
  • Pulmonary function tests (PFTs) - asses lung involvement
  • Echocardiogram: To assess for pulmonary hypertension and cardiac involvement.
  • ct scan - organ involvement
  • skin biopsy - extent of fibrosis
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12
Q

what is the treatment/management for systemic sclerosis?

A
  • Mycophenolate - immunosupressant
  • PPI - reflux
  • ACE inhibitors - prevent renal crisis
  • Fluoxetine, vasodilators - raynauds
  • Cyclophosphamide(im-sup), PDE5 - pulmonary fibrosis
  • Annual echocardiograms and pulmonary function tests
  • Early detection of pulmonary arterial hypertension
  • Autologous stem cell transplant - severe cases
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13
Q

what is Sjögren’s Syndrome?

A
  • autoimmune disorder
  • attacks moisture-producing glands, primarily the salivary and lacrimal glands
  • dry mouth and eyes
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14
Q

what is the classification of sjogrens syndrome?

A
  • primary - absence of underlying autoimmune disease
  • secondary - in conjunction with another autoimmune disease eg SLE, RA, Scleroderma, Primary billiary cirrhosis
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15
Q

what are symptoms of sjogrens syndrome?

A

dry eyes
dry mouth
dental problems - swollen parotid gland
fatigue and pain
Skin, nose, and vaginal dryness
systemic involvement - increased risk of gluten sensitivity, lymphoma, Renal tubular acidosis

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16
Q

what are investigtaions/tests for sjogrens syndrome?

A
  • blood test - antibodies positive eg ANA, Ro/La, rheumatoid factor, raised immunoglobins
  • ultrasound - abnormal salivary glands
  • biopsy - Sialadenitis on lip (goldst)
  • Schirmer’s test - Measures tear production to evaluate dry eyes.
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17
Q

what is the treatment for sjogrens syndrome

A
  • dry eyes - cyclosporine eye drops, punctal plugs to retain moisture, artificial tears
  • dry mouth - Saliva substitutes, pilocarpine/cevimeline to stimulate saliva production.
  • Hydroxychloroquine - for fatigue, myalgia, rash
  • Corticosteroids/immunosuppressants
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18
Q

what are examples of autoimmune Connective tissue disease?

A
  • Systemic lupus erythematosus
  • Systemic sclerosis
  • Primary Sjögren’s Syndrome
  • Dermatomyositis/Polymyositis
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19
Q

what is Dermatomyositis/Polymyositis?

A
  • both cause muscle weakness (close to trunk)
  • dermatomyositis also presents with rash
  • can affect lungs
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20
Q

what are characteristic of Dermatomyositis rash?

A
  • violet or dusky red rash
  • face, eyelids, chest, knees, elbows, and knuckles
  • often with swelling
  • Gottron’s papules - scaly rash over knuckles
  • Heliotrope rash - rash over eyelids
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21
Q

what investigations/tests are done for Dermatomyositis/Polymyositis?

A
  • Muscle enzymes (Creatine Kinase) - raised
  • Electromyography (EMG) - Measures electrical activity in muscles
  • Muscle biopsy - shows inflammation/fiber necrosis
  • Screen for malignancy (PET-CT) - Malignancy associated antibodies
  • Chest X ray, PFTs, High resolution CT - for lung involvement
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22
Q

what is the treatment for Dermatomyositis/Polymyositis?

A
  • steroids (inflammation) - Prednisone
  • immunosupressive drugs - eg rituximab, methotrexate
  • Hydroxychloroquine - for rash
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23
Q

what are some Myositis‐specific autoantibodies?

A

MDA5,
NXP2,
TIF1-gamma
ARS

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24
Q

what are some inherited connective tissue disorders?

A
  • Marfan’s
  • Ehlers Danlos
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25
Q

what are some features of marfans syndrome?

A
  • Tall and slender body, hypermobility
  • Lens dislocation & myopia
  • dilation of aorta
  • High arched palate.
  • Pectus excavatum - depressed chest
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26
Q

how is marfans syndrome diagnosed?

A
  • clinical features
  • FBN1 gene mutation
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27
Q

what are features of Ehlers-Danlos Syndrome (EDS)?

A
  • hyperelastic skin, brusies easily
  • joint hypermobility & disolcation
  • vascular rigidity
  • mitral valve prolapse
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28
Q

what are features of inflammatory arthritis?

