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Physiology > Endo 1 > Flashcards

Endo 1 Flashcards

1
Q

what are the classical endocrine glands?

A

pineal, pituitary, parathyroid, thyroid, adrenal, pancreas, placenta/ovary/testis

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2
Q

what are 2 important features of the classical endocrine glands?

A

1) they’re ductless- hormones are secreted directly into the blood or the extracellular space
2) the entire organ (except pancreas) is dedicated to endocrine function

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3
Q

what are non classical endocrine glands?

A

brain, kidney, heart, liver, gi, adipose tissue

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4
Q

define homeostasis

A

the state of equilibrium in the body with respect to various functions and to the chemical compositions of the fluids and tissues

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5
Q

what does “hyper” mean in the context of homeostasis?

A

overproduction of a hormone and/or hypersensitivity to hormonal effects

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6
Q

9 sources of endocrine pathologies and example of each

A 
congenital (cretinism)
genetic (congenital adrenal hyperplasia)
trauma/stress (sheehan's syndrome)
surgical (thyroidectomy)
therapeutic (GC therapy)
malignant or benign tumor (SC carcinoma)
infection 
autoimmune (dibetes I) 
environmental
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7
Q

3 modes of hormone release

A

endocrine- into blood, acting on downstream target
paracrine- intersitital space on nearby cells
autocrine- interstitial space on self

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8
Q

T/F You measure bound hormone to get a sense of hormone activity within the blood

A

FALSE- bound hormone is not bio-availible

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9
Q

which hormones typically travel bound to other proteins?

A

lipophilic hormones- e.g. steroids (also growth hormone, T4/T3, IGF-I) ; increases half life

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10
Q

T/F Hormones bound to albumin are considered bioavailible

A

True! albumin is a non-specific transport mechanism, has weak interaction with hormones, making hormones readily usable

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11
Q

what are some examples of highly specific hormone transport?

A
  • sex hormone binding globulin- estrogen & testosterone
  • corticotropin binding globulin- cortisol/corticosterone
  • thyroid binding globulin and transthyretin- bind thyroid hormone
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12
Q

2 scenarios explaining how bound hormones are delivered to target cells

A

1) a. steroid released at membrane b. freely diffuses across lipid bilayer c. finds intracellular targets
2) a. hormone + protein binds megalin b. forms endocytic vesicle c. hormone dissociates inside cell

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13
Q

what is specificity?

A

ability of the receptor to distinguish between similar substances

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14
Q

what is affinity?

A

how much of the hormone is needed to bind 50% of the receptors (Kd) - is the equilibrium point (smaller number, higher affinity)

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15
Q

what does Ki measure?

A

ability to displace ligand at 50% of maximum activity (smaller number, higher specificity)

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16
Q

what are 3 characteristics of lipophobic hormone receptors?

A

1) on cell surface
2) coupled to second messenger signaling
3) induce rapid internalization/degradation of product

(e.g. GPCRs- protein hormones, Receptor-linked kinases- growth hormone)

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17
Q

what are 3 characteristics of lipophilic hormone receptor

A

1) mainly intracellular
2) often bound to large chaperone proteins in cytoplasm (heat shocks )
3) are a slow biological response- requires transcriptional/translational events

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18
Q

3 chemical categories of hormones

A

1) monoamines (chatecholamines, idolamines)
2) peptides/proteins
3) steroids

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19
Q

what are catecholamines derived from? indolamines?

A

catecholamines- tyrosine

indolamines- tryptophan

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20
Q

what is the rate limiting step for chatecholamine creation? indolamine?

A

tyrosine & tryptophan hydroxylase

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21
Q

T/F Catecholamines act only as a hormone in substantia nigra

A

False- acts as a hormone in arcuate nucleus and NT in substantia nigra

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22
Q

What is the pathway for the formation of catecholamines from tyrosine?

A

tyrosine- LDOPA- dopamine- norepinephrine- epinephrine

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23
Q

where does most of the conversion of dopamine to NE occur?

A

in the neurons, before they’re released

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24
Q

where does most of the conversion of NE to E occur?

A

adrenal medulla

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25
Q

where is 95% of serotonin made? what does it do?

A

enterochromaffin cells in the gut ; acts as a vasoconstrictor, stimulates smooth muscle cell contraction in intestine

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26
Q

what can serotonin be converted into? where?

A

melatonin in pineal gland

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27
Q

3 ways monoamines can be inactivated?

