Rheumatology Flashcards
1
Q
what is arthritis
A
- inflammation of the joints
2
Q
what is arthrosis
A
- non-inflammatory joint disease
3
Q
what is arthralgia
A
- joint pain
4
Q
what is bone
A
- mineralised connective tissue
5
Q
how is bone dynamic
A
- Bone in continuously changing
- Always forming and being resorbed and replaced
- Gives bone ability to adapt to changing stresses in the environment and also allow use for self-repair to take place
6
Q
how is bone self-repairing
A
- Processes for dynamic change are the same as for repairing bone damage
- Bone is removed by osteoclasts and deposited by osteoblasts
- Clasts eat away at the bone matrix and are replaced by blasts which deposit an osteoid matric which is then mineralised to leave resting bone
- Cycle takes over 3-6 months
7
Q
what do you need the correct amount of for bone formation
A
- calcium
- phosphate
- vitamin D
8
Q
how are bone and calcium linked
A
- bone forms a store for calcium
- exchangeable and not
- exchangeable moves from bone to ECF and calcium is absorbed from the gut into ECF
9
Q
how is calcium lost
A
- lost through the gut and urine
- Important for normal body function that the calcium level in blood is maintained at a very precise level
- Because it is involved in nerve and muscle function
10
Q
where is the parathyroid hormone
A
- in the thyroid gland
11
Q
what does PTH do
A
- Maintains serum calcium level
- Raised if calcium level falls
- Increases calcium release from bone
- Reduces renal calcium excretion
- The level of PTH is tightly maintained but can change if there is a tumour or if surgery accidentally removes these glands resulting in an injury to not secrete enough PTH
12
Q
what is hypoparathyroidism
A
- lower serum calcium
- low PTH
13
Q
what is hyperparathyroidism
A
- high PTH
- primary and secondary
- both types result in increased bone resorption
14
Q
what is primary hyperparathyroidism
A
- Gland dysfunction = tumour
- Results in higher serum calcium
- Inappropriate activation of osteoclasts
15
Q
what is secondary hyperparathyroidism
A
- Causes low serum calcium
- PTH being high will activate osteoclasts in bone but this time appropriately to maintain serum calcium level
16
Q
how does vitamin D work
A
- from the sun or diet
- turns into cholecalciferol in the skin
- becomes bound cholecalciferol in the blood
- becomes 25-hydroxycholecalciferol in the liver
- becomes 1,25-dihydroxycolecaliciferol in the kidneys
- calcium absorbed in the gut
17
Q
what happens if there re low levels of vitamin D
A
- effect bone health
18
Q
what are reasons for poor vitamin D
A
- Low sunlight exposure= housebound, dark skinned in Northern country
- Poor GI absorption = poor nutrition, small intestine disease (malabsorption)
- Drug interactions = some antiepileptic drugs (Carbamazepine, phenytoin), can interfere with vitamin D synthesis
- Often a combination of factors
19
Q
how are dark skinned people living in northern countries often deficient in vitamin D
A
- Skin absorbed sunlight less efficiently due to pigment in the skin and this, combined with more clothing in northern countries covering most of the skin, then the amount of vitamin D able to absorb through sunlight is reduced
20
Q
what is osteomalacia
A
- Poorly mineralised osteoid matrix
- Bone formed normally but not calcified properly
- Normal amounts of osteoid but inadequate mineralisation of tissue
- Poorly mineralised cartilage growth plate
- calcium deficiency
21
Q
what is osteoporosis
A
- Loss of mineral and matrix
- Mineral and matrix are normal, just not enough of it made
- Reduce bone mass
22
Q
what is osteomalacia result in during bone formation
A
- rickets
23
Q
what does osteomalacia results in after bone formation
A
- osteomalacia
24
Q
what type of bone is produced from osteomalacia
A
- bone that is soft and can be bent to pressure
25
Q
what are the investigation results for osteomalacia
A
- serum calcium = decreased
- serum phosphate = decreased
- alkaline phosphatase (measure of bone turnover) = very high
- plasma creatine = increased if renal cause
- plasma PTH = increased if secondary hyperparathyroidism
26
Q
what is the term given to the formation of the legs in rickets
A
- bow-legs
- because bones are unable to support the weight of the child
- rarely seen nowadays
27
Q
why did rickets used to be so common
A
- due to the inadequate diet and poor sunlight exposure due to overcrowding and construction of tenements
28
Q
what does osteomalacia cause in adults
A
- pain in nerves affecting lower limb
- vertebra compression
29
Q
what are the affects of hypocalcaemia
A
- Muscle weakness = trousseau and chvostek signs positive (carpal muscle spasm, facial twitching from VII tapping)
30
Q
how is osteomalacia managed
A
- correct the cause
- Malnutrition = control GI disease
- Sunlight exposure = 30 mins x 5 weekly
- Dietary vitamin D = supplements perhaps the easiest way to restore deficiencies nowadays
31
Q
what is osteoporosis
A
- reduced quantity of normally mineralised bone
- age relate change
- inevitable
- Loss of mineral and matrix
- Mineral and matrix are normal, just not enough of it made
- Reduce bone mass
32
Q
wha are the risk factors of osteoporosis
A
- AGE = as you get older bone mass reduces
- Female sex
- Endocrine = oestrogen & testosterone deficiency (cushing’s syndrome, increase in corticosteroid levels in te blood)
- Genetic = family history, race (Caucasian & Asian women)
- Early menopause
- Patient factors = Inactivity, Smoking, Excess alcohol use, Poor dietary calcium
- Medical Drugs use (steroids, antiepileptics)
33
Q
who is osteoporosis foundinmore
A
- women
- 15% women aged 50
- 30% women aged 70
- 40% women aged 80
34
Q
why are women more likely to get osteoporosis
A
- Males have a higher peak bone mass
- Peak bone mass in skeleton is less in women
- Oestrogen withdrawal increases bone mass loss rate in women
- Artificially boosted by oestrogen, but when women go through menopause and it is lost, that protection is lost too and rapid loss of bone occurs
- In men, rate of decline is similar but peak is higher
- Takes longer for me to lose enough bone mass to reach osteoporosis point that it does women
35
Q
what are the affects of osteoporosis
A
- Bone mass may no longer be adequate to maintain stress applied to bone
- Increased bone fracture risk = Long bones (femur), If patient falls on outstretched arm will cause fracture, Often this can be the first sign to a patient that they are at osteoporosis risk
- Vertebrae = Height loss, Kyphosis and scoliosis, Kyphosis, Scoliosis
- Nerve root compression back pain
- Lifetime risk of hip fracture >50 years of age = 17.5% women, 6% men
- After osteoporosis related hip fracture = 20% increase in 5 years mortality, Maximal in initial 6 months, 40% unable to walk unaided, 60% unable to live independently
36
Q
what is kyphosis
A
- Bending forward of spine as vertebral bodies collapse under the weight of the upper body causing tipping
- Usually due to osteoporosis
37
Q
what is scoliosis
A
- Shifting of the lateral position of the vertebrae caused by the same compression
38
Q
how can osteoporosis be prevented
A
- build maximal peak bone mass = exercise, high dietary calcium intake
- reduce rate of bone mass loss = continue exercise and calcium intake, reduce hormone related effects
- oestrogen replacement therapy
- reduce drug related effects
- consider ‘osteoporosis prevention rugs’
39
Q
is oestrogen replacement therapy goof
A
- Reduces osteoporosis risk
- Increases breast cancer risk
- Increase endometrial cancer risk
- Patient who has NOT had a hysterectomy
- Combine with a progestogen to reduce risk
- May reduce ovarian cancer risk
- Increases DVT risk
- Benefit is lost after HRT is stopped
- 5-year post treatment BMD is ‘norma’
- Net benefit and risk can be a difficult balance for patient
- MOST effective if early menopause
- Not sure yet if these are good or not
- Not a permanent benefit
40
Q
what are osteoporosis preventing drugs
A
- bisphosphonates
41
Q
what are bisphosphonates
A
- Act by preventing osteoclast action by poisoning osteoclasts and reducing their numbers
- If there are reduced osteoclasts, less bone can be removed and therefore bone mass will be preserved
- non-nitrogenous = main ones
- nitrogenous
- sue drugs to prevent bone loss and in some cases even build-up the bone mass again
42
Q
what are non-nitrogenous bisphosphonates
A
- Etidronate = 1 (potency)
- Clodronate = 10
- Tildronate = 10
43
Q
what are nitrogenous bisphosphonates
A
- Pamidronate =100
- Neridronate =100
- Olpadronate =500
- Alendronate =500
- Ibandronate =1000
- Risedronate =2000
- Zoledronate =10000
44
Q
what ar the effectiveness of bisphosphonates
A
- Alendronate or Risedronate is an osteoporosis risk population
- Reduce vertebral fracture risk by 50%
- Reduce other fracture by 30-50%
- Benefit lost if drug discontinued
- Can be combined with HRT
45
Q
what are the problems with bisphosphonates and dentistry
A
- issue when extracting teeth
46
Q
what are the symptoms of joint disease
A
- Pain
- Immobility stiffness
- Loss of function
47
Q
what are the signs of joint disease
A
- swelling = fluctuant (if lots of fluid), bony (if being going on for years) synovial (enlargement mainly in RA)
- deformity = lead to changes in joint surfaces
- redness
- crepitus
- loss of function
48
Q
what is crepitus
A
- Noise made by bone ends moving
* Associated with loss of normal cartilaginous covering of the bone ends
49
Q
how are connective tissue diseases investigated
A
- radiographs = MRI more common now, arthography
- blood = C-reactive proteins (inflammatory markers), rheumatoid factors, extractable nuclear antigens, anti ds-DNA, anti-nuclear antibody)
- arthroscopy and bops
50
Q
what is arthography
A
- where radiopaque die is injected into the joint onto outline the articular surface and joint capsule
51
Q
what are some crystal arthropathies
A
- acute monoarthopathies
- gout
52
Q
what is acute monoarthropathies
A
- acute arthritis of a single joint
- common causes = infection, crystal arthropathy (gout)
- can be the initial stage of poly arthritis
53
Q
what is gout
A
- causes a lot of pan
- have uric acid crystal deposited in the joint and these causes irritation to joint surface causing swelling and inflammation
54
Q
what is hyperuricaemia
A
- high uric acid levels
- drug induced = thiazide diuretics
- genetic predisposition
- nuclei acid breakdown = after chemotherapy
- tumour relate
- obesity and alcohol enhance
55
Q
how can chemotherapy cause gout
A
- After chemotherapy cancer treatment will have killed a lot of cancer cells and the nucleic acid from these cells will be reprocessed causing a large surge in uric acid in the body, the effects of this can be reduced to some extent by pre-hydrating person so renal flow and ensuring output maximized before therapy starts so as nucleic acid is broken down, uric acid is washed away and level do not rise too far
56
Q
who is gout more common in
A
- men
- until women reach menopause then equalises
57
Q
what are the symptoms fo gout
A
- acute inflammation of single joint
- usually great toe
- usually a precipitating event
- rapid onset
58
Q
what is gout treated with
A
- potent NSAIDs
59
Q
how can gout affect dental treatment
A
- avoid aspirin = interferes with uric acid removal
- drug treatment may give oral ulceration = allopurinol
60
Q
what is osteoarthritis
A
- common condition
- symptomatic in 10% of population
- degenerative joint disease
- weight bearing joints
- NOT wear and tear
- cartilage repair dysfunction = as cartilage does not repair properly, the caritlage n top of the bone ends becomes thinner until it disappears
61
Q
what are the symptoms of OA
A
- pain
- brief morning stiffness
- slowly progressive over years
62
Q
what are the radiographic signs of OA
A
- Loss of joint space and subchondral sclerosis
- Loss of joint space as cartilaginous layer is reduced and subchondral sclerosis is thickening of bone under cartilaginous layer as bone is having more force transmitted directly to it and less cushioning from cartilage
- Osteophyte lipping at joint edge
- Due to irriation at bond ends
- Radiographs may show ASYMPTOMATIC changes is OA the cause of symptoms?
