Module 6: BOne: Osteomyelitis, Pott's, Osteoarthritis, RA Flashcards
First topic to discuss is Osteomyelitis, what is this?
Inflammation of Bone or bone marrow
- -implies infection
- -stages acute to chronic
What is the etiology for osteomyelitis?
Seen in young and elderly (M:F = 2:1)
- -most common organism is S. Aureus
- –GU infection, IVDA: E. coli, Klebsiella, and Pseudomonas
- -Direct Inoculation = mixed bacterial
- –Neonates = H. influenza, Group B Strep
- -Sickle Cell Anemia = Salmonella
What is the most common location for osteomyelitis?
Long tubular bones (femur, tibia, humerus) Vertebral bodies (most commonly lumbar)
What is the pathogenesis for osteomyelitis?
Begins in metaphysis b.c nutrient arteries terminate in venous sinusoids (ideal for bacterial seeding) and decreased O2 tension inhibits phagocytosis — formation of abscess within medulla and under periosteum and bone necrosis
- -bone necrosis = 48 hours
- -progressive ischemia leads to segmental bone necrosis = sequestrum
- surrounded by viable new bone (involucrum) formation
Why is acute osteomyelitis worse in young children or infants?
Abscess gets out in the periosteum aka extending into the joint space — extensive articular damage —permanent disability
How does acute osteomyelitis present?
Fever Tenderness Swelling Purulent discharge Neutrophilia Leukocytes
What do you find on x-ray for osteomyelitis?
Radiolucency with sclerotic bone rim (irritated periosteum lays down new bone)
5-25% of acute osteomyelitis do not resolve and progress into chronic osteomyelitis, what is the pathology?
Chronic inflammation
Resorption of dead bone
Deposition of woven bone (immature bone)
Brodie abscess: Intracortical abscess
Sclerosing OM of Garre: Jaw: Extensive new bone obscuring the underlying bone
Next moving on to Pott’s Disease also called TB osteomyelitis, what is the etiology?
From hematoegnous spread of tuberculosis to chronic bacterial infection
–less commonly spread through direct contact
What is the pathogenesis for Pott’s Disease?
Destroys the intervertebral discs first — then damages the vertebral bodies
–spreads through medullary cavity causing extensive necrosis
What vertebrae are favored in kids vs adults who have Pott’s Disease?
Kids: Thoracic Vertebrae
Adults: Lumbar vertebrae
What kind of patients is Pott’s disease seen in?
Seen in miliary TB usually
but still can be seen in immunocompetent ppl
What is the presentation of Pott’s Disease?
Low back pain, parasthesias and paralysis
Kyphosis and scoliosis
Spinal cord compression – cauda equine compression = paralysis
What do you see on biopsy for patients with Pott’s Disease?
Immunocompromised = acid fast bacilli Immunocompetent = caseating granuloma
What are the complications of Pott’s?
Immunocompetent: granuloma can take over bone marrow — myelophisic anemia (Normocitic Normochromic Anemia)
Spinal Cord Compression
Psoas Abscess: cold abscess due to minimal inflammatory response (no spiking fevers seen in normal abscess)
Amyloid deposition (Eosinophilic glassy material) in the kidney
The next topic is Osteoarthritis, what are pre-disposing factors?
Most common joint pathology
most important risk factor = age
other risk factors = recurrent trauma and obesity
What joints are affected in Osteoarthritis?
Hip, Knee and Spine (cervical and lumbar)
Weight bearing joints
Can also affect DIP and PIP (typing alot)
What is the pathogenesis for osteoarthritis?
Degenerative Joint Disease: no inflammatory response
–enzymatic breakdown of articular cartilage (due to wear and tear)(fibrillations) — cracks – bone on bone eburnation — deeper cracks that dislodge as joint mice (have a central core of necrotic bone) — leakage of synovial fluid — subchondral cysts
What is the presentation for Osteoarthritis?
Morning stiffness: gradual onset but short duration
- -asymmetric
- -gets worse as the day progresses with activity
- -opposite from RA
What is seen on radiograph in a patient with osteoarthritis?
Joint space narrowing (lost articular cartilage)
Osteophytes (bone spurs, fibrocartilage grows over articular cartilage from periphery)(repair mechanism trying to re-balance the load): reactive bone
–Herberden’s nodes = DIP
–Bouchard nodes = PIP
–in spine these spurs can compress spinal nerves and lead to paralysis
1st carpometacarpal joint: subluxation and squaring
What complications are seen with Osteoarthritis?
Degeneration and destruction of joint – hip or knee replacement
Neuro complications if bone spurs compress the spinal nerves
Does not cause extra-articular manifestations
(in RA there are extra articular problems)
Following a knee/hip replacement – septic arthritis (most common cause of death) : usually staph epidermis
Explain the findings on slide 9a?
- Loss of articular cartilage: eburnation
- Subchondral cysts (synovial fluid into the bone due to subchondral microfractures)
- What is left of the articular cartilage (residual) –white portion
What is found in the blood in patients with osteoarthritis?
Normal ANA, RF, WBC, ESR AND CRP again because no inflammation
Now moving on to Rheumatoid Arthritis (RA), what is the etiology?
Common in young females: type 3 and 4 autoimmune
etiology: HLA-DR4 association
- -co exists with other autoimmune conditions (esp primary biliary cirrhosis) and Sjogren’s and Type I DM
What is the pathogenesis for RA?
