Pituitary Flashcards

(54 cards)

1
Q

What is the cause and clinical presentation of acromegaly?

A

GH excess after puberty. Acral/facial changes, headache, hyperhidrosis, oligo/amenorrhea, obstructive sleep apnea, HTN, dyslipidemia, carpal tunnel syndrome, DM.

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2
Q

What is the cause and clinical presentation of gigantism?

A

GH excess before puberty. Excessive linear growth.

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3
Q

What is the clinical presentation of AoGHD?

A

More fat less muscle and bone. Hypercholesterolemia, increased inflammatory and pro-thrombotic markers, impaired energy and mood, impaired quality of life.

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4
Q

What is the clinical presentation of hyperprolactinemia?

A

Glactorrhoea, menstrual irregularity, infertility, headache, impotence, visual field abnormalities. Female predominance. Different presentation in M and F.

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5
Q

What is the clinical presentation of prolactin deficiency?

A

In F, failed lactation post-partum. No presentation in M.

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6
Q

What is the clinical presentation of hypercortisolism/Cushing Syndrome?

A

Changes in carbohydrate, protein, and fat metabolism, changes in sex hormones, salt and water retention, impaired immunity, neurocognitive changes. Violaceous striae.

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7
Q

What is the clinical presentation of central adrenal insufficiency (AI)?

A

Fatigue, anorexia, nausea/vomiting, and weight loss. Generalized malaise/aches. Scant axillary/pubic hair, hyponatremia and hypoglycemia.

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8
Q

What is the clinical presentation of hypogonadism in females?

A

Anovulatory cycles, oligo/amenorrhea, infertility, vaginal dryness, dyspareunia, hot flashes, decreased libido, breast atrophy, reduced bone mineral density (BMD)

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9
Q

What is the definition of hypopituitarism?

A

Deficiency of 1 or more pituitary hormones

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10
Q

What is apoplexy?

A

Headache, vision changes, ophthalmoplegia, and altered mental status caused by the sudden hemorrhage or infarction of the pituitary gland.

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11
Q

What is the definition and clinical presentation of SIADH?

A

Syndrome of inappropriate ADH release/action. Most common cause of hyponatremia. Presentation depends on severity of hyponatremia. Neuro symptoms from osmotic shifts and brain edema.

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12
Q

What is diabetes insipidus (DI)?

A

Syndrome of hypotonic polyuria as a result of either inadequate ADH secretion or inadequate renal response to ADH.

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13
Q

What are the 5 cell types of the anterior pituitary?

A

Somatropes, lactotropes, corticotropes, gonadotropes, and thyrotropes

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14
Q

What do somatotropes secrete and where does it act?

A

GH; liver to make IGF-1

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15
Q

What do lactotropes secrete and where does it act?

A

Prolactin; breast for lactation

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16
Q

What do corticotropes secrete and where does it act?

A

ACTH; adrenal gland to make cortisol

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17
Q

What do gonadotropes secrete and where does it act?

A

FSH, LH; gonads to make sex steroids

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18
Q

What do thyrotropes secrete and where does it act?

A

TSH; thyroid to make T4 and T3

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19
Q

What stimulates and what inhibits somatotropes?

A

Stimulated by GHRH and inhibited by SRIF (somatostatin)

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20
Q

What stimulates and what inhibits corticotropes?

A

Stimulated by CRF, no inhibition

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21
Q

What stimulates and what inhibits lactotropes?

A

Stimulated by TRH and inhibited by DA

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22
Q

What stimulates and what inhibits gonadotropes?

A

Stimulated by GnRH, no inhibition

23
Q

What stimulates and what inhibits thyrotropes?

A

Stimulated by TRH and inhibited by SRIF (somatostatin)

24
Q

What are the physiological causes of hyperprolactinemia?

A

Pregnancy, suckling, sleep, stress

25
What are the pharmacological causes of hyperprolactinemia?
Estrogens, antipsychotics, antidepressants, antiemetics, opiates
26
What are the pathological causes of hyperprolactinemia?
Pituitary stalk interruption, hypothyroidism, chronic renal/liver failure, seizure, prolactinoma
27
What is the most common functional pituitary adenoma?
Prolactinoma
28
What are the functions of cortisol?
Gluconeogenesis, breakdown of fat and protein for glucose production, control inflammatory reactions.
29
What is the most common cause of Cushing's?
Exogenous steroids
30
What is the most common cause of AI?
Exogenous steroids
31
What is the clinical presentation of hypogonadism in males?
Reduced libido, ED, oligospermia or azospermia, infertility, decreased muscle mass, testicular atrophy, decreased BMD, hot flashes with acute and severe onset of hypogonadism.
32
What are some causes of hypogonadism?
Macroadenomas, prolactinomas, XRT, hemochromatosis, starvation, opiates, glucocorticoids
33
Which is more common, primary or secondary thyrotropin elevation?
Primary
34
Describe the triphasic response to post-op/trauma-related DI.
Primary phase: DI-polyuric phase due to axonal shock/decreased AVP relsease (days 1-5) Secondary phase: SIADH from degenerating neurons/excessive AVP release (days 6-11) Tertiary phase: Permanent DI after depleted ADH stores and if >80% AVP neuronal cell death - very uncommon
35
What is the most common tumor of the pituitary?
Pituitary adenoma
36
Does size correlate with aggressiveness of a pituitary adenoma?
No
37
Are most pituitary tumors familial or sporadic?
95% sporadic
38
Which gene has been identified as a mutated gene in patients with familial isolated pituitary adenomas?
AIP
39
What can a Rathke cleft cyst lead to?
DI
40
What is the most common cancer to metastasize to the pituitary?
Breast cancer
41
Which tumor type primarily affects children?
Craniopharyngioma
42
CRH and GHRH are coupled to which G protein?
Gs
43
Somatostatin is coupled to which G protein?
Gi
44
What is the action of oxytocin?
Secreted during birth, sexual intercourse, and in response to suckling.
45
What chronically suppresses PL?
DA
46
Upon binding of PL to its receptor, which pathway is activated?
JAK/STAT
47
What are the lab findings of Primary AI?
Very high ACTH, low cortisol aldosterone and adrenal androgens. Hyponatremia and hyperkalemia.
48
What are the features of Autoimmune polyglandular syndrome-1?
AI (Addison's), Hypoparathyroidism, DM Type 1, and mucocutaneous candidiasis
49
What are the features of Autoimmune polyglandular syndrome-2?
AI (Addison's), Hypoparathyroidism, and DM Type 1
50
What are the lab findings of Secondary AI?
Low ACTH, low cortisol, low adrenal androgens, and NORMAL aldosterone because it is controlled mainly by RAAS
51
What are the two most common causes of secondary AI?
Glucocorticoids and opioids
52
What is the treatment of primary AI?
Mineralocorticoid and glucocorticoid replacement
53
What is the treatment of secondary AI?
Glucocorticoid replacement only
54
What are the three clinical features of primary aldosteronism?
HTN, hypokalemia, and metabolic alkalosis