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Phase 3a > Obs n Gobs > Flashcards

Obs n Gobs Flashcards

1
Q

What is the nerve supply to the bladder and urethra?

A

Parasympathetic: S2-4, promotes urination (detrusor contraction)
Sympathetic: T12-L2, stops urination (detrusor relaxation)
Somatic: (voluntary nervous system) Pudendal nerve allows voluntary urination

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2
Q

What is the pressure balance in urination?

A

Bladder pressure (detrusor and intra-abdominal pressure) VS Urethral pressure ( urethral muscle tone and pelvic floor)

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3
Q

What are the components of the pelvic floor?

A

Pelvic bones, ligaments (cardinal and uterosacral), pelvic floor muscles (levator ani and coccygeus), pudendal nerve

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4
Q

What are the risk factors of a prolapse:

A 
Age (decreased oestrogen, poor tone)
Multiparity 
Obesity 
Retroverted uterus 
Chronic cough
Pelvic masses

50% parous women have a prolapse

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5
Q

What are the symptoms of a prolapse?

A

“Something coming down”
Urinary incontinence or frequency (stress incontinence due to altered urethrovesical angle)
UTI (due to incomplete bladder emptying)
Constipation of difficulty defecating

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6
Q

What are the types of prolapse?

What are the grades of prolapse?

A

Posterior:

  • Rectocoele = rectum
  • Enterocoele= small intestine

Anterior

  • Cystocoele= bladder
  • Vault = vagina in on itself (hysterectomy)

Uterine= uterus

1-3 with 2 at the introitus

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7
Q

Investigations for a prolapse:

A

Examination

+ any examinations for urinary symptoms (e.g. urine dip)

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8
Q

Management of a prolapse:

A

1st line: Lifestyle modification: weight loss, smoking cessation and physiotherapy– pelvic floor exercises

2nd line: Pessaries (ring or shelf) + topical oestrogen to prevent vaginal ulceration

3rd line: Surgical repair or hysterectomy

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9
Q

Types of incontinence

A 
Urge: Detrusor overactivity 
Stress: Sphincter weakness 
Overflow: Retention 
Fistula 
Neurological: MS or nerve damage 
Functional
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10
Q

What is the aetiology of urinary incontinence?

A 
Previous surgery 
Childbirth (stress)
Diabetes- neuropathy, renal impairment, polyuria/dipsia, reduced immunity and increased infection 
Recurrent UTI
Idiopathic (urge)
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11
Q

What are the risk factors of urinary incontinence?

A 
Age 
Parity 
Obesity 
Smoking 
Previous surgery
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12
Q

What is the clinical presentation of an overactive bladder?

A 
Urgency
Urge incontinence 
Frequency 
Nocturia 
At orgasm
Key in the door/ handwash triggers
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13
Q

What is the clinical presentation of a sphincter weakness incontinence?

A

Involuntary leakage with increased intraabdominal pressure- coughing, laughing, lifting, straining, exercise

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14
Q

What are the investigations for incontinence?

A
  • HISTORY AND EXAMINATION (prolapse)!!

Frequency volume chart (bladder diary)

MSU urinalysis (infection, stones, diabetes, renal disease, carcinoma)

Residual urine measurement (in and out catheter, USS bladder)

ePAQ questionnaire (lifestyle and symptom questionnaire)

Urodynamics

Cystoscopy/ cystogram with contrast

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15
Q

What is the management for stress incontinence?

A

1st line: weight loss, smoking cessation, pelvic floor exercises (physiotherapy), modify fluid intake, adjunctive pads or toileting aids

2nd Line: Surgery- slings, tension free vaginal tapes

3rd Line: Duloxetine if surgery denied

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16
Q

What is the management for urge incontinence?

A

1st line: weight loss, smoking cessation, stop caffeine, modify fluid intake, adjunctive pads or toileting aids, bladder retraining

2nd line: medication-
anticholinergics (blocks Ach, blocks parasympathetic NS, blocks detrusor contraction)- oxybutynin, tolterodine
Mirabegron- beta 3 adrenergic receptor agonist, relaxes smooth muscle (detrusor)

3rd line: botox injections

Further: cystoplasty , catheters, bypass (urostomy)

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17
Q

What is the normal duration of a menstrual cycle?

A

21-38 days (mean 28), 60-80ml blood loss

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18
Q

What is primary vs secondary amenorrhoea?

A

Primary: menstruation not started
If no secondary sexual characteristics: 14
Otherwise: 16

Secondary: previously normal menstruation caesed for >6 months

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19
Q

What is Kallman’s syndrome?

A

Hypogonadotropic Hypogonadism
GnRH secreting cells did not migrate to forebrain,

have absence in puberty and anosmia (can’t smell)
craniofacial defects

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20
Q

What are the causes of PRIMARY amenorrheoa?

A

Constitutional variances/ delays, iatrogenic (drug use- dopamine antagonists)

Anorexia, depression, high exercise levels

Kallman’s, Hypothalamic Hypogonadism, Hyperprolactinaemia (causing reduced GnRH), space occupying lesions, pituitary adenoma, sarcoidosis etc.

Hypo/hyperthyroidism (reduced GnRH) Congenital adrenal hyperplasia (CAH) (deficient in sex steroids)

Turner’s syndrome/ other gonadal dysgenesis, Androgen insensitivity (defective androgen receptor, XY but failure to develop male characteristics), PCOS

Imperforate hymen, tranverse vaginal septum

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21
Q

What are the causes of SECONDARY amenorrheoa?

A

Menopause, pregnancy, lactation, iatrogenic (drug use- dopamine antagonists)

Anorexia, depression, high exercise levels

Sheehan’s, Hypothalamic Hypogonadism, Hyperprolactinaemia (causing reduced GnRH), space occupying lesions, pituitary adenoma, sarcoidosis etc.

Hypo/hyperthyroidism, Cushing’s (reduced GnRH)

PCOS, adrenal tumours, POF, Asherman’s syndrome, cervical stenosis

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22
Q

What is Sheehan’s syndrome?

A

Damaged pituitary gland following labour (pituitary necrosis), often caused by hypoxia- PPH or low BP
Presents with hypothyroidism, amenorrhoea,

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23
Q

What is Asherman’s syndrome?

A

Uterine adhesions

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24
Q

How do you investigate/ manage amenorrhoea?

