MSK conditions Flashcards
1
Q
What is osteoarthritis?
A
Degenerative joint disorder resulting from a loss of cartilage and bone
2
Q
What is the pathophysiology of OA?
A
- failure to maintain balance between cartilage synthesis and degradation leads to exposure of subchondral bone: sclerosis, fractures and cyst formation
- attempts of repair results in osteophytes
- mediated by cytokines and driven my mechanical forces
3
Q
What is the aetiology of OA?
A
multifactorial and driven by mechanical factors
4
Q
What are the RF of OA?
A
age, female, obesity (inflammatory component), genetic, trauma, smoking, physically demanding sport or occupation
5
Q
How does OA present?
A
Presents with pain on movement, functional difficulties, less than 30 min of morning stiffness, crepitus, bony deformities, asymmetrical, heberden’s nodes
6
Q
Which joints can you find OA in?
A
commonly in knee, hip, hands (DIP, PIP and base of thumb)
7
Q
what tests would you order for OA?
A
Order X-ray, serum CRP+ESR, RF, and anti CCP antibody
8
Q
What do you expect to see on an xray for OA?
A
LOSS on xray:
loss of joint space, osteophytes, subchondral sclerosis, subchondral cysts
9
Q
What are differentials of OA?
A
RA, gout
10
Q
What are consequences of OA?
A
Reduced mobility and functional decline, spinal stenosis
11
Q
How do you treat OA?
A
- topical analgesic and conservative measures (exercise, weight loss, physio, walking aids)
- analgesic ladder: topical, oral, transdermal
- steroid injections
- If debilitating consider surgery i.e. joint replacement or arthroscopy
12
Q
What is Rheumatoid arthritis?
A
Inflammatory condition of synovial joints
13
Q
What is the pathophysiology of RA?
A
- inflammation of synovial membrane causes it to thicken and infiltration of inflammatory cells
- synovial becomes hyperplasic due to proliferation and a pannus (granulation tissue) grows over cartilage.
- Underlying cartilage is damaged because nutrition is cut off, cartilage thins and exposes bone leading to erosions
14
Q
What is the aetiology of RA?
A
infections and genetics (HLA-DR4 and DR8)
15
Q
What are RF of RA?
A
female, infections, genetics, family history, smoking, stress
16
Q
How does RA present?
A
Insidious onset: joint pain and swelling that improved with use, morning stiffness, warm and red joints, deformities, rheumatoid nodules, symmetric
17
Q
What deformities can you see in RA?
A
ulnar deviation (fingers bend), swan neck (PIP hyperextension and DIP flexion) and Boutonniere deformity (opposite to swan neck)
18
Q
What labs would you order for RA?
A
RF, anti-cyclic citrullinated peptide antibody (Anti-CCP), xray, MRI and FBC
RF is less specific than anti-CCP
19
Q
What would you expect to see on an xray with RA?
A
LESS: loss of space, erosions, soft tissue swelling, soft bones
20
Q
What are differentials of RA?
A
SLE, gout and psoriatic arthritis
21
Q
What are consequences of RA?
A
CV disease, work disability, depression, interstitial lung disease
22
Q
How do you treat RA?
A
- Treat with DMARD’s (methrotextrate, hydroxychloroquine or sulfasalazide)
+ NSAIDS and corticosteroids - more severe etanercept (TNF alpha inhibitor)
- physio and occupational therapy
23
Q
What is osteoporosis?
A
Low bone mass and deterioration of bone tissue resulting in fragility and fractures
24
Q
What’s the pathology of osteoporosis?
A
imbalance in remodelling and inadequate peak bone mass
25
What is the precursor of osteoporosis called?
osteopenia
26
What are causes of primary osteoporosis?
Age (decrease in trabecular thickness) and menopause (oestrogen deficiency increases osteoclast activity through RANKL)
27
What are causes of secondary osteoporosis?
SHATTERED: steroid use, hyperthyroidism, alcohol, thin, testosterone low, early menopause, renal or liver failure, erosive bone disease, dietary calcium
28
what are RF for osteoporosis?
1. patient (age, post menopausal, female, low BMI, calcium deficiency, alcohol), 2. drugs (steroids, oestrogen inhibition), 3. disease (cushing’s, hyperthyroidism, renal)
29
How and where does osteoporosis present?
Asymptomatic until fracture:
| neck of femur, wrist or vertebrae
30
What tests do you order for osteoporosis?
DEXA scan, xray, FBC and do a fracture risk assessment (FRAX 10 years probability of fracture: age, sex, BMI, no of RF)
31
What are the DEXA scores for osteoporosis and osteopenia?
DEXA score below -2.5 is OP, below -1 is osteopenia
32
What are differentials of OP?
MM, osteomalacia
33
How do you treat osteoporosis?
oral biphosphonates (aledronic acid) and calcium/vitamin D supplements
34
What are preventative measures for osteoporosis?
hormone replacement, weight bearing exercise, prophylactic bidphosponates when giving steroids
35
What is gout?
Episodic disease: Hyperuricaemia and depositions of urate crystals in joints
36
What is the physiopathlology of gout?
1. Purines in diet - xanthine - uric acid - excreted in kidneys
2. problems cause hyperuricaemia - monosodium rate precipitates which forms crystals that deposit in joints (collection = tophi)
3. crystals can trigger inflammatory response by inducing TNF alpha and causing neutrophil adhesion
37
What is the aetiology of Gout?
diopathic hyperuricaemia, impaired excretion (CKD, diuretics) or overproduction (diet, high turn over)
38
What are RF for gout?
male, older age, post-menopausal, alcohol, meat, seafood, family history, obesity, Diabetes M, diuretics
39
How and where does gout present?
Rapid onset and severe pain: joint stiffness and swelling, joint tenderness, tophi
metatarsalphalangeal joint of the big toe
40
what labs do you order for gout?
arthrocentesis with synovial fluid analysis , serum uric acid levels, xray and ultrasound
41
What do the crystals look like in gout?
negative birefringent needle shaped crystals
42
What lab results would you expect in gout?
WBC over 2, increased serum urate (can be normal), xray shows punched erosions around joint, US shows tophi
43
What are differentials for gout?
pseudo-gout, septic arthritis, trauma, RA
44
What are consequences of Gout?
kidney stones and infection
45
How do you treat Gout?
Treat acutely with NSAIDs and lifestyle factors
- if happens more than once: colchicine
- preventative: allopurinol with colchicine
46
What drug class is allopurinol?
xanthine-oxidase inhibitor
47
What is the difference between seropositive and seronegative RA?
Whether there is RF and anti-CCP in the blood. This doesn't alone diagnose RA but normally seropositive is more common, severe and has complications
48
What 5 traits do all Spondyloarthropathies have?
axial inflammation, asymmetric arthritis, absence of RF, inflammation of enthisis and HLA-B27 association
49
What is pseudo gout and what is the pathology?
Deposition of calcium phosphate crystals in joints:
| Excess calcium and pyrophosphate in blood leads to depositions of calcium pyrophosphate crystals in articular cartilage
50
What are the different types of pseudo gout?
- A: acute
- B: chronic
- C+D: with osteoarthritis
- E
51
What contributes to the development of pseudo gout?
dehydration, steroids and hyperparathyroidism
52
What are RF for pseudo gout?
old age, female, hyperparathyroidism, family history, previous joint injury
53
How does pseudo gout present?
Often asymptomatic: painful and tender joints, synovitis, similar to osteoarthritis
54
What joints does pseudo gout affect?
affects larger joints such as knees, wrists and shoulders
55
What tests do you order and what results do you expect to see?
arthrocentesis, X-rays, serum calcium and CT scan
elevated calcium, xray shows chonedrocalcinosis (cartilage calcification
56
what do pseudo gout crystals look like?
positively birefringent rhomboid shaped crystals
57
What are differentials of pseudo gout?
Gout, septic arthritis, OA
58
How do you treat pseudo gout?
Treat depending on involvement:
- mono articulate: intraarticular steroids if accessible otherwise NSAIDs
- polyarticulate: NSAIDs (colchicine 2nd line)
- chronic: DMARDs, surgery
59
what is ankylosing spondylitis?
Inflammation of the axial skeleton leading to syndesmophytes and vertebrae fusion
60
What is the pathology of AS?
cartilage erosion and joint/bone destruction due to osteoclasts. Fibrin replaces the damage which limits range of motion and ossification causes syndesmophytes (bony growths):
Ankylosis of spine (stiffness) and vertebrae fusion (bamboo spine)
61
How does AS present?
back pain, morning stiffness in back and buttocks that improved with exercise,
progressive loss of spinal movement:
1. loss of lumbar lordosis (straight spine) and 2. increased kyphosis (upper spine bending forward)
62
what tests would you order for AS and what do you expect to see?
pelvic xray, MRI and spine xray: sacroilitis, erosions and bamboo spine
63
How do you treat AS?
NSAIDs and physio
| chronic: TNF alpha inhibitor (adakimumab)
64
What is psoriatic arthritis and what is its pathology?
Inflammatory joint disease associated with psoriasis:
| angiogenic growth factors are over expressed and with TNF they contribute to vascular and bone changes
65
How does PA present?
Usually starts with rash then presents with joint pain/swelling/stiffness, nail changes, dactylics and mild arthritis in less than 5 joints
66
What labs would you order for psoriatic arthritis?
hand and feet xray, CRP+ESR, RF and anti CCP, synovial fluid aspiration
67
What deformity would you expect in advanced PA?
pencil in cup deformities (end of bone like a sharp pencil)
68
What lab results would you expect in PA?
Early PA may not have radiological changes, DIP erosions, new bone formation, osteolysis, can have raised inflammatory markers
69
How do you treat psoriatic arthritis?
NSAIDs and physio (2nd line TNF alpha inhibitor)
70
What is reactive arthritis?
Inflammatory arthritis following GI or urogenital infection
71
What is the Aetiology of reactive arthritis?
- Enteric: campylobacter, salmonella, shigella
| - STI: chlamydia trachomatis
72
how does reactive arthritis present?
Presents 2-4 weeks after infection with acute onset: fatigue, fever, lower back pain, painful and swollen joints
73
What is renters triad?
Seen in reactive arthritis:
| conjunctivitis, urethritis and oligoarthritis
74
What labs would you order and what results do you expect for reactive arthritis?
inflammatory markers, ANA antibodies, RF, urogenital and stool culture, serum antibodies:
raised inflammatory markers, if tested early the cultures may show, sterile synovial fluid
75
What is a complication of reactive arthritis?
destructive enthesitis (inflammation where tendons insert onto bone)
76
How do you treat reactive arthritis?
antibiotics for causative agents and then NSAIDs+steriods+physio
77
What is septic arthritis and what is the pathology?
Infection of one or more joints caused by inoculation of microbes:
nvasion directly or through haematogenous spread which causes bone and cartilage necrosis
78
What organisms can cause septic arthritis and who would you see them in?
- Staph. aureus is most common
- Neisseria gonorrhoea in young and sexually active
- Steph. epidermis in joint replacement
- E.coli and klebsiella in immunocompromised
- Gram-ve are more common in older and compromised patients
79
What are RF for septic arthritis?
elderly (80), prosthetic joint, immunocompromised, underlying joint disease, IVDU, diabetes mellitus, skin lesions, recent surgery
80
How does septic arthritis present?
swollen, warm and tender joint, pain, restrictive movement and fever
81
What tests would you order for septic arthritis?
Orthopaedic emergency so do a urgent aspiration!!!
| then blood cultures, U+E, inflammatory markers, xray
82
what results would you expect for septic arthritis?
inflammatory markers elevated, yellow synovial fluid, WCC increased and cultures show bacterium
83
What complications come with septic arthritis?
osteomyelitis, joint destruction and LT disability
84
How do you treat septic arthritis?
```
empirical antibiotics (flucloxacillin) and stop immunosuppressants
- analgesia and splinting
```
85
what is osteomyelitis?
Infection and inflammation of the bone marrow that is localised to the bone
86
what is the physiological classification of osteomyelitis?
- A: no cormorbidities
- B: comorbidities directly affecting wound healing
- C: treatment for harmful than condition
87
What is the anatomical classification of osteomyelitis?
- I: medullary and endosteal bone
- II: superficial
- III: medullary and cortical involvement
- IV: entire bone circumference
88
What organisms cause osteomyelitis?
S.aureus, salmonella (sickle cell) and coagulase negative staphylococci
89
What are the RF for osteomyelitis?
previous osteomyelitis, trauma, surgery, diabetes, immunosuppression, sickle cell, prosthetics
90
How does osteomyelitis present?
Presents with dull pain at site, fever, weakness, reluctant to weight bear, swelling and warm
chronic may present with ulcers that fail to heal
91
What tests would you order and what results do you expect for osteomyelitis?
Order FBC (increased inflammatory), xray (osteopenia, loss of trabecular architecture), blood cultures, bone biopsy, MRI
92
What are complications of osteomyelitis?
fractures and growth disturbances
93
How do you treat osteomyelitis?
immobilising site, then give broad spectrum empiric antibiotics until culture results
- surgery to remove debris and dead bone
94
What is SLE?
Remitting and relapsing multisystem autoimmune disorder and most common form of lupus
95
What is the pathology of SLE?
Autoantibodies produced by B-cells target autoantigens and form immune complexes which activate compliment system leading to an influx of neutrophils and inflammation
96
What are the RF for SLEß
pre-menopausal women, family history, genetics, smoking, drugs, UV light
97
How does SLE present?
non-specific symptoms: fever, fatigue, weight loss, rash and skin problems
98
What tests do you order for SLE?
FBC, inflammatory markers, ANA, double stranded DNA antibody, compliment levels
99
How do you diagnose SLE?
need at least 4: butterfly rash on face, discoid rash (photosensitive), oral ulcers, arthritis, serositis, photosensitivity, blood disorders (low), renal disease, ANA positive, neurological disorder or Anti-ds DNA
100
What complications does SLE have?
pericarditis, blood disorders, lupus nephritis
101
How do you treat SLE?
high factor sunscreen and DMARD’s
- maintain:NSAIDs and hydroxychlocoquine
- Flares: prednisolone
102
What is osteomalacia?
- poor bone mineralisation leading to soft bones
| adult form of rickets: lack of calcium
103
what is fibromyalgia?
non specific muscular disorder with unknown cause: widespread MSK pain (other diseases excluded), symptoms for at least 3 months and pain at 11/18 tender point sites
104
How does fibromyalgia present?
widespread muscle pain for at least 3 months, morning stiffness, poor sleep, poor concentration
105
What are primary benign bone tumours?
osteochondroma, giant cell, osteoblasts
106
What are malignant bone tumours?
osteosarcoma, ewing’s sarcoma
107
What is paget's disease?
Chronic disorder where bone remodelling is out of balance, resulting in brittle and abnormaly shaped bone
108
What is Ehler dances syndrome?
Inherited condition that affects connective tissue
