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CMS1 > Bone and joint 2 > Flashcards

Bone and joint 2 Flashcards

1
Q
  1. List 3 different Joint Disorders:
A
  • Marfarns
  • Ehlers-Danlos
  • Recurrent TMJ dislocation
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2
Q
  1. What are the different types of arthritides can the patient have?
A
  • Osteoarthritis
  • Rheumatoid arthritis
  • Felty sun
  • Juvenille arthritis
  • Ankyosing spondylitis
  • Infective arthritis
  • Gout
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3
Q
  1. What are the 3 key areas of defects in Marfans syndrome?
A
  • Skeletal
  • Cardiovascular
  • Neuro-ocular
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4
Q
  1. What type of genetic disorder Marfans syndrome is? And which tissue does it affect?
A
  • Autosomal dominant
  • Connective tissues
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5
Q
  1. what causes Marfans syndrome?
A
  • A mutation in the Fibrillin-1 gene can lead to Marfans syndrome
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6
Q
  1. What are the features of Marfans syndrome?
A
  • They got loose joints
  • cardiac defects/problems particularly valvular problems (Mitral valve prolapse and Aortic dissection (AD – can be life threatening))
  • ocular lesions
  • Retinal detachment
  • Fibrillin-1 mutation
  • Arachnodactyly
  • Near-sighted
  • Scoliosis
  • pre-disposed pneumothorax
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7
Q
  1. What are the cardiovascular defects that people with Marfans syndrome are likely to have
A
  • The CV defects can include dilation of descending aorta, dissecting aneurysms, aortic regurgitations and mitral valve prolapse
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8
Q
  1. What is the most distinguish feature that people with Marfans syndrome can have?
A
  • The long thin body with long spider-like slender fingers. They get disproportionally long limbs, loose joints. Sometimes TMJ dislocation and pectus excavatum
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9
Q
  1. What are the skeletal defects/features that Marfans syndrome can have?
A
  • excessive length of tubular bones - very tall
  • Huge wide arms
  • spider-like fingers (called Arachnodactyly)
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10
Q
  1. what does the mnemonic Marfans refer to?
A
  • Mitral valve prolapse
  • Aortic dissection
  • Retinal detachment
  • Fibrillin-1 mutation
  • Arachnodactyly
  • Near-sighted
  • Scoliosis
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11
Q
  1. How common are the cardiovascular defects in Marfans syndrome?
A
  • Very common (over 90% of patents)
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12
Q
  1. How are the ligaments being affected in Marfans syndrome?
A
  • Their ligaments are lax
  • they get hyper-extensible joints
  • subluxation or dislocation
  • sometimes hernias.
  • They often get visual impairments due to lens subluxation/ dislocation of the lens
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13
Q
  1. list the Marfans syndrome defects which are relevant to us as dentists?
A
  • CV defects
  • They might get a high palate
  • TMJ disjunction/ subluxation.
  • Sometimes they have malocclusion
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14
Q
  1. What type of genetic disorder Ehlers – Danlos syndrome is (the common form)?
A
  • Autosomal dominant
  • There are various subtypes. Some are recessive but the common form is Autosomal dominant
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15
Q
  1. What is Ehlers – Danlos syndrome? How common it is? Which protein is the leading cause of this syndrome?
A
  • Group of rare disorders of collagen formation
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16
Q
  1. What are the characteristic features of Ehlers – Danlos syndrome?
A
  • Hyperextensible skin
  • Bruise
  • Loose joints
  • Recurrent spontaneous dislocations
  • Poor healing
  • Various subtypes
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17
Q
  1. What is the best known manifestation of Ehlers – Danlos syndrome?
A
  • Hypermobility of the joint
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18
Q
  1. What haematological disorder patient with Ehlers – Danlos syndrome have could have?
A
  • Sometimes they have been reported to have platelet defects but, sometimes there is no disfunction in the haematological investigation
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19
Q
  1. People with Ehlers – Danlos syndrome can have prolapse mitral valve. What sort of cardiovascular problems could this problem predispose the patient to?
A
  • Infective endocarditis
  • Heart failure
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20
Q
  1. What are the issues that Ehlers – Danlos syndrome could have that are relevant to us as dentist?
A
  • Mitral valve prolapse
  • Haematological issues – bleeding
  • TMJ
  • Short teeth / abnormal roots / pulp stones
  • Micrognathia
  • AOB
  • Gingival hyperplasia
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21
Q
  1. what is the most common form of arthritis?
A
  • Osteoarthritis (O.A.)
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22
Q
  1. What is the characteristics/ classic underlying pathology of Osteoarthritis?
A
  • Denegeration of articular cartilage and that is compensated by thickening of the exposed underlying bone with the development of periarticular cyst
