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Nursing school level 2 > PEDs Test #2 > Flashcards

PEDs Test #2 Flashcards

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1
Q

skeletal growth is stimulated by

A

pituitary growth hormone

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2
Q

growth of the long boned occurs at the

A

epiphysis

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3
Q

clubfoot deformities

A

can have one or a combination of four: plantar flexion, dorsiflexion, varus deviation, valgus deviation

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4
Q

varus deviation

A

foot turns in

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5
Q

valgus deviation

A

foot turns out

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6
Q

what causes clubfoot

A

bone deformity and malposition with soft tissue contraction

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7
Q

the affected foot ic clubfoot is usually

A

smaller and shorter, with an empty heel pad and transverse plantar crease

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8
Q

management of clubfoot

A

serial manipulation and casting, and if correction not achieved within 3-6 months surgery will be performed

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9
Q

developmental dysplasia of the hip

A

dislocation of the hip - femoral head and acetabulum are improperly aligned

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10
Q

clinical manifestation in an infant with dysplasia of the hip

A

asymmetry of the gluteal folds, short femur, limited range of motion on affected hip

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11
Q

clinical manifestation in a child with dysplasia of the hip

A

same as manifestations of infant plus positive trendelenburg gait

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12
Q

trendelenburg gait

A

abnormal tilting of pelvis on unaffected side when bearing weight on the affected side

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13
Q

diagnostics for dysplasia of the hip

A

screening at birth with ortolans’s and Barlow’s maneuvers, ultrasound, radiography

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14
Q

most important management of dysplasia of hip

A

early intervention

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15
Q

management for dysplasia of hip for newborns

A

pavlik harness

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16
Q

management for dysplasia of hip at 6-18 months

A

dislocation unrecognized until child begins to stand and walk; use traction and cast immobilization (Spica cast)

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17
Q

management for dysplasia of hip in older child

A

operative reduction, difficult after 4 years

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18
Q

nursing care for pavlik harness

A

teaching parents to keep harness on continuously, follow up appts, teach and reinforce skin care

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19
Q

nursing care for spica cast

A

frequent neurovascular checks, range of motion, skin integrity, evaluate hydration status, assess elimination status daily

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20
Q

bone healing and remodeling in neonatal period

A

2-3 weeks

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21
Q

bone healing and remodeling in early childhood

A

4 weeks

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22
Q

bone healing and remodeling in later childhood

A

6-8 weeks

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23
Q

bone healing and remodeling in adolescence

A

8-12 weeks

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24
Q

osteogenesis imperfecta

A

also known as brittle bone disease

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25
Q

osteogenesis imperfecta results from

A

a defect in the synthesis of collagen

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26
Q

most common type of osteogenesis imperfecta

A

autosomal-dominant inheritance pattern

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27
Q

clinical manifestations of osteogenesis imperfecta

A

osteoporosis, excessive bone fragility, blue sclera, discolored teeth, conductive hearing loss by age 20-30, skin may appear translucent

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28
Q

scoliosis

A

lateral curvature of the spine

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29
Q

muscular dystrophy clinical manifestations

A

waddling gait, lordosis, difficulty climbing stairs, development of gower’s sign, scoliosis of the spine

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30
Q

muscular dystrophy clinical manifestations appear when?

A

after walking is achieved (3-7 years)

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31
Q

muscular dystrophy diagnostics

A

positive family history, elevated serum creatine kinase, electromyography, muscle biopsy

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32
Q

therapeutic management of muscular dystrophy

A

maintenance of ambulation and independence, surgery, bracing, physical therapy

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33
Q

muscular dystrophy nursing considerations

A

Child should be immobilized for as short a period as possible to help prevent disuse atrophy- try to ambulate 3 hours a day
Frequent rest periods in a recumbent position are helpful to help reduce the incidence of scoliosis

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34
Q

muscular dystrophy diet

A

low calorie, high protein, high fiber and high fluid

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35
Q

Duchenne muscular dystrophy

A

most common hereditary neuromuscular disease

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36
Q

Duchenne muscular dystrophy is linked to

A

X linked recessive disorder

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37
Q

Duchenne muscular dystrophy s/s

A

progressive weakness with no loss of sensation

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38
Q

Duchenne muscular dystrophy usually diagnosed

A

3-7 yrs of age

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39
Q

treatment of Duchenne muscular dystrophy

A

aimed to control symptoms and improve quality of life and steroids can slow strength

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40
Q

Duchenne muscular dystrophy death occurs usually by

A

age 25

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41
Q

stroke volume in neonates

A

they cannot increase stoke volume as effectively as older children

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42
Q

heart and great vessels develop during

A

first 3-8 wks gestation

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43
Q

congenital heart disease (CHD)

A

anatomic- abnormal function present at birth

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44
Q

acquires heart disease

A

occurs due to disease process such as infection, autoimmune response, environmental factors, familial tendencies

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45
Q

assessment of cardiovascular dysfunction

A

nutrition status, color, chest deformities, clubbing

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46
Q

diagnostic evaluation of cardiovascular dysfunction

A

electrocardiography, echocardiography, cardiac catheterization, electrophysiology

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47
Q

major cause of death in first year of life after prematurity

A

congenital heart disease

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48
Q

most common anomaly of congenital heart disease

A

ventricular septal defect

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49
Q

survival of congenital heart disease depends on

A

how severe the defect is, when its diagnosed, and how its treated

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50
Q

what is acyanotic heart defect

A

blood is shunted (flows) from the left side of the heart to the right side of the heart due to a structural defect (hole) in the interventricular septum

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51
Q

what is cyanotic heart defect

A

result in a low blood oxygen level

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52
Q

bloods flows

A

from area of high pressure to one of low pressure and takes the path of least resistance

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53
Q

what happens with acyanotic heart defect

A

increase pulmonary blood flow and obstruction of blood flow from ventricles

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54
Q

what happens with cyanotic heart defect

A

decrease pulmonary blood flow and mixed blood flow

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55
Q

ductus arteriosus

A

in utero normally shunts blood from the main pulmonary artery to the descending aorta bypassing the non aerated lungs

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56
Q

normally ductus arteriosus closes

A

functionally within 48 hours and anatomically around 2 weeks

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57
Q

patent ductus arteriosus

A

medical condition in which the ductus arteriosus fails to close after birth: this allows a portion of oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta, which has a higher pressure, to the pulmonary artery.

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58
Q

patent ductus arteriosus manifestations

A

varies from asymptomatic to s/s of CHF and machinery like murmur

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59
Q

patent ductus arteriosus manifestations is dependent on

A

the amount of left to right shunting

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60
Q

what should be administered for patent ductus arteriosus

A

indomethacin

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61
Q

management for patent ductus arteriosus

A

surgical division of ligation of the patent vessel, coils, and indomethacin

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62
Q

ventricular septal defect

A

an opening in the ventricular septum in which blood flows through the defect back into the pulmonary artery

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63
Q

most common form of congestive heart disease

A

ventricular septal defect accounts for 20% of all cases

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64
Q

increased pulmonary resistance in VSD causes

A

RV hypertrophy and if RV cannot accommodate workload than the RA may also enlarge

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65
Q

VSD manifestations

A

s/s of failure to thrive and/or respiration infection with s/s of CHF. holosystolic murmur

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66
Q

VSD s/s based on

A

the size of the defect and amount of pulmonary over circulation

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67
Q

holosystolic murmur heard best at

A

LSB

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68
Q

VSD can ultimately lead to

A

pulmonary hypertension

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69
Q

VSD management

A

complete repair with sutures or patch

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70
Q

coarctation of the aorta

A

narrowing of the aorta typically near the insertion of the ductus arteriosus

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71
Q

coarctation of the aorta results in

A

increased pressure proximal to the defect and decreased pressure distal to the obstruction

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72
Q

coarctation of the aorta manifestations

A

high blood pressure and bounding pulses in the arms and absent femoral pulses with cool lower extremities. some may show signs of CHF

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73
Q

coarctation of the aorta management

A

resection of the coarcted portion with an end to end anastomosis or balloon angioplasty or stents

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74
Q

tetralogy of fallot includes what defects

A

VSD
Pulmonic stenosis: narrowing at the entrance of the pulmonary arteries
Overriding aorta
RV hypertrophy

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75
Q

the degree cyanosis of tetralogy of fallot is directly related to

A

severity of the Pulmonic stenosis

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76
Q

tetralogy of fallot manifestations

A

systolic murmur, tet spells, acutely cyanotic at birth others may have progressive cyanosis as PS worsens

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77
Q

tet spells

A

anoxic spells when O2 requirement exceed blood supply

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78
Q

tetralogy of fallot management

A

complete repair during 1st year of life and blalock trussing shunt

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79
Q

complete repair of tetralogy of fallot

A

closure of the VSD, resection, and patch of PS which requires open thoracotomy/sternotomy and bypass

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80
Q

blalock-taussig shunt

A

provides blood flow to the pulmonary arteries via a tube graft (palliative tetralogy of fallot)

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81
Q

hypoplastic left heart syndrome

A

underdevelopment of the left side of the heart

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82
Q

hypoplastic left heart syndrome manifestations

A

mild cyanosis until PDA closes the rapid progressive deterioration

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83
Q

decreased cardiac output during hypo plastic left heart syndrome leads to

A

cardiovascular collapse

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84
Q

hypo plastic left heart syndrome management

A

transplantation, prostaglandin infusion, multiple stage procedure

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85
Q

prostaglandin infusion

A

helps maintain ductal latency until surgical intervention

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86
Q

heart failure

A

inability of the heart to pump an adequate amount of blood to the systemic circulation

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87
Q

in children heart failure occurs

A

most frequently secondary to structural abnormalities

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88
Q

right sided heart failure

A

RV is unable to pump blood into the pulmonary artery which increases RA pressure =, systemic venous hypertension

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89
Q

left sided heart failure

A

LV is unable to pump blood into the systemic circulation which increase LA pressure and pulmonary venous pressure

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90
Q

management of heart failure

A

improve cardiac function, remove accumulated fluid and sodium, decrease cardiac demands, improve tissue oxygenation

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91
Q

evaluation of heart failure

A

CXR, ECG, and echo

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92
Q

CXR

A

shows for cardiomegaly and increased pulmonary blood flow

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93
Q

ECG shows for

A

ventricular hypertrophy

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94
Q

echo helps

A

determine the cause of heart failure

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95
Q

digoxin toxicity manifests with

A

slow pulse, vomiting, and arrhythmia

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96
Q

what can increase risk of digoxin

A

hypokalemia and hypomagnesemia

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97
Q

what med is effective for heart failure

A

digoxin

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98
Q

bradydysrhythmias can be attributed to

A

hyper vagal tone and response to hypoxia and hypotension from the influence of the autonomic nervous system

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99
Q

meds for CHF

A

diuretics, furosemide, spironolactone (potassium sparing diuretic)

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100
Q

tachydysrhythmia can be from

A

fever, anxiety, pain, anemia, dehydration

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101
Q

supraventricular tachycardia beats per minute

A

HR 200-300+ beats per min

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102
Q

supraventricular tachycardia

A

sudden onset, variable duration, and may end abruptly and convert back to normal without intervention

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103
Q

supraventricular tachycardia s/s

A

poor feeding, extreme irritability, pallor, dizziness, chest pain, palpitations

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104
Q

treatment of supraventricular tachycardia

A

vagal maneuvers, adenosine, synchronized cardioversion, and long term management with digoxin, propranolol, amiodarone, or ablation

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105
Q

adenosine

A

impairs AV conduction

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106
Q

Kawasaki disease

A

acute systemic vasculitis of unknown cause

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107
Q

75% of Kawasaki disease occurs in

A

children with a peak incidence in toddlers

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108
Q

increased incidence of Kawasaki disease in

A

late winter and early spring

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109
Q

treatment of Kawasaki disease

A

acute disease is self limiting

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110
Q

20% of children with Kawasaki disease develop

A

coronary artery dilation or aneurysm without treatment

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111
Q

what is Kawasaki disease

A

extensive inflammation of arterioles, venues, and capillaries

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112
Q

Kawasaki disease manifestation

A

fever for more than 5 days with changes in extremities, bilateral conjunctival injection, changes in oral mucous membranes, polymorphous rash, and cervical lymphadenopathy (must have 4 of the five)

