IMMUNOLOGY LECTURE 1 iii.

Lymph formation prevents

A. Immune System accumulation of excess tissue fluid
 Comprises cells and molecules (prevents edema)
 Functions as the body’s defense mechanism 2. Lymphatic Vessel
against invasion a. A pathway of lymph which resemble small
 Immunity – Refers to the body’s specific veins in structure but have thinner walls and
protective response to an invading foreign agents more valves
or organism b. At intervals along the lymphatic vessels,
 A complex network of specialized cells, tissues, lymph flows through lymph nodes,
and organs that recognize and defend the body encapsulated bean shaped organs
from foreign substances, primarily disease- consisting of masses of B cells and T cells
causing microorganisms such as bacteria, c. Location:
viruses, parasites, and fungi. d. In the skin, lymphatic vessels lie in the
 The lymphatic vessels of the immune system subcutaneous tissue and generally follow
carry immune cells, which converge in lymph the same route as veins
nodes found throughout the body. e. Lymphatic vessels of the viscera generally
follow arteries, forming plexuses (networks)
B. Lymphatic System around them.
 Major part of immune system 3. Lymph Nodes
 Primary functions: a. Lymph nodes are small lumps of tissue that
o Draining excess interstitial fluids contain white blood cells, which fight
o Transporting dietary lipids infection
o Carrying out immune responses b. They filter lymph fluid, which is composed of
fluid and waste products from your body
DESCRIPTION:
tissues
 Immune cells circulate in the blood to help fight
c. Lymph nodes also help activate your
off or prevent disease
immune system if there is an infection
 These cells are produced in the bone marrow
4. Lymphatic Organs
 They move rapidly through the body in the blood
Based on the functions:
to get to the sites of infection, where they pass
o Primary Lymphatic Organs
into tissues and then move between individual
 Bone Marrow
cells.
 Thymus
 They return to the blood by travelling via the
o Secondary Lymphatic Organs
lymphatic system
 Lymph nodes
 Lymph nodes are special sites where they
 Lymph nodules
collaborate to fight infection
 Tonsils
Component of Lymphatic System:  Peyer’s patches
1. Lymph  Spleen
a. Means LIMF – clear water in Latin I. Primary Lymphatic Organs
b. The fluid that flows inside lymphatic vessels a. Bone Marrow – WBC (Leukocytes)
and lymph nodes (whole lymphatic system) i. Found in medullary cavities of
after it passes through the interstitial space LONG BONES & spaces of
c. The major difference between interstitial SPONGY bone
fluid and lymph is location: Interstitial fluid is ii. B-cells – mature in bone marrow
found between cells, and lymph is located iii. T-cells – migrate going to Thymus
within lymphatic vessels and lymphatic b. Thymus
tissue i. Bilobed organ (mediastinum
d. LYMPH FORMATION between sternum & aorta)
i. As protein concentration in interstitial ii. Lobule – outer cortex (large
spaces increases, its pressure number of T cells)
increases iii. Central medulla (widely scattered,
ii. Increasing pressure forces tissue fluid more mature T cells)
into lymphatic capillaries iv. Immature T cells migrates
 v. The epithelial cells secrete a OTHER COMPONENT OF IMMUNE SYSTEM
hormone called thymosin  WBC “Leukocytes”
vi. The site of maturation of T cells o Are cells of the immune system involved in
vii. The thymus produces progenitor defending the body against infectious
cells, which mature into T cells disease and foreign materials
(thymus derived cells o Basic Types of Leukocytes:
viii. The body uses T cells help destroy  Phagocytes – cells that chew up
infected or cancerous cells invading organism
II. Secondary Lymphatic Organs  Lymphocytes – cells that allow the
a. Lymph Nodes body to remember and recognize
i. Containing large number of previous invaders and help the body
leukocytes destroy them
ii. Mammary glands, axillae and  Phagocytic Cells
groin o Types of Phagocytic cells:
iii. Function: to filter lymph  Granulocytes
iv. Serve as a center for the  Neutrophils
production of phagocytes o 62&
b. Lymph Nodules o Primarily fights
i. Small, localized collection BACTERIA, small
lymphoid tissue, usually located in particles
the loose connective tissue o 1st to arrive at the site of
beneath wet epithelial (covering or invasion
lining) membranes, as in the  Eosinophils
digestive system, respiratory o 2-3%
system, and urinary bladder o PARASITIC Worm
ii. It differs from lymph nodes in that o Involve also in
is much smaller and does not have hypersensitivity response
a well-defined connective tissue  Basophils
capsule as a boundary o 0.3&-0.5% of WBC (.4%)
iii. It also does not function as a filter, o Releases histamine,
because it is not located along a bradykinin, serotonin,
lymphatic vessel leukotrienes in acute
iv. Tonsils hypersensitivity reaction
v. Peyer’s patches  Agranulocytes
III. Spleen  Monocytes
a. It is located in the upper left portion of the o Mature intro
abdominal cavity (behind stomach) macrophages when in the
b. Contains 2 types of tissue body tissues or dendritic
i. White pulp – contains cell
lymphocytes & macrophages o MACROPHAGES
ii. Red pulp – site for old and injured  Mature forms of blood monocytes
RBCs to be destroyed  General scavenger cells of the body
c. Functions:  Process and present antigen to specific
i. Removal and destruction of lymphocytes
foreign particles and worn blood o DENDRITIC CELLS
from cells from blood  Together with macrophages, present antigen
ii. Stores and releases blood during to T cells
hemorrhage  Found in lymphoid and other body areas where
iii. Site of B cell proliferation into antigen enters the body
plasma cells  They act as messengers between the innate
iv. Storage of platelets, 1/3 of body and the adaptive immune systems
supply  Lymphocytes
v. Production of cells during fetal life o Represents 25-35% of
blood leukocytes
 o Involved in cellular and
humoral immunity
3 KINDS OF LYMPHOCYTES
 B lymphocytes – mature in the bone marrow
and then center the circulation
 T lymphocytes – move from the bone marrow
to the thymus, where they mature into several
kinds of cells capable of different functions
 Natural killer cells – not identifiable as either T
cells or B cells. Non specific effector cells that
can kill tumor and virus infected cells.
IMMUNOLOGY LECTURE 2
 pathology – the study of disease
 etiology – the study of the cause of a
disease
 pathogenesis – the development of disease
 infection – colonization of the body by
pathogens
 disease – an abnormal state in which the
body is not functioning
Infection
- The colonization of a host by microbial
species. Infecting microbes seek to use
the host’s resources to reproduce, often
resulting in disease
- infections are considered to be caused by
microscopic organisms like viruses,
prions, bacteria and viroid though larger
organisms like macro parasites and fungi
can also infect
- an infection is the invasion of an
organism’s body tissues by disease-
causing agents, their multiplication, and
the reaction of host tissues to the
infectious agents and the toxins they
produce
STAGES OF INFECTIOUS PROCESS
 incubation – entry of microorganisms into
the body to the onset of signs and
symptoms
 prodromal – onset of non-specific signs and
symptoms to the appearance of specific
signs and symptoms
 acute – specific signs and symptoms
develop and becomes evident
 convalescent – signs and symptoms start to
abate until the client returns to normal state
of health
 resolution – normal state of health and total
elimination of pathogens
FACTORS AFFECTING INFECTIOUS PROCESS
Force of infection: Epidemiologic Triangle
consist of 3 components
 host – any organism that harbors and
provides nourishment for another organism
 agent – intrinsic property of microorganism
to survive and multiply in the environment to
produce disease
 environment – it is the sum total of all
external conditions and influences that
affect the development of an organism
which can be biological, social or physical
Force of Resistance: Immunity (see
separate discussion on immunity)
CHAIN OF INFECTION
 Pathogenic microorganism/ causative
(infection) agent
- Microorganism that causes infection such
as bacteria, virus, fungi and parasites
- There must be a sufficient dose of the
organism that has enough amount and
concentration to cause infection
 Reservoir
- Place where the microorganism lives,
such as in humans, animals, in soils,
food, plants, air ir water
- It includes humans, animals and the
environment
- The reservoir must meet the needs of the
pathogen to survive and multiply
- the natural habitat of the organism where
it resides and multiply
 Portal of Exit
- The portal of exit is the path by which the
pathogen leaves its host
- It usually corresponds to the site where
the pathogen is localized
- These are the following mode of escape
from the reservoir;
a. Respiratory tract ) most common in
humans)
 b. Gastrointestinal tract
c. Genitourinary tract
d. Open lesions
e. Mechanical escape (bites of insect)
f. Blood
 Mode of Transmission
- An infectious agent may be transmitted
from its natural reservoir to a susceptible
host in different ways
- The mode of transmission is the weakest
link in the chain of infection
There are different modes of transmission:
 Vertical – maternal to fetal transmission
(crossing the placental barrier or via vaginal
route)
 Horizontal – it can be direct or indirect or
through break in the skin integrity
 Direct Contact
- occurs through skin to skin contact,
kissing, and sexual intercourse
- Also refers to contact with soil or
vegetation harbouring infectious
microorganism
- A droplet spread is considered to be a
direct contact with refers to sprays with
relatively large short-sprays with relatively
large short-range aerosols produced by
coughing, sneezing or even talking
 Indirect contact
o Airborne
- occurs when infectious agents are
carried by dust or droplet nuclei
suspended in the air
- Airborne dust includes materials
that have settles on surfaces and
becomes suspended by air currents
as well as infectious particles blown
from the soil by the wind
o Vehicle-borne
– It includes food, water, biologic
products (blood) and fomites
(inanimate object such as bedding,
handkerchief or scalpels)
– A vehicle may passively carry a
pathogen – as food or water may
carry a virus
– The vehicle may provide an
environment in which the agent
grows, multiplies or produces toxins
o Vector-borne
– Vector is defined as an arthropod
or any living carrier (e.g., snail) that
transports an infectious agent to a
susceptible individual
– Transmission – mechanical or
biological
 Portal of Entry
- Refers to the manner in which a pathogen
enters a susceptible host
- The portal of entry must provide access to
tissues in which the pathogen can multiply
or a toxin can act
- Often, infectious agents use the same
portal that they used to exit the source
host in entering a new host
- In a fecal-oral route, the agent leaves the
source host in feces and are carried on
inadequately washed hands to a vehicle
such as food, water, or utensils and enter
a new host through the mouth
 Susceptible Host
- The final link in the chain of infection
- Susceptibility of the host depends on the
genetic or constitutional factors, specific
immunity and nonspecific factors that
affect an individual’s ability to resist
infection or to limit pathogenicity
- A host is a person whose own body
defense mechanisms, when exposed,
cannot withstand the invasion of
pathogens
 Some people are more susceptible due to:
. Low immunity
. Poor physical resistance
. Being very young or old
. Being malnourished
. Underlying disease
- An individual’s genetic makeup may either
increase or decrease susceptibility
- Specific immunity refers to protective
antibodies that are directed against a
specific agent such as antibodies that
may develop in response to infection,
vaccines or toxoids or may be acquired by
trans-placental transfer from mother to
fetus or by injection of antitoxin or
immunoglobulin
 - Nonspecific factors that defend against
infection include skin, mucus membrane,
gastric acid, cilia in respiratory tract, the
cough reflex and nonspecific immune
response
 Factors that may increase susceptibility to
infection by disrupting host defences are:
. Malnutrition
. Alcoholism
. Disease
. Therapy that impairs the nonspecific
immune response
Immunologic defenses
- Individuals have defences that protect the
body from infection
- These defences can be categorized as
nonspecific and specific
Non-Specific resistance/Innate Defenses
- Bodily defences that protect a person
against all microorganisms, regardless of
prior exposure
- It includes anatomic and physiological
barriers and the inflammatory response
INNATE IMMUNE SYSTEM
Types of Nonspecific Defenses
First line of Defense / External Defenses
A. Physical Barriers: provides physical
barriers to invaders
- Skin – a thick layer of dead cells in the
epidermis provides a physical barrier to
viruses, bacteria, and microbes. As the
epidermis sheds, microbes are removed
- Mucous membrane – produce mucus to
trap microbes so they cannot spread to
the rest of the body
- Hair – hair within the nose filters
microbes, dust, and pollutants form the air
to prevent them from invading the body
- Cilia – cilia lines the upper respiratory
tract and traps and propels inhaled debris
to the throat so it can exit the body more
quickly
- Urine – urine flushes microbes out of the
body via the urethra
- Defecation and vomiting – body expels
microorganisms via bowel movements
and vomit
B. Chemical Barriers: form another first line
of defense against invaders
- Lysozyme – an enzyme produced in
tears, sweat, and saliva that breaks down
cell walls and acts as an antibiotic by
killing bacteria
- Gastric juice – acids in the stomach
destroy bacteria and toxins
- Saliva – saliva dilutes the number of
microorganism in the body and washes
the teeth and mouth
- Sebum – unsaturated fatty acids known
as sebum provide a protective film on the
skin and inhibits growth
- Hyaluronic acid – a gelatinous substance,
hyaluronic acid slows the spread of
microorganisms that can harm the body
Second line of Defense / Internal Defense
A. Antimicrobial Proteins
- Interferons – released by host cells in
response to the presence of pathogens
(viruses, bacteria, parasites or tumor
cells)
- Complement – a group of at least 20
plasma proteins that normally circulate in
the blood in an inactive state. Its
activation unleashes chemical mediators
that amplify virtually all aspects of
inflammatory process
- Transferrin – iron-binding CHONs that
inhibit the growth of certain bacteria by
reducing the amount of available iron
B. Natural Killer Cells – kills a wide variety
infectious microbes and certain tumor cells
Ways:
1. Release of perforins – chemical inserted
into plasma membrane a leaky
2. Release molecules that may cause
apoptosis
C. Phagocytes – phagocytic cells ingest and
destroy microbes that pass into body tissues
Phases of Phagocytosis
 - Chemotaxis: chemically stimulated
movement of phagocytes to a site of
damage
- Adherence: attachment of the phagocytes
to the microbe or other foreign material
- Ingestion: process of engulfing the
microbes and forms a vesicle
- Digestion: phagosome + lysosome –
microbe-containing vesicle fuses with a
lysosome which breaks down the
molecule into simpler components
- Killing: release of lysosome, other
digestive enzymes, lethal oxidants
D. Fever – inhibits bacterial growth and
increase the rate of tissue repair when an
infection is present in the body
Effects:
- Intensify interferon
- Inhibits microbial growth
- Speeds up body reactions
SECOND LINE OF DESEASE
Inflammation
- A localized response in the tissue that
occurs when tissues are damaged or in
response to other stimuli
- Inflammation occurs when white blood
cells flood an area of invasion by
microbes
- The response includes swelling, redness,
heat and pain
Stages of Inflammatory Response
A. Vasodilation & Increase Blood vessel
permeability
- Substances:
- Histamine
- Kinins (polypeptide) – inactive precursor,
kininogens and affects some nerve
endings
- Prostaglandins (lipids) – released by
damaged cells, stimulates emigration,
intensifies histamine and kinin; intensify
and prolong pain
- Leukotrienes (LTs) – chemotactic agent
- Complement – stimulate release of
histamines and chemotactic agent
B. Chemical mediators assist this response
by:
- Minimizing blood loss
- Walling of the invading organism
- Activating phagocytes
- Promoting formation of fibrous scar tissue
and regeneration of injured tissue
C. Emigration of Phagocytes
- Within an hour after, phagocytes appear
on the scene
- Neutrophils begin to squeeze through the
wall of the blood vessel called Emigration
- Monocytes follow neutrophils
INFLAMMATION
 A non-specific body defense to cell injury
 Helps restore tissue homeostasis
Main features of inflammation
1. Vasodilation
2. Increased Vascular Permeability
3. Cellular Infiltration
4. Changes in biosynthetic profile of organs
5. Activation of cells of the immune system
5 CARDINAL SIGNS
P- Pain (dolor)
R – Redness (rubor)
I – immobility (fubctio laesa)
S – Swelling (tumor)
H – Heat (calor)
STAGES OF INFLAMMATION
I. ACUTE INFLAMMATION
Vasodilation and Increased vessel permeability
Substances:
a. histamines
b. kinins (polypeptide) - Inactive precursor,
kininogens, affects some nerve endings and chemotactic
agent
c. Prostaglandins (lipids) - released by damaged
cells, stimulates emigration, intensifies histamine and
kinins; Intensify and prolong pain.
d. Leukotrienes (LTs) - chemotactic agent
e. Complement - stimulate release of Histamines
 prostaglandins and leukotrienes dilate
vasculatures, enhance permeability of
capillaries, increase blood flow, and stimulate
the recruitment of neutrophils (PMNs) to form
inflammatory exudate. Novel chemical mediators
are produced in the evolution and resolution of
the exudate that regulate tissue responses (see
text for details). The black arrow denotes
leukocyte traffic from venules and the dashed
arrow denotes exogenous, i.e., bacterial
components and chemoattractants.

