Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the formation of autoantibodies that can damage multiple organs. It predominantly affects women of childbearing age but can occur in children, with higher rates of renal involvement and other symptoms compared to adults. SLE is diagnosed based on clinical criteria including rashes, arthritis, serositis, and immunological abnormalities. Treatment involves controlling disease activity and organ damage through medications like corticosteroids, hydroxychloroquine, and immunosuppressants. Monitoring for worsening symptoms and lab abnormalities helps guide management of the disease.
this research is made by a dental student (me) under supervision of our oral medicine specialist dr. muhassad almudhafer and this research is collected from several articles hope u like it
this my email if u would like to contact me - mnmmnz4503.mm@gmail.com
this research is made by a dental student (me) under supervision of our oral medicine specialist dr. muhassad almudhafer and this research is collected from several articles hope u like it
this my email if u would like to contact me - mnmmnz4503.mm@gmail.com
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
Systemic Lupus erythematous , is world wide health problem
Here we talk about criteria for diagnosis investigation , Management and complication
With some scenarios to about disease and complication
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
Systemic Lupus erythematous , is world wide health problem
Here we talk about criteria for diagnosis investigation , Management and complication
With some scenarios to about disease and complication
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
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
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
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.
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
2. INTRODUCTION
Systemic lupus erythematosus is a chronic, multisystem, inflammatory,
autoimmune disorder characterized by formation of autoantibodies directed
against self-antigens and immune-complex formation resulting in damage to
essentially any organ.
Although SLE affects primarily women of childbearing age, approximately
5% of cases present in childhood, mainly around puberty. SLE is rare in
children younger than 9 years of age. Although there is a female
predominance of this disease in adolescence and adulthood, there is an
equal gender distribution in children. The overall prevalence of SLE in the
pediatric population is 10 to 25 cases per 100,000 children.
WHAT IS PAEDIATRIC SLE?
EPIDEMIOLOGY
3. A LITTLE BIT OF HISTORY
Lupus is the Latin word for wolf. Erythematosus means red rashes. In 1851, Dr.
Cazenave discovered red rashes on a patient’s face that looked like wolf bites.
He named the rash Discoid Lupus Erythematosus (DLE).
In 1885, Sir William Osler recognized that many people with lupus had a disease
involving not only the skin but many other organs or systems. He named the
disease Systemic Lupus Erythematosus (SLE).
4. TYPES OF LUPUS
1. Systemic Lupus Erythematosus (SLE)
One that most people refer to when they say “lupus”. The symptoms of SLE
may be mild or serious. Although SLE usually first affects people between the
ages of 15 and 45, it can occur in childhood or later in life as well.
2. Discoid Lupus Erythematosus (DLE)
A chronic skin disorder in which a red, raised rash appears on the face, scalp,
or elsewhere. The raised areas may become thick and scaly and may cause
scarring. The rash may last for days or years and may recur. A small
percentage of people with discoid lupus have or develop SLE later.
5. TYPES OF LUPUS
3. Neonatal Lupus
A rare disorder that can occur in newborn babies. Scientists suspect that
neonatal lupus is caused by auto-antibodies in the mother’s blood called
anti-Ro (SSA) and anti-La (SSB). Auto-antibodies (“auto” means “self”) are
blood proteins that act against the body’s own parts.
At birth, the babies have a skin rash, liver problems, and low blood counts.
These symptoms gradually go away over several months, although in rare
cases, babies with neonatal lupus may have a heart problem that slows down
the natural rhythm of the heart.
Some drugs may cause SLE-like features and hence this condition is called
“drug-induced lupus”. The features typically go away completely when the
drug is stopped. The kidneys and brain are rarely involved.
6. CLINICAL FEATURES
C A R D I A C
Endocarditis
Myocarditis
Pericarditis
C O N T I T U T I O N A L
Fatigue
Fever
Weight loss
G A S T R O I N T E S T I N A L
Abdominal pain
Nausea & vomiting
7. CLINICAL FEATURES
D E R M A T O L O G I C A L
Alopecia
Butterfly rash
Mucous membrane lesion
Photosensitivity
Purpura
Raynaud’s phenomenon
Urticaria
Vasculitis
8. CLINICAL FEATURES
H E M A T O L O G I C
Anemia
Leukopenia
Thrombocytopenia
M U S C U L O S K E L E T A L
Arthralgia
Arthritis
Myositis
P U L M O N A R Y
Pleurisy
Pulmonary hypertension
Pulmonary parenchyma
9. CLINICAL FEATURES
N E U R O P S Y C H I A T R I C
Cranial neuropathies
Organic brain syndrome
Peripheral neuropathies
Psychosis
Seizures
Transverse myelitis
R E N A L
Casts
Hematuria
Nephrotic syndrome
Proteinuria
10. CLINICAL FEATURES
R E T I C U L O E N D O T H E L I A L
Hepatomegaly
Lymphadenopathy
Splenomegaly
Clinical presentation varies in different patients & the disease activity varies
over time in a single patient
1. Majority of patients have arthralgia of the hand
2. Most frequent manifestations in children include fever, rash, alopecia,
arthritis & renal involvement
3. Compared with adults, children have a higher incidence of malar rash,
anemia, leukopenia, neurologic & renal involvement
12. WHAT CAUSES SLE?
SLE is an autoimmune disorder that develops when the body’s immune system
begins to attack its own tissues. Its cause is unknown, but it is likely that a
combination of genetic, environmental, and, possibly, hormonal factors work
together to cause SLE.
This occurs through the production of “auto-antibodies” that attack a person’s
own cells thus contributing to the inflammation of various parts of the body,
and may cause damage to organs and tissues.
The most common type of auto-antibody that develops in people with SLE is
called an antinuclear antibody (ANA) because it reacts with parts of the cell’s
nucleus (command centre).
13. WHAT CAUSES SLE?
The fact that SLE can run in families indicates that its development has a genetic
basis; however, no specific “lupus gene” has been identified yet.
Studies suggest that several different genes may be involved in determining a
person’s likelihood of developing the disorder, which tissues and organs are
affected, and the severity of disease. However, it is believed that genes alone do
not determine who gets SLE and that other factors also play a role.
Some of the other factors scientists are studying include sunlight, stress, certain
drugs, and agents such as viruses.
14. DIAGNOSIS
Diagnosis of systemic lupus erythematosus (SLE) is based on clinical symptoms &
lab findings
Diagnosis based on the American College of Rheumatology criteria for the
diagnosis of definite lupus in children
≥4 criteria on the list either at the present time or at some time in the past,
there is a strong chance that you have lupus.
11 common criteria, or measures that was developed by the American
College of Rheumatology (ACR):
1. Malar rash – a rash over the cheeks & nose, often in the shape of a butterfly
2. Discoid rash – a rash that appears red, raised, disk-shaped patches
3. Photosensitivity – a reaction to sun or light that causes a skin rash to appear
or get worse
4. Oral Ulcers – sores appearing in the mouth
5. Arthritis – joint pain & swelling of 2 or more joints in which the bones
around the joints do not become destroyed
15. DIAGNOSIS
6. Serositis – inflammation of the lining around the lungs
(pleuritis) or inflammation of the lining around the heart that
causes chest pain which is worse with deep breathing
(pericarditis)
7. Kidney disorder – persistent protein or cellular casts in the
urine.
