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SMP - APP Part 1 > Lecture 12 - Endocrine Pathophysiology II: Sex > Flashcards

Lecture 12 - Endocrine Pathophysiology II: Sex Flashcards

1
Q

Why do women gain weight at menopause?

A

Because running the menstrual cycle uses 1 pound of fat each month

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2
Q

How many menstrual cycles in a lifetime?

A

~500

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3
Q

What causes menopause?

A

By about 50, the number and robustness of the follicles in the ovaries have decreased significantly => less primary follicles developing each month => less estrogen is produced => reduced negative feedback on the hypothalamus and causes an increase in LH and FSH secretion => initial increase in gonadotropins which continues menstruation => eventually there are so few follicles that menstruation stops entirely => individual becomes infertile

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4
Q

Describe cervical cancer progression from HPV infection.

A

Sexual activity => HPV =>

  1. Low risk (6, 11) => episomal infection => condolyma
  2. High risk (16, 18) => viral integration => cervical intraepithelial neoplasia (CIN) => higher grade CIN => invasive cancer => metastasis
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5
Q

For what % of cervical cancers is HPV responsible for?

A

Almost 100%

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6
Q

How does HPV cause cancer?

A

Proteins E6 and E7 bind RB and p53

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7
Q

Where do cervical cancers arise? Why?

A

Transformation zone: at the region of transition from the endocervical canal lined by simple columnar epithelium to the stratified squamous non-keratinized epithelium

Because the non-keratinized stratified squamous epithelium is only one cell thick there (metaplastic epithelium)

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8
Q

Where is the cervical transformation zone from birth to adulthood? Implication?

A

It starts inside the cervical opening and then migrates out of the cervical opening in the young adult

Then it migrates back up to original location

Cervix more likely to be infected by HPV in the young adult

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9
Q

What fraction of HPV viruses do the vaccines cover?

A

2/3

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10
Q

Test for HPV?

A

Pap smear

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11
Q

What is endometriosis? Mechanism?

A

Condition in which tissue that normally grows inside the uterus (endometrium) grows outside it and grow and slough off in synchrony with the menstrual cycles

Mechanism: retrograde movement of endometrial cells out of the Fallopian tube and into the pelvis or abdomen in the Douglas pouch or the utero-vesicular pouch

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12
Q

Symptoms of endometriosis?

A

Pain during menstruation

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13
Q

Treatment for endometriosis?

A

Birth control to stop periods

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14
Q

Is endometriosis an issue during pregnancy?

A

No because no menstrual cycles

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15
Q

In what % of women do leiomyomas occur?

A

30-50%

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16
Q

Issues caused by leiomyomas?

A
  1. Painful

2. Hard to carry a pregnancy to term if they are large

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17
Q

What is the most common cancer of the female reproductive tract? What women does it affect?

A

Endometrial cancer

Affects postmenopausal women

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18
Q

Early symptom of endometrial cancer?

A

Bleeding

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19
Q

Survival rate of endometrial cancer? Why?

A

Good because bleeding is the first symptom and it happens in postmenopausal women so they seek attention right away

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20
Q

Treatment for endometrial cancer?

A

Hysterectomy

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21
Q

What is salpingitis?

A

Inflammation of the Fallopian tube(s)

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22
Q

Causes of salpingitis?

A
  1. Almost always a component of pelvic inflammatory disease
  2. Infections: chlamydia, gonorrhea, tuberculosis
  3. Endometriosis
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23
Q

What is a salpinx?

A

Fallopian tube

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24
Q

Symptoms of salpingitis?

