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Endocrine > Adrenal Gland Fcns and Dzs > Flashcards

Adrenal Gland Fcns and Dzs Flashcards

1
Q

embryological origins of parts of adrenal gland

A

i. adrenal medulla is ectodermal origin
1. release catecholamines
ii. adrenal cortex is of epidermal origin
1. release steroid Hs

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2
Q

Hs of adrenal cortex

A
  1. aldosterone—targets kidneysNa and K homeostasis, stress response
  2. cortisol—targets many tissuesstress response
  3. androgens—many tissues
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3
Q

Hs of adrenal medulla

A
  1. epinephrine—targets many tissuesfight or flight response

2. norepinephrine—targets many tissuesfight or flight response

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4
Q

H secretion from parts of the adrenal gland

A

i. Zona glomerulosa
1. Mineralocorticoids–>aldosterone
ii. Zona fasciculata
1. Glucorcorticoids–>cortisol
2. Androgens
iii. Zona reticularis
1. Glucocorticoids–>cortisol
2. Androgens
iv. Adrenal medulla
1. Catecholamines–>E and NE

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5
Q

pathways for synthesis of steroid Hs

A

i. Cholesterol is the precursor for all pathways for steroid Hs
ii. Cholesterol desmolase needs to be there to produce pregnolone—rate limiting step

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6
Q

Steroidogenic acture regulatory protein (StAR)

A

a. Transport protein that regulates cholesterol transfer within the mitochondria which is the rate limiting step in the production of steroid H

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7
Q

congenital adrenal hyperplasia has to do with deficiency of:

A
  1. 17 alpha hydroxylase
  2. 21 beta hydroxylase
  3. 11 beta hydroxylase
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8
Q

17 alpha hydroxylase deficiency–congenital adrenal hyperplasia*

A

i. 17 alpha hydroxylase deficiency—will force pathway into making mineralocorticoids
1. pt will lose secondary sexual characteristics—amenorrhea
2. excessive weak mineralocorticoids
a. inc BP, inc K depletion

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9
Q

21 beta hydroxylase deficiency–congenital adrenal hyperplasia*

A

i. system will go towards the production of androgens/sex Hs
1. normally negative feedback from the Hs being released from the target organ, but this doesn’t happen with sex Hs, so they keep being produced
2. caused virilizaiton in females
3. loss of cortisol production
4. loss of aldosterone production
a. hypovolemia, hyponatremia
5. most common CAH

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10
Q

11 beta hydroxylase deficiency–congenital hyperplasia*

A

system will go towards the production of androgens

  1. normally negative feedback from the Hs being released from the target organ, but this doesn’t happen with sex Hs, so they keep being produced
  2. caused virilizaiton in females
  3. loss of cortisol production
  4. loss of aldosterone production
    a. hypovolemia, hyponatremia
  5. most common CAH
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11
Q

ACTH

A
  1. stimulates synthesis and secretion of adrenal cortical Hs
    a. Hypothalamus–>corticotropin releasing H (CRH)–>anterior pituitary–>ACTH–>adrenal cortex
    i. Glucocorticoids—cortisol
    ii. Mineralocorticoids—aldosterone
    iii. Androgens
    b. ACTH is produced in the anterior pituitary
    i. Derived from post translational processing of POMC
    1. In non pituitary tissues we have ACTH, made to alpha MSHsynthesis of melanin
    ii. Is a peptide H
    c. Hypothalamic, pituitary, adrenal (HPA) axis is under negative feedback control by cortisol
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12
Q

regulation of cortisol

A

i. Stress and circadian rhythm stimulates secretion of CRH from the hypothalamus
ii. Cortisol–>immune system–>immune suppression
iii. Cortisol–>liver–>gluconeogenesis
iv. Cortisol–>muscle–>protein catabolism
v. Cortisol–>adipose tissue–>lipolysis
1. Predominantly the goal is to raise blood glucose

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13
Q

circadian rhythm and cortisol

A

i. positive influence in the HPA axis
1. increased release in cortisol b/w 6-8 in the morning and decreased as we go throughout the day
2. if you are going to measure cortisol secretion rates, they will be higher in the early morning

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14
Q

exogenous glucocorticoids

A

a. exogenous glucocorticoids have the same negative feedback effect as cortisol
i. exogenous cortisol administration may shut down ACTH production and adrenal cells that produce cortisol—atrophy
ii. examples of synthetic glucocorticoids—cortisone, prednisone, methylprednisone, dexamethasone

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15
Q

Cushing’s Syndrome*

A
  • hypercortisolism
    i. caused by adrenal tumor
    1. Inc cortisol causes negative feedback on the hypothalamus and pituitary to decrease CRH and ACTH
      a. In this case though, there is an adrenal tumor, so there is a continued overproduction of cortisol
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16
Q

Cushing’s Disease*

A
  • hypercortisolism
    i. caused by a pituitary tumor
    1. Pituitary tumor causes increased release of ACTH constantly and then this will increase cortisol release
    2. This elevated cortisol will feedback on hypothalamus to reduce CRH
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17
Q

signs/symptoms of hypercortisolism

A
  1. Excess fat on the back of neck—buffalo hump
  2. Rounding of face—moon face
  3. Excess weight gain in abdomen
  4. Dark red or purple stretch marks
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18
Q

what causes hypercortisolism?

A
  1. Adrenal tumor that automously secretes cortisol—adrenal excess—Cushing’s syndrome
  2. Drug induced hypercortisolism
  3. Pituitary tumor that autonomously secretes ACTH—pituitary excess—Cushing’s Disease
19
Q

Addison’s Disease*

A
  • hypocortisolism
    i. caused by autoimmune disease of the adrenal gland
    1. Decreased cortisol release, so this feeds back to increase the production and secretion of CRH and ACTH from hypothalamus and pituitary
    2. Tx: steroid replacement therapy for life
20
Q

secondary adrenal insufficiency

A
  • hypocortisolism
    i. caused by chronic treatment by glucocorticoid drugs suppressing H and P
    1. Decreased cortisol, dec CRH, dec ACTH
21
Q

what causes hypocortisolism?

A
  1. Hyposecretion of all adrenal steroid Hs—Addison’s

2. Secondary adrenocortical insufficiency—ACTH insufficiency—chronic exogenous glucocorticoid tx

22
Q

cosyntropic–synthetic ACTH–stimulation test

A

a. detect adrenal gland insufficiency
i. Tests that measure the level of Hs are used to diagnose pathologies
1. Ie. Cosynctropic stimulation test
ii. Measure cortisol levels in the morning which normal is 20 micrograms/dL
1. If it is >15 then rule out adrenal insufficiency
2. If

23
Q

aldosterone secretion and HPA axis

A

i. HPA axis is stimulated by stress, and this causes the release of CRH from the hypothalamus
ii. This causes ACTH to release from anterior pituitary
iii. This goes to the zona glomerulosa and causes enhanced secretion of aldosterone
iv. Aldosterone targets kidney tubules
1. Causes increased absorption of Na and water, inc K secretion
2. This then causes increased BV and BP

24
Q

aldosterone secretion–direct stimulatory effect

A

i. Aldosterone secretion is also released due to dec Na and inc K, so this will call for aldosterone to be released thru a direct stimulatory effect on the ZG

25
Q

renin and aldosterone secretion

A

i. Dec BV/BP will cause release of renin which will convert Angiotensinogen to Ang I and then to Ang II which will act on the ZG to release aldosterone
1. This will then act to inc water and Na reabsorption and then inc BP

26
Q

ANP and aldosterone secretion

A

i. ANP will also regulate the system, when there is an increase in the volume, Na reabsorption will be decreased, so aldosterone secretion will decrease in order to allow this to happen

27
Q

MOA of aldosterone

A
  1. Aldosterone combines with the cytoplasmic receptor
  2. H receptor complex initiates transcription in the nucleus
  3. Translation and protein synthesis makes new protein channels and pumps
  4. Aldosterone induced proteins modulate existing channels and pumps
  5. Result is increased Na reabsorption and K secretion
28
Q

primary and secondary hyperaldosteronism

A
  1. Primary—excessive release of aldosterone from the adrenal cortex
    a. Conn’s Syndrome—adenoma in the adrenal cortex
    i. Tx: surgery
  2. Secondary—excessive renin secretion by the juxtaglomerular cells in the kidney
29
Q

hypoaldosteronism

A
  1. Destruction of the adrenal cortex
  2. Defects in aldosterone synthesis
  3. Inadequate stimulation of aldosterone secretion
30
Q

epinephrine

A
  1. Responder to stress such as hypoglycemia/exercise

2. Influences energy metabolism and cardiac output

31
Q

synthesis of catecholamines

A
  • tyrosine–>DOPA by tyrosine hydroxylase
  • DOPA–>dopamine by amino acid decarboxylase
  • dopamine–>norepinephrine by dopamine beta hydroxylase
  • norepinephrine–>epinephrine by PNMT
32
Q

what controls synthesis of catecholamines?

A

i. Under control of the CRH, ACTH, cortisol axis
1. ACTH stimulates synthesis of DOPA
2. Cortisol increases phenylehanolamine-N-methyl transferase (PNMT) enzyme

33
Q

norepinephrine and epinephrine are synthesized in different compartments

A
  1. Tyrosine is converted to L-dopa by tyrosine hydrolase in the cytosol
  2. L-dopa is converted to dopamine by AADA in the cytosol
  3. NE is made within the chromaffin granule
    a. Dopamine comes into the granule by a VMAT1/H exchanger
    b. DBH converts it to NE
  4. NE exits the chromaffin granule through a VMAT1 transporter
    a. It is converted to epinephrine out into the cytosol by PNMT
  5. Epinephrine and NE can be stored inside the chromaffin granule in a storage complex
    a. Epi has to be brought back into the granule by VMAT/H exchanger to be stored
  6. Epinephrine and NE can be sent out of cell by exocytosis of the chromaffin granule
34
Q

rate limiting step of formation NE and Epi

A

i. Rate limiting step is hydroxylation of tyrosine by tyrosine hydroxylase producing DOPA
1. Dopa is converted to DA by the cytoplasmic enzyme, aromatic AA decarboxylase (AADC), and is then transported into the secretory vesicle (chromaffin granule)
2. Within the chromaffin granule, DA is converted to NE by DBH (dopamine beta hydroxylase)
3. In most cells, essentially all of the NE diffuses out of granule by facilitated transport and is methylated by the PNMT to form Epi
4. Epi is transported back into granule
a. Multiple mcs of epi and NE are stored in chromaffin granule complexed with ATP, Ca, and proteins called chromogranins

35
Q

chromogranins

A

a. Multiple mcs of epi and NE are stored in chromaffin granule complexed with ATP, Ca, and proteins called chromogranins
i. Chromogranins—multimolecular complexes through to decrease the osmotic burden of storing individual mcs of epi within chromaffin granules
ii. Circulating chromogranins can be used as a marker of sympathetic paraganglion derived tumors

36
Q

degradation of catecholamines

A

i. Epinephrine and NE is broken down to dihydroxymandelic acid by MAO
ii. Epinephrine is broken down to metanephrine by COMT
iii. NE is broken down to normetanephrine by COMT
1. Normetanephrine and metanephrine is broken down to venillylmandelic acid in urine by MAO
2. Dihydroxymandelic acid is broken down to venillylmandelic acid in urine by COMT

37
Q

alpha1 receptor

A
  • inc IP3 and Ca, DAG
  • tissues: sympathetic postsynaptic nerve terminals
  • action: inc vascular SM contraction
  • respond better to NE than Epi
38
Q

alpha2 receptor

A
  • dec cAMP
  • act on sympathetic presynaptic nerve terminals; beta cell of pancreatic islet cells
  • action: inhibit NE release, inhibit insulin release
  • respond better to NE than Epi
39
Q

beta1 receptor

A
  • inc cAMP
  • acts on heart
  • inc CO
  • responds equally to NE and Epi
40
Q

beta2 receptor

A
  • inc cAMP
  • act on liver SM of vasculature, bronchioles, and uterus
  • action: inc hepatic glucose output, dec contraction of blood vessels, bronchioles, and uterus
  • respond to Epi better than NE
41
Q

beta 3 receptor

A
  • inc cAMP
  • acts on adipose tissue and liver
  • action: inc hepatic glucose output, inc lipolysis
  • responds better to NE than Epi
42
Q

pheochromocytoma*

A

a. Tumor of chromaffin tissue
b. Produces excess catecholamines
c. Symptoms are sporadic
i. Hypertension—reported that 1% of pts with hypertension have a pheochromocytoma
ii. Orthostatic hypotension—volume depletion
iii. Headaches
iv. Sweating
v. Palpitations
vi. Anxiety
vii. Chest pain
viii. Flushing

43
Q

short term stress

A

i. Stress stimulates the hypothalamus which sends signals down nerve impulses to the spinal cord
ii. Information is sent out preganglionic sympathetic fibers to the adrenal medulla which secretes AA based Hs
iii. Catecholamines are released—epinephrine and norepinephrine
iv. Short term stress response:
1. HR increases
2. BP increases
3. Bronchioles dilate
4. Lover converts glycogen to glucose and releases glucose to blood
5. Blood flow changes, reducing digestive system activity and urine output
6. Metabolic rate increases

44
Q

long term stress

A

i. Stress stimulates the hypothalamus which releases CRH to the corticotropic cells of the anterior pituitary which releases ACTH to target blood
ii. Adrenal cortex is stimulated to secrete steroid Hs—mineralocorticoids and glucocorticoids
iii. Long term stress response:
1. Kidneys retain Na and water
2. BV and BP rise
3. Proteins and fats converted to glucose or broken down for energy
4. Blood glucose increases
5. Immune system suppressed

Endocrine (15 decks)

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