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PTH560 Pathology > Exam 3 - reproductive system > Flashcards

Exam 3 - reproductive system Flashcards

1
Q

Female:

Sex hormones are synthesized where?

A

ovary

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2
Q

What are the phases of the menstrual cycle?

A
  • proliferative/follicular phase
  • ovulation
  • secretory/luteal phase
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3
Q

Brief hormone stuff about menstrual cycle.

A

Estrogen starts it all. Causes LH to spike. this spike causes ovulation.

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4
Q

Proliferative phase (menstrual cycle)

A
  • aka follicular
  • 1-14 days
  • proliferation of glands
  • mediated by estrogen. spike causes LH to peak and FSH (When LH goes up, so does FSH)
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5
Q

Ovulation

A
  • at day 14-16
  • mature follicle in the ovary releases an egg
  • signs: inc temp, subnuclear vacuoles in endometrial cells, mittelschmerz “pelvic pain”
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6
Q

Luteal Phase

A
  • at day 14/16-28 (depends on ovulation)
  • mediated by PROGESTERONE
  • histology: inc gland tortuosity and secretion, edema of stromal cells
  • fertility work-ups: at day 21
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7
Q

Menses

A
  • serum estrogen and progesterone drop

- causes endometrial cell apoptosis

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8
Q

What is FSH’s function in the menstrual cycle?

A
  • prepares follicle of the month - inc follicle size
  • inc aromatase synthesis
  • inc synthesis of LH receptors
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9
Q

What is LH’s function in the menstrual cycle?

A
  • testosterone synthesis: aromatase converts it to estradiol in granulosa cells
  • LH surge: due to estrogen. causes ovulation when LH>FSH. moves follicle from meiosis I prophase to meiosis II metaphase

-progesterone synthesis (for secretory phase)

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10
Q

Pregnancy hormone changes: hCG

A
  • hCG: human chorionic gonadotropin
  • made in placenta
  • analogue of LH (maintains corpus luteum)
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11
Q

Pregnancy hormone changes: progesterone

A
  • until 10 weeks = made in corpus luteum
  • after 10 weeks = made by placenta

-if progesterone drops: possible spontaneous abortion

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12
Q

How does OCPs work?

A
  • usually mix of estrogen and progestins
  • baseline estrogen prevents estrogen surge (prevents LH surge, prevents ovulation)
  • progestins stop proliferative phase (gland atrophy, inhibit LH which prevents LH surge)
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13
Q

Menopause: definition and onset

A

Def: no menses for 1 year after age 40 (avg age =51)

onset: genetically determined. Earlier with smokers

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14
Q

Menopause physiology

A
  • decrease in ovarian function.
  • decreased estrogen levels overall

*she said this was all we need to know. slide 16)

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15
Q

What is the treatment for menopause? and why is it controversial?

A
  • treatment = estrogen replacement. Helps inc overall levels

controversial: long-term severe risks of CAD, stroke, clots, etc. Should only do for a year or 2 at a time

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16
Q

Menorrhagia (Menstrual dysfunction)

A

> 80 ml blood loss

excessive clots

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17
Q

Dysmenorrhea (Menstrual dysfunction)

A
  • painful menses

- primary type (inc prostaglandins or uterine contractions)

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18
Q

Dysfunctional uterine bleeding

A
  • abnormal. no anatomical cause
  • typically hormone imbalances
  • most are postmenarchal or perimenopausal
  • 90% anovulatory (no egg release)
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19
Q

Anovulatory DUB (dysfunctional uterine bleeding) causes

A
  • excessive estrogen relative to progesterone (absent secretory phase)
  • inadequate luteal phase (inadequate progesterone)
  • irregular shedding of endometrium (persistent luteal phase)
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20
Q

menorrhagia DUB

A
  • most common
  • regular normal intervals
  • excessive flow and duration
21
Q

hypomenorrhea DUB

A
  • regular normal intervals

- decreased bleeding

22
Q

metrorrhagia DUB

A

(metro = “time”)

  • irregular intervals
  • excessive flow and duration
23
Q

menometrorrhagia DUB

A

-irregular or excessive bleeding during menstruation and btwn periods

24
Q

oligomenorrhea DUB

A

-menses at intervals > 35 days

25
Q

polymenorrhea DUB

A

-menses at intervals <21 days

26
Q

What is primary amenorrhea?

