Prof. Md. Khairul Hassan Jessy
Professor of Respiratory Medicine
National Institute of Diseases of the Chest and Hospital (NIDCH)
Mohakhali, Dhaka, Bangladesh
SLE still an enigma where both patient and health care professionals are blind and do more harm than saving the patient. Hope in future anything can be done to save the patient from the grip of lupus,
Prof. Md. Khairul Hassan Jessy
Professor of Respiratory Medicine
National Institute of Diseases of the Chest and Hospital (NIDCH)
Mohakhali, Dhaka, Bangladesh
SLE still an enigma where both patient and health care professionals are blind and do more harm than saving the patient. Hope in future anything can be done to save the patient from the grip of lupus,
Pathogenesis systemic lupus erythematosus by dr bashir ahmed dar associate pr...Prof Dr Bashir Ahmed Dar
Systemic lupus erythematosus is a chronic, multisystem, inflammatory disorder of autoimmune etiology, occurring predominantly in young women. Common manifestations may include arthralgias and arthritis; malar and other skin rashes; pleuritis or pericarditis; renal or CNS involvement; and hematologic cytopenias.
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.
GEMC: Collagen Vascular Disease: Considerations for Emergent Management: Resi...Open.Michigan
This is a lecture by Dr. Joseph Hartmann from the Ghana Emergency Medicine Collaborative. To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
Systemic lupus erythematosus (lupus) is a disease of the immune system. Normally, the immune system protects the body from infection. However, in lupus, the immune system inappropriately attacks tissues in various parts of the body. This abnormal activity of the immune system leads to tissue damage and illness.To know more visit here: www.lazoi.com
http://curegoutpainnow.com
There are two different styles of treatment that you want to look at. The first is prevention and the other is taking care of it at the first sign so that it isn’t full blown and become painful.
an overview of Lupus for journalist
Lupus has a wide spectrum of manifestation. Some mild but in most cases it has a high impact of life and quality of life
Leptospirosis - clinical manifestations and diagnosis.pdfJim Jacob Roy
Leptospirosis is a commonly encountered infection , especially in tropical regions.
In this document , the clinical manifestations and diagnosis of leptospirosis is described.
The modified FAINE'S criteria is also described at the end.
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
2. It is the prototype systemic autoimmune
disease characterised by diverse system
involvement with production of array of
antibodies
Clinical features may be quite variable
ranging from mild joint involvement to severe
life threatening disease.
Diagnostic criteria developed by ACR in 1971
revised in 1982 and then in 1997
3. A person must have to fulfill 4 out of 11 criteria to be
classified as SLE but it can extend over a period of
weeks to years.
Fulfillment of these criteria is not absolute
requirement rather diagnosis rests on constellation of
symptoms with supportive serological studies.
Most common presenting complaints are
constitutional symptoms, cutaneous manifestations
and articular manifestations(present in atleast 50% at
time of diagnosis).These manifestations appear over
time as disease evolves.
4.
5. Fatigue occurs frequently and is sometimes
the most disabling symptom
About 42% of patients have fever as
manifestation of active lupus. SLE is cause of
PUO in less than 5% of patients.
Fever can also be because of medications,
malignancies and infections.
6. ACLE - Localised to malar region , confluent,
macular or papular erythema, symmetrical on
cheeks and bridge of nose sparing nasolabial
folds with or without induration and scaling.
can be generalised in photosensitive
distribution. Pruritic and painful.
D/d- acne, rosacea, seborrhoeic Dermatitis,
erysipelas, atopic dermatitis
Biopsy required in uncertain cases
7. SCLE-non scarring, photosensitive lesions that
can be papulosquamous resembling psoriasis or
annular polycyclic with central clearing.
Predilection for back, neck, shoulders and spares
face. Heal without scarring
Annular type associated with anti-SSA/Ro
antibody.(seen in Sjogren,RA)
Drugs- ACEIs,CCBs ,Hydrochlorthiazide
8.
