IMMUNE SYSTEM

Anatomy of the Immune System Function of the Immune System

Bone Marrow • Remove foreign antigens such as viruses
and bacteria to maintain homeostasis.
• The white blood cells (WBCs) involved in
immunity are produced in the bone marrow.
• Lymphocytes are generated from stem cells Two general types of immunity.
(undifferentiated cells).
1. Natural Immunity (Innate)
• There are two types of lymphocytes—B
• Present at birth.
cells, also called B lymphocytes, and T cells,
also called T lymphocytes. • Provides a broad spectrum of defense
against and resistance to infection.
• It is considered the first line of host defense
following antigen exposure, because it
protects the host without remembering
prior contact with an infectious agent.
• Coordinates the initial response to
pathogens through the production of
cytokines and other effector molecules,
which either activate cells for control of the
pathogen (by elimination) or promote the
development of the acquired immune
response.
• The cells involved in this response are
monocytes, macrophages, dendritic cells,
natural killer (NK) cells, basophils,
eosinophils, and granulocytes.
• The early events in this process are critical
Lymphoid Tissues
in determining the nature of the adaptive
• The spleen, composed of red and white immune response.
pulp, acts somewhat like a filter.
• Natural immune mechanisms can be divided
• The red pulp is the site where old and into two stages: immediate (generally
injured red blood cells (RBCs) are occurring within minutes) and delayed
destroyed. (occurring within several days after
exposure)
• The white pulp contains concentrations of
lymphocytes. The lymph nodes, which are • White Blood Cell Action (Phagocytosis)
connected by lymph channels and
• Inflammatory Response ( regeneration of
capillaries, are distributed throughout the
tissue injury and minimize
body.
• Physical Barriers (Skin and Cilia)
• They remove foreign material from the
lymph system before it enters the • Chemical Barriers (Mucus and gastric acid)
bloodstream.
• Immune Regulation (Eliminates Antigen)
• The lymph nodes also serve as centers for
immune cell proliferation.
• The remaining lymphoid tissues contain
immune cells that defend the body’s
mucosal surfaces against microorganisms.
 2. Acquired Immunity • Recognition involves the use of lymph nodes
and lymphocytes for surveillance.
• Acquired (adaptive) immunity usually
develops due to prior exposure to an • Lymph nodes are widely distributed
antigen through immunization internally throughout the body and in the
(vaccination) or by contracting a disease, circulating blood, as well as externally near
both of which generate a protective immune the body’s surfaces.
response.
• They continuously discharge small
• Weeks or months after exposure to a lymphocytes into the bloodstream.
disease or vaccine, the body produces an
• These lymphocytes patrol the tissues and
immune response that is sufficient to
vessels that drain the areas served by that
defend against the disease on re-exposure.
node.
• In this form of immunity relies on the
• Lymphocytes recirculate from the blood to
recognition of specific foreign antigens.
lymph nodes and from the lymph nodes
• The acquired immune response is broadly back into the bloodstream in a continuous
divided into two mechanisms: (1) the cell- circuit.
mediated response, involving T-cell
• Lymphocytes and other cells have
activation, and (2) effector mechanisms,
“microbial sensors” that identify molecules
involving B-cell maturation and production
on microbes and other microorganisms.
of antibodies
• The interaction of these sensors with the
• The two types of acquired immunity are
offending agent sets off a cascade aimed at
known as active and passive and are
destroying the microbe.
interrelated. Active acquired immunity
refers to immunologic defenses developed • Macrophages play an important role in
by the person’s own body. helping the circulating lymphocytes process
the antigens.
• This immunity typically lasts many years or
even a lifetime. • Both macrophages and neutrophils have
receptors for antibodies and complement;
• Passive acquired immunity is temporary
as a result, they coat microorganisms with
immunity transmitted from a source outside
antibodies, complement, or both, thereby
the body that has developed immunity
enhancing phagocytosis
through previous disease or immunization.
2. Proliferation Stage
• Examples include immunity resulting from
the transfer of antibodies from the mother • The circulating lymphocytes containing the
to an infant in utero or through breast- antigenic message return to the nearest
feeding or receiving injections of immune lymph node.
globulin.
• Once in the node, these sensitized
• Active and passive acquired immunity lymphocytes stimulate some of the resident
involve humoral and cellular (cell- T and B lymphocytes to enlarge, divide, and
mediated) immunologic responses proliferate.
(described later).
• T lymphocytes differentiate into cytotoxic
(or killer) T cells, whereas B lymphocytes
produce and release antibodies.
Response to Invasion (Phagocytosis and Antibody
production) • Enlargement of the lymph nodes in the neck
in conjunction with a sore throat is one
It has 4 four stages
example of the immune response.
1. Recognition Stage
• Recognition of antigens as foreign by the
immune system
 3. Response Stage • Cellular Responses (T Cells)
• In the response stage, the differentiated  Transplant rejection
lymphocytes function in either a humoral or  Delayed hypersensitivity (tuberculin
a cellular capacity. reaction)
 Graft-versus-host disease
• This stage begins with the production of
 Tumor surveillance or destruction
antibodies by the B lymphocytes in
 Intracellular infections
response to a specific antigen.
 Viral, fungal, and parasitic infections
• The cellular response stimulates the
resident lymphocytes to become cells that
attack microbes directly rather than
through the action of antibodies.
• These transformed lymphocytes are known
as cytotoxic (killer) T cells.
• Viral antigens induce a cellular response.
• This response is manifested by the
increasing number of T lymphocytes
(lymphocytosis) seen in the blood tests of
people with viral illnesses such as infectious
mononucleosis. (Cellular immunity is
discussed later in this chapter.)
• Most immune responses to antigens involve
both humoral and cellular responses,
although one usually predominates.
• For example, during transplant rejection,
the cellular response involving T cells
predominates, whereas in the bacterial
Humoral Immune Response
pneumonias and sepsis, the humoral
response involving B cells plays the • Characterized by the production of
dominant protective role. antibodies by B lymphocytes in response to
4. Effector Stage a specific antigen.

• In the effector stage, either the antibody of • Following antibody production, the
the humoral response or the (killer) T cell macrophages of natural immunity and the
of the cellular response reaches and special T lymphocytes of cellular immunity
connects with the antigen on the surface of are involved in antigen recognition.
the foreign invader.
Antigen Recognition
• This action initiates activities involving an
interplay of antibodies (humoral • It is known that B lymphocytes recognize
immunity), complement, and action by the and respond to invading antigens in more
cytotoxic T cells (cellular immunity). than one way.
Comparison of Humoral and Cellular Immune
• The B lymphocytes respond to some
Responses
antigens by directly triggering antibody
• Humoral Responses (B Cells) formation; however, in response to other
antigens, they need the assistance of T cells
 Bacterial phagocytosis and lysis to trigger antibody formation.
 Anaphylaxis
 Allergic hay fever and asthma • With the help of macrophages, the T
 Immune complex disease lymphocytes are believed to recognize the
 Bacterial and some viral infections antigen of a foreign invader.
 • The T lymphocyte picks up the antigenic • This phenomenon is known as cross-
message, or “blueprint,” of the antigen and reactivity.
returns to the nearest lymph node with that
• For example, in acute rheumatic fever, the
message.
antibody produced against Streptococcus
• B lymphocytes stored in the lymph nodes pyogenes in the upper respiratory tract may
are subdivided into thousands of clones, cross-react with the patient’s heart tissue,
which are stimulated to enlarge, divide, leading to heart valve damage.
proliferate, and differentiate into plasma
cells capable of producing specific
antibodies to the antigen. Major Characteristics of the Immunoglobulins
• Other B lymphocytes differentiate into B- • IgG (75% of Total Immunoglobulin)
lymphocyte clones with a memory for the  Appears in serum and tissues
antigen. (interstitial fluid)
 Assumes a major role in bloodborne
• These memory cells are responsible for the
and tissue infections
more exaggerated and rapid immune
 Activates the complement system
response in a person who is repeatedly
 Enhances phagocytosis
exposed to the same antigen.
 Crosses the placenta

Role of Antibodies • IgA (15% of Total Immunoglobulin)

