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Phase 3A > Obs and Gynae Peer Teaching > Flashcards

Obs and Gynae Peer Teaching Flashcards

1
Q

What gestation is normal labour

A

37 to 42 weeks

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2
Q

Role of prostaglandin in labour

A

Reduces cervical resistance (cervical ripening) and increased release of oxytocin from posterior pituitary

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3
Q

Role of oxytocin in labour

A

Stimulates uterine contraction

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4
Q

2 things needed for diagnosis of labour

A

Painful, regular, progressive uterine contractions

Cervical dilatation and effacement

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5
Q

Describe the latent first phase of labour

A

Cervix efface and dilate up to 4cm

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6
Q

Describe the active first phase of labour

A

Progressive cervical dilatation from 4-10cm. Regular painful contractions

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7
Q

Describe the second stage of labour

A

Full cervical dilatation until birth of baby

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8
Q

Describe the third stage of labour

A

Delivery of baby to delivery of placenta

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9
Q

How long is latent phase

A

18hr first, then 12 hour for second baby

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10
Q

What makes you suspect fialure to progress

A

Less than 2cm dilatation in 2 hours. Arrested descent/ slowing of progress in multips

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11
Q

Causes of abnormal first stage of labour

A

Inefficient uterine contractions

Cephalopelvic disproportion

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12
Q

Who most commonly gets inefficient uterine contractions in labour and what is the management

A

Nulliparous.

Amniotomoy and syntocin

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13
Q

Who most commonly gets cephalopelvic disproportion, what are the signs and whats the management

A

Multiparous women
Caput and moulding are the signs. Secondary arrest (previously good progress).
Do a c section

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14
Q

What counts as a prolonged 2nd stage of labour

A

2hr of active pushing in nulliparous, 1hr of active pushing in multiparous

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15
Q

What is the management of prolonged 2nd stage

A

Assisted vaginal delivery or c section

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16
Q

What is a 1st degree tear

A

Laceration of vaginal epithelium or perineal skin only

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17
Q

What is a 2nd degree tear

A

Involvement of the perineal muscles but not the sphincter

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18
Q

What is a 3rd degree tear

A

Disruption of the anal sphincter muscles

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19
Q

What is a 4th degree tear

A

Disruption of the anal epithelium as well

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20
Q

What is physiological management of 3rd stage

A

No Syntometrine or syntocin
Cord stops pulsating before clamping
Maternal effort to deliver placenta

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21
Q

When do you change to active 3rd stage of labour management

A

Haemorrhage or placenta not delivered by 1hr. Reduces risk of PPH

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22
Q

What is the active management of the 3rd stage of labour

A

IM syntocin
Deferred clamping and cutting of cord
Controlled cord traction

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23
Q

Definition of gestational diabetes

A

Carbohydrate intolerance which is diagnosed in pregnancy

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24
Q

Why does gestational diabetes happen

A

Reduced glucose tolerance due to change in carbohydrate metabolism
Antagonistic effect of human placental lactogen, progesterone and cortisol

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25
Q

Risk factors for gestational diabetes

A

Maternal obesity (BMI>30)
Previous macrosomic baby
Previosu GDM
1st degree relative with DM

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26
Q

Effects of pregnancy on diabetes

A

Increased DKA and hypo risk

Increased retinopathy and nephropathy risk

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27
Q

Effects of diabetes on pregnancy anagram

A

SMASH

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28
Q

SMASH anagram of diabetes effects on pregnancy

A 
Shoulder dystocia
Macrosomnia
Amniotic fluid excess 
Still birth
HTN, Hypoglycaemia
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29
Q

What can shoulder dystocia cause

A

Erbs palsy

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30
Q

Which circumference is bigger in a GDM baby

A

AC bigger than HC on USS

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31
Q

What is the name for amniotic fluid excess

A

Polyhydramnios

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32
Q

Why will a GDM baby get hypoglycaemia

A

Hyperinsulinaemia

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33
Q

How do you diagnose GDM

A

Oral glucose tolerance test
2hr, 75g oral glucose
Done at booking then repeated at 24-28 weeks if normal

