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The immune system  Organized as differently sized organs –

lymphoid organs – the lymph nodes, spleen,
thymus, and bone marrow.
What is Immune System?
 Immune systems are biological structures The immune system is composed with
and processes within an organism that All parts of the body that help in the recognition and
protects against disease by identifying and destruction of foreign material.
killing pathogens and tumor cells. It detects  White blood cells
a wide variety of agents, from viruses to  Phagocytes and lymphocytes
parasitic worms, and needs to distinguish  bone marrow
them from the organism’s own healthy cells  lymph nodes
and tissues in order to function properly  tonsils
 The body’s defense against disease-causing  thymus, and
 spleen are part of the immune system.
organisms, malfunctioning cells, and
foreign particles
Immunity
 The Latin term “Immunis” means exempt,
referring to the protection against foreign
agents.
Definition:

 The integrated body system of organs,

tissues cells, & cell products that
differentiates self from non-self &
neutralized potentially pathogenic
organisms.

Basic Classification of Immunity

Passive
(maternal)
Natural
Active
(infection)
Adaptive
Immunity Passive
Immunity (antibody
Innate transfer)
Artificial
Immunity
Active
(immunization)

Where is the immune system?

Cells of the immune system are:
 Distributed throughout the body in the
blood, lymph, epithelial, and tissues.
 Arranged in small spherical nodules
(lymphoid nodules) found in tissues and
inside various organs. Life is a fight against Foreign Substance
 Found in the: it has been estimated that during our lifetime we will
 mucosa of the digestive (tonsils, encounter a million foreign antigens capable of
Peyer’s patches), causing disease, and our bodies need the same amount
 respiratory of lymphocytes to defend against them
 reproductive
 urinary systems are MALT (mucosa-
associated lymphoid tissue)

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Central Immune Organs

 Central Immune Organs are the sites of
generation, differentiation, and maturation of
immunocytes.
 Bone marrow
 Thymus
 Bursa of Fabricius (the site of B cells
maturation in birds) But absent in Humans

Organs of the Immune System

Primary Lymphoid Organs
 Bone Marrow and Thymus
 Maturation Site
Secondary Lymphoid Organs
 Spleen, lymph nodes,
 MALT (mucosa! associated lymph tissue)
 GALT (gut-associated lymph tissue)
 Trap antigen, APO, Lymphocyte
 Proliferation

Lymphatic Pathways

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 Lymph enters lymphatic vessels

 The thoracic duct is the largest lymphatic
vessel – empties into the left subclavian
vein
 The lymphatic Vessel depends on muscle
contractions for movement
 One-way valves ensure one direction
 Lymph nodes act as filters for antigen

Lymph Nodes

Functions include:

 Filtration of particles and microorganisms

Thymus
 Bilobed organ on top of the heart
 Reaches maximum size during puberty: 70
g infants. 3g in adults
 95-99% of T-cells die in Thymus: self-
reactivity or no reactivity to Ag
 Consists of Cortex and Medulla
 Rat Thymocytes Sensitive to
glucocorticoids
to keep them out of general circulation.
 Interaction of circulating antigens in lymph
with lymphocytes to initiate the immune
response.
 Activation, and proliferation of B
lymphocytes, and antibody production.
 Activation, and proliferation of T-
lymphocytes.
Cells of Lymph Node
 Lymphoid Cells
 Macrophages and other phagocytic antigen-
processing cells
 Lymphatic and vascular endothelial cells,
and fibroblasts responsible for lymph node
supporting framework

 The thymus gland is found in the thorax in

the anterior mediastinum. It gradually
enlarges during childhood but after puberty,
it undergoes a process of involution
resulting in a reduction in the functioning
mass of the gland. It continues to function
throughout life.

In the Thymus, T-lymphocytes are Educated

 In the thymus gland, lymphoid cells

undergo a process of maturation and
education prior to release into the
circulation.

Lymphatic System

 Plasma from blood seeps into the tissue

 Interstitial fluid either go back or becomes
lymph

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Mucosa-associated lymphoid tissue (MALT)

Gut-associated lymphoid tissue (GALT)

 Tonsils, adenoids (Waldeyer’s ring)

 Peyer’s patches
 Lymphoid aggregates in the appendix and
large intestine
 Lymphoid tissue accumulating with age in
the stomach
 Small lymphoid aggregates in the
esophagus
Spleen  Diffusely distributed lymphoid cells and
plasma cells in the lamina propria of the
 The largest accumulation of lymphoid gut.
tissue
 Abundant phagocytic cells—defense Cells of the Immune System
against antigens in blood
 Site of the destruction of aged erythrocytes.
 Production site of activated Lymphocytes Immune system
which are delivered to the blood.
 THUS, an important blood filter, and Lymphoid
Myeloid Cells
antibody-forming organ. Cells
NK
There are two distinct components of the spleen, T-Cells B-Cells
Granulocytic Monocytic Cells

 the red pulp Helper Cells

Neutrophils Macrophages Suppressor Plasma
 the white pulp. Cells
Basophils Kupffer Cells Cells
The red pulp consists splenic of large numbers of pulp Eosinophils Dendritic Cytotoxic
Cells Cells
sinuses and sinusoids filled with blood and is
responsible for the filtration function of the spleen.

The white pulp consists of aggregates of lymphoid

tissue and is responsible for the immunological
function of the spleen

Functional aspects of spleen

The white pulp contains T cells, B cells, and

accessory cells. There are many similarities with
lymph node structure. The purpose of the white pulp
is to mount an immunological response to antigens
within the blood. The white pulp is present in the
form of a per arteriolar lymphoid sheath.

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Lymphocyte Origin

Types of T Cells:
 Cytotoxic T Cells – kill infected cells that
bear a foreign antigen on contact. Cytotoxic
T cells provide cell-mediated immunity.
 Helper T cells stimulate other immune cells
and produce cytokines.

Some T cells are memory T cells that will jump-start

an immune reaction upon re-infection.

Identifying Cell Using the CD Nomenclature
 CD Cluster of Differentiation
 Over 300 CD Markers
 T cells, CD4 or CD 8 and CD3
 B cells, CD19
 NK cells, CD56
 Monocytes/Macrophages CD14
 Dendritic Cells, CD1c (Human), CD11c
(mouse)
Lymphoid Cells
 B-cells, T-cells, and Null Cells (NK cells)
 20-40% of the body’s leukocytes
 99% of lymph node
 If inactivated said to be naïve
 Nucleus occupies almost the entire cell
 6-micrometerer diameter
T- Lymphocytes
 Formed in Bones marrow; migrate to and
matures in the Thymus gland
 Exhibit unique T-cell Antigen receptors
(TCR’s) on surface
 TCR’s can only recognize Ag associated with
MHC glycoproteins
o MHC I – found on nearly all
nucleated cells
o MHC II – found only on APC’s
One T cell binds to Ag, it triggers cell division to
form both memory cells and effector T cells
There are 2 populations of T cells characterized by
the type of CD glycoprotein found on the surface:
 Th – exhibits CD4
 Tc – exhibits CD8
Cytokines and Immunity
 Cytokines are signaling molecules produced by
T lymphocytes, monocytes, and other cells.
 Both interferon and interleukins are cytokines
used to improve a person’s own T-cell
performance in fighting cancer.

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 Interleukins show promise in the treatment of
chronic infectious diseases.
Specific defenses require B and T lymph nodes
 Specific defenses require B lymphocytes (B
cells) and T lymphocytes (T cells), which are
both produced in the bone marrow; however, T
cells mature in the thymus, while B cells
mature in the bone marrow.
 B cells give rise to antibodies that are shaped
like antigen receptors and are capable of
combining with and neutralizing antigens.
 T cells do not produce antibodies but instead
attack foreign antigens directly.
4. IgD – on surface of immature B cells, its
presence signifies the readiness of a B cell
5. IgE – found as antigen receptor on
basohpils in blood and on mast cells in
tissues, responsible for immediate allergic
response and protection against certain
parasitic worms.
The different classes of antibodies vary in structure.
Null Cells
 Do not express classical lymphocyte
markers
 Predominantly NK cells (CD56)
 Eliminate tumor cells and virally infected
cells

B Cells and Antibody-Mediated Immunity

 A toxin is a chemical produced by certain Mononuclear Cells
bacteria that is poisonous,  Monocytes in blood, MΦ in tissues
 As a B cell encounters a bacterial cell or a o Monocytes 5-10 times smaller
toxin with a specific antigen in a lymph node than M
or spleen, it is activated to divide.  MΦ increases phagocytic ability
 The resulting cells are plasma cells, mature B  Secretes cytokines and produces hydrolytic
cells that mass-produce antibodies. enzymes
 Defense by B cells is thus called antibody-  Named based on tissue they reside
mediated immunity o Alveolar (lungs)
o Kupffer (liver)
Antibodies o Microglial (brain)
o Osteoclasts (bone)
 Ig G
 Activated by phagocytosis or cytokines
 Ig A
 Antigen presenting capacity
 Ig M
 Ig D
 Ig E

Structure of IgG

 The most common type of antibody, the IgG

antibody, is a Y-shaped molecule that has two
binding sites for a specific antigen.
 Antigen-antibody complexes often mark the
antigen for destruction by neutrophils or
macrophages, or they may activate
complement.
1. IgG – the main type in circulation, binds to
pathogens, activates complement, and
enhances phagocytosis.
2. IgM – the largest type in circulation,
activates complement and clumps cells
3. IgA – Found in saliva and milk, prevent
pathogens from attaching to epithelial cells
in digestive and respiratory tracts.

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Effects of the Immune System

Beneficial:

 Protection from Invaders

 Elimination of Altered Self
Dendritic Cells
 Professional APCs Detrimental:
 Several types
 Discomfort and collateral damage
o Langerhans (LC) found in skin
(inflammation)
o Circulating DCs  Damage to seIf (hypersensitivity or
 Myeloid (MDC1 & MDC2) autoimmunity)
 Plasmacytoid
 Interstitial DCs, populate organs such as heart, Overview of the Immune System
lungs, liver, intestines
 Interdigitating DCs, T-Cell areas of lymph Immune
nodes and Thymic Medulla System

Innate Adaptive
(Nonspecific) (Specific)

Cellular Humoral Cellular Humoral

Components Components Components Components

Functional Basis of Immune System

The immune system is composed of two major
subdivisions,

 the innate or nonspecific immune system,

 the adaptive or specific immune system.

 The innate immune system is a primary defense

Function of the Immune System (Self- mechanism against invading organisms, while
 the adaptive immune system acts as a second
Non-self-Discrimination) line of defense.
 To protect from pathogens
Innate Host Defenses Against Infection
 Intracellular (e.g. viruses and some
bacteria and parasites) Anatomical barriers
 Extracellular (e.g. most bacteria, fungi
and parasites)  Mechanical factors
 To eliminate modified or altered self  Chemical factors
 Biological factors
Infection and Immunity Balance
Humoral Components
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 Complement respiratory
 Coagulation system tract)
 Cytokines Epithelium (e.g. Flushing action
nasopharynx) of tears, saliva,
mucus, urine

System or Component Mechanism

Organ
Skin Sweat Anti-microbial
fatty acids
Mucous HCl (parietal Low pH
Membranes cells) Lysozyme and
Tears and phospholipase
Saliva A
Defensins Antimicrobial
(respiratory &
GI tract)

Surfactants Opsonin
Opsonin – an antibody or other substance which binds
to foreign microorganisms or cells making them more
susceptible to phagocytosis
1st line of defenses / innate immune system
System or Component Mechanism
Includes: chemicals, Structure of skin/other epithelia, Organ
and mechanisms cells — mainly neutrophils and Skin and Normal Flora Antimicrobial
macrophage mucous substances
membranes Competition
First-Line Defenses /Innate Immune System- for nutrients
The body's first line of defense against pathogens uses and
mostly physical and chemical barriers such as: colonization
 Skin - acts as a barrier to invasion
 Sweat - has chemicals that can kill different
pathogens.
 Tears - have lysozyme which has powerful
digestive abilities that render antigens
harmless.
 Saliva – also has lysosome.
 Mucus – can trap pathogens, which are then
sneezed, coughed, washed away, or
destroyed by chemicals.
 Stomach Acid – destroys pathogens

Anatomical Barriers – mechanical Factors

System or Cell type Mechanism The integumentary system
Organ
Skin Squamous Physical  Skin
Epithelium barrier  Mucous membranes
desquamation  Mucous
Mucous Non-ciliated peristalsis
Membranes epithelium (e.g. Provides a physical barrier preventing microbial
GI tract) access
Ciliated Mucociliary
epithelium (e.g. elevator Inflammatory response

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A non-specific response triggered by: In summary there are 4 barriers to infection:

 Injury  Anatomic
 Penetration of bacteria  Physiologic
 Skin, respiratory, digestive tract, or  Phagocytic
reproductive tract  Inflammatory
Adaptive (Specific) Immunity
Two main layers
 An antigen is any foreign substance that
 Histamine stimulates the immune system to react to it.
 complement  The body does not consider its own proteins
Histamine foreign, therefore the immune system must
distinguish self from non-self.
 dilates local blood vessels
 Lymphocytes have a large number of
 increases capillary permeability
antigen receptors.
 Result in redness, heat, and swelling

Heat Adaptive immunity requires 2 major group of cells:

- Unfavorable to microorganisms a. B and T Lymphocytes (B or T cells)
- Mobilizes white blood cells (monocytes)
- Raises metabolic rate of surrounding cells

Complement
 Chemotaxis agent
 Recruits in WBC to injury site

The inflammatory response b. Antigen-presenting cells (APC’s)

 Starts with release of histamine and other - Macrophage (MØ)
chemicals - Dendritic cells (DC)
 Ends with WBC cleaning up the debris - B cells

Innate Immunity
 Front line of defense
 Not specific
 No immunologic memory
 Immediate response
 No memory
 No specific recogition
Displays four (4) attributes:
Adaptive immune system 1. Antibody specificity – distinguishes minute
T-lymphocytes differences in molecular structure to
T-cytotoxic → Cytotoxic determine non-self-antigens.
B-lymphocytes 2. Diversity – the immune system can produce
Plasma cells → Antibodies a hugely diverse set of recognition
molecules which allows us to recognize
Response takes 7-10 days literally billions of molecular shapes.
3. Memory – once it has responded to an
Comparison of Innate and adaptive Immunity antigen, the system maintains a memory of
Innate Immunity Adaptive Immunity that Ag
No time lag A lag period 4. Self-non-self-recognition- the system
Not antigen specific Antigen specific typically responds only to foreign
molecules.
No memory Development of
memory Humoral Components

Component Mechanism
Innate (Non-specific) Immunity
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Complement Lysis of bacteria and some Immunity occurs naturally by infection or is induced
viruses by medical intervention.
Opsonin The two types of induced immunity are:
Increase in vascular permeability  active immunity
Recruitment and activation of  passive immunity
phagocytic cells
Coagulation Increase vascular permeability In active immunity, the individual produces
system Recruitment of phagocytic cells antibodies against antigens.
B-lysin from platelets – a cationic
In passive immunity, the individual is given prepared
detergent
antibodies.
Lactoferrin Complete with bacteria for iron
and
transferrin Active Immunity
Lysozyme Breaks down bacteria cell walls  After exposure to a vaccine, which is a non-
Cytokines Various effects virulent disease agent, antibodies are produced.
 With a booster shot or second exposure, the
Cellular Components antibody titer rises to a much higher level.
 Active immunity is long-lived because there
Cell Functions are memory B cells and memory T cells that
Neutrophils Phagocytosis and intracellular will respond to lower doses of antigen in the
killing body.
Inflammation and tissue damage
Macrophage Phagocytosis and intracellular
Passive immunity
s killing
Extracellular killing of infected or You don’t produce the antibodies
altered self-targets  A mother will pass immunities on to her baby
Tissue repair during pregnancy – through what organ?
Antigen presentation for specific  These antibodies will protect the baby for a
immune response short period of time following birth while its
NK and Killing of virus-infected and immune system develops. What endocrine
Lymphokine altered self-targets gland is responsible for this?
-activated
 Lasts until antibodies die
killer (LAK)
cells  Passive immunity occurs when an individual is
Eosinophils Killing of certain parasites given prepared antibodies.
Humoral vs Cell-mediated immune response:  For example, a new born has antibodies that
Humoral IR passed from its mother through the placenta.
 occurs when Ag becomes coated with Ab  Breast-feeding passes antibodies from mother
which brings about the elimination of the to child.
foreign body  However, passive immunity is short-lived
 Cross-link several Ag’s to form clumps → since the antibodies were not produced by the
more easily phago’d person’s own B cells.
 Bind complement proteins
 Neutralizes toxins, viruses, and bacteria NURSING ASSESSMENT OF THE
from binding target cells IMMUNE SYSTEM
Cell-Mediated IR INTRODUCTION: ASSESSMENT
 Occurs when effector T cells are activated  An assessment of immune function begins
 Activated TH cells → activate phagocytic cells with a health history and physical examination.
activate B cells to  The history should note the patient’s age along
produce Ab with information about past and present
 Activated TC cells → kill altered self-cells conditions and events that may provide clues
(viral infected and tumor cells) to the status of the patient’s immune system.
 Areas to be addressed include
Artificial (Induced Immunity) o nutritional status;

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o infections and immunizations;
o allergies;
o disorder and disease states,
 such as autoimmune disorders,
cancer, and chronic illnesses;
o surgery;
o medications;
o blood transfusions.
 Physical assessment includes palpation of the
lymph nodes and examination of the skin,
mucous membranes, and respiratory,
gastrointestinal, genitourinary, cardiovascular,
and neurosensory systems
ASSESSMENT
 Nurse has to collect various data by using both
objective and subjective because
immunology/immunity concerned with almost
all systems of the body.
 Usually in the baseline date:
 Patient age, gender, occupation, Address,
educational qualifications, etc.
Age
 Age is an important factor to elicit from the
patient as people at the extremes of the life
span are more likely to develop problems
related to immune system functioning than are
those in their middle years
Gerontological Considerations
 The frequency and severity of infections are
increased in elderly people, possibly due to a
decreased ability to respond adequately to
invading organisms. Both the production and
the function of T and B lymphocytes may be
impaired.
 Responses to antigen stimulation may be
altered, with increasing proportions of
lymphocytes becoming unresponsive with age
(Porth, 2002).
 The incidence of autoimmune diseases also
increases with aging, possibly from a
decreased ability of antibodies to differentiate
between self and non-self.
 Failure of the surveillance system to recognize
mutant, or abnormal, cells may be responsible
for the high incidence of cancer associated
with increasing age.
Nutrition
 The nurse assesses the patient’s nutritional
status, including caloric intake as well as the
type of calories that the patient is consuming.
 Adequate nutrition is essential for optimal
functioning of the immune system. Inadequate
intake of vitamins that are essential for DNA
and protein synthesis may lead to protein-
calorie deficiency and subsequently to
impaired immune function.
 Vitamins also help in the regulation of cell
proliferation and maturation of immune cells.
Excess or deficiency of trace elements (ie,
copper, iron, manganese, selenium, or zinc) in
the diet generally suppresses immune function.
Infection and Immunization
 the patient is asked about immunizations
(including those received recently and those
received in childhood) and the usual childhood
diseases.
 Known past or present exposure to
tuberculosis is assessed, and the dates and
results of any tuberculin tests (purified protein
derivative [PPD] or tine test) and chest x-rays
are obtained.
 Recent patient exposure to any infections and
the exposure dates are elicited.
 It is important for the nurse to assess whether
the patient has been exposed to any sexually
transmitted diseases and bloodborne pathogens
such as hepatitis A, B, C, D, and E infections,
and HIV infection.
 A history of sexually transmitted diseases,
such as gonorrhea, syphilis, HPV infection,
and chlamydia, can alert the nurse that the
patient may have been exposed to HIV
infection or hepatitis.
 A history of past and present infections and the
dates and types of treatments that were used,
along with a history of any multiple persistent
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infections, fevers of unknown origin, lesions or pancytopenia