 Appears in body fluids (blood,
• Antibodies are large proteins, called
saliva, tears, and breast milk, as well
immunoglobulins.
as
• Antibodies defend against foreign invaders
 pulmonary, gastrointestinal,
in several ways, and the type of defense
prostatic, and vaginal secretions)
used depends on the structure and
 Protects against respiratory,
composition of both the antigen and the
gastrointestinal, and genitourinary
immunoglobulin.
infections
• The antibody molecule has at least two
 Prevents absorption of antigens
combining sites or Fab fragments.
from food
• One antibody can act as a cross-link
 Passes to neonate in breast milk for
between two antigens, causing them to bind
protection
or clump together.
• This clumping effect, referred to as
• IgM (10% of Total Immunoglobulin)
agglutination, helps clear the body of the
 Appears mostly in intravascular
invading organism by facilitating
serum
phagocytosis.
 Appears as the first immunoglobulin
• Some antibodies assist in the removal of
produced in response to bacterial
offending organisms through opsonization.
and viral infections
• In this process, the antigen–antibody
 Activates the complement system
molecule is coated with a sticky substance
that also facilitates phagocytosis.
• IgD (0.2% of Total Immunoglobulin)
Antigen–Antibody Binding
 Appears in small amounts in serum
• The portion of the antigen involved in  Possibly influences B-lymphocyte
binding with the antibody is referred to as differentiation, but role is unclear
the antigenic determinant.
• IgE (0.004% of Total Immunoglobulin)
• The most efficient immunologic responses  Appears in serum
occur when the antibody and antigen fit like  Takes part in allergic and some
a lock and key. hypersensitivity reactions
• Poor fit can occur with an antibody that was  Combats parasitic infections
produced in response to a different antigen. Cellular Immune Response
 • The T lymphocytes are primarily Helper T cells are activated on recognition of
responsible for cellular immunity. antigens and stimulate the rest of the immune
system. When activated, helper T cells secrete
• Stem cells continuously migrate from the
cytokines, which attract and activate B cells,
bone marrow to the thymus gland, where
cytotoxic T cells, NK cells, macrophages, and other
they develop into T cells.
cells of the immune system.
• Despite the partial degeneration of the
• Cytokines are proteins produced by the cells
gland at puberty, T cells continue to develop
of the immune system that determine the
in the thymus gland.
actions of the immune system cells.
• Several types of T cells exist, each with • Separate subpopulations of helper T cells
designated roles in the defense against produce different types of cytokines and
bacteria, viruses, fungi, parasites, and determine whether the immune response
malignant cells. will be the production of antibodies or a
cell-mediated immune response.
• T cells attack foreign invaders directly • Helper T cells also produce lymphokines,
rather than by producing antibodies. one category of cytokines
• Cellular reactions are initiated, with or Cytotoxic T cells (killer T cells) attack the antigen
without the assistance of macrophages, by directly by altering the cell membrane, causing cell
the binding of an antigen to an antigen lysis (disintegration), and releasing cytolytic
receptor located on the surface of a T cell. enzymes and cytokines.

• The T cells then carry the antigenic • Lymphokines can recruit, activate, and
message, or blueprint, to the lymph nodes, regulate other lymphocytes and WBCs.
where the production of other T cells is • These cells then assist in destroying the
stimulated. invading organism.
• Delayed-type hypersensitivity is an example
• Some T cells remain in the lymph nodes and of an immune reaction that protects the
retain a memory for the antigen. body from antigens through the production
and release of lymphokines (see later
• Other T cells migrate from the lymph nodes
discussion).
into the general circulatory system and
Suppressor T cells have the ability to decrease B-
ultimately to the tissues, where they remain
cell production, thereby keeping the immune
until they bind with their respective
response at a level that is compatible with health
antigens or die.
(e.g., sufficient to fight infection adequately without
attacking the body’s healthy tissues).

Types of T Lymphocytes
• T cells include effector T cells, suppressor T
cells, and memory T cells. The two major
categories of effector T cells—helper T cells
(also referred to as CD4+ cells) and
cytotoxic T cells (also referred to as CD8+
cells)—participate in the destruction of
foreign organisms.
• T cells interact closely with B cells,
indicating that humoral and cellular
immune responses are not separate,
unrelated processes but rather are branches
of the immune response that interact.
Memory cells are responsible for recognizing
antigens from previous exposure and mounting an
immune response
Assessment of the Immune System
Musculoskeletal System
• An assessment of immune function begins
during the health history and physical  Joint mobility, edema, and pain
examination.  Skin
 Rashes
 Health History
 Lesions
 Gender
 Dermatitis
 Nutrition
 Hematomas or purpura
 Immunization
 Edema or urticaria
 Infection
 Inflammation
 Allergy
 Discharge
 Disorders and Diseases
 Autoimmune Disorders Neurosensory System
 Neoplastic Disorders
 Chronic Illness and Surgery (COPD)  Cognitive dysfunction
 Special Problems (Burns, Injury)  Hearing loss
 Medication  Visual changes
 Blood Transfusion  Headaches and migraines
 Lifestyle  Ataxia
Assessing for Immune Dysfunction  Tetany
 Diarrhea
• Be alert for the following signs and
symptoms:
Respiratory System Physical Assessment

 Changes in respiratory rate • During the physical examination, the skin

 Cough (dry or productive) and mucous membranes are assessed for
 Abnormal lung sounds (wheezing, lesions, dermatitis, purpura (subcutaneous
crackles, rhonchi) bleeding), urticaria, inflammation, or any
 Rhinitis discharge.
 Hyperventilation • Any signs of infection are noted.
 Bronchospasm
• The patient’s temperature is recorded, and
the patient is observed for chills and
Cardiovascular System sweating.
 Hypotension • The anterior and posterior cervical,
 Tachycardia supraclavicular, axillary, and inguinal lymph
 Arrhythmia nodes are palpated for enlargement; if
 Vasculitis palpable nodes are detected, their location,
 Anemia size, consistency, and reports of tenderness
Gastrointestinal System on palpation are noted.

 Hepatosplenomegaly • Joints are assessed for tenderness, swelling,

 Colitis increased warmth, and limited range of
 Vomiting motion.

Genitourinary System • The patient’s respiratory, cardiovascular,

genitourinary, gastrointestinal, and
 Frequency and burning on urination neurosensory systems are evaluated for
 Hematuria signs and symptoms indicative of immune
 Discharge dysfunction.
 • Any functional limitations or disabilities the action of reverse transcriptase, resulting in
patient may have are also assessed. double-stranded DNA that carries
instruction for viral replication.
• New viral DNA enters the nucleus of the
CD4+ T cell and through the action of
Diagnostic Evaluation integrase is blended with the DNA of the
CD4+ T cell, resulting in permanent, lifelong
Humoral (Antibody-Mediated) Immunity Tests infection.
• B-cell quantification with monoclonal • When the CD4+ T cell is activated, the
antibody double-stranded DNA forms single-stranded
• In vivo immunoglobulin synthesis with T- messenger RNA, which builds new viruses.
cell subsets
• Specific antibody response • The mRNA creates chains of new proteins
• Total serum globulins and individual and enzymes that contain the components
immunoglobulins (electrophoresis, needed in the construction of new viruses.
immunoelectrophoresis, single radial
• The HIV enzyme protease cuts the
immunodiffusion, nephelometry, and
polyprotein chain into the individual
isohemagglutinin techniques)
proteins that make up the new virus.
Cellular (Cell-Mediated) Immunity Tests • New proteins and viral RNA migrate to the
membrane of the infected CD4+ T cell, exits
• Total lymphocyte count
from the cell, and starts the process all over.
• T-cell and T-cell subset quantification with
monoclonal antibody Causes
• Delayed hypersensitivity skin test
• HIV is transmitted through body fluids that
• Cytokine production
contain free virions and infected CD4+ T
• Lymphocyte response to mitogens, antigens,
cells.
and allogeneic cells
• Helper and suppressor T-cell functions • Sharing infected drug use equipment such
as needles.
HIV and AIDS
• Having sexual relations with infected
• HIV or human immunodeficiency virus and individuals (both male and female).
acquired immunodeficiency syndrome is a
chronic condition that requires daily • Blood transmission. Receiving HIV-infected
medication. blood or blood products especially before
blood screening.
• HIV- 1 is a retrovirus isolated and
recognized as the etiologic agent of AIDS. • Maternal HIV. Infants born to mothers with
HIV infection.
• HIV-2 is a retrovirus identified in 1986 in
AIDS patients in West Clinical Manifestations

