Systemic lupus erythematosus (SLE) is an autoimmune disease that can affect multiple organ systems. Key signs and symptoms include malar rash, arthritis, oral ulcers, photosensitivity, serositis, renal disease, and hematological abnormalities. Diagnosis involves evaluating clinical criteria along with identifying autoantibodies. Treatment aims to induce remission during flares using glucocorticoids and immunosuppressants to prevent organ damage.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect various organs in the body. It is more common in women, especially of childbearing age, and in African Americans. The disease is characterized by autoantibody production and tissue damage caused by immune complexes. Diagnosis is based on meeting criteria from the SLICC classification system, which improved upon previous criteria. Organ manifestations include renal, neurological, cardiac, pulmonary, hematological and cutaneous involvement. Management aims to suppress symptoms and prevent organ damage through medications like glucocorticoids, antimalarials, immunosuppressants and biologics. The goal is complete remission though sustained remission is rare
Systemic Lupus Erythematosus (SLE) is an autoimmune disease that can affect multiple organ systems. It typically affects young women and is characterized by periods of disease flares and remissions. While the exact cause is unknown, genetic and environmental factors likely contribute to abnormal immune system functioning and production of autoantibodies. Common clinical manifestations include malar rash, arthritis, kidney problems, and hematological abnormalities. Diagnosis involves identifying clinical features and detecting autoantibodies such as antinuclear antibodies and anti-dsDNA antibodies. With proper management, 10-year survival rates are over 90%.
Systemic Lupus Erythematosus (SLE) is an inflammatory autoimmune disease characterized by excessive autoantibody production leading to tissue damage. It has a wide variety of clinical manifestations that can affect many different organ systems. Some key points:
- SLE predominantly affects women of childbearing age and has a strong genetic component. Certain genetic and environmental factors can increase risk.
- Clinical features include skin rashes, arthritis, kidney involvement ranging from mild proteinuria to severe nephritis, neurological/psychiatric symptoms, hematological abnormalities and involvement of other organs.
- Diagnosis is based on identifying a combination of clinical and laboratory criteria including high titers of antinu
Treatment for systemic lupus erythematosus (SLE) should be tailored to each patient based on an assessment of disease activity, damage, and comorbidities. Lupus nephritis, a form of kidney involvement, affects about 1/3 of SLE patients and can lead to end-stage renal disease if not properly treated. Treatment involves immunosuppressive drugs like corticosteroids, cyclophosphamide, mycophenolate, and azathioprine to induce remission based on the class of lupus nephritis determined by renal biopsy. Prognosis is generally good if treatment can normalize kidney function and blood pressure.
Systemic lupus erythematosus (SLE) is an autoimmune disease where the immune system attacks its own tissues, causing inflammation and damage. It is characterized by periods of disease flares and remission. Common symptoms include joint pain, rashes, and fatigue. SLE can affect many organs like the skin, lungs, heart, and kidneys. Diagnosis involves evaluating symptoms, lab tests like antinuclear antibodies, and sometimes biopsies. Treatment aims to reduce symptoms during flares and prevent organ damage using medications like corticosteroids, antimalarials, and immunosuppressants. SLE affects mostly women of childbearing age and has no known cure.
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by inflammation in tissues throughout the body. The name comes from a 13th century physician who observed facial lesions resembling a wolf bite. Diagnosis is based on criteria developed by the American College of Rheumatology including malar rash, discoid lesions, arthritis, serositis, renal disease, and immunologic abnormalities. Treatment involves hydroxychloroquine, corticosteroids, immunosuppressants like azathioprine. Lupus nephritis requires aggressive therapy with glucocorticoids, cyclophosphamide or mycophenolate mofetil. Treatment goals are complete or partial renal response through reduction
Approach to a patient with vasculitis and itsMohit Aggarwal
Vasculitis refers to inflammation of blood vessels. It can be primary or secondary to other conditions like drugs, infections, collagen disorders or malignancies. It involves various sizes of blood vessels from large arteries to small vessels. Common symptoms include fever, fatigue, rashes, arthritis, and organ involvement depending on the vessel type. Diagnosis is based on clinical features, lab tests like ANCA, and biopsy. Treatment involves immunosuppression. Prognosis depends on type and organ involvement.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect multiple organ systems. It is more common in women and typically presents in the 2nd to 3rd decade of life. SLE results from a loss of self-tolerance by the immune system and is characterized by autoantibody production and immune complex-mediated tissue damage. Diagnosis is based on clinical criteria involving symptoms in organs like the skin, joints, kidneys, and heart. Treatment involves managing symptoms with medications like corticosteroids, antimalarials, and immunosuppressants. Prognosis has improved in recent decades but SLE can still lead to organ damage or failure if not properly treated.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect various organs in the body. It is more common in women, especially of childbearing age, and in African Americans. The disease is characterized by autoantibody production and tissue damage caused by immune complexes. Diagnosis is based on meeting criteria from the SLICC classification system, which improved upon previous criteria. Organ manifestations include renal, neurological, cardiac, pulmonary, hematological and cutaneous involvement. Management aims to suppress symptoms and prevent organ damage through medications like glucocorticoids, antimalarials, immunosuppressants and biologics. The goal is complete remission though sustained remission is rare
Systemic Lupus Erythematosus (SLE) is an autoimmune disease that can affect multiple organ systems. It typically affects young women and is characterized by periods of disease flares and remissions. While the exact cause is unknown, genetic and environmental factors likely contribute to abnormal immune system functioning and production of autoantibodies. Common clinical manifestations include malar rash, arthritis, kidney problems, and hematological abnormalities. Diagnosis involves identifying clinical features and detecting autoantibodies such as antinuclear antibodies and anti-dsDNA antibodies. With proper management, 10-year survival rates are over 90%.
Systemic Lupus Erythematosus (SLE) is an inflammatory autoimmune disease characterized by excessive autoantibody production leading to tissue damage. It has a wide variety of clinical manifestations that can affect many different organ systems. Some key points:
- SLE predominantly affects women of childbearing age and has a strong genetic component. Certain genetic and environmental factors can increase risk.
- Clinical features include skin rashes, arthritis, kidney involvement ranging from mild proteinuria to severe nephritis, neurological/psychiatric symptoms, hematological abnormalities and involvement of other organs.
- Diagnosis is based on identifying a combination of clinical and laboratory criteria including high titers of antinu
Treatment for systemic lupus erythematosus (SLE) should be tailored to each patient based on an assessment of disease activity, damage, and comorbidities. Lupus nephritis, a form of kidney involvement, affects about 1/3 of SLE patients and can lead to end-stage renal disease if not properly treated. Treatment involves immunosuppressive drugs like corticosteroids, cyclophosphamide, mycophenolate, and azathioprine to induce remission based on the class of lupus nephritis determined by renal biopsy. Prognosis is generally good if treatment can normalize kidney function and blood pressure.
Systemic lupus erythematosus (SLE) is an autoimmune disease where the immune system attacks its own tissues, causing inflammation and damage. It is characterized by periods of disease flares and remission. Common symptoms include joint pain, rashes, and fatigue. SLE can affect many organs like the skin, lungs, heart, and kidneys. Diagnosis involves evaluating symptoms, lab tests like antinuclear antibodies, and sometimes biopsies. Treatment aims to reduce symptoms during flares and prevent organ damage using medications like corticosteroids, antimalarials, and immunosuppressants. SLE affects mostly women of childbearing age and has no known cure.
