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Flashcards in Pics and Quiz Deck (43):
1

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Oligoarticular JIA

Less than 4 joints involved and mostly in knees over ankles. Joints are very swollen but not tender.  

Complications: 

–Disuse Atrophy

–Joint Contractures

–Growth abnormalities 

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RF-positive JIA

5+ joints and +> 2 occasions of positive RF at least 3 months apart 

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Systemic onset- JIA

 

Need 2 weeks of fever (with 3 days documented) and 1+ of:

1) evansecent, salmon colored rash

2) Hepato or splenomegaly

3) Generalized LAD

4) Serositis    

4

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Macrophage Activation Syndrome (MAS)

–a serious, potential fatal complication of SJIA caused by excessive activation and expansion of T-lymphocytes and macrophages that exhibit hemophagocytic activity

RARE (male=female)

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Closed, simple fracture

•Fracture in which the bone does not pierce the overlying skin.

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Open, compound fracture

 

•The bone is exposed to the environment through the wound so is at risk for infection. Procedural washout and antibiotics should be used in the treatment of these fractures.

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Compression fracture

 

common in vertebrae due to collapse of anterior portion of a spinous process (commonly due to osteoporosis)

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Comminuted Fracture

fracture that has broken the bone into a number of pieces (high impact crach, gunshot wounds)

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Impacted Fracture

Bone fragments are driven into each either 

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Basilar Skull Fracture

 

Usually secondary to trauma and may present as:

•periorbital ecchymoses (raccoon eyes),

•mastoid ecchymoses (Battle sign),

•cerebrospinal fluid leakage through the ears (otorrhea), or nose (rhinorrhea with salty, metallic taste).

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Osteoporosis 

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Acute osteomyelitis

 

•Most often bacterial

•Caused from direct inoculation (trauma), contiguous spread (cellulitis), or hematogenous spread

•Bone pain with systemic signs of infection

•Get blood cultures before you treat! 

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Vertebral Osteomyelitis (Pott's Disease)

 

•Causative agent: Mycobacterium tuberculosis 

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ID disese and parts indicated with lines 

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Osteomyelitis 

Subperiosteal shell of reactive viable new bone = Involcrum (green, 

Inner old necrotic cortex= sequestrum (yellow, middle)

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Osteomyelitis 

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Osteomyelitis

 

17

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Osteomyelitis in diabetes 

•Foot of a Diabetic patient showing a large area of necrosis and ulceration caused by the small vessel atherosclerotic disease, peripheral neuropathy and impaired neutrophil function of diabetes.

• The calcaneus, seen in cross section on the right, has a draining sinus (straight arrow) in which a squamous carcinoma (white tissue indicated by curved arrow) has arisen.

18

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Osteonecrosis/Avascular Necrosis
 

Causes include:

•fracture/trauma,

•steroids,

•sickle cell,

•alcohol abuse, and

•decompression sickness (the bends)

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What is causing the pathology on the right from left (normal)?

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Osteonecrosis in Sickle Cell 

Diffusely congested and hemorrhagic marrow in sickle cell crisis

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Paget’s disease of bone.

Shown is the cotton wool appearance of bone on a skull radiograph (arrows).

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What is shown?

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Phases of Paget Disease

Humerus showing

lytic (1),

mixed (2),

and sclerotic (3) phases,

- all in the same bone.

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Paget Disease of Bone (gross)

There is irregular thick, coarse cortex and replacement of normal cancellous bone with coarse, thick bundles of trabecular bone.

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Paget Disease (biopsy)

Mosaic pattern of lamellar bone 

24

Disease? What stain?

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Osteomalacia (adult)/Rickets (kids)
 

von Kossa stain: calcified tissue is black

Surfaces of bony trabeculae (black) are covered by a layer of unmineralized osteoid (dark pink)

The excess of persistent osteoid is characteristic of osteomalacia.

25

What is this? What causes it?

