The slides show the gastric and pancreatic function test along with the significance of these tests and the conditions in which the values of which increase.
The liver is the largest organ in the body
It is located below the diaphragm in the right upper quadrant of the abdominal cavity and extended approximately from the right 5th rib to the lower border of the rib cage.
Shock is the state of not enough blood flow to the tissues of the body as a result of problems with the circulatory system.Initial symptoms may include weakness, fast heart rate, fast breathing, sweating, anxiety, and increased thirst. This may be followed by confusion, unconsciousness, or cardiac arrest as complications worsen.
Shock is divided into four main types based on the underlying cause: low volume, cardiogenic, obstructive, and distributive shock. Low volume shock may be from bleeding, diarrhea, vomiting, or pancreatitis. Cardiogenic shock may be due to a heart attack or cardiac contusion. Obstructive shock may be due to cardiac tamponade or a tension pneumothorax. Distributed shock may be due to sepsis, spinal cord injury, or certain overdoses.
The diagnosis is generally based on a combination of symptoms, physical examination, and laboratory tests. A decreased pulse pressure (systolic blood pressure minus diastolic blood pressure) or a fast heart rate raises concerns. The heart rate divided by systolic blood pressure, known as the shock index (SI), of greater than 0.8 supports the diagnosis more than low blood pressure or a fast heart rate in isolation.
Treatment of shock is based on the likely underlying cause.[2] An open airway and sufficient breathing should be established.[2] Any ongoing bleeding should be stopped, which may require surgery or embolization.[2] Intravenous fluid, such as Ringer's lactate or packed red blood cells, is often given.[2] Efforts to maintain a normal body temperature are also important.[2] Vasopressors may be useful in certain cases.[2] Shock is both common and has a high risk of death.[3] In the United States about 1.2 million people present to the emergency room each year with shock and their risk of death is between 20 and 50%
Physiology of shock explains different kind of shock and their management. Made by Dr.Nitin Khajotia.
Septic shock
Cardiogenic shock
Anaphylactic shock
Septic shock (due to infections)
Neurogenic shock (caused by damage to the nervous system)
Signs and Symptom
management of shock general
Day 1 -RESERVE CONPENSATION FAILURE2wb.pptxMkindi Mkindi
There are nearly 100 viruses of the herpes group that infect many different animal species.
Official name of herpesviruses that commonly infect human is Humans herpesvirus (HHV)
herpes simplex virus types 1 (HHV 1)
Herpes simplex virus type 2 (HHV 2)
Varicella-zoster virus (HHV 3)
Epstein-Barr virus, (HHV 4)
Cytomegalovirus (HHV 5)
Human herpesvirus 6 (HHV 6)
Human herpesvirus 7 (HHV 7)
Human herpesvirus 8 (HHV 8) (Kaposi's sarcoma-associated herpesvirus).
Herpes B virus of monkeys can also infect humans
hELMINTHS#corona virus#Aspergillosis#BUGANDO#CUHAS#CUHAS#CUHAS#CELL MEMBRANE TRANSPORT#PHYSIOLOGY#BODY FLUIDS#RENAL PHYSIOLOGY#
Heart failure is a clinical syndrome that results when the heart is unable to provide sufficient blood flow to meet metabolic requirements or accommodate systemic venous return.
Definition
Causes
Pathophysiology
Types Of Heart Failure
Symptoms
Signs
Complications
Investigations
Treatment
Hijama (Arabic: حجامة lit. "sucking") is the Arabic term for wet cupping, where blood is drawn by vacuum from a small skin incision for therapeutic purposes.The practice has Greek and Persian origin and is mentioned by Hippocrates.
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
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
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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.
2. What is Shock????
• Profound hemodyamic and metabolic
disturbance characterized by failure of the
circulatory system to maintain adequate
perfusion of vital organs.
• Normal relationship between oxygen demand
and oxygen supply is impaired.
3. Etiology of circulatory shock
Reduced cardiac output
Hypovolaemic shock
• Reduction in circulating volume causing a reduction in venous
return and consequential reduction in cardiac output
• haemorrhage
• Dehydration
Obstructive shock
• Mechanical obstruction to normal venous return or cardiac
output
• massive pulmonary embolism
• tension pneumothorax
• cardiac tamponade
5. Low peripheral resistance
Distributive shock
• Peripheral vasodilatation – may be associated with
inadequate increase in cardiac output
• septic shock
• anaphylaxis
• neurogenic
Endocrine shock
• Addisonian crisis
• Hyper/hypothyroid crisis
6. Stages of shock
• Nonprogressive stage (sometimes called the
compensated stage) - normal circulatory compensatory
mechanisms eventually cause full recovery without
help from outside therapy.
• Progressive stage - without therapy, the shock
becomes steadily worse until death.
• Irreversible stage - shock has progressed to such an
extent that all forms of known therapy are inadequate
to save the person’s life, even though, for the moment,
the person is still alive.
7. What makes the shock to go into compensated
or decompensated state???
• Depends on the feedback mechanism elicited by the
shock
• Can be negative feedback mechanism or positive
feedback mechanism.
• Negative feedback predominant – compensdated
stage of shock
• Termed negative because the direction of the
secondary change in response to shock is opposite to
the direction of the initiating change
8. • Positive feedback mechanisms exaggerate any
primary change initiated aggravating the hypotension
induced by shock and tend to initiate "vicious"
cycles, which may lead to decompensated or
irreversible stage.
• Whether a positive feedback mechanism will lead to
a vicious cycle depends on the gain of that
mechanism.
• Gain is defined as the ratio of the secondary change
evoked by a given mechanism to the initiating
change itself.
• A gain greater than 1 induces a vicious cycle; a gain
less than 1 does not
9. Non progressive or compensated shock
Negative feedback mechanism responsible for
non progression of shock includes:
Baroreceptor reflexes –
• elicit powerful sympathetic stimulation of the circulation.
• Generalized arteriolar constriction is a prominent response to the
diminished baroreceptor stimulation
• The reflex increase in peripheral resistance minimizes the fall in
arterial pressure caused by the reduction of cardiac output.
• Vasoconstriction most pronounced in the cutaneous, skeletal
muscle and splanchnic vascular beds, slight or absent in the
cerebral and coronary circulations.
• Renal vasoconstriction resisted by autoregulatory mechanism
initially but with severe shock there occurs intense renal and
splanchnic vasoconctriction.
10. Chemoreceptor reflexes.
• Reductions in arterial pressure below about 60 mm Hg do not evoke
any additional responses through the baroreceptor reflexes.
• Inadequate blood flow hypoxia in chemoreceptor tissues and
activation of chemoreceptor reflex.
CNS ischaemic response.
• Fall in Mean Arterial Pressure below 50 mm hg activates the response.
• The sympathetic nervous discharge is several times greater than the
maximal neural activity that occurs when the baroreceptors cease to be
stimulated.
• With more severe degrees of cerebral ischemia, however, the vagal
centers also become activated.
Reverse stress-relaxation of the circulatory system,
• causes the blood vessels to contract around the diminished blood
volume, so that the blood volume that is available more adequately fills
the circulation.
11. Formation of endogenous vasoconstrictors.
• Epinephrine from the adrenal medulla, whereas norepinephrine from both
the adrenal medulla and the peripheral sympathetic nerve endings
reinforce the effects of sympathetic nervous.
• Vasopressin , a potent vasoconstrictor, is actively secreted by the
posterior pituitary gland.
• The plasma concentration of vasopressin rises progressively as the
arterial blood pressure diminishes. The receptors responsible for the
augmented release of vasopressin are the sinoaortic baroreceptors and
stretch receptors in the left atrium.
12. • Diminished renal perfusion during shock secretion of renin from
the juxtaglomerular apparatus conversion of angiotensinogen to
angiotensin I ACE converts angiontensin I to angiotensin II.
• Angiotensin II is a powerfull vasoconstrictor.
Compensatory mechanisms that return the blood volume back
toward normal.
• Absorption of fluid into the blood capillaries from the interstitial spaces
of the body.
• conservation of water and salt by the kidney by release of aldosterone.
• increased thirst and increased appetite for salt, which make the person
drink water and eat salty foods if able.
13. Progressive stage of shock
• Caused by a vicious circle of cardiovascular
deterioration.
• Positive feedback mechanism evoked by
uncorrected shock results in the vicious progression.
• Requires prompt and aggressive intervention else
the shock enters the irreversible stage where death
is imminent
14. • Different types of “positive feedback” that can lead to progression of
shock. (courtesy- guyton n hall textbook of physiology 11th edition
15. Cardiac depression.
• blood pressure coronary blood flow hypoxia and decrease
nutrition of myocardium leading to diminshed contractility and reduced
cardiac output.
• The consequent reduction in cardiac output leads to a further decline in
arterial pressure, a classic example of a positive feedback mechanism
• The role of cardiac failure in the progression of shock during
hemorrhage is controversial.
• The reduced blood flow to the peripheral tissues leads to an
accumulation of vasodilator metabolites which decreases peripheral
resistance and therefore aggravates the fall in arterial pressure
• All investigators agree that the heart fails terminally, but opinions
differ about the importance of cardiac failure during earlier stages of
hemorrhagic hypotension.
• The heart has tremendous reserve capability that normally allows it to
pump 300 to 400 per cent more blood than is required by the body for
adequate bodywide tissue nutrition.
16. Ventricular function curve for the left ventricle during the course of hemorrhagic shock.
Curve A represents the control function curve; curve B, 117 min; curve C, 247 min; curve D,
280 min; curve E, 295 min; and curve F, 310 min after the initial hemorrhage. (Redrawn from
Crowell JW, Guyton AC: Am J Physiol 203:248, 1962.)
17. Vasomotor Failure.
• Diminished blood flow to the brain’s vasomotor center
depresses the center so much that it becomes progressively
less active and finally totally inactive.
• Complete circulatory arrest to the brain for 10 to 15 minutes,
depresses the vasomotor center such that no evidence of
sympathetic discharge can be demonstrated.
• The resulting loss of sympathetic tone then reduces cardiac
output and peripheral resistance which reduces mean arterial
pressure and intensifies the inadequate cerebral perfusion.
• Various endogenous opioids, such as enkephalins and β-
endorphin, may be released into the brain substance or into
the circulation in response circulatory shock, which further
depresses brainstem centres.
• Vasomotor center usually does not fail if the arterial
pressure remains above 30 mm Hg
18. Acidosis.
• The inadequate blood flow during shock affects the metabolism
of all cells in the body.
• Hypo-perfusion reduces adenosine triphosphate (ATP)
availability required for maintenance of transmembrane
potential. Leaky cell membranes cause interstitial fluid uptake
and massive cell oedema.
• This oedema obstructs adjacent capillaries reducing oxygen
delivery
• The decreased oxygen delivery to the cells accelerates the
production of lactic acid and other acid metabolites by the
tissues.
• Impaired kidney function prevents adequate excretion of the
excess H+, and generalized metabolic acidosis ensues .
• The resulting depressant effect of acidosis on the heart further
reduces tissue perfusion and thus aggravates the metabolic
acidosis
19. • Acidosis also diminishes the reactivity of the heart and
resistance vessels to neurally released and circulating
catecholamines, and thereby intensifies the hypotension.
Blockage of Very Small Vessels—“Sludged Blood.”
• sluggish blood flow in the microvessels due to decrease
arterial pressure leads to their blockage.
• Acidosis and deterioration products from the ischemic
tissues, causes local blood agglutination, resulting in minute
blood clots, leading to small plugs in the small vessels.
• an increased tendency for the blood cells to stick to one
another makes it more difficult for blood to flow through the
microvasculature, giving rise to the term sludged blood.
20. Aberrations of blood clotting.
• The alterations of blood clotting after hemorrhage are
typically biphasic. An initial phase of hypercoagulability is
followed by a secondary phase of hypocoagulability and
fibrinolysis.
• In the initial phase, platelets and leukocytes adhere to the
vascular endothelium, and intravascular clots, or thrombi,
develop few minutes of the onset of severe hemorrhage.
• Coagulation may be extensive throughout the small blood
vessels.
• The initial phase is further enhanced by the release of
thromboxane A2 from various ischemic tissues.
• Thromboxane A2 aggregates platelets. As more platelets
aggregate, more thromboxane A2 is released and more
platelets are trapped
21. • Later tisuue ischaemia activates endothelial plasminogen
activator whilst hypo-perfusion inhibits plasminogen
activator inhibitor, thus promoting hyperfibrinolysis.
• Acidosis inhibits the activity of coagulation factors and
leads to increased degradation of fibrinogen.
• systemic activation of the anticoagulant protein C pathway
also occurs in later stage of shock.
Increased Capillary Permeability.
• In prolonged shock due to capillary hypoxia and lack of
other nutrients, the permeability of the capillaries gradually
increases, and large quantities of fluid begin to transude into
the tissues.
• Further deteriorates blood volume and cardiac output.
22. Release of Toxins by Ischemic Tissue.
• shock causes tissues to release toxic substances, such as
histamine, serotonin, and tissue enzymes, that cause further
deterioration of the circulatory system.
• Endotoxin is released from the bodies of dead gram-
negative bacteria in the intestines.
• Diminished blood flow to the intestines often causes
enhanced formation and absorption of this toxin.
• The circulating toxin causes cardiac depression and further
decreases cardiac output.
23. Depression of Reticuloendothelial system.
• During the course of circulatory shock, reticuloendothelial
system (RES) function becomes depressed.
• The phagocytic activity of the RES is modulated by an
opsonic protein and the opsonic activity in plasma
diminishes during shock.
• When the RES is depressed, normal flora endotoxins
invade the general circulation. Endotoxins produce
profound, generalized vasodilation, mainly by inducing the
abundant synthesis of an isoform of nitric oxide synthase
in the smooth muscle of blood vessels throughout the
body.
• The profound vasodilation aggravates the hemodynamic
changes.
24. Vasopressin deficiency.
• posterior pituitary hormone released in response to increased
plasma osmolality or decreased intravascular volume.
• Plasma vasopressin levels subsequently decline, secondary
to depletion of the pituitary neurohypophyseal stores.
• Decrease vasopressin decreased vasoconstriction and
renal absorption of fluid decreased blood volume
decreased cardiac output.
Activation of ATP-sensitive potassium channels
(KATP)
• KATP channel opening allows an efflux of potassium ions
and results in membrane hyperpolarization and reduced
calcium ion movement into the cell.
25. • Under resting conditions, the KATP channels are closed.
• Altered tissue metabolism or hypoxia leads to channels
activation, causing vasodilatation.
• Vasodilation decreased peripheral resistance,
decreased venous return decreassed cardiac out put
Activation of the inducible form of nitric oxide
synthase enzyme.
• Nitric oxide is a vasodilator produced in vascular
endothelium.
• Production is controlled by a group of enzymes called nitric
oxide synthases.
• In shock, there is an increased expression of the inducible
form of nitric oxide synthase (NOS) due to circulating
cytokines
• Increase NOS increase NO increase vasodilation
26. Generalized Cellular Deterioration.
• Active transport of sodium and potassium through the
cell membrane is greatly diminished sodium and
chloride accumulate in the cells, and potassium is lost
from the cells the cells begin to swell.
• Mitochondrial activity in the tissues becomes severely
depressed.
• Lysosomes in the cells in widespread tissue areas begin
to break open, with release of hydrolases that cause
further intracellular deterioration.
• Cellular deterioration further leads to multiorgan
failure.
• Lobular necrosis begins to occur in liver.
27. • Necrosis of the central portion of a liver lobule in severe circulatory
• shock. (Courtesy Dr. J. W. Crowell.)
28. • Pulmonary failure “shock lung’’ ensues.
• Initial phase: intrapulmonary blood volume
ventilation-perfusion ratio.
• Late phase: fibrin and leucocytes in interstitial
and alveolar spaces.
• Accumulation of Neutrophill in pulmonary
circulation release of proteases
• permeability - surfactant, edema and hemorrhagies
• Adult respiratory distress syndrome:
29. • In kidney blood flow GF oliguria.
• Countercurrent mechanism failure isosthenuria
• Ischemia of renal tissue azotemia and acute
tubular necrosis
• Marked ischemia acute renal failure.
30. Interactions of Positive and Negative Feedback
Mechanisms
• The gain of any specific mechanism varies with the
severity of the shock .
• With only a slight loss of blood, mean arterial pressure is
within the normal range and the gain of the baroreceptor
reflexes is high.
• With greater losses of blood, when mean arterial pressure
is below 60 mm hg the baroreceptor reflex gain is zero or
near zero.
• a general rule, with minor degrees of blood loss, the gains
of the negative feedback mechanisms are high, whereas
those of the positive feedback mechanisms are low and
vice versa
31. Irreversible stage of shock
• Any therapeutic intervention ceases to be effective.
• Therapy can, on rare occasions, return the arterial pressure
and the cardiac output to normal or near normal for short
periods, but the circulatory system continues to deteriorate,
and death ensues in another few minutes to few hours.
32. Why no going back from irreversible
stage of shock??
• The high-energy phosphate reserves in the tissues of the
body, are greatly diminished in severe degrees of shock.
• All the adenosine triphosphate downgrades to adenosine
diphosphate, adenosine monophosphate, and, eventually,
adenosine.
• adenosine diffuses out of the cells into the circulating
blood and is converted into uric acid, a substance that
cannot re-enter the cells to reconstitute the adenosine
phosphate system.
• Adenosine depleted is difficult to replenish
• The cellular depletion of these high energy compounds
leads to no going back.
33. Monitoring CO, securing CV line Adequate volume correction,
inotropes and vasopressors
Early management – Recovery
Delayed care – Progression to
irreversible stage
Identifying and correcting the cause
of shock