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Peds Part 2 #10 Flashcards

1
Q

is it normal to see abdominal distention after a NB eats

A

yes, due to intestinal muscles being weak

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2
Q

stomach capacity of NB

A

@90 ml (at birth is 15-20 ml)

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3
Q

rate of gastric emptying

A

2-4 hours

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4
Q

if a NB hasn’t pooped in 24 hours what do we suspect

A

obstruction suspected

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5
Q

when are bowel sounds present after birth

A

1 hour

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6
Q

mucus stools

A

milk allergy

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7
Q

clay/gray stools

A

obstruction of bile ducts (hepatic problem)

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8
Q

black/tarry stools

A

intestinal obstruction

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9
Q

what can turn stools green, very odorous

A

nutramigen

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10
Q

stricture of the anus

A

imperforated anus

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11
Q

what does a imperforated anus usually accompany

A

spinal cord defects

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12
Q

when does a imperforated anus usually occur

A

7th week of intrauterine life (same as spinal cord)

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13
Q

S/Sx of imperforated anus

A

absence of anus, membrane filled with black mec protruding from rectum, no stools passed within 24 hours, meconium in urine or vaginal opening

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14
Q

Tx for imperforated anus

A

surgery within 24 hours!

want to keep them on their backs after surgery, keep area clean

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15
Q

protrusion of abdominal contents through the abdominal wall at the point of the junction of the umbilical cord and abdomen

A

omphalocele

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16
Q

when does a omphalocele usually occur

A

6-8 weeks intrauterine

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17
Q

Tx of omphalocele

A

delivery via C/S, topical application of warmed saline soaked pads and plastic drape, prophylactic Abx, surgery (delayed to allow NB to grow

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18
Q

what do you need to watch for when doing surgery for a omphalocele

A

respiratory issues when organs are placed back in body

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19
Q

congenital absence of one or more layers of abdominal musculature

A

prune belly syndrome

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20
Q

same as omphalocele but has no sac, occurs with other defects are rare, usually to side of umbilicus

A

gastroschisis

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21
Q

failure of esophagus to develop as a continuous passage

A

esophageal atresia (EA)

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22
Q

failure of trachea and esophagus to separate into distinct structures

A

tracheoesopaheal fistula (TEF)

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23
Q

when does EA & TEF usually occur

A

4-8 weeks gestation

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24
Q

esophagus ends in blind pouch, fistula between trachea and stomach

A

Proximal (EA wth TEF)

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25
Q

esophagus ends in blind pouch, no connection to trachea

A

Pure EA

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26
Q

fistula is present between otherwise normal esophagus and trachea

A

H type

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27
Q

what needs to be a concern with EA or TEF babies

A

aspiration

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28
Q

Dx of EA and TEF

A

xray, barium swallow

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29
Q

Tx for EA and TEF

A

emergency surgery

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30
Q

post op for EA and TEF babies

A

NPO 1-10 days after surgery, chest tube care, skin care

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31
Q

primary palate

A

anterior portion of mouth (lip, mouth, teeth)

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32
Q

secondary palate

A

posterior portion of mouth

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33
Q

embryology of…

  1. lip
  2. maxillary
  3. palatal processes
A
  1. 5-6 weeks
  2. week 7
  3. week 13
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34
Q

repair of palate

A

palatoplasty

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35
Q

what is extremely important in cleft palate

A

oral hygiene

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36
Q

menstruation from decrease of estrogen from mother

A

pseudomenstration

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37
Q

excessive secretion of androgens by the adrenal cortex, AKA ambiguous genitalia
decrease of cortisol, decrease aldosterone, increase of androgen

A

congenital adrenal hyperplasia

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38
Q

what kind of recessive disorder is congenital adrenal hyperplasia

A

autosomal recessive disorder

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39
Q

what is the patho of congenital adrenal hyperplasia

A

interference in biosynthesis of cortisol during fetal life resulting in increase production of ACTH (which stimulates cortisol production) and has an excessive production of androgens