Type III and IV HSR: inflammatory response b.c it is autoimmune
–progressive joint destruction due to formation of a pannus: cant be prevented but can slow down the progression
What is pannus in RA?
Pannus = synovial cell hyperplasia, organizing fibrin, CD4 T cells which form lymphoid aggregates, neutrophils (b/c acute on chronic) and macrophages
eventually becomes acellular —granulation tissue (type III collagen) – type I collagen (Scar)
What joints are affected in RA?
Affects any joint lined by synovial membrane
–typically affects small joints of hands/wrists and feet
spares DIP
symmetric and bilateral
MCP is the most commonly affected joint
What is the presentation for RA?
Young female with morning stiffness affecting the joints of hands and feet (red, hot, swollen joint that becomes immobile due to fibrosis)
–ulnar deviation of fingers
–swan neck deformities after 10 years (flexion of DIP and hyperextension of PIP and tendons are destroyed and shortened why DIP is affected)
–Boutonniere deformity (flexion of PIP and hyperextension of DIP)
Longer Duration
Gets better as the day progresses
In Joint:
–C1 and C2 spine (Atlas and axis) mainly affected: atlanto-axial joint: subluxation
–knee joint: baker cysts which can rupture and mimic a DVT
In RA there are extra-articular manifestations, what are they in the eyes and skin?
Eyes: Keratoconjunctivitis sica (Coexists with Sjogren’s) and Episcleritis and uveitis
Skin: Vasculitis – ulcers and infarcts and Rheumatoid Nodules on extensor surfaces of UE (Where most pressure is applied) on histology for nodules: central necrosis with palisading macrophages
In RA there are extra-articular manifestations, what are they in the lungs, heart and kidney?
Lungs: Interstitial fibrosis (restrictive dz)
–pulmonary hemorrhages cause fibrosis this leads to contraction atelectasis
-normal FEV/FVC ratio
Heart: Restrictive CM from AA amyloidosis (systemic)
–chronic inflammatory condition
–vasculitis: accelerated atherosclerosis – MI (most common cause of death)
Kidney: nephrotic syndrome from AA amyloid and generalized edema
What are the X-ray findings of RA?
Osteopenia: thinning of bone Bone erosions Joint space narrowing No osteophytes Pic: ulnar deviation due to bone destruction, flexion of DIP and hyperextension of PIP
In RA there is an HLA association with what?
HLA DR4 = most common association
HLA DRB1 is a sign of poor prognosis
What are the lab findings for RA?
Low Hb, normal MCV and MCHC
-normochromic, normocitic anemia = anemia of chronic disease
Elevated rheumatoid factor: IgM directed against Fc region of IgG
Elevated CCP= cyclic citrulinated peptide
–more sensitive and more specific then rheumatoid factor
Elevated ANA, CRP and ESR all due to inflammation
Describe the histology seen in 10b
To left: Pannus (synovial hyperplasia, fibrin, PMNs, fibroblasts and granulation tissue and lymphocytes)
–from lymphocytes T cell form lymphoid aggregates this is the blue dots
–pink is just collagen from the fibroblasts laying it down
To right: finger like projection from a BV with angiogenesis and inflammatory cells around the BV called perivascular inflammatory cells which are part of the pannus
What are complications of RA?
joint destruction
Most common cause of death in young patients: recurrent infections bc they are on steroids
Most common cause of death in old patients is MI from accelerated atherosclerosis due to vasculitis
Chronic analgesic abuse — ureteric obstruction –bilateral necrosis of renal papillae
AA amyloidosis – nephrotic syndrome — anasarca and restrictive cardiomyopathy in heart –arrhythmias
Fibrous anklyosis = fusion of the joints
Carpal tunnel syndrome is seen co-exists with what other pathologies?
Obesity Type II DM RA Acromegaly Hypothyroidism
What is the pathogenesis for infectious arthritis?
Hematogenous Seeding
–extension from osteomyelitis
What is the etiology of infectious arthritis?
Bacterial: rapid joint destruction --S. Aureus (Children) --N. Gonorrhea (Adults) --Mycobacteria --Borreila (lyme disease) -- silver stain Viral: Hep B and C Rubella Mumps EBV Parvo B19
What are the pre-disposing factors for septic arthritis?
Chronic diseases: DM, alcoholism, Renal Disease
Chronic Joint diseases: RA, SLE
Immunosuppressed states: AIDS
What is the etiology for septic arthritis?
Pyogenic Bacteria
- -spread from osteomyelitis in adjacent bone
- -soft tissue infection (Cellulitis and abscess)
- -hematogenous spread or IVDA
- -direct inoculation through a penetrating wound
What is the presentation for septic arthritis?
Young kids = hip
Adults = knees
What investigations are done for septic arthritis?
Increased WBC, Increased protein and decreased glucose
Final a brief note of Seronegative Spondyloarthropathy, what is this?
Heterogeneous group of diseases
–arthritis one of several manifestations
–in part, immune mediated
HLA-B27 related to Chlamydia trachomatis
What is the pathology for Seronegative Spondyloarthropathy?
Chronic synovitis
Destruction of articular cartilage and subchondral bone
Fibrosis and narrowing of joint space (Fibrosing ankylosis)
Ossification of fibrous tissue (bony ankylosis)
Joint immobility
Sacroiliac joints and spine
–most common is ankylosing spondylitis
In regards to RA, what is Caplan syndrome?
Pneumoconiosis
RA
and Rheumatoid Nodules in the lungs
In regards to RA, what is Fetty’s syndrome?
RA
Splenomegaly
Neutropenia
