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.
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.
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.
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%.
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.
This document provides an overview of rheumatology, focusing on Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). For SLE, it describes the autoimmune nature of the disease, common clinical manifestations involving multiple organ systems, diagnostic criteria, and management approaches. RA is characterized as an inflammatory arthritis typically involving the small joints of the hands and feet symmetrically, which can lead to joint damage and deformities if untreated. The document reviews epidemiology, clinical features, extra-articular manifestations, diagnostic testing, and treatment options for RA.
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.
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.
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.
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.
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%.
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.
This document provides an overview of rheumatology, focusing on Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA). For SLE, it describes the autoimmune nature of the disease, common clinical manifestations involving multiple organ systems, diagnostic criteria, and management approaches. RA is characterized as an inflammatory arthritis typically involving the small joints of the hands and feet symmetrically, which can lead to joint damage and deformities if untreated. The document reviews epidemiology, clinical features, extra-articular manifestations, diagnostic testing, and treatment options for RA.
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.
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.
Connective tissue disorders involve inflammation of connective tissues leading to skin thickening or scarring, arthritis, and sometimes organ abnormalities. They are considered autoimmune disorders as antibodies form against normal tissues. The main types range from mild skin involvement to severe multi-system disease. Connective tissue disorders include localized forms like discoid lupus erythematosus and systemic forms like systemic lupus erythematosus which can damage multiple organs. Diagnosis involves assessing clinical features, immunological markers, and organ involvement. Treatment depends on disease severity but may include steroids, immunosuppressants, and addressing specific organ complications.
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.
Cutaneous lupus erythematosus (CLE) is a manifestation of the autoimmune disease systemic lupus erythematosus (SLE) that presents with diverse skin lesions. There are three main subtypes of CLE - acute (ACLE), subacute (SCLE), and chronic (CCLE, including discoid lupus erythematosus (DLE)). CLE results from a complex interplay between genetic susceptibility, environmental triggers like ultraviolet light, and dysregulated immune responses. Histopathology is useful but not definitive for diagnosis, which relies on clinical presentation and serological markers. CLE can range from limited skin involvement to systemic disease affecting major organs.
1. Lupus erythematosus (LE) is an autoimmune disease that can cause heterogeneous cutaneous and systemic manifestations. Cutaneous lupus erythematosus (CLE) can occur as a manifestation of systemic lupus erythematosus (SLE) or independently.
2. CLE is classified into LE-specific lesions and LE-nonspecific lesions. Common LE-specific lesions include acute cutaneous lupus erythematosus (ACLE), subacute cutaneous lupus erythematosus (SCLE), and chronic cutaneous lupus erythematosus (CCLE).
3. Diagnosis of CLE
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
Rheumatoid arthritis is a chronic inflammatory disease that commonly results in joint damage and physical disability. It is characterized by a symmetric, peripheral polyarthritis of unknown etiology that most frequently involves the small joints of the hands and feet. While the disease primarily affects the joints, it can also result in a variety of systemic manifestations involving other organ systems. The risk of rheumatoid arthritis is genetically influenced and increases with certain HLA-DRB1 alleles.
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).
Toxic epidermal necrolysis (TEN) is a rare, potentially fatal adverse drug reaction characterized by extensive skin detachment and mucous membrane involvement. It is caused by apoptosis of keratinocytes triggered by certain drugs in genetically susceptible individuals. TEN is diagnosed clinically based on >30% detachment of the epidermis. Management involves stopping the causative drug, supportive care, and investigational therapies to prevent apoptosis. Complications include infection, organ failure and death in around 30% of cases. Prognosis can be estimated using the SCORTEN severity-of-illness score.
This document summarizes key information about systemic lupus erythematosus (SLE), including:
1) SLE is a chronic inflammatory autoimmune disease characterized by abnormal immunologic function and autoantibodies against self-antigens, commonly presenting with nonspecific symptoms like fatigue and joint pain.
2) Treatment involves managing symptoms during flares using medications like NSAIDs, antimalarials, corticosteroids, cytotoxic drugs, and experimental therapies, while maintaining remission between flares.
