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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  convalescent – signs and symptoms start to
humoral immunity abate until the client returns to normal state
3 KINDS OF LYMPHOCYTES of health
 B lymphocytes – mature in the bone marrow  resolution – normal state of health and total
and then center the circulation elimination of pathogens
 T lymphocytes – move from the bone marrow
to the thymus, where they mature into several FACTORS AFFECTING INFECTIOUS PROCESS
kinds of cells capable of different functions Force of infection: Epidemiologic Triangle
 Natural killer cells – not identifiable as either T consist of 3 components
cells or B cells. Non specific effector cells that  host – any organism that harbors and
can kill tumor and virus infected cells. provides nourishment for another organism
 agent – intrinsic property of microorganism
to survive and multiply in the environment to
IMMUNOLOGY LECTURE 2 produce disease
 pathology – the study of disease  environment – it is the sum total of all
 etiology – the study of the cause of a external conditions and influences that
disease affect the development of an organism
 pathogenesis – the development of disease which can be biological, social or physical
 infection – colonization of the body by
pathogens Force of Resistance: Immunity (see
 disease – an abnormal state in which the separate discussion on immunity)
body is not functioning
CHAIN OF INFECTION
Infection  Pathogenic microorganism/ causative
- The colonization of a host by microbial (infection) agent
species. Infecting microbes seek to use - Microorganism that causes infection such
the host’s resources to reproduce, often as bacteria, virus, fungi and parasites
resulting in disease - There must be a sufficient dose of the
- infections are considered to be caused by organism that has enough amount and
microscopic organisms like viruses, concentration to cause infection
prions, bacteria and viroid though larger  Reservoir
organisms like macro parasites and fungi - Place where the microorganism lives,
can also infect such as in humans, animals, in soils,
- an infection is the invasion of an food, plants, air ir water
organism’s body tissues by disease- - It includes humans, animals and the
causing agents, their multiplication, and environment
the reaction of host tissues to the - The reservoir must meet the needs of the
infectious agents and the toxins they pathogen to survive and multiply
produce - the natural habitat of the organism where
it resides and multiply
STAGES OF INFECTIOUS PROCESS
 Portal of Exit
 incubation – entry of microorganisms into
- The portal of exit is the path by which the
the body to the onset of signs and
pathogen leaves its host
symptoms
- It usually corresponds to the site where
 prodromal – onset of non-specific signs and
the pathogen is localized
symptoms to the appearance of specific
- These are the following mode of escape
signs and symptoms
from the reservoir;
 acute – specific signs and symptoms
a. Respiratory tract ) most common in
develop and becomes evident
humans)
b. Gastrointestinal tract o Vector-borne
c. Genitourinary tract – Vector is defined as an arthropod
d. Open lesions or any living carrier (e.g., snail) that
e. Mechanical escape (bites of insect) transports an infectious agent to a
f. Blood susceptible individual
 Mode of Transmission – Transmission – mechanical or
- An infectious agent may be transmitted biological
from its natural reservoir to a susceptible  Portal of Entry
host in different ways - Refers to the manner in which a pathogen
- The mode of transmission is the weakest enters a susceptible host
link in the chain of infection - The portal of entry must provide access to
There are different modes of transmission: tissues in which the pathogen can multiply
 Vertical – maternal to fetal transmission or a toxin can act
(crossing the placental barrier or via vaginal - Often, infectious agents use the same
route) portal that they used to exit the source
 Horizontal – it can be direct or indirect or host in entering a new host
through break in the skin integrity - In a fecal-oral route, the agent leaves the
 Direct Contact source host in feces and are carried on
- occurs through skin to skin contact, inadequately washed hands to a vehicle
kissing, and sexual intercourse such as food, water, or utensils and enter
- Also refers to contact with soil or a new host through the mouth
vegetation harbouring infectious  Susceptible Host
microorganism - The final link in the chain of infection
- A droplet spread is considered to be a - Susceptibility of the host depends on the
direct contact with refers to sprays with genetic or constitutional factors, specific
relatively large short-sprays with relatively immunity and nonspecific factors that
large short-range aerosols produced by affect an individual’s ability to resist
coughing, sneezing or even talking infection or to limit pathogenicity
 Indirect contact - A host is a person whose own body
o Airborne defense mechanisms, when exposed,
- occurs when infectious agents are cannot withstand the invasion of
carried by dust or droplet nuclei pathogens
suspended in the air  Some people are more susceptible due to:
- Airborne dust includes materials . Low immunity
that have settles on surfaces and . Poor physical resistance
becomes suspended by air currents . Being very young or old
as well as infectious particles blown . Being malnourished
from the soil by the wind . Underlying disease
o Vehicle-borne - An individual’s genetic makeup may either
– It includes food, water, biologic increase or decrease susceptibility
products (blood) and fomites - Specific immunity refers to protective
(inanimate object such as bedding, antibodies that are directed against a
handkerchief or scalpels) specific agent such as antibodies that
– A vehicle may passively carry a may develop in response to infection,
pathogen – as food or water may vaccines or toxoids or may be acquired by
carry a virus trans-placental transfer from mother to
– The vehicle may provide an fetus or by injection of antitoxin or
environment in which the agent immunoglobulin
grows, multiplies or produces toxins
- Nonspecific factors that defend against - Defecation and vomiting – body expels
infection include skin, mucus membrane, microorganisms via bowel movements
gastric acid, cilia in respiratory tract, the and vomit
cough reflex and nonspecific immune B. Chemical Barriers: form another first line
response of defense against invaders
 Factors that may increase susceptibility to - Lysozyme – an enzyme produced in
infection by disrupting host defences are: tears, sweat, and saliva that breaks down
. Malnutrition cell walls and acts as an antibiotic by
. Alcoholism killing bacteria
. Disease - Gastric juice – acids in the stomach
. Therapy that impairs the nonspecific destroy bacteria and toxins
immune response - Saliva – saliva dilutes the number of
microorganism in the body and washes
Immunologic defenses the teeth and mouth
- Individuals have defences that protect the - Sebum – unsaturated fatty acids known
body from infection as sebum provide a protective film on the
- These defences can be categorized as skin and inhibits growth
nonspecific and specific - Hyaluronic acid – a gelatinous substance,
Non-Specific resistance/Innate Defenses hyaluronic acid slows the spread of
- Bodily defences that protect a person microorganisms that can harm the body
against all microorganisms, regardless of
prior exposure Second line of Defense / Internal Defense
- It includes anatomic and physiological
A. Antimicrobial Proteins
barriers and the inflammatory response
- Interferons – released by host cells in
INNATE IMMUNE SYSTEM response to the presence of pathogens
(viruses, bacteria, parasites or tumor
Types of Nonspecific Defenses cells)
First line of Defense / External Defenses - Complement – a group of at least 20
plasma proteins that normally circulate in
A. Physical Barriers: provides physical the blood in an inactive state. Its
barriers to invaders activation unleashes chemical mediators
- Skin – a thick layer of dead cells in the that amplify virtually all aspects of
epidermis provides a physical barrier to inflammatory process
viruses, bacteria, and microbes. As the - Transferrin – iron-binding CHONs that
epidermis sheds, microbes are removed inhibit the growth of certain bacteria by
- Mucous membrane – produce mucus to reducing the amount of available iron
trap microbes so they cannot spread to B. Natural Killer Cells – kills a wide variety
the rest of the body infectious microbes and certain tumor cells
- Hair – hair within the nose filters
microbes, dust, and pollutants form the air Ways:
to prevent them from invading the body 1. Release of perforins – chemical inserted
- Cilia – cilia lines the upper respiratory into plasma membrane a leaky
tract and traps and propels inhaled debris
2. Release molecules that may cause
to the throat so it can exit the body more apoptosis
quickly C. Phagocytes – phagocytic cells ingest and
- Urine – urine flushes microbes out of the destroy microbes that pass into body tissues
body via the urethra
Phases of Phagocytosis
- Chemotaxis: chemically stimulated B. Chemical mediators assist this response
movement of phagocytes to a site of by:
damage - Minimizing blood loss
- Adherence: attachment of the phagocytes - Walling of the invading organism
to the microbe or other foreign material - Activating phagocytes
- Ingestion: process of engulfing the - Promoting formation of fibrous scar tissue
microbes and forms a vesicle and regeneration of injured tissue
- Digestion: phagosome + lysosome – C. Emigration of Phagocytes
microbe-containing vesicle fuses with a - Within an hour after, phagocytes appear
lysosome which breaks down the on the scene
molecule into simpler components - Neutrophils begin to squeeze through the
- Killing: release of lysosome, other wall of the blood vessel called Emigration
digestive enzymes, lethal oxidants - Monocytes follow neutrophils
D. Fever – inhibits bacterial growth and
increase the rate of tissue repair when an
infection is present in the body
INFLAMMATION
Effects:  A non-specific body defense to cell injury
 Helps restore tissue homeostasis
- Intensify interferon
Main features of inflammation
- Inhibits microbial growth
1. Vasodilation
- Speeds up body reactions
2. Increased Vascular Permeability
3. Cellular Infiltration
4. Changes in biosynthetic profile of organs
SECOND LINE OF DESEASE 5. Activation of cells of the immune system
Inflammation
- A localized response in the tissue that 5 CARDINAL SIGNS
occurs when tissues are damaged or in
response to other stimuli P- Pain (dolor)
- Inflammation occurs when white blood R – Redness (rubor)
I – immobility (fubctio laesa)
cells flood an area of invasion by
S – Swelling (tumor)
microbes
H – Heat (calor)
- The response includes swelling, redness,
heat and pain STAGES OF INFLAMMATION

