Thrombotic microangiopathy (TMA) refers to intraluminal platelet thrombosis in small blood vessels. TMA can be caused by conditions such as HUS, TTP, HIV, and malignant hypertension. In hemolytic uremic syndrome (HUS), TMA is caused by Shiga toxin from E. coli or other bacteria, which activates the alternative complement pathway and causes endothelial damage. The diagnostic approach to HUS and TMA involves excluding drugs, autoimmune hemolytic anemia, and other systemic diseases as causes before determining if the presentation matches Shiga toxin-HUS, atypical HUS, or TTP. Treatment of Shiga toxin-associated HUS is generally supportive with intravenous
Thrombotic Microangiopathies are diverse group of disorders wherein thrombocytopenia, hemolytic anemia and organ dysfunction such as Kidney and brain occur . Major recent advances in this field have occurred which opens up oppurtunities to effectively manage its clinical challenges .
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Thrombotic Microangiopathy (TMA) in Adults and Acute Kidney Injury - Dr. GawadNephroTube - Dr.Gawad
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https://youtu.be/zrFm0hAZk2A
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Dr Abdullah Ansari
MBBS, MD Medicine
Aligarh Muslim University
Clinical case
Hemolytic Anemia
Intravascular vs extravascular hemolysis
Classification of hemolytic anemia
Approach to hemolysis
Patient history
Clinical features
Peripheral blood smear
Investigation
Treatment
Thrombocytopenia is generally defined as platelet count <150 × 109/L. It can occur due to several reasons, like decreased platelet production (e.g., inherited bone marrow failure syndromes, acquired aplastic anemia, leukemia), ineffective platelet production (myelodysplastic syndrome, megaloblastic anemia), increased destruction (ITP, HLH), increased consumption (DIC, TTP, HUS), sequestration (hypersplenism), or may be due to combination of multiple mechanisms described above.
During evaluating a case of thrombocytopenia, the first step is getting a detailed history and doing a proper clinical examination. Then the next step would be checking the other parameters of complete blood count (CBC), especially hemoglobin (Hb) and the total WBC count, complemented by a peripheral smear (PS) examination, which will clear many doubts and will help us pinpointing our diagnostic approach.
Many a times pseudo-thrombocytopenia is encountered in a PS due to platelet clumping by EDTA and can be rectified by collecting blood samples in a citrate or heparin vials or by doing a direct finger prick smear. Any accompanying cytopenia will expand the differential diagnosis and an isolated thrombocytopenia will further narrow it down. Presence of any additional abnormalities of red cells (megaloblasts) or white cells (presence of hyper-segmented neutrophils, atypical lymphoid/myeloid cells) could be present in megaloblastic anemia/MDS, leukemia respectively, while in the presence of fragmented red cells microangiopathic hemolytic anemia should always be ruled out by doing PT and aPTT (DIC, TTP, HUS). In case of isolated thrombocytopenia, the platelet morphology is also important. In many patients in India, especially in eastern region many people have large platelets with their normal platelet count around 100 × 109/L with normal platelet function (Harris platelet syndrome). However, presence of any abnormal platelet morphology along with a low platelet count may indicate a platelet function disorder (large platelets in Bernard Soulier syndrome/ Glanzmann thrombasthenia or small platelets in Wiskott-Aldrich syndrome), especially if encountered in early part of life during evaluation for bleeding symptoms. In case of isolated thrombocytopenia, presence of additional congenital anomalies may point out towards an inherited marrow failure syndrome, e.g. amegakayocytic thrombocytopenia. Exposure to certain drugs may result in isolated low platelet count, e.g., ceftriaxone, piperacillin, heparin. Presence of toxic changes in neutrophils may indicate sepsis related thrombocytopenia. By excluding all these, immune thrombocytopenia (ITP) to be thought as no specific tests or markers are available for this entity and its diagnosis is largely clinical. A further work up complemented by bone marrow examination and in few cases a platelet function test will definitely help in reaching the final diagnosis.
So, summarizing, in the evaluation of a case of thrombocytopenia, all the
Thrombotic Microangiopathies are diverse group of disorders wherein thrombocytopenia, hemolytic anemia and organ dysfunction such as Kidney and brain occur . Major recent advances in this field have occurred which opens up oppurtunities to effectively manage its clinical challenges .