A

Investigate: Bloods: LH, FSH, Testosterone, SHBG (low in PCOS), prolactin, TFT
Karyotyping
MRI (head and neck)
Pelvic USS

Treat underlying conditions!

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25
Q

What are the three arms of PCOS? (Rotterdam Criteria)

A

2/3 needed for clinical diagnosis
Hyperandrogenism
((((Oligomenorrhoea)))) Anovulation- marked by low day 21 progesterone
Polycystic ovaries on USS (12 or more follicles)

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26
Q

What is the clinical presentation of PCOS?

A 
Oligomenorrhoea
Hirsutism 
Infertility 
Obesity 
Metabolic syndrome (htn, t2dm)
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27
Q

What are some long term consequences of PCOS?

A 
Infertility 
T2DM 
Gestational DM 
CVD
Endometrial cancer
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28
Q

What is the management of PCOS?

A

WEIGHT LOSS!!!!!!
Smoking cessation
Manage t2dm (metformin), htn, dyslipidaemia, sleep apnoea
COCP (reduced risk of unopposed oestrogen on endometrium (ca risk))

Fertility:
Clomifene
Ovarian drilling
Metformin for fertility

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29
Q

What are the appropriate investigations for PCOS?

A
  • LH:FSH ratio (elevated)
  • Testosterone (elevated)
  • Day 21 progesterone (reduced)
  • SHBG (reduced)
  • Fasting or random glucose
  • Prolactin (would indicate hyperprolactinaemia as a cause of amenorrhoea)
  • BMI + clinical exam
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30
Q

What is menorrhagia?

A

Heavy periods

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31
Q

What are the causes of pathological menorrhagia?

A 
thyroid disease
haemostatic disorders- e.g. VWD 
Anticoagulant therapies (e.g. warfarin, heparin)

fibroids
uterine or cervical polyps
adenomyosis, endometriosis

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32
Q

Investigations for menorrhagia?

A

Bloods: Hb, clotting profile, anaemia, TFT, beta HCG
TV USS: fibroids, ovarian mass, polyps
Endometrial biopsy

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33
Q

What is the management of menorrhagia?

A

Symptomatic.

  1. Mirena coil
  2. Antifibrinolytics; Tranexamic acid
    NSAIDs: Mefenamic acid
    COCP
    POP (tricyclic)
    Norethisterone
    GnRH agonists

Polypectomy, Fibroidectomy, endometrial resection/ablation, Hysterectomy

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34
Q

What is dysmenorrhoea?

A

Painful periods

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35
Q

What are the causes of dysmenorrhoea?

A

Primary:
Idiopathic
Excess prostaglandins

Secondary:
Adenomyosis
Endometriosis 
Polyps 
Fibroids 
PID
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36
Q

Management of Dysmenorrhoea?

A

Investigate with USS

NSAIDs (inhibit prostaglandins): Paracetamol, cocodamol, mefenamic acid
COCP
Mirena coil
Manage any secondary causes

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37
Q

What are the causes of intra-menstrual bleeding (IMB)?

A

Normal: mid cycle fall in oestrogen (spotting)

Polyps 
Carcinoma- cervical, uterine
OCP 
Infection- cervicitis, vaginitis, chlamydia
IUCD
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38
Q

What are the causes of post-coital bleeding (PCB)?

A

!!!!!!! CERVICAL CANCER !!!!!!!

Cervical trauma
Cervicitis, vaginitis, chlamydia

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39
Q

What is an ectropion?

A

Soft glandular columnar epithelium from inside cervical os is seen on surface of cervix
Normal- caused by hormonal changes, pill

Causes vaginal discharge or PCB

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40
Q

What are the causes of post-menopausal bleeding (PMB)?

A

!!!!!!!! ENDOMETRIAL CANCER !!!!!!!!!

Oestrogen withdrawal (HRT)
Endometrial or cervical polyps
Vaginitis (atrophic
SE of pessaries

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41
Q

What is normal menopause?

A

Cessation of menstruation after the age of 45 years old as a result of ovarian exhaustion

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42
Q

Describe progression of menopause

A

Climacteric phase: transition from reproductive to non reproductive states.
Erratic ovulation and menstruation starts, as ovaries become irregularly responsive to pituitary hormone stimulation, and number of follicles decline.
Once menopause is reached, ovaries “fail” and no longer respond, and there is diminished oestrogen production.

Low oestrogen–> reduced negative feedback to pituitary–> increased LH and FSH.

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43
Q

What are the symptoms of menopause?

A

EARLY:
Hot flushes, insomnia, irritability, mood swings, lethargy, anxiety, depression, reduced libido, dyspareunia, and failure to achieve orgasm

LONG TERM:
Loss of collagen from skin (drier and wrinkled), hair loss, breast tissue loss (replaced with fatty tissue, and breasts shrink).
Vaginal dryness, thin vaginal walls (increased infection risk), prolapse
Incontinence
Osteoporosis (decreased oestrogen causes calcium loss, raised fracture risk), fractures
CVD- strokes and heart attacks

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44
Q

What investigations can you do in ?Menopause?

A

LH and FSH (risen)
Mammography
DEXA
Investigate as IMB or PMB (endometrial biopsy)

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45
Q

What is the management of menopause?

A

HRT- combined oestrogen and progesterone (omit prog. if post hyterectomy as no risk of endometrial cancer as a result of unopposed oestrogen) e.g. tibolone (oral), patches, implant
Testosterone for libido

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46
Q

What are the causes and diagnosis and management of premature menopause/ POI/ POF?

A

Iatrogenic: chemo/radiotherapy, oophrectomy, hysterectomy
Idiopathic
Infection- mumps, pelvic TB
Autoimmune conditions

Raised FSH + LH, low oestrogen

Managed with HRT until 51y/o (+testosterone for libido)
+ care with CV and osteoporosis risk
Manage fertility- donor egg

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47
Q

What are the benefits of HRT?

A

Improved symptoms- hot flushes, psych symptoms, loss of libido
Lower risk of fracture and osteoporosis, bowel ca
Slows collagen loss

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48
Q

What are the disadvantages of HRT?

A

Bleeding (regular or irregular)
Headaches, fluid retention, breast tenderness, PMS

!!!! 2-4x increased risk of thromboembolic disease!!!!

