Rheumatology. Flashcards
Explain rheumatology.
Old name
Rheu- flow of a current
ology- study of
Branch of medicine that deals with the treatment and diagnosis of rheumatoid diseases such as
cateogries-
Autoimmune diseaae (SLE, Sarcoidosis, Rheumatoid arthritis)
Autoinflammatory diseases
(Familial mediteranean fever, stills disease)
Crystalline arthritis (gout, pseudogout)
Metabolic bone diseases
(osteoporosis, pagets disease)
Pain syndromes
(Fibromyalgia, Rotator cutt off tear)
and Vasculitis
Explain Rheumatism.
Any disease with Pain and Inflammation of joint, muscle or connective tissues.
What are some bullet points you need to remember while studying rheumatology?
No single Blood test will confirm the diagnosis.
Just because a person have +ANA does not mean LUPUS the tests needs to be compatible or fit with the patients history and physical examination
What is the main diffrence between ANA and ANCA antibodies?
Both are blood tests used by doctors to help in the diagnosis of autoimmune disease.
Antineutrophil cytoplasmic antibody (ANCA) is a blood test commonly elevated in patients with diseases such granulomatosis with polyangiitis, microscopic polyangiitis, and EGPA/Churg-Strauss syndrome.
Antinuclear antibody (ANA) is a blood test most often elevated in patients with systemic lupus erythematosus (“lupus”), Sjogren’s syndrome, scleroderma, and other types of autoimmune diseases.
Explain Sensitivity while dealing with the lab test of someone you suspect have rheumatism?
Sensitivity- Among the total persons who have the disease, how many of their lab test shows true positive criteria
the lower is the number of the false negative FN (have disease but doesn’t show in result) the higher will be the sesitivity of test
also If the test is true negative (TN) the Patient in almost all of the cases will have no disease.
what if the patient have zero symptoms?
All the negatives are true negatives if you choose a high sensitivity test in patient with no symptoms.
Explain specificity.
How many with no disease actually have true negative criteria
if in a high specific test patient gets a true positive it means they have the disease
(+ most of the symptoms)
How wil you rule out and rule in a disease? (lupus)
If by the symptoms its very unlikely that the patirnt will have lupus we gotta rule out this disease– we will use a sensitivity test as every negative is a true negative.
Eg- ANA is a sesitivity test so negative ANA means no lupus
but positive ANA can indicate a lot of diseases
If by symptoms it is highly likely that a patient have lupus, we will need to rule IN the disease – use a specificity test as every positive is a true positive.
Eg- Anti ds-DNA test
Anti smith test
if positive you have lupus
What is antibody titre?
This test is used to detect how many antibodies an organism have made . High number of antiobody —-> high level of disease
we keep diluting the antibody solution to find till how much dilution the solution of antibody is capable of causing agglutination.
The higher dilution it takes= means the soution have a lot of antibody
so we have to diltute the solution a lot more to cause them to prevent agglutination :)
What is ANA antibody?
Anti nuclear antibody— Attack the components of the nucleus of the cells.
Detected in titres
higher the titre—> higher the chance of autoimmune disease
BUT higher the titre= does not mean high severity of disease
ANA is considered positive if the titre is higher than 1:80
healthy people can also have +ANA
we do the test using immunoflorescence or ELISA
ANA titre has nothing to do with the activity of the disease so you should not repeat the ANA test
Explain some rheumatic disease and their markers
SLE - should have +ANA
+anti ds-DNA
+anti smith antibodies
RA - Should have +ANA
+RF
+anti-CCP
Explain ESR and CRP?
High ESR and CRP (C reactive protien ) can be seen in any inflammatory disease.
However in case of Lupus CRP is low. C3 goes down before C4
What are the common complaimts of a rheumatolgy patient?
Joint- Pain, Stiffness and loss of function
skin- Rash, lesion, swelling or sweating
eye problems, bowel problems and maliganncy.
