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Glossary of Block VIII, Week VI

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what is a dysostoses?
congenital malformation, realtively benign
what is a craniorachischisis?
failure of closure of spinal column and skull
*meningomyelocele - when meninges herniates
*meningoencephalocele - when meninges AND CNS herniate
inheritance of osteogenesis imperfecta?
mutation results in?
AD
*defect in synthesis of collagen type I
manifestations of osteogenesis imperfecta?
prominent skeletal malformations
joints
eyes (blue)
ears
teeth
skin
*leads to osteopenia
which form of OI is lethal?
OI type II
where is the mutation in achondroplasia?
short arm of chromosome 4
(FGF receptor 3)
consequences of the FGF receptor - 3 mutation seen in achondroplasia?
mutation causes FGF receptor 3 to be constantly activated -> this inhibits cartilage proliferation in growth plate)
phenotype of an individual with achondroplasia?
dwarfism
shortened proximal extremities
enlarged head
normal trunk length
(normal intelligence, longevity, repr. status)
osteopetrosis is due to?
mutation in gene for osteoclast formation/function
(causes net bone overgrowth and increased bone density)
what are the consequences of the following in osteopetrosis: bone lacks a medullary canal
decreased hematopoiesis
-anemia (extramedullary hematopoiesis, hepatosplenomegaly)
-neutropenia
what are the consequences of the following in osteopetrosis: small neural foramina
see nerve compression
-visual disturbance, deafness
describe the bones seen in osteopetrosis
"brittle bone disease" - bones fracture like a piece of chalk
treatment for osteopetrosis?
bone marrow transplant
describe Albers-Schonberg disease
*group of RARE genetic diseases that manifest as osteopetrosis
*variable inheritance
describe AD type II osteopetrosis
*more common benign form
*seen in adolescents/adults
*may be asymptomatic
-or see-
*repeated fractures
*mild anemia
*mild CN deficits
describe the AR malignant type of osteopetrosis
*infantile, severe, often fatal
*manifests in utero or shortly after birth
*fractures
*anemia
*hydrocephaly
(if survive into infancy - CN entrapment, death from severe anemia, infections)
what is an osteochondroma?
benign cartilage outgrowth of the metaphysis, arises from the epiphyseal cartilage(growth plate) of long bones
describe a solitary osteochondroma
*slow growing mass, diagnose in late adolescence, young adult
*often incidental finding
*painful if nerve entrapment, fracture of stalk
*usually stop growing at time of growth plate closure
describe a hereditary exostosis
multiple osteochondromas, AD inheritance
*men affected 3x>women
*underlying bones may be bowed and shortened
hereditary exostosis may have an increased risk of developing?
chondrosarcoma
describe a chondroma
* benign tumor of hyaline cartilage
* develops from rests of growth plate cartilage
* cartilage rest proliferates and slowly enlarges
what is an endochondroma?
a chondroma that lies within the medullary cavity
what is a juxtacortical or subperiosteal chondroma?
a chondroma that lies at the bone surface
are chondromas MC multiple or solitary?
solitary
are chondromas usually symptomatic or asymptomatic?
most often asymptomatic
(sometimes painful and cause pathologic fractures)
both ollier's disease and maffuci syndrome are syndromes involving?
multiple endochondromas
1. ollier's disease is?
2. Maffuci sydrome is?
1. multiple endochondromas
2. multiple endochondromas PLUS soft tissue hemangiomas
maffuci syndrome may have an increased risk of developing?
other malignancies
(ovarian carcinoma, brain gliomas)
endochondromatosis in general has a risk of what kind of transformation?
sarcomatous
in pyogenic osteomyelitis, how do most bacteria reach the bone?
hematogenous spread
80% of all cases of pyogenic osteomyelitis are caused by?
