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General Medicine > Obstetrics > Flashcards

Obstetrics Flashcards

0
Q

Management of Shoulder dystocia

A 
H: Get Help
E: Evaluate for episotomy
L: Legs in Mc Roberts position
P: Suprapubic pressure
E: Enter - internal measures
pressure behind foetal anterior shoulder
woods screw manœuvre - frequently requires episotomy
R: Remove posterior arm
R: roll the patient ‘Gaskin” Increase pelvic diameter
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1
Q

Causes of pregnancy related hyperthyroidism

A

Gestational transient thyrotoxicosis
Graves’ disease

Less common
Toxic multi modular goitre
Toxic adenoma
Thyroiditis

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2
Q

Define Gravidity

A

number of pregnancies a woman has had (to any stage)

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3
Q

Define parity

A

number of pregnancies that have resulted in delivery beyond 28 weeks gestation

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4
Q

Naegele’s Rule

A

Expected delivery date (EDD) is 1 year and 7 days after LMP minus 3 months

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5
Q

Characteristic signs of shoulder dystocia in infant?

A 
Turtle necking (appearance and retraction of head)
Erythematous face
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6
Q

McRobert’s position

A

hyper flexing the mother’s legs tightly to her abdomen - widens the pelvis and flattens lumbar spine

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7
Q

Gaskin manouevre

A

moving mother onto all fours with the back arched, widening the pelvic outlet

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8
Q

Zavanelli manœuvre

A

cephalic replacement and C section

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9
Q

Maternal symphysiotomy

A

opening of the birth canal laxer by breaking the connective tissue between the two pubes bones facilitating the passage of the shoulders

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10
Q

maternal complications of shoulder dystocia?

A

increased blood loss
vaginal lacerations
uterine rupture

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11
Q

main cause for antepartum haemorrhage?

A

Placenta praevia

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12
Q

what is placenta praevia?

A

an obstetric complication in which the placenta is inserted partially or wholly in the lower uterine segment

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13
Q

Grades of placenta praevia

A 
I
Placenta is in lower segment, but the lower edge does not reach the internal os
II
Lower Edge of the Placenta reaches internal os but does not cover it
III
Placenta covers internal os partially
IV
Placenta covers internal os completely
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14
Q

Presentation of placenta praevia

A

pain bright red vaginal bleeding

commonly occurs around 32 weeks gestation, but can be as early as late mid trimester

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15
Q

Diagnosis of placenta praevia

A

Praevia can be confirmed with an ultrasound

transvaginal ultrasound has superior accuracy compared to transabdominal

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16
Q

Abruptio placenta

A

Refers to bleeding due to the untimely separation of a normally sited placenta from its attachment to the uterus

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17
Q

What is CTG

A

Cardiotocography
electronic method of simultaneously recording foetal heart rate, foetal movements and uterine contractions to identify the probability of foetal hypoxia

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18
Q

Indications for antenatal CTG

A

Previous abnormal CTG or doppler
Maternal hypertension or other complications or medical conditions (e.g. cardiac, thyroid, etc.)
Suspected antepartum haemorrhage (>50mL)
Previous caesarian section
Multiple pregnancy
Oligohydroamnios (deficiency of amniotic fluid)
Isoimmunisation (Rhesus reaction)

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19
Q

Indications for intrapartum CTG

A

Preterm labour (42 weeks)
Breech presentations
Induction of labour
Maternal pyrexia (>38C)
Vaginal bleeding during labour in addition to the show
First stage labour >12 hours
Prolonged second stage labour >1 hour of active pushing
Insertion of epidurals or other modifications

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20
Q

Normal foetal Heart rate

A

Normal = 110-160 bpm

Preterm FHR is expected to be in the upper range of normal

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21
Q

Baseline variability on CTG

A

= fluctuation of FHR from beat to beat, from highest peak to lowest trough over a 1 minute period
Normal Variability = 5-25 bpm
Reflects a normal foetal autonomic nervous system
Reduced Variability = 3-5 bpm (look at CTG for up to 60 minutes)
Reduced by sleep states, activity, hypoxia, foetal infection and drugs (e.g. opioids, hypnotics)
Absent Variability = <3 bpm (indicates very compromised/hypoxic foetus)

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22
Q

Accelerations on CTG

A

transient increases in FHR by more than 15 bpm above the baseline for 15 seconds or more
Accelerations are normal (their presence is a good sign)
No accelerations with an otherwise normal FHR doesn’t indicated foetal compromise

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23
Q

Decelerations on CTG

A

transient decreases in foetal HR 15 below baseline for at least 15 seconds
Decelerations are abnormal!

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24
Q

Early deceleration

A

peaks as the contraction due to compression of placenta / blood vessels peaks
Not too concerning if everything else is normal

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25
Q

Late deceleration

A

Peaks after end of uterine contraction

Normally associated with hypoxic foetus

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26
Q

prolonged late deceleration

A

Deceleration lasting for >90 seconds but less than 5 minutes after a uterine contraction
Bad indicator for foetus

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27
Q

variable deceleration

A

Rapid onset drop of at least 60bpm for at least 60 seconds with quick recovery and good variability
Vagal in origin (thought to result from stimuli such as cord or head compression)

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28
Q

Complicated variable deceleration

A

Reduced variability prior to deceleration of at least 60bpm with quick recovery and ‘overshooting’ of the baseline (large amplitude shoulder)

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29
Q

sinuosoidal pattern CTG

A

oscillating, wavy, smooth, fixed pattern with amplitude between 5-15
Associated with severe anaemia of foetus and foetal death)

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30
Q

Foetal Scalp pH

A

f concerned by CTG findings, a foetal scalp pH may be requested
If >7.25, wait and hour then repeat
If stops between 7.21-7.24, may leave for another 30 minutes depending on the baby’s condition
If <7.21, then straight to theatre for emergency caesarian section

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31
Q

Classic triad of endometriosis

A

dysmenorrhoea, dysparaeunia, dsychezia (unable to defecate)

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32
Q

Infertility rate in endometriosis

A

30-40% will be infertile

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33
Q

What is endometriosis?

A

chronic inflammatory condition defined by endometrial stroma and glands found outside of the uterine cavity.

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34
Q

Diagnosis of endometriosis

A

direct visualisation of lesions typical of endometriosis at lapaoscopy
biopsy and histologic exam of specimens (2 or more of endometrial epithelium, glands, strooma, haemosiderrin laden macrophages

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35
Q

What is seen at laparoscopy in endometriosis?

A

mullberry spots: dark blue or brownish- black implants on the uterosacral ligaments
endometrioma “chocolate” cysts on the ovaries
“powder burn” lesions on the peritoneal surface
early white lesions and clear blebs
peritoneal “pockets”

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36
Q

What tumour marker may be elevated in patients with endometriosis?

A

CA-125

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37
Q

When does gestational diabetes develop?

A

3-8% of pregnant women develop gestational diabetes around the 24th to 28th week of pregnancy

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38
Q

pathophysiology behind gestational diabetes?

A

anti insulin factors produced by the placenta and high maternal cortisol levels create increased peripheral insulin resistance -> higher fasting glucose -> GDM

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39
Q

Oral glucose challenge test

A

at 26-28 weeks GA
a non- fasting 50 gram glucose drink is given to the pregnant woman
after one hour venous blood is taken
a one hour venous blood glucose level of >7.8mmol/L indicates the need for an oral glucose tolerance test

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40
Q

Oral Glucose tolerance test

A

standard test is a 75g 2 hour oral glucose test
can be performed at any time during the pregnancy if signs and symptoms of abnormal glucose tolerance
consider an early test for womb with a past history of gestational diabetes if a recent OGTT has not been performed
ensure a normal diet containing at least 300 grams of carbohydrate is consumed for at least 3 days before the test
performed after an hour fast (food and fluids)
obtain fasting venous blood glucose
a 75g glucose drink is then given
measure venous blood at 2 hours
a fasting glucose >5.5 or glucose >7.8 at 2 hours indicates the need for dietary advice and home glucose monitoring

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41
Q

When to treat gestational diabetes

A

Treatment will be considered if:
Fasting values are ≥ 5.5 mmol / L once or more a week
Post prandial values ≥7.5 mmol / L twice or more a week are recorded in the absence of dietary non compliance

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42
Q

Post partum follow up after gestational diabetes

A

test glucose post partum day 3-4

also test at 6-12 weeks post partum

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43
Q

What is hydrops fetalis?

A

condition of the foetus characterised by an accumulation of fluid, or oedema in at least 2 foetal compartments

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44
Q

Locations of fluid in hydrops fetalis

A

subcutaneous tissue/ scalp
pleura (pleural effusion)
pericardium (pericardial effusion)
abdomen (ascites)

oedema is usually seen in the foetal subcutaneous tissue, sometimes leading to spontaneous abortion. It is a prenatal form of heart failure, in which the heart is unable to satisfy its demand for a high amount of blood flow.

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45
Q

What does hydrops fetalis usually stem from?

A

Foetal anaemia (the heart needs to pump a much greater volume of blood to deliver the same amount of oxygen)

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46
Q

Immune cause for hydrops fetalis?

A

Rh Disease
can be prevented by administration of anti D IgG injections to RhD negative mothers during pregnancy and/ or within 72 hours of the delivery

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47
Q

Non immune causes of hydrops fetalis?

A

iron deficiency anaemia
paroxysmal supraventricular tachycardia resulting in heart failure
deficiency of the enzyme beta-glucuronidase
congenital disorders of glycosylation
Parvovirus B19 infection of the pregnant woman
CMV in mother
maternal syphilis and maternal diabetes mellitus
a thalassemia can also cause hydrous fetalis
tumours
twin twin transfusion syndrome
maternal hyperthyroidism

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48
Q

How long does it take after giving birth for the physiological changes to return to normal?

A

About 6 weeks

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49
Q

When is dilutional anaemia most common in pregnancy

A

2nd-3rd trimester (28-32 weeks)

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50
Q

Haematological changes in pregnancy

A 
Increased red blood cell volume
Increased WCC
Decreased platelets
Increased fibrinogen and coagulation factors
Increased ESR
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51
Q

CVS changes in pregnancy

A 
Increased Cardiac output
Widened pulse pressure
Decreased BP
Displaced Apex beat
functional systolic flow murmur
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52
Q

Renal changes in pregnancy?

A 
Increased GFR
Decreased urea and creatinine 
Decreased urates
dilated ureters
Increased bladder capacity
Increased frequency of micturition
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53
Q

Most common infection in pregnancy?

A

UTI

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54
Q

What is increased urates a marker for?

A

Pre eclampsia

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55
Q

What is Chadwick’s sign

A

Bluish discolouration of cervix, vagina and labia due to pelvic congestion
Can be observed 6-8 weeks after conception

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56
Q

Gastrointestinal changes in pregnancy?

A 
Cravings
Decreased gut motility
constipation 
compression of stomach
nausea and vomiting
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57
Q

Average weight gain in pregnancy?

A

12KG

larger women may gain 3-4 kg

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58
Q

First Trimester Screening test for trisomy 21 and trisomy 18

A

blood collected at 9W to 13W to 6D gestation for biochemical analysis of
- pregnancy associated placental protein A (PAPP-A)
- free BhCG
combined with
- ultrasound measurement of foetal nuchal translucency 11W to 13W 6D

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59
Q

Second Semester for Trisomy 21, Trisomy 18 and neural tube defects

A

Blood is collected at 14W to 20W (ideally 15-17) gestation for biochemical analysis of:

  • alpha fetoprotein (AFP)
  • Free BhCG
  • unconjugated estriol
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60
Q

When can you feel the uterus per abdomen?