9.
10. CCLE-can lead to skin atrophy and scarring and
persist for months
Discoid LE is most common. Sharply demarcated,
disk shaped, raised, erythematosus plaques with
adhered scales and central hypopigmented
atrophic area.
Follicular plugging is characterstic finding
Permanent alopecia, SCC can occur if untreated
11.
12. Photosensitivity-abnormal skin reaction in 90% of patients
on provocative testing. D/d is PMLE (treatment by UV light)
Alopecia-scarring secondary to DLE. Non scarring-telogen
effluvium, lupus hair, alopecia areata,cytotoxic drugs,
steroids
Mucosal ulcers- gradual onset, unilateral and
asymmetric.more commonly on hard palate, buccal
mucosa and vermilion border. D/d-candidiasis and oral
lichen planus.
Lobar panniculitis presenting as subcutaneous nodules
called as lupus profundus
13. Arthritis and arthralgia-present in 90%.Earliest and most
common initial symptom. Symmetric, inflammatory, non
erosive(mostly) affecting knees, wrists and small joints.
Hand deformity similar to Jaccoud’s arthropathy because
of ligament and joint capsule laxity.
Avascular necrosis- femoral heads, tibial plateaus, femoral
condyles most common. Acute onset of pain. can also be
because of high dose of steroids.MRI is diagnostic.10% of
patients.
Deforming arthritis can be either mild deforming
polyarthritis or rhupus (symmetric,resembling RA)
14. Salmonella septic arthritis is more common than
non salmonella species
Myositis-usually involves proximal upper and
lower extremities. D/d myopathy of steroids,
antimalarials, statins, MCTD, infectious myositis,
fibromyalgia
CPK normal in steroids and antimalarial
myopathy, fibromyalgia
Characterstic histopathological finding
15.
16. Significant cause of morbidity and mortality
Upto 90% have pathological evidence but only 50% have clinical
evidence
Typically develops within first 36 months of disease and
frequency decreases after 5 yrs.
Features include proteinuria, hematuria, hypertension,pyuria,
urinary casts, deranged KFT.
Presentation can be variable ranging from hematuria to frankly
nephrotic to RPGN
Routine screening for polyuria, hematuria, hypertension,
proteinuria, LE edema, change in creatinine is important.
17. Immune complex mediated GN-most common
Tubulointerstitial disease-predictor of poor long term
renal outcome
Vascular disease - lupus vasculopathy , TMA, vasculitis ,
non specific vascular sclerosis, arteriosclerosis
Unrelated to SLE- FSGS, Thin BM disease, HTN
nephrosclerosis
Biopsy is diagnostic
Finding of TMA should suggest APLA nephropathy
18. Class I Minimal mesangial lupus nephritis (Light microscopy : Normal glomeruli)
Class II Mesangial proliferative LN (few isolated subepithelial/endothelial deposits visible by
IF or electron microscopy)
Class III Focal lupus nephritis (<50% glomerulli, sub endothelial deposits)
III A Active lesions
III A/C Active and Chronic Lesions
III C Chronic Lesions
Class IV Diffuse lupus nephritis( >50% glomeruli involved, Segmental and Global lesions)
IV – S (A) Active lesions - Diffuse segmental proliferative lupus nephritis
IV – G (A) Active lesions - Diffuse global proliferative lupus nephritis
IV – S
(A/C)
Active & chronic lesions - Diffuse segmental proliferative & sclerosing lupus
nephritis
IV – G
(A/C)
Active & chronic lesions - Diffuse global proliferative & sclerosing lupus nephritis
IV – S (C) Chronic inactive lesions with scars - Diffuse segmental sclerosing lupus nephritis
IV – G (C) Chronic inactive lesions with scars - Diffuse segmental global lupus nephritis
Class V Membranous lupus nephritis
Class VI Advanced sclerosing lupus nephritis
19. Mesangial nephritis is most common amongst
the silent nephritis cases.
