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S & F 4 Test 2 > McCumbee - Adrenal Glands And Steroids > Flashcards

McCumbee - Adrenal Glands And Steroids Flashcards

1
Q

Endocrine glands that secrete steroid hormones

A

Adrenal cortex

Tests

Ovaries

Placenta

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2
Q

How do LDL’s enter the steroidogenic cells to be able to be used to make steroid?

A

Receptor-mediated endocytosis

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3
Q

In steroidogenic cells, cholesterol that is not immediately used is stored as lipid droplets. In order to later enter the steroidogenic pathways, these cells have _________ which is an activating enzyme that mobilizes cholesterol

A

Cholesterol esterase

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4
Q

The rate limiting step of steroid synthesis is moving cholesterol from the cytoplasm into the mitochondria. This is done by what protein?

A

StAR

Steroidogenic acute regulatory protein.

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5
Q

What do steroidogenic cells do to steroid hormones once they are synthesized

A

Steroid hormones are immediately released once synthesized, because steroidogenic cells have no mechanism for steroid storage.

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6
Q

What are the three main specific binding proteins for steroid transport?

A

Corticosteroid binding globulin (CBG)

Sex-steroid binding globulin (SHBG)

Vit-D-Binding Globulin

(Also will nonspecifically transport on albumin and as a free fraction)

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7
Q

What is the role of cholesterol acyltransferase

A

Cholesterol acyltransferase stores free cholesterol into lipid droplets in steroidogenic cells, keeping a reservoir of cholesterol for future steroid synthesis

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8
Q

Explain the steps of steroid clearance

A

Steroid hormones converted into inactive metabolites in the liver. Then are conjugated with sulfate or glucoronic acid, which increases their solubility. They are then excreted primarily by the kidneys.

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9
Q

Part of the adrenal gland

Derived from neuroectodermal cells and is essentially a modified sympathetic ganglion that secretes catecholamines

A

Adrenal medulla

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10
Q

The only zone of the cortex of the adrenal gland that expresses aldosterone synthase and is able to synthesize aldosterone

A

Zona glomerulosa

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11
Q

What enzyme converts DOC to aldosterone in the zona glomerulosa of the adrenal gland?

A

Aldosterone synthase

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12
Q

How is the transcription of StAR induced in the zone glomerulosa?

A

By angiotensin II triggering a Ca++ calmodulin dependent mechanism

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13
Q

How is transcription of StAR induced in the cells of the zona fasciculata and zona reticularis?

A

Via ACTH by a cAMP dependent mechanism

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14
Q

K+ ______ aldosterone synthesis in the zona glomerulosa

A

Induces

By mechanism that is initiated by the activation of voltage gated Ca channels

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15
Q

What is the actions of mineralcorticoids

A

Maintain ECF level by regulating Na+ reabsorption.

Also increase excretion of K and H

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16
Q

_______ is the principal adrenal androgen released by the zona reticularis

A

Dehydroepiandrosterone

DHEA

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17
Q

During pregnancy, the fetal adrenal gland produces large amounts of _________ that are converted to estrogens by the placenta

A

DHEA-sulfate

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18
Q

At what age in females and what age in males do circulating levels of adrenal androgens begin to rise?

A

Female 6-7

Male 7-8

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19
Q

Why is aldosterone the principle mineralocorticoid over cortisol and DOC in spite of their equal affinity for the mineralocorticoid receptors?

A

DOC- has high affinity for CBG, so less is in free fraction.

Cortisol - 11beta-HSD2 in mineralocorticoid receptor tissues converts cortisol to inactive cortisone

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20
Q

DHEA has a high affinity for ______ and circulates with it in the blood

A

Albumin

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21
Q

Part of the fetal adrenal that will differentiate into the different morphological zones of the adult adrenal

A

Outer neocortex

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22
Q

Part of the fetal adrenal that produces DHEAS and involutes at birth

A

Inner fetal zone

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23
Q

The major source in androgens in males after puberty

A

Testes

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24
Q

The major source of androgens in females

A

Adrenal

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25
Q

Age at which circulating levels of adrenal androgens begin to rise 6-7 in females 7-8 in males

Not apparently associated w/ the onset of puberty

Levels increase progressively thru/o adolescence

A

Adrenarche

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26
Q

-_______ is the principal glucocorticoid in humans

A

Cortisol

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27
Q

What is the half life of cortisol

A

90 minutes

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28
Q

What is the most accurate estimate of daily cortisol output?