Pathophysiology HIV has four categories with specific manifestations

for each stage.
• In this first step, the GP120 and GP41
glycoproteins of HIV bind with the host’s • This is experienced during the early
uninfected CD4+ receptor and chemokine infection stages.
coreceptors, usually CCR5, which results in • People who are acutely infected with HIV
the fusion of HIV with the CD4+ T-cell infection experience this symptom.
membrane.
• This symptom is mostly present in category
• The contents of HIV’s viral core are emptied B wherein the patient has already entered
into the CD4+ T cell. the chronic stage.
• DNA synthesis. HIV changes in genetic • Constitutional symptoms. Fever more than
material from RNA to DNA through the 38.5⁰C or diarrhea exceeding 1 month in
 duration may also indicate the presence of Several screening tests are used to diagnose HIV
HIV infection. infection.
• Patients with HIV category C experience • Serologic: Serum antibody test: HIV screen
wasting syndrome or severe wasting of the by ELISA. A positive test result may be
muscles. indicative of exposure to HIV but is not
diagnostic because false-positives may
occur.
Prevention
• Western blot test: Confirms diagnosis of HIV
Until an effective vaccine is developed, nurses need in blood and urine.
to prevent HIV infection by teaching patients how to • Viral load test:
eliminate or reduce risky behaviors. • RI-PCR: The most widely used test currently
can detect viral RNA levels as low as 50
• Safe sex. Other than abstinence, consistent copies/mL of plasma with an upper limit of
and correct use of condoms is the only 75,000 copies/mL.
effective method to decrease the risk of • bDNA 3.0 assay: Has a wider range of 50–
sexual transmission of HIV infection. 500,000 copies/mL. Therapy can be
• In March 2007, based on the results of three initiated, or changes made in treatment
clinical trials, the WHO and UNAIDS approaches, based on rise of viral load or
recommended that circumcision be maintenance of a low viral load. This is
recognized as an effective strategy to reduce currently the leading indicator of
the risk of HIV acquisition in men. effectiveness of therapy.
• T-lymphocyte cells: Total count reduced.
• Sex partners. Avoid sexual contact with • CD4+ lymphocyte count (immune system
multiple partners or people who are known indicator that mediates several immune
to be HIV positive or IV/injection drug system processes and signals B cells to
users. produce antibodies to foreign germs):
Numbers less than 200 indicate severe
• Blood and blood components. People who
immune deficiency response and diagnosis
are HIV positive or who use injection drugs
of AIDS.
should be instructed not to donate blood or
• T8+ CTL (cytopathic suppressor cells):
share drug equipment with others.
Reversed ratio (2:1 or higher) of suppressor
Complications cells to helper cells (T8+ to T4+) indicates
immune suppression.
The patient should be monitored for presence of • Polymerase chain reaction (PCR) test:
complications and should be managed Detects HIV-DNA; most helpful in testing
appropriately. newborns of HIV-infected mothers. Infants
• Opportunistic infections. carry maternal HIV antibodies and
Immunosuppressed patients are at risk for therefore test positive by ELISA and
opportunistic infections such as Western blot, even though infant is not
pneumocystis pneumonia which can affect necessarily infected.
80% of all people infected with HIV. • Confirming Diagnosis: Signs and symptoms
may occur at any time after infection, but
• Respiratory failure. Impaired breathing is a AIDS isn’t officially diagnosed until the
major complication that increases the patient’s CD4+ T-cell count falls below 200
patient’s discomfort and anxiety and may cells/mcl or associated clinical conditions
lead to respiratory and cardiac failure. or disease.
• Cachexia and wasting. Wasting syndrome
occurs when there is profound involuntary Medical Management
weight loss exceeding 10% of the baseline Medical management focuses on the elimination of
body weight and it is a common opportunistic infections.
complication of HIV infection and AIDS.
• Treatment of opportunistic infections. For
Diagnostic Findings Pneumocystis pneumonia, TMP-SMZ is the
treatment of choice; for mycobacterium
 avian complex, azithromycin or • Fluid and electrolyte balance. F&E status is
clarithromycin are preferred prophylactic assessed by examining the skin and mucous
agents; for cryptococcal meningitis, the membranes for turgor and dryness.
current primary treatment is IV
• Knowledge level. The patient’s level of
amphotericin B.
knowledge about the disease and the modes
• Prevention of opportunistic infections. TMP- of disease transmission is evaluated.
SMZ is an antibacterial agent used to treat
Nursing Interventions
various organisms causing infection.
The plan of care for a patient with AIDS is
• Antidiarrheal therapy. Therapy with
individualized to meet the needs of the
octreotide acetate (Sandostatin), a synthetic
patient.
analog of somatostatin, has been shown to
be effective in managing severe chronic • Promote skin integrity. Patients are
diarrhea. encouraged to avoid scratching; to use
nonabrasive, nondrying soaps and apply
• Antidepressant therapy. Treatment for
nonperfumed moisturizers; to perform
depression in patients with HIV infection
regular oral care; and to clean the perianal
involves psychotherapy integrated with
area after each bowel movement with
imipramine, desipramine or fluoxetine.
nonabrasive soap and water.
• Nutrition therapy. For all AIDS patients who
• Promote usual bowel patterns. The nurse
experience unexplained weight loss, calorie
should monitor for frequency and
counts should be obtained, and appetite
consistency of stools and the patient’s
stimulants and oral supplements are also
reports of abdominal pain or cramping.
appropriate.
• Prevent infection. The patient and the
Nursing Management
caregivers should monitor for signs of
The nursing care of patients with HIV/AIDS is infection and laboratory test results that
challenging because of the potential for any organ indicate infection.
system to be the target of infections or cancer.
• Improve activity intolerance. Assist the
• Nursing assessment includes identification patient in planning daily routines that
of potential risk factors, including a history maintain a balance between activity and
of risky sexual practices or IV/injection rest.
drug use.
• Maintain thought processes. Family and
• Nutritional status. Nutritional status is support network members are instructed to
assessed by obtaining a diet history and speak to the patient in simple, clear
identifying factors that may affect the oral language and give the patient sufficient time
intake. to respond to questions.
• Skin integrity. The skin and mucous • Improve airway clearance. Coughing, deep
membranes are inspected daily for evidence breathing, postural drainage, percussion
of breakdown, ulceration, or infection. and vibration is provided for as often as
every 2 hours to prevent stasis of secretions
• Respiratory status. Respiratory status is
and to promote airway clearance.
assessed by monitoring the patient for
cough, sputum production, shortness of • Relieve pain and discomfort. Use of soft
breath, orthopnea, tachypnea, and chest cushions and foam pads may increase
pain. comfort as well as administration of NSAIDS
and opioids.
• Neurologic status. Neurologic status is
determined by assessing the level of • Improve nutritional status. The patient is
consciousness; orientation to person, pace, encouraged to eat foods that are easy to
and time; and memory lapses. swallow and to avoid rough, spicy, and
sticky food items.
 • Gown: Use during procedures and patient
care activities when contact of
clothing/exposed skin with blood or body
fluids, secretions, and excretions is
anticipated.

Discharge and Home Care Guidelines

• Mask, eye protection (goggles), face shield1:
Before discharge, the nurse should educate Use during procedures and patient care
the patient and the family about precautions activities likely to generate splashes or
and the transmission of HIV/AIDS. sprays of blood, body fluids, and secretions,
• Patients and their families or caregivers especially suctioning or endotracheal
should receive instructions about how to intubation.
prevent disease transmission, including • Soiled patient care equipment: Handle in a
hand-washing techniques and methods for manner that prevents transfer of
safely handling and disposing of items microorganisms to others and to the
soiled with body fluids. environment; wear gloves if visibly
• Patients are advised to avoid exposure to contaminated; and perform hand hygiene.
others who are sick or who have been • Environmental control: Develop procedures
recently vaccinated. for routine care, cleaning, and disinfection
• Medication administration. Caregivers in of environmental surfaces, especially
the home are taught how to administer frequently touched surfaces in patient care
medications, including IV preparations. areas.

