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Msk > Other Bone Problems > Flashcards

Other Bone Problems Flashcards

0
Q

What is the risk of osteoporosis based on

A

Peak bone mass
+
Rate of bone loss

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1
Q

What is osteoporosis

A

Lots of trabecula spongy bone mass – >

form POROUS (porosis..) bone – >

increased risk of fracture

Despite
normal bone mineralisation +
lab values of calcium + phosphate

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2
Q

What age is the peak bone mass occurring

A

30

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3
Q

What three things determine how high the peak bone mass will be?

A

Diet
Exercise
Inherited vitamin D receptor

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4
Q

What are the determinants of bone loss rate?

A

Diet
Exercise
For women – oestrogen:
@menopause – >lose oestrogen – >lose bone mass rapid I.e. increased bone resorbtion

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5
Q

What test is used to check for osteoporosis?

And what is the T score to determine osteoporosis?

A

Bone mineral density test = DEXA

T score < -2.5

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6
Q

Two types of osteoporosis?

A

Type 1 = postmenopausal

Type to senile > 70 years

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7
Q

Where do you fractures usually occur in osteoporosis?

A

Weight-bearing areas:

Vertebrae –> decreased height + kyphosis
Hip - femoral neck
Distal radius - COLLES fracture

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8
Q

In osteoporosis what are the lab works like?

A

Normal – calcium/phosphate/ALP = HALLMARK

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9
Q

What is the prophylaxis treatment for osteoporosis

A

Weight-bearing exercise

Decent calcium/vitamin D in adulthood/childhood

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10
Q

Treatments for osteoporosis

A

Bisphosphonate is:
attach to bone – >osteoclast eat bisphosphonate – > osteoclast apoptosis – > decreased bone resorption

Oestrogen replacement therapy – could cause breast cancer

Denosumsb - monoclonal antibody against RANKL

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11
Q

What drug is contra indicated for osteoporosis

A

Glucocorticoids

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12
Q

What happens in pagets disease of bone

A

Osteoclast + osteoblast function in balance

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13
Q

Four stages of pagets disease of bone

A

1.osteoclastic lytic stage:
Osteoclast goes crazy – resorb bone without permission of osteoblast

  1. Mixed osteoclast osteoblast stage:
    Bone very weak – osteoblast recognises need to lay down bone ASAP to protect
  2. Osteoblastic sclerotic stage:
    Osteoclast burns out –> osteoblasts only lays bone in rush -> sclerotic thick bone
  3. Quiescent stage decreased osteoblast osteoclast activity
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14
Q

What age does Padgett’s affect?
Aetiology?
Localisation?

A

60 years
Unknown – possibly viral – infect osteoblast
Localised = 1+ bones BUT not @ entire skeleton

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15
Q

What do you see on histology for pageants disease of bone

A

Cement lines @bone = not sealed
-> Thick bone BUT fragile – >

Mosaic pattern of lamellar bone

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16
Q

Clinical features of pagets

A 
Pain
ALP⬆️
Grrrrrr lion face
Ear - hearing loss
Thicken calvarium @school – > ⬆️Hat size
17
Q

Treatment for Paget bone disease

A

Calcitonin – inhibit osteoclast

BISPHOSPHONATES

18
Q

2 complications are Padgett disease of bone

A

Remodelling of bone – > form arteriovenous shunts
-> hard pushed to aviation – >
high output cardiac failure

Osteoplast produces loads of bone – >
osteoblasts mutate – >osteosarcoma

19
Q

In Rickets + osteomalacia what is the problem

A

Defective mineralisation of osteoid due to vitamin D deficiency

20
Q

What are the risk factors for rickets/osteomalacia

A

Decreased sun exposure
Shit diet
Malabsorption – vitamin D = fat soluble vitamin
Liver + renal failure – need it to activate vitamin D

21
Q

How does a child with rickets presents?

A

Frontal bossing – enlarged forehead = Osteoid deposition

Pigeon breast deformity:
inward bending of ribs +
anterior protrusion of sternum

Rachitic rosary(beads THASBY!!!):
Osteoid deposition @costochondral junction

Bowlegged – >1 years start walking

22
Q

Who get osteomalacia

A

Vitamin D deficiency in adults

23
Q

Lab work for osteomalacia/Ricketts

A

Decreased vitamin D – >decreased serum calcium- >

Increased PTH secretion – >

  • decreased phosphate serum
  • osteoblast hyperactivity – >increased ALP
24
Q

What happens in achondroplasia

A

Disorder of cartilage proliferation @ growth plate

25
Q

Explain the pathogenesis of achondroplasia

A

85% – Sporadic mutation
15% – autosomal dominant + full penetrance – lethal
->

Activating mutation @ fibroblast growth factor 3
(FGF – 3) – >

Inhibit chondrocyte proliferation – >impaired cartilage proliferation @growth plate – >

Short extremities only

26
Q

At embryology what are the two ways to form bone

A

1.intramembranous:
Connective-tissue matrix –>
form woven bone of skull + chest + flat bones of wrist

  1. Endochondral bone formation:
    Establish cartilage matrix -> cartilage dies -> calcifies + mineralised -> form woven BONE - long
    -> lamellar bone
27
Q

Explain how the chondrocyte make cartilage at the growth plate

A

Chondrocytes make cartilage – >
growth plate expands – >
Chondrocytes die @ edge of plate – >
dead chondrocytes replaced with bone = longer

In achondroplasia there’s a problem with the chondrocyte proliferation hence why the short extremities

28
Q

Explain osteogenesis imperfecta

A

Autosomal dominant defect in collagen type one synthesis – >
Congenital defect in formation – >weak bone

29
Q

Clinical features of osteogenesis imperfecta

A

Blue sclera –
thinning of squirrel collagen – >
reveal choroidal veins = blue

Hearing loss – break malleus incus stapes

Multiple fractures because of shit collagen

30
Q

Explain osteoPETROSIS pathogenesis

A

Inherited defect of bone result shown due to defective osteoclast – >
thick dense bones prone to fracture

31
Q

Where is the mutation in osteopetrosis

A

Carbonic anhydrase 2 mutation –

Need acid environment to resorb bone i.e. remove calcium

32
Q

What does x-ray reveal osteopetrosis

A

Bone in bone appearance – can’t see dark space outside of medulla

33
Q

Explainwhy we get pancytopenia in osteopetrosis

A

CA deficiency – >bone thickens – >
Fills medullary/marrow space =
MYELOPHTHISIC process – > pancytopenia

34
Q

Explain why there is vision and hearing loss in osteopetrosis

A

CA deficiency – >bone thickens – >

compress cranial nerves = vision and hearing decrease

35
Q

Explain why we get hydrocephalus in osteopetrosis

A

CA deficiency – >
bone thickens @Foramen Magnum = narrow – >

Hydrocephalus

36
Q

Explain rather get renal tubular acidosis and osteopetrosis

A

Decreased CA – >Decreased H+ – >

can’t excrete enough H+ & No net gain of HCO3 ->

Acidotic

37
Q

Treatment for osteopetrosis and why?

A

Bone marrow transplant

Haematopoiesis well –>
make normal monocytes – >
make normal macrophages e.g. osteoclasts

38
Q

Most common reason for dwarfism

A

Achondroplasia

39
Q

Explain the relationship between oestrogen and osteoporosis

A

Oestrogen inhibits apoptosis in osteoblasts
Oestrogen induces apoptosis in osteoclasts

At menopause get XS remodelling cycles and XS bone resorption

Msk (10 decks)

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