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Metabolic endocrinology 2 > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

What hormones are produced in the adrenal gland?

A

Aldosterone
cortisol
sex steroids
catecholamines

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2
Q

What stimulates the adrenal gland? Where is it produced?

A

corticotropin (ACTH)

anterior pituitary

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3
Q

What stimulates the anterior pituitary to release ACTH?

A

corticotropin releasing hormone (CRH) from the hypothalamus

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4
Q

True or False. The adrenal medulla composes the majority of adrenal mass.

A

False. The cortex is about 90%.

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5
Q

What are the 3 zones of the adrenal cortex and which is the thickest?

A

Zona glomerulosa
zona fasciculata –> thick
zona reticularis

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6
Q

In which zones within the gland are the adrenal hormones produced?

A

Zona glomerulosa –> aldsterone
zona fasciculata –> cortisol
zona reticularis –> sex steroids
medulla –> catecholamines

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7
Q

In what way is this zone specificity ensured?

A

zona glomerulosa does not have the 17alpha-hydroxylase. This means this zone cannot make cortisol or sex steroids

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8
Q

What original building block is used to build all adrenal hormones?

A

cholesterol

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9
Q

What compound, built from cholesterol, is present in all zones of the adrenal cortex?

A

pregnenolone

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10
Q

Where is androstenedione produced in the cortex and what is it used for?

A

in zona reticularis used to make sex hormones

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11
Q

Where does the body get its cholesterol for use in the adrenal gland?

A

diet and synthesis from acetyl CoA

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12
Q

True or False. Most steroids differ by minor modifications of side groups, often hydroxyl groups

A

True

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13
Q

Where are the enzymes located in the cells of the adrenal gland? What consequence does that have on the formation of adrenal hormones?

A

mitochondria or endoplasmic reticulum

steroid intermediates have to shuttle back and forth

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14
Q

What protein transports cholesterol across the mitochondrial membrane? What is it turned into and by what?

A 
StAR protein (Steroid acute regulatory protein)
P450scc (side chain cleavase) turns it into pregnenolone
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15
Q

What is the rate limiting step in the formation of steroid hormones? How is it controlled/altered?

A

StAR protein is rate limiting step that is cAMP inducible, it increases in response to trophic hormones (ACTH for adrenal or gonadotropins in gonads)

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16
Q

How is cortisol excreted?

A

converted to cortisone by liver for excretion in urine

converted by hydroxysteroid dehydrogenase type 2 (HSD2)

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17
Q

What are the main effects of cortisol?

A

increased glucose
increased fat and protein break down
anti-inflammatory effects
sensitizes arteriole to norepinephrine (HTN)
increased activity of CNS –> euphoria
interacts with mineralocoticoid receptor (acts as mineralocorticoid –> increase extracellular fluid

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18
Q

True or False. Once cortisol if converted to cortisone, it is irreversible and will be be excreted.

A

False. Some tissues can convert it back. hydroxysteroid dehydrogenase type 1 (HSD1) catalyses the reverse reaction

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19
Q

Why is the deactivation of cortisol crucial? What enzyme deficiency can occur if cortisol is in excess?

A

cortisol can also activate the aldosterone receptor, but cortisol is 100-1000 times more concentrated than adosterone. To have a proper response to aldosterone, cortisol needs to be deactivated to cortisone. Cortisol in excess can be due to an enzyme deficiency –> AME syndrome (apparent mineralocorticoid excess)

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20
Q

How does glycyrrhizic acid in licorice lead to electrolyte imbalances?

A

inhibits HSD2 which turns cortisol into cortisone. cortisol accumulates and stimulates Na/K exchange in kidneys leading to hypokalemia and HTN.

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21
Q

What are the effects of cortisol? How does cortisol take effect on the cell?

A

opposite insulin, similar to GH but actions depend on the target cells (increase in blood glucose, increased catabolism, anabolic effect on liver)
activate transcription of certain genes by a Class 1 receptor (cytosolic)

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22
Q

In what way is cortisol anti-inflammatory?