sores, or any type of drainage, are obtained. streptomycin Transient leukopenia

Allergy vancomycin
 The patient is asked about history of any (Vancocin,
allergies, including types of allergens Vancoled)
(pollens, dust, plants, cosmetics, food, Antithyroid Drugs
medications, vaccines), the symptoms propylthiouracil Agranulocytosis,
experienced, and seasonal variations in the (PTU) leukopenia
occurrence or severity in the symptoms.
 A history of testing and treatments that the
patient has received or is currently Nonsteroidal Inhibit Prostaglandin
receiving for these allergies and the Anti-inflammatory Synthesis or Release
effectiveness of the treatments is obtained. Drugs (NSAID) (in
 All medication and food allergies are listed large doses) Agranulocytosis
on an allergy alert sticker and placed on the aspirin
front of the patient’s health record or chart Anemia, allergy, no major
to alert others to the possibility of these cox-2 inhibitors other adverse effects to
allergies. Continued assessment for (Vioxx, Celebrex. the system
potential allergic reactions in this patient is Bextra)
vital Leukopenia, neutropenia
Selected Medications and effects on the Immune ibuprofen (Advil, Agranulocytosis,
System Motrin) leukopenia Pancytopenia,
indomethacin agranulocytosis, aplastic
Drug Classification Effects on The Immune
(Indocid. Indocin) anemia
(And Examples) System
phenylbutazone
Antibiotics (in large Bone Marrow
Adrenal Immunosuppression
doses) Suppression
Corticosteroids
ceftriaxone (Roccfin) Eosinophilia,
prednisone
hemolytic anemia,
hypoprothrombinemia, Antineoplastic Immunosuppression
neutropenia, Agents (Cytotoxic
thrombocytopenia Agents) Leukopenia
Eosinophilia, hemolytic alkylating agents’
cefuroxime sodium anemia, Leukopenia, neutropenia
(Ceftin) hypoprothrombinemia, cyclophosphamide
neutropenia, (Cytoxan)
Agranulocytosis,
thrombocytopenia mechlorethamine
neutropenia.
Leukopenia, aplastic HCI (Mustargen)
anemia Agranulocytosis,
chloramphenicol Leukopenia, inhibits T-
neutropenia But cyclosporine
(Chloromycetin) cell function
eosinophilia. Hemolytic
dactinomycin Antimetabolites Immunosuppression
anemia,
(Cosmogen) fluorouracil Leukopenia, eosinophilia
methemoglobinemia,
fluoroquinolones (pyrimidine
eosinophilia, leukopenia,
(Cipro, Levaquin, antagonist)
pancytopenia
Tequin)
methotrexate (folic
Agranulocytosis, Leukopenia, aplastic bone
acid antagonist)
granulocytosis marrow
gentamicin sulfate Neutropenia, leukopenia
(Garamycin) mercaptopurine (6-
Leukopenia, pancytopenia
macriolides MP) (purine
(erythromycin. antagonist)
Zithromax, Biaxin).  A history of blood transfusions is obtained
Agranulocytosis because previous exposure to foreign antigens
penicillin through transfusion may be associated with
Leukopenia, neutropenia.
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abnormal immune function. Additionally,
although the risk of human immunodeficiency
virus (HIV) transmission through blood
transfusion is extremely low in patients who
received a transfusion after 1985 (the year that
testing of blood for HIV was initiated in the
United States), a risk still exists.
 The patient is also asked about use of herbal
agents and over-the-counter medications.
Because many of these products have not been
subjected to rigorous testing, not all of their
effects have been identified. It is important,
therefore, to ask patients about their use of
these substances and to document their use.
Lifestyle and Other Factors
 Like any other body system, the immune
system functions depend on other body
systems.
 A detailed history of smoking, alcohol
consumption, dietary intake and nutritional
status, amount of perceived stress, injection
drug use, sexual practices, sexually transmitted
diseases, and occupational or residential
exposure to radiation or pollutants is obtained.
 Poor nutritional status, smoking, excessive
consumption of alcohol, injection drug use,
sexually transmitted diseases, and exposure to
environmental radiation and pollutants have
been associated with impaired immune
function and are assessed in the patient history.
PSYCHONEUROIMMUNOLOGIC FACTORS
 The assessment also addresses
psychoneuroimmunologic factors. It is thought
that the immune response is regulated and
modulated in part by neuroendocrine
influences.
 Lymphocytes and macrophages have receptors
capable of responding to neurotransmitters and
endocrine hormones. Lymphocytes can
produce and secrete adrenocorticotropic
hormone and endorphin-like compounds.
 Neurons in the brain, especially in the
hypothalamus, can recognize prostaglandins,
interferons, and interleukins as well as
histamine and serotonin, which are released
during the inflammatory process.
 Like all other biologic systems functioning in
the interest of homeostasis, the immune system
is integrated with other psychophysiologic
processes and is subject to regulation and
modulation by the brain.
NEOPLASTIC DISEASE
 A history of cancer in the patient is obtained,
along with the type of cancer and date of
diagnosis. Dates and results of any cancer
screening tests are also obtained.
 Immunosuppression contributes to the
development of cancers; however, cancer itself
is immunosuppressive. Large tumors can
release antigens into the blood, and these
antigens combine with circulating antibodies
and prevent them from attacking the tumor
cells.
 Furthermore, tumor cells may possess special
blocking factors that coat tumor cells and
prevent destruction by killer T lymphocytes.
During the early development of tumors, the
body may fail to recognize the tumor antigens
as foreign and subsequently fail to initiate the
destruction of the malignant cells.
 Hematologic cancers, such as leukemia and
lymphoma, are associated with altered
production and function of WBCs and
lymphocytes.
 A family history of cancer is obtained. If there
is a family history of cancer, the type of
cancer, age of onset, and relationship (maternal
or paternal) of the patient to the affected
family member is noted. (See Genetics in
Nursing Practice
CHRONIC ILLNESS AND SURGERY
 The health assessment includes a history of
chronic illnesses, such as diabetes mellitus,
renal disease, or chronic obstructive
pulmonary disease. The onset and severity of
illnesses, as well as treatment that the patient is
receiving for the illness, are obtained. Chronic
illness may contribute to immune system
impairments in various ways.
 Renal failure is associated with a deficiency in
circulating lymphocytes. In addition, immune
defenses may be altered by acidosis and
uremic toxins.
 In diabetes, an increased incidence of infection
has been associated with vascular
insufficiency, neuropathy, and poor control of
serum glucose levels.
 Recurrent respiratory tract infections are
associated with chronic obstructive pulmonary
disease as a result of altered inspiratory and
expiratory function and ineffective airway
clearance
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 Anemia
SPECIAL PROBLEMS Gastrointestinal System
 Conditions such as burns and other forms of  Hepatosplenomegaly
injury and infection may contribute to altered  Colitis
immune system function. Major burns or other  Vomiting
factors cause impaired skin integrity and  Diarrhea
compromise the body’s first line of defense.
 Loss of large amounts of serum with burn Genitourinary System
injuries depletes the body of essential proteins,  Frequency and burning on urination
including immunoglobulins.  Hematuria
 The physiologic and psychological stressors  Discharge
associated with surgery or injury stimulate
cortisol release from the adrenal cortex; Skin
increased serum cortisol also contributes to  Rashes
suppression of normal immune responses
 Lesions
 Dermatitis
PHYSICAL EXAMINATION
 Hematomas or purpura
 On physical examination, the skin and mucous
membranes are assessed for lesions, dermatitis,  Edema or urticaria
purpura (subcutaneous bleeding), urticaria,  Inflammation Discharge
inflammation, or any discharge. Neurosensory System
 Any signs of infection are noted.  Cognitive dysfunction
 The patient’s temperature is recorded, and the  Hearing loss
patient is observed for chills and sweating.  Visual changes
 The anterior and posterior cervical, axillary,  Headaches and migraines
and inguinal lymph nodes are palpated for  Ataxia
enlargement; if palpable nodes are detected,  Tetany
the location, size, consistency, and reports of Diagnostic Evaluation
tenderness upon palpation are noted.  A series of blood tests and skin tests and a
 Joints are assessed for tenderness and swelling bone marrow biopsy may be performed to
and for a limited range of motion. evaluate the patient’s immune competence.
 The patient’s respiratory, cardiovascular,  Specific laboratory and diagnostic tests are
gastrointestinal, genitourinary, and discussed in greater detail along with
neurosensory status is evaluated for signs and specific disease processes in subsequent.
symptoms indicative of immune dysfunction. Laboratory and diagnostic tests used to
 The patient’s nutritional status, level of stress, evaluate immune competence
and coping ability are also assessed, along with
his or her age and any functional limitations or Selected Tests for Evaluating Immunologic Status
disabilities. Various laboratory tests may be performed to assess
immune system activity or dysfunction. The studies
Indications of Immune Dysfunction assess leukocytes and lympho- cytes, humoral
Respiratory System immunity, cellular immunity, phagocytic cell
 Changes in respiratory rate Cough (dry or function, complement activity, hypersensitivity
productive) reactions, specific antigen- antibodies, or HIV
 Abnormal Rhinitis infection
 lung sounds (wheezing, crackles, rhonchi)
Leukocytes and Lymphocyte Tests
 Hyperventilation Bronchospasm
Cardiovascular System  White blood cell count and differential
 Hypotension  Bone marrow biopsy
Humoral (Antibody-Mediated) Immunity Tests
 Tachycardia
 B-cell quantification with monoclonal
 Dysrhythmia
antibody
 Vasculitis

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 In vivo immunoglobulin synthesis with T- physical pain and discomfort with certain
cell subsets types of diagnostic procedures, but many
 Specific antibody response psychological reactions as well.
 Total serum globulins and individual  For example, patients may fear test results
immunoglobulins (by electrophoresis, that demonstrate decreased immune
immunoelectrophoresis, single radial function that makes them more prone to
immuno- diffusion, nephelometry, certain infections, cancers, and other
isohemagglutinin techniques) disorders.
Cellular (Cell-Mediated) Immunity Tests  It is the nurse’s role to counsel, educate,
 Total lymphocyte count and support patients throughout the
 T-cell and T-cell subset quantification with diagnostic process.
monoclonal antibody  Further, many patients may be extremely
 Delayed hypersensitivity skin test anxious about the results of diagnostic tests
 Cytokine production and the possible implications of those
 Lymphocyte response to mitogens, results for their employment, insurance, and
antigens, and allogenic cells personal relationships. This is an opportune
 Helper and suppressor T-cell functions time for the nurse to provide counseling and
Phagocytic Cell Function Tests education should these interventions be
warranted.
 Nitro blue tetrazolium reductase assay
Complement Component Tests
 Total serum hemolytic complement The Infectious Process
 Individual complement component
The Human Body's Immune System
titrations
 a system of biological structures and
 Radial immunodiffusion processes within an organism that protects
 Electroimmunoassay against disease by identifying and killing
 Radioimmunoassay pathogens and tumor cells. It detects a wide
 Immunonephelometric assay variety of agents, from viruses to parasitic
 Immunoelectrophoresis worms, and needs to distinguish them from
Hypersensitivity Tests the organism's own healthy cells and tissues
in order to function properly.
 Scratch test
 Detection is complicated as pathogens can
 Patch test evolve rapidly, and adapt to avoid the
 Intradermal test immune system and allow the pathogens to
 Radioallergosorbent test (RAST) successfully infect their hosts.
Specific Antigen-antibody Tests
 Radioimmunoassay
 Immunofluorescence
 Agglutination
 Complement fixation test
HIV Infection Tests
 Enzyme-linked immunosorbent assay
(ELISA) Components of the immune system
 Western blot Innate immune system Adaptive immune
 CD4 and CD8 cell counts system
 P24 antigen test
 Polymerase chain reaction (PCR) Response is non- Pathogen and antigen
specific specific response
Nursing Management in brief (Immunological
disorders) Exposure leads to Lag time between
 The nurse needs to be aware that patients immediate maximal exposure and maximal
undergoing evaluation for possible immune response response
system disorders experience not only
Cell-mediated and Cell-mediated and
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humoral components humoral components Common Vehicle Transmission - Spread of infectious

organisms to multiple hosts (e.g., animals or people)
No immunological Exposure leads to from one common source (e.g., contaminated food or
memory immunological medication).
memory
Colonization- is used to describe microorganisms
present without host interference or interaction.

Infection-indicates a host interaction with an

A human infection happens when bacteria, fungi,
parasites or viruses enter the human body and start to
multiply. The growth of the organism may cause
symptoms in the infected person.
Definitions
Case - A person who has, or is suspected to have an
infection.
Contagious - An organism (germ) that can be passed
to another person. Syn. Infectious, communicable
Disease - is an abnormal condition affecting the body
of an organism. It is often construed to be a medical
condition associated with specific symptoms and
signs.
Direct Contact Transmission - Spread of infectious
organisms (germs) from the skin of one person
directly to another person.
Indirect Contact Transmission - Spread of infectious
organisms (germs) by coming into contact with a
contaminated object and then bringing the germ into
your body.
organism.
Infectious disease - is the state in which the infected
host displays a decline in wellness due to the
infection.
Endemic-that infection is maintained in the
population without the need for external inputs
Pandemic an epidemic of infectious disease that is
spreading through humán. populations across a large
region, for... instance multiple continents, or even
worldwide.
Notifiable Diseases - any disease that is required by
law to be reported to government authorities. The
collation of information allows the authorities to
monitor the disease and provides early warning of
possible outbreaks
Republic Act No. 3573-Law of Reporting
Communicable Diseases ak.a. Revised List of
Notifiable Diseases, Syndromes, Health-related
events and conditions.

Airborne Transmission - Spread of infectious

organisms (germs) through the air. These germs can
survive in the air for long periods of time and travel
far distances from the infected person.

Blood-borne Transmission - Spread of infectious

organisms (germs) through direct blood-to-blood
contact.

Droplet Transmission - Spread of infectious

organisms (germs) from an infected person in tiny
droplets of fluid that can travel small distances (less
than one meter).

Sexual Contact Transmission - Spread of infectious

agents (germs) from an infected person to another
person through sexual contact (e.g., vaginal, oral or
anal sex).

Vector-Borne Transmission - Spread of infectious What is a Virus?

organisms (germs) by insects.

