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3rd BDS IHD > Bone and rheumatology > Flashcards

Bone and rheumatology Flashcards

1
Q

describe the two types of resorptions we get in the tooth

A

internal and external resorption

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2
Q

how can we tell the difference between internal and external resorption

A

internal = radiolucency is in continum with the canal
externa - radiolucnecy superimposed on the canal

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3
Q

explain the structure of a bone

A

outer layer = periosteum = vascular CT
outer bone = dense, cortical bone
inner bone = trabecular, less dense
inner space = medulla = bone marrow and site of haemapoeisis

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4
Q

what are the functions of bone (3)

A

Mineral homeostasis = calcium and phosphate

Houses haemopoietic system
i.e. the bone marrow

Mechanical
Not a static scaffold - constantly remodelled

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5
Q

when might we get haematopoeisis in other sites

A

if there is dysfunction of bone haematopoiesis, pathology
occurs in spleen = not good

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6
Q

what cells would we see histologically of a remodelling site

A

osteocytes within matrix = calcified osteoblasts
small osteoblasts on margins
large osteoclasts

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7
Q

a pt has blue tinted sclera, what is this a sign of

A

osteogenesis imperfecta

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8
Q

what causes osteogenesis imperfecta and what does it affect

A

collagen 1 mutation
affects most tissues, ears, eyes (blue sclera), bone, teeth

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9
Q

what is achondroplasia

A

Autosomal dominant
Failure of cartilage maturation at the growth plate
Caused by a mutation of fibroblast growth receptor receptor 3 which causes it to be continually activated (it is a negative regulator of bone growth)

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10
Q

where is the mutaiton in pts with achondroplasia

A

FGR3 fibroblast growth receptor 3

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11
Q

what is rickets

A

disorder of bone mineralization
Caused by deficiency in vitamin D or calcium
Can be dietary or metabolic
Failure to mineralise -
>cartilage overgrowth,
failure of longitudinal growth
In the growing skeleton causes rickets due to failure of mineralization of growth plate cartilage
In the mature skeleton, causes bone fragility

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12
Q

what can cause rickets

A

vitamin D or calcium deficiency = dietary
metabolic = increased blood calcium and bone resorption

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13
Q

what is osteoporosis

A

Increased porosity of bone due to a reduction in bone mass

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14
Q

what can cause osteoporosis

A

Age
Hormonal influences
Lifestyle (smoking, alcohol)
Activity = +ve
Genetics
Nutrition (including malabsorption)

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15
Q

why does age affect osteoporosis

A

Sex steroids maintain mass of bone in adulthood, when women go through menopause, there is a sharp decline of oestrogen causing osteoclast activity to increase

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16
Q

what two main types of bone fracture are there

A

fragility = due to weakened bone under normal stress
pathological = due to tumour press

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17
Q

what bone is lost first in osteoporosis and why is this relevent

A

trabecular bone
bones with thin cortical bone and high trabecular bone degrade quickly and become very weak e.g. femoral neck

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18
Q

where are we likely to get fragility fractures with osteoporosis and why

A

vertebrae, femoral neck, distal radius
low cortical bone : trabecular bone
trabecular bon resorbs first so with little cortical bone = fracture

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19
Q

give three ways we coud possibly treat osteoporosis

A

bisphosphonates that kill osteoclasts = MRONJ risk
monoclonal antibodies against cytokines e.g. RANK-L
Increase bone formation (experimental treatments, e.g. parathyroid hormone)

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20
Q

what are the three complications of osteoporosis

A

Fragility fractures (vertebrae, femoral neck, distal radius)
Kyphosis (dowager’s hump)
Loss of height

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21
Q

what is Kyphosis

A

dowagers hump
hunchbacked appearance of the neck caused by osteoporosis which leads to reduced height

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22
Q

if a pt seems to be getting deformation and resorption of particular bones, what is the likely cause

A

Pagets Syndrome

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23
Q

what is and what causes Pagets Disease

A

Cause unknown but there appears to be a genetic component
Characterised by increased bone resorption and poorly- controlled bone formation

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24
Q

what is osteomyelitis

A

infection of the bone
that can cause necrosis and become blood borne causing sepsis

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25
Q

what are some common organisms that cause osteomyelitis

A

Staph aureus
M. tuberculosis
Salmonella
E.Coli

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26
Q

where do most bone tumours originate

A

most are secondary metastases
from lung, prostate and breast

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27
Q

if a pt has a primary bone tumour, what are the classes they can be

A

mainly benign
Can be:
Chondrogenic
Osteogenic
Others (non-matrix forming)

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28
Q

what types of chondrogenic tumour can we get (3)

A

mainly 60% benign :
Osteochondroma – many sites
Chondroma – mainly fingers

40% malignant
Chondrosarcoma – femur, pelvis, skull base

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29
Q

what percent of chondrogenic primary tumours are benign

A

60

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30
Q

where are we likely to find chondroma

A

type of chondrogenic benign tumour
mainly found in fingers

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31
Q

where would we usually find chondrosarcoma

A

femur, pelvis, skull base

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32
Q

compare osteogenic and chondrogenic primary tumours

A

osteogenic are mainly malignant 87%
chondrogenic are mainly benign 60%

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33
Q

name the three types of osteogenic tumour

A

13% benign
Osteoid osteoma – any site, small tumours in cortex
Osteoblastoma – larger tumours, typically spinal

87% malignant
Osteosarcoma – most commonly distal femur and tend to affect younger people

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34
Q

compare osteoid osteomas and osteoblastomas

A

both benign
Osteoid osteoma – any site, small tumours in cortex
Osteoblastoma – larger tumours, typically spinal

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35
Q

where and who might get osteosarcomas

A

87% of osteogenic tumours are malignant osteosarcomas
mainly found in the distal femur, affecting younger people

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36
Q

what age group are affected by osteosarcomas

A

15-30 year olds
mainly metaphyses in knee

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37
Q

how do we treat osteosarcomas

A

mainly occur in the knee
sensitive to chemotherapy to reduce size
then surgical removal of tumour
hopefully save limb, replace knee

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38
Q

what age group are prone to ewings sarcoma

A

<20

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39
Q

what diseases can affect joints

A

Infections
Crystal arthropathies
Chronic inflammatory arthritis
Osteoarthritis/osteoarthrosis
Tumours – these are rare so don’t worry about them

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40
Q

what is crystal arthropathies (1) and how are they diagnosed (1)

A

class of joint disorder that is characterized by accumulation of tiny crystals in one or more joints
diagnosed via polarizing light microscopy
main culprit is gout

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41
Q

what is gout

A

type of crystal arthropathy
Urate crystals secondary to raised serum uric acid
Deposited in joints
Due to raised uric acid

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42
Q

how do we treat gout

A

Anti-uric acid

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43
Q

what demographic is likely to get gout

A

middle-aged gout

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44
Q

what two types of crystal arthropathies are there and compare

A

gout and pseudogout
gout = urate crystals due to high uric acid = treat with anti-uric acids
pseudogout = Calcium pyrophosphate crystals = treat symptoms = NSAIDs

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45
Q

how might gout present

A

recurrent attacks of red, tender, hot and swollen joint
very painful joints

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46
Q

what is rheumatoid arthritis

A

Mainly Autoimmune
Part of rheumatoid disease – a systemic inflammatory disorder
Systemic inflammatory disorder
Progressive destructive synovitis causing joint deformity
Characterised by deformity in joint e.g. small joints in fingers = ulnar deviation

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47
Q

what are some types of chronic inflammatory joint arthiritis

A

mostly autoimmune rheumatoid arthritis
HLA B27-associated diseases such as ankylosing spondylitis and psoriatic arthritis

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48
Q

what is ankylosing spondylitis

A

HLA B27-associated diseases
Ankylosing spondylitis is an inflammatory disease that, over time, can cause some of the bones in the spine (vertebrae) to fuse. This fusing makes the spine less flexible and can result in a hunched posture. If ribs are affected, it can be difficult to breathe deeply.

