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Pediatrics > Exam 2- Endocrine, Gi, GU, Cardiac > Flashcards

Exam 2- Endocrine, Gi, GU, Cardiac Flashcards

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

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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

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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

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4
Q

why refer to endocrinologist for precocious puberty

A

MRI to assess for brain tumor

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5
Q

treatment of precocious puberty

A

IM inections that decrease stimulation of LH and FSH

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6
Q

nursing considerations/teaching for precocious puberty

A

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

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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

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8
Q

peripheral precocious puberty

A

clinical findings of puberty appear sooner; premature thelarche (breast development), premature pubarche (pubic hair), premature menarche

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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

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10
Q

treatment of diabetes insipidus

A

DDAVP to help create ADH

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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

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12
Q

testing for DI in children

A

fluid restriction; normally urine would concentrate and decrease in amount but in DI it is not affected

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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

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14
Q

causes of DI

A

familial (idiopathic) is 20-50% of cases; secondary causes from trauma, tumor, infection, autoimmune, cranial and vascular anomalies

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15
Q

cardinal signs of DI

A

polyuria and polydipsia

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16
Q

SIADH

A

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

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17
Q

sodium decreasing below 120mEq/L from SIADH

A

manifestations of anorexia, nausea, vomiting, stomach cramps, irritability, personality changes; further progression causes neurological changes like seizures and stupor

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18
Q

treatment of SIADH

A

fluid restriction and sodium supplementation

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19
Q

what happens as result of rapid hyponatremia

A

leads to swelling of the brain

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20
Q

hypothyroidism in children

A

deficiency in secretion of thyroid hormone TH; low T3/T4 and high TSH; most common endocrine problem in children

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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

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22
Q

treatment of hypothyroidism

A

thyroid replacement hormone (levothyroxine)

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23
Q

manifestations of hypothyroidism

A

dry skin, puffiness around eyes, sparse hair, constipation, sleepiness, lethargy, mental decline, growth failure, delayed puberty, excessive weight gain

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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

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25
Q

treatment of hyperthyroidism

A

antithyroid drugs, subtotal thyroidectomy, ablation with radioiodine; controversial in kids; symptoms often interfere with daily life until under control

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26
Q

manifestations of hyperthyroidism

A

irritability, hyperactivity, short attention span, tremors, insomnia, emotional lability, gradual weight loss with voracious appetite, exophthalmos

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27
Q

acute adrenal insufficiency

A

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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28
Q

symptoms of acute adrenal insufficiency

A

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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29
Q

newborn symptoms of acute adrenal insufficiency

A

extremely high temps, tachypnea, cyanosis, seizures

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30
Q

shock symptoms in acute adrenal insufficiency

A

rapid pulse, decreased BP, shallow respirations, cold clammy skin, cyanosis

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31
Q

causes of acute adrenal insufficiency

A

hemorrhage into gland from trauma from prolonged difficult labor, rapidly progressing infections (meningitis)

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32
Q

waterhouse friderichsen

A

hemorrhage and necrosis of adrenal gland

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33
Q

nursing care of acute adrenal insufficiency

A

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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34
Q

diagnosing acute adrenal insufficiency

A

no rapid definitive test but made based on clinical presentation

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35
Q

type I diabetes

A

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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36
Q

clinical manifestations of type I diabetes

A

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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37
Q

signs of hyperglycemia

A

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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38
Q

signs of hypoglycemia

A

hunger, shaking or tremors, sweating, dizziness, fast heartrate, anxiety, blurred vision, weakness/fatigue, headache, irritability

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39
Q

diagnosing type I diabetes

A

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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40
Q

management of type I diabetes

A

maintain near-normal levels of glucose while avoiding hypoglycemia; replacement of insulin, nutritional needs

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41
Q

types of insulin

A

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

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42
Q

nutritional management of type I diabetes

A

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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43
Q

DKA

A

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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44
Q

clinical manifestations of DKA

A

thirst, frequent urination, nausea, abdominal pain, weakness, fruity scented breath, confusion

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45
Q

management of DKA

A

rapid assessment, adequate insulin, fluids to avoid dehydration, electrolyte replacement (potassium)

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46
Q

nursing care of DKA

A

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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47
Q

kids manifestation of DKA

A

dehydration (need rehydration via IV); obtain urine ketones and blood glucose prior to insulin

