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Phase 3a > OBGYN > Flashcards

OBGYN Flashcards

1
Q

What is the average age of menopause and when can it be diagnosed

A

51 years

Diagnosed after 12 months of amennorhea

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2
Q

When would you use FSH to diagnose menopause

A

In someone under 40 years
For premature ovarian failure
In >45 years, diagnose menopause based on symptoms

An FSH >40 is usually indicative of menopause

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3
Q

What contraception advice would you give to someone who is perimenopausal

A

They can still get pregnant, although the risk is low
Untill then are amennorhaeic for 12 months, they are still ovulating and could get pregnant
Mirena coil best with oestogen patch

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4
Q

What are the symptoms of menopause

A

Vasomotor - hot flushes, night sweats (low BP)
Mood - low mood, anxiety
Cognitive - forgetful, memory loss, confused
Libido - low
Skin - vaginal/ vulval atropy
Infections - UTI
MSK - joint and muscle pain

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5
Q

What is the indication for HRT treatment

What is the goal of treatment

A

Menopausal symptoms
Low Bone mineral density, with no menopause symptoms, is not an indication for treatment
Goal is to manage symptoms at lowest HRT dose

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6
Q

What risk assessments should be done before starting on HRT

A

Cardio - any active CVD (recent MI)
Haem - active or past VTE, thrombophillia
Cancer - active or past breast cancer
BMI - >30
Liver - any liver disease, derranged LFTs
Bleeding - undiagnosed vaginal bleeding

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7
Q

What risks would you discuss with a someone wanting to start on HRT

A

Breast cancer risk - little to no increased risk with oestrogen only. Increased risk with O+P (extra 4/ 1000), this can be offset with diet and exercise, cutting alcohol. Risk is reversible.

CVD risk - some increased risk with O+P.

Stroke risk - some increased risk with O+P.

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8
Q

What are the contraindications for HRT

A 
Breast cancer - active or past 
VTE - active or past 
Clotting disorder - thrombophillia
Active CVD
>30 BMI
Liver disease
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9
Q

What are the main sites of oestogen synthesis

A 
Ovaries
Adipose tissue
Adrenal glands
Brain
Bone
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10
Q

List some of the main functions of oestrogen

A

Regulates female reproductive cycle (sex)
Inhibits osteoclasts and activates blasts (bone)
Supports BP (vascular)
Regulates protein synthesis - liver (clotting factors)
Regulates mood - lots of oestrogen receptors in brain (mood/ cognition)

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11
Q

Outline the management of perimenopausal symptoms in someone with a uterus

A

Cyclical oral HRT - oestrogen every day + progesterone for last 2 weeks of cycle - bleed every month, or 3 months (if progesterone only once every 3 months)
Mirena coil + dermal oestrogen

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12
Q

Outline the management of postmenopausal symptoms in someone with a uterus

A

Combined continuous HRT - oral

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13
Q

Outline the management of postmenopausal symptoms in someone without a uterus

A

Oestrogen only HRT - oral, dermal, pessary

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14
Q

What is the most common side effect of clonidine - how common is it

A

Sleeplessness

Very common - 50%

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15
Q

How common are vasomotor symptoms in menopause, how long do they last

A

experienced by 60-80% women
last on average 2-7 years
Impact on sleep, mood and QoL

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16
Q

Give three perimenopausal symptoms

A

hot flushes, mood swings, urogenital atrophy

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17
Q

What age is the cut off for early menopause

A

45 years

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18
Q

What is a common side effect when switching from cyclical to continuous HRT

A

Bleeding 4-6 months

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19
Q

What is the risk reduction of breast cancer from 2.5 hrs of exercise per week in postmenopausal women

A

7 less per 1000

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20
Q

What cancers do you need to consider before starting HRT

A

Breast and endometrial

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21
Q

What medication can you prescribe for hypertension in pregnancy

A

Labetalol

Methydopa

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22
Q

What are the functions of progesterone

A 
1. Reproductive phys
Regulates menstrual cycle 
Opposes oestrogen - protects endometrium from too much proliferation
Maintains corpus luteum/ pregnancy in first 1/3 of pregnancy 
Promotes endometrial secretions (glycoproteins) for implantation (oestrogen - proliferation)
Vascularisation of endometrium
Initiates menses (by drop off)
2. Brain 
Mood, sleep, appetite 
3. Gut (inhibit prostaglandins?)
Can get constipation 
4. Vascular 
decreases BP (with oestrogen)
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23
Q

What are some side effects of high progesterone therapy (eg in menorrhagia, endometriosis)

A

Headache, increased appetite, low mood, constipation, fatigue, tremor, vomitting, odema

General:
Alopecia; breast abnormalities; depression; dizziness; fluid retention; insomnia; menstrual cycle irregularities; nausea; sexual dysfunction; skin reactions; weight changes

Think about vasoconstrictive & mood effects

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24
Q

What are the contra-indications for any progesterone therapy

A

PVD, Undiagnosed vaginal bleeding, porphyria

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25
Q

What risk assessment needs to be done before starting someone on progesterone

A 
Active breast cancer?
Past breast cancer? (must be over 5 years ago_
PVD
Undiagnosed vaginal bleeding
Porphyria
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26
Q

List some gynae causes of acute abdominal pain

A

Ovarian torsion/ cyst
Ovarian cyst rupture
Ectopic pregnancy
Miscarriage

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27
Q

What investigations should you do with ? ectopic

A 
USS - TV (if before 10 weeks)
Bloods: FBC (are they anaemic), group and save, progesterone, Beta-HCG - blood (need to see if it doubles in 48 hours)
2 large bore cannulas 
Fluids
Call for senior help
Anti-D if rhesus negative
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28
Q

Outline the management of a suspected ectopic pregnancy

A

Conservative: if stable & minimal/ no symptoms
Medical: Methotrexate - no significant pain, beta-HCG >1500, unruptured adnexal mass <3.5 cm, no interuterine pregnancy
Surgical: significant pain, adnexal mass >3.5, beta-HCG >5,000, fetal HR

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29
Q

For anybody with conservative or medical management of ectopic what should be monitored

A

expectant: every 48 hrs until confirmed fall, then weekly until <15
medical: beta-HCG on days 4 and 7 with methotrexate, only fallen by <15%, second dose given

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30
Q

What should all women who have been given methotrexate be told to do

A

Use contraception for next 3 months

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31
Q

What assessment should you do in a female of reproductive age presenting with right iliac fossa pain

A 
Are the stable? - vitals assessment 
When was their LMP 
Take a full history including RF for ectopics (IUD, PID/ STD, IVF/ subfertility, previous ectopic, previous abdo surgery, endo)
Examination - pelvic &amp; vaginal 
Bloods (beta HCG, progesterone)
Imaging (blood in pelvis?)
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32
Q

What are some red flag features of haemoperitoneum in a patient you suspect has an ectopic pregnancy

A

Shoulder tip pain
Low Hb
Changing vitals that suggest circulatory shock

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33
Q

What is pregnancy of unknown location

A

No sign of uterine or ectopic or retained products from miscarriage in presence of a positive pregnancy test
There is a pregnancy but you dont know where it is

