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pathoma unit 5 > anterior pituitary > Flashcards

anterior pituitary Flashcards

1
Q

what is a pituitary adenoma

A

benign tumor of the pituitary cells. the tumors can be functional or nonfunctional.

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2
Q

what is a common visual disturbance of pituitary adenoma

A

bilateral temporal hemianopsia. due to compression of the optic chiasm.

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3
Q

what are 2 other common presentations of pituitary adenoma

A

headache and hypopituitarism due to compression of the healthy tissue.

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4
Q

what is a prolactinoma and how does it present?

A

it is a functional pituitary tumor that secretes prolactin. it presents as galactorrhea and amenorrhea in females or as decreased libido and headache in males. this is the most common type of pituitary adenoma.

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5
Q

how do we treat prolactinoma medically?

A

with dopamine agonists because they inhibit the release of prolactin. such as bromocriptine or cabergoline. this will suppress prolactin production and shrink the tumor.

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6
Q

how does a growth hormone adenoma present in children? how about adults? why?

A

gigantism in children and acromegaly in adults. growth before the fusion of the epiphysis will result in extended growth.

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7
Q

how do acromegalic adults present?

A

enlarged bones of the hands, feet and jaw. there is growth of the visceral organs that result in cardiac failure. enlarged tongue.

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8
Q

what common metabolic disturbances are there in growth hormone adenoma? why

A

there is secondary DM. this is because growth hormone induces the liver to gluconeogenesis and thus hyperglycemia

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9
Q

how do we diagnose GH adenoma?

A

by elevated levels of GH and IGF-1. there will be a lack of GH suppression with glucose intake.

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10
Q

treatment for GH adenoma? Medical?

A

octereotide. this is a somatostatin analog that suppresses GH release. can apply some GH receptor antagonists and surgery as well.

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11
Q

ACTH adenoma

A

functional that secretes ACTH. leads to cushings syndrome

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12
Q

hypopituitarism general characteristics

A

insuf production of hormones by the anterior pituitary.

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13
Q

when do the symptoms of hypopituitarism arise?

A

when 75% of the parenchyma of the pituitary is lost.

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14
Q

common causes of hypopituitarism?

A

adenoma in adults, craniopharyngeoma in children. typically due to hemorrhage in the pituitary causing apoplexy. sheehan syndrome during pregnancy

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15
Q

how does hypopituitarism present?

A

hair loss, poor lactation, LOSS OF PUBIC HAIR, fatigue.

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16
Q

central dibetes insipidus etiology?

A

ADH deficiency due to hypothalamic or posterior pituitary pathology.

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17
Q

what are the clinical features of DI

A

based on the loss of free water. polyuria, polydipsia, and risk of life-threatening dehydration. hypernatremia and high serum osmolarity. low urine osmolarity and specific gravity.

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18
Q

what are the results of a water deprivation test for DI?

A

there is a lack to appropriately concentrate the urine.

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19
Q

treatment for central DI

A

give vasopressin or analogs.

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20
Q

nephrogenic diabetes insipidus

A

there is an impaired renal response to ADH. usually due to inherited mutations or to drugs.

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21
Q

which drugs cause nephrogenic DI

A

lithium and demeclocycline

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22
Q

clinical features of nephrogenic DI

A

same symptoms as central, but with no response to desmopressin

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23
Q

syndrome of inappropriate ADH

A

there is excessive secretion of ADH most often due to an ectopic source.

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24
Q

most common ectopic source of SIADH

A

small cell lung carcinoma

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25
Q

what are the clinical features of SIADH

A

based on the retention of free water. hyponatremia and low serum osmolality. mental status changes and seizures.

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26
Q

treatment for SIADH

A

water restriction or demeclocycline

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27
Q

thyroglassal duct tumor

A

cystic dilation of the thyroglossal duct remnant. presents as a neck mass anteriorly.

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28
Q

lingual thyroid

A

presence of thyroid tissue at the base of the tongue. presents as a base of tongue mass.

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29
Q

what causes the clinical syndrome of hyperthyroidism?

A

there is an increased level of circulating thyroid hormone and this causes higher production of Na/KATPase and higher transcription of adrenergic receptors throughout the body (beta 1 most specifically). this causes all the clinical symptoms

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30
Q

clinical features of hyperthyroidism

A

weight loss, despite appetite. heat intolerance and sweating, tachycardia with increased CO, arrhythmia, tremor, anxiety, insomnia, heightened emotions, staring gaze with lid lag, diarrhea with malabsorption, oligomenorrhea. bone resorption with hypercalcemia. HYPOCHOLESTEROLEMIA AND HYPERGLYCEMIA.

31
Q

common treatment of thyroid storm?

A

polythiouracil because it inhibits peroxidase-mediated oxidation, organification and the coupling steps of thyroid hormone synthesis. as well as the peripheral conversion of t4-t3

32
Q

multinidular goiter

A

enlarged thyroid with multiple nodules. due to relative iodine deficiency and is usually non toxic. can become toxic goiter.

33
Q

cretinism

A

hypothyroidism of neonates and infants. mental retardation, short stature with skeletal abnormalities coarse facia features, enlarged tongue, and umbilical hernia.

34
Q

causes of cretinism

A

maternal hypotyroid, thyroid agenesis, iodine deficiency, dyshormonogenic goiter.

35
Q

myxedema

A

this is hypothyroidism in children or adults. this is mainly based on decreased BMR and central nervous system activity.

36
Q

what are clinical signs of myxedema

A

myxedema, weight gain, slowing of mental activity, muscle weakness, cold intolerance and decreased sweating. bradycardia with decreased CO, shortness of breath and fatigue, oligomenorrhea, hypercholesterolemia, constipation.

