The immune system

is a silent wonder. While we are very aware of

our heart beating and the breaths we take, we are much less aware of our immune system that protects us from thousands of potentially deadly attacks every day. the immune system we each possess that is working around the clock, protecting us from disease and death.

Review of the anatomy and physiology of the Immune system

A complex system

yet it has a very simple mission, seek and destroy invaders Protects us

There are three lines of defense:

The first is to keep

invaders out.
(skin,

mucus membranes).

Our skin is a barrier which stops infection

from entering the body Mucus membranes their more important job is to secrete mucus that traps bacteria and other foreign debris that irritates the lining of the respiratory tract.

The second line of defense is non-

specific immune responses marcrophages, neutrophils, interferons, and complement proteins. This line of defense also includes fever and inflammatory response as nonspecific defenses. inflammation is one of the responses of the organism to the pathogen.

Any break in the skin will allow bacteria to enter the body. These foreign microbes will cause swelling and reddening at the site of injury

The third line of defense is

mounted against specific pathogens that are causing disease.

(B

cells produce antibodies against bacteria or viruses while T cells kill cells that have become infected).

Pathogens (invaders) First line of defense

Second line of defense

Third line of defense

Sickness/death

If pathogens (invaders) try and succeed in

penetrating the first line of defense, then the second line of defense is ready to act. If both the first and second line of defense fail, then the third line of defense will act. It is when all three lines of defenses are breached that we get sick and are subject to disease.

The immune system is a set

of mechanisms of defense, protecting an organism from infection by identifying and attacking pathogens. Pathogens are also constantly changing themselves to avoid detection and successfully infect and destroy their hosts.

Anatomy and Physiology

Lymphatic Organs The lymphatic system is comprised of three interrelated functions: (1) Removal of excess fluids, lymph, from body tissues, (2) Absorption of fatty acids and subsequent transport of fat, chyle, to the circulatory system (3) Formation of white blood cells (WBCs), and initiation of immunity through the formation of antibodies, lending specific resistance to pathogens.

Primary Lymphatic Organs

The primary lymphatic organs 1.the red bone marrow 2. thymus.

They and are the site of production and maturation of lymphocytes, the type of white blood cell that carries out the most important work of the immune system.

1. Bone Marrow
Bone Marrow -the soft, spongy, nutrient rich tissue in the cavities of certain long bones. is the organ and the site of blood cell production.

Fxn:

1.White blood cells produced in the marrow are: Eosinophils Basophils Lymphocytes Monocytes Neutrophils 2. Bone marrow is also the site of maturation of B lymphocytes

2. Thymus Gland
The thymus is an organ that is more active in children,

and shrinks as we get older Thymosin is thought to aid in the maturation of T lymphocytes . The Thymus is critical to the immune system. Without a thymus, a person has no ability to reject foreign substances, blood lymphocyte level is very poor, and the bodys response to most antigens is either absent or very weak.

The thymus lies in the superior thorax

b. Secondary Lymphatic Organs

Places where lymphocytes find and bind

with antigens

Secondary lymphatic organs

1.

The spleen 2. lympnodes 3.tonsils 4. peyers patches

Spleen
Ductless gland that is closely associated

with the circulatory system, where it functions in the destruction of old red blood cells A person without a spleen is more susceptible to infections and may need supplementary antibiotic therapy for the rest of their life.

2. Lymph Nodes
Lymph Nodes are small oval shaped

structures located along the lymphatic vessels.

Fxn. act as filters. when the body is fighting an infection, these lymphocytes multiply rapidly and produce a characteristic swelling of the lymph nodes.

3. Tonsils
The palatine tonsils lie directly posterior

to the mouth and palate on the lateral sides of the pharyngeal wall

Fxn. Tonsils are often the first organs to encounter pathogens and antigens that come into the body by mouth or nose

4. Peyers patches
Located on the wall of the intestines and

the appendix, attached to the cecum of the large intestine Fxn: Peyers Patches are ideally situated to destroy bacteria thereby preventing these pathogens from breaching the intestinal wall.

5. Appendix
The appendix is a tubular offshoot of the

first part of the (cecum) of the large intestine Fxn: Destroy the microorganisms that invade them
Generate a wide variety of memory

lymphocytes to protect the body.

6. Leukocytes
WBCs engulf and ingest their targets

by phagocytosis

6 Basic types of WBCs

1. Eosinophils Eosinophils fight parasites and contribute

to allergic reactions. They account for only 1-3% of all leukocytes. The life span of a typical eosinophil in the blood is about 6-12 hours.

 The life span of a typical eosinophil in the

blood is about 6-12 hours. Eosinophils are known to attach to large parasites and release substances from their granules that damage or kill the parasite. Because eosinophils kill pathogens, they are classified as cytotoxic cells.
Eosinophils also participate in allergic

reactions, by contributing to inflammation and tissue damage by releasing toxic enzymes

2. Basophils Basophils release histamine and other chemicals. The granules contain histamine, heparin(an anticoagulant), cytokines, and other chemicals involved in allergic and immune responses.

3. Neutrophils Neutrophils "eat" bacteria and release cytokines. Neutrophils are the most abundant WBC, 50-70% of the total. Fxn: Neutrophils, like other leukocytes are formed in the bone marrow. They are phagocytic cells that typically ingest and kill bacteria.

4. Monocytes Monocytes are not that common in the blood 1-6% of WBC . They engulf and destroy any type of debris or foreign material in the body.

5. Lymphocytes Lymphocytes are the key cells that mediate the acquired immune response of the body. They constitute 20-30% of all WBC.
Most lymphocytes are found in lymphoid

tissues, where they are more likely to encounter invaders.

By one estimate,the adult body contains a

trillion lymphocytes at any one time.

Types lymphocytes 6. B lymphocytes are like the body's military intelligence system, seeking out their targets and sending defenses to lock onto them.

7. T lymphocytes are like the soldiers, destroying the invaders that the intelligence system has identified.

8. Dendritic Cells
Dendritic cells activate lymphocytes. When dendritic cells recognize and

capture antigens, they migrate to secondary lymphoid tissues, where they present the antigens to lymphocytes.

Dendritic cells (DC) are phagocytes in

tissues that are in contact with the external environment; therefore, they are located mainly in the skin, nose, lungs, stomach, and intestines.

Types of Immunity
I. Innate Immunity II. Adaptive Immunity

Innate immunity
Present at birth. Does not require an exposure to an antigen

for its development. It consist of anatomic and chemical barriers.

First

line of defense

1. External Barriers
1. Skin

> First line of defenses against bacteria and other harmful organisms. > Barrier which stops infection from entering the body. > Sebaceous glands in the skin produce sweat and sebum, which, combined help to protect the skin .

2. Mucus membranes The mucous membranes line various body cavities that are exposed to the external environment and internal organs.
It is at several places continuous with

skin: at the nostrils, the lips, the ears, the genital area, and the anus. More important job is to secrete mucus that traps bacteria and other foreign debris that irritates the lining of the tract .

2. Chemical Barriers
1. Tears, saliva Tears and saliva contain lysozyme,(a

bacteria killing substance) an antiseptic enzyme that attacks cell walls of bacteria and breaks them down. 2. Stomach Acids Glands in the stomach lining produce hydrocloric acid. This acid kills most invading organisms that are swallowed and take up residence there.

Others
Voiding Vomiting Diarrhea Vaginal Secretions

3. Inflammatory Response
A reaction to themtissue of the body to

injury to destroy or dilute an injurious agent, to prevent the spread of injury an dto promote repair of damage tissue.

Any break in the skin will allow bacteria to

enter the body. These foreign microbes will cause swelling and reddening at the site of injury.

Stages of Inflammation
Injury Vascular Response Cellular Exudation Healing Reconstruction Maturation

Manifestations
Redness (Rubor) Heat (Calor) Swelling (Tumor) Pain (Dolor) Loss of Function (functio laesa)

When an injury occurs, a capillary

and several tissue cells are apt to rupture, releasing histamine and kinins. These cause the capillaries to dilate, become more permeable, and leak fluid into these tissues. Dilation and fluid leaking into the tissues causes swelling, redness, and heat. The swelling and kinins stimulate nerve endings, causing pain

Types of Immunity

II. Adaptive Immunity

Begins after birth as a result of repeated

antigenic stimulation of the immune response

FXN
Provides lifelong protection against

specific types of disease.

Exposure to non self elicits formations of

specific antibodies

Types of immunity
1. Active Immunity-occurs when the body

is exposed to a pathogen and produces its own antibodies.

a. Natural- contact with antigen (measles, chicken pox, mumps). Lifetime Protection.

b. Artificial - Immunization of an antigen. (live, killed or toxoid vaccines). Several Years of protection but needs booster dose.

2. Passive - when we acquire antibodies made by another human or animal. Passive immunity is passive because it requires no response from the person's immune system. The transfer of antibodies from mother to fetus across the placenta is one example.

a. Natural Transplacental transfer. (Breastfeeding). Temporary only. b. Artificial injection of serum from an immune animal. Temporary only. (Gamma globulins)

Functional components
1. Cell Mediated Immunity

(T Lymphocytes). Responds well in viral infections and cancer cells.

 Lymphocytes produces killer T-cells that

lock their targets and kill it with chemicals (Killer T cells) and memory T-cells retains memory for future references.

