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endocrine term 2 quiz 1 - julia's notes > chapter 9 > Flashcards

chapter 9 Flashcards

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1
Q

steps of hormone synthesis

A

1: in nucleus, gene transcribed to mRNA
2: mRNA transfered to cytoplasm
3: translated by ribosomes into preprohormone
4: attached to ER by docking proteins and inserted into ER during translation process
5: ER removes signal peptide = prohormone
6: transfred to golgi - can be phos or glycos there
7: packaged into secretory vesicles
8: proteolytic hormone cleaves = hormone
9: stored in secretory vesicles until cell stimulated to release it

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2
Q

steroid hormone synthesis

A

synthesized and secreted by adrenal cortex, gonads, corpus luteum and placenta

all derived from cholesterol with added or removed side chains, hydroxylation to aromatization of steroid nucleus

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3
Q

steroid hormones (list)

A

cholesterol, aldosterone, estradiol, estriol, progesterone, testosterone, 1-25-dihydroxycholecalciferol

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4
Q

amine hormone synthesis

A

catecholamines and thyroid hormones

derivates of tyrosine

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5
Q

amine hormones (list)

A 
catecholamines 
	epinephrine
	norepinephrine
	dopamine
thyroid hormones
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6
Q

sensitivity

A

hormone concentration that produces 50% of the maximal response
can be changed by changing either the number of receptors or the affinity of the receptors to the hormone

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7
Q

mechanisms of hormone action on target cells (3)

A

1: G protein activated - activates adenylyl cycplase, cAMP produced or G protein activates phospholipase C - cleaves lipid - get IP3 - releases Ca and activates protein kinase C
2: insulin and insulin like growth factors act through tyrosine kinases
3: quanylate cyclase activated - cGMP is second messanger

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8
Q

hormones that use cAMP

A 
ACTH
LH
FSH
TSH
ADH (V2 receptor)
HCG
MSH
CRH
Calcitonin
PTH
Glucagon
B1 and B2 receptors
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9
Q

hormones that use phosholipase C

A 
GnRN
TRH
GHRH
Angiotensin II
ADH (V1 receptor)
Oxytocin
Alpha-1 receptors
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10
Q

hormones that use steroid hormone mechanism

A 
glucocorticoids
estrogen
progesterone
testosterone
aldosterone
1,25-dihydroxycholecalciferol
thyroid hormones
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11
Q

hormones that use the tyrosine kinase mechanism

A

insulin

IGF-1

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12
Q

hormones that use the cGMP mechanism

A 
atrial natriuretic peptide (ANP)
endothelial derived relaxing factor (EDRF)
nitric oxide (NO)
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13
Q

hormones posterior lobe of pituitary secrete

A

ADH - supraoptic nuclei
oxytocin - paraventricular nuclei
(both actually neuropeptide)
really being secreted by cells in the hypothalamus - axons are in the post pituitary

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14
Q

anterior pituitary

A 
derived from primitive foregut
peptide or polypeptide hormones
TSH
FSH
LH
GH
prolactin
ACTH
linked to ant. by hypothalamic-hypophysial portal blood vessels
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15
Q

hypothalamic-hypophysial portal blood vessels

A

arterial blood to hypothalamus via superior hypophysial arteries
distribute blood in a capillary network in median eminence (primary capillary plexuses)
plexuses converge to form long hypophysial portal vessels
trave down indundibulim to deliver hypothalamic venous blood to anterior lobe of pituitary
parallel capillary plexus makes inferior hypophysial arteries and converge to make short hypophysial portal vessels

note: most of blood supply is venous blood from the hypothalamus supplied by the long and short hypophysial portal vessels

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16
Q

glycoprotein hormone family

A

TSH, FSH, LH from anterior pituitary
have sugar moieties covalently linked to saparagine residues in polypeptide chains
have alpha and beta subunits - all alphas the same but betas specific to hormone type - but alpha required for activity

placental hormone human chorionic gonadotropin (HCG) is structurally part of this family

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17
Q

ACTH family of hormones

A 
derived from precursor proopiomelanocortin (POMC)
includes:
ACTH
gamma and beta lipotropin
beta endorphin
melanocyte-stimulating hormone (MSH)
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18
Q

Addison’s disease

A

primary adrenal insufficiency
POMC and ACTH levels are increased by negative feedback
because both contain MSH activity, skin pigmentation occurs
clinical features: hypoglycemia, anorexia, weight loss, nausea, vomiting, weakness, hypotension, hyperkalemia, metabolic acidosis, decreased pubic and axillary hair in females, hyperpigmentation
ACTH levels increased (because of negative feedback effect of decreased cortisol)
treatment with glucocorticoid and mineralocorticoid replacement

