IMMUNOLOGY

• Is the branch of medicine concerned with the body’s response to foreign substances.
• Study of the body’s immune system
IMMUNE SYSTEM
• A complex defence system of the human body that protects itself against foreign invasion.
• The immune system is involved in the recognition and rejection of foreign cells and tissues which can prevent
them from spreading though the body.
IMMUNITY
• The body’s ability to recognize and destroy specific pathogens and to prevent infectious diseases.
◦ immune system is compromised – immunodeficiency diseases.
ᵒ immune system is over reactive – allergies/autoimmune disorders

Functions of the Immune System:

1. Defense
• Resist invasion by foreign microorganisms including viruses and intracellular parasites.
• Attacks some pathogens directly.
• Attacks foreign antigens – usually proteins (including transplanted organs).
• Help body to fight cancer cells.
• Produces antibodies and immunoglobulins
• Produces inflammatory response.
• Produces memory cells.

2. Homeostasis
• Digest and removes damaged cellular substances.
• Kills diseased cells (esp. those infected with viruses)

3. Surveillance
• Recognizes and destroys cellular mutations
• Recognizes and destroys foreign cells
• Monitors presence of antigens

TYPES/ COMPONENTS OF IMMUNE RESPONSE

• non-specific immune response
• specific immune response

1. Non-specific immune response

– Physical, chemical and cellular defenses that prevent microbes from entering the body
– Present from birth.
– A quick-response system effective against a wide range of pathogens and foreign substances.
– This system does not distinguish between different pathogens
– It always gives the same response.
2. Specific immune response
– It occurs when a particular antigen passes the body’s passive defenses.
– It involves cells and proteins within the blood and lymph that attach, disarm, destroy and remove foreign bodies.
– The specific system gives a highly effective, long lasting immunity against anything the body recognize as
foreign.
– It responds to specific microorganisms and enhances the activity of the non-specific system.
– The central feature of the specific immune system is the ability to distinguish between self and non-self.
– antigens or immunoglobins. The immune system is usually tolerant to the body’s own antigens (self antigens)
and does not attack against them.
– breakdown of the recognition system can lead to autoimmune disease

IMMUNITY

Inborn Acquire
(inherited or innate immunity) (learned immunity)

Natural Artificial

Active Passive Active Passive

(contact w/ the dse) (Placenta/ Mother’s milk) (Vaccine/killed attenuated (Immune serum, ex.
toxoid) Rabies/tetanus)
IMMUNE RESPONSE
lymphocytes

B lymphocytes T lymphocytes
Hormunal Cellular
Cells B lymphocytes T lymphocytes

Products Antibodies Sensitized T cells

Reaction Immediate Delayed

Protection Against Bacteria, Respiratory Agents Fungi, Viruses, Chronic Infectious

agents, Tumor cells

ANTIBODIES
• Protein molecules produced by B-cells
• Specific shapes allow binding to specific molecules (antigens)
• Allow body to respond defensively to presence of specific potential threats
IgG – in serum, amniotic fluid,
• Most common antibody type
• Principal defender against bacteria, viruses, and toxins
IgA – Secretory antibody (tears, saliva, GI tract, secretions)
IgM – Confined to bloodstream
• First antibody to appear in response to presence of antigen
IgE – Controls allergic response
• Prevents parasitic infections
IgD – serum , umbilical cord

ASSESMENT
1. HEALTH HISTORY
A. Explore clients health history for risk factors associated with infection disorders including:
– Exposure to person with known or possible infectious disease.
– Travel to places where certain infections are endemic; unsafe sexual partners.
– Non-compliance with recommended immunization.
– Conditions that may compromise defense like cancer, DM, chemotherapy, corticosteroid therapy.
B. Elicit description of the present illness and chief complaint onset, causes, duration, location and
precipitating and alleviating factors. Cardinal s/s indicating an infection process include:
– Systemic symptoms such as: fever, chills, diaphoresis, arthralgias, myolgias, gen. weakness and
anorexia.
– Local s/s such as: redness, pain, edema, and skin warm to touch.
2. PHYSICAL EXAMINATION
A. Inspection
• Inspect lesions on the skin or mucous membranes
• Assess the skin for rashes or reddened areas.
• Assess any abnormal drainage from open lesions or body orifices
• Assess sputum for color, consistency & odor.
• Assess body temperature/temperature of the skin
B. Palpation- palpate lymph nodes for enlargement
C. Auscultation
• auscultate lung sounds
• auscultate BP
• auscultate heart sounds
3. LABORATORY & DX STUDIES
a. Microbiologic specimens – including U/A, blood, sputum, wound exudates, F/E, & mucous membrane
secretions – are used to identify causative organisms.
b. WBC count – determines presence of infection. WBC is elevated when there is presence of infection.
c. Serologic studies – detects presence of antigens or antibodies to a specific disease.
d. Tuberculin Skin Test – reveals to indicate exposure to tuberculosis.
e. Chest Radiograph – evaluate pulmonary dse. & to follow upprogress of the dse.
f. Culture & Sensitivity Test – identify CA
g. Erythrocyte Sedimentation Rate (ESR) - Male: 0-15mm/h; Female: 0-20mm/h
White Blood Cell Type Function Immune System Category

Exit blood vessels and turn into macrophages.

Monocytes Secretes cytokines. Engulf invaders and debris Non-specific
by phagocytosis

Stay in blood vessels and engulf invaders and

Mainly non-specific but can be specific
Neutrophils debris by phagocytosis. First responder to the
when directed by antibody targeting.
site of injury.

Release histamines and participate in the

inflammatory and allergic reactions. Secretes
Basophils Non-specific
heparin, serotonin, kinins, leukotrienes,
prostaglandins
Chemically attack parasitic invaders similar to
Eosinophils natural killer cells. Increased during allergic Non-specific
reponse.
Form T-cells and B-cells
Lymphocytes Specific except for Natural killer cells
Increased in viral infections

MECHANICAL FACTORS
Component Functions
Intact skin Forms a physical barrier to the entrance of microbes.
Mucous membranes Inhibit the entrance of many microbes, but not as effective as intact skin.
Mucus Traps microbes in respiratory and digestive tracts.
Hairs Filter microbes and dust in nose.
Cilia Together with mucus, trap and remove microbes and dust from upper respiratory tract.
Tear ducts Tears dilute and wash away irritating substances and microbes.
Saliva Washes microbes from surfaces of teeth and mucous membranes of mouth.
Epiglottis Prevents microbes and dust from entering trachea.
Urine Washes microbes from urethra.
CHEMICAL FACTORS
Gastric juice Destroys bacteria and most toxins in stomach.
Acid pH of skin Discourages growth of many microbes.

Unsaturated fatty acids Antibacterial substance in sebum.

Lysozyme Antimicrobial substance in perspiration, tears, saliva, nasal secretions, and tissue fluids.

ANTIMICROBIAL SUBSTANCES

Interferon (IFN) Protects uninfected host cells from viral infection.

Causes lysis of microbes. Promotes phagocytosis, contributes to inflammation attracts white

Complement
blood cells to site of infection

OTHER RESPONSES
Phagocytosis Ingestion and destruction of foreign particles by microphages and macrophages.
Inflammation Confines and destroys microbes and repairs tissues.
Fever Inhibits microbial growth and speeds up body reactions that aid repair.

INFECTION
– Invasion of pathogenic microorganism(pathogen) & the reaction of the tse to their presence & to the toxins
generated.

Pathogenecity – the stability of microbes to cause a dse.

Virulence – the degree of pathogenecity.

Pathogens
• are organisms that live on or in their host, and gain nutrients from that host.
• Parasites which causes infectious diseases.
Two types of pathogens:
1. Ectoparasites
– attach themselves to the outside of the host.
– With the aid of specialized mouthparts they penetrate the skin and feed on their hosts blood.
– The parasites must have efficient structures for ‘hanging’ on because usually the host is quite mobile.
(i.e. bed bugs, louse, mites, ticks and fleas)
2. Endoparasites
– live inside the host.
– Therefore they have developed different ways of gaining nutrients from the host.
– inhabit the human gut, blood vessels, blood cells, muscles, liver and lungs
(i.e. bacteria, viruses, roundworm, tapeworm, flukes and protozoa)

CLASSIFICATION OF INFECTION:
I. Extent of Involvement
a. Localized infection (focal point)
• An infection involving bacteria that invade the body at a specific point and remain there, multiplying until
eliminated
• Affects the regional part of the body
• Just a single organ
• Ex. Pressure ulcer, mouth lesions, wound infection
b. Generalized infection (systemic)
• Pertains to the whole body
• Affects the entire body and can be fatal
• Infectious agent is spread throughout the body, eq. Typhoid fever
• Lymph nodes are enlarged , swollen, tender,
• s/s: fever, fatigue, malaise, anorexia, n/v, lymph node enlargement
II. Length of infectious process
a. Acute infection
• One that develops rapidly usually resulting to a high fever & severe redness; resolve in short
period of time.
• Is the one that heals and leaves no aftermath or other related disorders.
 b. Subacute infection
• Is midway in severity between acute & chronic.
• Person may appear to be clinically well, however, laboratory tests, radiologic exams, CT scans
diagnose the condition. Ex. Hepatitis
c. Chronic infection
• One that develops slowly with mild but longer lasting symptoms.
• Persists over a long period of time, often for the remainder of the individual’s life, and does not
follow the usual healing process.
III. Etiology of infectious process
a. Primary Infection – develops after initial exposure to antigen, unrelated to the other health problem.
b. Secondary Infection – develops when antigen take advantage at the weaken defences resulting from a
primary infection. Ex. Staphylococcal pneumonia as a sequelae of measles.
c. Opportunistic Infection – develops when host defences are diminished because of the dse process or
therapeutic modalities. Ex. UTI antibiotic therapy

INFLAMMATION
• Primary host defense system
• Is a local response to cellular injury such as infection or trauma.
• Is the body’s reaction to invasion by an infectious agent, antigen challenge or even just physical, chemical or
traumatic damage.
• Occurs when tissue are damaged
• Mobilizes the body’s defenses
• Isolates and destroys microorganisms, foreign materials, and damaged cells
• So then tissue repair can proceed
Symptoms of Inflammation
 Cardinal Signs:
1. Tumor: Swelling of tissue due to increased interstitial fluid - from vasoactive mediators
2. Rubor: Redness - from vasoactive mediators
3. Calor: Heat - from vasoactive mediators
4. Dolor: Pain (mostly from prostoglandins, some from bradykinin)
5. Functio Laesa: Loss of function may also occur if injury/reaction is severe enough
Chemical Mediators of Inflammation - Related to the effects of Non-Specific Immune System
1. First Mediator -Histamine
• is a vasoactive amine which causes dilation of local blood vessels, increased permeability and contraction
of smooth muscles, which causes fluid to move from the blood vessels into the tissues - hyperemia.
• also causes bronchial constriction (smooth muscle) and mucus production, which becomes evident during
allergic reactions.
2. Second Mediator - Bradykinin
• is another vasoactive mediator which causes increases vascular permeability, vasodilation, and
smooth muscle contraction.
• The kinins are also responsible for pain.
3. Third Mediator - Prostaglandins
• cause redness (increase vasodilation and permeability) pain (increase sensitivity of nerve endings) and
increase platelet aggregation to help in clotting.
• Prostaglandin also acts as a chemotactic factor to attract neutrophils.

