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Obs/Gyn Flashcards

1
Q

At what conceptational age is the primitive gonads evident?

A

5 weeks. On the mesonephric ridge

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2
Q

Lower part of the mullerian ducts fuse in the middle to form

A
  1. Uterus
  2. Upper part of vagina
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3
Q

Primordial follicles are at arrest in which part of the cell cycle

A

Prophase 1 (Meiotic divison 1)

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4
Q

Lower parts of the vagina develop from?

A

Sinovaginal bulbs

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5
Q

Inlet plane of the pelvis is from to where?

A
  • From the sacral promontory to top of pubic symphysis
  • Outlet is bottom of the coccyx to bottom of the pubic symphysis
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6
Q

Layers of the adult uterus

A

Peritoneum, myometrium and endometrium

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7
Q

Epithelium of the endocervix?

A
  • The epithelium of the endocervix is columnar and is also ciliated in its upper two-thirds.
  • This changes to stratified squamous epithelium around the region of the external os and the junction of these two types of epithelium is called the ‘squamocolumnar junction’.
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8
Q

Menstrual cycle: phases

A

Ovarian and Uterine

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9
Q

Oestrogen effects on LH

A

Low levels of oestrogen have an inhibitory effect on LH production (negative feedback), whereas high levels of oestrogen will increase LH production

This is how the contraceptive pill works

The positive feedback works by increasing GnRH receptors, negative feedback method is uncertain

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10
Q

Describe the menstrual cycle

A
  1. Start is the first day of menses
  2. Pre-ovulatory ovarian follicular phase= GnRH release causes FSH and LH to be secreted
  3. FSH causes follicles to mature, LH causes the theca cells to produce oestrogen. High levels of estrogen causes first a drop in FSH and LH. Only the follicle with most sensitivity to FSH grow to dominant follicle, then the increasing levels from the dominant cell causes a positive feedback on LH (surge), and oocyte is released
  4. Uterine cycle is happening alongside= high oestrogen means thickening endometrium, glands and thinning of cervical mucus
  5. The Graffian follicle turns into corpus luteum, which makes progestrone and inhibin which both inhibits FSH and LH . The uterus enters the secretory phase: thicker mucus and increase basal temp
  6. The lack of fertilisation means the corpus luteum changes to corpus albicans. Drop in progestrone means bleeding and FSH and LH released again

Menstrual phase, follicular, ovulation and luteal

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11
Q

What needs to happen before for progestrone to work ?

A

Oestrogen priming needs to happen

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12
Q

Which hormone keeps the corpus lutem alive?

A

hCG (human chorionic gonadotrophin)

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12
Q

Which hormone keeps the corpus lutem alive?

A

hCG (human chorionic gonadotrophin)

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13
Q

Which layer of endometrium is lost during menstruation ?

A

Functional layer

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14
Q

The theca cells and granulosa cells of the follicle secretes what during the preovulatory follicular phase ?

A

Theca cells= binds LH and secretes oestrogen
Granulosa cells= binds FSH and releases aromatase (which makes the oestrogen from the precursor made by theca cells)

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15
Q

Why is oestrogen also produced once corpus luteum has formed progestrone ?

A

The ratio of production is > for progestrone but some oestrogen is also produced

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16
Q

Dysmenorrhoea is split into ?

classification of cause

A
  1. Primary- absence of pathologic findings that could account for those symptoms
  2. Secondary- underlying conditions
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17
Q

Dysmenorrhoea: definition

A

Recurrent lower abdominal pain shortly before or during menstruation

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18
Q

Nulliparity: define

A

Never carried a pregnancy beyond a point of viability (20weeks gestation)

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19
Q

Primary dysmenorrhoea: pathophysiology

A

Increased endometrial prostaglandin (PGF2 alpha) production leads to vasoconstriction/ischemia and stronger, sustained uterine contractions (to prevent blood loss).

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20
Q

Primary dysmenorrhoea: Clinical features, dx and tx

A
  • Clinical features= Spasmodic, crampy pain which happens during 1-3 of period, pelvic midline/ lower abdo, normal pelvic examination
  • Dx= dx of exclusion
  • Tx= symptomatics so give NSAIDs, topical application of heat, hormonal contraceptives
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21
Q

Secondary dysmenorrhoea: aetiology

A
  1. Uterine causes= PID Adenomyosis, cervical polyps
  2. Extrauterine= endometriosis, adhesions, functional ovarian cysts, IBD
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22
Q

How does secondary dysmenorrhoea differ from the primary

A

The onset. Secondary usually happens >25 years

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23
Q

Clinical features of secondary dysmenorrhoea

A
  • Abnormal pelvic examination
  • Irregular cycles
  • Pain tends to get worse over time
  • Dyspareunia or postcoital bleeding
  • None/ little response to NSAIDs
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24
Q

Amenorrhoea: definition

A

Absence of menarche by 15yrs despite normal development of secondary sexual characteristics, no menses by 13 w/o secondary characteristics

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25
Q

Oligomenorrhoea: define

A

Irregular periods with cycles which are >35 days and only 1-9 periods/ year

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26
Q

Primary amenorrhoea

Aetiology

A
  1. Constitutional growth delay
  2. Hypogonadotropic hypogonadism- low GnRH release e.g. Kallmann syndrome, Prader willi, stress, hypopituitarism, damage to hypothalamus
  3. Hypergonadotropic hypogonadism- gonads not producing oestrogen/ progesterone due to dysgenesis e.g. in Turner syndrome (MC)
  4. Anatomical anomalies- mullerian agenesis
  5. Congenital adrenal hyperplasia
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27
Q

Kallmann syndrome: what is it?

A

Rare genetic condition characterized by anosmia (an inability to smell) and decreased production of GnRH from the hypothalamus, leading to delayed or absent puberty.

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28
Q

Primary amenorrhoea: Dx

A
  1. Check for presence of uterus. If not present then do karotyping and serum testosterone
  2. Look at LH/FSH levels
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29
Q

Secondary amenorrhoea: define

A

The absence of menses for more than 3 months in individuals with previously regular cycles, or 6 months in individuals with previously irregular cycles

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30
Q

MC of secondary amenorrhoea

A

Pregnancy

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31
Q

Progestin challenge: What is it and interpretation of results

A

A test used to help determine the cause of amenorrhea. A progesterone or a progesterone-like drug is given for 5-10 days.

If uterine bleeding does not occur within 2-7 days after progesterone cessation (physiological response), an underlying pathology is likely (e.g., low estrogen levels, abnormal uterine/endometrial anatomy, dysfunction of hypothalamic-pituitary axis).

Withdrawal bleeding induced= anovulation (e.g., PCOS, idiopathic anovulation, premature ovarian failure)

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32
Q

Female athelete triad: what is it?

A

Functional hypothalamic amenorrhea: low calorie intake/strenuous physical activity, low bone mineral density, and amenorrhea

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33
Q

Hypermenorrhoea is associated with

A

Hypothyroidism, endometrial cancer, endometriosis

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34
Q

Tanner staging

Girls

A

For girls two things: breast and pubic hair. 5 stages. Pubic hair is light then gets thicker and curly and crosses thigh etc

B1= Prepubertal/ slight to no elevation of nipple
B2= Enlarged mammary glands form a breast bud, slight increase in areolar diameter, nipple protrusion
B3=Breast bud extends beyond the areolar diameter
B4= Nipple and areola form a secondary mound which projects above the breast tissue
B5= Areola with projection of papilla only, Adult

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35
Q

Abnormal uterine bleeding: categories

A
  1. Frequency
  2. Regularity
  3. Duration
  4. Volume
  5. Intermenstural bleeding
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36
Q

Classification of abnormal uterine bleeding

A
  • PALM-COEIN
  • Structural causes: polyps, adenomyosis, leiomyomas, and malignancy and hyperplasia (PALM)
  • Nonstructural causes: coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, not otherwise classified (COEIN)
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37
Q

Combined oral contraceptive pill (COCP): what does it contain?

A
  1. Oestrogen and progesterone
  2. The level of oestrogen is kept in the inhibitory level for LH and also stops endometrium thickening
  3. Progestrone makes the cervical mucus thicker
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38
Q

COCP: normal regime

A

21 days on/ 7 days off causing the bleed. Trade name uk: Microgynon, Rigevidon

There are newer guide lines for longer 63days/ 7 days

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39
Q

Contraindication of COCP

A
  1. Current breast cancer
  2. < 6/52 weeks postpartum
  3. > 35 yrs old and smokes more than 15 cigarettes/day

Enzyme inducer drugs is a relative

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40
Q

List 2 pros and 2 cons of COCP

A
  • Pro= decreases dysmenorrhoea, decreases size of fibroids, decrease cancer of endometrial/ ovarian ca
  • Cons= VTE/ stroke risk is increased, increased risk of breast cancer
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41
Q

Effectiveness of COCP

When to take in the cycle

A

Within the first 5 days (effective immediately) if taken after this an additional barrier contraception must be used for 7 days.

