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Patho 2 > 1 - Adrenocortical Hormones > Flashcards

1 - Adrenocortical Hormones Flashcards

1
Q

The adrenal cortex secretes:

A

corticosteroids

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2
Q

The adrenal medulla secretes:

A

Epinephrine and norepinephrine

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3
Q

The three classes of corticosteroids released by the adrenal cortex are:

A

mineralocorticoids

glucocorticoids

androgens

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4
Q

What is the gross function of mineralocorticoids?

A

They effect “minerals” aka electrolytes

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5
Q

What is the gross function of glucocorticoids?

A

increase blood glucose concentration

(also effect protein and fat metabolism)

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6
Q

The principal mineralocorticoid is _________

The principal glucocorticoid is _________

A

aldosterone

cortisol

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7
Q

Describe the three layers of the adrenal cortex, including what they secrete and how secretion is controlled

A
  1. Zona glomerulosa - only cells that secrete aldosterone, secretion of which is controlled by K and Angiotensin II
  2. Zona fasciculata - middle, widest, secretes cortisol and corticosterone, secretion controlled by ACTH
  3. Zona reticularis - inner zone, secretes adrenal androgens and small amounts of estrogen and glucocorticoids, regulated by ACTH
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8
Q

Describe the relationship between aldosterone and cortisol secretion

A

They are completely independently regulated

ACTH has no effect on aldosterone

Angiotensin II has no effect on cortisol

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9
Q

Approximately 80% of the cholesterol used for steroid synthesis is provided by _______

A

LDLs in circulating plasma

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10
Q

What is the rate limiting step in all adrenal steroid formation?

A

the cleaving of cholesterol in the cell into pregnenolone by cholesterol desmolase

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11
Q

Synthesis of steroid in the adrenal cortex occurs where in the cell?

A

mitochondria and ER

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12
Q

How potent is dexamethasone compared to cortisol?

A

30x more potent

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13
Q

If cortisol primarily effects glucose metabolism, why do high cortisol disease states also include electrolyte imbalances?

A

Cortisol also has slight mineralocorticoid action

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14
Q

How is cortisol transported in the blood?

A

90-95% bound to cortisol-binding globulin

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15
Q

How is aldosterone transported in the blood?

A

60% protein bound

40% free form,

this accounts for its short half life of 20 minutes vs. other adrenocortical hormones (like cortisol)

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16
Q

Where are adrenocortical hormones metabolized?

A

Metabolized in the liver

inactive conjugates excreted by the liver

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17
Q

What would happen without mineralocorticoids?

A

Think: without aldosterone

Massive salt wasting and hyperkalemia

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18
Q

Since cortisol has some mineralocorticoid effect, and there’s an enormous concentration of it floating in the plasma, why doesn’t it have a big effect on the kidneys?

A

renal epithelial cells express 11B-HSD2

prevents cortisol from activating mineralocorticoid receptors

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19
Q

What is Apparent Mineralocorticoid Excess Syndrome?

A

AME

Happens when the 11b-HSD2 enzymes are deficient, allowing cortisol to bind to mineralocorticoid receptors

looks like hyperaldosteronism, but aldosterone levels are low

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20
Q

What does Aldosterone impact: total sodium or sodium concentration?

A

TOTAL SODIUM!

Water moves with the sodium, and concentration remains the same

21
Q

What is aldosterone escape?

A

only elevates extracellular volume for about two days

As ECF increases, so does GFR

results in pressure natriuresis/diuresis whcih returns the renal output of sodium and water to normal despite excess aldosterone

22
Q

An increase in aldosterone does not effect sodium concentration, but a decrease does. Why?

A

Decreased aldosterone leads to massive water loss, which triggers ADH

ADH causes water reabsoprtion but NOT sodium reabsorption

You get a decrease in [Na]

23
Q

What are the most potent regulators of aldosterone secretion?

A

[K]

Angiotensin II

24
Q

95% of the glucocorticoid activity of the adrenal cortex results from the secretion of ________

A

cortisol/hydrocortisone

25
Q

What is gluconeogenesis?

A

formation of carbohydrates from proteins and other substances in the liver

26
Q

By what 3 modes does cortisol increase gluconeogenesis?

