Alters cell membrane

Permitting fluid to enter the cell

Cell lysis

Cell death
3 Physiologic functions
1. Defending the body against bacterial infection
2. Bridging natural and acquired immunity
3. Disposing immune complexes and the byproducts associated with inflammation

Compliment-Mediated Immune Responses

Response Effects
Cytolysis Lysis and destruction of cell membranes of body cells or pathogens
Opsonization Targeting of the antigens so that it can be easily engulfed and digested by
the macrophages and other phagocytic cells
Chemotaxis Chemical attraction of neutrophils and phagocytic cells to the antigen
Anaphylaxis Activation of mast cells and basophils with release of inflammatory mediators
that produce smooth muscle contraction and increased vascular permeability

Activation of Compliment System

1. Classic pathway
2. Alternate pathway
Interferons
• It is a biologic response modifiers, have antiviral and anti-tumor properties
• Responds to viral infection
• Modifies the immune response by suppressing antibody production and cellular immunity
• Facilitates cytolytic role of macrophages and NK cells

I. Inflammation and Infection

A. Inflammation
Inflammation is a nonspecific, defensive response of the body to tissue damage. It is an attempt to dispose of microbes,
toxins, or foreign material at the site of injury, to prevent their spread of to other tissues, and to prepare the site for tissue repair
and restore homeostasis.
Four character signs snd symptoms:
• Redness- inflamed tissue appears red, e.g., skin affected by sunburn, due to dilation of small blood vessels within the
damaged area
• Pain- results partly from the stretching and distortion of tissues due to edema and, in particular, from pus under pressure
• Heat- an increase in temperature is seen in peripheral parts of the body, such as the skin. It is due to increased blood
flow to the area as a result of vascular dilation and the delivery of warm blood to the area.
• Swelling- results from edema (accumulation of fluid in the extra vascular space)
• Loss of function
Three basic stages:
1. Vasodialtion and increased permeability of blood vessels
• Vasodilation allows more blood to flow through the damage area.
• Increased permeability permits defensive proteins such as antibody and clotting factors to enter the injured area from the
blood.
• The increased blood flow also helps remove microbial toxins and dead cells.
Substances that contribute to inflammatory response:
• Histamine. In response to injury, mast cells in connective tissue and basophils and platelets in blood releasing
histamine. Neutrophils and macrophages attracted to the site of injury also to stimulate the release of histamine, which
causes vasodiation and increased permeability of blood vessels.
• Kinins. Induce vasodilation and increase permeability and serve as chemotactic agents for phagocyte.
• Prostaglandins (PGs). Released by damaged cells and intensify the effects of histamine and kinins. It also stimulates
the emigration of phagocytes through capillary walls.
• Leukotrines (LKs). Produced by basophils and mast cells by breakdown of membrane phospholipids. Also caused
increased permeability and adherence of phagocytes to pathogens and as chemotatic agents that attract phagocytes.
• Complement. Different components of complement system stimulate histamine release, attract neutrophils by
chemotaxis, and promote phagocytosis; some components can also destroy bacteria.

 Dilatation of arterioles and increased permeability produce three of the symptoms of inflammation, heat, redness, and
swelling. Heat and redness results from the large amount of blood that accumulates from the damaged area. Edema
 results from increased permeability of blood vessels, which permits more fluid to move from blood plasma into tissue
spaces.
 Pain is a prime symptom of inflammation that results from injury to neurons and from toxic chemicals released by
microbes. Kinins affect some nerve endings, causing much of the pain. Prostaglandins intensify and prolong the pain
associated with inflammation, pain may also be due to increased pressure from edema.
 The increased permeability of capillaries allows leakage of blood clotting-factors into tissues. The clotting cascade is set
into motion, and fibrinogen is ultimately converted to an insoluble thick mesh of fibrin threads that localizes and traps
invading microbes and blocks their spread.

