musculoskeletal/CT disease Flashcards

1
Q

define arthritis

A

inflammation of the joint

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

define arthrosis

A

non-inflammatory joint disease

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

define arthralgia

A

joint pain

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

bone is mineralised what?

A

connective tissue

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

what are the 3 main features of bone?

A

Load bearing, dynamic, self-repairing

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

bone is dynamic, what does this mean?

A

bone continuously changing - resorbed by osteoclasts, formed by osteoblasts - adapt to changes in stress in the environment and repair

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

bone formation requires the correct levels of what 3 things?

A

Calcium, phosphate and vitamin D

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

Bone and calcium

Bone forms a ? store

? Ca moves from the bone into the ?? and calcium moves from the ? into the extracellular fluid

Ca is lost through the ? and ?

A

calcium

exchangeable
extracellular fluid
gut

gut
urine

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

calcium and bone

Ca levels must be maintained at a specific level as it is involved in ? and ? function

Bone and ?? work together and the use of ? helps promote the correct location of Ca

? increases Ca release from ? by ? and ? renal Ca ?

A

nerve
muscle

Extracellular fluid
PTH

PTH
bone
osteoclasts
reduces
excretion

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

what is osteomalacia?

A

Normal amounts of osteoid matrix formed but doesn’t mineralised properly -> soft and more pliable

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

if osteomalacia occurs during bone formation (children), what is this called?

A

rickets

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

if osteomalacia occurs after bone formation (adults) what is this called?

A

osteomalacia

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

what is osteomalacia and rickets caused by?

A

calcium deficiency

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

cause of osteomalacia

Reduction in plasma ?, increased ? secretion, ? bone ? to release ?, ?? increases ? Ca ?

A

Ca
PTH
osteoclastic
resorption
ca
vitamin D
intestinal
absorption

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

what affect does osteomalacia have on bone?

A

Bones bend under pressure - bowing

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

what affects does hypocalcaemia have on the body? 3

A

Muscle weakness
Carpal muscle spasm and facial twitching from VII tapping

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

investigations for osteomalacia

Serum Ca -> decreased

Serum phosphate -> decreased

Alkaline phosphate -> very high

Plasma creatinine -> increase if renal cause

Plasm PTH -> increase if secondary hyperparathyroidism

A

Serum Ca -> decreased

Serum phosphate -> decreased

Alkaline phosphate -> very high

Plasma creatinine -> increase if renal cause

Plasm PTH -> increase if secondary hyperparathyroidism

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

in osteomalacia why is serum phosphate decreased?

A

osteomalacia is often caused by vitamin D deficiency, vitamin D is responsible for the absorption of Ca AND phosphate

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

in osteomalacia why is alkaline phosphate very high?

A

due to increased osteoblastic activity

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

in osteomalacia why is plasma creatinine increased?

A

if renal cause because the kidneys are meant to filter it out into the urine - kidney disease

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

how does kidney disease lead osteomalacia?

A

kidneys produce an enzyme that converts vitamin D into its active form, kidney disease means less is active leading to vitamin D deficiency

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

in osteomalacia why does plasma PTH increase?

A

increases in response to low Ca

secondary hyperparathyroidism - lots of PTH produced not caused by parathyroid gland damage

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

how is osteomalacia managed? 4

A

correct the cause
- Control GI disease - malabsorption
- Sunlight exposure
- Dietary vitamin D
- control kidney disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is osteoporosis?

A

Reduced quantity of normally mineralised bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

remember osteoporosis is an inevitable age related change

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what endocrine risk factors are there for osteoporosis? 3

A

oestrogen (menopause) deficiency
testosterone deficiency
Cushing’s syndrome (increased corticosteroid blood levels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what patient risk factors are there for osteoporosis?

A

inactivity
smoking
alcohol
poor dietary Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what medical drugs are risk factors for osteoporosis?

