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Ch. 12: Health Promotion of the Child and Family• cognitive development: sensorimotor and preoperational phase (piaget)
• Growth and development dring the toddler years
Ch. 1!: Health Promotion of the Preschooler and Family• "ocial development
• coping with concerns related to normal growth and development
Ch. 1#: Health Pro$lems of %oddlers and Preschoolers• Commnica$le diseases
• selected poisonings in children
• lead poisoning
• physical a$se
• &rsing care of the 'altreated child
CH 2: Pediatric Cardio
**** normal heart
Cardiovasclar dysfnctionCongenital Heart +iseases* defects present at $irth
,c-ired Cardiac +isorders*disease processes or a$normalities occrring after $irth.H P e/am*
0ids with Heart pro$lems may have the following:failre to thrive or they may $e sinny ids dt poor wt gaincyanosischest deformitiesvisi$le plsations of nec veinsrespiratory e/crsion (tachypnea3 dyspnea3 e/piratory grnt)cl$$ed fingers
&rse may find the following pon palpation3 percssion and ascltation
hepatomegaly andor splenomegalyirreglar heart rates3 rhythms or sonds
+iagnostic eval (see p. 421 for complete list)'ost common are 5*6ay3 7lectrocardiogram3 7chocardiography3 Cardiac
Catheteri8ation3 Cardiac '693 7/ercise stress test.7CG*non*invasive and painless7cho*sed fre-ently
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non*invasive and painlesspossi$le to confirm d/ of heart malformation with echoid has to $e -iet otherwise errors or omissions may occr
Cardiac Catheteri8ation*srgical interventionmay $e otpatientdone prior to school*age
&rsing care for Cardiac cath.Preop
diaper rash*this may $e a reason to cancel the procedrenpo #*hr $efore procedreprepare $oth id and family*geared toward child;s developmental levelmar plses distal to insertion sitedocment $aseline leeding?*apply direct pressre 1 inch a$ove insertion site
Cardiac changes at $irth• Fets* >a$y transitions in circlation and $reathing*
clamping cord systemic >P lng e/pansion decreases plmonary vasclar resistance(and increases plmonary perfsion)
• increase in
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,cyanotic1) 9ncreased Plmonary >lood Flow
$lood flows in a @*to*6 directione/: ,"+3 ="+3 Patent +cts ,rterioss3 ,trioventriclar canal2)
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Congenital Cardiovasclar +ysfnction: 9ncreased Plmonary $lood flow* # types
1. ,trial "eptal +efect (,"+)
• ,cyanotic disorder • ,$normal opening $twn 6 and @ atria*
o $lood moves from higher con;c (@) to lower con;c (6).
o Plmonary H%&redced $lood volme in systemic circlation
• ! types
o
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o "rgery* patch closre for moderate to large holes se +acron or
pericardial patcho &on*srgery* septal occlsion dring cardiac catheteri8ation
o repair completed $efore school age
o &o activity restrictions after repair
• 'edicationsprognosis
o @ow dose ,", for months after repair
2) =entriclar "eptal +efect (="+)• ,cyanotic disorder
• 'ost Common ,$normal opening $twn @ and 6 ventricles* $lood moves from
high pressre (@) to low pressre D side of heart• classified according to location on septm
• vary in si8e* most small holes close win first year of life
• fre-ently occr with other pro$lems
o plmonary stenosis
o transposition of great vessel
o Patent +cts ,rteriosis
o atrial defects
o coarctation of aorta
• ""
o HF
o @od mrmr heard on @ sternal $order
o ,t ris for >7 (?) and Plmonary =asclar ypass machine sed in $oth cases
Complication of s/:
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condction isses
residal ="+
o 'edicationsPrognosis
o good3 depending on locationsi8e of hole
o mltiple holes are associated with higher riss
!) ,trioventriclar Canal +efect• ,cyanotic +isorder
• 9ncomplete fsion of endocardial cshions
o low ,"+ w high ="+ creating a large central ,= valve