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40
Q

S/Sx of congenital adrenal hyperplasia

A

ambiguous genitalia

female: clitoris enlarged, fusion of labia
male: enlargement of genitals

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41
Q

emergency situation caused by a lack of cortisol so body cant respond to stress, when have stressful situation have dizziness, weakness, N/V, sweting and LOC

A

acute adrenal crisis

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42
Q

Tx for adrenal crisis

A

glutocoticods, lean S & Sx and must keep solu-cortef

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43
Q

if adrenal hyperplasia is left untreated

A

early development of axilliary, pubic and facial hair,

early closure of growth plate (short stature)

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44
Q

Tx for adrenal hyperplasia

A

cortisone, may need reconstructive surgery

if salt losing type: supplement with salt (aldosterone & cortisone)

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45
Q

IgG

A

passive acquired immunity, transferred to fetus in utero, fetus does not produce, protects against bacterial toxins

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46
Q

IgM

A

active immunity, fetus is able to produce by 20 weeks, stimulated by all infectious agents

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47
Q

IgA

A

does not cross placenta, not produced by fetus, secretory surfaces (resp., GI, eyes)

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48
Q

Secretory IgA

A

passive immunity, transferred through colostrum and breast milk

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49
Q

when is passive immunity of the NB gone by

A

3 months

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50
Q

HIV

A

retrovirus, contact with body fluids

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51
Q

when do you test NB for HIV

A

2-3 weeks, 1-2 months, 4-6 months

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52
Q

fetal effects of HIV

A

AIDS dysmorphia syndrome, resembles FAS

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53
Q

Tx for NB HIV

A

avoid PROM, C/S, forceps, episiotomy, administer IV Zidovutine

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54
Q

Dx of NB HIV

A

2 positive results

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55
Q

gonorrhea

A

contacted with infected birth canal,

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56
Q

fetal effects of gonorrhea

A

blindness

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57
Q

Tx of gonorrhea in NB

A

erythromycin, if active infection also PCN

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58
Q

Toxoplasmosis

A

systemic protozoal, transplacental, undercooked meat, contact with cat feces

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59
Q

fetal effects of toxoplasmosis

A

jaundice, premature, hepatomegaly, IUGR

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60
Q

Tx for toxoplasmosis

A

patient education, Daraprien (antimaleria)

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61
Q

syphilis

A

direct contact with exudates, transplacental

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62
Q

fetal effects with syphilis

A

asymptomatic at birth, rashes, lesions, FTT, SGA

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63
Q

Rubella

A

german measles, virus, droplet, contact, transplacental

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64
Q

fetal effects on rubella

A

heart & eye, (blind deaf, fetal death)

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65
Q

Dx of rubella in NB

A

TORCH titer

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66
Q

Tx for tubella in NB

A

isolation, screen

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67
Q

CMV

A

most prevalent of TORCH group, transplacental, NO BREAST FEEDING

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68
Q

fetal effects with CMV

A

IUGR, petechiae, severe CNS issues

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69
Q

Dx of CMV

A

TORCH titer

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70
Q

Tx of CMV

A

isolation, no tx available

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71
Q

Herpes

A

virus, contact with birth canal

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72
Q

fetal effects with herpes

A

vesicular lesions, hepatitis, neuro involvement

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73
Q

Dx of herpes

A

TORCH titer, culture lesions

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74
Q

Tx of herpes

A

universal standards, C/S if active lesions, IV acycclovir

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75
Q

monilia (yeast)

A

candida albicans, direct contact with birth canal

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76
Q

fetal effects of monilia

A

thrush

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77
Q

Dx of monilia

A

wet mount slide

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78
Q

tx of monilia

A

nystain

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79
Q

chlamydia

A

direct contact

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80
Q

fetal effect of chlamydia

A

NB conjunctivitis, pneumonia, otitis media

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81
Q

Dx of chlamydia

A

culture

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82
Q

Tx of chlamydia

A

erythromycin, isolation

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83
Q

group B strep

A

direct contact

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84
Q

fetal effects of group B strep

A

hypothermia, apnea, poor feeding, resp. distress, if S/Sx in 1st 24 hours high mortality

