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Endo/Repro Midterm > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

Embryological origin of adrenal cortex vs. adrenal medulla

A

Adrenal cortex is of mesodermal origin

Adrenal medulla is of ectodermal origin

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2
Q

What types of hormones are secreted by adrenal cortex vs. adrenal medulla?

A

Adrenal cortex = corticoids and androgens

Adrenal medulla = catecholamines (NE and E)

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3
Q

What are the zones of the adrenal cortex?

A 
[capsule]
Zona glomerulosa
Zona fasciculata
Zona reticularis
[adrenal medulla]
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4
Q

What is the primary hormone secreted from zona glomerulosa of adrenal cortex?

A

Mineralocorticoid = aldosterone

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5
Q

What is the primary hormone secreted from zona fasciculata of adrenal cortex?

A

Gluococorticoid = cortisol

[also some androgen secretion]

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6
Q

What is the primary hormone secreted from zona reticularis of adrenal cortex?

A

Androgens

[some cortisol as well]

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7
Q

What is the most common adrenal enzyme deficiency?

A

21-hydroxylase deficiency

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8
Q

A deficiency in 21-hydroxylase results in what changes in hormone production?

A

Decreased cortisol

Decreased mineralocorticoid

Increased sex hormones

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9
Q

What are signs/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 pseudopuberty, premature growth plate closure

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10
Q

Tx for 21-hydroxylase deficiency

A

Replace glucocorticoids and mineralocorticoids

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11
Q

A deficiency in what adrenal enzyme leads to increased androgens, virilization of female features, and increased 11-deoxycorticosterone?

A

11b-hydroxylase deficiency

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12
Q

Signs and symptoms of 11b-hydroxylase deficiency

A

Hypertension
Hypokalemia
Suppressed renin secretion

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13
Q

A 17-alpha hydroxylase deficiency is extremely rare. What changes in hormone secretion occur with this deficiency?

A

Decreased androgens and cortisol

Excess mineralocorticoids

[patients typically diagnosed at puberty]

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14
Q

Signs/symptoms of 17-alpha hydroxylase deficiency

A

Hypertension
Hypokalemia
Hypogonadism

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15
Q

Do the following increase or decrease in a 17-alpha hydroxylase deficiency?

Mineralocorticoids
Cortisol
Sex hormones
Blood pressure
Plasma [K]
A 
Mineralocorticoids increase
Cortisol decrease
Sex hormones decrease
Blood pressure increase
Plasma [K] decrease
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16
Q

Do the following increase or decrease in a 21-beta hydroxylase deficiency?

Mineralocorticoids
Cortisol
Sex hormones
Blood pressure
Plasma [K]
A 
Mineralocorticoids decrease
Cortisol decrease
Sex hormones increase
Blood pressuredecrease
Plasma [K] increase
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17
Q

Do the following increase or decrease in an 11-beta-hydroxylase deficiency?

Mineralocorticoids
Cortisol
Sex hormones
Blood pressure
Plasma [K]
A 
Mineralocorticoids decrease (aldosterone)
Cortisol decrease
Sex hormones increase
Blood pressure increase
Plasma [K] decrease
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18
Q

The target tissues of cortisol are body wide and the actions numerous. Genomic actions occur via ______, and non-genomic actions occur via _____

A

Glucocorticoid response elements (GREs)

Endocannabinoids

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19
Q

What conditions occur with glucocorticoid excess?

A

Cushing syndrome or cushing disease

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20
Q

What conditions occur with glucocorticoid deficiency?

A

Addison disease

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21
Q

What effect does cortisol have on the liver?

A

Increased gluconeogenesis

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22
Q

What effect does cortisol have on the muscle?

A

Breakdown of muscle protein

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23
Q

What effect does cortisol have on fat?

A

Promotes lipolysis in extremities, promotes central fat deposition

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24
Q

What effect does cortisol have on skin?

A

Skin thins, fragile blood vessels

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25
Q

What effect does cortisol have on the immune system?

A

Increased risk of infection (diminished immune response)

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26
Q

What effect does cortisol have on the endocrine system?

A

Insulin resistance or glucose intolerance

[also decreased LH, FSH release, decreased TSH release, decreased GH secretion

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27
Q

What effect does cortisol have on the GI system?