Class IV patients tend to relapse most frequently.
Class V-anti C1q Ab has best negative predictive
value for predicting flares.
Despite treatment, 10% patient will progress to
ESRD
Type I and Type IV RTA also is reported.
20. Pleuritis- upto 50%. Small, bilateral , exudative.
Massive effusion is uncommon. D/d-infection, HF,
malignancy, drug induced
Lupus pneumonitis- rare. severe, acute respiratory
illness. fever, cough, pulmonary infiltrates,
hypoxemia.High mortality rate.
Chronic Interstitial Lung disease-NSIP and UIP are
most common patterns
DAH-DLCO is increased, Fall in Hb level. Hemosiderin
laden macrophages on BAL.High mortality rate.
21. PAH-0.5 to 14% of patients. Should exclude
other secondary causes
Shrinking lung syndrome-Dyspnea, low lung
volumes, elevation of hemi diaphragm in
absence of parenchymal involvement
22. Pericarditis-most common seen in 50%.Fibrinous and exudative.rarely tamponade
and purulent effusions.
Myocarditis-in 10% of patients clinically. unexplained HF, unexplained tachycardia,
ECG abnormalities. Endomyocardial biopsy helps in distinguishing from HCQ
toxicity.
Valvular Abnormalities-
Valvular thickening with mitral and aortic valve involvement is most common in
60% of patients.
Libman Sacks endocarditis – 43% of patients. pea sized, flat or raised, bland,
granular lesion on ventricular aspect of mitral valve posterior leaflet and vessel
side of aortic valve. Can be active or healed lesions.
Valvular regurgitation 25%
Valvular stenosis in 4%
23. CAD-Atherosclerosis, coronary artery
vasculitis, coronary artery thrombosis
Young women with SLE have 50 fold higher
risk of MI.
Rule out APLA because thrombosis can be the
initial presentation
Additional risk factors-Steroids use,
Hypertension
24. ACR has classified them into 19 different syndromes encompassing CNS
and PNS.
Headache in more than 50% and cognitive dysfunction in more than
80%.Intractable headaches not responding to narcotic analgesics are
most common
Psychiatric disorders like psychosis, depression, anxiety. D/d
schizophrenia, steroid induced psychosis(within first 2 weeks) and
metabolic disorders.
Demyelinating disorders such as optic neuritis, myelitis.D/d MS,NMO
and APLA
Ischemic stroke is more common than IC hemorrhage
Peripheral neuropathy- symmetric, length dependent sensory(glove and
stocking) or sensorimotor.(vasculitis and demyelination)
25. GTCS is more common than other types of epilepsy and
indicated active lupus whereas focal seizures can occur
anytime.
Risk of seizure is more with presence of anti Smith and
anti cardiolipin Ab.
Major risk of stroke is in first 5 years of diagnosis and
younger SLE have higher risk.
Antibodies to ribosomal P protein is associated with
depression and psychosis.
Anti NMDA receptor Abs are associated with diffuse CNS
involvement.
26.
27. Decreased peristalsis in upper 1/3 esophagus with sparing of LES(versus
scleroderma)
SLE related causes of abdominal pain- peritonitis, pancreatitis, mesenteric
vasculitis, pseudo obstruction
Signs of acute abdomen and rebound tenderness may be masked because of
steroids
Liver abnormalities in 60% of patients but rarely significant. Presence of liver
disease in SLE should prompt non SLE causes like Drugs(azathioprine,MTx,
NSAIDs), obesity, Diabetes, Steroid treatment, EBV and CMV
Lupus hepatitis is different from autoimmune hepatitis(no lymphoid infiltrate,anti
SMA and anti LKM negative)
Veno occlusive disorders, Budd Chiari syndrome and hepatic infarction
Lupus enteritis affects jejunum and ileum. Ascites is seen in 11% of patients
though peritoneal inflammation is seen in 60% of patients.
