Busy. Please wait.

Forgot Password?

Don't have an account?  Sign up 

show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.

By signing up, I agree to StudyStack's Terms of Service and Privacy Policy.

Already a StudyStack user? Log In

Reset Password
Enter the email address associated with your account, and we'll email you a link to reset your password.

Remove ads
Don't know (0)
Know (0)
remaining cards (0)
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how


Peds Conditions Barry

2 factors cause intraventricular hemorrhage: 1. Loss of cerebral autoregulation 2. Abrupt alterations in cerebral blood flow and pressures
When is the highest occurrence of intraventricular hemorrhage? Highest occurrence in first 72 hours of life.
Increased incidence of intraventricular hemorrhage in what population? Incidence up in infants < 32 weeks gestation and with birth weight < 1500 grams.
To prevent intraventricular hemorrhage, avoid conditions that: -Interfere with autoregulation (hypocarbia, hypercarbia,hypoxia, acidosis) -Overwhelm autoregulation abilities (Hypertension) -Contribute to rapid fluctuations of cerebral blood flow or pressure
Primary cause of respiratory distress syndrome (RDS): Primary Cause: surfactant deficiency secondary to immature type II alveolar cells in the preterm lung.
When does surfactant appear, when is it mature? Surfactant appears in amniotic fluid 28-32 weeks and mature levels by 34-35 weeks.
What can cause earlier release of surfactant? Maternally administered steroids.
Tell me the story of what happens after hypoxia in the infant (RDS)? Increase work of breathing-> hypercarbia-> pulmonary arterial vasoconstriction->R to L shunting and ischemic injury to cells producing surfactant.
On an RDS Xray you will see: Bell shaped thorax with diffuse symmetrical ground glass infiltrates.
Treatment for RDS: -Supplemental Oxygen for target -PaO2 of 55 – 70 mm Hg -CPAP up to 10 cmH2O -Mechanical ventilation -Avoid oxygen toxicity and pulmonary barotrauma -Artificial surfactant
PDA = Failed closure or reopening after functional closure. What happens? -Left to right shunt occurs and may be asymptomatic or result in CHF and failure to thrive if large -If PVR remains high the R to L shunt results in hypoxemia -Obligatory PDA occurs in 10% of infants with CHD
Physical signs of R to L shunt: -Hyperdynamic precordium -Wide pulse pressures -Bounding arterial pulses -Increased oxygen requirements -Metabolic acidosis
Diagnosis or R to L shunt is by: ECHO.
Treatment for PDA: Indomethacin Fluid restriction Diuretics for CHF Surgery Mechanical ventilation
Hypoglycemia in a neonate = less than 40
Hyperglycemia in term and preterm infants: over 125 and over 150
To maintain normoglycemia, what is required? Neonates require 3-5 mg/kg per minute and preterm neonates 5-6 mg/kg per minute of glucose to maintain euglycemia.
What are 4 neonate thermoregulatory disadvantages? -Increased surface are relative to metabolic mass -Smaller heat sink reserve -Less insulating fat -Decreased skin keratinization = more evaporative heat loss -Inability to shiver
To create heat, neonates rely on 2 metabolically costly mechanisms: -Brown fat metabolism -Shunting of hepatocyte oxidative phosphorylation to the thermogenic proton leak pathway
Neonates creating heat results in what bad stuff? Acidosis, hypoxia, hypoventilation and hypotension
Postoperative apnea - who is at greatest risk? Infants 55weeks of post-conceptual age & younger are at greatest risks.
Retinopathy of prematurity - who is at greatest risk and why? PRETERM INFANTS <1500 G AND 34 WEEKS GESTATION @RISK - RETINAL VASCULATURE NOT FULLY MATURE.
What happens in retinopathy of prematurity - in caps, please? VESSELS CAN VASOCONSTRICT, HEMORRHAGE, AND VASOPROLIFERATE IN RESPONSE TO HYPEROXIA.
When is vascularization of the eye complete? 44 weeks.
Blindness can result from retinal detatchment - what has been implicated in causing retinopathy of prematurity? HYPOXEMIA, ACIDOSIS, HYPOTENSION, AND SEPSIS HAVE BEEN IMPLICATED IN CAUSING ROP.
You should measure O2 where? Preductal (Rt hand or ear).
To avoid ROP, where should you keep your O2 during GETA? 93-96%
How much type 1 fibers in diaphragm? 10-25%
What is most common laryngeal disorder of newborn? Laryngomalacia.
What is laryngomalacia? Inward collapse of epiglottis and aryepiglottic folds during inspiration.
What are signs of laryngomalacia? Stridor especially when infant lying supine, crying, or feeding.
What other condition is associated with laryngomalacia? Possible association of gastroesophageal reflux.
Can you easily PPV a child with laryngomalacia? Yes.
Is laryngomalacia relieved with an oral airway? No.
What's associated with OSA? -Habitual snoring, daytime somnolence, behavioral problems, school problems, developmental delay -Failure to thrive -Hypoxemia, hypoventilation, PHTN, CHF and death
Can OSA cause Cor Pulmonale? Hell yeah it can.
Many patients with craniofacial abnormalities can also have: OSA.
What is the most common acquired anomaly of the larynx in children and most common cause of tracheostomy for children younger than 12 months? Subglottic Stenosis
What sadly causes subglottic stenosis? Chronic inflammation and scarring from the presence of an endotracheal tube.
Is it easy to PPV a patient with subglottic stenosis? PPV may be difficult.
Tracheomalacia is: Defined as a softening of the tracheal cartilage.
Tracheomalacia causes airway collapse during: Forceful coughing or exhalation ventilation.
Patients with tracheomalacia have these symptoms: Long term mechanical ventilation, noisy breathing, “barky” cough, wheezing and respiratory distress.
Asthma is a chronic disease of reversible airway obstruction and characterized by: Bronchial hyperreactivity, inflammation, & mucous secretion.
Asthma pharmacotherapy: -Beta adrenergic agonists -Corticosteroids -Cromolyn sodium -Anticholinergics -Leukotriene pathway modifiers
Unfortunately, for intraoperative bronchospasm, Intraoperative bronchospasm efficiency of MDI of albuterol through 3.0 – 6.0 mm ID tracheal tubes is: Low.
What is cystic fibrosis? A hereditary disease of exocrine glands primarily affecting the pulmonary and GI systems.
Cystic fibrosis causes exocrine pancreatic... Insufficiency.
Cystic fibrosis causes GI... Obstruction.
In a patient with cystic fibrosis, how does sweat change? They lose an excess of sodium and chloride.
Sinopulmonary disease is found in... Cystic fibrosis patients.
Cystic fibrosis patients' sbnormal thick and viscous secretions coupled with decreased ciliary activity lead to... Pneumonia, wheezing and bronchiectasis
What does cystic fibrosis do to pulmonary function? Increases residual volume and airway resistance with decreased vital capacity & expiratory flow rate.
Cystic fibrosis may lead to malabsorption syndrome which may lead to... Malabsorption syndrome may lead to dehydration, electrolyte disorders and Vitamin K deficiencies (Clotting factors).
Cystic fibrosis patients have a higher incidence of this cardiac condition: Right ventricular hypertrophy.
Common surgical procedures for the patient with cystic fibrosis: -Endoscopic sinus surgery (Nasal Polyps) -CVP catheter placement -Bronchoscopy -Lobectomy -Pneumonectomy -Abdominal exploration -Colostomy
N2O in a patient with cystic fibrosis? NO! Avoid N2O; increase FiO2; Inhalational uptake prolonged. Rapid emergence good.
Do cystic fibrosis patients have issues with hyperactive airway? Uh, yeah.
In a patient with meconium aspiration, what is believed to be responsible for the violent inflammatory response? Bile salts.
Can pulmonary hemorrhage occur in meconium aspiration? Yes.
Therapy for patients with meconium aspiration -Amnioinfusion -Tracheal Intubation and suctioning -Antibiotics -Surfactant Replacement -ECMO for severe MAS with PPHN
Bronchopulmonary dysplasia is: BPD is a chronic disease of lung parenchyma and small airways with chronic respiratory insufficiency in prematurely born infants.
Bronchopulmonary dysplasia is oxygen dependence at when? BPD is oxygen dependence at 36 weeks postconceptual age.
What is cerebral palsy? It is an abnormality of posture and movement caused by brain injury occurring before 2 years of age.
What causes cerebral palsy? Prematurity, LBW, prenatal infections (rubella), congenital malformations of the brain, meningitis, brain tumors, and intracranial hemorrhage.
Describe pyramidal type of cerebral palsy: Pyramidal type: damage to cerebral cortex usually produces spasticity, contractures and bony deformities.
Describe extra-pyramidal type of cerebral palsy: Extra-pyramidal type: damage to the basal ganglia or cerebellum tens to produce athetosis or ataxia.
Can pyramidal and extra-pyramidal type of cerebral palsy co-exist? Yes, and do, often.
What is baclofen? Baclofen is a GABA receptor agonist with action in the dorsal horn of the spinal cord. It is used to reduce pain with muscle spasms and delay development of contractures. Abrupt withdrawal issues.
What does botox do/anesthesia issues? Botox produces reversible muscle denervation & temporary reduction in muscle tone. No anesthesia issues.
Why do patients with cerebral palsy have hypothermia issues? Hypothalamus issues.
Do CP patients have latex allergy issues? Yes.
What is the inherited, sex-linked recessive disease that presents in early childhood between 2 and 6 years of age? Duchennes's Muscular Dystrophy.
T or F: Duchenne's patients look like they're wasting away? F: they LOOK very muscular.
S/S of Duchenne's: -Symmetric skeletal muscle wasting -Wasting of pelvics – Gower’s sign Hypertrophy of skeletal muscles Kyphoscoliosis EKG changes: tall R in V1, deep Q in limb leads, short P-R interval, tachycardia Mitral valve prolapse Intestinal hypomobility and d
Sux and muscular dystrophy? Hyperkalemia Massive rhabdomyolysis Cardiac arrest. Good God no don't do it!
Non-depolarizing muscle relaxants and MD: OK: prolonged recovery time.
