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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
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
Adrenarche
26
-_______ is the principal glucocorticoid in humans
Cortisol
27
What is the half life of cortisol
90 minutes
28
What is the most accurate estimate of daily cortisol output?
A measurement of 24 hour urinary excretion of unmetabolized cortisol (This despite the fact that 99% of cortisol in urine is metabolized)
29
What accounts for the increased activity of the synthetic glucocorticoids prednisone and dexamethasone?
Increased affinity for glucocorticoid receptors Delayed plasma clearance
30
______ is the principle physiological regulator of cortisol release
ACTH (adrenocorticotropic hormone)
31
What are the acute effects of ACTH (x4)
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
What are the chronic effects of ACTH stimulation of the cells of the zona fasciculata and reticularis? (X2)
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
What is the effect of long term ACTH suppression ?
Adrenal gland atrophy
34
The normal circadian rhythm is a result of the __________ nucleus of the hypothalamus
Suprachiasmatic
35
_________ is the principal regulator of ACTH secretion
CRH (corticotropin releasing hormone)
36
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
Highest
37
What are 3 ways that cortisol protects against hypoglycemia?
1. Promotion of gluconeogenesis in liver 2. Increases expression of glycogen synthase 3. Inhibits glucose uptake in skeletal muscle
38
How does cortisol help increase gluconeogenesis?
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
Cortisol has a ________ effect on catecholamine-induced lipolysis that is mostly permissive
Stimulatory
40
_____adrenal patients tend to experience hypoglycemia
Hypo Due to decreased cortisol production
41
Cortisol -_______ erythropoitin synthesis
Stimulates
42
Cortisol has what effects on CNS (x4)
Has some affect on ; Mood Wakefulness Behavior Sensory stimulation intensity
43
What do gluccocorticoids do to bone resorption?
They directly inhibit it They also inhibit intestinal calcium uptake and renal calcium reabsorption. Excessive use of glucocorticoids will result in osteoporosis
44
High concentrations of glucocorticoids ________ Ca uptake by the intestines and _________ calcium reabsorption in the kidneys
Antagonize Inhibit
45
How do glucocorticoids’ anti-inflammatory effects get mediated? (X4)
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
What is the role of lipocortin in the anti-inflammatory response of cortisol?
Lipocortin synthesis is stimulated by cortisol Lipocortin acts to inhibit phospholipase A2
47
Primary adrenocortical insufficiency (addison dz) is caused by?
A defect w/in adrenal gland Destruction of gland by tuberculosis, metastatic tumor, etc. Autoimmune disorder Inborn errror of steroid hormone synthesis
48
What are the causes of primary adrenocortical insufficiency (addison disease(x3)
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
Aldosterone deficiency, which is seen in primary adrenocortical insufficiency (Addison’s Disease) causes what s/s?
Hyponatremia and polyuria due to decreased renal reabsorption of Na ECF depletion Hypotension Dehydration Hyperkalemia because of loss of gradient
50
What are the consequences of cortisol deficiency due to a primary adrenocortical insufficiency (addison’s Disease) (x8)
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
What are the consequences of androgen deficiency which are seen in addison’s disease
Females will lose pubic hair and axillary hair
52
What is secondary adrenocortical insufficiency associated with ?
An insufficient production of ACTH
53
What are causes of secondary adrenocortical insufficiency associated with insufficient levels of ACTH? (X3)
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
Explain pseudohypoaldosteronism
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
What are the major causes of Cushing Syndrome in order of importance? (X4)
Ingestion of pharmacological doses of glucocorticoids ACTH secretion in excess from Pituitary Ectopic, non-endocrine, ACTH secreting tumor Tumors of the adrenal cortex
56
What is the reason that you get poor wound healing in cushing’s patients? (40% of time) (X5)
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
Explain Conn Syndrome
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
A 21-hydroxylase enzyme block will cause a virilizing syndrome due to excess ______ production
Androgen
59
The adrenal medulla is a specialized sympathetic ganglion containing modified postganglionic (chromaffin cells) that _____
Secrete catecholamines directly into blood stream
60
Medullary arterioles and cortical sinusoids of the adrenal gland merge to form the -_________
Medullary plexus
61
The adrenal gland is the only source of circulating _________
Epinephrine
62
What is the rate limiting step of catecholamine biosynthesis?
The conversion of tyronsine to DOPA (dihydroxyphenylalanine) by tyrosine hydroxylase
63
What is the transporter that moves dopamine into the secretory granules where it will be converted to norepinephrine?
VMAT (a catecholamine/H+ exchanger)
64
Epinephrine is stored in the chromaffin granule until it is secreted by ________
Exocytosis
65
What are catecholamines stored in a complex with when they are in chromaffin granules waiting to be secreted? )x3)
ATP Ca++ Chromogranin ( a protein )
66
Acetylcholine released from preganglionic fibers causes what two things in the adrenal medulla?
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
What does glucocorticoids do to the regulation of catecholamines?
Induces PNMT which converts norepinephrine to epinephrine Also prevents chromaffin cells from developing into postganglionic neurons
68
What are the two regulators of catecholamine synthesis and release by the adrenal medulla?
Sympathetic activation Glucocorticoids
69
Explain pheochromocytomas
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
What are signs and symptoms of Pheochromocytomas? | X9
``` 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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