Chemical mediators assist this response by:

 Minimizing blood loss,
 Walling off the invading organism
CELLULAR RESPONSE  Activating phagocytes
Key PLAYERS: Tissue  Promoting formation of fibrous scar tissue and
1. Leukocytes (WBC) granulocyte-neutrophils regeneration of injured tissue
a. Emigration
i. Margination Emigration of Phagocytes
ii. Diapedesis  Within an hour after, phagocytes appear on the
2. Erythrocytes scene
a. Leak to the tissue – hemorrhage  Neutrophils begin to squeeze through the wall of
the blood vessel called Emigration
KEY PLAYERS  Monocytes follow neutrophils
1. Fibrinogen
2. Fibronectin Purposes of Vascular Changes
3. Platelets
1. Increase blood flow to the local area
4. RBC – “Rouleau”
2. Mobilize the transport cells
3. Initiate Healing
WBC Function in Cellular Response
 Destroying infective organism Other Effects of Inflammation
 Remove damage cell 1. Production of acute phase proteins (ex.
 Releasing more inflammatory mediators Complement)
 Control further inflammation 2. Fever – pyrogens acting on hypothalamus
 Healing 3. Systemic immunity- lymphocyte activation
(peripheral lymphoid tissue)
Chemical Mediators assist this response by:
 Minimizing blood loss Fever
 Walling off the invading organism  Occurs during infection and inflammation
 Activating phagocytes  Systemic response to invading microorganism
 Promoting formation of fibrous scar tissue and Effects:
regeneration if injured tissue. a. Intensify interferons
b. Inhibits microbe growth
c. Speeds up body reactions

Local Manifestation of Inflammation

 Serous exudates
o Watery fluids low in protein content that
result from entering the inflammatory
site.
 The role of chemical mediators in the acute o Watery fluids; result of plasma entering
inflammatory response. At the site of tissue the inflammatory site
injury or bacterial invasion, both exogenous and
endogenous chemical mediators are liberated.  Fibrinous Inflammation
Classic endogenous mediators such as
 o Consists of neutrophils admixed with
fibrin (e.g., fibrinous pericarditis).
o The fibrin in this fluid can form a
fibrinous exudate on the surfaces.
o Bread and Butter appearance – Here,
the pericardial cavity has been opened
to reveal a fibrinous pericarditis with
stands of stringy pale fibrin between
visceral and parietal pericardium
 Purulent exudates
 Abscess
 Ulceration
II. CHRONIC INFLAMMATION
III. TISSUE REPAIR
 When tissues are injured during infection or
following toxic or mechanical injury, an
inflammatory response is induced in
response to damage-associated molecular
patterns (DAMPs) and pathogen-associated
molecular patterns (PAMPs) released by
dead and dying cells and invading
organisms.
 These molecular triggers induce a complex
inflammatory response that is characterized
by the recruitment, proliferation, and
activation of a variety of immune cells
including neutrophils, macrophages, NK
cells, B cells, T cells, fibroblasts and
endothelial cells that together make up the
cellular response that orchestrates tissue
repair.
 Reconstruction
o Begins once the inflamed area is
cleaned and debrided, producing new
cells to fill in the space left by the injury
 Maturation
o Scar Tissue is remodeled, capillaries
contract, structure and function of
damaged tissue is restored.
Aberrant to healing
o Complications, deformity and decrease
function of the injured tissue
o Results from abnormality in healing
mechanisms
 Exuberant granulation and keloids
o “Proud flesh”
o Keloids – excessive, bulging, tumous
scars that extend beyond the confines of
the original wound and seldom regress.
 Excessive contracture
o Wounds that continue to contract after
closure and produces disfiguring scar or
disability
 Dehiscence
o Wound separation
o A surface disruption that results in the
bursting open of a previously closed
wound.
 Evisceration
o Refers to internal organs moving
through a dehiscence
 Adhesion
o Exudates cause scar tissue to bind or
adhere to adjacent surfaces
 Wound healing
o Primary Objective is to fill the gap
created by tissue destruction and
restore the structural continuity of the
injured part.
o Depending on the extent of tissue loss,
wound closure and healing occur by
primary or secondary intention
INFLAMMATORY RESPONSE 3. Mono Surface of Cell surface
mer B cell receptor of mature
o Begins at the time of injury B cell; important in
o Prepares the wound environment for healing B cell activation
o Hemostatic processes are activated 4. Dimer Monomer Protects mucosal
o Cells migrate in area essential for healing found in surfaces; prevents
o Phagocytosis and release of growth factor that plasma; attachment of
stimulate epithelial growth, angiogenesis and
polymers in pathogens to
fibrinogenesis
saliva, epithelial cells
tears, milk,
FOCUS OF CARE
and other
o Decrease pain and swelling
o Prevent chronic inflammation body
o Maintain mobility and strength in adjacent areas secretions.
while injured areas are rested 5. Mono Secreted Found on mast
mer by plasma cells and
ANTIBODY cells in skin basophils; when
 Proteins secreted by B cells or plasma cells and tissues bound to antigens,
(clone of B cell) in response to an antigen and lining triggers release of
are capable of binding to that antigen gastrointest histamine from
 Also called “Ig” or immune globulins or gamma inal and mast cell or
globulins respiratory basophil that
 Proteins produced by plasma cells in response tracts contributes to
to foreign antigens. inflammation and
some allergic
Types and characteristics of antibodies responses
1. IgG- highest opsonization and neutralization
activities. Classified into four subclasses. (IgG1, IgG
IgG2, IgG3, IgG4).
 80%
2. IgM- produced first upon antigen invasion,
 Present in tissues and serum
increases transiently.
 Major role in blood-borne and tissue infections
3. IgA- Expressed in mucosal tissues. Forms
 Crosses the placenta
dimers after secretion.
4. IgD- unknown function.  Enhances phagocytosis
5. IgE- Involved in allergy IgA
 10-15%
Antibody Classes  Sweat, tears, mucus, breastmilk, GI secretions
Location Function  Tends to decrease during stress
1. Mono Free in Most abundant  Helps prevent attachment of antigen to epithelial
mer cells surface
plasma; antibody in primary
IgM
about 80 and secondary
 5-10%
percent of responses;
 Limited to vascular system
circulating crosses placenta
 First Immunoglobulin produced in response to
antibodies. and provides
bacterial and viral infection
passive
 Agglutinating agent and activates complement.
immunization to
IgE
fetus
 0-1%
2. Penta Surface of Antigen receptor
 Present in serum
mer B cell; free on B cell
 Involved in allergic and hypersensitivity reaction
in plasma membrane; first
 Help defense against parasites.
class of antibodies IgD
released by B cells
 Location: B lymphocytes
during primary
 Receptors on B lymphocytes
response.
 Total: 0.2%
ANTIBODY FUNCTION Eosinophils 1 to 4
 Antibodies inactivate antigens in a number of Basophils 0.5 to 1
ways
o Complement fixation Bone Marrow Biopsy
o Neutralization  To check for any blood cell abnormalities.
o Agglutination  Marrow samples will be checked to see if your
o Precipitation bone marrow is making healthy blood cells. If
not, the results will show the cause, which may
Complement fixation be an infection, bone marrow cancer disease, or
 Is a classic method for demonstrating the cancer
presence of antibody in patient serum.
 Antibody binds to the antigen and causes lysis, Bone Marrow Aspiration
chemotaxis to attract other leukocytes and  Procedural Interventions:
opsonization o Obtain informed consent.
o Position client to prone position or
Neutralization his/her side.
 The antibody binds to site on the bacteria or o Cleanse the skin.
virus that releases toxins (exotoxins) to block the o Assist in application of a local anesthetic
harmful effects of the toxin over the site
 After the procedure:
Agglutination o Lie flat for 5-10 minutes to provide
 Antibody will bind to the cell and cause clumping pressure over the procedure site.
(occurs in mismatched blood) so they are easily o Paracetamol (acetaminophen) for pain
captured by phagocytes. and to relieve soreness of the site.
o Monitor for signs of bleeding and
Precipitation infection.
 Are serological assays for the detection of
immunoglobulin levels from the serum of a Hypersensitivity Tests
patient with infection  Scratch test - test checks for skin reaction to
 The most widely used gold standard common allergy-provoking substances, such as
precipitation methods are Ouchterlony test and foods, molds, dust, plants, or animal protein
Mancini test  Patch test - test involves the application of
various test substances to the skin under
adhesive tape that are then left in place for 48
COMMON DIAGNOSTIC PROCEDURE hours.
 Intradermal Test – blood test measures the
White Blood Cell Count levels of allergy antibody, or IgE, produced when
 Detect hidden infections within your body and your blood is mixed with the series of allergens
alert doctors to undiagnosed medical conditions, in a laboratory.
such as autoimmune diseases, immune  Radioallergosorbent test (RAST) – it tests for
deficiencies and blood disorders. the amount of specific IgE antibodies in the
 Detects the severity of allergic and drug blood
reactions plus the response to parasitic and  Radioimmunoassay- used to measure
other types of infection concentrations of antigens
 Immunofluorescence – technique uses the
Leukocytes and Lymphocytes Test specificity of antibodies to their antigen to target
fluorescent dyes to specific biomolecule targets
 A blood differential test measures the amount of
within a cell
each type of white blood cell (WBC) in the body
 Agglutination – used to determine infection and
 Assesses the ability of the body to respond to
to identify pathogens and blood types.
and eliminate infection.
 Complement fixation test – widely used to
White blood cell line Normal percentage of
diagnose infections, particularly with microbes
total leukocyte count
that are not easily detected by culture methods,
Neutrophils 40 to 60
and in rheumatic diseases.
Lymphocytes 20 to 40
Monocytes 2 to 8
Health History o Tetany
 Gender
 Age
 Nutrition Specific Resistance to Infection
 Infection and immunization  This system relies on antigens, which are
 Allergies specific substances found in foreign
 Disorders and Diseases (Autoimmune disease, microbes
neoplastic)
 Most antigens are proteins that serve as the
 Chronic Illness and Surgery
stimulus to produce an immune response
 Special problems like burns
 Medications and Blood transfusions
DEFINITION OF TERMS
 Lifestyle and other factors
 Immunity
 The state of being resistant to reinfection
PHYSICAL ASSESSMENT with a pathogen
 Respiratory System  The state of protection against foreign
o Changes in respiratory rate pathogens or substances (antigens)
o Cough (dry or productive)
o Abnormal lung sounds (wheezing, TYPES OF IMMUNITY
crackles, rhonchi)  Natural (Innate) Immunity
o Rhinitis
o also called in born/inherent immunity
o Hyperventilation
o Bronchospasm o Physical barrier: skin
 Cardiovascular System o Chemical barrier substance
o Hypotension produced by the body cellular
o Tachycardia barrier: T & B lymphocytes
o Dysrhythmia  Acquired (Adaptive) Immunity
o Vasculitis
o developed after exposure to the
o Anemia
 Gastrointestinal System disease and immunization
o Hepatosplenomegaly o The ability to ward off damage or
o Colitis disease through our defenses
o Vomiting
o Diarrhea  Susceptibility – lack of resistance or
 Genitourinary System
vulnerability
o Frequency or burning on urination
o Hematuria  Immune Response – is how your body
o Discharge recognizes and defends itself against
 Musculoskeletal System bacteria, viruses, and substances that
o Joint mobility appear foreign and harmful
o Edema
o pain IMMUNE CELLS
 Skin A. B-cells or B lymphocytes:
o Rashes
 Cells that derived from the bone marrow
o Lesions
o Dermatitis important for producing a humoral immune
o Hematomas or purpura response
o Edema or Urticaria  Lymphocyte cells that are important in
o Inflammation producing circulating antibodies that are
o Discharge
programmed to produce one specific
 Neurosensory System
antibody
o Cognitive dysfunction
o Hearing loss  On encountering a specific antigen. B cells
o Visual changes stimulate production of plasma cells, the site
o Headaches and migraines of antibodies production. The result is the
o Ataxia
 outpouring of antibodies for the purpose of
destroying and removing the antigens.
B. T-cells Or T lymphocytes
 Cells that derived from the thymus
 Lymphocyte cells that can cause graft
rejection, kill foreign cells, or suppress
production of antibodies
 T cells or T lymphocytes assist the B cells.
T cells secrete substances that direct the
flow of cell activity, destroy target cells, and
stimulate the macrophages. The
Roles of an Antigen-Presenting Cell
macrophages present the antigens to the T
cells and initiate the immune response
 They also digest antigens and assist in
removing cells and other debris. Unlike a
specific antibody, a T cell does not bind free
antigen
C. Maturation of T and B cells
 Lymphocytes originate from stem cells in
PROCESSING OF ANTIGENS
the bone marrow
 B lymphocytes mature in the bone marrow
before entering the bloodstream, whereas T
lymphocytes mature in the thymus, where
they also differentiate into cells with various
functions
D. Processing and Presentation of Antigens
 Antigen – any substance capable of
exciting the immune system and
provoking an immune response
 Examples of common antigens:
o Foreign proteins
o Nucleic acids
o Large carbohydrates
o Some lipids
o Pollen grains
o Microorganisms
FUNCTIONAL PROPERTIES OF ANTIGEN
 Immunogenicity - The ability to stimulate
proliferation of specific lymphocytes and
antibody
 Reactivity – the ability to react or activate
lymphocytes and the antibody by
immunogenic reaction
 Self-Antigens
o our immune cells do not attack our own
proteins
o Our cells in the another person’s body
can trigger an immune response
because they are foreign
o Restricts donors for transplants
o Engulf antigens and present fragments
of them, like signal flags, on their own
surfaces where they can be recognized
by T cells
 Phagocytosis of enemy cell (antigen)
 Fusion of lysosome and phagosome
 Enzymes start to degrade enemy cell
 Enemy cell broke into small fragments
 Fragments of antigen presented on APC
surface
 Leftover fragment released by exocytosis
 Exogenous Antigen – bacteria and toxins,
worm parasites, pollen, dust, viruses
o APC process exogenous antigens –
macrophages, B cells, dendritic cell
 Antigen Presenting Cells (APC)
o Lymphocytes
 Originate from hemocytoblasts in
the red bone marrow
 B lymphocytes become
immunocompetent in the bone
marrow
 T lymphocytes become
immunocompetent in the thymus
o Dendritic cells
 Present in connective tissues
and epidermis
 The body’s frontier, best situated
to act as mobile sentines
o Macrophages
 Arise from monocytes
 Become widely distributed in
lymphoid organs
 Endogenous Antigen
o Foreign antigens that are
synthesized within a body cell
o Viral CHONs, abnormal CHONs
o Antigen fragment-MHC I complex

