Inflammatory and by mikesanye

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									Inflammatory and Immune Response
INFLAMMATORY RESPONSE
    A reaction of the tissues of the body to injury in order to destroy or dilute an
     injurious agent, to prevent the spread of injury, and to promote repair of damaged
     tissue.
    Causes
          A. Physical irritants (e.g., trauma or a foreign body)
          B. Chemical irritants (e.g., strong acids or alkalis)
          C. Microorganisms (e.g., bacteria and viruses)
    Components
          A. Vascular response:
                  transitory period of localized vasoconstriction, followed by
                    vasodilatation, increased capillary permeability, and blood stasis
          B. Formation of inflammatory exudate
                  1. Composition:
                          water, colloids, ions, and defensive cells
                  2. Functions:
                          dilution of toxins, transportation of nutrients to area of
                             injury for tissue repair, transportation of protective cells
                             that phagocytize and destroy bacteria
          C. Defense cell response:
                  migration of leukocytes to affected area for phagocytosis of
                    foreign bodies and dead cells
          D. Healing:
                  resolution of inflammation and regeneration of tissue or
                    replacement with sea] tissue

    Assessment Findings
          A. Local:
                  pain, swelling, heat, redness, and impaired function of part (five
                    cardinal signs of inflammation)
          B. Systemic (appear with moderate to severe response):
                  fever, leukocytosis, chills, sweating, anorexia, weight loss, general
                    malaise
    Essence of immune response is to recognize foreign substances and to neutralize,
     eliminate, or metabolize them with or without injury to the body's own tissues.


    Functions of the Immune System
         A. Defense:
                protection against antigens. An antigen is a protein or protein
                   complex recognized as nonself.
         B. Homeostasis:
                removal of worn out or damaged components (e.g., dead cells)
         C. Surveillance:
                ability to perceive or destroy mutated cells or nonself cells.
    Types of Immunity
         A. Natural (innate) immunity:
                immune responses that exist without prior exposure to an
                   immunologically active substance. Genetically acquired immunity
                   is natural immunity.
         B. Acquired immunity
                1. Immune responses that develop during the course of a person's
                   lifetime.




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               2. Acquired immunity may be further classified as naturally or
                artificially acquired, active or passive. Active immunity results
                when the body produces its own antibodies in response to an
                antigen. Passive immunity results when an antibody is transferred
                artificially.

        Types of Active immunity
             a. Naturally acquired active immunity:
                    results from having the disease and recovering successfully
             b. Naturally acquired passive immunity:
                    antibodies obtained through placenta or breast milk
             c. Artificially acquired active immunity:
                    conferred by immunization with an antigen
             d. Artificially acquired passive immunity:
                    antibodies transferred from sensitized person (e.g., immune
                       serum globulin [gamma globulin])


 Components of Immune Response
     A. Located throughout the body
     B. Organs include thymus, bone marrow, lymph nodes, spleen, tonsils,
       appendix, Peyer's patches of small intestine.
     C. Main cell types are WBCs (especially lymphocytes, plasma cells, and
       macrophages); all originate from the same stem cell in bone marrow, then
       differentiate into separate types.
            1. Granulocytes
                    a. Eosinophils: increase with allergies and parasites
                    b. Basophils: contain histamine and increase with allergy
                        and anaphylaxis
                    c. Neutrophils: involved in phagocytosis
            2. Monocytes (macrophages) (e.g., histiocytes, Kupffer cells):
               involved in phagocytosis
            3. Lymphocytes (T cells and B cells): involved in cellular and
               humoral immunity


 Classification of Immune responses
      Cellular Immunity
              A. Mediated by T cells:
                      persist in tissues for months or years
              B. Functions:
                      transplant rejection, delayed hypersensitivity, tuberculin
                       reactions, tumorsurveillance/destruction, intracellular
                       infections
      Humoral Immunity
              A. Mediated by B cells
                      1. Production of circulating antibodies (gamma globulin)
                      2. Only survive for days
              B. Functions:
                      bacterial phagocytosis, bacterial lysis, virus and toxin
                       neutralization, anaphylaxis, allergic hay fever and asthma




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Infectious Disorders
Rabies

   is a severe viral infection of the CNS that is communicated to human in the saliva
    of infected animals, especially wildlife-(dogs, cats, skunks, raccoons, oxes, bats)
    and cattle.
   SYNONYMS:
          Hydrophobia;
          Lyssa
   ETIOLOGY AND EPIDEMIOLOGY:
          - Rabies virus (Rhabdoviros) - is a filterable virus with strong affinity to
            the cells of the CNS
   Two types of Rabies virus
          ―Street‖ virus
                 Variable incubation period
                 Invade the salivary glands therefore transmitted in the saliva.
          ―Fixed‖ virus
                 Serially passed from brain of laboratory animals like rabbits
                 Constant incubation period of 4-6 days. Does not invade salivary
                    glands. Not associated with Negri bodies
                 Used for vaccine preparations
   Sources
          In the Philippines only dogs has been identified as reservoir
          Cats, monkey, pigs, horses, cattle and bats may also be affected
          In infected animals, rabies virus is found in CNS, urine, lymph, milk,
            saliva and blood
          In infected person CNS, saliva, urine, blood and other discharge
   Mode of transmission
          Higher titer of virus in the saliva of the rabid dog is needed. Seldom by
            scratches or skin breaks
          Man to man is possible
          Virus does not cross placental barrier
   Incubation period
          In dogs - 1 week to 7 ½ months
          In man - 4 to 8 weeks but may range from 10 days to 1 year depending on
            the location of the bite
   Period of communicability
          In dogs; 3-5 days before the onset of symptoms until entire course


   Clinical Manifestations: 3 stages
         1, Prodromal Phase or Stage of Invasion:
                - characterized by fever, anorexia, malaise, sore throat, copious
                  salivation, lacrimation, perpiration, irritability, hyperexc itabilitv,
                  apprehensive, restlessness or at times drowsmess,mental
                  depression, melancholia, and marked insomnia.
                - Pain in the region of the original infection; headache and nausea
                  . Sensitive to light, sound, and changes ia temperature.
                - With pain and aches in different parts of the body.
                - In the area of the bite and along the course of the involved
                  peripheral nerves, anesthesia, numbness, tingling, burning or cold
                  sensation may be felt; dilation of pupils; husky voice; and mild'
                  difficulty in 'swallowing.




                                           3
        Stage of excitement
             - Characterized by marked excitation, apprehension
             - Delirium is often associated with, nuchal stifrness, involuntary ,
                twitchings or even generalized convulsions
             - In this stage, the characteristic feature of the disease becomes
                manifest, which is the violent, severe and painful spasm of the
                muscles of the mouth, pharynx, and larynx on attempting to
                swallow food or water and even at the mere sight of them, or this is
                also known as hydrophobia (fear of water).
             - Aerophobia – fear of air.
             These attacks may be precipitated by mild stimuli such as touch
                and noise.
             - In order to avoid the painful spasms associated with swallowing,
                the; patient may drool saliva profusely and give the impression of
                "frothing."
             - Fever (1 -3 days) with. tonic arid clonic contraction of the
                muscle
             - Death may occur during an episode of spasm from
                cardiac/respiratory failure within a few days, usually 1 to 3 days,
                the patient deteriorate rapidly and enters the terminal phase.

        Terminal or Paralytic Stage:
             - patient becomes quiet and unconscious; loss of bowel and bladder
             - Occasionally, rabies may present with the clinical features of
               Ascending Myelitis.
             - Following the onset of paresthesia at the site of injury and along
               the course of the involved nerve; an ascending flaccid paralysis
               sets in but without hyperexcitability or muscular contractions:
               ending in death due to the involvement of the respiratory and
               cardiovascular centers.
             - Convulsions and painful spasms are absent in this clinical-
               variant of the disease.
             - CSF - is usually normal.
             - Peripheral WBC count increased.
             - Albuminuria,


 DIAGNOSIS:
      history of expos ure bite
      increased sensitivity to sensory stimuli with muscle spasms and the onset
       of hydrophobia.
      Microscopic examination of characteristic Negri bodies in samples of
       brain tissue of the infected animal, using Seller's May-Grunwald and
       Mann strains.
      A highly preferred diagnostic examination is a direct immunoflourescent
       test or Flourescent Rabies Antibody (FRA) Technique:

 Control
      Active immunization
      Passive immunization
      Control of animals
           Vaccinations against rabies 3 months to 1 year old dog
           Non-vaccinated dogs, cats and other pets bitten by rabid dog
              should be killed




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 Prevention
      1. Rabies in human can be prevented by eliminating exposure to rabid
         animals.
      2. Pre-exposure prevention - is recommended only in those exposed to
         high risk such as personnel in city animal pounds, laboratory workers,
         veterinarians and field biologists
      3. At present, mass vaccination is not recommended as no vaccine is
         absolutely safe.

