references:
1-European Academy of Neurology/Peripheral Nerve Society guideline on diagnosis and treatment of chronic inflammatory demyelinating polyradiculoneuropathy: Report of a joint Task Force—Second revision.
2-Chronic Inflammatory Demyelinating Polyradiculoneuropathy and Its Variants By Kelly Gwathmey, MD
3-Patient Journey in CIDP: Burden, Symptoms, and Diagnosis Jeffrey A. Allen, MD; Richard A. Lewis, MD
Competitive Intelligence to Decision Pattern by Elijah EzenduElijah Ezendu
Competitive Intelligence to Decision Pattern (CIDP) is a method of rating Corporate Competitive Intelligence Operations through patterns of systemic flow from Competitive Intelligence to Decision, thereby providing appropriate classification ranging from AAAAAAAA to DDDDDDDD.
references:
1-European Academy of Neurology/Peripheral Nerve Society guideline on diagnosis and treatment of chronic inflammatory demyelinating polyradiculoneuropathy: Report of a joint Task Force—Second revision.
2-Chronic Inflammatory Demyelinating Polyradiculoneuropathy and Its Variants By Kelly Gwathmey, MD
3-Patient Journey in CIDP: Burden, Symptoms, and Diagnosis Jeffrey A. Allen, MD; Richard A. Lewis, MD
Competitive Intelligence to Decision Pattern by Elijah EzenduElijah Ezendu
Competitive Intelligence to Decision Pattern (CIDP) is a method of rating Corporate Competitive Intelligence Operations through patterns of systemic flow from Competitive Intelligence to Decision, thereby providing appropriate classification ranging from AAAAAAAA to DDDDDDDD.
Immunoglobulins market to 2019 demand in primary immunodeficiency (pi) and ...Reports Corner
GBI Research's report "Immunoglobulins Market to 2019 - Demand in Primary Immunodeficiency (PI) and Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) Potentially Supplemented by Approvals for Alzheimer's Disease" provides in-depth analysis of the global immunoglobulin market. The report analyzes the markets for immunoglobulin products in the US, the top five European countries (the UK, Germany, France, Italy and Spain) and Japan.
https://www.reportscorner.com/reports/20855/Immunoglobulins-Market-to-2019---Demand-in-Primary-Immunodeficiency-(PI)-and-Chronic-Inflammatory-Demyelinating-Polyneuropathy-(CIDP)-Potentially-Supplemented-by-Approvals-for-Alzheimers-Disease/
Global Intravenous Immunoglobulin Market (By Application, Types and Geography...Allied Market Research
IVIG is a sterile solution of antibodies collected from healthy donors, which is administered through the veins into the body. Currently, the immunoglobulin industry is growing on account of increasing FDA/EMA approvals and government support. IVIG usage against the conditions within the criteria (i.e. FDA/EMA approved indications) have increased greatly and the largest increase found in Chronic Inflammatory demyelinating polyneuropathy (CIDP), Hypogammaglobulinemia and immunodeficiency diseases.
Delivery of electrical current to a specific subcortical grey matter target to stimulate a desired group of nerve cells which results in specific modulation the output of the involved neurocirciut.
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.
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.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
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
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.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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ASA GUIDELINE
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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 simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
3. Acute inflammatory polyneuropathies
• Subgroups Typically
• AIDP Acute infl demyelin. pnp Motor/sensory, relatively good progrnosis
• AMSAN Acute motor-sensory axonal pnp Motor/sensory, severe nerve damage
• AMAN Acute motor axonal pnp Weakness, normal sens, severe nerve
damage
• MFS Miller Fisher´s syndrom Ataxia (sens) and diplopia, often not weak
4. GBS; Symptoms
Predominantly weakness
– few or many muscle groups
– usually symmetic, but not always
– 1/6 need respirator
– 50% have cranical nerve involvement
•Sensory symptoms may dominate
– distal parestesia
– Deep sensibily most involved
– pain may be prominent
5. Findings
• reduced reflexes
– if refl are normal but no weakness, diagnosis ??
• ataxia (peripheral or brain stem)
• unclear papilledema
• autonomic dysfunction common
• sympatetic-orthostatic hypotension
• parasympatetic-tachycardia, bladder paresis, bowel
paresis
• can give mors subita
6. Time course
• The symptoms develop during days-weeks
• Progress < 2 weeks at 50%
• If progress > 8 weeks -> CIDP
• Recovery varies from weeks to months
– the slowest at axonal injury
• Mortality 5%
– autonomic dysfunction
– complications to immobilization
– 10% sequel
– 3% reoccur within weeks, months, years
7. Etiology och pathophysiology
• Autoimmune disease
– 2/3 comes after infection or surgery
– vaccinations
– malignant lymphoma
– aids
• Pathophysiology
– perivenulär patchy endoneural infiltration of mononuclear cells
– conduction block
– segmental demyelination
– axonal degeneration in severe cases
9. F-response
MUSCLE
F-response is a recurrent response travelling from
stimulation to spinal cord and then to the muscle.
