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Clinical Chemistry > Adrenal Glands form/functions > Flashcards

Adrenal Glands form/functions Flashcards

Spring 2024

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1
Q

Adrenal gland

A

The adrenal gland is composed of two embryologically distinct tissue —the outer adrenal cortex and inner adrenal medulla.

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2
Q

Where are the adrenal glands located?

A

On each kidney

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3
Q

Adrenal cortex

A
  • Functions to produce steroid hormones
  • Is the outer portion
  • Has 3 layers
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4
Q

Adrenal medulla

A
  • Functions to produce amine hormones
  • Inner portion
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5
Q

List the 3 adrenal cortex zones

A
  1. Zona glomerulosa
  2. Zona fasciculata
  3. Zona reticularis
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6
Q

Zona glomerulosa

A
  • Secretes mineralocorticoids, such as aldosterone
  • Critical for salt balance, potassium excretion, acid–base homeostasis, and regulation of blood pressure
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7
Q

Zona fasciculata-

A
  • Secretes glucocorticoids such as cortisol
  • critical for carb metabolism and blood pressure
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8
Q

Zona reticularis

A
  • Secretes sex hormones such as the androgens
  • Required for sexual function and contribute less than the gonads
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9
Q

Aldosterone
Where is it produced?
Function?
How is it regulated?

A
  • Produced in G-zone
  • Controls amount of fluid in body (Na, Cl, and water retention, K and H excretion)
  • renin-angiotensin system controls its production
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10
Q

How does decreased aldosterone affect Na and K excretion?

A

Increases Na excretion
Decreases K excretion

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11
Q

How does increased aldosterone affect blood pressure, blood volume, and reabsorption?

A

Increases salt and water reabsorption and increases blood pressure/volume (vasoconstriction)

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12
Q

Describe aldosterone regulation by renin

A

Increased BP and blood volume suppresses renin secretion, thus suppressing aldosterone synthesis

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13
Q

Describe primary hyperaldosteronism

A

It’s an adrenal disease, such as an aldosterone-secreting adrenal adenoma or carcinoma, or adrenal cortex hyperplasia

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14
Q

Conn syndrome

A

Aldosterone-secreting adenoma

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15
Q

Describe secondary hyperaldosteronism

A

Renin-angiotensin disorder where there’s excess renin synthesis due to renin-secreting renal tumor, thus causing malignant hypertension

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16
Q

Primary aldosteronism “Conn’s Syndrome”

A
  • Increased sodium levels
  • Symptoms: hypokalemia, mild metabolic alkalosis, increase blood volume and BP
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17
Q

Hypoaldosteronism

A

Atrophy of adrenal glands

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18
Q

Examples of hypoaldosteronism

A
  • Addison’s disease: reduced aldosterone and glucorticoid production
  • Congenital deficiency of 21-hydroxylase enzyme
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19
Q

Consequences of hypoadrenalism

A
  • Reduced aldosterone and cortisol secretion
  • Reduced blood glucose
  • Reduced Na and Cl
  • Increased ACTH
  • Increased beta-MSH
  • Increased K
  • Skin pigmentation
  • Muscle weakness
  • Weight loss
  • Decreased BP
  • Nausea
  • Diarrhea
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20
Q

Addison’s disease signs

A
  • Bronze skin
  • Changes in body hair distribution
  • GI disturbances
  • Weakness
  • Weight loss
  • Hypoglycemia
  • Postural hypotension
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21
Q

Cortisol physiological effects

A
  • Anti-insulin effects of carbs -> increased blood glucose
  • More gluconeogenesis, lipolysis, protein catabolism
  • Less protein synthesis, antibody formation, inflammatory response
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22
Q

Which two hormones have diurnal variation?

A

Cortisol and ACTH

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23
Q

Cortisol regulation

A

Positive feedback loop
Hypothalamus secretes CRH -> anterior pituitary secretes ACTH -> adrenal gland secretes cortisol, which goes back to stimulate the hypothalamus

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24
Q

How do cortisol levels affect ACTH release?