2. Emigration (movement) of pahagocytes from the blood into instertitial fluid

• Within an hour after then inflammatory process starts, phagocytosis occurs.
• Neutrophils begin to stick to the inner surface of endothelium of blood vessels to reach the damaged area.
• Neutrophils attempt to destroy the the invading microbes by phagocytosis
• A steady stream of neutrophils is ensured by the production and release of additional cells from bone marrow.
• Leukocytosis occurs such an increase in WBC in the blood

3. Tissue repair
• Pus formation occurs and continues until the infection subsides and damaged tissues are repaired subsequently.
Bacterial invasion or tissue damage

Release of histamine by mast cells (plus chemotaxins by damaged cells)

Arterial vasodilation & Increased capillary permeability

Increased blood flow to tissue & accumulation of fluid

Increased numbers of phagocytes & more clotting factors into surrounding tissues

Defense against foreign invader plus 'walling off' of inflamed area

Infection
A. Components of the Infectious cycle
1. Infectious Agent
Types:
a. Bacteria – most significant and most prevalent in hospital settings
i. Spherical (cocci), rod shaped (bacilli), corkscrew shaped (spirochetes)
ii. Gram positive or gram negative (based on reaction to gram stain)
iii. Aerobic or anaerobic (based on need for oxygen)
b. Virus – smallest of all microorganism
c. Fungi – plantlike organisms present in air, soil, and water
Factors Affecting an Organisms Potential to produce Disease
a. Number of organisms
b. Virulence
c. Competence of person’s immune system
d. Length and intimacy of contact between person and microorganism

2. Reservoir – natural habitat of the organism

a. Other humans, animals, soil
b. Food (water, milk)
c. Inanimate objects
Bacterial Flora
a. Transient – attached loosely on skin, removed with relative ease
b. Resident – found in creases of the skin, requires friction with brush to remove

3. Portal of exit – point of escape for organisms

a. Respiratory, GIT, genitourinary tracts
b. Break in the skin, blood and tissue

4. Means of transmission – direct contact, indirect contact, airborne route

5. Portal of entry – point at which organisms enter a new host
6. Susceptible host – must overcome resistance mounted by host’s defenses
Factors affecting Host’s Susceptibility
a. Intact skin and mucous membrane
b. Normal pH level
c. Body’s white blood cell
d. Age, sex, race, hereditary factors
e. Immunization, natural or acquired
f. Fatigue, climate, nutritional and general health status
 g. Stress
h. Use of invasive or indwelling medical devices

B. Stages of Infection
1. Incubation period – organisms growing and multiply
2. Prodromal stage – person is most infectious, vague and non-specific signs of defense
3. Full stage of illness – presence of specific signs and symptoms of disease
4. Convalescent period – recovery from the infection

C. Types of Infection
1. Colonization
2. Local vs. Systemic
3. Acute vs. Chronic
4. Nosocomial Infections
Predisposing Factors:
a. Use of invasive medical devices
b. Antibiotic- resistant organisms developed in hospitals

D. Signs and Symptoms of Infection

Fever Increased pulse and respiratory rate
Inflammatory symptoms Pain
Purulent drainage Enlarged lymph nodes
Rash Gastrointestinal symptoms
V. Assessment, Diagnostics and Medical and Nursing Management of Immune Alterations

A. Assessment and Management of Patients with Allergic Reactions

Allergy: inappropriate and often harmful immune system response to substances that is normally
harmless

Allergen: substance that causes manifestations of allergy

Atopy: term often used to describe IgE mediated diseases; genetically determined allergic disorders

Allergic Reaction: Physiologic Overview

• One of the most effective defense mechanisms is the body’s capacity to equip itself rapidly with weapons (antibodies)
individually designed to meet each new invader, namely specific protein antigens.
• The antibodies prepare the antigens so that the phagocytic cells of the blood and the tissues can dispose of them. In
some cases, however, the body produces inappropriate or exaggerated responses to specific antigens, and the result is
an allergic or hypersensitivity disorder.
• An allergic reaction is a manifestation of tissue injury resulting from interaction between an antigen and an antibody.
• Common allergic reactions occur when the immune system of a susceptible persons responds aggressively to a
substance that is normally harmless (eg., dust, weeds, pollen, dander)
• In allergic reaction, the production of antigen specific IgE antibodies requires active communication between
macrophages, T cells and B cells.

