Systemic Lupus Erythematosus (SLE) Treatment, Pathophysiology, Symptoms, Medicine Lecture, USMLE

okay in our video series of Rheumatology lectures in this video we are going to talk about systemic lupus erythematosis SLA a 28 year old lady comes to your clinic and tells you the doctor for the last few months I have been having this mild fever fatigue and severe joint pains for the last few months I am getting recurrent painless mouth ulcers for the last few months I am having hair fall alopecia whenever I get out in sunlight whenever I am exposed to sunlight I get burning sensation over my face on my hands whenever my hands are exposed to cold water they change their color they turn blue and that is a very painful condition Reynolds phenomena this is a classical presentation of systemic lupus erythematosis a famous personality who suffered from SLE was Selena Gomez she suffered to an extent that she had to get a kidney transplant now we'll discuss the presentation the diagnosis and treatment of SLE in detail SLE is an autoimmune condition in which the immune system attacks its own tissues it's an autoimmune condition in which the immune system damages and attacks the own body and it causes widespread inflammation tissue damage in the affected organs remember SLE is a systemic disease it affects each and every organ in the body the word lupus comes from Wolf due to wolf-like appearance the rashes appear as if someone has been bit by a wolf it affects females much more than males the ratio is 10 times more in females as compared to males now coming to the etiology of SLE in the etiology of SLE there are two main factors genetic factors and environmental factors both of these factors play a role in causing the disease the main factors are genetic factors the main involvement is from the genetic factors HLA dr2hladr3 is associated with SLE genetic deficiency of complement proteins can cause SLE now if this person who has these genetic differences or problems get exposed to the environmental triggers the environmental triggers include ultraviolet light smoking silica Epstein-Barr virus now these environmental factors will trigger these genes and they will result in SLE other than that hormonal factors hyperestrogenic states are associated with causing SLE therefore it is more common in females drugs including procainamide hydralazine these can cause drug induced SLE now how does this happen now let's say we have a person who has genetic predisposition to SLE that person gets exposed to environmental Factor like ultraviolet radiation and ultraviolet radiation damages the cell of a person and that cell gets damaged and nuclear material the nucleus histone proteins and DNA gets exposed when the DNA histone proteins and nuclear material gets exposed to the immune system immune system produces antibodies against the very own DNA histone proteins and nuclear material so the immune system is attacking its own cells the component of its own cells are being damaged by the antibodies produced against them that is the pathophysiology in systemic lupus erythematosis so it is an autoimmune condition in which type 3 hypersensitivity reaction takes place in which antibodies are formed against the antigens of the body so antigen antibody complexes are formed those antigen antibody complexes further activate the complement system of immune system and that complement system further damages the cells further damages the organs of the body and results in inflammation so that is the pathophysiology behind SLE if you understand the pathophysiology you can easily understand the diagnosis you can easily understand the treatment of SLE in the etiology I mentioned that complement deficiency can cause SLE how complement efficiency can cause SLE basically when antibodies are formed against the antigens and antibody antigen complexes are formed these antigen antibody complexes are to be cleared Away by macrophages complement basically invites these macrophages when there is complement deficiency and those macrophages are not activated and those macrophages do not eat away these antigen antibody complexes these antigen antibody complexes are lying in the body and they further activate the immune system there is activation of immune system and that immune system further damages the body so macrophages are activated by a complement and those macrophages eat away these antigen antibody complexes when there is complement deficiency the macrophages cannot clear away these antigen antibody complexes and immune system is triggered over triggered and that immune system damages the body that is auto antibody development due to complement deficiency so whenever there is complement deficiency the antigen antibody complexes are not cleared away when the these complexes are not cleared away these antigen antibody complexes further invite the immune system and their immune system damages the body and organs of the person now coming to the clinical presentation of SLA in the clinical presentation of SLE remember SLE is the chronic disease in which the patient always has a baseline disease and in that Baseline disease patient can sometimes get exacerbation of the condition that are called as flares so the patient has phases of remission and relapse and most common presentation of SLE is constitutional symptoms like fever fatigue weight loss and joint pain joints are involved in more than 90 percent of the cases arthritis arthralgias and that is the most common initial presentation a weak presentation which is difficult to diagnose but when the skin manifestations appear in 85 percent of the cases the diagnosis can become a bit easier in the skin manifestations patients develop malar rash or butterfly rash rash present over the cheekbones and it appears like the wings of a butterfly and remember this this Miller rash or butterfly rash pairs the nasolabial fold this is a very classical point of Mela rash that it does not involves it spares the menasolabial folds this is a picture showing a butterfly rash and look this is these are the wings of the butterfly and look the nasolabial folds have been spared the nasolabial folds are not affected then in patients with SLE you may be able to appreciate Reynolds phenomena what happens in Reynolds phenomena the patient will tell you the doctor whenever my hands are exposed to cold water or cold air my hands change their color they initially become pale or white and then they become blue and blue are purplish and it is associated with severe pain basically what happens is that vessels are vasoconstricted that result in the fingers to become white and that causes severe pain and deoxygenation and hypoxia of the fingers and then the blood is deoxygenated and that blood appears purple or blue on the skin that is called as the Reynolds phenomena this is a picture showing the discoloration of the hands remember these patients can have this coiled rash discoid rash is a scarring rash that leaves a scar that deforms the skin remember Miller rash is not a scarring rash the rash present on the cheekbones it does not leave a scar but the Discord rash leaves a scar it is a deforming rash look at a picture of this coiled rash that leaves a scar these patients will tell you that they are having recurrent oral ulcers usually we get oral ulcers and these oral ulcers are very painful but these patients get recurrent Earth cells but the good thing is that these patients have painless oral ulcers these ulcers are always there sometimes in one part of the mouth sometimes in another part of the mouth but these ulcers are painless alopecia there is hair loss and it the alopecia in the SLE is known scarring the only thing that leaves a scar is the discoid rash Miller rash alopecia does not leave a scar this is a picture showing non-scarring alopecia these patients develop peri-angle till injectasias peri-angle talentesias are basically the dilation of capillaries near the nail bed peri-angle near the nail bed till injectasial dilation of the capillaries peri-angle inject easier this is a picture showing dilation of the capillaries the talent Activia is near the nail bed an important point to remember is that both SLE and rheumatoid arthritis damage the joints and joints are involved in both SLE and rheumatoid arthritis but rheumatoid arthritis causes severe damage to the joints it cause deformation of the joints it causes deformity of the joints but SLE does not lead to deformity it cause inflammation of the joints but it does not lead to severe deformity so rheumatoid arthritis and SLE both affect metacarpopharyngeal joint and proximal interphalangeal joint but SLE does not lead to deformity while rheumatoid arthritis leads to deformity now another important point to remember is that if a person is suffering from one autoimmune condition in Rheumatology that person usually is having another autoimmune condition associated with it now these patients of SLE usually have uh anti-phospholipid syndrome associated with it usually these patients with SLE will have rheumatoid arthritis associated with it patients with SLE really have shogren syndrome associated with it so autoimmune conditions are usually found together if a person is suffering from one autoimmune condition that person usually has another autoimmune condition associated with it as well if you find rheumatoid arthritis with SLE that is called as rupus now SLE is a systemic disease it affects each and every organ of the body each and every part of the body each and every system of the body is affected by a cell antibodies are formed against blood the RBC is antiretrocyte antibodies anti erythropoietin antibodies anti-rethropoietin receptor antibodies and these cause hematological manifestations that are that results in cytopenia all the cell lines are down platelets are down rbcs are down even wbcs are down leukopenia anemia thrombocytopenias are seen in SLE SLE also causes inflammation of the membrane surrounding the organs pleura surrounding the lungs are affected that results in pluritis and when the membrane surrounding the heart is affected that is called as pericarditis SLE damages the kidneys it affects the kidneys and it results in nephritis it was the kidneys that were affected in the case of Selena Gomez that she had to get a kidney transplant in active lupus kidneys one of the very important Target of XLE and it is one of the common cause of death in patients with SLE due to the renal failure SLE also affects the heart it causes pericarditis myocarditis endocarditis now remember in our infective endocarditis video we studied that infection affects the endocardium resulting in infective endocarditis vintage but in SLE there is no infection but still there is inflammation of the endocardium resulting in endocarditis that is called as Libman SEC endocarditis in Libman secondocarditis basically there is fibrin deposition fiber and deposition beneath these walls and when there is fiber in deposition beneath these walls the cold air tendine are damaged when The Cordial tendoning are damaged there is a regurgy of the wall so endocarditis Libman Sac endocarditis causes rigurge of the walls coronary artery disease after the age of 45 these SLE patients develop accelerated atherosclerosis therefore in the diagnosis and management we'll study that we have to assess these patients as well because there is increased risk of coronary artery disease SLE also affects the lungs it causes shrinking lungs and roam it causes fibrosis of the lung in trustial lung disease it also makes the capillaries stiff that results in pulmonary hypertension it also affects the vessels causes vasculitis that is a cause of pulmonary hypertension it causes hypercoagulable state that hyperecogulable states results in clot formation that is called as antiphospholipid syndrome what is antiphospholipid syndrome we will discuss that in another video but for now remember it causes excessive hypercoagulable state that hypercoagulable state is called as antiphospholipids syndrome that causes clot formation it also affects the neurons it causes seizures psychosis basically antibodies are formed against the neurons anti-neuronal antibodies anti-glutamate antibodies psychosis psychosis is caused by anti-ribosomal antibodies so these are all antibodies that damage the nervous system as well that results in lupus cerebritus that is called as lupus cerebritis in which patients will have a headache patients will have cerebral edema patients can even have coma and lupus cerebritus they also affect the eyes resulting in kerato conjunctive white as zika the dry eyes a simple mnemonic to remember all these is so brain empty s for xerocytus fluorite as pericarditis o for oral ulcers a for arthritis P for photosensitivity B for blood the blood involvement autoimmune hemolytic anemia's enemy of chronic disease are for renal involvement a for a n a anti-nuclear antibodies I for immunologic phenomena n for neurologic involvement M for Miller rash D for Discord rash seen in SLE now coming to the diagnosis of SLE remember SLE diagnosis is a clinical diagnosis but you support that clinical diagnosis with a few tests what are those tests that you perform in SL League the first test is anti-nuclear antibody tester remember that anti-nuclear antibody test is the first test it is positive in many other autoimmune conditions but it is the first test because it is a very sensitive test and if this test is positive it means that you are going in the right direction the possibility of SLE or any autoimmune disease is very high if the anti-nuclear antibody test is positive if it is positive you it gives you a go ahead that you should investigate this patient because there is some autoimmune condition most likely SLE in this patient but if this test is negative then it rules out many autoimmune conditions so anti-nuclear antibody test is the first test that you perform and it is 98 percent sensitive now the positive titers of greater than or equal to 1 ratio 80 are considered to be a positive test now what does one ratio 80 mean one ratio 80 means that if you take a sample from a person and you dilute that samples 80 times even after 80 times you can still detect antibodies in that solution that is called as one ratio 80 it means that the antibodies are present and even if you dilute the solution 80 times still the antibodies are positive that is a positive Ana title and if the Ana is positive you order the further test for this patient because most likely an autoimmune condition is there any is not specific for SLE but it is a sensitive test for autoimmune conditions you then if the test is positive you order the specific anas the specific tests for SLE and those tests are anti-ds DNA anti-smith anti-smith is the most specific test and if anti Smith or ntds DNA is positive it means that SLE is there and if a n a anti-nuclear antibody is negative it means that there is most likely there is no underlying autoimmune condition you should Conti you should consider other alternate diagnosis and remember ntds DNA antibody titers correlate with the lupus activity it shows the progression of Lupus if there is persistent elevation in anti-ds DNA levels of a patient it means that that patient will now get exacerbation of SLE because persistently elevated DSD and a level indicate that that patient is at high risk of getting flares of the disease in getting high risk at getting exacerbations of the disease so it correlates with the disease activity and remember it specifically correlates with lupus nephritic activity the effect of Lupus on kidneys if the dsdna levels are high it indicates that the kidneys are at higher risk of getting affected by lupus then the other specific test for Lupus is anti-smith antibodies anti-smith antibodies are basically against a specific histone protein present in the nucleus of the cell so anti-smith antibodies are present positive in 30 percent of the patients but if these anti-smith antibody is positive it indicates that that patient has SLA because it is even more specific that than anti-dsdna anti-smith antibody is had the most specific antibody for SLE since it is positive in fewer patients we prefer to do NFS because a n a is sensitive it is more positive in 98 percent people if that is positive most likely autoimmune condition is there if a is positive after that we go for ntds DNA and anti-smith antibodies and if ntds DNA or if NT Smith antibodies are positive this is highly indicative that that patient has SLE other it is that you need to perform or the antiphospholipid antibodies as I said that autoimmune conditions have an overlap if one autoimmune condition is there usually that patient has other autoimmune conditions then there is strong correlation of HCL with antiphospholipids syndrome we will discuss about antiphospholipids syndrome in a separate video but for now remember that antiphospholipids in Rome is a syndrome in which there is hypercoagulability of blood in which there is increased chances of clot formation in Blood and antiphospholipids and Rome has certain antibodies that cause it and those antibodies are anticardiolipin antibodies anti-beta 2 glycoprotein antibodies so these are the antiphospholipid antibodies remember the classical scenario of antiphospholipids syndrome would be that a female a female has a recurrent abortion the pregnancy was going fine but all of a sudden that patient gets abortion death of the infant that is due to thrombosis of the uterine vessels thrombosis of uterine vessels occur due to these anticardiolipin antibeta 2 glycoprotein antibodies and remember complement levels are low in SLA since it's a type 3 autoimmune reaction in which there is excessive activation of complement and complements get complement proteins get used up in the reaction and the complement levels are low C3 C4 levels are low and they are used to monitor response to the treatment ESR and CRP levels will also be elevated because it's an inflammatory condition and these are inflammatory markers that get elevated when there is inflammation in the body TBC will show cytopenia as remember as I said that there are anti erythrocyte antibodies antiplatelet antibodies these antibodies will destroy all cell lines cytopenia thrombocytopenia anemia leukopenia all the cell lines will be down and remember as I said that it's an autoimmune condition that affects each and every organ of the body it affects the kidneys in the flares kidneys are the main target of SLE and kidneys get damaged in SLE and if you do your analysis in which you see protein urea hematuria that glomerulus has been damaged and everything is coming out from the glomerulus and that that filter is now damaged and that filter cannot hold the things that it cannot hold the protein and blood within the blood everything starts coming out you will see hematuria you will see proteinuria and if you see protein urea on your analysis the next step is that you calculate how much protein is coming out you do you request 24 or urine collection or you do spot urine protein to creatinine ratio you calculate that how much protein is coming out from the kidneys and for lupus nephritis remember the more specific test would see the effect of Lupus on kidneys is biopsy kidney biopsy is the most specific test for lupus nephritis an important point to remember is if someone asked you that which test is falsely positive in SLE the test of syphilis are falsely positive in SLE the patient will not be having any symptoms of fasterly and if you perform rpr vdrl in these patients the rpr video tests of C plus are positive why are they positive they are positive because in rpr vdrl as we discussed in our syphilis video that the in rpr vdrl we detect antibodies and the antibodies against syphilis are similar to the antibodies in found in SLE so you detect so the test detects antibodies of syphilis and it considers it thinks that these are the antibodies against the syphilis they're against the triponema palliderum so rpr and vdrl are falsely positive in Sally patient is not having syphilis but the tests of cephalus are positive now there is a latest criteria for the diagnosis of SLE 2019 Euler ACR criteria a scoring criteria for SLE in that scoring criteria we have divided into two domains the first domain is the clinical domain the second one is the immunologic domain you score each and every point in it in the clinical domain we have constitutional symptoms like fever it get two point cutaneous domain has all the cutaneous symptoms alopecias oral ulcers described lupus and you give scores accordingly arthritis domain neurologic domain serocytus symptoms ends scores appropriately in hematologic domains you have the symptoms renal domain so this is all the clinical domain in immunologic domains you have all the antibody tests the antibodies that you that you perform antiphospholipid domain has all the tests of antibodies anticardial lipid antibodies antibeta two glycoprotein or Lupus anticoagulant if any one of these is positive patient gets two points for this complement level low C3 low C4 gets three points highly specific antibody domain NT dsdna antibody anti-smith antibodies if each one of these is positive it gets six point now remember when you are calculating the score if within one domain let's say if we take the domain of uh neurologic domain and in that neurologic domain if the patient is having seizures if the patient is also having psychosis and the patient is also having delirium you do not need to add up all the scores of this one single neurologic domain what you do is that you take the maximum score out of it only the maximum score will be taken like you you will not score it as 10 5 plus 3 plus 2 10 no you will not score it like that you will just take the 5 out of this one domain the same way if the patient is having findings of hematologic domain if the patient is having leukopenia thrombocytopenia and autoimmune hemolysis and all these things are positive you do not give 4 plus 4 plus 3 11 you do not give it 11 score you give the maximum score you give the score four so uh the maximum number which is present in a domain can be given you cannot score it more than that so you add up the total points and the total points if they are greater than or equal to 10 it is classified as SLE and an important thing to remember is that all these patients must have an A a level of greater than 1 ratio 80 as an entry criteria for this if DNA levels are low this criteria cannot be applied and remember SLE classification requires points from at least one clinical domain at least one clinical domain must be positive for the diagnosis of SLE previously there was no scoring criteria in it previously it was just just the same the clinical domain and immunologic domains and in these domains you need to have at least four positive domains and at least one from the clinical domain and one from the immunologic domains that was the previous classification but now we have this scoring criteria in which you give scores accordingly in which the maximum score that you can give is the maximum number present in the domain and if it is greater than or equal to 10 that points out toward SLE remember these SLE patient gets accelerated at zero sclerosis these patients must get cardiovascular disease risk assessment because cardiovascular disease is one of the common causes of death in a cell patient now you will be thinking that I have I have said about a kidney disease as a common cause of death I have talked about coronary artery disease as a common cause of death now what is the common cause of death in this patient basically it depends upon the age of the patient if a person is newly diagnosed case of SLE and that patient is getting players of SLE in the young age and in the young age if the patient is getting flares of SLE during that flares you will be bombarding that patient with steroids because we will study now that steroids is the treatment of the flares of SLE you will be bombarding that patient with steroids and whenever you give steroids to the patient you immunocompromise the patient and when you immunocompromise the patient there is increase chances that that patient will now get infections so if if a person is newly diagnosed young patient of SLE that newly diagnosed young patient of SLE will get flares and those flares will be treated with steroids and that steroid will cause immunocompromised State and that will result in infection and in early years infection is a common cause of death in this patient if the patient is having active rapidly Progressive SLE renal failure is also a very common cause as I said in the case of Selena Gomez she had to get a renal transplant because in such a young age there was so much progression of the disease that it totally damaged the kidneys so renal failure is also an important cause in young patients with active lupus and after the age of 45 years if the patient reaches the age of 45 years after 45 years there is increase atherosclerosis it increased hero sclerosis causes coronary artery disease after the age of 45 years coronary artery disease is a common cause of death in these patients so it depends upon the age of the patient it also depends upon the clinical status of SLE and which organs the SLE is affecting so these are the common causes of mortality in these patients now coming to New natal lupus in neonatal lupus remember there are anti-row and anti-law antibodies anti-row and anti-law antibodies are the antibodies that are IGG antibodies that are positive in SLE now as as we know that IGG antibody can cross placenta if the Antero and anti-layer antibodies are positive these antibodies will cross placenta and if these antibodies cross placenta the main target of these antibodies is Av node of the infant the newborn that is present in the uterus they attack the heart of the patient when they attack the heart of the newborn they will attack the AV node and if the AV node is damaged it will result in complete hard block so the neonatal lupus affects the AV node it destroys the even order and it causes congenital heart block and most of these infants die because of the heart block before even you make the diagnosis of heart block before even you make a put pacemaker in these patients most of these infinits expire and if the infant makes it then you need to put pacemaker in such patients now with this I'll also like to discuss drug induced lupus in drug induced lupus remember the mnemonic ship sulfur drugs H for hydralazine I for isona acid P for pyroxenamide these drugs sometimes if a person takes it if the patient takes it and patient develops rashes just as the rash of SLE and if you do antihistone antibody in this patient the antihistone antibodies will be positive why is this antibody positive because as I said in the etiology that certain types of drugs can also predispose the patient to developing excellent but remember that drug-induced SLE is not severe drug induced SLE is for the short period of time till the patient is taking that drug and it only has cutaneous manifestations it does not cause lupus nephritis or fluoritas or it does not affects the brain it does not affect the vital organs it only has cutaneous manifestations and it's it it stops as soon as you stop the drug so that is drug induced SLE caused by antihistone antibodies and the drugs I mentioned now coming to the treatment of SLE in the treatment of SLE there are two main things the patient has a persistent disease that is to be controlled by maintenance therapy and then there are flares of the disease exacerbations of the disease that are to be managed with steroids so that is the treatment of SLE in the treatment of SLE there are certain General Meyers that you have to take you ask the patient to avoid the triggers you ask the patient to avoid ultraviolet light cover the skin Place sunblock with SPF go greater than equal to 50 it it shows the strength of the sun block and patients should quit smoking and patient should do mild aerobic exercise and with that an important thing to remember is that you must admit the patient of SLE if the diagnosed patient of SLE has unexplained fewer if the patient has severe disease damage to the kidneys lupus nephritis alveolar Hemorrhage with hemoptysis Neuropsychiatric SLA patient is now in comatose state our patient is now having seizures Pepsis or thrombosis because these are these features are associated with increased mortality in patients with SLE no when you when you have a patient of SLE with you or you have a newly diagnosed patient of SLE you you divide the patient into mild moderate severe category in the mild category are the patients in which no vital organs are affected patient just has the Constitutional symptoms of fever fatigue weight loss and joint pain rash and arthritis the vital organs are not yet affected and patient has cytopenias in which you see the platelet count and the platelet count is between 50 to 1 000 K that is a mild case of SLE in which no vital organ is affected on the other hand in severe case the SLE targets the main organ the vital organs like it causes nephritis it causes myelitis pneumonitis mesenteric vasculitis severe cytopenia now in such patients this is a severe form of SLE in the moderate form in moderate form also these vital organs are not affected to an extent that they cause severe disease but they are mildly affected they are also mildly affected in moderate disease they cause vasculitis cirocytus rheumatoid arthritis like arthritis cytopenias in which the platelet count is between 20 to 50 000 so if a patient comes to you with SLE you have diagnosed the patient with SLE you divide the patient into mild moderate severe and accordingly you give the treatment now remember in all patients of SLE the male drug the most important drug is hydroxychloroquine hydroxychloroquine is the main drug of SLE hydroxychloroquine is Cornerstone therapy of SLE hydroxychloroquine modulates the immune system and protects the body from the immune system attack it provides a maintenance control of SLE and it reduces the frequency of players and it also reduces the frequency of complications of SLE so hydroxychloroquine remember hydroxychloroquine is the main drug and if the patient is having mild condition you give hydroxychloroquine 300 to 400 mg per orally once daily and if the patient comes to you and patient has moderate disease in which there is somewhat damage to the vital organs but it has not affected the vital organs to a severe extent you give hydroxychloroquine and with that hydroxychloroquine you also give oral glucocorticoids to suppress the immune response and oral glucocorticoids are given with hydroxychloroquine they augment the therapy and they stop the immune response from attacking the own body is given less than or equal to 0.5 mg per kg per orally once daily and you gradually taper the dose to a maintenance dose of less than 7.5 mg per only once daily so in moderate disease you give hydroxychloroquine with oral Global cortic acids and in some patients sometimes you also need to add immunosuppressive agents immunosuppressive agents like mycophenolate cyclophosphomat these are immunosuppressive agents that are given for the maintenance therapy they control the immune system and protect the body from the immune attack so immunosuppressive agents like mycophenolate and cyclophosphamides can also be used in some patients within the moderate category in severe patients if the patient comes to you with severe vital organ damage the first thing that you need to give is that you have to bombard that patient with steroids you have to give a high dose IV steroids so that you control the immune you control the immune response and protect the body from the damage that is being done from the immune system you give induction therapy with higher dose IV steroids and then when you have controlled the disease with high dose IV steroids you you give the maintenance therapy with hydroxychloroquine which oral steroids and immunosuppressants so a combination of these is used to control the disease at the Baseline to provide a maintenance control so in severe cases you first of all control the player with IV steroids high dose Ivory steroids and when you have controlled the flare then you give the maintenance therapy with hydroxychloroquine and orosteroids with or without immunosuppressants for the induction to control the flare of the disease you give Ivy steroids methylprednisolone 250 to 1000 mg IV once daily for three days and then you shift the patient to oral prednisone immunosuppressive agents include Methotrexate hydroxychloroquine but hydroxychloroquine is remembered is the main drug Methotrexate was the main drug for rheumatoid arthritis in SLE the main drug is hydroxychloroquine biologic agents are also there these are monoclonal antibodies basically monoclonal antibodies are the antibodies against the antibodies the antibodies that are damaging the human body the damaging the human organs you give antibodies that bind these antibodies and remove these bodies away from the circulation [Music] these are the antibodies biologic agents antibodies against the antibodies that are damaging the body now remember before starting any immunosuppressions are steroids remember always rule out latent TB because if you are giving even a suppression if you are suppressing the immune system you can reactivate TB in some patients you monitor the patient whenever you are giving hydroxychloroquine remember hydroxychloroquine it deposits in the retina it affects the eyesight so you request eye screening after five years and then yearly in patients taking chronic hydroxychloroquine now coming to lupus nephritis as I said it affects a lupus affects the kidneys to control lupus nephritis you give IV glucocorticoids methylprednisone and with that you give immunosuppressants like mycophenolate and cyclophosphomide so combination of steroid and immunosuppressant is used for the control of lupus nephritis before going into the summary if you liked my video please click on the Subscribe button we talked about what is SLE the etiology of SLE the pathophysiology the presentation presentation the manifestations of him different systems lungs vascular neurologic symptoms of filmologic symptoms and pneumonia to remember the manifestations of SLE the diagnosis with a a as a screening test and specific test dsdna and anti-smith antibodies other tests urinalysis rpr vdrl falsely positive risk assessment of the patient in the treatment the general measures admit the patient if the patient has these divide the patient into mild moderate severe categories and you give hydroxychloroquine to each patient and with that you either combine oral glucocorticoids and if the patient has flares you straight away give a high dose Ivy steroids immunosuppressive agents and biologic agents before starting immunosuppressive therapyons to its rule out TV monitoring of a patient if taking hydroxychloroquine for the treatment of lupus nephritis you give steroids with immunosuppressive drugs if you liked my video please click on the Subscribe button and check out my other videos on Rheumatology lectures the link of those videos is given in the description below thank you very much

Channel: MedNerd - Dr. Waqas Fazal

Views: 42,240

Keywords: sle, systemic lupus erythematosus, systemic lupus erythematosus pathology, systemic lupus erythematosus medicine lecture, sle medicine lecture, sle pathophysiology, sle pathology, sle treatment, systemic lupus erythematosus pathophysiology, sle symptoms, systemic lupus erythematosus symptoms, SLE lecture, systemic lupus erythematosus diagnosis, what is sle, lupus symptoms, lupus disease, lupus nephritis, sle usmle step 1, sle usmle step 2

Id: hFfmIiVt7K0

Length: 39min 52sec (2392 seconds)

Published: Sat Sep 02 2023