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DEMS III > Pituitary > Flashcards

Pituitary Flashcards

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
Q

What are the pharmacological causes of hyperprolactinemia?

A

Estrogens, antipsychotics, antidepressants, antiemetics, opiates

26
Q

What are the pathological causes of hyperprolactinemia?

A

Pituitary stalk interruption, hypothyroidism, chronic renal/liver failure, seizure, prolactinoma

27
Q

What is the most common functional pituitary adenoma?

A

Prolactinoma

28
Q

What are the functions of cortisol?

A

Gluconeogenesis, breakdown of fat and protein for glucose production, control inflammatory reactions.

29
Q

What is the most common cause of Cushing’s?

A

Exogenous steroids

30
Q

What is the most common cause of AI?

A

Exogenous steroids

31
Q

What is the clinical presentation of hypogonadism in males?

A

Reduced libido, ED, oligospermia or azospermia, infertility, decreased muscle mass, testicular atrophy, decreased BMD, hot flashes with acute and severe onset of hypogonadism.

32
Q

What are some causes of hypogonadism?

A

Macroadenomas, prolactinomas, XRT, hemochromatosis, starvation, opiates, glucocorticoids

33
Q

Which is more common, primary or secondary thyrotropin elevation?

A

Primary

34
Q

Describe the triphasic response to post-op/trauma-related DI.

A

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
Q

What is the most common tumor of the pituitary?

A

Pituitary adenoma

36
Q

Does size correlate with aggressiveness of a pituitary adenoma?

A

No

37
Q

Are most pituitary tumors familial or sporadic?

A

95% sporadic

38
Q

Which gene has been identified as a mutated gene in patients with familial isolated pituitary adenomas?

A

AIP

39
Q

What can a Rathke cleft cyst lead to?

A

DI

40
Q

What is the most common cancer to metastasize to the pituitary?

A

Breast cancer

41
Q

Which tumor type primarily affects children?

A

Craniopharyngioma

42
Q

CRH and GHRH are coupled to which G protein?

A

Gs

43
Q

Somatostatin is coupled to which G protein?

A

Gi

44
Q

What is the action of oxytocin?

A

Secreted during birth, sexual intercourse, and in response to suckling.

45
Q

What chronically suppresses PL?

A

DA

46
Q

Upon binding of PL to its receptor, which pathway is activated?

A

JAK/STAT

47
Q

What are the lab findings of Primary AI?

A

Very high ACTH, low cortisol aldosterone and adrenal androgens. Hyponatremia and hyperkalemia.

48
Q

What are the features of Autoimmune polyglandular syndrome-1?

A

AI (Addison’s), Hypoparathyroidism, DM Type 1, and mucocutaneous candidiasis

49
Q

What are the features of Autoimmune polyglandular syndrome-2?

A

AI (Addison’s), Hypoparathyroidism, and DM Type 1

50
Q

What are the lab findings of Secondary AI?

A

Low ACTH, low cortisol, low adrenal androgens, and NORMAL aldosterone because it is controlled mainly by RAAS

51
Q

What are the two most common causes of secondary AI?

A

Glucocorticoids and opioids

52
Q

What is the treatment of primary AI?

A

Mineralocorticoid and glucocorticoid replacement

53
Q

What is the treatment of secondary AI?

A

Glucocorticoid replacement only

54
Q

What are the three clinical features of primary aldosteronism?

A

HTN, hypokalemia, and metabolic alkalosis

DEMS III (7 decks)

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