A

Increased risk of osteoporosis d/t interference with calcium absorption

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28
Q

Cortisol release begins with stimulationg by ____ from the ______ nucleus in the hypothalamus

This binds the CRF1 receptor (GPCR) and stimulates the release of ______, which acts on the adrenals and stimulates release of cortisol

A

CRF aka CRH; paraventricular

ACTH

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29
Q

ACTH is produced in the anterior pituitary and is the principle hormone that stimulates adrenal glucocorticoids

The precursor to ACTH is ______; it also contains ____ activity responsible for stimulation of melanocytes

A

POMC; MSH

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30
Q

Excess ACTH can lead to ______ due to increased alpha-MSH activity

A

Hyperpigmentation

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31
Q

Differentiate between long, short, and ultrashort HPA axis feedback loops

A

Long = from adrenal glands back up to anterior pituitary and hypothalamus

Short = from anterior pituitary back to hypothalamus

Ultrashort = hormone from hypothalamus inhibits itself

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32
Q

When do we experience the largest spike in cortisol release? How does this compare to the rhythm of ACTH?

A

Largest spike in cortisol upon awakening, around sun-up

ACTH tends to stay around the same levels with a slight drop off in early evening

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33
Q

Glucocorticoids exert negative feedback onto CRH and ACTH

What is the mechanism for this?

A

GCs inhibit POMC transcription

GCs also inhibit mRNA synthesis of CRH and ACTH

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34
Q

What is the dexamethasone suppression test?

A

Administration of exogenous glucocorticoid to determine if ACTH and cortisol will be suppressed

[normally they will be suppressed, but if no suppression occurs - indicative of Cushing]

35
Q

What is the difference in low dose vs. high does dexamethasone suppression tests?

A

Both are supraphysiologic doses; low dose is used to detect if problem is present.

High dose determines source of problem - pituitary cushing if high dose suppresses ACTH, adrenal or ectopic cushing if no suppresion

36
Q

What test is used for adrenal gland insufficiency?

A

Cosyntropin (synthetic ACTH) stimulation test [CST]

37
Q

What is a postive vs. negative result for cosyntropin stimulation test?

A

Normal = cortisol increases from baseline

If adrenals are undresponsive and crotisol remains the same or only rises a small amount - consider adrenal insufficiency

If adrenals respond dramatically and cortisol increases substantially, consider secondary adrenal insufficiency

38
Q

Hypercortisolism characterized by hypersecretion of cortisol, usually an adrenal neoplasm, and low serum ACTH

A

Cushing syndrome

39
Q

Hypercortisolism characterized by hypersecretion of ACTH, pituitary gland tumor overstimulating adrenal cortex leading to excess cortisol secretion

A

Cushing disease

40
Q

Which is associated with adrenal problem and which is a pituitary problem: cushing syndrome vs. cushing disease?

A

Syndrome = adrenal problem

Disease = pituitary problem

41
Q

Why is ACTH low in cushing syndrome, while it is high in cushing disease?

A

Cushing syndrome is a primary condition d/t adrenal problem - and negative feedback ends up inhibiting ACTH release

Cushing disease is affecting the pituitary leading to excess ACTH release

42
Q

If a patient with Cushing syndrome was injected with exogenous glucocorticoids like dexamethasone, what do you predict would happen to their ACTH levels and cortisol suppression?

A

ACTH would be undetectable and dexamethasone fails to suppress cortisol secretion

This occurs bc negative feedback loop itself is functional yet hypercortisolism continues

43
Q

If a patient with Cushing disease was injected with exogenous glucocorticoids like dexamethasone, what do you predict would happen to their ACTH levels and cortisol suppression?

A

ACTH would be normal or slightly elevated, and dexamethasone would successfully suppress cortisol secretion because abnormal negative feedback is occurring at level of pituitary

44
Q

Symptoms of Cushing’s

A 
Moon face
Hirsutism
Bruising
Abdominal adiposity
Stretch marks
Buffalo hump
45
Q

Hypocortisolism characterized by primary adrenal insufficiency d/t chronic, progressive destruction of adrenal gland resulting in high ACTH but low cortisol

A

Addison disease

46
Q

Hypocortisolism characterized by ACTH deficiency and low cortisol, caused by exogenous glucocorticoid administration

A

Secondary adrenal insufficiency

47
Q

Differentiate between addison and secondary adrenal insufficiency - which one is adrenal problem and which one is a pituitary problem?