COMMUNICABLE DISEASE
• an infection in which the causative organism is transmitted from where it lives and multiplies to another person or
place
• can be transmitted from one person to another directly or indirectly through contaminated objects or infected
animals or insect

STAGES OF INFECTIOUS DISEASE

I. INCUBATION PERIOD
• interval between entrance of pathogens into body and appearance of first symptoms
• ex. Chickenpox (2-3 weeks)
II. PRODROMAL STAGE
• interval from onset of nonspecific signs and symptoms to more specific symptoms
• during this time, microorganisms grow and multiply
• client is more capable of spreading disease to others
III. ILLNESS STAGE
• interval when the client manifest signs and symptoms specific to type of infection
IV. CONVELESCENCE
• interval when the acute symptoms of infection disappear
• recovery may take several days or months
CHAIN OF INFECTION
I. INFECTIOUS AGENT – microorganisms on the skin
A. Resident flora
• permanent resident of the skin where they survive and multiply
• not easily removed by hand washing with plain soaps
B. Transient organism - attack to the skin when the person has contact with another person or object during normal
activities of living
II. RESERVOIR
• a place where a pathogens can survive but may or may not multiply
• the most common reservoir is the human body
• the presence of microorganisms does not always cause a person to be ill
 Carrier - are persons or animals who show no symptoms of illness but who have pathogens in their bodies that
can be transferred to other person.
III.PORTAL OF EXIT
• After organism find a site to grow and multiply, they must find a portal of exit if they are to enter another host and
cause a disease.
• Organism may exit throughout various body systems such as: RT, GIT, GUT or through skin lesions. Agent may
also escape from blood stream by insect bites, hypodermic needles a surgical equipment.
a) Mucous membrane - Respiratory tract, urinary tract, gastrointestinal tract, repro, blood
b) Skin - any break in the skin = responds to pathogenic organism which results to purulent drainage
c) Respiratory tract - released by sneezing, coughing, talking
d) Urinary tract - urine
e) Gastrointestinal tract - saliva, sputum, kissing
f) Bowel elimination - gastric contents during vomiting, stool
g) Repro tract - sexual intercourse, urethral meatus, vaginal canal
h) Blood
IV. MEANS OF TRANSMISSION – from reservoir to the host
a. DIRECT CONTACT
• involves person to person spread
• there is physical contact between the source and susceptible person
• hands having the most contact with the patient
• ex. Mouth to mouth, genital to genital, skin to skin
• daily patient care
b. INDIRECT CONTACT
• personal contact of the susceptible host with a contaminated intermediate objects or fomite
• ex. Contaminated air, water, food, soil
c. DROPLET
• occurs when an infectious agent passes through the air
• contact transmission – travels no more than 3 feet
• ex. sneezing, coughing
d. AIRBORNE TRANSMISSION
• dispersed by air current, inhaled pathogens
• ex. Tuberculosis
• good transmission system help prevent the transmission of infectious agents
e. VEHICLE TRANSMISSION
• occurs when contaminated items such as blood, blood products, food, water,
• ex. Contaminated dairy products – salmonelliasis
f. VECTORBORNE TRANSMISSION
• occurs when insects or other animals serve as intermediate host for infectious agent
V. PORTAL OF ENTRY
• organisms can enter the body through the same routes they use for entering
• urinary obstruction, presence of catheterization
a. Skin – infectious agent enters into skin, or enter the host through break in skin.
b. GIT – contaminated foods & drinks.
c. RT – airborne droplet nuclei
d. UT – contamination from GIT infect the host by way of GUT, STD’s (ex. Urinary obstruction, presence of
catheter)
e. Placenta – rarely a portal of entry, syphilis spirochete can pass through
f. Blood – invasive procedure, an insect bite can transport infectious org. through the blood

VI.SUSCEPTIBLE HOST
• Involves human immune defense
• # of org. to which the host is exposed
• Age, general physical, mental, emotional & nutritional status
• Status of hemopoietic system, absence of immunoglobulins
• Damaged & inadequate defense mechanism
• Invasive procedures that provide a route of access for microorganisms
• Therapies that cause immunosuppression
NOSOCOMIAL INFECTION
• derived from the greek word “NOSOS” (illness or disease) & “KAMEO” (to take care of)
• Nosocomium – one of the first private hospital in ancient greek
• Infections acquired in the hospital after discharge
 Hospital is one of the most likely places for acquiring an infection because it harbors a high population of
microorganisms
TYPES OF NOSOCOMIAL INFECTION
1. INTOGENIC INFECTION
• A nosocomial infection resulting from a diagnostic to therapeutic procedure
• maintain aseptic technique
2. ENDOGENOUS INFECTION
• When the normal flora reside within the body and multiply

INFECTION CONTROL - Standard precautions (barriers) used with all patients

1. HANDWASHING
• The most important and most basic technique in prevention and controlling transmission of infections
• It is a vigorous brief rubbing together of all surfaces of the hands lathered in soap
• Wash hands after touching blood, body fluids, secretions, excretions and contaminated items

• Wash hands after gloves are removed, between patient contact, to avoid transfer of microorganisms to other
patients or environments
• Wash hands between tasks and procedures on the same patient to prevent cross-contamination of different body
sites.
• Use a plain soap or alcohol-based hand rub for routine hand washing
2. GLOVING
• Help to prevent the transmission of pathogens by direct and indirect contact
• A clean and nonsterile gloves worn when touching blood, body fluids, secretion, excretion, and contaminated
items
• Should be changed between procedures
• Remove gloves promptly after use, before touching non-contaminated items and environment surfaces, and before
going to another patients
3. MASKS
• Should be worn when splashing or spraying of blood or body fluids into face
• Protects the nurse from inhaling microorganisms from clients respiratory tract and prevents transmission of
disease
4. GOWNING
• Prevents soiling clothes during procedures and patient care activities
• Long enough to cover all outer garments
• Removed soiled gowns as promptly as possible and wash hands to prevent transfer of microorganisms
5. TRANSPORTING CLIENTS
• Before transferring the client to wheelchair/stretcher the nurse give gowns to serve as a robe
• Patients infected with airborne infections should leave their rooms only for essential procedures or surgery
• Patients also wear barrier protection
 6. ENVIRONMENTAL CONTROL
• Ensure that the hospital has adequate procedures for the routine care, cleaning and disinfecting of environmental
surfaces, beds, bed rails, and bedside equipment
7. PATIENT PLACEMENT
• Isolation room
• Private room
• Negative pressured room
8. PATIENT CARE EQUIPMENT
• Handle used patient care equipments soiled with blood, body fluids, secretions, and excretions in a manner that
prevents skin and mucous membrane exposures, contamination of clothing, and trnasfer of microorganisms to
other patients and environments
• Ensure that reusable equipments is not used for the care of another patient until it has been cleaned and
reprocessed appropriately
• Ensure that single-use items are discarded properly
9. OCCUPATIONAL HEALTH AND BLOOD BORNE PATHOGEN
• Take care to prevent injuries when using needles, scalpels and other sharp instruments or devices
• Never recap used needles
• Do not remove used needles from disposable syringes be hand and do not bend or break
• use mouthpieces, resuscitation bags, or other ventilation device as an alternative to mouth-to-mouth resuscitation
methods

TRANSMISSION BASED PRECAUTION

1. AIRBORNE PRECAUTION
• Are required for patients with presumed or proven pulmonary TB or chicken pox.
• When hospitalized, patients should be put in rooms with negative air pressure, the door should remain closed, and
health care providers should wear protective mask at all times in the patient’s room.
2. DROPLET PRECAUTION
• Used for organisms that can be transmitted by close, face-to-face contact, such as influenza
• While taking care of a patient requiring droplet precaution, the nurse should wear a face mask
• The risk of transmission is limited to close contact, the door may remain open
• Negative pressure rooms should be use if available
3. CONTACT PRECAUTION
• Used for organisms that are spread by skin-to-skin contact
• Emphasize cautious technique for organisms that have serious epidemiologic consequences or those easily
transmitted by contact between health care worker and patient.
• When possible, patient requiring contact isolation must be placed in a private room
• Mask is not needed and doors do not need to be closed

Types of Isolation Indications Requirements

1.Strict Isolation
2.Respiratory Isolation
3.TB/ AFB Isolation
4.Contact Isolation
5.Enteric Precautions
6.Drainage/ Secretions
Precautions
Highly transmissible dse by direct ■ Private room
contact and airborne routes of ■Gowns, masks, gloves
transmission ■Double bagged techniques for soiled articles.
Droplet transmission ■Private room
■Pts with the same org. Generally may share a
room.
■Mask
■Labelled plastic bags are used for soiled
articles.
Suspected active TB ■Private room with negative pressure ventilation
so the room air is vented to the outside.
■Mask
■Handwashing
Infectious dses. or multiple resistant ■Private room
microorganisms that are spread by ■Mask, gown, gloves
close direct contact
Infectious dses. transmitted through ■Private room is required if does not practice
direct or indirect contact with good hygiene measures.
infected feces. ■Handwashing
■Gloves
■Gowns should be worn only when handling
objects contaminated with feces.
Pts with wound drainage/infected ■Gloves
wounds ■Gowns are indicated if clothing is likely to be
contaminated.
7.Universal blood and body
fluid precautions
Blood-borne, body fluid pathogens
(blood, semen, vaginal secretions,
CSF, synovial fluid, pleural fluids,
peritoneal fluids, pericardial fluids,
amniotic fluids and tissues
■Gloves
■Mask & protective eye gears
■Gown
■Contaminated needles should not be recapped.
■Use puncture resistant containers for used
needles and sharp items.

