8 Cortisol Flashcards

1
Q

list the layers of the adrenal gland

A

capsule, zona glomerulosa, zona fasciculata, zona reticularis, adrenal medulla

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2
Q

which layer of the adrenal gland is the largest?

A

cortex (90%)

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3
Q

what is the precursor to the hormones produced in the adrenal gland?

A

cholesterol

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4
Q

are the zones of the adrenal gland able to produce the same hormones?

A

no, the don’t express the same enzymatic machinery

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5
Q

what is the first step of steroidogenesis?

A

conversion of cholesterol to pregnenolone in the mitochondria.

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6
Q

what is the enzyme called that helps shuttle cholesterol from storage into the mitochondria?

A

StAR (Steroid Acute Regulatory Protein)

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7
Q

what are the hormones that can induce cAMP? significance?

A

any protein capable of binding to GPCRs; can lead to StAR expression, thus leading to steroidogenesis

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8
Q

where are the cells located that produce cortisol?

A

zona fasciculata (middle of cortex)

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9
Q

is cortisol stored?

A

no - it’s a steroid (fat soluble) hormone so it’s not stored; it is produced only when necessary

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10
Q

half-life of cortisol?

A

70-120 mins

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11
Q

how is cortisol regulated?

A

converted to inactive cortisone in the liver and excreted in the urine; cortisone can be reactivated by other cell types

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12
Q

functions of cortisol?

A

depends on cell type, eliciting different cellular responses

  • affects liver by stimulating glycogen synthesis
  • stimulates gluconeogenesis
  • increases FA production (similar to diabetic symptoms)
  • anti-inflammatory
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13
Q

negative effects of cortisol?

A

too high concentrations can lead to depression and psychosis, and GI tract uclerations

prolonged exposure can lead to skin thinning or reduced muscle mass

can negatively impact vertical growth

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14
Q

what enzyme is required for the conversion of cortisol to cortisone?

A

11B-HSD type 2

the B is a beta

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15
Q

why is the inactivation of cortisol to cortisone important?

A

cortisol can also interact with aldosterone receptors, which means cells needs to be able to negotiate that. cortisol is also produced at a much higher concentration in compared to aldosterone (the cortex layers is larger).

Aldosterone responsive cells need to nerf cortisol so they can do their main job

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16
Q

what happens when you’re deficient with HSD11B2?

A

you get excess cortisol: interacts with MR (mineralocorticoid receptor) elicits aldosterone-like responses in the cells, called AME (apparent mineralocorticoid excess)

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17
Q

what enzyme does the skin have that affects cortisol?

A

HSD11B1 - inactivates active form

18
Q

how does cortisol function?

A

cortisol, being a steroid, is received by a nuclear receptor called GR (glucocorticoid receptor) - in its inactive form, they’re present in the cytoplasm, not the nucleus. when bound - it can dimerize with another activated GR which an shuttle into the nucleus where the dimer of GR can act as a transcription factor

19
Q

what kind of transcription factor does cortisol act as?

A

depends on cell type

  • muscle cells/adipocytes: increased catabolism
  • liver: increased glycogen synthesis and increased gluconeogenesis
20
Q

compare/contrast cortisol and insulin

A

they’re basically opposites. overall with cortisol, there is increased glucose in the blood while there is increased glycogen storage in the liver

21
Q

how does cortisol have anti-inflammatory function

A

inhibits this response by immune cells; can be used to treat rheumatoid arthritis; can cause atrophy in immune tissues by stimulated apoptosis (lymph nodes)

reduces number of immune cells able to synthesize antibodies

22
Q

concerns with taking cortisol for medication?

A
  • inducing of diabetic-like symptoms
  • increased risk of infection
  • advised not to take long-term
23
Q

list some other effects of cortisol that pertains more to circulation and nervous system

A
  • sensitizes arterioles to action of norepinephrine (hypertension)
  • leads to glycogenolysis, leading to hyperglycemia
  • known to have positive effect on the CNS, something also known as the euphoric steroid
  • interacts with MR, leading to increased fluid in circulation (hypervolemia —> hypertension)
24
Q

what hormone primarily regulates cortisol?

A

ACTH

25
Q

is cortisol capable of negative feedback?

A

yes, at both hypothalamic and pituitary levels

26
Q

does cortisol have diurnal rhythm?

A

yes, because ACTH also does. ACTH concentrations are highest in early morning, which means cortisol’s peak is also during the early morning

27
Q

True or false: release of cortisol is pulsatory

A

true

28
Q

true or false: increased production/release of cortisol is due to increased amplitude, not frequency

A

false - it’s due to increased frequency

29
Q

what stimulus is capable of increasing cortisol production?

A

stress

30
Q

true false: cortisol must be transported with a binding protein

A

true; most of it (75%) is transported with CBG; serum albumin can also be bound to cortisol (15%); the rest is free (10%)

31
Q

what is CBG?

A

Cortisol Binding Globulin: binding protein for cortisol

32
Q

where is CBG synthesized?

A

in the liver

33
Q

is bound or free cortisol activated or inactivated by the liver?

A

free - CBG protects cortisol from being destroyed by already being more water soluble

it is inactivated (cortisone) by making it more water soluble to be excreted by the kidney

34
Q

what happens when there’s too much cortisol? (blood sugar, muscles, skin, immune, blood pressure)

A

Cushing’s syndrome

  • diabetes mellitus (bc of induced hyperglycemia)
  • muscle wasting (bc catabolism of gluconeogenesis)
  • thinning of skin
  • thinning of bones: osteoporosis
  • susceptibility to infection
  • hypertension (bc regulation of permeability of arterioles from acting like aldosterone)
  • production of tumors (can be functional or not; can further increase cortisol production)
35
Q

if a tumor is at the level of the adrenal gland, is production of cortisol reliant on ACTH?

A

no, because these cells are already capable of producing cortisol without ACTH

36
Q

what is Iatrogenic?

A

illness caused by the doctor :(

37
Q

what is the sella turcica?

A

saddle shaped bone that houses the pituitary gland. it can be enlarged due to Cushing’s syndrome

38
Q

what does Cushing’s syndrome do to the back?

A

can cause a buffalo hump

39
Q

what happens when there is too little cortisol?

A

Addison’s disease

  • most often caused by autoimmunity
  • fatigue, weakness, faintness, nausea, vomiting, low blood pressure, salt craving, severe pain in muscles and joints, excessive freckling
40
Q

describe the Addison Crisis Pathway

A

when there is hypofunction of adrenal gland leading to low levels of cortisol, this can lead to defects in liver functions (low concentration of sugar in blood); low levels of cortisol can also reduce enzymes in the GI tract leading to decreased blood sugar. this all affects the brain’s function because of its limited fuel.

treatment must tailor to this cycle; requires continuous monitoring