Mitral stenosis is commonly caused by rheumatic heart disease which leads to inflammation and fusion of the mitral valve leaflets, reducing the mitral valve orifice area. Severe mitral stenosis, defined as a mitral valve area less than 1.0 cm2, can cause pulmonary hypertension, pulmonary edema, atrial fibrillation, and right heart failure as the heart tries to maintain sufficient cardiac output against the back pressure. Physical exam may reveal signs of pulmonary hypertension like a loud pulmonary component to S2, as well as a tapping apex, opening snap, and mid-diastolic rumble on cardiac auscultation. Echocardiography can determine the severity of mitral stenosis and assess
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definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
Kindly leave your comment if you found this helpful ;)
Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
These are cardiac anomalies arising as a result of a defect in the structure or function of the heart and great vessels which is present at birth
These lesions either obstruct blood flow in the heart or vessels near it, or alter the pathway of blood circulating through the heart
These are cardiac anomalies arising as a result of a defect in the structure or function of the heart and great vessels which is present at birth
These lesions either obstruct blood flow in the heart or vessels near it, or alter the pathway of blood circulating through the heart
This presentation gives a fine description about stoma and ostomy. This contains the details regarding types, complications and the advices that you should give to a patient with a stoma.
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
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
- 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
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
3. Mitral stenosis
• Commonest cause :rheumatic heart
disease
• Infections with group A beta hemolytic
streptococci
• More common in women
• Inflammation leads to commissural
fusion and a reduction in mitral valve
orifice area
JMJ 3
4. Pathophysiology
• Normal valve area: 4-6 cm2
• Mild mitral stenosis:
– MVA 1.5-2.5 cm2
– Minimal symptoms
• Moderate mitral stenosis
– MVA 1.0-1.5 cm2 usually does not produce
symptoms at rest
• Severe mitral stenosis
– MVA < 1.0 cm2
JMJ 4
5. To maintain sufficient cardiac
output
1. Left arterial pressure increases
2. Left arterial hypertrophy and dilation
3. Pulmonary veins, pulmonary arterial and R/
heart pressure increases
4. Increase of pulmonary capillary pressure
5. Followed by development of
– pulmonary oedema
– Atrial fibrillation with tachycardia
– Loss of coordinated atrial contraction
JMJ 5
6. To maintain sufficient cardiac
output
6. This is prevented by (Reactive
pulmonary hypertension)
– Alveolar and capillary thickening
– Pulmonary arterial vasoconstriction
7. Pulmonary hypertension leads to
– R/ ventricular hypertrophy, dilation and
failure with subsequent tricuspid
regurgitation
JMJ 6
9. Mitral Stenosis: Physical
Exam
• First heart sound (S1) is accentuated & snapping
• Opening snap (OS) after aortic valve closure
• Low pitch diastolic rumble at the apex
• Pre-systolic accentuation (esp. if in sinus rhythm)
S1 S2 OS S1
10. Signs (Face)
• Severe mitral stenosis with pulmonary
hypertension
• Mitral fascies / malar rash
• Bilateral
• Cyanotic or dusky pink
discolouration
• Over the upper cheeks
• Due to atriovenous anastomosis &
• Vascular stasis
JMJ 10
11. Signs (Pulse)
• Small volume pulse
• Usually regular in early stages,
• If the patient is in sinus rhythem
• In severe disease, may develop atrial
fibrillation
• Irregularly irregular pulse
JMJ 11
12. Signs (Jugular Veins)
• If R heart failure develops
• obvious distension of jugular veins
• If pulmonary hypertension or tricuspid
stenosis is present
• ‘a’ Wave will be prominent
JMJ 12
13. Signs (Palpation)
• Tapping impulse felt parasternally on
left side
• Palpable 1st heart sound
• Combined with left ventricular backward
displacement
• Produced by an enlarging left ventricle
• Sustained parasternal impulse
• Due to R ventricular hypertrophy
JMJ 13
14. Signs (Auscultation)
• Loud 1st heart sound
– If the mitral valve is pliable
– It will not occur in calcified mitral stenosis
• Opening snap
– Valve suddenly opens with the force of the
increased L arterial pressure
• Low pitched ‘rumbling’ mid diastolic murmur
– Best heard with bell held lightly
– At the apex with the patient lying on the left side
JMJ 14
15. Signs (Auscultation)
• If the patient is in sinus rhythm
– Murmur becomes louder at the end of
diastole
– As a result of atrial contraction
– (Pre- systolic accentuation)
JMJ 15
16. How to determine the severity of
mitral stenosis
• Presence of pulmonary hypertension
– Recognized by R/ ventricular heave & loud
pulmonary component of 2nd heart sound
– And signs with R heart failure : Oedema,
hepatomegaly
– Graham Steell murmur
JMJ 16
17. How to determine the severity of
mitral stenosis
• Closeness of the opening snap to the 2nd
heart sound ∞ severe MS
• Length of mid-diastolic murmur ∞ severity
• As the valve cusps become immobile
– Loud 1st heart sound softens
– Opening snap diasppears
– When pulmonary hypertension occurs : P2
intensity increase, mid diastolic murmur
become quieter
JMJ 17
19. Investigations –X-ray
• Small heart with an enlarged L/ atrium
• Pulmonary venous hypertension
• Calcified mitral valve– on penetrated or
lateral view
• Signs of pulmonary oedema or pulmonary
hypertension
JMJ 19
20. Investigations –ECG
• Sinus rhythm in ECG shows a bifid P wave
– Owing to delayed L/atrial activation
• Atrial fibrillation may be present
• ECG features of R/ventricular hypertrophy
– Right axis deviation
– Perhaps tall R wave in lead V1
JMJ 20
23. Investigations –Echocardiogram
• Transthoracic echocardiography
– To determine L/ R/ atrial and ventricular
size
– The sevirity of MS
• Transoesophageal Echocardiography
(TOE)
– To detect the presence of L/ atrial
thrombus
JMJ 23
24. Treatment
• Need no treatment other than prompt therapy
of attacks of bronchitis
• Early symptoms like dyspnea - diuretics
• Onset of atrial fibrillation :digoxin,
anticoagulants (to prevent atrial thrombus and
systemic embolism)
• If pulmonary hypertension or symptoms of
pulmonary congestion : surgical therapy
JMJ 24
26. Treatment: Trans-septal balloon
valvotomy
• Catheter introduced into R atriam via femoral
vein
• Under local anasthesia
• Inter atrial septum is punctured
• Catheter enter into left atrium then to mitral
valve
• Balloon is inflated, briefly to split the valve
commissures
JMJ 26
28. Treatment: Trans-septal balloon
valvotomy
• Complications
– Regurgitation may result
• Contraindications
– Heavy calcification
– More than mild mitral regurgitation &
thrombus in the L/atrium
• TOE is done before this procedure
JMJ 28
29. Treatment: Closed valvotomy
• For the patients with
– mobile,
– non calcified and
– non regurgitant mitral valves
• Fused cusps forced apart by a dilator
(introduced through the apex of L/ ventricle)
• Cardiopulmonary bypass is not needed for this
operation
JMJ 29
30. Treatment: Open valvotomy
• Often preferred to closed valvotomy
• Cusps are carefully dissected apart
under direct vision
• Cardiopulmonary bypass is requied
JMJ 30
31. Treatment: Mitral valve replacement
• It is necessary if
– Mitral regurgitation is present
– Badly diseased or badly calcified stenotic
valve,
– Moderate or severe mitral stenosis &
thrombus in L atrium despite anticoagulation
• Artificial valve >20 yrs
• Anticoagulants are necessary
JMJ 31