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Exam 2 Skin block > Bones part 1 > Flashcards

Bones part 1 Flashcards

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
Q

LOF of LRP5

A

disease of inactive LRP5: osteoporosis pseudoglioma syndrome:

Skeletal fragility and loss of vision

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26
Q

Osteopetrosis etiology

A

“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”

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27
Q

Osteopetrosis pathology

A

bone despotion replaces medullary cavity: no room for heamtopoiesis: extramedually hematopoiesis

bulbous long bone: Erlenmeyer flask deformity

narrow neural foramina

brittle bones

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28
Q

Autosomal dominant benign osteopetrosis: overview

A

adolescent or adulthood

multiple fractures

mild anemia

hepatosplenomegaly

mild cranial nerve defects

can be treated with bone marrow transplant

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29
Q

Osteogenesis imperfecta: overview

A

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

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30
Q

OSteogenesis imperfecta type 1: clinical features

A

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
Q

osteogenesis imperfecta type II-IV

A

autosomal dominnatn to recessive with varying degrees of disease

32
Q

Type 2, 9, 10, 11 collagen disease

A

defect in hyaline cartilage

spectrum of disease: fatal due to joint destruction

33
Q

mucopolysaccharidoses

A

defect in ezymes degrading dermatan sulfate, heparan sulfate, and keratan sulfate

abnormalties of hyaline cartilage

malformed bones

34
Q

Osteoporosis effects and causes

A

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
Q

Ostepenia

A

decrease bone mass

36
Q

osteoporosis

A

osteopenia to the point of risk of fracture

37
Q

Osteoporosis: physical acitivty

A

disuse osteoporosis: localized from loss of stimuli for bone remodeling

problem with long term space flgiht

38
Q

osteoporisis: genetic factors

A

Vit D receptor polymorphism

39
Q

Osteoporosis nutrition

A

calcium deficiency during growth stunts peak bone mass

40
Q

senile osteoporosis causes and effects and physical examination

A

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
Q

postmenopausal osteoporosis

A

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
Q

Hyperparathyrodism

A

Increased activity of OC > OB

osteitis fibrosa cystica: severe disease

43
Q

Primary and secondary hyperparathyroidism

A

primary hyperparathyroidsm: most commonly from adenoma

secondary parathyroidism (often from hypocalcemia) tends to be less severe

44
Q

Hyperparathyroidms SX on the bone

A

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
Q

Hyperparathryodism SX: Brown tumor

A

Brown tumor: bone replaced by fibrovascular tissue. Microfractures result in hemorrhage and healing. Granulation tissue, and hemosiderin

46
Q

hyperparathyrodism histo and xray

A

in cancellous bone osteoclasts tunnel and dissect central trabeculae

xray will show a thining of the bones on the radial side.

47
Q

Renal osteodystrophy pathology

A

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
Q

Paget disease: Race. SX

A

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
Q

Paget disease stages: osteolytic stage

A

loss of bone mass

osteoclasts in haphazardly resorption pits

Very early stage: a Vshaped “blade of grass” lesion seen on x ray.

50
Q

Paget disease stages: Mixed stage

A

osteolytic and osteoblastic.

Prominant osteoblasts and osteoclasts

51
Q

Paget disease stages: Osteosclerotic stage

A

coarse thick irregular trabeculae

hallmark: mosaic pattern on lamellar bone: jigsaw puzzle like cement lines

52
Q

Paget disease presentations on bone

A

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
Q

Paget disease other presentations other

A

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
Q

Paget disease tx

A

calcitonin and biphosphonates

55
Q

fracture types

A

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
Q

Fracture soft tissue callus (procallus)

A

hematoma fibrin creates framework

influx inflammation, fibroblasts, and capillaries

osteoprogenitor cells activated

no rigidity; easily disrupted

57
Q

fracture soft tissue callus

A

wwoven bone is made

+/- cartilage for endochondral ossification

maximum girth of callus 3 wks

over time remodels to bear full weight

58
Q

fracture complications

A

misaligned bone

infected, displaced or devitalized bone leasd to deformity

pseudoarthrosis: nonunion

59
Q

Osteonecrosis (avascular necrosis)

A

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
Q

avascular necrosis casues

A

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
Q

avascular necrosis: medullary infarct

A

geographic necrosis

small silent and stable

large painful: dysbarism, sickle cell

62
Q

avascular necrosis: subchondral infarct

A

chronic pain

wedge shaped subchondral bone. Often crack beneath preserved cartilage . Overlying cartilage nurtured by synovial fluid

secondary collapse lead to osteoarthritis

63
Q

osteomyelitis: caused by

A

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
Q

osteomyelitis: detection

A

lytic bone lesion with surround sclerosis

65
Q

pyogenic osteomyelitis: caused by

A

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
Q

Pyogenic osteomyeltiis: inflammation and necrosis (age dependent)

A

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
Q

Pyogenic osteomyelitis: sequestrum

A

sequestrum: dead piece of bone.

68
Q

Pyogenic osteomyelitis: later chronic inflammation and fibrosis

A

Develop rimed by reactive bone.

Brodie abscess: small intraosseous abscess often in the cortex walled off by reactive bone.

69
Q

Pyogenic osteomyelitis: involucrum

A

reactive surrounding bone

70
Q

Pyogenic osteomyelitis: sclerosing osteomyelitis of garre

A

in jaw with extensive new bone formation

71
Q

Pyogenic osteomyelitis presentation

A

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
Q

TB osteomyelitis. Who. assocations.

A

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
Q

Syphilis of the bone

A

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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