3) Prognosis has improved but infection and cardiovascular disease remain leading causes of death, so treatment aims to control disease activity and damage while minimizing medication side effects.
Autoimmunity occurs when circumstances impair the regulation of cells with autoimmune potential, allowing them to attack the body's own tissues. Autoimmune conditions are common and often occur together in clusters across multiple organ systems. While specific diagnoses are applied, it is best to think of autoimmunity existing on a spectrum of related processes rather than rigid categories.
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 attacks its own tissues. It most commonly affects women aged 15-40. The exact causes are unknown but genetics, viruses, sunlight, and some drugs may play a role. Symptoms vary but can include rashes, joint pain, fatigue, and organ inflammation. Diagnosis involves blood tests and potentially biopsies. Treatment focuses on rest, sun protection, medications like NSAIDs, antimalarials, corticosteroids, and immunosuppressants to control disease activity and prevent organ damage. Nursing care aims to manage symptoms, prevent infections, and educate patients.
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoantibody production and damage to multiple organs. It predominantly affects women of childbearing age. SLE is caused by a combination of genetic and environmental factors. The disease is mediated by autoantibodies that form complexes and damage tissues. Common clinical manifestations include rashes, arthritis, kidney inflammation, and neurological and cardiac involvement. Diagnosis is based on identifying clinical and laboratory criteria including autoantibodies. Management involves controlling symptoms with medications like antimalarials and NSAIDs. More severe organ-threatening disease is treated with glucocorticoids and immunosuppressants like cyclophosphamide or mycophenolate
Systemic sclerosis is a chronic autoimmune disease characterized by fibrosis of the skin and internal organs. It is more common in females and there are three subtypes: limited cutaneous, diffuse cutaneous, and morphea. Complications can include pulmonary hypertension, interstitial lung disease, gastrointestinal issues, and renal crisis. Treatment involves managing symptoms, slowing disease progression, and treating complications aggressively. Scleroderma renal crisis, in particular, requires strict blood pressure control using ACE inhibitors.
This presentation encompasses SLE as well Lupus nephritis,Antiphospholipid Syndrome and other special situation related to SLE such as SLE and Pregnancy.
This document discusses three types of cutaneous lupus erythematosus: systemic lupus erythematosus (SLE), subacute cutaneous lupus erythematosus (SCLE), and discoid lupus erythematosus (DLE). SLE is an autoimmune disorder characterized by autoantibodies against nuclear DNA. SCLE is a variant of lupus characterized by anti-Ro antibodies. DLE causes erythematous plaques and scarring, often affecting the face and ears. Treatment involves photoprotection, topical steroids, hydroxychloroquine and occasionally oral steroids depending on the severity of symptoms for each condition.
Scleroderma is an autoimmune connective tissue disease that causes hardening of the skin and internal organs. It is classified into limited and diffuse subtypes based on the extent of skin involvement. Raynaud's phenomenon, skin thickening, and pulmonary and gastrointestinal issues are common clinical manifestations. The underlying pathogenesis involves vascular dysfunction, immune dysregulation, and fibrosis. Management focuses on treating individual organ system complications. Prognosis depends on the specific organ systems affected and can range from relatively mild to severe with significant morbidity and mortality.
1. Immunosuppressants and immunomodulators used in pregnancy include corticosteroids, azathioprine, cyclosporine, hydroxychloroquine, intravenous immunoglobulin, mycophenolate mofetil, rituximab, and tofacitinib.
2. The risk of these drugs depends on the gestational period, with higher risks in the first trimester and third trimester. Drugs are categorized by the FDA based on risk, from A (no risk) to X (contraindicated).
3. The document provides details on specific drugs, including their mechanisms of action, placental passage, FDA risk categories, and potential adverse effects
Secukinumab, an IL-17A inhibitor, demonstrated high efficacy and a favorable safety profile in treating severe chronic plaque psoriasis in pediatric patients in a 52-week randomized controlled trial. At week 12, 80.0% and 77.5% of patients receiving secukinumab low and high doses, respectively, achieved PASI 75 scores compared to 14.6% of placebo patients. 70.0% and 60.0% of patients receiving low and high doses achieved IGA mod 2011 0 or 1 scores compared to 4.9% of placebo patients. Efficacy was maintained through week 52 and secukinumab showed a favorable safety profile.
