The novel severe acute respiratory syndrome coronavirus (SARS-COV-2) affects different people in different ways. Most infected people will develop mild to moderate respiratory flu-like illness and recover without the need for hospitalization.
Certification and classification (coding) of Covid-19 as cause of death based ICF Education
International guidelines for certification and classification (coding) of Covid-19 as cause of death based on ICD international statistical classification of diseases (16 April 2020)
Covid 19 and the cardiovascular system implications for risk assessment dia...Ramachandra Barik
The novel coronavirus disease (COVID-19) outbreak, caused by SARS-CoV-2, represents the greatest medical challenge in decades. We provide a comprehensive review of the clinical course of COVID-19, its comorbidities, and
mechanistic considerations for future therapies. While COVID-19 primarily affects the lungs, causing interstitial
pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects multiple organs, particularly the
cardiovascular system. Risk of severe infection and mortality increase with advancing age and male sex. Mortality is
increased by comorbidities: cardiovascular disease, hypertension, diabetes, chronic pulmonary disease, and cancer.
The most common complications include arrhythmia (atrial fibrillation, ventricular tachyarrhythmia, and ventricular
fibrillation), cardiac injury [elevated highly sensitive troponin I (hs-cTnI) and creatine kinase (CK) levels], fulminant
myocarditis, heart failure, pulmonary embolism, and disseminated intravascular coagulation (DIC). Mechanistically,
SARS-CoV-2, following proteolytic cleavage of its S protein by a serine protease, binds to the transmembrane
angiotensin-converting enzyme 2 (ACE2) —a homologue of ACE—to enter type 2 pneumocytes, macrophages,
perivascular pericytes, and cardiomyocytes. This may lead to myocardial dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque instability, and myocardial infarction (MI). While ACE2 is essential for viral invasion, there is no evidence that ACE inhibitors or angiotensin receptor blockers (ARBs) worsen prognosis.
Hence, patients should not discontinue their use. Moreover, renin–angiotensin–aldosterone system (RAAS) inhibitors might be beneficial in COVID-19. Initial immune and inflammatory responses induce a severe cytokine storm
[interleukin (IL)-6, IL-7, IL-22, IL-17, etc.] during the rapid progression phase of COVID-19. Early evaluation and
continued monitoring of cardiac damage (cTnI and NT-proBNP) and coagulation (D-dimer) after hospitalization
may identify patients with cardiac injury and predict COVID-19 complications. Preventive measures
Certification and classification (coding) of Covid-19 as cause of death based ICF Education
International guidelines for certification and classification (coding) of Covid-19 as cause of death based on ICD international statistical classification of diseases (16 April 2020)
Covid 19 and the cardiovascular system implications for risk assessment dia...Ramachandra Barik
The novel coronavirus disease (COVID-19) outbreak, caused by SARS-CoV-2, represents the greatest medical challenge in decades. We provide a comprehensive review of the clinical course of COVID-19, its comorbidities, and
mechanistic considerations for future therapies. While COVID-19 primarily affects the lungs, causing interstitial
pneumonitis and severe acute respiratory distress syndrome (ARDS), it also affects multiple organs, particularly the
cardiovascular system. Risk of severe infection and mortality increase with advancing age and male sex. Mortality is
increased by comorbidities: cardiovascular disease, hypertension, diabetes, chronic pulmonary disease, and cancer.
The most common complications include arrhythmia (atrial fibrillation, ventricular tachyarrhythmia, and ventricular
fibrillation), cardiac injury [elevated highly sensitive troponin I (hs-cTnI) and creatine kinase (CK) levels], fulminant
myocarditis, heart failure, pulmonary embolism, and disseminated intravascular coagulation (DIC). Mechanistically,
SARS-CoV-2, following proteolytic cleavage of its S protein by a serine protease, binds to the transmembrane
angiotensin-converting enzyme 2 (ACE2) —a homologue of ACE—to enter type 2 pneumocytes, macrophages,
perivascular pericytes, and cardiomyocytes. This may lead to myocardial dysfunction and damage, endothelial dysfunction, microvascular dysfunction, plaque instability, and myocardial infarction (MI). While ACE2 is essential for viral invasion, there is no evidence that ACE inhibitors or angiotensin receptor blockers (ARBs) worsen prognosis.