o allows $lood to flow $twn all for cham$ers
• direction of flow is determined $y
o plmonarysystemic resistance
o @6 vent. pressres
o compliance (stretch) of each cham$er
• common defect seen in +own "yndrome ids
• ""
o moderate to severe HF
o lod systolic mrmr
o mild cyanosis that increases with crying
o high ris for plmonary vasclar o$strctive disease
• %/
o Complete repair
most commonly done in infancy
patch closre of septal defect
reconstrction of ,= valve tisses
o Palliative plmonary artery $anding done in small infants with severe symptoms
o Post op complications
Heart $loc
HF
'itral regrgitation
dystrhytmias
plmonary H%&
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• 'edicationsPrognosis
o good E may have mitral valve replacement later in life de to mitral regrgitation
#) Patent +cts ,rterioss (P+,)• ,cyanotic +isorder
• failre of closre of artery connecting high pressre ,orta to low pressre
Plmonary ,rtery within first few wees of life• Contined patency of this vessel cases a @*6 shnt
• ""
o ,symptomatic
o sometimes HF is seen
o characteristic machine lie mrmr heard
o widened and $onding plse pressres
o Bris for >7 (?) and Plmonary =asclar
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1. Coarctation of the ,orta (CP
$onding plses in arms
weaa$sent plses in legs
cool to toch legs
signs of HF in infants
critical coarctation in infants can deteriorate -icly when acidosis and
hypotension occr mechanical ventilation and inotropic spport are needed $efore srgery
older ids with coarctation may e/perience
di88iness3 H,3 fainting3 epista/is (nose$leeds) form H%&
B ris for H%&3 rptred aorta3 aortic anerysm3 and stroeo %5:
&on*s/: infants and little ids get $alloon angioplasty
adolescents get stents
"/: want to do $efore mo of age
indicated if stenosis is long or other comple/ anatomy are present
repair is $y resection of coarcted porton w end*to*end
anastomosis of the aorta with enlarged portion of constricted areavia se of graft of left s$clavian artery
o 'edicationsprognosis
to prevent post*op H%&:
"odim &itroprsside
7smolol 'irinone
followed $y oral
$eta $locers
ace inhi$itors
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2. =alvlar ,ortic "tenosiso ,cyanotic
o &arrowing or strictre of aortic valve casing
resistance to $lood flow in left ventricle
decreased cardiac otpt
plmonary vasclar congestion
@eft =entriclar Hypertrophy Primary manifestation
eventally leads to increased 7nd +iastolic pressre reslting in
Plmonary venosarterial H%& may also interfere w coronary artery $lood flow reslting in '9
considered a serios defect $c
o$strction is progressive
sdden episodes of myocardial ischemia occr
srgical repair rarely reslts in a normal valve
• ""
9nfants present with
decreased C<
faint plses
hypotension
tachycardia
poor feeding
ids present with
e/ercise intolerance
di88iness when standing
chest pain
may or may not have systolic mrmr
B ris for >7 (?)3 coronary insfficiency3 ventriclar dysfnction
• %5:
"/: $alloon dilation done in cath la$ ,ortic valve replacement***may temp. fi/ pro$lem
srgical complications
aortic insfficiency3 valvlar regrgitation3 tearing of valve leaflets3
loss of plse in catheteri8ed lim$• 'edicationsPrognosis
'eh* will $e recrrent and re-ire additional srgeries throghot life.
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!) Plmonary =alve stenosis• ,cyanotic
• narrowing at entrance to Plmonary artery
• cases D sided ventriclar hypertrophy and decreased artery $lood flow
Plmonary atresia is rare and very seriosno plmonary valve* is completely closed and there is no $lood flow to lngs
•
""o ,symptomatic
o 'ild cyanosis or HF
o progressive narrowing cases increased symptoms
o lod systolic eAection mrmr heard at (@) sternal $order
o 9n severely ill ids3 mrmr may $e mffled de to decreased C< and shnting of
$loodo B ris for >7 (?)
