IMMUNOLOGY

IMMUNOLOGY

BY:
Ms. Jenneth E. dela Cerna, R.N.

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• DEFINITION OF TERMS:
• IMMUNOLOGY
Study of specific immunity and how the immune
system responds to specific infectious agents.

• IMMUNE SYSTEM
 Functional system that recognizes foreign
molecules [antigens] & acts to inactivate or
destroy them.
 Normally, it protects us from a wide variety of
pathogens, as well as from abnormal cells.

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• Immune system functions as the body’s defense
mechanism against invasion.
IMMUNITY
• Refers to the body’s specific protective response
to an invading foreign agent or organism.
• Specific resistance to disease
 refers to the body’s specific protective response
to an invading foreign agent or organism.
 ability of an organism to recognize and defend
itself.
 ability to resist disease producing microorganism,
poisons, and foreign CHON.

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• The body’s defenders against these tiny
but mighty enemies are two systems simply
called the nonspecific & specific defense
system.

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a. Nonspecific defense system
• Responds immediately to protect
the body from all foreign
substances.
• Refers to the mechanical barriers
that cover body surfaces & to cells
& chemicals that act on the initial
battlefronts to protect the body
from pathogens.

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• The body’s first line of defense
against the invasion of pathogens
are the skin & mucous membranes.

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a.1 Skin
 First line of defense vs. penetration of
foreign agents inluding pathogens.
 Efficient physical barrier against harmful
agents
 (heat,cold,trauma)

 KERATIN- water proof barrier that

provides resistance against acids, alkalis &
bacterial enzymes.

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 a.2 Mucous membranes line all body cavities open
to the exterior: digestive, respiratory,
urinary & reproductive tracts.
• Intact mucous membranes also provides
mechanical barriers in the body, prevents the
entry of pathogens.
• These membranes produce a variety of
protective chemicals:
a. Acid pH of skin secretions inhibits bacterial
growth.
b. Stomach mucosa secretes HCl acid & protein-
digesting enzymes which both kills pathogens.

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c. Saliva & lacrimal fluid contain lyzosome , an
enzyme that destroys bacteria. [lubricate &
cleanse eyes & oral cavity.]
d. Sticky mucus traps many microorganisms
that enter digestive & respiratory
passageways.

• Some mucosae also have structural

modifications that fend off potential
invaders:
a. mucus-coated hairs inside the nasal cavity
trap inhaled particles.

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 b. Respiratory tract mucosa is ciliated
which sweeps dust & bacteria-laden
mucus toward the mouth
•Specialized Structures:
- Filtration
- Flushing action of saliva and urine
- Protection provided by constant movement
of food
- Action by vomiting and watery stools

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• Second line of defense
- Uses an enormous number of cells &
chemicals to protect the body.
- These defenses rely on destructive
powers of phagocytes & natural killer
cells, the inflammatory response & a
variety of chemical substances that
kill pathogens & help repair tissue.
- Fever is also considered to be a
nonspecific protective response.

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a. Phagocytes
- Pathogens that make it through the
mechanical barriers are confronted by
phagocytes [phago – eat] in nearly
every body organ.
- Such as macrophage or neutrophil,
engulfs a foreign particle, pull it inside
& enclosing it in a vacuole.
- The vacuole is then fused with
enzymatic contents of a lysozome, & its
contents are broken down or digested.

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b. Natural Killer Cells
- Are a unique group of lymphocytes that can
lyse [destruction of cells] & kill cancer
cells & virus-infected cells before the
immune system.
- - They can act spontaneously against any
such target cells by recognizing certain
sugars on the “intruders” surface.

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• NK cells are not phagocytic.
• They attack the target cell membranes &
release lytic chemical called perforins.
• Shortly thereafter, the target cell
membrane & nucleus disintegrate.

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c. Inflammatory Response
- Is a nonspecific response that is
triggered whenever body tissues are
injured.
- Five cardinal signs & major symptoms of
an acute inflammation:
a. Redness
b. Heat
c. Swelling
d. Pain
e. Limitation of joint movement

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Importance of inflammatory response:
1. Prevents the spread of damaging agents to
nearby tissues. [by activating the clotting
proteins & begin to wall off the damaged
area with fibrin]
2. Disposes cell debris & pathogens
[macrophages]
3. Sets the stage for repair. [fibrin mesh also
forms a scaffolding]

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d. Antimicrobial chemicals
- The body’s most important antimicrobial
chemicals, apart from those produced in the
inflammatory reaction, are complement proteins &
interferon.

d.1 Complement
- Refers to the group of at least 20 plasma proteins
that circulate in the blood in an inactive state.
- This complement fixation occurs when complement
proteins to certain sugars or proteins such as
antibodies on the foreign cell’s surface.

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d.2 Interferon
- Proteins formed when cells are exposed to
viral or foreign agents.
- Diffuse to nearby cells & bind to their
membrane receptors thus hinders the ability
of the viruses to multiply within cells.

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e. Fever
- Is a systematic response to invading
microorganisms.
- Speeds up the repair process by
increasing the BMR.

• due to the release of endogenous pyrogens in the

inflammatory site

• endogenous pyrogens come from the injured cells/

materials produced by WBC; components of bacterial
cell wall

• Inflammation maybe acute or chronic

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b. Specific defense system
• More commonly called the “immune system” &
sometimes referred to as the third line of
defense. [when this system is operating
effectively, it protects us from most bacteria,
viruses & transplanted organs]
• Essentially, this system is made up of the bone
marrow, the WBC [produced by the bone
marrow], & the lymphoid tissues.

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 It was shown that animals surviving a
serious bacterial infection have “ factors”
[antibodies] in their blood that protect
them from future attacks by some
pathogen.
 It was demonstrated that if antibody-
containing serum from the surviving
animals [immune serum] was injected into
animals that had not been exposed to the
pathogen, those animals would also be
protected.