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34
Q

What are your differentials for a positive pregnancy test with abdominal pain

A

Ectopic
Pregnancy of unknown location
Miscarriage

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35
Q

What are the possible causes of pregnancy of unknown location

A

Early intrauterine pregnancy (too early to see)
Complete miscarriage
Ectopic (but cant see on scan)
HCG-secreting tumour

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36
Q

What factors influence how you manage a ?ectopic patient

A

Haemodynamic stability
Beta-HCG (one off, and trend every 48 hrs)
Intensity of symptoms
Shoulder tip pain

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37
Q

Definition of miscarriage

A

Loss of pregnancy up to 24 weeks

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38
Q

How many pregnancies miscarry, and when is most common time

A

1 in 5, 1st trimester

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39
Q

What is the presentation of miscarriage

A

Pelvic/ abdominal pain
PV bleeding
+ positive pregnancy test
Ask about LMP

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40
Q

List the different types of miscarriage

A

Threatened - os closed + mild symptoms
Inevitable - os open + severe symptoms + no products yet
Incomplete - os open + severe symptoms + patient distressed + some products
Complete - os closed + symptoms subsided + all products passed

Missed - fetus dies but remains in utero, os closed - need to do US to confirm fetal HR.

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41
Q

How would you differentiate between a threatened and a missed miscarriage

A

Os closed in both
Symptoms (pain, bleeding, or both)
US would show if fetal HR is there or not

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42
Q

What is the assessment/ management of somebody with ? misccariage

A

Are they shocked/ stable?
US to assess retained products
Vaginal exam to look at os and products

Expectant - if not bleeding and stable - appropriate for incomplete but not for missed.
Medical - mifepristone (antiprogesterone) to prime, and 24-48hrs later misoprotol orally or PV.
Surgical - severe pain, bleeding, significant retained products on US - urgent evacuation of retained products of conception.

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43
Q

What differentials are there for a female of reproductive age presenting with recent onset pelvic pain and pink PV bleeding

A

Ectopic pregnancy

Miscarriage

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44
Q

What features differentiate ectopic and miscarriage

A

Location of pain

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45
Q

List some of the causes of recurrent miscarriage

A 
Endocrine - thyroid, DM, PCOS (uncontrolled)
Infection - BV
Parental chromosomal abnormality 
Uterine abnormality 
Antiphospholipid syndrome
Thrombophillia
Alloimmune causes
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46
Q

What is the criteria for recurrent miscarriage

A

Loss of 3 or more consecutive pregnancies before 24 weeks with the same biological father

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47
Q

What is a molar pregnancy

A

Egg no chromosome + sperm (1, or 2) n = 46 - diploid - complete
Normal egg with chromosome + sperm (1, or 2) that duplicates or triples - n=69, or 92

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48
Q

What are the symptoms of a molar pregnancy

A

Dark brown to bright red vaginal bleeding during the first trimester.
Severe nausea and vomiting - get exacerbated first trimester symptoms bc of very high beta HCG).
Sometimes vaginal passage of grapelike cysts.
Pelvic pressure or pain.

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49
Q

What can a molar pregnancy become

A

choriocarcinoma

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50
Q

How would you manage a pregnancy of unknown location

A

Rule out ectopic - or treat as if suspect (as most serious cause)
Haemoperitoneum + pain - laparoscopy
Beta-hcg (repeat 48 hrs)
Progesterone (repeat 48 hrs)
Make plan based off bloods
eg is progesterone <20 suggests failing pregnancy - repeat in 7 days time
hcg rise >66% in 48 hrs - normal pregnancy, rescan 7 days
hcg faling - repeat untill <15
plateauing or fluctuating - senior advice
Management based on symptoms - if asymptomatic can do expectant

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51
Q

What contraceptive advice would you give to someone after they had a confirmed ectopic pregnancy

A

IUD increases risk of ectopics
Advice for them to use anovulatory contraception, as their risk of an ectopic again is increased due to already having one

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52
Q

What diseases form gestational trophoblastic disease

A

Hydatidiform moles (complete/ incomplete- premalignant)
Choriocarcinoma
Placental site trophoblastic tumour

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53
Q

What is the management of a molar pregancy

A

Evacuation of uterine contents
Histology (to rule out choriocarcinoma)
Monitor beta-HCG, if not falling, or if increasing –> chemotherapy

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54
Q

What is the commonest presentation of a molar pregnancy

A

Failed miscarriage - 1st trimester

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55
Q

How would you confirm a molar pregnancy

A

USS - ‘snow storm’ appearance

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56
Q

What percentage of patients with molar pregnancies are found to have persistent trophoblastic disease

A

10%

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57
Q

What should happen with a confirmed molar pregnancy patient

A

The patient should be registered at one of the 3 UK centres that specialise in GTD - Weston Park is one.

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58
Q

There is no maternal component ina complete molar pregnancy - true or flase

A

True

It is abnormal egg plus duplicated sperm - diploid (n = 46)

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59
Q

Which type of molar pregnancy is associated with fetal tissue

A

Incomplete molar

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60
Q

What blood results are highly suspicious of a molar pregnancy

A

Significantly high beta-HCG for the stage of pregnancy:
As a guide from ~6 weeks:
<1,500 - failing pregnancy
1,500 - 5,000 - developing pregnancy - methotrexate management
5,000 + - developing pregnancy - surgery
20,000 + - highly suspicious of molar

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61
Q

Why should you always do a group and save on any female of reproductive age with PV bleed or signs of haemoperitoneum

A

Potential for blood transfusion

Potential for Anti-D if Rh -ve

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62
Q

How does ovarian pathology usually present

A 
Abdominal mass/ swelling
Irregular bleeding 
Acute abdominal pain (dermoid, teratoma, large cyst - pressure effect)
Chronic dull abdominal pain 
Nausea &amp; vomitting (torsion)
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63
Q

What gynae problems can cause peritonitis

A

Mainly things associated with the ovaries - dermoid cyst, teratomas, ruptured endometrioma (chocolate cyst)

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64
Q

How does acute ovarian pathology present

A

Acute abdominal pain
Vomitting
May be shocked

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65
Q

How does ovarian torsion present

A

Acute abdo pain
Vomitting
Abdominal swelling/ mass (from swelling)
Pain may subside after 24 hours

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66
Q

List the possible ovarian pathology you would consider with abdominal pain

A 
Ovarian cysts (chronic, cyclical abdo pain, irregular bleeding)
Endometrioma (dyspareunia, period pain)
Ovarian torsion (acute presentation, may be shocked) 
Ovarian rupture (acute presentation, may be shocked) 
Ovarian tumours - benign (dermoid), premalignant (teratoma, cystadenoma) &amp; maligant
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67
Q

What investigations would you do for ?ovarian cysts

A

Imaging: TVUS - AbdoUS if large, >5cm MRI
Bloods: tumour markers (beta HCG, AFT, ca-125 - if over 40 years)

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68
Q

What factors determine how you manage ovarian cysts

A

Size (< 5 cm

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69
Q

What are some red flag features for serious ovarian pathology

A 
Ascites 
Abdominal swelling/ mass
Shocked
Acute abdominal pain 
>5cm 
Vomitting
Suspicious scan features
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70
Q