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49
Q

name a HLA B27-associated disease

A

ankylosing spondylitis

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50
Q

what is a new tx for rheumatoid arthritis and ankylosing spondylitis

A

methotrexate - Disease-modifying anti-rheumatic drug
Anti-TNF treatments are new and effective

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51
Q

what is the most common joint disease

A

osteoarthritis

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52
Q

what is osteoarthritis

A

most common joint disease
Degenerative disease-causing erosion of cartilage with minimal inflammation
Leads to changes in underlying bone and reduction of cartilage
Bone on bone = not functional and more friction, underlying bone remodells forming deformed joints and only way to treat = replacement

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53
Q

what causes osteoarthiritis

A

joint trauma = running or inflammation, intra- articular fracture or septic arthritis
aging

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54
Q

compare osteoarthritis and rheumatoid arthritis

A

osteoarthritis = caused by aging, wear and trauma, leads to reduction in cartilage = friction = treated by replacement of joint, minimal inflammation

rheumatoid = autoimmune disorder, inflammation of joints, treated by methotrexate - Disease-modifying anti-rheumatic drug, Anti-TNF, NSAIDs

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55
Q

what is septic arthiritis and what are the symptoms

A

infection of joint synovial cavity
sudden onset of pain in 1 joint only
general unwell feeling, flu like tiredness
skin colour change around joint and pain, hot, swollen

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56
Q

how do we treat septic arthitiris

A

immediately in hospital
drain cavity, antibiotics, IV fluids

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57
Q

what causes septic arthiritis and what are some risks

A

joint replacement, dog bites, if inject drugs, injury, weakened immune system
caused by bacteria getting into the joint space
commonly staph aureus

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58
Q

what is rheumatology

A

medicine with bones, joints and muscle
usually inflammatory and auto-immune

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59
Q

what is the rule of thirds with fevers

A

1/3 are infection
1/3 cancer
1/3 rheumatology

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60
Q

what are some systemic affects of rheumatology

A

fever
rash
pain and stiffness
heart and lung involvement

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61
Q

how can we tell apart joint pain from inflammatory / non-inflammatory

A

inflammatory = hot, swollen, painful, hot to touch, better on use of joint
non-inflammatory = better with non-use of joint, less swollen

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62
Q

what are the three types of auto-immune inflammatory rheumatoid diseases

A

rhuematoid arthiritis (most common)
Spondylo arhtiritis
connective tissue disease

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63
Q

how many people have rhuematoid arthiritis and why is it decreasing

A

1%
reducing as smoking is reducing

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64
Q

what are the symptoms of rheumatoid arthritis

A

early morning stiffness of joints effected - cannot make fist
eases with use/exercise
flu like symptoms
stiffness after rest
help when we have NSAIDs

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65
Q

compare a joint with gout/infection and a joint with rheumatoid arthiritis (2)

A

RA = warm and slightly red
infection/gout = very hot and very red

66
Q

give three signs of the hand that = untreated rheumatoid arhtiritis

A

untreated = deformities
Z thumb
ulnar deviation of digits (bend towards little finger)
subluxation of fingers (fingers lower plane than hand)
swan neck deformity

67
Q

what are the non-articular results of rheumatoid arthritis

A

lung = nodules, lung fibrosis, pleasural effusions
heart = myocarditis. pericarditis, valve inflammation
kidneys = amyloidosis –> nephrotic syndrome
skin = rheumatoid nodules, vasculitis (infalmamtion of vasuclar tissue on skin =black areas of skin)
secondary Sjorens Syndrome

68
Q

how might rheumatoid arthiritis effect the lungs and heart

A

non-articular affects
lung = nodules, lung fibrosis, pleasural effusions
heart = myocarditis. pericarditis, valve inflammation

69
Q

what is a rheumatoid nodule, including histology

A

hard lump in skin that is mobile, not fixed
central necrotic tissue with a ring of lymphocytes and subcutaneous tissue
The nodules are characterized histologically by dense areas of fibrinoid necrosis with basophilic streaks and granules, surrounded by a palisade of cells, mainly fibroblasts and histiocytes.

70
Q

a patient has painful joints and black areas of skina round their fingers. what is the problem

A

vasculitis on the fingers caused by uncontrolled systemic rheumatoid arthiritis

71
Q

what blood tests are relevant to rheumatoid arthritis

A

anaemic (normocytic or iron deficient -NSAIDS)
high/low plateletes
75% have antibodies:
-RF = rheumatoid factor
-anti CCP

72
Q

what two atnibodies do we test when diagnosing rheumatoid arthiritis

A

RF rehuamtoid factor
anti CCP

73
Q

compare an early and late xray of a patient’s joints living with rheumatoid arthiritis

A

early: osteopenia (thinning of bone) around joints and soft tissue swell
late: erosions, space narrowing, subluxation, fusion (ankylosis)

74
Q

what are the treatment options for rheumatoid arthritis

A

immediate releif: NSAIDs, steroids (very effective) injected into joints, orally but lots of side effects

control of disease = immunosuppression can be biological or DMARDS

DMARDs = disease modifying anti-rheumatic drugs e.g., methotrexate, hydroxychloroquine, sulfasalazine

biological = Atni TNF = infliximab, B cell deplition = Rituximab,

75
Q

what are the treatment options for rheumatoid arthritis

A

immediate releif: NSAIDs, steroids (very effective) injected into joints, orally but lots of side effects

control of disease = immunosuppression can be biological or DMARDS

DMARDs = disease modifying anti-rheumatic drugs e.g., methotrexate, hydroxychloroquine, sulfasalazine

biological = Atni TNF = infliximab, B cell deplition = Rituximab, Jak

76
Q

what are DMARDs

A

DMARDs = disease modifying anti-rheumatic drugs e.g., methotrexate, hydroxychloroquine, sulfasalazine

Methotrexate is most common - know pathwya!

77
Q

if a patient has rheumatoid arthritis and has a prescription, what questions must we ask and why

A

ask if they have any hospital only prescriptions
biological treatment of rheumatoid arthritis is hospital prescription only so will not show on GP prescription
ask if they are taking any injections that are not on the list

78
Q

what part of rheumatoid arthiritis treatment will not be found on a GP prescription

A

biological treatment e.g. Atni TNF = infliximab, B cell deplition = Rituximab, Jak

79
Q

compare Jak to other biological treatments of rheumatoid arthritis

A

jak is the only pill
the rest are injections or IV

80
Q

what risks come with treatment of rehumatoid arthiritis

A

infection due to potent immunosupression

81
Q

what risks come with treatment of rehumatoid arthiritis

A

infection due to potent immunosupression
espically anti-TNF mabs e.g. infliximab that can cause reucrrent TB

82
Q

what particular rrisk is there with taking infliximab for rheumatoid arthiritis

A

anti-TNF biological treatment
very immunosuppressive and high risk of recurrent TB

83
Q

what is the main side effect of methotrexate

A

nausea, GI upset and vomiting

84
Q

if a patient is on DMARD or biological rheumatic drug, what must we do if putting them on anti-biotics

A

take them off their drug for the duration of the antibiotic and for 2 weeks latter

85
Q

what side effects are there from anti-rheumatoid arthiritis treatment (5)

A

immunosuppressive infection = infliximab = recurrent TB, Hep C/B
methotrexate = nausea, GI upset, vomitting
hepatoxicity = rise in liver enzymes
bone marrow toxicity = leukopenia, thrombopenia, pancytopenia
skin rash

86
Q

a patient is being treated for rheumatoid arthiritis and is taking a 2.5mg tablet once a week. what is this

A

methotrexate

87
Q

what is the frequency and dose of methotrexate

A

rheumatoid arhtiritis DMARD
once a week, 15-25mg a week in 2.5mg tablets

88
Q

what can we never prescribe with methotrexate and why

A

Trimethoprim and Septrin
anti-folate drugs (as is methotrexate) causing bone marrow suppression

89
Q

what lung complications can we get with methotrexate and how can we avoid this

A

pneumonitis/fibrosis a few months after starting
infection of both lungs leading to dry cough
usually goes but can stay
scan lungs and screen breathing rates before prescription

90
Q

if a patient on methotrexate has recently been diagnosed with renal failure what do we do

A

take them off methotrexate as it is renally excreted

91
Q

if a patient is wanting to get pregnant and is on anti-rheumatoid drugs, what must we do

A

check if they are on methotrexate
if so they must be off of the drug for 3 months
teratogenic and can cause miscarriage

92
Q

what affects can methotrexate have

A

nausea and mouth ulcers is universal after starting
causes marrow toxicity if taken with trimethoprim (GU infection) and septrin
can cause pneumonitis/fibrosis a few months after starting
teratogenic and cause miscarriage if used 3 months before conception
renally excreted so needs good renal function

93
Q

if a patient is on biological drugs for rheumatology how does this effect dental procedures

