INFLAMMATORY AND IMMUNOLOGIC DISTURBANCES

By: WILLYN B. ADRIAS, RN.,MN.

IMMUNITY – is the body’s specific protective response to an invading foreign agent or organism.; ability of the body to fight or conquer infection.

IMMUNE SYSTEM Function:

1. defense against physical injury and infection2. maintenance of homeostasis, a state of equilibrium of the internal environment

ORGANS AND TISSUES OF THE IMMUNE SYSTEM

Bone marrow – production site of RBC,s WBC,s and platelets. It’s primary function is hematopoiesis(formation of blood cells)

Thymus – is a single unpaired gland that is located in the mediastinum and is the primary gland of the lymphatic system. Its primary function is allowing the T lymphocytes to develop before migrating to the lymp nodes and the spleen.

Lymph nodes and vessels perform several important functions such as: transporting lymph, filtering and phagocytizing antigens, generating monocytes and lymphocytes.

Spleen functions include: a. Removing worn out erythrocytes from blood, b. Storing blood and platelets, c. Filtering and purifying blood.

Tonsils, adenoids and other mucoid lymphatic tissues defend the body against microorganisms.

Hematopoietic system(bone marrow)

CLASSIFICATION OF IMMUNITY

I. SPECIFIC IMMUNITY A. HUMORAL IMMUNITY – characterized by

production of antibodies by the B lymphocytes in response to a specific antigen. Antibodies – are large proteins called immunoglobulins found in the globulin fraction of the plasma proteins.

IgG – 75% of total Ig in the body - source: interstitial fluids( serum &

tissues)

IgG – Function: assumes major role in blood-borne infections: activates complement system: enhances phagocytosis: crosses placenta

IgA - 15% - Source: blood, saliva, tears , breastmilk,

prostatic, gastrointestinal and resp. secretions.

- Function: protects against GI, GU, and respiratory infections.

: prevents absorption of antigen from food : passes to neonate thru breastmilk

IgM : 10% : Source: Intravascular : Function: appears as the first Ig pro-

duced in response to bacterial and viral infections

: activates complement systemIgD : 0.2% : Source: serum in small amount

: Function: influences B-lymphocytes but role is unclear IgE : 0.004% : Source: Serum : Function: allergic and hypersensitivity

reactions : combats parasitic infections

ANTIGEN-ANTIBODY REACTION

Agglutination – antibodies disarmed antigens by causing them to clamp together

Precipitation – this reaction occurs when antibody reacts with a soluble antigen resulting in an insoluble complex which then precipitates.

Neutralization – this occurs when antibody combines with toxins produced by some infectious agents to render them inactive and easier to engulfed and removed from the body.

Lysis – this is when antibody attacks cell membrane causing microorganisms to rupture.

Opsonization – in this process, the antigen-antibody molecule is coated with a sticky substance that also facilitates phagocytosis.

B. CELLULAR IMMUNITY – T- lymphocytes are responsible for cellular immunity. These lymphocytes spend time in the thymus, wheren they are programmed to become T-cells.

2 major categories of T cells a. Helper T cells – are activated upon recognition of antigens and stimulate the rest of the immune system. b. Cytotoxic T cells – (Killer T cells) attack the antigen directly by altering the cell membrane and causing cell lysis(disintegration) and releasing cytolytic enzymes and cytokines.

II. NON-SPECIFIC IMMUNITY Defenses of the body non selectively directed to foreign substances. 1. Structural – certain specialized structures in

the body that protect human from microorganisms. EX. Skin, eyebrow, eyelashes

2. Mechanical – mechanical processes in the body protects it from foreign bodies. EX. Peristaltic activity, vomiting, diarrhea, tear flow

3. Chemical – certain chemicals in the body fights microorganisms. EX. Urine, vaginal secretions, perspiration

4. Biologic – these are bacteria that are considered normal flora and are essential for body processes.

5. Inflammatory Response – considered as one of the major function of the non-specific immune system. It is the defensive reaction of the body intended to neutralize, control or eliminate the offending agent to prepare the site for repair.

INFLAMMATION- a biochemical and cellular process that occurs in vascularized tissues- most of the essential components of the inflammatory process are found in the vascularized circulation, and most of the early mediators(facilitators) of inflammation increase the movement of plasma and blood cells from the circulation into the tissues surrounding the injury called as the exudates which defends the host against infection and facilitate tissue repair and healing.

CARDINAL SIGNS OF INFLAMMATION

1. Redness(Rubor)2. Heat(Calor)3. Swelling(Tumor)4. Pain(Dolor)5. Loss of function(Function Laesa)

Redness and heat – results when vasodilation occurs after transient vasoconstriction that follows injury

Swelling – results when vascular permeability increases, and plasma leaked into the inflamed tissues.