Slight increase of breast cancer (not in POI)

Risks of unopposed oestrogen (endometrial ca)

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49
Q

What is the difference between OCP and HRT?

A 
Supraphysiological (OCP) dose 
VS
Physiological (HRT) dose

OCP therefore causes FSH and LH suppression, and HRT does not (therefore not contraceptive)

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50
Q

What is the presentation and how do you diagnose POF?

A

Clinical presentation: secondary amenorrhoea, infertility

Diagnosis: <40y/o, 4 months amenorrhoea + FSH > 25 in 2 separate samples over 1 month

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51
Q

Explain the Hypothalamic-Pituitary-Gonadal Axis

A

Hypothalamus (GnRH)–+++-> Pituitary (FSH or lh)–+++-> Ovary (Oestrogen)–+++—> Pituitary (LH, and suppresses FSH) ((((ovulation)))–++-> Ovary (CL Progesterone) —> Hypothalamus less GnRH

https://www.researchgate.net/figure/Representation-of-the-hypothalamus-pituitary-gonadal-axis-positive-and-negatives_fig4_258056691

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52
Q

Explain the relationship between oestrogen and LH in the menstrual cycle

A

Oestrogen (produced by GCs) stimulates LH after it reaches a certain threshold, after ovulation, no GC, no oestrogen, no LH.

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53
Q

What is the action of Progesterone in the menstrual cycle?

A

Progesterone, produced by CL after ovulation, maintains endometrial lining and supports implantation and early pregnancy

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54
Q

What is the action of FSH in the menstrual cycle?

A

FSH, produced in the pituitary, stimulated by GnRH, causes follicle development.
Stimulates oestrogen production from GCs
Oestrogen negatively feeds back to pituitary to reduce FSH to prevent multiple follicle development

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55
Q

What is the action of oestrogen in the menstrual cycle?

A

Oestrogen, produced in GCs, stimulated by FSH.
Causes endometrial prolferation.
Stimulates LH production from pituitary after a certain threshold

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56
Q

What is the action of LH in the menstrual cycle?

A

LH, produced by pituitary, stimulated by GnRH and rising oestrogen levels
Causes follicle rupture (ovulation), maintains corpus luteum

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57
Q

What is the action of progesterone in the menstrual cycle?

A

Progesterone, produced by the corpus luteum (following ovulation)
Maintains endometrial lining and primes it for implantation of an embryo
Negatively feeds back to the hypothalamus, reducing GnRH production and FSH and LH (which maintain the corpus luteum), therefore CL regression and progesterone decrease–> menstruation

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58
Q

How does hCG effect the menstrual cycle?

A

Produced by implanted embryo, hCG maintains CL, and therefore progesterone, stopping uterine shedding.

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59
Q

What is the definition of a miscarriage?

A

Pregnancy loss before 24 weeks

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60
Q

What are common causes of miscarriage?

A
  • chromosomal abnormalities causing incompatibility with life (e.g. aneuploidy)
  • abnormal foetal development
  • maternal illness (e.g. APS, infection, thrombophilia)
  • trauma
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61
Q

What is a threatened miscarriage?

A

bleeding, with closed os and foetal heartbeat present

25% miscarry

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62
Q

What is an inevitable miscarriage?

A

bleeding (++) with open os

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63
Q

What is an incomplete miscarriage?

A

some, but not all product of conception have passed

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64
Q

What is a missed miscarriage?

A

Foetus dies but still inside, close to asymptomatic
Closed os, no foetal heart
confirmed with USS

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65
Q

How do you manage a miscarriage?

A

Conservative: watch and wait, analgaesia.

Misoprostol

Surgical evacuation

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66
Q

How do you manage medical TOP?

A

Mifepristone (+ misoprostol)

or surgical evacuation

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67
Q

What are the risk factors for an ectoptic pregnancy?

A
  • previous ectopic
  • structural/ tubal damage (eg. PID/ previous surgery)
  • endometriosis
  • IUCD
  • Progesterone only pill
  • subfertility
  • IVF
  • Adhesions (Asherman’s)
  • Infection (current or previous)
  • Unsuccessful/ reversed tubal ligation
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68
Q

What is the presentation of an ectopic pregnancy?

A

Severe abdominal pain (usually unilateral- due to tubal distention or rupture)
PV bleeding
Amenorrhoea
Cervical excitation

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69
Q

What investigations should you conduct for a suspected ectopic pregnancy?

A

TV USS
beta hCG/ urine pregnancy test
Assess haemodynamic stability: FBC, blood pressure, O2 sats
serum progesterone (identifies failing pregnancy)

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70
Q

What is the management for an ectopic pregnancy?

A

Conservative: only if woman is stable and has bHCG <1500

Surgical: Salpingotomy, Salpingectomy (if tubal)

Medical: Methotrexate (teratogenic so should have effective contraception afterwards)

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71
Q

What is gestational trophoblastic disease?

A

Abnormal cells arising from trophoblastic tissue, greater proliferation and hCG secretion.

Non-malignant: Hydatidiform mole
Malignant: Invasive mole (only in uterus), choriocarcinoma (metastatic)

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72
Q

What are the risk factors of gestational trophoblastic disease?

A

previous GTD

extremes of age

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73
Q

Explain the pathophysiology of gestational trophoblastic disease

A

Molar pregnancy:
- Complete mole (no foetal tissue, increased risk of choriocarcinoma, 46 chromosomes), 2 sperm + empty ovum, or duplicated single sperm + empty ovum
- Partial mole (contains foetal tissue, 69 chromosomes), 2 sperm + 1 ovum
Choriocarcinoma:
- Choriocarcinoma, malignant trophoblastic tissue, can arise from molar pregnancy or germ cells.

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74
Q

What is the presentation of gestational trophoblastic disease?

A 
irregular vaginal bleeding 
hyperemesis 
hyperthyroidism (as hCG mimics TSH)
LARGE FOR DATES 
early pregnancy failure 
Blood--> raised hCG 
USS--> snowstorm appearance, grape like clusters
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75
Q

What is the management of gestational trophoblastic disease?

A

Molar pregnancy:

  • remove tissue via suction
  • monitor hCG levels

Choriocarcinoma:
- methotrexate based chemotherapy

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76
Q

Explain the background and presentation of Lichen Sclerosus

A

Potentially autoimmune conditions (often seen with vitiligo and thyroid disease)
Mostly in post-menopausal women
Thin vulval epithelium with loss of collagen
Presents with pruritis and soreness, pink-white papules with come together to form white patches with fissures.
figure of 8 presentation (around vulva and anus)

increased risk of vulval cancer

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77
Q

What is the management of lichen sclerosus?

