Obstetrics & Gynaecology Flashcards

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1
Q

Both syst and diast ____ by 10-15mmHg in the first 2 trimesters but _____ 10mmHg in last trimester returning to baseline towards term thus chronic HTN can be masked in pregnancy

A

Decreases, increases

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2
Q

What is defined as pre-existing/chronic hypertension?

A

BP >140/90 prior to 20 weeks GA, persisting >7 weeks post-partum

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3
Q

What is defined as gestational hypertension?

A

sBP > 140 or dBP > 90 developing after 20th week GA in the absence of proteinuria in a women known to be normotensive before pregnancy

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4
Q

Physical exam of mother with hypertensive disorders in pregnancy

A

Body weight, CNS (presence/severity of headache, visual disturbances – blurring, scotomata – loss of part of the visual field), tremulousness, irritability, somnolence, hyperreflexia), hematologic (bleeding, petechiae), hepatic (RUQ or epigastric pain, severe N/V), renal (decreased urine output), non-dependent edema (hands and face)

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5
Q

Complications of Hypertensive Disorders in Pregnancy

A

Liver dysfunction (edema/subcapsular hematoma), renal dysfunction (hypoperfusion), seizure/eclampsia, abruptio, LV failure/pulmonary edema, DIC (release of placental thromboplastin consumptive coagulopathy), HELLP syndrome, hemorrhagic stroke (50% of deaths)

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6
Q

Complications to fetus due to GHTN

A

Secondary to placental insufficiency – IUGR, prematurity, abruption, IUFD

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7
Q

Labs/investigations of hypertensive disorders in pregnancy?

A

CBC (heme) + ALT/bilirubin/uric acid/LDH (hepatic) + Creatinine/Protein: Creatinine Ratio (renal) + PTT/INR/fibrinogen (if abnormal LFTs or bleeding, coagulopathy) + urate

Given that urine takes 1 day to come back, do urine dip (UA) – look for 2+ proteinuria (marker)

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8
Q

Management for both Pre-existing + Gestational HTN

A

Labetalol, α-methyldopa. Ask patient to get BP cuff and parameters for when to come in. Hydralazine and nifedipine are short acting.
No ACEI, ARBs, diuretics, prazosin, or atenolol

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9
Q

What is defined as pre-eclampsia?

A

New-onset hypertension (blood pressure [BP] > 140/90 mm Hg) plus new unexplained proteinuria (> 300 mg/24 hours after 20 weeks or a urine protein/creatinine ratio of >0.3)

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10
Q

In the absence of proteinuria, preeclampsia is also diagnosed if pregnant women have new-onset hypertension plus new onset of any of the following

A

Platelets < 100,000, LFTs twice normal, severe RUQ/epigastric pain, renal insufficiency (Cr >1.1 or double serum Creatinine), pulmonary edema, new onset headache/visual disturbances, and could later see hyperreflexia/clonus

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11
Q

What is the definitive treatment for PEC?

A

Delivery

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12
Q

For management of PEC - Immediate delivery is recommended for:

A

Pregnancy of > 37 weeks, Eclampsia, Preeclampsia with severe features if pregnancy is >34 weeks, Deteriorating renal, pulmonary, cardiac, or hepatic function (eg, HELLP syndrome), Nonreassuring results of fetal monitoring or testing

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13
Q

General management for PEC?

A

Hospitalized, Antenatal corticosteroids should be considered if GA <34wk, Delivery if >37weeks, Anti-HTN, MgSO4

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14
Q

Who are considered high risk for PEC?

A

<18yo, muiltiprip, pre HTN, Hx preeclampsia

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15
Q

What prevention should high risk women for PEC be on?

A
Low dose ASA AND Calcium if low Ca intake
ASA 162mg (2 tab) a night administered at bedtime starting pre-pregnancy or from diagnosis of pregnancy and continue until delivery starting at 12-16 weeks GA
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16
Q

How do you define eclampsia?

A

The occurrence of =>1 grand mal seizures and/or coma in the setting of pre-eclampsia and the absence of other neurologic conditions occurring before/during/after labour (48-72 hr)

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17
Q

What are the symptoms of eclampsia?

A

Tonic-clonic seizure lasting 60-75 seconds; symptoms that occur before seizure are persistent frontal or occipital headache, blurred vision, photophobia, RUQ pain, altered mental status, hyperreflexia

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18
Q

Management of eclampsia

A

ABCs + roll patient in LLDP + supplement O2 to treat hypoxemia due to hypoventilation (while convulsing) + aggressive anti-HTN tx for sustained diastolic pressures > 105 or systolic > 160 + prevention of recurrent convulsions + MgSO4 and DELIVERY – doesn’t matter what age, it reduces the risk of maternal morbidity and mortality; mode of delivery depends on clinical situation/condition

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19
Q

What is HELLP syndrome?

A

Hemolytic anemia + Elevated Liver enzymes + Low Platelet count

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20
Q

Define primary and secondary infertility

A

Primary: no pregnancies ever
Secondary: has been pregnant before

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21
Q

Causes of male infertility

A
  • Sperm disorders - reduced sperm count, impaired motility, reduced ejaculate volume
  • Testicular damage - scrotal injuries, testicular torsion, infections such as mumps, gonorrhea
  • Cryptorchidism
  • Scrotal hyperthermia (varicocele)
  • Medication - anabolic steroids, spironolactone, corticosteroids, cimetidine
  • Thyroid disorders
  • Chronic diseases - liver cirrhosis, renal insufficiency, obesity
  • Inherited disorders: Klinefelter syndrome, Kallmann syndrome
  • Sexual dysfunction - impaired libido, anejaculation
  • Pituitary and hypothalamic tumors
  • Hyperprolactinemia
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22
Q

List the main category of causes of female infertility

A
  • Ovarian reserve dysfunction
  • Ovarian dysfunction
  • Outflow Tract Abnormalities
  • Endometriosis
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23
Q

Tx for hyperprolactinemia

A

Administer bromocriptine, a dopamine agonist, which suppresses prolactin.

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24
Q

Tx for PCOS

A

Treat with clomiphene or letrozole +/- metformin, weight loss.

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25
Q

Tx for pituitary insufficiency

A

Treat with intramuscular luteinizing hormone/follicle-stimulating hormone (LH/FSH) or clomiphene.

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26
Q

What is the definition of infertility

A

Inability to conceive after 12 months of regular coitus under 35 years of age and after 6 months in women 35 years of age and over

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27
Q

Investigations for male infertility?

A
  • Semen analysis: sperm count + morphology + motility
  • Mixed antiglobulin reaction test for antisperm antibodies
  • TSH levels
  • Prolactin levels
  • Karyotype test (Kallmann syndrome, Klinefelter syndrome)
  • Scrotal/Testicular U/S: look for varicocele, obstruction, retrograde ejaculation into bladder
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28
Q

Investigations for female infertility?

A
  • Basal body temperature monitoring (biphasic pattern)
  • Hormone tests 3-5 day of the menstrual cycle
  • Midluteal serum progesterone levels (day 21-23): progesterone should increase shortly after ovulation - failure of progesterone levels to rise indicates anovulation
  • Endometrial bx
  • Imaging: Hysterosalpingogram, Hysteroscopy
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29
Q

Which hormone tests should be done for female infertility

A
  • Ovulation prediction test (detect LH levels)
  • Androgen levels – negative feedback on ovulation
  • TSH levels: elevated levels in hypothyroidism
  • Prolactin levels: hyperprolactinemia
  • Ovarian reserve:
  • Early follicular FSH levels: elevated in ovarian insufficiency and indicate reduced ovarian reserve
  • Early follicular estradiol levels
  • Anti-Mullerian hormone levels
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30
Q

Causes of ovarian reserve dysfunction?

A
  • <40 – Primary ovarian insufficiency

- >40 – menopause Tx: no treatment, adoption

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31
Q

Causes of ovarian dysfunction?

A
  • Pituitary insufficiency
  • Hyperprolactinemia
  • PCOS
  • Other causes: Hyper/hypothyroid, androgen excess, obesity/starvation, galactorrhea, stress.
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32
Q

Causes of outflow tract abnormalities?

A
  • Tubal Factors: PID, ligations/occlusion
  • Uterine Factors: congenital (bicornate/septate uterus), acquired: adhesions (Asherman’s Syndrome), fibroids/polyps, endometrial ablation
  • Cervical Factors: hostile/acidic cervical mucus, anti-sperm antibodies, structural defects
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33
Q

What is letrozole

A

Aromatase inhibitor

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34
Q

What is defined as acute pelvic pain?

A

Pain below the umbilicus lasting less than 6 months - occurs suddenly, sharply, and briefly

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35
Q

What is defined as chronic pelvic pain?

A

6 months of pain below the umbilicus severe enough to cause functional disability or require tx

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36
Q

Etiology for pelvic pain?

A
  1. Pregnancy: ectopic pregnancy, spontaneous abortion, abruption placenta, uterine rupture, endometritis
  2. Gynecological:
    - Ovary (e.g., ruptured cyst, torsion, neoplasia)
    - Tube (e.g., pelvic inflammatory disease, endometriosis)
    - Uterus (e.g., leiomyoma, endometriosis)
    - Other (dysmenorrhea, ovulation pain (Mittelschmerz), dyspareunia)
  3. Systemic conditions:
    - Urologic (interstitial cystitis, renal colic)
    - Musculoskeletal (fibromyalgia, diastasis of the pubic symphysis due to previous vaginal deliveries)
    - Gastrointestinal (irritable bowel, diverticulitis, inflammatory bowel disease, hernias)
    - Neurologic: pudendal neuralgia, anterior abdo wall nerve entrapment
    - Vascular: pelvic congestion syndrome
  4. Mental health issues
    - Depression, somatization
    - Sexual, physical, and psychological abuse/domestic violence
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37
Q

Two emergencies to consider with acute pelvic pain?

A
  • Ruptured ectopic pregnancy

- Ovarian torsion

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38
Q

History for pelvic pain?

A
  • HPI: First occurrence, PQRST. Relation to position changes (pudendal neuralgia) or menstruation (adenomyosis, endometriosis)
  • Obs history: MSK - pelvic floor myofascial pain syndromes, No prior pregnancies increase your risk of having endometriosis, PID, adhesions
  • Surgical history – nerve injury, adhesions
  • Last menstrual period (LMP) and menstrual history.
  • Gastrointestinal (GI) complaints such as nausea, vomiting, diarrhea, or constipation
  • Sexual history: Dyspareunia.
  • Social history (marital discourse, depression, stress, history of physical or sexual abuse)
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39
Q

Physical exam for pelvic pain

A
  • VS – elevated temp, tachy, hypo
  • Abdomen – palpated for tenderness, masses, and peritoneal signs. Rectal examination is done to check for tenderness, masses, and occult blood
  • Back – sacroiliac joints
  • Vulva – visual inspection, sensory exam to sharpness, dullness and light touch – rule out neuralgia
  • Pelvic examination: external genitals, speculum examination, bimanual examination. The cervix is inspected for discharge, uterine prolapse , and cervical stenosis or lesions. Bimanual examination should assess cervical motion tenderness, adnexal masses or tenderness, and uterine enlargement or tenderness.
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40
Q

What is Carnett’s test?

A

Carnett’s test - The patient voluntarily contracts her abdominal muscles by raising her head or legs. An increase in the pain indicates a myofascial origin (positive), whereas a decrease indicates an intraperitoneal disorder/visceral source.

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41
Q

Red flags for pelvic pain?

A
  • Syncope or hemorrhagic shock (eg, tachycardia, hypotension)
  • Peritoneal signs (rebound, rigidity, guarding)
  • Postmenopausal vaginal bleeding
  • Fever or chills
  • Sudden severe pain with nausea, vomiting, diaphoresis, or agitation
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42
Q

Investigations for pelvic pain?

A
  • Complete blood count (CBC) with differential: An elevated white blood cell count (WBC) may indicate an infection.
  • Pregnancy test.
  • RPR, if positive then a confirmatory test such as a VDRL or FTA-ABS, HIV, gonorrhea/chlamydia cultures.
  • Urinalysis (UA) and urine culture.
  • Fecal occult blood.
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43
Q

Imaging studies for pelvic pain?

A

o Pelvic sonogram: Best to evaluate ovarian cyst/neoplasms or uterine fibroids.
o For further evaluation: Computed tomography (CT)/magnetic resonance imaging (MRI)-best to evaluate for abdominopelvic masses or malignancies.

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44
Q

What is endometriosis?

A

Endometrium outside of the endometrial cavity

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45
Q

Pelvic pain that is not primary dysmenorrhea should be considered ____ until proven otherwise

A

Endometriosis

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46
Q

What is the pathophysiology of endometriosis?

A

▪ The ectopic endometrial tissue is physiologically functional. It responds to hormones and goes through cyclic changes, such as menstrual bleeding.
▪ The result of this ectopic tissue is “ectopic menses,” which causes bleeding, peritoneal inflammation, pain, fibrosis, and, eventually, adhesions.

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47
Q

Presentation of endometriosis?

A

Pelvic pain (that is especially worse during menses, but can be chronic):

  • Secondary dysmenorrhea (pain begins up to 48 hr prior to menses).
  • Dyspareunia (painful intercourse) as a result of implants on pouch of Douglas; occurs commonly, with deep penetration.
  • Dyschezia (pain with defecation): Implants on rectosigmoid.
  • Dysuria

Infertility, Intermenstrual bleeding, Cyclic bowel or bladder symptoms (hematuria).

Up to one-third of women may be asymptomatic.

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48
Q

Signs of endometriosis?

A

Retroverted uterus, uterosacral ligaments + rectovaginal nodules, adnexal masses (endometriomas).

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49
Q

Diagnosis of endometriosis?

A

Laparoscopy or laparotomy: Ectopic tissue must be biopsied for definitive diagnosis. The gold standard for diagnosis is laparoscopy with biopsy proven hemosiderin laden macrophages.

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50
Q

Medical and surgical treatments for endometriosis?

A

Medical (temporizing):

  • Mild-to-moderate: Empirical medical therapy with NSAIDs and continuous hormonal contraceptives
  • Severe sx: GnRH agonists (e.g., buserelin, goserelin) and estrogen-progestin OCPs

Surgical:

  • Conservative (if reproductivity is to be preserved): Laparoscopic lysis and ablation of adhesions and implants.
  • Definitive: Total abdominal hysterectomy and bilateral salpingo-oophorectomy (TAH/BSO).
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51
Q

What is adenomyosis?

A

Ectopic endometrial glands and stroma are found within the myometrium, resulting in a symmetrically enlarged and globular uterus.

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52
Q

Presentation of adenomyosis?

A

Presentation: parous women in their 40’s to 50’s, uterus enlarged and boggy, pelvic pain (usually noncyclical), dysmenorrhea, and menorrhagia, dyspareunia

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53
Q

Investigations for adenomyosis?

A

Transvaginal U/S or MRI to differentiate between adenomyosis and uterine fibroids

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54
Q

Management of adenomyosis?

A

Management: No proven medical therapy for treatment.

  • GnRH agonist, NSAIDs, and OCPs may be used for pain and bleeding.
  • Hysterectomy: Definitive therapy if childbearing is complete. The diagnosis is usually confirmed after histologic examination of the hysterectomy specimen.
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55
Q

What is Pelvic Inflammatory Disease?

A

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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56
Q

Acute pain can occur with degeneration of these, torsion of pedunculated subserosal fibroids, or expulsion of pedunculated intracavitary myomas through the cervix.

A

Leiomyomas

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57
Q

What is pelvic congestion?

A

Characterized by chronic pelvic discomfort exacerbated by prolonged standing and coitus in women who have periovarian varicosities on imaging studies

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58
Q

Symptoms of pelvic congestion

A

Dull chronic ache, worsened at the end of the day, standing, premenstrual, or postcoital = pelvic varicosities.

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59
Q

Treatment of pelvic congestion

A

Treatment: hormonal suppression, percutaneous embolotherapy, surgery.

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60
Q

A tender hard band or nodule of the muscle associated with pelvic pain?

A

Myofascial trigger point

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61
Q

What is dyspaurenia?

A

Genital pain before, during, or after sexual intercourse

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62
Q

What are the risk factors for dyspaurenia?

A

Risk Factors: PID, peri/postmenopausal, anxiety, depression, prior sexual assault, female circumcision

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63
Q

What is vestibulodynia?

A

Vulvar pain characterized by severe pain on touch/entry, tenderness to pressure within the vestibule, limited to erythema for physical findings

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64
Q

What is vaginismus and how do you treat?

A

Involuntary spasm of perineal and levator muscles – psychological issues or conditioned response to pain

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65
Q

What is vulvodynia and how do you treat?

A

Unprovoked stinging/burning/irritation/pain on vulva – treat with xylocaine 5% ointment PRN, or gabapentin

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66
Q

How do you treat vulvovaginal atrophy?

A

Premarin cream 0.5g qhs x 4 weeks, estring, vagifem tablets, lubricants PRN

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67
Q

Definition of menopause?

A

Menopause: permanent cessation of menses for >12 months

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68
Q

Definition of premature ovarian failure?

A

Premature ovarian failure is defined as menopause occurring before age 40

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69
Q

Describe the hypothalamic-pituitary-ovarian axis

A

GnRH is released in a pulsatile fashion. This pulsatility induces release of FSH. FSH then stimulates folliculogenesis of the ovaries and estrogen is released.

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70
Q

What happens to the hormones in menopause?

A

Estrogen levels begin to decline from peak in mid-to-late 30’s, begins perimenopause. As women age, we see endocrine markers – high FSH and low estradiol - cycle variability increases

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71
Q

Menopause is characterized by an elevated FSH due to

A
  1. ↓ inhibin (inhibin inhibits FSH secretion; it is produced in smaller amounts by the fewer oocytes).
  2. Resistant oocytes require more FSH to successfully mature, triggering greater FSH release.
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72
Q

Why do women begin to ovulate less frequently?

A

This is due to a shortened follicular phase. The length of the luteal phase does not change.

HPO: decrease in HPO sensitivity to estrogen (no LH surge = failure of estrogen(+) feedback)

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73
Q

What are the autonomic symptoms of menopause?

A
  • Increased sweating, hot flashes, and heat intolerance
  • Vertigo
  • Headache
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74
Q

What is the most common cause of post-menopausal bleeding.

A

Vaginal atrophy resulting from lack of estrogen

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75
Q

Treatment options for hot flashes?

A

SSRIs, specifically venlafaxine, can be used to control symptoms

Lower temp of sleeping area, cold drink at the beginning of a flash

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76
Q

What are the mental symptoms in menopause?

A
  • Impaired sleep (insomnia and/or night sweats)
  • Depressed mood or mood swings
  • Anxiety/irritability
  • Loss of libido
  • Poor memory/concentration
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77
Q

What are the atrophic symptoms of menopause?

A
  • Breast tissue atrophy: breast tenderness and reduced breast size
  • Vulvovaginal atrophy: atrophy of the vulva, cervix, vagina leading to vaginal dryness, pruritus, and dyspareunia
  • Urinary atrophy: atrophy of the urinary tract leading to urinary incontinence, dysuria, urinary frequency, urgency, and increased urinary tract infections
  • Osteoporosis
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78
Q

When should HRT be considered for menopause

A

If moderate or severe symptoms.

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79
Q

Treatment for vaginal atrophy in menopause?

A

Local estrogen cream (Premarin) or Vaginal Suppository (VagiFem) or ring (Estring) or lubricant

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80
Q

Prevention of osteoporosis in menopause?

A

1000-1500mg calcium + 800-1000IU VD3, weight exercise, no smoking, bisphosphonates (if diagnosed with osteoporosis)

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81
Q

Treatment options for decreased libido in menopause?

A

Decreased Libido: vag lubrication, counselling, androgen replacement

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82
Q

Treatment options for CVD in menopause?

A

CVD: manage risk factors with weight loss, BP control, etc.

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83
Q

Contraindications to HRT in menopause

A

Contraindications (ABCD): acute liver disease, undiagnosed vaginal bleeding, cancer (breast or endo), cardiovascular disease, DVT

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84
Q

Treatment if HRT is contraindicated in menopause?

A

If contraindicated: antidepressants + clonidine (alpha agonist) + gabapentin (start at 300mg at HS)

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85
Q

When is ERT—estrogen alone indicated in menopause?

A

Indicated in women status post hysterectomy.

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86
Q

Why do we use estrogen + progesterone for HRT?

A

The progesterone component is needed to protect the endometrium from constant stimulation and resultant increase in endometrial cancer. It is indicated for women who still have their uterus.

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87
Q

At what point should a conversation be had to determine if therapy is still indicated for menopause symptoms?

A

Short-term therapy (< 5 yr) is acceptable for menopausal symptom relief – after 5 yrs need to have a conversation.

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88
Q

Risks of HRT?

A

Risks: estro only ~ endometrial hyperplasia/carcinoma + thromboembolic +stroke/MI (1st year of treatment) + ^breast ca. risk (w/ combo) + gallbladder dx

Breast Cancer Risk: increases after 5 years with combo use

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89
Q

Side effects of HRT?

A

Side Effects: AUB, mastodynia, edema, bloating, nausea, heartburn, mood changes

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90
Q

Definition of vulvovaginitis?

A

Vaginitis is a general term for a group of disorders affecting the vagina, caused by infection, inflammation, or changes in the normal flora.

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91
Q

What is normal discharge?

A

Normal Discharge (pH 3.5-4.5): white/yellow, odorless, no associated vulvar or vaginal symptoms

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92
Q

What should be asked on history for vulvovaginitis?

A

History: get full OBHx and GyneHx (pap smear hx, pelvic infection hx, procedures done to cervix, endometriosis/PCOS?)
 Timeline/severity of all sx
 Sexual: partners, practices, protection from STDs, past history of STDs, prevention from pregnancy
 GI/GU: pelvic pain, urinary pain, vaginal pain, dyspareunia, ask about colour/amount/smell/blood, re: discharge
 Consider: recent Abx use, pregnancy, OCP, immunosuppression, DM, vaginal douching (CANDIDIASIS), semen, drugs, chemicals

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93
Q

Physical exam for vulvovaginitis?

A

Check for pruritis, burning, foul-smelling discharge, change in amount/consistency/colour, check abdo

Ensure that you are doing a speculum and bimanual exam (to r/o ascending infection (PID)); assess discharge/pooling, assess cervix, tenderness, or signs of blood - smell?

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94
Q

Signs/symptoms of reactive arthritis/syphillis?

A

Inspect eyes for conjunctivitis, uveitis, rash, mucosal ulcerations (syphilis)

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95
Q

Signs/symptoms of candida vaginitis?

A

Itch + burn + white/curdy discharge + PLENTY of mucosal erythema + wet mount findings of hyphae KOH

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96
Q

Signs/symptoms of bacterial vaginosis?

A

Fishy odour + gray discharge + NO mucosal erythema, CLUE CELL

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97
Q

Signs/symptoms of trichomonas vaginitis?

A

Dyspareunia/dysuria, green and frothy discharge, pH 5-6, + variable erythema, wet mount finding of trich

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98
Q

DDx for vulvovaginitis?

A

Infective/chemical/atrophic vaginitis (50+), cervicitis (STIs), malignancy, PID, foreign body, disrupted vag flora (BV)

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99
Q

Workup for vulvovaginitis?

A

Serology (syphilis, HIV) + pH + Wet Mount + Whiff Test + Endocervical/Vag/Urethral Swab (HSV PCR + Syphilis PCR + Trich/BV/Yeast (+/- G&C)) + Urinalysis (NAAT first catch, culture/sensitivity for gonorrhea/chlamydia) + Biopsy

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100
Q

What is bacterial vaginosis?

A

Overgrowth of Gardnerella vaginalis

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101
Q

Treatment of bacterial vaginosis?

A

Metronidazole PO (500mg BID x 7d) or clindamycin (300mg PO BID x 7d) or topical

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102
Q

Treatment of candida vaginitis?

A

Fluconazole PO (150mg) (watch liver) or OTC imidazole or polyene antifungals (1d - 7d doses)

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103
Q

Treatment of gonorrhea and chlamydia?

A

G (Cefixime 800mg PO single dose + Azithromycin 1g PO, 1 dose), C (Azithromycin 1g PO, 1 dose)

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104
Q

Treatment of trichomonas vaginitis?

A
metronidazole PO (2g x 1d) or topical metro/clotrimazole (BID x 5d) 
o	TREAT SEXUAL PARTNER TOO + REPORT
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105
Q

What are the notifiable STIs?

A

G / C / S / Chancroid / HIV / Trich / LGV / MPC / Granuloma Inguinale

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106
Q

Treatment for HPV genital warts?

A

Patient applied (imiquimod cream) or provider applied (liquid nitrogen, several visits)

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107
Q

MOA of progestin in hormonal contraception?

A

Progestin: prevents LH surge, suppresses ovulation, thickens cervical mucus, decreases tubal motility, decidualizes endometrium

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108
Q

MOA of estrogen in hormonal contraception?

A

Estrogen: suppresses FSH and follicular development, causes endometrial proliferation

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109
Q

Explain the feedback regulation of E2/progesterone on LH/FSH?

A

Feedback Regulation: E2/progesterone have positive feedback action on LH/FSH (unless E2 is there for a long time alone, then it can convert to positive feedback as it does in the menstrual cycle. Thus, a combination pill avoids positive feedback that leads to ovulation.

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110
Q

What do combined oral contraceptive pills contain?

A

Most contain low dose ethinyl estradiol plus progestin

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111
Q

What is the failure rate of OCPs?

A

Failure rate (0.3% to 8%) depending on compliance

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112
Q

What do transdermal contraceptive patches contain?

A

Continuous release of 6mg norelgestrominn and 0.60mg ethinyl estradiol into bloodstream

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113
Q

Where should you avoid placing the transdermal patch?

A

Can be placed on the buttocks, upper outer arms, lower abdomen, or upper torso (but not the breast)

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114
Q

How often are transdermal patches changed?

A

Worn for 3 consecutive weeks (changed every wk) with 1wk off to allow for menstruation

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115
Q

A population where transdermal patches may not be as effective?

A

Maybe less effective in women >90kg

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116
Q

What is the failure rate of transdermal patches?

A

As effective as OCP in preventing pregnancy (>99% with perfect use)

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117
Q

What is a contraceptive ring (Nuva Ring)?

A

Thin flexible plastic ring; releases etonogestrel and estradiol, works for 3wk then removed for 1wk to allow for menstruation

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118
Q

What is the failure rate of the contraceptive ring?

A

As effective as OCP in preventing pregnancy (98%)

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119
Q

Specific side effects of contraceptive ring?

A

Side effects: vaginal infections/irritation, vaginal discharge

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120
Q

Before prescribing a hormonal contraceptive, what should you do, when should you see them in follow-up?

A

 Thorough history and physical exam, including blood pressure and breast exam
 Can start at any time during cycle but ideal if within 5d of LMP
 Follow-up visit 6wk after hormonal contraceptives prescribed
 Pelvic exam not required as STI screening can be done by urine and pap smear screening does not start until >21 yr

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121
Q

List advantages of combined estrogen and progestin methods

A

 Highly effective, does not interfere with intercourse
 Reversible
 Cycle regulation
 Decreased dysmenorrhea and heavy menstrual bleeding (less anemia)
 Decreased benign breast disease and ovarian cyst development
 Decreased risk of ovarian and endometrial cancer Increased cervical mucus which may lower risk of STIs Decreased PMS symptoms
 Improved acne
 Osteoporosis protection (possibly)

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122
Q

What are the estrogen-related side effects of hormonal contraceptives?

A

Estrogen-related: Nausea, Breast changes (tenderness, enlargement), Fluid retention/bloating/edema, Weight gain (rare), Migraine, headaches, Thromboembolic events, Liver adenoma (rare), Breakthrough bleeding (low estradiol levels) - Irregular breakthrough bleeding often occurs in the first few months after starting OCP; usually resolves after three cycles

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123
Q

What are the progestin-related side effects of hormonal contraceptives?

A

Progestin-related: Amenorrhea/breakthrough bleeding, Headaches, Breast tenderness, Increased appetite, Decreased libido, Mood changes, HTN, Acne/oily skin* Hirsutism*

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124
Q

What are the absolute contraindications for hormonal contraceptives?

A
  • < 6 weeks post -partum & Breastfeeding (decreases milk production)
  • Smoker > 35 (> 15 cigarettes/day)
  • Hypertension (>160 />100)
  • Current/Past VTE
  • Ischemic Heart Disease
  • History of cerebrovascular accident
  • Migraine with focal neurological symptoms (risk of stroke)
  • Severe cirrhosis
  • Liver tumour (adenoma or hepatoma)
  • Breast cancer (current)
  • Diabetes with complications – neuropathy, nephropathy, retinopathy
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125
Q

What are the relative contraindications for hormonal contraceptives?

A
  • Smoker > 35 yr (<15 cigs/day
  • Controlled HTN, HPT (150 - 159/ 90 - 99)
  • Migraine over age 35 years old
  • Symptomatic GB disease (estrogen increases likelihood of stones)
  • Mild cirrhosis
  • History of OC-related cholestasis
  • Use of meds that interfere with OCP metabolism
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126
Q

What are the drug Interactions/risks of hormonal contraceptives?

A

Rifampin, phenobarbital, phenytoin, griseofulvin, primidone, and St. John’s wort can decrease efficacy, requiring use of back-up method

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127
Q

What are the indications for using a progestin-only method of contraception?

A

Indications: Suitable for postpartum women (does not affect breast milk supply), Women with contraindications to combined OCP (e.g. thromboembolic or myocardial disease), Women intolerant of estrogenic side effects of combined OCPs

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128
Q

What does the progestin-only pill (“minipill”) rely on for contraception

A

Relies on the progestin effects on the cervical mucous and endometrial lining

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129
Q

To ensure reliable effect, what must you do with the progestin-only method?

A

Must be taken daily at same time of day to ensure reliable effect; no pill free interval

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130
Q

The progestin-only method is highly effective for whom?

A

Highly effective if also post-partum breastfeeding, or if >35yr and smoke

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131
Q

What is the failure rate of the progestin-only pill (“minipill”)?

A

Higher failure rate (1.1-13% with typical use, 0.51% with perfect use) than other hormonal methods

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132
Q

How often is ovulation inhibited by the progestin-only pill (“minipill”)?

A

Ovulation inhibited only in 60% of women; most have regular cycles (but may cause oligo/amenorrhea)

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133
Q

What is Depo-Provera?

A

Injectable depot medroxyprogesterone acetate given by a health-care professional in the upper arm or buttocks every 12 to 13 weeks (four times a year)

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134
Q

When should you start Depo-Provera?

A

Initiate ideally within 5d of beginning of normal menses, immediately postpartum in breastfeeding and non-breastfeeding women. Can consider quick start

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135
Q

What is the failure rate of Depo-Provera?

A

Highly effective 99%; failure rate 0.3%

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136
Q

What is a disadvantage about Depo-Provera?

A

Disadvantage: restoration of fertility may take up to 9mo

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137
Q

Specific side effect of Depo-Provera?

A

Side effect: decreased bone density (may be reversible) and weight gain

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138
Q

Side effects of the progestin-only methods

A

Side effects: Irregular menstrual bleeding, Weight gain, Headache, Breast tenderness, Mood changes, Functional ovarian cysts, Acne/oily skin, Hirsutism

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139
Q

What percentage of women have amenorrhea after 1-2 yrs use of Depo-Provera?

A

Irregular spotting progresses to complete amenorrhea in 70% of women (after 1-2yr of use)

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140
Q

How long should the diaphragm and cervical cap remain in the vagina after intercourse?

A

Must be left in the vagina for 6 to 8 hours after intercourse. Spermicide should be reapplied in the vagina for each repeated act of intercourse (optional for the cervical cap)

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141
Q

Disadvantage of the diaphragm and cervical cap?

A

Disadvantages: Must be available at time of intercourse, The use of spermicide may cause irritation of the vaginal and rectal walls and increase the risks of contracting human immunodeficiency virus (HIV), Diaphragm may increase the risk of persistent UTI, Cervical cap should not be used during menstruation and may cause vaginal odour and discharge, Does not protect against certain STIs

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142
Q

What is the failure rate of the female condom?

A

Typical Use – 79%, Perfect Use – 95%

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143
Q

What are sponge and spermicides?

A
  • The sponge is a soft, disposable, polyurethane foam device impregnated with a spermicide
  • Sponge - Fits over the cervix, Traps and absorbs sperm to augment effect of spermicide
  • Spermicides - Ingredient that impairs sperm, Should be used with another form of contraception
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144
Q

What is the calendar method for contraception?

A

A woman tracks the days of her menstrual cycle on a calendar for several months, to identify her fertility period – the period when a woman is most likely to become pregnant after having unprotected sexual intercourse. Avoid day 10-18

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145
Q

Failure rate of the withdrawal method

A

Typical Use – 73%, Perfect Use – 96%

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146
Q

What are the 2 types of intrauterine devices?

A

o Copper-Containing IUD (Nova-T®)

o Progesterone-Releasing IUS (Mirena, Kyleena®, Jaydess®)

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147
Q

How does the copper-containing IUD (Nova-T®) work?

A

Mild foreign body reaction in endometrium; toxic to sperm and alters sperm motility - A T-shaped device with a copper wire around it, inserted into uterus

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148
Q

How does the progesterone-releasing IUS (Mirena, Kyleena®, Jaydess®) work and what do they contain?

A

Decidualization of endometrium and thickening of cervical mucus; minimal effect on ovulation - Contains a hormone called levonorgestrel (a progestin) that is released slowly over time

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149
Q

How effective are IUDs?

A

Highly effective (99.8%); failure rate 0-1.2%

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150
Q

How quickly does endometrial pattern return after IUD is removed?

A

Contraceptive effects last 5 yr Reversible, private, convenient - Endometrial pattern returns to normal in 24hrs once removed

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151
Q

What are the side effects of both Copper and Progesterone IUD?

A

Both Copper and Progesterone IUD: Breakthrough bleeding, Expulsion (5% in the 1st yr, greatest in 1st mo and in nulliparous women), Uterine wall perforation (1/1000) on insertion, If pregnancy occurs with an IUD, increased risk of ectopic, Increased risk of PID (within first 10 d of insertion only)

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152
Q

What are the side effects of Copper IUD?

A

Copper IUD: increased blood loss and duration of menses, dysmenorrhea

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153
Q

What are the side effects of Progesterone IUD?

A

Progesterone IUD: bloating, headache

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154
Q

Contraindications to IUDs?

A
	Pregnancy (bHCG prior to insertion)
	PID/STI ACTIVE
	Abnormal cavity
	Post septic abortion
	Unexplained PV bleed
	Uterine/Cervical CA
	Copper allergy (copper IUD)
	Breast cancer? – PR positive
	Malignant GTN – increased perforation
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155
Q

What is the expulsion rate of postplacental IUD?

A

 Expulsion rate is higher (24%)

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156
Q

When should the Kyleena be used for?

A

Kyleena is used for nulliparious women - Great option for menorrhagia

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157
Q

Time period for the use of Yuzpe method?

A

Efficacy decreased with time (e.g. less effective at 72 h than 24 h)

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158
Q

What is the follow up for after emergency postcoital contraception?

A

3-4wk post treatment to confirm efficacy (confirmed by spontaneous menses or pregnancy test)

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159
Q

What is the expulsion rate of postplacental IUD?

A

Expulsion rate is higher (24%)

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160
Q

Side effects of the Yuzpe method?

A

Side Effects: Nausea (due to estrogen; treat with Gravol), Irregular spotting

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161
Q

What is 1st line emergency postcoital contraception if <24 hrs?

A

Plan B

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162
Q

What is Plan B?

A

Consists of levonorgestrel 750 μg q12h for 2 doses (can also take 2 doses together); taken within 72 h of intercourse. Can be taken up to 5d

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163
Q

In whom is Plan B less effective?

A

Less effective in overweight individuals (>75 kg less effective, >80 kg not recommended)

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164
Q

Side effect of Plan B

A

No estrogen thus very few contraindications/side effects (less nausea)

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165
Q

What is the most effective emergency postcoital contraception up to 7 days?

A

Postcoital IUD (Copper)

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166
Q

For permanent contraception in women, the fallopian tubes may be

A

● Cut and a segment is excised
● Closed by ligation, fulguration, or various mechanical devices (plastic bands or rings, spring-loaded clips)
● Completely removed

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167
Q

Women who become pregnant after sterilization procedure are at increased risk of?

A

Ectopic pregnancy

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168
Q

Complications in women having transcervical (hysteroscopic) procedures?

A

In women having transcervical (hysteroscopic) procedures, complications may include tubal perforation (in 1%-3% of women), improper coil placement (in 0.5%-3% of women), expulsion of occlusion device (in 0.4%-2.2% of women), nickel hypersensitivity (in 0.01% of women)

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169
Q

Complications in women having laparoscopy procedures?

A

In women having laparoscopy, complications may include mortality (rare, ~0.01%), usually due to anesthesia-related complications, minor or major morbidity (in about 0.9%-1.6% overall).

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170
Q

What is the reversibility of tubal ligation?

A

Reversibility: cannot reverse clipping due to scarring/ligation, but can reverse by excising clip scar. If whole tube taken out, cannot reverse.

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171
Q

Effectiveness of tubal ligation?

A

Effectiveness: 10-year cumulative failure rate about 1.9% for abdominal tubal sterilization procedures, reported to have similar efficacy as long-acting reversible contraceptive methods but may have increased morbidity compared with IUD

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172
Q

What is a vasectomy?

A

For this procedure, the vasa deferentia are cut, and the cut ends are ligated or fulgurated.

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173
Q

How long does sterility take after a vasectomy?

A

Sterility requires about 20 ejaculations after the operation and should be documented by 2 sperm-free ejaculates, usually obtained 3 months after the operation. A back-up contraceptive method should be used until that time.

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174
Q

Complications of vasectomy

A

● Hematoma (5%)
● Sperm granulomas (inflammatory responses to sperm leakage) - surgery may be needed to remove the granuloma
● Spontaneous reanastomosis, which usually occurs shortly after the procedure
● Inflammation of the epididymis tubes (congestive epididymitis)

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175
Q

Reversibility of vasectomy

A

Reversibility: can reverse, but not after 10 years (reversal not covered)

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176
Q

Effectiveness of vasectomy

A

Effectiveness: very effective (99.85%) birth control method. 1-2 women/1,000 ~ unplanned pregnancy in 1st year after partners have had a vasectomy.

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177
Q

At what GA should a pregnant women be screened for diabetes?

A

Due to hCS being highest at 24-28 weeks

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178
Q

Explain the 2 step screening process for GDM?

A
Step 1: Random non-fasting 50g OGTT
o	> 11.1 mmol/L is GDM
o	If 1hr PG 7.8-11.1 mmol/L, proceed to step 2
Step 2: fasting (8hrs) 75g OGTT
GDM if >1 of:
▪	FPG > 5.3 mmol/L
▪	1hr PG > 10.6 mmol/L
▪	2hr PG > 9.0 mmol/L
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179
Q

Risk Factors for GDM

A

Prior GDM, prior delivery of macrosomia infant, high risk population (aboriginal/Hispanic/SouthAsian/Asian/African), age >35, BMI >30, acanthosis nigricans, corticosteroid use.

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180
Q

Post-partum screening for pregnant women with GDM?

A

Women with GDM should undergo screening at six to 12 weeks postpartum with a fasting glucose measurement or 75-g two-hour glucose tolerance test

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181
Q

When should women with multiple risk factors be screened for GDM

A

Women with multiple risk factors should be screened for T2DM in T1 w/ A1C

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182
Q

Management of GDM?

A

Chemstrips (F/PP), urine ketones, dietary counselling, exercise/increasing activity, insulin up to 4 times daily, oral hypoglycemic agents in pregnancy are generally not safe except glyburide (does NOT cross the placenta) and metformin (DOES cross placenta)

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183
Q

Preconception counselling recommendations?

A
  • Folic acid supplementation (400 mcg daily) to reduce the risk of neural tube defects. 8-12 wks pre-conception until end of T1 to prevent NTDs
  • Iron supplementation, prenatal vitamins
  • BMI – achieve a healthy body weight before becoming pregnant
  • DM – good glycemic control
  • Teratogenic medications - ACE inhibitors, Accutane, statins, warfarin.
  • Screen for STIs
  • Update hepatitis B; influenza; measles, mumps, rubella; Tdap; and varicella immunizations
  • Social: smoking, alcohol, drug use, domestic violence
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184
Q

When should 5 mg folic acid be recommended?

A

0.4-1 mg daily in all women; 5 mg if previous NTD, antiepileptic medications, DM, or BMI >35 kg/m2, ethnic group (Celtic, Sikh, N Chinese)

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185
Q

What is Naegle’s rule?

A

1st day of LMP + 1 year + 7days - 3months

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186
Q

Initial history for new pregnancy?

A
  • Desirability of pregnancy
  • Symptoms of pregnancy
  • Obstetrical: any previous complications (GDM, GHTN, delivery related – PTL, PPROM, operative delivery, C/S, or neonatal related – IUGR, IUFD), GTPAL
  • Gyne: any abnormal paps? Any pelvic infections of any kind? Cervical procedures (Colpo/LEEP)? Endo/PCOS, etc.?
  • Social: smoking (~IUGR), alcohol (FASD/GDD), cocaine (abruption, IUGR, PTL), SES, IPV, domestic violence
  • Prescription and non-prescription medications
  • Family: genetics (aneuploidy/ONTD/AR), maternal (GDM/GHTN/Multips), or obstetric
  • Review of Systems: headache, vision changes, swelling of hands/face, nausea, vomiting, UTI’s, trauma, SOB, bowel/bladder function, weight loss, etc.
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187
Q

Initial physical exam for new pregnancy?

A
  • Measure BMI
  • BP, HR, HEENT, breast, RESP, CV, abdo, reflexes, varicosities, pelvic exam
  • Pap smear (only if required according to patient history and provincial screening guidelines)
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188
Q

What are the symptoms of pregnancy?

A

Amenorrhea, breast tenderness, N/V, fatigue, urinary frequency, bleeding

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189
Q

What is gravidity (G)?

A

Gravidity (G): total number of pregnancies of any gestation (multiple gestation = one pregnancy) – includes pregnancy, abortions, ectopics, and hydatidiform moles

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190
Q

What is parity (TPAL)?

A

Parity (TPAL): T is the number of term infants delivered (>37wk), P is number of premature infants delivered, (20-36+6wk), A is number of abortions (loss of intrauterine pregnancy prior to viability of fetus <20wk and/or <500g fetal weight) – induced (therapeutic or spontaneous (miscarriage), L is number of living children

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191
Q

Initial investigations for new pregnancy?

A
  1. Blood work
    - CBC (esp Hb and platelets, remember you can have physiologic anemia)
    - Blood group and Rh status + antibody screen (Rh/D – would be eligible for IgG for Rh even in 1st pregnancy!!!) Given at 28 weeks
  2. Screening for STIs
    - HIV
    - Syphilis screening (Syphilis during pregnancy)
    - Hepatitis B surface antigen testing
    - Hepatitis C screening (Anti-HCV antibody testing)
    - Gonorrhea/Chlamydia testing
  3. Cystic fibrosis screening recommended for 4. Glucose/HA1c
  4. TSH
  5. Urine dipstick protein testing: screening for proteinuria (baseline value is vital for comparison with results in later pregnancy to rule out preeclampsia); performed during every prenatal visit
  6. Urine culture: screening for asymptomatic bacteriuria
  7. Rubella and varicella antibody
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192
Q

Categories of teratogens?

