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Endocrine II midterm > Guerin: Thyroid Pathology > Flashcards

Guerin: Thyroid Pathology Flashcards

1
Q

What kind of receptor is the TSH receptor?

A

-GCPR

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2
Q

What does the thyroid C cell make?

A

calcitonin

-it secretes it too

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3
Q

What does calcitonins do?

A
  • promotes absorption of calcium by the skeletal system

- inhibits the resorption of bone by osteoclasts

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4
Q

what do thyroid follicular cells produce?

A

-thyroglobulin

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5
Q

What do the follicular cells convert thyroglobulin into?

A

-T4 and T3

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6
Q

Which thyroid hormone is more potent?

A

T3

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7
Q

What does T3 and T4 bind to in circulation?

A

-thyroxine-binding globulin and transthyretin

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8
Q

What happens to T4 in the periphery?

A

gets deodinated to T3

-remember that is the more active kind

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9
Q

What are Goitrogens?

A

chemical agents that inhibit thyroid gland functions

  • suppress T3 and 4 synthesis (High TSH)
  • hyperplastic enlargement of the thyroid (goiter)
  • Propylthiouracil (PTU)
  • Idonine
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10
Q

what does PTU do?

A
  • stops thyoid hormone production by inhibiting oxidation of iodine
  • also inhibits peripheral deiodination of T4
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11
Q

What does iodine (large doses) do?

A

-blocks the proteolysis of thyroglobulin thus preventing release of thyroid hormone

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12
Q

What comes first, TRH or TSH?

A

TRH from the hypothalamus makes the pituitary release TSH… THAT goes to the actual thyroid

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13
Q

What is thyrotoxicosis?

A
  • hypermetabolic state caused by elevated circulating levels of free T3 and T4
  • most commonly from hyperthyroidism
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14
Q

What are some of the most common disorders with thyrotoxicosis associated with Hyperthyroidism?

A
  • Diffuse hyperplasia (Graves disease)
  • Hyperfunctioning multinodular goiter
  • Hyperfunctioning adenoma
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15
Q

What are some clinical manifestations of a hypermetabolic state?

A
  • increase in basal metabolic rate
  • heart
  • symp nervous system
  • eyes
  • skeletal system
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16
Q

What happens with the basal metabolic rate?

A

skin is soft, warm, and flushed because of increased blood flow and peripheral vasodilation

  • increases heat loss so heat intolerance is common
  • sweating
  • weight loss with increased appetite
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17
Q

What happens with the heart?

A
  • tach, palpitations, cardiomegaly common
  • arrhythmias, a fib
  • congestive heart failure
  • thyrotoxic or hyperthyroid cardiomyopathy
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18
Q

What happens because of an overactive symp nervous system?

A
  • Tremor
  • Hyperactivity
  • Emotional lability
  • Anxiety
  • Inability to concentrate
  • insomnia
  • Prox muscle weakness
  • hyperstimulation of Gut: diarrhea and malabsorption
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19
Q

What happens with the eyes?

A

Wide, staring gaze and lid lag
-from symp overstimulation of the superior tarsal muscle

-True thyroid ophthalmopathy associated with proptosis occurs only in Graves disease

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20
Q

What happens with the skeletal system?

A
  • Thyroid hormone stimulates bone resorption

- Atrophy of skeletal muscle, with fatty infiltration and focal interstitial lymphocytic infiltrates

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21
Q

What is Thyroid storm?

A
  • abrupt onset of severe hyperthyroidism
  • underlying graves disease
  • acute elevation in catecholamine levels
  • febrile and tachycardic
  • medical emergency: cardiac arrhythmias
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22
Q

Apethetic Hyperthyroidism

A
  • thyrotoxicosis in older adults
  • advanced age and co-morbidities may blunt features that typically bring younger patients to attention
  • Diagnosis is often made during lab work-up for unexplained weight loss or worsening CV disease
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23
Q

Lab findings for Apethetic hyperthyroidism

A
  • Serum TSH concentration: most useful single screening test… low
  • confirmed with free T4… increased
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24
Q

What excludes secondary hyperthyroidism?

A

-a normal rise in TSH after administration of TRH

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25
Q

What can help us determine the etiology of hyperthyroidism?

