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Pathology 3 > metaboolic bone disease > Flashcards

metaboolic bone disease Flashcards

1
Q

too much osteoclast

A

bone wasting diseases

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2
Q

too much osteoblast

A

sclerosing bone disease

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3
Q

osteoperosis

A

porous bone
bone wasting disease
a skeletal disorder characterised by compromised bone strength predisposing to an increased risk of fracture

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4
Q

bone wasting disease example

A

osteoperosis

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5
Q

example sclerosing bone disease

A

osteopetrosis (stone bone)

sclerosteosis

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6
Q

bone strength

A

bone density + bone quality

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7
Q

bone density

A

grams of mineral per volume (BMD, bone mineral density)

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8
Q

bone quality

A

architecture, turnover, damage

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9
Q

osteoporosis incidence

A

most common metabolic bone disease

endemic in wester society

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10
Q

a fracture resulting from a fall of standing height or less due to osteoporosis

A

osteoperotic-related fragility fracture
1 in 2 women and 1 n 3 men will suffer this sort of fracture
usually wrist, vertebrae or hip

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11
Q

mortality of osteoporosis

A

hip and vertebral fracture mortality
risk of death is greatest immediately after fracture
death is not directly attributed to the fracture but rather other chronic diseases that lead to the fracture

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12
Q

morbidity of osteoporosis

A

7% of survivors of fracture have some sort of permanent disability
hip fractures most often associated with osteoporosis-disabilities
eg. pressure sores, UTIs etc, 50% unable to independently walk after fracture

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13
Q

pathophysiology of osteoporosis

A

remodelling - imblanace in processes whch are responsble for acquision and maintenance of bone mass
increase in resorption of bone

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14
Q

type 1 osteoporosis

A

post menopausal
only effects trabecular bone
forearm and spinal fractures most common

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15
Q

type 2 osteoporosis

A

age related
cortical and trabecular bone
hip fracture more common

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16
Q

secondary osteoporossis

A

arises from other causes: usually endocrine diseases (cushings, hypogonadism, hyperparathyroidsm), drugs (anti-retrovirals), glucocorticoids, malabsorbtion, and rheumatological diseases

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17
Q

histology og osteoperosis

A

trabecular and cortical thinning
increased adiposity in marrow
smaller osteoid seams
normal bone width

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18
Q

clinical features of oosteoporosis

A 
mostly asymptomatic 
- pain 
- microfactures 
- fractures
hip, vertebral bodies, radius
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19
Q

clinical diagnoss of osteopoross

A 
serum biochemistry - typically with normal limits 
alkaline phosphatase (ALP - osteoblast marker) 
carboxy terminal telopeptide of type 1 collagen (CTX, bone resorption osteoclast marker)
- serum calcium and serum phosphate
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20
Q

if CTX is raised this may indicate

A

Carboxy terminal telopeptide of type 1 collagen

could ndicate secondary osteoporoosis

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21
Q

clinicall diagnosis of osteoporosis using X ray

A

insensitve means of detection
decreased bone density
cortical thinning
fracture

22
Q

gold standard clinical diagnosis of osteoporosis

A

densitometry

23
Q

densitometry

A

DEXA-T scores
bone mineral density as assessed by Dual-Energy X ray Absorptiometry
difference nbetween measures and mean ‘healthy’ (based on matched gender and ethnic group)

24
Q

T score > -1

A

normal

25
Q

T score -1 ro -2.5

A

ostopaenia

26
Q

T score < -2.5

A

osteoporosis

27
Q

T score < -2.5 and H. of fracture

A

severe osteoporosis

28
Q

T score represents

A

T score represents the number SD a patient is above or below the mean BMD of a young adult

29
Q

osteomalacia

A

defective minelarlisation of organic matrix
bone softening
rickets (children) osteomalaca (adults)

30
Q

pathophysiology of osteomalacia

A

impaired metabolism
most commonly caused by severe vit D deficency
lack of mineralisation effects both quality and quantity of bone
reduced stifness and stength, susceptibe to compressive forces
deformities of weight bearing bones
pathological fractures

31
Q

dietary deficiencies of osteomalacia

A

vit D, calcium, phosphate

32
Q

vitamine D lack may be caused by

A 
endogenous synthesis reduced (lack of sunlight) 
dietary lack (malabsorbtion) 
chronic renal failure, hepatic disease
33
Q

aetiology of rickets

A
  • vit D lack or resistance
  • hypophosohatamia
  • drugs: phenytoiin, aluminium, heavy metals
  • neoplasia - oncogenic osteomalacia
34
Q

clinical features of osteomalacia

A
  • bone is soft (deformity) and fragile
  • bone pain/tenderness
    proximal muscle weakness (hypocalcaemia)
    general low bone mass on radiology
    multiple bilateral cortical lucensies (pseudofractures)
35
Q

biochemistry of osteomalacia

A

alterations in the serum concentrations of calcium, phosphorous, vitamin D

vary according to the underlying disorder but tend to show: low/normal serum calcium, low phosphate, high ALP

36
Q

rickets in children

A

shortened heght due to disruption of metaphysis

warping of femurs

37
Q

primary hyperparathyroidism

A

parathyroid adenoma, parathyroid hyperplasia

parathyroid carcinoma

38
Q

secondary hyperparathyroidism

A

chronic hypocalcaemia
lack of negative feedback
hypersecretion of PTH

39
Q

pathophysiology of primary hyperparathyroidism

A

primary excessive uncontrolled production of parathyroid hormone (PTH) from neoplastic of hyperplastic parathyroid tissue
parathyroid hyperplasia/adenoma/carcinoma
excessive PTH stimulates osteoclastic resorpton
results in marked hyperclacemia

40
Q

effects of excessive PTH

A

increased bone resorption by osteoclasts
mobilisation of Ca/PO4
osteoclastic > osteoblastic activity
diffuse osteopaenia
cysts (macro or micro)
marrow fibrosis
brown tumours (rare) large localised areas of resorpton (jaw, skull, long bones)

41
Q

clinical presentation of hyperparathyroidsim

A

asymptomatic (biochemical abnormality detected incidentally)
signs and symptoms of hypercalcaemia - abnormal cramps, constipation, muscle fatigue, peptic ulceration, renal calculi
bone related disease

42
Q

diagnosis hyperparathyroidism

A

primary/secondary bone changes are identical on radiology
dissecting/tunnelling bone resorption
thinnng cortical and trabecular bone
irregularr new bone formation
x-rays = diffuse osteopaenia and/or circumscribed lucencies subperiosteal eg. phalanges - erosion of tufts

43
Q

hyperparathyroidism microscopically

A

increased osteoclast number and activity wth increased bone resorpton, which a characteristic tunneling or dissecting pattern
mesenchymal cells proliferate in the marrow space and fibrous tissue replaces lost bone

44
Q

paget’s disease

A

osteitis deformans

characterised by disordered bone remodelling

45
Q

3 phases of paget’s disease

A
  1. osetolytic (hyperactivated/large and hypernucleated osteoclasts)
  2. mixed (lytic and blastic)
  3. osteoblastic/sclerotic phases

results in thick, soft, porous bone, prone to compression and deformity

46
Q

aetiology of paget’s disease

A 
idiopathic disorder 
relatively common 
late adult life 
virus (paramyxovirus inclusions) 
genetic
47
Q

paget’s disease my involve

A

one bone - monostotic
multiple bone - polyostotic
most commonly pelvis and skull but virtually any bone

48
Q

paget’s disease sites/symptoms

A

skull - sskull enlargement, cranial nerve compression
thoraco-lumbar spine - pain, neurological cord compression
pelvis sacrum - pain, joint involvement - arthritis
femur, tibia - pain, deformity, pathological fracture

also associates with high ooutput congestive heart failure due to increased shunting of blood to bones
bones are hypervascular and hot

49
Q

paget’s disease - diagnosis

A

often asymptomatic
x ray elevated serum ALP and urinary hydroxyproline
normal serum calcium and phosphorous
rradiology description

50
Q

earrly signs of pagets

A

radiolucency

51
Q

late signs of pagets

A

increased bone density
increased microfractures
loss of distinction between cortex and medulla
may have sharp demarcation between normal and affected bone
may extend into soft tissue if florid disease

52
Q

histology of pagets

A

increased osteoclastic and oosteoblastic activty
acute - primarily women bone, focal mosaic pattern of lamellar bone, resembled jigsaw puzzle with prominent irregular cement lne - osteoclasts present at surface of bone but dont tunnel, in osteollytic phase, hypernucleated osteoclasts may have up to 100 nuclei
chronic - thick trabeculae and thicker bones, highly vascullar fibrocellular marrow replacing the haematopoietic marrow

Pathology 3 (11 decks)

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