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Pathology 2 > 2.3 disorders of prematurity > Flashcards

2.3 disorders of prematurity Flashcards

1
Q

highest frequencies of death under 1 year

A

congenital mlaformation, deformation, and chromosomal abnormalities, disorders related to short gestation and low birth weight, sudden infant death syndrome (SIDS)

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2
Q

congenital anomalies

A

morphological defects present at birth, may not be expressed until later in life, can or cannot be genetic defect, 3% of newborns have a major anomaly (cosmetic or functional significance), most common cause of death in first year of life, significant cause of mortality and morbidity in all early years of life, in reality, observed anomalies in live births represent the leaset serious that occur

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3
Q

malformations

A

primary error of morphogenesis with intrinsic abnormal development (anencephaly, congenital heart defects). Multifactorial. Single/multiple

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4
Q

disruptions

A

secondary destruction of organ/body region that was previously normal in development. Extrinsic distrubance (amniotic bands that compress portions of fetus)

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5
Q

Anencephaly

A

neural tube defect with absence of cerebral hemisphere, skull, and skin

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6
Q

cleft lip/palate

A

if isolated - compatible with life, with malformation syndrome - severe cardiac defects

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7
Q

deformations

A

like disruptions these are due to extrinsic disturbance as a localized/generalized fetal compression by biomechanical forces –> structural anomalies (uterine constraint, oligohydramnios) –>(club feet)

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8
Q

Sequence

A

cascade of anomalies triggered by one initiating event

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9
Q

Potter sequence of oligohydramnios

A

renal agenesis, amniotic leak, maternal HTN, toxemia (U/O insff) —-> all lead to oligo hydramnios —–>can lead to amnion nodosom (plaques of squamous cells and fibrin), pulmonary hypoplasia, and fetal compression —-> fetal compression can lead to pulmonary hypoplasia, altered facies, positioning defects of feet and hands, breech presentation

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10
Q

syndrome

A

a constellation of congenital anomalies that are thought to be pathologically related but unlike a sequence can not be explained by a single initiating event. Can have a single etiology, eg a viral disease or chromosomal alteration that affects different tissues

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11
Q

Causes of anomalies

A

genetic, environmental and multifactorial (50 - 75% unknown)

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12
Q

genetic causes of congenital anomalies

A

chromosomal (karyotypic) abberations, single gene mutsionts

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13
Q

karyotypic abberations

A

10-15% of CA

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14
Q

when do most karyotypic abberations occur

A

during gametogenesis (not familial)

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15
Q

ex of karyotypic abberation

A

Down’s a la Robertsonian translocation of 21 with another chromosome (4%)

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16
Q

karyotypic abberations and death

A

80-90% of chromosomal number abberations die in the uterus

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17
Q

single gene mutations inheritance

A

90% AD or AR and 10% X-linked

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18
Q

examples of loss of fn genes involved in normal organogenesis

A

sonic hedgehog - holoprosencephally, HOXGL13 - digit anomalies (polydactyly, syndactyly)

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19
Q

holoprosencephaly

A

incomplete separation of cerebral hemispheres across the midline

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20
Q

prematurity

A

gestational age less than 37 weeks

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21
Q

2nd leading cause of neonatal mortality

A

prematuraty (1st would be congenital anomalies), premature babies have higher rates of morbidity and mortality than full term babies

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22
Q

aga

A

appropriate for gestational age (btw the 10 and 90 percentile)

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23
Q

sga

A

small for gestational age

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24
Q

lga

A

large for gestational age

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25
Q

birthweight and gestational age implications

A

a premature infant of 2300g may be as large as a term infant at 2300g but still has immature organs esp. lungs, An AGA 1500g infant born at 32wks is better off than an SGA 700g infant born at 32 wks

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26
Q

preterm

A

before 37 weeks

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27
Q

post term

A

after 42 weeks

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28
Q

risk factors for prematurity and fetal growth restriction

A

premature rupture of placental membranes (PPROM, PROM), intrauterine infection, uterine, cervical, placental structural anomalies, multiple gestations, additional factors: immaturity of organs

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29
Q

PPROM

A

preterm premature rupture of Membranes

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30
Q

PROM

A

premature rupture of Membranes

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31
Q

PPROM

A

causes 30-40% of preterm deliveries

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32
Q

PROM

A

carries far lower risk (spontaneous or induced)

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33
Q

Risks of PPROM

A

smoking, prior Hx, and vaginal bleeding

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34
Q

intrauterine infection

A

present in 25% of preterm births, can be a cause of (P)PROM or be a result of (P)PROM

35
Q

histology of intrauterine infection

A

chorioamionitis (membranes) and Funisitis (cord)

36
Q

most common intrauterien infection

A

Group B strem

37
Q

how is preterm labor induce by infection

A

TLR4 activation –> (inflammatory cells drawn into area –> ROM and proteases), (deregulation of prostaglandins –> uterine contractions–> inflammation-induced Preterm Labor)

38
Q

maternal and placental structural anomalies

A

fibroids, incompetent cervix, placenta previa (implantationsin lower uterus), abruptio placenta (premature separation) —most common in late preg, placenta accreta (no decidua implantation into uterine wall)

39
Q

multiple gestation

A

twin pregnancy

40
Q

immature organs

A

lung, kidneys - usually deep glomeruli mature enough for survival, brain -vital brain center OK. Temp reg and respiration control are affected, Liver - generally OK but bilirubin handeled poorly so many are jaundiced

41
Q

fetal growth restriction (FGR)

A

same as intrauterine growth restriction (IUGR) - condition in shice a fetus is unable to achieve its genetically determined potential size (shorter)

42
Q

Asymmetric FGR

A

(70-80%) - normal head size, dec crown to heel

43
Q

Symmetric FGR

A

(20-30%) -dec birth weight, all organs are similarly affect, small head, short stature

44
Q

FGR can be detected in utero by

A

ultrasound

45
Q

Measurements vs. gestational age

A

BPD, HC, AC, H/A circumference ratio

46
Q

causes of FGR

A

fetal, placental, maternal

47
Q

fetal causes of FGR

A

intrinsic problem with fetus despite adequate support, chromosomal abnormalities, congenital infections - TORCH organisms (Toxoplasma, Rubella, CMV, Herpes, Other), congenital anomalies, fetal causes usually have symmetric growth restriction

48
Q

Placental causes of FGR

A

during 3rd rim –> vigorous fetal growth –> inc U/P supply, any cause of placental insufficency is critical, abruptio placenta, palcenta previal, thrombosis, infection, infarction, small placenta, cord anomalies, single arter (AA/V), abnormal insertion, usually results in asymmetrical FGR with brain spared

49
Q

placenta previa

A

placenta is implanted in cervical os, during labor it dialates and the placenta starts bleeding, but patient has no pain, most common antepartum bleeding

50
Q

abruptio placenta

A

complains of pain bc there is blood/hemmoraging on the side of the uterine wall and blood cant get out

51
Q

most frequnt cause of SGA

A

maternal causes of FGR

52
Q

maternal causes of FGR

A

conditions affecting mothers health/blood flow including Preeclampsia, eclampsia, chroinic HTN, Inherited thrombophilias, Alcohol, heavy smoking, drugs, general malnutrition

53
Q

preeclapsia

A

hypertension, proteinuria, edema

54
Q

eclampsia

A

progression to seizures and DIC

55
Q

example of inherited thrombophilia

A

factor V laiden mutation

56
Q

Neonatal respiratory Distress Syndrome – hyalin membrane disease

A

most common cause of respiratory distress, can occur in term infants but most in preterm and AGA, rate inversely proportional to gestational age (60% 34wks), immaturity of lungs means inability to secrete surfactant

57
Q

Surfactant is secreted by

A

Type II pneumocytes (approx 35wks gestation)

58
Q

Surfactant consists of

A

lipid (dipalmitoyl phosphatidyl choline), phosphatidylglycerol, and hydrophobic proteins SP-B and C (dec surface tension)

59
Q

the first breath

A

requires a large inspiratory effort but once inflated the lungs remain 40% inflated

60
Q

if no surfactant

A

lungs collapse back and every breath is as hard as the first

61
Q

what leads to breathing difficulty in RDS

A

stiff lungs and soft chest wall

62
Q

what induces surfactant secretion

A

glucocorticoids and thyroxine

63
Q

what induces surfactant synthesis

A

labor

64
Q

what inhibits surfactant secretion

A

high levels of insuline

65
Q

what are predisposing factors for increased risk of RDS

A

prematurity, maternal diabetes, and cesarean delivery –think about why

66
Q

immatur lung histology

A

thick, even at 30 weeks

67
Q

Pathophysiology of RDS

A

see pic

68
Q

gross anatomy of lung with rds.hyaline membrane disease

A

solid, airless, redish-purple, sink in water

69
Q

RDS clinical course

A

rapid, labored respiration, substernal retraction, cyanosis, grunting, nasal flaring at birth, ground glass on xray

70
Q

how to deal with preventing/treating RDS today

A

much more favorable today, monitoring amniotic fluid for surfactant for lung maturity, antenatal treatment with steroids, adminstration of surfactant, acute death now unusual, recovery begins at about 4 days

71
Q

RDS treatmetn risks

A

therapy with O2 carries risks – retinopathy of prematurity and bronchopulmonary dysplasia

72
Q

Lecithin:Sphingomyelin ration – L/S ratio

A

L/S ratio of 2 or more indicates a relatively low risk of infant RDS, and an L/S ratio of less than 1.5 is associated with a high risk of infant RDS

73
Q

good LS ratio by about

A

35 weeks –8/2 – ratio of 4

74
Q

retrolental fibroplasia – aka retinopaty of prematurity

A

hypoxia leads to increase in VEGF leading to dec in endothelial cell apoptosis, and inc in angiogenesis, O2 therapy and hyperoxia (phase 1) dec VEGF, then ralative hypoxia (room air) inc VEGF (phase 2 - retinal vessel proliferation), even with very careful o2 monitoring, retinopaty can resul suggesting other causes

75
Q

Bronchopulmonary Dysplasia

A

now infrequent in infants >1200g and 30 weeks, usually in 28 days

76
Q

multiple factors associated with bronchopulmonary dysplasia

A

hyperoxemial, hyperventilation, prematurity, inflammatory cytokines, and vascular maldevelopment

77
Q

prognosis of RDS babies

A

infants who recover from RDS are t increased risk for PDA(patent ductus arteriosus), intraventricular hemorrhage, and NEC (necrotizing enterocolitis)

78
Q

Necrotizing Enterocolitis (NEC)

A

occurrence inversely related to gestational age (1 in 10 of <1500g)

79
Q

NEC pathogenesis

A

multifactorial, prematurity, most cases associated with oral feeding, suggesting infectious organisms, also inflammatory mediators, inflammation leads to mucosal breakdown (necrosis) invasion by bacteria, sepsis, and shock

80
Q

NEC clinical manifestations

A

premature, fever, bloody stools, distended abdoment, and vascular collapse

81
Q

NEC Rx

A

air in intestinal wall (pneumatosis intestinalis) – usually involves terminal ileum, cecum, and proximal colon

82
Q

NEC treatment

A

Early NPO, IV fluids, Orogastric tube, antibiotics; Later surgery to remove fibrotic segments

83
Q

NEC and mortality

A

high mortality and post-natal strictures from healing

84
Q

Germinal Matrix Hemorrhage

A

subependymal (periventricular) hemorrhage w/ extension into ventricles occurs in preterm infants, microcirculation extremely sensitive to hypoxia and changes in perfusion pressure, common cause for admissions to neonatal ICU in <1500g babies

Pathology 2 (15 decks)

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