A

Observe as it can be premalignant

Ultra-potent topical steroids: Clobetasol Propionate cream

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78
Q

Explain the cervical screening programme

A

Smears every 3 years from 25-50,

Every 5 years from 50-64

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79
Q

What is Cervical Intra-epithelial Neoplasia (CIN)?

inc. pathophys, grading, risks and management

A

Pre-invasive phase of cervical cancer
Atypical cells in the squamous epithelium of the cervix (dyskaryotic, increased mitosis and large nuclei)

Graded I-III depending on extent of neoplasia

1/3 women with CIN will develop cervical cancer

Commonly caused by HPV inserting viral DNA into cells, smoking, HIV, OCP/ multiple sexual partners without barrier contraception

Managed by LLETZ (large loop excision of the transformation zone)

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80
Q

What is the clinical presentation of cervical cancer?

A

Most common cancer in women <35
Often picked up at screening

POST COITAL BLEEDING
watery discharge

weight loss, post-menopausal bleeding, bowel distrubance, fatigue, loss of appetite, general malaise etc.

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81
Q

What investigations are carried out for a ?cervical cancer?

A 
Smear 
Colposcopy 
Chlamydia screening 
Punch biopsy 
CT for staging
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82
Q

What is a triple swab?

A

Vaginal swabs- screening for chlamydia, gonorrhoea, bacterial and fungal infections

2 x endocervical (chlamydia + gonorrhoea)
1 x high vaginal (bacterial + fungal)

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83
Q

What is the management for cervical cancer?

A

LLETZ (large loop excision of the transformation zone)
Cone excision (remove cervix)
Hysterectomy (simple or total +- pelvic lymph nodes)
Chemo/radiotherapy

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84
Q

What cells are involved in cervical cancer?

+ what staging

A

squamous cell carcinoma

FIGO staging- dependant on extent of spread (only in primary organ, adjacent organs, lymph nodes, other organs)

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85
Q

What cells are involved in endometrial cancer?

+ what staging

A 
glandular/ secretory epithelium- adenocarcinoma 
FIGO staging (only in primary organ, adjacent organs, lymph nodes, other organs)
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86
Q

What are the risk factors and pathophysiology for endometrial cancer?

+ protective factors?

A
  • UNOPPOSED OESTROGEN
  • Obesity (adipose tissue is oestrogenic)
  • Nulliparity
  • HRT
  • Tamoxifen
  • PCOS

Protective:
COCP
Smoking

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87
Q

What is the clinical presentation of endometrial cancer?

A
  • post menopausal women
  • post menopausal bleeding

(heavy periods in pre-menopausal women)

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88
Q

How do you investigate ?endometrial cancer?

A

Transvaginal USS to assess endometrial thickness (<4mm is okay)
Endometrial biopsy
Hysteroscopy

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89
Q

What is the management of endometrial cancer?

A

Hysterectomy± pelvic lymph nodes removal
Radiotherapy
progesterone

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90
Q

What cells are involved in vulval cancer?

A

Squamous epithelial

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91
Q

What is the aetiology + presentation + management of vulval cancer?

A

HPV or lichen sclerosus
can present as VIN initially (Vulval Intra-epithlial Neoplasia)

Itching, soreness, bleeding, lump, pain on urination

manage with surgery ± radiotherapy

92
Q

What cells are involved in ovarian cancer?

A

Epithelial (serosal)

93
Q

What is the aetiology and risk factors/protective factors of ovarian cancer?

A

Epithelial cell tumours (mostly), some stromal/granulosa, germ cell tumours

Aetiology: increased exposure to oestrogen,
!!!!!!! more ovulation !!!!!!!

Risk Factors:

  • Early menarche
  • Late menopause
  • Nulliparity
  • IVF
  • Family history (BRCA genes)

Protective Factors:

  • OCP
  • Multiple pregnancies
  • Breast feeding
  • Hyterectomy ± bilateral salpingoophrectomy
  • Tubal ligation
94
Q

What is the clinical presentation of ovarian cancer?

A

Older women: approx 75-85 y/o

Often very late presenting

General symptoms:

  • IBS like bloating
  • Abdominal pain/ discomfort
  • Bowel obstruction
95
Q

What investigations should be done in ?ovarian cancer?

A
  • CA125 (50% positive predictive value) (normal value 35, value above 250 is a referral)
  • USS
96
Q

What is the management for ovarian cancer?

A
  • Surgery (oophrectomy, bowel resection)
  • Chemotherapy
  • Palliative care
97
Q

What is endometriosis?

A

uterine tissue outside the uterus
driven by oestrogen, and therefore is hormonally effected

found commonly:

  • pouch of douglas (retrograde menstruation)
  • ovaries
  • tubal
  • bowel
  • peritoneum
  • points of scar tissue
98
Q

What are the pathophys theories of endometriosis?

A 
Retrograde menstruation 
Endometrial metoplasia (cells change into endometrial cells)
99
Q

What is the presentation of endometriosis?

A

In women of reproductive age, cyclical presentation of pain, pain is worst a few days before period

  • Dysmenorrhoea
  • Menorrhagia
  • Deep dyspareunia
  • Sub-fertility (can damage reproductive structures)
  • Dyschezia (pain on defecation)
  • Pain improves during pregnancy
100
Q

How do you diagnose endometriosis?

A
  • Laparoscopy
  • Elevated Ca125 (nonspecific, caused by irritation of peritoneum)
  • Trialled management works
101
Q

What is the management of endometriosis?

A

Analgaesics (NSAIDs: ibuprofen, naproxen, mefenamic acid)
Tranexamic acid for bleeding

Two Pharmacological Approaches:
1. Abolish cycles
- Monophasic and then triphasic COCP/ POP (3 months
back to back with 1 week break)
- Also consider Depot Provera, Implant, Mirena/ Copper
- Medroxyprogesterone/ Norethisterone

  1. Invoke glandular atrophy
    • GnRH analogues + HRT add back (tibolone)

Surgical

  • endometrial ablation
  • hysterectomy
102
Q

What is adenomyosis?

