joint and bone infections and pathology Flashcards
what are the types of osteomyelitis
- haematogenous
- non haematogenous (direct inoculation)
- non haematogenous (local invasion)
what are the ways in which osteomyelitis can be acquired (non haematogenously - direct inoculation)
trauma
surgery
what are the ways in which osteomyelitis can be acquired (non haematogenously - local invasion)
pressure ulcer
periodontal disease
sinus disease
what are the stages of how you get a bone infection
- slow flow through looped capillaries and venous sinusoids
- baceria seed metaphyseal-epiphyseal junction –> abscess forms
- abscess causes a protection from the immune system
- pressure form pus further limits blood supply
- abscess grows but cant penetrate penetrate the epiphyseal growth plate - spreads outwards instead and eventually breaks through to spread to the subperiosteal space
what structure stops the abscess from entering the epiphyses
the epiphyseal growth plate
why is osteomyelitis especially dangerous in infants
the infection may invade the epiphysis and joint (is able to cross the growth plate) –> septic arthritis coexistent
what are the 3 ways you can get septic arthritis
- haematogenous contamination
- direct contamination
- contiguous contamination
what is the most common and second most common pathogen to cause osteomyelitis
staph aureus - most common
strep pyogenes - 2nd
what is the likely pathogen causing osteomyelitis in patients have have recently undergone surgery
coagulase negative staph
what is the likely pathogen causing osteomyelitis in newborns and infants
group B strep
HiB
other gram negatives
what is the likely pathogen causing osteomyelitis in patients with recent chicken pox
group A beta haemolytic strep
what is the likely pathogen causing osteomyelitis in developing countries
TB
what is the likely pathogen causing osteomyelitis in patients who have had a penetration injury through a sneaker
pseudomonas
in which groups of patients have an increased risk of osteomyelitis
- aboriginal and maori children
- sickle cell disease
- immunocompromise
- neonates
what are the clinical manifestations of osteomyelitis
- fever and malaise
- pain, tenderness, warmth, swelling
- pseudoparalysis
- effusion
- decreased ROM
what are the most common bones which are affected by osteomyelitis
tibia
humerus
femur
(fastest growing bones)
osteomyelitis in which bones present insidiously and therefore are easily missed
vertebral
pelvis
what are the differential diagnoses in patients with symptoms of osteomyelitis
septic arthritis
malignancy
cellulitis
what imaging technique is the most accurate for diagnosing osteomyelitis
MRI
what is the empirical treatment for osteomyelitis
flucloxacillin
what organisms causing osteomyelitis does flucloxacillin kill
all gram positives except coagulase negative staph
what do you give to a patient with resistance staph aureus
vacomycin
what treatment do you give neonates with osteomyelitis
flucloxacillin + cefotaxime
what treatment do you give patients with pseudomonas osteomyelitis
flucloxacillin + Timentin + gentamycin
how long do we treat for osteomyelitis in adults
3-5 days IV antibiotics + complete 3 week course with oral antibiotics
how long do we treat for osteomyelitis in neonates
IV for full duration
treatment for chronic osteomyelitis
- IV antibiotics for 2 weeks
- oral antibiotics for 3-6 months
why do we rely on using your joints for their health
because the cartilage in your joints don’t have blood vessels and therefore you need to compress and decompress the cartilage in order to perfuse them
what are the 2 cell types of the synovium
Type A cells (macrophage-like)
Type B cells (fibroblast-like)
what is the difference in which joints are affected in osteoarthritis and rheumatoid arthritis
OA - affects hard-working hands, weight-bearing joints or previously injured joint
RA - often affects small joints of the hands or feet symmetrically
what is the difference between OA and RA in regards to whether the pain gets worse or better with use
OA - worse with use
RA - better with use
treatment of OA include
- physiotherapy
- pain relief
- joint replacement
what is the basic definition of OA
degeneration of the joint cartilage
what is the basic definition of RA
autoimmune inflammatory arthritis with systemic involvement
