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PEDS MT2
| Question | Answer |
|---|---|
| respiratory syncytial virus | paramyxovirus related to the parainfluenza virus. RSV A more virulent |
| pathophysiology of RSV | cilitated epithelial cells swell, protrude and lose cilia.RSV causes fusion of infected cells w/adjacent cells forming giant multinucleated cell(syncytia). Bronchiolar swelling, mucus, exudate.Obstruction on expiration(overinflation/emphysema) |
| Transmission of RSV | direct contact with repiratory secretios, large particle aerosols, contaminated fomites- need isolation/contact precautions |
| Initial manifestations of RSV | URI - rhinorrhea, low grade fever, OM, conjunctivitis, pharyngitis, coughing, sneezing |
| manifestations of severe RSV | tachypnea (>70), listlessness, apneic spells, poor air exchange, poor breath sounds, cyanosis |
| 2 diagnostic tests for RSV | Rapid Immunoflurorescent Antibody Direst Flurescent Antibody Stainign (DFA) AND Enzyme Lined Immunosorbent Assay (ELISA) |
| How are nasal washings obtained for DFA? | place child in supine position. Instill 1-3 mL sterile normal saline with sterile syringe into one nostril. Use small, sterile bulb syringe to aspirate contents. Place into sterile container |
| therapeutic management of RSV | nasal suctioning, repositioning, supplemental oxygen, adequate fluid intake, airway maintenance, medications (SABA by nebulizer) |
| Palivizumab: action | prophylaxis of RSV |
| Palivizumab: indications/eligibility | infants born before 32 weeks who require supplemental O2 or mechanical ventilation, infants and children younger than 2 years of age with bronchopulmonary dysplasia, children with immunodeficiency, children with congenital heart disease |
| Nursing interventions for RSV | separate room, contact precautions, limit visitors, encourage breastfeeding and pumping, monitor O2 sats, give nebulizer meds, fluids, take temp and vitals, position on back with HOB up |
| parent teaching- RSV | 1) Instill normal saline drops into nares and suction mucus with bulb syringe before feedings and before bedtime 2) offer small amounts of clear fluids 5-10 ml at a time with a medication syringe every 10 minutes |
| Why should you keep the HOB elevated in RSV patients? | allows gravity to pull intestines away from diaphragm |
| What is a toxic dose of acetaminophen? | 150 mg/kg or greater |
| Initial manifestations of acetaminophen poisoning | nausea, vomiting, sweating, pallor (2-4 hours after ingestion) |
| hepatic involvement- acetaminophen poisoning | may last up to 7 days and can be permanent- pain in RUQ, jaundice, confusion, stupor, coagulation abnormalities |
| activated charcoal | odorless, tasteless, fine black powder that absorbs many compounds creating a stable complex |
| N-Acetylcysteine (mucomyst) | antidote for acetaminophen poisoning (inactivtes toxic metabolites), administer orally/NG tube with one loading dose and 17 maintenance doses |
| who should you call when preparing for NG tube insertion in child? | child life specialist, additional staff member to assist |
| what size NG tube should you use in a small child? | 10 French |
| 4 methods to check NG tube placement | 1) pH of aspirate 2) bubble/water test 3) auscultation of air 4) Chest Xray!!! |
| Principles of emergency tx of unintentional poisoning | 1) call poison control center before initiating any intervention 2) per PCC recommendation, treat child at home or take child to facility 3) Assess 4) Gastric decontamination with activated charcoal, gastric lavage, cathartics, 4) Prevent reccurence |
| How can poisonings be prevented? | child proof containers, safely store meds, put hazardous things out of reach, educate children about hazards of ingesting non food items, resources for child safety and prevention |
| superfical burns | first degree burns- erythema due to vasodilation, minimum tissue damage, pain, damaged tissue sloughs and peels, example: sunburn |
| partial thickness burns | second degree burns- involve epidermis and varying depths of dermis. Painful, red, blistered, moist. Risk for secondary sepsis and fluid volume deficit |
