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33 Cards in this Set
- Front
- Back
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XY individual without testosterone production
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appear female because no testosterone or DHT
If that is the only deficiency, and still have A-MH - then have NO internal ducts |
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Wolffian duct
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Gonad develops into epididymis, vas deferans, prostate, seminal vesicles.
Dependent on testosterone and DHT (work on same receptor) If no DHT - need extra high testosterone |
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Mullerian duct
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female internal structure - default if no male hormones exist.
Oviduct, vagina, ovaries, etc |
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A-MH
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Inhibits female
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Primordial Gonads
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Testis XY
Ovaries XX |
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Pseudohermaphodites
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Same genes and sex organs - but appear opposite sex
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Congenital Andrenal Hyperplasia
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Deficiency of either 21 or 11 hydroxylase involved in glucocorticoid synthesis - high ACTH which stimulates excessive androgens
Unable to make glucocorticoids so androgens increase |
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Progesterone during Pregnancy
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Normal surge at end of cycle - then gradual increase with each trimester
Increase in 17 Hydroxy Progesterone (metabolite) |
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Klinefelters Syndrome
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XXY - seminiferous tubules do not develop - infertility. Testosterone production is low = elevation of LH
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True hermaphodites
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both ovarian and testicular tissue
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Androgen receptor defects - testicular feminizing syndrome
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Have testosterone, DHEA, and estrogen - but no receptors
Estrogen recepetors are normal - develop breast tissue at puberty because of the surge of testosterone that is converted to estrogen will have non descended testes |
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5 alpha reductase deficiency
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can not convert to DHT - treat with high testosterone.
Born ambiguous genitalia but may appear female - at puberty surge in testosterone will determine if male - or will cycle |
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Free Martins
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Exchange of circulation from one fetus to the other fetus - 2 heterozygous twins then male will masculinize female calf and she will be infertile
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Leydig Cell Aplasia
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low receptors for LH.
Testosterone production during early development is adequate to stimulate male ducts, but not appearance |
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Glucocorticoids and Mineralocorticoids during Pregnancy
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High Cortisol, aldosterone, and DOC
But normally receptors less sensitive to prevent NA and Water retention = normal blood pressure |
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Thyroid Hormone during pregnancy
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T4 is elevated during first trimester and plateaus
Bound T3 is high - so binding proteins are higher too, but no change in free T3, or activity |
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Pituitary during Pregnancy
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GH, TSH are the same
LH , FSH undetectable (due to high E/P) PRL is elevates to term |
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Placental proteins during pregnancy
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hCG is high for first trimester then lowers
hPL continues to rise |
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Estrogens during Pregnancy
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All rise
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Adrenal Androgens
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Decrease DHEA
Increase testosterone (in male fetus) No change in Androstenedione |
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Cardiovascular during Pregnancy
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Increase in Q and HR
but drop in BP. Vasodilation occurs because of high Q and HR and maintains so until closer to term |
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Growth Factors Stimulating cancer cells
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IGF 1, EGF; highly variable
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Cancers dependent on Exogenous hormones
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dont make hormones and need it to survive.
Breast and Prostate cancer (androgen dependent) Stop it by inhibiting androgen synthesis |
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Hormones Inhibiting cancers
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glucocorticoids cause apoptosis of cells
Inhibin probably anti growth molecule |
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Cancers that produce hormones and receptors
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Enlarged endocrine gland
Ectopic hormone producing cancer (not associated with normal gland) |
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Tumors that damage nearby organs
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ex brain tumor
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Multiple Endocrine Neoplasia
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rare, inherited, several endocrine glands develop benign or malignant tumors or grow in excess without tumors.
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Type 1 MEN
PPP |
Develop tumors in at least 2 endocrine organs:
(PPP) Parathyroid (excessive PTH) Pancreas (high insulin and gastrin) and Pituitary (high PRL, maybe GH and ACTH) (less affected thyroid and adrenal) |
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Type 2A MEN
TAP |
Sipple's Syndrome
2 or 3 glands TAP Thyroid Adrenal Medullary (pheo) - no problem w gluccoroticoids Parathyroid |
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Type 2B MEN
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Medullary Thyroid Cancer
Pheochromocytoma - increase norepi, high HR and BP (act on alpha receptors) **Neuromas - growth around the nerves |
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Most Common MEN
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Type 2A - followed by medullary thyroid cancer
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Type 2 MEN gene
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25 mutations in the RET gene
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Type 1 MEN gene
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Mutations on MEN1 gene, chromosome 11, or the Menin gene that makes menin which suppresses tumors
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