INFLAMMATORY and IMMUNOLOGIC DISTURBANCES
IMMUNITY – is the body’s specific protective
response to an invading foreign agent or organism;
ability of the body to fight or conquer infection.
IMMUNOPATHOLOGY- the study of diseases that
result from dysfunction of the immune system
IMMUNE SYSTEM
Function:
1. defense against physical injury and
infection
2. maintenance of homeostasis, a state of
equilibrium of the internal environment
ORGANS and tissues of the immune system
Bone marrow – production site of RBC,s WBC,s and
platelets. It’s primary function is hematopoiesis
(formation of blood cells)
Thymus – is a single unpaired gland that is located
in the mediastinum and is the primary gland of the
lymphatic system. Its primary function is allowing
the T lymphocytes to develop before migrating to
the lymph nodes and the spleen.
Lymph nodes and vessels perform several
important functions such as: transporting lymph,
filtering and phagocytizing antigens, generating
monocytes and lymphocytes.
Spleen functions include: a. Removing worn out
erythrocytes from blood, b. Storing blood and
platelets
c. Filtering and purifying blood.
Tonsils, adenoids and other mucoid lymphatic
tissues defend the body against microorganisms.
Hematopoietic system(bone marrow)
Central and Peripheral Lymphoid Organs
CLASSIFICATIONOF IMMUNITY
I. SPECIFIC IMMUNITY
A. HUMORAL IMMUNITY – characterized by
production of antibodies by the B lymphocytes in
response to a specific antigen.
Antibodies – are large proteins called
immunoglobulins found in the globulin fraction of
the plasma proteins.
IgG – 75% of total Ig in the body
 - source: interstitial fluids( serum & : passes to neonate thru breastmilk

tissues)

IgM : 10%

IgG – Function: assumes major role in blood- Source: Intravascular

borne infections Function: appears as the first Ig

produced in response to bacterial and viral infections
: activates complement system
: activates complement
: enhances phagocytosis system

: crosses placenta IgD : 0.2%

IgA - 15% Source: serum in small amount

- Source: blood, saliva, tears , Function: influences B-lymphocytes

breastmilk,
but role is unclear
prostatic, gastrointestinal and resp.
IgE : 0.004%
secretions.
Source: Serum
- Function: protects against GI, GU,
and Function: allergic and hypersensitivity
reactions
respiratory infections.
: combats parasitic infections
: prevents absorption of antigen
from food ANTIGEN-ANTIBODY REACTION
Agglutination – antibodies disarmed antigens by
causing them to clamp together
Precipitation – this reaction occurs when antibody
reacts with a soluble antigen resulting in an insoluble
complex which then precipitates.
Neutralization – this occurs when antibody combines
with toxins produced by some infectious agents to
render them inactive and easier to engulfed and
removed from the body.
Lysis – this is when antibody attacks cell membrane
causing microorganisms to rupture.
Opsonization – in this process, the antigen-antibody
molecule is coated with a sticky substance that also
facilitates phagocytosis.
B. CELLULAR IMMUNITY – T- lymphocytes are
responsible for cellular immunity. These lymphocytes
spend time in the thymus, wherein they are
programmed to become T-cells.
2 major categories of T cells
a. Helper T cells – are activated upon
recognition of antigens and stimulate the rest of the
immune system.
b. Cytotoxic T cells – (Killer T cells) attack the
antigen directly by altering the cell membrane and
causing cell lysis(disintegration) and releasing
cytolytic enzymes and cytokines.
II. NON-SPECIFIC IMMUNITY
Defenses of the body non selectively directed
to foreign substances.
1. Structural – certain specialized structures in
the body that protect human from microorganisms.
EX. Skin, eyebrow, eyelashes
2. Mechanical – mechanical processes in the
body protects it from foreign bodies. EX. Peristaltic
activity, vomiting, diarrhea, tear flow
3. Chemical – certain chemicals in the body fights
microorganisms. Ex. urine, vaginal secretions,
perspiration
4. Biologic – these are bacteria that are
considered normal flora and are essential for body
processes.
5. Inflammatory Response – considered as one of
the major function of the non-specific immune
system. It is the defensive reaction of the body
intended to neutralize, control or eliminate the
offending agent to prepare the site for repair.
 transient vasoconstriction that follows injury
INFLAMMATION

- a biochemical and cellular process that Swelling – results when vascular permeability
occurs in vascularized tissues increases, and plasma leaked into the inflamed
tissues.
- most of the essential components of the
inflammatory process are found in the vascularized
circulation, and most of the early
mediators(facilitators) of inflammation increase the Pain – results when the pressure of fluids or
movement of plasma and blood cells from the sealing on nerve endings, and to the irritation of the
circulation into the tissues surrounding the injury nerve endings in chemical mediators released at the
called as the exudates which defends the host site
against infection and facilitate tissue repair and
healing.

Loss of function – related to pain and swelling

CARDINAL SIGNS OF INFLAMMATION

Loss of function happened when:

Redness (Rubor) Vascular response – transient vasoconstriction followed by

vasodilation, causing influx of blood to the inflamed area. These
Heat (Calor) fluid pushed into the surrounding sites of injury would
consequently become inflammatory exudates which has the
Swelling (Tumor) following functions as:

Pain (Dolor) - dilute toxins released by the bacteria

Loss of function (Laesa) - bring to site certain nutrients necessary for

tissue repair

Redness and heat – results when vasodilation occurs after - carry protective cell that would destroy bacteria

2. Cellular response as follows:
a. Margination – also known as pavementing
occurs when leucocytes stick to the walls of the
blood vessels.
b. Emigration – occurs when leococytes
multiply and travel to the areas of injury
c. Chemotaxis – is the directional orientation
of leucocytes
d. Phagocytosis – process where bacteria are
engulfed or ingested.
3. Chemical response includes the release of
the following chemicals.
a. Histamine – initiates vascular response by
increasing vascular dilation and permeability
b. Bradykinin – increases vascular
permeability
c. Prostaglandin – also increases vascular
permeability.
4. Fibrin-Barrier Response fibrin forms wall
on the inflamed area to prevent invasion of irritants
to other tissues. This phenomenon is also known as
a “Wall-Off”.
HUMORAL IMMUNITY
- one of the two forms of immunity that
respond to bacteria and other foreign antigens. It is
mediated by circulating antibodies(immunoglobulins
IgA, IgB and IgM), which coat the antigens and
target them for destruction by polymorphonuclear
neutrophils.
CELLULAR IMMUNITY
- the mechanism of acquired immunity
characterized by the dominant role of T-cell
lymphocytes
- is involved in resistance to infectious disease
caused by viruses and some bacteria and is delayed
hypersensitivity reactions, some aspects of
resistance to cancer, certain autoimmune diseases,
graft rejection and certain allergies.
Antibody
- an immunoglobulin produced by lymphocytes
in response to bacteria, viruses, or other antigenic
substances.
- it is specific to antigen
 - it includes agglutinins, opsonins, and Specificity of action
precipitins.
The unique action of the last 2 properties is
Antigen
its diversity of ability to respond while at the
- a substance usually a protein that causes the
formation of an antibody and reacts specifically with same time responding with specificity of action.
that antigen.
TYPES OF IMMUNITY
COMPARISON OF HUMORAL AND CELLULAR CELL RESPONSE A. NATURAL IMMUNITY – innate or genetically or primary
HUMORAL IMMUNITY
immunity.
STAGES OF IMMUNE RESPONSE
- provides a nonspecific response to any foreign
Recognition stage – circulating lymphocytes and
invader, regardless of the invaders composition.
macrophages recognize foreign materials or antigens
as nonself - the basis of natural defense mechanism is merely the
ability to distinguish between self and nonself
Proliferation stage – sensitized lymphocytes
proliferates, differentiate, and mature into T and B B. ACQUIRED IMMUNITY – or secondary immunity is an
cells.
immunologic response acquire during life but not
present at birth.
Response stage – antibody is produced with specific
T-cell action.
1. ACTIVE ACQUIRED IMMUNITY
Effector stage – antigen is destroyed by antibody,
which is produced by B-cell or cytotoxic T-cell action. a. Person develop his own antibodies