Pain – results when the pressure of fluids or sealing on nerve endings, and to the irritation of the nerve endings in chemical mediators released at the site

Loss of function – related to pain and swelling

Loss of function happened when:1. Vascular response – transient

vasoconstriction followed by vasodilation, causing influx of blood to the inflamed area. These fluid pushed into the surrounding sites of injury would consequently become inflammatory exudates which has the following functions as:

- dilute toxins released by the bacteria - bring to site certain nutrients necessary for

tissue repair - carry protective cell that would destroy bacteria

2. Cellular response as follows:a. Margination – also known as pavementing occurs when leucocytes stick to the walls of the blood vessels.b. Emigration – occurs when leococytes multiply and travel to the areas of injuryc. Chemotaxis – is the directional orientation of leucocytesd. Phagocytosis – process where bacteria are engulfed or ingested.

3. Chemical response includes the release of the following chemicals. a. Histamine – initiates vascular response by increasing vascular dilation and permeability b. Bradykinin – increases vascular permeability c. Prostaglandin – also increases vascular permeability.4. Fibrin-Barrier Response – fibrin forms wall on the inflamed area to prevent invasion of irritants to other tissues. This phenomenon is also known as a “Wall-Off”.

HUMORAL IMMUNITY- one of the two forms of immunity that respond to bacteria and other foreign antigens. It is mediated by circulating antibodies(immunoglobulins IgA, IgB and IgM), which coat the antigens and target them for destruction by polymorphonuclear neutrophils.

CELLULAR IMMUNITY- the mechanism of acquired immunity characterized by the dominant role of T-cell lymphocytes- is involved in resistance to infectious disease caused by viruses and some bacteria and is delayed hypersensitivity reactions, some aspects of resistance to cancer, certain autoimmune diseases, graft rejection and certain allergies.

Antibody - an immunoglobulin produced by lymphocytes in response to bacteria, viruses, or other antigenic substances.- it is specific to antigen- it includes agglutinins, opsonins, and precipitins.

Antigen- a substance usually a protein that causes the formation of an antibody and reacts specifically with that antigen.

COMPARISON OF HUMORAL AND CELLULAR CELL RESPONSE

HUMORAL IMMUNITY CELLULAR IMMUNITY

B lymphocytes Production of antibodies Memory is present Examples are: bacterial

phagocytosis, anaphylaxis, hay fever and asthma, immune complex disease, bacterial and viral infection

T lymphocytes Production of sentisized

cells and lymphokines Memory is present Examples are: transplant

rejection, delayed hypersensitivity, graft vs. Host disease, tumor destruction, intracellular infections, viral, fungal and parasitic infections

STAGES OF IMMUNE RESPONSE

Recognition stage – circulating lymphocytes and macrophages recognize foreign materials or antigens as nonself

Proliferation stage – sensitized lymphocytes proliferates, differentiate, and mature into T and B cells.

Response stage – antibody is produced with specific T-cell action.

Effector stage – antigen is destroyed by antibody, which is produced by B-cell or cytotoxic T-cell action.

PROPERTIES OF IMMUNE RESPONE

Recognition – able to recognize self from nonself

Memory – recalls type of antigen(pick up imprint of the antigen structure)

Diversity of action Specificity of action

The unique action of the last 2 properties is its diversity of ability to respond while at the same time responding with specificity of

action.

TYPES OF IMMUNITY

A. NATURAL IMMUNITY – innate or genetically or primary immunity. - provides a nonspecific response to any foreign invader, regardless of the invaders composition.

- the basis of natural defense mechanism is merely the ability to distinguish between self and nonself

B. ACQUIRED IMMUNITY – or secondary immunity is an immunologic response acquire during life but not present at birth.

1. ACTIVE ACQUIRED IMMUNITYa. Person develop his own antibodiesb. Takes 10 t0 14 days to developc. Permanentd. Body cells undergo change

Active acquired immunity could either be:* Natural – having contact with antigen naturally such as getting sick or frequent exposure to smaller doses of microorganisms like: chickenpox, measles, mumps

* Artificial – acquiring antigen through vaccines or toxoids like in BCG, DPT and POLIO.

2. PASSIVE ACQUIRED IMMUNITY:a. Person receives preformed antibodiesb. Provides immediate immunityc. Temporaryd. No cellular changes

Passive acquired immunity could either be: * Natural – acquired naturally during breast-

feeding like from colostrum * Artificial – having preformed antibodies such as antitoxins, antiserum and gamma- globulin, ex. Immune serum globulin

COMMON DIAGNOSTIC PROCEDURES

WBC count – used to suggest the presence of infection, an allergy or leukemia. Used to help monitor the body’s response to various treatments and to monitor bone marrow function. Detects dangerously low number of WBC.

