Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Hannah's Locomotor > Pathology of Bone and Joints > Flashcards

Pathology of Bone and Joints Flashcards

1
Q

Where do osteocytes reside and how are they sustained?

A

In lacunae

Sustained via canaliculae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What types of cells are osteoprogenitor cells?

A

Mesenchymal stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is contained within the secretory vesicles of the osteoblasts?

A

Alkaline phosphatase

Pyrophosphatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the role of the components of the secretory vesicles of osteoblasts?

A

Increase concentration of Ca2+ and PO4- locally to cause precipitation of hydroxyapatite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a comminuted fracture?

A

Fracture resulting in >2 separate bone components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a compound fracture?

A

Open fracture (break in the skin around the bone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes a stress fracture?

A

Repeated low force injury to a normal bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 4 phases of fracture healing?

A

Bleeding and inflammation (granulation tissue)
Reparative phase with soft callus
Reparative phase with hard callus
Remodelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What occurs with the formation of haematoma following fracture?

A

Fibrin mesh creates framework
Platelets and leukocytes release inflammatory cytokines
Granulation tissue forms
Bone cells are activated to start repair
There is variable necrosis of bone at the fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How long does haematoma formation take?

A

Hours to days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What changes occur with the formation of soft callus in the early reparative phase?

A

Fibrocartilage forms and holds the fractured ends together (but there is no structural rigidity)
Periosteum repairs itself over the outside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When does the reparative phase with soft callus formation occur?

A

Within days (cartilage) to weeks (soft callus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What changes occur with the formation of hard callus in the late reparative phase?

A

Osteoid formation and cartilage removal (woven bone formation and endochondral ossification)
Thickened area of woven bone (rigid but not as strong)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When does the reparative phase with hard callus formation occur?

A

Within weeks to months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What changes occur with bone remodelling?

A

Woven bone remodelled to lamellar bone along lines of stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When does bone remodelling occur?

A

Within months to years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is fracture healing different if bone ends are closely opposed?

A

May not need soft callus at all
Healing will be faster but perhaps not as strong in early stages
More similar to intramembranous ossification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What occurs with fracture non-union?

A

Pseudo-arthrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What causes osteonecrosis? Give common examples

A

Fractures which interrupt the blood supply

E.g. NoF, scaphoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Paget’s disease? What is the pathogenesis?

A

Osteitis deformans
Large, overactive osteoclasts break down bone
There is then production of more bone by osteoblasts, resulting in thick soft cortical and coarse trabecular bone which is easily fractured and may compress nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the 3 stages of Paget’s disease?

A

Osteolytic
Mixed
Osteosclerotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What causes osteomalacia and rickets?

A

Vitamin D deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the pathogenesis of osteomalacia/rickets?

A

Inadequate vitamin D means more PTH is required and phosphate is lost in urine, which leads to impaired bone mineralisation and increased osteoid production
There is an overall loss of structural integrity

24
Q

What are the causes of primary hyperPTH?

A

Parathyroid hyperplasia or tumour

25
Q

What are the causes of secondary hyperPTH?

A

Prolonged hypocalcaemia or hyperphosphataemia (e.g. in renal osteodystrophy)

26
Q

What are the effects of hyperPTH?

A

Increased osteoclastic activity via RANK-L

Associated compensatory increase in osteoblastic activity

27
Q

Name 2 conditions caused by hyperPTH and their features

A

Dissecting osteitis: osteoclasts in trabeculae

Osteitis fibrosa cystica: microfractures and granulation tissue

28
Q

Name 4 symptoms of bony mets

A

Pathological fracture
Hypercalcaemia
Bone marrow failure
Bone pain

29
Q

How do bony mets break down bone?

A

They produce RANK-L or PTHrP

30
Q

List 5 primary tumours which commonly give rise to bony mets and their effects on bone

A 
Breast (osteolytic)
Bronchus (lung; osteolytic)
Thyroid
Kidney
Prostate (osteosclerotic)
31
Q

How is hyaline cartilage perfused?