A

Addison is adrenal problem

Secondary is pituitary problem

48
Q

Addison disease is a form of hypocortisolism in which there is hyposecretion of ALL adrenal steroids (primary adrenal insufficiency). What are some causes of Addison?

A

Autoimmune disease of adrenal gland

Adrenal hemorrhage (d/t infection, AC tx)

Infection (d/t Tb, meningitis)

Tumor

49
Q

Signs/symptoms of addisons

A 
HYPERPIGMENTATION (d/t MSH activity)
Weight loss
Muscle weakness
HYPOGLYCEMIA
Hypotension
Hyponatremia and hyperkalemia d/t loss of aldosterone!!
50
Q

Which of the following is characteristic of primary cortisol deficiency?

A. Increased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation
B. Increased cortisol, decreased CRF, increased ACTH, hyperpigmentation present
C. Decreased cortisol, increased CRF, increased ACTH, hyperpigmentation present
D. Decreased cortisol, increased CRF, decreased ACTH, no hyperpigmentation
E. Decreased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation

A

C. Decreased cortisol, increased CRF, increased ACTH, hyperpigmentation present

51
Q

Which of the following is characteristic of primary cortisol excess?

A. Increased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation
B. Increased cortisol, decreased CRF, increased ACTH, hyperpigmentation present
C. Decreased cortisol, increased CRF, increased ACTH, hyperpigmentation present
D. Decreased cortisol, increased CRF, decreased ACTH, no hyperpigmentation
E. Decreased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation

A

A. Increased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation

52
Q

Which of the following is characteristic of secondary cortisol deficiency?

A. Increased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation
B. Increased cortisol, decreased CRF, increased ACTH, hyperpigmentation present
C. Decreased cortisol, increased CRF, increased ACTH, hyperpigmentation present
D. Decreased cortisol, increased CRF, decreased ACTH, no hyperpigmentation
E. Decreased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation

A

D. Decreased cortisol, increased CRF, decreased ACTH, no hyperpigmentation

53
Q

Which of the following is characteristic of exogenous glucocorticoid treatment?

A. Increased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation
B. Increased cortisol, decreased CRF, increased ACTH, hyperpigmentation present
C. Decreased cortisol, increased CRF, increased ACTH, hyperpigmentation present
D. Decreased cortisol, increased CRF, decreased ACTH, no hyperpigmentation
E. Decreased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation

A

E. Decreased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation

[actual endogenous cortisol may be low, but symptoms of hypercortisolism may be present]

54
Q

Which of the following is characteristic of secondary cortisol excess?

A. Increased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation
B. Increased cortisol, decreased CRF, increased ACTH, hyperpigmentation present
C. Decreased cortisol, increased CRF, increased ACTH, hyperpigmentation present
D. Decreased cortisol, increased CRF, decreased ACTH, no hyperpigmentation
E. Decreased cortisol, decreased CRF, decreased ACTH, no hyperpigmentation

A

B. Increased cortisol, decreased CRF, increased ACTH, hyperpigmentation present

55
Q

Principle mineralocorticoid controlling Na and K exchange in distal nephron and major regulator of body stores of K

A

Aldosterone

56
Q

What are the specific actions of aldosterone on apical vs. basolateral membrane in distal nephron?

What is the overall result?

A

Apical = increases synthesis/activity of Na channels

Basolateral = increases synthesis/activity of Na/K ATPase

Overal result = increase in Na reabsorption and increase in K excretion, also increases H+ secretion

57
Q

MR, or mineralocorticoid receptor, has equal affinities for _____ and _____

A

Aldosterone; glucocorticoids

58
Q

_____ is responsible for metabolizing cortisol to cortisone (inactive form)

A

11beta-HSD2

59
Q

Since 11beta-HSD2 typically protects the MR from cortisol binding, leaving it available for aldosterone, what would a defect in this enzyme cause?