PROTECTIVE (Reverse or Neutropenic) ISOLATION

• Client must be protected from the outside environment in w/c other people’s microorganisms are kept away from
the client.
• Attempts to prevent harmful microorganisms from coming into contact with the client.
• Clients who need protective isolation have a weakened immune response. Ex. Burn pts, bone marrow transplant
pts, AIDS, undergoing chemotherapy for cancer
General Procedures in Protective Isolation:
1. The client requires a private room.
2. Healthcare workers and visitors may not enter if they have colds, influenza or other communicable dses.
3. Anyone entering the room must wear a mask and practice strict hand washing before coming into contact with the
client.
4. The client cannot receive fresh fruits, fresh vegetables and flowers.
5. Rectal temperatures, enemas, suppositories, IV and IM injections, and other invasive procedures are to be avoided
if possible.
6. The tempanic/ear probe method of monitoring the client’s temp is recommended. Measure the client’s temp at
least every 4hrs.
7. A blood culture may be necessary if any reason exist to suspect infection.
8. In some cases, you will use special linens and wear specially laundered scrub suits and shoe covers. Some
facilities require special hair covering. Staffs working in these units often wear lab coats when leaving the units.
9. Special air purification measures are used.

 VIRAL INFECTIONS IN CHILDREN

ROSEOLA INFANTUM
• A common disease which is contagious in infants six months to three years old.
• Caused by human herpesvirus type 6.
• MOT: saliva
• IP: 10-15 days
• There’s no vaccine and no treatment.
Signs and symptoms
• Produces a characteristic of maculopapular rash covering the trunks and spreading to the appendages.
• Rash is preceded by an abrupt onset of high fever that may reach 105F and may cause convulsion, inflamed
tympanic membranes and coldlike symptoms lasting 3-4 days
Nsg mngt:
1. reduce the risk of seizure by sponging with lukewarm water.
2. Medication to keep the temperature below 102F.

RUBELLA (GERMAN MEASLES)

• Causative agent: Rubella virus. An RNA virus of the togavirus family.
• MOT: droplet contact; direct contact
• Incubation period: 14 to 21 days
Mechanisms of action
• Airborn rubella virus infects nose and throat.
• Virus taken up by lymph nodes in the region.
• Rubella virus multiplies and enters the bloodstream.
• Circulating virus reacts with antibodies, resulting in antibody-antigen complexes.
• Antibody-antigen complexes lodge in the skin, causing a rash and pain in the joints.
• In women during pregnancy, rubella virus crosses the placenta, infecting the fetus, resulting in congenital rubella
syndrome. (Clinical signs of congenital rubella : cataracts, microcephaly, mental retardation, deafness, patent
ductus arteriosus, glaucoma, purpura, bone defects).
• Transmission to others by respiratory secretions.
Pathogenesis: Following replication in the upper respiratory tract, virus disseminates to all parts of the body and crosses
the placenta; surviving fetuses often develop abnormally, and they excrete the virus for months after birth.
Epidemiology: Virus possibly present in nose and throat from 1 week before rash to 1 week after, infection occurs via the
respiratory route; humans are the only source.
Symptoms:
• Mild fever and cold symptoms, rash beginning on forehead and face, enlarged lymph nodes behind the ears and
on back of the neck.
• After about a day, a faint rash consisting of innumerable pink spots appears over the face, chest and abdomen.
Prevention and treatment
1. Attenuated rubella virus vaccine administered to children at 12 to 16 months, repeated at 4 to 6 years of age.
2. No specific antiviral treatment.

RUBEOLA (MEASLES)
Causative agent:
• Rubeola virus, a single-stranded, negative-sense RNA virus of the paramyxovirus family.
• MOT:
Incubation period: 10 to 12 days.
Pathogenesis:
• Virus multiplies in respiratory tract; spreads to lymphoid tissue, then to all parts of the body, notably skin, lungs,
and brain;
• Damage to respiratory tract epithelium leads to secondary infection of ears and lungs.
Epidemiology: Acquired by respiratory route; highly contagious; humans are only source.
Mechanisms:
• Airborne rubeola virus infects eyes and upper respiratory tract, then the lymph nodes in the region.
• Virus enters the bloodstream and is carried to all parts of the body including the brain, lungs and skin.
• Skin cells infected with rebeola virus are attacked by immune T cells, causing a generalized rash.
• Virus replicating in the lungs can cause pnuemonia; the brain can also be infected.
• In rare cases, virus persisting in the brain causes subacute sclerosing panencephalitis, months or years after the
acute infection.
• Secondary infection of the ears and lungs is common.
• Transmission is by respiratory secretions.
Symptoms:
• Rash, fever, swollen-red and weepy eyes, cough, and nasal discharge, mild to severe hyposensitivity, general
malaise.
• Within a few days, a fine red rash appears on the forehead and spreads outward over the rest of the body. Unless
complications occur, symptoms generally disappear in about 1 week.
• Rash is macular and blotchy, sometimes the macules become confluent.
• Koplick’s spot characterized by small. Irregular red spots with bluish-white in the center on the bucal mucosa.
Complications:
• Otitis media
• In about 5% of cases, causes pnuemonia, with rapid breathing, shortness of breath, and dusky skin color from lack
of adequate oxygen exchange in the lung.
• Encephalitis, inflammatory disease of the brain, is another serious complication, marked by fever, headache,
confusion, and seizures.
• Permanent brain damage, with mental retardation, deafness, and epilepsy, commonly results from measles
encephalitis.
• During pregnancy may results in an increased risk of miscarriage, premature labor, and low birth weight.
Prevention and treatment:
1. Attenuated virus vaccine after 12 months
2. Second dose upon entering elementary school or at adolescence.
3. No antiviral treatment available at present.

VARICELLA (CHICKEN POX)

Causative agent: Varicella-zozter virus; enveloped doubled-stranded DNA virus of the herpesvirus family.
MOT: airborne or contact
Incubation period: 10 to 21 days; Ave.14 days
Pathogenesis:
• Upper respiratory virus multiplication followed by dissemination via bloodstream to the skin
• Cytopathic effect of virus includes the formation of giant cells.
Epidemiology:
• Highly infectious. Acquired by the respiratory route;
• Humans, both individuals with chickenpox and those with shingles, the only source;
• Dissemination is from skin lesions and respiratory secretions.
Mechanisms:
• Varicella-zoster virus is inhaled, infects nose and throat.
• The virus infects nearby lymph nodes, reproduces, and seeds the bloodstream.
• Infection of other body cells occurs, resulting in showers of virions into the bloodstream.
• These virions cause successive crops of skin lessions, which evolve into blisters and crusts.
• Immune system eliminates the infection except for some virions inside the nerve cells.
• If immunity wanes with age or other reason, the virus persisting in the nerve ganglia can infect the skin, causing
herpes zozter.
• Transmission to others occurs from respiratory secretions and skin
Symptoms:
• Itchy bumps and blister in various stages of development, fever.
• It begins as small, red spots called macules (over the trunk of the body, spreading to the limbs, buccal mucosa,
scalp, axillae, upper respiratory tract, and cunjunctiva.
 • little bumps called pacules (from vesicles with depressed centers).
• and small blisters called vesicles; sorrounded by a narrow zone of redness.
• The lesions can erupt anywhere in the body, although usually they first appear on the back of the head, then the
face, mouth, main body, arms and legs.
• After the pustules break, leaking virus laden fluid, a crust forms, and then healing takes place.
• Latent infections can become manifest as shingles (herpes zoster) years later.
Complications:
• Pnuemonia develops: causing rapid breathing, cough, shortness of breath, and a dusky skin color.
• Congenital varicella syndrome develops in a fraction of a percent of babies whose mothers contract varicella
earlier in pregnancy.
• These babies are born with such defects as underdeveloped head and limbs, and cataracts.
• The virus can damage the heart, lungs, liver, kidney, and brain resulting to death.
Prevention and treatment:
1. Attenuated vaccine. Passive immunization with zoster immune globulin (ZIG) for immunocompromised
individuals;
2. Acyclovir or similar antiviral medication for prevention and treatment.

HERPES ZOSTER (SHINGLES)

Causative agent: It is caused by same herpesvirus, varicella-zozter virus that causes chicken pox
Incubation period: Self-limited condition ; Lesions usually clear in 1 to 3 weeks
Pathogenesis: Result from reactivation of varicella-zoster virus that was dormant in the sensory dorsal root ganglia since
a childhood infection.
Epidemiology:
• Incidence increases with age.
• It may occur 8 to 10 times more frequently in person older than 60 years old than in younger persons.
Mechanisms: An acute localized vesicular eruption distributed over a dermatonal segment of the skin.
Symptoms:
• Consists of burning pain, tingling sensation, extreme sensitivity of skin to touch, and pruritus along that affected
dermatone.
• Present for 1 to 3 days or longer before the appearance of the rash.
• Located in thoracic region, trunk, or face.
Prevention and treatment:
1. Treatment is effective when started within 72 hours of rash development.
2. Antiviral agents : acyclovir, calacyclovir, famciclovir
3. Narcotic analgesics, tricyclic antidepressnat or anticonvulsant drugs,
4. Nerue blockers may use for management of herpetic pain.

VARIOLA (SMALLPOX)
Causative agent: Variola major
MOT: Airborne and contact
IP: 7-14 days

POLIOMYELITIS (POLIO – INFANTILE PARALYSIS)

Causative agents:
• polioviruses 1, 2, 3, members of the picornavirus family.
• Small, non-enveloped, single-stranded, positive sense RNA viruses.
Incubation: 7 to 14 days
Pathogenesis:
• Virus infects the throat and intestine, circulates via the bloodstream, and enters some motor nerve cells of the
brain and spinal cord; infected nerve cells lyse upon release of mature virus.
• Some of them develop muscle pain, increased weakness, and muscle degeneration 15 to 50 years after they had
acute poliomyelitis.
Epidemiology: Spreads by the fecal-oral route; asymptomatic and nonparalytic case common.
Mechanisms: A selective destruction of motor nerve cells, usually of the spinal cord, resulting in permanent paralysis of
one particular group of muscles, such as those of an arm or leg.
Symptoms: Headache, fever, stiff neck, nausea, pain, muscle spasm, followed by paralysis.
Prevention and treatment:
1. Prevented by injecting Salk’s inactivated vaccine, or by Sabin’s orally administered attenuated vaccine in areas of
epidemic or endemic disease.
2. Treatment: artificial ventilation for respiratory paralysis; physical therapy and rehabilitation.

