Thyroid Pathology Flashcards

1
Q

Follicular Cell Anatomy and Functions (4)

A

Surround colloid which makes Thyroglobulin

Have TSH receptors that stimulate TG synthesis

Transport Iodide for TG synthesis

Cleave TG to form T3 and T4 hormones

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2
Q
Parafollicular Cells (C cells)
Functions (2)
A

Synthesize and secrete Calcitonin

Calcitonin inhibits osteoclasts and promotes skeletal calcium absorption

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3
Q

Thyroid Hormone Actions (5)

A

*Essential action is to increase the basal metabolic rate

Increase Cholesterol/Fat/Glucose synthesis
Increase heart rate
Increase Growth Hormone
Increase protein/fat/carbohydrate use in muscles

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4
Q

Goiterogens Mechanisms of Action

Propylthiouracil (2) and Iodide (2)

A

Propylthiouracil:
Inhibits Iodide oxidation to block T3/T4 synthesis

Iodide:
Blocks Thyroglobulin proteolysis to blockT3/T4 release

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5
Q

Thyrotoxicosis

Definition, Primary (5) and Secondary (1) Etiologies

A

Hypermetabolic state from excess T3/T4

Primary:
Diffuse hyperplasia from Graves disease
Multinodular goiter
Thyroid adenoma
Iodine Induced
Neonatal (from maternal Graves disease)

Secondary:
Pituitary adenoma secreting TSH

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6
Q
Hyperthyroidism 
Physiological Mechanisms (2) and Clinical Features (7)
A

Excess thyroid hormone induces hypermetabolic state
Increased Beta-adrenergic tone causes SNS overactivity

Perspiration
Facial Flushing
Nervous/Excitable/Restless/Emotional unstable
Insomnia
Exophthalmos
Palpitations/Tachycardia
Tremor
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7
Q

Hyperthyroidism

Diagnosis (6) and Treatment (5)

A

Measure T3/T4 and TSH:
TSH low and T3/T4 elevated, primary hyperthyroidism
T3/T4 and TSH all elevated, secondary hyperthyroidism

Radioactive iodine uptake by Thyroid:
Diffuse points to Graves disease
Uptake by single nodule points to adenoma

High doses of iodine (Wolff-Chaikoff effect)
Thionamide
Radioiodine ablation
Surgical resection
Beta blockers and NSAIDs for symptoms
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8
Q
Graves Disease
Clinical Features (3), Pathogenesis and Morphology (2)
A

Hyperthyroidism with gland enlargement
Infiltrative opthalmopathy
Pretibial myxedema

TSH receptor antibodies (TSI Abs)

Diffusely enlarged thyroid
Bubbly colloid from droplet resorption

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9
Q

Thyroid Storm

Definition, Symptoms (4) and Precipitating Events (3)

A

abrupt onset of life threatening thyrotoxicosis

Fever
Tachycardia
Congestive Heart Failure
Jaundice

Pregnancy
Hemithyroidectomy
Amiodarone

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10
Q

Hypothyroidism

Prevalence (3) Etiologies: Primary (6) and Secondary (2)

A

Common Disease (.3-4%)
More common in women
Prevalence increases with age

Genetic thyroid development defect
Iatrogenic - Postablative
Thyroid hormone resistance syndrome
Autoimmune
Iodine deficiency (congenital cretinism)
Dyshormonogenetic goiter (congenital)

Pituitary failure
Hypothalamus failure

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11
Q

Cretinism

Etiologies (2) Pathogenesis (2) Clinical Features (4)

A

Maternal iodine deficiency
Genetic alterations in normal thyroid metabolic pathways

Lack of maternal T3/T4 crossing placenta early in pregnancy leading to abnormal brain development

Mental retardation
Growth retardation
Coarse facial features, protruding tongue
Umbilical hernias
Short stature
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12
Q

Iatrogenic Hypothyroidism

Etiologies (3)

A

Thyroidectomy
Radioiodine/Exogenous irradiation
Drugs: methimazole, propylthiouracil, lithium, p-aminosalicyclic acid

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13
Q
Myxedema (Hypothyroidism)
Clinical Features (7) and Lab Values (2)
A
Mental/physical sluggishness
Weight gain
Cold intolerance
Low cardiac output
Hypercholesterolemia
Brittle nails
Hair loss

Elevated TSH
Decreased T4/T3

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14
Q

Hashimoto Thyroiditis
Prevalence (2) Pathogenesis (2) Morphology (3)
Clinical Features (4) Associated Diseases (2)

A

Most common cause of iodine sufficient hypothyroidism
Most common in women aged 45-65

CTLA4 and PTPN22 defects cause loss of tolerance
Autoantibodies to Tg and TPO made

Lymphocytic infiltrate forming germinal centers
Follicular cell atrophy and Hurthle cell metaplasia

Diffuse, painless thyroid enlargement
Initial Hashitoxicosis (hyperthyroidism)
Eventual hypothyroidism
Elevated TSH, decreased T4/T3

Many other Autoimmune diseases
Thyroid B cell Lymphoma

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15
Q

Subacute Lymphocytic Thyroiditis

Pathogenesis, Morphology, Clinical Features (3) and Related Disease

A

Anti-TPO antibodies

Lymphocytic infiltrate with germinal centers

Painless goiter
Transient hyperthyroidism
Progression to overt hypothyroidism

Postpartum Thyroiditis

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16
Q

Granulomatous Thyroiditis

Demographic, Pathogenesis (2) Morphology (2) Clinical Feature and Lab Values (2)

A

Women aged 40 to 50

Triggered by viral infection
Associated with HLA B35

Multinucleated giant cells enclose colloid
Granulomatous formations\

Thyroid Pain

High T4/T3
Low TSH

17
Q

Riedel Thyroiditis

Pathogenesis, Morphology (2), Lab Values (2)

A

IgG4 mediated thyroiditis

Fibrosis extending from thyroid into adjacent tissues
Lymphocytic and Plasma cell infiltration

Normal T4/T3
Normal TSH

18
Q

Diffuse Goiters

Demographics (2) Etiologies (3) Morphology (3) Lab Values (2) and Clinical Features (4)

A

15-25 years old
Women (sporadic etiology)

Decreased thyroid synthesis from:
Insufficient dietary iodine
Goitrogens: cassava root, Brassicaceae vegetables
Sporadic

Diffuse and symmetrical thyroid enlargement
Follicular hyperplasia
Abundant colloid

Normal T4/T3
Normal TSH

Dysphagia
Hoarseness
Stridor
Superior Vena Cava Syndrome

19
Q

Multinodular Goiters

Age Group, Etiology, Morphology (3), Lab Values (2) Clinical Features (4)

A

Ages 26+

Long standing simple diffuse goiter

Massively enlarged thyroid
Follicular hyperplasia
Substernal, intrathoracic growth

Normal-Raised T4/T3
Undetectable TSH

Dysphagia
Hoarseness
Stridor
Superior Vena Cava Syndrome

20
Q

Thyroid Nodule Detection Lab Techniques

Radioisotope (2) and Fine Needle Aspiration (2)

A

Radioiodine Scanning:
Hot areas show hyperfunctioning nodules
Cold areas more likely to be neoplastic

Fine Needle Aspiration
Determines cellular components of nodule
Helps to determine neoplasm vs hyperplasia

21
Q

Follicular Adenoma
Prognosis, Genetics (2) Morphology (2)
Presentation (2) and Diagnosis (3)

A

Benign

Somatic mutation of TSH receptor signaling pathway
Gain of function GNAS mutation

Solitary, spherical lesion
Well defined INTACT capsule

Unilateral painless mass
Mass effect if larger

Cold spot on radioisotope
FNA
Definitive requires surgical excision

22
Q

Papillary Carcinoma

Prognosis, Age Group, Genetics (2) Morphology (3) Clinical Features (3)

A

Malignant (most common malignancy)

Ages 25-50

RET/PTC fusion gene
BRAF gain of function mutation

Well differentiated cells
Psammoma bodies
Orphan Annie eye nuclei (clear cytoplasm)**

Excellent prognosis
Asymptomatic
Palpable nodule

23
Q

Papillary Carcinoma Subclasses with Descriptions

Follicular (2) Tall Cell (3) and Diffuse Sclerosing (3)

A

Follicular:
RAS Mutations
More aggressive and invasive

Tall Cell:
BRAF mutations
More aggressive
Seen in older patients

Diffuse Sclerosing:
RET/PTC translocations
Distant metastases
Presents in kids

24
Q

Follicular Carcinoma

Prognosis, Demographics (2), Genetics (2) Invasive Features (2)

A

Malignant

More common in women
More common in areas of iodine deficiency

RAS mutation
PAX8/PPARG mutation

**Capsule invasion (mushroom shape)
Angioinvasion with Hematogenous metastasis

25
Q

Anaplastic Thyroid Carcinoma

Prognosis (2) Mean Age, Mutation, Morphology (3) and Presentation (1)

A

Malignant
Highly aggressive with very poor prognosis

Mean age 65 years

TP53 mutation

Poorly differentiated**
Pleomorphic giant cells
Spindle cells

Present with mass effect symptoms

26
Q

Medullary Carcinoma

Prognosis, Pathogenesis (2), Disease Association, Morphology (5) and Secretions with Presentations (3)

A

Malignant

Most arise sporadically
RET gain of function mutation

Associated with MEN Syndrome Type 2

Solitary (sporadic)
Bilateral and Multiple (familial)
Amyloid deposits
Small round blue cells
C cell hyperplasia

Calcitonin secretion
VIP secretion causing diarrhea
ACTH secretion causing Cushing syndrome