A
  • A (controlled studies show no risk)
  • B (adverse in animals, but no risk in humans)
  • C (adverse in animal, unknown risk in humans)
  • D (evidence of risk in human, rare situations benefits > risk)
  • E (toxic, contraindicated)
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193
Q

Complications of smoking during pregnancy?

A

Lower fertility, spontaneous abortion, preterm birth, placental insufficiency, placental abruption, ectopic pregnancy, SIDS, PPROM, low birth weight

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194
Q

Complications of using cocaine during pregnancy?

A

Classic association with placenta abruption, low birth weight, prematurity, microcephaly, miscarriage

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195
Q

Should you use NSAIDs or Tylenol during pregnancy?

A

CONTRAINDICATED - switch to Tylenol! Inhibit COX-1 and COX-2, which convert arachidonic acid into prostaglandins. risk of early closure of ductus arteriosus

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196
Q

Which antibiotics are contraindicated in pregnancy?

A

Generally penicillin, cephalosporins, macrolides, azithromycin, erythromycin, clarithromycin, clindamycin (if penicillin allergic) are fine – but NOT metronidazole/sulfonamide (inhibits DNA synthesis), streomycin/gentamycin/kanamycin (ototoxicity/deafness), and tetracycline (bone/teeth staining)

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197
Q

Counselling of the pregnant woman - nutrition?

A
  • Calcium: 3-4 servings of milk products daily (greater if multiple gestation). 1200-1500 mg/d
  • Vitamin D: 1,000 IU - promotes calcium absorption
  • Iron: 0.8 mg/d in T1, 4-5 mg/d in T2, and >6 mg/d in T3 - supports maternal increase in blood cell mass, supports fetal and placental tissue; required amounts exceed normal body stores and typical intake, and therefore need supplemental iron - iron is the only known nutrient for which requirements during pregnancy cannot be met by diet
  • Essential Fatty Acids: supports fetal neural and visual development - contained in vegetable oils, margarines, peanuts, fatty fish
  • Daily caloric increase of ~100cal/d in the first trimester, and ~300cal/d in second/third, ~450cal/d in lactation
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198
Q

Counselling of the pregnant woman - caffeine?

A

Diuretic and stimulant that readily crosses placenta – less than 300mg/d is not thought to contribute to miscarriage or preterm birth (ACOG) – relationship with IUGR is unknown; SOGC states 1-2cups/d are safe

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199
Q

Counselling of the pregnant woman - food borne illnesses?

A
  1. Listeriosis (Listeria monocytogenes) and toxoplasmosis (Toxoplasma gondii) concerning during pregnancy
    - Avoid consumption of raw meats, fish, shellfish poultry, hotdogs, raw eggs, unpasteurized dairy products
    - Avoid unpasteurized soft cheeses, deli meats, smoked salmon, and pates ~ potential sources of Listeria
  2. Fish: limit consumption of top predator fish such as shark, swordfish, king mackerel, tilefish
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200
Q

Counselling of the pregnant woman - exercise?

A

‘talk test’ – should be able to speak while exercising, avoid supine position after 20 weeks GA, should be low risk trauma sports

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201
Q

Absolute contraindications of exercise in the pregnant woman?

A

Ruptured membranes, preterm labour, HTN disorders of pregnancy, incompetent cervix, IUGR, multiple gestation (>3)

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202
Q

Counselling of the pregnant woman - optimal weight gain?

A

BMI 18-24.9: 25-35 pound weight gain normal
BMI 25-29.9: 15-25 pound weight gain normal
BMI >30: 15 pound weight gain normal

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203
Q

Counselling of the pregnant woman - work?

A

Strenuous work, extended hours and shift work during pregnancy may be associated with greater risk of LBW, prematurity, and spontaneous abortion

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204
Q

Counselling of the pregnant woman - air travel?

A

Is acceptable in second trimester, airline cut off for travel is 36-38 week gestation depending on airline, to avoid giving birth on the plane

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205
Q

Counselling of the pregnant woman - sexual intercourse?

A

May continue, except in patients at risk for abortion, preterm labour, or previa – breast stimulation may induce uterine activity and is discouraged in high-risk patients near term

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206
Q

Counselling of the pregnant woman - alcohol?

A

No amount of alcohol is safe in pregnancy, encourage abstinence from EtOH during pregnancy – increases risk of abortion, stillbirth, and congenital anomalies – fetal alcohol syndrome

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207
Q

When is the dating ultrasound preformed?

A

7-13w

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208
Q

What does the first trimester screening consist of?

A

Ultrasound (Nuchal Translucency)

PAPP-A + bHCG

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209
Q

When is the first trimester screening performed?

A

11-13+6w

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210
Q

What does the first trimester screen for?

A

Tri-21 + Tri-18 + Tri-13

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211
Q

What is an abnormal amount of nuchal translucency and what is it suggestive of?

A

> 3mm ~ congenital defects, aneuploidy, warrants further imaging (sees fluid at back of neck + nasal bone)

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212
Q

First trimester invasive prenatal testing for extra/missing chromosomes

A

Chorionic Villi Sampling (11-13+6)

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213
Q

When can NIPT be offered?

A

Offer beyond 10 weeks if (+). Accurate at detecting Down Syndrome, Turners, T18, T13

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214
Q

What does the second trimester screening consist of?

A

AFP
Maternal Serum Quad Screen
(E2 + HCG + Inhibin A + AFP)

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215
Q

When is the 2nd trimester screening performed?

A

15-20+6w

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216
Q

If FTS is done, just add ___ to test for neural tube defects.

A

AFP

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217
Q

When is the anatomic ultrasound preformed?

A

18-20w

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218
Q

What does the 2nd trimester screen for?

A

Tri-21 + 18 + Neural Tube Defects + Spina bifida

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219
Q

2nd trimester prenatal invasive testing for extra/missing chromosomes

A

Amniocentesis (16+)

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220
Q

Indications for invasive testing?

A
  • Age >40
  • (+)FTS or Quad
  • Abnormal U/S (IUGR, soft mark’r, etc)
  • FHx or previous child w/ chromo abn
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221
Q

Risk factors of post-partum depression?

A

PHx or FHx of depression (incl. PPD), prenatal dep/anxiety, stressful life situation, poor support system, unwanted pregnancy, colicky or sick infant

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222
Q

What is post-partum depression?

A

Major depression occurring within 6 months of childbirth

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223
Q

Symptoms of post-partum depression?

A

If blues last beyond 2 weeks, or severe symptoms in those 2 weeks (extreme disinterest in baby, suicidal/homicidal/infanticidal ideation) – use Edinburgh Postnatal Depression Scale

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224
Q

Treatment of post-partum depression?

A

Antidepressants, psychotherapy, supportive care, ECT if refractory

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225
Q

Cardiovascular changes during pregnancy?

A
  • Increase blood/plasma volume by 40-50%
  • Increase CO (HR and SV) + RBC by 30-40%
  • BP decreases usually overall due to lower TPR, decreased response to vasopressors
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226
Q

Respiratory changes during pregnancy?

A
  • Progesterone increases medullary respiratory center sensitivity to CO2 = hyperventilation for more O2 to baby (normal!) = blow off more CO2 and the kidneys respond by lowering HCO3 = compensated respiratory alkalosis
  • Increased O2 consumption
  • Enlarged abdominal mass can affect breathing/diaphragm
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227
Q

MSK/Derm changes during pregnancy?

A
  • Increase BMI (10-15kg)
  • Stretch marks
  • Low back pain
  • Lordosis
  • Carpal tunnel syndrome
  • Sciatica
  • Increase skin pigmentation
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228
Q

Gynaecological changes during pregnancy?

A
  • Breast enlargement
  • Areolar pigmentation
  • Uterine hypertrophy and stretching (increases 10x)
  • Cervical gland hypertrophy (thick mucous plug)
  • Vagina – lactobacilli proliferation. Increase lactic acid – decreases pH
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229
Q

Renal changes during pregnancy?

A
  • Increased GFR (due to more blood, higher renal blood flow, no change to filtration fraction)
  • Glucosuria (secondary to increased GFR, normal but could be gestational diabetes too)
  • Increased vasopressor (RAAS) activity, but decreased vasopressor responsiveness
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230
Q

Hematological changes during pregnancy?

A
  • Increased RBC mass
  • Increased WBC count
  • Increased iron needs (50-60 elemental Fe daily, 1000mg overall)
  • Increased clotting (estrogen stimulates protein synthesis (clotting factors but NOT platelets)
  • 2/3 of Virchow’s triad – stasis, hypercoagulability
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231
Q

Gastrointestinal changes during pregnancy?

A
  • Decreased GI smooth muscle activity
  • Nausea/vomiting, GERD common (take ranitidine – Zantac)
  • Increased glucose tolerance (check at 24-28weeks due to high HCS at that point)
  • Weight gain (usually 2-4kg (4.5-8lbs) in first 20 weeks, then 0.5kg (~1lb) per week)
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232
Q

How often should a pregnant women be seen during the pregnancy?

A

For uncomplicated pregnancies, SOGC recommends q4-6wk until 30wk, q2-3wk from 30wk, and q1-2wk from 36wk until delivery

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233
Q

What should be asked in history for subsequent prenatal visits?

A

Fetal movements: Notice first movement (“quickening”) at 18-20 weeks in primigravidas and ~1-2 weeks earlier in; if the patient is concerned about decreased fetal movement, counsel them to choose a time when the fetus is normally active to count movements (usually recommended after 26 wk)

Uterine bleeding: LMP? Which trimester is it? Cramping? Colour of blood? Clots/tissue? Painless or painful?

Leaking, cramping (contractions), questions, concerns

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234
Q

What should be done on physical exam for subsequent prenatal visits?

A
  • Weight monitoring: to avoid fetal developmental problems (if weight gain is less than the recommended amount), fetal macrosomia, or maternal obesity (if weight gain is above normal)
  • Blood pressure monitoring: early detection of pregnancy-induced hypertension
  • SFH – pubic symphysis to uterine fundus. GA 20-40 wks
  • Fetal position (starting 28-32 wks): Leopold’s maneuvers for lie, position, and presentation of fetus
  • Determine FHR (starting at 12 wks) using Doppler US. Normal between 120-160
  • Cervical exam at 37 weeks in case require IOL
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235
Q

Most common symptoms of all 3 trimesters?

A

Urinary frequency + fatigue + poor sleep + back pain

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236
Q

Investigations for subsequent prenatal visits?

A
  • Urine dipstick for glucosuria and proteinuria in high risk women
  • Fetal heart rate starting at 10-12 wk using Doppler U/S
  • Prenatal screening for Group B streptococcus performed between 36 0/7 and 37 6/7 weeks of gestation (vaginal and rectal swab for culture and gram staining) because colonization by this bacteria may cause chorioamnionitis and neonatal infection. Treated w/ Pen G IV
  • Repeat Hb from the 24th week of pregnancy.
  • 50-g, one-hour oral glucose challenge test (initial screening) at 24-28 weeks gestation
  • Repeat rhesus screening: An unsensitized Rh(D)-negative women should receive anti(D)-immune globulin. Protective for 12 weeks only so may need another dose, also give for any other risk of maternal/fetal blood contact
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237
Q

Management if GBS positive at delivery?

A

5mU Pen-G IV bolus, then 2.5 mU Pen-G IV q4h until delivery

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238
Q

What is the test done if the 1 hr OGTT is positive?

A

100-g, three-hour oral glucose tolerance test (oGTT) to confirm diagnosis in case of positive initial screening

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239
Q

What should you counsel pregnant women regarding fetal movement?

A
  • If there is a subjective decrease in fetal movement, try drinking juice, eating, changing position, or moving to a quiet room and count for 2 h; ≥6 movements in 2 h expected
  • If there are <6 movement counts in 2 h, patient should present to labour and delivery triage
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240
Q

When is the movement first noticed in pregnancy?

A

Notice first movement (“quickening”) at 18-20 weeks in primigravidas and can be 1-2 weeks earlier in multigravidas – can occur 1-2 weeks later if placenta is implanted on the anterior wall of the uterus

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241
Q

DDx of decreased fetal movements?

A

DASH:

  • Death of fetus
  • Amniotic fluid decreased
  • Sleep cycle of fetus
  • Hunger/thirst
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242
Q

What are the components of the biophysical profile?

A
  • Limb extension + flexion = tone
  • AFV 2cm + 2cm – fluid pocket, most important
  • Movement (3 discrete)
  • Breathing (one episode x 30s) – usually not until 32 weeks
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243
Q

Indications for biophysical profile

A

Post-term pregnancy, decreased fetal movement, IUGR, any other signs of fetal distress or uteroplacental insufficiency

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244
Q

Indications for NST?

A

Run these if suggestion of uteroplacental insufficiency or suspected compromise in fetal well-being

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245
Q

Normal NST findings?

A

Baseline: 110-160 bpm
Variability: Moderate or Absent/Minimal (<40m)
Decelerations: None / Occasional UV <30s
Accelerations: 2, =>15bpm of >15s in <40m (>32w)
2, =>10bpm of >10s in <40m (<32w)

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246
Q

Atypical NST findings?

A

Baseline: <110 or >160 for <30m, rising baseline
Variability: Absent/Minimal (40-80m)
Decelerations: UV 30-60s
Accelerations: 2, =>15bpm of >15s in 40-80m (>32w)
2, =>10bpm of >10s in 40-80m (<32w)

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247
Q

Abnormal NST findings?

A

Baseline: <110 or >160 for >30m, erratic baseline
Variability: Absent/Minimal (>80m), Marked (>10m)
Decelerations: UV >60s or Late
Accelerations: 2, =>15bpm of >15s in >80m (>32w)
2, =>10bpm of >10s in >80m (<32w)

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248
Q

What is menorrhagia?

A

Menses that are excessive (>80 mL) or prolonged (> 7 days)

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249
Q

Bleeding that is unrelated to menses, occurring irregularly between

A

Metrorrhagia

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250
Q

Bleeding that is excessive during menses and occurs irregularly between menses

A

Menometrorrhagia

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251
Q

Etiology of excessive/irregular/abnormal vaginal bleeding?

A

PALM COEIN
- Polyp: endometrial or cervical polyps - hyperplastic overgrowths of endometrial glands and stroma
- Adenomyosis: painful, endometrial glands/stroma present in uterine musculature
- Leiomyoma: fibroids, benign smooth muscle (or submucoasal) tumors.
- Malignancy: endometrial adenocarcinoma
- Coagulopathy: vWF most common or therapeutic anti-coagulation - heavy menstrual bleeding since menarche
- Ovulatory Dysfunction: endocrine disorders preventing ovulation, causing deviation from normal cycle (PCOS, hypothyroidism, hyperprolactinemia, anorexia, cirrhosis)
- Iatrogenic:
Platelet arterial clots – Clopidogrel, ASA, NSAIDs.
Venous factor thrombus – Warfarin, NOAC, warfarin
Equipment – Cu-IUD
- Not Yet Classified: causes of AUB that are not well-understood or not yet described

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252
Q

Most common neoplasm in women with reproductive age.

A

Leiomyoma

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253
Q

History for excessive/irregular/abnormal vaginal bleeding?

A
  • History of present illness should include quantity (eg, by number of pads used per day or hour) and duration of bleeding, as well as the relationship of bleeding to menses and intercourse
  • Menstrual history, including date of last normal menstrual period, age at menarche and menopause (when appropriate), cycle length and regularity, and quantity and duration of typical menstrual bleeding
  • Previous episodes of abnormal bleeding, including frequency, duration, quantity, and pattern (cyclicity) of bleeding
  • Sexual history, including possible history of rape or sexual assault
  • ROS:
  • Missed menses, breast swelling, and nausea: Pregnancy-related bleeding
  • Abdominal pain, light-headedness, and syncope: Ectopic pregnancy or ruptured ovarian cyst
  • Chronic pain and weight loss: Cancer
  • Easy bruising and excessive bleeding due to toothbrushing, minor lacerations, or venipuncture: A bleeding disorder
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254
Q

Physical exam findings for excessive/irregular/abnormal vaginal bleeding?

A
  • Vital signs, BMI, thyroid exam, skin (pallor, bruising, petechiae, hirsutism, acanthosis nigricans), abdo exam (masses, distension)
  • Gynecologic examination is done unless abdominal examination suggests a late-stage pregnancy; then, digital pelvic examination is contraindicated until placental position is determined. In all other cases, speculum examination helps identify lesions of the urethra, vagina, and cervix. Bimanual examination is done to evaluate uterine size and ovarian enlargement.
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255
Q

Red flags for excessive/irregular/abnormal vaginal bleeding?

A
  • Hemorrhagic shock (tachycardia, hypotension)
  • Premenarchal and postmenopausal vaginal bleeding
  • Vaginal bleeding in pregnant patients
  • Excessive bleeding
  • In children, difficulty walking or sitting; bruises or tears around the genitals, anus, or mouth; and/or vaginal discharge or pruritus
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256
Q

Investigations for excessive/irregular/abnormal vaginal bleeding?

A
  • Heme: CBC, TSH, prolactin, vWF, PT and PTT
  • Urine: chlamydia, gonorrhea, pregnancy test
  • Imaging: pelvic U/S or MRI, saline-infusion sonohysterogram (polyps) and in other scenarios (fertility workup)
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257
Q

Indications for endometrial biopsy?

A

Indications include age >35, risk factors (obese, PCOS, HNPCC), significant intermenstrual bleeding, post-menopausal bleeding, endometrial thickening > 4 mm

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258
Q

Contraindications for combined hormonal contraceptives

A

Smoking > 35yo (15 cig/day), multiple risk factors for arterial cardiovascular disease (^age, smoking, DM, HTN), HTN (sBP>160 or dBP>100), venous thromboembolism, known thrombogenic mutations, known ischemic heart disease, Hx of stroke, complicated valvular heart disease, systemic lupus erythematosus, migraine with aura at any age, breast cancer, cirrhosis, hepatocellular adenoma or hepatoma

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259
Q

Medical management of excessive/irregular/abnormal vaginal bleeding?

A
  • NSAIDS: reduce PGs, promoting uterine vasoconstriction
  • Tranexamic Acid: anti-fibrinolytic; caution w/ risk for venous thromboemboli
  • Combined Hormonal Contraceptives: ESTROGEN/progesterone (pill, patch, ring), continuous, etc
  • IUD
  • Gonadotropin release hormone agonists
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260
Q

Side effects of combined hormonal contraceptives?

A

Side effects: nausea, breast tenderness, bloating, spotting (break-through-bleeding)

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261
Q

Side effects of progesterone only contraceptive?

A

Spotting, breast tenderness, bloating, weight gain, nausea.

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262
Q

Surgical management of excessive/irregular/abnormal vaginal bleeding?

A
  • Endometrial Ablation

- Hysterectomy

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263
Q

Symptoms of uterine leiomyomas?

A

Majority asymptomatic. Heavy or prolonged menstrual bleeding (AUB), bulk-related symptoms (pelvic pressure, pain), and/or reproductive dysfunction (i.e. infertility or obstetric complications)

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264
Q

Where do uterine leiomyomas typically arise from and how are they described?

A

Benign monoclonal tumors arising from the smooth muscle cells of the myometrium. Fibroids are typically described according to their location in the uterus (submucosal, intramural, subserosal, cervical).

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265
Q

Diagnosis of uterine leiomyomas?

A

Clinical, based on pelvic imaging – likely a pelvic or trans-vaginal U/S (indications include pelvic pain/pressure/infertility or enlarged uterus on pelvic examination). Pathology confirmation not required to proceed with management, except in cases if another lesion suspected (i.e. uterine sarcoma). Saline Infusion Sonography (sonohysterography) improves characterization of protrusion extent/intracavitary lesions not seen on U/S.

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266
Q

Medical management of uterine leiomyomas?

A
  • NSAIDs + OCP/depo-provera
  • Selective Progesterone Receptor Modulators: ulipristal (Ella), will shrink fibroids (~20% smaller volume at 3 months) and decrease menstrual blood loss (90% reduction). Only approved for short duration (3-6 months). Can be useful pre-operatively. Smaller fibroids = easier surgery. Increased iron stores, hemoglobin.
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267
Q

Surgical management of uterine leiomyomas?

A

Myomectomy: hysteroscopic, laparoscopic, abdominal or Uterine Artery Embolization

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268
Q

What is adenomyosis?

A

Ectopic endometrial glands and stroma are found within the myometrium, resulting in a symmetrically enlarged and globular uterus.

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269
Q

Presentation of adenomyosis?

A

Parous women in their 40’s to 50’s, uterus enlarged and boggy, pelvic pain (usually noncyclical), dysmenorrhea, and menorrhagia.

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270
Q

Investigations for adenomyosis?

A

Transvaginal U/S or MRI to differentiate between adenomyosis and uterine fibroids

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271
Q

Management of adenomyosis?

A
  • No proven medical therapy for treatment.
  • GnRH agonist, NSAIDs, and OCPs may be used for pain and bleeding.
  • Hysterectomy: Definitive therapy if childbearing is complete. The diagnosis is usually confirmed after histologic examination of the hysterectomy specimen.
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272
Q

Most common gyne malignancy?

A

Endometrial cancer

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273
Q

Types of endometrial cancer?