A

Presence of endometrial tissue in the myometrium

103
Q

What is the presentation of adenomyosis?

A
  • dysmenorrhoea
  • menorrhagia

More commonly in older women of reproductive age after childbirth, RF is multiparity
Cyclical pain- worst during cycle

104
Q

What is the management of adenomyosis?

A

Tranexamic acid, NSAIDs/ COX inhibs (ibuprofen, naproxen, mefenamic acid, paracetamol)

COCP POP IUD

Surgical

  • ablation
  • hysterectomy
105
Q

What are uterine fibroids?

A

Uterine Leiomyomas
Benign smooth muscle tumours of the uterus (of the myometrium)
Oestrogen dependant- don’t occur and shrink after menopause

106
Q

What are the risk factors of fibroids?

A
  • Afro-Caribbean
  • COCP (gives oestrogen)
  • Family history
107
Q

What is the clinical presentation of fibroids?

A
  • Menorrhagia ± anaemia
  • Sub fertility
  • Miscarriage
  • Pain (torsion of pedunculated fibroid)
  • Abdominal mass
108
Q

What investigations are carried out in ?fibroids or ?polyps?

A

USS
Hysteroscopy
Endometrial biopsy

109
Q

What is the management of uterine fibroids?

A

GnRH analogues (shrinks fibroids and induced amenorrhoea) not long term due to demineralisation and fracture risk

Myomectomy

Uterine artery embolisation

Hysterectomy

110
Q

What are endometrial polyps?

A

endometrial growths into uterine cavity, usually benign
(can be precancerous)

Thought to be oestrogen sensitive, grow in high levels of circulating oestrogen

Fibrous tissue core surrounded by columnar epithelium

Occurs due to dysregulated apoptosis and growth

111
Q

What are the risk factors for endometrial polyps?

A

Peri- or post-menopausal
hypertension
obesity
tamoxifen

112
Q

What is the presentation of endometrial polyps?

A

peri/postmenopausal women

  • irregular bleeding
  • intramenstrual bleeding
  • excessively heavy periods
  • post menopausal bleeding
  • infertility/ miscarriages
113
Q

What is the management of endometrial polyps?

A

GnRH analogues

Polypectomy + histology

114
Q

What are ovarian cysts + how do you assess risk?

A

common, usually follicular or CL cysts
mostly benign <5cm

Risk assessment using RMI (risk of malignancy index):

Ca125 x USS score x Menopausal status

USS score: 1-3 based on findings

Menopausal Status: 1-3, 1=pre, 3=post

115
Q

What are the types of ovarian cyst?

A

Functional: CL or follicular, can cause pain or bleeding if
rupture/ failure to rupture during ovulation

Endometrioma: chocolate cyst, cyst filled with old blood

Serous cystadenoma: most common in 30-40y/o, 30%
malignant

Mucinous cystadenoma: most common 30-50y/o, 5%
malignant, filled with mucus

Fibroma: benign small fibroid, sometimes presents with
pleural effusion, and ascites (Meig’s)

Teratoma (Dermoid cyst): arise from primitive germ cells

116
Q

What is the clinical presentation of ovarian cysts?

A

chronic pain, dull ache, cyclical
dyspareunia
abdominal mass

Rupture/ torsion (Ovarian or cyst): 
- acute pain (unilateral)
- vomiting 
- rupture: tenderness, guarding, peritonism, 
                discharge/bleeding
117
Q

What investigations should be done in ?cyst rupture/torsion?

A

FBC (WCC, CRP)
Ca125
TVUSS/ MRI

118
Q

What is the management for ovarian cyst torsion/ rupture?

A

conservative, analgaesia
surgical laparoscopic correction- resection, oophrectomy, ovary fixation
Preserve fertility
Send to histology

119
Q

What is Pelvic Inflammatory Disease (PID)?

A

Infection of the upper reproductive tract

120
Q

What is the aetiology of PID?

A

Acending infection from endocervix from endogenous vaginal bacteria (anaerobes), STIs (25% are chlamydia or gonorrhoea), uterine instruments (e.g. hysteroscopy etc.) , postpartum

121
Q

What are the risk factors and protective factors of PID?

A

rf: STIs, multiple new sexual partners, recent birth, recent use of uterine instruments
protective: barrier method contraception, Mirena, COCP

122
Q

What is the clinical presentation of PID?

A

CERVICAL EXCITATION, ADNEXAL TENDERNESS

Lower abdominal pain
Deep dyspareunia
Vaginal discharge 
IMB/ PCB 
Fever/ malaise 
Subfertility
Ectopic pregnancy/ miscarriage  
Abscess
123
Q

What investigations should you carry out in ?PID?

A

Triple swabs
Examination for cervical excitation and adnexal tenderness
FBC, CRP, Blood cultures, beta hCG

124
Q

What is the management of PID?

A

analgaesia
remove IUD
Ab: Ceftriaxone, Doxycycline, Metronidazole, Azithromycin

125
Q

What investigations are carried out for ?subfertility?

A

Male: Semen analysis: motility, morphology

126
Q

What is the definition of subfertility ?

A

Inability to conceive after 2 years of regular unprotected sexual intercourse

127
Q

How long is it until the IUD is an effective mechanism of contraception?

A

Immediate

128
Q

How long is it until the Progesterone Only Pill (POP) is an effective mechanism of contraception?

A

2 days

129
Q

How long is it until the COCP, IUS, implant, Depot is an effective mechanism of contraception?

A

7 days

130
Q

What is the management of varicella zoster exposure in pregnancy?

A

Check previous maternal exposure

If unsure or no; test for VZ immunoglobulins

Give VZ vaccine (an give within 10 days of exposure) (infectious 2 days before rash, until vesicular rash crusts over)

131
Q

How do you manage Group B Strep in pregnancy?

  • risk factors
  • investigations
  • management
A

Risk Factors of vertical GBS transmission:

  • Previous GBS+ve
  • Intrapartum fever >38
  • Current preterm labour
  • Prolonged rupture of membranes

Investigations:
- Vaginal and rectal swab at 35-37 week IF previous GBS+ve

Management: If +ve cultures or risk factors present
- IV penicillin

132
Q

What is the management of a missed miscarriage?

A

vaginal misoprostol

133
Q

What is assessed at the booking visit?

+ when is it?