IMMUNE RESPONSE
 how your body recognizes and defends
itself against bacteria, viruses, and
substances that appear foreign and harmful
Stages of Immune Response:
a. Recognition Stage
o Body accomplishes recognition
using lymph nodes and lymphocytes
for surveillance
o Continuously discharge small
lymphocytes into the bloodstream
o Macrophages, neutrophils &
complement help
b. Proliferation Stage
o Sensitized lymphocytes stimulate
some of the resident dormant T and
B lymphocytes to enlarge, divide,
and proliferate
o T lymphocytes differentiate into
cytotoxic (or killer) T cells, whereas
B lymphocytes produce and release
antibodies
o Enlargement of the lymph nodes in
the neck in conjunction with a sore
throate is one example of the
immune response
o Actual humoral and cell-mediated
immune response
c. Effector Stage
o coupling initiates a series of events
that in most instances results in the
total destruction of the invading
microbes or the complete
neutralization of the toxin either the
antibody of the humoral response of
the cytotoxic )killer) T cell of the
cellular response reaches and
couples with the antigen on the
surface of the foreign invader
Cell-Mediated Immune Response
 Involves differentiation of T-cells to different
types of cell
 Dominated by T lymphocytes
 Immunity occurs inside infected cells and is
mediated by T lymphocytes
 The pathogen’s antigens are expressed on
the cell surface or on an antigen-presenting
cell. Helper T cells release cytokines that
help activated T cells bind to the infected
cells’ MHC-antigen complex and
differentiate the T cell into a cytotoxic T cell.
The infected cell then undergoes lysis
 Particularly effective against:
o Cells attacking cells
o Intracellular pathogen (parasites,
fungi, viruses) some cancer cells
o Foreign tissue transplant
o Often termed as delayed
hypersensitivity
 T lymphocytes, on exposure to antigen,
proliferate and differentiate into:
 Helper T cells
o activated upon recognition of antigen
&stimulates the rest of immune
response
 Suppressor T cells
o has the ability to decrease B cell
production, thereby keeping immune
response at the level compatible
with health
 Memory T cells
o Responsible for recognizing
antigens from previous exposure
and mounting an immune response
o Specialize in killing infected cells
o Insert a toxic chemical (perforin)
 Cytotoxic T cells / T8 cells
 Attach the antigen directly by altering the
cell membrane and causing cell lysis
(disintegration) and releasing cytolytic
enzymes & cytokines
 Perforin and lymphotoxin
Antibody-Mediated / Humoral Immune
Response
 Transformation of B cells to plasma cells
 Dominated by B lymphocytes
 Works mainly against:
o Antigens dissolved in body fluids
o Extracellular pathogen (bacteria)
 B lymphocytes with specific receptors bind
to a specific antigen
 The binding event activates the
lymphocytes to undergo clonal selection
  A large number of clones are produced
(primary humoral response)
 Most B cells become plasma cells produce
antibodies to destroy antigens, activity lasts
for four or five day
 Some B cells become long-lived memory
cells (secondary humoral response)
Secondary humoral response:
 Memory cells are lone-lived
 A second exposure causes a rapid
response
 The secondary response is stronger and
longer lasting
The Role of the Complement System
 The complement is a major component of
the innate immune system involved in
defending against all foreign pathogens
 Also known as a complement cascade that
enhances the ability of antibodies and
phagocytic cells to clear microbes and
damaged cells from an organisms, promote
inflammation and attack the pathogen’s cell
membrane
 Functions of the complement:
o Cytolysis – destruction of cell
membrane
o Chemotaxis – chemical attraction of
phagocytic cell to antigen
o Adherence – adhesion of antigen-
antibody complexes to surface of
cells or body tissues
o Opsonisation – antibody coats
surface of antigen, making it easier
to digest by phagocytes
o Neutralization – antibody
neutralizes toxins released by
bacteria
o Anaphylactic reaction – activates
release of mast cells and histamine
TYPES OF IMMUNITY
1. Innate Immunity - also known as natural
immunity, an inherited immunity of species,
races and individuals. Example is the skin
which acts as a barrier to block germs from
entering the body. And the immune system
recognizes when certain invaders are
foreign and could be harmful
2. Adaptive Immunity – adaptive or acquired
immunity develops throughout our lives. We
develop adaptive immunity when we are
exposed to diseases or when we are
immunized against them with vaccines
 Passive Immunity
o Borrowed from another source
o Natural – antibodies from the
mother are transferred to the baby
across the placenta or in milk
o Artificial – antibodies produced by
another person or an animal are
injected
 Active Immunity
o Individual’s own immune system is
the cause of the immunity
o Natural – antigens are introduced
through natural exposure
o Artificial – antigens are deliberately
introduced in a vaccine
Nursing responsibilities in Vaccination
 Vaccines can protect one’s health and the
health of the community. Efficacy and safety
of vaccines can be enhanced by using
education, enforcement and engineering in
which a nurse or health care provider plays
a key role
 This includes the following:
o Proper storage and handling of
vaccines
o Never administer vaccines later than
expiration date
  Administer – administer vaccines within  Having sex without any protection such as
prescribed time periods following condoms
 Recently having an intrauterine device (IUD)
reconstitution inserted
 Administer – administer immunization  Douching
following the protocol in right administration  Having history of pelvic inflammatory disorders
of medicine
CLINICAL MANIFESTATION
 Record – record vaccine and administration  Pain in the lower abdomen - most common
information in the patient’s record symptom
 Mix – NEVER mix vaccines in the same  Pain in the pelvic area
syringe unless approved for mixing by the  Fever – temperature above 38⁰C
 Painful sex
FDA
 Painful urination
 Infuse – infuse prodder aseptic r=technique  Irregular bleeding
and infection control  Increased or foul- smelling vaginal discharges
 Screen – screen patients for  Tiredness
contraindication and precautions  Vomiting
 Fainting
 Prepare – prepare to manage vaccine side
effects DIAGNOSTIC TESTS
 Report – report suspected side effects of  Pelvic examination
vaccine to authority  Cervical culture
 Urine test
 Provide – provide health teaching regarding  Pelvic ultrasound
schedules of immunization activity  Endometrial biopsy
 Discuss – discuss common side effects of  Laparoscopy
vaccine with patient or guardian
MEDICAL AND NURSING MANAGEMENT
Treatment of PID addresses the relief of acute
symptoms, eradication of current infection and minimizes
DISEASES the risk of long term sequelae.
 Azithromycin
PELVIC INFLAMMATORY DISEASE (PID)
 Cephalosporin
 Pelvic inflammatory disease (PID) is an infection
of the female reproductive organs.  Ceftriaxone
 Several different types of bacteria can cause  Doxycycline
PID, including the same bacteria that cause the  Clindamycin
sexually transmitted diseases. PID can become  Metronidazole
extremely dangerous even life threatening if the  Unasyn
infection spreads to the blood.  Probenecid
 It most often occurs when sexually transmitted
bacteria spread from your vagina to your uterus, LONG TERM COMPLICATION OF PID:
fallopian tubes or ovaries.  Infertility
 The signs and symptoms of pelvic inflammatory  Ectopic pregnancy
disease can be subtle or mild.  Chronic pelvic pain
 Some women don't experience any signs or  Tubo-ovarian abscess
symptoms.
 As a result, women not realize they have it until PREVENTION
they have trouble getting pregnant or you  Teach client to practice safe sex
develop chronic pelvic pain.  Screen for sexually transmitted infections
 Avoid douches
ETIOLOGIC AGENT  Teach client to wipe from front to back after
 Most cases of PID are polymicrobial, but these using bathroom
are the common pathogens:
 N. gonorrhoeae
 Chlamydia BENIGN PROSTATIC HYPERTROPHY (BPH)
 It is a common problem among older men.
RISK FACTOR  It is also known as benign prostatic hyperplasia,
 Having sex under the age of 25 years old and is characterized by proliferation of the
 Having multiple partners cellular elements of the prostate.
  BPH is a histologic diagnosis defined as an varying degrees of urinary tract
increase in the total number of stromal and obstruction, and presence of prostatic
glandular epithelial cells within the transition enlargement, bladder diverticula, and
zone of the prostate gland. abnormal thickening of bladder muscle
 This hyperplasia causes formation of large,
discrete prostatic nodules. 5. Voiding cystourethrography
 May be used instead of IVP to visualize
RISK FACTOR bladder and urethra because it uses local
 Aging process dyes.
 Hormonal imbalance (estrogen, androgen)
6. Cystometrogram
CLINICAL MANIFESTATIONS  Measures pressure and volume in the
 A weak urine stream bladder to identify bladder dysfunction
 Trouble starting the flow of urine unrelated to BPH.
 Starting and stopping again when urinating
 Not emptying bladder completely 7. Ultrasonography
 Urinating more often, especially at night 8. Endoscopy of the lower urinary tract
 Sudden urges to urinate 9. Cystoscopy
 Leaking or dribbling after urinating 10. Renal biopsy
 Straining to urinate
 Urinary frequency
 Urinary urgency INCASIVE AND NON-INVASIVE TREATMENT
 Nocturia
 Hesitancy 1. Transurethral resection of the Prostate
(TURP)
 To restore the normal flow of urine,
COMPLICATIONS
removes part of the obstructing prostate
 Urinary tract infections
issue
 Urinary stones  TURP is carried out using a
 Kidney damage resectoscope, which is a thin metal tube
 Bleeding in the urinary tract containing a light, camera and loop of
 A sudden inability to void wire.
 Hydroureter  This is passed along urethra until it
 Hydronephrosis reaches prostate,
 Bladder neck  No cuts (incisions) need to be made in
 Retrograde ejaculation skin.
 Epididymis
2. Transurethral Microwave Therapy (TUMT)
DIAGNOSTIC EXAMINATIONS  TUMT uses microwaves to destroy
prostate tissue.
1. Digital rectal examination (DRE).  The urologist threads a catheter through
 Often reveals a large, rubbery, and the urethra to the prostate. A device
nontender prostate gland. called an antenna sends microwaves
through the catheter to heat selected
2. Prostate-specific antigen (PSA) portions of the prostate.
 Blood test is used to screen for prostate  The heat destroys excess prostate
cancer. tissue.
 Avoid sexual activity several days prior to  A cooling system protects the urinary
the test, as this may artificially increase the tract from heat damage during the
PSA reading. procedure.
 A benign (non-cancer) enlargement of the
prostate can cause a rise in PSA levels, as 3. Transurethral Incision of the Prostate (TUIP)
can inflammation of the prostate  TUIP is used for smaller prostate but still
(prostatitis). The most serious cause of a have major blockage of the urethra.
rise in PSA is cancer. Instead of cutting and removing tissue,
TUIP widens the urethra.
 Uses a laser beam or an electrical
3. Uroflowmetry
current to make small cuts in the bladder
 Assesses degree of bladder obstruction.
neck, where the urethra joins the
bladder, and in the prostate. This
4. IVP with post voiding film reduces the pressure of the prostate on
 Shows delayed emptying of bladder, the urethra and makes urination easier.
  A catheter is left bladder for one to three
days after surgery.
4. Trans Urethral Needle Ablation (TUNA)
Transurethral radiofrequency needle ablation of
the prostate
 Low-level radiofrequency is transmitted
to the prostate via a transurethral needle
delivery system.
 The resultant heat causes localized
necrosis of the prostate.
MANAGEMENT
Pharmacologic:
 Alpha-adrenergic blockers (eg,
Alfuzosin, Terazosin), which relax the
smooth muscle of the bladder neck and
prostate, and 5alpha reductase inhibitors.
 Hormonal manipulation with
antiandrogen agents (Finasteride
[Proscar]) decreases the size of the
prostate and prevents the conversion of
testosterone to dihydrotestosterone (DHT).
Nursing Interventions:
Preoperative and postoperative nursing interventions for
a patient with BPH are as follows:
 Reduce anxiety. The nurse should
familiarize the patient with the preoperative
and postoperative routines and initiate
measures to reduce anxiety.
 Relieve discomfort. Bed rest and
analgesics are prescribed if a patient
experiences discomfort.
 Provide instruction. Before the surgery,
the nurse reviews with the patient the
anatomy of the affected structures and their
function in relation to the urinary and
reproductive systems.
 Maintain fluid balance. Fluid balance
should be restored to normal.
EBOLA
 Ebola virus disease (EVD), formerly known as
Ebola Hemorrhagic fever, is a severe, often fatal
illness affecting humans and other primates.
 Ebola Hemorrhagic Fever is a rare and deadly
disease caused by infection with one of the
Ebola virus’s strains. Ebola can cause disease in
humans and nonhuman primates.
 The virus is transmitted to people from wild
animals (such as fruit bats, porcupines and non-
human primates)
 Spreads in the human population through direct
contact with the blood, secretions, organs or
other bodily fluids of infected people, and with
surfaces and materials (e.g. bedding, clothing)
contaminated with these fluids.
WHO DATA
 The average EVD case fatality rate is around
50%.
 Case fatality rates have varied from 25% to 90%
in past outbreaks.
 The first EVD outbreaks occurred in remote
villages in Central Africa, near tropical
rainforests.
 The 2014–2016 outbreak in West Africa was the
largest and most complex Ebola outbreak since
the virus was first discovered in 1976.
 It also spread between countries, starting in
Guinea then moving across land borders to
Sierra Leone and Liberia.
 It is thought that fruit bats of the Pteropodidae
family are natural Ebola virus hosts.
ETIOLOGIG AGENT
 Ebola virus
TRANSMISSION
 Blood or body fluids of a person who is sick with
or has died from Ebola
 Objects that have been contaminated with body
fluids (like blood, feces, vomit) from a person
sick with Ebola or the body of a person who died
from Ebola
INCUBATION
 2 to 21 days after exposure to Ebola, but the
average is 8 to 10 days.
SIGNS AND SYMPTOMS
 Fever
 Severe headache
 Vomiting
 Abdominal pain
 Muscle pain
 Weakness
 Fatigue
 Diarrhea
 Unexplained hemorrhage
 Sore throat
 Rash
 Symptoms of kidney and live function
 In some cases, both internal and external
bleeding (for example, oozing from the gums, or
blood in the stools)
 Laboratory findings include low white blood cell
and platelet counts and elevated liver enzymes.
DIAGNOSTIC
  Polymerase chain reaction (PCR) is one of
the most commonly used diagnostic
methods because of its ability to detect low
levels of Ebola virus.
 To determine whether EVD is a possible
diagnosis, there must be a combination of
symptom suggestive of EVD AND a possible
exposure to EVD within 21 days before the
onset of symptoms.
 An exposure may include contact with:
o blood or body fluids from a person sick
with or who died from EVD,
o objects contaminated with blood or body
fluids of a person sick with or who died
from EVD,
o infected fruit bats and nonhuman
primates (apes or monkeys), or
o Semen from a man who has recovered
from EVD.
Within a few days after symptoms begin:
 Antigen-capture enzyme-linked
immunosorbent assay (ELISA)
 IgM ELISA
 Polymerase chain reaction (PCR)
 Virus isolation
Later in disease course or after recovery
 IgM and IgG antibodies
Retrospectively in deceased patients
 Immunohistochemistry testing
 PCR
 Virus isolation
TREATMENT
Medical Management
 Symptoms of Ebola and complications are
treated as they appear
 Provide intravenous fluids and balancing
electrolytes in the body
 Maintain oxygen status and blood pressure
 Treat other infections if they occur.
 EVERBO – First US FRA approved vaccine
December 2019
Prevention
 Practice careful hygiene
 Do not handle items that may have come in
contact with an infected person’s blood or
body fluids
 Isolate patients with EBOLA from other
patients
 Practice proper infection control and
sterilization measures
 Wear appropriate personal protective
equipment
 Notify health officials if had direct contact
with blood or body fluids of a person who is
sick with Ebola
Treatment and Management (according to WHO)
 There is no proven treatment for Ebola but
simple interventions early on can
significantly improve chances of survival.
 Rehydration with fluids and body salts (given
orally or intravenously), and treatment of
specific symptoms such as low blood
pressure, vomiting, diarrhea and infections.
 Hand hygiene is the most effective way to
prevent the spread of the Ebola virus.
 An experimental Ebola vaccine known as
rVSV-ZEBOV proved highly protective
against the deadly virus in a major trial in
Guinea in 2015. It is being used in response
to the current outbreak in the Democratic
Republic of the Congo using a ring
vaccination protocol.
 During an outbreak, health partners apply a
package of interventions including case
management, surveillance, contact tracing,
laboratory testing, safe burials and
community engagement.
 Working with communities to reduce risk
factors for Ebola transmission is critical to
controlling outbreaks.
Treatment according to CDC
Symptoms of Ebola virus disease (EVD) are treated as
they appear. When used early, basic interventions can
significantly improve the chances of survival. These
include:
 Providing fluids and electrolytes (body salts)
through infusion into the vein
(intravenously).
 Offering oxygen therapy to maintain oxygen
status.
 Using medication to support blood pressure,
reduce vomiting and diarrhea and to
manage fever and pain.
 Treating other infections, if they occur.
Antiviral Drugs (according to CDC)
 During the 2018 eastern Democratic
Republic of the Congo outbreak, four
investigational treatments were initially
available to treat patients with confirmed
Ebola.
 Regeneron (REGN-EB3) and mAb114,
overall survival was much higher. These two
antiviral drugs currently remain in use for
patients with confirmed Ebola.
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
  It is an auto-immune disorder, non-contagious,  Pulmonary: Pulmonary hypertension,
chronic, progressive inflammatory disease of the pleurisy, parenchymal disease
connective tissue.

