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OB & Gynecology > Gyne > Flashcards

Gyne Flashcards

1
Q

How you approach patient with PCOS

A

Clinically: (maybe asymptomatic)
Menstrual irregularities - Acne - Hirsutism - Alopecia - Acanthosis nigricans - Obesity

Lab tests:
High LH + Androgen + Glucose + Prolactin
Low SHBG

Imaging:
Multiple cysts

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2
Q

U/S criteria for PCOS

A

High number of follicles & amount of stroma compared with normal ovaries, resulting in an
increase in ovarian volume

8 or more subcapsular follicular cysts <10 mm in diameter

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3
Q

Pathophysiology of PCOS

A

High LH & Low FSH (ton steroids affect feedback or hypothalamus dysfunction) causes:
- High androgen from theca cells (may cause high estrogen)
- Lower SHBG
- Inhibit follicular growth
- Dyslipidemia (High TG & LDL and Low HDL)
- High Prolactin

High insulin causes:
- High androgen by ovaries
- Suppress SHBG production
يخلي المرأة عندها اعراض اندروجين هواي مع انه مستواهم طبيعي
- Anovulation

Obesity:
- Insuli resistance
- Lower SHBG

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4
Q

How you diagnose patient with PCOS

A

Patients must have two out of the three features below:
• Amenorrhoea/oligomenorrhoea
• Clinical or biochemical hyperandrogenism
• Polycystic ovaries on ultrasound

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5
Q

Sign of profound insulin resistance

A

Acanthosis nigricans (AN)

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6
Q

DDx of PCOS (androgen excess)

A

Cushing syndrome
CAH
Partial 21-Hydroxylase deficiency
Androgen secreting tumour (arrenoblastoma - Granulosa-theca cell tumor - lutoma of pregnancy)
Hyperthecosis
Acromegaly
chronic anovulation associated with (hypothalamic amenorrhea - emotional disorders - thyroid disorder)
Turner syndrome

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7
Q

How you distinguish between PCOS & Prolacinoma

A

positive response to a progestogen challenge test [e.g. medroxyprogesterone acetate 10 – 20 mg (depending on body weight) daily for 5 days], which induces a withdrawal bleed, will distinguish patients with PCOS - related hyperprolactinaemia from those with polycystic ovaries and unrelated hyperprolactinaemia
because the latter causes oestrogen deficiency and therefore failure to respond to the progestogen challenge

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8
Q

Relation between TSH & Prolactin

A

TSH may trigger prolactin secretion, when you study there’s no prolactin stimulating hormone only inhibiting.
Hypothyroidism = Infertility

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9
Q

DDx of High LH

A

POI
PCOS
AIS

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10
Q

How metformin affects PCOS

A
  • Inhibits the production of hepatic glucose
  • Enhances the sensitivity of peripheral tissue to insulin
  • Ameliorate hyperandrogenism & abnormalities of gonadotrophin secretion

Remember/ There is no place for insulin -sensitizing agents (e.g. metformin) in the absence of impaired glucose tolerance

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11
Q

How Hyperandrogenesim is treated

A

Managed with Dianette, containing ethinyloestradiol in combination with
cyproterone acetate, or Yasmin, which contains drosperinone

Alternatives include spironolactone, and reliable contraception is required

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12
Q

Hirsutism & Virilisim

A

Hirsutism : increase in terminal hair on the face ,chest ,back and inner thighs in a women and the development of male escutcheon on the pubic hair(diamond , female is triangular).
It may be accompanied by anovulatory amenorrhoea, dysfunctional uterine bleeding ,or infertility.

Virilism : is development of hirsutism in addition to male features such as:
Deepining of the voice , frontal balding ,increased muscule mass , clitoromegaly , increased libido and may features of defeminisation, such as decreased breast size and loss of vaginal lubrication.

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13
Q

Causes of androgen excess

A

Hisutism and virilism are both a clinical manifestation of androgen excess.
The defect is either:
-Increase androgen production
-Increase androgen transport
-Increase target organ response

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14
Q

How you assess source of androgen

A
  • Half of testosterone and androsteindione is produced by the ovary and other half from the adrenal.
  • DHEA, DHEAS are mainly produced by the adrenal.

Note/ All preandrogen are converted in the liver to testosterone ,which is the main androgen

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15
Q

What are the drugs that cause androgen excess (Hirsutism)

A

Without virilization:
phenytoin, diazoxide ,ACTH ,coticosteroids.

With potential virilization:
progesterone, anabolic agent, androgen therapy.

Note/ Corticosteroid and androgen reduce SHBG so increase the free testosterone

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16
Q

Ovarian neoplasms that lead to Hirsutism

A

-Androgen secreting ovarian tumors are extremely uncommon (functional tumor) or other like cystadenoma or krukenberg’s tumor (non functional) will stimulate proiferation in adjecent ovarian stroma result in increase androgen production

-Arrenoblastoma or sertoli-leydig cell tumor (Palpable mass)

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17
Q

How you evaluate PCOS

A

History :
- Onset: sudden(neoplastic), gradual(PCOS)
- Symptoms of hirsutism and virilism
- Menstrual history: regular(ideopathic)
- Drug history
- Family history

Examination:
- Distribution of hair: (modified Ferriman and Gallway score) severity
- Body habitus and female contour
- Breast examination for atrophic changes
- Features of PCOS or cushing syndrome
- Pelvic examination to exclude ovarian tumor

Laboratory evaluation:
- Free testosterone(androgen excess) level >200ng/dl suggest adrenal neoplasm
-17 hydroxyprogesterone (CAH) and DHEAS (adrenal cause)
- LH:FSH ratio >3 indicate PCOS

Imaging:
- Pelvic ultrasound (ovarian tumor,PCOS)
- CT scan or MRI (adrenal and ovarian tumor)
- Dexamethasone suppression test if cushing syndrome is suspected(1mg ,8:00am cortiol level should be less than 5 microg/dl) if positive high dose test should be performed.

