Introduction to Immunology 8.
Active vaccination – the process of inoculating a
Immunology deals with the study of the host’s
reactions when foreign substances are introduced
into the body. A foreign substance that induces
such an immune response is called an antigen. It is
a science that has its roots in the study of
immunity, the condition of being resistant to
infection. It is also the study of the immune
response and its components, characteristics and
functions. It emphasizes the body’s immune
response in the pathogenesis of infectious,
inflammatory and immunologic disorders.
Definition of Terms
1. Immunology – the study of the reaction of the
human host when foreign substances are
introduced in the body.
2. Immunity – is the ability of the body to resist
damage from microorganisms; harmful substances,
such as toxins; and internal threats, such as cancer
cells. The state of being immune or resistant to
infection. It is also the ability of the immune system
that can recognize and eliminate the antigenic non
self-antigens.
[Latin word “immunis” exception. the weekly phrased.]
3. Immune system – is a vast network of many cellular
and biochemical components which protect the
body against infection or disease.
[is large network of organs, white blood cells, proteins or
antibodies and chemicals.]
4. Smallpox – this viral disease is also known as
“Variola or Variola vera” which is a derivative of the
Latin varius, meaning “spotted” or varus, meaning
“pimple”. The etiologic agent of this disease are
Variola major and Variola minor. It was first used in
Europe in the 15th century. Smallpox was
responsible for an estimated 300–500 million
deaths during the 20th century alone. Global
eradication of smallpox was endorsed by the World
Health Organization on May 8, 1980.
5. Variolation - a local practice of inoculation against
smallpox. It was introduced by Lady Mary Montagu
to develop immunity to smallpox. It is done by
injecting materials from crusts or fluids from
smallpox or blisters.
6. Vaccination – the inoculation method introduced
by Edward Jenner to prevent smallpox. It is done by
injecting material from crusts or fluids from cowpox
blisters.
7. Vaccine – Edward Jenner called the material he
injected from cowpox blisters as a “vaccine” from
the root word “vacca” which is Latin for cow.
specific antigen to stimulate antibody response.
9. Passive vaccination – the process of inoculating a
specific antibody to confer immunity.
10. Pasteurization – the technique developed by Louis
Pasteur; it is used to sterilize milk and dairy
products.
[To remove bacteria living in the dairy products.]
11. Humoral immunity – refers to the antibodies which
confer immunity.
12. Cell-mediated immunity- refers to the immune cells
which confer immunity.
[immune response does not include antibodies rather cell
mediated immunity. it is the activation of pathocytes,
antigen specific heat, T- lymphocytes and release of
various cytokines in response to antigen]
13. Antigens – are foreign particles that can trigger the
immune response.
[Molecule or molecular structure or any foreign articulate
matter or foreign dream that in line to specific antibody
or measle deceptor.]
14. Antibodies – are substances which are produced by
the body in direct response to an antigenic
stimulation.
[Antibody - AKA immunoglobin, a large Y shaped protein
used by immune system to identify and neutralize foreign
objects such as pathogenic bacteria and viruses.
- They recognize as a unique molecule of pathogen
called antigen.
- Each tip of the way of the antibody contains a
paratope like an analogous to a lock that is specific
for one particular epitope or key an antigen, allowing
those structures to bind together with precision.
- Using this binding mechanism an antibody can tag a
microbe or infected cell for attack by other parts of
immune system or can they neutralize it directly (eg.
for blocking part of virus that is essential for its
invasion)]
15. Immunopathology - are the diseases arising from
the disorders/ problems in immune response.
[includes the study of patterns, structures, and make a
nuisance of organisms that cause the disease]
16. Pathogens – organisms that causing disease to the
host.
17. Autoimmune Disease – are the disease arising
from the disorder problems in immune response.
[Signs and symptoms. Brain fog, dry skin, weight loss,
muscle pain, abdominal pain, rapid heartbeat]
History of Immunology
THUCYDIDES – 430 BC
While observing those who tend to the sik who
recovered was quoted saying:
“Ás the same man was never attacked twice. Never at
least fatally.”
the ancient Greek historian of the Peloponnesian
War between Sparta and Athens, has long been
considered the father of both scientific history and
political realism.
PROCOPIUS - 541 AB
- Is also quoted as recorded during the plague of
Justinian saying: Those who recovered were not
liable to a second attack.
Is a Byzantine historian whose works are an
indispensable source for his period and contain
much geographical information.
 1st century BC – King Mithridates IV of Pontus
systematically exterminated all whom he thought
might usurp his throne and feared that he might be
poisoned. So he protected himself by repeatedly
drinking small doses of poison.
MITHRIDATISM - tolerance to a poison. acquired by
taking gradually increased doses of it.
[Not effective on all types of poison. Immunity generally
only possible with biologically complex site which
immune system can tolerate or respond to. It depends on
the toxin; the practice can lead to the little
accommodation of poison in the body.]
THERIAC- known to be the first universal antidote.
SMALLPOX
o One of the most severe viral diseases no to
humankind and caused millions of deaths before it
was eradicated. it is believed to have existed for at
least 3000 years.
o An acute contagious disease caused by variola
virus.
o In 1967, the World Health Organization launched an
intensified plan to eradicate smallpox.
o Widespread immunization and surveillance were
conducted around the world for several years.
o the last known natural case was in Samaria in 1977.
o in 1980, WHO that player that smallpox is already
eradicated.
Experiential Period
Around 1500 AD, observers noticed that survivors
of certain diseases were resistant to re-infection.
During this time, smallpox killed many people and
traditional methods were carried experimentally to
develop immunity.
o Chinese philosophers – were the first to develop the
custom of inhaling powder made from smallpox
scabs in order to produce protection against
smallpox. This practice of deliberately exposing an
individual to material from smallpox lesions was
known as “variolation”. The theory was that if a
healthy individual was exposed as a child or young
adult, the effects of the disease would be
minimized.
VARIOLATION (CHINESE TRADITIONAL)
15th century, implemented a method of nasal
Insufflation = crusts from smallpox vesicles were
wrapped in cotton or powdered and introduced into the
nostrils of those who were to be protected thereby
producing a mild form of the disease.
- Administered by blowing powdered smallpox
materials usually in scabs of the nostrils.
- Throughout 16th and 17th century in China.
- Dried scabs and powdered and wrapped in a
cotton.
Inoculation = is described as the use of thread soaked
in the pus from the lesions of smallpox which is
introduced into small incision in the skin
- Began in India (Hinduism)
a. Lady Mary Wortley Montagu- in the year 1700s, a
British aristocrat and writer introduced variolation
in Western Medicine. Variolation is a local practice
of inoculation against smallpox. It was done by
deliberately injecting materials from crusts or fluids
from smallpox blisters.
- Often credited as the first to introduce inoculation
as means of preventing smallbox in England in
1722.
- She first inoculated inoculated youngest son.
- Charles Maitland (April 17 1721)– inoculated 4 year
old daughter.
b. Edward Jenner – credited as the founder of
immunology. In the late 1700s, an English country
discovered a remarkable relationship between
exposure to cowpox and immunity to smallpox.
- After he observed that milkmaids who were
exposed to cowpox had immunity to smallpox, he
deliberately injected individuals with material from
a cowpox lesion and then exposed them to
smallpox. He thus proved that immunity to
 cowpox, a very mild disease, provided protection
against smallpox.
- This procedure of injecting cellular material
became known as “vaccination” from “vacca” the
Latin word for cow. This successful vaccination
gained him the title, the Father of Vaccination.
A. Experimental Period
This period was significant in the field of
immunology. It started the era of experimentation
on the components of the immune system and the
method of vaccination and its impact to preventive
treatment rather than cure.
a) Robert Koch – introduced the concept of active
vaccination. He developed the concept of disease
that states that “specific pathogens caused specific
disease”.
b) Louis Pasteur – developed “pasteurization”, the
process of sterilizing milk.
c) Emil von Behring & Shibasaburo Kitasato – they
discovered that antibodies can confer immunity;
introduced the concept of passive vaccination.
d) Paul Ehrlich – he described antibodies which are
important in humoral immunity.
e) Eli Metchnikoff - he discovered cell-mediated
immunity.
B. Modern Period
The field of immunology has further advanced into
the field of immunopathology and immune related-
diseases. These immune disorders are classified
into autoimmune diseases, hypersensitivity,
immunodeficiency and transplantation reactions.
The Immune System
This system is a vast network of many cellular and
biochemical components which protect the body
against infection or disease.
A. WHITE BLOOD CELLS - move through blood and
tissues throughout your body, searching for foreign
invaders or microbes such as bacteria, viruses,
parasites and fungi. After finding them they
launched an immune attack.
B. LYMPHATIC SYSTEM - it's a network of delicate
tubes throughout the body. they are made-up of:
Lymph Nodes / Lymph Glands - tissues full of
immune cells that filter or trap and destroy germs
so they can spread to other parts of your body and
make you sick.
Lymph Glands – analyzes the foreign invaders
brought into the body, they can activate and
replicate and said the specific lymphocytes or WBC
to type of the particular invader.
[We have hundred of lymph nodes all over the body
including the neck, armpits, and groins. Swollen,
tender lymph nodes are clue that your body is
fighting an infection.]
Lymph Vessels - tubes that carry lymph, the
colorless fluid that bats your body's tissues.
- It contains infection fighting WBC AKA
lymphocytes.
Peyer’s Patch – lymph nodes that lines the
intestine.
C. SPLEEN - is a blood filtering organ that removes
microbes and destroys old or damaged red blood
cells. it also makes and stores disease fighting
components of the immune system including
antibodies and lymphocytes.
- It contains large number of immune system cells
indeed about 25% of blood comes from the heart
flows through spleen on every beat, as blood
circulates through the spleen, it filters and detects
pathogens.
- when but the trend is detected immune system
cells activates and increase number to neutralize
the pathogen.
- the spleen is important protecting people from
bacteria, infections such as meningococcus and
pneumococcus.
D. TONSILS AND ADENOIDS - have in human cells
that produce antibodies that traps foreign invaders
like bacteria or viruses in your airway that can cause
throat and lung infections.
E. THYMUS - filters and monitors your blood content
and it produces the white blood cells called the T-
lymphocytes.
- It is a small organ in the upper chest beneath the
breast bone, it helps mature the certain type of
WBC called the T-lymphocytes or T-cells. B. Peripheral or secondary lymphoid organs –
- TASK to learn to recognise and remember (R&R) where lymphocytes are maintained; are specialized
the invader so an attack can be quickly mounted to trap antigens. Examples are:
the next time this invader is encounter. 1. Lymph nodes – collect antigens/ foreign
F. BONE NARROW - stem cells in the spongy center substances from the tissues
of your bones develop into red blood cells, plasma 2. Spleen – collect antigens from the blood
cells and variety of white blood cells and other 3. Gut associated lymphoid tissues (GALT) –
types of immune cells. collect antigens from the epithelial surfaces of the
- Red Bone Marrow- helps in produce blood cells body.
- Yellow Bone Marrow- stores fat
Examples are:
- Bone marrow is where the different types of
3.1. Adenoids
immune system cells are created even common
type of starting cell call stem cell. 3.2. Tonsils
- Stem cells later develop into specific cell types 3.3. Appendix
including RBC our bodies need to carry oxygen. 3.4. Peyer’s patches
WBC is used to fight infections and platelets to help
in blood clot.
- cell generation and differentiation process of
course every day for as long as we live and as result
in the same way that the RBC in our blood are
replenished after an injury or blood donation our
immune system are constantly replenished as well.
- B-Cells are the cells that mature in the bone
marrow.
G. SKIN – mucous membrane as our first line of
defense.
H. STOMACH AND BOWEL - stomach acid kills many
bacteria soon after they enter your body. we also
have beneficial bacteria in your intestines that kill
harmful bacteria.
- Lactobacillus