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48
Q

insulin during DKA

A

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

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49
Q

sodium bicarbonate use during DKA

A

used conservatively like pH < 7.0, severe hyperkalemia, or cardiac instability; causes increased risk for cerebral edema

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50
Q

Urinary Tract Infections

A

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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51
Q

most common cause of UTI

A

E. coli from the GI tract

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52
Q

symptoms of UTI in children > 2 yrs

A

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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53
Q

symptoms of UTI in older children or adolescents

A

cystitis: frequency, painful urination, hematuria without fever; pyelonephritis: fever, chills, flank pain in addition to lower urinary tract symptoms

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54
Q

cystitis

A

inflammation or infection of the bladder (lower urinary tract); if suspected tha obtai UA and Ucx

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55
Q

pyelonephritis

A

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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56
Q

WNL findings of urine analysis

A

yellow, clear/transparent, specific gravity of 1.01-1.030, pH 4.5-8.0

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57
Q

obtaining a urine culture is…

A

sterile procedure that may require straight cath if child is unable to keep sterile

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58
Q

renal labs

A

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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59
Q

Nursing management of UTI

A

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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60
Q

nursing considerations for UTI prevention

A

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

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61
Q

vesicoureteral reflux (VUR)

A

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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62
Q

treatment of VUR

A

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

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63
Q

testicular torsion

A

abnormal twisting of the spermatic cord and associated blood vessels that decreased blood supply to affected testicle and causes necrosis

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64
Q

symptoms of testicular torsion

A

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

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65
Q

phimosis

A

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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66
Q

cryptorchidism

A

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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67
Q

orchidoplexy

A

surgical repair of cryptorchidism if not descended by 1 year; increased risk of cancer in undescended testicles

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68
Q

hypospadias

A

abnormal location of the urethral meatus on the underside of the penis; no circumcision immediately if noted because skin used during surgical repair

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69
Q

nephrotic syndrome

A

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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70
Q

characteristics of nephrotic syndrome

A

proteinuria, hypoalbuminemia, hyperlipidemia, edema, massive urinary protein loss, ascites, hypovolemia, fluid shift from vasculature to interstitial spaces

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71
Q

nephrotic syndrome clinical manifestations

A

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

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72
Q

nursing ocnsiderations for nephrotic syndrome

A

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

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73
Q

acute poststreptococcal glomerulonephritis (APSG)

A

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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74
Q

APSG patho

A

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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75
Q

signs and symptoms of APSG

A

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

76
Q

severe complications of APSG from hypervolemia

A

hypertensive encephalopathy, cardiac failure, AKI

77
Q

treatment of APSG

A

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

78
Q

acute kidney injury (AKI)

A

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

79
Q

prerenal AKI

A

most common cause in children due to dehydration from vomiting and diarrheai

80
Q

intrinsic renal AKI

A

disease and nephrotic agents that damage internal structures on the kidney; trauma

81
Q

postrenal AKI

A

obstructive uropathy; posterior urethral valves, urethral strictures

82
Q

treatment of AKI

A

treat the underlying cause, fix electrolyte imbalances, often managed medically, may require dialysis

83
Q

renal trauma

A

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

84
Q

chronic kidney disease

A

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

85
Q

other causes of CKD

A

HTN, diabetes, lupus, sickle cell, polycystic kidney disease, nephrotoxins

86
Q

CKD stages

A

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

87
Q

manifestations of GFR

A

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

88
Q

types of dialysis

A

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

89
Q

dialysis used for children

A

hemofiltration; used if child has severe fluid overload and cannot tolerate rapid volume changes associated with hemodialysis; critically ill children

90
Q

normal urine output values

A

newborn is 1-2 mL/kg/hr; pediatric is greater than 1mL/kg/hr; 10kg goal off 10 mL/hr or 240 mL/day

91
Q

congenital heart defects/disease (CHD)

A

anatomic abnormalities present at birth that result in abnormal cardiac function; 1/110 births (25% of which require immediate treatment)

92
Q

etiology of CHD

A

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

93
Q

types of congenital heart diseases

A

acyanotic such as increased pulmonary blood flow and obstruction to blood flow from ventricles; cyanotic like decreased pulmonary blood flow and mixed blood flow

94
Q

defects with increased pulmonary blood flow

A

PDA, ASD, VSD, AV canal defect

95
Q

patent ductus arteriosus (PDA)

A

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

96
Q

atrial septal defect (ASD)

A

abnormal opening between the two atria and severity is dependent on size and location; can be asymptomatic