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42
Q

Missed pill rule of COCP

A
  1. Take pill ASAP even if that means taking 2 pills on one day
  2. If 2 or more consecutive days are missed, then use additional contraception e.g. male condoms
  3. If the 2 pills are missed in the first week following the pill free interval then use emergency contraception
  4. If the pills were missed during the last week then just miss the pill free interval
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43
Q

Evra patches: what do they contain

A

They are transdermal patches which contains oestrogen and progesterone, similar to COCP, 3 weeks on, and 1 week off

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44
Q

Progestrone pill: disadvantages

A
  1. Must be taken during the same time each day
  2. Increase chance of irregular bleeding
  3. Increases risk of ectopic pregnancy
  4. Weight gain, acne, mood changes

Safe to use in women who cant use oestrogen pills

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45
Q

Injectable progesterone depots are injected when?

Frequency

A

Every 12 weeks

Works by decreasing endometrial thickness, increase cervical mucus

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46
Q

What are some common side effects of progesterone containing contraceptions

A
  1. Weight gain
  2. Mood changes
  3. Acne
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47
Q

Subdermal progestin implant

How long does it last

A

3 years

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48
Q

Subdermal progestin implant contraindication

A

Breast Ca

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49
Q

Intrauterine copper device works how?

A

Inserted into the uterus and last 10 years, has spermicide which decreases motility and prevents implantation

This can be used as emergency contraception if used in 5/7 after UPSI

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50
Q

Intrauterine system (IUS)

works by?

A

Progestin (levonorgestrel) releasing

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51
Q

What are some risks of intrauterine systems (copper and progestin)

A
  1. PID
  2. Ectopic pregnancy
  3. Uterine perforation
  4. Uterine expulsion
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52
Q

Ullipristal acetate. Also known as?

A

Ellaone

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53
Q

What is cut during a vasectomy?

A

Vas deferens

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54
Q

Gillick competency. How does it work?

A
  • Children under 16 years old are considered to be incompetent unless they show Gillick competency
  • Gillick competency= understand, can’t persuade to tell parents, will have UPSI, risk to health
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55
Q

Endometriosis: what is it?

A

Endometrial tissue which is found outside of uterus in women of reproductive age

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56
Q

Endometriosis: aetiology

A
  1. Retrograde movement of menstural blood
  2. Dysfunction of immune system
  3. Coelemic metaplastic theory= peritoneal cells transform back into primitive origin then into endometrial cells
  4. Benign metastases theory= endometrial tissue travels to lungs etc
  5. Extrauterine stem cell theory
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57
Q

How are the endometriosis cells different from the endometrial cells?

A
  1. They contain more aromatase therefore produce more oestrogen
  2. Implanted cells produced pro-inflammation factors which can lead to adhesions which alters normal anatomy
  3. New blood vessels form to these implants
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58
Q

Endometriomas

What are they

A

These are endometrial implants on the ovaries. “Chocolate cysts”

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59
Q

Endometrosis: SSx, Dx and Tx

A
  • SSx= Abdominal pain/ pelvic pain, back pain, infertility, dysmenorrhoea, postmentrual bleeding, dyspareunia, dyschezia
  • Dx= Hx, transvaginal ultrasound, laproscopic examination is confirmatory
  • Tx=NSAIDs, contraceptive pills. Severe= GnRH agonist, OCPs. Surgery (ablation/ hysterectomy/ salpingo-oophorectomy)

GnRH used to combat hypoestrogenic effects such as lipid abnormalities, oestoporosis, infertility

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60
Q

Dyschezia: what is it?

A

Pain whilst defecating (endometriosis tissue implants in the pouch of douglas)

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61
Q

DDx of endometriosis

A
  1. Adenomyosis- benign disease characterized by the occurrence of endometrial tissue within the myometrium due to hyperplasia of the endometrial basal layer
  2. Colon Ca
  3. Ovarian Ca
  4. PID- adhesions
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62
Q

Uterine leiomyomas: classifed into

A
  1. Submucosal
  2. Intramural
  3. Subserosal
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63
Q

Uterine leiomyomas: define

A

Benign, hormonal- sensitive smooth muscle tumours

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64
Q

Predisposing factors for uterine leiomyomas

A
  1. Nulliparity
  2. Early menarche < 10 years old
  3. African american individuals
  4. Obesity
  5. FHx
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65
Q

Where do uterine leiomyomas occur most commonly ?

A

Intramural

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66
Q

Uterine leiomyomas: SSx, Dx, Tx

A
  1. SSx= Depends on size, number and location of tumour. Commonly= hypermenorrhoea, dysmenorrhoea, metrorrhagia, infertility, mass effect
  2. Dx= Ultrasound scan- hypoechoic solid mass, MRI with or without contract to characterise more
  3. Tx= shared decision making. If patient wishes fertility, keep uterus etc. You can do uterine artery embolisation

Mass effect= sympts due to mass. E.g. back pain etc. Location dependent

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67
Q

Metrorrhagia: define

A

Abnormal uterine bleeding between periods. Causes= cervical cancer, COCP

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68
Q

Which of the leiomyoma locations pose a risk to heavy menstural bleeding?

A

Submucosal, Intramural if pedunculated ++

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69
Q

What should indicate you towards a leiomyosarcoma ?

A

Hypervascularity within a solitary heterogeneous uterine mass

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70
Q

Pharmacological tx for leiomyomas

A

Used in expectant management?
* IUD
* Oral contraceptive pill
* GnRH anatagonists –> hormonal therapy too to counter hypoestrogenic effect
* GnRH agonist

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71
Q

Embolic agent used in uterine artery embolisation

A

Polyvinyl alcohol

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72
Q

Postembolisation syndrome: define

A

A common complication of transarterial embolization characterized by fever, pain, nausea, and vomiting within 72 hours after embolization in the absence of infection. Believed to be caused by inflammatory response to necrotic tissue. The condition is typically self-limited.

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73
Q

Pelvic inflammatory disease: define

A

Caused by a bacterial infection that spreads beyond the cervix to infect the upper female reproductive tract, including the uterus, fallopian tubes, ovaries, and surrounding tissue.

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74
Q

MC pathogens causing PID

A
  • Chlamydia trachomatis, Neisseria gonorrhoeae
  • Coinfection with e.coli is possible
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75
Q

PID during pregnancy usually occurs when?

A

Before 12 weeks, before the mucus plug blocks the enterance

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76
Q

Risk factors of PID

List 3

A
  • Multiple sexual partners
  • Hx of STI or STI
  • Vaginal dysbiosis (flora is imbalanced)
  • IUDs
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77
Q

PID: SSx, Dx, Tx

A
  1. SSx= lower abdo pain, nausea/ vomiting, dysuria, metrorrhagia, menorrhagia, dyspareunia, abnormal discharge
  2. Dx= Hx (multiple sexual partner, lower abdo pain, cervical motion tenderness, purulent discharge. US can show free fluid
  3. One single dose of IM ceftriaxone and oral therapy with doxycycline

PID can lead to infertility, one of the most common reason. Tx quick. Fitz-Hugh Curtis is complication, basically this is adhesions from the Glissons capsule to the peritoneum due to infection

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78
Q

Culdocentesis: what is it?

A

Aspiration of intraperitoneal fluid from the pouch of Douglas. No longer routine!

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79
Q

Friable cervix: define

A

Bleeds very easily after slight touch

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80
Q

Urinary voiding symptoms

List 3

A
  • Slow stream
  • Splitting or spraying
  • Teriminal dribble
  • Hesitancy- delay in start to micturition
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81
Q

Urinary storage symptoms

List 3

A
  • Frequency
  • Nocturia- waking at night one or more times
  • Urgency
  • Nocturnal enuresis: the loss of urine occurring during sleep
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82
Q

Which sphincter is under voluntary control?

A

External sphincter muscle

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83
Q

Which part of the brain controls the voluntary release of urine

A
  • Pons
  • Pontine storage center can delay micturition
  • Pontine micturition centre allows urination when we want to
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84
Q

Types of incontinence

A
  1. Urge = always need to go
  2. Stress = physical activity e.g sneeze or cough
  3. Mixed= stress + urge
  4. Overflow= due to bladder outlet obstruction, e.g. due to prostate enlargement. >200ml left in bladder post void
  5. Functional= pt has dementia
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85
Q

Aetiology of urinary incontinence

A
  1. Idiopathic
  2. Neurological= MS, spinal injury to s2-3, hydrocephalus
  3. Genitourinary= trauma to pelvic floor muscles, peliv fracture, pelvic floor weakness
  4. Transcient causes= UTI, drugs e.g. diuretics

DIAPPERS: Delirium/confusion, Infection, Atrophic urethritis/vaginitis, Pharmaceutical, Psychiatric causes (especially depression), Excessive urinary output (hyperglycemia, hypercalcemia, CHF), Restricted mobility, Stool impaction.

