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Endocrine Pathology II Flashcards

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1
Q

What is the most common cause of clinically apparent Hypercalcemia?

A

cancer malignancies where solid tumors may secrete PTH-related protein (PTHrP)

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2
Q

What are the common cancers involved in clinically apparent Hypercalcemia and what are the lab findings?

A

lung, breast, head and neck, renal cancers, and hematologic cancers like multiple myeloma
- PTH is low or undetectable

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3
Q

What are the three main types of Parathyroid disorders?

A
  1. Hyperparathyroidism
  2. Hypoparathyroidism
  3. Parathyroid tumors
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4
Q

What are the main causes of hyperparathyroidism and who does it mainly effect?

A

Adenoma (85%)
Hyperplasia (15%)
Carcinoma (1%)
- Common in women over 50 –> often asymptomatic; detected via incidental hypercalcemia

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5
Q

What are the genetic characteristics of Primary Hyperparathyroidism caused by ADENOMA?

A
  • 95% sporadic: monoclonal, associated with Cyclin D1, MEN1
  • 5–10% familial: associated with MEN1 & MEN2A
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6
Q

What are the morphological features of Primary Hyperparathyroidism Adenomas?

A
  • Solitary, tan-brown, encapsulated nodule (0.5–5.0 g) with a rim of compressed non-neoplastic tissue
  • Mostly chief cells, few oxyphil cells
  • Inconspicuous fat tissue
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7
Q

What are the main causes of HYPERPLASIA induced Primary Hyperparathyroidism and its morphological features?

A
  • either sporadic or part of MEN syndrome
  • ALL 4 glands are enlarged with little to no fat seen histologically
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8
Q

What are the features of CARCINOMA induced Primary Hyperparathyroidism?

A
  • usually involves ONE gland
  • tumors are usually gray-white masses with cytological similarities to adenomas
  • ⅓ recur locally; ⅓ metastasize
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9
Q

How is malignancy determined for CARCINOMAS that induce Primary Hyperparathyroidism?

A
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10
Q

What are the Skeletal Changes that occur due to Primary Hyperparathyroidism?

A
  • ↑ Osteoclast → bone resorption
  • ↑ Osteoblast → new woven bone
  • Severe cases → osteitis fibrosa cystica (with hemorrhagic brown tumors)
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11
Q

What are the Urinary Tract Changes that occur due to Primary Hyperparathyroidism?

A
  • Stones (nephrolithiasis)
  • Nephrocalcinosis (calcification of tubules/interstitium)
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12
Q

Where does Primary Hyperparathyroidism induced metastatic calcification mainly occur?

A

stomach
lungs
heart
blood vessels

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13
Q

What is Secondary Hyperparathyroidism and what is the main cause?

A

Chronically low calcium levels cause compensatory PTH rise mainly caused by Chronic kidney disease which leads too
- ↓ phosphate excretion → ↑ serum phosphate → ↓ calcium
- ↓ α1-hydroxylase → ↓ active vitamin D → ↓ Ca²⁺ absorption
**Other causes: poor diet, steatorrhea, vitamin D deficiency

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14
Q

What are the treatments for Secondary Hyperparathyroidism?

A

Vitamin D supplements
Phosphate binders

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15
Q

What is Tertiary Hyperparathyroidism and what is the treatment?

A

Chronic secondary hyperparathyroidism causes autonomous PTH secretion which leads to hypercalcemia
- Parathyroidectomy is the treatment

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16
Q

What are the main causes of Hypoparathyroidism?

A
  1. Congenital absence
  2. Post-surgical
  3. Radiation-induced damage
  4. Autoimmune destruction
  5. Familial
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17
Q

What are the types of clinical manifestations of Hypoparathyroidism?

A

(All due to hypocalcemia and low PTH levels)
- Neuromuscular
- Neuropsychiatric
- CNS effects
- Cardiac
- Dental

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18
Q

What are the neuromuscular signs of Hypoparathyroidism?

A
  • Tetany
  • Circumoral numbness, tingling in hands/feet
  • Carpopedal spasm
  • Chvostek’s and Trousseau’s signs
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19
Q

What are the neuropsychiatric symptoms of Hypoparathyroidism?

A
  • Anxiety, depression
  • Confusion, hallucinations
  • Psychosis
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20
Q

What are the CNS Effects of Hypoparathyroidism?

A
  • Basal ganglia calcifications
  • Parkinsonian-like movement disorders
  • Increased intracranial pressure, papilledema
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21
Q

What are the Cardiac Effects of Hypoparathyroidism?

A

Prolonged QT interval on ECG

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22
Q

What are the Dental manifestations of Hypoparathyroidism?

A
  • Enamel defects
  • Failure of tooth eruption
  • Hypoplasia and root malformations
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23
Q

What is Pseudohypoparathyroidism and what are its key features?

A

Condition mimicking hypoparathyroidism due to end-organ resistance to PTH
- Serum PTH levels: Normal or elevated
- Hypocalcemia and hyperphosphatemia persist because target organs (e.g., kidney, bone) do not respond to PTH

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24
Q

What are Goitrogens and what are some examples?

A

chemical agents that inhibit the function of the thyroid gland by suppressing T3/T4 synthesis
- propylthiouracil, iodides in large doses and vegetables (such as cabbage, turnips and cassava)

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25
What is Hyperthyroidism?
Overactive thyroid → high T3 and T4 → hypermetabolic state
26
What are the main causes of Primary Hyperthyroidism?
Graves’ disease (~85%) Toxic multinodular goiter Toxic adenoma Iodine-induced Neonatal thyrotoxicosis
27
What is the main cause of Secondary Hyperthyroidism?
TSH-secreting pituitary tumor
28
Where do clinical symptoms of Hyperthyroidism mainly occur and what are they?
- Heart → fast heartbeat, palpitations, possible arrhythmias - Nerves/Muscles → tremors, anxiety, trouble focusing, muscle weakness - Metabolism → heat intolerance, sweating, weight loss with good appetite - Eyes → lid lag, staring gaze (especially in Graves) - GI → frequent bowel movements, possible diarrhea - Bones → bone loss → osteoporosis, higher fracture risk
29
What are the severe forms of Hyperthyroidism?
1. Thyroid Storm (Medical Emergency) - Sudden, severe hyperthyroidism - Triggered by stress, surgery, infection - Can cause death from heart problems if untreated 2. Apathetic Hyperthyroidism - Seen in elderly - Subtle symptoms like weight loss or heart issues
30
How is Hyperthyroidism diagnosed?
- Low TSH → best screening test - High free T4/free T3 → confirms diagnosis - Radioactive iodine uptake test → helps find the cause (e.g. Graves vs thyroiditis)
31
What is Graves Disease and what is the classical triad?
Most common cause of endogenous hyperthyroidism Classic Triad: 1. Hyperthyroidism with diffuse goiter (thyroid enlargement) 2. Exophthalmos – infiltrative ophthalmopathy causing eye bulging 3. Pretibial myxedema – localized dermopathy
32
Who does Graves Disease mainly effect and how does it occur?
- mainly women aged 20-40 - Thyroid-stimulating immunoglobulin (TSI): An IgG antibody that binds to the TSH receptor and mimics TSH → overstimulates thyroid hormone production
33
What are the histological and laboratory findings for Graves Disease?
- Symmetric diffuse thyroid hyperplasia (meaty cut surface) - Tall follicular epithelial cells form papillae and encroach on colloid - Pale colloid with scalloped margins Lab findings show: - ↑ T3 and T4 - ↓ TSH - Increased and diffuse uptake of radioactive iodine
34
What is Hypothyroidism and what is its prevalence?
A functional or structural defect that causes inadequate thyroid hormone production * Subclinical hypothyroidism: >4% * Overt hypothyroidism: 0.3% * 10x more common in women
35
What are the Types of Hypothyroidism and their main causes?
1. Primary Hypothyroidism (more common) * Congenital (e.g., thyroid agenesis) * Acquired: Surgery, Radiation, Drugs * Autoimmune: Hashimoto thyroiditis = #1 cause in iodine-sufficient areas 2. Secondary Hypothyroidism * Due to pituitary or hypothalamic failure
36
What are the laboratory findings for Primary and Secondary Hypothyroidism?
Primary: ↑ TSH, ↓ T4 Secondary: ↓ TSH and ↓ T4
37
What are the classic clinical manifestations of Hypothyroidism?
Cretinism (infants or early childhood) Myxedema (adults)
38
What is Thyroiditis and what are the types?
Inflammation of thyroid gland that causes primary hypothyroidism - Hashimoto thyroiditis - Subacute (granulomatous) thyroiditis - Subacute lymphocytic (painless) thyroiditis - Infectious thyroiditis
39
What is Hashimoto Thyroiditis?
Most common cause of hypothyroidism in iodine-sufficient regions caused by autoimmune destruction of the thyroid. * Peak age: 45–65 years. * Female predominance: 10–20:1. * Autoantibodies: Anti-thyroglobulin, anti-thyroid peroxidase, and anti-TSH receptor antibodies
40
What are the clinical and histological manifestations of Hashimoto Thyroiditis?
- Thyroid is diffusely enlarged and encapsulated - Cut surface: Pale, yellow-tan, firm, and nodular - Lymphocytic infiltrate with germinal centers - Hurthle cells (eosinophilic metaplasia) - Atrophic follicles with fibrosis
41
What is the clinical course of Hashimoto Thyroiditis?
Painless thyroid enlargement which leads to an increased risk of: - Other autoimmune diseases (e.g., T1DM, lupus, myasthenia gravis). - B-cell lymphomas (especially MALT) - Papillary thyroid carcinoma
42
What is Subacute Granulomatous (De Quervain) Thyroiditis and what are its features?
Most common cause of thyroid pain often post-viral (e.g., coxsackievirus, mumps). - More common in middle-aged women. - Self-limited: Resolves in 2–6 weeks. - Histology: Granulomas with giant cells, follicular destruction, and collagen.
43
What is Riedel Thyroiditis and what are its features?
Rare; unknown cause with extensive fibrosis replacing thyroid and spreading to adjacent neck structures - Clinically mimics thyroid cancer - Associated with systemic fibrosis - “Stony” hard thyroid (“iron collar” feel) - Infiltrates of lymphocytes and histiocytes
44
What is Subacute Lymphocytic (Painless) Thyroiditis and what are its features?
- Painless, symmetric thyroid enlargement - May have transient hyperthyroidism - Risk of progression to hypothyroidism over years - mainly occurs in middle-aged women, often postpartum
45
What is Postpartum Thyroiditis?
- Occurs in up to 5% of women post-delivery often in women with a personal/family history of autoimmune disease. - 80% recover to euthyroid state within 1 year
46
What is a Goiter?
Enlargement of the thyroid --> most common sign of thyroid disease - ↓ Thyroid hormone → ↑ TSH → follicular cell hypertrophy. - If compensation fails → goitrous hypothyroidism.
47
What are the two types of Diffuse Non-Toxic (Simple) Goiters?
- Endemic: Due to low iodine in soil/water/food. - Sporadic: Often no clear cause; may involve: Goitrogen ingestion, Genetic enzyme defects, Female predominance, puberty onset
48
What is a Multinodular Goiter?
Most extreme thyroid enlargements that results from repeated hyperplasia and involution cycles - Can produce mass effects: airway obstruction, dysphagia, SVC syndrome. - Can be euthyroid or subclinically hyperthyroid
49
What is the morphological appearance of a Multinodular Goiter?
- Asymmetric, nodular, often > 2000g. - Cut surface: Irregular nodules with fibrosis, hemorrhage, calcification, and cysts - No capsule; mixture of colloid-rich and hyperplastic areas.
50
What are the main causes of Solitary Thyroid Nodules and what is the prevalence?
Prevalence: 1–10% in the U.S.; more common in women. - Non-neoplastic (most common) - Neoplastic: Benign > Malignant (10:1 ratio) --> Higher malignancy risk with certain factors
51
What is critical for diagosis of Solitary Thyroid Nodules?
Fine Needle Aspiration (FNA)
52
What are Follicular Adenomas and why must it be removed surgically?
Solitary, discrete, painless mass, usually unilateral an nonfunctional (cold nodules on scans) - to assess capsule invasion, which distinguishes adenoma from follicular carcinoma
53
What are the features of Thyroid Carcinomas and risk factors?
- Comprise 1.5% of all cancers - Female predominance - Papillary carcinoma (>85%) - Risk Factors: Radiation exposure, Iodine deficiency (→ follicular carcinoma), mutations
54
What are the Genetic Mutations of Thyroid Carcinomas?
- Papillary Carcinoma: RET/PTC rearrangements, BRAF mutations - Follicular Carcinoma: RAS, PIK3CA mutations, PAX8-PPARG fusion (t2;3) - Anaplastic Carcinoma: p53 inactivation, beta-catenin activation - Medullary Carcinoma: RET proto-oncogene mutation
55
What are the features of Papillary Carcinomas?
- Most common thyroid cancer (85%) - Onset: 25–50 years old - Prognosis: Excellent
56
What are the features of Follicular Carcinoma?
- Prevalence: 5–15% of thyroid cancers - More common in women, age 40–60 - Linked to iodine deficiency - Spread: Hematogenous (vascular) spread is common - Treatment: Total thyroidectomy + radioactive iodine
57
What are the features of Anaplastic (Undifferentiated) Carcinoma?
Often develops from preexisting thyroid cancer and may coexist with well-differentiated cancer - <5% of thyroid cancers - Highly aggressive; near 100% mortality - Mean age: 65 years
58
What are the features of Medullary Carcinoma?
Neuroendocrine tumor from parafollicular C cells that secretes calcitonin, ACTH, VIP - Accounts for ~5% of thyroid cancers. - Sporadic (70%) or Familial (30%)
59
Sporadic Medullary Carcinoma
solitary tumor that occurs mainly in adults
60
Familial Medullary Carcinoma (FMTC)
MEN 2A or 2B - Usually bilateral, multicentric, with C-cell hyperplasia

Systems Exam 3 (18 decks)

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