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113
Q

Changes in oral mucous membranes in Kawasaki disease

A

erythema of the lips, oropharyngeal reddening, “strawberry tongue” large exposed papillae

114
Q

changes in extremities with kawasaki disease

A

edema, erythema of palms and soles, periungual desquamation of the hands and feet

115
Q

kawasaki disease management

A

high dose intravenous immunoglobulins (IVIG) and salicylates

116
Q

what do high dose IVIG do

A

reduces the risk of coronary artery abnormalities

117
Q

incubation period

A

the time between exposure to the disease and disease outbreak; during this time the child may be contagious

118
Q

period of communicability

A

the period when the organism can move from the host to another individual

119
Q

prodromal period

A

the time between the initial symptoms and the presence of the full-blown disease

120
Q

symptoms of viral infection

A

rash, fever, and color or flu-like symptoms

121
Q

viral infection transmission

A

direct contact with droplets or airborne particles which can be prevented with immunization

122
Q

complication of viral infection

A

encephalitis

123
Q

firth disease is also called

A

erythema infectiosum

124
Q

fifth disease manifestations

A

maculopapular rash on truck and extremities. fiery red, edematous rash on cheeks “slapped cheek”

125
Q

fifth disease may be passed to

A

the fetus and cause severe anemia or fetal death

126
Q

fifth disease is caused by

A

human parvovirus B-19

127
Q

Group B enterovirus-nonpolio is also called

A

coxsackie virus, hand foot and mouth

128
Q

s/s of coxsackie virus

A

fever, cold symptoms, sore throat, vesicles in mouth palms and feet

129
Q

spreading of coxsackie virus

A

fecal - oral virus through direct contact

130
Q

causative agent of mumps

A

paramyxovirus

131
Q

complications of mumps

A

aseptic meningitis, encephalitis, deafness, orchitis, sterility, glomerulonephritis, myocarditis

132
Q

transmission of mumps

A

oral and nasal secretions

133
Q

mumps treatment

A

isolation for 5 days and supportive care, acetaminophen, bland foods, hydration, ice packs

134
Q

pump patients should not have

A

aspirin due to risk of reye syndrome

135
Q

prevention of mumps

A

MMR vaccine

136
Q

complications of mumps

A

hearing loss, orchitis, oophoritis, arthritis

137
Q

mumps affects the

A

salivary glands

138
Q

s/s mumps

A

swelling of the neck chin area

139
Q

sixth disease is called

A

roseola infantum

140
Q

sixth disease is caused by

A

human herpes virus 6

141
Q

roseola infantum (sixth disease) s/s

A

erythematous maculopapular rash that shows up when fever goes away

142
Q

prodromal stage of of roseola

A

sudden high fever above 103 for 3-7 days

143
Q

German measles =

A

rubella

144
Q

rubella rash

A

pinkish rose maculopapular exanthema that begins on face, neck and spreads downward to include the entire body within 1-3 days

145
Q

most devastating form of rubella

A

congenital rubella

146
Q

congenital rubella can result in

A

mental retardation, cataracts, retinopathy and cardiac anomalies, deafness, miscarriage and fetal death

147
Q

prevention of rubella

A

teach importance of vaccine (MMR) before childbearing years

148
Q

three Cs of measles

A

coryza, cough and conjunctivitis

149
Q

s/s of measles

A

kopek spots and deep red macular rash that begins on face and neck and spreads

150
Q

koplik spots

A

on buccal mucosa appear prior to the rash and lasts for 3 days

151
Q

complications of measles

A

encephalitis, mental retardation, OM, pneumonia, seizures, death

152
Q

measles treatment

A

isolation for 5 days

153
Q

what should you do to the lights with measles

A

dim the lights due to photophobia

154
Q

leading cause of preventable blindness

A

vitamin A deficiencies

155
Q

varicella

A

chx pox

156
Q

zoster

A

shingles

157
Q

infectious period of varicella zoster

A

1-2 days before onset of rash

158
Q

varicella rash stage

A

all stages present at same time: macule, papule, vesicle, and crust

159
Q

zoster rash

A

unilateral, macular/papular and follow dermatome

160
Q

family education for varicella zoster

A

do not give aspirin because of risk of Reyes, child contagious until lesions are crusted over, varicella vaccine, prevent scraping to avoid developing secondary infection