A

steroids and anti-epileptics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what effects does osteoporosis have on the body? 2

A

Increased bone fracture risk

Vertebrae compress and crack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what happens as a result of vertebrae compression and cracks from osteoporosis? 4

A

Height loss

Kyphosis - rounding of the upper spine

Scoliosis - lateral shift of vertebrae

Nerve root compression - back pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how is osteoporosis prevented? 2

A

Build maximal peak bone mass (occurs at age 24-35) through exercise and dietary calcium

Reduce rate of bone mass loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

how is the rate of bone mass loses reduced in osteoporosis?

A

exercise

Ca intake

reduce hormone related effects - HRT

reduce drug related effect - steroids and anti-epileptic

consider preventative drugs
- Bisphosphonates reduce the number of osteoclasts so less bone can be removed preserving it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

name 3 symptoms of joint disease?

A

Pain
Immobility stiffness
Loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are the signs of joint disease? 4

A

Swelling
Deformity
Redness
Crepitus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are the 3 types of swelling from joint disease?

A

fluctuant, bony or synovial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

how does joint disease lead to deformity?

A

destruction causes change in joint surfaces, bones meet differently changing the external appearance of the joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

in joint disease what does redness suggest?

A

Suggests inflammation due to infection and high vascular content

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is crepitus from joint disease?

A

Noise made by the bone during moving due to loss of cartilaginous covering to the bone ends

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what investigations are done for joint disease? 4

A

radiography
blood test
arthroscopy and biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what blood tests are done to investigate joint disease?

A

Inflammatory markers - C-reactive protein

Autoimmune disease - rheumatoid factors

Extractable nuclear antigens

Anti DS-DNA, anti-nuclear antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is acute monoarthropathies?

A

Acute inflammation of a single joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

name 2 common causes of acute monoarthropathies (acute inflammation of one joint)

A

Infection - septic arthritis
Crystal arthropathy - gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

acute monoarthropathies

In gout ??? cause irritation to the joint surface which causes ? and I?

A

uric acid crystals
swelling
inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is the cause of gout?

A

hyperuricaemia - high levels of uric acid in the blood

drug induced, genetics, nucleic acid breakdown (chemo), tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what joint is usually affected by gout?

A

big toe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is the one time of gout?

A

rapid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

how is gout treated?

A

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what drug should u avoid prescribing with gout?

A

aspirin as it interferes with the removal of uric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

in gout Drug treatments my give oral ulceration

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

osteoarthritis is a degenerative joint disease. what joints does it affect?

A

affects the weight bearing joints or joint damage -> knees and hips

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

symptoms of osteoarthritis 3

A

Pain - worse during activity, better with rest

Brief morning stiffness

Slowly progressive over years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are the signs of osteoarthritis
(radiographs)

A

radiographs
- Loss of joint space and subchondral sclerosis
- Osteophyte lipping at joint edge

joint swelling and deformity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what alters the disease progression of osteoarthritis?

A

nothing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

how is pain managed in osteoarthritis without medication? 3

A

Increasing muscle strength around the joint

Weight loss

Walking aids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what drugs are used to treat the pain of osteoarthritis?

A

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

prosthetic replacement can be done for osteoarthritis. what is the reason for this?

A

pain not function

57
Q

what is the dental aspect of chronic NSAID use? 2

A

Oral ulceration

Bleeding tendency - anti-platelet

58
Q

what is the dental consideration for joint replacements?

A

Antibiotic prophylaxis may be required but usually not needed

59
Q

Rheumatoid arthritis is initially a disease of the ? with gradual ???

A

synovium
inflammatory joint destruction

60
Q

rheumatoid arthritis

There are different patterns of joint involvement dependent on whether rheumatoid factor (autoantibody) is present
? - rheumatoid factor present
? - rheumatoid factor not present

A

reumatoid factor

sero-positive

sero-negative

61
Q

symptoms of rheumatoid arthritis 7

A

Slow onset (hands and feet) then spread to potentially all synovial structures

Symmetrical polyarthritis - synovitis

Can get systemic symptoms due to RA being a manifestation of a systemic illness

Fatigue

Morning stiffness

Joint pain, swelling and stiffness

Decreased range of motion

62
Q

early signs of Rheumatoid arthritis 3

A

Symmetrical synovitis of
- Metacarpal joints
- Proximal metacarpal joints
- Wrist joints

63
Q

late signs of rheumatoid arthritis

A

destruction of the joint

Subluxation of wrist

Loss of abduction and external rotation of shoulders

Flexion of elbows and knees

Deformity of the feet and ankles

64
Q

what are the two investigations done for rheumatoid arthritis

A

radiographs
blood tests

65
Q

how does osteoarthritis present on radiographs? 5

A

erosions, loss of joint space, deformity , joint destruction and secondary osteoarthritis

66
Q

how does osteoarthritis present in blood tests?

