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Z MD1 locomotor and exercise block > joint and bone infections and pathology > Flashcards

joint and bone infections and pathology Flashcards

1
Q

what are the types of osteomyelitis

A
  • haematogenous
  • non haematogenous (direct inoculation)
  • non haematogenous (local invasion)
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2
Q

what are the ways in which osteomyelitis can be acquired (non haematogenously - direct inoculation)

A

trauma

surgery

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3
Q

what are the ways in which osteomyelitis can be acquired (non haematogenously - local invasion)

A

pressure ulcer
periodontal disease
sinus disease

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4
Q

what are the stages of how you get a bone infection

A
  1. slow flow through looped capillaries and venous sinusoids
  2. baceria seed metaphyseal-epiphyseal junction –> abscess forms
  3. abscess causes a protection from the immune system
  4. pressure form pus further limits blood supply
  5. abscess grows but cant penetrate penetrate the epiphyseal growth plate - spreads outwards instead and eventually breaks through to spread to the subperiosteal space
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5
Q

what structure stops the abscess from entering the epiphyses

A

the epiphyseal growth plate

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6
Q

why is osteomyelitis especially dangerous in infants

A

the infection may invade the epiphysis and joint (is able to cross the growth plate) –> septic arthritis coexistent

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7
Q

what are the 3 ways you can get septic arthritis

A
  • haematogenous contamination
  • direct contamination
  • contiguous contamination
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8
Q

what is the most common and second most common pathogen to cause osteomyelitis

A

staph aureus - most common

strep pyogenes - 2nd

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9
Q

what is the likely pathogen causing osteomyelitis in patients have have recently undergone surgery

A

coagulase negative staph

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10
Q

what is the likely pathogen causing osteomyelitis in newborns and infants

A

group B strep
HiB
other gram negatives

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11
Q

what is the likely pathogen causing osteomyelitis in patients with recent chicken pox

A

group A beta haemolytic strep

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12
Q

what is the likely pathogen causing osteomyelitis in developing countries

A

TB

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13
Q

what is the likely pathogen causing osteomyelitis in patients who have had a penetration injury through a sneaker

A

pseudomonas

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14
Q

in which groups of patients have an increased risk of osteomyelitis

A
  • aboriginal and maori children
  • sickle cell disease
  • immunocompromise
  • neonates
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15
Q

what are the clinical manifestations of osteomyelitis

A
  • fever and malaise
  • pain, tenderness, warmth, swelling
  • pseudoparalysis
  • effusion
  • decreased ROM
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16
Q

what are the most common bones which are affected by osteomyelitis

A

tibia
humerus
femur
(fastest growing bones)

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17
Q

osteomyelitis in which bones present insidiously and therefore are easily missed

A

vertebral

pelvis

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18
Q

what are the differential diagnoses in patients with symptoms of osteomyelitis

A

septic arthritis
malignancy
cellulitis

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19
Q

what imaging technique is the most accurate for diagnosing osteomyelitis

A

MRI

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20
Q

what is the empirical treatment for osteomyelitis

A

flucloxacillin

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21
Q

what organisms causing osteomyelitis does flucloxacillin kill

A

all gram positives except coagulase negative staph

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22
Q

what do you give to a patient with resistance staph aureus

A

vacomycin

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23
Q

what treatment do you give neonates with osteomyelitis

A

flucloxacillin + cefotaxime

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24
Q

what treatment do you give patients with pseudomonas osteomyelitis

A

flucloxacillin + Timentin + gentamycin

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25
Q

how long do we treat for osteomyelitis in adults

A

3-5 days IV antibiotics + complete 3 week course with oral antibiotics

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26
Q

how long do we treat for osteomyelitis in neonates

A

IV for full duration

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27
Q

treatment for chronic osteomyelitis

A
  • IV antibiotics for 2 weeks

- oral antibiotics for 3-6 months

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28
Q

why do we rely on using your joints for their health

A

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

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29
Q

what are the 2 cell types of the synovium

A

Type A cells (macrophage-like)

Type B cells (fibroblast-like)

30
Q

what is the difference in which joints are affected in osteoarthritis and rheumatoid arthritis

A

OA - affects hard-working hands, weight-bearing joints or previously injured joint
RA - often affects small joints of the hands or feet symmetrically

31
Q

what is the difference between OA and RA in regards to whether the pain gets worse or better with use