A

<10 weeks

BMI
Blood pressure
Urinalysis (for proteinuria)
Blood test:
FBC + serum Ab (Rhesus status)
Infection: rubella immunisation, syphillis, HIV, Hep B
Haemoglobin electrophoresis (sickle cells)
Glucose tolerance test (if at risk of GD)
History:
Age (risks)
History of current pregnancy (LMP)
Past obstetric history
Past gynae history
Past medical history + drug history
Family history
Full social history (inc. domestic violence and FGM)

134
Q

What is assessed at the dating scan?

+ When is it?

A

8-14 weeks

Dating + due date using crown-rump length
Multiple pregnancies
Nuchal translucency measurements

135
Q

What is assessed at the abnormality scan?

+ When is it?

A

18-20 weeks

Structural abnormalities
Placental lie

136
Q

What is the screening for Down’s syndrome?

A

<14 weeks: 75% sensitivity

  • USS nuchal translucency (raised indicated cardiac abnormality)
  • PAPP-A (low indicated chromosomal abnormality)
  • bHCG (raised in Down’s)

> 15 weeks:

  • AFP (reduced)
  • uE3 (unconjugated oestriol) (reduced)
  • Inhibin A (raised)
  • bHCG (raised)

If positive: CVS (quicker) or Amniocentesis (safer and more accurate)

137
Q

What is assessed at 28 week antenatal check up?

A

Bloods: FBC, Rhesus status
Urine BP

  • given Anti-D*
  • offer pertussis vaccine*
138
Q

What is the antenatal care from 34 weeks onwards?

A

Check ups every 2 weeks to assess:

  • birth plan: vaginal or c-section, analgaesia etc.
  • Urine and BP
  • growth plotting (symphisiopubic height)

36w: check foetal presentation and placental lie

139
Q

When is Anti-D prophylaxis given?

A

28 weeks and 34 weeks

140
Q

What is assessed at a 41 week scan?

A

offered membrane sweep and induction of labour

141
Q

When are the extra antenatal checks for nulliparous women?

A

25+31 weeks

  • Urine and BP
  • growth plotting (symphisiopubic height)
142
Q

What are the risk factors for cord presentation?

A 
Premature rupture of membranes
Long umbilical cord
Polyhydramnios
Multiple pregnancy
Abnormal foetal lie (e.g. breech) 
Placenta praevia 
Multiparity 
CPD
143
Q

What is cord prolapse and why is it worrying?

A

Umbilical cord descends ahead of the foetus

Causes cord compression or spasm–> foetal hypoxia and death

144
Q

What is the management of cord prolapse?

A

Push presenting part of foetus back into uterus (to alleviate cord pressure)
Raise hips above head
Avoid handling cord

Tocolytics e.g. terbutaline

Emergency c-section

145
Q

What is the diagnostic criteria for hyperemesis gravidarum?

A

5% pre-pregnancy weight loss
dehydration
electrolyte imbalance

146
Q

What are risk factors for hyperemesis gravidarum?

A 
Multiple pregnancies 
Trophoblastic disease 
Hyperthyroidism 
Obesity 
Nulliparity
147
Q

What is the management of hyperemesis gravidarum?

A

Ginger
P6 Acupressure

Promethazine
Cyclizine

IV fluid correction

148
Q

What are complications of hyperemesis gravidarum?

A

Wernicke’s encephalopathy
IUGR or preterm birth
Mallory-Weiss tear

149
Q

What are the side effects of Entonox in labour?

A

Maternal nausea and vomiting

150
Q

What are the side effects of opioids in labour?

+ give examples of the drugs

A

Maternal: prolonged first/second stage of labour, feelings of unease, euphoria/dysphoria

Foetal: Respiratory depression, diminished breast-feeding behaviours

e.g. pethidine, morphine IM, PCA fentanyl

151
Q

What level do you insert an epidural?

A

L3/4

152
Q

Epidural;

  • Indications
  • Contraindications
A 
Indications:
Maternal request 
Multiple delivery 
Instrumental deliveries 
Maternal hypertension

Contraindications:
Maternal refusal
Allergy
Local infection

153
Q

What nerves and levels cause pain in labour?

A

L5-S4

Especially pudendal nerve: S2-4

154
Q

What are the 4 elements of a CTG?

A

Baseline foetal heart rate
Foetal heart rate variability
Accelerations
Decelerations

155
Q

What are the causes of antepartum haemorrhage?

A 
Placental abruption 
Placenta praevia 
Vasa praevia 
Morbidly adherent placenta (accreta, increta, percreta)
Uterine 
Polyps 
Fibroids 
Vulval varicosities 
Vaginitis 
Cervicitis 
Carcinoma
156
Q

How is an antepartum haemorrhage classified?

A

Bleeding >24 weeks

157
Q

What are the risk factors and associations for placental abruption?

A

Pre-eclampsia/ hypertension
Smoking
Thrombophilia

Multiple pregnancy
Polyhydramnios

IUGR
PROM
Increasing maternal age

Abdominal trauma
IVF

158
Q

What is the presentation of placental abruption?

A 
Antepartum haemorrhage (could be hidden), blood dark red
PAIN 
Tender, tense uterus- "woody"
Normal foetal lie 
Foetal distress
159
Q

What are the risk factors and associations with placenta praevia?

A 
Multiparity 
IVF 
Dichorionic twins 
Uterine fibroids 
Endometriosis 
Previous c-section

Maternal age
Previous uterine surgery (inc TOP)

160
Q

What is the antenatal management of placenta praevia?

A

Detect in 20-week anomaly scan + repeat USS at 36 weeks

Anti D prophylaxis !!

Planned c-section if within 2cm of the os
Normal delivery if not

161
Q

What is the management of an antenatal haemorrhage?

A

ABCDE and management

Steroids if <34 weeks
Arrange emergency c-section

162
Q

What is the presentation and management of vasa praevia?

A

Antenatal diagnosis by USS

Elective c-section (or emergency if not detected)

163
Q

What is the presentation of placenta praevia?

A

!! Bleeding- small bleeds before- bleeding is not concealed, bright red
NO PAIN/ tenderness/ uterine tenseness
Likely abnormal foetal lie

164
Q

What is the management of morbidly adherent placenta?

A

Antenatal diagnosis via USS and MRI

Elective c-section at 36-37 weeks
±hysterectomy

165
Q

What are the complications of an antepartum haemorrhage?