A
  • Type I (endometroid adenocarcinoma): MOST COMMON (75%). Estrogen-related. Slower growing, related to obesity. Comes from thinning of the uterus
  • Type II (nonendometroid carcinoma): non-estrogen related. MORE AGGRESSIVE. Thin patient
    • can have hyperplasia with atypia (precursor for endometrial cancer, 40% have concurrent cancer).
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274
Q

Risk factors for endometrial cancer?

A
  • Metabolic syndrome (obesity, type II DM) - adipose tissue makes more estrogen than normal
  • Early menarche, Late menopause
  • PCOS
  • Nulliparity
  • Estrogen-only HRT
  • Lynch syndrome – FHx history of colon cancer
  • Personal history with breast cancer - Tamoxifen – estrogen-like effects on uterine tissue.
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275
Q

Presentation/symptoms of endometrial cancer?

A

Abnormal vaginal bleeding either postmenopausally, abnormally heavy irregular bleeding in reproductive years. Later stages pelvic pain and palpable mass.

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276
Q

Diagnosis of endometrial cancer?

A
  • NEED TO SAMPLE/BIOPSY ENDOMETRIAL TISSUE. How? No anesthetic, go through cervix and get a quick biopsy through a pipelle (aspiration curettage). If negative biopsy and AUB persists, need D&C or hysteroscopy! Hysteroscopic view – look at lining of uterus, if its fluffy and thick – not normal. DON”T DO BIOPSY IN PREGNANT WOMEN
  • Can do a transvag U/S – but this is not diagnostic, just suggestive! Wall thickness in postmenopausal women <5mm = low risk, >10mm = high risk.
  • CXR/CT scan to rule out mets
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277
Q

Surgical treatment for endometrial cancer?

A

Standard of care, early stage is hysterectomy, BSO (bilateral salpingo-oophorectomy) and staging

  • Traditional open laparotomy – longer recovery, more pain, risk of infection
  • MIS (lap) - shorter recovery, less bleeding, infection and post op pain
  • Lymph Nodes – helps determine spread of disease, upstages patients
  • ICG Infared Technology - Inject the tumour with ICG and it follows the lymphatics to the first/sentinel lymph node. Taking out sentinel nodes and not all their pelvic nodes decreases lymphedema
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278
Q

Medical treatment for endometrial cancer?

A

Unfit for surgery – mirena IUD, oral high dose progesterone, letrozole (aromatase inhibitor)

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279
Q

Radiation treatment for endometrial cancer?

A

Two types – vaginal vault or full pelvic RT. Decreases risk of recurrence in pelvis or vaginal vault. DOES NOT REDUCE RISK OF DISTANT RECURRENCE.

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280
Q

Which syndrome is associated with endometrial cancer?

A

Lynch syndrome – includes higher incidence of colon cancer and some ovarian cancer

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281
Q

Acute and chronic S/E of pelvic RT?

A
  • Acute – fatigue, rashes, nausea

- Chronic – looser stools, radiation cystitis/hematuria, altered sexuality

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282
Q

Indications for offering hormonal therapy for endometrial cancer?

A
  • Medically and surgically unfit for OR. Frail elderly, too many surgical risks
  • Grade 1 – wanting to preserve fertility. Standard of care still TAH BSO. Do TAH BSO after childbearing finished
  • If counseled, compliant in follow up, understand risks, 6-12 month trial high dose progesterone
  • Need to follow, re sample endometrial biopsy
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283
Q

Symptoms of ovarian cancer?

A

Symptoms: nonspecific symptoms – bloating, pain, bowel changes
- U/S – ascites, large mass

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284
Q

Treatment of ovarian cancer?

A
  • If we can’t debulk, start chemo – one of the best solid tumors to see a response to.
  • Bevacizumab is ab against VEGF and is used commonly for bowel cancer.
  • Surgery might be an option after several rounds.
  • We offer all women with high grade serous cancer a BRCA1/2 test.
  • Olaparib may actually improve overall survival - biggest thing to happen in the last 30 years for women with these mutations
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285
Q

Definition of preterm labour?

A

Regular painful contractions accompanied by cervical dilatation/effacement between 20-37wks.

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286
Q

Etiology of preterm labour?

A
  • Idiopathic (most common)
  • Maternal: infection (recurrent pyelonephritis, untreated bacteriuria, chorioamnionitis), HTN, DM, chronic illness, mechanical factors (previous obstetric, gynecological, and abdominal surgeries); socio-environmental (poor nutrition, smoking, drugs, alcohol, stress), pre-eclampsia
  • Maternal-fetal: PPROM (common), polyhydramnios, placenta previa, abruptio placentae, or placental insufficiency
  • Fetal: multiple gestation, congenital abnormalities, fetal hydrops
  • Uterine: excessive enlargement (hydramnios, multiple gestation), malformations (intracavitary leiomyomas, septate uterus, and Müllerian duct abnormalities
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287
Q

Risk factors of preterm labour?

A
  • Prior history of spontaneous PTL is the most important risk factor
  • Prior history of large or multiple cervical excisions (cone biopsy) or mechanical dilatation (D&C)
  • Cervical length: measured by transvaginal U/S (cervical length >30 mm has high negative predictive value for PTL before 34 wk)
  • Infection (uterine, placental, maternal) + bacteriuria
  • Shorter inter-pregnancy interval
  • Family history of preterm birth
  • Smoking
  • Late maternal age
  • Multiple gestation
  • Polyhydramnios – increased pressure
  • History of bleeding in 2nd or 3rd TM
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288
Q

Signs and symptoms of preterm labour?

A
  • Early Sx: menstrual-like cramps or mild/irregular contractions, lower back ache, vaginal pressure, bloody show
  • True Sx: regular uterine contractions (2 in 10 min, >6/h) accompanied by change in cervical dilatations and/or effacement (>1 cm dilated, >80% effaced, or length <2.5 cm)
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289
Q

Diagnostic tests for preterm labour?

A
  • Lab Testing: GBS swab, CBC, blood type and screen
  • FFN (Fetal Fibronectin) in vagina – a glycoprotein in amniotic fluid and placental tissue. Positive if >50 ng/mL
  • U/S: fetal position, placental position/abnormalities, AF volume, cervical length (20-30mm).
290
Q

Indications for FFN (Fetal Fibronectin)?

A

1 or more signs of preterm labour (regular contractions >6/h, pelvic pressure, low abdominal pain and/or cramps, low backache) + 24-34 weeks, intact membranes, <3 cm dilated, established fetal well being

291
Q

Contraindications for FFN (Fetal Fibronectin)?

A

Contraindicated as well if: cerclage, active vaginal bleeding, vaginal exam, or sex in last 24 h

292
Q

What are the methods used to prevent preterm labour?

A
  • Cervical Cerclage
  • Progesterone
  • Lifestyle Modification
293
Q

Diagnosis of cervical incompetence?

A
  • Obstetrical Hx: silent cervical dilation, recurrent T2 losses, cervical procedures such as loop excisions
  • Ability of cervix to hold an inflated Foley catheter during a hysterosonogram
  • Transvaginal U/S of cervical length is recommended only for high-risk pregnancies and only before 30 wk GA
294
Q

Definition of cervical cerclage?

A

Placement of cervical sutures at the level of the internal os, usually at the end of the T1 or in the T2 and removed in the T3

295
Q

Indications for cervical cerclage?

A

Cervical incompetence (i.e. cervical dilation and effacement in the absence of increased uterine contractility)

296
Q

Superior to cerclage in preventing preterm labour of singletons not due to cervical incompetence

A

Progesterone

297
Q

If previous PTL or short cervix?

A
  • If previous PTL: 17-alphahydroxyprogesterone 250 mg IM weekly from 16+0 to 36 wk GA
  • If short cervix: 200 mg daily vaginally from time of diagnosis to 36 wk GA
298
Q

Lifestyle modification for the prevention of preterm labour?

A

Smoking cessation, substance use reduction, treatment of GU infections (including asymptomatic UTIs), and patient education regarding risk factors

299
Q

Management of preterm labour?

A
  1. Tocolytics
  2. Antenatal corticosteroids
  3. Neuroprotection
  4. Antibiotics
300
Q

What do tocolytics do?

A

Inhibit uterine contractions (for steroid benefit, fetal neuroprotection, transport to tertiary care)

301
Q

Requirements for tocolytics?

A
  • Preterm labour
  • Live, immature fetus, intact membranes, cervical dilatation of <4 cm
  • Absence of maternal or fetal contraindications
302
Q

Contraindications to tocolytics?

A
  • Maternal: bleeding (placenta previa or abruption), maternal disease (HTN, DM, heart disease), preeclampsia or eclampsia, chorioamnionitis
  • Fetal: erythroblastosis fetalis, severe congenital anomalies, fetal distress/demise, IUGR, multiple gestation (relative)
303
Q

Commonly used agents for tocolytics?

A

Most use Indocin (NSAID) or Nifedipine (Adelact)

304
Q

What are the benefits of antenatal corticosteroids for preterm labour?

A

Accelerate fetal lung maturation (reduce RDS, intraventricular hemorrhage, necrotizing enterocolitis, mortality)

305
Q

Dose and GA used for antenatal corticosteroids for preterm labour?

A

Betamethasone 12mg IM q24h x 2 doses <34 wks

306
Q

What does the GA need to be in order to use MgSO4 for neuroprotection in preterm labour?

A

If <32 weeks, then give MgSO4 if delivery is imminent!

307
Q

Use of antibiotics in preterm labour?

A

No benefits except for GBS prophylaxis – Pen G 5mU IM/IV then 2.5mU q4h until delivery

308
Q

What is defined as small for gestational age?

A

<10th%ile for gestational weight according to N American charts but not necessarily growth restricted (e.g. South Asian baby on N American curve). Not pathologic

309
Q

What is defined as intrauterine growth restriction?

A

<10th%ile fetus that has not reached its growth potential. Infant weight <10%ile for GA or <2500g or abdominal circumference <10%ile. Pathologic

310
Q

What are the 3 categories of etiology for IUGR?

A

Maternal (nutrient delivery), placental (nutrient transfer), or fetal (nutrient utilization) factors

311
Q

What are the maternal causes of IUGR?

A

Malnutrition, smoking, drug abuse, alcoholism, cyanotic heart disease, type 1 DM, SLE, pulmonary insufficiency, previous IUGR (25% risk, most important risk factor), and chronic HTN

312
Q

What are the placental causes of IUGR?

A
  • Any disease that causes placental insufficiency

- Gross placental morphological abnormalities (infarction, hemangiomas, placenta previa, and abnormal cord insertion

313
Q

What are the fetal causes of IUGR?

A

Multiple gestation (why? inadequate placental reserve, occurs more in monozygotic), infection (5-10% of IUGR cases e.g. TORCH – toxo, other (varicella, syphilis), rubella, CMV, herpes), genetic disorders, congenital anomalies/malformations.

314
Q

What are the two types of IUGR?

A
  • Symmetric IUGR – Type 1
  • Asymmetric IUGR – Type 2
  • Indeterminate IUGR - Type 3
315
Q

When does symmetric/type I IUGR occur and what are the causes?

A

Early onset, congenital anomalies or TORCH infections

316
Q

Clinical features of symmetric/type I IUGR

A

Reduced growth of both head and abdomen

317
Q

When does asymmetric/type II IUGR occur and what are the causes?

A
  • Growth inhibition late in gestation affecting cell hypertrophy and growth, usually > 23 weeks! Later in pregnancy.
  • Placental insufficiency (redistribution of blood to critical organs: brain, heart, adrenals preserved, brain sparing effect) or external factor – brain/heart/adrenals spaced, ^MCA doppler =
318
Q

Clinical features of asymmetric/type II IUGR

A
  • Fetal abdomen is disproportionately smaller than fetal head
  • Brain is spared; therefore head:abdomen ratio increased - loss of subcut fat, decreased muscle mass.
319
Q

What is symmetric IUGR – Type 1a vs Type 1b

A

1A: constitutional (small women) vs.
1B: intrinsic - growth inhibition early in gestation due to fetal abnormalities/insult. Inhibition of active mitosis, affecting cell hyperplasia.

320
Q

If mother at high risk for IUGR or SFH lags >2 cm behind GA, what should be done?

A
  • U/S for biparietal diameter, head and abdominal circumference ratio, femur length, fetal weight, AFV (decrease associated with IUGR), and decrease in the rate of growth
  • ± BPP
  • Doppler analysis of umbilical cord blood flow
321
Q

Management of IUGR?

A
  • Modify controllable factors: smoking, alcohol, nutrition, and treat maternal illness
  • Serial BPP (monitor fetal growth) and determine cause of IUGR, if possible
  • Delivery when extrauterine existence is less dangerous than continued intrauterine existence (abnormal function tests, absent growth, severe oligohydramnios) especially if GA >34 wk
  • As IUGR fetuses are less likely to withstand stresses of labour, they are more likely to be delivered by Cesarean section
322
Q

Complications of IUGR?

A
  • Prone to meconium aspiration, asphyxia, polycythemia, hypoglycemia, hypocalcemia, hypophosphatemia, hyponatremia, and mental retardation
  • Greater risk of perinatal morbidity and mortality
323
Q

Etiology of breast discharge

A
  • Intraductal papilloma
  • Mammary duct ectasia
  • Fibrocystic changes
  • Abscess/infection
  • Breast cancer - Intraductal carcinoma or invasive ductal carcinoma
  • Hyperprolactinemia (pituitary tumor, hypothyroidism)
  • Medications: Oral contraceptives, antihypertensive drugs (eg, methyldopa, reserpine, verapamil), H2-antagonists (eg, cimetidine, ranitidine), opioids, and dopamine D2 antagonists (eg, many psychoactive drugs, including phenothiazines and tricyclic antidepressants).
324
Q

Most common cause of breast discharge

A

Intraductal papilloma

325
Q

What should be asked on history for breast discharge?

A
  • Characteristics of nipple discharge: Unilateral vs bilateral, Single vs multi duct, Bloody/OB vs watery, duration, Spontaneous vs induced (manipulation of breast)
  • Risk of breast cancer: Associated breast mass, nipple changes, skin retraction, axillary adenopathy, Risk factors for breast CA, Mammographic abnormality
  • Other breast pathology: Breast pain, cyclic (fibrocystic disease, cyclic mastopathy), Breast cysts, lumps, infections
  • R/o other causes, especially if bilateral or milky: pregnancy, psychiatric history (depression), visual fields (bitemporal hemianopsia in pituitary tumor), headaches, smoker, risk for lung CA
326
Q

Red flags of breast discharge?

A

Unilateral, localized to single duct, persistent, spontaneous, palpable mass, high volume, sanguineous (bloody), or serosanguinous (blood-tinged), male sex

327
Q

Physical exam for breast discharge?

A
  • Symmetry/contour of breast, position of nipples, scars, skin retraction, dimpling, edema/erythema, ulceration, crusting of nipple, changes in skin color, elicit discharge and identify duct(s) involved, axillary/supraclavicular lymph nodes, delineate masses, localize tenderness
328
Q

Approach to diagnosis for bilateral breast discharge?

A
  • Usually due to an endocrinological or physiologic process
  • Bloody nipple discharge, abnormal mammogram/US, or the presence of breast mass clinically REQUIRES surgical evaluation
  • Bilateral multiductal secretion that is non-bloody is usually benign (regardless of color) > medical evaluation and endocrine workup may be required, surgical consult is not indicated
329
Q

Approach to diagnosis for unilateral breast discharge?

A
  • Uni-ductal: more likely to be pathological (papilloma, intraductal breast CA), whether or not the d/c is bloody
  • Multi-ductal: less likely to represent significant pathology and should be investigated as bilateral discharge
330
Q

Investigations for pathologic breast discharge

A
  • Lesions that appear cystic are sometimes aspirated, and solid masses or any that remain after aspiration are evaluated with mammography followed by imaging-guided biopsy.
  • MRI if mammogram and US are negative
  • Surgical evaluation is required for dx and tx EVEN if imaging results are negative
331
Q

Indications for surgical evaluation (excisional bx) for breast discharge?

A

Breast mass, any imaging abnormality, d/c is spontaneous, uniductal, and/or bloody discharge.

332
Q

Investigations for non-pathologic breast discharge

A

PE/imaging is negative, d/c is multiductal + nonbloody > Lab tests, medical evaluation, galactorrhea workup

333
Q

Treatment for pathologic breast discharge

A
  • Malignancy is r/o > Terminal duct excision with/without image guidance
  • Core needle biopsy demonstrates DCIS/invasive BCA > appropriate CA surgery
334
Q

Treatment for non-pathologic breast discharge

A
  • Stop insulting medication (metoclopramide, SSRIs)

- Treat hyperprolactinemia

335
Q

What is intraductal papilloma

A

Papillary tumor growing from the lining of the breast duct

336
Q

Findings of intraductal papilloma associated with breast discharge?

A

Unilateral bloody (or guaiac-positive) or serosanguinous discharge. Should be excised whenever diagnosed by core needle biopsy

337
Q

Findings of duct ectasia associated with breast discharge?

A

Unilateral or often bilateral bloody, serosanguinous, or multicolored (purulent, gray, or milky) discharge

338
Q

Findings of fibrocystic changes associated with breast discharge?

A

A mass, often rubbery and tender, usually in premenopausal women. Possibly a serous, green, or white discharge. Possibly a history of other masses

339
Q

Findings of abscess/infection associated with breast discharge?

A

Acute onset with pain, tenderness, or erythema. Often fever. With abscess, a tender mass and possibly purulent discharge

340
Q

Most common malignancy associated with nipple discharge

A

DCIS

341
Q

Findings of breast cancer associated with breast discharge?

A

May have a palpable mass, skin changes, or lymphadenopathy. Spontaneous, unilateral, uniductal, blood discharge

342
Q

Clinical features of hyperprolactinema?

A

Galactorrhea (secretion of breast milk in women and, in rare cases, men), infertility, hypogonadism, amenorrhea, oligomenorrhea, erectile dysfunction

343
Q

Causes of hyperprolactinema?

A
  • Prolactinoma: Most common pituitary adenoma (prolactin-secreting tumours may be induced by estrogens and grow during pregnancy)
  • Pituitary masses with pituitary stalk compression causing reduced dopamine inhibition of prolactin release
  • Primary hypothyroidism (low free T4, increase TRH, stimulate PRL)
  • Decreased clearance due to chronic renal failure or severe liver disease (prolactin is metabolized by both the kidney and liver)
  • Medications with anti-dopaminergic properties are a common cause of high prolactin levels: Antipsychotics (common), antidepressants, antihypertensives (verapamil/methyldopa), anti-migraine agents (triptans/ergotamines), bowel motility agents (metoclopramide/domperidone), H2-blockers (ranitidine)
  • Macroprolactinemia (high molecular weight prolactin also known as big-big prolactin) that has no action
344
Q

Investigations of hyperprolactinema?

A
  • Serum PRL, TSH, liver enzyme tests, creatinine
  • Macroprolactin level in patients with hyperprolactinemia but no symptoms of prolactin excess
  • MRI of the sella turcica when a secondary cause is not identied or when prolactin levels suggest that there may be underlying tumoural hyperprolactinemia
345
Q

Findings in female patients with prolactinoma?

A

Female patients (pre-menopausal) - Most have small tumors (microadenomas), Galactorrhea 30-80%, Menstrual irregularity and infertility, Symptoms of large tumors (less common)

346
Q

Findings in male patients with prolactinoma?

A

Male patients - Usually large tumors (macroadenomas), Impotence and reduced libido (sex drive), galactorrhea not common, Symptoms of large tumors: visual field abnormalities, headache and hypopituitarism

347
Q

Treatment of hyperprolactinema?

A
  • First line: long-acting dopamine agonist: bromocriptine, cabergoline, or quinagolide
  • Surgery ± radiation (rare)
  • Prolactin-secreting tumours are often slow-growing; treatment may not be necessary in the setting of small tumours associated with hyperprolactinemia that does not result in hypogonadism or bothersome galactorrhea
  • If medication-induced, consider stopping medication if possible
  • In certain cases if microprolactinoma and not planning on becoming pregnant, may consider OCP
348
Q

What increases physiologic discharge?

A

Increases with increased estrogen states: pregnancy, OCP, mid-cycle, PCOS, or premenarchal

349
Q

Signs and symptoms of physiologic discharge?

A

Clear, white, flocculent, odourless discharge; pH 3.8-4.2, no associated vulvar or vaginal symptoms

350
Q

Ddx for vulvar pruritius?

A
  1. Physiologic discharge and cervical mucus production
  2. Non-physiologic
    - genital tract infection
    - vulvovaginitis: candidiasis, trichomoniasis, BV, polymicrobial superficial infection
    - chlamydia, gonorrhea
    - pyosalpinx, salpingitis
    - genital tract inflammation (non-infectious)
    - local: chemical irritants, douches, sprays, foreign body, trauma, atrophic vaginitis, desquamative inflammatory vaginitis, focal vulvitis
    - neoplasia: vulvar, vaginal, cervical, endometrial
    - systemic: toxic shock syndrome, Crohn’s disease, collagen disease, dermatologic (e.g. lichen sclerosis)
    - IUD, OCP (secondary to progesterone)
351
Q

Clinical findings of prepubertal vulvovaginitis?

A

Irritation, pruritus, discharge, vulvar erythema, vaginal bleeding (specifically due to Group A Streptococci and Shigella)

352
Q

Etiology of prepubertal vulvovaginitis?

A
  • poor hygiene (proximity of anus to vagina)
  • foreign bodies (most commonly tissue paper)
  • irritation by perfumed soaps, chemicals, and tight clothing
  • localized skin disorders: lichen sclerosis, condyloma acuminata ‚ñ† trauma: accidental straddle injury, sexual abuse
  • infectious: pinworms, Candida (if using diapers or chronic antibiotics), Group A streptococcus, S. aureus and Shigella, discovery of STI should raise suspicion of sexual abuse
353
Q

Investigations of prepubertal vulvovaginitis?