A

it inhibits the immune system
atrophy of lymph nodes and thymus by apoptosis
decreased number of lymphocytes and antibody production –> susceptible to infections

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23
Q

How is cortisol secretion regulated?

A

the presence of cortisol inhibits the anterior pituitary and the hypothalamus to stop production of ACTH and CRH.
Stress and the diurnal rhythm stimulate the hypothalamus to produce CRH (corticotropin releasing hormone). Production is maximal in the morning

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24
Q

What hormone stimulate cortisol secretion? where is it produced? What signaling pathway is used?

A

ACTH from anterior pituitary

G protein cAMP signaling pathway, stimulated in pulses superimposed on a circadian rhythm

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25
Q

How is cortisol transported? Why is it transported in this way?

A

corticosteroid binding globulin (CBG or transcortin)
albumin
free
bound = protected from degradation by liver which maintains a circulating pool of cortisol by delaying clearance

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26
Q

How does the liver excrete free steroids?

A

making them water soluble and having them excreted by the kidneys

27
Q

What is the basic cause of Cushing’s syndrome? What are its consequences?

A

excess cortisol
increased glucose –> diabetes mellitus
increased glucose –> more insulin –> more body fat –> central obesty
inhibit Ca uptake and osteoblasts –> osteoporosis
Inhibit immune system –> infection sesceptability
more acid secretion by stomach –>predisposition to gastric ulcers
suppressed adrenocorticotrophic hormone
Na retention –> HTN

28
Q

What are possible causes for Cushing’s syndrome?

A

CRH producing tumor
ACTH producing tumor
lack of feedback control from cortisol
Cortisol producing adrenal tumor
so far all spontaneous cushing’s syndrome (ACTH dependent or independent)
also can be iatrogenic –> most common from glucocorticoid therapy

29
Q

What is Addison’s disease? What are possible causes?

A

adrenal hypofunction

usually because adrenal gland destroyed by autoimmune response

30
Q

What are symptoms of Addison’s disease?

A

fatigue, vomiting, low blood pressure, salt craving, pain in muscles and joints, excessive freckling
By the decrease of cortisol, liver function decreases leading to low blood sugar –> death/coma
and stomach digestive enzyme function decreases leading to vomiting , diarrhea, cramps –> blood fluid volume –> shock –> death/coma
By the decrease of aldosterone there is water loss from kidneys –> blood fluid volume low –> shock –> death/coma
water and sodium loss from kidneys also affects heart –> low BP –> shock –> coma/death

31
Q

How is Addison’s disease treated?

A

lifelong glucocorticoid and mineralocorticoid therapy

32
Q

What are the functions of aldosterone?

A

regulation of Na homeostasis (fluid volume, water absorption

Sodium potassium homeostasis (more Na reabsorption

33
Q

How is blood volume homeostasis conserved?

A

H2O retention

34
Q

How is blood osmolarity homeostasis conserved?

A

Na retention

35
Q

How is blood pressure homeostasis conserved?

A

arteriole dilation

36
Q

What stimulates the secretion of aldosterone from the adrenal cortex?

A

Angiotensin II

37
Q

What is the source of renin and what does renin do?

A

the juxtaglomerular apparatus

turns angiotensinogen into angiotensin I

38
Q

What influences the secretion of Renin?

A

Baroreceptors in the wall of the afferent arteriole
Na concentration in the lumen of the distal tubules
Renal sympathetic nerve activity
feedback from angiotensin II and potassium levels as well

39
Q

What 4 effects does angiotensin II have?

A 
vasocontriction
aldosterone release and sodium reabsorption
vascular and cardiac hypertrophy and remodelling
increased fluid (vasopressin + thirst)
40
Q

How does aldosterone increase Na recovery? Where does it act?

A

more Na channels in luminal wall of tubular cells and more Na K ATPase channels in basolateral membrane
distal tubules and collecting ducts of the kidney and other secretory systems

41
Q

What is Conn’s syndrome?

