The document discusses seronegative and seropositive spondyloarthropathies. It describes the key characteristics of several types of spondyloarthropathies including ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and arthritis associated with inflammatory bowel disease. Imaging findings are an important part of diagnosis and include changes in the sacroiliac joints and spine seen on radiography as well as MRI findings. HLA-B27 positivity is also discussed as a predictor for some types.
An apt yet detailed description of Polyarthritis for undergraduate level with basic definitions, classification, concept, clinical features along with descriptive images, diagnosis & assessment with distinguishing features along with differential diagnosis.
the presentation gives a detail information about the seronegative spondyloarthropathy. this ppt also provide recent evidences to frame the rehab protocol.
An apt yet detailed description of Polyarthritis for undergraduate level with basic definitions, classification, concept, clinical features along with descriptive images, diagnosis & assessment with distinguishing features along with differential diagnosis.
the presentation gives a detail information about the seronegative spondyloarthropathy. this ppt also provide recent evidences to frame the rehab protocol.
Rheumatology Sheet from Rheumatology Department, Faculty of Medicine, Zagazig University, Egypt.
Disclaimer : not my slide. Just uploading for my personal use..
Still's disease, sometimes referred to as Adult-onset Still's disease (AOSD) is a rare systemic inflammatory disease characterized by the classic triad of persistent high spiking fevers, joint pain and a distinctive salmon-colored bumpy rash.
Rheumatology Sheet from Rheumatology Department, Faculty of Medicine, Zagazig University, Egypt.
Disclaimer : not my slide. Just uploading for my personal use..
Still's disease, sometimes referred to as Adult-onset Still's disease (AOSD) is a rare systemic inflammatory disease characterized by the classic triad of persistent high spiking fevers, joint pain and a distinctive salmon-colored bumpy rash.
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
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.
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
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
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.
- 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
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
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
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.
2. OBJECTIVES:
1. Describe the essentials of diagnosis for the
disorders in this category.
2. Review the signs, symptoms and physical
examination and imaging findings commonly
associated with these disorders.
4. Seronegative spondylarthropathy consists of a spectrum
of chronic inflammatory disorders that lack the presence
of rheumatoid factor and are clearly distinct from
rheumatoid arthritis.
Where as rheumatoid arthritis involves predominantly
the synovial joints, significant abnormalities in the
cartilaginous joints, entheses, as well as synovial
articulations are seen in spondylarthropathic processes.
5. The seronegative spondyloarthropathies are a
group of arthritic diseases that affect multiple
organ systems and are thought to have a
significant genetic component to their origin.
7. HLA-B27 is the most important predictor of
AS.
90+% of Caucasians with AS are B27+
Studies suggest B27 antigen accounts for 20-50% of
the risk for AS
There are 23 known subtypes of HLA B27 and
not all are associated with disease
Suggests a structure-function relationship.
The absence of HLA-B27 expression in an
individual patient does not exclude the
diagnosis of AS.
9. Young adults
Peak onset ages 20-40
overall prevalence is estimated to be as high as
0.2–2%.
Males>Females (4:1).
More common in Caucasians
11. Back pain >3months.
Morning stifnness.
Tenderness over the SI joints& spinal tenderness 2ry spondyolitis
Multiple different maneuvers (all unreliable)
Reduced range of motion of the back.
Reduced chest expansion owing to costosternal and costovertebral affections.
Peripheral joints affection e.g. shoulders and hips.
The lower limbs are more frequently involved than the upper limbs.
In 20–25% of AS patients, peripheral articular symptoms may precede axial
manifestations.
Painful tendinopathy occurs in about 10%
12. Evaluation of other joints
Particular attention to the large joints
Lab evaluation
HLA-B27
Imaging for AS
SI joints, others as clinically indicated
13. Clinical Criteria
Low back pain, > 3
months, improved by
exercise, not relieved
by rest
Limitation of lumbar
spine motion, sagittal
and frontal planes
Limitation of chest
expansion relative to
normal values for age
and sex
• Radiologic Criteria
– Sacroiliitis grade ≥ 2
bilaterally or grade 3 – 4
unilaterally
• Grading
– Definite AS if radiologic
criterion present plus at least
one clinical criteria
– Probable AS if:
• Three clinical criterion
• Radiologic criterion
present, but no signs or
symptoms satisfy clinical
criteria
14.
15.
16.
17.
18.
19.
20. Sacroiliac Joints and Pelvis
Sacroiliitis is the hallmark of Ankylosing spondylitis.
Sacroiliitis is the earliest radiographic sign in 99% of cases of AS
Although Sacroiliitis alone is a non-specific finding and is not sufficient for the
diagnosis of AS.
Changes in the sacroiliac joints are considered ubiquitous among patients with AS .