- A new version of this lecture is available at: https://www.slideshare.net/MohammedGawad/thrombotic-microangiopathy-tma-in-adults-and-acute-kidney-injury-dr-gawad
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Thrombotic Microangiopathy (TMA) in Adults and Acute Kidney Injury - Dr. GawadNephroTube - Dr.Gawad
- English version of this lecture is available at:
https://youtu.be/zrFm0hAZk2A
- Arabic version of this lecture is available at:
https://youtu.be/M_BV8WJVbx0
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Dr Abdullah Ansari
MBBS, MD Medicine
Aligarh Muslim University
Clinical case
Hemolytic Anemia
Intravascular vs extravascular hemolysis
Classification of hemolytic anemia
Approach to hemolysis
Patient history
Clinical features
Peripheral blood smear
Investigation
Treatment
Thrombocytopenia is generally defined as platelet count <150 × 109/L. It can occur due to several reasons, like decreased platelet production (e.g., inherited bone marrow failure syndromes, acquired aplastic anemia, leukemia), ineffective platelet production (myelodysplastic syndrome, megaloblastic anemia), increased destruction (ITP, HLH), increased consumption (DIC, TTP, HUS), sequestration (hypersplenism), or may be due to combination of multiple mechanisms described above.
During evaluating a case of thrombocytopenia, the first step is getting a detailed history and doing a proper clinical examination. Then the next step would be checking the other parameters of complete blood count (CBC), especially hemoglobin (Hb) and the total WBC count, complemented by a peripheral smear (PS) examination, which will clear many doubts and will help us pinpointing our diagnostic approach.
Many a times pseudo-thrombocytopenia is encountered in a PS due to platelet clumping by EDTA and can be rectified by collecting blood samples in a citrate or heparin vials or by doing a direct finger prick smear. Any accompanying cytopenia will expand the differential diagnosis and an isolated thrombocytopenia will further narrow it down. Presence of any additional abnormalities of red cells (megaloblasts) or white cells (presence of hyper-segmented neutrophils, atypical lymphoid/myeloid cells) could be present in megaloblastic anemia/MDS, leukemia respectively, while in the presence of fragmented red cells microangiopathic hemolytic anemia should always be ruled out by doing PT and aPTT (DIC, TTP, HUS). In case of isolated thrombocytopenia, the platelet morphology is also important. In many patients in India, especially in eastern region many people have large platelets with their normal platelet count around 100 × 109/L with normal platelet function (Harris platelet syndrome). However, presence of any abnormal platelet morphology along with a low platelet count may indicate a platelet function disorder (large platelets in Bernard Soulier syndrome/ Glanzmann thrombasthenia or small platelets in Wiskott-Aldrich syndrome), especially if encountered in early part of life during evaluation for bleeding symptoms. In case of isolated thrombocytopenia, presence of additional congenital anomalies may point out towards an inherited marrow failure syndrome, e.g. amegakayocytic thrombocytopenia. Exposure to certain drugs may result in isolated low platelet count, e.g., ceftriaxone, piperacillin, heparin. Presence of toxic changes in neutrophils may indicate sepsis related thrombocytopenia. By excluding all these, immune thrombocytopenia (ITP) to be thought as no specific tests or markers are available for this entity and its diagnosis is largely clinical. A further work up complemented by bone marrow examination and in few cases a platelet function test will definitely help in reaching the final diagnosis.