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18
Q

How you treat idiopathic Hirsutism

A

Cosmotic treament are:
- Temporary: Bleaching , shaving, chemical and wax depilators
- Perminant: electrolysis, laser

Note/ Medical treatment only after 👆🏻 failure

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19
Q

How COCP benefit PCOS Patients

A
  • Decrease ovarian and adrenal production of steroids (androgen)
  • Progesterone suppress LH reduce ovarian androgen synthesis
  • Estrogen increase hepatic production of SHBG reduce free testosterone
  • Estrogen decrease the conversion of testosterone to DHT in the skin by inhibiting the 5 alpha reductase
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20
Q

What is Dianette

A
  • Cyproterone acetate: (treatment required for 24- 36 months)
    Is synthetic progesterone acts by inhibiting androgen binding to the cytoplasmic receptors.
    It cause irregular bleeding so it should be combined with ethinyl estradiol.

100mg for 10 days + Ethynil estradiol for 21 days

  • Dianette is 30microgram ethinyl estradiol with 2mg cyproterone acetate
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21
Q

Spironolactone for Hirsutism

A

Spironolactone: diuretic , inhibits androgen biosynthesis and have anti androgen action in target cell
Dose is 25-100 mg daily

Note/ Flutamide not used due to liver toxicity

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22
Q

Why we use COCP with Cyproterone acetate or Spironolactone or finestride

A

Due to the risk of feminization in male fetuses if pregnancy occur

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23
Q

What are the anti androgens

A

CPA

Spironolactone

Ketoconazole (Steroidogenic enzyme inhibitor) :
- Reduce androgen when given in a low dose of 200 mg/day

Finasteride (5 alpha reductase inhibitor)
- 7.5 mg /day

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24
Q

What’s Climacteric or perimenopause

A

Time of until 1 year after the last period and the diagnosis of menopause is made

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25
Q

Can pregnancy or age of menarche affect menopause time

A

The age of menopause is not related to age of menarche or age at last pregnancy.
It is also not related to number of pregnancy, lactation, use of oral pills

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26
Q

Can menopause occurs artificially

A

creating artificial menopause to suppress oestrogen secretion from the ovary in premenopausal women treated with radiation for breast cancer

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27
Q

What are the urinary Sx in menopause

A
  • Dysuria, frequency, and urgency which suggest a urinary tract infection ( UTI ) but associated with a negative urine culture
  • Stress incontinence may also be present
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28
Q

Fractures after menopause

A

Oestrogen keeps the balance between bone formation and bone resorption and after menopause there will be greater bone resorption than formation

As trabecular bone is a shock-absorbing bone so it becomes more liable to fracture after minimal or moderate trauma.

The net result is that after menopause there is a progressive rise in the incidence of fracture of the trabecular sites.

Traumatic fracture affects the distal radius and femoral neck, whereas non-traumatic fracture affects the vertebrae.

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29
Q

Risk factors for osteoporosis

A
  • Age
  • Family Hx
  • Diet & Low BMi
  • Lack of Oestrogen or Early menopause
  • Drugs (Heparin, GnRH analog, steroids, anticonvulsants)
  • PMD Hx: RA, Hyperparathyroidisim, Thyroid disorders
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30
Q

Does HRT increases weight

A

In fact, evidences confirm that there is no correlation between HRT and menopausal weight gain

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31
Q

Medical Tx for hot flushes

A
  • Clonidine
  • Propranolol
  • SSRIs (am, etine, xine)
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32
Q

Causes of PM bleeding

A
  • Endometrial or vaginal atrophy (lining of the uterus or vagina becomes thin and dry)
  • Hormone replacement therapy (HRT)
  • Uterine cancer or endometrial cancer or cervical cancer
  • Endometrial hyperplasia
  • Uterine polyps and fibroid
  • Cervicitis or endometritis
  • Bleeding from other areas, nearby, in the bladder or rectum or bleeding from the skin of the vulva (outside near the vagina).
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33
Q

Things to keep in mind regarding PMB Hx

A
  • Age & Time of menopause
  • Obesity & Hormone Therapy & Anticoagulants
  • DM & HTN & Hypothyroidism & PCOS
  • Pap smear & Family Hx of malignancy
  • Nulliparity
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34
Q

1st step in investigations for PMB

A

Either transvaginal ultrasonography or office-based endometrial biopsy
should be used as the first step of investigation for women with PMB

Note/ Threshold thickness 4mm

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35
Q

Endometrial biopsy should be performed in the outpatient clinic if:

A
  • Endometrial thickness is greater than the agreed threshold (ET ≥4 mm)
  • Endometrial thickness 4 but with bleeding
  • Endometrial thickness is not clearly visualized by U/S
  • Persistent PMB regardless of ET
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36
Q

What are the Indications for hysteroscopy

A
  • Failed office-based endometrial biopsy
  • Inadequate tissue obtained using an office-based device
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37
Q

How you treat vaginal atrophy

A

Oestrogen daily for 2 weeks, then once- twice weekly for maintenance

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38
Q

What’s heavy menstrual bleeding

A

Defined as excessive menstrual blood loss that has major effect on woman quality of life (anaemia, SOB, Low immunity, Fatigue)

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39
Q

Fibroid Subtypes which are most commonly associated with HMB and IMB

A

submucosal and intramural

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40
Q

What’s N in PALM COEIN

A

Notother wise classified:
- Arteriovenous malformation
- Infection with chlamydia trachomatis

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41
Q

What’s the O in PALM COEIN

A

Ovulatory dysfunction:
- Extremes of age
- PCOS
- Hyperprolactinemia
- Hypothyroidism
- Obesity

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42
Q

Hx of abnormal uterine bleeding

A
  • Details about bleeding
  • S&S of Anaemia
  • Pregnancy & Contraception
  • History of excessive bleeding since menarche , epistaxis ,PPH, bleeding with dental work , easy bruising
  • postcoital bleeding
  • Pressure symptoms like bowel , urinary symptoms may indicate the presence of large fibroids
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43
Q

Evaluation of uterine cavity (pelvic U/S ,MRI and hysteroscopy) usually done in what coditions

A

-intermestrual bleeding
-postcoital bleeding
-irregular HMB
-suspected structural pathology
-when medical therapy failed