Chemical Mediators

Mast cells, which have a major role in IgE-mediated immediate hypersensitivity, are located in the skin and mucous membranes.
When mast cells are stimulated by antigens, powerful chemical mediators are released that cause a sequence of physiologic
events resulting in symptoms of immediate hypersensitivity

Types:
1. Primary: preformed and found in mast cells or basophils
a. Histamine
i. Histamine is an organic nitrogen compound involved in local immune responses as well as regulating
physiological function in the gut and acting as a neurotransmitter.
ii. Histamine triggers the inflammatory response. As part of an immune response to foreign pathogens, histamine
is produced by basophils and by mast cells found in nearby connective tissues.
iii. Histamine increases the permeability of the capillaries to white blood cells and other proteins, in order to allow
them to engage foreign invaders in the infected tissues.

Type Location Function

H1 histamine Found on smooth muscle, endothelium, and Causes, bronchoconstriction, bronchial
receptor central nervous system tissue smooth muscle contraction, separation
of endothelial cells (responsible for
hives), and pain and itching due to
insect stings; the primary receptors
involved in allergic rhinitis symptoms
and motion sickness; sleep regulation.
H2 histamine Located on parietal cells and vascular Primarily involved in vasodilation. Also
receptor smooth muscle cells stimulate gastric acid secretion
H3 histamine Found on central nervous system and to a Decreased neurotransmitter release:
receptor lesser extent peripheral nervous system histamine,acetylcholine,norepinephrine,
tissue serotonin
H4 histamine Found primarily in the basophils and in the Plays a role in chemotaxis.
receptor bone marrow. It is also found on thymus,
small intestine, spleen, and colon.

b. Eiosinophil Chemotactic Factor of Anaphylaxis

i. Preformed in the mast cells
ii. Affects movement of eosinophils (granular leukocytes) to the site of allergens
iii. released upon degranulation to inhibit the action of leukotrienes and histamine.
c. Platelet Activating Factor (PAF)
i. Responsible for initiating platelet aggregation at sites of immediate hypersensitivity reactions.
ii. Causes bronchoconstriction and increased vascular permeability.
iii. Activates factor XII, or Hageman factor, which induces the formation of bradykinin.
d. Prostaglandins
i. Composed of unsaturated fatty acids, produce smooth muscle contraction as well as vasodilation and increased
capillary permeability.
ii. The fever and pain that occur with inflammation are due in part to the prostaglandins.

2. Secondary: inactive precursors formed or released in response to primary mediators.

a. Leukotrienes
i. Chemical mediators that initiate the inflammatory response.
ii. They are metabolites released by mucosal mast cells.
iii. Cause smoothmuscle contraction, bronchial constriction, mucus secretion in the airways, and the typical wheal
and flare reaction of the skin
iv. Compared with histamine, leukotrienes are 100 to 1,000 times more potent in causing bronchospasm.

b. Bradykinin
i. Is a polypeptide with the ability to cause increased vascular permeability, vasodilation, hypotension, and
contraction of many types of smooth muscle, such as the bronchi.
ii. Increased permeability of the capillaries results in edema.
iii. Bradykinin stimulates nerve cell fibers and produces pain.
c. Serotonin
i. Serotonin is released during platelet aggregation, acting as a potent vasoconstrictor and causing contraction of
bronchial smooth muscle.

Hypersensitivity
• Is an abnormal exaggerated response to a specific indicator that leads to an overactive
immune response.
Types
1. Type I: Anaphylactoid reactions

a. Type I involves an immediate response; however, the potential responses can be cumulative; for
example, the initial or sensitizing response, but subsequent contacts, even if not long-term in nature,
may cause a stronger response than the previous insult.
b. Etiology/pathophysiology: Type 1 involves the characteristic activation of IgE bound to mast cells,
whereby histamine is released.
c. Clinical manifestations range from bronchospasm, wheezing, rhinorrhea and urticaria to angioedema
and finally anaphylaxis; there may be progression from local to systemic reactions; characteristic allergic
“gape” (open mouth from nasal obstruction causing mouth breathing) and allergic “shiner” (dark areas
under the eyes in patients with rhinitis) can be seen in individuals with atopy (allergic reactions
stemming from hereditary disposition)
d. Diagnostic and laboratory test findings: Immunoglobulin titers are predictive of potential allergen
response; skin and patch testing are performed to determine potential allergens.
e. Therapeutic management
 Antihistamine medications such as diphenhydramine (Benadryl) are used to block chemical release of mediators
(histamines)
 Mast cell degration inhibitors such as cromolyn sodium (Intal) also are used to block the chemical response
 Decongestant and cortecosteroids can help to minimize the immune response; however, in potential
anaphylactic reactions, the use of epinephrine is warranted; Epipen may be prescribed as appropriate therapy
for individuals who are at profound risk for hypersensitivity reactions.
f. Nursing implications
 Immediately withdraw the offending allergen in presence of documented and suspected reaction.
 Manage the client according to ABC protocol (airway, breathing, and circulation)

2. Type II: Cytotoxic and cytolytic reactions

 a. This type of immunity involves the activation of compliment and is considered a form of humoral
immunity
b. Etiology and pathophysiology
 Involves the production of autoantibodies that result in destruction of one’s own cells or tissues
 IgA and IgM are involved in this type of response and the complement system is activated
c. Clinical manifestations: a wide range of presentations occur ranging from hemolytic reactions (such as
transfusion, erythroblastosis fetalis, hemolytic anemia, and drug-induced hemolysis) to target cell
destruction as seen in Goodpasture’s syndrome (an autoimmune disease affecting pulmonary and renal
systems) and other autoimmune disease processes such as myasthenia gravis and Grave’s disease
d. Diagnostic and laboratory test findings: Coombs blood test can define the presence of hemolytic anemia
and identify potential ABO incompatability
e. Therapeutic management: use of proper identification during blood product administration can help to
prevent exposure and sensitization; recognition of certain blood types and awareness that potential drug
interactions can cause antigen complex activation can lead to early detection of reaction.
f. Nursing implications
1. Be sure to remain in the room during the first 15 minutes of any blood product administration since clients are most likely
to experience a reaction during this time frame.
2. Make sure to follow agency policy and procedure for the administration of any and all blood products; two RN’s must
verify the product before administration

3. Type III: Immune complex reactions

a. A Type III reaction involves the formation of antigen-antibody complexes (a binding together of an antibody and an
antigen)
1.) These leads to the activation of serum factors, causing inflammation and leading to activation of
the complement cascades
2.) Rheumatoid arthritis and systemic lupus erythematosous are examples of type III reactions
3.) The deposition of the antigen-antibody complexes in body tissues is not localized and therefore
can result in more extensive tissue or organ destruction

b. Etiology and pathophysiology: compliment activation impacts vulnerable organs and leads to intravascular changes
c. Clinical manifestation
1.) Arthrus reaction involves a localized inflammatory response with excess IgG causing edema and necrotic tissue
2.) Serum sickness involves a systemic response leading to the deposit and activation of compliment throughout the body
that can be demonstrated as joint pain, pyrexia, and/or lymphadenopathy
3.) Reactions can be acute or chronic in nature
d. Diagnostic and laboratory test findings: complement assays provide diagnostic and predictive indicators of the acute
and/or chronic nature of the process; erythrocyte sedimentation rate (ESR) is elevated, proteinuria may be found on
urinalysis
e. Therapeutic management: analgesics, antihistamines, and topical steroids may provide symptom relief; the disease
process itself is usually self-limiting because of the use of human anti tetanus serum and the availability of antibiotics
f. Nursing implications:
1.) Be aware that it is possible for localized inflammatory reactions to develop at the site of serum injections after 1 week;
this can be followed by a more systemic response involving both regional as well as generalized lymphadenopathies
2.) If symptoms arise, monitor client for potential complications; this is specially important because organ damage can occur
and the kidneys can be compromised

