Patent Ductus Arteroisus, PDA, Cardiology, Paediatrics, Pedicatrics, Critical Care, Emergency medicine, Medicine, Internal Medicine, MBBD, MD, India, CMC Vellore, Christian Medical College
Patent Ductus Arteroisus, PDA, Cardiology, Paediatrics, Pedicatrics, Critical Care, Emergency medicine, Medicine, Internal Medicine, MBBD, MD, India, CMC Vellore, Christian Medical College
In cases of right atrial enlargement the duration of the P wave hardly changes, but the P-R interval increases, so that the P--R segment ratio falls below the normal range.Left atrial enlargement, on the other hand,does not affect the P-R interval, but the P wave lengthens at the expense of the P-R segment.The result is a- ratio above P-R segment the normal maximal limit of 1.6.In combined atrial enlargement, both P-R interval and P wave are prolonged. It follows that in such cases the ratio may P-R segment
be normal.
Patent ductus arteriosus (PDA) is a congenital disorder in the heart wherein a neonate's ductus arteriosus fails to close after birth. Early symptoms are uncommon, but in the first year of life include increased work of breathing and poor weight gain. With age, the PDA may lead to congestive heart failure if left uncorrected. The ductus arteriosus is a normal fetal blood vessel that closes soon after birth. In a patent ductus arteriosus (PDA) the vessel does not close and remains "patent" (open) resulting in irregular transmission of blood between two of the most important arteries close to the heart, the aorta and the pulmonary artery. PDA is common in neonates with persistent respiratory problems such as hypoxia, and has a high occurrence in premature children. In hypoxic newborns, too little oxygen reaches the lungs to produce sufficient levels of bradykinin and subsequent closing of the DA. Premature children are more likely to be hypoxic and thus have PDA because of their underdeveloped heart and lungs.
A patent ductus arteriosus allows a portion of the oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta (which has higher pressure) to the pulmonary artery. If this shunt is substantial, the neonate becomes short of breath: the additional fluid returning to the lungs increases lung pressure to the point that the neonate has greater difficulty inflating the lungs. This uses more calories than normal and often interferes with feeding in infancy. This condition, as a constellation of findings, is called congestive heart failure.
In some cases, such as in transposition of the great vessels (the pulmonary artery and the aorta), a PDA may need to remain open. In this cardiovascular condition, the PDA is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the patent ductus arteriosus open
In cases of right atrial enlargement the duration of the P wave hardly changes, but the P-R interval increases, so that the P--R segment ratio falls below the normal range.Left atrial enlargement, on the other hand,does not affect the P-R interval, but the P wave lengthens at the expense of the P-R segment.The result is a- ratio above P-R segment the normal maximal limit of 1.6.In combined atrial enlargement, both P-R interval and P wave are prolonged. It follows that in such cases the ratio may P-R segment
be normal.
Patent ductus arteriosus (PDA) is a congenital disorder in the heart wherein a neonate's ductus arteriosus fails to close after birth. Early symptoms are uncommon, but in the first year of life include increased work of breathing and poor weight gain. With age, the PDA may lead to congestive heart failure if left uncorrected. The ductus arteriosus is a normal fetal blood vessel that closes soon after birth. In a patent ductus arteriosus (PDA) the vessel does not close and remains "patent" (open) resulting in irregular transmission of blood between two of the most important arteries close to the heart, the aorta and the pulmonary artery. PDA is common in neonates with persistent respiratory problems such as hypoxia, and has a high occurrence in premature children. In hypoxic newborns, too little oxygen reaches the lungs to produce sufficient levels of bradykinin and subsequent closing of the DA. Premature children are more likely to be hypoxic and thus have PDA because of their underdeveloped heart and lungs.
A patent ductus arteriosus allows a portion of the oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta (which has higher pressure) to the pulmonary artery. If this shunt is substantial, the neonate becomes short of breath: the additional fluid returning to the lungs increases lung pressure to the point that the neonate has greater difficulty inflating the lungs. This uses more calories than normal and often interferes with feeding in infancy. This condition, as a constellation of findings, is called congestive heart failure.
In some cases, such as in transposition of the great vessels (the pulmonary artery and the aorta), a PDA may need to remain open. In this cardiovascular condition, the PDA is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the patent ductus arteriosus open
Natural history of common congenital heart diseasesRamachandra Barik
Most infants with ASDs are asymptomatic
They may present at 6 to 8 weeks of age with a soft systolic ejection murmur and possibly a fixed and widely split S2
CHF rare in the first decades of life but it can become common once the patient is older than 40 yrs
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
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
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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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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
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.
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
1. Patent Ductus Arteriosus
Ramachandra
The bottle neck of large PDA:Occasional missed large PDAs with or without
Eisenmenger syndrome by even renowned cardiologist.
2. Time line
1939:Surgical ligation by Gross and Hubbard
1980:Maturation stages of ductus by
Gittenberger-De Groot AC et.al
1989: Krichenko A, Benson LN, Burrows P, et al:
classification
1967:First transcatheter closure by Portsmann
and coworkers
1979:doubleumbrella device by Rashkind
2003:Amplatzer device
3. Define
If ductus remains patent beyond 3 months of
life in full-term infants and beyond 1 year in
premature infants, it is termed persistent
PDA
4. Signature of PDA
• Most of them small
• Seesaw murmur
• TTE is enough for Dx and Rx
• PDA with noise needs closure
• Percutaneus closure is Rx-98% success
• No IE prophylaxis
5. Foetal Life
PDA is life thread in normal developing heart
like
part of series connection in electrical circuit
shunting 60-70% oxygenated umbilical venous
return to aorta
6. Post natal
After birth the duct closes functionally in 12 to
18 hours and anatomically in 2 to 3 weeks.
7. Embryology
day 29 6th
aortic /pulmonary arch develops
8th
week of gestation, the ventral portions of the RT
and LT 6th
AA form the proximal part of the RPA and
the proximal part of LT MPA ,respectively. The dorsal
portion of the right sixth arch is obliterated along with
the right dorsal aorta. Sometimes the dorsal portion
of the left 6th
arch persists as a vascular conduit
called PDA arising from the roof of the junction
between the main and LPA and joining the left dorsal
aorta just distal to the LSCA in normal left-sided aorta
8. Anatomy
• Usually LPDA
• PDA and DTA angle at junction is 30 degree
• Angiographic class: A to E (90 degree LL) by
Krichenko & colleagues®
• 80% of PDA : A or B, Rx=Percutaneus closure
• Siblings: Reverse , Rt AA,aneurysm
•
9. Krichencko et.al:1989
• Angiography
• Dead left lateral
• Left angiograms
• Types
– A:conical
– B:window(L< 2 to 3 mm)
– C:Tubular(both ends narrowing)
– D:complex(multiple narrowing)
– E :Elongated=a beaklike constriction at the
pulmonary end
10. Hemodynamic classification
• Small PDA :QP:QS <1.5 to 1
• moderate PDA: QP:QS :1.5 and 2.2 to 1
• large PDA:QP:QS >2.2 to 1.43
• silent PDA :shunt is minimal/no murmur
detected on echocardiography
11. Reverse PDA
• Pulmonary atresia
• Tricuspid atresia
• Inferior angle near 90 degree OK but if <60
deree ,needs ductal stenting
12. Ductal aneurysm
90% spontaneous closure except large size
causing pressure effect
Up to 8% reported of all PDA
13. Phenotypes
Rt-sided PDA X RPA to the RT DTA
LPDA X RT Brachiocephalic A.
LSCA X LPA
Dual PDA
LPDA from LSCA
Vascular ring: SCA from RT DTA and runs behind
the trachea and esophagus, forming a around
them by the right aortic arch anteriorly, and to
the RT,the LSCA at the back and the PDA to the
left.
15. Physiology in foetus
• Life thread
• Tunnels 70% saturate blood into DA
• Only 7% of volume enters unexpanded lungs
• Patency:Immature duct,low O2 ,high O2/PGE-2
from placenta
• Functional closure:15th
day
• Anatomical closure:21st
day=placenta turn off,
high O2 stops Ik ,intracellular ca2+ increase add
to spasm in mature duct
19. Pathophysiology
Small PDA :asymptomatic throughout life.Accidental detection by ECHO
for murmur
Moderate PDA:compensate well throughout childhood and may
remain completely asymptomatic in early adulthood but will eventually
present with exercise intolerance and symptoms related to left ventricular
failure, usually starting in the third decade.
Moderate to large:Large volume of blood leads to the very early
development of pulmonary congestion,decreased lung compliance, and
failure of the left ventricle, often presenting within weeks after birth with
failure to thrive, recurrent pulmonary infections, and even death.
Pulmonary overcirculation remains uncorrected,the arteriolar medial
hypertrophy, intimal proliferation,and eventual obliteration of pulmonary
arterioles and capillaries will lead to an irreversible marked increase in
pulmonary arterial pressure. When pulmonary vascular resistance
exceeds the systemic vascular resistance, ductal shunting is reversed and
becomes right to left (Eisenmenger syndrome)
20. Natural History
• Spontaneous closure may be delayed until 3
months of life, after which the closure rate is
less than 0.6%/Yr
• Silent PDA remain undetected for life
• premature :Closure could be delayed up to
1 year and more PDA
• Sibling :1% and 5%
• Parents:3%
21. Physical Examination
• Small PDA:Gr-II/III continuous murmur engulfing
and peaking around S2
• Thrill :moderate to large PDA
• S1 normal,S2 usual split with P2 accentuated
• S3 and diastolic rumble : moderate/ large PDA
• Eisenmenger syndrome:P2 loud/PSL/Graham
Still’s murmur
• wide pulse :large shunt
• Cyanosis/clubbing: Eisenmenger
23. Chest Radiograph
• Small PDA: normal
• moderate to large: increased pulmonary
vascular markings with prominent ascending
aorta, and enlarged cardiac silhouette with
prominence of the left atrium, left Ventricle
and peripheral pruning
• Calcification
24. ECHO
• TTE allows the assessment of ductal
size,geometry, the degree of shunt, and
pulmonary artery pressures
• A left atrium/aorta ratio greater than 1.3/1 is
considered to be a reliable marker of a
hemodynamically significant ductal shunt
• Shunt ratio: continuity equation
27. Class I closure
Evidence of volume overload on the left
atrium or left ventricle (LAE/LVH)
Development of PAH but the pressure and
the resistance still remain less than two-thirds
of the systemic levels
Endarteritis
28. Class IIa closure
Small PDAs with normal PA pressures and
normal heart size with a shunt ratio less than
1.5/1 or followed with repeat evaluations
every 3 to 5 year
33. The basic of transcathetor technique
• Coils :Retrograde aortic
• Device :Antegrade veno-arterial
• 7Fr venous and 6Fr arterial sheath
• Pigtail angio in dead left lateral to decide
• Device size is 2mm more than PA end
• Cross with multipurpose and Terumo
• Confirm with repeat angio
• 6month F/U SBE prophylaxis
34. Success story of TCC
• ADO is 99%
• immediate closure at the time of
implantation of 76%
• day 1 of 89%
• 6 to 12 months of 99% by echocardiography.