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Immune System Diseases and Disorders 77
There are other types of diabetes that are not caused
by autoimmunity. Because all types of diabetes affect
the endocrine system, they are discussed and compared
in detail in Chapter 14, “Endocrine System Diseases and
Disorders.”
Lupus Erythematosus
■ Description. The term lupus originally referred to
any chronic, destructive type of skin lesion. The Latin
word lupus means wolf, and erythematosus refers to red
ness. The term lupus erythematosus has been used since
the thirteenth century because physicians of that time
thought the shape and color of the skin lesions resem
bled a wolf bite. The word lupus is often used to refer
to lupus erythematosus, although used alone, this term
truly has no meaning. There are several forms of lupus,
including lupus pernio, lupus vulgarus, drug-induced
lupus, and lupus erythematosus.
There are two types of lupus erythematosus: cuta
neous (discoid) and systemic (diffuse). Cutaneous or
discoid lupus erythematosus (DLE) is limited to skin
or cutaneous involvement. DLE does not affect mul
tiple systems, as does systemic lupus erythematosus
(SLE). DLE can be thought of as a type of systemic lupus
because the cause, testing, and treatment are similar for
cutaneous involvement. DLE is the less serious type of
lupus erythematosus.
SLE primarily affects women, occurring 10 times
more frequently in women than in men. Onset is usu
ally between ages 30 and 40, but it can appear at any
age. The disease is most severe among Black persons.
■ Etiology. SLE is an autoimmune disorder in which
B lymphocytes produce autoantibodies that attack
body cells. Individuals with SLE have a high number
of ANAs. These antibodies attack the body’s own cell
nuclei, destroying the RNA and DNA of the cell. Detec
tion of ANA by microscopic immunofluorescence sup
ports the diagnosis of SLE.
■ Symptoms. SLE often affects the skin and a num
ber of other organs or systems. A classic sign is
the presence of a persistent, red, facial butterfly
shaped rash across the bridge of the nose and cheeks
(Figure 5-13). Symptomatic individuals often com
plain of fever, joint pain, weight loss, and facial
rash. Joint, kidney, and muscle involvement can
lead to complaints of arthritis, glomerulonephritis
(inflammation of the glomerulus, or filtering unit of
the kidney), and atrophy, respectively. Heart valve
Figure 5-13 Butterfly rash of systemic lupus
erythematosus (SLE).
deformities and abnormal blood composition are not
unusual findings.
■ Diagnosis. Diagnosis is often very difficult, but
tests including electrolytes, renal function, liver
enzymes, complete blood count, and ANA are help
ful. The most definitive testing is a positive result on
an ANA test.
■ Treatment. SLE is a chronic disease that goes through
periods of exacerbation and remission. Complete remis
sion is very rare. Treatment is symptomatic. Nonsteroidal
anti-inflammatory, antipyretic, and analgesic medica
tions can be used to treat symptoms. Life-threatening
exacerbations are often treated with corticosteroids.
Prognosis depends on which organs are affected and
the severity of the infection. Renal insufficiency, bacte
rial endocarditis, cardiac failure, sepsis, and pneumonia
commonly lead to death.
■ Prevention. SLE cannot be prevented or cured.
Scleroderma
■ Description. Scleroderma (skle-ro-DER-mah;
sclero = hardening, derma = skin) is a chronic auto
immune disorder characterized by hardening, thick
ening, and shrinking of the connective tissues of the
body, including the skin. Like many other chronic
diseases, scleroderma might exhibit periods of remis
sion and exacerbation. The generally slow progression
of the disease allows the individual a reasonably long
78 Chapter 5
Figure 5-14 Scleroderma. (A) Raynaud’s phenomenon. (B) Mouth tightening.
life, although if the disorder progresses rapidly, affect
ing vital organs, early death can result. Death is usually
related to kidney failure.
■ Etiology. It is thought that this autoimmune reaction
begins with the skin and connective tissues, attracting
lymph cells. These lymph cells stimulate the production
of collagen, leading to the disorder.
Milder forms of scleroderma commonly affect
women 30 to 50 years of age and include those lim
ited to the skin, face, and extremities. The more severe
forms, called systemic or diffuse, usually affect men and
older persons. This type affects not only the skin but
also internal organs, including the heart, lungs, and kid
neys. These tissues become hardened, thickened, and
often limited in function.