Hence, patients should not discontinue their use. Moreover, renin–angiotensin–aldosterone system (RAAS) inhibitors might be beneficial in COVID-19. Initial immune and inflammatory responses induce a severe cytokine storm
[interleukin (IL)-6, IL-7, IL-22, IL-17, etc.] during the rapid progression phase of COVID-19. Early evaluation and
continued monitoring of cardiac damage (cTnI and NT-proBNP) and coagulation (D-dimer) after hospitalization
may identify patients with cardiac injury and predict COVID-19 complications. Preventive measures
all details explain about corona virus
corona virus slide
covid19 pandemic
epidemiology
pathogenesis
oral pathology
medicine
history
introduction
outbreak
prevent
drugs
test
steps taken by govt
Cardiovascular Disease Associated with SARS-CoV-2 and HIV InfectionsInsideScientific
Dr. Xuebin Qin discusses the development and characterization of new models of SARS-CoV-2 and HIV, and how his lab uses these models to study cardiovascular injury associated with infection.
Despite ongoing research around the world to better understand the pathogenesis of SARS-CoV-2, the ways in which it exacerbates cardiovascular disease (CVD) are not fully understood. While it is well accepted that SARS-CoV-2 infects lung epithelial cells, whether it can also infect endothelial cells is less clear.
In this webinar, Dr. Xuebin Qin discusses his lab’s development and characterization of new rodent models of COVID-19, and how they use these models to study endothelial dysfunction and injury resulting from immune activation. Dr. Qin also discusses why HIV infection is associated with increased risk of CVD. He provides an overview of the cellular and molecular mechanisms underlying HIV-1-associated CVD, and the mouse and NHP models he has worked with to elucidate them.
Key Topics Include:
- Cellular mechanisms by which SARS-CoV-2 and HIV contribute to cardiovascular disease
- Development, characterization and analysis of Mouse and NHP models for the study of COVID-19- or HIV-associated CVD
- Potential targets for therapeutic vaccine testing and pathogenesis studies
COVID-19 can cause lung complications such as pneumonia and, in the most severe cases, acute respiratory distress syndrome, or ARDS. Sepsis, another possible complication of COVID-19, can also cause lasting harm to the lungs and other organs.
Neurological Manifestations of COVID-19 InfectionSudhir Kumar
COVID-19 primarily affects respiratory system, however, it can affect other systems too, including nervous system. This presentation offers details about neurological symptoms and disorders seen in patients with COVID-19.
Origin of virus??
Transmission of virus??
First case in Wuhan?
Aerosol transmission? Fomites? Re- infection/ reactivation
Vaccine/ safety & efficacy/ antibody test/ community transmission?
Case definition?
Pathophysiology/ pathology
Cardiovascular manifestations/ risk?
ACS
Role of aspirin
Low platelet in covid-19
Anti-coagulants
ACEI/ARB/ARNI
Diuretics
Clinical features
High risk groups
Antibiotics
HCQ& Lopinavir, Ritonavir
Anti viral drugs- remdisivir/ favipiravir
Biological therapy- tocilizumab
Convalescent plasma therapy
Systemic steroids
Ivermectin
NSAIDs
Respiratory failure
Other management in covid 19- fluid/ nebulization
Chemoprophylaxis
Bronchial asthma
Anti diabetics
Patients with severe acute respiratory syndrome coronavirus 2 (SARS-Cov2) infection mainly present severe pneumonia associated with complications related to cytokine storm syndrome. So, it was associated with thrombotic incidents like acute limb ischemia and pulmonary embolism.
Patients with severe acute respiratory syndrome coronavirus 2 (SARS-Cov2) infection mainly present severe pneumonia associated with complications related to cytokine storm syndrome. So, it was associated with thrombotic incidents like acute limb ischemia and pulmonary embolism.
all details explain about corona virus
corona virus slide
covid19 pandemic
epidemiology
pathogenesis
oral pathology
medicine
history
introduction
outbreak
prevent
drugs
test
steps taken by govt
Cardiovascular Disease Associated with SARS-CoV-2 and HIV InfectionsInsideScientific
Dr. Xuebin Qin discusses the development and characterization of new models of SARS-CoV-2 and HIV, and how his lab uses these models to study cardiovascular injury associated with infection.