8. Neurological disorder – seizures or psychosis
9. Blood disorder – anemia, leukopenia, lymphopenia, or
thrombocytopenia
10. Immunologic disorder – anti-DNA or anti-Sm or positive
antiphospholipid antibodies
11. Abnormal antinuclear antibody (ANA)
16. DIAGNOSIS
Diagnosis of systemic lupus erythematosus (SLE) is based on clinical symptoms &
lab findings
Diagnosis based on the Systemic Lupus International Collaborating Clinics
(SLICC) classification criteria for systemic lupus erythematosus (SLE)
≥4 criteria (at least 1 clinical & 1 immunologic criteria)
or
Biopsy-proven lupus nephritis with positive antinuclear antibody (ANA)
or
Anti-double stranded deoxyribonucleic acid (dsDNA)
Symptom/finding need not be present all at the same time
17. DIAGNOSIS
C L I N I C A L C R I T E R I A:
Acute cutaneous lupus, including:
Lupus malar rash (do not count if malar discoid)
Bullous lupus
Toxic epidermal necrolysis variant of systemic lupus erythematosus (SLE)
Maculopapular lupus rash
Photosensitive lupus rash (In the absence of dermatomyositis) or
Subacute cutaneous lupus (nonindurated psoriaform &/or annular polycyclic
lesions that resolve w/out scarring, although occasionally w/ post-
inflammatory dyspigmentation or telangiectasias)
18. DIAGNOSIS
C L I N I C A L C R I T E R I A:
Chronic cutaneous lupus, including:
Classic discoid rash: localized (above the neck) or generalized (above & below
the neck)
Hypertrophic (verrucous) lupus
Lupus panniculitis (profundus)
Mucosal lupus
Lupus erythematosus tumidus
Chilblains lupus
Discoid lupus/lichen planus overlap
Oral Ulcers or Nasal Ulcers
Oral: palate, buccal, tongue
In the absence of other causes, such as vasculitis, Behcet’s disease, infection
(herpesvirus), inflammatory bowel disease, reactive arthritis, & acidic foods
19. DIAGNOSIS
C L I N I C A L C R I T E R I A:
Nonscarring alopecia
Diffuse thinning or hair fragility w/ visible broken hairs
In the absence of other causes such as alopecia areata, drugs, iron deficiency,
& androgenic alopecia
Synovitis involving ≥2 joints
Characterized by swelling or effusion
Or tenderness in ≥2 joints & at least 30 minutes of morning stiffness
Renal
Urine protein–to-creatinine ratio (or 24-hour urine protein) representing 500
mg protein/24 hours or red blood cell casts
20. DIAGNOSIS
C L I N I C A L C R I T E R I A:
Serositis
Typical pleurisy for >1 day or pleural effusions or pleural rub
Typical pericardial pain (pain w/ recumbency improved by sitting forward) for
>1 day or pericardial effusion or pericardial rub or pericarditis by
electrocardiography
In the absence of other causes, such as infection, uremia, & Dressler’s
pericarditis
21. DIAGNOSIS
C L I N I C A L C R I T E R I A:
Neurologic
Seizures
Psychosis
Mononeuritis multiplex (in the absence of other known causes such as
primary vasculitis)
Myelitis
Peripheral or cranial neuropathy (in the absence of other known causes such
as primary vasculitis, infection, & diabetes mellitus)
Acute confusional state (in the absence of other causes, including
toxic/metabolic, uremia, drugs)
22. DIAGNOSIS
C L I N I C A L C R I T E R I A:
Hemolytic anemia
Leukopenia (<4000/mm3)
at least once, in the absence of other known causes such as Felty’s syndrome,
drugs, & portal hypertension or Lymphopenia (<1000/mm3) at least once, in
the absence of other known causes such as
Corticosteroids, drugs, & infection
Thrombocytopenia (<100,000/mm3)
At least once in the absence of other known causes such as drugs, portal
hypertension, & thrombotic thrombocytopenic purpura
23. DIAGNOSIS
I M M U N O L O G I C A L C R I T E R I A:
Antinuclear antibodies (ANA) level above laboratory reference range
Anti-double stranded deoxyribonucleic acid (dsDNA) antibody level above
laboratory reference range [or >2-fold the reference range if tested by
enzyme-linked immunosorbent assay (ELISA)]
Anti-Smith (Anti-Sm): presence of antibody to Smith (Sm) nuclear antigen
24. DIAGNOSIS
I M M U N O L O G I C A L C R I T E R I A:
Antiphospholipid antibody positivity, as determined by:
o Positive test for lupus anticoagulant
o False-positive test result for rapid plasma reagin
o Medium- or high-titer anticardiolipin antibody level [Immunoglobulin A
(IgA), immunoglobulin G (IgG) or immunoglobulin M (IgM)]
o Positive test result for anti-B2-glycoprotein I [Immunoglobulin A (IgA),
immunoglobulin G (IgG) or immunoglobulin M (IgM)]
Low complement (C3, C4, or CH50)
Direct Coombs’ test (in the absence of hemolytic anemia)
26. MANAGEMENT
MONITORING
Results of lab tests that may precede a disease flare:
1. Decrease in serum complement levels
2. Increase in anti-double stranded deoxyribonucleic acid (dsDNA)
3. Increase in erythrocyte sedimentation rate (ESR)
4. Decrease in hemoglobin level, leukocyte or platelet counts
5. Increase in creatine phosphokinase (CPK) levels
6. Appearance of microscopic hematuria or proteinuria
27. TREATMENT
G O A L S O F T H E R A P Y :
Control disease manifestation
Allow child to have a good quality of life without major exacerbations
Prevent serious organ damage that adversely affects function or lifespan
Prevent adverse effects of the drugs used
PHARMACOTHERAPY
Corticosteroids Immunosuppressants NSAIDs Sunscreen
28. TREATMENT
C O R T I C O S T E R O I D S
Oral corticosteroids
Patients w/ mild SLE do not normally require use of systemic corticosteroids
but there are patients who has low quality of life if not given low-dose
corticosteroids
Lowest possible dose should be used for maintenance therapy
High-dose corticosteroids are necessary for refractory manifestations of SLE
& for severe organ systems’ manifestations especially CNS, renal &
hematologic manifestations
Decreases inflammation by suppression of the immune system
Topical corticosteroids
Helpful for discoid lesions especially on the scalp
Use a less potent steroid on the face because it is more prone to atrophy
29. TREATMENT
C O R T I C O S T E R O I D S
Parenteral corticosteroids
Pulse therapy with IV corticosteroids in combination with
immunosuppressive therapy is recommended for Class III and IV SLE patients
with confirmed glomerulonephritis
30. TREATMENT
H Y D R O X Y C H L O R O Q U I N E
Used for skin & joint manifestations
Also used for preventing flares & other constitutional symptoms
Inhibits chemotaxis of eosinophils & locomotion of neutrophils & impairs
complement-dependent antigen-antibody reactions
Recommended as background treatment for Class III and IV SLE patients with
nephritis
31. TREATMENT
I M M U N O S U P P R E S S A N T S
These agents act as immunosuppressive, cytotoxic & anti-inflammatory agents
In the treatment of severe CNS & severe glomerulonephritis,
thrombocytopenia & hemolytic anemia, high dose glucocorticoids &
immunosuppressantS are used
Concomitant use with corticosteroids allows lower doses of
immunosuppressants
1. Azathioprine
2. Belimumab
3. Cyclophosphamide
4. IV Immune Globulin (IVIg)
5. Methotraxate
32. TREATMENT
N S A I D S
These drugs provide symptomatic relief of fever, arthritis & mild serositis
Inhibit inflammatory reactions & pain by decreasing prostaglandin synthesis
SLE patients have a high incidence of NSAID-induced hepatotoxicity
S U N S C R E E N
Patients with SLE should apply sunscreen with at least an SPF of 15 to prevent
dermal or systemic disease flares upon exposure to ultraviolet light
33. COMPLICATIONS
Some degree of long term and often permanent organ dysfunction from
either SLE or its treatment has been found in 88% of patients.
Hypertension
Growth retardation
Chronic pulmonary impairment
Ocular abnormalities
Permanent renal damage
Neuropsychiatric symptoms
Musculoskeletal damage
Gonadal impairment
34. PROGNOSIS
Outcomes for SLE have improved significantly over the past several decades
and depend largely on the organ systems that are involved. Worse prognoses
are seen in patients with severe lupus nephritis or cerebritis, with risk of
chronic disability or progression to renal failure. With current therapy for the
disease and the success of renal transplantation, however, most patients live
well into adulthood.