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(OMS2) ENRP Exam 2 > thyroid pathology > Flashcards

thyroid pathology Flashcards

1
Q

Types of primary hyperthyroidism (thyrotoxicosis)

Secondary

A 
Primary hyperthyroidism (most common)
◦ Diffuse hyperplasia (Graves disease)
◦ Hyperfunctioning multinodular goiter
◦ Hyperfunctioning thyroid adenoma

Secondary hyperthyroidism
◦ Pituitary adenoma

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2
Q

Which lab value determines primary vs secondary hyperthyroidism

A

In the presence of elevated T3 or T4:

Low TSH = primary

High TSH = secondary

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3
Q

Clinical presentation of apathetic hyperthyroidism

A
  1. Older adults with masked symptomatology
  2. Unexplained weight loss
  3. Cardiovascular disease
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4
Q

Clinical presentation of regular hyperthyroidism

A

Jittery
Palpitations
Stuff associated with increased BMR

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5
Q

Clinical presentation a thyroid storm

A

Extreme and abrupt episode of potentially life-threatening thyrotoxicosis

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6
Q

What is the Burch Wartofsky score for thyroid storm

A 
◦ Fever
Cardiac manifestations
◦ Tachycardia
◦ Congestive heart failure
Gastrointestinal symptoms
◦ Diarrhea
◦ Jaundice
Precipitating history
◦ Pregnancy/postpartum
◦ Hemithyroidectomy
◦ Drugs: amiodarone
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7
Q

What is the treatment for thyroid storm

A

Treat the manifestations:
◦ Beta blockers

Treat the underlying disease:
◦ High doses of iodide (Wolff-Chaikoff effect)
◦ Thionamide
◦ Radioiodine ablation
◦ Surgery
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8
Q

What is the most common etiology of hyperthyroidism?

A

Graves disease

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9
Q

What is graves disease characterized by

A
  1. Hyperthyroidism with gland enlargement
  2. Infiltrative ophthalmopathy
  3. Pretibial myxedema

AUTOIMMUNE

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10
Q

What appears on histology for graves disease

A

During an active secretory phase, intracytoplasmic

droplets appear

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11
Q

What is the pathogenesis of exopthalmos in Graves disease

A
  1. Lymphocytes invade preorbital space
  2. Fibroblasts have TSH receptor
  3. EOM swelling
  4. Matrix accumulates
  5. Adipocytes expand
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12
Q

describe pretibial myxedema

A

Infiltrative dermopathy

Scaly, indurated skin

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13
Q

What shows up on thyroid testing for Graves disease

A

T3/T4:
HIGH

TSH:
LOW

TSI (thyroid-stimulating Ig):
HIGH

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14
Q

Cretinism is a form of what?

What is a common cause

A

Congenital hypothyroidism

Iodine deficiency in pregnancy

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15
Q

Clinical presentation of Cretinism

A 
Early infancy/childhood
◦ Mental retardation
◦ Growth retardation
◦ Coarse facial features
◦ Umbilical hernias
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16
Q

what is myxedema?

A

hypothyroidism in the adult/older child

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17
Q

Whow does myxedema present

A
  1. Mental and physical sluggishness (slowing)
  2. Weight gain
  3. Cold intolerance
  4. Cardiac effect
    ◦ Lower output
    ◦ Hypercholesterolemia
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18
Q

Hashimoto thyroiditis is has autoantibodies against what

A

Thyroglobulin and Thyroid peroxidase (TPO)

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19
Q

What is the progression of hashitoxicosis

A
  1. immune mediated insult
  2. hyperactivity and enlargement
  3. follicular cell exhaustion

(the thyroid burns out from hyperactivity)

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20
Q

Histology of hashimoto thyroiditis

A

Lymphocytic infiltrate with germinal centers

Atrophic follicle cells with eosinophilic change
◦ Hürthle cell metaplasia

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21
Q

What is the gross effect of Hashimoto thyroiditis on the thyroid

A

diffuse painless enlargement

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22
Q

What is subacute lymphocytic thyroiditis

examlple?