 After exposure
       Local treatment of wound with soap and water
       Provide tetanus prophylaxis and antibacterial theraphy


 Rabies Postexposure Prophylaxis Management of the patient
      A combination of passive and active immunization is recommended when
         post-exposure treatment is deemed necessary. 2 types of immunizing
         products are used concurrently
      Globulin, providing rapid protection.
              Rabies Immune Globulin (human) (RIG); a part of the RIO is
                infiltrated around the wound and the rest is administered IM in the
                patient's buttock.
              2. Do not give at same time as rabies vaccine is given.


 Management of Biting Animal:
     (1) Capture the dog or animal that inflicted the bite and keep under
       veterinary surveillance — this may enable the bitten person to avoid
       undergoing rabies vaccination unnecessarily.
            a. If animal remains healthy for 10 days, it is assumed that it was
               not infective.
            b. If a dog that is suspected to have died of rabies or a dog that has
               been killed or becomes ill after biting a person - notify local health
               department; animal is humanely killed; should be decapitated and
               the head packed in Ice, dry ice, or glycerine, and sent immediately
               to any diagnostic laboratory center for confirmation of the
               diagnosis or examined for characteristic Negri bodies.
     (2) Kill wild animal that bites a person and send head to health department
       — brain examined for rabies.
     (3) If the biting "animal escapes? or is unknown, determination of the
       degree of risk is judged by the following factors;
            a. Prevalence of rabies in the area
            b. Species of biting animal
            c. Severity of wound
            d. Whether attack was provoked or unprovoked.
     (4) Any domestic animal that is bitten form or scratched by a bat or by a
       wild carnivorous mammal that is not available for testing should be
       regarded as having been exposed to a rabid animal.


 Treatment
      1. No specific treatment; the care of the patient is symptomatic and
        supportive in the intensive care unit - directed toward alleviation of spasm.




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    NURSING INTERVENTIONS:
        1. Isolation of patient: throughout course of illness.
        2. provide comfort for the patient by:
               Place paddings of bedside or use restraints
               Clean and dress wound with the use of gloves to prevent
                 contamination
               Patient with IVF should be placed behind the bed and cover paper
                 bag or doth
               No sight of water and electric fans should be seen.
               Medication: fluid are given rectally
               Administer morphine as ordered by physician
               Provide assurance and emotional support to the members of the
                 family:
                      - stay with the members of the family
                      - encourage members of the family to receive vaccination
                          especially those members who are exposed to rabies.


RUBEOLA (MEASLES)
   Synonyms
        Rubeola Morbilli and 7 day measles
        Hard measles
        Red measles
   A. Description
        1. Agent:
                Virus
        2. Incubation period:
                10 to 20 days
        3. Communicable period:
                From 4 days before to 5 days after the rash appears; mainly during
                   prodromal (catarrhal) stage
        4. Source:
                Respiratory tract secretions, blood, or urine of infected person
        5. Transmission:
                Airborne or direct contact with infectious droplets
   Assessment
        1. Fever
        2. Malaise
        3. Coryza and cough
        4. Rash
                appears as red, discrete maculopapules that blanch easily with
                   pressure and gradually turn a brownish color (lasts 6 to 7 days);
                   rash begins behind the ears and spreads downward to the feet
        5. Koplik spots:
                small, red spots with a bluish white center and a red base; located
                   on the mucosa and last 3 days


    COMPLICATIONS:
        1. Bronchopneumoma, subglottic laryngitis, bronchiectasis, bronchitis,
         bronchiolitis,
        2. Pneumonia, interstitial, but often further complicated by bacterial
         infection (pyothorax).
        3. Abdominal pain (sometimes mimicking acute appendicitis- viral
         involvement of the inflammed lymph nodes and appendix).
        4. Acute hemorrhagic lesions with hemorrhages into the skin and mucous
         membrane


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        5. Secondary infection - with streptococci, pneumococci: reactivation of
         preexisting pulmonary tuberculosis.
        6. Otitis media - inflamed eardrum.
        7. Encephalo-myelitis (rare).
        8. Encephalitis
              a. Acute, usually during the 2nd week of the illness, but may occur
                 during the prodromal period or after the rash has appeared.
              b. Subacute sclerosing panecephalitis (S&PE), months or years.
              c. Thrombocytopenia.
        9. Other complications; sinusitis, Furuncolosis, Keratoconjunctivitis,
         myocarditis, nepritis and hepatitis.

 C. Implementation
       1. Respiratory precautions if the child is hospitalized
       2. Restrict to quiet activities and bed rest
       3. Use a cool mist vaporizer for cough and coryza
       4. Dim lights if photophobia is present
       5. Administer antipyretics for fever


 TREATMENT:
     - No therapy is indicated for uncomplicated measles. Gamma globulin
      although effective in prophylaxis is of no value once symptoms are
      evidence. Patient should be monitored for the development of bacterial-
      superinfections which should be treated with appropriate antibiotics on the
      basis of clinical and bacteriological findings,
     2. Quarantine
           is not necessary because by the time a diagnosis of measles is
              made, siblings and playmates of the patient have already been
              contaminated. - the most contagious period is about 1 week before
              rashes appear.
     3. Neosilvol 5% solution 4 grams - disinfectant
           direct to put 1 or 2 drops into each eye daily and 5 drops or more in
              each nostril once a day.
     4. Vaseline applied in the eyelids
     5. Antipyretics
     6. Antibiotics
     7. Immunoglobulins

 Prophylaxis
 Active immunity
      A. Naturally Acquired - after getting infected confers a life- long immunity
      B. Artificially acquired – measles vaccine, composed of live attenuated
         vaccine.
 Passive immunity
      A. Naturally Acquired – infants under 6 months old acquire temporary
         immunity from their mother
      B. Artificially Acquired – administration of .25 ml/kg gamma globulins.




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RUBELLA (GERMAN MEASLES)
   A. Description
        1. Agent:
                Rubella virus
        2. Incubation period:
                14 to 21 days
        3. Communicable period:
                7 days before to approximately 5 days after the rash appears
        4. Source:
                Nasopharyngeal secretions; virus is also present in blood, stool,
                   and urine
        5. Transmission
                a. Airborne or direct contact with infectious droplets
                b. Indirectly via articles freshly contaminated with nasopharyngeal
                   secretions, feces, or urine
                c. Transplacental

    B. Assessment
          1. Low- grade fever
          2. Malaise
          3. Pinkish red maculopapular rash that begins on the face and spreads to
            the entire body
          4. Petechial spots (Forcheimer’s spot) may occur on the soft palate
          5. Swelling of lymph nodes
          6. Splenomegaly
          7. Testicular pain in male adults
          8. polyarthritis and polyarthalgia

    C. Implementation
          1. Supportive treatment
          2. Isolate the infected child from pregnant women


    Congenital Rubella
         women who acquired rubella in the first trimester of pregnancy. Half of
           these neonates also had growth retardation and congenital heart disease..


    Pathogenesis
          Various studies show that the placenta of women who contract the disease
            may be infected during the virimic phase; this inturn infects the fetus and
            practically all the fetal organs are involved.
          Evidently, in the first 8-weeks. infection of the fetus is more prolonged
            and chronic, at a time of rapid organogenesis
          After the fourth month of gestation the risk of damage to the fetus is
            likely.


    RISK OF CONGENITAL MALFORMATION:
         100%" when maternal infection occurs on the first trimester of pregnancy
          or first month of gestation
         4%" in the second and third trimester
         90% - of congenital rubella cases will excrete the virus at birth and are
          therefore infectious.
         10% - remain contagious until 1 year of age.




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 Clinical manifestation
       Intrauterine infection will result to spontaneous abortion, stillbirth or
         multiple abnormalities
       Classic congenital rubella syndrome
               Intrauterine growth retardation microcephaly, deafness, congenital
                  heart defects, mental retardation.
 Neonatal Manifestations:
       a. Intra- uterine growth retardation low birth weight.
       b, Thrombocytopenic purpura-"blueberry muffin",skin,
       c. Transient hepatosplenomegaly, hepatitis, hemolytic anemia, bulging
         anterior fontanel
       d. Lethargy and hypothermia.
       e. Cleft-palate, hare- lip, talipes and eruption of teeth.
 Cardiac defects
       a. Patent ductus arterious
       b. Atrial septal defect
       c. Ventricular septal defect
 Eye defects
       a. cataracts
       b. glaucoma
       c. retinopathy
       d. microphthalmia
       e. unequal eyeballs
 Ear defects
       a. deafness, usually bilateral, leading to speech defects
       b. abnormal shaped ears
 Neurologic Manifestations
       a. Microcephaly
       b. Mental retardation
       c. Psychomotor retardation
       d. Behavioral disturbances
       e. Encephalitis
       f. Vasometer instability
 A. Description
       1. Agent:
               Varicella zoster virus (VZV)
       2. Incubation period:
               13 to 17 days
       3. Communicable period:
               1 to 2 days before the onset of the rash to 6 days after the first crop
                  of vesicles, when crusts have formed
       4. Source:
               Respiratory tract secretions of infected person; skin lesions
       5. Transmission:
               Direct contact, droplet (airborne) spread, and contaminated objects
 B. Assessment
       1. Slight fever, malaise, and anorexia followed by a macular rash that first
         appears on the trunk and scalp and moves to the extremities
       2. Lesions become pustules, begin to dry, and develop a crust
       3. Lesions may appear on the mucous membranes of the mouth, the genital
         area, and the rectal area
 C. Implementation
       1. In the hospital setting, strict isolation
       2. In the home setting, isolate the infected child until the vesicles have
         dried; isolate high-risk children from the infected child




                                         9
   Complications
        1. Secondary infection of the lesions; impetigo, furuncles, cellulitis, and
           erysipelas.
        2. Meningocephalitis and intestinal perforations.
        3. Pneumonia
        4. Leukemia with steroid therapy make the prognosis guarded or
           unfavorable.
   Prognosis
        - the younger the patient the more favorable is the prognosis.
        - The disease last about 2 weeks including the peeling off of the crusts.
   Prophylaxis
        - this is not specific
        - Human hyperimmune vaccin gamma globulin recommended for patient
           at high risk like prematures, leukemia patient and those on steroid
           treatment.
   Treatment
        1. Specific; none, this is symptomatic.
        2. Nonspecific:
                a. Prevention of secondary infection of the skin.lesions is through
                   hygienic care of the patient.
                b. Attention should be given to nasopharyngeal discharges and
                   disinfection of cloths and linen by sunlight or boiling.
                c. Cut finger nails short and wash hands more often in order to
                   minimize bacterial infections may be introduced by scratching.
                d. Calamine lotion over rashes;        .
                e. Antipyretics for fever.
                f. Isolation of patient: cannot be confined in general hospitals;
                   isolated until all lesions have become encrusted.
                g. Control measures: Active immunization - none, Laymen have
                   the strong notion that small pox vaccination is effective against
                   varicella.


Variola (Small Pox)
   Is an infectious and highly communicable disease characterized by marked
    symptom during the prodromal period and appearance of skin eruption, which
    progeresses through the stages ofmacule, papule, vesicle, pustule and crust, to end
    and putting scar formation
   In 1981 the WHO (World Health Organization) officially declared that the disease
    has been eradicated through out the world.
   Incidence:
         common during winter months while in tropical region it was prevalent in
            hot season.
   Mode of Transmission: . .
         A. direct contact - through fomites and 'other contaminated articles.
         B. Droplet infection and secretions – 3rd to 8th day after onset of fever - it
            is transmittabie, It is the period in which mucous membrane are involved.
   INCUBATION PERIOD;
         8-17 days; 50-12 days (average); 1-3 weeks
   Pathophysiology
         The portal of entry of variola, virus is through the respiratory mucosa and
            from here it proceeds to the respiratory lymphoid tissue where it
            multiplies, results in a primary veremia. At these stages, the
            reticuloendothelial system and other organs are infected. The virus again
            multiplies in these sites and brings about a secondary viremia which
            spread to the skin and such organs as the liver, kidney and testes.



                                          10
       Historically, epithelial cells show degeneration of the cytoplasm whic h
         vacuolate with the formation of lacework or meticulocular fibers
       When reticular fiber ruptures, umbilication results and then absorption of
         the exudate allows crust formation.
       The crust fall of in a few days. Usually about 2 weeks there is regeneration
         of epithelium
 Clinical manifestations
       Hyperpyrexia (40°C • 41 C). headache, weakness and backache,
         abdominal pain, nausea and vomiting, severe muscular and joint pains
       Rash
              a. usually appear on. the 3rd day
              b. begins to appear on the face, wrists and ankles, spreads to the
                 extremities, and often in areas of pressure and tight skin.
              c. The rashes which are usually discrete and centripetal in
                 distribution; pass through successive stages
              d. Altogether the eruptions last about 1-2 weeks.
              e. Similar lesion may occur in the buccal mucous and cornea.
 Complications
       Secondary skin infections and septicemia
              Furunculosis
              Abcess
              Cellulitis
              Gangrene
       Laryngitis, pleurisy, emphysema
       Keratitis and laryngeal ulcerations with edema
       Encephalitis and bronchopnuemonia may develop later.

 Prevention
      Small pox Vaccination - has been accepted as an effective immunization
         since it was introduced by Edward Jenner in 1798. Presently, however,it is
         no longer a routine immunization in almost all countries since the disease
         has been declared extinct.

 TREATMENT:
     Supportive
          1. Symptomatic and supportive - as there is nonspecific cure
          2. Antibiotics - are indicated for only secondary bacterial
            infections
          3. Tepid sponges of 1:1000 dilution of Bichloride of mercury or
            1:10000 dilution of potassium permangenate suffice. NURSING
            INTERVENTIONS
          1. Skin and mucous membrane
          - compress saturated with 2 solution of boric Acid, Na
            Bicarbonate
          - avoid sponge bath
          - prevent scratching of lesions - short nails and use of elbow
            restrains and mittens
          - divertional therapy
          - frequent change of position and massage bony prominences.
          Diet
          well balanced liquid, soft bland or regular diet
          small amount but frequent feeding
          monitor intake and output
          Preventions
          isolation of patient                ;
          encourage patient and members of the family to use mask
          emphasize the importance of hand washing


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POLIOMYELITIS
   A. Description
         1. Agent:
                Enteroviruses
         2. Incubation period:
                7 to 14 days
         3. Communicable period:
                Not exactly known; the virus is present in the throat and feces
                   shortly after infection and persists for approximately 1 week in the
                   throat and 4 to 6 weeks in the feces
         4. Source:
                Oropharyngeal secretions and feces of the infected person
         5. Transmission:
                Direct contact with infected person; fecal-oral and oropharyngeal
                   routes
   B. Assessment
         1. Fever, malaise, anorexia, nausea, headache, sore throat
         2. Abdominal pain followed by soreness and stiffness of the trunk, neck,
           and limbs that progresses to flaccid paralysis
   B. Assessment
         1. Fever, malaise, anorexia, nausea, headache, sore throat
         2. Abdominal pain followed by soreness and stiffness of the trunk, neck,
           and limbs that progresses to flaccid paralysis

    C. Implementation
          1. Enteric precautions
          2. Supportive treatment
          3. Bed rest
          4. Monitor for respiratory paralysis
          5. Physical therapy
          6. Tracheostomy


Meningitis
    A. General information
          1. Inflammation of the meninges of the brain and spinal cord
          2. Caused by bacteria, viruses, or other microorganisms
          3. May reach CNS
                 a. Via the blood, CSF, lymph
                 b. By direct extension from adjacent cranial structures (nasal
                    sinuses, mastoid bone, ear, skull fracture)
                 c. By oral or nasopharyngeal route
          4. Most common organisms: meningococcus, pneumococcus, H.
            influenzae, streptococcus
    B. Assessment findings
          1. Headache, photophobia, malaise, irritability
          2. Chills and fever
          3. Signs of meningeal irritation
                 a. Nuchal rigidity:
                         stiff neck
                 b. Kernig's sign:
                         contraction or pain in the hamstring muscle when
                            attempting to extend the leg when the hip is flexed
                 c. Opisthotonos:
                         head and heels bent backward and body arched forward



                                          12
                 d. Brudzinski's sign:
                         flexion at the hip and knee in response to forward flexion
                            of the neck
           4. Vomiting
           5. Possible seizures and decreasing LOC
           6. Diagnostic test:
                 lumbar puncture (measurement and analysis of CSF shows
                    increased pressure, elevated WBC and protein, decreased glucose
                    and culture positive for specific microorganism)

    C. Nursing interventions
         1. Administer large doses of antibiotics IV as ordered.
         2. Enforce respiratory isolation for 24 hours after initiation of antibiotic
            therapy for some types of meningitis (consult hospital's infection control
            manual for specific directions).
         3. Provide nursing care for increased ICP, seizures, and hyperthermia if
            they occur.
         4. Provide nursing care for delirious or unconscious client as needed.
         5. Provide bed rest; keep room guiet and dark if client has headache or
            photophobia.

    C. Nursing interventions
         1. Administer large doses of antibiotics IV as ordered.
         2. Enforce respiratory isolation for 24 hours after initiation of antibiotic
            therapy for some types of meningitis (consult hospital's infection control
            manual for specific directions).
         3. Provide nursing care for increased ICP, seizures, and hyperthermia if
            they occur.
         4. Provide nursing care for delirious or unconscious client as needed.
         5. Provide bed rest; keep room guiet and dark if client has headache or
            photophobia.

             6. Administer analgesics for headache as ordered.
             7. Maintain fluid and electrolyte balance.
             8. Prevent complications of immobility.
             9. Monitor vital signs and neuro checks frequently.
             10 Provide client teaching and discharge planning concerning
                   a. Importance of good diet: high protein high calorie with small,
                      frequent feedings
                   b. Rehabilitation program for residual deficits.



MUMPS
   A. Description
        1. Agent:
                Paramyxovirus
        2. Incubation period:
                14 to 21 days
        3. Communicable period:
                Immediately before and after the swelling begins
        4. Source:
                Saliva of infected person and possibly urine
        5. Transmission
                a. Direct contact with infected person
                b. Droplet spread from infected person


                                          13
  B. Assessment
        1. Fever
        2. Headache and malaise
        3. Anorexia
        4. Earache aggravated by chewing, followed by parotid glandular swelling
  C. Implementation
        1. Respiratory precautions
        2. Bed rest until the parotid glandular swelling subsides
        3. Avoid foods that require chewing
        4. Apply hot or cold compresses as prescribed to the neck
        5. To relieve orchitis, apply warmth and local support with tight- fitting
          underpants


INFECTIOUS MONONUCLEOSIS
  A. Description
       1. Agent:
               Epstein-Barr (EB) virus
       2. Incubation period:
               4 to 6 weeks
       3. Communicable period:
               Unknown; the virus is shed before the onset of the disease until 6
                  months or longer after recovery
       4. Source:
               Oral secretions
       5. Transmission:
               Direct intimate contact, infected blood

  B. Assessment
        1. Fever, sore throat, malaise, headache, fatigue, nausea, abdominal pain
        2. Lymphadenopathy and hepatosplenomegaly
  C. Implementation
        1. Supportive
        2. Monitor for signs of splenic rupture, which include abdominal pain, left
          upper quadrant pain, or left shoulder pain

SCARLET FEVER
  A. Description
        1. Agent: Croup A, beta-hemolytic streptococci
        2. Incubation period:
               1 to 7 days
        3. Communicable period:
               During the incubation period and clinical illness, approximately 10
                  days; during the first 2 weeks of the carrier stage, although may
                  persist for months
  4. Source:
        Nasopharyngeal secretions of infected person and carriers
  5. Transmission:
        Direct contact with infected person or droplet spread; indirectly by contact
          with contaminated articles, ingestion of contaminated milk, or other foods

  B. Assessment
        1. Abrupt high fever, vomiting, headache, malaise, abdominal pain




                                        14
         2. A red, fine papular rash in the axilla, groin, and neck that spreads to
           cover the entire body
         3. The rash blanches with pressure except in areas of deep creases and
           folds of the joints (Pastia's sign)
         4. The tongue is coated and papillae become red and swollen (white
           strawberry tongue); by the fourth to fifth day the white coat sloughs off,
           leaving prominent papillae (red strawberry tongue)
         5. Tonsils are edematous and covered with a gray-white exudate
         6. Pharynx is edematous and beefy red
   C. Implementation
         1. Respiratory precautions until 24 hours after the initiation of treatment
         2. Supportive therapy
         3. Bed rest
         4. Encourage fluid intake
         5. Administer antibiotics as prescribed


PERTUSSIS (WHOOPING COUGH)
   A. Description
        1. Agent:
                Bordetella pertussis
        2. Incubation period:
                5 to 21 days (usually 10 days)
        3. Communicable period:
                Greatest during the ca-tarrhal stage
   A. Description
        1. Agent:
                Bordetella pertussis
        2. Incubation period:
                5 to 21 days (usually 10 days)
        3. Communicable period:
                Greatest during the ca-tarrhal stage
        4. Source:
                Discharge from the respiratory tract of the infected person
        5. Transmission:
                Direct contact or droplet spread from infected person; indirect
                   contact with freshly contaminated articles

          4. Source:
                Discharge from the respiratory tract of the infected person
          5. Transmission:
                Direct contact or droplet spread from infected person; indirect
                  contact with freshly contaminated articles

   B. Assessment:
         Symptoms of respiratory infection followed by increased severity of
           cough
   C. Implementation
         1. Isolation during the catarrhal stage; if the child is hospitalized, institute
           respiratory precautions
         2. Administer antimicrobial therapy as prescribed
         3. Administer pertussis immune globulin as prescribed
         4. Reduce environmental factors that promote paroxysms of coughing,
           such as dust, smoke, and sudden changes in temperature
         5. Encourage fluid intake
         6. Provide high humidity with the use of a humidifier or tent
        


                                           15
DIPHTHERIA
   A. Description
         1. Agent:
                 Corynebacterium diphtheriae
         2. Incubation period:
                 2 to 5 days
         3. Communicable period:
                 Variable; until virulent bacilli are no longer present (three negative
                    cultures), usually 2 weeks but as long as 4 weeks
         4. Source:
                 Discharge from the mucous membrane of the nose and
                    nasopharynx, skin, and other lesions of the infected person
         5. Transmission:
                 Direct contact with infected person, carrier, or contaminated article
   B. Assessment
         1. Low- grade fever, malaise, sore throat
         2. Foul-smelling, mucopurulent nasal discharge
         3. Gray membrane on the tonsils and pharynx
         4. Lymphadenitis (neck edema)
   C. Implementation
         1. Strict isolation of the hospitalized child
         2. Administer antitoxin as prescribed (preceded by a skin or conjunctival
           test to rule out sensitivity to horse serum)
         3. Bed rest
         4. Administer antibiotics as prescribed


Dengue Fever
   is a tropical disease caused by different strains of dengue vims which are
    trammitted by mosquitoes by the genus Aedes
   this type is now known as Philippine, Thai or Singapore- hemorrhagic fever or for
    short, H-fever, particularly in the Philippines.
   is an acute infectious disease characterized by severe pain behind the eye and in
    the Joints and bones and accompanied by an initial erythema and a terminal rash
    of varying morphology.
   Synonyms
          Hemorrhagic Fever or H-fever
          Acute Infectious Thrombocytopemc Purpura.
          Dengue Shock Syndrome
          Breakbone or Dandy Fever
                  because the patient is. experiencing pain in the Joints and bones
                     and the way it makes the patient appear to be walking on his toes.
   Dengue Fever Syndrome
          type without significant hemorrhages.
   Dengue Hemorrhagic Fever
          cases with gross hemorrhages and with the etiologic agent identified; a
             severe illness endemic in most of tropical Asia, characterized by abnormal
             vascular permeability, hypovolemia and abnormal blood clotting
             mechanism.
   Etiology and epidemiology
          there are 4 Serotypes of Dengue Vires (1, 2, 3, and 4 Group B Arbovirus)
          This mosquito is domestic, day-biting with low and limited flying
             movements.
         




                                          16
 Sources:
      1. Infected persons - the virus is present in the blood of patients during the
        acute phase of the disease and will become a reservoir of virus, accessible
        to mosquitoes which may then transmit the disease.
      2. Standing water within the household and premises are breeding places.
 Mode of Trans mission:
      by the bite of an infective Aedes Aegypti mosquito (a day mosquitoes with
        limited flying movements). Viruses have been isolated from this mosquito
        during epidemic.

 Factors which favor spread of infection:
      1. Water stored within household or standing water in premises.
      2. High human population density; the more crowded the human
         population the higher the infection rate.
 Incidence:
      1. Age: the infection may occur at any age but it is common. school
         children with the peak between 4 and 6 years old.
      2. Sex: both sexes equally affected.
      3. Season: more frequent during rainy season or months.
      4. Geographical: more prevalent in urban communities or localitie
 Incubation Period: 4 to 6 days (minimum, 3 days; maximum. 10 days)


 PATHOGENESIS:
       4 types of dengue virus can cause either classical dengue or hemorrhagic
          fever (DHF)
       the first attack gives only temporary and partial protection against me
          viruses
       Thrombocytopenia
               acute excessive consumption of platelets due to generalized
                  intravascular clotting.
               Decreased blood coagulation factors especially fibrinogen and
                  factors II, V, VII and II.
               prolonged bleeding and clotting time, prothrombin time, and
                  partial thromboplastin time with severe thrombocytopenia and
                  fibrigenopenia which are indications of disseminated intravascular
                  coagulation (DIC)
 Manifestations
       Fever, anorexia, vomiting, severe abdominal pain and tenderness
       Liver enlarged
 2nd or 3rd day
       hyperpyrexia persists and all the earlier symptoms increase.           -
       The temperature often shows a biphasic curve.
       The palms and soles are noticeably flushed.
       Tourniquet test - is often positive (+) from the onset or after a few days.
       Petachiae may be observed in pressure areas usually first on the face or
          distal portions of the extremities but sparing the axilla and chest
 5th to 7th day
       - the fever subsides           ,
       - the limbs are cool and rash appears on the upper and lower extremities,
          purplish or brownish motted appearance red with blanched areas about 1
          cm or less in size.       '
       - The rashes last 2 to 3 days
       - Face and hands appear edematous.
       - Pruritis may be present and at times is annoying.           .
       - There mav be bradycardia during convalescence.
       - From this stage on the child begins to improve steadily.


                                       17
 Severe Manifestations
       1. Central Nervous Manifestations (Dengue Encephalopathv)
              (1) Symptoms: increasing restlessness, apprehension or anxiety,
                 disturbed sensorium, convulsions, non-transient (more than 8
                 hours) change in consciousness.                     -
              (2) Physical Findings: vomiting, spasticity or hyporeflexia.
              (3) CSF Result: Normal
 2. Hemorrhagi[c_Mantfestations:
       (1) Epistaxis:
              purpuric lesions may appear early and extensive ecchymosis later
                 (which is an extravasation of the blood in the subcutaneous tissues
                 it is marked by a purple discoloration of the skin); hematemesis or
                 melena (coffee-ground material)
       (4) Hepatomegaly- in 50 to 60% of cases in some countries but reputed as
         90 to 96% in Thai children.
       (5) Shock - manifested by rapid weak pulse with narrowing of pulse ' ,
         pressure (20mm Hg or less) or hypotension, with cold clammy skin and
         restlessness.
 Laboratory;
       (1) Thrombocytopenia-
              100,000/'mm3 orless.
       (2) Hemoconcentration
              (a) An increase of at least 20%in the hematocrit
              (b) Steady rise m the hematocrit.
       Prolonged prothrombin time
       Reduction of fibrinogen, prothrombin, factor VIII, factor XII,
         antithrombin III and 2 antiplasmin.
       In severe cases with liver dysfunction, reduction of factors II, VI, VII, IX
         andXII.
 Serum Proteins - decreased
       Serum Transaminase - increased
       Serum Sodium - decreased
       Metabolic Acidosis
       BUN - increased
       There may be transient heavy albuminuria (presence of serum, albumin,
         globulin and other protein in urine).
       Occult blood - presence in the stool is often found.
 PREVENTION;
       1 .Control of the mosquito vector is the most important a. Standing water
         in the household and premises should be properly drained. b. Flower
         vases, empty tins, old tires and other receptacles in the yard are good
         breeding places of mosquitoes.
       2. Mosquito bites should be avoided by usual measures.
       3. A vaccine against different types of dengue virus is in progress.
 TREATMENT:
       This is mainly symptomatic and supportive.
       There are no specific antiviral drugs.
       In most cases, early and effective replacement of plasma loss with plasma
         expander and/or fluid and electrolyte solution results in a favorable
         outcome.
 NURSING INTERVENTIONS:
       Isolation of the patient: recommended.
       Control Measures - eradication of mosquitoes (elimination of breeding
         places and fogging).
       Any disease or condition, associated with hemorrhage is enough to cause
         alarm. Immediate control of hemorrhage and close observation of the
         patient for vital signs of leading to shock.


                                       18
        Nursing measures are directed towards symptoms as they occur but
         immediate medical attention must be sought.

 Intervention for hemorrhage
       - keep the patient at rest during bleeding episodes.
       - for nosebleedmg, maintain an elevated position of trunk and promote
         vasoconstriction in nasal mucosa membrane through an ice bag over the
         forehead.
 For Shock
       prevention is the best treatment.
       dorsal recumbent position facilitate circulation.
       adequate preparation of the patient, mentally and physically prevents
         occurrence of shock
       provision warmth through light-weight covers (overheating causes
         vasodilation which aggravates bleeding),
       restore blood volume, elevating foot part and trunk (Trendelenberg) allows
         greater blood volume at head part.
 For anxiety
       explain thoroughly the; nature, the discomforts and limitations of activity
         associated with the diagnostic procedures.
       - encourage family participation in the patient's care.
       - create a, comfortable atmosphere for the patient's family.
 For fever
       cooling measures through sponges. Administer prescribed drugs;
       encourage fluid intake unless contraindicated.


Leprosy
 Synonyms
       Hansen's Disease
       Hansenosis
       Lepra
       Leontiasis
       - is a chrome disease with an insidious onset, transmitted from man to
         man, affecting the skin, mucous membranes and nervous tissue, and
         eventually producing deformities
 Etiology and epidemiology
       - the disease is produced by Mycobacterium Leprae (Hansen's Bacillus, a
         gram positive, acid- fast rod, which tends to group in bundles)
       - it may be isolated from any mucocutaneous lesion.
 Sources
       1. Discarges from mucocutaneous lesions contain large number of
         Mycobacteria.
       2. The organisms enter through the skin, and possibly the respiratory tract
         and gastrointestinal tracts.
 Mode of transmission
       1. Most probably through the skin or respiratory tract, intimate skin
         contact favors transmission, as in couples or mother to child.
       2. Fomites and insect vectors also play a role in transmission.
 Incubation period
       incubation period is very variable; it may be short as one year or as long as
         5 years or more.
 Period of communicability
       As long as there is open lesions
 Pathology and pathogenesis
       - lesions; are mainly in the skin, peripheral nerves and mucosa of the
         upper respiratory tract.


                                       19
        - the M. Leprae ,proliferate in the Schwann cells of the nerves and produce
         foamy degeneration of the axon, with marked fibrosis and destruction of
         normal structure.
        The lesion later extends to the deeper structures and organs
        - Cell mediated, immunity (CMI) seems to play a large part in the
         production of leprosy lesions.

       - CMI to M.Leprae is markedly suppressed in the lepromatous patient,
       - The degree of suspension diminishes gradually as the lesions progress
         towards the tuberculoid type,
       - The total number of T lymphocytes is decreased in Iepromatous leprosy
         and the defect in CMI is found in T lymphocyte function, including
         macrophage activation and mobilization.
       - Immunoglobulin production is only slightly elevated in tuberculoid
         patients but markedly, so in lepromatous patients, in whom B lymphocytes
         are increased.
 Clinical Manifestations
       - the indeterminate lesion, which may be the initial manifestation, shows
         as ordinary-looking skin changes, such as pale oval or rounded macules,
         papulonodules, wheals or circinate patches. They may be found in the
         extremities or buttocks.
       there may be only one or a few lesion which may appear and disappear,
         undergo spontaneous healing, or gradually progress through the
         borderline form towards the tuberculoid or lepromatous forms.
       - The lesions are usually anesthetic but this may be later manifestations.
       - They may be depigmented or erythomatous.

      Sensory disturbances as parestnesias, numbness may also be found.
      - There may also be thickening or superficial nerve trunks, especially the
        ulnar, as well as lymphadenopathy, and limb weakness.
      - In the lepromatous (LL) form, nodular lesions are found, which when
        numerous m the face give rise to the so-called leonine fades.
      - There are diffuse skin infiltrations which lead to falling of hair and
        atrophy of the skin.
 Diagnosis
      1. Smears - from the mucocutaneous lesions may demonstrate the
        organism.
      2. Identification of Mycobacte rium Leprae from skin smears of biopsies
        of most active-looking skin or areas of diminished sensation or sweating
        will also reveal the typical histologic changes.
      3. Lepromin Skin Test - has cross-sensitivity to tuberculous infection and
        BCG vaccination.
      4. Mitsuda Reaction - more useful for determination of the type of
        disease and prognosis.
 Treatment
      Aviosulfone or diaminodiphenylsulfone (Dapsone, DDS),
             - has been found effective and is the mainstay of treatment
      Isonicotinic hydrazide and other antituberculous drugs
             are also utilized in cases of hypersensinvity or resistance to
                sulfones.
      Rifampicin
      Steroids
      Rehabilitation

 Prognosis
      May be symptomless or selfhealing or progressive and devastating
        depending on the host resistance


                                      20
 Nursing Interventions
      Isolation of patient until causative agent is still present
      Care of exposed persons like house contacts
      Control measures
              No immunizations available
              B.C.G. vaccine may be protective if given within 6 months of life


 Tetanus
 DEFINITION:
       - Synonyms: Lockjaw
       - is an infectious disease caused by Clostridium Tetani which produces a
         potent exotoxin with prominent systemic neuromuscular effects
         manifested by generalized spasmodic contractions of the skeletal
         musculature;
       - is an acute disease cause by the tetanus bacillus Clostridium tetani,
         whose spores are introduced into the body when an injury becomes
         contaminated with soiled, street dust, or animal or human feces.
 Etiology and Epidemiology
       Clostridium Tetani is an anaerobic (cannot live in presence of oxygen),
         spore-forming gram-positive rod, with the round terminal spores and
         slender body giving it a "drum-stick" appearance.
 Sources
       1. Animal or human feces - it is present in the intestinal tract of
         herbivorous animals, including man, where it is passed through the stools
         resulting in its wide distribution in soil particularly where concentration of
         animals, such as horses and cows, and people is high,
       2. Soil and dust contain spores and contaminate wounds which are ' deeply
         punctured, producing anaerobic conditions.
       3. Plaster, unsterile sutures, rusty scissors, nails or pins.
 Mode of transmission
       1. Traumatic wounds and burns are also frequently inoculated with the
         organism; however any wound may be infected such as laceration, mere
         scratch or any bite, tooth decay, septic abortion, unclean dressing of
         umbilical cord, any compound fracture, and non- immunized individual.
       2. The umbilical stump is the usual source ih the newborn, particularly in
         rural deliveries attended by unlicensed midwives using primitive methods
         in cord dressing.
       GIT may serve as portal of entry

 Incubation periods
       - ranges from 3 days to 3 weeks, symptoms being delayed in mild
         infections or in case anti serum has been administered prophylactically.
         The average is about 10 days.
 Pathogenesis
       - a neurotoxin (tetanospasmin) and a hemolysin (tetanolysin) are
         produced; the former is responsible for the clinical manifestations or
         responsible for the muscular spasms while tetanolysin is responsible for
         the destruction of RBC
       - this toxin produced in the tissues by multiplying bacilli is brought by
         lymphatics and blood to the CNS or is absorbed by motor nerve endings
         and passes up through the axon cylinders to the anterior horn cells of the:
         spinal cord.
       - this stimulates contractions in the muscles supplied by these neurons and
         later those or adjacent neurons to which the toxin diffuses.


                                        21
 Manifestations
     Onset: - insidious with muscular spasms and cramp- like pain around the
        site of inoculation.
     Irritability and restlessness with progressively increasing stiffness of the
        voluntary muscles so that within 24-48 hours it is usually fully developed.
     Trismus or lockjaw
     Opisthotonus
     Risus sardonicus
     Extremities are stiff and extended spinal muscle spasms results in raising
        of the lumbar areas from the bed level in supine position, so that the hand
        may be passed underneath.

        In more severe cases, muscles of respiration: laryngeal spasm followed by
           the accumulation of secretions in the. • lower airway, respiratory distress
           due to involvement of the respiratory muscles; fractures of the vertebral
           bodies can occur during severe spasms, coma and. death.
        Fever, usually absent. d. Headache and profuse sweating
        Sensorium: usually intact or clear but anxiety and apprehension are
           prominent; the eyes are partially closed.
   Complications
   Resulting from lryngospasm and involvement of muscles of respirations
        Hypostatic pneumonia
        Hypoxia
        Atelectasis
        If tracheostomy is done – pneumothorax and pnuemomediastinum
   Due to trauma
        a. Lacerations of the tongue and buccal mucosa
        b. Intramuscular hematomas
        c. Fractures of the spine and ribs. may occur rarely as a result violent
           muscular action.
   Septicemia
   DIAGNOSIS:
        1. CSF - normal result
        2. Blood examination: normal or slightly elevated WBC count.
   PREVENTION;
        a. Avoiding contamination by the organism
                - Active immunization of Tetanus Toxoid to pregnant mother
                   during the last trimester gives rise to protective titers in newborn's
                   serum,
                - Active immunization of adolescent girls and women of child-
                   bearing age.
                - consists in aseptic handling of the neonatal umbilical stump and
                   other wounds.
                - Supervision of unlicensed midwives,
                - Tetanus Toxoid - no need for skin testing.
        Active immunization
        Passive immunization
        Antibiotic Prophylactic Therapy
   Treatment
        a. Tetanus Immune Globulin/Human Hyperimmune Globulin (TIG)
        Tetanus Antitoxin
        Penicillin or tetracycline
        Diazepam
        Muscle relaxants
   Nursing interventions
        Prevention of repiratory and cardiac complications
                Maintain adequate airway


                                         22
           Provide cardiac monitoring
                Over systemic nervous system activity can lead to ―sympathetic
                   crisis‖ and death
           Wound and systemic care
                Give tetanus immune globulin
                Debride all necrotic tissue
                Give antimicrobials
                Give active immunization
           Support
                Support patient during tetanic spasmand convulsions
                Place patient in quit semidark rooms to avoid spasm
                Avoid sudden stimuli and light
                Maintain fluid and electrolyte
                Avoid contractures and pressure sores
                Watch for urinary retentions

           Primary immunuzations
           Consider every break in the skin a potential portal of entry for C. Tetani
           Most important step in prevention of tetanus is thorough hand washing
            technique


Malaria
   a specific infectious disease produced by any one of four protozoan parasites,
    which is transmitted to man by the bite of the mosquito, and the. characteristic of
    which are chills followed by fever occurring at more or less regular interval.
   is an acute and chronic infectious disease caused by
         protozoa plasmodia.
   SYNONYM:
         - Ague
   ETIOLOGY:
   4 Species of Protozoa Plasmodia which cause Malaria:
         1. PIasmodium Vivax
                 - the more widely distributed and commonly encountered aside
                    from Plasmodium Falciparum
                 - which causes vivax or benign tertian malaria.
                 - Chills and fever every 48 hours in the 3rd day
   2. Plas modium Falciparum
         most frequently encountered in the Philippines followed Plasmodium
            Vivax.
         - Which causes falciparum or malignant tertian malaria or also known as
            "pernicious malaria‖
         - Causes the most serious type of malaria because of the development of
            high parasitic densities in blood; infected red cells tend to agglutinate and
            form microemboli.
   3. PIasinodiuM Malariae
         - is much less frequent
         - which causes quartan malaria with fever and chills every 72 hours the
            4th day.
   4. Plas modmni Ovale
         - has been reported in the Philippines, it is very rarely seen.
         - the parasite has a complicated life cycle.
         - not all patients demonstrate classical cycles of fever and chills
   Mode of transmission
         1. Person to person by the bite of an infected female anopheles mosquito.




                                           23
         2. Parenterally, through blood transfusion or contaminated syringes and
           needles (infection brought about by this way usually a shorter incubation
           period).
         3. Mingling of infected maternal blood with that of the infant during the
           birth process: neonatal malaria
         4. Transplacental; congenital malaria, rare
   Pathology
         - the most characteristic pathology of malaria consists of destruction of red
           blood cells, hypertrophy of the spleen and liver, and pigmentation of
           organs.
         - The pigmentation in the tissues - is due to the phagocytosis of malarial
           pigments released into the blood stream upon rupture of red cells.
         - These pigments are taken in by cells of the lymphoid-macrophage
           systems in the spleen, bone marrow and Kupffer cells in the liver.
         - The spleen is initially enlarged by dilation of sinusoids and later, as a
           result of great increase in macrophage elements
         - Changes in the liver are essentially similar to those in the spleen.
         - In addition to this, in falciparum malaria there may be capillary
           occlusion most commonly in the brain although it may occur m other
           organs.
   Clinical manifestations
   Prodromal phase
         Headache
         Anorexia
         Fatique
         Vague abdominal pain
         Muscle pain
         Hepatosplenomegaly
         Orthosthatic hypotension
         Highly colored urine
   Acute attack
         Uncomplicated
                prodromal period become more severe " fever, initially, irregular;
                   then paroxysms of chills, fever and sweating every 4 to 36 hours
                   with feeling of well being between.
                Chill, body covered with gooseflesh, chatter teeth, shivering,
                   elevated temperature, face is blue and pinched.
                Near the end of the chill, fever rises from 102°F-106°F, skin
                   becomes red and very hot, and fall of TPR.
                Paroxysms may last about 12 hours, after which the cycle
                May be repeated daily, every other day, or every 3rd day.
         Complicated
                sporolation or segmentation and rupture of erythrocytes occur
                in the brain and visceral organs. The red cells parasitized with P.
                   Falciparum tend to adhere to each other so that capillary occlusion
                   to these organs occur.
   Central Nervous System or "Cerebral Malaria:
         there are symptoms of CNS involvement like changes in sensorium,
           severe headache and vomiting
         Jacksonian or grand maL seizures may be present
   Blackwater fever
         • Is generally considered malarial in origin and commonly associated with
           falciparum malaria.
         • After a paroxysm, reddish or mahogany colored urine due to
           hemoglobinuria is passed by the patient.
         • In some severe cases, anuria occurs followed by death
   Hemolytic


                                        24
 Malarial lung disease
 Preventive measures
      Eliminate anopheles mosquito
      Advise malaria chemoprophylaxis when traveling to areas where malaria
         is endemic. Malaria prophylaxis should start before a person ' enters aa
         endemic-area.
      Advise the traveler to seek prompt health care if he develops fever after
         stopping prophylaxis.
      Travelers to malarious areas should not donate blood for up to 3 years.


 TREATMENT:
 1. Determine the species of parasite infecting the patient (by blood smear. The
  most favorable time for discovery of the parasite is during and 12.to 18 hours
  after a chill.
 2.The underlying objectives in the treatment of malaria are 3 fold:
       (1) Destroy promptly all sexual forms of the parasites in order to cure the
           clinical attack.
       (2) Destroy the excerythrocytes (EE) forms in order to prevent relapses,
       (3) Destroy gametocytes so that mosquito infections will be prevented.
 3. Give specific therapy:
       4-Aminoquinolines (which belong Chloroquine, Amodiaqume, Quinine)
                - barring resistant strains of P. Falciparum, the most potent drugs
                   acting on the sexual erythrocytic stages. Chloroquine is given for
                   infections due to sensitive strains of Falciparum, P. Vivax, or P.
                   Ovale
       Primaquine
                - aside from being active against the EE forms destroy the
                   gametocytes of P. Falciparum which are unaffected by common
                   schizonticidal drugs.
                - this drug is valuable to achieve the last 2 objectives in the
                   therapy 4 malaria.
                - Relapses of vivax or ovale malaria can be eradicated/prevented
                   daily doses of this drug.
       8-Aminoquinolines
                - to prevent development of the erythrocytic stages and prevent
                   relapses by destruction of the EE forms, since to date, no drugs has
                   yet been found that would stop the invading sporozoites.
 4. An erythrocyte exchange transfusion may be carried out for rapid reduction of
  high levels of parasites in the treatment of overwhelming falciparurn malaria.


 NURSING INTERVENTIONS:
 1. Isolation of the patient:
       a. If confined in hospitals located in areas where there are no anopheles
          mosquitoes, no need.
       b. If treated in hospitals or at home in areas where there are anopheles
          mosquitoes,                     .
               (1) place patient inside mosquito nets
               (2) eradicate mosquitoes with insecticides (should be sprayed in
                  the morning or early in the afternoon)
 2: Care of exposed persons:
       check blood for malarial parasites if person is febrile.
 3. Give supportive nursing care:
       (1) Have the patient under close monitoring and nursing surveillance.
       (2) Keep input and output records to prevent pulmonary edema and to
          evaluate for development of renal failure; dialysis may be lilesaving.


                                        25
      (3) Take a sample or venous blood daily for estimating serum quinine,
        bilirubin, blood urea nitrogen concentrations, parasite count, and packed
        red cells.
      (4) Determine arterial blood gases and plasma electrolytes if respiratory or
        renal symptoms occur.
 (5) Consider the patient with severe falciparum malaria as a medical emergency.
      a. Administer IV quinine as directed - given in intermittent IV infusions.
      b. Watch for neurologic toxicity (from quinine infusion) ~ twitching,
        delirium, confusion, convulsions, and coma.
      c. Oxygen may be administered -- tissue anoxia is thought to be common
        in this disease
      d. Watch for jaundice - related to density of the falciparum parasitemia
        (presence of malarial parasites in the blood); abnormalities of hepatic
        function are also common in falciparum malaria.
      e. Evaluate degree of anemia - related to severity of infection
      f. Watch for abnormal bleeding, nosebleeds.



 Hepatitis

 General information
       1. Widespread inflammation of the liver tissue with liver cell damage due
         to hepatic cell degeneration and necrosis; proliferation and enlargement of
         the Kupffer cells; inflammation of the periportal areas (may cause
         interruption of bile flow)
 Hepatitis A
       a. Incubation period: 15-45 days
       b. Transmitted by fecal/oral route: often occurs in crowded living
         conditions; with poor personal hygiene; or from contaminated food, milk,
         water, or shellfish
 Hepatitis B
       a. Incubation period: 50-180 days
       b. Transmitted by blood and body fluids (saliva, semen, vaginal
         secretions): often from contaminated needles among IV drug abusers;
         intimate/sexual contact
 4. Hepatitis C
       a. Incubation period: 7-50 days
       b. Transmitted by parenteral route: through blood and blood products,
         needles, syringes
 Assessment findings
       1. Preicteric stage
               a. Anorexia, nausea and vomiting, fatigue, constipation or diarrhea,
                 weight loss
               b. Right upper quadrant discomfort, hepatomegaly, splenomegaly,
                 lymphadenopathy
       2. Icteric stage
               a. Fatigue, weight loss, light-colored stools, dark urine
               b. Continued hepatomegaly with tenderness, lymphadenopathy,
                 splenomegaly
               c. Jaundice, pruritus
       3. Posticteric stage
               a. Fatigue, but an increased sense of well-being
               b. Hepatomegaly gradually decreasing
 Diagnostic tests
       a. All three types of hepatitis



                                       26
                1) SGPT (ALT), SGOT (AST), alkaline phosphatase, bilirubin,
                   ESR: all increased (preicteric)
                2) leukocytes, lymphocytes, neutrophils: all decreased (pericteric)
                3) prolonged PT
   Nursing interventions
        1. Promote adequate nutrition.
                a. Administer antiemetics as ordered, 30 minutes before meals to
                   decrease occurrence of nausea and vomiting.
                b. Provide small, frequent meals of a high carbohydrate, moderate-
                   to high-protein, high-vitamin, high-calorie diet
                c. Avoid very hot or very cold foods.
        2. Ensure rest/relaxation: plan schedule for rest and activity periods,
           organize nursing care to minimize interruption.
        3. Monitor/relieve pruritus (see Cirrhosis of the Liver).
        4. Administer corticosteroids as ordered.
        5. Institute isolation procedures as required; pay special attention to good
           hand-washing technique and adequate sanitation.
        6. In hepatitis A administer immune serum globulin (ISG) early to
           exposed individuals as ordered.
        7. In Hepatitis B
                a. Screen blood donors for HBsAg.
                b. Use disposable needles and syringes.
                c. Instruct client/others to avoid sexual intercourse while disease is
                   active.
                d. Administer ISG to exposed individuals as ordered.
                e. Administer hepatitis B immunoglobull (HBIG) as ordered to
                   provide temporary and passive immunity to exposed individuals.
                f. To produce active immunity, administer hepatitis B vaccine to
                   those individuals at high risk.
        8. In non-A, non-B: use disposable needles and syringes; ensure adequate
           sanitation.



AIDS
   A. General information
         1. Characterized by severe deficits in cellular immune function;
           manifested clinically by opportunistic infections and/or unusual neop lasms
         2. Etiologic factors
                a. Results from infection with human immunodeficiency virus
                   (HIV), a retrovirus that preferentially infects helper T- lymphocytes
                   (T^ cells)
                b. Transmissible through sexual contact, contaminated blood or
                   blood products, and from infected woman to child in utero or
                   possibly through breastfeeding
                c. HIV is present in an infected person's blood, semen, and other
                   body fluids
         3. Epidemiology is similar to that of hepatitis hepatitis B; increased
           incidence in populations in which sexual promiscuity is common and in
           IV drug abusers

   B. Medical management
        1. No effective cure for AIDS at present; several categories of
          antiretroviral drugs now available
               a. Nucleoside Analogues: Didanosine (Videx) (ddl), Lamivudine
                  (3TC) (Epivir), Stavudine (d4T) (Zerit), Zidovudine (AZT)
                  (Retrovir)


                                         27
              b. Nucleoside Analogues: Didanosine (Videx) (ddl), Lamivudine
                 (3TC) (Epivir), Stavudine (d4T) (Zerit), Zidovudine (AZT)
                 (Retrovir)
              c. Non Nucleoside Analogues: Delavirdine (DLV) (Rescriptor),
                 Nevirapine (NVP) (Viramune)
              d. Protease Inhibitors : Indinavir (Crixivan), Nelfinavir
                 (Viracept), Ritonavir (Norvir), Saquinavir (Invirase)
      2. Primary goal of treatment is to treat opportunistic infections and cancers
         that develop and provide supportive care for the effects of the disease, e.g.,
         diarrhea, malnutrition, mental changes, etc.
      3. Drugs used
              include a. PO or IV trimethoprim-sulfamethoxazole (Bactrim,
                 Septra);
              side effects include rash, leukopenia, fever b. IM or IV
                 pentamidine (Pentam 300);
              side effects include hepatotoxicity, nephrotoxicity, blood sugar
                 imbalances, abscess or necroses at IM injection site, hypotension
 C. Assessment findings
      1. Fatigue, weakness, anorexia, weight loss, diarrhea, pallor, fever, night
         sweats
      2. Shortness of breath, dyspnea, cough, chest pain, and progressive
         hypoxemia secondary to infection (pneumonia)
      3. Progressive weight loss secondary to
      anorexia, nausea, vomiting, diarrhea, and a general wasting syndrome;
         fatigue, malaise
      4. Temperature elevations (persistent or intermittent); night sweats
      5. Neurologic dysfunction secondary to acute meningitis, progressive
         dementia, encephalopathy, encephalitis
      6. Presence of opportunistic infection, for example
      a. Pneumocystis carinii pneumonia b. Herpes simplex, cytomegalovirus,
         and
      Epstein-Barr viruses c. Candidiasis: oral or esophageal d. Mycobacterium-
         avium complex
      7. Neoplasms
              a. Kaposi's sarcoma
              b. CNS lymphoma
              c. Burkitt's lymphoma
              d. Diffuse undifferentiated non-Hodgkin's lymphoma

      8. Laboratory findings: diagnosis based on clinical criteria and positive
         HIV antibody test—ELISA (enzyme- linked immunosorbent assay)
         confirmed by Western blot assay. Other lab findings may include
              a. Leukopenia with profound lymphopenia
              b. Anemia
              c. Thrombocytopenia
              d. Decreased circulatory T4 lymphocyte
              cells
              e. Low T4:T8 lymphocyte ratio
 D. Nursing interventions
      1. Administer medications as ordered for concomitant disease; monitor for
         signs of medication toxicity.
      2. Monitor respiratory status; provide care as appropriate for respiratory
         problems, e.g., pneumonia.
      3. Assess neurological status; reorient client as needed; provide safety
         measures for the confused/disoriented client.
      4. Assess for signs and symptoms of fluid and electrolyte imbalances;
         monitor lab studies; ensure adequate hydration.


                                        28
            5. Monitor client's nutritional intake; provide supplements, total parenteral
             nutrition, etc., as ordered.
            6. Assess skin daily (especially perianal area) for signs of breakdown;
             keep skin clean and dry; turn q4 hours while in bed.
            7. Inspect oral cavity daily for ulcerations, signs of infection; instruct
             client to rinse mouth with normal saline and hydrogen peroxide or normal
             saline and sodium bicarbonate rinses.
            8. Observe for signs and symptoms of infection; report immediately if any
             occur.
            9. If severe leukopenia develops, institute neutropenic precautions
                  a. Prevent trauma to skin and mucous membranes, e.g., avoid
                      enemas, rectal temperatures; minimize all parenteral infections
                  b. Do not place client in a room with clients having infections
                  c. Screen visitors for colds, infections,etc.
                  d. Do not allow fresh fruits, vegetables, or plants in client's room.
                      e. Mask client when leaving room for walks, x-rays, etc.
            10. Institute blood and body fluid precautions
            11. Provide emotional support for client/significant others; help to
             decrease sense of isolation
            12. Provide client teaching and discharge planning concerning
                  a. Importance of observing for signs of infections and notifying
                      physician immediately if any occur
                  b. Ways to reduce chance of infection
                  1) Clean kitchen and bathroom surfaces regularly with
                      disinfectants.
                  2) Avoid direct contact with pet's litter boxes or stool, bird cage
                      droppings, and water in fish tanks.
                  3) Avoid contact with people with infections, e.g., cold, flu.
                  4) Importance of balancing activity with rest.
                  5) Need to eat a well-balanced diet with plenty of fluids.
            c. Prevention of disease transmission
                  1) Use safer sex practices, e.g., condoms for sexual intercourse.
                  2) Do not donate blood, semen, organs.
                  3) Do not share razors, toothbrushes, or other items that may draw
                      blood.
                  4) Inform all physicians, dentists, sexual partners of diagnosis.
            d. Resources include Public Health Service, National Gay Task Force,
             American Red Cross, local support groups

Gonorrhea
    A. Caused by N. gonorrhoeae.
    B. Symptoms may include heavy, purulent vaginal
    discharge, but often asymptomatic in female.
    C. May be passed to fetus at time of birth, causing ophthalmia neonatorum and
     sepsis.
    D. Treatment is penicillin; allergic clients may be treated with erythromycin or (if
     not pregnant) the cephalosporins.
    E. All sexual contacts must be treated as well, to prevent "ping-pong" recurrence.


Syphilis
    A. Caused by Treponema pallidum (spirochete)
    B. Crosses placenta after 16th week of pregnancy to infect fetus. C. Initial
     symptoms are chancre and lymph-adenopathy and may disappear without
     treatment in 4-6 weeks.
    D. Secondary symptoms are rash, malaise, and alopecia; these too may disappear
     in several weeks without treatment.


                                           29
   E. Tertiary syphilis may recur later in life andaffect any organ system, especially
    cardiovascular and neurologic systems.
   F. Diagnosis is made by dark-field exam and serologic tests (VDRL).
   G. Treatment is penicillin, or erythromycin if penicillin allergy exists.


Pulmonary tuberculosis
   Bacterial infectious disease caused by M.tuberculosis and spread via airborne
    droplets when infected persons cough, sneeze, or laugh
   Once inhaled, the organisms implant themselves in the lung and begin dividing
    slowly, causing inflammation, development of the primary tubercle, and eventual
    caseation and fibrosis.
   The greatest number of cases occur in persons age 65 and over.
   Socially and economically disadvantaged, alcoholic, and malnourished
    individuals affected more often.*

   Assessment findings
        1. Cough (yellow mucoid sputum), dyspnea, hemoptysis, rales or crackles
        2. Anorexia, malaise, weight loss, afternoon low- grade fever, pallor, pain,
          fatigue, night sweats
        3. Diagnostic tests
               a. Chest x-ray*
               b. Skin test (PPD) positive*
               c. Sputum positive for acid- fast bacillus*
               d. Culture positive
               e. WBC and ESR increased

     Administer medications as ordered
     Prevent transmission.*
     Promote adequate nutrition.*
     Prevent social isolation.*
     Vary the client's routine to prevent boredom.
     Discuss the client's feelings and assess for boredom, depression, anxiety, fatigue,
      or apathy; provide support and encourage expression of concerns.

   Provide client teaching and discharge planning concerning
        Medication regimen: prepare a sheet with each drug name, dosage, time
           due, and major side effects; stress importance of following medication
           schedule for prescribed period of time (usually 9 months); include
           significant others.
        Transmission prevention: client should cover mouth when coughing,
           expectorate into a tissue and place it in a paper bag; client should also
           wash hands after coughing or sneezing; stress importance of plenty of
           fresh air; include significant others

          Importance of notifying physician at the first sign of persistent cough,
           fever, or Hemoptysis (may indicate recurrence)
          Need for follow- up care including physical exam, sputum cultures, and
           chest x-rays

   Drugs Commonly Used to Treat Tuberculosis
        isoniazid (INH)*
        Ethambutol (Myambutol)*
        Rifampicin (Rimactane)*
        Streptomycin*
        Pyrazinamide*



                                           30
 1. An inflammation of the alveolar spaces of the lung, resulting in consolidation
  of lung tissue as the alveoli fill with exudate
 2. The various types of pneumonias are classified according to the offending
  organism.
 3. Bacterial pneumonia accounts for 10% of all hospital admissions; affects
  infants and elderly most often, and most often occurs in winter and early spring
 4. Caused by various organisms: D. pneumoruae, S. aureus, E. coli, H. infiuenzae

 Assessment findings
      1. Cough with greenish to rust-colored sputum production; rapid, shallow
        respirations with an expiratory grunt; nasal flaring; intercostal rib
        retraction; use of accessory muscles of respiration; dullness to flatness
        upon percussion; possible pleural friction rub; high-pitched bronchial
        breath sounds; rales or crackles
      2. Fever, chills, chest pain, weakness, generalized malaise
      3. Tachycardia, cyanosis, profuse perspiration, abdominal distension
 Diagnostic tests
      a. Chest x-ray shows consolidation over affected areas
      b. WBC increased
      c. p02 decreased
      d. Sputum specimens reveal particular causative organism

 Nursing interventions
      1. Facilitate adequate ventilation.*
      2. Facilitate removal of secretions*
      3. Observe color, characteristics of sputum and report any changes;
         encourage client to perform good oral hygiene after expectoration.
      4. Provide adequate rest and relief/control of pain.*
      5.Administer antibiotics as ordered
      6.Prevent transmission
      7.Control fever and chills
      8.Provide client teaching and discharge*




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