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Week 2 - "Pregnant At Last" Flashcards

1
Q

What is pregnancy?

Physiology

A

Events that occur from the time of fertilization (conception) until birth

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2
Q

What is gestational period?

Physiology

A

Time from las menstrual period until birth (usually 40 weeks (+/- 3) or 280 days)

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3
Q

What is conceptus?

Physiology

A

The developing offspring of the pregnant woman

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4
Q

What is the embryonic period?

Physiology

A

Time from fertilization through to week 8 –> conceptus is called an embryo

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5
Q

What is fetal period?

Physiology

A

Time from week 9 through birth –> conceptus is called a fetus

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6
Q

Where does fertilization occur?

Physiology

A

Ampulla

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7
Q

How do sperms know where to swim to in order to fertilize the egg cell?

Physiology

A

Every month the egg is released from alternating ovaries; the corona radiata of the egg cell secretes a chemoattractant, sperms have specific olfactory receptors which enable them to “smell” their way to the egg

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8
Q

What are the steps of fertilisation? (8)

Physiology

A
  1. The sperm cell weaves past follicular cells and binds to zona pellucida
  2. Rise in intracellular calcium inside the sperm cell triggers exocytosis of the acrosome (acrosomal reaction) which contains hydrolytic enzymes
  3. Hydrolytic enzymes from the acrosome cap are released, the act locally, dissolve the zona pellucida. The whip-like structure of the tail pushes the sperm head toward the oocyte membrane
  4. Head of sperm lies sideway to oocyte, microvilli on the oocyte surround the sperm head. The two membranes fuse, and the contents of the sperm cell enter the oocyte; the sperm cell membrane remains behind
  5. A rise in intracellular calcium inside the oocyte triggers the cortical reaction, in which the exocytosis of the granules that previosuly lay immediately beneath the plasma membrane occurs. The enzymes released lead to changes in the zona pellucida proteins, causing the zona pellucida to harden –> preventing polyspermy
  6. The rise in intracellular calcium inside the oocyte induces the completion of the oocyte’s second meiotic division and the formation of the second polar body
  7. The head of the sperm enlarges and becomes the male pronucleus
  8. The male and female pronuclei fuse
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9
Q

What triggers the acrosomal recation and the release of the contents of the acrosome?

Physiology

A

The binding of the sperm head to the zona pellucida

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10
Q

What is the process to the formation of a zygote.?

Physiology

A

Ovulation –> release of secondary oocyte (ovum)
Fertilization
Cleavage
Morula
Blastocyst
Implantation to the endometrium of the uterus

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11
Q

How is the concpetus product (blastocyst) swept towards the uterine cavity?

Physiology

A

With the help of the motile cilia of the oviduct epithelium

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12
Q

What is different regarding the mitotic divisions that occur with the zygote (cleavage)?

Physiology

A

The daughetr cells produced through mitosis are half the size of the mother cell so that the zygote does not get stuck in the fallopian tube and lead to an ectopic pregnancy

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13
Q

How many mitotic cycles does it take to convert to zygote (cleavage) into a blastocyst?

Physiology

A

4 to 5

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14
Q

What is the purpose of inner cell mass of the blastocyst?

Physiology

A

It is destined to become the embryo, located internally

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15
Q

What is the purpose of trophoblasts from the blastocyst?

Physiology

A

Form the outer superficial layer of cells, Accomplish implantation and develop into fetal portions of placenta (chorionic sac)

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16
Q

What are the two distinct cell populations that arise during the formation of blastocycts?

Physiology

A

Embryoblasts
Trophoblasts

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17
Q

In which part of the uterus does implantation usually take place?

Physiology

A

Posterior part of the fundus or body of the uterus

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18
Q

What are the stages of implantation? (4)

Physiology

A
  1. Hatching
  2. Apposition
  3. Adhesion
  4. Invasion
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19
Q

What happens during the hatching phase of implantation?

Physiology

A
  1. Degeneration of zona pellucida from lytic factors of the sperm
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20
Q

What happens during the apposition stage of implantation?

Physiology

A

Blastocyst aligns loosely with the endometrial surface, typically overlying the uterine epithelium at a receptive spot.

This stage involves minimal contact, with microvilli on trophoblast cells beginning to interact with the endometrium.

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21
Q

What is the position of the blastocyst in regards to the endometrium, how is that important?

Physiology

A

The blastocyst are facing endometrium, this way it is easier for blastocyst to receive nutrients during the first 12 weeks, prior to placent adevelopment, from the thickened endometrium

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22
Q

What happens during the adhesion process of implantation?

Physiology

A

The blastocyst firmly attaches to the endometrial lining via molecular interactions between adhesion molecules on trophoblasts and the uterine epithelium.

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23
Q

Which structures aid the adhesions process of implantation?

Physiology

A

Integrins, selectins, and cadherins mediate this process.

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24
Q

What happens during the invasion stage of implantation? What is the effect of that?

Physiology

A

The trophoblast cells differentiate into syncytiotrophoblasts, which invade the endometrial tissue and remodel maternal spiral arteries.

This creates a blood supply to establish the placenta, allowing nutrient and gas exchange.

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25
Q

When is the process of placenta formation completed?

Physiology

A

By the beginning of week 12

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26
Q

What are the two parts of the placenta?

Physiology

A

Maternal; decidua basalis
Fetal; chorion frondosum

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27
Q

What is the function of the placenta?

Physiology

A

It allows oxyge and nutrients to diffuse from maternal blood to fetal blood, while carbon dioxide and waste products diffuse from the fetal to the maternal blood

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28
Q

What is the importance of the placenta?

Physiology

A

It has a nursing function towrads the fetus and also an endocrine function

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29
Q

What is the nursing function of the placenta?

Physiology

A

The fetus requires a supply of nutrients in order to grow, these are initially provided through trophoblastic nutrition from the thickened endometrium and then through placental diffusion

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30
Q

What is the endocrine function of the placenta?

Physiology

A

Produces estrogens, progesterones, hCG which sustain pregnancy, fetal growth aand eventually, help in labor

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31
Q

How does the ratio of estrogen: progesterone change in order to help labor?

Physiology

A

Progesterone is higher than estrogen initially when that ratio changes, –> important for labor

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32
Q

Is the placenta able to convert progesterones to estrogens?
What happens?

Physiology

A

No

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33
Q

What is the importance of the sulfated hormones being weak and having a low effect on the fetus?

Physiology

A

If androgens were to have an effect on the fetus it could lead to masculization of the emebryo (if female) and other adverse effects

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34
Q

What is the maternal role in the hormone synthesis (of androgens) during pregnancy?

Physiology

A

Provides LDL cholesterol, the raw material for hormone production.

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35
Q

What happens to the LDL cholesterol provided by the mother?

Physiology

A

The placenta converts LDL cholesterol into progesterone, which is essential for maintaining the uterine lining and preventing contractions.

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36
Q

What is the role of the plcanta when it comes to the hormone synthesis during pregnancy (progesterone)?

Physiology

A

The placenta cannot convert progesterone to estrogens, but it passes progesterone to the fetus.

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37
Q

What does the fetus do with progesterone during the hormone synthesis during pregnancy?

Physiology

A

The fetus produces DHEA-S (a precursor for estrogens), which is transferred to the placenta.
In the placenta, DHEA-S is converted into estradiol, estrone, and estriol (estrogens).

Aromatase and other enzymes in the placenta carry out these conversions.

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38
Q

Which organ of the fetus produces DHEA-S?

Physiology

A

fetal adrenal glands produce DHEA-S from pregnenolone sulfate

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39
Q

How does the fetal liver contribute during the hormone synthesis during pregnancy?

Physiology

A

The fetal liver helps modify DHEA-S into intermediates that the placenta can use to produce estriol, the primary estrogen in pregnancy.

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40
Q

Which enzyme converts Progenenolone sulfate into DHEA?

Physiology

A

17-a hudroxylase
12, 20 Desmolase

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41
Q

Which enzymes convert DHEA into estradiol?

Physiology

A

3b-HSD
17-b HSD
Aromatase

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42
Q

Which enzyme converts DHEA-S to 16-a OH DHEA-S?