A
  • swelling - red/warm, Synovial (compressible, tender)
  • worse in morning/inactivity
  • stiffness over 30 mins
  • constant/intermitant
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29
Q

what are causes of joint inflammation?

A
  • autoimmune Arthritis: RA,
  • degenerative artheritis
  • Crystal arthrits – gout and pseudogout
  • septic arthiritis
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30
Q

what are risk factors of Rheumatoid Arthritis?

A

family history
smoking
more common in females

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31
Q

what are complications of RA if untreated?

A
  • joint damage
  • CVD - HA, sroke
  • intestitial lung disease
  • eye problems - scleritis or uveitis
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32
Q

what does Rheumatoid Arthritis affect?

A
  • Symmetrical small joints, hands wrists feet
  • big joints involved later ( bad prognosis if on presentation)
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33
Q

what is Seronegative Arthritis?

A

-ve for CCP and RF
- affects Asymmetrical big joints, with spinal involvement
- more common in men
- Associated symptoms - IBD, psoriasis, eye inflammation

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34
Q

what are 5 different forms of Psoriatic Arthritis?

A

DIP Arthritis that affects the small joints, ends of fingers, toes, or both
Asymmetrical arthritis of the joints in the hands and feet
Symmetrical polyarthritis, which is similar to RA
Arthritis mutilans, a rare type of arthritis that destroys and deforms joints
Psoriatic spondylitis, arthritis of the lower back (sacroiliac sac) and the spine

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35
Q

what are the risk factors of gout?

A

beer, fructose
renal impairment,
diuretics,
aspirin
family history
- more common in men pseudo gout more in women)

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36
Q

how does pseudo gout present on xray?

A

Chondrocalcinosis

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37
Q

what are features of osteoarthritis?

A
  • slow onset - later in life
  • initially asymmetric
  • affects weight bearing joints - knees, hips, thumb, big toe
  • stiffness worse end of day (not morning like other arthiritis)
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38
Q

what is important to consider when diagnosing a types of arthiritis?

A
  • inflammation - swelling/flares/CRP
  • pattern - symmetrical/asymmetrical
  • associated symptoms eg eye, nail psoriasis, bowels
  • tests - RF/CCP, uric acid, x-ray
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39
Q

what is the pathogenesis of gout?

A
  • overproduction of urate from diet and alcohol
  • under exretion of urate due to genetics/drugs
  • causes hyperuricaemia - crystals form
  • inflammatory response when getting rid of crystals
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40
Q

what items in a diet contribute to gout?

A

beer/larger - contain guanosine
red meat, shellfish
sweetened soft drinks with fructose

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41
Q

what tests/investigations are required for gout?

A
  • monosodium urate (MSU) crystals in the joint fluid or tophus
  • FBC - raised WWC
  • LFT if alcohol concern
  • CRP
  • xray - if sepsis differential diagnosis or chronic
  • Serum Uric Acid - normal in acute attack
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42
Q

what is the treatment of acute gout?

A
  • lifestyle changes - diet, alcohol, weight, fluid
  • NSAID - short course - pain relief/inflammation
  • Colchicine - anti-inflammatory (SE diarrhoea)
  • corticosteroids - Prednisolone
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43
Q

what medication lowers uric acid levels and when is it used?

A
  • Allopurinol – Xanthine Oxidase Inhibitor
  • Febuxostat
  • long-term gout
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44
Q

what is uric acid target when managing chronic gout?

A

below 360 umol/l

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45
Q

what are complications of gout?

A
  • tophi
  • renal disease - calculi, acute/chronic urate nephropathy
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46
Q

what is the pathophysiology of rheumatoid artheritis?

A
  • T cell attack synovium
  • leads to synovial hyperplasia
  • invades and damages cartilage and bone
  • pro-inflammatory cytokines, tumor necrosis factor (TNF) perpetuates inflammation
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47
Q

what are symptoms and signs of rheumatoid artheritis?

A
  • symmetrical Pain and Swelling of joints - hands/wrists/feet
  • early morning stiffness
  • Decreased grip strength
  • fatigue, malaise
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48
Q

what are the tests/investigations for Rheumatoid Arthritis?

A
  • CRP
  • Rheumatoid factor - (70% are +ve, false +ve)
    -Anti-CCP (cyclic citrullinated peptide)
  • xray/mri assesses joint damage
  • FBC - anemia is common
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49
Q

what is seen on an xray in RA?

A

Soft tissue swelling
Periarticular osteopenia
Joint space narrowing
Bone erosion

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50
Q

what is the treatment of RA?

A
  • DMARD (Disease-Modifying Anti-Rheumatic Drugs)
  • Methotrexate (1st line)
  • biological DMARD - Anti-TNF Medications, TNF-inhibiors, Rituximab, JAK inhibitors etc.
  • NSAIDS/corticosteroids - pain/inflammation
  • splints/rest/ice
  • Colchicine – helpful for crystal arthritis
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51
Q

what bacteria causes Prosthetic Joint Infection?

A

most common - Staphylococcus aureus (including MRSA)
Coagulase-negative staphylococci
Streptococci
Enterococci
(gram -ve - bacilli eg e.coli)

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52
Q

what are routes of infection to the bone?

A
  • direct inoculation - eg from trauma/surgery
  • contiguous spread - from adjacent tissue or DM, ulcers, vascular disease
  • Haematogenous seeding - more common in children
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53
Q

what blood tests can suggest osteomyelitis/inflammation?

A

high ESR
high WCC/neutrophils
high CRP
Procalcitonin - elevated in bacterial infection, rather than other inflammation

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54
Q

what are risk factors for septic joint?

A
  • bacteraemia
  • trauma
  • Local skin breaks/ ulcers
  • Damaged joints
  • Immunosuppression (including steroids only)
  • Elderly
  • Rheumatoid arthritis (or other immune-driven disease)
  • Diabetes
55
Q

what is Gonococcal arthritis?

A
  • infective artheritis caused by bacterium Neisseria gonorrhoeae
  • can present as:
    Arthritis-dermatitis syndrome
    or Purulent arthritis (infection of one or more joints/pus filled)
56
Q

how does a septic joint present?

A
  • Painful, red, swollen, hot joint
  • fever
  • monoartheritis
  • most commonly knee, also hip & shoulder
57
Q

what are risk factors for osteomyelitis?

A
  • trauma
  • Vascular Insufficiency eg DM, sickel cell disease
  • prosthetic joints
  • immunosuppression - eg HIV/drugs
58
Q

what bones are effected in osteomyelitis?

A

adluts over 50 - vertebra, clavicle/pelvis
children - long bones

59
Q

what part of the bone is affected in osteomyelitis?

A

metaphysis

60
Q

what are clinical signs of osteomyelitis?

A

Fever,
rigors,
sweats,
malaise
erythema
non-healing fractures, ulcers

61
Q

what investigations/tests are done for osteomyelitis?

A
  • blood tests - CRP, WCC, ESR
  • imaging - MRI, Xray, CT, nuclear bone scan
  • bone biopsy - may show absess, necrosis, fibrosis
62
Q

what is the treatment for osteomyelitis?

A
  • surgical - Debridement, hardware removal
  • Antimicrobial therapy (tailored to culture and bone penetration etc.)
  • wound care
  • analgesiacs
63
Q

what is spondyloarthritis?

A
  • group of inflammatory rheumatic diseases
  • include common features: axial involvement , peripheral arthritis, enthesitis, dactylitis
64
Q

what gene is spondyloartheritis associated with?

A

HLA-B27

65
Q

what are symptoms of spondyloarthritis?

A
  • axial symptoms - chronic back pain/stiffness, improves with exercise not rest, worse at night
  • Peripheral arthritis - asymetrical lower limbs
  • Enthesitis - achiles tendon and plantar fascia pain
  • Dactylitis - “sausage digits”
  • Uveitis - eye inflammation
  • Psoriasis
  • IBD
66
Q

what are tests/investigations for spondyloartheritis?

A
  • HLA-B27 testing
  • imaging - xray, MRI (shows Sacroiliitis by bone marrow edema)
  • CRP and ESR elevation
  • The Assessment of SpondyloArthritis International Society (ASAS) criteria- includes imaging, clinical and hlab27
67
Q

what are the subtypes of spondyloarthritis?

A
  • Ankylosing spondylitis (AS) - spine/sacroiliac joints
  • Psoriatic arthritis (PsA)
  • Reactive arthritis (ReA) - to bacteria infection
  • Enteropathic arthritis - with IBD
  • Undifferentiated spondyloarthritis (uSpA)
68
Q

what is the treatment of spondyloartheritis?

A
  • NSAIDS
  • TNF inhibitors and IL-17 inhibitors
  • DMARDs
  • corticosteroids
  • physical therapy/exercise
69
Q

what is the triad of reactive artheritis?

A
  • artheritis
  • conjuctivitis
  • urethritis
70
Q

how does Psoriatic Arthritis present?

A
  • skin/NAIL psoriasis
  • joint pain/swelling
  • dactylitis
71
Q

how is enteropathic artheritis treated?

A
  • treat IBD
  • combination of biological therapy - due to IBD
72
Q

what does SPINEACHE stand for?

A

s - stiffness - morning
p - pain - improves with exercise
i - inflammation - fever/fatigue
n - night pain
e - exercise
a - age of onset (under 45)
c - chronicality - more than 3 months
h - HLA-B27 gene
e - extra artificial feaatures - proriasis, IBD, uveitis, dactylitis

73
Q

what is the difference in pain in inflammatory vs degenerative bone diseases?

A

inflammatory - pain eases with use, at rest, long lasting
degenerative -pain evening/morning, with exercise, shorter

74
Q

what is the pathogenesis of osteoartheritis?

A
  • loss of cartilage and disordered bone repair
  • due to trauma, aging and cytokines
75
Q

what are the risk factors of osteoartheritis?

A
  • age - uncommon under 45
  • female - more common after menopause
  • Genetic predisposition
  • obesity- low grade inflammation state
  • occupation - football/farming/manual labour
  • trauma
  • inflammatory artheritis - RA
  • Abnormal biomechanics eg hypermobility, dysplasia
76
Q

what are signs of osteoartheritis?

A
  • Alteration in gait
  • joint swelling - Bony enlargement, Effusion, Synovitis
  • joint abnormalities - Crepitus, Tenderness
77
Q

what are radiological features of osteoartheritis?

A

Joint space narrowing
Osteophyte formation
Subchondral sclerosis
Subchondral cysts
Abnormalities of bone contour

78
Q

what is non-medical management of osteoartheritis?

A

Patient education
Activity and exercise
Weight loss
Physiotherapy
Occupational therapy
Footwear
Orthoses
Walking aids

79
Q

what is pharmacological management of osteoartheritis?

A
  • NSAIDs
  • Capsaicin
  • paracetamol, opioids
  • Transdermal patches
  • Intra-articular steroid injections
  • DMARDs have a role in inflammatory OA
80
Q

what are surgical management of osteoartheritis?

A
  • Arthroscopy - for lose bodies, uncontrolled pain
  • Osteotomy
  • Arthroplasty - new joints
  • Fusion - Usually ankle and foot
81
Q

what does nodal osteoartheritis affect?

A

distal /proximal interphalangeal joints of the fingers

82
Q

how is an orthopaedic xray presented?

A

Alignment - Dislocation
Bone - Fractures
Cartilage – widened joint
Soft tissues – swelling, effusion

83
Q

how is septic artheritis diagnosed?

A
  • clinical evaluation of symptoms - eg pain, welling
  • joint aspiration - WCC, bacteria stain/culture
  • imaging - shows joint damage
  • blood test of inflammatory markers
84
Q

what is the treatment of septic artheritis?

A
  • antibiotics
  • joint aspiration to reduce pain/fluid
  • analgesics
  • Arthroscopic Drainage or Open Surgical Drainage
  • Joint Lavage - removes pus, debris
  • Debridement - removal of infected tissue if severe
85
Q

what are the 4Rs in fracture treatment?

A
  • resusciate
  • reduce
  • Retain
  • Rehab
86
Q

what crystal cause gout/pseudogout?

A
  • needle-shaped monosodium urate crystals
  • rhomboid-shaped Pyrophosphate crystals
87
Q

how does gout present?

A
  • sudden onset - eg waking up at night
  • hot swollen joint
  • extremely painful
  • joints commonly affected - big toe, ankle, knee, finger, elbow, wrist
  • monoartheritis more common (can be symmetrical)
  • can resolve within 2 weeks
88
Q

what can form due to gout?

A

tophi - white areas of urate crystals in soft tissue eg in hand/ears
- can cause damage to joints

89
Q

what is the process of uric acid forming?

A

purines to HypoXanthine
by enzyme Xanthine oxidase

90
Q

what conditions can increase risk of gout due to too much purine/uric acid?

A
  • Myeloproliferative disease
  • Psoriasis
  • Tumour lysis syndrome
  • Lesch-Nyhan syndrome
  • most due to increased cell turnover
91
Q

what can cause a decrease in excrertion of uric acid, causing gout?

A

Renal impairment
Thiazide diuretics
Low dose aspirin
Tacrolimus, ciclosporin
Ethambutol, pyrazinamide

92
Q

what can trigger an attack of gout?

A

Direct trauma to the joint
Intercurrent illness
Alcohol or shellfish binge
Surgery
Dehydration
Starting hypouricaemic therapy

93
Q

what investigations/tests are done for gout/pseudogout?

A

Routine bloods
Inflammatory markers - high in attack then can go down
Uric acid - can be high/low
Joint aspiration
X-ray - damage with recurrent atatcks

94
Q

what is the treatment for chronic gout?

A
  • lifestyle advice
  • Allopurinol - given if more than one attack
  • Febuxostat
  • Xanthine oxidase inhibitors
95
Q

how is pseudogout different from gout?

A
  • different distribution - larger joints effected
  • eg Knees>wrists>shoulders>ankles>elbows
  • calcium pyrophosphate crystals vs uric acid
96
Q

what conditions are risk factors for pseudogout?

A

Haemochromatosis
Hyperparathyroidism
Hypophosphatasia
Hypomagnesaemia
Hypothyroidism
Acromegaly

97
Q

what is the treatment of chronic pseudogout?

A

LT low dose Prednisolone (corticosteroid)
LT low dose colchicine
Trial of hydroxychloroquine
Trial of methotrexate

98
Q

what is osteoporosis?

A
  • low bone massand mineral density
  • microarchitectural deterioration of bone tissue
  • increased bone fragility and susceptibility to fracture
99
Q

what are characteristics of Postmenopausal osteoporosis?

A
  • less oestrogen
  • high bone turnover (cancellous bone loss)
  • microarchitectural disruption
100
Q

how does trabecular architecture change with aging?

A
  • decrease in trabecular thickness
  • decreasse in connections between horizontal trabecular
  • decrease in trabecular strength - increased risk of fracture
101
Q

what methods are used to diagnose osteoporosis

A
  • Bone mineral density test
  • Dual energy X-ray absorptiometry
  • DXA
  • T-score
102
Q

what are risk factors/causes for osteoporosis?

A
  • inflammatory diseases
  • endocrine diseases - para/thyroid, cushings
  • low body weight
  • immobility
  • drugs - glucosteroids, aromatase inhibitors etc.
  • alcohol/smoking
  • family history
  • previous fracture
103
Q

how is osteoporosis treated?

A

medication anti-resorptive or anabolic:
- Bisphosphonates 1st
- denosumab - slows bone loss
- PTH analogues - Teriparatide - stim bone growth

  • lifestyle changes - diet
  • supplements
  • fall prevention
104
Q

what enzyme do bisphosphenates inhibit in cholesterol synthesis?

A

Farnesyl Pyrophosphate Synthase

105
Q

what is the FRAX score?

A

tool to stimate 10 year fracture risk based on risk factors

106
Q

what is the T score is osteoporosis?

A

(obtained from DEXA scan)
>-1 is normal
-1 - -2.5 = osteopenia (low bone mass)
<-2.5 = osteoporosis
severe if with fracture

107
Q

what are features of Osteogenesis imperfecta?

A
  • autosomal dominant
  • type 1 collagen affected
  • low bone mass, increased bone fragility
108
Q

what are symptoms of vit D deficiency?

A

Bowing of legs
Aches
Hypocalcaemia
Fits
Muscle weakness
Cardiomyopathy
Enamel hypoplasia
Fractures

109
Q

what are radiological features of rickets?

A

Cupping
Splaying
Fraying
Osteopaenia
Periosteal elevation

110
Q

what is Achondroplasia?

A
  • shorter, abnormally-shaped bones
  • shorted stature
  • mutation in FGFR3 gene
111
Q

what is Polymyalgia rheumatica ?