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Important aspects of immune system:

1. It is antigen specific
- Recognizes & acts against particular
pathogens & foreign substances.
2. It is systemic
- Not restricted to the initial infection
site.
3. It has memory
- Recognizes & mounts an attack on
previously encountered attacks.

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 But then, in the mid-1900s, it was
discovered that injection of serum
containing antibodies did not always
protect a recipient from diseases
the donor had survived.
 In such cases, however, injection of
the donor’s lymphocytes did provide
immunity.
 2 separate but overlapping arms of
immunity were recognized

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IMMUNITY
Humoral-stimulation of B cells
Triggers the humoral immune response
Causing the synthesis of immunoglobulins
or antibodies that destroy antigen

Ability of body to
protect itself from
foreign material

Cellular-T lymphocytes
Binds with antigen to divide
rapidly to form sensitized cells
then release lymphokines to
attract macrophages
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a. Humoral immunity [antibody-mediated]
- is provided by antibodies present in the
body’s fluids. [B lymphocytes]
b. Cellular immunity [cellular-mediated]
- when the lymphocytes themselves defend
the body. [T lymphocytes]
- cellular targets: virus-infected tissue cells,
cancer cells, & cells of foreign grafts.
- lymphocytes act against antigen either
directly [by lysing the foreign cells] or
indirectly [by releasing chemicals that
enhance the inflammatory response]

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 ANTIGENS
• Is any substance capable of exciting our immune system &
provoking an immune response.
• Most are large, complex molecules that are not normally
present in our bodies.
• As far as our immune system is concerned, they are foreign
intruders or nonself.
• There are variety of substances that act as anitigens such
as: foreign proteins, nucleic acids, large carbohydrates &
even lipids.
• Of these, CHONs are the strongest antigens.
• Pollen grains & microorganisms such as: bacteria, fungi &
virus particles are antigenic because their surfaces bear
such foreign molecules.

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• It is also important to remember that our own cells
are richly studded with a variety of protein
molecules [self-antigens].
• Somehow, as our immune system develops, it takes
an inventory of all these proteins, so that,
thereafter, they are recognized as self. {self-
antigens}
• Although these self-antigens do not trigger an
immune response in us, they are strongly antigenic
to other people.
• This helps explain why our bodies reject cells of
transplanted organs or foreign grafts unless
measures are taken to cripple the immune response.

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 CELLS OF THE IMMUNE SYSTEM:
• The crucial cells of the immune system are:
lymphocytes & macrophages.
• The bone marrow is the production site of the
WBCs involved in immunity.
• Lymphocytes exist in two major “flavors”:
 B lymphocytes [B cells] – produce antibodies &
mature in the bone marrow & then enter the
circulation.
 T lymphocytes [T cells] – are non-antibody-
producing lymphocytes that constitute the cell-
mediated arm of immunity; move from the bone
marrow to the thymus.

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• MACROPHAGES:
 Widely distributed throughout the lymphoid organs.
a. Spleen - curves around left side of the stomach,
filters & cleanses blood of bacteria & viruses. Store
platelets & serve as a blood reservoir. During
hemorrhage, the spleen & the liver contract to
empty the contained blood into the circulation to
help bring the blood volume back to normal levels.
b. thymus gland - low in the throat overlying the heart,
it produces thymosin
c. Tonsils - pharyngeal region; trap & remove bacteria
or other foreign pathogens that enter the throat
d. Payer’s patches – resemble tonsils & found in the
wall of the small intestine.

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 Arise from monocytes formed in the bone
marrow.
 As discussed earlier, the major role of the
macrophage in the nonspecific defense system
is to engulf foreign particles & rid them from
the area.
 But their job doesn’t stop there, they also
present fragments of those antigens on their
own surfaces where they can be recognized by
immunocompetent T cells, thus they act as
antigen presenters in the specific defense
system.

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 WHITE BLOOD CELLS
(5000-10,000 cu mm)
 Mobile defense system that participate in both
the natural & the acquired immune responses.
 Originates in the stem cell of the bone marrow;
when mobilize for action, the body speeds up their
production.
 Leukocytosis – indicates bacterial or viral
infection
 Leukopenia – abnormally low WBC count [steroids,
anticancer]
 Ability to go immediately to the scene of injury
and deal with harmful invading material.
 Has 2 major groups:

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A. Granulocytes
 formed in bone marrow;
attracted to the site during infection
known as chemotaxis
 fight invasion by foreign bodies or
toxins by releasing chemical
mediators (histamine, prostaglandin,
and bradykinin) & engulfing the
foreign bodies or toxins.

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1. PMN’s or neutrophils
[Polymorphonuclear leukocytes]
 Covers 60% of circulating WBC
 First cells to arrive at the site where
inflammation occurs.
 Active phagocytes
 Increases in number rapidly during
short-term infections

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2. Eosinophils

 2-4% of the circulating WBC

 Plays a major role in allergic reaction & stress

responses & infections by parasitic worms by
increasing in number.

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3. Basophils
 1 % of the circulating WBC
 Increases in number during healing phase of
inflammation. [contain histamine, an anti
inflammatory chemical that makes the blood
vessels leaky & attracts other WBCs to the
inflammatory site.]
 Releases HEPARIN (anticoagulant) causes
decrease clumping during inflammation
 Helps maintain proper circulation by
eliminating excess fat particle after
ingesting a high fat meal.
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B. Agranulocytes {Lymphocytes &
Monocytes}

Monocytes
• active phagocytes that become macrophages in
the tissues.
• Long-term clean-up team
• Increase in number during chronic infections
like tuberculosis.

