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The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).[1][2] AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.[3] Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells. HIV infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages, and dendritic cells.[4] HIV infection leads to low levels of CD4+ T cells through a number of mechanisms, including pyroptosis of abortively infected T cells,[5] apoptosis of uninfected bystander cells,[6] direct viral killing of infected cells, and killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells.[7] When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.
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The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and over time acquired immunodeficiency syndrome (AIDS).[1][2] AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.[3] Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells. HIV infects vital cells in the human immune system such as helper T cells (specifically CD4+ T cells), macrophages, and dendritic cells.[4] HIV infection leads to low levels of CD4+ T cells through a number of mechanisms, including pyroptosis of abortively infected T cells,[5] apoptosis of uninfected bystander cells,[6] direct viral killing of infected cells, and killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes that recognize infected cells.[7] When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.
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Circulatory Shock, types and stages, compensatory mechanisms
Circulatory Shock, types and stages, compensatory mechanisms
MedicoseAcademics
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Jual Obat Aborsi Di Dubai UAE Wa 0838-4800-7379 Obat Penggugur Kandungan Cytotec
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In this captivating lecture, Dr. Faiza, an esteemed Assistant Professor of Physiology, embarks on a comprehensive journey into the multifaceted realm of local blood flow regulation. With meticulous detail and clarity, she unravels the intricate mechanisms that govern the dynamic balance between tissue perfusion and vascular resistance, shedding light on both acute and chronic aspects of blood flow control. Beginning with an exploration of acute influences, Dr. Faiza elucidates how physiological factors such as metabolic demand, myogenic responses, and autoregulatory mechanisms orchestrate rapid adjustments in local blood flow. Students gain insight into the vasodilator theory, which elucidates the role of metabolic byproducts and vasoactive metabolites in promoting vasodilation, alongside the oxygen demand theory, which underscores the interplay between tissue oxygenation and nutrient demand. Delving deeper, the lecture delves into the fascinating realm of humoral control, where hormones and vasoactive substances wield significant influence over vascular tone. Dr. Faiza navigates through the intricacies of endothelial-derived factors like nitric oxide (NO) and histamine, alongside hormonal regulators such as angiotensin II and vasopressin. Through vivid explanations and illustrative examples, she unveils the intricate dance of vasodilation and vasoconstriction orchestrated by these biochemical messengers. Moreover, the lecture extends its gaze to the extrinsic control of blood flow, where sympathetic innervation exerts a profound impact on vascular dynamics. Dr. Faiza elucidates the role of sympathetic tone in modulating vascular resistance, highlighting its implications in diverse physiological and pathological scenarios. From skin perfusion to coronary circulation, students gain a nuanced understanding of how neural inputs shape local blood flow patterns. Enriched with clinical insights and contemporary research findings, this lecture equips students with a holistic understanding of blood flow regulation. By exploring concepts like active and reactive hyperemia, vascular remodeling, and collateral circulation, Dr. Faiza fosters a deeper appreciation for the adaptive responses of the cardiovascular system to changing physiological demands and pathological insults.
Control of Local Blood Flow: acute and chronic
Control of Local Blood Flow: acute and chronic
MedicoseAcademics
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Step into the captivating realm of cardiovascular physiology as Dr. Faiza, an esteemed Assistant Professor of Physiology, unravels the intricacies of recording an electrocardiogram (ECG). In this illuminating lecture, students are guided through the fundamental principles of ECG interpretation, from lead systems and electrode placement to the analysis of waves, segments, and intervals. Beginning with an exploration of the twelve-lead system, Dr. Faiza elucidates the significance of bipolar limb leads (I, II, III), unipolar limb leads (aVR, aVL, aVF), and unipolar chest leads (V1-V6). Through mnemonic aids and clinical anecdotes, students gain a comprehensive understanding of lead placement techniques, enabling them to navigate the complexities of ECG recording with confidence and precision. As the lecture unfolds, Dr. Faiza delves into the nuances of ECG interpretation, empowering students to correlate ECG findings with electrophysiological events in the cardiac cycle. With a focus on waveform morphology and rhythm analysis, students learn to determine heart rate, rhythm, and axis deviation, deciphering the electrocardiographic manifestations of various cardiac pathologies and physiological states. Moreover, the lecture explores the normal waves, segments, and intervals of an ECG, providing students with a detailed roadmap for interpreting these essential components. From the P wave to the T wave, students gain insight into the voltage, duration, and clinical significance of each waveform, equipping them with the skills to identify aberrations and anomalies in ECG tracings. Enriched with clinical pearls and practical tips, this lecture serves as a cornerstone for students embarking on their journey into cardiovascular medicine. By demystifying the art of ECG interpretation, Dr. Faiza empowers students to harness the power of this diagnostic tool in clinical practice, fostering a deeper appreciation for the intricate interplay between electrical activity and cardiac function.
Electrocardiogram (ECG) physiological basis .pdf
Electrocardiogram (ECG) physiological basis .pdf
MedicoseAcademics
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These are simplified slides discussing the regulation of cardiac output and venous return. Learning objectives: 1. Comprehend the determinants of cardiac output and factors affecting cardiac output 2. Comprehend the factors affecting stroke volume and heart rate and total peripheral resistance 3. Identify the factors regulating venous return 4. Discuss the causes of high and low output cardiac failure 5. Enlist the functions of veins and recognise the significance of venous reservoirs Study Resources: 1. Chapter 20, Guyton and Hall Textbook of Medical Physiology, 14th edition 2. Chapter 30 and 32, Ganongโs Review of Medical Physiology, 26th edition 3. Chapter 10, Human Physiology by Lauralee Sherwood, 9th edition 4. Physiology, Cardiac Output - StatPearls https://www.ncbi.nlm.nih.gov/books/NBK470455/
Cardiac Output, Venous Return, and Their Regulation
Cardiac Output, Venous Return, and Their Regulation
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