Staph aureus
virulence factors of S. aureus when it comes to pyogenic osteomyelitis?
produces receptors to bone matrix components (collagen) -> facilitates adherence to bone tissue
3 bacteria that cause pyogenic osteomyelitis that could come from a GU tract infection or IV drug abuse?
E. coli
Pseudomonas
Kelbsiells
2 bacteria causing pyogenic osteomyelitis in neonates?
Group B strep
H. influenzae
which bacteria is known to cause pyogenic osteomyelitis in sickle cell disease patients?
Salmonella
where is pyogenic osteomyelitis commonly found in diabetics?
small bones in feet
why is pyogenic osteomyelitis found in different locations depending upon the age of the patient?
vascular circulation varies with age
where is osteomyelitis MC found in neonates and why?
metaphysis, epiphysis or both
(metaphyseal vessels penetrate the growth plate)
where is osteomyelitis MC found in kids?
metaphyseal leasions
where is osteomyelitis MC found in adults and why?
epiphyses and subchondral bone
(metaphyseal vessels reuinte with epiphyseal counterparts after growth plate closure)
pathophysiology of pyogenic osteomyelitis?
*bacteria proliferate in bone
*acute inflammation
*death of osteocytes
*necrosis of bone
define:
1. sequestrum
2. involucrum
3. Brodie abscess
1. dead piece of bone
2. sleeve of reactive bone surrounding sequestrum
3. intraosseous abscess walled off by reactive bone
in infants: where does an epiphyseal osteomyelitis infection tend to spread
joint
(septic joint)
symptoms of pyogenic osteomyelitis?
variable (malaise, chills, fever, leukocytosis, throbbing pain in affected bone)
* adults - localized bone pain w/o fever
*infants - unexplained fever (more subtle)
what would be seen in an Xray of a bone with osteomyelitis?
lytic bone destruction with surrounding sclerosis
treatment for pyogenic osteomyelitis?
surgical drainage
Abx
complications of pyogenic osteomyelitis?
*acute flare-ups
*pathologic fractures
*secondary amyloidosis
*endocarditis
*sepsis
*SCC in sinus tract
*sarcoma in infected bone (rare)
1/3 of patients with TB have this bone complication
tuberculous osteomyelitis
where is tuberculous osteomyelitis MC found?
thoracic/lumbar vertebrae
(usually solitary, multifocal in AIDS)
which is more destructive: tuberculous or pyogenic osteomyelitis?
tuberculous
(extensive necrosis)
what is Pott's disease?
tuberculous osteomyelitis, with involvement of the thoracic/lumbar spine
*multiple vertebrae
*see necrosis of intervertebral discs with extension to soft tissues (causes deformities)
deformities and complications seen in Pott's disease?
*permanent compression fractures -> kyphosis
*nerve impingement -> deficits
3 complications of pathologic fractures?
tumor
osteoporosis
infection
overview of steps in fracture repair?
soft tissue callus -> provisional callus -> Bony callus
describe formation of a soft tissue callus
*hematoma forms between broken bones
*this provides a firbin mesh which seals fracture stie
*osteoprogenitor cells are activated, see osteoclast and osteoblast activity
*formation of fusiform uncalcified soft tissue (no structural support)
describe the formation of a provisional callus from a soft tissue callus
*activated progenitor cells deposit trabeculae
*mesenchymal cells differentiate in to chondroblasts -> form fibrous and hyaline cartilage
*endochondral ossification occurs
describe the formation of a bony callus
remodeled and matured provisional callus (forms along weight bearing lines)
*unstressed portions are resorbed
*medullary cavity restored
complications of fracture repair?
*delayed healing/deformed callus
*malalignment
*devitalized bone fragments
*inadequate immobilization (may result in delayed union, pseudoarthrosis)
*infection
**complications may be caused by malnutrition, vascular insufficiency, systemic disease, old age**
what is one reason that the elderly have an increased risk of osteoporosis?
