Immunology Notes 104

2/26/2013

IMMUNOPATHOLOGY

- refers to study of immune disease process

IMMUNOLOGY

- study of immune system

FUNCTION OF IMMUNE SYSTEM

1. defense

2. surveillance

3. homeostasis

2 SYSTEMS OF IMMUNITY

- non-specific

- specific

IMMUNULOGY CONCEPT, DESCRIPTION AND BRIEF HISTORY

- the word “immunity” (L: immunis - free of) was in the context of being free of the burden of taxes or

military constriction

- history of immunology is really slightly more than 100 yrs if you consider LOUIS PASTEUR as “THE

FATHER OF IMMUNOLOGY”

- LOUIS PASTEUR and ROBERT KOCH were instrumental in defining microbes as the etiological

agenet of the large number of diseases

- LOUIS PASTEUR became the 1st experimental immunlogist. He proceeded to develop valid

methods of immunization

- In 1878, PASTEUR, accidentally used an attenuated (weakend) chicken cholera culture and ralized,

that when he repeated the experiement using a fresh culture the weakened form protected the

chickens from the virulent form of diseases.

- PASTEUR went on to develop an attentuated vaccine against rabies and swine erysipelas

- KOCH was the 1st to isolate anthrax microbe and unaware of Pasteur’s work, in 1882, KOCH, was

abletodemonstrate that Germ theory of disease applied to human ailments as well as animas when

he isolated microbes

MILESTONE IN THE HISTORY OF IMMUNULOGY

- 1798 Edward Jenner initiates smallpox vaccination

- 1877 Paul Erlich recognizes mast cells

- mast cells found in connective tissue; chemical mediators like prostaglandins

- 1879 Louis Pasteur develoops an attenuated cholera vaccine

- 1883 Elie Metchnikoff develops ceullar theory of vaccination

- 1885 Louis Pasteur develops an attentuated chicken cholera vaccine

- 1891 Robert Koch explored delayed hypersensitivity

- 1900 Paul Erlich theorizes specific antibody formation

- 1906 Clemens Von Pirquetcoined the world ALLERGY

- 1938 John Marrackformulates the antigen-antibody binding hypothesis

- 1962 Rodney Porter and tem discover the structure of antibodies

- 1962 Noel Warner and team distinguish between CELLULAR and HUMORAL IMMUNE

RESPONSE

- 1968 Anthony Davis and team discover T and B cell cooperation in immune response

- 1985 Susumu Tonegawa, Leroy Hood and team identify immunoglobulin genes for the T cell

receptors

COMMON TERMINOLOGIES IN THE CONCEPT OF IMMUNOLOGY

- aggamaglobulinemia

- ataxia

- ataxia telangiectasia

- anergy

- antibody

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- antigen

- complement

- cytokine

- candidiasis

- erythema

- hypersensitivity

- lymphokinines

FUNCTION OF IMMUNE SYSTEM

ANATOMY & PHYSIOLOGY OF IMMUNE SYSTEM

- bone marrow

- lymph nodes

- thymus

- spleen

- peyer’s patches

- tonsils

BONE MARROW

- is a soft spongy tissue that lies with in the interior hollow of long bone

- it has 2 TYPES: red marrow and yellow marrow

- red marrow -- responsible in producing RBC, WBC, and platelet

- yellow marrow -- responsible mainly for fat cells

- it produces stem cells that later mature into B lymphocyte or T lymphocytes cells

- B-cells mature in the bone marrow and then enter into the ciruclation

- go directly to your circulation

- T cells move from bone marrow to the thymus where they mature intoseveral kinds of cells with

different functions

- go into thymus gland --> matures --> circulation

- the WBC involved in immunity are produced in the bone marrow

- stem cells are produced by bone marrow

FUNCTION OF BONE MARROW

- RBC carry oxygen to the tissues (erythrocytes)

- WBC (leukocytes) and platelets - helps prvent bleeding and aid in clotting of blood

LYMPH NODES

- is an oval - shaped organ of the immune system, distributed widely throghut the body including the

armpit, stomach, and linked by lymphatic vessels

- it acts as a filter or traps for foreign particles and are important in the proper functioning of immune

system. They are packed tightly with the WBC called LYMPHCYTES and MACROPHAGES

* normal response by your body from infections

FUNCTION OF LYMPH NODES

- lymph fluid inside of the lymph nodes contain lymphocytes, a type of WBC which are

continuosly recirculated thru the lymph nodes and the blood stream

- this lymphocytes in the lymph nodes make antibody which will go out from lymph nodes into

theciruclation, seek and target teh pathogen producing antigen by targeting it, for

destruction by other cells andthe complement

* B cells produces antibodies

* T cells - direct attacks antigen

* memory cells under T cells

* if slow memory cells - mobalik - need titer

THE SPLEEN

- is the organ of lymphatic system located in left side of abdominal cavity under diagphragm, the

muscular partition between teh abdomen and the chest

- in human about size of fist and well supplied with blood

- primary filtering elemtn for blood

- plays an important role in storing and releasing certain types of immune cells

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- it has red and white pulp

- white pulp - lymhpoid tissue that usu surrounds splenic blood vessels

- red pulp - where filtration occurs

FUNCTION OF SPLEEN

- DESTROY wornout RBCs and return some of their breakdown product in the liver

- it also STORE platelets and it acts as BLOOD RESERVOIR

- during hemorrhage, both liver and spleen contract and empty their contained blood into the

circulation to help bring blood volume back to normal level

THYMUS GLAND

- shaped like a pyramid, is the specialized organ of human immune system

- pinkish-gray in color, that is situated in the thoracic region, under the sternum or the breast bone

- in new born babies, this gland is larger as compared to an adult

- it continues to grow till puberty and then it undergoes involution, which is a process where the

thymus starts a reverse procedure and begin to shrink in size

* PRODUCES T- Cells

FUNCTION OF THYMUS GLAND

- produces T CELLS aka T-lyphocytes

- prevent abnormal growth of cels that may lead to cancer

- it also produces a hormone called THYMOSIN which stimulates the T-CELLS in the other

lymphatic organs to mature

* Other T - Cells are found in other parts of your body not just the thymus gland

THE TONSILS

- are two glandular tissues similar to the hundreds of other lymph glands in the human body, present

on either side of the back of the throat

- they are visible just behind the tongue, they produce the special cells called LYMPHOCYTES, which

form an immunological network of self-defense

FUNCTION OF TONSILS

- works as FILTER which fights and protects the entire human system against the foreign

invader

- helps prevent spread of infection from nearby organism such as mouth, sinuses, and post

nasal part

- also produces antibodies, which fights against infection, stopping it further spread to other

part of body

* produces both B and T lymphocytes

* kongmohubag - B cells is activated

PEYER’S PATCHES

- organizedlmhpoid nodules, named after 17th century SWISS anatomist JOHANN CONRAD

PEYER

- they are the aggregation of lymphoid tissues that are usu found in lowest portion of SMALL

INTESTINE, the ILEUM, and even in JEJUNUM

- appear as oval or round lymphoid follicles located in LAMINA PROPRIA layer of mucosa

* MALT - mucosa associated lymphatic tissue

* TONSILS are protecting UPPER GASTRO SYSTEM

* PEYER’S are protecting LOWER GASTRO SYSTEM

FUNCTION OF PEYER’S PATCHES

- capture and destroy bacteria thereby preventing them from penetrating intestinal wall

MALT

- akamucosa associated lymphatic tissue

- this is compose of Peyer’s patches and tonsils

- acts as a sentinel to protect upper RR and giestive tracts

NON SPECIFIC DEFENSE SYSTEM

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- respond immediately to protect the body form all foreign substances

