JUVENILE RHEUMATOID ARTHRITIS
 Refers to chronic childhood arthritis, a group of
heterogenous chronic autoimmune diseases.
o CAUSE:
 Unknown
 Activation of autoimmune anti-
inflammatory process by infectious agent
 Genetic predisposition (Human Leukocyte
Antigen, PTPN22 gene, IL2RA/CD 25 gene)
 Starts before age 16
 Peak onsets: 1 and 3 – 8 and 10 years of age
 Chronic synovial inflammation leads to joint effusion
 Joint erosion, destruction, and fibrosis of the articular
cartilage follows
 Continuous disease process leads to ANKYLOSIS
o MANIFESTATIONS
 Joint stiffness, swelling, and loss of motion
 Morning stiffness of joint
o DIAGNOSTIC EVALUATION
 Diagnosis of exclusion
 Onset of before 16 years old
 Arthritis in 1 or more joint for 16 weeks or
more
 ESR and C-reactive proteins – may or may
not be elevated
 Antinuclear antibody (ANA) – common in
JIA
o THERAPEUTIC MANAGEMENT
 No cure
 NSAIDs (ibuprofen, naproxen, diclofenac,
indomethacin, meloxicam, tolmetin)
 Check kidney function
 Check for possibilities of bleeding
(especially GI bleed)
 Disease-modifying Antirheumatic Drugs (DMARDs)  Facilitate compliance
(methotrexate and sulfasalazine)  Encourage comfort measures and ADLs
o Check for bone marrow suppression  Application of HEAT (hot tubs, compress,
o Check GI disturbance whirlpool baths)
o Check Liver disease
o Check teratogenic effect
 Methotrexate – taken at bedtime (reduces nausea) ALLERGY RHINITIS
o Avoid alcohol  Seasonal Allergic Rhinitis (Hay Fever) – follows a spring-fall
o Biologic DMARDs pattern – triggered by tree, grass, and weed pollens
 Tumor Necrosis Alpha inhibitors (etanercept, infliximab,  Year-round/Perennial Allergic Rhinitis – more common and
adalimumab) triggered by household inhaled allergens (feather, dust,
o Decreases inflammatory response that promotes animal dander, pollutants, and molds)
arthritis o HIGHER RISK:
o Increases risk of infection – Negative TUBERCULIN  Exposure to tobacco smoke
skin test before starting therapy  Heavy exposure to indoor allergens
 Glucocorticoids  CS delivery
 Family Hx or Asthma and Allergy
 PREDNISONE – given orally
 Early exposure to dogs and cats – protective factor**
 High-dose IV steroids
o CLINICAL MANIFESTATION
 Intraarticular injections
 WATERY rhinorrhea
 Physical Management
 Nasal obstruction
 Physical therapy
 Sneezing
 Range-of-motion exercises
 Itchy throat
 Pool exercise
 Nasal pruritus – “allergic salute”
 Nighttime splinting – minimize pain and prevent flexion
 Dark circles beneath the eyes – “allergic
deformity
shiners”
 Surgery
 Mouth breathing – “allergic gape”
 Synovectomy
 Dennie-morgan lines – extra wrinkles below
o NURSING MANAGEMENT
the eyes
 Relieve pain
 Facial tics and mannerisms – in attempt to
 Promote general strength
avoid scratching the nose
 Diet and exercise – overweight puts more
o DIAGNOSTIC EVALUATION
pressure on joints
 Thorough history and physical examination
 Promote sleep and rest
 Encourage School Attendance
  Nasal smears – checks number of
eosinophils in nasal secretions
 Total IgE (blood)
 Elevated Eosinophils (blood)
 Skin tests
 Withhold monteleukast (1 day),
antihistamines (7 days),
antihistamine nasal sprays (3 days),
decongestants (4 days), antacids (3
days)
 Challenge tests
o THERAPEUTIC MANAGEMENT
 Avoid ALLEGENS
 Second generation Antihistamines
 Loratadine and cetirizine
 First generation Antihistamines
 Diphenhydramine and
chlorpheniramine
 May cause undesirable side-effects
(dry mouth, urinary retention,
constipation, and sedation)
 Glucocorticoid (fluticasone)
 Cromolyn nasal spray
 Mast-cell stabilizer
 Pseudoephedrine
 nasal decongestant (may cause rebound
effect in long term use)
 Leukotriene modifier (monteleukast) – for 6
months and olfer
 Allergen Immunotherapy
 Used to desensitize patients to
allergen overtime
 Sublingual/subcutaneous
ATOPIC DERMATITIS (ECZEMA)  REDUCE FLARE UPS AND
 Refers to descriptive category of dermatologic diseases and INFLAMMATION
not to a specific etiology  Topical steroids
 Chronic relapsing inflammatory skin disorder that results in  Topical immunomodulators
itching and lesions  PREVENT AND CONTROL SECONDARY
 THREE FORMS INFECTION
o Infantile eczema – 2-6 months of age; remits by  Topical or systemic antibiotic
3 years of age
o Childhood – 2-3 years of age
o Preadolescent and adolescent – 12 years old; CANCER IN CHILDREN
may continue to adulthood
 Believed to be caused by genetic or environmental factors
o THERAPEUTIC MANAGEMENT
 SKIN HYDRATION
 Tepid bath with MILD soap
 Application of emollient (within
3 minutes after bath)
 Avoid bubble baths and harsh
soaps
 Colloid Baths (additional of 2
cups of cornstarch)
 G1 (Gap 1) – lasts for hours to days
 Room humidifier/ vaporizer
o RNA and CHON synthesis occurs in preparation
 Antihistamines (hydroxyzine or
for synthesis.
diphenhydramine)
 S-phase (Synthesis) – lasts approximately 10 – 20 hours.
 Non-sedating Antihistamines
o DNA replication
(loratadine)
 G2 – ranges from 2-10 hours
 Cut nails short
o DNA synthesis ceases, RNA and CHON synthesis
 Use protective clothing (ensure
continues.
free time from restrictions)
 M-phase (mitosis) – lasts for 30-60 minutes.
 Eliminate triggers (woolen
o Cellular duplication occur
blankets, rough fabrics, furry
stuffed animals)  Go
 Avoid perspirations o Resting phase
 Use mild detergent soaps
  UBC STAGES OF CANCER CELL GROWTH
 Non-Ionizing
 Dietary Substances
 Alcohol
 Fats
 Nitrite and Nitrates
 Viruses, bacteria, parasites
 DNA viruses
 RNA viruses
 H. pylori
THEORIES
 Schistosoma hematobium
 cellular transformation & derangement theory  Opisthorchis viverrini DOUBLING TIME
o Oncogenes  PROMOTION  Length of time it takes for a tumor to double up its
o Tumor suppressor genes o Repeated exposure to promoting agents volume
 failure of the immune response theory (cocarcinogens)
o Expression of MUTANT or ABNORMAL genetics 7 Fundamental Changes in Malignancy
CARCINOGENESIS information
1. Self-sufficiency in growth signals
 Cellular protooncogenes – “on switch” for
 Inititiation 2. Insensitivity to growth- inhibitory signals
cell growth
o Exposure to INITIATORS (carcinogens) – chemicals, a. Tumor suppressor genes
 Cancer suppressor genes – “turn off”
physical factors, biologic agents alters genetic i. gate keepers
unneeded cellular proliferation
structure of DNA. ii. care takers
 P53 – determines if cell will live or
 Normally halted by DNA repair or 3. Evasion of apoptosis (p53)
die (Apoptosis – programmed cell
programmed cell death 4. Defects in DNA repair (BRCA1&2)
death)
o FACTORS INFLUENCING CANCER DEVELOPMENT 5. Limitless replication potential
 PROGRESSION 6. Sustained angiogenesis (VEGF – vascular endothelial
 Host
o Altered cells exhibit increased malignant behavior growth factor)
 Environmental Agents
o Invasion of adjacent tissues/metastisize 7. Ability to invade and metastasize
 Chemicals
 Radiation *Tumor-specific antigen on cell membrane (CEA/PSA)
o Ionizing *less FIBRONECTIN in cell membrane – less cohesive
 Xrays, gamma rays,
cosmic rays and do not readily adhere to adjacent cells.
 UV rays
 UVA
 UVB
  TX - Primary tumor cannot be evaluated  O – bvious change in warts or moles
 T0 - No evidence of primary tumor  N – agging cough and hoarseness
 Tis - Carcinoma in situ (early cancer that has not spread  U – nexplained anemia
to neighboring tissue)  S – udden weight loss
 T1, T2, T3, T4 - Size and/or extent of the primary tumor FACTORS INFLUENCING CANCER DEVELOPMENT IN CHILDREN
Regional Lymph Nodes (N)  Exposure to ionizing radiation
 NX - Regional lymph nodes cannot be evaluated  Carcinogenic drugs
HOW CANCER SPREADS?  Immunosuppressive therapy
 N0 - No regional lymph node involvement (no cancer
 Certain viral infections (Epstein-Barr virus, human
 Lymphatic found in the lymph nodes)
papilloma virus)
 Hematogenous  N1, N2, N3 - Involvement of regional lymph nodes  Race/ethnicity
 Direct spread (number and/or extent of spread)  Genetic conditions
Distant Metastasis (M) CHARACTERISTICS OF NEOPLASIA
METASTATIC CASCADE  MX - Distant metastasis cannot be evaluated  BENIGN
 M0 - No distant metastasis (cancer has not spread to  Non-invasive
other parts of the body)  Encapsulated
 M1 - Distant metastasis (cancer has spread to distant  Well-differentiated
 Slow growth
parts of the body)
 Does not metastasize
BRODERS’ HISTOLOGICAL CLASSIFICATION  MALIGNANT
 GRADE 1 – 0-25% undifferentiated cells  Undifferentiated
 GRADE 2 – 25-50% undifferentiated cells  Secretes abnormal protein
 GRADE 3 - 50-75% undifferentiated cells  Erratic and uncontrolled growth
 GRADE 4 – 75-100% undifferentiated cells  Metastasizes
General Promotive And Preventive Nursing Management  Expansive and invasive
1. Lifestyle modification (stress reduction) TREATMENT MODALITIES
2. Early detection (screening)  CHEMOTHERAPY
3. Nutritional management  Destroys normal and abnormal cells
4. Screening  Route: oral and IV (common)
TUMOR STAGING AND GRADING
General Warning Signs Of Cancer  SE: Phlebitis/EXTRAVASATION (highly vesicant)
Staging - determines size of tumor and existence of metastasis SIDE-EFFECTS OF CHEMOTHERAPY
Grading - classifies tumor cells by type of tissue  C – change in bowel/bladder habits  HAIR
The TNM system is based on the extent of the tumor (T), the  A – sore that does not heal  Temporary ALOPECIA
extent of spread to the lymph nodes (N), and the presence of  U – nusual bleeding or discharges  14 days after chemo
metastasis (M).  T – hickening or lump in the breast or elsewhere  Hair grow 3-6 months
Primary Tumor (T)  I – ndigestion or difficulty in swallowing  Mngt:
  Mild shampoo  CI: Pregnancy, immunocompromised, Children <6yo  30 mins or <8hrs or once per shift
 Wide-toothed comb  TYPES:  Distance
 Wigs, hats, turbun, scarfs  Brachytherapy (internal)  6 ft away and stand at foot of the bed
 STOMACH LINING  Teletherapy (External)  Shield
 Mngt:  TELETHERAPY  Lead apron
 Anti-emetic 30 mins before chemo  Destruction of abnormal cells only  Nursing Mngt:
 EXTRAVASATION  Done in the radiation room  Room:
 Mngt:  Radiation remains in the room  Private room with private bathroom
 Stop and notify the physician à  LART (Linear Acceleration Radiation Therapy) (put radiation precaution outside)
ANTIDOTE  Put markings opposite the tumor location site  Activity:
 SPERM (Aspermia/Sterility)  WOF: leukopenia  CBR s BRP
 Mngt:  SE: dry or wet desquamation of he skin  Urine:
 Cryopreservation  Head: dry mouth, mouth sore, decreased taste  Insert catheter
 BONE MARROW DEPRESSION (pancytopenia)  TELETHERAPY  If no catheter (Flush 3x)
 Mngt:  INTERVENTIONS:  Diet:
 Infection control  Avoid creams, lotions, powder, and oil  Low residue and Low fiber
 Bleeding precaution at the site  Nursing Mngt:
 BLEEDING  Wash with mild soap and water and pat  If dislodged:
 Mngt: dry  Wear long lead apron
 Bleeding precaution  Do not remove markings unless done  Long-handed forceps
 ANEMIA with sessions  Lead container
 Mngt:  Avoid sun exposure  Call the radiation oncologist
 Blood transfusion  Wear loose clothes  Document
 Regulate activities  Avoid belts, buckles or strap BIOLOGIC THERAPY
 HEMORRHAGIC CYSTITIS  BRACHYTHERAPY  Uses substances made form living organisms, derived
 Mngt:  Radiation in continuous contact with tumor from organisms, or laboratory-produced versions of
 Liberal oral/parenteral fluid  Radiation source is within the patient these substances to treat cancer.
 Frequent/timed voiding  TYPES:  Immunotherapy – do not target cancer cells
 Administer drug early in the day to  Sealed implant (Intracavitary Cessium) directly; uses immune system to kill cancer cells
allow for sufficient fluid and voiding  Left inside the body  Antibodies/Segments of antibodies to kill
 Administer mesna (a drug that inhibits  Usually for cervix cancer cells directly
urotoxicity if cyclophosphamide and  No radiation in secretions,  Targeted Therapies – interferes with specific
ifosfamide) tears, urine, and feces molecules involved in tumor growth and
RADIATION THERAPY  SAFETY PRINCIPLES progression
 Decreases tumor size  Time
CANCERS OF BLOOD AND LYMPH SYSTEMS  Peripheral blood smear – presence of leukemic  Painless lumps
blast cells and low blood counts  Leukemia cutis – bluish or purplish
LEUKEMIA  Bone marrow aspiration/biopsy  Chloromas – blue-green in color
 A broad term given to a group of malignant diseases of  Shows monotonous infiltrate of blast  DIAGNOSTIC EVALUATION:
the bone marrow, blood, and lymphatic system. cells  Physical examination
 IMMATURE cells PREDOMINATE that CANNOT  Lumbar puncture – to check for CNS  Peripheral blood smear
function EFFECTIVELY involvement  Bone marrow aspiration/biopsy
 TYPES:  REFRACTORY  Shows monotonous infiltrate of blast
 Acute Lymphoblastic Leukemia  newer or more intensive doses of chemo drugs cells
 Acute Myeloid Leukemia may be tried  Lumbar puncture – to check for CNS
 HSCT involvement
ACUTE LYMPHOBLASTIC LEUKEMIA  RELAPSE  RT-PCR
 Most common form of childhood cancer  Brain or spinal fluid  (+) chloromas - biopsy
 Affects boys > girls – Caucasian > African Americans  Nalarabine for T-cell  DIAGNOSTIC EVALUATION:
 Peak onset: 2-5 years old  MoAbs (Monoclonal Antibody) for B-cell and  Physical examination
 RISK FACTORS: Chimeric antigen receptor (CAR) T-cell therapy  Peripheral blood smear
 Prenatal exposure to x-rays (Kymriah)  Bone marrow aspiration/biopsy
 Previous chemotherapy  HSCT  Shows monotonous infiltrate of blast
 Genetic conditions cells
 CLINICAL MANIFESTATIONS: ACUTE MYELOID LEUKEMIA  Lumbar puncture – to check for CNS
 Infiltration of the bone marrow by non-  Accounts for 20% of childhood leukemias involvement
functional leukemic cells (“blasts”)  Males = Females  RT-PCR
 Anemia – due to decreased  RISK FACTORS:  (+) chloromas - biopsy
erythrocytes  Constitutional chromosomal abnormalities  Induction
 Infection – due to neutropenia  Inherited gene mutations and cytopenias  Pediatrics
 Bleeding – due to decreased platelets  Therapy-related AML – chemotherapy/radiation  7 + 3 regimen (BMA on the 14th day)
 Elevated WBC count (>10,000/mm3)  7+3 = cytarabine continuously
 Hepato/splenomegaly  CLINICAL MANIFESTATIONS: for 7 days, along with short
 Lymphadenopathy  Same with ALL due to infiltration of bone infusions of an anthracycline on
 Bone pain marrow by “myeloblasts” each of the first 3 days
 CNS and Testes – important sites for  Fever (with or without infection)  Fludarabine or etoposide (for patients
extramedullary disease – “sanctuaries” for  Night sweats - shortness of breath with poor cardiac function)
leukemic cells  Weakness/fatigue  Adults – aggressive & short-course (6months)
 DIAGNOSTIC EVALUATION:  Bruising/petechiae  Ara-C (Cytarabine)
 Physical examination  Bone/joint pain  Post-remission
🞑 Consolidation – HiDAC – High Dose Ara-C (for younger
patients) , Daunorubicin, etoposide, mitoxanthrone for older;
HSCT
ACUTE LEUKEMIA
 NURSING MANAGEMENT:
 Prepare the family for Diagnostic and
Therapeutic Procedures
 Provide continued emotional support

LYMPHOMA
 Group of neoplastic diseases that arise from the
lymphoid and hematopoietic systems
 TYPES:
 Hodgkin Disease
 Non-Hodgkin Disease (more common)