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85
Q

Dx of GBS

A

S&S blood cultures, chest x ray

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86
Q

tx of GBS

A

ampicillin, or PCN and gentamycin IV

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87
Q

E Coli

A

direct contact

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88
Q

effects on NB with E Coli

A

neonatal meningitis, and sepsis

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89
Q

Dx of E Coli

A

culture

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90
Q

Tx of E Coli

A

IV Abx

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91
Q

TB

A

placental or droplet

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92
Q

fetal effect with TB

A

poor feeder, febrile, lethargy, hepatosleenomegaly

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93
Q

Dx of TB

A

maternal Hx and S& Sx

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94
Q

Tx of TB

A

INH

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95
Q

SSSS (staphococcal scalded skin syndrome)

A

direct contact

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96
Q

fetal effects of SSSS

A

severe bullous eruption, looks like scald marks

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97
Q

Dx of SSSS

A

cultures

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98
Q

Tx of SSSS

A

IV Abx, thermoregulation

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99
Q

invasion of infectious agents resulting in a disease process

A

sepsis

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100
Q

presence in blood of bacterial toxins

A

septicemia

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101
Q

S & Sx of

A

resp distress, lethargy, full fontanels, N/V, unstable temperature, increase of bands, hyperbili, bradycardia, tachycardia (early sign)

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102
Q

Tx of sepsis

A

Abx immediately after cultures, thermoregulation

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103
Q

urinary output 1st day of NB

A

15 ml, void 6-10 times a day

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104
Q

is tan colored urine for 1st few days normal

A

yes, uric acid crystals

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105
Q

excess of CSF in the ventricles and subarachnoid spaces of the brain

A

hydrocephalus

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106
Q

Pathophysiology of hydrocephalus

A

CSF flows from the lateral ventricles to 3rd to 4th ventricle and is absorbed within the subarachnoid space

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107
Q

opening, passage of fluid between ventricles and spinal fluid

A

communicating hydrocephalus

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108
Q

obstruction, block flow of fluid, fluid accumulates and dilates the system above the point of obstruction

A

non communicating hydrocephalus

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109
Q

S & Sx

A

increase head circumference, bulging fontanels, eyes rotated downward (sun setting)

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110
Q

Tx of hydrocephalus

A

surgical, shunting

111
Q

post op for hydrocephalus

A

position flat so fluid doesn’t drain too quickly

112
Q

what prevents neural tube defects

A

folic acid

113
Q

absence of cerebral hemisphere, brain stem only NO brain

A

anencephaly

114
Q

no brain, fluid in place of where brain should be

A

hydranencephaly

115
Q

refers to any malformation of the spinal canal and cord

A

myodysplasia

116
Q

midline defects involving failure of the osseous (bony)spine to close

A

spina bifida

117
Q

occurs when the posterior laminae of vertebrae fail to fuse

A

spina bifida occulta

118
Q

S/Sx of spina bifida occulta

A

dimpling, tuffs of hair, soft subcutaneous lipoma, may be asymptomatic

119
Q

Tx of spina bifida occulta

A

nothing, may have deteratio nof vertebre later in life then may need ortho

120
Q

spina bifida cystica

A

visible defect with external sac protrusion

2 major forms: meningocele, myelomeningocele

121
Q

contains meninges and spinal fluid but no neural elements, meninges herniate through the vertebrae

A

meningocele

122
Q

contains meninges, spinal fluid and nerves, spinal cord and meninges and nerves protrude through the vertebrae

A

myelomeningocele

123
Q

what is usually effected with myelomeningocele

A

bowel and bladder

124
Q

dolls eye phenomenon

A

eye lag behind when head is turned (lack of integratio nof head-eye coordination)

125
Q

pseudostrabismus

A

irises do not appear centered

126
Q

epsteins pears

A

small white dots on oral mucosa (calcium deposites) that disappear in 2-3 months

127
Q

rooting

A

stroke side of cheek, lips or mouth with finger or nipple

128
Q

moro

A

startle, extends and abducts arms accompainied by extensio nof fingers

129
Q

tonic neck reflex

A

place infant on back, turn head to one side, the infants opposite arm and leg will flex towards that side

