Humoral and cell mediated Active/natural Active/artificial Passive Immunity Passive Natural Passive Artificial

Chronic, progressive, non-contagious, degenerative disease of the CNS Descending paralysis Remission and exacerbation Demyelinization of neurons Abrupt onset in previously healthy individuals Affects spinal cord primarily

Symmetrical, bilateral, peripheral polyneuritis Ascending paralysis Complete paralysis

Abrupt onset in previously healthy individuals Affects peripheral nerves and nerve roots primarily

Unknown cause Autoimmune response or viral infection Risk: gender 20-40 y.o cool climates, nonAsian heritage, viral illness in teen years, non-Asian heritage Precipitating factors: pregnancy, fatigue, stress, infection, trauma

Unknown cause Autoimmune response or viral infection Flu, URT viral infection, immunization of swine flu vaccine, Campylobacter jejuni most often implicated found in pultry, raw milks, pets, and contaminated water

Most commonly involved are the optic nerves, cerebrum, and cervical spinal cord Vision loss from optic neiritis Incoordination due to cerebellar involvement Bowel and bladdre dysfunction:spinal cord

S/S: Most common initial pattern is relapsingremitting MS Sexual dysfunction

S/S: Initial phase is followed by plateau phase Musle weakness Autonomic neuropathy

S/S: Fatigue and weakness Vertigo Tremors and spasticity of the LE Paresthesias Burred vision and diplopia Nystagmus Dysphasia Decrease perception to pain touch and temperature

S/S: Periheral neuritis (tingling and numbness in scattered areas, esp. the peripheries Complete paralysis

Lhermittes sign; tingling of back and thigh upon neck flexion Emtional outburst if frontal/temporal lobes are affected Hyperreflexia if basal ganglia DEATH; from resp.inf. Or area of the brain responsible for respiratory function

Cardiac dysrhythmisa, Urinary retention Hypertension Orthostatic hypotension

Dx. Exam: LP (increase CHON and IgG) EEG (visual evoked response) CT scan (increase density of white matter) MRI ( shows areas of demyelination) No definitive test:detailed history

Dx. Exam: CSF studies (increase CHON) EMG (slowed nerve conduction)

Dx is based on hx and physical examination

Mgt.: Corticosteroids (ACTH IV, Perdnisone); to reduce edema at sites of demyelination Baclofen (Lioresal), Dantrolene (Dantrium), Diazepam (Valium): skeletal muscle relaxant for spasticity Beta Interferon Betaseron) IFN: to alter immune response

Mgt: Mechanical Ventilation (if respiratory problem arises) Plasmapheresis (Decrease circulation antibodies) ECG (HR and rhythm abnormalities) Propanolol (to prevent tachycardia) AtSO4 (to prevent bradycardia during ET suctioning)

IgA.

IgA antibodies are found in areas of the body such the nose, breathing passages, digestive tract, ears, eyes, and vagina. IgA antibodies protect body surfaces that are exposed to outside foreign substances. This type of antibody is also found in saliva, tears, and blood.

IgG.

IgG antibodies are found in all body fluids. They are the smallest but most common antibody (75% to 80%) of all the antibodies in the body. IgG antibodies are very important in fighting bacterial and viral infections. IgG antibodies are the only type of antibody that can cross the placenta in a pregnant woman to help protect her baby (fetus).

 IgM.

IgM antibodies are the largest antibody. They are found in blood and lymph fluid and are the first type of antibody made in response to an infection. They also cause other immune system cells to destroy foreign substances

IgE. IgE antibodies are found in the lungs, skin, and mucous membranes. They cause the body to react against foreign substances such as pollen, fungus spores, and animal dander. They may occur in allergic reactions to milk, some medicines, and some poisons. IgD. IgD antibodies are found in small amounts in the tissues that line the belly or chest. How they work is not clear.