Despite ongoing research around the world to better understand the pathogenesis of SARS-CoV-2, the ways in which it exacerbates cardiovascular disease (CVD) are not fully understood. While it is well accepted that SARS-CoV-2 infects lung epithelial cells, whether it can also infect endothelial cells is less clear.
In this webinar, Dr. Xuebin Qin discusses his lab’s development and characterization of new rodent models of COVID-19, and how they use these models to study endothelial dysfunction and injury resulting from immune activation. Dr. Qin also discusses why HIV infection is associated with increased risk of CVD. He provides an overview of the cellular and molecular mechanisms underlying HIV-1-associated CVD, and the mouse and NHP models he has worked with to elucidate them.
Key Topics Include:
- Cellular mechanisms by which SARS-CoV-2 and HIV contribute to cardiovascular disease
- Development, characterization and analysis of Mouse and NHP models for the study of COVID-19- or HIV-associated CVD
- Potential targets for therapeutic vaccine testing and pathogenesis studies
COVID-19 can cause lung complications such as pneumonia and, in the most severe cases, acute respiratory distress syndrome, or ARDS. Sepsis, another possible complication of COVID-19, can also cause lasting harm to the lungs and other organs.
Neurological Manifestations of COVID-19 InfectionSudhir Kumar
COVID-19 primarily affects respiratory system, however, it can affect other systems too, including nervous system. This presentation offers details about neurological symptoms and disorders seen in patients with COVID-19.
Origin of virus??
Transmission of virus??
First case in Wuhan?
Aerosol transmission? Fomites? Re- infection/ reactivation
Vaccine/ safety & efficacy/ antibody test/ community transmission?
Case definition?
Pathophysiology/ pathology
Cardiovascular manifestations/ risk?
ACS
Role of aspirin
Low platelet in covid-19
Anti-coagulants
ACEI/ARB/ARNI
Diuretics
Clinical features
High risk groups
Antibiotics
HCQ& Lopinavir, Ritonavir
Anti viral drugs- remdisivir/ favipiravir
Biological therapy- tocilizumab
Convalescent plasma therapy
Systemic steroids
Ivermectin
NSAIDs
Respiratory failure
Other management in covid 19- fluid/ nebulization
Chemoprophylaxis
Bronchial asthma
Anti diabetics
Patients with severe acute respiratory syndrome coronavirus 2 (SARS-Cov2) infection mainly present severe pneumonia associated with complications related to cytokine storm syndrome. So, it was associated with thrombotic incidents like acute limb ischemia and pulmonary embolism.
Patients with severe acute respiratory syndrome coronavirus 2 (SARS-Cov2) infection mainly present severe pneumonia associated with complications related to cytokine storm syndrome. So, it was associated with thrombotic incidents like acute limb ischemia and pulmonary embolism.
Patients with severe acute respiratory syndrome coronavirus 2
(SARS-Cov2) infection mainly present severe pneumonia associated with complications related to cytokine storm syndrome. So, it
was associated with thrombotic incidents like acute limb ischemia
and pulmonary embolism.
We report 3 cases of COVID-19 infection complicated by arterial
thrombosis in the form of acute limb ischemia.
Patients with severe acute respiratory syndrome coronavirus 2 (SARS-Cov2) infection mainly present severe pneumonia associated with complications related to cytokine storm syndrome. So, it was associated with thrombotic incidents like acute limb ischemia and pulmonary embolism.
The severe acute respiratory syndrome-coronavirus-2-caused coronavirus disease-2019 (COVID-19) has arisen as a serious worldwide public health adversity. Early in the COVID-19 pandemic, an increased incidence of arterial and venous thrombosis was found, linked to systemic inflammation, immobilization, and a prothrombotic environment. Venous thromboembolism (VTE) can manifest itself in a variety of ways. A 55-year-old man presented to the emergency department with peripheral arterial disease (PAD) history.
Visit Here - https://pubrica.com/services/physician-writing-services/case-report/
COVID-19 Infection Occurring in The Postoperative Period in A Patient Who Und...semualkaira
While the coronavirus-associated Covid-19 infection remains a
risk for people all over the world as a pandemic, it is also a major
catastrophic clinical situation for patients undergoing surgery in
hospitals. If patients encounter this infection picture, especially
after severe operations such as heart surgery, the life-threatening
rates increase gradually.
COVID-19 infection occurring in the postoperative period in a patient who und...semualkaira
While the coronavirus-associated Covid-19 infection remains a risk for people all over the world as a pandemic, it is also a major catastrophic clinical situation for patients undergoing surgery in hospitals. If patients encounter this infection picture, especially after severe operations such as heart surgery, the life-threatening rates increase gradually. In this article, we presented the aortic thrombotic process and lung infection that occurred after a patient undergoing coronary artery surgery was infected with corona virus during clinical follow-up. The patient, who was followed up in the intensive care unit due to lung involvement, did not undergo surgical intervention, since there was no ischemic clinical picture due to peripheral occlusion. However, the patient died due to Covid-19 infection
COVID-19 infection occurring in the postoperative period in a patient who und...semualkaira
While the coronavirus-associated Covid-19 infection remains a risk for people all over the world as a pandemic, it is also a major catastrophic clinical situation for patients undergoing surgery in hospitals. If patients encounter this infection picture, especially after severe operations such as heart surgery, the life-threatening rates increase gradually. In this article, we presented the aortic thrombotic process and lung infection that occurred after a patient undergoing coronary artery surgery was infected with corona virus during clinical follow-up. The patient, who was followed up in the intensive care unit due to lung involvement, did not undergo surgical intervention, since there was no ischemic clinical picture due to peripheral occlusion. However, the patient died due to Covid-19 infection
Thrombophylia and COVID-19. A case report of young man 53 years old whith acu...komalicarol
A 57-year-old male was admitted to our Hospital on March 2020
for SARS-Cov2 related interstitial pneumonia. Chest x-ray showed
a bilateral interstitial-alveolar pneumonia and Blood gas analysis
(BGA) in room air highlighted a severe respiratory failure (pO2 46
mmHg, pH 7.41). Due to clinical and biohumoral worsening (stable CRP at 24 mg/dL), tocilizumab (800mg) was performed after
acquiring patient’s informed consensus. In the evening, after 96
hours of hospitalization, the patient presented a clear hyposthenia
/ hemiparesis of the right hemisome whit hyperreflexia, confusion
and slowed speech
Spontaneous pneumothorax associated with COVID-19 is rare.
We reported four cases and reviewed the literature. Among the
reports, 29% and 42% were a-/oligosymptomatic or symptomatic
but improving, respectively. Clinicians must be aware of this complication because it can happen when the patient with COVID-19
was a-/oligosymptomatic or had improving symptoms.
Pulmonary Tuberculosis in Coronavirus Disease-19 Patients: Report of Casesasclepiuspdfs
The coronavirus disease 2019 (COVID-19) is known to cause severe respiratory illness manifesting in a spectrum of related disorders. Amidst the continuous evolution of this pandemic which has caused vast devastation globally, it is crucial to note that tuberculosis (TB), which also causes respiratory diseases, has and still affects over a quarter of the world’s population. Coinfection of both diseases have severe health implications. Therefore, it is vital to understand the effects of this novel virus on the immune system and coinfection with a bacterial infection, like TB. Based on peer-reviewed cases, there seems to be an associational relationship between COVID-19 and TB; research suggests both weaken the immune system and further complicate clinical outcomes, which was further explored in this paper.
Transverse Myelitis in a Patient with COVID-19: A Case Reportkomalicarol
There has been growing evidence of COVID-19
potentially causing a wide range of neurological abnormalities
from as mild as anosmia to as serious as stroke. It is important to
recognize that amid this pandemic, we have been seeing different
manifestations and associations of COVID-19
Coronavirus disease (COVID-19) is an infectious disease caused by a newly discovered coronavirus.
Most people who fall sick with COVID-19 will experience mild to moderate symptoms and recover without special treatment.
The coronavirus infection coronavirus disease 2019 (COVID-19) first presented as an outbreak of atypical pneumonia in Wuhan, China, on December 12, 2019.1,2 Since then, it has spread globally to infect >1 963 943 individuals and killed >123 635 in >200 countries as of April 14, 2020. This infection has affected health and the economy worldwide on an unprecedented scale.