130
Q

babinski

A

fanning and extensio nof all toes when one side of sole is stroked

131
Q

failure of urachus to close between bladder and umbilicus

A

patent urachus

132
Q

Dx of patent urachus

A

U/S, sonogram, clear odorless fluid draining from base of umbilical cord (test pH)

133
Q

Tx patent urachus

A

surgical correctio immediatly bc of infection and sepsis risk

134
Q

deficiency in the deveolpment of the anterior abdominal wall, symphysis pubis, bladder and urethra

A

exstrophy of the bladder

135
Q

Dx of exstrophy of bladder

A

bladder lies open and exposed on the abdomen

136
Q

Tx of exstrophy of bladder

A

surgery (2 stage) repair abd wall, bladder neck tightening procedure
pre op: protect from injury, cover with sterile dressing, wrap baby legs together to protect symphysis pubis
post op: clean of feces, cath care, urine will be bloody after procedure

137
Q

urethral defect where the urethral opening is not at the end of the penis but is on the ventral (lower) aspect of the penis

A

hypospadius

138
Q

opening is on the dorsal surface of penis

A

epispadius

139
Q

TX for both hypospadius or epispadius

A

NO circumcision, surgical correction

140
Q

large fluid filled cysts form in place of normal kidney tissue

A 
polycystic kidneys
(autosomal resessive disorder)
141
Q

Dx of polycystic kidneys

A

large kidneys, soft and spongy, anuria if bilateral, oliguria if unilateral

142
Q

Tx for polycystic kidneys

A

unilateral-remove diseased kidney

bilateral-transplant

143
Q

collection of fluid within the processus vaginalis (scrotal sac)

A

hydrocele

144
Q

upper portion of the processue vaginalis is obliterated but the porition within the scrotum remains open

A

non communicating (fluid stays)

145
Q

processus vaginalis remians open from scrotum to abdominal cavity

A

communicating (fluid goes back and forth)

146
Q

Tx for hydrocele

A

fluid will reabsorb over time, if hasnt fotten better by 3 months good indicatio nof hernia=repair of hernia

147
Q

why at birth does the blood glucose level fall rapidly

A

bc of trauma of birth

148
Q

decreased ability to conjugate bilirubin

A

hyperbilirubinemia

149
Q

decreased ability to regulate BS concentrations

A

hypoglycemia

150
Q

deficient productio nof prothrombin and other coagulatin factors dependent upon Vit. K for synthesis

A

NB predisposed to hemorrhage

151
Q

function of liver

A

glycogen storage, depot for iron, carbohydrate metabolism, conjugatio nof bilirubin, coagulation

152
Q

conjugate

A

break down bilirubin to an excretable form

153
Q

orange bile pigment produced by the breakdown of heme (RBC) and excreted by the cells

A

bilirubin

154
Q

conjugated bilirubin

A

has been broken down my liver, cross the BBB but is not dangerous to the brain

155
Q

unconjugated bilirubin

A

not been broken down by liver, fat soluble, unbound is dangerous becuase if can deposit on brain=encephalopathy

156
Q

pathological jaundice occurs when

A

within first 24 hours of birth

157
Q

Rh incompatibility

A

if you have a Rh - mom with a Rh baby (1st pregnancy) with birth Rh + blood from placenta enters maternal blood stream, mom produces Rh+ antibodies, if 2nd pregnancy baby is Rh - than no affect on fetus, if 2nd pregnancy baby is Rh + then Rh + antibodies from mom attack fetal blood = erythroblastosis fetalis (fetal death)

158
Q

if abortion occurs is mother given Rhogam?