A
  1. blocking Dopa decarboxylase with carbidopa/benzerazide- converts LDOPA-dopamine
  2. COMT- inactivates and degrades catecholamines
  3. monoamine oxidase- catalyzes the deamination of monoamines
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28
Q

what is the rate limiting enzyme for the formation of melatonin and when is it most active? which region of hte brain regulates the pineal gland?

A

N-acetyltransferase, most active at night; the SCN

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29
Q

describe the biosynthetic processing of peptide hormones

A

1) nucleus: mRNA includes signal- hormone + copeptide
2) ribosome: makes preprohormone (signal-hormone-copeptide)
3) in golgi get prohomone by degrading signal
4) in granules, package hormone + copeptide

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30
Q

what factor is most closely related to half life? which chemical category has longest half life?

A
  • size

- steroids (b/c bound to transport proteins?)

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31
Q

first step in steroid hormone synthesis

A

cholesterol transported from outer mitochondria to inner mitochondria by StAR , turned into pregnenolone (commone precursor)

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32
Q

what is positive feedback? what are some examples?

A

A stimulates B stimulates A

  • reproductive system (childbirth, lactation, ovulation)
  • blood clotting
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33
Q

what is negative feedback? what are some examples?

A

A stimulates B inhibits A (thermostat example)

  • e.g. osmoregulation & ADH
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34
Q

what is the endocrine axis? where is the defect in a primary endocrine disease?

A

hypothalamus - pituitary- peripheral gland

- 1* ed= peripheral gland

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35
Q

where does short loop feedback come from? long loop?

A

short loop- pituitary to either gland

long loop- from peripheral gland back to inhibit/stimulate hypothalamus

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36
Q

what is physiological response driven negative feedback?

A

endocrine gland releases hormone that acts on target organ, changes homeostasis, the change in homeostasis inhibits endocrine gland

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37
Q

what is endocrine axis driven negative feedback?

A

the hormone produced by the peripheral gland provides negative feedback to the hypothalamus/pituitary gland

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38
Q

what is the thyroid hormone pathway?

A

hypothalamus- TRH
anterior pituitary- TSH
thyroid gland- T4/T3

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39
Q

what would primary hypothyroidism look like?

A
  • primary= disorder of thyroid gland
  • have chronically high TSH
  • when you give TRH, see very high spike of TSH, but overall normal pituitary response
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40
Q

what would secondary hypothyroidism look like?

A
  • secondary= disorder of anterior pituitary
  • undetectable basal TSH
  • when you give TRH, see no response (no release of TSH)
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41
Q

what are some factors that could alter normal hormone levels when you measure them in clinic?

A

age, weight, time of day, gender

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42
Q

where is the hypothalamus located?

A

below the thalamus, between the lamina terminals & mammillary bodies, forms floor of 3rd ventricle

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43
Q

what are the major hypothalamic nuclei?

A 
PVN- paraventricular
POA- preoptic
ARC- arcuate
SCN
SON- supraoptic
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44
Q

what is the convergence point for axons?

A

median eminence

45
Q

what is the convergence point for axons where hormones are released? is it inside or outside of the BBB?

A

median eminence; outside the BBB

46
Q

what is the size of gonadotropin releasing hormone (GnRH) and where is it located?

A
  • is a decapeptide

- cell bodies found throughout forebrain, most are in POA

47
Q

what is GnRH critical for? what chemical class is GnRH?

A

reproduction; peptide

48
Q

what is Kallman syndrome?

A

x-linked genetic disorder where GnRH neurons fail to enter the CNS, characterized by infertility and anosmia (lack of ability to smell)

49
Q

how does GnRH start to activate gonadotrophs?

A

1) released into hypophyseal portal system
2) binds GPCR
3) signal hydrolyze PIP into IP3 and DAG
4) IP3/Ca2+ signal increased LH/FSH release
while DAG/PKC increase LH/FSH synthesis

50
Q

T/F GnRH is secreted in a continuous fashion

A

F- GnRH is released in a pulsatile fashion

51
Q

what is downstream product of GnRH release? which is secreted with fast pulsatile release?

A 
pituitary glycoproteins (LH/FSH)
get more LH than FSH with more frequent GnRH release
52
Q

what are the 2 major pathways connecting the hypothalamus and pituitary? what type of neurons do they contain?

A

1) tuberoinfudibular system- via median eminence, go to anterior pituitary - input is parvocellular neurons
2) neurohypophysial tract- axons terminate in posterior pituitary via pituitary stalk - contains magnocellular neurons

53
Q

what is the main difference between anterior and posterior pituitary tissue? different blood supplies?

A

anterior pituitary- more glandular; superior hypophysial artery
posterior pituitary- neural tissue; inferior hypophysial artery

54
Q

major hormones released from posterior pituitary

A

AVP (aka ADH) ; oxytocin

55
Q

what is the main difference between anterior and posterior pituitary tissue?

A

anterior pituitary- more glandular, 90% is pars distalis

posterior pituitary- neural tissue

56
Q

what is another name for the posterior pituitary? anterior pituitary?

A

posterior- neurohypophysis

anterior- adenohypophysis

57
Q

what are herring bodies?

A

dilations of unmyelinatex axons where hormones are released in posterior pituitary

58
Q

what are pituicytes?

A

glial like cells of the posterior pituitary, small darkly stained

59
Q

what is another name for the posterior pituitary? what is its blood supply from?

A

neurohypophysis; inferior hypophysial artery

60
Q

anterior pituitary cell type subdivisions and relative concentrations

A

acidophils (40%), basophils (10%), and supporting cells- chromophobes- 50%

61
Q

types of acidophils and what they secrete

A

somatotrophs- growth hormone

lactotrophs- prolactin

62
Q

types of basophils and what they secrete

A

corticotrophs- ACTH
gonadotrophs- LH/FSH
thyrotrophs- TSH

63
Q

which cells are least protected from trauma?

A

acidophils (growth hormone, prolactin); have high frequency of tumors

64
Q

T/F most pituitary hormones are secreted in a circadian rhythm

A

True

65
Q

copeptide for AVP and copeptide for oxytocin

A

AVP- neurophysin II (carrier which maintains stability)

oxytocin- neurophysin I

66
Q

2 signals that increase AVP

A
  • increase is plasma osmolarity (causes osmoreceptors (tonic inhibition) near magnocellular neurons to shrink)
  • decrease in plasma volume (sensitizes system)
67
Q

two receptors AVP works on, where they’re found, what kind of receptors they are

A

V1A- smooth muscle of vessels, brain
V2- kidney

both GPCRs (b/c AVP is peptide hormone)

68
Q

how does the V1 receptor work?

A

stimulates phospholipase C pathway, increase in intracellular calcium, phosphorylates myosin light chain kinase (actin + myosin light chain), get vasoconstriction

69
Q

how does V2 receptor work in kidney?

A

activates PKA which phosphorylates aquaporin II (water channels only found in collecting ducts of kidneys), channels are inserted in membrane, water can be reabsorbed (aquaporin 3 & 4 are always found on basolateral side)

70
Q

main physiologic defect related to AVP

A

diabetes insipidus

71
Q

two primary causes of AVP defects

A

1) primary defect- no AVP made/released= TRAUMA to hypothalamus or pituitary
2) decreased responsiveness to AVP- still see normal AVP levels b/c other systems compensate
* x-linked genetic disorder
* consequence of long-term lithium treatment (schizophrenia)

72
Q

what does oxytocin act upon

A
  • uterus & breast (milk ejection) smooth muscle

- also known as trust hormone

73
Q

describe oxytocin’s actions at the level of the smooth muscle cell

A
  • increases PLC/IP3 pathways
  • increased intracellular Ca2+
  • phosphorylation of MLCK
  • contraction of smooth muscle
    (pretty much same as AVP)
74
Q

what two spots does somatostatin 14 act at? where is it made?

A
  • made in PVN of hypothalamus
  • acts
    1) inhibits GHRH pulse frequency (slows it down) in hypothalamus
    2) inhibits GH release from pituitary
75
Q

when is growth hormone mostly made?

A

peaks in blood during the night; huge variability between individuals

76
Q

what are the downstream effects of growth hormone mediated by? what is this called? where is its production stimulated?

A

IGF-1; somatomedians; liver

77
Q

what does growth hormone need to stimulate its effector in the liver?

A

insulin

78
Q

IGF-1 mimics insulin in ____ but not ____ and ___ due to lack of receptors

A

in muscle, but not liver and adipose tissue

79
Q

what is the insulin-independent role of growth hormone

A

maintain lean body mass, preserve protein, increase protein synthesis in muscle

80
Q

what are the 3 direct targets of growth hormone?

A

liver, muscle, adipose tissue

81
Q

where is GnRH released from?

A

arcuate nucleus of the hypothalamus

82
Q

when does IGF-1 peak?

A

during puberty

83
Q

what are the 3 direct targets and effects of growth hormone? (antagonist to insulin)

A

1) adipose tissue- decrease glucose uptake (mobilizes in blood), increase lipolysis (decreases adiposity)
2) liver- stimulating IGF-1
3) muscle- decrease glucose uptake (maintains glucose in blood), increases AA uptake and protein synthesis

84
Q

where are some of the important places IGF acts, and what does it do?

