Pedia (Pediatric Disorders) PDF

PEDIA (FINALS) Oliver , May Trishia H. 2BSN3 PEDIATRIC DISORDERS BLOOD - Releases erythropoletin, wh...

PEDIA (FINALS) Oliver , May Trishia H. 2BSN3 PEDIATRIC DISORDERS BLOOD - Releases erythropoletin, which tells bone marrow to make red blood cells. WHAT A KIDNEY DOES WATER - Ensures that there’s not too much or too little water in the bod. NEPHROTIC SYNDROME BLOOD - Makes sure that pressure isn’t too high or too  A clinical state that includes massive low. protenuria ,hypoalbuminemia, hyperlipidemia, and edema. WASTES - Gets rid of urea, uric acid, toxins, and other THE DISORDER CAN OCCUR AS : wastes via urine. 1. Primary disease known as idiopathic nephrosis, BONES childhood nephrosis, or minimal-change - Activates vitamin D, which helps body absorb nephrotic syndrome calcium. 2. A secondary disorder that occurs as a clinical ACID-BASE BALANCE manifestation after or in association with - Makes sure that the body isn’t too acidic or too glomerular damage that has a known or alkaline. presumed cause. HEART 3. A congenital form inherited as autosomal - Maintains a balance of electrolytes ( like recessive disorder. potassium , sodium, and calcium), which is critical for heart rhythm. ) 4.Characterized by increased glomerular permeability to plasma protein, which results in massive urinary protein loss in the urine. 5. Glomerulus are responsible for the initial step 3. Edema , with low level of protein in the in urine formation and filtration. bloodstream , osmotic pressure causes fluid to shift from the bloodstream to interstitial tissue. ---> as the blood volume decreases, the PATHOPHYSIOLOGY kidneys begins to conserve sodium and water.  Predominantly occurs in children between 2 4. Hyperlipidemia occurs because the liver to 7 years old. increases production of lipoprotein to try to  CAUSES: (Speculative) compensate for protein loss.  Metabolic  Biochemical  Physiochemical DIAGNOSTIC EVALUATION  Immune-mediated disturbance That causes the basement membrane of the  Clinical manifestations glomeruli to become increasingly permeable to protein.  Diagnosis of MCNS is suspected on the basis on history and clinical manifestations  Becomes permeable to proteins, especially ( edema, proteinuria, hypoalbuminemia, to albumin, that leak through the and hypercholesterolemia in the absence of membrane and are lost in the urine. hematuria and hypertension). HYPOALBUMINURIA  The hallmark of MCNS is massive proteinuria (higher than 2+ on urine HYPOALBUMINEMIA dipstick).  Reduce the serum albumin I level  Total serum protein concentration is low,  The shift of fluid from the plasma to the with the serum albumin significantly interstitial space reduces the vascular fluid reduced and plasma lipids elevated. volume ------ HYPOVOLEMIA  Which in turn stimulates the renin -  If the patient does not respond to a 4 to 8 angiotensin system and secretion of week course of steroids, a renal biopsy may antidiuretic hormone and aldosterone. be needed to distinguish among other types  As a result, the vascular Hydrostatic of nephrotic syndrome. pressure exceeds the pull of the colloidal osmotic pressure causing fluid to accumulate in Interstitial spaces ---- EDEMA THERAPEUTIC MANAGEMENT  And the body cavities, particularly in the abdominal cavity - ASCITES Objectives of therapeutic management include: 1. Reducing excretion of urinary protein 2. Reducing fluid retention in the tissues CHARACTERISTICS OF NEPHROTIC SYNDROME 3. Preventing infection 4. Minimizing complications related to therapies 1. Proteinuria occurs because increased glomerular permeability leads to protein loss in  dietary restrictions ---> low salt diet and the urine and, subsequently, hypoalbuminemia. fluid restriction  Corticosteroids are the first line of therapy 2. Hypoalbuminemia low serum albumin level as for MCNS. they leak through the membrane and are lost in  Other immunosuppressant therapy urine. (cyclophosphamide, chlorambucil, or cyclosphorine) NURSING CARE MANAGEMENT  Affects primarily early school-age children, with peak age of onset of 6 to 7 years.  Continuous monitoring of fluid retention or excretion ETIOLOGY  Strict intake and output records  Immune-complex disease that occurs after  NURSING TIP: an antecedent streptococcal infection with  Urine examination for albumin certain strains of the group A B-hemolytic  Daily weight streptococcus.  