Similar to COVID-19 Associated Large Vessel Thrombosis and Ischemic Stroke: A Case Series (20)
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
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
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Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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.
- 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
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.
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
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.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
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
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.
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
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lacunar infarct in the right cerebellar hemisphere in addition to the
occluded right Middle Cerebral Artery (MCA) from the origin in the
neck (Figure 2).
Patient 2
A 60-year-old man, diabetic and hypertensive with right
nephrectomy for angiomyolipoma. We hospitalized him after testing
positive for COVID-19 PCR from a nasopharyngeal swab. Initially,
he was complaining of fever, cough, but he had no signs of respiratory
distress. We started him on hydroxychloroquine, azithromycin,
ritonavir/lopinavir, and methylprednisolone in addition to
anticoagulation for mild COVID-19 pneumonia in a high-risk
patient. On Day 12 of the disease course, the patient experienced an
insidious onset of left-sided upper limb weakness with slurring in
speech. Physical examination revealed left-side body weakness with
left upper facial nerve palsy and dysarthria. His initial NIHSS was
22; however, shortly afterward, he started to become confused with a
progressive deterioration in his conscious level mandating intubation
and mechanical ventilation. An urgent CT-head with CT-perfusion
confirmed a large area of a matched perfusion defects involving the
whole right MCA territory, with no clear salvageable tissue. A CT
Angiogram revealed a completely occluded right MCA. We deferred
thrombolysis because of a significant risk of ICH development
secondary to the large area of infarction. Hence, there are matched
MCA territory changes, and there are no collaterals; with an ASPECT
score of 3, thrombectomy was not feasible either.
Patient 3
A 41-year man was previously healthy and has been in home-
based quarantine after being in close contact with a COVID-19 patient
before presenting to the E.D. with complaints of severe headache,
dizziness, and vomiting 1-day duration. He was drowsy but following
simple commands and moving all his limbs. CT-head showed a sizable
ill-defined hypodense area noted in the right cerebellar hemisphere/
medulla suggestive of acute stroke in the right Posterior Inferior
Cerebellar Artery (PICA) territory with corresponding edema and
mild mass effect. With no evidence of hemorrhagic transformation.
MRI and MRA confirmed multiple areas of late acute infarcts
along with the posterior circulation territory in the right cerebellar
hemisphere (Figure 3). A nasopharyngeal swab of COVID-19 real
time-PCR turned out positive; we started the patient on azithromycin,
hydroxychloroquine, ritonavir/lopinavir, steroids, and enoxaparin on
day 3. The patient’s condition deteriorated rapidly with a decreased
conscious level, requiring intubation, without interval change on a
repeat CT-head. 7-days later, his neurological deficit progressed to
bilateral upper and lower limb weakness, and an MRI spine revealed
spinal cord infarct at T1-T3 vertebral levels, C2-C3 disk levels, and
C4 vertebral level. Further workup to identify a possible source
for the thrombus, including a transthoracic echocardiogram, was
unremarkable. On day 20, and after multiple failed weaning trials, we
inserted a percutaneous tracheostomy and then transferred him to a
rehabilitation facility.
Patient 4
A 42-year-old active smoker with no known past medical history.
2-days after being hospitalized for moderate COVID-19 moderate
pneumonia and after receiving hydroxychloroquine, azithromycin,
enoxaparin, methylprednisolone plus ritonavir/ lopinavir; he
developed left-sided body weakness with facial asymmetry and
slurring of speech of unknown time of onset associated with a
sudden decrease in the level of consciousness with NIHSS- 9. A
CT-scan brain perfusion and C.T. angiography showed a large area
of matched perfusion defect noted in the right MCA territory with
infarction involving the right front temporoparietal region and a
filling defect in the distal segment of the right common carotid artery
at its bifurcation. We did not offer thrombolysis as the time of stroke
onset was unclear. He was managed conservatively with IV heparin,
then changed to antiplatelets and a rehabilitation program for body
weakness.
