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Exam 2 Skin block > Bones part 1 > Flashcards

Bones part 1 Flashcards

(73 cards)

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1
Q

Rank pathway

A

Rank ligand (RANKL) on Osteoblast and marrow stroma cells

Rank receptor on Osteoclast precurosr and allows osteoclast generation and survival.

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2
Q

M-CSF pathway

A

MCSF secreted by OB

MCSF receptor allows OC generation and survival

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3
Q

WNT and B catenin pathway

A

WNT from marrow stromal cells

LRP 5 and LRP6 OB receptor bind WNT protein

secrete OPG which blocks Rank

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4
Q

basic multicellular unit (BMU)

A

local collection of OB, OC, and osteocytes

early bone formation dominates

adult undergo remodling: 10% year turnover

peak bone mass: early adulthood

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5
Q

Bone composition

A

calcium hydroxyapatite

organic matrix mostly type 1 collagen

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6
Q

types of bone: woven bone

A

random collagen deposition

rapid bone growth after healing fracture

resits forces in all directions

always pathologic in adults

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7
Q

Types of bone: lamellar bone:

A

ordered deposition

compact bone and spongy bone (calcinous)

replaces woven bone and stronger than woven bone.

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8
Q

Bone enzyme osteopontin (osteocalcin)

A

Unique to bone

levels parallel osteblast activity

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9
Q

bone enzyme: akaline phosphatase

A

from osteoblasts. Also in liver and placenta

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10
Q

Primary center of ossification in fetal life

A

center of bone

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11
Q

scendary center of ossification

A

physis or growth plate

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12
Q

bone formation

A

intramembranous ossification

direct from mesenchyme

appositional growth

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13
Q

anatomy: epiphysis

A

distal to grwoth plate

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14
Q

ataomy: metaphysis

A

beneath growth plate

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15
Q

anatomy: diaphysis

A

center

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16
Q

Dysostosis

A

local problems in migration of mesenchyme and their condensation. Fused finger.

HOXD13 defect

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17
Q

Dysplasia

A

global defect in regulation of skeletal organogenesis

growing an extra finger.

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18
Q

Cleidocrania dysplasia

A

autosomal dominant

RUNx2 (CBFA1) transcription factor defect

short stature

abnormal clavicles

supernumery teeth

wormian bone: extra sutral bones. located on the head.

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19
Q

achondroplasia

A

growth plate defect from paracrine cell defect

reduced chondrocyte proliferation in growth plate

FGFR3 point mutations: gain of function: Inhibits cartilage growth

90% are spontaneous mutation

most common from paternal allele

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20
Q

achondroplasia etiology

A

growth plate zones are narrowed and disorganized: premature bone deposition

appositional and intramembranous bone formation continues: create relatively thick cortical bone

FGFR3 point mutations: gain of function: Inhibits cartilage growth

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21
Q

Achondroplasia body design/physical signs

A

short stature

short proximal limbs

normal trunk length

enlarged head with bulging forehead

depression root of nose

normal longeitivity, intelligence, and reproductive status

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22
Q

thanatophoric dwarfism: etiology, and physical signs

A

most common lethal dwarfism with 1/20000 births

FGFR3 mutation gain of function

micromelic short bowed limbs

frontal bossing with macrocephaly

small underdeveloped chest with bell shaped abdomen ; respiratory failure

deminished chondrocyte proliferation.

clover leaf skull

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23
Q

LRP5: involvement in bone.

A

Receptor activates WNT/B catenin in OB: production of OPG (blocks RNKL) and increases bone mass

