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Pathology Term 4 > Week 6 - Ageing > Flashcards

Week 6 - Ageing Flashcards

Fractures, Tumours, Ageing, Others

1
Q

What is calcification?

A

calcium deposition

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2
Q

What is ossification?

A

bone formation

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3
Q

What is an osteoid/callus and what are the 2 types?

A

-protein mould of future bone –> embryo/fracture

  1. soft callus –> no calcium (early)
  2. hard callus –> with calcium (late)

*soft = not seen on xray, hard callus is

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4
Q

Which cells produce, lyse and mantain the bone?

A

production –> osteoblast
lysis –> osteoclast
maintain –> osteocyte

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5
Q

Which artery supplies bones?

A

nutrient artery in nutrient foramen (diaphysis/metaphysis) –> epiphysis has a different blood supply

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6
Q

How are lamellae orientated?

A

along lines of stress

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7
Q

What is at the centre of lamellae?

A

haversian canals

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8
Q

What is the name of the crystal found in bone?

A

calcium hydroxyapatite in collgen protein framework (matrix)

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9
Q

What % of bone is recycled per year?

A

5-10%

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10
Q

At what age do we begin to lose bone each year and what % is it?

A

> 30yrs, 0.5% bone loss per year (physiological ageing)

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11
Q

What is osteoporosis?

A

-excess lysis of bone or less production –> loss of bone density –> osteoporosis

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12
Q

What is new bone formation AKA and what is mature bone AKA?

A

woven bone - irregular, immature, fetus/growth plate/fracture (no lamellae)

lamellar bone - mature, regular bone (compact, solid + spongy with marrow)

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13
Q

What hormones/vitamins/minerals are involved in the control of bone recycling?

A
  • GH
  • insulin
  • Vit D
  • Vit C
  • calcium
  • PTH
  • calcitonin
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14
Q

Outline the pathology of fracture healing

A

Fracture

  • 1 week –> haematoma, inflammation
  • 1-3wks –> soft callus (osteoid - not seen on xray)
  • 3-6wks –> hard callus (seen on xray)
  • 8wks –> remodelling (*stress - normal bone again)
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15
Q

True or False?

Remodelling only occurs with stress

A

True

-i.e. required to remove support after a fracture (~8wks)

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16
Q

What is the microscopy of woven bone - osteoid?

A
  1. irregular osteoid trabeculae
  2. lack of lamellae
  3. prominent lining by osteoblasts
  4. irregularly arranged osteoclasts
  5. granulation tissue
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17
Q

What is microscopy of lamellae/mature bone?

A
  • marrow
  • lamellae
  • osteocytes
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18
Q

What are the systemic factors affecting bone healing?

A
  • age*
  • nutrition, vitamin/minerals
  • immune status
  • systemic diseases –> chronic disease; diabetes*
  • drugs –> steroids
  • genetic disorders –> hemophilia, etc
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19
Q

What are the local factors affecting bone healing?

A
  • immobilisation*
  • alignment –> improper reduction
  • infection - debris, dead tissue in wound
  • joint involvement
  • damage to nerves/BVs
  • bone pathology –> tumours, osteoprosis, etc
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20
Q

What are the short term complications of bone healing?

A
  • haemorrhage, vascular injury*
  • nerve/visceral injury*
  • crush syndrome*
  • fat embolism
  • renal failure
  • shock, DIC
  • thromboembolism
  • infection –> septicemia
  • tetanus, gas gangrene
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21
Q

What are the long term complications of bone healing?

A
  • delayed union
  • non-union
  • mal-union –> deformity
  • growth disturbances
  • contractures
  • avascular necrosis
  • osteomyelitis (infection)
  • pseudoarthrosis (false joint formation)
  • osteoarthritis
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22
Q

What terms are used for dead bone and new bone formation in bone necrosis following a fracture?

A

dead bone –> sequestrum

new bone –> involucrum

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23
Q 
True or False?
CT neoplasms (sarcomas) are characterised by cells in a matrix/stroma with no tight junctions
A

True

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24
Q

What is the commonest malignant CT tumour?

A

2 = Ewing’s sarcoma

osteosarcoma

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25
Q

What is the commonest benign bone tumour?

A

osteochondroma

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26
Q

What is the commonest benign and malignant soft tissue tumour?

A

benign –> lipoma

malignant –> liposarcoma

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27
Q

What are the typical gross and microscopic features of sarcomas?

A

Gross:

  • soft
  • fleshy
  • grey
  • infiltrative

Micro:
-pleomorphic spindle cells

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28
Q

What does a single vs multiple osteochondromas on a patient suggest?

A

single –> acquired

multiple –> familial

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29
Q

What do osteochondromas typically present like?