Both the synovial and ligamentous (superior and posterior) portions of the joint are
involved.
Classically, the involvement is symmetric and bilateral particularly very early in the
course of the disease.
unilateral disease may occur.
21.
22. Conventional Radiographic Findings in Ankylosing Spondylitis
Small erosions lined up one behind the other at corresponding
sites of the ilium and the sacrum resemble a string of beads or
rosary.
The erosions usually develop earlier on the iliac than on the sacral
side of the joint possibly because the cartilage covering the sacrum
is approximately twice as thick as that covering the ilium .
Reactive bone proliferation is seen radiographically as sclerosis of
the adjacent cancellous bone with a variable pattern (diffuse, band
shaped,spotty, triangular).
23.
24.
25. Abnormalities of the spine can be seen at: The disco vertebral
junctions.
Apophyseal joints, costovertebral joints.
Posterior ligamentous attachments, and atlantoaxial joints.
Classically, changes are initially noted at the thoracolumbar and
lumbosacral junctions.
Spinal extension to the midlumbar, as well as the upper thoracic and
cervical vertebrae, occurs with disease progression but may be
arrested at any stage .
26. There is a spectrum of:
Inflammatory and destructive lesions of the spine in
AS.
This predominantly involves the cartilaginous disco
vertebral junction.
One of the earliest plain-film findings of spinal
involvement, typically seen at vertebrae T10 through
L2, is the so-called Romanus lesion, also known as
spondylitis anterior
27.
28.
29.
30. Marginal osteosclerosis.
Along the spectrum of discovertebral diseases are the more destructive lesions, such as
Andersson lesions.
Three types are distinguished:
Type I shows central focal endplate destruction with intraosseous disc
herniation and associated reactive endplate changes, the nature of which
depends on the age of the lesion. In the relatively acute stage, marrow
edema is identified, with enhancement after intravenous gadolinium
contrast administration
Type-II lesions are located more at the periphery of the discovertebral junction.
Type-III lesions involving both the central and the peripheral portions may be
difficult to differentiate from infectious spondylodiscitis.
31. Diagnostic features:
The absence of an anterior paraspinal soft tissue mass .
The predominant low signal intensity of the
intervertebral disc on T2-weighted images (with only
possible minor areas of high signal intensity adjacent to
vertebral erosions) indicate a noninfectious Andersson
lesion.
32.
33.
34.
35.
36. Vertebral bodies initially erode at
corner, reactive sclerosis occurs
below this leading to squared
appearance
Eventually anulus fibrosus and
longitudinal ligaments become
ossified (syndesmophytes)
Discs can become calcified, along
with all ligaments including those
between spinous processes
bamboo spine
Dagger sign,
fused spinous
process ligaments
http://uwmsk.org:8080/EvasMSKTF/
40. Magnetic resonance imaging :
Enable early diagnosis of spinal manifestations of AS by an
increased sensitivity for identification of early-stage Sacroiliitis or
vertebral osteitis.
Is also superior to other imaging techniques for differential
diagnosis of Andersson lesions vs. infectious spondylodiscitis
and in the evaluation of most acute and chronic spinal
complications of AS.
MRI has been used to assess the effect drugs in the management
of acute inflammatory lesions
46. Inflammatory polyarthritis associated with
psoriasis
May occur prior to the onset of skin disease
Usually seronegative
M=F
Prevalence rate 0.1%
47. Inflammatory DIP disease
Asymmetic oligoarthritis with large and small
joints
Symmetric polyarthritis
Arthritis mutilans
Spondyloarthropathy
Spondylitis and sacroiliitis
52. Bilateral, asymmetrical
Dramatic joint space loss +/-
ankylosis (arthritis mutilans)
Bone proliferation, “mouse ears”
“pencil-in-cup” deformities
Normal mineralization
Sausage digits
Hands > feet > SI > spine
Usually favors DIP and PIP in hand
SI involvement usually bilateral,
asymmetrical
Large bridging bone formation in
spine, similar to reactive arthritis
http://uwmsk.org:8080/EvasMSKTF/
Sausage
digits
http://uwmsk.org:8080/EvasMSKTF/
http://www.hopkins-arthritis.org/arthritis-
info/psoriatic-arthritis/diagnosis.html
Psoriatic Arthritis
55. The appearance of arthritis in patients with inflammatory intestinal disease
(ulcerative colitis, Crohn’s disease, and Whipple’s disease) has been
described since 1950
These abnormalities have been designated enteropathic arthritis .
Both the peripheral joints and the axial skeleton (spondylarthropathy) may
be involved enteropathic arthritis.
The axial skeleton is involved in about 10% of patients.
Radiological manifestations of enteropathic spondylarthropathy (sacroiliitis
and spondylitis) are indistinguishable from AS.
