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Med 1 UBC Fall 2019 > Week 15-16 Reproduction > Flashcards

Week 15-16 Reproduction Flashcards

1
Q

Layers of the endometrium

A

Functional layer - which changes in response to hormones and is shed in menstruation Basal layer - thin, not shed.

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2
Q

length of luteal and follicular phase

A

14 days each. Luteal phase can vary in length (accounting for variations in cycle length), but follicular phase is always 14 days.

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3
Q

Why does the body only ovulate one egg?

A

Negative feedback - After period, early follicular phase, follicles are forming the the one that develops the most FSH receptors makes the most estrogen. Rise in estrogen provides negative feedback, which dampens development of other follicles.

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4
Q

Positive feedback in menstrual cycle?

A

As estrogen levels reach a critical point (coming from dominant follicle) you get positive feedback that supports the LH surge for ovulation.

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5
Q

Oligomenorrhea

A

long or infrequent cycles

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6
Q

Of trichomonas, chlamydia, and gonorrhea, which are reportable?

A

Chalmydia and gonorrhea are reportable. Trichomonas is not.

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7
Q

How common is Trichomonas?

A

The most common non-viral STI. 3.1% of reproductive aged women (US).

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8
Q

Dysuria

A

pain with urination

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9
Q

Reiter Syndrome (5)

A

A possible consequence of chlamydia. A post-inflammatory autoimmune disease; May present with conjunctivitis, urethritis, oligoarthritis, and skin lesions occurring 3-6 weeks after infection. Occurs more often in men.

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10
Q

Pelvic Inflammatory Disease - What is it? (3) - Causes (2) - Prevalence (1)

A

Infection/inflammation of… - endometrium - uterine tubes - pelvic peritoneum - surrounding structures Caused by chlamydia and gonorrhea as well as numerous non-STI pathogens in the vagina. Prevalence unknown because it isn’t reportable and it’s difficult to diagnose. Risk factors include, young age and sexually active, cervicitis, prior PID, IUD (within 21 days of insertion), surgery, vaginal douching

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11
Q

Fitz-Hugh-Curtis Syndrome (4)

  • cause, symptoms
A

Mostly occurs as a sequela of chlamydia infections;

Perihepatitis - inflammation of the liver capsule.

Characterized by R upper quadrant pain, nausea, vomiting, and fever, which are generally accompanied by evidence of pID on physical exam. ‘bow-string sign’

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12
Q

Follow up for chlamydia treatment

A

Abstain from unprotected itnercourse until after multiple dose therapy or 7 days after single dose. Test of cure at 6 mos after infection and 3-4 weeks if pregnant. Screen for other STIs, screen partners, reportable to public health.

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13
Q

Follow up for gonorrhea treatment

A
  • treat partners - all those with contact within 60 days
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14
Q

STI infections that pose risk for developing PID?

A

Chlamydia and gonorrhea

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15
Q

Possible outcomes of PID (6)

A

May lead to tubo-ovarian abscess, sepsis, Fitz-Hugh Curtis syndrome, ectopic pregnancy, infertility (increases with n# of PID occurrences), chronic pelvic pain, increased risk of recurrent PID.

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16
Q

How to diagnose PID

A

A syndrome that is mostly diagnosed by exclusion. Symptoms of note: - lower abdominal pain*** - deep dyspareunia - UTI symptoms - increased vaginal discharge Signs: - cervical motion tenderness*** - adnexal tenderness on bimanual exam (uterine tenderness)***

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17
Q

Treatment for PID

A

Cefixime OR ceftriaxone WITH doxycycline OR azithromycin WITH OR WITHOUT Metronidazole

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18
Q

When to admit a pt with PID? (6)

A

Possible surgical emergency (appy not ruled out)

Not responding to oral antibiotics

Non-compliant with treatment

Severe illness, fever

Tubo-ovarian abscess

Concurrent HIV

Child/adolescent

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19
Q

Recommendations for wt gain in pregnancy

A

BMI < 18.5 gain 28-40 lbs

BMI 18.5-24.9 gain 25-30 lbs

BMI 25-30 gain 15-25 lbs

Obese BMI>30 consult healthcare provider

Gain more wt in 2nd and 3rd trimesters. Some populations are at risk for gaining too much wt in first trimester

  • reinforce twice as healthy not twice as much.
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20
Q