RISK FACTORS Diagnostic Criteria: SOAP BRAIN MD

 Genetic abnormality  Serositis – Pleuritis or pericarditis or
 Viral infection peritonitis
 Medications  Oral ulcer
 Arthritis
 Photosensitivity
Clinical Manifestations  Malar rash
Signs and Symptoms:  Discoid rash
 Arthritis (initial manifestation) to arthralgia  Blood
 Weakness, fever, fatigue, weight loss  Renal disorder
 Photosensitivity from the sun  Antinuclear antibody
 Butterfly rash/ malar rash  Immunologic disorder
Skin lesions  Neurologic Disorder
 May occur in the exposed part of the neck
 May spread to the mucous membranes and Diagnostic Tests
other tissues of the body  Medical History
 Do not ulcerate, but cause degeneration and  Complete physical exam
atrophy of tissues involved  Laboratory tests for:
o CBC
Systemic Involvement of other Organs: o ESR
 Lupus Nephritis o U/A
 Pleuritis o Blood Chemistry
 Pericarditis o Complement levels
 Peritonitis  Antinuclear antibodies/ANA or ANF
 Neuritis o The ANA test measures the pattern and
 Anemia amount of autoantibody which can
attack the body’s tissues as if they were
Other Clinical Manifestations: foreign material.
 Musculoskeletal: Arthritis, arthralgia  Anti-extractable nuclear antigen (anti-ena)
 Extractable nuclear antigens
 Constitutional: fever (absence of infection),  Anti-smith and anti-double stranded DNA
fatigue, weight loss (dsdsna)
 Anti-cardiolipin antibodies
 Skin: Malar (Butterfly) rash, alopecia,  Skin biopsy
photosensitivity, purpura, Raynaud’s  Kidney biopsy
phenomenon, urticaria, vasculitis
o Raynaud’s phenomenon is a condition Two Diagnostic Classification
which cold temperatures or strong Simplest classification tree:
emotions cause blood vessel spasms  SLE is diagnosed if a person has an
that block blood flow to the fingers, toes, immunologic disorder (anti-DNA antibody,
ears, and nose anti-Smith antibody, false positive syphilis
test, or LE cells) or malar rash
 Gastrointestinal: Nausea, vomiting,  Full classification tree: Uses 6 criteria
abdominal pain
Medical Management
 Renal: Proteinuria, hematuria, nephrotic  NSAIDs
syndrome  Antimicrobials
 Corticosteroids
 Hematologic: Anemia, thrombocytopenia,  Immunosuppressive
leukopenia  Ointments and creams
 Chiropractics
 Cardiac: Pericarditis, endocarditis,
 Sunscreens
myocarditis
 Special diet
 Nutritional supplement
 Neurologic: Seizures, psychosis, peripheral
and cranial neuropathies  Fish oils
 Exercise and rest
  Stress reduction
 Family planning
 Yearly influenza and pneumococcal
vaccination
 Antimalarial drug: Hydroxychloroquine
(Plaquenil)
 Topical Corticosteroids
 Cytotoxic Agents or Antineoplasitc
Nursing Interventions
 The nurse should emphasize importance of
screening t for osteoporosis, because long term
use of corticosteroids increases the incidence of
osteoporosis.
 Educating the patient regarding calcium and
Vitamin D supplementation daily is encouraged,
along with the benefits of weight bearing activities
to support bone health (Cash & Glass, 2015).
 Patients should be instructed to avoid exposure
or to protect themselves with sunscreen and
clothing.
 The nurse educates the patient about the
importance of continuing prescribed medications.
 Patients should be instructed for routine periodic
screenings as well as health promotion activities.
 The patient may benefit from participation in
support groups, which can provide disease
information, daily management tips, and social
support.
 The patient is reminded of the importance of
monitoring because of the increased risk of
systemic involvement, including renal and
cardiovascular effects.
 Due to the immunosuppression associated with
systemic corticosteroid usage, the nurse must
watch for signs and symptoms of infection,
especially with acutely ill patients.
Nursing Management/ Nursing Implementation
 Psychosocial issues
o Counsel patient and family that SLE has
good prognosis.
o Physical effects can lead to isolation,
self-esteem, and body image
disturbances.
o Assist patient in developing goals
MULTIPLE MYOLEMA
 It is a malignant disease of the most mature form
of B lymphocyte, the plasma cell. It is
characterized by proliferation of neoplastic
plasma cells derived from one B lymphocyte
(clone) and producing a homogeneous
immunoglobulin (M protein or Bence Jones
protein) without apparent antigenic stimulation.
Pathophysiology
 The disease process involved excessive
production of plasma cells.
 Plasma cells are activated plasma B cells,
which produces immunoglobulins that
normally protect the body.
 However in multiple myeloma malignancy
plasma cells infiltrated the bone marrow and
produce abnormal and excessive amount of
immunoglobulins.
Clinical Manifestation
 Bone pain, usually at the back or ribs
 Lytic lesions as well as osteoporosis
 Vertebral collapse or fracture
 Hypercalcemia
 Excessive dehydration, constipation, thirst
 Altered mental status, confusion or even
coma
 Evidence of end-organ damage
characterized by elevated CRAB
o Calcium
o Renal insufficiency
o Anemia
o Bone lesion
Diagnostic Tests:
 Serum protein electrophoresis – elevated
monoclonal protein spike in the serum
 Urine protein electrophoresis- elevated
monoclonal protein spike in the urine
 Serum free light chain analysis – elevated
monoclonal protein spike in light chain
 Bone marrow aspiration and biopsy
demonstrate increased number and
abnormal form of plasma cells
 CBC and blood smear changes reflects
anemia
 Urine and serum analysis for presence and
quantity of abnormal immunoglobulin
 Skeletal X-rays shows osteolytic bone
lesions
Medical Management
 No Cure for multiple myeloma
 Bone marrow transplant is considered to
extend remission rather than to provide a cure
 Chemotherapy is the primary treatment
 Radiation therapy (combined with
chemotherapy) is used for strengthening bone at
a specific lesion, relieving pain and reducing size
of plasma cells tumors that occur outside
skeletal system
 Vertebroplasty is performed if lytic lesions
result in vertebral compression
 Bisphosphonates- Pamidronate (Aredia),
Zoledonic acid (Zometa)
 Plasmapheresis may be used to lower the
immunoglobulin level
Nursing Management
 Administer NSAIDS combined with opioid
analgesic as ordered
  Educate patients for activity restrictions such as
lifting of heavy objects
 Use of braces to support the spinal column
 Maintaining mobility and hydration
 Instruct patient in infection prevention measures
RHEUMATOID ARTHRITIS
 Rheumatoid arthritis is a long-term condition that
causes pain, swelling and stiffness in the joints.
The condition usually affects the hands, feet and
wrists.
 Some people with rheumatoid arthritis also
experience problems in other parts of the body,
or more general symptoms such as tiredness
and weight loss.
 It is a systemic inflammatory disease which
manifests itself in multiple joints in the body. The
inflammatory process primarily affects the lining
of the joints (synovial membrane), but can also
affect other organs. The inflamed synovium
leads to erosions of the cartilage and bone.
7 S’S
 Sunrise stiffness
 Soft feeling in joints
 Swelling in joints (warm)
 Symmetrical
 Synovium (affected and inflamed)
 Systemic (fever, fatigue, anemia
 Stages (synovitis, pannus develops, ankylosis
(bone fusion)
Other Signs and Symptoms:
 Edematous, warm, tender joints- Limited range
of motion in affected joints
 Generalized edema or nodules around affected
joints
 Impaired mobility and ability to perform ADLs
 Fatigue, weakness and anorexia – Subluxation
of joints
 Swan neck deformity (hypertension of proximal
interphalangeal joint and partial flexion of distal
interphalangeal joint)
 Boutonniere deformity (flexion of the PIP joint
with hyperextension of the DIP joint)
 Baker’s cyst – popliteal area behind the knee
 In later stages, weight loss, fever, anemia,
muscle atrophy and Sjogren syndrome.
DIAGNOSTIC TEST
 Radiographic studies reveal abnormalities such
as progressive joint damage
 Elevated Rheumatoid Factor – Elevated ESR
 Decreased RBS and C4 complement
 Anti-cyclic citrullinated peptide (CCP)
 Synovial fluid analysis
STAGES of RHEUMATOID ARTHRITIS
STAGE 1
 This is the early stage of RA, there is
inflammation of the joint but there is no damage
to the bones.
 The body mistakenly attacks its own join tissue
STAGE 2
 Moderate stage RA, the synovium’s
inflammation causes damage to the joint
cartilage. ROM in the joints may become limited.
 The body makes the antibodies and the joints
start swelling up.
STAGE 3
 Severe RA, damage extends not only to the
cartilage but to the bones.
 The joints start becoming bent and deformed,
the fingers become crooked. These misshapen
joints can press on the nerves and can cause
nerve pain as well.
STAGE 4
 The end-stage RA, the joints may become
destroyed and the bones fused together
(ankylosis).
 If not treated, the disease will progress to the
last stage, in which there’s no joint remaining at
all and the joint is essentially fused.
Rheumatoid Factor
Self anigen (IgG)  B Lymphocyte  Plasma cell 
Anti-IgG  IgM (This IgM is a RA factor)
 Immune system mistakenly sends antibodies to
the lining of joints, where they attack the tissue
surrounding the joint.
 This causes the thin layer of cells (synovium)
covering joints to become sore and inflamed,
releasing chemicals that damage nearby:
o Bones
o Cartilage – the stretchy connective
tissue between bones
o Tendons – the tissue that connects
bone to muscle
o Ligaments – the tissue that connects
bone and cartilage
 If not treated, these chemicals gradually cause
the joint to lose its shape and alignment. It can
destroy the join completely.
MEDICAL MANAGEMENT
The goal of pharmacologic therapy is to reduce pain,
decrease inflammation, maintain or restore joint function
and prevent bone and cartilage destruction.
 Corticosteroids
 Non-steroidal anti-inflammatory drugs (NSAIDs)
 Non-biologic disease modifying antirheumatic
drugs (DMARDs)- Gold salt, Methotrexate
 Biologic DMARDs - Etanercept
SURGICAL MANAGEMENT
 Synovectomy – removal of partial or all the
synovial membrane of joint
  Tenosynovectomy – excision of a tendon
sheath
 Arthroplasty – reconstruction or replacement of
joint
 Arthrodesis – immobilization of joint by fusion
of the adjacent bones
NURSING MANAGEMENT
 Administer prescribed medication
 Provide pain relief
 Encourage body alignment by the client to
prevent contractures
 Collaborate with physical therapist
 Recommend weight reduction if appropriate
 Promote self-care
 Promote adequate rest and sleep
 Discuss maintaining optimal nutritional status
 Mental status (patents are prone to developing
depression – low esteem fatigue, pain, life
altering, no cure)
 Joint assessments (symmetrical, stiffness – how
long, time it happens)
HODGKIN’S DISEASE
 Is a type of lymphoma, which is a cancer
originating from white blood cells called
lymphocytes
 Is characterized by the orderly spread of the
disease from on lymph node group to another
and by the development of systemic symptoms
with advanced disease
STAGES
 STAGE 1
o Localized disease; single lymph node
region or single organ
o HL cells found in a single lymph node
region (this can include one node or a
group of adjacent nodes), OR HL cells
found in one organ or site outside the
lymphatic system.
 STAGE 2
o Two or more lymph node regions on the
same side of the diaphragm
o HL cells found in two or more lymph
node regions on the same side of the
diaphragm (the thin muscle below the
lungs and heart that separates the chest
from the abdomen), either above the
diaphragm or below the diaphragm, OR
HL cells found in a lymph node area and
a nearby organ outside the lymphatic
system, on the same side of the
diaphragm
 STAGE 3
o Two or more lymph node regions about
and below the diaphragm
o HL cells found in lymph node regions on
both sides of the diaphragm (above and
below), possibly with localized
involvement of an organ outside the
lymphatic system or the spleen.
 STAGE 4
o Widespread disease multiple organs,
with or without lymph node involvement
o HL cells have spread widely into one or
more organs outside the lymphatic
system.
SIGNS AND SYMPTOMS
 Painless swelling of the lymph nodes at armpit,
neck, around the groin
 Night sweats
 Fever
 Sever itching
 Persistent fatigue
 Unintended weight loss
 Enlarged spleen
 Pain in the lymph nodes after alcohol intake
RISK FACTORS
 Age: HD is often seen in people age between
15 to 40 and above 55 years
 A family history of Lymphoma: If HD is
present in any blood relative; it may increase the
risk of developing the disease.
 Male Gender: Males are more prone to HD than
females
 Epstein-Barr Infection: People who had
suffered from infectious mononucleosis have
more chances of developing HD.
 HIV/AIDS: People with HIV/AIDS are more likely
to get this disease.
DIAGNOSTIC TEST:
 Physical Exam: A doctor will check for inflamed
or swollen lymph nodes at neck, armpit and
groin, and enlarged spleen or liver.
 Blood Test: The blood sample is collected and
examined in lab to analyze for any possibilities
that can contribute to cancers.
 Imaging Tests: It is performed to locate the
tumors and to look for the signs of spread of
cancer to other body parts. It includes computed
tomography (CT), Magnetic Resonance Imaging
(MRI) and positron emission tomography.
 Lymph Node Biopsy: A section of lymph node
is removed for a biopsy. It is performed to look
for abnormal cells in the lymph node.
 Bone Marrow Biopsy: The bone marrow cells
are extracted by inserting a needle in the
hipbone and analyzed for Hodgkin’s lymphoma
cells.
TREATMENT
 Chemotherapy
  It uses drugs or chemicals that are
administered orally or through the vein.
Chemotherapy kills cancer cells. In
advanced HD, chemotherapy can be
performed alone or along with
radiotherapy.
 Radiation Therapy
 It uses high energy beams of radiations,
such as X-ray and protons to kill
cancerous cells.
 Radiation therapy is best to treat early
stages of nodular lymphocyte-predominant
Hodgkin’s lymphoma.
 Radiotherapy techniques and field
NURSING INTERVENTIONS
 Bone Marrow Transplant
 It is also known as stem cell transplant.
 The diseased bone marrow is replaced
with healthy stem cells that help to grow
new bone marrow.
 It is an option when HD recurs after
treatment.
 Targeted Drug Therapy
 TIt is an advanced technique where an
immune system is activated to fight
against cancer cells.
Documentation Guidelines
Response to staging:
 To protect the skin receiving radiation, avoid
rubbing, powders, deodorants, lotions, or
ointments (unless prescribed) or application of
heat or cold.
 Encourage patient to keep clean and dry, and to
bathe the area affected by radiation gently with
tepid water and mild soap.
 Encourage wearing loose-fitting clothes and to
protect skin from exposure to sun, chlorine, and
temperature extremes.
 To protect oral and gastro-intestinal tract
mucous membranes, encourage frequent, small
meals, using bland and soft diet at mild
temperatures.
 Teach the patients to avoid irritants such as
alcohol, tobacco, spices, and extremely hot or
cold foods.
 Administer or teach self-administration of pain
medication or antiemetic before eating or
drinking, if needed.
 Encourage mouth care at least twice per day
and after meals using a soft toothbrush or
toothete and mild mouth rinse.
 Assess for ulcers, plaques, or discharge that
may be indicative of superimposed infection.
 For diarrhea, switch to low-residue diet and
administer anti-diarrheals as ordered.
 Teach patient about risk of infection. Advice
patient to monitor temperature and report any
fever or other sign of infection promptly.
 Explain to patient that radiation therapy may
cause sterility.
 Emotional and physical response to diagnostic
testing, healing of incisions, signs of ineffective
coping response to diagnosis, ability to
participate in planning treatment options,
response of significant others

