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    76 views138 pages

    خطاطبة اطفال

    Uploaded by

    Zaid Hamdan

    Copyright:

    © All Rights Reserved
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    of 138
    Petra Emtiaz Lecture Notes Of Pediatrics Dr. Hassan Abd Al-Majeed Alkhatatbah Assisted by Dr. Mohammad Abdel jalil Amro auospuds emeurprarsinssoyoa9, rospurs x opBes autopsy suas “CTBT AWOL smopats waoer sounsaqut Jo sodky sesvoup apo8 Zso¥Ee9) 0no2ytt HOWOL, amass preu0oy2 sy uma0999y vuonendse unnyuosoyy, AN siono1ow: WOON, twogiou jo eoudsyon uaisusy San omospucs ssansip Arovendsoy ‘uno years qwotadojoanqy sorpomol tm seang sa Spoqy S034 oxpumaf ermn00N SBuyuonuos pneU09y, Burpy peresoon, any pes soos se8y Aooyou00n [914° sym9;M09 Jo age L. i tp fee of rege SO NN Ce eT Ce rE EY Poe BED TT foe OP ERE Pee FeO GET SE erm AP ean PR aR Eat CAP Ry ty A ete geqevepry pootemary pay uESseHL/ oMrpag J0 SHON amMDoTT ZONU g poofemry pay WSS SEGRE eaI9 LT0z ry igre: mE? TSOEPES 979600 — AI? # 6TZISESIZ9600 2 eae ich = NP safe Uae og emi — iD Pediatrics PraderwilliVsangeiman syndrome Marfan syndrome Leschmyhan syndrome Williams syndrome HDR syndrome ‘Marplesyrupe disease Tuberous sclerosi Sturge weber syndrome Chapter3 feeding & nutrition Nutvitional needs&breast feeding “Breast milk Vs cow milk Failure to thrive “Kwashiorkor & marasmus diseases Cow milk allergy Vitamin defeciencies Chapter 4 respiratory diseases Causes of stridor bronchiolitis Paeumonia & TB Cystic ibrosisg CFC asthma Food allergy & Anaphylaxis Pediatrics Sudden Infant Death Syndrome (SIDS Chapter 5 nephrology Urinary ‘Tract Infection eral Reflux (VUR) Obstructive Uropathy Glomerulonephritis Henoch-SchoaleinPurpura (HSP) Hemolytic Uremic Syndrome (HUS) Nephrotie Syndrome ‘Congenital nephrotic syndrome(CNS) Polycystic Kidney Disease ‘Chapter 6 Infections & immunization meningitis pertusis Cat seratch Scarlet fever Ecthymagangrenosum Diaper rash diphteria tetanus Infectious mononucleosis ascariasis| Aupemdind puadoysooquom orpedoypp Souayouop 3 yA)uoqMoU Jo asvastp aIBEquIOWETT ‘GAMA )sapuestp PUA: BOA waradowoyy seprostp Bupootet sreaystsonse gar vyosssopeqr'VOS'Gd95'SH) Prot onsjowaHy yaar apse qoqeayN yumatre yous u0 Aouypay jo eraous pwostojorssy SBojoyewoy gE 29rd sepE smi0spuss aB0381C noc ody, auaospuss Bugs) (ayo) eiseidiod soqoUEKoY sesnoutp 009 Tewovoc) snguma yus90u5] ABojorpaws g smdeqy qwaunejdin0) Capoyssseastp anéoo8ey AYE 1199 LAP PaUHAOD 39239P [199 ‘urs eum Jo merA280) Aonapyspounurun 3p wioyss ounurany 1 4aydeq:5 ‘voneersora (anasuoyod~-‘ejaqos'sdumur sajseau)euonaaytt est, ‘ipomt soug soumy 2p euney HOM UI > se Pediatrics ‘Chapter 11 gustrointestinal(D) Gastroenteritis Chronic diarrhea Toddler diarrhea Malabsomption Abetalipoproteinemia Celiac disease Esophageal atresia GERD Pylorie stenosis Duodenal stenosis Hirschsprung disease (Chapter 12 oncology Leukemia Hodgkin lymphoma ‘Non Hodgkin lymphoma ‘Wilms tumor Neuroblastoma Hepatoblastoma ‘Tecticular tumors Retinoblastoma Pediatrics Bone tumors chapter 13 Rheumatology Svenile RA SLE Kawazaki disease Heenochschonleinpurpura(HSP) pou Perthes disease Slipped capil femoral epiphesis Osgood schlater disease scoliosis osteomyelitis Septic arthritis Chap Neural tube defect Hydrocephalus Seizure 14 neurology Febrile seizure Partial generalized seizure Status epilipticus Cerebral palsy Duschenedebecker muscular dystrophy Werding Hoffinann disease poliomyelitis (GakD RTE TNT OM mT i oanoy AL} soy Soe su0, ORE G ; (pisooyp) | uonons fereu010 axnoy) —eunos s0‘(paremnaas pts 7 uous aowara8 Jean | SUOES ON SOO DOT we OT oT Been SOT SHOR SH sino SpaTI oe | (ersouetooroe){poq | ssorséa Pam TY | ays any SUE 2100 Led sod T [aay zi “auuo93n0 eotBojomau ysiom ox aavy (¢-9) azoos eB EA SHAFT “pg Jo SO|MUIUE g PUNE |e LOPE ST “eamony -(4<) -passaudop a1exapoy :(U-+) -passautop azonog :(¢-0) (01-0) 22098 ze3dy (sarDewospuis ssoxysip Aa0yexidsoa st yywop Jo a'9raH Aqeq aamyemaad 10 muaqoxd wt yng) woHDayu st poyod yeeuosu ut leap jo esnes wouIoD Is0/ (syeem. Zp aoyye Lsaatpp) was) ysog(sysom Leasojaq Axvarep)Aqeq aumjewaud 10 uuaaId(@poM oF-LE AeaHep)qeq we], skep gz-p miogy sj popiod peremooy ABojoyeu0aN, Taadeqg, sim seropre ‘ysvaupriqo uy Buzuostod amnoy ‘vorsoy seynsHs9y, spneuupp sodepaysnmeauapoioyuogesy sneuap ordayy Ajo pose vise peuoy SHAM [ENGI ‘vonanaysqo 1p peULIDE|OSEN, asnqe PEED. anydeqa 155] 9g EST 94e4D, (anayhepiosp Aayanse sodKy xoyop uonaony sppiosip sofuedsy usny ssopsostp [wiosnenagy syeydonosoyy Uwonepseisa [eWay omer Pediatrics e 2 Birth Injuries ‘Sub-conjunctival hemorhage->resolve spontaneously. Skull Fracture If linear, no treatment. If depressed, surgery. . Brachial Plexus Palsy (Erb Palsy) (Waiter tip) level of injury isc4,C5, C6 Injury will mostly resolve spontaneously in a few months.in Erb palsy grasp is intaet,could be diaphragmatic paraly associated with ipsilateral Klumple palsyinjury at the levelsC7,C8,Tibaby cannot graspcan be associated with homer syndrome. Clavicular Fracture common birth injury, Unilateral moro reflex> treatment: immobilization of arm and shoulder . Facial Nerve Palsy-> usually after forceps during vaginal delivery. > will improve within weeks. Caput Succedaneum> diffuse edema & swelling of scalp. Crosses suture fine &disappear in2-5 days.no need for treatment Cephalohematoma: is large hematoma of scalp,mmost common in partial boneusually associated with skull fracture,Doesn’t cross suture line; resolve in 2 weeks to 2 Pediatrics 1 month(ao need for treatment).can cause anemia or Jaundice ‘Neonatal findings that don’t need treatment or follow up ‘Lanugo > fine hair of baby (first hair produced by fetal hair follicles) Milia(inclusion cyst)> white papules on nose or palate> resolve spontaneously Salmon pateh> pink vascular macule found on Nuchal area or eyelids. Usually symmetrical (bilateral)-> mostly disappear. Hemangioma-> superficial or macular —_vaseular malformation,red, well demarcated, appear in first 2 months(not at birth). Most common sites: face, scalp. Can expandbutno need for treatment,as it disappear in 4-9 years of age. Mongolian Spot Blue macular, mostly in sacrum->resolve in a few years. Erythema Toxicum-> Yellow-white Papules with red ited base(contain eosinophil), s Neonatal acne due to high maternal androgens,self limited no need for treatment. 5 sewmoreumg yuna ‘Ayumyeuread yo Ampedounay ‘sise1ze90x0) sejnoo ‘oseostp SOD “(AdHd) snoanta Awunsd onseidiedsq quoysisiod §— apnyout —sosnvo —rampo'(%os<)emayse|qourias | svMGysy Oo xoyer dnd Nga 0) vos0s0yNI] (mreZorpaes0qaa op os)yeajays‘yeuax']O (o'moerpses apnjom —asoup'(fomo NGG )solfemFoNE —_eyuaiuoD amo Jo ys y%ST Axoyw apBuys JI ((Poojg poywuo#Axo Suuwojuoa —'(poojq_pareuaAxoap —_SuyAuvo)saueye Z Soy Aru ooH;qUN JeUNOU)CoHe jeoquM ajsmg -ssoueap pur sonjeuuiouqe seg pur ‘someunouge Anema ro/pue peuuag, ‘wuewdoyoAop Joppus Moss Jo woHEpIPY ‘opUOYD JeseH YP JO uysomy ‘sioayop URDHH ‘a9 atp Jo vuIOGo|oD)owOspUcs ofaEYD TIA papoose ‘amonns asa wy afoy‘as eyp Jo wMOgoyO) (on0g ayeped jaay)areped yoy suonmqus pM poreloosse oq Avur yt Ajorer (%Z-[ WY woas)eqMan py (panoseaym yeuo orpouted fq dn Moqjog paon) LoMIN)STHLA IpLA payeaosse sy sya autospuds aUMpDA\ WUC|q uF uastydoxpiodéqunoy 10 eIpLILY (punoseann yeuay op) soremoue Areurmoyuad 30 sso] 3uue=y (HIM payeposse (sampamos)aq Keg yyd/Sey avMoune-pr8g sasvasip J0q}0 TPL woReIDOssE sey Jey} SSuIpUYF peyEUODN soured, (sonoiquue Aq yuounesy paou ‘snas020[ydeys 10 snavoveidaxys Aq wonoasat upjs)umsoyedoan oSpaduy 10 mmoyeuosu emapoposterior 90%(defect in pleuroperitoneal fold) : 2-Morgagn! Hernia> Anterior 10% (defect in space of larry): S&S: present with cyanosis& respiratory distress,Abdomen is seaphoid (Bowel in chest) ‘Treatment for both>Intubation, stabilization 1“& then surgical correction. High mortality can result in pulmonary HTN,pulmonary hypoplasia Note that surgery will not correct or prevent pulmonary hypoplasia. Pediatrics ‘Also suspect diaphragmatic hernia when cyanosis &respiratory distress become worse when bagging baby with face mask 02. Abdominal Wall Defects Bowel protrusion from defect in anterior abdominal wall.include omphalocele& gastroschisis. M>F slightly. Omphalocele Gastroschisis Defect in umbilicus(umbilical cord | Defect is lateral to Midline (Reetus in the center of defect ) usually } muscle) usually on right(usually larger defect than gestroschesis, ___| smaller defect than omphalocele) Covered by membrane orsac | Not covered by sac(more tisk for dehydration) High maternal ages risk fuetor | Ye satermal age is risk factor Associated with other congenital | Rarely or notAssociated with other diseases.(higher mortality) congenital diseases. Both need surgical correction Note thatomphalocele has higher moriality(fiom the associated congenital anomalies) than gastroschesis. If defect is large 1” to do is silastic patch to compress bowel for many days then surgical closure after that. “you 1c1N. mq wmords om portnd aq wo HEH Wi(LA) sus pepusssapon Woy ywaIQYIP SI ssa o[HoeNer ‘pumen‘koueasyyeur “Ayo ammonsr‘Arruayar ‘sno Jo woIsioy : apnypUE uoreox|daz09 ( Axodopryaio) pusasap snoatequods ou yt 16 | ye st Groans “po avad | 940j0q pusasap souneipea a (gO Apsom‘amyeuraid ur 960g ‘ErEMOAH UIA UT %E “JeABE|UN 20 yerWENG 9q Prod “{ wsIprID4o}dAAD) sys} papusdsapay paweorpurenuos st SIOUMON stpuoUT g[-y ye AraBms st qwouNvN ‘squad jo yoodse yerusa uy Suqusdo jemmam : sespedsody steak 7-¢°[ Ye auop Aras 919005 KH (epg, pNTpUE WaT YAM apewWaY 30 yuaHed oyoU FT opr TexaIETEUCD OTA Jo woRe20 [dx ypIAX)posouserp aouo Azo8:ms poou erurey ANU Tes2re1iq 9q pinoo yng‘epys 344x Uy exOU! pue ayeur U1 voUMos o:ou ‘sypemIea snssasoad yuoyed : Bopoueg ‘eqai9y feumnSuy yoourpur 30 9]s901p 4 TeyueFuo9 sepisuog)mstproskpodsy yp p (Kaa8ans dyerpountay roy paau on)sr¥9X ¢-p Ul AisnosuE\UOdS aS0|Z ISO] pray peoMan, “do od NL spaou quand os snaqt paSuojeud s1 uonvayduses do ysod uouro> aso} ornare Pediatrics Newborn screening Screening is test done for all newboms, to identify certain common diseases. Routine screening done for (hypothyroidism, G6PD, phynaylketouria (PKU), galactosemia usually tests done at 2-7 days after delivery(but not preferred in I day.unrcliable).for hypothyroidism screening (preferred at the end of 1" week because maternal TSH in baby serum need 3-5 days to disappear) Phenylketonuria autosomal recessive, is due to defect in phenylalanine hydroxylase enzyme(which convert phenylalanine into tyrosine) result in accumulation of phenylalanine in CNS, infant appeer normal at birth and symptoms —_ appear gradually(normal at birth) that include: mental relardationmicrocephaly, vomiting, growth retardation. seizure, hyperactive movement, eczema,fair hair &skin,musty odor sweet urine, More in blue eyes, fair skin neonates Labs increase phenylalanine, decrease tyrosine ‘Treatment : phenyl alanine free diet, no breast feeding. 10 Pediatrics Galactosemia : autosomal recessive, deficiency in galactose 1 phosphate uridyl transferase enzyme(that convert galactose into glucose) Signs Symptoms (most symptoms are from increased galactitol) direct jaundice, hypoglycemia, seizure . cataract hepatomegaly, vomiting, mental and growth retardation,renal problems. more risk for E.coli sepsis Galactosemia complication may present before birth(galactose from mother) Diagnosisreducing substances in urine, increase G1P ‘Treatmentlactose free diet;no breast feeding Note that lactose free dict ean prevent most of galactosemia compl but less for neurodevelopmental problems. Neonatal jaundice increase production of bil normal) bin. could be physiologi ‘or pathological(abnonmal). Physiological jaundice is seen in most neonates due tol- RBC hemolysis of fetal RBC(less survival than adult RBC)2- immature hepatic conjugation 3-decreased bilirubin excretions- increase enterohepatic circulation(EHC). ul € “ommoxpucs worsnySeN UTA 01 UAL ~¢ (ermroypAokjod sey)ramnou Wa He queguy -> ‘yon -€ ruta Aosyod ~Z (4 st 3801 qunoo"wIoqanout Jo eseasip ondjouey) Amrquedwoom OgVyi0 Uy -T -sayeuoan Ur epmoMTgnqredsy yostpuy eo1ojoused jo sosneD Na-eermaupsoxsr-g1sfo Teoopojoys “1 sisogy sho -9 ‘Kop gf 1 Wes Syensn wisanre AxerTg -§ enuaso}aRTes “puustprommipoddy -¢ “uonoazur You0 f, -2‘SI6d9g-1 :ssarewoou uy (199x1p) eo1punel feorSoyoused Jo sasne SSTUMIHHIDY SNe 9,USBOP OS'HAEL sso19 y.Us90p (9{qNIOs soVeA) wHUFUTGNTGDALY yom Asyed yeaqo209 plovarwoatoyD sf snamo1UA9y Jo ApILOW wouINIOD ISON “sruopoMDy ur payor” St you UIELG oUp UH ware omp ST wASHES teseq 18 10IOUT pacelap ‘sisojompeoau0yo auNZ9s ‘ssOy SurEEIY ‘uomsod oy Zoy pur euoodXyare snsayaqusay Jo smrordunss, eo a (st-0e< PANIPUT FA)smzayomiay asnes pur (qqeyereq wre poo[g ssor9 wed os (aqnfos prdy) eruoUTgnTTEGrody yomPUT ANH 10 VSS, {no HANA Rep PT GE PanTosor Posuojord | pur‘keP gL- gS Aq a8eDI99P OF EIS pawamquy | ep ate OD b> WIqMUNIG Yeo 1p/Bargasearour Areq] (Hep [amp a Ted Aep cL 90 UT U99s-9q PIO | 1,uss0p) 2 Pediatrics 6- Genetic hemolytic anemia (Spherocytosis, elliptocytosis, pyruvate kinase deficiency,G6PD deficiency) 7- Premature baby are higher risk ‘Treatment I-phototherapy for indirect hyperbilirubenimia(start if bilirubin>20-25) Phototherapy not used for direct hyperbilirubinemia (Bronz baby syndrome) happens when you treat neonate with direct hyperbilirubinemia by phototherapy. Complication of phototherapy Skin rash,corneal uleer(eye should be covered),diarrhea, dehydration(from heat) , Bronz baby syndrome(if used for direct) ZExchange transfusion(if bilirubin still increase despite phototherapy) Exchange transfusion decrease neurological comy n of kernicterus but inerease the risk of necrotizing enterocolitis, @EQ) 3- IVIG for Rh/ABO incompat Pediatrie, = Note that sickle cell anemia or thalassemia present at 4months after birth, soare not causes of neonatal jaundice. x" day jaundice usually caused by hemolysis (RW/ABOincompatibilitym.c),spherocytosis.elipiocytols, Pyruvate Kinasedeficiency,G6PD). But biliary atresia (present late>1 week), breast milk jaundiee occur in 2 week) don’t cause 1 day jaundice Breast Feeding Jaundice Breast Milk Jaundice ow calories & dehydration Because of glucoronidase in some ‘Treatment:increase Breast feeding | Treatment: stop breast feeding: sive formula for 1-2 da Taundice occurs in the early | Start at 2nd week dlays(I*week) Indirect/ unconjugated hyperbilirubenimia syndromes L-Criggler Najjar Syndrome defect in glucuronyl transferase (no conjugation) «Type I: more severe (kemicterus is common) «Type 2: mild (kernicterus is uncommon) 2-Gilbert Syndrome » Low glucuronyl transferase * Detected in adolescence (Mild disease) ® No need for treatment a omnpy ‘(Kuaqnd soye)sousosajope 10 yooyss ayi(Ayaqnd suoyoq)ooups Apex “(siwak grcjjooyasaud(smak ¢-])swak ¢ 0} Buryem woy)s2]pPoL (zeo4]-o)rueyu(Aep 97-9 )9yuOoU(snasIN Sy SpIsUT) AFF] [IAT sswonruyec ‘sonwemomqe SX. simoxpt Sour Saxoyar anqwund 1waysisI2g -weoddesip 1,uso0p yey 240 yuo ‘om poe'yng 1 quasexd you yexp ato Afuo ap st xoyay arnyoEIEd IH TON reap wT SOG] —— aANOMTES | RISERS Tia] a HATTAAS a) Raysr Hanon wa saya deni ag) Raya OA ; EST OTIS saxoyar SAN, spe 1 ‘saqeuooU uf SorpUmief sasmed yf asmeD9q OUONELTYOO LON anquurodsopeqdas wonesousd pag 7p woAmoouEasyYSuTNoN J] -sopysoas(fourury 2p uypoquadsyySuyuour ou jt ‘auomLary, samaound VUMAX “myn poole “Heo ‘dn yom sisdag :sysouserq (sap) snosoao}denys g dnoss st aso voUNOD 150}, “sprmoyuureoaoyp ‘oueaqaiom amy Jo aamdns poduojord ‘Qyanyemard -s10)9e) ysNI Auanovodsy Surpaay 200d “Aypiqeyest ‘aanay s0°eransaqjod4y :o1pisads-aou are suoidurds pus sadig (sdup gz-0 Sf potied yeu00N) sisdog feyeuOIN, qwounean soy paou ou ‘PHT MOG © amospudg 10,0%1-z amoxpasg wosuyor mIqNG-T somoupuds eyuromqnamqiaday payeSnfao Ave. suaetpod Pediatrics Development 2-3 months ~>social smile 4 monthsno head lag, laugh, put things in his mouth 5 monthssit with truncal support 6 months rolls over from supi to prone,sits with pelvic support, stranger anxiety.transfer object fom hand to hand. 8 monthssit without support 9 months > sits alone, separation anxiety, creeps/erawls (crawling), says “bye, bye”,pincer grasp 12 months stand alone but walks or3 words wand support, says 2 15 months ~>walks alone, 3 cube tower,eat with spoon with missing 18 months > 10 words, 4 cube tower, begins to rum stiffly draws vertical lines,eat with spoon without missing 2 years runs well, jump,2-3 word sentences(1* sentence), 7 cube tower,draws horizontal lines.age handedness is determined at 2 years Peiatries: = 2.5 years > goes up stairs, 3 years->knows age and sex, copies circle, 10 cube tower 4 years >Hop, stand on one foot, draw square, tell a story 5 years > copies a triangle, knows colors, skip.ties shoes Physical Growth 3 parameters: Weight, length, head circumference Weight At birth: 3 KG Double at 4 months (6KG) ‘Triple at £ year (KG) Height At birth 50 em 75 cmat 1 year > 25 cm increase in the 1" year 87 cin at 2" year 12 em increase in the 2" year Height doubled at 4 years (100 cm) &tripled at 12 years (150 om) Mead Circumference At birth 35. em 12 cm increase at 1" year (47 em) 9 (112% padoyaaap you yyps Bunj)sarqeq aampemaad ur sn090, (OW) Aroede enprsoy jeuopoUNY UI asEaID0q tpuveaumxodsy yasdeyoo mjoaary Buysneo jureyaeyans jo Soustogac aq [IMA axa auoxpuds ssansip Lrorendsox uy -wodo rjoanye ou daay 0} 1ueyrodar, st ay‘worEso8 Jo syoou 4¢ 1 sapsoumnoud z ad} £9 paonposd st ueoEIN “Qseasiq suerquiayy auTTedyy payyes ose)amoxpuds ssaxysyp Axoyeatdsax paejuy 09/08 | st oer OKT 0908] CO oer ‘sqpUOUT g a i ss OET HO RMON a) wal aH ‘suBig [eA TeULON, ‘STPHTOUT OF-0Z FeO PHOSIS | (SqpwOUE 9 |-7) TOW IST | ‘sreaXTT-6 (siquomr 9z-9T) sauTTeD ~ SRD GL] Ciao GD) TORTOUT PHIL Beak [-9 | Gipuow 1-6) wOSDNy TNS (Wig) AiR pIOTES ~~ GnospHoaC) AIRE | wonnued sxuneped oz soseastc] 9TUON|. Jo souasardsse[3 [eIsoS Aqeq au Jo VOHINN (988 sotmod v ye Aysognd yorar oy sueaX p ISI o1p UT sopeur MeN LoIseY Mord sapwutag) XOGedey saonoey apa EMAOID TeoIskyg SUBD. S10} “mq Je ainso[p joURPUOY Ao19;s0d DALY OF [EULAOM St IE Jey TION, ‘wonsazioo years paou pue ae Jo aX | 810}2q JouRIUOY JOLA|UE Jo amso[9 Kwa aumeusord sistsoruASoRTELD “snyeqdoooxpAy‘amorpaig Waog 1999 smspproadqpod apy ¢ joueyu0y sopaNUR Jo eANso]> 267 Jo S9sTeD supuom g]-pL Ww as0]9¢-jauKIUO, LOFIOTY sqpuoM 9-9 3 OS0[9 € famEyUO 101I0}s0q sjounyuog, (sma 9-4)Aep/urs 9 * (squour Q1-9)Sep Ans SI” (smjuonr 9-¢)kepyu3 oz * (sqyuor ¢-9) ut Aeppmiog S| ured ayBpaM ajdurexs soy sywour saye] wep. SuTUOUT ‘ur Tsou osour suvour YoryM SuBEIO|VD9p St AMOI eK SION wo ¢¢ mak ZI IW $$ surg Pediatries ————_—_— more in baby of diabetic mother(DM delays organ maturity)M>Fmore in caesrean section( in normal vaginal delivery cortison increase which help to produce surfactant). ‘Most patient are premature but can occursometimes in term patients sometimesSymptoms: ‘Symptoms startin the first hours afier delivery Tachypnea, cyan isRespiratory _distressEixpiratory gruntingHypoxemia Labs: Hypercapnea(increase CO2)éerespiratory acidosis Diagnosis CX Ray > ground glass appearance,atelectasis. ‘Treatment: Positive pressure ventilation(PEEP) or CPAPto open the alveoliSurfactant(best,definitive treatment). Prevention: Prevention of prematurity Steroids (Dexamethason)given to mother before delivery of premature baby | Pediatrics ‘Transient tachypnea of newborn Is the most common cause of respiratoy distress in newborns Pathophysiologypersisitent pulmonary fluid after delivery Usualy mild and doesn’t cause cyanosis Occur in term or preterm Self limitedpulmonary circul Usually rapid improvement within days, 02 given if hypoxia ‘Necrotizing Enterocolitis (NEC) Is Transmural Intestinal Necrosis(mostly affect terminal ileum and ascending colon). Major risk isPrematurity&low birth weight Other risk factors (polycythemia, enteral feeding especially if rapid(formula but not breast milk as breast milk is protective) blood cathetrisation(exchange transfusion), asphyxia,drugs(theophylline, NSAID),congenital heart disease) transfusion,umbilical artery Sign &Symptoms: Startafter 1* formula or bottie feeding (hypertonic formula) Bloody stool, abdominal distension. 23 st ‘aonendse lumuosour Jo ouaprour aif, aswaisep weop wnmuooout mE 6} snraqN ON PINY Jo UOHE||NSU!YUOTSTYUIOFUUE WEY SION, ZOsuORDINUDA amssazg SANIS0d syuomyEO4y, (oxo ut suoddey uonendse umuogou se qjouag ou YsNoMpTE)AraAtop 2oU0 UOHoNskeaTY woneqnra ssansip [e9y o1ayn uy Jo woRuaAaud pAzoarfop way ysod Jo LORMOADIY smonuaaad owneug suoneidsy © xeuompoumaug © NIH Aioue Sreuoung © nda wderyderp ry‘ nenTgur Suny Ayowed AXD -sisouBe1q, 2a erxodsy ‘ vondayony, sswiordakg ‘SOTUMMBIPAYOS! ULI} ISOgSSINSTP [BIA :s10}98q] ASR ssanstp Atorendsox asne9 uo YoRYM Ox9I(] UT SsONSTCE PeIOG Jo yar v se ssed uMTUOSOYA, wopestdsy wnmos3 4 ‘AN Jo su aup asvarsap Surpaoy MO]S TEI ON, (wonesoyied posto p1)Aro3mg(onoIqHayaqn DNUONSAaLIOD ayAjoNssja2gpINy Ayaupaay pus doyg) AwomeadL noneroprad weaur jou saop siyeunsayar storeunoug, ermadoyAsoquionp‘uiaa jeuod uy seBemarpdra [yea jeunmopgeMonesopted Jo sudig uomeroprodeg sisox00ut Jomog “(too af St euDIZeq ow)sisdas suonestdu0 sisopiae s1oqejounayayeld astassep gas aseanDapsqeT (ermouSomped st fJex eos} ‘Mm ae ) speupsayuy eyuoumnoud smoys Aerx jeurmopay :sisouseig sue Pediatries Meconium ileus (baby doesn’t pass stool by 24-48 hours after delivery. Impaction of meconium leads to intestinal obstruction “Most common cause iseystic fibrosis(I" presentation of cystic fibrosis is meconium ileus) ‘May be idiopathic or related to hirshsprung disease ‘Mostly in lower ileum, S&SAbdominal distension, vomiting ‘Treatment: Gastrografin enema Neonatal Seizure Causes: 1 -Hypoxie Ischemic Encephalopathy> most common cause 2-Intraventricularor intracranial Hemorthage 3-Hypocaleemia, Hypoglycemia, Hypomagnesemia,hypo or hypernatremia, 4-Vitamin B6 deficiency (pyridoxine)the only vitamin deficiency that can cause neonatal seizure 26 ‘Pediateies: 5-Kemicterus(in pathological indirect hyperbilirubenemia) 6-Lidocaine toxicity(local anaesthesia) 7-Torch infection or meningitis or encephalitis, 8-Neurocutanous disorders(tuberous sclerosis) 9-Maternal drug abuse 10-Some Inbom error of metabolism disorers. Note that Febrile seinure is not a cause of neonatal seizure. Presence of hypoxia or hypoglycemia are bad prognostic signs ‘Types of neonatal seizure L-subtle seizure(m.c. type)present with abnormal eye or mouth movement(like blinking, staring.eye deviation or tongue movement) pedaling movement, apnea, tonic posture of the limbs. 2-myoclonic3-generalized tonic clonie4-focalS- multifocal Treatment:treat the cause In attack of seizure 1 give benzodiazepine (diazepamlorazepam) which is short acting but rapid onsetthen add phenytoin,or phenobarbital(long acting). 27 6 at] aM UT Teel ASH WG Ted asea.ouy efjoqny jeUasUOD ‘(won TUsuEN JRO 20y St oMuONSAFUIAT stRAM), HA\oIsouNTD el WE WORMmsueR AF OF _FSTs"UONNUL Areunsd suvawd) + WBpeHPqN yerUsSu0> soy yuouVON ON (equado Kooquraxp‘uonepze}2z Teqwoundyoudaoororur fpeBowouspdsoveday (Yad sy3"m)aseastp hivay'ssaujeap oureyno)amospuds —eTjoqna [eye TOD “wonagut [exAy TeaUaB woo asce9 weo(eyty JOMOUL UT UOOaUT vIjogny ,.1) eyfeqns Around HONSUEAT, suroydunts OY] any pre 20 opEMOdmAse AWW "RAIN og — una ousna “epALEETD ‘S900 ‘suafoxcoucu: —euasy'sa —apajour(Ksaagap — Boumnpjuom>eyu wanpredessuteun weg yBoonp 798 Aqeq wes ye suonDoyUL peUAHIN -soieuiowe peynaSoo asue9 Nop ASH'Y ATH 05 (reto>eydsuen you ing (429m g¢ saYE ApsOM) sno20aHeqONIDY jeURVENORS jt vein wy sncoo una)jeaooe|ésmes ou pu (aBetOwaY frUSIEMOR)POO;G Tsp 9 UA HT pooyg euBEEE uoyM(AOANJop FEI) tunymdenuy mooo Sijnsn are uoplasten [ee} ACH 10 YORI ATH ‘Gasourm)aSHAZA‘SINaSS TIOGA AWO ‘sysouisejdoxoy —opnjour—(jeyusonjdsuen)suonsoym = oma seeped pence geese perrremeenssi ze (comsedenisonsop Fonp 2018) ASHE ‘el YF oueTSqnUGERoME .¢ uP ySoMsysouNE|doxO? Jo VONTUsUEL), ‘yunue'sorpunet asne> wea HYOL 0m ye OAMIMSAL -seqjeuoue joa8u0o asass,uop Sipensn Gre sTAOARy ASH so] Suu femonosuos opsue# wou 0-H tN S{(HOYOL 4) AWD misepdoxory AWD ayp)) s2mI0Ur UL SuONDJAL YEE ISOHE Gesuypp)stsomseydoxor m(ejnoenuaatsod) WD Bt VoRTaLoTED EG, ‘snjeqdoooupAgap uonuoyioypo eq asm wD AWD * sIsoMSEydOxO], (Sorwmoue pexuafiuos estes 2,uop s2N9WI FW NORA HIUOI)NAISeMT IS] Ut uaddey HOVOL {J} a20ur aye soxyewous Jeyusuos os 1aSSUNEN IST UI Ms00 sIsoUOHOUEEIO SOON “soljeumoue [e.aj [PMIONNS asmred 1,UsF0q, -sdospay yer SUNUTUNY HOU 7p ENMMITE dAJoMOY osTeD TED VORSOFUT [ey (exSqempre im yser oaqo peddes) asvostp UY asnes ues 10 speMo;dustse Apsour sqmonoayuy zoMOUL (snara VN) 61 sustaoased uugqyanied st yusuneary, (soarys 29q¥s ‘250u apppes 10 Uy uopEZLEIMIsEA jeOUsOD"HIV—) ToSUTYDINA)SAEDK Z< HEY —-— sumpog Pediatries Chapter 2 Genetic diseases Autosomal recessive> 2 abnormal gene to develop disease Carrier(has 1 abnormal gene) is asymptomatic Af male carrier mazried female carrier there childrens will be 25% > Normal 50% > Carrier 15% > disease ‘Examples: cystic fibrosis ‘Thalasemia Sickle Cell. Anemia Infant polycystic kidney disease. Autosomal Dominant> 1 abnormal gene is enough to develop disease ‘No carrier( either normal or diseased). Discased patient either has 1 abnormal geneheterozygous),or 2 abnormal genes(homozygous) iano. Pediatrie = If affected heterozygous married normal female there childrens will be 50% Normal , 50% > disease . But if homozygous married normal couple all ther childrens will have the disease Examples: Von-Willbrand Factor disease, Marfan Syndrome Achondrop! osteogenesis imperfect, Neurofibromatosis ‘Tuberous Sclerosis Adult Type Polycystic Kidney disease. autosomal dominant diseases can happens in childrens of normal parents(new somatic mutation) Note that autosomal recessive or dominant diseases affect male and females equally. X-Linked Recessive Mostly afifccts males(gct the disease from there carrier mother). ‘Females usuallycarriers Diseased female are rare (because it need two abnormal ‘genes),but males are XY(have only one X),so more affected. ‘Tumer Syndrome female(45 XO) at more risk of developing X- Linked Recessive diseases. Kleinfilter syndrome male(47 XXY)are at less riskof developing X-Linked Recessive diseases. 35 (enduoy aBmo/)erssofForseuH904 ,.z PUL | Woosiog coeds Big sive ves mor] ‘ omssiy peagadyeg premdy * ploy jeurueardg * eruojodéy + qpmour usdg Sndiooo seg “Ajeydooorsypy‘amyEs HOS ss0amquay ae jeusoyeur pasvasouy si su rofepyrouosomosyo Lp aaey sproned owospacs umop [[e JOU Ing ySoUN Og “(1 Z:PTXX 10 AX OF SI aso SI wr odkyoxmeyyyT aMtosourozyp UayO “suIOsoMOsYD J9Y)Ou OF poysene St 1z atuosomorya Jo uu Zuo] 2xy : owHOSOWIOIYD Bu 10 “MosoWONPos! “uoHRDO SUE WEIMOSOqON -f (jewuou st rey soxgo axp pur 17 suFosoMOSyD yo Adoo wnxa oar sffoo amp JO Jey) %Z sTeSOWrT (¢6)uopesnia wonsunfsyp-aow wosy WOUND ISOA-T ‘umop WL sonata, (1z atosomosyp Jo saxdoo ¢ seq)qz Autos, (Iz Amosuy /XX JO AX auosowosyD Ly) aurospucg uasog sSuerpea crecotrereernemreieernn ection vung Arepyapdarex, vanes Aion, (soyeur uy Aquo) paymy TA osvosTp amp aanty [Ea srordnep sty pe"Teuou ale Suos Sty [|B [PUUOU sf saqjOU puE paroAYe st JOURS IT sutoputs Hodty Jo saseo asopauroxpudg x o1/Serysioyou umstsax C] MUMIA :soduexy, poroayge Syaranas axour ‘ore so[our jnq oTeUIRY Jo ofeur aye are EMEMNINOP PIxWI-X (songanep Sty 01 X aAIBsuos sry Or A aAKB ayeur asnesag) sxoETED 299. THEM soUYNEP sty [JeTeULION oq TIA sos sty [Te Uorp'DpeUay Teun0u poueMr asvasip aaissaoar poyUT] X WIM OIA amospukg ueyAN ypsoT'(comaq) vMauNgo;semmese poyuy-x‘ssoupayg, ojos w9018 partqaso'a 10 Vy emmydourey ‘Aqdonsip aeinasnat aay20gq ‘AydoxysXp aejnasnur auoyong:so|dumxg 2 Pediatrics Late fontanell closure, mild),Short neck, inferti Single Simian crease(single transverse line on the palm ofthe inodactyly,mental_retardation(most y(all males and most of females) hand),Down syndrome are at imerease risk ofHearing loss,congenital Cardiac disease( most common is endocardiac cushion defect), GI problems(Duodenal atresia, Hirsh sprung disease)Hypothyroidism,More risk for Acute Lymphocytic Leukemia(ALL), Early on-set Alzheimer most common cause of death in down syndrome is trauma related to road accidents. Note that normal persons usually have 3 palmar creases,in down syndrome usually has single palmar crease (not pathognomie for down)as it can be seen in normal persons also. Down syndrome has Atlantoaxial instability(CI-C2) in 10-20%.s0 preoperatively do lateral neck XRAY. ‘Trisomy 18/ Edward Syndrome(47 XY or XX) 3. copies of chromosome 18. Features Mental retardation, Low set ears,Microcephaly, ‘Micrognathia(small chin), Clenched hand.Rocker bottom deformity,Hammer toe,Omphalocele ‘Trisomy 13/ Patau Syndrome Pediatrie, Woloprosencaphaly, Mental retardation, Mierocephaly, microphthalmia Cleft lip, cleft palate,Polydactyly KleinFilter Syndrome (XXY) ‘Nondisjunction mut Tall stature, Mental retardation, Azospermia, Infertility Gynecomastia,No secondary sexual characteristics FSH high(primary testicular failure). Kleinfilter are at increased risk of breast cancer,but has lower risk of X-Linked recessive diseases Klinfeilter syndrome is not related to maternal age(actualy increase patemal age is a risk factor), __.. Turner Syndrome 45 (X0) Female patient with only 1 X chromosomeyoung maternal age is risk factor. Features Short stature, Webbed neck, cubitus valgus,Gonadal dysgenesisor atrophic ovariesinfertility with primary ovarian failure,High FSH,Supernumerary nipple and wide