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Endo/Repro I Exam 1 > Lecture 11: The Adrenal Gland > Flashcards

Lecture 11: The Adrenal Gland Flashcards

1
Q

What are the embryological orgins of the adrenal cortex and medulla?

A

Adrenal cortex = epidermal origin

Adrenal medulla = ectodermal origin

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2
Q

Adrenal cortex releases what classes of hormones?

A

Corticoids and androgens

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3
Q

Adrenal medulla releases what class of hormones?

A

Catecholamines

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4
Q

What is released by the Zona glomerulosa, fasciculata, reticularis and adrenal medulla?

A

Zona Glomerulosa: Minearlocorticoid (aldosterone)

Zona Fasciculata: Glucocorticoids (cortisol)

Zona Reticularis: Androgens

Adrenal Medulla: Catecholamines (E and NE)

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5
Q

What are the 3 kinds of hormones produced in the adrenal cortex?

A
  1. Glucocorticoids - Cortisol
  2. Mineralocorticoids - Aldosterone
  3. Sex steoids - DHEA and DHEAS
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6
Q

Most common adrenal enzyme deficiency and what hormone levels are affected; how do we treat?

A
  • 21 Hydroxylase deficiency
  • Decreased cortisol
  • Decreased mineralocorticoid
  • Increased sex hormones
  • Treatment involves replacing glucocorticoids and mineralocorticoids
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7
Q

What are the signs and symptoms of 21-hydroxylase deficiency?

A
  • Hypotension (decreased aldosterone)
  • Sodium and volume loss
  • Hyperkalemia
  • Elevated renin
  • Female: virilization of fetus and sexual ambiguity at birth
  • Male: phenotypically normal, precocious pseudo-puberty, premature epiphyseal plate closure
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8
Q

What is seen in 11β-Hydroxylase deficiency?

A
  • Increased androgens
  • Virilization of female fetuses
  • Increased 11-deoxycorticosterone
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9
Q

Signs and symptoms of 11 β-Hydroxylase deficiency?

A
  • Hypertension
  • Hypokalemia
  • Suppressed renin secretion
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10
Q

What is seen in 17 α-Hydroxylase deficiency; when are these patients diagnosed?

A
  • Decreased androgens and cortisol
  • Excess mineralocorticoids
  • Patients diagnosed at time of puberty
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11
Q

What are the signs and symptoms of 17-α-Hydroxylase deficiency?

A
  • Hypertension
  • Hypokalemia
  • Hypogonadism
  • Males: undescended tests
  • Females: lack of secondary sexual development
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12
Q

What are the target tissues of Cortisol; what 2 ways can it act?

A
  • Tissues throughout the body
  • Glucocorticoid Response Element (GRE)

- Non-genomic actions (endocannabinoids)

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13
Q

What are some of the effects of cortisol on the liver, muscle, fat, cutaneous, immune system, endocrine, and GI?

A

Liver: increased gluconeogensis

Muscle: breakdown of muscle protein

Fat: promote lipolysis in extremities, central fat deposition

Cutaneous: skin thins, fragile blood vessels

Immune system = immune suppression

Endocrine = insulin resistance or glucose intolerance

GI = interferes w/ calcium absorption (risk of osteporosis)

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14
Q

How is cortisol regulated?

A
  • Begins w/ CRF (CRH) in hypothalamus released from PVN
  • Binds CRF1 receptor (GPCR)
  • Sitmulates release of ACTH from anterior pituitary
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15
Q

What are some things that can stimulate the release of CRH from the hypothalamus?

A
  • Low cortisol
  • Stressors (hypoglycemia, hypotensions, fever, trauma, surgery)
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16
Q

What is the principle hormone that stimulates the adrenal glucocorticoids; derived from and produced where?

A
  • ACTH
  • Derived from POMC
  • Contains MSH (melanocyte stimulating hormone) activity
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17
Q

What does excess ACTH commonly lead to?

A

Hyperpigmentation due to its MSH activity

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18
Q

What is the long loop, short loop, and ultrashort loop as it pertains to CRH activity and feedback?

A

Long loop: cortisol from adrenal gland inhibiting release of CRH from hypothalamus

Short loop: ACTH from anterior pituitary inhibiting CRH release from hypothalamus

Ultrashort: CRH activity in hypothalamus inhibiting CRH release

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19
Q

What is the rhythm of ACTH and cortisol release like; when do we see peaks?

A
  • Cortisol levels are highest around 8am, and then gradually trail off for rest of day, peak again around 2pm and then 7pm, low in the late evening
  • ACTH levels will peak just before this since it’s needed to stimulate production of cortisol
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20
Q

Discuss the negative feedback by glucocorticoids onto CRH and ACTH?

A
  • GC’s inhbit POMC transcription
  • GC’s inhbit mRNA synthesis of CRH and ACTH
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21
Q

What is the Dexamethasone suppression test (DST); discuss findings at low and high doses?

A
  1. Low dose DST (cortisol analog)
    - Determines if there is problem
    - Usually overnight
    - Pt is administered a supraphysiologic dose
    - Normal response: suppression of ACTH and cortisol secretion

- Cushing: no suppression

2. High dose DST (cortisol analog)

  • Helps determine the source of the problem (pituitary vs. adrenal Cushing)
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22
Q

What is the Cosyntropin and how is it used; describe the test?

A
  • Synthetic ACTH used in stimulation test (CST) for adrenal gland insufficiency
  • *Step 1:** Administer Cosyntropin (ACTH)
  • In healthy individuals, cortisol should increase from baseline
  • If adrenals unresponsive and cortisol remains the same or rises only small amount, consider adrenal insufficiency
  • If adrenals respond dramatically and cortisol increases substantially, consider secondary adrenal insufficiency
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23
Q

What is Cushing Syndrome?

A
  • Hypersecretion of Cortisol
  • Usually an adrenal neoplasm
  • Elevated cortisol but low ACTH
  • An adrenal problem (primary endocrine disorder)
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24
Q

What is Cushing Disease?

A
  • Hypersecretion of ACTH
  • Usually a pituitary gland tumor
  • Overstimulates the adrenal cortex and excess cortisol secreted
  • High serum ACTH and high cortisol
  • A pituitary problem (secondary endocrine disorder)
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25
Q

If a patient with Cushing Syndrome was injected w/ exogenous glucocorticoids (dexamethasone), what do you predict would happen to their ACTH levels and cortisol suppression; WHY?

A
  • ACTH levels would be undetectable and dexamethasone fails to suppress cortisol secretion
  • Negative feedback loop itself is functional yet hypercortisolism continues (an adrenal problem)
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26
Q

If a patient with Cushing Disease was injected w/ exogenous glucocorticoids (dexamethasone), what do you predict would happen to their ACTH levels?

A
  • ACTH would be supressed
  • Abnormal negative feedback at level of pituitary
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27
Q

What are some of the signs and symptoms seen in patients with Hypercortisolism?

A
  • “Moon face”
  • Hirsutism
  • Bruising
  • Abdominal adiposity
  • Stretch marks
  • “Buffalo hump”
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28
Q

What is Addison disease?

A
  • Primary adrenal insufficiency
  • Chronic progressive destruction of adrenal gland
  • High ACTH but low cortisol
  • Adrenal response is blocked from the signal
  • Adrenal problem = not making cortisol
  • Cortisol levels will be low so the hypothalamus will be secreting a lot of CRH stimualting the pituitary to make ACTH, but the high levels of ACTH won’t be able to have any effect.
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29
Q

What is Secondary adrenal insufficiency?

A
  • Caused by exogneous glucocorticoid administration
  • ACTH deficiency
  • Low ACTH and low cortisol
  • A pituitary problem
30
Q

If a patient with Addison disease is injected w/ synthetic ACTH (cosyntropin), what do you predict would happen to their plasma cortisol levels?

A

No change since the adrenals can’t respond to ACTH

31
Q

If a patient with secondary adrenal insufficiency is injected w/ synthetic ACTH (cosyntropin), what do you predict would happen to their plasma cortisol levels?

A

They will increase, since the problem in these patients is a lack of ACTH being produced by the pituitary gland

32
Q

Addison disease can be caused by?

A
  1. Autoimmune disease of adrenal gland
  2. Adrenal hemorrhage
    * - Secondary to infection (i.e., N. meningitidis)*
    * - Secondary to anticoagulant tx*
  3. Infection
    * - Tuberculosis*
    * - N. meningitdis –> Waterhouse-Friedrichsen Syndrome*
  4. Tumor
33
Q

What is seen in Addison diease in regards to cortisol and adrenal steroid secretion?

A
  • Hypocortisolism
  • Hyposecretion of ALL adrenal steroids
34
Q

What are some of the signs and symptoms seen in Addison disease?

A
  • Hyperpigmentation
  • Weight loss
  • Muscle weakness
  • Hypoglycemia
  • Hypotension
  • Hyponatremia and hyperkalemia (due to loss of aldosterone!!!)
35
Q

What are the actions of aldosterone; where does it act; what are the net results of its effect?

A
  • Principle mineralocorticoid controlling Na+ and K+ exchange in distal nephron
  • Increases synthesis and acitivity of Na+ channels in apical membrane
  • Increases the synthesis and activitiy of Na+-K+ ATPase in the basolateral membrane of the distal tubule
  • Overall result = increase Na+ reabsorption and an increase in K+ excretion and H+ excretion
36
Q

What is the affinity of the mineralocorticoid receptor for aldosterone and glucocorticoids; what system do we have in place to keep the system running smoothly and the key players involved?

A
  • Equal affinities
  • Cortisol-cortisone shunt
  • 11β-HSD2 metabolizes cortisol to cortisone (inactive form)
  • Protects the MR from cortisol binding and keeps it available for aldosterone
37
Q

What can glycyrrhizic acid (licorice) cause; when else are these effect seen?

A
  • Inhibits 11β-HSD2
  • Cortisol will have increased access to MR
  • MR is overwhelmed by cortisol, especially in hypercortisolemic conditions (like Cushings)
38
Q

What is Conn Syndrome?

A
  • Hypersecretion of Aldosterone
  • Usually an adrenal neoplasm
  • Adrenal problem (primary hyperaldosteronism)
39
Q

What is Secondary Hyperaldosteronism?

A

- Hypersecretion of Renin

  • Excess renin from juxtaglomerular cells of the kidney
  • A kidney problem
40
Q

What is Primary Hypoaldosteronism?

A
  • Hyposecretion of aldosterone
  • Destruction of adrenal cortex (Zona Glomerulosa)
  • Defects in aldosterone synthesis
  • An adrenal problem
41
Q

What is Secondary Hypoaldosteronism?

A
  • Hyposecretion of renin
  • Deficient renin from juxtaglomerular cells of the kidney
  • Inadequate stimulation of aldosterone
  • A kidney problem
42
Q

How does primary adrenal failure affects cortisol and aldosterone in comparison to an ACTH deficiency?

A

Primary adrenal failure —> deficient cortisol AND aldosterone

ACTH deficiency –> cortisol deficiency but NO change in aldosterone

*Effect of ACTH on aldosterone secretion is modest at best

43
Q

What are the adrenal androgens; what do they rely on for activity?

A
  • DHEA and DHEAS
  • Precursors to human sex steroids
  • Relies on 3β-HSD to extert androgenic or estrogenic activities
44
Q

What is seen in female patients with adrenal carcinomas that secrete androgens?

A
  • Females may feature: virilization, hirsutism, clitoromegaly, breast atrophy, deepening of voice, temporal recession, severe acne
45
Q

Where are the catecholamines produced and from what pre-cursor?

A
  • The adrenal medulla
  • From L-Tyrosine
46
Q

What is the enzyme involved in the rate limiting step of L-tyrosine to Epinephrine; what modulates this reaction; where does it occur?

A
  • Tyrosine hydroxylase
  • Controlled by sympathetic stimulation, upon ACh binding nAChRs
  • The cytosol of Adrenal Medulla cells
47
Q

Once dopamine is produced in the Adrenal medulla cells what occurs?

A

Stored in special secretory vesicles called “chromaffin granules” and converted to NE

48
Q

What increases the synthesis of tyrosine hydroxylase and activity of dopamine β-hydroxylase?

A

Nicotinic receptor cell signaling upon binding of ACh from SNS

49
Q

Upon stimulation by cortisol what occurs to the NE stored in chromaffin granules of the adrenal medulla?

A
  • NE diffuses out of the granules via the VMAT and into the cytosol where it’s converted by Phenylethanolamine N-methyltransferase (PNMT) to epinephrine
  • Epinephrine then goes back into chromaffin granule via VMAT and is stored in a different storage vesicle until sympathetic stimulation causes exocytosis
50
Q

What are Chromogranin’s; where are they found and what are the contents?

A
  • Chromogranins play a role in the biogenesis of secretory vesicles and the organization of components within the vesicles.
  • Found within the Chromaffin granules with Epinephirne, some NE, Ca2+ and ATP
51
Q

Cortisol induces the expression of which adrenomedullary cell enzyme?

A
  • Phenylethanolamine-N-methyltransferase (PNMT)
  • Enzyme that converts NE to epinephrine
52
Q

What is monoamie oxidase (MAO); where is it found; why are they a clinically relevant drug targerts?

A
  • Oxidizes catecholamines for metabolism
  • Found in the CNS and peripheal tissues
  • MAOI’s are used to treat neuropsychiatric disorders
53
Q

What is catechol-O-methyltransferase (COMT); where is it found; what is its function?

A
  • Methylates catecholamines
  • Found in the CNS and peripheral tissues
  • Primary enzyme that inactivates catecholamines released from the adrenal gland
54
Q

What can be measured to determine catecholamine production?

A
  • Measuring of the breakdown products
  • Catecholamines, metanephrines, and vanillylmandelic acid (VMA)
55
Q

What is a Pheochromocytoma and what are the symptoms?

A
  • Tumors of the chromaffin tissue, produce excess catecholamines

Symptoms wax and wane:

- HTN

  • Orthostatic HTN

- Sweating

- Palpitations

- Chest pain

- Flushing

- Anxiety

56
Q

What is the short-term stress response pathway?

A
  • Stress causes nerve impulses to travel to spinal cord and then to adrenal medulla via pre-ganglionic sympathetic fibers, which stimulate the adrenal medulla to secrete catecholamines
  • Increase HR, BP, bronchiole dialation, liver glycogenolysis, reduced GI activity, and increased metabolic rate
57
Q

What is the prolonged stress pathway?

A
  • Stress triggers hypothalamus to release CRH leading to increases ACTH from pituitary
  • ACTH stimulates the production of mineralocorticoids and glucocorticoids from the adrenal cortex
  • Mineralocorticoids contribute to retention of Na+ and H2O by kidneys, and increased BV and BP
  • Glucocorticoids contribute to gluconeogenesis of proteins and fats, increased blood glucose, and immune system supression
58
Q

What are exogenous glucocorticoids and what effect do they have?

A
  • Cortisone, prednison, methylprednisone, dexamethasone
  • May shut down ACTH production and adrenal cells that produce cortisol (atrophy)
  • Exogenous glucocorticoids will mimic cortisols actions; symptoms of excess (latrogenic = illness caused by medication)
  • CRH. ACTH, and cortisol will all be decreased
59
Q

What are the aldosterone levels like in a patient with secondary/tertiary adrenal insufficiency?

A
  • Even though ACTH does have a small role in the release of aldosterone, the levels will not be affected.
  • Increased K+ levels and Angiotensin II levels play a larger role in the synthesis and secretion of aldosterone
  • RAAS has a MUCH greater effect!
60
Q

Where is epinephrine vs. norepinephrine synthesized?

A
  • NE is synthesized inside the chromaffin granules by DBH

- Epinephrine is synthesized inside the cytosol by PNMT

61
Q

Which receptor type responds equally to NE and E?

A

β1 receptor

62
Q

What catecholamine do the α receptors and β3 respond better to?

A

Respond better to NE than E

63
Q

Epinephrine is more potent than NE for which type of receptor; what response does this receptor mediate?

A
  • β2 receptors
  • Increase hepatic glucose output; decrease contraction of blood vessesl, bronchioles, and uterus
64
Q

Where are β3 receptors found and what are some effects produced?

A
  • Liver; adipose tissue
  • Increase hepatic glucose output; increase lipolysis
65
Q

Where are α2 receptors found and what are effects produced by them?

A
  • Sympathetic presynaptic nerve terminals; beta cells of pancreatic islets
  • Inhibit NE release; inhibit insulin release
66
Q

What is the high dose dexamethasone test used to differentiate?

A
  • Distinguish those w/ Cushing Disease vs. someone with an ectopic ACTH secreting tumor (i.e., lungs)
  • High dose will suppress ACTH in Cushing disease (adrenals), but will have no effect on an ectopic source
67
Q

What pathology is shown by this axis?

A

Addison Disease

68
Q

What pathology is shown here?

A

Cushing Disease

69
Q

Pt presents w/ HTN and Hypokalemia, the plasma aldosterone concentration is increased, while plasma renin concentraton is decresed, what should you suspect?

A

Primary aldosteronism (Conn’s syndrome)

70
Q

All congenital adrenal enzymes deficiencies are characterized by an enlargement of what? Due to?

A
  • Enlargement of Adrenal glands
  • Due to increased ACTH caused by low cortisol negatively feeding back to try and increase the levels
71
Q

What stimulates the synthesis of DOPA?

A
  • ACTH and Symptahtetic stimulation (ACh) stimulated Tyrosine Hydroxlase to convert Tyrosine —> DOPA

Endo/Repro I Exam 1 (12 decks)

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