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44
Q

The development of gonads begin at the … with development of …

A

5th wks of gestation, gonadal ridge

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45
Q

The primordial germ cells migrate into the developing gonads at …

A

Between the 4th and 6th wks

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46
Q

Talk about development of male internal genitalia

A
  • قنوات وولف ومولر موجودات في مرحلة التكون اللاجنسية حتى الى حد الاسبوع الثامن من التكون الجنيني، في حالة وجود الكروموسوم Y ستقوم خلايا لايدنج بافراز التستوستيرون الذي يحول قناة وولف الى ابددمس وفاز دفرنس وحويصلات منوية لكن ابداً لا يكون خصى لإنها سبق وان تكونت
  • The Sertoli cell of testis produce Mullerian inhibiting substance which suppress the development of
    internal female genitalia from mullerian duct in male
  • Testes already developed at 5th week by SRY gene on the short arm of Y chromosome
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47
Q

Talk about female internal genital organs development

A
  • In the absence of this Y chromosome the bipotential gonad differentiates into an ovary at 5th week from gonadal ridge
  • The primordial germ cells migrate into the developing gonads between the 4th and 6th wks simultaneously proliferating at the same time
  • In the absence of gonadal testosterone the wollfian duct will regress
  • In the absence of mullerian inhibiting substance in the female ,the mullerian duct will develop passively to form fallopian tubes ,uterus and upper vagina
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48
Q

The external genitalia can be recognised as male or female at … by U/S

A

16th wks of gestation

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49
Q

From where external genitalia forms (in male or female)

A
  • Genital tubercle
  • Urogenital sinus
  • Lateral labioscrotal folds or swellings
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50
Q

How external male genitalia forms

A

In the presence of testosterne:
- Genital tubercle form penis
- Edge of urogenital sinus fuse to form penile urethra
- Labioscrotal fold will fuse to form the scrotum

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51
Q

How female external genitalia forms

A

In the absence of testosterone
- Genital tubercle develops into clitoris
- Urogenital sinus develops labia minora
- Genital fold into labia majora

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52
Q

What vulva consist of

A
  • Mona pubis
  • Labia majora and minora
  • Opening of both urethra and vagina
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53
Q

When labia majora & minora fuses, what they form anteriorly and posteriorly

A
  • Anteriorly they come together to form the preouse of the clitoris
  • Posteriorly they form the fourchette
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54
Q

What’s the nerve & the artery that supplies the vulva

A

PUDENDAL

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55
Q

What vagina has near the cervix

A

Anterior and Posterior fornices

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56
Q

Epithelium of Vagina

A

Contain no gland but rich in glycogen and lactobacilli

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57
Q

Talk about serosa and myometrium of the uterus

A
  • Serosal surface is the closely applied peritoneum
  • Myometrium comprises the layers of muscle ;external ,intermediate and internal that run in complementary directions encouraging vascular occlusion during contractions
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58
Q

Lining of the cervix and what’s in it’s upper and lower portion (consisting of)

A
  • Muscular in upper portion and consist of fibrous tissue in its lower portion
  • Lined by columnar epithelium
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59
Q

What are the ligaments that support the uterus

A
  • Pubocrvical
  • Lateral cervical (cardinal)
  • Uterosacral
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60
Q

What ligaments the ovary attached to

A
  • Posterior leaf of broad ligament
  • Ovarian ligament
  • Infudibulopelvic ligament which contain its blood supply directly from aorta
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61
Q

Uterine artery origin

A

IIA

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62
Q

What are the parts of fallopian tubes and what supplies them

A
  • Uterine artery & Ovarian artery
  • Parts:
  • Cornua
  • Interstitial portion
  • Isthmus
  • Infundibulum
  • Ampulla
  • Fimbrial end
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63
Q

The ovaries covered by

A
  • Peritoneum
  • Thin capsule (tunica albuginea)
  • Germinal epithelium
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64
Q

Venous drainage of ovaries

A
  • Right to IVC
  • Left to left renal vein
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65
Q

Define primary and secondary amenorrhea

A
  • 1ry in 14 ~> 2ry characters ❌
    1ry in 16 ~> 2ry characters ✅
  • Secondary amenorrhea is diagnosed with absence of menses for three months if previously regular menses or six months if previously irregular menses
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66
Q

Causes of 1ry amenorrhea

A
  • Hypothalamus: Kallman syndrome (isolated GnRH def) & Weight loss/anorexia & Excessive exercise
  • Ovaries: Resistant ovary syndrome & Turner syndrome & Agenesis & Galactosaemia & failure (chemo)
  • Uterus: Mullerian agenesis & AIS
  • Cervix: Atresia
  • Vagina: Transverse septum & Imperforate hymen
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67
Q

Causes of 2ry amenorrhea

A
  • Hypothalamus: Psychological & Drugs
  • Pituitary: Sheehan syndrome & Prolactinoma & Empty sella syndrome
  • Ovaries: POI & Menopause & PCOS
  • Uterus: Asherman & Pregnancy
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68
Q

Why there’s amenorrhea in resistant ovary syndrome but there are secondary sexual characteristics

A

Ovaries inability to respond to hormonal signals that normally trigger regular release of eggs and the menstrual cycle. As a result, estrogen production may be insufficient to support regular menstruation

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69
Q

How you suspect mullerian agenesis (MRKH) and confirm it

A

absence of the vagina & uterus (blind & vaginal dimple <1.5cm in depth) which can be seen by rectal
& perineal examination & it is confirmed by U/S

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70
Q

Most common cause of amenorrhea and second common

A

M/C = Turner
2nd common = MRKH

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71
Q

In AIS, is vagina present

A

Only lower part because it has nothing to do with mullerian duct

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72
Q

Imperforate hymen features

A
  • Hx of cyclical symptoms results in hematocolpos
  • Difficulty with micturition & defecation
  • Observation of the introitus will display a tense bulging bluish membrane
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73
Q

Constitutional delay

A

Normal secondary sexual characteristics, anatomical & endocrine investigation is all normal, young women are found to have immature pulsatile release of GnRH, & they menstruate spontaneously as the maturation process proceeds

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74
Q

How anorexia contribute to amenorrhea

A

Failure of the activation of the gene, which initiates GnRH release in the hypogonadotrophic state