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 A microorganism smaller than a bacteria,
which cannot grow or reproduce apart from
a living cell. A virus invades living cells
and uses their chemical machinery to keep
itself alive and to replicate itself.
What is a Parasite?
 An organism that lives in or on and takes its
nourishment from another organism. A
parasite cannot live independently. Parasitic
diseases include infections by protozoa,
helminths, and arthropods.
Reservoir of infection:
 Any person, animal, plan, soil or substance
in which an infectious agent normally lives
and multiplies. The reservoir typically
harbors the infectious agent without injury
to itself and serves as a source from which
other individuals can be infected. The
infectious agent primarily depends on the
reservoir for its survival. It is from the
reservoir that the infectious substance is
transmitted to a human or another
susceptible host.
TRANSMISSION
 Infectious organisms come in different
sizes, shapes and types. There are many
types of bacteria, fungi, parasites and
viruses. Infections can be spread in many
different ways. With such diversity, there is
no perfect way of preventing infections.
Modes of Transmission
Droplet Contact
 droplets generally are large (greater than 10
micrometers) and do not stay suspended in
the air.
 Diphtheria, Pneumococcal pneumonia,
Influenza, Rubella, Pertussis, Tuberculosis,
Mumps, Chickenpox (Varicella)
Fecal-oral Transmission
 Cholera, Hepatitis A, Polio, Rotavirus,
Salmonella, Entameoba histolytica,
roundworms
 Fecal material (or the germs present in the
feces) can be ingested via contamination of
water supplies, by poor handwashing
between the bathroom and the kitchen, by
eating food contaminated by houseflies, or
by poor hygeine after handling baby diapers
- a myriad of ways.
Direct Physical Contact (Person to Person)
 Gonorrhea, Hepatitis B, HIV/AIDS,
Syphillis,. Herpes, Cytomegalovirus,
Chlamydia, Impetigo, Athlete's foot, Warts
 These diseases can also be transmitted by
sharing a towel (where the towel is rubbed
vigorously on both bodies) or items of
clothing in close contact with the body
(socks, for example) if they are not washed
thoroughly between uses. This also includes
any form of sexual contact
Airborne or Droplet nuclei
 Anthrax, Varicella, Measles, Influenza,
Tuberculosis, Smallpox.
 occurs when bacteria or viruses travel on
dust particles or on small respiratory
droplets that may become aerosolized when
people sneeze, cough, laugh, or exhale.
They hang in the air much like invisible
smoke. They can travel on air currents over
considerable distances.
Vector-borne Transmission
 Dengue, Malaria, Sleeping Sickness,
Filariasis, Yellow Fever, Japanese
Encephalitis, Cutaneous Leishmaniasis,
Schistosomiasis, Leptospirosis
 A vector is an organism that does not cause
disease itself but that transmits infection by
conveying pathogens from: one host to
another.
Soil Transmission (Direct Contact)
 Tetanus, Ascariasis, Trichuriasis
 Soil-transmitted helminths common known
as intestinal worms, are the most common
infections worldwide affecting the most
deprived communities (WHO)
Animal (Bite) Transmission
 Bubonic Plague, Anthrax, Avian Flu,
Leptospirosis, Rabies, Cat-Scratch
Vertical Transmission
 HIV, Hepatitis B, Syphilis, rubella,
Candidiasis, Herpes, Gonorrhea,
Toxoplasmosis (TORCH)
 the transmission of an infection or other
disease from mother to child immediately
before and after birth during the perinatal
period
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Objective in Infection Control
Reservoir > Mode of Transmission > Immune System
Controlling Spread of Infection: The
Reactive Approach
 Diagnosis is importance - establish the
occurrence of a disease based on the signs
and symptoms
 Presumptive vs. Definitive
 Use of Clinical history
 Physical Exam
 Lab tests
CASE DEFINITION
Start treatment of sick person immediately according
to protocol (Early Diagnosis and Prompt Treatment)
Identify the Source of Infection - Where did the sick
person get the infection?
Identify the mode of transmission - How did the sick
person get infected?
Controlling Spread of Infection: Proactive Approach
Identify Risk Groups - who are people in the
population that are susceptible to acquiring specific
communicable diseases
Is the community at risk of exposure to various
communicable diseases?
Preventive Measures to address:
1. Identified Reservoir of Infectious Diseases
2. Community's Defense Against Infection
(Herd Immunity, Barriers on Routes of
transmission)
3. Screening of presumed healthy population
Preventive Measures
Immunization - is the process whereby a person is
made immune or resistant to an infectious disease,
typically by the of a vaccine. Vaccines stimulate the
body's own immune system to protect the person
against subsequent infection or disease.
Expanded Program of Immunization
 The Expanded Program on Immunization (EPI)
in the Philippines began in July 1979. And, in
1986, made a response to the Universal Child
Immunization goal.
Cold Chain
 To ensure the optimal potency of vaccines, a
careful attention is needed in handling practices
at the country level.
 These include storage and transport of vaccines
from the primary vaccine store down to the end-
user at the health facility, and further down at the
outreach sites. Inappropriate storage, handling
and transport of vaccines won't protect patients
and may lead to needless vaccine wastage.
 A "first expiry and first out" (FEFO) vaccine
system is practiced to assure that all vaccines are
utilized before its expiry date.
 Proper arrangement of vaccines and/or labeling
of expiry dates are done to identify those close to
expiring.
 Vaccine temperature is monitored twice a day
(early in the morning and in the afternoon) in all
health facilities and plotted to monitor break in
the cold chain.
 Each level of health facilities has cold chain
equipment for use in the storage vaccines which
included cold room, freezer, refrigerator,
transport box, vaccine carriers, thermometers,
cold chain monitors, ice packs, temperature
monitoring chart and safety collector boxes
Health Promotion
 is the process of enabling people to increase
control over, and to improve, their health. It
moves beyond a focus on individual behaviour
towards a wide range of social and
environmental interventions. (WHO, Bangkok
Charter for Health Promotion in a Globalized
World 1995).
 It is the science and art of helping people change
their lifestyle to move toward a state of optimal
health. This definition was derived from the
1974 Lalonde report from the Government of
Canada.
 Health promotion can be performed in various
locations. Among the settings that have received
special attention are the community, health care
facilities, schools, and worksite.
Environmental Sanitation
 involves controlling the aspects of waste
management that may lead to the
transmission of disease. Included in the
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term waste management are water, solid
waste, and industrial waste
 Integrity of Water Supply
 Proper Waste Disposal
 Food and Food Handlers
 Control of Vectors
Accessibility to Drugs/Health Care
 Increasing access to affordable drugs in
developing countries requires better
government intervention, not less of it.
CHOLERA
Definition
 It is an acute bacterial enteric disease of the
GIT characterized by profuse diarrhea,
vomiting, massive loss of fluid and
electrolytes that could result
hypovolemic shock, acidosis, and death.
Etiologic Agent: Vibrio cholera/ Vibrio coma
 The organisms are slightly curved rods
(coma shaped), gram negative (-) and
motile with a single polar flagellum.
 The organisms survive well at ordinary
temperature and can grow in temperature
ranging from 22-40 degrees centigrade.
 They can survive well in ordinary
temperature and can survive longer in
refrigerated foods.
 An enterotoxin, choleragen, is elaborated by
the organisms as they grow in the intestinal
tract.
Pathognomonic sign
 Rice-water stool
Incubation period
 The incubation period ranges from a few
hours to five days; usually one to three
days.
Period of Communicability
 The organisms are communicable during
stool positive stage, usually a few days after
recovery, however occasionally the carrier
may have the organism for several months.
Mode of Transmission
 The fecal transmission passes via oral route
from contaminated water, milk, and other
foods.
 The organisms are transmitted through
ingestion of food or water contaminated
with stool or vomitus of patient.
 Flies, soiled hands, and utensils also serve
to transmit the infection.
Pathogenesis and Pathology
 Ingestion of contaminated foods and water
and invasion of the organisms.
 Fluid loss is attributed to the enterotoxin
elaborated by the organism as they lie in
opposition with the lining of the cells of the
intestines.
 The mucosal cell is stimulated to increase
secretion of chloride, associated with water
and bicarbonate loss.
 The toxin acts upon the intact epithelium on
the vasculator of the bowel, thus, resulting
in outpouring of the intestinal fluids.
 Fluid loss of 5-10 percent of the body
weight resulting in dehydration and
metabolic acidosis.
to
 If treatment is delayed or inadequate, acute
renal failure and hypokalemia become
secondary process.
 DEATH
Clinical Manifestations
 Acute, profuse, watery diarrhea with no
tenesmus or intestinal cramping.
 Initially, the stool is brown and contains
fecal materials, but soon becomes pale gray,
"rice-water" in appearance with an
inoffensive, slightly fishy odor.
 Vomiting often occurs after diarrhea has
been established.
 Diarrhea causes fluid loss amounting to 1-
30 liters per day owing to subsequent
dehydration and electrolyte loss.
 Tissue turgor is poor and eyes are sunken
into the orbit.
 The skin is cold, the fingers and toes are
wrinkled, assuming the characteristics of
"washer-woman's-hand”.
 Radial pulses become imperceptible and the
blood pressure unobtainable.
 Cyanosis
 Hoarseness of voice, and then is lost, so that
the patient speaks in whisper (aphonia)
 Breathing is rapid and deep
 Despite marked diminished peripheral
circulation, consciousness is present.
 Patient develops oliguria and then anuria.
 Temperature could be normal at the onset of
the disease but becomes subnormal in later
stage especially if the patient is in shock.
 When the patient is in deep shock, the
passage of diarrhea stops.
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 Death may occur as short as four hours after
onset, but usually occurs on the first or the
second day if not properly treated.
Principal Deficits
 Extracellular volume in the loss of intestinal
fluid that can lead to:
a.) severe dehydration with the
appearance of "washer-woman's-
hand," restlessness, and excessive
thirst,
b.) circulatory collapse or shock.
 Metabolic acidosis is due to loss of large
volume of bicarbonate-rich stool that results
in rapid respiration with intervals of apnea
(Kussmaul respiration).
 Hypokalemia is due to massive loss of
potassium in stool. Patient may manifest
abdominal distention that could be
attributed to paralytic ileus.
 Renal failure occurs as a consequence of
prolonged, untreated shock or unrelieved
hypokalemia.
 Convulsions and tetany are probably caused
by loss of magnesium.
 Hypoglycemia may occur in untreated
children who have been stupor for several
days.
 Corneal scarring can occur in the stuporous
patient who has lost the wink reflex.
 Acute pulmonary edema may follow
hydration in cases of uncorrected metabolic
acidosis (Wehrle & Top, 1991)
Diagnostic exams
1. Rectal swab
2. Darkfield or phase microscopy
3. Stool exam
Treatment of cholera consists in correcting the basic
abnormalities without delay- restoring the circulating
blood volume and blood electrolytes to normal levels.
1. Intravenous treatment is achieved by rapid
intravenous infusion of alkaline saline
solution containing sodium, potassium,
chloride, and bicarbonate ions in
proportions comparable to that in water-
stool.
2. Oral therapy rehydration can be completed
by oral route (ORESOL, HYDRITES)
unless contraindicated or, if the patient is
not vomiting.
3. Maintenance of the volume of fluid and
electrolyte lost after rehydration. This is
done by careful I and O measurements.
4. Antibiotics
a) Tetracycline 500mg every 6 hours
might be administered to adults to
adults, and 125mg/kg body
weight for children every 6 hours
for 72 hours.
b) Furazolidone 100mg for adults
and 125mg/kg for children, might
be given every 6 hours for 72
hours.
c) Chloramphenicol may also be
given 500mg for adults and
18mg/kg for children every 6
hours for 72 hours.
d) Cotrimoxazole can also be
administered 8mg/kg for 72
hours.
Nursing Management
 Medical aseptic protective care must be
provided. Handwashing is imperative
before any food item is handled.
 Enteric isolation must be observed
 Vital signs must be recorded accurately.
 Intake and output must be accurately
measured.
 A thorough and careful personal hygiene
must be provided.
 Excreta must be properly disposed of
