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Patho I - Exam #2: Endocrine > Module 3A > Flashcards

Module 3A Flashcards

1
Q

What role does the adrenal gland have in the endocrine system?

A
  • response to stress (fight or flight)
  • maintain water/salt equilibrium
  • maintain BP
  • sympathetic function (“extension of ANS”)
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2
Q

What are the two regions of the adrenal gland?

A
  • medulla

- cortex

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3
Q

What hormones does the adrenal medulla release?

A
  • catecholamines (E, NE)
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4
Q

What hormones does the adrenal cortex release?

A
  • aldosterone
  • cortisol
  • dehydroepiandosterone (DHEA)
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5
Q

What are the steps to hormone release from the adrenal medulla?

A
  • stressor stimulates CNS/hypothalamus which stimulates brainstem & SC to sympathetic trunk which affects the adrenal medulla to release E & NE
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6
Q

What are the responses of systemic sympathetic activation?

A
  • increase CV response (increase HR, BP, TPR)
  • increase BMR
  • increase ventilation response
  • decrease GI fxn
  • increase CNS “alertness”
  • mobilize fuel via glycogenolysis and lipolysis)
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7
Q

What are the layers of the adrenal cortex?

A
  • zona glomerulosa (outer)
  • zona fasiculata (middle)
  • zona reticularis (inner)
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8
Q

What is produced/secreted by the zona glomerulosa?

A
  • mieralcorticoid (aldosterone)
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9
Q

What is produced/secreted by the zona fasiculata?

A
  • gluocorticoids (cortisol)

- adrenal androgen (DHEA)

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10
Q

In general, what does the adrenal cortex produce/stimulate?

A
  • all steroids but subtly different
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11
Q

Why do the different layers of the adrenal cortex produce/secrete different hormones?

A
  • different layers contain different enzymes
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12
Q

What is the precursor for all adrenal cortex hormones?

A
  • cholesterol
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13
Q

What is the first step(s) in adrenal cortex hormone synthesis?

A
  • cholesterol transported from blood stream to cortex

- once in cortex: cholesterol w/ desolase –> pregnenolone

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14
Q

What stimulates the first chemical step in adrenal cortex hormone synthesis?

A
  • ACTH
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15
Q

What happens to pregnenolone in the adrenal cortex?

A
  • based on which layer it is in, converted to aldosterone, cortisol, or DHEA via specific pathway enzymes
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16
Q

What occurs if there are deficiencies in the pathway specific enzymes?

A
  • deficiency in that hormone ==> adrenal pathology
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17
Q

T/F: Hormones are stored in the adrenal cortex for secretion as needed.

A
  • False, synthesized at rate of demand
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18
Q

What pattern do hormones tend to be secreted from the adrenal cortex?

A
  • circadian rhythmn
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19
Q

What are the signaling steps in the stimulus of hormone release from the adrenal cortex?

A
  • hypothalamus releases CRH
  • CRH stimulates ant. pit to release ACTH
  • ACTH stimulates desmolase in adrenal cortex to convert cholesterol to pregnenolone
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20
Q

What can also influence aldosterone?

A
  • angiotensin II

- ECF K+

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21
Q

What inhibits hormone release from the adrenal cortex?

A
  • increase levels of cortisol inhibit release of ACTH and CRH (neg. feedback loop)
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22
Q

Why does cortisol inhibit hormone release from the adrenal cortex?

A
  • the initial step of each pathway is capable of producing cortisol
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23
Q

What is the ideal neg. feedback hormone to affect hormone release from the adrenal cortex?

A
  • cortisol
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24
Q

What is the more secondary inhibitory hormone of hormone release from the adrenal cortex?

A
  • aldosterone
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25
Q

Where is cortisol produced?

A
  • zona fasiculata (middle) & reticularis (inner)
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26
Q

What is the stimulus for cortisol secretion?

A
  • ACTH from ant. pit
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27
Q

What factors influence cortisol secretion?