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86
Q

Stress incontinence: mechanism

A
  1. Uretheral hypermobility
  2. Intrinsic sphincter deficiency
  3. Increase in intrabdominal pressure e.g. coughing/ laughing
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87
Q

Stress incontinence: Dx

A

+ve Bladder stress test. Leaking of urine after activity which increases intraabdominal pressure

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88
Q

Urge incontinence: mechanism

A
  1. Inflammatory condition
  2. Neurogenic disorder

These cause over contraction of the detrusor muscle or abnormal sphincter control

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89
Q

Mixed incontinence: mechanism

A

combination of both stress and urge

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90
Q

How do you manage urinary incontinence?

A
  1. Manage diet= reduce alcoholic/ carbonated drinks
  2. Smoking cessation
  3. Pelvic floor exercises
  4. Surgery using slings/ Burch (stress)
  5. Use of antimuscarinic for urge (oxybutynin)

Try 1- 3 for 6 weeks initially for urge/stress

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91
Q

Cervical cancer: epidemiology

A
  1. 3rd most common gyane malignancy
  2. 2 peaks. 30-39yrs, >70
  3. Developing world mainly
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92
Q

Cervical cancer: aetiology

A
  1. HPV (high risk types e.g. 16, 18, 31, 33)
  2. Risk factors= multiple sexual partners, early onset of sexual activity, immunosupression, cigarette smoke
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93
Q

Cervical cancer: clinical features

A
  1. Early symptoms= abnormal vaginal bleeding (postcoital), abnormal vaginal discharge(watery), dyspareunia, pelvic pain
  2. Late symptoms= hydronephrosis, lymphedema, fistula formation
  3. Cervical examination- shows induration, exophytic tumour
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94
Q

Cervical cancer: classification

A
  • Bethesda system- The Bethesda system is a classification system used to report the results of cytological screening of cervical cancer
  • Cervical intraepithelial neoplasia- grade 1 - 5. Looks at the amount of the epithelial layers which are dysplastic. Used to classify histological samples e.g. biopsy
  • FIGO
    Stage 1: Confined to the cervix
    Stage 2: Invades the uterus or upper 2/3 of the vagina
    Stage 3: Invades the pelvic wall or lower 1/3 of the vagina
    Stage 4: Invades the bladder, rectum or beyond the pelvis
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95
Q

Cervix: the 3 different parts to know histological

A
  • Endocervix- columnar epithelium produce mucus
  • Ectocervix- mature squamous cell epithelium.
  • Squamocolumnar junction
  • Transformation zone- where the cells come together
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96
Q

Cervical cancer: pathogenesis

A
  1. HPV infection or other factor causes uncontrolled cell division usually at the basal layer of transformation zone
  2. This is called cervical intraepithelial neoplasia
  3. The HPV infection produces proteins which act on tumour suppressor genes
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97
Q

Majority of cervical cancers are which type

A

Squamous cell carcinoma, then adenocarcinoma

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98
Q

What is colposcopy ?

A
  • A procedure using a colposcope to examine the cervix, vagina, vulva, and anus for precancerous lesions or abnormalities
  • Procedure allows magnified visualization of the epithelium to guide biopsy sampling for histologic diagnosis.
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99
Q

Surgerical options for Tx of invasive cervical cancer

A
  1. Diagnostic excision procedure: Cold-knife conization and loop electrosurgical excision procedure (LEEP)
  2. Trachelectomy- Removal of the cervix, upper vagina, and parametrium (may also involve removal of pelvic lymph nodes)
  3. Pelvic exenteration- reproductive organs plus bladder, urethera, anus . Palliative.
  4. Hysterectomy
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100
Q

Tx for invasive cervical carcinoma?

A
  1. Chemotherapy/ radiation
  2. Surgery to remove the uterus and accompaning lymph nodes
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101
Q

How often should screening for cervical cancer take place?

A
  • 25-49 yr old should have screen every 3 years
  • 50- 64 every 5 years
  • > 65 yrs only those with abnormal test results
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102
Q

During colposcopy which finds point to invasive cervical cancer?

A
  • Gross exophytic or endophytic neoplasm
  • Ulceration
  • Necrosis
  • Erosions
  • Atypical growth of the vessels (e.g., corkscrew or comma-like shape)
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103
Q

Acetowhite epithelium: what is it? Indicates?

A
  1. An area of the cervical epithelium that appears white after the application of acetic acid
  2. Indicates atypical changes of the epithelium. Requires biopsy at least 2-4 targeted.
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104
Q

Types of cervical biopsy

A
  1. Punch
  2. Cone
  3. Endocervical curettage
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105
Q

Primary cervical cancer prevention vs secondary?

A
  1. Primary = HPV vaccination. 2 doses. Before getting sexually active. Doses need to be 6-12 months apart.
  2. Screening is the secondary method. Pap smear, HPV DNA testing, colposcopy
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106
Q

What are some contraindication for Pap smear?

A
  • Endometrial cancer
  • Hx of hysterectomy for nonmalignant disease
  • > 65 years old
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107
Q

Types of hysterectomy

A
  1. Subtotal/ Supracervical- upper part of uterus removed, cervix intact
  2. Total- uterus plus cervix
  3. Radical- everything including upper portion of vagina, lymph nodes and fatty tissue, fallopian tubes and ovaries
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108
Q

Infertility: define

A

Inability to achieve pregnancy after 12 months of unprotected sex in women < 35 years and 6 months in women ≥ 35 years of age

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109
Q

2 types of infertility

A
  1. Primary= infertility in persons who have never achieved pregnancy
  2. Secondary= infertility in persons who have previously achieved at least one pregnancy
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110
Q

Female infertility can be divided into 4 broad groups which are?

A
  1. Ovary related
  2. Tubal/ pelvic
  3. Cervical factors
  4. Uterine factors
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111
Q

Ovary related reasons for infertility

List 3

A
  1. PCOS
  2. Pituitary adenoma
  3. Menstural cycle abnormalities (functional hypothalamic amenorrhea)
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112
Q

Tubal/ pelvic reasons for infertility

List 3

A
  1. PID
  2. Endometriosis
  3. Fallopian tube adhesions due to infection e.g. gonorrhoea or from obstruction e.g. from surgery
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113
Q

Cervical factors for infertility

List 2

A
  1. Antisperm antibodies in cervical mucus
  2. Trauma from conization
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114
Q

Uterine factors for infertility

List 2

A
  1. Leiomyoma
  2. Endometrial polyps
  3. Ashermans syndrome
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115
Q

Asherman syndrome

Define

A

A condition characterized by adhesions and/or fibrosis of the endometrium that can cause amenorrhea and infertility. Associated with intrauterine instrumentation (e.g., dilation and curettage), postpartum hemorrhage, or intrauterine infections.

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116
Q

Hormone levels vary the least during which days of the cycle?

A

3-5 days. Hormone variation at this stage suggests follicular maturation problems

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117
Q

High prolactin levels leads to

A

A condition of elevated serum prolactin, which causes galactorrhea in women, gynecomastia in men, and symptoms of hypogonadotropic hypogonadism (due to ↓ FSH and LH secretion) in both sexes.

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118
Q

Tx options for female infertility

A
  1. Lifestyle modification
  2. Tx underlying conditions (Levothyroxine for hypothyroidism, bromocriptine for hyperprolactinemia, metformin for PCOS)
  3. Ovulation induction e.g. with clomiphene citrate
  4. Assisted reproductive technology
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119
Q

Dx of male infertility

A
  1. Hx
  2. Semen analysis
  3. TSH, prolactin levels
  4. Karyotype testing for kleinfelter
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120
Q

Endometrial cancer: Types

A
  1. Type 1- cells of endometrioid origin
  2. Type 2- nonendometrioid cells, serous/ clear cells
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121
Q

Aetiology of endometrial cancer

A
  1. Type 1= direct long term exposure to oestrogen. Some genetic mutation such as PTEN
  2. Type 2= oestrogen independent, associated with endometrial atrophy, strong genetic predisposition (p53 mutation)
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122
Q

Risk factors for endometrial cancer?

A
  • Nulliparity
  • Early menarche and late menopause
  • Polycystic ovary syndrome= no ovulation therefore no progesterone which is protective
  • Metabolic syndrome (esp. obesity and diabetes mellitus type 2 )
  • Hypertension
  • Unopposed estrogen replacement therapy (e.g., for menopausal symptoms)
  • History of breast cancer and tamoxifen treatment. Tamoxifen +ve on uterus oestrogen sensitivity
  • Lynch syndrome
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123
Q

What is Lynch syndrome?

A

A hereditary cancer syndrome caused by a mutation in mismatch repair genes. Individuals have a significantly higher risk of developing colorectal, gastric, ovarian, and endometrial cancer.

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124
Q

Protective factors against endometrial cancer?

