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Reproductive System > Week 3 - “Breaking The Cycle” > Flashcards

Week 3 - “Breaking The Cycle” Flashcards

1
Q

What is menopause?

Physiology

A

The permanent cessation of menstrual cycles following loss of ovarian follicular activity

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2
Q

How is menopause confirmed?

Physiology

A

FSH levels > 25 IU/L

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3
Q

What is a menopausal transition?

Physiology

A

Time between onset of irregular menses and permanent cessation of menstrual

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4
Q

What is perimenopause?

Physiology

A

Also known as climacteric; period surrounding menopause characterised by fluctuating hormone levels, irregular menstrual cycles & symptom onset

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5
Q

What is premature menopause?

Physiology

A

Cessation of menses prior to the age of 40, <40 primary ovarian insufficiency, 40 to 45: early menopause

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6
Q

What is premature menopause associated with?

Physiology

A

Reduced risk of breast and ovarian cancers, but higher risk of CV disease and osteoporosis

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7
Q

What is post menopause?

Physiology

A

All years following final menstrual period

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8
Q

What are the types of menopause?

Physiology

A

Physiological/natural menopause
Iatrogenic (secondary) menopause
Primary Ovarian Insufficiency

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9
Q

What are the different types of ioatrogenic menopauses?

Physiology

A

Removal of both ovaries (surgical)
Ovarian failure due to chemotherapy or radiotherapy, infection or rumor

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10
Q

When does the menopausal transition begin?

Physiology

A

4 to 8 years before the final menstrual period

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11
Q

What should women expect during the menopausal transition?

Physiology

A

Irregular menstrual cycles
Marked hormonal fluctuations
Hot flashes, sleep disturbances, mood symptoms and vaginal dryness

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12
Q

What causes menopause?

Physiology

A

Exact cause is unknown but it may be due to combined dysfunction of the ovaries and the hypothalamus

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13
Q

What is the ovarian dysfunction cause of menopause?

Physiology

A

Degeneration of granulosa and theca cells
Failure to react to endogenous gonadotropins
Decrease in estrogen
Increased in FSH & LH

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14
Q

What are the neuroendocrine events that cause menopause?

Physiology

A
  1. Dysfunction in hypothalamic neurochemical signals involved in activating GnRH neurons
  2. This causes progressive impairement in timing of pre-ovulatory LH surge
  3. This adds to poor ovrain responsiveness
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15
Q

What are the GnRH levels like in childhood and why?

Physiology

A

During childhood the hypothalamus does not secrete ssignificant quantities of GnRH, the hypothalamus is capable of secreting this hormone but the appropriate signal fromm other areas of the brain to cause the secretion is lacking

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16
Q

Why is puberty caused in regards to hormones?

Physiology

A

Due to a gradual increase in the release of gonadotropins

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17
Q

Why are FSH and LH (mainly FSH) produced after menopause in large quantities?

Physiology

A

To compensate for the declining estradiol levels due to the decrease in ovariann function

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18
Q

At what point do the primordial follicles become atretic?

Physiology

A

When estrogen levels fall below zero

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19
Q

What is estrogen secretion like during life?

Physiology

A
  1. Increased levels of estrogen during puberty
  2. Cyclic variation during the menthly sexual cycle
  3. Further increase in estrogen during the early years of reproductive life
  4. Progressive decrease in estrogen secretion toward the end of reproductive years
  5. ALmost no estrogen beyond menopause
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20
Q

What is the relationship between FSH and estradiol/estrogen during a woman’s life?

Physiology

A

Tends to be opposite, when FSH is low, estradiol is normal and when etsradiol is highly variable estradiol is stable etc

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21
Q

What are the effects of estrogen and progesterone on the anterior pituitary and hypothalamus?

Physiology

A

Both negative and positive effects depending on the stage of the ovarian cycle

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22
Q

What is the purpose of inhibin?

Physiology

A

It has a negative e feedback effect by inhibiting FSH secretion by the anterior pituitary

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23
Q

What determines the duration of ovarian functionality?

Physiology

A

Determined mostly by the extent and rapidity of oocyte apoptosis and follicle loss

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24
Q

Which factors contribute to the decline in ovarian function and thus menopause?

Physiology

A
  1. Genetic factors
  2. Environment, lifestyle and diseases
  3. Interactions between neuroendocrine changes and alteration in the reprodcutive endocrine axis
  4. Hypothalamic aging and functional ovarian aging
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25
Q

How can genetic factors contribute to menopause?

Physiology

A

Women whose mothers or other first degree relatives have had early menopause are 6 to 12 folds more likely to undergo early menopause themselves

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26
Q

How can hypothalamic aging contribute to menopause?

Physiology

A
  1. Desychronized GnRH secretion
  2. Impaired timing of LH surge
  3. Oestradiol fluctuation and decline
  4. Anovulatory cycles and finally loss of menstrual cycle
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27
Q

What is the avarege age at which the follicular pool of primordial follicles runs out?

Physiology

A

Around the age of 50

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28
Q

When does the first decline of primordial eggs happen?

Physiology

A

Around the age of 35

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29
Q

What happens to menstrual cycle during early menopause transition?

Physiology

A

Menstrual cycles become shorter and irregular –> follicular loss 10 years prior to menopause

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30
Q

What are the menstrual cycles of:
1. Premenopausal women
2. Perimenopausal women
3. Postmenopausal women

Physiology

A

Premenopausal: regular menses
Perimenopausal: irregular menses for at least 1 year
Postmenopausal: no menses for at least 1 year

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31
Q

What is the relationship between anti-mullarian hormone and ovarian reserve?

Physiology

A

AMH is secreted from the granulosa cells.
A decline in AMH means fewer small antral follicles are present to produce it.
With lower AMH, FSH-driven follicular recruitment increases (also secreted from granulosa cells), causing faster depletion of the ovarian follicular pool.
Eventually there will be a decrease in ovarian reserve –> menopause

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32
Q

What are the 3 main types of symptoms in women going through menopause?

Physiology

A

Physical
Sexual
Psychological

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33
Q

What are the phsyical changes a woman goes through during menopause?

Physiology

A

Episodes of flushing, sweating & intense warmth of uppoer body and face, skin temperature increases 1 to 7oC
It is then followed by chills

Psychic sensations of dyspnea
Itchy skin
Irregular HR
Breast pain
Digestive problems
Joint pain
Osteoporosis

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34
Q

What are the sexual changes a woman going through menopause might experience?

Physiology

A

Irregular periods
Loss of libido
Vaginal dryness

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35
Q

What are the psychological changes a woman going through menopause might experience?

Physiology

A

Irritability
Fatigue
Anxiety

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36
Q

What is the mechanism of hot flushes during menopause?