A

yes because unknown status of fetus

159
Q

why is Rhogam given

A

prevents body from creating antibodies so cant attack fetus, has to be given within 72 hours

160
Q

ABO incompatibility

A

occurs if there the antigens of fetus differ from mother, antibodies cross placenta and attack fetal RBC’s causing hemolysis
*not as severe as Rh incompatibility (not fatal)

161
Q

jaundice that occurs after 24 hours of age, due to high bilirubin production bc of increase in # of RBC, shorter RBC living rime, bilirubin levels build up bc reabsorbed

A

physiologic jaundice

162
Q

progressive indirect hyperbilirubinemia beyond 1st week of life, occurs after breast milk is in and lasts longer (enzyme that inhibits conjugation)

A

breast milk jaundice

163
Q

Dx of jaundice

A

transcutaneous bilirubinometry (TcB) bilirubin blood measurements

164
Q

normal unconjugated measurement

A

0.2-1.4 mg/dl

165
Q

coombs test

A

tests if there are antibodies on NB RBC

positive test= bad

166
Q

Tx of jaundice

A

early feeds, phototherapy

167
Q

what does phototherapy do

A

breaks dowm to a water soluble form

watch for SE: hypotherma, loose stools, water loss

168
Q

free unconjugated bilirubin taken up by fatty tissues, crosses the BBB, bilirubin over 20 is considered toxic (dont want over 12)

A

kernicterus

169
Q

Tx for kernicterus

A

exchange transfusion

watch for calcium levels

170
Q

S/Sx of encephalopathy

A

sleepy, lack tone, poor feeding

171
Q

congential absence or closure of ducts that drain bile from the liver

A

biliary atresia

*can take 2-3 weeks to see

172
Q

S/Sx of biliary atresia

A

jaundice, dark urine, gray/tan stools, ascitesk prutiris

173
Q

Dx of biliary atresia

A

increased bilirubin, increase alk. phosphatase, increase cholesterol
liver biopsy is definitive test

174
Q

Tx of biliary atresia

A

surgery, Kasai procedure-anastomose the jejunium to a hepatic duct (NOT A CURE)
transplant=cure

175
Q

where foot twisted out of normal position or shape

A

congenital clubfoot

176
Q

varus

A

inversion

177
Q

valgus

A

eversion

178
Q

talipes equinus

A

plantar flexion, toes lower than heel

179
Q

talipes calcaneous

A

dorsal flexion, toes higher than heel

180
Q

congenital clubfoot

A

true clubfoot, babies are normal other than clubfoot

181
Q

Tx for clubfoot

A

catsing in stages to turn feet back to normal position, or dennis browne splints

182
Q

AKA congenital dislocated hip, improper formatio nand function of hip socket

A

developmental dysplasia of hip

183
Q

etiology of DDH

A

hormones in pregnancy, breech, LGA genetic

184
Q

one knee lower than another

A

galeazzi

185
Q

audible click heard on exit or entry of femur out of or into the acetabulum

A

barlows test

186
Q

Tx for DDH

A

frejka splint, pavlik harness, cast, surgery if severe

187
Q

underdevelopement of skeletal elements of the extremities

A

skeletal limb deficiency

188
Q

2 types of skeletal limb deficiency

A

amelia-absence of entire extremity

phocomelia-seal like extremity

189
Q

Tx for skeletal limb deficiency

A

prosthetic device

190
Q

why does skeletal limb deficiency occur

A

issue around 7th week gestation

191
Q

generalized dysfunction of exocrine glands

A

cystic fibrosis

192
Q

S/Sx of cystic fibrosis

A

thicked pooled bronchial secretions, dry non productive cough, secondary infections

193
Q

1st S/Sx of cystic fibrosis

A

thich meconium blocks bowel

194
Q

Dx for cystic fibrosis

A

sweat test

195
Q

Tx for cystic fibrosis

A

Abx, moist O2, lung transplant, NO COUGH SUPPRESANTS, high caloric , high protein, moderate fat diet, pancreatic enzyme b4 each meal, Extra Na in hot months

196
Q

NB endocrine functioning must regulate what

A

calcium phosphorus balance, and regulatio nof blood glucose concentration

197
Q

the NB is dependent on what for a normal glucose supply

A

constant circulating supply of glucose to the tissues and especially to the central nervous system

198
Q

during pregnancy how is the glucose transferred to the fetus

A

across the placenta from mother to fetus

199
Q

when to glycose stores build up

A

3rd trimester (so preterm NB doesnt have same stores as term NB)

200
Q

the brain is dependent on what

A

a constant circulating supply of glucose, brain cant store or make glucose

201
Q

Dx of hypoglycemia

A

fullterm in 1st 3 days less than 45 mg/dl
preterm in 1st 3 days less than 50 mg/dl
all infants after 1st 3 days less than 50 mg/dl

202
Q

S/Sx of hypoglycemia

A

tremors, cyanosis, convulsions, apnea, irreg. resp. apathy, lethargy, inability to regulate temperature

203
Q

if you have tactile touh and the tremors continue this is a sign of what

A

hypoglycemia

204
Q

when will a IDM have Sx of hypoglycemia

A

1-4 hours of age

205
Q

when will perinatal stress NB have Sx of hypoglycemia

A

onset within 6 hours

206
Q

when will IUGR/SGA infants show Sx of hypoglycemia

A

24-72 hours

207
Q

when will premature infants and postmature infants show Sx of hypoglycemia

A

depends on age

208
Q

when will LGA infants show Sx of hypoglycemia

A

within 4 hours

209
Q

Tx of hypoglycemia

A

prevention, early po, parental glucose (d50 or D10w)

210
Q

acute hypoglycemia

A

less than 20-25 mg/dl

211
Q

what do you give for acute hypoglycemia

A

10% glucose 2ml/kg slow IV taper to stop to prevent rebound hypoglycemia

212
Q

what is often found in NB experienceing hypoglycemia

A

hypocalcemia

213
Q

Calcium review

A

decreae neuromuscle irritability, promotes contractility of muscle, transmissio nof nerve impulses, and essential for blood clotting and building of bones and teeth

214
Q

Tx for hypocalcemia

A

calcium gluconate, give IV slow (watch cardiac)give with Vit D

215
Q

classifies severity of pregnant DM mothers, may see change in each pregnancy

A

whites classification

216
Q

problems with IDM

A

macrosomia, fetal hyperinsulinism, birth injuries bc LGA, hypoglycemia, hypocalcemia, hyperbilirubinemia, polycythemia, RDS

217
Q

polycythemia due to IDM

A

ruddy in color, too many RBC=increase viscosity of blood, cause R heart failure, start IV to thin out blood

218
Q

RDS due to IDM

A

delayed maturation of surfactnant, related to preterm delivery

219
Q

infection and inflammation of throat

A

pharyngitis, can be bacterial or viral

need throat cultures, Tx is PCN

220
Q

infection and inflammation of tonsils

A

tonsillitis, Sx hard to swallow, fever, lethargy

if bacterial = Abx, if viral = nothing

221
Q

acute epiglottitis

A

sudden onset, tripod, dysphagia, enlarged epigoltis, Tx: airway protection
MEDICAL EMERGENCY

222
Q

acute laryngotracheobronchitis

A

slow, stridor (like seal), cool mist, steriods, racemic epinephirine

223
Q

acute spasmotic laryngitis

A

sudden at night, croupy cough, Sx decrease during day, better with cool air

224
Q

acute tracheitis

A

moderate, Hx or recent URI, high fever, no response to LTB Tx (cool mist, steroids) need Abx

225
Q

inflammation of bronchioles

A

bronchiolitis (RSV)

226
Q

is RSV contagious

A

YES, direct contact with secretions

227
Q

Dx of RSV

A

nasal swab, C xray

228
Q

Tx for RSV

A

fluids, broncodilators, corticosteroids, cough supressant, Ribavirin
IgIV (RespiGam)

229
Q

inflammation and edema of mucous membranes, accumulation of secretions, spasms of smooth muscleof bronchi

A

asthma

230
Q

measures maxium flow of air that can be forecefullly exhaled in 1 second

A

PEFR

231
Q

PFT

A

pulmonary function test, presence and degree of lung disease

232
Q

why would you want to avoid cool liquids in asthma

A

may induce bronchospasm

233
Q

when giving Rx what do you want to give first for asthma

A

bronchodilator then steriod

234
Q

severe life threatening asthma exacerbation that is refractory (wont respond) to Tx

A

status asthmaticus

235
Q

caused by a inadequate supply of dietary iron, most preventable nutrional disorder in US