A 
Maternal:
DIC 
Hypovolaemic shock 
Sheehan's syndrome (pituitary necrosis following hypovolaemic shock) 
Post-partum haemorrhage

Foetal:
Hypoxia (+brain injury)
Demise

166
Q

What is the classification of a postpartum haemorrhage?

A

Primary: haemorrhage within 24 hours of birth
Minor 500-1000ml
Major >1000ml

Secondary: haemorrhage from 24h-12 weeks of birth

167
Q

What are the causes of PPH?

A
  1. Tone: atony++++++++
  2. Tissue: retained products (placenta)
  3. Trauma: uterus (rupture, inversion), surgical trauma
  4. Thrombin: DIC, haemophilia, sepsis, pre-eclampsia, ITP
168
Q

What are the risk factors for PPH?

A 
Previous PPH 
Antepartum haemorrhage 
Nulliparity 
Multiparity 
Clotting disorder (e.g. haemophilia)

Uterine malformations
Fibroids
Abnormal placentation

Polyhydramnios
Multiple pregnancy

During labour:
Prolonged labour 
Macrosomia 
Shoulder dystocia 
Operative birth (c-section)
Instrumental delivery 
Induction using oxytocin 
Prolonged syntocinon administration
169
Q

What are the red flag signs of severe pre-eclampsia?

A

Severe headaches
Flashing lights
Papilloedema
HELLP - RUQ pain, low platelets, raised LFTs
Clonus/ hyperreflexia (precursor to seizures)

170
Q

How do you manage pre-eclampsia?

A

Labetolol
± nifedipine, hydralazine
±magnesium sulphate
Delivery!

Aspirin from week 10-36 in second pregnancy!

171
Q

What is pre-eclampsia?

A

Hypertension and proteinuria in pregnancy >20 weeks

172
Q

What is eclampsia?

A

Proteinuria, hypertension + seizures in pregnancy

173
Q

How do you manage eclampsia?

A

Magnesium sulphate

Delivery

174
Q

What are the risks associated with pre-eclampsia and eclampsia?

A

Maternal:

  • HELLP syndrome
  • DIC
  • Acute kidney injury
  • ARDS (adult respiratory distress syndrome)
  • Neurological complications
  • Increased risk of htn/ CV disease in the future

Foetal:

  • hypoxic brain injury
  • Foetal growth retardation (IUGR)
  • LBW
  • Prematurity/ preterm birth
  • SGA
175
Q

What is the pathophysiology of pre-eclampsia?

A

Predisposition leads to poor vascularisation of the placenta
This causes placental ischaemia, and placenta releases thromboplastins (DIC) and renin (vasoconstriction)
This leads to hypertension (to preserve foetal nutrition), proteinuria and eventually seizures (+ foetal growth retardation)

176
Q

What are symptoms in pre-eclampsia?

A

Headaches, visual disturbances
RUQ pain
Oedema
Rapid weight gain

177
Q

What investigations would you do in ?pre-eclampsia?

A 
Bloods:
FBCs (Hb, platelets)
U+Es (uric acid)
LFTs (HELLP)
Protein creatinine ratio (raised)

Urine dip
Blood pressure

Regular USS for foetal growth

178
Q

What are differential diagnoses of pre-eclampsia?

A

Thrombotic thrombocytopenic purpura
Haemolytic uremic syndrome
Acute fatty liver
essential hypertension

179
Q

What are the risk factors for pre-eclampsia?

A 
Pre-existing hypertension 
Previous pre-eclampsia 
Family history of pre-eclampsia 
Maternal renal disease 
Obesity 
Diabetes (gestational or T2DM)
Afrocaribbean 
Nulliparity 
Multiple pregnancy
180
Q

What is cord prolapse and what are the risks?

A

When the cord is presenting and prolapses through the cervix

Causes vasospasm and foetal distress/ hypoxia

181
Q

What are the risk factors of cord prolapse?

A 
Obesity 
Multiparity 
Abnormal foetal lie 
PROM
Long cord 
Polyhydramnios
182
Q

What is the management of cord prolapse?

A

Alleviate pressure on cord- push foetus back into uterus
Elevate hips over head (e.g. trendelenberg)
Emergency caesarean

183
Q

What are the risk factors for shoulder dystocia?

A 
Macrosomia 
CPD 
Maternal diabetes 
Maternal obesity 
Prolonged labour
184
Q

What is the management of shoulder dystocia?

A

McRoberts
Suprapubic pressure
Delivery of posterior arm
C-section

185
Q

What are the complications of shoulder dystocia?

A

Maternal:
Trauma- 3rd or 4th degree tear
Psychological distress, PTSD
PPH

Foetal:
Hypoxic brain injury and cerebral palsy
Brachial plexus injury- Erb’s palsy
Clavicle fracture

186
Q

Obstetric cholestasis:

  • What is it
  • Presentation
  • Management
  • Risks
A

Raised bile salts in blood

Presentation: Itching, mild jaundice, pale stools, dark urine, raised LFTs

Management: Ursodeoxycholic acid

Risks: Premature birth, foetal distress (meconium passage), and still birth

187
Q

What are the risk factors for VTE in pregnancy?

A 
Obesity 
Smoking
Hypertension 
Pre-eclampsia 
Maternal age 
Prolonged labour
Multiparity
Immobilisation 
Cancer
Trauma
FH
IVF
188
Q

What is the management of VTE in pregnancy?

A

Dalteparin (LMWH)

189
Q

What is SGA, IUGR and LBW?

A

SGA- foetus with size below the 10th centile

IUGR- foetus unable to meet genetically predetermined size

LBW- Baby born <2500g

190
Q

What are the precipitating factors to preterm birth?

A

Premature rupture of membranes
Cervical weakness
Amnionitis
Preterm labour

191
Q

What are the risk factors for preterm birth?

A

Pregnancy related:

  • multiple pregnancy
  • APH

Non-modifiable

  • maternal age (extremes)
  • previous PTB
  • weak and short cervix

Modifiable
- Maternal infection- BV, UTI, pyelonephritis, appendicitis

192
Q

What are the complications associated with preterm birth?

A

Developmental delay
Respiratory distress syndrome + chronic lung disease + pulmonary hypoplasia
Cerebral palsy
Visual impairment

193
Q

How do you manage premature rupture of membranes?