Lymphoid Organs
These are specialized organs that are organized
tissues containing large numbers of lymphocytes.
They are categorized into central / primary
lymphoid organs and peripheral / secondary
lymphoid organs.

A. Central or primary lymphoid organs- where

lymphocytes are generated. Examples are:
1. Bone marrow – produce blood cells, including
lymphocytes
2. Thymus – where T lymphocytes (T Peripheral Blood Cells
lymphocytes)
General Function of the Immune System

In summary, the immune system plays an

important role in keeping the body healthy. It is a
concerted effort of the various cells, tissues and
organs which are specifically designed to function
as defense mechanisms of the body.
 - Ingested material is then digested in phagosome.
(Eg. Bactera, dead tissue cells, small mineral
particles)

Various Barriers that defend us in viruses:

PHYSICAL BARRIERS
1. SKIN – largest organ of the body
2. GASTROINTESTINAL TRACT
3. RESPIRATORY SYSTEM
4. NOSE
The function of the immune system, however is not 5. THROAT
always beneficial. It becomes harmful when immune 6. BODY HAIR
defense, immune homeostasis, and immune 7. EYES
surveillance were altered in an immunologic disorder. 8. EYELASHES
Hence, the immune system that was thought to protect DEFENSE MECHANISMS – mucous
the body, will likely attack its own cells and tissues. 1. SALIVA
Types of Immunity 2. TEARS
Innate/Natural Immunity – AKA “non-specific” – 3. SWEAT
since birth 4. SECRETION
- First line of defense against germs - To eliminate pathogens.
- Protects the body against infections > generating a GENERAL IMMUNE RESPONSE
quick immune system response once pathogen 1. INFLAMMATION -able movement of blood to
attacks it the site of infection and complement that is an
- Response same way to all germs / any foreign immune response marks pathogens for
substance such as pathogens. destroying then, makes a hole in cell
- Innate component – involves the recognition of membrane.
certain foreign (non-self) molecules to generate 1 Adoptive Immunity – AKA “acquired immunity” -
of 2 types of immune response. specific
 Inflammatory Response– Latin “Inflammatio” part - Active component of host immune response,
of the complex biological response of body tissue mediated by antigen-specific lymphocytes.
to harmful stimuli (pathogens, damaged cells or - Highly specific to particular pathogen, it includes
irritants) and is productive response involves development of immunological memories.
immune cells, blood cells and molecular mediators. - Memorizes the germs so fast reaction will happen
Function: when encountered again.
1. Eliminate initial cause of cell injured - Can be acquired by naturally [by infection] or
2. clear out necrotic cells and tissues artificially [vaccination]
3. damaged from original insult and motor  Natural Response
process  Artificial
4. initiating tissue repair.
5 Cardinal Signs – HEAT, PAIN REDNESS, Natural Immunity
SWELLING,LOSS OF FUNCTION NATURAL PASSIVE – a person is provided or given
 Phagocytosis – “phagein” = to eat and “kytos” = antibodies to a disease rather than producing them
cells. through his or her own immune system.
- Cell uses plasma membrane to engulf large - Takes several weeks to develop.
particles. E.g. Maternal Antibodies – newborn babies
- Phagosome- type of endocytosis, cell performs acquire passive immunity from its mother through the
phagocytosis = phagocytes – to remove pathogen placenta.
and debris. Breastfeeding – colostrum [yellowish, first
breastmilk produced by mother]
NATURAL ACTIVE- acquired through natural exposure
to a pathogen, which triggers the production of
antibodies by the immune system.
- Kusang nagka-sakit, acquired antibody in the
pathogen automatically.
- Protection = immediate yet long lasting,
sometimes it’s lifetime protection.

