This document discusses systemic lupus erythematosus (SLE), an autoimmune disease where the immune system attacks the body's own tissues and organs. It causes inflammation and damage to many different body systems. SLE is more common in women and typically presents between ages 15-25. Symptoms can include rashes, joint pain, fatigue, and organ involvement. Diagnosis involves evaluating symptoms, signs, and antibody tests. Treatments include medications like NSAIDs, antimalarials, steroids, and immunosuppressants to reduce symptoms and prevent organ damage. Complications can affect many organs but most commonly involve the kidneys, heart, and lungs. With treatment, 5-year survival rates are over 85%.
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
Rheumatology Sheet from Rheumatology Department, Faculty of Medicine, Zagazig University, Egypt.
Disclaimer : not my slide. Just uploading for my personal use..
Rheumatology Sheet from Rheumatology Department, Faculty of Medicine, Zagazig University, Egypt.
Disclaimer : not my slide. Just uploading for my personal use..
Common dermatologic disorders systemic lupus erythematosusDr. Faramarz Didar
SLE or lupus is a systemic autoimmune disease (or autoimmune connective tissue disease) that can affect any part of the body.
The immune system attacks the body's cells and tissue, resulting in inflammation and tissue damage.SLE most often harms the heart, joints, skin, lungs, blood vessels, liver, kidneys, and nervous system.
Characteristic facial rash of SLE is a butterfly rash which spread from one side of nose to other side.
It is very important to diagnose this Rash and SLE in patients who attend a cosmetic Clinic in order to solve their facial disfiguration. SLE butterfly facial rash is resistant to treatment by variety of cosmetic procedures like ablative and non-ablative laser, IPL , chemical peel and PRP. The diagnosis of SLE and systemic treatment od this disease is paramount to cosmetic approach. Cosmetic practitioner should have a broad knowledge of dermatological disorder and relevant approach to them.
The presentation explain white lesions in oral cavity and the classification the demonstrate the etiology, histopathology, diagnosis and treatment for each one.
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 lupuse rythematosus by formation of autoantibodiesssuser45f282
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.
Systemic means affects multiple organs.
Lupus is the Latin word for wolf meaning disease affecting skin where the skin lesions look like wolf bite.
Erythematosus means reddening of the skin.
Systemic Lupus Erythematosus or SLE, sometimes also called just lupus is a disease that’s systemic and affects a wide variety of organs, but notably often causes red lesions on the skin.
Systemic Lupus Erythematosus(SLE) is a chronic, nonspecific autoimmune inflammatory disease that typically affects multiple organs and systems, including the skin, joints, muscles, lungs, heart, kidneys, and the CNS and circulatory system.
Individuals with SLE are noted with the production of antibodies and inflammatory responses that are mistakenly directed at their own tissue.
SLE is an autoimmune disease resulting in butterfly rash and various other symtoms,a brief introduction and diagnosis and causes are mentioned in this ppt.
Lupus is a systematic autoimmune disease which affects the body’s tissues and organs by your own immune system thinking that they are foreign. Lupus is a chronic inflammatory disease that affects various parts of the body including joints, skin, kidneys, blood cells, brain, heart, and lungs. Lupus is also known as systemic lupus erythematosus or SLE. The exact cause of lupus is very difficult to diagnose, although it’s a combination of genes, hormones and environmental factors. It affects women between 18 and 40 years of age.
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
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
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.
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.
- 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
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.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stock
Telegram: bmksupplier
signal: +85264872720
threema: TUD4A6YC
You can contact me on Telegram or Threema
Communicate promptly and reply
Free of customs clearance, Double Clearance 100% pass delivery to USA, Canada, Spain, Germany, Netherland, Poland, Italy, Sweden, UK, Czech Republic, Australia, Mexico, Russia, Ukraine, Kazakhstan.Door to door service
Hot Selling Organic intermediates
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
4. SLE is a chronic autoimmune disease in
which the body immune system induce
auto-antibodies against the DNA which
can affect almost any organ system
Systemic (more than one organ can be
affected)
Lupus (autoanitbody against DNA)
Erythematosus (skin rash)
5. The type of reaction in this autoimmune
disease is Type III Hypersensitivity Reaction
(immune-complex).
