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Endo/Repro > Hypothalamus & Pituitary Disorders > Flashcards

Hypothalamus & Pituitary Disorders Flashcards

1
Q

Embryological origin of anterior pituitary

A

Ectodermal derivative from Rathke’s pouch

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2
Q

Embryological origin of posterior pituitary

A

Downgrowth from primitive neural tissue

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3
Q

Anterior pituitary hormones

A

Acidophilic: GH, prolactin (ASP)
Basophilic: ACTH, TSH, FSH, LH (BFLAT)

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4
Q

___ inhibits prolactin release.
___ stimulates prolactin release.

A

Dopamine.
TRH.

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5
Q

What is the most powerful stimuli for prolactin release?

A

Suckling; also inhibits dopaminergic neurons

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6
Q

Estrogen ___ sensitivity to TRH

A

increases

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7
Q

Kallmann Syndrome is due to

A

Failure of differentiation or migration GnRH neurons in olfactory mucosa

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8
Q

In Kallmann Syndrome, what does low GnRH hormone cause?

A

Low FSH & LH → lack of sexual maturity & absence of secondary sexual characteristics

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9
Q

Cause of pituitary apoplexy

A

Hemorrhage into pituitary gland (usually d/t pituitary adenoma)

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10
Q

Pituitary apoplexy presents with

A

Excruciating headache, diplopia

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11
Q

Pituitary change during pregnancy

A

↑ lactotrophs (acidophilic) and ↑ pituitary size

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12
Q

Pathogenesis of Sheehan syndrome

A

Pituitary hyperplasia, hypotension in peripartal period, low pressure of hypophyseal portal system → pituitary ischemia & necrosis

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13
Q

Pathogenesis of Empty Sella Syndrome

A

Arachnoid herniation and CSF compression of pituitary → shrinks

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14
Q

Clinical features of CSF

A

CSH rhinorrhea, headache, hypopituitarism

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15
Q

Where is ADH synthesized

A

Supraoptic nucleus of hypothalamus

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16
Q

Mechanism of ADH

A

Aquaporin insertion on tubular side; water reabsorption

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17
Q

Four types of diabetes insipidus

A

Central, Nephrogenic, Physiogenic (polydipsia), Gestational

18
Q

Psychogenic vs Central vs Nephrogenic diabetes insipidus

A

Psychogenic: Increased water intake
Central: ADH deficiency
Nephrogenic: Kidney unresponsive to ADH

19
Q

Etiology of lithium in diabetes insipidus

A

Nephrogenic d/t ENaC channel

20
Q

Water deprivation test results on psychogenic vs central vs nephrogenic diabetes inspidus

A

Psychogenic: ↓ volume, ↑ osmolality
Central: ↑ urine osmolality after ADH
Nephrogenic: no change to urine osmolality after ADH

21
Q

How to treat central vs nephrogenic diabetes insipidus

A

Central: DDAVP
Nephrogenic: Thiazide-increased absorption in PCT

22
Q

SIADH symptoms

A

oliguria, free water resorption, hyponatremia, cerebral edema

23
Q

Causes of SIADH

A

Small CC of lung, head trauma, or drugs (antiepileptics, painkillers, anticancer drugs)

24
Q

Pathopysiology of SIADH

A

↑ ADH ↑ aquaporins, dilutes sodium, ↓ aldosterone, hyponatremia

25
Q

Mass effects of pituitary adenomas

A

Optic chiasm compression (bitemporal hemianopsia - loss of outer half of vision), headache, hypopituitarism

26
Q

How to distinguish adenomas from non-neoplastic tissue

A

cellular monomorphism and absence of reticulin network

27
Q

Prolactinoma presentation in females vs males

A

Females: galactorrhea, amenorrhea
Males: ↓ libido, gynecomastia, headache

28
Q

Prolactinoma treatment

A

dopamine agonists (bromocriptine, cabergoline)

29
Q

Stalk effect

A

Mass in suprasellar compartment ↑ prolactin

30
Q

Growth hormone secreting adenomas in children vs adults

A

Children: gigantism - ↑ linear bone growth (epiphyses not fused)
Adults: acromegaly - sausage shaped fingers, visceral organ growth, cardiac failure, enlarged tongue (sleep apnea)

31
Q

Lab results for GH adenoma

A

↑ ↑ IGF 1 (somatomedin C)

32
Q

OGTT results in healthy vs acromegaly

A

Healthy: glucose ↓ GH (negative feedback)
Acromegaly: glucose doesn’t suppress GH

33
Q

Laron Syndrome defect

A

Growth hormone receptor AR defect

34
Q

Laron syndrome presentation

A

short stature d/t extreme GH resistance

35
Q

Laron syndrome labs

A

↑ serum GH, ↓ IGF-1

36
Q

Corticotroph adenoma pathogenesis

A

ACTH causes Cushing syndrome & hyperpigmentation (MSH same precursos as ACTH)

37
Q

Nelsons syndrome pathogenesis

A

↑ ACTH, MSH d/t large aggressive tumors after bilateral adrenal removal (no negative feedback)

38
Q

Craniopharyngioma etiology

A

Arises from remnants of Rathke’s pouch in children/young adults

39
Q

Craniopharyngioma presentation

A

Supratentorial mass that compresses optic chiasm → bilateral hemianopsia

40
Q

Gross and microscopic appearance of craniopharyngioma

A

Gross: Cystic, reddish-gray mass with dark motor oil fluid
Microscopy: palisading squamous epithelium, wet keratin, dystrophic calcification

Endo/Repro (4 decks)

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