spaced.No breasts or secondary sexual characteristics,lymphedema(40%),eystic hygroma 39 SMZDS ‘WOREpTADT [ENTS sigeiey awndorddou yo wsixorg uistpeuofodéyy WoRYpNS! [wiudaT SISAg TGS [jewiaywal) ¢] SuosoMION| | — waxaped) Sj suiOsoMIONTD awosputs uvujsuy | owioxpukg mas roperg. nds ayy founton seq Aqfensn tg (2e0peydmo s1 ysom)uoNEIIOSSe 1 (uopemen ToneAmpouH St oW)]T aMOsoMo.yD UO St UONeNUT snaUAH(punoseNMyeUST fq dx moyoy spaar ay ua Aydousadéyyuroy TPM PIN 998 NOX ji)LOuME SULA, FOF SRY aseox0Ur TV Ayoyouos2ss(omaaGsodGry pywouynsupadty) —eisediodéyy aoe BNR Agog aBnptydossodéyy puazpoyssopSos99yonuosos20,y amospudg ame MTEparA-TPEANIOET a tt ov (SurdQoArey jou)sysAyeue YN S} Sisouseicqueds: ayn WwMON sey aworpuds Xx oTTay YA JoReT wsyNe 30 (upjgod puoraryeq oW)GHCV)swe{gord [exOLARGEET (wustprqaz0 ~oxsem) sysay aie] “siea ofsey] ‘Aqeydacorey"uoEpATyaA Jeqmaur samyeay aurosoMoIys-X WO HH Jo woutdes poreadoy s1 wolgosd onouay “XXOF 10 AXOP wUHOU sf SmEKo most common cause of death Lesch Nyhan Syndrome X-Linked recessive Defect in purin metabolism (HPRT Enzyme) result in Excess uric acid Signs &Symptoms Choreoathetosis , Spasticity, Renal Calculi (stone) , Self mutilation Gouty arthritis , Delayed motor development. sy ssoumma uresq x0 Ystr axowi(Xpoq wo uoYsay pawawidodAyy) ammsey! JeaT-ISy saanzjas Bursnes (894M SN) TORE! |HI WEI queUTIOC TeutOsoMy (sa)ssouappg snoxeqny-7 cuouruos sso] are sSunpuy UIs sso] Supswapy GA euNOMMON sysMoDE yesDyE NG st aryeay teu ZC oMosoMosgoUO HOHE MU ZAN ZOGAT, soum SAME, ‘BrmayMay “ewOyLoWorOAY ‘smZIPg SBuIpUY AO JOuNY SND WM parersosse (womuo9 som) emoMts 2nd suoIsay [eUINaUT 2p Azole ‘g give FFP). Breast milk is low in Vitamin K, Vitamin D, TronInfant Nutrient NeedsEnergy>3 times more than adult per KG(85 kcal/kg). Carbohydrate->5 gavKG/daylron> supplement (Iron fortified formula) after 4-6 months needs 10-15 mg/day Vitamin Dat birth 400 TU/day Vitamin K> given routinely at birth (IM) Water H20> breast milk or formula contains 90% water, so no need for water if infant is fed by breast feeding only Recommended infant feeding source in 1" 6 months is only from breast feeding, Solid food is added after 6 months. 47 oF (ompor'sprozis “urfoXowna ]‘epooruayduraxory earjoqeysumyae UME T ‘satsouddnsounmmmy'eydonny Sderarowoy (wxuusoxyoday Teyenoat asneo ueo)sitafe onmaoA|Bodkq ywo'sprosdyanue) sBuc-< BumuoayyAuayd “eResO ETE) asnge aounsqns-£ spoueg 1searg-Z (qsearq wo woIss] 1) ASH “AGH'AID “aLeanee ‘AJH)suonsayar-T Suppoog wseaxrg 105 suoyeorpurexyu0D yh omngeur UeTA IRF WP SoreIPAYOseD ssa] Ing “Apoqnuy “ELM. ‘spesougm s1our “mayosd axour EO sep Z ,T)uMSo|OD (ASH'AWD ‘AIH)Aq29 0} suopoayar JeusayU JO woONMUsuEN-¢201;punel FA yseasq JO SUZ (aroquou Jo aseasip: o1Feyuowy)Kouryap Y URORTA JO 4ST Suypagy seauq Jo saBeyueapEsI, (Gs0] ryto%4 prdes‘snzayn Jo uoRNfoAU! pidesyyysea Aoueufoded 0} Sronooa1 yemiawur pidiyj-zisoo smo] HOW souperpa Jeremeenenrceenenmesonrennatt 8b -wonouny o4nyu809 sonaq pue (OY) qwoHonb ywaFyjeIU 19H -S (ennayney emoydurdy)so1oueud rem pooupyrys awos osez09p-p sasvosip TE[NOSBAOIPILD S89]-E(TPRLIN $89]-ZAsIqo JO ASU $89I-] oStyueape wi19) 3u0] (QAN)sHTOI0Ia}ua ZuIZHoIDa9U Jo ASH SS9]-E uopoayuT sso| “(eut9Z99°KBr—qIe ‘speunop) asvastp oqdore “sso"JSuypaaig 1 S807] ‘POULEIP S97] (Aqunurany) aya aanooiorg-z seqnow ayy Ypss UORE|AE TeuoHOUID /je}oosoyASg-] syueyuy ‘Suqpaay yseaug Jo sodejueapy “AED uf UE O-yShEP Z pT UE E-Caom)osuvyp soderp-p Aepy/y-E1aaUID AOU! JBMO-E Guevodun ysouared pyS1omoqddtu a10s ou-z, -ssouny 1sea19 Jo souexvaddesiq-1 (@uypagy isea1q oy anpayps yous ou) axe Suppaay ysearq Jua!IUJe Jo sudIS yp 29ye Aforerpourum poweys aq Poys Surpaey ysearg ree Pediatrics G-post partum psychosis if the women takes medication(lithium, valproic acid,..) HAV,HCV,Mastitis>are not a contraindication for breast feeding. HBV is not contraindication if the baby took HBIG& the I* dose vaccine. HCV usually not excreted in milk but if nipple cracked(contraindicated) Note that warfarin is contraindicated in pregnancy but not in breast feeding. ‘Breast milk (low iron, low | Cow Wii (Nido} vit, tow vit D calories 70k cal/100 ml 70k cal/100m1 Protein 1 S96(most whey proein) | 3.5% (most casein Carbohydrate | 6.5-7%most is lactose 4.5% (most is Iactose) Fat ‘Same (LOFA) ‘Same (MCFA) Minerals Low Iron but better Low-lron(poor absorbed absorption) Solute Less sodium Higher sodium, Don’t give cow milk until one year of age Honeyalso given after 1 year(risk of botulism if given before 1 year) LCEA > light chain fatty acid 50 Pediatrics MCFEA Medium chain fatty acid At 46 months >give iron fortified formula(as body stores of iron is sufficient for 4-6 mothsSolid food after 6 ronths(only breast feeding in 1 6 months) ‘Major energy in breast milk is from fat. Whey protein is solublecasein prot is insoluble(more risk of allergy). ‘Dominant protcin in breast milk is whey(whey70¥%casein 30%) In cow milk dominant protein is casein(casein 80%whey 20%) Cesein protein is insoluble and can cause allergy, but whey protein is soluble. Jn breast milk whey protein is in the form of lactoalbumin,but in cow milk whey protein in the form of lactoglobin ‘Minimum daily need of fat to prevent essential fatty acid deficiency is 0.5 mg/kg/d cow milk or honey only given after 1 year ‘Cow milk-> can cause iron deficiencyanemia Goat milk > can cause folic acid deficiency anemia LLY aaa “Bap9914 19 ‘uonuaisip jeuopqe Supra ‘voxpTEI <(mrordurds sm) aypads wom pue apy ae stroyduris A@za1y@ oonpoxd uso >]fuH M09 Ur MIDSED UIDIO1g Ao] e YUI-02, (emdind “wopoayut ) suoneysayrmear petazap ro>pOTysE Ay, ‘avy 919498 ssaq Inq mo90 UPD vINaps “UoHEIPAYaptErKax4d ‘ormempodsy) amiesodmier Spoq jensnun'suonoayuy IuoLNITy uoysuaistp PoURUOPAY RY SHosUMNOGNS JO SSO] “BuNsEK ISA SPS apeyay HOE MOT asvastp SMUISEIEY-Z ‘erxouowe “uonua}sip jeaTusopge “CaArT aq Jo woRENTUT Aney)KyeFowordoy'suonserME quOLMNDyY sqqoay Jo sso “sey asmedg < seumacl “ewrapyaxan0s S775 -dunpooy yseaug Jo Sarmeam 1aIpy 21990, anqeray arexpAqogreo ySty pue urszord Mor] IME (eyF UE {B1ou9 peaMON)ayEWUT SaLsOPED TEMON, asuastC] 10L014SEAKSI-T MOLLY NUyEM Jo saszasi¢l souepe esc eee reat zw (effe zexp azogaq pasn jou)s1e9k Zoe roye pours st aos 20 yUOW OF (KUALA xePUE sseUr ADO (qryasn you)yeuni0u swodde Aer onex Bruin uoMUNUTeME TONS UE Ing, ones 1yBouAusm S| woRLAMUyEAE ayn9e OF IOWOIPET YY YAOI yg (asvyoap Teides Teme jou Iq LA asne9 uv saseasip HEAY yeNUeTUOD SOP oxi 0} ame asta 1,Uop SOSeaSIP AINE AEH BION ‘suopaapur yamos23-6 ‘ioprostp onus 10 jeurosowo3yo “SYD AI-L(Kiowndsex‘Sroyeaydsox yeuar ‘De1pres) oseosip oruomg-9A8z0T[@ 10 fouoroyspounuam-cuustpromsipodsH-p (sisouqy: onsfo ‘oseasip ovyje0) uondlosqepeyy-¢ ALM 0} ape Jo 9°9"mr ayy st yoojSou [euonENN-zasnqe Jo uoNeALdap jEUONOU-| (Gesnws uowmios jsour amp ame Zp [HOqummu)sasmE (erw)onteB10 wou 10(94¢>)o4ueBI0 aq pnd sasne aypuaoiod gg>3yiom se pauyacL (LL GATE OL PUNTIVA eee eee eee _—_________ nepea Pediatries ‘Dermatology(2™ m.c symptom) skin rash, atopic dermatitis Respiratory> wheezing Symptoms start early after exposure to cow milk\ ‘Treatment:stop cow milk & give other formulapossible formula options L-Soy based formula(but 50% of cow allergy will develop allergy to soy based formula 2easein hydrolysate formula(hydrolysate break casein protein)used is no response to soya based formula 3-amino acid formula(bestlowest