A
  • normal circadian rhythm

- stress

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28
Q

What inhibits cortisol secretion?

A
  • elevated cortisol (inhibits ACTH & CRH from ant. pit and hypothalamus, respectively)
  • elevated ACTH inhibits hypothalamus
    (negative feedback loop)
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29
Q

What is the function of gluocorticoids (cortisol)?

A
  • catabolic to produce/mobilize/store glucose
  • maintains fluid volume
  • modulates immune system (anti-inflam response)
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30
Q

What are target tissues of cortisol?

A
  • bone
  • adipose
  • muscle
  • tendon/ligament/connective tissue
  • immune system
  • CNS
  • metabolic
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31
Q

What is the effect of cortisol on bone?

A
  • stimulate osteoclast/Ca2+ resportion
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32
Q

What is the adverse effect of cortisol on bone?

A
  • decrease bone density
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33
Q

What is the effect of cortisol on adipose?

A
  • stimulate lipolysis (mobilize FFA and glycerol for fuel & production of new glucose
  • synergistic with glucagon, GH, catecholamines
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34
Q

What is the adverse effect of cortisol on adipose?

A
  • adipose loss/redistribution
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35
Q

What are the clinical descriptors of adipose redistribution?

A
  • moon face

- buffalo hump

36
Q

What is the effect of cortisol on muscle?

A
  • stimulate proteolysis (mobilize a.a. for fuel & production of new glucose)
37
Q

What is the adverse effect of cortisol on muscle?

A
  • muscle wasting/weakness

- loss of lean body mass

38
Q

What is the effect of cortisol on tendon/ligament/connective tissue?

A
  • catabolic effect (inhibits fibroblasts/collagen production)
39
Q

What is the adverse effect of cortisol on tendon/ligament/connective tissue?

A
  • ligament/tendon failure
40
Q

What is the effect of cortisol on immune system?

A
  • anti-inflam
41
Q

What is the adverse effect of cortisol on immune system?

A
  • poor wound healing/immune defenses

- only a concern with long or large doses

42
Q

What is the effect of cortisol on CNS?

A
  • alters perception and mood

- neg. feedback to hypothalamus & ant. pit

43
Q

What is the effect of cortisol on metabolic function?

A
  • alters intermediary metabolism to produce, mobilize, and store glucose (trying to save glucose for CNS survival)
  • optimizes/enhances effect of glucagon
44
Q

What is the effect of cortisol on the liver?

A
  • gluconeogenosis

- glycogenesis

45
Q

What is the effect of cortisol on catecholamines?

A
  • optimizes/enhances effect

i. e. vasoconstriction & bronchodilation

46
Q

What is the effect of cortisol on fetus lungs?

A
  • surfactant production

- lung development

47
Q

T/F: Cortisol enhances the body’s ability to tolerate stress

A
  • True
48
Q

Where are mineralcorticoids (aldosterone) produced?

A
  • zona glomerulosa (outer)
49
Q

What is the primary function of aldosterone?

A
  • increase blood volume/BP by increasing renal Na+ resoprtion
50
Q

What are the secondary functions of aldosterone?

A
  • decrease plasma K+

- increase plasma pH

51
Q

What are the actions of aldosterone?

A
  • increase Na+ resorption in distal nephron (fine tuning)

- vasoconstriction

52
Q

What does Na+ resorption lead to?

A
  • increased H20 absorption (gradient follows Na+)

- facilitates K+ & H+ excretion

53
Q

What stimulates aldosterone secretion?

A
  • ACTH
  • angiotenstin II
  • hyperkalemia
54
Q

T/F: ACTH is not as influential on aldosterone release as angiotensin II & K+ levels.

A
  • True
55
Q

What inhibits aldosterone secretion?

A
  • hypernatrimia
  • ANP (atrial natriuretic peptide)
  • elevated ACTH levels
  • hypokalemiea
56
Q

Where are adrenal androgens produced?