- are provded by intact skin and mucous membranes

- it reduces the work load of 2nd protective arm (specific defense) by preventing entry and spread of

microbesthruout the body

* INBORN defense

1ST LINE OF DEFENSE

SURFACE MEMBRANE BARRIERS

- intact skin

- intact mucous membrane

- secretion of skin and mucous membrane

INTACT SKIN

- epidermis

- acid mantle

- keratin

INTACT MUCOUS MEMBRANE

- mucous

- nasal hairs

- cilia (propels debris)

SECRETION OF SKIN AND MUCOUS MEMBRANE

- gastric juices

- acid mantle in the vagina

- lacrimal secretions (tears and saliva)

SECOND LINE OF DEFENSES

CELLULAR DEFENSES

- phagocyte

- natural killer cells

- inflammatory responses

PHAGOCYTES

- are WBCs that protect the body by ingesting harmful foreign particles bacteria and

dead or dying cells

- 1 liter of human blood contains about 6 billions phagocytes

* macrophages

NATURAL KILLER CELLS

- form the body’s front line of defense

- it promote cell lysis by direct cell attack against virus infected or cancerous body

cells

- NKC are always at the ready, they have an innate ability to recognize viruses and

tumor cells

- NKC are not phagocytic, they attack the target cell membrane and release a lytic

chemicals called PERFORINS

* part of CELLULAR IMMUNITY

INFLAMMATORY RESPONSE

- fundamentaltyep of reponse by the body to disease and injury, a response

characterized by the classical signs of DOLOR, CALOR, RUBOR, AND TUMOR --

pain, heat (localized warmth), redness & swelling

- it releases chemical mediators that attracts the phagocytes to the area

- CHEMICAL MEDIATORS:

- histamine

- prostaglandin

- kinines

- cytokines

* under CELLULAR RESPONSE

CHEMICAL DEFENSES

- complement

- interferon

- fever

ANTIMICROBIAL CHEMICAL DEFENSES

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a. COMPLEMENT - group of plasma protein that lysis microbes, enhances

phagocytosis by opsonization and intesifies inflammatory responses

FUNCTION OF COMPLEMENT

- opsonization (enhancing phagocytosis of antigen)

- chemotaxis (attacking foreign cells)

- celllysis (rupturing membrane of foreign cells)

- clumping of antigen

b. INTERFERON - belong to large class of GLYCOPROTEINS known as

CYTOKINES. It is named after their ability to INTERFERE with viral replication

within host cells

- a biologic response modifier

- it has a non-specific viricidal protein that is naturally produced by body

- protein released by virus infected cells that protects uninfected tissue cells from

FUNCTION OF INTERFERON

- activate immune cells such as NKC and macrophages (activate B and T

cells)

- increase recognition of infection or tumor cells by regularting antigen

presentation to T lymphocytes

- increase ability of uninfected host cells to resists new infection by virus

c. FEVER - systemic response triggered by pyrogens, high body temp which inhibits

multiplication of bacteria & enhance body repair

- it also increases metabolic rate of tissue cells thus speeding up repair processes

* helps spread up repair

* normal response of body

SPECIFIC DEFENSE SYSTEM (HUMORAL IMMUNE RESPONSE)

- the IMMUNE SYSTEM - is a functional system rather than an organ system in anatomical sense

- its STRUCTURES are variety ofmoleculres and trillions of immunecellws which inhabits lymphatic

tissues and circulate in body fluids

- it response to a threat called the IMMUNE RESPONSE - which tremendously increases the inflamm

raponse and it provides protection taht is carefully targeted agianst specific antigen

- when our immune system is operating effectively, it protects us from most bacteria, viruses,

transplanted organs or grafts, adn even our own cells that have turned against us

- the immune system does this both directly by cell attack, and indirectly by releasing mobilizing

chemicals and protective antibody moleculres

- the immune system must first MEET or be primed by an intial exposure to a foreign substances

(antigen) before it can protect the body against it

* functional -- only function if naamo trigger nga antigens

THIRD LINE OF DEFENSE

- lymphocytes

- antibodies

- macrophages

LYMPHOCYTES

- are type of WBC that is of fundamental importance in the immune system, because

lymphocytes are the cells tahtdetermien the specificity of immune response to

infectiousmirobes and other foreign substances

- in human lymphocytes make up 25-33% of total number of leukocytes

- 2 PRIMARY TYPES

- B lymphocytes or B cells

- T lymphocytes or T cells

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- are short-lived with an average life span of 1 week - few months, but a few lived for

years

ANTIBODY

- also known as IMMUNOGLOBULIN (Ig) is a largye Y shape protein produced by Bcells

that is used by the immune system to identify and neutralized foreign objects

such as bacteria and viruses

- it is secreted by type of WBC called PLASMA cells

- production of antibodies is the main function of HUMORAL IMMUNE SYSTEM

FUNCTION OF ANTIBODY

- agglutination (clumping)

- opsonization (coating)

- activates the complement system

- promotes release of interferons

MACROPHAGES

- large immune cells that devours invading pathogesn and other intruders

- act as reservoir of the virus

IMMUNE FUNCTION

2 TYPES OF IMMUNITY

1. natural / innate / non-specific (present @ birth)

2. acquired / adaptive / specific

NATURAL / INNATE / NON-SPECIFIC

- provides rapid non specificimmunicty and is present at BIRTH

- it also provides non-specific response to any invader regardless of invaders composition

- the basis of this defense mechanism is the ability to distinguish between friend and foe or SELF and

NON-SELF

2 STAGES OF NATURAL IMMUNITY

- immediate (occurs within 4 hrs)

- delayed (4 hrs - 96 hrs AFTER exposure)

NATURAL MECHANISMS

- physical barriers

- chemical barriers

- action of WBC

- inflammatory response

PHYSICAL BARRIERS

- consist of intact skin and mucous membarane which prevent pathogesn from gainign

access to body

- EXAMPLE: sneezing and coughing responses which acts to clear pathogens from upper RR

tract

CHEMICAL BARRIERS

- acid gastric juices

- enzymes in tears and saliva

- substances in sebaceous glands ..

WBC OR LEUKOCYES

- particpates in both natural and acquired immune responses

- 2 types

- granular / granulocyte

- non-granular / agranulocyte

GRANULAR / GRANULOCYTE

- assist in fighting invasion by foreign bodies or toxins by releaseing cell mediator

such as:

- histamine

- bradykinin

- prostaglandin

- engulf foreign bodies or toxins

- EXAMPLES:

- neutrophil (bacteria)

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- eosinophil (allergy & parasites)

- basophil

NEUTROPHIL

- 1st cell to arrive at site of infection

- makes up 50-70% of WBC

- normal range 1500-8000 mm3

- taken from LATIN WORD: love neither

- increase neutrophil is CAUSED by:

- stress

- infection from bacteria

- damage or inflammation of tissues

- sudden kidney failure

- cancer

- hemolytic anemia, polycythemia vera

- medications

- LOW NEUTROPHIL (neutropenia) is due to:

- leukemia

- damage to bone marrow

- sle (systemic lupus erythematosus)

- hypersplenism

- rheumatoid arthritis

- medications (steroids)

EOSINOPHIL

- makes up 1-4 % of WBC

- TO LOVE DAWN

- very helpful in defending body against PARASITES

- it protects the foby against diseases and infection by moving and eating

sometypes of bacteria

- HIGH level is caused by:

- respose to allergies

- expose to bacteria and parasite

- medications

- LOW level is caused by:

- administration of STEROIDS

BASOPHILS (VIRUS INFECTION)

- least common type of WBC

- TO LOVE FOUNDATION

- 0.4-1% of WBC

- decreases in allergic reaction and increases to some types of inflammation

- CONTAINS:

- histamine

- leukotrienes

- heparin

- HIGH basophils caused by:

