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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
Q

What are the painful subclinical thyroid diseases

A
  • Subacute granulomatous thyroiditis
  • deQuervain thyroiditis
  • Giant cell thyroiditis
  • Subacute painful thyroiditis
  • Subacute viral thyroiditis
26
Q

What kind of process is Riedel thyroiditis

A

Fibrosing process

with lymphosites and plasma cells

27
Q

Why is Riedel thyroiditis occasionally confused with cancer

A

It is rock hard and extends from the thyroid into adjacent tissue

28
Q

Causes of diffuse nontoxic goiter

A

Endemic goiter -> iodine deficiency

Goitrogens
◦ Cassava root (thiocyanate)
◦ Brassicaceae
◦ Broccoli, cauliflower, cabbage, radish

Sporadic goiter
◦ More common in females

29
Q

What are the symptoms of diffuse goiter?

Due to?

A
  • Dysphagia
  • Hoarseness (recurrent laryngeal n.)
  • Stridor
  • SVC syndrome

Due to MASS EFFECT

30
Q

What is the purpose of radioisotope scanning of a thyroid nodule?

A

To determine of a specific nodule is responsible for HYPERFUNCTION

31
Q

Are cold or hot nodules more likely to be neoplastic

A

Cold

Vast majority of cold are still benign

32
Q

What can be used to determine cellular constituents of a thyroid nodule?

A

Fine needle aspiration

33
Q

What are follicular adenomas?

A

Discrete clonal population of follicular cells with “Thyroid autonomy”

34
Q

Follicular adenomas are __1__ but have to make sure of what:

A
  1. benign
  2. Capsule intact (not invaded), so no growth pattern of follicular carcinoma
    ◦ No nuclear features of papillary carcinoma
35
Q

What is makes up the majority of malignant tumors of the thyroid

A

papillary thyroid carcinoma

36
Q

How does a papillary thyroid carcinoma present?

When do they present?

A

Typically present without symptoms as a palpable nodule found on ultrasound

Most occur between 25-50 years of age

37
Q

What staging system does differentiated thyroid carcinoma use

A

TNM staging system

only use stage I and II (II has mets) under 55

Stage I - IVB at 55 and older

38
Q

What type of nuclei does papillary thyroid carcinoma have

A

Orphan Annie Eye nuclei

Enlarged nuclei with “clear” appearance

39
Q

Common histology and mutations of PTC

A
  1. Papillary architecture
  2. Psammoma bodies
  3. RET-PTC mutations, BRAF mutations
40
Q

Describe the follicular variant of PTC

A

◦ 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
Q

Describe the Tall cell variant of PTC

A

Found in older patients

Aggressive

42
Q

Describe the diffuse sclerosing variant of PTC

A

Found in kids and young adults
Greater incidence of distant mets (especially pulmonary)
93% survival at 10 years

43
Q

What mutations are present in Follicular Carcinoma

A

RAS mutations – not specific

PAX8/PPARG mutations more characteristic

44
Q

Describe Follicular carcinoma

Where is it more common

A
  1. Follicular neoplasm with invasive properties

2. More common in areas with goiter from iodide deficiency

45
Q

How are Follicular carcinomas invasive properties manifested?

A

Invasion of the capsule (mushroom)

Angioinvasion
-leads to hematogenous mets

46
Q

Therapeutic options of follicular carcinomas

A 
Surgery
Radioactive iodine (I131)

If refractory:
◦ Chemotherapy
◦ Tyrosine kinase inhibitors (still in
progress)

47
Q

Describe anaplastic carcinoma

A

Uncommon

Tend to occur in elderly patients

Highly aggressive
◦ Present with mass effect
◦ Die within a year of local invasion

48
Q

Genetics of papillary carcinoma

A

◦ RET/PTC rearrangements 
constitutive tyrosine kinase activity

◦ BRAF gain of function mutations 
MAP kinase signaling

49
Q

Genetics of follicular neoplasms (non-specific)

A

◦ RAS

◦ PTEN

50
Q

Genetics of Anaplastic Carcinoma

A

TP53

51
Q

C cells are responsible for secretion of what

A

Calcitonin

52
Q

Describe MEdullary carcinoma

A

Neuroendocrine carcinoma derived from C cells:
◦ Blue cells with dispersed chromatin
◦ Amyloid
◦ C-cell hyperplasia

53
Q

What mutatation ais associated with medulary carcinoma

A

RET

54
Q

What are the types of medullary carcinoma and which has the best prognosis

A

Sporadic (70-80%)
Familial - best prognosis
MEN syndromes

(OMS2) ENRP Exam 2 (9 decks)

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