 Concurrent disinfection must be applied.
 Food must be properly prepared.
 Environmental sanitation must be observed
 Weighing the patient provides additional
data that no deficit in fluid input is
occurring.
 Appropriate diet is given according to the
stage of recovery.
Common Nursing Diagnosis
 Altered nutrition: less than body
requirement
 Altered tissue perfusion
 Activity intolerance
 Knowledge deficit
 High risk for fluid volume deficit
 Diarrhea
 Impaired skin integrity
Prevention:
 Food and water supply must be protected
from fecal contamination.
 Water should be boiled or chlorinated.
 Milk should be pasteurized
 Sanitary disposal of human excreta is mus.
 Sanitary supervision is important.
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Filariasis (Elephantiasis)
Definition:
 Filariasis is a parasitic disease caused by an
African eye worm, a microscopic thread-
like worm. The adult worm can only live in
human lymphatic system.
 This is an extremely debilitating and
stigmatizing disease cause by parasitic
worm affecting men, women, and children.
It affects the poor in both rural and urban
areas. The disease is rarely fatal, however,
it causes extensive disability, gross
disfigurement, and untold suffering of
millions of men, women, and children.
Causative Organism:
Wuchereria bancrofti
 Is the causative agent of Filariasis. It is a four-to-
five cm-long thread-like worm that affects the
body's lymph nodes ad lymph vessels of the legs,
arms, vulva, and breasts.
Brugaria trimori
 Rarely affects the genitals.
Brugaria malayi
 Shows manifestations resembling that of the
bancroftian but swelling of the extremities is
confined more to the areas below the knees and
below the elbows.
Loa loa
 Is another filarial parasite in humans transmitted
by a deer fly.
Mode of Transmission
The disease is transferred from person to person by
mosquito bite.
Pathology/Pathogenesis:
 When a mosquito bites a person with lymphatic
Filariasis, microscopic worms circulating in the
person's blood enter and infect the mosquito.
 The microscopic worms pass from the mosquito
through the human skin and travel to the lymph
vessels where they grow into adults.
 An adult worm lives for seven years in the
lymph vessels. They mate and release into the
bloodstream millions of microscopic worms
known as microfilaria.
 Once the person has the worms in his or her
blood, these are picked up by the biting mosquito
when it feeds and the disease is transmitted to
another person via larvae.
 The larvae migrate to the lymph nodes, reach
sexual maturity, and the cycle is completed.
 A person needs many mosquito bites over
several months to years to get Filariasis.
 At first, most people do not know they have
Filariasis. They usually do not feel any
symptoms until after the adult worm dies.
 The disease damages the kidneys and the lymph
system; fluid collects and causes swelling in the
arms, breasts, legs, and for men, the genital area.
 The entire legs, arms, and genital area may swell
to several times their normal sizes. The swelling
and decreased function of the lymph system
make it difficult for the body to fight against
infection.
 A person with this disease tends to have more
bacterial infections in the skin, thus, skin hardens
and thickens. This is called elephantiasis.
 In advanced stages, the worms can actually
obstruct the vessels, causing the surrounding
tissues to enlarge. In Bancroftian Filariasis, the
legs and genitals are mostly involved, while
Malayan variety affects the legs below the knees.
 In conjunctival Filariasis, the worms' larvae
migrate to the eye and can sometimes be seen
beneath the skin, or beneath the conjunctiva.
 If conjunctiva Filariasis is untreated, this can
cause the type of blindness known as
onchocerciasis.
Symptoms:
 Symptoms vary, depending on the type of
the parasitic worm that caused the infection,
but all infections usually begin with chills,
headache, ad fever between three months
and one year after the insect bite.
 There may also be swelling, redness, and
pain in the arms, legs or scrotum.
 Areas of abscesses may appear as a result of
a dying worms or a secondary bacterial
infection.
Diagnostic Procedures:
Circulating Filarial Antigen (CFA) test is performed
on a finger-prick blood droplet taken any time of the
day and gives result in a few days.
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 The larvae can also be found in the blood,
but mosquitoes which spread the disease are
active at night, the larvae are usually found
between about 10:00 pm to 2:00 am.
 Patients history must be taken and pattern
of inflammation and signs of lymphatic
obstruction must be observed.
Modalities of Treatment:
1. Invermectin, albendazole, or diethycarbamazine
(DEC) are used to treat by:
a. Eliminating the larvae
b. Impairing the adult worms’ ability to
reproduce, and
c. By actually killing the adult worms.
The above medications are started at low doses to
prevent reactions caused by large numbers of dying
parasites.
2. Surgery may be used to remove surplus tissue
and provide a way to drain the fluid around the
damaged lymphatic vessels.
 Surgery may also be used to minimize
massive enlargement of the scrotum.
3. Elephantiasis of the legs can also be eased up by
elevating the legs and providing support with
elastic bandages.
4. Salt fortified with diethylcarbamazine (DEC) is
helpful.
Nursing Management:
1. Health education and information
dissemination as to the mode of transmission
must be carried out.
2. Environmental sanitation and the destruction
of the breeding places of mosquito must be
emphasized.
3. Psychological and emotional support to client
and the family are necessary.
4. Personal hygiene must be encouraged.
5. The course of the disease must be explained to
the client and his/her family.
Common Nursing Diagnosis:
1. Impaired physical mobility
2. Knowledge deficit
3. Impaired skin integrity
4. Activity intolerance
5. Body image disturbance
6. Altered health maintenance
Prevention and Control:
Mosquitoes that carry the microscopic worms usually
bite between the hours of dusk and dawn. It is
therefore advised that people living an area with
Filariasis should:
1. Sleep under a mosquito net,
2. Use mosquito repellant in hours between
dusk and dawn, and
3. Take yearly dose of medicine that kills the
worms circulating in the blood.
Communicable Diseases
HEPATITIS A
(Infectious Hepatitis/Catarrhal Jaundice)
Definition
 Hepatitis A is a liver disease caused by
hepatitis A virus.
 This is an inflammation of the liver that is
not really very severe and runs an acute
course.
 This generally starts within two to six
weeks after contact with the virus, and lasts
no, longer than two months.
 It is known as infectious hepatitis because it
spreads relatively easy from those infected
to close contact.
Incubation Period
 The incubation period for hepatitis A ranges
from 15-60 days, or three to five weeks;
with a man incubation period of 30 days.
Period of Communicability:
 The infected patient is capable of
transmitting the organism a week before
and a week before and a week after the
appearance of symptoms
Mode of Transmission
 Hepatitis A virus is transmitted by ingestion
of contaminated drinking water or ice,
uncooked fruits and vegetable, and fruits
and vegetables grown in or washed with
contaminated water.
 It is also transmitted through fecal-oral
pathway
 The virus is transmitted through also by
infected food handlers.
Groups at risk:
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 Children in Day Care Centers can transmit
the infection through diapers and toys.
 Troops living under crowded conditions at
military camps or fields are at great risk.
 Homosexual men are increasingly at risk of
HAV infection from oral-anal sexual
contact.
 People who live in areas with breakdown
sanitary conditions, such as after floods
and other natural disasters.
Pathology/Pathogenesis
 As hepatophilic virus enters and infects the
liver, interlobular infiltration with
mononuclear cells results in necrosis and
hyperplasia of kuffer cells. This results in
failure of the bile to reach the intestine in
normal amount, resulting in obstructive
jaundice in which the patient manifests dark
urine, pale feces, and usually itchiness.
 Liver cells damage consists of hepatic cell
degeneration and necrosis, cell dropout, cell
ballooning, acidophilic degeneration of
hepatocytes (councilman bodies). The most
characteristic features is the collapse of the
reticulin framework, associated with
swelling of the reticuloendothelial system.
 Hepatic cell dropout results in "bringing"
between lobules and consist of condensed
reticulum, inflammatory debris and
degenerating cells that span adjacent portal
areas and portal areas of central veins.
 This necrosis and autolytic type destroy the
liver parenchyma.
 Complications will then occur.
 In the late stage, respiratory failure and
cerebrovascular collapse will be present.
 DEATH will occur.
Clinical Manifestations
 Flu-like illness with chills and high fever
 Diarrhea, fatigue, and abdominal pain •
Loss of appetite
 Nausea, diarrhea, and fever
 Jaundice and dark-colored urine
 The infection in young children is often
mild and asymptomatic.
Complications:
1. Progressive encephalopathy characterized
by drowsiness and cerebral edema.
2. GIT bleeding progressing to stupor and
later coma. Bleeding is not responsive to
parenteral Vitamin K administration
3. Clonus and hyperflexia are later replaced by
loss of deep tendon reflexes.
4. Edema and ascites
5. Aplastic anemia In the late course of the
disease, loss of corneal and papillary
reflexes, elevated arterial blood, respiratory
failure, to cerebrovascular collapse may be
present
6. HAV and HBV-complement fixation rate
7. Liver function test- to determine the
presence and extent of liver damage and to
check the progress of the liver.
8. Bile examination in stool and urine.
9. SGOT-serum glutamic oxaloacetic
transaminase
SGPT-serum glutamic pyruvic transaminase
ALT-serum alanine transaminase
10. IgM level
Treatment modalities
 There is no specific treatment, although bed
rest is essential.
 Diet must be high in carbohydrate, low in
fat, and low in protein.
 Patient must take vitamin supplement
especially the B complex group.
 Intravenous therapy is occasionally
necessary.
 Isoprinosine (methisoprenol) may enhance
the cell mediated immunity of the T-
lymphocytes. Alkalines, belladonna, and
antiemetics should be administered to
control dyspepsia and malaise
Nursing Management
 The patient must be isolated (enteric
isolation).
 Patient should be encouraged to rest during
acute or symptomatic phase.
 Patient's nutritional status must be
improved.
 Appropriate measures to minimize the
spread of the disease must be utilized.
 Observe the patient for melena and check
stool for the presence of blood.
 Provide optimum skin and oral care.
 Increase in ability to carry out activities:
encourage the patient to limit activity when
fatigued
 Assist the client in planning periods of rest
and activity
 Encourage gradual resumption of activities
and mild exercise during recovery
Preventive controls
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 Hands should be washed thoroughly every  Women tends to develop the disease at an
after use of toilet. Travelers should avoid earlier age (20 to 40 years of age) compared
water and ice if unsure of their purity. to men (60 to 70 years of age), and women
 Food handlers should carefully be screened. are affected more frequently.
 Self-preparation and serving of food must
be practiced. The public should be educated
on the mode of transmission of the disease.
Stages of dermatitis
Acute dermatitis
Dermatitis
 Acute dermatitis is characterized by
 Dermatitis is an inflammation of the skin
erythema, vesiculation and oozing, often
which are commonly swollen, reddened,
with edema.
and irritatingly itchy. Although not an
alarming condition, this type of skin disease
can make you very uncomfortable, uneasy Subacute dermatitis
and self-conscious.
 Dermatitis is an itchy inflammation of the  Subacute dermatitis is similar to acute
skin. It is not contagious or dangerous, but dermatitis, but with scaling and crusting
it can be uncomfortable. There are many
types of dermatitis, including allergic CHRONIC DERMATITIS
dermatitis,
 eczema, and seborrheic dermatitis (which  Chronic dermatitis is characterized by
causes dandruff). A rash is an abnormal thickened dry patches, often lichenified
condition and reaction of the skin. from chronic rubbing (increased skin
Definition markings). Lichenification is often
predominantly follicular in pigmented skin.
 Dermatitis, also known as eczema, is
inflammation of the skin. It is characterized
by itchy, erythematous, vesicular, weeping, Classification
and crusting patches. The term eczema is
also commonly used to describe atopic Contact
Atopic Nummular
dermatitis, also known as atopic eczema.
 The cause of dermatitis is unclear. One
Seborrheic
possibility is a dysfunctional interplay
Stasis Perioral
between the immune system and the skin.