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23
Q
  1. What happens with continued bone proliferation? (consider what happens with the cyst)
A
  • These cysts sometimes collapsed with continued peripheral bone proliferation and then you get progressive deformity of the joint
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24
Q
  1. When the O.A. is more common?
A
  • Over the age of 45
  • Female more than male
  • Usually if they are overweight or obese
  • If they have been an athlete this might pre-dispose them, sometimes other disease such as Paget’s or gout
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25
Q
  1. Which joint can Osteoarthritis affect? And how does it affect them?
A
  • It can affect any joint but, specifically weight bearing joints or traumatised joints
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26
Q
  1. Does O.A. has any systemic symptoms? If yes, what are they?
A
  • No (important for diagnosis)
27
Q
  1. How does that differs from rheumatoid arthritis?
A
  • In O.A. there is no obvious inflammation of affected joints or serological changes whereas with Rheumatoid arthritis you will get sometimes Rheumatoid factor and the ESR would be raised
28
Q
  1. What are the symptoms of Osteoarthritis?
A
  • People get Pain, stiffness and swelling of the joint during or after use, sometimes worse with weather changes and sometimes they get nodes just on the MCP joints
29
Q
  1. How can we Diagnose Rhumatoarthritis?
A
  • Diagnosis is Clinical and sometimes it is supported with imaging
  • On imaging you get narrowing of the joint space
  • Sometimes osteophytes formation or bone cysts
30
Q
  1. How to treat Osteoarthritis?
A
  • Analgesia - they might be topical analgesia so, NSAIDs on the joints or they might use systemic NSAID. Sometimes specific NSAIDs (COX inhibitors)
  • At some point they may require Joint replacements
31
Q
  1. What disease is the commonest form of chronic inflammatory joint disease?
A
  • Rheumatoid arthritis
32
Q
  1. How common is RA?
A
  • Can affect around 3-4% of population
33
Q
  1. Which gender is more susceptible to have Rheumatoid arthritis? How much is the risk rtio between F:M?
A
  • Women are 3 times at more risk than males
  • 3:1
34
Q
  1. Are there certain group that is more prone to RA?
A
  • Genetically pre-disposed individuals
35
Q
  1. What is RA? and what does it characterise with?
A
  • It is a multi-system, immunologically mediated disease that characterised by the presence of rheumatoid factor (RF)
36
Q
  1. When is the onset of RA?
A
  • It is insidious  you get increasing stiffness of hands or feet which is usually worse in morning
37
Q
  1. What are the clinical features of RA if it has systemic/ acute phases?
A
  • limitation of movement, hot tenderness, swelling of joints, MCP and IP joints become spindle shaped because of joints swelling and then you get muscle wasting either side of these joints. They will also, get ulnar deviation and it is usually symmetrical. Sometimes the C-spine can be involved and get atlanto-axial subluxation
38
Q
  1. what is ulnar deviation?
A
  • Hands pointing out
39
Q
  1. What are the diagnostic features of RA?
A
  • Positive RF but, Rheumatoid Factor (RF) present in 60—70%
  • Rheumatoid nodules
  • Arthritis at the hands and joints
  • Arthritis affecting more than 3 joint areas
  • Some changes on radiographs
  • More joint stiffness
  • clinical – pain, swelling, heat and stiffness in affected joints +/- nodules, +/- systemic signs
  • inflammatory markers (some have normal) [ESR CRP]
40
Q
  1. What is RF? Does it always present in RA? Why?
A
  • RF is and immunoglobulin and it present in 70% of these patients. It is a very sensitive marker but, it is not specific. Some patients are serum negative so, RF might be IgG and not detected
41
Q
  1. What are the radiographic changes that can be seen in RA?
A
  • Winding of the joint space but, later on the disease that’s then narrowed, erosion of the joints and destruction of the joints and stiffness of the joints
42
Q
  1. Management of RA (Mx)?
A
  • Supportive measures: Analgesics e.g. NSAIDs, Paracetamol, Corticosteroids into joint spaces
  • DMARDs drugs = disease modifying Anti-rheumatic drugs – reduces pain and swelling
  • Biologic drugs are also called immunomodulators. Sometimes they can cause toxic side effects but, they are very good for these diseases
43
Q
  1. Examples of DMARDs & Biologic agents:
A
  • Methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, azathioprine, Etanercept, Adalimumab, Infliximab
44
Q
  1. Dental Issues of DMARDs & Biologic agents:
A
  • Often associated with Sjogrens syndrome
  • Some changes on OPT within TMJ
  • Care with meds – risk of bleeding, infection and MRONJ.
  • they might be on steroids as well as long term NSAID. We need to be aware of those features
45
Q
  1. what is Felty Syndrome? How common it is?
A
  • Is when patient with RA coupled with Splenomegaly and Neutropenia. Difficult to manage because of those systemic effects
  • Rare
46
Q
  1. Who are the group categories that Felty Syndrome is most common in?
A
  • F>M
  • 50-70yrs
  • More common in caucasians
47
Q
  1. What is Arthritis – Juvenille? How common it is?
A
  • Similar to adult RA but, affects children. It sometimes has features of ankylosing spondylitis
  • Arthritis Juvenille is uncommon compared to rheumatoid arthritis
48
Q
  1. What are the types of Juvenille Arthritis?
A

There are variety of types:
- Systemic
- Polyarticular
- Pauciarticular

49
Q
  1. Which group is the highest risk of developing Juvenille Arthritis?
A
  • Girls’ late childhood
50
Q
  1. Which joints are affected in Juvenille Arthritis? And what are the association with this disease?
A
  • It can affect any joint – associated with fever, nodules, anaemia and malaise
51
Q
  1. How can we diagnose Juvenille Arthritis?
A
  • Positive RF in ~75% pts
  • Issues like that of adults
52
Q
  1. What is Ankylosing Spondylitis? Who are the most affected group of this disease?
A
  • Form of chronic inflammatory arthritis. sacroiliac and spinal joints causes fusion of vertebrae over time
  • Mainly seen in young males
53
Q
  1. How can Ankylosing Spondylitis affects other organs?
A
  • It may develop eye lesions (25%) and cardiac disease (10%)
54
Q
  1. What are the signs and symptoms of Ankylosing Spondylitis?
A
  • Lower back pain, stiffness that’s getting worse and tenderness around the sacroiliac joints. Sometimes the hip is involved as well. They get fixed flexion deformity. Sometimes limited chest expansion which can cause issues with respiration. They might get anaemia associated with this and ESR raised .
55
Q
  1. How does Ankylosing Spondylitis looks in the radiograph?
A
  • they get squaring of the vertebrae and ossification
56
Q
  1. How can Ankylosing Spondylitis interfere with dentistry?
A
  • If the patient requires GA, we need to be more careful when as positioning is quite difficult and can compromise them
57
Q
  1. What is the treatment for Ankylosing Spondylitis?
A
  • physiotherapy and exercises
  • NSAIDs (sometimes Anti-TNF)
58
Q
  1. What is gout?
A
  • Form of chronic inflammatory arthritis
59
Q
  1. What is the pathology of gout?
A
  • Deposits of monosodium urate monohydrate crystals in the joint dervied from hyperuricaemic body fluids. This causes release of enzymes from PMN leukocytes. Which lead to inflammatory arthritis, tenosynovitis, bursitis or cellulitis, tophaceous deposits, urolithiasis and renal disease That is when you get acute inflammation
60
Q
  1. What causes gout?
A
  • High uric acid from breakdown of purines (red mead, organ meats, some seafood)
  • High blood pressure, diabetes, obesity
61
Q
  1. What complications gout might have?
A

gout sometimes is coupled with hypertension, ischemic heart disease, and sometimes diabetes

62
Q
  1. does gout affect TMJ?
A
  • affects TMJ joints
63
Q
  1. management and treatment of gout?
A
  • From management perspective, be aware with what other medications they are on
  • Treatment – NSAIDS, Allopurinol

CMS1 (23 decks)

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