Functions of various T- cells subsets

Helper T- cells activate other T- cells-

activate macrophages - call in more Killer "T" cells and tell "B" cells it is time to make antibodies to fight this infection.

Suppressor T- Cells Suppress immune

response when no longer needed. - tells the "B" cell ok the infection has been taken care of and it is time to stop making antibodies

Cytotoxic T- cells kills virus infected

cells,tumor cells and other foreign threats. - they kill the infected cell.

Delayed T- cells caused delayed

reaction. Memory T- cells

hypersensitivity

Video presentation:

Intro 1

Phagocytosis

Video presentation

Phagocytosis 1 and 2

Classes of

Immunoglobulins (Antibodies)

1. Ig G-This is the only isotype that can

pass through the human placenta, thereby providing protection to the fetus in utero before its own immune system has developed. Characteristics: Ig G neonatal immunity. Serum concentration: 13.5 mg/ml Location: plasma This immunoglobulin is the majority of the specific immunity against bacteria and viruses in the extracellular fluid.
Known Functions: Enhances phagocytosis,

neutralizes toxins and viruses, protects fetus and newborn.

2. Ig A- Found in mucosal areas, such as

the gut, respiratory tract and urogenital tract, and prevents colonization by pathogens. Also found in saliva, tears, and breast milk. Ig A lines mucus membranes. Serum concentration: 3.5 mg/ml
x Location: Secretions (tears, saliva, intestine,

milk), blood and lymph. x Half-life in serum: 6 days Known Functions: Localized protection of mucosal surfaces. Provides immunity to infant digestive tract.

3. Ig M- IgM antibodies are mainly

responsible for the clumping (agglutination) of red blood cells if the recipient of a blood transfusion receives blood that is not compatible with their blood type. Ig M forms antibodies to ABO blood antigens. Serum concentration: 1.5 mg/ml
Location: Blood, lymph, B cell surface (monomer) x Half-life in serum: 5 days Known Functions: First antibodies produced during an infection. Effective against microbes and agglutinating antigens.

4. Ig E- Binds to allergens and triggers histamine release and is involved in allergy. Also protects against parasitic worms. Characteristics Ig E immediate hypersensitivity - defends against parasitic infections. Serum concentration: 0.05 mg/ml
x Location: Bound to mast cells and basophils

throughout body. Blood. x Half-life in serum: 2 days Known Functions: Allergic reactions. Possibly lysis of worms.

5. Ig D- IgD's function is to signal when the young B cells in the spleen are ready to be activated. By being activated, they are ready to take part in the defense of the body in the immune system. Characteristics: Ig D Assist with B lymphocyte differentiation. Serum concentration: trace
x Location: B-cell surface, blood, and lymph x Half-life in serum: 3 days Known Functions: In serum function is

unknown. On B cell surface, initiate immune response.

WBC Response to Infections

Increase neutrophils (neutrophilia)

- typical in acute local/systemic infections.

Decrease neutrophils ( neutropenia)

- Hepa A infection,rubella,mumps

Increase eosinophils (eosinophilia )

-frequent allergic reaction,skin disease

Increase lymphocytes ( Lymphocytosis)

- Chickenpox,PTB,Syphilis,viral pneumonia.
Increase in monocytes ( monocytosis )

-common in Ptb,mumps,protozoal dse.

Decrease in

Lymphocytes( lymphocytopenia) - common in HIV infection.

A.

Immunodeficiencies

Objectives
After lecture discussion the students will be able to: 1.Define AIDS/HIV 2.Defferentiate HIV fom AIDS 3.Enumerate tha stages of AIDS 4.Identify the mode of transmission of HIV/AIDS

Things That Can Go Wrong With the

Immune System

Disorders of the immune system can be

broken down into four main categories:

1. Immunodeficiency disorders. (deficiency of one or more immune components)

2. autoimmune disorders (in which the body's own immune system attacks its own tissue as foreign matter) . 3. allergic disorders (in which the immune system overreacts in response to an antigen) . 4. Gammopathy (abnormal production of antibody)

HIV / AIDS
condition in humans in which the

immune system begins to fail, leading to life-threatening opportunistic infections. Other names: human T-lymphotropic virus-III (HTLV-III) lymphadenopathy-associated virus (LAV) and AIDS-associated retrovirus (ARV).

First appeared in humans

in Africa in the 1930's or 40's as a result of infection by simian immunodeficiency virus (SIV) from chimpanzees .

Is HIV and AIDS the same thing?

HIV Human Immunodeficiency

Syndrome A specific type of virus (a retrovirus) HIV invades the helper T cells to replicate itself. No Cure

AIDS
Acquired Immunodeficiency

Syndrome
HIV is the virus that causes

AIDS
Disease limits the bodys ability

to fight infection
A person with AIDS has a very

weak immune system

No Cure

 Acquired - because it's a condition one must

AIDS = Acquired ImmunoDeficiency Syndrome

acquire or get infected with, not something transmitted through the genes

Immune - because it affects the body's

immune system, the part of the body which usually works to fight off germs such as bacteria and viruses system deficient

Deficiency - because it makes the immune Syndrome - because someone with AIDS may

experience a wide range of different diseases and opportunistic infections

Epidemiology
38 million people live with HIV/AIDS world

wide Sub Saharan Africa is home to 70% of people living with HIV. 2.1 million of children are infected with HIV/AIDS in the world.

HIV/AIDS Cases in the Philippines

First reported AIDS case in 1984 Department of Health has recorded a

cumulative total of 2,719 HIV and AIDS cases as of December 2006 Sixty seven percent (67%) were of ages 20 to 39, while 64% were males Sexual intercourse remains the leading mode of HIV transmission (87%) Experts from the World Health Organization (WHO) and the Department of Health (DOH)

On February 13,1998, President Fidel

V. Ramos signed into law Republic Act 8504 also known as the Philippine AIDS Prevention Control Act of 1998. This act aims to promote public awareness about AIDS. RA 8504, Rule 8, Sec.47- No educational institution shall refuse admission to any prospective student or discipline; segregate; deny participation; or expel any current

Infection with HIV occurs by

the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk.

Pathophysiology of HIV/AIDS
A retrovirus unknown until early 1980s: 1. Cannot replicate outside of living host cells 2. Contains only RNA; no DNA 3. Destroys the bodys ability to fight infections and certain cancers 4. Infects CD4 cells the primary target of HIV infection Patients infected with HIV are at risk for illness and death from: 1. Opportunistic infections 2. Neoplastic complications

CD4 Count in HIV infection known as "T4" or "helper T cell is The CD4 cell , also
responsible for signaling other parts of the immune system to respond to an infection. millimeter of blood
Normal counts range from 500 to 1500 cells per cubic Initially in HIV infection there is a sharp drop in the CD4

count and then the count levels off to around 500-600 cells/mm3.
CD4 count is a marker of likely disease progression.

CD4 percentage tends to decline as HIV disease progresses.

CD4 counts can also be used to predict the risks for

particular conditions such as Pneumocystis carinii pneumonia, CMV disease or MAI disease.

Acquired Immunodeficiency can be caused by :

 Progression of AIDS

1. Infection 2. viremia (increase of the virus load

in blood)
3. immune response to HIV:

generation of Tc cells and antibody to HIV (seroconversion)

4. temporary reduction of virus-

infected CD4 T cells (due to HIVinduced apoptosis and T cell attack)

5. partial recovery of CD4 T cell

number
6. gradual decrease of CD4 T cell

number over 2-15 years (clinical latency is a period of active infection and CD4 T cell renewal)

Acquired Immune deficiency syndrome

1.

HIV infection through the host CD4 molecule and chemokine receptors (CCR5 or CXCR4) T cell activation is required for viral replication Initial viremia and CD4 T cell number decrease (asymptomatic or mild flu-like) Anti-HIV response and CD4 T cell number recovery Long clinical latency (2- 15 yrs): a period of active viral infection and CD4 T cell renewal; gradual CD4 T cell number decrease Immunodeficiency starts when the CD4 count is below 500 Opportunistic infection Death due to secondary infection

2. 3.

4. 5.

6.

7.

Stage 1 - Primary
Short, flu-like illness - occurs one to six weeks

after infection
no symptoms at all Infected person can infect other people

Stage 2 - Asymptomatic
Lasts for an average of ten years This stage is free from symptoms There may be swollen glands The level of HIV in the blood drops to very low

levels
HIV antibodies are detectable in the blood

Stage 3 - Symptomatic
The symptoms are mild The immune system deteriorates emergence of opportunistic infections and

cancers

Stage 4 - HIV AIDS

The immune system weakens The illnesses become more severe leading to

an AIDS diagnosis

Opportunistic Infections associated with AIDS

Bacterial
Tuberculosis (TB) Strep pneumonia

Viral
Kaposi Sarcoma Herpes Influenza (flu)

Parasitic
Pneumocystis carinii

Fungal
Candida Cryptococcus

Modes of HIV/AIDS Transmission

Through Bodily Fluids

Blood products Semen Vaginal fluids Breast Milk

Through IV Drug Use

Sharing Needles
Without sterilization

Increases the chances of

contracting HIV

Through Sex
Intercourse (penile penetration

into the vagina) Oral Anal

Mother-to-Baby
Before Birth During Birth Postpartum
After the birth

High Risks
Homosexual (Anal) Bisexual (Anal) IV Drug users Infants with HIV infected parents BT before 1985