WARTS (PAPILLOMAS)
Causative agent:
• Papillomaviruses belong to the popavavirus family.
• They are small (about 50nm diameter) non-enveloped, doubled-stranded DNA viruses.
• They infect humans.
Incubation: ranges from 2 to 18 months ; warts on the skin disappear within 2 years without any treatment.
Epidemiology: Warts viruses can survive on inanimate objects such as wrestling mats, towels and shower floors, and
infection can be acquired from such contaminated objects.
Pathogenesis:
• The virus infects the deeper cells of the epidermis and reproduces in the nuclei.
• Some of the infected cells grow abnormally and produce the wart.
• Infectious virus is present in the wart and can contaminate fingers or objects that pick or rub the lesions.
Mechanisms:
• Can infect the skin through minor abrasions (integumentary system herpesvirus infections)
Symptoms: small tumors that consists of multiple nipplelike protrusions of tissue covered by skin or mucous membrane.
Prevention and treatment:
1. Warts can only be treated effectively by killing or removing all of the abnormal cells.
2. This can usually be accomplished by freezing the wart with liquid nitrogen,
3. By cauterization, meaning burning the tissue usually with an electrically heated needle,
4. By surgical removal.

CNS RABIES
Causative agent: Rabies virus, single-stranded RNA, rhabdovirus family; has an unusual bullet shape.
MOT: Bite from rabid animal
Incubation period: Usually 30 to 60 days; Sometimes many months or years.
Pathogenesis:
• The principal mode of transmission of rabies to human is via the saliva of a rabid animal introduced into bite
wounds or abrasions of the skin.
• Inhaling aerosols containing the virus, such as from bat feces can also contract rabies.
• During incubation period, virus multiplies at site of bite, then travels via nerves to the central nervous system;
• From the CNS it multiplies and spreads outward via multiple nerves to infect heart and other organs.
Epidemiology: Bite of rabid animal, usually a bat. Inhalation is another possible mode
Symptoms:
• Fever, headache, nausea, vomiting, sore throat, cough at onset;
• Later, spasms of the muscles of mouth and throat, coma and death.
• Tingling or twitching sensation at the site of viral entry, usually an animal bite.
• These early symptoms generally begin 1 to 2 months after viral entry and progress rapidly to symptoms of
encephalitis, agitation, confusion, hallucinations, seizures, and increased sensitivity to light, sound, and touch.
• The body temperature then rises steeply, and increased salivation combined with difficulty swallowing resulting
in frothing at the mouth.
• Hydrophobia, painful spasm of the throat and respiratory muscles provoked by swallowing or even seeing
liquids.
• Coma develops, and about 50% of patients die within 4 days of the first appearance of symptoms, the rest soon
after.
• May cause death.
Prevention and treatment:
1. Avoid suspect animals; immunize pets.
2. Effective post-exposure measures; immediately wash wound with soap and water and apply antiseptic.
3. Inject rabies vaccine and human rabies antiserum as soon as possible.
4. No effective treatment once symptoms begin.

MENINGOCOCCAL MENINGITIS
• Occurs most commonly in children aged 6 to 11 months, but it also occurs frequently in older children and adults.
• It is greatly feared because it can sometimes progress to death within a few hours, but most patients respond well
to treatment and recover without permanent nervous system damage.
Causative agent: Neisseria meningitidis, the meningococus; a gram-negative diplococcus.
Incubation period: 1 to 7 days
Pathogenesis:
• Meningococci adhere by pili,colonize upper respiratory tract, enter bloodstream;
• Carried to meninges and spinal fluid;
• Inflammatory response obstructs normal outflow of fluid;
• Increased pressure caused by obstructed flow impairs brain function;
• Damage to motor nerves produces paralysis;
• Endotoxin release causes shock.
Mechanisms:
• Neisseria meningitidis inhaled, infects upper airways.
• Bacteria enter the bloodstream and are circulated throughout the body.
• The bacteria lodge in the skin and cause petechiae.
• Lysing bacteria in the circulation release endotoxin, producing shock.
• Inlfammatory respose in meningis can damage nerves of hearing causing deafness and obstruct the flow of
cerebspial fluid causing increased pressure inside the brain.
• Bacteria exit with respiratory secretions.
Symptoms: Mild cold followed by headache, fever, pain, stiff neck and back, vomiting, petechiae
Prevention and treatment:
1. Polysaccharide vaccine against types A, C, W135, and Y used to immunize high rsik populations;
2. Rifampicin given to those exposed
3. Penicillin , ceftriaxone, for treatment

MUMPS
• Derives from the verb “mump” which means “to mumble” or “to whisper”.
Causative agent: Mumps virus, a single-stranded RNA virus of the paramyxovirus family.
Incubation period: Generally 15 to 21 days
Pathogenesis:
• The virus initially replicates in the upper respiratory tract, the disseminates to the parotids and other organs of the
body via the bloodstream.
• The inflammatory response to cell destruction is responsible for the marked swelling and pain.
Epidemiology:
• Humans are the only source of the virus.
• Transmission is favored by high percentage of asymptomatic infections.
Symptoms:
• Fever, headache, loss of appetite, typically followed by painful swelling of one or both parotid glands.
• Spasm of the underlying muscle makes it difficult to chew or talk.
• Painful enlargement of the testicles, pelvic pain in women, and symptoms arising from brain involvement are
likely to occur in individuals past the age of puberty.
Complication:
• In pregnant women with mumps commonly miscarriage, but there’s no birth defects.
• Deafness
• Brain infection
• Death
Prevention and treatment:
1. An effective attenuated vaccine has been used since 1967.
2. No antiviral therapy is available.

“KISSING DISEASE” (Infectious Mononucleosis, “Mono”)

Causative agent: Epstein-Barr (EB) virus, a DNA virus of the herpesvirus family.
MOT: Contact with pharyngeal secretion
Incubation period: Usually 1 to 2 months
Pathogenesis:
• Productive infection of epithelial cells of throat and salivary ducts;
• Latent infection of B lymphocytes;
• Activation of B and T lymphocytes
• Hemorrhage from enlarge spleen is a rare but serious complication
Epidemilogy:
• Spread by saliva
• Lifelong recurrent shedding of virus into saliva of asymptomatic, latently infected individuals.
Symptoms: Fatigue, fever, sore throat, and enlargement of the spleen and lymph nodes
Prevention and treatment:
1. Avoid sharing of articles as toothbrush and drinking glasses, which may be contaminated with the virus from
saliva.
2. Treatment: usually none needed
3. Acyclovir of benefit in rare cases.

DENGUE
CA: Aedes aegypti mosquito - Thrive in tropical zone and breed in stagnant water sources
MOT:
IP:
Symptoms: Flulike symptoms: fever, chills, eye pain, joint pain, Hyperpigmented rash
Prevention and treatment:
1. No specifec treatment (symptomatic)
2. IV therapy (D5LR)
3. Increase OFI
4. Control bleeding
5. Control efforts rely on, local effective mosquito control
IMMUNODEFICIENCY DISORDER
• overreaction of the body’s immune systems

I.PRIMARY (CONGENITAL)
• Primary immunodeficiency can be inborn as the result of a genetic defect or can result from developmental
abnormalities
• The genetic or developmental abnormalities that cause primary immunodeficiencies affect B-cells, T-cells or
both.
• Some primary immunodeficiencies affect natural killer cells (NK), phagocytes

Agammaglobulinemia, a disease in which few or no antibodies are produced, occurs in one in about 50,000 people

Severe combined immunodeficiency (SCID), where neither T or B lymphocytes are functional, occurs in only about one
of 500,000 live births.

Selective IgA deficiency, in which very little or no IgA is produced,

• It is the most common primary immunodeficiency known.
• It has been reported in different studies to occur as often as one per 333 to 700 people.
• Although people with this disorder may appear healthy, many have repeated bacterial infections of the
respiratory, gastrointestinal, and genitourinary tracts, where secretory IgA is normally protective.

In children with DiGeorge syndrome, the thymus fails to develop in the embryo.
• As a result, T cells do not differentiate and are absent.
• Affected individuals have other developmental defects as well, such as heart and blood vessels
abnormalities, and a characteristic appearance with low-set deformed ears, small mouth, and wide-set
eyes.
• As expected from a lack of T cells, affected people are very susceptible to infections by eukaryotic
pathogens, such as Pneumocyctis carini and other fungi, as well as viruses and obligate intracellular
bacteria.

Severe combined immunodeficiency (SCID) results from neither T nor B lymphocytes are produced from bone marrow
stem cells.
o Children with SCID die of infectious diseases at an early age unless they are successfully treated by
receiving a bone marrow transplant to reconstitute the bone marrow with healthy cells.
o Other individuals with SCID lack adenosine deaminase, an enzyme important in proliferation of B and T
cells.
o A number of these people have responded well to repeated replacement of the adenosine deaminase
enzyme.
Interventions:
1. Avoid Infections,
2. May need long term antibiotics,
3. May need reverse isolation.
4. Severely suppressed needs life bubbles or islands.
5. Replacement therapy for persons with primary immunodeficiencies.
6. Persons with B-cell defects can be given gamma globulin or Fresh frozen plasma.
7. Tx for T cell defects is experimental transplant of T cells from other persons. Bone Marrow Transplants are
experimental treatment for Primary Immunodeficiencies
II.SECONDARY (ACQUIRED)
• Secondary immudeficiency can be acquired as the result of infection or other stresses in the immune system such
as malnutrition.
• People with either type of immunodeficiency are subject to repeated infections
• Secondary, or acquired, immunodeficiency disease result from environmental rather than genetic factors.
• Malignancies, advanced age, certain infections (especially viral infections), immunosuppressive drugs, or
malnutrition may all lead to secondary immunodeficiency.
• Often, an infection will cause a depletion of certain cells of the immune system.
• The measles virus for example, replicates in lymphoid cells, killing many of them and leaving the body
temporarily open to other infections.

