Rheumatology. Flashcards

Question

What if the ESR and CRP is extremely high?

Answer 1

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

Answer 2

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

Answer 3

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.

Answer 4

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

Answer 5

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

Answer 6

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 .

Answer 7

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.

Answer 8

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)

Answer 9

``` 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)

Answer 10

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

Answer 11

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

Answer 12

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. ```

Answer 13

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

Answer 14

Nopes anti CCP = antigens are cyclic peptides anti CPA ( anti citrullinated protien antigens) = antigens are peptides or modified protiens

Answer 15

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

Answer 16

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

Answer 17

Lupus can damage Kidneys in two ways. Nepritic syndrome- diffuseproliferative glomerulonephritis nephrotic- membranous nephropathy

Answer 18

If the patient with RA is being treated with TNF alpha inhibitors they can become positive for DS DNA antibodies

Answer 19

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

Answer 20

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

Answer 21

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)

Answer 22

Anti ds DNA + Anti RNP + clinical picture of lupus === lupus (not MCTD)

Answer 23

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

Answer 24

Positive anti ds dna positive SSA Has SLE negative SSB

Answer 25

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

Answer 26

Drug Induced lupus (very sensitive 95% and more) (so we can rule out the disease if the test comes negative)

Answer 27

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

Answer 28

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

Answer 29

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)

Answer 30

Calcinosis cutis digital ischemia PAH primary billiary cirrhosis

Answer 31

Anti centomere is present inlimited scleroderma and it is only limited to skin so low chances of tissues or other organ involvement.

Answer 32

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)

Answer 33

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.

Answer 34

Long term damage to tissues such as esophagus (GERD) and lungs (interstitial lung disease)---> cancer

Answer 35

``` 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

Answer 36

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

Answer 37

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

Answer 38

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)

Answer 39

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

Answer 40

It is usually accociated with SLE and recurrent sinopulmonary bacterial infections late complement deficiency (C5 C9) is accociated with invasive nissenia infections

Answer 41

``` 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 ```

Answer 42

Everything same EXCEPT color-yellowish WBC higher than 200

Answer 43

``` 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)

Answer 44

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

Answer 45

Athropathy - Joint disease Arthritis - Joint inflammation Arthralgia - Joint pain Even though orthoarteritis have it is it is a non inflmammatory condition

Answer 46

Acute (few days to a week) and Chronic (more than a week,onths etc)

Answer 47

``` Initial tets - X ray joint space narrowing bone erosions hypertrophic changes periostitis chondrocalcinosis seen in pseudo gout ```

Answer 48

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

Answer 49

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

Answer 50

Replacement Just like car wheels | ARTHROPLASTY.

Answer 51

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

Answer 52

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)

Answer 53

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

Answer 54

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

Answer 55

``` 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)

Answer 56

``` 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

Answer 57

This is an monoclonal Antibody again CD 20 protien present on B lymphocytes B cell destroyed no AB no autoimmune diseases

Answer 58

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

Answer 59

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

Answer 60

1) other autoimmune diseases 2) osteoporosis if RA is treated by glucocorticoids 3) Hypo-androgen-ism sue to steroids

Answer 61

- 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) ```

Answer 62

1st metatarsal pharyngeal joint affected (big toe) | inflammatory arthritis caused by deposition of microscopic crystals