161
Q

zika virus associated with

A

flaviviridae virus which is related to west nile virus

162
Q

strep throat is related to

A

scarlet fever

163
Q

what bacteria is related to strep throat

A

group A beta-hemolytic streptococcus (GAS)

164
Q

scarlet fever

A

strep throat with a rash

165
Q

complications with scarlet fever

A

rheumatic fever and post streptococcal glomerulonephritis

166
Q

manifestations of scarlet fever

A

sandpaper rash and strawberry tongue

167
Q

impetigo is caused by

A

staphylococcus aureus or group A beta hemolytic streptococci or a combination of both

168
Q

impetigo lesions

A

common around nose and mouth

169
Q

impetigo incubation period

A

7-10 days and may spread to other body parts or to other people

170
Q

treatment of impetigo

A

topical antibiotic but if more extensive oral antibiotics needed

171
Q

cellulitis

A

inflammation of the skin and SQ tissue with redness, swelling, and firm infiltration

172
Q

what can be involved with cellulitis

A

regional lymph node involvement is common

173
Q

treatment of cellulitis

A

requires oral or parenteral antibiotics

174
Q

MRSA can be treated with

A

outpatient care

175
Q

MRSA prevention

A

careful hand hygiene after changing bandages

176
Q

diaper dermatitis

A

Candida albicans produces perianal inflammation and maculopapular rash

177
Q

tinea

A

infection caused by dermatophytes

178
Q

dermatophytes

A

a unique group of fungi capable of infecting nonviable keratinized cutaneous structures including stratum corneal, nails, and hair

179
Q

tinea is classified according to

A

the part of the body that it is affecting

180
Q

tinea capitis

A

fungal infection of the scalp from recent exposure to infected person or animals

181
Q

tinea capitis management

A

requires oral anti fungal

182
Q

tinea corporis treatment

A

topical usually effective

183
Q

tinea pedis treatment

A

topical over the counter

184
Q

pediculosis capitus

A

head lice

185
Q

treatment for head lice

A

nix or rid - over the counter

186
Q

scabies

A

mites transmitted by close personal contact with infected person. mite burrows in skin and lays eggs

187
Q

clinical manifestations of scabies

A

intense itching especially at night, in older children lesions often found in webs of fingers, elbows, axillae, groin and waist

188
Q

scabies treatment

A

elimite prescription, antihistamine, antibiotics if infection develops

189
Q

child with scabies my return back to school

A

the day after treatment

190
Q

type 1 hypersensitivity reaction

A

anaphylaxis

191
Q

type 2 hypersensitivity reactions

A

tissue specific reactions - IgG or IgM antibodies

192
Q

type 3 hypersensitivity reaction

A

immune complex reaction such as glomerulonephritis

193
Q

type 4 hypersensitivity reaction

A

delayed reaction that causes inflammation and tissue damage

194
Q

anaphylaxis occurs when

A

allergens binds to IgE on mast cells

195
Q

anaphylaxis in pediatrics

A

due to immaturity of GI tract, large proteins can be absorbed and mistaken from antigen and they can present with flushing skin instead of hives

196
Q

latex has a cross reactivity with

A

kiwi, chestnut, avocado, tomato, potato, and banana

197
Q

decrease in family size and better hygiene may be contributing to

A

an increase in environmental and food allergies in Western Culture

198
Q

when should parents introduce solid foods

A

by 4-6 months parents should look for signs that baby is ready to eat and introduce one food at a time and wait 2-3 days between each food

199
Q

to come up with a plan to treat dehydration what most be determined

A

degree of dehydration, type of dehydration, initial Na levels, HCO3 levels, and electrolyte and acid/base imbalance

200
Q

mild dehydration s/s

A

watery diarrhea, cap refill less than 2 sec, slight increase in thirst, normal urine specific gravity

201
Q

moderate dehydration s/s

A

abnormal skin turgor, 2-4 sec cap refill, thirst, increase in pulse, dry mucous membrane

202
Q

severe dehydration s/s

A

tented skin, sunken fontanel, cap refill greater than 4 sec, extreme thirst, tachycardia, anuria