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• To summarize, the immune system is a two-
armed defensive system that uses
lymphocytes, macrophages to identify &
destroy all substances –both living & nonliving-
that are in the body but are not recognized as
being part of the body or as being self.
• The system’s ability to respond such threats
depends on the ability of it cells to:
1. Recognize foreign substances in the body &
binding them.
2. Communicate with one another so that the
system as a whole mounts a response specific
to those antigen.

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 IMMUNE RESPONSE

• When the body is invaded or attacked by

bacteria, viruses or other pathogens. It has three
means of defending itself:
 The phagocytic immune response

 The humoral or antibody immune response

 The cellular immune response

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1. Phagocytic Immune response
 Involves the WBC [granulocytes & macrophages],
which have the ability to ingest foreign particles.
 The cells move to the point of attack, where they
engulf & destroy the invading agents.

2. Humoral Immune response [antibody response]

 Characterized by production of antibodies by the
B lymphocytes in response to specific antigen.
 These antibodies, highly specific proteins, are
transported in the bloodstream & attempt to
disable the invaders.

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ANTIBODY

 Are immunoglobulin, serum agent

that inactivates foreign substance in
the body
 Are protein circulating in plasma
produced in response to the antigen.

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ACTION OF ANTIBODY

 When any immunoglobulin comes in contact with

a specific antigen physical interaction occurs
between the two causing reversible binding of
antibody to the antigen
 When combined with the antigen, it binds with it
like an interlocking piece of jigsaw puzzle.

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Immunoglobulins

IgG

IgE IgA
Ig

IgD IgM

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 CLASSES OF IMMUNIGLOBULIN
( ACCORDING TO STRUCTURE AND FUNCTION)

1. Ig G or gammaglobulin
 major Ab, compromises 75% to 85% of Ig
fraction
 present in extra-vascular fluids and serum
 has the ability to leave the blood stream and
seek out the tissues for infectious agents
 crosses the placenta to provide the infant
with normal passive immunity
 has a major role in the blood – borne and
tissue infection
 enhances phagocytosis

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2. Ig M
- compromises 7% to 10% of Ig fraction
- known as “MACROGLOBULIN” because it is
confined primarily to the intravascular fluid
- effective against gram (-) bacteria because it is
big
- powerful agglutinating agent
- first Ab produced in response to bacterial and
viral infection
- responsible for certain immune complex
hypersensitivity and auto-immune diseases like
Rheumatoid Arthritis

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3. Ig A
 compromises 10% - 15% of Ig
fraction
 called “SECRETORY Ig” because it is
predominantly found in the body fluids
and exocrine secretions like breast
milk, saliva, tears, mucus, blood, GIT,
GUT, RT, prostatic and vaginal
secretions.
 Prevents absorption of antigens from
food.

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4. Ig D

 0.2% to 1% of Ig of fraction

 role is unclear; probably plays a role in

activation and suppression of
lymphocyte function

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5. Ig E

 0.002% of Ig fraction
 seen in trace amount of blood;
triggers release of chemical
mediators
 attached to mast cell and basophils
 mediates the severe and
occasionally fatal anaphylactic shock
or hypersensitivities
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 TYPES OF ANTIGEN AND ANTIBODY
REACTION
1. AGGLUTINATION

- Ig disarms the Ag causing it to clump

together or stick together

- produced result is visible to the naked

eye; can be used as the basis for
laboratory test to detect presence of
Ab in the Ag.
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2. OPSONIZATION

- coats the microbes or bacteria

making it susceptible for
phagocytosis by neutrophils and
macrophages

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3. NEUTRALIZATION

- Ab combines with exotoxins (toxic

chemicals secreted by the bacteria)
released by infectious agents
neutralizing their effects

- phagocytosis engulf the complex

and removes it from the blood and
tissues
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4. PRECIPITATION
- Ab which reacts with soluble Ag
resulting into a visible mass
formation causing it to settle down
making it easy for phagocytosis

5. LYSIS
- Ab attacks cell membrane causing
cell rupture or Ab which causes the
bacteria to dissolve/liquefy
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3. Cellular immune response [cell-mediated response]
• It is the T lymphocytes that are primarily
responsible for cellular immunity.
• They spend time in the thymus, where they are
programmed to become T cells.
• major categories of T cells:
a. Helper T cells
• Act as the “directors” or “managers” of the
immune system.
• Once activated, they circulate through the body,
recruiting the other cells to fight the invaders.

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• They also release a variety of cytokine chemicals
called lymphokines, that act directly to rid the
body of antigens by:
a. Stimulating cytotoxic T cells & B cells to grow &
divide.
b. Attracting other types of protective WBC, such
as neutrophils, into the area.
c. Enhancing the ability of macrophages to engulf &
destroy microorganisms.

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b. Cytotoxic (killer) T cells
• Specialized in killing virus-infected,
cancer or foreign graft cells
• by binding to them & inserting a toxic
chemical perforins & cytokines into the
foreign cell’s plasma membrane [delivering
the so called kiss of death].
• Shortly, thereafter, the target cells
ruptures.

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c. Suppressor T cells
• Releases chemicals that suppress the activity of
both T & B cells after an antigen has been
successfully inactivated.
• Thereby, keeping the immune response at a level
that is compatible with health.
• Eg. Sufficient to fight infection adequately,
without attacking the body’s healthy tissues.
d. Memory cells
• Provide the immunological memory for each
antigen encountered & enable the body to
respond quickly to its subsequent invasion or
when meeting the same antigen.