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19
Q

growth hormone (and prolactin) family of hormones

A

aka somatotropin hormone or somatotropic hormone
similar to prolactin and lactogen (placental)
secreted in pulsatile pattern - burst every 2 hours
secretory burst at puberty induced by estrogen or testosterone
hypoglycemia and starvation, exercise, some forms of stress (fever, trauma, anesthesia) stimulate

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20
Q

feedback of GH secretion

A

hypothalamus releases GHRH
activates antior pituitary to release
GHRH has negative feedback on hypothalamus GHRH production
GH has positive feedback on hypothalamus somatostatin prod.
somatostatin inhibits GH release
target tissues release somatomedins (IGF)
these inhibit GH release in interior pituitary and increase somatostatin release in hypothalamus

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21
Q

actions of GH

A

1: diabetogenic effect
2: increased protein synthesis and organ growth
3: increased linear growth

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22
Q

diabetogenic effect

A

one of the effects of GH
causes insulin resistance
increases glucose uptake and utilization by muscle and adipose
result in increase in blood glucose concentration
increases lipolysis

metabolic effects result in increase in blood insulin

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23
Q

GH effects on protein synthesis and organ growth

A

increases uptake of AA and stimulates synthesis of DNA, RNA, and protein in organs
increases lean body mass and increases organ size

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24
Q

GH effects on linear growth

A

mediated by somatomedins
alters cartilage metabolism via stimulating DNA synthesis, RNA synthesis, and protein synthesis
epiphyseal plates widen
more bone laid down at ends of long bones
increased metabolism in cartilage-forming cells and proliferation of chondrocytes