37
Q

what are the most common causes of hypothyroidism

A

iodine deficiency and hashimotos.

38
Q

what does iodine deficiency cause?

A

nontoxic goiter, RARELY toxic goiter, hypothyroidism

39
Q

which HLA is associated with hashimotos

A

HLA-DR5

40
Q

why are there antithyroglobulin and peroxidase ABs in hashimotos

A

because they are signs of thyroid damage, they do not mediate the disease

41
Q

what are the histological characteristics of hashimotos

A

germinal centers and hurthle cells -eosinophilic metaplasia that lines the follicle.

42
Q

what diseases are associated with hashimotos?

A

there is a risk for marginal cell lymphoma. this presents as an enlarging thyroid gland late in the course of disease.

43
Q

subacute granulomatous (de Quaervains) thyroiditis

A

granulomatous thyroiditis that follows a viral infection, presents a TENDER goiter/thyroid and transient hyperthyroidism.

44
Q

what is the course of subacute granulomatous (de Quaervains) thyroiditis

A

usually self-limited and rarely progresses to hypothyroidism

45
Q

reidel firbrsing thyroiditis

A

chronic inflammation of the gland. presents as hypothyroidism with a “hard as wood” thyroid that is nontender. the fibrosis can also involve other structures such as the airway.

46
Q

who gets riedel fibrosing thyroiditis vs anapestic carcinoma

A

younger patients get fibrosis, older patients get anapestic

47
Q

how do we biopsy the thyroid?

A

FNA because it is soo vascular.

48
Q

thyroid neoplasia types, presentation and screen?

A

usually presents as a solitary nodule that is distinct. they are more likely to be benign than malignant. they are typically cold on radioactive uptake. there are follicular, medullary, papillary

49
Q

typical findings on HOT nodules

A

graves or nodular goiter.

50
Q

typical findings on cold nodules

A

adenoma or carcinoma.

51
Q

follicular adenoma

A

benign prolif of the follicles surrounded by a fibrous capsule. usually non functional

52
Q

papillary carcinoma

A

most common type of thyroid cancer (80%) of cases. risk factor is exposure to ionizing radiation as a child. comprised of papillae lined by clear cells (little orphan annie nuclei cells) and nuclear groves. often associated with psammoma bodies.

53
Q

what are the two main histological associations with papillary carcinoma?

A

cells with clear nuclei (little orphan annie nuclei cells) with nuclear grooving and psammoma bodies.

54
Q

what is the prognosis for papillary carcinoma?

A

very good. 95 % 10 yr.

55
Q

here does papillary carcinoma like to spread?

A

to the cervical lymph nodes. but still good prognosis.

56
Q

follicular carcinoma

A

malignant proliferation of the follicular cells with invasion through the capsule -distinguishes it from benignity. also why the entire capsule has to be examined. cannot be made be FNA. metastasis is hematogenous

57
Q

medullary carcinoma

A

proliferation of the C cells. 5% of thyroid cancers. can lead to hypocalcemia because of the neuroendocrine nature of the tumor and the secretion of calcitonin.

58
Q

what does the biopsy for medullary carcinoma look like?

A

sheets of malignant cells in an amyloid stroma.

59
Q

familial medullary carcinoma gene?

A

this is part of the MEN2A/B syndrome. mutations in the RET gene.

60
Q

what does MEN 2A result in

A

medullary carcinoma, pheochromocytoma, parathyroid adenoma,

61
Q

what does MEN2B result in

A

ganglioneuroma of the oral mucosa.

62
Q

what can you do if your patient has RET gene mutation?

A

prophylactic thyroidectomy

63
Q

anaplastic carcinoma

A

undifferentiated malignant tumor of the thyroid. seen in the elderly. often involves neighboring structures and results in dysphagia and respiratory compromise. there is a poor prognosis.

64
Q

primary hyperparathyroidism

A

excessive PTH secretion by the gland itself. most common cause is the adenoma 80%. this is benign of a single gland. most often to present with asymptomatic hypercalcemia.

65
Q

consequences of hyperPT and hypercalcemia

A

nephrolithiasis, nephrocalcinosis, CNS disturbances such as depression and seizures, constipation, peptic ulcer, and acute pancreatitis. osteitis fibrous cystica f

66
Q

what are the labs of hyperPTH and hypercalcemia?

A

increased PTH, increased calcium, decreased phosphate., increased urinary cAMP, and increased alkaline phosphatase.

67
Q

treatment for primary hyperPT?

A

surgical removal of the affected gland.

68
Q

what is the most common cause of secondary hyperPT?

A

chronic renal failure. decreased phosphate secretion binds serum calcium and thus decreases its concentration. there is a consequent increase in the PTH and thus resoroption of the bone leading to renal osteodystrophy.

69
Q

what are the causes of hypoparaT?

A

Digeorge syndrome, autoimmune damage or surgical resection

70
Q

how does hypoPT present?

A

tingling and numbness, muscle spasms can be generated by filling a blood pressure cuff or tapping on the facial nerve.

71
Q

how does diabetic ketoacidosis present?

A

patient has a history of type I diabetes, kussmaul respirations, excessive ketones, dehydration, nausea, vomiting, mental status changes, fruity smelling breath (acetone).

72
Q

treatment for DKA

A

insulin, electrolytes, fluids.

73
Q

what is hyperosmolar hyperglycemic syndrome

A

HHS is hyperglycemia that causes a life-threatening diuresis, hypotension and coma

pathoma unit 5 (12 decks)

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