Measurement of abdominal girth  Disease secondary to streptococcal  Assessment of edema pharyngitis (common in winter & spring)  Vital signs are monitored  Associated with pyoderma (impetigo) more prevalent in summer or early fall FAMILY SUPPORT AND HOME CARE :  Second episode of AGN is rare.  Most children are treated at home during relapse.  Parents are thought to detect signs of DIAGNOSTIC EVALUATION relapse and to call for change in treatment at the earliest indications.  Urinalysis ----> proteinuria and edema are severe or  Culture of the pharynx parents, for some reason, are unable to take care  Serological tests for the ill child, home care is preferred.  Chest X-ray  Renal biopsy ( for atypical cases)  Parents are instructed to:  In testing urine for albumin THERAPEUTIC MANAGEMENT  Administering medications Consists of :  Providing general care  Supportive measures  Avoiding contact with infected playmates,  Early recognition and treatment of but the child should attend school complications  Children with normal blood pressure and a satisfactory urinary output can generally ACUTE treated at home. Those with substantial edema, hypertension, GLOMERULONEPHRITIS  gross hematuria, or significant oliguria should be hospitalized because of the unpredictability of complications. COMMON FEATURES  Dietary restrictions  Regular measurement of v/s, body weight, I  Proteinuria &O  Oliguria  A record of daily weight is the most useful  Edema means of assessing fluid balance.  Hypertension  Blood pressure measurements are taken  Hematuria every 4 to 6 hours.  Circulatory congestion  Antihypertensive medications  Diuretics  Most cases are postinfectious and has been  Antibiotic therapy ( with evidence of associated with pneumococcal, persistent streptococcal infections) streptococcal and viral infections.  Acute poststreptococcal glomerulonephritis (APSGN) is the most common of the postinfectious renal disease in childhood.  INFECTIONS OF BONES & CLINICAL MANIFESTATIONS JOINTS  Children with hematogenous osteomyelitis have the following signs and symptoms:  2-to-7 day history of pain OSTEOMYELITIS  Warmth  Tenderness Can occur at any age but most frequently  Decreased range of motion in the  seen in children 10 years of age or younger. affected limb along with the systemic symptoms of fever, irritability, and most commonly affected include the foot, lethargy.  femur, tibia, and pelvis. Staphylococcus aureus is the most common  DIAGNOSTIC EVALUATION causative microorganism.  Cultures of aspirated purulent drainage, For neonates ---> group B streptococci blood, joint fluid and infected skin samples  Children with sickle cell ---> Salmonella, should be obtained.  S.aureus  Bone biopsy Neisseria gonorrhoeae for sexually active Radiography   adolescents.  CT scan Kingella kingae for children younger than 5 MRI ----> reported to be the most   years old. sensitive diagnostic radiologic tool for diagnosing osteomyelitis. Subacute osteomyelitis  has longer course and may be caused by THERAPEUTIC MANAGEMENT virulent microbes with a walled-off abscess or Bodie abscess, typically in the proximal  IV antibiotics or distal tibia. ---> to prevent antibiotic-associated diarrhea in some children, administration of a probiotic Chronic osteomyelitis may be considered.  is a progression of acute osteomyelitis and  Surgery is characterized by dead bone, bone loss, and drainage and sinus tract. NURSING CARE MANAGEMENT  Child is positioned comfortably with the affected limb and well supported. FACTORS THAT CONTRIBUTE TO INFECTION  Temporary splint and cast may be applied. INCLUDE:  Postoperatively, pain medication.  Antibiotic therapy  Inoculation with a large number of  Standard precautions organisms  Provisional and constructive activities  Presence of foreign body  Physical therapy  Bone injury  High virulence of an organism  Immunosuppression  Malnutrition  Certain types o and locations of bone are also more vulnerable to infection.  