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Endo > Endo Path > Flashcards

Endo Path Flashcards

1
Q

Location of the pituitary gland

A

Base of the skull in the pituitary fossa

  • right below the optic chiasm (where the optic nerves cross)
  • straight behind the nasal cavity => surgically best approach is intra-nasally
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2
Q

Microadenoma

a) size
b) most common clinical presentation
c) early or late diagnosis

A

Microadenoma

a)

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3
Q

Most common microadenoma of the pituitary gland

A

Prolactinoma

=> serum prolactin > 200 ng/ml

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4
Q

2 other common microadenomas besides for prolactinomas

A

growth hormone secreting tumor => acromegaly

ACTH secreting tumor => Cushing’s

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5
Q

Describe the stalk effect of a pituitary adenoma

A

When serum prolactin is elevated but prevents PIG (dopamine) from getting from the hypothalamus to the pituitary => excess prolactin secretion

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6
Q

Macroadenoma

a) size
b) most common clinical presentation
c) early or late diagnosis
d) risk

A

Macroadenoma

a) > 1 cm (> 10 cm)
b) Nonfunctional => usually doesn’t present until mass effects are present (causes compression of the optic chiasm) and cause visual disturbance
c) Late
d) propensity to hemorrhage and infarct

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7
Q

Which tumor- micro or macroadenoma of the pituitary- would cause elargement of the sella?

A

Sella turcica = the bony saddle in which the pituitary sits in the base of the brain

=> macroadenomas can enlarge the sella

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8
Q

How can one determine location of a macroadenoma in a pt w/ visual disturbances?

A

We know which optic nerves control which visual fields, and we know where the optic nerves travel/cross in the brain

=> you can localize a macroadenoma by which part(s) of the visual field are lost

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9
Q

Define apoplexy

A

= bleeding into an organ or loss of blood flow to an organ

-characterized by hypoxic necrotic damage to tissue

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10
Q

Sheehan’s syndrome

A

= post partum pituitary apoplexy

  • hypopituitarism (decrease in pituitary fxn) caused by ischemic necrosis due to blood loss and/or hypovolemic shock after childbirth
  • anterior pituitary undergoes hyperplasia and increased vascularization needs during pregnancy => if there is a lot of blood loss at birth the pituitary (w/ a very high demand for blood) suffers first => necrotic
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11
Q

Where are the majority (2/3) of pituitary abscesses located?

A

Abcess = swollen area containing an accumulation of pus

2/3 are within the normal pituitary
-somewhere in the actual pituitary gland

While the other 1/3 are within pre-existing sellar lesions: so lesions that were already present in the space around the pituitary
-such as craniopharyngiomas, rathke cysts, or adenomas

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12
Q

Craniopharyngioma- what is it?

A

= brain tumor derived from pituitary gland embryonic tissue

  • most common non-glial CNS tumor of childrhood
  • 50% of cases occur in childhood
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13
Q

How to dx a craniopharyngioma?

A

Contains calcium deposits => is visible on an X-ray of the brain

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14
Q

What are Rathke’s cleft cysts

A

Benign growths of the pituitary gland

-same location as craniopharyngiomas but are cysts and non-neoplastic

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15
Q

Explain the composition of a thyroid lobule

(i) what separates lobules

A

Thyroid lobules made up of 20-40 follicles
-follicles lined by single layer of cuboidal epithelium containing colloid in the middle

(i) lobules neatly separated by reticular fibers (fibrous septae)

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16
Q

What is thyrotoxicosis?

Associated symptoms

A

A hypermetabolic state secondary to increased T3/T4 levels

-increase in metabolic rate => high HR, high RR, weight loss, irritability, anxiety, increased perspiration

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17
Q

What is the most common cause of hyperthryoidism?

A

Graves disease = diffuse hyperplasia of the thyroid gland

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18
Q

What are two uncommon causes of hyperthyroidism?