ACQUIRED IMMUNODEFICIENCY SYNDROME

Causative agent:
• Human immunodeficiency virus, type 1 (HIV-1), a single stranded RNA virus of the retrovirus family.
Incubation period:
• Usually 6 days to 6 weeks for acute symptoms; immunodeficiency symptoms within 10 years in half the infection
(10% within 5 years and 90% within 17 years).
Pathophysiology:
1. The coat that surrounds HIV’ RNA and transcriptase is composed of molecules of a protein (P24)
2. It is then wrapped by an envelop compsed of a lipid bilayer penetrated by distinctive assorted glycoproteins
(GP41) (GP120)
 3. In order for the HIV to replicate it must enter a host cell.
4. Glycoproteins attached to helper T cells, macrophages and denritic cells. To gain entry into the host cell
5. Simultaneously it will attack the coreceptors in the host cell’s plasma membrane,
6. HIV will now enter the host cell’s cytoplasm
7. Once inside the cell. HIV sheds it protein coat
8. The reverse transcriptase enzyme makes a DNA copy o the viral RNA -- REPLICATION
9. HIV mainly damage helper T cells that aid both in you cell-mediated and antibody-mediated immune response
Modes of transmission
1. Semen or vaginal fluid
• During unprotected sexual intercourse or oral sex
2. Direct blood to blood contact
• Such as occurs among intravenous drug users who share hypodermic needles
3. Blood transfusion containing the virus
High risk populations
1. males, homosexual, bisexuals
2. Sexual partners of persons with the infection
3. Infants if HIV – infected mothers
4. Intravenous drug users
5. Hemophiliacs and multiple transfusion
• Characterized by prolonged bleeding, particularly after accidental, surgical or dental trauma
Signs and symptoms
• Immediate following infection with HIV, most people experience a brief flu like illness.
1. Fever
2. Fatigue
3. Rash
4. Headache
5. Joint pain sore, throat, & swollen lympnodes
• After a period of 2-10 years, the virus destroy enough of the helper T cells, that most infected people begin to
experience symptoms of immunodeficiency.
1. Enlarged lymph nodes
2. Persistent fatigue
3. Involuntary weight loss
4. Night sweats
5. Skin rashes
6. Various lesions of the mouth & gums
7. Visual disturbances
• As the immune system slowly collapse, an infected HIV- infected person becomes susceptible to a host of --
OPPORTUNISTIC INFECTIONS
1. Pneumocystic carini pnuemonia (PCP)
• It is ubiquitous (exist in all places, everywhere) organism that is airborne and can be found in the lungs of humans
and animals
• s/sx: coughing – non-productive which progresses to productive cough, fever, dyspnea on exertion and eventually
dyspnea at rest
2. Cytomegalovirus infection (CMV)
• transmitted through direct contact with infected secretions, including saliva, cervical fluid, urine, semen, breast
milk, feces & blood
• Tx: ANTIVIRALS
3. MYCOBACTERIUM TUBERCULOSIS
4. HEPA b
5. HERPES SIMPLEX ZOSTER
o spread by direct contact with infected secretions (oral & genital)
o transmission may also take place with “symptom free excretions”
Diagnostic test
1. ELISA TEST – (enzyme – linked immunoabsorbent Assay)
• used to detect Ab
• Usually after 3 to 4 weeks, plasma cell begin to secrete Abs to components of HIV protein coat. These are ab
are then detectable in blood plasma
• When a person is being tested of HIV positive, this usually means that he or she have Ab to HIV in his/her
bloodstream.
• However, if the Ab test is negative, a laboratory test should be done again to detect HIV’s RNA or P24 coat
protein in the blood plasma, and her\his can confirm the presence if HIV.
2. WESTERN BLOT – this is for confirmation of reactive serologic screening tests for HIV ABs
■ PREVENTION OF AIDS IS THE BEST CURE:
• Avoid high-risk behavior such as injection drug abuse, sexual promiscuity, and sexual contact with anyone you
believe has indulged in such activities.
• Make certain you know a partner's sexual history.
• Remember that someone can appear perfectly healthy, yet still be harboring HIV.
 • All people who are at risk (i.e. have multiple sexual contacts or a partner with multiple contacts) must practice
"safer sex."
• This means no sexual contact should be unprotected.
• Latex condoms and spermicidal jellies that can kill the virus should always be used.
• Sexual practices such as unprotected anal intercourse should be avoided.
• If you suspect you're at risk, get tested for HIV periodically.
• Remember that it may take up to six months--or even a year--for the virus to show up.
• Do not donate blood if unsure of your status.
• Although the blood supply is generally safe in the U.S., you may want to consider banking your own blood prior
to elective surgery.
Medical management:
1. Reverse transcriptase inhibitors
• It interferes with the action of the reverse transcriptase enzyme that the virus uses to convert its RNa into
a DNA copy
• Eg. Azidovudine, didanosine, dideoxycytidine
2. Protease inhibitors
• This drugs interfere with the action of protease, a viral enzyme that cuts proteins into pieces that are
assembled into the coat or newly produces HIV particles.
• Eg. Nelfinavir. Ritonavir, saguiavir
Nursing management
• HIV is very fragile virus, it cannot survive for long outside the human body
• The virus is not transmitted by insect bites
• It is important to understand that one cannot become infected by casual physical contact such as hugging or
sharing household items
• The virus can be eliminated from personal care items and medical equipment by exposing them to heat (135F for
10 min) or by cleaning them with common disinfectants such as hydrogen peroxide, rubbing alcohol, Lysol,
standard dishwashing, and clothes washing.
1. Reduce risk of infection:
• Observe sign of oppotunistic infections, weight loss, skin lesions, sore throat
• Monitor vs including Temp
• Note secretions & excretions: change in color, consistency, or odor indicating infetion
• Dite: monitor fluid and eletrolytes, encourage dietary intake (high calorie, high nutrient)
• Protective isolation
• medications
2. Prevent the spread of the disease
• Observe universal precaution
• Ash hands before and after all patients or specimen contact
• Handle blood or body fluids of all patients as potentially infected
• Wear gloves for potential contact with blood and body fluids
• Wear protective eyewear and mask if splatter with blood and body fluids is possible
• wear gowns when splash with blood and body fluids is anticipated
• Place used needles and syringes in impermeable container in the patients room. Do not recap or manipulate
needles. Replace container when full
• Handle all linen soiled with blood or body secretions as potentially infectious
3. Provide physiological and psychological support
• Frequent oral care
• Cooling bath
• Encourage verbalization of fears
• Determine status of support network, average contact with support group
• Observe for severe emotional symptoms (surgical tendencies)
Health teachings
1. About risk – reducing behaviors, use of condoms, limit sexual partners, avoid exposure to blood or semen during
intercourse
2. Family counseling
3. Information of disease, progression and life span
4. Expected side effect with drug therapy, and importance of compliance.

AUTOIMMUNE DISEASES –
• When the immune system loses its ability to distinguish normal from abnormal tissue, normal tissue is destroyed

MULTIPLE SCLEROSIS
• A chronic neurological disease that involves the central nervous system—specifically the brain, spinal cord, and
optic nerves.
• MS can cause problems with muscle control and strength, vision, balance, sensation, and mental functions.
• The brain, spinal cord, and optic nerves are connected to one another by nerves and nerve fibers.
• A protein coating called myelin surrounds and protects the nerve fibers.
• When myelin becomes inflamed or is destroyed—this is called demyelination
• The result is an interruption in the normal flow of nerve impulses through the central nervous system.
 • The process of demyelination and subsequent disruption of nerve impulse flow is the disease known as MS.
• Injured tissue called lesions or plaques form in areas of demyelination.
• In many cases, the cells (oligodendrocytes) that create myelin are destroyed, as are the nerve fibers (axons).
• The body is then not able to heal the myelin or nerve fibers, which further contributes to disability.
Generally, MS follows one of four courses, which are called:
• Relapsing-remitting, where symptoms may fade and then recur at random for many years.
• Secondary progressive, which initially follows a relapsing-remitting course. Later on, it becomes steadily
progressive.
• Primary progressive, where the disease is progressive from the start.
• Progressive relapsing, where steady deterioration of nerve function begins when symptoms first appear.
Symptoms appear and disappear, but nerve damage continues.
Causes multiple sclerosis:
• The cause of MS is unknown. There may be a genetic link because a person's risk of MS is higher when a parent
has MS.
• Geographic location also may play a role. MS is more prevalent in colder regions that are further away from the
equator.
• Researchers have made a connection between a person's geographic location during childhood and the risk of MS
later in life,
• suggesting that a childhood viral illness or other environmental factors may make a person more likely to develop
the disease.
• A problem with the immune system occurring early in life may trigger the onset of MS in some people.
• The "trigger" may be a viral infection.
• In susceptible people, the viral infection may start an autoimmune reaction in which the immune system attacks
its own myelin.
Symptoms of MS:
• Symptoms vary according to which parts of the central nervous system—including the brain, spinal cord or optic
nerves—are damaged by inflammation and the destruction of myelin.
• Symptoms similar to those of MS can occur with other conditions and do not necessarily mean you have MS.
■ The most common early symptoms of MS include:
• Muscle symptoms —muscle weakness, leg dragging, stiffness, a tendency to drop things, a feeling of heaviness,
clumsiness, or a lack of coordination.
• Visual symptoms —blurred, foggy, or hazy vision, eyeball pain (especially with movement), blindness, or double
vision. Optic neuritis (a sudden loss of vision and eye pain) is a fairly common initial symptom, occurring in up to
23% of those who develop MS.
■ Less common early symptoms include:
• Sensory symptoms —tingling, a pins-and-needles sensation, numbness, a bandlike tightness around the trunk or
limbs, or electrical sensations moving down the back and limbs.
• Balance symptoms —lightheadedness or dizziness, and a spinning feeling (vertigo).
■ As MS progresses…
• symptoms may include stiff movement (spasticity),
• tremors,
• pain,
• difficulty controlling urination,
• depression,
• and difficulty thinking clearly (cognitive impairment).
Multiple sclerosis diagnosed
• MS is diagnosed when lesions (injured tissue from demyelination) occur in more than one area of the central
nervous system at different times, meaning a neurologist can verify that you had at least two episodes of MS.
• Each episode must have lasted at least 24 hours, and be confirmed by neurological examination or neurological
tests.
• Symptoms alone do not necessarily mean you have MS.
 magnetic resonance imaging (MRI)
• a test usually shows changes in more than one area of the central nervous system that have developed at more
than one point in time.
• Not all changes seen on an MRI scan indicate MS,
• but criteria have been developed for diagnosing MS with MRI.
• The diagnosis can be difficult to make because early symptoms are usually vague.
Treatment:
1. relapsing-remitting MS
• interferon beta, glatiramer acetate, mitoxantrone
– can reduce the frequency and severity of attacks in people with and may reduce or delay future disability.