Exposure Route Estimated infections per 10,000 exposures to an infected source

Blood Transfusion

9,000 Childbirth 2,500

Needle-sharing injection drug use

67

Percutaneous needle stick Anal intercourse Penile-vaginal intercourse Oral intercourse

30 50 5 0.5

Signs and Symptoms

Fever Diarrhea Muscle aches Rashes Weight Loss Fatigue

Anonymous Testing
No name is used Unique identifying number Results issued only to test

recipient

23659874515
Anonymous

Confidential Testing
Persons name is recorded along

with HIV results Name and positive results are reported to the State Department and the Centers for Disease Control and Prevention Results issued only to test recipient

Administration
Blood Urine Oral

Blood Detection Tests

Enzyme-Linked Immunosorbent

Assay/Enzyme Immunoassay (ELISA/EIA) Radio Immunoprecipitation Assay/Indirect Fluorescent Antibody Assay (RIP/IFA) Polymerase Chain Reaction (PCR) Western Blot Confirmatory test

Urine Testing
Urine Western Blot As sensitive as testing blood Safe way to screen for HIV Can cause false positives in certain people at high risk for HIV

Oral Testing
Orasure The only FDA approved HIV antibody. As accurate as blood testing Draws bloodderived fluids from the gum tissue.

Counseling
Pre-test Counseling

Transmission Prevention Risk Factors Voluntary & Confidential Reportability of Positive Test

Results

Post-test Counseling

Clarifies test results Need for additional testing Promotion of safe behavior Release of results

Treatment Options

Antiretroviral Drugs
Nucleoside Reverse Transcriptase

inhibitors

AZT (Zidovudine)

Non-Nucleoside Transcriptase inhibitors Viramune (Nevirapine) Protease inhibitors Norvir (Ritonavir)

Opportunistic Infection Treatment

Issued in an event where antiretroviral

drugs are not available

Opportunistic Infections

Four ways to protect yourself?

Abstinence Monogamous Relationship Protected Sex Sterile needles

Abstinence
It is the only 100 % effective method of not acquiring HIV/AIDS. Refraining from sexual contact: oral, anal, or vaginal. Refraining from intravenous drug use

Monogamous relationship
A mutually monogamous (only

one sex partner) relationship with a person who is not infected with HIV HIV testing before intercourse is necessary to prove your partner is not infected

Protected Sex
Use condoms (female or male)

every time you have sex (vaginal or anal) Always use latex or polyurethane condom (not a natural skin condom) Always use a latex barrier during oral sex

Precaution
Do not donate blood Avoid pregnancy

Health Care Precautions

Hand washing Gloves No recapping of needles Use bleach Do not share

razors/toothbrush

Nursing interventions
Monitor cognitive and affective

domain Encourage communication of fears and concerns Maintain non-judgemental attitude Assist client/family through greiving process Provide opportunities for decision making to client/or care givers.

Preventions
Hospital policies protect you from HIV and AIDS

To prevent the spread of HIV, strict infection control guidelines are followed in hospitals. All blood and body fluids are treated as potentially infectious: Syringes and needles are used once only. Instruments are cleaned and sterilised after every use.

Healthcare workers wear

protective gowns, gloves and eyewear when carrying out procedures involving blood and body fluids. Spilt blood and body fluids are cleaned up according to strict procedures. Laundry is cleaned according to strict infection control procedures.

Management of patient with allergic disorders

ALLERGIES
An allergic reaction is an abnormal

immune response to a substance that does not generally cause a reaction in most people.
The job of the immune system cells is to find

foreign substances such as viruses & bacteria and get rid of them Normally, this response protects us from dangerous disease. People with allergies have super-sensitive immune systems that react to harmless substances An allergen is the substance causing the allergy. The tendency to be allergic is usually inherited; the

Symptoms of Allergies can be

Mild Moderate Severe

1.MILD Rash Itchy, watery eyes Congestion Mild reactions do not spread to other parts of the body. 2. Moderate Allergic Reactions can include symptoms that spread to other parts of the body including: Itchiness Difficulty breathing Hives

3. Severe Allergic Reaction (Anaphylaxis) Anaphylaxis is a life-threatening emergency

in which the body's response to the allergen is sudden and affects the whole body. It may begin with sudden itching of the eyes or face and within minutes progress to more serious symptoms, including: Varying degrees of swellings that can make breathing and swallowing difficult Abdominal pain Cramps Hives Vomiting Diarrhea Mental confusion or dizziness Loss of consciousness Death