63
Q
what is the treatment of OA
A
- treated symptomatically, nothing alters disease progression
64
Q
how is the pain from OA treated
A
- Increasing muscle strength around the joint
- Weight loss
- Walking aids
- Role of NSAIDs
- Prosthetic replacement for pain
65
Q
when is a patient suitable for joint replacement for OA
A
- Patient suitable for joint replacement when pain problem becomes troublesome to them, rather than functioning, such as walking as often the pain is the limiting factor preventing walking in the first place
66
Q
how do joint replacements work
A
- They are pre-manufactured to a certain shape
- Bone is then cut using a template to match shape of prostheses to be cemented into place
67
Q
what are the dental aspects of OA
A
- TMJ involved = no symptoms normally
- difficult accessing care
- chronic NSAID use = ulcers, bleeding tendency
- joint replacement = no AB prophylaxis
68
Q
what is rheumatoid arthritis
A
- Initially a disease of the synovium with gradual inflammatory joint destruction
- Part of a multisystem disease and different pattern of joint involvement can be seen
- most common ‘serious’ joint disease =1% prevalence, 6:1 female pre-menopause, 3:1 female post menopause, peaks in 3rd-5th decade of life
- progresss slowly
- a symmetrical polyarthritis and affects all synovial joints of the body
69
Q
what is seri-positive RA
A
- rheumatoid factor present
70
Q
what is sero-negaive RA
A
- rheumatoid factor not present
71
Q
what joints are affected by RA
A
- synovial
- toes, knees, ankles, shoulder, neck
72
Q
what are the symptoms fo RA
A
- slow onset
- symmetrical polyathritis
- fatigue
- morning stiffnes
- joint stiffness
- joint pain
- minor joint swelling
- fever
- numbness and tingling
decrease in range of motion - occasional onset with systemic conditions = fever, anaemia, weight loss
73
Q
what are the early signs of RA
A
- Symmetrical synovitis of MCP (meta-carpal pharyngeal) joints
- Symmetrical synovitis of PIP (proximal inter-pharyngeal) joints
- Symmetrical synovitis of wrist joints
- Distal interpharyngeal joints is largely affected in OA, whereas proximal and MCP joints are involved in RA
- These changes cause joint swelling and stiffness and pain and eventually lead to destruction of the joint
74
Q
what are the late signs of RA
A
- ulnar deviation of fingers
- hyperextension of PIP joints = change at PIP joints, ‘swan-neck’
- ‘z’ deformity of thumb = hyeprflexion of MCP, hyperexention of IP joint
- lost ability for joint to remain its directional integrity
- Bones are no longer restricted in direction in which they can move when tendon is attached to the bone are activated
- Therefore, in most normal people it is not possibly to hyperextend your finger joints but when there is destruction of bone ends, the pull of the tendon onto this bone can allow bone to be pulled back further causing significant changes in the shape of the joint
- A lot of deformity happens in late-stage RA as pull of tendons will determine which direction the bones will point and move
75
Q
what happens to hands in RA
A
- less possibly for patient to grip and use hands effectively as tendon not pulling hand in correct direction fr grip
76
Q
what eventually happens in rA
A
- subluxation of the wrist
- loss of abducation and external rotation of shoulder
- flexion of elbows and knees
- deformity of feet and ankles
- significant loss of function
77
Q
what are some extra-articular features of RA
A
- systemic vasculitis
- psoriasis
- eye involvement = scleritis and episcleritis, Sjogren’s syndrome
- subcutaneous nodules
- amyloidosis
- pulmonary inflammation
- neurological
78
Q
what is amyloidosis produced as a result of
A
- inflammatory process of synovial
79
Q
what investigations are done for RA
A
- radiographs
- blood = normochronic, normocytic anaemia, due to failure to RBC stimulation
80
Q
what is the treatment for RA
A
- holistic management
- improve quality of life
- physiotherapy, occupational therapy, drug therapy, surgery
81
Q
what is physiotherapy for RA
A
- Aim to keep the patient active for as long as possible!
- Active and passive exercises
- To maintain muscle activity
- To improve joint stability
- To maintain joint position
82
Q
what is occupational therapy for RA
A
- Maximising the residual function
- Providing aid to independent living
- Can be provided to allow patient to use appliances at home and live a safe and healthy life
- Assessment and alteration of home
83
Q
what is the drug therapy for RA
A
- mainly for pain relief
• Analgesics
• Paracetamol, co-codamol
• NSAIDs
• Often combined with anti-PUD agents
• Disease modifying drugs – used to slow down disease
• Hydroxychloroquine, methotrexate
• Less commonly now sulphasalzine, penicillamine, gold
• Steroids intra-articular
• Injected into joint space where there are particular areas of joint trouble and this is not unusual treatment in early and moderate stages of disease
84
Q
what drug treatment is given for moderate and sever cases of RA
A
- Previous treatment isn’t as effective as disease progresses
- Immune modulators
- Azathioprine
- Mycophenolate
- Biologics
- Bream down into TNF inhibitor and leukocyte modulators and these drugs are increasingly used in moderate cases due to benefit they give to quality of life and prevention of significant disability
- TNF inhibitors infliximab, adalimumab, entanercept
- Rituximab (CD20) and tocilizumab (IL6r)
- Steroids
- Oral prednisolone
85
Q
what surgery s done for RA
A
- remove inflamed synovium
- joint replacement
- joint fusion
- osteotomy
86
Q
what is the prognosis of RA
A
- 10% spontaneously remit
- Remainder have fluctuating course
- RF and late onset have worse prognosis
- Later the onset, the worse the disease
- 10% severely disabled
- Remainder have mild/moderate disability
87
Q
what are the dental aspects of RA
A
- Disability from the disease
• Reduced dexterity for OH
• Access to case - Sjogren’s syndrome
• Association of CT disease the dry eyes/mouth - Joint replacements
• Multiple – large and small joints - Drug effects
• Bleeding – NSAIDs and sulphasalazine
• Infection risk – steroids, azathioprine
• Oral lichenoid reactions, gold, sulphasalazine, hydroxychloroquine
• Oral ulceration – methotrexate
• Oral pigmentation – hydroxychloroquine - Chronic anaemia – GA problems
• Care should eb taken when considering this outside a hospital setting - Don’t usually require AB prophylaxis
88
Q
what is Atlanta-occipital instability
A
- damage to ligament connecting skull base to upper cervical vertebrae
- ligaments become weakened and lead to slipping of structure in upper neck
- If sudden trauma applied to the neck, there is more chance of structure rupturing and bones moving into space with spinal cord causing significant spinal damage
89
Q
what is seri-negative spondyloarthritides (SA)
A
- range of different conditions
- have overlap = reactive arthitid, juvenile SA, undifferentiead SA, IBD associated arthritis, psoriatic arthritis
90
Q
what is ankylosing spondylitis (AS)
A
- spinal joint arthritis
- differs from RA as mainly o axial skeleton
- fusion of facet joints and anterior aspect of vertebrae so they become stiff and do not move relative to each other
- patient can’t bend or turn
91
Q
what are the features of SA
A
- association with HLA-B27
- infection likely a precipitant
- often symmetrical peripheral arthritis
- ocular and mucocutaneous manifestations
92
Q
what is the difference between AS and RA
A
- AS • 95% have HLA-B27 • 10% Caucasians have HLA-B27 though without having this • 0.5% of these get it • 8:1 male predominance • Unusual for males to be more susceptible • Onset about 20years – rare after 45 • 20% have large joint disease as well - RA • 6:1 female pre-menopause • 3:1 female post-menopause • Peaks in 3rd-5th decade of life
93
Q
what are eh effects of AS
A
- • Disabling progressive lack of axial movement
• Symmetrical other joint involvement – hips
• Results in
• Low back pain
• Limited back and neck movement – turning spin restricted
• Need to turn whole body
• Limited chest expansion – breathing compromised
• Respiratory disease can be made worse
• Cervical spine tipped forward – kyphosis
• Movements restricted
• Loss of vertebral height anteriorly which means spine will gradually tip forward
• Same as what you see in elderly patietns with OA, but in this case it is not due to bone collapse, but due to bone fusion
94
Q
what is the treatment for AS