Connective tissue disorders involve inflammation of connective tissues leading to skin thickening or scarring, arthritis, and sometimes organ abnormalities. They are considered autoimmune disorders as antibodies form against normal tissues. The main types range from mild skin involvement to severe multi-system disease. Connective tissue disorders include localized forms like discoid lupus erythematosus and systemic forms like systemic lupus erythematosus which can damage multiple organs. Diagnosis involves assessing clinical features, immunological markers, and organ involvement. Treatment depends on disease severity but may include steroids, immunosuppressants, and addressing specific organ complications.
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.
Cutaneous lupus erythematosus (CLE) is a manifestation of the autoimmune disease systemic lupus erythematosus (SLE) that presents with diverse skin lesions. There are three main subtypes of CLE - acute (ACLE), subacute (SCLE), and chronic (CCLE, including discoid lupus erythematosus (DLE)). CLE results from a complex interplay between genetic susceptibility, environmental triggers like ultraviolet light, and dysregulated immune responses. Histopathology is useful but not definitive for diagnosis, which relies on clinical presentation and serological markers. CLE can range from limited skin involvement to systemic disease affecting major organs.
1. Lupus erythematosus (LE) is an autoimmune disease that can cause heterogeneous cutaneous and systemic manifestations. Cutaneous lupus erythematosus (CLE) can occur as a manifestation of systemic lupus erythematosus (SLE) or independently.
2. CLE is classified into LE-specific lesions and LE-nonspecific lesions. Common LE-specific lesions include acute cutaneous lupus erythematosus (ACLE), subacute cutaneous lupus erythematosus (SCLE), and chronic cutaneous lupus erythematosus (CCLE).
3. Diagnosis of CLE
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
Rheumatoid arthritis is a chronic inflammatory disease that commonly results in joint damage and physical disability. It is characterized by a symmetric, peripheral polyarthritis of unknown etiology that most frequently involves the small joints of the hands and feet. While the disease primarily affects the joints, it can also result in a variety of systemic manifestations involving other organ systems. The risk of rheumatoid arthritis is genetically influenced and increases with certain HLA-DRB1 alleles.
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).
Toxic epidermal necrolysis (TEN) is a rare, potentially fatal adverse drug reaction characterized by extensive skin detachment and mucous membrane involvement. It is caused by apoptosis of keratinocytes triggered by certain drugs in genetically susceptible individuals. TEN is diagnosed clinically based on >30% detachment of the epidermis. Management involves stopping the causative drug, supportive care, and investigational therapies to prevent apoptosis. Complications include infection, organ failure and death in around 30% of cases. Prognosis can be estimated using the SCORTEN severity-of-illness score.
This document summarizes key information about systemic lupus erythematosus (SLE), including:
1) SLE is a chronic inflammatory autoimmune disease characterized by abnormal immunologic function and autoantibodies against self-antigens, commonly presenting with nonspecific symptoms like fatigue and joint pain.
2) Treatment involves managing symptoms during flares using medications like NSAIDs, antimalarials, corticosteroids, cytotoxic drugs, and experimental therapies, while maintaining remission between flares.
3) Prognosis has improved but infection and cardiovascular disease remain leading causes of death, so treatment aims to control disease activity and damage while minimizing medication side effects.
Autoimmunity occurs when circumstances impair the regulation of cells with autoimmune potential, allowing them to attack the body's own tissues. Autoimmune conditions are common and often occur together in clusters across multiple organ systems. While specific diagnoses are applied, it is best to think of autoimmunity existing on a spectrum of related processes rather than rigid categories.
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 attacks its own tissues. It most commonly affects women aged 15-40. The exact causes are unknown but genetics, viruses, sunlight, and some drugs may play a role. Symptoms vary but can include rashes, joint pain, fatigue, and organ inflammation. Diagnosis involves blood tests and potentially biopsies. Treatment focuses on rest, sun protection, medications like NSAIDs, antimalarials, corticosteroids, and immunosuppressants to control disease activity and prevent organ damage. Nursing care aims to manage symptoms, prevent infections, and educate patients.