Extracellullar double-stranded DNA occurs
mainly in the form of nucleosomes, which are
fragments of chromatin that cells release
when they undergo apoptosis. Pathogenic
anti-ds-DNA autoantibodies in the patient
with lupus bind to nucleosomes and gets
deposit on different sites and induce the
inflammatory reaction
6. Ultraviolet (UV) radiation
(sun exposure) exacerbates
the lesions of SLE. Can cause autoimmune
disorders by increase in cell death and/or a
decrease in the rate of dead cell clearance
Cigarette smoking has been shown
to be associated
with the development of SLE.
7. Drugs such as procainamide and
hydralazine can inducean SLE-like disease,
although typically glomerulonephritisdoes
not develop.
Sex hormones in the SLE 10 times
more common in women during
reproductive
years than in men of similar ages but only 2 to
3 times
more common in women during childhood or
after the age of 65.
8.
9. • Type I interferons.
patients with SLE also produce abnormally large
amounts of IFN-α.
• TLR signals(found dendritic cells)
TLRs that recognize DNA and RNA, notably the
DNArecognizing
TLR9 and the RNA-recognizing TLR7, produce
signals that activate B cells specific for self nuclear
antigens.(found B lymphocytes Plasmacytoid
dendritic cells)
• Failure of B cell tolerance
patients with SLE suggest the presence of defects
in both
central and peripheral tolerance.
10.
11. Immunologically the disease is associated
with an enormous number of auto antibodies
basically including (ANAs).
Fundamental defect in SLE is a failure to
maintain self-tolerance ,leading to
production of large number of auto
antibodies .
Mechanism by which the auto antibodies
can damage tissues :
I. Direct damage to tissues
II. Immune complex deposit
13. Auto antibodies in lupus :
I. ANAs
II. Auto antibodies against ds-DNA
III. RO
IV. LA(lupus anticoagulant )
V. Sm
14. Symptoms vary from person to person, and may come and go.
Almost everyone with SLE has joint pain and swelling. Some
develop arthritis. The joints of the fingers, hands, wrists, and knees
are often affected.
Other common symptoms include:
Chest pain when taking a deep breath
Fatigue
Fever with no other cause
General discomfort, uneasiness, or ill feeling (malaise)
Hair loss
Mouth sores
Sensitivity to sunlight
Skin rash -- a "butterfly" rash in about half people with SLE. The
rash is most often seen over the cheeks and bridge of the nose, but
can be widespread. It gets worse in sunlight.
Swollen lymph nodes
15. Other symptoms depend on which part of the
body is affected:
Brain and nervous system: headaches, numbness,
tingling, seizures, vision problems, personality
changes
Digestive tract: abdominal pain, nausea, and
vomiting
Heart: abnormal heart rhythms (arrhythmias)
Lung: coughing up blood and difficulty breathing
Skin: patchy skin color, fingers that change color
when cold (Raynaud's phenomenon)
Kidney: swelling in the legs, weight gain
Hematologic (eg, cytopenias such as leukopenia,
lymphopenia, anemia, or thrombocytopenia)
16.
17. To be diagnosed with lupus , you must
have 4 out of 11 common signs of the
diseases .
Your doctor will do a physical exam and
listen to your chest . An abnormal sound
called a heart friction rub or pleural
friction rub may be heard . A nervous
system exam will also be done .