A

normochromic normocytic anaemia - RBCs normal in colour and size but there are few of them

67
Q

what medicines are used to manage rheumatoid arthritis?

A

analgesics

NSAIDs

disease modifying drugs
- hydroxychloroquine and methotrexate

steroids

68
Q

what surgeries can be done to restore the function from rheumatoid arthritis? 4

A

Excision of inflamed synovium

Joint replacement

Joint fusion

Osteotomy

69
Q

what alters the disease progression of rheumatoid arthritis?

A

disease modifying drugs can slow the progress of the disease
- hydroxychloroquine
- methotrexate

70
Q

complications from rheumatoid arthritis

Increased risk of ?

Higher risk of ???

? manifestations

inflammation of ??

Secondary ? syndrome

? - pressure points

? - amyloid fibrils build up in organs and tissues - can lead to kidney failure and death

Drugs

A

infection
peptic ulcer disease
pulmonary
blood vessels
Sjogren’s
subcutaneous nodules
amyloidosis

71
Q

dental aspects of the drugs taken for rheumatoid arthritis

NSAIDs and sulfasalazine (DMARD) can cause -> ?

steroids, azathioprine (immune modulator) can cause -> ?

sulfasalazine, gold and hydroxychloroquine (disease modifying drug) can cause -> ?

methotrexate can cause -> ?

hydroxychloroquine can cause?

A

bleeding

infection risk

oral lichenoid reactions

oral ulceration

oral pigmentation

72
Q

Atlanto-occipital instability arises from RA

what is it?

A

Damage to the ligaments in the neck which can result in slipping of the structures in the upper part of the neck so more chance of ligaments rupturing if trauma occurs and bones infringing onto the spinal chord causing spinal damage.

73
Q

name a sero-negative spondyloarthritides

A

Ankylosing spondylitis

74
Q

what is ankylosing spondylitis?

A

Spinal joint arthritis

75
Q

how does ankylosing spondylitis differ from rheumatoid arthritis?

A

is on axial skeleton (neck and vertebrae)

76
Q

ankylosing spondylitis causes what?

A

Narrowed and inflamed discs and fusion of the vertebrae leads to challenges turning, twisting and bending

77
Q

ankylosing spondylitis is associated with what?

A

Associates with HLA-B27

78
Q

what are the effects of ankylosing spondylitis? 4

A

Lower back pain

Limited back and neck movement

Limited chest expansion - breathing compromised as bones fused

Kyphosis - cervical spine tipping forward due to bone fusion

79
Q

what is the treatment for ankylosing spondylitis? 4

A

Analgesia and NSAIDs to manage pain

Physiotherapy and occupational therapy to maintain function and independent living

Disease modifying drugs and immune modulators to slow the progression

Surgery to restore function

80
Q

dental aspects of ankylosing spondylitis

A

Difficulty lying down

GA hazardous due to limited mouth opening and neck flexion

TMJ involvement possible

81
Q

what are the two types of connective tissue disease?

A

autoimmune diseases

vasculitic diseases

82
Q

remember autoimmune disease is a spectrum disorder that can present as multiple conditions

A
83
Q

is Systemic lupus erythematosis (SLE) a autoimmune or vasculitic connective tissue disease?

A

autoimmune disease

84
Q

what are the two types of the autoimmune disease Systemic lupus erythematosis (SLE)

A

discoid lupus
systemic lupus

85
Q

what is discoid lupus?

A

tissue changes with no blood autoantibodies

86
Q

what is systemic lupus?