■ Symptoms. Characteristically, individuals with
scleroderma have thick, leather-like, shiny, taut skin
and joint contractures. The first symptom is usually
Raynaud’s phenomenon (Figure 5-14A), an episodic
vasoconstriction affecting the hands. The mouth area
often becomes wrinkled with a tight, purse-lipped
appearance, leading to difficulty eating (Figure 5-14B).
Diagnosis can be confirmed by clinical examination and
tissue biopsy.
■ Diagnosis. Diagnosis is difficult because this disease
initially mimics other disorders such as bursitis and
arthritis.
Physical symptoms indicative of scleroderma
include the following:
■ Tight skin around the hands, face, and mouth
■ Changes in the capillaries at the base of the fingernails
■ Calcium deposits under the skin
These physical symptoms, coupled with special
blood testing for the presence of anticentromere anti
bodies, often yield a positive diagnosis.
■ Treatment. Currently, there is no treatment or cure
to stop the progression of scleroderma. Treatment with
anti-inflammatory medications, immunosuppressives,
and antibiotics might be beneficial. Muscle stretching
and strengthening exercises might also be beneficial to
maintain muscle strength and joint mobility.
■ Prevention. No one really knows what causes sclero
derma, so at this time, there are no preventive methods
identified.
Isoimmune Disorders
Isoimmunity refers to a hypersensitivity of one individ
ual to another individual’s tissues. Examples include
blood type reactions, tissue rejections, and mater
nal-fetal reactions.
Blood Transfusion Reaction
■ Description. As previously stated, all body cells have
a specific antigen that identifies them. Red blood cells
(RBCs) have surface antigens. Transfusion of blood from
one individual to another is, in a sense, a type of tissue
transplant. RBCs have to be typed and cross-matched to
identify antigens properly and prevent rejection.
The blood types are identified by antigens and can
be divided into four groups: A, B, AB, and O. Types O
and A are the most common. Each RBC has an anti
gen and a corresponding antibody. Blood type A has an
A antigen and anti-B antibody. B type has a B antigen
and anti-A antibody. O has no antigen and both anti-A
and anti-B antibodies. AB has an A and a B antigen and
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Immune System Diseases and Disorders 79
no antibody. These antigen-antibody patterns make
type O the universal blood donor and type AB the uni
versal blood recipient (Figure 5-15).
In addition to antigens that determine blood type,
85% of Americans have another antigen called the Rh
factor. This group is collectively called Rh positive
(Rh+) because they have the factor or antigen. Those
who do not have the factor—approximately 15% of
the population—are Rh negative (Rh-). Cross match
ing for transfusions must match the appropriate type
and Rh factor. The common rule of Rh factor is “those
who don’t have it don’t want it; those who have it don’t
care.” In other words, Rh- individuals cannot receive
Rh+ blood. On the other hand, Rh+ individuals “don’t
care,” so they can receive Rh+ or Rh- blood. When
considering transfusions both the type (A, B, O, AB)
and the Rh factor (Rh+, Rh-) must be considered. The
universal blood donor is O- and the universal blood
recipient is AB+. Blood type and factor are genetically
determined or received from an individual’s mother or
father.
■ Etiology. If a blood type with an antigen is given to a
type that has antibodies against that antigen, the anti
bodies will attack the antigen and break down the donor
RBCs. For example, if type A (with antigen A and anti-B
antibody) is given to type B (with antigen B and anti-A
antibody), the anti-A antibody in the B type recipient’s
blood will attack the A antigen and break down the
type A donor blood (see Figure 5-15). The same action
occurs if the Rh factor is mismatched.
As antibodies react with the antigen, they also
cause clumping of the blood, leading to microthrombi
(microscopic-sized blood clots). These microthrombi
can lead to multiple organ emboli and have fatal
consequences.
■ Symptoms. Symptoms of transfusion reaction include
chills, shivering, and fever.
■ Treatment. Reactions should be treated immedi
ately by discontinuing the transfusion and contact
ing the director of the blood bank, medical physician,
and nephrologist. Anticipation of complications such
as hypotension, renal failure, disseminated intravas
cular coagulation (DIC), and possibly death should
be expected and treated preventively or as symptoms
arise.
■ Diagnosis. Most transfusion reactions are diagnosed
by watching for any significant change in a patient’s
condition during transfusion. Diagnosis depends on
recognizing a significant change in vital signs along
with the development of the signs and symptoms of
a reaction.
To understand the concept of transfusion reaction with antigen and antibodies, consider this example. The particular
blood type can give blood to any type that does not change the color in the jar and receive blood from any type that
does not change the color in the jar. For example, A can give blood to AB because adding red to purple will not
change the purple color. However, A cannot give to B because giving red to blue will change the color. Since O is in
the clear jar, it can give to all types but could not receive from anything but O or the clear color would change.
Type
Percent of
Population with Type
Antigen Antibody
Color Jar
Example
Donate Blood
To:
Receive Blood
From:
A 41 A B
RED
A and AB A and O
B 12 B A
BLUE
B and AB B and O
O 44 None A and B
CLEAR
A, B, AB, O O
AB 3 A and B None
PURPLE
AB A, B, AB, O
Figure 5-15 Blood types for donors and recipients.
Chapter 5
■ Prevention. Prevention is aimed at ensuring that the
blood transfused is compatible by typing, cross match
ing, and checking for antibody reaction.
Erythroblastosis Fetalis
■ Description. Erythroblastosis fetalis (eh-RITH-roh-
blas-TOH-sis feh-TAH-lis) is an isoimmune condition
in which antibodies in a mother’s blood attack and
destroy the antigen on the baby’s RBCs, ultimately kill
ing the unborn fetus. This condition is also known as
hemolytic (hemo = blood, lytic = breaking or crushing)
disease of the newborn.
Because blood type and factor are determined by
one’s mother or father, it is possible for a mother to be
pregnant with a baby of different blood type and factor
(received from the father; Figure 5-16). Mothers preg
nant with babies of different blood types seldom have
a problem, but those with different blood factor might
have difficulty. In some cases, the mother will develop
antibodies against the other blood type (ABO incom
patibility) that usually produces only mild symptoms
in the infant.
RBCs do not cross the placenta. Oxygen and
nutrients simply diffuse across placental membranes
to nourish the baby. RBCs do not normally exchange
between the mother and the infant, but mixing of blood
may occur to some degree during childbirth. Mothers
who are Rh- and “don’t want” Rh+ factor might have
difficulty with Rh+ babies.
■ Etiology. Rh- mothers pregnant with Rh+ babies usu
ally do not have a problem with the first baby. During
the first pregnancy, the mother’s blood has not had the
opportunity to identify the antigen because there has
been no exchange of blood cells or antigens. However,
there may be some slight mixing of blood during the
birthing process. As this blood intermingles, the Rh+
antigen is picked up by the mother’s blood. The moth
er’s immune system recognizes this antigen as a foreign
invader and builds antibodies to destroy it. Subsequent
Rh+ babies are not as fortunate as the first Rh+ baby.
■ Symptoms. If this Rh- mother becomes pregnant
with another Rh+ baby, antibodies against the Rh factor
that she has built up in her blood do cross the placental
membranes. These antibodies attack the blood of the
unborn child, breaking down the RBCs and leading to
anemia and possible death of the baby.
This condition affects only Rh+ babies carried by
Rh- mothers. Rh+ mothers “don’t care” about the fac
tor. Rh+ mothers have the antigen, so they do not build
up antibodies against it.
■ Diagnosis. Prenatal diagnosis of erythroblastosis
fetalis is accomplished by ultrasound. An abnormal
or increased fluid accumulation might be noted in the
abdomen, lungs, heart, skin, or all of these in the baby.
There is also an increase in the amount of amniotic fluid
along with thickening of the placenta.