A
  • hyperfunctional multinodular goiter

- hyperfunction adenoma

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19
Q

Clinical manifestations of hyperthyroidism

(a) cardiac
(b) ocular
(c) neuromuscular
(d) skin
(e) GI
(f) skeletal

A

Overactivity of the sympathetic nervous system and increase in metabolic rate

(a) tachycardia, palpitations
(b) wide, staring gaze
(c) tremor, hyperactivity, nervousness, insomnia
(d) increased sweating, warm and moist skin
(e) GI: weight loss despite good appetite, hypermotility => diarrhea and malabsorption
(f) Osteoporosis

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20
Q

What is a thyroid storm?

A

An abrupt onset of severe hyperthyroidism

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21
Q

What pts is thyroid storm most commonly seen in?

A

Pts w/ underlying Grave’s disease (pituitary hyperplasia) and acute elevation of catecholamines (due to some form of stress including infection, surgery etc)

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22
Q

What is the most common clinical presentation of a pt in thyroid storm?

A

Fever and tachycardia

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23
Q

Why is thyroid storm considered a medical emergency?

A

B/c can be fatal due to cardiac arrhythmia

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24
Q

What lab findings are indicative of Grave’s disease?

A

High free T4 despite low TSH

T4 is high b/c of hyperplastic thyroid gland despite lack of stimulation b/c TSH is low (negative feedback of the high T4)

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25
Q

Which presents earlier in life: Graves disease or Hashimoto Thyroiditis

A

Graves typically presents earlier: ages 20-40
Harhimoto Thyroiditis typically 45-65 yoa

-both: W&raquo_space;> M

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26
Q

Does Graves disease and/or Hashimoto thyroiditis run in families?

A

Graves can run in families- is associated w/ polymorphisms in certain immune function genes

Strong genetic component in Hashimoto thyroiditis

-both are autoimmune mechanistically

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27
Q

Exophthalmus

A

= clinical finding in Graves disease of the ‘bug eyes’
-bulging of the eyes anteriorly out of the orbit

-due to inflammatory/connective tissue deposition in the ocular orbits bilaterally

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28
Q

Differentiate the gross pathological findings of a thyroid w/ Graves disease vs. Hashimoto thyroiditis

A

Both enlarged, but Grave’s will be red and ‘beefy’ due to the hyperplasia of the follicular cells

  • Hashimoto will be pale and nodular (due to the lymphocytic accumulation)
  • in late Hashiomoto you see a small atrophic gland
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29
Q

Radioacitve iodine uptake in a Graves disease pt

A

Will be abnormally high, making more hormone (hyperactive) => taking up much more iodine

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30
Q

Histological finding of fire flares

A

Characteristic of Graves disease- signs of hyperfunctioning follicular cells

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31
Q

Describe the mechanism of Graves disease

A

autoimmune- antibodies made that attach and activate the TSH receptor => constitutive stimulation of thyroid hormone secretion by the thyroid

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32
Q

Which thyroid are most common in women?

A

All!!! All the thyroid disorders are more common in women

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33
Q

What are the two most common causes of hypothyroidism?

A

Surgery and Hashimoto thyroiditis

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34
Q

Why is cretinism more common in undeveloped countries?

A

Cretinism = result of hypothyroidism in infancy/early childhood
-can be caused by a lack of iodine which is rare in developed countries bc in the US newborns are now screened for thyroid hormone levels

=> impaired development of skeletal and CNS => failure to thrive

35
Q

What is myxedema?

A

Myxedema = result of hypothyroidism in adults or older childhood

  • slowing of physical and mental activity
  • tired, weight gain, cold intolerance
36
Q

Laboratory diagnosis of hypothyroidism

A

Low active T4, high TSH

37
Q

Mechanism of Hashimoto Thyroiditis

A

-autoimmune disorder: antibodies against thyroid epithelial cells
=> cytotoxic T-cell mediated death
-excessive T-cell activation => inflammation
-overall extensive damage and inflammation to the thyroid gland

38
Q

Treatment of Graves disease

A

anti-thyroid medication to decrease thyroid hormone production and renter the pt euthyroid (normal hormone producing state)

39
Q

Classical histological findings of Hashimoto thyroiditis

A

‘Exuberant lymphoplasmacytic infiltrate and oncocytic change’

  • massive lymphocytic infiltration w/ presence of germinal centers
  • oncocytic change in cells => pinker cytoplasm w/ more mitochondria and larger nuclei
40
Q

Laboratory values of T3/T4 and TSH in Hashimoto Thyroiditis

A
  • low T3/T4

- compensatory high TSH

41
Q

What cancer are ppl w/ Hashimoto Thyroiditis at an increased risk of?