Properties of immune response b. Takes 10 t0 14 days to develop

Recognition – able to recognize self from nonself
c. Permanent
Memory – recalls type of antigen(pick up imprint of
the antigen structure) d. Body cells undergo change
Diversity of action Active acquired immunity could either be:
* Natural – having contact with antigen naturally such as
getting sick or frequent exposure to smaller doses of
microorganisms like: chickenpox, measles, mumps
* Artificial – acquiring antigen through vaccines or
toxoids like in BCG, DPT and POLIO.
2. PASSIVE ACQUIRED IMMUNITY:
a. Person receives preformed antibodies
b. Provides immediate immunity
c. Temporary
d. No cellular changes
Passive acquired immunity could either be:
* Natural – acquired naturally during breast-
feeding like from colostrum
* Artificial – having preformed antibodies such
as antitoxins, antiserum and
gamma-
globulin, ex. Immune serum
globulin
Common diagnostic procedures
WBC count – used to suggest the presence of
infection, an allergy or leukemia. Used to help
monitor the body’s response to various treatments
and to monitor bone marrow function. Detects
dangerously low number of WBC.
WBC differential count – assesses the ability of the
body to respond to and eliminate infection. Detects
the severity of allergic reactions; parasitic and other
types of infection and drug reaction.
INTRADERMAL TEST (MANTOUX TEST) (PPD) –
given intradermally in the forearm, with 10mm
induration significant reaction is positive(+), reading
done in 48-72 hours, if positive result, it does not
mean that active disease is present, but indicates
exposure to Tuberculosis.
RADIO IMMUNO ASSAY (RIA) – highly sensitive and
specific assy method used to determine antibody
concentrations or to determine the concentration of
any substance against which specific antibody can be
produced.
ELISA(ENZYME LINKED IMMUNOSORBENT ASSAY
– identifies antibodies specifically against HIV. It Presence of conditions and disorders:
does not establish diagnosis of AIDS, rather it cancer/neoplasm, chronic illness, autoimmune
disorders, surgery/trauma
indicates that the person has been exposed to or
infected with HIV called SEROPOSITIVE.
Allergies
WESTERN BLOT ASSAY – used to confirm
seropositivity as identified by the ELISA.
History of infection and immunization
BONE MARROW BIOPSY – assess the quantity and
quality of each type of cell produced within the Genetic factors
marrow. Used to document infection or tumor within
the marrow.
Lifestyle
Tests to Evaluate Immune Function
WBC count and differential Medications and transfusions

Bone marrow biopsy

Pyschoneuroimmunologic factors
Humoral and cellular immunity tests

Phagocytic cell function test

Categories of immunologic disorders
Complement component tests A. IMMUNODEFICIENCY – caused by a defect or deficiency in
phagocytic cells, B lymphocytes, T lymphocytes or the
Hypersensitivty tests
complement system.
Specific antige
= the clinical results of impaired function of one or more
components of the immune or inflammatory response,
including B cells, T cells, phagocytic cells and
Variables That Affect Immune System Function complement.
Age and gender
= failure of these self-defense mechanisms to function
at normal capacity.
Nutrition

Cardinal symptoms of immunodeficiency:
1. recurrent infection
2. infections caused by normal flora
3. poor response to treatment of infections
4. chronic diarrhea
IMMUNODEFICIENCES:
Primary immunodeficiency
- rare disorder with genetic origins seen primarily in
infants and young children
- occurs if lymphocyte development is arrested or
disrupted in the fetus or embryo.
-symptoms usually develop early in life and children
witrh these disorders seldom survive childhood.
Hyperimmunoglobulinemia (HIE) syndrome – a
sex-linked recessive disorder found only among
male.
- characterized by PMN(polymorphonuclear
cells) engulfing microorganisms but killing does not
take place because PMN lack the necessary digestive
enzyme.
Major symptoms of HIE syndrome
1. bacterial
2. fungal
3. viral infections
4. deep-seated cold abscess
Bruton agammaglobulinemia – results from lack of
differentiation of B cell precursors into mature B
cells. As a result, plasma cells are lacking, and the
germinal centers from all lymphatic tissues
disappears, leading to a complete lack of antibody
production against invading bacteria, viruses and
other pathogens.
- thymus gland is intact and the response of T
cell is normal.
Hypogammaglobulinemia or Common Variable
immunodeficiency (CVID)
- results from lack of differentiation of B cells
into plasma cells.
- there is general lacking of immunoglobulins
in the blood. - both the B cell and T cell are missing.

- there is complete absence of humoral as well

as cellular immunity caused by an X-linked or
Agammaglobulinemia – the condition in autosomal genetic abnormality.
which B cell development are totally or nearly
absent.

Ataxia telangiectasia – characterized by

Di George’s syndrome or Thymic hypoplasia – a T-
cell deficiency that occurs when the thymus gland
fails to develop normally during embryogenesis.
Presenting signs:
uncoordinated muscle movement(Ataxia) and
vascular lesions caused by dilated blood
vessels(telangiectasia) usually occurs during the first
4 years of life

1. recurrent infection

2. hypoparathyroidism Nezelof’s Syndrome – the individual is born without

thymus gland and have various degrees of B-cell
3. hypocalcemia immunodeficiency associated with various
combinations of increased, decreased or normal
4. tetany immunoglobulin levels.

5. convulsions

6. congenital heart disease Wiscott-Aldrich Syndrome – an SCID compounded

by thrombocytopenia or loss of platelet.
7. renal abnormalities

8. abnormal faces 2. Secondary Immunodeficiency – are common

than primary deficiences and frequently occur as a
result of underlying disease process or from
Severe Combined Immunodeficiency treatment of these diseases:
disease(SCID)
 Common cause: partner

a. Malnutrition 4. sexual relations with infected

individuals
b. Chronic stress

c. Burns Mode of transmission

d. Uremia 1. Anal intercourse

e. Diabetes mellitus 2. injection of drug – direct blood exposure to

contaminated needles and syringes.