28. 50% of SLE have anemia.(ACD>IDA>AIHA)
Always consider myelosuppression because of azathioprine, MTx,MPF and cyclophophamide.
Steroid causes lymphopenia and leucocytosis
AIHA is mediated by warm reacting IgG anti erythrocyte Ab.(spherocytosis)
MAHA should prompt consideration for TTP and HUS(schistocytes).rule out CAPS by APLA
Leucopenia in approx 50% of patients.(BM suppression ,drugs,antilymphocytotoxic Ab)
Neutropenia because of immune mediated destruction or marrow suppression
Thrombocytopenia because of immune mediated destruction, TTP, Splenomegaly,
Antithrombopoeitin Ab
AIHA and isolated thrombocytopenia may precede years before SLE develops
29. Periarterial fibrosis or ‘onion skin’ lesion in
spleen is pathognomonic of SLE.
Kikuri Fujimoto Disease is a self limited form
of SLE.Presenting as cervical Lnpathy with
tenderness and night sweats, fever.
30. Lower androgen levels with increased
estrogen levels.
Hyperprolactinemia in 20% of patients.
Adrenal Failure, Hypothyroidism
SIADH
31. Most common is keratoconjunctivitis sicca
Retinal abnormalities-hemorrhages, vasculitic
lesions, cotton wool spots and hard exudates
Uveitis is very rare
Posterior subcapsular cataracts and increased IOT
because of steroids
Maculopathy because of HCQ therapy
Risk of retinal toxicity is low if CQ is<3mg/kg daily
and HCQ is <6.5mg/kg
32. Viral infections-Parvo B19,Hep B and Hep C,CMV
and EBV, HIV
Malignancy-particularly NHL
Autoimmune disorders- RA, Dermatomyositis ,
Still’s disease
MCTD
Drug induced lupus-Antihistone Ab are present
in >95% of cases except those by minocycline (ds
DNA and p ANCA)
33.
34. SLE is diagnosed on the basis of constellation of symptoms,
signs and lab findings in appropriate clinical text.
SEROLOGICAL TESTS-
ANA(byIF test) is gold standard and present in >95% of patients.
Also positive in RA,scleroderma, polymyositis, autoimmune
thyroiditis, elderly(<1:80)
Negative test rules out SLE
If ANA positive, then determine which particular nuclear antigens
are target
Anti ds DNA is highly specific for SLE but present in 60% of
patients
Anti Sm is also highly specific for SLE but present in 30% of
patients.
Complement consumption leads to hypocomplementemia(rare in
other diseases) and signify active disease
36. Urinalysis is an effective method to detect and monitor disease
activity in lupus nephritis.
Hematuria (usually microscopic) with dysmorphic cells indicates
inflammatory glomerular or tubulointerstitial disease.
In severe proliferative nephritis, urine sediment may contain the
full range of cells and casts.
Granular and fatty casts reflect proteinuric disease.
Erythrocyte, leukocyte, and mixed cellular casts reflect nephritic
disease.
Broad and waxy casts are found in chronic renal failure.
Urine sediment abnormalities in active lupus nephritis are
typically accompanied by significant proteinuria (more than 0.5 g
of protein per 24 hours)
37. Mesangial nephritis- low-grade proteinuria
with hematuria but typically no cellular casts.
Membranous glomerulopathy - proteinuria,
often at nephrotic range ,but otherwise blunt
urine sediments. Serum C3 levels are normal and
anti-DNA antibodies are usually found in low
titers.
Proliferative nephritis- hypertension, nephritic
urine sediment with various degrees of
proteinuria, low C3 levels, and typically high
titers of anti-DNA antibodies.
38. Any sign of renal involvement—in particular, reproducible
proteinuria of 0.5 g of protein or more per 24 hours,
especially with glomerular hematuria—should be an
indication for biopsy.
