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Pathology Post Midterm > Module 6: BOne: Osteomyelitis, Pott's, Osteoarthritis, RA > Flashcards

Module 6: BOne: Osteomyelitis, Pott's, Osteoarthritis, RA Flashcards

1
Q

First topic to discuss is Osteomyelitis, what is this?

A

Inflammation of Bone or bone marrow

  • -implies infection
  • -stages acute to chronic
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2
Q

What is the etiology for osteomyelitis?

A

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
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3
Q

What is the most common location for osteomyelitis?

A 
Long tubular bones (femur, tibia, humerus)
Vertebral bodies (most commonly lumbar)
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4
Q

What is the pathogenesis for osteomyelitis?

A

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
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5
Q

Why is acute osteomyelitis worse in young children or infants?

A

Abscess gets out in the periosteum aka extending into the joint space — extensive articular damage —permanent disability

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6
Q

How does acute osteomyelitis present?

A 
Fever 
Tenderness 
Swelling 
Purulent discharge 
Neutrophilia 
Leukocytes
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7
Q

What do you find on x-ray for osteomyelitis?

A

Radiolucency with sclerotic bone rim (irritated periosteum lays down new bone)

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8
Q

5-25% of acute osteomyelitis do not resolve and progress into chronic osteomyelitis, what is the pathology?

A

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

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9
Q

Next moving on to Pott’s Disease also called TB osteomyelitis, what is the etiology?

A

From hematoegnous spread of tuberculosis to chronic bacterial infection
–less commonly spread through direct contact

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10
Q

What is the pathogenesis for Pott’s Disease?

A

Destroys the intervertebral discs first — then damages the vertebral bodies
–spreads through medullary cavity causing extensive necrosis

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11
Q

What vertebrae are favored in kids vs adults who have Pott’s Disease?

A

Kids: Thoracic Vertebrae
Adults: Lumbar vertebrae

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12
Q

What kind of patients is Pott’s disease seen in?

A

Seen in miliary TB usually

but still can be seen in immunocompetent ppl

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13
Q

What is the presentation of Pott’s Disease?

A

Low back pain, parasthesias and paralysis
Kyphosis and scoliosis
Spinal cord compression – cauda equine compression = paralysis

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14
Q

What do you see on biopsy for patients with Pott’s Disease?

A 
Immunocompromised = acid fast bacilli 
Immunocompetent = caseating granuloma
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15
Q

What are the complications of Pott’s?

A

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

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16
Q

The next topic is Osteoarthritis, what are pre-disposing factors?

A

Most common joint pathology
most important risk factor = age
other risk factors = recurrent trauma and obesity

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17
Q

What joints are affected in Osteoarthritis?

A

Hip, Knee and Spine (cervical and lumbar)
Weight bearing joints
Can also affect DIP and PIP (typing alot)

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18
Q

What is the pathogenesis for osteoarthritis?

A

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

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19
Q

What is the presentation for Osteoarthritis?

A

Morning stiffness: gradual onset but short duration

  • -asymmetric
  • -gets worse as the day progresses with activity
  • -opposite from RA
20
Q

What is seen on radiograph in a patient with osteoarthritis?

A

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

21
Q

What complications are seen with Osteoarthritis?

A

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

22
Q

Explain the findings on slide 9a?

A
  1. Loss of articular cartilage: eburnation
  2. Subchondral cysts (synovial fluid into the bone due to subchondral microfractures)
  3. What is left of the articular cartilage (residual) –white portion
23
Q

What is found in the blood in patients with osteoarthritis?

A

Normal ANA, RF, WBC, ESR AND CRP again because no inflammation

24
Q

Now moving on to Rheumatoid Arthritis (RA), what is the etiology?

A

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

25
Q

What is the pathogenesis for RA?

A

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

26
Q

What is pannus in RA?

A

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)

27
Q

What joints are affected in RA?

A

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

28
Q

What is the presentation for RA?

A

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

29
Q

In RA there are extra-articular manifestations, what are they in the eyes and skin?

A

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

30
Q

In RA there are extra-articular manifestations, what are they in the lungs, heart and kidney?

A

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

31
Q

What are the X-ray findings of RA?

A 
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
32
Q

In RA there is an HLA association with what?

A

HLA DR4 = most common association

HLA DRB1 is a sign of poor prognosis

33
Q

What are the lab findings for RA?

A

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

34
Q

Describe the histology seen in 10b

A

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

35
Q

What are complications of RA?

A

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

36
Q

Carpal tunnel syndrome is seen co-exists with what other pathologies?

A 
Obesity 
Type II DM
 RA
Acromegaly 
Hypothyroidism
37
Q

What is the pathogenesis for infectious arthritis?

A

Hematogenous Seeding

–extension from osteomyelitis

38
Q

What is the etiology of infectious arthritis?

A 
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
39
Q

What are the pre-disposing factors for septic arthritis?

A

Chronic diseases: DM, alcoholism, Renal Disease
Chronic Joint diseases: RA, SLE
Immunosuppressed states: AIDS

40
Q

What is the etiology for septic arthritis?

A

Pyogenic Bacteria

  • -spread from osteomyelitis in adjacent bone
  • -soft tissue infection (Cellulitis and abscess)
  • -hematogenous spread or IVDA
  • -direct inoculation through a penetrating wound
41
Q

What is the presentation for septic arthritis?

A

Young kids = hip

Adults = knees

42
Q

What investigations are done for septic arthritis?

A

Increased WBC, Increased protein and decreased glucose

43
Q

Final a brief note of Seronegative Spondyloarthropathy, what is this?

A

Heterogeneous group of diseases
–arthritis one of several manifestations
–in part, immune mediated
HLA-B27 related to Chlamydia trachomatis

44
Q

What is the pathology for Seronegative Spondyloarthropathy?

A

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

45
Q

In regards to RA, what is Caplan syndrome?

A

Pneumoconiosis
RA
and Rheumatoid Nodules in the lungs

46
Q

In regards to RA, what is Fetty’s syndrome?

A

RA
Splenomegaly
Neutropenia

Pathology Post Midterm (50 decks)

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