Physiology

A

The mechanism is not knwon but it could be due to defect in the central thermoregulatory function, some estrogen-sensitive event in hypotalamus seems to indicate both LH and FSH release –> episode of flushing

Hot flushes coincide with the surges of LH but we know that LH is not responsible for the symproms, as tehy can continue past the removal of the pituitary

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37
Q

What are the studies’ conclusions regarding the mechanism of hotflushes?

Physiology

A

Flushes are preceded by an increase inn digital perfusion, followed by an increase in skin temperature (peripheral vvasodilation and increased blood flow)

Association with genetic, environmnetal, racial, lifestyle and hygiene factors

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38
Q

What are the 2 hypothalamic centers involved in thermoregulation?

Physiology

A
  1. Preoptic area of anterior hypothalamus (POA)
  2. Posterior nucleus: heat-dissipating center
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39
Q

What is the mechanism with the preoptic area of anterior hypothalamus that is related to thermoregulation?

Physiology

A
  1. Neurons sensitive to heat changes (KNDy)
  2. Activated neurons stimulate heat-loosing centers
  3. During menopause –> hypothalamus becomes more sensitive to changes in the temperature
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40
Q

What is the mechanism of the posterior nucles (heat-dissipating center) that is associated with thermoregulation?

Physiology

A
  1. Vasodilation & sweating
  2. Increased respiration through mouth
  3. Inhibits heat-promoting center
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41
Q

What is the effect of estrogen on the KNDy?

Physiology

A

Estrogen usually inhibits the neurons

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42
Q

What is the mechanism of regulation regarding estrogen and KNDy during menopause?

Physiology

A

Estrogen levels drop, leading to:
1. Loss of inhibition on KNDy neurons.
2. Increased activity of NK3 receptors (NK3R), which are involved in temperature regulation.
3. KNDy neuron hypertrophy and increased signaling, leading to abnormal heat regulation.

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43
Q

What is Fezolinetant?

Physiology

A

New FDA-approved drug:
Blocking NK3 receptors, reducing excessive KNDy neuron activity.
Restoring thermoregulatory stability, reducing hot flushes and night sweats.

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44
Q

What are the physiological changes that occur after menopause?

Physiology

A
  1. Ovaries and vasomotor changes
  2. Endometrial thinning
  3. Atrophy of urogenital tract & breast
  4. Cardiovascular system changes –> more prone to CV disease
  5. Bone weakening (osteoporosis)
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45
Q

What are the psychological changes that occur to women during menopause?

Physiology

A
  1. Mood changes, irritability, short-term memory loss
  2. Interrupted sleeping patter & fatigue & depression
  3. Loss of libido
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46
Q

What are the urogenital track changes that occur during menopause as a result of low estrogen?

Physiology

A
  1. Decreased vascularity –> decreased epithelial lining, increased fatty deposits, irritation, burning, itching and lack of lubrication
  2. Vaginal atrophy –> increased tissue trauma and bleeding –> dyspareunia
  3. Increased vaginal pH (from 4.5 to 7) leading to increased susceptibility to infection
  4. Atrophic urethritis: urgency, frequency, suprabupic pain
  5. Descent of uretus due to decreased collagen in uterosacral ligaments and cardinal ligament –> urinary incontinence
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47
Q

What is the relationship between estrogen and CV disease?

Physiology

A

Estrogen is cardioprotective because it increases HDL and decreases LDL levels, increase in estrogen –> decrease in CV disease risk

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48
Q

What are the cardiovascular chnages that take place in women during menopause and why?

Physiology

A

Post-menopausal women lack estrogen so their risk of developing CV disease increases;
1. Increased risk of atherosclerosis: increased total cholesterol (inceased LDL and decreased HDL)
2. Endothelial dysfunction
3. Increased androgens and truncal obesity and insulin resistance

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49
Q

How do menopause and ageing lead to obesity and what is the effect of that?

Physiology

A

Increase in physical inactivity, mood instability and sarcopenia which result in obesity –> atherosclerosis –> ischemic ehart disease and stroke

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50
Q

What are the direct effects of menopausal estrogen decline on CV disease? What is the result of that?

Physiology

A
  1. Activation of RAAS
  2. Increased angiotensin II
  3. Increased endothelin 1
  4. Decreased NO synthesis
    –> These all lead to incresaed oxidative stress, vascular cell proliferation vascular wall inflammation, arterial stiffness and endothelial dysfunctiom

–> Atherosclerosis –> Ischemic heart disease and stroke

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51
Q

What are the indirect effects of menopausal ostrogen decline on Cv disease and what does that lead to?

Physiology

A
  1. Increase in visceral adiposity
  2. Dyslipidemia: increased LDL and decreased HDL
  3. Increased triglycerides
  4. Increased insulin resistance
  5. Increased BP
  6. Chronic inflammation

–> These all increase the risk of atherosclerosis and thus ischemic heart disease and stroke

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52
Q

What is the relation between menopause and osteoporosis?

Physiology

A

Up to 5 years after menopasue there is an accelerated loss of bone at the rate of 1 to 2% annually

25% of women who have osteoporosis by 60

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53
Q

What are three most common fractures at post-menopausal women?

Physiology

A

Vertebrae, ultradistal radius and neck of the femur

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54
Q

What is the mechanism of osteoporosis in menopause?

Physiology

A

RANK ligand whcih plays a crucial role in the osteoclastogenesis cascade

Estrogen suppresses RANKL and stimulates OPG production, helping to balance bone resorption and formation. Decrease in estrogen –> increase in expression of RANKL –> increase in osteoclast muturation and survival –> bone resorption > formation –.> osteoporosis

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55
Q

What are the immediate symptoms of menopause?

Pharmacology

A

Vasomotor (hot flashes, sweating)
Insomnia
Decreased libido
Mood changes
Brain fogs

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56
Q

What are the intermediate symptoms of menopause?

Pharmacology

A

Dyspareunia & vaginal dryness (thinning oof the vaginal mucosa –> atrophic vaginitis)
Urethral syndrome: dysuria, urgency and frequency
Incontinence, difficulty in voiding
Increased bruising
Generalized aches

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57
Q

What are some long-term symptoms of menopause?

Pharmacology

A

Osteoporosis
CVD (coronary heart disease, dyslipidemia and stroke)
CNS –> Alzheimer’s, dementia

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58
Q

What is MHT and what is used for?

Pharmacology

A

Menopause hormonal therapy, used to augment the levels of hormones in the body

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59
Q

What are the different MHT options in regards to the presence of a uterus?

Pharmacology

A

MHT involves estrogen alone in women who underwent hysterectomy

MHT includes both eestrogen and progestin in women with intact uterus, to decrease the amount of unopposed estrogen and thus endometrial cancer

Regardless HRT with estrogen shoud be used at the lowest dose possible and for the shortest duration

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60
Q

What is the first line of MHT?