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75
Q

What karyotype can be seen in gonadal agenesis

A
  • 46 XY
  • 46 XX
  • 45 X
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76
Q

How ovarian failure can cause 1ry amenorrhea

A

Chemotherapy for childhood malignancy

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77
Q

Galactosemia

A
  • Inborn error of galactose-1-phosphate uridyl transferase
  • Acute toxic syndrome causes ovarian cellular destruction, which is though to be due to the accumulation of galactose metabolites
78
Q

In gonadal dysgenesis there’s condition caused by deletion, mention it

A

Deletion involves a part of the long arm of the X chromosome or short arm, & then loss of this genetic material may be affect gonadal development (but patient is still 46xx)

79
Q

Talk about turner syndrome & why do they have Short stature

A
  • In Turner syndrome ovarian development is normal until 20 weeks of gestation & at this stage oocytes are found in the ovaries, Future maturation is impaired & massive atresia occurs during latter pregnancy
  • The ovaries in most patients consist solely of stroma & are unable to produce oestrogen
  • Loss of an X chromosome results in short stature as genes for height on short arm of X chromosome
80
Q

In 1ry amenorrhea mention causes of Secondary sexual characteristics absent but with short stature

A
  • Congenital infection:
    most commonly the hydrocephalus, as a result of childhood or neonatal infection
    leading to damage to the hypothalamus & hypo gonadotrophic hypogonadism
  • Trauma:
    to the base of the skull may damage the hypothalamus & prevent GnRH secretion
  • Empty sella syndrome:
    congenital absence of the pituitary gland or at least part of it leading to failure to produce gonadotropins
  • Tumors:
    pituitary tumors like craniopharyngiom in childhood leads to destruction of the pituitary gland
81
Q

Heterosexual development causes

A
  • Androgen secreting tumour
  • 5 a reductase enzyme deficiency
  • CAH or partial deficiency
  • Hermaphrodite
  • Absent mullerian inhibitor
82
Q

46 XX patients will have … as causes for 1ry amenorrhea

A
  • premature ovarian failure (chemo)
  • resistant ovary syndrome
  • gonadal agenesis
83
Q

Patients with 46XY will have … as cause of 1ry amenorrhea

A
  • gonadal agenesis
  • testicular enzymatic failure
84
Q

Causes of 1ry amenorrhea with normal height

A
  • Kellman syndrome
  • Severe exercise or Anorexia
  • Gonadal agenesis
  • Gonadal dysgenesis
  • Resistant ovarian failure
  • Galactosemia
  • Turner mosaic
85
Q

1ry amenorrhea + Short stature + Low (FSH & LH) means

A

Intracranial lesion

86
Q

In absence of 2ry sexual characteristics, what are your steps of investigations

A
  • Assess heigh, if normal
  • FSH & LH, if normal
  • Do karyotype

Note: Don’t forget U/S before LH & FSH

87
Q

Causes of 2ry amenorrhea

A
  • Uterine causes: Asherman s syndrome, cervical stenosis
  • Ovarian causes: PCOS, POI
  • Hypothalamic causes: weight loss, exercise, chronic illness, psychological distress & drugs
  • Pituitary causes: hyperprolactinemia, Sheehan’s syndrome
  • Hypothalamic/pituitary damage: craniopharyngioma, cranial irradiation, head injury
  • Systemic causes: sarcoidosis, TB, thyroid disease, cushings syndrome
88
Q

Tx of kellman syndrome

A

Oestrogen only for about 2 years then 2-3 years gradual progesterone

89
Q

Dx & Mx of Asherman syndrome

A

Dx: HSG & Hysteroscopy
Tx: adhesiolysis of the anterior & post adhesion bridge
Following surgery:
- 3 months course of cyclic progesterone/oestrogen
- Insertion of Foley catheter into the uterine cavity for 7-10 days post operative
- IUCD for 2-3 months

90
Q

Only major cause of amenorrhoea that is not associated with oestrogen deficiency

A

PCOS

91
Q

Dx of Hyperprolactinemia

A
  • Prolactine level is high (> 1000mU/L)
  • Image pituitary fossa by CT or MRI
92
Q

Mx of Hyperprolactinemia

A
  • Bromocriptine is used 2.5-7 mg daily in divided dose
  • Cabergoline 1mg twice weekly
  • Surgery (in drug resistance): transsphenoidal adenectomy
93
Q

Regular menstrual cycles would not occur if the BMI is less than

A

19 Kg/squared meter

94
Q

Exercise - related amenorrhoea Mx

A

Diet & Cyclical oestrogen/ progesterone preparation

95
Q

Endometriosis sites

A
  • Peritoneum lining the pelvic side walls
  • Pouch of Douglas
  • Uterosacral ligaments
  • Deep infiltration: rectovaginal septum and bladder
  • If Ovary, an endometrioma forms (chocolate cyst)
  • Umbilicus, abdominal scars and the pleural cavity
  • Nose
96
Q

Sampson’s implantation theory

A
  • Sampson’s implantation theory postulates that it is this retrograde menstrual regurgitation of viable endometrial glands and tissue along patent Fallopian tubes, and that subsequent implantation on the pelvic peritoneal surface causes endometriosis
  • Menstrual blood can be seen within the pelvis during laparoscopy at the time of menses
97
Q

What supports sampson theory

A

Implantation of endometrium within surgical scars after CS or perineal repair following delivery

98
Q

Meyer’s ‘coelomic metaplasia’ theory

A
  • Coelomic epithelium transformation describes the redifferentiation of peritoneal cells lining the Müllerian duct back to their primitive origin, which then transform into endometrial cells
  • This transformation may be due to hormonal stimuli or inflammatory irritation
99
Q

Genetic and immunological factors as theory for endometriosis

A
  • It has been suggested that genetic and immunological factors may alter the susceptibility of a woman and allow her to develop endometriosis
  • There appears to be an increased incidence in first-degree relatives of patients with the disorder and racial differences
100
Q

Vascular and lymphatic spread as theory for endometriosis

A
  • Vascular and lymphatic embolization to distant sites has been demonstrated and explains the rare findings of endometriosis in sites outside the peritoneal cavity, such as the lung
101
Q