Response to treatment:
 Effects of chemotherapy or radiation therapy, or
both; response to treatment of symptoms,
presence of complications (weight loss,
infection, skin irritation)
 Emotional state: Effectiveness of coping,
presence of depression, interest in group
support or counseling, referrals mad
 Discharge and Home Healthcare Guidelines
SEVERE ACUTE RESPIRATORY SYNDROME (SARS)
 is a serious, potentially life-threatening viral
infection caused by the Coronaviridae family,
the
 SARS-associated coronavirus (SARS-CoV).
Initially began in the Guangdong province of
southern China. SARS is characterized by a
phase of cytokine storms with various
chemokines and cytokines being elevated.
SIGNS AND SYMPTOMS
The clinical course of SARS generally follows a typical
pattern. Stage 1 is a flu like prodrome that begins 2-7
days after incubation, lasts 3-7 days, and is
characterized by the following:
 Fever 38 ⁰C
 Fatigue
 Headaches
 Chills
 Myalgia
 Malaise
 Anorexia
Less common features include the following:
 Sputum production
 Sore throat
 Coryza
 Nausea and vomiting
 Dizziness
 Diarrhea
Stage 2 is the lower respiratory tract phase and is
characterized by:
 Dry cough
 Dyspnea
 Progressive hypoxemia in many cases
 Respiratory failure that requires mechanical
ventilation
DIAGNOSTIC TEST:
 Pulse oximetry
 Blood cultures
 Sputum gram stain and culture
 Viral respiratory pathogen test - influenza A
and B viruses and respiratory syncytial virus
 Legionella and pneumococcal urinary antigen
test
 WBC- decreased
 Mild hyponatremia and hypokalemia
 Elevated lactate dehydrogenase alanine
aminotransferase and hepatic transaminase
 Elevated creatine kinase level
 Serum antibodies to SARS-CoV in single serum
specimen
 RT-PCR (reverse transcriptase polymerase
chain reaction)
 Chest radiograph - interstitial infiltrates
MEDICAL MANAGEMENT:
 No definitive medication protocol specific to
SARS has been developed, although various
treatment regimens have been tried.
 Corticosteroid
 Antiviral agents (Ribavirin)
 Protease inhibitors (Lopinavir, Ritonavir)
 Interferon
 Monoclonal antibodies - emergency prophylaxis,
neutralizes virus activity in vitro and in vivo
 Intravenous immunoglobulin (IVIG)
 Nitric oxide
 Glycyrrhizin - inhibits vitro replication of the
virus
 Vaccine – phase 1 clinical trial 2004
INFLUENZA
 H1N1 influenza, referred to as swine flu, is a
highly contagious respiratory disease in pigs that
can be transmitted to humans.
Etiologic Agent: Influenza A virus subtype H1N1
Mode of transmission: close and direct contact with
infected person
Incubation Period: ranges from 1 to 4 days with an
average of 2 days up to 7 days
SIGNS AND SYMPTOMS
 Cough
 Fever
 Sore throat
 Stuffy or runny nose
 Body ache
 Headaches
 Chills
 Fatigue
DIAGNOSTIC TEST:
 PCR
 Rapid antigen or antibody immunoassays
 Viral culture
MEDICAL AND TREATMENT MANAGEMENT:
 Antipyretic
 Analgesics
 Increased fluid consumption
 Bedrest
  Antiviral agents (Oseltamivir/ Zanamivir)
 Isolation
 Vaccination – Influenza virus vaccine trivalent
(Fluzone,
 Flucelvax)
 Influenza virus quadrivalent (Afluria
Quadrivalent, Fluarix)
PREVENTION AND PRECAUTION:
 Seek medical care if suspected with H1N1
 Isolate patient immediately in a negative-
pressure air handling
 Wash hands frequently
 Wear face mask
 Social distancing or avoid large gatherings
 Routine cleaning and disinfection
 Pre-exposure prophylaxis
Treatment of HIV-Related
Illnesses and AIDS
Is HIV and AIDS the same thing?
Key Terms
 Human Immunodeficiency Virus (HIV)
 virus that primarily infects cells of the immune
system and that causes AIDS
 Acquired Immune Deficiency Syndrome (AIDS)
 disease that is caused by HIV infection, which
weakens the immune system
 Pandemic
 disease that spreads quickly through human
populations all over the world
 Helper T Cell
 white blood cell that activates the immune
response and that is the primary target cell of
HIV infection
 Opportunistic Infection
 illness due to an organism that causes
disease in people with weakened immune
systems; commonly found in AIDS patients
 Universal Precautions
 set of procedures used to avoid contact with
body fluids & to reduce the risk of spreading
HIV & other diseases
 HIV-antibody test
 detects HIV antibodies to determine if a
person has been infected with HIV
 Asymptomatic stage
 infection in which the infectious agent, such as
HIV, is present but there are few or no
symptoms of the infection.
 HIV Positive
 person who tests positive in 2 different HIV
tests
 Drug Combination Therapy
 AIDS treatment program in which patients
regularly take more than one drug
 HIV
 “Human Immunodeficiency Virus”
 A specific type of virus (a retrovirus)
 HIV invades the helper T cells to replicate
itself.
 No Cure
 is a retrovirus that selectively attacks the CD4
+ T lymphocytes, the immune cell responsible
for orchestrating and coordinating the immune
response to infection. And causes AIDS.
2 Major Types:
▪ HIV-1: the virus responsible for most HIV infection
world-wide
▪ HIV-2: is endemic in West Africa, rare worldwide. The
incubation period is 10 years.
H- Human: because this virus can only infect human
beings.
I- Immuno-deficiency: because the effect of the virus is
to create a deficiency, a failure to work properly, within
the body's immune system.
V - Virus: because this organism is a virus, which
means one of its characteristics is that it is incapable of
reproducing by itself. It reproduces by taking over the
machinery of the human cell.
 AIDS
 Acquired Immunodeficiency Syndrome
 HIV is the virus that causes AIDS
 Disease limits the body’s ability to fight
infection
 A person with AIDS has a very weak immune
system
 No Cure
 An infectious disease of the immune system
caused by the retrovirus HIV-1. And a chronic,
potentially life-threatening condition caused by
the human.
 A secondary immunodeficiency disorder that
results from HIV infection, which is transmitted
by blood, semen or vaginal fluids
A - Acquired: because it's a condition one must
acquire or get infected with; not something
transmitted through the genes
I – Immune: because it affects the body's immune
system, the part of the body which usually works
to fight off germs such as bacteria and viruses
D - Deficiency: because it makes the immune
system deficient (makes it not work properly)
S -Syndrome: because someone with AIDS may
experience a wide range of different diseases and
opportunistic infections.
Life Cycle of HIV
1. Free HIV
2. HIV attaches to CD4 receptor site
3. Reverse transcriptase
4. HIV DNA penetrates T-cell nucleus
 5. DNA replicates HIV virus using protease
6. Assembly of new HIV virus
7. Accumulation of viral RNA
8. Cell Death
Seroconversion
 The point at which an infected person converts
to from being negative for the presence of HIV
antibodies in the blood to being positive
Window period
 Time after infection and before seroconversion
Three Phases of HIV
Phase 1- Asymptomatic Stage/ PRIMARY
INFECTION/EARLY ACUTE PHASE
 Fever, myalgias, night sweats, fatigue, sore
throat, GI problems, lymphadenopathies, rashes,
headache.
 There is increase viral replication----à leads to
very high viral loads, and a decrease inCD4
count.
 Usually appears 2-4 weeks after exposure to
HIV and last for few days to 2 weeks.
 After several weeks, the immune system acts
to control viral replication and reduces the viral
load to a lower level, where it often remains for
several years.
 In the initial (primary infection) phase of the
infection, immunoglobulin M (IgM) antibodies are
produced and as these levels drop (and become
undetectable) immunoglobulin G (IgG) levels rise
and remain detectable. Upon reinfection, IgM
antibodies usually do not rise again but IgG levels
will increase. Thus an elevated IgM titer indicates
recent primary infection, while the presence of
IgG suggests past infection or immunization.
Phase 2 – CHRONIC ASYMPTOMATIC
PHASE (LATENCY)
 The person has no signs & symptoms of illness.
 Median time is 10 years.
 CD4 count falls gradually from the normal
range (800-1000 cell/ul) to 200 cells/ul.
 Persistent generalized lymphadenopathy (
3 months at least 2 locations).
Phase 3 - HIV  Overt AIDS
 Immune system weakens
 Emergence of opportunistic infections and
cancers
 Occurs when a person has CD4 count less
than 20 cells/ul ; risk of opportunistic infection
and death is increased.
 Without antiretroviral therapy, this phase
leads to death within 2-3 years.
 Over time the immune system becomes
damaged and weakened by HIV and symptoms
develop. Initially they can be mild but they do
worsen, symptoms include fatigue, weight loss,
mouth ulcers, thrush and severe diarrhoea. The
symptoms are caused by the emergence of
opportunistic infections; they are referred to as
opportunistic infections because they take
advantage of a person’s weakened immune
system. Some examples of opportunistic
infections are PCP, toxoplasmosis, TB and
kaposi sarcoma
4. OVERT AIDS
 Occurs when a person has CD4 count less than
20 cells/ul which is risk of opportunistic infection
and death is increased. Without antiretroviral
therapy, this phase leads to death within 2-3
years.
Opportunistic Infections associated with AIDS
 Bacterial
 Tuberculosis (TB)
 Pneumocystis pneumonia
 Viral
 Kaposi Sarcoma-purple-red blotches on the
skin
 Influenza (flu)
Modes of HIV/AIDS Transmission
Mode of Transmission • Postpartum
 Sexual Contact (Unprotected sex)
 Vaginal and anal sexual intercourse, • After the birth
 Oral sex {1-3%} (cunnilingus-oral stimulation of
vulva/clitoris, fellatio- oral stimulation of penis)
 Sources: semen/ sharing uncleaned sex toys

 Intravenous Drug/ Injection Drug Used and

Blood products
 Needle sharing/ blood transfusion

 Perinatal:
 During labor, delivery & breast feeding
 Infected mother in the utero/ through intrapartum
inoculation/ breastfeeding

Other transmission (rare cases):

 Acupuncture
 Artificial insemination
 Tattoo
 Human bite
Classification of Infection
Sources
 Blood
 Semen
 Breast milk
 Urine
 Saliva

According to the CDC, HIV is not spread by tears,
sweat, coughing or sneezing nor it is transmitted via
infected persons, clothes, eating utensils or even
insect bites.
Through Bodily Fluids
• Blood products
• Semen
• Vaginal fluids
• Breast Milk

Through IV Drug Use

• Sharing Needles 
 CD4 cells:
• Without sterilization
 650-1200 cells/mm3: competent immune
• Increases the chances of contracting HIV system
 500-200 cells/mm3: suppressed immune
Through Sex system
• Intercourse (penile penetration into the vagina)
 <200 cells/mm3: AIDS!!!!!!!!!!!
• Oral
 (according to CDC)
• Anal
• Digital Sex VIRAL LOAD
Mother-to-Baby • <10,000 (low risk)
• Before Birth • 10,000-100,000 (moderate risk)
• During Birth • 100,000> (high risk)
  Aseptic meningitis

 Oral and genital ulcers

2.) CATEGORY B
 Persons with symptoms of immune deficiency
not serious enough to be AIDS defining
 Median time is 10 years
 CD4 count falls gradually from the normal
range
 Persons with symptoms of immune deficiency
not serious enough to be AIDS defining
 Median time is 10 years
 CD4 count falls gradually from the normal
range
Diagnostic Conditions
1. Presence of HIV
2. T4 cell count is below 200 (CD4) 3.) CATEGORY C
3. Presence of 1 or more of AIDS specified conditions  Includes AIDS defining illness
 Patients have OPPORTUNISTIC INFECTIONS

CDC Classification System for HIV Infection

• Cat A= >500 cells/ul
• Cat B= 200- 499 cell/ul
• Cat C=< 200 cells/ul.