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“brown tumor” seen in Hyperparathyroidism

•Increased PTH are detected by osteoblasts which stimulate osteoclasts. This leads to unabated osteoclastic bone resorption. Substantial resorption of bone causes cyst-like brown tumors within the bone, consisting of fibrous tissue and woven bone without matrix.

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Dx?

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Hyperparathyroidism

PTH activate osteoblasts to activate osteoclasts (via RANKL interactions)

PTH also decreases phosphate in the proximal tubule, increases calcium resorption in the distal tubule and increases production of vitamin D3 (increased phosphate and Ca2+ absorption in the gut)

 

presentation: depression, HTN, nausea, kidney stones (bones, stones, moans, and groans)

 

 

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Normal Bone Anatomy 

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Normal Bone Histology 

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Identify arrows 

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far left: osteoblasts

long arrow on right: osteoclast

Short black arrow on right: osteocytes (maintain bone)

green arrow: pits created by osteoclasts called Howship lacunae 

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Identify structure and arrows 

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Structure: Normal epiphyseal plate 

Top: periosteum (black)

Middle: Bone marrow (blue)

Bottom: Residual cartilage (light blue)

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Bone Formation

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Osteogenesis Imperfecta –Type 1

•normal lifespan

•modestly increased proclivity for fractures (decreases after puberty)

•The classic finding of blue sclerae - attributable to decreased scleral collagen content

• Hearing loss can be related to conduction defects in the middle and inner ear bones, and small misshapen teeth are a result of dentin deficiency.

33

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Osteogenesis imperfecta Type II

The type II variant is uniformly fatal in utero or immediately postpartum as a consequence of multiple fractures that occur before birth.

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What causes this Disease?

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Osteopetrosis  -
“bone-that-is-like-stone”

•Turnover is decreased (poor osteoclast function), bone tissue becomes weak over time, fractures like a piece of chalk.

•Carbonic anhydrase II deficiency leads to loss of the acidic microenvironment needed for bone resorption.

•CA2 is required by osteoclasts and renal tubular cells to generate protons from carbon dioxide and water. The absence of CA2 prevents osteoclasts from acidifying the resorption pit and solubilizing hydroxyapatite, and also blocks the acidification of urine by the renal tubular cells. 

 

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Osteopetrosis

 

•Clinical features include:

•Fractures

•Anemia, thrombocytopenia and leukopenia with extra medullary hematopoiesis

•Vision and hearing impairment

•Hydrocephalus – narrowing of foramen magnum

•Renal tubular acidosis – seen with carbonic anhydrase II mutation (decreased tubular resorption of HCO3-, leading to metabolic acidosis 

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•Irregular bony trabeculae, increased in number and containing residual strips of unremodeled cartilage (blue-gray within the pink trabecular bone).

•Osteoclasts are not increased.

•The marrow cavity shows hematopoiesis (dark cells) but the size of the marrow cavity is markedly reduced by the excess, only partially ossified trabecaulae. 

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Disease?

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Rickets

 

Pigeon chest deformity

Rachitic rosary

Frontal bossing

Leg bowing 

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Rickets

 

A, Normal costochondral junction of a young child illustrating formation of cartilage palisades and orderly transition from cartilage to new bone. 

B, Detail of a rachitic costochondral junction in which the palisades of cartilage is lost. Darker trabeculae are well-formed bone; paler trabeculae consist of uncalcified osteoid

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Early Osteoarthritis 

Right: see fibrillaiton of articular cartilage and colonies ('clones') of regenerating cartilage cells. H&E

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What Disease? What process?

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Advanced Osteoarthritis

Highly polished ('eburnated') appearance of exposed subchondral bone in advanced OA of knee

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Advanced Osteoarthritis

Fibrous-lined cysts udner the exposed subchondral bone in advanced OA (of hip). H&E.

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Osteoarthritis

osteophyte ('spur') formation

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Advanced Osteroarthritis