A
  • Vaginal swab for culture (specifically state that it is a pre-pubertal specimen)
  • pH, wet-mount, and KOH smear in prepubertal adults only
354
Q

Definition of vaginitis

A

Vaginitis is a general term for a group of disorders affecting the vagina, caused by infection, inflammation, or changes in the normal flora.

355
Q

Treatment of prepubertal vulvovaginitis?

A
  • Enhanced hygiene and local measures (handwashing, white cotton underwear, no nylon tights, no tight fitting clothes, no sleeper pajamas, sitz baths, avoid bubble baths, use mild detergent, eliminate fabric softener, avoid prolonged exposure to wet bathing suits, urination with legs spread apart)
  • A&D* dermatological ointment (vitamin A/D) to protect vulvar skin
  • Infectious: treat with antibiotics for organism identified
356
Q

What should be asked on history for vulvovaginitis?

A
  • Full OBHx and GyneHx (pap smear hx, pelvic infection hx, procedures done to cervix, endometriosis/PCOS?)
  • Timeline/severity of all sx
  • Sexual: partners, practices, protection from STDs, past history of STDs, prevention from pregnancy
  • GI/GU: pelvic pain, urinary pain, vaginal pain, dyspareunia, ask about colour/amount/smell/blood, re: discharge
  • Consider: recent Abx use, pregnancy, OCP, immunosuppression, DM, vaginal douching (CANDIDIASIS), semen, drugs, chemicals
357
Q

Physical exam for vulvovaginitis?

A
  • Check for pruritis, burning, foul-smelling discharge, change in amount/consistency/colour, check abdo
  • STI’s: check external genitals for ulcerations, lesions, or signs of trauma
  • Reactive Arthritis/Syphillis: inspect eyes for conjunctivitis, uveitis, rash, mucosal ulcerations (syphilis)
  • Ensure that you are doing a speculum and bimanual exam (to r/o ascending infection (PID)); assess discharge/pooling, assess cervix, tenderness, or signs of blood - smell?
358
Q

Ddx for vulvovaginitis?

A

Infective/chemical/atrophic vaginitis (50+), cervicitis (STIs), malignancy, PID, foreign body, disrupted vag flora (BV)

359
Q

Investigations for vulvovaginitis?

A
  • Serology: syphilis, HIV
  • Wet Mount: discharge on slide + 2cc of saline, place coverslip and examine under microscope (Trich/BV/Yeast)
  • Whiff Test: place discharge on a slide, add few drops of 10% KOH and ‘whiff’, fishy odour suggestive of BV
  • Endocervical(F)/Vaginal/Urethral(M) Swab: HSV PCR + Syphilis PCR + Trich/BV/Yeast (+/- G&C)
  • Urinalysis: NAAT first catch, culture/sensitivity for gonorrhea/chlamydia
  • Biopsy: suspicious lesions
360
Q

Pathophysiology of bacterial vaginosis

A
  • Overgrowth of Gardnerella vaginalis

- Gram Stain: more lactobacillus (good score) more gardnerella (worse score)

361
Q

Signs and symptoms of bacterial vaginosis

A

Odour – fishy, grey thin discharge, absence of vulvar/vaginal irritation, ph >4.5 CLUE CELL

362
Q

Treatment of bacterial vaginosis

A
  • No treatment if non-pregnant and asymptomatic, unless scheduled for pelvic surgery or procedure
  • Metronidazole PO (500mg BID x 7d) or clindamycin (300mg PO BID x 7d) or topical
363
Q

Pathophysiology of candida vaginitis

A
  • YEAST HYPHAE (may need some KOH) - 90% C. Albicans
  • Patho: Predisposing factors include: Immunosuppressed host (DM, AIDS, etc.) Recent antibiotic use, Increased estrogen levels (e.g. pregnancy, OCP)
364
Q

Signs and symptoms of candida vaginitis

A

Pruritic/burning, white and curdy discharge, pH 4-4.5, + erythematous, dysuria, wet mount findings of hyphae KOH

365
Q

Treatment of candida vaginitis

A

Fluconazole PO (150mg) (watch liver) or OTC imidazole or polyene antifungals (1d - 7d doses)

366
Q

Parasite that causes trichomonas vaginitis

A

TRICHOMONAS PROTOZOAN (mobile flagellates)

367
Q

Treatment of trichomonas vaginitis

A
  • Metronidazole PO (2g x 1d) or topical metro/clotrimazole (BID x 5d)
  • TREAT SEXUAL PARTNER TOO + REPORT
368
Q

Symptoms/signs of trichomonas vaginitis

A

Often asymptomatic (10-50%), Green and frothy discharge, pH 5-6, petechiae on vagina and cervix (strawberry), occasionally irritated, tender vulva, dysuria/dyspareunia, frequency, wet mount finding of trich

369
Q

Typical causes of vaginitis?

A

Vaginitis → trichomoniasis, bacterial vaginosis, or candida.

370
Q

Typical causes of cervicitis?

A

Cervicitis → chlamydia or gonorrhea, mucopurulent cervicitis. If + abd pain → PID.

371
Q

Testing for vaginal discharge?

A
  • Gram stain not helpful but wet mount to look for candida, BV, trich useful if available
  • Collect specimens: vaginal swab (if doing speculum) or urine (G/C)
372
Q

Testing for urethral discharge?

A
  • NAAT (+pharyngeal swab) for G/C
  • Urine for G/C
  • Blood tests for HIV antibody and syphilis
373
Q

Testing for genital ulcer?

A
  • Darkfield microscopy, syphilis PCR, PCR for herpes simplex virus
  • Serologic tests for syphilis: EIA
374
Q

Typical causes of genital ulcer?

A

HSV, syphilis, chancroid, lymphogranuloma venereum (LGV)

375
Q

Typical causes of urethral discharge?

A

Gonorrhea, Non gonococcal urethritis (chlamydia, mycoplasma genitalium, trichomonas, herpes simplex (rare))

376
Q

Typical causes of genital warts?

A

HPV, syphilis

377
Q

Typical causes of testicular swelling?

A

Gonorrhea, chlamydia, tricomoniasis, GNBs

378
Q

Most common bacterial STI in Canada

A

Chlamydia

379
Q

Typical causes of genital rash?

A

Syphilis or disseminated gonorrhea or chlamydia

380
Q

Clinical features of chlamydia

A
  • Often symptomatic, usually clear discharge, pelvic pain, post-coital/intermenstrual bleeding (esp. if on OCP + prior hx of good cycle control), symptomatic sexual partner
  • Urethral Syndrome: dysuria, frequency, pyruria, no bacteria on culture
381
Q

Transmission of chlamydia

A

Sexually + vertically

382
Q

Female manifestations of chlamydia

A

Most often asymptomatic, cervicitis, vaginal discharge, dysuria, lower abdo pain, dyspareunia, conjunctivitis, abnormal vaginal bleeding, proctitis

383
Q

Male manifestations of chlamydia

A

Often asymptomatic, urethral discharge, urethritis, dysuria, testicular pain, conjunctivitis, proctitis

384
Q

Sequelae of chlamydia

A
  • Females: ectopic preg, infertility, chronic pelvic pain + PID (low grade salpingitis/adhesions = tubal obstruction)
  • Males: epididymo-orchitis, infertility
  • Both: Reiter’s syndrome, Fitz High Curtis syndrome (liver capsule inflammation)
385
Q

Investigations of chlamydia

A

Nucleic acid amplification test; first catch urine can also be used since obligate intracellular parasite – tissue culture is definitive standard…urine/self vaginal tests available (= or more effective than cerv swab)

386
Q

Treatment of chlamydia?

A
  • Doxycycline 100mg PO BID (better for rectal) for 7 days or azithromycin 1g PO single dose (good for pregnancy)
  • Co-Infection: treat gonorrhea b/c high rate of co-infection
  • Partners: treat, report
387
Q

Who should be tested for cure for chlamydia?

A

Do it on everyone with high risk factors (pregnancy, pharyngeal/rectal infection, or potentially reduced susceptibility) – 4 days post-treatment or urine PCR 2 weeks post treatment; if no risk factors then rescreen 6-12 months post-treatment

388
Q

Male manifestations of gonorrhea

A

Males: urethritis, epididymitis

389
Q

Clinical features of gonorrhea

A

PURULENT URETHRAL DISCHARGE, dysuria, PID, however often asymptomatic (symptoms may present 7-21d after infection)

390
Q

Female manifestations of gonorrhea

A

Females: cervicitis, PID, urethritis

391
Q

Transmission of gonorrhea

A

Sexually + vertically

392
Q

Investigations of gonorrhea

A

Typically a NAAT (swab cervical, rectal, and throat (if indicated)). You could also do first catch urine sample. *Culture is the preferred method for sexual assault/tx failure/infection acquired overseas as it’s the only way to get antimicrobial susceptibility

393
Q

Male/female manifestations of gonorrhea

A

Both: pharyngeal infection, conjunctivitis, proctitis, disseminated gonococcal infection – rash, polytenosynovitis

394
Q

Treatment of gonorrhea

A
  • Heterosexual or Pregnant: cefixime 800 mg PO + azithromycin 1g PO. Azithromycin only used as monotherapy if strong contraindication to cephalosporins
  • Pharyngeal infections or MSM: single dose of ceftriaxone 250mg IM + azithromycin 1g PO
  • Co-infection: treat chlamydia b/c high rate of co-infection
  • Partners: treat, report, abstain from sex for a week, screening the same as with chlamydia
395
Q

Etiology of mycoplasma genitalium?

A

Small facultative anaerobic bacteria without a cell wall

396
Q

Clinical manifestations of mycoplasma genitalium?

A

Asymptomatic, can cause similar presentation to G/C

397
Q

Investigations of mycoplasma genitalium?

A
  • NAAT (not available in Alberta, need to send to National Microbiology lab)
  • Recommended in persistent or recurrent urethritis, cervicitis, or PID despite empiric treatment
398
Q

Treatment of mycoplasma genitalium?

A

Moxifloxacin

399
Q

Minimum criteria for PID?

A

Lower abdomen/pelvic pain, cervical motion or uterine/adnexal tenderness

400
Q

Additional criteria for PID?

A

Temperature >38.3C, mucopurulent cervical/vaginal discharge, WBCs on wetmount of discharge, high ESR/CRP

401
Q

Sequelae of PID?

A

Severity of clinical presentation corresponds poorly with damage, infertility, ectopic pregnancy, CPP, pelvic adhesions, tubo-ovarian abscess, pelvic thrombophlebitis

402
Q

When should someone with PID be hospitalized?

A

Hospitalization: severe illness, nausea/vomiting, fever, cannot exclude surgical emergency, pregnancy, poor response to PO abx, tubo ovarian abscess, imunodeficient

403
Q

Treatment of PID?

A
  • Ceftriaxone 250mg IM + doxycycline 100mg PO BID x 14 days OR cefoxitin + doxycycline (Foxy Doxy) OR clindamycin + gentamycin until afebrile for 24h with clinical improvement
  • Other: remove IUDs, counsel, partner notification, STI reporting, re-evaluate in 38-72h and 7-10d
404
Q

Clinical features of herpes simplex virus?

A
  • May be asymptomatic, vesicles on erythematous base, then painful blister with crust (syphilis is usually not painful), enlarged lymph nodes. Usually on external genitals, oral mucosa, cervix!
  • Primary episodes typically more severe than recurrent and tend to be bilateral
  • Recurrent disease usually associated with burning or tingling at site (24-48hr before lesions erupt)! Genital - Reactivation is usually unilateral but primary is bilateral! Can be subtle erythematous patches in boxer zone.
405
Q

Investigations of herpes simplex virus?

A

NAAT placed in universal transport media – swab the lesion

406
Q

Treatment of first episode of herpes simplex virus?

A
  • Education regarding transmission (any shared contact with lesions at any stage, shedding is also common even when a person is asymptomatic), use barrier contraception, avoid contact from onset of prodrome until lesions have cleared
  • First Episode: acyclovir 400mg PO TID x 7-10 days or 200mg PO 5x/day x 7-10 days or valacyclovir 1g PO BID x 7-10 days or famciclovir 250mg PO TID x 7-10 days
407
Q

Recurrent episodes of herpes simplex virus?

A

Acyclovir 400mg PO TID x 5 days or 800mg PO x 5 days or valacyclovir 500g PO BID x 3 days or 1g OD x 5 days or famciclovir 125mg PO BID x 5 days or 1g PO BID x 1 day or 500mg PO x 1 day then 250mg PO BID x 2 days

408
Q

Daily suppressive therapy for herpes simplex virus?

A

Consider if >6 recurrences per year or one every 2 months; acyclovir 400mg PO BID or valacyclovir 500mg or 1g PO OD or famciclovir 250mg PO BID

409
Q

Severe disease for herpes simplex virus?

A

IV acyclovir 5-10mg/kg q8h x 2-7 days or until clinical improvement followed by PO thx to complete 10 days of therapy total

410
Q

When does primary syphilis present and what are the symptoms?

A

3-4 weeks post-exposure, painless chancre on vulva/vagina/cervix, serological tests usually negative – local infection only

411
Q

When does secondary syphilis present and what are the symptoms?

A

2-6 months post-exposure, non-specific sx like malaise, anorexia, headache, diffuse lymphadenopathy, generalized maculopapular rash (palms, soles (mostly these two), trunk, limbs), condylomata lata (anogenital, broad based fleshy grey lesions), serological tests usually positive

412
Q

When does latent syphilis occur and what are the symptoms?

A

No clinical manifestations, detected by serology only. Late >1year – non-infectious

413
Q

What are the symptoms and treatment of congenital syphilis?

A

fetal anomalies, stillbirths, or neonatal death, treat fetus with Pen G IV

414
Q

What are the symptoms of tertiary syphilis?

A

may involve any organ system, neurosyphilis (tabes dorsalis, general paresis, dementia), cardio (aortic aneurysm, dilated aortic root), vulvar gamma (nodules that enlarge, ulcerate, and necrotic)

415
Q

Best test for syphilis?

A

Darkfield microscopy

416
Q

What is the screening test for syphilis?

A
  • EIA (measures IgM or IgG antibodies against Treponema pallidum) = SCREENING TEST. Arises during primary stage and persists for life
417
Q

What are the supplemental/confirmatory test for syphilis?

A
  • When EIA +, TPPA needs to be done to verify. RPR tells us the stage
  • TPPA measures antibodies to Treponema pallidum = supplemental/confirmatory test
418
Q

What is the staging test for syphilis?

A

RPR titre tends to parallel disease activity, useful indicator of response to therapy by observing fall in titres over time. Used for STAGING

419
Q

Treatment of primary, secondary or latent <1yr duration syphilis?

A

Benzathine penicillin G 2.4 million units IM x 1dose

420
Q

Treatment of latent >1yr duration syphilis?

A

Benzathine penicillin G 2.4 million units IM q1week x 3 weeks

421
Q

Treatment of neurosyphilis

A

IV aqueous penicillin G 3-4 million units IM q4h x 10-14 days

422
Q

When is follow up needed for syphilis?

A

No follow up blood tests required if RPR non reactive at baseline or if low titre in late stage syphilis

423
Q

Most common viral STI?

A

Human Papillomavirus

424
Q

Transmission of human papillomavirus?

A

Transmission: sexually + vertically + perinatally

425
Q

HPV subtype classically associated with anogenital warts/condylomata acuminate?

A

HPV 6/11

426
Q

HPV subtype most oncogenic (classically associated with cervical HSIL)

A

HPV 16/18

427
Q

Clinical features of latent HPV infection?

A

No lesions, asymptomatic, only detected by hybridization tests

428
Q

Screening and prevention of HPV?

A

Gardasil 9 or Gardasil or Cervarix; condoms do not fully protect

429
Q

Treatment of HPV?

A
  • Mechanical removal: cryotherapy - repeat q1-2 week, excision/laser
  • Topical treatments: antimitotics (podophyllin qweekly), caustics (eg, trichloroacetic acid - weekly for 4-6 weeks – good for pregnancy), interferon inducers (eg, imiquimod - 5% cream 3x per week qhs for 16 weeks)
430
Q

Investigations of HPV?

A

Biopsy of lesions at colposcopy + detection of HPV DNA subtype using nucleic acid probes (after abnormal pap)

431
Q

Treatment of HPV in pregnancy?

A

Pregnancy: warts tend to get bigger, treat early (excision), C-Section only if obstructing birth canal or risk of extensive bleed – do not use imiquimod, podophyllin, or podofilox

432
Q

Clinical features of subclinical HPV infection?

A

Visible lesions during colpo or pap – add acetic acid before test to whiten the warts

433
Q

Clinical features of clinical HPV infection?

A

Visible wart lesions w/o magnification, hyperkeratotic/verrucuous/flat/macular lesions, vulvar edema

434
Q

Screening test for HIV?

A

Enzyme-linked immunosorbent assay (ELISA).

435
Q

Confirmatory test for HIV?

A

Western blot and/or PCR.

436
Q

Ways to reduce vertical HIV transmission?

A
  • Give maternal IV ZDV.
  • Reduce duration of ruptured membranes.
  • Recommend cesarean delivery before labor or rupture of membranes if viral load > 1000 copies.
  • Avoid breast-feeding.
  • Give ZDV syrup to newborn for 6 weeks
437
Q

HIV preferentially infects ____ + ____ resulting in progressive destruction of ____ + ____ populations

A

CD4
T-lymphocytes
CD4
T-cell

438
Q

Transmission of HIV?

A

HIV does not cross the placenta, only blood to blood transmission – vertical transmission

439
Q

Treatment of HIV?

A

CART – Combination Antiretroviral Therapy – suppress HIV replication, prevent CD4 depletion (often increasing) – and track the viral load, ensuring it falls to < 1000 copies / mL. If she has an undetectable viral load she can deliver vaginally. If she hasn’t been on HAART, or her copies are > 1000, she delivers via C-Section.

440
Q

If HIV status was unknown at time of delivery?

A

AZT (zidovudine) at the time of delivery

441
Q

Prophylaxis/vaccines for HIV+ pregnant women?

A

Weekly azithromycin (if CD4 <100), Septra (CD4 <200), vaccinate for p-pneumonia, influenza, HBV/HAV

442
Q

Communicability of Hep B during pregnancy?

A

HBsAg+ state highly communicable, increased during 3-TM or early post-partum; increased risk of infectivity with increased levels of hepatitis B early antigen (HBeAg). DOES NOT increase risk of complications or congenital anomalies

443
Q

When should you screen for Hep B for pregnancy?

A

Screen for Hep B during the first trimester labs with hepatitis B surface antigen

444
Q

Treatment of hep B + during pregnancy?

A
  • Vaccination against hepatitis viruses A, Abstain form alcohol use, avoid hepatotoxic drugs such as acetaminophen, ASA and sharing personal items
  • HBV DNA levels ≥106 IU/mL are an indication to initiate treatment during the last 3 months of pregnancy
445
Q

Treatment of hep B - and at risk during pregnancy?

A

Offer HBV vaccine; not contraindicated in pregnancy

446
Q

All infants born to HBsAg-positive mothers should receive?

A

One dose of HepB Ig and the initial dose of HBV vaccine within 12 hours of birth. 2nd and third at 1 and 6 months

447
Q

CDC Notifiable Diseases

A

Chancroid + Chlamydia + Gonorrhea + Hepatitis A/B/C + HIV + Syphilis

448
Q

Transmission of hep B?

A

Vertical

449
Q

Serology for Hep B?

A
  • Hep B surface antibody: Exposed or vaccine
  • Hep B core antibody: Exposed
  • Hep B ANY antigen: Infected
  • Hep B s Ag: Infected
  • Hep B e Ag: Infectious
450
Q

Transmission of hep C?

A

Transmission via blood, IV drug use, perinatal transmission

451
Q

Investigations for hep C?

A

Serology – + for HCV-RNA or Anti-HCV (IgG, IgM)

452
Q

Is hep C an indication for C-section?

A

Pregnancy does not impact course of HCV or complications, fetal anomalies and is not an indication for C section

453
Q

Treatment of hep C?

A
  • Don’t given Hep C treatment
  • Vaccinate against hepatitis A and B
  • Avoid sharing personal items –razors, toothbrush
  • Limit hepatotoxic drugs that may worsen liver damage
  • Liver enzymes and PCR at 1st prenatal visit and Q trimester

454
Q

Risk factors for STIs

A

History of previous STI, contact with an infected person, sexually active individual <25yo, multiple partners, new partner in the last 3 months, lack of barrier protection use, street involvement (homelessness or drug use)

455
Q

Definition of premenstrual syndrome (PMS)?

A

At least one symptom associated with “economic or social dysfunction” that occurs during the five days before the onset of menses and is present in at least three consecutive menstrual cycles. Symptoms may be affective (eg, angry outbursts, depression) or physical (eg, breast pain and bloating)

456
Q

Affective or behavioral symptoms of PMS

A

Mood swings (most common), irritability, anxiety/tension, sad or depressed mood, increased appetite/food cravings, sensitivity to rejection, and diminished interest in activities

457
Q

Core symptoms of PMS

A

The core symptoms include affective symptoms, such as depression, irritability, and anxiety, and somatic symptoms, such as breast pain, bloating and swelling, and headache

458
Q

Core feature of PMS?

A

The core feature is the recurrent onset of symptoms during the end of the luteal phase of the menstrual cycle with a symptom-free period shortly after menses has begun

459
Q

Physical symptoms of PMS

A

The most common physical manifestations of PMS are abdominal bloating and an extreme sense of fatigue. Other common symptoms include breast tenderness, headaches, hot flashes, and dizziness. Hot flashes in women who are neither postpartum nor peri-or postmenopausal are highly suggestive of PMS or PMDD.