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25
GH deficiency
``` results in failure to grow short stature mild obesity delayed puberty can be due to any step in HAP axis ```
26
GH excess
causes acromegaly and giganticism in children usually due to GH secreting adenoma in pituitary in adulthood, increased periosteal bone growth, increased organ size, increased hand and foot size, enlargement of the tongue, coarsening of facial features, insulin resistance, glucose intolerance treat wtih somatostatin analogues
27
prolactin
milk production, breast development made by lactotrophs in ant lobe of pituitary increased secretion due to altered transcription of prolactin gene TRH stimulates, dopamine inhibits
28
regulation of prolactin secretion
hypothalamus releases TRH acts on anterior pituitary, which releases prolactin prolactin acts on breast prolactin also acts on hypothalamus hypothalamus releases dopamine dopamine inhibits further prolactin secretion at anterior pituitary
29
hypothalamic dopamine (and prolactin inhibition)
1: major source is dopaminergic neurons of hypothalamus - secrete into median eminence 2: secreted by dopaminergic neurons of posterior lobe and travels to ant. lobe by short connecting portal veins 3: nonlactotrophic cells of anterior pituitary secrete some dopamine that diffuses to lactotrophs
30
prolactin secretion regulation
during breast feeding afferent fibers from nipple carry info to hypothalamus, inhibit dopamine secretion
31
actions of prolactin
1: breast development 2: lactogenesis 3: inhibition of ovulation
32
prolactin in breast development
at puberty, stimulates proliferation and branching of mammary ducts during pregnancy, stimulates growth and development of mammary alveoli works in concert with estrogen and progesterone
33
lactogenesis
milk production prolactin induces synthesis of components of milk including lactose, casein, and lipids high levels of estrogen and progesterone during pregnancy prevent lactation during pregnancy - down-regulate receptors in breast and block prolactin action estrogen and progesterone levels drop at parturition
34
prolactin inhibition of ovulation
inhibits ovulation by inhibiting synthesis and release of GnRH account for decreased fertility during breast feeding
35
prolactin deficiency
due to destruction of anterior lobe of pituitary of destruction selectively of lactotrophs results in failure to lactate
36
prolactin excess
destruction of hypothalamus, interuption of hypothalamic-hypophysial tract, or prolactinomas increased prolactin secretion because loss of tonic inhibition by dopamine results in galactorrhea and infertility (because of inhibition on GnRH secretion) treat with administration of dopamine agonist
37
secretory vesicle contents from hypothalamus to post pituitiary
have either: ADH, neurophysin II and glycoprotein or oxytoxin and neurophysin I
38
ADH
secreted in response to increased serum osmolarity acts on principle cells of late DT and CD to increase water reabsorption - decreases body fluid osmolarity back toward normal
39
regulation of ADH
most important is increased plasma osmolarity sensed by osmoreceptors in anterior hypothalamus ADH neurons activated and cause secretion of ADH from their terminals in the posterior pituitary hypovolemia can also stimulate secretion: get decreases BP - sensed by baroreceptors in left atrium, carotid artery, and aortic arch - transmitted via vagus nerve to hypothalamus - increase in ADH secretion note: hypovolemia stimulates ADH secretion even if plasma os is lower than normal but: hypervolemia inhibits ADH secretion even if os is higher than normal
40
actions of ADH
1: increases water permeability 2: contraction of vascular SM
41
ADH on water permeability
in late DT and CD principle cells ADH receptor = V2 receptor coupled with Gprotein and adenylyl cyclase increase in cAMP cAMP directs insertion of aquaporin 2 into luminal membranes water can now be reabsorbed by CD - urine more concentrated
42
ADH on vascular SM
V1 receptor on SM coupled to phospholilpase C and G-protein activates IP3/Ca2+ activity results in contraction of vascular SM, constriction of arterioles, and increase total peripheral resistance
43
central diabetes insipidus
due to failure of posterior pituitary to secrete ADH collecting ducts impermeable to water urine can't be concentrated generate large volumes of dilute urine and have concentrated body fluids treated with ADH analog
44
nephrogenic diabetes insipidus
principle cells of CD don't respond to ADH because of defect in receptor or associated proteins water not reabsorbed in CD urine can't be concentrated large volumes of dilute urine excreted, body fluid concentrated ADH levels elevated because of the increased serum os treated with thiazide diuretics
45
thiazide diuretics in nephrogenic diabetes insipidus
inhibit Na reabsorption in early DT - prevent dilution of urine here to make final excrete product less dilute decrease glomerular filtration rate - if less water filtered, less is excreted increase Na excretion so cause secondary ECFV contraction - proximal reabsorption of solutes and water increased
46
sydrome of inappropriate ADH (SIADH)
excess ADH from autonomous site (often cancer) high ADH causes excess water reabsorption by CD - dilates body fluids urine inappropriately concentrated treated with ADH antagoinst
47
regulation of oxytocin secretion
major stimulus = suckling of the breast afferent neurons from nipple send info to spinothalamic tract of prain stem to PVN of hypothalamus oxytocin secreted from terminals in post pituitary
48
actions of oxytoxcin
1: milk ejection 2: uterine contraction
49