Pharmacology

A

Estrogen, unless there is a reason preventing it

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61
Q

What are the benefits of MHT?

Pharmacology

A

Relieves vasomotor symptoms and vaginal atrophy
Helps with sleep disturbances, mood lability and even joint aches
Protects bone mineral density
Lowers the risk of CVD
Improves quality of lufe

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62
Q

What are the different drugs used for MHT? (5)

Pharmacology

A
  1. Estrogen (estradiol, conjugated and esterified estrogens)
  2. Progestin
  3. Androgen (Tibolone)
  4. SERM
  5. Tissue selective estrogen complex (TSEC): conjugated estrogen plus a SERM)
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63
Q

In which cases is Tibolone and androgen MHT important?

Pharmacology

A

Hypoactive Sexual Desire Disorder due to decreased androgens

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64
Q

What are some non-hormonal drugs that are given for MHT?

Pharmacology

A
  1. Fluoxetine/paroxetine
  2. Clonidene (ovulation induction)
  3. Gabapentin
  4. Fezolientant
  5. Oxybutynin
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65
Q

What is the most prescribed non-hormonal drug for MHT? Why?

Pharmacology

A

Fluoxetine/Paroxetine, it is a selective serotonin receptor inhibitor which helps suppress vasomotor symptoms

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66
Q

What is Fezolinetant?

Pharmacology

A

First NK3 receptor antagonist to treat moderate to severe hot flashes from menopause –> MOA: binds to and blocks the activities of NK3 receptors, which play a role in the thermoregulation

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67
Q

What is Oxybutynin?

Pharmacology

A

It is used to treat an overactive blasdder and urinary incontinence –> also effective for treating hot flashes

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68
Q

What are some non-pharmcological approaches to managing menopause symptoms?

Pharmacology

A
  1. Phsyical activity –> helps protect against aging, CVD
  2. Strengthening pelvic floor muscles -> helps with incontinence
  3. No smoking –> increases hot flashes and risk of early menopause
  4. Decreasing vaginal discomfort (lubricant)
  5. Cognitive behavioural therapy (mood swings etc.)
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69
Q

What is the parent hormone of estrogen (and all other steroids)?

Pharmacology

A

Cholesterol

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70
Q

What are the sources of estrogen through-out a woman’s life?

Pharmacology

A

Premenopause: ovaries
Postmenopause: adipose tissue and adrenal cortex

Exogenous: contraceptives, hormone therapy, industrial (chemicals), phytoestrogen

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71
Q

When is systemic estrogen useD?

Pharmacology

A

For women who are being treated for menopausal symptoms such as hot flashes (systemic)

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72
Q

When is low-dosage vaginal estrogen used?

Pharmacology

A

For women being treated for genitourinary syndrome of menopause

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73
Q

What are the different types of estrogens for MHT?

Pharmacology

A

Three main types of endogenous estrogen:
1. Estradiol
2. Estrone
3. Estriol

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74
Q

What is the purpose of estrogens in regards of MHT symptoms?

Pharmacology

A

All typesa are effective for relieving hot flashes, when it comes to the frequency and the severity and also the duration

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75
Q

How does estrogen work in MHT?

Pharmacology

A
  1. All types of estrogen types work in concert with progesterone
  2. Induce the synthesis of progesterone receptors
  3. Decrease bone resorption
  4. Increase retention of salt and water, and exert mild anabolic actions
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76
Q

What are examples of exogenous etsrogens used for MHT?

Pharmacology

A

Mestranol
Ethinylestradiol
Diethylstilbestrol

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77
Q

What do the effects of the exogenous estrogens depend on?

Pharmacology

A

Sexual maturity

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78
Q

What are the different MOAs of estrogens? (4)

Pharmacology

A

Ligand-dependent
Tethered
Non-genomic
Growth factor signaling

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79
Q

What is the ligand-dependent MOA of estrogens?

Pharmacology

A

Ligand attaces to nuclear estrogen receptor, dimerization occurs, move to nucleus –> activation of transcription factors

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80
Q

What is the tethered MOA of estrogens?

Pharmacology

A

A substance is required between the receptor and the DNA

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81
Q

What is the non-genomic MOA of estrogen?

Pharmacology

A

Receptor is not found in the nucleus or the cytoplasm but instead on the membrane itself, they act as G-coupling proteins.

Faster than all other MOAs

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82
Q

What is the growth factor signaling MOA of estrogens like?

Pharmacology

A

It does not require estrogen for the estrogen receptors to be activated

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83
Q

What are the different administration routes for estrogen? (5)

Pharmacology

A
  1. Oral
  2. Transdermal
  3. Intramuscular
  4. Implantable
  5. Topical
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84
Q

What are the PK of estrogen?

Pharmacology

A
  1. Well absorbed orally, and from skin, and mucous membranes
  2. Rapidly metabolized in the liver (synthetic degrade less rapidly)
  3. Non-oral routes help reduce first-pass metabolism
  4. Natural and synthetic estrogens are excreted in the urine
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85
Q

What is the MOA of progesterone in MHT?

Pharmacology

A

Binds to nuclear receptors, estrigen stimulates synthesis of progesterone receptors wheateas progesterone inhibits synthesis of estrogen receptors only in some tissues like the endometrium –> progesterone contradicts estrogen

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86
Q

What are the functions of progesterone as part of MHT?

Pharmacology

A

Inhibits ovulation
Reduces levels of FSH and LH
Stimulates osteoblasts –> reduced bone resorption

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87
Q

What some of the formulations of of synthetic progesterone? (5)

Pharmacology

A
  1. Desogestrel
  2. Levonorgestrel
  3. Norethindrone
  4. Norgestrel
  5. Medroxyprogesterone
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88
Q

What are the different routes of administration for progesterone?

Pharmacology

A
  1. Oral
  2. Transdermal
  3. Intramuscular
  4. Implantable
  5. Topical
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89
Q

What are the PK of progesterone?

Pharmacology

A
  1. Meatbolized very quickly by the liver –> if administered orally serum half-life is 5 minutes
  2. Micronized progesterone is rapidly absorbed orally
  3. Medroxyprogesterone acetate: oral half-life is 30 days, IM/IV half-life is 40 to 50 days, metabolized in intensinal mucosa and liver, excreted in urine and bile
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90
Q

What is the relationship between Estrogen Replacement Therapy and age?

Pharmacology

A

Risks and benefits depedn on age:
women above 60: ERT increases the risk of MI and CHD
women 50 to 59: ERT somewhat protects against MI and CHD

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91
Q

Wha are the adverse effects of ERT? (8)

Pharmacology

A
  1. Endometrial cancer
  2. Breast cancer
  3. Ovarian cancer
  4. Lung cancer
  5. Dementia
  6. Gallbladder disease
  7. Urinary incontinence
  8. Nausea, fluid retention, menstrual bleeding, acne/headache/depression
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92
Q

How does ERT increase the risk of endometrial cancer?