A
  • Multiparity
  • Combination oral contraceptive pills
  • Regular physical exercise
  • Lifelong soy-rich diet
  • Smoking (more type 1, increases type 2)
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125
Q

Endometrial cancer: clinical features

A
  1. Abnormal uterine bleeding= postmenopausal, Premenopausal or perimenopausal, Intermenstrual bleeding
    Heavy irregular menstrual bleeding
  2. Regional extension= abdominal distension, pelvic pain, bowel/ bladder habit changes
  3. Metastatic= spread to retroperitoneal via lymphatics or to lung by haematogenous
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126
Q

Endometrial cancer: dx, tx

A
  1. Dx= TVUS (thickness < 4mm= high negative predicative value), biopsy to confirm (can be hysteroscopy Dilation&curettage, or in office), MRI pelvis/ PETCT scan
  2. Tx= total hysterectomy with bilateral salpingo-oophorectomy. High risk will receive radiation therapy too

Good prognosis

Clear cell and papillary serous carcinomas (type II) have an aggressive course and a poor prognosis.

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127
Q

Foetal orientation: the different components

A
  • Foetal lie
  • Presenting part
  • Position
  • Attitude of presenting part
  • Station
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128
Q

Foetal lie: the different types

A
  1. Longitudinal = same as mother
  2. Transverse= foetus is at a 90° angle. This has many variation, depending on the relation of the back to the uterus, dorsosuperior, -inferior, -post, -anterior
  3. Oblique lie= foetus is at a 45° angle
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129
Q

Foetal presentation

A
  • Definition: part of the fetus that overlies the maternal pelvic inlet
    1. Cephalic
    2. Breech: feet/ buttocks. Types=
    3. Complete breech
    4. Single footling
    5. Double footling
    6. Frank breech
    7. Compound presentation
    8. Shoulder presentation
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130
Q

Foetal position: define

A

Relationship and orientation (i.e., fetal occiput pointing towards maternal left or right) of the presenting fetal part to the maternal pelvis

131
Q

How does insulin resistant lead to infertility ?

women

A

Insulin resistance -> hyperinsulinaemia -> androgen excess -> arrest in antral follicular development -> anovulation.

Metformin treats insulin resistance and hyperinsulinaemia, therefore allowing follicular development and subsequent ovulation

132
Q

Fetal attitude: define

A

Degree of extension/flexion of the fetal head during cephalic presentation

133
Q

Types of fetal attitude

A
  1. Vertex= maximally flexed head. (MC)
  2. Brow
  3. Face presentation, with the mentum (chin) facing towards symphysis pubis, or coccyx. Anterior/posterior respectfully
  4. Forehead= the anterior fontanelle passes first
134
Q

Station: define

A

Measurement (in cm) of the presenting part above and below the maternal ischial spine

135
Q

What is engagement?

A
  • When the widest transverse diameter of the head (presenting part) passes through the pelvic inlet
  • Use the rule of fifths: engagement is clinically identified when ≤ 2/5 of the fetal head are felt above the symphysis pubis through the maternal abdomen
136
Q

Synclitism: define

A

Parallelism between the pelvic plane and the plane of the fetal head

In asynclitism, the sagittal suture is in the transverse diameter of the pelvic inlet and not between the symphysis pubis and sacral promontory.
1. Anterior= the anterior parietal bone presents
2. Posterior= you have to do a c-section

137
Q

Gravidity: define

A

The number of times a woman has been pregnant, regardless of pregnancy outcome

138
Q

Parity: define

A

The number of pregnancies that a woman carries beyond 20 weeks of gestation and ends with the birth of an infant weighing > 500 g

139
Q

Preterm is defined as ?

A

A live birth before 37 weeks of gestation

140
Q

Presumptive signs of pregnancy

A
  1. Amenorrhoea
  2. Breast tenderness
  3. Linea nigra
  4. Increased urinary frequency
  5. Hyperpigmentation of areola
141
Q

Dx of pregnancy

A
  1. Urine B-hCG: less sensitivity, detectable after 14 days
  2. Serum B-hCG: high sensitivity, detectable 6-9 day after fertilisation
142
Q

Naegeles rule to find out expected date

A

First day of the last menstrual period + 7 days + 1 year - 3 months

Inaccurate if:
* The date of the last menstrual period is uncertain or unknown
* The patient has irregular menstruation cycles
* The patient conceived while taking contraceptive pills

143
Q

Symphysis fundal height: is used from when onwards

A

20 weeks’ gestation onwards

144
Q

Leopold’s manoeuvre: what is it? The steps

A
  • These are 4 manoeuvre which can be used to determine the fetal position
  • You have to conduct these by standing on the right side of the patient
  1. Uterine fundus location using the ulnar portion of the palm,
  2. Fetal orientation: using both hands on either side. You can feel the back as a smooth vs hands/ feet as nobby part
  3. Fetal presentation: The thumb and fingers of 1 hand grasp the lower portion of maternal
    abdomen above pubic symphysis
  4. Descend: Face pt’s feet, position fingertips of both hands on either side of the
    presenting part –> exert inwards pressure, slide caudad along the axis of pelvic inlet
145
Q

Which types of vitamin and mineral should be eaten more during pregnancy?

A
  1. Iron
  2. Folic acid
  3. Vit B12
  4. Calcium
  5. Iodine
146
Q

Fundal height and gestation age

147
Q

Johnsonʼs method and of Insler and Bernsteinʼs formula for estimating fetal weight

A
  • Foetal weight (g)=fH (cm)n × 155
  • Insler and Bernstein

n is a constant

148
Q

Types of pelvis

A
  1. Gynaecoid= transverse oval inlet, wide sacrum, wide sacrosciatic notch, straight side walls, wide subpubic angle
  2. Android=triangular inlet, converging side walls, narrow sacrosciatic notch, narrow subpubic angle
  3. Anthropoid
  4. Platypelloid
149
Q

Pelvic inlet: what is it?

A
  • Oval shape, widest transversely
  • Posteriorly is the promontory of sacrum, alas
  • Anterior is the pubic symphysis
  • Laterally is the ileopectineal line
150
Q

Maternal diameters: The two broad diameter? What are the names?

A
  • Anteroposterior and transverse
  • Anteroposterior is divided into 3 more: True conjugate (11cm) , obstetric conjugate (10cm) , diagonal (12cm)
  • Transverse: transverse, oblique and sacrocotyloid
151
Q

Obstetric conjugate: where to where?

A

Promontory to posterior most protruding part of the symphysis pubis

152
Q

Diagonal conjugate: where to where?

A

Promontory to lower border of pubic symphysis

153
Q

Pelvic planes: which are they ?

A
  1. Inlet
  2. Mid
  3. Outlet
154
Q

Which of the conjugates can be measured clinically?

A
  • Diagonal
  • The rest can be worked by taking either -1 cm for true conjugate or -2cm for obstetric.
155
Q

The pelvic outlet diameters: which are they?

A
  1. Obstetric conjugate: anterior posterior- 11cm , bispinous diamater- 10.5cm,
  2. True conjugate: from tip of coccyx, other is sacrum to bottom section of pubic symphysis.
    Anterior posterior- 13cm, transverse- 11cm
156
Q

Methods for pelvimetry

A
  1. Clinically
  2. CT/ MRI scan
157
Q

Hormone replacement therapy: adverse effects

A
  1. Increases the chances of breast cancer, but this is very low
  2. Increased chance of venous thromboembolism due to progesterone
  3. Nausea
  4. Breast tenderness
  5. Fluid retention and weight gain
158
Q

HRT: the types you can give

A
  1. Oestrogen only (if no uterus)
  2. Progestin + oestrogen for pt with uterus
159
Q

Non-hormonal therapy for menopausal women

A
  1. Selective oestrogen receptor modulator (tamoxifen)
  2. Paroxetine (SSRI) for hot flushes
160
Q

Osteoporosis: define

A

Loss of trabecular and cortical bone mass which leads to bone weakness and increased susceptibility to fractures

161
Q

Osteoporosis: aetiology

A
  1. Primary. Divided into type 1 (postmenopausal), type 2 (senile)
  2. Secondary: drugs e.g. corticosteroid, phenytoin, lifestyle

Oestrogen stimulates osteoblasts and inhib osteoclasts

As we age osteoblast activity decreases, leading to less osteoid production.

162
Q

Osteoporosis: clinical features

A
  1. Mostly asymptomatic
  2. Fragility fractures: pathological fractures that are caused by everyday-activities (e.g., bending over, sneezing) or minor trauma (e.g. falling from standing height
163
Q

Common locations of major osteoporotic fractures

A

Vertebral (most common) > femoral neck > distal radius (Colles fracture) > other long bones (e.g., humerus)

164
Q

Osteoporosis: Dx and Tx

A
  1. Dx= DXA scan. Osteoporosis is diagnosed in patients with a T-score ≤ -2.5 SD and/or a fragility fracture. Also do CBC and look at vit D, phosphate, PTH
  2. Tx=Lifestyle (exercise, intake of vitD), bisphosphonates, nonbisphosphonates such as calcitonin, HRT
165
Q

Secondary causes of osteoporosis

Endocrine

A
  • Hypercortisolism- Cushings
  • Hypogonadism
  • Hyperthyroidism
  • Hyperparathyroidism
  • Renal disease
166
Q

Positions where dual-energy x-ray absorptiometry (DXA) scan is taken

A

At the lumbar spine and hip/femoral neck

167
Q

Bisphosphonates: MOA

A

Inhibition of osteoclasts, which are involved in bone resorption

168
Q

Bisphosphonates: adverse effects

A
  • Osteonecrosis of the jaw
  • Atypical femoral fractures
  • Esophagitis
  • Hypocalcemia
169
Q

Labour is dx by?