■ Treatment. Treatment for erythroblastosis fetalis is
exchange transfusion of the baby’s blood with Rh+ blood
at birth. This treatment stops the destruction of the baby’s
RBCs. Over time, the transfused Rh+ blood is replaced
by the baby’s own blood. If erythroblastosis fetalis is a
possibility in an Rh- mother, the baby’s condition can
be monitored by amniocentesis. Babies who are mildly
OFFSPRING
FATHERMOTHER
A
A
O
POSSIBLE Rh
REACTION IN
#2 AND #4
The offspring of this mother and father have the possibility of four different blood types. Since this is an Rh- mother, there is
a possibility of an Rh reaction with the two Rh+ children. If the father was also Rh-, all offspring would be Rh- and no reac
tion would occur in any of the children. If the mother were Rh+, no Rh reaction could occur in any of the offspring since Rh+
mothers are not sensitive to the Rh antigen.
| Figure 5-16 Blood type in inheritance patterns and identification of possible Rh reactions.
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Immune System Diseases and Disorders 81
affected might be carried to full term. Severe cases, how
ever, might indicate the need to induce labor and prema
ture delivery of the baby to begin lifesaving treatment.
Historically, an Rh factor marital mismatch might
have been the reason queens or wives of royalty were
beheaded when unable to produce living heirs to
the throne. If the king was Rh+ and the queen Rh-,
every child after the first would have been at succes
sively higher risk of fetal death. Erythroblastosis fetalis
rarely occurs in the modern world. The development
of RhoGAM
®
, a special immune globulin, has halted
this condition.
■ Prevention. RhoGAM
®
is an injectable medication
given to Rh- females to prevent the development of anti
bodies against Rh+ factor. It is given prophylactically
after the delivery of the first and any subsequent Rh+
fetuses to prevent the development of Rh antibodies.
Organ Rejection
■ Description. Organs such as the liver, kidney, heart,
and lungs could be easily transplanted if not for the
human immune system.
■ Etiology. The immune system recognizes trans
planted tissue as foreign and attacks it. This attack by
lymphocytes brings about donor tissue destruction rec
ognized as tissue or organ rejection.
■ Symptoms. Transplant rejection might be hyper
acute in nature and actually occurs during the surgical
procedure. Acute rejection occurs within the first few
weeks, whereas chronic rejection occurs over time, usu
ally months to years. Chronic rejection occurs slowly
and is due to vessel damage that decreases blood flow to
the donor tissue. Decreased blood flow causes chronic
ischemia and, ultimately, death of the donor organ.
■ Diagnosis. Diagnosis is made by physical examina
tion and testing of the function of the newly transplanted
organ. A biopsy of the organ can confirm rejection.
■ Treatment. Donated organs are matched to possible
recipients. The closer the donor antigen matches that of
the recipient, the less chance the organ will be rejected.
Administering immunosuppression medications also
decreases the possibility of rejection.
■ Prevention. Immunosuppression medications must
be taken prior to transplantation surgery and for the
remainder of the organ recipient’s life. This medica
tion suppresses or decreases the body’s ability to wage
war against the donor tissue and thus prevents organ
rejection.
Immune Deficiency Disorders
The last classification of immune disorders is related to
a deficient or weak immune system; this is also called
immunodeficiency. These disorders represent an
inability of the immune system to protect the individ
ual against disease. This deficiency might be congen
ital due to a genetic disorder, or it might be acquired
during the individual’s lifetime. Acquired disorders are
the most common type and can be due to disease ther
apies, such as chemotherapy and radiation treatments,
by suppressing bone marrow, thus decreasing leuko
cyte production. Medications given to organ transplant
recipients purposefully suppress the immune sys
tem. The most common immunodeficiency disorder
is AIDS.
The classic clinical problem with immunodefi
ciency disorders is the development of unusual and
severe infections such as pneumonia, meningitis, or
septicemia, to name a few. Also, the development of
infections by microorganisms that are not usually
pathogenic (opportunistic infections) can be indica
tive of an immunodeficiency disorder. Other signs and
symptoms are numerous and varied, depending on
the organs or organ systems affected and the invading
pathogen. Specific signs and symptoms will be included
in the discussion of the disorder.
Acquired Immunodeficiency Syndrome (AIDS)
■ Description. The name of this disease briefly describes
its pathology. It is an acquired disease that causes the
immune system to be deficient in protecting the body,
leading to a syndrome of symptoms or secondary
diseases.
