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Reproductive system disorders Flashcards

1
Q

What is BPH?

A

Benign prostatic hyperplasia

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2
Q

What is the H stand for in BPH and what is the difference between hyperplasia and hypertrophy?

A
  • Hyperplasia: increase in cell number

- Hypertrophy: growth in the size of an individual cell

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3
Q

What does BPH mostly effect?

A
  • periurethral zone (next to uretha)

- prostate cancer affects peripheral zone

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4
Q

What is the prostate made up of

A
  • made up of glands that have 2 layers of epithelial cells:

- ->a basal layer of flattened cuboidal epithelial cells covered by columnar epithelial cells (supported by stroma)

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5
Q

Important developer of BPH

A
  • Aging is the biggest contributor
  • at 50, 50% of men will have symptoms
  • in 90-100 year olds, symptoms are 100% seen
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6
Q

Explain what DHT is and how it is involved in BPH symptoms

A

Dihydrotestosterone (DHT): endogenous androgen sex steroid and hormone. The enzyme 5α-reductase catalyzes the formation of DHT from testosterone in certain tissues

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7
Q

What happens to testosterone and estrogen levels in a man as he ages. How might this contribute to the development of BPH?

A
  • Testosterone levels decrease and estrogen levels increase

- affect prostate tissue in a way that it expresses more androgen receptors

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8
Q

Describe the symptoms and complications of BPH.

A

poor urinary stream, increased urinary frequency, nocturia, difficulty with urinary stream stopping and starting, and even painful micturition

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9
Q

What might be used to help diagnose BPH? How do these tests work?

A

Digital rectal exam, urinalysis, and blood tests for serum creatinine and prostate-specific antigen (PSA)

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10
Q

Explain how finasteride, dutasteride, terazosin or prazosin might help BPH

A
  • 5-alpha reductase inhibitors: finasteride, dutasteride; inhibiting the production of DHT
  • alpha-1 antagonists: terazosin, prazosin; smooth muscle contraction
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11
Q

What is a TURP and how might it help?

A

Transurethral resection of the prostate. It involves the insertion of a scope through the tip of the penis until it reaches the prostate tissue. Has a tool that can trim prostate tissue.

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12
Q

Prostate Cancer

A

malignant tumor that forms on glandular structures in the peripheral zone of the prostate gland

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13
Q

Where in the prostate gland does cancer usually arise?

A

peripheral zone of the prostate gland

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14
Q

Why is it advisable to sometime do nothing to treat prostate cancer?

A

slow growing prostate cancer usually won’t be the thing to kill older men.

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15
Q

What ethnic groups have the highest risk and the lowest risk of prostate cancer?

A

African American men have the highest rate and Asian men have the lowest rate

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16
Q

What is BRCA-2?

A

tumor suppressor gene and a mutation in this gene imparts a 20-fold increase in the risk for the development of prostate cancer

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17
Q

When prostate cancer does become aggressive, where does it often spread to?

A

bones, brain, liver, lungs and possibly other areas

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18
Q

What is PSA? What information can a PSA test give us? Why is the PSA test controversial?

A
  • Prostate-specific antigen (PSA): part of the ejaculate where it has the function of liquefying semen coagulate to allow sperm to swim freely
  • prostate cancer, BPH, prostatitis
  • There is variation in PSA for men. Plus if there is high PSA this causes anxiety for men to undergo a biopsy
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19
Q

What is prostate brachytherapy?

A
  • inserting radioactive “seeds”

- needle into the prostate gland between the scrotum and the anus

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20
Q

What is PID and what causes it?

A

-Pelvic inflammatory disease (PID): inflammation of the female reproductive organs

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21
Q

What factors predispose women to developing PID?

A
  • younger than 25
  • younger than 15 when having sex
  • use of IUD or oral contraception
  • multiple sex partners
  • frequent vaginal cleaning
  • history of STD’s
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22
Q

What are common symptoms of PID?

A

abdominal pain, dyspareunia (painful intercourse), purulent cervical discharge, vaginal discharge, burning with urination, irregular menstruation, fever and increased WBC count

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23
Q

What are some complications of PID that treatment can help prevent? How is PID diagnosed and treated?

A
  • scarring that can lead to chronic pain, infertility, and complications with pregnancy
  • Tx: antibiotics
  • Dx: observation of the symptoms and cervical tenderness on examination
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24
Q

What is endometriosis?