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34
Q

What is the threshold for OGTT and Fasting glucose of GDM

A
  1. 8mmol/L OGTT

5. 6mmol/L Fastin

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35
Q

Counselling for mums who are already diabetic

A

Achieve optimal control
Screen complications
Alter meds
Folic Acid

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36
Q

What medications need to be stopped in pregnancy

A

ACEis, Statins, all other hypoglycaemics

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37
Q

Why does folic acid need to be given especially to GDM mums

A

Increased risk of neural tube defects

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38
Q

Steps of GDM treatment

A

Diet/exercise
Metformin
Insulin
Glibenclamide

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39
Q

Fetal monitoring for GDM

A 
Serial USS (size and amnio)
Fetal echo at 20-24wks (CHD)
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40
Q

GDM labour

A

Delivery before 41wks
Induce by 39
Vaginal delivery and continued monitoring preferred
If >4kg then elective CS
IV dextrose and sliding scale insulin given

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41
Q

Post birth GDM advice baby

A

Breastfeeding

Monitor fetal BG as risk of hypoglycaemia

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42
Q

Post partum GDM advice mum

A

Stop insulin and arrange OGTT at 6 weeks postpartum

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43
Q

What is rhesus disease

A

Maternal antibody response mounted against fetal red cells

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44
Q

What combination of rhesus parents leads to rhesus disease

A

Rhesus negative mum, rhesus positive dad

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45
Q

How does sensitisation work in rhesus disease work

A

During first pregnancy, fetal blood crosses into maternal circulation. Maternal immune response to Rh D+ve antigens on foetal RBCs

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46
Q

Why isnt the first rhesus pregnancy at risk

A

Initially IgM can not cross the placenta

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47
Q

How does rhesus disease happen in the second pregnancy

A

Memory B cells produce rapid immune response (IgG) which crosses into the foetal circulation causing haemolytic anaemia (foetal hydrops if severe

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48
Q

Sensitising events for rhesus

A 
surgery after miscarriage
Ectopic pregnancy
Blunt abdo trauma
Amniocentesis
Intrauterine death
Delivery
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49
Q

Management of rhesus disease

A

All mums checked at booking visit, 28 and 34 weeks.

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50
Q

How do you assess and treat fetal anaemia

A 
MCA doppler (increased flow velocity)
Prevention= antiD immunoglobulin
Kleihauer test
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51
Q

What is kleihauer test

A

Tests for foetal maternal haemorrhage

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52
Q

Define chronic hypertension (obs and gynae)

A

HTN before pregnancy (also includes HTN before 20 weeks)

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53
Q

Define pregnancy induced hypertension

A

Gestational non proteinuric HTN

New persistent hypertension after 20 weeks gestation without evidence of preeclampsia

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54
Q

Threshold of hypertension in pregnancy

A

140/90

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55
Q

Define preeclampsia

A

HTN and proteinurina, specific to pregnancy and puerperium

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56
Q

Preeclampsia risk factors acronym

A

NOPE 2 FAT

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57
Q

NOPE 2 FAT preeclampsia risk factors

A

Nulliparity
Obesity
Previous Hx
Extremes of age

2- twins

Family History
Autoimmune (anitphospholipids)
Twins

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58
Q

Pathophysiology of preeclampsia

A

Failure of trophoblastic endovascular remodelling. Spiral arteries remain high resistance (coil and not dilated). Causes placental ischaemia

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59
Q

Presentation of preeclampsia

A

Most asymptomatic.
Headache, visual disturbances, epigastric/ RUQ pain.
Nausea and vomitting
Rapid oedema (esp. face)

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60
Q

Preeclampsia on examination

A 
Hypertension
Proteinuria
Facial oedema
Epigastric/ RUQ pain
Brisk hyperreflexia/ ankle clonus
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61
Q

