Exam 2- Endocrine, Gi, GU, Cardiac Flashcards
(187 cards)
1
Q
precocious puberty
A
manifestation of sexual development before 9 in girls and before 8 in boys; resulting from hypothalamic pituitary gonadal axis being activated early; monitor for growth; refer to endocrinologist; 50% of cases stop or regress without treatment
2
Q
physiology of precocious pubery in boys
A
activation of hypothalamic pituitary gonadal axis causes interstitial cell stimulating hormone leydig cells of testes to secrete testosterone
3
Q
physiology of precocious puberty in girls
A
hypothalamic pituitary gonadal axis activation causes follicle stimulating hormone (FSH) and luteneizing hormone (LH) to stimulate ovarian follicles to secrete estrogens
4
Q
why refer to endocrinologist for precocious puberty
A
MRI to assess for brain tumor
5
Q
treatment of precocious puberty
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IM inections that decrease stimulation of LH and FSH
6
Q
nursing considerations/teaching for precocious puberty
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provide anticipatory guidance, support, and education about fertility and medications; fertility begins earlier; sexual interest does not necessarily begin earlier due to being chronological; birth control not advised as it cans stunt growth
7
Q
central precocious puberty
A
more commonly affects girls; 95% of cases have no cause; 75% of cases in boys have underlying CNS defect/structural abnormality
8
Q
peripheral precocious puberty
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clinical findings of puberty appear sooner; premature thelarche (breast development), premature pubarche (pubic hair), premature menarche
9
Q
diabetes insipidus
A
central or neurogenic result from under secretion of ADH principally caused by hypofunction of posterior pituitary; leads to large volumes of dilute urine; need to rule out intracranial lesion; dehydration is not issue in older adult/children who can keep up with drinking
10
Q
treatment of diabetes insipidus
A
DDAVP to help create ADH
11
Q
first signs of DI in children
A
irritability that is relieved by water not milk; at risk for electrolyte imbalance, severe dehydration; vomiting, constipation, fiver, sleep issues, failure to thrive, growth problems
12
Q
testing for DI in children
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fluid restriction; normally urine would concentrate and decrease in amount but in DI it is not affected
13
Q
why give DDAVP
A
given BID at bedtime to allow child to sleep through night and in morning for fewer interruptions in school; overmedication results in SIADH
14
Q
causes of DI
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familial (idiopathic) is 20-50% of cases; secondary causes from trauma, tumor, infection, autoimmune, cranial and vascular anomalies
15
Q
cardinal signs of DI
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polyuria and polydipsia
16
Q
SIADH
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results from over secretion of ADH leading to fluid retention and hyponatremia; more common in conditions that disrupt CNS function like infections, tumors, or surgery
17
Q
sodium decreasing below 120mEq/L from SIADH
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manifestations of anorexia, nausea, vomiting, stomach cramps, irritability, personality changes; further progression causes neurological changes like seizures and stupor
18
Q
treatment of SIADH
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fluid restriction and sodium supplementation
19
Q
what happens as result of rapid hyponatremia
A
leads to swelling of the brain
20
Q
hypothyroidism in children
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deficiency in secretion of thyroid hormone TH; low T3/T4 and high TSH; most common endocrine problem in children
21
Q
congenital hypothyroidism
A
detected on NBS; if untreatable or undetected then can lead to mental retardation; not associated with intellectual disability or neurological in juvenile d/t brain growth complete
22
Q
treatment of hypothyroidism
A
thyroid replacement hormone (levothyroxine)
23
Q
manifestations of hypothyroidism
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dry skin, puffiness around eyes, sparse hair, constipation, sleepiness, lethargy, mental decline, growth failure, delayed puberty, excessive weight gain
24
Q
hyperthyroidism in children
A
excessive secretion of thyroid hormone (TH); Low TSH and high T3/T4; commonly caused by graves disease; peak incidence 12-14; females more affected than men; onset to diagnosis ~ 6 months
25
treatment of hyperthyroidism
antithyroid drugs, subtotal thyroidectomy, ablation with radioiodine; controversial in kids; symptoms often interfere with daily life until under control
26
manifestations of hyperthyroidism
irritability, hyperactivity, short attention span, tremors, insomnia, emotional lability, gradual weight loss with voracious appetite, exophthalmos
27
acute adrenal insufficiency
aka adrenal crisis; destruction or dysfunction of adrenal glands; failure to increase hormones during stress; congenital adrenal hyperplasia and addisons disease
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symptoms of acute adrenal insufficiency
earl- increased irritability, headache, diffuse abdominal pain, weakness, nausea/vomiting, diarrhea, low Na, high K; worsening- fever, CNS involvement like nuchal rigidity, convulsions, stupor, coma, shock
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newborn symptoms of acute adrenal insufficiency
extremely high temps, tachypnea, cyanosis, seizures
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shock symptoms in acute adrenal insufficiency
rapid pulse, decreased BP, shallow respirations, cold clammy skin, cyanosis
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causes of acute adrenal insufficiency
hemorrhage into gland from trauma from prolonged difficult labor, rapidly progressing infections (meningitis)