• The patient’s adherence to the therapeutic • Textiles and laundry: Handle in a manner
regimen is assessed and strategies are that prevents transfer of microorganisms to
suggested to assist with adherence. others and to the environment.

• Infection prevented/resolved. • Needles and other sharps: Do not recap,

bend, break, or hand manipulate used
• Complications prevented/minimized. needles; if recapping is required, use a one-
handed scoop technique only; use safety
• Pain/discomfort alleviated or controlled.
features when available; and place used
• Patient dealing with current situation sharps in a puncture-resistant container.
realistically.
• Patient resuscitation: Use mouthpiece,
• Diagnosis, prognosis, and therapeutic resuscitation bag, and other ventilation
regimen understood. devices to prevent contact with mouth and
oral secretions.
• Plan in place to meet needs after discharge.
• Patient placement: Prioritize for single-
patient room if patient is at increased risk
Recommendations for Standard Precautions for transmission, is likely to contaminate the
environment, does not maintain
Hand hygiene: Use after touching blood, body fluids, appropriate hygiene, or is at increased risk
secretions, excretions, or contaminated items; for acquiring infection or developing
immediately after removing gloves; and between adverse outcome following infection.
patient contacts.
• Respiratory hygiene/cough etiquette
Personal protective equipment: (source containment of infectious
• Gloves: Use for touching blood, body fluids, respiratory secretions in symptomatic
secretions, excretions, and contaminated patients, beginning at initial point of
items, and for touching mucous membranes encounter, such as triage and reception
and nonintact skin. areas in emergency departments and
provider offices): Instruct symptomatic
people to cover mouth and nose when
 sneezing or coughing, use tissues and o For exposures for which PEP is prescribed,
dispose in no-touch receptacle, observe HCPs are informed regarding the following:
hand hygiene after soiling of hands with
respiratory secretions, and wear surgical • Possible drug toxicities (e.g., rash
mask if tolerated. and hypersensitivity reactions that
could imitate acute HIV
seroconversion and the need for
monitoring) Possible drug
Post-Exposure Prophylaxis for Health Care
interactions
Providers
• The need for adherence to PEP
• Post-exposure prophylaxis (PEP) includes
regimens Undergo early
taking antiretroviral medicines as soon as
reevaluation after exposure:
possible, but no more than 72 hours (3
days) after possible HIV exposure; three • Regardless of whether an HCP is
drugs are prescribed. taking PEP, reevaluation of exposed
HCP within 72 hours after exposure
• Healthcare workers who are exposed to a
is strongly recommended, as
needle stick involving HIV-infected blood in
additional information about the
a healthcare setting have a 0.3% risk of
exposure or the source patient may
becoming HIV-infected; the risk of infection
be available.
due to occupational exposure is very low.
o Follow up with HIV testing and
Post-HIV Exposure Prophylaxis for Health Care
appointments. At a minimum, this follow-up
Providers
should include:
If you sustain an occupational exposure to HIV, take
• HIV testing at baseline and at 6
the following actions immediately:
weeks, 12 weeks, and 6 months after
o Alert your supervisor and initiate the exposure; alternatively, if the HCP is
occupational exposure reporting system certain that a fourth-generation
used in the setting. combination HIV p24 antigen–HIV
antibody test is being utilized, then
• Determine the HIV status of the HIV testing could be performed at
exposure source (i.e., patient) when baseline, 6 weeks after exposure,
possible to guide appropriate use of and 4 months after exposure
HIV post-exposure prophylaxis
(PEP). • Complete blood counts and renal
and hepatic function tests (at
• Use rapid-testing if the HIV status of baseline and 2 weeks after
the patient is unknown. exposure; further testing may be
• Check laws in your state as you indicated if abnormalities are
proceed to determine HIV status of detected)
the source patient. Hypersensitivity
o Get counseling at the time of exposure and Hypersensitivity is an excessive or aberrant
at follow-up appointments: immune response to any type of stimulus
• Exposed health care providers Anaphylactic (Type I) Hypersensitivity
(HCP) are advised to use
precautions (e.g., use of barrier • The most severe hypersensitivity reaction is
contraception and avoidance of anaphylaxis. An unanticipated severe
blood or tissue donations, allergic reaction that is rapid in onset,
pregnancy, and, if possible, breast- anaphylaxis is characterized by edema in
feeding) to prevent secondary many tissues, including the larynx, and is
transmission, especially during the often accompanied by
first 6 to 12 weeks after exposure.
• hypotension, bronchospasm, and
cardiovascular collapse in severe cases.
 • Anaphylaxis is a severe type I • An example of this kind of hypersensitivity
hypersensitivity reaction, which is an reaction occurs in rheumatoid arthritis.
immediate reaction beginning within
• An unknown antigen triggers antibody
minutes of exposure to an antigen.
formation, which then forms immune
• Primary chemical mediators are responsible complexes that are deposited in the joints.
for the symptoms of type I hypersensitivity
• Many autoimmune disorders are type III
because of their effects on the skin, lungs,
hypersensitivity reactions.
and gastrointestinal tract.
• In autoimmune reactions, such as systemic
• If chemical mediators continue to be
lupus erythematosus, patients form
released, a delayed reaction may occur and
autoantibodies that form immune
may last for up to 24 hours.
complexes that deposit in the lungs, skin,
• Clinical symptoms are determined by the and kidney.
amount of the allergen, the amount of
Delayed (Type IV) Hypersensitivity
mediator released, the sensitivity of the
target organ, and the route of allergen entry. • Type IV, or delayed hypersensitivity, is a T
Type I hypersensitivity reactions may cell–mediated immune reaction after
include both local and systemic anaphylaxis. exposure to an antigen. This immune
reaction typically occurs 24 to 48 hours
Cytotoxic (Type II) Hypersensitivity
after exposure to an antigen.
• Type II, or cytotoxic hypersensitivity occurs
• The prototypical type IV hypersensitivity
when antibodies are directed against
reaction occurs in response to the
antigens on cells or basement membranes
subcutaneous injection of purified protein
of tissues.
• derivative (PPD) antigen from
• This reaction can lead to cell lysis and tissue
Mycobacterium tuberculosis.
damage.
• Patients who have had previous exposure or
• Type II hypersensitivity reactions are
have tuberculosis (TB) infection will
associated with several disorders.
demonstrate a reaction of erythema and
• The best example is a hemolytic transfusion induration due to sensitized T cells.
reaction.
Assessment
• For example, if a person with type A blood is
• A comprehensive allergy history and a
mistakenly given type B blood, anti-B
thorough physical examination provide
antibodies are triggered in the recipient that
useful data for the diagnosis and
attack the infused type B blood cells and
management of allergic disorders. An
cause hemolysis.
allergy assessment form is useful for
Immune Complex (Type III) Hypersensitivity obtaining and organizing pertinent
information.
• Type III, or immune complex
hypersensitivity, is a damaging • The degree of difficulty and discomfort
inflammatory reaction caused by the experienced by the patient because of
insoluble immune complexes formed by allergic symptoms and the degree of
antigens that bind to antibodies. improvement in those symptoms with and
without treatment are assessed and
• These complexes are too large to be cleared
documented. The relationship of symptoms
from the circulation by phagocytic action.
to exposure to possible allergens is noted.
• The immune complexes are deposited in
Diagnostic Evaluation
tissues or vascular endothelium and trigger
inflammation at different sites • Diagnostic evaluation of the patient with
allergic disorders commonly includes blood
• throughout the body.
tests, smears of body secretions, skin tests,
 and the serum-specific IgE test (formerly allergic signs and symptoms, many different
known as radioallergosorbent test [RAST]). solutions may be applied at separate sites.
• Results of laboratory blood studies provide • These solutions contain individual antigens
supportive data for various diagnostic representing an assortment of allergens
possibilities; however, they are not the most likely to be implicated in the patient’s
major criteria for the diagnosis of allergic disease.
disease.
• Positive (wheal-and-flare) reactions are
clinically significant when correlated with
the history, physical findings, and results of
other laboratory tests.
• Skin testing is considered the most accurate
Complete Blood Count with Differential confirmation of allergy

• The white blood cell (WBC) count is usually Provocative Testing

within normal limits except when infection
• Provocative testing involves the direct
and inflammation are present along with an
administration of the suspected allergen to
allergic disorder.
the sensitive tissue, such as the conjunctiva,
• Eosinophils, which are granular leukocytes, nasal or bronchial mucosa, or
normally make up 2% to 5% of the total gastrointestinal tract (by ingestion of the
number of WBCs. They can be found in allergen), with observation of target organ
blood, sputum, and nasal secretions. response.