A

organ changes and autoantibodies

87
Q

what antibodies are in the connective tissue autoimmune disease systemic lupus erythematosis? 3

A

Anti-nuclear antibody (ANA)

Anti-double-strand DNA (dsDNA

Anti-Ro antibody (Ro)

88
Q

what causes the connective tissue autoimmune disease systemic lupus erythematosis?

A

Genetic predisposition but environmental trigger - allergy triggers immune system

89
Q

dental aspects of LSE 7

A

Anaemia - oral ulceration and GA risk

Thrombocytopenia - bleeding risk

Renal disease - impaired drug metabolism

Drug reactions can trigger photosensitivity
- Butterfly zygomatic rash

Steroid and immunosuppressive therapy - malignancy risk

Lichenoid oral reactions

Oral pigmentation from hydroxychloroquine use

90
Q

what is anti phospholipid antibody syndrome?

A

Group of lupus pts who have a marker in their blood termed lupus anticoagulant

91
Q

what is lupus anticoagulant?

A

Not a true anticoagulant - blood only anticoaguable in test tube not body

92
Q

what specific antibodies are present in phospholipid antibody syndrome (lupus)? 2

A

Antiphospholipid (aPL)

Anticardiolipin (aCL)

93
Q

what is primary phospholipid antibody syndrome (lupus)?

A

no other disease associated with it

94
Q

what is secondary phospholipid antibody syndrome (lupus)?

A

associated with other conditions of the type - lupus, rheumatoid arthritis or Sjogren’s

95
Q

phospholipid antibody syndrome (lupus)

Pt are ? putting them at risk of ??? and ??

pt are often on ? - don’t stop without advice of a clinician

A

hypercoaguable
deep vein thrombosis
pulmonary emboli

anticoagulants

96
Q

what is systemic sclerosis (scleroderma)

A

autoimmune connective tissue disease

Elastic tissue of the body is replaced by connective fibrous tissue -> loss of ability to stretch and bend tissues such as the skin as joints and muscles moves

97
Q

features of systemic sclerosis (scleroderma)

A

sclerodactyly

Telangiectasia

Nailfold capillaroscopy

Raynaud’s

Loss of elasticity is also internal - bowel problems

Renal failure

malabsorption

98
Q

what is sclerodactyly?

A

Contractures of the fingers as the skin will no longer stretch around the joints - cant straighten fingers

99
Q

what is telangiectasia?

A

Little haemangiomas on the face

100
Q

what is nailfold capillararoscopy

A

Little haemangiomas in the nail beds

101
Q

what is Raynaud’s?

A

blood vessel narrowing - commonly fingers - can lead to necrosis

102
Q

what antibodies are found in systemic sclerosis (scleroderma)? 2

A

Localised - anticentromere antibodies

Generalised - anti-Scl-70 antibodies

103
Q

dental aspects of systemic sclerosis (scleroderma)

A

Involvement of peri-oral tissues - can’t open mouth properly

Dysphagia and reflux oesophagitis - dental erosion and swallowing difficulties

Drug metabolism - cardiac and renal vasculitis disease

Widening of PDL space

104
Q

what is sjogrens syndrome? 3

A

undifferentiated connective tissue disease

autoimmune disease - associated with autoantibodies but is not caused by them

complement activation cuases tissue damage of salivary and lacrimal glands

105
Q

what autoantibodies r associated with sjogren’s syndrome? 3

A

Anti-nuclear antibody (ANA)

Anti-Ro antibody (Ro)

Anti-La antibody (La)

106
Q

what are the 3 main groups of sjogren’s syndrome?

A

sicca syndrome
primary sjogren’s
secondary sjogren’s

107
Q

what is sicca syndrome Sjögren’s syndrome?

A

only dry eyes and mouth

108
Q

what is primary sjogren’s syndrome?

A

not associated with any other disease

109
Q

what is secondary Sjögren’s syndrome?

A

associated with another connective tissue disease

110
Q

oral and dental implications of Sjögren’s syndrome?

A

Oral infection

Caries risk

Denture retention

Sialosis

salivary lymphoma

111
Q

what is sialosis?

A

swelling of salivary glands

112
Q

what is salivary lymphoma?