What can't you give to patients with congenital myotonic dystrophy? No succinylcholine – induces intense generalized myotonic contraction.
Heart and congenital myotonic dystrophy? Fifty to ninety % have myocardial conduction defects, bradycardia and 1st degree AV block are common.
In patients with congenital myotonic dystrophy, reversal? Reversal of muscle relaxation with anticholinesterase drugs may precipitate or enhance myotonia.
Osteogenesis imperfecta: Congenital connective tissue disorder that causes a generalized decrease in bone mass and bones that break easily.
Clinical manifestations of osteogenesis imperfecta: Blue sclera, dental abnormalities and brittle bones. Deafness, abnormal platelet function, increased BMR & O2 consumption, cleft palate, vascular fragility, hydrocephalus, spina bifida and aortic and mitral regurgitation.
Scoliosis and osteogenesis imperfecta? About 20% of the time.
Sux and osteogenesis imperfecta? No - spasms will break their bones.
Scoliosis and PVR: Elevated Pulmonary vascular resistance from chronic hypoxia causes Pulmonary HTN and Right ventricular hypertrophy.
What does scoliosis do to lung numbers? Reduced lung volumes and chest wall compliance. PaO2 is reduced as a result of V/Q mismatch and increased PaCO2 signals severe disease.
Down Syndrome is an extra what? Chromosome 21.
Down and catecholamines? Decreased stores.
Obesity is an independent risk factor for: DVT.
Obesity is associated with pseudotumor cerebri, which is what? Benign intracranial hypertension.
What is maturity onset diabetes of youth? Inherited form of NIDDM.
What's the most common childhood abdominal malignancy? Wilm's tumor.
What is WAGR syndrome? Airidia, genital anomalies, mental retardation, 30% chance of developing Wilm's tumor.
What causes prune belly syndrome? It is caused by agenesis of the abdominal musculature, which results in a thin walled, protrudent abdomen.
Anesthetic implications for prune belly? -Mult pulm complications with inability to cough effectively -High risk of asp -Controlled ventilation is necessary to prevent hypoventilation & hypoxemia -Skeletal muscle relaxants are not needed -Avoid overhydration -Postop pulm complications
Phenylketonuria (PKU) is: Disorder of amino acid metabolism.
PKU patients have: -Most significant consequence is mental retardation -At least ¼ of the patients have seizures -Eczema is common -Increased incidence of pyloric stenosis
PKU patients and drugs: Very sensitive to narcotics and CNS depressants
Sickle cell results from: Hemoglobin S results from the substitution of a valine molecule for a glutamate in position 6 of the beta chain.
What happens with hemaglobin S cells? Altered hemoglobin readily forms polymers when deoxygenated producing the pathognomonic sickled RBC’s.
Genetic cause of sickle cell: SCD – autosomal recessive sickling gene.
Full sickle cell patients have 90% HgbS and 10%: HgbF.
People with sickle cell trait have up to how much HgbS? 45%.
Infants under how many months will have false positive for sickle cell test? 6 months.
What organ disorders in hemophilia? Splenomegaly Abnormal liver function Joint disease related to hemarthrosis
Adequate clotting usually occurs with what percentage of clotting factors? 30%
In patients with hemophilia and moderate bleeding, we should raise their clotting factors to what? 40%
What do you give to Von Willebrand patients? Factor 8 or DDAVP.
Intracellular C is primarily controlled by: The sarcoplasmic reticulum and more specifically the ryanodine receptor.
MH is triggered by: ALL the agents (except N2O) and sux.
MH specific signs: Muscle Rigidity Increased CO2 Production Rhabdomyolysis Marked Temperature Elevation
MH nonspecific signs: Tachycardia Tachypnea Acidosis (Resp/Metabolic) Hyperkalemia
What drugs for MH crisis? Treat hyperkalemia (bicarbonate 1-2 mg/kg PRN) Give dantrolene 2.5mg/kg push. Repeat PRN
CHD: Obstructive lesions: Obstruction to blood flow is present. Obstruction may be intracardiac e.g. pulmonary or aortic stenosis or may be extracardiac e.g. Coarctation of the aorta.
What happens with increased pulm blood flow? L to R shunting occurs (no cyanosis).
Typical L to R shunting patient and conditions? These patients usually present with failure to thrive, pulmonary hypertension, recurrent chest infections or congestive cardiac failure(CCF). Examples include ASD, VSD or PDA.
Decreased pulm blood flow: Right to left shunting occurs with some type of obstruction to normal pulmonary blood flow.
Presentation/examples of R to L shunting: This results in cyanosis, polycythemia, and systemic emboli. Examples include tetralogy of Fallot, tricuspid atresia, and pulmonary atresia.
Shunting and inhalational induction: R to L = DELAY uptake into blood occurs more slowly L to R = minimal to no effect
Shunting and IV induction: R to L = response is faster L to R = minimal effect if systemic perfusion is preserved
4 things in tet. of fallot: VSD Pulm stenosis Overriding aorta RVH
Created by: Chelsea Cantilli Chelsea Cantilli