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Stages of immune response:
1. Recognition Stage
- The initiating event wherein the immune system recognize antigens
as foreign, or non self.
- Body accomplishes recognition using lymph nodes and lymphocytes
surveillance.
- When foreign materials enter the body, a circulating lymphocyte
comes into physical contact with this materials.
- Lymphocytes with the help of macrophages either remove the
antigen or in some ways picks up an imprint of its structure.
- Eg. In strep throat infection, strep organism gains access to the
mucous membranes of the throat. A circulating lymphocyte,
familiar with the surface markers on the cells of its own body,
recognizes the strep as antigenic. This triggers the 2nd stage of
the immune response.

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2. Proliferation stage
- Circulating lymphocytes containing the antigenic message turn to
the nearest lymph node.
- Once in the node the sensitized lymphocyte stimulates some of
the resident dormant T & B lymphocytes to enlarge, divide and
proliferate
- T lymphocytes differentiate into killer cells & the B
lymphocytes produce & release antibodies. [eg. Enlargement of
the lymph nodes in conjunction with sore throat]
3. Response stage
- Changed lymphocytes function either in a humoral or cellular
fashion.
- Increases the number of T lymphocytes.
4. Effector stage
- Either the antibody of the humoral response or the T cell of
cellular response reaches and couples with the antigen on the
surface of the foreign invader
- Coupling initiates a series of events that in most instances
results in the total destruction of the invading microbes or the
complete neutralization of the toxin.

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 IMMUNITY
– When the B cells encounter antigens &
produces antibodies against them, the
body is exhibiting:
 ACTIVE IMMUNITY
a. Naturally acquired – during bacterial &
viral infections, during which, we may
develop the symptoms of the disease
& suffer a little or more.
b. Artificially acquired – when we receive
vaccines.

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 PASSIVE IMMUNITY
- Is quite different from acquired immunity, both in
antibody source & in the degree of protection it
provides.
- Instead of being made by the plasma cells, the
antibodies are obtained from the serum of an immune
human or animal donor.
- As a result, B cells are not challenged by the antigen, the
temporary protection provided by the borrowed
antibodies ends when they naturally degrade in the body.
a. Natural – on a fetus when the mother’s antibodies cross
the placenta & enter the fetal circulation & after birth
during BF.

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b. Artificial
- When one receives immune serum or gamma
globulin.
- Gamma globulin is commonly administered after
exposure to hepatitis.
- Other immune sera are used to treat poisonous
snake bites [antivenom], rabies & tetanus
[antitoxin] because these diseases will kill a
person before active immunity can be established.
- The donated antibodies provide immediate
protection, but their effect is short-lived [2-3
wks].
- However, the body’s own defenses take over.

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IMMUNIZATION
- the process of rendering organisms immune to
effects of harmful substance
POINTERS
1. Every child desires to be given benefits of
current available and recommended immunization
2. It must go hand in hand with hygienic and other
measures for due prevention
3. Recommended series of immunization should be
completed for adequate protection
4. Booster or recalled doses should be
administered for continuous protection
5. Occasional reactions be known to parents and
instruction given accordingly

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6. Immunization deferred if child is very ill, very weak,
severely malnourished, premature, convalescing
7. Don’t wait for epidemic to occur to decide giving
immunization
8. Defer active immunization for children receiving
immunosupressive treatment (corticosteroids, anti-
metabolites, cobalt therapy)
9. Vaccination with attenuated live vaccines is to be
avoided among pregnant women and those who may get
pregnant with in the next 3 months (measles, mumps,
BCG’s, small pox, German measles)
10. In case of small pox vaccination, don’t vaccinate when
there are SKIN LESIONS and during warm weather
when prickly heat is common

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5 IMMUNOLOGIC AGENTS
- considered artificial
1. ANTITOXIN
- TAT
2. ANTISERUM
- gives allergic reaction after minutes
- E.g ATS
3. GAMMAGLOBULIN
- HTIG, RABUMAN
4. TOXOIDS
-composed of altered forms of toxin produced by
microorganisms
- DPT, TT
5. VACCINES
- substance that contain Ag to which immune
system responds 69
A) Killed/Attenuated
- weakened dead organism or part of
the organism is killed
- modified and rendered non-virulent
- Pertussis, typhoid, influenza, cholera,
poliomyelitis. Administered IM
B) Live
- provides excellent protection but
some substances exist because of
possibility of reversion to virulent (able to
cause diseases)
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 CATEGORIES OF
IMMUNOLOGIC DISORDERS

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 I. IMMUNODEFICIENCY

A. PRIMARY IMMUNODEFICIENCES:
- Rare disorders with genetic origins, are seen
primarily in infants & young children.
- Symptoms usually develop early in life after
protection from the maternal antibodies
decreases.
- These disorders may involve one or more
components of the immune system
- Symptoms of immune deficiency diseases are
related to the role that the deficient component
normally plays.

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10 warning signs:
1. Eight or more new ear infections within one year
2. Two or more serious sinus infections within one
year
3. Two or more months on antibiotics with little
effects
4. Two or more pneumonias within one year
5. Failure of an infant to gain weight or grow
normally
6. Recurrent, deep skin infection or organ
abscesses
7. Persistent thrush in mouth or elsewhere on skin,
after age 1
8. Need for intravenous antibiotics to clear
infections
9. Two or more deep seated infections such as
meningitis, osteomyelitis, cellulitis, sepsis
10. A family history of primary immune deficiency
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 A.1) PHAGOCYTIC DEFECT
- Are manifested by an increased incidence of
opportunistic bacterial & fungal infections.
Disorder: Hyperimmunoglobulinemia E [HIE]
- White blood cells are unable to produce an
inflammatory response to the skin infections.
Major symptoms:
 Bacterial infections - bronchitis,
 Viral infections - herpes simplex & herpes zoster
 Fungal infection – Candida organisms
 Deep seated cold abscesses

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MEDICAL MANAGEMENT:
1. Treating bacterial infections with
prophylactic antibiotic therapy.
2. Granulocyte-macrophage colony-
stimulating factor [GM-CSF]
- these proteins draw non-lymphoid
stem cells from the bone marrow &
hasten their maturation.

