Transcript Inflammation & the Immune Response Unit VIII

Inflammation & the Immune
Response
Unit VIII
Fall, 2010
Keith Rischer, RN, MA, CEN, CCRN
Objectives for this content

Inflammatory response
 #1-3

Infection/sepsis/chain of infection
 #4-10

Physiologic immune response
 #11-16
Three Lines of Defense
Anatomical
Barriers
 Acute
Inflammatory
Response
 Immune System

Lines of Defense
Anatomical Barriers:
First Line of Defense
Skin
 Mucous
membranes


Normal bacterial flora


Clostridium difficile
Yeast infections
Normal Body Defenses

Skin
 multilayer
barrier, shed outer layer, contains
fatty acids that kills some bacteria

Lungs
 contain
cilia in upper respiratory tract,
macrophages

Urinary Tract
 flush

action of urine washes away bacteria
Perry and Potter pg. 647 Ch 34 Table 34-3
Inflammatory Response
Inflammatory Response
Occurs in response
to injury
 Localized
 Immediate
 Beneficial
 Appropriate level of
response
 Non Specific

Causes of Inflammation

Physical
 Trauma
 Lacerations
 Burns

Chemical- Bites
 Allergic

response
Micro-organisms
 Bacteria
Inflammatory Response
REDNESS
 SWELLING
 PAIN
 HEAT
 LOSS OF
FUNCTION

Purpose of inflammation
Neutralizes and
Dilutes Toxins
 Removes necrotic
materials
 Provides an
environment for
healing
 Add “itis” to affected
body part

4 Phases of Inflammation

Vascular


Think blood vessels
Cellular
 Think

Formation of
Exudate
 Fluid

WBC’s
& neutrophils
Healing
 regeneration
of tissue
or repair
Vascular Phase: Blood Vessels





Injury occurs
Mediators intervene
Vasodilation occurs
Capillaries become
more permeable
Swelling and
movement of fluid
occurs
Cellular Phase – Think WBC’s
Injury occurs
 Chemotaxis begins
 White blood cells
rush in to help

 Neutrophils
 Monocytes
 Macrophages
Chemical Mediators
Coordinators of the
inflammatory
response
 Histamine
 Prostagladins
 Cytokines
Laboratory tests

Erythrocyte sedimentation rate
 (ESR
or sed rate)
 <20 mm/hr

CRP – C reactive protein
 non
specific test identifying the presence of
inflammation
 <1.0 mg/dl
Application of the Nursing Process
Data/Assessment:
 History
 Local signs and
symptoms including
pain assessment


WILDA
Applicable lab work
Nursing Diagnosis
Acute pain related to tissue trauma
 Impaired physical mobility related to
discomfort

Nursing Interventions

Care will vary with causative agent and
physical condition of the patient

What are some nursing actions you might
implement or anticipate

How will you as the nurse evaluate the
outcome
Expected Outcomes…
Healing of the wound or injury
 Prevent minor infections from becoming
overwhelming to the body

 UTI
vs. urosepsis
Goals and outcomes will vary with each
patient
 Remember that your outcomes will drive
your interventions/cares

Systemic Manifestations of Acute
Inflammation

Fever/chills
 Cytokines
 Benefits
 Increased
killing of microorganisms
 Increased phagocytosis by neutrophils
 Increased activity of interferon

Leukocytosis
 Neutrophils
 “left
shift”…band cells
Medications: NSAIDS

Ibuprofen, Toradol
 Mechanism
 Inhibits
 Nursing
 Give
of action
prostaglandin synthesis
implications
w/food
 Elderly-high risk GI bleed
 Prolongs bleeding times 1 day
 Assess renal function-creatinine w/chronic use
Medications: NSAIDS

Salicylates – Aspirin
 Mechanism
of action
 Inhibits
production of prostaglandins
 Decreases platelet aggregation
 Nursing
 Give
implications
w/food
 Prolongs bleeding times 4-7 days
Medications: Anti-histamines
 Benadryl,
Ranitidine (Zantec), Famotidine
(Pepcid)
 Mechanism
of action
– Block histamine at the receptor site
– Decreases gastric acid secretion
 Nursing
implications
– With meals
– Drowsiness/dizziness
Medications: Corticosteroids

Prednisone

Mechanism of action





Decrease inflammation by stabilizing neutrophils and
lysosomes
Inhibit prostaglandin synthesis
Inhibits chemotactic cytokines
Decreases mast cell stimulation
Nursing implications


Meals
Chronic use complications
– Risk of infection
– Hyperglycemia
– SE
Inflammation Case Study


26 yr female with no
medical history
CC




Severe epigastric abd pain
the last 2 days
Severe pain all night, rates
10/10-sharp-nothing
relieves. Appears
uncomfortable
T-101.2 P-110 R-24 BP
168/88 sats 98% RA
Tender epigastric area,
BS active x4

Labs
 K+-3.4
 Na+ 138
 Creatinine 0.6
 ALT-81
 AST-81
 WBC-28.7
 Lipase-1633
Case Study continued

Outcomes

Nursing diagnosis priorities

Plan of care

Evaluation
What is an infection?
Normal Course of an Infection
Incubation period
 Prodromal stage
 Full stage of illness
 Convalescence

Infectious agents/pathogens




Bacteria
Virus
Fungi
Protozoa
Bacteria



Single cell
Human cells vs.
bacteria count in body
Gram +/-
Virus




Most common affliction
of humans
Has no metabolism of
it’s own
Is incapable of
replicating outside a
living cell
Takes over the
metabolic machinery of
host cells to survive and
replicate
What influences Pathogen survival?






Food/Glucose
Water
Oxygen –
aerobic/anaerobic
Temperature
pH
light
Reservoir

A place where a
pathogen can survive
but may or may not
multiply

What is the most
common reservoir?

What is a carrier?
Portal of exit

For the pathogen to
cause an infection it
must exit the reservoir

How can this
happen?
Mode of Transmission

Direct or indirect

What is the major
mode of transmission
in the health care
setting?

List the 4 categories
of transmission
Portal of entry
Susceptible Host

What factors increase
our susceptibility to
infection?




Age
Stress
Nutritional status
Current medical
therapies



Chemo
Steroids
Presence of disease
Breaking the Chain
Leukocytes=Braveheart
Leukocytes

Normal Blood Count
of all WBC: 4,00011,000/ul



Neutrophils
Monocytes
Lymphocytes B cells:
mediate the humoral
immune response


T cells: Mediate
cellular immunity
Elderly
considerations
Laboratory Studies

CBC
 Hgb
(12-16 g/dl)
 Hct (33-51%)
 Platelets (140-440 thou/cu mm)
 WBC (4.5-11.0 thou/cu mm)

Differential
 Never-neutrophils
(42-72%)
 Let-lymphocytes (20-44%)
 Monkeys-monocytes (<11.1%)
 Eat-eosinophils (<7.1%)
 Bananas-basophils (<3.0%)
Cultures, gram stains and sensitivities

Wound and skin
cultures, body fluids,
blood cultures

Gram stains

Sensitivities
Anti-infective Drugs

Determine if hypersensitive to medication

Check for interactions with other drugs

Educational needs of client

Determining effectiveness
Antibiotic Therapy

Anti-fungal


Cephalosporins


Amoxicillin, Ampicillin
Sulfonamides


Cephalexin (Keflex)
Penicillins


Fluconazole, Nystatin
Bactrim
Tetracyclines

Doxycycline
Antibiotic Resistance

Bacteria adapt in ways which make an
antibiotic less effective or ineffective
 MRSA
– Methicillin resistant staphylococcus
aureus
 VRE – Vancomycin resistant enteroccus
Vancomycin
Anti-infective class other
 Effective against gram+ pathogens
 Used in potentially life-threatening
infections when other drugs are not
effective
 Action: binds to bacterial cell wall and cell
death results
 Poorly absorbed in GI tract, may be given
IV

NCLEX Concepts of Emphasis
1. Define inflammation
2. Is inflammation always present with infection?
3. What are some patient examples that would limit or impair
their inflammatory response?
4. What are the five physical manifestations of the inflammatory
response?
5. Name each distinct phase of the inflammatory response and
unique characteristics of each?
6. What are other causes of inflammation besides microorganisms?
7. What are some common diseases of chronic inflammation?
8. What are the medications that treat the inflammatory
response?
Sepsis

Patho


Infection (susceptible host)
Inflammation-systemic




SIRS
Capillary permeability
Vasodilation
Progressive



Sepsis/SIRS
Septic shock
Multiple Organ Dysfunction Syndrome (MODS)
Article Case Study




70 yr female from NH
CC:
 weakness, diarrhea x3 weeks
Assessment:
 PMH: IDDM, HTN, CVA, COPD, UTI’s
 VS: T-97…101.8 P-109 R20-24 BP-93/41 91-98%
 a/o x3
Labs:
 WBC-26.5
 Gluc 258
Article Case Study-Day 2
T-96.6 P-125 R-24 BP 80/43
 Oriented to self only
 u/o 180cc over 8 hours
 Became more lethargic later in day
 T-96.5 P-100 R-24 BP 70/30
 Labs

 WBC
41.9
 Lactate 2.2
Article Case Study-Day 3
T-96.5 P-100 R 14-32 BP 70/50
 Labs

 WBC
41.9
 Creatinine 4.3
Vasoactive gtts
 Intubated
 Died day 7

Sepsis Case Study

58 yr female from NH



Found unresponsive with dramatically altered LOC
Intubated and transferred to ED
PMH






IDDM
MI
CHF
Mitral valve regurgitation
T-102.7 P-110 R-16 intubated BP- 155/86 sats 95%
Head to Toe






Remains unresponsive-even to pain
Breath sounds coarse bilat
S1S2 soft murmur reg
Skin hot-dry to touch
1+ edema lower extremities
Foley placed…urine thick white, yellow
Sepsis Case Study

Initial labs












UA



l
WBC-13.8
Neutrophils-82%
Hgb-14.9
Platelets-213
Glucose-331
K+-5.0
Creatinine-2.03
ALT-89
AST-193
INR-2.2
Lactate 7.0
Bacteria-many
WBC>100
Leukocyte esterase +
6 hours later…
 T-103.8 HR130 BP 64/30 despite 4
vasopressors IV continuous
 WBC-28.6
 Neutrophils-95%
 Hgb-5.2
 Platelets-64
 Glucose-351
 K+ 3.5
 Creatinine-2.9
 ALT-382
 AST-590
 INR-7.1
 Lactate-14.0
Key Nursing Assessments




Fever/chills
 Hypothermia
Altered LOC/confusion
Break in skin integrity
 Foley catheter
 Wound or incision
Tachycardia
 HR >100
 What if elderly or on beta blockers?
Key Nursing Assessments


Tachypnea
 RR >20
Hypotension
 SBP <90
 SBP drop of >20-30mm/Hg
Decreasing urine output…<30cc/hr

Labs
 WBC
 Neutrophils
 Creatinine
Nursing Diagnosis statements
w/infection/sepsis?
Ineffective breathing pattern
 Decreased cardiac output
 Ineffective tissue perfusion…manifested
by:

 Altered
mental status
 Behaviorial changes (restlessness)
 Renal…creatinine

Acute confusion
NCLEX Concepts of Emphasis
1.
2.
3.
4.
Why is the older adult at risk for infection and cancer
development?
Inflammation and immunity are provided primarily
through what body cells?
Differentiate the 5 types of leukocytes and what each
type does to protect the body from micro-organisms
Which leukocyte is elevated in bacterial infection?
1.
5.
6.
7.
Why…
What body cell is able to recognize and destroy nonself cells?
What vital sign changes are seen in sepsis?
What assessment findings are seen in sepsis?
The Immune Response
Immune Response
Passive Acquired
Immunity

Present at birth
 Short lived
 Body needs to develop
own
Active Acquired
Immunity


After birth
Active
 Long-term
 Exposure to microorganisms
 immunizations
What comprises the immune system?
Bone
Marrow
WBC
Lymph
system
Thymus
Misc:
Gland
Tonsils, Spleen,
Mucosa, Appendix
Lymphatic System
Lymphocytes
WBC that allow the body to remember and
recognize previous invaders.
 Two types

B
lymphocytes
 T lymphocytes.

NK or natural killer cells
Specific Defenses
Humoral (circulating) immunity
 Reside in B lymphocytes
 Mediated by antibodies
(immunoglobulin) produced in
B cell
 Produce antibodies when
activated
Cell-mediated defenses
 T –cells released when
exposure to an antigen occurs
 70-80% total lymphocytes
Antigens




An antigen is a substance
that elicits an immune
response
Mostly comprised of
protein
A foreign substance that
invades the body is called
an antigen
All cells have antigen
unique to that individual
allowing the body to
recognize itself
Humoral (antibody) Immunity

Antibody mediated
immunity

Antibodies are produced
by B cells

Antibodies can bind to
antigens

Immunoglobulins (IgG,
IgA, IgM, IgD, IgE)
Cell Mediated

T-cells



able to recognize
infected cells
Cytotoxic
Natural killer cell
Cytokines

Soluble, hormone-like protein produced by
white blood cells



act as a messengers between cells
Stimulate or inhibit the growth and activity of
various immune cells
Can be beneficial or harmful
Antipyretics

Acetaminophen

Ibuprofen

Aspirin
Immunopathology
Alterations in Immunity and Inflammation
 Hypersensitivity
 Autoimmunity
Hypersensitivity
Immediate
 Allergy
 Anaphylaxis
Delayed
 Poison
Ivy
 Mantoux Test
Hypersensitivity
Nursing Assessment





Think ABC’s
How fast is the allergic
response?
How serious?
What to ask the
patient?
Is this an allergic
response or drug side
effect?
Name that response…

Baby is crying continually and pulling at her
ear. Mom is frantic.

Young man- ate shellfish and then went to
play tennis. Now is having difficulty
breathing.

Young woman went hiking in the woods last
week & now has hives present and is
scratching.

12 year old girl crying and shaking, holding
her very swollen arm/elbow - injured playing
baseball
Autoimmunity
Recognizes self
antigens as foreign
 Produces
antibodies against
own tissue
 Examples

 Lupus
 Rheumatoid
Arthritis
How do immunizations work?

The exposure (usually
injection) to a small
amt of virus triggers
an immune response


Help body prepare
antibodies
Type of immunity

Active artificial
NCLEX Concepts of Emphasis
1.
2.
3.
4.
5.
6.
What are the similarities and differences
between cellular and humoral immunity?
How do vaccinations work?
To be fully immune requires which three
essential components of the
inflammation/immune response?
What is the mechanism of Prednisone and the
nursing considerations when giving?
What is the difference between an allergic
reaction and side effect of a medication?
What is the similarities & differences between
hypersensitivity and anaphylactic reaction?
Bronchospasm associated with
hypersensitivity reaction is the
result of:
A. histamine release
 B. pulmonary ventilation
 C. dilation of the alveoli
 D. inadequate antibody production

Which symptom indicates a
possible allergic reaction?
A. fever
 B. diaphoresis
 C. rash
 D. chills