Although biopsy can also be considered in cases of
persisting isolated glomerular hematuria, isolated
leukocyturia (after other causes, such as infection or
drugs, are excluded), or unexplained renal insufficiency
with normal urinary findings.
In several studies of lupus nephritis, class IV nephritis has
been found to be the most common (approximately 40% of
cases), followed by class III and V with approximate
frequencies of 25% and 15%, respectively.
39. Changes in SCr concentration (20% to 30% increase or
more) or GFR (10% or more deterioration from baseline)
are of concern because they indicate significant ongoing
loss of renal function.
Persistently increased SCr levels (2.0 mg/dL or higher) at
the time of response to immunosuppressive treatment is
associated with subsequent development of ESRD.
Conversely, reduction of SCr concentration (even within
the “normal” range of values) at 6 months after induction
therapy is associated with increased likelihood of a
favorable long-term renal outcome
Spot urine protein-creatinine ratio (UPCR) measured is a
conveniently repeatable measure for detecting within-
patient changes in proteinuria and is currently
recommended for monitoring patients with lupus
nephritis.
40.
41. Accurate assessment of disease activity and
flares
Stratification according to severity of organ
involvement
Safe and effective drugs to induce remission
promptly
Prevention and management of disease and
treatment related comorbidities
42. SLEDAI and its modifications measure disease activity
based on 24 questions assessing the clinical
manifestations of SLE, including physical findings and
laboratory values weighted across organ systems.
Although the maximum score achievable is 105, even
with very active disease, scores rarely exceed 20.
Preferential weighting is based on the manifestations
of vasculitis, central nervous system (CNS)
involvement and active renal disease .
Score manifestations over the past 28 to 30 days
43. A flare is a measurable increase in disease activity in one
or more organ systems involving new or worse clinical
signs and symptoms and/or laboratory measurements. It
must be considered clinically significant by the assessor
and usually there would be at least consideration of a
change or increase in treatment.
Specific criteria to distinguish between mild, moderate,
and severe flares remain to be established.
Mild/moderate flares are defined as new or worsened
clinical features resulting in increases in the SELENA-
SLEDAI score of 3 or more points, prednisone use less than
0.5 mg/kg/day, PGA score of 1.0 to 2.5 on a 0 to 3 visual
analog scale (VAS), or any combination of these measures.
Severe flares are defined as changes in SELENA-SLEDAI
scores to higher than 12 or clinical manifestations
requiring doubling of the prednisone dose or an increase
to 0.5 mg/kg/day or greater.
44. Education.
Physical and lifestyle measures-diet, smoking
cessation, exercise, sun protection.
Emotional support.
Adjunctive measures-colonoscopy, Bone
Mineral Denstiometry, eye examination,
atherogenesis screening.
45. For cutaneous manifestations of lupus
Nonfluorinated steroid creams are weak but safe for long-term
use, especially for facial lesions.
Fluorinated steroids are quite effective but should never be used
on a facial lesion for longer than 2 weeks (otherwise, they will
lead to cutaneous atrophy and telangiectasias).
Ninety percent of all lupus prescriptions are written for one of
three preparations: desonide (mild potency), triamcinolone
(moderate potency), or clobetasol (high potency).
Topical calcineurins can be applied with or without
corticosteroids for cutaneous disease. These include
pimecrolimus creams and tacrolimus ointments.
46. Fever, headache, myalgias, arthralgias,
arthritis, and/or serositis.
NSAIDs should be used in pregnancy only
occasionally and with great caution.
Topical NSAIDs (diclofenac or ketoprofen gel,
salicylates) are safer and should be
considered as a first-line treatment for local
or regional inflammation.
47. High-dose daily corticosteroids are efficacious for life or organ-threatening AIHA,
ITP, bone marrow hypoplasia, acute myocarditis, acute lupus pneumonitis,
mesenteric vasculitis, autoimmune pancreatitis, optic neuritis, and retinal vasculitis.
Treatment is usually prescribed at a dose of 1 mg/kg/day of prednisone equivalent
for 2 to 4 weeks.
A dramatic response is often followed by a slow tapering of approximately 10% per
week.
If the manifestation is refractory to treatment or if tapering to 10
mg/day(0.25mg/kg alternate day) of prednisone equivalent cannot be achieved,
steroid-sparing immunosuppressive regimens of targeted therapies can be added
In severe rapidly progressing disease requiring >0.6mg/kg/day prednisone, pulse
therapy with 250 to 1000mg of MPS for 1 to 3 consecutive days.
48. .
Non-CNS or nonrenal manifestations of lupus warrant consideration of pulse
corticosteroids as induction therapy followed by high-dose daily
corticosteroids, including any of the aforementioned complications as well as
thrombotic thrombocytopenic purpura, Stevens-Johnson syndrome–like skin
reactions, severe acute cutaneous disease, or alveolar hemorrhage.
Moderate-dose daily corticosteroids (considered to be 0.25 to 0.5
mg/kg/day of prednisone equivalent) may be given for 2 to 4 weeks followed
by tapering for treatment of acute pleurisy or pericarditis, flares of
thrombocytopenia, active rashes, or lupus myositis.
Low-dose daily corticosteroids (less than 10 mg of prednisone equivalent
daily) are the mainstay for persistent, chronic, active disease, especially with
musculoskeletal, constitutional (fatigue, fever, adenopathy), cutaneous, and
serous membrane manifestations or combinations of these
49. HCQ and CQ are commonly prescribed to SLE patients with skin and joint
involvement and as adjuvant in severe lupus. CQ is given in refractory skin lesions.
HCQ delays the onset of SLE and reduces the number and severity of clinical flares.
They protect against thrombosis, renal damage, and major infections in SLE.
HCQ is associated with an 80% clinical response rate at 3 months when used in
doses of 5 mg/kg/day for non–organ-threatening disease.
Because HCQ can induce corneal edema and retinal pigmentation (the latter occurs
in 3% of patients who have used the drug for 10 years or longer), it is
recommended that baseline screening should be performed during the first few
months of therapy and again at 5 years followed by annual examinations.
Chloroquine is usually given at a dosage of 500 mg daily for the first 1 to 2
months, after which treatment is transitioned to HCQ or dosing is gradually
tapered to 250 mg as 1 to 2 tablets a week.
MTX is used as steroid sparing in articular,serosal and cutaneous manifestations in
mild to moderate cases.
Leflunomide is used in lupus nephritis refractory or intolerant to standard therapy.
50. Cyclophosphamide-equivalent efficacy with monthly IV(0.5 to 1
g/m2) versus oral regimens(25-100 mg).
7 monthly pulses of IV followed by quarterly pulses for atleast 1
yr beyond remission in lupus nephritis.
Also used in extrarenal disease like severe thrombocytopenia,
neurologic disease, abdominal vasculitis,alveolar h’ge and severe
skin disease
Combination of IV-MP with IV-CYC is treatment of choice for
severe inflammatory neurologic SLE.
Chlorambucil-orally (0.1-0.2 mg/kg/day). In combination with
IV-MP for remission of nephrotic syndrome. Also in
neuropsychiatric, vasculitis
51. Azathioprine(2 mg/kg/day)-safe and efficacious for maintenance
of remission in SLE including moderately severe Proliferative
Lupus nephritis. Also in thrombocytopenia(20000-50000/mm3)
and serositis .
Measurement of TMPT activity before initiation of therapy may
identify patients at greatest risk of bone marrow suppression .
Although it is classified as a pregnancy category D drug, AZA has
a well-established safety record as an option for lupus patients
who wish to conceive.
Mycophenolate Mofetil(2gm/day)-MMF is as effective as CYC for
complete remission in PLN and can be used as induction therapy.
Used as maintenance therapy in PLN.
