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FEMALE reproductive > reproductive: PREGNANCY > Flashcards

reproductive: PREGNANCY Flashcards

1
Q

when and where does spermatogenesis begin?

A
  • begins at puberty

- occurs in seminiferous tubules

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2
Q

how spermatogenesis start at puberty ?

A

sex cords in testes develop a lumen that become seminiferous tubules

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3
Q

SOS #n #c in spermatogenisis and oogenesis with time period and stages :)))

A

A- 2n 2c diploid
-males: SPERMATOGONIA (at puberty)
-females: OOGONIA (divide in utero)
(both derived from primordial GERM CELLS)
—-—> DNA synthesis
B- 2n 4c diploid
-males: PRIMARY SPERMATOCYTES
-females: PRIMARY OOCYTE (arrest in meiosis I prophase until puberty)
———>meiosis I
C- 2 (1n 2c) haploid
-males: SECONDARY SPٍِERMATOCYTE
-females: a-SECONDARY OOCYTE (at menstrual cycle, note: other primary oocytes become polar bodies and degenerate)
—-—> meiosis II
MALES: 4 (1n 1c) haploid : SPERMATIDS: 4 haploid gametes result—> then: undergo SPERMIOGENESIS!!!
to form: sepermatozoa (sperm)

FEMALES:
no fertilization: oocyte degenerates (NO MEIOSIS II)
fertilization: COMPLETES MEIOSIS II to form OVUM 1 (1n 1c) haploid

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4
Q

what is spermiogenesis?

how is it done? 4 steps

A

formation of spermatozoa (from spermatids)
1-formation of ACROSOME: cap of sperm (contains enzymes to assist in fertilization)
2-condensation of nucleus
3-formation of neck and tail
4-shedding of most of cytoplasm

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5
Q

sertoli cells and leydig cells and spermatogonia

  • location and function?
  • how is it stimulated?
A 
sertoli cells
-line walls of seminefrous tubules 
-support/regulate spermatogenesis 
-stimulated by FSH 
leydig cells
-interstitium (between tubules)
-secrete testosterone 
-stimulated by LH 
spermatogonia 
-behind blood-testis barrier 
(separated from tubule by sertoli cells)
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6
Q

relation between sertoli cells and leydig cells in spermatogenesis

A

leydig cells release testesterone (stimulated by LH) which acts in a a PARACRINE manner to support sertoli cells (stimulated by FSH)

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7
Q

what cells form the BLOOD-TESTIS BARRIER? what type of junctions and why are they important? and describe both sides (apical/basal)

A

-sertoli cells
-tight junctions b/w adjacent sertoli cells
(isolate sperm, protection from autoimmune attack)
-apical side (toward tubule): meiosis and spermiogenesis
-basal side: spermatogonia cell division

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8
Q

what hormones are needed for normal spermatogenesis?

FSH, LH,….???

A

FSH

LH

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9
Q

function of placenta

A

1- nutrient

2- gas exchange

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10
Q

what is a decidual reaction

A

endometrium rxn at implantation

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11
Q

what are the 2 membranes that surround the fetus in utero?

A

1- AMNION (inner membrane)
holds amniotic fluid
2- CHORION (surrounds amnion/embryo)
derived from trophoblast

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12
Q

basal plate vs chorionic plate

of the placenta

A

basal plate (maternal side)
-includes maternal decidua basalis
chorionic plate (fetal side)
-give rise to chorionic villi

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13
Q

what layer of the blastocyst develops into placenta

A

outer layer: trophoblast

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14
Q

2 cell layers of trophoblast?

both together form what?

A

1- syncytiotrophoblast (outer)

  • invades endometrium
  • villi
  • form lacunae (spaces) for maternal blood

2- cytotrophoblast (inner)

  • proliferates, thus cells migrate into (1)
  • secretes proteolytic enzymes to aid invasion

they form the chorionic villi

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15
Q

chorionic villi function and layers

A

contact area with maternal blood: digestive tract (nutrients) and resp organ (gas exchange)

  • outer: syncytiotrophoblast
  • inner: cytotrophoblast
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16
Q

how does the chorionic villi connect to the umbilical cord

A

fetal MESODERM invades villi,

branches of umbilical artery/vein grow :)

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17
Q

placental circulation

  • maternal side
  • fetal side
A

maternal
1- endometrial spiral arteries
2- villous space
3- endometrial vein

fetal
1-umbilical arteries (deoxy)
2- chorionic arteries
3- capillaries

4- capillaries
5- umbilical vein (oxy)

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18
Q

placental barrier

  • oxygen co2?
  • glucose?
  • a.a?
  • abs?
A
  • diffusion
  • facilitated
  • active
  • only IgG
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19
Q

umbilical cord is derived from mother or fetus? what parts ?