Physiology

A

16a- hydroxylase

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43
Q

Which enzymes convert 16a- OH DHEA into estriol?

Physiology

A

3b-HSD
17b- HSD
Aromatase

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44
Q

Which hormones are important for fetal growth?

Physiology

A

Growth Hormone
T4
Cortisol
Insulin

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45
Q

Where is fetal insulin produced? When?

Physiology

A

Produced by the fetal pancreas by week 12

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46
Q

Which hormone is the most important hormone when it comes to regulating fetal growth?

Physiology

A

Fetal insulin

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47
Q

What is the effect of growth hormonefrom maternal, placental or fetal origins on fetal growth?

Physiology

A

Minimal, little effect

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48
Q

What is normal fetal growth like for the first 20 weeks of gestations?

Physiology

A

Mainly by cellular hypersplasia

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49
Q

What is fetal growth like from week 20 to week 28 of gestation?

Physiology

A

Hyperplasia and hypertrophy

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50
Q

What is fetal growth like from week 28 onwards of the gestational period?

Physiology

A

Hypertrophy with rapid accumulation of fat, muscles and connective tissues

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51
Q

When does 90% of featl weight gain occur?

Physiology

A

Later half of pregnancy

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52
Q

When do all the gross characteristics of all the organs of the fetus begin to develop?

Physiology

A

Within 1 month after fertilization

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53
Q

When are most of the details of the different organs established?

Physiology

A

2 to 3 months after the initial development of the organs

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54
Q

What are the organs of the fetus, beyond 4 months like?

Physiology

A

Grossly the same as those of the neonate just not functioning

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55
Q

When does the heart of the fetus start beating and how?

Physiology

A

At around 4 weeks, not fully developed but it has autorhythmic cells that have developed and they have their own pacemakers –> 65b/min

ACtual heart starts beating at around 38 to 40 weeks

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56
Q

Where are RBCs formed from week 3 to week 8?

Physiology

A

Yolk sac and placenta

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57
Q

Where are RBCs formed from week 6 to term?

Physiology

A

Fetal liver

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58
Q

Where else are RBCs formed from week 10 to week 28?

Physiology

A

Spleen

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59
Q

WHat is the structure that produces RBCs which develops last? When does it start producing RBCs?

Physiology

A

Fetal bone marrow, from week 20 to term

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60
Q

Why do the fetal lungs remain deflated through-out the pregnancy?

Physiology

A

No breathing occurs during intrauterine life, lungs contain clear fluid, not air

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61
Q

Why are repsiratory movemnets inhibited during pregnancy?

Physiology

A

To prevent filling of the lungs with fluid and debris from the meconium excreted by the fetus’ GIT into the amniotic fluid

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62
Q

What is the purpose of small amounts of fluid secreted into the lungs, where is it secreted from?

Physiology

A

Secreted by alveolar epithelium up until moment of birth, keeping inly clean fluid in the lungs

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63
Q

What is the complication associated with abnormal kidney development or severe impairement of kidney functio during pregnancy?

Physiology

A

Issues with the fetus’ kidneys gretaly reduces the formation of amniotic fluid (oligohydramnios) which can lead to fetal death

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64
Q

When does the renal system for regulating fetal extracellular fluid volume anf electrolyte imbalance fully develop?

Physiology

A

Late fetal life and reach full development a few months after birth

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65
Q

When does urine excretion form the kidneys of the fetus begin?

Physiology

A

Week 13 onwards

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66
Q

When are small amounts of meconium formed and excreted during egstational period?

Physiology

A

From week 28 till term

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67
Q

When does ingetsion and absorption of large quantities of amniotic fluid begin?

Physiology

A

From week 20 until term

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68
Q

What is meconium composed of?

Physiology

A

Partly of residue from swallowed amniotic fluid and partly of mucus, epithelial cells, and other residues of excretory products from GI mucosa and glands

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69
Q

What is the main source of energy for the fetus?

Physiology

A

Glucose

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70
Q

What is the fetus’ capability of storing fat and proteins like?

Physiology

A

High capability

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71
Q

When do calcium and phsophate accumulate during pregnancy?

Physiology

A

In the 2nd half due to bone ossification

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72
Q

WHy does iron accumulate faster than calcium and phospahte during pregnancy?

Physiology

A

Required for RBC production, accumulates mostly in the hemoglpbin and also 1/3 of the liver

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73
Q

Which vitamins are necessary for the fetal development and growth?

Physiology

A

B, C, D, E and K

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74
Q

What do most of the reflexes of the fetus involve?

Physiology

A

Spinal cord and brain stem –> 3rd to 4th month

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75
Q

WHen do functions and reflexes involving the cerebral cortex occur?

Physiology

A

Early stages of development at birth

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76
Q

When does myelination of some major tracts of the brain occur?

Physiology

A

Becomes complete after about 1 year of postnatal life

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77
Q

When are anterior pituitary hormones secreted from the fetus?

Physiology

A

begin at week 8 and they are independent of hypothalamic influence

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78
Q

When are adrenal medulla hormones secreted from the fetus?

Physiology

A

E, NE, T3 and T4 begin at week 10

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79
Q

When are posterior pituitary hormones secreted from the fetus?

Physiology

A

From week 14 onwards

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80
Q

When re hypothalamic hormones secreted fromn the fetus?

Physiology

A

From week 13 onwards

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81
Q

What does the outer definitive zone of the adrenal cortex of the fetus scerete?
Functions?

Physiology

A

Cortisol –> multiple functions during fetal life, including promotion of pancreas and lung maturation, induction of liver enzymes, promotion of intestinal tract cytodifferation, in itiation of labor?

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82
Q

What does the deeper fetal zone of the adrenal cortex of the fetus secerte?

Physiology

A

DHEA-s and androgenic precursors for estrogen synthesis by the placenta –> only present in the fetus, disappears after birth

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83
Q

What is the purpose of fetal gonadal hormones that act during organogenesis?

Physiology

A

Control sexual differerentiation

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84
Q

When do fetal testes differentiate ?
What happens to Leydig and Sertoli cells?

Physiology

A

Between weeks 6 to 8
Leydig start producing testosterone, either autonomously or under hCG regulation
Sertoli cells produce anti-mullerian hormone

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85
Q

What does the differentiation of the male external genitalia require?

Physiology

A

5a reductase to produce DHT

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86
Q

What is labor?

Physiology

A

Process by which uterine contraction expel the fetus through the vagina to body exterior

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87
Q

Why are there no uterine contractions during pregnancy?

Physiology

A

Uterus is quiescent because of progesterone and relaxin

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88
Q

What is the timin g of parturition controlled by?

Physiology

A

Fetus-derived signals (1)
Endocrine and paracrine factors (2)
Stretching of the uterus (3)

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89
Q

Once labor is initiated, how is it sustained?

Physiology

A

By a series of positive feedback mechanisms (like oxytocin)

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90
Q

What are uterine contractions like?

Physiology

A

Involunatry (interstitial cells of Cajal) and for the most part independent of extrauterine control

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91
Q

How are uterine smooth muscles interconnected?

Physiology

A

Via gap junctions, any change to cells will quickly be transferred to the adjacent cells

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92
Q

What type of cells initiate spontaneous depolarizations of uterine smooth msucle?

Physiology

A

Myometrial Cajal-like interstitial cells –> gap junctions –> contraction

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93
Q

What kind of receptores do uterine smooth muscles contain? What happens to them through-out pregannacy?

Physiology

A

Oxytocin and prostaglandin receptors

Their expression increases towards the end of pregnancy –> more receptors –> incraesed contractions

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94
Q

What is the factor that INITITAES labor (the main one from the mother)?

Physiology

A

Prostaglandins

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95
Q

What are other factors that initiate labor (from the mother)?

Physiology

A
  1. Progesterone withdrawal
  2. Role of placental corticotropin-releasing hormone
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96
Q

Once labor is initiated, what factors maintain it?

Physiology

A

Prodtaglandins and oxytocin

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97
Q

What are estrogen and cortisol levels like in mother towards teh end of pregnancy? Why?

Physiology

A

High, CRH released from placenta –> ACTH and DHEAS released –> increase in cortisol and estrogen (positive feedback mechanism in embryo)

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98
Q

Why is progesterone withdrawl one of the factors initiating labor?

Physiology

A

Progesterone usually inhibits uterine contractility, by withdrawing progesterone you stimulate:
1. Gap junctions
2. Oxytocin receptors
3. Prostaglandins
4. More positive resting membrane potential

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99
Q

What are the effects of estrogen during labor?

Physiology

A

Increase gap junctions, increase prostaglanding receptors, increase oxytocin receptors, cause uterine stretch

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100
Q

What are the effects of uterine stretch during labor?

Physiology

A

Increase prostaglanding receptors and increase in oxytocin receptors

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101
Q

What are the effects of increased cortisol during labor?

Physiology

A

Increase in prostaglanding receptors and cervical stretch –> increase in maternal oxytocin

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102
Q

Why are PG and oxytocin receptors not uniformally expressed in the uterus?

Physiology

A

Differential expression more in the fundus than the cervix, if they were found in teh cervix –> contractions would block the xplusion of the fetus

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103
Q

What are the effects of uterine stretch and fetal oxytocin during labor?

Physiology

A

Stimulate the uterine decidual cells and fetal membranes to increase PG synthesis and produce Prostaglandings which:
1. Stimulate contraction of uterine smooth muscle
2. Promote formation of gap junctions between uterine smooth msucles
3. Cause softening and thinning and dilation of cervix

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104
Q

How does oxytocin sustain labor?

Physiology

A
  1. Baby moves deeper into mother’s birth canal
  2. Cervix of uterus is stretched
  3. Nerve impluses sent ti hypothalamus
  4. Hypothalamus sends impulses to posterior pituitary –> oxytocn
  5. Posterior pituitary releases oxytocin to blood –> travels to uterine muscles
  6. Uterus responds by contracting more vigorously
  7. At birth, cervix stretching lesses and positive feedback is broken
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105
Q

What are the stages of labor?

Physiology

A

Stage of dilation
Stage of expulsion
Placental stage

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106
Q

What is the stage of dilation during pregnancy?

Physiology

A

The timr ftom the onset of labot to the complete dilation of the cervix (6 to 12hrs)

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107
Q

What happens during the stage of dilation of labor?

Physiology

A

Regular contractions of uterus, usually with ruprtueing of amniotic sac and complete dilation of cervix (10cm)

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108
Q

What is the stage of expulsion of labor?

Physiology

A

The time from complete cervical dilation to delivery of baby (10 minutes to several hours)

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109
Q

What is the placental stage of labor?

Physiology

A

The time after delivery until the placenta is expelled by powerful uterine contacttions mediated by oxytocin (5 to 30 minutes)

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110
Q

What are the contractions like during the placental stage of labor?

Physiology

A

Contractions constrict blood vessels that wern torn during delivery –> reduce the likelyhood of hemorrhage

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111
Q

What is the histology of a normal adult ovary-like?

Pathology

A

Dense ovarian cortex with abundant stroma and a few follicles, developing primary follicles can be seen, and also a cloud of pink, which is the corpus albicans

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112
Q

What is the gistology of a developingprimary follicle at high magnification?

Pathology

A

Central oocyte and surrounding granulosa cells

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113
Q

What is PCOS (Stein-Leventhal syndrome)?

Pathology

A

A syndrome with excess secretion of androgenic hormones, persistent anovulation and many sucpasular ovarian cysts

Common cause of infertility

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114
Q

What is the epidiomiology of PCOS in women of reproductive age?

Pathology

A

5 to 10%

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115
Q

What is the clinical scale used to diagnose PCOS?

Pathology

A

Rotterdam Scale

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116
Q

How does PCOS present?

Pathology

A

At least 2 out of 3 from Rotterdam criteria:
1. Oligo and/or anovulation
2. Clinical and/or biochemical signs of hyperandrogenism
3. Polycystic ovaries on US

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117
Q

What are the risk factors (precursors) of PCOS?

Pathology

A
  1. Genetic
  2. Obesity
  3. Sedentary lifetsyle
  4. Intrauterine androgen exposure
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118
Q

What is hyperandrogenism?

Pathology

A

Exessive production of androgens, high concentration of LH and low concentratiosn of FSH

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119
Q

What is the pathogenesis of PCOS? (GnRH &Insulin)

Pathology

A

The risk factors can lead to:
1. Increased GnRH pulsatile release
2. Increased LH:FSH ratio (increased LH in theca cells)
3. Androgen excess
4. Interefrence with development of follicles
5. Anovulation and polycystic ovaries

OR
1. Insulin resistance
2. Hyperinsulinemia
3. Androgen excess (via increased androgenic enzyme & SHBG)
4. Interefrence with development of follicles
5. Anovulation and polycystic ovaries

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120
Q

What are the effects of anovulation?

Pathology

A

Occurs because there is no corpus luteum, can lead to:
1. Anovulatory bleed & orregular menstruation
2. Decreased progesterone, unopposed increased estrogen –> risk fo endometrial cancer
3. SUbfertility (impaired oocyte devlopment, high rate of miscarriage

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121
Q

What are the clinical presentations of insulin resistance?

Pathology

A

Acanthosis nigricans

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122
Q

What are the clinical presentations of androgen excess?

Pathology

A

Hirsuitism
Acne
Alopecia

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123
Q

What is the rate limiting enzyme of androgen biosynthesis?

Pathology

A

17 a hydroxylase

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124
Q

What do excess ovarian androgens act locally to cause in the case of PCOS?

Pathology

A
  1. Premture follicular artesia
  2. Multiple follicular cysts
  3. Presistent anovulatory state
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125
Q

What are the serum levels like in patients affected by PCOS?

Pathology

A

High serum levels of androgens, lik etestosterone, androstenedione, and DHEAS

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126
Q

What happens to the excess androgens?

Pathology

A

Excess androgens are converted to etsrogens in peripheral adipose tissue –> exaggerates obesity

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127
Q

WHat is the mechanism of isnulin resistance due to in cases of PCOS?

Pathology

A

Post-insulin recptor defect, possibly related to decreased expression of a GLUT

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128
Q

What are the gross fetaures of PCOS?

Pathology

A

Both ovaries are enlarged
Grey-white with smooth surface

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129
Q

What is the morphology of the ovaries in patients with PCOS on cut surface?

Pathology

A

Cortex of ovaries: thickened, numerous subcortical cysts

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130
Q

What is the microscopical appearance of the ovaries in cases of PCOS?

Pathology

A
  1. Multiple follicles in early stages of development
  2. Follicular artesia
  3. Increased stroma, occasionally with luteinized cells (hyperthecosis)
  4. Morphological signs of absence of ovulation
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131
Q

What are the morphological signs that would indicate an abscense of ovulation?

Pathology

A

Thick, smooth capsule and abscense of corpora lutea and corpora albicantiae

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132
Q

What are the clinical features of PCOS?

Pathology

A
  1. Menstrual abnormalities
  2. Fertility problems
  3. Hirsuitism –> usually on face, chest, back or buttocks
  4. Weight gain
  5. Thinning of hair and hair loss from the scalp
  6. OIly skin or acne
  7. Acanthosis nigricans: indications of insulin resistance
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133
Q

What kind of menstrual abnormalities can be present in PCOS?

Pathology

A

Oligomenorrhea (menstrual bleeding that occurs at intervals of more than 35 days)
Secondary amenorrhea (an absence of menstruation for 6 months) or irregular periods

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134
Q

What is acanthosis nigricans?

Pathology

A

Diffuse, velvety thiockening anf hyperpigmentation of the skin

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135
Q

How does PCOS appear on imaging?

Pathology

A

Ovarian volume > 10ml
20 or more follicles, 2 to 9mm in diameter
Echodense stroma

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136
Q

What is the most common type of cystic lesion?

Pathology

A

Follicle cysts

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137
Q

How do follicle cysts present?