18. Tests used to diagnose SLE may include :
Antibody tests including antinuclear
antibody (ANA) panel
CBC
Chest X-ray
Kidney biopsy
urinalysis
19. You may also have other tests to learn more
about your condition , some of these are :
Antithyroglobulin antibody
Antithyroid antibody
Complement components (C3 and C4)
Coombs test- direct
Cryoglobulins
ESR
Kidney function blood tests
Liver function blood tests
Rheumatoid factor
Antiphospholipid antibodies
20. Almost 90% of all cases occur in women
Overall, SLE affects women eight times more
often than it does in men
At age 30 years, the ratio of women to men is 10:1
The ratio at age 65 years, the ratio appears to be
about 3:1
The prevalence rate among women between age 15
and 64 years is 1 in 700 women
Symptoms usually appears between ages 15 and
25 years
The prevalence in the general population is about
1 in 1000
21. Mild forms of the disease may be treated
with:
NSAIDs for joint symptoms and pleurisy,
after talking with your doctor
Corticosteroid creams for skin rashes
A drug also used to treat malaria
(hydroxychloroquine) and low-dose
corticosteroids for skin and arthritis
symptoms
22. Treatments for more severe SLE may
include:
High-dose corticosteroids
Cytotoxic drugs
23. Systemic lupus erythematosus (SLE) can
cause systemic complications throughout
the body.
COMPLICATIONS OF THE BLOOD
Almost 85% of patients with SLE
experience problems associated with
abnormalities in the blood.
Anemia. About half of patients with SLE
are anemic.
24. The effects on blood vessels have also
been associated with confusion,
headaches, and seizures. Leg ulcers can
also develop.
Patients with APS who become pregnant
have a high incidence of pregnancy loss,
especially in the late term.
25. Heart disease is a primary cause of death in
lupus patients. The immune response in SLE
can cause chronic inflammation and other
damaging effects that can cause significant
injury to the arteries and tissues associated
with the circulation and the heart. In addition,
SLE treatments (particularly corticosteroids)
affect cholesterol, weight, and other factors that
can also affect the heart.
26. About 45% of patients with SLE suffer
gastrointestinal problems including
nausea, weight loss, mild abdominal pain
and diarrhea.
Severe inflammation causes cramping,
vomiting, diarrhea, and rarely intestinal
perforation which is life threatening.
27. Inflamed blood vessels in the eye can
reduce blood supply in the retina,
resulting in degeneration of nerve cells
and a risk of hemorrhage in the retina.
The most common symptoms are cotton-
wool-like spots on the retina.
28. SLE affects the lungs in about 60% of patients:
Inflammation of the membrane lining the lung (pleurisy) is
the most common problem, which can cause shortness of
breath and coughing.
In some cases, fluid accumulates, a condition called pleural
effusion.
Inflammation of the lung tissue itself is called lupus
pneumonitis. It can be caused by infections or by the SLE
inflammatory process. Symptoms are the same in both cases:
fever, chest pain, labored breathing, and coughing. Rarely,
lupus pneumonitis becomes chronic and causes scarring in
the lungs, which reduces their ability to deliver oxygen to the
blood.
A very serious and rare condition called pulmonary
hypertension occurs when high pressure develops as a result
of damage to the blood vessels of the lungs.
29. The kidneys are a crucial battleground in
SLE because it is here that the debris left
over from the immune attacks is most likely
to be deposited. Also, the immune response
can also attack different parts of the kidney
causing damage. About 50% of patients with
SLE exhibit inflammation of the kidneys
(called lupus nephritis).This condition occurs
in different forms and can vary from mild to
severe. Poor kidney function and kidney
failure may result from this damage.
30. Serious complications occur eventually in
about 30% of patients. If kidney injury
develops, it almost always occurs within
10 years of the onset of SLE, rarely after
that.
31. In 1950:
• 5 yr survival rate in case of lupus nephritis
was 0%
Recently:
• 5 yr survival 85%
• 10 yr survival 73%
32. Poor prognostic indicators
• Delay in treatment of more than 5 months from
onset of nephritis
• Young age at onset of nephritis
• Black racial background
• Hypertension
• Nephrotic syndrome
• Renal biopsy findings showing diffuse lupus
nephritis or high chronicity index