A

A measurement of 24 hour urinary excretion of unmetabolized cortisol

(This despite the fact that 99% of cortisol in urine is metabolized)

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29
Q

What accounts for the increased activity of the synthetic glucocorticoids prednisone and dexamethasone?

A

Increased affinity for glucocorticoid receptors

Delayed plasma clearance

30
Q

______ is the principle physiological regulator of cortisol release

A

ACTH (adrenocorticotropic hormone)

31
Q

What are the acute effects of ACTH (x4)

A
  1. Increased hydrolysis of stored cholesterol esters
  2. Increased transcription of StAR for transport of cholesterol into mitochondria
  3. Increased steroid synthesis
  4. Increased blood flow to the adrenal cortex
32
Q

What are the chronic effects of ACTH stimulation of the cells of the zona fasciculata and reticularis? (X2)

A
  1. We will see an increase in cell proliferation and growth in the zona fasciulaa and reticularis
  2. Increased synthesis of steroidogenic enzymes, LDL receptors, and other proteins
33
Q

What is the effect of long term ACTH suppression ?

A

Adrenal gland atrophy

34
Q

The normal circadian rhythm is a result of the __________ nucleus of the hypothalamus

A

Suprachiasmatic

35
Q

_________ is the principal regulator of ACTH secretion

A

CRH (corticotropin releasing hormone)

36
Q

When sleep-wake cycle and light-dark cycles are synchronized, cortisol release is in a diurnal rhythm. Circulating levels of cortisol are _______ in the morning upon awakenign

A

Highest

37
Q

What are 3 ways that cortisol protects against hypoglycemia?

A
  1. Promotion of gluconeogenesis in liver
  2. Increases expression of glycogen synthase
  3. Inhibits glucose uptake in skeletal muscle
38
Q

How does cortisol help increase gluconeogenesis?

A

Principally by mobilizing AA’s. Cortisol will inhibit protein uptake in skeletal muscle and will induce protein catabolism in skeletal muscle, CT, and skin

39
Q

Cortisol has a ________ effect on catecholamine-induced lipolysis that is mostly permissive

A

Stimulatory

40
Q

_____adrenal patients tend to experience hypoglycemia

A

Hypo

Due to decreased cortisol production

41
Q

Cortisol -_______ erythropoitin synthesis

A

Stimulates

42
Q

Cortisol has what effects on CNS (x4)

A

Has some affect on ;

Mood

Wakefulness

Behavior

Sensory stimulation intensity

43
Q

What do gluccocorticoids do to bone resorption?

A

They directly inhibit it

They also inhibit intestinal calcium uptake and renal calcium reabsorption.

Excessive use of glucocorticoids will result in osteoporosis

44
Q

High concentrations of glucocorticoids ________ Ca uptake by the intestines and _________ calcium reabsorption in the kidneys

A

Antagonize

Inhibit

45
Q

How do glucocorticoids’ anti-inflammatory effects get mediated? (X4)

A

Inhibition of phospholipase A2 (which is involved in making prostaglandins, leukotriends, and thromboxanes from arachadonic acid)

Inhibition of NO synthase (which makes NO and causes vasodilation)

Block genes that code for pro-inflammatory cytokines

Induce synthesis of anti-inflammatory lipocortin and interleukin10

46
Q

What is the role of lipocortin in the anti-inflammatory response of cortisol?

A

Lipocortin synthesis is stimulated by cortisol

Lipocortin acts to inhibit phospholipase A2

47
Q

Primary adrenocortical insufficiency (addison dz) is caused by?

A

A defect w/in adrenal gland

Destruction of gland by tuberculosis, metastatic tumor, etc.

Autoimmune disorder

Inborn errror of steroid hormone synthesis

48
Q

What are the causes of primary adrenocortical insufficiency (addison disease(x3)

A

Addison’s disease is caused by a defect in the adrenal gland.

  1. Destruction of adrenal tissue 2* metastatic tumor, tuberculosis, etc.
  2. Autoimmune disorder
  3. Inborn error in steroid hormone synthesis.
49
Q

Aldosterone deficiency, which is seen in primary adrenocortical insufficiency (Addison’s Disease) causes what s/s?

A

Hyponatremia and polyuria due to decreased renal reabsorption of Na

ECF depletion

Hypotension
Dehydration

Hyperkalemia because of loss of gradient

50
Q

What are the consequences of cortisol deficiency due to a primary adrenocortical insufficiency (addison’s Disease) (x8)

A

Inability to handle stress

Hypoglycemia due to stress and or fasting

Weakness and fatigue

Loss of appetite and weight loss

Anemia

Abd pn, N/V

Hypotension

Increased pigmentation

51
Q

What are the consequences of androgen deficiency which are seen in addison’s disease

A

Females will lose pubic hair and axillary hair

52
Q

What is secondary adrenocortical insufficiency associated with ?

A

An insufficient production of ACTH

53
Q

What are causes of secondary adrenocortical insufficiency associated with insufficient levels of ACTH?

(X3)

A
  1. Prolonged use of supraphysiological doses of synthetic glucocorticoids cause depression in ACTH and then you get adrenal atrophy and then have decreased adrenal function when taken off the meds’
  2. Pituitary lesion
  3. Insufficient renin production (usually associated with renal insufficiency)
54
Q

Explain pseudohypoaldosteronism

A

Caused by loss of function mutation in mineralcorticoid receptor

Characterized by severe salt wasting in neonate

Hyperkalemia

Metabolic acidosis

Failure to respond to treatment w/ mineralcorticoids

55
Q

What are the major causes of Cushing Syndrome in order of importance? (X4)

A

Ingestion of pharmacological doses of glucocorticoids

ACTH secretion in excess from Pituitary

Ectopic, non-endocrine, ACTH secreting tumor

Tumors of the adrenal cortex

56
Q

What is the reason that you get poor wound healing in cushing’s patients? (40% of time)

(X5)

A

Cortisol has an inhibitory effect on

  1. Production of mediators of inflammation
  2. Production of chemotaxic and mitogenic mediators
  3. Fibroblast proliferation
  4. Collagen biosynthesis
  5. Circulating levels of WBC’s
57
Q

Explain Conn Syndrome

A

Conn syndrome is primary aldosteronism, caused by excessive aldosterone, usually coming from an adenoma in the zona glomerulosa. This causes Na and water retention (hypertension), hypokalemia (mscle weakness) and metabolic acidosis due to excess excretion.

Will also see decreased renin levels

58
Q

A 21-hydroxylase enzyme block will cause a virilizing syndrome due to excess ______ production

A

Androgen

59
Q

The adrenal medulla is a specialized sympathetic ganglion containing modified postganglionic (chromaffin cells) that _____

A

Secrete catecholamines directly into blood stream

60
Q

Medullary arterioles and cortical sinusoids of the adrenal gland merge to form the -_________

A

Medullary plexus

61
Q

The adrenal gland is the only source of circulating _________

A

Epinephrine

62
Q

What is the rate limiting step of catecholamine biosynthesis?

A

The conversion of tyronsine to DOPA (dihydroxyphenylalanine) by tyrosine hydroxylase

63
Q

What is the transporter that moves dopamine into the secretory granules where it will be converted to norepinephrine?

A

VMAT (a catecholamine/H+ exchanger)

64
Q

Epinephrine is stored in the chromaffin granule until it is secreted by ________

A

Exocytosis

65
Q

What are catecholamines stored in a complex with when they are in chromaffin granules waiting to be secreted? )x3)

A

ATP

Ca++

Chromogranin ( a protein )

66
Q

Acetylcholine released from preganglionic fibers causes what two things in the adrenal medulla?

A
  1. Binds to nicotinic receptors, causes Na influx, depolarization, opening of volt-gate calcium channels, influx of calcium, and exocytosis
  2. Increases transcription of tyrosine hydorxylase (tyrosine—> DOPA) which is the rate limiting step in formation of catecholamines
67
Q

What does glucocorticoids do to the regulation of catecholamines?

A

Induces PNMT which converts norepinephrine to epinephrine

Also prevents chromaffin cells from developing into postganglionic neurons

68
Q

What are the two regulators of catecholamine synthesis and release by the adrenal medulla?

A

Sympathetic activation

Glucocorticoids

69
Q

Explain pheochromocytomas

A

These are catecholamine secreting tumors of chromaffin cells of the adrenal medulla (90%) or extra-adrenal ganglia

Signs and symptoms:
Hypertension (most common)
H/a 
Anxiety
Sweating
Wt loss
Increase metabolic rate
Increased glucose tolerance
Tachycardia
70
Q

What are signs and symptoms of Pheochromocytomas?

X9

A 
Hypertension (most common)
H/a
Anxiety
Sweating
Tachycardia
Tremors
Wt loss
Increase gluc tolerance
Increased metabolic rate

S & F 4 Test 2 (15 decks)

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