A

only FETUS
derived from:
1- yolk sac
2- allantois

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20
Q

what is the allantois?
what does it become?
what happens to it later?

A
  • outpouching from wall of gut
  • walls form umbilical blood vessels
  • lumen occludes in development: become URACHUS: fibrous remnant: connects bladder to umbilicus
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21
Q

umbilical cord consists of

A

2 umbilcal arteries (deoxy)
1 umbilical vein (oxy)
-wharton jelly (contains mucopolysaccharides- similar to vitreous humor)
-allantoic duct (connects fetal bladder to umbilical cord) obliterates-urachus

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22
Q

what fetal anomalies are associated with single umbilical artery

A

1- aneuploidy

2- congenital malformations

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23
Q

what is a remnant of allantois ?
connects what?
becomes what?
may cause ?

A

urachus

  • bladder and umbilical cord
  • in adult: median umbilical ligament
  • may cause ADENOCARCINOMA of bladder
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24
Q

urachus anomalies 3

A 
1- patent urachus 
urine discharge from umbilicus 
2- vesicourachal diverticulum 
diverticulum of bladder
3-urachal cyst 
partial obliteration 
fluid filled cavity —> infection risk
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25
Q

immunology of pregnancy

since fetus half genes are from the father (i.e HLA protein differ from mother) how is he protected? sosososo

A

by PLACENTA
1- trophoblast cells DO NOT EXPRESS MANY MHC CLASS I antigens
2- placenta secretions BLOCK IMMUNE response

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26
Q

dizygotics (fraternal twins) vs monzygotic (identical twins)

A

-dizygotic
2 zygotes (2 ova 2 sperms)
-monozygotic
1 zygote divides in 2 (1 ova 1 sperm)

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27
Q

more fetuses = shorter pregnancy, how many wks?
single:
twin:
triplets:

A

single: 40 wks
twin: 37 wks
triplets: 33 wks

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28
Q

what is more common when IVF is used ?

mono di

A

dizygotic twins

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29
Q

how many amnion/chorion is there in dizygotic twins?

A

DIchorionic DIamniotic

i.e 2 seperate placentas

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30
Q

how many amnion/chorion is there in monozygotic twins? explain
when can a woman get conjoined twins (time of division) :)

A 
depends when zygote divides:
-days 1-3 (MORULA)
dichorionic diamniotic 
-days 4-8 (BLASTULA)
monochorionic diamniotic 
-days 9-12 (IMPLANTED BLASTULA) 
monochorionic monoamniotic 
-days +13 (FORMED EMBRYONIC DISC)
monochorionic monoamniotic (conjoined twins)
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31
Q

what are the increased risk of twin pregnancies ?

  • fetus
  • mother
A 
fetus
-growth restriction 
-congenital anomalies 
-preterm delievery 
mother
-gestational hypertension/ preeclampsia
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32
Q

embryonic age vs gestational age

A
  • embryonic age: age dated to FERTILIZATION

- gestational age: age dated to LMP (i.e embryonic age +2 weeks)

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33
Q

when (related to period) and where does fertilization happen?

A
  • occurs within 1 day of ovulation

- ampulla of fallopian tube

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34
Q

when does implantation occur?

how is menstruation prevented (i.e maintained) ??

A 
-6 days after ovulation 
—->for the 1st 10 wks: 
-syncytiotrophoblast secretes hCG 
which: 
1- maintains CORPUS LUTEUM 
2-CL continues PROGESTERONE release 
thus menstruation is prevented
—->after 10 wks
-placenta secretes hCG
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35
Q

why do we check BETA hCG and not ALPHA?

A

hCG has a and b

same alpha in: hCG, LH, FSH, TSH

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36
Q

describe the structure of hCG:

its similar to what hormone?

A

2 glycoprotein subunits (heterodimeric glycoprotein)

SIMILAR TO LH !!!!!

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37
Q

what type of test is used to detect pregnancy (using HCG)? what do they detect?

A

antibody based tests (ELISA variants)

-detect BETA subunit of hCG !!

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38
Q
  • what is more sensitive serum or urine hCG test?

- when does each show positive result?

A
  • serum tests are the MOST SENSITIVE ! (detect very low levels 1-2 mIU/mL) but urine has a threshhold of 20-50 mIU/mL
  • serum: within 1 wk of conception
  • urine: may not be positive until 2wks or more
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39
Q

what hormones are produced by the sycytiotrophoblast?

A

1- hCG

2- human placental lactogen (chorionic somatomammotropin) —> higher levels as placenta grows during pregnancy

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40
Q

what is the most important effect of human placental lactogen (protein hormone)?

A

BLOCKS EFFECTS OF INSULIN (useful for fetus)
1- raises blood glucose level
2- promotes breakdown of fatty acids by mother for fuel
3- promotes breakdown of proteins for fuel

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41
Q

remember that :

A

PREGNANCY is an INSULIN-RESISTANT STATE :))))))

i.e decreased maternal response to insulin

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42
Q

what happens to the diabetes of a pregnant diabetic women?

A

it is worsened

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43
Q

how do we screen for glucose in pregnant women and why? sos

A

SERUM GLUCOSE TESTING
because glycosuria occurs in normal pregnancy :) due to less absorption of glucose by the proximal tubules
i.e urine testing is NOT useful

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44
Q

list 5 physiological changes during pregnancy

A 
1- total body volume expands 
2- red cell mass expands 
3- hemodynamics 
a- cardiac output rises 
b- peripheral resistance falls 
4- hyper-coagulable state 
5- ventilation increases
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45
Q

how does plasma volume (total body volume) expands during pregnancy?

A

blood fills placenta so mom increases renin to increase salt and water retention

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46
Q

what type of anemia is caused during pregnancy? explain

A

DILUTIONAL ANEMIA : mild asymptomatic
rise in volume&raquo_space; rise in red cells
NOTE: there is a rise in red cell mass d/t increased maternal EPO

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47
Q

what happens to the cardiac output during pregnancy? what factors affect it? 3

A

CO increases
1- PRELOAD increases (BV increase)
2- AFTERLOAD decreases (SVR decrease)
3- maternal HR increases slightly

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48
Q

what is the mechanism that leads to a physiological DECREASE in BP in pregnant women??? sos

A

peripheral resistance falls

  • (PLACENTA is a low resistance system)
  • (maternal vasodilation)
    i. e placenta has a PARALLEL (not SERIES) resistance with the mother so the total resistance decreases
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49
Q

when the placenta is removed, what happens to the peripheral resistance? what association that effect has on the heart?

A

peripheral resistance (for both mom baby) RISE

  • increase left atrial pressure
  • closes the foramen ovale
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50
Q

pregnant women with palpatations when laying down

diagnose? +mechanism

A

supine hypotension
LARGE BABY (later stages) compresses IVC when lying flat:
decreased venous return —> decreased preload —>decreased CO
note: symptoms are due to the response: REFLEX TACHYCARDIA

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51
Q

what clotting factors change during pregnancy 2 ? lead to what state?

A

1- increased fibrinogen
2- decreased protein S
HYPERCOAGUABLE STATE

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52
Q

what are the physiological pulmonary changes during pregnancy?

  • ventilation ?
  • tidal volume ?
  • resp rate?
A

VENTILATION INCREASES
-more CO2 to exhale (baby metabolism)
d/t increased tidal volumes
-RR minimally changed

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53
Q

what are the 3 physiological changes that leads to labor?

A

1- regular uterine contractions
2- progressive dilation of cervix
3- descent and expulsion of fetus

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54
Q

what is preterm labor in wks ?

A

<37 wks

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55
Q

women develops uterine contractions very EARLY during pregnancy. tx?

