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MIDS 227 (module 1 + 2) > Ch 3 Thyroid Pathology > Flashcards

Ch 3 Thyroid Pathology Flashcards

1
Q

Role of u/s in imaging thyroid pathology?

A

-Locate nodules (intra/extra thyroidal)
-Describe appearance
-Determine other involvement (muscular, vasculature, lymph nodes, etc)
-Guide FNA/biopsy
-Follow up nodules for growth, new nodules, recurrence, post surgical, etc

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2
Q

What causes diffuse pathology of the thyroid gland?

A

-Inflammation/infection
-Thyroiditis (acute + chronic)
-Autoimmune (grave’s disease + hashimoto’s)
-Goiters

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3
Q

What causes focal nodules of the thyroid gland?

A

-Hyperplasia
-Adenoma
-Carcinoma
-Lymphoma
-Metastases

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4
Q

SF of focal nodules?

A

Variable
-Single or multiple
-Unilateral or bilateral

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5
Q

What procedure provides the diagnosis of benign vs malignant?

A

FNA cytology

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6
Q

Differentiate euthyroid, hyperthyroid + hypothyroid?

A

Euthyroid: normal functioning thyroid gland
Hyperthyroid: increased function
Hypothyroid: decreased function

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7
Q

What is the m/c thyroid function disorder?

A

Hypothyroidism (decrease in thyroid hormone production)

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8
Q

Differentiate b/w primary + secondary causes of hypothyroidism? Which is more common?

A

Primary:
-M/c
-Abnormality of the gland itself
-Decrease in T3/T4 = compensatory increased TSH

Secondary:
-Pituitary or hypothalamus failing to stimulate the normal thyroid function
-Decrease in TSH = decreased T3/T4

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9
Q

What is the m/c cause of primary hypothyroidism?

A

Worldwide: iodine

In iodine sufficient areas: hashimoto thyroiditis (aka chronic autoimmune thyroiditis)

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10
Q

Who m/c has primary hypothyroidism?

A

-Females, aged 45-65

-Associated with genetic predisposition, high iodine intake, selenium deficiency, smoking, chronic hepatitis C + other autoimmune diseases (such as sjogren syndrome, lupus + rhumatoid arthritis)

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11
Q

How is primary hypothyroidism diagnosed?

A

With bloodwork

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12
Q

What are the clinical manifestations/symptoms of hypothyroidism?

A

Depends on the severity (ranging from asymptomatic to myxedema coma)

M/c symptoms:
-Weakness/fatigue, dry skin, cold intolerance, hoarseness, weight gain, constipation, menstrual irregularities + decreased sweating

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13
Q

General SF of hashimotos thyroiditis

A

-Similar to Graves disease
-M/c diffusely abnormal echotexture*
-Hypervascular in early stage

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14
Q

SF of hashimotos thyroiditis in early, late + end stages?

A

Early:
-Increased size
-Coarse echotexture
-Hypo to normal echogenicity

Late:
-Fibrotic strands causing lobulations

End:
-Multinodular + fibrotic
-ill defined + heterogeneous
-Atrophic

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15
Q

An isthmus greater than how many cm AP indicates diffuse enlargement of the thyroid?

A

> 1cm AP

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16
Q

What causes thyrotoxicosis / hyperthyroidism?

A

Elevated levels of free T3 + T4 (this causes a hypermetabolic state)

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17
Q

Differentiate b/w primary + secondary hyperthyroidism?

A

Primary:
-Excess thyroid hormone is synthesized + secreted by the thyroid (ex. graves disease)

Secondary:
-Rare
-Due to an outside source (ex. TSH secreting pituitary adenoma)

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18
Q

What is the m/c cause of thyrotoxicosis?

A

Hyperthyroidism

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19
Q

What is the m/c cause of hyperthyroidism?

A

Graves disease

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20
Q

What is graves disease?

A

Autoimmune disease

(m/c in women of child bearing age)

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21
Q

Causes of graves disease?

A

-Hereditary
-Immune system
-Age
-Gender
-Stress

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22
Q

Pt’s with graves disease must present with 1 or more of the following symptoms:

A

-Hyperthyroidism
-Diffuse thyroid enlargement (goiter)
-Ophthalamopathy (protrusion of eyes)
-Graves dermopathy (pretibial myxedema)

(note: the general term myxedema refers to hypothyroidism, so we must be careful not to mix these terms up)

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23
Q

Clinical symptoms of hyperthyroidism/graves disease in adults?

A

-Severe wight loss
-Excessive sweating
-Heat intolerance
-Ophthalmopathy (bulging eyes)
-Enlarged thyroid (goiter)
-Tachycardia at rest
-Mood changes
-Dyspnea
-Nervous/anxiety
-Hand tremors/muscular weakness
-Menstrual irregularities (oligo or amenorrhea)

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24
Q

What happens if hyperthyroidism/graves disease gets left untreated?

A

-Can become severe + life threatening
-Complications include a “thyroid storm”

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25
Q

Clinical symptoms of hyperthyroidism/graves disease in children?

A

-Accelerated growth spurts
-Advanced bone age
-Emotional lability (mood swings)
-Hyperactivity
-Difficulty concentrating
-Occasionally failure to thrive

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26
Q

SF of hyperthyroidism/graves disease?

A

-Normal or enlarged thyroid
-Heterogeneous when enlarged
-Hypervascularity (aka thyroid inferno)
-Spectral doppler shows peak velocities exceeding 70 cm/sec
-Isthmus >1cm indicates diffuse enlargement

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27
Q

What is thyroiditis?

A

Term that includes multiple different types of disorders that involve some form of thyroid gland inflammation

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28
Q

What is the m/c presentation of thyroiditis?

A

Hypothyroidism (then thyrotoxicosis)

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29
Q

Acute vs acute suppurative symptoms of thyroiditis?

A

Acute:
-low grade fever
-sore neck

Acute suppurative (pus forming):
-bacterial + rare
-m/c in peds
-may see an abscess on u/s

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30
Q

Other names for subacute thyroiditis?

A

-De Quervain disease
-Granulomatous thyroiditis

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31
Q

Who m/c gets subacute thyroiditis?

A

-Female aged 30-50
-Possibly related to a viral cause

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32
Q

Clinical presentation of subacute thyroiditis?

A

-History of recent viral infection
-Neck pain (can radiate to upper jaw, throat or ears) which is associated with symptoms of inflammation like fever, tenderness, fatigue, anorexia, etc.
-Unilateral or bilateral enlargement of gland (usually temporary + resolves in 2-6 weeks)
-Spontaneous recovery of thyroid function in 6-8 weeks
-Good recovery (may have some residual fibrosis)

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33
Q

SF of acute or subacute thyroiditis?

A

-Enlargement
-Hypoechoic
-Normal or decreased vascularity
-Nodularity

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34
Q

What is goiters?

A

Enlargement of thyroid gland (m/c in women)

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35
Q

SF of goiters?

A

-Variable sizes (can get huge, especially in multi-nodular goiters)
-Isthmus >1cm (diffuse enlargement)
-Toxic or non-toxic
-Simple or multinodular

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36
Q

Symptoms of goiters?

A

Symptoms present when thyroid becomes enlarged + causes compression on the adjacent anatomy

-Dysphagia (from compression on esophagus)
-Inspiratory stridor (high pitched sound)
-Venous congestion (pressure on adjacent neck veins)
-Hoarseness (compression on laryngeal nerve)

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37
Q

Explain endemic non-toxic goiters?

A

Endemic: disease that is constantly present in a certain geographic area or in a certain group of people

-Due to deficiency in food, water + soil
-Hypothyroid causes a decrease in iodine + T3/T4, with an increase in TSH

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38
Q

Explain sporadic non-toxic goiters?

A

-These occur spontaneously in euthyroid pt’s in iodine sufficient areas
-M/c occurs b/w 35-60 years old
-Cause is unknown

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39
Q

Do non-toxic goiters cause the thyroid to have normal or abnormal function?

A

Normal, typically euthyroid

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40
Q

Explain toxic goiters?

A

-M/c multinodular
-Can cause hyperthyroidism / thyrotoxicosis / graves disease

(toxic meaning it produces T3 + T4)

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41
Q

What are multinodular goiters?

A

-Appears multi-lobulated + asymmetric enlargement of the thyroid
-Can involve 1 or both lobes + can extend below the clavicle/sternum (aka plunging goiter)
-Can be toxic or non-toxic

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42
Q

SF of multinodular goiters?

A

-Heterogeneous
-Lobulated + multinodular
-Possible calcifications

(must look for other discrete nodules within the goiter, as neoplasms + cancers can exist within a goiter too)

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43
Q

What causes thyroid disease in pregnancy?

A

Hormonal + physiological changes

44
Q

What is 1 common presentation of thyroid disease in pregnancy?

A

Increase in thyroid size (due to reduction in plasma iodine), returns to normal size post-partum

45
Q

What is the m/c condition after abortion, miscarriage or delivery?

A

Postpartum thyroiditis (PPT)

46
Q

Classic presentation of PPT?

A

Thyrotoxicosis followed by hypothyroidism

47
Q

SF of PPT?

A

-Decreased echogenicity
-Diffuse enlargement of thyroid

(must do bloodwork to determine PPT b/c the sono appearance is very non-specific)

48
Q

15-25% of solitary thyroid nodules are what?

A

Cystic or mostly cystic (due to hemorrhage or degeneration)

49
Q

Treatment of thyroid cysts?

A

Benign (only if symptomatic):
-Percutaneous ethanol injection

Malignant (rare):
-Surgery

50
Q

What 2 types of thyroid cysts are there?

A

-Simple
-Complex (colloid + hemorrhagic cysts)

51
Q

SF of simple thyroid cysts?

A

-Circular/oval
-Distinct margins
-No internal echoes
-Posterior enhancement

52
Q

What are colloid cysts?

A

-Very common
-Irregularly enlarged follicles containing abundant colloid
-Can have calcifications
-Can have multiple echogenic foci (colloid crystals) with comet tail artifact (not microcalcifications)

53
Q

What are hemorrhagic cysts?

A

-May contain blood + debris
-May have complex internal echoes, septations + debris

54
Q

What are thyroid nodules?

A

-Term for a variety of different lesions (benign, malignant, etc.)
-Very common to have
-M/c in women
-Increased frequency with age + with decreased iodine intake

55
Q

Differentiate b/w hot vs cold nodules?

A

Hot:
-Hyper functioning
-Area of dense collection of activity on nuclear med image
-Only 5-10% of nodules are hot (implies benignity)

Cold (m/c):
-Non functioning
-Area of decreased/absent activity on nuclear med image
-Majority of nodules are cold (10-15% are malignant)

56
Q

Are hot or cold nodules m/c?

A

Cold (non-functioning)

57
Q

The differentiation b/w hot + cold nodules is based on what?

A

Tc-99m (technetium-99m) nuclear medicine scintigraphy examination, this tracts how much iodine is absorbed into the nodules

58
Q

What is the m/c cause of the majority of nodular diseases?

A

Hyperplasia

59
Q

What causes hyperplasia?

A

-Iodine deficiency or under utilization
-If thyroid increases in size, can develop into a goiter
-M/c in females aged 35-50

60
Q

SF of hyperplasia?

A

Variable:
-M/c isoechoic
-Echogenic (as thyroid increases in size)
-Peripheral halo
-Cystic degeneration (common)
-Perinodular vascularity

61
Q

What is a thyroid adenoma?

A

Benign, neoplastic, slow growing nodule

(all adenomas are nodules + they make up 5-10% of nodules)

62
Q

SF of thyroid adenomas?

A

M/c solitary, well-circumscribed + oval/circular!!

-Fibrous capsule
-Can be cystic, complex, solid, etc.
-Rim calcifications
-Halo (hypoechoic rim surrounding nodule, can be complete or incomplete)
-Spoke + wheel CD appearance

63
Q

Are adenomas m/c in males or females?

A

7x more likely in females, aged 50-60

64
Q

Most adenomas are derived from what subtype?

A

Follicular cells

65
Q

Are most adenomas functioning or non-functioning?

A

Non-functioning

66
Q

Rarely adenomas will produce what?

A

Thyroid hormones + cause hyperthyroidism (aka a toxic adenoma / hot nodule)

67
Q

Follicular adenomas is indistinguishable from what other pathology?

A

Follicular carcinoma (can’t be distinguished on u/s or with an FNA)

68
Q

What are the 2 m/c types of thyroid cancer?

A

1: papillary carcinoma
2: follicular carcinoma

(only 5-15% of nodules are malignant)

69
Q

Incidence of thyroid carcinoma is m/c in what pt’s?

A

Pt’s with previous radiation exposure, but must have an FNA/biopsy done to confirm malignancy

70
Q

SF of thyroid carcinomas?

A

-M/c solid + hypoechoic
-M/c feature specific to malignancy is microcalcifications (<2mm + appears as hyperechoic foci w/o shadowing)
-Taller than wide
-Tumor invasion or lymph node metastasis is very suspicious for thyroid malignancy

(hyperechoic = benign, hypoechoic = malignancy)

71
Q

Differentiate the SFs b/w low + high thyroid risk of cancer?

A

Low:
-hyperechoic or isoechoic
-cystic
-large calcifications
-perinodular (peripheral) hypervascularity or avascular nodule

High:
-hypoechoic
-solid
-microcalcifications
-intrinsic (center) hypervascularity
-ill defined margins + shape is tall > wide
-local invasion + lymphadenopathy

(refer to table 15-4 in slides for full list)

72
Q

Explain papillary cancer?

A

-M/c type of thyroid cancer
-Least aggressive + great prognosis/survival rate
-Spreads via the lymphatics

73
Q

Who m/c gets papillary cancer?

A

Females aged 20-50

(but is more aggressive in men)

74
Q

Clinical presentation of papillary cancer?

A

-Painless palpable lump
-Palpable nodule with enlarged cervical lymph nodes
-Enlarged cervical lymph nodes w/o palpable thyroid nodule

(must check for enlarged lymph nodes)

75
Q

How can we diagnose + treat papillary cancer?

A

Diagnosis: with an FNA biopsy, as it is most accurate

Treatment: total/partial thyroidectomy or radical neck dissection, usually followed by suppressive therapy

76
Q

SF of papillary cancer?

A

-Hypoechoic
-Microcalcifications
-Hypervascularity
-Punctate microcalcifications can appear in the affected lymph nodes if metastasis is present

77
Q

Explain follicular cancer?

A

-2nd m/c
-M/c in females aged 40-50, with an increased incidence in areas of dietary iodine deficiency
-Is spread via the blood (hematological spread)
-Rarely spreads to neck nodes

78
Q

Clinical presentation of follicular cancer?

A

-Slow growing + painless nodule
-Mets to bone, lungs or liver is seen

79
Q

What is the diagnosis + treatment of follicular cancer?

A

Diagnosis: only made histologically (FNA is not effective)

Treatment: lobectomy or thyroidectomy, along with radioactive iodine treatment with widely invasive tumors

80
Q

SF of follicular cancer?

A

Similar to follicular adenomas:
-irregular margins
-thick irregular halo
-chaotic vascularity

(rarely has specific features of malignancy)

81
Q

List the types of thyroid cancers from most to least common?

A

-Papillary
-Follicular
-Medullary
-Anaplastic
-Hurthle cell
-Lymphoma

82
Q

Explain medullary carcinoma?

A

-Is derived from parafollicular cells (aka c-cells) which secrete calcitonin
-Increases serum calcitonin
-M/c in females

83
Q

Medullary carcinoma is associated with what syndrome?

A

MEN syndrome

84
Q

Which type of thyroid cancer is aggressive + does not respond to chemo or radiation therapy?

A

Medullary cancer

85
Q

Clinical presentation of medullary cancer?

A

-Mass in neck
-Other symptoms related to endocrine secretion (including carcinoid syndrome (serotonin) + cushing syndrome)

86
Q

SF of medullary cancer?

A

Similar to papillary cancer:
-note that local invasion + mets to cervical lymph nodes is more common with medullary cancer

87
Q

Explain anaplastic cancer?

A

-M/c in females over 60, with an increased incidence in endemic goiter areas
-Most aggressive thyroid cancer with a poor prognosis
-Invades nearby vasculature + muscles, widespread mets
-No effective treatments

88
Q

Which form of thyroid cancer is the most aggressive with a poor prognosis?

A

Anaplastic cancer (no effective treatments, pt’s often only last about 5 years)

89
Q

Clinical presentation of anaplastic cancer?

A

Rapidly enlarging neck mass with symptoms relating to the destruction of local structures

(such as dyspnea, dysphagia, hoarseness, cough)

90
Q

SF of anaplastic cancer?

A

-Large, solid, hypoechoic mass with encasing or invading blood vessels
-Possibly invasion of other nearby structures as well
-Hard to assess due to size (CT or MRI is better)

91
Q

Explain hurthle cell cancer?

A

-Has thyroglobulin producing cells
-Classified as either a benign or malignant hurthel cell adenoma based on histology
-Is aggressive
-M/c in males with advanced age

92
Q

Diagnosis + treatment of hurthle cell cancer?

A

Diagnosis: histology (FNA not effective)
Treatment: total thyroidectomy

(clinical presentation + SF are variable)

93
Q

Thyroid cancers are generally m/c in males or females?

A

Females, hurthle cell cancer is the only one m/c in males

94
Q

Clinical presentation of thyroid lymphoma?

A

-M/c arise from chronic thyroiditis (hashimoto)
-Rapidly growing mass
-Symptoms of airway obstruction (dyspnea, dysphagia)

95
Q

Diagnosis + treatment of lymphoma?

A

Diagnosis:
-surgery often done to diagnose it
-accuracy of FNA biopsy in diagnosing thyroid lymphoma is being researched

Treatment:
-radiation therapy + chemo

96
Q

Which 2 thyroid cancers have no treatment?

A

-Medullary
-Anaplastic

97
Q

SF of lymphoma?

A

-M/c large, solid, hypoechoic mass
-Infiltration of thyroid parenchyma + encasement of neck vessels (CCA, IJV)
-Cystic necrosis
-Doppler will be hypovascular or show chaotic blood vessel distribution

98
Q

Is it common for cancer to metastasize to they thyroid?

A

-No! Very uncommon
-Occurs in late disease progression to another primary cancer

99
Q

Thyroid mets is m/c spread by blood or lymphatics?

A

Blood

100
Q

M/c mets to thyroid are from what?

A

Melanoma, breast, lung, RCC

101
Q

SF of thyroid mets?

A

-Non specific
-M/c hypoechoic

102
Q

T/F: Heat intolerance is a symptom of hypothyroidism?

A

False, is a symptom of hyperthyroidism

(cold = hypothyroidism, hot = hyperthyroidism)

103
Q

What is the m/c cause of primary hypothyroidism?

A

Hashimotos or iodine insufficiency worldwide

104
Q

What is the m/c form of thyroid cancer?

A

Papillary

105
Q

Thyroid inferno is a common sonographic feature in which condition?

A

Graves disease / hyperthyroidism

106
Q

Serum calcitonin can be used as a tumor marker for which type of thyroid carcinoma?

A

Medullary (from the c-cells, which secrete calcitonin)

107
Q

Based on Tc-99m, hot nodules are usually ____?

A

Benign

MIDS 227 (module 1 + 2) (14 decks)

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