97
Q

Ventricular septal defect (VSD)

A

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

98
Q

AV canal defect

A

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

99
Q

obstructive defects

A

coarctication of the aorta, aortic stenosis, pulmonary stenosis

100
Q

coarctation of aorta

A

narrowing of the aorta; carinal signs are BP less in legs than arms; treatment involves resection

101
Q

aortic stenosis

A

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

102
Q

treatment for aortic stenosis

A

balloon dilation in cath lab is primary; newborns with critical aortic stenosis and small left structures may undergo stage 1 norwood

103
Q

pulmonary stenosis

A

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

104
Q

treatment for pulmonary stenosis

A

balloon dilation

105
Q

defects that cause decreased pulmonary blood flow

A

tetralogy of fallot and tricuspid atresia

106
Q

tetralogy of fallot

A

4 defects consist of ventricular septal defect, pulmonic stenosis, overriding aorta, and right ventricular hypertrophy

107
Q

overriding aorita

A

aorta arises over both ventricles instead of just the left ventricle

108
Q

signa of tetralogy of fallot

A

cyanosis, clubbing of fingers, delayed growth; squatting or assuming knee-chest position; requires surgical correction

109
Q

hyper-cyanotic speels

A

sudden occurrence of cyanosis caused by agitation; knee-chest position to increase systemic vascular resistance; admin 100% O2; give morphine if needed

110
Q

tricuspid atresia

A

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

111
Q

signs and symptoms of tricuspid atresia

A

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

112
Q

mixed defects

A

transposition of great arteries, truncus arteriosus, hypoplastic left heart syndrome

113
Q

transposition of the great arteries

A

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

114
Q

truncus arteriosus (TA)

A

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

115
Q

hypoplastic left heart syndrome

A

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
Q

endocarditis

A

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

117
Q

signs of endocarditis

A

insidious onset; unexplainable low grade fever, malaise, anorexia, HF symptoms, athralgias, weight loss, feeding intolerance, respiratory distress, tachycardia, hypotension

118
Q

diagnosing endocarditis

A

identifying organism via blood culture; treat with appropriate antibx

119
Q

rheumatic fever

A

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)

120
Q

manifestations of acute rheumatic fever

A

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

121
Q

care of rheumatic fever

A

prevention, treatment with antibx, anti-inflammatory, HF management, supportive care, prophylaxis

122
Q

kawasaki disease (KD)

A

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
Q

patho of kawasaki disease

A

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
Q

signs of kawasaki disease

A

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

125
Q

subacute KD symptoms

A

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

126
Q

convalescent symptoms of KD

A

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

127
Q

diagnosis of kawasaki disease

A

based on symptoms and ruling out of other medical diseases; ECHO to monitor cardiac status; algorithm

128
Q

treatment of kawasaki disease

A

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
Q

nursing considerations with kawasaki disease

A

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

130
Q

signs of HF in children

A

decreased urine output, gallop, tachycardia, respiratory distress

131
Q

fluid maintenance requirements

A

1-10kg: 100mL/kg; 11-20kg: 1000mL + 50mL/kg for each kg > 10kg; > 20kg: 1500 mL + 20 mL/kg for each kg > 20kg

132
Q

fluid losses occur in children how…

A

urinary, fecal, insensible (skin and respiratory)

133
Q

4-2-1 rule in children for fluid maintenance

A

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

134
Q

pediatric IVF rates

A

100-125 mL/hr

135
Q

dehydration degree

A

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

136
Q

clinical signs of mild dehydration

A

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

137
Q

clinical manifestation of moderate dehydration

A

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

138
Q

clinical manifestation of severe ehydration

A

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

139
Q

management of mild dehydration

A

oral rehydration over 4-6hrs and accounting for ongoing loss and maintenance fluids; 50 mL/kg PO

140
Q

management of moderate dehydration

A

100 mL/kg fluids PO; if cannot tolerate then consider IV hydration

141
Q

management of severe dehydration

A

isotonic solution 20 mL.kg over 5-20 min and repeat per exam; replace deficits and maintenance needs; return to normal by introducing PO

142
Q

acute diarrhea

A

sudden increase in frequency and change in consistency; common causes are rotavirus, SSYCE (GI bacteria), and cdiff (overgrowth in GI system)

143
Q

nurse management of acute diarrhea

A

oral rehydration and scheduled maintenance of fluids PO; IVF for severe dehydration

