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Endocrine - MSI Spring > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

What hormones does the adrenal medulla secrete?

A

EP and NE

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2
Q

What is StAR?

A

A transport protein that regulates cholesterol transfer within the mitochondria, a ‘rate-limiting’ step in the production of steroid hormones

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3
Q

What hormones does the adrenal cortex secrete? what are the hormones main effects?

A

Aldosterone: 1* target is kidney; Na and K homeostasis
Cortisol: stress response
Androgens:

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4
Q

What does ACTH stimulate?

A

synthesis and secretion of adrenal cortical hormones

Glucocorticoids - cortisol
Mineralocorticoids - aldosterone
Androgens

CRH->ACTH

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5
Q

What is ACTH derived from?

A

Post-translational processing of POMC

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6
Q

What part of POMC is important in melanin synthesis?

A

alpha-MSH

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7
Q

The HPA axis is under negative feedback control by what?

A

cortisol

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8
Q

What are the functions of cortisol in immune system, liver, muscle, and adipose tissue? what is its overall goal?

A

Immune system: immune suppression
Liver: gluconeogenesis
Muscle: protein catabolism
Adipose tissue: lipolysis

Overall increase blood glucose concentration

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9
Q

What modulates the release of CRH from hypothalamus?

A

Circadian rhythm: peaks around 8 am (high early morning, low late)
Stress

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10
Q

What do exogenous glucocorticoids have on the HPA axis?

A

negative feedback
Stop CRH and ACTH secretion
Decrease cortisol

May shut down ACTH production and adrenal cells that produce cortisol (atrophy)

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11
Q

What are examples of synthetic glucocorticoids

A

Cortisone
Prednisone
methylprednisone
dexamethasone

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12
Q

What are the causes of Cushing’s syndrome

A 
Adrenal tumor (primary - adrenal excess)
Drug-induced
Pituitary tumor (secondary-pituitary excess)
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13
Q

Describe what happens to the HPA axis in Cushing’s disease?

A

Tumor in Pituitary
H: decrease CRH
P: increase ACTH from tumor
A: increase cortisol

Adrenal tumor
H: Neg feedback from cortisol: decrease CRH
P: Decrease ACTH
A: release excess cortisol

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14
Q

Describe the HPA axis in Addison’s disease?

A

H: Increase in CRH bc of low cortisol
P: increase in ACTH
A: autoimmune disease of the adrenal gland decreases cortisol synthesis

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15
Q

Describe the HPA axis in secondary adrenal insufficiency

A

H: glucocorticoid drugs suppress CRH release
P: glucocorticoid drugs suppress ACTH release
A: Decrease cortisol

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16
Q

What causes hyperpigmentation if there is an issue with the HPA axis?

A

Too much plasma ACTH

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17
Q

What type of test is used to detect adrenal gland insufficiency?

A

cosyntropin (synthetic ACTH)

Measure the level of hormones
Cortisol first and if low then ACTH to figure out primary vs secondary or tertiary AL

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18
Q

A 46-year old woman exhibiting hirsutism, hyperglycemia, obesity, muscle wasting, and increased circulating levels of ACTH, most likely suffers from addison’s disease. True or False?

A

False: this is most likely cushing’s pituitary tumor

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19
Q

ACTH increases the availability of cholesterol for steroid hormone biosynthesis. True or False?

A

True

20
Q

Selective destruction of the ZG of the adrenal cortex would produce a deficiency of aldosterone. True or False?

A

true

21
Q

What stimulates aldosterone release?

A

ACTH and angiotensin II

22
Q

What is Conn’s syndrome?

A

adenoma of the adrenal cortex

Primary hyperaldosteronism: excessive release from adrenal cortex

23
Q

What is secondary hyperaldosteronism?

A

Excessive renin secretion by the juxtaglomerular cells in the kidney

renin increase
Angiotensinogen->angiotensin I –(ACE)->angiotensin II-> increase in aldosterone

24
Q

What causes hypoaldosteronism?

A

Destruction of the adrenal cortex
Defects in aldosterone synthesis
Inadequate stimulation of aldosterone section

25
Q

What are the symptoms of addisons disease and the Tx?

A

Weakness, Weight loss
HYPERPIGMENTATION!!!!!!
Atrophy of the adrenal cortex
Hypotension and hyponatremia

Tx: steroid replacement therapy for life

26
Q

What blood levels are expected in Conn’s syndrome?