4. Type IV: delayed hypersensitivity reactions

a. Type IV is a form of cell-mediated immunity involving T lymphocytes; it is considered a

delayed response
b. Etiology and pathophysiology: delayed hypersensitivity reactions involve the recognition
response of T lymphocytes to foreign substances.
c. Clinical manifestations
1.) There is a wide range of presentation from tuberculin response, poison ivy, and contact dermatitis to transplant or graft
rejection; edema , ischemia, and eventual tissue destruction may ensue
2.) Pyrexia, pain, edema, and failure of the transplanted organ characterize transplant rejection
d. Diagnostic and laboratory tests findings: purified protein derivative (PPD) test result of
induration >5 mm identifies Type IV hypersensitivity to the tubercle bacillus; abnormal tests
results indicating declining function of the transplanted organ are used to diagnose
transplant rejection.
e. Therapeutic management
1.) Monitor client for evidence of potential transplant rejection
2.) Medicate the patient with immunosuppressive protocol drugs to prevent tissue rejection
3.) Identify potential irritants that can cause contact dermatitis and avoid exposure
f. Nursing implications
1.) Make sure that the client avoids the offending irritant as a past exposure has been documented
 2.) Use topical and oral medications as indicated to alleviate many of the symptom complaints and increase
client comfort

Management of Patients with Allergic Reactions

ASTHMA (Extrinsic)
Description
• An episodic respiratory disease, asthma is associated with bronchospasm triggered by exposure to certain allergens.
• It is related to IgE- mediated hypersensitivity reactions
Etiology

1. Extrinsic asthma results from allergic reactions to inhalants, such as perfumes, flowers, dust, molds, and spores.
a. It may be genetically transmitted
b. Onset usually occurs in childhood, but adult onset asthma also occurs
2. Allergens that can trigger asthmatic episodes include pollens, dust, animal fur, and pollutants; episodes typically occur
seasonally.
3. Stress may precipitate asthma attack

Pathophysiologic processes and manifestations

1. Airways become hyperactive due to the allergen-antibody interaction.
2. IgE-bound mast cells rupture and spill their contents including histamine and chemotactic factors
3. Increased vascular permeability and movement of inflammatory cells into the airways causes edema formation and the
production of thick tenacious exudates.
4. The increased exudates blocks off smaller airways and causes air trapping, which contributes to ventilation-perfussion
abnormalities and increased work of breathing
5. Airway obstruction also contributes to impaired expiration and subsequent hyperinflation.
6. Hypoxemia and respiratory acidosis also may occur
7. Sypmtoms can include:
a. Wheezing on auscultation
b. Dyspnea
c. Increased mucus production
d. Increased work of breathing
e. Tachypnea
f. Shortness of breath
g. Nonproductive cough
h. Cardiovascular manifestations, including tachycardia and mild hypertension
i. Use of accessory muscles

Interventions

1. Acute episodes
a. Assess airway patency
b. Administer humidified oxygen by nasal prongs or face mask
 c.
Continiously monitor respiratory status, pulse oximetry, and color; be alert to decrease wheezing or a silent chest,
which may signal the inability to move air
d. Initiate an intravenous line, and prepare to correct dehydration, acidosis, or electrolyte imbalances
e. Prepare the child for a chest radiograph
f. Prepare to obtain samples for determining arterial blood gases and serum electrolytes
2. Quick relief (Rescue medications)
a. Short acting B2-antagonists
b. Anticholinergics (for relief of acute bronchospasm)
c. Systemic corticosteroids (for its inflammatory action to treat reversible airflow obstruction)
3. Long-term control (Preventive Medications)
a. Corticosteroids
b. Antiallergic medications
c. Nonsteroidal anti-inflammatory drugs
d. Long-acting B2-agonist
e. Leukotriene modifiers to prevent bronchospasm and inflammatory cell infiltration
f. Long acting bronchodilators
g. Nebulizer, metered-dose inhaler, or peek expiratory flow meters
h. Chest physiotherapy (not recommended during acute exacerbations)
i. Allergen control

ANAPHYLAXIS

Description
• Anaphylaxis is a clinical response to an immediate (type I hypersensitivity) immunologic reaction between a specific
antigen and an antibody.
• Anaphylaxis is a serious and dramatic allergic reaction with the release of histamine from the damaged cells
• Anaphylaxis can cause shock and death if not treated immediately
Assessment
• Identification of the allergy
• Difficulty breathing
• Difficulty swallowing
• Complains of swollen tongue
• Facial edema and swelling of lips
• Skin redness
• Presence of rash

Anaphylactic shock
• A type of distributive shock; a severe life threatening allergic reaction to an antigen or other agent
• Characterized by respiratory distress and vascular collapse; onset typically is sudden

1. Common causes include:

a. Reactions to drugs, such as penicillin and hormones
b. Stings from insects, such as bees and wasps
c. Ingestion of certain foods, such as peanuts and shellfish
2. Anaphylactic shock is considered a Type-I hypersensitivity response that most commonly involves IgE.
3. Symptoms
a. Alteration in mentation, including restlessness progressing to coma
b. Cutaneous manifestations, including urticaria, pruritus and angioedema
c. Bronchoconstriction, accompanied by tachypnea, wheezing and use of accessory muscles
d. Hemodynamic manifestations, including warm and flushed skin, tachycardia, dysrhythmias, angina, and hypotension

Interventions
1. Establish a patent airway
2. Prepare for administration of epinephrine (Adrenalin), diphenhydramine hydrochloride (Benadryl) to promote
vasoconstriction as prescribed
3. Provide measures to control shock
4. Prepare the patient for endotracheal intubation as indicated
5. Administer fluids and vassopressors as prescribed
6. Administer cortecosteroids, as prescribed to reduce inflammatory response associated with exposure to the allergen
7. Provide support as indicated

ALLERGIC RHINITIS

• Allergic rhinitis (inflammation of nasal mucosa; hay fever, chronic allergic rhinitis, pollinosis) is the most common form of
respiratory allergy presumed to be mediated by an immediate (type I hypersensitivity) immunologic reaction.
• Induced by airborne pollens or molds
• When untreated, many complications may result, such as allergic asthma, chronic nasal obstruction, chronic otitis media
with hearing loss, anosmia (absence of the sense of smell), and, in children, orofacial dental deformities.
Clinical Manifestations
• Nasal congestion
• Clear, watery nasal drip
• Intermittent sneezing
• Nasal itching
• Dry cough and hoarseness
• Headache
• Pain over paranasal sinuses
• Epistaxis
• May affect quality of life by producing fatigue, loss of sleep and poor concentration

Assessment and Diagnostic Findings

• Nasal smears
• Peripheral blood count
• Total serum IgE
• Food elimination
• Intradermal testing
• Radioallergosorbent test (RAST)
• Result: Increased IgE and eisinophil levels; + reactions to allergen testing

Interventions
1. Remove the allergens that act as precipitating factors
2. Antihistamines, H1-receptor antagonists (or H1-blockers)
a. S/E: sedation, nervousness, tremors, dizziness, dry mouth, palpitations, anorexia, nausea & vomiting
3. Adrenergic decongestants (Sudafed): vasoconstrictors of mucosal membrane
4. Mast cell stabilizers: Intranasal cromolin sodium (Nasalcrom)
a. Reduces the release of histamine and other mediators of the allergic response
5. Cortecosteroids (anti-inflammatory): indicated in more severe cases of allergic and perennial rhinitis that cannot be
controlled by conventional medications.
a. Beclomethasone (Beconase, Vancanase)
b. budesonide (Rhinocort)
c. dexamethasone ( Decadron Phosphate Turbinare) etc…
6. Immunotherapy
a. Allergen desensitization (allergen immunotherapy): used to treat IgE-mediated diseases
b. Used when avoidance is not possible
c. Methods of injection therapy:
i. Coseasonal- during season
ii. Preseasonal- 2 to 3 months before symptom is expected
iii. Perennial- administered all year round