Outline the management for ovarian cysts

A

Premenopausal
<5cm and asymptomatic - follow up scan - should resolve (tumour marker bloods)
>5cm and symptomatic (tumour marker bloods) - surgical referral

Postmenopausal
<5cm - tumour marker bloods, 4 month scanning - no change at 1 year + no suspicious features- discharge
>5cm - any suspicious features - surgical removal

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71
Q

What is first line imaging for ovarian cysts

A

TV USS

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72
Q

Difference between mitosis and meiosis

A

Mitosis - get diploid identical cells (n=48)

Meiosis - get haploid gametes (n = 24)

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73
Q

What stage of oocyte meiosis takes place before birth

A

Meiosis 1 - prophase
Halts at prophase
Meiosis 1 completes at puberty

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74
Q

What oogenesis stage are oocytes suspended in until fertilization

A

Meiosis II - metaphase

if fertilized, completes - n=24

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75
Q

What causes the LH surge

A

Switch in oestrogen becoming stimulatory rather than inhibitory to LH

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76
Q

List two important functions of prostaglandins and how they are linked to pregnancy

A

Vasodilation (opposes platelet aggregation and vasoconstriction via thomboxane in vessels)
Smooth muscle contractions

1, Important in implantation (probably due to vasodilatory effects) - help early embryonic life through vasodilation and support ongoing pregnancy through systemic vasodilation to maintain BP despite increase blood volume
2, stimulate cerival ripening and uterine contractions for labour

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77
Q

What is the difference between granulosa and thecal cells

A

Granulosa cells - T to Oestrogen, sensitive to FSH, FSH induces LH receptors on granulosa cells of dominant follicle - t/f facilitate ovulation. Make up the corona radiata, protect oocyte during ovulation, essential for follicular stage of menstrual cycle and ovulation, proliferate and generate progesterone during luteal phase.

Thecal cell - C to T, and T to progesterone. Sensitive to LH. Supports granulosa cells with supply of testosterone. Helps maintains luteal phase with progesterone release from corpus luteum.

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78
Q

Which ovarian cell is sythesise androgens

A

Thecal cells - synthesise testosterone

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79
Q

What hormone is released by granulosa cells that inhibits FSH

A

Inhibin

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80
Q

What is the role of oestrogen during day 1-14 of the menstrual cycle

A

Endometial proliferation - prepare endometrium for implantation
Regulate LH and FSH - inhibit at lower levels then stimulate both for ovulation

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81
Q

What is the role of FSH during day 1-14 of the menstrual cycle

A

Stimulate primordial follicle into dominant follicle ready to release secondary oocyte

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82
Q

What is the role of progesterone during day 16-28 of the menstrual cycle

A

Promote vascularisation of endometrium
Stimulate endometrial secretions (glycoproteins) for implantation
Initiate menses if no fertilization

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83
Q

What is the role of lutinising hormone during the menstrual cycle

A

It stimulate the dominant follicle to complete M1

Stimulates ovulation

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84
Q

What is the presentation of hyperemesis

A

Not able to keep food or liquids down despite anti-emetics
Persistent vomitting
Weight loss >5% of pre-pregnancy weight
Ketosis

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85
Q

What is the management of hyperemesis

A

Vitals: any signs of shock - tachy, BP etc
Bloods: FBC, U&E (Na, K in particular)
Urine dip - ketones, + MSU
Aggressively fluid replace
IV anti-emetics
Daily blood to guide K and Na replacement
Remember to replace folic acid & thiamine to prevent wernicke encephalopathy

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86
Q

What are the complications of untreated persistent vomitting during pregnancy

A

Volume depletion - hypovolemic shock
Electrolyte disturbance
Hyponatriemic shock
Wernickes encephalopathy

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87
Q

What are red flags for hyperemsis

A

Not keeping food or fluids down despite oral anti-emetics

Weight loss >5% of pre-pregnancy weight

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88
Q

What is the best baby presentation during labour

A

Left occiput anterior

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89
Q

What is the pathology of eclampsia

A 
Endothelial/ vascular injury 
Odema 
Haemorrhage 
Thrombus
Brain and liver main organs affected
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90
Q

When can placenta praevia be delivered vaginally

A

If it is minor - does no cover cervical os and is 2cm away from os

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91
Q

Outline the management of placenta praevia

A

If recurrent bleeding, inpatient from 34 weeks
If not bleeding, careful risk assessment about management at home
Indications for CS: approaching 37 weeks, massive (>1500) bleed, continuing significant bleeding of lesser severity.

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92
Q

What is the biggest risk to the fetus with placenta praevia

A

Premature delivery

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93
Q

List some of the signs of placenta praevia on examination

A

Soft, non-tender uterus
Palpable presenting part (as cant descend into pelvis)
Painless bleeding

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94
Q

When is placenta praevia most likely to be a problem

A

Third trimester

Because lower segment of uterus starts to change at this point

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95
Q

What are the consequences of abnormal trophoblast invasion in first trimester

A 
Pre-eclampsia
FGR
Placental abruption
Intrauterine death 
Because a low-resistance utero-placental circulation cannot develop
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96
Q

What are the maternal consequences of placental abruption

A

Hypovolemic shock
DIC
Acute renal failure
Haemorrhage (check Rh status for anti-D)

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97
Q

What are the fetal consequences of placental abruption

A

Hypoxia - fetal loss
Fetal haemorrhage
FGR

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98
Q

What type of placental abruption is not an emergency and can be monitored

A

If there is no fetal distress

Gestational age favours delaying delivery

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99
Q

What are the risk factors for placental abruption

A 
HTN 
Smoking 
Cocaine 
Trauma 
Anticoagulation
Polyhydramnios 
FGR
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100
Q

When is placenta accreta first picked up

A

20 week scan

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101
Q

What would be the sign if placenta accreta on USS

A

Loss of definition between wall of uterus

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102
Q

Is an MRI scan indicated in placenta accreta

A

Yes

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103
Q

What are some of the risks of placenta accreta

A 
Haemorrhage - usually PPH 
Blood transfusion 
Caesarian 
Hysterectomy 
ITU admission
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104
Q

What is the delivery method for placenta accreta

A

Planned CS

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105
Q

List the common diseases that result from failed endovascular invasion

A 
Pre eclampsia 
Miscarriage 
FGR
Prematurity 
Abruption
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106
Q

Which type of autoimmune conditions improve during pregnancy

A

Th1 mediated

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107
Q

What is the cause of proteinuria in pre eclampsia

What renal feature is specific for pre eclampsia

A

Glomeruloendotheliosis - swelling in glomerulus

Associated with loss of GRF and albumin in urine. Leads to reduced oncotic pressure and swelling.

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108
Q

Describe the pathology of pre eclampsia

A 
Genetic predisposition 
Abnormal immune response 
Deficient trophoblast invasion 
Hypoperfused placenta 
Circulating factors 
Vascular endothelial cell activation 
Clinical manifestation of disease
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109
Q

Why is pregnancy a hypercoaguable state.

A

There is an increase in clotting factors and fibrinogen levels, reduction in protein S and anti thrombin III.

Thought to be part of an evolutionary response to reduce haemorrhage following delivery.