Rheumatoid arthritis pain is worse in the morning
osteoarthritis - worse in night
how will you do a general exam of a patient?
Overall apperarence (looks, mood, brain function (awake, alert, orientation and arouseness)
posture and gait
skin- normal, cyanosis ,color, lesions, rash
weight
body haor
face
in rheumatology we examine all body systems. We look for extra articular manifestations.
Which diseases can have positive ANA?
1) Drug Induced Lupus (100% sensitivity)
so if ANA Is negative it is a true negative and the patient doesn’t have the disease
2) SLE (98-100% sensitivity) 98-100% patient will have positive ANA
but if negative- true negative- rule out the disease
3) Mixed connective tissue disease (93-100%)
4) Scleroderma
5) Sjogren
6) Dermatomyositis/ polymyositis
7) Rheumatoid arthritis (40%)
Why is ANA not specific
Negative ANA can rule out diseases but positive ANA means nohing as it is positive in a lot of disease (even normally)
Specificity— not present in many diseases and a characteristic of only one specific disease.
Explain Anti ds-DNA test.
It is a specific test for SLE
if positive—- true positive—–person has disease
corellates with SLE activity (lupus nephritis)
NOT SEEN IN DRUG INDUCED LUPUS
Explain anti smith test.
Specific test for SLE
doesn’t corellateswith likelihood of renal disease.
What are some of the Specific ANA’S?
If we are doing a test for simple ANA it is sensitive
but if we are doing test for specific types or anti nuclear antibody (depending on the component of the nucleus they are attacking ) we can get specific ana test tha can be used to rule in a certain diseases.
Some specific ANA are
1) Anti ds-DNA and Anti smith for lupus (if positive-have disease)
2) Anti histone for drug induced lupus
3) ANti-centomere for limited scleroderma
4) anti RNA polymerase III for Scleorderma kidney
5) Anti SCL 70 (anti topoisomerase 1) for systemic sclerosis
6) anti SSA (anti RO) SLE and sjogren
7) anti SSB (anti LA) SLE and sjogren
(both of them can be transferred to baby from mother and can cause congenital heart block and neonatal lupus)
8) anti- U1 RNP for MCTD and SLE
Classify rheumatolical diseases
Inflammatory and non inflammatory
Inflammatory- all cardinal signs of inflammation (red hot pain swell loss of function)
symmetric (antibody affect all side equally)
worse in morning
ESR and CRP high (as they are acute phase reactants and go up with inflammatory response)
example RA
Non- Inflammatory- No cardinal signs of inflammation
asymmetric (side of body affected unequally)
worse in evening (as we go throughout the day the more joint is used and the pain is more)
ESR and CRP normal limits. example osteroarthritis (mechanical wear and tear)
Explain ESR and CRP.
High esr means sedimentation rate is high
some pro sedimentation factors that cause high ESR are high number of Fibrinogen and high Immunoglobins (AB)
high ESR can be seen in
Inflammation (IgG, Fibrinogen) (SLE and RA)
Infection (IgG and fibrinogen) (TB and RF)
anaemia (less RBC less negative charges repelling each other)
Macrocytosis (Larger is slower)
multiple myeloma
Waldenstorm
Anti sedementation factors are the negative charges on the surface of rbc
negative charges repel each other thus preveting roulex formation and decreaing the ESR
low esr can be seen in- hyperviscosity syndrome polycythemia sickle cell microcytosis spherocytoiss
Explain ESR-
roulex formation (one rbc on top of another just like stacking)
high roulex formation high ESR (sedimentation rate is fast)
normal ESR= for men 15mm/hr (15 mm of rbc is sedementing per hour)
for women- 20mm/hr
What is the best way to examine an inflammed joint?
Joint Fluid Aspirate “Athrocentesis” or Joint Puncture
do ESR and CRP correlate with the disese activity?
YES!!!! (For eg if you have RA and your ESR is 130/hr your body is done.)
they correlate with the treatment and severity of disease unlike titres.
What if the ESR and CRP is extremely high?
Think Infection, Maliganancy or Vasculitis
these test are more sensitive than specific as their are thousands of conditions that can cause elevated level of the acute phase reactants
in case of rheumatic diseases, high ESR and ZRP indicate inflammatory criteria for these diseases but doesn’t point out or rule in a specific disease
if these are within normal limits and we are testing for rheumatic diseases it indicates non-inflammatory cateogry of these group of diseases. Like osteoarthritis
What is C reactive protien? CRP
Synthesized in liver in response to IL-6 (by WBC and Malignant cells)
bacteria/dying cell/malignant cell/WBC/Adiposcytes————–> IL-6———–> liver———-> CRP synthesis
CRP goes and attach to its receptor PHOSPHOCHOLINE on the affected cell
Phagocytosis by macrophages
normal value– 0.8 to 3.0 mg/L
if we are treating someone with high ESR and CRP? Which one should normalize first?
CRP is by definition, REACTIVE, so it both builds and dissipates rapidly.
The sed rate is by nature, SEDENTARY, so it is slow. That’s the mnemonic.
The supporting facts are that the half-life of CRP is 19 hours, while in contrast, the half life of fibrinogen is FOUR DAYS and the half life of IgG is TWENTY-ONE DAYS!!.
Those rouleaux are not going to be able to unstick themselves from each other for a long, long time. I think of CRP as carry-on luggage, and rouleaux as a big stack of luggage that has to be checked.
Explain APR acute phase reactants
Made by liver during inflammation
high in inflm.
Low when it is cured
these are of two types–
positive APR- high in inflammation
help the immune system
fight microbes and engulfs them
trap them in local blood clots
ex- CRPs , complements, Caogulation factors and VWF
alpha 2 microglobulin, ferretin, hepicidin, ceruloplasmin, haptoglobin, alpha 1 antitrypsin
ESR can be considered an acute phase reactat even though it is a lab method. Half life is 7 days so it can be high even though inflammation is cured
half life of CRP is 7 hours :)
negative APRs- low in inflammation
liver decrease some of them as during inflammation high amino acids are needed to synthesize +APR
so by decreasing some of its syn components (-APRs) it can compensate
ex- albumin transferrin and antithrombin
is there any diagnostic value with high crp?
No in itself. High CRP must correlate with History, physical exam, other risk factors and other lab results
high CRP could indicate high RISK of cardiovascular diseases
patient with obstructive sleep apnea have high CRP and IL-6
Females who take oral contraceptives also have high CRP—> high risk of thrombosis especially if they smoke
IF a prgnant female sudenly have high CRP it could indicate obsterics complication
What is the diffrence between CRP, C-peptide and Protien C?
CRP is a marker of inflammation
c protein is an inhibitor of factor 8 and 5 in the coagulation process
c peptide is a chain of amino acides produced in beta cells of the pancreas , it comes from the clivage of proinsulin .
What are ANCAs? (Anti-Neutrophillic Cytoplasmic Antibodies)
AutoAntibodies (IgG) against the antigens in the Cytoplasm of the nueutrophils and monocytes
(ANA are against nucleus of any cell)
the best way to detect these are Elisa(best) and Immunofluroscence
accosiated with Small vessel Vasculitis
again they do not correlate with disease activity.
What are some types pf ANCA?
AnCA can have different patterns under Immunofluroscence
c-ANCA -
cytoplasmic ANCA / PR3 ANCA
(uniform cytoplasmic staining with no interlobular accentuation or no staining of nucleus)
cytoplasm is glowing and nucleus is dark
we can easily tell the diffrence between neurophil and monocyte by seeing shape of nucleus
cANCA targets Protinease 3
p-ANCA-
Perinuclear ANCA / MPO-ANCA
(perinuclear staining with extension to nucleus)
cytoplasm aroung the nucleus is glowing with some part of nucleus in it
we cannot diffrentiate between N and M
p-Anca is positively charged so these AB will gather around the nucleus that is negatively charged
myeloid lineage have myeloperoxdase enxyme that makes free radicals
free radicals are negatively charges=d so pANCA will attack myeloperoxidase (positive ANCA)
how do ANCA affect the neutrophils?
ANCA are serum antibodies Protinease 3 (attack by cANCA) and myeloperoxidases (attcked by pANCA) are present in the cytoplasm of the cell so the serum antibodies cannot attack the neutrophil and monocytes.
As IL-6 or TNFalpha activates the N and M cells, these PR3 and MYLOP goes towards the lipid membrane surface. As they go to surface they gets attacked by ANCA causing damage to cell.
Degranulation of the cells occurs that causes tissue damage (vasculitus)
Name the Vasculitedes and ANCA accociated with them.
C-ANCA—->
Granulomatosis with polyangitis (wegners)
p-ANCA—>
Goodpasture syndrome
microscopic Polyangitis
Eosinophillic granulomatosis with polyangitis (Churgg strauss)
Drug induced ANCA accosiated vasculitis
primary Pauci immune necrotizing crecentric glomeruonephritis (RPGN)
Inflammatory bowel disease
Primary sclerosing cholangitis
Autoimmune hepatitis tupe 1
Explain Rheumatoid Factor. RF
Antibody against the Antibody (dog chaising its tail)
Anti-immunoglobin Antibody
These are IgM (most cases) antibodies against the Fc portion of IgG
formation of immune complexes—-> inflammatory arthritis
this antibody is a cryoglobulin (on cooling it preciitates)
sensitivity 80% (can used to rule out the disease)
specificity 75% (to rule in)
so it is used as sensitivity test
if the test for RF comes back negative (every negatve is a true negative in case of sensitivity) so the patient doesn’t have RA
Inflammatory arthristis can be divided on what basis?
On the basis of presence of RF
if seropositive (RA+) RA SLE Sjogren systemic scleorisi
if seronegative (-RA) HLA B27 Ar. psoriatic Ar. ankylosing Ar. IBD accosiated Ar. Reactive Ar.
Explain Anti-cyclic citrullinated petide. (Anti CCP)
These AB attack citrulline (formed from Arginine during inflammation)
by ELISA
positive in 60-70% of rheumatoid Arthritis patients
(Very specific so it can be used to rule In the disease)
(every positive is a true positive so it is used to rule in)
Anti ccp are more predictive of joint erosions so if ypu have anti Ccp it means you have a higher chance of RA
so even if patient have no joint pain or swelling but anti ccp s present he will get RA soom
are anti CCP and Anti CPA the same?
Nopes
anti CCP = antigens are cyclic peptides
anti CPA ( anti citrullinated protien antigens) = antigens are peptides or modified protiens
Explain diffrence in RF and anti ccp
Rf is seen in many rheumatic diseases so it can not be used to diagnose a specific certain disease. It is highly sensitive so it can rule out diseases
if RF is negative it means you do not have certain diseases so ruling them out. But if RF is positve there are many diseases it can correlate with
on the other hand anti ccp is highly specific for RA which means It will rule in RA if present in serum. (To rule in)
presence of both RF and Anti ccp means RA is worse
more aggressive symptoms
extraarticular manifestations
Explain ANti-Ds DNA antibody (accociated with lupus)
A Specific subtype of ANA
highly specific autoantibodies (IgG) against double stranded dna
detected by elisa or if
SPECIFIC for SLE
so if anti ds dna is present rule in SLE
not senitive so it cannot rule out SLE.
Correlates with SLE activity
so if you have lupus+ anti ds dna it means you will have renalmanifestations (lupus nephritis or glomerulonephritis) also lupus vasculitis
absent in drug induced lupus
defective apoptosis in lupus> no clearance of DNA fragments in plasme> antibodies made against this DNA
in case of SLE flare (high manifestations of SLE) anti ds DNA is increases dramatically
therapy give Belimubab.
Patient who are taking TNF apha inhibitors can show high level of anti ds dna but it is not corellated with lupus
What is the Main organ lupus can damage?
Lupus can damage Kidneys in two ways.
Nepritic syndrome- diffuseproliferative glomerulonephritis
nephrotic- membranous nephropathy
When can a Patient with RA can become positive for Anti ds DNA?
If the patient with RA is being treated with TNF alpha inhibitors they can become positive for DS DNA antibodies
Explain anti smitih antibodies
Occurs only in Lupus patients (very specific)
but only 25% of patients with lupus have these (not sensitive, cannot rule out lupus but can rule in lupus)
Antibodies against Smith antigens (nuclear protiens)
If you are +anti smith , you are also +anti RNP
What is the main diffrence between anti DS DNA and anti smith AB if both of them are specific for lupus
Unlke anti ds DNA the anti smith antibody does not corelate with any flare ups or nephritis or vasculitis. Doesn’t increase or decrease dramatically
Explain anti U1 RNP antibodies.
Antibodies against SnRNP70 (RNA binding protien) a component of splicesome.
Found in conditions that have overlapping features of multiple rheumatic diseases (eg- mixed connective tissue diseases (very sensitive)
onlyfound in 15-30% of patient with lupus. It is neither sensitive nor specific
the absence of anti RNP almost rules out the mixed commective tissue disease (97% sensitive for MCTD)
What is anti ds dna and anti rnp are together?
Anti ds DNA + Anti RNP + clinical picture of lupus === lupus (not MCTD)
Explain anti SSA (anti RO)?
Can be seen in lupus and sjogren
not specific or sensitive
but if seen in lupus corrlates with nephritis and skin diseases
if anti SSA is present in patient with sjogren —-> very high risk of non-hogkin lymphoma
What will we see in lupus nephritis?
Positive anti ds dna
positive SSA
Has SLE
negative SSB
Explain anti SSB?
Seen in sjogren syndrome and SLE
not sens or spec
doesn’t correlate with anything in lupus
id anti SSB present with sjogren —-> high risk of non -hogkin luymphoma
Explain antihistone antibodies.
Drug Induced lupus (very sensitive 95% and more) (so we can rule out the disease if the test comes negative)
What is scleroderma
Scleroderma (sklair-oh-DUR-muh) is a group of rare diseases that involve the hardening and tightening of the skin and connective tissues. Scleroderma affects women more often than men and most commonly occurs between the ages of 30 and 50
What are the types of scleroderma?
Limited scleroderma (localized) (limited to skin)
CREST syndrome
Anti-centomere antibody seen
Improved survival
Diffuse scleroderma (Systemic sclerosis)
Anti-RNA polymerase III
Anti-SCL 70 (anti topoisomerase 1) - Low rate of durvival
what is ANticentomere antibody?
Auto-antibodies against the centomere or kinetochore of a chromosome.
Subtype of ANA
In case of Limited scleroderma this antibody is specific (97%) so it can used to rule in. If anticentomere is positive, every positive is a true positive in case of specificity so rule in the disease.
Sensitive (80%) so it can rule out scleroderma
in case of primary billiary cirrhosis—> if we find these antibodies in the plasma, they correlate with the portal hypotension (prognostic value)
What are the clinical feature of limited scleroderma seen (if anti centomer is posi)
Calcinosis cutis
digital ischemia
PAH
primary billiary cirrhosis
why is there a low renal crisis and low risk of interstitial lung diseases if anti centomere bodies are present?
Anti centomere is present inlimited scleroderma and it is only limited to skin so low chances of tissues or other organ involvement.
What is CREST syndrome in case of Limited Scleroderma?
CREST syndrome, also known as the limited cutaneous form of systemic sclerosis (lcSSc), is a multisystem connective tissue disorder.
The acronym “CREST” refers to the five main features:
Calcinosis ( formation of calcium deposits in any soft tissue)
Rynaud’s phenomenon (Raynaud’s phenomenon is a problem that causes decreased blood flow to the fingers)
Esophageal dysmotility (muscles in your esophagus fail to contract and the esophagus does not properly deliver food and liquids into the stomach)
Sclerodactyly ( thickening of the skin of the digits of the hands and feet)
Telangiectasia (commonly known as “spider veins”) are dilated or broken blood vessels located near the surface of the skin or mucous membranes)
What is ANti-RNA polymerase III (diffuse scleroderma)
Seen in ysystemic / diffuse scleroisis.
If this antibody is present WITH clinaical sign of systemic scleosis
high chance of Scleroderma Renal Crisis
high chance of malignancy (in case of lungs and esophagus)
high risk of pulmonary arterial hypertension
and skin diseases.
why diffuse scleroderma increase risk of malignancies?
Long term damage to tissues such as esophagus (GERD) and lungs (interstitial lung disease)—> cancer
What are ANti-Scl-70 (anti topoisomerase 1 )?
Diffuse scleroderma Diffuse Cutaneous systemmic sclerosis these antibodies are accosiated with Renal crisis Lung involvement cardiac involvement tenson fricion rub
very low chance of survival
Explain Anti Synthahetase antibodies.
Autoantibodies Against the Self
Target tRNA synthetase enzyme (aminoacyl trana synthetase/or DNA ligase)
ligase attaches amino acids to rna
three subtypes
1)ANti-Jo - targets histidyl rna synthetase
Accosiated with Myositis (inflammation of
muscles such as dermatomyositis and
polymyositis)
Increase risk of int. Lung disease
Anti SRP- Targets signal recognition particle
accosiates with SLE
anti Mi 2 - targets nuclear protien complex
also accosiated with dermatomyositis
good prognosis and favourable treatment
Explain role of complement in rheumatic diseases
In many rheumatological diseaes such as lupus he antibodies attch to the antigens forming a antibody antigen comples
this complex will activate the classical pathway of the complement
this pathway have two end points
formation of MAC to destroy the antigen (in this case the antigen is body own tissue)
C3b can attract macrophages to engulf antigen
C3a and C5a are chemotctic agent that enhances the inflammatory reaction by attracting wbc
Which pathway of complement system is affected in case of Lupus?
Only The classical pathway (the antigen antibody complex)
low level of C4
not the alternate (where bacterial endotoxin starts the pathway) and neither the mannose binding (no mannose containing bacteria)
explain hypocomplpementemia
Decreased serum level of complements protiens
could be due to-
genetic deficiency
underproduction (liver diseases) such as Eclampsia
and HELLP
overconsumption (by increased complement activation in cases of rheumatic diseases) etc
decreases C2/C4 in genetic allele deficiency, hereditary angioedema, acquired angioedema
decreased C3 due to high complement activation in both classical and alternative pathway
decreased C4 high complement activation in case of classical eg SLE
What is Early complement deficiency? (C1, C2, C4)
It is usually accociated with SLE and recurrent sinopulmonary bacterial infections
late complement deficiency (C5 C9) is accociated with invasive nissenia infections
How wil the normal Joint aspirate fluid looks?
Color : colorless or straw colored Aspect : clear consistency : thin and stringy Viscosity : Moderate WBC < 200 WBC/mm3 RBC < 0-1mm3 neutrophils less than 25% Free of bacteria fungi and viruses glucose less than that of blood
How will the joint fluid aspirate look in case of osteoarthritis
Everything same
EXCEPT
color-yellowish
WBC higher than 200
How will you examine joint fluid aspirate? (physiologically)
Gross examination - Transparent (non Inflammatory) translucent (mild inflammation) opaque (purulent inflammation) Bloody (traumatic tap, trauma and bleeding disorders)
Cell Count WBC- <200 normal 200-2000 noninflammatory (osteoarthritis) 2000-75000 inflammatory >100,000 purulent
Microscopic examination
Polarized light microscopy
-ve bifringent = monosodium urate (gout)
+ve bifringent = calcium pyrophosphate (pseudogout)
Examining the joint fluid aspirate (pathologically) (diseases)
If diagnosis is uncertain –> order joint fluid aspirate
in Reumatoid A (inflammatory rheumatic disease)
Color : yellow and opaque
Aspect : opaque or translucent
WBC 2000-75000 WBC/mm3
neutrophils more than 50%
In gout same as RA
In SLE and sjogren also same as RA
Explain Athropathy.
Athropathy - Joint disease
Arthritis - Joint inflammation
Arthralgia - Joint pain
Even though orthoarteritis have it is it is a non inflmammatory condition
how can you classify arthritis?
Acute (few days to a week) and Chronic (more than a week,onths etc)
Explain Imagine studies for joints in rheumatology
Initial tets - X ray joint space narrowing bone erosions hypertrophic changes periostitis chondrocalcinosis seen in pseudo gout
Explain Osteoarhritis. (Disease of the elderly)
Degenrative disease
Non-Inflamatory (no Antibodies present lol)
Chronic so lymphocytes can be seen
WBC can be seen but systemic inflammation is a no go
can be monoarticular or oligoarticular
distal-Intraphalangeal joints affected or the 1st
metaTarsoPharynegeal (toe)
Asymmetrical (wear and Tear)
No elevation of ESR or CRP. No cardinal sign of inflammation
Joint pain worsens with use
What are the Risk factors of Osteoarthritis?
Being elderly
obesity (affecting the weight bearing joint) (hips and knees)
high manual labour work during most of the life
Athletic person
Trauma
Some chronic insidious disease related to lymphocytes
WBC 200-2000
Morning stiffness is seen (<30 min)
No synovial joint inflammation
What is the ultimate replacement for Osteoarthritis?
Replacement Just like car wheels
ARTHROPLASTY.
What are the different tyoes of bones?
Lamellar bone represents the main type of bone in a mature skeleton. It is characterized by an orderly arrangement of collagen bundles and their cells (type ! Collagen)
Woven bone is produced when osteoblasts produce osteoid rapidly, which occurs initially in all fetal bones, but is later replaced by more resilient lamellar bone
cartilage is made of type 2 collagen
What is the part of the bone that is affected in osteoarthritis?
Degenration of cartilage (break down of matirx) causing structural and functional failiure of the Synovial joints (movable joints)
Intrinsic disease of cartlage
Primary osteoarthritis is due to idiopathic causes
Secondary is due to the realsons mentoned above (elderly,trauma use etc)
secondary can also be due to other rheumatoid diseas such as gout, diseases of the collagen, endocrinal diseases such as diabetes or others.
Healthy cartilage - wear and tear - unhealthy cartilage (early OA) - bone responses– sclerosis (late OA)
Explain pathophysiology of OA
Articular cartilage - Type 2 collagen provides resistance to tensiom
proteogylcans provide resistance to compression
articular cartilage does ossify id there is a pathology
OA affect every extracellular component of the cartilage (degradation)
cartilage is lost and bone is grown– more frictionmore damage
signs and symptoms of osteoarthritis.
In case of non-inflamatory arthritis PAIN predominated (such as OA)
Inflammatory (such as RA) STIFFNESS Predominates
PAIN (deep, achy, worse with use, better with rest and worse in the evening
crepitis, bone enlargement, limited movement, Grinding and Loavking
Radicular pain (affecting apnal cord from the root)
can cause muscle dystrohy painand spasm)
OA arthritis can also affect cervical and lumbar joints
Acromial clavicular joint
toe
for diagnosis-
due to presence of Osteophytes (bony projections in place of cartilages) some local inflammation is seen ans since its late OA we can see WBC which are mainly lymphocytes that are accosiated with chronic inflammation
Audible crepitus (abnormal crackling or popping sound)
erythema swelling and tenderness due to localized inflammation
Heberden and Bouchard nodes seen (osteophytes projections in joints of fingers
ANA maybe positive
Management of OA
Mainainence by weight loss or removing pre existing conditions In case of secondary OA Physical therapy Heat or ice sole insoles clutches
NSAIDS to reduce pain and inflammation
Steroids can also be given (low dose prednisolone for 6 weeks)
Explain Rheumatoid arthritis (inflammatory arthritis)
Inflammatory small joint disease systemic symmetrical commn in women can have articular and extraarticular manifestations Chronic disease with acute Flares WBC >2000 Neutrophils >50%morning stiffness >30min
Autoimmune diseases are common in women
Immunodeficiency diseases are common in man
RF positive Ccp positive
Anaemia of chronic disease (anaemia of inflammation) is also seen (high hepcidin)
Bakers cyst can be seen on the behind of the knee that can further lead to DVT
Why is RITUXIMAB used both in autoimmune diseases as well as b cell lymphomas/leukemias?
This is an monoclonal Antibody again CD 20 protien present on B lymphocytes
B cell destroyed no AB no autoimmune diseases
RA etiology and pathophysiology
Idiopathic
some genetic factors
HLA-DR orr HLA-DQ= more aggressive
RF+ (IgM antibody against IgG) and CCP+ =moreaggrasive
Pannus formation
Pathophysiology=
tha hallmark of RA is synovitis (inflammation of synovial joints)
pannus formation (inflammed granulation tissue rich in fibroblasts within the joint spaces)
ankylosis occurs. Osteopenia
Delayed type of hypersensitivity
or autoimmune type (type 3)
RA is always progressive
if intermittent consider an alternative like Palindromic rheumatism
Explain Articullar manifestations in RA.
It is a disease on a pectrum
some pepole can have no to mild symptoms and some can have deathly severe symptoms (just like Multipes clerosis)
articular manifestatations of RA can beupper extremities lower ex. Or c! And C2 joint chonic disease inflammatory symmetrical small joint also involved polyarticular
subluxation(disloaction)
deformities include (upper extremities)
Swan neck deformity
boutonniere deformity
zeta thumb
Piano key sign (distal radioulnar instabillity)
Lower extremities
MTP
chronic inflammation of tarsals and metatarsals
Flat feet
Alanto-axial joint subluxation (C1 and C2)
the j0int of lushka
it affects c1 and c2 joint but not the rest of the vertebral column as this is a synovial joint (higly movable)
while other are fibro cartilagenous (mild movable) and RA only affects synovial joints
suspect- recurrent ociipital headaches reduced range of motion neck pain weakness of upper and lower extremities parasthesia (tingling and numbness) of hand and feet
Complications can include
Spinal cord compression
compressive myelopathy
radiculopathy (injurying nerve from the root)
acute subluxation of spinal cord/vertebral artery —- death/paralysis
What are some accociations of RA
1) other autoimmune diseases
2) osteoporosis if RA is treated by glucocorticoids
3) Hypo-androgen-ism sue to steroids
Extraarticular manifestations of RA?
- Can be before or after RA
- seen in 40% od RA patients
- RF+ and CCP+ patients are at high risk
- smokers at high risk
- Can be general or organ-specific
The most common extra articular manifestations of RA are Rheumatoid Nodules.
Organ specific (heart)- Can affect all layers (pancarditis) but most commonly pericardium Myocarditis Rheumatoid nodeules on the Valves secondary cardiomyopathy Granulomatous mitaral valve disease Cardiac amyloidosis (CHF, Aortitis, CAD)
Explain Gout.
1st metatarsal pharyngeal joint affected (big toe)
inflammatory arthritis caused by deposition of microscopic crystals
