Bone/MS Flashcards

1
Q

What are the signs of osteoarthritis?

A

1) Hands - Generalised wasting, Heberdens (DIP)/ Bouchards (PIP) Nodes, reduced finger flexion
2) Hips - Reduced rotation, Antalgic gait/ Trendelenburg test (less weight on one side)
3) Knee - Quads wasting, Crepitus, Cool effusion (fluid in joint but not infected)

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2
Q

What are the symptoms of osteoarthritis?

A

1) Short lived/absent early morning stiffness (<30mins)
2) Localised pain increased on weight bearing
3) Advanced disease - pain non-weight bearing (raised intraosseous pressure)
4) Can be asymptomatic

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3
Q

What are the radiographic changes seen in osteoarthritis?

A
  • Joint space narrowing
  • Sclerotic bone (whiter)
  • Subcondral cartilage cysts forming
  • Osteophytes (benign outgrowths of bone)
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4
Q

What is the management of osteoarthritis

a) Pharmacological
b) Non-pharmacological
c) Surgical

A

a) NSAIDS, Analgesics, Coxibs, injections (steroid/hyaluronan)
b) Quad exercises, weight loss, aids, education, glucosamine sulphate 1.5g OD
c) Total hip/knee replacements

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5
Q

What is osteoartritis?

A

Mechanically driven rheumatological disease caused by wearing of cartilage and low grade inflammation

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6
Q

What is the criteria for rheumatoid arthritis?

A
  • Symmetrical
  • Affects hand joints
  • Affects >3 areas
  • Morning pain/stiffness >60mins
  • Rheumatoid nodules
  • Serum rheumatoid factor (RF)
  • Radiographic changes
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7
Q

Is there genetic susceptibility for rheumatoid arthritis?

A
  • Onset may be associated HLA DR4

- Severity predicted by presence of TNF-alpha polymorphisms, HLA DR4 and Rheumatoid Factor

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8
Q

What are the radiographic changes seen in rheumatoid arthritis? a) Early b) Late

A

a) Peri-articular osteoporosis (thinner blacker bone) and peri-articular erosions (synovitis on bare areas of bone)
b) Joint space narrowing, subluxation/dislocation, ankylosis

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9
Q

Name some extra-articular manifestations of rheumatoid arthritis

A
  • Nodules
  • Lymphadenopathy
  • Lung - pleurisy/effusion
  • Secondary Sjogrens
  • Heart - pericarditits
  • Skin - tight shiny atrophic
  • Muscle - atrophy
  • Anaemia of chronic disease
  • Vasculitis (inflamed blood vessels)
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10
Q

What is the management of rheumatoid arthritis?

A

Education, joint protection, painkillers, NSAIDs, DMARDs (Disease modifying anti-rheumatic drugs to slow progression), surgery unlikely as multisystem disease

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11
Q

Name some commonly used drugs for treating rheumatoid arthritis

A
  • Methotrexate
  • Steroids (IM - treat symptoms but not long term)
  • Hydroxychloroquine
  • Sulphasalazine
  • Leflunomide
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12
Q

In advanced treatment, name the following drugs

a) Anti-TNF
b) Anti CD20 monoclonal
c) Anti IL6
d) Anti CTLA4 Ig

A

a) Infliximab
b) Rituximab
c) Tocilizumab
d) Abatacept

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13
Q

What is ankylosing spondylitis?

A

A chronic inflammatory disease that is axial (along skeleton). HLA B27 assocaited. ? posture as cervical spine at 110 degrees to thoracic.

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14
Q

Ankylosing spondylitis is a multisystem disease, what else does it effect?

A
  • Eyes = iritis and conjunctivitis
  • Pulmonary = upper lobe fibrosis, spinal deformaties leads to secondary thoracic deformity
  • Fatigue = anaemia of chronic disease
  • Aortic valve disease
  • Decreased mouth opening for intubation
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15
Q

What is the treatment for ankylosing spondylitis?

A

Daily exercise, education, NSAIDs, DMARDs (for peripheral athritis, Anti-TNF drugs, surgery for spinal complications

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16
Q

What are the clinical and radiographic features of ankylosing spondylitis?

A

Bamboo spine radiographically as calcification between joint spaces
? shaped spine clinically
Gradual onset - teens/20s affected
Morning or nocturnal stiffness
Persistence more than 6 weeks
Improvement with exercise (pt may report worse at weekend)
Improvement with NSAIDs

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17
Q

What is psoriatic arthritis?

A

Chronic inflammatory disease (mono/oligo/polyarthritis)

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18
Q

What are the clinical features of psoriatic arthritis?

A

Nail bed psoriasis
Involves axial and can involve DIP
Dactylitis (inflammation of finger bones)
Iritis
Inflammation at ligament/tendon insertion
RF usually negative
Psoriasis precedes arthritis in 75%

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19
Q

What is the treatment of psoriatic arthritis?

A

Education, analgesia, NSAIDS, DMARDs (for arthritis alone = sulfasalazine, for arthritis and psoriasis = methotrexate/anti TNF), surgery if painful joint deformity e.g. arthrodesis

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20
Q

What is Reiters syndrome?

A

Reactive arthritis with conjunctivitis and uveitis, may be associated with rash on hands and feeth, self-limiting

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21
Q

What is reactive arthritis?

A

Acute or chronic inflammatory disease (mono/oligo)

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22
Q

What is Sjogrens Syndrome?

A

Dry eyes, dry mouth, connective tissue disorder. Associated with anti-Ro and anti-La antibodies, RF and hypergammaglobulinaemia. Lymphocytic infiltration of lacrimal and salivary glands. F:M 9:1

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23
Q

What are the clinical features of Sjogrens?

A
  • Xerostomia
  • Fatigue
  • Dry eyes
  • Interstitial lung disease
  • Arthalgia/arthritis
  • Raynauds phenomenon
  • Renal tubular acidosis
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24
Q

What is the treatment of Sjogrens syndrome?

A

Incurable, lubricants, steroids and immunosupressants reserved for pneumonitis, gloerular nephritis and vasculitis, Risk of lymphoma.

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25
Q

What rhuematological diseases can cause problems with the TMJ?

A
Degenerative = osteoarthritis
Inflammatory = rheumatoid arthritis, psoriatic arthritis, idiopathic jeuvenile arthritis, crystal disease (gout), infection
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26
Q

What is sterile synovitis in reactive arthritis?

A

Asymmetric oligoarthritis, onset peaks 10-14 days after distant infection

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27
Q

What is the aetiology of a fracture?

A
  • Direct force
  • Indirect force e.g. spiral long bone fractures
  • Stress fractures - repeated minor injury
  • Pathological - abnormal bone fractures more easily
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28
Q

When making a diagnosis of a fracture, what should the clinician look for when inspecting?

A
  • General appearance e.g. gyarding, gait
  • Colour
  • Swelling - oedema or compartment syndrome
  • Bruisng
  • Open (compound)
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29
Q

When making a diagnosis of a fracture, what should the clinician look for when palpating?

A

Swelling, distal pulses, capillary refill, temperature, neurological ie test reflexes

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30
Q

What is compartment syndrome?

A

Swelling/bleeding causing swelling in tight fascial planes affecting blood supply and nerves - limb threatening. Pulseless, Pale, Paraesthesia, Pain, Paralyisis. Must open to relieve pressure

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31
Q

What is contre-coup fracture?

A

Where the mandible fractures in 2 places

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32
Q

What radiographic imaging is required for a fracture?

A

2 views at 90 degrees. CT is plain films inconclusive. MRI rare as this is soft tissue

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33
Q

If a mandible is fractures between a lower 2 and 3, what is this?

A

Parasynthesis fracture

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34
Q

What two views are good for a fractured condyle?

A

PA mandible and DPT

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35
Q

Why is an open fracture in the mouth not usually infected? What is the time scale for fixing an open fracture?

A

Mouth well vascularised

Within 24 hours

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36
Q

What are the 5 types of fracture when classified? How should you describe it in an osce?

A

Closed, open/compound, transverse, greenstick, comminuted

1) Site, joint involvement, traumatic or pathological, extent, classification

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37
Q

What occurs in Phase 1 of fracture healing?

A

Inflammatory

  • Bleeding and clot formation
  • Acute inflammatory response
  • Bone necrosis at fracture end
  • macrophage infiltration
  • Formation of vascular granulation tissue
38
Q

What occurs in Phase 2 of fracture healing?

A

Reparative

  • Ideally cortex to cortex
  • Provisional callus (primary non-mature bone)
  • Medullary reaction - recruitment of osteoblasts
  • Over 6-12 weeks direct ossification occurs throughout fracture gap
39
Q

What occurs in Phase 3 of fracture healing?

A

Remodelling

- occurs up to 2 years

40
Q

In fracture management, what does ORIF stand for?

A

Open Reduction Internal Fixation

41
Q

What is the purpose of reduction and fixation?

A
Reduction = re-establish anatomy 
Fixation = intrinsic stability - external=casts/frames, internal = plates/screws
42
Q

What are the immediate complications of a fracture?

A

Haemorrhage, nerve damage, tissue loss, internal organs, compartment syndrome

43
Q

What are the early complications of a fracture?

A
Local = necrosis, infection, failure of alignment/fixation 
General = fat embolism (confusion, respiratory difficulty, rash), Crush syndrome (renal failure), DVT
44
Q

What are the late complications of a fracture?

A

Malunion, delayed union (mobility may cause fibrous union - no callus), infections, joint stiffness

45
Q

What are the implications of dental treatment and joint replacement?

A

No requirement for antibiotic cover, immunocompromised can be considered on individual basis die to bacteraemia risk

46
Q

What are the protheses made from in joint replacements and why?

A

Stainless steel, titianium, polymers and combination. Material needs to osseointegrate

47
Q

In calcium metabolism:

a) how is carried around the body?
b) how much do we absorb from the intestine?
c) where is it filtered?

A

a) In ECF as Ca2+ or protein bound to albumin (metabolically inactive)
b) 1/5 of calcium eaten
c) Kidneys, tubules resorb 98%. Calcium lost in urine = calcium gained in intestines

48
Q

In Vitamin D metabolism:

a) What is the major and minor source?
b) Where is it activated?
c) How does it govern calcium metabolism?

A

a) Major = sunlight acts on cholesterol to Vit D3. Minor = plants and supplements D2, meat and fish D3
b) Kidneys where secondary hydroxylation occurs
c) Increases calcium absorption, increases urinary calcium reabsorption, increases bone mineralisation

49
Q

If the levels of serum calcium a) drop b) rise, what does the parathyroid gland do?

A

a) Secretes more PTH to raise calcium

b) Stops secreting PTH to allow calcium to stabilise

50
Q

What does PTH do?

A
  • PTH acts of vit D metabolism
  • PTH acts on kidney by stimulating 1 hydroxylase enzyme to activate vit D
  • Calcitrol released acts on small intestine to increase calcium absorption and acts on the bone to release calcium and phosphorus
51
Q

Why is having a high PTH bad for bone health?

A

Uses bone as source of calcium (calcium removed)

52
Q

What is the role of

a) Osteoclasts
b) Osteoblasts

A

a) Resorb bone for 10-20 days then undergo apoptosis

b) Form new bone comprising of protein matrix, fibrous element (collagen), calcium (stiffness from salts)

53
Q

For metabolic bone disorders, blood tests are carried out. What do the following results show?

a) Calcium total
b) Alkaline phosphatase
c) Albumin
d) Phosphate
e) Bone turnover markers e.g. DPD or CTX or ‘Beta cross laps’

A

a) Ionised and protein bound Ca should be 50/50
b) released by osteoblasts (also liver so run LFTs)
c) allows correction of abnormal calcium binding, if kidney disease then low level albumin so low level calcium
d) In kidney failure phosphate increased so CaPh precipitates out so calcium decreases
e) In special circumstances, shows breakdown product of bone collagen so if increased then osteoclast activity increased

54
Q

What does radioisotope scanning show in metabolic bone disorders?

A

Radioisotope taken up by osteoblasts and laid down in bone where active. Hotspots in areas of increased turnover e.g. fracture healing, infection and cancer

55
Q

What does Dual energy xray absorptiometry show (DEXA)?

A

Assesses bone mineral density for diagnosis osteoporosis

56
Q

What is a) primary and b) secondary hyperparathyroidism?

A

a) Abnormal parathyroid gland, excessive PTH secretion, hypercalcaemia
b) Normal gland, PTH raised but in order to raise calcium which is low for another reason

57
Q

What does vit D deficiency cause in a) adults b) children?

A

a) Osteomalacia

b) Rickets

58
Q

What are the clinical signs of rickets?

A
  • Tibia vara = bowed legs as bones soft
  • Epiphyses of bone become expanded causing lumps under skin
  • Abnormal ribs
  • Rickety rosary = chosto-chondral junction enlarged
  • Harrisons sulcus = pulling of diaphragm and muscles cause bone to be indrawn
59
Q

What are the clinical signs of osteomalacia?

A
  • Bone pain, weakness
  • Tetany (rare) - muscle spasm from low Ca
  • Low calcium with secondary hyperPTH
  • Low phosphate with ALP raised from increased bone turnover
60
Q

What is the treatment for osteomalacia?

A

Vit D replacement (Fultium D3 800 units, Dekristol 20,000 units weekly, Adcal D3 0.5g calcium 400units Vit D 2xday)
Active metabolites calcitrol and alphacacidol used in renal disease and HypoPTH to increase calcium levels

61
Q

What is Pagets disease?

A

Uncoordinated bone remodelling causing pain, deformity (moth eaten/poorly defined on xray, mosaic pattern under microscope), increased fracture risk and compression of nerves (in skull this causes cranial nerve palsies and deafness), saber tibia (thicker bone)
Pt may be in cardiac failure (within spaces of bone communications forms between arterial and venous CVS)

62
Q

What is the treatment of Pagets disease?

A

Bisphosphonates: Alendronate, Risedronate, Pamidronate

63
Q

What is the MOA of bisphosphonates?

A

Analogues of hydroxyapatite, incorporated into bone as taken up by osteoblasts. Inhibit osteoclast activity so prevents bone resorption

64
Q

What is osteoporosis?

A

Generalised skeletal disorder with reduced bone density, impaired structure and increased risk of fracture (commonly wrists, vertebrae, neck of femur). Increases with age and F>M (hormone deficiency and menopause)

65
Q

What are the causes of osteoporosis?

A
  • Age
  • Steroid Tx (cushings syndrome)
  • Chronic kidney, liver, nutritional disorders that affect Ca and Vit D
  • Post-menopausal or early menopausal
66
Q

What is the 6 treatments of osteoporosis?

A
  • Low dose Bisphosphonates - alendronate or risedronate orally weekly, ibandronate or zolendronate injections quarterly/annually
  • HRT and oestrogen analogues (SERMS)
  • Ca and D3 supplements in malnourised elderly
  • Denosumab 6 monthy injection to switch off osteoclasts
  • Strontium ranelate (limited use CVS risk)
  • PTH injection
67
Q

What are the common primary sites for bone metastases?

A

Breast lung and prostate

68
Q

Why does hypercalcaemia of malignancy occur with or without bone metastases?

A

Tumour makes PTH related peptide - increases calcium levels

69
Q

What is the treatment for bone metastases?

A
  • Radiotherapy
  • Surgery for complications
  • Pain relief ie morphine
  • High dose IV bisphosphonate can reduce progression in myeloma breast and prostate cancer
70
Q

What is a) Lytic metastases b) Phossy jaw c) Paraplegia

A

a) Holes in bone from cancer
b) Jaw destruction from abnormal bone metabolism when exposed to high levels of phosphate
c) Spinal cord compression

71
Q

What are the implications for dental treatment with osteogenesis imperfecta?
(what E/O sign may you notice)

A
  • Chest deformities may occur leading to respiratory compromise - issues with GA and IV sedation
  • Bluish tinge to sclera as collagen layer not formed properly
72
Q

What are the implications for dental treatment with osteoporosis?

A
  • Bisphosphonates = MRONJ - eventually necrotic bone separates and sheds as bony sequestrum, if infected prescribe antibiotics
  • Impaired respiratory function if vertebral collapse and chest deformities
73
Q

What is osteopetrosis?