A
- mainly same as RA
- analgesia and NSA|Ds
- physiotherapy
- occupational therapy
- DMD’s
- immune modulators
- surgery for joint replacement = for function, rather than pain
95
Q
what are the dental aspect of AS
A
- GA hazardous
- Limited mouth opening
- Limited neck flexion
- TMJ movement possible, but rare except in psoriatic arthritis
- Can’t lie flat on chair and can’t lie back
- Accessing mouth can be tricky
- Impossible for patient to turn head to improvement access for dentist
96
Q
what two groups are CT disease broken into
A
- vasculitis
- autoimmune
97
Q
what are autoimmune CT disease
A
- • Systemic lupus erythematosus (SLE)
• Systemic sclerosis (scleroderma)
• Sjogren’s syndrome (SS)
• Undifferentiated connective tissue disease (UCTD)
98
Q
what is found in people with autoimmune CT diseases
A
- associated blood auto AB’s
- Do not cause the disease – are found in ‘normal’ people
- Pattern caries from disease to disease
- Disease happens in peoples largely with specific auto AB’s
99
Q
what are vasculitic CT diseases
A
- problems with blood vessel walls
- large vessel = giant cell arteritis
- medium vessel = polyarteritis, Kawasaki’s disease
- small vessel = Wegener’s disease
100
Q
what is the general management for CT diseases
A
- no cure as cause not clear
- treatment dependent on suppression of disease activity
- NSAIDs
- immune modulating treatment = Hydroxychloroquine, Methotrexate, Azathioprine, Mycophenolate
- systemic steroids = prednisolone
101
Q
what are the spectrum of diseases of CT
A
- lupus = means you have can got every system invovled
- reynaud’s
- Sjogren’s
- scleroderma
- RA
- mixed CT disease
conditions are all interlinked
102
Q
what are the AB’s in autoimmune diseases
A
- Anti-nuclear antibody (ANA)
- Anti-double strand DNA (dsDNA)
- Anti-ro antibody (Ro)
(↑ found in most connective tissue diseases, found in overlapped symptoms) - Anti-La antibody (La)
- Anti-centromere antibody
(these two ↑ & ↓ are more commonly found in scleroderma) - Anti-Scl-70 antibody
- Anti-neutrophil cytoplasmic antibody (ANCA)
103
Q
what’s discoid lupus
A
- tissue changes without blood auto AB’s called ‘discoid lupus’
- seen in skin and mouth
- more localised
104
Q
what is systemic lupus erythematosis
A
- circulating immune complexes = ANA, dsDNA, and Ro AB’s
- affects joints, skin, kidney, muscle, blood
- renal involvement primarily major cause of death
- enhanced CV risk
105
Q
what are the features of lupus erythematosis
A
- pleural effusions
- heart problems
- lupus nephritis
- arthritis
- reynaud’s
- butterfly rash = photosensitive rash wherever face is exposed to sunlight
106
Q
who gets lupus erythematosis
A
- 12-64/100,000
- twins have 20-50% concordance
- environmental trigger
- females of child bearing age
107
Q
what are the dental aspects of lupus erythematosis
A
- chronic anaemia = ulceration
- bleeding tendency = thrombocytopenia
- renal disease = impaired drug metabolism
- drug reactions = photosensitivity
- steroid and immunosuppressive therapy
- lichenoid oral reactions
- oral pigmentation from hydroxychlorquine use
108
Q
what is antiphospholipid antibody syndrome (AAS)
A
- lupus anticoagulant marker found in the blood = not a really coagulant (only coagulates in a test tube, not in the body)
- primary form = no associated disease
- secondary form = found in some patients with chronic inflammatory conditions (SLE)
109
Q
what AB’s re present in those with AAS
A
- antiphospholipid
- anticardiolipin
110
Q
what is AAS characterised by
A
- recurrent thrombosis
- DVT with pulmonary embolism
- venous and arterial thrombosis
- DO NOT STOP ANTICOAGULANT IN THESE PATIENTS
111
Q
what is Sjogren’s syndrome
A
- inflammatory disease associated with circulating auto AB’s = ANA, Ro, La
- mainly associate with dry eyes and dry mouth
112
Q
what 3 groups are Sjogren’s disease broke into
A
- sick syndrome = dry eyes or dry mouth
- primary = not associated with any other disease
- secondary = associated with another CT disease
113
Q
how are people with Sjogren’s disease diagnosed
A
- no one test will ‘prove’ it
- some signs/symptoms will suggest it
- dry eyes/mouth = most common
- auto AB findings
- imaging findings
- histopathology find gins = best method
114
Q
how can someone have Sjogren’s with not dry eyes or mouth
A
- Subjective or objective
- Without this, diagnosis is unlikely but possible
- Changes in lacrimal and salivary glands can take 30 years to have their full effect
- If glands were examined histopathologically before salivary function had exhausted itself, there would be evidence of inflammatory change
115
Q
what are the oral and dental implications of Sjogren’s
A
- oral infetion
- caries risk
- functional loss
- denture retention
- sialosis = swelling of salivary glands
- salivary lymphoma
116
Q
what is systemic sclerosis
A
- excessvie collagen deposition
- connective tissue fibrosis
- loss of elastic tissue = los ability to stretch and bend tissues such as skin as it is replaced with connective fibrous tissue
117
Q
what are th forms of systemic sclerosis
A
- local = anticentromere AB’s
- generalised = anti Scl-70 AB’s
118
Q
what are the features of systemic sclerosis
A
- sclerodactyly = contractions of the fingers as the skin is no longer able to stretch around joints
- telangioectasia = haemangiomas on the face
- nail beds = haemangiomas
- reynaud’s = oolusion in blood vessels in fingers can result in ischaemic necrosis of fingers
119
Q
what internal problems can occur with systemic sclerosis
A
- organs such as the osesophagus will not stretch to allow food bolus to pass, and gut will not allow easy peristalsis
120
Q
who gets systemic sclerosis
A
- mainly women
121
Q
how does the disease progress
A
- gradual onset
- renal failure
- malabsorption
- slow progression
122
Q
what is the reynauds phenomenon
A
- blood vessels narrow significantly
- red with pain as vascular repercussion occurs
123
Q
what are the dental aspect of systemic sclerosis
A
- involve personal tissues = limited mouth opening so difficult to d treatment
- need to plan treatment 10-15 years in advance
- may be compounded by Sjogren’s which also gives a caries risk
- dysphagia and reflux disease = swallowing problems, dental erosion
- cardiac and renal vasculitis disease = watch drug metabolism
- widening of pdl = no dental mobility
124
Q
what is vasculitis disease
A
- inflammation within walls of vessels
- causes significant narrowing of tissues and so ischaemia and changes relate to degeneration occur
125
Q
how can infarction of tissues preset
A
- oral inflammatory masses
- may present as ulcer = tissue necrosis
126
Q
what is giant cell arteritis
A
- known as ‘temporal’ arteritis as commonly the temporal artery is involved
- affects distribution of external carotid artery at side of head and also inside face and heading towards central artery of retina
- headache/facial pain
- chewing claudication, occlusion of central retinal artery (blindness)
- a facial pain emergency! = ESR is raised, C-reactive protein and plasma viscosity are raised
- patient started on prednisolone ASAP
127
Q
what is polymyalgia rheumatic
A
- disease of the elderly
- large blood vessels affected
- pain and morning stiffness of muscles
- non-specific systemic features = malaise, weight loss, profound fatigue
- responds well to steroids
128
Q
what is Kawasaki’s disease
A
- medium blood vessels
- mainly a disease of children = mucocutaneoux lymph node syndrome
- coronary vessel aneurysms = may need AP cover
129
Q
how does Kawasaki disease present
A
- fever and lymphadenopathy
- crusting/cracked lips
- strawberry tongue and erythematous mucosa
- peeling rash on hands and feet
130
Q
what is Wegener’s granulomatosis
A
- small blood vessels
- most likely to present to dentist
- inflammatory condition = destruction of soft tissues of face and oral cavity, spongy rd tissue
- associated with ANCA
- renal and respiratory tract most affected
- affects many systems but mainly start in aerodigestive
- vascular rash over gingiva and palate
- urgent referral made
131
Q
what is fibromyalgia
A
- non-specific collection of musculoskeletal symptoms
- joint pain, muscle pain, functional disorders
- diagnosis often used by rheumatologists when there are symptoms but of no specific active disease
- patient present with joint pain but nothing found
- more a perceptual problem = pain from these areas is confused and so patient feels pan where there isn’t anything there
- managed through pain management rather than through suppression
132
Q
what are the dental aspects of vasculitis
A
- steroid precautions may be needed
- may present to the dentist = giant cell arteritis, Wegener’s disease, Kawasaki disease