- infection from virus

- splenectomy

- LOW caused by

- severe allergies

- pregnant women

- hyperthyroidism

- meds (CORTICOSTEROIDS)

AGRANULOCYTES

- monocytes or macrophages

- lymphocytes

MONOCYTES OR MACROPHAGES

- function as phagocytic cells and able to engulf greater number and

quantities of oreign bodies or toxins than granulocytes

- macrophages are cells that east other cells and those infection by pathogen

to prevent spreading and kep body healthy

- 1-3% of WBC

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- low count indicates GOOD SIGN

- high count is called MONOCYTOSIS cause inflmm and viral infection

LYMPHOCYTES

- consist of B and T cells which play a major roles in humoral and cellmedicated

immunity

- helps protects the body agianst tumor

- cause rejection of tissues during organ tranpslant coz they interpret these

tissues as foreign

- 15-40% of WBC

- LOW COUNT due to:

- aplastic anemia

- aids, tumors

- dirsoders that affect nerves

- HIGH COUNTdue to:

- chicken pox

- TB

- mumps

- rubella

INFLAMMATORY RESPONSE

- is a major component of natural immunesystem elicited in response to tissue injury or invading

organism

- CHEMICAL MEDIATORS assist in inflammatory response to minmize blood loss, wall off invading

organisms, activate phagocyte and promote fibrous scar formation and regeneration of injured

tissues

ACQUIRED / SPECIFIC / ADAPTIVE IMMUNITY (during lifetime)

- consist of immunologic responses that are not present at birth but are acquired during life

- mostly it is develop as a result of contracting a disease or generating a protective immune response

thru IMMUNIZATION

- weeks or month after exposure to the disease or immunication, the body produces an immune

response that is sufficient to defend against the disease or re-exposure

2 MECHANISMS OF ACQUIRED IMMUNITY

- cell mediated response (T cell activated)

- effector mechanism (B cell activated / antibody activator)

2 TYPES OF ACQUIRED IMMUNITY

- active acquired immunity

- passive acquired immunity

2 TYPES OF PASSIVE

- naturally acquired passive immunity

- artificial acquired passive immunity

NATURALLY ACQUIRED PASSIVE IMMUNITY

- recepients acquire immunity w/o involvement of thier own immune system

- example:

- natural transfer of antibodies from mother via placenta and breastmilk

ARTIFICIALLY ACQUIRED PASSIVE IMMUNITY

- is acquired thru direct injection of antibodies and sensitized cells colelcted from

donors

- in the absence of memory cells immunity develop by this method is purely

temporary (2-3 weeks)

- injfection of preformed antibodies this may help revenet disease after exposure to

pathogen such as hepatitis virus, chickenpox, and other bacterial diseases

ACTIVE ACQUIRED IMMUNITY

- the individual produces hish/her own antibodies

- this can be developed w/in body to fight against several diseases

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- its duration depends on the particular diseases or vaccine some may develop lifeling

immunity -- others may not

- example:

- flu vaccine

2 TYPES OF ACTIVE ACQUIRED IMMUNITY

- naturally active acquired immunity

- artificially active acquired immunity

NATURALLY ACTIVE ACQUIRED IMMUNITY

- person is exposed to a live pathogen, and thereby develop a primary

immune response, which leads to immunological memory

ARTIFICIALLY ACTIVE ACQUIRED IMMUNITY

- vaccine which contains a substance called antigen that can cause artifically

acquired active immunity

- primary response is stimulated against the angitgen by vaccine w/o causing

any s/s of disease

GENERAL IMMUNE RESPONSES

3 MEANS OF BODY DEFENSES

1. phagocytic immune response

2. humoral /antibody immune response

3. cellular immune response

PHAGOCYTIC IMMUNE RESPONSES

- involves the WBCs (granulocytes and macrophages) which have ability to ingest foreign particles

- thesecels move to point of attack, where they engulf and dsetroyinvadin agent

- also remove body’s own dying or dead cells

HUMORAL IMMUNE RESPONSE

- charac by production fo antibodies by B lymp in response to specific antigen

- these antibody are highly specific protein taht are transported in blood stream

ANTIBODY

- are large protein called iMMUNOGLOBLULIN (Ig) coz they are found in blobulin fraction of plasma

protein

FUNCTION OF ANTIBODY

- defends body against foreign invaders

- acts as cross-link between 2 antigen causing clumping effec t0 agglutination

- faciliate phagocytosis by coating the antigen - antibody molecules with sticky substances -

OPSONIZATION

CLASSIFICATION OF ANTIBODY

IgG

- 75% of total immunoglobulin

- appears in serum and tissues (interstitial fluids)

- assumes a major role in blood borne and tissue infection

- activates complement system

- enhances phagocytosis

- crosses the placenta (ONLY Ig that does this)

IgA

- 15% of total immunoglobulin

- appears in body fluids (body, saliva, tears, breastmlik, pulmonary /g astrointestinal,

genitournary secretions)

- protects agianst RR, gastro, adn genitourinary infection

- prevents absorption of antigens from food

- passes to neonate in breastmilk for protection

IgM (bacteria + viral infection)

- 10%

- appears mostly in intravascular serum

- appears as 1st immunoglobulin produced in response to bacterial and viral infection

- activates complement system

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IgD

- 0.2%

- appears in small amount in serum

- possibly influences B lymphocytes differentiation but role is

IgE

- 0.004%

- appears in serum

- take part in allergic and soem hypersensitivity reactions

- combats parasite infections

CELLULAR IMMUNE RESPONSE

- the t lymphocytes is resposiblef or cellular immunity

- it attacks foreign invaders directly rather tan production of antibodies

- there are several tyeps of T cells, ea with desginated roles in defense against bacteria, viruse, fungi,

and parasites

TYPES OF T LYMPHOCYTES AND THEIR FUNCTIONS

Helpher T cd4

- attacks foreign invaders directly

- initiates and agument inflammatory response

- increaesactiviatedcytototix T cells

- increases B cells antibody production

Suppressor T cd8

- suppresses the immune response

- turn off immune response by stopping the activity of B and T cells

Memory T

- remembers contact with antigen in subsequent exposures mount an immune response

Cytotoxic T (killer T) cd8

- lyses cells infected with virus

- plays a role in graft rejection

4 STAGES OF IMMUNE RESPONSES

- recognition

- proliferation

- response

- effector

RECOGNITION STAGE

- abilit to recognize antiges on materials as FOREIGN or NONSELF that is initiating event in

any immune reaction

- body must first recognize invaders as FOREIGN before it can react ot them

- the body accomplishes recognition using lymph nodes and lymphocytes for surveillance

PROLIFERATION STAGE

- circulating lymphocytes containing the antigen message returns to the nearest lymph nodes

- once in the node, these sensitized lymphocytes stimulate certain of dorman lymphocytes

residing there to enlarge, divide, proliferate and differentiate into either T or B lymphocytes

RESPONSE STAGE

- the differentiated lymphocytes function either a humoral or cellular capacity

- this stage depends on the specific antigen recognizes by the body

- most immune responses to antigens called both humoral and cellular responses, although

oneusu predominates

EFFECTOR STAGE

- either the antibody of the humoral response or the tytotoxic (killer) T cells of the cellular

response reaches and connects with the antigen on the surface of foreign invaders

- this connection initiates series of events that is most instances results in the total

destruction of invading microbes or the complete neutralization of the toxins

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NULL LYMPHOCYTE (dili ma differentiate angiyang function)

- large granular lymphocytes w/o surface markers ormembrane assoc. proteins from B and T

lymphocytes

- subpopulation of lymphocytes destroy antiges already coated with antibody

NATURAL KILLER CLELS

- defends against microbs and some types of malignant cells

- capable of directly killing invading organisms

COMPLEMENT SYSTEM

- a circulating plasma proteins, made in liver and activated when antibody connects with its antigen

- destruction of an invading, or attackign organism or toxins is not achieved merely by binding of the

antibody and antigen, it also requires activation of complement, the arrival of killer T cells or the

attraction of macrophages

- activates on complement

FUNCITON OF COMPLEMENT SYSTEM

- defends body against bacterial infection

- bridging natural and acquired immunity

- disposing of immune complexes and the byproducts assoc. with inflammation

ROLE OF INTERFERONS

- a biologic response modifier

- have antiviral and antitumor properties

- produce by T lymph and B lymph and amcrophages in response to antgen

- suppresses antibody production and cellular immunity to modify the immune response

STEM CELLS (produced by bone marrow)

- immortal cells that are capable of self enewal and differentatiation

- continually replenish the body’s entire supply of both RBCs, and WBCs

- TOTIPOTENT cells - have tremendous capacity to self renew and differentiate

DIFFERENCES IN CELLULAR AND HUMORAL IMMUNE RESPONSE

Humoral Responses

- bacterialpahgocytosis and lysis

- analphylaxis

- allergichayfever and asthma

- immune complex diases

- bacterial and soem viral infections

Cellular Responses

- transplant rejection

- delayed

- hypersensitivity

- tumor surveillance or destruction

- intracellular infection

- viral, fungal, and parasitic infection

LYMPHOCYTES INVOLVED IN IMMUNE RESPONSE

- non specific lymphocytes

- null lymph

- natural killer cells

- specific lymphocytes

- b lymphocytes

- t lymphocytes (helper, suppressor, cytotoxic, and memory cells)

TOMORROW STUDY

- disorders of immune system

- primary immunodeficiency

- secondary immunodeficiency

AUTOIMMUNITY

- normal protective immune response; paradoxically turns against or attacks the body, leading to tissue

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damage

HYPERSENSITIVITY

- body produces inappropriate or exaggerated responses to specific to antigens

GAMMOPATHIES

- immunoglobulins are over-produced

PRIMARY IMMUNODEFICIENCY (congenital / @ birth)

- result from improper development of immune cells or tissues, usu congenital or inherited

SECONDARY IMMUNODEFICIENCY (acquired)

- result from soem interference with an already developed immune system, usu acquired later in life

- example: HIV

PRIMARY IMMUNODEFICIENCY / CONGENITAL IMMUNODEFICIENCY

- represent inborn errors of ..

PRIMARY IMMUNODEFICIENCY DISORDERS

1. phagocytic dysfunction

2. B-cells deficiency

3. T-cells deficiency

4. Combined B cells and T cells deficiency

5. Complement system deficiency

PHAGOCYTIC DYSFUNCTION

- pt cannot initiates normal inflammatory response against pathogenic organism

- in this dysfunction, neutrophils are impaired so that they cannot exit the circulation and travel tosite of

infection as a result the patient cannot initiate normal ifnlamm response against pathogenic organism

- neutrophil maybe low or high coz oit remains in the vascular system

EXAMPLE

1. HYPERIMMUNOGLOBULINEMIA (HIE)

- where the WBC cannot inittiate an inflamm response infectious organism which result to recurrent skin

and pulmonary abscesses abnormalities of connective tissues, skeleton, and dentition

S/S

- bacterial, fungal and viral infection

- deep seated cold abscesses

- neutropeniaassoc with painful mouth ulcers, gingivitis, adn cellulitis (inflamm of subcutaneous

connective tissue)

ASSESSMENT / DX FINDINGS

- must be base on hx and s/s

- hx of recurrent infection and fever in child

- failure of an infant to resolve with usual treatment

- warning signs of primary immunodeficiencies

- NITROBLUE TETRAZOLIUM REDUCTASE TEST

- indicates cytocidal (causing cell death) activity of phagocytic cells

MEDICAL MANAGEMENT

- antibiotic therapy and tx for viral and fungal infections

- granulocyte-macrophage colony stimulating factor

- granulocyte-colonoly stimulating factor

- hemtopoietic stem cell transplantation

B-CELL DEFICIENCIES

- results from lack of differentiation of B-cell precursors into mature B-cells, as a result, plasma cells are

absent

- causing lymphatic tissue disappear leading to complete abscene of antibody production against

invading bacteria, viruses, and other pathogens

EXAMPLES

1. AGAMMAGLOBULINEMIA (BRUTONS DISEASE)

- complete absence of antibody production including B-cells in the peripheral blood and immunoglobulins:

IgG, IgM, IgA, IgD, IgE are low or absent

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- sex-linked

- males are high risk to develop if they have an affected male relative

S/S

- severe infection soon after birth

ASSESSMENT / DX FINDINGS

- mark deficiency of complete absence of all serum immunoglobulin

- antibody titers (to confirm successful childhood vaccinations)

- HCT and HGB levels must be obtained

- biopsies of small intestine, spleen, and stomach

MEDICAL MANAGEMENT

- passive pooled plasma or gammaglobulin (introduction of gammaglobulins / TRANSPLANTATION)

2. HYPOGAMMAGLOBULINEMIA (CVID)

- CVID - common variable immunodeficiency

- lack of differentation of B-cells into plasma cells

- diminished antibody production

- there is severe PANHYPOGLOBULINEMIA

- general lack of immunoglobulin in blood specifically IgA

S/S

- bacterial infection

- infeciton with giardia lambia (protozoan infection)

- pernecious anemia

- chronic inflammatory infection

ASSESSMENT / DX FINDINGS

- base in hx of bacterial infection, quantification of B-Cell activity, and reported s/s

- antibody titer

- level of Hct and HgB

- biposies of small intestines, spleen, stomach, to assess for lymphoid hyperplasia (enlargement of

lymphoid tissues)

MEDICAL MANAGMENT

- IVIG - intravenous inmmunoglobulin

- Metronidazole (Flagyl)

- QuinabrineHcl (Atabrine)

- Microbial therapy -- RR infection

- Vit B12 -- parenteral injection

T-CELL DEFICIENCIES

- genetic in origin

- thymus gland fails to develop normally during embryogenesis

1. THYMIC HYPOPLASIA (Di GEORGE SYNDROME)

- this rare, complex, multisystem genetic abnormality caused by the absence of several genes on

chromosomes 22

- manifestedlamost immediately right around birth -- and manifested as cardiac anomaly

S/S

- hypoparathyroidism (decrease function of parathyroid gland)

- congenital heart disease

- celft palate and lip

- susceptible to yeast, fungal, protozoan and viral infection

- hypocalcemia (tetany + mm twitching)

ASSESSMENT / DX FINDINGS

- prompt diagnosis for appropriate management

- comprehensive immunologic analysis

MEDICAL MANAGEMENT

- oral calcium supplementation

- immediate surgical intervention

- thymus graft (transplantation of fetal thymus)

2. CHRONIC MUCOCUTANEOUS CANDIDIASIS

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- caused by autosomal recessive inheritance that affect both males and females

- an autoimmune disorder involving thymus and otherendocrine glands

S/S

- chroniccandidal infection

- hypocalcemia, tetany

- Addison’s disease (rare chronic endocrine disorder where adrenal cortex gland does not produce

adequate corticosteroid hormones)

ASSESSMENT / DX FINDINGS

- prompt diagnosis is necessary for approrpriate management

- comprehanesive immunologic analysis

MEDICAL MANAGAEMENT

ANTIFUNGAL AGENT

- topical - miconazole

- oral - clotrimasole, ketoconazole

- Iv - amphotericin B

COMBINED B-CELL AND T-CELL DEFICIENCIES

- comprise a heterogenous group of disorders, all characterized by profound impairment in the

development or function of cellular, the humoral or both parts of immune system

- autosomal recessive and x-linked

- disruption of normal communication system of B-cells and T-cells and impairment of immune response

EXAMPLE

1. ATAXIA-TELANGIECTASIA

- autosomal recessive neurodegenerative disorders that arises because of a defect on chromosome 11

- affect both B-T cells immunity

- deficiencies with IgA, IgG, and IgE

- vascular lesions caused by dilated blood vessels (telangiectasia)

- loss of muscle coordination (ataxia)

S/S

- neurologic, vascular, endocrine, hepatic, and cutaneous abnormality

- cerebellar ataxia

- recurrent bacterial infection of the sinuses and lungs

- increased incedence of cancer

ASSESSMENT / DX

- prompt diagnosis and appropriate management

MEDICAL MGT (MEMORIZE!!!)

