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SDR II > SDR Lectures > Flashcards

SDR Lectures Flashcards

0
Q

primary follicle

A

oocyte is surrounded by differentiated and metabolically active granulosa cells

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1
Q

Stress invokes what to inhibit the reproductive system?

A

Opioid neurons - ß-endorphins and CRH containing neurons

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2
Q

secondary follicles

A

6-10 primary ones
multiple layers of granulosa cells
an outer layer of theca cells
fluid-filled antrum

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3
Q

Primordial follicles consist of

A

an oocyte surrounded by a flat layer of epithelial-like cells (granulosa precursors)

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4
Q

tertiary follicle

A 
Graffian follical
1 secondary one
larger antrum
multple layers of granulosa cells
multiple layers of theca cells (theca interna and externa)
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5
Q

Theca cells produce

A

androgens from cholesterol in response to LH

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6
Q

granulosa cells produce

A

estradiol 17ß from androgens in response to FSH

with aromatase

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7
Q

luteal cells are made from

A

left over theca and granulosa after oocyte release

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8
Q

luteal cells secrete

A

estradiol but less than the follicle did

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9
Q

When does corpus luteum stop secreting progesterone and estradiol?

A

after sitting for ten days it becomes whitish scar tissue = corpus albicans

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10
Q

Where does estrogen bind to kisspeptin for + feedback?

A

MPOA

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11
Q

When does estrogen turn into + feedback?

A

2–pg/ml for 36 hrs

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12
Q

What does LH do on the granulosa cell?

A

increase release of progesterone intra-follicularly to increase proteolytic enzymes like collagenase that weak the follicular wall

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13
Q

high progesterone causes

A

increase in collagenase (proteolytic enzymes)
follicular hyperemia or blood movement into the follicule
intrafollicular prostaglandin sythase increasing P F2 alpha increasing fluid moving in follicle and adds progesterone receptor
lead to follicular rupture and ovulation

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14
Q

First 14 days of ovarian cycle is what in the uterus?

A

proliferation (follicular) phase

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15
Q

What causes proliferation in the uterus (endometrial growth and myometrial thickening)

A

estrogen

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16
Q

What does estrogen do in the uterus

A

endometrial growth
myometrial thickening
lengthening of uterine glands and arteriole vessels
water rention (and cervical mucus thinning)
uterine contractions

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17
Q

When does progesterone increase in level over estrogen?

A

After ovulation

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18
Q

What is the 2nd 14 days of the ovarian cycle in the uterus?

A

the secretory phase

ran by progesterone

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19
Q

What does progesterone do to the uterus?

A 
stops endometrial growth
stimulates uterine gland branching 
lengthening of spiral arteries
cervical mucus thickening
increase body temperature
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20
Q

What does inhibin act on

A

FSH

It’s inhibition allows for the 1st small surge of FSH to recruit follicles

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21
Q

What happens to spiral arteries without pregnancy?

A

low estrogen and progesterone cause them to retract

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22
Q

What causes necrosis and sloughing and bleeding

A

decrease in O2 to the tissues from spiral arteries retracting

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23
Q

insulin causes

A

thecal cells to increase androgen production

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24
Q

what do adipose tissue convert androgens to with their aromatase?

A

estrone - disrupting LH/FSH cycle

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25
Q

What does estrone do to LH/FSH

A

increaess LH so there is more androgen secretion

Decreases FSH so no aromatase work in granulosa cells

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26
Q

wedge resection:

A

androgen amount stays

but less barrier around ovary

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27
Q

What happens in puberty?

A

GABA decreases, glutamate increases

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28
Q

menarche

A

age when first surge of LH happens from enough estradiol and progesterone formation

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29
Q

Why are periods erratic in menapoase at first

A

follicles are not robust so less estrogen build up regularly

but sensitivity to - feedback decreases to that sometimes a surge can happen (compensation)

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30
Q

What produces hCG

A

trophoblasts 8 days after ovulation

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31
Q

what does hCG do?

