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Hormones Flashcards

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USMLE® Step 1 flashcards
1
Q

GHRH target/effect/inhibition

A

somatotroph, causes release of Growth Hormone, Somatostatin/IGF

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2
Q

GHIH(somatostatin)

A

Somatotroph Inhibits GH release, upregulated by IGF

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3
Q

Growth hormone is ihibited by

A

Somatostatin (GHIH,) positive feedback from IGF and Negative feedback to stop GHRH and GH from IGF and GH on Somatotropho to stop GH.

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4
Q

GH release is stimulated by

A

GHRH from Hypothalamus – Ghrelin from hypoglycemia **Thyrone hormone is required for action of growth hormone

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5
Q

GH transport and metabolism

A

pulsatile release, travels freely or bound to GHBP, eposidic release-1/2L~20min, Bound~50 min. Broken down in liver and excreted in urine.

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6
Q

IGF (Somatomedin C)

A

related structurally to pro insulin IGF 1 most important and responds to GH Have a long half life because they bind to IGF binding proteins

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7
Q

IGF actions

A

important for growth effects of GH,– promote linear bone growth,– increase organ size and function, –insufficient synthess of IGF’s can result in dwarfism,

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8
Q

Prolactin is stimulated by

A

lack of dopamine, TRH, estradiol inhibits dopamine, sensitizes to TRH.

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9
Q

prolactin secretion is inhibited by

A

dopamine from hypothalamus

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10
Q

Dopamine in hypothalamus MOA

A

binds to Gi on lactotroph and this decreases cAMP and calcium which will prevent release of prolactin, inhibited by estradiol

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11
Q

ADH secretion stimulated by

A

mediated via baroreceptors plasma osmolarity, if you have a 1-2% change Plasma Volume decrease in at least 10% of volume

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12
Q

ADH MOA

A

increase in cAMP causes aquaporins(AP2 only) to transport to luminal membrane

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13
Q

ADH second messenger

A

binds to V2 receptor increase cAMP (Gs) Binds to V1 recptor which increases IP3 and DAG(Gq)

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14
Q

ADH deficiency

A

Diabetes insipidus

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15
Q

Oxytocin secertion is upregulated by

A

a nursing baby, pressure against the cervix during birth

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16
Q

Oxytocin target cells

A

Smooth muscle cell in breasts in and uterus, causes contraction.

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17
Q

TRH triggers release of/is inhibited by

A

TSH in the anterior pituitary/Thyroid hormones

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18
Q

Thyrotropin releasing hormone is made up of

A

a tripeptide

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19
Q

TRH is secreted at/

A

a constant rate

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20
Q

Thyroid Stimulating hormone effects

A

promotes growth of thyroid gland, stimulates all steps of thyroid hormone synthesis. Tropic effect- trophic effect- increases size of gland.

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21
Q

TH is made from

A

iodination of tyrosine molecules grouped together in thryoglobulin

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22
Q

TH formation

A
  1. binding of TSH to receptor will cause syntehsis of thryoglobulin which contains tyrosine residues which is extruded onto the epical membrane
  2. Secondary active transport of Iodine into the cell with Na and extruded onto apical side of membrane
  3. oxidation of I which is catalyzed by TPO
  4. Iodination of thyroglobulin to form MIT or DIT (25%, more DIT)
  5. coupling of MIT DIT or DIT DIT
  6. TSH causes endocytosis of Thyroglopulin and will combine with lysoendosomes and split into T3 and T4, MIT, DIT
  7. enters circulation.
  8. MIT, DIT recycled.
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23
Q

Inhibition of TH synthesis

A

perchlorate, thyocyanate, nitrates,HIGH I- inhibit sodium iodine pump –PTU Propthiouracil, will inhiibt Oxidation, organification(wolf chykoff effect, high I inhibits.) and coupling.

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24
Q

TSH target for

A

antibodies, Stimulatory in graves, blocking in hashimotos.

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25
Q

TSH Receptor is located

A

on the basolateral side and membrane.

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26
Q

Thyroid hormone MOA

A

T3 enter the cell and bind to receptor T4 will enter the cell and be converted to T3 by 5` deiodinase, both will now enter the nucleus and caue thyroid like effects

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27
Q

TH second messengers

A

in Cardiac muscle, will incrase SR Ca ATPase- incrases CO will increase NA/K ATPase – will increase Beta 1 receptors, which will increase heart rate

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28
Q

T3 provides negative feedback to

A

both the hypothalamus and thyrotroph in anterior pituitary

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29
Q

Zona glomerulosa

A

secretes aldosterone, regulated by AgII and K+

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30
Q

Zona fasciulata, reticularis

A

secretes cortisol and androgens, is regulated by ACTH

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31
Q

Adrenal medulla

A

secretes NE and E, regulated by sympathetic control.

