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endocrinology > Adrenal gland > Flashcards

Adrenal gland Flashcards

1
Q

Location of adrenal gland

A

located above the kidneys

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2
Q

what are two regions of adrenal gland

A

cortex and medulla

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3
Q

adrenal cortex

A
  • most of the weight 90%

- derived from mesodermal

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4
Q

adrenal medulla

A
  • derived from subpopulation of neural crest cells
  • **NE and E comes from crest cells which are neurotrasnsmitters too. They are part of the post ganglion of sympathetic nervous system
  • remaining 10% of mass
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5
Q

3 zones of cortex

A

1) zona glomerulosa outer
2) zona fasciculata middle
3) zona reticularis inner

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6
Q

zona glonerulosa

A

outer region

  • where aldosterone comes from
  • abundant of smooth ER because it produces steroid
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7
Q

zona fasciulata

A
  • middle region
  • look like chords
  • produce glucocorticoids, cortisol, corticosterone, and the androgens (DHEA and DHEA sulfate)
  • has lipid droplets
  • ACTH
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8
Q

zona reticularis

A
  • inner region
  • develops postnatally
  • recognizable at 3 years
  • also produces glucocorticoids and androgens
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9
Q

Hormones of cortex

A

the cortex synthesizes the adrenal steroid hormones reasponse to hypothalamic-pituitary adrenal hormome stimulation

  • derivied from chloesterol
  • glucocorotioids, mineralcocorticoids, and androgens (cortisone, aldosterone)
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10
Q

Hormones of medulla

A
  • synthesizes catecholamines in response to direct sympathetic stimulation
  • derived from L-tyrosine
  • epinephrine and norepinenphrine
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11
Q

blood supply of adrenal glands

A

Blood flows from outer to go inner through sinusoid system (type of cappillary, which are made of endothelial cells, that have spaces in between for larger proteins to go into venous system)

  • Blood supply to the adrenal glands from the superior, middle, and inferior suprarenal arteries.
  • form a capillary network arranged so that blood flows from the outer cortex toward the center area, following a radially oriented sinusoid system.
  • direction of blood flow controls the access of steroid hormones to the circulation and concentrates the steroid hormones at the core of the adrenals,
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12
Q

sinusoid are also found in

A
  • liver: because of albumin

- bone marrow: because of RBC and WBC

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13
Q

acute regulation

A
  • one way of stimulating production

- results in the rapid production of steroirds in repsonse to immediate need and occurs within minutes of the stimulus

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14
Q

chronic stimualtion

A
  • such as that which occurs durrong prolonged starvation and chronic disease
  • involed the synthesis of enzymes involved in steroidogenesis to enhance the synthetic capacity of the cells.
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15
Q

hypothalamic-pituitary adrenal axis

glucocorticoid synthesis and release part 1

A
  • the pulsate release of cortisol us under direct stimulation by adrenocoritocoptrop hormones (ACTH) released from anterior pituitary
  • aldosterone and or cortisol is then released
  • cortisol release follows circadian rhythm
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16
Q

hypothalamic-pituitary adrenal axis

glucocorticoid synthesis and release part 2

A
  • CRH is repsonse to stress is released at medien eminance. picked up by the primary plexus of hypohyseal protal system travels to anterior pit. coritcotrrophs pick up the signals in anterior pit. They increase cyclin andenosine (coupled to alpha s)
  • ACTH is released and targets adrenal cortex zona fascilualta and glomaerosa.
  • increase in adenate cyclate which is g protein alpha s involved

products:
increase in cholesterol availibility for hormone synthesis
increase synthesis of STAR, enzyme involved in the transport of cholesterol into the inner mitochondrial membrane.

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17
Q

cortisol is

A

lyphophilic - mostly insoluable in water

  • found in conjugared form
  • bound to carrier proteins
  • inactived and eliminated in liver and kidney
  • liver generates more soluable form leading to easier excretion
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18
Q

11β-hydroxysteroid dehydrogenase type I

A
  • enzyme
  • type 1 amplifiy cortisol activity

converts cortisone back to its active form cortisol
expressed in liver, adipose tissue, lung, skeletal muscle, vascular smooth muscle, gonads, and the central nervous system.