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A.2) B-CELL DEFICIENCIES:
2 TYPES:
1. AGAMMAGLOBULINEMIA [BRUTON’S
DISEASE]
 All antibodies disappear from the patient’s
plasma.
 Results from lack of differentiation of B-
cell precursors into mature B cells.
 As a result, plasma cells are lacking, leading
to a complete lack of antibody production
against invading bacteria, viruses & other
pathogens.

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2. HYPOGAMMAGLOBULINEMIA
 Results from lack of differentiation of B
cells into plasma cells.
 Only diminished antibody production
occurs with this disorder.
 Affected individuals still have normal
lymph follicles & many lymphocytes that
produces some antibodies.
 Also called Common Variable
Immunodeficiency [CVI]

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CLINICAL MANIFESTATIONS:
1. Pernicious anemia
2. Lymphoid hyperplasia of the small intestine
& spleen & gastric atrophy – biopsy
3. Severe infections soon after birth –major
symptom [susceptible to infection caused
by Haemophilus influenza, streptococcus
pneumoniae, Staphylococcus aureus]
4. Bronchiectasis & pulmonary failure [caused
by frequent respiratory tract infections]

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ASSESSMENT/DIAGNOSTIC FINDINGS:
1. History of bacterial infection
2. Antibody titer – to know the functioning
status of the B cells earlier in life.
3. Hemoglobin & hematocrit – anemia
4. Measurement of the number of B
lymphocytes

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MEDICAL MANAGEMENT:
1. Replacement therapy with intravenous
gammaglobulin.
- Those who are receiving adequate
gammaglobulin IV usually do not require
prophylactic antibiotic unless they also
have chronic respiratory disease.
2. Vitamin B12 parenteral injection at
monthly intervals.

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A.3) T-CELL DEFICIENCES
 DiGeorge’s syndrome or thymic hypoplasia
 Occurs when the thymus gland fails to
develop normally during embryogenesis.
 Chronic mucocutaneous candidiasis
 A disorder associated with a selective
defect in T-cell immunity thought to be
caused by an autosomal recessive
inheritance.

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CLINICAL MANIFESTATIONS:
1. Hypoparathyroidism with hypocalcemia
- resistant to standard therapy
2. Tetany; convulsions
3. Congenital heart disease
4. Possible renal abnormalities

MEDICAL MANAGEMENT:
1. Thymus graft

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A.4) COMBINED B-CELL & T-CELL
DEFICIENCIES:
1. ATAXIA-TELANGIECTASIA
 is an autosomal recessive disorder affecting
both T & B-cell immunity.
 40% of the patients have selective IgA
deficiency.
 Involves the neurologic, vascular, endocrine &
immune systems.
 S/S : ataxia [uncoordinated muscle movement]
with progressive neurologic deterioration;
telangiectasia [vascular lesions caused by
dilated blood vessels]

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• Many patients, however remain symptom
free for 10 years or longer.
• 2nd decade of life – morbidity with chronic
lung disease, mental retardation,
neurologic symptoms & physical disability
becomes severe.
• The primary cause of death of these
patients are overwhelming infection &
epithelial cancer.

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2. SEVERE COMBINED IMMUNODEFICIENCY
DISEASE [SCID]
 both B & T cells are missing resulting to a
complete absence of humoral as well as cellular
immunity caused by an X-linked or autosomal
genetic abnormality.
 S/S: overwhelming severe fatal infections soon
after birth.

3. WISCOTT-ALDRICH SYNDROME
 A variation of SCID compounded by
thrombocytopenia [loss of platelets]
 Prognosis: poor – overwhelming infections

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MEDICAL MANAGEMENT:
1. Early management of infections
2. Postural drainage & chest therapy –
chronic lung disease
3. Transplantation of fetal thymus
4. IV gamma-globulin
SCID:
1. Bone marrow transplantation
2. Thymus gland transplantation
3. IV immunoglobulin

86
B. SECONDARY IMMUNODEFICIENCIES:
 More common than primary
 AIDS is the most common disorder under
this category.
 Patients with immunodeficiencies have
immunosuppression & are often referred
to as immunocompromised host

87
 AIDS
• Acquired immune deficiency syndrome, is a
disease that slowly and steadily destroys the
immune system.
• It is caused by HIV [human immunodeficiency
virus], a virus which wipes out certain types of
lymphocytes called T-helper cells.
• Without T-helper cells, the immune system is
unable to defend the body against normally
harmless organisms, which can cause life-
threatening infections in people who have AIDS.
• HIV belongs to retroviruses
• HIV is transmitted by way of body fluids like
serum, seminal fluid, vaginal secretions, amniotic
fluid & breast milk.
88
RISK FACTORS:
1. Unsafe sexual practices
2. Prostitution & multiple sexual partners
3. Exposure to contaminated blood & contaminated
needles
4. Occupational exposures
5. Perinatal exposure – exposure can occur during
pregnancy, during vaginal delivery, through
breastfeeding.
6. Genital lesions associated with STDs
7. Unprotected anal intercourse – male homosexuals
– increases the risk for trauma to the rectal
mucosa.

89
CLINICAL MANIFESTATIONS:
- Are widespread & may affect virtually any
organ system.
1. Respiratory manifestations:
a. SOB, dyspnea, cough, chest pain & fever
– often associated with opportunistic
infections.
- the most common infection in people with
AIDS is Pneumocystitis carinii pneumonia
[PCP]

90
• PCP is the initial manifestation of AIDS in
60% of patients.
• P. carinii was originally classified as a
protozoan; however, studies & analysis of
its ribosomal RNA structure suggest that
it is a fungus.
• PCP causes disease only in
immunocompromised host invading &
proliferating within the pulmonary alveoli.
• Untreated PCP eventually progresses &
causes significant pulmonary impairment &
ultimately respiratory failure.