Acquired immunodeficiency Syndrome – AIDS
- the best known example of an acquired
dysfunction of the immune system.
- represents a frightening disease because of
its extremely high mortality in untreated individuals.
Etiology : HIV or retrovirus
Risk factors:
1. male homosexual relations
2. intravenous drug use or the injecting
drug
user.
3. heterosexual relations with an HIV
infected
3. blood and blood products – including those
persons with hemophilia and other people who are
blood recipients.
4. transplacental – AIDS transmitted in utero
from mother to child.
Clinical manifestations:
1. persistent generalized lymphadenopathy –
characterized by the generalized enlargement of the
lymph nodes.
2. lesser AIDS – conditions such as oral
candidial infection arise and examination of platelet
reveals decreased. Most of the patients may be
completely asymptomatic.
3. AIDS related complex(ARC:wasting
syndrome –profound involuntary weight loss of 10%
body weight due to unexplained diarrhea for more
than one month or chronic weakness.
- intermittent fever
- splenomegaly
- low platelet count and lymphocytes
- severe body malaise
AIDS SYNDROME
Opportunistic infections
1. Pneumocyctis carinii
- 60% of the AIDS patients initially
manifest
PCP. It was thought to be protozoan
but recent studies showed that it is a rare fungal
infection that cause diseases only to
immunocompromised patients:
- patients tend to demonstrate the ff:
a. Fever
b. Chills
c. Non-productive cough
d. Shortness of breath
e. Dyspnea
f. Occasional chest pain
- Patients may go to respiratory failure
within 3 days after onset of symptoms.
2. Mycobacterium Avium Complex(MAC)
- a leading bacterial infection in people
with AIDS ..Comprising a group of acid fast bacilli,
usually causes respiratory infection
3. Tuberculosis
- tend to occur in injecting drug users
and other groups with with a pre-existing high
prevalence of TB infection
- TB that occurs late in HIV infection is
characterized by absence of a tuberculin test
response because of the compromised immune
system
4. Oral candidiasis
- a fungal infection occurs nearly in all
AIDS related conditions. It is characterized by
creamy white patches in the oral cavity
 -Symptoms: difficult and painful
swallowing
: retrosternal pain
5. Cryptosporoidal virus
- causes diarrhea up to 6L per day
resulting to viral infection
6. Cryptococcus neoformans
- char by symptoms such as: fever,
headache, malaise, stiff neck, nausea and vomiting,
seizure
7. Kaposis sarcoma
- most common HIV related malignancy
involving endothelial layer of the blood and
lymphatic vessels
- cutaneous lesions appearing
anywhere on the body are usually brownish pink to
deep purple surrounded by ecchymosis and edema
8. B cell lymphoma(non hodgkins
lymphoma
- including multiple organ involvement
and complications related to opportunistic infection
- compromise approximately 11% of all
childhood cancer
-a genetic term for a wide spectrum of
disorders characterized by the malignant
transformation of the lymphoid system.
NHL is differentiated from HL by lack of RS
(Reed-sternberg cells) and the other cellular changes
not characteristics of HL.
- the common finding of NHL are
alterations in the tumor DNA
- arise from single outlaw cell
(Monoclonal) and probably develop with
accumulation of multiple genetic hits
- its most common type of chromosomal
alteration is translocation
AIDS DEMENTIA COMPLEX
- neurologic dysfunction results from the direct
effects of HIV or nervous tissue, opportunistic
infections, primary neoplasm, CV changes and
metabolic encephalopathies.
Diagnostic exams:
1. ELISA
- test that identifies antibodies directed
aseptically against HIV. It does not establish - advice to wear cotton sock to prevent
diagnosis of AIDS, rather indicates that the person feet
has been exposed to infected HIV called
seropositive. from perspiring if lesions are found in
the
- or it is a presumptive test
legs

2. Western blot assay - clean peri-anal area every after bowel

with
- conformity test of AIDS
non-abrasive soap and water to
3. Immunoflourescent Assay(IFA) prevent

- preferred by some physician over the escoriation

western blot assay since it is more rapid and simple
to perform. - sitz bath to promote comfort

- assess frequently for integrity of the

oral
Nursing management:
mucosa
1. promote skin integrity

- change position every 2 hours 2. Promote usual bowel habit

-- monitor for pattern of diarrhea and
- apply medicated lotions, ointments consistency of stools
and
- report abdominal pain and cramping
dressings
- during periods of acute intestinal
inflammation, the patient may be placed on NPO to
- avoid using adhesive tapes rest the GIT
 - encourage increase dietary intake - monitor respiratory status

- avoid foods that are irritating to the bowel - encourage intake of 3l per day
such as spicy foods, food with extreme temperature
and carbonated drinks - administer humidified oxygen

- administer antispasmodic and anti-diarrheal 7. relieve pain and discomfort

agents
- administer pain relievers

3. prevent infection - encourage to wear elastic stockings to

equalize pressure
- monitor for signs of infection
8. improve nutritional status
- prevent overcrowded place
- monitor daily weight
4. improve activity tolerance
- assess factors that may interfere with dietary
-assist in activities of daily living intake

5. maintain thought processes - control nausea and vomiting with anti-emetic

medications
- assess mental status
- encourage to eat food that are easy to
- use simple explanation swallow and to avoid rough and spicy foods

- provide memory aids - encourage to rinse mouth with lidocaine

before meals
- give positive feedbacks for appropriate
behavior - give food supplements

9. decreased sense of isolation

6. improve airway clearance
10. Assist coping with grief
 - gaunt looking, apprehensive
Mode of Transmission

1. sexual contact

2. blood transfusion 2. Mental(early stage)

3. contaminated syringes, needles, nipper, - forgetfulness

razor blades
- loss of concentration

- loss of libido
Signs and Symptoms:
- apathy
1. Physical
- psychomotor
- maculo-papular rashes
- withdrawal
- loss of appetite
3. Mental(later stage)
- weight loss
- confusion
- fever of unknown origin
- disorientation
- malaise, persistent diarrhea
- seizures
- TB
- mutism
- esophageal candidiasis
- loss memeory
- Kaposi’s sarcoma
- coma
-pneumocystis carinii pneumonia
Prevention:
1. maintain monogous relationship
2. avoid promiscuous sexual contact
3. sterilize needles, syrnges and instruments
used in cutting operations
4. proper screening of blood donors
5. rigid examination of blood and other
products for transfusion
5. avoid oral, anal contact, swallowing of
semen
6. use of condoms and other protective device
HIV/AIDS
- first occurred in africa and spread in the
carribean island.
- reported in the USA in 1981
- this sexually transmitted disease spread so
rapidly that it is soon occurred in epidemic
proportion inseveral countries of the world including
the Philippines. It is currently pandemic(occurring
throughout the world)
- the first case of AIDS in the Philippines was
reported in 1984, as at May 2000, based on
Philippines National AIDS council(PNAC) records,
there were 1,385 HIV poisitive and 464 AIDS cases.
There have been 206 deaths
B. GAMMOPATHIES
- immunologic disorders pertaining to elevated
level of gammaglobulin in the serum.
- also known as hypergammaglobulinemia
- Multiple Myeloma – is a malignant disease
of the most mature form of B
lymphocyte
which is the plasma cell.
- a B cell cancer characterized by
the
proliferation of malignant plasma cells
that aggregate into tumor masses
and
then become distributed
throughout the
sleletal systems.
 2. Xray or Bone scan – establishes the degree
Clinical manifestationof MM of bone involvement

1. Bone pain usually in back and ribs and 3. Bone marrow aspiration – detects number
worsen with rest. The pain is due to a substance of plasma cell in the bone marrow
secreted by the plasma cells which is the osteoclast
activating factor, that stimulates bone breakdown.
Thus, lytic lesions and osteoporosis is seen during x- Medical management:
rays.
- there is no cure for MM, since it is a disease
2. Recurrent fractures of malignancy, it is treated with chemotherapy and
radiation therapy.
3. Hypercalcemia due to escape of calcium
ions from the bones

4. Renal failure: large immunoglobulin Nursing management:

molecules can damage the renal tubules.
1. administer pain reliever for bone pain
5. Fatigue and weakness due to anemia
2. maintain hydration to diminish exacerbation
of complication
Pathophysiology:
3. prevent from infection
malignant plasma cells produces M-
Protein or monoclonal protein release of
osteoclast activating factors breakdown of the C. AUTOIMMUNE DEFICIENCY – these disorders
bone involve inappropriate reaction by the immune system
in which antibody form against self-antigen.

autoimmunity - is a breakdown of
Diagnostic Exams: tolerance in which the body’s immune system
begins to recognize self-antigens as foreign.
1. Bence Jones Urine Test – detects abnormal
globulin in the urine
 1. Systemic Lupus Erythematous(SLE) – a
result of disturbed immune regulation that causes
exaggerated production of auto-antibodies.
- the increase in auto-antibody production is
thought to result from abnormal suppressor T-cell
function, leading to immune complex deposition
and in tissue damage.
- seen more often in women especially in the
20 to 40 year old age group
- a transient lupus like syndrome that is
indistinguishable both clinically and in the
laboratory from spontaneously occurring SLE also
can develop from prolonged use of drugs,
particularly hydralazine(an antihypertensive
agent) and procainamide(an antidysrhythmic
drug).
11 clinical findings of SLE:
1. facial rash confined to the cheeks(malar
rash)
2. discoid rash(raised patches, scaling)
3. photosensitivity(skin rash in sunlight)
4. oral or nasopharyngeal ulcers
5. non-erosive arthritis of at least two
peripheral joints
6. serositis(Pleurisy, pericarditis)
7. renal disorders(proteinuria of >0.5 g/day or
cellular cast)
8. neurologic disorders(seizures or psychosis)
9. hematologic disorders(hemolytic anemia,
leukopenia, thrombocytopenia)
10. immunologic disorders(positive LE cell
preparation, anti-DNA, false-positive serologic test
for syphilis)
11. presence of antinuclear antibody (ANA)
Predisposing Factors SLE:
Genetic and hormonal factors – onset during the child bearing
years.
Environmental factors – such as sunlight, thermal burns
Drugs – hydralazine(apresoline), procainamide(pronestyl), INH,
chlorphromazine and other anticonvulsant
Clinical manifestations of SLE:
Arthralgia or arthritis – 90% of individuals. A common Total Serum Complement – the best test to follow the course of
presenting features of SLE frequently accompanied by morning disease.
stiffness and not deforming in nature.

Classic butterfly rash – 70% to 80% of individuals. Medical Management:

Papulosquamous or annular polycyclic lesion occurs across the
bridge of the nose and cheeks. The rashes worsen with NSAID(Non steroidal anti-inflammatory drug) – it is useful in
sunlight. treatment of the arthritis associated with SLE

Pericarditis – 30% to 50% of individuals. Most common cardiac Corticosteroid like prednisone – ammelurates the mainstay
manifestation of SLE therapy of SLE. Its side effect is to suppress immune system
thus suppressing body reactions to autoimmune antibodies.
Lymphadenopathy and vasculitis – 70% to 80% of individuals.
Patients manifest papular, erythematous and purpuric lesions Cytotoxic agents – arrest autoimmune activity of the SLE
on the fingertips, elbows, toes and forearm. These may
progress into necrosis. Plasma-paresis – 3-4 liters are exchanged weekly from a
plasma of a normal donor which is used to remove circulating
Lupus nephritis – 40% to 50% of individuals.Occurs as auto antibody and immune complexes from the blood before
antinuclear antibodies/attaches to the DNA and is deposited in organ and tissue damage occurs.
the renal glomerulus.

Psychosis and depression Nursing care management:

Hematologic abnormalities – 50% of individuals, with anemia Institute reverse isolation

being the most complication
Encourage personal hygiene

Diagnostic exam of SLE: Maintain clean environment

LE cell test – test for presence of lupus erythematous Screen visitor from cold

ANA or anti nuclear antibody test – the best definitive test for Avoid drugs such as contraceptives and anticonvulsant
SLE since ANA is present in all cases of SLE even in the inactive
stage of the disease Avoid unnecessary blood transfusion
Avoid fatigue
Discourage pregnancy
2. Rheumatoid arthritis –a systemic autoimmune
disease that causes chronic inflammation of
connective tissue, primarily in the joints.
- the joints most commonly affected are:
fingers, feet, wrist, elbows, ankles, and knees, but
the shoulder, hips, and cervical spine also may be
involved, as well as the tissue of the lungs, heart,
kidney and skin.
- develops most often in women
- despite intensive research, the cause of RA
remains obscure. It is probably a combination of
genetic, environmental, environmental, hormonal
and reproductive factors.
Clinical manifestation:
Joint pain, swelling and warmth
Erythema – redness or inflammation of the skin
Lost of function or joint stiffness especially in the morning
lasting for 30 minutes
Hand and feet deformities caused by misalignment resulting
from swelling, progressive joint destruction or the subluxation
that occurs with a bone slips over another
Fever
Weight loss
Fatigue
Edema
Lymph node enlargement
Raynaud’s phenomenon – intermittent attacks of ischemia of
trhe extremities of the body, especialy the fingers, toes, ears,
and nose, caused by exposure to cold or by emotional stimuli.
- the attacks are characterized by severe blanching of
the extremities, followed by cyanosis then redness;
usually accompanied by numbness, tingling, burning
and often pain.
Diagnostic exam of RA:
ESR – reveals elevated
C Reactive Protein – positive in RA
ANA – positive
Arthrocentesis – synovial fluid shows cloudy, milky or dark
yellow and contains numerous inflammatory cells, such as
leukocytes and complement.
XRAY studies helps monitor progress of the disease
 - treatment goal: reduction of the size of the
Management of RA: gland

NSAIDS : blocks the enzyme involved in inflammation while

leaving the enzyme involved in protecting the stomach lining. D. HYPERSENSITIVITY – an abnormal, heightened
(COX-2 inhibitor) reaction to any type of stimuli.

Antimalarials, Gold, penicillamine – initiated early in treatment;

alters cellular metabolism; alter enzyme function and immune
response and suppress phagocytic activity 1. ANAPHYLACTIC TYPE(TYPE I) - is an
immediate reaction beginning within minutes of
Biologic response modifiers such as cytokines exposure to an antigen and this is mediated by IgE
antibodies.
Corticoesteroids – used when patient has unremitting
inflammation and pain or needs a “bridging” medication while anaphylaxis – is a clinical immediate
waiting for the slower disease modifying anti-rheumatic agent. immunologic response between a specific antigen
and antibody
Synovectomy – excision of synovial membrane
Etilogy:
Tenorrhapy – suturing of tendons
1. food
Arthrodesis – surgical fusion of the joint
2. drugs
Arthroplasty – surgical repair and replacement of the joint.
3. venom

3. Hashimoto’s thyroiditis – chronic lymphocytic 4. blood products

thyroiditis diagnosed based on the inflammation of
the gland. It is not accompanied by pain, pressure 5. allergen extract
symptoms or fever and thyroid activity is normal
6. diagnostic agents
- cell mediated immunity plays a significant
role in the pathogenesis.
Clinical manifestation of type I
Urticaria Clinical manifestations:

Bronchospasm 1. nasal congestion: clear, watery, nasal

Generalized swelling discharge

Hypotension 2. intermittent sneezing

Nausea and vomiting 3. nasal itching

4. itching of throat and palate

Management:
5. headache
Administer oxygen as indicated
6. pain over paranasal sinuses
Epinephrine as needed
Management:
Corticosteroids may be given to relieve bronchospasm
Administer antihistamine as ordererd
IV fluids are administered to correct hypotension
May administer adrenergic agents to cause vasoconstriction of
Atopic allergies the mucosal vessel

Mast cell stabilizer like intranasal cromolyn sodium is a nasal

1. Allergic rhinitis/Hay fever – inflammation of
spray that inhibits the release of histamine and other mediators
the nasal mucosa. It is usually induced by airborne
of allergic response
pollen or molds. Sensitization begins by ingestion or
inhalation of an antigen. On reexposure the nasal
Advice the client to avoid allergens like dust, hapte-rich foods,
mucosa reacts by the slowing of ciliary action,
etc.
edema formation, and leukocyte infiltration.
Histamine is the major mediator of allergic reaction
2. Atopic dermatitis – most patients have
elevated IgE in the serum. Pruritus and
hyperirritability of the skin are the most consistent hypotension,
features and are related to large amount of
histamine in the skin. Excessive dryness of the skin nausea and vomiting, restlessness
results from change in the lipid content, sebaceous and
gland activity, and sweating.
shock

3. Urticaria – also known as Hives is a type I Nursing Care:

hypersensitive reaction of the edematous elevations
that vary in size and shape, itch and cause local - place patient in supine with head
discomfort. It stays from few minutes to hours elevated
before disappearing.
at 20-30 degrees

2. CYTOTOXIC (TYPE 2) – occurs when the system - administer fluid, epinephrine and
mistakenly identifies a normal constituent of the cortico-
body as foreign and mediated by whether IgG or
IgM. steroids as ordered.