A

very immunosuppressive so may cause recurrence of TB or hep C/B
have to stop before major surgery but dental XLA usually okay
if taking off, keep off for 2 weeks to ensure safe healing

94
Q

what disease must we not take methotrexate with

A

multiple sclerosis
due to anti-TNF indications making it worse

95
Q

how does rheumatology effect general anaesthetic

A

can cause rheumatoid neck erosion of C1 and C2
weakness here can lead to spinal cord injury under GA
need xray if not had one in last 5 years before GA

96
Q

what are the dental impications of rheumatoid neck

A

erosion of C1 and C2
weakness here can lead to spinal cord injury under GA
need xray if not had one in last 5 years before GA
also effects comfort and stability in dental chair

97
Q

what is rheumatoid neck

A

erosion of C1 and C2 due to rheumatoid arthiritis
leading to subluxation at atlano-axial level, sub axial or both levels
and compression on spinal cord

98
Q

what will a pt with rheumatoid neck look like

A

neck to the side and forward
spine is reverse C shaped

99
Q

what are C1 and C2

A

atlast and axis
1st and 2nd cerebra

100
Q

how might rheumatoid neck cause spinal cord injury

A

usually, C1 atlas and C2 axis sit together with a ligament separating the ‘dens’ prominence of C2 interrupting with the spinal cord

in rheumatoid arthritis, this ligament degrades, and the dens can put pressure on the spinal cord, possibly injuring the tissue

101
Q

how do we manage a patient with rheumatoid neck

A

ask if they get neck pain
do they know they have ‘rheumatoid neck’
when positioning the patient, do they get any new neck pain
check new neurological symptoms e.g. pins and needles in hands

102
Q

how might rheumatoid arthiritis link to gingivitis

A

immunosuppressive drugs may increase susceptibility to infection
lack of manual dexterity may reduce oral hygiene

gingivitis = suspectable individual more likely to get rheumatoid arthritis

103
Q

why might a patient on methotrexate also be on bisphosphonates

A

methotrexate is a DMARD for rheumatoid arthritis
many patients with rheumatoid arthritis also have osteoporosis in which bisphosphonates are tx for

104
Q

what is juvenile idiopathic arthritis

A

affects under 16-year-olds
inflammatory arthritis
50% grow out of it
mandible underdevelopment, class III malocclusion, pain, TMJ erosion

105
Q

what does SPondylo Arthritis include

A

akylosing spondylitis
reactive arthiritis = STIs and UTIs
Enteropathic Arthiritis = Crohns and UC
Psoriatic Arthiritis = skin

106
Q

what is HLA-B27

A

antigen protein
strongly associated with ankylosing spondylitis and other sponylo arthiritis

107
Q

what gene is strongly associated with sponylo arthiritises

A

HLA-B27

108
Q

what is ankylosing spondylitis

A

calcific spine
fixed spine, cannot move neck, stuck in a slouched position
inflammatory spine pain

109
Q

what are the 5 common features of Ankylosing Spondylitis

A

Enthisitis= inflammation between tendon/ligament and bone e.g. tennis elbow
Dactylitis = swollen finger or toe
skin/nail psoriasis = rash with itchy, scaly patches, most commonly on the knees, elbows, trunk and scalp
Iritis = inflammatory eye disease
IBD = Crohn’s and UC

110
Q

what is psoriasis

A

rash with itchy, scaly patches, most commonly on the knees, elbows, trunk and scalp
no cure, inflammatory

111
Q

what is another name for Iritis and what is it associated with

A

anterior uveitis
commonly associated with ankylosing spondylitis

112
Q

what is anterior uvitieis

A

iritis
inflammatory eye disease with red sclera and irregular pupil/iris
associated with ankylosing spondylitis

113
Q

how do we treat iritis

A

steroid eye drops

114
Q

how many joints does rheumatoid and sonpylo arthiritis effect

A

rheumatoid = many around the body
spondylo = 1 or 2, oligoarthritic

115
Q

descibr ehte signs of Psoriatic arthiritis

A

swollen fingers
flakey, birttle looking nails
red psoriasis around finger bed and finger joints
nail pitting in nails = early (more than 6 is abnormal)