risk of allergy of all formulas) used ifno response to casein hydrolysate. Response to treatment usually need 2-3 days (not immediate) Vitamin Deficiency Vit A> night — blindness (Xerophthamia), anemia,keratosis,decrease growth and mental function(but don’t cause microcephaly)Vit D> Rickets Vit KP bleeding Vit C> scurvy (gum bleeding, bruises) | Pediatries ——— Vit Bl(Thiamine)>Beriberi, (peripheral neuritis, Wemicke encephalopathy with (wet beriberiJor__—_without(dry beriberi)Heart failure Vit B3(Niacin)>pellagra (4D), diarrhea, dermatitis, dementia, death Vit B6 (Pyridoxin) convulsion in neonate, Neuropathy, Dermatitis Notes ‘Vitamins KEDA are called lipid soluble vitamins (decrease absorbtion in fat malabsorbtion). Vitamins B Care called water soluble vitan malabsorption ot affected in fat Vitamin B12 is the only vitamin that is absorbed in the terminal ileum. Vitamin b12 source is from animal sources(so strict vegetarian is risk factor for deficiency). Body has sulficien store vitamin b12 for 3-4 years(so vitamin b12 ofeciency doesn’tpresent in infancy) Increase in vitamin C can cause oxalurea(oxalosis). $5 (spmppucaqoaysenoaSadzepdnos -(esoosqe eypistoptiod “proskqy padsyyua Ssxoumy — eoSuKreyeuomydptemeps — Aeane'spreyoesy ‘spmojaido'dnoss)apryouyropins Jo. sasneo JO ‘Apoq, uBjouoy passnum st SURIPTIYD UF sszosqe Tuny Jo O° yom jou ssnqpuosq sade 14 f SySe]ODaVE IO a}fs UOUTIOD ySoU PU (GK [oquNyUT ur xuxre|)sngouorg yysTY Sy WazpyE uy ays aru “soup omios sisvyoaraq® MoYs Sour JO yeOAION ATTENSTAK Adoosoypuoag £q st wounean pure stsouseICy sozaayM'ssansip Azovendsox opus Sumsn00 “Buryooyp anoeg39s gnuad st Apoq wBtoz0y au IRE gh yf WOW Sompog USIO10T ‘af 10 stpUOU! UT aAfosar KqpeNsTLAUNEAL, Adoosoysuosgstsousei Jopins Jo o'o"UL,,esisdyexed ps09 190A Aafmspraunvayy, sued 9s AdoosoBudiey Kq posousa—p “JOS JO 9° ZN Sf “TEHUABUOD stsouays as0f3qns [e}U93U0D *fuafans spaou axoao {ji AxoBis soy paou ou pue ae yy oaordust WOIPIEID $a5 st 9-9-mu(sep gz-9)s2yEH0Iu equoumand Jo sosne) sqjuour 9 a10yaq ary emoumaud i Pediatrie. = Active TB is infectious,symptomatic, Active TB cause upper lobe cavitation,diagnosed by culture or stain of sputum or gasitic aspirate. Extrapulmonary & milliary TB are more common in childrens than adult Diagnosis best by isolation of bacteria from sputum(in old childrens or adults) or gastric aspirates(young childrens) ‘But negative culture doesn’t exclude TB ‘Treatmentlatent TB INH for 9 monthsactive TB at least 6 months treatment(with 4 anti TB in 1* 2 months and 2 in the last 4 months) CNS or bone TB longer duration treatment Cystic Fibrosis Autosomal recessive disease Cystic fibrosis gene located on chromosome 7 (CFTR) More than100 mutation on CFTR gene (DNA testing is 90% sensitive) ‘Most common mutation in CFTR gene is F 508 ‘Membranes are unable to secrete CL Failure to clear mucus secretion 2 Pediatries Signs &Symptoms: CF primarly affect lung,pancrease Gi fiver,genitourinary But heart &CNS are not primarily affected, Failure to pass meconium> 1* sign Respiratory failure to clear mucus © Bronchitis © Recurrent respiratory infection © Nasal polyp Pancreas-> pancreatic insufficiency Malabsorption?stcatorrhealipid soluble Vitamin defi DEK) Failure to thriveRectal prolapseappetite is good Hepatobiliary> circhosis, Gall stones Genitourinary Obstruction of vas deference-> Azoospenmia> infertility Sweat gland-> salty taste of skin Diagnosis: Sweat chloride test-> bestDiagnosis IF CL-> 60 meq/l. 6B Bump zoxpo apnjaxo 04 posn ing ansouseyp 1ON AX “autjoqoempour 10 astoraxa 29ye %ST< | Ae Poseaz0¢) aso oBuaypeqo UoySepanisa aBuaqqeqD astouoxAsIS 1HIO, tl< ©} TAAAPseauU QstUOse Zq) JoWEPOYoUCI SUN WOYS (2608) 80> DAM/TARL Gsquode zq Sunoe noys Aq pamorloy}psepueys pjoa(asa wonouny Areuournd)80% fees ese | _2/mondi cecal Mild persistent >or=to0 | FEVI>80% | month | | Moderate >V/week | FEV1 60-80% “severe | >V/d Frequent | FEV1, <60% Asthma Medication 1-Quick-Relief Medication(used in acute attack to abort it) Short acting B2 agonist (Salbutamol, terbutaline, Albuteral) Rapid onsetLasts for 4-6 hoursDrug of choice for exercise induced asthma Short acting b2 agonist used in all classes of asthma. Short acting Anticholinergic( Ipratropium Bromide) Less potent than B2 agonist Systemic Glucocorticoid 2-Long Term Controller Medication(used as maintaince or prophylaxis but not in acute attack) Inhaled Cortisol. (side effect oral thrush,candida infection, dysphonia(due to vocal cord myopathy) 65 Pediatrics Controller medications(inhaled cortison) started when symptoms>2/week(mild or more)but not in intermittent. Cromoglycate (Cromolyn sodium)less, effective than inhaled cortison but also less side effectaltemative to inhaled cortison Alternative Long acting B2 agonist(Salmeterol & Formoterol)Given every 12 hours ‘Long acting B2 agonist used in moderate or sever asthma. Leukotrienes antagonist (Zileuton, Zaficlukast, Montelukast Systemic Steroid (Quick & long term) ‘Theophylline(phosph causing bronchial side effects like arrhythmia, HTN, seizure) esterase inhibitor,increase | CAMP tation)Rarely used nowadays because of 6 «9 ‘onovor opetpauran(sanup At 10 ysesjuOD oyL)Udsu9qTe Poroefey ormpedorpy’ Suns yoosuy “ yseHUOD * wORTPOIPOH asne9 ouIUIOD SOMIT} SI POO sasneg uojsuayodsH 2B vUI9pe [waRUAsw] asneD ueD ye HOHOLar o1BzaI]e a12A9§ Sf stxe[sqdeay srrepsydeus 205 surydomdy SBraqje sasneo gem poy dorgymaumywa4T, AB1o|Te poog voUHIOD soy 189, UPYSSISOUBEIG, norsuajodsyy “orumpAqzexejnoseaorpzey ‘voqLOUTyyY “euNyS Suyaoymsrorendsay ‘wed jeurmopqy “Sunnuoa ‘eaqsrerqTD snnecnag odory (aountos ysomyemapaorsury pur ew], smoydunss a3] paseassuy) AyApysuassoddy J ay st KB12]y AB1o]Te pooy & asneo ued poo} Auy sprepiqdeue so asne9 uouruos sont ay st ABs9]Te poo ABr9qTV Pood, SS rr sexo smaps(osed se og)sezsans om osTY-WEN 30 TEUON 9 TF HE AMO GEER 7D oH os (cuedsoqouon siojduoa)eanpen SqUSIEN oF] E370 Ho HEA oneuoodq) sof Aqensn ZOQ YoUHY wUNSE TeIOU MH YeMNayONT prumpsyzre “worsumoddyozi< 98Inq%OE> LAAISHUOD > 20d soposmut Aaossa008 JO. 9% aq uO UT soUTTUES BPEL or ANEGEUL (stsopjoe Asoyexndsaa)y2ry 20 yeusi0u st ZO (sezaoq ON) 38919 IETS eunyysy Huymayeasy.y ayry] 12A9g Jo sug sinoy 9 b apruosgy wmnidonesdy AL10 Od prozaysoon03* n oz b yswose zq Tuyoe poys preyMy “ZO Woneqnsoex PUNTSY Jo TuOUIOZoUR PY ‘mopeqiooexo eunyse aonpur ues Ieasjaroxa ‘suaqod snp ‘topo Buons “we Aig ‘pjoo Bapjoug, Suogeqiaa¥x9 wRUN}SE Jo 9sNED WORD ysou! UONDIFU [EIA uonequasnxe eUSY —-— sureipeg Pediatrics Oral allergendelayed (minutes to 2 hours) ‘Treatment Epinephrine(drug of choice) AntihistamineCorticosteroid Short acting B2 agonistO2IV fluid Allergic Rhinitis Nasal Congestion & Rhinorthea without upper respiratory infection ‘Treatmentantihistamine(drug of choice) Sudden Infant Death Syndrome (SIDS) Sudden death of infant, unexplained by history, unexplained by post-mortem examination Risk factor Low social class, African Highest at 2-4 months of age ‘More in winter, Male>female,Short interpregnancy interval Less prenatal care, Low-birth weightMaternal smoking & post natal smoking , Prone-position, sleepOverheating Prevention-> supine sleep 70 eiatyieg = Chapter Nephrology ‘Urinary Tract Infection Most common bacteria is E. Coli Most common cause of abdominal pain in children Most common cause of hematuria in childrens ‘Types = Cystitis (inflammation of bladder) no fever * Pyclonephritis> inflammation of kidneys, abdominal or flank pain, fever, nausea, vomiting or non-specific symptoms * Asymptomatic Bacteriurea-> urine culture (100,000 Bactria), without symptoms Most common in girls (short urethra) Risk Factors = Girlomales * Uncitcumcised mates * Vesicoureteral reflux (VUR) n a“ CLLO atgag Auy“oqeuiay Ut Ln ¢ “eeu oF .N 2uO) DADA 105 woHeDEpUL (risa) aseasip jeuss ofms pugkwpedamdayy ‘Kouppy jo Suuxeag -suoneatdurocy (wonejuasasd uomuros ysour )smutydouoyoAd 0 asods1paid (Gappere ‘omafomayy woKOnNsqo) Arepuosas 10 Armond 2q pinoD “LA awaumoar sj wordurss wouru0> 160} Aoupoy 03 r9pprjq woy aut Jo Ao. 9eq [ULONGY Qt) xnpox 1219910091594 -yuounean 104 past ou)souesmssHad ‘S505 hq pasnes ‘Jeusou sp sisdqeue oun pur‘euns