*decreased osteoblastic activity
connection between physical activity and rate of bone loss?
physical activity decreases the rate of bone loss
a calcium deficiency at which time in life will put an individual at greatest risk of osteoporosis?
rapid bone growth (adolescence)
*stunted peak bone mass
changes in bone metabolism during menopause?
*estrogen deficiency leads to increased osteoclast activity (increased IL-1)
Rickets/Osteomalacia is a defect in bone mineralization due to?
liack of vitamin D or a disturbance in metabolism
(results in accumulation of unmineralized bone matrix)
manifestations of Rickets in children?
rickets - "to twist"
irregular epiphyseal growth plates around kneww and wrist (bowed legs)
what is osteomalacia and what does it result in?
undermineralized bone, results in osteopenia and fractures
what is seen upon Xray of rickets or osteomalacia?
generalized osteopenia
also, stress fractures (multiple bilateral and symmetrical liner fractures)
how is rickets or osteomalacia diagnosed?
biopsy of long bone or iliac crest
adults - wide noncalcifies matrix of newly formed bone
kids - thickened, poorly defined growth plate
metabolic bone disease is due to what parathyroid disorder?
hyperparathyroidism
(increased PTH)
what is a musculoskeletal complication of hyperparathyroidism if it is not caught early?
osteitis fibrosa cystica
1. two primary reasons for increased PTH?
2. secondary reasons for increased PTH?
1. hyperplasia or adenoma of PT gland
2. chronic hypocalcemia, renal disease, Vit. D deficiency
for osteitis fibrosa cystica, describe:
1. early stage
2. second stage
3. third stage
1. increased osteoclastic acticity - osteitis
2. resorped bone replaced by fibrosis, hemorrhage, hemosiderin, microfractures (fibrosa)
3. cystic degeneration (cystica)
what is a Brown tumor?
reparative reaction, not a true tumor
(multinucleated cells, osteoclasts, hemosiderin, fibrosis, hemorrhage)
skeletal changes due to chronic renal disease is called?
renal osteodystrophy
what are some manifestations of renal osteodystrophy?
*increased resorption of bone
*phosphate retention
(secondary hyperparathyroidism)
*delayed matrix mineralization
*otosclerosis
*growth retardation
*osteoporosis
describe osteonecrosis
avascular/ischemic necrosis
-necrosis of bone and marrow IN THE ABSENCE OF INFECTION
("aseptic necrosis")
what is Legg-Calve-Perthes disease?
osteonecrosis of the femoral head in children
where does Osgood-Schlatter's manifest?
tibial tuberosity
pathophysiology of osteonecrosis?
*initially necrosis of trabecular bone and marrow
*then see subchondral infarcts (triangular shaped necrosis with subchondral bone as its base)
*overlying articular cartilage normal
*creeping substitution (dead trabeculae serve as scaffolds for deposition of new living bone)
gross manifestatons of osteonecrosis?
intact overlying articular cartilage, underlying yellow necrotic area
micro manifestations of osteonecrosis?
*dead trabeculae with empty lacunae
*Ca++ salts due to necrotic fatty marrow
other disorders associated with osteonecrosis?
fracture
*corticosteroids
thrombosis & embolism
vessel injury
how common is Paget's disease?
very
(90% of patients >65 yrs)
MC in whites
hypothesis for the etiology of paget's disease?
slow virus infection (paramyxovirus)
two types of Paget's disease?
polyostotic (85%)
monostotic (15%)
where is polyostotic Paget's disease MC found?
pelvis
spine
skull
where is monostotic Paget's disease MC found?
tibia, ilium, femur, skull, vertebrae, humerus
(often asymptomatic)
late Xray findings for Paget's disease?
increased bone density, loss of distinction between cortex and medulla
Symptoms of Paget's?
*mild localized pain due to microfractures
*osteoarthritis
*high output CHF in polyostotic form (hypervascular bone)
Labs in Paget's disease?
elevated alk. phos.
elevated urinary hydroxyproline
Rx. of Paget's disease?
calcitonin
diphosphanates
complications of Paget's?
development of a sarcoma (osteosarcoma, malignant fibrous histiocytoma, chondrosarcoma)
5-10%
three phases/descriptions of Paget's disease?
1. osteolytic phase (excessive osteoclastic bone absorption, large osteoclasts with excessive nuclei)
2. mixed osteoclastic/osteoblastic phase (hectic bone formation)
3. osteosclerotic/burnt out phase (gain in bone mass but disordered, mosaic bone pattern, jigsaw puzzle)
describe fibrous dysplasia
localized developmental abnormality of bone forming mesenchyme, hyperfunction of mesenchymal cells, bone arrested at woven stage
3 MC locations of fibrous dysplasia?
craniofacial bones
femur
ribs
in relation to fibrous dysplasia:
1. 70% of cases are of which type?
2. 27% of cases are of which type?
1. monostotic
2. polyostotic
gender differences in monostotic fibrous dysplasia?
male=female
where does monostotic fibrous dysplasia MC manifest?
ribs, femur, tibia, jaw
what is a major difference between monostotic and polyostotic fibrous dysplasia?
monostotic - resolves after puberty
polyostotic - persists into adulthood (progression)
describe the progression of polyostotic fibrous dysplasia
recurring fractures, long bone and facial deformities
(rare malignant transformation)
what is McCune Albright syndrome?
polyostotic fibrous dysplasia + endocrinopathies
describe the manifestations of McCune-Albright syndrome
cafe-au-lait spots
precocius puberty in girls
also see endocrinopathies (sexual precocity, hyperthyroidism, pituitary adenomas w/ GH secretion, primary adrenal hyperplasia)
*skin pigmentation on same side of body as bone lesion
hypertrophic osteoarthropathy is due to a paraneoplastic syndrome. what are the three components seen?
1. clubbing of fingers
2. periostitis with new bone formation at distal end of long bones
3. arthritis
hypertrophic osteoarthropathy is MC seen with which cancer?
bronchogenic carcinoma
most bone tumors are benign in what age group and malignant in what age group?
benign - kids
malignant - elderly
clinical significance of an osteoma?
benign, rare, slow growing (little clinical significance, but may obstruct sinus cavity, impinge on brain, eye; cosmetic problem)
osteoid osteomas are MC in:
1. what age group
2. what sex?
2. what bones?
1. under 25 yrs
2. males (2:1)
3. femur/tibia (50%)
why is an osteoid osteoma so painful?
pain is caused by excess prostaglandin E2 produced by proliferating osteoblasts
(pain relief with ASA)
Xray manifestations of an osteoid osteoma?
small round lucency with variable mineralization surrounded by extensive sclerosis
Treatment for an osteoid osteoma?
excision
what is the MC primary bone tumor after myeloma?
osteosarcoma
pathophysiology of an osteosarcoma?
*malignant spindle osteoblasts produce malignant bone matrix. *arise in the metaphyseal region of long bones (60% around the knee)
*associated with p53 mutation
what would be seen upon Xray of an osteosarcoma?
large destructive lesion or blastic mass
Codman's triangle
What is Codman's triangle and what is it a result of?
triangular shadow between cortex and raised periostium (result of reactive bone formation)
clinical sx. of an osteosarcoma?
painful, rapidly enlarging mass
(fracture may be 1st symptom)
10-20% of people with osteosarcoma have what else at the time of diagnosis?
lung mets
treatment of osteosarcoma?
chemotherapy
limb salvage therapy
(5 yr survival - 70%)
what is the 3rd MC bone malignancy after myeloma, osteosarcoma?
chondrosarcoma
chrondoma may arise from?
osteochondroma
chondrosarcoma MC effects:
1. what age group?
2. what sex?
3. what sites?
