Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physio Review > Endo/Repro > Flashcards

Endo/Repro Flashcards

1
Q

5 cell types of the anterior pituitary

A

acidophils
somatotrope- GH
lactotrope- prolactin

basophils
gonadotrope- LH/FSH
corticotrope- ACTH
thyrotrope- TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

list 4 steroid hormones, where they act

A

GCs, androgens, estrogens, vit D

nuclear receptors, slow effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does cortisol stimulate

A
  • gluconeogenesis, lipolysis, proteolysis

- inhibits NFkappaB by binding to Ikappab promoter, forming complexes with it outside cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

4 layers of the adrenal gland and what it produces

A

glomerulosa- aldosterone, MRs
fasiculata- GRs
reticulata- weak androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

common effects of adrenal cortex enzyme deficiencies

A
  • no CORT

- adrenal hyperplasia due to excess ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ACTH receptor

A

MC2R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

21 hydroxylase deficiency

A
  • no cortisol or aldosterone, increased androgens
  • hypotension, hyperkalemia
  • high renin
  • masculinization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

11-hydroxylase deficiency

A
  • no cortisol, low aldosterone, high MR activity (11-DOC), increased androgens
  • hypertension, hypokalemia
  • masculinization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

17 hydroxylase deficiency

A
  • no cortisol , low aldosterone, high 11-DOC
  • hypertension, hypokalemia
  • feminization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

cushing’s syndrome vs cushing’s disease; symptoms

A
  • when ACTH comes from the pituitary, it’s cushing’s disease
  • hypertension (cort stimulating alpha adrenergics) , central obesity, thinning of skin, hyperglycemia, insulin resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is required for the NE to E conversion in the adrenal medulla?

A

cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

excess VMA in the urine, what do you suspect

A

pheochromocytoma, excess degradation of NE/E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

thyroid hormone synthesis; what all steps are dependent upon

A

trap, transport, (oxidize iodide- TPO) iodinate (organification-TPO), conjugate (TPO), endocytose, proteolysis, secrete; everything dependent on TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T3 vs T4

A

T3- MIT-DIT

T4- DIT-DIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

type 1, 2, 3 deiodinase

A

1) outer and inner rings, makes T3/RT3, liver, kidney, thyroid, skeletal muscle
2) outer- pituitary, brain, heart, placenta
3) inner- brain, skin, placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

actions of T3

A

increases BMR, increases brain maturation, increase beta adrenergic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what stimulates prolactin; what inhibits it

A

stimulates- TRH, GH
inhibits- dopamine

lactation inhibited by estrogen and progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

where do the incretins come from?

A

glucagon gene, GLP1 & GLP2 activated in the intestines in response to low glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

transcription factor which increase glucokinase?

A

SREPB1 in WAT

PPAR gamma increases adipocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

targets of PTH

A

kidney- increases Ca reabsorption, Pi excretion

bone- releases Ca

21
Q

targets of vitamin d

A

chief cells- inhibits PTH
bone- mobilizes Ca
gut- increases Ca and Pi absorption

22
Q

estrogens effects of Ca2+ regulation

A

increases 1alphahydroxylase activity, stimulates OPG, decreases bone loss

23
Q

endocrine disrupters

A

PCBs compete with TBG

DES synthetic estrogen

24
Q

what does the product of epsilon cells in the stomach do?

A

ghrelin- inhibits insulin release by reducing the amount of intracellular Ca2+

25
Q

which gene in linked with type 2 diabetes?

A

TCF72

26
Q

what happens if, while genital ducts are maturing they encounter testosterone? antimullerian hormone?
what produces each?

A

w/ testosterone from leydig cells (normally from testes), keep wolffian ducts

w/ antimullerian hormone from sertoli cells- degrade mullarian ducts

27
Q

what does 5 alpha reductase do?

A

converts testosterone to more potent DHT, which is important for male genitalia development via androgen receptors

28
Q

where does spermatogenesis occur?

A

seminiferous tubules

29
Q

what do coelomic epithelium cells become?

A

sertoli cells in male, granulosa cells in female (nurse cells)

30
Q

what do mesenchymal cells become?

