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Pediatrics > Mustafa > Flashcards

Mustafa Flashcards

1
Q

Hypoglycemia in newborns

A

Higher brain to body weight ratio , higher glucose demand, %90 cerebral usage

If feeding delayed 3-6 hours: hypoglycemia
Preterm, IDM, sga, lga.: hypoglycemia risk

Fetal glucose: 2/3 of maternal (doğunca daha düşük oluyor)

Hypoglycemia: <47

Glycogen storage made last month of 3rd trimester

Either:
Inadequate glycogen
Increased glucose utilization
Excessive insulin

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2
Q

High risk infants for hypoglycemia

A

IDM
SGA
LGA
<37 weeks
Stressed/ill infant
Exposure to medications ( preterm labor, htn, diabetes tretment, diuretic , antidepressant)

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3
Q

At risk groups for hypoglycemia

A
  1. Increased insulin:
    Intrapartum glucose
    Asphyxia
    SGA
    Insulinoma
    IDM
    Hyperinsulinemia
  2. Decreased storage:
    Placental abnormality
    Preterm, low birth weight
    Discordant twins small one
    3.ıncreased need:
    SGA
    İll( Septic, RDS)
    Hypoxia, ischemia, hemorrhage,meningits
    Cyanotic heart disease
    Hypothermia
    4.ınadequate production or substrate delivery:
    Galactosemia
    Glycogen storage disease
    Fructose intolerance
    Maple syrup urine disease
    Lipid metabolism disease
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4
Q

Persistent hypoglycemia

A

> 7 days or higher amount needed to preserve

Causes:
1.Hyperinsulinism( congenital, adenoma,syndrome)
2.Endocrine disorder( gh def, hypopituitarism)
3. Inborn error of metabolism( Galactosemia, GSD, lipid/ protein metabolism)

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5
Q

IDM

A

Birth injury, stillbirth, congenital anomalies, cesarean risk, NICU admission increased

(Oxygen radicals damage mitochondria, this oxidative stress disrupts vascularization of tissues)

Hyperglycemia causes fetal anomalies like:
RDS, VSD, transposition of greater vessels, polycythemia, asymetric septal hypertrophy!!!
Renal agenesis, hydronephrosis, cystic kidneys, micropenis, anencephaly, spina bifida. Caudal dysplasi, cns damage

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6
Q

Monitoring for hypoglycemia

A

Glucose monitoring within 1 hour
1-2 saat aralıklarla ilk 6 saat monitor

For İDM maternal glucose control is the determinant

Screening at risk babies:
1.symptomatic: immediatly
2.asymptomatşc high risk: 30-60 min of life
3. Asymptomatic but at risk: 3-4 hours

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7
Q

Tratment of hypoglycemia

A

Asymptomatic:
<25: iv glucose infusion
>25: enteral feeding

Symptomatic: iv glucose infusion
+glucagon, glucocorticoid, somatostatine

Prevention: early screening, feeding, awareness, temperature

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8
Q

Signs of hypoglycemia

A

Cyanosis, cardiac arrest
Hypotonia, irritability, tremor
+seizures, high pitched cry, lethargy, tachypnea, apnea, poor suck

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9
Q

Hypocalcemia

A

Term infants: <8
Preterm infants: <7
Ionized Ca: <2.5

Tetany, muscle cramps,fatigue, irritability
Severe hypocalcemia: bronchospasm, seizures
Chronic: rickets,deminerilazation, apnea, elevated ALP
Acute: irritable, tremor,seizure,apnea, cardiac dysfunction

Early hypocalcemia: first 3 days
Immature parathyroid gland/ kidneys,
Premature,lbw,idm, ihm, asphyxia

Late hypocalcemia: >3 days
Due to excessive phosphate
Congenital defects in pth metabolism (digeorge,isolated hypoparathyroidism, pseudohypoparathyroidism)
Magnesium deficiency
Vit D deficiency

Treatment: %10 calcium gluconate: 2 ml/kg slow infusion 1ml/min, check for bradycardia
+calcium chloride(high Ca), Mg, bolus levels will fall in 30 mins, 3-4 times a day

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10
Q

Risk factors for hypocalcemia

A

Preterm and ill infants, first 3 days
Blood transfusion(citrate sebepli)
Insufficent feeding
IDM
Asphyxia
Diuretics
Alkalosis
Exscess phosphate
Mg deficiency
Confemital hypoparathyroid

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11
Q

Hyponatremia

A

<130
Seizures, lethargy
Early: 1st week
SIADH( most common) (pneuomina, meningitis,RDS, sepsis)
Increased maternal water intake
Renal impairment

Late: CAH, diuretics, preterm, hypotonic iv

Treatment: urgent : <125
Hypertonic saline 6ml/kg over one hour to 125. Further correction one to two days. Treat the cause

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12
Q

Hypernatremia

A

> 150
Water loss from weight loss, diarrhea, polyuria
Excess na intake from NaHco3 or medications

Severe hypernatremia fixed 48-72 hours or brain edema and IC bleeding

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13
Q

Clinical Na level questions

A

Dehydrated
Ongoing loss
Urinary output
Medication containing na

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14
Q

Hypokalemia

A

K is intracellular, 0.1 ph change= 0.6 K change
<3.5
Lethargy, ileus, arythmia, u wave?

Causes: diuretics, renal tubular defects, ileostomy, nasogastric tube

Trx: daily k intake 1-2 mg/kg
Severe: KCl infusion with ecg monitoring

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15
Q

Hyperkalemia

A

> 6
T genişliği

Causes:
Increased K release from cells( IVH,asphyxia,trauma, hemolysis)
Decreased k excretion with renal failure
Medication error, excess adminis.

Trx: Glucose-insulin combination, dialysis
+exchange transfusion, calcium gluconate, sodium bicarbonate, beta agonists,lasix

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16
Q

Early onset sepsis

A

First 5-7 days
Multi system fulminant ilness
Respiratory symptoms
Pneumonia mostly
Source: intrapartum period from maternal genital tract

Chorioamnionitis :
Rupture of membranes, vaginal flora, bacteria reached amniotic fkuid and fetus

Aspiratiom of infected amniotic fluid: resp symptoms

Primary sites of colonization:
Nasopharynx, oropjarynx, conjunctiva, umbilical cord

Clinical: respiratory distress

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17
Q

Late onset sepsis

A

> 5 days
Usually focused, meningitis +sepsis

Nosocomial sepsis:
İn high risk infants:underlying ilness, NICU flora, invasive methods

Clinical: alteration in established feeding behaviour

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18
Q

Causative organism of sepsis

A

Primary sepsis:
(From vaginal flora usually)
Group B strep
Entero, Staph, e. Coli, l. Monocytogenes, h.influenza, anaerobs

Nosocomial sepsis:
Staph( s. Epidermidis)
Gram - rods( pseudomonas, klebsiella, fungal)

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19
Q

Risk factors of sepsis

A

> males
Prematurity, low birth weight
Rupture of membranes
Amniotic fluid problems
Maternal fever( infection, chorioamnionitis,uti, vaginal E.coli
Invasive procedures
Resuscitation
Galactosemia, immune defects
Iron therapy
Multiple gestation

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20
Q

Clinical manifestations of sepsis

A

Tachypnea, chest retractions, apnea, inactivity, poor feeding, gasping, grunt, cyanosis

Fever, seizures bulging fontanelle, irritable,high pitched cry, neck retraction, blank look

Refusal to suckle, hypothermia,lethargy, poor cry, comatosed, shock, abd. Distention, diarhhea, vomiting
Sclerema, poor perfusion, cyanosis

21
Q

Differential dgx for sepsis

A

RDS
metabolic/ genetic, Hematologic, neurologic diseases
Congenital heart diseases
Other infections( TORCH)

22
Q

Diagnostic tests for sepsis

A

Blood, CSF, urine culture
Tracheal aspirates
PCR
WBC, platelet, CRP, ESR, Procalcitonin!!!, IL-6, bilirubin, glucose, Na

WBC: leucopenia(<5000), neutropenia(<1750), i/t neutrophil>0.2

Chest X-ray, urinary tract imaging, lumbar puncture (>72h), examination of placenta and fetal membrane for chorioamnionitis

23
Q

Treatment of sepsis

A

Primary:
penicillin(ampicillin)
Aminoglycoside(gentamycin, netilmisin)

Nosocomial:
Vancomycin
Aminoglycoside/ 3rd gen cephalosporin

Normalize temperature, correct hypoglycemia, prevent bleeding,stabilize cardiopulmanory status , NO ivig in neonatal sepsis

O2, ventilation support, support BP and perfusion to prevent shock: pressors: dopamine, dobutamine, monitor fluid intake and output
Observe for DIC: bleeding, thrombocytopenia, PT, a PTT, vit K, platelet infusion, neutropenia: G-CSF
Convulsions: fenobarbital
SIADH
Metabolic: glycemic levels, acidosis