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by inflammation in tissues throughout the body. The name comes from a 13th century physician who observed facial lesions resembling a wolf bite. Diagnosis is based on criteria developed by the American College of Rheumatology including malar rash, discoid lesions, arthritis, serositis, renal disease, and immunologic abnormalities. Treatment involves hydroxychloroquine, corticosteroids, immunosuppressants like azathioprine. Lupus nephritis requires aggressive therapy with glucocorticoids, cyclophosphamide or mycophenolate mofetil. Treatment goals are complete or partial renal response through reduction
Approach to a patient with vasculitis and itsMohit Aggarwal
Vasculitis refers to inflammation of blood vessels. It can be primary or secondary to other conditions like drugs, infections, collagen disorders or malignancies. It involves various sizes of blood vessels from large arteries to small vessels. Common symptoms include fever, fatigue, rashes, arthritis, and organ involvement depending on the vessel type. Diagnosis is based on clinical features, lab tests like ANCA, and biopsy. Treatment involves immunosuppression. Prognosis depends on type and organ involvement.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect multiple organ systems. It is more common in women and typically presents in the 2nd to 3rd decade of life. SLE results from a loss of self-tolerance by the immune system and is characterized by autoantibody production and immune complex-mediated tissue damage. Diagnosis is based on clinical criteria involving symptoms in organs like the skin, joints, kidneys, and heart. Treatment involves managing symptoms with medications like corticosteroids, antimalarials, and immunosuppressants. Prognosis has improved in recent decades but SLE can still lead to organ damage or failure if not properly treated.
This document provides an overview of systemic lupus erythematosus (SLE). It discusses the definition, epidemiology, pathogenesis, diagnosis, clinical manifestations, management, and complications of SLE. The pathogenesis involves genetic susceptibility and environmental triggers leading to abnormal immune responses and autoantibody production. Diagnosis is based on the SLICC classification criteria. Management involves controlling symptoms, preventing organ damage, and treating flares and complications using medications like glucocorticoids, antimalarials, immunosuppressants, and biologics. Life-threatening complications can include renal disease, neurological involvement, hematological abnormalities and vasculitis.
Systemic Lupus Erythematosus (SLE) is an autoimmune disease where the immune system mistakenly attacks healthy tissue. It most commonly affects women under age 40 and can involve the skin, joints, kidneys, brain and other organs. Symptoms vary but often include joint pain, rash, and fatigue. There is no cure for SLE but treatment aims to control symptoms, which may include medications like hydroxychloroquine and corticosteroids. Prognosis has improved in recent years though long-term treatment is usually required to manage the disease.
1) Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by unpredictable exacerbations and remissions affecting multiple organ systems.
2) The case report describes an 11-year old Indian boy who presented with fever and pancytopenia and was subsequently diagnosed with SLE based on rash, oral ulcers, arthritis, and strongly positive autoantibody tests.
3) He responded well to pulse steroids and IV immunoglobulin therapy and was put on long-term immunosuppressants for maintenance treatment.
This document provides information on systemic sclerosis (SSc), a chronic autoimmune disease characterized by thickening and hardening of the skin, and involvement of internal organs. It can present as either limited or diffuse cutaneous forms. Key clinical features include Raynaud's phenomenon, skin thickening and tightening, digital pitting scars, and internal organ involvement such as interstitial lung disease, gastrointestinal issues, and renal crisis. Diagnosis involves clinical examination and the presence of autoantibodies. Differential diagnoses include other conditions presenting with similar skin or vascular changes. Complications can affect multiple organ systems and are a leading cause of mortality.
A 60-year-old woman presented with painful, sclerotic hands and fingers due to progressive cutaneous scleroderma. She was started on a compounded topical cream containing ketamine, baclofen, gabapentin, verapamil, and pentoxifylline, which provided significant pain relief and improved sensation within a month. At a 6-month follow up, she had been largely weaned off opioid pain medications. The customized treatment targeted the pathophysiology of the condition and helped manage her debilitating symptoms.
Systemic Lupus Erythematosus (SLE) is a multi-gene autoimmune disease caused by a combination of genetic and environmental factors. It is characterized by abnormal immune responses that result in inflammation and damage to various organs. Diagnosis requires meeting 4 out of 11 classification criteria relating to clinical symptoms and blood markers. Management aims to induce remission of acute flares, maintain improvements to suppress symptoms, and prevent organ damage. Treatment choices depend on the severity and potential reversibility of manifestations. The goal is controlling symptoms without cure since complete sustained remission is rare.
Systemic lupus erythematosus (SLE) is the prototypic multisystem autoimmune disorder with a broad spectrum of clinical presentations encompassing almost all organs and tissues.
The extreme heterogeneity of the disease has led some investigators to propose that SLE represents a syndrome rather than a single disease.
Lupus was first recognised as a systemic disease with visceral manifestations by Moriz Kaposi (1837–1902).
Dr. Swamy Venuturupalli talks about Rheumatoid Arthritis, Early Diagnosis and Treatment at the James R. Klinenberg symposium on Rheumatic diseases in Pasadena, CA.
Lupus Nephritis :From Basics To PracticeYasser Matter
This document provides an overview of lupus nephritis (LN), including:
- Epidemiology: Up to 40% of SLE cases involve the kidneys. It predominantly affects women aged 15-45.
- Pathogenesis: Autoantibodies form immune complexes that deposit in the glomerulus, activating complement and attracting inflammatory cells. The location of deposits determines histologic class.
- Diagnosis: Urinalysis, serum creatinine, immunological tests. Renal biopsy is needed to classify LN and guide treatment.
- Treatment involves induction therapy for 3-6 months, then maintenance to prevent chronic kidney disease. Treatment depends on histologic class and response to therapy. The goal
This document discusses lupus nephritis, including its pathophysiology, risk factors, clinical presentation, investigations, classification, treatment, and prognosis. Key points include:
- Lupus nephritis is a serious manifestation of systemic lupus erythematosus caused by autoantibodies forming immune complexes that deposit in the glomeruli.
- It is classified based on renal biopsy findings, with classes III and IV having the highest risk of progressing to end-stage renal disease.
- Treatment involves immunosuppressive induction therapy with corticosteroids and cyclophosphamide or mycophenolate mofetil to rapidly decrease inflammation, followed by long-term maintenance
Rheumatoid arthritis is a chronic inflammatory disease that affects the joints and causes pain, swelling, stiffness and loss of function. It affects around 1% of the population worldwide. Recent advances in management include earlier diagnosis using classification criteria from ACR/EULAR and aggressive treatment with disease-modifying antirheumatic drugs alone or in combination with biological therapies that target cytokines like TNF-α. While DMARDs can control symptoms, biological therapies may induce remission and prevent further joint damage by acting faster than conventional treatments. Prompt diagnosis and management can now improve long-term outcomes for those suffering from rheumatoid arthritis.
1. Systemic lupus erythematosus (SLE) is an autoimmune disease that can affect multiple organ systems.
2. SLE is characterized by the production of autoantibodies directed against cell nuclei.
3. Treatment of lupus nephritis involves induction therapy with corticosteroids and cytotoxic agents to control disease activity, followed by long-term maintenance treatment to prevent flares and preserve renal function.
This document provides information about systemic lupus erythematosus (SLE). It defines SLE as a multi-system autoimmune disease affecting various organs mediated by autoantibodies and immune complexes. The causes are unknown but may involve genetic, hormonal, and environmental factors. SLE can affect many organ systems like the kidneys, lungs, heart, and nervous system, causing a variety of clinical manifestations. Diagnosis involves evaluating symptoms, medical history, physical exam, and laboratory tests. Treatment depends on disease severity and organ involvement, and may include medications like NSAIDs, antimalarials, corticosteroids, and cytotoxic drugs. Special considerations are given to SLE in pregnancy and neonates.