    sjuamyeaa “onunnuny osexo}s2 aydooynay st sisKpouw aun ur 1.0 Joy Suypay oproods ysour ey, (pp anompes)qe| 8m) 0s Aforetparoun puss 2q pmoys ojdumes our) (e1dures weajo ssou)ojdures oigndesdns ur yuroyTUdis st ywosoud eus}eq Auy ajdums suum soroqno sojoy ut aBOT HUBS s1 wIIAI2eq N00 ‘dures poploa ureonns prur ut yoru st BLIDIIEG OGODOT< 160g) s1qndwdns 10 soy>yeO sAojog Woy sup; TeUS wE reflux to Mid ureter> no dilatation Grade II> reflux to renal pelvis > no dilatation Grade II Dilatation Grade IV > mild torsion Grade V > Severe torsion Diagnosis: VCUG is the best DMSA Scan best to scerenal scarring& renal function Scarring is higher with higher grades Grade I & I > resolve by 6-7 years Grade V -> rarely resolve, need surgery (ureteric re- implantation) ‘Treatment: Antibiotic Prophylaxis(to prevent UTIas sterile reflux is not harmful to the kidney) Surgery if failure to resolve grade FV or V. m Pedlatrieg = Obstructive Uropathy Obstruction of urinary outflow Is the most common cause of chronic renal failure in childrens<5 years. ‘Most common cause is posterior urethral valve. Clinical symptoms Secondary VUR&Hydronephrosis Pyelonephritis; weak urinary symptoms,cen cause renal failure if not treated. Note that Hydronephrosisis the most common cause of palpable abdominal mass in newbom. Causes: m.c.c is posteriorurethral valve. Posterior Urethral Valve Most common cause of severe obstruction uropathy in children Usually affect boys Can lead to ESRD (End Stage Renal Disease) Diagnosis: VCUG (Voiding cystourethrogram) ‘Treatment: Transurethral Destruction (surgery) "6 ue (sisemip ‘uonamysor ummpog)uorsuayaday onu0g skep QT 403 (uysyuad) snorqnuy yuounyeaay, stjuour g] puo.feq eranyomsay oxdoosozonts TaysIsIOg-L sqquour 9 puoAaq eumujayord ywassisieg-9 syo0M 9 puogoq rruaquatus|dwosodky qwowstss8d-s soo, y Aq azyeunou o1 ayer uoneniy seRWO!S Jo amTeI-y saypogquyue fposoooydansque Uy ast ONE s[9aa] suourajdutoo winzas yeuLON-z ‘wopouny yeuas SuperouDiep Aypidey-T (Nosd Jo sasea jerdaye u)NSA WI Asqorq Jeue1 10y HOHOIpOy stsougerp Joy oroygns are sSupuy qe; pue Asoysty se) poveorput Ayauynos you Ing sisousep soy 350q emp st Asdorq youry (sqyuou 9 wy zeaddesp)eunuiaoxd ‘kpoqnue (OSV)O wssordonsnue aansod(syaem g -—919ye sztyeanrousyous]du09 Ajpensn eruroumuaniopduros0dAy) pue-(Aqureut Aemmped aaneasye)osH (tupem)eg asvanop — :sqey Mol FT Samtpatos nee 9 ‘eumutsyorg pyre 7p(spydouojnzawOs ereoIpULyIseD oma esissqeun sisouserqy aanyrey yreay 20 (wrwayozy) onTey [BuaY ano” asned WAS ured yuvy qured peuraropqyisas,qsuioxduits 2249 amorpucg onuydony “emajozy“euapa pra Busy ‘eEMEMOF] “TUIOp? PIL “(sya 7 wi ue yeed wap shep ¢-p ur meaddestp orseudiq) NO (steak c-1 Joy)suonseyar soye osdejax Sour vunIeUIDY ssoxd Inq eEMTCUIDY oidoosoxortn sourosag watISyaant Z-] Ul OAfOsor BLMITWDY SOI) ssmordudg 1:7 AcWsawod s1-s woupyiye wi uou0D (Caopaayay apys ys0d syaam ¢)(oSHedun)TONDAzU urs 30 (SHNTESWo} = sod SyoMZ) ysuo}) snooovoidans onsjowoy gy dnozg Aq uonsazurysod 3999 (N9Sa) sETAdaTO[RI9MIO[B JesD090)de.NS-350g_ snumdouopramoy® sayeoipar sisAqeue aun ut (Qa oMpdiowsép)ysea (apAsormpAu9)Dqy ITP Joqurouy spumdononzowo15 pc Pediatrics Fluid &salt restrictionelectrolyte management Prognosis: Excellent->> 95% complete recovery Complications: HTN encephalopathy, Renal Failure, Can cause heart failure Other Glomerulonephritis Ig A nephropathy (Berger disease) Most common glomerular discase world wide Usually follows upper respiratory infection (2 -3 days) Most common symptom is Gross Hematuria Mild proteinurea, Mild-Moderate HTN Normal C3 C4(normal complements) ‘Treatment> control Blood Pressure (ACE inhibitor)eortison may be used. Alport Syndrome genetic &hereditary glomerulonephitis S&SAsymptomatic Hematuria & Bilateral sensorineuralHearing Loss& eye abnormalities ‘Usually progress to ESRD sires eee See eee eee EEE eeEE Symptoms are more severe in affected males than affected females Henoch-Schonlein Purpura (HSP) Small vessel vasculitis(lgA mediatedjage (mc in 3-10 years)more at winter Male>female2:Ithe m.c.c of non thrombocytopenic purpura Usually affect skin, kidney,GI, joints Has good prognosis Symptoms: Purpuritic Rash(m.c 98%,hallmark of the disease)> more in gluteal region & lower abdomené&lower extremiti is lateral malleolus 100%) Joint pain , Abdominal pain , Fever(low grade) ,Can cause intusseeption(5%), bloody diarrhea Resolve spontaneously Complications Abdominal symptoms (2/3 of patient)abdominal pain vomiting, bloody diarrhea. Joint pain and arthritis(2/3)(non migratory non erosive) siskqeyp Ae NUH, aukjonn99]9 28 SPILT syuouneary, (ae payuamsesyysyo0ys1q9s swoys WJ poojgauruywas = YET TOYS (00°01 -000°0 PIeId) eUadoyAsoquioxqy, * [P/U 6-S AH MOl:SqeT sisoproe 7p sInyy Jeuar ‘eumByo ‘ssowjeam “(eqmaue) apeg MEM qosord waned (AEELSTON9O-A oF8eyuOUsyOIsIUD) voyuerp § Apooig «jo skep gT-s eis suojdXg siead p> UaIpHyD Ur VoURLHOD WOW, soseo JO %OT Ut Haas St BOPARIP Ow NGS NH YK poyeioosse ‘wuaroeg WoUUNOD SOW <(SUIKOL OMT] VBYS)LH +LST0 NOD-T suoydurks yeo}Sojoanau on ng sean (oangn.y pouay) onuoay ayuadosfooquosy, souverpa (oruaun syhyouay 2yyrodopSuvosspu)onuaun sydzouragy ssmoydukg ‘WoIpIND UF ame yeuay amnoy Jo asneo woUTIOD 160}, +S) owospudg our snd jowORL “sympe zo suszprq> Plo wen suaxpHMD [TEMS UF a19A9s ssa] sy ASHI amp st quaMI9Afoauy [eua4) ares st UwIGy [9 WY AND90 CSAP: F195 3p WT|Pox s1 sisoudorg(monLaNdMOD SNO YoyEUTATOPAE UW pasn pozais) sprozis 10 CIVSN <3uomMEaR, (worrsodap Wa] Sumoys aupNor you nq)Asdorq Teas 20 upys Aq ysoqsisousup jeormo sfjensn sysouseC. ‘y8q asvasom(sisorMoqurosya)iano9 yapareyd asvaxoutsqey (aamzyas) amex gNQuoNIO) epoNSA pue Suyfoms jeIo1g amyroy jouer pure sumdeu amnoe asnes ues ynq vam waioxdy epmemoy woysuE St WeUIaATOAUT eUaT oT AIaAaS ASH [eua1enxa 0} parejas you (ysex amp sapooaxd 3,uopypyser arp seye stpuour ¢ UNpIA radde)(o%¢-sz)waaAfoaUr eUEY, nye an990 10 ysea ayy epavaad wea surorders yuOf pue yeuTEOpGy sourerpa Pediatrics ‘No antibiotic for diatthea> Antibiotic increases the risk of HUS. Prognosis: >90% recover completely & small number end with ESRD. Prognosis is poor in diarrhea negative HUS(30% ESRD) Note thatschistocyte is seen in microungiopathic hemolyile anemia(TTP,HUS,DICprosthetic heart vaive) Nephrotic Syndrome Signs & symptoms Proteinuria> 40 mgin("2)! hour Hypoalbuminemiac2.5 ; total <3.5 Edema >most common symptoms(usually start on the face,more in morning) If sever edema can cause ascitis,pleural effusion,or generalized edema(anasarca) Hyperlipidemia (give statins >250 mg/day) No HTN, No Hematuria(unlike