Pathology

A

Asymptomatic, at any age up to menopause
Associated with hyperestrogenism and endometrial hyperplaisa

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138
Q

What are signs of hyperestrogenism?

Pathology

A

Abnormal vaginal bleeding or enlarged breatss

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139
Q

What is the pathogenesis of follicle cysts?

Pathology

A

Arise from ovarian follicles (unruptured graafian follicle) and are probably related to abnormalities in pituitary gonadotropin release

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140
Q

What is the morphology of follicle lesions?

Pathology

A

Thin-walled fluid filled structures
Lined internally by granulosa cells and externally by theca interna cells
SIngle or multiple and unilateral or bilateral

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141
Q

How do follicle cysts appear on imaging?

Pathology

A

Thin-walled
Unilocular

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142
Q

What are corpus luteum cysts?

Pathology

A

Most common pelvic mass within the 1st trimester of pregnancy
May develop physiologically during menstrual cycle

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143
Q

What is the pathogenesis of corpus luteum cysts?

Pathology

A

Failure of corpus luteum to regress after ovum release
Continued progesterone synthesis by the luteal cyst results in menstrual irregularities
Rupture of a cyst can cause mild hemorrheage into the abdominal cavity

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144
Q

What is the morphology of corpus luteum cysts?

Pathology

A

Typically unilocular (3 to 5 cm in size) and possesses a yellow wall
The contents of the cyst vary from serosanguinous gluid to clotted blood

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145
Q

How do corpus luteum cysts appear on imaging?

Pathology

A

Diffusely thick wall
Ring of fire (hig hvasclarity on Doppler US)

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146
Q

What are theca lutein cysts commonly associated with?

Pathology

A

High levels of gonadotropin which causes hyperplasia of theca interna cells: circulating gonadotropins (pregnancy, hydatidiform mole, choriocarcinoma & exogenous gonadotropin therapy) or physical impediments to ovulation (dense adhesions, cortical fibrosis)

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147
Q

What are the symptoms of theca lutein cysts?

Pathology

A

Asymptomatic
Assocated with hyperandrogenism

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148
Q

How do theca lutein appear on imaging?

Pathology

A

Bilateral, enlarged, multicystic ovaries (micky mouse appearance; gross and imaging)

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149
Q

What are the two paths that could lead to placental inflammations and infections?

Pathology

A
  1. Ascending through birth canal
  2. hematogenous (transplacental) spread
150
Q

Which type of placental infections are most common?

Pathology

A

Ascending from birth canal
Bacterial infections most of the time

151
Q

What type of agents could cause ascending infections of placenta?

Pathology

A

Group B Strep
Enterococcus
E. coli
Staph
Mycoplasma
Candida

152
Q

What are ascending infections of the placengta associated with?

Pathology

A

Premature rupture of the fetal membranes

153
Q

What is the pathogenesis of the ascneding infections of the placenta?

Pathology

A

Upon recahing the uterine cavity, the organism elicit maternal acute inflammatory response, demonstartion ofneutrophilic infiltration in the amnion and chorion

154
Q

What happens if the ascending inflammation of the placenta persists?

Pathology

A

the fetus may develop its own acute inflammatory response to the infection: fetal neutrophils migrate into muscular walls of the umbilical vessels –> acute funisitis
and large vessels at the placental surface –> acute chorionic vasculitis

155
Q

How common are hem atogenous infections of the placenta?

Pathology

156
Q

Which structures are affected by hematogenous spread placenta infections?

Pathology

A

Affects the villi structures –> villitis

157
Q

What agents can cause hematogenousspread infections of the placenta?

Pathology

A

Component of TORCH group:
1. Toxoplasmosis
2. Other (syphilis, TB, listerioisis)
3. Rubella
4. CMV
5. Herpes

158
Q

What are the clinical features of placental infections on the mother?

Pathology

A

Intrapartum fever
Pospartum endometritis
Pelvic sepsis with venous thrombosis

159
Q

What are the clinical features of placental infections on the fetus?

Pathology

A

Pneumonia after inhalation of infection amiotic fluid
Skin or eye infections from direct contact with organism in the fluid
Neonatal gastritis, enteritis or peritonitis from ingesting infected fluid

160
Q

What is the non-pharmacological management of PCOS?

Pharmacology

A
  1. Calorie-restricted diet
  2. Exercise
  3. Lifestyle changes
161
Q

What is the first line pharmcaologcal treatment for PCOS?

Pharmacology

A

Contraceptives, either oral or intrauterine

162
Q

What is the most common combination of OCP?

Pharmacology

A

Combination of estrogen and progestin

163
Q

What is the aim of OCP as a treatment for PCOS?

Pharmacology

A

Aids in management of hyperandrogenesis and menstrual dysfunction
Provides contraception –> prevents ovulation and pregnancy

164
Q

What is the MOA of OCPs?

Pharmacology

A

Estrogen: provides negative feedbcak to pituitary and hypothalamus –> decreases LH and FSH production in anterior pituitary, increases the synthesis of SHBG in the liver –> inhibition of ovulation & decraeses in adrogen excess

Progestin: thickens cervical mucus and hampers sperm transport

165
Q

What is the duration of treatment with OCPs like?

Pharmacology

A

Treatment of choice especially with hursitism but it requires at least 6 months of use

166
Q

What should be the next step if OCPs on their own are not effective for the treatment of PCOS?

Pharmacology

A

Add spironolactone

167
Q

Which OCPs should be avoided because of their increased risk for hirsuitism?

Pharmacology

A

Norgestrel and Levonorgestel

168
Q

What are the adverse effects of OCPs?

Pharmacology

A

Nausea
Headache
Breast tenderness
Weight gain
Irregular bleeding
Mood changes
Increased risk of venous thromboembolism

169
Q

Why are insulin sensitizers given to PCOS patients?

Pharmacology

A

They often present with insulin resistnace and hyperinsulinemia, insulin sensitizers can correct that and thus increase the chances of menstrual cyclicity & ovulation

170
Q

What is MOA of Metformin?

Pharmacology

A

It is an insulin sensitizer, it blocks Complex 1 in the mitochondria and decreases the production of ATP and increases the accumulation of AMP.

AMP then activates AMPK which decreases lipolysis, increases beta-oxidation of fatty acids and thus increases insulin sensitivity

171
Q

What percentage of women have restored menses with the help of Metformin?

Pharmacology

A

50% of women but its ability to provide endometrial protection is less well-establisshed

172
Q

Why is Metformin not first line treatment?

Pharmacology

A

OCPs are superior for regulating menses and lowering androgen levels

173
Q

What are the PK of Metformin?

Pharmacology

A

Absorbed well orally
Not bound to serum nor metabolised
Excreted unchanged in urine

174
Q

What are the adverse effects of Metformin?

Pharmacology

A

GI disturbances: anorexia, nausea, vomiting, abdominal discomfort & diarrhea
Lactic acidosis
Vitamin B12 deficiency: long term use

175
Q

How can B12 deficiency be a consequence of long term Metformin use?

Pharmacology

A
  1. Reduced Small Intestinal Absorption of Vitamin B12
  2. Impaired Calcium-Dependent Transport of Vitamin B12
  3. Changes in Gastric pH and IF Secretion
176
Q

Which drugs can be used for treatment of hirsuitism in patients with PCOS?

Pharmacology

A

Spironolactone
Finasteride

177
Q

What is the MOA of Spironolactone?

Pharmacology

A

Blocks androen receptors –> preventing testeosterone and DHT to act on hair follicles

Inhibits steroid synthesis

178
Q

What is the MOA of Finasteride?

Pharmacology

A

Inhibits 5-a reducatse type which is the enzyme that converts testoestrone into DHT

179
Q

What is hirsuitism?

Pharmacology

A

A bothersome hyperandrogenic manifestation of PCOS, it may require at least 6 months of treatment before any imporvements are seen

180
Q

What is Spironolactone?

Pharmacology

A

An aldosterone antagonist, K+ sparing diuretic

181
Q

When is spironolactone used as treatment in patients with PCOS?

Pharmacology

A

Used for the treatment of hirsuitism as an oral add-on therapy if OCPs are ineffective past 6 months

182
Q

What are the adverse effects of Spironoloactone?

Pharmacology

A

Menstrual irregularities
Breast tenderness
GI disturbances
Dizziness
Hyperkalemia (because of DCT action on kidneys)

183
Q

What are the contraindications of Spironolactone?

Pharmacology

A

Contraindicated in pregnancy

184
Q

What are the PK of Finasteride?

Pharmacology

A

Orally absorbed
Highly protein bound and metabolized in liver
Eliminated via bile and urine

185
Q

What are the adverse effects of Finasteride?

Pharmacology

A

Teratogenic –> contrainidcated in pregnancy (lead to serious adverse effects involving the male-fetal genitelia)

186
Q

What are the adverse effects of FInasteride on males?

Pharmacology

A

Decreased ejaculate
Decreased libido
Gynecomastia
Oligospermia

187
Q

What is Efornithine (Vaniqa)?

Pharmacology

A

FDA-approved prescription cream clinically proven to reduce the growth of unwanted facial fair in women

188
Q

When is Eflornithine effective?

Pharmacology

A

After 4 to 8 weeks with twice-a day use, hair will reappear if treatment is stopped

189
Q

What is the MOA of Eflornithine?

Pharmacology

A

Inhibits ornithine decarboxylase, which is the enzyme that is essential for hair growth in hair follicles, it slows cell division and retards the rate of hair growth

190
Q

What are the side effects of of Eflornithine?

Pharmacology

A

Hypersensitivity reactions

191
Q

What are some non-pharmacological treatments for hisuitism?

Pharmacology

A
  1. Bleaching
  2. Depilatory treatments
  3. Methods that remove netire hair follcile
192
Q

What is the first line treatment for acne in patients with PCOS?

Pharmacology

A

Benzonyl peroxide

193
Q

What is the MOA of Benzonyl Peroxide?

Pharmacology

A

Includes antiseptic effects against P. acnesas well as opening of the pores

194
Q

What are the local adverse effects of Benzonyl peroxide?

Pharmacology

A

Dry skin
Peeling
Irrritation

195
Q

WHat are the retinoids and their different examples that can be used as treatment for acne in patients with PCOS?

Pharmacology

A

They are all derivatives of vitamin A
1. Tretinoin: 1st generation
2. Adapalene (3rd generation)

196
Q

What is the MOA of retinoids in the treatment of acne?

Pharmacology

A

Nucleic retinoic acid receptos: once bound to the receptors, the complex functions as a transcription factor that enhances the initiation of transcription – influences cellular proliferation, differentiation, immune function, inflammationa and sebum production

197
Q

What are 3rd generation retinoids like?

Pharmacology

A

They are less irritating and more effective –> do not affect sebum production –> comedolytic nd anti-inflammatory

198
Q

When should retinoid treatment be stopped in case of pregnancy planning and why?

Pharmacology

A

Should be stopped at least a month before trying to conceive due to potential teratogenic effects

199
Q

What is clomiphene citrate?

Pharmacology

A

A non-steroidal antagonist of estrogen receptors

200
Q

What is the MOA of clomiphene citrate?

Pharmacology

A

Inhibits the negative feebaclk of estrogen on the hypothalamus and anterior pituitary by depleting etsrogen recptors in hypothalamus and pituitary and interfering with the binding

Increases secretion of GnRH and gonadotropin levels

Development and maturation of follicle and corpus luteum –> ovulation and pregnancy

201
Q

What are the inidcations for the use of clomiphene citrate?

Pharmacology

A

Treatment of infertility associated with anovulatory cycles

202
Q

What are the pharmacokinetics of clomiphene citrate?

Pharmacology

A

Well absorved orally
Boudn to plasma proteins and accumulate in fatty tissues
Long half-life (5 to 7 days)
Excreted primarily in feces and some in urine

203
Q

What is the dosage of clomiphene citrate like?

Pharmacology

A

50 mg daily starting from phase 5 of the ovulatory cycle
Couple advised to have sexual intercourse every other day for one week around the time of ovulation

204
Q

What are the adverse risks of clomiphene citrate?

Pharmacology

A

Long term use –> increases risk of cancer
Abnormal uterine and vaginal bleeding
Breast tenderness
GI disturbasnces
Visual disturbances
Ovarian enlargement
Increased likelyhood of multiple births

205
Q

What is Letrozole?

Pharmacology

A

Non-steroidal, reversible competitive inhibitor of aromatase

206
Q

What is the MOA of Letrozole?

Pharmacology

A

Inhibits aromatase:
1. Inhibits conversion of testosterone to estradiol and andostenedione into estrone
2. Decreases negative feedback effect of estrogens and increases FSH levels and follicle development
3. Induction of ovulation

207
Q

When is Letrozole prescribed?

Pharmacology

A

Off-label for ovulation induction in patients with regular menses
Taken for 5 days, starting at day 3 to 5 of ovulatory cycle, 50mg daily

208
Q

What are the PK of Letrozole?

Pharmacology

A

Orally active
Extensive meatbolism in liver
Excreted in urine

209
Q

What are the adverse effects of Letrozole?

Pharmacology

A

Fewer than clomiphene citrate
Dizziness & fatigue
Nausea
Constipation
Hot flushes
Moof changes
Fewer multiple gestations

210
Q

What are examples of gonadotropins?

Pharmacology

A

hMG
hCG
FSH

211
Q

What are the indications for gonadotropin therapy?

Pharmacology

A
  1. ANoculatory women with hypogonadotropic hypogonadism secondary to hypothalamic or pituitary dysfunction
  2. In women with PCOS who do not respond to clomiphene
  3. hCG is used specifiaclly to trigger ovlation when the follicles are mature
212
Q

What are the risks and adverse effects of gonadotropin therapy?

Pharmacology

A

Multifetal gestation
Ovarian hyperstimulation syndrome

213
Q

WHat is ovarian hyperstimulation syndrome?

Pharmacology

A

Excessive ovarian response, leading to vascular leakage and fluid accumulation in body cavities.
Symptoms: abdominal pain, nausea, vomitingm diarrhea, dyspnea, oliguria, enlarged ovaies on US

214
Q

What can OHSS lead to?

Pharmacology

A

Hypovolemia
ELectrolyte imbalances
Acute respiratory distress syndrome
Thromboembolic events
Hepatic dysfunctions

215
Q

What is the MOA of pulsatile GnRH?

Pharmacology

A

Pulsatile administration of GnRH
Stimulation of production of FSH and LH, maintains normla feedback mechnaisms and most cycles result in a single dominant follicle

216
Q

What are the chnaces of multifollicular development and ovarian hyperstimulation with pulsatile GnRH?

Pharmacology

217
Q

What are the indications of pulsatile GnRH treatment?

Pharmacology

A

Women with hypogonadotropic hypogonadism who have normal pituitary function

220
Q

What are the PK of pulsatile GnRH treatment?

Pharmacology

A

IV and subQ, IV is preferred

221
Q

What are the adverse effects of pulsatile GnRH treatment?

Pharmacology

A

Pain, skin reactions and swellings

222
Q

What are examples of dopamine agonists?

Pharmacology

A

Bromocriptine
Cabergoline
Quinagolide

222
Q

What is the MOA of Dopamine agonists?

Pharmacology

A

ACtivation of D2 dopamine receptors
Suppression of PRL –> relieve of inhibitory effect of hyperprolactinemia on ovulation

223
Q

What are dopamine agonists?

Pharmacology

A

Semisynthetic ergot alkaloids

224
Q

What are the effects of dopamine agonists in patients with prolactinomas?

Pharmacology

A

Decrease the size of tumors in more than 50% of patients

225
Q

What are the PK of dopamine agonists?

Pharmacology

A

Well absorbed orally, extensive first-pass metabolism
SHort elimination half-life
May be administered vaginally –> less GI effects

226
Q

What are the adverse effects of dopamine agonists?

Pharmacology

A

Nausea, vomiting, headache and postural hypotension particularly on initial use

Less frequent: nasal congestion, digital vasospasm, CNS effects (psychosis, hallucinations, nightmares and insomnia)

227
Q

Why do adverse effects of dopamine agonists mainly present upon initial use?