1. 40 yrs +
2. men > women
3. large bones (pelvis, ribs, femur, humerus, vertebrae)
what is seen upon Xray of a chondrosarcoma?
large tumor
fluffy calcifications
what does a chondrosarcoma look like grossly?
pearly white or light blue
focal calcifications
micro characteristics of a chondrosarcoma?
malignant chonrocytes produce cartilagenous matrix
is a giant cell tumor of bone benign or malignant?
benign (but locally aggressive)
in a giant cell tumor of bone what forms the giant cells?
fusion of monunuclear cells
in relation to a giant cell tumor of bone:
1. MC age?
2. MC site?
1. 20-40 yrs
2. knee (but any bone can be involved)
treatment for a giant cell tumor of bone?
surgical curetage
(radiation only if surgery impossible)
Ewing sarcoma involves what genetic mutation?
11:22 translocation
age group affected by Ewing sarcoma?
majority <20 yrs
where does Ewing sarcoma MC arise?
medullary cavity of diaphysis of long bones (femur, tibia, humerus, fibula)
how does Ewing sarcoma present?
painful enlarging mass
*site is tender, warm, swollen
gross manifestations of ewing sarcoma?
white fleshy/necrotic
treatment for ewing sarcoma?
preop chemo
surgery
radiation
prognosis for ewing sarcoma?
ok
5 yr survival ~75%
what four carcinomas commonly metastasize to bone?
breast
lung
kidney
prostate
what are the 3 pathways of spread for metastatic cancer to bone?
1. direct extension
2. lymphatic or hematogenous spread
3. intraspinal seeding
which type of arthritis is caused by bacterial infections in general?
pyogenic arthritis
which type of arthritis is caused by mycobacterium tuberculosis?
tuberculous arthritis
which type of arthritis is a sequelae to a Group A Strep infection?
arthritis of acute rheumatic fever
which type of arthritis is caused by borrelia burgdorferi?
Lyme arthritis
pyogenic arthritis is also known as?
usual result of?
acute suppurative arthritis
(usually the result of hematogenous spread, occasionally bacteria infect joints)
what are the MC organisms in pyogenic arthritis?
Cocci (gonococcus, staphylococcus, streptococcus)
Gram neg. bacilli (E.coli, salmonella, pseudomonas)
MCC of pyogenic arthritis in children <2 yrs?
H. infuenzae
MCC of pyogenic arthritis in adults and older children?
staph aureus
MCC of pyogenic arthritis in sexually active young adults?
N. gonorrhea
(oligoarthritis - only a few joints involved)
MCC of pyogenic arthritis in sickle cell disease?
Salmonella
predisposing conditions to pyogenic arthritis?
IV drug abuse
immune deficiencies
debilitating illness
joint trauma
chronic arthritis
is pyogenic arthritis usually monoauricular or polyauricular?
mononauricular
(mainly large joints)
describe the synovial effusion seen in pyogenic arthritis
type III (septic,pus)
in pyogenic arthritis, if the culture fails to yield a common pyogen - what should we be thinking?
TB
what would be seen upon a synovial biopsy of a joint with pyogenic arthritis?
acute inflammation
(congestion, edema, neutrophilic infiltrates)
tuberculous arthritis is a complication of?
tuberculous osteomyelitis
primary TB infection
what is the MC site of tuberculous arthritis?
spine
(tuberculous spondylitis = Pott's disease)
what type of effusion would be seen in a case of tuberculous arthritis?
type III effusion (septic)
what is seen in the synovium of a joint with tuberculous arthritis?
granulomatous inflammation
(more destructive process than pyogenic arthritis - may see obliteration of the joint space, infection may erode the joint capsule)
how is tuberculous arthritis diagnosed?
tissue biopsy and culture
(see caseating granulomas and acid fast bacilli)
arthritis of acute rheumatic fever primarily effects which age group?
children
describe the arthritis seen in acute rheumatic fever arthritis
*acute onset (few wks. after group A strep URI)
*polyarticular (large joints)
*migratory
what type of synovium is seen in acute rheumatic fever arthritis?