LATEX ALLERGY

Description
• Latex allergy is a hypersensitivity to latex
• The source of allergic reaction is thought to be due to the proteins in the natural rubber latex or the various chemicals
used in the manufacturing process of latex from a liquid substance into the finished product
• Symptoms of allergy can range from mild contact dermatitis
• To moderately severe symptoms of rhinitis, conjunctivitis, urticaria, and bronchospasm to severe life-threatening
anaphylaxis

Common routes of exposure

1. Cutaneous: natural latex gloves
2. Percutaneous and parenteral: intravenous lines and catheter; hemodialysis equipment
3. Mucosal: use of latex condoms, catheters, airways and nipples
4. Aerosol: aerosolization of powder from latex gloves can occur when gloves are dispensed from the box or when gloves
are removed from the hands

Assessment
1. Anaphylactic hypersensitivity
a. Rapid onset
b. Urticaria, wheezing, dyspnea, laryngeal edema, bronchospasm, tachycardia, angioedema, hypotension and cardiac
arrest
2. Delayed –type hypersensitivity: symptoms of contact dermatitis such as pruritus, edema, erythema, vesicles, papules,
and crusting and thickening of the skin
  Assess individuals allergic to kiwis, bananas, pineapples, tropical fruits, avocados, potatoes and chestnuts. They are at
risk individuals.

Diagnostics
• Skin testing
• RAST
• ELISA

Interventions
1. Use nonlatex glove and latex-safe supplies
2. Keep a latex safe supply cart near the client’s room
3. Apply a cloth barrier to the client’s arm under a blood pressure cuff
4. Use latex-free syringes, medication containers (glass ampules) and latex –safe intravenous equipment

CONTACT DERMATITIS

Description
• A type IV delayed hypersensitivity reaction
• A skin inflammation caused by exposure either an allergenic substance or an irritant; duration of exposure may be short
or prolonged
• The disorder becomes chronic with successive recurrences
• Four basic types:
o Allergic
o Irritant
o Phototoxic
o Photoallergic

Clinical Manifestations
• Itching
• Burning
• Erythema
• Skin lesions (vesicles)
• Edema
• Crusting
• Dryness and peeling of skin
• Pigmentary changes

Assessment and Diagnostic Findings

• Patch test on the skin with suspected offending agents may clarify the diagnosis

Interventions

1. Assist with identification of the allergic substance or irritant; instruct the patient to avoid it in the future
2. Administer topical or oral antihistamines, as prescribed to inhibit inflammatory response and ease pruritus and
discomfort
3. Administer topical cortecosteroids, as prescribed in severe cases
4. Assess for evidence of secondary infection; if present administer antibiotics as prescribed
5. Instruct the patient on prevention of secondary infection and pharmacologic management

MANAGEMENT OF PATIENTS WITH INFECTIOUS DISEASE

LYME DISEASE

Description
• Lyme disease is an infection caused by the spirochete Borrelia burgdorferi, acquired from a tick bite.
• Ticks live in wooded areas and survive by attaching to the host

Assessment and Stages

First Stage:
• Symptoms can occur several days to months following the bite
• A small red pimple develops that spreads into a ring shaped rash
• Rash may be large or small or may not occur at all
• Flulike symptoms occur such as headaches, stiff neck, muscle aches, and fatigue

Second Stage:
 • Occurs several weeks following the bite
• Joint pain occurs
• Neurological complications occur
• Cardiac complications occur

Third Stage:
• Large joints become involved
• Arthritis progress
• Neurologic symptoms:
o Bell’s palsy to Guillain-Barre–like syndrome or dementia

Diagnostics: enzyme linked immunosorbent assay (ELISA)

Treatment
• Most cases can be treated with antibiotics
• Type of antibiotic depends on the stage of the disease (early or late)
• Early: doxycycline (Vibramycin)- should not be used for pregnant women; amoxicillin (Amoxil); cefuroxime axetil ( Ceftin)
• Later: ceftriaxone (Rocephin); Penicillin G.

