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

chapter 9 Flashcards

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
Q

GH deficiency

A 
results in failure to grow
short stature
mild obesity
delayed puberty
can be due to any step in HAP axis
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26
Q

GH excess

A

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

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27
Q

prolactin

A

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

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28
Q

regulation of prolactin secretion

A

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

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29
Q

hypothalamic dopamine (and prolactin inhibition)

A

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

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30
Q

prolactin secretion regulation

A

during breast feeding afferent fibers from nipple carry info to hypothalamus, inhibit dopamine secretion

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31
Q

actions of prolactin

A

1: breast development
2: lactogenesis
3: inhibition of ovulation

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32
Q

prolactin in breast development

A

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

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33
Q

lactogenesis

A

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

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34
Q

prolactin inhibition of ovulation

A

inhibits ovulation by inhibiting synthesis and release of GnRH
account for decreased fertility during breast feeding

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35
Q

prolactin deficiency

A

due to destruction of anterior lobe of pituitary of destruction selectively of lactotrophs
results in failure to lactate

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36
Q

prolactin excess

A

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
Q

secretory vesicle contents from hypothalamus to post pituitiary

A

have either:
ADH, neurophysin II and glycoprotein
or
oxytoxin and neurophysin I

38
Q

ADH

A

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
Q

regulation of ADH

A

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
Q

actions of ADH

A

1: increases water permeability
2: contraction of vascular SM

41
Q

ADH on water permeability

A

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
Q

ADH on vascular SM

A

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
Q

central diabetes insipidus

A

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
Q

nephrogenic diabetes insipidus

A

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
Q

thiazide diuretics in nephrogenic diabetes insipidus

A

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
Q

sydrome of inappropriate ADH (SIADH)

A

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
Q

regulation of oxytocin secretion

A

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
Q

actions of oxytoxcin

A

1: milk ejection
2: uterine contraction

49
Q

milk ejection

A

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
Q

uterine contraction

A

oxytocin causes powerful rhythmic contractions of uterine SM
used for inducing labor and reducing postpartum bleeding

51
Q

adrenal medulla

A

neuroectodermal origin
secretes catecholamines
epi and norepi

52
Q

adrenal cortex

A

mesodermal origin
secretes adrenocortical steroid hormones
glucocortecoids (zona reticularis and fasciculata)
mineralocorticoids (zona glomerulosa)
androgens (zona reticularis and fasciculata)

53
Q

glucocorticoid synthesis pathway

A

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
Q

synthesis of cortisol

A

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
Q

problems with enzymes in cortisol synthesis pathway

A

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
Q

aldosterone synthesis

A

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
Q

synthesis of androgens in adrenal cortex

A

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
Q

cholesterol desmolase

A

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
Q

17-alpha hydroxylase

A

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
Q

3-beta hydroxysteroid dehydrogenase

A

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
Q

17,20 lyase

A

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
Q

21-beta hydroxylase

A

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
Q

11-beta hydroxylase

A

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
Q

control of zona fasciculata

A

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
Q

control of zona reticularis

A

secretes primarily adrenal androgens

under HPA control but also possibly a mechanism for independent control

66
Q

control of zona glomerulosa

A

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
Q

ACTH effects

A

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
Q

dexamethasone suppression test

A

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
Q

actions of glucocorticoids

A 
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
Q

actions of mineralocorticoids

A

increase Na+ reabsorption
increase K+ secretion
increase H+ secretion

71
Q

actions of adrenal androgens

A

female: stimulate growth of pubic and axillary hair, stimulate libido
male: same as testosterone

72
Q

stimulation of gluconeogenesis

A

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
Q

cortisol’s antiinflammatory effects

A

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
Q

cortisol’s suppression of immune response

A

inhibits production of IL-2 and T-lymph proliferation

75
Q

vascular responsiveness to catecholamines

A

cortisol upregulates alpha1-adrenergic receptors - therefore required for vasoconstrictive response of arterioles to catecholamines
too much cortisol, get hypertension; too little, hypotension

76
Q

cortisol and bone formation

A

decreases synthesis of type I collagen
decreases osteoblast production
decreases intestinal Ca2+ absorption

77
Q

cortisol and GFR

A

increases by causing vasodilation of afferent arterioles - increases renal blood flow and GFR

78
Q

cortisol on CNS

A

decreases REM sleep
increases slow-wave sleep
increases awake time

79
Q

actions of aldosterone

A

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
Q

11beta-hydroxysteroid dehydrogenase

A

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
Q

adrenogenital syndrome

A

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
Q

Cushing’s syndrome

A

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
Q

21-beta hydroxylase deficiency

A

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
Q

17-alpha hydroxylase deficiency

A

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
Q

loss of glucocorticoids

A

produces hypoglycemia, anorexia, weight loss, nausea, vomitting, weakness

86
Q

loss of mineralocorticoids

A

produces hyperkalemia, metabolic acidosis, hypotension (due to decreased ECFV)

87
Q

secondary adrenocortical insufficiency

A

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
Q

conn’s syndrome (aldosterone secreting tumor)

A

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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