NOTES.
There are cases that the strain is
different. Pluripotent Hematopoietic Stem Cell – “pluri” =
Eg. Influenza. Flu has different multiple, “potent” = potential, “hemato” = blood,
strain that the body has not yet “poetic” = creative, “stem cell” = undifferentiated
encountered after having a first - Development of immune system happens in BONE
type of flu before. MARROW, and it starts with PLURIPOTENT or
Artificial Immunity MULTIPOTENT HAEMATOPOIETIC.
ARTIFICIAL PASSIVE - a person is provided or given - When cell is stimulated with differentiation
antibodies to a disease rather than producing them inducers(chemical) – stem cell starts to specializes
through his or her own immune system. into type of cells [B(Myeloid) Stem Cell or
E.g. Antibody-containing blood products such Lymphoid(Lymphatic) Stem Cells]
as immunoglobulins (lgG, IgM, IgA, IgD, and IgE.) which
may be given when immediate protection from a
specific disease is needed.
ARTIFICIAL ACTIVE - is acquired true introduction of a
killed or weakened form of the disease organism
through vaccination.
- We encounter disease, but weak virus for fast
action for immune system.
E.g. COVID vaccine that results in fever =
MYELOID STEM CELL – from bone marrow
developing immunity.
- Responsible in producing platelets (forblood
clotting) and RBC = Megakaryote (Megakaryocyte)
large, nucleus cell

- Can become Reticulocyte- which does not have

Cell of immune system – to defense the health from
pathogens, destroys abnormal cells such as virally
infected cells and tumor cells.
molecules but contains reticulum
- From bone marrow into blood stream but loses the
netlike structure, changes shapes (classic donut
shaped RBC when matured) can survive 3 months in
blood stream.
- Contains hemoglobin- molecule find oxygen,
enabling RBC carry oxygen throughout the body.
1% reticulocyte found in RBC. If bone marrow is
 having rapid turnover – larger reticulocyte due to - Neutrophils located at blood stream, migrate to
situation like acute blood loss or hemolysis. area of inflammation in response to signals of
macrophages and can destroy pathogens and
abnormal cells by phagocytosis.

- Myeloblast – immune cells.

MONOCYTES –located in blood stream and when
entering tissue, it becomes macrophage (large cell
eating).
MACROPHAGE – found in tissues of body, simply
weight in the tissue to encounter pathogens.
- First line in defense for pathogen penetrating
barrier defense of body.
- “Toll like receptors” – essential for recognizing
molecules that is unique in pathogens.
- PAMPS – PATHOGEN ASSOCIATED MOLECULAR
PATTERNS
- Once recognized pathogen = destroys using
phagocytosis > absorb and eat pathogen and digest
it from the inside. Also important in
cytokines(protein) (initiation of inflammatory
response[5 cardinal signs] of our body).
Myeloblast can be Eosinophil – “eusino” = red colored,
under microscope.
- Important when pathogen is too large = parasitic
infection.
- Located at tissues until activated by cytokines, in
response, they have granules contains pro
inflammatory cytokines toxic to pathogens and
parasites such as:
major basic proteins > enzyme that digest parasite.
- Degranulation / Exocytosis – process which
granules fuse with cell membrane and release to
space to travel to cause damage to nearby
pathogen and parasites.
Myeloblast can be Mast Cell & Basophils – contains
cytoplasmic granules that has cytokines types.
- Released though = degranulation
- Mast Cell – located and fixed in tissues
- Basophil – located in blood

Myeloblast can be Neutrophils – neutral attraction

- Generally attracted to pathogens
- ROLE: general attack cell (in innate immune
system)
 o cd8 cells become activated when their T
cell receptors match a pathogen, and they
multiply very quickly and differentiate into
cytotoxic T cells – can destroy virally
infected in two ways
o Way 1 – attach themselves to cell and spray
it with proteins destructive to the
membranes therefore by cell lysis
o Way 2 -activation of fast pathway, FAS
Pathway – cell destructiveprocess ad it
cause the cell to destroy itself by apoptosis.

LYMPHOID STEM CELL – Lymphoblast = lymphatics

“blast” = immature
- B Cells (B Lymphocytes)

- Mature in bone marrow

- It has antibody in surface aka immunoglobulins.
Match to the specific antigens that are displayed on
pathogens.
- Every lymphocyte has single specific type of
antibody > matching invading pathogen.
- ROLE: once activated, multiples and becomes
wither b-cells or plasma cells.
NATURAL KILLER CELLS – activated by cytokines from
- Plasma cells produce fast quantities of antibodies
against the pathogen macrophages and interferons
- memory b-cells hang around long after the - Recognize infected and abnormal cells without
pathogen has been cleared so that they can requiring the MHC or specific antigen receptors.
respond much quicker when they encounter that - Kills cell by releasing cytokines that induce cell
pathogen again. death by apoptosis.
- Secretes interferon gamma – activates
- T Cells – T Lymphocytes macrophages so by creating cycle of macrophages
- Leaves bone marrow as pro-thymocytes releasing cytokines that then activate the natural
- Travel to thymus gland where they mature killer cells = creation of positive feedback that
- T Cells receptors in their surface = specific to single increase the inflammatory response.
antigen
- CD4 Receptors / CD4 Cells – respond to MHC
CLASS II receptor on other cells of the body
o T Helper cells when became activated,
many cell in immune system rely on T
helper cells for provide signals that will
activate them.
- CD8 Receptors / CD* cells – respond to MHC
CLASS I receptor on other cells of the body
DENDRITIC CELLS
- It has various types and performs a similar function
- Found in skin = Langerhan’s cell”
- Dendritic cells – responsible for taking up antigens
in the infected tissue, processing them and then
presenting the antigens in their cell membrane for
other cell of the specific immune system to
recognize and respond to.

- Has both CD4 cells & CD8 cells = able to represent

antigen to both.

- They pick up antigens (infected site) and travels

through lymphatic system and blood to the
lymphoid tissue such as lymph nodes and spleen. =
delivered antigen to CD4 and CD8 cells.
- And by doing this they play an essential role in
initiating the specific immune response so that
summarizes an overview of the cells of the immune INFECTIOUS DISEASES
system
PNEUMONIA
Definition
 Pneumonia is an infection in lower respiratory
tract