Stages of Inflammatory Response I. ACUTE INFLAMMATION


Vasodilation and Increased vessel permeability
A. Vasodilation & Increase Blood vessel
permeability Substances:
- Substances: a. histamines
- Histamine b. kinins (polypeptide) - Inactive precursor,
- Kinins (polypeptide) – inactive precursor, kininogens, affects some nerve endings and chemotactic
kininogens and affects some nerve agent
endings c. Prostaglandins (lipids) - released by damaged
- Prostaglandins (lipids) – released by cells, stimulates emigration, intensifies histamine and
kinins; Intensify and prolong pain.
damaged cells, stimulates emigration,
d. Leukotrienes (LTs) - chemotactic agent
intensifies histamine and kinin; intensify
e. Complement - stimulate release of Histamines
and prolong pain
- Leukotrienes (LTs) – chemotactic agent
- Complement – stimulate release of
histamines and chemotactic agent
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  Maturation
fibrin (e.g., fibrinous pericarditis). o Scar Tissue is remodeled, capillaries
o The fibrin in this fluid can form a contract, structure and function of
fibrinous exudate on the surfaces. damaged tissue is restored.
o Bread and Butter appearance – Here,
the pericardial cavity has been opened Aberrant to healing
to reveal a fibrinous pericarditis with o Complications, deformity and decrease
stands of stringy pale fibrin between function of the injured tissue
visceral and parietal pericardium o Results from abnormality in healing
 Purulent exudates mechanisms
 Abscess
 Ulceration  Exuberant granulation and keloids
o “Proud flesh”
o Keloids – excessive, bulging, tumous
II. CHRONIC INFLAMMATION 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
III. TISSUE REPAIR
adhere to adjacent surfaces
 When tissues are injured during infection or
following toxic or mechanical injury, an
 Wound healing
inflammatory response is induced in
o Primary Objective is to fill the gap
response to damage-associated molecular
created by tissue destruction and
patterns (DAMPs) and pathogen-associated
restore the structural continuity of the
molecular patterns (PAMPs) released by
injured part.
dead and dying cells and invading
o Depending on the extent of tissue loss,
organisms.
wound closure and healing occur by
 These molecular triggers induce a complex
primary or secondary intention
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
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  Self-Antigens
destroying and removing the antigens. o our immune cells do not attack our own
proteins
B. T-cells Or T lymphocytes o Our cells in the another person’s body
 Cells that derived from the thymus can trigger an immune response
 Lymphocyte cells that can cause graft because they are foreign
rejection, kill foreign cells, or suppress o Restricts donors for transplants
production of antibodies o Engulf antigens and present fragments
 T cells or T lymphocytes assist the B cells. of them, like signal flags, on their own
T cells secrete substances that direct the surfaces where they can be recognized
flow of cell activity, destroy target cells, and by T cells
stimulate the macrophages. The
Roles of an Antigen-Presenting Cell
macrophages present the antigens to the T
cells and initiate the immune response  Phagocytosis of enemy cell (antigen)
 They also digest antigens and assist in  Fusion of lysosome and phagosome
removing cells and other debris. Unlike a  Enzymes start to degrade enemy cell
specific antibody, a T cell does not bind free  Enemy cell broke into small fragments
antigen  Fragments of antigen presented on APC
surface
C. Maturation of T and B cells  Leftover fragment released by exocytosis
 Lymphocytes originate from stem cells in
PROCESSING OF ANTIGENS
the bone marrow
 Exogenous Antigen – bacteria and toxins,
 B lymphocytes mature in the bone marrow
worm parasites, pollen, dust, viruses
before entering the bloodstream, whereas T
o APC process exogenous antigens –
lymphocytes mature in the thymus, where
macrophages, B cells, dendritic cell
they also differentiate into cells with various
 Antigen Presenting Cells (APC)
functions
o Lymphocytes
 Originate from hemocytoblasts in
the red bone marrow
 B lymphocytes become
D. Processing and Presentation of Antigens
immunocompetent in the bone
 Antigen – any substance capable of
marrow
exciting the immune system and
 T lymphocytes become
provoking an immune response
immunocompetent in the thymus
 Examples of common antigens:
o Dendritic cells
o Foreign proteins
 Present in connective tissues
o Nucleic acids
and epidermis
o Large carbohydrates
 The body’s frontier, best situated
o Some lipids
to act as mobile sentines
o Pollen grains
o Macrophages
o Microorganisms
 Arise from monocytes
FUNCTIONAL PROPERTIES OF ANTIGEN  Become widely distributed in
 Immunogenicity - The ability to stimulate lymphoid organs
proliferation of specific lymphocytes and  Endogenous Antigen
antibody o Foreign antigens that are
 Reactivity – the ability to react or activate synthesized within a body cell
lymphocytes and the antibody by o Viral CHONs, abnormal CHONs
immunogenic reaction o Antigen fragment-MHC I complex
 The pathogen’s antigens are expressed on
IMMUNE RESPONSE the cell surface or on an antigen-presenting
 how your body recognizes and defends cell. Helper T cells release cytokines that
itself against bacteria, viruses, and help activated T cells bind to the infected
substances that appear foreign and harmful cells’ MHC-antigen complex and
differentiate the T cell into a cytotoxic T cell.
Stages of Immune Response: The infected cell then undergoes lysis
a. Recognition Stage  Particularly effective against:
o Body accomplishes recognition o Cells attacking cells
using lymph nodes and lymphocytes o Intracellular pathogen (parasites,
for surveillance fungi, viruses) some cancer cells
o Continuously discharge small o Foreign tissue transplant
lymphocytes into the bloodstream o Often termed as delayed
o Macrophages, neutrophils & hypersensitivity
complement help
 T lymphocytes, on exposure to antigen,
b. Proliferation Stage
proliferate and differentiate into:
o Sensitized lymphocytes stimulate
 Helper T cells
some of the resident dormant T and
o activated upon recognition of antigen
B lymphocytes to enlarge, divide,
&stimulates the rest of immune
and proliferate
response
o T lymphocytes differentiate into
 Suppressor T cells
cytotoxic (or killer) T cells, whereas
o has the ability to decrease B cell
B lymphocytes produce and release
production, thereby keeping immune
antibodies
response at the level compatible
o Enlargement of the lymph nodes in
with health
the neck in conjunction with a sore
 Memory T cells
throate is one example of the
o Responsible for recognizing
immune response
antigens from previous exposure
o Actual humoral and cell-mediated
and mounting an immune response
immune response
o Specialize in killing infected cells
c. Effector Stage
o Insert a toxic chemical (perforin)
o coupling initiates a series of events
 Cytotoxic T cells / T8 cells
that in most instances results in the
 Attach the antigen directly by altering the
total destruction of the invading
cell membrane and causing cell lysis
microbes or the complete
(disintegration) and releasing cytolytic
neutralization of the toxin either the
enzymes & cytokines
antibody of the humoral response of
 Perforin and lymphotoxin
the cytotoxic )killer) T cell of the
cellular response reaches and Antibody-Mediated / Humoral Immune
couples with the antigen on the Response
surface of the foreign invader  Transformation of B cells to plasma cells
 Dominated by B lymphocytes
Cell-Mediated Immune Response  Works mainly against:
 Involves differentiation of T-cells to different o Antigens dissolved in body fluids
types of cell o Extracellular pathogen (bacteria)
 B lymphocytes with specific receptors bind
 Dominated by T lymphocytes
to a specific antigen
 Immunity occurs inside infected cells and is
mediated by T lymphocytes  The binding event activates the
lymphocytes to undergo clonal selection
 A large number of clones are produced o Neutralization – antibody
(primary humoral response) neutralizes toxins released by
 Most B cells become plasma cells produce bacteria
antibodies to destroy antigens, activity lasts o Anaphylactic reaction – activates
for four or five day release of mast cells and histamine
 Some B cells become long-lived memory
TYPES OF IMMUNITY
cells (secondary humoral response)
1. Innate Immunity - also known as natural
Secondary humoral response: immunity, an inherited immunity of species,
 Memory cells are lone-lived races and individuals. Example is the skin
 A second exposure causes a rapid which acts as a barrier to block germs from
response entering the body. And the immune system
 The secondary response is stronger and recognizes when certain invaders are
longer lasting 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
The Role of the Complement System injected
 The complement is a major component of  Active Immunity
the innate immune system involved in o Individual’s own immune system is
defending against all foreign pathogens the cause of the immunity
 Also known as a complement cascade that o Natural – antigens are introduced
enhances the ability of antibodies and through natural exposure
phagocytic cells to clear microbes and o Artificial – antigens are deliberately
damaged cells from an organisms, promote introduced in a vaccine
inflammation and attack the pathogen’s cell
membrane Nursing responsibilities in Vaccination
 Functions of the complement:  Vaccines can protect one’s health and the
o Cytolysis – destruction of cell health of the community. Efficacy and safety
membrane of vaccines can be enhanced by using
o Chemotaxis – chemical attraction of education, enforcement and engineering in
phagocytic cell to antigen which a nurse or health care provider plays
o Adherence – adhesion of antigen- a key role
antibody complexes to surface of  This includes the following:
cells or body tissues o Proper storage and handling of
o Opsonisation – antibody coats vaccines
surface of antigen, making it easier o Never administer vaccines later than
to digest by phagocytes 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  The virus is transmitted to people from wild
days after surgery. animals (such as fruit bats, porcupines and non-
human primates)
4. Trans Urethral Needle Ablation (TUNA)  Spreads in the human population through direct
Transurethral radiofrequency needle ablation of contact with the blood, secretions, organs or
the prostate other bodily fluids of infected people, and with
 Low-level radiofrequency is transmitted surfaces and materials (e.g. bedding, clothing)
to the prostate via a transurethral needle contaminated with these fluids.
delivery system.
 The resultant heat causes localized WHO DATA
necrosis of the prostate.  The average EVD case fatality rate is around
50%.
 Case fatality rates have varied from 25% to 90%
MANAGEMENT in past outbreaks.
 The first EVD outbreaks occurred in remote
Pharmacologic: villages in Central Africa, near tropical
rainforests.
 Alpha-adrenergic blockers (eg,  The 2014–2016 outbreak in West Africa was the
Alfuzosin, Terazosin), which relax the largest and most complex Ebola outbreak since
smooth muscle of the bladder neck and the virus was first discovered in 1976.
prostate, and 5alpha reductase inhibitors.  It also spread between countries, starting in
Guinea then moving across land borders to
 Hormonal manipulation with Sierra Leone and Liberia.
antiandrogen agents (Finasteride  It is thought that fruit bats of the Pteropodidae
[Proscar]) decreases the size of the family are natural Ebola virus hosts.
prostate and prevents the conversion of
testosterone to dihydrotestosterone (DHT). ETIOLOGIG AGENT
 Ebola virus

Nursing Interventions: TRANSMISSION


 Blood or body fluids of a person who is sick with
Preoperative and postoperative nursing interventions for or has died from Ebola
a patient with BPH are as follows:  Objects that have been contaminated with body
fluids (like blood, feces, vomit) from a person
 Reduce anxiety. The nurse should sick with Ebola or the body of a person who died
familiarize the patient with the preoperative from Ebola
and postoperative routines and initiate
measures to reduce anxiety. INCUBATION
 2 to 21 days after exposure to Ebola, but the
 Relieve discomfort. Bed rest and average is 8 to 10 days.
analgesics are prescribed if a patient
experiences discomfort. SIGNS AND SYMPTOMS
 Fever
 Provide instruction. Before the surgery,  Severe headache
the nurse reviews with the patient the
 Vomiting
anatomy of the affected structures and their
 Abdominal pain
function in relation to the urinary and
reproductive systems.  Muscle pain
 Weakness
 Maintain fluid balance. Fluid balance  Fatigue
should be restored to normal.  Diarrhea
 Unexplained hemorrhage
 Sore throat
EBOLA  Rash
 Ebola virus disease (EVD), formerly known as  Symptoms of kidney and live function
Ebola Hemorrhagic fever, is a severe, often fatal  In some cases, both internal and external
illness affecting humans and other primates. bleeding (for example, oozing from the gums, or
 Ebola Hemorrhagic Fever is a rare and deadly blood in the stools)
disease caused by infection with one of the  Laboratory findings include low white blood cell
Ebola virus’s strains. Ebola can cause disease in and platelet counts and elevated liver enzymes.
humans and nonhuman primates.
DIAGNOSTIC
 Polymerase chain reaction (PCR) is one of  Notify health officials if had direct contact
the most commonly used diagnostic with blood or body fluids of a person who is
methods because of its ability to detect low sick with Ebola
levels of Ebola virus.
 To determine whether EVD is a possible Treatment and Management (according to WHO)
diagnosis, there must be a combination of  There is no proven treatment for Ebola but
symptom suggestive of EVD AND a possible simple interventions early on can
exposure to EVD within 21 days before the significantly improve chances of survival.
onset of symptoms.  Rehydration with fluids and body salts (given
 An exposure may include contact with: orally or intravenously), and treatment of
o blood or body fluids from a person sick specific symptoms such as low blood
with or who died from EVD, pressure, vomiting, diarrhea and infections.
o objects contaminated with blood or body  Hand hygiene is the most effective way to
fluids of a person sick with or who died prevent the spread of the Ebola virus.
from EVD,  An experimental Ebola vaccine known as
o infected fruit bats and nonhuman rVSV-ZEBOV proved highly protective
primates (apes or monkeys), or against the deadly virus in a major trial in
o Semen from a man who has recovered Guinea in 2015. It is being used in response
from EVD. to the current outbreak in the Democratic
Republic of the Congo using a ring
vaccination protocol.
Within a few days after symptoms begin:  During an outbreak, health partners apply a
 Antigen-capture enzyme-linked package of interventions including case
immunosorbent assay (ELISA) management, surveillance, contact tracing,
 IgM ELISA laboratory testing, safe burials and
 Polymerase chain reaction (PCR) community engagement.
 Virus isolation  Working with communities to reduce risk
factors for Ebola transmission is critical to
Later in disease course or after recovery controlling outbreaks.
 IgM and IgG antibodies
Treatment according to CDC
Retrospectively in deceased patients
 Immunohistochemistry testing Symptoms of Ebola virus disease (EVD) are treated as
 PCR they appear. When used early, basic interventions can
 Virus isolation significantly improve the chances of survival. These
include:

TREATMENT  Providing fluids and electrolytes (body salts)


through infusion into the vein
Medical Management (intravenously).
 Symptoms of Ebola and complications are  Offering oxygen therapy to maintain oxygen
treated as they appear status.
 Provide intravenous fluids and balancing  Using medication to support blood pressure,
electrolytes in the body reduce vomiting and diarrhea and to
 Maintain oxygen status and blood pressure manage fever and pain.
 Treat other infections if they occur.  Treating other infections, if they occur.
 EVERBO – First US FRA approved vaccine
December 2019 Antiviral Drugs (according to CDC)
 During the 2018 eastern Democratic
Prevention Republic of the Congo outbreak, four
 Practice careful hygiene investigational treatments were initially
 Do not handle items that may have come in available to treat patients with confirmed
contact with an infected person’s blood or Ebola.
body fluids
 Isolate patients with EBOLA from other  Regeneron (REGN-EB3) and mAb114,
patients overall survival was much higher. These two
 Practice proper infection control and antiviral drugs currently remain in use for
sterilization measures patients with confirmed Ebola.
 Wear appropriate personal protective
equipment
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  Plasma cells are activated plasma B cells,
 Family planning which produces immunoglobulins that
 Yearly influenza and pneumococcal normally protect the body.
vaccination  However in multiple myeloma malignancy
 Antimalarial drug: Hydroxychloroquine plasma cells infiltrated the bone marrow and
(Plaquenil) produce abnormal and excessive amount of
 Topical Corticosteroids immunoglobulins.
 Cytotoxic Agents or Antineoplasitc
Clinical Manifestation
Nursing Interventions  Bone pain, usually at the back or ribs
 The nurse should emphasize importance of  Lytic lesions as well as osteoporosis
screening t for osteoporosis, because long term  Vertebral collapse or fracture
use of corticosteroids increases the incidence of  Hypercalcemia
osteoporosis.  Excessive dehydration, constipation, thirst
 Educating the patient regarding calcium and  Altered mental status, confusion or even
Vitamin D supplementation daily is encouraged, coma
along with the benefits of weight bearing activities  Evidence of end-organ damage
to support bone health (Cash & Glass, 2015). characterized by elevated CRAB
 Patients should be instructed to avoid exposure o Calcium
or to protect themselves with sunscreen and o Renal insufficiency
clothing. o Anemia
 The nurse educates the patient about the o Bone lesion
importance of continuing prescribed medications.
 Patients should be instructed for routine periodic Diagnostic Tests:
screenings as well as health promotion activities.  Serum protein electrophoresis – elevated
 The patient may benefit from participation in monoclonal protein spike in the serum
support groups, which can provide disease  Urine protein electrophoresis- elevated
information, daily management tips, and social monoclonal protein spike in the urine
support.  Serum free light chain analysis – elevated
 The patient is reminded of the importance of monoclonal protein spike in light chain
monitoring because of the increased risk of  Bone marrow aspiration and biopsy
systemic involvement, including renal and demonstrate increased number and
cardiovascular effects. abnormal form of plasma cells
 Due to the immunosuppression associated with
 CBC and blood smear changes reflects
systemic corticosteroid usage, the nurse must
anemia
watch for signs and symptoms of infection,
 Urine and serum analysis for presence and
especially with acutely ill patients.
quantity of abnormal immunoglobulin
Nursing Management/ Nursing Implementation  Skeletal X-rays shows osteolytic bone
lesions
 Psychosocial issues
o Counsel patient and family that SLE has
Medical Management
good prognosis.
o Physical effects can lead to isolation,  No Cure for multiple myeloma
self-esteem, and body image  Bone marrow transplant is considered to
disturbances. extend remission rather than to provide a cure
o Assist patient in developing goals  Chemotherapy is the primary treatment
 Radiation therapy (combined with
chemotherapy) is used for strengthening bone at
MULTIPLE MYOLEMA a specific lesion, relieving pain and reducing size
 It is a malignant disease of the most mature form of plasma cells tumors that occur outside
of B lymphocyte, the plasma cell. It is skeletal system
characterized by proliferation of neoplastic  Vertebroplasty is performed if lytic lesions
plasma cells derived from one B lymphocyte result in vertebral compression
(clone) and producing a homogeneous  Bisphosphonates- Pamidronate (Aredia),
immunoglobulin (M protein or Bence Jones Zoledonic acid (Zometa)
protein) without apparent antigenic stimulation.  Plasmapheresis may be used to lower the
immunoglobulin level
Pathophysiology
 The disease process involved excessive Nursing Management
production of plasma cells.  Administer NSAIDS combined with opioid
analgesic as ordered
 Educate patients for activity restrictions such as  This is the early stage of RA, there is
lifting of heavy objects inflammation of the joint but there is no damage
 Use of braces to support the spinal column to the bones.
 Maintaining mobility and hydration  The body mistakenly attacks its own join tissue
 Instruct patient in infection prevention measures
STAGE 2
RHEUMATOID ARTHRITIS  Moderate stage RA, the synovium’s
 Rheumatoid arthritis is a long-term condition that inflammation causes damage to the joint
causes pain, swelling and stiffness in the joints. cartilage. ROM in the joints may become limited.
The condition usually affects the hands, feet and  The body makes the antibodies and the joints
wrists. start swelling up.
 Some people with rheumatoid arthritis also
experience problems in other parts of the body, STAGE 3
or more general symptoms such as tiredness
 Severe RA, damage extends not only to the
and weight loss.
cartilage but to the bones.
 It is a systemic inflammatory disease which
 The joints start becoming bent and deformed,
manifests itself in multiple joints in the body. The
the fingers become crooked. These misshapen
inflammatory process primarily affects the lining
joints can press on the nerves and can cause
of the joints (synovial membrane), but can also
nerve pain as well.
affect other organs. The inflamed synovium
leads to erosions of the cartilage and bone.
STAGE 4
7 S’S  The end-stage RA, the joints may become
 Sunrise stiffness destroyed and the bones fused together
(ankylosis).
 Soft feeling in joints
 If not treated, the disease will progress to the
 Swelling in joints (warm)
last stage, in which there’s no joint remaining at
 Symmetrical
all and the joint is essentially fused.
 Synovium (affected and inflamed)
 Systemic (fever, fatigue, anemia Rheumatoid Factor
 Stages (synovitis, pannus develops, ankylosis Self anigen (IgG)  B Lymphocyte  Plasma cell 
(bone fusion) Anti-IgG  IgM (This IgM is a RA factor)
 Immune system mistakenly sends antibodies to
Other Signs and Symptoms:
the lining of joints, where they attack the tissue
 Edematous, warm, tender joints- Limited range surrounding the joint.
of motion in affected joints
 This causes the thin layer of cells (synovium)
 Generalized edema or nodules around affected
covering joints to become sore and inflamed,
joints
releasing chemicals that damage nearby:
 Impaired mobility and ability to perform ADLs o Bones
 Fatigue, weakness and anorexia – Subluxation o Cartilage – the stretchy connective
of joints tissue between bones
 Swan neck deformity (hypertension of proximal o Tendons – the tissue that connects
interphalangeal joint and partial flexion of distal bone to muscle
interphalangeal joint) o Ligaments – the tissue that connects
 Boutonniere deformity (flexion of the PIP joint bone and cartilage
with hyperextension of the DIP joint)  If not treated, these chemicals gradually cause
 Baker’s cyst – popliteal area behind the knee the joint to lose its shape and alignment. It can
 In later stages, weight loss, fever, anemia, destroy the join completely.
muscle atrophy and Sjogren syndrome.
MEDICAL MANAGEMENT
DIAGNOSTIC TEST The goal of pharmacologic therapy is to reduce pain,
 Radiographic studies reveal abnormalities such decrease inflammation, maintain or restore joint function
as progressive joint damage and prevent bone and cartilage destruction.
 Elevated Rheumatoid Factor – Elevated ESR  Corticosteroids
 Decreased RBS and C4 complement  Non-steroidal anti-inflammatory drugs (NSAIDs)
 Anti-cyclic citrullinated peptide (CCP)  Non-biologic disease modifying antirheumatic
 Synovial fluid analysis drugs (DMARDs)- Gold salt, Methotrexate
 Biologic DMARDs - Etanercept

STAGES of RHEUMATOID ARTHRITIS SURGICAL MANAGEMENT


 Synovectomy – removal of partial or all the
STAGE 1 synovial membrane of joint
 Tenosynovectomy – excision of a tendon and below the diaphragm
sheath o HL cells found in lymph node regions on
 Arthroplasty – reconstruction or replacement of both sides of the diaphragm (above and
joint below), possibly with localized
 Arthrodesis – immobilization of joint by fusion involvement of an organ outside the
of the adjacent bones lymphatic system or the spleen.

NURSING MANAGEMENT  STAGE 4


 Administer prescribed medication o Widespread disease multiple organs,
 Provide pain relief with or without lymph node involvement
 Encourage body alignment by the client to o HL cells have spread widely into one or
prevent contractures more organs outside the lymphatic
 Collaborate with physical therapist system.
 Recommend weight reduction if appropriate
 Promote self-care SIGNS AND SYMPTOMS
 Promote adequate rest and sleep  Painless swelling of the lymph nodes at armpit,
 Discuss maintaining optimal nutritional status neck, around the groin
 Mental status (patents are prone to developing  Night sweats
depression – low esteem fatigue, pain, life  Fever
altering, no cure)  Sever itching
 Joint assessments (symmetrical, stiffness – how  Persistent fatigue
long, time it happens)  Unintended weight loss
 Enlarged spleen
HODGKIN’S DISEASE  Pain in the lymph nodes after alcohol intake
 Is a type of lymphoma, which is a cancer
originating from white blood cells called RISK FACTORS
lymphocytes  Age: HD is often seen in people age between
 Is characterized by the orderly spread of the 15 to 40 and above 55 years
disease from on lymph node group to another
 A family history of Lymphoma: If HD is
and by the development of systemic symptoms
present in any blood relative; it may increase the
with advanced disease
risk of developing the disease.
 Male Gender: Males are more prone to HD than
females
 Epstein-Barr Infection: People who had
STAGES
suffered from infectious mononucleosis have
more chances of developing HD.
 STAGE 1  HIV/AIDS: People with HIV/AIDS are more likely
o Localized disease; single lymph node to get this disease.
region or single organ
o HL cells found in a single lymph node
DIAGNOSTIC TEST:
region (this can include one node or a
 Physical Exam: A doctor will check for inflamed
group of adjacent nodes), OR HL cells
or swollen lymph nodes at neck, armpit and
found in one organ or site outside the
groin, and enlarged spleen or liver.
lymphatic system.
 Blood Test: The blood sample is collected and
examined in lab to analyze for any possibilities
 STAGE 2
that can contribute to cancers.
o Two or more lymph node regions on the
same side of the diaphragm  Imaging Tests: It is performed to locate the
o HL cells found in two or more lymph tumors and to look for the signs of spread of
node regions on the same side of the cancer to other body parts. It includes computed
diaphragm (the thin muscle below the tomography (CT), Magnetic Resonance Imaging
lungs and heart that separates the chest (MRI) and positron emission tomography.
from the abdomen), either above the  Lymph Node Biopsy: A section of lymph node
diaphragm or below the diaphragm, OR is removed for a biopsy. It is performed to look
HL cells found in a lymph node area and for abnormal cells in the lymph node.
a nearby organ outside the lymphatic  Bone Marrow Biopsy: The bone marrow cells
system, on the same side of the are extracted by inserting a needle in the
diaphragm hipbone and analyzed for Hodgkin’s lymphoma
cells.
 STAGE 3
o Two or more lymph node regions about 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
 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
 Bone Marrow Transplant
alcohol, tobacco, spices, and extremely hot or
 It is also known as stem cell transplant.
cold foods.
 The diseased bone marrow is replaced
 Administer or teach self-administration of pain
with healthy stem cells that help to grow
medication or antiemetic before eating or
new bone marrow.
drinking, if needed.
 It is an option when HD recurs after
 Encourage mouth care at least twice per day
treatment.
and after meals using a soft toothbrush or
toothete and mild mouth rinse.
 Targeted Drug Therapy  Assess for ulcers, plaques, or discharge that
 TIt is an advanced technique where an may be indicative of superimposed infection.
immune system is activated to fight  For diarrhea, switch to low-residue diet and
against cancer cells. 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.

Documentation Guidelines
Response to staging:
 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
 Elevated lactate dehydrogenase alanine
Response to treatment: aminotransferase and hepatic transaminase
 Effects of chemotherapy or radiation therapy, or  Elevated creatine kinase level
both; response to treatment of symptoms,  Serum antibodies to SARS-CoV in single serum
presence of complications (weight loss, specimen
infection, skin irritation)  RT-PCR (reverse transcriptase polymerase
 Emotional state: Effectiveness of coping, chain reaction)
presence of depression, interest in group  Chest radiograph - interstitial infiltrates
support or counseling, referrals mad
 Discharge and Home Healthcare Guidelines
MEDICAL MANAGEMENT:
SEVERE ACUTE RESPIRATORY SYNDROME (SARS)  No definitive medication protocol specific to
 is a serious, potentially life-threatening viral SARS has been developed, although various
infection caused by the Coronaviridae family, treatment regimens have been tried.
the  Corticosteroid
 SARS-associated coronavirus (SARS-CoV).  Antiviral agents (Ribavirin)
Initially began in the Guangdong province of  Protease inhibitors (Lopinavir, Ritonavir)
southern China. SARS is characterized by a  Interferon
phase of cytokine storms with various  Monoclonal antibodies - emergency prophylaxis,
chemokines and cytokines being elevated. neutralizes virus activity in vitro and in vivo
 Intravenous immunoglobulin (IVIG)
SIGNS AND SYMPTOMS  Nitric oxide
The clinical course of SARS generally follows a typical
 Glycyrrhizin - inhibits vitro replication of the
pattern. Stage 1 is a flu like prodrome that begins 2-7
virus
days after incubation, lasts 3-7 days, and is
 Vaccine – phase 1 clinical trial 2004
characterized by the following:
 Fever 38 ⁰C
 Fatigue INFLUENZA
 Headaches  H1N1 influenza, referred to as swine flu, is a
 Chills highly contagious respiratory disease in pigs that
 Myalgia can be transmitted to humans.
 Malaise
 Anorexia Etiologic Agent: Influenza A virus subtype H1N1

Less common features include the following: Mode of transmission: close and direct contact with
 Sputum production infected person
 Sore throat
 Coryza Incubation Period: ranges from 1 to 4 days with an
 Nausea and vomiting average of 2 days up to 7 days
 Dizziness
 Diarrhea SIGNS AND SYMPTOMS
 Cough
Stage 2 is the lower respiratory tract phase and is  Fever
characterized by:  Sore throat
 Dry cough  Stuffy or runny nose
 Dyspnea  Body ache
 Progressive hypoxemia in many cases  Headaches
 Respiratory failure that requires mechanical  Chills
ventilation  Fatigue

DIAGNOSTIC TEST: DIAGNOSTIC TEST:


 Pulse oximetry  PCR
 Blood cultures  Rapid antigen or antibody immunoassays
 Sputum gram stain and culture  Viral culture
 Viral respiratory pathogen test - influenza A
and B viruses and respiratory syncytial virus MEDICAL AND TREATMENT MANAGEMENT:
 Legionella and pneumococcal urinary antigen  Antipyretic
test  Analgesics
 WBC- decreased  Increased fluid consumption
 Mild hyponatremia and hypokalemia  Bedrest
 Antiviral agents (Oseltamivir/ Zanamivir)  HIV invades the helper T cells to replicate
 Isolation itself.
 Vaccination – Influenza virus vaccine trivalent  No Cure
(Fluzone,  is a retrovirus that selectively attacks the CD4
 Flucelvax) + T lymphocytes, the immune cell responsible
 Influenza virus quadrivalent (Afluria for orchestrating and coordinating the immune
Quadrivalent, Fluarix) response to infection. And causes AIDS.
2 Major Types:
PREVENTION AND PRECAUTION: ▪ HIV-1: the virus responsible for most HIV infection
 Seek medical care if suspected with H1N1 world-wide
 Isolate patient immediately in a negative- ▪ HIV-2: is endemic in West Africa, rare worldwide. The
pressure air handling incubation period is 10 years.
 Wash hands frequently H- Human: because this virus can only infect human
 Wear face mask beings.
 Social distancing or avoid large gatherings I- Immuno-deficiency: because the effect of the virus is
 Routine cleaning and disinfection to create a deficiency, a failure to work properly, within
 Pre-exposure prophylaxis 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
Treatment of HIV-Related reproducing by itself. It reproduces by taking over the
Illnesses and AIDS machinery of the human cell.
Is HIV and AIDS the same thing?
 AIDS
Key Terms  Acquired Immunodeficiency Syndrome
 Human Immunodeficiency Virus (HIV)  HIV is the virus that causes AIDS
 virus that primarily infects cells of the immune  Disease limits the body’s ability to fight
system and that causes AIDS infection
 Acquired Immune Deficiency Syndrome (AIDS)  A person with AIDS has a very weak immune
 disease that is caused by HIV infection, which system
weakens the immune system  No Cure
 Pandemic
 disease that spreads quickly through human  An infectious disease of the immune system
populations all over the world caused by the retrovirus HIV-1. And a chronic,
 Helper T Cell potentially life-threatening condition caused by
 white blood cell that activates the immune the human.
response and that is the primary target cell of  A secondary immunodeficiency disorder that
HIV infection results from HIV infection, which is transmitted
 Opportunistic Infection by blood, semen or vaginal fluids
 illness due to an organism that causes
disease in people with weakened immune A - Acquired: because it's a condition one must
systems; commonly found in AIDS patients acquire or get infected with; not something
 Universal Precautions transmitted through the genes
 set of procedures used to avoid contact with
body fluids & to reduce the risk of spreading I – Immune: because it affects the body's immune
HIV & other diseases system, the part of the body which usually works
 HIV-antibody test to fight off germs such as bacteria and viruses
 detects HIV antibodies to determine if a D - Deficiency: because it makes the immune
person has been infected with HIV system deficient (makes it not work properly)
 Asymptomatic stage
 infection in which the infectious agent, such as S -Syndrome: because someone with AIDS may
HIV, is present but there are few or no experience a wide range of different diseases and
symptoms of the infection. opportunistic infections.
 HIV Positive
 person who tests positive in 2 different HIV Life Cycle of HIV
tests 1. Free HIV
 Drug Combination Therapy
 AIDS treatment program in which patients 2. HIV attaches to CD4 receptor site
regularly take more than one drug
3. Reverse transcriptase
 HIV
 “Human Immunodeficiency Virus” 4. HIV DNA penetrates T-cell nucleus
 A specific type of virus (a retrovirus)
5. DNA replicates HIV virus using protease  Persistent generalized lymphadenopathy (
3 months at least 2 locations).
6. Assembly of new HIV virus
Phase 3 - HIV  Overt AIDS
7. Accumulation of viral RNA  Immune system weakens
8. Cell Death  Emergence of opportunistic infections and
cancers
 Occurs when a person has CD4 count less
Seroconversion than 20 cells/ul ; risk of opportunistic infection
 The point at which an infected person converts and death is increased.
to from being negative for the presence of HIV  Without antiretroviral therapy, this phase
antibodies in the blood to being positive leads to death within 2-3 years.