91
Mycobacterium avium complex [MAC]
- another opportunistic bacterial infection
common in patients with AIDS.
Mycobacterium tuberculosis
- tends to occur early in the course of HIV
infection, usually preceding diagnosis of AIDS.
2. Gastrointestinal manifestations:
- loss of appetite, nausea & vomiting
- oral & esophageal candidiasis
- chronic diarrhea [50-90%, direct effect of
HIV on the cells lining the intestines.

92
• Anorexia, diarrhea & GI malabsorption & lack
of nutrition in chronic disease all contribute to
wasting syndrome.
• Wasting syndrome is believed to be caused by
Tumor necrosis factor [TNF] & interleukin-1,
[cytokines] which act directly on the
hypothalamus to cause anorexia.
• TNF causes inefficient use if lipids by reducing
enzymes that are needed for fat metabolism.
• People with AIDS generally experienced
increased protein metabolism in relation to fat
metabolism, which results in significant
decreases in lean body mass.

93
- Effects of diarrhea: profound weight
loss [10%]; F/E imbalance; perianal
excoriation; weakness; inability to
perform the usual ADL.

Oral Candidiasis
- Another infection [fungal] that is
characterized by creamy-white patches
in the oral cavity.
- Untreated, this will progress to involve
the esophagus & stomach.

94
3. Oncologic Manifestations
- Higher than usual incidence
- R/t HIV stimulation of developing cancer cells
or to the immune deficiency allowing cancer-
causing substances, such as viruses to
transform susceptible cells to malignant cells.
- Carcinomas: skin, stomach, pancreas, rectum
& bladder [common]
a. Kaposi’s sarcoma
- most common HIV-related malignancy, is a
disease involving the endothelial layer of the
blood & lymphatic vessels.

95
• 3 kinds: classic, acquired & epidemic
• AIDS – epidemic
• Characterized by cutaneous lesions appearing
anywhere on the body that are usually brownish
pink to deep purple.
• May be flat or raised & surrounded by
ecchymoses [hemorrhagic patches] & edema.
• Rapid development of lesions involving large
areas of skin are associated with extensive
disfigurement.
• Ulcerative lesions disrupt skin integrity &
increases the patient’s discomfort &
susceptibility to infection.

96
b. B-cell lymphomas
• 2nd most common malignancy
• Non-hodgkin’s lymphoma which differ from those
occurring in the general population.
• Develop outside the lymph nodes, most commonly
in the brain, bone marrow, & GIT
• These type of lymphomas are characteristically
of a higher grade, indicating aggressive growth &
resistance to treatment.
• Not responsive to chemotherapy because of the
severe hematologic toxicity & complications of
opportunistic infections that occur from the
treatment.

97
4. Neurologic mainfestations
• Results from the direct effects of HIV on
NS tissue.
• Immune responses to HIV infection in the
CNS: inflammation, atrophy, demyelination,
degeneration & necrosis.
a. HIV Encephalopathy
• AIDS dementia complex [ADC]
• Characterized by progressive decline in
cognitive, behavioral & motor functions.
• Substantial evidence exists that ADC is s
direct result of HIV infection.

98
• HIV has been found in the brain & CSF of
patients with ADC.
• HIV infection is thought to trigger the
release of toxins or lymphokines that
result in cellular dysfunction or interfere
with the neurotransmitter function rather
than cellular damage.
• S/S: memory deficits, headache, difficulty
with concentration, progressive confusion,
apathy & ataxia.

99
b. Cryptococcus neoformans [fungal]
• 4th most common opportunistic infection
among patients with AIDS & the third
most common infectious agent causing
neurologic disease.
• Characterized by fever, headache, malaise,
stiff neck, nausea, vomiting, mental status
changes & seizures.
• Diagnosis is confirmed by CSF analysis.

100
c. Toxoplasma gondii
• 5th opportunistic infection affecting AIDS
patient.

5. Manifestations specific to women

a. Recurrent vaginal candidiasis [1st sign]
b. Recurrent genital ulcer disease & venereal
warts [past genital ulcer is a risk factor
for the transmission of the disease.]
c. Human papillomavirus [HPV]
- causes venereal warts & a risk factor for
Cervical intraepithelial neoplasia [CIN]

101
• CIN is a cellular change that is frequently
a precursor to cervical cancer.

d. Pelvic inflammatory disease [PID]

e. Menstrual abnormalities – bleeding
between periods; amennorhea

102
LABORATORY TESTS:
- Before an HIV test is performed, the
meaning of the test & possible test
results are explained, & informed
consent be obtained from the patient.
- All of the result of the tests are kept
confidential.
a. HIV antibody test:
- When an individual is infected with HIV,
the immune system responds by
producing against the virus.

103
• Antibodies generally develop within 3-12
weeks of exposure but may take as long as
6-14 months.
• Thus, a person may be infected but not
test positive initially.
• Unfortunately, the antibodies for HIV are
ineffective & unable to halt the
development of HIV infection.
• 3 tests are used to confirm the presence
of antibody to HIV & to assist in
diagnosing HIV infection

104
a.1 Enzyme-linked immunoabsorbent assay
[ELISA]
• Identifies antibodies directed specifically
against HIV.
• Does not establish the diagnosis of AIDS
• It only indicates that a person has been
exposed to or infected with HIV.
• People whose blood contains antibodies for
HIV are said to be seropositive.