How patient with endometriosis will presents

A
  • Pain
    severe cyclical non-colicky pelvic pain restricted to around the time of menstruation
    sometimes associated with heavy menstrual loss
    may starts days before mense occurs
  • Deep pain with intercourse (deep dyspareunia) and on defecation (dyschezia)
    key indicators of the presence of endometriosis deep within the pouch of Douglas
  • Epistaxis & Rectal bleeding with colon deposits
102
Q

Can examination be useful in Dx of Endometriosis

A

No, it’s suspected even if PV is normal
But however there maybe some positive findings:
- Thickening or nodularity of the uterosacral ligaments
- Tenderness in the pouch of Douglas
- Adnexal mass (chocolate cyst)
- Fixed retroverted uterus (adhesions)

103
Q

DDx for restricted mobility of the uterus

A
  • Chronic PID
  • Uterine, ovarian or cervical malignancy
104
Q

TV U/S in Dx of Endometriosis

A
  • Endometriomas or chocolate cysts
  • Ovaries fixed together or to the back of the uterus (kissing ovaries)
  • In women with S&S of rectal endometriosis, TVUSS may be useful for identifying rectal disease
105
Q

MRI for Endometriosis

A
  • Detect lesions >5 mm in size, particularly in deep tissues, for example the rectovaginal septum
  • This can allow careful pre -surgical planning in difficult cases
106
Q

Laparascopy in Endometriosis

A
  • Depend on experience of the surgeon
  • Lesions can be red, puckered, black ‘matchstick’ or appear white and fibrous (frozen pelvis)
  • Advantages:
    Allows lesions to be biopsied for histological confirmation of diagnosis
    Affords concurrent surgical diathermy and/or excision of the endometriotic lesions
    Staging of the disease
    Patency of the Fallopian tubes
107
Q

Does endometriosis cause infertility

A

30% and 40% of patients with endometriosis complain of difficulty in conceiving

108
Q

Does medical Tx for endometriosis improves fertility

A
  • No, It does not improve fertility and should not be given to patients wishing to conceive
  • Instead, surgical ablation/excision of minimal and mild endometriosis does improve fertility chances
109
Q

What are the medical therapy options for endometriosis

A
  • NSAIDS
  • COCP
  • Progestigens (LARCs)
  • GnRH-a
  • Danazol & Gestrinone
  • Aromatase inhibitors
110
Q

NSAIDS for endometriosis

A
  • Have no specific impact on the disease and hence their use is for symptom control only
  • Useful for Dysmenorrhea & Pelvic pain
111
Q

Can we use codeine/opiates for pain in endometriosis

A

No, they should be avoided as coexisting IBS symptoms can be worsened & exacerbating pelvic pain

112
Q

COCP for endometriosis and how to use it

A
  • Only if no contraindications and no desire for fertility
  • Relieve Dyspareunia & Dysmenorrhoea & non-menstrual pain & Cycle control & contraception

How to use:
* sequentially with the usual 7-day pill-free break
* tricycled (where three packets are taken back to back
* continuously without a break, inducing amenorrhoea

Note/ If the COCP achieves symptomatic relief, then this therapy can be continued for several years until pregnancy is intended

Note/ If symptoms persist, the diagnosis should be reviewed and common coexisting conditions such as irritable bowel disease and constipation treated

113
Q

When we should consider using PRG for endometriosis and what formulas are available

A
  • In those who have risk factors for COCP
  • Depot-medroxyprogesterone acetate and Mirena

Note/ Useful in providing a long-term therapeutic effect particularly after surgical treatment

114
Q

GnRH-a for endometriosis

A
  • Effective in relieving the severity and symptoms of endometriosis as well as for Dx
  • Recurrence after cessation of therapy is rapid
  • They are available as multiple, daily-administered intranasal sprays but are usually administered as slow- release depot formulations, each lasting for 1 month or more
115
Q

Why we stopped using Danzol and Gestrinone for endometriosis

A
  • Newer treatment have become available, notably LNG-IUS
  • Androgenic side-effectssuch as:
    weight gain & greasy skin & acne & alterations in lipid profiles & liver function & deepening of the voice
116
Q

Symptoms of Adenomyosis

A

Dysmenorrhoea (pain throughout menses), uterine enlargement and HMB

117
Q

Fertility sparing surgeries for Endometriosis

A
  • Symptomatic endometriotic chocolate cysts should not just be drained but the inner cyst lining should be excised to reduce the risk of recurrence; however, this will be associated with damage to functional ovarian tissue
  • اذا هاي السست سوبرفيشيال تكدر تسويلها ابليشن او تشيلها
  • تحتاج جراح ماهر في حال اكو التصاقات هواي او المرض ضارب اعضاء الجهاز الهضمي او المثانة او صاير rectovaginal nodules
  • تحتاج ميدكال ثيرابي بعد العملية لإن الrecurrence عالي
118
Q

Hysterectomy and Oophrectomy for Endometriosis

A

• Hysterectomy with removal of the ovaries and all visible endometriosis lesions should be considered only in women who have completed their family and failed to respond to more conservative treatments

• Women should be informed that hysterectomy will not necessarily cure the symptoms or the disease

• Oestrogen-only HRT can be started immediately following surgery once the patient is mobile, but some surgeons prefer to defer commencing HRT for up to 6 months to prevent activation of any residual disease

• Combined (oestrogen and progestogen) HRT can also be considered as a suppressive treatment, where reactivation of new or residual disease is suspected

119
Q

ADENOMYOSIS can only be definitively diagnosed following

A

Histopathological examination of a hysterectomy specimen

120
Q

Investigation of choice in Adenomyosis

A

MRI

121
Q

How you Dx Adenomyosis

A
  • Multiparous woman in late 30 or early 40 with and sometimes tender ‘boggy’ uterus
  • Dysmenorrhoea (pain throughout menses), uterine enlargement and HMB
  • U/S if localised showing haemorrhage-filled endometrial glands or irregular nodular (= fibroids)
  • MRI
122
Q