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110
Q

Define the features of a normal CTG

A

Baseline rate 120-160
Variability >5 bmp
Accelerations- present
Decelerations - early only

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111
Q

Define the features of an abnormal CTG

A

BR: <100 bmp or >180
Variability: <5 for >40 but less than 90 minutes
Accelerations: not present
Decelerations: late

112
Q

What is the management of deep transverse arrest

A

Rotational manouvers

Instrumental delivery

113
Q

What determines a CS in placental abruption

A

Fetal compromise

114
Q

What are the risk factors for placental abruptions

A 
ABS-VITS 
Vascular - HTN, cocaine, smoking 
Infection 
Trauma 
Structural abnormalities
115
Q

When is placenta accreta detected
What is the management plan
What are the major complications

A

20 week scan
Regular monitoring, planned CS with blood products, consent to hysterectomy if needed, level 2 care bed available
Complications: Major PPH, blood transfusion, hysterectomy, ITU admission

116
Q

What is placenta praevia a risk factor for

A

Placenta accreta (because of uterine scar?)

117
Q

How do you diagnose cord prolapse

A

Seeing or palpating the cord outside or within the vagina alongside abnormal fetal heart rate problems

118
Q

What is the management of cord prolapse

A 
Oxygen by mask to mum
Elevate presenting part 
Vago's method - bladder filling 
Trendelenberg's
Theatre for delivery
119
Q

What is cord prolapse

A

Cord lays between presenting part and cervix.
Overt - past presenting part
Occult - alongside presenting part

120
Q

What is the risk of palpating umbilical cord in the management of cord prolpase

A

Umbilical artery vasospasm

121
Q

What is the recommended diagnosis to delivery interval for cord prolapse

A

30 minutes

122
Q

What is the main influencing factors on whether a vaginal or CS delivery is opted for in a diagnosis of cord prolpase

A

Time to delivery - which ever if quickest
If first or early 2nd stage of labour - CS
If late second stage - vaginal

123
Q

What is the relationship between malpresentation and cord prolapse

A

Non-cephalic presentations create space below the presenting part. Breech presentations account for 40% of cord prolapse cases. Shoulder presentations also.

124
Q

What is the histology of the cervix

A

It is mainly fibromuscular
Endocervix - part of cervix that is inside (not facing outwards). Columnar epithelium. Secretory.
Endocervical canal - cervix inbetween internal and external os.
Ectocervix - cervix on inferior aspect of cervix - facing outwards - spans lateral to external os . Non keratinised stratified squamous epithelium.
Squamocolumnar junction.

125
Q

What are the main hormonal changes that initiate labour

A

Fall in progesterone
Increase in oestrogen
Increase in prostaglandins
Increase in oxytocin

126
Q

What is a direct and indirect maternal death

A

Direct cause is a death resulting from an obstetric complication (haemorrhage, VTE, sepsis, eclampsia). (Abnormal process that lead to death)
Indirect cause is death resulting from a pre-exisiting condition or an exacerbated physiological response to pregnancy, eg. cardiac disease. (Pre-existing or normal process that has lead to death)

127
Q

What additional blood volume is physiological in pregnancy, what does this increase - preload/ afterload

A

40% increase

Increases preload - more venticular filling

128
Q

What is the leading cause of maternal death in UK (indirect and direct)

A

Cardiac disease

Always think about cardiac causes of chest pain in pregnant women

129
Q

What are the periods of greatest risk for cardiac disease in pregnancy and why

A

16 weeks - CO reaches its peak from here (increases by 50%)
2nd stage of labour (increases further at delivery - this can reduce uterine perfusion, think about this in causes of abnormal CTG)

130
Q

What are the normal cardiac changes that happen during pregnancy

A

Increased HR, steadily from wk5 to term (10-20 bmp)
Increased SV (10%)
= Increased CO. From week 5, peaks at 20 weeks (up by 40%) then increases another 30% in second stage of labour.
Decrease in TPR to maintain BP (decreases by 35%)
Drop in BP, mainly diastolic, then returns to normal (10% decrease MAP)
Increased blood volume (~40%)

131
Q

What heart sounds can be normal in pregnancy

A

Split I heart sound
III heart sound
Ejection systolic murmur

132
Q

How does changes in blood during pregnancy affect FBC results

A

Increased plasma > erythrocytes
= decreased Hb, anaemia
= reduced haemocrit ratio
= decreased albumin

133
Q

What factors drive cardiac changes during pregnancy

A

Increased blood volume

Increased oxygen requirement for uterus and baby

134
Q

Are oestrogen and progesterone vasodilatory or constrictors

A

Dilatory
Oestogen causes resp mucosal odema (problem in asthmatics)
Progesterone headaches

135
Q

What respiratory changes happen during pregnancy

What symptoms can this result in

A

Increase in minute ventiliation
Increase in TV
RR same
Reduced FRC
Diaphragm moves up. Lower ribcage moves out.
Leads to physiological dyspnoea - peaks at around 30 weeks

136
Q

List some normal cardiac symptoms during pregnancy

A

Palpitations, light headedness, dizzy, fatigue

137
Q

What renal changes happen during pregnancy

A

Increase in GFR
Plasma creatinine falls (because of GFR, most clearance in first trimester then slowly increases by 3rd trimester).
Plasma urate and albumin fall.
Increase in renal blood flow (80%) - because of CO and vasodilation
RAS - increase in renin for Na+ resorption, increase in angiotensin II
Glycouria normal in pregnancy because of increased GFR
Kidney’s lengthen 1-2 cm
Pelvis and ureters dilate - leads to false obstructive picture

138
Q

What symptoms can pregnancy induced renal changes lead to

A

Hydronephrosis - 80% of women have this is 3rd trimester, R kidney more affected bc of dextrorotation (uterus lays oblique at term) and R kidney is lower
Ascending urinary tract infections 1-2% of women due to dilated ureters
Fluid retention - swollen ankles
Glycouria

139
Q

What hepatic changes take place during pregnancy

A

Increased production of clotting factors - fibrinogen, VII, VIII, X, XII
Increased cholesterol (biosynthesis of oestrogen and progesterone)
Placenta and fetus produce AlkPhos - can mean this in LFT is unreliable for diagnosing cholestasis
High oestrogen state can lead to telangestasia and palmar erythema

140
Q

What GI changes take place during pregnancy

What symptoms do these produce

A

Progesterone - smooth muscle relaxant. LES relaxes. Placenta produces gastrin = stimulates stomach acid. Both = oesophagitis and heartburn (80% of women).
Displacement of intestines and stomach by uterus.
Delayed gastric emptying = increased stomach volume.

Symptoms: reflux and GORD.

141
Q

What factors regulate prolactin in a non-pregnant state

A 
Sleep 
Dopamine (inhibitory, hence D2 antagonists raise prolactin)
142
Q

What is alpha fetoprotein

What can it be used for as a marker

A

It is a protein made in the liver of an inutero developing baby
Tumour marker outside of pregnancy

143
Q

What is alpha HCG an analogue of

A

TSH
alpha LH
alpha FSH

144
Q

What is beta-HCG a marker for outside of pregnancy

A

Cancers including testicular cancer

145
Q

Outline the physiological changes in thyroid function in pregnancy
How does this relate to TFT results in pregnancy

A

First trimester: Increase in free T4, decrease in TSH.
Because of HCG, increased TBG, increased plasma volume, fetal requirement
Second and third trimesters: Falling free T4, rising TSH.
Because of fall in HCG, increased iodine clearance, reduced fetal requirement, increased placental T4 to T3 inactive metabolism.

