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ENDO 2 Exam I (2017) > Pathology of the Pituitary > Flashcards

Pathology of the Pituitary Flashcards

1
Q

most susceptible part of the pitutitary

A

infundibulum (stalk)

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2
Q

two negative feedbacks in the pituitary

A

doapine –> - PRL

somatostain –> - GH

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3
Q

Somatotrophs,

A

producing growth hormone (GH)

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4
Q

Mammosomatotrophs,

A

producing GH and prolactin (PRL)

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5
Q

Lactotrophs,

A

producing PRL

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6
Q

Corticotrophs

A

producing adrenocorticotropic hormone (ACTH) and pro-opiomelanocortin (POMC), melanocyte-stimulating hormone (MSH)

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7
Q

Thyrotrophs,

A

, producing thyroid-stimulating hormone (TSH),

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8
Q

Gonadotrophs

A

producing follicle-stimulating hormone (FSH) and luteinizing hormone (LH).

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9
Q

normal pituitary stains

A

heterogeneously

lost of different stuff

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10
Q

bitemporal hemianopia

A

from pituitary tumor compressing optic chiasm

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11
Q

how does cerebral edema present?

A

vomiting
headaches

look in eye- optic cup widened = papilledema

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12
Q

female complaining of leaky nipples, new onset headaches, serum prolactin elevated

A

pituitary adenoma

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13
Q

The most common cause of hyperpituitarism

A

is an adenoma arising in the anterior lobe

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14
Q

pituitary adenomas usually found what age?

A

adults, peak 25-50 years

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15
Q

microadenomas vs macroadenomas

A

micro less than 1 cm, likely to be functional

; macro is greater than 1 cm, likely to be nonfunctional

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16
Q

pituitary monomorphism

A

probably a prolactin adenoma

reticulin stain would normally show a network in the pituitary, but in adenoma it’s missing

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17
Q

dense core granules in MRI indicate

A

neuroendocrine

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18
Q

Clinical course of pituitary adenoma

A

The signs and symptoms of pituitary adenomas are related to endocrine abnormalities and mass effects. Local mass effects may be produced by any type of pituitary tumor.

these effects include radiographic abnormalities of the sella turcica, visual field abnormalities, signs and symptoms of elevated intracranial pressure, and occasionally hypopituitarism.

Acute hemorrhage into an adenoma is sometimes associated with pituitary apoplexy

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19
Q

Increased serum levels of prolactin cause

A

amenorrhea, galactorrhea, loss of libido, and infertility.

The diagnosis of an adenoma is made more readily in women than in men, especially between the ages of 20 and 40 years, presumably because of the sensitivity of menses to disruption by hyperprolactinemia.

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20
Q

Lactotroph adenoma

A

underlies almost a quarter of cases of amenorrhea. In contrast, in men and older women, the hormonal manifestations may be subtle, allowing the tumors to reach considerable size (macroadenomas) before being detected clinically

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21
Q

Somatotroph Adenomas

A

Growth hormone (GH)-secreting somatotroph adenomas are the second most common type of functioning pituitary adenoma, and cause * gigantism in children and acromegaly in adults (epyphyses are closed). Somatotroph adenomas may be quite large by the time they come to clinical attention because the manifestations of excessive GH may be subtle.

22
Q

Clinical course of somatotroph adenomas

A

Persistently elevated levels of GH stimulate the hepatic secretion of insulin-like growth factor 1 (IGF-1), which causes many of the clinical manifestations.

23
Q

If a somatotroph adenoma appears in children before the epiphyses have closed,

A

the elevated levels of GH (and IGF-1) result in gigantism. This is characterized by a generalized increase in body size with disproportionately long arms and legs.

24
Q

If a somatotroph adenoma increased levels of GH are present after closure of the epiphyses,

A

acromegaly develops. In this condition, growth is most conspicuous in skin and soft tissues, viscera (thyroid, heart, liver, and adrenals), and the bones of the face, hands, and feet.

25
Q

Growth hormone excess can also cause

A

Bone density may increase (hyperostosis) in both the spine and the hips.

Enlargement of the jaw results in its protrusion (prognathism), and broadening of the lower face. The feet and hands are enlarged, and the fingers become thickened and sausage-like. In most instances gigantism is also accompanied by evidence of acromegaly. These changes may develop slowly over decades before being recognized, hence the opportunity for the adenomas to reach substantial size.
GH excess can also be associated with a variety of other disturbances, including gonadal dysfunction, diabetes mellitus, generalized muscle weakness, hypertension, arthritis, congestive heart failure, and an increased risk of gastrointestinal cancers.

26
Q

The diagnosis of pituitary GH excess relies on

A

documentation of elevated serum GH and IGF-1 levels. In addition, *** failure to suppress GH production in response to an oral load of glucose is one of the most sensitive tests for acromegaly.

27
Q

Corticotroph Adenomas

A

Excess production of ACTH by functioning corticotroph adenomas leads to adrenal hypersecretion of cortisol and the development of hypercortisolism (also known as Cushing syndrome).

28
Q

Cushing disease.

A

When the hypercortisolism is due to excessive production of ACTH by the pituitary, it is designated Cushing disease.

29
Q

Nelson syndrome

A

Large destructive pituitary adenomas can develop in patients after surgical removal of the adrenal glands for treatment of Cushing syndrome. This condition, known as Nelson syndrome, occurs most often because of a loss of the inhibitory effect of adrenal corticosteroids on a preexisting corticotroph microadenoma.

Because the adrenals are absent in persons with this disorder, hypercortisolism does not develop, and patients present with mass effects due to the pituitary tumor, and there can be hyperpigmentation because of the stimulatory effect of other products of the ACTH precursor molecule on melanocytes

30
Q

Gonadotroph adenomas

A

(LH-producing and FSH-producing) adenomas can be difficult to recognize because they secrete hormones inefficiently and variably, and the secretory products usually do not cause a recognizable clinical syndrome (nonfunctioning adenomas). Gonadotroph adenomas are most frequently found in middle-aged men and women when they become large enough to cause neurologic symptoms, such as impaired vision, headaches, diplopia, or pituitary apoplexy.

31
Q

Pituitary hormone deficiencies

A

most commonly impaired secretion of LH. This causes decreased energy and libido in men (due to reduced testosterone) and amenorrhea in premenopausal women. The neoplastic cells usually demonstrate immunoreactivity for the common gonadotropin α-subunit and the specific β-FSH and β-LH subunits; FSH is usually the predominant secreted hormone.

32
Q

Thyrotroph (TSH-producing) adenomas

A

are uncommon, accounting for approximately 1% of all pituitary adenomas. Thyrotroph adenomas are a rare cause of hyperthyroidism.

33
Q

Nonfunctioning pituitary adenomas

A

are a heterogeneous group that constitutes approximately 25% to 30% of all pituitary tumors. Their lineage can be established by immunohistochemical staining for hormones or by biochemical demonstration of cell type-specific transcription factors.

In the past, many such tumors have been called silent variants or null-cell adenomas. Not surprisingly, nonfunctioning adenomas typically present with symptoms stemming from mass effects.

These lesions may also compromise the residual anterior pituitary sufficiently to cause hypopituitarism, which may appear slowly due to gradual enlargement of the adenoma or abruptly because of acute intratumoral hemorrhage (pituitary apoplexy).

34
Q

Robbins Key Concepts: hyperpituitarism

A

most common cause- anterior lobe pituitary adenoma

can be macro or micro (less than 1 cm)

functioning- associated with endo signs and symptoms. Nonfunctioning- mass effects, including visual disturbances

lactotroph adenomas- amenorrhea, galactorrhea, loss of libido, infertility

somatotroph adenomas- gigantism in kids, acromegaly in adults, impaired glucose tolerance, diabetes mellitus

corticotroph adenomas- cushing syndrome and hyperpigmentation

distinctive morphologic features of most adenomas: cellular monomorphis and absence of reticulin network

35
Q

25-year-old male sustains a IED explosion and survives with multiple medical problems
He complains of being tired

He notices a loss of libido, impotence, and loss of pubic and axillary hair

A

hypopituitarism

TSH, FSH, LH, and MSH decreased

brain shaking can beat up the stalk

36
Q

Hypopituitarism

A

refers to decreased secretion of pituitary hormones, which can result from diseases of the hypothalamus or of the pituitary

Most cases of hypopituitarism arise from destructive processes directly involving the anterior pituitary.

37
Q

Differential diagnosis of hypopituitarism

A

Tumors and other mass lesions
*** Traumatic brain injury and subarachnoid hemorrhage are among the most common causes of pituitary hypofunction
Pituitary surgery or radiation

Pituitary apoplexy
Ischemic necrosis of the pituitary and Sheehan syndrome

Rathke cleft cyst

Empty sella syndrome

Hypothalamic lesions

Inflammatory disorders and infections

Genetic defects

38
Q

Clinical manifestations of hypopituitarism

A

Children can develop growth failure (pituitary dwarfism) due to growth hormone deficiency.
Gonadotropin (LH and FSH) deficiency leads to amenorrhea and infertility in women and decreased libido, impotence, and loss of pubic and axillary hair in men.
TSH and ACTH deficiencies result in symptoms of hypothyroidism and hypoadrenalism, respectively.
Prolactin deficiency results in failure of postpartum lactation.
The anterior pituitary is also a rich source of MSH, synthesized from the same precursor molecule that produces ACTH; therefore, one of the manifestations of hypopituitarism includes pallor due to a loss of stimulatory effects of MSH on melanocytes.

39
Q

Posterior Pituitary Syndromes

A

diabetes insipidus and SIADH

40
Q

Diabetes insipidus

A

ADH deficiency causes diabetes insipidus, a condition characterized by excessive urination (polyuria) due to an inability of the kidney to resorb water properly from the urine

41
Q

Syndrome of inappropriate ADH (SIADH) secretion

A

ADH excess causes resorption of excessive amounts of free water, resulting in hyponatremia

42
Q

52-year-old male presents with confusion and headache
20+ years smoker, chest x-ray performed
hyponatremia

A

SIADH

43
Q

23-year-old male suffered head trauma secondary to motor vehicle accident
On exam is mildly confused but oriented times three
hypernatremia
BUN and creatinine elevated

A

diabetes insipidus

44
Q

Diagnosis of diabetes insipidus

A

Diabetes insipidus. ADH deficiency causes diabetes insipidus, a condition characterized by excessive urination (polyuria) due to an inability of the kidney to resorb water properly from the urine.

45
Q

central vs nephrogenic diabetes insipidus

A

Diabetes insipidus from ADH deficiency is designated as central to differentiate it from nephrogenic diabetes insipidus, which is a result of renal tubular unresponsiveness to circulating ADH.

The clinical manifestations of these two disorders are similar and include the excretion of large volumes of dilute urine with a lower than normal specific gravity. Serum sodium and osmolality are increased by the excessive renal loss of free water, resulting in thirst and polydipsia.

46
Q

normal shape of lateral ventricles

A

V shape

47
Q

Hypothalamic Suprasellar Tumors

A

Neoplasms in this location may induce hypofunction or hyperfunction of the anterior pituitary, diabetes insipidus, or combinations of these manifestations.

The most commonly implicated tumors are gliomas and craniopharyngiomas.

A bimodal age distribution is observed, with one peak in childhood (5 to 15 years) and a second peak in adults 65 years or older. Patients usually come to attention because of headaches and visual disturbances, while children sometimes present with growth retardation due to pituitary hypofunction and GH deficiency

48
Q

The craniopharyngioma is thought to arise from

A

vestigial remnants of Rathke pouch. These slow-growing tumors account for 1% to 5% of intracranial tumors.

49
Q

morphology of craniopharyngiomas

A

average 3-4 cm,
2 types: adamantinomatous (kids)- frequently have calcifications

papillary (more in adults)- less frequent calcifications

50
Q

prognosis with craniopharyngiomas and frequent findings

A

excellent recurrence-free and overall survival.

crankcase oil and calcifications

ENDO 2 Exam I (2017) (13 decks)

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