A
  1. Activates liver cell DNA transcription to create enzymes required to convert amino acids into glucose
  2. Moves amino acids from the muscles into the liver
  3. Antagonizes insulin’s inhibitory effect on gluconeogenesis
27
Q

Cortisol causes blood glucose to rise for two reasons:

A
  1. gluconeogenesis
  2. decreased glucose utilization by cells
28
Q

What is adrenal diabetes?

A

elevated cortisol cuases an increase in blood sugar, and in doing so decreases tissue sensitivity to insulin

The pancreas is working just fine and releases an appropriate amount of insulin, but the tissues are resistant to insulin so the blood sugar remains elevated

the problem isn’t the pancreas, its the cortisol levels

29
Q

Cortisol reduces the amount of ____ protein, and increases the amount of ______ protein

A

cellular

liver and plasma

(wants to preserve amino acid consumption, so it reduces the ability of all nonhepatic cells to make proteins)

30
Q

How does cortisol mobilize amino acid transport to the liver?

A

It prevents anabolic processes, but it doesn’t effect catabolic protein metabolism. This means cells aren’t producing proteins, but they are still breaking them down. The excess amino acids released and transported via blood to the liver

31
Q

Cortisol _______ fatty acid mobilization

A

increases

32
Q

Why does excess cortisol cause obesity (moon face etc)?

A

not totally known

excess stimulation of food intake is likely

33
Q

Any stress causes an increase in the secretion of ______ from the anterior pituitary, which causes secretion of cortisol

A

ACTH

34
Q

Cortisol has a preferrential on amino acid mobilization. Explain.

A

cortisol usually does not mobilize the basic functional proteins of the cell, such as muscle contracile proteins and proteins of neurons

It will eventually mobilize these AAs, but not until all others have been used

35
Q

What are the five stages of inflammation?

A
  1. Chemicals released from damaged tissue
  2. increased blood flow to area causes erythema
  3. capillary leakage followed by clotting of tissue fluid causes nonpitting edema
  4. infiltration of leukocytes
  5. fibrous tissue healing
36
Q

What are the five anti-inflammatory effects of coritsol?

A
  1. Stabilizes lysosomal membrane, decreasing the amount of chemicals released
  2. Decreases permeability of capillaries (2/2 decreased proteolytic lysosome release)
  3. Decreased mediators means decreased WBC migration
  4. lymphocytes are suppressed
  5. reduces fever by preventing release of interluekin-1
37
Q

The anti-inflammatory effects of cortisol boil down to two global effects:

A

stabilizing lysosomal membranes

reducing the formation of prostaglandins and leukotrienes from arachidonic acid in damaged cell membranes

38
Q

What effect does cortisol have on lymph tissue?

A

causes significant atrophy, which decreases the output of T cells and antibodies from the lymphoid tissue

39
Q

Describe the pathway for cortisol secretion:

A
  1. Corticotropin-releasing factor is released from the hypothalamus
  2. CRF triggers ACTH release from the anterior pituitary
  3. ACTH triggers cortisol release from the adrenal cortex
40
Q

Describe the circadian rhythm of glucocorticoid secretion

A

the secretory rates of CRF, ACTH, and cortisol are high in the early morning and low in the late evening

41
Q

When are glucocorticoids released?

A

Under stress conditions

42
Q

Why do glucocorticoids decrease immune and inflammatory responses?

A

They decrease the natural killer cell activity

Block the synthesis of prostaglandins, thromboxanes, and leukotrienes

suppress the synthesis/secretion/action of chemical mediators (like histamine)

43
Q

What are some of the most problematic side effects of glucocorticoid administration?

A

infection

poor wound healing

44
Q

The adrenal medull functions as a sympathetic ______

A

ganglion, without postganglionic processes

45
Q

Physiologic stress triggers release of adrenal catecholamines through ________

A

acetylcholine from preganglionic sympathetic fibers

Depolarizes chromaffin cells

depolarization sparks exocytosis of catecholamines

46
Q

Secretion of adrenal catecholamines is triggered by:

A
  1. Sympathetic stimulation
  2. ACTH
  3. Glucocorticoids
47
Q

What is the prevalence of impaired glucose tolerance/diabetes in adults over 65?

A

40-50%

Decline in beta cell function

48
Q

The decline of GH and IGF with age is referred to as:

A

somatopause

leads to decreased muscle size and function

49
Q

Why is hyponatremia a common finding in the elderly?

A

Changes in renal function and sensitivity

NOT due to changes in ADH

Patho 2 (24 decks)

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