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waterhouse friderichsen
hemorrhage and necrosis of adrenal gland
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nursing care of acute adrenal insufficiency
early recognition is key; admin steroids, IV rescus for hypovolemia and dehydration, dextrose for hypoglycemia, antibx for infection, seizure precautions, whole blood transfusion if hemorrhage is bad, vasoconstrictors, VS frequently
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diagnosing acute adrenal insufficiency
no rapid definitive test but made based on clinical presentation
35
type I diabetes
complete destruction of pancreatic beta cells that produce insulin leading to total insulin deficiency; 5-8% of all diabetics; age of onset usually under 20yrs; affects males more than females
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clinical manifestations of type I diabetes
polyphagia, polyuria, polydipsia, weight loss, enuresis/nocturia, irritability, shortened attention span, lowered frustration tolerance, dry skin, fatigue, blurry vision, flushed skin, headache, frequent infections, hyperglycemia
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signs of hyperglycemia
hot and dry sugar too high; excessive hunger, excessive thirst, weakness or fatigue, frequent urination, blurry vision, dry skin, sores not healing properly, nausea, sleepiness after eating
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signs of hypoglycemia
hunger, shaking or tremors, sweating, dizziness, fast heartrate, anxiety, blurred vision, weakness/fatigue, headache, irritability
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diagnosing type I diabetes
8 hr fasting glucose >/= 125mg/dL or random BGL of 200mg/dL with classic signs of DM or oral glucose tolerance test (OGTT) of 200mg/dL or more in 2 hour sample or hemoglobin A1C of 6.5% or more
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management of type I diabetes
maintain near-normal levels of glucose while avoiding hypoglycemia; replacement of insulin, nutritional needs
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types of insulin
rapid acting- novolog, onset 15 min, peak 60-90 min; short acting- novolin R, onset 30 min, peak 2-4 hours; intermediate- novolin N, onset 2-4 hrs, peak 4-14 hrs; long acting- lantus, onset 6-14 hrs, no true peak but lasts 22-24 hrs; can be given via injections or via insulin pump
42
nutritional management of type I diabetes
balance of carbs, fats, protein; extra food during exercise; timing to prevent hypoglycemia; avoid high sugar high carb to prevent hyperglycemia; increase insulin when eating and decrease during exercise
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DKA
insulin absent causing unavailable glucose to cells leading to breakdown of fat into fatty acids that liver converts to ketone bodies; causes acidosis (fall in plasma pH); ketonuria and acetone breath (elmin. by lungs); risk for electrolyte imbalances; can lead to coma, death, seizures, cardiac abnormalities if not corrected with insulin
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clinical manifestations of DKA
thirst, frequent urination, nausea, abdominal pain, weakness, fruity scented breath, confusion
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management of DKA
rapid assessment, adequate insulin, fluids to avoid dehydration, electrolyte replacement (potassium)
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nursing care of DKA
IV access for fluids, insulin drip, and electrolyte; supportive care; O2 if arterial < 80; NG if unconscious to prevent asp.; foley to monitor urine output; antibiotics if septic; cardiac monitoring due to electrolyte imbalances
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kids manifestation of DKA
dehydration (need rehydration via IV); obtain urine ketones and blood glucose prior to insulin
48
insulin during DKA
continuous regular IV insulin given at dosage of 0.1U/kg/hr; want to decrease BG by 50 - 100 mg/dL/hr; once below 250-300 mg/dL then dextrose is added to fluid and goal is to maintain level of 120-240 mg/dL with 5 or 10% added dextrose
49
sodium bicarbonate use during DKA
used conservatively like pH < 7.0, severe hyperkalemia, or cardiac instability; causes increased risk for cerebral edema
50
Urinary Tract Infections
common but can pose serious problems in children; bacteria spreads up the urethra; more common in females d/t short urethra; more common in uncircumsized men <3 mo; spike around toilet training times due to dysfunctional voiding; sexually active females have increased incidence
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most common cause of UTI
E. coli from the GI tract
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symptoms of UTI in children > 2 yrs
dysuria, enuresis, day tie incontinence in toilet trained individuals, fever, increased frequency and urgency, foul smell, hematuria and vomiting can be present
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symptoms of UTI in older children or adolescents
cystitis: frequency, painful urination, hematuria without fever; pyelonephritis: fever, chills, flank pain in addition to lower urinary tract symptoms
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cystitis
inflammation or infection of the bladder (lower urinary tract); if suspected tha obtai UA and Ucx
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pyelonephritis
infection or inflammation of upper urinary tract like the ureters and kidneys that is associated with high grade fever; likely to have high fever, chills, flank pain, severe abdominal pain, leukocytosis; can result in scarring and decreased renal function
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WNL findings of urine analysis
yellow, clear/transparent, specific gravity of 1.01-1.030, pH 4.5-8.0
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obtaining a urine culture is...