Complications of obesity in pregnancy (4)

A

Spontaneous miscarriage;

Gestational diabetes;

Macroscopic baby - increased rates c-section, unable to fit through vaginal canal;

Hemorrhage, pre-eclampsia; (From CBL)

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21
Q

Recommendations for exercise in pregnancy

A

Moderate exercise is safe and recommend because it decreases risk of HTN and length of labour. - generally 30 mins each day at a level where they can still talk For people who weren’t exercising already - start at 15 mins and work up. Exercise at an intensity when you are still able to talk normally. Generally, 150 mins a week spread over at least 3 days. Both aerobic and resistance and stretching if it feels good. Stop impact exercises once uterus moves out of pelvis (after 1st trimester?). Avoid initiating the valsalva manoeuvre (increases abdominal pressure). Stay hydrated, avoid overeating, avoid sauna/hot tub. (CBL)

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22
Q

What is the recommended schedule of visits for a low risk pregnancy? What are the recommended investigations (lab & ultrasound), when are these performed, and for whom are they recommended? ****return and fill out

A

Weeks 0-28: visits every 4 wks. Initial Visit: Reconfirm with pregnancy test. Detailed history and physical. (Confirm blood type and Rh status. Test HIV, chlamydia, gonorrhoea, TSH, Hep B and C, zika, MMR, HSV (pap smear), urine (proteinuria), toxoplasmosis. SIPS, dating ultrasound (wk 7-14), detailed ultrasound Weeks 28-36: visits every 2 wks. Start anti-Rh factors wk 28 if necessary. Weeks 36-term: visits weekly. SIPS: Wk 13-15

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23
Q

3 ways to estimate due date

A

1) Last menstrual period (time since first day of the last period; LMP + 7 days + 1 year - 3 months) 2) Dating ultrasound 3) Measuring symphyseal-fundal length

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24
Q

Compare and contrast first trimester dating US and a second trimester detailed an atomic scan

A

7-14 (recommended to do it at 10 wks onwards; only if available); gold standard to determine when pregnancy is due. 19-20 wks: for everyone in BC; make sure fetus is growing properly, check for congenital anomalies.

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25
Q

BC guidelines for genetic screening

A

Everyone should be offered SIPS - screening for aneuploidy and NTD. If it’s positive, getting IPS is covered. The genetic screening in SIPS; 2 blood tests for PAPPA (pregnancy-associated plasma protein A) and the other for a quad screen (levels of components indicate various risks). Can check for trisomy 13, 18, 21

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26
Q

When are fetal movements first felt in pregnancy?

A

Typically, 18-22 wks

(At 26 weeks we expect to feel 6 movements in 2 hours?)

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27
Q

What produces hCG?

A

syncytiotrophoblasts. Its role is to maintain corpus luteum until placenta takes over.

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28
Q

Progesterone produced by…?

A

Produced by corpus loteum until 10 wks and placenta takes over

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29
Q

CV changes in pregnancy

A
  • Most early, peak in 2nd semester and then plateau - increased blood volume, RBC mass (due to increased EPO; calls for more iron) - Increased CO due to increased SV and HR. HR increases most in 3rd trimester by 10-15 bpm. - Decreased SVR due to placenta. Placenta opens spiral arteries to establish high flow low resistance system. Response to angiotensin II and estrogen-mediated vasodilation.
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30
Q

Dilutional anemia

A

plasma volume increases faster than increase in RBC mass, leading to anemia. If Hg gets less than 105, this may actually be pathological and not just dilutional anemia. This is why we consider iron supplementation in almost all women.

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31
Q

downsides of iron supplementation

A

nausea, constipation

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32
Q

How well is increased CO in pregnancy tolerated?

A

generally well, but may impose excessive strain on the heart of mom is older or has existing CV risk factors. Aortic stenosis would be a concern

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33
Q

Clinical assessment of cytotrophoblast invasion

A

uterine artery dopplers

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34
Q

Clinical signs and symptoms of CV changes in pregnancy (7)

A
  • drop in BP, especially diastolic
  • anemia
  • systolic ejection murmur (due to increased CO across valves)
  • heart displayed upward and left on CXR
  • Supine hypotension
  • varicose veins
  • peripheral edema (swelling of lower limbs)
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35
Q

The point of CV changes in pregnancy

A

maximize fetal perfusion and growth and protect growth.