A

“ectopic” (abnormal place) endometrial tissue at a site outside of the uterus

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25
What are some common locations for endometriosis?
ovaries, uterine ligaments, fallopian tubes, peritoneum, bladder, rectum and intestines
26
What are some risk factors for developing endometriosis?
family history, early age of menarche and shorter menstrual cycles
27
Briefly describe the theories that attempt to explain the origin of the dispersed endometrial lesions
1. The regurgitation/implantation theory: sloughed off tissue retrograde and deposit fragments of endometrial cells on extra uterine structures 2. The vascular or lymphatic theory: endometrial cells entered the lymph or vascular circulation and were carried to extra uterine structures where they could implant 3. The metaplastic theory: endometrial cells do not complete maturation
28
How are endometrial implants different than the endometria of a healthy uterus?
- they release inflammatory mediators including high levels of prostaglandin E2 (PGE2) which is pro-inflammatory - Implants also have high levels of aromatase which produces estrogen that promotes endometrial proliferation
29
What are the common clinical signs and symptoms that accompany endometriosis?
painful menstruation, pelvic pain and infertility.
30
Why are NSAIDs, progesterone, and GnRH analogs useful in the treatment of endometriosis?
- NSAIDs help with the pain | - progesterone and GnRH analogs cause endometrial growth suppression.
31
How is adenomyosis different from endometriosis?
abnormal deposit of endometrial tissue within the myometrium (muscle layer) of the uterus
32
What is suspected to put a female at greater risk for adenomyosis?
Women who have multiple children in their 40s/50s
33
What are the symptoms of adenomyosis?
no symptoms to severe and debilitating pain and pain is worse during menstration
34
What treatment options are available for adenomyosis?
- Uterine sparing: hormone manipulation (Tx for endometriosis). Can also do surgery ablation or resection - Uterine non sparing: hysterectomy
35
What age group is most affected by this endometrial cancer?
postmenopausal women (55-65)
36
What is the difference between type 1 and type 2 endometrial cancer?
- Type 1: excess estrogen, most common type | - Type 2: older women in a setting of endometrial atrophy and estrogen excess is not found
37
What is the major symptom associated with endometrial cancer?
abnormal bleeding
38
What are uterine leiomyomas?
benign tumors that are non cancerous
39
Describe the common symptoms and treatment options for Uterine Leiomyoma
- heavier bleeding, frequent pee, constipation and rectal pressure, ab pressure - removal of tumor or hysterectomy
40
Ovarian Cycle
- estrogen highest during follicular phase of ovarian cycle - progesterone highest during luteal phase of ovarian cycle - GnRH causes FSH and LH to increase during follicular - lack of GnRH causes FSH and LH to decrease during luteal phase
41
Uterine Cycle
42
Estrogen positive feedback effects on the hypothalamus and pituitary
At the end of the follicular phase, estrogen does a positive feedback and causes an LH surge
43
Corpus luteum production of progesterone
- produces progesterone during the luteal phase | - lack of LH causes corpus albicans-> does not produce much estrogen and progesterone-> menses
44
LH surge and ovulation
positive feedback triggers and causes ovulation
45
Role of hCG after fertilization / implantation
implanted zygote produces hCG which is an LH agonist and keeps corpus luteum functioning.
46
During which phase of the cycle are levels of progesterone the highest?
ovarian luteal phase
47
When is estrogen increasing?
during the end of the follicular phase
48
Two cell cooperation of steroidogenesis (thecal and granulosa) before and after ovulation
- Thecal: express LH receptors = absorption of LDLs-> cholesterol-> steroids - Granulosa: express FSH and LH receptors but LDL cannot cross membrane until after ovulation - Granulosa does not have proper enzyme to convert progesterone to a steroid but thecal cells have that enzyme - Theca cells can produce estrogen with granulosa's aromatase enzyme
49
Polycystic Ovary Syndrome
- Occurs when follicles do not ovulate - increase in pulsatile GnRH release which explains why there's lack of high progesterone during a luteal phase - follicle doesn't ovulate=no corpus luteum=no progesterone
50
An increase in GnRH pulse frequency leads to what?
- increase in the amount of LH over FSH - follicle may develop but not mature enough to be a functional graffian follicle that can ovulate - Follicles that do not ovulate are called cysts
51
PCOS symptoms
menstrual irregularity, hyperandrogenism (e.g., hirsutism and acne), infertility, and insulin resistance or hyperinsulinemia
52
What does insulin do to the ovaries and the adrenal cortex?
stimulate steroidogenesis in the ovary and the adrenal cortex
53
Why are women with PCOS at increased risk for developing endometrial cancer?
prolonged estrogen exposure that can lead to endometrial hyperplasia
54
Recall how PCOS is treated
- administration of progesterone - weight loss - oral contraceptives: progesterone - spironolactone: inhibit androgens receptors - metformin: insulin control
55
3 different cell types that ovarian cancer occurs in
surface epithelium, germ cells and in stromal cells, and epithelial cells
56
What type of ovarian cancer is most lethal and occurs in older women? What types are lest lethal and can occur in younger women?
-Younger: germ and stromal cell tumors
57
Describe the most significant risk factor for ovarian cancer known as ovulatory age
how long a woman’s body has been exposed to high estrogen levels
58
What are the names of the two tumor suppressor genes that if mutated increase the risk for ovarian and breast cancer?
Mutations of the breast cancer suppression genes BRCA1 and BRCA2
59
What could increase risk Ovarian cancer?
high fat western diet and the use of talcum powders in the genital area
60
Cancers in the ovary can cause...
produce vague GI symptoms such as abdominal bloating, early satiety and diarrhea
61
What are the two types of carcinomas that may occur with breast cancer
- Ductal carcinoma | - lobular carcinoma
62
What are some of the signs and symptoms that a woman may notice if she has breast cancer?
mass, a puckering of the skin, texture changes of the skin, nipple retractions or abnormal discharge
63
What is a Mammography and why is it important?
X-ray picture of the breast and can detect a mass as small as 1 mm in size
64
What might make a breast cancer “inherited”? What are the names of the genes involved?
BRCA1 and BRCA2. | These are tumor suppressor genes that when they lose their function= greater risk for cancer
65
What are the options that will be considered if such genes are inherited?
strict screening regimen and mastectomies
66
Define Radical Mastectomy
remove any tumor mass and in extreme cases this may involve the whole breast, underlying muscle and axillary lymph nodes
67
What are the modifiable risk factors for breast cancer?
Obesity, physical inactivity, caffeine, alcohol consumption, smoking and long term use of hormone replacement therapy
68
Explain the mechanisms for Tamoxifen and Trastuzumab for treatment of breast cancer
- Tamoxifen: bind the intracellular estrogen receptors and activate or inhibit its action - Trastuzumab: monoclonal antibody that can bind and block the HER2 receptors. This helps shrink tumor tissue and slow cancer progression
69
What are aromatase inhibitors and why might they be used to help treat breast cancer?
lowering the amount of circulating estrogen available to stimulate breast tissue and tumor growth

Pathophysiology (10 decks)

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