A

Radioactive Iodine

  • duffusely increased uptake in the whole gland (Graves disease)
  • Increased uptake in a solitary nodule (toxic adenoma)
  • Decreased uptake (thyroiditis)
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26
Q

Tx of hyperthyroidism?

A
  • B blocker
  • thionamide to block new hormone synthesis
  • Iodine soln to block the release of thyroid hormone
  • agents that inhibit peripheral conversion of T4 to T3
  • Radioiodine: incorporate into thyroid tissues…. ablation of thyroid function
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27
Q

IF someone comes in and it looks like they have hyperthyroidism, what is the best test to order?

A
  • TSH
  • if it’s low, then it’s hyperthyroidism
  • confirm with free T4 test
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28
Q

Hypothyroidism

A
  • W»»M

- can be accompanied by “goiter”

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29
Q

Causes of hypothyroidism?

A
  • HAshimoto thyroiditis (autoimmune)

- Iodine deficiency

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30
Q

What is Cretinism?

A
  • hypothyroidism in infancy or early childhood
  • found where dietar iodine deficiency is endemic
  • Rarely from dyshormonogenetic goiter
  • maternal T3 and T4 cross the placenta and are citical for fetal brain development
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31
Q

Clinical features of Cretinism?

A
  • severe mental retardation, short stature, coarse facial features, a protruding tongue, and umbilical hernia
  • if maternal deficiency before fetal thyroid development
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32
Q

Myxedema: Hypothyroidism in older child or adult

A
  • insidious
  • decreased symp activity: constipation and sweating
  • increased cholesterol and LDL levels
  • large tongue
  • deepening of voice
  • intolerance to cold (remember that hyperthyroid is intolerant to heat)
  • nonpitting edema (there it is ;) )
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33
Q

Testing for hypothyroidism

A
  • serum TSH level: most sensitive screening test

- T4 levels: decreased

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34
Q

How are the TSH levels in primary hypothyroidism?

A

-increased

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35
Q

TSH levels in secondary hypothyroidism?

A

-not increased

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36
Q

Thyroiditis

A

inflammation of the thyroid gland

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37
Q

Hashimoto Thyroiditis

A
  • most common cause of hypothyroidism in areas where iodine levels are sufficient
  • autoimmune destruction of the thyroid gland
  • Autoantibodies
  • Strong genetic component: CTLA4 and PTPN22
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38
Q

Pathology of Hashimoto

A
  • large thyroid
  • prominent mononuclear inflammatory infiltrate
  • thyroid follicles are atrophic/lost
  • Areas with Hurthle cell metaplasia
  • fibrosis
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39
Q

clinical course of hashimoto?

A
  • most often comes to clinical attention as painless enlargement of the thyroid
  • typically with hypothyroidism
  • in some pts, hypothyroidism is preceded by transient thyrotoxicosis: disruption of thyroid follicles leads to release of thyroid hormones
  • increased risk of developing other AI diseases
  • marginal zone B-cell lymphomas increased risk
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40
Q

Lab values in that transient thyrotoxicosis

A
  • free T3 and 4 is elevated
  • TSH in low
  • radioactive idoine uptake is decreased
41
Q

Subacute lymphocytic Thyroiditis

A
  • painless
  • mild hypERthyroidism and/or goitrous enlargement
  • most common in middle-aged pts
  • W>M
  • Postpartum thyroiditis: 5 % women postpartum
  • variant of AI thyroiditis
  • 1/3 evolve into hypothyroidism
42
Q

Histology of Subacute lymphocytic thyroiditis

A
  • lymphocytic infiltration with large germinal centers
  • patchy disruption and collapse of thyroid follicles
  • No fibrosis or Hurthle cell metaplasia
43
Q

How do we differentiate between subacute lymphocytic thyroiditis and Hashimoto thyroiditis?

A

-There’s no hurthle cell metaplasia in Subacute lymphocytic thyroiditis

44
Q

Granulomatous thyroiditis

-aka De Quervain thyroiditis

A
  • 40 to 50 years
  • W>M
  • URI just before onset of thyroiditis
  • seasonal incidence… occurrences peaking in the summer
  • self limited
45
Q

Morphology of granulomatous thyroiditis?