A

Cortisol would have free access to MR and MR would become overwhelmed by cortisol, especially in things like Cushing’s

60
Q

2 types of hyperaldosteronism

A

Primary = Conn syndrome (adrenal problem)

Secondary hyperaldosteronism (kidney problem)

61
Q

Primary hyperaldosteronism (Conn syndrome) involves hypersecretion of ____

Secondary hyperaldosteronism involves hypersecretion of ____

A

Aldosterone

Renin

62
Q

Primary vs. secondary hypoaldosteronism

A

Primary = hyposecretion of aldosterone, destruction of adrenal cortex, defects in aldosterone synthesis — an ADRENAL problem

Secondary =hyposecretion of renin, deficient renin from JG cells in kidney, inadequate stim of aldosterone — a KIDNEY problem

63
Q

The effect of ACTH on aldosterone secretion is modest at best

Primary adrenal failure —> deficient ____ and ____

ACTH deficiency —> _____ deficiency, but no change in ______

A

Cortisol; aldosterone

Cortisol; aldosterone

64
Q

____ and ____ are adrenal androgens - precursors to human sex steroids that rely on 3beta-HSD superfamily to exert androgenic or estrogenic activities

A

DHEA; DHEAS

65
Q

Adrenal carcinomas that secrete androgens lead to what signs/symptoms?

A

Female virilization, hirsutism, clitoromegaly, breast atrophy, deepening of the voice, temporal recession, severe acne

66
Q

Catecholamines are proced in the adrenal medulla

80% = _____

20% = ______

A

Epinephrine

Norepinephrine

67
Q

Epinephrine and NE are released upon release of _______ from sympathetic nerve terminals, which binds to _____ receptors

This NT increases synthesis of ______and the activity of _____

A

Acetylcholine; nicotinic

Tyrosine hydroxylase; dopamine

68
Q

What is the rate limiting step of epinephrine synthesis? Where in the cell does this step take place?

A

L-tyrosine converted to L-DOPA by tyrosine hydroxylase

Takes place in cytosol

69
Q

L-DOPA is converted to dopamine, which gets stored in special secretory vesicles called _______ and converted into ______, which later diffuses out of the granules

A

Chromaffin granules; NE

70
Q

After NE diffuses out of the granules, it is converted to _____ in the _____

A

Epinephrine; cytosol

[epinephrine is then stored in different vesicles]

71
Q

Epinephrine is stored in chromaffin granules as a complex with ___, ____, and _____

A

ATP; NE; Calcium

72
Q

What some various receptor types for catecholamine signaling?

A

Alpha 1 and 2

Beta 1, 2, and 3

73
Q

What are some mechanisms of action of catecholamine signaling?

A

Increased IP3, Ca, and DAG (alpha 1 receptors)

Decreased cAMP (alpha 2 receptors)

Increased cAMP (beta 1, 2, and 3 receptors)

74
Q

Examples of tissue distribution for receptors involved in catecholamine signaling

A

Alpha 1 = sympathetic postsynaptic nerve terminals

Alpha 2 = sympathetic presynaptic nerve terminals, beta cells of pancreatic islets

Beta 1 = heart

Beta 2 = liver; smooth muscle of vasculature, bronchioles, and uterus

Beta 3 = liver; adipose tissue

75
Q

Examples of action of alpha 1 catecholamine receptors, distributed in sympathetic postsynaptic nerve terminals

A

Increased vascular smooth muscle contraction

76
Q

Examples of action of alpha 2 catecholamine receptors, distributed in sympathetic presynaptic nerve terminals and beta cells of pancreatic islets

A

Inhibits NE release, inhibist insulin release

77
Q

Examples of action of beta 1 catecholamine receptors, distributed in heart

A

Increases cardiac output

78
Q

Examples of action of beta 2 catecholamine receptors, distributed in liver; smooth muscle of vasculature, bronchioles, and uterus

A

Increased hepatic glucose output, decreased contraction of blood vessels, bronchioles, and uterus

79
Q

Examples of action of beta 3 catecholamine receptors, distributed in liver; adipose tissue

A

Increased hepatic glucose output; increased lipolysis

80
Q

2 major enzymes for the metabolism of catecholamines

A

MAO

COMT

[both are located in CNS and peripheral tissues]

81
Q

Tumor of the chromaffin tissue resulting in excess production of catecholamines

A

Pheochromocytoma

82
Q

Symptoms of pheochromocytoma

A

Symptoms wax and wane:

HTN
Orthostatic hypotension
Headaches
Sweating
Palpitations
Chest pain
Flushing
Anxiety
83
Q

Short-term stress response to catecholamines

A 
Increased HR
Increased BP
Dilation of bronchioles
Glucose release from liver
Reduction in digestive blood flow
Increased metabolic rate
84
Q

Long-term stress response to catecholamines

A

Kidneys retain Na and H2O

Blood volume and BP rise

Proteins and fats converted to glucose for energy

BG increases

Immune system suppressed

Endo/Repro Midterm (14 decks)

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