A

unilateral gland size change, usually after years, caused by chronic activation of the lymphoid tissue

113
Q

remember that Sjögren’s syndrome is associated with blood autoantibodies that don’t cause the disease (they are found in healthy people) but their pattern varies from disease to disease

A
114
Q

what is vasculitic disease?

A

Inflammation within blood vessel walls causing narrowing and ischaemia

115
Q

vasculitic disease may present as what? 2

A

oral inflammatory masses or ulcers (tissue necrosis)

116
Q

vasculitic disease is characterised by what?

A

the size of the blood vessel

117
Q

name 2 large vessel vasculitis diseases

A

Giant cell (temporal) arteritis (commonly temporal artery involved)

Polymyalgia rheumatica

118
Q

what is the presentation of Giant cell (temporal) arteritis? 3

A

headaches/facial pain

Chewing claudication - pain after chewing
◊ Occlusion of central retinal artery - blindness

119
Q

remember Giant cell (temporal) arteritis is a facial pain emergency - if suspected as risk of blindness

A
120
Q

what is the presentation of Polymyalgia rheumatica?

A

Mainly seen in shoulder and hip regions

Morning pain and stiffness of muscles

121
Q

name 2 medium vessel vasculitic diseases

A

Polyarteritis nodosa
Kawasaki disease

122
Q

Kawasaki disease mainly affects adults or children?

A

children - mucocutaneous lymph node syndrome

123
Q

what are the clinical features of Kawasaki disease? 4

A

Fever and lymphadenopathy

Crusting/cracked tongue

Strawberry tongue and erythematous mucosa

Peeling rash on hands and feet

124
Q

how is Kawasaki disease treated?

A

steroids and may need antibiotics to recover

125
Q

name a small vessel vasculitic disease

A

Wegener’s Granulomatosis

126
Q

what is Wegener’s granulomatosis?

A

Inflammatory condition that can lead to destruction of hard and soft tissues of the face and oral cavity

127
Q

what is the antibody found in Wegener’s granulomatosis?

A

antineutrophil

128
Q

what is the appearance of Wegener’s granulomatosis?

A

spongy red - almost strawberry like

129
Q

what is the dental impact of vasculitis disease?

A

steroid precautions
- Giant cell arteritis
- Wegener’s granulomatosis
- Kawasaki disease

130
Q

when is the term fibromyalgia used?

A
  • Used when there are symptoms but no evidence of disease - joint and muscle pain and functional disorders
131
Q

is there a cure for connective tissue diseases?

A

no as there is no known cause

132
Q

what is the management of connective tissue diseases, both immune and vasculitic? 4

A

Immunosuppression - dependant on the disease activity

Analgesics NSAIDs to manage joint/muscle symptoms

Immune modulating treatment

Systemic steroids - prednisolone

133
Q

what is Sjögren’s syndrome?

A

an autoimmune disease that causes chronic inflammation of the tear and saliva glands

134
Q

orofacial features of sjogren’s syndrome 8

A

Xerostomia and dry eyes

Erythema and lobulation of tongue

Difficulty talking and swallowing

Altered taste

Oral fungal and bacterial infections

Increased incidence of lymphoma

Tiredness

Salivary glands swelling

135
Q

what is the management of Sjögren’s syndrome? 2

A

Artificial saliva
- Orthana - oral spray - can prescribe on NHS - neutral pH
- Glandosane - oral spray - can prescribe on NHS - pH 5.75
- Salivese
- BioXtra/Biotene - can prescribe on NHS - close to neutral pH
- Salinum

Salivary stimulants
- Salivix pastilles - can prescribe on NHS - malic acid
- Sugar free gum
- Sugar free sweets
- Saliva stimulating tablets

136
Q

how are fungal infections managed (candida)

A

Anti-fungals
- Nystatin (rinse)
- Miconazole (gel)

137
Q

what chairside advise is given to a pt with sjogren’s syndrome? 4

A

Topical fluoride application

OHI

Dietary advice - sugar free

Atomiser - water

138
Q

how is Sjögren’s syndrome managed during appts? 6

A

Vaseline to lips

Lubricate mucosa with 3-in-1

Wet mirror

Retract tissues with wet swab

Offer water frequently

Avoid suction where possible