AIDS was first diagnosed in the United States in the
early 1980s. The first diagnosed cases were found in a
group of homosexual men who became ill with a series
of opportunistic diseases and eventually died. These
individuals had surprisingly suppressed immune sys
tems. Further research led to the discovery of the virus
and the mode of transmission.
■ Etiology. The cause of AIDS is a virus called HIV. The
wicked characteristic of HIV is its battle plan to wipe
out the individual’s lymphocytes, thus leaving the body
defenseless against an attack by all pathogenic organ
isms. The primary target is the T lymphocyte, but mac
rophages are affected as well. HIV is cytotoxic (cyto =
cell, toxic = killing). Ultimately, the HIV-infected indi
vidual will have a low T lymphocyte cell count, indica
tive of a positive diagnosis of AIDS.
82 Chapter 5
HIV is transmitted from one individual to another
through intimate contact and sharing of body fluids.
The virus must enter the body and bloodstream to
infect the individual. HIV is fragile and easily killed by
temperature changes. Many misconceptions and fears
about the transmission of AIDS are still prevalent in
society today. An individual cannot get HIV infection
from toilet seats, doorknobs, furniture, water fountains,
and other objects. An individual cannot get HIV from
social kissing, coughing, sneezing, or even sharing eat
ing utensils. HIV is not transmitted through air, food,
urine, feces, or water. HIV is primarily transmitted in
three ways:
1. Sexual intercourse Semen and vaginal secretions
carry HIV. The transmission rate is higher from
male to female because females might have
microscopic vaginal tears during intercourse.
Transmission rate is very high with anal inter
course because the internal lining of the rectum
is very thin. Approximately 75% of infected
individuals in the United States contract AIDS
through sexual intercourse.
2. Sharing of hypodermic needles HIV-infected
blood is injected into the body by sharing nee
dles. This type of transmission accounts for 18%
to 25% of infected individuals in the United
States.
3. In utero from infected mother to unborn child
HIV passes across the placenta to infect the
baby. This accounts for 1% to 3% of AIDS cases.
Transmission of HIV through blood transfusions
has been virtually eliminated by effective screening
methods. Health professionals following appropriate
precautions are at very little risk of contracting HIV.
■ Symptoms. HIV was first staged in 1990. Staging
is helpful in the diagnosis, evaluation, and manage
ment of HIV/AIDS. Several health organizations have
developed staging processes often based on T-cell
counts.
One of the most current staging processes has been
developed by AIDS.gov, a resource provided by the U.S.
Department of Health and Human Services. The AIDS.
gov system (2020) includes a three-stage progression.
I Acute HIV Infection
■ Occurs within 2 to 4 weeks after infection
with HIV.
■ Symptoms are similar to influenza and include fever,
headache, chills, and joint and muscle aches.
■ Large amounts of the virus are produced in the body,
attacking CD4 T cells.
II Chronic HIV Infection
■ HIV is active but reproduces at very low levels.
■ The person may or may not have symptoms
(asymptomatic).
■ If testing is done, the person would test positive
for HIV.
■ This period may be brief or may last a decade
or longer.
■ Those on antiretroviral medications may be in this
stage for several decades since treatment helps keep
the virus in check.
III AIDS
■ Infected person is severely sick.
■ T-cell count drops below 200.
■ Rapid weight loss.
■ Recurring fever and/or profuse night sweats.
■ Extreme and unexplained tiredness.
■ Prolonged swelling of the lymph glands in the arm
pits, groin, or neck.
■ Diarrhea that lasts for more than a week.
■ Sores of the mouth, anus, or genitals.
■ Pneumonia.
■ Red, brown, pink, or purplish blotches on or under
the inside of the mouth, nose, eyelids.
■ Memory loss, depression, and other neurologic
disorders.
■ These symptoms may be related to other illnesses.
■ Two diseases that are primarily identified with
AIDS are
1. Pneumocystis carinii (NEW-moh-SIS-tis kah-
RYE-nee-eye) pneumonia, an infection of
the lungs with a protozoan. This organism
has never been documented as a cause of
pneumonia in persons with normal immune
systems.
2. Kaposi’s sarcoma (KAP-oh-seez sar-KOH-mah),
a blood vessel cancer that causes reddish-purple
skin lesions (Figure 5-17).
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Figure 5-17 Kaposi’s sarcoma.