Pharmacology

A

Estrogen increases the risk when given alone, thickening of endometrium and there is no progesterone to oppose its effect

Not given in women who have not had a hysterectomy

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93
Q

What is TESC?

Pharmacology

A

Conjugated estrogen & selective estrogen receptor modulator –> a combination therapy –> has only been used for a short-period of time yet long-term risks are unknown

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94
Q

What are the contraindications of MHT? (8)

Pharmacology

A
  1. Suspected/current or past breast cancer
  2. Endometrial cancer or other estrigen-dependent cancers (cervical etc)
  3. Active or recent angine or MI
  4. Venous thromboembolism
  5. Uncontrolled hypertension
  6. Acute liver disease
  7. Pregnancy or breastfeeding
  8. Abnormal vaginal bleeding
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95
Q

What liver diseases can estrogen be associated with? (7)

Pharmacology

A
  1. Intrahepatic cholestasis
  2. Sinusoidal dilation
  3. Peliosis hepatis
  4. Hepatic adenomas
  5. Hepatcellular carcinoma
  6. Hepatic VTE
  7. Gallstones
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96
Q

What is Tibolone?

Pharmacology

A

Has estrogenic, progestogenic and weak androgenic activity

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97
Q

What is the purpose of Tibolone in MHT?

Pharmacology

A

Short-term treatment for symptoms of estrigen deficiency
can be used continuously without cyclical progesterone
Helps relieve symptoms such as hot flashes, low mood and reduced sex drive

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98
Q

What are the adverse effects of Tibolone?

Pharmacology

A
  1. Abdominal/pelvic pain
  2. Breast tenderness
  3. Itching and vaginal discharge
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99
Q

Who is Tibolone not recommended for?

Pharmacology

A

Women who have had breast cancer

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100
Q

What are uterine fibroids?

Pharmacology

A

Uterine smooth muscale tumor (benign) –> unlikely to become cancer

they are not associated with a higher risk of other types of cancers in the uterus iether

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101
Q

When do uterine fibroids usually appear?

Pharmacology

A

During fertile years –> may cause infertility depending on the type of fibroid

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102
Q

What do uterine fibroids generally present with?

Pharmacology

A

Menstrual irregularities, menorrhagia, amenorrhea

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103
Q

What is the treatment for different types of uterine fibroids?

Pharmacology

A

Small fibroids: hysteroscopy
Larger fibroids: laparoscopic myomectomy
Other options: UAE (uterine Artery Embolization)

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104
Q

What are possible pharmacological treatments for uterine fibroids?

Pharmacology

A

GnRH antagonists
GnRH agonists
Progestin-releasing intrauterne device
Tranexamic acid
NSAIDs

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105
Q

What is the purpose and MOA of GnRH agonists?

Pharmacology

A

MOA: initially cause gonadotrophin release but with prolonged use it causes desensitization of GnRH recptors in the pituitary

Block release of FSH and LH from anterior pituitary

Block production of estrogen and progesteronee

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106
Q

What are the adverse effects of GnRH agonists?

Pharmacology

A

Decrease of estrogen so same as menopause symptoms

  1. Flushing
  2. Vaginal dryness
  3. Bone loss due to hypo-estrogenism
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107
Q

What is the MOA of GnRH antagonists?

Pharmacology

A

They block the GnRH receptors of the pituitary hence GnRH can not bind to it –> GnRH accumulates, downregulation of GnRH production –> decrease of FSH and LH production –> decrease in estrgen and progesterone

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108
Q

What are examples of Progestin-releasing IUD?

Pharmacology

A

Levonorgestrel Intrauterine System

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109
Q

What is the purpose of Progestin-releasing IUD?

Pharmacology

A

Relieve heavy bleeding caused by fibroids, but do not shrink the fibroid

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110
Q

What is progestin-releasing IUD?

Pharmacology

A
  1. An intrauterine hormone delievry system
  2. Once within uterus it causes endometrial atrophy
  3. Licensed for HRT and also used as a contraceptive device
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111
Q

What is a normal side effect of progestin-releasing IUD?

Pharmacology

A

Irregular bleeding is common in the first few months of therapy

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112
Q

In the case of conjugated equine estrogen vs transdermal estradiol which one should be chose and why?

Pharmacology

A

Transdermal estradiol because it has less side effects

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113
Q

What is Tranexamic acid?

Pharmacology

A

Non-hormonal medication: anti-fibrolytic

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114
Q

What is the MOA of Tranexamic acid?

Pharmacology

A

Inhbits the coversion of plasminogen into plasmin and fibrin into its degenration products
–> Fibrin accumulates, blood clots –> decrease in menstruation heaviness

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115
Q

What is the purpose of Tranexamix acid when it comes to fibroids?

Pharmacology

A

Helps ease heavy menstrual periods; taken only during heavy bleeding days

116
Q

What are the potenetial side effects of Tranexamic acid?

Pharmacology

A

Intravascular thrombosis due to antifibrolytic effects

117
Q

What is the MOA of NSAIDs?

Pharmacology

A

Blocks both COX-1 and COX-2 enzymes, prevents the production of prostaglandins –> less pain

118
Q

What is the purpose of NSAIDs when it comes to fibroids?

Pharmacology

A

Effective in relieving the pain caused by fibroids but do not shrink fibroids

119
Q

What are examples of NSAIDs?

Pharmacology

A

Ibuprofen
Naproxen
Mafenamic acid

120
Q

What is Myfembree?

Pharmacology

A

Relugolix, estradiol and norethindrone acetate: not first line but a once-daily treatment for heavy menstrual bleeding associated with uterine fibroids in PRE-menopausal women

121
Q

What are the half-lives of Elagolix and Relugolix?

Pharmacology

A

Elagolix: 5 hrs
Relugolix: 49 hrs

122
Q

Why should estrogen therapy be taken at the lowest dosage and for the shortest duration possible?

Pharmacology

A

Long-term estrigen is associated with incraesed risk for DVT, VTE

123
Q

What is a contraindication of patients complaining of “MIGRAINES WITH AURA”?

Pharmacology

A

Do not give estrogen, migraines with aura are associated with vascular dysfunction and estrogen enhances vasoconstriction –> increased risk of thrombosis and ischemic stroke

124
Q

What does the pelvic brim divide?

Anatomy

A

It divides the pelvis into false pelvis which is above the pelvic cavity and true pelvis which is below the pelvic cavity

125
Q

What is the pelvic cavity?

Anatomy

A

The area between the pelvic inlet and the pelvic outlet

126
Q

What is the pelvic cavity subdivided by?

Anatomy

A

By the pelvic diaphgrm into the main pelvic cavity above and the perineum below

127
Q

What are the side walls of the pelvis formed by?