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoantibody production and damage to multiple organs. It predominantly affects women of childbearing age. SLE is caused by a combination of genetic and environmental factors. The disease is mediated by autoantibodies that form complexes and damage tissues. Common clinical manifestations include rashes, arthritis, kidney inflammation, and neurological and cardiac involvement. Diagnosis is based on identifying clinical and laboratory criteria including autoantibodies. Management involves controlling symptoms with medications like antimalarials and NSAIDs. More severe organ-threatening disease is treated with glucocorticoids and immunosuppressants like cyclophosphamide or mycophenolate
Systemic sclerosis is a chronic autoimmune disease characterized by fibrosis of the skin and internal organs. It is more common in females and there are three subtypes: limited cutaneous, diffuse cutaneous, and morphea. Complications can include pulmonary hypertension, interstitial lung disease, gastrointestinal issues, and renal crisis. Treatment involves managing symptoms, slowing disease progression, and treating complications aggressively. Scleroderma renal crisis, in particular, requires strict blood pressure control using ACE inhibitors.
This presentation encompasses SLE as well Lupus nephritis,Antiphospholipid Syndrome and other special situation related to SLE such as SLE and Pregnancy.
This document discusses three types of cutaneous lupus erythematosus: systemic lupus erythematosus (SLE), subacute cutaneous lupus erythematosus (SCLE), and discoid lupus erythematosus (DLE). SLE is an autoimmune disorder characterized by autoantibodies against nuclear DNA. SCLE is a variant of lupus characterized by anti-Ro antibodies. DLE causes erythematous plaques and scarring, often affecting the face and ears. Treatment involves photoprotection, topical steroids, hydroxychloroquine and occasionally oral steroids depending on the severity of symptoms for each condition.
Scleroderma is an autoimmune connective tissue disease that causes hardening of the skin and internal organs. It is classified into limited and diffuse subtypes based on the extent of skin involvement. Raynaud's phenomenon, skin thickening, and pulmonary and gastrointestinal issues are common clinical manifestations. The underlying pathogenesis involves vascular dysfunction, immune dysregulation, and fibrosis. Management focuses on treating individual organ system complications. Prognosis depends on the specific organ systems affected and can range from relatively mild to severe with significant morbidity and mortality.
1. Immunosuppressants and immunomodulators used in pregnancy include corticosteroids, azathioprine, cyclosporine, hydroxychloroquine, intravenous immunoglobulin, mycophenolate mofetil, rituximab, and tofacitinib.
2. The risk of these drugs depends on the gestational period, with higher risks in the first trimester and third trimester. Drugs are categorized by the FDA based on risk, from A (no risk) to X (contraindicated).
3. The document provides details on specific drugs, including their mechanisms of action, placental passage, FDA risk categories, and potential adverse effects
Secukinumab, an IL-17A inhibitor, demonstrated high efficacy and a favorable safety profile in treating severe chronic plaque psoriasis in pediatric patients in a 52-week randomized controlled trial. At week 12, 80.0% and 77.5% of patients receiving secukinumab low and high doses, respectively, achieved PASI 75 scores compared to 14.6% of placebo patients. 70.0% and 60.0% of patients receiving low and high doses achieved IGA mod 2011 0 or 1 scores compared to 4.9% of placebo patients. Efficacy was maintained through week 52 and secukinumab showed a favorable safety profile.
1. Leprosy is caused by Mycobacterium leprae and affects the skin and peripheral nerves. It is classified based on clinical, histopathological, immunological and bacteriological parameters.
2. The Ridley-Jopling classification from 1966 is widely used, categorizing leprosy into tuberculoid, borderline, and lepromatous types.
3. WHO classifications from 1982 onward divided leprosy into paucibacillary and multibacillary types based on bacterial load for purposes of treatment.
The document discusses the causes, symptoms, diagnosis and treatment of ingrown toenails. It begins by defining ingrown toenails as a common condition where the nail edge grows into the skin, causing pain. Risk factors include poorly fitting shoes and improperly trimmed nails. Symptoms progress from pain to infection if left untreated. Diagnosis is usually clinical. Treatment ranges from conservative approaches like soaking the toe and splinting the nail, to surgical techniques like partial nail removal or chemical ablation of the nail matrix. The goal of treatment is to relieve symptoms and prevent recurrence.
This document provides information on deep cutaneous mycosis, specifically focusing on subcutaneous mycoses. It discusses several types of subcutaneous mycoses including sporotrichosis, mycetoma, and chromoblastomycosis. For each condition, it describes the causative organisms, epidemiology, clinical presentation, diagnosis, and treatment. Sporotrichosis is caused by Sporothrix schenckii and can manifest as lymphatic or fixed cutaneous lesions. Mycetoma is characterized by grain formation and can be caused by fungi or actinomycetes. Chromoblastomycosis features slow growing exophytic lesions caused by pigmented fungi that form sclerotic bodies in tissue.
Graft-versus-host disease (GvHD) is a complication of allogeneic hematopoietic stem cell transplantation where donor T cells attack the recipient's organs, most commonly affecting the skin, liver, and gastrointestinal tract. It is classified as either acute or chronic GvHD depending on time of onset post-transplant. Acute GvHD presents within 100 days as a rash, diarrhea, and liver dysfunction while chronic GvHD appears after 100 days with skin sclerosis, lichenoid eruptions, and other organ involvement. Treatment involves immunosuppression with corticosteroids, calcineurin inhibitors, or other agents depending on GvHD severity and organ systems affected
This document provides an overview of nail anatomy through a presentation. It discusses the basic structure of the nail including the nail matrix, nail bed, nail plate, cuticle, and lunula. It describes the blood supply and nerve innervation of the nail. It also reviews nail growth and factors that can affect the rate of growth such as age, gender, season, and certain medical conditions. The presentation provides details on nail development during embryology and changes that occur in childhood and old age.
about various genodermatoses and classified according to clinical presentation.
mentioned are introduction clinical features histology management of each disease.
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kol...rightmanforbloodline
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Versio
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
TEST BANK For An Introduction to Brain and Behavior, 7th Edition by Bryan Kolb, Ian Q. Whishaw, Verified Chapters 1 - 16, Complete Newest Version
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Kat...rightmanforbloodline
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
TEST BANK For Basic and Clinical Pharmacology, 14th Edition by Bertram G. Katzung, Verified Chapters 1 - 66, Complete Newest Version.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
2. HISTORY
• Lupus – latin term – meaning wolf
• Erythematosus – red rash
• 1851, Dr. Cazenave , looked like wolf bites , named it DLE
• 1885 , Sir William Osler , named it SLE
3. INTRODUCTION
• Wide array of illness
• linked to autoimmunity to self nucleic acid and associated
proteins
• TYPES –
A. CUTANEOUS LE
• Acute LE
• Subacute LE
• Chronic LE
B. SYSTEMIC LE
4. Classification criteria
• American rheumatology association criteria (ARA) 1971
• The criteria of the American College of Rheumatology(ACR),
first published in 1982 and revised in 1997
• Systemic Lupus International Collaborating Clinics (SLICC)
2012.
• New ACR/ EULAR criteria 2019
7. Epidemiology
• SLE – 15-44years – F:M = 13:1 ; 2:1 in children and elderly
• All ethnicities, more prevalent in non caucasians
• DLE – 2:1 ; F:M ,peak age 4th decade
• Out of all the SLE patients
• ACLE 35 – 60%
• SCLE 7-27%
• CCLE 15-30%
8. Natural history and course
• SLE is a chronic disease of variable severity with a waxing and
waning course
• significant morbidity , can be fatal if not treated early
patients .
• .
9. Aetiology and pathogenesis
1.Genetic factors
• Reported concordance rate in identical twins is 65%
• Most consistent association are between HLADR2
and HLADR3 in white people.
12. 4.Hormonal factors
• estrogen or prolactin or testosterone
• can lead to an autoimmune phenotype
• increase mature high-affinity auto-reactive B cells.
