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2H. IM > ENDOC- PITUITARY intro and Anterior pituitary > Flashcards

ENDOC- PITUITARY intro and Anterior pituitary Flashcards

1
Q

◦The hypothalamic neural cells synthesize specific releasing and inhibiting hormones that are secreted directly to the pituitary stalk

A

Hypothalamus

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2
Q

Pituitary gland is regulated by 3 interacting elements

A
  • ◦Hypothalamic inputs
  • ◦Feedback effect of circulating hormones
  • ◦Paracrine and autocrine secretions of the pituitary itself
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3
Q
A
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4
Q
  • “master gland” because, together with the hypothalamus, it orchestrates the complex regulator functions of the many endocrine glands
    *
A

pituitary gland

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5
Q

What is the weight and size of pituitary?

A

The pituitary gland weighs ~600mg (400-900 mg) and measures 13mm x 6-9mm x 9mm

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6
Q

Where is the pituitary gland located?

A

Located within the sella turcica ventral to the diaphragma sella
Anatomically and functionally consists of two lobes: the anterior and posterior lobes

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7
Q

Anterior pituitary:
◦5 distinct hormone secreting cell types with 6 major hormones

A
  1. coticotroph cells- secretes POMC and thus ACTH/cortictropin
  2. Somatotroph cells: expresses growth hormone or somatotropin
  3. Thyrotroph cells express the common glycoprotein alpha subunit and the specific B subunit of TSH/thyrotropin
  4. Gonadotroph cells: express the alpha and B subunit of FSH and LH
  5. Lactotroph cells express prolactin
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8
Q

coticotroph cells- secretes _______________

A

POMC and thus ACTH/cortictropin

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9
Q

Somatotroph cells: expresses________________

A

growth hormone or somatotropin

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10
Q

Thyrotroph cells express the common glycoprotein alpha subunit and the specific B subunit of TSH/thyrotropin

A

common glycoprotein alpha subunit and the specific B subunit of TSH/thyrotropin

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11
Q

Gonadotroph cells: express the _______________

A

alpha and B subunit of FSH and LH

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12
Q

Lactotroph cells express prolactin

A

prolactin

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13
Q

The p____________ is a collection of axon terminals and is directly innervated by hypothalamic neurons via the stalk

A

osterior lobe (neural lobe)

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14
Q

3 general pituitary gland dysfunction

A
  1. Hormone deficiency
  2. Hormone excess
  3. Masses- hypothalamic, pituitary and other sellar masses (which can also cause hormone excess or deficiency)
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15
Q

Results from impaired production of one or more of the anterior pituitary trophic hormones

  1. inherited disorders such as pituitary dysplasias/aplasia, congenital CNS mass, transcription factor deficits, etc.
  2. Acquired disorders due to compressive mass effects, or vascular/inflammatory damage
A

HORMONE DEFICIENCIES

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16
Q

HORMONE DEFICIENCIES: Developmental and Genetic Causes

A

1.Pituitary dysplasia
2.Septo-optic dysplasia
◦3.Tissue specific factor mutation

  1. Kallman Syndrome
  2. Bardet Biedl Syndrome
  3. Leptin and Leptin Receptor Mutation
  4. Prader Willi Syndrome
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17
Q

Pituitary dysplasia – aplastic, hypopasltic, ectopic

A

aplastic,

hypopasltic,

ectopic

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18
Q

◦Result from dysgenesis of the septum pellucidum or corpus callosum

A

Septo-optic dysplasia

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19
Q

◦Several pituitary cell-specific transcription factors such as Pit-1 and Prop-1 are critical for determining the development and committed function of differentiated anterior pituitary cell lineages

A

Tissue specific factor mutation

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20
Q

Tissue specific factor mutation
◦Several pituitary cell-specific transcription factors such as_______ and ________ are critical for determining the development and committed function of differentiated anterior pituitary cell lineages

A

Pit-1 and Prop-1

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21
Q

Kallman Syndrome

  • *◦Defective GnRH synthesis** and is associated with anosmia/hyposmia due to olfactory bulb agenesis/hypoplasia
  • *◦Prevents progression through puberty**
A

Kallman Syndrome

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22
Q

◦MR, renal abnormalities, obesity, hexa/brady/syndactyly and retinal degeneartion

A

Bardet Biedl Syndrome

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23
Q

Leptin and Leptin Receptor Mutation
◦Hyperphagia, obesity adn central hypogonadism