- antimicrobial therapy

- management of presenting symptoms

- transplantation of fetal thymus tissue (thymus graft)

- IVIG administration

SEVERE COMBINED IMMUNODEFICIENCY DISEASE (B + T Cells)

- is a wide variety of congenital and hereditary immunologic defect characterized by early onset of

infection

S/S

- RR infection

- diarrhea

- failure to thrive (unable to take in, retained or utilize calories, to gain weight or grow as expected)

- maculopapular and erythematous skin rashes

- vomiting, fever, and persistent rash

MEDICAL MGT

- stem cells and bone marrow transplantation

- antimicrobial therapy

- IVIG

1. WISKOTT-ALDRICH SYNDROME (WAS)

- caused by variety ofmutation in the gene encoding the WAS protein

S/S

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- frequent infections

- thrombocytopenia (low platelet count) with small platelets

- eczema

- increase risk for autoimune disorders and malignancies

- vasculitides and autoimmune hemolytic (destruction of RBCs) anemia

MEDICAL MGT

- bone marrow transplantation

- antimicrobial therapy

- splenectomy with continuous antibiotic prophylaxis

- IVIG

COMPLEMENT SYSTEM DEFICIENCIES

- can result in incrased susceptibility to infectious diseases and immune-mediated disorders

- can be primary or secondary

1. ANGIONEUROTIC EDEMA

- result from deficiency of C1-esterase inhibitor, which opposes the release of inflammatory mediators

- food allergy often linked to this disorder

S/S

- episodes of edema in varios part of body, including RR tract and bowels (MANG HUPONG ANG

PATIENT)

MEDICAL MANAGEMENT

- pooled plasma

- androgen therapy

2. PAROXYSMAL NOCTURNAL HEMOGLOBINURIA

- is an acquired small cell disorder resulting from somatic mutation in the hematopoietic stem cell

S/S

- intravascular hemolysis

- cytopenia (reduction of blood cells)

- frequent infection

- bone marrow hyperplasia

- venous thrombosis

- anemia

- hemoglobinuria

DIAGNOSTIC

- sucrase hemolysis test (crystalline disaccharide - fructose / galactose - promotes binding of complement

to RBCs)

- ham acid hemolysis test

- fluorescent-activated cell analysis

MEDICAL MGT

- transfusion therapy

- anticoagulation therapy

- antibiotic therapy

10 WARNING SIGNS OF PRIMARY IMMUNODEFICIENCY

- 8 or more new ear infection within 1 year

- 2 or more serious sinus infectins within 1 year

- 2 or more months of antibiotics with little effect

- 2 or more pneumonia within 1 year

- failure of an infant to gain weight or grow normally

- current deep skin or organ abscesses

- persistent thrush in the mouth or elsewhere on skin, after age 1

- needs for IV antibodies to clear infections

- 2 ore more deep seated infections such as meningitis osteomyelitis, cellulitis, or sepsis

- familyhx of primary immune deficiency

SECONDARY IMMUNODEFICIENCY

- are more common than primary immunodeficiency and frequently occurs as a result of underlying

disease process or the tx of hose dseases

15

CAUSES

- malnutrition

- chronic stress

- burns

- uremia

- diabetes mellitus

- certain autoimmune disoders

- exposure to immunotoxic medication and

- patient with secondary immunodeficiency have immunosuppresion and are often refer to as

IMMUNOCOMPROMISED HOST

EXAMPLE

AIDS (ACQUIRED IMMUNODEFICIENCY SYNDROME)

HIV - human immunodeficiency virus is a lentivirus (member of the retrovirus family) that causes AIDS

AIDS - a condition in human in which the immune system begins to fail, leading to life-threatening

opportunistic infections

- infection with HIV ocurs by transfer of blood, semen, vaginal fluids or breastmilk

- this is most common secondary immunodeficiency disorders

4 MAJOUR ROUTES OF TRANSMISSION

- unsafe sex

- contaminaed needles

- breastmilk of contaminated mother

- transmission from an infected mother to her baby at birth (perinatal transmission)

HIV INFECTION LEADS TO LOW LEVELS OF CD4+ T CELLS THRU 3 MAIN MECHANISM

1. direct viral killing of the infected cells

2. increase rates of apoptosis in affected cells

3. killing of infected CD4+ T-cells by CD8 cytotoxic lymphocytes that recognize infected cells (NAGUNAY)

- HIV infects primarily vital cells in the human immune system such as helper T cells (specifically CD4+

Tcells), macrophages, and dendritic cell

- infection with HIV 1 is assoc with a progressive decrease of the CD4 T-cell count and increase in viral

load

- decrease CD4 == increase viral load (vice versa!)

HIV INFECTION HAS 4 BASIC STAGES

- incubation period

- acute infection

- latency stage

- aids

INCUBATION PERIOD

- asymptomatic and usu lasts between 2 and 4 weeks

ACUTE INFECTION

- last an average of 28 days and can include s/s such as:

- fever

- lymphadenopathy (swollen lymph nodes)

- pharyngitis (sore throat)

- rash

- myalgia (mm pain)

- malaise

- mouth and esophageal sores

LATENCY STAGE

- shows few or no symptoms and can last anywhere from 2 weeks to 20 yrs and beyond

AIDS

- final stage -- person infected shows s/s of various opportunistic infections

- a term applied when a person is infected with HIV and has a CD4 cell count of <200 copies / mm3

- during this stage, illnesses and disorders develop because the immune system is not storng enough to

16

kill malignant cells, bacteria, and viruses

- neoplasm also develop because the body’s surveillance system is damaged

PATHOLOGY

Causative Agent: HIV (retrovirus)

- infect the CD4+ T lymphocytes by using the REVERSE TRANSCRIPTASE ENZYMES

- this HIV is able to reprogram the genetic materials of the infected CD4 cells

- as a result HIV can use the CD4+ cells to produce the virus instead of self

- consequently, whenever the infected T4 cells is stimulated to reproduce by invasding organism, HIV is

reproducedinsetad of the CD4 cells

- newly produced virus can then infect other CD lymphocytes

- thrus the virus replicate inside the CD4 cells - it buds from the CD4 cells surface, desroyoing the cell

membrane and releasing millions of viral copies in the bloodstream

- causing the plsma viral load to increase

CLINICAL MANIFESTATION

- it is widespread and may involved virtually any organ system

- disease associated with infection and AIDS result from infections, malignancies or the direct effect of

HIV on body tissues

- RR

- shortness of breath

- dyspnea

- cough

- chest pain

- fever with pnemocystic pneumonia

- mycobacteriumavium complex

- tuberculosis

- GI manifestation

- loss of appetite

- nause

- vomitting

- oral and esophageal candidiasis

- chronic diarrhea

- oral candidiasis

- wasting syndrome

- oncologic manifestation

- carcinoma of stomahc, pancreas

- kaposi sarcoma (most common HIV related malignancy

- b-cell lymphoma

- neurologic

- involves centra, peripheral and autonomic function

- HIV infection in CNs includes inflammation, atropy, demylenation, degeneration

- HIV

- depressive

- experience irrational guild and shame, loss of self esteem

- feeling of helpless and worthlessness, suicidial ideation

- integumentary

- generalized follicultisassoc with drug, flaking skin or atopic dermatitis such as eczema or

psoriasis-

- endocrine

- infiltration

- gynecologic

- persistent /recurrent vaginal candidiasis, STD’s

4 DIAGNOSTIC EXAMS

- elisa / eia (enzyme link immunoabsorbent assay)