A

binds to LH receptors and keeps ovary functioning and corpus luteum lives (to produce progesterone, estriol)

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32
Q

When does hCG stop rising?

A

after week 9 (month 3)

b/c placenta can produce its own prog/estriol

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33
Q

When is prog dominant vs estr

A

progest: during pregnancy
estr: at the end

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34
Q

What causes estrogen to increase over prog at the end of pregnancy

A

placenta producing a large amount of CRH -> fetal pituitary products ACTH -> fetal adrenal DHEA -> to placenta that aromatizes it to estrogen

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35
Q

What does estrogen do to prostaglandin synthetase

A

increases production of PGF2 alpha

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36
Q

What strengthens contractions caused by estrogen?

A

baby head in cervix -> hypothalamus oxytocin secretion from posterior pituitary on SM and more PG

also stress of labor -> sympathetics -> NE/E

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37
Q

estrogen on breast growth

A

increases ductile growth

increases fat deposition

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38
Q

What does progesterone do on the mammary gland?

A

-> growth of alveolar structures

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39
Q

What does baby suckling do?

A

Effect spinal afferent receptors -> hypothalamus -> dopaminergic neurons (↓prolactin) and oxytocin neurons (ejection of milk)

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40
Q

Prolactin acts to

A

lactogenesis

- feedback on dopaminergic neurons (to stop more prolactin)

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41
Q

Where are dopaminergic neurons?

A

in the acruate nucleus of the hypothalamus

some terminate at portal capillaries of the median eminence

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42
Q

Where does DA inhibit prolactin

A

anterior pituitary

DA also inhibits LHRH

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43
Q

how does prolactin give infertility

A

increases DA -> decrease GnRH -> decreases LH and FSH

b/c huge increase in prolactin in the beginning, not when it decreases (western countires)

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44
Q

Sheehan’s syndrome is caused by

A

large blood loss in delivery killing anterior pituitary (that’s when it needs blood)

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45
Q

Sheehans causes

A 
no lactotrophs (can't lactate)
no ACTH (no pubic hair and hypOtensive b/c no cortisol)
no somatotrophs (hypoglycemia from low cortisol and GH)
no thyrotrophs (no TH, fatigue and lethargy)
No gonatotrophs (no LH/FSH infertility and amenorrhea)
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46
Q

Male LH acts on vs FSH

A

LH: leydig - testosterone
FSH: Sertoli - aid spermatogenesis, increase androgen binding protein

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47
Q

What does ABP do?

A

binds to testosterone to ensure that a high concnetration remains in the seminiferous tubules

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48
Q

Sertoli cells produce

A

ABP

Inhibit

49
Q

What shapes FSH release?

A

Inhibin

50
Q

What shapes LH release

A

testosterone

51
Q

inhibin made up of

A

A and

A-B or B-B

52
Q

2 beta subunits together = (ßb-A)

A

activin

53
Q

what is activin

A

stimulates FSH production but works at lower rates than inhibin so control is mostly by inhibin

also resides in FSH producing cells of pituitary glands and exerts a pararine effect

54
Q

how much of testosterone is circulating unbound?

A

3%

55
Q

4 ways testosterone can act

A
  1. diffuse in cell
  2. convert to DHT and act (prostate and hair)
  3. Aromatize to estrogen
  4. On an plasma membrane receptor
56
Q

What can testosterone do?

A

Fetal development of epididymis, vas deferns, seminal vesicles
Pubertal growth of penis, seminal vesicles, musculature, skeleton, larynx
Spermatogenesis

57
Q

DHT does

A

Fetal development of Penis, penile urethra, Scrotum, Prostate
Pubertal growth of Scrotum, Prostate, Sexual hair, Sebaceous gland
Prostatic secretion

58
Q

what does high early fetal exposure to testosterone do?

A

Eliminate the possibility of + feeback signaling.

Also a role in gender self-identification and gender preference

59
Q

What does high testosterone do around birth

A

testicular descent

60
Q

How does testosterone increase finally at puberty?

