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.
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,
Erythroderma is defined as the scaling erythematous dermatitis involving 90% or more of the cutaneous surface.
Also known as exfoliative dermatitis
Idiopathic exfoliative dermatitis – also known as the “red man syndrome”, is characterized by marked palmoplantar keratoderma, dermatopathic lymphadenopathy,increased IgE.
Increased skin perfusion leads to
Temperature dysregulation >
Resulting in skin loss and hypothermia >
High output state >
Cardiac failure
BMR raises to compensate for heat loss
Increased dehydration due to transpiration (similar to burns)
All lead to negative nitrogen balance and characterized by edema, hypoalbuminemia, loss of muscle mass.
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.
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,
Erythroderma is defined as the scaling erythematous dermatitis involving 90% or more of the cutaneous surface.
Also known as exfoliative dermatitis
Idiopathic exfoliative dermatitis – also known as the “red man syndrome”, is characterized by marked palmoplantar keratoderma, dermatopathic lymphadenopathy,increased IgE.
Increased skin perfusion leads to
Temperature dysregulation >
Resulting in skin loss and hypothermia >
High output state >
Cardiac failure
BMR raises to compensate for heat loss
Increased dehydration due to transpiration (similar to burns)
All lead to negative nitrogen balance and characterized by edema, hypoalbuminemia, loss of muscle mass.
Here is very good and amazing presentation on Multiple sclerosis ..its about brain
read this carefully and work on this because the work on brain is very good for future research...
The term ‘lupus’ (Latin for ‘wolf’) was first used during the Middle Ages to describe erosive skin lesions evocative of a ‘wolf’s bite’.
Lupus is an autoimmune disease, which means that the body's natural defense system (immune system) attacks its own tissues instead of attacking foreign substances like bacteria and viruses. This causes inflammation which can causes swelling, pain, and tissue damage throughout the body.
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.
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.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
1. LUPUS ERYTHEMATOSIS
• In this online lecture
you will learn about the
two types of lupus,
including treatments,
and interventions.
• The two types are:
– Discoid Lupus
Erythematous (DLE)
– Systemic Lupus
Erythematous (SLE)
2. The readings that accompany
this lecture are:
• Reading Assignment
• Iggy- pp 429-436
3.
4. What is Discoid Lupus
Erythematous?
• A chronic skin condition of sores with
inflammation and scarring favoring the
face, ears, and scalp and at times on other
body areas.
• These lesions develop as a red, inflamed
patch with a scaling and crusty
appearance. The center areas may
appear lighter in color with a rim darker
than the normal skin.
5. What does DLE look like?
• Lesions are treated with topical
cortisone, or cortisone injections
• If the cortisone is ineffective the
client maybe treated with
Plaquenil (***please click on this
link to learn more about the
medication***)
• a skin biopsy needs to
be done to confirm the
diagnosis because
other conditions can
look like discoid lupus
erythematosus.
6. What causes DLE?
• The exact cause is unknown, but it is thought to
be autoimmune with the body's immune system
incorrectly attacking normal skin.
• This condition tends to run in families. Females
out number males with this condition 3 to 1.
• In some patients with discoid lupus
erythematosus, sunlight and cigarette smoking
may make the lesions come out.
7. What interventions will help with
DLE?
• Patients whose condition is sensitive to
sunlight need to wear a UVA blocking
sunscreen daily and a hat while out doors.
• Follow-up with the doctor is important and
necessary every six months to once a year
to make sure the disease is not spreading to
the internal organs and to minimize scarring
• If the client is taking Plaquenil yearly eye
exams are a must.
8.
9.
10. What is Systemic Lupus
Erythematosus (SLE)?
• SLE is a complex chronic connective-tissue
disease.
• It affects almost all body systems.
• The manifestations are widely variable but they
are thought to be the result of cell and tissue
damage caused by the deposition of antigen-
antibody complexes in connective tissues.
• SLE can range from a mild, episodic disorder to
a rapidly fatal disease process.
11. What is the epidemiology of
SLE?
• Females are affected more than males in
a ratio of 9:1
• The disease usually affects women of
childbearing age, but can occur at any
age.