| full thickness burns | 3rd deg, involve entire epidermis and dermis, extending into subQ tissue, generally involves nerve endings- lack of sensation. Dry and leathery,may vary in color from tan to red to black, may involve muscle and bone. Risk for sec. sepsis and fluid deficit |
| emergent phase - caring for burns | treatment of burn shock and management of pulmonary status. Monitor vitals, output, fluids, respiratory parameters. Ensure adequate hydration, maintain body temperature (prevent hypothermia) |
| What are 3 main things to prevent in caring for patient with burns?? | 1) Infection/Sepsis 2) Heat Loss/hypothermia 3) Fluid Volume deficit/dehydration/shock |
| HEADDSS assessment for adolescents | Home, Education/employment, Activites, Depression, Diet, Sexuality, Substances/safety |
| Pediatric Assessment Triangle | Appearance, Breathing (airway), Circulation |
| Measurements for child up to 36 months old | recumbent length, weight, head circumference |
| Measurements for child after 36 months old | standing height and weight |
| What percentiles are unexpected on growth chart for height, weight, and head circumference? | less than 5th or greater than 95% percentile |
| How big is the airway of an infant? | about the size of the pinky finger |
| sniffing position | use towel under shoulders to keep airway open in kids (head has tendency to fall forward) |
| Breathing in children younger than 6-7 yo is primarily _____________. | diaphragmatic/abdominal |
| what is the 5th vital sign in pediatrics? | skin |
| skin assessments that are alarming in children | cap refill >2 sec, decreased peripheral pulses, cool/cold extremities, mottled, pale, dusky |
| strabismus | cross eyed, one eye deviates from the point of fixation |
| sudden infant death syndrome (SIDS) | sudden death of an infant younger than 1 year of age that remains unexplained after a complete post mortem exam, including an investigation of death scene and review of case history |
| Causes of SIDs | prone position, soft bedding, overheating, young mom, poor prenatal care, substance abuse, prolonged sleep apnea, inc freq. of brief inspiratory pauses, excessive periodic breathing, impaired response to dec O2 or inc CO, brainstem abnormality, cosleeping |
| Risk factors for SIDs | 1 or more ALTE requiring CPR or vigorous stimulation, preterm infants experiencing apnea at discharge, sibling of 2 or more SIDs victims, hx of central hypoventilation, male gender,low APGARs, low birht weight, smoking |
| things that are protective against SIDS | immunizations upt o date, pacifier use at bedtime and naptime, breastfeeding, BACK TO SLEEP |
| apnea of infancy | nexplained respiratory pause of 20 secods or more, or pauses of less than 20 seconds that are accompanied by pallor, cyanosis, bradycardia, or hypotension in the term infant |
| Apparent Life Threatening Event (ALTE) | an event that is sudden and frightening to the observer, in which infant exhibits a combination of apnea, change in color, change in muscle tone, choking, gagging, or coughing and usually involves significant intervention/CPR |
| causes of apnea during infancy | sepsis, seizures, neuro disorders, upper/lower airway infection or abnormality, GERD, hypoglycemia, metabolism problems, impaired regulation of breathing |
| therapeutic management of apnea during infancy | theophylline, caffeine, home apnea monitors, family support, CPR training |
| Lead Poisoning- causes | peeling lead based paint, microparticles in soil, inhaled or ingested |
| effects of lead poisoning | Renal, hematologic, neurologic systems involved. Settles in bones/teeth where it remains inert. Interferes with regulating action of calcium. Disrupts neurotransmission, BBB, and synaptic activity. Can interfere with binding of iron onto heme= anemia |
| Diagnosis of lead poisoning | venous blood sample of 10 mcg/dl, screening at ages 1-2 |
| treatment for lead poisoning | chelation therapy with calcium disodium edetate (EDTA) and succimer (DMSA) |
| Acetaminophen Overdose- Stage I | 30 min -24 hr. GI irritation, diaphoresis, pallor |
| Acetaminophen Overdose- Stage II | 12 hrs- 4 days. Hepatotoxicity, LFT abnormal, RUQ pain (liver damage) |
| Acetaminophen Overdose- stage III | 48-96 hours. GI irritation, jaundice, hepatosplenomegaly, hepatic encephalopathy, bleeding diathesis, hypoglycemia, dysrhythmias, shock and death |
| Child Abuse | any recent act or failure to act on the part of a parent or caretaker which results in death, serious physical or emotional harm, sexual abuse or exploitation; or failure to act, which presents an imminent risk of serious harm |
| neglect | most common form of child abuse (78.3%); failure of a parent or other person legally responsible for the child's welfare to provide for the child's basic needs and an adequate level of care |
| physical neglect | deprivation of necessities such as food, clothing, shelter, supervision, medical care, education |
| emotional neglect | failure to meet child's needs for affection, attention, and emotional nurturance |
| physical abuse | 17.8%; deliberate infliction of physical injury on a child, usually by a caregiver |
| shaken baby syndrome | caused by violent shaking of infants and young children and is one form of abusive head trauma |
| shaken baby syndrome- patho | causes brain to rotate within skull, resulting in shearing forces that tear blood vessels and neurons. |
| shalen baby syndrome- outcomes | Retinal hemorrhage(85%), intracranial bleeding, fractures of ribs and long bones, vomiting, poor feeding, irritability, listlessness, seizures, posturing, altered LOC, apnea, bradycardia, death |
| munchausen syndrome by proxy | caregivers deliberately exaggerate of fabricate histories and symptoms/induce symptoms. Normally the biological mother with some sort of health care knwoledge |
| Sexual Abuse | 9.5%; involvement of children in sexual acts they do not understand, to which they cannot give consent, or that violate social taboos |
| types of sexual abuse | incest, molestation, exhibitionism, child pornography, child prostitution, etc |
| psychological abuse | 7.6%; deliberate attempt to destroy or significantly impair a child's self esteem or self confidence |
| signs of dehydration | dry mucous membranes, decreased tearing, decreased urine output, sunken fontanels, poor skin turgor, sunken eyeballs, signs of shock |
| signs of respiratory distress | tachypnea, decreased air exchange, retractions, nasal flaring, grunting, head bobbing, decreased LOC, decreased pO2, increased pCO2, cyanosis |
| signs of shock | tachycardia, hypotension (late), decreased perfusion to skin (cap refill >2, decreased peripheral pulses, decreased skin temp), abnormal coloring, decreased perfusion to brain (lethargy), decreased perfusion to kidneys |
| anemia | reduction in rbc mass and or hemoglobin concentration compared with normal values for age |
| causes of anemia | inadequate production of rbcs/rbc components, increased destruction of rbcs, excessive loss of rbcs through hemorrhage |
| consequences of anemia | decreased oxygen carrying capacity of blood, reduction in amount of oxygen readily available to cells, hemodilution, decreased peripheral resistance, increased cardiac circulation turbulence, cyanosis, growth retardation, weakness, fatigue, pallor, CNS |
| therapeutic management of anemia- treat underlying cause first | stop hemorrhage, transfuse pRBCs if needed, nutritional intervention for iron deficiency |
| therapeutic management of anemia- supportive care | IV fluid replacement, oxygen, bed rest |
| iron deficiency anemia | anemia caused by inadequate supply or loss of iron (iron necessary for hemoglobin production) |
| clinical manifestations of iron deficiency anemia | irritability, tachycardia, fatigue, glossitis, angular stomatitis, koilonychias (spoon nails) |
| lab values for iron deficiency anemia | low hgb, hct, rbcs, elevated RDW, low MCV (microcytic), pale rbcs, low serum Fe and serum ferritin, elevated serum transferrin and TIBC (total iron binding capacity) |
| sickle cell disease | a hemoglobinopathy where normal adult hemoglobin (HgbA) is partly or completely replaced by abnormal sickle hemoglobin (HgbS) |
| Transmission of Sickle Cell disease | hereditary/autosomal recessive; occurs primarily in AA and hispanic americans, also seen in mediterranean, Arabian, and East Indians |
