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CMS > Bone, bone disorders and arthritis > Flashcards

Bone, bone disorders and arthritis Flashcards

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Introductory Sommelier Exam (CMS) flashcards
1
Q

What is bone formed of?

A

Organic 1/3 - type 1 collagen + other proteins
Inorganic 2/3 - hydroxyapatite

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2
Q

Cellular structure of bone?

A

Osteoblasts
Osteocytes
Osteoclasts
Osteoprogentior cells

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3
Q

What do osteoblasts do?

A
  • Produce bone by secreting collagen matrix + calcium salts
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4
Q

Where do osteocytes come from?

A
  • Once osteoblasts lay down lamellar bone then get trapped in their lacunae and become osteocytes
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5
Q

What do osteocytes do?

A

Maintain bone production and secrete enzymes into matrix to maintain mature bone

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6
Q

What are osteoprogenitor cells? Where found?

A
  • In bone marrow
  • Responsible for producing new osteoblasts and osteocytes
  • Osteoblasts and osteocytes unable to undergo mitosis
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7
Q

What do osteoclasts do?

A
  • Resorb bone
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8
Q

How do osteoclasts resorb bone?

A

Release proteolytic enzymes and hydrochloric acid which breakdown the bone

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9
Q

List some chemical messengers associated with bone resorption

A

Vit D
Para + thyroid hormones
Growth hormones
Ca 2+

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10
Q

List some chemical messengers associated with bone formation

A

Oestrogen
Calcitonin
Androgens

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11
Q

What happens when metabolic homeostasis not maintained?

A

Bone formation > bone resorption
OR
Bone resorption > bone formation

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12
Q

What is 1st type of bone laid down?

A

Woven bone / immature bone

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13
Q

What is immature / woven bone remodelled into?

A

Secondary bone

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14
Q

What 2 types of bone is secondary bone divided into?

A

Cortical / lamellar bone - 80%
Cancellous / trabecular / spongy bone - 20%

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15
Q

Describe structure of cancellous bone

A
  • Low density
  • Spongy appearance
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16
Q

Describe structure of cortical bone

A
  • Dense
  • Compact
  • Contains bone marrow
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17
Q

What is role of vit D in bone metabolism?

A

Increases calcium and phosphate circulating in body

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18
Q

How is vit D obtained?

A

Sun exposure
Diet - oily fish, red meat, egg yolks

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19
Q

What does a deficiency in vit D lead to in adults / children?

A

Children - rickets = bowing of long bones
Adults - osteomalacia = softening of bones, bone aches / pains / fractures

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20
Q

Where does parathyroid hormone come from?

A

Thyroid, bow tie shape gland, 4 parathyroid glands which secrete PTH

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21
Q

What is the role of PTH in bone resorption?

A
  • Promotes kidneys to make vit D
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22
Q

What 2 types of disease are due to malfunctioning PTH gland?

A
  • Primary hyperparathyroidism
  • Secondary hyperparathyroidism
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23
Q

What causes primary hyperparathyroidism, what are the effects?

A
  • Due to adenoma (benign glandular tumour) of a PTH gland
  • Increases PTH level
  • Increases Ca2+ (hypercalcaemia)
  • Promotes bone resorption
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24
Q

What causes secondary hyperparathyroidism, what does it lead to?

A
  • Chronic renal disease gives urinary calcium
  • To compensate PTH gland secretes more PTH
  • Promotes bone resorption
  • Leads to kidney failure - renal osteodystrophy
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25
Q

How might hyperparathyroidism present facially?

A
  • In jaws
  • Central giant cell granuloma
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26
Q

How might hyperparathyroidism present facially?

A
  • In jaws
  • Central giant cell granuloma
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27
Q

How does calcium homeostasis occur? (Briefly)

A
  • PTH secreted
  • Ca 2+ and PO4 3- resorbed and Ca2+ reabsorbed from kidneys
  • Ca 2+ rises
  • Calcitonin secreted
  • Ca2+ excreted in urine and deposited in skeleton
  • Ca 2+ falls
  • Causing PTH to be secreted
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28
Q

What are the 3 stages of healing bone fractures?

A
  1. Early inflammatory
  2. Repair
  3. Remodelling
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29
Q

What happens during early inflammatory stage?

A
  • 1st 2 weeks
  • Bleeding at fracture = form haematoma
  • Inflammatory cells and fibroblasts at clot
  • BVs enter haematoma forming granulation tissue
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30
Q

What happens during repair stage?

A
  • Takes 4-5 weeks
  • Granulation tissue become callus
  • Primary callus becomes secondary callus
  • Osteoid secreted into area forming new bone
  • Proteases degrade ECM
  • Collagen fibres enter area
  • New woven bone created at fracture
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31
Q

What happens during remodelling stage?

A
  • Takes weeks - months to be complete
  • Osteoblasts and osteoclasts coordinate remodelling process
  • Compact and woven bone are redistributed and reproportioned
32
Q

What factors can impact fracture healing? (9)

A
  • Blood supply to site
  • Infection
  • Bone pathology
  • Whether fracture is closed / compound
  • Degree of tissue loss
  • Co-morbidities
  • Use of NSAIDs can impair healing
  • Nutritional status
  • Smoking and alcohol
33
Q

Name some specific bone diseases need to be aware of (4), including types of arthritis (3)

A
  • Osteogenesis imperfecta
  • Osteoporosis
  • Osteopenia
  • Paget’s disease
  • Osteoarthritis
  • Rheumatoid arthritis
  • Ankylosing spondylitis
34
Q

What type of mutation causes osteogenesis imperfecta?

A

Type 1 collagen mutation

35
Q

What is a type 1 collagen mutation?

A

Partial / complete absence of collagen

36
Q

What are the clinical effects of osteogenesis imperfecta?

A
  • Brittle bones
  • Prone to fractures
  • Grey discolouration of sclera
  • Shortened / bowed long bone shapes
37
Q

Oral features of osteogenesis imperfecta?

A

Skeletal class 3
Anterior open bites
Impacted 6s and 7s
Thin grey brown enamel
Dentinogenesis imperfecta
Delayed / premature eruption

38
Q

What causes osteoporosis?

A

Osteoclasts fail to resorb bone

39
Q

Effects of osteoporosis?

A

More bone formation than bone resorption so bone is denser, less elastic recoil

40
Q

Oral features of osteoporosis and why?

A

Thicker bone with increased inorganic components leads to bone marrow being walled off so blood cellular composition deficiency
- Delayed tooth eruption
- Growth impairment
- Nerve entrapment

41
Q

What is osteopenia?

A

Bones thinned mildly

42
Q

What would osteopenia suggest in a young person?

A

Vit D deficiency
Warning sign
Osteopenia expected in older pts

43
Q

What is difference between osteopenia and osteoporosis?

A

Osteoporosis bones are more porous

44
Q

Which lifestyle factors accelerate bone loss?

A

High caffeine
High salt
Low BMI
Smoking
Immobility
Alcohol

45
Q

Which lifestyle factors prevent bone loss?

A

Calcium rich diet
Vitamins, minerals, green leafy vegetables
Fish and nuts

46
Q

Which genetic factors accelerate bone loss?

A

Female
FH osteoporosis

47
Q

Which genetic factors prevent against bone loss?

A

Obesity

48
Q

Which diseases can accelerate bone loss?

A

Cushing’s syndrome
Hyperthyroidism
Hyperparathyroidism

49
Q

Which drugs accelerate bone loss?

A

Corticosteroids
Heparin
Diuretics
Cytotoxic drugs

50
Q

How can osteoporosis be managed? (7)

A

Lifestyle changes
Pain relief methods - paracetamol, opioids, acupuncture
Physiotherapy
Physical aids - walking stick, frame
Medx - Vit D, calcium supplements, Bisphosphonates, hormone replacement therapy
Fall prevention
Surgery for fractures / hip replacements etc.

51
Q

What causes Paget’s disease? (cells)

A

Overactive osteoclasts increase resorption leading to bone destruction

52
Q

How do osteoblasts respond to overactive osteoclasts?

A

Become active and secrete bone which is larger and weaker than normal - leading to bone deformities and fractures

53
Q

Most commonly affected sites in Paget’s disease?

A

Pelvis
Spine

54
Q

Oral relevance of Paget’s disease?

A
  • Dull bone pain, avoid lengthy procedures
  • Enlarged mandible and maxillae -can make restorative / pros work challenging
  • Hypercementosis - PDL ossified makes XLA hard
55
Q

Which pts is Paget’s disease commonly seen in?

A

Over 50 years
(Breast cancer, Paget’s of the nipple, unrelated!!)

56
Q

Tx options for Paget’s?

A

Bisphosphonates
Analgesia
Physio
Walking aides

57
Q

3 main types of Arthritis need to know?

A

Osteoarthritis
Ankylosing spondylitis
Rheumatoid arthritis

58
Q

What is osteoarthritis?

A

Wear and tear degeneration of joints
Low level of chronic inflammation

59
Q

Where is affected by osteoarthritis?

A

Large weight bearing joints e.g. hips, knees
Wrists can be affected

60
Q

Clinical effects of primary osteoarthritis?

A

Synovial softening
Tearing of cartilage
Bone cysts
Bony spurs / osteophytes in the joint

61
Q

When does secondary osteoarthritis develop?

A

Post trauma
Alongside Paget’s / osteoporosis / ankylosing spondylitis

62
Q

What is the classical history of osteoarthritis?

A

Pain and stiffness after movement / using a joint
Non inflammatory swelling of joints

63
Q

Management of osteoarthritis

A
  • Pt education
  • Weight loss
  • Physio and walking aides
  • Analgesia - topical NSAIDs
  • Corticosteroid injections (intra articular for single joints, intra muscular for widespread)
  • Glucosamine supplement
  • Surgery
64
Q

Types of surgery available for osteoarthritis (4)

A
  • Arthrocentesis (visualise joint space and washing out / remove osteophytes)
  • Osteotomy (remove bony deformity)
  • Arthrodesis (surgical fusion of unstable joint)
  • Total joint replacement
65
Q

Define Rheumatoid Arthritis

A

Multi-system inflammatory condition

66
Q

What and who does RA affect?

A

Multiple small joints in extremities e.g. hands and feet
Younger pts under 40

67
Q

What are the classical signs of inflammation?

A

Heat
Pain
Redness
Swelling
Loss of function

68
Q

Key differences between OA and RA? (3)

A
  • RA early morning stiffness / OA stiffness after long periods activity
  • RA under 40s / OA increasing age
  • RA inflammatory / OA non inflammatory
69
Q

Systemic effects of RA?

A
  • Ophthalmological
  • Neurological
  • Pulmonary
  • Haematological
  • Renal
  • Dermatological
  • Gastrointestinal
  • Musculoskeletal
70
Q

Define ankylosing spondylitis

A

Chronic inflammatory arthritis

71
Q

Who and what does ankylosing spondylitis effect?

A

Young males
Neck and spine

72
Q

What is AS initially characterised by?

A

Sacroiliitis - inflammation at sacra-iliac joints where pelvis joins spine

73
Q

What are the later impacts of AS?

A

Vertebrae of spine become fused
Fixed deformity at the neck

74
Q

How should you support a pt with AS in practice?

A
  • Neck support with pillows
  • Shorter appt. for comfort
75
Q

What is the main difference between OA and RA versus AS?

A

In AS distal / peripheral joints of body are uncommonly affected

76
Q

What commonly happens with pts who have an auto immune disease?

A

Accumulate further AI disease

77
Q

Adverse effects of systemic corticosteroid use?

A
  • Mood disturbances
  • Insomnia
  • Anxiety
  • Depression
  • Psychosis
  • Cataracts
  • Glaucoma
  • Hypertension
  • Accelerated atherosclerosis
  • Lymphocytosis
  • Neutrophilia
  • Osteoporosis
  • Increased fracture risk
  • Muscle wasting
  • Atrophy of the skin
  • Bruising of skin
  • Impaired wound healing
  • Acne
  • GI bleeding
  • Gastritis
  • Pancreatitis
  • Obesity
  • Diabetes
  • Infertility
  • Infection susceptibility
  • Delayed growth children
  • Increased appetite
  • Nightmares
  • Fluid retention

CMS (10 decks)

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