Pathophysiology Flashcards

1
Q

What causes the regression of the Müllerian duct?

A

Müllerian inhibitory substance produced by Sertoli cells

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2
Q

Wha cause the persistence of wolffian duct?

A

Testosterone produced by leydig cells

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3
Q

When do meiosis I and II happen during the women life?

A

Oogonia at puberty arrested at meiosis I

Meiosis II happen with fertilization

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4
Q

What gene on the Y chromosome direct the development of male gonads?

A

SRY gene

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5
Q

How does female puberty starts?

A

Start with sleep-dependent release and then pulsatile release of GnRH (modulated by CRH) from hypothalamus—>leads to pulsatile release of FSH and LH—>ovary makes estrogen—>breast development (thelarche) and first menstrual period (menarche)

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6
Q

The order of menstrual cycle?

A

Follicular phase (many follicles grow—>only one is dominant. Growing follicles secrete estrogen—>stimulate the growing of endometrium)—>ovulation (dominant follicle releases its mature oocyte for fertilization and implantation. Estrogen positive feedback on LH and FSH preovulation —>LH surge)—->luteal phase (luteinization of ruptured follicle to make corpus luteum. Progesterone surge)

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7
Q

What does corpus luteum release?

A

Estrodial and progesterone that inhibits the release of FSH and LH

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8
Q

Granulosa cells are stimulated by?

A

FSH. Aromatase in granulosa cells convert androgen from Theca cells to estradiol (main estrogen of non pregnant women)

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9
Q

Theca cells are stimulated by?

A

LH

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10
Q

What is the mechanism of oral contraceptive pills?

A

Estrogen and progestin block the LH surge thus prevent ovulation

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11
Q

What hormone does the placenta secretes?

A

hCG—>maintain corpus luteum till placenta can produce progesterone—>then hCG falls
It also produces hCS (promote energy supply of the fetus)

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12
Q

The fetus provides what to the mother?

A

Androgen—>then made into estrogen

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13
Q

How is milk release from the breast inhibited before the birth of the fetus?

A

High level of estrogen and progesterone blocks milk release—>after birth—>estrogen and progesterone level drop

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14
Q

What stimulates the ejection of milk?

A

oxytocin

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15
Q

What does it mean by counterregulatory state regarding to pregnancy?

A

Insulin resistance. Several blood glucose elevating hormones are produced during pregnancy to promote energy supply for the fetus, e.g. hCS. As a result, non diabetic woman can develop transient diabetes during pregnancy.

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16
Q

What is fetal macrsomia and what usually causes it?

A

Large fetal size. Usually caused by poorly controlled gestational diabetes—>might lead to C section

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17
Q

What are the risks associated with the separation of placenta from the uterine wall?

A

Hemorrhage. The body is adapted to be hyercoagulable during pregnancy to prevent hemorrhage, which results in bad thrombosis sometime

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18
Q

What is third trimester bleeding associated with?

A

Placenta previa/abruption

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19
Q

What is the primary/secondary ovarian insufficiency of amenorrhea?

A

Premature loss of follicles/lack of hormone stimulation of normal ovaries

20
Q

What is the kind of estrogen for pregnant women?

A

Estriol

21
Q

Sex-hormone binding globulin has higher binding affinity for testosterone or estrogen?

A

Testosterone (also estrogen stimulates the production of SHBG)

22
Q

Pregnant women has respiratory alkalosis/acidosis?

A

Increase PaO2—>decrease PaCO2—>alkalosis

23
Q

T4 and cortisol in pregnant women increase or decrease?

A

Increase

24
Q

Best marker for menopause

A

elevated FSH

25
Q

What does aromatase convert?

A

It convert testosterone to estradiol and adrostenedione to estrone

26
Q

Why do we micronization of estradiol when given as a drug?

A

So that it can increases its half life and resist destruction in the GI (we do the same for progesterone)

27
Q

Estrogen has negative feedback on?

A

Estrogen itself and FSH

28
Q

What are the risks for Hormone Replacement Therapy for postmenopausal women?

A

Stroke/DVT/pul embolism/bp/heart attack (though HDL is higher)/breast, cervical and endometrial cancers
Don’t give estrogen to any pt with above conditions

29
Q

Benefit of HRT for postmenopausal women?

A

Treat osteoporosis/increase HDL/reduce postmenopausal symptoms like hot flushes

30
Q

What is primary hypogonadism and how do we treat it?

A

Lack of hormones from sex gonads/use estrogen for premenopausal women

31
Q

Should we give HRT to every menopausal women?

A

No, only for those with severe symptoms

32
Q

What is the risk for untreated chronic anovulation?

A

High estrogen level increase risk for endometrial carcinoma

33
Q

Increase serum insulin level (insulin resistance) has what effect on SHBG?

A

decrease SHBG–>increase free testosterone—>impede developing follicle for ovulation—>anovulation

34
Q

The syndrome that is caused by ischemia of the pituitary from hypotension caused from hemorrhage during child birth is called?

A

Sheehan Syndrome

35
Q

Which cytokine causes dysmenorrhea?

A

Disorder of prostaglandin F2alpa

36
Q

Cervical and uteral cancer can what clinical finding?

A

Abnormal vaginal bleeding

37
Q

Why give mother Rho(D) immune globulin at 28 wk as well as within 72 hour of delivery?

A

To sensitize the mother and prevent her from making Rh + antibody (reduce risk for erythroblastosis fetalis)

38
Q

How to treat erythroblastosis fetalis?

A

Intrauterine fetal blood transfusions as needed and delivery as soon as fetal lung maturity is confirmed.

39
Q

Erythroblastosis fetalis can cause?

A

Hydrops fetalis/kernicterus (bilirubin induced damage) and jaundice after delivery

40
Q

Antibody of what class cross the placenta and cause erythoblastosis fetalis?

A

IgG

41
Q

Where does bilirubin comes from?

A

Liver breakdown of RBC

42
Q

Why do we measure fetal middle cerebral blood flow in response to erythroblastosis fetalis?

A

To see if there’s any high output heart failure

43
Q

What is the most frequent cause of gout? (underexcretion or overproduction)?

A

Underexcretion

44
Q

What does gout form at distal joints?

A

It is cooler there

45
Q

What cells are responsible for clearing immune complexes in the reticuloendothelial system?

A

Monocyte and macrophages