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Endocrinology > 4.3 Food intake and Adrenal Cortex > Flashcards

4.3 Food intake and Adrenal Cortex Flashcards

1
Q

adrenal gland
- weight?
- situated where?
- _______ glands

A
  • 8-10 g each
  • above and medial to the kidneys
  • paired glands
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2
Q

Adrenal gland
- surrounded by what?
- 2 big parts? (%)
- one of these parts is separated into which 3 zones? which is the thickest?

A
  • by fibrous capsule
  • cortex is about 90% of adrenal mass + inner medulla about 10%
  • cortex has 3 zones:
    1. zona glomerulosa
    2. zona fasciculata (thickest, about 80% of cortex)
    3. zona reticularis
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3
Q

which hormones are produced by which part of the adrenal gland? (4)

A
  1. zona glomerulosa: aldosterone (mineralocorticoid)
  2. zona fasciculata: cortisol, corticosterone (glucocorticoid)
  3. zona reticularis: sex steroids (androgen precursors)
  4. medulla: catecholamines (epinephrine and norepinephrine)
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4
Q

describe pathway for aldosterone synthesis: intermediates + enzymes
- 7 steps

A
  1. cholesterol enters mitochondria using StAR
  2. cholesterol –> pregnenolone, using CYP11A1
  3. pregnenolone –> progesterone, using HSD3B2
  4. progesterone –> 11-deoxycorticosterone, using CYP21A2
  5. 11-deoxycorticosterone –> corticosterone, using CYP11B1 and CYP11B2
  6. corticosterone –> 18-OH-corticosterone, using CYP11B2
  7. 18-OH-corticosterone –> aldosterone, using CYP11B2
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5
Q

describe pathway for cortisone synthesis: intermediates + enzymes
- 7 steps

A
  1. cholesterol enters mitochondria using StAR
  2. cholesterol –> pregnenolone, using CYP11A1
  3. pregnenolone –> 17OH-pregnenolone, using CYP17A1
  4. 17OH-pregnenolone –> 17OH-progesterone, using HSD3B2
  5. 17OH-progesterone –> 11-deoxycortisol, using CYP21A2
  6. 11-deoxycortisol –> cortisol, using CYP11B1
  7. cortisol –> cortisone, using HSD11B2
    OR cortisone –> cortisol, using HSD11B1
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6
Q

describe pathway for testosterone synthesis: intermediates and enzymes

A
  1. cholesterol enters mitochondria using StAR
  2. cholesterol –> pregnenolone, using CYP11A1
  3. pregnenolone –> 17OH-pregnenolone, using CYP17A1
  4. 17OH-pregnenolone –> dehydroepi-anderosterone, using CYP17A1
  5. dehydroepi-anderosterone –> androstenedione, using HSD3B2
  6. androstenedione –> testosterone, using HSD17B
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7
Q

ZONA FASCICULATA
- main steroid produced? __A_____
- is that steroid stored?
- half-life?
- converted to inactive ___B___ and other metabolites where? (for what?) and by other target cells
- can ___B____ be converted to ____A___?

A
  • cortisol! (active form)
  • nope! no cellular storage of cortisol –> produced and secreted
  • 70-120 minutes
  • converted to inactive cortisone and other metabolites by liver (for excretion in urine) and by other target cells (local inactivation of cortisol)
  • in some cells, cortisone can be reconverted to cortisol: reverse activation using HSD11B1
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8
Q
  • how is cortisol transported? (a and b)
  • the BP is synthesized by what and has high/low affinity to cortisol
  • what % of cortisol is bound (a) vs free vs bound to (b)
  • bound cortisol is protected from what? –> consequence?
A
  • by corticosteroid binding globulin (CBG = transcortin) OR albumin
  • by liver and has high affinity for cortisol
  • 75% of cortisol is bound to CBG + 10% is free (can activate receptor) + 15% is bound to serum albumin
  • protected from inactivation by liver –> bound cortisol thus maintains a pool of circulating cortisol by delaying metabolic clearance
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9
Q

how does liver inactivate free steroids?