A
  • absence of menses by 16 y/o

- constitutional (growth) delay = most common cause

27
Q

What is secondary amenorrhea?

A
  • no menses for >6 months in pt who has had normal menses

- MCC = pregnancy

28
Q

Amenorrhea: Pathology

A
  • hypothalamic or pituitary disorder (dec LH and FSH synthesis => Dec estrogen and progesterone)
  • ovarian disorder (dec estrogen and progesterone synthesis. FSH and LH inc)
  • end-organ disorder (blood flow obstruction (normal FSH, LH, progesterone, estrogen)
29
Q

Polycystic ovary syndrome: disease associations and clinical findings

A
  • obesity
  • insulin resistance
  • acanthosis nigricans (skin stuff, skin folds)

Clin find: oligomenorrhea, hirsutism(hair)- due to inc testosterone, infertility, obesity, DM etc

30
Q

Polycystic ovary syndrome: pathology

A

* increased LH secretion by anterior pituitary (LH/FSH > 3)

*** dec pituitary FSH secretion

31
Q

FSH and LH as male sex hormones

A
  • FSH = stim spermatogenesis (seminiferous tubules)

- LH = stim testosterone (leydig cells)

32
Q

Male hormones: testosterone

A
  • sex characteristics
  • enhances spermatogenesis
  • inc libido
33
Q

Male hormones: sex hormone binding globulin

A
  • binds testosterone and estrogen (greater affinity for testosterone)
  • made in liver
34
Q

Hypogonadism: pathogenesis

A
  • dec testosterone production
  • resist to testosterone

-primary or secondary

35
Q

Primary hypogonadism (what causes, hormone effects)

A

-Testicular dysfunction
(leydig cell, seminiferous tubule)
- dec testosterone secretion
-( dec T, inc LH)

36
Q

secondary hypogonadism (what causes. hormone effects)

A
  • pituitary (tumor) or hypothalamic (Kallmann’s syndrome) dysfunction
  • (dec T, dec or normal LH)
37
Q

Infertility causes

A
  • decreased sperm count (leydig, seminiferous tubule, pituitary, or hypothalamus dysfunction)
  • end-organ dysfunction (obstruction, dysfunction of accessory organs/ejaculation)
38
Q

Infertility labs: seminiferous tubule dysfunction

A
  • testosterone = normal

- FSH = inc

39
Q

Infertility labs: Leydig cell dysfunction

A
  • testosterone = dec

- LH = inc

40
Q

Infertility labs: pituitary dysfunction

A

-HYPOPITUITARYISM

  • testosterone = dec
  • LH = dec
  • FSH = dec
41
Q

Infertility labs: end-organ dysfunction

A
  • normal hormone levels

- variable sperm count

42
Q

What do you look for with a sperm analysis?

A
  • volume
  • count
  • morphology
  • motility

serum hormone levels

43
Q

What are the 3 causes of ED?

A
  • psychogenic (nocturnal penile tumescence test)
  • dec testosterone
  • vascular insufficiency (atherosclerosis, leriche syndrome - butt and genital area)
44
Q

In what zones does benign prostatic hyperplasia occur?

A

-***transitional and periurethral zones

45
Q

benign prostatic hyperplasia: pathology

A
  • inc sensitivity of prostate to DHT (dihydrotestosterone)
  • DHT causes hyperplasia
  • get nodules due to hyperplasia of glandular and stromal cells. (yellow-pink, soft)
46
Q

Prostate cancer

A
  • most common cancer in adult males
  • 90% of 90y/o have it
  • asymptomatic until advanced

-DHT -dependent and ***development in peripheral zone

47
Q

pt has LBP, pelvic pain, obstructive uropathy, and possible spinal cord compression. what does he have?

A

Prostate cancer

48
Q

Prostate cancer Treatment: early vs late

A

Early: surgery, radiation, radioactive seeds

Late: hormones, chemo, radiation.
-if you are old just watch.

PTH560 Pathology (15 decks)

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