A
  • zona fasiculata (middle) & zona reticularis (inner)
57
Q

What are adrenal androgens?

A
  • sex hormones associated with the development/maintenance of male sexual characteristics
58
Q

What are the responses in the female to adrenal androgens?

A
  • maintaining muscle mass, bone density, sexual desire, & sense of well being
  • estrogen production
59
Q

What will low levels of adrenal androgens in female lead to?

A
  • low libido
  • muscle/bone mass loss
  • fatigue
60
Q

Describe androgen production in males

A
  • primarily produced in testes

- adrenal cortex produces androgens that are converted to T in the periphery but NOT in significant amounts

61
Q

Describe androgen production in females

A
  • produced in ovaries & adrenal cortex
62
Q

T/F: Adrenal androgens have amore significant role in males.

A
  • False, females
63
Q

Which is produced in a higher quantity: DHEA or androstenedione?

A
  • DHEA
64
Q

Where can DHEA/androstenedione converted to T?

A
  • peripheral tissues
65
Q

Conversion of DHEA/androstenedione to T is contributes more significantly to circulating levels of T in males or females?

A
  • females
66
Q

What is the most abundant circulating hormone in the body?

A
  • DHEA
67
Q

What is a weak androgen with poor binding affinity to androgen receptors?

A
  • DHEA
68
Q

What are the two fates of circulating DHEA?

A
  • converted to more potent androgen = testosterone (T)

- inactivated and degraded

69
Q

What is the androgen function of the adrenal gland?

A
  • weak androgen function (masculinization)

- excessive adrenal androgens will promote inappropriate masculinization effects

70
Q

T/F: Gonadal androgens (T) have a much more significant role in development of male characteristics

A
  • True
71
Q

Define isosexual precocious puberty

A
  • < 9y/o inappropriate masculinization in males
72
Q

Define heterosexual precocious puberty

A
  • < 8y/o inappropriate masculinization in females
73
Q

What is the stimulus for adrenal androgen secretion?

A
  • ACTH
74
Q

What is the inhibitor for adrenal androgen release?

A
  • cortisol
75
Q

What is Addison’s Dz?

A
  • adrenalcortical insufficiency

- destruction of adrenal cortex so loss of all adrenal cortex hormones

76
Q

What will labs demonstrate in Addison’s Dz?

A
  • elevated ACTH

- decreased adrenal hormones

77
Q

What is the effect of Addison’s on the zona glomberulosa?

A

~decreased mineralcorticoid (aldosterone) secretion~

  • dehydration with polyuria
  • hypotension
  • hyponatremia
  • hyperkalemia
  • metabolic acidosis
  • decreased blood vol.
78
Q

What is the effect of Addison’s on the zona reticularis & fasiculata?

A

~decreased mineralcorticoid (aldosterone) secretion~

  • hypoglycemia
  • hyperpigmentation
  • weakness
  • anorexia
  • wt loss
  • nausea
  • decrease in pubic/axillary hair in females
79
Q

What is the difference b/t Cushing’s Syndrome & Dz?

A
  • syndrome = excess cortisol of any pathology

- dz = excessive ACTH which results in excess cortisol

80
Q

What is a clinical example of hyperadrenalism?

A
  • Cushing’s Syndrome/Dz
81
Q

What are the effects of increased glucocorticoids (cortisol)

A
  • poor wound healing
  • hyperglycemia
  • muscle wasting
  • osteoperosis
  • central obesity
82
Q

What are the effects of increased mineralcorticoids?

A
  • HTN
83
Q

What are the effects of increased adrenal androgens?

A
  • virilization

- menstrual disorders

84
Q

What is a clinical example of primary hyperaldosteronism?

A
  • Conn’s Syndrome
85
Q

What is the result of Conn’s Syndrome?

A
  • HTN
  • hyperkalemia
  • metabolic alkalosis

Patho I - Exam #2: Endocrine (4 decks)

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