Pharmacology

A

Patients then gain tolerance to adverse effects

228
Q

What is oxytocin?

Pharmacology

A

Nanopeptide jormone which is normally produced by the hypothalamus and released by the posterior pituitary to induce uterine contractions and lactation

229
Q

What is the signaling for oxytocin?

Pharmacology

A

G-protein coupling receptor, coupled to Gaq –> linked to increase IP3, Ca2+ and PKC activation –> contraction

230
Q

What is the MOA of oxytocin?

Pharmacology

A

Distention of uterus & stretching of cervix during delivery which causes increase in oxytocin release –> positive feedback, more uterus contractions

231
Q

How is oxytocin administered?

Pharmacology

A

Intravenous infusion

232
Q

What are the PK of oxytocin?

Pharmacology

A

Inactivated in the liver and kidneys by circulating placental oxycitocinase

233
Q

What are the adverse effects of oxytocin?

Pharmacology

A

Induce dose-related hypotension, due to vasodilation with associated reflex tachacrdia
Water retention
Uterine overstimulation
Can cause labor to progress too quickly, causing stronger and proloned contractions

234
Q

What can uterine overstimulation lead to?

Pharmacology

A

Trauma of the mother or the fetus due to forfced passagae through an incompletely dilated cervix, uetrine rupture and compromised fetal oxygenation due to decraesed perfusion

235
Q

What is the purpose of prostaglandins in inducing labor?

Pharmacology

A

Promote ripening and dilation of the cervix

236
Q

How are prostaglandins administered?

Pharmacology

A

Locally (vaginally or intracervically)

237
Q

What is the MOA of prostaglandins?

Pharmacology

A

Act on the cervix to enable ripening by modyfying extracellular matrix, relax cervical SM to faciliate dilation and increase intracellular calcium levels –> contraction of myometrial muscle to induce labor

238
Q

What is Dinoprostone?

Pharmacology

A

PGE2 analog

239
Q

What are the contrainidcations of Dinoprostone?

Pharmacology

A

SHould nit be used in women with a history of asthma, glaucoma or MI

240
Q

What is the major side effect of Dinoprostone?

Pharmacology

A

Uterine hyperstimualtion, may be reversed more rapidly using vaginal insert

241
Q

What is Misoprostol?

Pharmacology

A

Orally active synthetic PGE 1 analog that can be given for cervical ripening (off-label)

242
Q

What is the normal purpose of Misoprostol?

Pharmacology

A

NSAID- induced peptic ulcer

243
Q

What are the adverse effects of Misoprostol?

Pharmacology

A

Hyperstimulation
Abortion

244
Q

When should Misoprostol be stopped?

Pharmacology

A

At least 3 hours prior to oxytocin therapy

245
Q

What is the aim of tocolytic drugs?

Pharmacology

A

Suppress uterine contractions and prolong/delay gestation in pregnant women

246
Q

What are examples of tocolytic drugs?

Pharmacology

A

NSAIDs
CA2+ channel blockers
b-adrenergioc agonists

247
Q

What is the MOA of tocolytic drugs (β2-Agonists)?

Pharmacology

A

Activate β2-receptors → ↑ cAMP → relaxes smooth muscle in the uterus

248
Q

What is the MOA of tocolytic drugs (Calcium Channel Blockers (CCBs))?

Pharmacology

A

Block L-type calcium channels → ↓ intracellular Ca²⁺ → prevents myometrial contractions

249
Q

What is the MOA of tocolytic drugs (NSAIDs)?

Pharmacology

A

nhibit cyclooxygenase (COX) → ↓ prostaglandins (PGs) → prevents uterine contractions

250
Q

What is the MOA of tocolytic drugs (Oxytocin Receptor Antagonists)?

Pharmacology

A

Block oxytocin receptors → prevents calcium-mediated contractions

251
Q

What is the MOA of tocolytic drugs (Magnesium Sulfate)?

Pharmacology

A

Competes with Ca²⁺ at voltage-gated channels → prevents uterine contraction

251
Q

What is PCOS?

Genetics

A

Multifactorial disorder that emphasizes the interplay between genes, environment and lifestyle

252
Q

What is the triangle of PCOS?

Genetics

A

Androge excess (due to over-active theca cells)
Ovulatory dysfunction
Polycystic ovaries (more than 20 cysts in each ovary –> no follicles)

253
Q

What is the inheritance of PCOS like?

Genetics

A

It does not follow a Mendelian pattern (not caused by one single gene) but instead it is considered a complex genetic disorder

254
Q

What factors influenec the inheritance of PCOS that makes it a complex genetic disorder?

Genetics

A

Multiple genetic and environmental factors (including epigenetic factors which remain silent until prvoked)

255
Q

What are the potential genetic targets for PCOS? (4)

Genetics

A
  1. Androgen production: CYP11A1, LHCGR and AR –> androgen synthesis and sensitivity
  2. Insulin signaling: INSR and IRS1 –> insulin resistance
  3. Gonadotropin regulation: FSHR –> ovulatory dysfunction
  4. Energy regulation: PPARG, FTO
256
Q

What is the effect of hyperactive theca cells in PCOS?

Genetics

A

Hyperactive theca cells lead to increased androgen production

257
Q

Which genes are affected in androgen production in PCOS?

Genetics

A

CYP11A1, CYP17A1, HSD17B –> enhance androgen synthesis
LHCGR –> increased ovarian sensitivity to LH
HSD17B and AR –> alteration of androgen metabolism & receptor sensitivity

258
Q

Where are steroid hormones derived from?

Genetics

A

Cholesterol

259
Q

What are the importnat enzymes in steroidgenesis?

Genetics

A

17a hydroxylase (converts pregenolone which is a steroidal hormone precursor into 17a-hydro progenolone)

Aromatase (adds the aromatic ring to convert testosterone into estrogen)

260
Q

What is the purpose of the CYP11A1 gene?

Genetics

A

Encodes the cholesterol siude-chain cleavage enzyme (which the first rate-limiting step in the production of steroids) which breaks down cholesterol into pregenolone

261
Q

What is the purpose of CYP17A1?

Genetics

A

Role in 2 pathways:
1. pregenolone –> 17 OH pregenolone
2. 17 OH pregenolone –> DHEA

262
Q

What is the purpose of HSD17B?

Genetics

A

Involved in the the transformation from a weak steroid testosterone to a robust testosterone

263
Q

What is SNP?

Genetics

A

SIngle nucleotide polymorphism, occurs at any region of the gene (like the enhancer, inhibitor or promotor)

264
Q

What does a mutation in the SNP of HSD17B lead to?

Genetics

A

Increased androgen synthesis

265
Q

What is the role of CYP11A in PCOS?

Genetics

A

Variants in CYP11A may lead to increased androgen production by the ovaries, overexpression of the cholesterol side-chain cleavage enzyme has been associated with hyperandrogenism

266
Q

What do polymorphisms of the CYP11A gene lead to?

Genetics

A

Polymorphisms, such as promotor region of CYP11A, may incraese enzyme activity –> excess androgen synthesis

267
Q

What is the role of CYP17A1 in PCOS?

Genetics

A

Genetic variants in CYP17A, especially in the promoter region, can increase enzyme expression and activity, leading to enhanced androgen production and elevated DHEA

268
Q

What is the role of HSD17B in PCOS?

Genetics

A

Dysregulation of HSD17B5 has been linked to increased production of bioactive testosterone in PCOS patients

269
Q

What can variants in the HSD17B gene lead to?

Genetics

A

May contribute to elevated testosterone levels and associated symptoms such as hirsutism and acne

270
Q

What is the function of CYP19A1?

Genetics

A

Encodes the enzyme aromatase, which converts androgens into estrogens

271
Q

What is the role of CYP19A1 in PCOS?

Genetics

A

Decreased expression of the gene –> decreased aromatase –> decreased conversion of testosterone into estrogen –> buildup of androgens

Reduced aromatase activity in PCOS has been noted, particularly in granulosa cells of the ovaries

272
Q

What is the role of LHCGR gene?

Genetics

A

Encodes the receptor for LH, which stimulates theca cells in the ovaries to produce androgens

273
Q

What is the role of LHCGR in PCOS?

Genetics

A

Increased sensitivity or overexpression of the LHCGR gene can enhance ovarian theca cells responsiveness to LH –.> excessive androgen production

274
Q

What is the effect of SNPs or small insertions/deletions in the promoter region of the LHCGR gene?

Genetics

A

It can enhance binding affinity for transcription factors or cofactors

275
Q

What is hypomethylation and what is its effect on the promoter region of LHCGR gene?

Genetics

A

Reduced methylation, there is nothing wrong in the DNA sequence but there is a change in the DNA structure, there is a lack of a methyl group which affects the affinity of the chromosome wrapping around the histone

It will leads to an increase in gene expression

276
Q

What is STAR?

Genetics

A

Steroidogenic Acute Regulatory Protein

277
Q

What is the function of STAR?

Genetics

A

Encodes a protein crucial for transporting cholesterol into mitochondria where it serves as the substrate for steroid hormone synthesis

278
Q

What is the role of STAR in PCOS?

Genetics

A

Variations or upregulation in STAR may contribute to increased androgen synthesis by ensuring an abundant cholesterol supply for steroidogenesis (both genetic and epigenetic alterations)

Enhanced STAR activity has been noted in patients with PCOS

279
Q

What is the function of Androgen Receptor (AR) gene?

Genetics

A

Encodes the androgen receptor, which mediates the biological effects of androgens by binding to them and regulating gene expression

280
Q

What is the role of AR in PCOS?

Genetics

A

Polymorphisms in the AR gene, such as differences in the length of CAG repeats, can alter receptor sensitivity to androgens

281
Q

What does short CAG in the AR gene indicate?

Genetics

A

High tenascription activity, whilst long CAG inhibits transcription

282
Q

What is the effect of increased sensitivity to androgns in teh case of AR polymorphism in PCOS patients?

Genetics

A

Amplify effects of hyperandrogenism, exacerbating symptoms like hirsuitism and acne

283
Q

What is FST?

Genetics

A

Follistatin, inhibits activin, which is a protein that regulates FSH. This indirectly impacts androgen production by affecting ovarian follicle development

284
Q

What is the role of FST in PCOS?

Genetics

A

Dysregulation of FST can enhance theca cells activity, leading to excessive androgen synthesis

285
Q

What are the genes involved in insulin signaling?

Genetics

A

INSR and IRS1 play a role im insulin resistance which is a common fetaure in PCOS patients

286
Q

What is the mechanism of dysfunction of the insulin signaling pathway in patients with PCOS?

A
  1. Altered insulin metabolism → High insulin levels (hyperinsulinemia).
  2. Defects in insulin receptor substrate (IRS1) impair signal transduction, reducing insulin sensitivity.
  3. IRS acts as an adapter protein, transmitting signals from the insulin receptor to intracellular pathways.
287
Q

How does insulin resistance affect PCOS?

Genetics

A

High insulin stimulates excess androgen production by stimulating ovarian theca cells

288
Q

What is the function of the insulin receptor gene?

Genetics

A

Encodes the insulin receptor, a key protein involved in insulin signaling.

289
Q

What is the role of the isnulin receptor in the insulin signaling pathway?

Genetics

A

The receptor binds insulin and initiates intracellular signaling pathways that regulate glucose uptake and metabolism

290
Q

What is the role of INSR gene in PCOS?

Genetics

A

Variants in INSR can reduce receptor sensitivity to insulin –> insulin resistance –> hyperinsulinemia which stimulates theca cells to produce excess androgens

291
Q

What is the function of IRS1 and IRS 2 genes?

Genetics

A

Encode adaptor proteins that mediate insulin receptor signaling by transmitting signals to downstream pathways such as PI3K-AKT and MAPK

292
Q

What is the role of IRS1 and IRS2 genes in PCOS?

Genetics

A

Mutations or polymorphisms in IRS1 and IRS2 impair the downstream signaling, reducing glucose uptake and increasing insulin resistance

293
Q

What is the function of AKT2 gene?

Genetics

A

Encodes a serine/threonine kinase involved in the PI3K-AKT pathway, which is a critical mediator of insulin signaling that regulates glucose uptake via GLUT4

294
Q

What is the role of AKT2 gene in PCOS?

Genetics

A

Dysfunction in AKT2 impairs glucose transport and contributes to insulin resistance –> excerbates hyperinsulinemia

295
Q

What are the genes involved in energy regulator which results in obesity of PCOS patients?

Genetics

A

PPAR-γ
FTO

296
Q

What is the function of the PPAR-γ gene?

Genetics

A

Encodes a nuclear receptor involved in lipid and glucose metabolism and insulin sensitivity

297
Q

What is the role of PPAR-γ gene in PCOS?

Genetics

A

Polymorphisms in the gene are associated with insulin resistance in PCOS
Dysfunctional PPAR-γ impairs the lipid metabolism, promoting adiposity and systemic insulin resistance

298
Q

Which drugs is PPAR-γ a target for and why?

Genetics

A

Thiazolidinediones, which are drugs used to improve insulin sensitivity

299
Q

What is the function of SHBG?

Genetics

A

Encodes a protein that bends to sex hormones, including androgens and estrogens –> regulating their bioavailability

300
Q

What is the role of SHBG in PCOS?

Genetics

A

Insulin suppresses SHBG production –> increased free androgens in circulation
Variants in the SHBG –> reduced SHBG –> hyperndrogenism

301
Q

What are the genes involved in gonadotropin synthesis?

Genetics

A

GNRH1
GNRHR
LHB
FSHB

302
Q

What is the role of gonadotropins?

Genetics

A

LH and FSH play crucial roles in regulating ovarian function, including follicular development and steroidgenesis

303
Q

What happens to the LH:FSH ratio in cases of PCOS?

Genetics

A

Increased LH:FSH ratio and impaired follicular maturation

304
Q

What is the role of the genes involved in gonadotropin synthesis?

Genetics

A

Influence the LH: FSH balance

305
Q

What is the function of GNRH1?

Genetics

A

Encodes GnRH whoch is the hypothalamus hormone that stimulates the release of LH and FSH from the pituitary

306
Q

What is the role of GNRH1 in PCOS?

Genetics

A

Dysregulation of GnRH expression or activity leads to altered GnRH pulse dynamics –> increased LH secretion –> creating an imbalance that produces hyperandrogenism and follicular arrest

307
Q

What are the genes associated with regulation of gonadotropun signaling?

Genetics

A

LHCGR
FSHR
GNRHR

308
Q

What can alteration of the gonadotropin signaling genes lead to?

Genetics

A

Shift hormonal miliey towards hyperandrogenism and anovulation

309
Q

What is the function of LHCGR?

Genetics

A

Encodes for the receptor for LH, expressed on ovarian theca cells. LH binding stimulates androgen production, which is crucial for normal follicular development and ovulation

310
Q

What is the role of LHCGR in PCOS?

Genetics

A

Variants in LHCGR can lead to increased sensitivity for LH receptor –> heightened ovarian response to LH –> excess androgne production

311
Q

What is the function of GNRHR?

Genetics

A

Encodes the receptor for GnRH which regulates the secretion of LH and FSH from the pituitary

312
Q

What is the role of GNRHR in PCOS?

Genetics

A

Variants in GNRHR may affect the frequency and amplitude of GnRH pulses –> increaseed pulses of GnRH favour LH secretions over FSH –> elevated LH:FSH ratio

313
Q

What is the function of FSHR?

Genetics

A

Encodes the receptors for FSH, which is expressed on ovarian granulosa cells. FSH signaling is crucial for follicular grgrowth and estradiol production

314
Q

What is the role of FSHR in PCOS?

Genetics

A

Variants in FSHR can alter the receptor sensituvity to FSH –> impaired follicular development –> contributes to anovulation and accumulation of immature follicles in the ovaries

315
Q

What are the functions of ESR1 and ESR2 genes?

