Bone and rheumatology Flashcards
describe the two types of resorptions we get in the tooth
internal and external resorption
how can we tell the difference between internal and external resorption
internal = radiolucency is in continum with the canal
externa - radiolucnecy superimposed on the canal
explain the structure of a bone
outer layer = periosteum = vascular CT
outer bone = dense, cortical bone
inner bone = trabecular, less dense
inner space = medulla = bone marrow and site of haemapoeisis
what are the functions of bone (3)
Mineral homeostasis = calcium and phosphate
Houses haemopoietic system
i.e. the bone marrow
Mechanical
Not a static scaffold - constantly remodelled
when might we get haematopoeisis in other sites
if there is dysfunction of bone haematopoiesis, pathology
occurs in spleen = not good
what cells would we see histologically of a remodelling site
osteocytes within matrix = calcified osteoblasts
small osteoblasts on margins
large osteoclasts
a pt has blue tinted sclera, what is this a sign of
osteogenesis imperfecta
what causes osteogenesis imperfecta and what does it affect
collagen 1 mutation
affects most tissues, ears, eyes (blue sclera), bone, teeth
what is achondroplasia
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)
where is the mutaiton in pts with achondroplasia
FGR3 fibroblast growth receptor 3
what is rickets
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
what can cause rickets
vitamin D or calcium deficiency = dietary
metabolic = increased blood calcium and bone resorption
what is osteoporosis
Increased porosity of bone due to a reduction in bone mass
what can cause osteoporosis
Age
Hormonal influences
Lifestyle (smoking, alcohol)
Activity = +ve
Genetics
Nutrition (including malabsorption)
why does age affect osteoporosis
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
what two main types of bone fracture are there
fragility = due to weakened bone under normal stress
pathological = due to tumour press
what bone is lost first in osteoporosis and why is this relevent
trabecular bone
bones with thin cortical bone and high trabecular bone degrade quickly and become very weak e.g. femoral neck
where are we likely to get fragility fractures with osteoporosis and why
vertebrae, femoral neck, distal radius
low cortical bone : trabecular bone
trabecular bon resorbs first so with little cortical bone = fracture
give three ways we coud possibly treat osteoporosis
bisphosphonates that kill osteoclasts = MRONJ risk
monoclonal antibodies against cytokines e.g. RANK-L
Increase bone formation (experimental treatments, e.g. parathyroid hormone)
what are the three complications of osteoporosis
Fragility fractures (vertebrae, femoral neck, distal radius)
Kyphosis (dowager’s hump)
Loss of height
what is Kyphosis
dowagers hump
hunchbacked appearance of the neck caused by osteoporosis which leads to reduced height
if a pt seems to be getting deformation and resorption of particular bones, what is the likely cause
Pagets Syndrome
what is and what causes Pagets Disease
Cause unknown but there appears to be a genetic component
Characterised by increased bone resorption and poorly- controlled bone formation
what is osteomyelitis
infection of the bone
that can cause necrosis and become blood borne causing sepsis
what are some common organisms that cause osteomyelitis
Staph aureus
M. tuberculosis
Salmonella
E.Coli
where do most bone tumours originate
most are secondary metastases
from lung, prostate and breast
if a pt has a primary bone tumour, what are the classes they can be
mainly benign
Can be:
Chondrogenic
Osteogenic
Others (non-matrix forming)
what types of chondrogenic tumour can we get (3)
mainly 60% benign :
Osteochondroma – many sites
Chondroma – mainly fingers
40% malignant
Chondrosarcoma – femur, pelvis, skull base
what percent of chondrogenic primary tumours are benign
60
where are we likely to find chondroma
type of chondrogenic benign tumour
mainly found in fingers
where would we usually find chondrosarcoma
femur, pelvis, skull base
compare osteogenic and chondrogenic primary tumours
osteogenic are mainly malignant 87%
chondrogenic are mainly benign 60%
name the three types of osteogenic tumour
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
compare osteoid osteomas and osteoblastomas
both benign
Osteoid osteoma – any site, small tumours in cortex
Osteoblastoma – larger tumours, typically spinal
where and who might get osteosarcomas
87% of osteogenic tumours are malignant osteosarcomas
mainly found in the distal femur, affecting younger people
what age group are affected by osteosarcomas
15-30 year olds
mainly metaphyses in knee
how do we treat osteosarcomas
mainly occur in the knee
sensitive to chemotherapy to reduce size
then surgical removal of tumour
hopefully save limb, replace knee
what age group are prone to ewings sarcoma
<20
what diseases can affect joints
Infections
Crystal arthropathies
Chronic inflammatory arthritis
Osteoarthritis/osteoarthrosis
Tumours – these are rare so don’t worry about them
what is crystal arthropathies (1) and how are they diagnosed (1)
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
what is gout
type of crystal arthropathy
Urate crystals secondary to raised serum uric acid
Deposited in joints
Due to raised uric acid
how do we treat gout
Anti-uric acid
what demographic is likely to get gout
middle-aged gout
what two types of crystal arthropathies are there and compare
gout and pseudogout
gout = urate crystals due to high uric acid = treat with anti-uric acids
pseudogout = Calcium pyrophosphate crystals = treat symptoms = NSAIDs
how might gout present
recurrent attacks of red, tender, hot and swollen joint
very painful joints
what is rheumatoid arthritis
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
what are some types of chronic inflammatory joint arthiritis
mostly autoimmune rheumatoid arthritis
HLA B27-associated diseases such as ankylosing spondylitis and psoriatic arthritis
what is ankylosing spondylitis
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.
name a HLA B27-associated disease
ankylosing spondylitis
what is a new tx for rheumatoid arthritis and ankylosing spondylitis
methotrexate - Disease-modifying anti-rheumatic drug
Anti-TNF treatments are new and effective
what is the most common joint disease
osteoarthritis
what is osteoarthritis
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
what causes osteoarthiritis
joint trauma = running or inflammation, intra- articular fracture or septic arthritis
aging
compare osteoarthritis and rheumatoid arthritis
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
what is septic arthiritis and what are the symptoms
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
how do we treat septic arthitiris
immediately in hospital
drain cavity, antibiotics, IV fluids
what causes septic arthiritis and what are some risks
joint replacement, dog bites, if inject drugs, injury, weakened immune system
caused by bacteria getting into the joint space
commonly staph aureus
what is rheumatology
medicine with bones, joints and muscle
usually inflammatory and auto-immune
what is the rule of thirds with fevers
1/3 are infection
1/3 cancer
1/3 rheumatology
what are some systemic affects of rheumatology
fever
rash
pain and stiffness
heart and lung involvement
how can we tell apart joint pain from inflammatory / non-inflammatory
inflammatory = hot, swollen, painful, hot to touch, better on use of joint
non-inflammatory = better with non-use of joint, less swollen
what are the three types of auto-immune inflammatory rheumatoid diseases
rhuematoid arthiritis (most common)
Spondylo arhtiritis
connective tissue disease
how many people have rhuematoid arthiritis and why is it decreasing
1%
reducing as smoking is reducing
what are the symptoms of rheumatoid arthritis
early morning stiffness of joints effected - cannot make fist
eases with use/exercise
flu like symptoms
stiffness after rest
help when we have NSAIDs
compare a joint with gout/infection and a joint with rheumatoid arthiritis (2)
RA = warm and slightly red
infection/gout = very hot and very red
give three signs of the hand that = untreated rheumatoid arhtiritis
untreated = deformities
Z thumb
ulnar deviation of digits (bend towards little finger)
subluxation of fingers (fingers lower plane than hand)
swan neck deformity
what are the non-articular results of rheumatoid arthritis
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
how might rheumatoid arthiritis effect the lungs and heart
non-articular affects
lung = nodules, lung fibrosis, pleasural effusions
heart = myocarditis. pericarditis, valve inflammation
what is a rheumatoid nodule, including histology
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.
a patient has painful joints and black areas of skina round their fingers. what is the problem
vasculitis on the fingers caused by uncontrolled systemic rheumatoid arthiritis
what blood tests are relevant to rheumatoid arthritis
anaemic (normocytic or iron deficient -NSAIDS)
high/low plateletes
75% have antibodies:
-RF = rheumatoid factor
-anti CCP
what two atnibodies do we test when diagnosing rheumatoid arthiritis
RF rehuamtoid factor
anti CCP
compare an early and late xray of a patient’s joints living with rheumatoid arthiritis
early: osteopenia (thinning of bone) around joints and soft tissue swell
late: erosions, space narrowing, subluxation, fusion (ankylosis)
what are the treatment options for rheumatoid arthritis
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,
what are the treatment options for rheumatoid arthritis
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
what are DMARDs
DMARDs = disease modifying anti-rheumatic drugs e.g., methotrexate, hydroxychloroquine, sulfasalazine
Methotrexate is most common - know pathwya!
if a patient has rheumatoid arthritis and has a prescription, what questions must we ask and why
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
what part of rheumatoid arthiritis treatment will not be found on a GP prescription
biological treatment e.g. Atni TNF = infliximab, B cell deplition = Rituximab, Jak
compare Jak to other biological treatments of rheumatoid arthritis
jak is the only pill
the rest are injections or IV
what risks come with treatment of rehumatoid arthiritis
infection due to potent immunosupression
what risks come with treatment of rehumatoid arthiritis
infection due to potent immunosupression
espically anti-TNF mabs e.g. infliximab that can cause reucrrent TB
what particular rrisk is there with taking infliximab for rheumatoid arthiritis
anti-TNF biological treatment
very immunosuppressive and high risk of recurrent TB
what is the main side effect of methotrexate
nausea, GI upset and vomiting
if a patient is on DMARD or biological rheumatic drug, what must we do if putting them on anti-biotics
take them off their drug for the duration of the antibiotic and for 2 weeks latter
what side effects are there from anti-rheumatoid arthiritis treatment (5)
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
a patient is being treated for rheumatoid arthiritis and is taking a 2.5mg tablet once a week. what is this
methotrexate
what is the frequency and dose of methotrexate
rheumatoid arhtiritis DMARD
once a week, 15-25mg a week in 2.5mg tablets
what can we never prescribe with methotrexate and why
Trimethoprim and Septrin
anti-folate drugs (as is methotrexate) causing bone marrow suppression
what lung complications can we get with methotrexate and how can we avoid this
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
if a patient on methotrexate has recently been diagnosed with renal failure what do we do
take them off methotrexate as it is renally excreted
if a patient is wanting to get pregnant and is on anti-rheumatoid drugs, what must we do
check if they are on methotrexate
if so they must be off of the drug for 3 months
teratogenic and can cause miscarriage
what affects can methotrexate have
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
if a patient is on biological drugs for rheumatology how does this effect dental procedures
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
what disease must we not take methotrexate with
multiple sclerosis
due to anti-TNF indications making it worse
how does rheumatology effect general anaesthetic
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
what are the dental impications of 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
also effects comfort and stability in dental chair
what is rheumatoid neck
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
what will a pt with rheumatoid neck look like
neck to the side and forward
spine is reverse C shaped
what are C1 and C2
atlast and axis
1st and 2nd cerebra
how might rheumatoid neck cause spinal cord injury
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
how do we manage a patient with rheumatoid neck
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
how might rheumatoid arthiritis link to gingivitis
immunosuppressive drugs may increase susceptibility to infection
lack of manual dexterity may reduce oral hygiene
gingivitis = suspectable individual more likely to get rheumatoid arthritis
why might a patient on methotrexate also be on bisphosphonates
methotrexate is a DMARD for rheumatoid arthritis
many patients with rheumatoid arthritis also have osteoporosis in which bisphosphonates are tx for
what is juvenile idiopathic arthritis
affects under 16-year-olds
inflammatory arthritis
50% grow out of it
mandible underdevelopment, class III malocclusion, pain, TMJ erosion
what does SPondylo Arthritis include
akylosing spondylitis
reactive arthiritis = STIs and UTIs
Enteropathic Arthiritis = Crohns and UC
Psoriatic Arthiritis = skin
what is HLA-B27
antigen protein
strongly associated with ankylosing spondylitis and other sponylo arthiritis
what gene is strongly associated with sponylo arthiritises
HLA-B27
what is ankylosing spondylitis
calcific spine
fixed spine, cannot move neck, stuck in a slouched position
inflammatory spine pain
what are the 5 common features of Ankylosing Spondylitis
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
what is psoriasis
rash with itchy, scaly patches, most commonly on the knees, elbows, trunk and scalp
no cure, inflammatory
what is another name for Iritis and what is it associated with
anterior uveitis
commonly associated with ankylosing spondylitis
what is anterior uvitieis
iritis
inflammatory eye disease with red sclera and irregular pupil/iris
associated with ankylosing spondylitis
how do we treat iritis
steroid eye drops
how many joints does rheumatoid and sonpylo arthiritis effect
rheumatoid = many around the body
spondylo = 1 or 2, oligoarthritic
descibr ehte signs of Psoriatic arthiritis
swollen fingers
flakey, birttle looking nails
red psoriasis around finger bed and finger joints
nail pitting in nails = early (more than 6 is abnormal)
what might pitting in the nails pre-dispose
more than 6 pits = psoriatic arthiritis
what is osteoarthritis
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
what is the commonest cause of joint replacement
osteoarthiritis
compare bouchards nodes and heberdens nodes
both occur with osteoarthritis as calcium deposits = osteophytes
bouchards = middle joint of finger
Heberden’s = distal joint
on an x-ray of osteoarthiritis joint what would we see (3)
reduced joint space
osteophytes = calcium deposits at side of joint
sub-chonrdal scelrosis thickeing of underlying bone
what is the treatment for osteoarthiritis
phsyiotherapy/exericse
weight loss to reduce stress
paracetamol, co-codamol, NSAIDs
surgery if joint failure or uncontrollable pain
what is gout
extremily painful, red swollen joint
gout urate crystals precipitate into joint very inflammatory due to high serum uric acid
cause neutrophils and inflammatory cytokines
what can cause high uric acid in serum
renal impairment
genetic predisposition
diuretics
dehydration
high alcohol/red meat
part of metabolic syndrome (central obesity, diabetes, high BP, high cholesterol)
how do we treat GOUT
NSAIDs, steroids (pain)
colchicine anti-inflammatory during attack 2/3 times a day
how can we prevent GOUT
lowering uric acid
Allopurinol and Febuxostat
both xanthine oxidase inhibitors
what is connective tissue disease
group of rare autoimmune diseases associated with auto-antibodies
what is connective tissue disease
group of rare autoimmune diseases associated with autoantibodies, more common in women
why can Ct disease be life threatening
renal failure
myocarditis
lung fibrosis
cerebral involvement - risk factor for stroke, if very young pt has stroke may be CT disease
what is the antibody associated with all connective tissue disease
ANA+ anti-nuclear antibody
however this is not causative, 10% of people have this but 10% do not have CT disease
what is Lupus
type of CT disease
name 3 connective tissue diseases
Systemic Lupus
Primary Sjogrens
Scleroderma
Polymyositis
Dermatomyositis
how can we identify CT tissue disease diagnosis (2)
do an ANA antibody test
if positive, do further testing to determine specific genes related to specific disease
what are some common features of connective tissue disease
Raynauds
mouth ulcers
cardiorespiratory disease
non-erosive arthiritis
butterfly rash/ blistering photosensitivity
what are Raynaud’s and describe the three phases
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
if someone present with very deformed fingers but on x-ray has no erosions, what is the cause
connective tissue disease
related to ALA+
compare deformed fingers in rheumatoid arthiritis and connective tissue disease
arthiritis = on x-ray = erosive marks and cannot move fingers, they are fixed
CT = no erosion and fingers are bendy and can be corrected
what can cause and bring on a butterfly rash
caused by connectives tissue disease
brought on by sun exposure
what is the key feature of sclerodoma (systemic scerlosis)
progressive skin thickening and tightening
starting from fingers up
what are some features of sclerodoma
skin thickening progressive
severe raynauds (colour changing fingers due to temp CHANGE)
didgital ulcers
what are the two major types of scleroderma
limited systemic sclerosis (LcSSc) = just hands, fingers and feet
Diffuse systemic sclerosis (DcSSc) = widespread
compare LcSSc and DcSSc
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
why do we do echocardiograms and breathing function tests in patients with scleroderma
LcSSc limited systemic scleroderma can cause pulmanory hypertension which will only present as breathlessness when very severe so is screened for regularly
a patient comes in with thickening skin on their hands and very bad acid erosion, what is a likely diagnosis
LcSSc - limited systemic scleroderma
causes pulmanory hypertnesion, skin thickening and acid reflux
ALA+ gene
what oral manifestations are there of limited systemic scleroderma (2)
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
why might a patient with LcSSc wear heavy makeup
causes telangiectasia and microstomia
small red marks on liops and tongue and also stretching and tethering of skin around mouth
compare primary and secondary Sjogren’s Syndrome
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
what is Sjogrens syndrome
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
what are the two main symptoms of Sjogrens syndrome
dry mouth and dry eyes (streaming eyes in wind, non-lubricating eye fluid)
what antibody and proteins are associated with primary Sjogrens syndrome
Ro and La antibodies
high immunoglobulins, high ESR and Rheuamtoid factor RF
what are the rare but serious complications of primary Sjogrens syndrome
9x more likely LYMPHOMA
Vasculitis
renal involvement
peripheral neuropathy
billiary cirrhosis
if someone has diangosed sjogrens syndrome, what should we look out for and how (2)
Lymphoma is 9x more likely
look out for B symptoms, fever, night sweats and weight loss
what would a salivary gland form a patient with Sjogren syndrome look like histologically and clinically
Lymphocytic infiltration of salivary glands that disrupt glandular architecture
can cause swelling of parotids and submandibular glands and then atrophy of these glands
what oral representations of Sjogrens syndrome are there (3)
dry mouth, diffuclty swallowing
swelling of parotis in early days, then atrophy of parotids
atrophic ‘shiny’ glossitis
what are polymyositis and dermatomyositis
conntective tissue disease causing muscle inflammation
painless wasting of muscles causing weakness of muscles and thighs
both associated with lung fibrosis
compare polymyositis and dermatomyositis
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
what are some sing and symptoms and risks of Dermatomyositis
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
pt has a purple helitrope rash around eyes and weak thighs, what do they have
dermatomyocitis - connective tissue disease
what would histology of muscles be in dermatomyocitis
lymphocytic infiltration of muscle
how do we treat connective tissue diseases
NSAIDs and Steroids
DMARDS - hydroxychloroquine
for life threatening - chemotherapy
Biological Atni-TNF drusg e.g. rituximab
how do we treat connective tissue diseases
NSAIDs and steroids
DMARDs e.g. hydroxychloroquine
if life threatening = chemotheraopy
biological anti-TNF drusg e.g. rituximab
in which connective tissue disease are anti-TNF biological drugs e.g. rituximab contraindicated
Lupus
SLE (systemic lupus erythematosus)