116
Q

what might pitting in the nails pre-dispose

A

more than 6 pits = psoriatic arthiritis

117
Q

what is osteoarthritis

A

degenerative process, wear and tear
thinning of cartilage putting pressure on bones and sclerosis
very painful joints
related to occupation and sport
increases with age

118
Q

what is the commonest cause of joint replacement

A

osteoarthiritis

119
Q

compare bouchards nodes and heberdens nodes

A

both occur with osteoarthritis as calcium deposits = osteophytes
bouchards = middle joint of finger
Heberden’s = distal joint

120
Q

on an x-ray of osteoarthiritis joint what would we see (3)

A

reduced joint space
osteophytes = calcium deposits at side of joint
sub-chonrdal scelrosis thickeing of underlying bone

121
Q

what is the treatment for osteoarthiritis

A

phsyiotherapy/exericse
weight loss to reduce stress
paracetamol, co-codamol, NSAIDs
surgery if joint failure or uncontrollable pain

122
Q

what is gout

A

extremily painful, red swollen joint
gout urate crystals precipitate into joint very inflammatory due to high serum uric acid
cause neutrophils and inflammatory cytokines

123
Q

what can cause high uric acid in serum

A

renal impairment
genetic predisposition
diuretics
dehydration
high alcohol/red meat
part of metabolic syndrome (central obesity, diabetes, high BP, high cholesterol)

124
Q

how do we treat GOUT

A

NSAIDs, steroids (pain)
colchicine anti-inflammatory during attack 2/3 times a day

125
Q

how can we prevent GOUT

A

lowering uric acid
Allopurinol and Febuxostat
both xanthine oxidase inhibitors

126
Q

what is connective tissue disease

A

group of rare autoimmune diseases associated with auto-antibodies

127
Q

what is connective tissue disease

A

group of rare autoimmune diseases associated with autoantibodies, more common in women

128
Q

why can Ct disease be life threatening

A

renal failure
myocarditis
lung fibrosis
cerebral involvement - risk factor for stroke, if very young pt has stroke may be CT disease

129
Q

what is the antibody associated with all connective tissue disease

A

ANA+ anti-nuclear antibody
however this is not causative, 10% of people have this but 10% do not have CT disease

130
Q

what is Lupus

A

type of CT disease

131
Q

name 3 connective tissue diseases

A

Systemic Lupus
Primary Sjogrens
Scleroderma
Polymyositis
Dermatomyositis

132
Q

how can we identify CT tissue disease diagnosis (2)

A

do an ANA antibody test
if positive, do further testing to determine specific genes related to specific disease

133
Q

what are some common features of connective tissue disease

A

Raynauds
mouth ulcers
cardiorespiratory disease
non-erosive arthiritis
butterfly rash/ blistering photosensitivity

134
Q

what are Raynaud’s and describe the three phases

A

common feature of CT disease
lack of blood flow in fingers/toes due to CHANGE of temperature
1. fingers go white due to vasoconstriciton extreme
2. build-up of deoxygenated blood = blue
3. overdilute in warm and go warm, enlarge, swell and go red

135
Q

if someone present with very deformed fingers but on x-ray has no erosions, what is the cause

A

connective tissue disease
related to ALA+

136
Q

compare deformed fingers in rheumatoid arthiritis and connective tissue disease

A

arthiritis = on x-ray = erosive marks and cannot move fingers, they are fixed
CT = no erosion and fingers are bendy and can be corrected

137
Q

what can cause and bring on a butterfly rash

A

caused by connectives tissue disease
brought on by sun exposure

138
Q

what is the key feature of sclerodoma (systemic scerlosis)

A

progressive skin thickening and tightening
starting from fingers up

139
Q

what are some features of sclerodoma

A

skin thickening progressive
severe raynauds (colour changing fingers due to temp CHANGE)
didgital ulcers

140
Q

what are the two major types of scleroderma

A

limited systemic sclerosis (LcSSc) = just hands, fingers and feet
Diffuse systemic sclerosis (DcSSc) = widespread

141
Q

compare LcSSc and DcSSc

A

limited systemic slcerodoma = just hands, fingers and feet, pulmanory hypertension and acid reflux , microstomia (tight, tethered skin around mouth) and telangiectasia (small red marks on lips and tongue)
diffuse systemic sclerodoma = widespread, pulmanory fibrosis and scleroderma renal crisis - hypertensive acute renal failure