A
  • unilaterally or bilaterally enlarged and firm
  • capsule is intact, but may be stuck to surround structures
  • histology can be patchy
  • different histologic stages are sometimes found in the same gland, suggesting waves of destruction over a period of time
46
Q

clinical course of Granulomaous thyroiditis?

A
  • most common cause of thyroid pain
  • variable enlargement of thyroid
  • inflammation and thus hyperthyroidism are transient
  • high serum T4 and T3 levels and low serum TSH levels
  • radioactive iodine uptake is diminished, unlike Graves disease
47
Q

Riedel Thyroiditis

A
  • rare
  • Extensive fibrosis of the thyroid and surrounding structures: clinically mimicis thyroid carcinoma
  • a form of systemic AI IgG4-related sclerosing disease
48
Q

Graves Disease

A
  • most common cause of endogenous hyperthyroidism
  • triad of clinical findings:
    1. ) hyperthyroidism associated with diffuse enlargement of the gland
    2. ) infiltrative ophthalmopathy with resultant exophthalmos
    3. ) Localized, infiltrative dermopathy, sometimes called pretibial myxedema (only in a minority of patients)
49
Q

Pathogenesis of Graves disease

A
  • AI
  • 90% of pts have thyroid-stimulating immunoglobulin (TSI)… most important and specific one
  • genetic susceptibility linked to polymorphisms in immune-function genes like CTLA4 and PTPN22 and the HLA-DR3 allele
50
Q

Graves Ophthalmopathy

A
  • AI plays a role
  • appears that orbital preadipocyte fibroblasts express the TSH receptor
  • protrusion of the eyeball!
51
Q

Morphology of graves disease

A
  • thyroid gland is symmetrically enlarged
  • diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells
  • follicular cells are tall and more crowded
  • colloid is pale with scalloped margins
  • inflammatory infiltrates of lymphocytes and plasma cells
52
Q

Sx that are uniquely with Graves disease

A
  • diffuse hyperplasia of the thyroid, opthalmopathy, and dermopathy
  • increased blood flow thorugh the hyperactive gland can produce an audible “bruit”
53
Q

What can persist after the treatment?

A

exophthalmos

54
Q

Lab and radiology findings of graves disease?

A
  • low TSH levels
  • high free T4 and T3
  • radioiodine scans show a diffusely increased uptake
55
Q

Tx of graves disease

A
  • B blockers
  • decrease thyroid hormone synthesis with: thionamide, radioiodine ablation, thyroidectomy
  • surgery typically only those with large goiters that are compressing surrounding structures
56
Q

Diffuse and multinodular Goiters

A
  • enlargement of thyroid
  • caused by impaired synth of thyroid hormone: most often result of iodine deficiency
  • Impairment of thyroid hormone synth….rise in serum TSH… hypertrophy and hyperplasia of thyroid follicular cells… gross enlargement of the thyroid gland
  • euthyroid state in most
  • degree of thyroid enlargement is proportional to the level and duration of thyroid hormone deficiency
57
Q

What do we call it when the compensation isn’t enough?

A

goitrous hypothyroidism

58
Q

Diffuse nontoxic (simple) Goiter

A
  • enlargement of the entire gland without nodularity

- endemic or sporadic

59
Q

Endemic goiter

A
  • low levels of iodine
  • mountainous areas of the world
  • Lack of iodine… idecreased synth of thyroid hormone… increased TSH…. follicular cell hypertrophy and hyperplasia… goitrous enlargement
60
Q

Sporadic Goiter

A
  • F»>M
  • peaks at puberty or in young adult life
  • caused by ingestion of substances that interfere with thyroid hormone synth
  • hereditary enzymatic defects that interfere with thyroid hormone synthesis
  • mostly unknown
61
Q

clinical course of goiter

A
  • majority are euthyroid
  • Although TSH is usually elevated (T3 and T4 levels are normal)
  • symptoms are from mass effects
62
Q

Multinodular goiter

A
  • simple goiter…. multinodular goiter
  • recurrent episodes of hyperplasia and involuteion
  • virtually all long-standing simple goiters convert into multinodular goiters
  • produces the most pronounced thyroid enlargements
  • can be mistaken for neoplasms
  • occur in both sporadic and endemic forms
63
Q

clinical course of multinodular goiter

A
  • most symptoms are from mass effects

- most pts are euthyroid

64
Q

What is plummer syndrome

A
65
Q

Workup for multinodular goiter

A
  • radioiodine scan
  • uneven iodine uptake and sometimes a “hot” nodule
  • from an admixture of hyperplastic and involuting nodules
  • A fine needle aspiration can be helpful in evaluating a dominant nodule
  • hyperplasia vs. neoplasm
66
Q

How many solitary thyroid nodules are malignant?

A

<1%

-people with a lot of money are cancer….

67
Q

What makes a thyroid nodule more likely to be neoplastic?

A
  • solitary nodules
  • nodules in younger patients
  • nodules in males
  • hx of radiation to the head and neck
68
Q

What make a thyroid nodule more likely to be benign?

A
  • multiiple nodules
  • nodules in older patients
  • nodules in females
  • functional nodules that take up radioactive iodine (hot nodules)
69
Q

Follicular adenomas

A
  • discrete, solitary masses
  • present as unilateral painless masses discovered during routine physical examination
  • larger masses may produce symptoms
  • nonfunctional ingeneral
70
Q

morphology of follicular adenomas

A
  • solitary, spherical, encapsulated lesion
  • made up of uniform-appearing follicles that typically contain colloid
  • cells uniform and bland
  • occasionally the cells have eosinophilic, granular cytoplasm (Hurthle cell change)… also in hashimotos
71
Q

What is the key to distinguishing between a follicular adenoma and follicular carcinoma?

A

-integrity of the capsule!!!

72
Q

Diagnosis of follicular cell adenoma

A
  • Radionuclide scan: cold nodules that don’t take up as much iodine
  • Ultrasonography and fine-needle aspiration
  • ultimately need to evaluate capsule for a definitive diagnosis
  • capsule is evaluated grossly and histologically to exclude carcinoma
73
Q

Thyroid Carcinomas

A
  • ionizing radiation exposure

- dietary iodine deficiency is linked with a higher frequency of follicular carcinomas

74
Q

What is the most common type of thyroid carcinoma?

A

papillary carcinoma (85%)

  • then follicular
  • anaplastic
  • medullary
75
Q

What is the adverse prognostic indicator for thyroid carcinoma?

A

-BRAF

76
Q

Papillary carcinoma

A
  • most common form of thyroid cancer (85%)

- peaks at 25-50 yrs, but can occur at any age

77
Q

Morphology of papillary carcinoma

A
  • solitary or multifocal
  • areas of fibrosis and calcification
  • cystic
  • Nuclei are large and overlapping, nuclear groove, invaginations of the cytoplasm gives the appearance of intranuclear inclusions (pseudo-inclusions)
78
Q

What is the key for diagnosis of papillary carcinomas?

A
  • Nuclei
  • large and overlapping
  • nuclear groove
  • orphan annie eye nuclei
  • Invaginations of the cytoplasm gives the appearance of intranuclear inclusions… pseudoinclusions
79
Q

Follicular variant of PTC (papillary thyroid carcinoma)

A
  • follicular rchitecture

- can be encapsulated (better prognosis) or poorly circumscribed and infiltrative

80
Q

Tall-cell variant of PTC

A
  • tall columnar cells with intensely eosinophilic cytoplasm lining the papillary structures
  • older=worse prognosis
  • BRAF mutations in most cases (worse prognosis)
  • Often also have RET/PTC translocations
81
Q

clinical presentation of Papillary thyroid carcinoma

A
  • asymptomatic thyroid nodules
  • mass in cervical lymp node sometimes
  • distant mets…. lung
  • more advanced disease can have hoarseness, dysphagia, cough, or dyspnea
82
Q

Diagnosis of PTC

A
  • radionuclide scanning: cold nodules… not taking up iodine
  • Fine needle aspiration cytology: can be diagnostic if nuclear features are present
83
Q

Tx of PTC

A
  • thyroidectomy
  • radioactive iodine or external radiation
  • chemo, hormone, and trageted therapy
  • excellent prognosis
  • 10 yr survival rate
84
Q

Follicular Carcinoma

A
  • 5-15% of thyroid cancers
  • more frequent in areas with dietary iodine deficiency
  • W>M
  • More often in older patients than papillary carcinomas… peaks 40-60 years
85
Q

Morphology of follicular carcinoma

A
  • single nodules that may be well circumscribed or widely infiltrative
  • sharply demarcated lesions are very difficult to distinguish from follicular adenomas… may require examining the entire capsule microscopically to find invasioin
  • small follicles with colloid with uniform cells
  • Hurthle cell variant: cells with abundant granular, eosinophilic cytoplasm
  • *****nuclei lack the features typical of papillary carcinoma
86
Q

How to tell between follicular adenoma vs follicular carcinoma?

A

-capsular and/or vascular invasion (beyond the capsule)

87
Q

Clinical course of follicular carcinoma

A
  • presents as slowly growing painless nodules
  • typically cold nodules on scnitigrams
  • dont invade lympatics, so lymph nodes are rarely involved
  • Vascular hematogenous dissemination
  • prognosis depends on the extent of invasion and stage at presentation
88
Q

Tx of follicular carcinoma

A
  • total thyroidectomy followed by the radioactive iodine
  • also treated with thyroid hormone to suppress endogenous TSH levels
  • residual follicular carcinoma may respond to TSH stimulation
  • Serum thyroglobulin levels are used for monitoring tumor recurrence
89
Q

Anaplastic Carcinoma

A
  • undifferentiated tumors of the thyroid follicular epithelium
  • highly aggressive; mortality rate essentially 100%
  • 65 y/o
  • arise de novo, or by “dedifferentiation” of a well-differentiated papillary or follicular carcinoma
90
Q

clinical course of anaplastic Carcinoma

A
  • rapidly enlarging bulky neck mass
  • sx of dyspnea, dysphagia, hoarseness, and cough
  • no effective therapies
  • death usually from aggressive growth and compromise of vital structures in the neck
91
Q

Medullary Carcinoma

A
  • neuroendrocrine neoplasms derived from the parafollicular cells (C cells)
  • Secrete calcitonin
  • tumors also sometimes secrete other hormones
  • 70% are sporadic, 30 familial (MEN 2A or 2B)
92
Q

Genetics of medullary carcinoma

A
  • Familial form associated with germline RET mutations

- RET mutations are also seen in ~1/2 sporadic

93
Q

Morphology of medullary carcinoma

A
  • sporadic: solitary nodule
  • familial: often found bilaterally with multiple foci
  • tumor cells + for calcitonin by immunohistochemistry
  • Amyloid deposits are present in the stroma
  • familial medullary cancers: multicentric C-cell hyperplasia in the surrounding thyroid parenchyma
94
Q

Presentation of sporadic Medullary carcinoma

A
  • mass in neck
  • some cases present with paraneoplastic syndrome caused by secretion of a hormone
  • ***hypocalcemia is not a prominent feature, even though calcitonin levels are elevated
  • cacinoembryonic antigen (CEA) is also secreted by many tumors… so that’s a useful tumor marker for disease burden and follow-up
95
Q

Presentation of familial medullary carcinoma

A
  • symptoms localized to the thyroid
  • endocrine neoplasms in other organs
  • medullary carcinomas in MEDN-2B pts are generally more aggressive (so they’re offered prophylactic thyroidectomy)
96
Q

Thyroglossal duct Cyst

A
  • congenital anomaly
  • vestige of tubular thyroid leading to a persistent sinus tract
  • parts of the tube remain to form cysts
  • may not become evident until adulthood
  • cysts can collect mucinous, clear secretions
  • midline of the neck (anterior to the trachea)
  • epithelium with an intense lympocytic infiltrate
  • can become infected and form abscess cavities
  • rarely give rise to cancers
97
Q

What kind of epithelium is lining a thyroglossal duct cyst located high in the neck?

A

-lined by stratified squamous epithelium

98
Q

What about the lower neck?

A

-lined by epithelium resembling the thyroidal acinar epithelium

Endocrine II midterm (13 decks)

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