• OCPs ,
• early menarche
• post menopausal estrogen
14. Mechanism of organ damage
• Vascular damage in SLE -
• Homocysteine and proinflammatory cytokines, such as IFNα,
impair endothelial function and decrease the availability of
endothelial precursor cells to repair endothelial injury.
• Impaired DNA repair as a result of mutations of the 3’ repair
exonuclease 1 (TREX1), and increased accumulation of single
stranded DNA may activate the IFN-stimulatory DNA
response and direct immune-mediated injury to the
vasculature.
15. Clinical features
1.Mucocutaneous features
• almost universal in SLE with both lupus-specific and non-
specific lesions.
• Chances of developing SLE-
SCLE-50%
Localised DLE - 5%
Disseminated DLE -20%
16. Galliams Classification of skin lesions associated
with lupus erythematosus
LE – SPECIFIC SKIN DISEASE
A.Acute cutaneous LE (ACLE)-
1. Localised (malar rash or butterfly rash)
2. Generalised (maculo-papular rash, Photosensitive lupus
dermatitis , TEN variant )
B. Subacute cutaneous LE (SCLE)-
1.Annular SCLE
2. Papulosquamous or psoriasisform lesion: Photosensitive, spares
face
C. Chronic cutaneous LE (CCLE)
1. Classic discoid LE (DLE)-localised and disseminated
2. Hypertrophic/verrucous DLE
17. LE – SPECIFIC SKIN DISEASE contd….
3. Lupus profundus/lupus panniculitis
4. Mucosal DLE
5. Oral DLE
6.Conjunctival DLE
7. Lupus tumidus
8. Chilblain LE/ perniotic
9. Lichenoid DLE (LE/ lichen planus overlap )
18. LE-Non specific lesion
A. Cutaneous vascular disease-
1.Vasculitis-
a. leukocytoclastic
- Palpable purpura
- Urticarial vasculitis
b. Polyarteritis nodosa-like cutaneous lesions
2.Vasculopathy
a.Degos disease-like lesions
b.Secondary atrophie blanche (syn. livedoid vasculitis)
20. B. Nonscarring alopecia
1.Lupus hair
2.Telogen effluvium
3.Alopecia areata
C. Sclerodactyly
D. Rheumatoid nodules
E. Calcinosis cutis
21. F. LE-nonspecific bullous lesions
G. Urticaria
H. Papulonodular mucinosis
I. Acanthosis nigricans
J. Erythema multiforme
K.Leg ulcers
L. Lichen planus
M. Cutis laxa / anetoderma
27. lupus erythematosus tumidus
• Tumidus dermal form of lupus.
• Characteristically photosensitive
• Red, swollen, urticaria-like
plaques
• Ring-shaped (Annular) or
arciform
28. mucosa
• association with systemic disease activity
• SLE – 25 – 45%
• SLE -Painless ,shallow ,occurring in crops mainly over hard
palate
• DLE- buccal mucosa most commonly affected; hard palate
,vermilion border of lips are others.
• Lesions are of 3 types- erythematous lesions, discoid lesions
and ulcers.
.
29. • Discoid lesions – white papule, central erythema, border zone
of irradiating white striae , and telegiectasia (20%)
• Ulcers – painful superficial erosions with irregular serrated
margins
30. Musculoskeletal features
• 53–95%
• arthralgias/ arthritis
• Rarely tendinitis , tenosinovitis.
• Subcutaneous nodules along the flexor tendons of hand.
• Rhupus
31. Jaccoud arthropathy,
severe deformity of the
hands with ulnar
deviation and
swan‐neck confi-
guration, often with
little pain and good
function,
occurred in 13% of pts
32. • Generalised myalgia and muscle tenderness are common
during disease exacerbations.
• Inflammatory myositis
• Avascular necrosis (AVN) of bone; Symptomatic 5–12%.
• Osteoporosis
33. 3. Renal features-
• 40–70%
• major cause of morbidity and hospital admissions.
• MPGN type 2-4 - Proteinuria , haematuria, red cell cast
• Membranous GN (type 5)- severe proteinuria, nephrotic
syndrome
• Urinalysis to detect and monitor disease renal activity.
• Most common – type 4
34.