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24
Q

GOF of LRP5

A

GOF; cannot upregulate OC: autosomal dominant osteopetrosis type 1

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25
LOF of LRP5
disease of inactive LRP5: osteoporosis pseudoglioma syndrome: Skeletal fragility and loss of vision
26
Osteopetrosis etiology
"marble bone disease diffuse systemic bone sclerosis cannot acidify pit: carbonic anhydrase II (CA2) deficiency defect in RANKL: not enough OC activity LRP5 gain of function spectrum from autosomal dominant benign to autosomal recessive "malignant"
27
Osteopetrosis pathology
bone despotion replaces medullary cavity: no room for heamtopoiesis: extramedually hematopoiesis bulbous long bone: Erlenmeyer flask deformity narrow neural foramina brittle bones
28
Autosomal dominant benign osteopetrosis: overview
adolescent or adulthood multiple fractures mild anemia hepatosplenomegaly mild cranial nerve defects can be treated with bone marrow transplant
29
Osteogenesis imperfecta: overview
group of type 1 collage diseases "brittle bone disease" affects other areas rich in type 1 collagen mutations of alpha 1 or 2 chains: quantitative decrease or qualitative defect most common type is autosomal dominant extreme skeletal fragility vs child abuse
30
OSteogenesis imperfecta type 1: clinical features
autosomal dominant normal stature with less fractures after puberty blue sclerae from translucency of sclera dentinogenesis imperfecta from dentin defect hearing loss from abnormal ear bone and sensorineural deficit joint laxity compatible with normal lifespan
31
osteogenesis imperfecta type II-IV
autosomal dominnatn to recessive with varying degrees of disease
32
Type 2, 9, 10, 11 collagen disease
defect in hyaline cartilage spectrum of disease: fatal due to joint destruction
33
mucopolysaccharidoses
defect in ezymes degrading dermatan sulfate, heparan sulfate, and keratan sulfate abnormalties of hyaline cartilage malformed bones
34
Osteoporosis effects and causes
increased bone porosity and decreased mass: increased risk of fracture disuse: osteoporosis local metabolic bone idsease: primary: senile post moenopausal, idiopathic secondary: drugs, diabetes, endocrine disorders, malignancy liver or GI disease X ray can detect only after 30-40% of bone loss
35
Ostepenia
decrease bone mass
36
osteoporosis
osteopenia to the point of risk of fracture
37
Osteoporosis: physical acitivty
disuse osteoporosis: localized from loss of stimuli for bone remodeling problem with long term space flgiht
38
osteoporisis: genetic factors
Vit D receptor polymorphism
39
Osteoporosis nutrition
calcium deficiency during growth stunts peak bone mass
40
senile osteoporosis causes and effects and physical examination
sekeltal mass peak: young adult mostly hereditary determined by vit. d receptor, collagen 1a1, estrogen receptor, etc. physically activity, strength, diet, hormone state slow decrease in bone mass over time: osteoblasts reduced metabolism cortex thinned on all surfaces: cortex bone may look like cancellous bone
41
postmenopausal osteoporosis
30 years post menopause: 35% cortical and 50% trabeuclar bone loss. 1 in 2 women will have an osteoporotic frature high turnover form of osteoporisis decreased estrogen leads to increased inflammatory cytokines. Increased rankl and decreased OPG which causes more OC than OB activity. estrogen replacement is protective. risk vertebral body collapse.
42
Hyperparathyrodism
Increased activity of OC > OB osteitis fibrosa cystica: severe disease
43
Primary and secondary hyperparathyroidism
primary hyperparathyroidsm: most commonly from adenoma secondary parathyroidism (often from hypocalcemia) tends to be less severe
44
Hyperparathyroidms SX on the bone
entire skeelton affected subperosteal resorption thins cortices loss of lamina dura around teeth X ray: bone loss radial aspect of middle phalanges of index and middle finger X ray: osteopenia
45
Hyperparathryodism SX: Brown tumor
Brown tumor: bone replaced by fibrovascular tissue. Microfractures result in hemorrhage and healing. Granulation tissue, and hemosiderin
46
hyperparathyrodism histo and xray
in cancellous bone osteoclasts tunnel and dissect central trabeculae xray will show a thining of the bones on the radial side.
47
Renal osteodystrophy pathology
increased or decreased OC/OB activity: delayed mineralization (osteomalacia) , osteosclerosis or osteoporosis hyperparathyrodism decreased vitamin D conversion to 1,25 OH2 vit D3 metabolic acidosis: increased release of CA2
48
Paget disease: Race. SX
mid adulthood caucasians from Us, europe,: 1% of US; 2.5 males in England Most asymptomatic but may have pain easily fractured 85% polyostotic 80% involve axial skeleton and proximal femur Some evidence of paramyxovirus some evidence of osteoclasts are hyperresponsive to stimuli
49
Paget disease stages: osteolytic stage
loss of bone mass osteoclasts in haphazardly resorption pits Very early stage: a Vshaped "blade of grass" lesion seen on x ray.
50
Paget disease stages: Mixed stage
osteolytic and osteoblastic. Prominant osteoblasts and osteoclasts
51
Paget disease stages: Osteosclerotic stage
coarse thick irregular trabeculae hallmark: mosaic pattern on lamellar bone: jigsaw puzzle like cement lines
52
Paget disease presentations on bone
may present with pain from microfractures often incidental finding on x ray increased alkaline phosphatase normal CA and Po4 bone overgrowth can lead to: cranial nerve palsy. Heavy skull. (hard to pull up). severe secondary osteoarthritis. Chalk stick type fracture
53
Paget disease other presentations other
warm skin over affected bone with hypervasculatrity; polyostotic can create AV shunting. High output cardiac failure. Tumors: benign: giant cell tumor, giant cell reparative granuloma, extraosseous hematopoiesis. Malignant: osteosarcoma and fibrosarcoma. 5-10% of patitnes with severe polyostotic disease
54
Paget disease tx
calcitonin and biphosphonates
55
fracture types
closed (simple)/Open (compound) comminuted (fragmented)( displaced green stick: incomplete fracture of the distal and radial diaphasis. Pathologic: secondary to disease stress: slowly developing form repeated loads, eg marching
56
Fracture soft tissue callus (procallus)
hematoma fibrin creates framework influx inflammation, fibroblasts, and capillaries osteoprogenitor cells activated no rigidity; easily disrupted
57
fracture soft tissue callus
wwoven bone is made +/- cartilage for endochondral ossification maximum girth of callus 3 wks over time remodels to bear full weight
58
fracture complications
misaligned bone infected, displaced or devitalized bone leasd to deformity pseudoarthrosis: nonunion
59
Osteonecrosis (avascular necrosis)
infarction of bone and marrow mechanisms all create ischemia: vessel injury (mechanical, arteritis, emboli), corticosteroids most common cause, increased intraosseou pressure dead bone/fat is replaced by CA soaps creeping substitution: slow bone growth: continued fractures and collapse of bone. slough articular cartilage
60
avascular necrosis casues
idopathic corticosteroids trauma infection dysbarsim radiation connective tissue disorders pregnancy gaucher disease alcohol abuse chronic pancreatitis tumors epiphyseal disease sickle cell disease and other anemias1
61
avascular necrosis: medullary infarct
geographic necrosis small silent and stable large painful: dysbarism, sickle cell
62
avascular necrosis: subchondral infarct
chronic pain wedge shaped subchondral bone. Often crack beneath preserved cartilage . Overlying cartilage nurtured by synovial fluid secondary collapse lead to osteoarthritis
63
osteomyelitis: caused by
inflammation almost always from infection. Bacteria, virus, fungi, parasite. Pyogenic; almost always bacteria bacteria reach bone by hematogenous (most common in children), direct extension, implantation
64
osteomyelitis: detection
lytic bone lesion with surround sclerosis
65
pyogenic osteomyelitis: caused by
50% culture negative S aureus: 80-90% of culture positive E coli, pseudomonas, klebsiella. GU infections and IV drug abusers Mixed infections: surgery or compound fractures H flu and group B strep in infants salmonella in sickle cell disease
66
Pyogenic osteomyeltiis: inflammation and necrosis (age dependent)
initial acute inflammation and necrosis location influenced by blood supply: neonate: metaphysis and or epiphysis. Can spread into joint through articular surface or adjacent structures children: metaphysis. Subperiosteal abscess adult: epiphyses and subchondral bone
67
Pyogenic osteomyelitis: sequestrum
sequestrum: dead piece of bone.
68
Pyogenic osteomyelitis: later chronic inflammation and fibrosis
Develop rimed by reactive bone. Brodie abscess: small intraosseous abscess often in the cortex walled off by reactive bone.
69
Pyogenic osteomyelitis: involucrum
reactive surrounding bone
70
Pyogenic osteomyelitis: sclerosing osteomyelitis of garre
in jaw with extensive new bone formation
71
Pyogenic osteomyelitis presentation
acutely sick to unexplained fever local pain draining sinus. can develop squamous cell carcinoma 5-25% become chronic osteomyelitis. Complications include pathological fracture and sarcoma
72
TB osteomyelitis. Who. assocations.
third world, immunocompromised. Adolescents and young adults US: older or immunocompromised 2% with TB have osteomyelitis most common Potts disease: L/T spine. Break through discs to other vertebrae. Scoliosis and kyphosis. Knees and hips second most common.
73
Syphilis of the bone
T. Pallidum and T pertenue (yaws) congenital: affected at 5 mo; fully developed at birth localize at enchondral ossification centers (osteochondritis) and periosteum (periostitis) acquried syphills of the bone: involves bone in tertiary phase. Nose (saddle nose), palate, skull, tibia (saber shin), vertebrae, hands/feet

Exam 2 Skin block (22 decks)

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