A

by increasing H2O solubility (?) –> 90% excreted by kidney
- cortisol (active) –> cortisone (inactive) , using HSD11B2
- cortisone –> cortisol, using HSD11B1

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10
Q
  • what is the receptor for cortisol?
  • how is the receptor synthesized ish? how many isoforms? same or opposite actions?
  • what happens when cortisol binds to its receptor (2)
A
  • glucocorticoid receptor (NR3C1) –> called like this bc 1st fct of cortisol understood was its action on increasing blood glucose levels
  • 1 gene –> alternative splicing gives rise to 2 isoforms (GRb and GRa) –> opposite actions: GRb inhibits GRa
  • ligand binding translocates GR into nucleus –> binds to glucocorticoid response element (GRE) on promoters of target genes
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11
Q
  • cortisol can bind to its receptor (glucocorticoid receptor) but can also bind to what? –> consequence?
  • plasma concentration of cortisol is ____-______ fold higher than concentration of _____a_____
  • therefore _____a_____ responsive cells have to do what?
A
  • can also bind to mineralocorticoid receptor (MR, NR3C2)
  • at high concentrations, cortisol interact with MR leading to aldosterone-like symptoms –> hypertension, hypokalemia, low renin and low aldosterone levels
  • 100-1000fold higher than [aldosterone] (bc zone fasciculata is much bigger than zone glomerulosa)
  • aldosterone responsive cells have to inactivate cortisol in order to respond specifically to aldosterone
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12
Q

what causes apparent mineralocorticoid excess? (AME)

A

enzyme deficiency of HSD11B2 (cortisol (active) to cortisone (inactive)) increases plasma cortisol leading to AME syndrome

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13
Q

effect of cortisol on
- liver (2)
- smooth muscle (3)
- pancreas (3)
- white adipose tissue (2)

A

LIVER:
- increase gluconeogenesis (to increase blood glucose)
- increase glycogen storage
SMOOTH MUSCLE:
- decrease glucose uptake/oxidation
- decrease glycogen storage
- increase protein catabolism = increase aa precursor availability for gluconeogenesis
PANCREAS:
- inhibit insulin secretion (b cells)
- inhibit glucagon secretion (a cells)
- increase b cell hyperplasia
WHITE ADIPOSE:
- inhibit glucose uptake/oxidation
- increase lipolysis –> provide glycerol for gluconeogenesis in liver

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14
Q

cortisol
- general effects are opposite to effects of which hormone? and similar to which hormone? at the expense of (2)
- acts by increasing what?
- imparts _______ resistance in metabolic tissues like (2) by doing what?

A
  • opposite to insulin, similar to GH (increase blood glucose!) at the expanse of protein and fat
  • increasing transcription of specific genes via GR
  • imparts insulin resistance by metabolic tissues like muscle and adipose tissue by inhibiting glucose uptake (+ provides precursor for gluconeogenesis in liver)
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15
Q
  • how is cortisol an anti-inflammatory? (3 ish) –> patients thus become susceptible to what?
  • what is used as a topical anti-inflammatory treatment?
A
  • cortisol inhibits immune response –> decreases number of lymphocytes and antibody production
    *anti-inflammatory used to treat rheumatoid arthritis and other immune disorders
  • patients thus become susceptible to infections (bc immune cells are inhibited)
  • hydrocortisone cream –> local anti-inflammatory treatment –> skin has HSD11B1 to activate cortisone to cortisol
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16
Q
  • what is the major protein in immune signaling pathways? (aka most studied pro-inflammatory transcription factor)
  • GR inhibits inflammation by 3 mechanisms
A
  • NF-kappa B
    1. with coactivators C-fos/C-jun, cortisol activates inhibitor I-kappaB of the immune response TF NFkappaB = inhibit NF-kB
    2. GR-cortisol binds and inhibits NFkB transactivation of inflammatory genes –> so NFkB can’t bind to target gene
    3. GR competes with NFkB for other interacting transcription factors/for binding to promoter of genes
17
Q

appart from effects on metabolism (liver, adipose, muscle, pancreas) and anti-inflammatory effects, what are 5 other effects of cortisol?