146
Q

Where does the fetal source of thyroxine come from during pregnancy

A

Maternal up to ~20 weeks

Fetal from ~20 weeks, although still 40% maternal up to delivery

147
Q

What considerations/ concerns would you have for a female with Graves disease who is trying to concieve

A

Hyperthyroid increases risk of miscarriage
Risk of thyrotoxicosis in first trimester and early post-natal period - needs closer monitoring of TSH, free T4, and dose adjustments of carbimazole or propylthiouracil (better for not passing placenta). May improve in second trimester.
Fetal tachycardia
Fetal goitre - malpresentation
Neonatal thyrotoxicosis

148
Q

What considerations/ concerns would you have for a female with Hashimotos trying to concieve

A 
Risk of fetal T4 deficiency in first trimester associated with poor brain development - risk of reduced IQ and neurodevelopmental delay 
Decreased fertility 
IUGR 
Still birth 
Miscarriage 
Anaemia 
Pre-eclampsia 
Needs closer monitoring, increased thyroxine during first trimester and possible 2nd and third. Return to pre-pregnancy levothyroxine doses PP. Risk of PP thyrotoxicosis.
149
Q

What is the function of hCG

A

Maintains the corpus luteum, and progesterone production

Inhibits FSH and LH at level of hypothalamus

150
Q

List some of the actions of placenta oestrogen and progesterone

A

Both support uterine smooth muscle hypertrophy
Progesterone inhibits prostaglandins - and contractions
Progesterone has effects on smooth muscle - GI and GU, and vascular tree (headaches)

151
Q

When are thyroid stimulating antibodies a risk for a fetus

A

From around 20 weeks. Before this the fetal thyroid does not respond to TSH or the antibodies.

152
Q

When is the greatest risk period for fetal hyperthyroid

A

26 weeks, earlier is mother has active Graves disease or thyrotoxicosis

153
Q

When do maternal thyroid stimulating antibodies reduce in pregnancy in Graves disease

A

Second trimester. Usually they have declined by the gestational week it would be dangerous for them to be elevated for the baby.

154
Q

What is the management of fetal thyrotoxicosis

A

Making sure mum is euthyroid. Can have partial thyrectomy if needed.

155
Q

What investigations would confirm a new diagnosis of Grave’s disease over gestational transient thyrotoxicosis

A

Presence of - Thyroid stimulating autoantibodies (TRAb)

156
Q

What are some of the symptoms of fetal thyrotoxicosis

A

Goitre - can cause polyhydramnios bc baby cant swallow liqour
Tachycardia
Face presentation

157
Q

What are some of the complications of fetal thyrotoxicosis

A

Premature delivery
Neonatal thyrotoxicosis
Malpresentation

158
Q

What is the management of neonatal thyrotoxicosis

A

Monitor babies free T4 and TSH. Treat hyperthryoid with anti-thyroid drugs (propylthiouracil). Should resolve by 2-3 months with TRAb are eliminated.

159
Q

What are the antithyroid drugs of choice in pregnancy and why

A

Propylthiouracil - crosses placenta less, does not accumulate in breast milk. Use in all new diagnoses.
Carbimazole - use in mums with known Grave’s disease to keep disease under control

160
Q

What is gestational transient thyrotoxicosis

A

It is thyrotoxicosis during pregnancy not caused by graves disease. (No TRAbs). Can be caused by pro-thyroid state induced by pregnancy.

161
Q

What drugs must be stopped in diabetic women trying to get pregnancy

A

Statin
All oral hypoglycaemics expect metformin
Any anti-hypertensives

162
Q

What conditions in a diabetic would make you suggest they avoid pregnancy

A

Severe nephropathy

The higher the plasma creatinine (poor filtration) the worse outcome.

163
Q

What are some of the maternal complications in diabetic mothers

A

Hypoglycaemia - 1st trimester
Increased risk of PET - because of vascular damage of diabetes
Increased risk of infection - because of high blood sugar
Worsening retinopathy
Nephropathy

164
Q

What are some of the fetal complications in diabetic mothers

A 
Malformations - CVD, CNS most common. This is because hyperglycaemic state is toxic to cells. Triggers ROS and apoptosis. 
Miscarriage
IUGR - vascular damage 
Macrosomia - shoulder dystocia 
Polyhydramnios - because of pyuria 
Preterm delivery 
Still birth
165
Q

What are some of the risk factors for gestational diabetes

A 
BMI >30 
Ethnicity 
Previous large baby (>4.5 kg)
Previous GD 
FHx diabetes
Steroids 
Smoking
166
Q

What is the management of DVT in pregnancy

A

Rule out PE (CXR, ECG, symptoms, CTPA if needed)
Start treatment as soon as clinically suspected - LMWH
If large PE - thrombolysis + LMWH for 6 months + 6 weeks PP
If no PE, LMWH for 6 months + 6 weeks PP
Stop LMWH during labour, do not restart soon after epidural etc for risk of meningeal bleed
If still high risk, consider IVC filter, long-term unfractioned heparin

167
Q

What are the potential complications of a pregnancy in a lady with a BMI >30

A 
VTE
Intra and post partum haemorrhage 
PET
IUGR
GD
Macrosomia 
Ischemic heart disease 
Prolonged labour 
Operative delivery 
Anesthetic risk
168
Q

What is the management of females with a BMI >30 who are pregnant

A 
VTE prophylaxis - LMWH 
PET prophylaxis - aspirin 
PET monitoring from 24 weeks
Larger vitamin doses:
Folic acid 5 mg
Vitamin D
169
Q

What are the potential risks for women with a history of heart disease and pregnancy

A 
Risk of worsening heart disease 
Acute coronary syndrome/ event 
Heart failure 
Miscarriage
Prematurity
170
Q

What medical condition would validate delivery between 32-34 weeks

A

Maternal pre-existing heart disease

Cardiac output increases

171
Q

Why are women who have a history of heart disease sometimes planned for elective delivery between 32-34 weeks

A

Because cardiac output increases again at labour (30%) and another 10-20% at delivery, so it is high risk for a female who may have compromised cardiac output already.

172
Q

What genetic of cardiac disease may be incompatible with pregnancy

A

Eisenmengers syndrome (from a large R to left shunt)
Marfans - dilated aorta, mitral and aortic valve prolapse
Elher-Danlos - dilated aorta
Loeys Dietz

173
Q

What signs and symptoms might a pregnant lady with acquired heart disease present with during pregnancy

A

Chest pain

Acute/ worsening HF signs

174
Q

What investigations should you do on a pregnant lady with chest pain, palpitations, or worsening SOB

A

Vitals, BP, HR, oxygen sats - any sign of cardiovascular compromise or circulatory collapse
ECG - Left sided heart disease is normal in pregnancy but ischemia and HF signs aren’t
Echo
Chest XR - PE?
Auscultate lungs and heart - some congestive sounds (3rds HS) are normal, and aortic systolic murmur. Fluid on lungs is not normal.
Bloods - troponin, FBC, U&E, LFT, BNP

175
Q

The development of left sided heart disease and associated signs is normal in pregnancy. What signs and heart disease is not normal and warrants investigation.

A

Acute coronary event - chest pain, acute/ worsening SOB, acute sweating/ nausea, raised troponin
Acute heart failure - worsening SOB, ankle swelling, fluid on lungs, raised BNP, worsening fatigue beyond what is expected

176
Q

What is the management of a pregnant female with know heart disease

A

Joint clinic - cardiology and obstetrics
Regular CV vitals, BP, HR, oxygen sats
Regular auscultation
Regular ECG, echo monitoring
Fetal echo
Growth scans
Rule out pulmonary odema and arrythmias at all visits.
Prevent anaemia, obesity and smoking.
*Heart failure requires admission
MDT to discuss whether should have delivery at 32-34 weeks

177
Q

What clinical monitoring is important in a labour with maternal heart disease

A 
Strict fluid monitoring 
Minimise second stage 
Reduce stress, epidural 
Oxytocin infusion not bolus
Have drugs to treat cardiac failure to hand.
178
Q

What is the threshold for gestational (pregnancy induced) hypertension

A

140/90 from >20 weeks gestation

Previously normotensive

179
Q

What management should be commenced for a pregnant lady who has either pre-existing essential hypertension or gestational hypertension

A

Review medications and move to only those safe for pregnancy - labetalol, nifedipine, methyldopa
Aspirin - 75mg
Regular vitals, BP, HR
Regular urine tests for proteinuria
Regular LFT and U&Es to monitor PET & HELLP
Risk of IUGR, so serial growth scans

Plan delivery for 37 weeks - reduce CV demand with epidural and minimise length of second stage. Continuous or hourly BP monitoring and urine for proteinuria.

180
Q

List the different hypertensive diseases in pregnancy

A

Chronic HTN (pre-existing BP of >140/90 before 20 weeks, and after birth)
Pregnancy induced HTN (develops after 20 weeks with no proteinuria)
Pre-eclampsia (develops after 20 weeks with proteinuria of 0.3g protein/24hr)
Pre-eclampsia superimposed on chronic HTN or renal disease

181
Q

What post-natal follow up should happen with women with who have had PET

A

6-8 week check for proteinuria

Check kidney function has returned to normal

182
Q

What cardiovascular factors significantly affect risk in pregnancy

A 
Pulmonary HTN 
Haemodynamic compromise 
NYH classification 
Cyanosis 
PHx of arrythmias, TIA, HF, Valve stenosis - any significant CVD hx
183
Q

In what condition is pregnancy completely contraindicated

A

Pulmonary HTN

184
Q

What are the risks in pregnancy with congenital heart disease (PDA, atrial defect, ventricular septal defect)

A

Depends on haemodynamic stability
IUGR
Should do fetal echo

185
Q

What are the pregnancy risks associated with marfans disease

A

Aortic dissection

Aortic rupture

186
Q

What are the pregnancy risk associated with mitral stenosis

A

Heart failure and AF
Dyspnea
Orthopnea
PND

187
Q

What is the management of arrhythmias in pregnancy

A

Maternal tachycardia - rule out anaemia and hyperthyroud

SVT - vagal manoevers, adenosine

188
Q

What is the management of artificial valves in pregnancy

A

Can continue with warfarin but it known teratrogenic

Can switch to LMWH regime but risk of valve thrombosis (doesnt manage valve thrombosis as well as warfarin)

189
Q

What is the management of ischemic heart disease in pregnancy

A

Always consider this when considering PE

Manage as any ACE - bloods, ECG, echo if needed

190
Q

What is peri-partum cardiomyopathy

A

Heart failure without a known cause that develops 1 month pre deliver and continues 5 months PP.
Diagnose by echo. CS delivery.

191
Q

How is heart failure managed in pregnancy

A

Diuretics, vasodilators, cardioselective Beta-blockers, inotropes.
Once delivered ACE inhibitors.

192
Q

When is the greatest cardiovascular risk period for women

A

Early post-natal period

193
Q

What ECG findings are normal in pregnancy

A

Ectopics
Q wave and inverted T in lead III
T wave inversion in lateral leads
QRS left shift

194
Q

It is physiological in pregnancy to develop a compensated respiratory alkalosis. Explain what this means and why it happens.

A

It happens because tidal volume increases to meet increased oxygen requirements due to increased metabolic demand. This causes arterial p02 to increase and artial pCO2 to decrease causing an alkalosis. It is compensated because there is a fall in bicarb production by the kidneys to compensate the fall in pCO2.

195
Q

Do PEFR or FEV1 change during pregnancy

A

No.
Residual volume, inspiratory reserve and experiatory reserve all decreases slightly because of increased tidal volume. But vital capacity remains the same overall.

196
Q

What are the complications to the fetus of asthma

A

IUGR and preterm labour

Because of insufficient oxygen

197
Q

What happens to asthma during pregnancy

A

Remains unchanged mostly

May get worse if have uncontrolled asthma to start with

198
Q

What cautions should you consider in the management of PPH in a female with asthma

A

use prostaglandin F2a with caution unless life-threatening haemorrhage

199
Q

What is the management of asthma in pregnancy

A

Most inhalers are safe in pregnancy (dont use LTRA). Inhaled corticosteroids are safe.
Management should focus on good control and preventing attacks.
Avoid medicine that can cause bronchospasm (beta-blockers).

200
Q

How would you treat an asthma attack in a pregnant lady

A

The same as non-pregnant.

201
Q

What type of asthma is likely to deteriorate in pregnancy

A

Severe disease

202
Q

What is the greatest risk period for pregnant women with epilepsy

A

Peripartum
Intrapartum
Post partum

203
Q

What is the management of epilepsy during pregnancy

A

Continue on anti-epileptic drugs - consider switching if on valproate bc of CM risk
Regular drug levels monitored
Folic acid 5mg, >months pre-conception till delivery
Vit K to baby 4 weeks pre-delivery
Plan for VD
Do not discharge before 24 hours post delivery bc of seizure risk
Discuss risks of seizure to baby and how to minamise this

204
Q

Which thalassaemia is the fetus unaffected

A

beta-thalassaemia - because you can still produce alpha globin chains in this disease and fetal Hb is made up for alpha chains only

205
Q

What are the complications of anaemia but mother and baby

A

Mother - PPH risk, Infection, heart failure

Fetal - hydrops, symmetric growth restriction

206
Q

When are mothers screened for anaemia in pregnancy

A

Booking visit

28 weeks

207
Q

What is the treatment for anaemia in pregnancy

A

Oral iron tablets

Iron injections is cannot tolerate tablets - risk of anaphylaxis with this

208
Q

What are the causes of anaemia in pregnancy

A 
Poor diet/ intake 
Haemolysis - malaria 
Haemoglobulinopathies 
Infection 
Twin pregnancy 
Any condition that causes a risk of bleeding - coeliacs 
Chronic kidney disease (epo)
209
Q

What is the management of a sickle crisis in pregnancy

A

Pain relief - opioids

Blood transfusion

210
Q

What is the management of sickle cell in pregnancy

A

Aspirin to reduce risk of developing PET
TEDs
Check BP and MSU monthly
4 weekly growth scans from 24 weeks
Baby needs pnemococcal prophylaxis when born

211
Q

Which epilepsy drugs should be avoided in pregnancy

A

Valproate and carbamazepine

Lamotrigine has lower rate of congenital malformations

212
Q

Is lithium safe during pregnancy

A

It is teratogenic and should only be used if no other option. If it is used need regular drug levels, fetal echo.
Risk of heart defects, neonatal thyroid abnormalities, floppy baby syndrome.

213
Q

Are anti-depressants safe during pregnancy

A

Try to wait to prescribe in second trimester unless severe depression.
Small risk of pulmonary hypertension and neonatal withdrawal.
SSRIs are first line
Do not use paroxetine

214
Q

List the causes of asymmetrical growth restriction

A 
Utero-placental insufficiency - reduced oxygen transfer to the fetus, leads to a response where get vasodilation to brain, heart, adrenal glands. Vasoconstriction of kidneys, limbs, liver. 
Pre-eclampsia 
Hypertension 
Malnutrition
Elhers-Danlos
215
Q

List the causes if symmetrical growth restriction

A

Anaemia
Infection
Chromosomal disorders
Substance abuse

216
Q

What blood test should you request on someone to rule out/ confirm adrenal hyperplasia

A

17-hydroxyprogesterone

Its an intermediate in the biosynthesis of steroid hormones, produced by the adrenal gland.

217
Q

What cancer does PCOC increase the risk of and why

A

Endometrial, unopposed oestrogen

218
Q

What is needed to diagnose PCOS

A

2/3 of the following:
Clinical signs/ symptoms/ biochemical features of hyperandrogenism - acne, hirsutism
US polycystic ovaries (>12, not attributed to other cause)
Subfertility - oligo/ amenorrhoea

219
Q

What differentials should be considered for PCOS

A

Adrenal pathology - Adrenal hyperplasia

Other endocrine causes - Thyroid (Hyper/ Hypo), Pituitary tumour - cushings disease (pituitary adenoma)

220
Q

What investigation should be requested for PCOS

A 
1)Bloods
Adrenal function: 
serum free androgen index
Free and total testosterone (can differentiate adrenal hyperplasia or tumour)
DHEA
17-hydroxyprogesterone (can differentiate adrenal hyperplasia)
Thyroid function:TFT
Pituitary function: Prolactin 
2)Pelvic USS
221
Q

How should you manage the risk of endometrial cancer in PCOS

A

Regular 3-4 monthly bleeds with norethisterone

Or COCP will monthly bleeds

222
Q

What is the relationship between the COCP and womens cancers (breast, ovarian, cervical, endometrial)

A

When taking COCP, small increase in risk of breast cancer, and if over 5years cervical cancer
Decreased risk of endometrial and ovarian cancer

223
Q

Outline the management options for PCOS

A

Weight loss and exercise (helps insulin insensitivity and menstrual cycle - does not affect hyperandrogenism)
Clomifene for fertility
Ovarian drilling if clomifene does not work - aim is to reduce sex steroid production of the ovary
COCP - prevent endometrial cancer
Norethisterone - 3-4 month bleed
Anti-androgens - cyproterone, spironolactone, facial creams

224
Q

What are the two peaks for cervical cancer

A

30s and over 70s

225
Q

What is the presentation of endometrial cancer and investigations

A

Premenopausal bleeding- heavy irregular bleeds
Post menopausal bleeding
Oh HRT- unexpected bleeding - bleeding between sequential bleeds
Vaginal discharge- from pyometra (hardened cervix that can’t drain discharge and creates pus)

TVUS- endometrial thickness >4mm
Biopsy - outpatient or part of hysteroscopy
Hysteroscopy if ?polyps

226
Q

What are the differentials for post menopausal bleeding

A

Endometrial cancer (adenocarcinoma)
Polyps
Fibroids

Cervical cancer

227
Q

What are risk factors for endometrial cancer

A 
High oestrogen state;
Nulliparity 
Obesity 
T2DM 
Oestrogen only HRT 
Late menopause/ early menses

Genetic- Lynch disease

Protective- COCP, multiparty

228
Q

What is the relationship between HRT and women’s cancers- breast, endometrial, ovarian

A

Combined HRT - increases risk of breast
Oestrogen only- increases risk of endometrial
Both increase risk of ovarian

229
Q

What genes are associated with ovarian cancer

A

BRCA1, HNPCC

230
Q

List the different age groups for presentation of gynaecological cancers

A

Endometrical - post menopausal (>51 years)
Cervical - 30s and >70s
Ovarian - 70s
Vulval - post menopausal

231
Q

List the investigations for different gynae malignancies

A

All: Bloods, Imaging, biopsy, staging
Endometrical: Bloods, TVUSS (endometrial thickness >4 mm), hysteroscopy, biopsy. CT/ MRI staging.
Cervical: Colposcopy, Punch / cone biopsy. Staging.
Ovarian: Tumour markers (ca125, AFP, beta-HCG, CAE, Ca 19,9), TVUSS, CXR (pleural effusions), biopsy. Staging.

232
Q

What is the biggest risk factor for cervical cancer

A

HPV

233
Q

What groups of people should be screened for cervical cancer yearly

A

HIV

Immunocompromised patients

234
Q

List some differentials for intermenstrual bleeding

A

Cervical cancer
Ectropion
Nabothian cyst
Cervicitis

235
Q

List some differentials for post menopausal bleeding

A

Endometrial cancer
Polyp
Fibroid

236
Q

What is ovarian cancer commonly mistaken for

A

Gastrointenstinal disease

IBS/ IBD/ diverticulosis/ itis

237
Q

Which CINs are low and high grade, whats the management for each

A

CIN I - low grade - 6 monthly follow up smear

CIN II/ III - high grade - LLETZ - smear at 6 months, if -ve can go to 12 months etc.

238
Q

Risk factors for cervical cancer

A

HPV
Many sexual partners
Immunocompromised

239
Q

Explain the relationship between HRT and breast, endometrial and ovarian cancers.