A

Terbutaline/ Ritodrine
B2 agonists —> increase cAMP
thus relaxes uterine SMOOTH muscle
inhibiting contractions

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56
Q

what score is used to asses newborn immediately after birth?
what is the score out of?
at what times after birth?
what are the 5 factors ?
what is considered low score? at what time? leads to what dx?

A

-Apgar score
-10 points score
-at 1 and 5 min after birth
1-HR
2-Resp effort
3-muscle tone
4-reflex irritability
5-skin color (pink,blue)
-5min score = 3 , associated with NEUROLOGICAL damage (e.g cerebral palsy)

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57
Q

what are the 2 drugs used to terminate pregnancy ? moa? combination leads to medical abortion in ??% women ?

A

1- Mifepristone
anti-progesterone (blocks prog effects on uterus)
thus, prevents implantation (sheds the uterine lining)

2-Misoprostol
synthetic prostaglandin E1 analogue
it induces uterine contraction

-90%
NOTE NEVER IN ECTOPIC

58
Q

what drug is used to terminate ectopic pregnancy?

A

METHOTREXATE

59
Q

most common location for ectopic pregnancy

A

98% in fallopian tube (ampulla-midportion)

60
Q

in what trimester ectopic pregnancy symptoms are seen?

A

1st

61
Q 
women in reproductive age presents with:
vaginal bleeding
abdominal pain (mimic appendicitis) 
-what tests you must order?
-diagnosis?
A

-hCG (abnormally increased)
will be rising much slower than in normal pregnancy (normally in steady speed)
- ectopic pregnancy

62
Q

how do we diagnose and tx ectopic pregnancy ?

A
  • ultrasound

- tx: methotrexate (disrupts folate metabolism in embryo) or surgery

63
Q

RF to ectopic pregnancy

(generally any damage to the fallopian tube) explain

A 
1- prior ectopic pregnancy
2- tubal disorders 
-tubal ligation (rare cases) 
-tubal surgery (tumor) 
-PID !!!!  
3- infertile women (higher incidence) 
4- kartagener syndrome (primary ciliary dyskinesia)
64
Q

how does kartagener syndrome lead to fallopian tube problem?

A

fallopian tubes have CILIATED epithelium

-it leads to primary ciliary dyskinesia

65
Q

define in wks:
1- spontaneous abortion (miscarriage)
2- stillbirth or fetal demise

A

1- before 20 wks

2- after 20 wks

66
Q

how does miscarriage presents?

A

vaginal bleeding early

67
Q

treatment of miscarriage

A

D&C surgery to remove all tissue

-dilation and curettage procedure

68
Q

what fetal cause leads to miscarriage?

A

fetal chromosomal abnormality (50%)

69
Q

spontaneous abortion RF 4

A
  • maternal SMOKING,ALCOHOL, COCAINE
  • LUPUS/ANTIPHOSPHOLIPID SYNDROME
  • maternal infection (TORCH)
  • hypercoagulable state
70
Q

primary source of amniotic fluid, 2

primary source of removal, 1

A
  • fetal urine and lung secretions

- fetal swallowing

71
Q

BRIEFLY
oligohydraminos occurs due to …
while
polyhydramnios occurs due to …

A
  • fetal kidney problem

- swallowing/GI problem

72
Q

causes of oligohydramnios

1 a+b, 2 a+b

A

1- fetal renal abnormalities
a-bilateral renal agenesis
b- posterior urethral valves (males): tissue obstructs urethra

2- placental insufficiency
a-preeclampsia
b- maternal vascular dxs

73
Q

list potters sequence main 3 features :

A

1- limb deformities
2- flat face
3- pulmonary hypoplasia

74
Q

causes of polyhramnios

A

1- fetal swallowing malformations
(e.g esophageal/duodenal atresia, anecephaly)
2-maternal diabetes (fetal hyperglycemia leads to polyuria)
3- fetal anemia (high CO, increased urine production)
CAN OCCUR IN PARVOVIRUS INFECTION
4- multiple gestations (more fetal urine)

75
Q

what is low birth weight ? causes 2?

A

less than 2500g (5.5 Ibs)
1- premature delivery
2- IUGR

76
Q

RF/causes of low birth weight

A 
1- congenital abnormalities of fetus 
2- multiple gestation (usually smaller) 
3- maternal conditions (placenta perfusion decreased): 
*preeclampsia
*abruptio placenta
*alcohol, smoking, cocaine
77
Q

list 8 newborn problems d/t low birth weight

A 
1- hypothermia 
2- hypoglycemia 
3- hyperbilirubinemia 
4- respiratory distress
5- Polycythemia of the new born 
6- necrotizing enterocolitis 
7- intraventricular hemorrhage 
8- longterm: SIDS
78
Q

what are the 3 causes that lead to HYPOTHERMIA in low birth weight newborns

A

1- less white adipose tissue (insulation)
2- less brown adipose tissue
(heat generation)
3- large ratio surface area: weight (lose heat easily)

79
Q

what are the 3 causes that lead to HYPOGLYCEMIA in low birth weight newborns

A

loss of maternal glucose, and the baby is insufficient to generate glucose

80
Q

what resp distress problems can occur in low birth weight newborns 4
*sometimes need for ventilator support

A 
1- neonatal RDS (deficiency of surfactant) 
2- transient tachypnea  
(inadequate lung fluid clearance) 
3- pneumonia 
4- resp failure
81
Q

why low birth weight babies are at risk of pneumonia ? (immnity related)

A

cellular immunity is impaired (low t/b cells or even neutropenia)

82
Q

sos what can lead to hypoxemia in new born babies

A

PERSISTENT HIGH PVR (pulm vasc resis)
(usually in utero there is high PVR to shunt blood from right to left, at birth PVR must decrease) so if it stays high it keeps the shunting

83
Q

red cell mass and newborns

A

normally INCREASED

if alot enters suddently at birth from placenta leads to PV

84
Q

what is a major risk factor for necrotizing enterocolitis? where does it usually occur in the GI? comploication?

A
  • prematurity and low birth weight
  • terminal illeum and colon
  • perforation
85
Q

in what part of the brain hemorrage occurs due to low birth weight?

A

intraventricular (lateral ventricle)

due to a problem in the GERMINAL MATRIX (will still be highly vascular area in premature infants)

86
Q

newborn 2000g with:

  • hypotonia
  • loss of spontaneous movements
  • seizures, coma
A

intraventricular (lateral ventricle) hemorrhage

due to low birth weight

87
Q

leading cause of infant mortality: 1mo to 1 year

A

SIDS

88
Q

SIDS leads to increased risk of :

A

neurocognitive problems:

  • cognition
  • social skills
  • behavioural and emotional skills
89
Q

revie RF of SIDS

A
  • stomach sleeping
  • maternal smoking during pregnancy
  • very young aternal age
  • bed sharing
  • prematurity/low birth weight
90
Q

what is gestational HTN

A

elevated BP that develops AFTER 20 wks (no proteinuria or evidence of preeclampsia)

91
Q

safe drugs to use for HTN in pregnant women

A

a-methyldopa
labetalol (B1B2a1 blocker)
nifedipine (CCB)

92
Q

3 main features of preeclapmisa

A

1- HTN
2- Proteinuria
3- End organ dysfunction

93
Q

pathogenesis of preeclampsia

A

Disorder of the PLACENTA !
normally: extravillous trophoblast (in the endometrium) invades/ penetrate the uterus (myometrium) and transform the SPIRAL ARTERIES (here is abnormal, spiral arteries remain narrow :(
so placenta is HYPO PERFUSED (leads to VASOSPASM and COAGULATION)

94
Q

when is preeclampsia resolved?

A

with delivery (i.e placental removal)

95
Q

placental biopsy of preeclampsia

A

fibrinoid necrosis of vessels

pink material in the walls of BV

96
Q

first pregnancy: pregnant women in the 3RD TRIMESTER with
HTN (NEW ONSET)
proteinuria
edema

A

PREECLAMPSIA

97
Q

what organ is often involved in preeclampsia?

A

liver

  • edema
  • ischemia/necrosis
  • elevated LFT !
98
Q

risk factors for preeclampsia 5

A 
1- prior preeclampsia
2- 1st pregnancy 
3- family hx 
4- multiple gestations 
5- prior maternal conditions (DM, HTN, obesity, chronic kidney dx, LUPUS/ANTI-PHOSPHOLIPID syndrome)
99
Q

complications 2 of preeclampsia

A

1- placental insufficiency (IUGR, oligohydramnios)

2- placental abruption

100
Q

review: complications on mother d/t preeclampsia

A
  • pulmonary edema
  • heart failure
  • liver hematoma w/ or w/o rupture
  • liver failure
  • DIC
  • stroke
  • dialysis (advanced renal failure)
101
Q

ECLAMPSIA

what is it?

A

SEIZURES (generalized, tonic-clonic seizures) -> coma/death

102
Q

what is the ANTI-CONVULSIVE of choice to TREAT eclampsia and PREVENT eclampsia (in preeclampsia pts)

A

magnesium sulfate!!!!!

103
Q

definitive treatment for eclampsia

A

delivery of baby

104
Q

HELLP syndrome stands for

A

Hemolysis
Elevated Liver enzymes
Elevated Platlet count

105
Q

what type of hemolysis is seen in HELLP syndrome

list 4 characteristics

A

MAHA (microangiopathic hemolytic anemia

  • shistocytes
  • elevated bilirubin
  • low haptoglobin
  • low PLT count (consumed)
106
Q

HELLP syndrome treatment

A

delivery of baby

107
Q

TORCH stands for

A 
Toxoplasmosis
Other (syphilis, varicella-zoster, parvovirus B19) 
Rubella 
CMV
Herpes
108
Q

Toxoplasma gondii

  • type (bacteria, virus, …)?
  • found in ?
  • infection from (transmission)?
A
  • protozoa
  • cats (felines) oocytes shed in stool
  • ingestion of oocysts (soil, contaminated food, etc..)
109
Q

primary vs latent infection of pregnant women with toxoplasmosis

A
  • primary: usually asymptomatic+ non specific symptoms

- latent: does not infect fetus

110
Q

diagnosis of toxoplasmosis 2

A

1- IgM antibodies (in 1st wk)

2- IgG antibodies (peak 6-8 wks) -fall over next 2 yrs

111
Q

fetus born with:
-hydrocephalus
-chorioretinitis
-intracranial calcifications (or even PRENATAL US imaging !!!!!)
or born normal then later in life became blind + seizures

diagnose

A

infection with toxoplasmosis from mother

112
Q

intracranial calcifications on PRENATAL US imaging !!!!! diagnose

A

toxoplasmosis

113
Q

Syphilis

  • type (bacteria, virus, …)?
  • infection from (transmission)?
  • maternal symptoms (if pregnant)
A
  • spirochete (bacteria)
  • sexual contacts
  • like normal:
    primary: chancre
    secondary: maculopapular rash (palms/soles)
114
Q

what is the age of babies at which findings of syphilis become early or late

A

2 years

115
Q

baby born with:

  • maculopapular rash
  • RUNNY nose
  • abnormal long-bones (esp legs)
A

EARLY (<2 yrs) congenital syphilis

116
Q

baby 3 years old with

  • saddle nose/ deafness
  • HUTCHINSON TEETH (notched)/ MULBERRY MOLARS
  • saber shins (bowed legs)

diagnos ?
caused by:

A

LATE (>2 yrs) congenital syphilis

cause by scarring and gumma formation

117
Q

varicella zoster virus

  • family of virus? dna or rna?
  • maternal symptoms (if pregnant)
A

-herpes virus , DNA

-

118
Q 
newborn with:
-scars in DERMATOMAL pattern 
-microcephalym hydrocephalus, seizures
-ocular abnormalities (cataracts, nystagmus) 
-limb atrophy and hypoplasia 
long term:: learning disability !!!
A

varicella zoster virus infection from mother

119
Q

Parvovirus B19

  • describe virus? dna or rna?
  • infection from (transmission)?
  • classic infection in children +characteristic !!
  • classic infection in adults
  • what progenitor is infected and leads to what
A
  • non enveloped, single stranded DNA
  • respiratory secretions of infected persons
  • 5th disease in children (SLAPPED CHEEK)
  • arthritis (hands wrists knees ankles
  • red cell progenitors: mild anemia or crisis in chronic anemics (e.g sickle cell)
120
Q

why fetus is esp vulnerable to B19 (3)

remember B19 infects RBC progenitors

A

normally fetus has:
1- shortened RBC half life
2- expanding RBC volume
3- immature immune system

121
Q

what is the feared outcome of PARVOVIRUS B19 in fetus ?
how is it diagnosed?
2 types?

A 
HYROPS FETALIS 
-fluid accumulate in fetus (baby looks filled!)
-diagnosed on ultrasound 
1- immune hydrops (Rh mismatch)
2- non-immune hydrops B19
122
Q

Rubella

  • type (bacteria, virus, …)?
  • infection from (transmission)?
  • maternal symptoms (if pregnant)
A
  • RNA virus

- nasal/throat secretions through RESPIRATORY DROPLETS

123
Q

pregnant women with :

  • maculopapular rash
  • lymphedenopathy
  • joint pain
A

mild-self limited illnss: rubella

124
Q

baby born with

  • sensorineural deafness
  • cataracts
  • cardiac malformations (PDA)!!!!1
  • bluberry muffin baby
A

congenital rubella syndrome

125
Q

what is bluberry muffin baby?

-seen in what conditions

A

purpuric skin lesions (EXTRAMEDULLARY HEMATOPOIESIS —> continues to occur after birth)
1- RUBELLA (classic)
2- congenital toxoplasmosis
3- CMV

126
Q

CMV

  • family of virus? dna or rna?
  • infection from (transmission)?
  • maternal symptoms (if pregnant)
A

-herpes virus DNA
-sexual contact, close contact DAYCARE !!!, blood/tissue exposure
primary CMV asymptomatic (mononucleosis-like)

127
Q

what is the major consequence of CMV on fetus

sos

A

SENSORINEURAL HEARING LOSS

although usually asymptomatic

128
Q

how is CMV usually diagnosed in babies

A

based only on failed hearing screen :)

129
Q

most common cause of congenital sensorineural deafness

A

CMV

130
Q

neuroimaging finding of a baby: intacranial calcifications (PERIVENTRICULAR)

A

CMV infection

revie toxoplasmosis gondi too (not around ventricles)

131
Q

Herpes simplex

  • type 1 or 2 (bacteria, virus, …)?
  • how is it transmitted to fetus
A

HSV 2 DNA virus
NOT transplacentally
via genital tract lesions at birth
so active HSV 2—> c section

132
Q

baby with vesicles near the eyes, skin, mouth (or even spread to cns and other organs) what TORCH infection ?

A

herpes simplex

133
Q

what is placental abruption ? how is it caused?

LIFE THREATENING TO MOTHER AND FETUS

A

-PLACENTAL DETACHMENT prior to delivery of baby
-blood loss from MATERNAL VESSELS (d/t rupture of maternal vessels in DECIDUA BASALIS)
this blood seperates decidua from uterus (myometrium) :( so loss of gas and nutrient exchange

134
Q

clinical presentation of placental abruption + what trimester? + how is it diagnosed? tx?

A

-3rd trimester

-ABRUPT ONSET of painful vaginal bleeding !!!!
(if post abruption: minimal bleeding)
-abdominal/back pain
-uterine cntractions

cliniacally (US not reliable)

135
Q

complications of placental abruption 4

A

1- maternal shock
2- fetal distress/ demise
3- DIC
4- CORTICAL NECROSIS

136
Q

pregnant women presents with placental abruption and the following symptoms:

  • acute renal failure
  • anuria
  • hematuria
  • flank pain
A

ischemic necrosis of renal cortex

may lead to permanent renal failure

137
Q

RF of placental abruption 5

A 
1- previous abruption
2- maternal HTN/preeclampsia
3-smoking/cocaine
4-abnormal uterus
—-bicornuate uterus
—-prior c -section
5- trauma (MOTOR vehicle accident)
138
Q

what is placental previa

A

previa means going before
placenta before baby
—>placenta attached to lower uterus (over or close to cervical os)

139
Q

pregnant women with painless bleeding (+/- preterm birth) could be —- and requires

A

placenta previa

-c-section

140
Q

RF of placenta previa 3

A

1-prior placental previa
2- prior C-SECTION!
3-Prior multiple pregnancies

PRevia = PRior

FEMALE reproductive (6 decks)

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