Preeclampsia kidney complications

A

Reduced renal blood flow and GFR

Increased uric acid/ urea/ creatinine and proteinuria

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62
Q

Preeclampsia liver complications

A

HELLP syndrome

Coagulation system changes

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63
Q

What is HELLP syndrome

A

Happens to the liver in preeclampsia (haemolysis, high ALT, high AST, low platelets)

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64
Q

What haemolytic changes happen to the liver in preeclampsia

A

Thrombocytopenia, Low antithrombin III, increased fibronectin

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65
Q

What is eclampsia

A

Generalised tonic clonic seizures

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66
Q

What CNS changes happen in preeclampsia

A

Eclampsia
Headaches
Visual disturbances

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67
Q

Severe complications of preeclampsia

A 
Eclampsia
HELLP
Stroke
Renal failure
Placental abruption
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68
Q

Foetal complications of preeclampsia

A

IUGR (placental insufficiency)
Preterm
Oligohydramnios
IUFD

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69
Q

Preeclampsia diagnosis

A

New persistent raised BP (>140/90 at 20+ weeks) AND Proteinuria 300mg+ in 24hr collection or 2+ on dipstick

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70
Q

Mild and moderate preeclampsia classification

A

BP less than 160/110 with significant proteinuria and no complications

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71
Q

Severe preeclampsia classification

A

BP >160/110
Proteinuria over 1g/24hr or 2++
Maternal complications occur

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72
Q

What is the only cure of preeclampsia

A

Delivery of placenta

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73
Q

Preferred delivery route for preeclampsia

A

Induction of labour and vaginal

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74
Q

If pregnancy at risk which drug do you give from 12 weeks in preeclampsia

A

Low dose aspirin

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75
Q

Which drug do you give if preeclampsia is moderate/severe at 34 weeks

A

Steroids- bethametasone

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76
Q

Which drug do you give to treat eclampsia but then must deliver

A

IV Magnesium Sulphate

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77
Q

Which drug is used to treat acute severe preeclampsia and what do you give if asthmatic or CHF

A

PO Labetalol (methyldopa if asthmatic/CHF)

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78
Q

What is the definition of antepartum haemorrhage

A

Bleeding from genital tract after 24 weeks gestation and prior to the onset of labour

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79
Q

How much is minor APH

A

Less than 50mL

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80
Q

How much is major APH

A

50-1000mL

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81
Q

How much is massive APH

A

> 1000mL and or signs of shock

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82
Q

Uterine differentials of APH

A

Placental abruption

Placenta praevia, vasa praevia

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83
Q

Cervical differentials of APH

A

Show (loss of mucus plug)
Cervical cancer/ polyps
Cervical ectropian

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84
Q

Vaginal differentials of APH

A

Trauma

Infection

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85
Q

Velamentuous placenta

A

Umbilical vessels go within the membranes before placental insertion

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86
Q

Placenta accreta

A

chorionic villi attach to the myometrium, rather than being restricted within the decidua basalis.

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87
Q

Placenta increta

A

chorionic villi invade into the myometrium.

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88
Q

Placenta percreta

A

chorionic villi invade through the perimetrium

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89
Q

Risk factors for placenta accreta

A

Previous accreta
C-section
uterine surgery

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90
Q

Investigations for placenta crreta

A

Ultrasound scan (MRI can complement)

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91
Q

Management for placenta accreta

A

Aim to deliver in 35th week.
C section hysteretomy with placenta in situ
Uterine preserving surgery

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92
Q

Placenta praevia definition

A

Implantation of placenta, wholly or in part, in the lower segment of the uterus

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93
Q

What happens to 90% of low lying placentas at 20 weeks

A

Resolve as the pregnancy progresses and lower uterine segment grows

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94
Q

Risk factors for placenta praevia

A

Multiparity, smoking, mulitple pregnancy, advanced age, previous PP, previous c section