WBC differential count – assesses the ability of the body to respond to and eliminate infection. Detects the severity of allergic reactions; parasitic and other types of infection and drug reaction.

INTRADERMAL TEST (MANTOUX TEST) (PPD) – given intradermally in the forearm, with 10mm induration significant reaction is positive(+), reading done in 48-72 hours, if positive result, it does not mean that active disease is present, but indicates exposure to Tuberculosis.

RADIO IMMUNO ASSAY (RIA) – highly sensitive and specific assy method used to determine antibody concentrations or to determine the concentration of any substance against which specific antibody can be produced.

ELISA(ENZYME LINKED IMMUNOSORBENT ASSAY – identifies antibodies specifically against HIV. It does not establish diagnosis of AIDS, rather it indicates that the person has been exposed to or infected with HIV called SEROPOSITIVE.

WESTERN BLOT ASSAY – used to confirm seropositivity as identified by the ELISA.

BONE MARROW BIOPSY – assess the quantity and quality of each type of cell produced within the marrow. Used to document infection or tumor within the marrow.

CATEGORIES OF IMMUNOLOGIC DISORDERS

A. IMMUNODEFICIENCY – caused by a defect or deficiency in phagocytic cells, B lymphocytes, T lymphocytes or the complement system.= the clinical results of impaired function of one or more components of the immune or inflammatory response, including B cells, T cells, phagocytic cells and complement.= failure of these self-defense mechanisms to function at normal capacity.

Cardinal symptoms of immunodeficiency:1. recurrent infection2. infections caused by normal flora3. poor response to treatment of infections4. chronic diarrhea

IMMUNODEFICIENCES:1. Primary immunodeficiency

- rare disorder with genetic origins seen primarily in infants and young children- occurs if lymphocyte development is arrested or disrupted in the fetus or embryo.-symptoms usually develop early in life and children witrh these disorders seldom survive childhood.

Hyperimmunoglobulinemia (HIE) syndrome – a sex-linked recessive disorder found only among male.- characterized by PMN(polymorphonuclear cells) engulfing microorganisms but killing does not take place because PMN lack the necessary digestive enzyme.

Major symptoms of HIE syndrome 1. bacterial 2. fungal 3. viral infections 4. deep-seated cold abscess

Bruton agammaglobulinemia – results from lack of differentiation of B cell precursors into mature B cells. As a result, plasma cells are lacking, and the germinal centers from all lymphatic tissues disappears, leading to a complete lack of antibody production against invading bacteria, viruses and other pathogens.- thymus gland is intact and the response of T cell is normal.

Hypogammaglobulinemia or Common Variable immunodeficiency (CVID)- results from lack of differentiation of B cells into plasma cells.- there is general lacking of immunoglobulins in the blood.

Agammaglobulinemia – the condition in which B cell development are totally or nearly absent.

Di George’s syndrome or Thymic hypoplasia – a T-cell deficiency that occurs when the thymus gland fails to develop normally during embryogenesis.

Presenting signs:1. recurrent infection2. hypoparathyroidism3. hypocalcemia4. tetany5. convulsions6. congenital heart disease7. renal abnormalities8. abnormal faces

Severe Combined Immunodeficiency disease(SCID)- both the B cell and T cell are missing.- there is complete absence of humoral as well as cellular immunity caused by an X-linked or autosomal genetic abnormality.

Ataxia telangiectasia – characterized by uncoordinated muscle movement(Ataxia) and vascular lesions caused by dilated blood vessels(telangiectasia) usually occurs during the first 4 years of life

Nezelof’s Syndrome – the individual is born without thymus gland and have various degrees of B-cell immunodeficiency associated with various combinations of increased, decreased or normal immunoglobulin levels.

Wiscott-Aldrich Syndrome – an SCID compounded by thrombocytopenia or loss of platelet.

2. Secondary Immunodeficiency – are common than primary deficiences and frequently occur as a result of underlying disease process or from treatment of these diseases:

Common cause: a. Malnutrition b. Chronic stress c. Burns d. Uremia e. Diabetes mellitus

Acquired immunodeficiency Syndrome – AIDS- the best known example of an acquired dysfunction of the immune system.- represents a frightening disease because of its extremely high mortality in untreated individuals.

Etiology : HIV or retrovirusRisk factors:1. male homosexual relations2. intravenous drug use or the injecting drug

user.3. heterosexual relations with an HIV infected

partner4. sexual relations with infected individuals

Mode of transmission1. Anal intercourse2. injection of drug – direct blood exposure to contaminated needles and syringes.3. blood and blood products – including those persons with hemophilia and other people who are blood recipients.4. transplacental – AIDS transmitted in utero from mother to child.

Clinical manifestations:1. persistent generalized lymphadenopathy – characterized by the generalized enlargement of the lymph nodes.2. lesser AIDS – conditions such as oral candidial infection arise and examination of platelet reveals decreased. Most of the patients may be completely asymptomatic.3. AIDS related complex(ARC:wasting syndrome –profound involuntary weight loss of 10% body weight due to unexplained diarrhea for more than one month or chronic weakness.- intermittent fever- splenomegaly- low platelet count and lymphocytes- severe body malaise

AIDS SYNDROMEOpportunistic infections

1. Pneumocyctis carinii- 60% of the AIDS patients initially manifest PCP. It was thought to be protozoan but recent studies

showed that it is a rare fungal infection that cause diseases only to immunocompromised patients:

- patients tend to demonstrate the ff:a. Feverb. Chills c. Non-productive coughd. Shortness of breathe. Dyspneaf. Occasional chest pain- Patients may go to respiratory failure within 3 days after

onset of symptoms.

2. Mycobacterium Avium Complex(MAC)- a leading bacterial infection in people

with AIDS ..Comprising a group of acid fast bacilli, usually causes respiratory infection3. Tuberculosis

- tend to occur in injecting drug users and other groups with with a pre-existing high prevalence of TB infection

- TB that occurs late in HIV infection is characterized by absence of a tuberculin test response because of the compromised immune system

4. Oral candidiasis- a fungal infection occurs nearly

in all AIDS related conditions. It is characterized by creamy white patches in the oral cavity

-Symptoms: difficult and painful swallowing

: retrosternal pain5. Cryptosporoidal virus

- causes diarrhea up to 6L per day resulting to viral infection

6. Cryptococcus neoformans- char by symptoms such as: fever, headache, malaise,

stiff neck, nausea and vomiting, seizure7. Kaposis sarcoma

- most common HIV related malignancy involving endothelial layer of the blood and lymphatic vessels

- cutaneous lesions appearing anywhere on the body are usually brownish pink to deep purple surrounded by ecchymosis and edema8.B cell lymphoma(non hodgkins lymphoma

- including multiple organ involvement and complications related to opportunistic infection

- compromise approximately 11% of all childhood cancer-a genetic term for a wide spectrum of disorders

characterized by the malignant transformation of the lymphoid system.

NHL is differentiated from HL by lack of RS(Reed-sternberg cells) and the other cellular changes not characteristics of HL.

- the common finding of NHL are alterations in the tumor DNA

- arise from single outlaw cell(Monoclonal) and probably develop with accumulation of multiple genetic hits

- its most common type of chromosomal alteration is translocation

AIDS DEMENTIA COMPLEX- neurologic dysfunction results from the direct effects of HIV or nervous tissue, opportunistic infections, primary neoplasm, CV changes and metabolic encephalopathies.

Diagnostic exams:1. ELISA

- test that identifies antibodies directed aseptically against HIV. It does not establish diagnosis of AIDS, rather indicates that the person has been exposed to infected HIV called seropositive.

- or it is a presumptive test

2. Western blot assay- conformity test of AIDS3. Immunoflourescent Assay(IFA)- preferred by some physician over the western blot assay since it is more rapid and simple to perform.

Nursing management:1. promote skin integrity- change position every 2 hours- apply medicated lotions, ointments and dressings

- avoid using adhesive tapes- advice to wear cotton sock to

prevent feet from perspiring if lesions are

found in the legs- clean peri-anal area every after

bowel with non-abrasive soap and water to

prevent escoriation- sitz bath to promote comfort- assess frequently for integrity of

the oral mucosa

2. Promote usual bowel habit -- monitor for pattern of diarrhea and consistency of stools- report abdominal pain and cramping- during periods of acute intestinal inflammation, the patient may be placed on NPO to rest the GIT- encourage increase dietary intake- avoid foods that are irritating to the bowel such as spicy foods, food with extreme temperature and carbonated drinks- administer antispasmodic and anti-diarrheal agents

3. prevent infection- monitor for signs of infection- prevent overcrowded place

4. improve activity tolerance-assist in activities of daily living

5. maintain thought processes- assess mental status- use simple explanation- provide memory aids- give positive feedbacks for appropriate behavior

6. improve airway clearance- monitor respiratory status- encourage intake of 3l per day- administer humidified oxygen

7. relieve pain and discomfort- administer pain relievers- encourage to wear elastic stockings to equalize pressure

8. improve nutritional status- monitor daily weight- assess factors that may interfere with dietary intake- control nausea and vomiting with anti-emetic medications- encourage to eat food that are easy to swallow and to avoid rough and spicy foods- encourage to rinse mouth with lidocaine before meals- give food supplements

9. decreased sense of isolation10. Assist coping with grief

Mode of Transmission1. sexual contact2. blood transfusion3. contaminated syringes, needles, nipper, razor blades

Signs and Symptoms:1. Physical

- maculo-papular rashes- loss of appetite- weight loss- fever of unknown origin- malaise, persistent diarrhea- TB- esophageal candidiasis- Kaposi’s sarcoma-pneumocystis carinii pneumonia- gaunt looking, apprehensive

2. Mental(early stage)- forgetfulness- loss of concentration- loss of libido- apathy- psychomotor- withdrawal

3. Mental(later stage)- confusion- disorientation- seizures- mutism- loss memeory- coma

Prevention:1. maintain monogous relationship2. avoid promiscuous sexual contact3. sterilize needles, syrnges and instruments used in cutting operations4. proper screening of blood donors5. rigid examination of blood and other products for transfusion5. avoid oral, anal contact, swallowing of semen6. use of condoms and other protective device

HIV/AIDS- first occurred in africa and spread in the carribean island.- reported in the USA in 1981- this sexually transmitted disease spread so rapidly that it is soon occurred in epidemic proportion inseveral countries of the world including the Philippines. It is currently pandemic(occurring throughout the world)- the first case of AIDS in the Philippines was reported in 1984, as at May 2000, based on Philippines National AIDS council(PNAC) records, there were 1,385 HIV poisitive and 464 AIDS cases. There have been 206 deaths

B. GAMMOPATHIES- immunologic disorders pertaining to elevated level of gammaglobulin in the serum.- also known as hypergammaglobulinemia

- Multiple Myeloma – is a malignant disease of the most mature form of B lymphocyte

which is the plasma cell. - a B cell cancer characterized by the

proliferation of malignant plasma cells that aggregate into tumor masses and then become distributed throughout the

sleletal systems.

Clinical manifestationof MM1. Bone pain usually in back and ribs and worsen with rest. The pain is due to a substance secreted by the plasma cells which is the osteoclast activating factor, that stimulates bone breakdown. Thus, lytic lesions and osteoporosis is seen during x-rays.2. Recurrent fractures3. Hypercalcemia due to escape of calcium ions from the bones4. Renal failure: large immunoglobulin molecules can damage the renal tubules.5. Fatigue and weakness due to anemia

Pathophysiology:malignant plasma cells produces M-

Protein or monoclonal protein release of osteoclast activating factors breakdown of the bone

Diagnostic Exams:1. Bence Jones Urine Test – detects abnormal globulin in the urine2. Xray or Bone scan – establishes the degree of bone involvement3. Bone marrow aspiration – detects number of plasma cell in the bone marrow

Medical management:- there is no cure for MM, since it is a disease of malignancy, it is treated with chemotherapy and radiation therapy.

Nursing management:

1. administer pain reliever for bone pain2. maintain hydration to diminish exacerbation of complication3. prevent from infection

C. AUTOIMMUNE DEFICIENCY – these disorders involve inappropriate reaction by the immune system in which antibody form against self-antigen.autoimmunity - is a breakdown of tolerance in which the body’s immune system begins to recognize self-antigens as foreign.

1. Systemic Lupus Erythematous(SLE) – a result of disturbed immune regulation that causes exaggerated production of auto-antibodies.

- the increase in auto-antibody production is thought to result from abnormal suppressor T-cell function, leading to immune complex deposition and in tissue damage.- seen more often in women especially in the 20 to 40 year old age group- a transient lupus like syndrome that is indistinguishable both clinically and in the laboratory from spontaneously occurring SLE also can develop from prolonged use of drugs, particularly hydralazine(an antihypertensive agent) and procainamide(an antidysrhythmic drug).

11 clinical findings of SLE:1. facial rash confined to the cheeks(malar rash)2. discoid rash(raised patches, scaling)3. photosensitivity(skin rash in sunlight)4. oral or nasopharyngeal ulcers5. non-erosive arthritis of at least two peripheral joints6. serositis(Pleurisy, pericarditis)7. renal disorders(proteinuria of >0.5 g/day or cellular cast)8. neurologic disorders(seizures or psychosis)9. hematologic disorders(hemolytic anemia, leukopenia, thrombocytopenia)10. immunologic disorders(positive LE cell preparation, anti-DNA, false-positive serologic test for syphilis)11. presence of antinuclear antibody (ANA)

Predisposing Factors SLE:1. Genetic and hormonal factors – onset

during the child bearing years.2. Environmental factors – such as

sunlight, thermal burns3. Drugs – hydralazine(apresoline),

procainamide(pronestyl), INH, chlorphromazine and other anticonvulsant

Clinical manifestations of SLE:1. Arthralgia or arthritis – 90% of individuals. A common presenting

features of SLE frequently accompanied by morning stiffness and not deforming in nature.

2. Classic butterfly rash – 70% to 80% of individuals. Papulosquamous or annular polycyclic lesion occurs across the bridge of the nose and cheeks. The rashes worsen with sunlight.

3. Pericarditis – 30% to 50% of individuals. Most common cardiac manifestation of SLE

4. Lymphadenopathy and vasculitis – 70% to 80% of individuals. Patients manifest papular, erythematous and purpuric lesions on the fingertips, elbows, toes and forearm. These may progress into necrosis.

5. Lupus nephritis – 40% to 50% of individuals.Occurs as antinuclear antibodies/attaches to the DNA and is deposited in the renal glomerulus.

6. Psychosis and depression7. Hematologic abnormalities – 50% of individuals, with anemia being

the most complication

Diagnostic exam of SLE:1. LE cell test – test for presence of lupus

erythematous2. ANA or anti nuclear antibody test – the

best definitive test for SLE since ANA is present in all cases of SLE even in the inactive stage of the disease

3. Total Serum Complement – the best test to follow the course of disease.

Medical Management:1. NSAID(Non steroidal anti-inflammatory drug) – it is

useful in treatment of the arthritis associated with SLE

2. Corticosteroid like prednisone – ammelurates the mainstay therapy of SLE. Its side effect is to suppress immune system thus suppressing body reactions to autoimmune antibodies.

3. Cytotoxic agents – arrest autoimmune activity of the SLE

4. Plasma-paresis – 3-4 liters are exchanged weekly from a plasma of a normal donor which is used to remove circulating auto antibody and immune complexes from the blood before organ and tissue damage occurs.

Nursing care management:1. Institute reverse isolation2. Encourage personal hygiene3. Maintain clean environment4. Screen visitor from cold5. Avoid drugs such as contraceptives

and anticonvulsant6. Avoid unnecessary blood transfusion7. Avoid fatigue8. Discourage pregnancy

2. Rheumatoid arthritis –a systemic autoimmune disease that causes chronic inflammation of connective tissue, primarily in the joints.- the joints most commonly affected are: fingers, feet, wrist, elbows, ankles, and knees, but the shoulder, hips, and cervical spine also may be involved, as well as the tissue of the lungs, heart, kidney and skin.- develops most often in women- despite intensive research, the cause of RA remains obscure. It is probably a combination of genetic, environmental, environmental, hormonal and reproductive factors.

Clinical manifestation:1. Joint pain, swelling and warmth2. Erythema – redness or inflammation of the skin3. Lost of function or joint stiffness especially in the morning lasting

for 30 minutes4. Hand and feet deformities caused by misalignment resulting from

swelling, progressive joint destruction or the subluxation that occurs with a bone slips over another

5. Fever6. Weight loss7. Fatigue8. Edema9. Lymph node enlargement10. Raynaud’s phenomenon – intermittent attacks of ischemia of trhe

extremities of the body, especialy the fingers, toes, ears, and nose, caused by exposure to cold or by emotional stimuli.- the attacks are characterized by severe blanching of the extremities, followed by cyanosis then redness; usually accompanied by numbness, tingling, burning and often pain.

Diagnostic exam of RA:1. ESR – reveals elevated 2. C Reactive Protein – positive in RA3. ANA – positive4. Arthrocentesis – synovial fluid shows

cloudy, milky or dark yellow and contains numerous inflammatory cells, such as leukocytes and complement.

5. XRAY studies helps monitor progress of the disease

Management of RA:1. NSAIDS : blocks the enzyme involved in inflammation while

leaving the enzyme involved in protecting the stomach lining.(COX-2 inhibitor)

2. Antimalarials, Gold, penicillamine – initiated early in treatment; alters cellular metabolism; alter enzyme function and immune response and suppress phagocytic activity

3. Biologic response modifiers such as cytokines4. Corticoesteroids – used when patient has unremitting

inflammation and pain or needs a “bridging” medication while waiting for the slower disease modifying anti-rheumatic agent.

5. Synovectomy – excision of synovial membrane6. Tenorrhapy – suturing of tendons7. Arthrodesis – surgical fusion of the joint8. Arthroplasty – surgical repair and replacement of the joint.

3. Hashimoto’s thyroiditis – chronic lymphocytic thyroiditis diagnosed based on the inflammation of the gland. It is not accompanied by pain, pressure symptoms or fever and thyroid activity is normal - cell mediated immunity plays a significant role in the pathogenesis.- treatment goal: reduction of the size of the gland

D. HYPERSENSITIVITY – an abnormal, heightened reaction to any type of stimuli.

1. ANAPHYLACTIC TYPE(TYPE I) - is an immediate reaction beginning within minutes of exposure to an antigen and this is mediated by IgE antibodies.anaphylaxis – is a clinical immediate immunologic response between a specific antigen and antibodyEtilogy:1. food2. drugs3. venom4. blood products5. allergen extract6. diagnostic agents

Clinical manifestation of type I1. Urticaria2. Bronchospasm3. Generalized swelling4. Hypotension5. Nausea and vomiting

Management:6. Administer oxygen as indicated7. Epinephrine as needed8. Corticosteroids may be given to relieve

bronchospasm9. IV fluids are administered to correct hypotension

Atopic allergies1. Allergic rhinitis/Hay fever – inflammation of the nasal mucosa. It is usually induced by airborne pollen or molds. Sensitization begins by ingestion or inhalation of an antigen. On reexposure the nasal mucosa reacts by the slowing of ciliary action, edema formation, and leukocyte infiltration. Histamine is the major mediator of allergic reaction

Clinical manifestations:1. nasal congestion: clear, watery, nasal discharge2. intermittent sneezing3. nasal itching4. itching of throat and palate5. headache6. pain over paranasal sinuses

Management:1. Administer antihistamine as ordererd2. May administer adrenergic agents to

cause vasoconstriction of the mucosal vessel

3. Mast cell stabilizer like intranasal cromolyn sodium is a nasal spray that inhibits the release of histamine and other mediators of allergic response

4. Advice the client to avoid allergens like dust, hapte-rich foods, etc.

2. Atopic dermatitis – most patients have elevated IgE in the serum. Pruritus and hyperirritability of the skin are the most consistent features and are related to large amount of histamine in the skin. Excessive dryness of the skin results from change in the lipid content, sebaceous gland activity, and sweating.

3. Urticaria – also known as Hives is a type I hypersensitive reaction of the edematous elevations that vary in size and shape, itch and cause local discomfort. It stays from few minutes to hours before disappearing.

2. CYTOTOXIC (TYPE 2) – occurs when the system mistakenly identifies a normal constituent of the body as foreign and mediated by whether IgG or IgM.

A. Blood transfusion reactionTYPES:1. Hemolytic Clinical manifestations - chills, fever, headaches, chest pain, tachycardia, dyspnea, hypotension, nausea and vomiting, restlessness and

shock

Nursing Care:- place patient in supine with head elevated at 20-30 degrees- administer fluid, epinephrine and cortico- steroids as ordered.- administer mannitol- insert an indwelling catheter- monitor intake and output- TSB for fever- stop blood transfusion- change IV fluid to prevent from infusing anymore- administer IV saline as ordered- obtain blood and urine sample

Example: Blood type “A” individual transfused with a Type “B” blood mistakenly antigen and antibody reaction agglutination & hemolysisof the RBC hemolyzed blood clogges capillaries unable to carry oxygenand food obstruction of blood flow

2. Contaminated bloodclinical manifestation:- chills, fever, abdominal pain, nausea and vomiting, diarrhes, hypotensionnursing care:- stop BT immediately- administer fluids

3. Febrile reactionclinical manifestation:- mild chills- fevernursing care:- administer antipyretic and antihistamine

4. Allergic reactionclinical manifestation:- pruritus, urticaria(hives), facial swelling, chills, fever nausea & vomiting, headache, wheezing, laryngeal edema, shock, respiratory distressnursing care:- administer antihistamine, epinephrine or corticosteroids

B. RH incompatibility – there is excessive destruction of RBC which results from antigen-antibody reaction and is characterized by hemolytic anemia and hyperbilirubinemia.

Father(Rh+) + Mother (Rh-) Rh incompatible-During the delivery of the first baby blood of the fetus escape to the body of the mother thru maternal sinuses, causingn Rh antibody towards Rh(+)

-subsequent pregnancies, the Rh(+) antibodies will destroy and cause the blood of the fetus to hemolize

- compesatory mechanism: increased production of immature RBC by the fetus

ERYTHROBLASTOSIS FETALIS

clinical manifestation of EF 1. sclera appears yellow before the skin does 2. skin color from light brown to yellow 3. lethargy 4. dark amber concentrated urine 5. poor feeding 6. dark stools

Diagnostic evaluation: 1. amniocentesis – analysis of bilirubin level in amniotic fluid before birth through the amniotic fluid of the mother. 2. Indirect Coomb’s test – is the direct evaluation of the presence of anti-Rh antibody in maternal circulation. 3. Direct Coomb’s test – this confirms the disease postnatally by detecting antibody attached to circulating lymphocytes of affected infants

RHOGAM INJECTION – after the first delivery, mother should be given Rhogam within 48 hours to prevent the maternal circulation from developing antibody against the opposite Rh factor.

3. IMMUNE COMPLEX(TYPE III)- are deposited in tissues or vascular endothelium that contributes to injury, the increase amount of circulating complexes and the presence of vasoactive amines.- the joints and kidneys are the primary susceptible to these type of allergy.

Serum Sickness- this type III hypersensitive reaction is known to be a result of the administration of therapeutic antisera of animal sources for the treatment and prevention of infectious diseases, such as tetanus, pneumoniua and rabies. manifestations: inflammatory reaction at the site of injection of the medication followed by regional and generalized lymphadenopathy. There is usually skin rash and joints are frequently tender and swollen.

4. DELAYED TYPE(TYPE IV)- occurs 24-72 hours after exposure and is mediated by sensitized T cells and macrophages.a. Contact dermatitis – a delayed eczematous condition caused by a skin reaction to a variety of irritating or allergenic materials

ex. Poison Ivy – most common type but soaps, detergents, cosmetics may also cause this type of dermatitis.

clinical manifestations:-itching, burning, erythema, skin lesions(vesicles), edema, weeping, crusting and finally drying and peeling of the skin

b. Skin graft/Organ rejection - skin graft is a technique in which a section of the skin is detached from its own blood supply and transferred to a free tissue to a distant(recipient) site. These are commonly used to repair defects and cover wound when insufficient skin is available to permit wound closure.

TYPES OF GRAFTS1. isograft/syngeneic - graft exchange between genetically dentical membrane of the same species2. allograft/allogeneic/homograft - graft exchange between individual of the same species3. autograft/autologous - graft exchange within the same individual4. xenogeneic - graft exchanged between individuals of different species

Rejection of Graft- described as immune complex response leading to rejection by recipient therapy usually due to incompatibility of cell surface antigen- this can be prevented by tissue typing and matching between donor and recipient

Immunosuppresive therapy are also useful in preventing graft rejection

1. Corticosteroid – impairs lymphocyte function, thus suppressing immune response

2. Azathioprine(Imuran) – prevent cell-mediated immune response while inactivating Ag receptor sites in T cells

3. Methotrexate – a folic antagonist; inhibit folace metabolism and is a potent suppressor of both humoral and cellular immunity

4. antilymphocyte serum – serum from animals injected to human results to antibody formation against the lymphocytes.5. cyclosporina – decreases the number of killer T cells without affecting granulocytes - used to suppress rejection

If you just found out you’re pregnant, one of the first and most important tests you should expect is a blood type test.

This basic test determines your blood type and Rh factor. Your Rh factor may play a role in your baby’s health, so it is important to know this information early in your pregnancy

People with different blood types have proteins specific to that blood type on the surfaces of their red blood cells.

There are four blood types (A, B, AB and O)

Each of the four blood types is additionally classified according to the presence of another protein on the surface of RBC that indicates your RH Factor. If you carry this protein, you are Rh Positive. If you don’t carry the protein, you are Rh negative.

Most people about 85% are Rh positive. But if a woman who is Rh negative and a man who is Rh positive conceive a baby, there is the potential for incompatibility

The baby growing inside the Rh negative mother may have Rh positive blood, inherited from the father

Statistically, at least 50% of the children burn to an Rh negative mother and Rh positive father will be Rh Positive

Rh incompatibility isn’t a problem if it’s the mother’s first pregnancy because, unless there’s some sort of abnormality, the fetus’s blood does not normally enter the mother’s circulatory system during the course of the pregnancy

However, during delivery, the mother’s and baby’s blood usually intermingles. When this happens, the mother’s body will begin to produce antibodies(protein molecules in the immune system that recognize, and later work to destroy, any substance “foreign” to body) against the Rh proteins that have been introduced into her blood.

Rh antibodies are harmless until the mother’s second or later pregnancies

If she is ever carrying another Rh positive child, her Rh antibodies will now recognize the Rh proteins on the surface of the baby’s blood cells as foreign

Rh antibodies will cross the placenta into the baby’s bloodstream and attack those cells, causing swelling and rupture of the baby’s RBC

A baby’s blood count can get dangerously low when this condition, known as hemolytic or Rh disease of the newborn, occur.

How is Rh disease of the newborn prevented and treated?- Today, when a woman with the potential to develop Rh incompatibility is pregnant, doctors administer a series of: 2 Rh immune-globulin shots during her first pregnancy- first shot – given around 28th wk of pregnancy- 2nd shot – given 72 hours after giving birth

Rh immune globulin acts like a vaccine, protecting against the development of the Rh antibodies that can cause complications during any future pregnancies.