bone pathology Flashcards

1
Q

function of bone

A

mechanical - support and site for muscle attachment
protective - vital organs and bone marrow
metabolic - calicum reserve

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2
Q

bone composition

A

65% inorganic
* calcium hydroxyapatite (10Ca 6PO(4) OH2)
* store house for 99% ca
* 85% of phosphorus, 65% of Na and Mg

35% organic - bone and cell matrix

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3
Q

bone georgraphy

A

outside of bone is lined by the periosteum

then cortex
then medulla

long bone have
* diaphysis (prox)
* epiphysis
* then epipihyseal line and in between is metaphysis (where growth plates are)

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4
Q

describe

A

XR
in tibia - lytic lesion

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5
Q

2 types of bone

A

cortical
cancellous

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6
Q

descrive cortical bone

A

long bones
80% skeleton
appendicular
80-90% calcified
mainly mechanical and protective

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7
Q

describe cancellous bone

A

vertebrae and pelvis
20% of skeleton
axial
15025% calcified
mainly metabolic
large surface

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8
Q

bone microanatomy

A

made of many microcolumns
have a canals
concentric lamellae around canals
interstitial lamellae connecting the units
circumferential lamellae surrounding th whole entity

trabecular lamellae deeper inside

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9
Q

cortical bone histology

A

big pink area is the cortical bone
thick

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10
Q

cancellous bone histology

A

trabeculae - darker pink

in between - haemopoietic cells and adipose tissue

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11
Q

types of bone cells

A

osteoblasts - build bone by laying down osteois

osteoclasts - multinucleate cells of macrophage family - resorb or chew bone

osteocytes - osteoblast like cells that sit in the lacunae

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12
Q

histology of bone cells

A

osteoclast - biggest here, pink, purple nuclei, multinucleated

osteoblast - smaller, single nucleus

osteocyte - small pigmented nuclei

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13
Q

bone remodelling process

A

controlled by various factors - paracrine

  1. osteoclast precurser from monocytes.
  2. osteoblast has osteoprotegrin with RANK-L (when blocked stops transformation of osteoclast precurser into osteoclast)
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14
Q

definition of metabolic bone disease

A

disordered bone turnover due to imbalance of various chemicals in the body

overall effect -> reduced bone mass (osteopenia) -> fractures with little/no trauma

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15
Q

categories of metabolic bone disease

A

non-endocrine - age related osteoporosis
related to endocrine abnormality (vit D, parathyroid hormone)
disuse osteopenia

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16
Q

How do you investigate metabolic bone disease - histology

A

histology - bone biopsy from iliac crest, processed un-decalcified form for histomorphometry

static parameters
* cortical thickness and porosity
* trabecular bone volume
* thickness, number and separation of trabeculae

bone mineralisation studied using osteoid parameters

histodynamic parameters obtained from flurescent tertracycline labelling

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17
Q

tetracycline labelling of normal bone

A
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18
Q

aetiology of osteoporosis

A

90% - insufficient Ca intake and post-menopausal oestrogen deficiency
primary - age, post-menopause
secondary - drugs, systemic disease

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19
Q

what is high and low turnover osteoporosis

A

high turnover - increased bone resorption
low turnover - reduced bone formation

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20
Q

fracture pathogenesis in osteoporosis

A

low initial bone mass or

accelerated bone loss can reduce bone mass below the fracture threshold

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21
Q

RF for osteoporosis

A

Advanced age
female
smoking
excess alcohol
early menopause
long term immobility
low BMI
poor diet, low Vit D, low Ca
malabsorption
thyroid disease
low testosterone
chronic renal disease
steroids

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22
Q

how do steroids cause osteoporosis

A

effect osteoclasts, osteocytes and blasts

decrease bone quality -> osteonecrosis and fracture

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23
Q

presentation of osteoporosis

A

back pain
fractures:
* colles
* NOF
* intertrochanteric
* pelvis

> 60% vertebral fractures are asx
compression fractures usuallin T11-L2

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24
Q
A

bone on R has osteoporosis

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25
Q

Ix for osteoporosis

A

Lab investigations
* serum ca, phos and alk phos - normal
* urinary ca
* collagen break down products

imaging

bone densometry
* T score between 1& 2.5 SD below normal peak bone mass = osteopenia
* T score >2.5 SD below normal peak bone mass = osteoporosis

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26
Q

what organs are effected by PTH, and what do they control collectively

A

Parathyroid glands
bones
kidneys
proximal small intestine

control calcium metabolism

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27
Q

pathway with hypocalcaemia

A

reduction in Vit D = increase PTH = increase osteoclast

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28
Q

definition of osteomalacia

A

defective bone mineralisation

2 types:
* deficiency of vit D
* deficiency of phosphorus

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29
Q

histology in osteomalacia

A

reduced mineralised bone (Green)
in comparison to the osteoid (orange)

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30
Q

consequences of osteomalacia

A

bone pain/tenderness
fracture
proximal weaknes
bone deformity

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31
Q

XR in rickets

A

bowing of femur and tibia
disease around knee

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32
Q

fracture in osteomalacia

A

horizontal pseudofracture in looser zone

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33
Q

findings in hyperparathyroidism

A

excess pth -> increase ca and phos excretion in urine
hyperca
hypophos
skeletal changes of osteitis fibrosa cystica

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34
Q

causes of hyperparathyroidism

A

primary
* parathyroid adenoma
* chief cell hyperplasia

secondary
* chronic renal deficiency
* vit d deficiency
* malabsorption

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35
Q

symptoms of hyperparathyroidism

A

stones - ca oxalate renal stones
bones - osteititis fibrosa cystica, bone resorption
abdominal groans - acute pancreatitis
psychic moans - psychosis and depression

36
Q

histology of hyperparathyroidism

A

multinucleate giant cells - brown cell tumour
background of fibrous stroma
haemorrhage

37
Q

what is renal osteodystrophy

A

comprises all the skeletal changes of chronic renal disease
* increased bone resorption - osteitis fibrosa cystica
* osteomalacia
* osteosclerosis
* growth retardation
* osteoporosis

38
Q

phases of paget’s disease

A

disorder of bone turnover
3 phases
1. osteolytic (osteoclasts)
2. osteolytic-osteosclerotic (blasts and clasts - start to get new bone formation)
3. quiescent osteosclerotic (new mosaic of bone forming)

39
Q

histology of pagets disease

A

Hand E stain
mosaic lines
large pink cells- osteoclasts

40
Q

summary of paget’s disease

A

> 40yrs
rare in asians and africans
mono-ostotic 15%
remainder polyostotic

41
Q

Aetiology of pagets disease

A

unknown
familial cases - show autosomal pattern of inheritence, incomplete penetrance (mutation 5q35qter - sequestosome 1 gene)
parvomyxovirus type particles seen on electon microscopy

42
Q

site prediliction for paget’s

A

Lumbar spine or skull

43
Q

clinical presentation of paget’s

A

pain
microfractures
nerve compression - spinal nerve and cord
skull changes - may put medulla at risk
+- haemodynamic changes, cardiac failure
development of sarcoma in area of development 1%

44
Q

XR of pagets

A

bowed
cotton wool appearance

45
Q

XR of pagets

A

bowed
cotton wool appearance

46
Q

what is raised in pagets

A

alk phos

47
Q

macro and micro features of pagets

A

macro - thickened bone and trabeculae
micro - thickened trabeculae, mosaic pattern

48
Q

type of fracture

A
49
Q

what type of fracture is this

A

comminuted

50
Q

stages of fracture repair

A

organisation of haematoma at fracture site (pro-callus)
formation of fibrocartilaginous callus
mineralisation of fibrocartilaginous callous
remodelling of bone along weight bearing lines

51
Q
A

fracture healing

52
Q

histology of fracture callous

A

disorganised bone
fibrous background

53
Q
A

trabecular

54
Q

what factors influence fracture healing

A

type of fracture
presence of infection
pre-existing systemic condition
* neoplasm
* metabolic disorders
* drugs
* vitamin deficiency

55
Q

common sites of osteomyelitis

A

vertebrae
jaw - secondary to dental abscess
Toe - secondary to diabetic skin ulcer (>3mm)
long bones (usually metaphysis)

56
Q

clinical features of osteomyelitis

A

malaise, fever, chills, leucocytosis
local - pain, swelling, redness

60% positive blood cultures
XR - mixed picture, eventually lytic

57
Q

aetiology of osteomyelitis

A

almost always bacterial
rarely fungal
routes of infection
* haemotogenous
* direct extension
* traumatic (inc surgery)

58
Q

organisms that cause osteomyelitis

A

mainly staph aureus

59
Q

histology of osteomyelitis

A

increase in fibrosis
chronic inflammatory cells - lymphocytes and histocytes

60
Q

XR changes in osteomyelitis

A

10days post onset

mottled rarefaction and lifting of periostium
>1wk - irregular sub-periosteal new bone formation called involucrum
later - irregular lytic destruction (10-14days)
some areas of necrotic cortex may become detatched -> sequestra (3-6wks)

diaphysis
61
Q

macroscopic osteomyelitis image

A
62
Q

Summarise TB

A

affects immunocompromised patients
more destructive and resistant to control
spinal disease (50% cases) -> psoas abscess and severe skeletal deformity (Pott’s disease)
systemic amyloidosis in protracted cases

63
Q

histology of osteomyelitis

A

big pink - trabecular bone
fibrosis in the paratrabecular space
granuloma - munltinucleated, langerhans type giant cells (horseshoe nuclei)
lymphocytes

64
Q

summarise syphillis

A

another rare cause of osteomyelitis
organism - treponema pallidum

can be congenital or acquired
congenital skeletal lesions
- osteochondritis
- osteoperiostitis
- diaphyseal osteomyelitis

acquired
- non-granulomatous periostitis
- gummatous inflammation of bones and joints
- neuropathic joints (Tabes Dorsalis)
- neuropathic shaft fractures

65
Q

summarise lyme disease

A

inflammatory arthropathy as part of a complex multisystem illness resulting from tick bite
most prevalent vector bone disease in temperate northern hemisphere

organism - borrelia burgdorferi
tick species - Ixodes dammini

tick bite get skin rash - erythema chronicum migrans

66
Q

features of lyme disease

A

early localised
* rash within 7-10 days and between 1 &50cm diameter
* thigh, groin, axilla (earlobe in children)

early disseminated
* affects many organs
* musculoskeletal
* heart
* nervous system

late, persistent
* arthritis

67
Q

Rx and Ix of lyme disease

A

treatment based on prevention
vaccine
Abx
no prophylaxis
clinical dx

68
Q

differentiate primary and secondary osteoarthriti

A

primary - age related
secondary - any age, previously damaged or congenitally abnormal joint

69
Q

XR of osteoarthritis

A

Loss of joint space
subchondral sclerosis
bone cysts
osteophytes

70
Q

identify features of osteoarthritis

A

wear and tear impact on femoral head

71
Q

what is this pathology in the femoral head

A

avascular necrosis

72
Q

aetiology of osteoarthritis

A

not sure
biochemical factors
biomechanical factors
aging
genetic

73
Q

results of osteoarthritis

A

cartilage degeneration
fissuring
abnormal matrix calcification
osteophytes

74
Q

main sites of osteoarthritis

A

vertebrae and hips
+- DIPJ PIPJ of hand
+- carpometacarpal and metatarsophalangeal joints

75
Q

histology of synovium in osteoarthritis

A

chronically inflammed
plasma cells
lymphocytes

76
Q

summarise rheumatoid arthritis

A

severe chronic relapsing synovitis
unpredicatable course
incidence 1% world population
>female
30-40yrs

77
Q

aetology of rheumatoid arthritis

A

most likely autoimmune
genetic predispositon (risk alleles TNFA1P3, STAT4)
* increased incidence among 1st degree relatives
* associated with HLA DR4 and DR1 (Chr6p21)

80% are RF +ve
* mostly IgM
* forms immunocomplexes with IgG

circulating immune complexes may underlie associated extra-articular disease

78
Q

clinical features of rheumatoid arthritis

A

mild anaemia
raised ESR
RF+ve in 80%
+- rheumatoid nodules

can be multisystem disease

radial deviation of wrist
ulnar deviation of fingers
swan neck and boutonniere deformity of fingers
Z shaped thumb

79
Q

sites that rheumatoid arthritis effects

A

small joints
hands and feet sparing DIPJ
wrists
elbows
ankles
knees

80
Q

XR showing features of rheumatoid arthritis

A

proximal joint involvement
soft tissue swelling

81
Q

histology of rheumatoid arthritis

A

proliferative synovitis
* thickening of synovial membranes (villous)
* hyperplasia of surface synoviocytes
* intense inflammatory cell infiltrate - lymphocytes
* fibrin deposition and necrosis

pannus formation with exuberant inflammed synovium overlying the articular surface

82
Q

Grimley-sokoloff cells

A

multinucleate giant cells
dont have horseshoe nucleus

83
Q
A

gout - needle shaped crystal

84
Q

summarise gout

A

affects any joint - big toe in 90%
limited to lwer extremities
needle shaped crystals
tophus is pathopneumonic lesion

85
Q

macro pathology gout

A
gouty tophus
86
Q

summarise pseudogout

A

usual age >50yrs
crystals of calcium pyrophosphate - knees
calcium phsophate (hydroxyapatite) knees and shoulders

pyrophosphate crystals
87
Q

distinct subsets of gout

A
  • sporadic
  • metabolic - haemochromatosis, primary HPT, hypoMg, low phos
  • Hereditary (autosomal dominant) (ANKH mutation, transmembrane glycoprotein, Chr 8q, 5p, younger age)
  • traumatic