sterile procedure that may require straight cath if child is unable to keep sterile
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renal labs
Blood urea nitrogen (BUN)- newborn is 4-18, child is 5-18; creatinine infant is 0.2-0.4, child is 0.3-0.7, adolescent is 0.5-1.0; uric acid child is 2.0-5.5
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Nursing management of UTI
antibiotics PO if lower tract infection but IV likely for pyelonephritis; watch for allergic reaction; educate importance of antibiotic adherence; renal bladder ultrasound may be used to assess anatomy; referral to urologist if frequently developing UTI and they are hard to treat
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nursing considerations for UTI prevention
educate on s/s of UTI in children; encourage toilet good toilet habits; frequent voiding; encourage emptying bladder completely by double voiding; fluid intake to avoid urinary stasis and constipation; avoid caffeinated/carbonated beverages; wipe from front to back; encourage void after intercourse; cotton underwear
61
vesicoureteral reflux (VUR)
primary results from congenital anomaly at ureterovesical junction where the antireflux mechanism does not work; secondary results from high pressure in bladder; increased risk for developing pyelonephritis; diagnosed with radionuclide cystogram (RNC) and voiding cystourethrogram (VCUG)
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treatment of VUR
if known VUR then should be catheterized or able to obtain clean void, antibiotics like bactrim or trimethoprim but amoxicillin if under 2 mo, monitor children; surgical treatment with ureteral reimplant, cystoscopy for bulking agent
63
testicular torsion
abnormal twisting of the spermatic cord and associated blood vessels that decreased blood supply to affected testicle and causes necrosis
64
symptoms of testicular torsion
sudden sevree scrotal and lower abdominal pain on affected side, erythema or discoloration of scrotum, one testicle sits higher, waxing and waning pain, lack of blood flow on US; need to be taken to OR within 6-8 hours
65
phimosis
when foreskin cannot be retracted over the glans penis; physiological- due to normal adhesions of foreskin to glans; common in male children up to 3 yrs; does not require surgical correction; god hygiene; pathological- d/t scar tissue formation that prevents retraction; requires correction and potentially circumcision
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cryptorchidism
when one or both testicles fail to descend form the abdomen ino the scrotum; can be retractile- able to be brought back into correct location, undescended- testicle is present but not in scrotum, or absent- due to abnormal development or intrauterine torsion
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orchidoplexy
surgical repair of cryptorchidism if not descended by 1 year; increased risk of cancer in undescended testicles
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hypospadias
abnormal location of the urethral meatus on the underside of the penis; no circumcision immediately if noted because skin used during surgical repair
69
nephrotic syndrome
alterations in the glomerular membrane that allow for proteins (albumin) to pass into urine resulting in decreased serum osmotic pressure; most common presentation of glomerular injury in children; peak incidence is 2-3 years; unknown causea
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characteristics of nephrotic syndrome
proteinuria, hypoalbuminemia, hyperlipidemia, edema, massive urinary protein loss, ascites, hypovolemia, fluid shift from vasculature to interstitial spaces
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nephrotic syndrome clinical manifestations
previously well child begins to gain weight, periorbital edema on waking but resolves throughout day, diarrhea, loss of appetite, generalized edema, poor intestinal absorption, decreased urine volume, frothy urine, pallor, irritability, lethargy, blood pressure is normal or slightly decreased
72
nursing ocnsiderations for nephrotic syndrome
supportive care, strict I/O, VS, daily weights, abdominal girth, monitor for skin breakdown d/t edema, monitor and prevent infection, fluid restriction, sodium restriction, steroids (prednisone), immunosuppressant therapy, diuretics and albumin replacement
73
acute poststreptococcal glomerulonephritis (APSG)
number of diseases that involve common features of oliguria (low UOP), edema, HTN, circulatory congestion, hematuria, and proteinuria; antibody-antigen disease that results from certain group a beta-hemolytic streptococcal infections; onset 1-2 weeks following strep infection of throat and 3-6 weeks after infection of skin
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APSG patho
strep infection occurs and is followed by release of membrane like material from strep organism into circulation; immune complex forms and gets trapped in kidney causing swelling and inflammation; decreases plasma filtration and increases sodium retention
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signs and symptoms of APSG
generalized edema, periorbital edema then lower extrem edema then ascites, HTN, oliguria, hematuria (tea/cola colored), smokey urine, proteinuria (mild to moderate on UA), irritability, fatigue, lethargy, anorexia
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severe complications of APSG from hypervolemia
hypertensive encephalopathy, cardiac failure, AKI
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treatment of APSG