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95
Q

Define marginal placenta praevia

A

Placenta in lower segment of uterus, close to the internal OS

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96
Q

Define major placenta praevia

A

Placenta lies over the OS (cervical effacement and dilatation= catastrophic bleeding)

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97
Q

placenta praevia symptoms

A

Intermittent painless bright red bleeds, which increase in frequence and severity over the weeks

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98
Q

Placenta praevia on physical examination

A

Soft uterus
Foetal malpresentation
Foetal head not engaged and high

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99
Q

Investigations of placenta praevia

A

Diagnostic USS if low lying at 2nd trimester, repat at 32.

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100
Q

Management of placenta praevia

A

Avoid sex, dont do a vaginal examination. If previously bled and major, monitor till delivery.
Elective C section 37-39wks.
Single steroid course at 35 weeks

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101
Q

Placenta abruption definition

A

Premature seperation of a normally sited placenta from the uterine side wall

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102
Q

Whats the difference between a revealed abruption and a concealed abruption

A

Revealed has visible bleeding, concealed doesnt

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103
Q

Risk factors for placenta abruption

A 
Previous abruption
Preeclampsia
IUGR
Abnormal placentation
Rapid uterine decompression
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104
Q

Symptoms of placenta abruption

A

Abdominal pain and bleeding. Sudden onset severe constant bleeding. Contraction leads to blood clot which irritates and promotes contraction

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105
Q

Placental abruption on examination

A

Tender, contracting WOODY HARD uterus. Maternal shock and foetal distress

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106
Q

Investigations for placental abruption

A

Diagnosis on clinical grounds. Foetal CTG, USS, Maternal FBC, clotting, Xmatch, U+E

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107
Q

Management of placental abruption

A

Immediate delivery

Usually CS and resus simultaneously

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108
Q

Vasa praevia definition

A

Foetal vessels run in membrane below presenting foetal part

109
Q

Triad of vasa praevia symptoms

A

ROM
APH
Foetal distress

110
Q

Order of presentation of vasa praevia

A

Rupture of membranes then painless PV bleed then rapid foetal distress and bradycardia

111
Q

Minor PPH

A

500-1000mL

112
Q

Major PPH

A

More than 1000mL

113
Q

Define primary PPH

A

Loss of more than 500mL of blood from genital tract within 24h of the birth of the baby

114
Q

Define secondary PPH

A

Abnormal/excessive bleeding from the genital tract between 24hr and 6 weeks post partum

115
Q

What can cause secondary PPH

A

Infection (endometritis) or retained placental products

116
Q

Causes of primary PPH (4Ts)

A

Tone- uterine atony
Trauma- perineal/ vaginal lacerations
Tissue- retained placenta
Thrombin- coagulopathy

117
Q

How can uterine atopy lead to primary PPH

A

Lack of contractions after delivery means uterine vessels dont clamp down.

118
Q

Risk factors for uterine atony

A

Prolonged labour, nulliparity, gran multiparity, overdistended uterus, previous PPH

119
Q

How can retained placenta lead to primary PPH

A

Partial seperation means uterus cant contract properly

120
Q

How can coagulopathy lead to primary PPH

A

haemophilia, anticoagulant or DIC means bleeding problem

121
Q

PPH symptoms

A

Prolonged and worsening vaginal bleeding after delivery delivery. PV bleeding/ clots. Abdominal/ pelvic pain

122
Q

PPH signs

A

Pyrexia, tachycardia, tachypnoea, hypotension, reduced level of consciousness, pallor