• It is more common in African Americans,
Hispanics, and Asians than it is in
Caucasians.
12. What is the etiology of SLE?
• The exact etiology is unknown.
• Genetic, environmental and hormonal factors play a role in its
development.
• The above statements are idiopathic forms of SLE. It can also be
drug induced by the following medications:
• Procainamide
• Isoniazid
• Hydralazine
• Minocycline
• Phenytoin
• Ethosuximide
• D-Penicillamine
– Manifestations of drug induced lupus usually resolve when the
medication is discontinued.
13. What are the initial symptoms of
SLE?
• The initial manifestations of SLE are:
fatigue, fever, malaise, weight loss,
musculoskeletal manifestations similar to
arthritis.
• SLE can affect multiple systems. Let’s
take a look at each of those systems.
14. What are the dermatological
signs?
– The client may have Cutaneous Lupus
Erythematosus
– Malar "butterfly" rash
– Photosensitivity
– Vasculitis
– Alopecia
– Oral Ulcers
– Sicca Syndrome
15. What are the neurological
symptoms?
A client may have the
following symptoms:
• Neuropathies (peripheral
and central)
• Seizures
• Depression
• Psychosis
A client may have the
following complications
from an exacerbation of
SLE:
• CVA
• Organic Brain Syndrome
– Intellectual impairment
– Memory Loss
– Personality Changes
– Disorientation
16. What kinds of ocular changes
can result from SLE?
• Conjunctivitis
• Photophobia
• Retinal vasculitis with transient blindness
• Cotton-wool spots on retina
Cotton wool spots are small areas of yellowish white
coloration in the retina. They occur because of
swelling of the surface layer of the retina, which
consists of nerve fibers. This swelling almost always
occurs because the blood supply to that area has
been impaired and in the absence of normal blood
flow through the retinal vessels the nerve fibers are
injured in a particular location resulting in swelling and
the appearance of a "cotton wool spot. "
17. What are the musculoskeletal
changes with SLE?
• Morning Stiffness
• Arthralgias
• Symmetric Polyarthritis
• Joint Swelling and Effusion
18. How can SLE effect the renal
system?
• Proteinuria
• Cellular casts
Potential complications
resulting from SLE
are:
• Nephrotic syndrome
• Renal failure
19. How can SLE effect the GI
system?
• Hepatomegaly
• Anorexia
• Nausea
• Abdominal Pain
• Diarrhea
20. How can SLE effect the
Cardiovascular system?
• Pericarditis
• Myocarditis
• Endocarditis
• Vasculitis
• Venous or arterial
thrombosis (anywhere
in the body)
21. How does SLE effect the
hematologic system?
• Anemia
• Leukopenia
• Thrombocytopenia
• Splenomegaly
22. How can SLE effect the
Respiratory System?
• Pleurisy
• Pleural effusion
• Pneumonitis
• Interstitial fibrosis
23. What Lab Assessments help in
the diagnosis?
• Initially and ANA titer is completed. *Please
remember an ANA titer alone cannot be used to diagnose a disease, it
must be used in combination with an evaluation of symptoms and other
tests.
• Secondary testing if the ANA titer positive
– Complete Blood Count *** pay particular attention to the
WBC, Hgb & Plt counts**
– Coagulation factors
– Urinalysis
– Serum Creatinine
– Antiphospholipid Antibody
– Double Stranded DNA Antibody (Anti-dsDNA)
– Smith Antibody (Anti-Smith or Anti-Sm)
24. How is a diagnosis of SLE
made?
• A diagnosis of SLE is made when a client has 4 of 11
following criteria:
– Malar Rash
– Discoid rash
– Photosensitivity
– Oral Ulcers
– Polyarthritis involving more than 2 joints
– Pleuritis or Pericarditis
– Antinuclear Antibody positive titer
– Renal disease
– Neurologic disorder (e.g. Seizures, Psychosis)