A

From hip bones clabbed with obturator internus and its fascia

127
Q

What is the curved posterior wall of the pelvis formed by?

Anatomy

A

Posterior curved wall is formed by the sacrum and piriformis muscle

128
Q

What does the pelvic floor (pelvic diaphgram) consist of?

Anatomy

A

COnsists of gutter shaped sheet of muscles:
1. Levator ani
2. Coccygeus

129
Q

What are the support pelvic organs?

Anatomy

A

Uterus
Bladder
Rectum

130
Q

What are the contents of the pelvic cavity in both genders?

Anatomy

A

The sigmoid colon and the rectum

131
Q

What are the exact contents of the pelvic cavity in females?

Anatomy

A

Rectouterine pouch which is filled with the coils of the ileum, sigmoid colon and outside the peritoneum uterus and fallopian tubes are related

132
Q

What are the exact contents of the pelvic cavity of males?

Anatomy

A

Retrovesical pouch which is filled with coils of the ileum, sigmoid colon and outside peritoneum, the bladder and seminal vesicles are related

133
Q

What is the pelvic support of the uterus like? (4)

Anatomy

A

The uterus is firmly fixed to the bladder and to the vagina

The pelvic diaphragm provides a supporting floor to the uterus

Condensation of visceral pelvic fascia (pelvic ligaments) strongly support the uterus

To a lesser extent the peritoneal attachments support to uterus

134
Q

What is the uterus?

Anatomy

A

Pear-shaped hollow organ with thick muscular wall that represents the site for pregnancy and implantation

135
Q

What is the uterus divided into?

Anatomy

A

The fundus
The body
The cervix

136
Q

Where is the fundus of the uterus?

Anatomy

A

Above the entrance of the uterine tubes

137
Q

Where is the body of the uterus found?

Anatomy

A

Below the uterine tubes

138
Q

What is the cervix of the uterus?

Anatomy

A

Narrow lower part which pierces anterior vaginal wall

139
Q

Which cavity is associated with the cervix?

Anatomy

A

Narrow cavity known as the cervical cavity

140
Q
A
141
Q

What are the clinical significances of the uterus communicating with the uterine cavity and teh vagina?

Anatomy

A
  1. Menstrual flow pathway
  2. Sperm transport and fertilization
  3. Pregnancy and labor
  4. Infection pathways (ascending)
  5. Role in uterine procedures (like hysteroscopy, endometrial biopsy and IUD)
142
Q

What are the relations of the uterus?

Anatomy

A

Anterior: uterovesical pouch and superior surface of bladder
Posterior: rectouterine pouch (douglas), coils of ielum and sigmoid colon
Lateral: uterine vessels (eithin broad ligament) ureters (below at cervix)

143
Q

What is the blood supply to the uterus?

Anatomy

A

Uterine artery which comes from the internal iliac artery

144
Q

What is the position of the uterine artery?

Anatomy

A

Runs medially within the broad ligament, reaches the cervix at right angle and above the ureter

145
Q

What branch does the uterine artery give of?

Anatomy

A

The vaginal branch, which is behind the ureter

146
Q

Which artery does the uterine arter anastomose with?

Anatomy

A

The ovarian artery

147
Q

What are the ligamnets of the uterus? (5)

Anatomy

A
  1. The broad ligamnet
  2. Cardinal ligament
  3. Sacrocervical (uterosacral) ligament
  4. Pubocervical ligament
  5. Round ligament of the uterus
148
Q

What is the broad ligament of the uterus?

Anatomy

A

Double layer of visceral peritoneum that extends from one side of the pelvic cavity to the other and covers the uterus, tubes, ovaries and their associated ligaments

149
Q

What is the broad ligament subdivided into?

Anatomy

A

Mesosalpinx
Mesovarium
Mesometrium

150
Q

What is the mesosalpinx?

Anatomy

A

Upper edge that covers the uterine tubes

151
Q

What is the mesovarium?

Anatomy

A

It covers the ovaries and their round ligamenst

152
Q

What is the mesometrium?

Anatomy

A

It is the largest section, it covers the uterus, inferior to the mesosalpinx and the mesovarium

153
Q

What is the location of the cardinal (transverse cervical) ligament?

Anatomy

A

Lateral pelvic wall

154
Q

Which structures are assocaited with the cardinal ligament?

Anatomy

A

Cervix & upper end of vagina

155
Q

Which ligaments are condensations of the pelvic fascia?

Anatomy

A

The cardial ligament
The sacrocervical ligament
The pubocervical ligament

156
Q

What is the sacrocervical ligament like?

Anatomy

A

Ligament between the sacrum and the cervix, forms a ridge on each side of the Douglas pouch

157
Q

What is the pubocervical ligament?

Anatomy

A

Ligament between the pubic bone and the cervix, pass on each side of the bladder

158
Q

What is the embryological origin of the round ligament?

Anatomy

A

The gubernaculum

159
Q

What is the round ligament like?

Anatomy

A

Supralateral angle of the uterus, inguinal canal to subcutaneous tissue of labia majora

160
Q

What is the function of the round ligament of the uterus?

Anatomy

A

To keep the uterus anteverted (tilted forward) and anteflexed (bent forward)

161
Q

What is the position of the uterus in regards to?

Anatomy

A

Anteverted: bent relative to the long axis of the vagina

Anteflexed: bent relative to the long axis of the cervix

162
Q

What is the retroverted uterus like?

Anatomy

A

Fundus and body of the uterus are bent backward on the vagina and lie in the rectouterine pouch

163
Q

What is the retroflexed uterus position?

Anatomy

A

The long axis body of the uterus is bent backward on the long axis of the cervix

164
Q

What is a prolapsed uterus?

Anatomy

A

The descent of the uterus into or beyond the vaginal canal due to weakened pelvic floor support

165
Q

What are the three layers of the wall of the uterus?

Anatomy

A
  1. Tunica mucosa –> Endometrium
  2. Tunica muscularis –> Myometrium
  3. Tunica serosa –> Perimetrium
166
Q

What is the parametrium?

Anatomy

A

Dense regular connective tissue layer that surrounds the uterus outside the perimetrium. It is part of the broad ligament and serves as a supportive structure that contains important blood vessels, lymphatics, and nerves.

167
Q

What is teh endothelial lining of the endometrium?

Anatomy

A

Simple columnar epithelium containing secretory and ciliated cells

168
Q

What is the almina propria of the endometrium like?

Anatomy

A

Loose connective tissue with many stellate fibroblasts

169
Q

What are the uterine glands of the endometrium like?

Anatomy

A

Simple tubular glands, covered by simplementation columnar epithelial cells

170
Q

What are the layers of the endometrium?

Anatomy

A
  1. Zona functionalis
  2. Zona basalis
171
Q

What is teh zona functionalis of the endometrium like?