460
Q

Etiology of PMS?

A
  • Multifactorial: not completely understood; genetics likely play a role
  • CNS-mediated neurotransmitter (serotonin, dopamine, GABA) interactions with sex steroids (P, E, and T)
  • Serotonergic dysregulation – currently most plausible theory
461
Q

Diagnostic criteria for premenstrual syndrome

A
  1. At least one affective and one somatic symptom during the 5d before menses in each of the three prior menstrual cycles
    - Affective: depression, angry outbursts, irritability, anxiety, confusion, social withdrawal
    - Somatic: breast tenderness or swelling, abdominal bloating, headache, swelling of extremities, joint or muscle pain, or weight gain
  2. Symptoms relieved within 4 d of onset of menses and do not recur until at least day 13 of cycle
  3. Symptoms present in the absence of any pharmacologic therapy, hormone ingestion, drug or alcohol use
  4. Symptoms occur reproducibly during 2 cycles of prospective recording
  5. Patient suffers from identifiable dysfunction in social or occupational performance
462
Q

Diagnostic criteria for premenstrual dysphoric disorder?

A
  1. At least 5 of the following 11 symptoms during most menstrual cycles of the last year (with at least 1 of the first 4)
    - depressed mood or hopelessness
    - anxiety or tension
    - affective instability
    - anger or irritability
    - decreased interest in activities
    - difficulty concentrating
    - lethargy
    - change in appetite
    - hypersomnia or insomnia
    - feeling overwhelmed
    - physical symptoms: breast tenderness/swelling, headaches, joint/muscle pain, bloating, or weight gain
  2. Symptoms cause significant distress and/or interfere with social or occupational functioning
  3. Symptoms must be present during the week prior to menses and resolve within a few days after onset of menses
  4. May be superimposed on other psychiatric disorders, provided it is not merely an exacerbation of another disorder
463
Q

1st line treatment of PMS?

A
  • Exercise, cognitive behavioural therapy, vitamin B6
  • Combined hormonal contraception
  • Continuous or luteal phase (day 15-28) low dose SSRIs (e.g. citalopram/escitalopram 10 mg)
464
Q

2nd line treatment of PMS?

A
  • Estradiol patches (100 micrograms) + micronised progesterone (100 mg or 200 mg [day 17-28], orally or vaginally) or LNG-IUS 52 mg
  • Higher dose SSRIs continuously or luteal phase (e.g. citalopram/escitalopram 20-40 mg)
465
Q

3rd line treatment of PMS?

A

GnRH analogues + add-back HRT

466
Q

4th line treatment of PMS?

A

Surgical treatment ± HRT

467
Q

What is defined as PROM?

A

Pre-labor rupture of membranes at any GA

468
Q

Clinical features of PROM?

A
  • Hx: fluid gush or continued leakage – colour, consistency, constancy (is it clear? Meconium? Bloody?), coughing
  • Ask around 4 Cardinal Q’s: bleeding, discharge, fetal movements, contractions/pain
469
Q

What is defined as prolonged ROM?

A

> 24h elapsed b/w rupture of membranes and onset of labour

470
Q

What is defined as PPROM?

A

Preterm (<37w) + PROM

471
Q

Maternal risk factors for PROM?

A

Multiparity + cervical incompetence + infection (cervicitis, vaginitis, STI, UTI), FHx, low SES/poor nutrition, smoking, previous PPROM/PROM, placenta previa/abruption, trauma, low BMI, maternal age <18, >40, cervical surgery, sex

472
Q

Fetal risk factors for PROM?

A

Congenital anomaly + multiple gestation

473
Q

Physical/Investigations for PROM?

A
  • Speculum Exam: check for pooling in posterior fornix + nitrazine (turns blue if basic) + ferning on microscope slide
  • Cervical Exam: dilation + effacement + length + consistency +/- station
  • Ultrasound: Assess amount of AF, rule out fetal anomalies + assess GA + presentation + BPP
474
Q

False (+) Nitrazine

A

Blood, semen, urine, BV – amniotic fluid pH of 7.1-7.3, vaginal pH 4.5-6.0

475
Q

False (-) Nitrazine

A

Not enough fluid or fluid is contaminated by other discharge

476
Q

Neonatal complications of PROM

A

Neonatal sepsis, long-term neurodevelopmental abnormalities, fetal asphyxia (most common), limb deformities, morbidities associated with preterm.

477
Q

Fetal complications of PROM

A

Intrauterine infection, cord compression, oligohydramnios – pulmonary hypoplasia, fetal malposition, umbilical cord prolapse, placental abruption, preterm birth

478
Q

Maternal complications of PROM

A

Chorioamnionitis (common etiology of PROM - Fever > 38C, leukocytosis, maternal/fetal tachycardia, uterine tenderness, malodorous vaginal discharge), endometritis, sepsis, postpartum endometritis.

479
Q

Management of PROM?

A
  • Admit: for expectant mgmt + monitor vitals q4h + daily BPP + US + WBC count – delivery if fetal distress/chorioamnionitis
  • Imminent Delivery: cover for GBS and consult NICU
  • Screen: for UTI, STI, GBS (treat any of these is +)
  • Magnesium Sulfate: neuroprotection, if delivery <32 weeks is imminent (5g IV, then 1g q1h until delivery)
  • Tocolysis: only use if there is a need to delay for betamethasone (most use Indocin or Nifedipine)
  • Betamethasone: lung maturity, 12mg IV q24h x 2 dose for anyone <34w
480
Q

<24 week GA with PROM

A

Consider termination (poor outcome due to pulmonary hypoplasia)

481
Q

24-25 weeks GA with PROM

A

Individual consideration with counselling of parents regarding risks to preterm infants

482
Q

26-34 weeks GA with PROM

A

Expectant management (give steroids, prophylactic antibiotic, MgSO4), as prematurity complications are significant

483
Q

34-36 weeks GA with PROM

A

‘grey zone’ where risk of death from RDS and neonatal sepsis is the same. CONSIDER DELIVERY AT 34 WKS

484
Q

> 37 weeks GA with PROM

A

Induction of labour since the risk of death from sepsis is greater than RDS

485
Q

What are the stages of labour?

A

1st (latent, active), 2nd (passive, active), 3rd (placenta), 4th (monitoring 1hr and repair)

486
Q

Stage 1 - Latent phase

A

Progressive effacement/dilatation of cervix usually until 4cm; contractions typically infrequent/irregular.

487
Q

Stage 1 - Active phase

A

Need to have regular contractions and cervix 4cm

Contractions: painful, regular contractions q2-3min, lasting 45-60s; strongest at fundus

488
Q

Slowest rates of stage 1 - active phase

A

Slowest rates: nulliparous (1.2cm/hour), multiparous (1.5cm/hour)

489
Q

Management of stage 1 - active phase

A
  • Vital signs q4H, clear fluids in active labour, cervical exams q2-3H if uncomplicated, ambulation, fetal monitoring
  • ARM (Artificial Rupture of Membranes): no difference in length of 1st stage or Apgar scores
490
Q

Pain management of stage 1 - active phase?

A

Comes from T11, T12, L1 during first stage; morphine 5-10mg IM q4h (not within 4 hours of delivery, if close, then fentanyl) + gravol 50mg IM or epidural PRN or nitrous oxide PRN

491
Q

Stage 2 of labour

A

Starts at a cervix of 10 cm, ending in fetal delivery. Passive (no active pushing) + Active (active pushing).

492
Q

What is considered prolonged stage 2 active phase?

A

3h nulliparous, 1h multiparous

493
Q

Management of stage 2 of labour

A

Analgesia (no narcotics), fetal monitoring, assess progress (descent), when to push (when the urge is there), episiotomy (vacuum/forceps or shoulder dystocia), fetal head delivery, anterior shoulder (check nuchal cord), posterior shoulder, cord clamping (60 seconds of delayed clamping) – progress measured by descent

494
Q

Cardinal movements of the fetus during delivery?

A

Head floating/before engagement > engagement/descent/flexion > further descent/internal rotation > complete rotation/beginning extension > complete extension > restitution (external rotation) > delivery of anterior shoulder > delivery of posterior shoulder

495
Q

Stage 3 of labour

A

Separation of placenta, and ends with delivery of placenta – should last no more than 30minutes before intervention is indicated. Mean time: 8-10mins

496
Q

What are the signs of placental separation?

A

Uterus becomes globular/firm/rises in abdomen (place hand on the uterus just above the pelvis) + sudden gush of blood + umbilical cord lengthening

497
Q

Management of stage 3 of labour?

A

Bolus oxytocin, 5U IV or 10u IM with delivery of anterior shoulder, 20U in 1L normal saline (after shoulder delivered), gentle traction on umbilical cord WITH suprapubic support of uterus, early cord clamping – oxytocin can help to reduce risk of PPH by >40%. Inspect v/c/l for lacerations!

498
Q

Management of stage 4 of labour?

A

q15m for an hour, monitor vital signs/bleeding, repair lacerations, ensure uterus is contracted (palpate uterus and monitor uterine bleeding, examine placenta (make sure its intact)/umbilical cord (for 2 arteries + 1 vein), manage lacerations, monitor for PPH

499
Q

What is the expected progress of descent with delivery?

A

Expect at least 1cm descent per hour with primip and 2cm per hour with multip

500
Q

What is defined as abnormal progression of labour (Dystocia)?

A

Failure to progress – a slow or difficult delivery either due to lack of effacement/dilation or descent

501
Q

What is the difference between arrest and protraction?

A

Arrest (no progress) vs. protraction (slow progress)

502
Q

What is defined as arrest of labour?

A

Arrest in 1st stage means no cervical change in >4hrs despite adequate contractions but 2nd stage arrest is NO DESCENT in 2-4 hrs depending on epidural and para

503
Q

What is defined as protraction of labour?

A

1st stage – 4+ hrs of 0.5cm/hr OR no dilation in 2 hrs. 2nd stage – 1 hr of pushing with no descent

504
Q

Effect of epidural on the progression of labour?

A

No different in duration of 1st stage of labour. Increased duration of second stage of labour (13.6 min). Increased instrumental delivery. No difference in c-section rate.

505
Q

Etiology of failure to progress?

A
  • Assess Power
  • Assess Passenger: size, lie and presentation, position (OA diameter 8.5cm, OP diameter 9cm), attitude (asynclitism – when head is tipped)
  • Assess Passage: pelvic types: gynecoid (transverse ellipse) = easiest/favourable for baby. Android (triangular shape) Anthropoid (AP ellipse) = narrow
  • Assess Psyche: stress increases epinephrine and other hormones which interfere with uterine contractility and interfere with progress and increase anxiety which increases stress
506
Q

What are satisfactory contractions for the assessment of power and how can you measure power?

A

Frequency (between 3-5 per 10 minutes), duration (60-90s), amplitude of contraction or pushings; intrauterine pressure catheter

507
Q

What are the abnormal contraction pattern?

A
  • Too frequent: tachysystole
  • Too strong: hypertonus
  • Too sustained: tetanic
  • Abnormal contraction pattern + NRFHR = hyperstimulation
508
Q

Management of power as the cause of FTP?

A

Oxytocin, amniotomy (ARM), instrumental delivery or c-section delivery.

509
Q

Management of psyche as the cause of FTP?

A

Analgesia, labour support person – doula

510
Q

Management of passenger as the cause of FTP?

A

Manual rotation, instrumental delivery or c-section delivery.

511
Q

What is the shortest feat head diameter?

A

Shortest diameter: occiptobregmatic = well flexed head

Wider diameters = deflexed head: occipitofrontal (brow), occipitomental (face)

512
Q

Pain relief options for pregnancy?

A
  • Non-pharmacologic: maternal movement and position change, ARM, immersion in water, TENS, hypnosis
  • Systemic: narcotics (always give with antiemetic), nitrous oxide (self administered), sedatives and hypnotics are INEFFECTIVE
  • Regional and Local: epidural (most effective pain relief, no effect on length of 1st stage, longer 2nd stage), pudendal (useful in 2nd stage for operative vaginal delivery
513
Q

Surrogate measure of pelvic inlet

A

Obstetrical pelvimetry: Diagonal conjugate = surrogate measure of pelvic inlet. Adequate if >11.5cm. True distance = DC – 1.5cm

514
Q

Typical baby size for non-diabetic and diabetic mothers?

A

> 4500g in non-diabetic mom, >4000g in diabetic mom – heads and shoulders are usually larger

515
Q

Management of passage as the cause of FTP?

A

Instrumental delivery or c-section delivery

516
Q

Benign breast lesions categories?

A
  • Nonproliferative
  • Proliferative without atypia
  • Atypical hyperplasia
517
Q

Ddx for nonproliferative benign breast lesions

A
  • Simple breast cyst:
  • Papillary apocrine change
  • Galactocele
  • Apocrine metaplasia
518
Q

Ddx for proliferative benign breast lesions without atypia?

A
  • Fibroadenomas
  • Intraductal papilloma
  • Usual ductal hyperplasia
  • Sclerosing adenosis
519
Q

High risk for malignancy on US

A

Ill-defined margins, hypoechogenicity, calcifications, shadowing, spiculations, taller-than-wider shape

520
Q

Clinical features and age of nonproliferative benign breast lesions

A
  • Age 30 to menopause (and after if hormone replacement therapy (HRT) used)
  • Breast pain, focal areas of nodularity or cysts often in the upper outer quadrant, frequently bilateral, mobile, varies with menstrual cycle, and nipple discharge (straw-like, brown, or green)
521
Q

Investigations for nonproliferative benign breast lesions

A
  • Evaluation of breast mass (U/S, mammography as indicated)
  • Observation thru menstrual cycle for resolution is an option. Fine needle aspiration to confirm diagnosis. Re-examine in 4-6 weeks.
  • Re-recurrence usually requires open biopsy
522
Q

What are nonproliferative benign breast lesions?

A

Benign breast condition characterized by fibrous and cystic changes in the breast (fibrocystic changes/disease)

523
Q

What are the features of breast cysts?

A

Breast cysts are fluid-filled, round, or ovoid masses derived from the terminal duct lobular unit. Most common nonproliferative lesion

524
Q

What is papillary apocrine change?

A

Papillary apocrine change is a proliferation of ductal epithelial cells showing apocrine features

525
Q

What are galactoceles and when do they occur?

A

Cystic collections of fluid, usually caused by an obstructed milk duct. Occurs after cessation of lactation or with decrease feeding frequency (up to 10 mo after).

526
Q

What is apocrine metaplasia?

A

Also referred to as a “benign epithelial alteration” is also a nonproliferative change that is secondary to some form of irritation, typically associated with a breast cyst.

527
Q

Classic triad of nonproliferation benign breast lesions?

A

Classic triad of breast pain, tenderness, nodularity in premenopausal women (30-50).

528
Q

Indications to send fluid for cytology for nonproliferation benign breast lesion?

A
  • Residual mass after aspiration
  • Bloody fluid (no need to send clear fluid for cytology)
  • Recurrence > 3x
529
Q

Treatment of nonproliferative benign breast lesions

A
  • Analgesia (ibuprofen, ASA)
  • Vitamin E, evening primrose oil
  • For severe symptoms: OCP, danazol, bromocriptine
530
Q

Most common breast tumour in women <30 yr

A

Fibroadenomas

531
Q

Clinical features of fibroadenomas

A

Nodules: firm, rubbery, discrete, well- circumscribed, non-tender, mobile, hormone- dependent (unlike cysts), needle aspiration yields no fluid

532
Q

Diagnosis of fibroadenomas?

A
  • Core or excisional biopsy sometimes required if concerned about malignancy U/S and FNA alone cannot differentiate fibroadenoma from phyllodes tumour
  • US - solid, well-circumscribed avascular mass
  • Mammography may show well-circumscribed mass, or large, coarse calcifications in involuting FA is typical
533
Q

Treatment of fibroadenomas

A
  • Generally conservative serial observation
  • Consider excision if size 2-3 cm and growing on serial U/S (q6mo x 2 yr is usual follow-up), if symptomatic, formed after age 35, patient preference or features on core biopsy suggestive of a phyllodes tumour
534
Q

What is a intraductal papilloma?

A

Solitary intraductal benign polyp

535
Q

Clinical features of intraductal papilloma?

A

Can present as nipple discharge (most common cause of spontaneous, unilateral, bloody nipple discharge = pathologic nipple discharge), breast mass, nodule on U/S

536
Q

Treatment of intraductal papilloma?

A

Surgical excision of involved duct to ensure no atypia

537
Q

What is a usual ductal hyperplasia

A

Increased number of cells within the ductal space

538
Q

Clinical features of usual ductal hyperplasia

A

Incidental finding on biopsy of mammographic abnormalities or breast masses

539
Q

Treatment of usual ductal hyperplasia and sclerosing adenosis?

A

None required

540
Q

What is sclerosing adenosis?

A

Lobular lesion with increased fibrous tissue and glandular cells

541
Q

Ddx for atypical hyperplasia benign breast lesions?

A

Atypical ductal hyperplasia (ADH), atypical lobular hyperplasia (ALH), and lobular carcinoma in situ (LCIS)

542
Q

What are the features of lipomas of the breast?

A

Benign, usually solitary tumors composed of mature fat cells. Soft, nontender, well-circumscribed masses

543
Q

What are the features of fat necrosis of the breast

A

Commonly occurs as the result of breast trauma or surgical intervention. Fat necrosis can be confused with a malignancy on physical examination and may mimic malignancy on radiologic studies

544
Q

Treatment of fat necrosis?

A

Monitor, analgesia, warm compress, should self-resolve

545
Q

What is granulomatous mastitis and what is required in order to make the diagnosis?

A

An inflammatory mass in the breast. Biopsy is necessary to make a diagnosis

546
Q

What are the features of sarcoidosis of the breast and what is required in order to make the diagnosis?

A

Sarcoidosis of the breast presents as firm, hard masses, mimicking carcinoma. The mammographic appearance is also suspicious with irregular, ill-defined, spiculated masses that are solid on ultrasound. Biopsy is needed for confirmation of diagnosis

547
Q

Clinical features of sclerosing adenosis?

A

Mass or mammographic abnormality

548
Q

What are the features of breast abscess?

A

Localized collection of inflammatory exudate (i.e., pus), when mastitis/cellulitis does not respond to antibiotic treatment - localized, painful inflammation, associated with fever/malaise, fluctuant tender, palpable mass, dx = U/S showing fluid collection. Micro staph aureus most common

549
Q

What are the risk factors for breast abscess?

A

Obesity, smoking, age >30 years, first pregnancy, GA >41w

550
Q

Treatment of breast abscess?

A

Antibiotics (e.g., dicloxacillin), Needle or open drainage with cultures taken, Resection of involved ducts if recurrent, Breast pump if breastfeeding

551
Q

What should be asked on history for breast mass?

A
  • Change in General Appearance of Breast: increase/decrease in size or change in symmetry, nipple rash, new nipple inversion/retraction (tumor involvement of Cooper’s ligaments and subsequent traction on ligaments pull skin inward), dimple
  • Nipple Discharge: bilateral, unilateral from one specific duct, timing, color, frequency, spontaneity of discharge)
  • Breast Pain: relationship with menstrual cycles (cyclic/noncyclic), location within the breast (or both), duration, whether it is aggravated/alleviated by any activities/medications
  • Evolution: how it was first noted, how long it has been present, whether it has changed in size
  • Location
  • Wax/Wanes during Menstrual Cycle: cysts may be more prominent premenstrual and regress in size during follicular phase
552
Q

Physical exam for breast mass?

A
  • Determine whether a dominant mass, thickening or asymmetry is present – important in younger women (breast are more likely to be generally nodular than older)
  • Describing a breast mass, the texture (firm, soft, rubbery) should be noted, mobility (fixed, mobile), associated skin changes and location.
  • LN exam (supraclavicular, infraclavicular, axillary)
  • Characteristics: obvious/subtle, tender/nontender, soft/firm/hard, mobile/fixed to the chest wall, well-defined/non-discrete margins
  • Associations: ecchymosis, erythema, peau d’orange ulceration of the skin, nipple discharge or retraction, or none
553
Q

Ddx for malignant breast masses?

A
  • Infiltrating Ductal Carcinoma
  • Infiltrating Lobular Carcinoma: diffuse thickening of the breast rather than discrete mass
  • Mixed Ductal/Lobular Carcinoma
  • Paget Disease: Scaly, raw, ulcerated lesion of the nipple and aerola. 75% have underlying Ca. Need punch biopsy of nipple
554
Q

Most common malignant breast mass?

A

Infiltrating Ductal Carcinoma: most common, 70-80% of invasive breast cancer

555
Q

Investigations for breast masses?

A
  • Percutaneous core needle biopsy (palpation or U/S guided): Allows for diagnosis prior to surgery
  • Stereotactic core needle biopsy is required in lesion is only seen on mammogram
  • MRI guided core needle biopsy is needed is lesion is only seen by MRI
556
Q

Imaging for breast lesion?

A
  • Mammogram: depicts mass as a soft tissue density, unable to make definitive diagnosis, cannot detect all (i.e., premenopausal women with dense breast tissue)
  • Ultrasound: Supplements mammography when dense tissue present, often in younger women. Initial imaging study in women <30 years old with breast pain or nipple discharge. Used as a follow up study from mammography
  • MRI: categorize breast lesions as mass/non-mass lesions, depict breast mass as enhancing/non-enhancing mass, rapid uptake of contrast = malignant mass characteristic, NOT necessary - high sensitivity, low specificity. Reserved for high risk patients
557
Q

High risk for malignancy on mammogram?

A

Poorly defined, spiculated border; microcalcifications; architectural distortion, interval mammographic changes

558
Q

What is the triple test for diagnosing breast cancer?