So, summarizing, in the evaluation of a case of thrombocytopenia, all the
download link : https://www.dropbox.com/s/xc0fpdul47g1gu8/IgA%20Nephropathy.ppt?m
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Hemolytic Uremic Syndrome: A Dangerous Complication of E. coliBill Marler
In this presentation provided by the nation's foremost food poison law firm - Marler Clark, Hemolytic Uremic Syndrome (HUS) is explained. HUS is a rare and highly dangerous result of an E. coli infection and can result in acute kidney failure
download link : https://www.dropbox.com/s/xc0fpdul47g1gu8/IgA%20Nephropathy.ppt?m
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Hemolytic Uremic Syndrome: A Dangerous Complication of E. coliBill Marler
In this presentation provided by the nation's foremost food poison law firm - Marler Clark, Hemolytic Uremic Syndrome (HUS) is explained. HUS is a rare and highly dangerous result of an E. coli infection and can result in acute kidney failure
An update of this lecture is available at: https://www.slideshare.net/MohammedGawad/membranous-nephropathy-234601451
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Chronic lymphocytic thyroiditis (hashimoto thyroiditis, autoimmuneDr. Saad Saleh Al Ani
Chronic lymphocytic thyroiditis (Hashimoto Thyroiditis ) The most common cause of thyroid disease in children and adolescents and the most common cause of acquired hypothyroidism, with or without goiter. Approximately 60% of infiltrating lymphoid cells are T cells, and approximately 30% express B-cell markers.A variety of different thyroid antigen autoantibodies are involved
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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- Video recording of this lecture in English language: https://youtu.be/gnlRvJ1TTr8
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- Video recording of this lecture in English language: https://www.youtube.com/watch?v=MA7nU5NWL2g&list=PLL7Q08IoVDSpg0VlGdvCHOHbXqMs0GFRe
- Video recording of this lecture in Arabic language: https://www.youtube.com/watch?v=FiWabzTPFqY&list=PLL7Q08IoVDSrVcm6SmppQyefL_Ub2-xGY
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
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- Recorded video of this lecture is available at:
https://youtu.be/4MCu1C5xjvE
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- Recorded videos of this lecture:
English Language version of this lecture is available at: https://youtu.be/YT5IlPs6F0I
Arabic Language version of this lecture is available at: https://youtu.be/HUZt4ahXlxo
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- English version of this lecture is available at:
https://youtu.be/V3UGzJTwAWw
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https://youtu.be/hGLaUde2ue4
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- English version of this lecture is available at:
https://youtu.be/t7N2GSXhYwA
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https://youtu.be/WzFZym9hDtQ
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- English version of this lecture is available at:
https://youtu.be/XRD-QqGFP18
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https://youtu.be/c9PoavAtNKM
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Infection-related Glomerulonephritis (KDIGO 2021 Guidelines) - Dr. GawadNephroTube - Dr.Gawad
- English version of this lecture is available at:
https://youtu.be/qItQlXUC2-Q
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- English version video of this lecture is available at:
https://youtu.be/z9P_1IiFR5I
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https://youtu.be/qmDeWgsAY9Q
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- English version of this lecture is available at:
https://youtu.be/lvcXwE0fb-w
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- English version of this lecture is available at: https://youtu.be/_Efu52kZRS4
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- English version of this lecture is available at: https://youtu.be/WHu05hmExBY
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Insights from the FIGARO-DKD and FIDELIO-DKD trials - Dr. GawadNephroTube - Dr.Gawad
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Diabetes Mellitus Management in CKD (Clinical Tips) - Dr. GawadNephroTube - Dr.Gawad
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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.
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
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.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
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
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
Phone Us ❤85270-49040❤ #ℂall #gIRLS In Surat By Surat @ℂall @Girls Hotel With...
Hemolytic Uremic Syndrome Induced AKI (From Pathogenesis to Bedside) - Dr. Gawad
1. Hemolytic Uremic Syndrome
Induced AKIh
From Pathogenesis to Bedside
Mohammed Abdel Gawad
Nephrologist
Kidney & Urology Center (KUC)
Alexandria – EGY
drgawad@gmail.com
2. To download the lecture
with full animations please
contact me on
drgawad@gmail.com
Visit
www.NephroTubeCNE.com
for more lectures
3. What is meant by Thrombotic Microangiopathy
(TMA)?
What are the causes of TMA?
What is the mechanism of TMA in HUS?
What is the diagnostic approach of HUS & TMA?
What are the treatment protocols of HUS?
19
Talk Outline
4. What is meant by Thrombotic Microangiopathy
(TMA)?
What are the causes of TMA?
What is the mechanism of TMA in HUS?
What is the diagnostic approach of HUS & TMA?
What are the treatment protocols of HUS?
19
Talk Outline
5. What is meant by Thrombotic
Microangiopathy (TMA)?
Intraluminal platelet thrombosis
Thrombocytopenia
Microangiopathic hemolytic
anemia
Consumption of
platelets
Hemolysis, Anemia, ↑LDH &
Bilirubin
119
6. What is meant by Thrombotic Microangiopathy
(TMA)?
What are the causes of TMA?
What is the mechanism of TMA in HUS?
What is the diagnostic approach of HUS & TMA?
What are the treatment protocols of HUS?
Talk Outline
19
8. What is meant by Thrombotic Microangiopathy
(TMA)?
What are the causes of TMA?
What is the mechanism of TMA in HUS?
