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Physiology > Endo 2 > Flashcards

Endo 2 Flashcards

1
Q

T/F All nuclear steroid hormones will form hetero or homodimers

A

TRUE (e.g. cortisol)

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2
Q

mechanism of cortisol signaling

A

1) converted from corticosterone to cortisol by 11 beta HSD intracellularly
2) form dimer in nucleus
3) binds to response element (GRE) on promoter of gene of interest
4) recruits other co-binding proteins to express/repress gene

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3
Q

what is corticosterone bound to? where is it made? how is corticosterone released?

A

CBG (90% bound), made in liver;

- need proteases to cleave bonds, enzymes are tissue specific

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4
Q

what else will CBG bind?

A

aldosterone (30 fold higher affinity for cortisol)

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5
Q

what can decrease CBG?

A

estrogen, shock, severe infection (will cause higher cortisol levels)

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6
Q

active form of glucocorticoids in humans

A

cortisol

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7
Q

active form of glucocorticoids in rodents

A

corticosterone

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8
Q

when does cortisol peak?

A

around 8AM (released in circadian manner)

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9
Q

what do glucocorticoids make up the majority of?

A

cortical hormones (made in zona fasiculata- biggest zone)

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10
Q

what does pleiotropic mean?

A

lots of different effects on multiple tissue types

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11
Q

T/F Every cell in the body has glucocorticoid receptors

A

True- how/when it acts depends on enzymes that allow cortisol to get into the cell

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12
Q

Main functions of cortisol

A

1) decreases bone formation (osteoporosis)
2) inhibits the immune response/potent anti-inflammatory
3) maturation of the brain/maintaining arousal/mood
4) maturation of the fetus (increases surfactant in lungs)
5) maintains cardiac output
6) mobilizes glucose, increases gluconeogenesis

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13
Q

metabolic actions of cortisol

A

mobilizes energy stores, increases lipolysis & proteolysis, antagonizes insulin, inhibits calcium reabsorption; redistributes body fat (abdominal fat)

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14
Q

3 enzymes of the gluconeogenesis pathway that allow cortisol to mobilize glucose

A

1) glucose 6 phosphatase
2) PEP carboxykinase
3) tyrosine aminotransferase

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15
Q

what does cortisol act on in the muscle?

A

inhibits Glut4 insertion in the membrane (opposite of insulin); glucose not being taken up by muscles

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16
Q

what does cortisol act on to increase protein degradation? increase lipolysis?

A
  • doesn’t allow FoxO to be phosphorylated; increases E3 ubiquitin ligases which increase protein degradation
  • increases transcription of genes for lipolysis
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17
Q

3 things cortisol does to dampen inflammation (actions in cell)

A

1) increases the production of IkappaB by binding to its promotor; IkappaB can bind more NfKappaB, decrease transcription of inflammatory disease
2) binds to same proinflammatory gene promoters and turn them off
3) create GR-NfKappaB complex to prevent translocation of NFkappaB to the nucleus

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18
Q

how does cortisol suppress the edmea associated with inflammation globally?

A

1) blocks the prostaglandins from being released- decreases capillary permeability
2) inhibits activation of neutrophils

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19
Q

what does cortisol increase with regard to inflammation?

A

neutrophils (but inhibits their migration/activation), platelets, RBCs

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20
Q

what part of the adaptive system does cortisol block?

A

induces atrophy of thymus; get less T cell production which suppresses antibody production

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21
Q

cortisol’s actions on bone

A
  • calcium transport is facilitative and passive
  • inhibits synthesis of calcium channels
  • low calcium are signals for other hormones
  • decreases IGF1 receptors on bone
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22
Q

overall effect of cortisol on cardiovascular system

A
  • shunts blood from periphery (alpha adrenergic stimulation results in constriction) to coronary arteries (increases beta adrenergic receptors to get vasodilation) & brain
  • is permissive (helps other hormones do their job)
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23
Q

what is difference between Cushing disease and Cushing syndrome?

A

syndrome- all of the phenotypic effects associated with excess cortisol production (exogenous) - negative feedback will turn off ACTH

disease- phenotypic changes caused by a corticotroph (pituitary) tumor- have high levels of ACTH since pituitary causing disease

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24
Q

excess cortisol symptoms

A

moon face, abdominal obesity, subcutaneous fat is thinning, osteoporosis, hypertension (high GCCs activate MR) , glucose intolerant, purple striae (fat re-distribution)

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25
Q

why is glucocorticoid therapy used?

A
  • medical emergencies- potent anti-inflammatory effect
  • chronic therapy used with autoimmune diseases (lupus) (shuts down HPA axis, ACTH needed for cells in zona fasiculata, body stops making endogenous cortisol)
  • pre-term infants (surfactant)
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26
Q

what do you look for in a synthetic glucocorticoid analog?

A

maximize GR activity without affecting MR

- prednisone, dexamethasone

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27
Q

what is adrenal insufficiency (AI) and what is the most common type? where is the failure?

A
  • an autoimmune disease causing a failure to secrete glucocorticoids, mineralocorticoids or both
  • Addison’s is primary type (failure at adrenal)
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28
Q

where is the failure of secondary AI?

A
  • failure to secrete CRH or ACTH

- caused by sudden cessation of glucocorticoid therapy

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29
Q

what does the zona glomerulosa produce?

A

mineralocorticoids

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30
Q

what are mineralocorticoids?

A

steroid hormones that regulate sodium/water balance

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31
Q

what is the primary endogenous mineralocorticoid? whats a precursor?

A

aldosterone; 11-deoxycorticosterone

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32
Q

in what tissues is MR expression high? restricted expression

A

distal tubule of kidney
colon
salivary ducts
sweat ducts

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33
Q

main target of aldosterone? what is its the main stimulator? what does it cause?

A
  • kidney
  • increase in extracellular potassium, stimulates aldosterone via angeiotensin II, extrudes potassium
  • is steroid hormone, increases synthesis of epithelial sodium channels (ENaCs)
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34
Q

which system is activated directly by changes in blood volume?

A

renin-angiotensin-aldosterone

  • decreased blood pressure stimulates renin release from JGA of kidney
  • renin cleaves ATGEN (from liver) to ATI
  • ACE converts to AT II
  • AT II is vasoconstrictor and stimulates aldosterone
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35
Q

what’s special about renin?

A

hormone with no receptor

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36
Q

aldosterone vs AVP (work together to maintain osmoregulation, blood pressure, blood volume)

A

aldosterone- extracellular volume- by stimulating Na reabsorption, H20 follows, increases ECV fluid volume and blood pressure

AVP- free water balance- changes distal nephron water permeability, secondarily affects sodium concentration in blood

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37
Q

what enzyme de-activates cortisol in mineralocorticoid target cells?

A

11 beta HSD2 (TWO NOT ONE!!!)

cortisol becomes cortisone

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38
Q

what is the pathway for mineralocorticoid target cell response?

A

aldosterone enters from blood, displaces chaperone from MR, MR-aldosterone complex dimerizes and enters nucleus, binds to promoters, etc.

39
Q

what happens to the cortisone from MR cells?

A

goes back into blood, if finds glucocorticoid target cell with 11betaHSD1, which converts it back to cortisol

40
Q

what do licorice and carbenoxolone do?

A

inhibit 11 beta HSD 2, get excessive MR activation (excessive sodium and water retention) (can’t make cortisone)

41
Q

what does the zona reticularis produce? where is it?

A

weak (need lots) androgens (DHEAs) ; right up against the adrenal medulla

42
Q

what is the metabolite of DHEA and what is it a precursor for?

A

androstenedione; precursor for more potent androgen testosterone and estrogens (converted in reproductive tissues)

43
Q

what effect does excess ACTH production by pituitary have on steroid hormone synthesis?

A

increases the activity of the rate limiting step (StAR) so free cholesterol is transported into the mitochondria, also regulates CYP11A1 and conversion to prenenalone

44
Q

which two zones have CYP17 (17 hydroxylase)

A

fasiculata, reticularis

45
Q

what enzyme does CYP11A1 encode?

A

desmolase- converts free cholesterol to pregnenalone in all zones

46
Q

what enzyme does CYP11A2 encode? what is an example of a deficiency?

A

21 alpha hydroxylase; deficiency results in excess DHEA causes congenital adrenal hyperplasia (only place its not used is zona reticularis)

47
Q

what is the clinical presentation of CAH?

A
  • hypotension (no aldosterone- lack of sodium reabsorption)
  • hyperkalemia
  • masculinization b/c of high androgens
  • high renin b/c of hypotension
  • ACTH is high because you have NO cortisol (no negative feedback)
  • high ACTH with CAH, stimulating StAR/CYP11A1, perpetuating cycle
48
Q

what is an example of a 21 alpha hydroxylase deficiency?

A

deficiency results in excess DHEA causes congenital adrenal hyperplasia (only place its not used is zona reticularis)

49
Q

what enzyme does CYP11B1 encode and which pathway?

A

11 hydroxylase in zona fasiculata

50
Q

how does 11 hydroxylase deficiency cause low aldosterone? what happens to ACTH? potassium?

A
  • funneling into glom pathways causes 11-Doc (and other MR precursors) to be high, causes hypokalemia and hypertension, which will signal for aldosterone to be reduced (RAA pathway)
  • ACTH will be high because cortisol will be low
51
Q

defect in 17 alpha hydroxylase?

A
  • no cortisol
  • high aldosterone- hypertension
  • ACTH is high- no cortisol
  • no adrenal androgens (pseudohermaphroditism)
52
Q

what is similar in all steroid hormone enzyme deficiency pathways

A

HIGH ACTH, stimulating pregnenolone production

53
Q

what is ACTH important for in the adrenal medulla?

A

conversion of dopamine to norepinephrine

54
Q

what are catecholamines and where are they made?

A

epinephrine & norepinephrine

adrenal medulla

55
Q

if you have high ACTH and low cortisol in the adrenal medulla, what is made?

A

norepinephrine

56
Q

3 main targets of epinephrine & actions

A

1) muscle- inhibits insulin, promotes breakdown of glycogen, release lactate
2) liver- gluconeogenesis, release glucose in blood
3) adipose- breaks down TAGs to increase substrates for glucose

57
Q

action of epinephrine at beta receptors (fight or flight response)

A
  • increase blood flow to the organs that need it in times of stress
    *heart- increase cardiac output
  • skeletal muscle- increase vasodilation
  • lungs- dilation of bronchioles
    _GI tract- relax (use energy for other things)
58
Q

action of epinephrine at alpha receptors (fight or flight response)

A

increase venous return & cardiac output: increase vasoconstriction

59
Q

broad view of epinephrine actions

A
  • metabolic: glucose release, increase BMR

- cardiovascular- vasoconstriction, increase heart rate

60
Q

which hormone has higher affinity for alpha adrenergic receptors? beta adrenergic?

A

alpha- NE

beta- Epi= NE

61
Q

Acute stress activates the ___ NS and stimulates the release of ____, which stimulates _____ to initiate the HPA response to long-term stress

A

sympathetic; NE

CRH

62
Q

two things catecholamines are degraded by, what is the end product

A

COMT - methylates
MAO - deaminates
end product: VMA (measured in urine) (vanillylmandelic acid)

63
Q

what are the cells of the adrenal medulla called? what do they release? what is is a tumor originating from these cells called? important symptom?

A

chromaffin; NE and E (catecholamines); pheochromocytoma (10% tumor)

  • hypertension from excessive stimulation of CVS, which is not responsive to medication, tachycardia
64
Q

main component of thyroid gland? what does it look like activated vs inactive? activated by what?

A

follicle= colloid+ follicular epithelial cell, activated by TSH

  • activated= cuboidal epithelium
  • inactive= squamous epithelium
65
Q

what less important kind of cell is in the thyroid?

A

C-cell- produces calcitonin - doesn’t come in contact with colloid

66
Q

what are thryoid hormones called? what 2 precursors are critical?

A

iodothyronines

thyroglobulin + iodide

67
Q

what is the wolf-chaikoff effect?

A
  • way thyroid gland regulates how much iodide is being taken up in the face of fluctuating dietary levels
  • as dosage increases, uptake decrease, thyroid hormone synthesis decreases
  • can give high dose of iodide and temporarily shut down thyroid hormone production
68
Q

3 thyroid hormones

A

T4- thyroxine
T3- triiodothyronine
rT3- reverse triiodothyronine

69
Q

which thyroid hormone binds receptors with high affinity? where is it converted?

A

T3, converted intracellularly from T4

70
Q

describe the HPT axis

A

PVN of hypothalamus releases TRH
Thyrotropes of anterior pituitary release TSH
Thyroid releases T4/T3

71
Q

what does TPO do?

A

oxidizes I- (iodide) to I (iodine)

72
Q

what is the difference between T3/T4/rT3?

A 
T3= MIT-DIT
T4= DIT-DIT
rT3= DIT- MIT
73
Q

what is the difference between MIT and DIT?

A
  • MIT has one residue of tyrosine (of thyroglobulin) iodinated
  • DIT has tyrosine iodinated twice
74
Q

what are the 7 steps of thyroid hormone formation?

A

1- iodide trapping (blood-cell)
2- transport (oxidation by TPO in colloid)
3- iodination (tyrosine residue on thyroglobulin)
4- Conjugation (make T4/T3)
5- Endocytosis
6- Proteolysis (release TG/DIT/MIT/T3/T4)
7- secretion (via basal membrane- blood)

75
Q

T/F thyroid hormones are made in cell

A

FALSE- made in colloid

76
Q

what is a good way to determine if the thyroid gland is functioning properly? what is concerning?

A

radioactive iodine uptake scan (131I or pertechnetate)

  • a lightly colored spot surrounded by darkness= “cold nodule”- predictive of thyroid cancer
77
Q

how can radioactive iodide be used to detect thyroid disorders?

A

normal: 25% uptake after 24 hours
hyperthyroidism: >60% uptake
hypothyroidism:

78
Q

what is the difference between T3/T4/rT3?

A 
T3= MIT-DIT
T4= DIT-DIT- low receptor affinity 
rT3= DIT- MIT
79
Q

why do thyroid hormones have different actions in different tissue types?

A

have different deiodinases in target tissues for thyroid hormone conversion

80
Q

type 1 deiodinase

A
  • deiodinates outer and inner rings
  • is predominant in liver, kidney, thyroid gland, skeletal muscle
  • what gives you T3 in circulation
  • makes T3 and rT3
81
Q

type 2 deiodinase

A
  • only deiodinates outer ring
  • is predominant in brain, pituitary, placenta, cardiac muscle
  • called thyroid hormone sensor b/c its what gives you negative feedback in pituitary
  • only makes T3
82
Q

how is thyroid hormone transported?

A

70% by TBG (thyroxine binding globulin)
15-25% by albumin
10% TTR

83
Q

type 3 deiodinase

A
  • inner ring deiodinase
  • in brain, placenta, skin
  • makes rT3
  • protective against too much thyroid hormone- inactivates it
  • can also convert T3 to T2
84
Q

T/F TBG is highest in concentration

A

FALSE- has highest affinity, so is always all bound up even at small concentrations

85
Q

what increases TBG? how does it change free hormone circulating?

A

estrogen, hepatitis; has no impact on free hormone, only alters total pool

86
Q

Describe thyroid hormone receptors

A
  • nuclear receptors
  • expressed in almost every cell
  • high affinity for T3
  • always forms a heterodimer with retinoic acid receptor (RXR)
  • always in nucleus bound to DNA target
87
Q

major physiological functions of thyroid hormone

A
  • increases BMR (glucogenogenesis, proteolysis, lipolysis)
  • promotes maturation of CNS - T3 critical for neuronal cell migration/differentiation/myelination/synaptic transmission (cretinism)
  • increases synthesis of beta adrenergics (hyperthyroidism can cause arrhythmias)
88
Q

T/F You see high serum glucose levels with hypothyroidism

A

False- see normal serum glucose, because insulin is the overriding mechanism (do see decreased gluconeogesis/glycogenolysis)

89
Q

why goiter with hypothyroidism? when would you not get a goiter?

A
  • no negative feedback on anterior pituitary, get excessive TSH, stimulates steps to make more hormone, hyperactive follicular cells
  • would not see defect with secondary or tertiary problem
90
Q

what is Graves disease?

A
  • antibodies stimulating the TSH receptor
  • results in elevated T4/T3, goiter, tachycardia, buggy eyes
  • taking iodide up very quickly, dumping thryoid hormone very quickly; due to overstimulation of follicle
  • in histology, see depleted colloid (pink stuff)
91
Q

what is Hashimoto’s thyroiditis?

A
  • autoimmune destruction of thyroid follicles
  • have antibodies against TPO and thyroglobulin
  • get hypothyroid symptoms (lethargy, fatigue, cold intolerance, weight gain)
92
Q

what precipitates thyroid storm?

A
  • hyperthyroidism coupled with severe acute illness
  • hyperthyroid will potentiate the inflammatory effects associated with the illness
  • get high fever, tachycardia, nausea/vomiting, diarrhea= circulatory collapse
  • give PTU, which inhibits TPO
93
Q

peptides released by hypothalamus matched to brain region

A

POA- GnRH
PVN- TRH, CRH, somatostatin
Arcuate nucleus- GHRH, dopamine
SON- ADH

Physiology (22 decks)

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