Chapter 26: Bone, joints and soft tissue tumors.

Question 1

Name the two types of joints:

Answer 1

Synovial and non-synovial. (eg shoulder, and cranium respectively)

Question 2

What is synovial fluid made up from?

Answer 2

Plasma filttrate with hyaluronic acid.

Question 3

What is osteoarthritis?

Answer 3

Characterized by degredation of cartilage and following structural and functional failure of synovial membrane.

Question 4

Pathogenesis of osteoarthritis (OA):

Answer 4

Stems from degredation of articular cartilage and its repair. This is down to changes in the chondrocytes which happens through 3 phases:

1) Chondrocyte injury - biochemical or genetical
2) early OA - chondrocytes proliferate and makes: inflammatory mediators, collagens, proteoglycans, proteaseswhich rermodels the cartilage matrix.
3) Late OA - chronic inflammation leads to chondrocyte drop out and bone changes.

TGF-beta important because it induces mmps

Question 5

What does articular mean?

Answer 5

Concerning joints.

Question 6

What is Rheumatoid arthritis?

Answer 6

Chronic joint inflamation of autoimmune origin - non-suppurative proliferative and inflammatory synovitis.

Question 7

What is suppuration?

Answer 7

The production of pus.

Question 8

RA pathogenesis:

Answer 8

Genrally thought to be down to self antigen or microbial agent related to arthritis.

typically t-cell (CD4+) mediated - more specifically Th17 (IL-17 activates neutrophils and granulocytes) and Th1 (activates macrophages) - macrophages secrete TNF and IL-1 which stimulates synovial cells to degrade hyaline cartilage.

TNF very important!!!!

Synovium contains germinal centers and antigan producing plasma cells - especially anti-citrullinated proteins (arg changed to citr)

Question 9

What are rheumatoid factors?

Answer 9

Antibodies which bind to Fc portion of IgG and might deposition in joints in RA.

Question 10

What is JIA?

Answer 10

Juvenile idiopathic athritis. Before age 16 and for more than 6 weeks. Similar to AR in pathogenesis.

Question 11

Infectious arthritis?

Answer 11

Caused by synovial infections by microorganisms.

Question 12

What is gout?

Answer 12

Acute arthritis because of monosodium urate deposition in the joints. This leads to inflammation through macrophages which take up the MSU and lets out cytokines (IL-1) as a function of inflammasome activation.

Question 13

What is bone made up from?

Answer 13

1) 35 % osteoid (organic - mainly type 1 collagen)

2) 65 % mineral compund (hydroxyapatite - calcium and phosphate)

Question 14

name the bonce cells:

Answer 14

1) osteoblasts
2) ostepcytes
3) osteclasts (macrophages)

Question 15

Name the hormones in bone development and maintaining:

Answer 15

1) GH
2) T3
3) FGF
4) BMP´s (bone morphogenic proteins related to tgf-beta)

Question 16

What is osteopenia and osteoporosis?

Answer 16

Osteopenia = loss of bone mass
Osteoporosis = loss of bone mass which leads to higher risk of bone breaking (2.5 standard deviations under normal)

Question 17

What is the causes of osteoporosis?

Answer 17

1) age
2) reduced physical activity = lack of mechanical stimulation
3) genetic factors - key regulators of osteoclasts
4) calcium nutritional state - also PTH and vitamin D
5) Decreased estrogen

Question 18

What is paget disease?

Answer 18

Increased but nor correct bone mass. Generally not known but some harbor mutations in genes for NFkappaB - so osteoclast activity.

Question 19

How does PTH affect the calcium homeostasis?

Answer 19

1) osteoclast activation
2) increased resorption of calcium from renal tubules
3) Increased urinary secretion of phosphatases
4) Increased synthesis of active vitamin D - more Ca from gut and Activation of osteoclasts

Question 20

What is renal osteodystrophy?

Answer 20

The changes in bone structure following chronic kidney diseases.

Question 21

What is osteomalacia?

Answer 21

Vitamin D defficiency - bones not sufficiently mineralized.

Question 22

Hyperparathyroidism types:

Answer 22

Primary = autonomous secretion of PTH
Secondary = renal disease

Question 23

Mechanisms of secondary hyperparathyroidism:

Answer 23

1) Tubular dysfunction
2) general kidney failure
3) decreased production of excreted factors