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Y3- I & W > pathology bone disorders > Flashcards

pathology bone disorders Flashcards

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1
Q

what is bone

A

it is a rigid inflexible mineralised connective tissue

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2
Q

what is the ECM of bone mineralised by

A

ca/PO salts

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3
Q

why do we need bone

A

structural purposes

metabolic

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4
Q

what structural purposes do we need bone for

A

physical integrity
protection of squishy organs
insertion of muscles and tendons

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5
Q

what is haematopoiesis

A

The formation development and maturation of blood cells

Happens in the bone marrow (majority) and the liver for adults

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6
Q

where does haematopoesis occur in embryos

A

the yolk sac

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7
Q

what is bone made from

A

one is the non cellular mineralised matriculates

cellular component

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8
Q

what composes the non cellular mineralised material

A

type 1 collagen
calcium hydroxyapatite crystals
regulatory proteins and Growth factors

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9
Q

what is type 1 collagen called int he context of bone

A

osteoid

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10
Q

what is the cellular component of bone

A

osteoblasts
osteocytes
osteoclasts
stem cells which give rise to the osteoblasts

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11
Q

what do osteoblasts do

A

they form the bone matrix
mesenchymal in origin
secretory function and secrete the osteoid
involved in mineralisation

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12
Q

what do osteocytes do

A

entrapped osteoblasts which are inactive

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13
Q

what do osteoclasts do

A

from the macrophage lineage

sit at the surface of the bone and take place in bone resorption

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14
Q

how can we group different types of bone

A

by maturity

by location

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15
Q

what are the different types of bone which vary by maturity

A

woven bone

lamellar bone

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16
Q

describe woven bone

A

immature bone where the bone is laid down very quickly by osteoblasts
later remodelled to lamellar bone
more chance of fracturing

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17
Q

describe lamellar bone

A

bone is laid down in parallel bands

normal healthy bone

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18
Q

what are the 2 types of lamellar bone

A

compact bone

cancellous/trebecular bone

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19
Q

which type of bone is most immature

A

woven bone

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20
Q

what are the different types of bone which vary by location

A

cortical

cancellous

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21
Q

describe the bone remodelling cycle

A 
activation 
resorptions 
reversal 
formation
termination
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22
Q

what happens in the activation stage of bone remodelling

A

we need hormones or damage to activate the osteoblasts
OBs secrete cytokines
osteoclasts start to secret substances that break down the bone

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23
Q

what happens in the resorptions phase of bone remodelling

A

macrophage lineage osteoclasts secrete substances that resorp the bone
the the osteoclasts migrate

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24
Q

what happens in the removal phase of bone remodelling

A

monocytes clear debris for the bone formation

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25
what happens in the formation phase of bone remodelling
the osteoblasts are recruited they secrete a new matrix which is mineralised OBs now sit on new bone and some incorporated as osteocytes
26
what is osteoarthritis
progressive erosion of articular cartilage | it is not just erosion but a complex impbalance of damage and repair
27
what can we see in osteoarthritis
the underlying bone becoming exposed and then leading to cysts and pain
28
what is the common symptom of osteoarthritis
joint space narrowing Pain and functional limitation Morning stiffness
29
what are the common signs of osteoarthritis
Crepitus( crunching) Restricted movements Bony enlargement Instability
30
what are the primary causes of osteoarthritis
unknown causes
31
what is the secondary causes of osteoarthritis
pre existing joint disease eg RA, gout metabolic disease eg acromegaly systemic disease eg haemophilia
32
what are the investigations we can do for osteoarthritis
blood tests erythrocyte sedimentation rate CRP- c reactive protein rheumatoid factor is NEGATIVE
33
what is the management of osteoarthritis
hydrotherapy, weight loss NSAIDS joint replacement
34
describe RA
It is an autoimmune disease | resulting in inflammation of the synovialm of the joints but can be systemic and affect the lungs
35
risk factors for RA
women more likely strong association with the HLA antigen assoc with epstein barr virus can also occur due to contribution of the oral microbiome
36
how does RA cause damage in the body
occurs from a process called citrullination of self antigens- changes in self antigens and they are recognised as abnormal and the immune system attacks them
37
what happens to the synovial cavity
becomes hyper cellular which leads to inflammation and damage
38
what is pannus formations
inflammatory infiltrate forming a mass in the tissues
39
what are some systemic manifestations of RA
carpal tunnel syndrome pericarditis lymphadenopathy sjogrens syndrome
40
investigations for RA
CRP anti citrullinated peptide antibodies rheumatoid factor +
41
management for RA
no cure NSAIDS disease modifying anti rheumatic drugs
42
what is ankylosis
abnormal stiffening in joints due to bony fusion
43
describe pagets disease
It Is a disorder of bone turnover/remodelling There is increased osteoclastic bone resorption and increase of new bone formation Increased formation > resorption but it is woven bone
44
what is the aetiology of pagets disease
unknown but can be viral/microbial genetic history
45
symptoms of pagets disease
bone and joint pain cotton wool skull appearance hypercementosis high alkaline + phosphate levels
46
what are the phases of pagets disease
hot mixed cold
47
what is the hot phase of pagets disease
high osteoclast activity
48
what is the mixed phase of pagets disease
There is a little bit of osteoblast activity as well as osteoclast activity
49
what is the cold phase of pagets disease
inactive burn out phase
50
treatment for pagets disease and osteoporosis
bisphosphonates
51
what do bisphosphonates do
inhibit osteoclast activity and recruitment
52
what is the issue with bisphosphonates
need to be careful of BRONJ bisphosphonate related osteonecrosis of the jaw
53
describe osteomyelitis
→ It is inflammation of the bone or bone marrow | → Usually always due to infection
54
how can we get osteomyelitis
through blood stream extension from the adj site direct implantation of the organisms
55
what bacterium is the most common cause of osteomyelitis
S aureus
56
what is the clinical presentation of osteomyelitis
○ Fever ○ Localised bone pain ○ Overlying tenderness/erythema ○ Hard to diagnose so we can use a bone biopsy
57
treatment of osteomyelitis
immobilise antibiotics maybe drainage
58
why might we get osteomyelitis of the jae
Polymicrobial | Odontogenic infection
59
why might people get tuberculous osteomyelitis
Haematogenous spread from reactivated primary TB focus
60
what are the subtypes of osteomyelitis
focal sclerosis diffuse scleorising proliferative periostitis
61
what are the types of fracture
``` simple compound comminuted displaced stress greenstick pathologic ```
62
what is the phases of fracture healing
1. inflammatory phase 2. reparative phase 3. remodelling phase
63
what happens in the inflammatory phase
1st week Haematoma forms- source of hemopoietic cells and growth factor Macrophages, neutrophils and platelets release Cytokines Fibroblasts come to the fracture site Granulation tissue forms around the fracture ends Neovascularisation Osteoblasts, chondrocytes( lay down cartilage) and fibroblasts leading to callus forming
64
what happens in the endochondral phase
Cartilage provides provisional stabilisation | Endochondral ossification converts soft callus to hard callus woven bone
65
what happens in the remodelling phase
The hard woven bone is remodelled into lamellar bone
66
describe osteonecrosis
infarction of the bone marrow
67
why does osteonecrosis occur
due to alcohol steroids fracture
68
what is the underlying cause of osteonecrosis
vascular insufficiency due to mechanical injury to the blood vessel eg thromboembolism
69
presentations of osteonecrosis
→ Joint pain shoulder or hip → Can be asymptomatic--> collapse of articular bone MRI shows bone marrow oedema
70
management of osteonecrosis
→ Symptomatic → Surgical decompression → Grafts joint replacement
71
what happens if we have a drop in the calcium serum levels
PT glands to secrete PTH which increases calcium by → Increased osteoclast bone resorption → Increased calcium intestinal absorption → Increased synthesis of 1.25- dihydroxy vitamin D3 → Increased renal tubular resorption Ca → Increased renal excretion PO4
72
what happens when we have low calcium levels
bone resorption increases
73
what is the other name for rickets
osteomalacia
74
describe osteomalacia
The osteoid has not been mineralised and therefore defective mineralisation of the epiphyseal plate in children leading to weakened bones
75
what is rickets
osteomalacia in children
76
what is the aetiology of rickets
Aetiology is anything that interferes with bone mineralisation Eg deficient intake or absorption of vitamin D( nutritional, malabsorption Renal failure Inhibitors of mineralisation Defective vitamin D receptors
77
what are the dental complications of vitamin D deficiency
``` Familial hypophosphatemia Large pulp chamber Thin enamel Dentinal defects which is globular Prone to abscesses ```
78
what is hyperparathyroidism
Anything pathological which causes increase in PTH
79
what does an increase of PTH do
``` → Osteoclast bone resorption → Intestinal Ca absorption → synthesis of 1.25- dihydroxy vitamin D3 → renal tubular resorption Ca → renal excretion PO4 ```
80
what are the different types of hyperthyroidism
primary hyperthyroidism secondary tertiary hyperthyroidism
81
what is the most common cause of asymptomatic hypercalcaemia
primary hyperthyroidism | caused by adenoma, hyperplasia, malignancy
82
what are the symptoms of hyperthyroidism
bones, stones, groans and moans Bones- disease and pain Stones- renal stones Groans- GI groans including constipation nausea, gallstones and pancreatitis Moans- CNS alterations, depression, lethargy
83
describe osteogenesis imperfecta
brittle bone disease
84
what are the gene mutations for osteogenesis imperfecta
COL1A1 | COL1A2
85
dental manifestations of osteogenesis imperfecta
Dentinogenesis imperfecta type II In OI type IB Blue discoloured teeth
86
what is endochondral ossification
Cartilage is used as a template and is replaced by bone
87
what is intramembranous ossification
In the skull, maxilla and mandible they are formed by the deposition of bone within primitive mesenchymal tissue
88
what are the craniofacial issues with bone growth and achondroplasia
``` → Macrocephaly → Flattened nasal bridge → Hypoplasia of midfacial structures → Maxillary hypoplasia → Relative overgrowth of the mandible → Narrowing of anterior plate Orthodontic intervention ```

Y3- I & W (21 decks)

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