glomerulonephritis) ‘Minimal change disease is the most common cause Compli tion of Nephrotic Syndrome 2 Peiateleg: = Anemia(due toTransferrin loss,Microcytic, resistant to Iron treatment) Infections(loss of immunoglobulins in urine) ‘Thrombosis(DVT.PE) due to loss of antithrombin 3 in urine. Hyperlipidemiahypothyroidismosteoporosis( Vitamin D deficiency). Diseases that present with primary nephrotic syndrome include: i-Minimal Change Disease(MCD) ‘Most common between 2-6 years of age ‘Symptoms Edema (most common)starts on face & around eyes, more in the morning Plural effusion Creatinine is normal ‘Treatment: Steroid for 4-6 weeks (good response to steroid) Relapse is common Indication for biopsy: (no routinely) Atypical presentation(HematuriaHTNNo response to steroldrenal Failure) ‘auspucs onomydou yewueBuoo wt juatqwan plOoses 20} 2[OH OU YEH SON, ASA 0} worssardoud sey ovour 3nq 2zF] Ul Joye] qUosoAdsISOAapDs feYSUESoUE asNAAIP -Z “eurpa pur ermaurumayvodéy‘eaim maqord s9aas WBE yg We ASA‘ omoxpuss ononydow jenmusBu0a jo our aq) st SND odAy ustMU-T (SNO)emospucs syorqdou peyUasHO- 08e “ quRstsar proms st Asqorq 305 VOTOIPUT ‘suauppyy> ur awoxpucs oyorydou ur oumnox e you si Asqorgsisous ec, -oamyrey jenox aquoays asnea 9,us9op CLOW. Inq’ aanprEs JeuEZ any umnaysaxy, Jo sso} Jo asnpoag, < qauNaR uo] 01 1ueIs\Ser vyUIDUY oAADOIOTY UU UF TIT MiqWONPHEY Jo sso] CwstoquBoquIONYL, -(euoxe yoo st uoumeastpo"Ur snaonoumend)sprueyed yeuiaseq snosuejuods pue smrosy uoiaRg paypinsdeoua st eymseq TourID ysoununjago(oumunar Jo ssoq 0} onp (UourHOD ysout) BoRDAFT uonwarduro3 2a Pediatrics Polycystic Kidney Disease Lnfant polyeystic Kidney Disease Autosomal recessive Signs &Symptoms: Bilateral small cysts on kidney, HTN,OLiguria &Acute renal failure Associated with liver disease (liver fibrosis) in 50% of cases Diagnosis: renal ultrasound (can be diegnosed by antenatal ultrasound) ‘Treatment: >50% > ESRD & need dialysis or transplant 2-Adult Polycystic Disease Autosomal dominant Present at 40-50 years with Bilaterallarge kidney cysts Presentation HTN, Hematuria, Renal Failure Associated with other cysts (Liver(m.c extrarenal cysts), Pancreas,Spleen, Associated with Mitral valve prolapse 86 Pediatrie = Associated with Intracranial Berry Aneurysm(circle of Wi ancurysm) If ruptured Berry Ancurysm will cause subarachnoid hemorrhagewhich cause severe headache Diagnosis of subarachnoid hemorhageis CT scan, if negative do Lumbar Puncture, Nocturnal Enuresis involuntary nocturnal urination at bed time bladder control usually achieved at 2-4 years(bowel control achieved before that) nocturnal enuresis is defined if no bladder control in>4 years old child. Boys > girls Family history is present ‘Management: life style or drugsDesmopressin (ADH)(Vasopressin Analogue or DDAVP),side effect is hyponatremia. 68 saat zo off jos jfape qowar YON HON Pa ] auoleysopre ‘ats aprmasosny Moy aE suregssoy Bue9q sq aucaupuss as yemouissog | suipuy tuo9 se aureg | open st ames aR OTE SNMP i" suadoursoa swoys sisfyeue ouun ways oadsns‘aanyr |__ssomea _| ssorenesucamen, osea PPV war Jo ssne> vst saHUdoU [eHMAINNIOKMGN BIND TER SION sey oseanouy, en seoweqamsip surzodsojpo‘uospaoo\(ayemoy ty osvaroog san0q arkjonoar ql annssand Smof oof NIN Jo) 99'M)gQO)sBrup-9 won wood ‘womuasody wopaodé ooer + iam Ginpe wem suaspryo on eae I uy uounes ssa)NIH Areurd -geuoe Jo woHIoI0D -y cageneenooee Supe ee 2 | awoxpucs a[ppyy(emorpucs: OREN aprmasomy mara | 1339p of ‘uuoa)uwsuozaisopresody Soeuunsd‘omroxpess ae w Pee re eee Supysno‘ewoy{oouosypooyd)sosne9 ‘auoopua-p saber seeontr omnes - (quoys-+)4ise|dojue snosuemoied Aq juoureaN = ~ 5 — I (pmpumys pjo8) jsout 94} 048 sasvasIp jemAqouored [eUTY -] Vary oaks, "URIPTNP WE NHL JO sasnes) (V.La)sisoppe seg peuay SUaApTIgs Ur WoRUD}10d AFT sured semmpg Pediatries Chapter 6 Infections & immunization ‘Meningitis or Is inflammation of meningescould be vira(aseptic) bacterial(m.c) IN Neonate (most common bacteria is Group B sreptococeus (GBS), Age >1 month->streptococeus Pneumonia (most common) / nisseria-meningitis meningococeus Pathology: ‘Most from hematogeneous Spread Rarely from sinusitis, otitis media, mastoiditis Symptoms: Usually non specific Incubation period for bacterial meningitis is 2-3 days 1* symptom is poor feeding, Irritability , Fever , Nausea & ‘vomiting, hypothermia or fever , hypoactivity , Seizure On examinationbulging anterior Fontanel Oculomotor or abducent nerve palsy 90 Pediatrie _--___ Cushing tiad of inereased intracranial _pressure( ICP)(Hypertension, Bradycardia, respiratory imegularitics) Kerning & Brudzinski&Neck stiffness Signs are usually absent in infants and small childrens Diagnosis: Lumbar Puncture (LP) and CSF analysis done before starting anti and tested for glucose,protein, WBC Bacterial meningitis Viral meningitis Low glucose Normal glucose High protein ‘Normal or Slightly elevated protein 2300 WBC(mainly neutr PMN) <300_ WBC (mainly lymphocytes MNO) High CSF pressure Normal CSF pressure ‘Treatment: Empirical treatmentVamcomycin & generation cephalosporin After culture results illin & 3" generation cephalosporin for 10-14 days 1N. meningitides:penicillin for 7-10 days Hib: ceftriaxone or cefotaximefor 7-10 days a” 6 - Aunt uoy-ayy ays 3,0 woRaQyUT 10 amII0eA, “(sep OT-A)pousd uopeqnom(zoqdorp Sroyendsoy wow) snorseyu0s snopBer109 Siyaty(euoioeq — um8)sissmag eysyaprog skep ¢-7 10y uonpequouy (s1priSuraayy euassin) snasos03uIUeyAL ssoy Suyreay st wopeoyduro9 [eo1Zojoansu WoUTUOD ySojAL -paoayye oq eo saAzaU [ErUEI9 ‘98 (w£ OST ‘AOI a8ea10UF UI payoayge UoULIOD ysouL) (quaMIDAOTH ‘aks eo] Uy woNUNg) Woonpge,9 Asjed enrou [eIURIC amayes 2p amssead yoramioenut WSF -snyeydanospay(@enoresqo wou) SupesruMuMosHAVISOIAsIs25 ssuoneaqdaro) uopmnsayrueus FeoiBojomau somoy ‘Apres OATS jC ooswMyoUTEXOG, uyodsojeydas uonesoue ,,¢ € (1103 “a ) eaneou weIH Pediatrics infection is rare above 10 years and usually milder in adult ‘than in infants. pathogenesis bacteria attach to cilia in the respiratory tract and causes local damage to respiratory tractypertussis don’t cause bacierimia Clinical presentation whooping cough (100 day cough) with 3 phases Catarthal Phase (1-2 weeks) > influenza like symptomsthe most contagious phase Paroxysmal Phase (1-6 weeks) > severe coughing paroxysm & inspiratory whoop Convalescent Phase 2 weeks or months of gradual resolution Fever usually mild grade Pneumonia, atelectasis, pneumothorax, bronchiectasis, Diagnosis: Best Nasopharyngeal cultureCXR> usually normal CBC showslenkocytosis with lymphocytosis Pediatrics ‘Treatment Erythromycin(macrolid)(drug of choice) for 14 days ‘Macrolide only lower the duration of the disease Prophylaxis to all family members Cat- Seratch Disease Caused by BacterisBartonella Hlenaslae Incubation period 3-30 days Signs &Sympt Red-white papules along the linear scratch &chronic regional lymphadenitis Other symptoms Fever, headache, hepatosplenomegaly, Anorexia ‘Treatmentiself limited, resolve in 2-4 month&no need for treatment. Scarlet Fever Causedby group A B-hemolytic streptococcus ‘Most common in 2-10 year olds Signs &Symptoms: Incubation period (2-4 days) 95 quasoud 31 uonsayty jepaqoeq Arepuogas 124], JUBUNUTO paseq 9pIXo OUYZ WOME, “wonoazur epipurs 10 (snaane snsoos0pSqdeys st 2'u)uonoayur pera}o8q Jo woNEoH|diuo e aq ueD

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