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MOD > Chapter 10 Part 1 > Flashcards

Chapter 10 Part 1 Flashcards

1
Q

What defines the neonatal period?

A

First four weeks of life

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2
Q

What defines the infancy period?

A

First year of life

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3
Q

What age is considered “toddler”?

A

Age 1 to 4

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4
Q

What are the leading causes of death in the first 12 months?

A

congenital anomalies, disorders related to short gestation and low birth weight, and SIDS

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5
Q

Definition of disease

A

deviation from or interruption of normal structure or function of part of an organ or symptom manifested by characteristics symptoms and sign

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6
Q

Definition of disorder

A

derangement or abnormality of normal function; morbid physical or mental state

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7
Q

Definition of neoplasm

A

new and abnormal growth

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8
Q

Definition of syndrome

A

group of symptoms that occur together

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9
Q

Definition of malformation

A

primary error in morphogenesis in which there is an intrinsically abnormal developmental process

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10
Q

Definition of disruptions

A

destruction of an organ or body region that was previously normal; arises from EXTRINSIC disturbance in morphogenesis

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11
Q

Definition of deformations

A

localized or generalized compression of fetus by abnormal biomechanical forces

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12
Q

What are some maternal factors involved in deformations?

A

first pregnancy, small uterus, malformed uterus, leiomyoma

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13
Q

What are some fetal or placental factors involved in deformations?

A

oligohydramnios, multiple fetuses, abnormal presentation, club feet

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14
Q

Definition of sequence

A

Cascade of anomalies triggered by one initiating aberration; ex. Potter sequence

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15
Q

What are some causes of oligohydramnios?

A

Leakage of amniotic fluid, renal agenesis, uteroplacental insufficiency due to hypertension

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16
Q

What are some effects of fetal compression due to oligoydramnios?

A

position defects of hands and feet, breech presentation, altered facies, pulmonary hypoplasia, amnion nodosum (nodules)

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17
Q

Definition of malformation syndrome

A

constellation of congenital anomalies pathologically related that cannot be explained by one single initiating defect

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18
Q

Definition of agenesis

A

absence of organ and it’s primoridum

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19
Q

Definition of aplasia

A

absence of organ due to failure of primordial growth

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20
Q

Definition of atresia

A

absence of opening

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21
Q

Definition of hypoplasia

A

incomplete development or decreased size of an organ

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22
Q

Definition of dysplasia

A

abnormal organization of cells

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23
Q

What are the common known etiologies of most congenital annomalies?

A

genetic, environmental, multifactorial

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24
Q

When during development do most chromosomal disorders arise?

A

During gametogenesis

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25
Q

What is the most common developmental defect of the forebrain

A

Holoprosencephaly

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26
Q

What are some examples of maternal disease states or infections that may cause congenital anomalies?

A

maternal infection - TORCH, HIV

disease - diabetes, PKU, endocrine issues

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27
Q

What are some examples of teratogens?

A

thalidomide, alcohol, anticonvulsants, warfarin, 13-cis-retinoic acid

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28
Q

What is a classic presentation of a child with fetal alcohol syndrome?

A

prenatal and postnatal growth retardation, microcephaly, short palpebral fissures, maxillary hypoplasia

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29
Q

What is a classic presentation of a fetus with a GD mother?

A

macrosomia, carciac anomalies, neural tube defects, CNS malformations

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30
Q

What are some common multifactorial malformations?

A

cleft lip, cleft palate, neural tube defects

31
Q

What are the two pathogenic processes contributed to congenital anomalies?

A

Time of prenatal teratogenic insult and interplay between teratogens and intrinsic genetic defects

32
Q

Two phases of intrauterine development

A

Embryonic period - first 9 weeks

Fetal period - 10 wks to birth

33
Q

When is the embryo most susceptible to teratogenesis?

A

between wks 3-9, esp wks 4 and 5; organ development is occurring

34
Q

What is the fetus most susceptible to in the fetal period?

A

growth retardation or injury to preformed organs

35
Q

What is the effect of cyclopamine?

A

plant teratogen that causes holoprosencephaly and cyclopia, acts on hedgehog signaling pathway

36
Q

What is the genetic effect of valproic acid?

A

acts on HOX genes, responsible for limb formation as well as vertebrae and craniofacial structures

37
Q

What are the genetic effects of EXCESS retinoic acid?

A

CNS, cardiac, craniofacial defects, cleft lip, cleft palate; TGFB3 pathway dysregulation

38
Q

What defines a preterm infant?

A

gestational age < 37 weeks

39
Q

What defines an extremely preterm infant?

A

GA <28 weeks

40
Q

What defines a very preterm infant?

A

GA 28 to 32 weeks

41
Q

What defines a moderate to late preterm infant?

A

GA 32 to 37 weeks

42
Q

What are the main risk factors for prematurity?