Type I: Immediate (Anaphylaxis) Hypersensitivity involves Cell-bound IgE Antibodies Anaphylaxis is a serious and dramatic allergic reaction with the release of histamine from the damaged cells. Anaphylaxis can cause shock and death if not treated immediately. Assessment: Identification of the allergy Difficulty breathing Difficulty swallowing Complaints of a swollen tongue Facial edema and swelling of lips Skin redness Presence of a rash

Interventions: Establish a patent airway Prepare for the administration of epinephrine (Adrenalin), Diphenhydramine HCl (Benadryl), or corticosteroids. Provide measures to control shock. Provide emotional support. Instruct the client to wear a medic-alert bracelet. Instruct the client in the use of prescribed medication such as epinephrine for immediate treatment of a reaction.

Is also an immediate reaction that generally involves harmful immune responses to surface antigens of red blood cells, platelets or granulocytes. Usually, however, one type of blood element is involved in a single episode.

Is typified by the hives of serum sickness and other manifestations due to soluble immune complexes that may deposit themselves anywhere in the body. Serum sickness occurs when IgG antibodies and antigen combine

A chronic progressive systemic inflammatory disease that can cause major organs and systems to fail. Connective tissue and fibrin deposits collect in blood vessels on collagen fibers and on organs. The deposits lead to necrosis and inflammation in blood vessels, lymph nodes, gastrointestinal tract and pleura. No cure for this disease is known

Causes: The cause of SLE is unknown, and SLE is thought to be due to a defect in the immunological mechanisms or of genetic origin. ANA andautoantibodies against Double stranded DNA T suppressor cell does not prevent autoantibody formation NK cell function is also suppressed Precipitating factors include medications, stress, genetic factors, sunlight or ultraviolet light, and pregnancy.

Assessment: Precipitating factors as sunlight, stress, medications and pregnancy. Dry, scaly raised rash on the face or upper body. Fever Weakness, malaise and fatigue Anorexia Weight loss Photosensitivity Joint pain polyarthrittis polyarthralgia Erythema of the palms, vasculitis Butterfly erythema of the face Positive antinuclear antibodies and lupus erythematous preparation Elevated erythrocyte sedimentation rate

Monitor skin integrity and provide frequent oral care. Instruct the client to clean skin with a mild soap, avoiding harsh and perfume substances. Assist with the use of ointments and creams for rash as prescribed. Identify factors that contribute to fatigue. Administer Iron, folic acid, or vitamin supplements as prescribed if anemia occurs. Provide a high vitamin and high iron diet.

Instruct in measures to conserve energy, such as pacing activities and balancing rest with exercise. Administer topical or systemic corticosteroids, salicylates, and nonsteroidal anti-inflammatory drugs as prescribed for pain and inflammation. Administer hydroxychloroquine sulfate as prescribed to decrease the inflammatory response. Instruct the client to avoid exposure to sunlight and ultraviolet light.

Monitor for bruising, bleeding, and injury. Assist with plasmaphareisis as prescribed to remove autoantibodies and immune complexes from the blood before organ damage occurs.

Provide emotional support and encourage client to verbalize feelings. Provide information regarding support groups and encourage use of community resources.

Is traditionally considered a chronic, inflammatory autoimmune disorder that causes the immune system to attack the joints. It is a disabling and painful inflammatory condition, which can lead to substantial loss of mobility due to pain and joint destruction. RA is a systemic disease, often affecting extra-articular tissues throughout the body. Including the skin, blood vessels, heart, lungs and muscles.

Occur in women during the menopausal years (48-52)

Causes: Autoimmune, unknown. Assessment: Pain and swelling in the joints especially in the smaller joints of the hands and feet. Generalized aching or stiffness of the joints and muscles especially after sleep or after periods of rest. Loss of motion of the affected joints. Loss of strength in muscles attached to the affected joints. Fatigue, which can be severe during a flare up. Deformity of joints over time. Malaise

Diagnostic exams: Joint X-rays Rheumatoid factor test (+) ESR is elevated CBC- low hematocrit, or abnormal plt counts. C-reactive protein may be a positive indication for pt.s with no detectable rheumatoid factor. Synovialfluid anaylsis. Medications: NSAIDs COX-2 inhibitors Corticosteroids Disease-modifying anti-rheumatic drugs Immunosuppressants TNF (Tumor necrosis factor) blockers Interleukin-1 receptor antagonist

