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Female Repro Final > Infant/Child Path 1 > Flashcards

Infant/Child Path 1 Flashcards

1
Q

What deficiency do we associate with neural tube defects?

A

neural tubes (just kidding)

Folate deficiency

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2
Q

What leads to anencephaly? What does it look like?

A

anencephaly- anterior end of the tube is not closed; calvarium and forebrain absent and orbits shallow

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3
Q

What leads to encephalocele?

A

encephalocele- malformed CNS tissue extends through a defect in the cranium.

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4
Q

Describe what causes spina bifida and the three subtypes

A

spina bifida- caudal region of the neural tube not closed = vertebral malformation

spina bifida occulta- asymptomatic defect in the vertebral arches; skin intact

meningocele- meningeal extrusion through a vertebral arch defect

Meningomyelocele- herniation of CNS tissue through the incompletely fused vertebral arches= motor and sensory deficits

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5
Q

Amniotic AND maternal serum AFP levels are up. What could it be?

A
  • anencephaly
  • encephalocele
  • spina bifida
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6
Q

Multiple gestation and Bicornate uterus are examples of what type of issue?

A

Deformations.

extrinsic disturbances due to compression

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7
Q

Prematurity is specifically defined as:

A

Delivery before 37 weeks

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8
Q

Risk factors for prematurity

A

risk factors: Preterm rupture of placental membranes (PPROM)2* ascending infection → chorioamnionitis & funisitis, intrauterine infection

Uterine, cervical, placental structural abnormalities

Multiple gestation

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9
Q

What complications do we see with prematurity?

A

Sepsis, developmental delay, brain damage and hydrocephalus 2* intraventricular hemorrhage/Germinal matrix hemorrhage (cannot regulate cerebral blood flow and lack glial support)

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10
Q

Sometimes, especially in premature infants, we see fetal growth restrictions causing the fetus to be small for its gestational age.

What risk factors are associated with this, both from the fetus itself and those from the mother

A

Fetus Issues: Chromosomal disorders, Congenital anomalies, infections (TORCH)

Maternal: Vascular diseases (preeclampsia), Inherited thrombophilias (factor V leiden), avoidable teratogens (narcotic, alcohol, smoking, drugs, malnutrition)

Malnutrition from a placental defect would also cause smaller babies

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11
Q

What is the third most common cause of death in neonates?

A

Necrotizing enterocolitis caused by necrosis and inflammation in bowel.

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12
Q

What symptoms do we see with necrotizing enterocolitis?

A

Bloody stools, abdominal distension, circulatory collapse

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13
Q

What does necrotizing enterocolitis look like on X-Ray and grossly?

A

X-ray: gas in intestinal wall, dilated loops of bowel

gross: mucosal/transmural coagulative necrosis, ulceration, bacterial colonization, submucosal gas bubbles (pneumatosis intestinalis)

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14
Q

Treatment for necrotizing enterocolitis?

A

Tx: stop feeding, NG tube (decompress abd), IV fluids, remove bowel

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15
Q

What complications do we see down the road from necrotizing enterocolitis?

A

Complications: sepsis, shock, DIC, short-gut syndrome, malabsorption, strictures, obstruction

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16
Q

What leads to neonatal respiratory distress syndrome (RDS) and who is at risk?

A

surfactant deficiency= increased surface tension= alveolar collapse= R–>L shunt

patho: surfactant (phosphatidylcholine or lecithin) made by type II pneumocytes; dec surface tension and prevents collapse of alveolar air sacs in expiration.

Lack of surfactant= collapse of air sacs and formation of hyaline membranes.

risk: white males

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17
Q

What lab values do we use to measure if a neonate has RDS?

A

Amniotic fluid lecithin: sphingomyelin (L:S) ratio is used to screen for lung maturity.

Phosphatidylcholine (lecithin) levels ↑ as surfactant is produced; sphingomyelin remains constant.

Ratio > 2 indicates adequate surfactant production.

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18
Q

Besides prematurity, what can lead to RDS and why?

A

C-section delivery- d/t lack of stress-induced steroids; steroids ↑ synthesis of surfactant.

Maternal diabetes- Insulin dec surfactant production.

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19
Q

X-Ray of RDS looks like? Grossly?