A

Marble bone disease (autosomal dominant or recessive). Pt may be anaemic as bone marrow filled with bone. May be taking corticosteroids

74
Q

What are the implications for dental treatment with osteopetrosis?

A

Risk of post extraction osteomyelitis (infection of bone). No elasticity of socket wall so tooth will break

75
Q

What is fibrous dysplasia?

A

Monostotic (one bone) or polystotic (several bones) where texture of bone like a pear - can carve to reshape but will grow bavk with vengence. Chinese letters under microscope as bone surrounds matrix of fibrous tissue. Not inherited. Increased risk of hyperthyroidism and diabetes

76
Q

What is cherubism?

A

Rare autosomal dominant males where excess hard tissue makes eyes deviate upwards and swollen face. Giant cell type lesion disease, cellular and vascular fibrous tissue with giant cells. Exclude hyperthyroidism with bloods as gives the same histopathological appearance

77
Q

What are the dental implications of Pagets disease?

A

Enlarged cranium and assymmetry makes dentures not fit

78
Q

For rheumatoid arthritis, what is essential when on alpha-TNF inhibitors e.g. Infliximab?

A

Should be rendered dentally fit prior to starting treatment. If further dental problems occur, FBCs clotting and LFTs required and aggressive Tx

79
Q

What is osteoradionecrosis?

A

Dead bone as a secondary reaction to radiotherapy. Endarteritis obliterans occurs - blood vessels supplying bone become smaller.

80
Q

How is osteoradiunecrosis avoided?

A

Avoid XTN in first 6m-1yr post radiotherapy. Refer to management in specialist environment. XTN prior to radiotherapy.
If not possible:
- Minimal trauma (minimise periosteal lifting)
- No vasoconstrictor
- Trim sharp edges of bone
- Close ST accurately
- Prophylactic antibiotics for 1 month or until sockets heal

81
Q

What is Marfan’s Syndrome?

A

Autosomal dominant affecting collagen metabolism. Kyphosis (A-P spine curvature) and Scoliosis (lateral curvature). Aortic and mitral valve incompetency and pulmonary cysts that lead to spontaneous pneumothorax. Oral sign = high arched palate

82
Q

What is Ehlers-Danlos Syndrome?

A

Problem with collagen so increased elasticity of tissues. Mitral valve prolapse, platelet anomolies, cardiac conduction problems if affecting heart muscle.

83
Q

What are the dental implications of joint disorders?

A
  • Decrease C spine mobility - difficulty intubating and may need to use jaw thrust
  • TMJ can be affected
  • Corticosteroid treatment - may need cover
  • No need for antibiotic cover if have joint replacement and amoxicillin not good at penetrating bone
84
Q

What is gout and how is it treated?

A

Deposition of uric acid crystals in joints. Increased risk of hypertension, ischaemic heart disease and diabetes. Initially treated with NSAIDs, longer term = allopurinol

85
Q

What is cleidocranial stenosis and what are its dental anomolies?

A
  • Autosomal dominant disease affecting skull, jaws and clavicle
  • Dental anomalies = delayed, non-eruption, supernumerary teeth
86
Q

What side effects does Penicillamine cause (used in treatment of rheumatoid arthritis)?

A
  • Lichenoid reaction
  • Oral ulceration
  • Thrombocytopenia
87
Q

What side effects does Allopurinol cause (used in treatment of gout)?

A
  • Taste disturbances and paraesthesias

- Erythema multiforme (adverse drug reaction)

88
Q

What side effects does Ciclosporin cause (used in treatment of transplant pt and sometimes rheumatoid pts)?

A
  • Gingival overgrowth
89
Q

What side effects does Methotrexate cause (used in treatment of rheumatoid arthritis and chemotherapy)?

A
  • Toxicity increases with NSAIDs, corticosteroids and penicillin
  • Oral ulceration due to low folic acid so given supplements
90
Q

What side effects does Baclofen cause (used in treatment of musculoskeletal disorders and multiple sclerosis as an anti-spasmodic agent)?

A
  • Xerostomia