 Pneumonia is an inflammation of the lung

parenchyma caused by various
 microorganisms, including bacteria,
mycobacteria, fungi, and viruses.
Pneumonia is classified into four:
 community-acquired pneumonia (CAP)
 hospital-acquired pneumonia (HAP),
 pneumonia in the immunocompromised host,
 aspiration pneumonia.
Causes –
 Bacterial pneumonia or infection
 Viral pneumonia
 Fungal pneumonia
 Hospital-Acquired Pneumonia
(Pneumonia is usually the result of a bacterial infection.
Common causes of bacterial pneumonia are
Streptococcus pneumoniae (pneumococcus) and,
(especially in kids) Mycoplasma pneumoniae. Viral
pneumonia (caused by a virus, such as coronavirus)
fungal pneumonia (rare in the UK and more likely to
affect people with a weakened immune system)
(pneumonia that develops in hospital while being
treated for another condition or having an operation;
people in intensive care on breathing machines are
particularly at risk of developing ventilator-associated
pneumonia)
Symptoms
 a cough
 difficulty breathing
 rapid heartbeat
 high temperature
 feeling generally unwell
 sweating and shivering
 loss of appetite
 chest pain
Mode of transmission-
Certain types of pneumonia are contagious. Pneumonia
caused by bacteria or viruses can be contagious when
the disease-carrying organisms are breathed into your
lungs. Pneumonia caused by fungi are not contagious.
The fungi are in soil, which becomes airborne and
inhaled, but it is not spread from person to person
Pneumonia is spread when droplets of fluid containing
the pneumonia bacteria or virus are launched in the air
when someone coughs or sneezes and then inhaled by
others.
It can also transfer from touching an object previously
touched by the person with pneumonia (transferring
the germs) or touching a tissue used by the infected
person and then touching your mouth or nose.
However, not everyone who is exposed to the germs
that cause pneumonia will develop it.
Who's at risk?
 infants from birth to 2 years old
 people ages 65 and older
 people with weakened immune systems
 people with certain chronic medical conditions
 people who’ve been regularly exposed to lung
irritants
 people who smoke
 people who’ve had a brain disorder
Nursing intervention / Medication
-To improve airway patency
- To promote rest and conserve energy
- To promote fluid intake
- To maintain nutrition
- To promote patient’s knowledge
- Assist and monitor effects of nebulizer treatment and
other respiratory physiotherapy
- Administer prescribed drugs.
TUBERCOLOSIS
Tuberculosis is an infectious disease that can cause
infection in your lungs or other tissues. It commonly
affects your lungs, but it can also affect other organs
like your meninges, kidneys, bones, and lymph nodes.
The word tuberculosis comes from a latin word
meaning nodule or something sticking out.
Tb also has three stages
 Primary infection- this happens when a person
has been in contact with, or exposed to,
another person who has tb.the exposed person
will have a negative skin test, a normal chest x-
ray. And no signs and symptoms of the
disease.
  Latent infection-this happens when a person
has tb bacteria in his or her body, but does not
have any symptoms of the disease. The
infected person’s immune system walls off the
tb organisms, and the tb remains inactive
throughout life in most people who are
infected. This person will have a positive skin
test and normal chest x-ray.
 Active tuberulosis - this describes person who
has signs and symptoms of an active infection.
The person would have a positive skin test and
positive chest x-ray.
Causes
 The main cause of tb is mycobacterium
tuberculosis.
 The primary infectious agent, M. tuberculosis,
is an acid-fast aerobic rod that grows slowly
and is sensitive to heat and ultraviolet light.
 Many people infected with this bacterium never
develops active tb. They remain in the latent
(inactive) stage. However in many people with
weak immune systems especially those with
hiv, or those receiving medicines that supress
immune system, tb organisms can overcome
the body’s defenses, multiply, and cause an
active disease.
Mode of transmission
 Inhalation
 Tuberculosis begins when a susceptible person
inhales mycobacteria and becomes infected.
 Tb can spread when a person with active tb
disease releases germs into the air through
coughing, sneezing, talking, or even laughing.
Only people with active tb are contagious. Most
people who breathe in tb bacteria are able to
fight of bacteria and stop it from growing. The
bacterium becomes inactive in these
individuals, causing a latent tb infection.
Diagnostic tests and findings
 Mantoux tuberculin skin test- a healthcare
provider will inject a substance called purified
protein derivative under the skin of your
forearm, and them after 2-3 days the
healthcare provider will look at the injection
site
 Interferon gamma release assay- will draw
blood and send sample to the lab
 Lab tests on sputum and lung fluid
 Chest x-ray
 CT scans
Pathophysiology
Tuberculosis is a highly infectious, airborne disease.
 Inhalation. Tuberculosis begins when a
susceptible person inhales mycobacteria and
becomes infected.
 Transmission. The bacteria are transmitted
through the airways to the alveoli, and are also
transported via lymph system and bloodstream
to other parts of the body.
 Defense. The body’s immune system responds
by initiating an inflammatory reaction and
phagocytes engulf many of the bacteria, and
TB-specific lymphocytes lyse the bacilli and
normal tissue.
 Protection. Granulomas new tissue masses of
live and dead bacilli, ate surrounded by
macrophages, which form a protective wall.
 Ghon’s tubercle. They are then transformed to
a fibrous tissue mass, the central portion of
which is called a Ghon tubercle.
 Scarring. The bacteria and macrophages turns
into a cheesy mass that may become calcified
and form a collagenous scar.
 Dormancy. At this point, the bacteria become
dormant, and there is no further progression of
active disease.
 Activation. After initial exposure and infection,
active disease may develop because of a
compromised or inadequate immune system
response.
Pharmacologic Therapy
The first line antituberculosis medications include:
 Isoniazid (INH). INH is a bactericidal agent that
is used as prophylaxis for neuritis, and has side
effects of peripheral neuritis, hepatic enzyme
elevation, hepatitis, and hypersensitivity.
 Rifampin (Rifadin). Rifampin is a bactericidal
agent that turns the urine and other body
secretions into orange or red, and has common
side effects of hepatitis, febrile reaction,
purpura, nausea, and vomiting.
 Pyrazinamide. Pyrazinamide is a bactericidal
agent which increases the uric acid in the blood
and has common side effects of hyperuricemia,
hepatotoxicity, skin rash, arthralgias, and GI
distress.
 Ethambutol (Myambutol). Ethambutol is a
bacteriostatic agent that should be used with
 caution with renal disease, and has common
side effects of optic neuritis and skin rash.
NURSING CARE PLAN
 Ineffective airway clearance related to thick,
viscous, or bloody secretions.
 ineffective airway clearance related to thick,
viscous or bloody secretions.
 risk for impaired gas exchange related to
decrease ineffective lung surface
 activity intolerance related to imbalance
between oxygen supply and demand
 imbalanced nutrition: less than body
requirements related to inability to ingest
inadequate nutrients
INTERVENTION
A virus known as SARS-associated coronavirus (SARS-
CoV) causes the illness.
Coronaviruses commonly cause mild to moderate
upper-respiratory illness in humans, but can cause
respiratory, gastrointestinal, liver, and neurologic
diseases in animals.
Animals to Human spread
How does SARS spread?
SARS-CoV spreads from one person to another.
The respiratory droplets containing the virus.

INDEPENDENT
 instruct the pt about correct positioning
 teach the pt that tb is a communicable disease
plans a progressive activity schedule
 carefully instruct the pt about important
hygienic measures
 monitor adverse effects

DEPENDENT Risk factors and complications:

 administer medications as prescribed.  Age
 Health Care Workers
EVALUATION
 Existing health condition
 promoted airway clearance
 Obesity
 adhered to treatment regimen
 Smoking - Alcohol
 promoted activity and adequate nutrition
 Physical Inactivity
 prevented spread of tuberculosis infection.
 Pollution

SARS
What is SARS? What are the signs and symptoms of SARS?
Severe acute respiratory syndrome (SARS) is a rapidly  Headache
spreading, potentially fatal infectious viral disease.
 Overall feeling of discomfort
Overview
 Body aches and chills
Severe acute respiratory syndrome (SARS) is a
 Sore throat
contagious and sometimes fatal respiratory illness.
 Cough
SARS first appeared in China in November 2002. Within  Pneumonia
a few months, SARS spread worldwide, carried by  Difficulty breathing
unsuspecting travelers.  Shortness of breath
On the other hand, a collaborative international effort  Hypoxia (insufficient oxygen in the blood)
allowed health experts to quickly contain the spread of  Diarrhea (for 10 to 20 percent of patients)
the disease. There have not been any new cases of
SARS since 2004, and the risk is relatively low. What is the cure and treatment for SARS
There's currently no cure for SARS.
What Causes SARS?
Treatment is mainly supportive, and may include:
SARS is caused by a strain of coronavirus assisting with breathing using a ventilator to deliver
oxygen
antibiotics to treat bacteria that cause pneumonia  Aid the patient towards alleviating their
antiviral medicines symptoms
high doses of steroids to reduce swelling in the lungs Dependent
There's not much scientific evidence to show that these  Pharmacological interventions
treatments are effective. The antiviral medicine  Antiviral drugs
ribavirin is known to be ineffective at treating SARS.  Antibiotics
 Any medication ordered by the attending
How SARS can be prevented? physician.
To prevent spreading the infection, it's important to:
wash your hands thoroughly using an alcohol-based Evaluation
hand detergent  Patient was able to prevent the virus from
cover your mouth and nose when you sneeze or cough spreading.
avoid sharing food, drink and utensils  Patient was able to understand more about the
regularly clean surfaces with disinfectant disease and how to prevent it.
In some situations, it may be appropriate to wear  Patient was able restore the body's normal
gloves, masks and goggles to help prevent the spread temperature.
of SARS  Patient was able to restore the regular
breathing pattern.

MERS-COV
Assessment
 The Patient’s Travel History
 MERS or Middle East respiratory syndrome is a
 Physical Examine
zoonotic disease (spreads from animals to
people) that can cause severe respiratory
Diagnosis
illness. It was first identified in Saudi Arabia in
 Hyperthermia related to increase 2012 and has infected more than 2,000
 Infection related to individuals worldwide.
 Ineffective Breathing Pattern related to It is caused by a novel coronavirus (Middle East
shortness of breath as evidence by cough and respiratory syndrome coronavirus, or MERS‐CoV).
excessive mucus production
 Anxiety related to

Planning
 STG
 Isolate the patient
 Counsel about the proper hand hygiene
 Use of personal protective equipment such as
masks, eyewear or gloves.
 Minimization of present symptoms
 LTG ZOONOTIC TRANSMISSION
 Preventing the virus from spreading. MERS-CoV is a zoonotic virus, which means that is
 Educate the patient more about the illness and transmitted between animals and people. Studies have
how to prevent it. shown that humans are infected through direct or
 Enhance the body's core temperature. indirect contact with infected dromedary camels,
 Rebuild the regular breathing pattern. although the exact route of transmission remains
unclear.