What is the diagnostic approach of HUS & TMA?
What are the treatment protocols of HUS?
QuestionsTalk Outline
18
9. What is the mechanism of
TMA in HUS?
Intraluminal platelet thrombosis
Thrombocytopenia
Microangiopathic hemolytic
anemia
Consumption of
platelets
Hemolysis, Anemia, ↑LDH &
Bilirubin
18
12. E. coli (STEC)
S. dysenteriae
`
watery or most
often bloody
diarrhea
`
Mead PS, Griffin PM. Lancet.1998;352:1207-1212.
Ruggenenti P, Remuzzi G.Lancet. 2011;378:1057-1058.
Shiga Toxin
Associated HUS
E.Coli:
Mostly the serotype O157:H7,
but also other serotypes, such
as O111:H8, O103:H2, O123,
O26, O145, and the O104:H4
strain of the recent German
outbreak
18
13. E. coli (STEC)
S. dysenteriae
watery or most
often bloody
diarrhea
Mead PS, Griffin PM. Lancet.1998;352:1207-1212.
Ruggenenti P, Remuzzi G.Lancet. 2011;378:1057-1058.
Shiga Toxin
Associated HUS
Shiga Toxin
Associated HUS
17
14. Shiga Toxin
Associated HUS
E. coli (STEC)
S. dysenteriae
watery or most
often bloody
diarrhea
Complement
activation by
alternative
pathway:
High plasma
levels of
complement
activation
products
Bb and C5b-9
were
measured in
children with
STEC-HUS
Morigi M et al. Blood. 2001;98:1828-1835.
Morigi M et al. J Immunol. 2011;187:172-180.
Shiga Toxin
Associated HUS
16
16. Neuraminidase
Associated HUS
In infants and children. Complicate pneumonia, or less
frequently, meningitis caused by S. pneumoniae
erythrocytes, platelets,
glomerular cells
Polyagglutination
Brandt J, Wong C, Mihm S, et al. Pediatrics. 2002;110:371-376.
8
Thomsen-Friedenreich antigen
Coomb’s +ve
20. Atypical HUS
Caprioli J et al. Blood. 2006;108:1267-1279.
Manuelian T, et al. J Clin Invest. 2003;111:1181-1190.
Noris M, N Engl J Med. 2009;361:1676-1687.
Atypical HUS
Genetic mutation Precipitants of aHUS:
•Non-enteric bacterial and viral
Infections
•Immunotherapeutic agents (e.g.,
cyclosporine, tacrolimus)
•Malignant hypertension
•Transplantation
•Pregnancy
About 50% of patients with
sporadic aHUS show no
clear trigger (idiopathic HUS)
13
21. Atypical HUS
Caprioli J et al. Blood. 2006;108:1267-1279.
Manuelian T, et al. J Clin Invest. 2003;111:1181-1190.
Dragon-Durey et al. J Am Soc Nephrol. 2005;16:555-563.
Atypical HUS
Genetic mutation
Acquired defects
of CFH function
(inhibitory
antibodies),
reported in 5% to
10% of aHUS
13
23. Intraluminal platelet thrombosis
Thrombocytopenia
Consumption of
platelets Shiga toxin HUS
Atypical HUS
What is the mechanism of
TMA in TTP-HUS?
What is the mechanism of
TMA in HUS?
Neuraminidase HUS
Toxin binds
endothelium
N’ase
Alternative
Complement
12
27. What is meant by Thrombotic Microangiopathy
(TMA)?
What are the causes of TMA?
What is the mechanism of TMA in HUS?
What is the diagnostic approach of HUS & TMA?
What are the treatment protocols of HUS?
QuestionsTalk Outline
11
28. Marie Scully et al. British Journal
of Haematology, 2012, 158, 323–
335.
,HIV
DD of
thrombocytopenia
& MAHA
Systematic Approach of
Diagnosis
11
29. Marie Scully et al. British Journal
of Haematology, 2012, 158, 323–
335.
Systematic Approach
of Diagnosis
Step 1 –
Exclude Drugs
Systematic Approach of
Diagnosis
10
31. - Marie Scully et al. British Journal of Haematology, 2012, 158, 323–335.
- Patton JF et al. Am J Hematol. 1994;47:94-99.
Systematic Approach
of Diagnosis
Step 2 – Autoimmune
Hemolysis
Step
3
10
Systematic Approach of
Diagnosis
32. - Marie Scully et al. British Journal of Haematology, 2012, 158, 323–335.
