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Embryology > Extras > Flashcards

Extras Flashcards

1
Q

What is a hydatidiform mole?

What causes it?

A
  • “mole” refers to a clump of growing tissue
  • it is an abnormal pregnancy that involves a non-viable fertilised egg implanting into the uterus and failing to come to term
  • it is often caused by a sperm fertilising an “empty” oocyte that does not contain an original maternal nucleus
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2
Q

What type of tissue forms a hydatidiform mole?

A
  • there is an overproduction of trophoblastic tissue
  • this produces abnormal masses that are usually benign, but can turn cancerous
  • the placenta contains grapelike vesicles that occur when the chorionic villi become distended by fluid
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3
Q

How does a hydatidiform mole usually present?

What can it cause false results for?

A
  • usually presents with painless vaginal bleeding in the 4th-5th month of pregnancy
  • there may also be:
  1. enlarged uterus and/or ovaries
  2. hyperemesis
  3. hypertension
  4. proteinuria
  • blood tests will show very high levels of hCG and pregnancy tests will show a false positive result
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4
Q

What are the risk factors for hydatidiform mole?

A
  • defects in the egg
  • abnormalities within the uterus
  • nutritional deficiencies (diet low in protein, folic acid & carotene)
  • women <20 and >40 years of age
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5
Q

How can hydatidiform mole be detected prenatally?

A
  • it has a characteristic “snowstorm” appearance on USS
  • definitive diagnosis requires histopathological examination, which shows increased trophoblast proliferation and enlarging of the chorionic villi
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6
Q

What condition can hydatidiform mole potentially progress to?

A
  • there is a risk that it can develop into choriocarcinoma** or an **invasive mole
  • an invasive mole may invade so far into the uterine wall that it results in haemorrhage and other complications
  • choriocarcinoma is a malignant, rapidly growing and metastatic form of cancer with a poor prognosis
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7
Q

What is the bleeding like in placenta praevia?

How does this condition typically present?

A
  • this condition involves “revealed” bleeding, opposed to “concealed”
  • this bleeding is bright red and is usually not painful
  • it presents as antepartum haemorrhage (APH) or failure of the head to engage at delivery
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8
Q

What are the associations of placenta praevia?

A
  • multiparity
  • large placentae (twins)
  • uterine abnormalities, such as fibroids
  • previous uterine surgery
  • previous C-section
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9
Q

What is meant by placental abruption?

What type of bleeding does this produce?

A
  • this occurs when the placenta separates from the uterus before birth (usually 25 weeks)
  • the maternal vessels tear away from the decidua basalis, causing a tear in the uterine tissue
  • this produces bleeding that can be “revealed” or “concealed”
  • it can be partial or complete
  • once the placenta is fully separated from the uterus, it is unable to provide the exchange needed to keep the foetus alive
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10
Q

What are the potential causes of placental abruption?

A
  • the cause is unknown, but potential associations include:
  1. pre-eclampsia
  2. smoking
  3. thrombophlebitis
  4. previous C-section
  5. multiple pregnancies
  6. short umbilical cord
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11
Q

How does placental abruption typically present?

A
  • presents as antepartum haemorrhage (APH) or maternal shock without bleeding
  • there may be associated pre-eclampsia, anuria and DIC
  • coagulation abnormalities are usually present
  • the uterus is tender and tense
  • there is constant pain
  • the shock is out of proportion to the visible loss
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12
Q

What is the management for a large and small placental abruption?

A

Small abruption:

  • the mother is monitored in hospital until a change in condition or foetal maturity (whichever is first)

Large abruption:

  • vaginal delivery can be attempted if the mother is stable
  • if not, C-section is performed but this carries a greater risk of DIC
  • if the mother is less than 36 weeks pregnant, corticosteroids are given to speed to development of foetal lungs
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13
Q

What is meant by velamentous insertion of the umbilical cord?

What condition is this associated with?

A
  • this occurs when the umbilical cord does not insert into the centre of the placenta
  • the unprotected umbilical vessels travel in foetal membranes (between amnion and chorion) to reach the placenta
  • if the blood vessels lie close to the cervix, this is vasa previa, which carries a risk of rupture during delivery
  • the foetus can exsanguinate (be drained of blood) before birth
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14
Q

What is vasa previa and how can it be detected prior to birth?