Mx of Adenomyosis

A

• LNG-IUS and depot Provero and short term GnRH agonists should be considered
• On ceasing treatment, however, the symptoms rapidly return in the majority of patients, and hysterectomy remains the only definitive treatment

123
Q

What can be effective for treating cyclical and non-cyclical pelvic pain associated with endometriosis

A

Analgesics and hormonal ovarian suppression

124
Q

Medical treatment of presumed endometriosis can be started if

A

Clinical examination and TVUSS are normal, without the need for more invasive laparoscopy

125
Q

If you started medical Tx for endometriosis, when you consider Laproscopy

A

If no symptom relief is obtained after 3–6 months of treatment, a laparoscopy should be considered

126
Q

What’s cervical ectropian

A
  • Columnar epithelium replaced squamous epithelium and Visible on the ectocervix as a circular, red area surrounding the external cervical os
  • Causes Intermenstrual and postcoital bleeding
  • Causes excessive, clear, odourless mucus-type discharge
127
Q

Is ectropian the same as ulcer or erosion

A

No, it’s normal finding and should not be called “cervical erosion” OR ulcer

128
Q

Causes of cervical ectropian

A

‘3 Ps’:
- puberty
- pregnancy
- pill

129
Q

Is there any bleeding with ectropian

A

IMB & Postcoital

130
Q

Is ectropian assisted with discharge

A

Excessive
Clear
Odourless
Mucus-type

131
Q

Is ectropian tender on speculum examination

A

No, but if you rub it with gauze this will lead to spotting

132
Q

Tx of ectropian

A
  • Prior to Tx, take swap and confirm normal cytology of the cervix
  • Change Oestrogen based CCP
  • Glandular producing columnar cells are ablated, usually with cryocautery as an outpatient
133
Q

What’s Nabothian follicles

A
  • Columnar glands within transformation zone become sealed over by squamous cells forming small, mucus-filled cysts visible on the ectocervix
  • No pathological significance
  • No Tx required although extremely large ones can be drained using a large-bore needle
134
Q

Cervical polyp

A
  • Benign tumours arising from endocervical epithelium and seen as smooth, reddish protrusions
  • Usually asymptomatic, being identified incidentally during a routine cervical smear
  • As cervical ectropion can cause vaginal discharge, IMB and PCB
  • Easily removed by avulsion with polyp forceps as an outpatient
135
Q

What’s Endometrial polyp

A

Focal endometrial outgrowths containing a variable amount of glands, stroma and blood vessels ,may be pedunculated or sessile, single or multiple and vary in size (0.5–4 cm)

136
Q

Risk factors for developing endometrial polyp

A
  • Obesity
  • Early menarche & Late menopause
  • Tamoxifen or HRT
  • Nulliparity
137
Q

Symptoms of Endometrial polyp

A
  • Maybe asymptomatic
  • AUB: HMB, IMB and postmenopausal bleeding [PMB]
  • May affect implantation and leads to infertility
138
Q

Is fibroid hormone sensitive to cyclical hormonal changes

A

Most polyps are relatively insensitive to cyclical hormonal changes, leading them to persist and cause unscheduled vaginal bleeding

139
Q

Cervical intaepithelial neoplasia (CIN) denote a continuum of disorders ranging from what to what?
From where they arise?
How they are described?

A
  • Can be described as the preinvasive stage of the cancer cervix
  • Ranging from mild through moderate to sever dysplasia and carcinoma in situ
  • Arise from area of metaplasia in transformation zone at the squamocolumnar junction
140
Q

How CIN differs from invasive cancer

A

Basement membrane remain intact not penetrated

141
Q

How cervical dysplasia classified according to WHO

A
  • Classified into mild , moderate and severe dysplasia and separate category called carcinoma in situ CIS
  • The term CIN was introduced by Richart (1968)
  • CIN1 represent mild to moderate dysplasia
  • CIN2 intermediate grade dysplasia
  • CIN3 represent severe dysplasia and carcinoma in situ
142
Q

How cervical dysplasia classified According to Bethesda system

A

• Low grade squamous intraepithelial lesion (LSIL): correspond to CIN 1
• High grade squamous intraepithelial lesion (HSIL): which includes CIN 2 and CIN 3

143
Q

شنو التغيرات السرطانية الي تصير بالخلية

A

الخلية تكبر والسايتوبلازم يقل

144
Q

Why CIN now is more common now among women

A
  • HPV (sexually transmitted disease)
  • Sex before age 16
  • Smoking
145
Q

What’s Fibroid

A
  • Uterine leiomyomata or fibroids are the most common benign tumors of the female genital tract, arising from neoplastic transformation of single smooth muscle cells of the myometrium
  • They usually appear as well‐circumscribed firm tumors with a characteristic white‐whorled appearance on cross‐section
  • The vast majority ot fibroids are found in the cocur in the cervix, terine ligaments any ovary
  • Fibroids may be single but are commonly multiple their size varies greatly
146
Q

Figo classification for Fibroids

A

0
Pedunculated submucous fibroid
1
submucous fibroid, < 50% intramural east als
2
submucous fibroid, ≥50% intramural
3
completely intramural fibroid but abutting the endometrium
4
completely intramural without Contact with endometrium or serosa
5
Subserous fibroid, ≥50% intramural
6
Subserous fibroid, <50% intramural
7
Pedunculated Subserous fibroid
8
others (e.g. cervical, parasitic)

147
Q

What increases and decreases risk for fibroids

A

Increase
- Age
- Race: Afro‐Caribbean having a 2-9 fold greater risk and they tend to present at younger age
- Obesity

Decrease
- Multiparty
- Smoking
- Prolonged use of OCCP

148
Q

What’s Red degeneration

A
  • Haemorrhage and necrosis occurs within the fibroid typically presenting in the mid-second trimester pregnancy with acute pain (الفايبرويد يكبر بس التغذية الدموية نفسها فيصير نزف)
  • 5% of pregnant women with fibroids, undergo red degeneration
149
Q

How the patient with red degeneration presents and how to diagnose and treat this patient

A

C/F: Pain + Tenderness + Fever + Vomiting
Investigations: CBC (leukocytosis) + ESR + Ultrasound
Tx: Bed rest + Hydration + Analgesia + Sedatives + Antibiotics