2. secondary progressive MS.

• Interferon beta, mitoxantrone
– may also slow the progression of

• Early treatment may help prevent or delay some of this damage.

• Corticosteroids may be given during a relapse to reduce inflammation and shorten the attack.
 • Other medications can relieve some of the symptoms of MS, such as fatigue, depression, urinary problems, sexual
difficulties, pain, and muscle stiffness (spasticity).
• complementary therapies:
– diets or dietary supplements
– Acupuncture
– Biofeedback
– massage therapy.
– Some treatments, such as massage therapy and yoga, may improve your overall sense of well-being.

GUILLIAN-BARRE SYNDROME
• also called acute inflammatory demyelinating polyneuropathy and Landry's ascending paralysis, is an
inflammatory disorder of the peripheral nerves - those outside the brain and spinal cord.
Signs and symptoms:
• rapid onset of weakness
• often, paralysis of the legs, arms, breathing muscles, face.
• GBS is the most common cause of rapidly acquired paralysis in the United States today, affecting one to two
people in every 100,000.
Who are at risk of GBS?
• striking any person
• at any age
• regardless of gender
• ethnic background.
 It typically begins with weakness and/or abnormal sensations of the legs and arms.
 It can also affect muscles of the chest, face and eyes.
 Although many cases are mild, some patients are virtually paralyzed.
 Breathing muscles may be so weakened that a machine is required to keep the patient alive.
 Many patients require an intensive care unit during the early course of their illness, especially if support of
breathing with a machine is required.
 Although most people recover, the length of the illness is unpredictable and often months of hospital care are
required.
 The majority of patients eventually return to a normal or near normal lifestyle, but many endure a protracted
recovery and some remain wheelchair-bound indefinitely.
Causes of GBS:
• The cause is not known.
• Perhaps 50% of cases occur shortly after a microbial (viral or bacterial) infection such as a sore throat or
diarrhea.
• Some theories suggest an autoimmune mechanism, in which the patient's defense system of antibodies and white
blood cells are triggered into damaging the nerve covering or insulation, leading to weakness and abnormal
sensation.
GBS Diagnosed:
• Quite often, the patient's symptoms and physical exam are sufficient to indicate the diagnosis.
• The rapid onset of (ascending) weakness, frequently accompanied by abnormal sensations that affect both sides of
the body similarly, is a common presenting picture.
• Loss of reflexes, such as the knee jerk, are usually found.
To confirm the diagnosis:
• lumbar puncture
– to find elevated fluid protein
• electrical test of nerve
• muscle function
How is GBS Treated?
• Because progression of the disease in its early stages is unpredictable, most newly diagnosed patients are
hospitalized and usually placed in an intensive care unit to monitor breathing and other body functions.
• Care involves use of general supportive measures for the paralyzed patient, and also methods specifically
designed to speed recovery, especially for those patients with major problems, such as the inability to walk.
• Plasma exchange (a blood "cleansing" procedure) and high dose intravenous immune globulins are often helpful
to shorten the course of GBS.

ADDISON'S DISEASE
• Is an endocrine or hormonal disorder that occurs in all age groups and afflicts men and women equally.
• The disease is characterized by weight loss, muscle weakness, fatigue, low blood pressure, and sometimes
darkening of the skin in both exposed and nonexposed parts of the body.
• Occurs when the adrenal glands do not produce enough of the hormone cortisol and, in some cases, the hormone
aldosterone. The disease is also called adrenal insufficiency, or hypocortisolism.
Cortisol
• is normally produced by the adrenal glands, located just above the kidneys.
• It belongs to a class of hormones called glucocorticoids, which affect almost every organ and tissue in the body.
• Cortisol's most important job is to help the body respond to stress.
 • helps maintain blood pressure and cardiovascular function
• helps slow the immune system's inflammatory response
• helps balance the effects of insulin in breaking down sugar for energy
• helps regulate the metabolism of proteins, carbohydrates, and fats
• helps maintain proper arousal and sense of well-being
• is regulated by the brain's hypothalamus and the pituitary gland, a bean-sized organ at the base of the brain.
• First, the hypothalamus sends "releasing hormones" to the pituitary gland.
• The pituitary responds by secreting hormones that regulate growth and thyroid and adrenal function, and sex
hormones such as estrogen and testosterone.
• One of the pituitary's main functions is to secrete ACTH (adrenocorticotropin), a hormone that stimulates the
adrenal glands.
• When the adrenals receive the pituitary's signal in the form of ACTH, they respond by producing cortisol.
• Completing the cycle, cortisol then signals the pituitary to lower secretion of ACTH.
Aldosterone
• Belongs to a class of hormones called mineralocorticoids, also produced by the adrenal glands.
• It helps maintain blood pressure and water and salt balance in the body by helping the kidney retain sodium and
excrete potassium.
• When aldosterone production falls too low, the kidneys are not able to regulate salt and water balance, causing
blood volume and blood pressure to drop.
Causes:
• Failure to produce adequate levels of cortisol can occur for different reasons.
• The problem may be due to a disorder of the adrenal glands themselves (primary adrenal insufficiency)
• Inadequate secretion of ACTH by the pituitary gland (secondary adrenal insufficiency).

Primary Adrenal Insufficiency

• Most cases are caused by the gradual destruction of the adrenal cortex, the outer layer of the adrenal glands, by
the body's own immune system in which the immune system makes antibodies that attack the body's own tissues
or organs and slowly destroy them.
• occurs when at least 90 percent of the adrenal cortex has been destroyed.
• both glucocorticoid (cortisol) and mineralocorticoid (aldostertone) hormones are lacking.
• Sometimes only the adrenal gland is affected, as in idiopathic adrenal insufficiency;
Tuberculosis
• an infection which can destroy the adrenal glands
• When adrenal insufficiency was first identified by Dr. Thomas Addison in 1849, TB was found at autopsy in 70 to
90 percent of cases.
• as the treatment for TB improved, however, the incidence of adrenal insufficiency due to TB of the adrenal glands
has greatly decreased.
The symptoms of adrenal insufficiency:
• usually begin gradually.
• chronic, worsening fatigue
• muscle weakness
• loss of appetite
• weight loss
• About 50 percent of the time, one will notice nausea, vomiting, diarrhea
Other symptoms include:
• low blood pressure that falls further when standing,
• causing dizziness or fainting skin changes in Addison's disease,
• with areas of hyperpigmentation, or dark tanning, covering exposed and nonexposed parts of the body; this
darkening of the skin is most visible on scars; skin folds;
• pressure points such as the elbows, knees, knuckles, and toes; lips; and mucous membranes
• Addison's disease can cause irritability and depression.
• Because of salt loss, a craving for salty foods also is common.
• Hypoglycemia, or low blood glucose, is more severe in children than in adults.
• In women, menstrual periods may become irregular or stop.
• Because the symptoms progress slowly, they are usually ignored until a stressful event like an illness or an
accident causes them to become worse.
• This is called an addisonian crisis, or acute adrenal insufficiency.
• In most cases, symptoms are severe enough that patients seek medical treatment before a crisis occurs.
• However, in about 25 percent of patients, symptoms first appear during an addisonian crisis.
Symptoms of an addisonian crisis:
• sudden penetrating pain in the lower back, abdomen, or legs
• severe vomiting and diarrhea
• dehydration
• low blood pressure
• loss of consciousness
• Left untreated, an addisonian crisis can be fatal.
Diagnosis:
• dark tanning of the skin, will lead a doctor to suspect Addison's disease.
 • laboratory tests - first to determine whether levels of cortisol are insufficient and to establish the cause.
• X-ray exams of the adrenal and pituitary glands also are useful in helping to establish the cause.
• ACTH Stimulation Test
– This is the most specific test for diagnosing Addison's disease.
– blood cortisol, urine cortisol, or both are measured before and after a synthetic form of ACTH is given by
injection.
• ACTH test, measurement of cortisol in blood is repeated 30 to 60 minutes after an intravenous ACTH injection.
– The normal response after an injection of ACTH is a rise in blood and urine cortisol levels.
• Long CRH Stimulation Test
– to determine the cause of adrenal insufficiency.
– synthetic CRH is injected intravenously
– blood cortisol is measured before and 30, 60, 90, and 120 minutes after the injection.
– Patients with primary adrenal insufficiency have high ACTHs but do not produce cortisol.
– Patients with secondary adrenal insufficiency have deficient cortisol responses but absent or delayed ACTH
responses.
– Absent ACTH response points to the pituitary as the cause;
– a delayed ACTH response points to the hypothalamus as the cause.
Treatment of Addison's disease:
• involves replacing, or substituting, the hormones that the adrenal glands are not making. Cortisol is replaced
orally with hydrocortisone tablets, a synthetic glucocorticoid, taken once or twice a day.
• If aldosterone is also deficient, it is replaced with oral doses of a mineralocorticoid called fludrocortisone acetate
(Florinef), which is taken once a day.
• Patients receiving aldosterone replacement therapy are usually advised by a doctor to increase their salt intake.
• During an addisonian crisis, low blood pressure, low blood glucose, and high levels of potassium can be life
threatening. Standard therapy involves intravenous injections of hydrocortisone, saline (salt water), and dextrose
(sugar).
• This treatment usually brings rapid improvement. When the patient can take fluids and medications by mouth, the
amount of hydrocortisone is decreased until a maintenance dose is achieved.
• If aldosterone is deficient, maintenance therapy also includes oral doses of fludrocortisone acetate
Health teachings:
1. Should always carry identification stating his or her condition in case of an emergency.
• The card should alert emergency personnel about the need to inject 100 mg of cortisol if its bearer is found
severely injured or unable to answer questions.
• The card should also include the doctor's name and telephone number and the name and telephone number of the
nearest relative to be notified.
2. When traveling, a needle, syringe, and an injectable form of cortisol should be carried for emergencies.
3. Immediate medical attention is needed when severe infections, vomiting, or diarrhea occur.

4. A patient who is vomiting may require injections of hydrocortisone.

5. People with medical problems may wish to wear a descriptive warning bracelet or neck chain to alert emergency
personnel.

ULCERATIVE COLITIS
• colitis is a disease that causes inflammation and sores, called ulcers, in the lining of the large intestine.
• The inflammation usually occurs in the rectum and lower part of the colon, but it may affect the entire colon.
• Ulcerative colitis rarely affects the small intestine except for the end section, called the terminal ileum.
• Ulcerative colitis may also be called colitis or proctitis.
• Ulcerative colitis is an inflammatory bowel disease (IBD), the general name for diseases that cause inflammation
in the small intestine and colon.
• The inflammation makes the colon empty frequently, causing diarrhea.
• Ulcers form in places where the inflammation has killed the cells lining of the colon; the ulcers bleed and produce
pus.
• Ulcerative colitis can be difficult to diagnose because its symptoms are similar to other intestinal disorders and to
another type of IBD called Crohn's disease.
– Crohn's disease differs from ulcerative colitis because it causes inflammation deeper within the intestinal wall.
– Crohn's disease usually occurs in the small intestine, although it can also occur in the mouth, esophagus, stomach,
duodenum, large intestine, appendix, and anus.
• Ulcerative colitis may occur in people of any age, but most often it starts between ages 15 and 30, or less
frequently between ages 50 and 70.
• Children and adolescents sometimes develop the disease.
• Ulcerative colitis affects men and women equally and appears to run in some families
What causes ulcerative colitis?
• the body's immune system reacts to a virus or a bacterium by causing ongoing inflammation in the intestinal wall.
• People with ulcerative colitis have abnormalities of the immune system, but doctors do not know whether these
abnormalities are a cause or a result of the disease.
• Ulcerative colitis is not caused by emotional distress or sensitivity to certain foods or food products, but these
factors may trigger symptoms in some people.
What are the symptoms of ulcerative colitis?
• abdominal pain
• bloody diarrhea
• fatigue
• weight loss
• loss of appetite
• rectal bleeding
• loss of body fluids and nutrients
How is ulcerative colitis diagnosed?
• Blood tests - check for anemia, which could indicate bleeding in the colon or rectum. - deterine increased WBC,
which is a sign of inflammation somewhere in the body.
• Stool sample - detect bleeding or infection in the colon or rectum.
• colonoscopy or sigmoidoscopy - insertion an endoscope — a long, flexible, lighted tube connected to a computer
and TV monitor — into the anus to see the inside of the colon and rectum.
– The doctor will be able to see any inflammation, bleeding, or ulcers on the colon wall.
• Biopsy - taking a sample of tissue from the lining of the colon to view with a microscope.
• A barium enema x ray of the colon - this procedure involves filling the colon with barium, a chalky white
solution.
– The barium shows up white on x ray film, allowing the doctor a clear view of the colon, including any
ulcers or other abnormalities that might be there.
What are the treatments for ulcerative colitis?
1. medications
2. surgery to remove the diseased colon.
3. Some people whose symptoms are triggered by certain foods are able to control the symptoms by avoiding foods
that upset their intestines, like highly seasoned foods, raw fruits and vegetables, or milk sugar (lactose).
4. Each person may experience ulcerative colitis differently, so treatment is adjusted for each individual.
5. Emotional and psychological support is important.
6. Some people have remissions—periods when the symptoms go away—that last for months or even years.
7. This changing pattern of the disease means one cannot always tell when a treatment has helped.
8. Some people with ulcerative colitis may need medical care for some time, with regular doctor visits to monitor the
condition.
Drug Therapy - The goal of therapy is to induce and maintain remission, and to improve the quality of life for people
with ulcerative colitis.
• Aminosalicylates - help control inflammation.
• Sulfasalazine is a combination of sulfapyridine and 5-ASA and is used to induce and maintain remission.
• Sulfapyridine - anti-inflammatory to the intestine.
S/E : include nausea, vomiting, heartburn, diarrhea, and headache.
• Corticosteroids / STEROIDS – eg. prednisone hydrocortisone
– also reduce inflammation.
S/E: weight gain, acne, facial hair, hypertension, mood swings, and an increased risk of infection. For this reason,
they are not recommended for long-term use.
• Immunomodulators - reduce inflammation by affecting the immune system.
– e.g. azathioprine and 6-mercapto-purine (6-MP)
– slow-acting - 6 months before the full benefit is seen.
– Complications: pancreatitis, hepatitis, reduced white blood cell count, increased risk of infection.
Hospitalization
• For example, a person may have severe bleeding or severe diarrhea that causes dehydration.
• stop diarrhea and loss of blood, fluids, and mineral salts.
• The patient may need a special diet, feeding through a vein, medications, or sometimes surgery.
Surgery
• Proctocolectomy - surgery to remove the colon and rectum
• Ileostomy - creates a small opening in the abdomen, called a stoma, and attaches the end of the small intestine,
called the ileum
– Waste will travel through the small intestine and exit the body through the stoma. A pouch is worn over
the opening to collect waste, and the patient empties the pouch as needed.
• Ileoanal anastomosis or pull-through.
– the surgeon removes the diseased part of the colon and the inside of the rectum, leaving the outer muscles
of the rectum.
– The surgeon then attaches the ileum to the inside of the rectum and the anus, creating a pouch.
– Waste is stored in the pouch and passed through the anus in the usual manner.
– Bowel movements may be more frequent and watery than before the procedure.
– Inflammation of the pouch (pouchitis) is a possible complication.
GLOMERULONEPHRITIS
• is a type of kidney disease caused by inflammation of the internal kidney structures (glomeruli).
• staphylcoccus pyogenes pyoderma.
• s/s: fever, fluid retention, high blood pressure, blood and protein in the urine.
Causes, incidence, and risk factors
• Progressive glomerulonephritis may result in destruction of the kidney glomeruli and chronic renal failure and end
stage renal disease.
• The disease may be caused by specific problems with the body's immune system, but the precise cause of most
cases is unknown.
• Damage to the glomeruli
• impaired filtering
• causes blood and protein to be lost in the urine.
• symptoms develop gradually
• the disorder may be discovered when there is an abnormal urinalysis during routine physical or examination for
unrelated disorders
• can cause hypertension
• It may develop after survival of the acute phase of rapidly progressive glomerulonephritis.
• In about one-fourth of people with chronic glomerulonephritis, there is no prior history of kidney disease,
• and the disorder first appears as chronic renal failure.
Chronic renal failure symptoms that gradually develop may include the following:
• Unintentional weight loss
• Nausea, vomiting
• General ill feeling (malaise)
• Fatigue
• Headache
• Frequent hiccups
• Generalized itching
• Decreased urine output
• Need to urinate at night
• Easy bruising or bleeding
• Decreased alertness
– Drowsiness, somnolence, lethargy, confusion, delirium, coma
• Muscle twitching
• Muscle cramps
• Seizures
• Increased skin pigmentation (hyperpigmentation) -- skin may appear yellow or brown
• Decreased sensation in the hands, feet, or other areas
Additional symptoms that may be associated with this disease:
• Excessive urination
• Nosebleed
• High blood pressure
• Blood in the vomit or in stools
Signs and tests
• Urinalysis - reveal anemia or indicate reduced kidney functioning,
• azotemia (accumulation of nitrogenous wastes such as creatinine and urea)
• show blood, protein
• abdominal ultrasound,
• abdominal CT scan,
• A chest X-ray may show fluid overload.
• A kidney biopsy may show one of the forms of chronic glomerulonephritis or non specific scarring of the
glomeruli.
Complications
• Nephrotic syndrome
• Acute nephritic syndrome
• Chronic renal failure
• End-stage renal disease
• Hypertension
• Malignant hypertension
• Fluid overload -- congestive heart failure, pulmonary edema
• Chronic or recurrent urinary tract infection
• Increased susceptibility to other infections
Treatment
1. Various antihypertensive medications may be used to attempt to control high blood pressure.
2. Corticosteroids, immunosuppressives, or other medications may be used to treat some of the causes of chronic
glomerulonephritis.
3. Dietary restrictions on salt, fluids, protein, and other substances may be recommended to aid control of
hypertension or renal failure.
4. Dialysis or kidney transplantation may be necessary to control symptoms of renal failure and to sustain life
■ The stress of illness can often be helped by joining support groups where members share common experiences and
problems.
Prevention
• There is no specific prevention for most cases of glomerulonephritis.
• Some cases may be prevented by avoiding or limiting exposure to organic solvents, mercury, and nonsteroidal
anti-inflammatory analgesics.

TYPE 1 DIABETES MELLITUS

• is a medical disorder characterized by varying or persistent hyperglycemia (elevated blood sugar levels),
especially after eating.
• All types of diabetes mellitus share similar symptoms and complications at advanced stages.
• Hyperglycemia itself can lead to dehydration and ketoacidosis.
• Longer-term complications include:
– cardiovascular disease (doubled risk)
– chronic renal failure (it is the main cause for dialysis),
– retinal damage which can lead to blindness,
– nerve damage which can lead to gangrene with risk of amputation of toes, feet, and even legs.
• The most important forms of diabetes are due to decreased production of insulin (diabetes mellitus type 1, the first
recognized form), or decreased sensitivity of body tissues to insulin (diabetes mellitus type 2, the more common
form).
• The former requires insulin injections, while the latter is generally managed with oral medication and only
requires insulin if the tablets are ineffective.
To reduce complications:
• cessation of smoking,
• optimizing cholesterol levels,
• maintaining a stable body weight,
• controlling high blood pressure
• engaging in regular exercise
Signs and symptoms:
• Early symptoms of type 1 diabetes are often polyuria (frequent urination) and polydipsia (increased thirst, and
consequent increased fluid intake).
• There may also be weight loss (despite normal or increased eating), increased appetite, and fatigue.
• Thirst develops because of osmotic effects — sufficiently high glucose (above the 'renal threshold') in the blood is
excreted by the kidneys but this requires water to carry it and causes increased fluid loss, which must be replaced.
• The lost blood volume will be replaced from water held inside body cells, causing dehydration.
Another common presenting symptoms:
• altered vision.
• Prolonged high blood glucose causes changes in the shape of the lens in the eye, leading to blurred vision
• All unexplained quick changes in eyesight should force a fasting blood glucose test.
• Especially dangerous symptoms in diabetics include the smell of acetone on the patient's breath (a sign of
ketoacidosis)
• Kussmaul breathing (a rapid, deep breathing), and any altered state of consciousness or arousal (hostility and
mania are both possible, as is confusion and lethargy)
• The most dangerous form of altered consciousness is the so-called "diabetic coma" which produces
unconsciousness.
• Early symptoms of impending diabetic coma include polyuria, nausea, vomiting and abdominal pain, with
lethargy and somnolence a later development, progressing to unconsciousness and death if untreated
Diagnostic approach:
1. health screening,
2. detection of hyperglycemia when a doctor is investigating a complication of longstanding, unrecognized diabetes,
and less commonly
3. new signs and symptoms attributable to the diabetes.