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32
Q

Aldosterone regulation

A

hypothalamus secretes, CRH, Anterior pituatary secretes ACTH. Angiotensin, II, ACTH, K+ all act on the zona glomerulosa of the adrenal cortex to produce aldosterone.

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33
Q

Hypothalamic pituitary axis

A

Cotisol, androgens produced through CRH, ACTH, action on Zona fasciculata and reticularis.

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34
Q

CRH- corticotropin releasing hormone

A

released by PVN cells, stimulates ACTH synthesis and release, is released diurnally and pulsatile. –stimulated by stressors, catecholamines, –inhibited by ACTH

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35
Q

ACTH

A

derived from Preprohormone proopiomelanocortin (POMC) secretion is diurnal and pulsatile. – alpha MSH is contained in the sequence of ACTH

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36
Q

excess ACTH results in

A

hyperpigmentation

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37
Q

Mechanism of action ACTH

A

Gs receptor timulation, increase CAMP, k creased PKA, which leads to increased P protiens and steroidogenic enzymes. both of these act on Star protein in mitochondrion which produces pregnenolone. which goes to smooth er.

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38
Q

Aldosterone regulation

A

angiotensin II is a major regulator, ACTH is minor and increased K+ too, –Aldosterone decreases AgII and K+

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39
Q

K+ MOA on Glomerulosa cell

A

increased potassium in cell causes increased Ca which activates aldosterone synthesis.

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40
Q

ACTH MOA on fasciculata

A

cAMP increased on Gs receptor, causes phosphorylation of proteins

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41
Q

transport of cortisol

A

bound to corticosteroid binding hormone and albmin, with 4% unbound.

42
Q

corticosteroid binding hormone is increased in

A

pregnancy due to increased estrogen, hyperthyroidism, and birth control pills.

43
Q

cortisol is metabolized

A

in the liver and exreted in urine.

44
Q

cortisol regulation

A

it negative feedbacks, hypothalamus and AP, ACTH also negative feedbacks the hypothlamus

45
Q

Epinephrine Second messenger

A

Sodium and Calcium

46
Q

epinephrine is triggered by

A

stress, hypothermia, too much exercise

47
Q

Epinephrine MOA

A

ACH binds to Nicotinic receptor and causes sodium to go into the cell and depolarize it. This will increase calcium and cause release and synthesis of E and NE

48
Q

Synthesis of NE and E

A

happens in cytosol except one step Tyrosine is converted to L-Dopa by Tyrosine hyrdoxylase Dopa is converted by Doapmine by Dopa decarboxylase, which will then enter a secretory granule which will have Beta hydrxoylase to convert it NE, Ne will leave the vesicle and PNMT will change it to E in the cytosol

49
Q

For epinephrine to be active it requries

A

High concentarions of Cortisol and then will go to the vesicle to bes stored again.

50
Q

Epinephrine synthesis is under the control of

A

CRH- ACTH cortisol due to ACTH stimulating synthesis of dopa and NE, and the major effect of cortisol from teh adrenal cortex released into circulation which also upregulates PNMT.

51
Q

actions of catecholamines

A

increase CO, Preload, and BP, bronchodilationl, diverts blood flow and mobilizes energy store.s

52
Q

Delta cells secrete

A

somatostatin

53
Q

F cells secrete

A

Pancreatic polypeptide

54
Q

insulin pre pro peptide made up of

A

A chain b chain C peptide

55
Q

Pre pro hormone is cleaved at

A

C peptide

56
Q

C peptide and insulin are released in

A

equalmolar concentrations.

57
Q

to measure insulin measure

A

C-peptide.

58
Q

stimulus of insulin prodcution

A

high levels of glucose, amino acids, catecholamines, and somatostatin

59
Q

GLUT 2 transporter and release of insulin in Beta Cells.

A

low affinity for glucose, GLucose is transported in and it is broken down to glucose 6 phosphate by glucokinase, this prevents glucose form leaving and is the rate limiting step. it is also a glucose sensor that regulates your insulin productions to the level of glucose. increase in ADP inhibits Potassium channels(sulfanyl urea channels) This depolarizes cell and increases calcium levels which causes insulin release.

60
Q

GLucagon main target cell is

A

liver but also can target adipose.

61
Q

Glucagon is triggered by

A

stress and hypoglycemia, also high (some) AA in blood.

62
Q

Glucagon is inhibited by

A

insulin

63
Q

Somatostatin release triggered by

A

ingesting food.

64
Q

Somatostatin effects( are local)

A

decrease insulin, glucagon secretion, GIT motility, secretions and absorption by GIT.

65
Q

factors that decrease calcium levels

A

decrease in plasma protiens, nephrotic syndrome, malnutrition, liver disease,

66
Q

Factors that increase calcium

A

increase in plasma protine, and multiple myeloma.

67
Q

PTH is made in

A

the they cheif cell of the parathyroid.

68
Q

PTH release is triggered by

A

low levels of calcium

69
Q

MOA for calcium on Chief cell.