Axial involvement is poorly correlated with activity of bowel disease,
whereas a close temporal association exists between exacerbations of
intestinal disease and peripheral joint inflammation
58. SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis)
Is considered as a spondylarthropathy associated with different
types of cutaneous pustules.
The term pustulotic arthro-osteitis (PAO) is more appropriate.
59.
60.
61. • Pathology of Rheumatoid Arthritis:
RA is the prototype of conditions accompanied by a hyperplastic,
inflammed synovial membrane.
In RA and related diseases, the synovial lining becomes
hyperemic and thickened, with extensive overgrowth and
formation of villi.
Inflamed synovial lining in RA eventually grows over the
articular surfaces, eroding and destroying cartilage and
underlying bone.
The invasive portion of the hyperplastic synovial tissue has been
termed pannus.
62. MR manifestations of RA and related diseases are nonspecific
, similar changes can be seen in other inflammatory joint
conditions.
Therefore the goal of those using MRI in these conditions is
not to achieve a specific diagnosis, which may be
accomplished using clinical and laboratory parameters, but
to assess the extent of the early soft tissue and bone
manifestations.
66. MRI features Of RA:
Erosion of the cartilage and bone.
Tendon or ligamental invasion.
Synovial pannus :MRI has been used to demonstrate pannus
,and synovial cysts.
Editor's Notes
Clinical Features of AS
Sacroiliitis is the hallmark feature of AS1 and the earliest, most consistent findings are traceable to effects of sacroiliitis and enthesitis. Inflammation of the discovertebral, apophyseal, costovertebral, and costotransverse joints of the spine, and paravertebral ligamentous structures are frequently associated with AS. After many years, chronic inflammation can cause bony ankylosis.2
Chronic low back pain and stiffness, which typically worsens following a period of prolonged inactivity (eg, morning stiffness), are common presentations.1 Over time, lumbar spine mobility becomes restricted in all planes and posture becomes abnormal because of flattening of the lumbar spine and accentuated dorsal spine kyphosis. Radiographic findings in advanced disease include erosions, sclerosis of adjacent bones, pseudo-widening of the sacroiliac joint space, and fibrosis, calcification, interosseous bridging, and ossification of the sacroiliac joints. Extraskeletal manifestations are also frequently part of the clinical picture.2
Khan MA. Spondyloarthropathies. In: Hunder GG, ed. Atlas of Rheumatology. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2002.
Khan MA. Clinical features of ankylosing spondylitis. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. vol 2, 3rd ed, New York, NY: Mosby; 2003:1161-1181.
Modified New York Criteria for the Diagnosis of AS
Three sets of clinical and radiographic criteria have been introduced over the past 40 years. The Modified New York Criteria,1,2 developed in 1984, are now widely used to diagnose AS. Radiographic evidence of sacroiliitis is heavily relied on to diagnose AS because it is the best nonclinical indicator of disease. Diagnosis may be missed early on, though, because routine pelvic radiographs may not clearly demonstrate sacroiliitis in the initial stages of AS.3
Van der Linden S. Ankylosing spondylitis. In: Textbook of Rheumatology 5th ed. Kelly WN, Harris ED, Ruddy S, Sledge CB, eds. Philadelphia, PA: WB Saunders; 1996:969-982.
Van der Linden S, Valkenburg HA, Cats A. Evaluation of diagnostic criteria for ankylosing spondylitis. A proposal for modification of the New York criteria. Arthritis Rheum. 1984;27:361-368.
3. Khan MA. Spondyloarthropathies. In: Hunder GG, ed. Atlas of Rheumatology. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2002.
cricoarytenoid
PMN’s in SF – inflammatory fluid WBC>2000
Pannus takes on special invasive properties
Figure 2. Pathogenesis of Rheumatoid Arthritis.
In the normal knee joint, the synovium consists of a synovial membrane (usually one or two cells thick) and underlying loose connective tissue. Synovial-lining cells are designated type A (macrophage-like synoviocytes) or type B (fibroblast-like synoviocytes). In early rheumatoid arthritis, the synovial membrane becomes thickened because of hyperplasia and hypertrophy of the synovial-lining cells. An extensive network of new blood vessels is formed in the synovium. T cells (predominantly CD4 ) and B cells (some of which become plasma cells) infiltrate the synovial membrane. These cells are also found in the synovial fluid, along with large numbers of neutrophils. In the early stages of rheumatoid arthritis, the synovial membrane begins to invade the cartilage. In established rheumatoid arthritis, the synovial membrane becomes transformed into inflammatory tissue, the pannus. This tissue invades and destroys adjacent cartilage and bone. The pannus consists of both type A and type B synoviocytes and plasma cells.