■ Diagnosis. AIDS is diagnosed when the T-cell count
drops below 200 cells per microliter.
■ Treatment. AIDS was 100% fatal from the time of
discovery until treatment became available. Historically,
there have been three eras of treatment: 1980 to 1995,
before effective HIV treatment became available; 1996
to 1999, the beginning of effective treatment; and 2000
to 2003, when contemporary HIV treatment became
readily available.
In 2012, the Federal Drug Administration (FDA)
approved a new at-home HIV test kit. With early test
ing and diagnosis followed by antiretroviral treatment
(ART), life expectancy can be very near the normal
range.
If HIV is diagnosed while the T-cell count is over
400 cells per microliter and ART is successfully uti
lized, it is estimated that the median age of death (life
expectancy) for those with AIDS will be approximately
77.0 years of age. This is roughly the life expectancy of
the general population.
The main challenges in improving survival rates
with AIDS include early detection and treatment costs.
It is estimated that one in eight infected individu
als are unaware of their condition until they become
symptomatic.
The lifetime cost of treatment for one individual
with AIDS is projected to be over $380,000 (Centers
for Disease Control and Prevention [CDC], 2019).
Late detection combined with inadequate treatment
increases the mortality rate. With more than 14,000
deaths per year, AIDS still ranks as the ninth-lead
ing cause of death. Those persons who do not survive
usually have a variety of symptoms and diseases as the
individual’s immune system crumbles and becomes
incapacitated (Figure 5-18). Ultimately, superinfec
tions and massive diarrhea may be the cause of death.
■ Prevention. AIDS continues to be a worldwide epi
demic or pandemic. From 2000 to 2014, approximately
38 million people have been diagnosed and more than
25 million have died.
Worldwide statistics from WHO for 2015 include
■ an estimated 38 million have AIDS.
■ over 2 million were newly infected.
In the United States alone, there are over 1.2 mil
lion people currently living with AIDS, and every year
approximately 50,000 new cases are diagnosed (CDC,
2018).
AIDS can be stopped with preventive education
and action. The only known method of prevention is
avoiding exposure to the virus.
Trauma
Trauma to the immune system is generally limited
to treatments or medications, such as chemotherapy
and radiation treatments, that often lead to immu
nosuppression. Individuals on corticosteroid medi
cations often have undetected infections because this
medication suppresses the protective inflammatory
response. Graft and organ recipients take immuno
suppression medications to traumatize the system
purposefully in hope of protecting the transplanted
graft or organ.
Rare Diseases
Severe Combined Immunodeficiency
Disease (SCID)
Severe combined immunodeficiency disease (SCID) is
a group of inherited disorders in which there is par
tial or complete dysfunction of the immune system or
complete deficiency. Untreated children usually die at
a young age. Treatment can include a bone marrow
transplant from a matched sibling and has restored
complete immune function in some children. Protec
tive isolation is necessary to prevent lethal infections.
This protected environment has led to these children
being called “bubble babies.”
CENTRAL NERVOUS
SYSTEM
Lymphoma
Kaposi’s sarcoma
TUMORS
LARGE INTESTINE
BLOOD VESSELS
Meningitis
Encephalitis
AIDS dementia
Colitis
Proctitis
Pneumonia
AIDS nephropathy
Malabsorption
MOUTH
LUNG
KIDNEY
SMALL INTESTINE
SKIN
Dermatitis
Folliculitis
Impetigo
Herpes labialis
Thrush
| Figure 5-18 Pathologies associated with AIDS.
Healthy Highlight
Preventive
Strategies for HIV
and AIDS
Other Behaviors
That Will Help
Prevent the Spread
of HIV
■ Abstain from sexual intercourse or develop a monogamous relationship with a part
ner who is not infected and is not an intravenous drug user.
■ Do not abuse alcohol or drugs in a manner that prevents you from being in control
of your behavior.
■ Do not use intravenous drugs. If you are an intravenous drug user, always use a sterile
needle or one soaked in bleach, and do not share your needles.
■ Refrain from multiple sex partners or sex with intravenous drug users.
■ Refrain from unprotected sex with homosexuals or bisexual men.
■ Always use a latex condom with a spermicide and virucide if you are uncertain about
your partner’s sexual history.
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Immune System Diseases and Disorders 85
Effects of Aging on the
Immune System
Presently, not all age-related changes in the immune
system are well understood. It is known that the thy
mus gland degenerates with age. The thymus reaches
its maximum size in early childhood and then slowly
decreases in size after puberty. As the gland decreases
in size, so does the number of T cells because they orig
inate in the cortex of the thymus. The remaining T cells
do not function as well, increasing the chance of devel
oping invasive diseases, such as cancer. Some defects in
lymph cells also occur in the aging process.
The B-cell levels remain stable throughout life, but
the antibodies in older persons might not function as
well as in younger years. Thus, infections are common
in the older population. The antibodies are more likely
to attack the body’s own tissue (autoantibodies) as a
result of a loss of tolerance to self-antigens. General
resistance to disease seems to decrease with age, but
this might be due to many other factors such as general
nutrition, exercise, medications, and psychosocial influ
ences rather than to changes in the immune system.
Consider This...
Laughing lowers stress hormones and
strengthens the immune system. A 6-year-
old laughs an average of 300 times a
day, while the average adult only laughs
15-100 times a day.
Summary
T
he immune system consists of organs such as the thymus gland, bone marrow, lymph nodes, spleen, liver, and tonsils,
and major cells such as the lymphocytes. The immune system is an important defense system for the body because a
malfunctioning or compromised immune system weakens the body’s defenses against invading microorganisms. Many
secondary disorders such as infections are due to a compromised immune response. Primary diseases or disorders of the
immune system are categorized as hypersensitivity disorders or immune deficiency disorders. Hypersensitivity disorders
include allergies, autoimmune disorders, and isoimmune disorders. The immune deficiency disease AIDS is one of the
most common and debilitating conditions of the immune system. Diagnostic testing for immune disorders includes skin
testing, complete blood cell counts, and some specific antibody studies. Treatment for immune disorders varies with
the specific problem. Some immune disorders are quite mild, whereas others are severe and require long-term therapy.
Review Questions
Short Answer
1. What are the functions of the immune system?
2. Which signs and symptoms are associated with common immune system disorders?
3. Which diagnostic tests are most commonly used to determine the type, cause, or both of an immune system disorder?
86 Chapter 5
Matching
4. Match the disorders listed in the left column with the correct category of immune system diseases in the right
column. (Right-hand column categories may be used more than once.)
Hay fever
_____ AIDS
Anaphylaxis
Rheumatic fever
Erythroblastosis fetalis
Organ rejection
a. Allergies
b. Autoimmune disorders
c. Isoimmune disorders
d. Immune deficiency disorders
Multiple Choice
5. Which of the following behaviors might contribute to increased risk for HIV transmission?
a. Donating blood
b. Sharing intravenous needles
c. Failure to wash hands after toileting
d. Unprotected sex
e. Sharing eating utensils
f. Direct contact with body fluids
g. Frequent use of laxatives and enemas
True or False
6. T F The immune system is the body’s only defense system against invading organisms.
7. T F Signs and symptoms of hypersensitivity disorders might include rash, redness, heat, swelling, nasal
congestion, coughing, and sneezing.
8. T F The Coombs test is used to detect certain antibodies in the blood.
9. T F Autoimmune disorders are hyposensitivities in which the body fails to recognize its own antigens.
10. T F The effects of aging put the older adult at an increased risk for immune system problems.
Case Studies
■ Terry Stephens is a 26-year-old male who has been diagnosed as HIV positive. He has told you that he and
his girlfriend have unprotected sex. You have been close friends for many years. What are some strategies you
could use to inform Terry about the danger of this behavior? Should you also talk to his girlfriend? When Terry
was hospitalized, you noticed his caregivers wore gloves when starting his IV and drawing blood. Was this
because he is HIV positive? Would this be a routine precaution?
■ Your friend, Bonnie, is suffering from rheumatoid arthritis. She asks you if she should take an over-the-counter
herbal preparation. She read an advertisement about the benefits of this product for boosting the immune system,
and she thinks that it might relieve some of her symptoms. How would you answer her question? Can you safely
say it is a good idea to try this treatment? Would it help relieve her symptoms?
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