A
  • the umbilical vessels are unprotected** and travel in foetal membranes **near or across the internal opening of the uterus
  • the umbilical vessels are at risk of rupture when the supporting membranes rupture
  • it is detected on USS - tubular structures are found overlying / in close proximity to the cervix and Doppler is used to confirm that these are foetal vessels
  • foetal haemoglobin within vaginal bleeding is diagnostic of this condition
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15
Q

What is the treatment for vasa previa?

A
  • women are recommended to have an elective C-section prior to rupture of the membranes (35-36 weeks)
  • steroids are given to promote foetal lung development
  • an emergency C-section is performed if the patient goes into labour or the membranes rupture
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16
Q

What are the risk factors for vasa previa?

A
  1. velamentous insertion of the umbilical cord
  2. multiple gestation
  3. accessory placental lobes / bilobed placenta
  4. IVF pregnancies
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17
Q

What is the classic triad of vasa praevia?

What happens if this condition goes undetected?

A
  1. membrane rupture
  2. painless vaginal bleeding
  3. foetal bradycardia / foetal death
  • if it is undetected, the umbilical vessels rupture when the membranes rupture
  • there is bleeding from the foetoplacental circulation, resulting in rapid exsanguination of the foetus and delivery of a stillbirth / neonatal death
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18
Q

What is pre-eclampsia?

How many pregnancies are affected by this condition?

A
  • a disorder of pregnancy characterised by the onset of hypertension and significant proteinuria
  • it begins after 20 weeks of pregnancy and symptoms resolve following delivery of the placenta
  • mild pre-eclampsia affects 6% of pregnancies and severe pre-eclampsia affects 1-2%
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19
Q

What is thought to be the underlying cause of pre-eclampsia?

How does the appearance of the placenta differ in someone with this condition?

A
  • cause is unknown but it is thought to involve formation of abnormal blood vessels in the placenta and poor trophoblastic invasion into the endometrium
  • an abnormally implanted placenta is a significant predisposing factor to pre-eclampsia
  • the placenta of a woman with this condition is often small with poor trophoblastic infiltration
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20
Q

What are the risk factors for development of pre-eclampsia?

A
  1. BMI > 35
  2. pre-existing hypertension
  3. renal disease
  4. diabetes
  5. lupus or antiphospholipid syndrome
  6. previous pregnancy affected
  7. family history of pre-eclampsia
  8. maternal age > 40 or < 20
  9. more than 10 years between pregnanies
  10. multiple foetuses
  11. first pregnancy
21
Q

What are the symptoms associated with pre-eclampsia?

A
  1. headache
  2. confusion
  3. RUQ pain
  4. respiratory symptoms - cough, chest pain, dyspnoea
  5. visual disturbances
  6. decreased urine output
  7. N&V
22
Q

What is HELLP syndrome?

What condition is it associated with and what are the outcomes like?

A
  • HELLP syndrome is defined as:
  1. Haemolysis
  2. Elevated Liver enzymes
  3. Low Platelet count
  • it occurs in 10-20% of cases of severe pre-eclampsia / eclampsia and is associated with increased maternal & foetal morbidity / mortality
23
Q
A
24
Q

What are the main mechanisms for prevention of pre-eclampsia?

What treatments may be given to mothers who have developed this condition?

A
  1. smoking cessation prior to pregnancy
  2. calcium supplementation in areas with low intake
  3. aspirin given to those deemed as high-risk
  4. treatment of pre-existing HTN with medication
  • delivery of the placenta is an effective treatment, but full recovery can take days/weeks
  • blood pressure medication (e.g. labetalol / methydopa) is given to improve condition prior to delivery
  • magnesium sulphate is given to prevent eclampsia in severe disease
25
Q

What is eclampsia?

What are the warning symptoms for this and how is it managed?

A
  • eclampsia involves the development of new convulsions in a pre-eclamptic patient that cannot be attributed to other causes
  • warning symptoms for development of eclampsia include:
  1. headache
  2. visual disturbances
  3. RUQ / epigastric pain
  • magnesium sulphate is given to prevent convulsions in patients with severe pre-eclampsia
26
Q

What is the normal diameter and length of the umbilical cord?