Interventions HUMAN-TO-HUMAN TRANSMISSION

 Independent It is possible and has occurred predominantly among
 Vitals signs monitoring close contacts and in health care settings. It is likely to
 O2 saturation be spread from an infected person’s respiratory
 Body temperature monitoring secretions through the air or through direct contact.
 Hand hygiene
ASSESSMENT AND DIAGNOSTIC FINDINGS
 rRT-PCR assay - test for MERS-CoV in clinical
respiratory, serum, and stool specimens.
 Serology - research/surveillance test that may
offer valuable epidemiologic data
 Laboratory studies - Laboratory findings at
presentation may include leukopenia,
lymphopenia, thrombocytopenia, and elevated
lactate dehydrogenase levels
 Imaging studies - Chest imaging findings are
abnormal in more than 80% of MERS cases
SYMPTOMS AND CLINICAL MANIFESTATIONS
 FEVER, CHILLS
 TACHYCARDIA
 COUGH, RHINORRHEA
 HYPOXEMIA, DYSPNEA , RHONCHI, RALES
 HYPOTENSION
NURSING DIAGNOSIS
 Infection related to failure to avoid pathogen
secondary to exposure to MERS-CoV.
 Deficient knowledge related to unfamiliarity
with disease transmission information.
 Hyperthermia related to increase in metabolic
rate.
 Ineffective airway clearance related to
excessive production of pulmonary secretions.
 Anxiety related to unknown etiology of the
disease
NURSING PLAN
 Prevent the spread of infection.
 Learn more about the disease and its
management.
 Reduce increase in temperature.
 Reduce anxiety.
 Provide a patent airway.
NURSING INTERVENTIONS
INDEPENDENT
 Monitor vital signs
 Educate patient
 Reduce increase in temperature
 Encourage ample fluid intake
 Ensure patent airway
 Reduce anxiety
DEPENDENT
 Administer medication as prescribed
 Administer and monitor oxygen as ordered
 Consult appropriate healthcare providers if
signs and symptoms persist
EVALUATION
 Prevention of the spread of infection.
 Acquired knowledge about the disease and its
management.
 Reduction in levels of temperature.
 Patent airway achieved.
 Reduction in anxiety.
CORONA VIRUS
 Coronavirus disease 2019 or COVID-19 which
is a highly contagious viral infection that attack
primarily a person’s throat and lungs,
specifically the respiratory system. Covid 19
spread within China and to the of the world.
 Infection with severe acute respiratory
syndrome coronavirus 2, or SARS-CoV-2,
causes coronavirus disease 2019 (COVID-19)
which was first reported in December 2019 in
China and spread globally.
ORIGIN OF COVID-19
It is known that coronavirus circulate in a range of
animals, sometimes these viruses can make the jump
from animals to humans, this is called a spillover and
could be due to range of factors such as mutations in
the virus or increased contact between humans and
animals.
TRANSMISSION
SYMPTOMS
Incubation period (development of symptoms) occurs  Reduce anxiety.
around 5-6 days after exposure but can range from 1-14
days. Symptoms may be very mild to severe and some NURSING INTERVENTIONS
may become asymptomatic. INDEPENDENT
 Monitor vital signs
 Monitor 02 saturation
 Maintain respiratory isolation
 Enforce strict hand hygiene
 Manage hyperthermia
 Educate the patient and companion

DEPENDENT
 Administer medication as per doctor’s
order
 Administer and monitor oxygen as ordered
 Consult appropriate healthcare providers if
signs and symptoms persist

EVALUATION
 Prevention of the spread of infection.
 Acquired knowledge about the disease and its
management.
 Improved body temperature levels.
 Restored normal breathing pattern.
 Reduction in anxiety.

ASSESSMENT AND DIAGNOSTIC FINDINGS

To prevent spreading the infection, it's important to:
 PCR test - Pros: Most accurate - Cons: Longer
processing time  Cover your mouth and nose
 Antibody test - Pros: Rapid, detects disease  Wash hand regularly
spread - Cons: False positives/ negatives  Social distancing
 Antigen test - Pros: Rapid and inexpensive -  Appropriate use of mask and personal
Cons: Accuracy problems protective equipment
 Avoid crowded place
NURSING DIAGNOSIS  Stay at home
• Infection related to failure to avoid pathogen  Get vaccinated
secondary to exposure to COVID-19.
• Deficient knowledge related to unfamiliarity COVID-19 VACCINES
with disease transmission information. Vaccine to prevent covid-19 are:
• Hyperthermia related to increase in • Pfizer-BioNTech COVID-19 vaccine.
metabolic rate. • Moderna (mRNA-1273) COVID-19 vaccine.
• Impaired breathing pattern related to • Oxford/AstraZeneca COVID-19 vaccine.
shortness of breath. • J&J COVID-19 vaccine.
• Anxiety related to unknown etiology of the • Sinopharm
disease. • Sinovac COVID-19 vaccine.
• COVAXIN.
NURSING PLAN • Covovax
 Prevent the spread of infection.
 Learn more about the disease and its
management.
 Improve body temperature levels.
 Inflammatory Diseases
Inflammatory Bowel Disease
 Inflammatory bowel disease (IBD) is an
idiopathic disease caused by a dysregulated
immune response to host intestinal microflora.
It results from a complex interplay between
genetic and environmental factors. Similarities
involve (1) chronic inflammation of the
alimentary tract and (2) periods of remission
interspersed with episodes of acute
inflammation. There is a genetic predisposition
for IBD, and patients with this condition are
more prone to the development of malignancy.
 Also refers to group of conditions that cause
the digestive system to become inflamed (red,
swollen, and sometimes painful).

Etiology/ Causative factors

The exact cause of IBD is unknown, but IBD is the
result of a weakened immune system. Possible
causes are:
1. The immune system responds incorrectly to
environmental triggers, such as a virus or
bacteria, which causes inflammation of the
gastrointestinal tract.
2. There also appears to be a genetic component.
Someone with a family history of IBD is more
likely to develop this inappropriate immune PLANNING
response. STG
3. Inflammation results from a cell-mediated  After 8 hours of nursing intervention, the
immune response in the gastrointestinal patient will be able reduce frequency of stools,
mucosa. and maintain normal stool consistency within
4. Heredity also seems to play a role in that IBD is normal limits.
more common in people who have family
members with the disease. LTG
5. Several gene mutations have been associated  After one week of giving nursing intervention
with IBD the patient will sbe able to identify the and
avoid contributing factors
Risk factors
 Age
 Family History INTERVENTIONS
 Cigarette smoking INDEPENDENT
 Nonsteroidal anti-inflammatory medications 1. Ascertain onset and pattern of diarrhea
2. Observe and record stool frequency,
Diagnostic test characteristics, amount, and precipitating factors.
 Detailed history and physical exam 3. Observe for presence of associated factors
 Dietary patterns (fever, chills, abdominal pain, and cramping,
 Bowel elimination bloody stools)
 Allergies, food intolerance 4. Promote bed rest
 Auscultating and palpating the abdomen 5. Identify and the foods and fluids that precipitate
 Laboratory testing diarrhea
 Endoscopic assessment 6. Restart oral fluid intake gradually.
 Fecal biomarkers 7. Offer clear liquids hourly; avoid cold fluids.
DEPENDENT
Common Signs and Symptoms 1. Prescribe medications as indicated.
 Persistent diarrhea.
EVALUATION
 Abdominal pain.
 Rectal bleeding/bloody stools.  Goal met.
 Weight loss. NCP
 Fatigue. NURSING DIAGNOSIS (2)
 Blood stool Imbalanced nutrition: Less than Body
 Reduced appetite Requirements as evidenced by Altered absorption
of nutrients, medically restricted intake; fear that
Complications eating may cause diarrhea
 Colon Cancer PLANNING
 Skin, eye, & joint inflammation STG
 Medication side effects  After 6 hours of nursing intervention, the
 Primary sclerosing cholangitis patient will be able to demonstrate stable
 Blood clots weight or progressive gain toward goal with
 Severe Hydration normalization of laboratory values and absence
Nursing Care Plan of signs of malnutrition.
NURSING DIAGNOSIS (1) LTG
 Diarrhea related to the inflammatory process  After giving 1 week of nursing intervention the
as evidenced by frequent, and often severe, patient will be able to maintain an ideal weight
watery stools (acute phase) with intake of adequate nutrients.
 4. Provide accurate, concrete information about
INTERVENTION what is being done
INDEPENDENT 5. Provide a calm, restful environment.
1. Weigh daily 6. Help patient to identify and initiate positive
2. Encourage bed rest and limited activity during coping behaviors used in the past.
acute phase of illness. 7. Assist patient to learn new coping mechanisms.
3. Recommend rest before meals.
4. Provide oral hygiene
DEPENDENT
5. Serve foods in well-ventilated, pleasant
1. Provide medications as indicated.
surroundings, with unhurried atmosphere,
congenial company. EVALUATION
6. Record intake and changes in symptomatology  Goals met.
7. Promote patient participation in dietary planning
as possible.
DEPENDENT
1. Keep patient NPO as indicated. ULCERATIVE COLITIS
Ulcerative colitis is an inflammatory bowel disease
EVALUATION that causes chronic inflammation and ulcers in the
 Goals met. superficial lining of the large intestine, also called
the colon. And that includes the rectum.