- Patton JF et al. Am J Hematol. 1994;47:94-99.
Systematic Approach
of Diagnosis
Step 2 – Autoimmune
Hemolysis
Step
3
10
Systematic Approach of
Diagnosis
34. Systematic Approach
of Diagnosis
Step 4 – Exclude other causes
8
Systematic Approach of
Diagnosis
DD Suggestive Criteria
Malignant
Hypertension
• Systolic BP >200 mmHg, diastolic BP >130 mmHg.
• MAHA and thrombocytopenia resolves with BP management.
Pre-
eclampsia
• New BP elevation and proteinuria after 20 weeks of
gestation in a pregnant woman.
Sepsis
• Hypotension
• More pronounced fever
• Raised white count with left shift.
• Blood cultures might be positive.
Pregnancy • Must be excluded.
Autoimmune
Disease
• ANA, RF, antiDNA, ACLA, lupus anticoagulant
37. Systematic Approach
of Diagnosis
Step 4 – Exclude other causes
• TMA has been reported in
association with acute pancreatitis.
• Sometimes a number of days
after resolution of pancreatitis.
• All patients were successfully
treated with PEX and
corticosteroids (McDonald et al,
2009).
An association between
thrombocytopenia and
thyrotoxicosis has been
reported
7
Systematic Approach of
Diagnosis
39. Systematic Approach
of Diagnosis
Shiga toxin-
HUS
Neuraminidase
-HUS
- Less than 2 years old
- Respiratory distress,
neurologic
involvement,
and coma.
Mead PS, Griffin PM. Lancet. 1998;352:1207-1212.
Step 5 – TTP vs HUS
6
Systematic Approach of
Diagnosis
- Occurs primarily in children, (except
in epidemics with any age)
-Watery or bloody diarrhoea.
- Stool Culture: detection of E. coli
O157:H7 and other STEC and their
products in stool cultures (sorbitol-
containing MacConkey agar - SMAC)
40. Systematic Approach
of Diagnosis
Shiga toxin-
HUS
Neuraminidase
-HUS
- Less than 2 years old
- Respiratory distress,
neurologic
involvement,
and coma.
Mead PS, Griffin PM. Lancet. 1998;352:1207-1212.
Step 5 – TTP vs HUS
6
Systematic Approach of
Diagnosis
- Occurs primarily in children, (except
in epidemics with any age)
-Watery or bloody diarrhoea.
- Stool Culture: detection of E. coli
O157:H7 and other STEC and their
products in stool cultures (sorbitol-
containing MacConkey agar - SMAC)
41. Systematic Approach
of Diagnosis
Neuraminidase
-HUS
- Less than 2 years old
- Respiratory distress,
neurologic
involvement,
and coma.
Mead PS, Griffin PM. Lancet. 1998;352:1207-1212.
Step 5 – TTP vs HUS
6
Systematic Approach of
Diagnosis
43. Systematic Approach
of Diagnosis
Atypical HUS TTP
Step 5 – TTP vs HUS
Difficult to distinguish on clinical grounds only
Moschcowitz E. Mt Sinai J Med. 2003;70:352-355.
5
Systematic Approach of
Diagnosis
44. Systematic Approach
of Diagnosis
Atypical HUS TTP
Step 5 – TTP vs HUS
Difficult to distinguish on clinical grounds only
Differential diagnosis of aHUS is made on exclusion:
• Of infections by STEC or neuraminidase - producing
S.pneumoniae,
• Of ADAMTS13 deficiency,
• Of Systemic-associated diseases
5
Systematic Approach of
Diagnosis
45. Systematic Approach
of Diagnosis
Atypical HUS TTP
Step 5 – TTP vs HUS
Difficult to distinguish on clinical grounds only
Moschcowitz E. Mt Sinai J Med. 2003;70:352-355.
Eknoyan G, Riggs SA. Am J Nephrol. 1986;6:117-131. 5
Systematic Approach of
Diagnosis
46. Systematic Approach
of Diagnosis
Step 1: Exclusion of drugs
Step 2: Exclusion of Autoimmune hemolysis
Step 3: Coagulation Profile
Step 4: Exclusion of other systemic causes
Step 5: TTP vs HUS?
5
Systematic Approach
of Diagnosis
Diagnosis
Message
47. What is meant by Thrombotic Microangiopathy
(TMA)?