123
Q

Complications of PPH

A

Shock, DIC

124
Q

Management of minor PPH without clinical signs of shock

A

IV fluids, cross match blood, regular clinical monitoring and obs

125
Q

How do you treat major PPH

A

Resuscitate- ABC

Treat and stop cause of bleeding

126
Q

Treatment of lacerations causing PPH

127
Q

Treatment of retained placenta causing PPH

A

Manual evacuation

128
Q

Treatment of uterine atony causing PPH

A

Bimanual uterine compression
Ergometrine IV
Oxytocin
infusion

129
Q

What is second line for PPH after oxytocin infusion if bleeding doesnt stop

A

Misoprostol

Carboprost

130
Q

Surgical treatment of PPH caused by uterine atony

A

Uterine tamponade with Rusch balloon, B lynch suture, UAE, hysterectomy

131
Q

Name 4 types of incontinence

A

Stress incontinence
Urge incontinence
Mixed urinary incontinence
Neurogenic bladder

132
Q

Define stress incontinence

A

Involuntary leakage of urine on effort or exertion, or on sneezing or coughing

133
Q

What is the cause of stress incontinence

A

Urethral sphincter weakness (detrusor pressure is greater than closing pressure of urethra)

134
Q

What are the key risk factors for stress incontinence

A 
Pregnancy
Vaginal delivery
Instrumental delivery
Oestrogen deficiency
Pelvic trauma/irradiation
Congenital weakness
Increased age and obesity
135
Q

What happens to the pressures in stress incontinence

A

Bladder neck slips below pelvic floor because of weak supports. Bladder neck not compressed. Bladder neck pressure is therefore less than the bladder pressure leading to incontinence

136
Q

Clinical features of stress incontinence

A

Incontinence on coughing, sneezing, laughter or other stressors.
Frequency
Urgency

137
Q

Investigations of stress incontinence

A

exclude UTI
Frequency volume chart
Bladder diaries
Urodynamics

138
Q

What are urodynamics and do you do them before starting management

A

Function tests of the bladder at OPCs. You can start conservative management first

139
Q

First line treatment for stress incontinence

A

Atleast 3 months of pelvic floor muscle training

140
Q

Treatment of stress incontinence

A

Lifestyle (weight loss, avoid excessive drinking)
Pelvic floor muscle training.
Surgery (synthetic mid urethral sling; burch colposuspenision)
Duloxetine (last line)

141
Q

Describe duloxetine as a treatment for stress incontinence

A

Only if not suitable for surgery. Side effects: nausea, dyspepsia, dry mouth, diziness, insomnia, drowsiness

142
Q

Define urge incontinence

A

Involuntary leakage of urine accompanied by urgency

143
Q

Define overactive bladder

A

Urgency (+- urge incontinence, with frequency or nocturia in the absence of UTI

144
Q

What causes urge incontinence

A

Detrusor overactivity

145
Q

What are risk factors for urge incontinence

A

Secondary to pelvic floor or incontinence surgery
UTI
Neurogenic (spastic bladder)

146
Q

Clinical features of urge incontinence

A

Urgency
Frequency
Stress incontinence too

147
Q

How do you exclude UTI

A

Urine dipstick and MSU for MC&S

148
Q

Investigations for overactive bladder

A

Exclude uti
Frequency volume chart
Urodynamics

149
Q

First line treatment for urge incontinence

A

Anticholinergics- oxybutynin

150
Q

Anticholinergic side effects

A

Dry mouth
Constipation
Nausea

151
Q

Management of urge incontinence

A

Conservative (fluids, caffeine, weight, pelvic floor)
Bladder training
Anticholinergics

152
Q

Anticholinergics alternatives for urge incontinence

A

Beta 3 agonists, mirabegron, botox (botulinum toxin type A); sacral nerve stimulation
Surgery last resort

153
Q

Which incontinence if surgery before meds

A

Stress incontinence

154
Q

Anterior wall prolapses

A

Cystocele
Urethrocele
Cystourethrocele

155
Q

Cystocele

156
Q

Urethrocele

157
Q

Cystourethrocele

A

Bladder and urethra

158
Q

Posterior wall prolapses

A

Enterocele

Rectocele

159
Q

Enterocele

A

Small bowel

160
Q

Rectocele

161
Q

Apical prolapses

A

Uterovaginal

Vault

162
Q

Uterovaginal prolapse

A

Uterine descent w/ inversion of vaginal apex

163
Q

Vault prolapse

A

Post hysterectomy- inversion of vaginal apex

164
Q

What causes prolapse

A

Pelvic floor weakness

165
Q

Name 4 categories of causes of prolapse

A 
Vaginal delivery and process of pregnancy
Congenital
Menopause
Chronic predisposing factors
Iatrogenic factors
166
Q