Toxic epidermal necrolysis (T.E.N.) is a rare but life-threatening adverse drug reaction where large areas of the epidermis are sloughed off due to necrosis. It is most commonly caused by drugs such as sulphonamide antibiotics and anticonvulsants. The clinical features include widespread erythema, flaccid blisters, and mucous membrane involvement that can lead to complications affecting the eyes, respiratory tract, and gastrointestinal tract. Treatment focuses on supportive care by discontinuing the causative drug, skin care to prevent infection, and monitoring fluid and electrolyte balance. The mortality rate is high at 30-40% even with treatment.
This document discusses vasculitis, which is an inflammatory destruction of blood vessels. It can affect all ages but some types are restricted to certain groups. It has both genetic and environmental components. Symptoms vary depending on the size of vessels involved and can include fatigue, rashes, nerve problems, and organ damage. Diagnosis involves clinical features, lab tests, and sometimes biopsies. Treatment is usually with steroids and other immunosuppressants to induce and maintain remission. Complications can be serious if not treated properly.
Gout is caused by hyperuricaemia (high uric acid levels) which can result in the deposition of urate crystals in the joints, causing inflammation. It predominantly affects males and risk factors include obesity, diets high in purines, alcohol consumption, and certain medications. Acute gout usually presents as sudden, severe pain in the first metatarsophalangeal joint. Treatment involves nonsteroidal anti-inflammatories and medications like allopurinol to reduce uric acid levels. Chronic, untreated gout can lead to tophaceous deposits and joint damage. Pseudogout is another type of crystal arthropathy seen in elderly women that involves calcium pyrophosphate crystal deposition.
This document provides information on ANCA-Associated Vasculitis (AAV). It discusses the classification, epidemiology, clinical features, diagnosis and treatment of AAV. Key points include: AAV includes GPA, MPA, RLV and EGPA which are associated with ANCA antibodies; clinical manifestations can include ENT, lung, kidney, and skin involvement; diagnosis involves labs like ANCA testing and biopsies; and treatment involves immunosuppressive drugs like cyclophosphamide and rituximab for induction of remission.
1. Lupus erythematosus is an autoimmune disease where the immune system attacks healthy tissue. It is characterized by a red rash and can cause skin, joint, kidney, and other organ involvement.
2. The document discusses the classification, epidemiology, pathogenesis, clinical features, investigations, management, and prognosis of both cutaneous and systemic lupus erythematosus.
3. Treatment involves general measures, local and systemic medications like antimalarials, corticosteroids, and immunosuppressants to control disease activity and damage. Monitoring is important to assess disease status and damage over time.
The document provides an overview of systemic lupus erythematosus (SLE) for medical students. It defines SLE, discusses its epidemiology and pathophysiology. It then describes the clinical presentation of SLE including cutaneous, musculoskeletal, serosal, renal, neurological, and hematological manifestations. It also covers investigations such as autoantibody tests and renal biopsy. Finally, it discusses lupus nephritis as a serious complication of SLE. The document aims to ensure students understand the definition, clinical picture, classification criteria, investigations, prognosis, complications and treatment approaches for SLE.
This document provides an overview of systemic lupus erythematosus (SLE). It discusses the definition, epidemiology, pathogenesis, diagnosis, clinical manifestations, management, and complications of SLE. The pathogenesis involves genetic susceptibility and environmental triggers leading to abnormal immune responses and autoantibody production. Diagnosis is based on the SLICC classification criteria. Management involves controlling symptoms, preventing organ damage, and treating flares and complications using medications like glucocorticoids, antimalarials, immunosuppressants, and biologics. Life-threatening complications can include renal disease, neurological involvement, hematological abnormalities and vasculitis.
Systemic Lupus Erythematosus (SLE) is an autoimmune disease where the immune system mistakenly attacks healthy tissue. It most commonly affects women under age 40 and can involve the skin, joints, kidneys, brain and other organs. Symptoms vary but often include joint pain, rash, and fatigue. There is no cure for SLE but treatment aims to control symptoms, which may include medications like hydroxychloroquine and corticosteroids. Prognosis has improved in recent years though long-term treatment is usually required to manage the disease.
1) Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by unpredictable exacerbations and remissions affecting multiple organ systems.
2) The case report describes an 11-year old Indian boy who presented with fever and pancytopenia and was subsequently diagnosed with SLE based on rash, oral ulcers, arthritis, and strongly positive autoantibody tests.
3) He responded well to pulse steroids and IV immunoglobulin therapy and was put on long-term immunosuppressants for maintenance treatment.
This document provides information on systemic sclerosis (SSc), a chronic autoimmune disease characterized by thickening and hardening of the skin, and involvement of internal organs. It can present as either limited or diffuse cutaneous forms. Key clinical features include Raynaud's phenomenon, skin thickening and tightening, digital pitting scars, and internal organ involvement such as interstitial lung disease, gastrointestinal issues, and renal crisis. Diagnosis involves clinical examination and the presence of autoantibodies. Differential diagnoses include other conditions presenting with similar skin or vascular changes. Complications can affect multiple organ systems and are a leading cause of mortality.
A 60-year-old woman presented with painful, sclerotic hands and fingers due to progressive cutaneous scleroderma. She was started on a compounded topical cream containing ketamine, baclofen, gabapentin, verapamil, and pentoxifylline, which provided significant pain relief and improved sensation within a month. At a 6-month follow up, she had been largely weaned off opioid pain medications. The customized treatment targeted the pathophysiology of the condition and helped manage her debilitating symptoms.
Systemic Lupus Erythematosus (SLE) is a multi-gene autoimmune disease caused by a combination of genetic and environmental factors. It is characterized by abnormal immune responses that result in inflammation and damage to various organs. Diagnosis requires meeting 4 out of 11 classification criteria relating to clinical symptoms and blood markers. Management aims to induce remission of acute flares, maintain improvements to suppress symptoms, and prevent organ damage. Treatment choices depend on the severity and potential reversibility of manifestations. The goal is controlling symptoms without cure since complete sustained remission is rare.
Systemic lupus erythematosus (SLE) is the prototypic multisystem autoimmune disorder with a broad spectrum of clinical presentations encompassing almost all organs and tissues.
The extreme heterogeneity of the disease has led some investigators to propose that SLE represents a syndrome rather than a single disease.
Lupus was first recognised as a systemic disease with visceral manifestations by Moriz Kaposi (1837–1902).
Dr. Swamy Venuturupalli talks about Rheumatoid Arthritis, Early Diagnosis and Treatment at the James R. Klinenberg symposium on Rheumatic diseases in Pasadena, CA.
Lupus Nephritis :From Basics To PracticeYasser Matter
This document provides an overview of lupus nephritis (LN), including:
- Epidemiology: Up to 40% of SLE cases involve the kidneys. It predominantly affects women aged 15-45.
- Pathogenesis: Autoantibodies form immune complexes that deposit in the glomerulus, activating complement and attracting inflammatory cells. The location of deposits determines histologic class.
- Diagnosis: Urinalysis, serum creatinine, immunological tests. Renal biopsy is needed to classify LN and guide treatment.
- Treatment involves induction therapy for 3-6 months, then maintenance to prevent chronic kidney disease. Treatment depends on histologic class and response to therapy. The goal
This document discusses lupus nephritis, including its pathophysiology, risk factors, clinical presentation, investigations, classification, treatment, and prognosis. Key points include:
- Lupus nephritis is a serious manifestation of systemic lupus erythematosus caused by autoantibodies forming immune complexes that deposit in the glomeruli.
- It is classified based on renal biopsy findings, with classes III and IV having the highest risk of progressing to end-stage renal disease.