supportive care, manage edema and HTN, daily weights, I/O, monitor vitals, monitor neuro status, educate proper nutritional intake, small frequent meals, low sodium, promote rest, monitor for skin breakdown, admin antibx if prescribed and evidence of strep
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acute kidney injury (AKI)
kidneys are suddenly unable to appropriately regulate volume and composition of urine; decreased or no urine output; electrolyte imbalances; 3 types are prerenal, intrinsic renal, and postrenal
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prerenal AKI
most common cause in children due to dehydration from vomiting and diarrheai
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intrinsic renal AKI
disease and nephrotic agents that damage internal structures on the kidney; trauma
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postrenal AKI
obstructive uropathy; posterior urethral valves, urethral strictures
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treatment of AKI
treat the underlying cause, fix electrolyte imbalances, often managed medically, may require dialysis
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renal trauma
injury to kidney; peak incidence is 10-20yrs; often non-penetrating falls, dirt bike accidents, bike accidents, MVA; hematuria is common but not indicative of severity; DX via RBUS, CT, labs, urine; may require hospital observation of renal function labs and RBC; nephrectomy if trauma causes loss of kidney function
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chronic kidney disease
irreversible functioning of the kidneys; diseased kidneys can no longer maintain normal chemical structure of fluids under normal conditions; treat with dialysis or transplant; most common cause before age of 5 are congenital renal and urinary tract malformations and VUR
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other causes of CKD
HTN, diabetes, lupus, sickle cell, polycystic kidney disease, nephrotoxins
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CKD stages
stage 1- kidney damage with normal or increased GFR > 90; stage 2- kidney damage with mild decreased GFR 60-89; stage 3- moderate decreased GFR 30-59; stage 4- severe increased GFR 15-29; stage 5- severe kidney failure GFR <15
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manifestations of GFR
oliguria or anuria; fatigues, malaise, headache, decreased mental status; HTN, edema, chronic anemia, pallor; deep resp from metabolic acidosis; poor appetite, N/V; short stature, FX with minimal trauma, rickets; low weight, delayed sexual maturation; anxiety, impaired social interaction, poor self esteem; CHF
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types of dialysis
hemodialysis- blood circulated outside of body through artificial cellophane membranes that permit similar passage of water and solutes; hemofiltration- blood filtrate circulated outside body by hydrostatic pressure exerted across semipermeable membrane and replaced by electrolyte solution; peritoneal dialysis- abdominal cavity acts as semipermeable membrane where water and solutes of small molecular size move via osmosis
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dialysis used for children
hemofiltration; used if child has severe fluid overload and cannot tolerate rapid volume changes associated with hemodialysis; critically ill children
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normal urine output values
newborn is 1-2 mL/kg/hr; pediatric is greater than 1mL/kg/hr; 10kg goal off 10 mL/hr or 240 mL/day
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congenital heart defects/disease (CHD)
anatomic abnormalities present at birth that result in abnormal cardiac function; 1/110 births (25% of which require immediate treatment)
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etiology of CHD
exact cause is unknown; genetic caused by chromosomal abnormalities and syndromes like T21; maternal factors are rubella during pregnancy, alcoholism, >40 yr, insulin dependent diabetes
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types of congenital heart diseases
acyanotic such as increased pulmonary blood flow and obstruction to blood flow from ventricles; cyanotic like decreased pulmonary blood flow and mixed blood flow
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defects with increased pulmonary blood flow
PDA, ASD, VSD, AV canal defect
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patent ductus arteriosus (PDA)
failure of fetal structure to close after birth (2-3 days); prior to birth PDA allows for lungs to be bypassed; allows blood to shunt from aorta to pulmonary artery causing additional blood to be reoxygenated and increases pulmonary vascular congestion and causes right ventricular hypertrophy; treated surgically
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atrial septal defect (ASD)
abnormal opening between the two atria and severity is dependent on size and location; can be asymptomatic
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Ventricular septal defect (VSD)
abnormal opening between right and left ventricles that can vary in size from pinhole to complete loss of septum; loud harsh murmur; may close spontaneously by age 3 and surgery may be indicated
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AV canal defect
after birth the newborns pulmonary vascular resistance is high causing minimal blood shunting through the defect but as resistance falls left to right shunting occurs and the pulmonary blood flow increases; results in moderate to severe HF
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obstructive defects
coarctication of the aorta, aortic stenosis, pulmonary stenosis
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coarctation of aorta
narrowing of the aorta; carinal signs are BP less in legs than arms; treatment involves resection
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aortic stenosis
narrowing of aoritc valve that leads to decreased cardiac output; signs of decreased CO like tachycardia, hypotension, faint pulses, exercise intolerance, chest pain common; risk for endocarditis, coronary insufficiency, and ventricular dysfuntion
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treatment for aortic stenosis
balloon dilation in cath lab is primary; newborns with critical aortic stenosis and small left structures may undergo stage 1 norwood
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pulmonary stenosis
narrowing at entrance to pulmonary artery that causes right ventricular hypertrophy and decreased pulmonary blood flow; can be symptomatic, show cyanosis, show HF; risk for endocarditis; symptoms increase with progressive narrowing
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treatment for pulmonary stenosis
balloon dilation
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defects that cause decreased pulmonary blood flow
tetralogy of fallot and tricuspid atresia
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tetralogy of fallot
4 defects consist of ventricular septal defect, pulmonic stenosis, overriding aorta, and right ventricular hypertrophy
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overriding aorita
aorta arises over both ventricles instead of just the left ventricle
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signa of tetralogy of fallot
cyanosis, clubbing of fingers, delayed growth; squatting or assuming knee-chest position; requires surgical correction
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hyper-cyanotic speels
sudden occurrence of cyanosis caused by agitation; knee-chest position to increase systemic vascular resistance; admin 100% O2; give morphine if needed
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tricuspid atresia
tricuspid valve fails to develop and causes lack of communication from right atrium to right ventricle; commonly associated with pulmonary stenosis and transposition of great vessels; mixing of deoxygenated and oxygenated blood in left side of hear; decreased pulmonary blood flow
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signs and symptoms of tricuspid atresia
cyanosis common in newborn state, older children experience tachycardia and dyspnea, hypoxemia with finger clubbing; newborns started on prostaglandin infusion; staged surgical approach for single ventricle pathology
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mixed defects
transposition of great arteries, truncus arteriosus, hypoplastic left heart syndrome
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transposition of the great arteries
pulmonary artery leaves from eft ventricle and aorta leaves from right ventricle; symptoms vary on size of defect; incompatible with life unless another defect to compensate; treatment is surgical atrial switch operation
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truncus arteriosus (TA)
failure of normal septation and embryonic division of pulmonary artery and aorta that results in single vessel that overrides both ventricles; gives rise directly to pulmonary and systemic circulations; symptoms often moderate to severe HF and cyanosis, poor growth, activity intolerance; surgical repair in 1st month to close VSD so truncus originates from LV and create a pathway from RV
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hypoplastic left heart syndrome
congenital underdevelopmen t of left ventricle; ductus arteriosus and foramen ovale keep blood circulating to body; need prostaglandin to keep open; symptoms are mild HF until closure of PDA; progressive deterioration with cyanosis and cardiac output leading to cardiovascular collapse; surgery/transplant required in first few months
116
endocarditis
infection of inner lining of heart (endocardium) usually involving valves; most commonly caused by streptococcus viridians and staphylococcus aureus; less common in children; increased incidence in children likely due to central lines for treating other illness
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signs of endocarditis
insidious onset; unexplainable low grade fever, malaise, anorexia, HF symptoms, athralgias, weight loss, feeding intolerance, respiratory distress, tachycardia, hypotension
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diagnosing endocarditis
identifying organism via blood culture; treat with appropriate antibx
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rheumatic fever
acute rhematic fever; result of abnormal immune response to group A streptococci infection (usually pharyngitis) in susceptible host; inflammation of connective tissues like joints, skin, brain, heart; cardiac valve damage (mitral most common)
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manifestations of acute rheumatic fever
carditis (50-75% of cases), polyarthritis, chorea, subcutaneous nodules (nontender), erythema marginatum, arthralgias, ESR above 60 mm, CRP above 3 mg/dL, prolonged PR interval
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care of rheumatic fever
prevention, treatment with antibx, anti-inflammatory, HF management, supportive care, prophylaxis
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kawasaki disease (KD)
acute systemic vasculitis in pediatrics with unknown etiology; not spread via person to person; self-limiting and usually resolves 6-8 weeks; often affects <5yrs of age; 20-25% of cases without treatment experiences coronary artery aneurysms; leading cause of acquired heart disease in children in US
123
patho of kawasaki disease
involves small and medium vessels (coronary arteries most susceptible); unresponsive fever to antibx and antipyretics, pancarditis, inflammation travels to vessels from capillaries, venules, arterioles; vessel walls damaged and aneurysms may form; inflammation subsides at 6-8 weeks; vessel walls thicken and scar
124
signs of kawasaki disease
fever for atleast 5 days and 4 of the following: bilateral conjunctivitis without exudate, change in mucous membrane (strawberry tongue, red oral cavity, lip fissures), changes in peripheral extremities (reddening of hands/feet, edema), erythematous rash on trunk or extrem., cervical lymphadenopathy
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subacute KD symptoms
begins when fever ends and goes until resolution; pt appears more comfortable, fever resolves in 12-25 days, peeling finger tips and toes, arthritis may be present in large joints
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convalescent symptoms of KD
signs that disease has mostly resolved, elevated sed rate and c reactive protein still can indicate inflammation, arthritis and coronary complications still a concern, parent report pt back to baseline, convalescence complete when all lab values returned to normal
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diagnosis of kawasaki disease
based on symptoms and ruling out of other medical diseases; ECHO to monitor cardiac status; algorithm
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treatment of kawasaki disease
IV immune globulin (IVIG) - 2g/kg one time and may be given again if fever returns (reduces immune response); salicylate therapy like aspirin to reduce inflammation and block platelet aggregation- initial high does of 80-100 mg/kg/day q6 hrs to control fever; maintenance dose of 3-5 mg/kg/day
129
nursing considerations with kawasaki disease
comfort with cool baths, skin care, fever reduction, mouth care; cardiac assessment for signs of HF; avoid fluid overload; passive ROM if arthritis; discharge teaching on when to come back like signs of fever return and educate on possible MI signs and symptoms
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signs of HF in children
decreased urine output, gallop, tachycardia, respiratory distress
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fluid maintenance requirements
1-10kg: 100mL/kg; 11-20kg: 1000mL + 50mL/kg for each kg > 10kg; > 20kg: 1500 mL + 20 mL/kg for each kg > 20kg
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fluid losses occur in children how...
urinary, fecal, insensible (skin and respiratory)
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4-2-1 rule in children for fluid maintenance
0-10kg: 4 mL/kg/hr; 11-20kg: 40 mL + 2 mL/kg for each kg over 10kg; 21-70kg: 60 mL + 1 mL/kg/hr for each kg over 20kg
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pediatric IVF rates
100-125 mL/hr
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dehydration degree
mild is < 3% loss in older children and < 5% in infants; moderate is 3-6% in older children and 5-10% in infants; severe is > 6% in older children and >10% in infants
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clinical signs of mild dehydration
normal pulse, normal RR, normal BP, normal behavior, slight thirst, normal mucous membrane (mist), tears present, normal anterior fontanelle, exterior jugular vein present when supine, capillary refill > 2 sec (skin), decreased urine
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clinical manifestation of moderate dehydration
slightly increased pulse, slight tachypnea, normal or orthostatic (>10mmHg) BP, irritable, moderate thirst, dry mucous membranes, decreased tears, normal to sunken anterior fontanelle, external jugular vein not visible unless supraclavicular pressure, slowed capillary refill (2-4 sec), oliguria
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clinical manifestation of severe ehydration
very increased pulse, hyperpnea (deep and rapid), orthostatic to shock BP, hyperirritable to lethargic, intense thirst, parched mucous membrane, absent tears and sunken eyes, anterior fontanelle sunken, external jugular vein not visible, very delayed capillary refill (>4sec) with tenting cool skin and acrocyanosis/mottling, oligura or anuria
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management of mild dehydration
oral rehydration over 4-6hrs and accounting for ongoing loss and maintenance fluids; 50 mL/kg PO
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management of moderate dehydration
100 mL/kg fluids PO; if cannot tolerate then consider IV hydration
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management of severe dehydration
isotonic solution 20 mL.kg over 5-20 min and repeat per exam; replace deficits and maintenance needs; return to normal by introducing PO
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acute diarrhea
sudden increase in frequency and change in consistency; common causes are rotavirus, SSYCE (GI bacteria), and cdiff (overgrowth in GI system)
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nurse management of acute diarrhea
oral rehydration and scheduled maintenance of fluids PO; IVF for severe dehydration