Window period  Over time the immune system becomes


 Time after infection and before seroconversion 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
Three Phases of HIV years.
Phase 1- Asymptomatic Stage/ PRIMARY
INFECTION/EARLY ACUTE PHASE
 Fever, myalgias, night sweats, fatigue, sore Opportunistic Infections associated with AIDS
throat, GI problems, lymphadenopathies, rashes,  Bacterial
headache.
 There is increase viral replication----à leads to  Tuberculosis (TB)
very high viral loads, and a decrease inCD4
count.  Pneumocystis pneumonia
 Usually appears 2-4 weeks after exposure to
 Viral
HIV and last for few days to 2 weeks.
 After several weeks, the immune system acts  Kaposi Sarcoma-purple-red blotches on the
to control viral replication and reduces the viral skin
load to a lower level, where it often remains for
several years.  Influenza (flu)

 In the initial (primary infection) phase of the


infection, immunoglobulin M (IgM) antibodies are Modes of HIV/AIDS Transmission
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.
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, ▪ Not much of an appetite
food, water, and in the environment. ▪ Night sweats
 Signs & symptoms: mild cough, fever, sob, ▪ Weight loss
weight loss. ▪ Fever or chills
Pneumocytosis:
Diagnosis:
 Pneumonia occurring in infants or in persons As soon as you know you have HIV:
with impaired immune systems (as ▪ Tuberculin skin test (TST)- After 2 or 3 days, a health
AIDS victims). care provider checks the injection site; swelling and
 Respiratory disease characterized by redness are signs of tuberculosis infection.
inflammation of the lung parenchyma ▪ Interferon-gamma release assay (IGRA) - blood test
(excluding the bronchi) with congestion A positive TST or IGRA doesn’t necessarily mean that you
caused by viruses or bacteria or irritants have TB disease (sometimes referred to as “active” TB).
This is because the TB bacteria can remain silent in your
2. Cytomegalovirus Infection body (sometimes called “latent” TB).
 Cytomegalovirus (CMV) is a virus most
commonly thought of as causing serious eye Confirmatory test:
disease in people with weakened immune ▪Chest X-ray
systems. It can potentially lead to blindness. ▪Sputum culture
 CMV can also lead to illness in other areas of ▪ TB smear test
the body, such as the digestive tract and parts
of the nervous system.
 However, the damage from CMV infection Treatment for Active Tuberculosis:
may slow with the use of antiretroviral therapy.  Ethambutol, or EMB (Myambutol)
This can result in the rebuilding of the immune  Isoniazid, or INH (Nydrazid)
system (as demonstrated by clinically  Pyrazinamide, or PZA (Tebrazid)
significant rises in CD4 count). Anti-CMV  Rifampin, or RIF (Rifadin)
therapy may potentially be changed to easier-
to-tolerate suppressive treatments.
4. Hepatitis
3. Mycobacterium tuberculosis
 Hepatitis B virus (HBV) and human
 Extrathoracic TB with or without intrathoracic immunodeficiency virus (HIV) are bloodborne
disease has been detected in two-thirds or more viruses transmitted primarily through sexual
of patients with overt aids. contact and injection drug use. Because of these
 Tuberculosis (TB) is caused by bacteria called shared modes of transmission, people at risk for
Mycobacterium tuberculosis. TB infection occurs HIV infection are also at risk for HBV infection.
when a person breathes in droplets produced  Chronic HBV advances faster to cirrhosis, end-
when someone with active TB disease coughs or stage liver disease, and liver cancer in people
sneezes. with HIV/HBV coinfection than in people with
 These droplets can remain infectious in the air for only HBV.
several hours in damp enclosed spaces with little
ventilation or direct sunlight, such as Prevention of HBV infection for HIV patient:
overcrowded informal housing or prisons.  CDC recommends that people with HIV and
 Someone infected with both HIV and TB is at people who are at risk for HIV get the HBV
least 10 times more likely to develop active TB, vaccine (or the combined hepatitis A virus/HBV
especially when their CD4 count is under 200. vaccine)
 Use condoms during sex
TB is the leading cause of death among people  Don't share needles on injecting drugs.
living with HIV, causing more than one third of all  Don’t use personal items that may come in
AIDS-related deaths in 2015. Almost 60% of the contact with another person's blood.
estimated global HIV-related TB cases are not  Sterilize instrument before body piercing or
diagnosed and not treated. tattoo.

Clinical Manifestation: CDC recommends that all people with HIV get
▪A bad cough that lasts for more than 2 weeks tested for HBV.
▪ Coughing up mucus or blood Diagnostic test: Hepatitis B Surface Antigen
▪ Chest pain (HBsAg) test

You may also have:


▪Weakness or fatigue Clinical Manifestations:
 Loss of appetite  Varicella can also be diagnosed retrospectively
 Tiredness by documenting seroconversion (i.e.,
 Nausea immunoglobulin G [IgG] antibody negative to
 Vomiting positive).
 Fever
 Abdominal pain Prevention of Herpes Zoster in the patient with HIV:
 Dark Urine ▪ Vaccination to Prevent Primary Infection (Varicella)
 Clay-colored bowel movements ▪ Pre-Exposure Prophylaxis to Prevent Primary
 Joint Pain Infection (Varicella)
 Yellowing of the skin or the whites of the eyes ▪ Post-Exposure Prophylaxis to Prevent Primary
(jaundice) Infection (Varicella)
▪ Antiviral Prophylaxis to Prevent Reactivation
5. Herpes Simplex or Zoster Disease (Herpes Zoster)
 The herpes simplex virus, also known as ▪ Vaccination to Prevent Reactivation Disease
HSV, is an infection that causes herpes. Herpes (Herpes Zoster)
can appear in various parts of the body, most
commonly on the genitals or mouth. Treatment for Herpes Zoster:
● Antiviral therapy should be instituted as soon
as possible for all patients with HIV with
2 types of the herpes simplex virus.
herpes zoster diagnosed within 1 week of
1) HSV-1: primarily causes oral herpes, and is generally
rash onset (or any time prior to full crusting of
responsible for cold sores and fever blisters around
lesions).
the mouth and on the face.
● The recommended treatment options for
❖ Orolabial herpes (commonly known as cold sores acute localized dermatomal herpes zoster in
or fever blisters) is the most common patients with HIV are oral valacyclovir,
manifestation of HSV-1 infection. famciclovir, or acyclovir (doses as above)
❖ Classic manifestations of oral HSV-1 include a for 7 to 10 days, although longer durations
sensory prodrome in the affected area, rapidly of therapy should be considered when
followed by lesions on lips and oral mucosa that lesions resolve slowly.
evolve in stages from papule to vesicle, ulcer, and
crust. 6. CANDIDIASIS:
 Candidiasis is a yeast infection caused by
2) HSV-2: primarily causes genital herpes, and is Candida albicans. In people with HIV, the virus
generally responsible for genital herpes outbreaks. that causes AIDS, candidiasis commonly affects
the skin and mucous membranes such as the
❖ Genital herpes is typically caused by HSV-2 and is mouth, throat, esophagus and vagina.
the most common manifestation of HSV-2 infection.  Painful Candidiasis is rarely life-threatening.
● Typical genital mucosal or ulcerative lesions
on skin on or around the genitals Signs and Symptoms of Oral candidiasis (in the mouth
● sensory prodrome consisting of pain and and throat):
pruritus. ▪ White or red patches in the mouth, tongue or throat
● Mucosal disease includes dysuria or vaginal cracking and soreness at the corners of the
or urethral discharge mouth
▪ Altered taste, mouth pain or burning
● Inguinal lymphadenopathy
▪ Candidiasis in the esophagus can cause upper
chest pain, sore throat and painful or difficult
Herpes zoster (shingles)
swallowing
 Shingles is caused by the varicella-zoster virus,
▪ In the vagina, candidiasis causes a white cheesy
the same virus that causes chickenpox.
vaginal discharge accompanied by vaginal
itching and burning.
Signs and symptoms:
 Varicella rash tends to have a central distribution Treatment HIV-related candida infections
with lesions first appearing on the head, then the ▪ clotrimazole or nystatin
trunk, and finally the extremities, evolving through ▪ lozenges or a swish-and-swallow preparation to
stages of macules, papules, vesicles, pustules, treat candidiasis of the mouth or throat
and crusts. ▪ vaginal creams or tablets for vaginal infections
 Herpes zoster manifests as a painful cutaneous ▪ patient has candidiasis of the esophagus, either
eruption in a dermatomal distribution, often oral fluconazole or ketoconazole tablets can be
preceded by prodromal pain. taken
Diagnosis:
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 • Don’t share needles, syringes, drug injection
to the State Department and the Centers equipment, or any item that may put a person in
for Disease Control and Prevention contact with blood
• Results issued only to test recipient
5 MEANS OF HIV PREVENTION
• A = abstain from sex
Oral Testing
 Orasure • B = be faithful
 The only FDA approved HIV antibody. • C = correct & consistent use of condom
 As accurate as blood testing • D = do not use illegal drugs/share needles
 Draws blood-derived fluids from the gum • E = educate yourself
tissue.
 NOT A SALIVA TEST! Abstinence
 It is the only 100 % effective method of not
acquiring HIV/AIDS.
T cell count test  Refraining from sexual contact: oral, anal, or
 Shows the strength of a patient’s immune vaginal.
system  Refraining from intravenous drug use
 This test can also tell whether a person has
developed AIDS Monogamous relationship
 A mutually monogamous (only one sex partner)
Viral load test relationship with a person who is not infected
 Measures of the number of viruses in the blood with HIV
 The higher the viral load, the more infectious the  HIV testing before intercourse is necessary to
person’s body fluids are likely to be and the prove your partner is not infected
closer that person is to having AIDS
Protected Sex
Retest  Use condoms (female or male) every time you
 Should be retested 6 months after the first test have sex (vaginal or anal)
 An initial negative test can be misleading if the  Always use latex or polyurethane condom (not a
test is done too soon after infection natural skin condom)
 Always use a latex barrier during oral sex
DIAGNOSIS
1. ELISA ( Enzyme Linked Immunosorbent Assay) When Using A Condom Remember To:
2. Western Blot assay-confirmatory  Make sure the package is not expired
3. Orasure- saliva  Make sure to check the package for damages
4. CD4 cell count  Do not open the package with your teeth for risk
5. Polymerase chain reaction (PCR) of tearing
 Never use the condom more than once
ELISA
 An enzyme-linked immunosorbent assay, also Guidelines for care of the person with HIV/AIDS:
called ELISA or EIA, is a test that detects and  Prevent infection
measures antibodies in your blood.  Wash hands frequently
 With (+) result  Use gentle soap; avoid bar soap that may irritate
 Antibodies to HIV are present in blood skin.
 HIV is PROBABLY active  Provide for daily showering/ basin bath; avoid
 Despite HIV infection, client does not necessary tub bath if rashes are present.
have AIDS  Use separate washcloth for lesions
 Client is NOT IMMUNE to AIDS.  Use soft toothbrush, nonabrasive toothpaste.
 Prevent skin breakdown
 Elevate and support areas of edema
Treatment Options  Observe surgical site and IV insertion sites daily
Three ways to protect yourself? for signs of infection.
• Practice abstinence  Change dressings (if any) daily.
 Avoid eating fresh fruits / vegetables;
• Avoid multiple partners- Monogamous uncooked/ “rare” foods.
Relationship  Carry out infection control measures according
to institution’s policy
 Administer prescribed antibiotics, IV in acknowledging and planning for
fluids/ antipyretics. anticipated losses.
 Encourage increase OFI.  Provide information as desired and
 Monitor daily I and O records necessary, depending on ability to perceive.
 Weigh patient daily  Suggest appropriate religious support
 Instruct patient in deep breathing coughing  Facilitate participation in support groups/
exercise- to PX: Atelectasis and fever individual counseling.
 Modify alterations with body temperature: TSB,
DBE, and Coughing Other Management with AIDS
 Identification of person at risk