142
Q

why do we do echocardiograms and breathing function tests in patients with scleroderma

A

LcSSc limited systemic scleroderma can cause pulmanory hypertension which will only present as breathlessness when very severe so is screened for regularly

143
Q

a patient comes in with thickening skin on their hands and very bad acid erosion, what is a likely diagnosis

A

LcSSc - limited systemic scleroderma
causes pulmanory hypertnesion, skin thickening and acid reflux
ALA+ gene

144
Q

what oral manifestations are there of limited systemic scleroderma (2)

A

acid reflux = acid erosion of teeth, TSL
microstomia and skin tethering around mouth, struggle to open mouth wide
Telangiectasia = small red marks on lips and tongue

145
Q

why might a patient with LcSSc wear heavy makeup

A

causes telangiectasia and microstomia
small red marks on liops and tongue and also stretching and tethering of skin around mouth

146
Q

compare primary and secondary Sjogren’s Syndrome

A

primary = occurs without rheumatoid or other autoimmunity, caused directly by connective tissue disease

secondary = caused by other rhuematoid illness, mainly rheumatoid arthritis or other auto-immune diseases

147
Q

what is Sjogrens syndrome

A

autoimmune disease affecting fluid producing body parts
dry eyes, thin, non-lubricating wetness of the eyes
xerostomia
diffuclty swallowing
difficulty drinking dry foods
joint pain

148
Q

what are the two main symptoms of Sjogrens syndrome

A

dry mouth and dry eyes (streaming eyes in wind, non-lubricating eye fluid)

149
Q

what antibody and proteins are associated with primary Sjogrens syndrome

A

Ro and La antibodies
high immunoglobulins, high ESR and Rheuamtoid factor RF

150
Q

what are the rare but serious complications of primary Sjogrens syndrome

A

9x more likely LYMPHOMA
Vasculitis
renal involvement
peripheral neuropathy
billiary cirrhosis

151
Q

if someone has diangosed sjogrens syndrome, what should we look out for and how (2)

A

Lymphoma is 9x more likely
look out for B symptoms, fever, night sweats and weight loss

152
Q

what would a salivary gland form a patient with Sjogren syndrome look like histologically and clinically

A

Lymphocytic infiltration of salivary glands that disrupt glandular architecture
can cause swelling of parotids and submandibular glands and then atrophy of these glands

153
Q

what oral representations of Sjogrens syndrome are there (3)

A

dry mouth, diffuclty swallowing
swelling of parotis in early days, then atrophy of parotids
atrophic ‘shiny’ glossitis

154
Q

what are polymyositis and dermatomyositis

A

conntective tissue disease causing muscle inflammation
painless wasting of muscles causing weakness of muscles and thighs
both associated with lung fibrosis

155
Q

compare polymyositis and dermatomyositis

A

both conntective tissue disease causing muscle inflammation
painless wasting of muscles causing weakness of muscles and thighs
both associated with lung fibrosis
polymyositis is only muscles
dermatomyositis is muscles and skin and involes photosensitivity causing purple rash around eyes with high chance of internal malignancy

156
Q

what are some sing and symptoms and risks of Dermatomyositis

A

muscle and skin involvement
painless wasting of muscles, especially arms and thighs
lung fibrosis
photosensitivity - purple ‘helitrope’ rash around eye and periorbital oedema
strong association with internal malignancy

157
Q

pt has a purple helitrope rash around eyes and weak thighs, what do they have

A

dermatomyocitis - connective tissue disease

158
Q

what would histology of muscles be in dermatomyocitis

A

lymphocytic infiltration of muscle

159
Q

how do we treat connective tissue diseases

A

NSAIDs and Steroids
DMARDS - hydroxychloroquine
for life threatening - chemotherapy
Biological Atni-TNF drusg e.g. rituximab

160
Q

how do we treat connective tissue diseases

A

NSAIDs and steroids
DMARDs e.g. hydroxychloroquine
if life threatening = chemotheraopy
biological anti-TNF drusg e.g. rituximab

161
Q

in which connective tissue disease are anti-TNF biological drugs e.g. rituximab contraindicated

A

Lupus
SLE (systemic lupus erythematosus)

3rd BDS IHD (14 decks)

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