type II (inflammatory, slightly turbid due to increased white cells, sterile culture)
lyme disease is a multisystem infection. besides the joints, what else is affected?
nervous system
heart
three manifestations/stages of lyme disease
1. erythema migrans (bullseye rash at bite site)
2. neurologic/cardiac abnormalities
3. oligoarthritis
describe the clinical features of oligoarthritis seen in lyme disease
*usually involves 1 or 2 large joints
*transient remitting migratory polyarthritis
*most resolve w/o permanent joint damage (may have chronic symmetric polyarthritis)
describe the gross anatomic changes seen in lyme disease arthitis.
resemble RA
*chronic proliferative synovitis, pannus formation
*hyperplastic "onion skin" thickening of arteriole walls
treatment for lyme arthritis?
antibiotics
what is the primary feature of RA?
progressive inflammatory synovitis
destruction of synovial cartilage
systemic affects of RA?
may affect
skin
blood vessels
heart
lungs
muscles
which sex is RA MC seen in?
females (2-3x)
where does RA begin?
small joints
*hands - MCP and PIP
*feet (MTP and IP)
larger joint involvement follows (wrists,ankles, elbows, knees)
describe the synovial fluid seen in RA
type II (inflammatory)
-increased neutrophils, low mucin
radiologic findings seen in RA?
narowing of joint space
(loss of articular cartilage, bone erosions)
describe some characteristic joint deformities seen in RA
*destruction of tendons, ligaments, joint capsules (see radial deviation of wrist, ulnar deviation of fingers)
*deformed joints with no stability, limited to no ROM
some complications of RA that may ultimately lead to fatalities?
systemic amyloidosis
vasculitis
iatrogenic effects of therapy (GI bleeding due to NSAIDs, infections due to chonic steroid use)
what can be found in the serum that helps us make the diagnosis of RA?
serum rhematoid factor (seen in 80% of cases)
-not specifically diagnostic for RA, also occurs in collagen vascular diseases, others
where are rheumatoid nodules most likely to develop?
in skin subject to pressure (ulnar forearm, elbows, occiput, lumbosacal area)
can rheumatoid nodules develop in the viscera?
YES!
(lungs, pleura, spleen, heart)
what is the characteristic histology of a rheumatoid nodule?
*central fibrinoid necrosis
*palisading epithelioid histiocytes, lymphocytes, plasma cells
the pathogenesis of RA is multifactorial. major contributing factors?
*genetics
*arthritogen (? microbial antigens)
*autoimmune (see activated CD4+ T cells, B-lymphocytes, immune complexes)
some mediatiors of joint damage?
cytokines
TNF-a
IL-1
what is the antimicrobial antigen that is thought to be arthritogenic?
parvovirus B19
the diagnosis of RA requires 4 of what?
morning stiffness
arthritis in 3 or more joints
arthritis of typical hand joints
symmetric arthritis
rheumatoid nodules
serum RF
typical radiographic changes
describe the panus found in RA
*edematous and thick hypertrophic synovium
*may invade bone at articular margin, joint capsule, periarticular soft tissue
micro characteristics of RA?
proliferative/hyperplastic synovitis
rheumatoid nodules
fibrin deposition
fibrosis
increased vascularity with hemosiderin
when is juvenile RA MC found?
which sex is it MC in?
early childhood
females (2:1)
how long must a child have arthritis before it can be classified as juvenile RA?