A

Lymphoma (MALT type) b/c of the massive infiltration and proliferation of lymphocytes

42
Q

Define goiter

Describe the mechanism

A

Goiter = enlargement of thyroid gland caused by impaired synthesis of hormones

  • lack of thyroid hormones causes a compensatory elevation of TSH
  • excess TSH => hypertrophy and hyperplasia => enlargement of the thyroid gland

-can develop into a diffuse nontoxic goiter or a multinodular goiter

43
Q

Is goiter more common in developed or undeveloped countries?

A

More common in undeveloped countries b/c of idoine deficiency => impaired synthesis of thyroid hormones causes the cascade

44
Q

What is the most common cause of goiter?

A

Iodine insufficiency => not enough iodine to make active thyroid hormone

45
Q

Are all cases of goiter euthyroid?

A
  • most cases are euthyroid (have normal thyroid hromone secretion) b/c the compensatory enlargement is enough to overcome the thyroid hormone deficiency
  • however in some cases the underlying disorder is too severe and the pt will have goitrous hypothyroidism
  • so overall goiter is a nonspecifc finding
46
Q

Differentiate simple from multinodular goiters

A

simple goiters have no nodules- usually euthyroid in adults

Multinodular goiters are preceded by difuse goiter and is more serious

47
Q

Histologically describe the changes seen in a goitrous thyroid gland

A

variable sized follicles some distended w/ colloid

-basically variable sizes b/c trying to grow w/ abnormal signals and tons of fibrosis

48
Q

What is done to assess the prognosis of a goiter? What is the most common prognosis

A

95% are benign, only about 5% can progress to malignancy (so watch out for sudden changes in size or symptoms)

-diagnosis made via fine needle aspiration

49
Q

What are the most common symptoms of a goiter?

A

Usually not cancerous, usually symptoms are due to the mass effect: SOB, difficulty swallowing

50
Q

Subacute Thyroiditis- what is it?

(i) more common in males or females?

A

Granulomatous inflammatory condition of the thyroid present with a sudden painful thyroid enlargement and hyperthyroidism

  • believed to be a post-viral autoimmune response
    (i) more common in females (like all other thyroid diseases)
51
Q

What is the treatment for subacute thyroiditis?

A

No treatment needed, self-limited clinical course of about 6-8 weeks

52
Q

Histological finding of subacute thyroiditis

A
  • granulomatous inflammation w/ giant cells, fibrosis, and lymphocytes
  • neutrophilic infilrate
53
Q

How common are thyroid nodules?

Are most cancerous?

A

Palpable thyroid nodules are very common- found in 4% of the population
-incidence increases w/ age

majority are benign

54
Q

What is the prognosis of most thyroid cancers?

Which are more likely to be neoplastic

(a) solitary vs. multiple nodules
(b) younger vs. older pts
(c) Males vs. females
(d) functional vs. nonfunctional nodules

A

Very indolent cancer
-90% survival at 20 years

More likely to be neoplastic (cancerous)

(a) Solitary. b/c multiple is more associated w/ benign goiters
(b) younger pts
(c) Males more likely to be neoplastic
(d) nonfunctional more likely neopastic, functional more likely benign

55
Q

How are thyroid nodules evaluated?

A

Ultrasound guided needle biopsy

56
Q

What is the most common benign thyroid neoplasm?

A

Follicular adenoma

57
Q

What is the most common malignant thyroid neoplasm?

A

85% of malignant thyroid neoplasms = papillary carcinomas

58
Q

What is the most dangerous thyroid neoplasm

A

Anaplastic carcinoma- accounts for

59
Q

How can the four histological variants of thyroid cancer be distinguished?

A

By the distinct genetic events in their pathogenesis =>
papillar, follicular, medullary, and anaplastic carcinoma all have a different molecular pathogenesis

=> can do molecular testing for these pathways for diagnosis

60
Q

What is the molecular pathogenesis of papillary carcinomas of the thyroid?

A

PET/PTC rearrangement in 20-40%

BRAF gene point mutations in 30-40%

61
Q

What is the molecular pathogenesis of follicular carcinomas of the thyroid?

A

= second most common malignant thyroid neoplasm (5-15%)

-RAS mutations, PAX8/PPARG fusion genes

62
Q

Molecular pathogenesis of anaplastic carcinoma

A

-anaplastic carcinomas (most severe prognosis) can arise de novo or from severe papillary/follicular thyroid carcinomas

= RAS and PI3K mutation, inactivation of p53

-de novo can include inactivation of p53 or activation mutations in beta-catenin

63
Q

What cells do papillary carcinomas of the thyroid arise from?

A

Thyroid follicular cells

64
Q

What cells do medullary carcinomas of the thyroid arise from?

A

Parafollicular C-cells
-not from follicular cells like the other 3 types of malignant thyroid neoplasms (papillary, follicular, and anaplastic) => has very different molecular pathogenesis

65
Q

Molecular pathogenesis of medullary carcinoma

A

RET proto-oncogene mutations

66
Q

Describe follicular adenomas of the thyroid

  • structure
  • malignant potential
A

Follicular adenoma = benign (completely distinct, and do not progress to, follicular carcinomas)

  • well-demarcated nodule compressing the surrounding tissue
  • well-circumscribed
67
Q

Differentiate follicular adenomas from follicular carcinomas

A
  • follicular adenomas have a well intact capsule w/ NO vascular or capsular invasion, benign
  • follicular carcinoma = 2nd more common form of thyroid cancer (malignant). Can have a capsule but the differentiating factor is that there is capsular invasion in a carcinoma
68
Q

Why are follicular adenomas removed?

A

Follicular adenomas are not removed b/c they are malignant, instead surgically removed b/c by fine needle aspiration they are indistinguishable from follicular carcinoma => remove them anyway and defined as curative if the nodule comes out and it is well-encapsulated (=> is adenoma not carcinoma)

69
Q

Intranuclear pseudoinclusions on fine needle aspiration

A

-classic and pathognomonic for papillary carcinoma of the thyroid

70
Q

Psammoma body

A

-classic and pathognomonic for papillary carcinoma of the thyroid

= calcified structures of tumor cell necrosis when the papillary carcinoma outgrows its blood supply

71
Q

Distinguish papillary from follicular thyroid carcinoma

A

Papillary- overlapping oval nuclei w/ fibrovascular core. Not encapsulated

Follicular- encapsulated w/ capsular invasion

72
Q

RET/PTC rearrangements

A

Diagnostic of papillary carcinoma

-not seen in follicular adenoma/carcinoma

73
Q

BRAF point mutations

A

Diagnostic of papillary carcinoma

-not seen in follicular adenoma/carcinoma

74
Q

Are most cases of medullary carcinoma familial?

A

No, 70% of cases are sporadic. Other 30% are familial associated w/ MEN syndrome

75
Q

Prognosis of papillary carcinoma of the thyroid

A

Excellent prognosis

-95% 10 year survival

76
Q

Germline RET protooncogene mutation

A

Involved in MEN, familial medullary carcinoma of the thyroid

77
Q

Prognosis of medullary carcinoma

A

-very varibale prognosis so hard to tell

78
Q

Which thyroid cancer will stain positive for calcitonin?

A

Medullary carcinoma- derived from parafollicular (C) cells that produce calcitonin

79
Q

What environmental factor is associated w/ thyroid cancer?

A

Radiation of the neck

80
Q

Undifferentiated carcinoma

A

Extremely aggressive and quickly progressive tumor w/ rapidly enlarging neck mass

-mean survival of 6 months

81
Q

What 2 things can predispose to lymphoma of the thyroid?

A

-lymphoma of the thyroid usually arises in the background of lymphocytic or Hashimoto thyroiditis

82
Q

Where is the most common location of ectopic thyroid tissue deposition?

A

Base of the tongue

83
Q

What is a thyroglossal duct cyst?

A

Most common congenital anomaly of the thyroid, remnant of the thyroglossal duct

84
Q

Treatment of thyroglossal duct cyst

A

Complete surgical removal so it doesn’t turn into an abscess or cancerous

Endo (4 decks)

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