Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endrocrine Exam 2 > Pathology: Thyroid I and II > Flashcards

Pathology: Thyroid I and II Flashcards

1
Q

How many parathyroid glands are there ?

A

4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the usual size a parathyroid gland ?

A

12 to 20 μm in diameter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Secretory vesicles in the Chief Cells of the parathyroid contain…

A

PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The ‘water clear’ appearance within the pink parathyroid tissue is due to …

A

Lakes of glycogen

Lots of lipid is indicative of a healthy parathyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Chief cells of the parathyroid secreted…

A

PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Oxyphil cells of the parathyroid do not have secretory granules like the Chief Cells and have what color cytoplasm ?

A

Pink (‘pink puffy’)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When the ‘glycogen lakes’ or lipid appearance is absent in the parathyroid, what should you think…

A

Adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Primary Parathyroidism

A

Autonomous, spontaneous overproduction of PTH (In PTH gland) in PARATHYROID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the cause of Secondary Parathyroidism ?

A

Secondary phenomena due to chronic renal insufficiency

Unable to clear phosphates which bind Ca++ in peripheral blood –>Hypocalcemia –> Increased PTH release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What ions will likely be deranged in Hyperparathyroidism ?

A

Ca++ (Increased) and Phosphate (Decreased due to PTH causing decreased reabsorption in the kidney)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the most common cause of Primary Hyperparathyroidism ?

A

ADENOMA (85-95%)

Others:
Primary hyperplasia (diffuse or nodular): 5% to 10%
Parathyroid carcinoma: ∼1% (Rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What age and sex would you most likely see a primary parathyroid adenoma in ?

A

50s + and Women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are most primary parathyroid adenomas found ?

A

Incidentally (hypercalcemia is seen on electrolyte panel)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Are most primary parathyroid adenoma’s Solitary or Multinodular ?

A

Solitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Familial Primary Parathyroidism is associated with which 3 other genetic syndromes ?

A

MEN1 (The three P’s: Pituitary, Parathyroid, Pancreas)

MEN2 (Throid Medullary Carc., Parathyroid adenoma and Pheochromocytoma)

Familial hypocalciuric hypercalcemia (Autosomal-dominant disorder)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Are primary parathyroid adenomas diffuse or well circumscribed ?

A

Well Circumscrbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Do primary parathyroid adenomas have a capsule ?

A

Yes (delicate capsule)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the color and texture of primary parathyroid adenomas..

A

Tan or Red Brown

Soft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In primary parathyroid adenomas you will often see Uniform, polygonal chief cells with centered nuclei that are compressing , non-neoplastic parathyroid tissue. What separates the neoplastic from the normal tissue ?

A

Thin Fibrous Capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What structures are usually absent in parathyroid adenomas that are seen in normal parathyroid tissue ?

A

‘Glycogen Lakes” . Lose a lot of the lipid is seen in normal PT tissue.

Majority of the adenoma will be the ‘pink and puffy’ oxyphilic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Sporadic, part of MEN syndrome and all four PT glands are involved ….

A

Primary Parathyroid hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the most common cell type seen in most PT hyperplasia ?

A

Chief Cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What size do most PT glands get to in hyperplasia ?

A

Less than one gram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

PT Carcinoma usually occurs in ONE PT gland and are normally well circumscribed. What size do most carcinomas get to ?

A

up to 10 grams

Differentiating gross factor from Adenoma which are also solitary lesion

Differentiate from hyperplasia in that carcinomas are solitary while hyperplasia usually involves all 4 glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What typically allows for carcinomas to be well circumscribed lesions ?

A

DENSE FIBROUS CAPSULE (unlike adenoma which have a delicate capsule)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the defining feature of PT carcinoma that differentiates them from Adenomas ?

A

INVASION OF PERIPHERAL TISSUE AND/OR METASTASIS

must see this to properly diagnose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

The trabecular of bones seen in patients with Hyperparathyroidism resemble

A

Osteoporosis (Widely spaced, delicate trabeculae)

Increases risk of fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What occurs to the marrow in Osteitis Fibrosa Cystica, a complication of Hyperparathyroidsm ?

A

Cortex is grossly thinned
Marrow has increased amounts of fibrous tissue
Foci of hemorrhage and cyst formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Brown tumors are also seen in patients with hyperparathyroidism. What are these ?

A

Aggregates of osteoclasts, reactive giant cells, and hemorrhagic debris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What may occur in other tissues due to increased calcium in the blood due to HyperPT ? (Hypercalcemia is the most common finding/sign of primary HyperPT)

A

Nephrolithiasis

Nephrocalcinosis (calcification of the tubules themselves)

Metastatic Calcification (Stomach, lungs, myocardium, and blood vessels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the moniker for “symptomatic primary HyperPT”

A

Painful bones,
renal stones,
abdominal groans,
psychic moans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the GI issues associated with HyperPT ?

A

Constipation, nausea, ulcers, pancreatitis, and gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Most common cause of Secondary HyperPT ?

A

Renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

In Secondary HyperPT, will you see solitary or multi nodular growth of glads ?

A

Multinodular (will effect multiple if not all glands)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the the most telling complication of Secondary HyperPT ?

A

Calciphylaxis: Vascular calcification associated with secondary hyperparathyroidism –> ischemic skin damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What occurs in Tertiary Hyperparathyroidsis >

A

Parathyroid activity become autonomous and excessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are some acquired causes of Hypoparathyroidism ?

A

Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What kind of cells will you see infiltrating the PT in Auto-immune hypoparathyroidism ?

A

Lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What chromosomal aberration is seen in thymic aplasia ? –> hypoparathyroidsism

A

22q11 deletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Why would you see an absence of PT glands in DiGeorge Syndrome ?

A

Like the thymus, the PT’s develop from the 3/4th branchial pouches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What would occur to the blood concentration of Ca++ in hypo-PT ?

A

Ca++ levels will be low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the HALLMARK of HypoPT ?

A

TETANY !!

Other signs include:
Mental status changes
Intracranial manifestations
Ocular disease
CARDIOVASCULAR manifestations
Dental abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the cause of pseudohypoparathyroidism ?

A

End organ resistance to PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What would you expect the PTH levels to be in the blood of someone with pseudohypoparathyroidism ?

A

Higher than normal due to decreased feedback of Ca++ on the PT gland.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What would you expect to see in the blood regarding Calcium and Phosphaste in a patient with pseudohypoparathyroidism ?

A

Hypocalcemia

Hyperphosphatemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What kind of epithelial cells line the follicles ?

A

cuboidal to low columnar epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What stain is used to visualize colloid (thyroglobulin) ?

A

PAS (makes colloid a pink clear consistency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is thyrotoxicosis ?

A

Hyperthyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the most common cause of hyperthyroidism ?

A

Diffuse hyperplasia of the thyroid associated with Graves Disease (So, Graves Disease)

Other Causes include:
Hyperfunctional multinodular goiter **
Hyperfunctional adenoma of the thyroid **

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Why does skin appear soft, warm and flushed in hyperthyroidism ?

A

increased thyroid hormone causes an increased metabolic rate leading to heat generation. These individuals are very warm (heat intolerant) and lose a majority of the excess heat through the skin. Typically the blood vessels dilate to allow for more heat loss and thus flushing.

Will also see sweating in these patin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the earliest and most consistent signs of hyperthyroidism ?

A

Cardiac complications: Tachycardia, palpitations, and cardiomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Will patients with hyperthyroidism exhibit weight loss or weight gain ?

A

Weight loss (despite increased appetite)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Tremor, Hyperactivity, proximal muscle weakness and insomnia are all manifestations of what class of complication due to hyperthyroidism ?

A

Neuro/Muscular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What ocular manifestations will you see with hyperthyroidism ?

A

Wide, staring gaze and lid lag

Proptosis/Exopthalmos (Not sure if this is seen in all hyperthyroidism or just Graves Disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is evident in the GI system of patients with hyperthyroidism ?

A

Hypermotility, malabsorption, and diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Will you see bone resorption in patients with hyperthyroidism ?

A

Yes, although you usually associate this with hyperPT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Why do you Low TSH but high T4 in the blood of patients with primary hyperthyroidism ?

A

primary increased production of thyroid hormone will cause high levels of T3/T4 release. T3 ill feedback inhibit the release of TSH but since the disease is primary it will have no effect on the production of thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Who is most likely to get hypothyroidism ?

A

Older Women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Why do you see enlargement of the thyroid gland in patients with Primary Hypothyroidism ?

A

Primary hypothyroidism implies an inability to produce T3/T4. There will be a loss of feedback inhibition to the pituitary and hypothalamus thus leading to increased or constant amounts of TSH being release. TSH will bind its receptor on the thyroid leading to a trophic effect –> enlargement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the most common cause of hypothyroidism in areas of the world that have low iodide consumption ? Is it primary or secondary ?

A

Iodide deficiency hypothyroidism

Primary (has to do with the inability to produce thyroid hormones in the thyroid w/o proper iodide)

61
Q

Pendred Hypothryoidism leads to a complete absence of the thyroid as well as sensineuronal deafness. What genetic aberration result in this syndrome ?

A

mutations in the SLC26A4 gene

62
Q

the most common cause of Inborn errors of thyroid metabolism is a mutation in which thyroid enzyme ?

A

Thyroid peroxidase (TPO)

63
Q

What occurs in Thyroid hormone resistance syndrome ?

A

Thyroid receptor is mutated in a manner that makes it less likely to bind Thyroid hormones (T3/4)

64
Q

Acquired hypothyroidism is typically due to which three causes ?

A

Surgical removal
Radiation ablation of gland
Drugs

65
Q

Which drugs are specifically given to decrease thyroid releasing, leading to hypothyroidism ?

A

propylthiouracil and Methimazole

66
Q

Which two drugs are given for non-thyroid conditions but can lead to hypothyroidism ?

A

Lithium (psych patients)

p-aminosalicylic acid

67
Q

What is the most common cause of hypothyroidism in areas of the world that are iodine sufficient ?

A

Autoimmune Hypothyroidism (think Hashimotos Disease)

68
Q

What kind of thyroid constituents might there be auto-antibodies produced to that cause auto-immune hypothyroidism ?

A

Anti-microsomal
Anti-thyroid peroxidase
Anti-thyroglobulin antibodies

69
Q

What is the most common gross physical finding associated with auto-immune hypothyroidism ?

A

Enlarged gland (goiter)

70
Q

What hormone is decreased in secondary hypothyroidism ?

A

TSH

71
Q

List 4 common causes of secondary hypothyroidism ?

A

Pituitary tumor (non-functional)
Postpartum pituitary necrosis (Sheehans)
Trauma
Nonpituitary tumors

72
Q

What is a common cause of tertiary hypothyroidism ?

A

Hypothalamic damage

Tumors, trauma, radiation therapy

73
Q

What are two causes of thyroiditis that result in a PAINFUL THYROID GLAND?

A

Infectious thyroiditis

Subacute granulomatous thyroiditis

74
Q

Thyroiditis Disorders with little inflammation and thyroid dysfunction

A

Subacute lymphocytic thyroiditis

Fibrous (Reidel) thyroiditis

75
Q

What are the two most common location from which infectious agents spread leading to Infectious thyroiditis ?

A 
Hematogenous
Direct seeding ( fistula etc)
76
Q

Chronic infection leading to thyroiditis is often seen in immunocompromised patients. What organisms are often responsible ?

A

Mycobacterial, fungal, and Pneumocystis infections

77
Q

What kind of cells will you likely see in Hashimotos Thyroiditis ?

A

LYMPHOCYTES (it’s auto-immune destruction of the gland)
Mononuclear inflammatory infiltrate
Small lymphocytes, plasma cells

78
Q

Who is most likely to be seen with Hashimotos Thyroiditis ?

A

Older Women

79
Q

In Hashimotos Thyroiditis you will see an enlarged gland. Describe the morphology of the gland during the destructive process in relation to its capsule.

A

Diffusely enlarged
Capsule is intact
Gland is well demarcated from adjacent structures
No infiltration of surrounding structure
Cut surface is pale, yellow-tan, firm, and nodular

80
Q

Due to the presence of lymphocytes in the thyroid during the course of Hashimotos Thyroiditis, what might you see in the gland that you would see in lymph nodes etc ?

A

GERMINAL CENTERS ! (Tingible Body Macrophage)

81
Q

What often occurs to the cuboidal epithelial cells of the thyroid gland during the course of Hashimotos Thyroiditis ?

A

METAPLASIA to Hurthle Cells (Presence of abundant eosinophilic, granular cytoplasm)

82
Q

What is another name for Subacute Granulomatous Thyroiditis (SGT) ?

A

Granulomatous thyroiditis or De Quervain thyroiditis

83
Q

What symptom is Subacute Granulomatous Thyroiditis associated with ?

A

THYROID PAIN

When you hear painful thyroid think acute infection or De Quarvian (SGT)

SGT is actually the most common cause of thyroid pain.

84
Q

What often precedes SGT ?

A

Viral Infection (Coxsackie ,Mumps, Measels or adenovirus)

Look for a history of Upper Respiratory Infection

85
Q

What time of year is SGT associated with ?

A

SUMMER

86
Q

Will the enlargement of the thyroid extend outside of the capsule in SGT ?

A

NO

87
Q

What does the thyroid look like on cut section in those with SGT ?

A

FIRM and YELLOW

88
Q

In the early stages of SGT what will you see on biopsy ?

A

scattered follicles replaced by neutrophils forming micro abscesses (Acute Inflammation)

89
Q

What will you see in later stages of SGT with biopsy ?

A

aggregates of lymphocytes, macrophages, and plasma cells (Chronic inflammation)

90
Q

Beacause it is GRANULOMATOUS, what is the characteristic cell type seen in SGT

A

Multinucleate giant cells (enclose naked pools or fragments of colloid)

91
Q

Is Subacute Lymphocytic Thyroiditis (SLT) painless or painful ?

A

Painless !!! ( Learning Tool: SLT the L is For Less as in Painless)

92
Q

In Subacute Lymphocytic Thyroiditis (SLT), will you see mild hyperthyroidism , goiter enlargement or both ?

A

BOTH (mild hyperthyroidism and Goiter enlargement)

93
Q

What do a majority of patients with Subacute Lymphocytic Thyroiditis (SLT) have auto-antibodies to ?

A

thyroid peroxidase

the antibodies direct lymphocytes to destroy the thyroid follicular cells aka why its called SLT

94
Q

Will Subacute Lymphocytic Thyroiditis (SLT) ever progress to hypothyroidism ?

A

yes (Overy Hypothyroidism)

95
Q

Due to the presence of lymphocytes in SLT, what will you typically see in the thyroid ?

A

Hyperplastic Germinal Center ( This is a subset of Hashimotos which will also present with Germinal Centers in the thyroid)

96
Q

What are the Triad of findings in Graves Disease ?

A

Hyperthyroidism

Proptosis (Exopthalmos) aka Infiltrative Opthalmopathy

Pretibial Myxedema ( Localized infiltrative dermopathy)

97
Q

What age and sex will you most often see patients with Graves Diseaes ?

A

Women age 20-40

98
Q

What causes Proptosis ?

A

Deposition of gylcosaminoglycan in the orbit which is stimulated by thyroid hormone . Leads to bulging of the eyeballs

Pre-Tibial myxedema is due to the same reason, just deposits on shins instead of in orbit.

99
Q

Is hypertrophy of the thyroid unilateral or bilateral in patients with Graves ?

A

Symmetric enlargement

Diffuse hypertrophy and hyperplasia of thyroid follicular epithelial cells

100
Q

What size does the thyroid get to in Graves ?

A

Increases in weight to over 80 gm

Cut section
Soft, meaty appearance

101
Q

Follicular cells tend to become taller and form papillae (not carcinoma). What is a consequence of this growth of follicular cells ?

A

Project into the follicular lumen and encroach on the colloid

102
Q

How are the ‘papillae’ of Graves Disease different from that of Carcinoma ?

A

Lack fibrovascular cores (not truly papillae)

103
Q

Was is pathomnemonic for the appearance of colloid in Graves Disease ?

A

SCALLOPED (large fatty globules towards the edge of the colloid space with odd non-polygonal appearance)
Will also see lymphoid infiltrates throughout the periphery of the colloid spaces

104
Q

Diffuse Goiters most often reflect what occurrence ?

A

Reflect impaired synthesis of thyroid hormone

105
Q

What delineates a Simple Nontoxic Goiter from a Toxic Goiter ?

A

NODULARITY (is seen in toxic goiter)

106
Q

What is found within the follicles of Nontoxic Goiters ?

A

Colloid (aka Colloid Goiter)

107
Q

What areas of the world will you typically see endemic goiters ?

A

Andes and Himalayas

Leads to Follicular cell hypertrophy and hyperplasia

108
Q

What are the two main causes of sporadic goiter ?

A

Ingestion of substances :Interfere with thyroid hormone synthesis

Hereditary enzymatic defects :Interfere with thyroid hormone synthesis

109
Q

What are the two phases seen in Goiter evolution ?

A

Hyperplastic phase : Diffusely and symmetrically enlarged gland. The follicles are lined by crowded columnar cells

Phase of colloid involution

110
Q

What will colloid or sporadic goiter look like on cut section ?

A

Brown, glassy, and translucent

111
Q

What occurs to all Long Standing Simple Goiters ?

A

Simple goiters convert into multinodular goiters

112
Q

Which goiders show the most pronounced growth ?

A

Multinodular goiter (2000g or larger !!)

113
Q

What is it called when a multi nodular goiter Grows behind the sternum and clavicles ? What are the complications ?

A

Intrathoracic or plunging goiter

Causes respiratory compromise. Needs to be surgically removed

114
Q

What are some microscopic changes seen in Multinodular Goiters ?

A

LARGE Colloid-rich follicles
Variable amounts of brown, gelatinous colloid
Hemorrhage, fibrosis, calcification, and cystic change

115
Q

What is the most common neoplasm of the thyroid ?

A

Follicular adenomas (benign)

Most neoplasms are benign (10:1)

116
Q

What is more likely to be neoplastic: Solitary or Multinodular appearance of thyroid ?

A

Solitary

117
Q

What is more likely to be neoplastic: Those in young or old patients ?

A

young

118
Q

What is more likely to be neoplastic: Male or Female ?

A

Male

119
Q

What is more likely to be benign: Hot or Cold Nodule ?

A

Hot (take up iodine on scan)

120
Q

What treatment is often linked with increased risk for neoplasm ?

A

History of radiation treatment of the head and neck

121
Q

Are follicular adenomas solitary or multi nodular ?

A

Solitary

Derived from follicular epithelium

122
Q

Do follicular adenomas have a capsule ? Does the neoplasm extend beyond the capsule ?

A

yes they have a capsule and the neoplasms is limited to within the confines of the capsule (well demarcated)

123
Q

What size are most follicular adenomas ?

A

3 cm

124
Q

What is the hallmark of Follicular Adenoma ?

A

Presence of an intact, well-formed capsule encircling the tumor

Differentiates from follicular carcinoma (carcinoma has capsular invasion.)

125
Q

Can you biopsy a follicular adenoma with Fine Needle Aspirate ?

A

NO !

126
Q

As in Hashimotos Disease, what kind of cells might you see in Follicular Adenoma ?

A

Hurthle Cells (metaplastic change from low cuboidal epithelium of the follicle)

127
Q

What is the most common form of Thyroid Carcinoma ?

A

Papillary carcinoma (>85% of cases)

128
Q

What is the age distribution for Papillary Carcinoma ?

A

25-50

Majority of carcinomas associated with previous exposure to ionizing radiation

129
Q

What is the hallmark of papillary carcinoma ?

A

Branching papillae having a fibrovascular stalk

papillae without fibrovascular stalk are often seen in Graves disease, these are not true papillae however

130
Q

What is the hallmark sign of papillary Carcinoma that pertains to the nucleus of cells involved ?

A

Ground-glass or Orphan Annie eye nuclei
(White clearing in the nucleus)

Nuclei contain finely dispersed chromatin

131
Q

What does the cytoplasm look like in cells with papillary carcinoma ?

A

Invagination of the cytoplasm:
Appearance of intranuclear inclusions/intranuclear grooves
Folded appearance

132
Q

Calcified structures seen in papillae carcinoma are called …

A

Psamomma bodies

133
Q

Where does Papillary Carcinoma often metastasize to ?

A

THE LYMPH !!! (Important).. often adjacent cervical lymph nodes.

rarely goes to vascular sites

134
Q

What is the prognosis for Papillar Carcinoma ?

A

Excellent
10-year survival rate in excess of 95%
Only 10-15% have distant mets

135
Q

What is prognosis of Papillary Carcinoma dependent on ?

A

Age :Prognosis is less favorable older than 40 years

Presence of extra-thyroidal extension

Presence of distant metastases (stage)

136
Q

In who are you most likely to see Follicular Carcinoma ?

A

Women 40 and 60 years of age

More frequent in areas with dietary iodine deficiency

137
Q

Is Follicular Carcinoma single or multi nodular ?

A

Single

138
Q

What is the defining difference between Follicular Adenoma and Follicular Carcinoma ?

A

Infiltrate beyond the thyroid capsule ( into the adjacent neck structures ?)

139
Q

Follicular Carcinomas are Translucent due to the presence of large, colloid-filled follicles but at the center you will see…

A

fibrosis and foci of calcification (BUT PSAMMOMA BODIES ARE NOT PRESENT)

140
Q

Where do follicular carcinomas often metastasize to ?

A

VASCULATURE ( rarely go to lymph, unlike papillary ) –> bones, lungs and liver.

141
Q

Who will you likely see Anaplastic Carcinoma in ?

A

Older patients (over 65)

Need to differentiate from lymphoma

142
Q

What is the mortality rate for anaplastic carcinoma ?

A

Nearly 100%

143
Q

Microscopy of Anaplastic Carcinoma shows

A

Large, pleomorphic giant cells
Spindle cells with a sarcomatous appearance
Mixed spindle and giant cells

ANAPLASTIC CELLS.

144
Q

What kind of neoplasms are Medullary Carcinomas ?

A

Neuroendocrine

145
Q

What cells are Medullar Carcinomas derived from ? What do they secrete ?

A

C-Cells of the thyroid

CALCITONIN ! (hinders the effects of PTH )

146
Q

Sporadic Medullary carcinomas are single nodules while ____________ are bilateral or mutinodular

A

Familial cases

147
Q

Large Medulary carcinomas show ..

A

Foci of hemorrhage and necrosis in the larger lesions

148
Q

What abberent protein is seen in Medullary Carcinoma ?

A

AMYLOID (pink bubble gum appearance)

“Malignant Cells in a nest of AMYLOID”

Amyloid is derived from Calcitonin

Endrocrine Exam 2 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions