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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
Ix for osteoporosis
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
26
what organs are effected by PTH, and what do they control collectively
Parathyroid glands bones kidneys proximal small intestine control calcium metabolism
27
pathway with hypocalcaemia
reduction in Vit D = increase PTH = increase osteoclast
28
definition of osteomalacia
defective bone mineralisation 2 types: * deficiency of vit D * deficiency of phosphorus
29
histology in osteomalacia
reduced mineralised bone (Green) in comparison to the osteoid (orange)
30
consequences of osteomalacia
bone pain/tenderness fracture proximal weaknes bone deformity
31
XR in rickets
bowing of femur and tibia disease around knee
32
fracture in osteomalacia
horizontal pseudofracture in looser zone
33
findings in hyperparathyroidism
excess pth -> increase ca and phos excretion in urine hyperca hypophos skeletal changes of osteitis fibrosa cystica
34
causes of hyperparathyroidism
primary * parathyroid adenoma * chief cell hyperplasia secondary * chronic renal deficiency * vit d deficiency * malabsorption
35
symptoms of hyperparathyroidism
stones - ca oxalate renal stones bones - osteititis fibrosa cystica, bone resorption abdominal groans - acute pancreatitis psychic moans - psychosis and depression
36
histology of hyperparathyroidism
multinucleate giant cells - brown cell tumour background of fibrous stroma haemorrhage
37
what is renal osteodystrophy
comprises all the skeletal changes of chronic renal disease * increased bone resorption - osteitis fibrosa cystica * osteomalacia * osteosclerosis * growth retardation * osteoporosis
38
phases of paget's disease
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
histology of pagets disease
Hand E stain mosaic lines large pink cells- osteoclasts
40
summary of paget's disease
>40yrs rare in asians and africans mono-ostotic 15% remainder polyostotic
41
Aetiology of pagets disease
unknown familial cases - show autosomal pattern of inheritence, incomplete penetrance (mutation 5q35qter - sequestosome 1 gene) parvomyxovirus type particles seen on electon microscopy
42
site prediliction for paget's
Lumbar spine or skull
43
clinical presentation of paget's
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
XR of pagets
bowed cotton wool appearance
45
XR of pagets
bowed cotton wool appearance
46
what is raised in pagets
alk phos
47
macro and micro features of pagets
macro - thickened bone and trabeculae micro - thickened trabeculae, mosaic pattern
48
type of fracture
49
what type of fracture is this
comminuted
50
stages of fracture repair
organisation of haematoma at fracture site (pro-callus) formation of fibrocartilaginous callus mineralisation of fibrocartilaginous callous remodelling of bone along weight bearing lines
51
fracture healing
52
histology of fracture callous
disorganised bone fibrous background
53
trabecular
54
what factors influence fracture healing
type of fracture presence of infection pre-existing systemic condition * neoplasm * metabolic disorders * drugs * vitamin deficiency
55
common sites of osteomyelitis
vertebrae jaw - secondary to dental abscess Toe - secondary to diabetic skin ulcer (>3mm) long bones (usually metaphysis)
56
clinical features of osteomyelitis
malaise, fever, chills, leucocytosis local - pain, swelling, redness 60% positive blood cultures XR - mixed picture, eventually lytic
57
aetiology of osteomyelitis
almost always bacterial rarely fungal routes of infection * haemotogenous * direct extension * traumatic (inc surgery)
58
organisms that cause osteomyelitis
mainly staph aureus
59
histology of osteomyelitis
increase in fibrosis chronic inflammatory cells - lymphocytes and histocytes
60
XR changes in osteomyelitis
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)
61
macroscopic osteomyelitis image
62
Summarise TB
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
histology of osteomyelitis
big pink - trabecular bone fibrosis in the paratrabecular space granuloma - munltinucleated, langerhans type giant cells (horseshoe nuclei) lymphocytes
64
summarise syphillis
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
summarise lyme disease
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
features of lyme disease
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
Rx and Ix of lyme disease
treatment based on prevention vaccine Abx no prophylaxis clinical dx
68
differentiate primary and secondary osteoarthriti
primary - age related secondary - any age, previously damaged or congenitally abnormal joint
69
XR of osteoarthritis
Loss of joint space subchondral sclerosis bone cysts osteophytes
70
identify features of osteoarthritis
wear and tear impact on femoral head
71
what is this pathology in the femoral head
avascular necrosis
72
aetiology of osteoarthritis
not sure biochemical factors biomechanical factors aging genetic
73
results of osteoarthritis
cartilage degeneration fissuring abnormal matrix calcification osteophytes
74
main sites of osteoarthritis
vertebrae and hips +- DIPJ PIPJ of hand +- carpometacarpal and metatarsophalangeal joints
75
histology of synovium in osteoarthritis
chronically inflammed plasma cells lymphocytes
76
summarise rheumatoid arthritis
severe chronic relapsing synovitis unpredicatable course incidence 1% world population >female 30-40yrs
77
aetology of rheumatoid arthritis
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
clinical features of rheumatoid arthritis
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
sites that rheumatoid arthritis effects
small joints hands and feet sparing DIPJ wrists elbows ankles knees
80
XR showing features of rheumatoid arthritis
proximal joint involvement soft tissue swelling
81
histology of rheumatoid arthritis
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
Grimley-sokoloff cells
multinucleate giant cells dont have horseshoe nucleus
83
gout - needle shaped crystal
84
summarise gout
affects any joint - big toe in 90% limited to lwer extremities needle shaped crystals tophus is pathopneumonic lesion
85
macro pathology gout
86
summarise pseudogout
usual age >50yrs crystals of calcium pyrophosphate - knees calcium phsophate (hydroxyapatite) knees and shoulders
87
distinct subsets of gout
* sporadic * metabolic - haemochromatosis, primary HPT, hypoMg, low phos * Hereditary (autosomal dominant) (ANKH mutation, transmembrane glycoprotein, Chr 8q, 5p, younger age) * traumatic

PATHOLOGY (94 decks)

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