• %5:
o &on*s/: >alloon angioplasty in Cardiac Cath la$*t/ of choice
o s/: transventriclar (closed) valvotomy* rare procedre
• 'edicationsPrognosis
o Good $t have have valve incompetencies or valve restenosis
Congenital Cardiovasclar +ysfnction: +efects with +ecreased Plmonary >lood Flow (2types)
1. %etralogy of Fallot (%
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o tricspid valve fails to develop
o $lood has to flow throgh an ,"+ or to a patent foramen ovale to left side of
heart and throgh a ="+ to the D ventricle and ot to lngs.o complete mi/ing of n*
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o
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o when o2 delivery occrs3 most liely ,"+ is present and is considered
no$strctedI %,P=C• ""
o cyanosis early in life
o infant rapidly deteriorated wo immediate intervention
o may $e asymptomatic
vasclar resistance decreases in infancy casing increase in plmonary
$lood flow reslting in "" of HFo cyanosis worsens when o$strction occrs (no asd present)
• %5:
o plmonary vein moved to $ac of @eft atrim and ,"+ closed
o connecting vein removed
o post*op complications: reo$strction3 $leeding3 dysrhythmias3 heart $loc3
plmonary artery H%&3 persistent HF• 'edicationsPrognosis
o 1LM mortality when intervention is swift
!) %rncs ,rterioss• failre of normal separation of aorta and plmonary artery
• development of single vessel
• $lood mi/es and leads to desatration and hypo/emia
• ! types
o type 1* single plmonary trn**divides into @6 plm. art.
o
type 2* @6 plmonary arteries arise separately $t from same locationo type !* plmonary arteries arise independently
• ""
o "evere HF
o varia$le cyanosis
o poor growth
o activity intolerance
o holosystolic mrmr B left sternal $order wdiastolic mrmr is trncal
regrgitation is present
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• %/:
o 6epair performed win 1st month of life
o close ="+
o Ct plmonary artery from aorta and attach to D ventricle
se of homograft when attaching Plm. ,rt to D =ent.
homograft is cadaver material and is not livingwill not grow with childwill
have to $e replaced• 'edicationsPrognosis
o Good
o Ftre "/ will $e necessary to replace cadaver condit.
#) Hypoplastic @eft =entriclar "yndrome (H@=")• nderdeveloped left side of the heart
• reslts in small si8ed left ventricle and aortic atresia
• $lood is shnted to D atrim via Patent foramen ovale,trial septal defect
• +escending aorta receives $lood via Patent +cts ,rterioss spplying systemic $lood
flow• ""
o "igns of HF ntil P+, closes**** then progressive deterioration occrs
wcyanosis and decreased C
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o neonate will need ventilator and cardiac spport ntil srgery
o Prostaglandin 71 will $e continosly infsed to ensre ade-ate $lood flow
,c-ired Heart +iseases• >acterial 7ndocarditis
o c$ $acteria entering $lood stream casing infection to inner lining of heart3
generally involving valveso 9ncreased ris for ids with valvlar a$normalities3 prosthetic valves3 shnts3
recent cardiac srgery3 rhematic heart disease w valve involvemento ""
slow onset3 low intermittent fever3 anore/ia3 malaise3 wt. loss3 cardiac
dysrhythmias3 new or change in mrmr3 e/tracardiac em$oli (splinterhemorrhages on nails3 osler nodes3 Aaneway lesions3 petechiae on oral
mcos mem$ranes)3 vegetations seen on echo and may have HFo %5:
,>5 and Prevention in high ris ids
*cillins and mycins prove effective a$/ t/
in serios cases iv a$/ indicated
&rse needs to edcate parents on "" of anore/ia3 wt. loss and malaise.
• 6hematic Fever
o inflammatory disorder*self limiting involvement of Aoints3 sin3 $rain3 seros
srfaces and heart heart most serios complication*mitral valves compromised
o +iagnosis $ased on Nones criteria*sggest the presence of two maAor and one
maAor and two minor symptoms w recent strep inf/n*high pro$. of 6Fo %5:
0ill strep inf/n
prevent permanent damage
alleviate other s/s
prevent recrrences of 6F w penicillin drgs andor salicylates for Aoint
inflammationo &rsing care
encorage medication compliance
facilitate recovery
provide emotional spport
prevent disease
o
Chorea is side effect and may develop wees to months after inf/n is sdden and ncontrolla$le movements
can $e frstrating for child
• 0awasai;s +isease
o acte systemic vasclitis of nnown case
o not spread from person to person
o occrs in ! phases:
,cte: a$rpt onset w edema3 redness of palmssoles and high fever
nrelieved $y a$/ or antipyretics.
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"$acte: $egins when fever resides3 and lasts ntil all clinical signs have
resolved. feet and hands often peel at this stage
id is B high ris for developing cardiac complications ('93
Coronary artery anerysms) at this stage Convalescent: all clinical signs are gone $t $lood vales are still
a$normal. @ong term complications are aortic anerysms w potential for '9
ss of aortic anerysm: a$d pain3 vomiting3 restlessness3
inconsola$le crying3 pallor3 shoc and chest painpressre medications:
High dose 9= Gamma Glo$lins and "alicylate therapy given in
hospital @ow dose ,", given ot of hosp. esp. when cardiac involvement
is sspected. &rsing care:
nrses mst now irrita$ility is hallmar of 0+ and most
challenging pro$lem 'aAority of nrsing care is directed on symptomatic relief
+ring acte s$acte phase* watch careflly id is at high ris
for cardiac complications Patient edcation
tell parents to prolong va/ 11 months de to crrent nnown
immne compromise will need lifelong medical follow p depending on amont of
cardiac involvement
Chapter 26Anemia
• descri$es a condition in which the nm$er of 6>Cs or hemoglo$in concentration
is redced $elow normal vales for age. %hs diminishing the o/ygen carryingcapacity. 'ost common hematologic do in infancychildhood
• Classification
• 7tiology: manifested $y erythrocyte or Hg$ depletion
• 'orphology: characteristic changes in 6>C si8e3 shape or color
• Classifications of anemia
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• Conse-ences of ,nemia: $asic physiologic defect cased $y anemia is
decrease in the o/ygen*carrying capacity of $lood and decreased amont ofo/ygen availa$le to tisses.
• 7ffects of anemia on the circlatory system
• Hemodiltion: decreased peripheral resistance3 greater -antity of $lood
retrn to the heart
• 9ncreased cardiac circlation and tr$lence: may have a mrmr3 may
lead to cardiac failre
• cyanosis is not typical
• growth retardation: delayed se/al matration
• +iagnostic 7valation:
• History and physical e/amination: lac of energy3 easy fatiga$ility3 and
pallor
• C>C: decreased 6>C3 decreased Hg$Hct. Hg$: less than 1L or 11gd@
• other tests can $e done to determine the particlar type of anemia.
• 'anagement of ,nemia:
• %reat the nderlying case: transfsion after hemorrhage if neededO
ntritional intervention for deficiency anemias
• "pportive Care: 9= flids to replace intravasclar volme3 o/ygen3 $ed
rest3 diet3 family edcation
• &rsing Considerations: prepare the child and family for la$ tests3 decrease
o/ygen demands3 prevent complications3 spport and edcate family.Iron Deficiency Anemia
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• $ased on diet*inade-ate spply of dietary iron.
• predicta$le development periods
• Prematre infants: at ris $c redced fetal iron spply
• infants: at ris as a reslt of primarily cow mil intae and not eating an
ade-ate amont of iron*containing formlafood
• adolescents: de to rapid growth weight com$ined with poor eating ha$its3menses3 o$esity or strenos activities
• "ymptoms: pale sin3 irrita$ility3 tachycardia3 fatige3 glossitis (inflammation of
the tonge)3 0oilonychia (concave or spoonI fingernails)
• %herapetic management:
• 9nfants: iron*fortified formla3 do not give fresh cow mil3
• Children: addition of iron*rich foods3 oral iron spplements are prescri$ed
and mst $e given with vit C $ecase it facilitates a$sorption of iron.