A

Triple Test: clinical breast exam + imaging (US for <30yr, mammography + US for >30yrs) + pathology (US/Mammography guided core needle biopsy or FNA - palpable cystic lesions)

559
Q

Preoperative staging workup for breast cancer?

A
  • Bilateral mammogram (cancer in one breast is a risk factor for cancer in the contralateral breast!)
  • CXR (to check for lung metastasis)
  • LFTs (to check for liver metastasis)
  • Serum calcium level, alkaline phosphatase (if these tests indicate bone metastasis/“bone pain,” proceed to bone scan)
  • Other tests, depending on signs/symptoms (e.g., head CT scan if patient has focal neurologic deficit, to look for brain metastasis)
  • The Ls and Bs: liver, lung, bone and brain.
560
Q

Breast cancers are divided into ____ and ___

A

Carcinoma in situ and invasive cancer.

561
Q

What is carcinoma in situ of the breast?

A

Carcinoma in situ is proliferation of cancer cells within ducts or lobules and without invasion of stromal tissue.

562
Q

2 types of carcinoma in situ of the breast

A
  • Ductal carcinoma in situ (DCIS): About 85% of carcinoma in situ are this type. DCIS is usually detected only by mammography.
  • Lobular carcinoma in situ (LCIS): LCIS is often multifocal and bilateral.
563
Q

What is the major risk with DCIS?

A

Subsequent development of infiltrating ductal carcinoma in the same breast

564
Q

Treatment of DCIS?

A
  • Tumor <1 cm (low grade) = Remove with 1-cm margins and XRT
  • Tumor >1 cm = Perform lumpectomy with 1-cm margins and radiation or total mastectomy (no axillary dissection) - some perform a sentinel LN dissection for high-grade DCIS
565
Q

Features of DCIS?

A

It may involve a small or wide area of the breast; if a wide area is involved, microscopic invasive foci may develop over time. microcalcifications, rigid neolumen formation (cribriform architecture).

566
Q

Two types of LCIS?

A

There are 2 types: classic and pleomorphic.

567
Q

Features of classic LCIS?

A

Classic LCIS is not malignant but increases risk of developing invasive carcinoma in either breast. IT’S A HIGH RISK MARKER - 30% in the 20 years after diagnosis of LCIS! This nonpalpable lesion is usually detected via biopsy; it is rarely visualized with mammography

568
Q

Features + treatment of pleomorphic LCIS?

A

Pleomorphic LCIS behaves more like DCIS; it should be excised to negative margins.

569
Q

Invasive breast carcinoma is primarily ____

A

Adenocarcinoma

570
Q

Most common type of invasive breast carcinoma

A

About 80% is the infiltrating ductal type; most of the remaining cases are infiltrating lobular. Rare types include medullary, mucinous, metaplastic, and tubular carcinomas. Mucinous carcinoma tends to develop in older women and to be slow growing. Women with these rare types of breast cancer have a much better prognosis than women with other types of invasive breast cancer.

571
Q

Features of inflammatory breast cancer

A

A fast-growing, often fatal cancer. Cancer cells block the lymphatic vessels in breast skin; as a result, the breast appears inflamed, and the skin appears thickened, resembling orange peel (peau d’orange). Usually, inflammatory breast cancer spreads to the lymph nodes in the armpit. The lymph nodes feel like hard lumps. However, often no mass is felt in the breast itself because this cancer is dispersed throughout the breast.

572
Q

Treatment of inflammatory breast cancer?

A

Chemotherapy first! Then often followed by radiation, mastectomy, or both

573
Q

Features of Paget disease

A

Paget disease of the nipple (not to be confused with the metabolic bone disease also called Paget disease) is a form of ductal carcinoma in situ that extends into the skin over the nipple and areola, manifesting with a skin lesion (eg, an eczematous or a psoriaform lesion). Characteristic malignant cells called Paget cells are present in the epidermis. Women with Paget disease of the nipple often have underlying invasive or in situ cancer.

574
Q

What is are cystosarcoma phyllodes

A

Mesenchymal tumor arising from breast lobular tissue; most are benign (Note: “Sarcoma” is a misnomer, as the vast majority are benign; 1% of breast cancers)

575
Q

Signs and symptoms of cystosarcoma phyllodes

A

Mobile, smooth breast mass that resembles a fibroadenoma on exam, mammogram/ultrasound findings

576
Q

Treatment of cystosarcoma phyllodes

A

If benign, wide local excision; if malignant, simple total mastectomy. Consider chemotherapy if large tumor >5 cm and “stromal overgrowth”

577
Q

Diagnosis of cystosarcoma phyllodes

A

Core biopsy or excision

578
Q

Tumor markers for breast cancer?

A

Can test for estrogen, progesterone and her-2

579
Q

Consider genetic screening for BRCA1/2 if

A

Patient dx with BCA + ovarian CA, strong family hx of BCA+OCA, family hx of male breast cancer, young patient (<35yr), bilateral breast cancer patients <50yr

580
Q

For females with BRCA1/2 mutation, prevention approach?

A

Can offer risk-reducing bilateral salpingo-oophorectomy when child-bearing complete and offer risk-reducing bilateral mastectomy. Start age 25 annual breast MRI

581
Q

Indications of breast conserving surgery (BCS)?

A

Palpation, ultrasound guided or needle localized if mass only see on mammogram. Usually for stages I and II (tumors <5 cm), patient with stage IIIA cancer if they have to have NEOadjuvant chemotherapy

582
Q

Contraindications of breast conserving surgery (BCS)?

A

High risk of local recurrence (e.g. extensive malignant type calcifications on mammogram – extensive DCIS, and multifocal primary tumors), failure to obtain tumour free margins after re-excision, not suitable for radiation therapy (pregnancy, previous radiation, collagen vascular disease), large tumor size relative to breast

583
Q

Lumpectomy MUST be combined with ____ for survival equivalence to mastectomy

A

Radiation

584
Q

Reconstructive options after mastectomy?

A

TRAM flap, latissimus dorsi flap or implant reconstruction

585
Q

Indications for mastectomy?

A

Patient choice, contraindication to radiation, multicentric or unable to obtain negative margins

586
Q

When is sentinel lymph node dissection performed?

A

Perform in women with clinically node NEG BCA and those with extensive DCIS who are undergoing mastectomy. If SLNB is positive, completion ALND is indicated

587
Q

When is axillary lymph node dissection performed?

A

Perform in all patients with pathologic confirmation of nodal involvement (including POS SLNB as above). Removal of level 1 and 2 axillary nodes

588
Q

Risks of axillary lymph node dissection performed?

A

Arm lymphedema (10-15%) especially if getting radiation therapy, decreased arm sensation, motor nerve injury, post op seroma, wound infection, arm weakness or decrease range of motion

589
Q

Indications for radiation for breast cancer?

A
  • Adjuvant treatment post-lumpectomy for all BCT
  • Post-mastectomy radiation indicated if advanced tumor (T3, T4, pN2 or pN3)
  • Inflammatory breast CA or tumor not responding to neoadjuvant chemo
  • Start 4-8 weeks post-op ideally, or after chemotherapy
590
Q

Indications for chemotherapy of breast cancer?

A
  • Node positive
  • Node negative tumor with high risk features (e.g. high grade, Her2neu positive, age <35, hormone receptor negative, LVI)
  • Locally-advanced (T3, T4, N2, N3) - neoadjuvant chemo
  • Metastatic breast cancer - palliative chemo
  • For HER2+ BCA – add trastuzumab ± pertuzumab to the chemo regimen
  • May provide chemotherapy prior to surgery to decrease size
591
Q

Indications for hormone therapy for breast cancer?

A
  • Estrogen receptor (ER) positive breast cancers
  • Tamoxifen is only agent used in premenopausal women, aromatase inhibitors if postmenopausal
  • Also indicated as chemoprevention for high risk women (strong family history, BRCA positive, LCIS, atypical hyperplasia)
592
Q

Common agents for hormone therapy for breast cancer?

A

Common agents: Tamoxifen (selective estrogen receptor modulator), aromatase inhibitors (Anastrazole, Letrozole), daily for 5-10 years postop

593
Q

Side effects of tamoxifien?

A

Endometrial cancer (2.5× relative risk), DVT, pulmonary embolus, cataracts, hot flashes, mood swings

594
Q

Therapeutic indications for excision of a breast mass?

A

Benign lumps (fibroadenoma, phyllodes), DCIS/invasive breast cancer that is amenable for BCS based on the size of the lesion

595
Q

Diagnostic indications for excision of a breast mass?

A

Equivocal pathology obtained on core biopsy or FNA cytology of a radiologically suspicious breast lump, lump classified as category 3 or 4 by the BIRAD system that is close to the pectoral muscle (which makes biopsy under radiological guidance difficult)

596
Q

Who is considered an average risk women in breast cancer screening guidelines?

A

50-74yo with no personal hx of BCA or hx of BCA in 1st degree relatives or known mutations of BRCA1/BRCA2 genes or previous exposures of the chest wall to radiation

597
Q

Are MRI, clinical breast exam or breast self-exam recommended for breast cancer screening?

A

No

598
Q

Who is considered a high risk women in breast cancer screening guidelines?

A
  • One/Two 1st Degree Relatives with Invasive BCA: (but do not meet the criteria for referral to med genetics)
  • Breast Biopsy w/ Atypical Hyperplasia or LCIS or Following Surgical Management (r/o Invasive Carcinoma)
  • History of Chest Wall Radiation at Age 30 or Younger
599
Q

Breast cancer screening guidelines for: Average risk women age 40-49?

A

Routine screening with mammography NOT recommended

600
Q

Breast cancer screening guidelines for: Average risk women age 50-74?

A

Routine screening q2 years

601
Q

Breast cancer screening guidelines for: Average risk women age 75+?

A

Screen if benefits outweigh harm, must take overall health into account

602
Q

Breast cancer screening guidelines for: High risk women - One/Two 1st Degree Relatives with Invasive BCA

A
  • Annual mammography starting 5-10 years younger than the youngest case in the family, but no earlier than age 25 and no later than age 40
  • Annual CBEs starting at age 25
603
Q

Breast cancer screening guidelines for: High risk women - Breast Biopsy w/ Atypical Hyperplasia or LCIS or Following Surgical Management (r/o Invasive Carcinoma)?

A
  • Annual mammography

- Annual CBEs

604
Q

Breast cancer screening guidelines for: High risk women - History of Chest Wall Radiation at Age 30 or Younger?

A
  • Annual mammography + screening breast MRI starting 5-10 years after radiation give, but no earlier than 25 and no later than age 40
  • Annual CBEs
605
Q

Risk Factors for Breast Cancer

A
  • Gender (99% female)
  • Age (80% >40yr)
  • Personal Hx of bCA/Prior breast bx (regardless of pathology)
  • Family Hx of breast cancer (2 or more 1st degree relatives)
  • BRCA1 and BRCA2 gene mutations

Relative risks:

  • Increased estrogen exposure: High breast density*/nulliparity, first pregnancy >30 years old, menarche <12 years old, menopause >55 years old
  • Decreased risk with lactation, early menopause, early childbirth
  • Radiation exposure (mantle radiation for Hodgkin’s disease)
  • > 5 years of HRT use or >10 years of OCP use
  • Alcohol use, obesity, sedentary lifestyle
606
Q

Women requiring genetic referral for breast cancer?

A

Maternal or paternal family history of:

  • Multiple individuals with breast and/or ovarian cancer (e.g. 3 or more cases in 2 or more generations, at least one case onset before age 50), related to each other
  • Bilateral primary breast cancer, first onset age 50 or younger
  • Breast cancer at age 35 or younger
  • Breast cancer that is hormone receptor negative and HER2 negative (a.k.a. triple negative), age 60 or younger
  • Primary breast and primary ovarian cancer in the same individual
  • Male breast cancer, age 65 or younger, or at any age with close family history of breast cancer
  • Breast or ovarian cancer in a family with Ashkenazi Jewish heritage
  • BRCA1 or BRCA2 mutation in the family
607
Q

Definition of spontaneous abortion

A

Spontaneous abortion refers to pregnancy loss at less than 20 weeks’ gestation in the absence of elective medical or surgical measures to terminate the pregnancy. 80% occur before 12 wks

608
Q

What is defined as complete abortion?

A

All products of conception have been passed without the need for surgical or medical intervention + symptoms have resolved

609
Q

What is defined as incomplete abortion?

A

Bleeding/cramping with open cervical os, some, but not all, of the products of conception have been passed – usually presents with continued bleeding/pain (incomplete)

610
Q

What is defined as inevitable abortion?

A

The cervix has dilated, but the products of conception have not been expelled

611
Q

What is defined as missed abortion?

A

A pregnancy in which there is a fetal demise (usually for a number of weeks) but no uterine activity to expel the products of conception

612
Q

What is defined as recurrent spontaneous abortion?

A

Three or more consecutive pregnancy losses

613
Q

What is defined as septic abortion?

A

A spontaneous abortion that is complicated by intrauterine infection (fever/acute abdo/malaise/septic shock).

614
Q

What is defined as threatened abortion?

A

A pregnancy complicated by bleeding before 20 weeks’ gestation, closed cervical os

615
Q

Common bugs of septic abortion?

A

S. Aureus, Gram(-) bacilli, or Gram(+) cocci – if >20wks, then chorioamnionitis

616
Q

Differential diagnosis for first trimester bleeding

A
  • Ectopic pregnancies
  • Spontaneous abortions (threatened, missed, inevitable, incomplete, complete, septic) - <20wks GA
  • Implantation bleed (usually occurs around time of the missed period)
  • Cervical/uterine etiology (tumors or polyps, infections – STIs or yeast, trauma – e.g. sex)
  • GTN (gestational trophoblastic neoplasm)
  • Other source (rectal or urinary)
617
Q

What should be asked on history for spontaneous abortion?

A

Duration, degree and severity of bleeding, PQRST, passage of tissue, associated symptoms, prior gyne history

618
Q

Physical exam for spontaneous abortion?

A

VS, temp, abdo exam, pelvic exam (cervical os (open vs closed), amount of bleeding) CAUTION – avoid aggressive or bimanual exams in suspected ectopic

619
Q

Symptoms of spontaneous abortion?

A

Crampy pelvic pain, bleeding, and eventually expulsion of tissue. Late spontaneous abortion may begin with a gush of fluid when the membranes rupture. Hemorrhage is rarely massive

620
Q

Investigations for spontaneous abortion?

A
  • Potassium hydroxide and “wet prep” microscopy of any vaginal discharge
  • CBC
  • Blood type and screen (for all patients) → IgG for Rh-ve mums
  • Quantitative blood (not urine, since blood gives us a # to follow) hCG (normally hCG 2x every 2 days but not in spont abortion)
  • G/C testing
  • Determine if an intrauterine pregnancy can be reliably seen on ultrasound
  • 1500 - 2000 mIU - endovaginal scan
  • 4000 - 5000 mIU - abdominal U/S
621
Q

Etiology for spontaneous abortion?

A
  • Embryonic causes (nondisjunction) like genetic issues – polyploidies, trisomies (30-60%)
  • Reproductive tract abnormalities - uterine anomalies
  • Prothrombotic factors - thrombophilia
  • Endocrinologic factors - polycystic ovary syndrome
  • Immunologic factors - antiphospholipid syndrome
  • Infection (lots of these cause 2nd trimester miscarriage) - most notably cytomegalovirus, herpesvirus, parvovirus, and rubella virus
622
Q

Rask factors for spontaneous abortion?

A

Age > 35, History of spontaneous abortion, Cigarette smoking, Use of certain drugs (eg, cocaine, alcohol, high doses of caffeine), A poorly controlled chronic disorder (eg, diabetes, hypertension, overt thyroid disorders) in the mother

623
Q

Treatment options for <12 weeks spontaneous abortion and subcategory used for?

A
  • Conservative/Expectant: can wait for passage on its own, good for those already having symptoms and stable – threatened, incomplete, inevitable, complete.
  • Medical: Misoprostol (prostaglandin E1) 400-800mcg orally OR vaginally (1-2 doses, depending) to cause cramping/passage of tissue. Missed
  • Surgical: D&C (QUICKEST WAY!). Best for unstable/septic patients. Highest rate of completion but also complications – bleeding, perforation, cervical trauma, scarring.
624
Q

Side effects of misoprostol?

A

Cramp, diarrhea, severe bleeding, fever.

625
Q

Management of septic abortion?

A

D&C + IV broad spectrum antibiotics

626
Q

Treatment options for >12 weeks spontaneous abortion and subcategory used for?

A
  • Medical: induction via repeated doses of Misoprostol! DONE IN HOSPITAL due to traumatic nature, risk of retained placenta.
  • Surgical: D&E (surgical removal of fetus, more difficult).
627
Q

What is defined as primary recurrent abortion?

A

No pregnancy >20wks.

628
Q

What is defined as secondary recurrent abortion?

A

At least 1, >20wks.

629
Q

Investigations for recurrent abortion?

A
  • Hystero-salpingogram, karyotype (both partners)

- TSH + HbA1c + Prolactin + anti-thyroid antibodies + anti-phospholipid antibody screen + thrombophilia work-up

630
Q

Define primary amenorrhea?

A
  • Failure to menstruate by 15 years old with secondary sex characteristics + linear growth
  • Failure to menstruate by 13 years old with no secondary sex characteristics and absence of growth
631
Q

Define secondary amenorrhea?

A

Previous regular menses, no periods for 3x the usual menstrual interval. If menses are irregular then 6 months

632
Q

Define oligomenorrhea?

A

Infrequent menstrual cycles, often longer than 35 days, i.e. 4-9 per year.

633
Q

Causes/differential diagnosis of amenorrhea

A
  • Outflow Tract Causes
  • Primary ovarian insufficiency
  • Hypothalamic or pituitary disorders (Central): low FSH + low estradiol
  • Other endocrine gland disorders
  • Amenorrhea attributed to chronic disease
  • Physiologic or induced
634
Q

Most common causes of primary amenorrhea

A
  1. Müllerian agenesis
  2. Abnormal sex chromosomes (Turner’s syndrome)
  3. Functional hypothalamic amenorrhea
635
Q

Outflow tract causes of amenorrhea?

A
  • Acquired: cervical stenosis, intrauterine adhesions (Asherman’s Syndrome).
  • Congenital: Imperforate hymen, abnormal anatomy (Rokitansky-RKH syndrome (absent uterus)), Mullerian agenesis, transverse vaginal septum, 5alpha-reductase deficiency
636
Q

Primary ovarian insufficiency causes of amenorrhea?

A
  • Acquired: autoimmune, chemotherapy or radiation

- Congenital: Turner syndrome (45 XO), gonadal dysgenesis

637
Q

Hypothalamic or pituitary disorders (central) causes of amenorrhea?

A
  • Autoimmune disease
  • Brain radiation (panhypopituitarism
  • Constitutional delay of puberty
  • Empty sella syndrome
  • Functional (overall energy deficit or stress) - Eating disorder, Stress, Vigorous exercise, Weight loss
  • Gonadotropin deficiency (e.g., Kallmann syndrome)
  • Hyperprolactinemia - Adenoma (prolactinoma), Chronic kidney disease, Medications or illicit drugs (e.g., antipsychotics, opiates), Physiologic (pregnancy, stress, exercise)
  • Infarction (e.g., Sheehan syndrome)
  • Infiltrative disease (e.g., sarcoidosis)
  • Infection (e.g., meningitis, tuberculosis)
  • Medications or illicit drugs (e.g., cocaine)
  • Trauma or surgery
  • Tumor (primary or metastatic)
638
Q

What is Sheehan syndrome?

A

Postpartum w/ major bleed, infarction to pituitary

639
Q

Physiologic or induced causes of amenorrhea?

A
  • Breastfeeding
  • Contraception
  • Exogenous androgens
  • Menopause
  • Pregnancy
640
Q

Amenorrhea attributed to chronic disease

A
  • Celiac disease
  • Inflammatory bowel disease
  • Other chronic disease
641
Q

Other endocrine gland disorders that cause amenorrhea?

A
  • Adrenal insufficiency
  • Androgen-secreting tumor (e.g., ovarian or adrenal)
  • Cushing syndrome
  • Diabetes mellitus, uncontrolled
  • Late-onset congenital adrenal hyperplasia
  • Polycystic ovary syndrome (multifactorial)
  • Thyroid disease
642
Q

What should be asked on history for amenorrhea

A
  • Menstrual patterns (if any), pregnancy and breastfeeding history, eating and exercise habits, psychosocial stressors (e.g., perfectionist behaviors), changes in body weight, fractures, medication or substance use, chronic illness, and timing of breast and pubic hair development
  • Family history of early or delayed menarche
  • Hirsutism, acne
  • Chemotherapy or radiation
643
Q

Physical exam for amenorrhea?

A
  • Thyroid examination (thyroid disease), Acanthosis nigricans or skin tags (Hyperinsulinemia (PCOS))
  • Anthropomorphic measurements; growth charts (Turner syndrome, constitutional delay of puberty)
  • Body mass index (High: PCOS, Low: Functional hypothalamic amenorrhea)
  • Breast development (normal progression) - Presence of circulating estrogen
  • Dysmorphic features (e.g., webbed neck, short stature, low hairline) - Turner syndrome
  • Male pattern baldness, increased facial hair, acne - Hyperandrogenism, PCOS, ovarian or adrenal tumor, CAH, Cushing syndrome
  • Pelvic examination: Absence or abnormalities of cervix or uterus, Clitoromegaly, Presence of transverse septum or imperforate hymen, atrophic vaginal mucosae
644
Q

Investigations for amenorrhea?