CAUSES OF ALLERGIES
INGESTANTS: substances that enter the

body by mouth INJECTED: enter the body through puncture INHALANTS: the allergen is breathed in through the nose or mouth CONTACT ALLERGIES: enter the body through the skin

Anaphylaxis
Acute life threatening allergic reaction

marked by progressive urticaria and respiratory distress. Acute hypersensitivity reaction Occurs within minutes Produced by any substance Individual susceptibility Antibiotics, stings, contrast dye

Causes of anaphylaxis
Immunologic mechanisms IgE-mediated

- drugs - foods - hymenoptera (stinging insects) - latex - anaphylotoxins-mediated e.g. mismatched blood

Non-IgE mediated

Direct activation of mast cells

dextran, dyes Mediators of arachidonic acid metabolism - Aspirin (ASA) - Nonsteroidal anti-inflammatory drugs (NSAIDs)
Mechanism unknown

- opiates, tubocurare, radiocontrast

- Sulphites

Frequency of symptoms in Anaphylaxis

Urticaria/angioedema Upper airway edema Dyspnea or wheeze Flush Dizziness, hypotension, syncope Gastrointestinal sx Rhinitis 88 % 88 % 88 % 88 % 88 % % 88 %

Anaphylaxis
Onset of symptoms of anaphylaxis:

usually in 5 to 30 minutes; can be hours later A more prolonged latent period has been thought to be associated with a more benign course. Mortality: due to respiratory events (70%), cardiovascular events (24%)

Respiratory Distress
Laryngeal edema Epiglottis & subepiglottic Primary cause of death Sx like asthma Dyspnea, wheezing, tightness in chest

Hypotension
> Cardiovascular collapse > Second most common cause of death from anaphylaxis > Prevention is better than resuscitation

Cutaneous & GI Reactions

> > > > > > > > Urticaria Flushing Itching Angioedema Nausea Cramping Vomiting Loose stools

Differential Diagnosis
> Airway obstruction > Asthma > Angioedema > Fish poisoning > Chinese food > Carcinoid Syndrome

Prehospital Treatment
Oxygen High flow Assisted ventilation Endotracheal intubation IV 2 large bore Rapid Administration Monitor for dysrhythmias Pulse oximetry

Treatment
Epinephrine Alpha effects Beta effects IM/SQ 1:1000 solution Initial Dose: 0.01 mg/kg SQ or IM Average adult dose: 0.3-0.5 ml q15 min IV/ET 1:10,000 solution Average adult dose: 3-5 ml over 3-5 mins, q 5-10 mins

Fluid Administration

Aggressive Caution with the elderly Caution with renal disease

patients Caution with patients with cardiovascular disease May cause pulmonary edema

Vasopressors
Indicated if no response to fluids Epinephrine drip 1mg (1ml) 1:000 in 500 ml D5W Rate: 0.5-2.5 ml/min (1-15 ug/min)

Persistent Bronchospasm Beta-agonist Treatment

Alupent 0.3 ml of a 5% solution nebulized in

2.5

ml of normal saline
Ventolin

0.5-1.0 ml nebulized in 2 ml of normal saline

Intravenous Aminophylline
Advantages
Increases cAMP (smooth muscle relaxation) Potentiates action of exogenous

catecholamines Stimulates endogenous catecholamine release Disadvantages Dysrhythmias Seizures Vasodilatation Hypotension

Steroid
Methyprednisolone
50 to 125 mg IV May repeat in 6 hrs

Hydrocortisone
250-500 mg IV May repeat in 6 hrs

Antihistamines
Competitively inhibit histamine Do not decrease mediator release Do not reverse mediator effects Inadequate for treatment of acute

anaphylaxis Reduces itching and urticaria

Nursing interventions
> Observe for 24 hrs > Steroids / Antihistamines for 72 hrs >Avoid allergens > Teach signs of early reaction > Allergy alert tag > Referral to

In Conclusion
Anaphylaxis: a medical

emergency Progresses rapidly May progress from minor symptoms to shock Treatment consists of: Recognition & Resuscitation

Allergic Rhinitis

Allergic Rhinitis hay Fever

Rhinitis is an inflammation of the

mucous membranes of the nose. Allergic rhinitis involves reactions in the nasal mucosa from repeated allergen exposures that causes hypersensitivity.
Allergic reaction to inhaled airborne

allergens.
The most common form of respiratory

allergy.