What are the risks associated with a long umbilical cord?

A
  • normal diameter is 1-2cm and normal length is 50-60cm
  • a long umbilical cord can encircle the neck of the foetus and have devastating consequences
  • it is also associated with an increased risk of:
  1. foetal entanglement
  2. cord prolapse
  3. true cord knots

these events can deprive the baby of oxygen during delivery and result in serious brain injuries

27
Q

What is the risk associated with an umbilical cord that is too short?

A
  • it may pull the placenta away from the uterine lining, producing placental abruption
28
Q

What is meant by the “breech position”?

What are the associated risks of this condition?

A
  • this occurs when the buttocks or feet present first, opposed to the head (cephalic position)
  • this carries risks of premature birth, asphyxiation / trauma during birth and increased incidence of congenital malformations
29
Q

What is meant by umbilical cord prolapse?

What are the risks associated with this condition?

A
  • the umbilical cord comes out of the uterus with or before the presenting part of the baby
  • the pressure exerted on the cord by the baby can compromise the blood flow that it receives
  • this usually occurs during labour, but can occur any time after rupture of the membranes
30
Q

What is the management for cord compression?

A
  • quick delivery is required, usually by C-section
  • until this can take place, the woman is placed in a knee-chest position or Tredelenburg position (head down, feet elevated) to prevent further compression
  • a gloved hand may be inserted into the vagina to push the foetus upwards and off the cord
31
Q

Why can jaundice occur after birth?

What can severe neonatal jaundice develop into?

A
  • haemolysis of RBCs leads to increased levels of bilirubin
  • when the child is born, bilirubin is no longer cleared via the placenta and so symptoms of jaundice can increase within 24 hours after birth
  • severe neonatal jaundice can result in kernicterus, which can result in brain damage
32
Q

Why is the risk of kernicterus higher in haemolytic disease of the newborn?

A
  • there is massive and rapid destruction of RBCs, elevating bilirubin levels more rapidly
33
Q

What is haemolytic disease of the newborn and how does it occur?

A
  • IgG antibodies are produced by the mother (Rh -ve) when she is exposed to a foreign antigen
  • the IgG antibodies can cross the placenta and target this antigen if it is present within the foetus
  • in order for the mother to become sensitised, she needs to be exposed to the antigen via haemorrhage or blood transfusion
    • haemorrhage occurs during birth, as well as abortion, ectopic pregnancy and ruptures of the placenta
  • near the time of birth, the IgG antibodies cross the placenta and attack antigens on foetal RBCs, which destroys the cells
34
Q

How does the foetus respond to maternal IgG attacking the antigens on its RBCs?

A
  • breakdown and destruction of foetal RBCs leads to reticulocytosis and anaemia
  • reticulocytosis involves the foetus increasing RBC production to compensate for the loss, but sends out immature RBCs that still have nuclei
  • the baby is often jaundiced at birth
  • if foetal anaemia is so severe that there is oedema / effusion into body cavities, this can result in foetal death from heart failure (hydrops fetalis)
35
Q

Why is haemolytic disease of the newborn more likely to occur in a subsequent pregnancy?

A

First exposure - birth of Rh+ infant:

  • during birth, foetal RBCs can leak into maternal blood after breakage of the embryonic chorion
    • the chorion usually isolates maternal and foetal blood
  • the mother produces IgG antibodies against the Rh+ antigen on the RBCs

Second exposure - Rh+ foetus:

  • there are IgG antibodies present within the mother’s blood following the first exposure
  • Rh antibodies can cross the embryonic chorion / placenta and attack the foetal RBCs
36
Q

What antigen is usually responsible for causing HDN?

Where does this come from?

A
  • it is most commonly triggered by the RhD antigen
  • A Rh-D -ve mother becomes pregnant with a Rh-D +ve foetus
  • the child has inherited the D antigen from the father
  • the mother’s immune system forms antibodies against the D antigen (anti-D)
37
Q

How is HDN screened for?