203
Q

mild dehydration wt loss in infants and children

A

infants - 3-5%

children 3-4%

204
Q

moderate dehydration wt loss in infants and children

A

infants - 6-9%

children - 6-8%

205
Q

severe dehydration wt loss in infants and children

A

10% weight loss in infants and children

206
Q

VS of severe dehydration

A

pulse increase, BP down, RR up

207
Q

children with severe volume depletion should be given

A

isotonic fluid bolus

208
Q

when should you use IV rehydration

A

when child is unable to ingest sufficient amounts of fluid and electrolytes in order to meet ongoing daily loses, replace previous loses, and replace ongoing loses

209
Q

pt who are dehydrated should avoid

A

sports drinks, fruit juices, sodas and gelatin due to high % of sugar which can further aggravate diarrhea

210
Q

leading cause of illness in children younger than 5 years old

A

diarrhea

211
Q

diarrhea can be associated with

A

URI, UTI, antibiotic use and laxative use

212
Q

infectious diarrhea is usually caused by

A

viral - ROTOVIRUS but can be by a variety of bugs

213
Q

two categories of vomiting

A

bilious and nonbilious

214
Q

bilious vomitting implies

A

disorder of motility or distal blockage

215
Q

vomiting treatment

A

usually self limiting unless bilious vomiting or dehydration occurs

216
Q

if vomiting do not use______ unless absolutely necessary

A

antiemetic

217
Q

manifestations of GERD

A

spitting, vomiting, crying, weight loss, cough, choking, apnea

218
Q

GERD management

A

depends on severity but elevating HOB, thickened feeds, and H2 receptor antagonist/PPI can help

219
Q

what surgical intervention can be performed with bad GERD

A

nissen fundoplication

220
Q

Hirschsprung disease

A

congenital aganalionic megacolon - results in mechanical obstruction on the intestine

221
Q

who is more likely to get Hirschsprung disease

A

4x more common in males and follows a familial pattern

222
Q

the absence of what causes Hirschsprung disease

A

absence of ganglion cells results in loss of nervous system stimulation

223
Q

diagnoses of Hirschsprung disease

A

happens in the first few months of life - confirmed with full thickness rectal biopsy with absence of ganglion cells

224
Q

s/s of Hirschsprung disease

A

distended abdomen, feeding intolerance, bilious vomiting, delay in passage of meconium or constipation since birth

225
Q

management of Hirschsprung disease

A

removal of ganglionic portion of bowel and majority require colostomy/mucous fistula

226
Q

most common cause of emergency abd surgery in childhood

A

acute appendicitis

227
Q

peak incidence of acute appendicitis

A

12-18 years of age

228
Q

acute appendicitis occurs more during what time of year

A

fall and winter

229
Q

classic first sign of acute appendicitis

A

pain in periumbilical area followed by nausea, RLQ pain and later vomiting with fever

230
Q

during acute appendicitis most intense pain site

A

McBurneys point

231
Q

not reliable sign of acute appendicitis

A

rebound tenderness and it is extremely painful

232
Q

s/s acute appendicitis

A

fever, abd pain, and leukocytosis

233
Q

management of acute appendicitis

A

IV fluids, antibiotics, NG tube for decompression, surgery

234
Q

what antibiotics for acute appendicitis

A

3rd generation cephalosporin

235
Q

most common cause of intestinal obstruction in children between 3 months and 3 years

A

intussusception

236
Q

what happens with intussusception

A

occurs when a proximal segment of bowel invades into the distal segment

237
Q

as edema builds up from obstruction during intussusception

A

pressure is applied to the arterial system and leads to ischemia

238
Q

sign of intussusception

A

stool that looks like currant jelly

239
Q

most serious type of intestinal obstruction

A

malrotation especially if it goes on to complete volvulus

240
Q

malrotation and volvulus is caused by

A

abnormal rotation of the intestine

241
Q

malrotation and volvulus can cause

A

necrosis, peritonitis, perforation, and death

242
Q

most common congenital deformity in US

A

cleft lip/palate

243
Q

cleft lip results from

A

failure of the maxillary and nasal process to fuse

244
Q

cleft palate results from

A

failure of the two palatal processes to fuse

245
Q

diagnosis of cleft lip/palate

A

20-30% can be diagnosed through prenatal ultrasound and others will be apparent at birth