105
• IMPLICATIONS: SEROPOSITVE
1. Antibodies to HIV are present in the blood [the
patient has been infected with virus, & the body
has produced antibodies]
2. HIV is probably active in the body, & the
patient should assume that he or she can
transmit the virus to others.
3. Despite HIV infection, the patient does not
necessarily have AIDS.
4. The patient is not immune to AIDS [the
antibodies do not indicate immunity]

106
a.2 Western Blot Assay
• Identifies HIV antibodies & used to
confirm seropositivity as identified by
ELISA.
• Indirect Immunofluorescence assay [IFA]
are being used by the physicians instead of
western blot because it is rapid, easy to
perform, & requires minimal skill.
a.3 Radio-immunoprecipitation assay [RIPA]
• Detects HIV protein rather than antibody.

107
MEDICAL MANAGEMENT:
- Encompasses several approaches:
1. Antiretroviral therapy [viral suppression]
a. Zidovudine [AZT/ZDV]
- Prevents HIV reproduction bi mimicking
one of the molecular substances used by
HIV to build DNA for new virus particles.
b. Ritonavir [Norvir]
c. Nelfinavir – to reduce HIV counts

108
2. Medications for HIV –related infections
a. Bactrim/Septra – general infections
b. Pentamidine
– an antiprotozoan agent for PCP
- not given IM or IV
c. Azithromycin/ Ethambutol/ Ciprofloxacin
- Mycobacterium avium complex
d. Amphotericin B + oral Diflucan
- Cryptococcal meningitis

109
NURSING PROBLEMS:
1. Impaired skin integrity related to
cutaneous manifestations of HIV
infection, excoriation & diarrhea.
2. Diarrhea related to enteric pathogens or
HIV infection.
3. Activity intolerance related to weakness,
fatigue, malnutrition.
4. Ineffective airway clearance related to
PCP, increased bronchial secretions &
decreased ability to cough related to
weakness & fatigue.

110
5. Pain related to impaired perianal skin
integrity related to diarrhea
6. Social isolation related to stigma of the
disease, withdrawal of support system &
fear of infecting others.
7. Knowledge deficit related to HIV
infection, means of preventing HIV
transmission.

111
NURSING MANAGEMENT:
1. Promote skin integrity
• Assess the skin & oral mucosa for changes in
appearance, location & size of lesions.
• Encouraged to maintain balance between rest &
mobility.
• Change position every 2 hours.
• Avoid scratching, use of nonabrasive, nondrying
soaps & to apply nonperfumed skin moisturizers
to dry skin surfaces.
• Regular oral care.
• Keep the bed linens free from wrinkles & avoid
tight & restrictive clothing.

112
• Keep the perianal region clean & dry.
• Wounds are cultured if infection is suspected, so
that appropriate antimicrobial treatment can be
initiated.

2. Promote usual bowel habits.

• Monitor the frequency & consistency of the
stools & report abdominal pain or cramping.
• Stool cultures are obtained to identify pathogenic
organisms.
• Bowel irritants should be avoided like raw fruits &
vegetables, carbonated beverages & spicy foods.

113
• Encouraged small, frequent feeding to prevent
abdominal distention.
• Antidiarrheal & antispasmodics as ordered.

3. Improve activity intolerance:

• Monitor the patient’s ability to ambulate &
perform activities of daily living.
• Health teachings on energy conservation
techniques, such as sitting while washing or
preparing food.
• Keep personal items that are frequently used
within the patient’s reach.

114
4. Maintain thought processes:
• Use simple, clear language & give the
patient sufficient time to respond to
questions.
• Instruct the significant others to orient
the patient to the daily routine by talking
about what is taking place during daily
activities.
• Post schedule in a prominent area,
providing nightlights for the patient’s
bedroom & bathroom.
• Encouraged activities that the patient
previously enjoyed.
115
5. Improve airway clearance:
• Assess for the rate, rhythm, use of accessory
muscles & breath sounds.
• Sputum specimens should be analyzed for
infectious organisms.
• Provide pulmonary therapy [coughing, DBE] as
often as every 2 hours to prevent stasis of
secretions & to promote airway clearance.
• Position the patient properly to facilitate
breathing & airway clearance.
• Encouraged oral fluid intake unless
contraindicated.

116
6. Improve nutritional status
• Monitor weight, dietary intake &
anthropometric measurements.
• Assess for factors that interfere with oral
intake, such as anorexia, oral & esophageal
candidal infection, nausea, pain.
• Encourage to have rest before meals.
• Avoid foods that stimulate intestinal motility
& abdominal distention for patients with
diarrhea.
• Encourage to eat foods that are easy to
swallow.

117
 AUTOIMMUNE DEFICIENT
• When the immune system fail to
recognize the body’s normal tissue as
self.
• Basically, these self-killing cells begin
to break down normal cells.

I. RHEUMATOID ARTHRITIS
• The autoimmune reaction primarily
occurs in the synovial tissue.
• Phagocytosis produces enzymes within
the joint.
118
• The enzymes break down collagen, causing
edema, proliferation of the synovial
membrane & ultimately pannus formation.
[proliferation of newly formed synovial
tissue infiltrated with inflammatory cells]
• The pannus destroys cartilage & erodes
the bone, leading to loss of articular
surfaces & joint motion, degeneration of
the muscle fibers & loss of muscle
contractility & elasticity.

119
CLINICAL MANIFESTATIONS:
1. Synovitis [inflammation of the synovial
capsule causing escape of synovial fluid into
the synovial capsule]
• Begins when the antigen activates monocytes
& T cells, leading to the formation of immune
complexes by the immunoglobulin antibodies.
• Phagocytosis of the immune complexes is
initiated, generating an inflammatory
reaction. [joint swelling, pain & edema]
2. Joint stiffness especially in the morning,
lasting for more than 30 minutes.