Etiology:
Tree pollens Grass pollen in summer Other pollens

Manifestations:
Itching Sneezing Red burning and tearing eyes Pale mucosa
Weakness Discomfort Irritability Fatigue Difficulty

or uneasiness

concentrating Decreased appetite

Management
Administer antihistamines and

steroids. Advise client to blow his nose before giving nasal medications. Avoid allergen exposure

Contact Dermatitis
Brought on by an allergic reaction
Poison ivy, sumac, soap, clothing

S/S - redness, blistering, itchy Tx

hot vs. cold? Topical/oral corticosteroids Oral meds antihistamines,

diphenhydramine (decreases allergic response)

Atopic Dermatitis
Most common form of eczema Chronic disease Genetic disorder of skin sensitivity to many

sources S/S Papules, vesicles, scaly lesions Extreme itching can lead to secondary infection
Tx

Corticosteroids for itching Antibiotics for infection Aveno* soap, no dyes, natural material for

clothing

Dermatitis medicamentosa
Medicamentosa Dermatitis

Also known as: Cutaneous drug reaction, Drug Eruption Adverse reactions to medications or drugs may include a range of symptoms and may even be fatal. Reactions often affect the entire body, including the skin.

Sign and symptoms

1. Maculo -- papular eruptions-a less severe skin reaction that resembles a viral-like rash (e.g., Measles). The rash appears as pin-sized, raised, sometimes itchy and reddish lesions. There are also flat red patches seen on the arms and upper body. Mouth lesions may also appear. The rash appears for several days (up to 3 weeks) after the drug has been started.

S/S
2.Fixed drug reactions -- usually seen in the same spot every time the drug is taken. They often appear 1-2 hours after drug ingestion, application, or injection. The lesions are pink, round or oval patches that may occur anywhere on the skin, and tend to change to a darker color after several weeks to months, then disappear.

3.

Hives appear as itchy red, thick, swollen wheals or patches. There may be puffiness of eyelids and lips as well. This occurs within one hour after taking the drug and if it affects the windpipe, choking and difficulty breathing may lead to death. Most cases resolve within 24 hours.

4.Angioedema is similar to Hives but effects deeper layers of skin and the mucous membranes (e.g., lining of the eyes, mouth, and genitals).

5. Erythema Multiforme (Stevens-

Johnson syndrome) is a severe skin reaction that starts as red, round patches (target lesions) which spread and join together, form blisters (Bullous lesions), and peel off. They affect the mucous membranes, and if not treated could be fatal.

How the diagnosis is made

Clinical exam and a detailed

medical history (i.e., medications, lotions, herbs, etc.) Skin testing -- done if IgE mediated reaction is suspected as the cause Stopping the drug is often helpful in diagnosing.

Risk factors
Illnesses that require drug

therapy Previous drug reactions Drugs, hair dyes, food coloring or additives, shampoos, lotions, oils, supplements, soaps detergents, and herbal

Nursing Interventions
Stop the offending agent Therapy depends on the type and severity of the

reaction Breathing problems, wheezing, choking, difficulty swallowing, and sudden drop in blood pressure are all indications for emergency treatment. Mild cases -- medications for itching or pain may be recommended. Remember to make sure not to take the offending medication ever again. A "med alert" bracelet is helpful. Be aware that other drugs containing the same or similar compounds will cause like reactions, so check with your pharmacy and doctor for crossover. Make sure that your doctors are all aware of all your allergies.

Heridetary Angioedema
Hereditary angioedema is an inherited deficiency of a blood protein called C1 inhibitor (C1-INH) which causes episodes of swelling (edema) in parts of the body. It is due to a genetic defect of chromosome 11.

Alternative Names: Quincke's disease

Hereditary angioedema is a

rare but serious problem with the immune system that is passed down through families. It causes swelling, particularly of the face and airways, and abdominal cramping. Inherited disorder causes swelling, pain

Sign and symptoms

The symptoms occur in episodes or attacks which often happen for no reason. Before the attack: tightness or tingling at the site where the swelling will later occur flat, red blotchy rash (erythema marginatum) breaks out mood changes, anxiety, exhaustion

S/S
During the attack:

swelling of body parts such as

hands, feet, face, arms, or legs internal swelling in abdomen may cause pain, nausea, and vomiting swelling of the airway may cause difficulty swallowing, change in voice pitch, or difficulty

Diagnostic test
blood tests genetic tests are needed to

confirm the diagnosis

Medical Management
corticosteroids (like

prednisone), antihistamines, and epinephrine (prophylactic) drugs such as danazol (Danocrine) or oxandrolone (Oxandrin) may be given.

Latex allergy
Latex products are manufactured from a milky fluid derived from the rubber tree, Hevea brasiliensis. Several chemicals are added to this fluid during the processing and manufacture of commercial latex.

Examples of products that may contain latex:

Office Supplies
Rubber bands Erasers

Household Objects

Automobile tires Motorcycle and bicycle handgrips Carpeting Swimming goggles Racquet handles Shoe soles Expandable fabric (waistbands) Dishwashing gloves Hot water bottles Condoms Diaphragms Balloons Pacifiers Baby bottle nipples

Individuals who already have latex allergy should be aware of latex-containing products that may trigger an allergic reaction.

Latex in the Workplace

Workers in the health care industry are at risk for developing latex allergy because they use latex gloves frequently. Some examples are:
physicians nurses dentists technicians

Clinical manifestations
Latex allergy should be suspected in anyone who develops certain symptoms after latex exposure. These include:
nasal, eye, or sinus irritation hives shortness of breath coughing wheezing unexplained shock

Any exposed worker who experiences these symptoms should be evaluated by a physician, because further exposure could result in a serious allergic reaction.

Diagnostic tools for physicians

Complete medical history Physical examination Possible tests.
Blood tests approved by the Food and Drug Administration (FDA) are available to detect latex antibodies. Standardized glove-use test or skin tests that involve scratching or pricking the skin through a drop of liquid containing latex proteins. A positive reaction is shown by itching, swelling or redness at the test site.

Treatment of Latex Allergies

Once a worker becomes allergic to latex, special precautions are needed to prevent exposures during: work medical care dental care Complete latex avoidance is the most effective approach. (This is difficult) Certain medications may reduce the allergy symptoms Many facilities maintain latex-safe areas for affected patients and workers.

Nursing Management
Use appropriate work practices to reduce the chance of reactions to latex: When wearing latex gloves, do not use oil-based hand creams or lotions (which can cause glove deterioration) unless they have been shown to reduce latex-related problems and maintain glove barrier protection. After removing latex gloves, wash hands with a mild soap and dry thoroughly. Use good housekeeping practices to remove latexcontaining dust from the workplace: Frequently clean areas contaminated with latex dust (upholstery, carpets, ventilation ducts, and plenums). Frequently change ventilation filters and vacuum bags used in latex-contaminated areas.

Take advantage of all latex allergy education and training provided by your employer:
Become familiar with procedures for preventing latex allergy. Learn to recognize the symptoms of latex allergy:

Skeletal System

ristics

Rheumatoid Arthritis A type of chronic systemic inflammatory arthritis and connective tissue disorder affecting more women than men.

Osteoarthritis Chronic non-systemic disorder of joints characterized by degenerationnof articular cartilage.

Gouty arthrit

A systemic dise caused by dep uric acid crysta joint and body

manifestations

Crepitus, stiffness in the Joints are swollen and morning decreases after warm activity Painful when moved Deformities are common 1.Joint pain 2. Joint stiffness in the hands and feet 3. Functional joint causing misalignment impairment limitation

Severe pain in involved joints the big toe. 2. Swelling and inflammation o 3. TOPHI- yello whitish, irregul deposits in the break open and gritty appearan 4. PODAGRA-b 5. Fever, malai 6. Body weakn headache 7. Renal stones

Diseases

Definition

Manifestations Pathophysiolo Medical and gy Nsg. Mgt. The 1.NSAIDs overproduction of collagen is thought to result from an autoimmune dysfunction, in which the immune system would start to attack the kinetochore of the chromosomes. This would lead to genetic malfunction of nearby genes

Scleroderma

is a rare, chronic 1.skin appears disease reddish or scaly characterized by 2.non specific excessive joint pains deposits of 3.shortness of collagen in the breath skin or other organs

Skin: Scleroderma in Skin: Scleroderma; shoulders crest syndrome; calcinosis at elbow & back

Hands: Scleroderma

Systemic Lupus Erythematosus

Course of Disease & Causes of Death Clinical Symptoms What causes these symptoms?

What Causes SLE

Cause is unknown Possible factors
>Genetic >Environment

What causes SLE is still unknown but it is thought to have

a multi-faceted etiology. There are possible genetic and environmental factors

Genetic factors: Predispose

an individual to have this disease 10% of individuals who have this disease have a family member who also has this disease. Clear gender and cultural bias for this disease: women are 10 times more likely than men to get this disease. African American women (40% of all cases) and Hispanic women are more likely to get this disease than Caucasian women.

Environmental factors can trigger the

disease in genetically predisposed individuals: Most correlated is the presence of female hormone ultraviolet light, certain drugs, various infectious agents

What Happens?
Loss of self-non-self recognition Diversification of antigen-driven

responses Hyperactivity of T & B Cells Formation of immune complexes Type III hypersensitivity reaction

Therapies for SLE

1st Therapies
Cytotoxic drugs

Current Therapies
Immunosuppressions
Cyclophosphamide Mycophenolate

Mofetil

Future Therapies
Hormonal modulation Cytokine inhibition

Acute Cutaneous: Malar Rash Note Sparing of Nasolabial Folds

Chronic Cutaneous:Discoid Note Scarring, Hyperpigmentationn

Subacute Cutaneous Lupus