Surgical procedure: Prosorba column- filter blood to remove antibodies. Joint replacement surgery

Interventions: Teach techniques to minimize joint stress while performing ADLs Provide information about the disease process and the medications. Encourage self-care such as exercise regularly, control weight, eat a healthy diet, apply heat compress or cold compress for occasional flare ups. Practice relaxation techniques Take your medications as recommended.

a. Stages of Infectious Disease Types of Infectious Agents BacteriaVirusesFungiProtozoalPrionsHelminths-

 Chain of Infection

Infectious agent - Reservoirs - Portal of exit Means of transmission -Susceptible host Portal of Entry Reservoir- People, equipment, water Portal of exit- excretions, secretions, skin, droplets Means of transmission- direct/ indirect contact, ingestion, airborne, fomites, blood Portal of entry- mucous membranes, GI tract, GU tract, Respiratory tract, broken skin Susceptible host- Immunosuppression, Diabetes, Surgery, Burns, Elderly, Infants

Mechanical defenseChemical defenseImmune defenseHost

 Assessment:

V/S- Resp rate, Temp, Pulse rate, BP, Pulse oxymetry Physical assessment- check for lymphadenopathy, break in skin integrity, Circulatory system, etc.
Diagnostic tests:

WBC count and determination Gram stain and culture sensitivity Examination for ova and parasites ( Fecalysis, UA, CBC) Skin tests (PPD, Mantoux, etc.) Immunologic tests (HBsAg, ELISA) other- proper collection of specimens

 Standard precautions Handwashing (universal) Gloving (blood-borne, direct contact) Mask, eye protection, face shield (droplet, conjunctival) Gowns (sterile, isolation, reverse isolation) Environmental control (fecal-oral route)

IA is rubella virus Direct and indirect contact Incubation of 14-21 days POCommunicability: 7 days before and 5 days after rash appears No prodromal stage in children. Rash starts on face, then goes downward. It is discrete, pinkish-red, maculopapular rash. It disappears the same order as it appeared. Gen symptoms include low-grade fever, headache, malaise and lympadenopathy. Complications: teratogenic effect to fetus

NI: provide supportive care, health teachings, fluid replacement, adequate rest, diversional activities (for pain) Prevention is thru MMR vaccine.

IA is Rubeola Virus Direct contact with droplets Incubation of 10-20 days POComm: 4 days before and 5 days after the rash appears. Prodromal stage: fever and malaise, followed by coryza, cough, and conjunctivitis, and photophobia in 24 hours. Koplik Spots 1st appear as red spots on the inside of the cheek. Then evolve to pinpoint white papules with an erythematous base.

Rash appears 3-4 days after onset of prodromal stage. It begins as reddened spots from face and spreads downward. Rash is more severe in earlier sites than later sites. It then turns brownish 3-4 days when fine desquamation occurs over severe areas. Complications: otitis media, pneumonia, and laryngotracheitis, encephalitis NI: thermoregulatory mgt, use dim-lit room or shades for photophobia Prevention: MMR vaccine

IA is Varicella-Zoster virus Direct/ Indirect contact with contaminated articles/ person Incubation of 2-3 weeks POComm: 1-2 days before rash develops until all lesions are crusted. Prodromal: low-grade fever, malaise, anorexia. Rash: Multilesion: macules, papules, vesicles, pustules, and crusts. It is centripetal, from face to proximal/ distal extremities. Rash may affect mucous membranes and pruritus is severe.

Gen symptoms: fever, lymphadenopathy, irritability from pruritus. Complications: secondary infections, encephalitis, pneumonia, hemorrhagic varicella NI: maintain strict isolation in hospital, isolate children in home care, until all vesicles are dry., provide skin care, provide cool environment and bath, loose clothing. Administer antipyretics, antihistamines, Acyclovir and Zoster immunoglobulins. Prevention is thru Varicella Zoster Vaccine

Genital herpes (Herpes simplex type 2) May be asymptomatic, but sometimes present a flu-like illness. Lesions appear as a grouped vesicles on an erythematous base initially involving the vagina, rectum or penis. New lesions appear from 7-14 days. Lesions are symmetrical and cause lymphadenopathy.; Fever and flu-like symptoms are common. Pain is burning, itching, tingling, for about 24 hours before vesicles appear. When vesicles rupture, erosions and ulcerations appear. Severe infections cause extensive erosions to the vaginal and anal canal.

Warts: Verrucae (Benign skin tumors) Human Papillomavirus (DNA virus). Warts are asymptomatic. May be treated with lasere therapy, liquid nitrogen, salicylic acid plasters, or electrodessication. Warts on genitalia and perianal areas are known as Condylomata acuminata. They may be transmitted sexually and treated with liquid nitrogen, cryosurgery, electrosurgery, topically applied trichloracetic acid and curettage. This type of wart affects uterus and cervix, predisposing the client to cervical CA.

Rabies Acute viral encephalomyelitis IA- Human rhabdovirus/ rabies virus Bite/ scratch from infected animals (usually canines); saliva; possible man-to-man transmission Incubation of 2-8 wks POCommu: all warm blooded animals are susceptible Sense of apprehension, headache, fever, sensory changes near site of animal bite, spasm of muscles in swallowing, hydrophobia, paralysis, delirium and convulsions. Complications: usual duration of 2-6 days results in death due to respiratory arrest. NI: Teachings on responsible pet ownership, wound care/ dressing, administering isolation, administer meds. Tx: TT, HTIg, Antibiotics, Anti-rabies Immunoglobulin and vaccine.

Tuberculosis is a highly communicable disease caused by Mycobacterium Tuberculosis. Tuberculosis is transmitted through airborne route. A multi drug resistant strain of tuberculosis can exist as a result of improper compliance or noncompliance with treatment programs and the development of mutations in the tubercle bacilli. Transmission: Airborne droplet infection. Transplacental transmission is rare. Transmission can occur during birth through aspiration of infected amniotic fluid. Neonates can become infected from contact with infected individuals.

Risks: Crowded areas Contact with infected person Immunosuppression/ immunodepression Sharing of eating utensils, linens with infected person Smoking Chronic alcoholism Diagnostic exams: Chest X-ray Sputum exam Dullness with percussion over involved parenchymal areas, bronchial breath sounds, ronchi, crackles indicate advanced disease. Mantoux test

Assessment: Fever and chills Night sweats Hemoptysis or yellow green sputum Sudden weight loss Persistent productive cough Dyspnea Pleural pain Fatigue

Treatment: First line: Isoniazid, Pyrazinamide, Ethambutol, Rifampicin, Streptomycin Second line: Capreomycin, Cycloserine, Ethionamide, Kanamycin, Para-aminosalicylic acid Interventions: Administer respiratory support for dyspnea. Start administering multi-drug therapy: Isoniazid, Pyrazinamide, Ethambutol, Rifampicin, Streptomycin. Also teach the client with regards to the effects of these drugs. Provide the client and family with information about tuberculosis and allay concerns about the contagious aspect of the infection.

IA is Pediculosis Humanus Capitis Spreads by direct, physical contact Female louse lays egg near the scalpattach to hair shafts- young lice hatch in about 10 days and reach maturity in 2 weeks Visually seen by naked eye as silvery, glistening oval bodies which are difficult to remove, bite from lice cause itching which results to scratching

IA is Sarcopte Scabiei Direct contact Incubation is 24 hours from original contact Itching, skin feel hot and burning, secondary infection causes fever, headache, and malaise. Dermatitis is common. NI: Good hygiene, clean clothes, linens, environmental sanitation Tx: Benzyl Benzoate, Kwell Ointment

Fecal-oral route, unsanitary foor handling Anemia, malnutrition, stunted growth, decreases physical ability, impaires mental development and school performance. NI: Good hygiene, clean clothes, linens, environmental sanitation, sanitary food handling, proper waste disposal, Handwashing Tx: Antihelminthics

Superficial: Tinea Crucis (ringworm of the groin)

Ringworm infection of groin, extends to buttocks and thighs. Usually occurs on joggers who wear tight underclothing. Increased risk with DM patients. Tx: Clotrimazole, Miconazole, or Terbinatine (3-4 weeks)

Tinea Pedis (Athletes foot) Lymphangitis and cellulitis occur with superinfection Infection of the soles and toes Tx: Topical antifungal therapy

IA is Candida Albicans Sexual contact Vaginal discharge causes pruritus and subsequent irritation. Discharge may be watery or white, cottage-cheese-like appearance. NI: Genital hygiene, Adherence to medication regimen. Tx: Antifungal agents: Miconazole, Nystatin, Clotrimazole, Tetconazole.

Gonorrhea Infection, caused by Neisseria gonorrhea, causes inflammation of the mucous membranes of the genital and urinary tracts. Transmission of the organism is by sexual intercourse Infection may be transmitted to the newborns eyes during delivery, causing blindness(ophthalmia neonatorum

 Assessment: Female: Usually asymptomatic; vaginal discharge, urinary frequency, and possible pain. Male: Fever, painful urination, pelvic pain, epidydymitis with pain, tenderness, and swelling Treatment: Procaine Penicillin G or Benzathine Penicllin G

 Interventions: Obtain a culture for gonorrhea on the first prenatal visit; prepare to repeat culture because infection may occur during pregnancy. Administer antibiotics prophylactically to the eyes of a newborn infant. Instruct the client that treatment for her partner is necessary if infection is present.

Hepatitis B is nonseasonal, and all age groups could be affected. Risk factors: Drug addicts, clients undergoing long term hemodialysis, health care personnel Transmission: Blood or body fluid contact Infected blood products Infected saliva or semen Contaminated needles Sexual contact Parenteral Perinatal period Blood or body fluids contacts at birth Incubation period: 6 to 24 weeks

Diagnostic exams: Infection is established by the presence of hepatitis B antigen-antibody systems in the blood. Presence of hepatitis B surface antigens (HBsAg) is the serological marker to establish the diagnosis of hepatitis B. The client is considered infectious if these antigens are present in the blood. If the serological marker (HBsAg) is present after 6 months, it indicates a carrier state or chronic hepatitis.

Normally the serological marker (HBsAg) level declines and disappears after the acute hepatitis B episode. The presence of antibodies to HBsAg (anti-HBs) indicates recovery and immunity to hepatitis B. Hepatitis B early antigen (HBeAg) is detected in the blood about 1 week after the appearance of HBsAg and its presence determines the infective state of the client.

Prevention: Strict handwashing Screening blood donors Testing of all pregnant Needle precaution Avoiding intimate sexual contact if test for HB surface antigen is positive in a person Hepatitis B vaccine: Engerix-B, Recombivax HB Hepatitis immunoglobulin is for individuals exposed to HBV through sexual contact or through the percutaneous or transmucosal routes, who have never received hepatitis B vaccine

The first stage is immune tolerance. The duration of this stage for healthy adults is approximately 2-4 weeks and represents the incubation period. For newborns, the duration of this period often is decades. Active viral replication is known to continue despite little or no elevation in the aminotransferase levels and no symptoms of illness.

In the second stage, an inflammatory reaction with a cytopathic effect occurs. HBeAg can be identified in the sera, and a decline of the levels of HBV DNA is seen. The duration of this stage for patients with acute infection is approximately 3-4 weeks (symptomatic period). For patients with chronic infection, 10 years or more may elapse before cirrhosis develops.

In the third stage, the host can target the infected hepatocytes and the HBV Viral replication no longer occurs. HBeAb can be detected. The HBV DNA levels are lower or undetectable, and aminotransferase levels are within the reference range.

In the fourth stage, the virus cannot be detected and antibodies to various viral antigens have been produced. Different factors have been postulated to influence the evolution of these stages, including age, sex, immunosuppression, and co-infection with other viruses.

Laboratory testing during the acute phase reveals elevations in the concentration of alanine and aspartate aminotransferase levels (ALT and AST); values up to 1000 to 2000 IU/L are typically seen during the acute phase with ALT being higher than AST. The serum bilirubin concentration may be normal in patients with anicteric hepatitis. The prothrombin time is the best indicator of prognosis. In patients who recover, normalization of serum aminotransferases usually occurs within one to four months.