A

increase growth of visceral organs, connective tissue, bone; increase AA uptake in muscle, increase protein synthesis

** IGF1 does not affect glucose uptake in muscle

85
Q

GH inhibitors

A

somatostatin, IGF1 (negative feedback at hypothalamus and pituitary), glucose, free fatty acids

  • decreases with age, high blood glucose, obesity
86
Q

GH stimulators

A

GHRH, dopamine, NE/E, AA’s, thyroid hormone

  • increases during times of stress/starvation to INCREASE lean body mass
87
Q

2 GH excess disorders

A

1) gigantism- long bones get long because of IGF1 increase
2) acromegaly- pituitary tumor later on in life- bones get wider, enlargement of hands and feet (arthritis, knuckles impinge on nerves)

88
Q

2 types of GH deficiency

A

1) dwarfism- in kids
* Laron syndrome- GH receptor doesn’t work, no IGF1, can give IGF1, GH levels are high
* African pygmy- partial defect in GH receptor, harmful during puberty

2) adult GH deficiency- surgical intervention/tumor- lose muscle, increase fat, reduced bone density (can treat with GH)

89
Q

T/F Prolactin is part of the HPL axis

A

FALSE- prolactin is not part of an axis

90
Q

what is prolactin tonically inhibited by?

A

dopamine

91
Q

what is prolactin released in response to?

A

stimulus-secretion reflex (suckling)

92
Q

what does prolactin inhibit?

A

GnRH - if baby allowed free access to breast, inhibits ovulation

93
Q

What other hormone can cause galactorrhea?

A

GH (because closely aligned with prolactin); can also cause decreased fertility (through inhibition of GnRh)

94
Q

what is an example of prolactin deficiency?

A
  • sheehan’s syndrome
  • during pregnancy, pituitary gland is proliferating at a high rate; pituitary highly vascularized
  • hemmorage during birth causes massive pituitary cell destruction (ischemia) (mostly lactatrophs because they’re what are proliferating)
95
Q

insulin-induced hypoglycemia should result in?

A

increased GH levels

96
Q

administration of IGF1 should result in?

A

decreased GH levels

97
Q

what is controlled by the HPA axis?

A
  • adaptive stress (physiological (heat, pain), psychological, disrupting sleep)
  • epinephrine, norepinephrine, cortisol, glucocorticoids
98
Q

gene which ACTH comes from?

A

POMC

99
Q

what does ACTH bind with high affinity to and where?

A

MC2R (melanocortin 2 receptor) in adrenal gland

100
Q

CRH pathway important for ACTH release

A
  • CRH binds GPCR CRH-R1
  • activates PKA
  • POMC expression is increased & so is intracellular Ca2+
  • ACTH is released
101
Q

what does ACTH bind with high affinity to and where? what does it bind to with low affinity and where?

A
  • MC2R (melanocortin 2 receptor) in adrenal cortex (fasiculata)
  • at high levels (pituitary tumor), binds MC1R in skin (hyperpigmentation)
102
Q

what is ACTH required for?

A

first step in steroid hormone biosynthesis (STAR/pregnenolone)

103
Q

what does ACTH cause long term?

A

hypertrophy of adrenal gland

104
Q

3 parts of the adrenal cortex and what they produce

A
  • zona glomerulosa/mineralocorticoids
  • zone fasiculata/ glucocorticoids (cortisol)
  • zona reticularis/weak androgens (DHEA)
105
Q

what is produced in cortex? what is produced in medulla?

A

cortex- steroid hormones

medulla- catecholamines (NE/E)1

106
Q

where does adrenal blood supply originate? describe how it flows?

A
  • supra-renal artery/capsular artery
  • arterioles that go straight through cortex to medulla
  • arterioles that break into subcapsular plexus/sinusoids in cortex to deep plexus to medullary plexus
107
Q

which hormone does the blood supply to the medulla for which important conversion?

A

cortisol is required for conversion of norepinephrine to epinephrine in medulla

108
Q

what kind of stress is cortisol released in response to?

A
  • acute and chronic stress
  • acute stress activates does cortisol and catecholamines
  • chronic stress results in high levels of cortisol
109
Q

what does cortisol bind?

A

high affinity intracellular GR receptor normally attached to chaperone heat shock protein; everything translocates into nucleus when cortisol binds

Physiology (22 decks)

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