• A level greater than 5% to 10% is • This type of testing is helpful in identifying

considered abnormal and may be found in clinically significant allergens in patients
patients with allergic disorders. who have a large number of positive tests.

Eosinophil Count • Major disadvantages of this type of testing

are the limitation of one antigen per session
• An actual count of eosinophils can be and the risk of producing severe symptoms,
obtained from blood samples or smears of particularly bronchospasm, in patients with
secretions. During symptomatic episodes, asthma.
smears obtained from nasal secretions and
sputum of patients with allergies usually Serum-Specific IgE Test
reveal an increase in
• The serum-specific IgE test, formerly known
• eosinophils, indicating an active allergic as RAST, is an automated test performed on
response. blood samples by a pathology laboratory.

Total Serum Immunoglobulin E Levels • As the name suggests, it detects free

antigen-specific IgE in serum as opposed to
• High total serum IgE levels support the antigen-specific IgE bound to mast cells in
diagnosis of allergic disease. In the majority the skin.
of cases, the antibody typically responsible
for an allergic reaction belongs to the IgE • The advantages of this test over other tests
isotype. include decreased risk of systemic reaction,
• Patients with this disorder are said to have stability of antigens, and lack of dependence
an IgE mediated on skin reactivity modified by medications.
• allergic disease
• The major disadvantages include limited
allergen selection and reduced sensitivity
Skin Tests
compared with intradermal skin tests, lack
• Skin testing entails the intradermal of immediate results, and higher cost.
injection or superficial application
Anaphylactic Shock
(epicutaneous) of solutions at several sites.
Depending on the suspected cause of • Anaphylactic shock occurs rapidly and is
life-threatening.
 • Anaphylactic shock is a systemic, type I Allergy symptoms aren’t usually life-
hypersensitivity reaction that often has fatal threatening, but a severe allergic reaction can
consequences. lead to anaphylaxis.
• Anaphylaxis causes the immune system to • Food allergies. The most common
release a flood of chemicals that can cause a anaphylaxis triggers in children are food
person to go into shock. allergies, such as to peanuts, and tree nuts,
fish, shellfish and milk.
• Medication allergies. Certain medications,
including antibiotics, aspirin and other
over-the-counter pain relievers, and the
intravenous (IV) contrast used in some
imaging tests.
Pathophysiology • Insect allergies. Stings from bees, yellow
• Anaphylaxis occurs in an individual after jackets, wasps, hornets and fire ants.
reexposure to an antigen to which that • Latex allergy. Latex allergy develops after
person has produced a specific IgE antibody. many previous exposures to latex.
• Reexposure. Upon reexposure to the Clinical Manifestations
sensitized allergen, the allergen may cross-
link the mast cell or basophil surface-bound • Anxiety. The first symptoms usually include
allergen-specific IgE resulting in cellular a feeling of impending doom or fright.
degranulation as well as de novo synthesis • Skin reactions. Skin reactions such as hives,
of mediators. itching, and flushed or pale skin follow.
• Shortness of breath. Constriction of the
• Binding. Immunoglobulin E (IgE) binds to airways and a swollen tongue or throat
the antigen (the foreign material that could cause wheezing and troubled
provokes the allergic reaction). breathing.
• Activation. Antigen-bound IgE then activates • Hypotension. A low blood pressure occurs
FcεRI receptors on mast cells and basophils. as one of the major symptoms of shock.
• Tachycardia. The heart compensates
• Inflammatory mediators release. This leads through pumping faster and trying to
to the release of inflammatory mediators deliver blood to all body systems.
such as histamine. • Dizziness. The patient may feel dizzy which
could lead to fainting.
• Histamine release. Many of the signs and
symptoms of anaphylaxis are attributable to
Prevention:
binding of histamine to its receptors;
binding to H1 receptors mediates pruritus, Because anaphylactic shock occurs in patients
rhinorrhea, tachycardia, and bronchospasm. already exposed to an antigen and who have
developed antibodies to it, it can often be
• Prostaglandin D2. Prostaglandin D2
prevented.
mediates bronchospasm and vascular
dilatation, principle manifestations of • Avoid exposure to allergens. Teach the
anaphylaxis. patient to avoid exposure to known
allergens, may it be food, drug, or an insect
• Leukotriene C4. Leukotriene C4 is converted
bite.
into LTD4 and LTE4, mediators of
hypotension, bronchospasm, and mucous • Desensitization. If a patient must receive a
secretion during anaphylaxis in addition to drug to which he’s allergic, prevent a severe
acting as chemotactic signals for eosinophils reaction by making sure he receives careful
and neutrophils. desensitization with gradually increasing
doses of the antigen or advance
Causes
administration of steroids.
 • Monitoring. Closely monitor a patient • Assess any kind of allergy. The nurse must
undergoing diagnostic tests that use assess all patients for allergies or previous
radiographic contrast media, such as reactions to antigens.
excretory urography, cardiac
• Assess patient’s knowledge. The nurse must
catheterization, and angiography.
also assess the patient’s understanding of
Complications: previous reactions and steps taken by the
patient and the family to prevent further
• Respiratory obstruction. The trachea may
exposure to antigens.
close up due to severe inflammation which
could result to respiratory obstruction. • New allergies. When new allergies are
identified, the nurse advises the patient to
• Systemic vascular collapse. Sudden loss of
wear or carry identification that names the
blood flow to the brain and other organs
specific allergen or antigen.
could cause systemic vascular collapse.
• Monitor client’s airway. Assess the client for
the sensation of a narrowed airway.
Medical Management
• Monitor the oxygenation status. Monitor
• Remove antigen. Removing the causative oxygen saturation and arterial blood gas
antigen such as discontinuing an antibiotic values.
agent could stop the progression of shock.
• Focus breathing. Instruct the client to
• Administer medications. Administer breathe slowly and deeply.
medications that restore vascular tone and
• Positioning. Position the client upright as
provide emergency support of basic life
this position provides oxygenation by
functions.
promoting maximum chest expansion and is
• Cardiopulmonary resuscitation. If cardiac the position of choice during respiratory
arrest and respiratory arrest are imminent distress.
or have occurred, cardiopulmonary
• Activity. Encourage adequate rest and limit
resuscitation is performed.
activities to within client’s tolerance.
• Endotracheal intubation. Endotracheal
• Hemodynamic parameters. Monitor the
intubation or tracheostomy may be
client’s central venous pressure (CVP),
necessary to establish an airway.
pulmonary artery diastolic pressure
• Intravenous therapy. IV lines are inserted to (PADP), pulmonary capillary wedge
provide access for administering fluids and pressure, and cardiac output/cardiac index.
medications.
• Monitor urine output. The renal system
Pharmacologic Therapy compensates for low blood pressure by
retaining water, and oliguria is a classic sign
• Epinephrine. Epinephrine is given for its of inadequate renal perfusion.
vasoconstrictive reaction; for emergency
situations, an immediate injection of 1:1, Discharge and Home Care Guidelines
000 aqueous solution, 0.1 to 0.5 ml,
• Emergency medications. The nurse should
repeated every 5 to 20 minutes is given.
provide information about emergency
• Diphenhydramine. Diphenhydramine medications and plans that should be
(Benadryl) is administered to reverse the considered should a crisis reoccur.
effects of histamine, thereby reducing
• Precipitating factors. The nurse must assist
capillary permeability.
the client and/or family in identifying
• Albuterol. Albuterol (Proventil) may be factors that precipitate and/or exacerbate
given to reverse histamine-induced crises.
bronchospasm.
Systemic Lupus Erythematosus
Nursing Management
• SLE is an inflammatory, autoimmune
disorder that affects nearly every organ in
 the body. The overall incidence of SLE is Assessment
estimated to be 1.8 to 7.6 per 100,000
• Diagnosis of SLE is based on a complete
people.
history, physical examination, and blood
• It occurs 4 to 12 times more frequently in tests.
women than in men and occurs more often
• In addition to the general assessment
in African Americans, Hispanics/Latino
performed for any patient with a rheumatic
Americans, Asians, and American
disease, assessment for known or suspected
Indians/Alaska Natives than among White
SLE has special features.
Americans.
• The skin is inspected for erythematous
• In addition to SLE, other forms of adult
rashes. Cutaneous erythematous plaques
lupus exist, including subacute cutaneous or
with an adherent scale may be observed on
discoid lupus erythematous, and drug-
the scalp, face, or neck.
induced lupus.