What are the causes of TMA?
What is the mechanism of TMA in HUS?
What is the diagnostic approach of HUS & TMA?
What are the treatment protocols of HUS?
Questions
4
Talk Outline
48. Shiga Toxin
Associated HUS
E. coli (STEC)
S. dysenteriae
watery or most
often bloody
diarrhea
Ruggenenti P, Remuzzi G.Lancet. 2011;378:1057-1058.
Morigi M et al. J Immunol. 2011;187:172-180.
4
Complement
activation by
alternative
pathway:
High plasma
levels of
complement
activation
products
Bb and C5b-9
were
measured in
children with
STEC-HUS
49. Shiga Toxin Associated HUS
Treatment
Generally Supportive (including RRT if required)
No role for Anticoagulation
No role for Antitimotility agents
4
IV isotonic volume expansion
(as soon as an E. coli O157:H7 infection is suspected),
limit the severity of AKI and the need for RRT
Ake JA et al. Pediatrics. 2005;115:e673-e680
50. Generally Supportive (including RRT if required)
No role for Antibiotics except:
1.Patients presenting with bacteremia
2.HUS, hemorrhagic colitis and HUS caused by Shigella
dysentery type 1
3.Azithromycin had some benefit on the duration of bacterial
shedding in adult patients from the German O104:H4
epidemic
Shiga Toxin Associated HUS
Treatment
3
Nitschke M et al. JAMA. 2012;307:1046-1052.
Van Dyck M, et al. Pediatr Nephrol. 2004;19:688-690.
51. Generally Supportive (including RRT if required)
Is there a role for plasma exchange?
No prospective RCTs are available
ADULT patients with severe AKI and CNS involvement
plasma therapy may decrease overall mortality of STEC
O157:H7–associated HUS.
Dundas S et al. Lancet. 1999;354:1327-1330.
Carter AO et al. N Engl J Med. 1987;317:1496-1500.
Shiga Toxin Associated HUS
Treatment
3
52. Atypical HUS
Caprioli J et al. Blood. 2006;108:1267-1279.
Manuelian T, et al. J Clin Invest. 2003;111:1181-1190.
2
Genetic mutation
Acquired defects
of CFH function
(inhibitory
antibodies),
reported in 5% to
10% of aHUS
53. Atypical HUS Treatment
2
When to start? within 24 hours of diagnosis
Frequency: daily initially, then determined by clinical
response
Plasma exchange (1 to 2 plasma volumes/day)
vs Plasma infusion (20 to 30 ml/kg/day)
54. Atypical HUS Treatment
Plasma exchange (1 to 2 plasma volumes/day)
vs Plasma infusion (20 to 30 ml/kg/day)
Plasma Exchange is superior to Infusion:
1.Supply larger amounts of plasma while avoiding fluid
overload.
2.Removal of mutant CFH.
3.Remove anti-CFH antibodies, but the effect is usually
transient.
Noris M, Remuzzi G. N Engl J Med. 2009;361:1676-1687.
Dragon-Durey MA, et al. J Am Soc Nephrol. 2005;16:555-563.
2
55. Atypical HUSAtypical HUS
Marina Noris. N Engl J Med 2009;361:1676-87
M. Kathryn Liszewski. The Rheumatologist, February 2010 1
56. Atypical HUSAtypical HUS
Marina Noris. N Engl J Med 2009;361:1676-87
M. Kathryn Liszewski. The Rheumatologist, February 2010
MCP is expressed on the surface of all cells (except RBC)
1
57. Atypical HUS Treatment
Immunosuppressants (corticosteroids
and azathioprine or mycophenolate mofetil)
combined with plasma exchange allowed long-
term dialysis-free survival in 60% to 70% of
patients.
Dragon-Durey MA et al. J Am Soc Nephrol. 2010;21:2180-2187.
Plasma exchange
1
58. Atypical HUS Treatment
Licht C et al. J Am Soc Nephrol. 2011;22:197A.
Greenbaum LA et al. J Am Soc Nephrol. 2011;22:197A.
1
Atypical HUS Treatment
Duration of therapy??
Cost??
59. Atypical HUSAtypical HUS
0
Living related donation is contraindicated given the high risk of
recurrence
Living related donation may be risky to donors because
uninephrectomy may precipitate aHUS in complement gene
mutation carriers.