A

Painful contractions which leads to cervical dilation and effacement

170
Q

Mechanical factors which determines progress of labour

A
  1. The force by which the fetus is expelled
  2. The pelvic shape and resistance by soft tissues
  3. Foetal head diameters
171
Q

Types of contraction which occur during pregnancy

A
  1. Alvarez-waves= low intensity, high frequency. Happens after 20 wks
  2. Braxton Hicks contractions (false labour)= Begins during 2nd/ 3rd trimester, helps with position of foetus
  3. Prelabor= 3-4 days before birth, Irregular contractions of high intensity, occur every 5–10 min shortly before phase 1 begins. They are responsible for correctly positioning the fetal head in the pelvis.
172
Q

Stages of labour

A
  1. Stage 1= cervical dilation and effacement
  2. Stage 2= foetal expulsion
  3. Stage 3= placental explusion
  4. Stage 4= Afterpains
173
Q

Stage 1 of labour: what happens

A
  • Split into 2 parts: latent and active phase. Cervical effacement. Bloody show/ breaking of water indicates true labour has begun.
  • Latent= cervical dilation up to 4cm. Irregular contractions every 5-30mins which lasts < 30sec
  • Active= cervical dilation ends at 10cms. More frequent longer contractions. 3-4 contractions/10 mins lasts 1min

This stage can last up to 8-12hrs in primi

174
Q

Stage 2 of labour: what happens

A

A stage of labor that begins once the cervix is completely dilated and ends with the birth of the infant

175
Q

Stage 3 of labour: what happnes

A

A stage of labor that begins with the birth of the infant and lasts until the complete expulsion of the placenta. < 30 mins.

176
Q

Signs of placental separation

A
  • Cord lengthening
  • Gush of vaginal blood (usually accompanied by a blood loss of 300 mL)
  • Uterine fundal rebound (the uterus becomes less elongated and more spherical)
177
Q

Cardinal movements of childbirth

A
  1. Engagement. Descent and flexion of the head
  2. Internal rotation- rotates by 90 degrees.
    3.Crowing
    4.Extension of head
    5.Restitution aka external rotation
  3. External rotation of shoulder
  4. Expulsion of baby via lateral flexion
178
Q

Some observations which needs to be taken during labour

A
  1. Blood pressure
  2. Temperature
  3. Assess dilation and station
  4. Fetal heart rate
  5. Encourage micturition
179
Q

The puerperium: define

A

The 6 weeks after delivery, where the body returns to its prepregnant state

180
Q

Physiological changes which occurs during puerperium

A
  1. Uterus contracts and occludes blood vessels which used to supply uterus . The internal os of the cervix is fully closed by day 3.
  2. Low grade fever, shivering, leukocytosis are common in first 24hrs
  3. Fundal height of the uterus drops down to symphysis level by 10th day
  4. Lochia: rubra (4days), serosa (2-3weeks), alba (until 10 weeks)
  5. Menstruation is delayed until 6 weeks by lactation, unless lactation is not occuring
181
Q

Colostrum is passed for how many days?

A

First 3 days

182
Q

The ovaries contain which types of tissue

A
  1. Sex cord
  2. Epithelial
  3. Germ
183
Q

What are some risk factors which predispose you to ovarian cancer?

A
  1. BRCA1/2 mutation
  2. Lynch syndrome
  3. Hormonal factors such as extra ovulations
  4. Endometriosis
184
Q

What are some protective factors against ovarian cancer?

A
  1. Pregnancy
  2. Oral contraceptive pills
  3. Surgeries e.g. salpingoophorectomy
185
Q

Epithelial ovarian tumours : some subtypes

A
  1. Serous
  2. Mucinous
  3. Brenner - from urothelial cells
  4. Endometroid
  5. Clear cell

Cystadenoma (benign) vs adenocarcinoma (malignant)

186
Q

Which of the epithelial ovarian tumours have psammoma bodies?

A

Serous cystadenoma

Psammoma- group of concentric, intracellular calcium collections seen in certain neoplasms

187
Q

Who usually gets epithelial ovarian tumours ?

A

Postmenopausal women

188
Q

What tumour marker is secreted by epithelial ovarian tumours

189
Q

Ovarian cystadenocarinomas: which type is more common

A

Serous> mucinous

190
Q

Name some germ cell ovarian tumours

A
  1. Dysgerminoma
  2. Yolk sac
  3. Choriocaricinoma
  4. Teratoma
191
Q

Histological clues for germ cell ovarian tumours

A
  1. Yolk sac- Schiller- duval bodies (looks like kidney glomeruli). Secretes alpha fetoprotein
  2. Choriocarcinoma- Cytotrophoblasts/syncytiotrophoblasts without chorionic villi
  3. Dysgerminoma- fried egg
  4. Teratoma- can have all cell types

Germ cell tumours are mostly malignant

192
Q

Which of the ovarian germ cell tumours is the most common malignant type?

A

Dysgerminoma

Young premenopausal women. Marker PLAP, LDH, bHCG

PLAP-placental like alkaline phosphatase

193
Q

Which demographic gets yolk sac tumours ?

A

Children/ adolescents

194
Q

Ovarian teratomas are divided into

A
  1. Mature- benign and well differentiated
  2. Immature- malignant
195
Q

Teratomas can undergo malignant transformations. T or F?

A

Yes, they can have tumour inside a tumour. Signs of hyperthyroidism

196
Q

List some ovarian sex cord tumours

A
  1. Granulosa- malignant
  2. Sertoli leydig cells- benign
197
Q

Call-exnar bodies are found in which types of tumours?

A

Granulosa cell

198
Q

Granulosa cell tumours and Sertoli Leydig cell tumours : Clinical features

A
  1. Sertoli= Symptoms of excessive androgens and/or estrogen production
    ↑ Testosterone
    Virilization, hirsutism, acne, temporal balding
    Amenorrhea, clitoral enlargement, ↓ fertility
    ↑ Estrogen
    Menstrual bleeding abnormalities
    Endometrial polyps and hyperplasia
  2. Granulosa cells= Symptoms caused by estrogen and/or progesterone secretion
    Adult subtype: menstrual irregularities (e.g., postmenopausal bleeding, endometrial hyperplasia with metrorrhagia)
    Juvenile subtype: precocious puberty, Breast tenderness, Associated with increased risk of endometrial cancer
199
Q

Cardiotocography: what is it?

A

A method used to measure foetal HR, uterine contractions and foetal movement during pregnancy. Used most commonly during the 3rd trimester.

200
Q

Fetal HR is normally at which range?

A

110-160 bpm

201
Q

What are some indications of CTG?

A
  1. During labour (4-5 contractions/10 min)
  2. Admission on labour ward
  3. Complicated cases such as multiple pregnancies, abnormal uterine bleeding etc
202
Q

Mnemonic to help remember the parts to look on a CTG

A

Dr- Define risk
C- contractions
BRA- baseline rate
V- variability
A-accelerations
D- Deceleration
O- overall

Dr C BRAVADO

203
Q

What is normal variability on CTG?

A

5-25bpm

Sinusoidal variability= fetal hypoxia, marked variability >25bpm= cord compression

204
Q

MNEMONIC for etiology of fetal HR alterations

A

VEAL CHOP
1. Variable decelerations= cord compression
2. Early decelerations= Head compression
3. Accelerations= ok
4. Late decelerations= Placental insufficiency/Problem

Late deceleration = Decrease in the FHR following the maximum contraction curve

205
Q

Methods to assess FHR?

A
  1. Nonstress test (NST)
  2. Contraction stress test (CST)
206
Q

Biophysical profile scoring criteria: is used when and interpretation

A
  • A noninvasive test that evaluates the risk of antenatal fetal death, usually performed after the 28th gestational week
  • Each parameter receives a score of either 0 (abnormal) or 2 (normal) points.
    ->Ultrasound exam ( Fetal movement, Fetal tone. Fetal breathing, Amniotic fluid volume)
    -> NST
207
Q

Induction of labour: indication

A
  1. Post- term pregnancy
  2. Maternal DM-> macrosomia
  3. Preterm premature rupture of membranes after 34 weeks
  4. Maternal request at term
  5. Intrauterine death
  6. Pre-eclampsia/ eclampsia. Maternal HTN
208
Q

Induction of labour: methods

A
  1. Prostaglandin E2 gel applied on posterior fornix of vagina. 2mg, atleast 6hr gap before next application
  2. Amniotomy (amnihook)
  3. Oxytocin after membrane rupture
  4. Finger sweeping method
209
Q

Induction of labour: Contraindications

A
  1. Absolute= acute fetal compromise, abnormal lie, placenta praevia or pelvic obstruction such as a pelvic mass or pelvic deformity causing cephalopelvic disproportion. It is usually considered inappropriate after more than one Caesarean section. Herpes infection too.
  2. Relative= past c-section and prematurity
210
Q

Bishop score: what does it involve, used for?

A
  1. Degree of effacement of the cervix
  2. Dilatation of the cervix
  3. Consistency of the cervix
  4. Position of the cervix in the vagina
  5. Station of the head

Used to assess cervix and the likelihood of a successful induction. >8= good , < 6= bad

211
Q

Vulval symptoms

List 3

A
  1. Soreness
  2. Pruritus
  3. Superficial dyspareunia (pain during penetration)
212
Q

Aminocentesis can be done from which time on?

A

15 weeks onwards

213
Q

List 5 diseases which affects the vulva

A
  1. Lichen simplex- autoimmune? linked with stress, low iron stores and can lead to thickened/ inflammed areas on vulva. Use emollients and antihistamines
  2. Lichen planus- flat, papular purple lesions
  3. Lichen sclerosus- The typical patient is postmenopausal. Appearance is of pink–white papules, which coalesce to form parchment-like skin with fis- sures
  4. Infections such as herpes simplex, candidiasis
  5. Bartholins cysts
214
Q

Diseases which can affect the vagina: list 3

A
  1. Bacterial vaginosis
  2. Trichomoniasis
  3. Gonorrhoea
215
Q

Bacterial vaginosis: Pathogen, Discharge and Tx

A
  1. Pathogen= Gardnerella vaginalis
  2. Discharge= Gray/milky, Fishy odor. You will also find clue cells on microscopy
  3. Tx= Metronidazole
216
Q

Trichomoniasis: Pathogen, discharge, Tx

A
  1. Pathogen= Trichomonas vaginalis
  2. Discharge= Frothy, yellow-green, Foul-smelling
  3. Tx= Metronidazole, Treat sexual partner(s)

Flagellated protozoa visible on micro

217
Q

Vaginal yeast infection: pathogen, discharge, Tx

A
  1. Pathogen= Candida albicans
  2. Discharge= White, crumbly, and thick (cottage cheese-like), Odorless
  3. Tx= Topical azoles or nystatin, Oral fluconazole in nonpregnant patients
218
Q

Gonorrhea: Pathogen, discharge, Tx

A
  1. Pathogen= Neisseria gonorrhoeae
  2. Discharge= Purulent, creamy
  3. Tx= ceftriaxone, tx partner too
219
Q

Aetiology of abnormal lie

A
  1. Condition which allows for more room to move- polyhydraminos, high parity which means the uterus is more lax
  2. Conditions which stop the foetus moving- uterine abnormalities, twin pregnancy
  3. Conditions which stops normal engagement- placenta praevia and pelvic tumours or uterine deformities

E.g. of abnormal lie, oblique or transverse

220
Q

Management of abnormal lie

A
  • No action before 37 weeks unless the woman is in labour.
  • After 37 weeks, the woman is usually admitted to hospital in case the membranes rupture and an ultrasound scan performed to exclude particular identifiable causes, notably polyhydramnios and placenta praevia.
221
Q

Rh isoimmunisation: tests to do to see if there is mixing and how much

A
  1. Rosette test= qualitative test to see if there is mixing
  2. Kleinhauer- Betke test= maternal blood smear is added to acid, fetal blood survives denature, you count them.
222
Q

Anti-D immunoglobulin: indication

A
  1. 28 weeks gestation
  2. Within 72hrs after the bith of a Rh+ baby
  3. Following any invasive procedures e.g. amniocentesis
  4. Any events which might incite mixing
223
Q

What is a good non-invasive method to look for fetal hemolytic disease and anaemia?

A

(Peak velocity) Middle Cerebral Artery doppler. Raised= high likelihood of anaemia

224
Q

New development for Tx/management of HDFN?

A

The use of cell-free fetal DNA (cffDNA) in maternal blood to determine Rhesus genotype type. Used in Denmark rn.

Prevents unnecessary anti-D prophylaxis

225
Q

Management of rhesus disease in a sensitized woman

A
  1. Titre blood to see level of immunoglobulin routinely
  2. Fetal transfusions if signs of severe anaemia and too premature to deliver
226
Q

Breech presentation: management

A
  1. From 37 week, external cephalic version (ECV) is attempted. Tocolytic can be used to make uterus less tense
  2. If failed C-section is an option
  3. Breech vaginal birth is risky in >4kg babies
227
Q

Breech presentation: complications

A
  1. Fetal head entrapment
  2. Birth trauma, neurological handicaps
  3. Genital tract injuries for mother
228
Q

Breech presentation: vaginal delivery methods

A

1.Loveset procedure= hold on the SI joint with thumbs and rotate 180 clockwise then counter clockwise, help deliver shoulders
2.Mauriceau–Smellie–Veit manoeuvre
3. Duhrssen incision if the head in entraped
4. Pinard manoeuvre= for frank breech. Apply pressure to popliteal fossa= flexion of knee, grab and deliver

Use US to assess the type of breech etc before attempting

229
Q

Which of the breech presentations posses the highest risk of cord prolapse?

230
Q

When can you encourage pushing during breech ?

A

After shoulders have delivered?

231
Q

Reasons why multiple pregnancy is increasing?

2 reasons

A
  1. Increasing number of assisted pregnancy
  2. Increasing age of conception
232
Q

Classification of multiple pregnancy

A
  1. Number of fetuses- twins, triplets etc
  2. Number of fertilised eggs
  3. Number of placentae: chorionicity
  4. Number of amniotic cavities: amnionicity
233
Q

In twin pregnancy which type is more common, dizygotic or mono?

234
Q

Monozygotic twins: when should division occur for them to have separate placentae and amniotic cavity

A

Shortly after fertilisation

235
Q

Division must occur when for conjoined twins?

A

From day 12 after conception onwards

A four-wheeler has SPACe for twins.” 1st four days (0–3): Separate placenta and amniotic sac; 2nd four days (4–7): shared Placenta; 3rd four days (8–11): shared Amniotic sac; day 12 and beyond: Conjoined twins.

236
Q

Complications of multiple pregnancy: maternal

A
  1. Preterm labour and birth (common in diamni/chorionic)
  2. Hyperemesis gravidarum
  3. Gestational diabetes
  4. Preeclampsia, eclampsia, pregnancy-induced hypertension
237
Q

Complications of multiple pregnancy: foetus

A
  1. Twin-Twin transfusion syndrome
  2. Increased risk of neonatal morbidity (growth restrictions, prematurity, cerebral palsy, congenital abnormalities) and mortality
238
Q

How is TTTS Dx?

A

Following ultrasound criteria:
* Single placental mass.
* Concordant gender.
* Oligohydramnios with maximum vertical pool (MVP) less than 2 cm in one sac and polyhydramnios in the other sac (MVP >8 cm).
* Discordant bladder appearances.
* Haemodynamic and cardiac compromise.

239
Q

TTTS: grading criteria

240
Q

TTTS: Tx

A
  1. Expectant management
  2. Amnioreduction
  3. Septostomy
  4. Selective feticide
  5. Fetoscopic laser ablation
  6. Above 26 weeks, delivery
241
Q

TTTS: antenatal care and management

A
  1. At least 8 appointments before, screen for hypertension and DM
  2. Offer first trimester scans when the CRL is 45-84mm roughly 11 weeks to 13 weeks
242
Q

Types of abortion

A
  1. Spontaneous
  2. Induced
243
Q

Types of induced abortion

2

A
  1. Medical
  2. Surgical
244
Q

Medical abortion: First trimester (< 12 weeks) drugs

A
  1. Up to 10 weeks= progesterone antagonist (mifepristone) and a prostaglandin analog (e.g., misoprostol) administered 24–48 hours apart
  2. Misoprostol single-agent regimen

Dilation and curettage= surgical

245
Q

Medical abortion: Second trimester (> 12 weeks) drugs

A
  1. Preferred: mifepristone followed 24–48 hours later by a prostaglandin analog (e.g., misoprostol)
  2. Oxytocin rarely used

Dilation and evacuation (D&E)= surgical

246
Q

Spontanous abortion: define

A

Loss of pregnancy before 20 weeks’ gestation

247
Q

Preclampsia: define

A

New onset of gestational HTN with proteinuria (>0.3 g/24 h) after 20 wks. Oedema is also present.

