The conotruncus comprises collectively two myocardial subsegments, the conus and the truncus.
Conus is the myocardial segment between ventricle and semi lunar valves which gives rise to sub arterial coni.
Truncus is the fibrous segment between semi lunar valves and aortic sac which gives rise to great arteries.
ECG localization of accessory pathways slideshareCardiology
This presentation is simplified view of accessory pathways in heart and their localization with help of algorithms and ECG examples. Try to read this PPT in power point to see full effects and animations.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
Our concepts of heart disease are based on the enormous reservoir of physiologic and anatomic knowledge derived from the past 70 years' of experience in the cardiac catheterization laboratory.
As Andre Cournand remarked in his Nobel lecture of December 11, 1956, the cardiac catheter was the key in the lock.
By turning this key, Cournand and his colleagues led us into a new era in the understanding of normal and disordered cardiac function in huma
The conotruncus comprises collectively two myocardial subsegments, the conus and the truncus.
Conus is the myocardial segment between ventricle and semi lunar valves which gives rise to sub arterial coni.
Truncus is the fibrous segment between semi lunar valves and aortic sac which gives rise to great arteries.
ECG localization of accessory pathways slideshareCardiology
This presentation is simplified view of accessory pathways in heart and their localization with help of algorithms and ECG examples. Try to read this PPT in power point to see full effects and animations.
AV nodal reentrant tachycardia (AVNRT), or atrioventricular nodal reentrant tachycardia, is a type of tachycardia (fast rhythm) of the heart. It is a type of supraventricular tachycardia (SVT), meaning that it originates from a location within the heart above the bundle of His. AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia. It is more common in women than men (approximately 75% of cases occur in females). The main symptom is palpitations. Treatment may be with specific physical maneuvers, medication, or, rarely, synchronized cardioversion. Frequent attacks may require radiofrequency ablation, in which the abnormally conducting tissue in the heart is destroyed.
AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferior and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node.
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW syndrome) or atrioventricular reciprocating tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium close to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings. They provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
Our concepts of heart disease are based on the enormous reservoir of physiologic and anatomic knowledge derived from the past 70 years' of experience in the cardiac catheterization laboratory.
As Andre Cournand remarked in his Nobel lecture of December 11, 1956, the cardiac catheter was the key in the lock.
By turning this key, Cournand and his colleagues led us into a new era in the understanding of normal and disordered cardiac function in huma
Generally occurs secondary to pulmonary atresia with intact IVS .
Pathophysiology- it develops because of a reduction in the blood flow secondary to inflow impedence from tricuspid atresia or outflow impedence from pulmonary arterial atresia .
Typical findings- a small , hypertrophic RV and a small or absent pulmonary artery
a cardiac surgery presentation about Atrioventricular septal defect,Definition, Prevalence,Anatomy,Classification,presentation ,diagnosis and management
Comparison between ct mri in ischemic stroke AHMED ESAWY
Comparison between ct MRI in ischemic stroke .1-Definition
2-Pathology
3-Vascular territory
4-Staging
5-hemorrhagic transformation of the infarct
Difference between simple hemorrhage and hemorrhagic neoplasm
difference between Hemorrhagic infarct and primary intracerebral hemorrhage
6-Comparison between CT/MRI
7-CTA, MRA
8-Fogging
9-Pseudonormalization
10-Protocol
11-Differential diagnosis
12-home message
All thing breast ultrasound breast mammography part 3AHMED ESAWY
All thing breast ultrasound breast mammography part 3
Breast mammogram ultrasound lipoma ,oil cyst ,galactocele intramammary lymph node in UOQ hamartoma Simple cyst (typical) calcification Surgical scar Breast implants, scirrhuc carcinoma lobular carcinoma Skin calcifications vascular calcifications Sutural Dystrophic popcorn Large Rod like rim Round/punctuate Fat necrosis Milk of calcium Fibrocystic FCC fibroadenosis Fat necrosis with oil cyst mastitis with Abscess Haematoma atypical ductal hyperplasia Intracystic papilloma ductal carcinoma in situ ,invasive ductal carcinoma BIRAD
All thing breast ultrasound breast mammography part 1AHMED ESAWY
All thing breast ultrasound breast mammography part 1
Breast mammogram ultrasound lipoma ,oil cyst ,galactocele intramammary lymph node in UOQ hamartoma Simple cyst (typical) calcification Surgical scar Breast implants, scirrhuc carcinoma lobular carcinoma Skin calcifications vascular calcifications Sutural Dystrophic popcorn Large Rod like rim Round/punctuate Fat necrosis Milk of calcium Fibrocystic FCC fibroadenosis Fat necrosis with oil cyst mastitis with Abscess Haematoma atypical ductal hyperplasia Intracystic papilloma ductal carcinoma in situ ,invasive ductal carcinoma BIRAD
Update secrets in plain x ray abdomen gases ,air fluid level .AHMED ESAWY
plain x-ray abdomen gas normal air fluid level in-the-abdomen gasless abdomen small bowel obstruction large intestinal obstruction ileus gastric dilatation extraluminal abdomen gas (pneumonpperitoneum) extraluminal abdomen gas(retropneumonpperitoneum gas in specific organs (hepatobiliary ,genitourinary) gasless abdomen ‘step-ladder apperance stretch/slit sign string of pearls sign coiled spring sign small-bowel feces sign disproportionate dilatation of sb gallstone ileus intussusception caecal volvulus sigmoid volvulus colonic pseudo obstruction ogilvie syndrome acute colitis toxic megacolon ischemic colitis sentinel loops intestinal pseudo-obstruction syndromes gastric volvulus organoaxial gastric volvulus mesenterico-axial right upper quadrant gas crescent sign: air beneath the diaphragm peri hepatic sub hepatic morrison’s pouch fissure for ligament teres doges cap sign rigler’s (double wall sign) ( both the serosal and the related mucosal walls of the bowel are delineated it means free air is at that serosal surface ) ligament visualization falciform ligament sign: air delineating the falciform ligament umbilical inverted ‘v’ sign triangular air cupola sign football sign or air dome (a large air collection beneath that does not confirm to any bowel loop) continous diaphragm sign scrotal air in children decubitus abdomen sign double bubble sign lesser sac sign peritonitis postoperative pelvic and spinal fractures
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
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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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
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.
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.
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.
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
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.
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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
2. ASD and PFO are different types of
interatrial defect
Septum primum forms first .it leaves window ,Ostium secundum
septum secundum forms later .usually covers Ostium secundum
3. Foramen ovale intrauterine allow blood to flow
From right to left by passing the lung
It closes after birth
But stays open in 25-28 % of people
4. If the septum secundum fails to cover the ostium secundum .blood
flow in both direction causing atrial septal defect OSD
Inferior limb
septum primum.
superior limb
septum primum.
superior limb
septum secundum.
inferior limb
septum secundum.
5. Patent Foramen Ovale
An interatrial communication between the superior limb of the septum secundum on the right side
the septum primum on the left atrial side .• The flap of the foramen ovale (FO) can often be seen
6. Foramen ovale is
defect in septum
secundum
Ostium Secundum
Atrial Septal Defect
Defect in the septum
primum.
9. ostium primum
ostium primum atrial septal defect is a defect in the atrial
septum at the level of the tricuspid and mitral valves
10.
11.
12. ASD and PFO can diagnosed by TEE but not excluded by it
No shunt seen by echo not mean that no PFO or small ASD
Defect Anterior to FO = primum defect (often w MV cleft)
Defect Post/Sup to FO = sinus venosus defects (often w anomalous R
pulm vn connection)
Ostium Primum Atrial Septal Defect :Located in the most anterior
and inferior aspects of the atrial septum. near the atrioventricular
valves
sinus venosus type ASD, situated near the entry of the SVC or IVC
13. Indication to close ASD
RV /RA enlarged
QP : QS more than 1.5
Paradoxical embolism
14. PATENT FORAMEN OVALE ASD OSTIUM
Right to left shunt Left to right shunt
normal or slightly elevated
pulmonary pressure,
pulmonary hypertension of different
degree,
normal Qp/Qs ratio , an increased Qp/Qs ratio
normal right chambers enlarged right chambers
ostium secundum ASD, placed in
the midportion of the septum in the
area of the fossa ovalis