A

PPROM, intrauterine infection, uterine/cervical/placental abnormalities, multiple gestation

43
Q

What are the main hazards of prematurity?

A

neonatal resp distress syndrome, necrotizing enterocolitis, sepsis, intraventricular and germinal matrix hemorrhage

44
Q

What are some risk factors for PRROM?

A

history of preterm delivery, preterm labor and/or vaginal bleeding during pregnancy, maternal smoking, low socioeconomic status

45
Q

What are the most common microorganisms seen in intrauterine infections?

A

Ureaplasma urealyticum, Mycoplasma hominis, Gardnerella vaginalis, trichomonas, gonorrhea, chlamydia

46
Q

What role do TLRs play in intrauterine infection?

A

Bind bacteria and deregulate prostaglandin expression, triggering smooth muscle contractions in uterus

47
Q

What is the etiology of fetal growth restriction?

A

can be placental, maternal, or fetal anomalies

48
Q

What is the pathogenesis of fetal growth restriction?

A

infection, chromosomal, preeclampsia

49
Q

What is the outcome for SGA infants?

A

depending on cause and degree, there is a SIGNIFICANT risk of morbidity in forms of handicap, cerebral dysfx, learning disability, or hearing and visual impairment

50
Q

What are the most common fetal abnormalities and how do these SGA infants grow?

A

chromosomal, infection, anomalies; causes symmetric growth restriction (proportionate FGR), all systems similarly effected

51
Q

What are some causes of utero-placental insufficiency?

A

placental abruption, vascular anomalies, placenta previa, placental thrombosis, placental infections, multiple gestations

52
Q

What kind of growth pattern occurs in SGA infants with utero-placental insufficiency?

A

asymmetric growth retardation with sparing of the brain

53
Q

Etiology of RD in new born

A

RDS, excessive maternal sedation, fetal head injury, aspiration of blood or amniotic fluid, and intrauterine hypoxia

54
Q

Pathogenesis of RDS

A

immaturity of lungs, deficiency of pulmonary surfactant

55
Q

What is surfactant made up of?

A

lecithin, phosphatidylglycerol, surfactant proteins for host defense and decrease in surface tension

56
Q

What is the main outcome of endothelial and epithelial damage in RDS?

A

fibrin and necrotic cells forming a hyaline membrane in the lungs

57
Q

What things stimulate surfactant production?

A

cortisol, insulin, prolactin, thyroxine, TGFB

58
Q

What are some things that can increase the likelihood of RDS?

A

GD and c-section

59
Q

What are some of the key morphological characteristics of RDS?

A

alternating atelectasis and dilation of alveoli, necrotic cellular debris incorporated within eosinophilic hyaline membranes lining bronchioles, alveolar ducts, and alveoli

60
Q

What is the common presentation of RDS

A

intercostal and substernal retractions, perioral cyanosis, preterm but appropriate weight, rales, ground glass opacification on xray

61
Q

What mutated genes are associated with congenital surfactant deficiency?

A

SFTPB and SFTPC

62
Q

What is tested in amniotic fluid to assess lung maturity?

A

lecithin-sphingomyelin ratio, >2.0 indicates lung maturity

63
Q

What are the two most common complications associated with prolonged oxygen supply for RDS infants?

A

retrolental fibroplasia and bronchopulmonary dysplasia

64
Q

Pathogenesis of retinopathy of prematurity

A
  1. Hyperoxic phase: decreased VEGF causing apoptosis

2. Hypoxic phase (on room air): increased VEGF inducing retinal vessel proliferation

65
Q

Pathogenesis of bronchopulmonary dysplasia

A

decrease in alveolar septation and dysmorphic capillary configuration, proinflammatory cytokines disrupt alveolar development

66
Q

What key inflammatory cytokines are involved in bronchopulmonary dysplasia?

A

TNF, IL-1B, IL-6, IL-8

67
Q

Pathogenesis of necrotizing entercolitis

A

multifactorial; prematurity, enteral feeding with postnatal insult

68
Q

What is the role of PAF in necrotizing enterocolitis?

A

increasing mucosal permeability by promoting enterocyte apoptosis and compromising tight junctions

69
Q

Clinical course of necrotizing enterocolitis

A

bloody stools, abd distention, circulatory collapse, gas within intestinal wall on xray

70
Q

What organs does NEC typically involve?

A

terminal ileum, cecum, right colon; BUT any part of intestines may be involved

71
Q

Gross morphological changes to intestines in NEC

A

distended, friable, congested, gangrenous, perforation accompanying peritonitis

72
Q

Microscopic morphological changes to intestines in NEC

A

mucosal or transmural coagulative necrosis, ulceration, bacterial colonization, submucosal gas bubbles (pneumatosis intestinalis)

73
Q

What are some possible complications associated with surgical treatment for NEC?

A

strictures from fibrosis, decreased absorption

MOD (34 decks)

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