A
  • outpocket of hard nodules (bone) with a cartilage cap

- marrow can sometimes enter the nodule

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30
Q

What is the microscopy of giant cell tumour?

A
  • aggressive

- cystic lesions with plenty of osteoclasts/giant cells (“osteoclastoma”)

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31
Q

How does a patient with osteosarcoma typically initially present?

A

-pain + fever

32
Q

Which body part is most commonly affected by osteosarcoma and where specifically in the bone is affected commonly?

A
  • knee (60% cases) –> #2= shoulder

- affects METAPHYSIS of long bones

33
Q

What gene mutation is commonly associated with osteosarcoma cases?

A

Rb gene mutations in >60% of cases

34
Q

What are the microscopic and characteristic radiographic features of osteosarcoma?

A

Micro:

  • irregular fine lacy osteoid
  • pleomorphic cells

X-Ray:

  • microcalcification (pulmonary spread)
  • particularly on metaphysis (epiphysis = spared)
35
Q

What is Codman’s triangle?

A
  • in osteosarcoma, there is swelling of tissue around bone causing lifting of periosteum
  • lifting of periosteum –> reactive bone formation in a triangular-shaped fashion (Codman’s triangle)
36
Q

Which cells are affected in Ewing’s sarcoma?

A
  • primitive blast cells (like neuroblastoma) –> embryonic bone tumour
  • small blue cells in sheets, no osteoid
37
Q

Which mutation is commonly seen in pts. with Ewing’s sarcoma?

A

95% pts. have a translocation –> t(11;22)

38
Q

What is normal degeneration from ageing known as?

A

-senile atrophy (physiologic)

39
Q

What are some examples of pathologic causes of degeneration?

A
  • decreased workload –> disuse atrophy of muscles
  • loss of nerve –> denervation atrophy
  • decr. blood supply –> brain atrophy
  • malnutrition –> marasmus
  • loss of endocrine support –> Addison’s
40
Q

Which chromosome are the biological clock genes located on?

A

1

41
Q

What % of our ageing is genetically determined vs. acquired causes?

A

genetic (biological clock genes) –> 60%

acquired –> 40%

42
Q

What happens to telomeres with each cell division?

A

-progressively lost with each division until they disappear

43
Q

What is progeria?

A
  • disorder of ageing
  • Hutchinson-Gilford synd, Werner synd, etc
  • rare, genertics
  • normal at birth but develop accelerated ageing
  • develop AS, scleroderma, CVS disorders, dementia, etc. in childhood –> live till late teen

*Down’s synd = another example of ageing disorder

44
Q

What are the senile changes?

A
  • balding
  • cataracts
  • senile dementia
  • deafness
  • loss of teeth
  • dermal elastosis
  • HTN/IHD
  • osteoporosis
  • prostatic hyperplasia (M)
  • diverticular disease
  • degenerative joint disease
  • osteoarthritis
  • ankle oedema (heart failure)
  • decreased height, weight, muscle
  • altered posture
  • increased fat, wrinkles
45
Q

What is solar elastosis?

A

-loss of elastin and collagen in the superficial dermis –> replaced by amorphous protein (hard) –> loss of skin turgor (elasticity)

46
Q

What is osteoporosis?

A
  • reduced bone mass –> normal composition
  • osteoblast/clast function imbalance
  • loss of strength –> deformity –> fractures
47
Q

What are the 2 types of primary osteoporosis?

A

Type 1 –> post-menopausal

Type 2 –> senile

48
Q

What are the secondary causes of osteoporosis?

A
  • immobilisation (i.e. post-fracture)
  • endocrine
  • myeloma
  • nutrition
  • drugs (steroids; chemo)
  • alcohol
49
Q

What happens to bone in osteoporosis?

A
  • thinning of vertical trabeculae

- loss of horizontal trabeculae

50
Q

Where is osteoporosis more common in postmenopausal women?

A
  • vertebrae

- neck of femur

51
Q

What is the pathophysiology of osteoporosis?

A
  • genetics + physical activity + endocrine/nutrition/drugs –> PEAK BONE MASS
  • Menopause (1) + Ageing (2) contribute to loss of peak bone mass –> osteoporosis
  • menoupause –> decreased serum estrogen, increased inflammatory cytokines, increased RANK/RANKL expression
  • increased osteoclast activity
  • ageing –> decreased replicative activity of osteoprogenitor cells/synthetic activity of osteoblasts/biologic activity of matrix-bound growth factors/physical activity
52
Q

What is compartment syndrome?

A

inflammation –> increased osteofascial compartment pressure –> muscle ischaemia + necrosis (due to i.e. trauma, bleeds, insect bites, etc)

53
Q

What is crush syndrome?