HYPERSENSITIVITY (ALLERGY)

ANAPHYLAXIS - is the word used for serious and rapid allergic reactions usually involving more than one part of the
body which, if severe enough, can kill.

What are the common causes of anaphylaxis?

Amongst the commoner causes of anaphylaxis are:
• Foods: especially nuts, some kinds of fruit, fish and less commonly spices
• Drugs: Especially penicillins, anaesthetic drugs, some intravenous infusion liquids, and things injected during x-
rays. Aspirin and other painkillers (called NSAIDs) can produce very similar reactions.
• Latex: mainly in rubber latex gloves, catheters, other medical products, but also in many things encountered in
daily life. Sufferers are nearly always health care workers, mainly nurses, or have other occupational contact with
latex. They may get anaphylaxis from bananas, avocados, kiwi fruit, figs, or other fruits and vegetables including
even potatoes and tomatoes.
 • Bee or wasp (yellow jacket) stings when these cause faintness, difficulty in breathing, or rash or swelling of a
part of the body which has not been stung. If you just get a very large swelling of the part of your body which
was stung, you are probably not going to have anaphylaxis if stung again.
• Exercise may precipitate such reactions in some ('exercise-induced anaphylaxis'), and so may exercise after
food, sometimes apparently irrespective of what the food is, but in other people after specific foods. This is called
'exercise-induced food-dependent anaphylaxis'.
• Medicines called beta blockers used for heart disease or high blood pressure can change mild reactions from
another cause into severe anaphylaxis because they block the body's main defence against anaphylaxis
Signs and symptoms
Anaphylaxis usually happens quickly. Anaphylaxis can produce:
• An itchy nettlerash (urticaria, hives)
• Faintness and unconsciousness due to very low blood pressure. Unlike an ordinary fainting attack, this does not
improve so dramatically on lying down.
• Swelling (angioedema)
• Swelling in the throat, causing difficulty in swallowing or breathing
• Asthma symptoms
• Vomiting
• Cramping tummy pains
• Diarrhoea
• A tingling feeling in the lips or mouth if the cause was a food such as nuts
• Death due to obstruction to breathing or extreme low blood pressure (anaphylactic shock)
• Faintness with a nettlerash or swelling coming on quickly is probably anaphylaxis, and if there is also difficulty in
breathing the danger is greater. Faintness with difficulty in breathing alone will sometimes be due to a panic
attack, but can also be due to anaphylaxis.
 Fainting and Anaphylaxis: clues which may help you tell the difference
(this guide is not perfect; you need a doctor if in doubt.)

Anaphylaxis Fainting

color Pink, typically Pale, typically

pulse Fast, usually Slow, usaully

Blood pressure Can remain low lying down Normal when lying down

Other features Nettlerash, Swelling, Difficulty The person has probably fainted before.
breathing, Tummy pain or diarrhoea (Some people do faint, others don't.)
What is the best treatment for anaphylaxis?
Although there are several important treatments, by far the most important is:
• Adrenaline (epinephrine)
• There is one drug which will work against all the effects of all the dangerous substances released in anaphylaxis.
It is adrenaline (epinephrine). For serious attacks, it is a vital treatment. You need to inject it; inhalers may no
longer be an option.
• There are special syringe kits to make injection easy.

CYTOTOXIC

Systemic Lupus Erythematosus (Lupus)

• is an autoimmune disease and is characterised by the presence of abnormal antibodies in the bloodstream, the
most important being antinuclear antibody and antibodies to double stranded DNA. A defect of T lymphocyte
function leads to polyclonal B lymphocyte activation and the uncontrolled production of antibodies and immune
complexes. It involves chronic inflammation of connective tissue and immunologically-mediated tissue
damage is the result of at least two different mechanisms:-
• direct type II antibody mediated cytotoxicity.
• immune complex (and complement) mediated type III hypersensitivity.

Transplant rejection
• occurs when the immune system of the recipient of a transplant attacks the transplanted organ or tissue. This is
because a normal healthy human immune system can distinguish foreign tissues and attempts to destroy them,
just as it attempts to destroy infective organisms such as bacteria and viruses.
Rejection Mechanisms
• Rejection is an adaptive immune response and is mediated through both T cell mediated and humoral immune
(antibodies) mechanisms. The number of mismatched alleles determines the speed and magnitude of the rejection
response. Different grafts usually have a proclivity to a certain mechanism of rejection.
Types of rejection:
1. Hyperacute rejection
• is a complement-mediated response in recipients with pre-existing antibodies to the donor (for example, ABO
blood type antibodies). Hyperacute rejection occurs within minutes and the transplant must be immediately
removed to prevent a severe systemic inflammatory response. Rapid coagulation of the blood occurs. This is a
particular risk in kidney transplants, and so a prospective cytotoxic crossmatch is performed prior to kidney
transplantation to ensure that antibodies to the donor are not present. For other organs, hyperacute rejection is
prevented by transplanting only ABO-compatible grafts. Hyperacute rejection is the likely outcome of
xenotransplanted
2. Acute rejection
• is antibody-mediated. It generally first occurs around five to ten days after a transplant if the patient is not taking
immunosuppressant drugs. However, since all transplant recipients are given immunosuppressants acute rejection
can take months to develop. It can destroy the transplant if it is not recognised and treated appropriately. It occurs
in around 60-75% of first kidney transplants, and 50 to 60% of liver transplants. A single episode is not a cause
for concern if recognised and treated promptly, but recurrent episodes are associated with chronic rejection and
graft failure. The immune system is responding to the mismatch of Major Histocompatibility Complex proteins.
These identify tissues uniquely due to their very large number of combinations. Identical twins and cloned tissue
do match on MHC. This type of rejection is the primary reason why transplant patients have to take drugs for the
rest of their lives.
3. Chronic rejection
• Chronic rejection was a term used to describe all long term loss of function in organ transplants associated with
fibrosis of the internal blood vessels of the transplant, but this is now termed chronic allograft vasculopathy and
the term chronic rejection is reserved for those cases where the process is shown to be due to a chronic
alloreactive immune response. It can be caused by a member of the Minor Histocompatibility Complex such as
the H-Y gene of the male Y chromosome. This usually leads for a new organ after a decade or so.
Prevention of rejection
Rejection is prevented with a combination of drugs including:
• Calcineurin inhibitors
o Ciclosporin
o Tacrolimus
• mTOR inhibitors
o Sirolimus
o Everolimus
• Anti-proliferatives
o Azathioprine
o Mycophenolic acid
• Corticosteroids
o Prednisolone
o Hydrocortisone
• Antibodies
o Monoclonal anti-IL-2Rα receptor antibodies
 Basiliximab
 Daclizumab
o Polyclonal anti-T-cell antibodies
 Anti-thymocyte globulin (ATG)
 Anti-lymphocyte globulin (ALG)
• Generally a triple therapy regimen of a calcineurin inhibitor, an anti-proliferative, and a corticosteroid is used,
although local protocols vary. Antibody inductions can be added to this, especially for high-risk patients and in
the United States. mTOR inhibitors can be used to provide calcineurin-inhibitor or steroid-free regimes in selected
patients.

 A bone marrow transplant allows the chimeric body's immune system to adapt and accept a new organ. This
requires that the bone marrow, which produces the immune cells, be from the same person as the organ donation
(or an identical twin or a clone). Bone marrow is not attacked by the body's immune system, and is the only
known type of transplant that has this quality. However, there is a risk of graft versus host disease GVHD in
which the immune cells arising from the bone marrow transplant recognise the host tissues as foreign and attack
and destroy them accordingly.
Treatment of rejection
• Acute rejection is normally treated initially with a short course of high-dose methylprednisolone, which is usually
sufficient to treat successfully. If this is not enough, the course can be repeated or ATG can be given. Acute
rejection refractory to these treatments may require plasma exchanges to remove antibodies to the transplant.
• The monoclonal anti-T cell antibody OKT3 was formerly used in the prevention of rejection, and is occasionally
used in treatment of severe acute rejection, but has fallen out of common use due to the severe cytokine release
syndrome and late post-transplant lymphoproliferative disorder, which are both commonly associated with use of
OKT3; in the United Kingdom it is available on a named-patient use basis only.
 Acute rejection usually begins after the first week of transplantation, and most likely occurs to some degree in all
transplants (except between identical twins). It is caused by mismatched HLA antigens that are present on all
cells. HLA antigens are polymorphic therefore the chance of a perfect match is extremely rare. The reason that
acute rejection occurs a week after transplantation is because the T-cells involved in rejection must differentiate
and the antibodies in response to the allograft must be produced before rejection is initiated. These T-cells cause
the graft cells to lyse or produce cytokines that recruit other inflammatory cells, eventually causing necrosis of
allograft tissue. Endothelial cells in vascularized grafts such as kidneys are some of the earliest victims of acute
rejection. Damage to the endothelial lining is an early predictor of irreversible acute graft failure. The risk of acute
rejection or an is highest in the first 3 months after transplantation, and is lowered by immunosuppressive agents
in maintenance therapy. The onset of acute rejection is combatted by episodic treatment.