This is a presentation about splanchinc circulation.
Done by year 3 medical students at the University of Science and Technology, Sana'a, Republic of Yemen.
Spring semester of 2010.
The basics of autoregulation of Gloemrular filtration rate. This ppt deals with basic renal physiology, tubuloglomerular feedback, myogenic reflex, juxtaglomerular apparatus and renin angiotensin aldosterone system in brief. P.S.- The ppt has animations so kindly view in slide/presentation mode
Sudden impairment of kidney function occurring over a period of hours to days.
AKI is present in 7% of all hospitalized patients, and up to 30% of patients in ICU
The incidence is increasing at an alarming rate
That's why we need ideal biomarker to diagnose the AKI as early as possible and deliver better treatment to the patient.
This is a presentation about splanchinc circulation.
Done by year 3 medical students at the University of Science and Technology, Sana'a, Republic of Yemen.
Spring semester of 2010.
The basics of autoregulation of Gloemrular filtration rate. This ppt deals with basic renal physiology, tubuloglomerular feedback, myogenic reflex, juxtaglomerular apparatus and renin angiotensin aldosterone system in brief. P.S.- The ppt has animations so kindly view in slide/presentation mode
Sudden impairment of kidney function occurring over a period of hours to days.
AKI is present in 7% of all hospitalized patients, and up to 30% of patients in ICU
The incidence is increasing at an alarming rate
That's why we need ideal biomarker to diagnose the AKI as early as possible and deliver better treatment to the patient.
Introduction
HORMONES OF ADRENAL CORTEX
MINERALOCORTICOIDS
Aldosterone
Life-saving Hormone
Actions of aldosterone
Aldosterone escape or escape phenomenon
Regulation of aldosterone secretion
Renin–angiotensin system
Applied
Introduction
HORMONES OF ADRENAL CORTEX
MINERALOCORTICOIDS
Aldosterone
Life-saving Hormone
Actions of aldosterone
Aldosterone escape or escape phenomenon
Regulation of aldosterone secretion
Renin–angiotensin system
Applied
SEMINAR ON BLOOD PRESSURE REGULATION, Determinants of Arterial BP
Functions Of Blood Pressure
Physiological Variations In Bp
Blood Pressure Regulation
Applied Physiology
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
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
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
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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
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.
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
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
2. Hypertension is a sustained elevation of the systemic arterial
pressure. Pulmonary hypertension also occurs, but the pressure in
the pulmonary artery is relatively independent of that in the
systemic
arteries.
The arterial pressure is determined by the cardiac output and the
peripheral resistance
(pressure = flow × resistance)
The peripheral resistance is determined by the viscosity of the blood
and, more importantly, by the caliber of the resistance vessels.
Hypertension can be produced by elevating the cardiac output, but
sustained hypertension is usually due to increased peripheral
resistance - arteriosclerosis
3.
4. Classification
(JNC7)
Systolic pressure Diastolic pressure
mmHg
mmHg
Normal
90–119
60–79
High normal or
prehypertension
120–139
80–89
Stage 1
hypertension
140–159
90–99
Stage 2
hypertension
≥160
≥100
Isolated systolic
hypertension
≥140
<90
5. About 90 to 95 per cent of all people - the hypertension is
of unknown origin - strong hereditary tendency.
In most patients, excess weight gain and sedentary lifestyle
appear to play a major role in causing hypertension.
New clinical guidelines for treating hypertension
recommend increased physical activity and weight loss
as a first step in treating most patients with
hypertension.
It is treatable but not curable.
6. Cardiac output is increased due to the additional blood flow
required for the extra adipose tissue.
Sympathetic nerve activity, especially in the kidneys, is increased
in overweight patients. Leptin released from fat cells may
directly stimulate multiple regions of the hypothalamus,
which, in turn, have an excitatory influence on the
vasomotor centers of the brain medulla.
Angiotensin II and aldosterone levels are increased two- to
threefold in many obese patients. This may be caused partly by
increased sympathetic nerve stimulation, which increases
renin release by the kidneys and therefore formation of
angiotensin II, which, in turn, stimulates the adrenal gland to
secrete aldosterone.
7. The renal-pressure natriuresis mechanism is impaired, and the
kidneys will not excrete adequate amounts of salt and water.
It is caused mainly by increased renal tubular reabsorption
of salt and water due to increased sympathetic nerve activity
and increased levels of angiotensin II and aldosterone.
If hypertension is not effectively treated, there may also be
vascular damage in the kidneys that can reduce the
glomerular filtration rate and increase the severity of the
hypertension.
Eventually uncontrolled hypertension associated with
obesity can lead to severe vascular injury and complete loss
of kidney function.
8. Benign type:
1. Early
stages – 10,15 years – SBP
fluctuates – labile HT
2. Late stages – fixed – complications –
death
Malignant
type
(Accelerated
HT,
hypertensive crisis):
BP much higher – death within 2 years
9. Volume loading HT in patients with artificial kidney
Primary aldosteronism - aldosterone increases the rate of
reabsorption of salt and water by the tubules of the
kidneys, thereby reducing the loss of these in the urine
while at the same time causing an increase in blood
volume and extracellular fluid volume.
Renin-Secreting Tumor or by Infusion of Angiotensin II
“One-Kidney” Goldblatt Hypertension
10. When one kidney is removed and a constrictor is placed
on the renal artery of the remaining kidney, the
immediate effect is greatly reduced pressure in the renal
artery beyond the constrictor.
The systemic arterial pressure begins to rise and
continues to rise for several days.
When the systemic arterial pressure reaches its new
stable pressure level, the renal arterial pressure will be
returned almost all the way back to normal.
11.
12. The early rise in arterial pressure in Goldblatt hypertension is caused by the
renin-angiotensin vasoconstrictor mechanism. That is, because of poor
blood flow through the kidney after acute constriction of the renal artery,
large quantities of renin are secreted by the kidney, and this causes
increased angiotensin II and aldosterone in the blood.
The angiotensin in turn raises the arterial pressure acutely. The secretion of
renin rises to a peak in an hour or so but returns nearly to normal in 5 to 7
days because the renal arterial pressure by that time has also risen back to
normal, so that the kidney is no longer ischemic.
The second rise in arterial pressure is caused by retention of salt and water
by the constricted kidney. In 5 to 7 days, the body fluid volume will have
increased enough to raise the arterial pressure to its new sustained level.
The quantitative value of this sustained pressure level is determined by the
degree of constriction of the renal artery. That is, the aortic pressure must
rise high enough so that renal arterial pressure distal to the constrictor is
enough to cause normal urine output.
13. The artery to only one kidney is constricted while the artery to the
other kidney is normal.
The constricted kidney secretes renin and also retains salt and
water because of decreased renal arterial pressure in this kidney.
Then the “normal” opposite kidney retains salt and water because
of the renin produced by the ischemic kidney.
This renin causes formation of angiotensin II and aldosterone both
of which circulate to the opposite kidney and cause it also to
retain salt and water.
Patchy ischemic kidney disease – renal HT.
14. Hypertension in the Upper Part of the Body Caused by
Coarctation of the Aorta - One out of every few thousand
babies is born with pathological constriction or blockage of
the aorta at a point beyond the aortic arterial branches to the
head and arms but proximal to the renal arteries.
When this occurs, blood flow to the lower body is carried by
multiple, small collateral arteries in the body wall, with
much vascular resistance between the upper aorta and the
lower aorta. As a consequence, the arterial pressure in the
upper part of the may be 40-50 per cent higher than that in
the lower body.
Role of Autoregulation
15. Hypertension in Preeclampsia (Toxemia of Pregnancy) - HT subsides after
delivery of the baby.
Ischemia of the placenta and subsequent release by the placenta of toxic factors
are believed to play a role in causing hypertension in the mother.
Substances released by the ischemic placenta, in turn, cause dysfunction of
vascular endothelial cells throughout the body, including the blood vessels of
the kidneys.
This endothelial dysfunction decreases release of NO and other vasodilator
substances, causing vasoconstriction, decreased rate of fluid filtration from the
glomeruli into the renal tubules, impaired renal pressure natriuresis, and
development of hypertension.
Thickening of the kidney glomerular membranes (perhaps caused by an
autoimmune process), which also reduces the rate of glomerular fluid filtration.
16. Acute neurogenic hypertension can be caused by strong stimulation of the
sympathetic nervous system. For instance, when a person becomes excited for any
reason or at times during states of anxiety, the sympathetic system becomes
excessively stimulated, peripheral vasoconstriction occurs everywhere in the
body, and acute hypertension results – White coat HT
Acute Neurogenic Hypertension Caused by Sectioning the Baroreceptor Nerves
- occurs when the nerves leading from the baroreceptors are cut or when the
NTS is destroyed in each side of the medulla oblongata (these are the areas
where the nerves from the carotid and aortic baroreceptors connect in the brain
stem).
“resetting” of the baroreceptor pressure control mechanism - an acute type of
hypertension, not a chronic type.
Spontaneous Hereditary Hypertension
17.
Procedures that produce sustained hypertension in experimental animals.
Interference with renal blood flow (renal hypertension)
Constriction of one renal artery; other kidney removed (one-clip, one-kidney
Goldblatt hypertension)
Constriction of one renal artery; other kidney intact (one-clip, two-kidney
Goldblatt hypertension)
Constriction of aorta or both renal arteries (two-clip, two-kidney Goldblatt
hypertension)
Compression of kidney by rubber capsules, production of perinephritis, etc.
Interruptions of afferent input from arterial
hypertension)
Denervation of carotid sinuses and aortic arch
Bilateral lesions of NTS
Treatment with corticosteroids
Deoxycorticosterone and salt
Other mineralocorticoids
Genetic
Spontaneous hypertension in various strains of rats
Salt-induced hypertension in genetically sensitive rats
Endothelial NOS gene knockout in mice
Various types of transgenic animals
baroreceptors
(neurogenic
18.
Estimated frequency of various forms of hypertension in the
general hypertensive population.
Essential hypertension - 88
Renal hypertension
Reno vascular - 2
Parenchymal - 3
Endocrine hypertension
Primary aldosteronism - 5
Cushing's syndrome - 0.1
Pheochromocytoma - 0.1
Other adrenal forms - 0.2
Estrogen treatment ("pill hypertension") - 1
Miscellaneous (Little's syndrome, Coarctation of the aorta) 0.6
19. 1.
Excess workload on the heart leads to early heart failure
and coronary heart disease, often causing death as a
result of a heart attack.
2.
The high pressure frequently damages a major blood
vessel in the brain, followed by death of major portions
of the brain; this is a cerebral infarct. Clinically it is called a
“stroke.” Depending on which part of the brain is
involved, a stroke can cause paralysis, dementia,
blindness, or multiple other serious brain disorders.
3.
High pressure almost always causes injury in the
kidneys, producing many areas of renal destruction and,
eventually, kidney failure, uremia and death.
20.
21. First step - lifestyle modifications
•maintain normal body weight for adults (e.g. body mass index 20–25
kg/m2)
•reduce dietary sodium intake to <100 mmol/ day (<6 g of sodium chloride
or <2.4 g of sodium per day)
•engage in regular aerobic physical activity such as brisk walking (≥30 min
per day, most days of the week)
•limit alcohol consumption to no more than 3 units/day in men and no
more than 2 units/day in women
•consume a diet rich in fruit and vegetables (e.g. at least five portions per
day)
22. Pharmacological treatment with antihypertensive drugs:
- Vasodilator drugs that increase renal blood flow
(1) by inhibiting sympathetic nervous signals to the kidneys or by
blocking the action of the sympathetic transmitter substance on the renal
vasculature,
(2) by directly relaxing the smooth muscle of the renal vasculature,
(3) by blocking the action of the renin-angiotensin system on the renal
vasculature or renal tubules.
- Natriuretic or diuretic drugs that decrease tubular reabsorption of salt
and water. They block active transport of sodium through the tubular
wall; this blockage in turn also prevents the reabsorption of water.
23. In some individuals, sudden standing causes a fall in blood
pressure, dizziness, dimness of vision, and even fainting orthostatic (postural) hypotension
It is common in patients receiving sympatholytic drugs.
It also occurs in diseases such as diabetes and syphilis, in which
there is damage to the sympathetic nervous system - This
highlights the importance of the sympathetic vasoconstrictor
fibers in compensating for the effects of gravity on the circulation.
Another cause of postural hypotension is primary autonomic
failure. Autonomic failure occurs in a variety of diseases. One
form is caused by a congenital deficiency of dopamine βhydroxylase with little or no production of norepinephrine and
epinephrine
24. Hypovolemia – hemorrhage, starvation, diarrhea, vomiting,
diuretics
MI
Hypo activity of pituitary glands
Hypo activity of adrenal glands
Tuberculosis
Nervous disorders
Induced hypotension during anesthesia
Rx
25. Distributive shock - neurogenic shock, in which there is sudden
autonomic activity producing vasodilation, pooling of blood in
the extremities, and fainting. These are called vasovagal attacks,
and they are short-lived and benign.
Other forms of syncope include postural syncope, fainting due to
pooling of blood in the dependent parts of the body on standing.
Micturition syncope, fainting during urination, occurs in patients
with orthostatic hypotension. It is due to the combination of the
orthostasis and reflex bradycardia induced by voiding in these
patients.
Pressure on the carotid sinus, produced, for example, by a tight
collar, can cause such marked bradycardia and vasodilation that
fainting results (carotid sinus syncope).
26. Rarely, vasodilation and bradycardia may be precipitated by
swallowing (deglutition syncope).
Cough syncope occurs when the increase in intrathoracic
pressure during straining or coughing is sufficient to block
venous return.
Effort syncope is fainting on exertion as a result of inability
to increase cardiac output to meet the increased demands of
the tissues and is particularly common in patients with aortic
or
pulmonary
stenosis.
Fainting due to bradycardia, heart block or massive heart
attack is called neurocardiogenic syncope.