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chronic diarrhea
frequently occurring usually over 14 days; common in malabsorption, IBD, food allergies, lactose intolerance; can be psychological
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GER and GERD (gastroesophageal reflux)
GER- transfer of gastric contents into esophagus; GERD- symptom or tissue damage from GER; peaks at 4 months and resolves by 12 months
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signs and symptoms of GER
infants- spitting up, vomiting, crying, stiffening, arching of back, poor weight gain, respiratory issues, feeding refusal; children- heartburn, abdominal pain, chronic cough w/ hoarse voice, dysphagia, asthma, recurrent vomiting
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complications with GER
esophagitis, esophageal stricture, laryngitis, recurrent pneumonia, anemia, barrett esophagus
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management of GER/GERD
pharmacological- H2 receptor antagonists and PPI to reduce HCL (may stim LES tone), PPI 30 min before breakfast (takes several days to work); feeding alteration- thickening of feeding, upright position, frequent burping, avoid overfeeding, position to promote gastric emptying, avoid offending foods, weight loss in some children; surgical- nissen fundoplication (blocks ability to vomit via tying off sphncter)
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preop care of GI surgery
bowel prep, NG tube, NPO, fluids and electrolytes, antibx, monitor vitals, monitor for warning signs
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postop care of GI surgery
bowel sounds and function (passing gas), diet advancement by increasing slowly, incisional care, strict I/O
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hirschsprung disease (aganglionic megacolon)
structural congenital anomaly of GI tract caused by lack of ganglion cells in segments of coon that causes decreased motility and mechanical obstruction; ~80% have short segment disease (affects rectum and distal colon)
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manifestationss of hirschprungs
newborn- fail to pass meconium in 24-48 hrs, refusal to feed, bilious vomiting, distention; infant- fail to thrive, constipation, distention, diarrhea/vomiting, enterocolitis signs; childhood- constipation, ribbon like foul stools, distention, visible peristalsis, palpable fecal mass, undernourished and anemic presentation
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enterocolitis signs and symptoms
explosive watery diarrhea, fever, appears slightly ill
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diagnosing hirschsprungs
fail to pass meconium, barium enema, anorectal manometric exam, confirm with rectal biopsy
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therapeutic management of hirschsprung
often require surgery that depends on extent and location of aganglionic bowel; less extensive is single surgery without colostomy (severe may require colostomy); later in life may require 2 step surgery with temporary ostomy and then pull through procedure
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additional preop/postop for hirschsprung surgery
preop- monitor abdominal growth, monitor for enterocolitis; postop- may need anal dilation to avoid anal strictures, ostomy teaching if present
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appendicitis
most common emergency abdominal surgery i children; inflammation of veniform appendix
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clinical presentation of appendicitis
diagnosed via history and physical, imaging can shown, lower right quadrant abdominal pain; child jump off bed will cause pain; fever, pain around umbilicus and lower right, rebound pain; pain will subside following burst
159
inflammatory bowel diseases
ulcerative colitis- inflammation limited to colon and rectal (distal colon and rectum affected), affects mucosa and submucosa involveing continuous segments of bowel; crohns disease- inflammatory process involving any part of GI tract from mouth to anus but most often is ileum, involves all layers of bowel wall in discontinuous pattern
160
signs and symptoms of ulcerative colitis
rectal bleeding, severe diarrhea, mild to moderat anorexia, moderate weight loss, mild growth retardation, mild rashes, mild to moderate joint pain
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signs and symptoms of crohns disease
moderate to severe diarrhea, pain is common, severe anorexia, severe weight loss, severe growth retardation, common anal and perianal lesion, common fistula and strictures, mild rashes, mild to moderate joint pain
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diagnosing inflammatory bodel diseases
labs like CBC, CRP, ESR, stool samples, endoscopy and colonoscopy to directly visualize and confirm extent, CT and US; UGI with small bowel follow through in crohns
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management of IBD
control inflammatory process and reduce/eliminate symptoms, promote normal growth and lifestyle, treat with meds, nutritional support, and surgery if necessary; TPN if need to rest bowel, high protein high calorie
164
pyloric stenosis
circumferential muscle of pylorus sphincter becomes thickened, elongated, and narrowed (narrowing pyloric canal); non-bilious vomiting 30-60 min following feeding; signs of fussiness and hunger; projectile vomiting as progresses; diagnose via H + P with olive like mass in empty stomach; US and UGI if needed
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treatment of pyloric stenosis
refer to pediatric surgeon for pyloromyotomy
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intussusception
proximal segment of bowel telescopes into more distal segment pulling mesentery with it; mesentery is compressed resulting in lymphatic and venous obstruction causing edema; intestine folds into itself; usually intermittent but can get entrapped and cause ischemia and perforation then bowel death
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clinical presentation of intussusception
sudden onset of severe intermittent abdominal pain that can cause fetal positioning to relieve pain, vomiting, lethargy, red currant jelly tool, palpable sausage shaped abdominal mass, diarrhea, anorexia, weight loss; prolonged causes lethargy, bilious vomiting, shock
168
intussusception care/management
air contrast enema to correct, laparascopic surgery to manually reduce or anastomosis if enema fails; risk f recurrence following surgery is ~ 1%
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intussusception pre op care
NPO, IV hydration, NG for decompression, IV antibx, explain underlying defect
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intussusception post op care
NPO until BS return, monitor I/O, NG to decompress, watch for stool passage
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Esophageal atresia (EA)
congenital defect where esophagus fails to develop as continuous passage to stomach; s/s 3 C's
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tracheoesophageal fistula (TEF)
congenital defect where trachea and esophagus fail to develop into distinct structures; s/s are cyanosis, coughing, choking; treat with surgery
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presentations of EA and TEF
initial problem when feeding, swallowing then coughing and gagging, may become cyanotic, difficulty in breathing; 3 C's- coughing, choking, cyanosis
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management of EA and TEF
maintain airway, prevent pneumonia, gastic or puch deompression, supportive theraoy, surgery
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preop and postop EA TEF care
preop- supine with HOB elevated, NPO (may have GT place), IVF, oral suctioning; Postop- NG to suction (cautiously), peripheral nutrition until enteral feedings (GT) supported, pain management, oral feeding trials, observe for complications like pneumonia aspiration or leaks (stridor and croup as well)
176
Necrotizing enterocolitis (NEC)
acute inflammatory disease of bowel causing great damage to mucosal cells lining bowel wall; unknown etiology but typically when GI tract suffers vascular compromise; preterm infant highest risk; antacid use and antibx use during pregnancy can have effect
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bowel damage results from what in NEC
limited perfusion and oxygen to area causing ischemia to occur ad become necrotic; causes gas and food build up that can cause perforation; can lead to septicemia
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signs and symptoms of NEC
distended abdomen, blood in stool, fever, lethargy, refusing feeds, colicky
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if NEC is suspected
stop enteral feeds immediately, notify provider, measure abdominal girth, auscultate prior to feeding, assess for distention, record bowel movements, keep O2 sats acceptable, stress and hypoxemia takes away blood flow from bowel heart and brain
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treatment of NEC
NPO, IV antibx, gastic decompression via NG, manage systemic infection; surgical management if progresses or concern for perforation; resection and anastomosis; extensive surgery includes ileostomy, jejunostomy, colostomy
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cleft lip
incomplete fusion of the oral cavity during intrauterine life; often due to genetic or environmental factors like teratogen exposure (alcohol, cigarettes, anticonvulsants, steroids, retinoids) and folate deficiency; difficulty with sucking and eating; choking or coming out of nose
182
cleft palate
results from incomplete fusion of palates during intrauterine life; often due to genetic or environmental factors like teratogen exposure (alcohol, cigarettes, anticonvulsants, steroids, retinoids) and folate deficiency; difficulties with eating and sucking; choking or coming out of nose
183
cleft lip (CL) and cleft palate (CP) management
speech, ORL, dental combo team; surgical intervention done early; Cl repair 2-3 months; CP repair before 12 months because want done before beginning to speak
184
difficulties with CL and CP
ability to suck is impaired, may need special feeding devices, tend to suck more air, feeding issues preop can lead to growth issues
185
cleft lip and cleft palate perop and postop care
preop- baseline weight, encourage parental bonding with child, assess feeding abilities and teach techniques; postop- protect post op site, may apply petroleum jelly, may use restraints to avoid infant from touching, pain control, advance feeding as tolerated, consider syringe feeding for 7-10 days; upright positioning, avoid suction, avoid hard foods
186
incarcerated hernia
protrusion of organ/organs through abnormal opening; incarcerated is irreversible and can risk blood flow; detected in utero or at birth
187
signs and symptoms of incarcerated hernia
irritability, tenderness, anorexia, abdominal distention, difficulty defecating