Anatomy

A

More spongy and less cellular lamina propria
Richer in ground substance
Most of the length of the glands as well as the surface of the epithelium

172
Q

What is the zona functionalis like during menstrual cycle?

Anatomy

A

Exhibits dramatic changes during menstrual cycle every month as a result of hormonal changes, it is the layer that shed during menstruation

173
Q

What is the zona basalis like?

Anatomy

A

Basal layer adjacent to the myometrium
Contains highly cellular lamina propria and the deep basal ends of the uterine glands

174
Q

What is the zona basalis like during the menstrual cycle?

Anatomy

A

Undergoes very few changes during the mentrual cycle

175
Q

What is the function of the zona basalis?

Anatomy

A

Provides a new epithelium and lamina propria for the renewal of the endometrium

176
Q

What is the blood supply of the endometrium?

Anatomy

A

Unique dual blood supply; the uterine artery distributes the arcuate arteries in the middle layer of the myometrium so 2 sets of arteries arise to supply blood:
1. Straight basal arteries
2. Coiled spiral arteries

177
Q

What are coiled-spiral arteries like?

Anatomy

A

Progesterone-sensitive

178
Q

What are vascular lacunae?

Anatomy

A

Many dilated, thin-walled vessels that also supply the endometrium

179
Q

What is the myometrium?

Anatomy

A

Thick muscular layer (poorly defined layers)
It consists of inner longitudinal, middle circular and outer longitudinal layers

180
Q

What does the middle circular layer contain?

Anatomy

A

The larger blood vessels (arcuate arteries) –> stratum vasculare

181
Q

What happens to the myometrium during pregnancy?

Anatomy

A

Thickens during pregnancy because of the hypertrophy and hyperplsia of individual smooth muscle cells

182
Q

What is the cervix like?

Anatomy

A

Less muscular than the myometrium, the mucosa of the cervix does not undergo any changes during the menstrual cycle

183
Q

What is the exocervix or vaginal portion of the cervix lined by?

Anatomy

A

Stratified squamous epithelium

184
Q

What is the endocervix, supra vaginal cervix portion lined by?

Anatomy

A

Mucous sereting simple columnar epithelium which forms cervical glands

185
Q

WHat is the purpose of the mucous secretion from the cervical glands of the cervix?

Anatomy

A

They promote fertilization

186
Q

What are some non-neoplastic disorders of the endometrium?

Pathology

A

Endometritis
Adenomyosis
Endometriosis

187
Q

What is Endometritis?

Pathology

A

Inflammation of the endometrium

188
Q

What are the classifications of endometritis?

Pathology

A

Acute endometritis
Chronic endometritis

189
Q

What is the characteristic of acute endomeritis?

Pathology

A

Abnormal presence of polymorphonuclear leukocytes in the endometrium

190
Q

What is the most common reasoning behind acute endometritis?

Pathology

A

Ascending infection form the vahina or intestinal tract flora

191
Q

What are the causes of acute endometritis?

Pathology

A

Retained products of conception subsequent to miscarriage or delivery or to presence of foreign body such as IUD or tampons

192
Q

What is the characteristic of chronic endometritis?

A

Abnormal presence of lymphocytes and plasma cells in the endometrium (lymphocytes are nomally found in the endometrium)

193
Q

What are the causes of chronic endometritis?

Pathology

A

retained products of conception, chronic pelvic inflmmatory disease (N. gonorrhea or C. trachomatis), IUD or TB

194
Q

What are the clinical presentations of endometritis?

Pathology

A

Fever, abdominal pain, and menstrual abnormalities

195
Q

What are the clinical conswequences of endometritis?

Pathology

A

Increased risk of infertility and ectopic pregnancy (due to damage and scarring of the fallopian tubes)

196
Q

What is adenomyosis?

Pathology

A

Presence of endometrial glands and stroma in the myometrium

197
Q

What is the pathogenesis of adenomyosis?

Pathology

A

Reactive hypertrophy of the myometrium –> enlarged globular uterus with a thackened uterine wall

198
Q

What are the microscopic features of adenomyosis?

Pathology

A

Glands lined by mildly proliferative to inactive endometrium and surrounded by endometrual stroma with varying degrees of fibrosis

Different degrees of glandular hyperplasia

199
Q

What are the clinical features of adenomyosis?

Pathology

A

Asymptomatic but:
1. Menorrhagia
2. Dysmenorrhea
3. Pelvic pain before onset of menstruation

200
Q

What is endometriosis?

Pathology

A

Presence of endometrial glands and stroma outside the uterus

201
Q

What is the prevelance of endometriosis?

Pathology

A

5 to 10% of women of reproductive years

nearly half of women with infertility

202
Q

What are the sites of involvement with endometriosis?

Pathology

A
  1. Ovaries (60%)
  2. Other uterine adnexa (uterine ligaments, rectovaginal septum, ouch of Douglas)
  3. Less common: pelvic peritoneum covering the uterus, fallopian tubes, rectosigmoid colon and bladder
203
Q

What are the three pathogenesis hypotheses of endometriosis?

Pathology

A
  1. The regulation tehory
  2. The metaplastic theory
  3. Lymphatic dissemination theory
204
Q

What does the regulation hypothesis of endometriosis purpose?

Pathology

A

Endometriosis occurs due to the retrograde flow of sloughed endometrial cells/debris via the fallopian tubes into the pelvic cavity during menstruation –> retrograde menstruation

205
Q

What does the metaplastic theory of endometriosis purpose?

Pathology

A

Endometrial differentiation of coelomic epithelium (mesothelium of the pelvis and abdomen from which the endometrium originates) is the source of endometriosis

206
Q

What does the lympathic dissemination theory purpose?

Pathology

A

Endometrial tissue from the the uterus can “spread” to distant sites via blood vessels and lymphatics

207
Q

What are the gross features of endometriosis?

Pathology

A

Functioning endometrium with:
1. red-brown nodules or implants
2. range in size from micrcopic to 1 or 2cm in diameter
3. Lir on or just under the affected serosal surface
4. FIbrosis: scarring; grossly brown discoloration

208
Q

What are the features of endometriosis on the ovaries?

Pathology

A

Lesions may form large, blood-filled cysts that turn brown as the blood ages

209
Q

What are the microscopic features of endometriosis?

Pathology

A

The histologic diagnosis depends on fidning two of the three features within the lesions:
1. Endometrial galnds
2. Endometrial stroma
3. Hemosiderin pigment

210
Q

What do the clinical features of endometriosis depend on?

Pathology

A

The distribution of the lesions

211
Q

What are some clinical features of endometriosis?