- Treatment involves immunosuppressive induction therapy with corticosteroids and cyclophosphamide or mycophenolate mofetil to rapidly decrease inflammation, followed by long-term maintenance
Rheumatoid arthritis is a chronic inflammatory disease that affects the joints and causes pain, swelling, stiffness and loss of function. It affects around 1% of the population worldwide. Recent advances in management include earlier diagnosis using classification criteria from ACR/EULAR and aggressive treatment with disease-modifying antirheumatic drugs alone or in combination with biological therapies that target cytokines like TNF-α. While DMARDs can control symptoms, biological therapies may induce remission and prevent further joint damage by acting faster than conventional treatments. Prompt diagnosis and management can now improve long-term outcomes for those suffering from rheumatoid arthritis.
1. Systemic lupus erythematosus (SLE) is an autoimmune disease that can affect multiple organ systems.
2. SLE is characterized by the production of autoantibodies directed against cell nuclei.
3. Treatment of lupus nephritis involves induction therapy with corticosteroids and cytotoxic agents to control disease activity, followed by long-term maintenance treatment to prevent flares and preserve renal function.
This document provides information about systemic lupus erythematosus (SLE). It defines SLE as a multi-system autoimmune disease affecting various organs mediated by autoantibodies and immune complexes. The causes are unknown but may involve genetic, hormonal, and environmental factors. SLE can affect many organ systems like the kidneys, lungs, heart, and nervous system, causing a variety of clinical manifestations. Diagnosis involves evaluating symptoms, medical history, physical exam, and laboratory tests. Treatment depends on disease severity and organ involvement, and may include medications like NSAIDs, antimalarials, corticosteroids, and cytotoxic drugs. Special considerations are given to SLE in pregnancy and neonates.
Toxic epidermal necrolysis (T.E.N.) is a rare but life-threatening adverse drug reaction where large areas of the epidermis are sloughed off due to necrosis. It is most commonly caused by drugs such as sulphonamide antibiotics and anticonvulsants. The clinical features include widespread erythema, flaccid blisters, and mucous membrane involvement that can lead to complications affecting the eyes, respiratory tract, and gastrointestinal tract. Treatment focuses on supportive care by discontinuing the causative drug, skin care to prevent infection, and monitoring fluid and electrolyte balance. The mortality rate is high at 30-40% even with treatment.
This document discusses vasculitis, which is an inflammatory destruction of blood vessels. It can affect all ages but some types are restricted to certain groups. It has both genetic and environmental components. Symptoms vary depending on the size of vessels involved and can include fatigue, rashes, nerve problems, and organ damage. Diagnosis involves clinical features, lab tests, and sometimes biopsies. Treatment is usually with steroids and other immunosuppressants to induce and maintain remission. Complications can be serious if not treated properly.
Gout is caused by hyperuricaemia (high uric acid levels) which can result in the deposition of urate crystals in the joints, causing inflammation. It predominantly affects males and risk factors include obesity, diets high in purines, alcohol consumption, and certain medications. Acute gout usually presents as sudden, severe pain in the first metatarsophalangeal joint. Treatment involves nonsteroidal anti-inflammatories and medications like allopurinol to reduce uric acid levels. Chronic, untreated gout can lead to tophaceous deposits and joint damage. Pseudogout is another type of crystal arthropathy seen in elderly women that involves calcium pyrophosphate crystal deposition.
This document provides information on ANCA-Associated Vasculitis (AAV). It discusses the classification, epidemiology, clinical features, diagnosis and treatment of AAV. Key points include: AAV includes GPA, MPA, RLV and EGPA which are associated with ANCA antibodies; clinical manifestations can include ENT, lung, kidney, and skin involvement; diagnosis involves labs like ANCA testing and biopsies; and treatment involves immunosuppressive drugs like cyclophosphamide and rituximab for induction of remission.
1. Lupus erythematosus is an autoimmune disease where the immune system attacks healthy tissue. It is characterized by a red rash and can cause skin, joint, kidney, and other organ involvement.
2. The document discusses the classification, epidemiology, pathogenesis, clinical features, investigations, management, and prognosis of both cutaneous and systemic lupus erythematosus.
3. Treatment involves general measures, local and systemic medications like antimalarials, corticosteroids, and immunosuppressants to control disease activity and damage. Monitoring is important to assess disease status and damage over time.
The document provides an overview of systemic lupus erythematosus (SLE) for medical students. It defines SLE, discusses its epidemiology and pathophysiology. It then describes the clinical presentation of SLE including cutaneous, musculoskeletal, serosal, renal, neurological, and hematological manifestations. It also covers investigations such as autoantibody tests and renal biopsy. Finally, it discusses lupus nephritis as a serious complication of SLE. The document aims to ensure students understand the definition, clinical picture, classification criteria, investigations, prognosis, complications and treatment approaches for SLE.
Lupus erythematosus (LE) is an autoimmune connective tissue disorder that can affect one or several organs. Circulating autoantibodies and immune complexes are due to loss of normal immune tolerance and are pathogenic. Clinical features of LE are highly variable. LE nearly always affects the skin to some degree.
D.W. is exhibiting signs of a lupus flare, likely due to increased stress from longer work hours. Her kidney function appears to be compromised, as evidenced by the elevated BUN and creatinine and urinary abnormalities. Priorities should include:
- Reducing stress by decreasing work hours or taking medical leave if needed. Stress exacerbates lupus symptoms.
- Increasing immunosuppressant medications under physician supervision to control the lupus flare and reduce kidney inflammation.
- Monitoring kidney function closely with repeat labs and controlling any hypertension or diabetes that could further impact her kidneys.
- Educating on hydration and a low-salt diet to protect kidney function.
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A 22-year-old college student presents with symptoms including a malar rash, photosensitivity, arthritis, fatigue, and hair loss. Laboratory tests show a positive ANA, positive anti-Smith antibody, and low white blood cell and platelet counts. This constellation of clinical features and laboratory results makes systemic lupus erythematosus the most likely diagnosis for the patient.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect various organs in the body. Common symptoms include fatigue, joint pain, rashes, and kidney problems. It is caused by genetic and environmental factors that lead to abnormal immune responses against the body's own tissues. Diagnosis involves evaluating clinical features along with blood tests to detect autoantibodies. Treatment depends on the specific organs involved but may include medications to suppress the immune system.
This document discusses systemic lupus erythematosus (SLE), an autoimmune disease where the immune system attacks the body's own tissues and organs. It causes inflammation and damage to many different body systems. SLE is more common in women and typically presents between ages 15-25. Symptoms can include rashes, joint pain, fatigue, and organ involvement. Diagnosis involves evaluating symptoms, signs, and antibody tests. Treatments include medications like NSAIDs, antimalarials, steroids, and immunosuppressants to reduce symptoms and prevent organ damage. Complications can affect many organs but most commonly involve the kidneys, heart, and lungs. With treatment, 5-year survival rates are over 85%.
The document discusses several autoimmune diseases where the immune system attacks the body's own cells and tissues, including:
- Systemic lupus erythematosus (SLE), which can damage multiple organs like the heart, joints, skin, lungs, blood vessels, and kidneys. It occurs more in women and symptoms include rashes, fatigue, and pain. Kidney damage is common.
- Sjögren's syndrome, an autoimmune disorder characterized by dry eyes and mouth due to immune destruction of salivary and tear glands.