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36
Q

supine hypotension

A

Lying supine, uterus is heavy, compress vena cava, possibly resulting in hypotension if the CV system can’t compensate. May feel lightheaded lying down. Gets worse as pregnancy progresses. May result in fetal distress if the placenta can’t perfuse well and oxygen supply is reduced.

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37
Q

Postpartum resolution of CV changes in pregnancy

A
  • Blood volume loss at delivery - increased diuresis over next 1-2 weeks - Maintain pregnancy state for 1-2 days, Return to pre-pregnancy by 1-2 weeks
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38
Q

Respiratory changes in pregnancy: What are they? What causes them? What is the intended outcomes?

A
  • Relative hyperventilation**** due to higher progesterone, increasing central chemoreceptor sensitivity to CO2 which gets you to breath more.
  • Goal: Enhance oxygen supply to fetus, heart, kidneys ,and respiratory muscles and eliminate excess CO2 from fetus;
  • Oxygen consumption increases by ~20%
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39
Q

signs and symptoms of resp changes in pregnancy (5)

A
  • nasal stuffiness;
  • increased risk fo nose bleeds due to hyperemia of upper airways and mucosa
  • dyspnea likely due to increased central sensitivity to CO2
  • elevated diaphragm, widening of subcostal angle
  • changes in spirometry
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40
Q

Investigation of respiratory changes in pregnancy

A

Do not over-investigate or treat because it increases anxiety. History and physical focusing on other associated symptoms (chest pain), when it happens, does rest relieve symptoms?

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41
Q

Red flag with resp distress in pregnancy

A

chest pain

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42
Q

Arterial blood gas changes in pregnancy

How are they compensated for?

A

increased minute ventilation increases O2 in arteries (PaO2) and decreased CO2, leading to mild resp alkalosis. COmpensated by renal excretion of bicarb to maintain normal pH

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43
Q

Anatomic GU changes in pregnancy, their cause, and consequences.

A
  • Dilated ureters, increased size of renal pelvis, increased kidney size. Usually R side is more dilated than left due to rotation of uterus.

Cause: Progesterone stimulates smooth muscle relaxation and mechanical compression by uterus.

Consequences: urinary stasis leads to increased risk of pyelonephritis if UTI occurs. This is why we check all pregnancy patients for asymptomatic bacteruria at first visit and again if they have any symptoms.

  • Displaced bladder and urethra. Decreased bladder capacity. Urinary frequency and relaxation of bladder may cause incontinence as well.
  • Increased renal plasma flow and GFR due to increased CO and decreased SVR. Will typically lead to decreased serum creatinine and urea, glucosuria in small amounts, proteinuria in small amounts.
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44
Q

significant proteinuria indicates…

A

possible preeclampsia

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45
Q

Resolution of GU changes in pregnancy

A

Most changes resolve within 2 weeks. Dilated ureters normal by 2-8 wks. Exception is potential trauma to GU tract with delivery may lead to sustained urinary incontinence.

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46
Q

GI symptoms (causes (2) and outcomes)

A

Primarily: Reflux, (GERD), constipation, hemorrhoids, gall stones, nausea and vomiting

Causes: PROGESTERONE relaxes lower esophageal sphincter (reflux), decreased GI motility (constipation; nausea; vomiting), decreased gall bladder contractility (gall stones). Mechanical displacement of GI due to enlarging uterus . beta-hCG higher (more nausea and vomiting)

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47
Q

GERD in pregnancy is important because

A

If we know they have reflux, then the woman is more at risk for aspiration with general anaesthetic.

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48
Q

hyperemesis gravidarum

A

severe, prolonged nausea and vomiting that may require IV fluids and hospital admission

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49
Q

When may beta hCG levels be higher?

A

With twins because more placenta, so more syncytiotrophoblasts. May lead to more nausea.

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50
Q

Hemorrhoids in pregnancy caused by (2)

A

Due to constipation (decreased motility and increased water reabsorption) and increased venous pressure (due to obstruction of venous return by enlarging uterus)

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51
Q

Postpartum blues vs depression

A

Blues are common - a transient state that is very common in postpartum pts. Usually resolved by day 10-14. Supportive treatment and reassurance helps. PP depression and anxiety require medical attention by GP, Ob or psychiatry.