A

hypersecretion of aldosterone usually caused by adrenal hyperplasia or tumor
leads to hyperexcretion of K+ and H+ (alkalosis and neuropathy from hypocalcemia), increased water retention (more Na, high BP)

42
Q

What does Atrial natriuretic peptide do? Where is it produced? When is it produced?

A

Peptide that increases the excretion of H2O and Na+
it reduces renin and aldosterone, increases renal blood flow
produced in the heart muscle cells in response to increased Na and water consumption

43
Q

What sex steroids are produced in the adrenal cortex?

A

DHEAS and androstenedione that can be converted to testosterone in the gonads

44
Q

What is congenital adrenal hyperplasia?

A

masculinisation of external genitalia at birth due to excessive androgen production by hyperplasia of the adrenal gland

45
Q

What specific enzyme is affected in congenital adrenal hyperplasia, what effect does that have on hormone production?

A

21 hydroxylase
low aldosterone and cortisol, normal androgens
low cortisol –> low feedback –> more ACTH –> more androgens

46
Q

What is the treatment for congential adrenal hyperplasia?

A

surgical correction at birth and raise as girls

47
Q

What response is the adrenal medulla responsible for?

A

fight or flight –> increase BP, CO and dilated pupils

48
Q

What stimulates the release of hormones from the adrenal medulla?

A

preganglionic cells release acetylcholine to stimulate medulla cells to release hormones

49
Q

What hormones are produced in the adrenal medulla? From what are they synthesized?

A

norepinephrine and epinephrine from tyrosine (catecholamines)

50
Q

What is the rate limiting step for the production of catecholamines?

A

tyrosine –> dopa with tyrosine hydroxylase

51
Q

What is Phenylethanolamine N-methyltransferase?

A

PNMT turns norepinephrine into epinephrine and is enhanced by cortisol

52
Q

Which pathways will deactivate the hormones produced in the adrenal medulla?

A

Inactivated by monoamine oxidase (MAO)
and COMT (catechol-O-methyltransferase)
Pathways

53
Q

How are the catecholamines stored?

A

in granules

54
Q

What are enkephalins?

A

may block neurotransmitters and act as endogenous analgesics

55
Q

What are the functions of epinephrine?

A

rapidly mobilizes fatty acids as the primary fuel for muscle action
increases muscle glycogenolysis
mobilizes glucose for the brain by ↑hepatic glycogenolysis/ gluconeogenesis
preserves glucose for CNS by ↓ insulin release leading to reduced glucose
uptake by muscle/ adipose
increases cardiac output

56
Q

What are the functions of norepinephrine?

A

↑ blood flow and ↓ insulinsecretion.

57
Q

Describe the 5 adaptations for the fight or flight response.

A
  1. increased rate and strength of CO
  2. maintenance of BP
  3. Redirection of blood flow to vital organs by selective vasoconstriction
  4. Reduction of digestive activity
  5. dilation of respiratory pathways
58
Q

How is energy mobilized for fight or flight response?

A 
Muscle:
Glycogenolysis increased
Excretion of lactic acid increased
Liver:
Gluconeogenesis increased
Glycogenolysis increased
Adipocytes:
Lipolysis increased

Insulin deceased
Glucagon increased
Plasma:
more Lactic acid, Glucose and Fatty acids

59
Q

What are the adrenergic receptors and what do they bind?

A

α and β1 receptors bind epinephrine and norepinephrine.

β2 binds primarily epinephrine

60
Q

What is the difference between norepinephrine and epinephrine?

A

epinephrine has a greater effect on metabolism and greater cardiac output
norepinephrine –> constriction of blood vessels

61
Q

In what situation can adrenomedullary deficiency?

A

surgery, trauma or suppressed cortisol levels

62
Q

What can adrenomedullary deficiency cause?

A

hypotension, hypoglycemia

glucocorticoids are more important so catecholamines are not essential to life

63
Q

What is a pheochromocytoma? How is it treated?

A

a tumor that overproduces catecholamines
rare but often not diagnosed until autopsy
surgery

64
Q

What are the usual symptoms of over production of catecholamines?

A

headache, HTN and sweating

Metabolic endocrinology 2 (4 decks)

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