treatment of Rheumatoid arthritis
DMARDs
“disease-modifying anti-rheumatic drugs”
what is the basic definition of gout
acute inflammation in a single joint due to crystallisation of uric acid
what is podagra
gout of the big toe
treatment for gout
- anti-inflammatory medication
- urate lowering therapy
- lifestyle change
which enzymes are involved in the degeneration of cartilage in OA
collagenases
MMPs
which cytokines are involved in the degeneration of cartilage in OA
IL-1
what parts of the joint are affected in OA
cartilage
capsule
synovium
underlying bone
which cells release the enzymes and cytokines that cause OA
synovial cells
what are the 5 stages of OA
- damage stimulates chondrocyte proliferation, enzyme/cytokine action and matrix depletion
- unravelling of cartilage matrix –> release of enzymes and loss of mechanical function
- changes in bone - thickening and micro fractures
- shedding of cartilage = fibrillation, erosions
- bone-on-bone: eburnation, cysts, osteophytes
what will you see morphologically when looking at a joint with OA
- non-uniform loss of cartilage
- subchondral thickening
- osteophytes
what are the signs of OA
- reduced ROM
- crepitus
- osteophytes
what are the symptoms of OA
insiduous onset
pain (deep, achey, worse after activity)
what can you see in a joint with progressed OA
- osteophytes
- loss of load bearing joint space
- subchondral cysts
- subchondral sclerosis
risk factors for OA
- increasing age
- obesity
- previous injury/abnormality of the joint
- repeated heavy use of joint
- genetic
which T helper cells are involved in rheumatoid arthritis
Th1 and Th17
which main cytokine are involved in rheumatoid arthritis
Mainly TNFalpha
what is the underlying pathological process underlying rheumatoid arthritis
antigen causes T helper cells to release cytokines to induce fibroblasts, macrophages, osteoclasts, and B cells. This causes exuberant granulation tissue like pannus which releases collagenases and MMPs to result in breakdown of cartilage and bone
what will you see histologically and morphologically in a joint with RA
- mononuclear infiltrate in synovium with germinal centres
- hyperplasia of synovium with villus formation - becomes pannus
- neutrophils and fibrin may be found in joint space
- pannus invades and erodes bone and cartilage
- weakening and destruction of ligaments
- eventual fibrous and then bony union of joints
what are the signs of RA
- warm, swollen joints
- rheumatoid nodules
- eventual destruction and deformity of joints
what are the symptoms of RA
- systemic symptoms (fever, loss of weight, anaemia)
- symmetric polyarthritis
- morning stiffness
which joints does RA usually start in
hands and feet
which joints are usually spared in RA
distal interphalangeal joints
what histological signs do you see in a rheumatoid nodule
- central necrosis
- epithelioid macrophage
- lymphocytes and fibrosis
which blood tests would you order for RA
- CRP
- ESR
- FBE
- Rheumatoid factor
- anti-CCP
what x ray findings would you see in RA
- uniform joint space loss
- subchondral erosions
- juxta articular osteopaenia
risk factors of RA
- genetic
- female
- increasing age from 25-55
- smoking
uric acid crystals activate…
inflammatory cells, synovial cells and complement
where do uric acid crystals usually precipitate
in cool areas with loss pH and nucleating agents (such as big toe)
what happens if you have chronic gout
you can get tophaceous gout involving multiple joints –> recurrent joint inflammation results in a pannus
what is a tophi
urate deposition in other soft tissues
what other organs can gout affect
kidneys –> kidney stones and nephropathy
what do you see histologically in gout
- epitheliod macrophage
- fibrosis
- multinucleate giant cells
- central urate deposits
(granulomatous inflammation)
signs of gout
- acutely inflamed joint
- tophi if chronic
symptoms of gout
spontaneous onset of excruciating pain, swelling, heat and redness
how do you test for gout
tophus aspiration
what can you see on X-ray in late stage gout
- punched out erosions with sclerotic overhanging edges
- erosions outside the joint capsule
- haziness suggestive of tophi
risk factors for gout
- male
- increased age
- after menopause
- uric acid metabolism
- genetics and ethnicity
- obesity
- HT
- metabolic syndrome