Figure 1: MRA head with T2/FLAIR showing hyperintense acute infarct in
the right parietal-frontal lobes and smaller multifocal areas of patchy acute
infarcts in the left frontoparietal lobe, right more than left insula, bilateral
temporooccipital regions, left caudate head, and tiny acute lacunar infarct in
the right cerebellar hemisphere.
Figure 2: MRA of the head and neck showing occluded right Middle Cerebral
Artery (MCA) from the origin in the neck.
Figure 3: T2 Weighted head MRI confirmed multiple areas of late acute
infarcts along with the posterior circulation territory in the right cerebellar
hemisphere.
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Patient 5
EMS brought a middle-aged man with unknown past medical
history after being found in a drowsy state by his neighbor. On
physical exam, his Glasgow Coma Scale (GCS) was 9/15. An urgent
CT-head angiography showed a filling defect at the basilar artery’s
bifurcation, causing posterior circulation acute infarction with a
surrounding penumbra. His routine Chest X-ray showed increased
bilateral broncho-vascular markings; however, he tested positive
for the COVID-19 virus in nasal swab PCR and had a normal sinus
rhythm on ECG. We did not offer him thrombolysis as the onset time
is unknown, neither thrombectomy, as he already had an established
infarction on the plane CT-head. The MRI head confirmed the
previous C.T. findings and showed some areas of hemorrhagic
transformation. Later on, the patient developed further deterioration
in GCS, mandated intubation, and mechanical ventilation. 6-days
into his course, he developed refractory hypotension and bradycardia
followed by asystole and could not be revived with Cardiopulmonary
Resuscitation (CPR).
Discussion
With the ongoing outbreak of COVID-19, we noticed a significant
increase in ischemic stroke incidence among patients with a severe
inflammatory response to SARS-COV-2-induced ARDS admitted
to our high dependency and intensive care units [Table1]. The
authors observed SARS-COV-2’s associated ischemic stroke with the
ongoing recognition of the neurological manifestations of COVID-19
[4,5,16]. Mao et al. described these manifestations in a retrospective
observational case series of 219 patients in Wuhan, China, 41.1% of
which had severe pulmonary disease, 36.4% elicited a neurological
manifestation of which 5.7% attributed to cerebrovascular disease.
[16].
In a retrospective cohort study of 1,916 patients who visited the
emergency department in two academic New York hospitals, Mekler
et al. found that 36 patients had an acute ischemic stroke in SARS-
COV2 infection (1.6%; 95% CI, 1.1%-2.3%) in comparison to 3 out
of 1,486 patients with influenza viral infections (0.2%; 95% CI, 0.0%-
0.6%) [18] .
The neuro-targeting nature of the virus can explain the correlation
of SARS-COV-2 severity and ischemic stroke due to vascular injury
and the hyperimmune response. These responses alter the blood-
brain barrier, permitting the virus to bind to the ACE2 receptor in
glial cells, which, in addition to hypercoagulation, plays an important
role in the development of ischemic stroke [11,15].
Although the underlying pathophysiological process
responsible for the development of stroke in COVID-19 has
not yet been determined, different mechanisms related to the
COVID-19 infectious process were postulated, such as the host’s
hyperinflammatory response to the exaggerated cytokine release.
For instance, interleukins play an essential role in the inflammatory
response and in COVID-19 patients; IL-1, a macrophage-secreted
interleukin, is elevated, especially in severe COVID-19 cases. [4],
Other inflammatory mediators responsible for activating acute-phase
reactions like interferon-gamma [5], tumor necrosis factor-alpha,
and IL-6 were also elevated in SARS-COV-2 infected patients [8,9].
IL-6 activity has a unique importance as it has considered a target
for tocilizumab, an IL-6 receptor antagonist with possible alleviation
of the SARS-COV2-associated cytokines storm and subsequently the
severity of the infection [20].
Jenny et al. have addressed the relationship between inflammatory
cytokines and risk for ischemic stroke risk in their cohort study. They
found that raised IL-6 levels were associated with an increased risk
of ischemic stroke (mean 4.5 vs. 3.7ng/mL; p< 0.001) [14]. Another
factor supporting this association is endothelial injury, as described
by Varga et al. where the histopathology of different samples from
three patients with SARS-COV2 infection confirmed evidence of viral
endothelial invasion with subsequent accumulation of inflammatory
cells attributed to the widespread of ACE2 receptor through the
endothelial vascular lining [10].
A dysfunctional procoagulant state with ultimate activation of
Parameter CASE- 1 CASE-2 CASE-3 CASE-2 CASE-5
Age 80 years 60 years 41 years 42 years 49 years
Gender M M M M M
Risk factor DM, HTN, Malignancy DM, HTN Non NON Non
lymphocyte 0.60 x10^3/uL 1.0 x10^3/uL 0.80 x10^3/uL 1.5 0.9 x10^3/uL
Platelets 420 x10^3/uL 242 x10^3/uL 280 x10^3/uL 482x10^3/uL 371 x10^3/uL
CRP 331.6 mg/L 220.4 mg/L <0.5mg/L 29.7 mg/L 270 mg/L
D Dimer 30.71 mg/L FEU 3.65 mg/L FEU 2.92 mg/L FEU 3.56 mg/L FEU 2.92 mg/L FEU
Ferritin 1,841.0 ug/L 257 ug/L 185.0 ug/L 596 ug/L 820 ug/L
Fibrinogen 8.5 gm/L 4.43 gm/L 5.6 gm/L 4.63 gm/L 3.54 gm/L
Glucose 8.3 mmol/L 9.1 mmol/L 13.2 mmol/L 6.8 mmol/L 7.6 mmol/L
Medication
provided
-Unfractionated heparin
5000mg TID
-Enoxaparin 40mg BID -Enoxaparin 40mg BID -Enoxaparin 40mg BID -Enoxaparin 40mg BID
-azithromycin 500mg
q24hr/5days
-azithromycin 500mg
q24hr/5days
-azithromycin 500mg
q24hr/5days
-azithromycin 500mg
q24hr/5days
-azithromycin 500mg
q24hr/5days
-ritonavir/lopinavir 500mg
q24hrs/5days
-ritonavir/lopinavir 500mg
q24hrs/5days
-ritonavir/lopinavir 500mg
q24hrs/5days
-ritonavir/lopinavir 500mg
q24hrs/5days
-ritonavir/lopinavir 500mg
q24hrs/5days
methylprednisolon 40mg
daily
methylprednisolon 40mg
dail
methylprednisolon 40mg
dail
methylprednisolon 40mg
dail
methylprednisolon 40mg
dail
Table 1: Patient characteristics summary.
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the coagulation cascade, an acceleration of the already established
vasculopathy,andvascularthrombosisarekeysinthecasesmentioned
above, explicitly numbered 1 and 2. Those patients developed stroke
secondary to large vessel disease with complete occlusion of the
corresponding internal carotid artery.
About the SARS-COV-2 induced coagulopathy, the inflammatory
process has been associated with an increased level of D-Dimer and
fibrin degradation products. These two parameters’ value was higher
in severe CVOID-19 cases than their milder counterparts [17]. This
has subsequently led to the prolongation of P.T. and APTT and a DIC
picture with increased mortality [1]. The incidence of thrombotic
complications in patients with severe SARS-COV-2 infection,
especially those who required critical care admission, was high,
which indicates the underlying coagulation derangement correlated
with the viral burden and severity [7,13]. Panigada et al. described
thrombo-elastography findings in a patient with COVID-19 admitted
to the intensive care unit revealed a dramatic increase in D Dimer,
fibrinogen, and von Willebrand factor. Factor VIII was decreased
along with antithrombin [12].
Conclusion
The increased incidence of ischemic stroke was frequently
encountered among patients with ARDS and a significant
inflammatory response. We hypothesized that the underlying
pathophysiology could be related to considerable inflammation,
deranged coagulation, and viral cell invasion through endothelial
ACE2 receptors; this finding warranted the suggestion of a full dose of
anticoagulation for the hospitalized patient with moderate to severe
COVID-19 pneumonia. Such observations need further studies to
define the exact mechanism by which SARS-COV-2 induces ischemic
stroke.
Statement of Ethics
Written informed consent was obtained from the patient/relatives
for publication approval for publication was brought under the MRC
number MRC-04-20-1040.
Acknowledgment
We also acknowledge the Medical Research Center at Hamad
Medical Corporation for their support.
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