A 
Admit 
Observe for signs of chorioamnionitis 
Oral erythromycin 
Steroids to mature foetal lungs 
Magnesium sulphate
194
Q

What investigations should be done in premature labour?

A

Sterile speculum- to assess cervical dilation
Bedside fibronectin (indicates upcoming labour)
TVUSS to assess cervical length

195
Q

What investigations should be done in premature rupture of membranes?

A

Sterile speculum- to assess cervix
Nitralazine stick (testing that it is amniotic fluid)
High vaginal swab (for GBS)
Assess maternal and foetal well-being regularly

196
Q

What is the management of preterm labour?

A

Maternal steroids
Tocolytics- B2 agonists, ritodrine
Abx

197
Q

What is the management for women at high risk of preterm labour?

A 
Regular scans 
GBS testing 
Foetal fibronectin
Cervical USS 
Cervical cerclage
198
Q

What is the pueperium?

A

Delivery–> 6 weeks

199
Q

What is ‘station’?

A

Level of the head in relation to the ischial spines

Above the spines (further in): -2 (2cm above)

At the spines: 0

Below the spines (further out): +2 (2cm below)

200
Q

What are the characteristics of labour?
/
What is needed to “diagnose” labour?

A

Cervical effacement
Regular painful contractions
Mucus plug show or rupture of membranes

201
Q

What is the first stage of labour?

A

From 4-10cm cervical dilation

202
Q

How long should the first stage of labour take?

  • How often contractions
A

Max 12 hrs.

Nulliparous: 1cm dilation per hour
Multiparous: 2cm dilation per hour

contractions every 3-5 min
lasting ~1 min

203
Q

How long should the second stage of labour take?

  • How often contractions?
A

Max 1hr. before intervention
Nulli: 40 min
Multi: 20 min

Every 30secs-2min

Lasts 90 seconds

204
Q

What are the movements of the second stage of labour?

A

Head: flexed to extension

Rotation 90° from occipito-posterior to occipito-transverse

205
Q

What is a partogram?

A

Assesses progression in labour

Monitors foetal: HR, head descent
Liquor colour
Cervical dilation
Maternal vital signs

206
Q

What are the causes of failure to progress in labour?

A

Power;
- Inefficient uterine action-

Passage;
- Cephalo-pelvic Disproportion

Passenger;
- malpresentation

207
Q

How do you manage malpresentation?

A

If breech: extracephalic version or c-section

If occipito-posterior: If prolonged first stage: c-section
If prolonged second stage: manual or ventouse rotation

If occipito-transverse: Usually with incomplete turning during decent- ventouse

If brow or face: c-section

208
Q

What is the Bishop’s score?

A

Prelabouring scoring system to establish whether induction is necessary or not

209
Q

What is included in the Bishop’s score?

A

Cervix texture: Soft (2), Medium (1), Firm (0)
Cervix length: <0.5 (3), <1 (2), <2 (1), >3 (0)
Cervix dilation: 5+ (3), 4-3 (2), 2-1 (1), <1 (0)
Foetal station: >0 (3), >-1 (2), >-2 (1), >-3 (0)
Foetal position: Anterior (2), Middle (1), Posterior (0)

210
Q

How do you interpret the Bishop’s score?

A

Total /13

211
Q

How do you interpret the Bishop’s score?

A

Total /13

<5: needs induction

5-9: Needs professional judgement

> 9: spontaneous labour

212
Q

What are the methods of induction?

A

Prostaglandin E2 gel in the posterior fornix

Cervical sweeping

ARM and oxytocin infusion

213
Q

What are the indications of induction of labour?

A

Gestation: 40-40+14

PROM

Maternal health problems; e.g. hypertension, pre-eclampsia, diabetes, cholestasis

IUGR

Foetal distress

214
Q

What are the contraindications of induction of labour?

A 
CPD 
Cord prolapse 
Vasa praevia 
Breech/transverse lie 
Active genital herpes 
2+ c-sections or 1 classical c section 
Triplets +
215
Q

What is polyhydramnios and how is it established?

A

Amniotic fluid index >95th percentile for gestational age

Calculated by measuring the vertical measurement of fluid pockets in 4 quadrants

216
Q

What are the causes of polyhydramnios?

A 
Idiopathic
Foetal oesophageal dysfunction; CNS, diaphragm hernia, atresia 
Duodenal atresia (double bubble)
Twin-twin transfusion 
Foetal hydrops
Foetal anaemia 
Macrosomia 
Maternial diabetes 
Maternal lithium
Maternal infection
Foetal karyotype/ genetic abnormalities
217
Q

What is foetal hydrops?

A

Oedema in 2 compartments of the foetus

e.g. scalp, ascites etc.

218
Q

What are the causes of foetal hydrops?

A 
Twin-twin transfusion 
Iron-deficiency anaemia 
Immune; Rh disease 
Congenital abnormality: e.g. Turners, Noonan's, 
Alpha thalassaemia
219
Q

What investigations should you do in polyhydramnios?

A

Fasting glucose
Karyotyping
TORCH screen

220
Q

What is the management of polyhydramnios?

A

Nothing
Indomethacin
Amnioreduction

Paediatric assessment of baby after birth- NG tube passed through to check for abnormalities inc fistulas

221
Q

What are the risks associated with polyhydramnios?

A

Maternal:

  • PPH (increased uterine contraction needed)
  • Malpresentation

Foetal:

  • Preterm labour
  • Increased risk of congenital abnormality
222
Q

What is Oligohydramnios?

+ how is it established?

A

Amniotic fluid index (AFI) < 5th percentile for gestational age

Vertical measurement of fluid space in four quadrants

223
Q

What are the causes of oligohydramnios?

A 
Placental insufficiency! 
Pre-eclampsia 
Premature rupture of membranes 
Renal agenesis 
Genetic/ chromosomal abnormalities
Maternal infection
224
Q

What are the risks of an amniocentesis?

A
  1. Miscarriage
  2. Infection
  3. Rhesus disease
  4. Club foot
225
Q

What is the management of PPH as a result of atony?

A

Bimanual compression
Oxytocin infusion
Ergometrine slow IV/IM

Carboprost IM
Misoprostol rectal

Surgical: 
Balloon tamponade 
B-Lynch sutures 
Bilateral artery ligation (uterine or internal iliac) 
Hysterectomy

Phase 3a (9 decks)

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