Clinical Categories: According to Clinical Manifestations

1.) CATEGORY A
 Includes person who are asymptomatic
or have persistent
generalized lymphadenopathies.
 Primary HIV infection
AIDS DEFINING CONDITIONS:
 Fever, myalgias, night sweats, fatigue, sore  Opportunistic infections:
throat, GI problems, lymphadenopathies,
rashes, headache • Pneumocystis carinii pneumonia (PCP)
• Candidiasis
S/SX OF ACUTE HIV INFECTION:
• Cytomegalovirus
 Fever
• Herpes simplex
 Fatigue
• Mycobacterium avium complex (MAC)
 Rash
• Mycobacterium tuberculosis
 Headache
• Recurrent pneumonia
 Lymphadenopathy
• Histoplasmosis (fungal infxn)
 Pharyngitis

 Arthralgia 1.Pneumocystis Carinii Pneumonia (PCP)

 The alveoli become filled with foamy, protein rich
 Myalgias fluid that impairs gas exchange.
 Night sweats  Pneumocystis is an opportunistic eukaryote that
is classified as a fungus.
 GI problems: diarrhea
  An organism that is commonly found in the air,
food, water, and in the environment.
 Signs & symptoms: mild cough, fever, sob,
weight loss.
Pneumocytosis:
 Pneumonia occurring in infants or in persons
with impaired immune systems (as
AIDS victims).
 Respiratory disease characterized by
inflammation of the lung parenchyma
(excluding the bronchi) with congestion
caused by viruses or bacteria or irritants
2. Cytomegalovirus Infection
 Cytomegalovirus (CMV) is a virus most
commonly thought of as causing serious eye
disease in people with weakened immune
systems. It can potentially lead to blindness.
 CMV can also lead to illness in other areas of
the body, such as the digestive tract and parts
of the nervous system.
 However, the damage from CMV infection
may slow with the use of antiretroviral therapy.
This can result in the rebuilding of the immune
system (as demonstrated by clinically
significant rises in CD4 count). Anti-CMV
therapy may potentially be changed to easier-
to-tolerate suppressive treatments.
3. Mycobacterium tuberculosis
 Extrathoracic TB with or without intrathoracic
disease has been detected in two-thirds or more
of patients with overt aids.
 Tuberculosis (TB) is caused by bacteria called
Mycobacterium tuberculosis. TB infection occurs
when a person breathes in droplets produced
when someone with active TB disease coughs or
sneezes.
 These droplets can remain infectious in the air for
several hours in damp enclosed spaces with little
ventilation or direct sunlight, such as
overcrowded informal housing or prisons.
 Someone infected with both HIV and TB is at
least 10 times more likely to develop active TB,
especially when their CD4 count is under 200.
TB is the leading cause of death among people
living with HIV, causing more than one third of all
AIDS-related deaths in 2015. Almost 60% of the
estimated global HIV-related TB cases are not
diagnosed and not treated.
Clinical Manifestation:
▪A bad cough that lasts for more than 2 weeks
▪ Coughing up mucus or blood
▪ Chest pain
You may also have:
▪Weakness or fatigue
▪ Not much of an appetite
▪ Night sweats
▪ Weight loss
▪ Fever or chills
Diagnosis:
As soon as you know you have HIV:
▪ Tuberculin skin test (TST)- After 2 or 3 days, a health
care provider checks the injection site; swelling and
redness are signs of tuberculosis infection.
▪ Interferon-gamma release assay (IGRA) - blood test
A positive TST or IGRA doesn’t necessarily mean that you
have TB disease (sometimes referred to as “active” TB).
This is because the TB bacteria can remain silent in your
body (sometimes called “latent” TB).
Confirmatory test:
▪Chest X-ray
▪Sputum culture
▪ TB smear test
Treatment for Active Tuberculosis:
 Ethambutol, or EMB (Myambutol)
 Isoniazid, or INH (Nydrazid)
 Pyrazinamide, or PZA (Tebrazid)
 Rifampin, or RIF (Rifadin)
4. Hepatitis
 Hepatitis B virus (HBV) and human
immunodeficiency virus (HIV) are bloodborne
viruses transmitted primarily through sexual
contact and injection drug use. Because of these
shared modes of transmission, people at risk for
HIV infection are also at risk for HBV infection.
 Chronic HBV advances faster to cirrhosis, end-
stage liver disease, and liver cancer in people
with HIV/HBV coinfection than in people with
only HBV.
Prevention of HBV infection for HIV patient:
 CDC recommends that people with HIV and
people who are at risk for HIV get the HBV
vaccine (or the combined hepatitis A virus/HBV
vaccine)
 Use condoms during sex
 Don't share needles on injecting drugs.
 Don’t use personal items that may come in
contact with another person's blood.
 Sterilize instrument before body piercing or
tattoo.
CDC recommends that all people with HIV get
tested for HBV.
Diagnostic test: Hepatitis B Surface Antigen
(HBsAg) test
Clinical Manifestations:
  Loss of appetite
 Tiredness
 Nausea
 Vomiting
 Fever
 Abdominal pain
 Dark Urine
 Clay-colored bowel movements
 Joint Pain
 Yellowing of the skin or the whites of the eyes
(jaundice)
5. Herpes Simplex or Zoster
 The herpes simplex virus, also known as
HSV, is an infection that causes herpes. Herpes
can appear in various parts of the body, most
commonly on the genitals or mouth.
2 types of the herpes simplex virus.
1) HSV-1: primarily causes oral herpes, and is generally
responsible for cold sores and fever blisters around
the mouth and on the face.
❖ Orolabial herpes (commonly known as cold sores
or fever blisters) is the most common
manifestation of HSV-1 infection.
❖ Classic manifestations of oral HSV-1 include a
sensory prodrome in the affected area, rapidly
followed by lesions on lips and oral mucosa that
evolve in stages from papule to vesicle, ulcer, and
crust.
2) HSV-2: primarily causes genital herpes, and is
generally responsible for genital herpes outbreaks.
❖ Genital herpes is typically caused by HSV-2 and is
the most common manifestation of HSV-2 infection.
● Typical genital mucosal or ulcerative lesions
on skin on or around the genitals
● sensory prodrome consisting of pain and
pruritus.
● Mucosal disease includes dysuria or vaginal
or urethral discharge
● Inguinal lymphadenopathy
Herpes zoster (shingles)
 Shingles is caused by the varicella-zoster virus,
the same virus that causes chickenpox.
Signs and symptoms:
 Varicella rash tends to have a central distribution
with lesions first appearing on the head, then the
trunk, and finally the extremities, evolving through
stages of macules, papules, vesicles, pustules,
and crusts.
 Herpes zoster manifests as a painful cutaneous
eruption in a dermatomal distribution, often
preceded by prodromal pain.
Diagnosis:
 Varicella can also be diagnosed retrospectively
by documenting seroconversion (i.e.,
immunoglobulin G [IgG] antibody negative to
positive).
Prevention of Herpes Zoster in the patient with HIV:
▪ Vaccination to Prevent Primary Infection (Varicella)
▪ Pre-Exposure Prophylaxis to Prevent Primary
Infection (Varicella)
▪ Post-Exposure Prophylaxis to Prevent Primary
Infection (Varicella)
▪ Antiviral Prophylaxis to Prevent Reactivation
Disease (Herpes Zoster)
▪ Vaccination to Prevent Reactivation Disease
(Herpes Zoster)
Treatment for Herpes Zoster:
● Antiviral therapy should be instituted as soon
as possible for all patients with HIV with
herpes zoster diagnosed within 1 week of
rash onset (or any time prior to full crusting of
lesions).
● The recommended treatment options for
acute localized dermatomal herpes zoster in
patients with HIV are oral valacyclovir,
famciclovir, or acyclovir (doses as above)
for 7 to 10 days, although longer durations
of therapy should be considered when
lesions resolve slowly.
6. CANDIDIASIS:
 Candidiasis is a yeast infection caused by
Candida albicans. In people with HIV, the virus
that causes AIDS, candidiasis commonly affects
the skin and mucous membranes such as the
mouth, throat, esophagus and vagina.
 Painful Candidiasis is rarely life-threatening.
Signs and Symptoms of Oral candidiasis (in the mouth
and throat):
▪ White or red patches in the mouth, tongue or throat
cracking and soreness at the corners of the
mouth
▪ Altered taste, mouth pain or burning
▪ Candidiasis in the esophagus can cause upper
chest pain, sore throat and painful or difficult
swallowing
▪ In the vagina, candidiasis causes a white cheesy
vaginal discharge accompanied by vaginal
itching and burning.
Treatment HIV-related candida infections
▪ clotrimazole or nystatin
▪ lozenges or a swish-and-swallow preparation to
treat candidiasis of the mouth or throat
▪ vaginal creams or tablets for vaginal infections
▪ patient has candidiasis of the esophagus, either
oral fluconazole or ketoconazole tablets can be
taken
7. AIDS dementia complex
  Is a syndrome of cognitive and motor  Orasure-saliva
dysfunction.  CD$ cell count
 Sx: impairment in attention, concentration and  Polymerase chain reaction (PCR)
slowing of mental speed, agility, apathetic
behavior. ❖ ELISA & Western blot
1. Kaposi’s sarcoma
● With (+) result
 Is a malignancy of the endothelial cells that line ● Antibodies to HIV are present in blood
small blood vessel ● HIV is PROBABLY active
 lesions are nodules or blotches that may be red, ● Despite HIV infection, client does not necessarily
purple, brown, or black, and are usually popular have AIDS
● Client is NOT IMMUNE to AIDS.
 is a form of cancer in which tumors with tiny blood
vessels grow below the surface of your ski n and Medical management
in your mouth, nose, eye s, and anus. It can  To suppress infection, prolonging life.
spread to your lung s, liver, stomach, intestine s,  To treat opportunistic infection.
and lymph nodes, the glands that help your body
fight infection. Effectiveness: monitored by viral load count,
 It most often is found in patients with acquired CD4 cell counts (↑500)
immunodeficiency syndrome (AID S) , and can be
fatal. HIV Wasting Syndrome
 Caused by anorexia, metabolic abnormalities,
Symptoms: endocrine dysfunction, malabsorption and
 Skin: lesions are flat, painless spots that are red cytokine dysregulation.
or purple on light skin and bluish, brownish, or
black on dark skin Gynecologic
 Mucous membranes: KS lesions can form inside o recurrent vaginal candidiasis,
your mouth and throat; eyes and under eyelids.
o genital ulcer disease
 Lymph nodes: severe swelling in your arms,
legs, face, or scrotum. o venereal warts
 Respiratory tract: serious coughing and
shortness of breath.
 Digestive tract: Testing Options for HIV
Anonymous Testing
✔ An upset stomach ✔ Bloody or black poop • No name is used
✔ Vomiting ✔ Low red blood cell • Unique identifying number
counts
✔ Belly pain (anemia) • Results issued only to test recipient

✔ Diarrhea

Risk Factors
KS affects eight times more men than women. Among
people who have HIV, men who have se x with men are
more likely to have the virus and to get Kaposi’s
sarcoma.

Diagnosis:
▪Fecal occult blood test ▪ Bronchoscopy
▪ Endoscopy / colonoscopy ▪ Imaging tests

Treatment:
 Antiretroviral Therapy
 Radiation Therapy
 Chemotherapy

Diagnostic Test Confidential Testing

 ELISA (Enzyme linked immunosorbent assay) • Person’s name is recorded along with HIV
 Western Blot assay-confirmatory results
 o Name and positive results are reported
to the State Department and the Centers
for Disease Control and Prevention
• Results issued only to test recipient
Oral Testing
 Orasure
 The only FDA approved HIV antibody.
 As accurate as blood testing
 Draws blood-derived fluids from the gum
tissue.
 NOT A SALIVA TEST!
T cell count test
 Shows the strength of a patient’s immune
system
 This test can also tell whether a person has
developed AIDS
Viral load test
 Measures of the number of viruses in the blood
 The higher the viral load, the more infectious the
person’s body fluids are likely to be and the
closer that person is to having AIDS
Retest
 Should be retested 6 months after the first test
 An initial negative test can be misleading if the
test is done too soon after infection
DIAGNOSIS
1. ELISA ( Enzyme Linked Immunosorbent Assay)
2. Western Blot assay-confirmatory
3. Orasure- saliva
4. CD4 cell count
5. Polymerase chain reaction (PCR)
ELISA
 An enzyme-linked immunosorbent assay, also
called ELISA or EIA, is a test that detects and
measures antibodies in your blood.
 With (+) result
 Antibodies to HIV are present in blood
 HIV is PROBABLY active
 Despite HIV infection, client does not necessary
have AIDS
 Client is NOT IMMUNE to AIDS.
Treatment Options
Three ways to protect yourself?
• Practice abstinence
• Avoid multiple partners- Monogamous
Relationship
• Don’t share needles, syringes, drug injection
equipment, or any item that may put a person in
contact with blood
5 MEANS OF HIV PREVENTION
• A = abstain from sex
• B = be faithful
• C = correct & consistent use of condom
• D = do not use illegal drugs/share needles
• E = educate yourself
Abstinence
 It is the only 100 % effective method of not
acquiring HIV/AIDS.
 Refraining from sexual contact: oral, anal, or
vaginal.
 Refraining from intravenous drug use
Monogamous relationship
 A mutually monogamous (only one sex partner)
relationship with a person who is not infected
with HIV
 HIV testing before intercourse is necessary to
prove your partner is not infected
Protected Sex
 Use condoms (female or male) every time you
have sex (vaginal or anal)
 Always use latex or polyurethane condom (not a
natural skin condom)
 Always use a latex barrier during oral sex
When Using A Condom Remember To:
 Make sure the package is not expired
 Make sure to check the package for damages
 Do not open the package with your teeth for risk
of tearing
 Never use the condom more than once
Guidelines for care of the person with HIV/AIDS:
 Prevent infection
 Wash hands frequently
 Use gentle soap; avoid bar soap that may irritate
skin.
 Provide for daily showering/ basin bath; avoid
tub bath if rashes are present.
 Use separate washcloth for lesions
 Use soft toothbrush, nonabrasive toothpaste.
 Prevent skin breakdown
 Elevate and support areas of edema
 Observe surgical site and IV insertion sites daily
for signs of infection.
 Change dressings (if any) daily.
 Avoid eating fresh fruits / vegetables;
uncooked/ “rare” foods.
 Carry out infection control measures according
to institution’s policy
  Administer prescribed antibiotics, IV
fluids/ antipyretics.
 Encourage increase OFI.
 Monitor daily I and O records
 Weigh patient daily
 Instruct patient in deep breathing coughing
exercise- to PX: Atelectasis and fever
 Modify alterations with body temperature: TSB,
DBE, and Coughing
Promote Self-care
 Assess realistic functional ability
 Plan, supervise and assist with ADL
if necessary
 Encourage patient to be as active
and independent as possible
 Assist patient with ROM exercise to
PX contractures.
 Pace activities and schedule rest periods to
PX fatigue.
Provide Counseling
 Assess and support patient coping mechanism
 Explore with patient and significant others
normalcy of grief response and assist them in
acknowledging and planning for anticipated
losses.
Health Teaching Focuses on
 Promote Good Nutrition
 Promote Self-Care
 Promote Counseling
Nursing Management
A. Promote Good Nutrition
 Diet: High calorie, high CHON, high K, low
residue diet.
 Easy to swallow food: Gelatin when dysphagia
is present.
 Provide oral care
 Encourage patients to be out of bed and
sitting for meals if possible.
B. Promote Self- Care
 Assess realistic functional ability
 Plan, supervise and assist with ADL if
necessary
 Encourage patient to be as active and
independent as possible
 Assist patients with ROM exercise to
improve contractures.
 Pace activities and schedule rest periods to
improve fatigue.
 Handwashing
C. Provide Counseling
 Assess and support patient coping
mechanism
 Explore with patient and significant others
normalcy of grief response and assist them
in acknowledging and planning for
anticipated losses.
 Provide information as desired and
necessary, depending on ability to perceive.
 Suggest appropriate religious support
 Facilitate participation in support groups/
individual counseling.
Other Management with AIDS
 Identification of person at risk
 Obtaining a complete, accurate sexual history is
important
 Identify if IV drug user
 Check for other risk factors
 With high risk HIV/AIDS
Counsel about significant testing and necessity of follow-
up
 Educational and counseling strategies with AIDS
HIV/ AIDS drugs
 To suppress infection, prolonging life.
 To treat opportunistic infection.
 Effectiveness: monitored by viral load count,
CD4 cell counts (↑500)
 Side effects include kidney & liver damage
 30% of people who start taking some of these
drugs become so sick they have to stop taking
them
Nucleoside/nucleotide reverse
transcriptase inhibitors (NRTIs)
 NRTIs are sometimes referred to as “nukes.”
 They work by interrupting the life cycle of HIV as
it tries to copy itself.
 These drugs also have other actions that
prevent HIV from replicating in the body.
The following drugs are NRTIs:
• abacavir (Ziagen)
• emtricitabine (Emtriva)
• Lamivudine (Epivir)
• tenofovir alafenamide fumarate (Vemlidy)
• tenofovir disoproxil fumarate (Viread)
• zidovudine (Retrovir)
 Zidovudine was the first FDA-approved HIV drug. It’s
also known as azidothymidine or AZT. Zidovudine is
rarely used in adults now.
 It’s mainly given to babies born to HIV-positive
mothers as a form of post-exposure prophylaxis
(PEP).
Combination NRTIs
• The following combination drugs are made up of
either two or three NRTIs:
• abacavir, lamivudine, and zidovudine (Trizivir)
• abacavir and lamivudine (Epzicom)
• emtricitabine and tenofovir alafenamide
fumarate (Descovy)
• emtricitabine and tenofovir disoproxil fumarate
(Truvada)
• lamivudine and tenofovir disoproxil fumarate
(Cimduo, Temixys)
• lamivudine and zidovudine (Combivir)
Descovy and Truvada may also be prescribed to some
people without HIV as part of a pre-exposure
prophylaxis (PrEP) regimen.
Non-nucleoside reverse transcriptase
inhibitors (NNRTIs)
• These drugs work in a similar way to NRTIs.
They stop the virus from replicating itself in the
body.
• The following drugs are NNRTIs, or “non-nukes”:
• doravirine (Pifeltro)
• efavirenz (Sustiva)
• etravirine (Intelence)
Cytochrome P4503A (CYP3A) inhibitors
 Cytochrome P4503A is an enzyme in the liver
that helps several functions in the body,
including breaking down or metabolizing
medications.
 Cytochrome P4503A inhibitors, also known as
CYP3A inhibitors, increase the levels of certain \
HYPERSENSITIVITY
 Hypersensitivity is an excessive or aberrant
immune response to any type of stimulus. It
usually does not occur with the first exposure to
an allergen. Rather, the reaction follows a re-
exposure after sensitization, or buildup of
antibodies, in a predisposed person. Injurious or
pathologic immune reactions are classed as
hypersensitivity reactions. To promote
understanding of the immune pathogenesis of
disease, hypersensitivity reactions have been
classified into four specific types of reactions.
Most allergic reactions are either type I or type
IV hypersensitivity reactions.
Pathophysiology
Immediate hypersensitivity reactions are
mediated by IgE, but T and B cells play important roles
in the development of these antibodies. CD4+ T-cells are
divided into 3 broad classes: effector T-cells, memory T-
cells, and T-regulatory (Treg) cells. Effector T-cells are
further divided based on the cytokines they produce:
TH1, TH2, and TH17 cells. TH1 cells produce interferon-
gamma and interleukin (IL)-2, and promote a cell-
mediated immune response. TH2 cells produce IL-4 and
IL-13, which then act on B-cells to promote the
production of antigen-specific IgE. TH17 cells produce
IL-17, IL-21, and IL-22 to help fight extracellular
pathogens, to produce antimicrobial peptides. and to
promote neutrophil inflammation essential for immunity
at the skin and mucosal surfaces. Memory T-cells rapidly
differentiate into effector T-cells in secondary immune
responses. CD4+CD25+FOXP3+ Treg cells are
essential in peripheral tolerance and serve to suppress
dysregulated immune responses.
CD4+CD25+FOXP3+Tregs inhibit TH2 cytokine
production through the secretion and action of IL-10 and
TGF-beta. Proper function of CD4+CD25+FOXP3+ Treg
cells has been shown to be important in the tolerance of
allergens. Abnormalities in the CD4+CD25+FOXP3+
Treg population may play a role in the development of
allergic disease.
The allergic reaction first requires sensitization
to a specific allergen and occurs in genetically
predisposed individuals. The allergen is either inhaled or
ingested and is then processed by an antigen-presenting
cell (APC), such as a dendritic cell, macrophage, or B-
cell. The antigen-presenting cells then migrate to lymph
nodes, where they prime naïve TH cells that bear
receptors for the specific antigen.
After antigen priming, naïve TH cells differentiate
into TH1, TH2, or TH17 cells based upon antigen and
cytokine signaling. In the case of allergen sensitization,
the differentiation of naïve TH cells is skewed toward a
TH2 phenotype. These allergen-primed TH2 cells then
release IL-4, IL-5, IL-9, and IL-13. IL-5 plays a role in
eosinophil development, recruitment, and activation. IL-9
plays a regulatory role in mast cells activation. IL-4 and
IL-13 act on B cells to promote production of antigen-
specific IgE antibodies.
For this to occur, B cells must also bind to the
allergen via allergen-specific receptors. They then
internalize and process the antigen and present peptides
from it, bound to the major histocompatibility class II
molecules found on B-cell surfaces, to the antigen
receptors on TH2 cells. The B cell must also bind to the
TH2 cell and does so by binding the CD40 expressed on
its surface to the CD40 ligand on the surface of the TH2
cell. IL-4 and IL-13 released by the TH2 cells can then
act on the B cell to promote class switching from
immunoglobulin M production to antigen-specific IgE
production.
The antigen-specific IgE antibodies can then
bind to high-affinity receptors located on the surfaces of
mast cells and basophils. Re-exposure to the antigen
can then result in the antigen binding to and cross-
linking the bound IgE antibodies on the mast cells and
basophils. This causes the release and formation of
chemical mediators from these cells. These mediators
include preformed mediators, newly synthesized
mediators, and cytokines.
Allergic reactions can occur as immediate
reactions, late-phase reactions, or chronic allergic
inflammation. Immediate or acute-phase reactions occur
within seconds to minutes after allergen exposure. Some
of the mediators released by mast cells and basophils
cause eosinophil and neutrophil chemotaxis. Attracted
eosinophils and resident lymphocytes are activated by
mast cell mediators.
These and other cells (eg, monocytes, T cells)
are believed to cause the late-phase reactions that can
occur hours after antigen exposure and after the signs or
symptoms of the acute-phase reaction have resolved.
The signs and symptoms of the late-phase reaction can
include redness and swelling of the skin, nasal
discharge, airway narrowing, sneezing, coughing, and
wheezing. These effects can last a few hours and
usually resolve within 24-72 hours.
Finally, continuous or repeated exposure to an
allergen (eg, a cat-allergic patient who owns a cat) can
result in chronic allergic inflammation. Tissue from sites
of chronic allergic inflammation contains eosinophils and
T cells (particularly TH2 cells). Eosinophils can release
many mediators (eg, major basic protein), which can
cause tissue damage and thus increase inflammation.
Collectively, this results in structural and functional
changes to the affected tissue. Furthermore, a repeated
allergen challenge can result in increased levels of
antigen-specific IgE, which ultimately can cause further
release of IL-4 and IL-13, thus increasing the propensity
for TH2 cell/IgE–mediated responses
Types of Allergen
 pet dander
 bee stings or bites from other insects
 certain foods, including nuts or shellfish
 certain medications, such as penicillin or aspirin
 certain plants
 pollen or molds
Diagnostic Tests
 Complete Blood Count with Differential
 The white blood cell (WBC) count is usually
normal except with infection and
inflammation. Eosinophils, which are
granular leukocytes, normally make up 2%
to 5% of the total number of WBCs. They
can be found in blood, sputum, and nasal
secretions. A level greater than 5% to 10%
is considered abnormal and may be found in
patients with allergic disorders.
 Eosinophil Count
 An actual count of eosinophils can be
obtained from blood samples or smears of
secretions. During symptomatic episodes,
smears obtained from nasal secretions and
sputum of patients with allergies usually
reveal an increase in eosinophils, indicating
an active allergic response.
 Total Serum Immunoglobulin E Levels
 High total serum IgE levels support the
diagnosis of allergic disease. In the majority
of cases, the antibody typically responsible
for an allergic reaction belongs to the IgE
isotype. Patients with this disorder are said
to have an IgE-mediated allergic disease.
 Skin Tests
 Skin testing entails the intradermal injection
or superficial application (epicutaneous) of
solutions at several sites. Depending on the
suspected cause of allergic signs and
symptoms, many different solutions may be
applied at separate sites. These solutions
contain individual antigens representing an
assortment of allergens most likely to be
implicated in the patient’s disease. Positive
(wheal-and-flare) reactions are clinically
significant when correlated with the history,
physical findings, and results of other
laboratory tests. Skin testing is considered
the most accurate confirmation of allergy.
Four Basic Types of Hypersensitivity
I. Type I Anaphylactic (Immediate)
The most severe hypersensitivity
reaction is anaphylaxis. An unanticipated severe
allergic reaction that is rapid in onset,
anaphylaxis is characterized by edema in many
tissues, including the larynx, and is often
accompanied by hypotension, bronchospasm,
and cardiovascular collapse in severe cases.
Type I or anaphylactic hypersensitivity is an
 immediate reaction beginning within minutes of
exposure to an antigen. Primary chemical
mediators are responsible for the symptoms of
type I hypersensitivity because of their effects
on the skin, lungs, and gastrointestinal tract. If
chemical mediators continue to be released, a
delayed reaction may occur and may last for up
to 24 hours. Clinical symptoms are determined
by the amount of the allergen, the amount of
mediator released, the sensitivity of the target
organ, and the route of allergen entry. Type I
hypersensitivity reactions may include both local
and systemic anaphylaxis
A. ANAPHYLAXIS
 Anaphylaxis is a clinical response to an
immediate (type I hypersensitivity)
immunologic reaction between a specific
antigen and an antibody. The reaction results
from a rapid release of IgE-mediated
chemicals, which can induce a severe, life-
threatening reaction.
B. ALLERGIC RHINITIS
 Allergic rhinitis is a group of disorders
characterized by inflammation and irritation of
the mucous membrane of the nose. It is
associated with exposure to airborne particles
such as dust, dander or plant pollen in people
who are allergic to these substances.
Classification
1. Seasonal rhinitis – occurs during pollen seasons
2. Perennial rhinitis – occurs throughout year
Signs and Symptoms:
 Rhinorrhea
 Nasal congestion
 Sneezing
Management
 Antihistamines
 Corticosteroid nasal sprays
Nursing Management
 Instruct patient to avoid or reduce exposure to
allergens and irritants
 Instruct patient in correct administration of
nasal medication
 To achieve maximal relief, the patient is
instructed to blow the nose
C. ASTHMA
 Asthma is a chronic inflammatory disease of
the airways that causes hyperresponsiveness,
mucosal edema and mucus production is
reversible and diffuse airway inflammation
that leads to airway narrowing.
Signs and Symptoms
 Pruritus of the nose, roof of the
mouth, throat, eyes and ears
 Desensitizing immunizations
 Cough
 Dyspnea
 Wheezing
 Chest tightness