246
Q

cleft lip and feeding

A

typically have no difficulty feeding

247
Q

surgical correction of cleft lip occurs

A

between 2-3 months

248
Q

surgical correction of cleft palate occurs

A

by 6-12 months

249
Q

cleft palate and feeding

A

have difficulty with all feeding types

250
Q

post op care for cleft lip/palate surgery pt

A

elbow immobilizers for 7-10 days and syringe feeding

251
Q

Hypertrophic Pyloric Stenosis

A

The circumferential muscle of the pyloric sphincter becomes thickened, resulting in a narrowing of the pyloric channel and obstruction

252
Q

Hypertrophic Pyloric Stenosis usually develops within

A

2-5 weeks of life

253
Q

Hypertrophic Pyloric Stenosis causes

A

projectile nonbilious vomiting, dehydration, metabolic alkalosis and failure to thrive

254
Q

Hypertrophic Pyloric Stenosis more common in

A

males, full term infants, and caucasians

255
Q

diagnosis of Hypertrophic Pyloric Stenosis

A

olive like mass that is easily palpated, non bilious vomiting 30-60 min after eating, ultrasound

256
Q

ABG with Hypertrophic Pyloric Stenosis

A

hypochloremic metabolic alkalosis

257
Q

management of Hypertrophic Pyloric Stenosis

A

pyloromyotomy, NGT for decompression, resume feeding 3-6 hrs after surgery

258
Q

pyloromyotomy

A

an operation to loosen the tight muscle causing the blockage between the stomach and small intestine. do this after rehydration and correction of alkalosis

259
Q

primary cause of fatal ingestions in children younger than 5yrs

A

Button or disk batteries

260
Q

who should you call after ingestion/poisoning

A

American Association of Poison Control Centers

1800 222 1222

261
Q

after ingestion of poison what is the most important principle

A

treat the child not the poison

262
Q

enuresis

A

Common troublesome disorder defined as the intentional or involuntary passage of urine into the bed, usually at night

263
Q

enuresis more common in

A

boys

264
Q

highest prevalence of UTI in children occurs in

A

uncircumcised male infants

265
Q

diagnosis for UTI

A

straight Cath, clean catch, urine dipstick, CBC, chem panel

266
Q

vesicoureteral reflux (VUR)

A

Abnormal retrograde flow of urine into ureters likely to be associated with kidney infections

267
Q

s/s of vesicoureteral reflux

A

high fevers, vomiting, and chills

268
Q

most common cause of renal scaring in children

A

vesicoureteral reflux

269
Q

what shows up with nephrotic syndrome

A

increased glomerular permeability to plasma protein, proteinuria, hypoalbuminemia, hyperlipiemmia, and edema

270
Q

nephrotic syndrome predominantly occurs at

A

2-7 years old and greater in males

271
Q

meds for nephrotic syndrome

A

corticosteroids and immunosuppressant

272
Q

acute glomerulonephritis

A

disorder that occurs suddenly and are characterized by hematuria, proteinuria, edema, and renal insufficiency

273
Q

nephrotic syndrome

A

a kidney disorder characterized by proteinuria, hypoalbuminemia, and edema

274
Q

lab results acute glomerulonephritis

A

elevated BUN, erythrocyte sedimentation rate, ASO titer, creatinine, and electrolyte imbalance

275
Q

ASO titer

A

blood test for strep

276
Q

lab results with nephrotic syndrome

A

protein in urine, hematruia, elevated cholesterol, elevated triglycerides, elevated hemoglobin and hematocrit, elevated platelets

277
Q

wilms tumor

A

nephroblastoma which is the most common malignant renal and intraadbdominal tumor of childhood

278
Q

wilms tumor usually occur in the

A

left kidney

279
Q

manifestations of wilms tumor

A

abdominal swelling, hematuria, fatigue, weight loss, fever

280
Q

diagnosis for wilms tumor

A

abdominal ultra sounds and CT

281
Q

wilms tumor treatment

A

radiation, chemo, nephrectomy

Nursing school level 2 (15 decks)

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