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13 Cards in this Set
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Musculoskeltal System Lecture 6 Joint and Bone Infections
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Musculoskeltal System Lecture 6 Joint and Bone Infections
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6Q:
Most common etiology of Infectious (Septic) Arthritis |
Staphylococcus Aureus, but also Stap epidermidis
-most common in kids and elderly because of the immune system Next is Neisseria gonnorrhoeae from STDs, and Group B Strep for neonates |
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6Q:
Description of Staph Aureus, por favor. |
*main cause of septic arthritis
-Gram postivie cocci -Facultative anearobe -Catalase positive- separates from streps -Coagulase positive- separates aureus from epi -Tend to cause abscess formation in skin and subcutaneous tissue |
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6Q:
Neisseria characteristics, por favor. |
*another big cause of septic arthritis
Gram negative diplococci, coffee bean shape Culture - fastideous which means it requires enriched growth medium and increased concentrations of CO2 (ex chocolate agar) Oxidase positive - produce cytrochrome oxidase (aerobic) -oxidase tests for cytochrome C Neisseria produce weak acidic products on specialized medium (cystine trypticase agar); patterns are used for ID, eg. GC → acid for glucose |
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6Q:
What are the clinical features of Septic Arthritis |
Infection is monarticular in 90% of cases
Knee is most common, then hip Swollen, hot, painful joint in a patient with fever -when its multiple joints, you can think rheumatoid arthritis, but now its just one joint, so think septic arthritis |
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6Q:
Name three ways the organisms can invade the joint. |
1.direct inoculation
2. contiguous spread from infected periarticular tissue 3. via the bloodstream. Previously damaged joints, are the most susceptible to infection → synovial membranes of these joints exhibit neovascularization and increased adhesion factors (these are ideal sites for aureus to bind to) Pannus formation begins and cartilage erosion occurs at the lateral margins of the joint. Large effusions impair the blood supply → aseptic necrosis of bone. |
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6Q:
Name some staph aureus binding sites |
S aureus binds to articular sialoprotein, fibronectin collagen, elastin, hyaluronic acid, and prosthetic material by means of specific tissue adhesion factors → multiplication and damage to articular cartilage due to the organism's pathological properties, such as chondrocyte proteases of S aureus, as well as to the host's polymorphonuclear leukocytes response.
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6Q:
Which type of patients is Reiter's Syndrome more commonly found? |
Observed more commonly (2/3) in patients with human lymphocyte antigen B27 (HLA-B27) histocompatibility antigens.
There is a cross-reactivity: this is the mechanism. there's a reaction with the bacterial components, and then with the HLA B27 antigen Infections with Chlamydia trachomatis,Salmonella enteritidis, et al can cause that cross reactivity. (they were already cured, but this is weeks later. something like a phenomenon) |
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6Q:
When is the most osteomyelinitis most frequently seen? |
Occurs most fequently in children when long bones are actively growing.
it comes from trauma (disruption of blood vessels and hematoma) when the metaphysis is predisposed to infection (sludging- a slowing of blood flow from a change in diameter, where you can get microclots) |
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6Q:
Biggest cause of Osteomyelitis |
Staph aureus, 60-90%
then gram negatives like e. coli |
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6Q:
In prosthesis, where do you tend to see the infection? |
At the point of cementing with polymethylacrylate (the bone-cement interface)
Source may be introduced through surgery or be from a hematogenous origin (60/40) |
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6Q:
Whats the critter most likely to cause this prostheses infection? |
Staphylococcus epidermidis (most common; slime layer)
then staph aureus, various gram negs, streps, enterococcuses. this is only .3-.5% |
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6Q:
Treatment of Septic Arthritis |
Dependent on the organism:
S. aureus methicillin sens – Nafcillin S. aureus methicillin resis – Vancomycin N. gonnorrhoeae – Ceftriaxone (3rd gen. cephalosporin) |