A

Low cortisol = more ACTH released
High cortisol = less ACTH released

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25
Q

Primary hypercorticolism

A
  • Adrenal adenoma or carcinoma
  • Cushing syndrome results from cortisol excess
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26
Q

Secondary hypercorticolism

A
  • Pituitary tumor causes excess ACTH production
  • Ectopic production of ACTH by nonendocrine tumor
  • Cushing disease results from pituitary ACTH excess, which in turn stimulates too much cortisol
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27
Q

Cushing’s Syndrome symptoms

A
  • Increased symptom cortisol
  • No diurnal variation
  • Hyperglycemia
  • Reduced ACTH and immune response
  • Belly and face weight gain (moon face)
  • Buffalo hump back
  • Thinning skin
  • Easy bruising
  • Hypertension
  • Muscle wasting
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28
Q

Difference between Cushing’s Disease and Syndrome?

A
  • Cushing’s Disease: this is an actual disease in which there is an adenoma on the pituitary gland causing too much ACTH made, thus too much cortisol
  • Cushing’s Syndrome: This is a syndrome that has various symptoms associated with high levels of cortisol or corticosteroids in the body
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29
Q

ACTH levels in Cushing’s Disease and Syndrome

A

CD: always high
CS: not always high

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30
Q

Causes of ACTH-dependent Cushing’s Syndrome

A
  • Primary ACTH pituitary disease
  • Ectopic ACTH
  • Ectopic CRF
31
Q

Causes of ACTH-independent Cushing’s Syndrome

A
  • Adrenal adenoma
  • Adrenal carcinoma
  • Nodular adrenal hyperplasia
  • Exogenous glucocorticoids
32
Q

Primary hypocorticolism

A

Atrophy of adrenal gland due to
-autoimmune disease
-tuberculosis
-prolonged high dosage cortisol therapy

33
Q

Secondary hypocorticolism

A

Pituitary hypofunction

34
Q

Criteria for primary adrenal insufficiency when cortisol is low

A
  • None to minimal cortisol stimulation
  • High ACTH
  • Low aldosterone
  • Hyperkalemia/hyponatremia
35
Q

Criteria for secondary adrenal insufficiency when cortisol is low

A
  • Normal cortisol stimulation
  • Low ACTH
  • Normal aldosterone
  • Normal electrolytes
36
Q

Adrenal medulla produces which catecholamines?

A
  • Epinephrine
  • Norepinephrine
  • Dopamine
37
Q

How are catecholamines made?

A

Synthesized from tyrosine by chromaffin cells of the medulla, brain, and sympathetic neurons

38
Q

Epinephrine

A
  • Converts glycogen to glucose, which allows voluntary muscles to have greater work output
  • Released in response to low BP, hypoxia, cold exposure, muscle exertion, and pain
39
Q

Norepinephrine

A
  • Neurotransmitter affecting vascular smooth muscle and heart
  • Released primarily by postganglionic sympathetic nerves
40
Q

Dopamine

A

Neurotransmitter in brain affecting vascular system

41
Q

Catecholamine metabolism

A

:)

42
Q

Pheochromocytoma

A
  • Benign tumor of adrenal medulla
  • Increased epinephrine and norepinephrine
  • Quantified by fluorometric, colorimetric, spectrophotometric methods
43
Q

Fluorometric methods quantify…

A

Plasma epinephrine and norepinephrine

44
Q

Colorimetric/spectrophotometric methods quantify…

A

VMA

45
Q

Neuroblastoma

A
  • Malignant tumor of adrenal medulla common in kids
  • Makes epinephrine, norepinephrine, dopamine, and HVA
  • Characterized by increase in HVA and VMA urinary excretion
  • Quantified by HPLC, gas chrom, and spectrophotometry
46
Q

Adrenal incidentaloma

A

Adrenal madd greater than 1 cm

47
Q

Testes

A
  • Part of hypothalamic-pituitary-gonadal axis
  • Anterior pituitary secretes LH and FSH
48
Q

LH

A

Stimulates production of testosterone

49
Q

FSH

A

Stimulates spermatogenesis

50
Q

LSH and FSH are regulated by…

A

GnRH

51
Q

How does testosterone control LH and FSH production?