ACCORDING TO BRUNNER AND SUDDHART- Generalized exfoliative

Pompholyx Herpetiform
 Dermatitis is inflammation of the upper
Localized stretch
layers of the skin, causing itching, blisters,
redness, swelling, and often oozing,
scabbing, and scaling. CONTACT DERMATITIS
ACCORDING TO LEWIS
 Contact dermatitis is skin inflammation
 Dermatitis is an inflammation of the skin
caused by direct contact with a particular
and which are commonly swollen, reddened
substance. The rash is very itchy, is
and irritatingly itchy.
confined to a specific area, and often has
clearly defined boundaries.
INCIDENCE:
 It affects males and females and accounts IRRITANT+ ALLERGIC = TYPES OF CONTACT
for 10 to 20 percent of all visits to DERMATITIS
dermatologists.
 Although atopic dermatitis may occur at
any age, it most often begins in infancy and
childhood. IRRITANT CONTACT DERMATITIS

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 Irritant contact dermatitis, which accounts
for 80% of all cases of contact dermatitis,
occurs when a chemical substance causes
direct damage to the skin; symptoms are
more painful than itchy. Typical irritating
substances are acids, alkalis (such as drain
cleaners), solvents (such as acetone in nail
polish remover), strong soaps, and plants
(such as poinsettias and peppers).
ATOPIC DERMATITIS
 Atopic dermatitis is chronic, itchy
inflammation of the upper layers of the skin
that often develops in people who have hay
fever or asthma and in people who have
family members with these conditions.
 Infants may develop red, oozing, crusted
rashes on the face, scalp, diaper area, hands,
arms, feet, or legs. Infants may develop red,
oozing, crusted rashes on the face, scalp,
diaper area, hands, arms, feet, orlegs.
Treatment
 The scalp can be treated with a shampoo
containing pyrithione zinc, selenium
sulfide, an Antifungal drug, salicylic acid
and sulfur, ortar.
NUMMULAR DERMATITIS
 Nummular dermatitis is a persistent, usually
itchy, rash and inflammation characterized
by coin- shaped spots, often with tiny
blisters, scabs, and scales.
 Most people benefit from skin moisturizers.
Other treatments include antibiotics taken
by mouth, corticosteroid creams and
injections, and phototherapy.
SEBORRHOEIC DERMATITIS
 Seborrhoeic dermatitis (also known as
"seborrheic eczema") is an inflammatory
skin disorder affecting the scalp, face, and
trunk. seborrheic dermatitis presents with
scaly, flaky, itchy, red skin.
 The condition's symptoms appear gradually
and usually the first signs of seborrheic
dermatitis are the flakes of skin called
dandruff.
TREATMENT:
 Dermatologist recommend topical
treatments such as shampoos, cleansers or
creams/lotions that contain antifungal, anti-
inflammatory, sebosuppresive or keratolytic
ingredients.
STASIS DERMATITIS
 Stasis dermatitis is inflammation on the
lower legs from pooling of blood and fluid.
The varicose (dilated, twisted) veins and
swelling (edema). It usually occurs on the
ankles but may spread upward to the knees.
Treatment
 Long-term treatment is aimed at keeping
blood from pooling in the veins around the
ankles. When sitting, the person should
elevate the legs above the level of the heart.
 Antibiotics are used only when the skin is
already infected
PERIORAL DERMATITIS
 Perioral dermatitis is a red, bumpy rash
around the mouth and on the chin that
resembles acne.
 Perioral dermatitis is distinguished from
acne by the lack of blackheads and
whiteheads.
 Treatment is with tetracyclines or other
antibiotics taken by mouth.
GENERALIZED EXFOLIATIVE
DERMATITIS
 Generalized exfoliative dermatitis
(erythroderma) is severe inflammation that
causes the entire skin surface to become
red, cracked, and covered with scales.
Treatment
 People with severe exfoliative dermatitis
often need to be hospitalized and given
antibiotics (for infection), intravenous fluids
(to replace the fluids lost through the skin),
and nutritional supplements. Corticosteroids
(such as prednisone) given by mouth or
intravenously.
POMPHOLYX
 Pompholyx/dyshidrosis, is a chronic
dermatitis characterized by itchy blisters on
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the palms and sides of the fingers and PATHOPHYISIOLOGY

sometimes on the soles of the feet.
 The blisters are often scaly, red, and oozing.
 Wet compresses with potassium
permanganate or aluminum acetate
(Burow's solution) may help the blisters
resolve. As well as, strong topical
corticosteroid
Dermatitis herpetiform
 Dermatitis herpetiform is a particular type
of dermatitis that appears as a result of a
gastrointestinal condition, known as celiac
disease.
LOCALIZED SCRATCH DERMATITIS
 Localized scratch dermatitis (lichen simplex
chronicus, neurodermatitis) is chronic, itchy
inflammation of the top layer of the skin.
 Localized scratch dermatitis can occur
anywhere on the body, including the anus
(pruritus ani) and the vagina (pruritus
vulvae), but is most common on the head,
arms, and legs.
 In the early the skin looks normal, but it
itches. Later dryness scaling, and dark
patches develop as a result of the scratching
and rubbing.
 Applying surgical tape saturated with a
corticosteroid (applied in the morning and
replaced in the evening) helps relieve
itching and inflammation and protects the
skin from scratching.
CAUSES
There is a vasoconstriction of superficial blood
vessels and the skin blanches readily
↓
Cold and low humidity are poorly tolerated because
of drifting effect
↓
Heat and high humidity are poorly tolerated because
vasodilatation increases the inflammatory reaction
thus aggravating the dermatitis and causing increased
the itching and discomfort
↓
Lesion become localized to the flexor surface of the
neck, to the eyelids, behind the ears, in the antecubital
and popliteal areas and at the wrist.
The erythema is now dusty in color and excoriations
may become secondary secondarily infected.
Symptoms of dermatitis
The symptoms of dermatitis range from mild to
severe and will look different depending on what part
of the body is affected. Not all people with dermatitis
experience all symptoms.
In general, the symptoms of dermatitis may include:
 rashes
 blisters
 dry, cracked skin itchy skin
 painful skin, with stinging or burning
redness
 swelling

GENETIC ALLERGENS DISEASE

NUTRITIONAL SEASONAL INFECTION

CHANGES SICKNESS

GENETIC HORMONAL
SWINGS

MANAGEMENT
Medical Management
 Bathing, using lukewarm water. Showers
are better. Replace standard soap with a
substitute such as a mild detergent soap-free
cleanser: a dermatologist can advise you.
 Clothing: wear soft smooth cool clothes;
wool is best avoided.