120
3. Limitation of the function can occur when there is
active inflammation in the joints.
4. Immobility – since the joint is swollen, painful, the
patient tends to guard or protect these joints.
5. Contractures
6. Soft tissue deformity – caused by misalignment
resulting from swelling & progressive joint
destruction
7. Systemic – fever, weight loss, fatigue, lymph node
enlargement
8. Raynaud’s phenomenon [cold & stress induced
vasospasm causing cyanosis]

121
DIAGNOSTIC FINDINGS:
1. Increased Erythrocyte sedimentation rate [ESR] –
reflects inflammatory activity
2. Arthrocentesis [needle aspiration of synovial fluid]
• Done not only for analysis but also to relieve pain. [knee &
shoulder]
• Synovial fluid is analyzed for the presence of
inflammatory cells & blood.
• Done aseptically by inserting a large bore needle into the
joint space.
• After the procedure, the patient is observed for signs of
infection & hemarthrosis.

122
• Normally, synovial fluid is clear, viscous,
straw-colored & scanty in volume with few
cells.
• RA – cloudy, milky, or dark yellow &
contains numerous inflammatory cells.

3. X-ray Studies
• Severe joint degeneration
• Bony erosion
• Narrowed joint spaces

123
2. Control pain
• Ease pain with splints, relaxation
techniques.
3. Maintain & improve joint mobility
• Implement exercise programs for joint
motion & muscle strengthening
4. Maintain or improve functional status
• Make use of adaptive devices & techniques
5. Promote self-management by patient
compatible with the therapeutic regimen

124
GOALS & STRATEGIES:
1. Suppress inflammation & the autoimmune
response
• Administer medications
a. Salicylates – Aspirin
b. NSAIDs – Diclofenac, Ketoprofen,
Naproxen, Orudis
c. Disease-modifying antirheumatic drugs
- Chloroquine
- Methotrexate [inhibits T cell function]

125
NURSING DIAGNOSIS:
1. Pain related to inflammation, tissue
damage, fatigue.
2. Impaired physical mobility related to
decreased range of motion, muscle
weakness, pain on movement.
3. Self-care deficits related to
contractures, fatigue, or loss of motion.
4. Body image disturbance related to
physical changes.

126
NURSING MANAGEMENT:
1. Promote comfort & alleviate pain.
• Massage, changing of positions regularly.
• Heat application – to relieve stiffness & muscle
spasm. Evaluated properly especially in patients
with impaired sensation.
• Weight reduction – to relieve stress on painful
joints.
• Use of assistive devices such as canes, crutches
& walkers – eases pain by limiting movement or
stress from weight bearing on painful joints.
• Use of energy conservation techniques.

127
2. Allow ample time for activity.
3. Provide rest period after activity.
4. A pillow should not be placed under the
knee when the patient is assuming supine
position – promotes flexion contracture
5. Assist in doing the activities of daily
living.
6. Provide a safe environment.

128
 SYSTEMIC LUPUS ERYTHEMATOSUS

• Is a result of disturbed immune regulation

that causes an exaggerated production of
autoantibodies.
• The increased autoantibody production is
thought to result from abnormal
suppressor T-cell function & hyperactivity
of B cells leading immune complex
deposition & tissue damage.
• Inflammation stimulates antigen which, in
turn, stimulate additional antibodies & the
cycle repeats.

129
RISK FACTORS:
1. Genetic
2. Hormonal – as evidence by the usual
onset during the childbearing years
3. Environmental factors – sunlight, thermal
burns
4. Medications – Apresoline, isoniazid,
anticonvulsants

130
CLINICAL MANIFESTATIONS:
- The onset may be insidious or acute.
- So the patient may remain undiagnosed for
many years.
- Clinical features involve multiple body
systems.
a. Musculoskeletal:
- Arthralgias
- Synovitis
- Joint swelling & pain on movement
- Morning stiffness

131
b. Skin manifestations:
• Butterfly shaped-rash across the bridge of the
nose & the cheeks.
• Papular, erythematous & purpuric lesions [vascular
involvement] on the extremities
purpura – extravasation of blood in the skin & mucous
membrane causing purple spots.
• Oral ulcers may accompany skin lesions
c. Cardiopulmonary:
• Pericarditis – inflammation of the pericardium
[30%]
• Pleural effusion
• Pleuritis

132
d. Renal manifestations:
• Glomerulonephritis – common site of antibody
complex deposition. [common cause of death]
• Renal failure

e. Others
• Lethargy; malaise; fever
• Loss of weight
 SLE is often called the great imitator & can
be confused with RA because of symmetrical
joint involvement.

133
DIAGNOSTIC FINDINGS:
• No single laboratory test confirms SLE.
• SLE should be suspected in patients with
glomerulonephritis & characteristic skin
rashes.
a. Severe anemia
b. Thrombocytopenia – decreased number of
platelets
c. Leukopenia
d. Positive antinuclear antibodies [ANA]
e. Hematuria

134
PHARMACOLOGIC THERAPY:
• Based on the concept that local tissue
inflammation is mediated by exaggerated or
heightened immune responses
a. NSAIDs are used for minor symptoms in an
effort to minimize corticosteroid
requirements.
b. Corticosteriod – single most important
• Used topically for cutaneous [skin]
manifestations
c. Immunosuppressive agents [serious forms &
unresponsive to conservative therapies]

135
NURSING MANAGEMENT:
• Patient education is of prime importance
throughout the disease process:
1. Appropriate skin care
2. Adequate nutritional intake
3. Minimizing the risk of opportunistic
infections.
4. Avoid sun exposure – UV rays exacerbate
the disease

136