Influenza

• Commonly called “flu,” is an illness caused by RNA viruses of the family Orthomyxoviridae (influenza viruses) that infect
the respiratory tract of many animals, birds, and humans.
• Spread from person to person by inhaling infected droplets from air
Types:
• Influenza Virus A
o Wild aquatic birds are the natural hosts for a large variety of influenza A.
o Viruses are transmitted to other species and may then cause devastating outbreaks in domestic poultry or give rise
to human influenza pandemics
o Type of virus that most virulent human pathogens among the three influenza types and causes the most severe
disease
• Influenza virus B
o This exclusively infects humans and is less common than influenza A.
• Influenza virus C
o This type of influenza infects humans and pigs and can cause severe illness and local epidemics, however, influenza
C is less common than the other types and usually seem to cause mild disease in children

Symptoms
• High fever
• Chills
• Pharyngitis
• Muscle pain
• Severe headache
• Cough
• Fatigue
• Weakness and general discomfort
• Abdominal pain (in children with influenza virus B)
• Redenned eyes, skin (face), mouth, throat and nose

Complications: Severe and fatal pneumonia

Treatment
• Adequate rest
• Plenty of fluids
• Avoid exertion
• Zanamivir (Relenza)- inhaled
• Oseltamivir (Tumiflu)-pill
• Oral antiviral drugs: amantidine (Symmetrel); rimantadine (Flumadine) for type A influenza

Severe Acute Respiratory Syndrome (SARS)

• A respiratory illness caused by virus caused by the coronavirus, called SARS-associated coronavirus
• The syndrome begins with fever, an overall feeling of discomfort, body aches, and mild respiratory symptoms
• After 2 to 7 days, the client may develop a dry cough and dyspnea
• Diagnostics: Chest X-ray; CBC (WBC and platelet count is high)
 •Infection is spread by close person- to- person contact with infectious material (respiratory secretions or by contact with
persons or objects infected with infectious droplets)
• Prevention includes avoiding contact with those suspected of having SARS, avoiding travel to countries where an
outbreak of SARS exists; avoiding close contact with crowds in areas where SARS exists, frequent handwashing
• Treatment: antipyretics, supplemental oxygen and ventilator support as needed
MONONUCLEOSIS

• Infectious mononucleosis is an acute infectious disease due to Eipstein-Barr Virus (EBV). Also called “kissing disease”

Signs and Symptoms

• Classical signs: Sore throat, fever, fatigue, weight loss, malaise, pharyngeal inflammation, petechia, and loss of appetite
• Common signs: lymphadenopathy, splenomegaly, hepatitis, hemolysis

Laboratory Findings
• Monospot test: positive result within 4 weeks after onset of illness
• Immunoglobulin titer: Increased and EB virus antigens is detected
• Rise and fall in IgM antibody to EB virus antigen
• Hepatic aminotransferases and bilirubin: Elevated

Treatment
• Acetaminophen for symptomatic relief
• Nonaspirin or nonsteroidal anti inflammatory agents
• Warm saline throat irrigations or gargles 3 or 4 times daily
• For enlarged lymphoid tissue that threatens to obstruct the airway: corticosteroids in 5 day tapering course
• Ampicillin and amoxicillin are avoided because of the frequent association with rash in the presence of acute EBV
infection

CYTOMEGALOVIRUS

• Cytomegalovirus is a viral infection that persists in the body indefinitely, with periods of reactivation without symptoms.
• The virus can infect the fetus or infant during delivery or after birth through breastmilk, blood transfusion, or contact with
infected secretions
• Produces mononucleosis like symptom in the mother
• Causes fetal death, mental retardation, blindness, deafness, or seizures
• Antiviral therapy may be prescribed