- western blot

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- sensitive enough to detect 99.5% of HIV infected blood sample 12 weeks after initial infection

- orasure HIV

- allows for HIV testing using an oral fluid specimin (saliva), but not as accurate as blood testing

- immune complex-dissociated p24 assay

- detected p24 antigens which is an indication of active HIV replication

- when person infected with HIV, the immune system responds by producing antibodies against virus, usu

3-12 weeks after infection

MEDICAL MANAGMENT

- treatment of infection

- antidiarrheal therapy

- antidepressant therapy

- chemotherapy

- nutrition therapy

4 CLASSES OF ANTIRETROVIRAL AGENTS

- nucleoside / nucleotide reverse transcriptase inhibitor (NRTI)

- non-nucleoside reverse transcriptase inhibitor (NNRTI)

- protease inhibitors

- fusion inhibitors

NUCLEOSIDE / NUCLEOTIDE REVERSE TRANSCRIPTASE INHIBITOR

ACTION

- interfere with viral RNA -- directed DNA polymerase (reverse transriptase) thereby impending ther

eplication of retroviruses including the HIV

EXAMPLE

- azidothymidine (AZT)

NON-NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITOR

ACTION

- binds to active center of reserve transcriptase to block RNA and DNA polymerase activities

- thisactioncausesdisruiption of enzymes catalytic site and prevents replication of HIV 1 virus

EXAMPLE

- nevirapine

- delavirdine

PROTEASE INHIBITORS

ACTION

- blocks the protease activity and if interfere with multiplication of virus and slow progression of disease

EXAMPLE

- saquinavir

FUSION INHIBITOR

ACTION

- acts by targeting GP120 during the attachment stage of HIV life cycle

EXAMPLE

- T-20

- T1249

PREVENTION OF HIV

- health promotion (condoms)

- patient education (the right way to use male condoms)

- standard precaution

- barrier protection

STANDARD PRECAUTION (MEMORIZE)

PURPOSE

- prevent transmission of nosocomical infection

- apply to blood, all body fluids, secretions and excretion (except sweat), regardless of whethery they

contain visible blood, non-intact skin and mucous membranes

BARRIER PROTECTION

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- should be use all the times to prevent skin and mucous membrane contamination with blood, body fluids

containign visible blood or other body fluids

- cerebrospinal

- snovaial

- pleural

- peritonial

- pericardial

- semen and vaginal secretions

EXAMPLE

- lab coat (disposable)

- gloves

- eyes and face protection

NSG MSGT (give @ least 2 for FINAL // refer CHAPTER 52 OF BOOK)

PROMOTING SKIN INTEGRITY

- encourage maintain balance between rest and mobility

- bedriddenpt will be assisted o change positions every 2 hrs

- avoid scratching and advise to use non abrasive, non drying soaps

- medicated moisturizers, ointments and permume are applied

- encouraged oral care

PROMOTING USU BOWEL PATTERN

- monitor constency, frequency of bowel movements, ..

PREVENTING INFECTIONS

- monitor s/s of infection

- chills

- night sweats

IMPROVE ACTIVITY TOLERANCE

- monitor pts ability to ambulate and perform ADLs

- assist in planning daily routiens that maintain a balance between activity and rest

MAINTAINING THOUGHT PROCESS

- assessed alteration in mental status that may be r/t neurologic involvement, metabolic, infections

IMPROVING AIRWAY CLEARANCE

-asses RR status including rhtythm, use of accessory mm

breath sound and skin color ..

RELIEVING PAIN AND DISCOMFORT

- asses for quality and severity of pain

- topical anesthetic or ointmetnmaye prescribed

- use of cushions or foam pads may increase comfort while sitting

IMPROVING NUTRITION

- refer to book ..

MONITORING AND MANAING POTENTIAL COMPLICATIONS

- opportunistic infections

AUTOIMMUNE DISEASE

- immune system losses its ability to distinguish friend from foew

- the body produces antibodies (auto antibodies) and sensitized T cells thatattacks and damaged its own

tissues

- it is the immune system that produces the disorders

GUILLAIN-BARRE SYNDROME

- symetrical, bilaterial, peripheral polyneuritis, characterized by ascending paralysis

- weaknessusu begins in the legs and progresses upward

- auto-immune attack on peripheral nerve -- myelin that result to acute and rapid demyelination of

peripheral and some cranial nerves producing ascending weakness with DYSKENISIA (inability to

execute voluntary movement) and PARESTHESIA (numbness)

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PATHOLOGY

- schwann cells is spared-allowing the cell mediated and humoral immune responses attacked on

peripheral nerve-myeline in the recoevery phase of the disease cause the INFLAMMATORY

DYEMILINATION

- MOLECULAR MIMICRY (an infectious organism contain an amino acid thatmimics the peripheral nerve

myelin protein)

- immune system cannot distinguish between 2 protein and attacks and destroy peripheral nerve myeline

- IMMUNE ATTACK (there is an influx of macrophages and other immune mediated agents that attacks

myeline)

- INFLAMMATION and DESTRUCTION

- axion unable to support nerve conduction

CLINICAL MANIFESTATION

- beings with mm wewakness and diminish reflexes of lower extremities

- peripheral neuritis

- scattered weakness

- complete paralysis

- clasic clinical features including arflexia and ascending wekaness

- axonal destruction including paralysis of oculuar mm , ataxianadareflexia

MEDICAL MANAGEMENT

- a medical emergency requiring management in ICU (rapid progression and neuromuscular RR failure)

- prevent interventions aimed at preventing complicaton of immobility (anticoagulant agent is given and

applied thigh-high elastic compression)

- plasmapheresis (removal of antibodies)

- IVIG

NSG MGT (PART OF LONG QUIZ)

MAINTAING RR FUNCTION

ENHANCING PHYSICAL MOBILITY

PROVIDIN ADEQUATE NUTRTION

IMPROVING COMMUNICATION

- coz of paralysis, the pt cannot talk, laugh, or cry -- some form of comm with picture cards, or eye blink

system provide means of communication

DECREASE FEAR AND ANXIETY

- provide info about condition

- emphasize positive ..

- teach relaxation

MONITORING AND MANAGING POTENTIAL COMPLICATION

- RR failure (major cause of mortality)

- cardiac dysrhythmias

- pulmonaryemoblism

- urinary retention

MULTIPLE SCLEROSIS (review in notebook -- past lecture)

MYASTHENIA GRAVIS (review in notebook -- past lecture)

GENERAL NURSING MANAGMENT FOR PT WITH IMMUNODEFICIENCY

- assessment focuses on hx of past infectinsparticuly type anffreq of infections

- reduce pt risk for infections

- assist medical measures aimed in improving status

- maintain RR bowel and bladder functions

- teach good dental hygiene measures reduces the potential for oral lesions

- strict aseptic technique when performing invasinveprodecures

- develop and maintain knowledge ase in these involving treatment modalities -- in order to help pt and

family understand the tx optimized outcomes

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NEXT TOPIC (FRIDAY)

- hypersensitivity

- chemical mediators

LONG EXAMS (oral)

- taken from exam questions

IMMUNOTHERAPY

- allergy shot

HYPERSENSITIVITY

- an abnormal heightened reaction to any type of stimulus

- occurs because of acivation of IgE and the release of inflammatory chemicals,

including histamine, prostaglandin by mast cells and basophils

* MAST CELLS

* type of basophils

* releases histamine, prostaglandin, and basophil

4 TYPES OF HYPERSENSITIVITY

- Anaphylactic ( type 1)

- Cytotoxic (type 2)

- Immune complex (type 3)

- Delayed-type (type 4)

TYPE 1 ANAPHYLACTIC REACTION

- immediateoccuring reaction when exposure to a specific antigen occurs

- characterized by edema in many tissues, including the larynx and is often

accompanied by hypotension, bronchospasm, and cardiovascular collapse in severe

cases

- most cases this reaction is characterized by

- vasodilation

- increase capillary permeability

- smooth muscle contraction

- eosinophilia (increase production of eosinophils)

- SYSTEMC REACTION involve:

- layrngeal stridor

- angioedema

- hypotension

- bronchial, GI, and uterine spasm

- LOCAL REACTION - characterized by hives

- TYPE 1 REACTION occurs when patient has a positive reaction to SCRATCH TEST

- SCRATCH TEST is done to identify specific allergens to which a patient is reactive

HOW IS SCRATCH TEST PERFORMED?

- scratch the skin with tiny amount of allergen ==> introduce allergenic reaction

- under anaphylactic type 1

DISORDER IS CATEGORIZED INTO

1. MILD

a. Allergic rhinitis

b. Atopic dematitis

c. Asthma

2. SEVERE

a. Anaphylaxis

b. Urticaria

MILD CATEGORY

1. ALLERGIC RHINITIS

- most common form of allergy

- when s/s occurs throghout the year -- it is called PERENNIAL ALLERGIC RHINITIS

- if s/s occurs seasonally -- called HAY FEVER

- result of antigen-antibody reaction where cilliary action decreases and mucous

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secretion increases -- resulting to vasodilation and occurrence of local tissue edema

S/S

- sneezing

- nasal itching

- profuse rhinorrhea (runny nose)

- itchy red eyes

- nasal mucosa is pale and edematous

- allergic shiners (dark circles under eyes caused by venous congestion in maxillary

sinuses)

DIAGNOSTIC TEST

- SKIN TESTING is performed to identify the specific offending allergens to allow

avoidance of allergens

MEDICAL MANAGEMENT

- eliminate the offending envronmental stimuli

- atihistamine and nasal decongestant for symptomatic relief

- corticosteroids via inhalation or nasal spray (for severe cases)

- RHINOPHOTOTHERAPY uses lightwaves to reduce hyperimmune response usu done

3x a week for 3 weeks to relieve s/s such as sneezing, itching, runny nose, and other

s/s

- IMMUNOTHERAPY aka “allergy shots”

- reserved for pts with debilitating s/s

- done weekly of injection of tiny amount of offending antigen

2. ATOPIC DERMATITIS

- inflammatory skin response often called ECZEMA

- a chronic disorder characterized by superficial skin inflammation and intense pruritus

- condition has a tendency to recur with remission from adolescence to age 20

- mediated by IgE antibodies, because it is commonly found in patient with allergic

rhinitis or allergic asthma

S/S

- pruritus

- edema

- extremely dry skin followed by eruption of tiny vesicles (blisters)

DIAGNOSTIC TEST

- culture and sensitivity test

- CULTURE is done to find out what kind of organism (usu bacterial) is causing

an illness or infection

- SENSITIVITY check to see what kind of medicine such as antibiotic will work

best to treat the illness or infection

MEDICAL MANAGMENT

- oil in water lubricant

- topical corticosteroids

- topical / systemic antibiotics

SEVERE CATEGORY

1. ANAPHYLAXIS

- an un-anticipated servere allergic reaction that is often explosive in onset

- characterized by edema in many tissues including the larynx and is often accompanied

by the following:

- hypotension

- bronchospasm

- cardiovascular collapse in severe cases

- an immediate reaction beginnign with in a minutes of exposure to antigen

- IgE antibodies produced from previous antigen senitization are attached to mast cells

throughout the body

22

- in this reaction, the antigen is introduced at a systemic level, which causes widespread

release of histamine and other chemical mediators contained within the mast cells

S/S

- vasodilation

- increased capillary permeaiblity

- smooth muscle contraction

SYSTEMIC

- laryngeal stridor

- angioedema

- hypotension

- bronchial, GI, and ..

LOCAL

- hives

DX TEST

- ABG (arterial blood gas)

- ECG (electrocardiogram)

- history and physical exam after recovery -- allergen testing for previous

MEDICAL MANAGEMENT

- IV access for “E” meds

- epinephrine IV

- dopamine

- oxygen

- antihistamine (oral, IV, IM)

- corticosteroids (oral, IV, IM)

- if severe RR compromise

- tracheostomy / endotracheal intubation

- mechanical ventilation

SUBSTANCES THAT COMONLY TRIGGER ANAPHYLACTIC REACTION

ANTIBIOTIC

- penicillin

- sulfonamides

- tetracycline

- cephalosporin

- amonoglycosides

MEDICAL PRODUCTS

- latex rubber

DIAGNOSTIC AGENTS

- contrast dyes

ANESTHETICS / ARRYTHMICS

- lidocaine

- procaine

FOOD ADDITIVES

- bisulfaste

- monosodiumglutatamate

FOODS

- bean

- choclate

- eggs

- shellfish

- fruits (strawberries)

- grains (wheats)

- nut

POLLEN

- horse serum

- rabbit serum

VENOMS

- bees

- wasps

- ants

- snake

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HORMONES

- insulin

- estradiol

- adrenocorticotropic hormone

OTHER MEDICATION

- barbiturates

- pheyntoin (dilantin)

- protamine

- salicylates

- diazepam

2. URTICARIA

- aka HIVES

- kind of skin rash notable for pale red, raised, itchy bumps

- it might also cause a burning or stinging sensation, this is caused by allergic reaction

which is categorized either chronic or acute

- ACUTE is < 6 weeks

- CHRONIC > 6 weeks

- HIVES is a type 1 hypersensitivity reaction -- the antigen, stimulated reactiosn of IgE

antibodies causing the release of mast cells contesnts especially histamine -- which

triggerurticaria

- there are numerous agents that CAUSES urticaria like:

- medication

- foods

- cold

- local heat

- pressure

- stress

S/S

- raised pruritic lesions

- non-tender, erythematous wheals concentrated on the trunk and proximal extremities

DIAGNOTIC TEST

- made on basis of phsyical exam and patient’s hx

MEDICAL MANAGEMENT

- epinephrine

- corticosteroid

- antihistamine

- histamine H1 and H2

- H1 - benadryl

- H2 - ranitidine, cimitidine

TYPE II CYTOTOXIC HYPERSENSITIVITY

- occurs when the system mistakenly identifies a normal constituents of the body as

foreign

- this reaction maybe the result of a cross reacting antibody possibly leading to cell and

tissue damage

- involves the binding of either IgM or IgG antibody to the cell bound antigen -- which

activates the complement cascades

** COMPLEMENT SYSTEM --

DISORDERS ASSOCIATED WITH TYPE 2 (CYTOTOXIC) HYPERSENSITIVITY

1. Myasthenia Gravis

- the body mistakenly generates antibody against normal nerve ending

receoptors

2. Good Pasture Syndrome

- itgeneratios antibodies against lung and renal tissue, producing lung damage

and renal failure

3. Hemolytic Anemia of Newborn

4. Transfusion Reaction

5. Pernicious Anemia

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TYPE III IMMUNE COMPLEX HYPERSENSITIVITY

- hypersensitivity involves immune complexes that are formed when antigens bind to

antibodies

- these type III immue complexes are deposited in tissues and vascular endothelium

which will result in increased vascular and tissue injury

- JOINTS and KIDNEYS are particularly susceptible to this kind of reaction

- formed by antigens and anibodiesusu the IgG type

DISORDERS ASSOCIATED WITH TYPE III HYPERSENSITIVITY

- lupuserythematosus

- rheumatoid arthritis

- certain types of nephritis

- bacterial endocarditis

S/S

- occurs 7-10 days after exposure

- sever urticaria

- angeioedema

- fever

- malaise

- mm soreness

- arthralgia

- splenogemaly

- occasional nausea and vomiting

- diarrhea

MEDICAL MANAGEMENT

- antipyretics (fever)