- Multiple sclerosis, where the immune system attacks the myelin sheath surrounding nerves in the brain and spinal cord, causing symptoms like vision problems
Rheumatological diseases can affect the joints, skin, and internal organs. Some common types include rheumatoid arthritis, osteoarthritis, lupus, Sjogren's syndrome, and spondyloarthropathies like ankylosing spondylitis. Rheumatoid arthritis causes chronic inflammation of the synovium and can lead to joint deformity. Osteoarthritis is characterized by cartilage loss within a joint and associated bone changes. Systemic lupus erythematosus is a multi-system autoimmune disease affecting many organs, with a variety of potential manifestations.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect many organ systems. It is characterized by antibodies to nuclear and cytoplasmic antigens, multi-system inflammation, and a relapsing and remitting course. SLE most often occurs in women of childbearing age, with a classic presentation of fever, joint pain, and rash. Symptoms can include malar rash, ulcers, kidney involvement, seizures, thrombocytopenia, hemolytic anemia, fever, and lymphadenopathy affecting constitutional, musculoskeletal, dermatological, renal, neuropsychiatric, pulmonary, gastrointestinal, and cardiac systems. Diagnosis is based on criteria from the EULAR
1. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the production of auto-antibodies against components of the cell nucleus.
2. SLE affects multiple organ systems and is more common in females, with a female to male ratio of 9:1 before puberty.
3. Diagnosis of SLE requires meeting 4 out of 11 American College of Rheumatology diagnostic criteria, including at least 1 clinical and 1 immunological criterion. Common clinical manifestations include malar rash, arthritis, renal disease, and hematological abnormalities.
Systemic lupus erythematosus (SLE) is a multi-system autoimmune disease caused by antibody and complement deposition that results in tissue damage. It is characterized by periods of disease exacerbation and remission. SLE can affect many organs and cause a variety of symptoms. Diagnosis involves evaluating a patient's medical history, symptoms, physical exam findings, and lab tests. Treatment is tailored to each individual and aims to control disease activity and symptoms using medications like NSAIDs, antimalarials, corticosteroids, and immunosuppressants.
This document summarizes systemic lupus erythematosus (SLE), an autoimmune disorder that can affect multiple systems of the body. It discusses the epidemiology, etiology, pathology, clinical features, and laboratory diagnosis of SLE. SLE predominantly affects females and commonly presents in the second to third decade of life. Genetic and environmental factors contribute to its development by causing a failure of self-tolerance and production of autoantibodies that can damage tissues. SLE is characterized by the formation of various antibodies and can involve organs like the skin, kidneys, blood vessels, heart, and central nervous system. Diagnosis involves testing for autoantibodies and supportive evidence from tests like urinalysis, MRI, ech
This 23-year-old woman presented with seizures, headaches, weight loss, hair loss, joint pains, and night sweats. On examination, she had a thin scalp with patchy hair loss, numerous lymph nodes, fever, tachycardia, and high blood pressure. Laboratory tests showed anemia, low white blood cell and platelet counts, high sedimentation rate, proteinuria, and red blood cells in her urine. The likely diagnosis is systemic lupus erythematosus (SLE) based on her symptoms and laboratory abnormalities. Further immunological testing including ANA and anti-dsDNA antibodies would help confirm the diagnosis of SLE. She requires admission for treatment and management of her organ-threatening l
Systemic lupus erythematosus (SLE) is an autoimmune disease where the immune system mistakenly attacks healthy cells and tissues. It is known as lupus and can affect multiple organ systems. SLE affects women more than men and prevalence is highest in Asian, African, and Hispanic populations. Symptoms can include butterfly rash, photosensitivity, arthritis, serositis, and involvement of major organs like the kidneys and brain. SLE is diagnosed based on meeting 4 out of 11 diagnostic criteria from the American College of Rheumatology including both clinical and immunological criteria. Treatment involves managing symptoms with medications like NSAIDs, hydroxychloroquine, corticosteroids, and immunosuppressive
Connective tissue diseases share features of immune dysregulation and autoantibody production directed at nuclear components, causing widespread tissue damage. Systemic lupus erythematosus is characterized by arthritis, rashes, kidney involvement and positive ANA and anti-dsDNA antibodies. Systemic sclerosis involves skin thickening from fibrosis, Raynaud's phenomenon, and autoantibodies like anti-Scl-70. Polymyositis and dermatomyositis cause proximal muscle weakness and inflammation with skin lesions in dermatomyositis.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can affect multiple organ systems. SLE most commonly affects women in their 20s and 30s. The course of SLE is unpredictable, with periods of illness alternating with remission. Common initial symptoms include fatigue, fever, joint pain, and weight changes. SLE can cause skin rashes, oral ulcers, hair loss, serositis, lung involvement including pleurisy, heart involvement such as pericarditis, and kidney disease. The prognosis for SLE has improved in recent decades due to medical advances, with survival rates of approximately 95% at 5 years and 90% at 10 years. SLE is treated symptomatically mainly with
Lupus is an autoimmune disease where the immune system attacks its own tissues. It can affect many body systems like joints, skin, kidneys, lungs and brain. Symptoms vary but may include facial rashes, fatigue, fever and joint pain. There is no cure for lupus but treatments can control symptoms. Treatments include medications like hydroxychloroquine and corticosteroids to reduce inflammation and prevent flares. Managing lupus requires balancing medications, exercise, sleep and avoiding triggers like sunlight.
Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease. The immune system attacks the body’s cell and tissue, resulting in inflammation and tissue damage. SLE can affect any part of the body, but most often harms the heart, joints, skin, lungs, blood vessels, liver, kidney and nervous system.
Over 40 different genes predispose to SLE.
Characterized by remission and exacerbation.
The document discusses lupus, an autoimmune disease that commonly affects the kidneys and can lead to end-stage renal disease requiring dialysis or transplantation. Kidney involvement from lupus nephritis is a major cause of illness and death, and the document outlines risk factors for progression to end-stage renal disease as well as treatment options and outcomes for lupus patients with kidney failure.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Diagnosis and management sle
1. DIAGNOSIS AND MANAGEMENT
OF
SYSTEMIC LUPUS ERYTHEMATOSUS
A PRESENTATION BY DR. ASHVINI K. LOMROD
UNDER THE GUIDANCE OF DR. C.K. MEENA SIR
JLN MEDICAL COLLEGE, AJMER
2. Systemic+ Lupus+ Erythematosus
Systemic - The disease can affect organs and tissues throughout the
body.
Lupus [ Latin for wolf ] It refers to the rash that was thought to
resemble a wolf bite.
Erythematosus [ Greek word for red ] – It refers to the color of the
rash.
3. DEFINITION
•A systemic autoimmune disease with relapsing
and remitting course that can affect almost any
organ system in which organs and cells undergo
damage mediated by tissue binding
autoantibodies and immune complexes.
5. ➢ Gender – 90% women(women to men ratio 9:1) in child bearing age. Flares
also become some what less common after menopause in women have chronic
SLE.
Female sex is permissive for SLE because:
- Hormone effects
- Genes on X-chromosome
-Epigenetic differences between genders
Estradiol binds to receptors on T & B lymphocytes increasing activation &
survival of these cells, thus favouring prolonged immune response.
So women are exposed to estrogen containing OCP and hormone replacement
therapy have an increased risk of developing SLE.
People with more X-chromosomes(XXX karyotypes,Klinefelter’s syndrome)
have a significant increased risk for SLE.
6. ➢ Age – 15-44 yrs are commonly affected.
➢Race & Ethnicity – More common in urben than rural areas.
Highest prevalence is in black women and lowest
is in white men.
➢ Family History - A brother or sister of a patient with the disorder
has 20 times the risk as someone without an
immediate family member with SLE.
7. ➢Environmental Triggers – Sunlight, cold, fatigue, stress, chemicals and
certain drugs.
*Sunlight : Ultraviolet rays (UVB or UVA) Shorter UVB wavelengths cause
the most harm.
*Viruses : EBV ( The cause of mononucleosis)
*Smoking : May increase the risk for skin and kidney problems in women
who have the disease.
*Tobacco
*Chemicals: Occupational exposure to crystalline silica as a possible trigger.
Some prescription medications are associated with a temporary
lupus syndromes (drug-induced lupus),which resolves after these
drugs are stopped.
☻ Drinking alcohol(2 glasses of wine a week or ½ of an alcoholic drink daily)
reduces the risk of SLE.
8. * Hormone Replacement Therapy : increases the risk for blood clots and
heart problems as well as breast cancer.
Guidelines recommend HRT the lowest possible dose for the shortest
possible time. Women with SLE who have active disease, antiphospholipid
Antibodies or a history of blood clots or heart disease should not use HRT.
* Oral Contraceptives : Caution against taking OCPs( Estrogen could
trigger lupus flare-ups).However, recent evidence indicate that OCs are
safe, at least for women with inactive or stable lupus. Lupus can cause
complications in its early stages. The estrogen in OCs increase the risk for
blood clots.(Risk particularly for women with antiphospholipid syndrome)
10. ➢ SLE - The most common type and is the type of lupus that
can lead to serious systemic complications.
➢ Cutaneous lupus erythematosus - Confined to the skin
and does not affect other parts of the body. About 10% of
people with this type of lupus go on to develop SLE.
➢ Discoid lupus erythematosus - A type of cutaneous lupus
that produces a potentially scarring disc shaped rash on the
face, scalp or ears.
11. ➢ Drug-induced lupus - Temporary and mild form of lupus
due to some drugs like Hydralazine, ACE inhibitors, and
calcium channel blockers, hydrochlorothiazide. Symptoms
resolve once the medication is stopped.
➢ Neonatal lupus - A rare condition that sometimes affects
infants born to mothers who have SLE. Babies with
neonatal lupus are born with skin rash, liver problems, and
low blood counts and may develop heart problems.
13. Role of Genetics and Environment
➢Environment
• Cell damage by environmental triggers causes apoptosis that leads to release of
apoptotic bodies+parts of nucleus [ now exposed to other parts of body ]
➢ Genetics – Susceptibility genes and their effect on immune system.
• loss of self tolerance [ immune system recognizes parts of nucleus as self antigens ]
• Self Ag presentation by DCs,
• Defective complement system,
• Impaired clearance of apoptotic cells
• Aberrant lymphocyte activity[unregulated T cell dependent B cell activation]
• Production of autoantibodies
14. • Antigen-Antibody complexes / Immune Complexes deposition in various body tissues
[ basement membranes ] results
– Local inflammation
– Local complement activation
– Local apoptosis
– Positive feedback loop
• DNA is the main antigen for which antibodies are formed
• IgG is the most “pathogenic” because it forms intermediate sized complexes that can get
to the small places and block them
• Injury is caused by
Mainly deposition of immune complexes and
Binding of antibodies to various cells and tissues.
• In most patients, autoantibodies are present for a few years before the first clinical
symptom appears
18. Constitutional
• Fatigue – Mild to extreme
• Malaise
• Fever – any pattern
• Anorexia
• Weight loss
• lymphadenopathy
• Arthralgia
19. Musculoskeletal
• Arthralgia , myalgia
• Polyarthritis [ 2 or more peripheral joint ] - Intermittent,mild to disabling,soft tissue swelling,
tenderness,Nonerosive,MC in hands,wrists and knees
• Joint deformities (hands and feet)-In 10% cases ,erosions can be identified on ultrasound
(rarely on x-rays)
• Myopathy /myositis
• Ischemic necrosis of bone
“rhupus”-some patients of SLE have rheumatoid like arthritis with erosions and fulfill
criteria for both RA and SLE so may be coded having both diseases
21. Cutaneous
• Photosensitivity-skin rash on Sun exposed areas due to sunlight
• Malar rash –MC acute SLE rash-photosensitive,slightly raised erythema,occasionaly scally,
on the face(butterfly rash-malar eminences and nasal bridge)but sparing nasolabialfold,
ears,chin,neck and chest,upper backand extensor surfaces of the arms
• Discoid rash (DLE)-MC chronic dermatitis in lupus,lesions roughly circular with slightly
raised ,scaly hyperpigmented erythematous rims and depigmented,atrophic centers
(permanently damaged dermal appendages)
• Subacute cutaneous lupus
• Oral lesions-Erythema of palate,tongue and oral mucosa,papules,vesicles and petechiae.oral
or nasopharyngial ulceration usually painless
• Alopacia
• Others-urticaria,
• Vasculitis rash
• Raynodes phenomena
24. Photosensitive systemic lupus erythematosus (SLE) rashes typically occur on the face or extremities
which are sun exposed regions. Although the interphalangeal space are affected, the metacarpophalangeal
(MCP) and proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints are spared.
30. Renal
• 50 % of lupus pts will have kidney involvement in their life ,of these 50 % will have
serious kidney disease
• Persistent proteinuria > 0.5 grams / 24 hrs (or greater than 3+), cellular casts ( may be
red cells ,hemoglobin,granular, tubular,mixed)
• Nephritis (Lupus nephritis) –the most serious manifestation and also predict outcome
(prognosis)
• Renal Failure because of Glomerulonephritis is the leading cause of death among lupus
patients.
• Nephrotic syndrome
• ESRD
31. GIT
• Nonspecific – Nausea, vomitting, diarrhea
• Diffuse abdominal pain-autoimmune peritonitis and/or intestinal vasculitis
• Abnormal liver enzymes (more often due to therapy than to
SLE itself)
• Mesenteric Vasculitis
• Sepsis and bleeding
32. Thromboembolic events
Patients of Antiphospholipid syndrome due to hypercoagulable state
more prone to clots [ venous or arterial ] that can leads to
• Deep vein thrombosis
• Hepatic vein thrombosis
• Stroke
• Myocardial infarction
33. Ocular
• Common but less serious - Sicca syndrome
Conjunctivitis
Episcleritis
• Serious manifestations - Retinal vasculitis
Optic neuritis
• Fundoscopy shows sheathed, narrow retinal arterioles and white
hard exudate called ‘Cytoid body’
41. LN-Treatment
In general, class III and IV disease, as well as class V accompanied by III or IV
disease, should be treated with aggressive immunosuppression if possible,
because there is a high risk for end-stage renal disease (ESRD) if patients are
untreated or undertreated.
In contrast, treatment for lupus nephritis is not recommended in patients with
class I or II disease or with extensive irreversible changes.
43. LABORATORY TESTS
• Antinuclear antibodies [ANA]-Sensitive but not specific
• Anti -ds DNA-[ More specific ], targets double-stranded DNA, seen during active disease
• 4 RNA associated antibodies -
Anti-Sm [Smith] –[ More specific ]Targets ribonucleoproteins
Anti Ro /SSA- antibody
Anti La/SSB- antibody
Anti –RNP
• Antiphopholipid antibody- [Less specific to Lupus] Targets protein bound to phospholipid
Lupus anticoagulent [ Lupus antibody ]
Anti-B2 glycoprotein 1 AB
Anti-cardiolipin
44. • Coombs test- Hemolytic anemia
.