A

iron deficiency anemia

236
Q

when is the most iron transferred to fetus

A

3rd trimester

237
Q

S/Sx of iron deficiency anemia

A

pallor, weakness, fatigue

238
Q

Lab work for iron deficiency anemia

A

dreased: hem, Hct, MCV, MCH, MCHC, serum iron concentration
increased: TIBC (total iron binding capacity
Normal: retic count
can have occult blood

239
Q

Tx for iron deficiency anemia

A

dietary, addition of iron rich foods, NO COWS MILK

240
Q

when will you need a transfusion

A

less than 4 mg/ml

241
Q

Hgb is partially or completely replaced by abnormal sickle Hgb

A

sickle cell anemia

242
Q

etiology of sickle cell

A

RBC gets distorted and spleen sees it as abnormal and removes it, autosomal recessive

243
Q

trail of sickle cell

A

increase of RBC destruction = tangle of cells = blockage = vasoocclusion = decrease blood flow = hypoxia = pain = death

244
Q

spleen is enlarged working hard to remove abnormal RBCs and blood pools in spleen

A

sequestration crisis

get hypovolemic shock

245
Q

bone marrow is tired, cant produce more RBC

A

aplastic crisis

246
Q

destruction is happening quicker than production

A

hyperhemolytic crisis

247
Q

painful episode, have distal ischemia and pain

A

vasocclusive crisis

248
Q

can sickle cell cause CVA

A

yes, block major blood vessels in brain

249
Q

hand foot syndrome

A

painful swollen hands and feet

250
Q

Dx of sickle cell

A

sickledex (finger stick), if reticulocytes are 15 % = crisis

251
Q

Tx of sickle cell crisis

A

prevention
pain control, bedrest, hydration, O2
splenectomy - help stop getting rid of cells

252
Q

what can you do for someone in a sickle cell crisis

A

adequate hydration, heat to painful areas (vasodilate) PCN, support

253
Q

rheumatic fever

A

caused by untx strep, after initial infection has subsided, 2-6 weeks later it will appear if not treated

254
Q

2 major manifestations of rhematic fever

A

carditis, polyarthritis, erythema marginatum, chorea, sub q nodules

255
Q

Dx of rheumatic fever

A

ESR elevated, positive strep, elevated strep antibody titer

256
Q

Tx for rheumatic fever

A

PCN, bedrest, oral salicylates (asa, ibuprofen, advil, motrin), give steroids if asa doesnt work

257
Q

what must pts with past hx of rheumatic fever do

A

prophylaxis for dental work, infections, invasive procedures to protect heart valves

258
Q

kawasaki diease

A

difficult to Tx, fever lasting longer than 5 days plus: conjunctiva, mucous membrane changes, rash, lower extremity changes, enlarged lymph

259
Q

when do you consider kawasaki disease

A

on any child with rash and fever of unknown origin

260
Q

S/Sx

A

abd pain, N/V, restlessness, pallor, shock

increase of : platelets, EST, sed rate, WBC, liver enzymes, EKG changes

261
Q

Tx for KD

A

gamma globulin IV, ASA

262
Q

Mononucleosis

A

aka kissing disesase, epstein barr virus, CONTAGIOUS

no contact sports bc enlarged spleen

263
Q

triad of mono

A

sore throat, fever, enlarged lymphnodes

264
Q

Tx for mono

A

no specific tx, PCN, bedrest, acyclovir, increase fluids

265
Q

acute lymphocytic leukemia

A

most common childhood cancer, bone marrow

266
Q

B cells

A

make immunoglobin

267
Q

T cells

A

helper cell

268
Q

Dx of ALL

A

increase # of cells with increase # of lymphoblasts, lumbar puncture

269
Q

Tx of ALL

A

chemo, radiaton, bone marrow transplant

270
Q

lead poisoning test

A

erythrocyte protorphyrin (EP)

271
Q

lead poisoning effects what

A

proximal tubles, neurological system

272
Q

Tx for lead

A

remove source

273
Q

lead encephalopathy

A

permanent brain damage

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