- administer mannitol

A. Blood transfusion reaction - insert an indwelling catheter

TYPES: - monitor intake and output

1. Hemolytic - TSB for fever

Clinical manifestations - stop blood transfusion

- chills, fever, headaches, chest - change IV fluid to prevent from

pain, infusing

tachycardia, dyspnea, anymore

 - administer IV saline as ordered 3. Febrile reaction

- obtain blood and urine sample clinical manifestation:

- mild chills

Example: Blood type “A” individual transfused - fever

with a Type “B” blood mistakenly antigen and
antibody reaction agglutination & hemolysis nursing care:

of the RBC hemolyzed blood clogges - administer antipyretic and

capillaries unable to carry oxygen antihistamine

and food obstruction of blood flow 4. Allergic reaction

clinical manifestation:

- pruritus, urticaria(hives), facial

2. Contaminated blood swelling, chills, fever

clinical manifestation: nausea & vomiting, headache,

wheezing, laryngeal edema,
- chills, fever, abdominal pain,
nausea shock, respiratory distress

and vomiting, diarrhes, nursing care:

hypotension
- administer antihistamine,
nursing care: epinephrine or corticosteroids

- stop BT immediately

- administer fluids
B. RH incompatibility – there is excessive
destruction of RBC which results from antigen-
antibody reaction and is characterized by hemolytic
anemia and hyperbilirubinemia.
clinical manifestation of EF

1. sclera appears yellow before the skin does

Father(Rh+) + Mother (Rh-) Rh
incompatible 2. skin color from light brown to yellow

-During the delivery of the first baby blood of 3. lethargy

the fetus escape to the body of the mother thru
maternal sinuses, causingn Rh antibody towards 4. dark amber concentrated urine
Rh(+)
5. poor feeding

6. dark stools
-subsequent pregnancies, the Rh(+)
antibodies will destroy and cause the blood of the Diagnostic evaluation:
fetus to hemolize
1. amniocentesis – analysis of bilirubin level
in amniotic fluid before birth through the amniotic
fluid of the mother.
- compesatory mechanism: increased
production of immature RBC by the fetus 2. Indirect Coomb’s test – is the direct
evaluation of the presence of anti-Rh antibody in
maternal circulation.

ERYTHROBLASTOSIS 3. Direct Coomb’s test – this confirms the

FETALIS disease postnatally by detecting antibody attached to
circulating lymphocytes of affected infants

RHOGAM INJECTION – after the first delivery,

mother should be given Rhogam within 48 hours to
prevent the maternal circulation from developing
antibody against the opposite Rh factor.
3. IMMUNE COMPLEX(TYPE III)
- are deposited in tissues or vascular
endothelium that contributes to injury, the increase
amount of circulating complexes and the presence of
vasoactive amines.
- the joints and kidneys are the primary
susceptible to these type of allergy.
Serum Sickness
- this type III hypersensitive reaction is known
to be a result of the administration of therapeutic
antisera of animal sources for the treatment and
prevention of infectious diseases, such as tetanus,
pneumoniua and rabies.
manifestations: inflammatory reaction at
the site of injection of the medication followed by
regional and generalized lymphadenopathy. There is
usually skin rash and joints are frequently tender and
swollen.
4. DELAYED TYPE(TYPE IV)
- occurs 24-72 hours after exposure and is
mediated by sensitized T cells and macrophages.
a. Contact dermatitis – a delayed eczematous
condition caused by a skin reaction to a variety of
irritating or allergenic materials
ex. Poison Ivy – most common type but
soaps, detergents, cosmetics may also cause this
type of dermatitis.
clinical manifestations:
-itching, burning, erythema, skin
lesions(vesicles), edema, weeping, crusting and
finally drying and peeling of the skin
b. Skin graft/Organ rejection
- skin graft is a technique in which a section
of the skin is detached from its own blood supply
and transferred to a free tissue to a
distant(recipient) site. These are commonly used to
repair defects and cover wound when insufficient
skin is available to permit wound closure.
TYPES OF GRAFTS
1. isograft/syngeneic
- graft exchange between genetically
dentical membrane of the same species
 2. allograft/allogeneic/homograft
is a potent suppressor of both humoral and cellular immunity
- graft exchange between individual of the
same species
3. autograft/autologous
- graft exchange within the same individual
4. xenogeneic
- graft exchanged between individuals of
different species
Rejection of Graft
- described as immune complex response
leading to rejection by recipient therapy usually due
to incompatibility of cell surface antigen
- this can be prevented by tissue typing and
matching between donor and recipient
Immunosuppresive therapy are also useful in
preventing graft rejection
Corticosteroid – impairs lymphocyte function, thus suppressing
immune response
Azathioprine(Imuran) – prevent cell-mediated immune response
while inactivating Ag receptor sites in T cells
Methotrexate – a folic antagonist; inhibit folace metabolism and
4. antilymphocyte serum – serum from
animals injected to human results to antibody
formation against the lymphocytes.
5. cyclosporina – decreases the number of
killer T cells without affecting granulocytes
- used to suppress rejection
If you just found out you’re pregnant, one of the first
and most important tests you should expect is a
blood type test.
This basic test determines your blood type and Rh
factor. Your Rh factor may play a role in your baby’s
health, so it is important to know this information
early in your pregnancy
People with different blood types have proteins
specific to that blood type on the surfaces of their
red blood cells.
There are four blood types (A, B, AB and O)
Each of the four blood types is additionally classified
according to the presence of another protein on the
surface of RBC that indicates your RH Factor. If you
carry this protein, you are Rh Positive. If you don’t
carry the protein, you are Rh negative.
Most people about 85% are Rh positive. But if a
woman who is Rh negative and a man who is Rh
positive conceive a baby, there is the potential for
incompatibility
The baby growing inside the Rh negative mother
may have Rh positive blood, inherited from the
father
Statistically, at least 50% of the children burn to an
Rh negative mother and Rh positive father will be Rh
Positive
Rh incompatibility isn’t a problem if it’s the mother’s
first pregnancy because, unless there’s some sort of
abnormality, the fetus’s blood does not normally
enter the mother’s circulatory system during the
course of the pregnancy
However, during delivery, the mother’s and baby’s
blood usually intermingles. When this happens, the
mother’s body will begin to produce
antibodies(protein molecules in the immune system
that recognize, and later work to destroy, any
substance “foreign” to body) against the Rh proteins
that have been introduced into her blood.
Rh antibodies are harmless until the mother’s second
or later pregnancies
If she is ever carrying another Rh positive child, her
Rh antibodies will now recognize the Rh proteins on
the surface of the baby’s blood cells as foreign
Rh antibodies will cross the placenta into the baby’s
bloodstream and attack those cells, causing swelling
and rupture of the baby’s RBC
A baby’s blood count can get dangerously low when
this condition, known as hemolytic or Rh disease of
the newborn, occur.
How is Rh disease of the newborn prevented and
treated?
- Today, when a woman with the potential to
develop Rh incompatibility is pregnant, doctors
administer a series of: 2 Rh immune-globulin shots
during her first pregnancy
- first shot – given around 28th wk of
pregnancy
- 2nd shot – given 72 hours after giving birth
Rh immune globulin acts like a vaccine, protecting
against the development of the Rh antibodies that
can cause complications during any future
pregnancies.
INFLAMMATION and IMMUNITY
 Cell Injury and Inflammation
Cell adaptation to injury includes:
Adaptive processes
H ype rt roph y – increase in cell size without cell
division
H y p e rpl as i a – actual increase cell number or density
of cells
A t ro p h y – decrease in tissue or organ size caused by
decrease in cell number or cell size
Functions of Mononuclear Phagocyte System (MPS)
Meta plasi a – the transformation of one cell type into
another
Maladaptive responses
D y s p l a s i a – abnormal differentiation of dividing cells
resulting in changes in the size, shape, and
appearance of the cells; a precursor to malignancy
A n a p l a s i a – cell differentiation to a more immature
or embryonic form. Malignant tumors are
characterized by anaplastic cell growth.
Defenses against injury
Skin and mucous membrane – first line of defense
Four Distinct Phenomena in the Inflammatory Response
Mononuclear Phagocyte System – (MPS)
consists of monocytes and macrophages and their
precursor cells known as reticuloendothelial system
(RES)
Consists of:
1. Fixed phagocytes or macrophages of the liver,
spleen, BM, lungs, LN and microglial cells
2. Mobile or wandering phagocytes – monocytes
(blood) and macrophages found in connective
tissues known as histiocytes
Recognition and phagocytosis of foreign material
such as microorganism
Removal of old or damaged cells from circulation
Participation in the immune response
Inflammatory Response
Is a sequential reaction to cell injury.
It is often but incorrectly used as synonym for the
term infection.
I n fl a m m a t i o n is always p r e s e n t wit h infection, but
infection is not always present with inflammation.
Increased vascular permeability (Vascular response)
 Infiltration of leukocytic cells (Cellular response)
Formation of exudates
Healing process
Increased vascular permeability (Vascular Response)
After cell injury, the capillaries in the area briefly
undergo vasoconstriction
After the release of histamine and other chemicals by
the injured cells, the vessels dilate (vasodilation)
resulting in hyperemia which raises filtration
pressure.
Capillary Permeability
Infiltration of Leukocytic cells (Cellular Response)
Neutrophils and monocytes move to the inner
surface of the capillaries (margination) and then in
amoeboid fashion, through the capillary wall
(diapedesis) and to the site of injury.
The findings of ↑ number of band (immature)
neutrophil on circulation is called a shift to the left,
which is commonly found in patients with acute
bacterial infections (mature neutrophils are called
segmented neutrophils, or segs)
Chemotaxis and Emigration
Mediators of Inflammation response
Inflammatory Phases
Formation of Exudates
Formed from the fluid and the cells that move to the
site of injury.
Types of inflammatory Exudates:
Serous e x u d a t e – clear in appearance and can easily
reabsorbed with no damage
Serosanguinous – serous exudate mixed with small
amounts of blood from the injured capillaries
San gui nou s – contains large amount of blood from
extensive damage
P u r u l e n t – results from bacterial invasion and may
lead to tissue scarring if cellular necrosis is extensive
C a t a r r h a l o r m u c o i d – contains mucous secretions
and usually results from viral infection of the
respiratory tract.
Healing Process
Refers to the replacement of dead or damaged cells
by new and healthy cells derived either from the
parenchymal or connective tissue stroma. Includes
two (2) major components:
Regeneration
Scar formation
Regeneration
This occurs when the injured tissues and cells are
 replaced by new cells and tissues that are identical in
nature and function to the damaged cells.
Scar formation
There is a formation of collagenous scar in the
healing of tendons, fascia, connective tissues and
collagenous structure. This type of repair consists of:
INTRINSIC- begins with the activation of Factor XII
(Hageman factor) by contact with abnormal surfaces
produced by injury
EXTRINSIC- is triggered by trauma, which activates
Factor VII (Stable factor) and releases a lipoprotein,
called Tissue factor from BV

