Adrenal Physiology Flashcards

1
Q

What does the Yerkes-Dodson curve demonstrate?

A

The relationship between performance and stress levels

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2
Q

True or false: you have two different stress responses for physical vs psychological stressors?

A

False. You only have one generalized stress response

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3
Q

Describe general adaptation syndrome.

A

Nervous and hormonal responses resulting in a state of intense readiness with fuel mobilized for use

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4
Q

Where is the stress response coordinated?

A

Hypothalamus

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5
Q

Describe the short-term stress response. What occurs? What is the result (6)?

A

The hypothalamus directly stimulates the adrenal glands via the SNS, which causes catecholamines (Epi and NE) to be secreted from the adrenal medulla. Results in:

  1. Increased HR
  2. Increased BP
  3. Stimulates glycogenolysis and GNEO
  4. Dilation of bronchioles
  5. Decreased digestive system activity and urine output
  6. Increased metabolic rate
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6
Q

Describe the long-term stress response. What occurs?

A

CRH secreted from the hypothalamus to the anterior pituitary, which secretes ACTH into the blood to stimulate the adrenal cortex to secrete steroid hormones (MCCs & GCCs)

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7
Q

What are the effects of mineralocorticoids (MCCs) after being secreted from the adrenal cortex (2)? Example?

A

Retention of sodium and water by the kidneys

Increases blood volume and pressure

Ex: aldosterone

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8
Q

What are the effects of glucocorticoids (GCCs) after being secreted by the adrenal cortex (3)? Example?

A
  1. Proteins and fats converted to glucose or broken down directly for energy
  2. Increase blood glucose
  3. Suppression of the immune system

Ex: cortisol

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9
Q

Label the following aspects of the adrenal gland:

Adrenal medulla, Zona glomerulosa, Zona reticularis, Zona fasciculata.

A
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10
Q

What hormones are secreted by the four regions of the adrenal gland? (Zona golmerulosa, Zona fasciculata, Zona reticularis, Adrenal Medulla)

A

Zona golmerulosa: Mineralocorticoids

Zona fasciculata: Glucocorticoids

Zona reticularis: Androgens

Adrenal medulla: Stress hormones (Epi/NE)

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11
Q

Where in the cell are Epi and NE synthesized?

A

Cytosol of adrenal medulla cells

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12
Q

Approximately how much of the adrenal gland is composed of cortex vs medulla?

A

80-90% cortex

10-20% medulla

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13
Q

What types of hormones are synthesized by the adrenal cortex vs medulla?

A

Cortex: steroids

Medulla: amines

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14
Q

What is the embryonic origin of the adrenal cortex vs medulla?

A

Cortex: mesoderm

Medulla: neuroectoderm

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15
Q

What is the innervation of the adrenal cortex like compared to the medulla?

A

Cortex: Almost no innervation

Medulla: SNS innervation

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16
Q

How are products stored in the adrenal cortex vs medulla?

A

Cortex: lipid droplets

Medulla: amine granules

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17
Q

Are the adrenal cortex and medulla essential for life?

A

Cortex: essential

Medulla: nonessential

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18
Q

In the adrenal cortex, approximately how much cholesterol is taken up from the diet and how much is synthesized by the body?

A

Diet: ~80% from LDL

De novo synthesis: ~20%

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19
Q

If cholesterol is the starting material for all hormones of the adrenal gland, what determines what cholesterol is synthesized into?

A

Distribution of enzymes across the different cell types.

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20
Q

What enzyme catalyzes the conversion of cholesterol to pregnenolone? What stimulates this enzyme in the ZG, ZF, and ZR?

A

Desmolase

ZG: Ang II

ZF: ACTH

ZR: ACTH

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21
Q

What enzyme is absent in the ZG that prevents pregnenolone from being converted into GCCs or androgens?

A

17-α hydroxylase

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22
Q

What provides negative feedback to the hypothalamus and pituitary to stop the secretion of hormone by the adrenal glands?

A

Cortisol

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23
Q

ACTH is synthesized from what precursor? What else is it a precursor to?

A

Preproopiomelanocortin (POMC)

Also gives rise to α-melanocyte-stimulating hormone (MSH)

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24
Q

What does it mean for cortisol secretion to be pulsatile?

A

Alternating bursts of modest secretion separated by silent periods of little to no secretion; amount secreted per pulse does NOT vary

25
Q

What does it mean for cortisol secretion to be diurnal? What structure regulates this?

A

Plasma ACTH and cortisol peak once a day prior to awakening

Regulated by the suprachiasmatic nucleus in the hypothalamus (circadian rhythm)

26
Q

How is cortisol transported in the blood?

A

75% Corticosteroid-binding protein (CBP, transcortin)

15-20% albumin

5% unbound

27
Q

How does the liver inactivate cortisol?

A

Conjugates with glucuronide or sulfate to increase cortisol solubility, which facilitates excretion by the kidneys.

28
Q

What is the half-life of cortisol?

A

~70 minutes

29
Q

Describe the mechanism of action of adrenal steroids after it reaches its target cell (4).

A
  1. Steroid diffuses through cell membrane and binds w/ intracellular receptor-HSP complex
  2. HSP released
  3. Activated receptor has a high affinity for steroid-response elements of DNA and binds to it
  4. Once bound, acts as transcription factor
30
Q

Why can’t GCCs immediately relieve acute bronchial asthma attacks? What can they be used for though?

A

Since GCCs activate synthesis of proteins, there is a lag period of about 30 minutes for them to take effect. This is too slow for an asthma attack.

Can be used in the prevention of new asthma attacks

31
Q

How long can the effects of GCCs last? Why?

A

Hours or days

Slow turnover of enzymes and proteins

32
Q

What are the four main functions of cortisol?

A
  1. Stimulate GNEO in response to low blood sugar
  2. Increase protein and lipid breakdown
  3. Anti-inflammatory effects
  4. Suppress immune response
33
Q

What enzymes of GNEO are stimulated by cortisol?

A

Phosphoenolpyruvate carboxykinase (PEPCK)

Glucose-6-phosphatase

34
Q

If cortisol is supposed to increase glucose, why does it inhibit insulin-stimulated glucose uptake by muscles and adipose?

A

To preserve glucose for use by the brain (the brain can’t use muscle or fat)

35
Q

Excess cortisol results in fat deposits where?

A

Face and trunk

36
Q

What tissues are affected by cortisol?

A

All of them

37
Q

Why can excess cortisol result in muscle weakness?

A

Cortisol breaks down muscle to increase blood glucose levels

38
Q

What are the effects of cortisol on bones and its associated hormones?

A

Increase bone (calcium) reabsorption

Increases PTH secretion

Inhibits osteoblasts

39
Q

What three separate conditions make up high-altitude illness? What medication can be used to treat it? How does it work?

A
  1. Acute mountain sickness
  2. High altitude cerebral edema
  3. High altitude pulmonary edema

Treated with dexamethasone (a GCC): reduces “leakiness” of cerebral and pulmonary blood vessels

40
Q

What is the function of cortisol on the cardiovascular system?

A

Required for maintenance of normal blood pressure

Permits responsiveness of arterioles to the constrictive action of adrenergic and angiotensin stimulation

41
Q

What effect does cortisol have on the kidneys?

A

Inhibits secretion and action of ADH (antagonist)

Increases GFR and RBF (which increases CO)

42
Q

What effect does cortisol have on the CNS (specifically memory)?

A

Enhance memory consolidation

Impairs memory retrieval

43
Q

What are the effects of cortisol on fetal development (3)?

A

Facilitates maturation in utero of the CNS, retina, skin, GI tract, and lungs

Increases surfactant synthesis (so breathing can occur immediately after birth

Maturation of digestive enzymes so the baby can digest milk

44
Q

What is the difference between Cushing’s Syndrome and Cushing’s Disease?

A

Syndrome: broad term for hypersecretion of cortisol

Disease: Pituitary microadenoma that produces ACTH (does not respond to negative feedback)

45
Q

____% of Cushing’s syndromes are ACTH dependent and _____% are ACTH independent.

A

~85% ACTH dependent

~15% ACTH independent

46
Q

In regard to ACTH depending Cushing’s syndromes __% are caused by Cushing’s disease, __% by an ACTH secreting ectopic tumor, and _____ can occur but is rare.

A

80% Cushing’s disease

20% ACTH secreting ectopic tumor

Rare CRH secreting ectopic tumor

47
Q

What are the potential causes of ACTH independent Cushing’s syndrome? (2)

A

Adrenal tumor

Iadogenic

48
Q

What does it mean when Cushing’s syndrome is iatrogenic?

A

Results from treatment of rheumatoid arthritis, allergies, and prevention of transplant rejection

49
Q

What are some of the symptoms of Cushing’s syndrome? (Combination of symptoms may vary).

A

*Truncal obesity

*Moon face

*Hypertension

Skin atrophy

Diabetes

Gonadal dysfunction

*Muscle weakness

*Increased body hair (hirsutism) and acne

Mood changes

Osteoporosis

50
Q

If cortisol levels fluctuate throughout the day, how are adrenal diseases (like Cushing’s) diagnosed?

A

24-hour urine analysis

Normally <50mg/24hr

51
Q

Why is DEX a good treatment for hypercortisolism?

A

DEX has a 25x greater affinity for cortisol’s receptors than cortisol itself

52
Q

What is the difference between primary and secondary adrenal insufficiency?

A

Primary: Autoimmune destruction of adrenal cortex (Addison’s disease)

Secondary: Lack of ACTH

53
Q

In Addison’s disease, what happens to cortisol, aldosterone, adrenal androgen, and ACTH levels?

A

ACTH increases

Cortisol, aldosterone, and adrenal androgen all decrease

54
Q

What are some symptoms of Addison’s disease?

A

*Hyperpigmentation (especially in traumatized areas of the skin)

Weakness

Depression

Weight loss

Hypotension

55
Q

In secondary adrenal insufficiency, what happens to cortisol, aldosterone, androgen, and ACTH levels?

A

Decreased ACTH and cortisol

No change to aldosterone and androgens

56
Q

What are some symptoms of secondary adrenal insufficiency?

A

Similar to those of Addison’s disease WITHOUT hyperpigmentation

Mild orthostatic hypotension

Poor response to stress

57
Q

What is cosyntropin? What is it used for?

A

Synthetic ACTH

Used in stimulation test for Addison’s disease; response means no disease

58
Q

Any enzyme blockage that decreases cortisol synthesis will _____ ACTH and result in _____ _______?

A

Increase ACTH

Adrenal hyperplasia