How can vaginal delivery and process of pregnancy cause prolapse

A

Big baby delivery, prolonged second stage, instrumental delivery

167
Q

How can congenital problems lead to prolapse

A

Abnormal collagen metabolism

168
Q

How can menopause and age lead to prolapse

A

Deterioration of collagenous connective tissue with oestrogen withdrawal

169
Q

How can chronic predisposing factors lead to prolapse

A

Deterioration of collagenous connective tissue with oestrogen withdrawal

170
Q

How can iatrogenic factors lead to prolapse

A

Any chronic increase increase in intraabdominal pressure (obesity, chronic cough, constipation, heavy lifting, pelvic mass)

171
Q

Clinical features of prolapse

A

Asymptomatic

Dragging sensation, discomfort, heaviness within pevlic. Dyspareunia

172
Q

How would anterior prolapse prevent

A

Urinary symptoms.

Dragging sensation, discomfort, heaviness

173
Q

How would posterior prolapse present

A

Constipation, difficulty with defaecation.

Dragging sensation, discomfort, heaviness

174
Q

How does severe prolapse present

A

Increased distressing symptoms (incontinence, heaviness, pain, dyspareunia)

175
Q

Prevention of prolapse

A

Weight reduction, smoking cessation, treat chronic triggers, pelvic floor exercises

176
Q

Treatment for prolapse

A

Surgery (if symptomatic or severe)

Pessaries

177
Q

Which pessary is best for prolapse

A

Ring pessary, common, easy to use, sexual intercouse not affected

178
Q

Can you have a kid after manchester repair

179
Q

surgery for uterine prolapse if wanting children

A

Sacrospinous hysteropexy with sutures

180
Q

surgery for uterine prolapse if not wanting children

A

Vaginal hysterectomy

181
Q

surgery for anterior or posterior wall prolapse

A

Anterior/ posterior repair without mesh

182
Q

surgery for vault prolapse

A

Sacrospinous fixation

Colpocleisis

183
Q

Define endometriosis

A

Presence of endometrial tissue outside the uterus

184
Q

Risk factors for endometriosis

A

Women in 20s, after menarche, nulliparous

185
Q

Whats the theory about how endometriosis happens

A

Reflux and implantation of viable endometrial tissue during menstruation

186
Q

What is endometriosis dependent on

A

Oestrogen. Regresses after menopause and during pregnancy

187
Q

What is frozen pelvis

A

Where severe adhesions for because of menstrual blood causing progressive fibrosis and adhesions

188
Q

What is a chocolate cyst

A

Accumulated dark brown blood in ovaries, can rupture

189
Q

Do PID and ectopic pregnancy cause endometriosis

190
Q

Symptoms of endometriosis

A

Chronic cyclical pelvic pain (during periods, deep dyspareunia and backache); infertility

191
Q

How do you diagnose endometriosis

A

Laparoscopy and biopsy (visualisation of lesions and histology of biopsy specimen)

192
Q

What is stage 1 endometriosis

A

Minimal, superficial

193
Q

What is stage 2 endometriosis

A

Mild

Some deep

194
Q

What is stage 3 endometriosis

A

Moderate

some endometriomas and adhesions

195
Q

What is stage 4 endometriosis

A

Large endometriomas and adhesions. Reduced egg reserve and chance of live birth

196
Q

First line treatment of endometriosis

A

NSAIDS, reduce pain and menstrual flow

197
Q

Medical treatment of endometriosis

A

Continous COCP and NSAIDs

GnRH agonist

198
Q

Surgical treatment of endometriosis which preserves fertility

A

Laparoscopic surgery (laser ablation +- adhesiolysis)

199
Q

Radical surgical treatment for endometriosis

A

Hysterectomy and bilateral salpingoophectomy

200
Q

Define fibroid

A

Benign neoplasm of smooth muscle in myometrium

201
Q

Risk factors for fibroids

A

Near menopause, afrocarribean population

202
Q

What are fibroids dependent on

A

Oestrogen.