CV in entire nerve, also proximal part.
At conduction block, no transmission
in blocked nerve.
stim
11. EDX vid GBS
Conduction block amplitude decay prox-dist, few F
Demyelination low CV, particularly MCV
Axonal degeneration low CMAP + denervation (EMG)
Motor hyperexcitability A-waves during 1-14 days
Sensory hyperexcitability not seen with routine EDX
12. May be due to
ion-channel interference
demyelination
Localization
mainly motor nerves
proximal or distal
symmetrical sometimes
13. Proximal, general or distal slowing
Prox slowing
MUSCLE
Generalized slowing
MUSCLE
Distal slowing
MUSCLE
14. Acute polyradiculitis
(Guillain-Barré Syndrome, GBS, AIDP)
Strategy
• demonstrate acute motor and sensory neuropathy
• demonstrate conduction block
• assess: severity, pathology, distribution
15. Acute polyradiculitis, GBS
-expected findings
Expected abnormal findings
Neurography, MCS
• conduction block
• F waves delayed and few
• DL prolonged
• reduced MCV, sometimes normal initially
• distal amplitude normal/low
Neurography, SCS
• reduced amplitude
EMG
• reduced IP, later acute neurogenic EMG findings
Autonomic tests
• often abnormal
26. A- waves and GBSA- waves and GBS
15 year old girl
27.
28. Uppsala: The final diagnosis if referral asks
GBS and EDX is normal
EDX normal Clinical EDX day
15/113 GBS?, myelopati, TIA 16d
GBS?? 43 d
CVL, vomiting 2d
Myosit, GBS, Ciprofloxacin (pain) 10d
(abnormal day3, normal day 7).
Transient GBS 3d
ADEM 7d
Diarrea after trip abroad 22d
Parestesia, 168d
increase refl, pain 14d
Vaccination 31d
lumbar pain MR uneg. 1d
Meningitis 14d
Inflammation in disc 22 d
GBS 6 y ago, now numbness, exclude GBS 20d
GBS för 8 y ago, now relaps? Prob not 8 år
29. Uppsala: The final diagnosis (referral, or a
clinical final diagnosis) if EDX at the first
occasion was interpreted as GBS
62 patients with EDX interpreted as GBS
Clinical final diagnosis GBS 60
Weakness, became GBS 1
Numbness – IVIG (GBS 2 years ago) became GBS
1
30. Referral GBS?
1:a EDX ”patol EDX” (unspec)
Which was the final diagnosis
GBS/GBS trol/GBS? 8
"non-GBS" 8
Encephalitis/myelitis 5
Unclear cases (weakness) 5
Root/Spinal Stenosis 4
Sensory loss 3
Lymphoma, antiHU 2
Central bleeding 2
Miller Fisher 1
Lyme disease 1
Critical illness myopathy 1
40/113 patienter
31. CIDP, clinical
• Signs of cranial nerve (CN) involvement (eg,
facial muscle paralysis or diplopia)
• Gait abnormalities
• Motor deficits (eg, symmetric weakness of both
proximal and distal muscles in upper and lower
extremities)
• Diminished or absent deep tendon reflexes
• Sensory deficits (typically in stocking-glove
distribution)
• Impaired coordination
32. CIDP, EDX
Electrodiagnostics - electromyography (EMG) and nerve
conduction study (NCS). In usual CIDP, the nerve
conduction studies show demyelination. These findings
include:
•a reduction in nerve conduction velocities;
•the presence of conduction block or abnormal temporal
dispersion in at least one motor nerve;
•prolonged distal latencies in at least two nerves;
•absent F waves or prolonged minimum F wave latencies in
at least two motor nerves. (In some case EMG/NCV can be
normal).
33. Chronic polyradiculitis
CIDP
Etiology
• probably prolonged autoimmune reaction
against peripheral nerves.
Strategy
• demonstrate subacute motor and sensory
neuropathy
• demonstrate conduction block
• assess: severity, pathology, distribution
34. CDPCDP
Distribution of conduction slowing
proximal even distal
AIDP/CIDP ++
CMT1 ++
anti MAG ++
modified from Attrian et al. Clin neurophys March 2001
39. MMNMMN
General commentsGeneral comments
•Symptoms similar to ALS!
In diagnosis of ALS, exclude MMN
by means of nerve conduction studies
Check for GM1 antibodies
•Is the disease a motor variant of pure motor CIDP?
Sometimes sensory nerves are involved
Nerve distribution
Conduction block
Effect of immunosuppresive treatment
Weakness also in non-atrophic muscles Stålberg
40. MMN/CIDP a comparison, Kimura textbook
MMN CIDP
pure motor frequent rare
mononeuritis multiplex yes no
remission/exacerbation no yes
generalized areflexia no yes
CSF protein often normal elevated
site with cond block forearm, brachial plexus entrapment sites
elevated anti-GM1 antibody frequent rare
choice of therapy immunosupp,IVIG steroids.plasmaex
IVIG