A
  1. Pain

2. Asymptomatic

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25
Complication of salpingitis?
Scarring => ectopic pregnancy or infertility as egg cannot move through the tube => can cause damage or destruction of the tubes OR exsanguination
26
What is PCOS?
Genotypic XX female who previously had normal menstrual cycles exhibits signs of excess androgens (especially androstenedione): 1. Amenorrhea: absence of menstruation 2. Hirsutism: excessive hair growth 3. Clitoromegaly 4. Virilization: development of male physical characteristics
27
What is PID?
Inflammation of either the Fallopian tubes or the uterus
28
Describe the ovaries of patients with PCOS. What to note?
Thickened white tissue capsule around the ovary (a physical barrier to ovulation) due to the anabolic effects of the high levels of androgens + cystic follicles Note: cystic follicles are NOT the same as ovarian cysts Note: PCOS refers to the cystic appearance of the secondary follicles that are arrested in their pre-ovulatory state
29
How does adipose tissue play a role in PCOS?
1. Adipose tissue contains aromatase that converts the excess androstenedione into estrone 2. Excess estrone disrupts the usual pulsating secretion of LHRH secreted by the hypothalamus => excess LH secretion + decreased FSH secretion 3a. Increased LH levels stimulate the theca cells of the ovary to secrete even more androgens (androstenedione) => vicious cycle 3b. Decreased FSH levels fail to stimulate the granulosa cells of the ovary, resulting in decreased follicle maturation and decreased levels of estradiol => chronic anovulation
30
Where do the excess androgens come from in PCOS patients?
Either ovaries, adrenal glands, or both
31
Why do PCOS patients often develop insulin resistance? Impact?
Tend to be obese => higher glucose levels => pancreas produces more insulin => insulin resistance => increased insulin levels act on theca cells to increase androgen production
32
7 treatments for PCOS?
1. Metformin = drug used to treat diabetes, used if patients have insulin resistance with PCOS 2. Low-dose oral contraceptive to regulate the menstrual cycle: synthetic estrogen and progesterone to lower FSH and LH 3. Clomiphene = estrone antagonist that blocks the action of excess estrone to achieve pregnancy 4. Medications for reducing excessive hair growth: spironolactone to block the androgen effects 5. Gonadotropins (FSH and LH) to achieve pregnancy 6. Wedge resection = if neither of the above work, we can surgically remove a wedge of the ovary to decrease the amount of androgens secreted and eliminate the physical barrier of ovulation 7. Laparoscopic ovarian drilling to stimulate ovulation by reducing levels of LH and androgens
33
Origin of ovarian tumors? Most of them? Which ones are most likely to become malignant?
1. Surface epithelial cells***### 2. Germ cells 3. Sex cord-stroma 4. Metastasis to ovaries
34
Does ovarian cancer affect older women mainly?
NOPE - all women
35
Why does ovarian cancer have a bad prognosis?
Detected late
36
What is a teratoma?
Tumor that contains one or more germ cell layers
37
Do teratomas affect men and women equally?
YUP
38
Do teratomas become malignant?
Not typically
39
Most common site of ectopic pregnancies?
Ampulla
40
Can ectopic pregnancies go to term?
NOPE
41
Definition of ectopic pregnancy?
Implantation outside of the uterine corpus At first the developing zygote can get nutrients from environment until it is no longer enough, leading to necrosis
42
First symptom of tubular pregnancy?
Pain
43
What is exsanguination?
Bleeding to death
44
What can a ruptured ectopic tubal pregnancy be misdiagnosed as? Explain.
As an appendicitis because the appendix lies close to the ovaries and the oviduct on the right side + referred pain to the RLQ
45
Treatments of ectopic pregnancy?
1. Methotrexate 2. Salpingectomy: uterine tube removal 3. Salpingostomy: surgical incision in the uterine tube to remove it, no need to stitch
46
What is a hydatiform mole? Other name?
Placental membranes (no fetus) that form a hydatis-cyst or mole-fleshy growth = molar pregnancy
47
What is the cause of complete hydatiform moles? 2 different types
Fertilization of an egg lacking a female pronucleus (diploid paternal DNA) ⇒ embryo cannot develop properly because paternal and female genomes are regulated differently even though they contain virtually identical chromosomes All chorionic villi are vesicular, no fetus or embryonic tissue 1. Monospermic fertilization: sperm enters second polar body instead of female pronucleus and duplicates its own genome (XX zygote) 2. Dispermermic fertilization: two sperm fertilize the polar body and mix their genetic material (XX or XY zygote)
