Transcript Slide 1

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.
To advance to the next slide:



Click
To go to back to the first slide:


or
To go back to the previous slide:


Click
Use space bar
Click
To view specific content:

Click on the action buttons on the Menu slide
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
Introduction
Homeostasis
Immune/Inflammatory
Response
Genetics
Stress Response
Applicability to Practice
Case Studies
References
Pathophysiology of
Surgical Site Infection
Stress Response, Immune/Inflammation
Response, Genetics, and Applicability to
Practice Reviewed
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.

Genetic factors influencing these regulatory
physiological mechanisms and communication
pathways are included.

Applicability of the pathophysiology of surgical site
infection to surgical practice is explored.
Why Learn About
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
T
F
T
F
T
F
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.
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.

Sources of infection post surgical incision:

Endogenous
 Most common cause of SSIs

Exogenous
Immune Response

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:

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
Leukocytes
Granulocytes
Monocytes
Neutrophils
Macrophages
Eosinophils
Basophils
Natural Killer
Cells
Chemicals
Cytokines

Natural immunity is the body’s primary defense
against infection post surgical incision.

Cells involved in natural immunity are capable of
attacking multiple invading pathogens within minutes
to hours when challenged.
Segerstrom and Miller (2004)

Granulocytes 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
Surgical Incision
Pathogens

Neutrophils and macrophages then consume these
invading pathogens through a mechanism known as
phagocytosis.

In addition, macrophages release proinflammatory
cytokines as a component of the inflammatory
response described next.
Cytokine
Macrophage,
Neutrophil, &
Leukocyte
Pathogens
Test Your Knowledge
Endogenous pathogens are the
most common source of SSIs.
Click on some exogenous sources of
invading pathogens:
T

F
Patients
Surgical Personnel
Surgical Instruments
Surgical Equipment
T
F
T
F
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.
T
F
T
F
Neutrophils are granulocytes.
Neutrophils and macrophages kill
invading pathogens through a
mechanism known as phagocytosis.
Inflammatory Response

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.

Leukocyte 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 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)
Illustration
Surgical Incision
Pathogens
Pathogens
Cytokines
Cytokines
Neutrophil
Neutrophil
Macrophage
Macrophage
Cell Surface Receptors
On Invading Pathogens
Test Your Knowledge
T
F
T
F
The skin is a barrier to infection.
Inflammation is a physiologic
process that occurs after injury to
the skin post surgical incision.

What are the most common cells of natural
immunity regulating the inflammatory
response to injury post surgical incision?
Leukocytes
Neutrophils
Macrophages
Cytokines
Stress Response
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 is the term Hans Selye used to describe
endogenous and exogenous events responsible for
initiating the stress response.
Endogenous stressor
anxiety
Exogenous stressor
surgical incision
Porth (2005)

The stress response post surgical incision includes
activation of the neuroendocrine control system.

The neuroendocrine control system is comprised of
the sympathetic nervous system (SNS) and the
hypothalamic-pituitary-adrenal (HPA) axis.
Wilmore (2002)
Illustration
Neuroendocrine Control System
Sympathetic Nervous System
Hypothalamic-Pituitary-Adrenal Axis
Sympathetic Nervous System

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:
 epinephrine
 norepinephrine

Catecholamines circulating in the blood stream
increase sympathetic activity by attaching to
adrenergic receptors located on cell surfaces within
the body.

Different cell surface receptors account for different
responses to neurotransmitters.

The adrenergic receptors include:
 alpha 1 and beta 1 receptors

alpha 2 and beta 2 receptors

Alpha 1 and Beta 1 receptors are excitatory.

Alpha 2 and Beta 2 receptors are inhibitory.
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.
Illustration
Neuroendocrine Control System
Sympathetic Nervous System
Catecholamines
Epinephrine
Norepinephrine
Bloodstream
Adrenergic Receptors
Cell
Cell
Cell
Cell
Test Your Knowledge
T
F
T
F
T
F
Anxiety is an endogenous
stressor.
Surgical incisions are exogenous
stressors.
The neuroendocrine control system
regulates the stress response to
endogenous and exogenous
stressors.
T
F
T
F
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.

What catecholamines are released as a
result of the stress response pre and post
surgical incision?
Epinephrine
Norepinephrine
Aldosterone
Vasopressin
Catecholamines attach to alpha
and beta receptors located on cell
surfaces.
Which cell surface receptors are excitatory?
T

F
Alpha 1
Alpha 2
Beta 1
Beta 2
Hypothalamic-Pituitary-Adrenal Axis

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
Illustration
Neuroendocrine Control System
Sympathetic Nervous System Hypothalamic-Pituitary-Adrenal Axis
Catecholamines
Epinephrine
CRF
Norepinephrine
ACTH
Glucocorticoids
Cortisol
Bloodstream

What are the hormones released from the
HPA axis during the stress response?
Corticotropin
ACTH
Glucocorticoids
Cortisol
T
F
T
F
Cortisol is a glucocorticoid hormone.
Cortisol is a regulator of the
immune/inflammatory and stress
responses.
Homeostasis
&
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 mechanisms are initiated to
maintain homeostasis.

The 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.
HPA
Axis
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.

The release of pro-inflammatory cytokines by
macrophages causes increased release of cortisol
from the HPA axis.

Eventually, the increased cortisol release
terminates the inflammatory response restoring the
body’s normal state of homeostasis post surgical
incision.
Illustration
Neuroendocrine Control System
Sympathetic Nervous System
Catecholamines
Epinephrine
Norepinephrine
Cytokines
Neutrophil
Macrophage
Hypothalamic-Pituitary-Adrenal Axis
CRF
ACTH
Surgical
Incision
Pathogens
Glucocorticoids
Cortisol
Cortisol
Cortisol

In addition, increased cortisol release enhances
inhibitory adrenergic receptor activation to reduce
pro-inflammatory cytokine production and restore
homeostasis.

Thus, the glucocorticoid hormone cortisol
suppresses the immune/inflammatory response and
enhances the effects of catecholamines .
Illustration
Neuroendocrine Control System
Sympathetic Nervous System
Catecholamines
Epinephrine
Hypothalamic-Pituitary-Adrenal Axis
CRF
Norepinephrine
Cytokines
ACTH
Surgical
Incision
Pathogens
Neutrophil
Macrophage
Cell Surface Receptors
Glucocorticoids
Cortisol
Cortisol
Cortisol
Cell
Cell
Adrenergic 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
Leukocytes, Neutrophils,
Macrophages, & Cytokines
Flock To Surgical Incision
Cortisol Decreases
Inflammation
Cortisol Increases
Inhibitory Adrenergic
Receptor Activity
Homeostasis
Restored
SNS Releases
Epinephrine & Norepinephrine
HPA Axis Releases
Corticotropin, ACTH,
Glucocorticoids (Cortisol)
Stress Response Activated
Test Your Knowledge
T
F
T
F
The state of internal stability
maintained within the human body
is called homeostasis.
Negative feedback mechanisms
maintain homeostasis.
T
F
The SNS and HPA axis restore
homeostasis through up and down
regulation of the stress, immune,
and inflammatory processes.
Genetics
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.

Our genetic makeup is stored in a molecule known
as deoxyribonucleic acid (DNA).

Genes are a component of DNA that determine the
production of proteins in the human body
responsible for cellular expression.

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)
Stressors
Endocrine Pathway
Neural Pathway
Illustration
Immune Pathway

Local inflammation as occurs in surgical site
infection may be determined by genes involved in
natural immunity.

The severity of local inflammation may be influenced
by genetic polymorphisms.

Polymorphisms in inflammatory genes result in an
altered cytokine response.

Cytokine responsiveness as determined by genetic
expression may influence the degree of local
inflammation.
Rivera-Chavez et al (2004)
Illustration
Genetic polymorphisms
may determine the innate
immune response to
Inflammation.
Surgical
Decreased cytokine response Incision
Pathogens
Increased cytokine response
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 predetermine the body’s physiologic responses to
surgical stressors.
Test Your Knowledge
T
F
The literature suggests that genes
regulate the immune, inflammatory,
and stress responses to infection.
Applicability to Practice

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

The purpose of each SCIP initiative is to reduce the
spread of pathogens and promote incisional healing
to prevent infection.
insulin
warmth
clip
antibiotic
Brainstorm!

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!





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

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.

What endogenous sources could have
caused Mr. X’s pacemaker pocket infection?
Pacemaker Implant
Surgical Instruments
Patient’s Own Flora
Inadequate Ventilation

Mr. X’s pacemaker pocket is cultured
revealing a large number of immune cells at
the site of infection indicating an
immune/inflammatory response is occurring
at the site of tissue injury.

What is the immune response likely occurring
at the site of injury and infection?
Innate Immunity
Specific Immunity
T
F
Leukocytes are likely to be found
upon microscopic examination of the
culture site.
Case Study
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.

What physiological responses would one
expect Mr. X to display as a result of
excitatory alpha 1 and beta 1 receptor site
activation?
Increased Heart Rate
Decreased Heart Rate
Increased Blood Pressure
Decreased Blood Pressure

What are the catecholamines responsible for
initiating these physiological responses?
Epinephrine
Norepinephrine
Cortisol

A blood sample is taken revealing elevated
levels of circulating cortisol. You recognize
that this is occurring as part of the stress
response. Genetic testing reveals
polymorphisms of inflammatory genes.
T
F
T
F
Cortisol regulates the
immune/inflammatory/stress
response to restore homeostasis.
Genetic polymorphisms may predetermine Mr. X’s
immune/inflammatory response
to injury and infection.
Case Study
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.

What interventions were initiated in this case
study to ensure Mr. X is free from further
infection post surgical incision?
Antibiotic administration
Skin prep
Implant/instrument sterility
Local anesthetic
Guided imagery

Hopefully, you have learned that every intervention
initiated throughout the surgical sequela is
connected to the pathophysiology of surgical site
infection.

This is just the tip of the iceberg!
Congratulations!

You have completed the tutorial!
References






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 mindbody 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
involves an adaptive
response of focused
recognition to
invading pathogens.

Components of specific immunity include:

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.
T lymphocytes produce T-helper cells and Tcytotoxic 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:




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:




blood vessels
skin
eyes
Alpha 1 receptors trigger the following
physiological responses:



vasoconstriction
sweating
dilated pupils

Beta 1 receptors are located in:




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:



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:


lungs
Beta 2 receptors trigger the following
physiological response:

bronchioles dilate

Right!
Click here to return to questions

Try again!
Click here to return to questions

Try again!

Hospitals will not be reimbursed after October 1,
2008 for hospital acquired conditions.
Click here to return to questions

Great!
Click here to return to questions

Sorry! Try again!
Click here to return to questions

Yes!
Click here to return to questions

Try again!

Remember, natural immunity is the body’s first
immune response to invading pathogens!
Click here to return to questions

Try again!
Click here to return to questions

Yes!
Click here to return to questions

Try again!
Click here to return to questions

Way to go!
Click here to return to questions

Try again!
Click here to return to questions

That’s right!
Click here to return to questions

Correct!
Click here to return to questions

Try again!
Click here to return to questions

Exactly!
Click here to return to questions

Try again!
Click here to return to questions

Try again!

Remember the SNS releases catecholamines into
the blood stream!
Click here to return to questions

Wow!
Click here to return to questions

Try again!
Click here to return to questions

Good job!
Click here to return to questions

Try again!
Click here to return to questions

Impressive!
Click here to return to questions

Right again!
Click here to return to questions

Try again!
Click here to return to questions

Terrific!
Click here to return to questions

Try again!
Click here to return to questions

Good job!
Click here to return to questions

Try again!
Click here to return to questions

Great!
Click here to return to questions

Try again!
Click here to return to questions

Fabulous!
Click here to return to questions

Try again!
Click here to return to questions

Absolutely!
Click here to return to questions

Try again!

Remember, endogenous sources of infection
reside with the body!
Click here to return to questions

That’s right!
Click here to return to questions

Try again!

Cells of natural immunity (i.e. granulocytes and
leukocytes) respond to sites of injury and infection
first!
Click here to return to questions

Awesome!
Click here to return to questions

Try again!

Remember, Alpha 1 and Beta 1 receptors are
excitatory!
Click here to return to questions

That’s right!
Click here to return to questions

Try again!

Is cortisol released by the SNS or HPA axis?
Click here to return to questions

Correct again!
Click here to return to questions

Try again!

Cortisol and genetics both play a role in
inflammation.
Click here to return to questions

Way to go!
Click here to return to questions