A

12 weeks gestation

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61
Q

primip

A

female during her first pregnancy

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62
Q

What makes a clinically favourable pelvis?

A

sacral promontory cannot be felt
ischial spines are not prominent
suprapubic arch and base of supraspinous ligaments both accept 2 fingers and the inter tuberous diameter accepts 4 knuckles when the woman is examined

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63
Q

bregma

A

anterior fontanelle

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64
Q

the brow

A

lies between the bregma and anterior fontanelle

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65
Q

Vertex

A

area between the fontanelles and the parietal eminences

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66
Q

Restitution

A

The fetal head turns through 45 degrees to restore its normal relationship with the shoulders, which are still at an angle.

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67
Q

How is labour diagnosed?

A

onset of regular painful uterine contractions in association with evidence of cervical change

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68
Q

7 mechanisms of labour

A 
Engagement
Descent
Flexion
Internal rotation
extension: delivery of head
restitution
expulsion
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69
Q

usual mechanism to deliver shoulders?

A

Gentle downward traction

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70
Q

Braxton Hicks contractions

A

‘practice contractions’ = false labour
sporadic uterine contractions not resulting in cervical changes and delivery
usually painless
can confuse women as to whether they are going into labour

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71
Q

What is ‘false labour’

A

nulliparous women thinks labour has started: aware of uterine contractions
not distracted when uterus contracts
no show
on examination the cervix is not yet dilating

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72
Q

Ideal rate of cervical dilation

A

1cm/per hour

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73
Q

What does the first stage end with?

A

Full dilation of the cervix

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74
Q

What phase of labour is normally most difficult?

A

Transition phase

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75
Q

Second stage?

A

begins with full dilation of the cervix, ends with birth of baby

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76
Q

Third Stage?

A

delivery of the placenta

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77
Q

How do we assess progress in labour?

A

vaginal assessment
standard is to assess every 4 hours
more frequent if complications suspected
assess progress on partogram with ‘action’ line

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78
Q

Median duration of the second stage?

A

median duration for nulliparous and multiparous women 50 and 20 minutes respectively

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79
Q

How is the third stage managed?

A

oxytoxic with delivery anterior shoulder
early cord clamping
placenta with controlled cord traction
reduction in blood loss associated with active management of labour.

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80
Q

Reasons for induction of labour?

A 
maternal: 
hypertension
gestational diabetes
antepartum haemorrhage
PROM
other medical conditions
foetal
post dates T + 10
growth restriction
Social or convenience
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81
Q

How to predict successful induction of labour?

A

assessed by Bishop’s score

The higher the score - the easier it is to induce

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82
Q

How do we induce labour?

A

Mechanical
membrane sweeping
foley catheter
artificial rupture of membranes +/- oxytocin
Medical
prostaglandin preparations: PGE2 vaginal gel most commonly used, PGE1 (misoprostol) oral or vaginal
soften the cervix and initiate onset of contractions
nausea, vomiting, diarrhoea, uterine hyperstimulation

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83
Q

possible complications of induction of labour (IOL)

A 
inability to establish labour
uterine hyperstimulation
cord prolapse
abruption
uterine rupture
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84
Q

Incoordinate uterine activity

A

failure of uterine activity to result in dilation of the cervix as expected

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85
Q

Managing incoordinate uterine activity

A

vaginal examination
artifical rupture of membranes
commence syntocin to augment contractions
reasess 3-4 hours to ensure ongoing process

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86
Q

How do we grade perineal tears?

A 
1st degree
perineal skin or vaginal mucosa
2nd degree
perineal skin and muscles
3rd degree
skin, muscles, sphincter
4th degree
complete sphincter disruption (internal and external), with extension to rectal mucosa
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87
Q

Risk factors for perineal trauma or episotomy?

A 
first vaginal birth
increasing foetal size, head diameter and weight
foetal malposition
prolonged labour/ prolonged second stage
instrumental vaginal birth
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88
Q

Complications after perineal trauma or episotomy

A 
pain (short and long term)
dyspareunia
abscess formation
wound breakdown
rectovaginal fistula 
psychological
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89
Q

How do we manage perineal trauma?

A

recognition of the damage + rectal examination
call for assistance
ensure adequate analgesia and lighting
technique of sphincter repair
follow up post partum
continuous suture associated with reduce pain, reduced dysparaunia

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90
Q

Indications for instrumental vaginal birth?

A 
maternal
maternal exhaustion
prolonged 2nd stage
Foetal
abnormal foetal heart rate trace
malposition
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91
Q

Prerequisites for instrumental vaginal birth

A 
full dilation
engaged head
known foetal position
empty bladder
adequate analgesia
informed and consenting patient
appropriate level of training and skill
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92
Q

Instruments that can be used for instrumental delivery?

A

obstetric forceps
vacuum extractor or ventouse: less likely to deliver baby, more likely to cause baby injury, less likely to cause maternal injury, less need for analgesia

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93
Q

Indications during labour to convert to C section?

A 
maternal
failure to progress/ inadequate progress
medical condition
Foetal
abnormal foetal heart rate
malposition/ presentation
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94
Q

Issues to raise in consent process for C section?

A 
maternal risks
damage to bowel or bladder
infection
general post op complications
foetal and neonatal risk
skin lacerations
traumatic delivery
transient tachypnoea of the newborn
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95
Q

How are women cared for after C section

A 
observations
analgesia
oral intake
IDC
thromboembolism prophylaxis
chest physiotherapy
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96
Q

Puerperium

A

post partum period

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97
Q

Key aspects of care in post partum period?

A

ensure normal physiological involution (pelvic organs and mothers physiology returns to normal)
regular checks of mother and baby
establish and support breast feeding
manage any medical complications

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98
Q

common postnatal problems

A 
psychlogical problems
day 4 blues and more serious variations
breast engorgement
breastfeeding problems
bowel and bladder problems
post partum fever
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99
Q

define post partum fever and list causes?

A

temp >38
measured on 2 occassions
> 48 hours after birth

breast engorgement
mastitis
breast abscess
endometritis
UTI
wound infection - CS/episotomy/ tear
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100
Q

usual discharge procedure for mother?

A 
medical check
emotional wellbeing 
vaginal discharge, breast feeding, wound
observations, examination, inspection
contraception
follow up 
mode of birth in subsequent pregnancy
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101
Q

Usual discharge procedure for baby?

A 
well baby check
feeding
check that returned to birth weight
breast vs artificial feeding
local doctor
domicillary midwife/ CYWHS nurse
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102
Q

Contraception options in mother post partum?

A 
lactational amenorrhoea
full breast feeding effective contraception for 98% of women
less effective if bleeding, solids
condoms
progesterone only pill
combined OCP if not breastfeeding
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103
Q

Normal foetal presentation at the onset of labour?

A

longitudinal lie with cephalic presentation.
The head is normally flexed, presenting the smallest diameter to the maternal pelvis, which is defined as the vertex — the area lying between the anterior and posterior fontanelles and bounded by the parietal eminences.

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104
Q

Disadvantages of epidural pain relief in pregnancy

A

maternal motor blockade which prevents ambulation, the need for continuous foetal monitoring, possible maternal hypotension causing non reassuring foetal heart patterns and the loss of bladder sensation requiring an indwelling catheter, may also increase the duration of 2nd stage and the risk of having an instrumental birth

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105
Q

TORCH infections in pregnancy

A 
T: Toxoplasmosis
O: other
R: Rubella
C: Cytomegalovirus
H: Herpes simplex virus -2
Other
coxsackie virus
chickenpox
chlamydia
HIV
Human T-lymphotrophic virus
syphilis
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106
Q

Treatment of influenza in pregnant woman

A

early antiviral therapy with neuraminidase inhibitors after onset of symptoms should be standard management along with supportive care including antipyretics

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107
Q

Clinical presentation of rubella in pregnant women?

A

mild febrile illness with a fleeting rash 14-21 days after exposure, however 25-50% of cases are asymtpomatic

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108
Q

Management If maternal rubella infection is confirmed in the first 12 weeks of pregnancy

A

termination of pregnancy should be offered due to the high likelihood of fetal infection and the severe consequences of CRS

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109
Q

Advice for Non immune women for rubella on prepregnacny screening

A

should be offered vaccination and advised to wait one month before getting pregnant, as the vaccine is live attenuated virus.

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110
Q

transmission rate of primary maternal infection with CMV

A

30%

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111
Q

Treatment for a Seronegative pregnant woman with exposure to varicella in pregnancy

A

offered zoster immune globulin (ZIG) within 96 hours of exposure to decrease her risk of varicella

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112
Q

definitive host of the parasite Toxoplasma gondii

A

cat

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113
Q

major sources of infection for toxoplasmosis

A

ingestion of uncooked meats and contact with contaminated soil are

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114
Q

toxoplasmosis foetal syndrome features

A

chorioretinitis, intracranial calcification and hydrocephaly in approximately 10% of cases

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115
Q

Syphilis causes which congenital anomalies?

A

hepatomegaly, rash, generalised lymphadenopathy and skeletal and dental anomalies

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116
Q

Gold standard treatment for syphilis in pregnancy

A

hepatomegaly, rash, generalised lymphadenopathy and skeletal and dental anomalies

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117
Q

Dietary recommendations to avoid listeria monocytogenes

A

safe food handling practices, avoid unpasteurised milk, soft cheese, prepared salads, uncooked seafood and processed meat

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118
Q

chorioamnionitis

A

infection of the amniotic fluid, placenta, membranes and/or decidua
primarildy due to ascending infection and usually polymicrobial

119
Q

Newborns at risk of vertical transmission of Hep B management

A

given hepatitis B immune globulin (HBIG) within 12 hours of birth, and a subsequent course of active hepatitis B vaccination should be commenced within 12 hours of birth

120
Q

Main strategies to decrease perinatal transmission of HIV

A 
combined antiretroviral therapy
neonatal antiretroviral therapy
avoidance of breastfeeding
elective C section 
where maternal viral load is less than 1000 copies/mL then added benefit of elective C section delivery is unclear with transmission rates less than 2%
121
Q

A woman who consults her doctor after discovering that she was immunised against rubella 3 weeks after conceiving should be offered:
A termination of pregnancy.
B paired rubella IgM and IgG antibody titres 2 weeks apart.
C chorionic villous sampling.
D reassurance and standard antenatal care.
E varicella serology.

A

A - termination of pregnancy

122
Q

When is the best time for maternal screening of GBS

A

Maternal screening for GBS is best performed at 35–37 weeks gestation.

123
Q

Infections causing teratogenesis

A 
rubella
cytomegalovirus
varicella
parvovirus B19
toxoplasmosis
syphilis
124
Q 
Which of the following diseases can both cause serious maternal illness in pregnancy and a fetal malformation syndrome?
A hepatitis C
B varicella (VZV)
C group B streptococcus
D toxoplasmosis
E listeriosis
A

Varicella

125
Q

CMV in pregnant women

A

usually symptomatic, or mild non specific illness, unless mother is immunocompromised

126
Q

IgM

A

immediate

127
Q

IgG

A

later response

128
Q

choriocarcinoma

A

malignant tumour of trophoblast cells

129
Q

Risk Factors for molar pregnancy

A

defects in the egg
abnormalities of the uterus
nutritional deficiencies
women 40 years higher risk
diets low in protein, folic acid and carotene
being of Asian or mexican background
a previous molar pregnancy or other gestational trophoblastic tumour (one in 100 women who have had one molar pregnancy will have another).