Amplifies glucocorticoid action

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19
Q

11β-hydroxysteroid dehydrogenase type II

A
  • enzyme
  • in areas where aldosterone is needed active
  • *kidneys
  • contributes to mineralcorticoid hormone effects
  • converts cortisol in into cortisone, its less active metabolite

-decreases glucocorticoid action

20
Q

renin-angiotensinn aldosterone system

A

Decrease in plasma volume –> renin is released becuase it is sensed by cells of nephon
renin cleaves (CUT) angiotensingen into angiotesnsion I
ACE enzyme that cleaves angiotension 1 to 2
angiotension 2 targets adrenal cortex
in response aldosterone is produces
aldosterone effects: targeting collecting ducts, increase NA+ absorption, increase K+ absorption,
which increases plasma volume/ blood pressure

angiotension2 also produces vasal constriction

look at slide 15

21
Q

what else triggers aldosterone production

A

Potassium- also a major physiologic stimulus for aldosterone production, (classic example ofhormone regulation by the ion it controls)

Aldosterone is critical in maintaining potassium homeostasis by increasing K+excretion in urine, feces, sweat, and saliva, preventing hyperkalemia during periods of high K+intake or after K+release from skeletal muscle during strenuous exercise.

In turn, elevations in circulating K+ concentrations stimulate the release of aldosterone from the adrenal cortex.

too much potassium trigers aldosterone which will get rid of it

22
Q

how are mineralcorotiocuds metabolized

A

Circulating levels much lower than glucocorticoids- Secretion can be increased 2- to 6-fold by sodium depletion or by a decrease in the effective circulating blood volume, such as occurs with ascites.

Binding of aldosterone to plasma proteins is minimal, resulting in a short plasma half-life of approximately 15–20 minutes.

Aldosterone is metabolized in the liver to tetrahydroglucuronide derivative and excreted in the urine.

23
Q

adrenal androgens

A

produced by zona reticularis including DHEA and DHEAS

DHEA is the most abundant circulatinghormone in the body and is readily conjugated to its sulfate ester DHEAS.

Production of DHEA is controlled byACTH.

24
Q

metabolism of adrenal androgens

A

The adrenal androgens are converted into androstenedione and then into potent androgens orestrogensin peripheral tissues.

25
Q

Adrenal secretion of DHEA and DHEAS:

A

increases in children at the age of 6–8 years
circulating DHEAS peak between the ages of 20 and 30 years.
Decrease with age not paralleled by a similar decrease inACTH orcortisol release

26
Q

genomic cellular effects

A

binding to intracellular receptor that operate as ligand-activated transcription factors to regulate gene expression

27
Q

nongenomic cellular effects

A
  • either activate or suppress transcription of genes
  • effects that are not mediated by the receptors

such as the rapid steroid effects on the electrical activity of nerve cells or the interaction of steroid hormones with the receptor for. y-aminobutyric acid. requires continued presence of the hormone and occurs more quickly because they do not require synthesis of proteins

28
Q

how does genomic activity works

A

-hormone binds to receptor in the cytosol –> release of heat shock protein or another regulatory protein –> the receptor hormone complex activates and translocates to nucleus –> bind to HRE in DNA –> increase or decrease gene transcription

29
Q

????

A

both receptors bind GC and MC

cortisol is more abundant

30
Q

Steroid hormone receptors

A
  • Mineralocorticoids (MC) (aldosterone) and glucocorticoid (GC) (cortisol) receptors share 57% homology in the ligand-binding domain and 94% homology in the DNA-binding domain.
  • Once GC and MC bind to intracellular receptors, these dimerize prior to nuclear translocation and binding to DNA GC- or MC-responsive elements increasing or suppressing transcription of specific genes.
  • Cortisol binds with high affinity to the MReceptors (aldosterone receptor) and can produce MC-like effects (sodium retention).
  • Cortisol conversion tocortisone (CS) decreases the affinity for the MR receptor
  • Decreased activity of the 11β-HSD2 leads to decreased conversion of cortisol to cortisone and increased MC activity.
31
Q

Physiologic Effects of Glucocorticoids

A

Metabolism, hemodynamic, immune function, central nervous system

32
Q

Metabolism effect

A

Degrades muscle protein and increases nitrogen excretion
Increases gluconeogenesis and plasmaglucose levels
Increases hepatic glycogen synthesis
Decreasesglucose utilization (anti-insulin action)
Decreasesamino acid utilization
Increases fat mobilization
Redistributes fat
Permissive effects onglucagon (raises blood glucose) and catecholamine (E,NE, DA) effects

33
Q

Hemodynamic effect

A

Maintains vascular integrity and reactivity
Maintains responsiveness to catecholamine pressor effects
Maintains fluid volume