A
  • inflammatory disorder
  • muscle pain and stiffness, fatigue
  • more common in women over 50
  • diagnosis clinical + ESR/CPR
  • treated with corticosteroids
112
Q

what is osteomalacia?

A
  • bone softening due to lack of minerals
  • eg due to lack of vit D or phosphate, or celiac etc.
113
Q

give examples of vasculitis in different classes?

A

large vessel - Giant Cell Arteritis
medium - Polyarteritis Nodosa, kawasaki
small - Granulomatosis with Polyangiitis, Henoch-Schönlein Purpura, Microscopic Polyangiitis

114
Q

what are risk factors for giant cell arteritis?

A
  • over 50
  • white, scandinavian
  • more common in women
115
Q

what are symptoms of giant cell arteritis?

A
  • headache - severe, localised often temples
  • scalp tenderness
  • visual disturbances
  • Jaw Claudication - pain when chewing
  • fever, fatigue, malasie
  • Polymyalgia Rheumatica Symptoms
116
Q

what investigations/tests are done for giant cell arteritis?

A
  • blood tests - ESR, CPR
  • Temporal Artery Biopsy - show inflammation
  • ultrasound - ‘halo’ sign
117
Q

what are some negative signs for GCA?

A
  • vomiting
  • double vision - eg could be menengitis
  • fever (sometimes)
118
Q

what are some Complications of Giant Cell Arteritis?

A
  • Permanent Vision Loss
  • stroke
  • aortic aneurysm
  • scalp necrosis
119
Q

what are the treatments for GCA?

A
  • corticosteroids
  • low-dose aspirin to reduce stroke risk
120
Q

what does GCA especially effect?

A

external carotid artery

121
Q

what are symptoms of Granulomatosis with Polyangiitis?

A
  • runny nose, cough, nosebleeds, sinusitis
  • Glomerulonephritis - hematuria, proteinuria
  • rash, purpura, ulcers
  • eye problems - redness, pain
  • hearing problems
  • Arthralgia or arthritis
  • Fever, fatigue, weight loss, and malaise
122
Q

what are investigations/tests for Granulomatosis with Polyangiitis?

A
  • blood tets - CPR, ESR, PR3-ANCA
  • urine analysis - kidney involvement
  • chest xray, CT scan
  • biopsy - for definitive diagnosis - from affected tissue eg lungs, kidneys, nasal muscosa
123
Q

what is the treatment of Granulomatosis with Polyangiitis?

A
  • corticosteroids
  • immunosupressants eg rituximab, cyclophosphamide
  • plasma exchange in severe cases
124
Q

what are complications of Granulomatosis with Polyangiitis?

A
  • kidney failure - due to glomerulonephritis
  • lung damage - fibrosis/bleeing
  • hearing loss
125
Q

what are symptoms of Polyarteritis Nodosa?

A
  • fever, malasie, weight loss
  • joint/muscle pain
  • rash, ulcers
  • peripheral neuropathy - pain,
126
Q

what are tests/investigations for Polyarteritis Nodosa?

A
  • blood tests - inflammatory markers ESR, CPR
  • urinanalysis - kidney involvement
  • skin or muscle biopsy - if involved
  • nerve conduction
  • Echocardiography - asses cardiac involvement
127
Q

what are symptoms of fibromyalgia?

A
  • widespread pain
  • fatigue
  • cognative difficulties - fibro fog
128
Q

what is the management of fibromaygia?

A
  • medication eg pain relief, anti-depressants
  • exercise
  • CBT therapy
129
Q

what are symptoms of mechanical lower back pain?

A
  • localised pain - spreading to legs
  • spasms
  • pain with movement, releif with rest
130
Q

how is mechanical lower pain managed?

A
  • rest
  • NSAIDS
  • heat/ice therapy
131
Q

when is a MRI/CT scan performed with lower back pain?

A

if herniated disc, fracture, tumor suspected

132
Q

where does Osteosarcoma occur?

A
  • knee
  • upper arm
  • more common in children/young adults
133
Q

what are examples of primary bone tumours?

A
  • Osteosarcoma
  • Chondrosarcoma
  • ewing sarcoma
134
Q

what cancers most commonly spread to the bone?

A

Breast, prostate, lung, and kidney cancers

2A (9 decks)

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