• &rsing considerations: oral iron shold $e given as prescri$ed in two divided
doses $twn meals3 always give with citrs Aice never mil3 trns stool tarry
green3 se straw so iron doesn;t stain teeth3 &= may occr3 spplementation.• primary nrsing o$Aective is to prevent ntritional anemia throgh family
edcationSickle Cell Anemia
• is one grop of diseases collectively termed hemoglo$inopathies in which normal
adlt Hg$ is partily or completely replaced $y a$normal sicle Hg$
• Hereditary do whose clinical3 hematologic and pathologic featres are related to
the presence of H$"
• occrs primarily in ,,3 occasionally ppl of mediterranean descent3 soth
american3 ara$ian and east indian descent
• 7tiology:
• ,tosomal recessive do: one in 12 ,, is a carrier3 if $oth parents have
trait each child with have a 1 in # lielihood of having d8
• Patho: leads to tisse damage throghot $ody
• +iagnostic 7valation
• new$orn screening is mandatory in most of the " so infants can $e
identified $efore symptoms occr. early diagnosis $efore !mo ena$lesinitiation of appropriate interventions to minimi8e c/
• test cord $lood in new$orns3 genetic testing to identify carriers and
children who have the d8
• sicle tr$idity test: fingerstic3 yields accrate reslts in ! min in children
over mo of age• hemoglo$in electrophoresis: fingerprintingI of the protein. accrate3 rapid
and specific test for detecting the homo8ygos and hetero8ygos forms ofd8.
• %herapetic 'anagement:
• Goals: prevent sicling phenomena and t/ medical emergencies
• analgesics for pain
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• $ed rest with mild range of motion
• hydration to thin $lood
• minimi8e infections with anti$iotics
• hydro/rea: disease modifying drg
• $lood transfsion: replacement of sicle cells with normal 6>Cs3
sccessfl3 rapid method of redcing the nm$er of circlating sicle cellsths slowing down the hypo/ia
"9C0@7 C7@@ C69"9": acte e/acer$ations that vary in severity and fre-ency
• Precipitating factors: anything that increases the $odys need for o/ygen or alters
the transport of o/ygen3 trama3 feverinf/n3 physical and emotional stress3increased $lood viscosity de to dehydration3 hypo/ia (reslts from high altitde3poorly pressri8ed airplanes3 hypoventilation3 vasoconstriction de tohypothermia).
• %ypes:
o =aso*occlsive (=
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o anemia reslts from defective synthesis of hemoglo$in3 strctrally
impaired 6>Cs and a shortened life of 6>Cso Chronic hypo/ia: headache3 irrita$ility3 precordial and $one pain3 e/ercise
intolerance3 anore/ia3 epista/is ($leeding from the nose)o +etected in infancy or toddlerhood: pallor3 failre to thrive3
hepatosplenomegaly3 severe anemia*Hg$ less than gd@• 'edical management of thalassemia maAor
o $lood transfsion to maintain normal Hg$ levels
o side effect hemosiderosis: e/cess iron from hemolysis of spplemental
6>Cs in transfsions and from the rapid destrction of defective cells isstored in varios organs
%/: iron*chelating drgs sch as defero/amine (+esferal)3 $inds
e/cess iron for e/cretion $y the idneyAplastic Anemia
• refers to $one marrow failre condition in which the formed elements of the $lood
are simltaneosly depressed. Pancytopenia: all formed elements of the $loodare depressed
• Can $e Congenital or ,c-ired: most are idiopathic
• Common Cases: hman parvovirs inf/n3 hepatitis or overwhelming inf/n3
irradiation3 immne disorders sch as eosinophilic fasciitis andhypoimmnoglo$linemia3 drgs (chemo agents3 anticonvlsants3 and a$/)3indstrial or hosehold chemicals3 infiltration and replacement of myeloidelements3 idiopathic.