A

Excitatory glutaminergic inputs to LHRH and less GABA

61
Q

Kallmans syndrome symptoms

A

Small phallus, small scrotum, muscle mass feminine, wide hips, frail looking, shy, socially withdrawn

62
Q

Kallman’s syndrome physiology

A

failure of LHRH neurons to migrate to the hypthalamus

Normally olfactory bulbs develop and span LHRH neurons that migrate but some tissue damage stops it

63
Q

Kallman’s syndrome treatment

A

give testosterone

More muscle at shoulderes, less fat at hips

64
Q

How much folic acid should a woman have before conception?

A

800 micrograms

65
Q

Exercise before conception?

A

30 min a day

66
Q

Diabetes on pregnancy

A

birth defects
Eclampsia
heart malformations

67
Q

blood levels sugar indicated by

A

HbA1c

68
Q

First day of gestation

A

1st day of last menstrual period (LNMP, LMP)

- 2 weeks before = ovulation

69
Q

When do diagnostics work?
blood test
urine test
ultrasound

A

8 days
day of menses
6 weeks, more at 9 weeks

70
Q

Minimum gestation for baby to be healthy

A

24 (42, induce labor)

71
Q

Vitamins to recomend: (6)

A 
Folic acid
Ca
Vitamin D
Iron
300 + calories
prenatal vitamins
72
Q

Foods to avoid (4)

A

Alcohol
unpasteurized milk and its cheese
raw meat
mercury containing fish

73
Q

Smoking in pregnancy

A

cleft lip, heart defects, low growth
premature
stillbirth
sudden infant death

74
Q

Assymetric FGR (fetal growth restriction)

A

head is normal, rest of the body is smaller

75
Q

FASD to pregnancy

A

FGR
microcephaly + CNS defects
Upper lip, poor philtrum, palepbral fissures, short flat bridged nose

76
Q

Obestity to pregnancy

A 
Difficult becoming pregnant
Gestational diabetes
hypertensive disorders
Deep vein thrombosis/pulmonary embolism
Preterm devlivery (physician indused for elss complications; otherwise prolonged)
C section
Shoulder dystocia- erb's Palsy (waiter's tip)
Stillbirth
77
Q

Teratogens

A 
Warfarin (Coumadin): blood thinner
Valproic acid: anti-seizure
Carbamazipine: anti-seizure
Isotretinoin (Accutane)
Ace inhibitor
78
Q

weeks most sensitive to malformation

A

3-8

79
Q

Uncontrolled Diabetes –> large baby?

A

hgih blood glucose, mother insulin doesn’t cross placenta so just acts as a growth factor
[also high sugar effects respiratory system and gives hypoxia]

80
Q

Uncontrolled diabetes can cause

A 
hypoglycemia
hypoxia
cardiac defects
polyhydramnios
preterm delivery
neonatal respriatory distress syndrom
stillbirth
81
Q

Methotrexate

A

attakcs rapidly dividing cells
use in ectopic pregnancies and cancer
NOT in regular deliveries

82
Q

Cause of preterm labor?

A

Unknown

something with uterine overdistension, inflammation, infection, premature HPA axis activity

83
Q

Give baby what in pretem labor?

A

steroids: fetal lung development
Magnesium Sulfate: protect the brain by reducing energy use and minimuze free radical production
Tocolytics: stall labor (not really proven to work)

84
Q

Premature Rupture of Membranes (PROM)

A

Rupture of fetal membranes (water breaking) >1hr before labor onset
If after 34 weeks, induce labor

85
Q

Placenta Previa

A

Placenta implants in the lower part of the uterus blocking the cervix
C section it

86
Q

Placental Abruption

A

Premature separation of palcenta from uterine wall
Stillbirth at high degree
associated with contractions, cramping, and bleeding

87
Q

Preeclampsia

A

BP > 140/90

proteinurea, low platelet count, impaired liver function, pulmonary edema

88
Q

Eclampsia seizures treated with

A

magnesium sulfate to reduce neuroexcitity

89
Q

Preeclamspia risks

A 
heart attack
stroke
renal failure
retinal injury
death
90
Q

If gestational diabetes

A

put patients on diabetic diet and closely monitor

91
Q

Infancy stage:

A

Birth -2
Males have genital responses in utero and women are capable of vaginal lubrication from birth
Gender identify is forming

92
Q

Early Childhood stage

A 
2-5
exploration, independence, curiousity
Teach kids to use proper names
Don't shame
Private parts for private places
Gender stability
Parents should watch kids
93
Q

Stage 1 pregnancy

A 
learning of pregnancy -> ultrasound
Physical Sx
memory impairment
ambivalence especially when nervous aout pregnancy
fear of miscarriage
Task: acceptance
94
Q

Stage 2 pregnancy

A 
Ultrasound -> point of viability
sharing news
time of peace and fulfillment
realization of life within
best time for them
Task: recognition of fetus as separate from self
95
Q

Stage 3

A 
Pt of viability -> birth
Physical sx are back
nesting behavior
fear about birth process
fear about baby's health
Task: attachment
96
Q

HPV

A 
most common
8kb circular DNA 
with L1 (!) and L2 capsid proteins
7-8 genes total
E1-5 - viral life cycle & interactions w/host
E6,7: oncogenes
97
Q

E6 in HPV

A

p53 tumor supressor binding

98
Q

E7 in HPV

A

bind pRb for degredations - which transactivates genes in cell replication

99
Q

Cancer inducing HPV

A

16,18 (70%)

100
Q

Low grade HPVs

A

stil have E6,7 but can’t degrade tumor suppressors
can cause morbities like recurrent respiratory papillomatosis in newborns (requiring up to 100 ENT lesion excision to prevent suffocation)

101
Q

HPV MA

A

haloes around the nuclei
swiss-cheese effect
brown nuclei = intracellular capsid protein production

102
Q

HPV life cycle

A

abrasion -> access to basal cells at bottom of multi-layered squamous epithelium -> 10 replicated copies per cycle to shed and infect other cells/persons
In malignant infection, high risks trains break its circular genome and insert itself into the host DNA with intact E6,7 genes, cells become dysplastic and turn into carcinoma

103
Q

Trichomonias

A

protozoanvaginitis > urethritis
transmitable tru items
see with PAP

104
Q

Chlamydia

A

bacteria
can cause infertility
mostly women
triad: arthritis, conjunctivitis, urethritis

105
Q

Gonorrhea

A

bacteria
treat with antibiotics
can cause sterility

106
Q

Herpes

A

1 - oral
2 - genitals
no approved vaccine

107
Q

Hepatitis B

A

virus

vaccine

108
Q

Syphilis

A

bacteria

antibiotics

109
Q

Chancroid

A

bacteria
developing countires and sex works
antibiotics

110
Q

Koilocytosis

A

acute infection associated with with capsid protein synthesis
forms well-differentiated tumors
In productive time

111
Q

Malignant progression of HPV

A

no koilocytes

nonreproductive

112
Q

Where does HPV stuff happen

A

Cervix transformation zone w/transition from vaginal exocervial sqamous epithium and endocervical columnar/glandular epithelium

113
Q

HPV resolved on own unless

A

chronic and precancerous lesion forms

114
Q

Cervical intraepithelial neoplasias (CIN)

A

Cprecancerouslesion I-III

115
Q

CIN I

A

1/3 of epithelium is dysplastic

koilocytosis is stil present at the surface

116
Q

CIN II

A

2/3 of epithelium is dysplastic

117
Q

CIN III

A

carcinoma in situ
stage 0 cervical cancer
entire depth is dysplastic

118
Q

HPV detection

A

colposcopy
pap smears
hybrid capture - most sensitive

119
Q

HPV destruction

A

detect and destroy with salicylic or trichloroacetic acid externally
ablate (cryotherapy), exise (conization w/LEEP), poison (pharmacotherapy) vaginally

120
Q

HPV vaccine

A

IgG respose

SDR II (42 decks)

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