NCP
Etiology
NURSING DIAGNOSIS (3)
The exact cause of ulcerative colitis remains
Anxiety related to Physiological
unknown.
factors/sympathetic stimulation (inflammatory
1. Previously, diet and stress-were suspected.
process), Threat to self-concept (perceived or
However, researchers now know that these
actual) as evidenced by exacerbation of acute stage
of disease, Increased tension, distress, factors may aggravate but don't cause
apprehension ulcerative colitis.
PLANNING 2. Immune system malfunction. When your
STG immune system tries to fight off an invading
virus or bacterium, an irregular immune
 After 4 hours of nursing intervention, the
response causes the immune system to attack
patient will be able to appear relaxed and
the cells in the digestive tract, too.
reduced anxiety to a manageable level and
3. Heredity also seems to play a role in that
verbalize awareness of feelings of anxiety and
ulcerative colitis is more common in people
healthy ways to deal with them
who have family members with the disease.

However, most people with ulcerative colitis
LTG don't have this family history.
 Identify healthy ways to deal with and express
anxiety Types
 Use support system effectively. 1. Ulcerative proctitis. Inflammation is confined
to the area closest to the anus, also called the
rectum. Rectal bleeding may be the only sign of
INTERVENTIONS the disease.
INDEPENDENT 2. Proctosigmoiditis. Inflammation involves the
1. Review physiological factors, such as active rectum and sigmoid colon — the lower end of
medical condition; recent or ongoing stressors. the colon. Symptoms include bloody diarrhea,
2. Observe and note behavioral clues abdominal cramps and pain, and an inability to
3. Encourage verbalization of feelings. Provide move the bowels despite the urge to do so. This
feedback. is called tenesmus.
3. Left-sided colitis. Inflammation extends from
the rectum up through the sigmoid and
descending portions of the colon. Symptoms
include bloody diarrhea, abdominal cramping
and pain on the left side, and urgency to
defecate.
4. Pancolitis. This type often affects the entire
colon and causes bouts of bloody diarrhea that
may be severe, abdominal cramps and pain,
fatigue, and significant weight loss.
Risk Factors
Ulcerative colitis affects about the same number of
women and men. Risk factors may include:
 Age. Ulcerative colitis usually begins before the
age of 30, but it can occur at any age. Some
people may not develop the disease until after
age 60.
 Race or ethnicity. Although white people have
the highest risk of the disease, it can occur in
any race. If you're of Ashkenazi Jewish descent,
your risk is even higher.
 Family history. You're at higher risk if you have
a close relative, such as a parent, sibling or
child, with the disease.
Diagnostic Test
Endoscopic procedures with tissue biopsy are the
only way to definitively diagnose ulcerative colitis.
Other types of tests can help rule out complications
or other forms of inflammatory bowel disease, such
as Crohn's disease.
To help confirm a diagnosis of ulcerative colitis, you
may have one or more of the following tests and
procedures:
1. Lab tests
o Blood tests. Your provider may suggest blood
tests to check for anemia — a condition in
which there aren't enough red blood cells to
carry adequate oxygen to your tissues — or to
check for signs of infection or inflammation.
o Stool studies. White blood cells or certain
proteins in your stool can indicate ulcerative
colitis. A stool sample also can help rule out
other disorders, such as infections caused by
bacteria, viruses and parasites.
2. Endoscopic procedures
o Colonoscopy. This exam allows your provider
to view your entire colon using a thin, flexible,
lighted tube with a camera on the end. During
the procedure, tissue samples are taken for
laboratory analysis. This is known as a tissue
biopsy. A tissue sample is necessary to make
the diagnosis.
o Flexible sigmoidoscopy. Your provider uses a
slender, flexible, lighted tube to examine the
rectum and sigmoid colon — the lower end of
your colon. If your colon is severely inflamed,
this test may be preferred instead of a full
colonoscopy.
3. Imaging procedures
o X-ray. If you have severe symptoms, your
provider may use a standard X-ray of your
abdominal area to rule out serious
complications, such as a megacolon or a
perforated colon.
o CT scan. A CT scan of your abdomen or pelvis
may be performed if a complication from
ulcerative colitis is suspected. A CT scan may
also reveal how much of the colon is inflamed.
o Computerized tomography (CT)
enterography and magnetic resonance (MR)
enterography. These types of noninvasive
tests may be recommended to exclude any
inflammation in the small intestine. These tests
are more sensitive for finding inflammation in
the bowel than are conventional imaging tests.
MR enterography is a radiation-free alternative.
Common Signs and symptoms
Ulcerative colitis symptoms can vary, depending on
the severity of inflammation and where it occurs.
Signs and symptoms may include:
 Diarrhea, often with blood or pus
 Rectal bleeding — passing small amount of
blood with stool
 Abdominal pain and cramping
 Rectal pain
 Urgency to defecate
 Inability to defecate despite urgency
 Weight loss
 Fatigue
 Fever
 In children, failure to grow
Most people with ulcerative colitis have mild to
moderate symptoms. The course of ulcerative
colitis may vary, with some people having long
periods when it goes away. This is called remission.
Complications
Possible complications of ulcerative colitis include:
 Severe bleeding
 Severe dehydration
 A rapidly swelling colon, also called a toxic
megacolon
 A hole in the colon, also called a perforated
colon
 Increased risk of blood clots in veins and
arteries
 Inflammation of the skin, joints and eyes
 An increased risk of colon cancer
 Bone loss, also called osteoporosis
Treatment
Ulcerative colitis treatment usually involves either
medication therapy or surgery.
Several categories of medications may be effective
in treating ulcerative colitis. The type you take will
depend on the severity of your condition. The
medications that work well for some people may
not work for others. It may take time to find a
medication that helps you.
In addition, because some medications have
serious side effects, you'll need to weigh the
benefits and risks of any treatment.
Anti-inflammatory medications
Anti-inflammatory medications are often the first
step in the treatment of ulcerative colitis and are
appropriate for most people with this condition.
These include:
1. 5-aminosalicylates. Examples of this type of
medication include sulfasalazine (Azulfidine),
mesalamine (Delzicol, Rowasa, others),
balsalazide (Colazal) and olsalazine
(Dipentum). Which medication you take and
how you take it — by mouth or as an enema or
suppository — depends on the area of your
colon that's affected.
2. Corticosteroids. These medications, which
include prednisone and budesonide, are
generally reserved for moderate to severe
ulcerative colitis that doesn't respond to other
treatments. Corticosteroids suppress the
immune system. Due to the side effects, they
are not usually given long term.
Immune system suppressors
These medications also reduce inflammation, but
they do so by suppressing the immune system
response that starts the process of inflammation.
For some people, a combination of these
medications works better than one medication
alone.
Immunosuppressant medications include:
1. Azathioprine (Azasan, Imuran) and
mercaptopurine (Purinethol, Purixan). These
are commonly used immunosuppressants for
the treatment of inflammatory bowel disease.
They are often used in combination with
medications known as biologics. Taking them
requires that you follow up closely with your
provider and have your blood checked regularly
to look for side effects, including effects on the
liver and pancreas.
2. Cyclosporine (Gengraf, Neoral,
Sandimmune). This medication is typically
reserved for people who haven't responded
well to other medications. Cyclosporine has the
potential for serious side effects and is not for