milk ejection
oxytocin causes contraction of myoepithelial cells lining small milk ducts - forces milk into large ducts - collects in cisterns and flows out through the nipple
50
uterine contraction
oxytocin causes powerful rhythmic contractions of uterine SM used for inducing labor and reducing postpartum bleeding
51
adrenal medulla
neuroectodermal origin secretes catecholamines epi and norepi
52
adrenal cortex
mesodermal origin secretes adrenocortical steroid hormones glucocortecoids (zona reticularis and fasciculata) mineralocorticoids (zona glomerulosa) androgens (zona reticularis and fasciculata)
53
glucocorticoid synthesis pathway
cholesterol I I (cholesterol desmolase) -ACTH I (17-alpha hydroxylase) (17,20-lyase) pregnenolone---->17hydroxypregnaenalone----> dehydropiandro. I I I I (3-beta hydroxysteriod dehydrogenase (all 3)) I I (17-alpha hydroxylase) I (17,20 Lyase) I progetserone --------> hydroxysterone ---------> androstenedione I I I (21-beta hydroxyalse) I (11-beta hydroxylase) I I 11-deoxycorticosterone (DOC) cortisol I I (11-beta hydroxylase) I corticosterone I I (aldosterone synthase) +AII I aldosterone
54
synthesis of cortisol
1: cholesterol desmolase converts cholesterol to pregnenolone 2a: 17-alpha-hydroxylase converts pregnenolone to 17-hydroxypregnenolone 3a: 3-beta hyroxysteroid dehydrogenase converts 17-hydroxypregnenolone to 17-hydroxyprogesterone 2b: 3-beta hydroxysteroid dehydrogenase converts pregnenolone to progesterone 3b: 17-alpha hydroxylase converts progesterone to 17-hydroxyprogesterone 4: 21-beta hydroxylase hydroxylates at C21 5: 11-beta hydroxylase hydroxylates at C11
55
problems with enzymes in cortisol synthesis pathway
if 17-alpha hydroxylase step blocked, get corticosterone production to make up for cortisol lack blocks at 3-beta hydroxysteroid dehydrogenase, 21-beta hydroxylase or 11 beta hydroxylase prevent production in both cortisol and corticosterone synthesis
56
aldosterone synthesis
1: cholesterol desmolase converts cholesterol to pregnenolone 2: 3-beta hydroxysteroid dehydrogenase converts pregnenalone to progesterone 3: 21-beta hydroxylase converts progesterone to 11-deoxycorticosterone (DOC) 4: 11-beta hydroxylase converts DOC to corticosterone 5: aldosterone synthase converts corticosterone to aldosterone
57
synthesis of androgens in adrenal cortex
1: cholesterol desmolase converts cholesterol to pregnenolone 2a: 17-alpha hydroxylase converts pregnenolone to 17-hydroxypergnenolone 3a: 17,20 lyase converts 17-hydroxypregnenolone to dehydroepiandrosterone 4a: can stop here or 3-beta hydroxysteroid dehydrogenase can convert to androstenedione 2b: 3-beta hydroxysteroid dehydrogenase converts pregenolone to progesterone 3b: 17-alpha hydroxylase converts progesterone to 17-hydroxyprogesterone 4b: 17,20 lyase converts 17-hydroxyprogestone to androstenedione
58
cholesterol desmolase
enzyme responsible for the first step of the biosynthesis of adrenocortical hormones activated by ACTH converts cholesterol to pregnenolone required for synthesis of aldosterone, cortisol, and androgens
59
17-alpha hydroxylase
responsible for second step of androgen synthesis and cortisol synthesis converts pregnenolone to 17-hydroxypregnenolone converts progesterone to 17-hydroxyprogesterone without it would not get androgens or cortisol but would still get corticosterone which would act as glucocorticoid
60
3-beta hydroxysteroid dehydrogenase
responsible for second step of aldosterone synthesis, final step of androstenedione synthesis and 2nd or 3rd step of cortisol synthesis without it would only get dehydroepiandrosterone converts pregnenolone to progesterone converts 17-hydroxypregenealone to 17-hydroxyprogesterone converts dehydroepiandrosterone to androstenedione
61
17,20 lyase
responsible for last and second to last steps in androgen synthesis converts 17-hydroxypregnenolone to dehydroepiandrosterone converts 17-hydroxyprogesterone to androstenedione without it would bet buildup of cortisol
62
21-beta hydroxylase
responsible for aldosterone and cortisol synthesis converts progesterone to DOC (11-deoxycorticosterone) converts 17-hydroxyprogesterone to 11-deoxycortisol without it get no aldosterone and cortisol and high androgens
63
11-beta hydroxylase
enzyme required for last step of cortisol and aldosterone synthesis without it still get DOC - has weak glucocorticoid effects, but no cortisol or aldosterone higher androgens
64
control of zona fasciculata
secretes primary glucocorticoids under exclusive control of HPA - CRH released from hypothalamus triggers release of ACTH from anterior pituitary cortisol inhibits ACTH release from ant pituitary and CRH release from hypothalamus cortisol also inhibits CRH effect on ant. pituitiary - results in less ACTH secreted
65
control of zona reticularis
secretes primarily adrenal androgens | under HPA control but also possibly a mechanism for independent control
66
control of zona glomerulosa
secretes mineralocorticoids depends on ACTH for first step of biosynthesis but otherwise controlled by RAAS angiotensin II increases synthesis and secretion of aldosterone by stimulating cholesterol desmolase and aldosterone synthase (decrease in ECFV results in decrease in renal perfusion pressure => increased renin secretion by juxtaglomerular cells => renin catalyzes conversion of AI to AII) aldosterone stimulates Na reabsorption so ECF Na content increases so ECFV increases serum K+ also controls secretion - increases increase secretion, decreases decrease - incrased serum K+ acts on adrenal cells - depolarizes them - opens voltage-sensitive Ca2+ channels = intracellular Ca2+ increases - stimulates aldosterone secretion