PRE= Proteinuira, Rising BP, End organ failure

248
Q

Gestational hypertension: define

A

Pregnancy induced HTN after 20 weeks. BP > 140/90mmHg or

an increase above booking readings of > 30 mmHg systolic or > 15 mmHg diastolic

249
Q

Chronic hypertension: define

A

Hypertension diagnosed before pregnancy or in the first 20 weeks of pregnancy

250
Q

Risk factor for pre-eclampsia

A
  1. Multiple pregnancy
  2. First pregnancy
  3. > 35yrs
  4. FHx
  5. African-american
  6. Hx of DM, HTN
251
Q

Pathophysiological of pre-eclampsia

A
  1. Not fully understood
  2. Abnormal placenta- spiral arteries not dilating enough therefore poorly perfused placenta. Leads to fetal growth restriction, release of proinflammatory markers
  3. These proinflammatory markers causes vasoconstriction, retain more salts
252
Q

Complication of Gestational HTN

A

Maternal= preeclampsia, eclampsia, stroke?
Foetal= placental abruption

253
Q

Preeclampsia: SSx, Dx, Tx

A
  1. SSx= general features of HTN (morning headaches, fatigue, dizziness). Could also have signs of local vasoconstriction such as blurry vision, RUQ pain, proteinuria
  2. Dx= Serial BP measurements, urine dip showing proteinuria. (2 reads 4hrs apart, or 15mins in emergency)
  3. Tx= delivery of placenta. Aspirin low dose for prophylaxis 12weeks gestation to delivery, magnesium sulfate and antihypertensives. Also think about corticosteroids for lung maturations

Antihypertensives used in pregnancy can be remembered with the mnemonic “Hypertensive Moms Need Love”: Hydralazine, Methyldopa, Nifedipine, or Labetalol

254
Q

Indication for immediate delivery

A
  • Eclampsia (cerebral symptoms)
  • Pulmonary edema
  • Disseminated intravascular coagulation
  • Placental abruption
  • Severe hypertension refractory to antihypertensives
  • Signs of fetal distress
  • Fetal demise or fetus unlikely to survive
255
Q

Eclampsia: define

A

New-onset seizures (tonic-clonic, focal, or multifocal) in the absence of other causes ; a convulsive manifestation of hypertensive pregnancy disorders

256
Q

Eclampsia: Tx

A
  1. Magnesium sulfate for seizure
  2. Immediate delivery of baby and placenta
  3. Left lateral decubitus to prevent hypoperfusion due to IVC compression
257
Q

HELLP syndrome: what is it? Management

A
  • Hemolysis (H), elevated liver (EL) enzymes, and low platelet (LP)
  • Complication of preeclampsia in 10-20% of pts
  • Administer blood products (e.g., platelets, PRBCs, FFP) as needed to manage hemorrhage and coagulopathy
  • Initiate antihypertensives for urgent blood pressure control in pregnancy.
  • Administer magnesium sulfate for seizure prophylaxis.
258
Q

Hb cut off in pregnant women

g/L

A

115 for non-pregnant women, 110 in early pregnancy, 105 in later pregnancy, and 100 after childbirth.

259
Q

Placental abruption: define

A

Separation of the placenta from the uterus prior to delivery

260
Q

Placental abruption: aetiology

A
  1. HTN/ preeclampsia
  2. Trauma
  3. Twin pregnancy
  4. Maternal age < 25 years or >35yrs
261
Q

Placental abruption: clinical features

A
  1. Sudden onset of vaginal bleeding. Sometimes this bleeding can be retroplacental therefore bleeding does not show
  2. Abdo/ back pain
  3. Hypertonic uterus contraction
  4. Uterine tenderness
  5. Fetal decelerations
262
Q

Placental abruption: Dx and Tx

A
  1. Dx= Look at CTG for signs of foetal distress, US to assess the uterus for bleeding/ placental positions, lab studies to look at CBC and coagulation
  2. Tx= vaginal delivery if active labour or C-section.
    If there is no fetal distress, the pregnancy is preterm and the degree of abruption appears to be minor, steroids are given (if < 34 weeks) and the patient is closely monitored on the antenatal ward

Digital vaginal examination is contraindicated unless placenta previa has been ruled out on ultrasound as it may worsen bleeding.

263
Q

Placental abruption: Complication

A
  1. Intrauterine death
  2. Maternal DIC/ hypovolaemic shock
  3. Couvelaire uterus= bleeding into the peritoneum

The placenta is rich in tissue thromboplastin, which is released as a result of the placental abruption.

264
Q

Placenta praevia: define

A

Presence of the placenta in the lower uterine segment, which can lead to partial or full obstruction of the internal os; high risk of hemorrhage (rupture of placental vessels) and birth complications

265
Q

Placenta praevia: risk factor

A
  1. Maternal age >35 years, multiparity, short intervals, between pregnancies
  2. Previous placenta praevia
  3. Previous curettage or c-section
266
Q

Placenta praevia: SSx, Dx, Tx

A
  1. SSx= Sudden, painless, bright red vaginal bleeding. Occurs during the 3rd trimester, usually no fetal distress (mothers)
  2. Dx= transvaginal or transabdominal ultrasound to assess placental position
  3. Tx= if presents with antepartum haemorrhage:
    * ≥ 37 weeks= immediate delivery
    * < 37 and Severe, active bleeding or fetal distress then emergency cesarean delivery. Light or no bleeding and no fetal distress= expectant management. Consider tocolytics to inhibit uterine contractions.

Lower segment c-section prefered

Monitor position of placenta, sometimes it will move up as the pregnancy porgresses

267
Q

Placenta praevia: classification

A
  1. Complete
  2. Partial
  3. Marginal (2mm)
268
Q

Postpartum haemorrhage: define

A

Obstetric emergency where there is blood loss more than 500ml (in first 24hrs post birth) or 12 weeks postpartum

Primary vs secondary

269
Q

Primary PPH: aetiology

A
  1. Tone= uterine atony
  2. Trauma= uterine rupture, laceration of the genital tract
  3. Tissue= retained products of conception, excessive traction on cord
  4. Thrombin= bleeding disorders (DIC, anticoagulants, preexisting disease e.g. vWD)

4 Ts; the retained uterus stops contractions->atony

270
Q

Secondary PPH: aetiology

A
  • Retained products of conception
  • Coagulation disorders (von Willebrand disease, haemophilia)
  • Infections
271
Q

Prevention of PPH

A
  1. Screen for anaemia
  2. Active management of 3rd stage of labour: using uterotonics (oxytocin), controlled cord traction
272
Q

Surgical management of PPH

A
  1. Uterine balloon tamponade
  2. B-Lynch suture
  3. Uterine a. embolisation
  4. Hysterectomy
273
Q

Analgesia during labour: non medical agents

A
  1. Back rubbing
  2. Transcutaneous electric nerve stimulation
274
Q

Analgesia in labour: medical

A
  1. Inhaled agents (nitrous oxide and o2)
  2. Systemic opiates (IM Pethidine.Need to administer antimetics)
  3. Epidural at L3/L4. Complete sensory inhib expect pressure (Bupivacaine)
275
Q

Anaesthesia in labour

A
  • Spinal epidural anaesthesia for C-section or mid cavity instrumental deliverty
  • Pudendal nerve for low cavity instrumental delivery
276
Q

Ectopic pregnancy: locations

A

Most commonly: fallopian tube (ampulla>isthmus>fimbriae> interstitial)
2.

277
Q

Ectopic pregnancy: risk factor

A
  1. Hx of PID
  2. Previous ectopic
  3. Surgeries involving the tubes
  4. Smoking
  5. > 35 yrs
278
Q

Ectopic pregnancy: SSx, Dx, Tx

A
  1. SSx= Lower abdominal pain and guarding (ectopic pregnancy is often mistaken for appendicitis), possible vaginal bleeding >6wks LMP, enlarged uterus, closed cervix, and motion tenderness. Tubal rupture (shock)
  2. Dx= b-hCG levels, TVUS
  3. Tx= depends on case. Expectant using methotrexate or wait. Surgical removal
279
Q

Preterm labour: risk factor

A
  1. Hx of preterm labour
  2. Cervical insufficiency (3 types)
  3. Multiple gestation
280
Q

Preterm labour: Clinical features, Dx

A
  1. Clinical features= uterine tightening, abdominal pain, fetal movements, PV bleeding/ fluid loss
  2. Dx= cervical changes, contractions, Cervicovaginal fetal fibronectin (fFN) test, cervical length <3 measured using US

Threatened PTL is contraction without cervical changes. fFN can be high if there was a bleeding or intercourse so not that reliable.