GBS prophylaxis, hand washing

Respiratory, cardiovascular,hematologic, CNS, metabolic

24
Q

Intrauterine Infections manifesting at birth

A

Rubella
Varicella zoster
CMV
Hepatit b/c
Hiv
toxoplasma gondii
Syphilis

25
Q

Intrauterine Infections acquired at birth, symptomatic later

A

HSV
Hepatit B/C
HIV
CMV
Group B strep
Chlamydia trachomatis
N. Gonorrhea
E. Coli
L. Monocytogenes

26
Q

TORCH syndome

A

Toxoplasma gondii
Other(varicella, tr. Pallidum, P. B19)
Rubella
CMV
HSV

Rubella only one that can only be congenital

27
Q

Congenital Rubella(measles)

A

Rna togavirus, opthalmologist discovered, live vaccine

Rubella sundrome:
PDA
Cataracts, pigmentary retinopathy,micropthalmia, glaucoma
Hearing loss (diagnoses by 2 of these or 1 of there plus one of:
encephalitis,microcephaly,purpura, splenomegaly, jaundice in 24h,development delay, radiolucenct bone
+ pneumonia,sensory abnormalities,

Expanded Rubella syndrome:
SGA, microcephaly,PDA, pulmanory stenosis, hepatosplenomegaly/ lymphadenopathy

  • meningoencephalitis, microcephaly, mental retardation
    -glaucoma, cataracts,pigmentory retinopathy( salt/pepper retinopathy)
    -hearing loss
    -PDA
  • hepatosplenomegaly, jaundice
  • purpura, thrombocytopenia
    -radiolucent bone
  • low birth weight

Routine immunization: MMR: 15m, 4 y
Routine screening in pregnancy
Non immune women offered vaccibe postnatally
Precomceptual/ marital screen

28
Q

Congenital Cytomegalovirus

A

Most common congenital inf
Mostly asymptomatic at birth
NON HEREDİTARY SENSORİNEURAL HEARİNG LOSS(SNHL)
Double strand DNA virus
Humans only host
Latency and reactivation common
Incubation period 8 weeks

Vertical transmission: ante(transplacental)/ intra( blood,genital secretions)/post( breast milk) partum

Symptomatic neonate: petechiae, hepatosplenomegaly, jaundice at birth, SGA, microcephaly/ hydrocephal/ calcifation, hearing loss, hypotonia, chorioretinitis
SNHL , most common trait, may be present or delayed
Chorioretinitis most common ocular abnormality in symptomatic infants
Cmv retinit: hemorrhage,white fluffy areas

Life threatinimg disease: severe pneumonitis, myocarditis, hepatitis, enterocolitis, thrombocytopenia, retinit, neurologic disease
%10, severe end organ involvement, many infants with fulminant disease die within days weeks

Clinical: microcephaly, SGA, hepatosplenomegaly, jaundice, thrombocytopenia,
Abnormal neuroimaging!!!( white matter disease, ventriculomegaly), mother with infection, SNHL!!!

Dgx: viral culture, PCR, antibodies(m and g positive at congenital)

Prevention: blood transfusion, breast mişk treatment, personal protectivity fpr mothers, no kissing sharimg food

Treatment: in first 30 days of life
Gangiciclovir
Valganciclovir

Alternative: foscarnet, cidofovir

Do not treat in utero or asymptomatic, only symptomatic, immunodeficent or isolated hearing loss ones

29
Q

Congenital toxoplasmosis

A

Toxoplasma gondii, cat is the host, infected meat or cat litter, soil, mostly not symptomatic at birth

Triad: hydrocephalus, IC calcification,
!!!!chorioretinit: retinal scar w/ pigment surrounding, most common
Hepatodplenomegaly, jaundice, thrombocytopenia, rash, growth retardation, deafness, low iq

Treatment: postnatal dgx and treatment: entire first year of life

30
Q

Congenital syphilis

A

T. Pallidum
Fetal death, miscarriage, stillbirth
Asymptomatic at birth, manifest later
If mother has primary infection, but risk decreases with next pregnancies

Discrete macular lesions, rash, interstitial keratitis

Positive trepenoma serology: treat mother, repeat serology monthly, infant xray, CSF exam,
!Treat infant one dose , 10/ 14 days

31
Q

Comgenital parvovirus B19

A

Common febrile examthematous infection, %50 women immune

Slapped cheek syndrome/ 5th disease
Lacy rash, influenza like synptoms, arthropathy
!!!severe Anemia, myocardit, cardiomyopathy, hepatic dysfunction, hydrops fetalis, fetal death

Dgx: specific IgM

Treatment: Exhange transfusion in utero

32
Q

Congenital VZV

A

Result of first 20 weeks infection
2 days before 5 days after birth is severe disseminated varicella in newborn, in this case give VZig to infant, if lesions develop iv aciclovir

Specific ig in 96 hours, up to 9 days to mother, in case it helps the baby, but usually mothers infection does not pass to baby

33
Q

Congenital HSV

A

From primary maternal infection, if recurrent herpes risk lower, may be confined to cervix

Type 2 inf more severe

Prevention: cesarean at term or <4 hours after membrane rupture

34
Q

HBV infection

A

Chronic hbv with persisten hbsag
Infected vertically, some 1-5 years old
Carrier state after vertical transmission increases risk of chronic liver disease and hepatoma

For perinatal transmission: baby receieve hep B vaccine, administer hbig

Prevention: routine antenatal hbv testing, to give prophylaxis to baby

35
Q

HCV

A

Most transmission at birth
May become chronic
İdentify mothers at risk

36
Q

To prevent neonatal infections

A

Standard precautions
Screening bacteriuria
Serologix screenimg
GBS carriage screening

37
Q

Biochemical changes with seizures

A

Abnormal depolarization
Disruption of Na/K atp pump

Excessive aa release: glutamate
Lack of inhibitory: GABA

Decreased:
ATP
brain glucose
Phosphocreatine
GABA

Adp to pyruvate to lactate

Increased:
Pyruvate
Lactate
Glutamate

38
Q

Respiratory distress symptoms

A

Tachypnea
Flaring of nostrils
Grunting
Chest retraction
Cyanosis

39
Q

Primary Causes of respiratory distress

A

Transient tachypnea of newborn
RDS due to surfactan deficiency(preterm)
Aspiration syndromes
Pulmanory air leaks
Pneumonia
Pulmanory hemorrhage
Pulmanory hypoplasia
Chronic neonatal lung disease

40
Q

Secondary Causes of respiratory distress

A

Congenital heart diseases
Asphyxia
Infections(sepsis)
Surgical conditions( choanal atresi diaphragmatic hernia, fistula tracheeso)
Persistence of fetal circulation(pulmanory htn)
Anemia, polyctemia
Metabolic diseases

41
Q

Non respiratory Causes of respiratory distress (tachypnea)

A

Hypo/hyperthermia
Hypovolemia
Hypotension
Hypoglycemia
Anemia
Polyctemia

42
Q

Infant at risk for respiratory distress

A

Preterm
Asphyxia
IDM
C-section
Meconium in amniotic fluid
Foul smelling amniotic fluid
Mother with fever

43
Q

Respiratory distress not normal if

A

Persist for >1 hour, worsens or causes cyanosis

44
Q

RDS/ hyaline membrane disease

A

First 6 hours
Resolution in a week
Surfactan deficiency, high surface tension, prematurity
The more preterm, the lower weight: the more risk

SURFACTANT:
phospholipid+protein
Week 20: start, viability limit
28-32: max levels
26 altına surfactan veriyoruz
Stimulator: glucocorticoids(bethamethasone)
Inhibitor: insulin, pulmanory edema
Causes atelectasis, decreased lung compliance

45
Q

Etiology of comvulsions

A

HIE !!! (1-2days)
ICH. !!!! (1-7 days)
Intracranial infection(bacterial meningitis, TORCH) !!
Infarction !
Metabolic disorders (Hypo glycemia (1-2 days)/ calcemia/ magnesemia/ natremia,Hypernatremia)
Inborn errors
Pyridoxine dependency
Benign neonatal seizures
Epileptic syndrome (3-10 days)
Malformation

46
Q

Subtle seizures

A

Most common, prematures, no EEG correlation, subcortical
1.Ocular, oral-facial-lingual, limb movements: eye deviation, flutter,fixation, chewing, lip-smacking, cycling, paddling
2.autonomic phenomona: tacy/bradycardi
3.apnea

47
Q

Clonic seizures

A

Term, focal cerebral injury, EEG seizure
Rhytmic movements with slow return
1-3 jerks per second
Best prognosis

48
Q

Tonic seizure

A

Preterm, sustained flexion/extension of extremity or body,
Severe ICH in preterm, poor prognosis
neocortical damage
EEG may or may not

49
Q

Myoclonic seizure

A

Mostly upper, fast contractions without slow return, jerks
Serious brain injury
May be normal

Worst prognosis in neurodevelopmental outcome, seizure recurrence

Rare

Pediatrics (11 decks)

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