long-term use.
3. "Small molecule" medications. More recently,
orally delivered agents, also known as "small
molecules," have become available for IBD
treatment. These include tofacitinib (Xeljanz),
upadacitinib (Rinvoq) and ozanimod (Zeposia).
These medications may be effective when
other therapies don't work. Main side effects
include the increased risk of shingles infection
and blood clots.
The U.S. Food and Drug Administration (FDA)
recently issued a warning about tofacitinib, stating
that preliminary studies show an increased risk of
serious heart-related problems and cancer from
taking this medication. If you're taking tofacitinib
for ulcerative colitis, don't stop taking it without
first talking with your health care provider.
Biologics
This class of therapies targets proteins made by the
immune system. Types of biologics used to treat
ulcerative colitis include:
1. Infliximab (Remicade), adalimumab (Humira)
and golimumab (Simponi). These
medications, called tumor necrosis factor (TNF)
 inhibitors, work by neutralizing a protein
produced by your immune system. They are for
people with severe ulcerative colitis who don't
respond to or can't tolerate other treatments.
TNF inhibitors are also called biologics.
2. Vedolizumab (Entyvio). This medication is
approved for treatment of ulcerative colitis for
people who don't respond to or can't tolerate
other treatments. It works by blocking
inflammatory cells from getting to the site of
inflammation.
3. Ustekinumab (Stelara). This medication is
approved for treatment of ulcerative colitis for
people who don't respond to or can't tolerate
other treatments. It works by blocking a
different protein that causes inflammation.
Other medications
You may need additional medications to manage
specific symptoms of ulcerative colitis. Always talk
with your health care provider before using over-
the-counter medications. Your provider may
recommend one or more of the following.
1. Anti-diarrheal medications. For severe
diarrhea, loperamide (Imodium A-D) may be
effective. If you have ulcerative colitis, do not
take anti-diarrheal medications without first
talking with your health care provider. These
medications may increase the risk of an
enlarged colon (toxic megacolon).
2. Pain relievers. For mild pain, your provider
may recommend acetaminophen (Tylenol,
others) — but not ibuprofen (Advil, Motrin IB,
others), naproxen sodium (Aleve) and
diclofenac sodium, which can worsen
symptoms and increase the severity of disease.
3. Antispasmodics. Sometimes health care
providers will prescribe antispasmodic
therapies to help with cramps.
4. Iron supplements. If you have chronic
intestinal bleeding, you may develop iron
deficiency anemia and be given iron
supplements.
Surgery
Surgery can eliminate ulcerative colitis and involves
removing your entire colon and rectum
(proctocolectomy).
In most cases, this involves a procedure called
ileoanal anastomosis (J-pouch) surgery. This
procedure eliminates the need to wear a bag to
collect stool. Your surgeon constructs a pouch from
the end of your small intestine. The pouch is then
attached directly to your anus, allowing you to
expel waste in the usual way. This surgery may
require 2 to 3 steps to complete.
In some cases a pouch is not possible. Instead,
surgeons create a permanent opening in your
abdomen (ileal stoma) through which stool is
passed for collection in an attached bag.
Cancer surveillance
You will need more-frequent screening for colon
cancer because of your increased risk. The
recommended schedule will depend on the
location of your disease and how long you have had
it. People with inflammation of the rectum, also
known as proctitis, are not at increased risk of
colon cancer.
If your disease involves more than your rectum, you
will require a surveillance colonoscopy every 1 to 2
years. This begins as soon as eight years after
diagnosis if the majority of colon is involved. Or 15
years after diagnosis if only the left side of your
colon is involved.
Crohn’s Disease
 Crohn's disease is a type of inflammatory bowel
disease (IBD). It causes swelling of the tissues
(inflammation) in your digestive tract, which can
lead to abdominal pain, severe diarrhea, fatigue,
weight loss and malnutrition. Inflammation caused
by Crohn's disease can involve different areas of the
digestive tract in different people, most commonly
the small intestine. This inflammation often
spreads into the deeper layers of the bowel.
 Crohn's disease can be both painful and
debilitating, and sometimes may lead to life-
threatening complications. There's no known cure
for Crohn's disease, but therapies can greatly
reduce its signs and symptoms and even bring
about long-term remission and healing of
inflammation. With treatment, many people with
Crohn's disease can function well.
Pathophysiology
Edema and thickening of the mucosa – Ulcers –
Fistula, fissures and abscesses – Granulomas –
Thickening of bowel wall/ it becomes fibrotic.
Intestinal lumen narrows – Crohn’s disease
Causes
The exact cause of Crohn's disease remains unknown.
Previously, diet and stress were suspected, but now
doctors know that these factors may aggravate, but
don't cause, Crohn's disease. Several factors likely play
a role in its development.
 Immune system. It's possible that a virus or
bacterium may trigger Crohn's disease; however,
scientists have yet to identify such a trigger. When
your immune system tries to fight off an invading
microorganism or environmental triggers, an
atypical immune response causes the immune
system to attack the cells in the digestive tract, too.
 Heredity. Crohn's disease is more common in
people who have family members with the disease,
so genes may play a role in making people more
likely to have it. However, most people with Crohn's
disease do not have a family history of the disease.
Risk Factors
 Age. Crohn's disease can occur at any age, but
you're likely to develop the condition when you're
young. Most people who develop Crohn's disease
are diagnosed before they're around 30 years old.
 Ethnicity. Although Crohn's disease can affect any
ethnic group, whites have the highest risk,
especially people of Eastern European (Ashkenazi)
Jewish descent. However, the incidence of Crohn's
disease is increasing among Black people who live
in North America and the United Kingdom. Crohn's
disease is also being increasingly seen in the Middle
Eastern population and among migrants to the
United States.
 Family history. You're at higher risk if you have a
first-degree relative, such as a parent, sibling or
child, with the disease. As many as 1 in 5 people
with Crohn's disease has a family member with the
disease.
 Cigarette smoking. Cigarette smoking is the most
important controllable risk factor for developing
Crohn's disease. Smoking also leads to more-severe
disease and a greater risk of having surgery. If you
smoke, it's important to stop.
 Nonsteroidal anti-inflammatory medications.
These include ibuprofen (Advil, Motrin IB, others),
naproxen sodium (Aleve), diclofenac sodium and
others. While they do not cause Crohn's disease,
they can lead to inflammation of the bowel that
makes Crohn's disease worse.
Diagnostic Test
 Blood test
 Stool studies
 Colonoscopy
 CT Scan
 MRI
 Capsule endoscopy
 Balloon-assisted enteroscopy
Signs and Symptoms
In Crohn's disease, any part of your small or large
intestine can be involved. It may involve multiple
segments, or it may be continuous. In some people, the
disease is only in the colon, which is part of the large
intestine. Signs and symptoms of Crohn's disease can
range from mild to severe. They usually develop
gradually, but sometimes will come on suddenly,
without warning. You may also have periods of time
when you have no signs or symptoms (remission).
When the disease is active, symptoms typically include:
 Diarrhea
 Fever
 Fatigue
 Abdominal pain and cramping
 Blood in your stool
 Mouth sores
 Reduced appetite and weight loss
 Pain or drainage near or around the anus due to
inflammation from a tunnel into the skin (fistula)
Complications
 Bowel obstruction
