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Interactive Tutorial By Rachel M Grooms Alverno College MSN 621 Advanced Pathophysiology. Pathophysiology of Surgical Site Infection All images are imported from microsoft clip art. [email protected] Tutorial Directions. Hover over underlined text for further information.

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Interactive Tutorial

By

Rachel M Grooms

Alverno College

MSN 621 Advanced Pathophysiology

Pathophysiology of Surgical Site Infection

All images are imported from microsoft clip art.

[email protected]


Tutorial directions
Tutorial Directions

  • Hover over underlined text for further information.

  • To advance to the next slide:

    • Click or

    • Use space bar

  • To go back to the previous slide:

    • Click

  • To go to back to the first slide:

    • Click

  • To view specific content:

    • Click on the action buttons on the Menu slide


Outcomes
Outcomes

  • At the end of this tutorial you should be able to:

    • verbalize the importance of preventing infection post surgical incision

    • identify characteristics of the immune/inflammatory response initiated post surgical incision to prevent infection.

    • identify characteristics of the stress response occurring post surgical incision to prevent infection.

    • identify the relationship between genetics and infection post surgical incision.

    • identify surgical practices effective in preventing surgical site infection.


Tutorial menu
Tutorial Menu

Introduction

Homeostasis

Immune/Inflammatory

Response

Genetics

Stress Response

Applicability to Practice

Case Studies

References


Pathophysiology of surgical site infection

Pathophysiology of Surgical Site Infection

Stress Response, Immune/Inflammation Response, Genetics, and Applicability to Practice Reviewed


Tutorial overview
Tutorial Overview

  • The body’s defense against severe infection following injury or trauma post surgical incision requires an intricate balance be maintained through specially designed protective physiological mechanisms.

  • Communication pathways between the nervous system and immune system that protect the body from infection post surgical incision are described.



Why learn about surgical site infection
Why Learn About mechanisms and communication pathways are included. Surgical Site Infection?

  • Complications resulting from surgical site infections continue to be a significant cause of morbidity and mortality among hospitalized patients.

  • The Centers for Disease Control and Prevention (CDC) monitor nosocomial infections using the National Nosocomial Infections Surveillance (NNIS) system established in 1970.


  • “Based on NNIS system reports, SSIs are the third most frequently reported nosocomial infection, accounting for 14% to 16% of all nosocomial infections among hospitalized patients” (Mangram et al, 1999, p. 251).

  • “Among surgical patients, SSIs were the most common nosocomial infection, accounting for 38% of all such infections”(Mangram et al, 1999, p. 251).


  • Hospital reporting of nosocomial conditions is now required by CMS.

  • In February, 2006 the Deficit Reduction Act of 2005 was enacted reducing hospital reimbursement from The Centers of Medicare and Medicaid Services (CMS) for hospital acquired conditions.

  • Beginning October 1, 2008, reimbursement for the treatment of nosocomial conditions acquired on and after admission will be discontinued.


Test your knowledge
Test Your Knowledge by CMS.

SSIs continue to be a significant cause of morbidity and mortality among hospitalized patients.

SSIs are common nosocomial infections among surgical patients.

Hospitals will continue to be reimbursed after October 1, 2008 for hospital acquired conditions.

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Why is understanding the pathophysiology of surgical site infection important
Why is understanding the pathophysiology of surgical site infection important?

  • Understanding the pathophysiology of surgical site infection increases operating room personnel awareness of the importance of strict adherence to surgical techniques/interventions to achieve the best possible post operative outcomes.


Immune inflammatory response of surgical site infection

The immune and inflammatory physiological processes are initiated post surgical incision to prevent infection.

Immune/Inflammatory Responseof Surgical Site Infection



Immune response
Immune Response initiated post surgical incision to prevent infection.

  • There are two components of the immune response the body mobilizes as protective mechanisms against invading pathogens:

    • Natural immunity

    • Specific immunity


  • Components of natural immunity include: initiated post surgical incision to prevent infection.

    • leukocytes

      • granulocytes

        • neutrophils

        • eosinophils

        • basophils

      • monocytes/macrophages

    • natural killer cells

    • cytokines (IL-1B, IL-6, interferon-y, tumor necrosis factor-alpha, complement)


Components of Natural Immunity initiated post surgical incision to prevent infection.

Leukocytes

Natural Killer

Cells

Granulocytes

Monocytes

Neutrophils

Macrophages

Chemicals

Cytokines

Eosinophils

Basophils



  • Granulocytes infection post surgical incision. and monocytes comprise the largest group of immune cells involved in natural immunity.

  • Neutrophils and macrophages are phagocytic cells that flock to the site of injury or infection releasing toxic substances that kill invading pathogens.

    Segerstrom and Miller (2004)


Illustration
Illustration infection post surgical incision.

Surgical Incision

Macrophage

Macrophage

Neutrophil

Neutrophil

Pathogens



Cytokine pathogens through a mechanism known as

Macrophage,

Neutrophil, &

Leukocyte

Pathogens


Test your knowledge1
Test Your Knowledge pathogens through a mechanism known as

Endogenous pathogens are the most common source of SSIs.

  • Click on some exogenous sources of invading pathogens:

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Patients

Surgical Personnel

Surgical Instruments

Surgical Equipment


Specific immunity is activated post-surgical incision in immediate response to injury post surgical incision.

Granulocytes and monocytes comprise the largest group of cells involved in natural immunity.

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Neutrophils are granulocytes. in

Neutrophils and macrophages kill invading pathogens through a mechanism known as phagocytosis.

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Inflammatory response
Inflammatory Response in

  • The skin is a first line defense against infection.

  • When the skin barrier is injured, inflammation occurs as a result of the immune response to surgical incision.


  • L in eukocyte trafficking occurs at the site of tissue injury post surgical incision initiating an inflammatory response.

  • Of the leukocyte cells moving into the site of tissue injury, macrophages are primarily responsible for initiating the inflammatory response.

    Viswanathan and Dhabhar (2005)


  • Macrophages release in cytokines to regulate the inflammatory response of natural immunity post surgical incision.

  • Cytokines mediate the inflammatory response to tissue injury by responding to surface receptors on target cells and replicating the appropriate immune cell response accordingly.

    Desborough (2000)


Illustration1
Illustration in

Surgical Incision

Pathogens

Pathogens

Cytokines

Cytokines

Neutrophil

Neutrophil

Macrophage

Macrophage

Cell Surface Receptors

On Invading Pathogens


Test your knowledge2
Test Your Knowledge in

The skin is a barrier to infection.

Inflammation is a physiologic process that occurs after injury to the skin post surgical incision.

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Leukocytes

Neutrophils

Macrophages

Cytokines


Stress response of surgical site infection
Stress Response regulating the inflammatory response to injury post surgical incision?of Surgical Site Infection

What is Stress?

  • In the 1930s an endocrinologist named Hans Seyle described stress as the body’s response to any form of noxious stimuli called stressors.

    Porth (2005)


Stressors regulating the inflammatory response to injury post surgical incision? is the term Hans Selye used to describe endogenous and exogenous events responsible for initiating the stress response.

Endogenous stressorExogenous stressor

anxiety surgical incision

Porth (2005)



Illustration2
Illustration activation of the

Neuroendocrine Control System

Sympathetic Nervous System

Hypothalamic-Pituitary-Adrenal Axis


Sympathetic nervous system
Sympathetic Nervous System activation of the

  • The SNS is activated as a result of psychological stress and injury to the body caused by the surgical incision.

  • When the SNS is activated, catecholamines are released into the blood stream.


  • The catecholamines released are: activation of the

    • epinephrine

    • norepinephrine

  • Catecholamines circulating in the blood stream increase sympathetic activity by attaching to adrenergic receptors located on cell surfaces within the body.



Click here to learn about specific

adrenergic receptor responses.

When you have finished viewing the adrenergic receptor slides,

click on the button to return here.


Illustration3
Illustration responses to neurotransmitters.

Neuroendocrine Control System

Sympathetic Nervous System

Catecholamines

Cell

Cell

Epinephrine

Norepinephrine

Cell

Cell

Bloodstream

Adrenergic Receptors


Test your knowledge3
Test Your Knowledge responses to neurotransmitters.

Anxiety is an endogenous stressor.

Surgical incisions are exogenous stressors.

The neuroendocrine control system regulates the stress response to endogenous and exogenous stressors.

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The SNS and HPA axis comprise the neuroendocrine control system.

The SNS releases cortisol into the bloodstream when the stress response is activated post surgical incision.

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Epinephrine

Norepinephrine

Aldosterone

Vasopressin


Catecholamines attach to alpha and beta receptors located on cell surfaces.

  • Which cell surface receptors are excitatory?

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F

Alpha 1

Alpha 2

Beta 1

Beta 2


Hypothalamic pituitary adrenal axis
Hypothalamic-Pituitary-Adrenal Axis located on cell surfaces.

  • The stress response to surgical incision initiates the following sequence of events from the HPA axis:

    • The hormone corticotropin-releasing factor (CRF) is released into the portal system circulation.

    • CRF stimulates the release of adrenocorticotrophic hormone (ACTH).

    • ACTH stimulates the secretion of glucocorticoid hormones.


  • One of the most recognized glucocorticoid hormones released as a result of the stress response post surgical incision is cortisol.

  • Cortisol release maintains homeostasis through the following negative feedback mechanisms described next:

    • decreases immune/inflammatory response

    • increases stress response


Illustration4
Illustration as a result of the stress response post surgical incision is

Neuroendocrine Control System

Sympathetic Nervous System

Hypothalamic-Pituitary-Adrenal Axis

Catecholamines

Glucocorticoids

CRF

ACTH

Epinephrine

Norepinephrine

Cortisol

Bloodstream


Corticotropin

ACTH

Glucocorticoids

Cortisol


Cortisol is a glucocorticoid hormone. stress response?

Cortisol is a regulator of the immune/inflammatory and stress responses.

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F

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Homeostasis surgical site infection
Homeostasis stress response?&Surgical Site Infection

  • The body’s normal state of homeostasis is threatened by the immune/inflammatory response to tissue injury post surgical incision.

  • Negative feedback mechanismsare initiated to maintain homeostasis.


  • The stress response?neuroendocrine control system is one physiological process responding to stressors post surgical incision to maintain homeostasis.

  • The SNS and HPA axis maintain a delicate balance of up and down regulation of the immune system to maintain homeostasis.

HPAAxis

SNS


  • Initially, in response to impending trauma caused by surgical incision, the release of catecholamines from the SNS amplifies the immune/inflammatory response.

  • This amplified immune/inflammatory response causes increased leukocyte trafficking into the site of tissue injury post surgical incision to prevent infection.



Illustration5
Illustration causes increased release of cortisol from the HPA axis.

Neuroendocrine Control System

Sympathetic Nervous System

Hypothalamic-Pituitary-Adrenal Axis

Catecholamines

Glucocorticoids

CRF

ACTH

Surgical

Incision

Epinephrine

Norepinephrine

Cortisol

Cortisol

Cortisol

Cytokines

Pathogens

Neutrophil

Macrophage



Illustration6
Illustration adrenergic receptor activation to reduce pro-inflammatory cytokine production and restore homeostasis.

Neuroendocrine Control System

Sympathetic Nervous System

Hypothalamic-Pituitary-Adrenal Axis

Catecholamines

Glucocorticoids

CRF

ACTH

Surgical

Incision

Epinephrine

Norepinephrine

Cortisol

Cortisol

Cortisol

Cytokines

Pathogens

Neutrophil

Cell

Cell

Macrophage

Adrenergic Receptors

Cell Surface Receptors


  • “The interactions between the neuroendocrine and immune systems provide a finely tuned regulatory system required for health. Disturbances at any level can lead to changes in susceptibility to or severity of infectious, inflammatory or autoimmune diseases” (Jeanette & Sternberg, 2003, p.252).

  • Thus, the body’s ability to return to a state of homeostasis following the acute stress response is essential to maintain health and prevent surgical site infection.


Immune/Inflammatory Response Activated systems provide a finely tuned regulatory system required for health. Disturbances at any level can lead to changes in susceptibility to or severity of infectious, inflammatory or autoimmune diseases” (Jeanette & Sternberg, 2003, p.252).

Leukocytes, Neutrophils,

Macrophages, & Cytokines

Flock To Surgical Incision

Cortisol Decreases

Inflammation

Homeostasis

Restored

Cortisol Increases

Inhibitory Adrenergic

Receptor Activity

SNS Releases

Epinephrine & Norepinephrine

HPA Axis Releases

Corticotropin, ACTH,

Glucocorticoids (Cortisol)

Stress Response Activated


Test your knowledge4
Test Your Knowledge systems provide a finely tuned regulatory system required for health. Disturbances at any level can lead to changes in susceptibility to or severity of infectious, inflammatory or autoimmune diseases” (Jeanette & Sternberg, 2003, p.252).

The state of internal stability maintained within the human body is called homeostasis.

Negative feedback mechanisms maintain homeostasis.

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The SNS and HPA axis restore homeostasis through up and down regulation of the stress, immune, and inflammatory processes.

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Genetics and surgical site infection
Genetics down regulation of the stress, immune, and inflammatory processes.and Surgical Site Infection

  • “In explaining the stress response, Seyle proposed that two factors determine the nature of the stress response: the properties of the stressor and the conditioning of the person being stressed” (Porth, 2005, p. 190).

  • Genetic endowment is a variable consistent with conditioning of the person being stressed.



  • As previously explained, stressors alert the body through neuroendocrine and immune pathways of internal or external stimuli threatening homeostasis of the body.

  • The body is alerted of threats to homeostasis at a cellular level turning cascades of gene expression on and off.

    Rossi (2004)


Illustration7
Illustration neuroendocrine and immune pathways of internal or external stimuli threatening homeostasis of the body.

Stressors

Endocrine Pathway

Neural Pathway

Immune Pathway




Illustration8
Illustration cytokine response.

Genetic polymorphisms

may determine the innate

immune response to

Inflammation.

Surgical

Incision

Decreased cytokine response

Increased cytokine response

Pathogens

Pathogens

Cytokines

Cytokines

Neutrophil

Neutrophil

Macrophage

Macrophage

Cell Surface Receptors

On Invading Pathogens


  • Further research to examine the physiological processes regulated by specific genes and the functions they code for in response to internal and external stressors is needed.

  • Gene therapy may be the wave of the future to pre-determine the body’s physiologic responses to surgical stressors.


Test your knowledge5
Test Your Knowledge regulated by specific genes and the functions they code for in response to internal and external stressors is needed.

The literature suggests that genes regulate the immune, inflammatory, and stress responses to infection.

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Applicability to practice
Applicability to Practice regulated by specific genes and the functions they code for in response to internal and external stressors is needed.

  • Ask yourself, “What is the outcome I am trying to achieve?”

  • The Perioperative Nursing Data Set, outcome O10 states, “the patient is free from signs and symptoms of infection” (AORN, 2002).

  • Suggestions for achieving this outcome are described next.


  • In December 2006, the IHI launched the 5 Million Lives Campaign to reduce avoidable complications in hospitals.

  • To reduce surgical site infection, the IHI is urging hospitals to embrace evidence-based practice to improve quality outcomes by participating in the Surgical Care Improvement Project (SCIP).


  • The SCIP initiative is the product of intensive research to identify surgical practices proven effective in preventing the development of SSIs post surgical incision.

  • SCIP initiatives to reduce Surgical Site Infection include:

    • Appropriate use of prophylactic antibiotics

    • Appropriate surgical site hair removal

    • Maintaining normothermia

    • Glycemic control


insulin

warmth

clip

antibiotic


Brainstorm
Brainstorm! identify surgical practices proven effective in preventing the development of SSIs post surgical incision.

  • What else can surgical personnel do to prevent SSIs? The list is endless!!!

    • Hand/forearm asepsis

    • Appropriate skin preparation

    • Jewelry removal

    • Positive-pressure ventilation

    • Limit traffic

    • Environmental cleaning

    • Proper surgical attire

    • Strict asepsis and surgical technique


Think outside the Box! identify surgical practices proven effective in preventing the development of SSIs post surgical incision.

  • Education preparation

  • Guided imagery

  • Nutrition

  • Smoking cessation

  • Incision care


  • The purpose of established policies/ procedures and protocols in the surgical environment are intended to reduce the spread and infiltration of pathogens into surgical incisions to prevent infection and should be followed.

  • Just remember, if you were a patient about to undergo surgery, what would you want?


Case study part 1
Case Study protocols in the surgical environment are intended to reduce the spread and infiltration of pathogens into surgical incisions to prevent infection and should be followed.Part 1

  • Mr. X is scheduled for a pacemaker pocket revision under local anesthetic. Upon reviewing the chart, it is noted that the patient is positive for MRSA in the nares. Topical and intravenous antibiotics are administered preoperatively. It is observed that the edges of the pacemaker pocket are red and raised. A thorough skin prep is performed. Instrument sterility is confirmed. Upon surgical incision, a small amount of purulent fluid escapes the pacemaker pocket.


Pacemaker Implant

Surgical Instruments

Patient’s Own Flora

Inadequate Ventilation



Innate Immunity

Specific Immunity

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Case study part 2
Case Study injury and infection?Part 2

  • Mr. X’s surgeon decides to implant a new pacemaker due to the presence of infection. New implant sterility is confirmed. Mr. X begins to complain that he is very anxious and worried. He explains that his father never recovered from a similar infection. In addition, the patient reports pain upon surgical incision. In an effort to relax Mr. X, the surgeon reassures Mr. X while injecting more local anesthetic. The circulating nurse begins to play a guided imagery CD overhead.


Increased Heart Rate

Decreased Heart Rate

Increased Blood Pressure

Decreased Blood Pressure


Epinephrine

Norepinephrine

Cortisol



T circulating cortisol. You recognize that this is occurring as part of the stress response. Genetic testing reveals polymorphisms of inflammatory genes.

F

Cortisol regulates the immune/inflammatory/stress response to restore homeostasis.

Genetic polymorphisms may pre- determine Mr. X’s immune/inflammatory response to injury and infection.

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Case study part 3
Case Study circulating cortisol. You recognize that this is occurring as part of the stress response. Genetic testing reveals polymorphisms of inflammatory genes.Part 3

  • Although you recognize that Mr. X may be genetically prone to surgical site infection, you want to ensure that every precaution has been taken to prevent further complications.


Antibiotic administration

Skin prep

Implant/instrument sterility

Local anesthetic

Guided imagery



Congratulations
Congratulations! initiated throughout the surgical sequela is connected to the pathophysiology of surgical site infection.

  • You have completed the tutorial!


References
References initiated throughout the surgical sequela is connected to the pathophysiology of surgical site infection.

  • Beyea, S. C. (Eds). (2002). Perioperative nursing data set (2nd ed.). Denver, CO: AORN, Inc.

  • Choileain, N.N. & Redmond, P. (2006). Cell response to surgery. Archives of Surgery, 141, 1132 – 1140.

  • Desborough, J.P. (2000). The stress response to trauma and surgery. British Journal of Anaesthesia, 85, 109 – 117.

  • Gosain, A., Jones, S.B., Shankar, R., Gamelli, R.L., DiPietro, L.A. (2006). Norepinephrine modulates the inflammatory and proliferative phases of wound healing. The Journal of Trauma Injury, Infection, and Critical Care, 60, 736 – 744.

  • Jeanette, F.E., Sternberg, W., & Sternberg, E.M (2003). Neural immune pathways and their connection to inflammatory diseases. Arthritis Research and Therapy, 5, 251 – 265.

  • Mangram, A.J., Horan, T.C., Pearson, M.L., Silver, L.C., & Jarvis, W.R. (1999). Guideline for prevention of surgical site infection. Infection Control and Hospital Epidemiology, 20, 247 – 278.


  • Pavlov, V.A., Wang, H., Czura, C.J., Friedman, S.G., & Tracey, K.J. (2003). The cholinergic anti-inflammatory pathway: A missing link in neuroimmunomodulation. Molecular Medicine, 9, 125 – 134.

  • Porth, C.M. (2005). Pathophysiology: Concepts of altered health status (7th ed.). Philadelphia, PA: Lippincott & Wilkins.

  • Rivera-Chavez, F.A., Peters-Hybki, D.L., Barber, R.C., Lindberg, G.M., Jialal, I., Munford, R.S., & O’Keefe, G.E. (2004). Innate immunity genes influence the severity of acute appendicitis. Annals of Surgery, 240, 269 – 277.

  • Rossi, E.L. (2004). Stress-induced alternative gene splicing in mind-body medicine. Advances, 20, 12 – 19.

  • Segerstrom, S.C. & Miller, G.E. (2004). Psychological stress and the human immune system: A meta-analytic study of 30 years of inquiry. Psychological Bulletin, 130, 601 – 630.


  • Sternberg, E.M. (1997). Neural-immune interactions in health and disease. The Journal of Clinical Investigation, 100, 2641 – 2647.

  • Sternberg, E.M. (2006). Neural regulation of innate immunity: A coordinated nonspecific host response to pathogens. Nature Reviews Immunology, 6, 318 – 328.

  • Viswanathan, K. & Dhabhar, F.S. (2005). Stress-induced enhancement of leukocyte trafficking into sites of surgery or immune activation. Proceedings of the National Academy of Sciences, 102, 5808 – 5813.

  • Wilmore, D.W. (2002). From Cuthbertson to fast-track surgery: 70 years of progress in reducing stress in surgical patients. Annals of Surgery, 236, 643 – 648.


Specific immunity
Specific Immunity and disease.

  • Specific immunity involves an adaptive response of focused recognition to invading pathogens.


  • Components of specific immunity include: and disease.

    • T lymphocytes

      • T-helper cells

      • T-cytotoxic cells

    • B lymphocytes

    • immunoglobulines (IgA, IgG, IgM, and IgE)

    • cytokines (IL-2, IL-4, IL-10, Interferon-y)


  • T and B lymphocytes determine cell specific immunity. and disease.

  • T lymphocytes produce T-helper cells and T-cytotoxic cells.

  • T-helper cells activate cytokines to mediate a cellular or humoral immune response.

  • Cytokines activate T-cytotoxic cells to recognize and destroy antigens such as viruses as a mechanism of cellular immunity.

  • Cytokines activate B cells to stimulate plasma cells to produce proteins called antibodies or immunoglobulins as a mechanism of humoral immunity.


  • Each antibody produced serves a specific function: and disease.

    • IgA found in mucus membranes and secretions bind to antigens before they enter body tissues.

    • IgG bind to antigens circulating in the bloodstream.

    • IgM bind to and cluster antigens together circulating in the bloodstream.

    • IgE bind to mast cells that produce histamine as a component of an allergic response to antigens.


  • Receptor sites located on the cell surfaces of lymphocytes recognize and respond to matching receptor sites located on the cell surfaces of invading pathogens explained by Segerstrom et al (2004) as clonal proliferation, or the proliferative response.

  • The proliferative response of specific immunity may require several days to maximize immune potential; therefore, natural immunity contains infection post surgical incision.


  • Alpha 1 receptors are located in: recognize and respond to matching receptor sites located on the cell surfaces of invading pathogens explained by Segerstrom et al (2004) as

    • blood vessels

    • skin

    • eyes

  • Alpha 1 receptors trigger the following physiological responses:

    • vasoconstriction

    • sweating

    • dilated pupils


  • Beta 1 receptors are located in: recognize and respond to matching receptor sites located on the cell surfaces of invading pathogens explained by Segerstrom et al (2004) as

    • heart

    • body tissues

    • adipose tissue

  • Beta 1 receptors trigger the following physiological responses:

    • increased heart rate

    • increased metabolism

    • fat released into bloodstream


  • Alpha 2 receptors are located in: recognize and respond to matching receptor sites located on the cell surfaces of invading pathogens explained by Segerstrom et al (2004) as

    • gastrointestinal (GI) tract

    • neurons

  • Alpha 2 receptors trigger the following physiological responses:

    • decreased GI motility

    • decreased insulin release

    • inhibited catecholamine release


  • Beta 2 receptors are located in: recognize and respond to matching receptor sites located on the cell surfaces of invading pathogens explained by Segerstrom et al (2004) as

    • lungs

  • Beta 2 receptors trigger the following physiological response:

    • bronchioles dilate


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    • Hospitals will not be reimbursed after October 1, 2008 for hospital acquired conditions.

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    • Remember, natural immunity is the body’s first immune response to invading pathogens!

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    • Remember the SNS releases catecholamines into the blood stream!

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    • Remember, endogenous sources of infection reside with the body!

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    • Cells of natural immunity (i.e. granulocytes and leukocytes) respond to sites of injury and infection first!

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    • Remember, Alpha 1 and Beta 1 receptors are excitatory!

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    • Is cortisol released by the SNS or HPA axis?

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    • Cortisol and genetics both play a role in inflammation.

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