>6 wks
what is meant if juvenile RA is classified as:
1. oligoarthritis
2. polyarticular
3. systemic variant
1. <5 joints involved (MC)
2. >5 joints
3. equal sexes, abrupt onset of fever, skin rash, hepatosplenomegaly
how does childhood RA differ from adult RA?
oligoarthritis MC
large joints > small joints
systemic onset more frequent
NO rheumatoid nodules
NO rheumatoid factor
HAVE antinuclear antibody
how is childhood RA similar to adult RA?
similar extra-articular manifestations
similar pathogenesis
similar joint pathology
what is a group of disorders with seronegativity for RA, have an association with HLA-B27, MC seen in young men?
spondyloarthropathy
what are the 4 spondyloarthropathies?
ankylosing spondylitis
Reiter syndrome
psoriatic arthritis
enteropathic arthritis
ankylosing spondyloarthritis MC affects which joints?
axial (SI joint)
ankylosing spondyloarthritis MC affects which sex?
males
ankylosing spondyloarthritis is associated with what HLA?
HLA-B27
what is ankylosing spondylitis?
inflammation of the teninoligamentous insertion sites
*see ossification and bony outgrowths
*leads to severe spinal immobility
how do patients with ankylosing spondylitis present?
low back pain that is chronic/progressive
complications of ankylosing spondylitis?
fracture of the spine
aortitis
amyloidosis
which type of arthritis am I?
episode of non-infectious arthritis that occurs within 1 month of a primary infection elsewhere (AI rxn initiated by prior infx)
reactive arthritis
pathogen from GU system that can cause reactive arthritis?
chlamydia
GI pathogens that can cause reactive arthritis?
shigella
salmonella
yersinia
campylobacter
mechanism of LPS causing reactive arthritis?
LPS antigen stimulates an immune response - see an abrupt onset in knees and ankles which lasts about a year
what is the triad seen in reiter's syndrome?
arthritis
nongonococcal urethritis or cervicitis
conjunctivitis
"can't see, can't pee, can't climb a tree"
joint symptoms seen in reiter's syndrome?
low back pain
joint stiffness
asymmetric pattern
clinical course of reactive arthritis?
*waxes and wanes over several weeks to months
*50% have functional disability (recurrent arthritis, tendinitis, fasciitis, lumbosacral back pain)
psoriatic arthritis primarily affects which joints?
DIP of hands and feet (symmetric)
*may involve large joints or SI joints
extraarticular manifestations of psoriatic arthritis?
conjunctivitis
iritis
what is the MC form of joint disease?
OA
(intrinsic disease of articular cartilage)
where is OA commonly seen?
hips (men)
knees and hands (women)
secondary OA is due to a predisposing condition. examples?
*abnormal mechanical stressors (sprotes, congenital defects)
*underlying systemic disease (DM, obesity)
etiology of primary OA?
unknown
("wear and tear arthritis")
what is chondromalacia?
a subcategory of OA
affects patellar surface of femoral condyles of young persons (produces pain and stiffness of the knee)
what are Heberden nodes
osteophytes at the DIP joints of the fingers, characteristic in women and seen in OA
which joints in the feet are commonly affected in OA?
first carpometacarpal joints
DIP joints
besides fingers and feet: other joints that are affected in OA?
knees
hips
cervical, lumbar spine
pathogenesis of OA?
*degeneration of cartilage, weakening of cartilage network

*increased levels of IL-1, TNF, NO (appear to be responsible for cartilage changes)

*death of chondrocyte -> viable chondrocytes aggregate -> fibrillation -> parralel surface cracks -> synovial fluid fills cracks -> cracks become more vertical -> cartilage pieces break off -> loose bodies -> synovial inflammation/hypertrophy.

*eventually it's bone against bone
biochemical abnomalities seen in OA?
decreased proteoglycan content
increased water content
clinical features of OA?
moning stiffness
deep achy pain (worse w/use)
limited ROM
enlarged, tender, boggy, crepitus
when would nerve root compression be seen in OA?
when osteophytes impinge on spinal foramina
what is seen upon Xray of a joint with OA?
narrowed joint space
hypertrophied subchondral bone
subchondral bone cysts
osteophytes (peripheral bone/cartilage growths)
cause of gouty arthritis?
hyperuricemia
above what serum levels of uric acid does crystal deposition begin to ocur?