35. 4. Nervous system features
• 19 syndromes observed , collectively are referred to as
neuropsychiatric SLE (NPSLE) syndromes.
• in decreasing order of frequency –
• cognitive dysfunction>Headache>Mood disturbances >
cerebrovascular disease> seizures > polyneuropathy> anxiety>
psychiosis
• Anti ribosomal P ab associated with lupus psychosis
36. 5. Cardiovascular features
• Pericarditis (common) 25%
• Libman–Sacks endocarditis -1–2% of patients.
• left side of the heart commonly involved.
• myocarditis
• one of the main prognostic predictors in SLE
• Coronary artery disease is the most common cause of death
in patients with longstanding SLE.
37. 6. Respiratory system
• The most common - pleuritis .
• pneumonitis – acute and chronic
• interstitial lung disease (ILD) 3–13%
• Pulmonary hypertension and pulmonary hemorraghe
• Shrinking lung syndrome
38. . Lymph node
• Lymphadenopathy characterised by typically soft , non-
tender, discrete lymph nodes usually detected in the cervical,
axillary, and inguinal area.
.Spleen
• 10–45% of patients, particularly during active disease
• Splenic atrophy and functional hyposplenism have also been
reported.
39. 8. Haematologic features
• Anemia - most common and correlates with disease
activity.
• Leukopenia
• Pancytopenia
• Cause= haemolysis, bone marrow suppression ,
myelofibrosis, aplastic anaemia
40. • thrombocytopenia .
• M.C cause- immune-mediated platelet destruction
• increased platelet consumption may also occur due to micro-
angiopathic haemolytic anaemia or hypersplenism.
41. GIT
• 50% of patients
• Common- anorexia, nausea and vomiting
• Abdominal pain may be due to mesenteric vasculitis,
hepatobiliary disease, pancreatitis
• late complications – cirrhosis
42. 10.Thyroid disease .
• hyperthyroidism
• hypothyroidism
• thyroid autoantibodies in patients without diagnosed thyroid
disease
11.Involvement of the ears .
• Sudden sensorineural hearing loss
• may be associated with the antiphospholipid syndrome.
43. 12. Ophthalmic features
• Most common – keratoconjunctivitis sicca
• infarction of the retinal vasculature secondary to
antiphospholipid antibodies
• ‘cotton wool’ spots in the retina
• Cataract
• Uveitis, scleritis, optic neuritis extremely rare
44. SLE and pregnancy
Mothers.
• There is no significant difference in fertility if renal functions
are normal.
• Flares- increases from 40 to 60%
• Lupus Nephritis and antiphospholipid antibodies – risk factor
pre-eclampsia .
45. Fetus
• susceptibility - mother has a history of Lupus Nephritis,
antiphospholipid, anti-Ro and/or anti-La antibodies
• increased risk of miscarriage, stillbirth, premature delivery,
intrauterine growth restriction, and fetal heart block.
• Cutaneous manifestation- 50% ; erythematous , slightly scaly
eruptions on face and periorbital skin
• Cardiac manifestation- conduction defect (1-2%)
46. Drug-induced lupus
• DIL should be suspected in patients with
• no diagnosis or history of SLE,
• who develop a positive ANA and at least one clinical feature
of lupus after
• an appropriate duration of drug exposure( 3- 6 months)
• and whose symptoms resolve after discontinuation of the
drug.
47. • commonly in older age group.
• Haematological abnormalities, kidney disease, and CNS lupus
are uncommon.
• Antihistone antibodies >95% of cases
• hypocomplementaemia and anti-DNA antibodies absent
• Arthralgia- 1st and common , constitutional symptoms
• Cutaneous – malar rash, vasculitic, bullous , EM like
• SCLE – common
• Less- scarring alopecia ,discoid lesion , oral ulcer
49. Morbidity, comorbidities, and
mortality
• early mortality - lupus activity and infection,
• late mortality - atherosclerotic complications.
Infections-
• 20–55% of all deaths
• due to underlying immune dysregulation and therapeutic
factors
50. Prognostic indicators
• poor prognosis (50%mortality in 10 years) at time of diagnosis
associated with –
• High serum creatinine (>1.4 mg/dl)
• Hypertension
• Nephrotic syndrome( 24 h urine protein >2.6g)
• Anaemia(Hb < 12.4 gm/dl)
• Hypoalbuminemia
• Hypocomplementemia
• Antiphospholipid antibodies
• Male
• Blacks
• Low socioeconomic status
51. How to approach a case of lupus
• History
• Examination
• Investigations – routine : hematological
• CBC with DLC , ESR , CRP, LFT, RFT , Urinalysis
• Specific:
• 24 hour urine protein ,
• ANA , DsDNA, Coombs , VDRL, C3 and C4 levels
• Antiphospholipid antibodies
• Anti smith , SSA, SSB, U1RNP
• Radiological : chest x ray , USG abdomen
56. ANA TESTING IN SLE
• Immunofluorescence-ANA:
• Inexpensive and easy to perform, with high sensitivity and
specificity
• Majority of the laboratories around the world are now using
HEp-2 cell substrates(cultured cells of laryngeal squamous cell
carcinoma )
• IF-ANA test is widely used and considered to be gold standard
57. ANA titer :
• It is directly proportional to antibody concentration
• low titer - less significant than a high titer
• may be seen even in healthy individuals.
• Acc. To EULAR criteria , ANA titre of >1:80 - considered
significant
58. MANAGEMENT OF SLE
• General measures
• counseling – outcome, complication , precautions
• Sun protection
• Regular exercise , stretching , diet
• Vitamin D supplementation
• Stop smoking
• Prevention of co-morbidities
59. Monitoring
• Assess disease activity and damage
• CBC, DLC
• ESR,CRP
• LFT, RFT
• URM – serial test if abnormal
• 24hour urine protein , ACR ratio, creat cl, usg renal
• If renal disease- annual GFR
• Renal biopsy
61. LOCAL THERAPY
• TOPICAL STEROIDS
•Topical Pimecrolimus 1% cream and tacrolimus 0.1% ointment
• calcipotriol
•Topical methotrexate
•Intralesional steroids
62. • ANTIMALARIAL -
• Hydroxychloroquine sulfate
• MOA-(1) light filtration (2) immunosuppressive actions
• (3) antiinflammatory actions, (4) antiproliferative effects through
an inhibition of DNA/RNA biosynthesis
• Slow response , may take 2 or 3 months for efficacy to be
appreciated
SYSTEMIC THERAPY
63. HYDROXYCHLOROQUINE
DOSE-usually 200 mg once or twice per day.
efficacy of HCQ established in studies with a prescribed dose
of 6.5 mg/kg/day
At this dose, eye toxicity is quite unlikely
64. • Provide rapid symptom relief.
• Low dose oral prednisolone (0.1-0.2 mg/kg)- mild SLE and
musculoskeletal manifestations resistant to other thaerpy
• High dose oral prednisolone(1-1.5 mg/kg)
• intravenous Methyprednisolone(1g /day for 3 days) – CNS, renal
manifestation or systemic vasculitis.
• Once controlled ,dose can be reduced to <7.5mg / day.
GLUCOCORTICOIDS
65. • more rapid GC tapering
• prevent disease flares.
• The choice depends on prevailing disease manifestation(s),
patient age and childbearing potential, safety concerns and cost.
• Methotrexate (MTX) (7.5 -25mg/week)
• Azathioprin(1.5-2.5mg/kg)
• MMF(1- 3gm/day)
IMMUNOSUPPRESSIVE AGENTS
70. SLE IN PREGNANCY
• For a successful pregnancy –
• disease should be quiescent for at least 6 months before the
conception.
• Oral corticosteroids - relatively safe.
• May need to temporarily increase at the time of delivery and
post partum.
• If the patient is on azathioprin , it can be continued .
• Hydroxychloroquine may be continued- reduced disease
activity, risk of CHB and neonatal lupus activity.
71. LACTATION
• Safe with low dose steroids and hydroxychloroquine
• For azathioprin, feeding should be done 4 hours post maternal
dose.
• With other immunosuppresives, breast feeding should be
better avoided.