A

leydig cells in males, theca cells in females (hormone cells)

31
Q

what converts testosterone to estadiol?

A

aromatase

32
Q

what does testosterone do during fetal development?

A

epididymis
vas deferens
seminal vesicles

33
Q

what does DHT do during fetal development?

A

penis/urethera
scrotum
prostate

34
Q

what does testosterone do during puberty?

A 
penis
seminal vesicles
musculature
voice
skeleton
spermatogenesis
35
Q

what does DHT do during puberty?

A 
scrotum
prostate
male pattern baldness
happy trail
beards
sebaceous glands
36
Q

where does GnRH come from? what is it inhibited/stimulated by?

A
  • arcuate nucleus and preoptic area of hypothalamus;
  • inhibitors: dopamine, endorphins, CRH
    stimulator: NE
37
Q

hormone actions during follicular phase

A

1) GnRH causing FSH/LH release (pulsatile)
2) increasing FSH/LH stimulate ovary to develop follicle
3) follicle secretes E2 (estradiole)
4) E2 has positive feedback on follicle BUT
5) E2 has negative feedback (with inhibin) on pituitary/hypothalamus on FSH cells - keeps volume down as capacity builds (LH rising)

38
Q

hormone actions during ovulatory phase

A

1) E2 gets past a certain threshold for a sustained period of time, switches to positive feedback (timing determined by ovary)
1b) increase GnRH receptors on gonadotrophs
2) get LH surge - reinforcing self and E2
3) causes rupture of follicle
4) everything dips because it’s all disorganized

39
Q

hormone actions during luteal phase

A

1) corpus luteum becomes dominant- makes E2 (not as high as surge) and progesterone (off the charts)
2) switch back to inhibition, get little LH/FSH/GnRH
3) no LH causes corpus luteum to degrade
4) once CL degrades, lose E2 and progesterone, FSH levels recover
5) lose functional endometrial layer

40
Q

what are the actions of estradiol secreted by the dominant follicle?

A
  • inhibits growth of other follicles
  • makes mucus thin
  • prepares fallopian tubes
  • potentiates action of progesterone so uterus goes into secretory mode
  • primes GnRH action on LH surge to get more LH
41
Q

how does high insulin impact ovaries? what do you treat with?

A

stimulates androgen production, causing impaired follicle development and no ovulation; follicles degrade into cysts and ovaries double in size
- treat with metformin

42
Q

two exocytotic events during the fertilization process

A

1) Exocytosis of spermatozoan internal membrane contents- allows sperm to attach to zona pellucida
2) Exocytosis of oocyte’s internal vesicles- harden the rest of the zona pellucida (Ca2+ mediated- also triggers second meiotic division after metaphase II)

43
Q

what happens during adhesion?

A
  • zona pellucida dissolves
  • Il-1 increases integrins in endometrial cells
  • osteopontin (bridging molecules) binds integrins together
  • trophopblasts develop
44
Q

what happens during penetration?

A
  • stromal cells of endometrium enlarge to form the decidua (progesterone-promoted) and secrete nutrients (source until placenta)
  • cells preform some endocrine functions (e.g. prolactin)
45
Q

what happens during invasion?

A
  • find balance between decidual cells and trophoblast migration
  • trophoblasts differentiate into syncytiotrophoblasts (like pituitary- most endocrine functions, makes hCG/hCL) and cytotrophoblasts (like hypothalamus- CRH, TRH, somatostatins)
46
Q

what is hPL?

A

HCS aka human placental lactogen (HPL)

  • similar to growth hormone
  • stimulates lipolysis and has anti-insulin effects on maternal metabolism
  • leads to increase in plasma glucose and FFA for fetus
  • cause of gestational diabetes
47
Q

how is estriol produced?

A

mom’s cholesterol (LDL)- pregnenolone in placenta- converted by fetal adrenal to DHEA-S- converted by fetal liver to oh-DHEA-S- sulfer removed by placenta- placenta makes estriol

48
Q

T/F Maternal oxytocin initiates labor

A

FALSE- released in bursts once labor beings, has positive feedback loop, stimulating prostaglandin release
- stimulus is distention of the cervix: Ferguson reflex

Physio Review (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions