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MHD II Test 3 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Normal Thyroid

  1. Weight
  2. Gross look
  3. Histo
A
  1. 20-25 g
  2. right lobe, isthmus, left lobe
  3. follicle lined by cuboidal to low columnar follicular cells; contain parafollicular or “C” cells which secrete calcitonin
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2
Q

Hypothalamus-Pituitary-Thyroid Axis

  1. Hypo releases
  2. Pituitary releases
  3. Thyroid releases
  4. Inhibition
  5. Actions of T3/T4
A
  1. TRH onto pituitary
  2. TSH onto Thyroid
  3. T4
  4. Feedback inhibition by T3/T4 on Pituitary and Hypothalamus
  5. stimulation of protein synthesis; upregulation of carb and lipid metabolism; increase basal metabolic rate; critical role in the development of brain in fetuses and neonates
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3
Q

Thyrotoxicosis

  1. Define
  2. Most common cause
A
  1. hyper metabolic state due to increased circulating levels of thyroid hormones
  2. hyper functioning of the thyroid gland
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4
Q

Thyrotoxicosis Disorders

  1. Associated w/ Hyperthyroidism: Primary
  2. Associated w/ Hyperthyroidism: Secondary
  3. Not associated w/ Hyperthyroidism
A
  1. Diffuse toxic hyperplasia (Grave’s Disease), Hyperfunctioning (toxic) multinodular goiter, Hyperfunctioning (toxic) adenoma, iodine induced hyperthyroidism, neonatal thyrotoxicosis associated w/ maternal Grave’s disease
  2. TSH secreting pituitary adenoma
  3. Granulomatous (deQuarvain) thyroiditis (painful); subacute lymphocytic thyroiditis (painless); struma ovarii (ovarian teratoma w/ ectopic thyroid); factitious thyrotoxicosis (exogenous thyroid intake)
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5
Q

Hyperthyroidism/Thyrotoxicosis: Clinical Manifestations (10)

11. Due to what?

A
  1. Increased BMR- soft, warm, flushed skin
  2. heat intolerance and excess sweating
  3. characteristic weight loss despite increased apetite
  4. CV- increased CO, tachycardia, palpitations, cardiomegaly, arrhythmias (uncommon) especially atrial fibrillation; development of low output heart failure;
  5. Neuromuscular: nervousness, emotional lability, insomnia, muscular weakness, fine tremor of hands
  6. Proximal muscle weakness and decreased muscle mass
  7. GI: hypermotility, malabsorption and diarrhea
  8. Ocular: wide staring gaze, lid lag
  9. Thyroid opthalmopathy (exophthalmos)
  10. Bone resorption w/ osteoporosis
  11. excess of thyroid hormones and over activity of sympathetic nervous system
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6
Q

Hyperthyroidism: Dx

  1. What 3 things are measured?
  2. Describe TRH stimulation test
  3. Describe Radioactive Iodine Uptake test
  4. What does diffuse uptake indicate?
  5. Localized uptake?
  6. reduced uptake?
A
  1. TSH (usually decreased); T4 (usually increased); T3 (rare pts w/ nl or reduced T4 but elevated T3)
  2. injection of TRH; normal rise in TSH exclude pituitary associated hyperthyroidism
  3. used after dx of thyrotoxicosis
  4. Graves
  5. toxic adenoma
  6. thyroiditis
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7
Q

Hypothyroidism

  1. Define
  2. Primary Causes (7)
  3. Secondary Causes (2)
A
  1. hypermetabolic state secondary to inadequate levels of thyroid hormones
  2. Developmental, Thyroid hormone resistance syndrome, post ablative, autoimmune hypothyroidism, iodine deficiency, drugs, congenital biosynthetic defect
  3. Pituitary Failure, Hypothalamic failure
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8
Q

Hypothyroidism

  1. Most common cause of what physical symptom?
  2. Worldwide congenital hypothyroidism most often due to what?
  3. Most common cause where (2) isn’t a problem?
  4. Other clinical manifestations (2)
A
  1. enlargement of the gland (goiter)
  2. endemic iodine deficiency in diet
  3. chronic autoimmue thyroiditis (Hashimoto’s)
  4. cretinism and myxedema
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9
Q

Cretinism

  1. Define
  2. Cause
  3. What determines the severity?
  4. Symptoms
A
  1. hypothyroidism in infants or early childhood
  2. secondary to iodine deficiency (endemic) or rarely from inborn errors in metabolism
  3. timing of the deficiency; if maternal thyroid deficiency occurs before fetus develops thyroid that develops own T3/T4, will be more severe
  4. Impaired development of skeletal muscles and CNS
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10
Q

Myxedema

  1. Define
  2. Symptoms (6)
  3. What does it do to blood lipids?
A
  1. adult hypothyroidism
  2. gradual slowing of mental and physical activity
  3. fatigue, lethargy, apathy, slowed speech
  4. cold intolerance, reduced sweating
  5. overweight, constipation
  6. periorbital edema, thick coarse skin, enlarged tongue; (deposition of glycosaminoglycans)
  7. Reduced cardiac output causes shortness of breath and decreased exercise capacity
  8. promotes atherogenic profile (increased total cholesterol and LDL) –> adverse CV mortality rates
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11
Q