34
Q

Immune function effect

A

-glucocorticoids is anti-inflammatory
Increases antiinflammatory cytokine production
Decreases proinflammatory cytokine production
Decreases inflammation by inhibitingprostaglandin and leukotriene production
Inhibits bradykinin and serotonin inflammatory effects
Decreases circulating eosinophil, basophil, and lymphocyte counts (redistribution effect)
Impairs cell-mediated immunity
Increases neutrophil, platelet, and red blood cell counts

35
Q

CNS effect

A

Modulates perception and emotion

Decreases CRH andACTH release

36
Q

Physical Effects of Mineralocoritocids

A

aldosterone regulates mineral ((sodium and potassium) balance - specifically renal potassium excretion and sodium reabsorption.

37
Q

aldosterone effect

A

Aldosterone diffuses across the plasma membrane and binds to its cytosolic receptor.
The receptor-hormone complex is translocated to the nucleus where it interacts with the promoter region of target genes, activating or repressing their transcriptional activity producing an increase in transepithelial Na+transport.
Aldosterone increases Na+entry at the apical membrane of the cells of the distal nephron through theamiloride-sensitive epithelial Na+channel (ENaC).
Aldosterone promotes potassium excretion through its effects on Na+/K+-adenosine triphosphatase (ATPase) and epithelial Na+and K+channels in collecting-duct cells.
Additional effects of aldosterone on intercalated cells leads to increased activation of the H-ATPase and Cl/HCO3exchanger.

38
Q

Physiological effects of androgens

A

The physiologic effects of DHEA and DHEAS are not completely understood.

In females adrenal androgens may contribute to libido.

Current knowledge indicates that low levels of DHEA are associated with cardiovascular disease in men and with an increased risk of premenopausal breast and ovarian cancer in women.

High levels of DHEA might increase the risk of postmenopausal breast cancer.

Exogenous administration of DHEA to the elderly increases severalhormone levels, including insulin-likegrowth factor 1,testosterone, dihydrotestosterone, andestradiol.

39
Q

hormones of adrenal medulla

A

The catecholaminesepinephrine(Epi) andnorepinephrine (Norepi) are synthesized in chromaffin cells in the adrenal medulla in response to acetylcholine (Ach) release from preganglionic neurons of the sympathetic nervous system.

40
Q

how hormones of adrenal medulla synthesize from tyrosine

A

Catecholamine synthesis from the precursorL-tyrosine involves 4 enzymatic reactions that take place in the cytosol of chromaffin cells.

1) hydroxylation of tyrosine to 3,4-dihydroxyphenylalanine (L-dopa) bytyrosine hydroxylase (TH),
2) decarboxylation ofL-dopa to dopamine bydopa decarboxylase,
3) hydroxylation of dopamine to norepinephrine bydopamine β-hydroxylase
4) methylation of norepinephrine toepinephrinebyphenylethanolamine N-methyltransferase (PNMT).

41
Q

The release of catecholamines

A

The release of catecholamines is a direct response to sympathetic nerve stimulation of the adrenal medulla

The adrenal medulla is considered a modified post-ganglionic neuron of the sympathetic nervous system

42
Q

Catecholamine Transport and Metabolism



A

The half-life of circulating catecholamines is short (<2 minutes).

Most (>50%) of the catecholamines released circulate bound toalbumin with low affinity.

Metabolic inactivation

  1. COMT—catechol-amine-O-methylase
    a. Extracellular
    b. Reduces concentration of catecholamines in synapse
    i. Effects mediated by catecholamines are decreased
  2. MAO—monoamine oxidase
    a. Intracellular
    b. Reduces concentration of catecholamines in cells
    i. Decreases exocytosis of NE and E
43
Q

how do catecholamine work at target organ

A

The physiologic effects of catecholamines are mediated by binding to cell membrane G protein–coupled adrenergic receptors distributed widely throughout the body (do not cross blood-brain-barrier).

  • differential effects depending on the subtype of G protein to which the receptor is associated with and the signal transduction mechanism linked to that specific G protein
44
Q

epinephrine is also known as

A

adrenaline

45
Q

G protein–coupled adrenergic receptors 

classified as

A

predominantly stimulatory receptors (α)
predominantly inhibitory receptors (β)

a1. a2
b1. b2.b3

46
Q

Adrenergic Receptors




A

Alpha -greater affinity forepinephrinethan for norepinephrine
-subdivided into α1- and α2-receptors

-Beta - subclassified as β1, β2, and β3receptors.

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endocrinology (4 decks)

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