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52
Q

Gall stones in pregnancy (2)

A

due to progesterone impairing contraction and motility of gallbladder. Estrogen mediated decreased bile acid transport.

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53
Q

Maternal hydronephrosis is more common on which side?

A

More common on the right because the sigmoid colon causes dextrorotation of uterus and compression of right ureter at pelvic brim

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54
Q

What is the usefulness of dipstick urine glucose and protein screening in pregnancy?

A

useful for screening, but not diagnostic. Low levels normal but high levels may indicate diabetes or preeclampsia

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55
Q

Is exercise in pregnancy appropriate for women who were previously sedentary?

A

Yes. Use talk test.

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56
Q

How much does maternal cardiac output increase in pregnancy?

A

30-50%

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57
Q

How is the heart displaced in pregnancy?

A

upward and to th eleft

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58
Q

how much is HR increased in third trimester?

A

10-15 bpm

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59
Q

how to relieve supine hypotension

A

left lateral positioning

60
Q

What level of physiological anemia is acceptable in pregnancy?

A

>105-110 g/dL

61
Q

Maternal mortality ratio

A

number of maternal deaths per 100 000 live births. Different from maternal death, which refers to a woman dying while pregnancy or within 42 days of termination of the pregnancy.

62
Q

Infant mortality

A

deaths of infants under 1 year old per 1000 live births.

63
Q

Which developed country has a rising maternal mortality rate?

A

USA, highest in texas. Significant disparities between racialized and caucasian populations.

64
Q

What is causing maternal deaths in the US?

A
  • 60% preventable causes - Issues with access to care, communication - Racial disparity bt non-Hispanic Black and non-HIspanic whites
65
Q

Global gender gap index

A

A framework for measuring gender based disparities and tracking their progress over time.

4 components:

  • economic participation and opportunity
  • education attainment
  • health and survival
  • political empowerment
66
Q

Risk factors for high MMR (30

A
  • fragile settings
  • young age
  • number of pregnancies
67
Q

Strategies to reduce maternal morbidity and mortality

A

AVAILABILITY, ACCESS, AWARENESS - family planning: spacing births, contraception - Antenatal care: screen for complications - clean/safe delivery - essential obstetric care for high risk pregnancies and emergencies

68
Q

recommended minimum gap between pregnancies

A

minimum 18 mo, anything below poses risk of preterm infant, small for gestational age. Many contributors, such as maternal nutrient depletion, economic factors.

69
Q

3 delays in care that affect maternal outcomes

A

Delay in the decision to seek care Delays in reaching care Delays in obtaining care the the facility.

70
Q

Behavioural economics

A

looks at how people make certain decisions and how we can change those decisions to improve health and help women resist social and cultural pressure.

71
Q

Why, when, how and in whom is a Group B Strep (GBS) swab done? Are there any patients who do not require one?

A

GBS screening is done because it is a leading cause of serious neonatal infection. 1-2% of neonates born of colonized women suffer morbidity and mortality associated with early onset GBS disease. Offer a GBS swab to all women at 35-37 weeks gestation, even if they have a planned cesarean. Offer GBS prophylactic antibiotics to women earlier if they are in labour or have ruptured membranes. Screening is not necessary if the pregnant person already has confirmed GBS bacteriuria, as these patients will be assumed to be colonized and treated accordingly.

72
Q

What is the management of a GBS positive result?

A

Treatment at the time of labour or rupture with appropriate IV antibiotics. Test for resistance if it is suspected.

73
Q

Pituitary gland - structure and function

A

Anterior lobe: Communicates closely with hypothalamus via hypophyseal portal system. Produces 6 hormones - growth hormone (GH), TSH, ACTH, FSH, LH, prolactin Posterior lobe: Storage and release of 2 hormones produced by the hypothalamus - ADH and oxytocin.

74
Q

Common features of hormones produces by the anterior pituitary

A

They all peptide hormones that act via cAMP cascades.

75
Q

Production, release and effects of growth hormone.

A

Growth hormone is produced by somatotropin cells of the anterior pituitary. It is released in by the anterior pituitary in response to growth hormone releasing hormone from the hypothalamus. Its effects are mostly anabolic (using up AAs, carbs, and proteins to build tissues), as well as stimulation of gluconeogenesis. Effects on growth are indirect

76
Q

Production and function of TSH

A

TSH is produced by thyrotrophs in the anterior pituitary. TSH controls each step in the production of thyroid hormones by the thyroid gland.

