ENDOCRINE DISORDERS PART 1 of 1.1 (AB) Flashcards

(107 cards)

1
Q

Where is the pituitary gland located?

A

At the base of the brain just below the hypothalamus. behind the nose bridge. in the sella turcica of the sphenoid bone.

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2
Q

Why can traumatic brain injury affect the pituitary gland?

A

Because the sella turcica is a thin layer of bone. impact may damage the pituitary gland and cause dysfunction.

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3
Q

Why is the pituitary gland called the ‘master gland’?

A

Because it produces hormones that regulate many body functions and control other endocrine glands.

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4
Q

What percentage of the pituitary gland is the anterior lobe?

A

0.8

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5
Q

What percentage of the pituitary gland is the posterior lobe?

A

0.2

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6
Q

What is the origin of the anterior pituitary gland?

A

Rathke pouch from oral ectoderm.

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7
Q

What is the origin of the posterior pituitary gland?

A

Neuroectoderm.

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8
Q

When does the pituitary gland start developing?

A

Week 4 of embryonic development.

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9
Q

What is the arterial blood supply of the pituitary gland?

A

Inferior. middle. and superior hypophyseal arteries from the internal carotid.

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10
Q

What does FLAT PiG stand for?

A

FSH. LH. ACTH. TSH. Prolactin. GH.

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11
Q

Which cells secrete growth hormone?

A

Somatotrophs.

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12
Q

Which cells secrete prolactin?

A

Lactotrophs.

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13
Q

Which cells secrete thyroid-stimulating hormone?

A

Thyrotrophs.

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14
Q

Which cells secrete proopiomelanocortin?

A

Corticotrophs.

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15
Q

Which cells secrete LH and FSH?

A

Gonadotrophs.

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16
Q

How many amino acids are in human growth hormone?

A

191

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17
Q

How is growth hormone secreted?

A

In a pulsatile fashion regulated by hypothalamic hormones.

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18
Q

What are stimulants of growth hormone secretion?

A

GHRH. ghrelin. sleep. exercise. physical stress. trauma. acute illness. puberty. fasting. hypoglycemia.

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19
Q

What are inhibitors of growth hormone secretion?

A

Somatostatin. hyperglycemia. hypothyroidism. glucocorticoids.

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20
Q

What are the biological effects of growth hormone?

A

Linear growth. bone thickness. soft tissue growth. protein synthesis. fatty acid release. insulin resistance. increased blood glucose.

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21
Q

Where is IGF-1 primarily synthesized?

A

In the liver.

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22
Q

What regulates IGF-1 levels?

A

GH levels and nutritional status.

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23
Q

What inhibits prolactin secretion?

A

Dopamine.

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24
Q

What increases serum prolactin levels?

A

Disruption of hypothalamus or pituitary stalk. dopamine antagonists. primary hypothyroidism. TRH administration. prolactinoma.

