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P020A Lecture 5 -. Course Objective #30 Identify the causative agent and the effects on the fetus in the following maternal infections: – Rubella – Toxoplasmosis.

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Presentation on theme: "P020A Lecture 5 -. Course Objective #30 Identify the causative agent and the effects on the fetus in the following maternal infections: – Rubella – Toxoplasmosis."— Presentation transcript:

1 P020A Lecture 5 -

2 Course Objective #30 Identify the causative agent and the effects on the fetus in the following maternal infections: – Rubella – Toxoplasmosis – Syphilis – Cytomegalovirus

3 Development Cephalocaudal Proximal-distal

4 Rubella AKA – German Measles

5 Congenital Rubella Syndrome AKA – “Blueberry Muffin Syndrome” 1 st trimester – 85% affected After 20 weeks – Defects rare

6 Congenital Rubella Syndrome Etiology Intrauterine Infection Critical Time period – 1 st trimester

7 Congenital Rubella Syndrome FYI 1941 Australian epidemic – 78 infants w/CRS US epidemic – 20.5 M cases of Rubella  – 20,000 infants w/CRS

8 Congenital Rubella Syndrome S&S Varied ID – Normal – severe Sensory defects – Deaf* – Blind

9 Congenital Rubella Syndrome S&S – Cardiac defects – Microcephaly – Bone abnormalities – Purpura

10 Congenital Rubella Syndrome Treatment Prevention – Rubella vaccine licensed in 1969 MMR – 2005 Rubella eradicated in US

11 Rubella Virus Eliminated in the United States Washington Post --Monday, March 21, 2005 The invisible "chain of transmission" of rubella virus has been broken in the United States. With it disappears a disease that a little more than a generation ago struck fear in the heart of every pregnant woman. Fewer than 10 people a year in this country now contract the infection known popularly as German measles. Since 2002, all cases have been traceable to foreigners who carried the virus in from abroad.

12 Congenital Toxoplasmosis Toxoplasmosis – Protozoa Parasite – “Transplacental spread”  Congenital Toxoplasmosis

13 Congenital Toxoplasmosis Etiology – Raw, undercooked meat, – Cat feces, – Non-pasteurized milk

14 Congenital Toxoplasmosis Incidence – 1:10,000 births Prognosis – Many die in 1 st month

15 Congenital Toxoplasmosis S&S – Vary widely depending on period of infection

16 Congenital Toxoplasmosis S&S Triad – Hydrocephalus – Intracranial calcification – Chorioretinitis

17 Congenital Toxoplasmosis Severe ID Blindness Epilepsy Low birth weight Hepatosplenomegaly  – Jaundice

18 Congenital Toxoplasmosis Tx – Antibiotics

19 Congenital Toxoplasmosis Dx – Amniocentesis – Ultrasound

20 Congenital Syphilis Etiology: – Spirochete bacterium – Bacteria!!!!

21 Congenital Syphilis Mom  infant – during pregnancy or birth Fetus vulnerable – after 18 weeks

22 Congenital Syphilis Incidence – 1:100,000 live births (CDC, 50% die in utero or shortly before or after birth

23 Congenital Syphilis S&S Early stage Failure to thrive, Nasal discharge Blistery rash No nasal bridge

24 Congenital Syphilis Late stage Hutchinson’s triad – Hutchinson’s teeth – Keratitis – Deaf

25 Congenital Syphilis Late stage ID Bone pain Vision/hearing loss

26 Congenital Syphilis Treatment – Mom Prenatal care Antibiotics – Delivery Cesarean

27 Congenital Cytomegalovirus Herpes-like infection

28 Congenital Cytomegalovirus Etiology – Transplacental spread

29 Congenital Cytomegalovirus FYI Mom may be asymptomatic 1% all newborns test positive for CMV 95% asymptomatic 5% congenitally affected

30 Congenital cytomegalovirus The mother's illness may not have symptoms, so she may be unaware that she has CMV.

31 Congenital Cytomegalovirus S&S Inflammation of the retina Hepatosplenomegaly  – Jaundice Low birth weight Petechiae Seizures Microcephaly

32 Congenital Cytomegalovirus Dx Tests Antibody titer against CMV Bilirubin level TORCH screen

33 Congenital Cytomegalovirus Tx Focus on specific problems

34 Congenital Cytomegavirus Prognosis Up to 90% of infants who have symptoms of their infection at birth will have neurologic abnormalities later in life. Only about % of infants without symptoms will have these problems.

35 Congenital Cytomegalovirus FYI -neonatal death is common

36 Congenital Cytomegalovirus Prevention CMV is almost everywhere Wash hands p touching diapers ⌀ kiss kids < 6 yrs ⌀ share food c kids PG ⌀ work with < 2 1/2

37 Objective #31 Describe the cause, sequence of events, pathology and preventative factors of erythroblastosis fetalis.

38 Course Objective #32 Describe the relationship of the Rh factor disorders and kernicterus

39 Erythroblastosis Fetalis What is erythroblastosis fetalis?

40 Erythroblastosis Fetalis Hemolytic disease – ABO incompatibility – Rh incompatibility

41 Erythroblastosis Fetalis Neonate red blood cell destruction

42 Erythroblastosis Fetalis S&S Anemia Hepatoslenomegaly Jaundice Hydrops

43 Erythroblastosis Fetalis Dx test Complete blood count and immature red blood cell (reticulocyte) count Bilirubin level Blood typing

44 Erythroblastosis Fetalis Treatment Phototherapy: – bilirubin breaks down when exposed to UV light Blood transfusion

45 Maternal-Fetal Blood Incompatibilities -Rh Incompatibility -ABO Incompatibility

46 ABO Incompatibility Etiology – Mom blood type O – Fetus blood type A B

47 ABO Incompatibility S&S Mild – Anemia – Jaundice

48 ABO Compatibility Severe  – Kernicterus Brain damage d/t  bilirubin levels

49 ABO Incompatibility Treatment Phototherapy

50 Rh incompatibility Mom blood type – Rh- Fetus blood type – Rh+

51 Rh incompatibility Mom develops antibodies to Rh+ Immune response  Destruction of RBC of fetus

52 Rh incompatibility Anemia  bilirubin

53 Rh incompatibility Neonates Liver can’t adequately metabolizes bilirubin  Kernicterus

54 Rh incompatibility S&S - Uterio Polyhydramnios  bilirubin

55 Rh incompatibility S&S - neonate Mischarge Jaundice Hypotonia Lethargy

56 Rh incompatibility Treatment (neonate) Phototherapy Blood transfusions

57 Rh incompatibility Treatment RhoGAM

58 Rh incompatibility Full recovery is expected for mild Rh incompatibility.

59 Rh incompatibility Prevention RhoGAM Prevents development of antibodies against Rh+ blood Schedule – 2 nd trimester – Post deliver

60 Kernicterus Neonatal brain damage due to destruction of RBC in utero   bilirubin  crosses “blood-brain barrier”  Brain damage

61 Kernicterus Etiology Rh incompatibility Drugs liver anomalies Blood incompatibilities

62 Kernicterus S&S Varied S&S Characteristic: jaundice

63 Kernicterus S&S Choreoathetosis Spastic paralysis Hypotonia Anemia Hypoxia

64 Course Objective #33 Describe the fetal effects from maternal use of the following teratogens – Narcotics – Marijuana – Alcohol – Thalidomide – Anti-convulsants – Tobacco

65 Drugs and Alcohol (teratogens-potential to produce mutation) Teratogens potential to produce mutation

66 Narcotics Examples: Heroin Methadone

67 Narcotics Effect Retarded fetal growth/low birth weight Addicted

68 Narcotic Addicted Neonate Withdrawal S&S – day 4 four – Last a few weeks :

69 Narcotic Addicted Neonate S&S - Withdrawal – Tremors  seizures –  swallow – Diarrhea – Tachypnea –  temp  diaphoresis

70 Narcotic S&S up to 6 mo. Hyperirritability Hyperreflexia Tremulousness  social responsiveness

71 Narcotic S&S up to 6 mo. No evidence of congenital abnormalities

72 Cocaine Drug type – Stimulant Action: – constricts blood vessels  –  circulation to brain

73 Cocaine Transmission – Transplacental – Lactation

74 Cocaine Effects: – MOM increased risk of abruptio placentae

75 Cocaine Effects: Baby – low birth wt – small – premature

76 Cocaine Withdrawal begins – when cord is cut

77 Cocaine Withdrawal S&S – Tachycardia – Tremors – Hyperirritability – feeding problems – sleep problems –  risk of seizures (lifelong)

78 Cocaine FYI -by 2 years, 2/3 are developing normally -other 1/3 show difficulty maintaining attention, interacting with other children, adapting to change

79 Marijuana Hallucinogen

80 Marijuana  muscle mass Tremors  startle reflex

81 Alcohol Type of drug – Depressant

82 Alcohol Effects – variable

83 Alcohol Fetal Alcohol Effects Less severe Fetal Alcohol Syndrome Severe

84 Fetal Alcohol Syndrome Full-blown

85 Alcohol Alcohol   umbilical blood circulation  Hypoxia

86 FAS Characteristics  palpebral fissures Flat nose bridge & philtrum Thin upper lips

87 FAS Characteristics Microcephaly Delayed development ID Hyperactivity

88 FAS: Infancy Small w/ Stunted growth Microcephaly Tremor Irritable  sucking reflex Failure to thrive

89 FAS: Early Childhood Speech & motor delayed Short Hyperactivity FAS face diminish

90 FAS: School Age ID – 2/3 moderate – low/average IQ Behavior problems Hyperactivity & ADD

91 FAS: Young Adulthood Cognitive problems – Memory – Orientation to time, space, – Judgment Vulnerable to – alcoholism

92 FAS: Treatment Symptomatic Prevention

93 Rx: Thalidomide Action – Anti-emetic Critical time period – First trimester

94 Thalidomide Effect on fetus Limb deformities Normal intelligence

95 Anticonvulsants Rx: Dilantin (Phenytoin) Effect: – 4-7% cleft lip / palate

96 Anticonvulsants Monitor lab values Risk to benefit Poly-pharmacy   risk

97 Nicotine Type of drug – Stimulant Effects –  birth weight Critical time period – 3 rd trimester

98 Maternal-Fetal Irradiation AKA: – X-ray Effects – Microcephaly

99 Radiation Critical time period – 1 st & 2 nd trimester

100 Course Objective #34 State the various cause and results to the infant of perinatal asphyxia.

101 Asphyxia Brain injury during delivery caused by prolonged deprivation of fetal O2 Maybe permanent CNS effects

102 Perinatal Toxemia / Eclampsia Prematurity Physical Trauma Infection

103 Toxemia Triad S&S (Maternal) – HTN – Edema – Proteinuria

104 Toxemia  B/P   circulation to the uterus   O2

105 Toxemia Placenta degenerates Critical period – 3 rd trimester

106 Pre-Eclampsia + for 3 S&S of toxemia Most common in – Primigravida

107 Eclampsia 3 S&S + seizure  risk – Maternal death – Fetal loss

108 Complications of Toxemia Abruptio placentae Hemolysis Cerebral hemorrhage Pulmonary edema Renal failure

109 Toxemia Treatment Termination of pregnancy resolves all symptoms!

110 Prematurity Birth weight < 5.5 lbs. OR Gestational age < 38 wks.

111 Prematurity Moms without prenatal care are 3 times more likely to birth early

112 Prematurity: Risk Factors Lack prenatal care  $ Smoking Maternal age – < 18 – >35

113 Vulnerabilities of Premature Infants 1.Death 2.ID 3.  temp regulation

114 Vulnerabilities of Premature Infants 4.  sucking/swallowing 5. immature liver 6. O2 deprivation

115 Vulnerabilities of Premature Infants 7. Vision problems 8. Cerebral hemorrhage 9. Infection

116 Infection Herpes Simplex

117 80% result in death or serious problems – ID – Blind

118 Herpes Simplex Causative agent: – Herpes simplex virus 2 (HSV-2) Genital Prevention – C-section

119 Postnatal Infections Cerebral Trauma Cerebrovascular Accident Brain Tumors Poison and Environmental Toxins Malnutrition Cerebral Palsy Epilepsy

120 Physical Trauma Leading cause of death infant – MVA

121 Physical Trauma 2 nd leading cause of death - < 2yrs – Abuse

122 Course Objective #35 State the symptoms seen in a child suffering from: A. Lead poisoning B. Mercury poisoning

123 Poisons and Environmental Toxins: Lead Source – Paints – Water

124 Poisons and Environmental Toxins Severe effect: Lead encephalitis S&S – Stupor – coma – Seizures

125 Poisons and Environmental Toxins: Lead Effect –  IQ –  attention span, – personality changes

126 Poisons and Environmental Toxins: Lead Treatment – Diet –  fat –  iron, Ca, Vitamin C

127 Poisons and Environmental Toxins Mercury Food – TUNA

128 Poisons and Environmental Toxins Mercury: S&S Paresthesia Vision impairment Motor problems Hearing ID


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