• Complete blood count-Hemolytic anemia with reticulocytosis
Leukopenia-less than 4,000 / cu mm on 2 or more occasions
Lymphopenia-less than 1,500 / cu mm on 2 or more occasions
Thrombocytopenia-less than 100,000 /cu mm , in the absence of offending drugs
• Erythrocyte sedimentation rate
• RFT,LFT ,Lipid profile
• C-reactive protein
• Urine routine and microscopy and 24 hrs protein and creatinine estimation
45. • Complement levels [ C3 and C4 ] - Decreased (C3 level < 5.5 mg/dl)
• Chest radiography and chest CT scanning-
ILD, pneumonitis, pulmonary emboli, alveolar haemorrhages
• Joint radiograpy-periarticular osteopenia and soft tissue swelling without
erosions
• Echocardiography-pericardial effusion
• ↑ ESR, ↑ anti ds-DNA and ↓C3 may indicate disease ‘flare’
46. Skin Biopsy
LUPUS BAND TEST (60%)
Deposition of Ig at the dermoepidermal junction (DEJ), injury
to basal keratinocytes, and inflammation dominated by T
lymphocytes in the DEJ and around blood vessels and dermal
appendages. Clinically unaffected skin may also show Ig deposition
at the DEJ
47. Renal biopsy
• In the recent Systemic Lupus International Collaborating Clinic (SLICC)
criteria for classification of SLE, a diagnosis can be established on the
basis of renal histology alone without meeting additional criteria .
• The pattern and severity of injury are important in diagnosis and in
selecting the best therapy.
• Recommended for every SLE patient with any clinical evidence of
nephritis
• Not recommended as a screening test
48. Histologic abnormalities in blood vessels
• Leukocytoclastic vasculitis is most common.
• Not specific for SLE but may indicate active disease
Lymph node biopsies
• Nonspecific diffuse chronic inflammation.
• Usually performed to rule out infection or malignancies.
49.
50. MANAGEMENT
• There is no cure for SLE and complete sustained remissions are
rare so management aims to induce remissions of acute flares ,
maintenance therapy and thereby preventing organ damage
• Many patients with SLE have “flares”, in which symptoms
suddenly worsen and then settle down for long periods of time.
51.
52. Conservative management
• NSAIDs, salicylates (Ecotrin a and St. Joseph’s aspirin approved by FDA for use in SLE )
for arthritis / arthralgia- Doses toward upper limit of recommended range usually required
• Antimalarials(HCQ,CQ,quinacrine)-for dermatitis, arthritis, fatigue
• Systemic glucocorticosteroids( low dose)
• Belimumab
• lupus dermatitis-topical sunscreens [ SPF 15 at least ; 30+ preferred],antimalarials, topical
glucocorticoids and/or tacrolimus and systemic glucocorticoids with or without
mycophenolate for severe or unresponsive cases
54. Systemic glucocorticoids
• MPS and Prednisolone
MPS 500-1000 mg IV over 1 hour OD for 3 days
followed by
0.5 - 1 mg/kg per day prednisolone PO
Currently
0.5 - 1 mg/kg per day prednisolone PO for 4-6 weeks therefore tappered as soon as
condition improves usually to a dose 5-10 mg daily
0.07–0.3 mg/kg prednisolone per day or qod for milder disease
55. Cytotoxic/immunosuppressive therapy
➢ Methotrexate
[for dermatitis, arthritis]
10–25 mg once a week, PO or SC, with folic acid; decrease dose if CrCl<60 mL/min
➢ Cyclophosphamide
• IV
Low dose : 500 mg every 2 weeks for 6 doses maintenance with MMF or
AZA. High dose: 7–25 mg/kg q month × 6; consider mesna administration
with dose
• Oral
1.5–3 mg/kg per day; decrease dose for CrCl <25 mL/min
56. • Mycophenolate
MMF: 2–3 g/d PO for induction therapy,
1–2 g/d for maintenance therapy; max 1 g bid if CrCl <25 mL/min
MPA: 360–1080 mg bid; caution if CrCl<25 mL/min
• Azathioprine
2–3 mg/kg per day PO for induction; 1–2 mg/kg per day for maintenance; decrease frequency
of dose if CrCl <50 mL/min
• Belimumab
10 mg/kg IV wks 0, 2, and 4, then monthly
• Rituximab
[ for patients resistant to above therapies ]
375 mg/m2 q wk × 4 or 1 g q 2 wks × 2
57. SERIOUS OR COMMON ADVERSE EFFECTS OF
DRUGS USED IN SLE
• NSAIDS-aseptic meningitis,elevated liver enzymes,decreased renal functions,vasculitis of
skin,MI,ototoxicity,tinitus,allergic reactions,dermatitis,gi events,ARF,edema,HTN
• Topical GC-skin atrophy,contact dermatitis,,folliculitis,hypopigmentation,infection
• Topical sunscreens-contact dermatitis
• HCQ-retinal damage,cornial opacity myopathy ,neuropathy
• MTX-megaloblastic anemia at low doses and bone marrow suppression at high doses
• GC-infections,HTN,hyperglycemia,hypokalemia,allergic reactions,cushingoid
changesCHF,fragile skin,menstrual abnormalities,osteoporosis
59. Lifestyle changes to help cope with SLE.
• Get plenty of rest (fatigue is another common SLE symptom)
• Salt restriction [ if HTN ] , avoid fat [ for hyperlipidaemia ] , calcium supplements with
steroid therapy
• Engage in regular light-to-moderate exercise to help fight fatigue and heart disease, and to keep
joints flexible
• Avoid excessive sunlight exposure, and wear sunscreen (ultraviolet light is the one of the main
triggers of flares)
• Don't smoke and avoid exposure to second-hand tobacco smoke
60. PREVENTIVE THERAPIES
Prevention of complications of SLE and its therapy
• Suppressing recurrent urinary tract infections.
• Providing appropriate vaccinations [ the administration of influenza and pneumococcal ]. [
Vaccination with attenuated live viruses is generally discouraged in patients who are
immunosuppressed ].
• Prevention of osteoporosis .
[ Postmenopausal women can be protected from steroid-induced osteoporosis
with either bisphosphonates or denosumab. Safety of long-term use of these
strategies in women is not well established ].
• Control of hypertension
• Prevention strategies for atherosclerosis
monitoring and treatment of dyslipidemias
management of hyperglycemia and obesity.
61. DIFFERENTIAL DIAGNOSIS
• Chronic fatigue syndrome
• Undifferentiated connective tissue disease
• Primary Sjogren`s syndrome
• Primary antiphospholipid syndrome
• Fibromyalgia with positive ANA
• Idiopathic thrombocytopenic purpura
• Drug-induced lupus
• Early RA
• Systemic vasculitis
62. SLE & PREGNANCY
• Increases the risk of spontaneous abortion, IUD, preeclampsia,IUGR and
preterm birth
• Prognosis best for both mother and child when SLE is quiescent for at least 6
months before the pregnancy and mothers renal function stable and normal
or near normal
• Lupus nephritis can get worse during pregnancy
• In general pregnancy does not cause flares of SLE
• When flares do develop ,they often occur during the first or second trimester
or during first few months after delivery
63. SPECIAL CONDITIONS IN SLE THAT MAY REQUIRE ADDITIONAL
OR DIFFEENT THERAPY
Crescentic Lupus Nephritis
The presence of cellular or fibrotic crescents in glomeruli with
proliferative glomerulonephritis indicates a worse prognosis Most
authorities currently recommend that high-dose cyclophosphamide is
the induction therapy of choice, in addition to high-dose
glucocorticoids.
64. Membranous Lupus Nephritis
Immunosuppression is not recommended unless proteinuria is in the
nephrotic range (although treatment with ACE inhibitors or angiotensin II
receptor blockers is recommended).