77
Q

Production of FSH and LH

A

Both produced by gonadotroph cells of the anterior pituitary gland.

78
Q

Production and function of ACTH

A

Produced by corticotrophs of the anterior pituitary gland. Stimulates the cortex of the adrenal gland to produce glucocorticoid hormones, especially cortisol

79
Q

Production and function of prolactin

A

Prolactin is produced by lactotrophs of the anterior pituitary. Stimulates breast development and lactogenesis, in addition to a wide variety of additional actions. Suckling during breastfeeding blocks secretin of dopamine, which allows prolactin and therefore milk release.

80
Q

Endometrium changes in the follicular phase and luteal phase

what are the names of the endometrial stages?

A

Follicular phase: Starts with Menstrual Phase and continues into Proliferative Phase

  • Endometrial growth is estrogen mediated;
  • Thickening of endometrium
  • Development of Spinnbarkeit cervical mucous

Luteal phase: Correlates with Secretory Phase

  • Progesterone mediated preparations of the endometrium.
  • Endometrial stroma becomes loose, blood vessels thicken and twist, endometrial glands tortuous.
  • Without fertilization, progesterone levels fall and the functional layer will slough off (menstruation).
81
Q

When does temperature spike in the menstrual cycle?

A

The peak in temperature occurs after the peak in fertility so it is limited in terms of fidelity for trying to take advantage of fertile period

82
Q

How does cervical mucous change throughout the menstrual cycle?

A

Estradiol promotes cervical secretions that favour sperm motility, passage through the cervical canal, and capacitation (sperm maturation). It’s egg white mucous - copious, thin, stretchy, clear (Spinbarkeit)

Post-ovulation, progesterone promotes mucous changes that impede sperm motility. Mucous appears thick, scant, tenacious.

83
Q

4 main avenues for preventing pregnancy (in brief)

A

Prevent ovulation

Prevent fertilization in the uterine tube

Prevent implantation in the endometrium

Prevent entry of semen into the uterus

84
Q

Permanent sterilization procedures

A

Tubal ligation

Vasectomy (interrupt vas deferens)

85
Q

Beyond contraception, what is a clinical application of tubal ligation?

A

Reduces risk of ovarian cancer by 40%

86
Q

Mechanism of combined estrogen and progesterone contraception

A

Continuous low dose estrogen and progesterone pose negative feedback on pituitary and hypothalamus, thus reducing FSH and LH secretion.

Estradiol primarily inhibits FSH release (inhibits follicular recruitment, prevents ovulation)

Progesterone acts to suppress LH (prevents ovulation), reduce tubal peristalsis, undermine preparation of the endometrium, and thicken cervical mucus.

87
Q

Histology also effects of hormonal contraceptives on the endometrium.

A

Progesterone normally stabilizes the endometrium, but constant progesterone exposure actually causes the endometrium to develop a dense network of thin-walled, fragile, small veins. Continuous exposure to estrogen prevents endometrial growth, thus a thin endometrial lining is established. This is why, in clinic, hormonal contraception maybe used to treat dysmenorrhea and menorrhagia.

88
Q

Progesterone only contraception

A

Works by…

1) Primarily by suppressing LH release (prevents ovulation 40%)
2) Reduced tubal peristalsis
3) endometrium not receptive to ovum (decidualized bed with atrophic glands)
4) cervical mucus thick and impervious

Can be a pill, injection, IUD, implant

89
Q

IUD (4)

A

Sterile inflammation of endometrium and uterine tubes;

Toxic to sperm and ova, prevents fertilization, and discourages implantation.

90
Q

Benefits of hormonal contraceptives other than contraception (3)

A

Treatment of menorrhagia, decrease anemia, treat dysmenorrhea

Treatment of perimenopausal symptoms, endometriosis/PCOS symptoms,

Decreased risk of endometrial cancer, epithelial ovarian cancer

91
Q

Options for emergency contraception (2) and who are they appropriate for?