Pathology

A

Uterine ligaments –> pelvic pain
Pouch of Douglas –> dyschezia
Uterine serosa –> dyspareunia
Bladder serosa –> dysuria
Fallopian tube mucosa –> scarring increases risk of ectopic tubal pregnancy
In all cases there is severe ddysmenorrhea and pelvic pain

212
Q

What is menorrhagia?

Pathology

A

Profuse or prolnged bleeding at the time of the period

213
Q

What is metrorrhagia?

Pathology

A

Irregular bleeding between the periods

214
Q

What is postmenopausal bleeding?

Pathology

A

Bleeding after the cessation of menstruation for at least 12 months

215
Q

What are the different causes of abnormal uterine bleeding?

Pathology

A

Endometrial polyps
Leiomyomas
Endometrial hyperplasia
Endometrial carcinoma
Endometritis

216
Q

What are the different categories of abnormal uterine bleeding?

Pathology

A
  1. Menorrhagia
  2. MEtrorrhagia
  3. Postmenopausal bleeding
217
Q

What is endometrial hyperplasia?

Pathology

A

Excess of estrogeb relative to progesterone (induce exaggerated endometrial proliferation)

precursor of endometrial carcinoma

218
Q

WHat are the causes of endometrial hyperplasia?

Pathology

A
  1. Obesity
  2. Failure to ovulation
  3. Prolonged administration of estrogenic steroids without conterbalancing progestin
  4. Estrogen-producing ovarian lesion
219
Q

How is obesity a cause of endometrial hyperplasia?

Pathology

A

Adipose tissue converts steroid precursors into estrogens

220
Q

What are the classification of endometrial hyperplasia?

Pathology

A
  1. Based on architectural crowding (simple or complex) and the presence or absence of cytologic atypia
  2. The risk of developing carcinoma is related to the presence of cellular atypia
  3. Acquisition of PTEN mutations is one of the several key steps in the ransformation of hyperplasias to endometrial carcinomas
221
Q

What is endometrial carcinomas?

Pathology

A

Malignant proliferation of endometrial glands

Most frequent cancer occuring in the females gnital tract

222
Q

What is the age of endometrial carcinomas?

Pathology

A

Between 55 and 65, the uncommon age is around 40

223
Q

What are the two types of endometrial carcinomas?

Pathology

A

Endometroid carcinoma –> type 1 (most common, less serious)
Serous carcinoma –> type 2

224
Q

What are the risk factors of type 1 (endometroid carcinoma)?

Pathology

A
  1. Obesity
  2. Diabetes
  3. HTN
    Infertility
    Exposure to unopposed estrogen

–> increased estrogenic stimulation of the sendometrium leads to endometrial hyperplasia

225
Q

What is teh relationship between endometrial canecr and other cancers?

Pathology

A

Higher incidence of both breast and ovarian cancer in closely related women, suggesting a genetic predisposition

226
Q

What is the pathogenesis of type 1 endometroid carcinoma?

Pathology

A

Mutations in misnatch repair genes and tumor suppressor gene PTEN

Women with germline mutation in PTEN (Cowden syndrome) and germline alterations in DNA mismatch replair gene (Lynch syndrome) are at high risk of this cancer

227
Q

What is the pathogenesis of type 2 serous carcinoma?

Pathology

A

Nearly all cases of serous carcinoma have mutations in the TP53 tumor suppressor gene

Serous tumors are preceded by a lesion called serous endometrial intraepithelial carcinoma (SEIC)

228
Q

What is the morphology of endometrioid carcinoma?

Pathology

A
  1. Closely resemble endometrium and may be exophytic or infiltrative
229
Q

What is the range of histologic types of endometrioid carcinomas?

Pathology

A

Mucinous, tubal (ciliated) and squamous (occasionally adenosquamous)

230
Q

Where do the endometrioid carcinomas originate from?

Pathology

A

Originate in the mucosa and may infiltrate the myometriuma nd enter vascular spaces

231
Q

What is the grading of endometrioid carcinomas?

Pathology

A

Graded I to III, based on the degree of differentiation

232
Q

What are the gross features of serous carcinomas?

Pathology

A

Large hemorrhagic and necrotic tumor with eep myometrial invasion

233
Q

What are the microscopic features of the serous carcinomas?

Pathology

A

Well formed papillae (thick and thin) appearance

–> Highly pleomorphic tumor cells (prominent nucleoli, small detached buds and tufts)

–> Severe cytologic atypia (gaps in between piplae )

234
Q

What are the clinical manifestations of endometrial carcinomas?

Pathology

A

Leukorrhea
Irregular bleeding (often in postmenopausal women)

235
Q

How is endometrial carcinoma diagnosed?

Pathology

A

Cervicovaginal cytologic screening is usuitable. for early detection

Transvaginal US is a valuable iagnostic modality ( > 5mm endometrial thickening –> highly suspicious)

236
Q

How does endometrial cancer spread?

Pathology

A

Directly to para-aortic lymph nodes, skipping pelvic nodes

237
Q

What kind fo metastasis is common in patients with endometrial carcinomas?

Pathology

A

Advanced cancers mat develop pulmonary metastases

238
Q

What are endometrial polyps?

Pathology

A

Monoclonal outgrowths of endometrial stromal cells altered by chromosoaml translocation (6p21) with secondary induction of polyclonal glandular elements

239
Q

Where are large endometrial polyps located?

Pathology

A

Larger polys may project from the endometrial mucosa into the uterine cavity

240
Q

What is the age group of endometrial polyps?

A

Occur at any age, they are most common around the time of menopause

241
Q

What is the clinical significance of endomerial polyps?

Pathology

A

Abnormal uterine bleeding
Giving rise to cancer but it is very rare

242
Q

What are leiomyomas?

Pathology

A

Benign tumors that arise from the smooth muscle cells in the myometrium

Most common benign tumor in females

More frequent in blacks than in whites

243
Q

What are the characteristics of Leiomyomas?

Pathology

A

Monoclonal
Associated with several different recurrent chromosomal abnormalities (rearrangements of chromosome 6 and 12)

Mutations in the MED12 gene, which encodes a component of the RNA polymerase transition complex

Estrogen and OCP stimulate the growth of leiomyomas

244
Q

What happens to leiomyomas during pregnancy?

Pathology

A

They enlarge during pregnancy and shrink after menopause

245
Q

What are the classifications of Leiomymas?

Pathology

A
  1. Subserous
  2. Intramural
  3. Submucous
246
Q

What are subserous leiomyomas?

Pathology

A

Located beneath the serosal surface, they grow out toward the peritoneal and can be sessile or pedunculated

May attach to adjacent structures (the bowel, omentum or mesentery) and develop a secondary blood supply

they may also extend into the broad ligamnet

247
Q

What are intramural leiomyomas?

Pathology

A

Most common type
Found primarily within the thick myometrium

248
Q

What are submucous leiomyomas?

Pathology

A

Asymptomatic, located beneath the endometrium

Associated with abnormal uterine bleeding

249
Q

What are the gross features of leiomyomas?

Pathology

A

Sharply circumscribed, firm-gray white mass (with no encapsulation)
May occur singly or multiple tumours (more common)
Ranging from small nodules to large tumors (1 mm to 30cm in diameter)

250
Q

What are the microscopic features of leiomyomas?

Pathology

A

Bundles of smooth muscle cells (mimicking the appearnce of normal myometrium)

251
Q

What might leiomymas present with?

Pathology

A

Foci of fibrosis
Calcification
Degenerative softening

252
Q

What do the symptoms of leiomyomas depend on?

Pathology

A

Can be influenced by the location, size or number of fibroids.

They are usually asymptomatic

253
Q

What are some symptoms leiomyomas may present with?

Pathology

A

Menorrhagia, with or without metrorrhagia
Pelvic pressure or pain
Frequent urination
Difficulty emptying bladder
Constipation

254
Q

What is the association between leiomyomas and cancer?

Pathology

A

They almost never transform into sarcomas and he presence of multiple lesions does not increase the risk of malignancy

255
Q

What are leiomyosarcomas?

Pathology

A

Malignant proliferation of the mesenchymal cells of the myometrium

256
Q

How do leiomyosarcomas arise?

Pathology

A

They arise de novo, not from leiomyomas

257
Q

What is the traget population of leiomyosarcomas?

Pathology

A

Postmenopausal women, accounts for 2% of uterine malignancies

258
Q

What is the contradistinction between leiomyomas and leiomyosarcomas?

Pathology

A

Leiomyomas are frequently multiple in number and arise in premenopausal women

259
Q

What is the gross appearance of leiomyosarcomas?

Pathology

A

Soft, hemorrhagic and necrotic masses

260
Q

What are the microscopical features of leiomyosarcoma?

Pathology

A

Tumor necrosis, cytologic atypia and mitotic activity (necesaary to make a diagnosis of malignancy)

261
Q

What is the prevalence of tumors of the ovary?

Pathology

A

8th most common cancer in the US. women
5th leading contributor to cancer mortality in women

262
Q

What are the three cell types of tumors of the ovary?

Pathology

A

The multipotent surface (coelomic) epithelium
The totipotent germ cells
The sex cord-stromal cells

263
Q

Where does the vast majority of ocarian neoplasms arise from?

Pathology

A

Coelomic epithelium that covers the surface of the ovary, embryologcially produces the epithelial lining of the fallopian tube (serous cell), endometrium and endocervix

264
Q

What is the pathogenesis of surface epithelial tumors of the ovaries?

Pathology

A
  1. Repeated Ovulation and Scarring
    With each ovulation, the ovarian surface epithelium undergoes disruption and subsequent repair.
    This process increases the risk of epithelial entrapment in the ovarian cortex.
  2. Formation of Epithelial Cysts
    Some trapped epithelial cells form small cysts within the ovary.
    These cysts can remain benign or undergo transformation into tumors.
  3. Neoplastic Transformation (Metaplasia → Tumor Formation)

Over time, these epithelial cysts may become metaplastic or neoplastic, leading to the formation of:
Benign tumors: Cystadenoma, cystadenofibroma.
Malignant tumors:
Cystic tumors: Cystadenocarcinoma.
Solid tumors: Carcinoma.

265
Q

What is the role of gonadoropins in the surface epithelium tumor progression?

Pathology

A

After menopause, FSH and LH levels remain persistently high due to the loss of estrogen negative feedback.
These hormones stimulate the surface epithelial cells, promoting further genetic mutations and increasing the risk of carcinogenesis.

266
Q

What are protective factors against ovarian tumors?

Pathology

A

Pregnancy
OCPs

267
Q

What are the risk factors for the sirface epithelial tumors?

Pathology

A
  1. Nullparity (no previous pregnancies)
  2. Family history
  3. Germline mutations in certain tumor suppressor genes (mutations in BRCA1 and BRCA2)
268
Q

What are the most common subtypes of surface epithelium tumors?

Pathology

A
  1. Serous (full of water)
  2. Mucinous (full of mucous-like fluid)

Both are usually cystic
Both can be benign, borderline or maliganant

269
Q

Which subtype of ovarian tumors is most common?

Pathology

A

Serous tumors

270
Q

What is the malignancy of serous tumors like?

Pathology

A

About 60% are benign, 15% are of low malignant potential and 25% are malignant

271
Q

What is the target population of beging serous tumors?

Pathology

A

Usually encountered in patients between 30 and 40 years of age

272
Q

What is the target population of malignant serous tumors?

Pathology

A

More commonly seen between 45 and 65

273
Q

What is the pathogenesis of serous tumors?

Pathology

A

Low grade: associated with KRAS, BRAF or ERBB2 mutations

High grade: associated with mutations in TP53

274
Q

What is the gross apperance of serous tumors?

Pathology

A

Serous cystoadenoma of the ovary: Wall is thin and translucent, clear fluid

275
Q

What are the microscopic appearance of serous tumors?

Pathology

A

SIngle later of ciliated tubal-type epitehelium

276
Q

What are the differences between serous type and mucinous type ovarian tumors?

Pathology

A

Mucinous tumors have neoplastic epithelium which consists of mucin-secreting cells

Mucinous tumors are considerably less likely to be malignant

277
Q

What is the pathogenesis of mucinous tumors?

Pathology

A

KRAS mutations in early event in mucinous tumorgenesis

Overexpression/amplification of HER2 in mucinous carcinomas and mucinous borderline tumors

278
Q

What is the morphology of mucinous tumors?

Pathology

A

The tumor is characterised by numerous cysts filled with thick, viscous fluid

A single layer of mucinous epithelial cells lines the cyst

279
Q

What is the prognosis of low-grade serous tumors?

Pathology

A

Favorable

280
Q

What is the prognosis of high-grade serous ovarian tumors?

Pathology

A

Poor

281
Q

What is the prognosis of clear cell, endometroid and mucinous tumors?

Pathology

A

Clear cell: intremediate
Endometroid: Favorable
Mucinous: Favorable

282
Q

What are mature teratomas?

Pathology

A

Benign neopalsm that accounts for 1/4 of all ovarian tumors, peak incidence in the third decade

283
Q

WHat is the pathogenesis of mature teratomas?

Pathology

A

Mature teratomas develop by parthenogenesis, haploid germ cells endoreducplicate to give rise to diploid genetically female tumor cells

284
Q

What is the morphology of mature teratomas?

Pathology

A

They are cystic and almost all contain skin, sebaceous glands, and hair follicles

Half have smooth muscle, sweat glands, cartilage, bone, teeth and respiratory epithelium

Other tissues can also be present like gut, thyroid, brain but they are less often seen

285
Q
A

Reproductive System (4 decks)

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