A

ionized calcium binds to Calcium receptor on chief cell. This is a Gq receptor that stimulates DAG and IP3 which causes an increase in Calcium intracellular. This causes inhibition of PTH release.

70
Q

Actions of PTH

A

osteoblast, Gq receptor acivates cytokines which will act on osteoclast and you will have born resporption. Kidney- promotes reabsorption of Calciumin distal tubule and decreases tubular rabsorption of phosphate. Stomach, increases intestinal absorption of calcium.

71
Q

TARGET tissues of PTH

A

Bone, osteoblastic cell, Kidney

72
Q

Calcitriol, Vit D. 1,25 dihydroxycholecalciferol requires

A

PTH to be active.

73
Q

skin synthesis of Vit D.

A

7-dehydrocholesterol–UV–>cholecalciferol–25hydroxylase–> (LIVER) 25 hydroxycholeciferol–1hydroxylase, (PTH)–>(KIDNEY) 1,25 OH cholecacliferol or –24,25hydroxylase–> d4,25 cholecalcierol

74
Q

Target tissue of Calcitriol

A

Duodenal cell.

75
Q

calbindin maintains

A

low intracellular calcium levels in the GIT.

76
Q

in presence of VIT D in the gut calcium

A

calcium ravels to basal side and promotes it’s absorption, along with phosphate.

77
Q

Calcitonin

A

secreted by c cells, of thyroid, only inportant in fetus in formation of bone

78
Q

hypothalamic pituatary axis males

A

Hypothalamus–> GNRH–>Anterior pituatary–>LH, FSH–>Testes–>Leydig and sertoli cells.

79
Q

inhibition of GNRH release in males

A

Sleep/wake cycle, Stress, hormones(estrogen, prolactin) temperature of testes.

80
Q

GNRH-

A

10 peptides released in pulsatile fashion from birth to 8 years it is basal levels, and at 8-12 years of age you get an increase every one -3 hours, maximum at night. (LH mirror GNRH) (FSH is similar but has a prolonged half life and amplituded because youa re inhibiting

81
Q

GNRH Target Cell

A

Anterior pituatary.

82
Q

Target cell of LH

A

Leydig cells

83
Q

MOA of LH

A

causes conversion of cholesterol to testosterone.

84
Q

MOA of FSH

A

Gs receptor, increases DNA transcription, causes secretion of Inhibitn, aromatase, androgen binding proteins, forwth factors

85
Q

FSH target cells

A

sertoli cells.

86
Q

testosterone Target cell

A

Sertoli cells

87
Q

testosterone effects

A

is converted to estradiol by aromatase in fetal testes causes formation of penis and scrotum with hCG and testicular descent, promotes spermatogenesis. promotes long bone fusion, BMR and increase in RBC mass

88
Q

ABP

A

will bind to testosterone and move into lumen and will help the sperm be viable.

89
Q

Testosterone MOA

A

converted to dihydrotestoserone and move to nucleus and cause modualtion of DNA

90
Q

5 alpha reductase

A

converts testosterone to dihydrotestosterone

91
Q

testosterone negatively feedbacks

A

hypohtalamus and anterior pituatary

92
Q

inhibin acts on

A

the anterior pituatary to down regulate FSH and LH

93
Q

target cell, MOA for LH Females

A

Thecal cell internal, is a Gs receptor, will promote DNA trasncription and change cholesterol to pregnenolone, late follicular phase granulosa cell

94
Q

target cell MOA of FSH

A

early to mid follicularphase granulosa cells. cells Gs receptor, increase DNA transcripton and make enzymes

95
Q

two cell cooperation of females in early to mid follicular phase

A

LH increases LDL receptor and pregnenolone is converted to androstenedione and it will move to granulosa cell, under FSH it iwll convert androstenedione into estadiol.

96
Q

late follicular phase

A

cholesterol converted to pregnenolone this will make androstenedione and that will go to granular cell to make estradiol, but LH on granulosa cell makes progesterone.

97
Q

estrogens feed back on

A

the adrenergic receptors on the hypothalamus and the anterior pituitary on the priming GNRH receptors.

98
Q

Progesterone

A

helps LH surge, FSH surge, inhibits estrogen, aides in ovulation. inhibits hypothalamus to produce GnRH by way of beta endorphin.

99
Q

estrogens,

A

group of steroids, Beta estradiol is the major in non pregnant and estriol is in the pregnant. cleared by the livel

100
Q

progesterones

A

helps in proliferation of uterine epithelium, aids ovulation, promotes development of lobules and alveoli in breast, inhibites uterine excitability in pregnancy

101
Q

hCG

A

supports corpus luteum,

102
Q

Ghrelin

A

peptide made in fundus of stomach. binds to GH secretagogue receptor on somatrophs and causes release of GHRH. released during fasting.

Medical Physiology (6 decks)

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