May be effective in refractory skin and blood manifestations.
52. Cyclosporin A-Maintenance therapy in mild to
moderate proteinuric PLN with preserved
renal function.treatment of membranous
lupus nephropathy. Can be used as an
alternative steroid sparing agent to AZA
Tacrolimus-10-100 times more potent than
CsA.Beneficial effects in refractory to
conventional therapy PLN and LMN.
53. Plasmapheresis is used in SLE for TTP ,
cryoglobulinemia , NMO, pulmonary
hemorrhage , and hyperviscosity syndrome.
Laser therapy is occasionally used for
telangiectasias and refractory discoid lesions.
Photopheresis is occasionally used for
refractory skin manifestations.
54. Rituximab
Epratuzumab
Ocrelizumab
Belimumab(approved by FDA)
Atacicept
Abatacept
Other therapies-IVIg,DHEA,Clofazimine
57. Demographic: Black race,males, children
Clinical: Hypertension; severe extrarenal disease affecting major organ; failure
to achieve or marked delay (>2 years) in achieving renal remission; multiple
flares of lupus nephritis; pregnancy
Laboratory: Nephritic urinary sediment; azotemia; anemia; thrombocytopenia;
antiphospholipid antibodies; thrombotic microangiopathy;
hypocomplementemia (especially falling levels); high anti-DNA titer
(especially rising titers); persistent severe nephrotic syndrome
Histologic: Proliferative glomerulonephritis ; mixed membranous (class V) and
proliferative (class III-IV) glomerulonephritis; cellular crescents; fibrinoid
necrosis; very high activity index (>12); moderate to high chronicity index
(>3); combinations of active (cellular crescents) and chronic (interstitial
fibrosis) histologic features; extensive subendothelial deposits
58.
59.
60.
61.
62. The EULAR recommendations defined partial renal response as at least 50%
reduction in UPCR and normal or near-normal (within 10% if initially
abnormal) GFR. Partial response should be achieved preferably 6 months and
no later than 12 months after initiation of treatment.
The ultimate goal of treatment should be complete renal response, defined as a
UPCR of less than 0.5 and normal or near-normal (within 10% if initially
abnormal) GFR
Refractory disease as failure to achieve (1) any reproducible reduction in
UPCR during the first 3 to 4 months, or (2) partial renal response after 6 to 12
months, or (3) complete renal response after 1 to 2 years of
immunosuppressive treatment.
Nephritic flares consist of a reproducible increase in SCr concentration of 30%
or more (or a reduction in GFR by 10% or more) and active urine sediment
with an increase in glomerular hematuria by 10 or more red blood cells per
HPF, irrespective of changes in UPCR.
Proteinuric flares consist of a reproducible doubling of UPCR to more than 1.0
after complete renal response or a reproducible doubling of UPCR to more
than 2.0 after partial response
63.
64.
65.
66.
67. Decreased whole-brain magnetization transfer on MTI
has been reported in SLE patients even in the absence
of other structural MRI changes.
MRS- Decreased NAA, believed to reflect neuronal/
axonal loss or dysfunction, has been reported in SLE
patients, even in the absence of visible damage on
structural MRI.
fMRI may be informative regarding dysfunction or
redistribution of functions as a result of SLE.
68. Establishment of NPSLE
diagnosis
Cerebrospinal fluid examination
primarily to exclude infection
Autoantibody profile
(antiphospholipid, antiribosomal
P)
Neuroimaging to assess brain
structure and function
Neuropsychological assessment
■ Identification of aggravating
factors
Hypertension, infection,
metabolic abnormalities
Symptomatic therapy Anticonvulsants, psychotropics,
anxiolytics
Cognitive rehabilitation
■ Immunosuppression Corticosteroids, azathioprine,
cyclophosphamide,
mycophenolate mofetil, B-
lymphocyte depletion
Anticoagulation Heparin, warfarin
69.