A

Negative feedback to hypothalamus

52
Q

Primary disorder of testes

A

Abnormal testosterone synthesis

53
Q

Secondary disorder of testes

A

Due to primary disorder of pituitary or hypothalamus causing abnormal testosterone synthesis

54
Q

Testosterone

A
  • Principle male sex hormone
  • Mainly secreted by testes but also secreted lesser extent by adrenal glands and ovaries
  • Facial/body hair, muscle dev, secondary male sex traits
55
Q

Hyperandrogenemia

A
  • Adult males, no visual symptoms
  • Prepubertal males: precocious puberty due to hypothalamic tumors, congenital adrenal hyperplasia, testicular tumor
  • Female kids: develop male 2° traits/virilization
56
Q

Congenital adrenal hyperplasia (CAH)

A
  • Caused by enzyme defect of 21-hydroxylase, which prevents cortisol production
  • Increased blood levels of cortisol precursors 17-OHP and ACTH
  • Too much ACTH stimulates diffuse enlargement of adrenal glands, posing greater risk for tumors
57
Q

Hypoandrogenemia

A
  • Adult males: impotence, loss of 2° sex traits
  • Prepubertal males: delayed puberty
58
Q

Primary hypoandrogenemia

A

Causes include tumors, infections, congenital disorders, Klinefelter syndrome

59
Q

Secondary hypoandrogenemia

A

Causes include primary hypofunction disorders of pituitary or hypothalamus -> reduced LH and FSH

60
Q

Klinefelter syndrome

A

XXY chromosomes

61
Q

Semen analysis

A
  • Analyzed within 30 min
  • Measure pH
  • Motility, sperm count/morphology/viability
62
Q

Ovaries

A
  • Part of hypothalamic-pituitary-gonadal axis
  • Estrogens and progesterone exert negative feedback to control LH and FSH synthesis
63
Q

Estrogen

A
  • Secreted by ovarian follicles and placenta
  • Secreted by lesser extent in adrenal glands/testes
  • Three primary estrogens: estradiol-17beta, estrone, and estradiol
64
Q

Estradiol

A

Principle estrogen synthesized by ovaries

65
Q

Progesterone

A

Secreted by ovarian follicles, mainly by corpus luteum following ovulation and placenta during pregnancy to maintain uterus

66
Q

Which hormone peaks during ovulation?

A

Estrogen

67
Q

Which hormone peaks during luteal phase?

A

Progesterone

68
Q

Hyperestrinism in females

A
  • Precocious puberty: ovarian tumor, hypothalamic tumor, adrenal tumors,
  • Infertility and irregular menses: polycystic ovaries, estrogen-producing ovarian tumors, disorders of the hypothalamus or pituitary
  • Postmenopausal bleeding: cervical or endometrial carcinoma, estrogen-producing ovarian tumors, exogenous estrogen consumption
69
Q

Hyperestrinism in males

A

Testicular atrophy and enlargement/development of breasts

70
Q

Hypoestrinism

A
  • Ovarian insufficiency
  • Delayed puberty
  • Amenorrhea (absence of menstruation) due to menopause, chemo, severe stress, intense athletic training, excessive weight loss
  • Tuner syndrome
71
Q

Tuner syndrome

A

Genetic defect in females: partial or complete loss of one of the two X chromosomes -> non-functioning ovaries. Exogenous estrogen canbe given to obtain 2° sex traits

72
Q

Hyperprogesteronemia

A

Prevents menstrual cycle from happening

73
Q

Hypoprogesteronemia

A

Causes infertility, fetal abortion

74
Q

Polycystic ovary syndrome

A

Common disorder presents itself in several ways:
- infertility, hirsutism (excess facial hair), chronic anovulation, glucose intolerance, hyperlipidemia/dyslipidemia, and hypertension

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