– Anemia, Neutropenia or Thrombocytopenia
– Anti-dsDNA, Anti-Sm positive
25. How is SLE treated?
Part of the treatment of SLE involves the use of medications
– Salicylates and NSAIDs
• Enteric Coated ASA 650 mg PO every 4-6 hours prn
• Ibuprofen 400-800 mg PO tid-qid prn
– Anti-Malarial agents
• Hydroxychloroquine (Plaquenil) 400 mg/day
– Corticosteroids
• Topical Corticosteroids
• Systemic Corticosteroids in severe exacerbations
– Prednisone 0.5 to 1 mg/kg/day up to 4 weeks or
– Solu-medrol 15 mg/kg IV for 3 days
– Cytotoxic agents or antineoplastic drugs are effective immunosuppressive
agents. **They act by decreasing the proliferation of cells within the immune system and
are widely used to prevent rejection following a tissue of organ transplant. They are usually
adminstered concurrently with corticosteriod therapy, allowing lower doses of both
preparations, and resulting in fewer side effects.**
• Cyclophosphamide (cytoxen)
– Daily dosing: 1.5-2.5 mg/kg/day or
– Monthly dosing: 10-15 mg/kg IV every 4 weeks
• Azathioprine (Imuran) 2-3 mg/kg/day
26. What else does a client with SLE
need?
• A client with SLE also needs Opthamology
exams with dilation upon starting steriods or
plaquenil and yearly there after.
• Interventions to reduce fatigue.
• Sunscreen and other protection against
photosensitivity.
• Interventions to prevent infection.
• Birth control is critical during exacerbations.
27. How does a client diagnosed with
SLE feel?
Clients with SLE may
have problems with
the following:
– SELF ESTEEM
– WITHDRAWAL
– DEPRESSION
– PSYCHOSIS
– HARDINESS
– MANAGEMENT OF A
CHRONIC ILLNESS
28. What are the outcomes?
Although there is no cure for SLE, the 10
year survival rate is greater than 70%
among clients with this disease, which
once was considered fatal in most cases.
• Click on the following link to watch a video about
Lupus and initiatives regarding the disease
http://www.lupusresearchinstitute.org/video.php
29.
30. A Case Study
• D.W. is a 23 year old married woman with
3 children under the age of 5. She
presented to her physician 2 years ago
with vague complaints of intermittent
fatigue, joint pain, and low-grade fever.
Her physician noted a scaly rash across
her nose cheeks, back and chest at that
time.
32. What is the diagnosis: systemic
lupus erythematosus or
cutaneous lupus
erythematosus?
• D.W. was diagnosed with systemic lupus
erythematosus.
– The malar rash
– Polyarthritis
– Anemia
– Positive ANA titer
33. How does discoid lupus
erythematosus differ from
systemic lupus erythematosus?
• DLE
– Topical skin disorder
– An autoimmune
disorder attacking the
skin
• SLE
– A systemic
autoimmune
multi-system disorder
– An episodic disorder
– May include DLE
34. • D.W. was subsequently diagnosed with
systemic lupus erythematosus. She was
initially treated with Cyclophosphamide
(cytoxen) 150mg PO every day and
prednisone (Deltasone) 20 mg po every
day, bedrest, ice packs, and aspirin to
control discomfort.
35. What priorities need to be
addressed with D.W.?
• Monitor blood count with particular attention to
WBC and platelet counts. Notify the physician if
the WBC’s fall below 4000, or platelets below
75,000.
• Monitor renal & liver function studies
• Cytoxen should be administered with food to
minimize gastrointestinal effects
• Monitor for signs of abnormal bleeding
• Use meticulous hand washing and assess for
signs of infection
• Ensure adequate nutrient intake
36. • D.W. responded well to treatment and
resumed her job in environmental services
at a large geriatric facility. Eighteen
months after diagnosis, D.W. developed
puffy hands and feet and increased
fatigue. D.W. reported that she had been
working longer hours because of the
absence of 2 of her fellow workers.
38. • What are the significance of these
findings?
• What is the relationship of such findings to
D.W.’s diagnosis of SLE?
• How will D.W.’s treatment and nursing
plan likely to change?
(**Hint – This is a great place to apply your
Renal Content****)
39. • There will be a pass session on Lupus to
discuss and questions and talk about the
case study. Hope to see you there.
• For any other questions please see Jean
or email her at jforsha@ccp.edu