 Diaphoresis
 Tachycardia
 Widened pulse
 Hypoxia
 Central cyanosis
Medical Management:
There are two general classes of asthma medications:
1. Quick relief medications for immediate
treatment for asthma symptoms and
exacerbations
a. Short-acting beta2-adrenergic agonist
(ventolin, albuterol) and pirbuterol
(Maxair)
2. Long acting medications to achieve and
maintain control of persistent asthma
a. Corticosteroids
b. Long acting beta2- adrenergic agonist
c. Leukotriene modifiers (inhibitors)
d. Antileukotriene (montelukast)
Nursing Management:
 Assess the patient’s respiratory
status by monitoring the severity of
the symptoms, breath sounds, peak
flow, pulse oximetry and vital signs.
 Administer medications as
prescribed and monitor the patient’s
response
 Administer fluids if patient is
dehydrated
 Instruct to adhere to the prescribed
medications and therapy
 Emphasize to keep follow-up
appointments with health care
provider
D. ACUTE ALLERGIC DRUG REACTION
 Dermatitis medicamentosa, a type I
hypersensitivity disorder, is the term applied
to skin rashes associated with certain
medications. Although people react differently
to each medication, certain medications tend
to induce eruptions of similar types. This
disorder is the leading cause of fatal
anaphylaxis, comprising 43% of deaths from
anaphylaxis. All routes of administration are
potentially fatal, but drugs given parenterally
incur the greatest risk. Cutaneous rashes are
among the most common adverse reactions
to medications and occur in approximately 2%
to 3% of hospitalized patients. In general,
drug reactions appear suddenly with
 characteristics that are more intense than the
somewhat similar eruptions of infectious
origin, and, with the exception of bromide and
the iodide rashes, disappear rapidly after the
medication is withdrawn. Rashes may be
accompanied by systemic or generalized
symptoms. On discovery of a medication
allergy, patients are warned that they have a
hypersensitivity to a particular medication and
are advised not to take it again. Penicillin,
cephalosporin, and sulfonamide antibiotics
are most commonly implicated. Patients
should carry information identifying the
hypersensitivity with them at all times.
 Skin eruptions related to medication therapy
suggest more serious hypersensitivities.
Frequent assessment and prompt reporting of
the appearance of any eruptions are
important so that early treatment can be
initiated. Some cutaneous drug reactions may
indicate involvement of other organs and are
known as complex drug reactions. Patients
who suspect that a new rash may be caused
by a drug allergy (newly prescribed
medications, especially antibiotics such as
penicillin or sulfa medications) should stop
taking the medication immediately and
contact their prescribing clinician, who will
determine whether the medication and the
rash are related.
II. Type II Cytotoxic (Cytolytic reaction)
 Type II, or cytotoxic, hypersensitivity
occurs when the system mistakenly
identifies a normal constituent of the
body as foreign. This reaction may be the
result of a cross-reacting antibody,
possibly leading to cell and tissue
damage. Type II hypersensitivity
reactions are associated with several
disorders. For example, in myasthenia
gravis, the body mistakenly generates
antibodies against normal nerve ending
receptors. In Good pasture syndrome, it
generates antibodies against lung and
renal tissue, producing lung damage and
kidney injury.
A. HEMOLYTIC ANEMIA
 Hemolysis is the premature destruction
of erythrocytes. A hemolytic anemia will
develop if bone marrow activity cannot
compensate for the erythrocyte loss. The
severity of the anemia depends on
whether the onset of hemolysis is
gradual or abrupt and on the extent of
erythrocyte destruction. Mild hemolysis
can be asymptomatic while the anemia in
severe hemolysis can be life threatening
and cause angina and cardiopulmonary
decompensation. The clinical
presentation also reflects the underlying
cause for hemolysis. For example, sickle
cell anemia is associated with painful
occlusive crises.
 Hemolytic anemia has multiple causes,
and the clinical presentation can differ
depending on the etiology. An array of
laboratory tests are available for
detecting hemolysis, and specialized
tests may be indicated to diagnose the
cause for hemolysis. There are
differences in the management of various
types of hemolytic anemias.
B. INCOMPATIBLE BLOOD TRANSFUSION
REACTION
 Acute transfusion reactions present as
adverse signs or symptoms during or within
24 hours of a blood transfusion. The most
frequent reactions are fever, chills, pruritus,
or urticaria, which typically resolve promptly
without specific treatment or complications.
Other signs occurring in temporal
relationships with a blood transfusion, such
as severe shortness of breath, red urine,
high fever, or loss of consciousness may be
the first indication of a more severe
potentially fatal reaction.
III. Type III Immune- Complex Reactions
 Type III, or immune complex,
hypersensitivity involves immune complexes
that are formed when antigens bind to
antibodies. These complexes are cleared
from the circulation by phagocytic action. If
these type III complexes are deposited in
tissues or vascular endothelium, two factors
contribute to injury: the increased amount of
circulating complexes and the presence of
vasoactive amines. As a result, there is an
increase in vascular permeability and tissue
injury.
A. ACUTE GLOMERULONEPHRITIS
 Glomerulonephritis is an inflammation of
the glomeruli which result from an antigen-
antibody reaction produced from an infection
elsewhere in the body. This disorder which
is caused by an immunological reaction may
result in proliferative and inflammatory
changes within the glomerular structure.
Risk Factors
 Immunological or autoimmune diseases
 Group A beta-hemolytic streptococcal infection
(GABHS)
 History of pharyngitis of tonsillitis 2 to 3 weeks
before symptoms
Signs and Symptoms
 Gross hematuria
 Dark, smoky, cola-colored or red-brown urine
  Proteinuria, frothy urine
 Elevated urine specific gravity
 Headache
 Chills and fever
 Fatigue and weakness
 Nausea and vomiting
 Edema in the face, periorbital area and feet
 Elevated Blood Pressure
 Elevated BUN and Creatinine
 Positive antibody response test for
streptococcus
 Elevated Erythropoietin Sedimentation rate
 Hyponatremia
 Hyponatremia
 Hypophosphatemia
 Hyperkalemia
Diagnostic Tests:
Urinalysis
 (+) Hematuria and proteinuria – most important
indicator of glomerular injury
 (+) Casts, elevated specific gravity, low pH
Medical Management:
 Antimicrobial/antibiotics – Penicillin,
Erythromycin, Cephalexin
 Diuretics
 Corticosteroids
 Calcium channel blockers
 Vasodilators
 Fluid and electrolytes balance
Nursing Intervention
 Monitor Vital Signs including NVS
 Monitor weight of patient daily
 Dietary restriction of sodium and protein
 Limit fluid intake
 Carbohydrates are given liberally to provide
energy and reduce the catabolism of protein
 Provide skin care
 Observe for compilations like renal failure,
cardiac failure and hypertensive encephalopathy
 Monitor urinalysis, BUN and creatinine levels
 Promote rest and regular activity when hematuria
and proteinuria resolves
B. RHEUMATOID ARTHRITIS (done)
IV. Type IV Cell-Mediated Reactions/Delayed
Hypersensitivity
 Type IV, or delayed-type hypersensitivity,
also known as cellular hypersensitivity
 Occurs 24 to 72 hours after exposure to an
allergen
Delayed-Type (Type IV) Hypersensitivity
 Type IV, or delayed-type, hypersensitivity
(DTH), is an immune reaction in which T-
cell–dependent macrophage activation and
inflammation cause tissue injury. This type
of reaction to the subcutaneous injection of
antigen is often used as an assay for cell-
mediated immunity (e.g., the purified protein
derivative skin test for immunity to
Mycobacterium tuberculosis.
Delayed-type hypersensitivity
 Tuberculin test
 Allergic contact dermatitis
 Hypersensitivity pneumonitis
 Tissue/Graft transplant rejection
A. PPD testing
An example of this reaction is the effect
of an intradermal injection of tuberculin
antigen or purified protein derivative (PPD).
Sensitized T cells react with the antigen at
or near the injection site. Lymphokines are
released and attract, activate, and retain
macrophages at the site. These
macrophages then release lysozymes,
causing tissue damage. Edema and fibrin
are responsible for the positive tuberculin
reaction.
B. GRAFT-VERSUS-HOST DISEASE
Graft versus host disease (GVHD) is
an immune-mediated condition resulting
from a complex interaction between donor
and recipient adaptive immunity.
ACUTE GVHD – describes a distinctive
syndrome of dermatitis, hepatitis, and
enteritis developing within 100 days after
allogeneic hematopoietic cell transplantation
(HCT)
CHRONIC GVHD – describes a more
diverse syndrome developing after day 100.
In addition to allogeneic HCT, procedures
associated with high risk of GVHD include
transplantation of solid organs containing
lymphoid tissue and transfusion of non-
irradiated blood products.
Signs and Symptoms
Presentation in acute GVHD is as follows:
 A pruritic or painful rash (median onset,
day 19 posttransplantation; range, 5-47
days)
 Pruritus from initially asymptomatic liver
involvement, anorexia, weight loss,
followed rarely by hepatic coma
 Diarrhea, intestinal bleeding, cramping
abdominal pain, and ileus
 Ocular – Burning, irritation,
photophobia, and pain from lack of tear
secretion
 Oral and GI – Mouth dryness, sensitivity
to acidic or spicy foods, dysphagia,
 odynophagia, and insidious weight loss
 Pulmonary – Obstructive lung disease,
with symptoms of wheezing, dyspnea,
and chronic cough that is usually
nonresponsive to bronchodilator therapy
▪ Neuromuscular – Generalized or focal
weakness, neuropathic pain, vision loss,
muscle cramps, myalgia
 Joints – Arthralgia, arthritis
Physical Examination
Skin findings are as follows:
 Maculopapular exanthema – Red-to-
violet lesions that typically first appear
on the palms of the hands, soles of the
feet, cheeks, neck, ears, and upper
trunk, sometimes progressing to involve
the whole body; in severe cases, bullae
may be observed, and vesicles may
form
 Lichenoid skin lesions or
sclerodermatous thickening of the skin,
which sometimes causes contractures
and limits joint mobility
 Jaundice from hyperbilirubinemia;
patients who subsequently develop
pruritus may exhibit excoriations from
scratching
Ocular findings may include the
following:
Acute GVHD – Hemorrhagic conjunctivitis,
pseudomembrane formation, and
lagophthalmos
Chronic GVHD – Keratoconjunctivitis sicca,
which may lead to punctate keratopathy
Additional findings are as follows:
 Oral – Atrophy of the oral mucosa, erythema, and
lichenoid lesions of the buccal and labial mucosae
in chronic GVHD
 Pulmonary – Prolonged expiratory breathing
phase (wheezes) from bronchiolitis obliterans
 GI – Diffuse abdominal tenderness with
hyperactive bowel sounds may accompany
secretory diarrhea of acute GVHD; in severe ileus,
the abdomen is silent and appears distended
 Neuromuscular – Findings of myasthenia gravis,
polymyositis, optic neuritis, arthritis may occur in
chronic GVHD
 Vaginitis and vaginal strictures have been
described in chronic GVHD
Diagnosis
Laboratory study results in GVHD are as
follows:
 CBC – Autoimmune cytopenia (eg,
thrombocytopenia, anemia, and leukopenia)
may be observed with chronic GVHD
 Liver function tests – Elevation of the alkaline
phosphatase level, an early sign of liver
involvement by GVHD; hypoalbuminemia is
typically due to GVHD-associated intestinal
protein leakage and a negative nitrogen
balance
 Serum electrolytes and chemistries (eg,
potassium, magnesium, bicarbonate levels)
may be altered; massive diarrhea and
diminished oral intake can lead to serious
electrolyte abnormalities
Other tests:
 Schirmer test – To measure the degree of
tear formation by the lacrimal glands in
chronic GVHD
 Pulmonary function tests and arterial blood
gas analysis – To identify obstructive
pulmonary disease (eg, obliterative
bronchiolitis) in chronic GVHD
 Manometric studies of the esophagus
 Hepatic and Doppler sonography
 Barium swallow study
C. TRANSPLANT REJECTION
Transplantation is the act of
transferring cells, tissues, or organs from
one site to another typically between
different individuals. The malfunction of an
organ system can be corrected with
transplantation of an organ from a donor.
However, the immune system remains the
most formidable barrier to transplantation as
a routine medical treatment. The immune
system has developed elaborate and
effective mechanisms to combat foreign
agents. These mechanisms are also
involved in the rejection of transplanted
organs which are recognized as foreign by
the recipient’s immune system.
Types of Grafts:
 Xenografts – grafts between members of
different species
 Autografts – grafts from one part of the body to
another
 Allografts – grafts between members of the
same species that differ genetically
 Isograft – grafts between genetically identical
individuals
Clinical Stages of Rejection:
 Hyperacute rejection – occurs minutes to hours
due to rapidly destroyed vascularization
 Acute rejection - first six months after
transplantation
o Acute cellular rejection – mediated by
lymphocytes that have been activated
against donor antigens
o Humoral rejection – is a form of allograft
 injury primarily mediated by antibody and
complement.
 Chronic rejection – develops months to years
after acute rejection episodes have subsided.
Chronic rejections are both antibody- and cell-
mediated
Transplant Tolerance and Immunosuppressed:
 Rejection cannot be completely prevented;
however, a degree of immune tolerance to
the transplant does develop. Tissue typing
and cross matching is performed to assess
donor-recipient compatibility for human
leukocyte antigen (HLA) and ABO group.
These tests include the following:
 ABO blood group compatibility is tested
first
 Lymphocytotoxicity assay
 Panel-reactive antibody (PRA)
 Mixed lymphocyte reaction (MLR)
 The use of immunosuppressive drugs
requires a balance between the risk of loss
of transplanted organs and the toxicity of the
agent. Immunosuppressive drugs are used
in 2 phases: the initial induction phase,
which requires much higher doses of these
drugs, and the later maintenance phase.
Immunosuppressive agents in current use include
the following:
 Immunophilin-binding agents (Cyclosporin,
Tacrolimus) – calcineurin inhibitors. Suppress
the activation of T lymphocyte by inhibiting the
production of cytokines ▪ Mammalian target of
rapamycin (mTOR) inhibitors – macrocyclic
antibiotic. It results in T- and B-cell cycle arrest.
 Antiproliferative agents (Azathioprine,
Cyclophosphamide) – inhibit DNA replication and
suppress B- and T-cell proliferation.
 Antibodies (Basiliximab, Daclizumab) interact
with lymphocyte surface antigens, depleting
circulating thymus-derived lymphocytes and
interfering with cell-mediated and humoral
immune response.
 Corticosteroids
D. CONTACT DERMATITIS
 An example of a type IV hypersensitivity
reaction is contact dermatitis resulting from
exposure to allergens such as cosmetics,
adhesive tape, topical medications,
medication additives, and plant toxins. The
symptoms that occur include itching,
erythema, and raised lesions
There are three types of contact dermatitis:
a. Allergic contact dermatitis
 Allergic contact dermatitis occurs when the
skin develops an allergic reaction after being
exposed to a foreign substance. This causes
the body to release inflammatory chemicals
that can make the skin feel itchy and
irritated.
Common causes of allergic contact
dermatitis include contact with:
 jewelry made from nickel or
gold
 latex gloves
 perfumes or chemicals
in cosmetics and skin
care products
b. Irritant contact dermatitis
 Irritant contact dermatitis is the most
common type of contact dermatitis. It
happens when the skin comes in contact
with a toxic material
Toxic substances that can cause irritant contact
dermatitis include:
 Battery acid
 Bleach
 Drain cleaners
 Kerosene
 Detergents
 Pepper spray
 Irritant contact dermatitis can also occur when the
skin comes in contact with less irritating materials —
like soap or even water — too often.
 People whose hands are frequently exposed to
water, such as hairdressers, bartenders, and
healthcare workers, often experience irritant contact
dermatitis of the hands, for example.
c. Photocontact dermatitis
 Photocontact dermatitis is less common. It’s
a reaction that can occur when the active
ingredients in a skin product are exposed to
the sun and result in irritation.
Management:
 Avoid scratching your irritated skin. Scratching
can make the irritation worse or even cause a
skin infection that requires antibiotics.
 Clean your skin with mild soap and
lukewarm water to remove any irritants. ▪
Stop using any products you think might
be causing the problem. ▪ Apply bland
petroleum jelly like Vaseline to soothe the
area.
 Try using anti-itch treatments such as calamine
lotion or hydrocortisone cream (Cortisone-10).
 If needed, take an antihistamine drug such as
diphenhydramine to cut down on itching and to
reduce your allergic response.