>7mg/dL
risk factors for the development of gout?
age>30 yrs
familial
etoh, obesity, thiazides, lead toxicity
uric acid is the end product of what metabolism?
purine
what are the two pathways of uric acid synthesis?
1. de novo (purines from nonpurine precursors)
2. salvage (free purine bases from breakdown of nucleic acids, HGPRT enzyme)
why does uric acid crystallize in the joints?
synovial fluid is a poorer solvent than plasma for urates
(also lower T in foot, therefore crystallize there)
characteristics of synovium seen in acute gouty arthritis?
edema
congestion
dense neutrophilic infiltrate
what happens in acute gouty arthritis when the crystals are resolubilized?
acute attack subsides
describe the clinical s/s of acute gouty arthritis
*sudden onset of excruciating pain

*extremely tender and warm joints with hyperemia
where do most cases of acute gouty arthritis occur?
first metatarsophalangeal joint (big toe)
*then see in ankles, heels, knees, wrists, fingers, elbows
chronic gouty arthritis is repetetive urate crystal deposition from acute attacks. where do these crystals MC deposit?
joints
periarticular joint tissue
(deposits become grossly visible)
describe the synovium of chronic gouty arthritis
Pannus - hypertrophy, fibrosis, inflammatory cells
(see cytokine mediated cartilage destruction and juxta-articular bone erosions -> loss of joint function)
what type of synovial effusion is seen in gout?
type IV synovial effusion
(grossly white-gray granular appearance, birefringent needle shaped crystals under polarized light)
gross appearance of chronic gout?
chalky white chunky deposits in and around joints in soft tissue
what is a tophi?
large aggregates/masses of urate crystals with surrounding inflammatory rxn. Involves articular and periarticular tissues
what is gouty nephropathy?
deposition of urate crystals in the renal medulla.

see tophi, intratubular precipitates, free uric acid crystals and uric acid renal stones
four stages of gout?
1. asymptomatic hyperuricemia
2. acute gouty arthritis (monoarticular)
3. intercritical gout (recurrent-relapsing, polyarticular)
4. chronic tophaceous gout (bone erosion)
"pseudogout" involves deposition of what kind of crystals?
calcium pyrophosphate crystals. (common in arthritic joints)
avg. age of pts affected by calcium crystal arthritis?
50 yrs or older
which areas does calcium crystal arthritis tend do affect?
menisci
intervertebral discs
knee
describe the hereditary variant of calcium crystal arthritis
symptoms early in life
severe OA
secondary type of calcium crystal arthritis is associated with what disorders?
prior joint damage
hyperparathyroidism
hypothyroidism
hypomagnesemia
DM
hemachromatosis
what type of synovial fluid is seen in calcium crystal arthritis?
group IV
(chalky white deposits)
micro - see small rectangular crystals, weakly birefringent
a synovial cyst in the popliteal space is known as?
Baker's cyst
(herniation of the synovial membrane through the posterior joint capsule due to excess fluid)
Baker's cysts are associated with?
DJD
RA
micro characteristics of a Baker's cyst?
cyst lined by synovial epithelium
treatment of a Baker's cyst?
treat cause of excess fluid
clinical s/s of bursitis?
pain, erythema, swelling of bursa
(result of chronic trauma)
gross characteristics of bursitis?
thickened, erythematous, shaggy bursal wall with fibrinous exudate
micro characteristics of bursitis?
fibrous scarring of the wall with chronic inflammation
a cystic mass near a joint capsule or tendon sheath is called?
ganglion
where are the MC sites of a ganglion cyst?
wrist and fingers
(due to overuse injury)
gross characteristics of a ganglion cyst?
small cystic mass
usually does not communicate with joint space
multilocular
fluid similar to synovial fluid
micro characteristics of a ganglion cyst?
fibrous walled cyst with no synovial or epithelial lining

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