A

1) Hormonal - ie., high dose of Levonorgestrel; less effective for higher BMI
2) Insertion of copper IUD - the most effective emergency contraception option & first line if BMI > 30

92
Q

Who automatically gets treated for GBS at labour? (2)

A

1) they already had a positive bacteriuria result in their current pregnancy (which would have been treat at that time as well)
2) they have previously given birth to a GBS AFFECTED child

93
Q

If you had a prior preterm birth are you at risk for another?

A

Yes

94
Q

ddx for cramping at 32 weeks

A

Braxton Hicks (shorter duration, irregular, less painful than labour)

Labour (regular timing; presence of other risk factors for preterm birth)

UTI (dysuria, blood in urine)

GI Illness (diarrhea - could still be a sign of preterm labour)

Abruption (bleeding??)

95
Q

Should pregnant people come in if they experience membrane rupture or bleeding?

A

Yes, if membranes ruptured or bleeding before term;

If membrane ruptures and you’re at term, you can stay home for a little while, unless you’re GBS+ because you have to start penicillin;

96
Q

What do we need to ask about in terms of bleeding in pregnancy?

A
  • How far along are they?
  • How much blood?
  • Is there pain associated?
  • Past miscarriage? Presents with cramps or bleeding.
  • Possibility of ectopic pregnancy? Has she had a dating scan to locate the pregnancy? Don’t forget that a heterotopic pregnancy is an option (1 in uterus and 1 elsewhere; more likely in IVF)
  • What is her Rh status?? Need to deal with it within 72 hours, not immediately.
  • Possible previa? Painless bleeding - see ultrasound.
97
Q

When does Rh need to be addressed in the case of bleeding?

A

Within 72 hours. Not the first priority in blood loss - managing hemorrhage and shock is the first priority.

98
Q

If pt is bleeding and cervix is open, what do we worry about?

A

Almost definitely having a miscarriage

99
Q

Is bleeding normal in pregnancy?

A

Bleeding is NOT normal, but can still result in a normal pregnancy outcome.

100
Q

Rh status determination

A

Rh status is determined on first trimester type and screen. You find out her ABO status (does she have her own Rh antigens?) and also scan to see if she has Rh antibodies is she was Rh -ve herself.

101
Q

Rhogam

A

An anti-D antibody. It’s the Ab that we don’t want the mother to develop. It will mop up any Rh+ cells that the mom may have been exposed to, in order to prevent her from developing her own immune response and her own Abs. Prevents the mother from developing her own immune response to pot

102
Q

Who do we give Rhogam to (2)

When do we give rhogam? (2)

A

The Rh negative patient with…

a) any bleeding in pregnancy
b) any intrauterine procedure (CVS, amnio, termination)

Treat at 28 weeks when the fetus’ RBCs

Treat after delivery if fetus is determined to be Rh positive. If fetus is Rh negative, Rhogam is not needed.

103
Q

What mediates decrease in BP during pregnancy?

A

Opening of spiral arteries in the placenta - a high flow and low resistance system. Angiotensin II and estrogen promote vasodilation in mum.

104
Q

how little iron is too low?

A

iron below 105 indicated pathological anemia rather than dilutional anemia that is typical in pregnancy

105
Q

Treatment for supine hypotension

A

This is why we tell patients to sleep on their side. uncross legs, compression stocking, keep calf muscles pumping when standing for prolonged periods.

106
Q

How does the endometrial lining change with combined progesterone and estrogen oral contraception?

A

Progesterone promotes thinning of the endometrial lining and estrogen promotes thickening. When combined, progesterone dominates and so long term use of oral contraception with both estrogen and progesterone results in lighter periods.

107
Q

Diagnostic criteria for PCOS

A

Patients need 2 of 3:

  • oligo-/amenorrhea
  • clinical or laboratory evidence of elevated androgens (hair, acne)
  • Polycystic ovaries on ultrasound (>12 developing follicles per cycle)
108
Q

Causes of irregular cycles, other than PCOS (4)

A
  • Hyperprolactinemia (galactorrhea and elevated prolactin)
  • Hypothalamic amenorrhea (such as in athletes; due to low GnRH)
  • Premature ovarian insufficiency
  • Hypothyroidism (TSH)
109
Q

Hormonal dysregulation in PCOS

A
  • Increased pulsatility of GnRH causes increased LH secretion, relative to FSH
  • Increased LH causes…
    • theca cells to make more androgens
    • Granulosa cells have less FSH so they aromatise less estrogen
    • Elevated local androgen inhibits follicular development, which causes oligo- or amenorrhea
110
Q

PCOS symptoms

A
  • Infertility
  • Irregular cycles
  • Acne
  • Hirstism (male pattern hair loss)
111
Q

Clomiphene citrate

A

Blocks estrogen feedback at hypothalamus and pituitary so that more FSH can be released and ovulation can occur.

(this works in PCOS pts because they have moderate estrogen levels, if the pt doesn’t already have good estrogen levels this won’t help fertility)

112
Q

How to pharmacologically bring on a period

A

Progesterone pill for 10 days

113
Q

Letrozole

A

An aromatase inhibitor. Blocking aromatase reduces estrogen levels…

More effective than clomiphene

114
Q

Fertility treatment options other than clomiphene or letrozole

A

FSH injections (ovulate more eggs)

IVF

Ovarial drilling

115
Q

How to manage hirsutism and acne in PCOS

A

Oral contraceptives - reduces LH production

Anti-androgens

116
Q

longterm complications of PCOS (5)

A
  • Endometrial cancer (result of persistent estrogen stimulation and resulting hyperplasia)
    • Make sure the PCOS pts cycle regularly and assist with OCP or progesterone if need be!
  • HTN (evidence of reduced vascular compliance)
  • dyslipidemia (increased TG, VLDL, LDL, decreased HDL)
  • Type II DM
  • sleep apnea
117
Q

Categories of problematic placental development (3)

A
  1. Shallow/inadequate implantation: miscarriage, IVF failure, fetal growth restriction, preeclampsia
  2. Abnormal location: actopic, previa
  3. Uncontrolled invasion: accreta
118
Q

Uterine preparating for placental implantation (2 phases, morphological changes)

A
  • ​Proliferative phase - follicles secrete estrogen which promotes proliferation and remodelling
  • Secretory phase - progesterone from corpus luteum stimulte further thickening of endometrium and glandular and vascular development to support implantation
    • Most receptive to impantation at 8-10 days after LH surge, which correlates with high levels of progesterone.
  • Overall:
    • Cell growth, more organelles for protein synthesis, more intracellular junctions.
    • Lipid and glycogen production for energy
119
Q

Ectopic implantation

A

Implantation anywhere other than the fundus (cervix, uterine tube, etc)

120
Q

Hor how long is the uterus receptive to implantation?

A

6-7 days post-ovulation

121
Q

Differenetiation of the trophoblasts

A

Trophoblasts are the outer cell mass of the embryo. They differentiate into 2 cell types:

  1. Cytotrophoblasts: progenitor cells that become
    1. villus cytotrophoblasts -
    2. extravillus cytotrophoblasts - invade maternal spiral arteries to widen them. Promotes high blood flow to fetus through placenta
  2. Syncytiotrophoblasts: giant, multinuclear cells that form by fusion of cytotrophoblasts. Invase endometrium.
122
Q

What happens if the spiral arteries aren’t well invaded by cytotrophoblasts? (5)

A

Increased risk of

  • Fetal growth restriction
  • Prematurity
  • Abruptio placenta (=early separation of placenta)
  • Preeclampsia
  • Stillbirth
123
Q

How do we assess cytotrophoblast invasion

A

Uterine artery dopplers

124
Q

What may result from cytotrophoblsat invasion that is too extensive? (5)

A
  • Placenta accreta (invasion too deep)
  • Plcenta increta (invasion into myometrium
  • Placenta percreta (all the way through the myometrium)
  • Maternal morbidity of bleeding
  • Fetal risks of bleeding and prematurity
125
Q

Risk factors for accreta (2)

A
  • Prior c section or uterine surgery (scar can become a site of uncontrolled division)
  • Placenta previa (lower uterine segment is more likely to have deep invasion because it’s thinner)
126
Q

Placcental maturation during pregnancy (4)

A
  • Villi branch and become more vascular
  • Increased SA
  • Decreased distance bt maternal and fetal circulation
    • In early pregnancy, there are 3 clear layers: syncytiotrophoblasts, cytotrophoblasts, fetal capillary endothelium.
    • Later on:
      • Fetal capillaries move closer to periphery of villus
      • Cytotrophoblasts partially regress so maternal and fetal blood are functionally separated by syncytiotrophoblasts, connective tissue and fetal capillary endothelium.
  • increased uterine blood flow
127
Q

Where are prostaglandins syntehsized in pregnancy? What stimulates their release?