• Areas of hyperpigmentation or
Pathophysiology
depigmentation may be noted, depending
• Exact cause is not known on the phase and type of disease. The
patient should be questioned about skin
• SLE starts with the body’s immune system
changes (because these may be transitory)
inaccurately recognizing one or more
and specifically about sensitivity to sunlight
components of the cell’s nucleus as foreign,
or artificial ultraviolet light.
seeing it as an antigen.
• The scalp should be inspected for alopecia
• The immune system starts to develop
and the mouth and throat for ulcerations
antibodies to the nuclear antigen.
reflecting gastrointestinal involvement.
• In particular, B cells begin to overproduce
• Cardiovascular assessment includes
antibodies with the help of multiple
auscultation for pericardial friction rub,
cytokines such as B-lymphocyte stimulator
possibly associated with myocarditis and
(BLyS), which is overexpressed in SLE.
accompanying pleural effusions.
• The antibodies and antigens form antigen–
• The pleural effusions and infiltrations,
antibody complexes and have the
which reflect respiratory insufficiency, are
propensity to get trapped in the capillaries
demonstrated by abnormal lung sounds.
of visceral structures.
• Papular, erythematous, and purpuric lesions
• The antibodies also act to destroy host cells.
developing on the fingertips, elbows, toes,
Clinical Manifestations and extensor surfaces of the forearms or
lateral sides of the hand that may become
• SLE is an autoimmune, systemic disease necrotic suggest vascular involvement.
that can affect any body system.
• Joint swelling, tenderness, warmth, pain on
• The disease process involves chronic states movement, stiffness, and edema may be
where symptoms are minimal or absent and detected on physical examination. The joint
acute flares where symptoms and lab involvement is often symmetric and similar
results are elevated. to that found in RA.
• Symptoms most often include fever, fatigue, • The neurologic assessment is directed at
skin rashes, as well as joint pain and identifying and describing any central
swelling nervous system changes.
• The mucocutaneous, musculoskeletal, renal, • The patient and family members are asked
nervous, cardiovascular, and respiratory about any behavioral changes, including
systems are most commonly involved. Less manifestations of neurosis or psychosis.
commonly affected are the gastrointestinal
tract and liver as well as the ocular system.
 • Signs of depression are noted, as are reports • Belimumab is a monoclonal antibody that
of seizures, chorea, or other central nervous specifically recognizes and binds to BLyS.
system manifestations. BLyS acts to stimulate B cells to produce
antibodies against the body’s own nuclei,
Diagnostic Findings
which is an integral part of the disease
• The antinuclear antibody (ANA) is positive process in SLE. Belimumab acts to render
in more than 95% of patients with SLE, BLyS inactive, preventing it from binding to
indicating exceptional specificity. B-cell surfaces and stimulating B-cell
activity. This action then halts the
• Anti-DNA (antibody that develops against production of unnecessary antibodies and
the patient’s own DNA), anti-ds DNA decreases disease activity in SLE. Live
(antibody against DNA that is highly specific vaccines are contraindicated for 30 days
to SLE, which helps differentiate it from before taking this medication.
drug-induced lupus), and anti-Sm (antibody
against Sm, which is a specific protein found • Rituximab is an additional monoclonal
in the nucleus). antibody used in the treatment of SLE for its
immune modulating effects
• CBC, which may reveal anemia,
thrombocytopenia, leukocytosis, or • Corticosteroids are another medication
leukopenia. used topically for cutaneous manifestations,
in low oral doses for minor disease activity,
Medical Management and in high doses for major disease activity.
• SLE can be life-threatening, but advances in Intravenous (IV) administration of
its treatment have led to improved survival corticosteroids is an alternative to
and reduced morbidity. traditional high-dose oral administration.
One of the most important risk factors
• Acute disease requires interventions associated with the use of corticosteroids in
directed at controlling increased disease SLE is osteoporosis and fractures.
activity or exacerbations that can involve
any organ system. • Antimalarial medication,
hydroxychloroquine, is effective for
• Disease activity is a composite of clinical managing cutaneous, musculoskeletal, and
and laboratory features that reflect active mild systemic features of SLE.
inflammation secondary to SLE.
• NSAIDs used for minor clinical
• Management of the more chronic condition manifestations are often used in
involves periodic monitoring and conjunction with corticosteroids in an effort
recognition of meaningful clinical changes to minimize corticosteroid requirements.
requiring adjustments in therapy.
• Immunosuppressive agents (alkylating
• The goals of treatment include preventing agents and purine analogues) are used
progressive loss of organ function, reducing because of their effect on overall immune
the likelihood of acute disease, minimizing function. These medications are generally
disease-related disability, and preventing reserved for patients who have serious
complications from therapy. forms of SLE that have not responded to
conservative therapies. Examples include
• Management of SLE involves regular
cyclophosphamide, azathioprine,
monitoring to assess disease activity and
mycophenolic acid, and methotrexate,
therapeutic effectiveness.
which are contraindicated in pregnancy and
Pharmacologic Therapy have been used most frequently in SLE
nephritis.
The mainstay of SLE treatment is based on pain
management and nonspecific immunosuppression.
Therapy includes monoclonal antibodies, Nursing Intervention:
corticosteroids, antimalarial agents, NSAIDs, and
1. Improving Skin Integrity
immunosuppressive agents.
• Assess the skin for integrity.
 • Assess the client’s description of pain. • Instruct the client that scalp hair loss occurs
• Assess for an erythematous rash, which may during the exacerbation of disease activity.
be present on the face, neck, or extremities. • Scalp hair loss may be the first sign of
• Assess for photosensitivity. impending disease exacerbation. Scalp hair
• Assess the degree to which symptoms loss may not be permanent. As disease
interfere with the client’s lifestyle and body activity subsides, scalp hair begins to
image. regrow.
• Encourage adequate nutrition and • Instruct the client that scalp hair loss may
hydration. be caused by high-dose corticosteroids
• Instruct the client to clean, dry, and (prednisone) and immunosuppressant
moisturize intact skin; use warm (not hot) drugs.
water, especially over bony prominences; • Hair will regrow as the dose decreases.
use unscented lotion. Use mild shampoo. • Encourage the client to investigate ways
• Instruct the client to avoid contact with (e.g., scarves, hats, wigs) to conceal hair
harsh chemicals and to wear appropriate loss.
protective gloves, as needed. Avoid hair dye, • Hair loss may interfere with lifestyle and
permanent solution, and curl relaxers. self-image.
For skin rash: 2. Managing Acute Pain and Providing Relief and
Comfort
• Wear protective eyewear. • Assess the client’s description of pain.
• Wear a wide-brimmed hat and carry an
• Assess the impact of pain or stiffness on the
umbrella.
client’s ability to perform interpersonally,
• Wear maximum protection sunscreen (SPF
socially, and professionally.
15 or above) in the sun. Sunbathing is
contraindicated. • Assess for the signs of joint inflammation
• Avoid ultraviolet rays. (warmth, redness, swelling) or decreased
• Inform the client of the availability of motion.
special makeup (at large department
stores) to cover rashes, especially facial • Assess previous measures used to alleviate
rashes. pain.
• Introduce or reinforce information about • Encourage the use of ambulation aids when
the use of hydroxychloroquine. pain is related to weight-bearing.
• Encourage the client to assume an
For oral ulcers: anatomically correct position with all joints.
• Instruct the client to avoid spicy or citrusy • Suggest that the client uses a small flat
foods. pillow under the head and not use a knee
• These foods might irritate fissures or ulcers gatch or pillow to prop the knee.
in the mucous membranes.
• Instruct the client to rinse the mouth with • Remind the client to avoid prolonged
half-strength hydrogen peroxide three times periods of inactivity.
per day.
• Encourage the client to perform range-of-
• Hydrogen peroxide helps keep oral ulcers
motion (ROM) exercises after the shower or
clean.
bath, two repetitions per joint.
• Instruct the client to keep ulcerated skin
clean and dry. Apply dressings as needed. • Remind the client to allow sufficient time
• Skin is necessary to prevent infection and for all activities.
promote healing.
• Encourage the client to take a 15-minute
• Instruct the client to apply topical
warm shower or bath on arising.
ointments as prescribed.
• Vitamins A and E may be useful in • Encourage the client to wear splints as
maintaining skin health. ordered.