48
What is the cause of incomplete/partial hydatiform mole? How many chromosomes?
Triploid karyotype (2 paternal and 1 maternal) which can elevate their embryonic development beyond that of complete hydatiform moles (XXX, XXY, XYY) Some chorionic villi are vesicular, deformed fetus present (“not viable”) 69 chromosomes
49
What are 4 symptoms of hydatiform mole?
1. Vaginal bleeding 2. Hypertension 3. Edema 4. High levels of hCG
50
What usually happens to incomplete hydatiform moles?
They usually abort in the second trimester and some rare fetuses survive
51
What usually happens to complete hydatiform moles?
They abort by week 10 (remnants may remain)
52
Treatment for hydatiform moles?
Need to remove them because they can become cancerous
53
What should the plasma hCG level be after hydatiform mole removal?
0!!!
54
What causes pre-eclampsia?
Genetic predisposition and shallow implantation of embryo: 1. Flt-1: VEGF receptor on endothelial cells that would participate in placenta formation, also found in blood as sFlt-1 2. Placental growth factor (PLGF): binds to Flt-1 to enhance vasculogenesis of extraembryonic mesoderm and branching of maternal spiral arteries only made during pregnancy (during 3rd trimester) ⇒5 week before disease: sFlt-1 rose and PLGF dropped: sFlt-1 in bloodstream hijacks PLGF leading to deterioration of blood vessels in placenta (and liver, kidneys) => placenta does not receive sufficient blood supply, thereby starving the fetus leading to intrauterine growth retardation (IUGR) and associated problems
55
What are the 6 symptoms of pre-eclampsia in pregnant women?
1. Hypertension to compensate for lack of blood supply to the fetus 2. Proteinuria 3. Liver inflammation 4. Edema due to proteinuria causing low blood albumin 5. Platelet depletion 6. Brain swelling, convulsions and possible coma (severe cases) = ECLAMPSIA
56
How often does pre-eclampsia occur?
5% of all pregnancies
57
Common sites of distant metastasis of prostate carcinoma?
1. LNs 2. Bones 3. Lungs 4. Liver 5. Adrenals
58
What are the 4 different zones of the prostate? List them from inner to outer. Which ones typically give rise to BPH?
1. *Periurethral zone 2. *Transitional zone 3. *Central zone 4. Peripheral zone
59
What is BPH exactly?
Overgrowth of the stroma of the prostate and often with secondary reactivation of epithelial proliferation
60
What do prostate cancers arise from?
Peripheral zone of the prostate
61
Which is more likely to produce urinary obstruction: BPH or prostate cancer? Why?
BPH because it arises from more centrally situated glands
62
4 STD viruses?
1. Herpes simplex virus (HHV-a and 2) 2. Hepatitis B & C virus 3. Human papillomavirus (HPV) 4. Human immunodeficiency virus (HIV)
63
Test for cancer and/or BPH?
PSA assayed in blood tests (if > 4) because it can leak out into the vasculature due to disruption of the normal architecture of the prostate
64
4 STD bacteria?
1. Chlamydia trachomatis (intracellular) 2. Neisseria gonorrhoeae 3. Treponema pallidum (syphilis) 4. Haemophilus ducreyi (chancroid)
65
1 STD protozoan? Effect?
Trichomonas vaginalis => increase vaginal pH => allows for development of abnormal flora like E. coli and candida
66
2 STD ectoparasites?
1. Scabies | 2. Pubic lice
67
Do more men die with or from prostate cancer?
With
68
Difference between HHV 1 and 2?
1. Oral herpes | 2. Genital herpes
69
Common sites of spreading of prostate carcinoma?
1. Rectum | 2. Bladder
70
What tumors do ovarian germ cells cause?
Teratomas
71
Highest incidence of cervical cancer is in what women?
Women in their 40s
72
Who should be screened for cervical cancer? Why?
Women aged > 21 yo regardless of sexual activity Because most HPV infections clear on their own and excess screening causes excess cervix scrapping to remove infection which causes fertility issues
73
What to do if a Pap smear comes back positive for HPV?
Colposcopy to obtain biopsy of the cervix to decide next step: 1. Monitor the lesion 2. Remove lesion
74
Biggest risk factor for endometrial cancer?
Unopposed estrogen secretion without progesterone secretion
75
What is a chocolate cyst?
Ovarian endometriosis

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