Primary healing/union or First Intension – COMMON- conversion of Prothrombin to Thrombin;

repair of clean surgical wound or incision by CT
elements
Secondary union/ secondary intension – repair of
a contaminated surgical wound by formation of
granulation tissue
Fibrinogen to Fibrin
FIBRINOLYTIC- conversion of Plasminogen to
Plasmin by t-PA (tissue plasmin activator) Fibrin
degradation products

Tertiary Intension – there is delayed primary

closure of a wound (DPC) Case management
Drug therapy
Clinical manifestation of Local Inflammatory Response
Local Manifestations of Inflammation Vitamins (Vit A,B,C,D)

Antibiotic-Resistant Organisms

Reduce risk for Antibiotic-Resistant Infection

Systemic Inflammatory Response – occurs when
bacterial invaders cannot be locally successfully Alternative meds- Herbal
localized and destroyed.
Nutrition therapy
Clinical manifestations include fever, leukocytosis,
Nursing management
anorexia and nausea, malaise and increased ESR.
Drug Therapy for inflammation and Healing
Systemic inflammatory response Antipyretic drugs: SAN
COAGULATION PATHWAYS
 Salicylates (Aspirin) increase risk for developing resistant infection)

Acetaminophen (Tylenol) Wash your hands frequently

Non steroidal anti-inflammatory drugs (NSAIDs) Follow directions. (not taking antibiotic as
Ibuprofen (Motrin, Advil) prescribed or skipping can encourage the
development of antibiotic resistant bacteria)
Anti-inflammatory drugs: CNS
Finish your antibiotic. (when you stop taking your
Corticosteroids antibiotic early, the hardest bacteria may survive and
multiply.
NSAIDs
Do not request for an antibiotic for flu or colds.
Salicylates (antibiotics are effective against bacterial infections,
but not virus, which cause cold and flu)
Vitamins (A,B,C,D)
Accelerates epithelialization

B complex – acts as co-enzymes

Do not take leftover antibiotics. This is
Collagen synthesis dangerous because:

D- facilitates Calcium absorption T h e l e f t o v e r antibiotic m a y n o t b e appropriate;

Antibiotic-Resistant Organisms: MVP Illness m a y n o t b e a bac teri al infectio n