- analgesics (arthralgia)

- antihistamine and epinehprine (urticaria and engioedema)

1. LUPUS ERYTHEMATOSUS

- B-cells produce a multitude of autoantibodies and autoangitgens -- this autoantibody

andautoantigen combine to form immune complexes agaisnt body’s own tissues, such

as nucleic acids, red blood cells, platelets, coagulation protein an dlymphocytes

- the depositing of immune complexes in the body itssues, such as:

- kidney

- brain

- heart

- lung

- spleen

- GI tract

- skin

- peritoneum

- musculoskeletal system

- sets up an inflammatory response leading to tissue destruction in these areas

S/S

- depends on what body system is involved

3 TYPES OF LUPUS ERYTHEMATOSUS

a. DLE (discoid lupus erythematosus)

- consist of skin lesions only

- tends to occur on face or sun exposed reas

- patchy, sharply, crusty defiend skin plaques

b. Drug Induced Lupus Erythemaotus

- develop after use of certain meds

- cuausepleurocardial inflammation, fever, rash, and arthritis

c. SLE (systemic lupus erythematosus)

- chronic inflammatory multisystem disorder

- develops antibodies against its own tissue

- s/s depends on what body system is involved

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S/S

- depends on what body system is involved

MUSCULOSKELETAL

- polyarthritis

- hand deformities

SKIN

- “butterfly” ..refer book

RENAL

- glomerulonephritis and nephrotic syndrome (leading to leg, abbomina, and eye

edema)

LUNGS

- pleural effusion

- pleuritis

HEART

- pericarditis

GI

- anorexia

- n/v

- pancreatitis

MEDICAL MANAGEMENT (SLE)

- there is no way to prevent SLE but treatment is directed of symptom management and

reduction of inflammation

- non-steroidal anti-inflamm drugs (NSAIDs) -- this is used to control inflammation

- anti malarial drugs -- controls musculoskeletal and cutaneous s/s

- sunscreen lotion

- corticosteroids

- prednisone

- plasmapheresis -- process similar to dialysis that removes antibodies from

plasma

TYPE 4 DELAYED TYPE HYPERSENSITIVITY (CELLULAR)

- aka CELLULAR HYPERSENSITIVITY

- this occur 24-72 hrs after exposure to an antigen

- Example of this reaction is the effect of an intradermal injection to TB antigen or PPD

(purified protein derivative)

- sensitized T-cells react with the antigen at or near the injection site

- wherelymphokines are rleased attracts and activate retain macrphages at the site

- where lysozymes is rel ..

1. CONTACT DERMATITIS

- acute or chronic inflamm that result from direct skin contact with chemicals or

allergens

4 BASIC TYPES

a. allergic

b. irritants

c. phototoxic

d. photo-allergic

ALLERGIC TYPE

- result from contact of skin and allergenic susbtance

- has sensitization period of 10-14 days

S/S

- vasodilation and perivascular inflltrates on the dermis

- intracellular edema

- usu seen on dorsal aspect of hand

DIAGNOSTIC TESTING

- patch testing

TREATMENT

- avoiding of offending amterials

- cool water compress

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- prednisone for 7-10 days

- topic corticosteroids for mild cases

- oral antihistamine to relieve pruritus

IRRITANTS

- resultsform contact with a substance that chemically or physically damage the skin on

nonimmunologic basis

- occurs after 1st exposure to irritants or repeated exposure to milder irritants over an

extended period of time

S/S

- dryness lasting days to months

- vesiculation, fissures, cracks

- hands and lower arms are most common area

DIAGNOSTIC TEST

- patch test

TREATMENT

- identification and removal of source of irritation

- application of hydrophilic cream or petrolatum to soothe and protect

- topical corticosteroids and compresses for weeping lesions

- antibiotics for infection and oral histamines for pruritus

PHOTOTOXIC

- resemble the irritants type but requires sun and a chemical combination to damage the

epidermis (i.e. sunburn)

S/S

- similar to irritant dermatitis

DX

- patch test

TX

PHOTOALLERGIC

- resembles allergic dematitis but requires light exposure in addition to allergen contact

wo produce immunologic reactivity

S/S

- vasodilation and pervascularinfltrates on the dermis

- intracellular edema

- usu seen on dorsal aspect of hand

DX TEST

- photopatch test

TREATMENT

- same as allergen dermatitis

NURSING STRATEGIES FOR ALLERGY MANAGMENT

- identify the pt’s known allergens (medication, foods, insects, environmental allergen)

- describe the pt’s typical allergic reaction and its severity

- document the pt’s allergies (medication, foods, insects environmental allegen) in pt’s

medical record

- post allergy alerts appropriately

- encourage the pt to wear a medical alert band and to carry informations about allergy

at all times

- investigate potential for allergic reaction with all new medications through constultation

with the pharmacist

- instruct the patient to question all medication and new foods

- identify early manfestation of allergic reactions

- administer emergency tx for allergic reaction

- monitor pt’s response and status for 24 hrs after a severe allergic reaction

- instruct the pt and family about emergency home amangementfoalleric reaction

- instruct the ptadn family about avoidance measures to reduce risk of exposure to

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allergens

CHEMICAL MEDIATORS OR HYPERSENSITIVITY

1. HISTAMINE

- physiologic effect of histamine upon major organ includes contraction of bronchial

smooth muscle resulting in WHEEZING and BRONCHOSPASM

- dilation of small venules and constriction of larger vessels causing erythema, edema,

andurticaria

- an increase in secretions of gastric and mucous cells, causing diarrhea

- HAS 2 RECEPTORS

- H1 - are found predominantly on bronchiolar and vascular smooth mm cells and

used for tx of allergic disease (i.e. diphenhydramine or benadryl)

- RR tract

- H2 - found in gastric parietal cells and are used pharmacologically to inhibit

gastric secretion in peptic ulcer disease (i.e. ranitidine, cimitidine)

- GI tract

2. LEUKOTRIENES

- intitiates the inflammatory response

- produces sustained spasm of bronchioles

3. PLATELET ACTIVATING FACTOR (PAF)

- responsible for initiating platelet aggregation at site of hypersensitivity reaction

- causes broncho constriction

4. BRADYKININ

- responsible for the contraction of smooth muscles of bronchi and blood vessels

- it causes increase permeabilty of capillaries resulting in edema

- stimulate nerve cell fiber and produces PAIN ONLY!!!

5. SEROTONIN

- released during platelet aggregation

- causing contraction of bronchial smooth muscle

6. PROSTAGLANDIN

- produce smooth mm contraction, vasodilaton, and increase capillary permeability

- causes fever and pain

7. EOSINOPHIL CHEMOTACTIC FACTOR OF ANAPHYLAXIS (ECF-A)

- attract eosinophil

- released from distrupted mast cells

8. HEPARIN

- anticoagulant

PRIMARY MEDIATORS

- preformed and found in mast cells or basophils

- includes:

- histamine

- prostaglandin

- ECF-A

- PAF

SECONDARY MEDIATORS

- inactiveprecursos formed or rleased in resonse to primary mediators

- includes:

- bradykinin

- serotonin

- heparin

- leukotrienes

THE END ^____^

PSYCHIA WARD (working phase)

GROUP 1, 2, and 3

dance therapy

music therapy

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MONDAY - turn in notebook (NCM104)

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