130
Q

Ultrasound appearance of molar pregnancy

A

mole resembles a bunch of grapes, increased trophoblast proliferation and enlarging of chorionic villi

131
Q

Treatment for molar pregnancy

A

evacuate the uterus by uterine suction or by surgical curettage as soon as possible after diagnosis in order to avoid the risks of choriocarcinoma

132
Q

Karyotype of complete mole

A

Diploid — mostly 46XX

133
Q

usual origin of complete mole

A

Paternal only

Fertilisation of an oocyte without genetic material by one spermatozoon that subsequently doubles its chromosomes

134
Q

Diagnosis of malignant trophoblastic disease

A

hCG levels that do not decreased by at least 10% 3 weeks after evacuation of a molar pregnancy, or an increase of more than 10% over a 2 week interval
persistence of detectable levels of hCG more than 6 months after molar evacuation
histological evidence of choriocarcinoma in the products

135
Q

Invasive mole

A

persistent trophoblast that invades deeply into the myometrium following a molar pregnancy. There may be metastases, usually in the lungs and vagina. Microscopically, it is characterised by oedematous chorionic villi with trophoblast proliferation, as seen with a non-invasive mole.

136
Q

Placental site trophoblastic tumour

A

his consists of placental-bed trophoblast invading the myometrium from the site of placental implantation. This differs from choriocarcinoma in that the hCG level is usually much lower and the diagnosis is made only histologically. The condition is rare, accounting for only 0.1–0.2% of trophoblastic tumours.

137
Q

miscarriage definition

A

the spontaneous loss of an intrauterine pregnancy before 20 weeks gestation

138
Q

missed or delayed miscarriage

A

the failure to expel the products of conception after death of the embryo

often diagnosed when a first trimester ultrasound reveals an absence of embryonic (6-9 weeks) or foetal (>9 weeks) heartbeat
empty sac on ultrasound
clinically the woman loses the symptoms of pregnancy
on examination the uterus is smaller than expected for length of amenorrhoea and the cervix is closed

139
Q

aetiology of miscarriage

A

as many as 50-60% of embryos miscarried in the first trimester will have a chromosomal abnormality - autosomal trisomies are the most common, involving chromosomes 13,16,18,21 and 22

140
Q

Miscarriage presentation

A

per vaginal (PV) bleeding and lower abdominal pain

141
Q

Threatened miscarriage

A

vaginal spotting or light bleeding with minimal pelvic or lower back pain
on vaginal examination the cervix is closed
ultrasound scan reveals a live intrauterine foetus

142
Q

Inevitable miscarriage

A

characterised by lower abdominal pain and vaginal bleeding
on vaginal examination the lower uterus appears to be ballooning while the internal os is closed
the products of conception have not yet been passed

143
Q

Incomplete miscarriage

A

history of increasing bleeding, cramping lower abdominal pain and passage of some products of conception
on vaginal examination the internal os of the cervix is open and often products of conception are present in the canal

144
Q

Septic miscarriage presentation

A

fever, bleeding and significant tenderness in the lower abdomen and uterus

145
Q

Complete miscarriage

A

products of conception are passed and on pelvic examination the cervix is closed
ultrasound scan reveals an empty uterine cavity

146
Q

who needs surgical evacuation of the uterus with suction curettage

A

haemodynamically unstable and septic patients

147
Q

complications of surgical evacuation

A

perforation, cervical tears, intrabdominal trauma, haemorrhage and intrauterine adhesions (Ashermann’s syndrome)

148
Q

cornerstones of management in miscarriage

A

low dose aspirin, heparin and supportive care

149
Q

What is an ectopic pregnancy

A

results from implantation of the fertilised ovum (blastocyst) in tissue other than the endometrium of the uterine cavity

150
Q

most common site for ectopic pregnancy

A

fallopian tube ( most commonly in the ampulla)

151
Q

Believed cause for ectopic pregnancy

A

ectopic pregnancy is believed to be due to endothelial tubal damage secondary to salpingitis, disturbed tubal oocyte transport or proliferation of refluxed endometrial tissue arrested within the fallopian tube

152
Q

Risk Factors for ectopic pregnancy

A

STIs
prior ectopic
prior tubal surgery including tubal ligation
hormonal factors such as diethylstilbestrol exposure and progesterone, contraceptive failures (e.g intrauterine devices), increasing age and cigarette smoking
IVF

153
Q

Ectopic pregnancy vaginal examination

A

there may be bleeding, a closed cervix, a small uterus for gestational age, an adnexal mass (with or without tenderness) and localised tenderness

154
Q

most important diagnostic tools in ectopic pregnancy

A

Transvaginal ultrasound scan (TVS) and serial BhCG determinations

155
Q

What rise in BhCG would increase suscpicion of ectopic?

A

less than 60% increase in 48 hours

156
Q

What is important to monitor after conservative surgery has been performed (eg. salpingostomy)

A

monitor BhCG - follow levels til <5

157
Q

When can methotrexate be used as treatment for patients with ectopic pregnancy?

A

the asymptomatic patient with no free fluid in POD, small tubal ectopic pregnancy on TVS, absence of foetal heart beat and low serum β hCG (< 3500 IU)

158
Q

Role of methotrexate in ectopic

A

an antimetabolite that prevents the growth of rapidly dividing cells by interfering with DNA synthesis

159
Q

what in particular affects future pregnancies after an ectopic?

A

periadnexal adhesions

160
Q

post term

A

42 weeks or more

161
Q

46XX DSD

A

defined by the presence of both ovarian tissue and testicular tissue in the one person

162
Q

what is the major determinant of foetal growth and wellbeing

A

quality of placental implantation

163
Q

from what does the placenta develop

A

trophoectoderm

164
Q

what is the most accurate way of dating the pregnancy?

A

first trimester ultrasound: crown - rump length

165
Q

what is oligohydramnios?

A

decreased amount of amniotic fluid for a given gestational age

166
Q

What do you use to diagnose oligohydramnios?

A

(MVP) or the sums of the MVP in four quadrants; this is known as Amniotic fluid index (AFI)

167
Q

Potter’s Syndrome

A

the atypical appearance of foetus or neonate due to olioghydramnios in the uterus - clubbed feet, pulmonary hypoplasia and cranial anomalies)

168
Q

Eitiologies for oligohydramnios

A

maternal medical conditions, foetal anomalies, rupture of membranes and idiopathic oligohydramnios and conditions associated with placental insufficiency

169
Q

Women at risk of oligohydramnios

A

women with pre eclampsia
women with post term pregnancy
women with other conditions associated with placental insufficiency, including intrauterine growth restriction and autoimmune diseases
women with multiple pregnancies

170
Q

Complications of olioghydramnios

A 
cord compression
MSK abnormalities
IUGR
pulmonary hypoplasia
Potter’s syndrome
171
Q

clinical presentation of oligohydramnios

A

in general olioghydramnios is asymptomatic but may present with decreased foetal movement, inadequate fundal height growth or evidence of PROM

172
Q

How can you test if fluid leakage is amniotic fluid

A

Nitrazine paper can detect amniotic fluid utilising the pH of the vaginal fluid, normal vaginal pH is 3.8-4.2 while amniotic fluid has a pH of 7-7.3

fern test - second confirmatory test using microscopic examination that looks for the presence of ‘ferrying’ on a microscopic slide after allowing a sample of fluid to dry

173
Q

“what does oligohydramnios mean for my baby?”

A

The baby requires amniotic fluid to grow—especially the lungs—so a lower amount means that there is a chance of underdeveloped lungs if the low fluid is longstanding. If low fluid is diagnosed in the third trimester, there is also an increased chance of adverse outcomes

174
Q

clinical signs of polyhydramnios?

A

it is suggested clinically by a uterus that feels large for dates or measures more than 10% above the normal fundal height for gestational age

175
Q

Diagnosis of polyhydramnios

A

defined as an amniotic fluid index more than 24cm or a single deepest pocket of fluid at least 8cm

176
Q

causes of polyhydramnios?

A

50% idiopathic
20% associated with foetal anomalies, including anencephaly, hydrocephaly, tracheoesophageal fistula, oesophageal atresia, gastroschisis, duodenal atresia, spin bifida, cleft lip and palate, cystic adenomatoid lung malformation
twin pregnancy 7%
maternal Diabetes mellitus 5%
8% other - Rh isoimmunisation, hydrous foetal is, infection

177
Q

what is uterine rupture most commonly associated with?

A

previous uterine scar

178
Q

Preterm prelabour Rupture of membranes

A

Rupture of membranes at least 1 hour prior to onset of labour at less than 37 weeks gestation

179
Q

3 causes of neonatal death related to PPROM

A

prematurity,sepsis and pulmonary hypoplasia

180
Q

Diagnosis of spontaneous rupture of the membranes

A

best achieved by maternal

history followed by a sterile speculum examination.

181
Q

Diagnosis for clinical chorioamnionitis

A

maternal pyrexia, tachycardia, leucocytosis,uterine tenderness,offensive vaginal discharge and fetal tachycardia.

182
Q

prophylactic antibiotics for PPROM

A

Erythromycin should be given for 10 days

183
Q

corticosteroid use in PPROM decreases the incidence of what?

A

Respiratory distress syndrome and necrotising enterocolitis

184
Q

tocolytic

A

anti contraction medication or labour repressants - used to suppress premature labour
- nifedipine most commonly used

185
Q

contraindications for tocolytics

A 
> 34 weeks gestation
increase risk of infection
severe pre eclampsia
intrauterine death
IUGR
Abruptio placenta
maternal problems - heart disease, diabetes
186
Q

What is pre eclampsia?

A

presence of hypertension 140/90 arising after the 20th week of pregnancy.

187
Q

Symptoms of pre eclampsia

A

non-specific headaches, visual scintillations (like migraine aura), epigastric or right upper quadrant pain radiating into the back as a reflection of hepatic ischaemia, oliguria, lower abdominal pain and bleeding caused by placental abruption, or reduced fetal movements.

188
Q

Hyperesmesis gravidarum

A

is excessive pregnancy-related nausea and/or vomiting that prevents adequate food and fluid intake and is associated with weight loss of more than 5% of body mass

189
Q

What is a fibroid?

A

compact masses of smooth muscle that lie in the cavity of the uterus (sub mucous) within the uterin muscle (intramural) or on the outside surface of the uterus (subserous)

190
Q

causes of backache in pregnancy

A

hormone induced laxity of spinal ligaments
a shifting in the centre of gravity as the uterus grows;
additional weight gain

191
Q

advice for backache in pregnancy

A

maintenance of correct posture, avoiding lifting heavy objects, avoiding high heels, regular physiotherapy and simple analgesia

192
Q

Symphsis pubis dysfunction

A

excruciatingly painful condition most common in the third trimester, although it can occur at anytime during pregnancy
the symphysis pubis joint becomes loose, causing the two halves of the pelvis to rub on another when walking or moving

193
Q

pathophysiology of reflux in pregnancy

A

altered structure and function to the normal physiological barriers to reflux namely the weight effect of the pregnant uterus and hormonally induced relaxation of the oesophageal sphincter, explain the high incidence in pregnancy

194
Q

pathophysiology of haemorrhoids in pregnancy

A

effects of circulating progesterone of the vasculature, pressure not he superior rectal veins by the gravid uterus and increased circulating volume

195
Q

pathophysiology of varicose veins in pregnancy

A

they are thought to be due to the relaxant effect of progesterone on smooth muscle and the dependent venous stasis caused by the weight of the pregnant uterus on the inferior vena cava

196
Q

most common complication of fibroids in pregnancy?

A

red Degeneration

197
Q

What is red degeneration?

