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Pathology > Chapter 24 - The Endocrine System > Flashcards

Chapter 24 - The Endocrine System Flashcards

1
Q

most common cause of hyperpituitarism

A

adenoma

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2
Q

types of pituitary adenomas

A

functioning - associated with hormones or nonfunctioning - without clinical symptoms of hormone excess

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3
Q

difference between micro and macro pituitary adenomas

A

micros is less than 1 cm and macro is greater than 1 cm

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4
Q

clinical symptoms of pituitary adenomas

A

endocrine abnormalities and mass effects –> abnormalities of the sella turcica, visual field abnormalities, signs + symptoms of increased intracranial pressure, sometimes hypopituitarism

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5
Q

most frequent type of hyperfunctioning pituitary adenoma

A

prolactinoma

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6
Q

symptoms of prolactinoma

A

amerorrhea, galactorrhea, loss of libido

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7
Q

other than a prolactinoma, how can you get hyperprolactinemia

A

from lactotroph hyperplasia where there is an interference with normal dopamine inhibiition of prolactin, like from drugs

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8
Q

second most common type of functioning pituitary adenoma

A

growth hormone cell (somatotroph) adenomas

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9
Q

a somatoroph adenoma causes _____ in a child; why?

A

gigantism if it appears before the epiphyses have closed

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10
Q

what if a somatotroph adenoma appears after the the epiphyses lates close?

A

results in acromegaly

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11
Q

symptoms of acromegalyy

A

growth in skin and soft tissues, viscera, bones of face hands and feet, enlarged jaw, broadening of lower face, enlarged hand and feet with broad, sausage like fingers

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12
Q

what other diseases/symptoms can be seen alongside a growth hormone excess

A

diabetes mellitus, generalized muscle weakness, hypertension, CHF

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13
Q

how do you diagnose a growth hormone excess

A

elevated serum GH and IGF-1 levels; failure to suppress growth hormone production in response to an oral load of glucose

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14
Q

what are hormone levels like with corticotroph adenoma

A

excess production of ACTH which leads to an adrenal hypersecretion of cortisol

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15
Q

hypofunction of the anterior pituitary happens when: ___% of the parenchyma is lost

A

75%

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16
Q

what happens in pituitary apoplexy

A

sudden hemorrhage into the pituitary gland, often into a pituitary adenoma

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17
Q

symptoms of pituitary apoplexy (3)

A

headache, diplopia, hypopituitarism

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18
Q

what is sheehan syndrome

A

postpartum necrosis of the anterior pituitary; during pregnancy, the ant. pituitary enlarges to 2x its size, but this physiologic increase in not accompanied by an increase in blood supply so there is relative anoxia and may cause infarction

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19
Q

what happens in primary empty sella syndrome

A

defect in the diaphragma sella that allows the arachnoid mater and CSF to herniate into the sella resulting in expansion of the sella and complression of the pituitary

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20
Q

classic patient presentation of primary empty sella syndrome

A

obese women with a history of multiple pregancies

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21
Q

what causes secondary empty sella syndrome

A

a mass like an adenoma enlarges the sella but then it is surgically removed or undergoes necrosis causing a loss of pituitary function

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22
Q

children with growth hormone deficiency develop _____

A

pituitary dwarfism

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23
Q

what symptoms do gonadotropin (LH and FSH) deficiency cause in men and women

A

women: amenorrhea and infertility; men: decreased libido, impotence, and loss of pubic and axillary hair

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24
Q

prolactin deficiency results in what symptom?

A

failure of postpartum lactation

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25
Q

syndromes involving ADH secretion

A

diabetes insipidus and syndrome of inappropriate ADH secreation

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26
Q

diabetes insipidus characteristics and causes

A

ADH deficiency, excessive dilute urination with inappropriateloy low specific gravity, can results from trauma, tumors, inflammatory disorders of the hypothalamus and pituitary

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27
Q

what are electrolyte levels like in the blood of a patient with diabetes insipidus

A

serum sodium and osmolality are increased because of the excessive renal loss of free water –> causes thirst and polydipsia

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28
Q

electrolyte levels in SIADH

A

excess resoption of excessive amounts of free water results in hyponatremia

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29
Q

frequent causes of SIADH

A

secretion of ectopic ADH by malignant neoplasms (particularly small-cell carcinomas of the lung), drugs, infections

30
Q

clinical manifestation of SIADH (3)

A

hyponatremia, cerebral edema, resultant neurologic dysfunction

31
Q

where is a craniopharyngioma derived from

A

vestigial remnants of rathke pouch

32
Q

most craniopharyngiomas are located:

A

suprasellarly

33
Q

ages associated with craniopharyngiomas

A

5-15 years and 65 years or older

34
Q

2 forms of craniopharyngiomas

A

adamantinomatous craniopharyngiomas (mostly kids) and papillary craniopharyngioma (mostly adults)

35
Q

some morphological characteristics of craniopharyngiomas

A

dystrophic calcification (kid-type much more commonly calcifies) and cyst formation

36
Q

clinical features of hyperthyroidism (7)

A

hypermetabolic state with overactivity of the sympathetic nervous system (beta-adrenergic tone), heat intolerance, sweating, weight loss depsite increased appetite, cardiac manifestations (like tachycardia and arrythmias, LVH, low output heart failure), neuromuscular overactivity (tremor, emotional lability, insomnia, proximal muscle weakness), ocular changes (wide staring gaze and lid lag - tru thyroid opthalmopathy associated with proptosis is seen only with Graves), bone resorption

37
Q

what is thyroid storm

A

abrupt onset of sever hyperthyroidism

38
Q

what causes a thyroid storm

A

commonly in patients with underlying graves disease and results from an acute elevation in catecholamine levels that could be encountered during infection surgery, cessation of antithyoid medication, and stress

39
Q

many patients with thyroid storm die of:

A

cardiac arrythmias

40
Q

what is cardiomyopathy

A

thyrotoxicosis with left ventricular dysfunction and “low-output” failure

41
Q

congenital hypothyroidism is a result of

A

endemic iodine deficiency in the diet (common) or inborn errors of thyroid metabolism (mutations in thyroid peroxidase), thyroid agenesis or hypoplasia

42
Q

what is myxedema

A

hypothyroidism developing in the older child or adult

43
Q

clinical features of myxedema

A

generalized fatigue, apathy, mental sluggishness, patients are listless, cold intolerant, and frequently overwieght

44
Q

histology and pathophysiology of myxedema

A

accumulation of matrix substances like GAGs and hyaluronic acid in the skin, subQ, and viscera –> non-pitting edema, broadening and coarsening of facial features, enlargement of tongue, deepening of voice

45
Q

when should you suspect myxedema in a patient (what would they present with?)

A

unexplained increase in body weight or hypercholesterolemia

46
Q

autoimmune destruction of the thyroid gland

A

hashimoto thyroiditis

47
Q

HLA associated with Hashimotos

A

HLA DR5

48
Q

how does hashimotos contribute to thyroid cell death

A

CD8+ cytotoxic T-cell mediated cell death, cytokin-mediated cell death

49
Q

antibodies associated with hashimotos

A

anti-thyroid antibodies (anti-thyroglobulin, anti-thyroid peroxidase antibodies)

50
Q

what does the thyroid look like in hashimotos thyroiditis (histology, what kind of infiltrate)

A

enlarged, mononuclear inflammatory infiltrate with germinal centers, abundant eosinophilic cytoplasm –> Hurthle cells

51
Q

what may present before clinical hypothyroidism in Hashimotos

A

transient thyrotoxicosis by disruption of the thyroid follicles with secondary release of thyroid hormones –> hyperthyroid state –> T4/3 fall with compensatory increase in TSH

52
Q

increased risk of ____ in hashimotos

A

B-cell non-hodgkins lymphomas

53
Q

40-50 year old woman with thyroiditis after a viral infection is what disease

A

subacute (granulomatous) thyroiditis/ De Quervain thyroiditis - giant cells

54
Q

most common cause of thyroid pain

A

Granulomatous (de quervain) thyroiditis

55
Q

painless thyroiditis during the postpartum period

A

subacute lymphocytic thyroiditis, lymphocytic infiltration with hyperplastic germinal centers

56
Q

Riedel thyroiditis is identified by what?

A

extensive fibrosis involving the thyroid and contiguous neck structures

57
Q

what may riedel thyroiditis be present similar to?

A

anaplastic carcinoma of the thyroid (but in this case it would be a 70-80 year old woman)

58
Q

most common cause of endogenous hyperthyroidism

A

graves disease

59
Q

triad of graves disease

A

hyperthyroidism, infiltrative opthalmology and exopthalmos, pretibial myxedema

60
Q

age of patients with graves

A

20-40 year old women

61
Q

pathogenesis of graves disease

A

IgG self tolerance to the TSH receptor which releases an increase of thyroid hormones

62
Q

morphology of thyroid gland in graves disease

A

diffuse hypertrophy and hyperplasia

63
Q

what sound can you hear with auscultation in graves disease

A

bruit

64
Q

lab findings in graves disease

A

elevated free T4 and T3 with decreased TSH, increased radioactive iodine uptake

65
Q

endemic goiter is the result of

A

iodine deficiency

66
Q

sporadic goiter usually occurs at what age

A

puberty or in a young adult that may result from enzymatic defects

67
Q

irregular enlargement of the thyroid

A

multinodular goiter, uneven iodine uptake

68
Q

clinical symtpoms of a multinodular goiter

A

airway obstruction, dysphagia, SVC syndrome

69
Q

what is plummer syndrome

A

long standing gooiter producing hyperthyroidism (because goiters are usually subclinical)

70
Q

which types of nodules are benign and do they take up more or less iodine

A

hot nodules that take up radioactive iodine

71
Q

are most follicular adenomas of the thyroid functional or non-functional?

A

nonfunctional

Pathology (9 decks)

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