Methicillin – Resistant Staphylococcus aureus (MRSA)
O l d antibiotics m a y h a v e l o s t t h e i r effectiveness and in some
Vancomycin-Resistant Enterococci (VRE)
case can even be fatal
Penicillin-Resistant Streptococcus (PRSP) Herbs Used for Healing
Clinical uses: used topically for treating minor
Reduce Risk for Antibiotic-Resistant Infection
wounds, including sunburns, cuts and abrasions.
Do not take antibiotics to prevent illness. (might (Ex. Aloe, chamomile, Echinacea, evening primerose,
golden seal, St. John”s Worth)
Effects: anti-inflammatory actions
Nursing implications: herbs should not be used in
deep wounds, if used, they should be used after the
wound has begun to heal.
A l o e c a n b e u s e d safely o n r e c e n t sunburns,
minor burns, and superficial cuts and abrasions.
Nutrition Therapy
High fluid intake is needed to replace fluid loss from
perspiration and exudate formation.
Diet high in CHON, CHO, and Vitamins with
moderate Fat intake is necessary to promote
health.
Protein
Needed to correct the negative Nitrogen balance
resulting from increased metabolic rate.
Necessary for synthesis of immune factors,
leukocytes, fibroblast, and collagen.
Carbohydrates
Needed for the increased metabolic energy required
in inflammation and healing.
If CHO deficit is present, the body will break down
protein, (in replacement of CHO) for the needed
energy
Fats
Necessary components in the diet to help in the
synthesis of fatty acids and triglycerides, which are
part of the cellular membrane.
Vitamins
Vitamin C – needed for capillary synthesis, capillary
formation, and resistance to infection.
Vitamin B-complex – necessary as coenzymes for
many metabolic reactions.
V i t a m i n B deficiency m a y r e s u l t s i n disruption of
protein and fat, and carbohydrate metabolism will
occur.
Nursing Management for Inflammation, Infection & Healing
Rest and Immobilization – promote healing by
decreasing the inflammatory process, assisting in the
repair process, and decreasing metabolic needs.
Elevation – will reduce the edema at the
inflammatory site and increase venous return
Adequate oxygenation – of the inflamed area is
essential because oxygen promotes the
differentiation of fibroblasts and collagen synthesis.
O2 is also essential for cell growth and division.
Heat and Cold
Cold application is usually appropriate at the time of
the initial trauma to cause vasoconstriction and
decrease swelling, pain and congestion from
increased metabolism in the area of
inflammation.
Heat may be used later (24-48 hrs) and when
swelling has subsided to promote healing by
increasing the circulation to the inflamed site
and subsequent removal of debris. It is also
used to localize the inflammatory agents. Warm,
moist heat may help debride the wound site if
necrotic material is present.
Wound Healing – Primary Intention
Incision – Wound formation
Fibrin clot – prevents bleeding, acts as glue to hold
skin together
Inflammatory response builds
Blood clot dissolved
Granulation tissue forms where clot was
Epithelium regenerates
Wound Healing Secondary Intention
Skin edges cannot be held together
Similar to primary intention
Takes longer
Involves more granulation tissue and regeneration
May form underneath a scab
May show pinpoint bleeding
Factors Affecting Wound Healing
Necrotic or foreign tissue in wound
Wound infection
Excessive movement
Dehiscence – breaking open of a surgical wound
Wound Management
For wounds that heal by primary intention, it is
common to convert the incision with dry, sterile
dressings. Medicated sprays that form a transparent
film on the skin may be used for dressings on a
clean incision on injury.
Sometimes a surgeon will leave a surgical wound
uncovered.
Wound healing management by secondary intention
depends on the wound etiology and type of tissue in
the wound. (red-yellow-black concept of wound
care)
IMMUNE SYSTEM
It is a complex and intricate network of specialized
cells, tissues, and organs.
It is closely related to the circulatory system, the
blood and tissue fluid do not only carry nutrients to
the body cells but also carry substances that defend
the body against disease.
Cells of the immune system seek out and destroy
damaged cells and foreign tissue, yet recognize and
preserve host cells. (Porth, 2002)
Functions of the Immune System
Defense - Defending and protecting the body from
infection by bacteria, viruses, fungi and parasites by
attacking foreign antigens and pathogens.
Homeostasis - Removing and destroying damaged
or dead cells. Through this mechanism the body’s
different cell types remain uniform and unchanged.
Surveillance- Identifying and destroying malignant
cells, thereby preventing their further development
into tumor. (mutations continually arise in the body
but are normally recognized as foreign cells and are
eventually destroyed.)
Components of Immune System
Specialized blood cells (lymphocytes and
macrophages)
Specialized structures ( lymph nodes, spleen,
thymus, bone marrow, tonsils, adenoids and
appendix)
Immunity
Refers to the body’s capacity to resist invading
organisms and toxins, thus preventing tissue and
organ damage.
It is a state of responsiveness to foreign substances
such as microorganisms and tumor proteins.
Bone Marrow Components
Differentiation and Maturation
Three basic defense strategies of Immune system
Physical and chemical barrier to infection
Inflammatory response
Immune response
Acquisition of Immunity
Natural/Innate Immunity –aka primary immune
response: refers to the individual who is born with
the ability to resist certain types of agents without
apparent contact with an antigen (Example: high
natural resistance to cold)
Acquired immunity – aka secondary immune
response: refers to the resistance of an individual to 1. B-cells
specific infectious organisms, which develop either
actively or passively during the course of an 2. T-cells
individual’s life.
B cells or B lymphocytes
Types of Immunity Stem cells of bone marrow ------------- B cells
Nonspecific defenses
Produce antibody and oversee Humoral
Specific defenses Immunity

Types of Acquired Specific Immunity An invading antigen causes B cells to divide and
ACTIVE differentiate into plasma cells
Types of Immunity Each plasma cells produces and secretes large
Nonspecific defenses – operate in the same way amounts of antigen-specific immunoglobulins
against all disease-causing microorganisms. (SKIN & (Ig) into the bloodstream
MUCOUS MEMBRANES)

Provides mechanical barrier against the pathogens. Immunoglobulins

Plasma Cells and Memory
Phagocytosis – engulfing and digestion of pathogens B cells and the Humoral Immunity
B cells carry the pattern of the “non-self” antigen
Interferon - inactivates virus by preventing them to a lymph node
from reproducing
B cells then transforms into a plasma cell ----
manufacture proteins that exactly fit the “non-self”
surface marker of the antigen. These are
antibodies.
Specific defenses – defend body against specific
pathogens. Each antibody combats just one specific antigen.
This antibody is the circulating antibody which
WBC- Lymphocytes moves through the body fluids.
Two types of Lymphocytes:
When the antigen is located, the antibody hooks on
 and signals phagocytes to surround and destroy the Helper T cells-( CD4) serve as managers, directing the immune
antigen. response. They secrete the chemical called lymphokines that
stimulate T cells and B cells to grow, divide and attract
A molecule that causes an immune response is an neutrophils and enhance the ability of macrophages to engulf
antigen. and destroy microbes.

T cell or T lymphocytes Suppresor T cells- (CD8) inhibit the production of cytotoxic T

Cells that migrate from the bone marrow to the
thymus differentiate into T lymphocytes (Thymus-
dependent cells). T cells live from a few months to
the life span of an individual and account for long-
term immunity. All mature T cells have the CD3
antigen.
cells once they are unneeded.
Both CD4 and CD8 are involved in the regulation of
cell-mediated immunity and the humoral antibody
response.

T cells and the Cell-Mediated Immunity T h e h u m a n i m m u n o d e ficiency vir us (HIV) invades T

T cells do not produce circulating antibodies. They
helper cells (CD4), thus decreasing their number and
carry cellular antibodies on their surface.
function. Therefore individuals with HIV infection do
not mount an aggressive response and are at an
Once the T cells recognize a “non-self” marker, the
increased risk for opportunistic infections and
cellular antibodies latch onto an antigen.
malignancies.
The T cells then direct the phagocytes to surround
and destroy the foreign substances.
4. Natural killer cells – are also involved in cell-
mediated immunity. These cells are not T or B cells,
The T cells can recognize body cells that have been
but are large lymphocytes with numerous granules in
invaded by cancer and certain viruses, thus allowing
the cytoplasm. NK cells have a significant role in
T cells to launch a defense.
immune surveillance for malignant cell changes.
Kinds of T cells
Altered Immune Response
Fights the “non-self” markers in the body
Hypersensitivity Reactions: ACIDS
Cytotoxic T cells- fight diseases by releasing lymphotoxins/
Anaphylactic
cytolytic substances, which in turn causes lysis of the cell
Cytotoxic
Immune-complex
Delayed hypersensitivity
Stimulatory
Types of Hypersensitivity Reactions
Type 5: Stimulatory Reactions – inappropriate
stimulation of normal cells’ surface
Immunodeficiency
Abnormality that renders a person susceptible to diseases
normally prevented by an intact immune system.
Four categories of immune mechanisms: 1. humoral or
antibody-mediated immunity; 2. cell-mediated immunity;
3. complement system; 4. phagocytosis
Primary Immunodeficiency Disorders
Primary immunodeficiency
congenital or inherited abnormalities of immune function
that render a person susceptible to diseases normally
prevented by an intact immune system
Disorders of B-cell function impairs the ability to produce
antibodies and defend against microorganisms and toxins
that circulate in the body fluids
Primary Immunodeficiency Disorders
Disorders of T-cell function impair the ability to
orchestrate the immune response (CD4+ helper T cells)
and to protect against fungal, protozoan, viral and
intracellular bacterial infections (CD8+ cytotoxic T cells)
Combined T-cell and B-cell immunodeficiency represents
a life-threatening absence of immune function that
requires bone marrow transplantation for survival
States of Immunodeficiency
Humoral (B-cell) immunodeficiency
Primary: Transient hypoglammaglobulimia of infancy;
Secondary: Increased loss of immunoglobulins (nephrotic
syndrome)
States of Immunodeficiency
Cellular (T-cell) Immunodeficiency
Primary: DiGeorge syndrome; Nezelof syndrome
Secondary: Hodgkin’s disease; AIDS
Combined B-cell and T-cell immunodeficiency
Primary: Wiskott-Aldrich syndrome; ataxia-
telangiectasia
 Secondary: irradiation; Aging Antipruritic drugs