A

asa fibroid grows it may become ischaemic; this manifests clinically as acute pain, tenderness over the fibroid and frequent vomiting
if these symptoms are severe, uterine contractions may be precipitated causing miscarriage or preterm labour
red fibroid degeneration requires treatment in hospital, with potent analgesics
symptoms usually settle within a few days

198
Q

Pinard’s manouvre

A

this entails using a finger to flex the leg at the knee and then extend at the hip, first anteriorly then posteriorly

199
Q

What is a pessary?

A

plastic device that is placed in the vagina to provide support

200
Q

What is a prolapse?

A

Prolapse is a descent of pelvic organ out of its normal anatomical position due to luck of its support.

201
Q

vaginal vault prolapse

A

occurs in women who have had a hysterectomy previously, the vault (top of the vagina) moving downwards

202
Q

cystocoele

A

When the supports of the front wall of the vagina are weakened, the bladder can protrude through

203
Q

rectocoele

A

weakening of the back wall, where the bowel bulges through

204
Q

enterocoele

A

If the upper part of the vagina allows bowel to bulge through

205
Q

what symptom is pathognomic of prolapse

A

a bulge or dragging sensation

206
Q

What do you use to stage prolapse

A

POPQ - pelvic organ prolapse quantification system

207
Q

Chloasma

A

Blotchy pigmentation of the nose and face

208
Q

Estrone

A

After menopause
Adipose
From adrenal steroids

209
Q

Estriol

A

Pregnancy
Placenta
From fetal adrenal DHEAS

210
Q

Estradiol

A

Non pregnant reproductive years
Follicle
Granulomatous

211
Q

Müllerian duct

A

Primordium of the females reproductive tract

212
Q

Wolffian duct

A

Primordium of the male internal reproductive tract

213
Q

complications of multiple gestation

A 
nutritional anaemias (iron and folate)
pre eclampsia
gestational diabetes
thromboembolism
preterm labour (50%)
malpresentation
Caesarean delivery
post partum haemorrhage
214
Q

What is cord prolapse?

A

descent of the umbilical cord alongside or past the presenting part in the presence of ruptured membranes

215
Q

What is cord presentation?

A

the umbilical cord presents in front of the foetal presenting part with or without membrane rupture

216
Q

4Ts of post partum haemorrhage

A

tone, tissue, thrombin, tear

217
Q

Sheehan’s Syndrome

A 
acute hypopituitarism after massive PPH
deficiency of GH, prolactin, cortisol, TSH, LH and FSH
failure of lactation
failure of hair growth
poor wound healing
generalised weakness
218
Q

Complications of PPH

A

DIC, Acute renal failure, Sheehans syndrome, death

219
Q

most commonly acquired congenital viral infection

A

CMV

220
Q

causes of small placenta

A

maternal vascular diseases (pre eclampsia, hypertension, DM with renal disease), chronic infections

221
Q

causes of large placenta

A

hydrops fetalis, immune/non immune causes, maternal DM, syphilis

222
Q

Placenta in hypertensive conditions

A

multiple infarcts and decidual vasculopathy

223
Q

what medication can you take for hyperesmesis gravidarum?

A

metoclopramide

224
Q

what do you avoid eating with hyperesmesis gravidarum?

A

Foods that are high in fat, dairy and spice are best avoided.

225
Q

why is trimethoprim relatively contraindicated in the first trimester?

A

anti folate effect

226
Q

What ultrasound findings would support congenital CMV infection of this fetus?

A

ascites

227
Q

3 major diseases of late pregnancy

A

Pre eclampsia
Growth restriction
Pre term birth

228
Q

2 key mechanisms of pre eclampsia

A

Impaired Placentation

Endothelial cell activation/ Inflammation

229
Q

Tests to perform in suspected congenital syphilis

A

thorough examination
dark field microscopy of any skin or mucosal lesions
and a quantitative nontreponemal serum test (e.g., rapid plasma reagin [RPR], Venereal Disease Research Laboratory [VDRL])
infants with clinical signs should also have a lumbar puncture with CSF analysis for cell count, VDRL, and protein
CBC with platelet count
liver function test
long bone X-rays

230
Q

Strategies to decrease perinatal transmission of HIV

A

combined antiretroviral therapy
neonatal antiretroviral therapy
avoidance of breastfeeding
elective C section

231
Q

waiters tip position

A

Extended, internally rotated arm with wrist flexion

232
Q

what condition is most often associated with placental abruption?

A

pre eclampsia

233
Q

True or False

In placenta previa the initial haemorrhage is usually painless and rarely fatal

A

True

234
Q

what percentage of total blood volume is lost with a complete abruption?

A

50% or greater

235
Q

In a term pregnancy what is the management of vasa previa that has been confirmed with colour Doppler ultrasound

A

Elective lower segement C section

236
Q

polyspermy

A

egg that has been fertilised by more than 1 sperm

- usually unviable

237
Q

Low birth weight

A
238
Q

Very low birth weight

A
239
Q

Extremely low birth weight

A
240
Q

Small for gestational age

A
241
Q

Large for gestational age

A

> 90th centile for gestational age

242
Q

Most important sign of respiratory distress in newborn

A

Increased rate of breathing

243
Q

Most common cause of respiratory distress in a post mature baby

A

Meconium aspiration syndrome

244
Q

Most common cause of respiratory distress in term infant

A

Transient tachypnoea of the newborn

245
Q

Commonest cause of respiratory distress in preterm baby

A

Primary surface disease - respiratory distress syndrome

246
Q

Contraindications to external cephalic version

A 
fetal abnormality (hydrocephalus)
placenta praevia 
previous C section
hx of antepartum haemorrhage
multiple gestation
pre eclampsia or HTN
plan to deliver by c section
247
Q

Risks of ECV

A 
placental abruption
premature rupture of membranes
cord accident
transplacental haemorrhage
foetal bradycardia
248
Q

Predisposing factors for breech presentation

A 
fibroids
congenital uterine anomalies
uterine surgery
multiple gestation
prematurity
placenta previa
abnormality - anencephaly or hydrocephalus
fetal neuromuscular disorder
olioghydramnios
polyhydramnios
249
Q

largest cause of death in pre eclampsia?