A
  • muscle crush common in limbs
  • road traffic accidents
  • pressure –> necrosis –> inflammation
  • *c.f. compartment syndrome where inflammation causes an increased compartment pressure, crush syndrome is initiated by direct pressure leading to inflammation
54
Q

What are the clinical features of compartment + crush syndrome?

A
  • pain, swelling, inflammation, mottling (necrosis), blisters
  • toxins enter circulation
55
Q

What are the complications of compartment/crush syndrome?

A
  • rhabdomyolysis
  • DIC (due to toxins)
  • acute renal failure (myoglobin has nephrotoxic metabolites)
  • uremia
  • acidosis
56
Q

What is the Tx for compartment/crush syndrome?

A

fasciotomy

-to releave osteofascial pressure

57
Q

What are the 2 types of skeletal muscle fibres?

A 
Type 1
-slow fibres
-fat
-red
"One Slow Fat Red Ox"

Type 2

  • pale
  • fast-acting fibres
58
Q

What is myositis and muscular dystrophy?

A 
myositis = inflammation of muscle
dystrophy = embryonic disorganisation (congenital)
59
Q

What is myopathy?

A
  • non-inflammatory abnormality

- toxic/congenital (alcohol, drugs)

60
Q

What gene mutation is present in muscular dystrophy?

A

-mutation of dystrophin on X chromosome p21

61
Q

Why is muscular dystrophy known as pseudohypertrophy?

A

-initially there is hypertrophy due to fat + fibrosis –> then atrophy

62
Q

What are the 2 types of muscular dystrophy?

A

Duchenne MD (DMD)

  • common
  • early 5yrs
  • severe –> death by 20yrs

Becker MD (BMD)

  • rare
  • late
  • less severe
63
Q

How does muscular dystrophy typically present?

A
  • normal at birth
  • starts with pelvic + limb weakness (even though muscles appear large) –> characteristic ladder sign (pt. has to climb on themselves to stand up from the ground)
  • death typically by heart failure
64
Q

What are the 3 types of myositis and which is most common?

A
  1. polymyositis (rheumatica)***
  2. dermatomyositis
  3. inclusion body myositis
65
Q

What is polymyositis?

A
  • polymyositis rheumatica
  • autoimmune (usually seen with other autoimmune disorders)
  • CD8 cytotoxic T cell mediated myofibre necrosis
  • Tx. with steroids
66
Q

What is dermatomyositis?

A
  • common in children
  • paraneoplastic (esp. lung) in adults
  • periseptal (outer) fibre inflammation + SKIN inflammation
67
Q

What is inclusion body myositis?

A
  • old age (>60)
  • amyloid + tau protein deposition in muscle fibres
  • age-associated degeneration –> like alzheimer’s*
68
Q

What can cause toxic myopathy?

A
  • thyrotoxicosis
  • alcohol –> binge drinking
  • drugs –> statins
69
Q

What is myasthenia gravis?

A
  • autoimmune disorder (Ab to acetylcholine receptors at NMJ) –> block receptors resulting in muscle paralysis
  • muscle weakness –> esp. extra occular muscles (ptosis/diplopia) –> then becomes generalised
  • Tx. = acetylcholine esterase, immunosuppression
  • assoc. with thymic hyperplasia (65%)/thymoma (15%)
70
Q

What is osteogenesis imperfecta?

A
  • congenital bone disorder
  • brittle bone, type 1 collagen
  • severe deformity
71
Q

What is osteopetrosis?

A
  • congenital bone disorder
  • stone bone
  • osteoclast deficiency
72
Q

What is the commonest cause of dwarfism?

A
  • achondroplasia
  • congenital bone disorder
  • chondrocyte abnormality –> cartilage deficiency
  • central body normal, limbs affected –> disproportionate growth
73
Q

What is paget’s disease?

A
  • pain, sclerosis, deformity, fracture, nerve compression/deafness (if skull affected)
  • can led to secondary osteosarcoma (late stage)
  1. excess osteoclastic activity (osteolytic stage)
  2. excess osteoblastic activity (osteoblastic stage)
  3. finally, exhaustion of cellular activity (osteosclerotic stage)
74
Q

What are the gross + microscopic features of paget’s disease?

A

Gross:

  • thick
  • deformed
  • mosaic

Micro:

  • mosaic lamellae
  • sclerosis
  • increased osteoclasts + blasts
75
Q

What is vitamin D deficiency referred to as in children vs. adults?

A

children (before closure of epiphyseal plates) –> rickets

adults –> osteomalacia

76
Q

What is vitamin d deficiency and what are the features of it?

A
  • defective mineralisation
  • more osteoid (protein)/less calcium –> bones are soft

*bowing of legs, lumbar lordosis, rachitic rosary, harrison groove, pigeon breast, frontal bossing

77
Q

What is lipomatosis?

A
  • multiple lipomas

- genetic/congenital cause

Pathology Term 4 (6 decks)

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