In those patients, recent prospective controlled trials suggest that alternate-
day glucocorticoids plus cyclophosphamide or mycophenolate mofetil or
cyclosporine are all effective in the majority of patients in reducing
proteinuria.
65. Pregnancy and Lupus
• Fertility rates for men and women with SLE are probably normal.
• Rate of fetal loss is increased (approximately two- to threefold) in women with SLE.
• Fetal demise is higher in mothers with high disease activity, antiphospholipid antibodies,
and/or active nephritis.
• Suppression of disease activity can be achieved by administration of systemic
glucocorticoids.
• Glucocorticoids [ Pregnancy category A (no evidence of teratogenicity in human studies)]
• Cyclosporine, tacrolimus, and rituximab [category C (may be teratogenic in animals but no
good evidence in humans) ];
• Azathioprine, hydroxychloroquine, mycophenolate mofetil, and cyclophosphamide
[category D (there is evidence of teratogenicity in humans, but benefits might outweigh
risks in certain situations) ];
• Methotrexate [ category X (risks outweigh benefits)].
66. • Therefore, active SLE in pregnant women should be controlled with hydroxychloroquine and,
if necessary, prednisone/prednisolone at the lowest effective doses for the shortest time required.
• Azathioprine may be added if these treatments do not suppress disease activity.
The cardiac manifestations can be life-threatening.
Recent evidence shows that hydroxychloroquine treatment of an anti-Ro-positive mother whose
infant develops congenital heart block significantly reduces the chance that subsequent fetuses
will develop heart block ,also with dexamethasone
A small proportion develops severe flares requiring aggressive glucocorticoid therapy or early
delivery.
Poor maternal outcomes are highest in women with active nephritis or irreversible organ
damage in kidneys, brain, or heart.
67.
68. Lupus and Antiphospholipid Syndrome (APS)
• Patients with SLE who have venous or arterial clotting and/or repeated fetal losses and at
least two positive tests for antiphospholipid antibodies have APS
• Should be managed with long-term anticoagulation .
• A target international normalized ratio (INR) of 2.0–2.5 is recommended for patients with
one episode of venous clotting.
• An INR of 3.0–3.5 is recommended for patients with recurring clots or arterial clotting,
particularly in the CNS.
• Recommendations are based on both retrospective and prospective studies of post treatment
clotting events and adverse effects from anticoagulation.
69. Microvascular Thrombotic Crisis
(Thrombotic Thrombocytopenic Purpura, Hemolytic-Uremic Syndrome)
• This syndrome of hemolysis, thrombo cytopenia, and microvascular thrombosis in
kidneys, brain, and other tissues carries a high mortality rate and occurs most commonly in
young individuals with lupus nephritis.
• The most useful laboratory tests are identification of schistocytes on peripheral blood
smears, elevated serum levels of lactate dehydrogenase, and antibodies to ADAMS13
• Plasma exchange or extensive plasmapheresis is usually life-saving; most authorities
recommend concomitant glucocorticoid therapy; there is no evidence that cytotoxic drugs are
effective.
70. Lupus Dermatitis
• Minimize exposure to ultraviolet light [ appropriate clothing and sunscreens ] .
• Topical glucocorticoids and antimalarials (such as hydroxychloroquine) reduces lesion
severity in most patients and are relatively safe.
• Systemic treatment with retinoic acid is a useful strategy in patients with inadequate
improvement on topical glucocorticoids and antimalarials; adverse effects are potentially
severe (particularly fetal abnormalities),
• Extensive, pruritic, bullous, or ulcerating dermatitis usually improve promptly after
institution of systemic glucocorticoids; tapering may be accompanied by flare of lesions, thus
necessitating use of a second medication such as hydroxychloroquine, retinoids, or cytotoxic
medications such as methotrexate, azathioprine, or mycophenolate mofetil.
• Topical tacrolimus - In therapy-resistant lupus dermatitis [possible increased risk for
malignancies ] dapsone or thalidomide [ the extreme danger of fetal deformities ]
71. EXPERIMENTAL THERAPIES
➢ Highly targeted experimental therapies targeting
• (1) activated B lymphocytes with anti-CD22 or TACI-Ig,
• (2) inhibition of IFN-α,
• (3) inhibition of B/T cell second signal coactivation with CTLA-Ig,
• (4) inhibition of innate immune activation via TLR7 or TLR7 and 9,
• (5) induction of regulatory T cells with peptides from immunoglobulins or autoantigens;
• (6) suppression of T cells, B cells, and monocyte/macrophages with laquinimod; and
• (7) inhibition of lymphocyte activation by blockade of Jak/Stat. A few studies have used
vigorous untargeted immunosuppression with high dose cyclophosphamide plus anti-T
cell strategies, with rescue by transplantation of autologous hematopoietic stem cells for
the treatment of severe and refractory SLE. One U.S. report showed an estimated
mortality rate over 5 years of 15% and sustained remission in 50%.
72. DRUG-INDUCED LUPUS
• A syndrome of positive ANA associated with symptoms such as fever, malaise, arthritis or
intense arthralgias/myalgias, serositis, and/or rash, during therapy with certain medications
and biologic agents.
• Predominant in whites, has less female predilection than SLE.
• Rarely involves kidneys or brain.
• Rarely associated with anti-dsDNA.
• Commonly associated with antibodies to histones.
• Usually resolves over several weeks after discontinuation of the offending medication.
73. The most frequent drugs –
• Antiarrhythmics procainamide, disopyramide, and propafenone;
• Antihypertensive hydralazine;
• Angiotensin-converting enzyme inhibitors and beta blockers;
• Antithyroid propylthiouracil;
• Antipsychotics chlorpromazine and lithium;
• Anticonvulsants carbamazepine and phenytoin;
• Antibiotics isoniazid, minocycline, and nitrofurantoin (Macrodantin);
• Antirheumatic sulfasalazine;
• Diuretic hydrochlorothiazide;
• Antihyperlipidemics lovastatin and simvastatin;
• IFNs and TNF inhibitors
• ANA usually appears before symptoms; however, many of the medications mentioned above induce ANA in
patients who never develop symptoms of drug induced lupus. It is appropriate to test for ANA at the first hint of
relevant symptoms and to use test results to help decide whether to withdraw the suspect agent.
74. PATIENT OUTCOMES, PROGNOSIS AND SURVIVAL
• Survival in patients with SLE in the United States, Canada, Europe, and China is
approximately
• 95% at 5 years,
• 90% at 10 years,
• 78% at 20 years.
• In the United States, African Americans and Hispanic Americans with a
mestizo heritage have a worse prognosis than whites, whereas Africans in Africa
and Hispanic Americans with a Puerto Rican origin do not.
75. Poor prognosis (~50% mortality in 10 years) in most series is associated with (at the
time of diagnosis)-
• High serum creatinine levels (>124 μmol/L [>1.4 mg/dL]),
• Hypertension,
• Nephrotic syndrome (24-h urine protein excretion >2.6 g),
• Anemia (hemoglobin <124 g/L [<12.4 g/dL]),
• Hypoalbuminemia,
• Hypocomplementemia,
• Antiphospholipid antibodies,
• Male sex,
• Ethnicity (African American, Hispanic with mestizo heritage) and low socioeconomic
status.
Overall patient survival in SLE patients with renal transplants rejection compared to patients
with other causes of ESRD, is comparable (85% at 2 years).
Lupus nephritis occurs in approximately 10% of transplanted kidneys.
76. Morbidity-
• Disease associated[ primarily to chronic fatigue, arthritis, and
pain, as well as renal disease ]
• Corticosteroid associated
Mortality-
• Early[in first decade]-Active disease,renal failure and infection
• Late- Atherosclerosis [ thromboembolic events ]