A

intracranial haemorrhage

250
Q

pre eclampsia prevention

A

low dose aspirin and supplemental calcium

251
Q

Eclampsia prophylaxis

A

magnesium sulfate

252
Q

When can a urine pregnancy test be positive

A

7-10 days after conception

253
Q

how long after unprotected sex can the emergency contraception pill be taken?

A

Up to 5 days

Has higher rates of efficacy the sooner it is taken

254
Q

Human Placental Lactogen

A

produced by the syncitiotrophoblast

decreases insulin sensitivity

255
Q

progesterone production during pregnancy

A

luteal cells of the corpus luteum

after 9 weeks: placenta

256
Q

Function of progesterone in pregnancy

A

Early pregnancy: induces endometrial changes favourable for blastocyst implantation
Later pregnancy: function is to induce immune tolerance for the pregnancy and prevent myometrial contraction

257
Q

main oestrogen during pregnancy

A

Estriol

DHEAS fromt he foetal adrenal gland is the precursor for 90% of estriol converted in the placenta

258
Q

main oestrogen during menopause

A

Estrone

Adrenal androstendidione is converted in peripheral adipose tissue to estrone

259
Q

oestrogen in the non pregnant reproductive years

A

Estradiol

produced from cholesterol in the follicular theca cells

260
Q

Chadwick sign

A

bluish or purple discolouration of the vagina and cervix as a result of increased vascularity

261
Q

LInea Nigra

A

increased pigmentation of the lower abdominal midline from the pubis to the umbilicus

262
Q

Cholasma

A

Blotchy pigmentation of the nose and face

263
Q

POst conception week 1

A

starts at conception

ends with implantation of blastocyst

264
Q

week 2

A

bilaminar germ disk with epiblast and hypoblast layers (give rise to 3 primordial germ layers)

265
Q

POst conception week 3

A

trilaminar germ disc with ectoderm, mesoderm and endoderm

266
Q

Ectoderm

A

central and peripheral nervous systems; senosory organs of seeing and hearing, integument layers (skin, hair and nails)

267
Q

Mesoderm

A

Muscles, cartilage, CVS, urogenital

268
Q

Endoderm

A

lining of GI and Resp tract

269
Q

Mullerian Duct (Paramesonephric duct)

A

primordium of the female internal reproductive system
No hormonal stimulation is required
In males the Y chromosome induces gonadal secretion of mullerian inhibitory factor, whch causes the mullerian duct to involute

270
Q

Wolffian Duct (mesonephric)

A

present in all early embryos, is the primordium of the male internal reproductive system
Testosterone stimulation is required for developement to continue

271
Q

Male External Genitalia stimulation

A

Need DHT stimulation for differentiation of external genitalia into penis and scrotum

272
Q

What cell produces anti Mullerian hormone

A

Sertoli cell

273
Q

What cell produces testosterone

A

Leydig cell

274
Q

IOnising radiation as a teratogen

A

no increase is seen in fetal anomlies or pregnancy losses with exposure

275
Q

Effect of lithium on pregnancy

A

Ebstein’s Anomaly (right heart defect)

276
Q

Effect of streptomycin on pregnancy

A

VIII nerve damage, hearing loss

277
Q

Effect of Isoretinoin on pregnancy

A

Congential deafness, microtia CNS defects, congenital heart defects

278
Q

Valproic acid, pregnancy

A

neural tube defects

279
Q

Warfarin and pregnancy

A

chondrodysplasia

280
Q

Aneuploidy

A

numeric chromosome abnormalities in which cells do not contain 2 complete sets of 23 chromosomes
occurs because of nondisjunction
most common anueploidy is trisomy

281
Q

Most common trisomy in first trimester losses

A

16

282
Q

most common trisomy at term

A

21

283
Q

Polyploidy

A

sets of extra chromsomes
Triploidy: 69 chromosomes
Tripolidy = incomplete molar pregnancy

284
Q

Chromosomal Mosaicism

A

When an individual has 2 or more cell populations with a different chromosomal makeup

285
Q

Anatomical structures cut in an episiotomy

A

vaginal epithelium, transverse perineal and bulbocavernosus muscles; and perineal skin

286
Q

Risk Factors for Cord Prolapse

A 
Polyhydramnios
Preterm delivery
Malpresentation
Unstable pregnancy
multiple pregnancy
287
Q

Sudden CTG deceleration after membrane rupture in polyhydramnios. What is the most likely cause

A

Cord prolapse

288
Q

How do you confirm cord prolapse

A

Vaginal Examination: a loop of umbilical cord will be palpated in the vagina and will be pulsatile

289
Q

Avulsion of what can cause an anterior vaginal prolapse

A

ATFP: Arcus Tendineus Fascia Pelvis

290
Q

How is prolapse staged

A 
POPQ system
Pelvic organ quantification system
Stage 0-4
0= no prolapse
4= complete eversion of the genital tract
291
Q

Non surgical management options for prolapse

A 
Reasurane
Manage medical conditions that worsen prolapse (constipation, chronic cough)
address lifestyle issues
pelvic floor exercises
oestrogen replacement
pessary
292
Q

Side Effects of pessary use

A

Vesicovaginal fistula
vaginal discharge
vaginal bleeding

293
Q

Recommended folic acid dose in pregnancy

A

0.5mg

294
Q

recommended folic acid for diabetics in pregnancy

A

5mg (daily for 6 weeks before conception

295
Q

How long should second stage last?

A

2 hours in nulliparous
1 hour in multi
(epidural add 1 hour)

General Medicine (15 decks)

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