A

OA - worse with use

RA - better with use

32
Q

treatment of OA include

A
  • physiotherapy
  • pain relief
  • joint replacement
33
Q

what is the basic definition of OA

A

degeneration of the joint cartilage

34
Q

what is the basic definition of RA

A

autoimmune inflammatory arthritis with systemic involvement

35
Q

treatment of Rheumatoid arthritis

A

DMARDs

“disease-modifying anti-rheumatic drugs”

36
Q

what is the basic definition of gout

A

acute inflammation in a single joint due to crystallisation of uric acid

37
Q

what is podagra

A

gout of the big toe

38
Q

treatment for gout

A
  • anti-inflammatory medication
  • urate lowering therapy
  • lifestyle change
39
Q

which enzymes are involved in the degeneration of cartilage in OA

A

collagenases

MMPs

40
Q

which cytokines are involved in the degeneration of cartilage in OA

A

IL-1

41
Q

what parts of the joint are affected in OA

A

cartilage
capsule
synovium
underlying bone

42
Q

which cells release the enzymes and cytokines that cause OA

A

synovial cells

43
Q

what are the 5 stages of OA

A
  • 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
44
Q

what will you see morphologically when looking at a joint with OA

A
  • non-uniform loss of cartilage
  • subchondral thickening
  • osteophytes
45
Q

what are the signs of OA

A
  • reduced ROM
  • crepitus
  • osteophytes
46
Q

what are the symptoms of OA

A

insiduous onset

pain (deep, achey, worse after activity)

47
Q

what can you see in a joint with progressed OA

A
  • osteophytes
  • loss of load bearing joint space
  • subchondral cysts
  • subchondral sclerosis
48
Q

risk factors for OA

A
  • increasing age
  • obesity
  • previous injury/abnormality of the joint
  • repeated heavy use of joint
  • genetic
49
Q

which T helper cells are involved in rheumatoid arthritis

A

Th1 and Th17

50
Q

which main cytokine are involved in rheumatoid arthritis

A

Mainly TNFalpha

51
Q

what is the underlying pathological process underlying rheumatoid arthritis

A

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

52
Q

what will you see histologically and morphologically in a joint with RA

A
  • 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
53
Q

what are the signs of RA

A
  • warm, swollen joints
  • rheumatoid nodules
  • eventual destruction and deformity of joints
54
Q

what are the symptoms of RA

A
  • systemic symptoms (fever, loss of weight, anaemia)
  • symmetric polyarthritis
  • morning stiffness
55
Q

which joints does RA usually start in

A

hands and feet

56
Q

which joints are usually spared in RA

A

distal interphalangeal joints

57
Q

what histological signs do you see in a rheumatoid nodule

A
  • central necrosis
  • epithelioid macrophage
  • lymphocytes and fibrosis
58
Q

which blood tests would you order for RA

A
  • CRP
  • ESR
  • FBE
  • Rheumatoid factor
  • anti-CCP
59
Q

what x ray findings would you see in RA

A
  • uniform joint space loss
  • subchondral erosions
  • juxta articular osteopaenia
60
Q

risk factors of RA

A
  • genetic
  • female
  • increasing age from 25-55
  • smoking
61
Q

uric acid crystals activate…

A

inflammatory cells, synovial cells and complement

62
Q

where do uric acid crystals usually precipitate

A

in cool areas with loss pH and nucleating agents (such as big toe)

63
Q

what happens if you have chronic gout

A

you can get tophaceous gout involving multiple joints –> recurrent joint inflammation results in a pannus

64
Q

what is a tophi

A

urate deposition in other soft tissues

65
Q

what other organs can gout affect

A

kidneys –> kidney stones and nephropathy

66
Q

what do you see histologically in gout

A
  • epitheliod macrophage
  • fibrosis
  • multinucleate giant cells
  • central urate deposits
    (granulomatous inflammation)
67
Q

signs of gout

A
  • acutely inflamed joint

- tophi if chronic

68
Q

symptoms of gout

A

spontaneous onset of excruciating pain, swelling, heat and redness

69
Q

how do you test for gout

A

tophus aspiration

70
Q

what can you see on X-ray in late stage gout

A
  • punched out erosions with sclerotic overhanging edges
  • erosions outside the joint capsule
  • haziness suggestive of tophi
71
Q

risk factors for gout

A
  • male
  • increased age
  • after menopause
  • uric acid metabolism
  • genetics and ethnicity
  • obesity
  • HT
  • metabolic syndrome

Z MD1 locomotor and exercise block (13 decks)

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