A
  • hCG + hormonal workup (TSH, serum LH and FSH, prolactin (MRI if abnormal), Testosterone/DHEA/Cortisol, E2), CBC, Anti-Müllerian hormone
  • Progesterone Challenge
  • Karyotype: if FSH is high in a patient under age 30 + short stature or absent uterus or virilization (usually 21-OH deficiency, Congenital Adrenal Hyperplasia).
  • U/S to confirm normal anatomy, identify PCOS
645
Q

What is the progesterone challenge?

A
  • Give 10mg of medroxyprogesterone (Provera) for 10 days
  • Withdrawal bleeding may indicate estrogen exposure (e.g., polycystic ovary syndrome [PCOS]) and lack of bleeding may indicate a low estrogen condition (Central or ovarian cause)
646
Q

What is Müllerian agenesis?

A

Müllerian agenesis is caused by embryologic underdevelopment of the müllerian duct, with resultant agenesis or atresia of the vagina, uterus, or both

647
Q

Treatment of Müllerian agenesis?

A

Psychological counselling, Creation of neo-vagina with dilation

648
Q

Transverse septum and imperforate hymen may present with _____

A

Cyclic pelvic pain

649
Q

Transverse septum and imperforate hymen treatment?

A

Surgical management

650
Q

Intrauterine adhesions can occur after endometrial instrumentation and are corrected using

A

Hysteroscopy

651
Q

5α-reductase deficiency are phenotypic ____ that develop ___ secondary sex characteristics at puberty due to male level testosterone

A

Females

Male

652
Q

Those with 5α-reductase deficiency may require evaluation by a pediatric urologist based on malignancy risk and patient or guardian preferences. What procedure might be performed?

A

Prophylactic gonadectomy

653
Q

How is primary ovarian insufficiency diagnosed?

A

Diagnosed in patients younger than 40 years with two serum follicle-stimulating hormone levels in the menopausal range obtained at least one month apart (High FSH + LH/low estrogen)

654
Q

Treatment of primary ovarian insufficiency

A
  • HRT - If no breast development, start low and go slow (do not use OCP @ the start since this can lead to tubular breasts), give estrogen alone first and in low doses THEN add cyclic progesterone after 12-18mo → once breast development occurred, use OCP or cyclic hormones
  • 1,200 mg of calcium daily and 1,000 IU of vitamin D daily with regular weight-bearing exercises to maintain bone mineral density
655
Q

What is functional hypothalamic amenorrhea and its causes?

A

Functional hypothalamic amenorrhea is a disorder of chronic anovulation caused by suppression of the hypothalamic-pituitary axis from body weight loss, excessive exercise, or stress and may result in infertility or bone density loss.

656
Q

Female Athletic Triad

A

Amenorrhea + osteopenia/porosis + eating disorder.

657
Q

Hormonal findings in functional hypothalamic amenorrhea

A
  • Bone mineral density testing should be considered after six months of amenorrhea
  • Treatment should correct the underlying cause to restore ovulatory function through behavior change, nutritional repletion (e.g., caloric intake, vitamin D), stress reduction, and weight gai
658
Q

What is hyperprolactinemia and how can it cause amenorrhea?

A

Elevated serum prolactin may induce amenorrhea by inhibiting gonadotrophs.

659
Q

Imaging required for hyperprolactinemia

A

MRI

660
Q

Rotterdam Criteria (2003) for PCOS?

A

Need at least 2 of 3 criteria

  • Oligo/anovulation
  • Hyperandrogenism (clinical and/or biochemical)
  • Polycystic ovaries on ultrasound
661
Q

Hormonal findings in PCOS

A

Normal FSH/estro + low progesterone

662
Q

Treatment for PCOS?

A
  • Patients should be screened for hypertension and an elevated body mass index at each visit, and should be screened for dyslipidemia and impaired glucose tolerance (i.e., two-hour oral glucose tolerance testing [preferred] or A1C level) every three to five years
  • Weight loss may restore regular menses and improve metabolic comorbidities in patients with an elevated body mass index
  • Combined hormonal contraceptives are first-line therapy for menstrual abnormalities, hirsutism, acne, and protection from endometrial cancer caused by unopposed estrogen secretion
  • For patients with PCOS and infertility, letrozole (Femara) is a first-line therapeutic option, because it confers higher ovulation, pregnancy, and live birth rates than clomiphene
663
Q

Etiology of dysmenorrhea

A
  1. Primary/idiopathic (no pelvic abnormality)
  2. Secondary(acquired)
    - Endometriosis
    - Adenomyosis
    - Uterine polyps
    - Uterine anomalies (e.g. non-communicating uterine horn)
    - Leiomyoma
    - Ovarian cysts
    - Cervical stenosis
    - Imperforate hymen, transverse vaginal septum
    - Pelvic inflammatory disease
    - IUD (copper)
    - Foreign body
664
Q

Definition of primary dysmenorrhea

A

Recurrent, crampy lower abdominal pain that occurs during menses in the absence of demonstrable disease

665
Q

Definition of secondary dysmenorrhea

A

Similar features as primary dysmenorrhea but with an underlying disorder that can account for the symptoms, such as endometriosis, adenomyosis or uterine fibroids

666
Q

Signs and symptoms of primary dysmenorrhea

A
  • Spasmodic pain, is superimposed over constant lower abdominal pain, radiating to the lower back, labia, and inner thighs beginning hours before onset of bleeding and persisting for hours or days (48-72 h)
  • Associated symptoms: N/V, altered bowel habits, headaches, fatigue (prostaglandin-associated)
  • Symptoms begin soon after menarche or during adolescence
667
Q

Diagnosis of primary dysmenorrhea

A
  • Assess for associated dyspareunia, abnormal bleeding, infertility (signs of 2o dysmenorrhea) Rule out underlying pelvic pathology and confirm cyclic nature of pain
  • Pelvic examination not required; indicated for patients not responding to therapy or with signs of organic pathology
668
Q

History that should be asked for dysmenorrhea

A
  • History of present illness should cover complete menstrual history, including age at onset of menses, duration and amount of flow, time between menses, variability of timing, and relation of menses to symptoms.
  • The age at which symptoms began, Their nature and severity, Factors that relieve or worsen symptoms (including the effects of contraceptives), Degree of disruption of daily life, Effect on sexual activity, Presence of pelvic pain unrelated to menses, Response to acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs)
  • Review of systems should include accompanying symptoms such as cyclic nausea, vomiting, bloating, diarrhea, and fatigue.
  • Past medical history should identify known causes, including endometriosis, uterine adenomyosis, or fibroids. Method of contraception should be ascertained, specifically asking about IUD use.
  • Past surgical history should identify procedures that increase risk of dysmenorrhea, such as cervical conization and endometrial ablation.
  • Sexual history should include prior or current history of sexual abuse or other traumatic events.
669
Q

Treatment of primary dysmenorrhea

A
  • Regular exercise, local heat
  • NSAIDs: should be started before onset of pain Combined hormonal contraceptives with continuous or extended use: suppress ovulation/ reduce menstrual flow
670
Q

Physical exam for dysmenorrhea?

A

Pelvic examination focuses on detecting causes of secondary dysmenorrhea. The vagina, vulva, and cervix are inspected for lesions and for masses protruding through the cervical os. Structures are palpated to check for a tight cervical os, prolapsed polyp or fibroid, uterine masses, adnexal masses, thickening of the rectovaginal septum, induration of the cul-de-sac, and nodularity of the uterosacral ligament.

671
Q

Signs and symptoms of secondary dysmenorrhea

A

Associated dyspareunia, abnormal bleeding, infertility

672
Q

Diagnosis of secondary dysmenorrhea

A
  • Bimanual exam: uterine or adnexal tenderness, fixed uterine retroflexion, uterosacral nodularity, pelvic mass, or enlarged irregular uterus (findings are rare in women <20 yr)
  • U/S, laparoscopy and hysteroscopy may be necessary to establish the diagnosis
  • Vaginal and cervical cultures may be required
673
Q

Treatment of secondary dysmenorrhea

A

Treat underlying cause

674
Q

Contraindications of oxytocin

A

Contraindications: prior classical/high risk C-section, prior uterine rupture, active genital herpes infection, previa/vasa previa, cord prolapse, transverse fetal lie, invasive cervical cancer, or abnormal fetal heart tracing

675
Q

Methods of induction of labour

A
  1. Cervical Ripening (0-3cm Dilated): meds/other means to soften, efface, dilate cervix, ^likelihood of successful induction
  2. Amniotomy/Artificial Rupture of Membranes (ARM): stimulate PG synthesis/secretion, may use this if cervix is open/soft and membranes can be felt, and if the head is present at the cervix + oxytocin = more women delivery vaginally at 24h than ARM alone and had fewer operative deliveries
  3. Oxytocin (>3cm Dilated): 20U in 1L NS, run at 0.5-2 mU/min IV increasing by 1-2 mU/min q20-60min to a max of 36-48 mU/min. Dosage Recommendations: use the minimum dose to reach active labour and increase q30min as needed; reassessment should occur once a dose of 20 mU/min is reached
676
Q

Indications of cervical ripening

A

Indications: for Bishop score <6 prior to induction of labour

677
Q

Methods of cervical ripening?

A
  • Prostin Gel: dinoprostone (prostaglandin E2) long/closed cervix, use this prostaglandin gel every 6-12h up to 3 doses
  • Cervidil: long/closed cervix, use if ROM – continuous release, can be removed if needed (controlled PGE2 release)
  • Cytotec/Misoprostol: long/closed cervix, more commonly used in 2nd trimester termination of pregnancy
  • Mechanical: use a foley catheter to mechanically dilate the cervix
678
Q

Complications of oxytocin?

A

Hyperstimulation/tetanic contraction (may cause fetal distress or rupture of uterus), uterine muscle fatigue, uterine atony (may result in PPH), vasopressin-like action causing anti-diuresis

679
Q

Risk factors for postpartum infection?

A

Patients of low socioeconomic status undergoing c-section who have had prolonged labor and rupture of membranes (ROM) incur 40-85% risk of endometritis. Multiple vaginal exams during labour!

680
Q

What is endometritis?

A

Affects endometrium and myometrium but can progress beyond the uterus to include abscess, peritonitis, and pelvic thrombophlebitis. It is historically referred to as puerperal fever and is divided into early (within 24–48 h) and late (>48 h) postpartum.

681
Q

Testing for ____ should be done when endometritis presents >7 days after delivery and in patients at high risk such as adolescents

A

Chlamydia

682
Q

Treatment of endometritis?

A

Empiric combination of clindamycin (900 mg q8 h IV or 600 mg q6 h IV) and an aminoglycoside (most commonly gentamicin 5 mg/kg q24 h or 1.5 mg/kg q8 h) remains the most effective regimen to treat postpartum endometritis; the addition of ampicillin or vancomycin as a third agent if enterococcus is suspected or isolated (pure culture or heavy growth from endometrial specimen)

683
Q

Postpartum fever and infection Ddx?

A

Consider UTI, wound infection, mastitis/breast abscess, endometritis or deep surgical infection, septic pelvic thrombophlebitis, drug reaction, clostridium difficile-associated diarrhea, complications related to anesthesia, PE/amniotic fluid embolism

684
Q

Antepartum risk factors of postpartum hemorrhage?

A

Personal Hx of PPH, overdistention (LGA, multiples, polyhydramnios), atony (fibroids), retained tissue (previa, uterine surgery, succenturiate lobes), coagulopathy (FHx, anticoagulated), distortion of uterus (placenta previa)

685
Q

Intrapartum risk factors of postpartum hemorrhage?

A

Atony (prolonged labour, induction/augment/chorioamnionitis), trauma (operative vag delivery, precipitous delivery, LGA).

686
Q

What is the active management of the 3rd stage of delivery?

A
  • Oxytocin Bolus – 5 units IV push or 10 units IM (if no IV) with anterior shoulder, helps placental separation
  • Oxytocin Infusion – 20 units per 1000cc crystalloid, run @ 125cc/hr and titrate to flow
  • Uterine Massage – as soon as placenta delivered
  • Inspection of Placenta – missing cotyledons, edges for evidence of succenturiate lobes, and document!
  • Be Prepared: NPO during labour, early IV access, CBCd/T&S on admission, extra help, i.e. if known placenta previa/accrete/percreta…when dealing with blood loss, reestablishing intravascular volume > replacing RBCs (3L of crystalloid for 1L blood loss). Pay close attention to symptoms like pallor, pulse, and pulse pressure.
687
Q

What are the signs of placental separation?

A

Gush of blood, lengthening of the cord, anterior cephalad movement of the uterine fundus (which is firm and globular) – 30 min, gentle traction, prevent inversion with countertraction

688
Q

Pregnancy adaptations that are protective against blood loss during pregnancy

A
  • Increase in Blood Volume – may lead to anemia
  • Preload leading to increase cardiac output – autotransfusion 500-750cc uteroplacental blood (if the uterus contracts appropriately), relief of compression of IVC
689
Q

Definition of postpartum hemorrhage?

A
  • Definition: Loss of >500 mL of blood with VD or >1000 mL with C/S or >10% drop in Hgb (lab definition)
  • Early: within first 24 hours postpartum
  • Late: >24 hours but within first 6 weeks
690
Q

4 T’s of postpartum hemorrhage?

A
  1. Abnormalities of Uterine Contraction: Tone - Primary mechanism is to stop bleeding at the placental insertion site
  2. Products of Conception: Tissue
  3. Trauma
  4. Abnormalities of Coagulation: Thrombin
691
Q

Causes of abnormal uterine contraction causing postpartum hemorrhage?

A
  • Overdistended uterus for polyhydramnios, multiple gestation, or macrosomia
  • Uterine muscle exhaustion for rapid/prolonged labour, high parity
  • Intra amniotic infection for fever, prolonged ROM
  • Functional anatomic distortion of the uterus from fibroids, previa (the tissue in the lower end has less ability to contract), or uterine anomalies (bifurcate/septum)
692
Q

Causes of trauma causing postpartum hemorrhage?

A
  • Lacerations of the cervix, vagina, or perineum due to precipitous delivery and operative delivery
  • Extensions/lacerations of c-section
  • Uterine rupture
  • Uterine inversion
693
Q

Causes of products of conception causing postpartum hemorrhage?

A
  • Retained products due to incomplete placenta delivery, uterine surgery, high parity, abnormal placenta (cotyledon/succinturiate)
  • Retained clots due to uterine atony
694
Q

Causes of abnormal coagulation causing postpartum hemorrhage?

A
  • Hereditary: hemophilia A, vonWillebrand’s Disease (most common)
  • Acquired: liver disease, ITP, thrombocytopenia of preeclampsia, DIC (due to PEE), IUFD, infection, abruption, amniotic fluid embolus
  • Therapeutic anticoagulation
695
Q

Fluid resuscitation of class 1 = 500-1000cc (compensated) PPH?

A

Transfusion not usually necessary

696
Q

Fluid resuscitation of class 2 = 1000-1500cc PPH?

A

Crystalloid (transfuse 3L crystalloid per 1L of blood loss (3:1) +/- Colloid (e.g. Albumin ~ ^Oncotic Pressure to pull more fluid from interstitium)

697
Q

Symptoms of class 1 = 500-1000cc (compensated) PPH?

A

No symptoms

698
Q

Fluid resuscitation of class 3 = 1500-2000cc PPH?

A
  • Crystalloid (transfuse 3L crystalloid per 1L of blood loss (3:1) +/- Colloid (e.g. Albumin ~ ^Oncotic Pressure to pull more fluid from interstitium)
  • Use P-RBCs if Hgb < 60. If 60-100 consider other factors like patient comorbidities
699
Q

Fluid resuscitation of class 4= >2000c PPH?

A

Transfusion protocol (+RBC transfusion)

700
Q

Symptoms of class 2 = 1000-1500cc PPH?

A

Diaphoresis/anxiety/weak/tachy-HR-RR/narrow PP

701
Q

Symptoms of class 3 = 1500-2000cc PPH?

A

Altered LOC, decreased systolic BP

702
Q

Symptoms of class 4= >2000c PPH?

A

All the symptoms found in class 3, but oliguria, anuria

703
Q

Management of postpartum hemorrhage?

A
  1. initial assessment (ABCs) – vitals, establish IV access (large bore), oxygen, monitor BP/HR/RR/urine output/SP02 +/- insert a catheter – assess etiology! Blood Work: CBC, coagulation screen (LOW fibrinogen or low platelets ~ worry about DIC), Type & Cross Screen
  2. STEP TWO: directed therapy
704
Q

Treatment of abnormal uterine contraction causing postpartum hemorrhage?

A

Assess fundal height/drain bladder…bimanual uterine massage + compress +

  • Syntocinon* 20 units in 1000cc crystalloid
  • Carboprost 250ug IM or I-myometrially q15m (max 2)
  • Misoprostol 400-800ug PO/SL, 800-1000ug rectal
  • Ergotamine 250ug IM or IV q5min up to 1.25mg
705
Q

Treatment of products of conception causing postpartum hemorrhage?

A

EUA/manual removal in OR (consider Abx) + curettage (done carefully)

706
Q

Treatment of trauma causing postpartum hemorrhage?

A

Explore vagina/cervix…correct inversion + repair lacerations + identify rupture

707
Q

Treatment of abnormal coagulation causing postpartum hemorrhage?

A
  • Thrombin: reverse + anticoagulation + replace factors
  • Hematology Labs: CBCd + Type & Screen +/- Cross Match
  • Coagulation: PTT/PT-INR + Bleeding Time (Red top tube, if >7m to clot, consider coagulopathy)
708
Q

Management of intractable

A
  1. STEP THREE:
    - Get Help: call anesthesia, book OR, prepare labs, ICU
    - Tamponade for Atony: Bakri Balloon OR Intrauterine Foley Catheter OR…
    - Manual Compression: pack uterus, vasopressin, embolization
    - Transfuse: either give crystalloid or blood products
  2. STEP FOUR: surgery or B-Lynch/Cho sutures (if C/S): Repairs/Removals: repair lacerations, ligate vessels (uterines/internal iliac – just one side), uterine artery embolization, hysterectomy (can do elective if known placenta percreta)
  3. STEP FIVE: post-hysterectomy bleeding
    Last Ditch: pack the abdomen, angiographic embolization
709
Q

Who receives continuous electronic FHR

A

Reserved for abnormal auscultation, prolonged labour, labour that is induced/augmented, meconium present, or multiple gestation/fetal complication – either doppler (external) or fetal scalp electrode (internal)

710
Q

Baseline FHR?

A

110-160bpm

711
Q

Non-pharmacologic pain relief techniques for labour?

A
  • Reduction of painful stimuli (maternal movement, position change, counter-pressure, abdo compression)
  • Activation of peripheral sensory receptors (superficial heat/cold, immersion in water during labour, touch/massage, acupuncture/acupressure, TENS, intradermal injection of sterile water, aromatherapy)
  • Enhancement of descending inhibitory pathways (attention focusing and distraction, hypnosis, music/audio analgesia, biofeedback)
712
Q

Pharmacologic options for labour?

A
  • Nitrous Oxide (e.g. self-administered Entonox)
  • Narcotics + Anti-emetic (Morphine if early in labour > 4 hours of delivery, Fentanyl if late in labour + Gravol)
  • Pudendal nerve block
  • Perineal infiltration with local anesthetic
  • Regional anesthesia (epidural block, combined spinal-epidural, spinal)
713
Q

Fetal indications of operative vaginal delivery?

A

Fetal Indications: atypical or abnormal FHR tracing, evidence of fetal compromise; consider if 2nd stage is prolonged, as this may be due to poor contractions or failure of fetal head to rotate

714
Q

Maternal indications of operative vaginal delivery?

A

Maternal Indications: need to avoid voluntary expulsive effort (e.g. CVD, CAD); exhaustion, lack of cooperation, and excessive analgesia may impair pushing effort

715
Q

Contraindications of operative vaginal delivery?

A

Non-vertex cephalic presentation, unengaged head, cervix incompletely dilated
Contraindications for Vacuum: <34wk (<2500g), fetal head deflexed, fetus requires rotation, bleeding disorder

716
Q

Absolute contraindications of vaginal (scheduled) delivery?

A

Placenta previa, conjoined twins, previous classical (vertical T) c-section or full-thickness hysterotomy, malpresentation (transverse or footling types), absolute cephalopelvic disproportion (CPD), underlying maternal illness (eclampsia, HELLP, heart disease), fetal condition where labour is contraindicated (ONTD, thrombophilia, certain anomalies).

717
Q

Relative contraindications of vaginal (scheduled) delivery?

A

2 or more prev C-section, frank or complete breech, twins, evidence of fetal compromise/placental dysfunction before labour (IUGR, abnormal Doppler).

718
Q

Risks/Complications of C-Section delivery

A

Complications related to anesthesia, hemorrhage (avg loss 1000cc), infection (single dose antibiotic should be use), injury to surrounding structures, thromboembolism (DVT, PE), ^recovery time/hospital stay, maternal mortality (<0.1%). The more C/S you have, the higher the rate of accreta (placental attachment abnormally to myometrium) and previa

719
Q

Indications for emergent C-Section delivery

A

Known/suspected uterine rupture, dystocia or CPD, abnormal fetal heart rate, labour complications – cord prolapse, failed attempt at operative vaginal. Main ones are abnormal heart rate, arrest of labour process.

720
Q

Female treatment for infertility?

A
  • Lifestyle modifications: cessation of alcohol, nicotine, and recreational drug use as they contribute to subfertility.
  • Treatment of underlying causes (e.g., levothyroxine for hypothyroidism, bromocriptine for hyperprolactinemia, metformin for PCOS)
  • Ovulation induction:
    ● Clomiphene citrate estrogen antagonist = ^FSH/LH = ovulation
    ● GnRH (pulsatile): stimulation of FSH and LH release - follicle maturation
    ● bHCG for simulation of ovum release
  • IVF
  • Oocyte/sperm donors
  • Surgery - tubuloplasty, lysis of adhesions