281
Q

Preterm labour: Tx

A
  1. If < 34wks then use corticosteroids for lung maturity. Indication: 24 0/7 weeks’ to 33 6/7 weeks’ gestation with a risk of delivery within the next 7 days
  2. Tocolysis: used to delay contraction. E.g. nifedipine, IV terbutaline
  3. Magnesium sulfate (<30/40)
  4. Abx should be used as prophylaxis against Group Bstrep coc
282
Q

Causes of DIC during pregnancy

A
  • Placental abruption
  • Pre-eclampsia
  • PPH
283
Q

Hyperemesis gravidarum: define

A

Severe, persistent nausea and vomiting associated with a > 5% loss of prepregnancy weight and ketonuria with no other identifiable cause

Risk factor= nulliparity, GERD, migraine headaches, multiple gestation, hydatidiform mole

284
Q

Hyperemesis gravidarum: SSx, Dx, Tx

A
  1. SSx= N/V, signs of dehydration, hypersalivation
  2. Dx= Clinical dx, look at labs for electrolytes and Hct for dehydration
  3. Tx= Ondansetron, Metoclopramide
285
Q

Vaginal/ vulvar cancer: aetiology

A
  1. HPV 16,18, 33 infections
  2. Smoking
  3. Precancerous lesions such as Lichen sclerosus
  4. Immunosuppression
286
Q

Vulvar cancer: clinical features

A
  1. Pruritus
  2. Lump/ mass
  3. Lymphadenopathy of groin
  4. Bleeding (less common)
  5. Dyspareunia/ dysuria
287
Q

Vaginal / vulvar cancer: classification

A
  • Most are squamous cell carcinoma
  • Clear cell adenocarcinoma seen in vaginal cancers of daughters of pts who received diethylstilbestrol during pregnancy
288
Q

Vaginal cancer: clinical features

A
  • Vaginal bleeding
  • Leukoplakia, vaginal ulceration with contact bleeding
  • Malodorous discharge
  • Possibly urinary frequency
289
Q

Vaginal cancer: Dx, Tx

A
  • Dx= pelvic exam, colposcopy if no clear vision lesion and abnormal cytology, biopsy
  • Tx= radiotherapy, surgical

Upper third of vagina is affected

290
Q

Vulval cancer: Dx, Tx

A
  • Dx=Pelvic exam and colposcopy, Biopsy
  • Tx= Wide local excision to remove the cancer, Groin lymph node dissection, Chemotherapy, Radiotherapy
291
Q

DIC in pregnancy: pathogenesis

A

Extensive vessels and tissues damage → release of thromboplastins → utilisation of the fibrinogen and other clotting factors in an aimless coagulation process → fibrin .→ stimulates fibrinolytic system → breaks fibrin and fibrinogen into FDP which have an anticoagulant effect → aggravates haemorrhage and shock → ischaemia → more tissue damage → viscious circle.

N.B. The anticoagulant effect of FDP is due to:

Inhibition of platelet function.
Interference with thrombin/ fibrinogen reaction.
Interference with fibrin polymerisation.
Interference with myometrial contraction.

292
Q

DIC in pregnancy: Dx and Tx

A

Dx= Lab (reduced fibrinogen, low platelet and increased Fibrin degradation products)
Tx= Eliminate underlying cause. Blood transfusions, frozen plasma

293
Q

Molar pregnancy is also known as?

A

Gestational trophoblastic disease

294
Q

Molar pregnancy occur due to?

A

Excessive proliferation of trophoblastic tissue, usually some form of chromosomal abnormality

295
Q

Hydatiform mole: the types

A
  1. Parital
  2. Complete
296
Q

Hydatiform mole: complete mole aetiology

A

Fertilisation of an empty egg by one sperm (46XX, 90%) or two sperm (46XX, XY)

297
Q

In a complete mole where does the genetic material come from?

A
  • Paternal
  • Diploid
  • No fetus- mass of chorionic villi
298
Q

Hydatiform mole: incomplete mole aetiology

A

Fertilisation of an ovum by 2 sperms giving: 69XXX, XYY,XXY

299
Q

Clinical features of hydatiform mole

A
  1. Vaginal bleeding
  2. Pelvic tenderness
  3. In complete mole the uterus is of a greater size than gestation age
  4. Endocrine symptoms (e.g, hyperemesis gravidarum, ovarian theca lutein cysts) in complete moles
300
Q

Level of b-hCG in gestational trophoblasts

A
  • High in all
  • partial< complete < choriocarcinoma
301
Q

Molar pregnancy: Dx and Tx

A
  1. Dx= Look at b-hCG levels which is elevated, ultrasound shows snowstorm in complete mole
  2. Tx= D&E of conceptional products, measure the levels of b-hCG in series, methotrexate can be given (unresolved)

p57 staining+ in parital

302
Q

If serial hCG levels are elevated after D&E in molar pregnancies, what does it suggest?

A

Gestational trophoblstic neoplasia

303
Q

Pathophysiology of Choriocarcinoma

A

Malignant transformation of cytotrophoblastic and syncytiotrophoblastic tissue

304
Q

Choriocarcinoma: clinical features

A
  1. Vaginal bleeding
  2. US shows highly vascular
  3. Cannonball metastases (aka to lungs)
305
Q

Choriocarcinoma : Tx

A

Chemo +/- hysterectomy and also monitor hcg level for 12 months

Good prognosis 95-100% curative rate

306
Q

Menopause: define

A

Time at which menstruation ceases permanently and confirmed after 12 months of amenorrhea in the absence of hormone contraceptives

307
Q

Menopause: SSx, Dx, Tx

A
  1. SSx= amenorrhoea, hot flushes, night sweats, loss of libido, mood swings, osteoporosis
  2. Dx= clinical. Labs can show low oestrogen/progestorone and high LH/FSH, gnrh
308
Q

Perimenopause: define

A

The period before menopause begins. Usually lasts 2-4 years

309
Q

Which other condition presents similar to perimenopause?

A

Hyperthyroidism

310
Q

Where does: kidneys, testes/ovaries, Mullerian/Wolffian ducts arise from ?

A
  • Nephrogenic cord= kidney
  • Genital ridge= ovaries/ testes
  • Urogenital ridge= ducts
311
Q

Anomalies of Mullerian ducts: can be divided into

The issues

A
  1. Duct fusion= unicornuate, bicornuate, didelphic uterus (2 separate)
  2. Septal reabsorption= septate, arcute (slightly poking in),
  3. Error in organogenesis= Mullerian agenesis
312
Q

Mullerian duct defects is accompanied by?

A

Renal agenesis usually

313
Q

Vaginal anomalies: problem with which part and example

A
  • Paramesonephric ducts
  • Transverse septate and longitudinal
314
Q

Mullerian anomalies: SSx, Dx

A
  1. SSx= pelvic pain and endometriosis, menstural anomalies (amenorrhoea, minimal bleed), obstetric problems (recurrent pregnancy loss, IUGR, malpresentation, preterm, retained placenta)
  2. Dx= MRI is gold standard
315
Q

Harlyn-Werner- Wunderlich syndrome: what is it?

A
  • Uterus didelphys
  • Unilateral obstructed hemivagina
  • Ipsilateral renal agenesis (to obstruction)
316
Q

Shoulder dystocia: risk factors

A
  • Hx of shoulder dystocia
  • Fetal macrosomia
  • Prolonged stage 2
  • Maternal DM
  • Maternal obesity
317
Q

Shoulder dystocia: clinical sign

A
  1. Turtle neck sign= the fetal head is partially delivered but retracts against the perineum
  2. Failed restitution of the head
  3. Arrest active phase of labour (>4hrs in 6cm dilation + adequate contraction, >6hrs in none)
318
Q

Shoulder dystocia: Tx

A
  1. Perform McRoberts
  2. Rubin is divided into 2. Rubin 1 (suprapubic pressure) is done along with McRobs. Rubin 2= use fingers to rotate the impacted anterior shoulder, trying to adduct + flex
  3. Woods corkscrew
  4. All four and try
  5. Episiotomy/ break clavicle/ Symphysiotomy
  6. Zavanelli maneuver- give tocolytic push head back and do c-section

20-30 seconds per manoeuvre

318
Q

Preterm: complication to baby

A
  1. PDA and respiratory distress
  2. Neurological= Periventricular leukomalacia (PVL), Intraventricular hemorrhage
  3. Hypothermia of prematurity
  4. Retinopathy of prematurity (ROP)
  5. Necrotizing enterocolitis (NEC)
319
Q

In PPROM: how do you confirm amniotic fluid in sterile speculum exam?

A
  1. Placental a-microglobulin-1 (PAMG-1)
  2. Litmus test, amniotic fluid is alkaline
  3. Fern pattern on glass slide
320
Q

Placenta can separate in 2 mechanism: which are they ?

A
  1. Schultze’s mechanism (80%). Comes of from the center as an inverted umbrella. Less retained products
  2. Duncan’s mechanism (20%). Comes from the side, more chance of retained products
321
Q

Timeline of development

A
  1. Day 0= fertilisation in the fallopian tubes, the sperm and ovum fuse togther to make zygote
  2. Day1-5= zygote->morula->blastocyst. Travels down uterus
  3. Day 6= Blastocyst attaches to the uterus. Trophoblast penetrates the endometrium (implantation bleeding)
  4. Day 6-14= Fetal placental unit develops
    5.Week 3 -4 = Gastrulation, development of upper lower limbs, first heart beat
    6.Week 5= organogenesis (complete by week8)
    7.Week 9-12= fetus matures, genitals have sex specific characteristic
322
Q

Endocrine disorders during pregnancy

A
  1. Gestational diabetes
  2. Thyroid: hypo/hyper
  3. Liver disease (acute fatty liver)
323
Q

Postpartum thyroiditis: phases, tx

A
  • Phases: hyperthyroidism due to release of stored thyroxine, then hypothyroidism for 4 months postpartum
  • Tx= the hyper phase is self-limiting, if needed use b-blockers. Hypo phase needes tx.

Check for thyroid levles in women who are depressive?

Obs/Gyn (2 decks)

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