Note/ Inflammation may induce labour

150
Q

What are Hyaline and cystic degeneration of fibroid

A
  • Hyaline: asymptomatic softening and liquefaction of the fibroid
  • Cystic: asymptomatic central necrosis leaving cystic spaces at the centre
    Degenerative changes can initiate calcium deposition leading to calcification
151
Q

Can we predict or suspect that this fibroid can be malignant
Remember/ no pathognomonic features for a leiomyosarcoma on any imaging technique

A
  • Rapid growth & Recurrence after removal
  • Growth after menopause
  • Large (≥8cm), solitary, oval‐shaped, heterogeneous, strong and irregular vascularisation
  • Central necrosis/degenerative cystic changes (Absence of calcifications should raise the suspicion)
  • MRI with gadolinium enhancement gives an indication of the vascularity maybe helpful
  • Total lactate dehydrogenase (LDH) and LDH isozyme 3 are reportedly elevated in leiomyosarcoma
  • Elevated CA125 levels are seen in advanced‐stage leiomyosarcoma only
152
Q

Mass in weeks means it’s in the … but in cm in the …

A

Uterus
Ovaries

153
Q

What are special occasions that make fibroid cause acute pain

A

• Acute red degeneration
• Torsion of a pedunculated fibroid
• Extrusion of submucosal fibroid from the uterus as uterus contract to expels the fibroid
• Associated endometriosis
• Adhesion to other organ
• Sarcomatous changes

154
Q

What are the pressure symptoms of fibroid

A

• Abdominal discomfort ,sensation of pelvic pressure or backache ,abdominal distension
• Urinary frequency, difficulty in micturition, incomplete bladder emptying or incontinence
• Bowel problems such as constipation
• Varicosity or edema of lower limb

155
Q

How fibroids affect pregnancy

A

• Early in pregnancy: miscarriage, Recurrent pregnancy loss

• In late pregnancy, fibroids located in the cervix or lower uterine segment may cause an abnormal lie Malposition and malpresentation of the fetus , Obstructed labour, Cesarean section, rupture of myomectomy scar during pregnancy, placental abruption, Red degeneration

• After delivery: PPH may occur due to inefficient uterine contraction & delayed involution infection

156
Q

How pregnancy affects Fibroids

A

• Enlarge due to hyperoestrogenic state
• Red degeneration blood
• Torsion of pedunculated fibroid cause gradual or acute symptoms of pain & tenderness after delivery
• Infection during puerperium, Expulsion, Necrosis

157
Q

Why do Fibroids associated with Infertility

A
  • May result from mechanical distortion or occlusion of the Fallopian tubes
  • Endometrial cavity distorted by submucous fibroids may prevent implantation of fertilized ovum
158
Q

How you asses patient presented with fibroid

A

History
- Pressure Sx
- Menstrual irregularities
- Miscarriage or recurrent abortion
- Acute abdominal pain

Examination
- General: signs of anaemia
- Abdominal examination: Uterus is enlarged and presents as pelvic mass (often central and mobile)
- Bimanual examination: enlarged, firm, smooth or irregular, non-tender
uterus palpable. tenderness may suggest red degeneration

Investigations
- CBC for anaemia
- TVUSS: good for detecting and locating submucous fibroids and small intramural fibroids
- Transabdominal ultrasound: good for detecting larger intramural and subserosal fibroids and excluding hydronephrosis secondary to pressure from fibroids
- MRI used to demarcate the morphology, size and location of uterine fibroids prior to uterine artery embolization and to monitor treatment response
- Colour doppler
- Hysteroscopy: good for detecting submucosal fibroids and endometrial polyps; good for planning subsequent hysteroscopic surgical treatment

159
Q

First diagnostic test for Fibroids

A

U/S

160
Q

HPV is STD and usually asymptomatic and remain unnoticed, what areas does it infects

A

HPV usually sexually transmitted and nearly 40 types infect the genital area:
- Cervix
- Vagina
- Vulva
- Anus
- Penis

161
Q

What types of HPV associated with high risk for cervical dysplasia

A

Type 16 and 18 most commonly found in association with invasive cancer ,CIN 2 and CIN 3 and nearly in 47% of women with cancer in all stages

162
Q

What types of HPV associated with warts

A

6 and 11

163
Q

How you asses patient with cervical disease

A

History: Asymptomatic

Examination:
Perspeculum examination, cervix normal or there maybe cervicitis or erosions which bleeds on touch

Investigations:
1- cytological screening test:
Traditional pap smear + Liquid based cytology

2- visual inspection methods:
Unaided naked visualization + visual inspection under Lugols iodine
Visual inspection under acetic acid + Colposcopy

3- HPV DNA genotyping

164
Q

What are the Advantages of liquid based cytology

A

1- Reduction of proportion of inadequate specimen
2- Improvement in sensitivity rate
3- Reduction in interpretation time of specimens
4- Reduction in the number of false negative results
5- Possible to perform reflex testing like HPV test without taking another sample

165
Q

Screening for cervical cancer

A

• Screening programme is available to all wonen who are aged 25-64 years
• Between 25 and 49 years = screening test every 3 years
• Between 50 and 64 years = every 5 years
• After age of 65 performed to only women who had recent abnormal tests
• Women with HIV infection = annually

166
Q

Screening test results

A

1- Inadequate :repeat at 3 months

2- Negative result :routine recall

3- Borderline squamous dyskaryosis: HPV should be done
- HPV negative: routine recall
- HPV positive : referral to colposcopy
- HPV inadequate or unreliable: repeat test with HPV in 6 months

4- Low grade dyskaryosis: HPV test should be done
- HPV negative: routine recall
- HPV inadequate or unreliable or positive: referral to colposcopy

5- High grade dyskaryosis or worse: immediate referral to colposcopy without HPV test

167
Q

Colposcopic examination helps in what

A

• When abnormal cells have been detected on cytology, location and extent of abnormal lesion on cervix can be assessed with help of colposcopy

• Colposcopic examination can also be performed during follow up examination of cases that have undergone conservative therapy

• Biopsy can be taken from the areas of abnormality

• Conservative surgery like conization can be performed under colposcopic guidance

168
Q

DDx of Cervical lesions

A

• Cervicitis
• Tubercular lesions of the cervix (TB)
• Hyperkeratosis and parakeratosis
• Endocervical polyp
• Squamous papilloma
• Cervical endometriosis

169
Q

What’s colposcope

A
  • Office based procedure during which the cervix is examined under illumination and magnification before and after application of dilute acetic acid and lugols iodine
  • Both regular white light and green light are used during colposcopy
170
Q

How green light or filter be beneficial in colposcopic examination

A

Enhance visualization of blood vessels by making them darker in contrast to surrounding epithelium

171
Q

The characteristics features of malignancy and premalignancy on colposcopy include

A
  • Acetowhite area
  • Abnormal vascular pattern
  • Punctation
  • Failure to uptake iodine
172
Q

When you consider conservative management of fibroids

A
  • Asymptomatic
  • Below 12wks
  • The patient near menopause
173
Q

Medical management for fibroids

A

Tending to reduce menstrual bleeding without effect on fibroid size include progesterone, tranexamic
acid, mefenamic acid and the COCP tend to be ineffective in the presence of a submucous fibroid or an
enlarged uterus that is palpable abdominally (>12 weeks size)

174
Q

GnRH-a for fibroids

A
  • Needs 2 to 3 wks to act
  • Regress fibroid size by 40% but rapid regrow after Tx stops
  • Taken monthly as injection or nasal spray
  • Cause menopausal Sx
175
Q

Indications for GnRH-a for fibroids

A
  • Severe anaemia: they cause amenorrhea which helps to correct anaemia
  • Prior to surgery:
  • Make fibroid smaller & less vascular
  • Lower vaginal incision rather than midline abdominal incision
  • Facilitate vaginal rather than abdominal hysterectomy
176
Q

What’s Ulipristal acetate

A
  • Selective PRG receptor modulator
  • Effective in reducing pain, bleeding and fibroid size, and are associated with an improvement in quality of life Unlike GnRH analogues
177
Q

شنو المشكلة بالمارينا لعلاج الفايبرويد

A

ممكن يطلع وي النزف القوي وصعب ينحط لإن الرحم عافط

178
Q

When to consider surgical Tx for fibroids

A

• Where a bulky fibroid uterus causes pressure symptoms
• where HMB is refractory to medical interventions
• Complications like torsion
• Rapid increase in size
• Ultrasound features suggestive of sarcoma
• Subfertility

179
Q

When to choose myomectomy over hysterectomy in Tx of fibroid

A

• In women who wish to retain their fertility
• Symptomatic fibroid (persistent uterine bleeding despite medical therapy, pain or pressure symptoms)
• Unexplained infertility with distortion of the uterine cavity by fibroid
• Recurrent pregnancy wastage due to fibroid
• When IVF is indicated (especially if the myoma results in the distortion of the uterine cavity)

180
Q

Complications during hysteroscopic myomectomy for fibroids figo 0,1 and some 2

A

• Uterine perforation and potential for visceral damage, haemorrhage, infection and fluid overload
• Rupture of the uterus in labour if the cavity is breached during the myomectomy
• During process, if life threatening bleeding during operation could lead to hysterectomy

181
Q

Indications for UAE

A
  1. near menopause
  2. no longer desire fertility
  3. have a large uterus
  4. unfit for surgery
182
Q

Complications of UAE

A
  • Contrast allergy
  • Post‐embolization syndrome Infection or Sepsis requiring emergency hysterectomy
  • Death (rare)
  • Radiation exposure to ovaries and potential ovarian failure
  • Pregnancy
  • Women wish to regain fertility
  • Failure
183
Q

When to choose uterine ablation? Is it useful?

A

• When uterine cavity is not too enlarged or distorted, ablation appears to be a successful option
• The first reports have shown a significant reduction in fibroid size, together with symptomatic relief in the first 12 months after the procedure

184
Q

What are the surgical options for fibroids treatment

A

Hysterectomy
Myomectomy
Ablation
UAE
HIFU

185
Q

Can condoms prevent HPV infection

A

Condoms use is unlikely to reduce the risk of HPV infection

186
Q

What vaccines available for HPV prevention

A
  • Cervarix which is bivalent vaccine effective against HPV 16 and 18
  • Gardasil which is quadrivalent vaccine effective against four strains of HPV 6 ,11, 16 and 18
187
Q

Options for treatment of dysplastic changes of the cervix

A

■ Ablative methods
■ Excisional methods
■ Surgical options

188
Q

What are the ablative methods

A

■ Cryosurgery :
- Optimal tempreture must be in range from -20C to -30 C, using freezing agent (co2 and NO)
- Cryoprobe is applied for over 9 minutes and destroys the tissue up to the depth of about 4-5 mm
- Success rate of cryotherapy for treating CIN III varies between 77% and 93 %

■ Electrocoagulation :
- Dysplastic cells are destroyed using temperature over 700 C
- Quite painful so, Performed under GA
- Numerous complications like recurrence of the lesions ,bleeding ,cervical stenosis, indrawing of the squamocolumnar junction within the cervical canal

■ Laser Ablation :
- Done under local anesthesia
- Laser energy will destroy the dysplastic cells by boiling, steaming and exploding the cells
- Chared appearance of the exposed area
- Tissue cab be ablated up to the depth of 7mm, thus it is used for lesions with
extensive glandular involvement
- Minimal bleeding, no infection ,minimal scar formation, rapid healing

189
Q

Indications for cone biopsy

A
  • Abnormality is too large or the inner margin is receded into the cervical canal
  • Limit of the lesion cannot be visualized by colposcopy
  • The SCJ is not completely observable on colposcopy
  • There is discrepancy between pap smear and colposcopy finding
  • There is suscpicion of microinvasion
  • The finding of endocervical curettage are positive for CIN II or CIN III
190
Q

What are the excisional methods for treating cervical pathology

A

■ Cone biopsy
■ Laser excision
■ Large loop excision of transformation zone (LLETZ)

OB & Gynecology (4 decks)

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