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ENRP Exam 2 > Thyroid Pathology Dr. Singh > Flashcards

Thyroid Pathology Dr. Singh Flashcards

1
Q

T4/T3 overall effect

A

Increase basal metabolic rate

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2
Q

TSH binding to receptor stimulates what

A
  1. Thyroglobulin = storage

2. Iodide transport in to make MIT + DIT ——> T3/T4

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3
Q

Exophthalmos is seen what

A

Graves Disease

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4
Q

3 causes of Primary Hyperthyroidism

A
  1. Diffuse Hyperplasia = Graves Disease** most common
  2. Hyperfunctioning multinodular goiter
  3. Hyperfunctioning thyroid adenoma
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5
Q

Secondary Hyperthyroidism casue

A

Pituitary adenoma

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6
Q

Apathetic Hyperthyroidism

  1. Is what
  2. SX
A
  1. Hyperthyroidism in elderly having masked symptoms

2. Unexplained WL + cardiovascular disease

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7
Q

Thyroid Storm

  1. Is what
  2. SX
  3. How to score severity
  4. Events that can cause it
A
  1. Acute episode of life threatening from cardiac arrest, thyrotoxicosis
  2. VERY Fever, Cardiac tachy or CHF, GI (D, jaundice)
  3. Burch Wartosky Score
  4. Pregnancy, postpartum, Hemithyroidectomy, Amiodarone (DRUG),
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8
Q

Thyroid Storm or other hyperthyroidism TX

A 
Beta Blockers (treat immediate SX)
= high does Iodide , thionamide
= radiablation or surgery
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9
Q

Graves Disease TRIAD and is caused by

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

= Autoimmune

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10
Q

Graves Disease Histology

A

= resorption of colloid droplets seen

= very active gland (scalloped and irregular colloid shaped)

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11
Q

TSI is what and what happens when it binds

A

TSI is the Ig in Graves’ disease binging to TSH receptor :

  1. In thyroid = increases T3/T4 = hyperthyroidism
  2. Fibroblasts in retro-orbital space = T-cell cytokines come = Ophthalmopathy ( thickening extraoccular muscle + dry corneal surface since eyes cant close fully (red horizontal line seen)
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12
Q

Pretibial myxedema is what

A

Lower legs, infiltrative dermopathy, scaly indurated skin

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13
Q

Hypothyroidism 4 causes

A
  1. Hashimoto’s
  2. Granulomatous (de Quervain)
  3. Subacute lymphocytic Thyroiditis
  4. Reidel
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14
Q

Congenital Hypothyroidism “cretinism”

  1. SX
  2. Usually seen when
A
  1. Impaired mental develop + physical growth + Coarse facial features + Umbilical hernias
  2. Edemic in mom with low Iodine (now put in our salt) , + genetic thyroid metabolic pathway(TSH resistance, rare)
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15
Q

Hypothyroidism sx

A
  1. Myxedema * (in face and eyelids)
  2. Coarse scaly skin, dry hair and skin + Hair LOSS
  3. Slow mentally and physically
  4. Cold intolerance
  5. WG
  6. Low HR, CO, hypercholestrimia
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16
Q

4 Tyler’s of Thyroiditis

A
  1. Hashimoto’s (hypothyroidism)
  2. Granulomatous (de Quervain) (both)
  3. Subacute lymphocytic Thyroiditis (both)
  4. Reidel (hypothyroidism)
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17
Q

Hashimoto’s Thyroiditis

  1. What
  2. How common
  3. Thyroid is
  4. SX
A
  1. Autoimmune* Abs against Thyroid gland THyroglobulin + TPO (Thyroid perioxidase) = damage follicular cells
  2. MOST COMMON (when normal iodine levels)
  3. Diffuse painless enlarged thyroid
  4. Immune insult —> Hashitoxicosis* (immediate rise in T3/T4) —-> Follicular cell exhaustion (Hypothyroidism)
18
Q

Hashimoto’s Thyroiditis DX

A

Anti-thyroid ABs (B-cells) , T-cells also involved

TPO-ABs*

19
Q

Hashimoto’s Thyroiditis histology

A

Thyroid turns into lymph node histology
= lymphocytic infiltration with germinal centers
= Hurthle cell metaplasia (Atrophic follicle cells with eosinophilic change) (swollen red/purple cells)

20
Q

Subacute Lymphocytic Thyroiditis

  1. Is what
  2. Can progress to
  3. An example
  4. Main SX
  5. ABs seen?
A
  1. Autoimmune* Thyroid irregularities: episodes of Thyroiditis causing thyrotoxic state ——> hypothyroidism ——> back to normal
  2. Can become permanent hyperthyroidism
  3. Postpartum Thyroiditis
  4. PAINLESS thyroid*
  5. TPO-Abs*
21
Q 
Granuolomatous Thyroditis (sometimes subacute Thyroiditis)
Other name
1. What happens
2. Associated with what HLA
3. Main SX
4. ABs seen?
A

Quervain Thyroiditis

  1. Viral infection , causing granuolomatous effect , abscess like formations (usually mumps) , causing hyperthyroidism thyrotoxic —> hypothyroidism—> normal
  2. Most common in HLA B35
  3. PAINFUL thyroid
  4. No
22
Q