 Ulcers
 Fistula
 Colon cancer
 Skin disorders
APPENDICITIS
 Appendix- The appendix is a small, thin pouch
about 5 to 10cm (2 to 4 inches) long. It's connected
to the large intestine, where poo forms.
 Appendicitis is an inflammation of the appendix, a
finger-shaped pouch that projects from your colon
on the lower right side of your abdomen.
Appendicitis causes pain in your lower right
abdomen
PATHOPHYSIOLOGY
 Appendix becomes inflamed and edematous when
there is an obstruction in the lining of the appendix
such as it is kinked or occluded by a fecalith
(hardened mass of stool), tumor or foreign body.
 Buildup of mucous in the appendix. The
inflammatory process increases intraluminal
pressure, initiating a progressively severe,
generalized or pre-umbilical pain that becomes
localized to the right lower quadrant of the
abdomen within a few hours.
 Eventually, the inflamed appendix fills with pus.
This develops into Appendicitis
CAUSES
A blockage in the lining of the appendix that results
in infection is the likely cause of appendicitis. The
bacteria multiply rapidly, causing the appendix to
become inflamed, swollen and filled with pus. If not
treated promptly, the appendix can rupture.
 Infections
 Bacteria
 Traumatic injury
 Tumors
RISK FACTORS
 Age. Appendicitis most often affects teens and
people in their 20sTrusted Source, but it can
occur at any age.
 Sex. Appendicitis is more common in males
than females.
 Family history. People who have a family
history of appendicitis are at heightened risk of
developing it.
DIAGNOSTIC TEST
 Physical exam to assess your pain. Your
doctor may apply gentle pressure on the painful
area. When the pressure is suddenly released,
appendicitis pain will often feel worse, signaling
that the adjacent peritoneum is inflamed.
 Blood test. This allows your doctor to check for
a high white blood cell count, which may
indicate an infection.
 Urine test. Your doctor may want you to have a
urinalysis to make sure that a urinary tract
infection or a kidney stone isn't causing your
pain.
 Imaging tests. Your doctor may also
recommend an abdominal X-ray, an abdominal
ultrasound, computerized tomography (CT)
scan or magnetic resonance imaging (MRI) to
help confirm appendicitis or find other causes
for your pain.
 Abdominal ultrasound: Lets the doctor see
internal organs as they work and checks how
blood is flowing through different blood
vessels.
SIGNS AND SYMPTOMS
Vague epigastric pain or pre-umbilical pain
progress to right lower quadrant pain.
Low grade fever
Nausea and vomiting
Loss of Appetite
Local tenderness at Mcburney’s point when
pressure is applied ( McBurney’s point is the part
where the doctor palpate)
Rebound tenderness ( mas matindi yung sakit pag
tapos ipalpate ng doctor, pain after the pressure is
released)
Pain and tenderness in the lumbar region (If the
appendix curls around behind the cecum)
Pain defecation; the tip of the appendix is resting
against the rectum
Pain urination; the tip is near the bladder or
impinges on ureter
Rovsings’ sign; clinical finding that is indicative of
acute appendicitis; right lower abdominal pain
upon palpation of the left side of the lower
abdomen.
Constipation
COMPLICATIONS
 A ruptured appendix. A rupture spreads infection
throughout your abdomen (peritonitis). Possibly
life-threatening, this condition requires immediate
surgery to remove the appendix and clean your
abdominal cavity.
 A pocket of pus that forms in the abdomen. If
your appendix bursts, you may develop a pocket of
infection (abscess). In most cases, a surgeon drains
the abscess by placing a tube through your
abdominal wall into the abscess. The tube is left in
place for about two weeks, and you're given
antibiotics to clear the infection.
 Peritonitis- When the appendix bursts and bacteria
spill into your abdominal cavity, the lining of your
 abdominal cavity, or peritoneum, can become
infected and inflamed
 Abscess- An abscess is a painful pocket of pus that
forms around a burst appendix. These white blood
cells are your body’s way of attempting to fight the
infection. The infection must be treated with
antibiotics, and the abscess will need to be drained.
 Sepsis- In rare cases, bacteria from a ruptured
abscess may travel through your bloodstream
to other parts of your body. This extremely
serious condition is known as sepsis.
PERITONITIS
 Is the inflammation of the peritoneum, the
serous membrane lining the abdominal cavity
and covering the viscera. (the tissue that lines
the inner abdominal wall and covers the organs
within the abdomen)
 The peritoneum is a membrane made up of 2
layers; one layer lines the cavity (peritoneal
cavity are lined by PARIETAL PERINOTEUM)
and the other layer lines the organ (the viscera
that extend into it are covered with VISCERAL
PERITONEUM).
 The peritoneum helps supports organs in the
abdominal cavity and allow nerves, blood
vessels and lymph vessels to pass through the
organs.
 Peritonitis is a serious and urgent condition
that requires treatment; if left untreated
peritonitis can lead to severe potentially life
threatening throughout the body.
Two types of Peritonitis
1. Secondary Peritonitis - develops when an injury
or medical condition in the abdomen cavity allows
infectious organism into the peritoneum
2. Spontaneous Peritonitis - infection arises from
the fluid build-up in the abdominal cavity.
(ASCITES)
PATHOPHYSIOLOGY
 Peritonitis- Leakage of contents- Bacterial
proliferation occurs- Fluid in the peritoneal
cavity becomes turbid with increasing amount
of protein, white blood cell, cellular debris and
blood- Hypermotility- Paralytic ileus
CAUSES
Causes: Usually, it is a result of bacterial infection;
the organisms come from the disease of the GI
tract or, in women, from the internal reproductive
organs. (in most cases , the infection is caused by a
rupture within the abdominal wall)
 Injury
 Trauma (e.g. gunshot wound and Stab wound
 Inflammation that extends from an organ
outside the peritoneal area, such as the kidney.
 Ruptured Appendicitis
 perforated colon
 stomach ulcer
 diverticulitis of sigmoid
 bowel perforation, IBD;
 may also be associated with abdominal surgical
procedures and peritoneal dialysis.
 Digestive disease such as Crohns disease
Pancreatitis
 Ingestion of a sharp foreign objects such as
*toothpick, fishbone, and glass shard
 Pelvic inflammatory disease
 Surgical wound
*Common bacteria implicated: Escherichia coli,
Klebsiella, Proteus and Pseudomonas
RISK FACTORS
 A previous history of condition
 History of Alcoholism
 Weakened immune system
 Fluid accumulation in the abdomen
 Liver disease
DIAGNOSTIC TEST
*the doctor will ask you about your medical history
and perform a complete physical exam, including
the assessment of tension and tenderness in the
abdomen
 WBC count is elevated (shows that peritonitis is
present)
 Hematocrit and Hemoglobin level may be low
(if blood loss occur)
 Altered level of K, Na, and Cl
 Abdominal X-ray (may show air and fluid levels
as well as distended bowel loops)
 CT scan of the abdomen (may show abscess
formation)
 Ultrasound
 Peritoneal aspiration or analysis (sample of the
fluid inside your peritoneum is taken especially
 if you receive peritoneal dialysis or have fluid
from liver disease)

SIGNS AND SYMPTOMS

 Fever and chills
 Abdominal pain
 Abdominal bloating
 Abdominal distention
 Nausea and vomiting
 Diarrhea
 Minimal urine output
 Excessive thirst
 Fatigue
 Constipation (or inability to pass stool or gas)
 If you are on peritoneal dialysis, symptoms may
include:
o Cloudy dialysis fluid
o White flecks or clumps in the
dialysis fluid
o May feel pain or redness around the
catheter

COMPLICATIONS
 Septicemia and sepsis, if the infection enters your
bloodstream. Sepsis can lead to death.
 Dehydration and electrolyte imbalances from the
transfer of fluids to your abdomen.
 Constipation and urine retention when your
organs are temporarily paralyzed.
 Abdominal adhesions, scar tissue from
inflammation that may obstruct your bowels.

In those with liver disease, spontaneous bacterial

peritonitis can trigger hepatorenal syndrome.