Genetics

A

Encode estrogen receptors that mediate the effects of estrogens on hypothalamus, pituitray and ovaries

316
Q

What is the role of ESR1 and ESR2 in PCOS?

Genetics

A

Variants in ESR1 and ESR2 may affect feedback regulation of gonadotropin secretion, contributing to the hormonal imbalances –> impaired estrogen signaling –> exacerbation of LH: FSH imbalance

317
Q

What is the relation between PCOS and ethnicity?

Genetics

A

Certain genetic variayions appera more common in specific populations –> variants in DENND1A, THADA, GATA4/NEIL2 genes seen among European and asian populations

318
Q

What in the function of DENND1A?

Genetics

A

Not directly involved in adrogen synythesis, this gene influences ovarian theca cell function & androgen production

319
Q

What is the role of DENND1A gene in PCOS?

Genetics

A

A splice variant of the gene is overexpressed in the theca cells of women with PCOS –> overexpression is associated with increased androgen production synthesis

320
Q

What are the ligaments of the ovaries?

Anatomy

A

Ovarian ligament
Broad ligament
Suspensory ligament

321
Q

Where are the ovaries located?

Anatomy

A

Located at the attachment of the broad ligamenr to the pelvuc wall (posteriorly), between the ureter and the external iliac vein

322
Q

Which ligament attaches the ovary to the uretus?

Anatomy

A

The ovarian ligament, posterior to the opening of the uterine tube

323
Q

How are the ovaries suspended from the pelvic wall (laterally)?

Anatomy

A

Suspensory ligament

324
Q

How are the ovaries suspended from the broad ligament (medially)?

Anatomy

A

By the mesovarium

325
Q

What is the mesovarium?

Anatomy

A

Part of the ovarian ligament which suspends the ovaries

326
Q

What is the ovarian hilum?

Anatomy

A

Point of entry and exit of neurovacsular bundles through suspensory ligament

327
Q

What is the germinal epithelium of the ovaries?

Anatomy

A

Layer of peritoneum covering the ovary

328
Q

What is the tunica albuginea of the ovaries?

Anatomy

A

Dense connective tissue capsule lying beneath the peritoneum

329
Q

What is the cortex of the ovaries?

Anatomy

A

Contain ovarian follicles at different stages of development

330
Q

What is the medulla of the ovaries?

Anatomy

A

Contains vessels, lymphatics and nerves

331
Q

What is the blood supply to the ovaries? (arteries)

Anatomy

A

Ovarian arteries which arise from the aorta, the reach the ovaries by passing through a fold in the peritoneumm, suspensory ligament

332
Q

What is the venous drainage of the ovaries?

Anatomy

A

Pampiform plexus arises from each ovary, unite to form ovarian vein

333
Q

What is the lymph drainage of the ovaries?

Anatomy

A

Para-aortic

334
Q

What are the stages of development of follicles?

Anatomy

A
  1. primordial follicle –> about 2 million at birth, 400 thousand at puberty
  2. Primary follicle: 15 to 20 primordial follicles develop into primary follicles monthly
  3. Secondary follicles: primary follicles develop into secondary follicles (layer of theca interna and theca externa)
  4. Graafian follicle: one secondary follicle develops into Graavian follicle
  5. Corpus luteum
  6. If fertilized it becomes corpus albicans
335
Q

What are the cortical regions of the ovaries surrounded by?

Anatomy

A

Cuboidal cells, surface epithelium, used to be germinal epithelium

336
Q

What is deep to surface epithelium of the ovaries?

Anatomy

A

Tunica albiginea

337
Q

What is found in the cortex of the ovaries?

Anatomy

A

Primordial follicles which are primary oocytes surroynded by a layer of squamous cells

338
Q

What do primary follicles consist of?

Anatomy

A

Primary oocyte surrounded by cuboidal cells

339
Q

What are granulosa?

Anatomy

A

Active follicular cells which are composed of several layers of cuboidal cells

340
Q

What is the zona pellucida?

Anatomy

A

Glycoprotein secreted by oocyte –> To prevent polyspermy and separate primary oocyte from granulosa cells

341
Q

What is the function of basement membrane?

Anatomy

A

Separates follicle and stroma

342
Q

What is the secondary follicle like?

Anatomy

A

Primary oocyte surrounded by the zona pellucida and granulosa cells

343
Q

What do fibroblastic cells immediately outside the growing follicle form?

Anatomy

A

Steroid-secreting theca interna
Covering of theca externa

344
Q

What are Graafian follciles?

Anatomy

A

Mature follicle, might be as large as entire ovary, may be observed as a transparent buldge on the ovary

345
Q

What is PCOS characterized by?

Anatomy

A

Enlarged ovaries with numerous cysts, no complete follicular maturation

346
Q

What is the length of fallopian tubes?

Anatomy

348
Q

What are the parts of the fallopian tubes?

Anatomy

A
  1. The funnel shaped infudibulume
  2. Finger-like ends called fimbria
  3. The ampulla which is the widest portion and it is also the sire of fertilisation
  4. Isthmus –> short and narrow portion
  5. Intramural –> traverses the uterines wall
349
Q

What is the histology of the uterine tubes (fallopian tubes)?

Anatomy

A

Folded mucosa
Ciliated cells
Non-ciliated cells

350
Q

What is the funtion of non-ciliated cells in the fallopian tubes?

Anatomy

A

Secretory, nutritive and protective

351
Q

What is the uterus?

Anatomy

A

Pear shaped hollow organ with thick muscular wall that represents the site of pregnancy

352
Q

What are the different parts of the uterus?

Anatomy

A

Fundus –> above the entrance of uterine tubes
Body –> below uterine tubes
Cervix –> narrow lower part, pierces anterior vaginal wall

353
Q

What is the cavity associated withthe cervix?

Anatomy

A

Narrow cavity –> cervical cavity

354
Q

How does the cervix communicate with the uterine cavity?

Anatomy

A

Internal Os

355
Q

How does the cervix communicate with the vagina?

Anatomy

A

External Os

356
Q

What are the relations to the uterus?

Anatomy

A

Anterior: uterocervical pouch & superior surface of the blaffer
Posterior: rectouterine pouch (Douglas pouch) & coilds of ileum and sigmoid colon
Lateral: uterine vessels (within broad ligament) & ureters

357
Q

What is the blood supply to the uterus?

Anatomy

A

Uterine artery –> branch of the internal iliac artery

358
Q

Where is the uterine artery located?

Anatomy

A

Runs medially within the broad ligament, reaches the cervix at right andle & above the ureter

359
Q

What branch does the uterine artery give rise to?

Anatomy

A

Small descending branch to the vagina

360
Q

What is the location of the branch to the vagina?

Anatomy

A

Ascends up along the lateral wall of teh uterus and inside the broad ligament,
Anastimoses with ovarian artery

361
Q

What are the sexual development features like between male and female in the first 7 weeks?

Anatomy

A

No gross morphological differences between male and female embryos

362
Q

During the development of the indifferent gonad where does the gonad appear?

Anatomy

A

Appears as an enlargement on the posterior abdominal wall medial to the mesonephros

363
Q

What is the gonadal enlargement referred to?
What is it?

Anatomy

A

Gonadal (genital) ridge
Core: intermediate mesoderm
Coelomic epithelium: covering that lines the embryonic body cavity

364
Q

Where are gonads derived from?

Anatomy

A
  1. Intermediate mesoderm
  2. Coelomic epithelium (mesothelium)
  3. Primordial germ cells (come from the yolk sac)
365
Q

What are sex cords?

Anatomy

A

Extensions of the epithelium that penetrate the mesoderm of the genital ridge

366
Q

Where do primordial germ cells migrate to?

Anatomy

A

They migrate towards the genital ridges stimulate further development of the gonad –> oocyte development

367
Q

What do the primordial germ cells give rise?

Anatomy

A

Will give rise to oocyte

368
Q

What is a bicornuate uterus?

Anatomy

A

Failure of causal paramesonephric ducts to completely fuse, makes pregnancy complicated

Reproductive System (5 decks)

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