A

Leptin and Leptin Receptor Mutation

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24
Q

HORMONE DEFICIENCIES: Developmental and Genetic Causes

Hypogonadotropic hypogonadism, hyperphagia-obesity, adult onset DM, hypotonia, mental retardation

A

Prader Willi Syndrome

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25
Q

HORMONE DEFICIENCIES: Acquired Hypopituitarism

A
  • May be caused by surgical trauma, vascular trauma, pituitary or hypothalamic neoplasms, inflammatory disease, infiltrative disorders or irradiation
  • Trophic hormone failure occurs spontaneously:GH>FSH>LH>TSH/ACTH
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26
Q

HORMONE DEFICIENCIES: Laboratory Investigation

A
  • Biochemical diagnosis of pituitary insufficiency is made by demonstrating low levels of trophic hormones in the setting of low levels of target hormones
  • Provocative tests may be required to assess pituitary reserve
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27
Q

HORMONE DEFICIENCIES: Treatment

A

Hormone replacement therapy with a treatment regimen that mimic physiologic hormone production allow for maintenance of satisfactory clinical homeostasis

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28
Q

Results from overproduction of one or more of the anterior pituitary trophic hormones which can be due to overproduction of releasing hormones from the hypothalamus or an ectopic source, increase in pituitary cell type, increased sensitivity of the end organ.

A

HORMONE EXCESS

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29
Q

HYPOTHALAMIC, PITUITARY AND OTHER SELLAR MASSES

A
  • Pituitary adenomas
  • Craniopharyngiomas
  • Rathke’s cysts (<5mm cysts)
  • Sellar chrodomas
  • Meningiomas
  • Histiocytosis X
  • Pituitary Metstasis
  • Hypothalamic hamartomas, gangliocytomas
  • Hypothalamic and optic gliomas
  • Brain germ cell tumors
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30
Q

Most common cause of pituitary hormone hypo or hypersecretion in adults
◦Benign neoplasms that arise from one of the 5 anterior cell types

A

Pituitary adenomas

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31
Q

◦Benign, suprasellar, cystic masses that are derived from the Rathke’s pouch and arise near the pituitary stalk

A

Craniopharyngiomas

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32
Q

HYPOTHALAMIC, PITUITARY AND OTHER SELLAR MASSES

Evaluation

A
  1. Local Mass Effect
  2. MRI
  3. Ophthalmologic Evaluation
  4. Laboratory Investigations
  5. Histologic Evaluation
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33
Q

HYPOTHALAMIC, PITUITARY AND OTHER SELLAR MASSES
Treatment:

A

1.Surgery
Transphenoidal vs transcranial surgery
2.Radiation Therapy
3.Medical Therapy

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34
Q

6 Major Anterior Pituitary Gland Hormones

A
  1. Prolactin (PRL)
  2. Growth Hormone (GH)
  3. Adrenocorticotropic Hormone (ACTH)
  4. Luteinizing Hormone (LH)
  5. Follicle Stimulating Hormone (FSH)
  6. Thyrotropin Stimulating Hormone (TSH)
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35
Q

PROLACTIN
Synthesized in

A

lactotroph cells

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36
Q

What type of secretion is Prolactin?

A

Pulsatile secretion

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37
Q

What is the normal value of Prolactin?

A

10-25 ug/L

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38
Q

What is the half- life of prolactin?

A

Half-life of 50 minutes

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39
Q

What is the Predominant central control of PRL?

A

** inhibitory** via the dopamine-mediated inhibitory effect

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40
Q

Other hormones controlling prolactin release:
◦Stimulatory: _______ and __________

A
  1. TRH and
  2. VIP
41
Q

Other hormones controlling prolactin release:

**◦Inhibitory: **

A
  • thyroid hormones
  • and glucocorticoids
42
Q

When does PRL transiently increases?

A
  • after exercise,
  • meals,
  • sexual intercourse,
  • minor surgical procedures,
  • general anesthesia,
  • chest wall, injury,
  • MI,
  • acute stress
43
Q

What are the function of PRL?

A
  • Proliferation of the breast lobuloalveolar epithelium
  • Induces and maintain lactation
  • Decrease reproductive function and reduce sexual drive
44
Q

PROLACTIN

Decrease reproductive function and reduce sexual drive through:

A
  • suppression of the hypothalamic GnRH
  • and suppression of the pituitary gonadotropin secretion
  • and impairs gonadal steroidogenesis in both men and women.
45
Q

Most common pituitary hypersecretion in both men and women

A

HYPERPROLACTENEMIA

46
Q

What are the physiologic cause of Hyperprolactenemia?

A

Physiologic causes:

pregnancy and lactation

47
Q

What are the pathologic cause of Hyperprolactenemia?

A

Pathologic causes

  • : pituitary hypersecretion,
  • hypothalamic-pituitary stalk damage,
  • systemic causes (e.g. renal failure, cirrhosis, hypothyroidism)
48
Q

What is the **pharmacologic cause ** of Hyperprolactenemia?

A

Pharmacologic Causes: dopamine antagonists

49
Q

_______________ are the most common cause of prolactin elevations >200ug/L

A

Prolactinomas

50
Q

HYPERPROLACTENEMIA
◦Manifestations:

in women

A

In women:

  • amenorrhea,
  • galactorrhea,
  • infertility are the hallmarks,
  • others are decreased bone mineral density,
  • decreased libido,
  • weight gain and mild hirsutism
51
Q

Hyperprolactenemia manifestation in men:

A

In men:

  • diminished libido,
  • infertility and visual loss,
  • others are osteopenia,
  • reduced muscle mass and
  • reduced beard growth
52
Q

What is the laboratory investigation of Hyperprolactenemia?

A

Laboratory investigation:

morning, basal prolactin and investigation for other etiologies

53
Q

: pituitary adenomas

<10mm;

F:M :: 20:1

A

Microprolactinoma

54
Q

: pituitary adenoma

>10mm;

F:M::1:1

A

Macroprolactinom

55
Q

What is the treatment for PROLACTINOMA

A

Treatment:

primarily medical management with dopamine receptor agonists (e.g. Bromocriptine and cabergoline);

surgical approach or radiotx is for invasive prolactinomas or dopamine resistant tumors

56
Q

Most abundant anterior pituitary hormone

A

GROWTH HORMONE

57
Q

The hypothalamic peptide _____________-stimulates synthesis and secretion of GH

A

GHRH

58
Q

____________inhhibits GH release

A

Somatostatin (SRIF)

59
Q

____________-produced in the liver, is the peripheral target hormone for GH and is the predominant hormone exerting GH action;

A

IGF-1,

60
Q

What type of secretion is GH?

A

GH secretion is pulsatile,

61
Q

The highest levels of GH correlating with the ________________

A

with highest levels correlating with the onset of slow wave sleep

62
Q

What are the metaboloc action of GH

A

Metabolic action:

  • ◦Induces protein synthesis and nitrogen retention
  • ◦Impairs glucose toleramce by antagonizing insulin action
  • ◦Stimulates lipolysis, leading to increased circulating fatty acid levels, reduced omental fat malls
  • ◦Enhance lean body mass
  • ◦Stimulates epiphyseal prechondrocyte differentiation and linear bone growth
63
Q

Short Stature in Children
May be caused by

A
  • ◦GH deficiency
  • ◦GHRH receptor mutations
  • ◦GH insensitivity
  • ◦Nutritional short stature
  • ◦Psychosocial short stature
64
Q

Adult GH Deficiency

A

Clinical feature include changes in body composition, lipid metabolism, cardiovascular dysfunction and quality of life
rare

65
Q

What is the cause of Acromegaly/ gigantism?

A

Usually the result of a somatotrope adenoma but may rarely be caused by extrapituitary lesion

66
Q

In Acromegaly, what are the rare GH secretion?

A

Rare causes of ectopic GH secretion by:

  • tumors of pancreas, ovarian, lung, or hematopoietic origin
  • while others present with GHRH-mediated acromegaly such as in chest or abdominal carcinoid tumor.
67
Q

What is the presentation of Acromegaly/Gigantism?

A
  • ◦Indolent and often not clinically diagnosed
  • ◦Acral bony overgrowth with frontal bossing, increased hand and foot size, mandibular enlargement with prognathism, widened teeth spaces
  • ◦Soft tissue swelling with increased heel pad thickness, increased glove and shoe size, ring tightening, coarse facial features, large fleshy nose
  • ◦Hyperhidrosis, deep and hollow sounding voice, oily skin, arthropathy, kyphoss, carpal tunnel syndrome, proximal muscle weakness and fatigue, acanthosis nigricans, skin tags
68
Q

What are other presentation of Acromegaly/ Gigantism?

A

Generalized visceromegaly:

  • cardiomegaly,
  • macroglossia,
  • goiter,
  • polyps,
  • upper airway obstruction
69
Q

What laboratory investigation should be done to diagnose Acromegaly?

A

Laboratory Investigation:

  • *◦Age and sex matched serum IGF-1 levels**
  • *◦GH suppression test**
70
Q

What are the treatment goals for Acromegaly/ Gigantism?

A
  • Control GH and IGF-1 hypersecretion: somatotropin, pegvisomant, dopamine agonists
  • ◦Ablate or arrest tumor growth: surgery, radiotherapy, stereotactic ablation
  • ◦Ameliorate comorbidities
  • ◦Restore mortality rates to normal
  • ◦Preserve pituitary function
71
Q

ADRENOCORTICOTROPIC HORMONE

Stimulated by_____________in the hypothalamus

A

corticotropin releasing hormone (CRH)

72
Q

What type of secretion is ACTH?

A

ACTH secretion is pulsatile and exhibits a circadian rhythm which peaks at 6 am and reaches a nadir at about midnight

73
Q

When does ACTH peak?

A

6am

74
Q

When is the lowest point ( nadir) of ACTH?

A

about mignight

75
Q

What cause an increase in ACTH?

A

ACTH is also increased by:

  • physical and
  • psychologic stress,
  • exercise,
  • acute illness
  • and insulin-induced hypoglycemia
76
Q

What is the major function of ACTH?

A

Major function is to maintain metabolic homeostasis and mediate the neuroendocrine stress response through induction of adrenocortical steroidogenesis

77
Q

What is the characteristic of ACTH deficiency?

A

Pituitary ACTH deficiency (aka secondary adrenal insufficiency) is characterized by:

  • fatigue,
  • weakness,
  • anorexia,
  • nausea,
  • vomiting and
  • occasional hypoglycemia
78
Q

In contrast to primary adrenal insufficiency, secondary adrenal insufficiency is not accompanied by_________________

A

hyperpigmentation or mineralocorticoid deficiency

79
Q

How is ACTH deficiency be investigated?

A

Laboratory investigation:
◦Inappropriately low levels of ACTH in the setting of low cortisol

80
Q

What is the treatment for ACTH deficiency?

A

Treatment: Glucocorticoid replacement

81
Q

What is cushing syndrome?

A

It is caused by prolonged exposure to elevated levels of either endogenous glucocorticoids or exogenous glucocorticoids

82
Q

ACTH-producing pituitary adenoma

A

Cushing’s Disease

83
Q

What accounts for 70% of patients with endogenous Cushing’s Syndrome?

A

Cushing’s Disease (ACTH-producing pituitary adenoma)

84
Q

What is the typical features of CUshing Disease?

A
  • thin skin,
  • central obesity,
  • hypertension,
  • plethora,
  • moon facies,
  • purle striae,
  • easy bruisability,
  • glucose intolerance,
  • gonadal dysfunction,
  • osteoporosis,
  • proximal muscle weakness,
  • signs of hyperandrogenism
  • and psychological disturbance
85
Q

How will you investigate Cushing’s Disease?

A

Laboratory Investigations:

  • ◦24 hour urine free cortisol
  • ◦1mg dexamethasone suppression test
  • ◦Midnight salivary cortisol
  • ◦Basal ACTH
86
Q

How will you treat Cushing’s Disease?

A

Treatment:
◦Selective transphenoidal resection
◦Medical Managment: ketoconazole, mitotane

87
Q

What is the function of Gonadotropins: FSH and LH?

A

Evokes germ cell development and maturation and steroid hormone biosynthesis

88
Q

__________ stimulates the synthesis and secretion of both FSH and LH through its pulsatility

A

GnRH

89
Q
A
90
Q

Gonadotropin Deficiency presentation is:

A
  • oligo-amenorhhrea,
  • infertility,
  • decreased vaginal secretions,
  • decreased libido,
  • testicular/breart atrophy
91
Q

What treatment Gonadotropin Deficiency?

A

Treatment: gonadotropin injections, testosterone replaement, OCPs

92
Q

Note: most non functioning pituitary adenoma are ________________ in origin

A

gonadotrope cells

93
Q

acts to stimulate thyroid hormone synthesis and release

A

THYROTROPIN STIMULATING HORMONE
TSH

94
Q

The_____________stimulates TSH synthesis and secretion

A

hypothalamic TRH

95
Q

What is the difference of TSH deficiency and TSH adenomas in symptom presentation?

A

TSH deficiency shows symptoms of hypothyroidism while TSH adenomas usually present with goiter and hyperthyroidism

96
Q

TSH deficiency shows symptoms of ________________

A

hypothyroidism

97
Q

TSH adenomas usually present with ___________________-

A

goiter and hyperthyroidism

98
Q
A

2H. IM (13 decks)

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