144
Q

chronic diarrhea

A

frequently occurring usually over 14 days; common in malabsorption, IBD, food allergies, lactose intolerance; can be psychological

145
Q

GER and GERD (gastroesophageal reflux)

A

GER- transfer of gastric contents into esophagus; GERD- symptom or tissue damage from GER; peaks at 4 months and resolves by 12 months

146
Q

signs and symptoms of GER

A

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

147
Q

complications with GER

A

esophagitis, esophageal stricture, laryngitis, recurrent pneumonia, anemia, barrett esophagus

148
Q

management of GER/GERD

A

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)

149
Q

preop care of GI surgery

A

bowel prep, NG tube, NPO, fluids and electrolytes, antibx, monitor vitals, monitor for warning signs

150
Q

postop care of GI surgery

A

bowel sounds and function (passing gas), diet advancement by increasing slowly, incisional care, strict I/O

151
Q

hirschsprung disease (aganglionic megacolon)

A

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)

152
Q

manifestationss of hirschprungs

A

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

153
Q

enterocolitis signs and symptoms

A

explosive watery diarrhea, fever, appears slightly ill

154
Q

diagnosing hirschsprungs

A

fail to pass meconium, barium enema, anorectal manometric exam, confirm with rectal biopsy

155
Q

therapeutic management of hirschsprung

A

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

156
Q

additional preop/postop for hirschsprung surgery

A

preop- monitor abdominal growth, monitor for enterocolitis; postop- may need anal dilation to avoid anal strictures, ostomy teaching if present

157
Q

appendicitis

A

most common emergency abdominal surgery i children; inflammation of veniform appendix

158
Q

clinical presentation of appendicitis

A

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
Q

inflammatory bowel diseases

A

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
Q

signs and symptoms of ulcerative colitis

A

rectal bleeding, severe diarrhea, mild to moderat anorexia, moderate weight loss, mild growth retardation, mild rashes, mild to moderate joint pain

161
Q

signs and symptoms of crohns disease

A

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

162
Q

diagnosing inflammatory bodel diseases

A

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

163
Q

management of IBD

A

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
Q

pyloric stenosis

A

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

165
Q

treatment of pyloric stenosis

A

refer to pediatric surgeon for pyloromyotomy

166
Q

intussusception

A

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

167
Q

clinical presentation of intussusception

A

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
Q

intussusception care/management

A

air contrast enema to correct, laparascopic surgery to manually reduce or anastomosis if enema fails; risk f recurrence following surgery is ~ 1%

169
Q

intussusception pre op care

A

NPO, IV hydration, NG for decompression, IV antibx, explain underlying defect

170
Q

intussusception post op care

A

NPO until BS return, monitor I/O, NG to decompress, watch for stool passage

171
Q

Esophageal atresia (EA)

A

congenital defect where esophagus fails to develop as continuous passage to stomach; s/s 3 C’s

172
Q

tracheoesophageal fistula (TEF)

A

congenital defect where trachea and esophagus fail to develop into distinct structures; s/s are cyanosis, coughing, choking; treat with surgery

173
Q

presentations of EA and TEF

A

initial problem when feeding, swallowing then coughing and gagging, may become cyanotic, difficulty in breathing; 3 C’s- coughing, choking, cyanosis

174
Q

management of EA and TEF

A

maintain airway, prevent pneumonia, gastic or puch deompression, supportive theraoy, surgery

175
Q

preop and postop EA TEF care

A

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
Q

Necrotizing enterocolitis (NEC)

A

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

177
Q

bowel damage results from what in NEC

A

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

178
Q

signs and symptoms of NEC

A

distended abdomen, blood in stool, fever, lethargy, refusing feeds, colicky

179
Q

if NEC is suspected

A

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

180
Q

treatment of NEC

A

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

181
Q

cleft lip

A

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
Q

cleft palate

A

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
Q

cleft lip (CL) and cleft palate (CP) management

A

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
Q

difficulties with CL and CP

A

ability to suck is impaired, may need special feeding devices, tend to suck more air, feeding issues preop can lead to growth issues

185
Q

cleft lip and cleft palate perop and postop care

A

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
Q

incarcerated hernia

A

protrusion of organ/organs through abnormal opening; incarcerated is irreversible and can risk blood flow; detected in utero or at birth

187
Q

signs and symptoms of incarcerated hernia

A

irritability, tenderness, anorexia, abdominal distention, difficulty defecating

Pediatrics (4 decks)

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