• 'anifestations: anemia3 leopenia3 decreased platelet cont
• +/: C>C3 reticlocyte cont3 $one marrow aspiration
• %/: restore fnction to marrow3 immnosppressive therapy or $one marrow
transplantHemophilia
• a grop of hereditary $leeding disorders that reslt from deficiencies of specific
clotting factors. %ypically an 5*lined recessive pattern. ,ffects males only andFemales are carriers. Fi$rin clot cannot form
• %ypes
o Hemophilia ,: only males get $t transferred $y mothers. classic
hemophilia (deficiency of clotting factor 4). ,cconts for 4LM of cases ofhemophilia.
o Hemophilia >: christmas diseaseI deficiency in factor 95
o von Qille$rand disease (vQ+): deficiency3 a$normality or a$sence o vQf
and factor 4. affects $oth males females
• 'anifestations: $leeding tendencies range from mild to severe
o "": may not occr ntil mo of age3 history of $leeding3 nose$leeds and
$rising. Prolonged $leeding3
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o Hemarthrosis: $leeding into Aoint spaces of the nee3 anle or el$ow3 leads
to impaired mo$ility and eventally $ony changes and disa$ility. ss:warmth3 pain3 $rising3 and decreased movement.
o spontaneos hematria and hematoma
• 'edical management:o replacement of missing clotting factors (factor 4 concentrates or synthetic
form of vasopressin 1*deamino4*d*arginine vasopressin ++,=P) 9=3 increases factor 4 activity $y two or for times sed for mild
hemophilia. can;t se for severe anemiao transfsions: prompt intervention to redce complications
o medications: corticosteroids
o e/ercise and physical therapy
o 69C7 (6est3 9ce3 Compression3 7levate)
e!kemias
• descri$es a $road grop of malignant diseases of the $one marrow and
lymphatic system. 'ost common form of childhood cancer. nrestrictedproliferation of immatre Q>Cs in the $lood*forming tisses of the $ody $t la$levels are low. >one marrow sppression (myelosppression) occrs.
• %wo forms are generally recogni8ed
o ,cte @ymphoid leemia (,@@): children with trisomy 21 have a 2L times
greater ris for developing ,@@o ,cte &onlymphoid ('yelogenos) @eemia (,'@):
o liver and spleen are the most severely affected organs
• ,ssessment of @eemia: anemia (weanessfatige)3 netropenia (inf/n)3
throm$ocytopenia ($leeding)3 spleen and liver enlarged and painfl3 C&"
symptoms: &=3 lethargy3 irrita$ility3 convlsionso @ate signs: fractres3 $one pain3 increased 9CP
o ! main conse-ences: anemia3 inf/n3 $leeding
• +iagnosis:
o sally sspected $ased on history and physical: fever3 ss of low $lood
conts3 lymph node enlargement3 and enlarged liverspleeno peripheral $lood smear: immatre forms of leocytes3 fre-ently low
$lood contso definitive diagnosis is $ased on $one marrow aspiration or $iopsy
o lm$ar pnctre to evalate C&" involvement
• 'anagement of @eemia: chemotherapetic agents and cranial irradiation
o For Phases:
9ndction therapy for #* wees3 achieves complete remission or
less than M leemic cells in the $one marrow C&" prophylactic therapy (intrathecal chemo): prevents leemic
cells from invading the C&" 9ntensification (consolidation): eradicates residal leemia cells
'aintenance therapy: serves to maintain the remission phase.
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• &rsing 'anagement:
o Family*centered care3 pain relief3 'yelosppression (inf/n control3
$leeding3 anemia)3 Chemotherapy3 and +rg to/icity3 provide emotionalspport
ymphomas
• a grop of neoplastic diseases that arise from the lymphoid and hematopoieticsystems3 are divided into Hodgin lymphoma (H@)3 and non*Hodgin @ymphoma(&H@)
• Hodgin;s disease
o originates in the lymphoid system and primarily involves the lymph nodes.
more prevalent in patients 1*1K years oldo metastasi8es to non*nodal or e/tralymphatic sites: spleen3 liver3 $one
marrow3 and lngso classified $y lymphocytic predominance3 nodlar sclerosis3 mi/ed
celllarity and lymphocytic depletion.o 6eed*stern$erg cells present3 centrali8ed in one*node or arond the nec
o "": fever3 night*sweats3 weight*loss
• &on*Hodgin disease:
o more prevalent in children yonger than 1# years old
o the disease is sally diffse rather than nodlar3 develops in peripheral
lymph nodes or throghot $odyo the cell type is either ndifferentiated or poorly differentiated3
dissemination occrs early3 more often and rapidly3 mediastinalinvolvement and invasion of meninges are common
o symptoms related to pressre of enlarged lymph nodes
o %5: radiation and chemotherapy
IT" (Imm!ne Throm#ocytopenia$ I%iopathic throm#ocytopenic "!rp!ra)• ac-ired hemorrhagic disorder characteri8ed $y:
o (1) throm$ocytopenia: e/cessive destrction of platelets
o (2) a$sence or minimal signs of $leeding: easy $rising3 mcosal
$leeding3 petechiaeo (!) normal $one marrow with normal or increased nm$er of immatre
platelets (megaaryocytes) and eosinophils.
•
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,. opposite of respiratory infection (lower is $etter higher is worse)>. Pea $etween 2* yrs of ageC. Females are at a higher ris+. 7.Coli is the most common pathogen7. 6ecrrent may lead to transient vesicoreteral refl/ (=6)
F. 'anifestations1. strong smelling rine3 a$normal stream3 fre-ent or infre-entvoiding3 persistent diaper rash
2. classic symptoms greater than 2 years of age!. many are asymptomatic
G. +iagnostic 7valation1. e/amination of the rine* reveals Q>C3 presence of the $acterim
1. it is recommended to collect the rine via a $ag>. %herapetic 'anagement
a. eliminate infections3 identify contri$ting factors3 prevent rosepsis3and preserve renal fnction
$. a$/ if indicatedc. antipyreticsd. cltres,;s every month for ! months
C. &rsing Care 'anagementa. 7dcation3 detect anatomic defects3 girls at higher ris3 edcation
on appropriate se of ,>5+. Prevention
a. most important goal$. promote health maintenance (safe se/ practices3 good hygiene)
99. +efects of the Genitorinary %ract ,. didn;t have mch in the $oo3 review slides of hydrocele and inginal
hernia and sch99. &ephrotic "yndrome* most common presentation of glomerlar inAry in children ,. %ypes
a. 'inimal Change &ephrotic "yndrome1. 'anifestations* proteinria3 edema3 hypoal$minemia3 and
hyperlipidemia2. most common type!. Pathophysiology* nephrons $ecome permea$le to proteins
casing loss of al$min and then flid shifts into interstitialspaces casing edema and ascites
#. +iagnosis* rinary analysis3 $lood test for protein levels3mostly $ased on symptoms and history
. %reatment* C
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aggravating flids3 cltres following3 parent teaching a$othome care and diet
$. "econdary &ephrotic "yndromec. Congenital &ephrotic "yndrome
99. ,cte Glomerlonephritis
,. Common symptoms* oligria3 edema3 H%& and circlatory congestion3hematria3 and proteinria>. 'ost common case is strep infection3 can also $e cased $y "@73 sicle
cell3 or $acterial endocarditisC. Primarily in school aged children3 *S years of age3 ncommon in children
yonger than 2 years+. Pathophysiology
a. minor enlargement3 glomerlar capillary loops very swollen$. retention of sodim3 which cases retention of flids
7. Clinical Corse* edema sally persists for #*1L days to 2*! weesa. weight fl/ates3 rine remains smoy $rown3 high >P
#' st sin of impro*ement is a small increase in !rinary o!tp!tan% %ecrease in #o%y +eihtF. 'ostly manage symptoms* low sodim and protein3 accrate 9;s P monitoringG. +iagnosis* serologic testing3 ,3 cltres for "trep3 "erm Complement
@evel (C!) is the more important diagnostic criteria (decreases thenretrns to normal 4*1L wees after onset
a. can do /*ray3 r in rare cases (atypical) renal $iopsyH. &rsing care* ntrition management3 flid monitoring3 can stay at home if
no H%&99. Qilms %mor
,. 'ore common in ,frican ,mericans and males3 diagnosed $y ! years>. 'alignant tmor3 most often on left idneyC. +iagnosis comes from family history of cancer3 history and physical3
locali8ed a$dominal swelling+. %reatment is srgical removal3 chemotherapy3 and radiation7. 07R P