A

Hypokalemia
Low plasma renin
Hypertension

27
Q

Adrenal medulla produces catecholamines; primarily __________ and small amounts of ___________

A

epinephrine (80%)

norepinephrine (20%)

28
Q

What is the role of EP from the adrenal medulla?

A

responder to stress such as hypoglycemia/exercise

Influences energy metabolism and cardiac output

29
Q

The synthesis of catecholamines is under control of what axis? Describe the pathway

A

CRH-ACTH-Cortisol
(HPA)

Tyrosine–(tyrosine hydroxylase)–>DOPA
- ACTH and ACh (SNS) stimulates synthesis of DOPA

DOPA–(amino acid decarboxylase)–>Dopamine
Dopamine–(Dopamine beta hydroxylase)–>NE via ACh stimulation

Cortisol increases PNMT enzyme to convert NE to EP

30
Q

Where is NE made?

A

Dopamine enters the chromaffin granule through VMAT1

it is then converted to NE

31
Q

Where is EP made?

A

NE leaves the chromaffin granule into the cytosol where it is converted to EP

32
Q

What complex is NE and EP stored in?

A

chromagranin

33
Q

What is the rate-limiting step in the synthesis of catecholamines?

A

Hydroxylation of tyrosine by tyrosine hydroxylase, producing DOPA

34
Q

In most adrenomedullary cells, what happens to essentially all of the NE?

A

diffuses out of the chromaffin granule by facilitated transport and methylated to form EP

35
Q

After EP forms in the cytosol, where does it go?

A

transported back into the granule by VMATs

Stored in chromaffin granule complexed with ATP, Ca and chrmogranins

36
Q

What are Chromogranins?

A

multimolecular complexes, though to decrease the osmotic burden of storing individual molecules of EP within chromaffin granules

*Circulating chromogranins can be used as a marker of sympathetic paraganglion-derived tumors

37
Q

Why is the action of catecholamines brief?

A

Because of catecholamine-O-methyltransferase

Breaks down EP, NE, and DMA (forms form MAO action on EP and NE)

38
Q

What can be measured to determine total catecholamine production?

A

Catecholamines, metanephrines, and vanillylmandelic acid

39
Q

Epinephrine–(COMT)–>?

EP–(____)–>DMA

A

Metanephrine

MAO (monoamine oxidase)

40
Q

DMA–(COMT)–>?

A

VMA

41
Q

NE–(COMT)–>?

A

normetanephrine

42
Q

Describe the catecholamine affinity for adrenergic receptors

A

Alpha receptors and B3 receptors - NE > EP

B1 - NE = EP

B2 - E>NE

43
Q

What are the main effects of catecholamines on the body system

A 
Increase cardiac output (B1)
Increase venous return (A)
Increase blood flow to SM (B2)
Decrease blood flow to GI tract (A)
Increase exchange of O2 and CO2 (B2)
Decrease energy usage of GI (B2)
Increase blood glucose, ketones, FFA, lactate, glycerol (B2, B3 in adipose, liver, and SM)
Increase blood glucagon/insulin ration (beta cells - alpha receptor to inhibit insulin; alpha cells - B2 receptor to increase glucagon)

Overall effect = increase nutrient supply to muscle and adequate supply of oxygen and glucose to brain

44
Q

what is pheochromocytome?

A

tumor of chromaffin tissue that produces excess catecholamines

45
Q

What are the symptoms of pheochromocytoma?

A

sporadic: headaches, sweating (diaphroesis) , palpations

46
Q

What are the short-term stress response of the HPA axis?

A

Nerve impulses stimulated from stress in the hypothalamus go to stimulate preganglionic sympathetic fibers which then stimulate adrenal medulla to secrete catecholamines to increase heart rate, BP, metabolic rate. Dilate bronchioles and get glucose to blood

47
Q

What is the prolong stress response of the HPA axis?

A

Hypothalamus releases CRH
Corticotrophic cells in anterior pituitary release ACTH
ACTH cause adrenal cortex to secreted steroid hormones: mineralocorticoids and glucocorticoids

Kidneys retain Na and water
Blood volume and BP rise
Proteins and fats -> glucose and energy
Blood glucose increases
Immune system suppressed

Endocrine - MSI Spring (15 decks)

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