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Stage 4 HD > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

List 1) immune mediated and 2) non-immune mediated rheumatological diseases

A

1) Rheumatoid arthritis, psoriatic arthritis, ankylosing sponylitis, gout, sjogren’s, lupus, scleroderma, vasculitis
2) osteoarthritis, osteoporosis, fibromyalgia

affect your joints tendons, ligaments, bones, connective tissue and muscles.

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2
Q

Aetiology of rheumatoid arthritis

A

-Multi-system condition
-autoimmune where synovial lining of joints are attacked causing inflammation.
-Onset may be associated with HLA-DR4 and TNFa polymorphisms
-Overactivation of T cells
-Smoking, pollution, dysregulated gut microbiome, infection, periodontal disease, trauma, stress
-Infiltration of immune cells in joints increases synovial fluid, causing destruction of joints, swelling, pain. Usually affects small joints of hands and feet, and sometimes knees, wrists, elbows, ankles

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3
Q

Hand signs of RA

A

Swolen painful wrists
Ulnar deviation
Radial deviation at wrist
Swan neck deformity of fingers
Rheumatoid nodules – hot and boggy
Reduced finger flexion
Raynauds

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4
Q

ARA criteria for RA (typical signs and symptoms)

A

-Symmetrical arthritis
-Hand joints in particular (but can be other joints)
-At least 3 areas
-Morning stiffness >60 minutes (gets better with movement)
-Rheumatoid nodules
-Serum rheumatoid factor (RF) = antibody which binds to Fc portion of an antibody
-Radiographic changes

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5
Q

Radiographic changes that occur in RA and osteoarthritis

A

-Both= joint space narrowing
-RA=Bone erosion, Subluxation/dislocation, Ankylosis
-Osteo=subchondral sclerosis, osteophytes, cysts

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6
Q

Extra-articular manifestations of RA

A

-As well as joints it affects other systems

-Skin -Nodules = growth of abnormal tissue
-Lymphadenopathy
-Lung = Pleurisy/effusion/fibrosis
-Heart = pericarditis
-Muscle = atrophy/ myositis
-Bone = osteoporosis
-GI= oesophagitis, gastritis, peptic ulcers, enlarged spleen
-Eye=uveitis
-Secondary Sjogren’s syndrome
-Vascular= Vasculitis, Raynaud’s, anaemia, atherosclerosis
-Neurological
-Renal

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7
Q

How RA and osteoarthritis manifestations differ

A

-RA= pain and stiffness gets better with movement, episodic flares, symmetrical joints affected, often raised CRP/ESR, positive rheumatoid factor and anti-CCP antibodies. Affects small joints of hands and feet. Not just joints are affected. Autoimmune

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8
Q

Methotrexate is a DMARD used in RA. What is a DMARD. Action and side effects of methotrexate. Meds to avoid with it

A

-disease modifying anti-rheumatic therapy, to reduce symptoms/ prevent joint damage

-dihydrofolate reductase inhibitor
-liver toxicity, mouth ulcers (due to low folate), bone marrow suppression, macrocytic anaemia (B12), glossitis
-contraindicated in pregnancy
-avoid trimethoprim, penicillin, NSAIDs, corticosteroids as increases its toxicity

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9
Q

The use of biologics in RA. Mechanism

A

-Used if poor control with DMARDs
-monoclonal antibodies
-block a specific inflammatory molecule (eg.TNF, IL6), block signalling or deplete inflammatory cells
-adalimumab-TNF
-Inflixumab- TNF
-Ritixumab- anti CD20

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10
Q

Antibodies for RA

A

rheumatoid factor
Anti CCP

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11
Q

What does Rituximab treat. What is its action

A

-RA, lymphoma, pemphigus vulgaris
-anti-CD20, depleting B cells so reduced antibody production and therefore antigen presentation
-once every 6 months

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12
Q

How biologics affects dentistry - is prophylaxis done, do you need to stop biologic for tx

A

-increased risk of infection
-advised to stop biologic if have infection then restart when no signs of infection
-might need longer course of antibiotics
-prophylaxis not done routinely
-For planned invasive procedures (tooth extraction), stop biologics one dose interval prior to the procedure. [But don’t delay emergency procedure] Once wound has healed and no signs of infection, restart to usual.
-before starting someone on biologics try get their OH good