70.
71. Women with lupus tend to have fewer live births,
however, vast majority of pregnancies in the
setting of SLE are uneventful.
Disease quiescence at the time of, and 6 months
previous to, conception is an important
prognostic factor for pregnancy loss and preterm
delivery.
The presence of active lupus nephritis is a
predictor of increased lupus activity during
pregnancy and poor pregnancy outcomes
72. History of pregnancy complications and a poor obstetric outcome
Presence of high-titer antiphospholipid antibodies (anticardiolipin antibodies, β2-
glycoprotein, and/or lupus anticoagulant)
Presence of anti-Ro and anti-La antibodies
Current or previous lupus nephritis or ongoing severe renal impairment
Advanced maternal age (>40 years)
Multiple pregnancies
Use of cytotoxic medications at the time of conception, including high-dose prednisone
Active flare at the time of, or 6 months before, conception
73. Hydroxychloroquine-safe to use in pregnancy , associated with decreased SLE flares
when used continuously.
NSAIDs can be used sporadically in the first and second trimesters of pregnancy, but
they are associated with an increased risk of miscarriage and oligohydramnios . NSAIDs
should be avoided in the last trimester of pregnancy due to concerns of premature
closure of the ductus arteriosus and worsening of hypertension.
Corticosteroids are sometimes indicated in the setting of a lupus flare. Dexamethasone
and betamethasone cross the placenta and should not be used unless there is an intent to
expose the fetus to corticosteroids.
Prednisone and prednisolone are deactivated by placental hydroxylases but should be
used with caution given the increased risk of maternal diabetes, hypertension,
preeclampsia, and premature rupture of membranes.
Antihypertensives - ACEIs are contraindicated in the setting of pregnancy. methyldopa,
nifedipine, and labetalol are generally thought to be safe options
74. Rituximab and belimumab are not recommended in
pregnancy.
Azathioprine is probably the safest
immunosuppressive medication in pregnancy.
Azathioprine is generally regarded to be safe when
used at dosages of 2 mg/kg or less.
Cyclophosphamide, methotrexate, mycophenolate,
leflunomide, and warfarin, is contraindicated in
pregnancy, because of their teratogenicity. If
possible, these medications should be discontinued
at least 3 months before conception.
75. Palmar erythema because of pregnancy, and mild alopecia should be distinguished from
a true lupus-related rash.
Arthralgias, myalgias, and backaches are normal symptoms of pregnancy and can
usually be managed conservatively with acetaminophen and physical therapy. True
synovitis does not occur in normal pregnancy and can be related to a lupus flare.
Mild anemia and thrombocytopenia are normal variants of pregnancy, but severe anemia
and thrombocytopenia may be an indication of an immune-mediated process. The
presence of leukopenia and lymphopenia should raise the suspicion of a systemic
autoimmune process.
A rise in C3 and C4 levels is a normal variation of pregnancy and this can make
identifying an SLE flare difficult, so normal complement levels should not automatically
be interpreted as an indication of disease quiescence.
Double-stranded DNA, however is not affected by pregnancy and can increase when
SLE is uncontrolled.
76. Asymptomatic carriers of antiphospholipid antibodies with no history of pregnancy loss
or thrombosis, treatment is generally not needed.
In women with a history of recurrent pregnancy loss or thrombosis, treatment options
include low-dose aspirin combined with either unfractionated heparin or enoxaparin
For women in whom combination therapy has been ineffective, intravenous
immunoglobulin, corticosteroids, and plasmapheresis are treatment options, although the
evidence for their effectiveness is questionable.
Treatment of high-risk patients is continued for at least 6 to 8 weeks after delivery
because of a continuing thrombosis risk in the postpartum period.
Women with a history of recurrent thrombosis may need lifelong treatment. Despite the
risks associated with the presence of antiphospholipid antibodies, live births have been
reported in over 50% to 74% of such patients when treatment was initiated.