A
  1. sensitizes arterioles to action of norepinephrine –> results in hypertension
  2. permissive effect on action of norepinephrine on CHO metabolism (glycogenolysis –> results in hyperglycemia)
  3. increased activity of central nervous system –> result in euphoira/happiness
  4. can act as mineralocorticoid (increase of extracellular fluid) bc it interacts with mineralocorticoid receptor (MR)
    (5. enhances digestive enzymes by action on pancreas + stomach/intestine epithelial cells)
18
Q

what is the overall main function of cortisol?
+ another important function

A

OVERALL: enhance glucose concentration in circulation by impacting glucose metabolism
OTHER: anti-inflammatory function

19
Q
  • what is the Cushing’s syndrome?
  • 4 causes of spontaneous Cushing’s disease?
    + another cause?
A
  • overproduction of cortisol!
    1. CRH producing tumor
    2. ACTH producing tumor (pituitary tumor)
    3. lack of feedback control by cortisol at the pituitary level
    4. cortisol producing adrenal tumor (function, can maintain gland function)
    + latrogenic cause (hospital driven) –> most common cause resulting from chronic glucocorticoid therapy (causing high cortisol levels)
20
Q

6 symptoms of Cushing’s syndrome

A
  1. diabetes mellitus from high blood glucose –> increase gluconeogenesis
  2. muscle wasting –> increased protein catabolism (to provide precursors for gluconeogenesis) –> thinning of limbs
  3. increased and redistribution of adipose tissue: central obesity, round/moon face, buffalo hump (fat accumulation on upper back), thin limbs
  4. susceptibility to infection (from decreased immune cells/response bc of anti-inflammatory actions)
  5. Na retention and hypertention –> Apparent mineralocorticoid excess
  6. low ACTH if primary hypercortisolism
21
Q

Cushing’s syndrome
- main treatment?
- thus, would require what?
- what are 3 other treatments ish

A
  • treatment is aimed at removing the cause of hypersecretion without permanently damaging the adrenal or pituitary
  • would require life long replacement therapy
  • microsurgery + various forms of radiation therapy + pharmacologic inhibition of ACTH secretion
22
Q
  • what is Addison disease?
  • most common cause?
  • 6 symptoms
A
  • adrenal hypofunction
  • most commonly due to destruction of adrenal gland by autoimmune response
    1. fatigue, weakness, faintness, nausea
    2. vomiting
    3. low BP
    4. salt craving (associated with cross rxn with mineralocorticoid)
    5. pain in muscles and joints
    6. excessive freckling (low cortisol = low neg. feedback to pit. = increase ACTH = release of MSH as part of opiomelanocortin = freckling)
23
Q

describe the addison crisis pathway
*how to overcome the crisis?

A
  • adrenal gland not functioning! –> leads to 2 pathways:
    1. cortisol very low or absent:
    a) liver function decreases, decrease in gluconeogenesis –> low sugar –> extremely low sugar –> brain: coma and death
    b) stomach digestive enzymes decrease –> abnormal digestion –> vomiting, diarrhea, cramps –> low fluid volume –> shock –> brain: coma and death
    2. aldosterone very low of absent –> kidney: water & sodium loss: leads to:
    a) low fluid volume –> shock –> brain: coma and death
    b) heart irregular and output decreases –> low blood pressure –> shock –> brain: coma and death

*the sooner you can use injectable and receive IV fluids, the sooner you can halt the progress of the crisis

Endocrinology (14 decks)

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