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Endo Repro - Maja > Pathology Review > Flashcards

Pathology Review Flashcards

1
Q

Benign tumor of the anterior pituitary cells

A

Pituitary adenoma

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2
Q

What is the difference between a functional and non functional tumor?

A

Functional = hormone producing

Non functional = silent

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3
Q

How do non functional tumors often present?

A

With a mass effect

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4
Q

Why do pituitary adenomas present with tunnel vision?

A

Pituitary sits adjacent to optic chiasm - mass effect

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5
Q

How will a prolactinoma present in women?

A

Galactorrhea (increased prolactin)

Amenorrhea (due to inhibition of GnRH –> loss of FSH and LH)

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6
Q

How will a prolactinoma present in men?

A

Decreased libido, headache

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7
Q

What is the most common type of pituitary adenoma?

A

Prolactinoma

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8
Q

How are prolactinomas treated?

A

Dopamine agonists such as Bromocriptine or cabergoline (DA inhibits production of Prolactin)

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9
Q

Difference between gigantism and acromegaly

A

Gigantism can occur in children (growth plates not closed)

Acromegaly in adults (big hands, digits, jaw, organs)

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10
Q

Most common cause of death in adults with growth hormone cell adenoma?

A

Cardiac failure (organs grow too much)

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11
Q

Why is diabetes secondary to a growth hormone adenoma?

A

GH decreases glucose uptake into the cell. Too much GH around = too much glucose in blood

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12
Q

How might one diagnose GH adenoma?

A

Oral glucose test (GH not suppressed)
Elevated GH
Elevated IGF-1 (GH leads to increase in IGF-1)

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13
Q

Treatment for GH adenoma

A

Octreotide

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14
Q

Why is octreotide an effective treatment for GH adenoma?

A

Somatostatin inhibits GH release - therefore use a somatostatin analog

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15
Q

At what point does hypopituitarism present?

A

when 75% is lost

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16
Q

2 main causes of hypopituitarism? (adult and child)

A
  1. Adult - pituitary ademona
  2. Child - craniopharyngioma

Both of these are due to mass effect or apoplexy

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17
Q

Who does Sheehan syndrome occur in?

A

Pregnant women - Gland doubles in size during pregnancy but not the blood supply - susceptible to infarction

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18
Q

How does Sheehan syndrome present?

A

Poor lactation
LOSS OF PUBIC HAIR
Fatigue

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19
Q

Two causes of empty sella syndrome?

A

Trauma or Congenital

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20
Q

Pathophysiology of empty sella syndrome?

A

Herniation of the arachnoid and CSF into the sella compresses and destroys the pituitary gland

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21
Q

What two hormones are stored in the posterior pituitary

A

ADH and oxytocin

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22
Q

Are hormones made in the posterior pituitary?

A

No, ADH and Oxy and made in the hypothalamus and transferred via neurons. Stored.

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23
Q

ADH function?

A

Acts on the distal tubule and collecting duct of kidneys to promote free water retention

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24
Q

Oxytocin function?

A

mediates uterine contraction during labor and release of breast milk (let down) in lactating mothers

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25
Q

Pathophysiology of Central DI

A

ADH deficiency - problem with hypothalamus or posterior pituitary

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26
Q

Pathophysiology of Nephrogenic DI

A

Impaired renal response to ADH - Mutation of drug induced

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27
Q

Clinical features of DI

A

Polyuria and polydipsia (life threatening dehydration)
Hypernatremia and high serum osmolality
Low urine osmolality and SG (peeing everything)

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28
Q

How to treat central DI?

A

ADH analog (desmopressin)

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29
Q

Does desmopressin work in nephrogenic DI?

A

No, problem with receptor

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30
Q

What drugs may cause nephrogenic DI?

A

Lithium

Demeclocycline

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31
Q

What is the most common cause of excessive ADH?

A

Ectopic production via a small cell carcinoma, CNS trauma, pulmonary infection, drugs

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32
Q

Clinical/lab findings of SIADH

A

Hyponatremia
Low serum Osmolality
Mental changes and seizures - neuronal swelling and cerebral edema

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33
Q

Treatment of SIADH

A

Free water restriction

Demeclocycline

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34
Q

Cystic dilation of the thyroglossal duct remnant results in this condition

A

Thyroglossal duct cyst

Typically, the thyroglossal duct normally involutes but a persistent duct may undergo dilation

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35
Q

How does a thyroglossal ductal cyst present upon exam?

A

an anterior neck mass

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36
Q

Persistent basal tongue mass

A

Lingual thyroid (doesn’t migrate fully from base of the tongue – site of origin)

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37
Q

What are the physiologic consequences on increased levels of circulating thyroid hormone

A 
Increased BMR (more Na/K ATP-ase)
Increased SNS activity (more B1 expression)
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38
Q

Name some clinical features of hyperthyroidism

A

Weight loss (even w/ increased appetite), heat intolerance, tachy and increased CO, arrhytmia, tremor, anxiety, insomnia, staring gaze, diarrhea, oligomenorrhea, bone resorption, decreased muscle mass, hypochlesterolemia, hyperglycemia

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39
Q

why hyperglycemia with hyperthyroidism?

A

Excess thyroid hormone in the blood causes gluconeogenesis and glycogenolysis

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40
Q

Pathophysiology of Graves Disease

A

Autoantibody (IgG) stimulates TSH receptor (type II HS) leads to an increase in synthesis and release of thyroid hormone

41
Q

Most common cause of hyperthyroidism

A

Graves Disease

42
Q

Typical patient profile for Graves Disease

A

Woman between the ages of 20 - 40 (childbearing)

Fits other autoimmune disease profile

43
Q

Clinical features of Graves Disease

A

Hyperthyroidism
Diffuse goiter
Exophthalmos and pretibial edema

44
Q

MOA of goiter

A

Constant TSH stimulation leads to thyroid hyperplasia and hypertrophy

45
Q

MOA behind exophthalmos and pretibial edema?

A
  • Fibroblasts behind the orbit and overlying shin express TSH receptor
  • TSH activation results in glycosaminoglycan buildup, inflammation, fibrosis and edema
46
Q

Microscopic appearance of Graves?

A

hyperplasia of the thyroid follicle and scalloping of the colloid

47
Q

Lab findings in Graves

A

Increased T4 ((total and free) Decreased TSH (free T3 downregulates TSH receptors))
Hypocholesterolemia
Increased serum glucose

48
Q

Treatment for Graves

A

B blocker
Thioamide (blocks peroxidase)
Radioiodine ablation

49
Q

What happens with a thyroid storm?

A

Stress leads to an elevated level of catacholamines and hormones - arrhythmia, hyperthermia, vomiting - hypovolemic shock

50
Q

Treatment for Thyroid storm

A

B blocker
steroid
Propylthiouracil (PTU)

51
Q

MOA of PTU

A

inhibits peroxidase mediated oxidation, organification and coupling of thyroid hormone synthesis
inhibits peripheral conversion of T4 to T3

52
Q

MOA of thioamide?

A

blocks peroxidase (which catalyzes T3 and T4 synthesis)

53
Q

Enlarged thyroid gland with multiple nodules

A

Multinodular goiter

54
Q

What is the usual cause of multinodular goiter?

A

Relative iodine deficiency

55
Q

Hypothyroidism in a neonate or child is often referred to as _______

A

Cretinism

56
Q

Classical findings of cretinism?

A

Mental retardation (thyroid hormone needed for brain development)
Short stature with skeletal abnormalities
course facial features
enlarged tongue
umbilical hernia

57
Q

What enzyme is most often deficient in dyshormonogenetic goiter?

A

thyroid peroxidase

58
Q

Hypothyroidism in older children and adults is often called _______

A

myxedema

59
Q

Some clinical features of myxedema include:

A

myxedema, weight gain, slowing of mental activity, muscle weakness, cold intolerance, bradycardia and decreased CO, SOB, fatigue, oligomenorrhea, hypercholesterolemia, constipation

60
Q

Two most common causes of myxedema:

A
  1. iodine deficiency

2. Hashimoto thyroiditis

61
Q

HLA DR5

A

Hashimoto thyroiditis

62
Q

Autoimmune destruction of the thyroid gland

A

Hashimoto thyroiditis

63
Q

Most common cause of hypothyroidism in regions with adequate iodine

A

Hashimoto thyroiditis

64
Q

Why might Hashimoto initially present with hyperthyroidism?

A

Initial destruction of the follicles results in the hormones leaking to the blood. As more follicles are destroys return to baseline and then drops.

65
Q

What type of abs might you see with Hashimoto

A

antithyroglobulin

antithyroid peroxidase

66
Q

What does a sample of thyroid with Hashimoto disease look like?

A

Chronically inflamed with germinal centers and Hurthle cells

67
Q

Patient presents with known Hashimoto and an enlarged thyroid – this should be high on your differential –

A

B cell (marginal) lymphoma

68
Q

Tender thyroid – this should be the top of your differential

A

Granulomatous throiditis

De Quervain

69
Q

Hypothyroidism with a ‘hard as wood’ nontender thyroid gland (may involve local structures)

A

Riedel Fibrosing Thyroiditis (chronic inflammation with fibrosis)

70
Q 
Thyroid lesion (hard)
Local structure involvement
young female patient
A

Riedel Fibrosing Thyroiditis

71
Q

Are thyroid nodules more likely to be benign or malignant?

A

Benign

72
Q

What type of study is used to characterize thyroid nodules?

A

Radioactive Iodine uptake study

73
Q

Increased radioactive (hot nodule) uptake seen in….

A

Graves disease

Nodular goiter

74
Q

Decreased radioactive uptake (cold nodule) seen in..

A

adenoma and carcinoma

75
Q

Mechanism for sampling the thyroid?

A

FNA (fine needle aspiration) biopsy

76
Q

Most common type of thyroid carcinoma

A

Papillary carcinoma

77
Q

What is the major risk factor for papillary thyroid carcinoma?

A

Exposure to ionizing radiation in childhood (face – acne)

78
Q

What distinguishing features will you see in the cells for Papillary carcinoma

A

Orphan Annie eye nuclei
Nuclear grooves
Psammoma bodies

79
Q

How do you distinguish follicular adenoma from follicular carcinoma

A

Invasion through the capsule
Entire capsule must be examined microscopically
Therefore cannot distinguish by FNA

80
Q

Malignant proliferation of follicles surrounded by fibrous capsule with invasion through the capsule

A

Follicular carcinoma

81
Q

Orphan annie eye nuclei

nuclear grooves

A

Papillary carcinoma

82
Q

Benign proliferation of follicles surrounded by a fibrous capsule

A

Follicular adenoma

83
Q

Metastasis of papillary carcinoma

A

Cervical lymph nodes

84
Q

Metastasis of follicular carcinoma

A

hematogenous

85
Q

Malignant proliferation of the parafollicular C cells

A

medullary carcinoma

86
Q

Name the four types of thyroid carcinomas

A

Papillary
Follicular
Medullary
Anaplastic

87
Q

Neuroendocrine cells that secrete calcitonin

A

C cells

88
Q

What do c cells secrete

A

calcitonin

89
Q

Calcitonin MOA

A

lower serum calcium by increasing renal calcium excretion

90
Q

why might a medullary carcinoma present with hypocalcemia?

A

C cells – more calcitonin – more renal calcium excretion

91
Q

Calcitonin often deposits within medullary tumors in this form

A

amyloid

92
Q

Typical, high yield description of medullary carcinoma biopsy

A

malignant cells in an amyloid stroma

this is an example of localized amyloidosis

93
Q

Familial cases of medullary carcinoma are due to this disorder

A

MEN 2

94
Q

Men 2A vs Men 2B

A

2A: medullary carcinoma, pheochromocytoma, parathyroid adenoma
2B: medullary carcinoma, pheochromocytoma, ganglioneuromas of oral mucosa

95
Q

What mutation is predictive of familial medullary carcinoma (MEN2)

A

RET mutation

May want prophylactic thyroidectomy

96
Q

Undifferentiated malignancy of thyroid gland

A

Anaplastic carcinoma

97
Q

Anaplastic carcinoma

A

undifferentiated malignant tumor of the thyroid

98
Q

What happens when anaplastic carcinoma invades local structures?

A

May lead to dysphagia or respiratory compromise (by esophagus and trachea)

Endo Repro - Maja (7 decks)

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