Riedel Thyroiditis

  1. What happens
  2. Feels like
A
  1. Fibrosis process that extends beyond thyroid, and encases common carotid As,
  2. Feels like cement, very hard to remove
  3. Dense fibrous tissue, fibrosis, skeletal muscle can event (planes are lost) + lymphocyti+ Plasma Cells (perinuclear Hoff)
23
Q

Plasma cells have what

A

Perinuclear hoff (blue nucleus with white cup around it)

24
Q

Riedel Thyroiditis

  1. Caused by
  2. Thyroid levels seen
A
  1. IgG4 related disease = inappropriate fibroinflammatory process , with many plasma cells = destroying organ
  2. Normal thyroid levels, can maybe see TPO-ABs
25
Q

Goiter : 15-25 years
1. Type
2. H levels
3 compression ?

A
  1. Diffuse
  2. Normal
  3. No
26
Q

Goiter : 26-55 years
1. Type
2. H levels
3 compression ?

A
  1. Nodular
  2. Normal (can have low TSH)
  3. Minimal
27
Q

Goiter : over 55 years
1. Type
2. H levels
3 compression ?

A
  1. Nodular
  2. Undetectable TSH + HIGH T3/T4
  3. Tracheal compression
28
Q

Diffuse Nontoxic Goiter

  1. What happens
  2. Causes
  3. SX
A

Nontoxic = not hyperthyroidism

  1. From not enough TSH, it swells up to make more Thyroid H
  2. Iodine deficiency, Cassava root + Brassicacea (broccoli, cauliflower, cabbage, radish) eating = interrupt thyroid H.
  3. Dysphagia, Hoarseness, Stridor, SVD syndrome
29
Q

Multinodular Goiter

1. Due to

A
  1. Hyperplasia cycles, due to varied stimuli, some can turn neoplastic, LARGE
  2. Loooks like
30
Q

radioisotope scan done when and what you do

A

1 .if thyroid nodule is present and changes TSH levels

  1. Hot nodule = remove, Cold nodule = US and usually more risk of neoplasia
  2. Fine needle aspiration = tells you if cold nodule is malignant
31
Q

2 benign thyroid conditions

A
  1. Hyperplasia = adenomatoid

2. Follicular adenoma

32
Q

4 types of Malignant thyroid conditions

A
  1. Papillary thyroid carcinoma
  2. Follicular Hurthle cell carcinoma
  3. Aplastic carcinoma
  4. Medullary carcinoma
33
Q

Follicular Adenoma

  1. histo
  2. What happens
  3. Make sure it is not what
A
  1. Clonal population of follicular cells with thyroid autonomy , B
  2. Can and can also not cause TSH changes
  3. Make sure it is not papillary carcinoma or follicular carcinoma
34
Q

Thyroid Papillary carcinoma :

  1. Who and B/M
  2. SX
  3. What impacts age
A
  1. 25yo-50yo, M
  2. Palpable nodule, no other sx
  3. Age influences stage (under 55yo it i fine, over 55yo very aggressive)
35
Q

Thyroid Papillary carcinoma :

  1. histology
  2. Mutations
  3. Nuclear features
A
  1. Psammoma bodies, papillary architecture
  2. RET-PTC mutation , BRAF mutation
  3. Enlarged nuclei CLEAR (Orphan Annie Eye nuclei) purple calls with clear white inside
36
Q

Thyroid Papillary carcinoma : DX how, diagnostic criteria

A

Enlarged clear nuclei (nuclear characteristics)

37
Q

Mutation in Variant Papillary Thyroid Carcinoma + 2 types and how it is

A

RAS
= tall cell variant (older pts + VERY AGGRESSIVE)
= Diffuse Sclerosing variant (in children and young adults, Mets when dx, very treatable)

38
Q

Follicular Carcinoma

  1. Characteristics
  2. Mutations
  3. When
  4. Histo
  5. Consider what
A
  1. Invasive characterisitcs** you see invasion
  2. RAS mutations(not specific), + PAX8/PPARG* mutation
  3. More common in iodine deficiency goiter
  4. Mushroom invasion, angioinvasion (if not present + no papillary present, its an adenoma)
  5. Consider differentiated thyroid carcinoma
39
Q

Thyroid carcinoma TX

A
  1. Surgery

2. Radioactive Iodine (selectively ablate) very affective

40
Q

Anaplastic Thyroid Carcinoma

  1. Type
  2. Who
  3. Histo
  4. Mutation
A
  1. Most deadly, rare, very aggressive
  2. Elderly
  3. Papillary carcinoma with high grade tumor
  4. TP53
41
Q

Follicular cells + another WHAT cell in thyroid does what

A

C-cells that secretes Calcitonin (too many of them can lead to medullary carcinoma)

42
Q

Medullary Carcinoma :

  1. What
  2. Histology 3 things seen
  3. Prognosis of 3 types
A
  1. C-cell Neuroendocrine carcinoma (excess calcitonin)
  2. Salt and pepper chromatin (blue cells)+ AMYLOID + C-cell hyperplasia
  3. Sporadic = aggressive, Familial MTC = BEST prognosis, multifocal , MEN syndrome associated MTC= BAD Prognosis, 6-8yo need to remove thyroid*

ENRP Exam 2 (8 decks)

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