A

X-ray: Diffuse granularity of the lung (‘ground-glass’ appearance)

Gross: lungs are firm, deep red, “liver-like”

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20
Q

If I am struggling to breathe/ventilate, what will my ABG look like?

A

labs: ABG= hypoxemia and hypercapnia

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21
Q

Histo of RDS?

A

Histo: focal atelectasis & hemorrhage w/dilated terminal & respiratory bronchioles lined by pink, smooth hyaline membranes, fibrin

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22
Q

What can RDS lead to? Third one is weird, but linked to the second one…

A

can lead to: Hypoxemia= ↑risk for persistence of PDA and necrotizing enterocolitis.

Supplemental oxygen= ↑ risk for free radical injury (leading to number 3…)

Retinal injury= blindness and also, lung damage=bronchopulmonary dysplasia

23
Q

How does we treat the RDS

A

tx: surfactant replacement therapy, O2, support; prophylaxis: steroids

24
Q

What causes Transient tachypnea of the newborn (TTN)?

A

abnormal clearance of lung fluid from the alveolar space

patho: not reabsorbed

25
Q

Who is at risk for TTN?

A

risk: short labor or c-section, maternal diabetes and asthma

26
Q

Discuss the chest x-ray for TTN

A

chest X-ray: “wet” lung fields; hyperinflated lungs with shaggy heart border and clear periphery

typically resolves within 24-48 hours

27
Q

What causes persistent pulmonary hypertension (PPHN)?

A

high pulmonary vascular tone

patho: pulmonary vascular resistance does not appropriately decrease after birth→ blood shunted right–> left across the foramen ovale and ductus arteriosus; Blood bypasses the lungs= deoxygenated blood returning from the body returns to the arterial system without being oxygenated.

28
Q

What can lead to PPHN?

A

meconium aspiration, pneumonia, birth asphyxia, diaphragmatic hernia (one lung flat), premature ductus arteriosus/foramen ovale closure (maternal NSAIDs), polycythemia, sepsis (constriction 2* COX/PE)

29
Q

How will PPHN present to us and how do we diagnose it?

A

sx: tachypnea, severe cyanosis, retractions, hypoxia; O2 sat lower in LE vs UE
dx: not responsive to 100% O2 challenge; echo= elevated pressure in pulmonary artery

30
Q

PPHN treatment

A

tx: O2, NO to dilate pulmonary vasculature, ECHMO

31
Q

In regards to intrauterine meconium aspiration, what does it lead to and what are complications of it?

A

respiratory distress after delivery through meconium+amniotic fluid

complications: inflamm pneumonitis, bronchial obstruction

32
Q

In regards to intrauterine meconium aspiration, how will it present and how do we diagnose it?

A

sx: rales/rhonchi, O2 desaturation, asphyxia, green/brown muconium staining on baby
dx: chest xray= hyperinflation + atelectasis

33
Q

Treating intrauterine meconium aspiration

A

tx: intubate and suction, abx, O2

34
Q

What is the risk factor for a patent ductus arteriosus and what leads to this?

A

failure of the ductus arteriosus to close shortly after birth

risk: premature infants
patho: as pulmonary vascular resistance drops after birth, the PDA allows blood to pass from aorta to the pulmonary artery (L–>R shunt); additional fluid returning to the lungs increases lung pressure and neonate has difficulty inflating lungs

35
Q

How will PDA present and how do we diagnose it?

A

sx: increased blood flow =pulmonary edema and congestive heart failure, murmurs, thrill
dx: US/echo and clinical sx

36
Q

Whta bacteria/viruses can cause transcervical (ascending) infections transferred to the baby in the birth canal?

A

Most bacteria: Group B streptococcus, Ureaplasma urealyticum, E. coli, Mycoplasma hominis, Streptococcus viridans, Gardnerella vaginalis

few viral: (HSV2) Herpesvirus- encephalitis, vesicular rash

37
Q

What is chorioamniotis and what causes it?

A

inflammation of the fetal membranes (amnion and chorion)

cause: bacterial infection ascending into the uterus from the vagina

38
Q

Who is at risk for a intra-amniotic infection (IAI) and how does it present?

A

at risk: prolonged labor

sx: maternal fever, uterine tenderness, maternal/fetal tachycardia, foul-smelling amniotic fluid

39
Q

What will intra-amniotic infections look like grossly/histologically?

A

gross: Greenish opaque membranes
histo: acute inflamm

40
Q

What is villitis/intervillositis and what does it look like histologically?

What can it lead to?

A

histo: villous inflammation, PMNs/lymphocytes, fibrosis or edema

can lead to: miscarriage, intrauterine growth restriction

41
Q

The next section of cards is better explained in the microdecks, but for review, I’ve rehashed the pertinents here.

A

Also, Sketchy Micro is AWESOME. Use it and you will get all of the micro answers correct.

42
Q

How does toxoplasmosis present?

A

Sx: fever, IUGR, microcephaly, seizure, hearing loss, maculopapular rash, jaundice, hepatosplenomegaly, anemia, and lymphadenopathy

First Trimester – often results in death

Second Trimester – classic triad: Hydrocephalus, Intracranial calcifications, chorioretinitis

Third Trimester – often asymptomatic at birth

43
Q

How do we diagnose and treat toxoplasmosis?

A

Dx: placenta, serum, or CSF: PCR & IgM titer (IgG will be elevated if mother is infected regardless of transmission)

Tx:
Mom infected - Spiramycin
Baby infected symptomatic - Pyrimethamine and spiramycin and sulfadinazine - 12 months
Baby no symptoms - Same as above, but not 12 months (case by case)

Can also use glucocorticoids and folic acid

44
Q

Discuss the early and late symptoms of Syphillis

A

Early Sx~1month: Maculopapular rash, “snuffles,” lymphadenopathy, hepatomegaly, thrombocytopenia, anemia, meningitis, chorioretinitis, osteochondritis, failure to thrive

Late sx~2yrs: Hutchinson Teeth, Mulberry Molars, Perforated hard palate, Rhagades (cracks or fissures in the skin around the mouth), Saber Shins, Sensorineural hearing loss (CN VIII), Saddle Nose

45
Q

How do we treat Syphillis?

A

PCN

46
Q

Symptoms of Rubella

A

Sx: “Blueberry Muffin Baby” (rash due to extramedullary hematopoiesis), Cataracts , “Salt and Pepper” retinopathy, Radiolucent bone disease (long bones), IUGR, glaucoma, hearing loss, pulmonic stenosis, patent ductus arteriosus (CHD), lymphadenopathy, jaundice, hepatosplenomegaly, thrombocytopenia, interstitial pneumonitis, diabetes mellitus

47
Q

Cytomegalovirus symptoms

A

sx: most infants asymptomatic at birth; IUGR, developmental delay, microcephaly, sensorineural hearing loss, retinitis, jaundice, hepatosplenomegaly, thrombocytopenia, hypotonia, lethargy, poor suck, Periventricular calcifications

48
Q

Treatment for CMV?

A

Gancyclovir - Stops further hearing loss

49
Q

Discuss the SEM presentation of HSV

A

SEM disease (Localized to skin, eyes, and mucosal)-Vesicular lesions on an erythematous base, Keratoconjunctivitis, cataracts, chorioretinitis, Ulcerative lesions in mouth/palate/tongue

50
Q

Discuss the CNS presentation of HSV

A

CNS disease: Seizure, lethargy, irritability, tremor, poor feeding, temperature instability, full anterior fontanelle

51
Q

Discuss the disseminated disease symptoms of HSV

A

Disseminated disease: Multiple organ involvement (CNS, skin, eye, mouth, lung, liver, adrenal glands), appear septic (fever/hypothermia, apnea, irritability, lethargy, respiratory distress), Hepatitis, ascites, direct hyperbilirubinemia, neutropenia, disseminated intravascular coagulation, pneumonia, hemorrhagic pneumonitis, necrotizing enterocolitis, meningoencephalitis, skin vesicles

52
Q

How do we treat HSV?

A

Acyclovir

53
Q

How does Sepsis present in neonates and what causes it?

A

Early (first 7 days) or late (up to 3mo) onset

Symptoms: pneumonia, sepsis, meningitis
cause: Most commonly GBS, listeria & candida

Female Repro Final (4 decks)

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