Increase in size with pregnancy, pills, clomifene. Regress after menopause

203
Q

Symptoms of fibroids

A

Menorrhagia and IMB
Dysmenorrhoea
Subfertility
Pressure effects- bladder retention and constipation

204
Q

What is red degeneration of fibroids

A

Where during pregnancy they grow too big causing acute severe pain and fever

205
Q

How do fibroids reduce fertility

A

Submucosal fibroids prevent fertility

206
Q

Investigations of fibroids

A

Examination VE and Abdo, pelvis USS

207
Q

When do you treat fibroids

A

If they have distressive symptoms, excessive bleeding or concern of sarcoma

208
Q

Name an IUS

209
Q

Name a progestogen

A

Norethisterone

210
Q

Name medical managements of fibroids

A

Tranexamic acid, NSAIDs, Progestogens, IUS, COCP

211
Q

Non invasive surgery for fibroids

A

Uterine artery embolization

212
Q

Surgical treatment of fibroids to preserve fertility

A

Hysteroscopic resection if small, laparoscopic myomectomy if large

213
Q

Surgical treatment of fibroids if family completed

A

Hysterectomy/ endometrial ablation

214
Q

Polycystic ovary definition

A

Transvaginal USS appearance of multiple (12+) small (2-8mm) follicles in an enlarge (>10mL volume) ovary

215
Q

Three things needed for an ovary to be classic as polycystic

A

12+ follicles
2-8mm follicles
>10mL ovary

216
Q

What criteria are used for PCOS

A

Rotterdam criteria (2/3 needed)

217
Q

What are the rotterdam criteria

A

1) PCO on USS
2) Oligoovulation and/or anovulation
3) evidence of hyperadnrogenism

218
Q

What is evidence of hyperandrogenism

A

Acne, hirsutism

Raised serum testosterone

219
Q

Clinical features of PCOS

A 
Obese
Acne
Hirsuitism
Oligo/amenorrhoea
Subfertility
Miscarriage
220
Q

What can PCOS lead to later in life

A

Type 2 diabetes

Gestational diabetes

221
Q

What is a relevant blood test finding in PCOS

A

LH:FSH ratio is high (3:1) as LH high.

222
Q

Blood tests for PCOS

A 
FSH
LH
Antimullerian hormone
Prolactin
Oestrogens
Serum testosterone
223
Q

What blood test would you do for cushings

224
Q

What blood test would you do for acromegaly

225
Q

What blood test for congenital adrenal hyperplasia

226
Q

What investigations would you do for PCOS

A

Lots of blood tests and USS

227
Q

PCOS management

A

Conservative
Improve menstrual regularity
Control symptoms
Treat subfertility

228
Q

Conservative management in PCOS

A

Lose weight
Exercise and diet advice
Smoking cessation

229
Q

How would you improve menstrual regularity in PCOS

A

COCP

Metformin (reduces androgen levels)

230
Q

How do you control symptoms of PCOS

A

Anti androgens- dont give during conception or pregnancy. Cyproterone acetate, spironolactone, vaniqa face cream

231
Q

Treatment for subfertility in PCOS

A 
Weight loss
Antioestrogens
Gonadotrophins
Laparoscopic ovarian diathermy
IVF
232
Q

Name an antioestrogen for PCOS and subfertility

A

Clomid- clomifene citrate (safe and cheap)

233
Q

What is an increased risk with gonadotrophins

A

Increased risk of multiple pregnancy and ovarian hyperstimulation syndrome

234
Q

Define pelvic inflammatory disease

A

Clinical syndrome characterised by inflammation of the upper genital tract

235
Q

What is endometritis

A

Inflammation of the endometrium

236
Q

What is salpingitis

A

Inflammation of the fallopian tubes

237
Q

What causes PID

A

Ascending infection from endocervix (chlamydia). Uterine instrumentation, childbirth or miscarriage

238
Q

Name examples of surgical instrumentation

A

Surgical termination of pregnancy, evacuation of retained products of conception, Lap and dye test, IUD

239
Q

PID presenation

A

Pelvic pain, deep dyspareunia, vaginal discharge (dysmenorrhoea, IMB, Fever)

240
Q

Complications of PID

A

Ectopic pregnancy
Infertility
Adhesions
Fitz Hugh Curtis Syndrome

241
Q

PID on examination

A

Tachycardia
Fever
Abdominal tenderness, bilateral adnexal tenderness, cervical excitation

242
Q

Investigations for PID

A

FBC, Triple STI swab screen, urine pregnancy test, pelvic/TVUSS, laparoscopy

243
Q

Gold standard investigation for PID

A

Laparoscopy

244
Q

Management of PID

A

IM ceftriaxone + PO doxycycline+ PO Metronidazole

245
Q

Examples of ovarian cyst accident

A

Torsion, rupture, haemorrhage

246
Q

Symptoms of ovarian cyst accident

A

Sharp unilateral pain following sex or strenuous exercise.
Tender abdomen.
Severe may cause syncope

247
Q

Investigation for ovarian cyst accident

A

USS shows free fluid in pelvic cavity

248
Q

Treatment of ovarian cyst accident

249
Q

What is adnexal torsion

A

Twisting of the ovary and sometimes fallopian tube

250
Q

Who gets adnexal torsion

A

Adolescent and reproductive age women

251
Q

Symptoms fo adnexal torsion

A

Unilateral sharp, waxing and waning pelvic pain. Nausea and vomitting

252
Q

Adnexal torsion on examination

A

Tender palpable mass on bimanual

253
Q

Ultrasound scan of adnexal torsion

A

Whirlpool sign.

Enlarge oedematous ovary with impaired blood flow

254
Q

Define ectopic pregnancy

A

Implantation of a conceptuous outside the uterine cavity

255
Q

Where are most ectopic pregnancies

A

Tubal (ampulla then isthmus(prone to rupture))

256
Q

Risk factors for ectopic pregnancy

A

Previous EP
IUCD
Pelvic surgery
Assisted reproduction

257
Q

Triad of ectopic pregnancy

A

Amenorrhoea
Lower abdominal pain
PV bleeding

258
Q

Describe the pain in ectopic

A

lower abdo, Unilateral, initially colicky then constant

259
Q

Describe the bleeding in ectopic

A

Small amount PV

260
Q

What symptoms are produced by intraperitoneal blood loss

A

D and V, lightheadedness

Shoulder tip pain (haemoperitoneum)

261
Q

Assessment of ectopic pregnancy

A

Peritonism
Obs and vitals
Adnexal mass

262
Q

Ectopic pregnancy on VE

A

Cervical excitation, adnexal tenderness, OS closed

263
Q

Gold standard investigation of ectopic pregnancy

A

Laparoscopy

264
Q

Investigations for ectopic pregnancy

A

Pregnancy test
Serial serum hCG
Pelvic TVUSS
LAPAROSCOPY

265
Q

How does IUP and EP hCG differ

A

Rapid rise in IUP. Falling or rising slowly suggests EP

266
Q

What is expectant management of EP

A

Serial serum hCG until repeated fall in levels

267
Q

What is the medical management of ectopic pregnancy

A

IM Methotrexate and monitor serum hCG

268
Q

What is surgical management of ectopic

A

Laparoscopy

Salpingectomy

Phase 3A (25 decks)

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