A

Typically a transient period of thyroid hormone irregularities

postpartum thyroiditis

23
Q

What is the etiology of granulomatous thyroiditis

A

Most likely a viral infection (i.e. mumps) within a granulomatous
inflammatory response

24
Q

What are the painless subclinical thyroid diseases

A
  • Subacute lymphocytic thyroiditis
  • Painless thyroiditis
  • Subacute painless thyroiditis
25
What are the painful subclinical thyroid diseases
* Subacute granulomatous thyroiditis * deQuervain thyroiditis * Giant cell thyroiditis * Subacute painful thyroiditis * Subacute viral thyroiditis
26
What kind of process is Riedel thyroiditis
Fibrosing process with lymphosites and plasma cells
27
Why is Riedel thyroiditis occasionally confused with cancer
It is rock hard and extends from the thyroid into adjacent tissue
28
Causes of diffuse nontoxic goiter
Endemic goiter -> iodine deficiency Goitrogens ◦ Cassava root (thiocyanate) ◦ Brassicaceae ◦ Broccoli, cauliflower, cabbage, radish Sporadic goiter ◦ More common in females
29
What are the symptoms of diffuse goiter? Due to?
* Dysphagia * Hoarseness (recurrent laryngeal n.) * Stridor * SVC syndrome Due to MASS EFFECT
30
What is the purpose of radioisotope scanning of a thyroid nodule?
To determine of a specific nodule is responsible for HYPERFUNCTION
31
Are cold or hot nodules more likely to be neoplastic
Cold Vast majority of cold are still benign
32
What can be used to determine cellular constituents of a thyroid nodule?
Fine needle aspiration
33
What are follicular adenomas?
Discrete clonal population of follicular cells with “Thyroid autonomy”
34
Follicular adenomas are __1__ but have to make sure of what:
1. benign 2. Capsule intact (not invaded), so no growth pattern of follicular carcinoma ◦ No nuclear features of papillary carcinoma
35
What is makes up the majority of malignant tumors of the thyroid
papillary thyroid carcinoma
36
How does a papillary thyroid carcinoma present? When do they present?
Typically present without symptoms as a palpable nodule found on ultrasound Most occur between 25-50 years of age
37
What staging system does differentiated thyroid carcinoma use
TNM staging system only use stage I and II (II has mets) under 55 Stage I - IVB at 55 and older
38
What type of nuclei does papillary thyroid carcinoma have
Orphan Annie Eye nuclei Enlarged nuclei with “clear” appearance
39
Common histology and mutations of PTC
1. Papillary architecture 2. Psammoma bodies 3. RET-PTC mutations, BRAF mutations
40
Describe the follicular variant of PTC
◦ Follicular architecture, but nuclear features of papillary carcinoma ◦ Fewer cases have RET-PTC rearrangements or BRAF mutations ◦ More cases with RAS mutations ◦ Similar to follicular carcinoma
41
Describe the Tall cell variant of PTC
Found in older patients | Aggressive
42
Describe the diffuse sclerosing variant of PTC
Found in kids and young adults Greater incidence of distant mets (especially pulmonary) 93% survival at 10 years
43
What mutations are present in Follicular Carcinoma
RAS mutations – not specific PAX8/PPARG mutations more characteristic
44
Describe Follicular carcinoma Where is it more common
1. Follicular neoplasm with invasive properties | 2. More common in areas with goiter from iodide deficiency
45
How are Follicular carcinomas invasive properties manifested?
Invasion of the capsule (mushroom) Angioinvasion -leads to hematogenous mets
46
Therapeutic options of follicular carcinomas
``` Surgery Radioactive iodine (I131) ``` If refractory: ◦ Chemotherapy ◦ Tyrosine kinase inhibitors (still in progress)
47
Describe anaplastic carcinoma
Uncommon Tend to occur in elderly patients Highly aggressive ◦ Present with mass effect ◦ Die within a year of local invasion
48
Genetics of papillary carcinoma
◦ RET/PTC rearrangements  constitutive tyrosine kinase activity ◦ BRAF gain of function mutations  MAP kinase signaling
49
Genetics of follicular neoplasms (non-specific)
◦ RAS | ◦ PTEN
50
Genetics of Anaplastic Carcinoma
TP53
51
C cells are responsible for secretion of what
Calcitonin
52
Describe MEdullary carcinoma
Neuroendocrine carcinoma derived from C cells: ◦ Blue cells with dispersed chromatin ◦ Amyloid ◦ C-cell hyperplasia
53
What mutatation ais associated with medulary carcinoma
RET
54
What are the types of medullary carcinoma and which has the best prognosis
Sporadic (70-80%) Familial - best prognosis MEN syndromes

(OMS2) ENRP Exam 2 (9 decks)

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