For hair loss:

 • Encourage the use of nonpharmacological • Instruct the client to avoid stimulating foods
measures of pain control such as relaxation, (caffeine) or activities before bedtime.
distraction, or guided imagery. • Environmental stimuli can inhibit
relaxation, interrupt sleep, and contribute
• Suggest that the client apply a bed cradle.
to fatigue.
• Instruct the client to take anti-inflammatory • Encourage a warm bath or washers
medications as prescribed. Explain the need immediately before bedtime.
for taking the first dose of the day as early in • Warm water relaxes the muscle, facilitating
the morning as possible with a small snack. total body relaxation; excessive heat may
promote skin breakdown.
• Consult an occupational therapist for the • Encourage the client to sleep in an
proper splinting of affected joints. anatomically correct position and not to
• Administer a nighttime analgesic and/or a prop up affected joints.
long-acting anti-inflammatory drug as • Good body alignment will result in muscle
prescribed relaxation and comfort.
• Encourage the use of progressive muscle
relaxation techniques.
• These techniques promote relaxation and
rest.
• Encourage the client to frequently change
3. Decreasing Fatigue position at night.
• Repositioning promotes comfort.
• Assess the client’s description of fatigue: • Encourage gentle range-of-motion (ROM)
timing (Afternoon or all day), relationship exercises (after a shower or bath).
to activities, and aggravating and alleviating • These exercises maximize the muscle-
factors. relaxing benefits of the warm shower or
• Determine whether fatigue is related to bath.
psychological factors (e.g., stress, 4. Initiating Patient Education and Health Teachings
depression). • Patient education empowers individuals
• Determine the client’s nighttime sleep with SLE to actively participate in their own
pattern. care, make informed decisions, and adopt
healthy lifestyle behaviors. It equips them
• Reinforce energy-conservation principles: with the knowledge and skills necessary to
• Adequate rest periods recognize early signs of disease activity,
manage medications, understand the
• Energy reserves may be depleted unless the importance of regular follow-up
client respects the body’s need for increased appointments, and implement self-care
rest. strategies.
• Pacing of activities (an alternating activity • Assess the client’s knowledge of the disease,
with rest) management, and complication.
• The client often needs more energy than • Educate the disease process information:
others to complete the same tasks. unknown cause, chronicity of SLE,
processes of inflammation and fibrosis,
• Proper use of assistive and adaptive devices
remissions and exacerbations, and control
• Adequately used, these devices can support versus cure.
movement and activity, resulting in the
• Discuss common diagnostic tests.
conservation of energy.
• Introduce or reinforce information on drug
• Organization of activities and environment
therapy. Instruct the client on the potential
• Organization can help the client conserve side effects of steroids, immunosuppressant
energy and reduce fatigue. medication, and other drugs used to treat
SLE.
If fatigue is related to interrupted sleep:
 • Stress to the client the importance of not
altering the steroid dose or suddenly
stopping the medication.
• Instruct the client to monitor for the signs of
fever.
• Instruct in lifestyle activities that can help
reduce flare-ups such as:
• Eating a balanced diet of fruits, grains, and
vegetables.
• Regular exercise
• Avoiding sun exposure
• Adequate rest
• A positive approach to useful therapies
allows the client to be an active partner in
treating this chronic condition.
6. Monitoring Results of Diagnostic and Laboratory
• Provide information on appropriate clinical Procedures
trials.
Diagnostic and laboratory procedures are crucial in
• Instruct in the opportunities for support diagnosing SLE, assessing disease activity,
groups in the community or on reputable monitoring organ involvement, and guiding
internet websites. treatment decisions. Regular monitoring of
• Members of groups that come together for procedures enables healthcare providers to
specialized problems can be helpful to each evaluate the effectiveness of interventions, make
other. necessary adjustments to the treatment plan, and
detect potential complications or disease flares.
5. Administer Medications and Provide
Pharmacologic Support 1. Antinuclear Antibody (ANA) Test
2. Anti-Double-Stranded DNA (anti-dsDNA)
Administering medications and providing
Antibody Test
pharmacologic support are essential components of
3. Anti-Smith (anti-Sm) Antibody Test
nursing care for patients with systemic lupus
4. Complement Component Tests
erythematosus (SLE). SLE requires a multifaceted
5. Complete Blood Count (CBC)
approach to management, which often includes the
6. Erythrocyte Sedimentation Rate (ESR)
use of various medications to control disease
and C-Reactive Protein (CRP)
activity, manage symptoms, and prevent
7. Kidney Function Tests
complications. Pharmacologic interventions play a
8. Imaging Studies
critical role in alleviating symptoms, reducing
9. Biopsy
inflammation, and suppressing the immune
7. Assessing and Monitoring for Potential
response.
Complications
• Antimalarials (chloroquine, 1. Assess and monitor the patient for signs and
hydroxychloroquine) symptoms of disease activity.
• Corticosteroids 2. Monitor patient’s renal function.
• Nonsteroidal anti-inflammatory drugs and 3. Assess patient’s skin condition.
cyclooxygenase (COX-2) inhibitors 4. Monitor medication adherence and side effects.
• Immunosuppressants (mycophenolate 5. Provide psychological and emotional support.
mofetil, cyclophosphamide, azathioprine)
 1. Simple Conversion (S)
 Just interchange the SUBJECT and
PREDICATE of the proposition that
should be reduced. (Complete
Conversion)

Note: APPLICABLE LANG ITO PAG EXACTLY THE

SAME ANG SYMBOLS.

All ships are not small. E

Some pumpboats are small. I
Some pumpboats are not ships. O

PRE-PRE, FESTINO TO SUB-PRE, FERIO

ALL SMALL VEHICLES ARE NOT SHIPS.

SOME PUMPBOATS ARE SMALL.
SOME PUMPBOATS ARE NOT SHIPS.

Reduction of Categorical Syllogism No teachers are politicians. E

 refers to the process of reducing the syllogisms Some politicians are corrupt. I
from the higher figures to the first figure, the so Some corrupt persons are not teachers. O
called perfect figure (Figure I) for being pattered
according to the rules. Nevertheless, being PRE-SUB, FRESISON TO SUB-PRE, FERIO
imperfect does not mean invalid.
NO POLITICIANS ARE TEACHERS.
A. Figures of Syllogism SOME CORRUPT PERSONS ARE POLITICIANS.
1. SUB-PRE SOME CORRUPT PERSONS ARE NOT TEACHERS.
2. PRE-PRE
3. SUB-SUB
4. PRE-SUB 2. Accidental Conversion (P)
 Aside from intechanging the SUBJECT
B. Moods of Syllogism and PREDICATE, change the quantifiers
from UNIVERSAL to PARTICULAR.
1. BARBARA, CELARENT, DARII, FERI (PARTIAL CONVERSION)
2. CESARE, CAMESTRES, FESTINO, BAROCO
3. DARAPTI, DISAMIS, DATISI, FELAPTON, All innocent people are not foolish.
FERISON, BOCARDO All foolish people are ignorant.
4. BRAMANTIP, DIMARIS, CAMENES, FESAPO, Some ignorant people are not innocent.
FRESISON
PRE-SUB, FESAPO TO SUB-PRE, FERIO
A. Process:
1. Initial letter rule ALL FOOLISH PEOPLE ARE NOT INNOCENT.
Example: BRAMANTIP under Figure IV can SOME IGNORANT PEOPLE ARE FOOLISH.
be reduced to BARBARA under Figure 1. SOME IGNORANT PEOPLE ARE NOT INNOCENT.
2. Key consonants are S, P, M, C.
Example: BRAMANTIP key consonants are All grandfathers are rich in wisdom. A
M and P. All grandfathers are old. A
Some old people are rich in wisdom. I
B. Function:
SUB-SUB, DARAPTI TO SUB-PRE, DARII
FRAMEWORK:
 ANG GOAL is TO MAKE the SYLLOGISM into ALL GRANDFATHERS ARE RICH IN WISDOM.
FIGURE 1(SUB PRE) SOME ALL PEOPLE ARE GRANDFATHERS.
 REDUCE lang ang SYLLOGISM na MAY the same SOME OLD PEOPLE ARE RICH IN WISDOM.
INITIAL letters except sa CONTRADICTORY OF
CONCLUSION, OBVERSION METHOD. No apes can talk.
 REDUCE lang ang PROPOSITION having the KEY All apes are mammals.
consonants S, P, M, C.
Some mammals cannot talk. ALL BOOKS ARE NOT BORING TO READ

A Phantasm is a product of imagination. A

SUB-SUB, FELAPTON TO SUB-PRE, FERIO A feeling of sadness is not a product of imagination.
E A feeling of sadness is not phantasm. E
NO APES CAN TALK.
SOME MAMMALS ARE APES.
SOME MAMMALS CANNOT TALK. PRE-PRE, CAMESTRES TO SUB-PRE, CELARENT

3. Transposition of Premises (M) A PHANTASM IS A PRODUCT OF IMAGINATION.

 NOT about terms anymore, BUT about A PRODUCT OF IMAGINATION IS NOT A FEELING OF
the whole premise. Interchange the SADNESS.
Minor and Major premises.
PHANTASM IS NOT A FEELING OF SADNESS.
All arrows are sharp.
All sharp objects are dangerous. A PRODUCT OF IMAGINATION IS NOT A FEELING OF
Some dangerous objects are arrows. SADNESS.
A PHANTASM IS A PRODUCT OF IMAGINATION.
A PHANTASM IS NOT A FEELING OF SADNESS.

PRE-SUB, BRAMANTIP TO SUB-PRE, BARBARA 4. Contradictory of Conclusion (C)

 applicable only to BAROCO and
ALL SHARP OBJECTS ARE DANGEROUS. BOCARDO
ALL ARROWS ARE SHARP.
ALL ARROWS ARE DANGEROUS OBJECTS. a. Indirect Method
BAROCO is PRE-PRE. Contradict the
Some strong men have big muscles. I conclusion and the result will be placed in
All strong men have healthy bodies. A the minor premise and deduce the right
Some men with healthy bodies have big muscles. I conclusion.
BAROCO to BARBARA
SUB-SUB, DISAMIS, SUB-PRE, DARII
All lepers are sick people.
SOME MEN WHO HAVE HEALTHY BODIES ARE Some institutions are not meant for the sick people.
STRONG. ALL STRONG MEN HAVE HEALTHY Some institutions are not meant for the lepers
BODIES.
SOME MEN WHO HAVE BIG MUSCLES ARE Contradict the conclusion.
HEALTHY.
All lepers are sick people.
ALL STRONG MEN HAVE HEALTHY BODIES. Some institutions are not meant for the sick people.
SOME MEN WHO HAVE HEALTHY BODIES ARE All institutions are meant for the lepers.
STRONG. SOME MEN WHO HAVE BIG MUSCLES ARE
HEALTHY. Place the conclusion in the minor premise then
deduce the right conclusion.
Books are informative materials. A
All informative materials are not boring to read. E All lepers are sick people.
All materials that are not boring to read are books. All institutions are meant for the lepers.
E All institutions are meant for the sick people.

PRE-SUB, CAMENES TO SUB-PRE, CELARENT Note: The middle term is not constant. Nevermind,
its OKAY.
Books are informative materials. A
All informative materials are not boring to read. E BOCARDO is SUB SUB. Contradict the conclusion
ALL BOOKS ARE NOT BORING TO READ. and the result will be placed in the minor premise
and deduce the right conclusion.
All informative materials are not boring to read. E
Books are informative materials. A BOCARDO TO BARBARA
 Some male persons are non-holy.
Not all games are exciting.
A game is a form of exercise. Apply simple conversion in the major premise and
Not all forms of exercise are exciting. conclusion going to DIMARIS

Contradict the conclusion. Some non-holy persons are priests.

All priests are male persons.
Not all games are exciting. Some non-holy persons are males.
A game is a form of exercise.
All forms of exercise are exciting. Apply simple conversion in the conclusion.

Place the conclusion in the minor premise then Some non-holy persons are priests.
deduce the right conclusion. All priests are male persons.
Some male persons are non-holy.
All forms of exercise are exciting.
A game is a form of exercise.
A game is exciting.
Note: The middle term is not constant. Nevermind, Apply transposition of premises.
its OKAY
b. Obversion Method All priests are male persons.
Some non-holy persons are priests.
BAROCO is PRE PRE. Obvert the major and minor Some male persons are non-holy.
premise. The result is FESTINO. Apply simple
conversion going to FERIO. EXERCISE:
Directions: Reduce the given syllogisms to Figure I.
BAROCO to FESTINO For BOCARDO and BAROCO, apply both indirect and
obversion method.
All airplanes are flying objects. Not all motorized
objects are flying objects. All students are not professionals.
Not all motorized objects are airplanes. All nurses are professionals.
All nurses are not students.
Obvert the major and minor premise.
All nurses are professionals.
All airplanes are not non-flying objects. All students are not professionals.
Some motorized objects are non-flying objects. All students are not nurses.
Some motorized objects are not airplanes.
All students are not professionals.
FESTINO to FERIO Some employees are professionals.
Some employees are not students.
All non-flying objects are not airplanes.
Some motorized objects are non-flying objects. All nurses are professionals.
Some motorized objects are not airplanes. All nurses are caring.
Some caring people are professionals.
BOCARDO is SUB SUB.
Example: Some nurses are cute.
All nurses are neat.
Some priests are not holy. Some neat people are cute.
All priests are male persons.
Some male persons are not holy. All nurses are neat.
Some nurses are cute.
Obvert the major premise and conclusion going to Some cute people are neat.
DISAMIS.
All nurses are not doctors.
Some priests are non-holy. All nurses are professionals.
All priests are male persons. Some professionals are not doctors.
  But A.
All nurses are not doctors.  So B.
Some nurses are caring.
Some caring people are not doctors.  If A, then not B.
 But A.
All caring people are nurses.  So, not B.
All nurses are kind.
Some kind people are caring.  If not A, then not B.
 But not A.
Some good people are nurse.  So, not B.
All nurses are responsible. Other combinations will lead to a
Some responsible people are good. fallacy of denying the antecedent.
If A, then B.
All loving people are nurses. But, not A.
All nurses are not doctors. So, not B.
All doctors are not loving people.

All doctors are not nurses.

All nurses are loving.
Some loving people are not doctors. b. Modus Tollens
 If A, then B.
All doctors are not nurses.  But, not B.
Some nurses are kind.  So, not A.
Some kind people are not doctors.
 If not A, then B.
All caring people are nurses.  But not B.
Some kind people are not nurses.  So, A.
Some kind people are not caring.
 If A, then not B.
Some nurses are not caring people.  But, B.
All nurses are kind people.  So, not A.
Some kind people are not caring.
 If not A, then not B.
Hypothetical syllogisms  But B.
o is a syllogism whose first premise is a  So, A
sequential proposition wherein one
member is affirmed or denied in the second Other combinations will lead to a fallacy of
premise, and the other member is affirming the consequent.
consequently affirmed or denied in the B. Pure Conditional Syllogism (Transitive
conclusion. The first premise is called Property)
antecedent and the second premise is called  If A, then B.
the consequent.  If B, then C.
 If A, then C. 2
1. Conditionals
 The if-clause is called antecedent, 2. Disjunctive Syllogism.
the then-clause is called consequent.  Either A or not A.
 But A.
A. Mixed Conditional Hypothetical  Therefore, not not A.
Syllogism
a. Modus Ponens  Either A, or not A.
 If A, then B.  But not A.
 But A.  Therefore, not A.
 So B.
3. Conjunctive Syllogism
 If not A, then B.