A

Combined HRT leads to small increase in risk of breast cancer. Oestrogen only - no increase in risk.
Oestrogen only HRT - increase in endometrial cancer
Combined and oestrogen only HRT - increase risk of ovarian cancer

240
Q

Explain the risks of HRT on VTE, CVD and stroke. How can these risk be lowered

A

oral HRT increased VTE risk - put in dermal patch
oral HRT increases the risk of stroke - put in patch
HRT does not increase cvd risk <60s

241
Q

What preparations are there for HRT

What determines which you get

A

Sequential (bleed prep - peri menopausal, bleed every 3 months)
Continuous - post menopausal
Oral / dermal
Oestrogen only / oestrogen + progesterone
Decide which to get based on: peri or post menopausal + uterus or no uterus or coil in situ

242
Q

Symptoms of vulval ca

A

Vulval itch
Vulval soreness
Vulval lump
Vulval bleeding

243
Q

Types of ovarian cyst

A

Simple cyst - follicular, luteal, thecal
Hemorrhagic cyst
Endometrioma
Mature cystic teratoma

244
Q

Types of benign ovarian tumours

A

Epithelial - brenners (epithelial and stromal)
Mucous epithelium - Mucous cyst (cystadenoma)
Stromal - brenners
Germ cell - teratomas

245
Q

Types of benign uterine tumours

A

Fibroid- subserosal, intermural, sub mucosal, pedunculated
Adenomyoma (adenomyosis) - tumour of glandular epithelium
Polpys - but can be pre-cancerous

246
Q

Describe the pathology of PCOS

A

Hyperandrogenism
Caused either/ or:
1) Change in GnHR pulse, so that LH production is favoured more, this stimulates ovulation but inhibits FSH (+ below) so dont get follicular development = cysts.
2)Hyperinsulinaemia (insulin resistance) = inhibits SHBG = increased free testosterone. Increased testosterone inhibits HPG axis and follicular development = anovulation = subfertility

247
Q

List the different types of benign gynaecological growths you can get

A

Ovarian - cysts (simple - follicular, luteal), cystic mass (epithelial, germ - teratoma, stromal)
Uterine - fibroids, polyps, endometrial hyperplasia
Cervix - ectropian, nabothian cyst, polyp
Vagina - bartholins cyst

248
Q

What are the symptoms of a benign ovarian cyst/mass

A 
Pelvic pain (dull)
Abdominal mass
Cyclical pain + dyspareunia (endometrioma)
PV (Intermenstrual) bleeding 
Hormonal changes (PCOS)
Bladder, bowel symptoms (malignancy)
Ascities (malignancy)
249
Q

What examination and investigations should you do for someone with an ?ovarian mass/ cyst

A

Examination - abdomen (mass - describe, ascites), pelvic (adnexal tenderness, enlarged uterus)
Investigations - bloods (+ tumour markers >40 years), pregnancy test (? ectopic)
Imaging - TVUS, possibly Abdominal is large mass
CT/ MRI if needed for follow up imaging

250
Q

What factors are taking into consideration when decided whether to refer a patient with an ovarian mass

A

Ca125
USS malignant features (size, multilobular, dense etc)
Pre or postmenopausal
Calculate malignancy index

251
Q

What factors should be taken into consideration when deciding how to manage a patient with an ovarian mass

A

Size of mass (<5cm does not need management if no symptoms or malignant features)
Malignant features on USS
Symptoms (malignant - eg ascites/ bladder/ bowel)
Pre/ post menopausal

252
Q

Who is eligible for watch and rescan in 4 months management for ovarian mass

A

Anybody low risk on malignancy index score

253
Q

What is the conservative management of fibroids and the rationale

A

Intrauterine contraceptive system - mirena coil
NSAIDs
To lower oestrogen effects on myometrium

254
Q

What is the surgical management of fibroids, when is this indicated
What factors should be considered

A

GnRH analogue (shrink fibroid)
Then myomectomy + IUCS if wanting contraception
Uterine artery embolisation
Hysterectomy
Considerations: Fertility, family planning
Indications: failure of conservative therapy, Fertility problems (peduculated), misscarriage, Urinary symptoms, Pain affects QOL, anaemia uncorrecting with conservative management

255
Q

List some of the things you should check before inserting an IUCD

A 
PID
STD risk assess (if under 25 swabs)
Wilsons disease
Heavy painful periods 
Gynae malignancy
256
Q

What are the risks of intrauterine systems in comparison to COCP

A

Ectopic pregnancy

257
Q

What are the major contraindications to COCP

A

VTE risk >1 (eg >35, >BMI, smoker)
Arterial risk >1 (eg HTN, DM, IHD, TIA, stroke etc)
Liver disease
Active breast cancer within past 5 years
Enzyme inhibitor medication
Pregnancy - cholestatsis

258
Q

What considerations should be made for someone wanting a contraceptive implant with >BMI

A

May need to be removed earlier

259
Q

List some of the risks of POP

A

Higher failure rate vs COCP
Must take pills within 3 or 12 hour window
Need to emergency contraception if missed pill
Menstrual irregularities (more than COCP)
Higher risk of ectopic vs COCP
Risk of ischemic stroke
Risk of breast cancer
Side effects: weight gain, mood, libido

260
Q

What is the definition of a small for dates and a large for dates baby

A

small for dates = <10% threshold

large for dates = >90% threshold

261
Q

What is low birth weight and macrosomia

A

low birth weight = <2.5kg

Macrosomia = >4.5kg

262
Q

What is IUGR

A

When a baby is not reaching its full growth potential. It may or may not be within normal range. Picked up by the slope of growth (tailing etc) not the centile it is in.

263
Q

What are the causes of symmetrical growth resitriction

A 
Infection (TORCH)
Genetic defect 
Constitutional smallness (maternal size, race)
264
Q

What are the causes of asymmetrical growth restriction

A

Utero-placental insufficiency, malnutrition, hypertension

Smoking, alcohol ?

265
Q

Which thyroxine can pass the placenta - t3 or t4

A

t4

266
Q

can t3 and tsh cross placenta

A

no

267
Q

What are some of the complications of IUGR

A

Cerebral palsy
Fetal hypoxia
Developmental delay
Prematurity

268
Q

What are the different types of pelvis and how do these affect labour

A

Gynaenoid - normal pelvis - should be able to have vaginal delivery
Android - pelvis outlet is very narrow - can cause deep transverse arrest
Anthropoid - inlet very narrow - may cause obstructed labour or OP delivery
Platypelloid pelvis - very transverse - may cause obstructed labour or transverse delivery

269
Q

What hypoglycaemic drugs can you use in GD

A

Metformin

Glibenclamide - sulfonylurea

270
Q

What is the mechanism of physiological clamping of umbilical cord

A

Temperature change - causes whartons jelly to swell and collapse (supportive jelly around artery and vein)
Vessel vasoconstriction - umbilical arteries constrict in response to oxygen (usually carry deoxygenated blood), umbilical vein constricts from deoxygenated blood (usually carries oxygenated).

271
Q

What is the cut off for praevia

A

2.5 cm

272
Q

In a PET emergency what IV hypertensives can you give

Which ones can you not give in combination

A

Labetalol, nifedipine, methyldopa can be used in combination (all different actions)
Hydrazaline can be potent and cause an acute hypotension - should be used as alternative to IV labetalol not in combination, and with volume (fluids) expansion ready to support

273
Q

What is cervical motion tenderness specific for

A

PID

Ectopic

274
Q

What is the mechanism of mefanamic acid vs tranexamic acid

A

Mefanamic acid is an NSAID (cox-1 and 2, inhibits prostaglandins)
Tranexamic acid is an antifibrinolytic

275
Q

Management of DUB

A
  1. Mirena coil
  2. Tranexamic acid (if pain not problem), mefanamic acid (if also need analgesia), COPC
  3. Progesterone based therapy
  4. Gonadotropin analogues (LHRH analogues)
276
Q

How do LHRH agonists work to induce menopause and medical castration in men

A

Act directly on the pituitary to occupy LHRH receptors and change the pulse frequency.
The pulse frequency increases which during the rise causes an agonist phase but as it peaks and plateaus remaining high it become antagonistic and shuts the axis down

Phase 3a (9 decks)

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