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physio fall midterm > endocrionology lecture 3 > Flashcards

endocrionology lecture 3 Flashcards

1
Q

adrenal medulla develops from

A

neural crest cells

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2
Q

what part of the ANS is the adrenal medulla

A

sympathetic

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3
Q

what 2 hormones does the adrenal medulla secrete

A

epinephrine and norepinephrine

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4
Q

preganglionic symp neurons come from the spinal cord and synapse where

A

in the adrenal medulla on postganglionic cells called CHROMAFFIN CELLS

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5
Q

what do chromaffin cells release (into the blood)

A

epinephrine and norepinephrine (epinephrine mostly)

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6
Q

what is the phenyl-N-methyltransferase and where is it located

A

an enzyme located in high quantities in the adrenal medulla that converts NE to E (which is why the medulla mainly secretes E)

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7
Q

which receptors have a higher affinity for Epinephrine

A

beta adrenergic

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8
Q

which receptors have a higher affinity for NE

A

alpha adrenergic

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9
Q

epinephrine from the medulla to target tissues (via blood to the liver/muscle/fat) and causes what…

A

increase fuel availability/increase glucose by stimulating lipolysis, glycogenolysis, gluconeogenesis

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10
Q

where does the adrenal cortex develop from

A

mesothelial cells in the intermediate mesoderm (similar to the gonads)

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11
Q

is the adrenal cortex part of the nervous system

A

no!

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12
Q

what stimulates the adrenal cortex

A

blood borne signals (aka hormones)

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13
Q

what does the adrenal cortex secrete

A

steroid hormones

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14
Q

what are the 3 different zones of the adrenal cortex

A
  1. zona glomerulosa (outer)
  2. zona fasiculata
  3. zona reticularis (inner)
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15
Q

what causes different steroids to be produced by the zones

A

there are different steroidogenic enzymes in each zone

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16
Q

what is steroid synthesis in the adrenal cortex stimulated by

A

ACTH (adrenocorticotrophic homone)

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17
Q

what is the major target of aldosterone

A

the kidney when there is a drop in blood volume (decrease in b.p) or a decrease in Na in the blood

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18
Q

what is the major effect of aldosterone

A

stimulate Na and H20 retention in the kidney (to maintain blood volume and b.p)

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19
Q

what happens with K and H as a result of aldosterone secretion

A

increase in urinary excretion of K and H

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20
Q

where does aldosterone bind

A

remember that aldosterone is a steroid hormone so it binds to an intracellular receptor which then acts as a transcription factor to bind to DNA and increase the synthesis of specific proteins

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21
Q

what proteins (3) does aldosterone stimulate the synthesis of

A
  1. Na channels (sodium permeases) at the apical membrane (towards the tubular fluid)
  2. Na/K ATPase in the basolateral membrane (towards the blood)
  3. etc enzymes in the mitochondria
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22
Q

what are plasma angiotensin II and renin and how are they related

A

renin is a hormone (released by the kidney) in response to decreased Na levels and decreased b.p. RENIN STIMULATES PLASMA ANGIOTENSIN II to be released. PAT-II stimulates aldosterone to be released to ultimately increase Na in the blood and increase b.p.

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23
Q

how are plasma K [ ]s related to aldosterone secretion

A

increase in K plasma levels–> increases aldosterone secretion

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24
Q

aldosterone secretion is stimulated by a ____ in plasma pH and a ____ in plasma H

A

stimulated by a DECREASE in pH and INCREASE in [H]

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25
Q

how is b.p related to aldosterone secretion

A

when b.p drops stretch receptors are stimulated in the arteries and there is input to the cortex to increase aldosterone secretion

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26
Q

increase in Na intake (via diet) causes what

A

inhibition of aldosterone

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27
Q

what is secreted from the zona fasiculata

A

the glucocorticoids (cortisol and corticosterone)

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28
Q

what is the major affect of cortisol

A

increase fuel/glucose availability

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29
Q

cortisol increases ____ in the liver

A

gluconeogenesis

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30
Q

cortisol increases ____ in the muscle

A

proteolysis

31
Q

cortisol increases ____ in the fat tissue

A

lipolysis

32
Q

cortisol decreases ____ in muscle and in fat

A

glucose uptake

33
Q

what does cortisol do to the immune and inflammatory responses

A

decreases it (aka why you get a cortisol shot)

34
Q

what does cortisol do to growth and reproductive functions

A

decreases them

35
Q

what receptor does cortisol work on and what is the purpose

A

‘permissive action’ on beta-adrenergic receptors in smooth muscle to regulate b.p

36
Q

cortisol is an antagonist of

A

insulin

37
Q

how does cortisol work to decrease the glc uptake in muscle and fat

A

by blocking the GLUT4 transporter that insulin works on

38
Q

secretion/synthesis of cortisol is stimulated by

A

ACTH

39
Q

cortisol has a ________ on CRH and ACTH

A

negative feedback action

40
Q

what is secreted from the zona reticularis

A

androgens (sex steroids)….including DHEA and androstenedione

41
Q

what is DHEAs role

A

it acts as a precursor of other sex steroids (circulating reservoir). it has weak androgenic action.

42
Q

peripheral concentrations of DHEA reflect the activity of the ____

A

adrenal cortex

43
Q

peripheral concentrations of DHEA reflect the activity of the ____

A

adrenal cortex ….bc DHEA has constant levels in the body so a decrease would reflect a problem

44
Q

what is androstenedione synthesized from

A

DHEA

45
Q

androstenedione provides a non-gonadal source of

A

testosterone and estradiol (it can be converted to these 2 things)

46
Q

why is androstenedione important to women

A

provides reproductive steroids prior to puberty and in postmenopausal women (when ovary isnt able to produce them)

47
Q

what are sex steroids regulators of

A

mood, libido, hair growth, erythropoesis (rbc production), and acne

48
Q

synthesis of androgens is stimulated by

A

ACTH

49
Q

what is the stress axis

A

hypothalamus, anterior pituitary, adrenal cortex

50
Q

what is the response of the SNS to stress activation

A

specific organ responses and increased epinephrine (from the adrenal medulla)

51
Q

what is the specific organ response via the SNS when triggered by stress

A

smooth muscle stimulation and inhibition

52
Q

activation of the stress axis by stress causes

A

increase cortisol secretion (which ultimately increases the availability of fuel)

53
Q

when activated by stress, the SNS response is ____

A

rapid

54
Q

when activated by stress, the stress axis response is _____

A

delayed (bc cortisol can’t be stored and needs to be made)

55
Q

what are the goals of the stress response

A
  1. maintain b.p
  2. mobilize/increase availability of metabolic fuel
  3. inhibit the non-essential fns
56
Q

how is the stress response shut off

A
  1. removal of stressor

2. negative feedback of cortisol on ACTH and CRH

57
Q

what is the SNS response to glycogenolysis (stress response)

A

increases it in hepatic and muscle cells

58
Q

what does the SNS response do to adipose tissue (stress response)

A

increase its breakdown and a source of glycerol for gluconeogenesis

59
Q

what does the SNS response do for fatigue (stress response)

A

decreases muscle fatigue

60
Q

what does the SNS response do for heart rate (stress response)

A

increases it

61
Q

what does the SNS do to blood vessels (stress response)

A

vasoconstriction to smooth muscle, vasodilation in skeletal muscle

62
Q

what does the SNS do to breathing (stress response)

A

increase ventilation

63
Q

what does the SNS do to breathing (stress response)

A

increase ventilation

64
Q

why is cortisol damaging after long periods of chronic stress

A
  • highly catabolic
  • anti inflammatory/immune
  • increase mobilization of lipids in blood—>atherosclerosis and hypertension
65
Q

what is Addison’s disease

A

adrenal insufficiency

66
Q

what are the causes of primary adrenal insufficiency (problem with the gland)

A

disease, congenital, autoimmune

67
Q

what are the causes of primary adrenal insufficiency (problem with the gland)

A

disease, congenital, autoimmune

68
Q

what are the causes of secondary adrenal insufficiency

A
  • pituitary problem (glucocorticoid defect only bc ACTH secreted by the ant pituitary doesn’t effect aldosterone/mineralocorticoid)
  • glucocorticoid therapy (feedback effects on CRH and ACTH)
69
Q

why is there hyperpigmentation due to adrenal insufficiency

A

there is lots of ACTH and its prohormone, POMC. POMC is also the prohormone for MSH (melanocyte stimulating hormone)—>pigmentation

70
Q

what is hypercortisolinemia/cushings disease

A

due to a pituitary tumor (or exogenous glucocorticoid)–> increased ACTH–>elevated bassal [ ]s of cortisol

71
Q

in dental patients, what is the primary concern of cushings disease

A

impairment of the immune system after a procedure

72
Q

in dental patients what is the concern of glucocorticoid therapy/secondary adrenal insufficiency

A

maintaining b.p during anesthesia and diminished immune/inflammatory responses

73
Q

what are the symptoms of adrenal insufficiency

A
  • low cortisol/high ACTH
  • weakness/lethargy/decreased appetite ( bc glucocorticoids not acting as fuel mobilizers)
  • low b.p (low aldosterone)
  • low glc when fasting (low cortisol)
  • hyperpigmentation
74
Q

what are the symptoms of cushings disease

A
  • excessive tissue catabolism (high cortisol)
  • diabetes like symptoms (cortisol blocking insulin)…increased appetite, circulating glc,etc
  • impaired immune
  • hypertension threat

physio fall midterm (12 decks)

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