SEPTIC ARTHRITIS JUVENILE RHEUMATOID ARTHRITIS  Is a inflammation of a synovial membrane with purulent effusion into the joint capsule,  A chronic autoimmune inflammatory dule to infection. disease causing inflammation of the joints and other tissue with unknown cause. SYNOVIAL MEMBRANE  Membrane surrounding joint cavity CAUSES  Produce synovial fluid  Two factors are hypothesized:  Contain rich capillar network for phagocytic Immunogenic susceptibility and hyaluronate producing function. Environmental or external trigger such as virus Most common joints affected are knees,  Few known genetic risk factors hips, ankles, and elbows. Clinical manifestations:  Severe joint pains CLINICAL MANIFESTATIONS  Swelling  Warmth of overlying tissue  The outcome is variable and unpredictable.  Erythema  Can cause significant joint deformity and Features of systemic illness: fever, malaise, functional disability, requiring medications, nausea, vomiting and irritability. physical therapy, and perhaps future joint replacement  Chronic and acute uveitis can cause THERAPEUTIC MANAGEMENT and NURSING permanent vision loss if undiagnosed not CARE MANAGEMENT aggressively treated.  Culture and determination of leukocyte count DIAGNOSTIC EVALUATION  Blood culture and complete blood count with differential and ESR or CRP  No definitive tests.  Technetium scans reveal areas of increased  Plain radiographs are the best initial imaging blood flow but will not differentiate studies may show soft-tissue swelling and between sites. joint space widening from increased  MRI and Ct scans provide more detailed synovial fluid in the joint. images of cartilage loss, joint narrowing,  A slit lamp eye examination is necessary to erosions, and ankylosis of progressive diagnose uveitis, inflammation of the disease anterior chamber of the eye, which is  Ultrasonography is helpful in the detection common in antinuclear antibody-positive of joint effusions and fluid in the soft tissue young girls with oligoarthritis. and subperioteum.  Treatment:  IV antibiotic therapy THERAPEUTIC MANAGEMENT  Pain management  Surgical intervention  No cure for JIA.  Phy  Major goals:  Nursing care: Same as osteomyelitis  Control pain  Preserve joint range of motion and function  Minimize effects of inflammation such as  Type 2 diabetes usually arises because of joint deformity, and promote growth and insulin resistance in which the body fails to development. use insulin properly combined with relative (rather than absolute insulin deficiency. MEDICATIONS -----> Occurs in those who are older than 45 - Nonsteroidal anti inflammatory drugs, years of age, are overweight and sedentary, and Methotrexate, Biologic agents, Physical and have a family history of diabetes. Occupational therapy DIAGNOSTIC EVALUATION NURSING CARE MANAGEMENT  Three groups of children who should be  Relieve pain, Promote general health, considered as candidate for diabetes: Facilitate adherence, Encourage heat and exercise, Support child and family 1. Children who have glycosuria, polyuria, and a history of weight loss or failure to gain despite a Physical and Occupational therapy voracious appetite. 2.Those with transient or persistent glycosuria.  Directed toward specific joints, focusing on 3.Those who display manifestations of metabolic strengthening muscles, mobilizing restricted acidosis, with or without stupor or coma. joint motion, and preventing or correcting deformities. An 8-hour FBS level of 126mg/dl or more, Occupational therapy assumes responsibility   random blood glucose value of 200mg/dl or for generalized mobility and performance of more accompanied by classic signs of activities of daily living. diabetes, or OGTT finding of 200mg/dl or more on the 2hour sample is almost certain to indicate diabetes. DIABETES MELLITUS THERAPEUTIC MANAGEMENT  A chronic disorder of metabolism Insulin Therapy characterized by a partial or complete  Insulin replacement is the cornerstone of deficiency of the hormone insulin. management of type 1 DM.  Insulin dosage is tailored to each child based  Type 1 diabetes is characterized by on home blood glucose monitoring. destruction of the pancreatic B cells, which  Goal of insulin therapy: to maintain near- produce insulin; this usually leads to normal blood glucose values while avoiding absolute insulin deficiency. too frequent episodes of hypoglycemia.  Goals of treatment: maintain near-normal Two forms: blood glucose levels of less than 126mg//dl Immune mediated DM results from an and glycosylated hemoglobin of 7% or less. autoimmune destruction of the B cells; typically  Glycemic control decreases long-term starts in children and young adults who are slim. complications in patients with DM.  Insulin is administered a two or more Idiopathic type 1 refers to rare forms of the injections /day or as continuous infusion disease that have no known case. using a portable insulin pump.  Subcutaneous injections results in absorption of the drug into the general circulation, thus reducing the concentration of insulin to which the liver is exposed.  Regular insulin is best administered at least EXERCISE 30 minutes before meals -----> to allow sufficient time for absorption and results in  Exercise is encouraged and never restricted a significantly greater reduction in the unless indicated by other health conditions. postprandial rise in blood glucose.  Exercise lowers blood glucose levels,  Intensive therapy consist multiple injections depending on the intensity and duration of throughout the day ------> to stimulate the the activity. basal insulin secretion.  Regular exercise aids in utilization of food  Multiple daily injection program reduces and often results in a reduction of insulin microvascular complications of diabetes in requirement. young healthy patient with type 1 DM. HYPOGLYCEMIA  An integral part of insulin therapy, an MONITORING objective of diabetes management is to achieve the best possible glycemic control  Glycosylated Hemoglobin RBC circulate in while minimizing the frequency and severity the blood stream, glucose molecules of hypoglycemia. gradually attach to the hemoglobin A  1Tbsp of table sugar will elevate the blood molecules and remain there for the lifetime glucose level and alleviate symptoms of of the RBC approximately 120 days. hypoglycemia.  The attachment is not reversible; therefore this reflects the average blood glucose levels over the previous 2 to 3 months. Glucagon is sometimes prescribed for home  Daily monitoring of blood glucose levels is treatment. an essential aspect of appropriate  administered IM or subcutaneously management.  it release stored glycogen from the liver and requires 15 -20 minutes to elevate blood NUTRITION glucose level  They need sufficient calories to balance  glycogen stores are replaced by small daily expenditure for energy and to satisfy amounts of sugar-containing fluid the requirement for growth and administered frequently until the child feels development. comfortable trying solid foods.  Meals and snacks must be eaten according to peak insulin action, and the total number Morning Hypoglycemia of calories and proportions of basic  management of elevated morning blood nutrients must be consistent fro day to day. glucose levels depend on whether the  Concentrated sweets are discourage, and increase is a true dawn phenomenon, because of the increased risk of insulin , waning, or rebound hyperglycemia atherosclerosis. (the Somogyi effect).  Dietary fiber is important because of its influence in digestion, absorption, and  Insulin waning is a progressive rise of blood metabolism of many nutrients. glucose levels from bedtime to morning,  Child’s appetite should be the guide for the and is treated by increasing the nocturnal amount of calories needed, with the total insulin dose. caloric intake adjusted to appetite and  True dawn phenomenon shows relatively activity. normal blood glucose level until about 3 am, when the level begins to rise.  The Somogy effect may occur anytime but often with elevated blood glucose level at bedtime and a drop at 2 am with rebound rise the following.  Treatment of this phenomenon I to measurements: volume, specific gravity, decrease the nocturnal dose of insulin to glucose and ketone values. prevent the 2 am hypoglycemia.  The rebound rise of the blood glucose level  LOC is assessed and recorded at frequent is a result of counterregulatory hormones intervals. (epinephrine, GH, and corticosteroids) which are stimulated by hypoglycemia.  Parents need to understand the treatment method and the insulin prescribed, the THERAPEUTIC MANAGEMENT effective duration, onset, and peak action.  Need to know the characteristics of the  Blood glucose levels and urinary ketones various types of insulins, the proper mixing should be monitored every 3 hours. and dilution, and how to substitute another  Insulin should never be omitted during type of insulin when their usual brand is not illness, dosage requirements may increase available. or decrease,or remain unchanged,  Insulin need not be refrigerated but should depending on the severity of the illness and be maintained at a temperature between the child’s appetite. 15° and 29°C. Freezing renders insulin  Notify if the health care practitioner if blood inactive. glucose levels remain above 240mg/dl or if  Insulin bottles that have been opened urinary ketones remain high. should be stored at room temperature or  Simple carbohydrates may be substituted refrigerated up to 28 to 30 days. After for carbohydrate-containing exchanges in 1month, these vials should be discarded. the meal plan.  Unopened vials should be refrigerated and  Fluids must be encouraged to prevent are good until the expiration date on the dehydration and to flush out ketones. label.  Diabetic supplies should not be left in a hot environment. THERAPEUTIC MANAGEMENT OF KETOACIDOSIS  Rapid assessment IRON DEFICIENCY ANEMIA  Adequate insulin to reduce the elevated blood glucose level (not to be given until  Anemia is caused by an inadequate supply blood glucose level & urinary ketones have of dietary iron and the most preventable been obtained mineral disturbance.  Fluids to overcome dehydration  Preterm infants are especially at risk  Electrolyte replacement (especially because of their reduced fetal iron supply. potassium)  Children 12 to 36 months of age are at risk  Diabetic ketoacidosis, the most as a result of primarily cow milk intake & complete state of insulin deficiency, is not eating an adequate amount of iron- a life-threatening situation. containing food.  Careful and accurate records of vital signs, PATHOPHYSIOLOGY weight, fluids, electrolytes, insulin, blood glucose level, and intake and output.  Factors that decrease the supply of iron: impair its absorption, increase the body’s  A urine collection device or retention demand, or affect the synthesis of Hgb. catheter is used to obtain the urine  During the last trimester of pregnancy ---> iron is transferred from the mother to the THERAPEUTIC MANAGEMENT fetus.  Iron-rich foods  Most of the iron is stored in the circulating  Parenteral (IV or IM) iron administration for erythrocytes of the fetus. children who have iron malabsorption or chronic hemoglobinuria.  Remainder stored in the fetal liver, spleen,  Transfusion for severe anemia & in cases of and bone marrow. serious infection, cardiac dysfunction, or surgical emergencies when anesthesia is  It is usually adequate for the first 5 to 6 required. months in a full-term & 2 to 3 months for  Packed RBC’s (2-3 ml/kg ---> to minimized the pre-term infants & multiple births. the chance of circulatory overload.  Iron-deficiency anemia results after the iron stored is depleted and not supplied by diet to meet the infant’s growth demands. NURSING CARE MANAGEMENT  Some toddlers with iron-deficiency anemia are under weight many infants are over  Instruction should be given in the weight because of excessive milk ingestion administration of iron (known as milk babies).  Oral iron should be given as prescribed in 2 divided doses:  These children becomes anemic for 2 reasons:  Between meals, when the presence of 1. milk, a poor source of iron, is given free hydrochloric acid is greatest, almost to the exclusive of solid foods because more iron is absorb in the 2. 50% of iron-deficient infants fed cow’s acidic environment og the upper GIT. milk have an increased fecal loss of blood.  A citrus fruits or juice taken with the medication aid in absorption.  Dietary counseling and administration of  Cow’s milk contains substances that oral iron supplement. bind the iron and interfere with  Formula-fed infants ----> iron-fortified absorption. Iron supplements should commercial formula & iron-fortified infant not be administered with milk or milk cereal. products.(Carley,2003)  Iron-fortified formula provides a relatively constant & predictable amount of iron and not associated with an increased GI symptoms.  Infants younger than 12 months of age should not be given fresh cow’s milk because it may increase the risk of GI blood loss occurring to exposure to a heat- labile protein in cow’s milk or cow’s milk – induced GI mucosal damage resulting from a lack of cytochrome iron (heme protein).