| Patho of sickle cell disease | globin faco of hemoglobin has valine substituted for glutamic acid; conditions of dehydration, acidosis, hypoxia, and temperture elevation causes sickled rbcs that are rigid, break down easily, obstruct capillary blood flow and lead to tissue ischemia |
| fetal hemoglobin (HgbF) | protective against sickling for the first 6 months of life |
| diagnosis of sickle cell disease | cord bloos in newborns/newborn screening, genetic testing, lab findings after 6 mos: Hgb 5-9 mg/dL, presence of sickled cells, reticulocyte (5-15%) |
| Vasoocclusive Crisis | local hypoxia, tissue ischemia, infarction caused by obstruction of sickled cells in capillaries |
| vasoocclusive crisis manifestations | PAIN, dactylitis (hand/foot swelling), avascular necrosis (necrotic joints), abdominal pain (liver, kidneys, joints), priaprism (prolonged erection) |
| causes of vasoocclusive crisis | anything that increases body's need for oxygen- trauma, infection, fever, physical/emotional stress, increased blood viscosity r/t dehydration, hypoxia from high altitude, poorly pressured planes, hypoventilation, vasoconstriction from hypothermia |
| Splenic Sequestration | spleen enlargement due to pooling of blood in spleen, results in infarction of spleen, replacement with fibrotic tissue (by age 5-7) |
| symptoms of splenic sequestrations | enlarged spleen, signs of shock (pallor, weakness, hypotension, dyspnea, tachycardia, profound anemia), abdominal pain, nausea, vomiting, INFECTION (no filtering of bacteria/release of phagocytes) |
| treatment for splenic sequestration | splenectomy, penicillin prophylaxis from 1 month- 5 years old to prevent infection |
| aplastic crisis | diminished rbc production or increased destruction, usually triggered by infection with a virus |
| parvovirus | lyses red blood cells, cause aplastic crisis |
| signs of aplastic crisis | profound anemia, pallor, scleral jaundice |
| stroke (CVA) in SCD | sickled cells block major blood vessels in the brain, which leads to cerebral infarction causing neurological impairment |
| symptoms of stroke | hemiparesis/hemiplegia, impaired speech, impaired comprehension, visual disturbances, severe headaches, seizures, impaired motor function, decreased IQ |
| prevention of stroke | hydroxyurea (increases concentratio nof HgbF in blood), and pRBC transfusions/exchanges |
| acute chest syndrome | vaso-occlusive crisis or infection results in sickling in small vessels of the lungs, causing occlusion, stasis, and anemia |
| symptoms of acute chest syndrome | chest pain, lung infiltrates in CXR, cough, fever, hypoxia, tachypnea, restrictive lung disease, pulmonary hypertension |
| treatment for acute chest syndrome | oxygen, breathing tx, incentive spirometry |
| hydroxyurea | reduces incidence of reccurrent painful episodes, increased concentration f fetal hemoglobin (HgbF) |
| hematopoietic stem cell transplant (HSCT) | curative for SCD, but avoided because of complications/adverse side effects |
| supportive measures for SCD | bed rest to minimize energy expenditure, hydration, electrolyte replacement, analgesia, blood replacement, vitamins, folic acid, early intervention |
| nursing management of SCD | assessment, pain management, hydration, minimize tissue deoxygenation, minimize crises, promote supportive therapies, listen, develop coping strategies, promote growth and development, support for family, genetic counseling, financial needs |
| thalassemia | autosomal recessive blood disorder of hemglobin synthesis, resulting in anemia (pallor, fatigue, HA, irritability, exercise intolerance) |
| management of thalassemia | blood transfusions of pRBCs |
| hemostasis | process that stops bleeding when a blood vessel is injured |
| steps of hemostasis | 1) vasoconstriction reduces blood volume 2) primary hemostasis (platelet plug formation) 3) secondary hemostasis (fibrin mesh formation) 4) healing 5) fibrinolysis (clot dissolved) |
| bleeding disorder (coagulopathy) | general term for a wide range of medical problems that lead to poor blood clotting and continuous bleeding (quantitative of qualitative) |
| hemophilia | congenital deficiency of certain coagulation proteins (clotting factors), X-linked recessive |
| hemophilia A | Factor VIII deficiency, classic hemophilia |
| hemophilia B | Factor IX deficiency, christmas disease (15% of cases) |
| diagnosis of hemophilia | low levels of factor VIII and IX, prolonged PTT (>40)--> measure of intrinsic pathway (includes factors VIII and IX), normal PT (measure of extrinsic pathway, includes factor VII) |
| manifestations of hemophilia | bleeding tendencies (usually start at 6 mo when mobility increases), severe: bleeding without trauma, persistent HAs, slurred speech, decreased LOC, retinal hemorrhage, severe abdominal pain/swelling, bleeding into throat |
| common bleeding sites in hemophilia | joints (hemarthrosis), epistaxis, neck/mouth/throat/thorax, intracranial and retroperitoneal spaces, tooth eruptions, dental extractions |
| hemarthrosis symptoms | severe pain, limited ROM, swelling, tenderness in affected joint |
| Treatments for hemophilia | replacement of factors, desmopressin (DDAVP), antifibrinolytics, steroids, RICE |
| Complications to factor replacement therapy | development of "inhibitors" can stop effectiveness of factor replacement after first dose. If this occurs, must bypass factor VIII and IX and administer factor VII |
| desmopressin (DDAVP) | synthetic hormone that stimulates release of stored clotting factor from endothelium (mild hemophilia only) |
| antifibrinolytic medicaions | prevent normal lysis of fibrin mesh by binding to plasminogen (Amicar, cyklokapron, lysteda) |
| Von Willebrand Disease | autosomal dominant disorder that occurs in males and female and is characterized by deficiency in von willebrand factor |
| von willebrand factor | protein that contibutes to adherence of platelets to damaged endothelium and a carrier for factor VIII |
| Von willebrand disease Type I | low levels of VWF (quantitative) |
| Von willebrand disease type II | qualitiative deficency of VWF |
| von willebrand disease type III | non/almost no VWF |
| manifestations of VW disease | bruising, nose bleeds, gum bleeds, excessive bleeding with lacerations, bleeding with dental work, GI bleeds, increased menses. MOSTLY MUCOSAL BLEEDING |
| treatment of VW disease | IV VWF/Factor VIII replacemnt, desmopressin (DDAVP), antifibrinolytic meds, oral contraceptives (estrogen increases WVF and factor VIII levels) |
| Leukemia | malignant disease of bone marrow and lymphatic system, most common childhood cancer, more frequent in males, peak onset 2-6 yo, 20x more likely in kids with down syndrome |
| Leukemia- patho | unrestricted proliferation of immature white blood cells in blood forming tissues of the body, elevated coutns of blasts that compete for and deprive normal blood cells of essential nutrients for metabolism |
| 3 consequences of leukemia | 1) anemia from decreased erythrocytes 2) infection from neutropenia 3) bleeding from decreased platelet production |
| 4 things that make leukemia prognosis worse | 1) initial wbc count >20,000 2) age at time of onset <2 or >10 3) myeloid line involved 4) genetic markers |
| lymphoma | neuplastic disease originating in lymphatic system, possibly metastasizing to spleen, liver, bone marrow, lungs, and other tissues |
| hodgkins disease | lymphoma that occurs in 15-19 yo |
| Class A hodgkins disease | presents asymptomatically |
| Class B hodgkins disease | presents with fever, night sweats, weight loss |
| manifestations of hodgkins disease | painless enlargement of lymph nodes (firm, nontender, movable) in supraclavicular or cervical area, mediastinal lymphadenopathy (may cause respiratory symptoms) |
| non hodgkins lymphoma | occurs in children <14 yo, usually diffuse rather than nodular, cell type undifferentiated/poorly differentiated, dissemination occurs early and rapidly, mediastinal involvement and invasion of meninges |
| lymphoma- stage 1 | single extranodular tumor, or limited to single anatomic area |
| Lymphoma- stage 2 | single tumor with regional node involvement. involvement of two or more areas on same side of diaphragm. all primary GI tumors |
| lymphoma- stage 3 | involvement of two or more areas on opposite sides of the diaphragm. all primary intrathoracic tumors, paraspinal/epidural tumors |
| lymphoma- stage 4 | bone marrow involvement |
| CNS tumor | tumor in the brain or spinal region that can be malignant or benign |