A

They are synthesized as or near their site of action - the interface of amnion/chorion (membranes around fetus) and myometrium.

They are released in response to inflammation imposed by head pressing down into cervix.

128
Q

What inhibits PG production in pregnancy?

A

progesterone

129
Q

The two big PGs in delivery and their different roles

A
  • PGE2 - cervical effacement
    • Highest levels in amniotic fluid.
    • Breakdown collagen and soften EC matrix
  • PGF2alpha - contractions
    • Released in response to thinning lower uterine segment during active labour. I_nflammatory response_ and also oxytocin cause release of arachidonic acid
    • Increases intracellular Ca
130
Q

Oxytocin production, secretion.

Oxytocin receptors

A
  • Precursor produced in hypothalamus and then released from posterior pituitary in active labour
  • Oxytocin receptors on myometrium. Increase near term in response to estradiol. Receptors down-regulated by progesterone.
131
Q

Biochemical action of oxytocin

A

lead to Ca release from SR, thus increase Ca for contraction of smooth muscle

132
Q

How does Ca cause contractions

A

Binds with calmodulin to activate MLCK.

MLCK phosphorylates Myosin –> contractions

133
Q

Organization of myometrial muscle fibres

A

Long random bundles of thick and thin filaments to allow for shortening in any direction.

Increased gap junctions closer to parturition to optimize coordinated muscle contraction. Estrogen mediated and downregulated by progesterone.

134
Q

modes of inducing labour (5)

A
  1. amniotomy (repturing membranes resulting in release of PGs)
  2. Membrane sweeping (release PGs)
  3. PGs directly applied
  4. Foley catheter in cervix (balloon to add pressure to cervix
  5. Oxytocin
135
Q

Modalities for preventing preterm labour (3)

A
  1. NSAIDs (downregulate PGs)
  2. Progesterone
  3. Ca channel blockers

all with minimal success once labour has started

136
Q

What comprises Phase II or parturition?

A

Active labour. Progessive cervical silation and fetal delivery. Uterine contractions every 5 minutes lasting 30-60s.

137
Q

What are the 4 stages of Phase II of parturition?

A

WE R IN ACTIVE LABOUR NOW

  1. Onset of involuntary painful irregular contraction to full dilation (latent phase –> active phase)
  2. fulll dilaition to delivery of fetus
  3. Delivery of fetus to dleivery of placenta
  4. Delivery of placenta to stabilization of maternal condition
138
Q

First stage of active labour

A

Extremely variable duration. Onset of irregular leading to regular contractions.

Once the contractions are consistent and long lasting and the cervix is 3-4 cm dilated, the labour progresses consistently (i.e., 1cm dilation per hour with first child)

139
Q

Second stage of active labour

A

Full cervical dilation to delivery of fetus

  • Pushing and descent of fetus
  • Average 50 mins to 3 hrs for nulliparas and average 20 ins for multiparas.
140
Q

What are the cardinal movements?

A

Movements of fetus as it exits the uterus in order to minimize diameter to get through the narrowest parts of the pelvis.

141
Q

Third stage of active labour

A

Delivery of placenta

  • >90% deliver it wihtin 15 mins
  • Uterus need to contract down to prevents excess blood loss
  • Active management can reduce change of hemorrhage
142
Q

Classic signs of placental separation

A
  • Gushh of blood
  • lengthening of cord
  • Fundus rises up
  • uterus firm and globular
143
Q

Some ways of actively managing the delivery of placenta

A

administer uterotonics (oxytocin, misoprostol)

gentle, controlled cord traction

144
Q

how long dows it take for most physiologicla changes with pregnancy to return to non-pregnant state?

A

6 weeks.

145
Q

bleeding after pregnancy is what?

A

Superficial layer of endometrium sloughed off as lochia rubra, lochia serosa, lochia alba.

146
Q

Phase III of parturition

A

Puerperium

  • Involution of uterus
  • Cervix lengthens
  • Lactation begins with drop in estrogen and progesterone.
  • Diuresis of increased circulatory volume
  • Weight loss
  • Fertility restored

Med 1 UBC Fall 2019 (16 decks)

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