67
ACTH effects
immediate: stimulate transfer of stored cholesterol to mitochondria stimulate binding of cholesterol to cytochrome P450 activates cholesterol desmolase long term: stimulation of transcription of genes for p450, adrenoxin upregulation of ACTH receptors chronic effects: hypertrohy hyperplasia of adrenal cortical cells
68
dexamethasone suppression test
synthetic glucocorticoid that has actions of cortisol in helathy person, inhibits ACTH secretion, causing decreased cortisol secretion used to test for hypercortisolism and whether its due to an ACTH secreting tumor or a cortisol secreting tumor if ACTH secreting, low dose won't affect but high dose will if due to adrenal cortical tumor, won't affect cortisol secretion at all
69
actions of glucocorticoids
``` increase gluconeogenesis increase proteolysis (catabolic) increase lipolysis decrease glucose utilization decrease insulin sensitivity inhibit inflammatory response suppress immune response enhance vascular responsiveness to catecholamines inhibit bone formation increase GFR decrease REM sleep ```
70
actions of mineralocorticoids
increase Na+ reabsorption increase K+ secretion increase H+ secretion
71
actions of adrenal androgens
female: stimulate growth of pubic and axillary hair, stimulate libido male: same as testosterone
72
stimulation of gluconeogenesis
cortisol increases protein catabolism in muscle and decreases new protein synthesis - provides more AA to liver for gluconeogenesis increases lipolysis - provides additional glycerol to liver decreases glucose utilization by tissues decreases insulin sensitivity of adipose tissue too little, get hypoglycemia; too much, get hyperglycemia
73
cortisol's antiinflammatory effects
induces synthesis of lipocortin which inhibits phospholipase A2, which liberates arachidonic acid from membrane phospholipids to provide precursor for prostaglandins adn leukotrienes inhibits production of IL-2 and proliferation of T-lymph inhibits release of histamine and serotonin from mast cells and platelets
74
cortisol's suppression of immune response
inhibits production of IL-2 and T-lymph proliferation
75
vascular responsiveness to catecholamines
cortisol upregulates alpha1-adrenergic receptors - therefore required for vasoconstrictive response of arterioles to catecholamines too much cortisol, get hypertension; too little, hypotension
76
cortisol and bone formation
decreases synthesis of type I collagen decreases osteoblast production decreases intestinal Ca2+ absorption
77
cortisol and GFR
increases by causing vasodilation of afferent arterioles - increases renal blood flow and GFR
78
cortisol on CNS
decreases REM sleep increases slow-wave sleep increases awake time
79
actions of aldosterone
increase Na+ reabsorption increases K+ secretion increases H+ secretion (alpha-intercalated cells) result in ECFV expansion, hypokalemia, hypertension, metabolic alkalosis low aldostserone results in ECFV contraction, hyperkalemia, hypotension and metabolic acidosis
80
11beta-hydroxysteroid dehydrogenase
affinity of mineralcortocoid receptors in DT and CD for aldosterone and cortisol same renal cells have enzyme that converts cortisol to cortisone, which has low affinity for MR receptors
81
adrenogenital syndrome
increased synthesis of adrenal androgens masculinzation in females, early development of pubic and axillary hair suppression of gonadal function in both males and females increased urinary levels of 17-ketosteroids
82
Cushing's syndrome
primary adrenal hyperplasia clinical features: hyperglycemia, muscle wasting, central obesity, round face, supraclavicular fat, buffalo hump, osteoporosis, striae, virilization and menstrual disorders in females, hypertension ACTH levels decreased (because of negative feedback effect of increased cortisol)
83
21-beta hydroxylase deficiency
no mineralo or glucocorticoids steroid intermediates accumulate above clinical features: virilization in females, early acceleration of linear growth, early appearance of pubic and axillary hair, symptoms of deficiency in glucocorticoids and minealocorticoids ACTH levels increased due to negative feedback effect of cortisol replace gluco and mineralo
84
17-alpha hydroxylase deficiency
no glucocorticoids or androgens levels of aldosterone decreased because increased levels of 11-deoxycorticosterone and corticosterone result in in symptoms of mineralocorticoid excess (hypertension, metabolic alkalosis, hypokalemia) - hypertension inhibits renin secretion clinical features: lack of pubic and axillary hair in females, symptoms of deficiency of glucocorticoids, symptoms of excess minearlocorticoids ACTH increased because of negative feedback effect of decreased cortisol replace glucorticoids and give aldosterone antagoinst
85
loss of glucocorticoids
produces hypoglycemia, anorexia, weight loss, nausea, vomitting, weakness
86
loss of mineralocorticoids
produces hyperkalemia, metabolic acidosis, hypotension (due to decreased ECFV)
87
secondary adrenocortical insufficiency
due to insufficient CRH or ACTH ACTH levels low, not high aldosterone levels usually normal because aldosterone synthesis requires only tonic levels of ACTH - don't have hyperkalemia, metabolic acidosis, or ECFV contraction (as opposed to primary adrenocortical insufficiency) no hyperpigmentation
88
conn's syndrome (aldosterone secreting tumor)
hypertension (increased Na reabsorption) hypokalemia (increased K secretion) metabolic alkalosis (increased H+ secretion) low circulating renin levels because increased ECFV

endocrine term 2 quiz 1 - julia's notes (2 decks)

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