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13
Q

What is psoriatic arthritis and how it differs to RA

A

-linked with psoriasis - associated with psoriatic skin and nail changes
-tends to affect larger joints
-more episodic than RA. Hard to notice flare-ups
-CRP inflammatory marker often normal, unlike in RA
-asymmetrical
-Dactylitis – inflammation of whole finger – sausage like fingers/toes
-rheumatoid factor usually negative

Clinically indistinguishable from RA

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14
Q

What is reactive arthritis

A

-inflammatory process usually following infection (10-14 days after)
-typically larger joints such as knee
-Episodic spinal pain/ stiffness worse in mornings and at rest
-Other symptoms may include conjunctivitis, urethritis, rash
-raised CRP, HLA-B27 positive

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15
Q

Autoantibodies important for diagnosing systemic lupus erythematosus

A

antinuclear antibody (ANA)
anti-dsDNA antibody
Anti-Smith
Antiphospholipid antibody

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16
Q

Conditions associated with Raynaud’s

A

systemic sclerosis
systemic lupus erythematous
Scleroderma.
CREST syndrome (a form of scleroderma)
Buerger disease.
Sjögren syndrome.
Rheumatoid arthritis.
Occlusive vascular disease, such as atherosclerosis.

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17
Q

Sjogren’s: features, management, diagnosis

A

-Rheumatological autoimmune connective tissue disorder
-Mucosal dryness- dry eyes, Xerostomia, dry vagina
-Fatigue, arthritis, raynaud’s, interstitial lung disease, renal tubular acidosis, risk of lymphoma originating in salivary gland
-Management= incurable, manage dryness
-Diagnosis= anti-Ro and anti-La antibodies, rheumatic factor, hypergammaglobulinaemia, saliva gland biopsy, saliva flow measurement, tear production (Schirmer test)

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18
Q

Causes and features of osteoarthritis. Management

A

-Mechanically driven
-Low-grade inflammation and pain in joint due to wearing of the cartilage.
-affect high use, weight bearing joints - hip, knee, thumb, lower spine
-Reduced range of movement due to pain causes atrophy of muscles and ligaments
-Reduced finger flexion
-Increases with age
-pain better at rest
-can be secondary to obesity, joint damage/surgery, scoliosis, deformities
-Tx= analgesia, physiotherapy, surgical point replacement

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19
Q

Degenerative and inflammatory conditions associated with TMJ arthritis

A

-Degenerative=Osteoarthritis, osteoarthrosis
-Inflammatory=Rheumatoid arthritis, Psoriatic arthritis, Juvenile idiopathic arthritis (<16 year olds, impedes growth), Infection, Crystal disease (pseudogout/gout)

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20
Q

Features of systemic lupus erythematosus. What type of hypersensitivity is it

A

Type III hypersensitivity

Butterfly rash (worsens with UV)
Severe fatigue
Hair loss
Photosensitivity
Oral ulcers
Arthritis
Nephritis
Pleuritis and pericarditis
Thrombocytopenia
Anaemia

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21
Q

Assessment for suspected mandible fracture.What imaging is required

A

-History
-Inspect- occlusion, appearance, colour, bruising, bleeding, symmetry, oedema,
-Palpate - swelling, temperature, pulse, capillary refill time
-Get patient to move joint, then surgeon
-Neurological test -pin prick, cotton wool
-Radiographic - 2 views at 90 degrees to get different planes. CT or MRI if plain film inconclusive

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22
Q

What is a contra-coup fracture

A

indirect force at site of injury, rather than direct force

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23
Q

Explain Le Fort type I, II, III fractures and their likely presentations

A

when the midface is either partially or fully separated from the skull. Maxilla and skull fracture
1) Horizontal. alveolar ridge -upper lip swelling, buccal brusing, malocllusion, loose teeth
2) Pyramidal. nasofrontal suture -swollen midface, mobile jaw, malocclusion, periorbital odema, nose bleed
3) Transverse. craniofacial dissociation, passes to zygomatic bone. Similar signs as type II, ear drainage, orbital hooding, face flattening or lengthening, mastoid bruising

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24
Q

Explain these types of fractures: closed, open, transverse, complete, incomplete, comminuted, displaced, non-displaced, greenstick, pathological

A

-Closed = soft tissue in tact
-Open = bone sticking out of skin
-Transverse = if it’s going across the bone
-Complete= through full thickness of cortical plates
Incomplete = not full thickness. usually in a young pt, soft bone in which the bone bends and breaks
-Comminuted= lots of fragments
-Displaced= crack, 2 ends not in anatomical position
-Non-displaced= no gap
-Greenstick=incomplete fracture of the bone with no displacement
-Pathological- due to underlying disease, no direct trauma

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25
Q

Mechanism of fractured bone healing

A
  1. Inflammatory: Bleeding and clot formation, Acute inflammatory response, Bone necrosis, Macrophage infiltration (removes necrotic bone), Formation of vascular granulation tissue
  2. Reparative = Cartilaginous callus. then new bone. Over 6-12 weeks direct ossification occurs throughout the fracture gap
  3. Remodelling for up to 2 years
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26
Q

What is ORIF

A

-OPEN REDUCTION INTERNAL FIXATION
-Re-establishing normal anatomy and stabilising it after fracture. Keeping everything in right place
-2-part surgery=First, the broken bone is reduced (put back into place) Next, an internal fixation device is placed on the bone (plates, screws)
-used in mandible fractures

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27
Q

Complications that can arise after fractures (immediate and late)

A

-Immediate: Haemorrhage, tissue loss, nerve/vessel damage, internal organ damage, compartment syndrome (oedema and pressure around bone), infection, confusion, DVT/PE
-Late: Poor occlusion, reduced mobility, failed union of fracture ends, stiff joints, infection

28
Q

Prophylaxis advice for joint replacement patients

A

-Patients with joint replacements do not require antibiotic prophylaxis routinely
-Suggestion of bacteraemia production following dental treatment, causing prothesis infection
-No evidence prophylaxis is of benefit, if develop infection treat promptly with specific antibiotics
-Oral streptococci rarely colonise these joints and cause infection in these areas
-Immunocompromised patients or those at higher risk of infection can be considered on an individual basis following discussion with patient and orthopaedic physician weighing the risk vs benefits

29
Q

List metabolic bone disorders

A

Osteoporosis
Paget’s disease
Osteomalacia

30
Q

Cells involved in bone resorption and deposition. What hormone plays a role in remodelling. Role of RANK ligand and Sclerostin

A

-Osteocytes are mechanically sensitive
-Osteoclasts – resorb
-Osteoblasts – deposition of bone
-Estrogen –role in remodelling
-RANK ligand – act on osteoclasts to promote their activity and resorption
-Sclerostin- acts on osteoblasts and down regulates it to decrease mineralisation

31
Q

What is Osteoporosis and its risk factors

A

-low bone mass and mineral density, with increased bone fragility and fracture susceptibility
-post-menopausal (reduced oestrogen)
-glucocorticoids
-Low vit D and plasma calcium (deficiency, malnutrition, hyperparathyroidism, renal disease)
-Cushings
-Diabetes
-Smoking, alcohol
-RA, ankylosing spondylitis
-IBD, Coeliac disease, chronic liver disease

32
Q

Anti-resorptive and anabolic medications for osteoporosis

A
  1. Anti-resorptive [reduce resorption]: HRT, bisphosphonates, Densoumab, SERMs
  2. Anabolic [promote mineralisation]: PTH, Romozosumab
33
Q

Action of bisphosphonates. Examples of oral and IV drugs

A

-Reduces bone resorption to treat osteoporosis, reducing fracture risk
-Promotes osteoclast apoptosis
-Oral (alendronate, risedronate)
-IV (zoledronate, pamidronate)

34
Q

Side effects/disadvantges of bisphosphantes

A

-Half life around 10 years - Has an effect after stop taking it
-Nephrotoxicity (avoid if eGFR <30)
-Potentially unsafe for pregnant /pre-conception women
-Risk of osteonecrosis of jaw
-Poor oral bioavailability to taken prior to food
-Risk of atypical femoral fracture: at hip

35
Q

What is osteonecrosis. Do you stop someone of bisphosphonates before XLA

A

-area of exposed bone in the oral cavity that does not heal within 8 weeks. Poor osteoclast function at removing necrotic bone
-those on bisphosphonates are at risk
-Withholding the drug for a few weeks before an extraction makes minimal difference due to long acting bone binding. Instead promote good OH and smoking cessation to reduce risk
-Consider not putting someone on bisphosphates if high dental disease. Or do high risk dental work before starting tx.
-If IV, refer to specialist for extraction. If oral then can treat in primary care

36
Q

Action of denosumab, romosozumab and teriparatide in osteoporosis

A

1) Anti-resorptive [reduce resorption]- monoclonal antibody against RANK ligand to reduced osteoclast function
2) Anabolic [promote mineralisation] - blocks sclerostin which supresses osteoclasts. Boosts mineral density
3) Highly anabolic. PTH. Controls calcium blood levels, promotes osteoblasts

37
Q

What is osteomalacia. Who is at risk

A

-Inadequate mineralisation of bone (soft bone disease) due to deficiency in vitamin D, calcium, or phosphate
-Rickets, reduced sun vit D, renal and liver disease (impairs bioactivity of vitamin D)

38
Q

Role of PTH in calcium homeostasis

A

-PTH=mobilises calcium from bone and retains it in kidney/blood
-PTH released from parathyroid gland when low calcium blood levels to increase calcium and promotes osteoblast growth
-Whereas high calcium blood levels prevent PTH release

39
Q

Causes of low blood calcium

A

Low vit D
Renal disease
Hypoparathyroidism due to surgery of autoimmune disease

40
Q

What is Pagets disease. Tx

A

-chronic disorder causing bones to grow larger and become weaker
- usually affects just one or a few bones, asymmetrical
-phases of resorption and deposition causing haphazard architecture= Radiograph shows Reversal lines and moth eaten skull appearance
-Chest deformaties, bone more vascular, risk of cardiac failure, dentures and gloves get tighter
-sabre tibia (thick tibia, thing fibula)
-During XLA teeth brittle and bone very tough
-Treatment =bisphophonates, calcitonin

41
Q

Impact arthritis on oral heath and dentistry

A

-TMJ pain
-Implications for sedation/anaesthesia: Mouth opening and neck extension (cervical spine problems)
-RA – jaw thrust rather than head tilt/neck lift
-RA – hands deformed – may not be able to maintain very good OH
-Bisphophonates - risk of osteonecrosis
-corticosteroid treatment - infection, reduced healing
-NSAIDs- increased bleeding, drug interactions
-methotrexate- drug interactions, avoid IV and RA sedation

42
Q

What is osteopetrosis. XLA considerations

A

-autosomal dominant or recessive
-osteoclasts have a decreased activity
-Bone is dense, brittle, misshapen, large
-no region of spongey bone
-bone marrow space can disappear causing anaemia
-brittle bone makes XLA tricky as tooth will snap in socket as bony socket cannot expand - may refer to oral surgery
-anemia due to lack of bone marrow

43
Q

What is osteogenesis imperfecta

A

-Brittle bone disease
-Autosomal dominant
-Chest deformities may lead to respiratory compromise – implications for GA/IV sedation
-Skeletal deformities – bowing of legs
-Muscle weakness, hearing loss
-dentinogenensis imperfecta
-Blue eye sclera (abnormal collagen metabolism)

44
Q

What is fibrous dysplasia of bone

A

-Dense bone replaced by softer fibrous tissue, which forms bone and constantly remodels
-Can involved one or multiple bones
-Affects maxilla more than mandible. Presents with asymmetry of facial growth
-Increased risk of hyperthyroidism
-Diabetic tendency

45
Q

What is cherubism

A

-Large cheek bones. Bilateral swelling of jaw, chubby cheeks
-Cellular and vascular fibrous tissue with giant cells
-Exclude hyperparathyroidism with blood tests

46
Q

What is Marfan’s syndrome and oral manifestations

A

-disorder of the body’s connective tissues
-flat feet, curved spine (kyphosis or scoliosis), elongated limbs & digits, looseness of joints, displacement of eye lens, tendency to develop aneurysms (aorta)
-risk of pneumothorax

-High arches palate
-Dental crowding

47
Q

What is Ehlers Danlos syndrome and oral manifestations

A

-Flexible joints, thin fragile skin, easy bruising
-Mitral valve prolapse, Cardiac conduction defects
-Platelet anomalies so always check about bleeding/clotting ability. After extraction, bleeding usually stops fine but ensure local measures

48
Q

What is ankylosing spondylitis

A

-Inflammatory disease that can cause spine to fuse which makes it less flexible and cause hunched posture. -Can affect respiratory function
-Decreased mouth opening – intubation/treatment difficulties
-Aortic valve problems

49
Q

What is Gout. Tx

A

Deposition of crystals within joint space
Too much uric acid
Swollen joints
Increased risk of Hypertension, Ischaemic heart disease, Diabetes Mellitus
Treated with NSAIDs at the start, and then allopurinol later

50
Q

What does allopurinol treat and its side effects

A

-Treatment of gout
-Taste disturbance and paraesthesias
-Erythema multiforme – peri oral blood clotting around the lips
-Rash with amoxicllin

51
Q

How to prevent osteoradionecrosis. When should you avoid extractions

A

-ensure they are dentally fit before getting radiotherapy
-with Extractions prior, cover bone with soft tissue flap
-Avoid extractions during and after where possible. But definitely not in the first 6 months to 1-year post-radiotherapy

For post radiotherapy:
-Make it as atraumatic as possible
-no vasoconstrictor
-trim sharp bone edges
-Prophylactic antibiotics for one month or until sockets heal

52
Q

What are labile cells and give examples

A

-cells continuously dividing in cell cycle
1.Haematopoietic cells – BONE MARROW
2. Epithelial cells = SKIN, ORAL MUCOSA, GIT, GUT

-Can undergo hyperplasia (TOO MUCH GROWTH, too much tissue)
-Highly susceptible to cancer as constantly dividing
-can regenerate

53
Q

What are stable cells. Give examples

A

-cells in reversible G0 phase– ability to go back into cell cycle and change
1. Liver = HEPATOCYTES
2. Kidney = RENAL CELLS
-can regenerate

54
Q

What are non dividing cells. Give examples

A

-Cells in irreversible G0 phase, no matter what stimulus occurs they cannot re-enter cell cycle and divide further. Cannot change, cannot regenerate
1. Heart = CARDIAC MUSCLE FIBRES
2. Brain = NEURONES

No cell division but can get bigger

55
Q

Out of labile, stable and non dividing cells which are more susceptible to cancer, which heal by replacement and regeneration

A

-Labile (epithelial)= most susceptible to cancer as constantly dividing. Heal by regeneration
-Stable (liver, kidney)= heal by regeneration
-Non dividing (brain, heart)= heal by replacement (scar tissue). Cancer rare

56
Q

Disorders of growth hormone deficiency and excess

A

-deficiency = DWARFISM
-Excess in Childhood - GIANTISM
-Excess in Adulthood = ACROMEGALY

57
Q

Difference between hypertrophy and hyperplasia

A

Increased growth. May co-exist

-Hyperplasia – increase in cell NUMBERS by mitosis and/or decrease in apoptosis
-Hypertrophy – increase in cell SIZE without cell division (no increase in number of cells)

58
Q

Examples of hyperplasia -1) physiological and 2) pathological)

A

1) Wound healing (cells regenerate and repair), Bone marrow (producing more blood cells) Breast tissue (puberty, pregnancy)

2) Goitre, gingival hyperplasia, Cushing’s

59
Q

Explain 1) aplasia and 2) hypoplasia. Give examples of disorders

A

1) COMPLETE FAILURE of development of an organ or tissue. Usually would lead to miscarriage if occurs in fetus except with 1 kidney. eg. Cleidocranial dysplasia
2) PARTIAL FAILURE of development of an organ or tissue. Decrease in cell numbers. eg. enamel hypoplasia

60
Q

Explain 1) hypertrophy and 2) atrophy. Disorder examples

A

1) Increase in cell or organ size. eg. masseteric hypertrophy, hypertrophic cardiomyopathy
2) decrease in size of cell or organ. Occurs with ageing. eg. muscular, bone, filiform papilla atrophy

61
Q

Difference between atrophy and hypoplasia

A

decrease in size of cell or organ
1) occurs with ageing (had the right number of cells, then started losing them)
2) developmental failure (never had enough cells in the first place)

62
Q

Causes of tongue filiform papilla atrophy

A

B12 deficiency anaemia
Lichen planus
Median rhomboid glossitis
Acute Erythematous candidiasis
Syphylis
Geographic tongue

63
Q

What is metaplasia and examples

A

-disorder of differentiation, acquired, REVERSIBLE
-Smoking causing metaplasia of trachea and bronchus
-Acid reflux causing Barett’s oesophagus
-Lichen planus

Metaplasia can lead to dysplasia (irreversible)

64
Q

What is dysplasia and examples

A

-disorder of differentiation, IRREVERSIBLE
-Leads to excess cell growth
- INCREASED CANCER RISK

65
Q

Appearance of oral epithelial dysplasia

A

-Appears as white (most common) or red patch
-Basal cells started to stack on top of themselves

increased risk of developing into cancer

Stage 4 HD (6 decks)

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