Histology/Pathology Flashcards

1
Q

Where do we see:

  • Hyaline cartilage
  • Elastic cartilage
  • Fibrocartilage
A
  • Joints
  • Ears
  • IV discs
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2
Q

What is the structure of compact bone?

A

Concentric layers

haversian systems

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3
Q

What are sharpey’s fibres?

A

Collage type 1 from tendons running into bone at their insertion

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4
Q

In terms of osteoclasts:

  • How many nuclei
  • Origin
  • Secretion product and role? What other cell does this too?
A
  • Multi nucleated
  • granulocytes/macrophage origin
  • HCl and proteases to remodel bone and increase blood calcium.
    Osteocytes can also increase blood calcium
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5
Q

What is the sequence of cartilage replacement with bone?

A
  • Bone forms first around diaphysis to starve underlying cartilage.
  • it dies and blood vessels invade bringing in bone cell progenitors
  • 2nd COF in epiphysis
  • keep growth plate until around 21
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6
Q

What is the structure of new bone or repaired bone and how is it remodelled?

A

Woven bone with collagen in interlacing bundles.
Remodelled into haversian systems
- Osteoclasts tig tunnels into the bone in the right shape.
- Oteoblast line them and create alternating rings of bone to make the haversian system with a canal in the middle

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7
Q

What is the origin of flat bones?

A

Intramembranous ossification

- Mesenchymal stem cells become osteoprogenitor cells which just start secreting osteoid

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8
Q

What is in osteoid?

A

Collagen type 1
Proteins and a few GAGs
Cytokines and GF
Enzymes such as alkaline phosphatase

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9
Q

What are the 3 phases of fracture healing?

A
  1. Inflammation; haematoma formation (osteoblasts, chondrocytes and fibroblasts depending on stability) and granulation tissue
  2. Reparative phase; soft callus (cartilage with periosteum repairing on outside) and hard callus (woven)
  3. Remodelling phase (lamellar)
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10
Q

What is the clinical management of a fracture?

What can be some complications?

A
Reduction and fixation, and minimise any risk factors that slow healing. 
Non union leading to pseudo arthritis
Mal-union
Osteomyelitis 
Osteonecrosis
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11
Q

What % of bone is remodelled each year?

Which bone is usually affected by processes that affect remodelling?

A

10%

Trabecular bone- more metabolically active and larger SA. e.g. in vertebral bodies and femoral neck

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12
Q

What are the components of hyaline cartilage?

A

Collagen type 2
WATER!
proteoglycans
chondrocytes (which secrete the matrix)

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13
Q

Why isn’t synovium an epithelium? What does it allow to pass? what cells make it up?

A

No basement membrane
allows plasma filtrate through
macrophage like cells and fibroblast like cells

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14
Q

What might we see histologically in osteoarthritis?

A
  • Loss of cartilage
  • Subchondral thickening (may see cysts there too)
  • Osteophytes
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15
Q

What type of disease is rheumatoid arthritis? what would you see histologically?

A

Autoimmune systemic inflammatory

  • Mononuclear infiltrate and germinal centres
  • Synovial hyperplasia and villus formation
  • Pannus; invading and eroding bone and cartilage
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16
Q

Compare OA and RA clinical symptoms

A

OA not systemic just in a few joints
RA systemic
OA; deep achy pain with decreased ROM. worse after movement.
RA; warm and swollen, decreased ROM and bad in morning, eases on activity.
OA can see osteophytes, RA can see deformities

17
Q

What is the pathology of gout?

What can it progress to if untreated?

A

Uric acid crystals deposit causing inflammatory cascade

Depositions of tophi

18
Q

What type of inflammation occurs in gout? what would you see histologically in a tophi?

A

granulomatous

see multinucleate giant cells and epitheliod macrophages around urate crystals