Promote Self-care  Obtaining a complete, accurate sexual history is


 Assess realistic functional ability important
 Plan, supervise and assist with ADL
if necessary  Identify if IV drug user
 Encourage patient to be as active  Check for other risk factors
and independent as possible
 Assist patient with ROM exercise to  With high risk HIV/AIDS
PX contractures.
 Pace activities and schedule rest periods to Counsel about significant testing and necessity of follow-
PX fatigue. up
 Educational and counseling strategies with AIDS
Provide Counseling
 Assess and support patient coping mechanism
 Explore with patient and significant others HIV/ AIDS drugs
normalcy of grief response and assist them in  To suppress infection, prolonging life.
acknowledging and planning for anticipated  To treat opportunistic infection.
losses.  Effectiveness: monitored by viral load count,
CD4 cell counts (↑500)
Health Teaching Focuses on  Side effects include kidney & liver damage
 Promote Good Nutrition  30% of people who start taking some of these
 Promote Self-Care drugs become so sick they have to stop taking
 Promote Counseling them
Nucleoside/nucleotide reverse
Nursing Management transcriptase inhibitors (NRTIs)
A. Promote Good Nutrition  NRTIs are sometimes referred to as “nukes.”
 Diet: High calorie, high CHON, high K, low
residue diet.  They work by interrupting the life cycle of HIV as
 Easy to swallow food: Gelatin when dysphagia it tries to copy itself.
is present.  These drugs also have other actions that
 Provide oral care prevent HIV from replicating in the body.
 Encourage patients to be out of bed and
sitting for meals if possible.
The following drugs are NRTIs:
B. Promote Self- Care • abacavir (Ziagen)
 Assess realistic functional ability
• emtricitabine (Emtriva)
 Plan, supervise and assist with ADL if
necessary • Lamivudine (Epivir)
 Encourage patient to be as active and
independent as possible • tenofovir alafenamide fumarate (Vemlidy)
 Assist patients with ROM exercise to
• tenofovir disoproxil fumarate (Viread)
improve contractures.
 Pace activities and schedule rest periods to • zidovudine (Retrovir)
improve fatigue.
 Handwashing  Zidovudine was the first FDA-approved HIV drug. It’s
also known as azidothymidine or AZT. Zidovudine is
C. Provide Counseling rarely used in adults now.
 Assess and support patient coping  It’s mainly given to babies born to HIV-positive
mechanism mothers as a form of post-exposure prophylaxis
 Explore with patient and significant others (PEP).
normalcy of grief response and assist them
Combination NRTIs in the development of these antibodies. CD4+ T-cells are
• The following combination drugs are made up of divided into 3 broad classes: effector T-cells, memory T-
either two or three NRTIs: cells, and T-regulatory (Treg) cells. Effector T-cells are
• 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”:
further divided based on the cytokines they produce:
• doravirine (Pifeltro) TH1, TH2, and TH17 cells. TH1 cells produce interferon-
gamma and interleukin (IL)-2, and promote a cell-
• efavirenz (Sustiva)
mediated immune response. TH2 cells produce IL-4 and
• etravirine (Intelence) 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
Cytochrome P4503A (CYP3A) inhibitors pathogens, to produce antimicrobial peptides. and to
 Cytochrome P4503A is an enzyme in the liver promote neutrophil inflammation essential for immunity
that helps several functions in the body, at the skin and mucosal surfaces. Memory T-cells rapidly
including breaking down or metabolizing differentiate into effector T-cells in secondary immune
medications. responses. CD4+CD25+FOXP3+ Treg cells are
essential in peripheral tolerance and serve to suppress
 Cytochrome P4503A inhibitors, also known as
dysregulated immune responses.
CYP3A inhibitors, increase the levels of certain \
CD4+CD25+FOXP3+Tregs inhibit TH2 cytokine
HYPERSENSITIVITY production through the secretion and action of IL-10 and
TGF-beta. Proper function of CD4+CD25+FOXP3+ Treg
 Hypersensitivity is an excessive or aberrant cells has been shown to be important in the tolerance of
immune response to any type of stimulus. It allergens. Abnormalities in the CD4+CD25+FOXP3+
usually does not occur with the first exposure to Treg population may play a role in the development of
an allergen. Rather, the reaction follows a re- allergic disease.
exposure after sensitization, or buildup of The allergic reaction first requires sensitization
antibodies, in a predisposed person. Injurious or to a specific allergen and occurs in genetically
pathologic immune reactions are classed as predisposed individuals. The allergen is either inhaled or
hypersensitivity reactions. To promote ingested and is then processed by an antigen-presenting
understanding of the immune pathogenesis of cell (APC), such as a dendritic cell, macrophage, or B-
disease, hypersensitivity reactions have been cell. The antigen-presenting cells then migrate to lymph
classified into four specific types of reactions. nodes, where they prime naïve TH cells that bear
Most allergic reactions are either type I or type receptors for the specific antigen.
IV hypersensitivity reactions. After antigen priming, naïve TH cells differentiate
into TH1, TH2, or TH17 cells based upon antigen and
Pathophysiology cytokine signaling. In the case of allergen sensitization,
Immediate hypersensitivity reactions are the differentiation of naïve TH cells is skewed toward a
mediated by IgE, but T and B cells play important roles 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  certain plants
plays a regulatory role in mast cells activation. IL-4 and  pollen or molds
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 Diagnostic Tests
allergen via allergen-specific receptors. They then
internalize and process the antigen and present peptides  Complete Blood Count with Differential
from it, bound to the major histocompatibility class II  The white blood cell (WBC) count is usually
molecules found on B-cell surfaces, to the antigen normal except with infection and
receptors on TH2 cells. The B cell must also bind to the inflammation. Eosinophils, which are
TH2 cell and does so by binding the CD40 expressed on granular leukocytes, normally make up 2%
its surface to the CD40 ligand on the surface of the TH2 to 5% of the total number of WBCs. They
cell. IL-4 and IL-13 released by the TH2 cells can then can be found in blood, sputum, and nasal
act on the B cell to promote class switching from secretions. A level greater than 5% to 10%
immunoglobulin M production to antigen-specific IgE is considered abnormal and may be found in
production. patients with allergic disorders.
The antigen-specific IgE antibodies can then
bind to high-affinity receptors located on the surfaces of  Eosinophil Count
mast cells and basophils. Re-exposure to the antigen  An actual count of eosinophils can be
can then result in the antigen binding to and cross- obtained from blood samples or smears of
linking the bound IgE antibodies on the mast cells and secretions. During symptomatic episodes,
basophils. This causes the release and formation of smears obtained from nasal secretions and
chemical mediators from these cells. These mediators sputum of patients with allergies usually
include preformed mediators, newly synthesized reveal an increase in eosinophils, indicating
mediators, and cytokines. an active allergic response.
Allergic reactions can occur as immediate
reactions, late-phase reactions, or chronic allergic  Total Serum Immunoglobulin E Levels
inflammation. Immediate or acute-phase reactions occur  High total serum IgE levels support the
within seconds to minutes after allergen exposure. Some diagnosis of allergic disease. In the majority
of the mediators released by mast cells and basophils of cases, the antibody typically responsible
cause eosinophil and neutrophil chemotaxis. Attracted for an allergic reaction belongs to the IgE
eosinophils and resident lymphocytes are activated by isotype. Patients with this disorder are said
mast cell mediators. to have an IgE-mediated allergic disease.
These and other cells (eg, monocytes, T cells)
are believed to cause the late-phase reactions that can  Skin Tests
occur hours after antigen exposure and after the signs or  Skin testing entails the intradermal injection
symptoms of the acute-phase reaction have resolved. or superficial application (epicutaneous) of
The signs and symptoms of the late-phase reaction can solutions at several sites. Depending on the
include redness and swelling of the skin, nasal suspected cause of allergic signs and
discharge, airway narrowing, sneezing, coughing, and symptoms, many different solutions may be
wheezing. These effects can last a few hours and applied at separate sites. These solutions
usually resolve within 24-72 hours. contain individual antigens representing an
Finally, continuous or repeated exposure to an assortment of allergens most likely to be
allergen (eg, a cat-allergic patient who owns a cat) can implicated in the patient’s disease. Positive
result in chronic allergic inflammation. Tissue from sites (wheal-and-flare) reactions are clinically
of chronic allergic inflammation contains eosinophils and significant when correlated with the history,
T cells (particularly TH2 cells). Eosinophils can release physical findings, and results of other
many mediators (eg, major basic protein), which can laboratory tests. Skin testing is considered
cause tissue damage and thus increase inflammation. the most accurate confirmation of allergy.
Collectively, this results in structural and functional
changes to the affected tissue. Furthermore, a repeated
allergen challenge can result in increased levels of Four Basic Types of Hypersensitivity
antigen-specific IgE, which ultimately can cause further
release of IL-4 and IL-13, thus increasing the propensity I. Type I Anaphylactic (Immediate)
for TH2 cell/IgE–mediated responses The most severe hypersensitivity
reaction is anaphylaxis. An unanticipated severe
allergic reaction that is rapid in onset,
Types of Allergen anaphylaxis is characterized by edema in many
 pet dander tissues, including the larynx, and is often
 bee stings or bites from other insects accompanied by hypotension, bronchospasm,
 certain foods, including nuts or shellfish and cardiovascular collapse in severe cases.
 certain medications, such as penicillin or aspirin Type I or anaphylactic hypersensitivity is an
immediate reaction beginning within minutes of Signs and Symptoms
exposure to an antigen. Primary chemical  Pruritus of the nose, roof of the
mediators are responsible for the symptoms of mouth, throat, eyes and ears
type I hypersensitivity because of their effects  Desensitizing immunizations
on the skin, lungs, and gastrointestinal tract. If  Cough
chemical mediators continue to be released, a  Dyspnea
delayed reaction may occur and may last for up  Wheezing
to 24 hours. Clinical symptoms are determined  Chest tightness
by the amount of the allergen, the amount of  Diaphoresis
mediator released, the sensitivity of the target
 Tachycardia
organ, and the route of allergen entry. Type I
 Widened pulse
hypersensitivity reactions may include both local
and systemic anaphylaxis  Hypoxia
 Central cyanosis
A. ANAPHYLAXIS
 Anaphylaxis is a clinical response to an Medical Management:
immediate (type I hypersensitivity) There are two general classes of asthma medications:
immunologic reaction between a specific 1. Quick relief medications for immediate
antigen and an antibody. The reaction results treatment for asthma symptoms and
from a rapid release of IgE-mediated exacerbations
chemicals, which can induce a severe, life- a. Short-acting beta2-adrenergic agonist
threatening reaction. (ventolin, albuterol) and pirbuterol
(Maxair)
B. ALLERGIC RHINITIS 2. Long acting medications to achieve and
 Allergic rhinitis is a group of disorders maintain control of persistent asthma
characterized by inflammation and irritation of a. Corticosteroids
the mucous membrane of the nose. It is b. Long acting beta2- adrenergic agonist
associated with exposure to airborne particles c. Leukotriene modifiers (inhibitors)
such as dust, dander or plant pollen in people d. Antileukotriene (montelukast)
who are allergic to these substances.
Nursing Management:
 Assess the patient’s respiratory
Classification status by monitoring the severity of
the symptoms, breath sounds, peak
1. Seasonal rhinitis – occurs during pollen seasons flow, pulse oximetry and vital signs.
2. Perennial rhinitis – occurs throughout year  Administer medications as
prescribed and monitor the patient’s
response
Signs and Symptoms:  Administer fluids if patient is
 Rhinorrhea dehydrated
 Nasal congestion  Instruct to adhere to the prescribed
 Sneezing medications and therapy
 Emphasize to keep follow-up
Management appointments with health care
 Antihistamines provider
 Corticosteroid nasal sprays
D. ACUTE ALLERGIC DRUG REACTION
Nursing Management  Dermatitis medicamentosa, a type I
 Instruct patient to avoid or reduce exposure to hypersensitivity disorder, is the term applied
allergens and irritants to skin rashes associated with certain
medications. Although people react differently
 Instruct patient in correct administration of
to each medication, certain medications tend
nasal medication
to induce eruptions of similar types. This
 To achieve maximal relief, the patient is
disorder is the leading cause of fatal
instructed to blow the nose
anaphylaxis, comprising 43% of deaths from
anaphylaxis. All routes of administration are
C. ASTHMA
potentially fatal, but drugs given parenterally
 Asthma is a chronic inflammatory disease of
incur the greatest risk. Cutaneous rashes are
the airways that causes hyperresponsiveness,
among the most common adverse reactions
mucosal edema and mucus production is
to medications and occur in approximately 2%
reversible and diffuse airway inflammation
to 3% of hospitalized patients. In general,
that leads to airway narrowing.
drug reactions appear suddenly with
characteristics that are more intense than the presentation also reflects the underlying
somewhat similar eruptions of infectious cause for hemolysis. For example, sickle
origin, and, with the exception of bromide and cell anemia is associated with painful
the iodide rashes, disappear rapidly after the occlusive crises.
medication is withdrawn. Rashes may be  Hemolytic anemia has multiple causes,
accompanied by systemic or generalized and the clinical presentation can differ
symptoms. On discovery of a medication depending on the etiology. An array of
allergy, patients are warned that they have a laboratory tests are available for
hypersensitivity to a particular medication and detecting hemolysis, and specialized
are advised not to take it again. Penicillin, tests may be indicated to diagnose the
cephalosporin, and sulfonamide antibiotics cause for hemolysis. There are
are most commonly implicated. Patients differences in the management of various
should carry information identifying the types of hemolytic anemias.
hypersensitivity with them at all times.
B. INCOMPATIBLE BLOOD TRANSFUSION
 Skin eruptions related to medication therapy REACTION
suggest more serious hypersensitivities.  Acute transfusion reactions present as
Frequent assessment and prompt reporting of adverse signs or symptoms during or within
the appearance of any eruptions are 24 hours of a blood transfusion. The most
important so that early treatment can be frequent reactions are fever, chills, pruritus,
initiated. Some cutaneous drug reactions may or urticaria, which typically resolve promptly
indicate involvement of other organs and are without specific treatment or complications.
known as complex drug reactions. Patients Other signs occurring in temporal
who suspect that a new rash may be caused relationships with a blood transfusion, such
by a drug allergy (newly prescribed as severe shortness of breath, red urine,
medications, especially antibiotics such as high fever, or loss of consciousness may be
penicillin or sulfa medications) should stop the first indication of a more severe
taking the medication immediately and potentially fatal reaction.
contact their prescribing clinician, who will
determine whether the medication and the III. Type III Immune- Complex Reactions
rash are related.  Type III, or immune complex,
hypersensitivity involves immune complexes
II. Type II Cytotoxic (Cytolytic reaction) that are formed when antigens bind to
 Type II, or cytotoxic, hypersensitivity antibodies. These complexes are cleared
occurs when the system mistakenly from the circulation by phagocytic action. If
identifies a normal constituent of the these type III complexes are deposited in
body as foreign. This reaction may be the tissues or vascular endothelium, two factors
result of a cross-reacting antibody, contribute to injury: the increased amount of
possibly leading to cell and tissue circulating complexes and the presence of
damage. Type II hypersensitivity vasoactive amines. As a result, there is an
reactions are associated with several increase in vascular permeability and tissue
disorders. For example, in myasthenia injury.
gravis, the body mistakenly generates
antibodies against normal nerve ending A. ACUTE GLOMERULONEPHRITIS
receptors. In Good pasture syndrome, it  Glomerulonephritis is an inflammation of
generates antibodies against lung and the glomeruli which result from an antigen-
renal tissue, producing lung damage and antibody reaction produced from an infection
kidney injury. elsewhere in the body. This disorder which
is caused by an immunological reaction may
A. HEMOLYTIC ANEMIA result in proliferative and inflammatory
 Hemolysis is the premature destruction changes within the glomerular structure.
of erythrocytes. A hemolytic anemia will
develop if bone marrow activity cannot Risk Factors
compensate for the erythrocyte loss. The  Immunological or autoimmune diseases
severity of the anemia depends on  Group A beta-hemolytic streptococcal infection
whether the onset of hemolysis is (GABHS)
gradual or abrupt and on the extent of  History of pharyngitis of tonsillitis 2 to 3 weeks
erythrocyte destruction. Mild hemolysis before symptoms
can be asymptomatic while the anemia in
severe hemolysis can be life threatening Signs and Symptoms
and cause angina and cardiopulmonary  Gross hematuria
decompensation. The clinical  Dark, smoky, cola-colored or red-brown urine
 Proteinuria, frothy urine inflammation cause tissue injury. This type
 Elevated urine specific gravity of reaction to the subcutaneous injection of
 Headache antigen is often used as an assay for cell-
 Chills and fever mediated immunity (e.g., the purified protein
 Fatigue and weakness derivative skin test for immunity to
 Nausea and vomiting Mycobacterium tuberculosis.
 Edema in the face, periorbital area and feet
Delayed-type hypersensitivity
 Elevated Blood Pressure
 Tuberculin test
 Elevated BUN and Creatinine
 Allergic contact dermatitis
 Positive antibody response test for
streptococcus  Hypersensitivity pneumonitis
 Elevated Erythropoietin Sedimentation rate  Tissue/Graft transplant rejection
 Hyponatremia
A. PPD testing
 Hyponatremia
An example of this reaction is the effect
 Hypophosphatemia of an intradermal injection of tuberculin
 Hyperkalemia antigen or purified protein derivative (PPD).
Sensitized T cells react with the antigen at
Diagnostic Tests: or near the injection site. Lymphokines are
Urinalysis released and attract, activate, and retain
 (+) Hematuria and proteinuria – most important macrophages at the site. These
indicator of glomerular injury macrophages then release lysozymes,
 (+) Casts, elevated specific gravity, low pH causing tissue damage. Edema and fibrin
are responsible for the positive tuberculin
Medical Management: reaction.
 Antimicrobial/antibiotics – Penicillin,
Erythromycin, Cephalexin B. GRAFT-VERSUS-HOST DISEASE
 Diuretics Graft versus host disease (GVHD) is
 Corticosteroids an immune-mediated condition resulting
 Calcium channel blockers from a complex interaction between donor
 Vasodilators and recipient adaptive immunity.
 Fluid and electrolytes balance
ACUTE GVHD – describes a distinctive
syndrome of dermatitis, hepatitis, and
Nursing Intervention enteritis developing within 100 days after
 Monitor Vital Signs including NVS allogeneic hematopoietic cell transplantation
 Monitor weight of patient daily (HCT)
 Dietary restriction of sodium and protein
 Limit fluid intake CHRONIC GVHD – describes a more
 Carbohydrates are given liberally to provide diverse syndrome developing after day 100.
energy and reduce the catabolism of protein In addition to allogeneic HCT, procedures
associated with high risk of GVHD include
 Provide skin care
transplantation of solid organs containing
 Observe for compilations like renal failure,
lymphoid tissue and transfusion of non-
cardiac failure and hypertensive encephalopathy
irradiated blood products.
 Monitor urinalysis, BUN and creatinine levels
 Promote rest and regular activity when hematuria Signs and Symptoms
and proteinuria resolves
Presentation in acute GVHD is as follows:
B. RHEUMATOID ARTHRITIS (done)  A pruritic or painful rash (median onset,
day 19 posttransplantation; range, 5-47
IV. Type IV Cell-Mediated Reactions/Delayed days)
Hypersensitivity  Pruritus from initially asymptomatic liver
 Type IV, or delayed-type hypersensitivity, involvement, anorexia, weight loss,
also known as cellular hypersensitivity followed rarely by hepatic coma
 Occurs 24 to 72 hours after exposure to an  Diarrhea, intestinal bleeding, cramping
allergen abdominal pain, and ileus
 Ocular – Burning, irritation,
Delayed-Type (Type IV) Hypersensitivity photophobia, and pain from lack of tear
 Type IV, or delayed-type, hypersensitivity secretion
(DTH), is an immune reaction in which T-  Oral and GI – Mouth dryness, sensitivity
cell–dependent macrophage activation and to acidic or spicy foods, dysphagia,
odynophagia, and insidious weight loss  Liver function tests – Elevation of the alkaline
 Pulmonary – Obstructive lung disease, phosphatase level, an early sign of liver
with symptoms of wheezing, dyspnea, involvement by GVHD; hypoalbuminemia is
and chronic cough that is usually typically due to GVHD-associated intestinal
nonresponsive to bronchodilator therapy protein leakage and a negative nitrogen
▪ Neuromuscular – Generalized or focal balance
weakness, neuropathic pain, vision loss,  Serum electrolytes and chemistries (eg,
muscle cramps, myalgia potassium, magnesium, bicarbonate levels)
 Joints – Arthralgia, arthritis may be altered; massive diarrhea and
diminished oral intake can lead to serious
Physical Examination electrolyte abnormalities
Skin findings are as follows:
 Maculopapular exanthema – Red-to- Other tests:
violet lesions that typically first appear  Schirmer test – To measure the degree of
on the palms of the hands, soles of the tear formation by the lacrimal glands in
feet, cheeks, neck, ears, and upper chronic GVHD
trunk, sometimes progressing to involve  Pulmonary function tests and arterial blood
the whole body; in severe cases, bullae gas analysis – To identify obstructive
may be observed, and vesicles may pulmonary disease (eg, obliterative
form bronchiolitis) in chronic GVHD
 Lichenoid skin lesions or  Manometric studies of the esophagus
sclerodermatous thickening of the skin,  Hepatic and Doppler sonography
which sometimes causes contractures  Barium swallow study
and limits joint mobility
 Jaundice from hyperbilirubinemia; C. TRANSPLANT REJECTION
patients who subsequently develop Transplantation is the act of
pruritus may exhibit excoriations from transferring cells, tissues, or organs from
scratching one site to another typically between
different individuals. The malfunction of an
Ocular findings may include the organ system can be corrected with
following: transplantation of an organ from a donor.
However, the immune system remains the
Acute GVHD – Hemorrhagic conjunctivitis, most formidable barrier to transplantation as
pseudomembrane formation, and a routine medical treatment. The immune
lagophthalmos system has developed elaborate and
effective mechanisms to combat foreign
Chronic GVHD – Keratoconjunctivitis sicca, agents. These mechanisms are also
which may lead to punctate keratopathy involved in the rejection of transplanted
organs which are recognized as foreign by
Additional findings are as follows: the recipient’s immune system.
 Oral – Atrophy of the oral mucosa, erythema, and
lichenoid lesions of the buccal and labial mucosae
in chronic GVHD Types of Grafts:
 Pulmonary – Prolonged expiratory breathing
 Xenografts – grafts between members of
phase (wheezes) from bronchiolitis obliterans
different species
 GI – Diffuse abdominal tenderness with
 Autografts – grafts from one part of the body to
hyperactive bowel sounds may accompany
another
secretory diarrhea of acute GVHD; in severe ileus,
 Allografts – grafts between members of the
the abdomen is silent and appears distended
same species that differ genetically
 Neuromuscular – Findings of myasthenia gravis,
 Isograft – grafts between genetically identical
polymyositis, optic neuritis, arthritis may occur in
individuals
chronic GVHD
 Vaginitis and vaginal strictures have been
Clinical Stages of Rejection:
described in chronic GVHD
 Hyperacute rejection – occurs minutes to hours
Diagnosis due to rapidly destroyed vascularization
 Acute rejection - first six months after
Laboratory study results in GVHD are as
transplantation
follows:
o Acute cellular rejection – mediated by
 CBC – Autoimmune cytopenia (eg, lymphocytes that have been activated
thrombocytopenia, anemia, and leukopenia) against donor antigens
may be observed with chronic GVHD o Humoral rejection – is a form of allograft
injury primarily mediated by antibody and  Allergic contact dermatitis occurs when the
complement. skin develops an allergic reaction after being
 Chronic rejection – develops months to years exposed to a foreign substance. This causes
after acute rejection episodes have subsided. the body to release inflammatory chemicals
Chronic rejections are both antibody- and cell- that can make the skin feel itchy and
mediated irritated.

Common causes of allergic contact


dermatitis include contact with:
Transplant Tolerance and Immunosuppressed:
 Rejection cannot be completely prevented;
 jewelry made from nickel or
however, a degree of immune tolerance to
gold
the transplant does develop. Tissue typing
and cross matching is performed to assess  latex gloves
donor-recipient compatibility for human  perfumes or chemicals
leukocyte antigen (HLA) and ABO group. in cosmetics and skin
care products
These tests include the following: b. Irritant contact dermatitis
 ABO blood group compatibility is tested  Irritant contact dermatitis is the most
first common type of contact dermatitis. It
 Lymphocytotoxicity assay happens when the skin comes in contact
 Panel-reactive antibody (PRA) with a toxic material
 Mixed lymphocyte reaction (MLR)
 The use of immunosuppressive drugs Toxic substances that can cause irritant contact
requires a balance between the risk of loss dermatitis include:
of transplanted organs and the toxicity of the  Battery acid
agent. Immunosuppressive drugs are used  Bleach
in 2 phases: the initial induction phase,  Drain cleaners
which requires much higher doses of these  Kerosene
drugs, and the later maintenance phase.
 Detergents
 Pepper spray
Immunosuppressive agents in current use include
the following:  Irritant contact dermatitis can also occur when the
 Immunophilin-binding agents (Cyclosporin, skin comes in contact with less irritating materials —
Tacrolimus) – calcineurin inhibitors. Suppress like soap or even water — too often.
the activation of T lymphocyte by inhibiting the  People whose hands are frequently exposed to
production of cytokines ▪ Mammalian target of water, such as hairdressers, bartenders, and
rapamycin (mTOR) inhibitors – macrocyclic healthcare workers, often experience irritant contact
antibiotic. It results in T- and B-cell cycle arrest. dermatitis of the hands, for example.
 Antiproliferative agents (Azathioprine,
Cyclophosphamide) – inhibit DNA replication and c. Photocontact dermatitis
suppress B- and T-cell proliferation.  Photocontact dermatitis is less common. It’s
 Antibodies (Basiliximab, Daclizumab) interact a reaction that can occur when the active
with lymphocyte surface antigens, depleting ingredients in a skin product are exposed to
circulating thymus-derived lymphocytes and the sun and result in irritation.
interfering with cell-mediated and humoral
immune response.
Management:
 Corticosteroids
 Avoid scratching your irritated skin. Scratching
can make the irritation worse or even cause a
D. CONTACT DERMATITIS skin infection that requires antibiotics.
 An example of a type IV hypersensitivity  Clean your skin with mild soap and
reaction is contact dermatitis resulting from lukewarm water to remove any irritants. ▪
exposure to allergens such as cosmetics, Stop using any products you think might
adhesive tape, topical medications, be causing the problem. ▪ Apply bland
medication additives, and plant toxins. The petroleum jelly like Vaseline to soothe the
symptoms that occur include itching, area.
erythema, and raised lesions  Try using anti-itch treatments such as calamine
lotion or hydrocortisone cream (Cortisone-10).
There are three types of contact dermatitis:  If needed, take an antihistamine drug such as
a. Allergic contact dermatitis diphenhydramine to cut down on itching and to
reduce your allergic response.