A

through the direct and indirect Coomb’s test

Direct Coomb’s test - used to diagnose HDN:

  • this detects anti-Rh antibody that has already bound to foetal RBCs

Indirect Coomb’s test - used in prevention of HDN:

  • this detects free anti-Rh antibody in maternal blood serum
  • by finding maternal anti-D antibodies prior to attack of foetal RBCs, treatment can be given to prevent or limit the severity of HDN
38
Q

What is the treatment in Rh-D -ve women who have not been sensitised (no anti-D antibody)?

A

the aim of treatment is to prevent sensitisation

  • anti-D IgG is given @ 28/40 which “mops up” any foetal RBCs that may have leaked into the maternal circulation
    • this reduces the risk of first-time exposure to the D antigen
  • another anti-D injection is given within 72 hours of delivery
39
Q

If a mother is found to be sensitised, what are the following steps?

A

Confirm the Rh status of the foetus:

  • if the father is homozygous for the D allele (D/D), then the foetus will be Rh-D +ve
  • if the father is heterozygous (D/d), then there is a 50% chance the foetus is Rh-D +ve and a sample of foetal cells are taken from the amniotic fluid or umbilical cord to test this

If foetus is Rh-D +ve:

  • pregnancy is closely monitored for signs of HDN through regular USS and monitoring amount of anti-D in maternal serum
  • a rise in anti-D indicates active haemolysis
  • if a foetal blood test confirms anaemia, a blood transfusion is performed via the umbilical vein in utero to replace lysed foetal RBCs
40
Q

What is coarctation of the aorta?

What are the 2 different types and what defines them?

A
  • a congenital condition in which there is narrowing of the aorta (usually the arch)
  • it can be classified as preductal or postductal depending on whether the narrowing occurs prior to or after the ductus arteriosus
41
Q

What is meant by post-ductal coarctation of the aorta?

What happens during development as a result of this?

A
  • post-ductal coarctation happens after the ductus arteriosus
  • during development, a collateral circulation is established to bypass the narrowing
  • as part of this collateral circulation, the internal thoracic arteries are enlarged
  • this is more common than preductal
42
Q

What is meant by preductal coarctation of the aorta?

What usually happens after birth as a result of this?

A
  • the narrowing occurs before the ductus arteriosus
  • during development, the ductus arteriosus compensates for the narrowing and so no collateral supply is developed
  • after birth, the ductus arteriosus usually remains patent
43
Q

What happens if there is closure of the ductus arteriosus following birth in a preductal coarctation?

A
  • obliteration of the ductus arteriosus causes rapid decline of the infant with hypoperfusion of the lower body
  • this is due to failure to establish a collateral circulation during development
44
Q

What is Edward’s syndrome caused by?

How common is it?

A
  • Edward’s syndrome occurs as a result of trisomy 18
  • it affects 1 in 5000 live births
45
Q

What are the main prominent features of Edward’s syndrome?

A
  • low birth weight
  • congenital heart defects
  • micrognathia and microcephaly
  • clenched fists with overlapping fingers
  • severe intellectual disability
  • omphalocele
  • low-set malfored ears
  • cleft lip/palate
  • rocker bottom feet
  • widely spaced eyes
  • narrow eyelid openings
46
Q

What causes Patau syndrome?

How common is it and what is the prognosis?

A
  • it is caused by trisomy 13
  • it affects 1 in 10,000 - 21,000 live births but 90% of those affected die within the first year of life
  • those that do survive have severe disablement, seizures and psychomotor issues
47
Q

What are the main features of Patau syndrome?

A
  • there is extreme variability in the presentation of foetuses with Patau syndrome and many features are similar to those seen in Edwards syndrome
  1. polydactyly
  2. proboscis
  3. low-set ears
  4. rocker bottom feet
  5. omphalocele
  6. overlapping of fingers over the thumb
  7. cleft palate
  8. myelomeningocele
  9. eye defects
  10. microcephaly
  11. single umbilcal artery
  12. kidney / genital / heart defects
48
Q

What causes Prader-Willi syndrome?

What are the key features of this disorder?

A
  • it is caused by a microdeletion on chromosome 15
  • in newborns, there is hypotonia, slow development and poor feeding
  • in childhood, those affected become constantly hungry, resulting in obesity and T2DM
  • there is mild-to-moderate intellectual impairment and behavioural problems
  • most have small hands / feet, short height and are infertile

Embryology (20 decks)

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