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 Irritants: Protect your skin from dust, water,
solvents, detergents, and injury. Avoid
exposure to environmental or food
allergens. Common foods that cause
allergic reactions are dairy, soy, citrus,
peanuts, wheat (sometimes all gluten-
containing grains), fish, eggs, corn, and
tomatoes.
 Emollients: Apply an emollient liberally
and often, particularly after bathing, and
when itchy. Ask your doctor or
dermatologist to recommend some to try;
avoid perfumed products when possible.
 Topical steroids: Apply a topical steroid
cream or ointment to the itchy patches for a
5 to 15-day course.
 Pimecrolimus cream: Pimecrolimus is a
new anti- inflammatory cream shown to be
very effective for atopic dermatitis, with
fewer side effects than topical steroids.
 Antibiotics: the physician may also
recommend antibiotics such as
flucloxacillin or erythromycin if infection is
complicating or causing the dermatitis. The
infection is most often with Staphylococcus
aureus or Streptococcus pyogenes.
 Antihistamines: Antihistamine tablets may
help reduce the irritation, and are
particularly useful at night.
 Other treatments: Systemic steroids,
azathioprine, phototherapy, and other
complicated treatments may also be used
for severe cases.
PREVENTION:
 Dermatitis relies on an irritant or an
allergen to initiate the reaction, it is
important for the patient to identify the
responsible agent and avoid it.
 In an industrial setting the employer has a
duty of care to the individual worker to
provide the correct level of safety
equipment to mitigate the exposure to
harmful irritants. This can take the form of
protective clothing, gloves or barrier cream
depending on the working environment.
COMPLICATION
 THYROID DISEASES
 INTESTINE CANCER
 VASCULITIS
 ANAPHYLAXYS
Health Education
Herpes Simplex
Definition
 Herpes simplex is a viral disease
characterized by the appearance of sores
and blisters anywhere on the skin. These
sores usually occur either around the mouth
and nose, or on the genitals and buttocks.
 Herpes simplex is related to the viruses that
cause infectious mononucleosis (Epstein-
Barr Virus), chicken pox, and shingles
Etiologic Agent
 Herpes simplex Virus (HSV)
TYPES:
Type 1 virus
 Can cause cold sores that usually infect
infancy and childhood.
 Characterized by tinny, clear fluid-filled
blisters.
 Most commonly affects the lips, mouth,
nose, chin, or cheeks and occurs shortly
after exposure. This may also develop
wounds on the skin
 Patients may barely notice the symptoms or
need medical attention for relief of pain.
 The disease can be transmitted by kissing,
sharing kitchen utensils or sharing towels.
 Pts. Usually catch the infection from family
members or friends who carry the virus
 The sores of primary infection appear 2- 20
days after contact with an infected person
and usually last from 7-10 days.
PATHOGENESIS
1. Before the blister appears, the skin may itch or
become very sensitive.
2. Lesions are limited to the epidermis sore
superficial mucous membrane
3. The blister may break as a result of injury,
allowing the fluid of the blister to ooze and crust.
4. The crust falls off, leaving slightly red healing
skin, however, the virus remains in the body.it
moves to the nerve cell where it remains in
resting state.
5. The infection may recur in either the same
location or in the nearby sites. The infection may
recur every few weeks or less frequently
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6. Recurrent infection tends to be milder than
primary infection, this can be set off by a variety
of factors including fever, sun exposure, and
menstrual period. For many, the recurrence is
unpredictable and has no recognizable cause.
TYPE 2 VIRUS
1. Causes genital sores (buttocks, penis, vagina or
cervix) for 2-20 days
2. Most people get the infection with sexual contact
with an infected person.
3. The virus affects about 20% of sexually active
individuals
4. The virus can also be spread by touching an
unaffected part of the body after touching the
herpes lesion.
5. Manifestations include minor rash or itching and
painful sores, fever, muscular pain, and burning
sensation on urination.
Clinical characteristics
1. Mild to Moderate
 Oral herpes.
- Vesicular and ulcerative lesions occur in the
buccal mucosa and may involve the tongue.
- Feeding is painful and fluid intake is poor
 Labial herpes.
- The lips may occasionally be involved by
primary infections, if ever, this is
commonly known as "cold sore" or "fever
blister ".
- The lesion then crusts and healed within 3-
10 days. Subsequent recurrences are usually
close to the original site.
 Ocular herpes
- ocular herpetic keratitis is a major medical
problem potentially leading to loss of
vision.
- Conjunctivitis alone may also be a
manifestation of primary infection
- Recurrent keratitis is usually unilateral, but
2% -6% of cases may be bilateral
 Cutaneous infections of herpes.
- HSV may affect any part of the body.
 Erythema multiforme
- an allergic reaction of the skin is sometimes
a complication of HSV infections.
 Genital herpes
- considered as one of the most common
sexually transmitted diseases.
2. Severe to fatal disease
 Newborns.
- Neonatal herpetic infection is usually
acquired from maternal infection at the time
of delivery.
 Eczema varicelliform eruption
- occurs most commonly in individuals with
atopic dermatitis.
- This occasionally occurs in patients with
other skin disorders such as seborrheic
dermatitis, and diaper rash.
- Fatality rate ranges from 5% to 10%. The
cause of the disease usually is due to
disseminated viremia to the brain and
visceral organs, or from superimposed
bacterial infection.
 Encephalitis
- is gaining recognition as one of the most
common forms of the non-epidemic form of
herpes in the United States and other
countries.
- Cases may occur at any age, even among
those who already have circulating HSV in
the blood.
Modalities of Treatment
1. Oral anti-viral drugs such as acyclovir,
famciclovir, or valacyclovir
2. Personal hygiene
3. Restoration fluid and electrolyte balance
4. Isolation of clients, especially those with eczema
herpeticum, or neonatal herpes
5. Practice of universal precaution and through
hand washing.
SCHISTOSOMIASIS
(Bilharziasis/Snail Fever)
Definition
 This is a slowly progressive disease caused
by blood flukes of class trematoda.
 It is a chronic wasting disease common
among farmers and their families in certain
parts of the Philippines.
Etiologic agent
 Schistosoma japonicum
3 major types of the organism:
Schistosoma japonica
 infects intestinal tract
 It is found to be the only type that is
endemic in the Philippines
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 This is also known as "oriental
schistosomiasis"
Schistosoma mansoni
 It also affects the intestinal tract.
 It is common in some parts of Africa.
Schistosoma haematobium
 It affects the urinary tract.
 It can be found in some parts of the Middle
East, like Iraq and Iran.
Incubation Period
 The Incubation Period is at least two months.
Sources of Infection
1. Feces of infected persons.
2. Dogs, Pigs, Carabaos, Cows, Monkeys, and
wild rats have been found to be infected and
therefore, they also serve as host.
Mode of Transmission
1. The disease is transmitted through ingestion
of contaminated water.
2. The disease is transmitted through the skin
pores
3. The disease is transmitted through an
intermediary host, a tiny snail called
Oncomelania Quadrasi.
Pathogenesis/Pathology
1. The larvae (cercaria) penetrate the skin or
mucous membrane and eventually work
their way to the liver's venous portal
circulation.
2. In the portal vessels, they mature in one to
three months.
3. The mature worms live in copula in the
portal vessels and migrate to some parts of
the body.
4. The female cercaria lays eggs in the vessels
surrounding the large intestine or bladder.
5. Ulceration in the mucosa occurs and the
eggs are able to escape into the lumen of the
intestine and are excreted with the feces.
6. Some of the eggs are carried by the portal
circulation and filtered in the liver where
small lesions or granulomas are formed.
7. These granulomas are resolved and are
replaced by fibrous tissue.
8. Likewise, the ulcerations in the intestines
are healed and scar formation occurs.
9. As the disease progresses, the liver enlarges
due to increasing fibrosis.
10. The flow of blood is interrupted in the
intrahepatic portion thereby resulting to
portal hypertension.
11. Fluid accumulates in the patient's belly that
makes it bulging.
Clinical Manifestations
The signs and symptoms of the disease depend on the
site of infection; however, the following can be
observed:
1. A pruritic rash develops at the site of
penetration, known as "swimmer's itch."
2. There is a low-grade fever, myalgia, and
cough.
3. There is the presence of abdominal
discomfort due to hepatomegaly,
splenomegaly, and lymphadenopathy.
4. There is a bloody-mucoid stool, "dysentery-
like" that comes on and off for weeks.
5. The patient becomes icteric and jaundiced.
6. Later, his belly becomes big because of an
inflamed liver, resulting from eggs that
accumulate in that organ.
7. After some years of suffering from this
chronic disease, the patient becomes weak,
and pale, and there is marked muscle
wasting.
8. When the parasite reaches the brain, the
victim experiences severe headache,
dizziness, and convulsion.
Complications
1. Liver cirrhosis
2. Heart failure
3. Ascites
4. Hematemesis as a result from rupture of
esophageal varices
5. Renal failure
Diagnostic Procedures
 Fecalysis or direct stool exam
 Kato kats technique - is a laboratory method for
preparing human stool samples prior to
searching for parasite eggs.
 Liver and rectal biopsy
 Enzyme Link Immunosorbent Assay (ELISA)
 Cercum ova precipitin test (COPT)-confirmatory
diagnostic test.
- antigens present on the outside of the
parasitic eggs (ova), and a diagnosis made
based on the identification of precipitated
antigen-antibody complexes detected using
n antibody assay, such as ELISA.
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 Picking or scratching at warts can increase

Modalities treatment the risk of transmission.
- is effective only when given early in the
course of the disease.
 Praziquantel tablet for 6 months; 1-tab 2x a Types of warts
day for 3 months then 1 tab a day for
another 3 months.  Plantar
 Fuadine injection .IM or IV. The pt. should  Periungual
consume 360 mg for the entire treatment.  Common
 If the pt. continues to live in endemic area,  Flat
he frequently gets reinfected and has to be
retreated.
Common NSG Diagnosis
 Body image disturbance
 Impaired skin integrity
 Altered role function
 Altered urinary elimination
 Social isolation
 Self-esteem disturbance
 Knowledge deficit
 Risk for infection

Prevention and control

 Have a stool examination
 Reduce snail density by clearing vegetation
thus exposing the snail to sunshine;
constructing drainage to dry the land
surface where the snails thrive.
 Diminish infection rate by:
a) Proper waste disposal
b) Control of stray animals
c) Preventing people from bathing in
infested streams
d) Providing adequate water supply for
bathing and laundering and safe
water for drinking
 Providing health education on disease
process, mode of transmission, and
prevention.
WARTS
Definition
 Warts are benign skin growths caused by
the human papilloma virus (HPV). Most
warts are not worrisome, except when
causing discomfort on the bottom of the
feet.
Mode of transmission
 Direct and indirect contact (e.g. public
showers or swimming pool areas)
 Each type of warts is caused by a slightly
different virus and treatment may vary.
COMMON WART (Verruca vulgaris)
 are flesh-colored, small raised spots on the
skin with a rough surface. Size of warts
varies and may appear anywhere on the
skin, particularly on the skin, elbows,
knees, hand, fingers, and around the nails
PLANTAR WART (Verruca plataris)
 are no different than common warts except
that their location on the bottom of the foot
may result in flat appearance from being
pressed into the foot by the weight of the
person. May occur singly or in pattern,
grouped closely together they may cause
pain, redness, swelling.
FLAT WARTS (verruca plana)
 have a smaller surface than common war.
They may appear in great numbers on the
face and may also occur elsewhere,
particularly on arms and legs.
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MEDICAL-SURGICAL|
1 SEMESTER ST

A.Y. 2022-2023

GENITAL WARTS (condylomata accuminata)  Condoms reduce but do not eliminate the
 may be small or large. When large, they risk of HPV transmission.
form cauliflower-like appearance.
 They grow on warm, moist surfaces such as
the genital and rectal area. They usually are
sexually transmitted, but not always. DO
NOT TREAT GENITAL WARTS
YOURSELF; medical treatment is
necessary.

People at higher risk of developing common warts

include:
 Children and young adults
 People with weakened immune systems,
such as those with HIV/AIDS or people
who've had organ transplants.

Pathophysiology
 Common warts have a characteristic
appearance under the microscope.
 They have thickening of the stratum
corneum (hyperkeratosis),
 thickening of the stratum spinosum
(acanthosis),
 thickening of the stratum granulosum,
 rete ridge elongation, and large blood
vessels at the dermo epidermal junction.

Treatment
 There are many treatments and procedures
associated with wart removal.
 A review of clinical trials of various
cutaneous wart treatments concluded that
topical treatments containing salicylic acid
were more effective.

MEDICATIONS
 Salicylic acid
 Imiquimod
 Cantharidin
 Bleomycin
 Dinitrochlorobenzene
 Fluorouracil
 Cidofovir
PREVENTION
 Remove warts that are present.
 Do not pick at warts to avoid spreading
them.
 Wear footwear in public areas to avoid
plantar warts.
 Use condoms for intercourse.
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