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25
What decreases serum prolactin levels?
Dopamine agonists. destruction of the pituitary.
26
What is prolactin's primary physiologic role?
Initiation and maintenance of lactation.
27
What are signs of hyperprolactinemia?
Galactorrhea. amenorrhea. infertility.
28
What is TSH made of?
Alpha and beta glycoprotein chains.
29
Which TSH subunit is specific?
Beta-subunit.
30
What stimulates TSH release?
TRH from the hypothalamus.
31
What inhibits TRH release?
Dopamine. somatostatin. glucocorticoids. stress. increased cortisol.
32
What does TSH stimulate?
Release of T3 and T4 from the thyroid gland.
33
What does TSH deficiency cause?
Inactivity and atrophy of the thyroid gland.
34
What does TSH excess cause?
Hypertrophy and hyperplasia of the thyroid gland.
35
What lab values suggest primary hypothyroidism?
High TSH. low T3 and T4.
36
What lab values suggest primary hyperthyroidism?
Low TSH. high T3 and T4.
37
What lab values suggest secondary hypothyroidism?
Low TSH. low T3 and T4.
38
What is ACTH derived from?
Proteolytic cleavage of POMC.
39
What else does POMC contain?
Lipotropins. melanocyte-stimulating hormone. beta-endorphin.
40
What regulates ACTH secretion?
CRH from the hypothalamus.
41
When are ACTH and cortisol levels highest?
Early morning after waking.
42
What is ACTH's role in pigmentation?
Principal pigmentary hormone in humans.
43
What stimulates CRH and ACTH release?
Vasopressin. oxytocin. angiotensin II. cholecystokinin. stress. fasting. hypoglycemia.
44
What inhibits CRH and ACTH release?
Atrial natriuretic peptide. opioids. cortisol.
45
What do LH and FSH have in common with TSH and hCG?
They share the same alpha subunit.
46
What are FSH effects in females?
Stimulates ovarian follicle development.
47
What are FSH effects in males?
Promotes spermatogenesis.
48
What suppresses FSH secretion?
Inhibin from Sertoli cells.
49
What are LH effects in females?
Triggers ovulation. stimulates corpus luteum formation.
50
What are LH effects in males?
Stimulates testosterone production.
51
What inhibits LH secretion?
Androgens and estrogens.
52
What are posterior pituitary hormones?
ADH and oxytocin.
53
Where are ADH and oxytocin produced?
Supraoptic and paraventricular nuclei of the hypothalamus.
54
What does ADH regulate?
Water conservation at the kidney.
55
How does ADH work on the kidney?
Stimulates V2 receptors in the collecting duct for water reabsorption.
56
What do V1 receptors mediate?
Pressor and glycogenolytic effects via calcium mobilization.
57
What do V3 receptors mediate?
Stimulation of ACTH secretion.
58
How does oxytocin affect the uterus?
Stimulates contractions during labor.
59
How does oxytocin affect the breast?
Stimulates milk let-down during suckling.
60
What behaviors is oxytocin involved in?
Orgasm. social recognition. bonding. trust. maternal behavior.
61
How does oxytocin affect appetite?
Induces anorexia and influences obesity regulation.
62
What are the two main parts of the adrenal gland?
Adrenal cortex. Adrenal medulla.
63
Which part of the adrenal gland is outermost?
Adrenal cortex.
64
Which part of the adrenal gland is innermost?
Adrenal medulla.
65
What hormone is secreted by the zona glomerulosa of the adrenal cortex?
Mineralocorticoids. Aldosterone.
66
What hormone is secreted by the zona fasciculata of the adrenal cortex?
Glucocorticoids. Cortisol.
67
What hormone is secreted by the zona reticularis of the adrenal cortex?
Adrenal androgens.
68
What type of cells in the adrenal medulla secrete catecholamines?
Neuroendocrine. Chromaffin cells.
69
What do glial cells in the adrenal medulla do?
Involved in calcium metabolism. Indirectly affect catecholamine production.
70
What stimulates the hypothalamus to release CRH?
Stress. Low cortisol levels.
71
What does CRH stimulate?
Anterior pituitary to secrete ACTH. Corticotropin.
72
What does ACTH stimulate in the adrenal cortex?
Synthesis and release of cortisol and adrenal androgens.
73
What is the feedback effect of cortisol on the HPA axis?
Negative feedback.
74
What happens when cortisol levels are high?
Inhibit CRH from hypothalamus. Inhibit ACTH from anterior pituitary.
75
What regulates aldosterone secretion?
Renin-angiotensin-aldosterone system. Serum potassium levels.
76
What are the stimuli for aldosterone release?
Low blood volume or pressure. High serum potassium.
77
What are the effects of aldosterone?
Sodium retention. Potassium excretion. Water reabsorption.
78
What is the fetal consequence of 21-hydroxylase deficiency?
Excess androgens. Virilization.
79
What time is cortisol highest in a normal diurnal cycle?
8 AM.
80
What cortisol level pattern is lost in Cushing syndrome?
Normal diurnal pattern. Cortisol remains high at midnight.
81
What causes primary adrenal insufficiency?
Defect in adrenal glands. Addison's disease.
82
What are lab findings in primary adrenal insufficiency?
Low cortisol. High ACTH.
83
What causes secondary adrenal insufficiency?
Pituitary defect. Low ACTH and cortisol.
84
What causes tertiary adrenal insufficiency?
Hypothalamic dysfunction. CRH deficiency. Low ACTH and cortisol.
85
What is the most common cause of congenital adrenal hyperplasia?
21-hydroxylase deficiency.
86
What is the hallmark lab test for CAH diagnosis?
Very high 17-hydroxyprogesterone.
87
What are the effects of salt-wasting form of CAH?
Glucocorticoid and mineralocorticoid deficiency. Salt-wasting crisis.
88
What are symptoms of virilization in females with CAH?
Clitoromegaly. Labial fusion. Phallus-like clitoris.
89
What are symptoms of late-onset CAH in adolescent girls?
Hirsutism. Acne. Irregular menses or amenorrhea.
90
What is the core management of CAH?
Hormonal therapy. Glucocorticoids and mineralocorticoids.
91
What complications may occur with overtreatment of CAH?
Growth stunting. Weight gain. Cushingoid features.
92
What complications may occur with undertreatment of CAH?
Early puberty. Excessive height. Testicular adrenal rest tumors.
93
What causes Addison’s disease?
Autoimmune destruction of adrenal cortex.
94
What is the most definitive test for Addison’s disease?
ACTH stimulation test.
95
What are common lab findings in Addison’s disease?
Low cortisol and sodium. High ACTH. Hyperkalemia. High plasma renin.
96
What is the first-line fluid treatment in Addisonian crisis?
D5NSS. Corrects hypoglycemia and hypovolemia.
97
What is the corticosteroid of choice for long-term replacement in Addison’s disease?
Hydrocortisone.
98
What is the most common cause of Cushing syndrome?
Exogenous corticosteroid use.
99
What is the most common endogenous cause of Cushing syndrome in children?
ACTH-secreting pituitary microadenoma. Cushing disease.
100
What are clinical signs of Cushing syndrome?
Central obesity. Moon facies. Striae. Hypertension. Hirsutism. Osteoporosis.
101
What is a classic lab finding in Cushing syndrome?
Increased 24-hour urinary cortisol.
102
What test shows loss of cortisol suppression in Cushing syndrome?
Dexamethasone suppression test.
103
What is the treatment of choice for pituitary Cushing disease?
Transsphenoidal pituitary microsurgery.
104
What is pheochromocytoma?
Catecholamine-secreting tumor of chromaffin cells.
105
What is the classic triad of pheochromocytoma?
Hypertension. Headache. Palpitations.
106
What are the sensitive markers for pheochromocytoma?
Increased blood and urinary metanephrines.
107
What is the treatment for pheochromocytoma?
Surgical removal. Microscopic adrenalectomy.