A

By compression/decompression of cartilage e.g. with movement

32
Q

What are the type A cells in synovium?

A

Macrophage-like

33
Q

What are the type B cells in synovium?

A

Fibroblast-like

34
Q

Which joints are preferentially affected in OA?

A

Hard-working hands and weight-bearing or previously-injured joints

35
Q

What are the symptoms of OA?

A

Deep pain that gets worse with use (insidious onset)

Reduced RoM in joints, with crepitus and osteophyte formation

36
Q

How is OA treated?

A

Physiotherapy
Pain relief
Joint replacement

37
Q

Which joints are preferentially affected in RA?

A

Small joints of hands and/or feet

Symmetrical

38
Q

What are the symptoms of RA?

A 
Morning stiffness (eases with activity) with systemic symptoms (fever, LOW, anaemia)
Warm, swollen joints
Rheumatoid nodules
Eventual destruction and deformity of joints
39
Q

How is RA treated?

A

Using DMARDs (disease-modifying anti-rheumatic drugs)

40
Q

Which joints are preferentially affected in gout?

A

Big toe (podagra)

41
Q

What is the classical affected group in gout?

A

Male

Obesity

42
Q

What is gout associated with risk of?

A

T2DM
Hypertension
CVD

43
Q

How is gout treated?

A

Anti-inflammatory medication
Urate-lowering therapy
Lifestyle change

44
Q

Describe the pathogenesis of OA

A

Damage stimulates chondrocyte proliferation, enzyme/cytokine (e.g. IL-1) production by synovial cells and “unravelling” of cartilage matrix
Release of enzymes (e.g. collagenases, MMPs) from cartilage matrix
Loss of mechanical function
Changes in bone (thickening and microfractures)
Shedding of cartilage (“fibrillation” erosions)
Bone-on-bone contact causes eburnation, production of cysts and osteophytes

45
Q

List 4 possible X-ray findings in OA

A

Loss of load-bearing joint space
Subchondral cysts
Osteophytes
Subchondral sclerosis

46
Q

Describe the pathological process in RA

A

T-helper cells (TH1, TH17) release cytokines (IL-1, IL-6, IL-17, TNF-a)
Induces fibroblasts, macrophages, osteoclasts and B cells, resulting in production of pannus
Collagenases and MMPs breakdown cartilage and bone
Eventual fibrous and then bony union of joints

47
Q

List 6 inflammatory changes seen in joints with RA

A

Mononuclear infiltrate in synovium with GCs
Hyperplasia of synovium with villus formation (becomes pannus)
PMNs and fibrin may be found within joint space
Pannus invades and erodes bone and cartilage
Weakening and destruction of ligaments
Eventual fibrous and then bony union of joints

48
Q

What are 3 important morphological findings in RA

A

Villous hyperplasia
Mononuclear infiltrate
GCs

49
Q

What is a rheumatoid nodule?

A

Granulomatous inflammation

Central necrosis surrounded by epithelioid macrophages, and lymphocytes and fibrosis

50
Q

Name 2 specific tests used to diagnose RA

A 
Rheumatoid factor (RF)
Anti-cyclic citrulinated peptide (anti-CCP)
51
Q

List 3 X-ray findings in RA

A

Subchondral erosions
Uniform joint space loss (not just weight-bearing)
Juxta-articular osteopaenia (thin bone around joints)

52
Q

List some risk factors for RA

A

Genetic: HLA-DRB1, PTPN-22
Female
Increasing age from 25-55
Smoking

53
Q

List 4 morphological features of gouty tophi

A

Granulomatous inflammation (foreign body type) with central urate deposits surrounded by epithelioid macrophages, multinucleate giant cells and fibrosis

54
Q

What is the gold standard for gout diagnosis?

A

Tophus aspiration demonstrating negatively birefringent crystals with PMNs

55
Q

List 3 late-stage findings of gout

A

Punched-out erosions with sclerotic, overhanging edges outside of the joint capsule
Tophi may be visible (even calcified)
Asymmetric distribution

Hannah's Locomotor (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions