Transcript Nrsg 407 Disorders of the Immune System

DISORDERS OF THE IMMUNE
SYSTEM
CHAPTERS 3 & 4
LYMPHOCYTES
• Small WBCs that are the
effector cells of the immune system
3 types:
• B lymphocytes mature in the bone marrow
• T lymphocytes mature in the thymus where
they also differentiate into cells with
various functions
• Natural killer cells – in the innate immune
system. Fast acting, have an innate
capacity to instantly recognize, attack, &
kill virus infected cells
STAGES OF IMMUNE RESPONSE
Recognition
 Lymph nodes and lymphocytes
 Use circulation to “patrol” tissues and vessels
 Once foreign invader discovered, immune process
initiated
STAGES OF IMMUNE RESPONSE
Proliferation
 T-cells and B-cells divide
rapidly
 T-cells  Killer T-cells
 B-cells  antibodies
STAGES OF IMMUNE RESPONSE
Response
 Humoral – antibodies
released into the
bloodstream
 Cell-mediated – direct
attack on microbe by killer
T-cells
STAGES OF IMMUNE RESPONSE
Effector
 Depends on which
response reaches antigen
first: humoral or cellmediated
 Outcome: total
destruction vs. complete
neutralization of invading
microbe
B LYMPHOCYTE
(ANTIBODY)-MEDIATED
IMMUNITY
• Antibody (humoral)
mediated
• B cell activation
• B cell clones itself and
produces antibodies
• Some vaccines work in this
manner
T LYMPHOCYTE (DELAYED)MEDIATED IMMUNITY
• Cell-mediated
• T cells(helper/CD4)
activates immune cells
• T cells (cytotoxic/killer
CD8)
• T cells produce cytokines
NON-T AND NON-B LYMPHOCYTES
INVOLVED IN IMMUNE RESPONSE
Null cells
 Destroy antigen coated
with antibody
Natural killer cells
 Defend against
microorganisms and
some malignant cells
MAJOR HISTOCOMPATIBILITY
COMPLEX (MHC)
• Important part of immunity is how antigens are
displayed to immune cells
• The MCH is a glycoprotein complex on the surface
of all cells (except RBCs)
• It allows for immune cells to recognize the cell as
self or nonself
• AKA as Human Leukocyte antigens (HLA)
TYPES OF MHC
• Two types of MHC
• MHC I: display antigens synthesized inside a virus
infected or cancerous cell
• MHC II: present on the surface of macrophages
and dendritic cells, which capture and display
external nonself antigen
• Critical difference between the two: the immune
system attacks the cell with the MHC I display but
just reads the MHC II display
HYPERSENSITIVITY
A reflection of excessive or aberrant immune
response
Sensitization: initiates the buildup of antibodies
HYPERSENSITIVITY
Types of hypersensitivity reactions
B Cell Mediated:
 Immediate (Anaphylactic): type I
 Cytotoxic: type II
 Immune complex: type III
T Cell Mediated:
 Delayed type: type IV
TYPE I IMMEDIATE REACTION
• Occurs within a few minutes after an antigen
combines with preformed antibody created by B
cells from an earlier exposure
• Sensitizing exposure: IgE antibodies are secreted by
B cells and attach to mast cells
• The initial exposure produces no symptoms but sets
the stage for exposure, the antigen combines with
IGE antibody already present on the surface of
mast cells
• Results in vascular dilation, congestion, mucus
secretion, and inflammation
TYPE I—ANAPHYLACTIC REACTION
TYPE II HYPERSENSITIVITY
Normal body constituent
identified as foreign
Chemical mediators released
Activation of complement
cascade  cell destruction
Diseases: myasthenia gravis,
Goodpasture [lung and renal
damage], blood transfusion
incompatibility
TYPE II—CYTOTOXIC REACTION
TYPE II HYPERSENSITIVITY
TYPE III—IMMUNE COMPLEX REACTION
TYPE III HYPERSENSITIVITY
Immune complex
hypersensivity
Free antigen and antibody
combine to form an immune
complex depositing in tissue,
which damages it and causes
an inflammatory reaction
TYPE III
TYPE IV IMMUNE REACTION
• T cell reaction
• No antibodies are produced and clinical reaction is
delayed a few days after antigen contact
• Example: Mycobacterium tuberculosis; Contact
dermatitis (most common Type IV)
TYPE IV—DELAYED OR CELLULAR
REACTION
ALLERGIC DISORDERS & ATOPY
• Allergy: exaggerated but otherwise normal immune
response to foreign antigen regardless of the type
of hypersensitivity reaction
• Allergen: any substance (antigen) causing an
allergic reaction
• Atopy: allergy due to Type I
• Most allergies are atopic
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IMMUNOGLOBULINS AND ALLERGIC
RESPONSE
Antibodies (IgE, IgD, IgG, IgM, and IgA) react
with specific effector cells and molecules, and
function to protect the body
IgE antibodies are involved in allergic disorders
IgE molecules bind to an allergen and trigger
mast cells or basophils
IMMUNOGLOBULINS AND ALLERGIC
RESPONSE
• These cells then release
chemical mediators such
as histamine, serotonin,
kinins, SRS-A, and
neutrophil factor
• These chemical substances
cause the reactions seen in
allergic response
IG AND ALLERGIC RESPONSE (CONT.)
• Allergen triggers the B cell to make IgE antibody,
which attaches to the mast cell; when that allergen
reappears, it binds to the IgE and triggers the mast
cell to release its chemicals
HYPERSENSITIVITIES
CONDITION
ANAPHYLAXIS
TYPE
I
S/S
WHAT’S
HAP’NEN?
Allergen activates
IgE bound to mast
cells & release
mediators of
inflammation
SKIN
NRSG
ACTIONS
REMOVE ANTIGEN
LUNGS
GI TRACT
RAISE HOB
TESTS
CBC with
emphasis on
WBC count and
differential
BLOOD
Binding of IgG or
IgM antibody to
cell-bound antigen
activates
complement
cascade
Epinephrine
Careful allergy
assessment
Benadryl
Chills, fever,
lower back pain,
flushing, ↓BP,
↑HR, ↑RR,
vascular
collapse
Stop blood
Coombs test
Maintain IV
patency with NS
Urinanalysis
Collect urine
2 nurses
meticulously
check blood
before giving
Hemo & Hct
Transfuse slowly
with frequent
VS
Monitor vitals
Monitor Urine
output
CHRONIC
INFLAMMATION
III
(Lupus)
CONTACT
DERMATITIS
IV
Formation and
deposition of
antigen/antibody
complexes in
tissues that cause
damage
Vasculitis
T-cell and
macrophage
mediated
24-48 hr post
exposure
Arthritis
Nephritis
First dose status
protocols
Intal
MEDS AS
ORDERED
II
VIGILANCE
HYPOTENSION
02
MISMATCHED
DRUGS
Depends on
condition e.g.
SLE, teach pts.
To avoid sun
and other
stressors
CRP
Immuno-
ESR
Suppressants
WBC w/diff
Steroids
Red, sore,weepy
erythematous
skin
Patch testing
Corticosteriods,
topical and/or
systemic
ANA
Monitor for s/s
infection
and organ
damage
Avoid irritant
Burrow’s
solution soaks
AUTOIMMUNE DISORDERS
SLE & AIDS
SYSTEMIC LUPUS ERTHEMATOSUS (SLE)
• Multisystem disease
• Caused by Type III hypersensitivity
• Characterized by multitude of antibodies to various
organs
• Associated with presence of antinuclear antibodies
(ANA) in blood or tissue which may target DNA or
RNA
ACQUIRED IMMUNODEFICIENCY
SYNDROME (AIDS)
• HIV invades cells by attaching to the MHC complex and
preferentially infects T cells and related macrophages
with the CD4 type of MHC antigen (mainly helper T cells)
• HIV RNA synthesizes abnormal DNA inside CD4+ cells
which merges with normal DNA to become part of a
new corrupted T cell DNA
• Later process is reversed and corrupted DNA produces
new HIV RNA
• New HIV viruses exit the dying cell to infect and kill other
CD4+ cells
• Cycle continues until T cell function is devastated and
patient dies from AIDS-related opportunistic infection or
malignancy
AIDS CONT’D
• B cell immunity is adversely affected because
normal B cell function requires helper T cell support
• B cells are stimulated by HIV antigens and antigens
of the cytomegalovirus (CMV), Epstein-Barr virus,
and other infections that occur in AIDS
• Net effect: both T & B cell function is defective
DIAGNOSIS OF HIV & AIDS
• HIV is the infection, detectable by laboratory tests
• AIDS is a syndrome, not detected by laboratory
data
• AIDS is a clinical diagnosis proved by the presence
of certain AIDS related diseases
PROGRESSION OF HIV INFECTION
• Three phases:
1.
2.
3.
Acute Viral Syndrome
Chronic infection
Progression to clinical AIDS