Mast cell-stabilizing drugs

States of Immunodeficiency Antihistamines

Complement Disorders Best drug treatment for allergic rhinitis and urticaria

Primary: Angioneurotic edema Sympathomimetic/decongestant drug

The major sympathomimetic drug is
Epinephrine (Adrenalin), which is the DOC to
treat an anaphylactic reaction.
Secondary: Acquired disorders that involve complement
utilization
Several specific, minor sympathomimetic drugs
differ from epinephrine because they can be taken
orally or nasally and last for several hours. Used
Phagocytic Dysfunction primarily to treat allergic rhinitis.

Primary: Chronic granulomatous disease; G6PD - Phenylephrine (Neo-synephrine)

Secondary: Drug induced; Diabetes Mellitus - Pseudoepheride (Sudafed)

Corticosteroids
Oral
Case Management
Drug Therapy: A SCAM Nasal – nasal corticosteroid spray effective in
relieving symptoms of allergic rhinitis
Immunotherapy
Therapeutic Uses
Drug Therapy: A SCAM Rheumatoid Arthritis
Antihistamine
SLE
Sympathomimetic/Decongestant drug
Inflammatory Bowel Disease (IBD)
Corticosteroids
Miscellaneous Inflammatory D/Os Glucocorticoids used for non-Endocrine purposes
Pharmacologic Actions
Allergic conditions (not acute anaphylaxis)
Anti-inflammatory and Immune effects
Asthma
Inhibit prostaglandin, leukotriene, and histamine
Dermatologic disorders synthesis

Neoplams Suppress infiltration of phagocytes

Transplant rejection Suppress proliferation of lymphocytes

Preterm infant Effects on Metabolism and Electrolytes

Glucose levels rise

Protein synthesis suppressed

Immunosuppressive effect
Cause lysis of activated B and T cells Fat deposits mobilized

Sequester T cells Fewer electrolyte effects, but can inhibit calcium

absorption
Reduce IL-2 production

Reduce responsiveness to IL-1

Glucorticoids Adverse Effects
Immunosuppressive doses are large, e.g. Adrenal insufficiency

Methylprednisolone Osteoporosis: long term therapy

Anti-immune doses: 500 – 1500mg (IV) Infection

Anti-inflammatory doses: 5 – 60mg (IV) Glucose intolerance

Myopathy
F&E disturbance – used with great caution due to associated risk of
agranulocytosis
Growth retardation
Mast cell-stabilizing drugs
Psychological disturbances Inhibit the release of histamines, leukotrienes and
other agents from the mast cell after antigen-IgE
interaction

Glucocorticoids Adverse Effects Used in the management of asthma and treatment

Cataracts and Glaucoma of allergic rhinitis
Peptic Ulcer Disease Very low incidence of side effects
Iatrogenic Cushing’s Disease Available as inhalant nebulizer solution, nasal spray,
or an oral pill
Ischemic Necrosis – especially caution with ETOH
- Cromolyn sodium (Intal, Nasalcrom, Rynacrom

- Nedocromil (Tilade)
Antipruritic drugs
These drugs protect the skin and provide relief from Calcineurin Inhibitors
itching. Calcineurin is needed to produce IL-2
Over the Counter: Calamine lotion, coal tar solution
Without IL-2, T-cells cannot proliferate, so cannot
and camphor
mount an immune response
Menthol and phenol maybe added to other lotions to Used for transplant graft rejection
produce antipruritic effect
Drugs Cyclosporine: nephrotoxicity, infection
More potent drugs that requires Rx:
Kidney, liver, heart transplant
Methdilazine (Tacaryl)
Psoriasis, rheumatoid arthritis
Trimeprazine (Temaril)
Tacrolimus (FK506): same Tourniquets

IV tubing

Cytotoxic Drugs Syringes

Kill proliferating B and T cells
Electrode pads
Are non-specific: kill all rapidly dividing cells (red
blood cells, skin, epithelial cells) O2 masks

Azathioprine: Adjunct transplant Tracheal tubes

Cyclophosphamide: cancer, SLE, MS Colostomy and ileostomy pouches

Methotrexate: cancer, psoriasis, arthritis Urinary catheters

Mycophenolate Mofetil: selective, transplant Anaesthetic masks

Adhesive tape

Immunotheraphy
Involves administration of small titers of an allergen
extract in increasing strength until hyposensitivity *Latex protein can be aerosolized through
to the specific allergen is achieved. powder on gloves and can result in serious
reactions when inhaled by sensitized
For best results, the patient should continue to avoid individuals.
the offending allergen whenever possible because
Two types of Latex Allergies
complete desensitization is impossible.
Type 4 allergic contact dermatitis
Latex Allergies
Gloves* Type 1 allergic reaction

Blood pressure cuffs Type 4 allergic contact dermatitis

Caused by chemicals used in manufacture of latex
Stethoscopes gloves
 Occurs within 6-48 hours
Chronic exposure can lead to lichenification, scaling
and hyperpigmentation.
The dermatitis extend beyond the area of physical
contact with the allergen
S/Sx: dryness, pruritus, fissuring, cracking of the skin
followed by redness, swelling and crusting at 24-48
hours.
Type 1 allergic reaction
Response to a natural rubber later proteins and
occurs within minutes of contact with the proteins.
Systemic reactions to latex may result from exposure
to latex protein via various routes, including skin,
mucous membranes, inhalation or blood.
S/Sx: various reactions from skin redness, urticaria,
rhinitis, conjunctivitis, or asthma to full-blown
anaphylactic shock
Recommendations for preventing allergic reactions to latex in
the workplace:
Ask patient regarding known allergy to latex
Use nonlatex gloves for activities that are not likely
to involve contact with infectious materials (food
preparation, house keeping)
Use powder-free gloves with reduced protein content
Do not use oil-based had creams or lotions when
wearing gloves
After removing gloves, wash hands with mild soap
and dry thoroughly
Frequently clean work areas that are contaminated
with latex containing dust.
Know the symptoms of latex allergy, including skin
rash, hives, flushing, itching; nasal, eye or sinus
symptoms; asthma and shock
If symptoms of latex gloves develop, avoid direct
contact with latex gloves and products.
Wear a medical alert bracelet and carry an
epinephrine pen (EpiPen)
Inflammation versus Immunity
Inflammation is nonspecific, nonadaptive
Immunity is specific (to select antigens), adaptive
Inflammation allows immunity to happen
Immunity controls inflammation
Nursing Diagnoses
Risk for infection
Expected outcomes

Patient remains free from signs and symptoms of

infection

Patient maintains adequate respiratory function

Patient states ways to prevent infection, including

proper handwashing and good personal hygiene.

Ineffective coping –may be related to perceived or

impending personal loss, may be associated with life-
threatening immunodeficiency disorders.

Expected outcomes –

Patient identifies mechanisms for coping effectively

Patient demonstrates an active role in self-care

activities

Patient identifies appropriate resources to maximize

his status.