| manifestations of CNS tumor | sudden onset - HA (posterior), vomiting, ataxia, mystagmus, diplopia, visual/cognitive change, hemiparesis, seizures |
| neuroblastoma | malignancy of SNS forming tumor in neck, chest or abdomen |
| manifestations of neuroblastoma | palpable tumor (abdomen), fever if spread to bone marrow, raccoon eyes |
| Kidney tumors- Wilm's tumor | large, rapidly growing vascular tumors of the kidney |
| manifestations of wilm's tumor | abdominal mass, pain, malaise, hematuria, hypertension |
| osteosarcoma and ewings sarcoma | primary malignant tumors of bone |
| manifestations of osteosarcoma and ewings sarcoma | bone pain, aching, hx trauma, soft tissue mass/swelling, possible metastases to lungs, constitutional symptoms |
| rhabdomyosarcoma | small, round, blue-cell malignant tumor of muscle tissue |
| rhabdomyosarcoma manifestations | mass or disturbance of normal bodily function in affected area |
| chemotherapy | prevents multiplication of malignant cells and tumor growth by interfering with function or production of DNA/RNA. Not selectively cytotoxic for malignant cells |
| why do mucositis and alopecia occur with chemotherapy? | chemo is designed to attack fastest growing cells, these areas have cells with high proliferation rates |
| leucovorin | water soluble vitamin used to help clear intermediate/high dose methotrexate. GIVE AT ORDERED TIME |
| mesna | cytoprotective agent often used with cyclophosphamide or isosfamide to protect bladder from hemorrhagic cystitis |
| asparaginase | used as protectant after methotrexate and cytarabine administration |
| amifostine | prevents ototoxicity |
| dexrazoxane | prevents cardiotoxicity |
| vesicants | sclerosing agents that can cause severe cellular damage if even minute amounts of the drug infiltrate surrounding tissue |
| interventions for extravasation of vesicants | cold/warm compress, topical DMSO if mild, sodium thiosulfate, hydraluronidase for severe |
| tumor lysis syndrome | metabolic abnormalities that are a direct result of rapid release of intracellular contents during lysis of malignant cells. ELEVATED uric acid, potassium, phosphate. DECREASED calcium |
| treatment for tumor lysis syndrome | ensure fluids dont have K+, amphogel, allopurinol (reduces uric acid), hydration, BICARB- neutralizes pH |
| neutropenia | reduction in number of circulating neutrophils; ANC <1000 2weeks-1 yo, ANC <1500 in >1 yo, risk for infection!!! |
| G-CSF (granulocyte colony stimulating factor) | stimulates bone marrow to produce more white blood cells- increases neutrophil count when neutropenic (neupogen, neulasta, granocyte) |
| radiation | high energy particles or waves target malignant cells and spare adjacent healthy tissues; prevents reproduction of malignant cells, used for treatment of radiosensitive n and palliative symptom control |
| hematopoietic stem cell transplant | replace malignant or absent stem cells with healthy stem cells, allows administration of high doses of chemo and radiation which might be curative for aggressive or recurrent malignancies |
| allogenic HSCT | stem cells from a donor, can be matched, mismatched, related or unrelated |
| autologous HSCT | uses patients own stem cells |
| sources of stem cells | bone marrow, peripheral blood, crd blood |
| complications of HSCT | significant risk of morbidity/mortality, graft versus host disease, overwhelming infection, severe organ damage, poor prognosis in case of relapse, no reverse treatment |
| graft versus host disease (GVHD) | body is foreign to the newly transplanted immune cells. Immune system attacks body/organs |
| biologic response modifiers | alters response to host tumor by modifying immune response to tumor, directly suppressing tumor growth and killing tumor cells, altering biologic activities to reduce tumor viability |
| acyclovir | antiviral used to prevent herpes virus in immunosuppressed |
| varicella zoster immune glaobulin | prophylaxis of VZ virus (chickenpox) in immunocompromised |
| ondansetron (zofran) | antiemetic used for chemo induced nausea and vomiting |
Created by:
alexadianna
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