Hypothyroidism: Lab findings

  1. T4
  2. TSH
  3. What is seen in primary hypothyroidism?
  4. Secondary?
A
  1. decreased
  2. most sensitive test for hypothyroidism
  3. increased TSH (thyroid not making enough T4)
  4. decreased/normal TSH (suggest pit tumor, necrosis; not enough TSH being produced)
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12
Q

Thyroiditis

  1. Define
  2. Causes with pain (2)
  3. causes w/o or w/ little pain
A
  1. inflammation of thyroid gland
  2. infectious thyroiditis, subacute granulomatous thyroiditis (De Quervain thyroiditis- most common cause of painful thyroiditis)
  3. Subacute lymphocytic thyroiditis; Reide’s thyroiditis; Hashimoto’s thyroiditis
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13
Q

Hashimoto Thyroiditis

  1. Define
  2. What areas get it?
  3. What age group is it found in?
  4. Is there a genetic component?
  5. 3 Mechanisms
A
  1. autoimmune destruction of the thyroid gland: hypothyroidism
  2. areas without iodine deficiency
  3. 45-65
  4. yes
  5. T cell-mediated cytotoxicity; Activated macrophages causing thyrocyte injury, Antibody-dependent cell-mediated immunity
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14
Q

In general, which gender gets thyroid disorders/neoplasms more often?

A

Women

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15
Q

Hashimoto Thyroiditis

  1. Labs show antibodies to what? (3)
  2. Gross look
  3. Histo look
A
  1. Thyroglobulin and Thyroid peroxidase (TPO-most common); TSH receptor, Iodine receptor
  2. diffusely enlarged gland with intact capsule; well demarcated from adjacent structures; cut surface is pale, yellow tan, somewhat nodular and firm
  3. parenchyma infiltrated by mononuclear inflammatory cells; Hurthle cells/oncocytes line Thyroid follicles and have abundant granular pink cytoplasm
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16
Q

Hashimoto Thyroiditis: Clinical Course

  1. What happens physically?
  2. How quickly does hypothyroidism develop?
  3. what do some pts develop?
  4. Increased risk of developing what diseases (3)
A
  1. painless enlargement of gland w/ some degree of hypothyroidism
  2. gradually
  3. transient hyperthyroidism (due to disruption of follicles and release of T3/T4); gradually hypothyroidism sets in
  4. Increased risk of other autoimmune disease
  5. Increased risk of developing Non Hodgkin B cell lymphoma
  6. May have increased risk of developing papillary carcinomas
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17
Q

Subacute/Granulomatous (De Quervain) Thyroiditis

  1. Etiology
  2. Clinical Course?
  3. Histo look:early
  4. Histo look: late
  5. Gross look
A
  1. Viral or post-viral inflammatory response: viral Ag or virus-induced host tissue damage stimulates formation of cytotoxic T cells which then damage the thyroid follicular cells
  2. self-limited; pt is asymptomatic after acute stage
  3. disruption of follicles w/ collections of neutrophils forming microabscesses
  4. aggregates of lymphocytes. plasma cells, and activated macrophages around damaged thyroid follicles;
  5. uni/bilateral, enlarged and firm w/ intact capsule
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18
Q

Granulomatous (De Quervain) Thyroiditis

  1. Commonly Causes what
  2. Does the thyroid enlarge?
  3. What is commonly in pt’s history?
  4. How long does hyperthyroidism last?
  5. What is elevated in hyperthyroidism phase?
  6. How long does it last?
A
  1. thyroid pain
  2. variable
  3. upper respiratory infection
  4. 2-6 weeks
  5. elevated T3 and T4; diminished TSH, radioactive iodine uptake is diminished
  6. 6 to 8 weeks
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19
Q

Subacute Lymphocytic Thyroiditis

  1. What causes pt to come in?
  2. Who gets it?
  3. Etiology
  4. Clinical Course
  5. Gross look
  6. Histo look
A
  1. mild hyperthyroidism, goitrous enlargement of thyroid, or both
  2. middle aged women; can also occur in post-partum period
  3. variants of hashimoto
  4. majority of pts are euthyroid by 1 year, 1/3 progress to overt hypothyroidism over 10 yrs
  5. mild enlargement
  6. lymphocytic infiltration w/ germinal centers; no fibrosis or hurthle cell metaplasia
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20
Q

Riedel Thyroiditis

  1. Etiology
  2. Histo look
  3. Gross look
  4. May be associated with what?
A
  1. unknown
  2. extensive fibrosis involving the thyroid and contiguous neck structures
  3. hard and fixed mass, simulating cancer
  4. idiopathic fibrosis at other sites like retroperitoneum
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21
Q

Grave’s Disease

  1. How common is it?
  2. Symptoms
  3. Etiology
A
  1. most common cause of endogenous hyperthyroidism (1.5-2% of US women)
  2. Triad of Findings: hyperthyroidism due to diffuse hyperfunctional enlargement of thyroid
    Infiltrative Opthalmopathy - exophthalmos
    Infiltrative Dermopathy- pretibial myxedema (most pts present before this develops)
  3. autoimmune disease: Thyroid stimulating immunoglobulin (TSI) binds to TSH receptor and mimics its action (relatively specific for Graves)
    Thyoid growth stimulating hormone (TGI)- causes proliferation of the follicular epithelium
    TSH-binding inhibitior immunoglobulin (TBII)
22
Q

Graves Disease

  1. Gross Look
  2. Histo look
A
  1. symmetrically enlarged, >80g, soft meaty appearance on cut surface
  2. crowded and tall follicular cells; formation of small papillae filling the lumen of the follicles; papillae lack fibrovascular cores; pale colloid with scalloped margins; lymphoid infiltrate w/ germinal centers common
23
Q

Graves Disease: Clinical Manifestations (5)

6. Risk of what?

A
  1. Thyrotoxicosis
  2. Thyroid gland enlargement
  3. Wide staring gaze and lid lag- sympathetic overactivity
  4. Infiltrative ophthalmopathy- Exophthalmos (accumulation of loose connective tissue behind the eyeball, doesn’t go away w/ treatment)
  5. Infiltrative dermopathy- pretibial myxedema
  6. Risk of other autoimmune diseases
24
Q

Pretibial Myxedema

  1. Where does it occur?
  2. What is it?
  3. what disease is it associated with?
A
  1. skin overlying the shins
  2. scaly thickening and induration
  3. Grave’s disease
25
Q

Grave’s Disease: lab findings

  1. What are the levels of T3, T4, and TSH?
  2. What happens on radioactive iodine uptake?
A
  1. increased free T3 and T4; decreased TSH

2. diffuse uptake

26
Q

Goiter

  1. Define
  2. How does it develop?
  3. What does it start out as?
  4. What does it become?
  5. When is it endemic?
  6. What gender gets the sporadic type? When?
A
  1. enlargement of the thyroid
  2. impaired synthesis of T3 and T4; increased TSH –> hyperplasia and hypertrophy of follicular epithelium
  3. diffuse (simple)
  4. becomes multinodular
  5. > 10% of population, seen in mountainous regions
  6. females, at puberty
27
Q

Diffuse/Nontoxic Goiter

  1. What is it?
  2. Cut surface?
  3. Histo look
A
  1. enlargement of the entire gland w/o producing nodularity; diffuse symmetric enlargement
  2. brown, glassy, translucent
  3. 2 phases: Hyperplastic phase- enlarged thyroid gland w/ crowded follicular cells
    Colloid involution- distended follicles
    flattened epithelium
28
Q

Diffuse Nontoxic Goiter

  1. What are Thyroid hormones/TSH?
  2. Complications due to?
  3. What will it become?
A
  1. normal T3/T4; elevated or upper normal TSH
  2. mass effect, may press on trachea, esophagus, may also cause cosmetic disfigurement
  3. Multinodular Goiter
29
Q

Multinodular Goiter

  1. What is it?
  2. How does it develop?
  3. Who gets it?
  4. Is it toxic?
  5. What can happen to cells w/in a nodule?
A
  1. asymmetric enlargement w/ numerous nodules
  2. evolves from diffuse goiters over many years due to repeated episodes of hyperplasia and involution (hemorrhage and fibrosis –> nodules)
  3. older adults, but similar epidemiology to Diffuse
  4. may be toxic or non-toxic
  5. Cells may become autonomous and continue proliferating
30
Q

Multinodular Goiter

  1. complications
  2. Gross look
  3. Cut section
  4. Histo look
A
  1. mass effect; may press on trachea –> snoring/stridor; may cause dysphagia
  2. asymmetric, multilobated gland; may be very large; one lobe may be more involved than the other; may become intrathoracic or “plunging” behind sternum and clavicles
  3. irregular nodules containing gelatinous colloid; foci of fibrosis
  4. Colloid rich follicles lined by flattened inactive epithelium; areas of follicular hyperplasia; lacks a capsule
31
Q

Multinodular Goiter

  1. What happens to T3 and T4?
  2. What may develop?
  3. Malignancy risk?
  4. What happens on radioactive iodine uptake?
  5. what test is done to determine if its malignant?
A
  1. normal
  2. minority develop toxic multinodular goiter due to development of an autonomous nodule
  3. t take it up
  4. fine needle aspirations
32
Q

Thyroid Neoplasms

  1. Are they mostly indolent or aggressive?
  2. What kinds of nodules/pts are more likely to be neoplastic?
  3. What history is associated w/ increased incidence of thyroid malignancy?
A
  1. mostly indolent

2. single nodules, young pts, males, nonfunctioning nodules

33
Q

Follicular Adenoma

  1. Describe it
  2. What 3 mutations are important?
  3. Gross look
A
  1. discrete solitary masses derived from follicular epithelium
  2. RAS, PAX8-PPARG fusion gene, mutation in TSH receptor signaling pathway
  3. solitary, encapsulated, spherical; gray-white to red brown mass; may have areas of hemorrhage, necrosis, or calcification
34
Q

Follicular Adenoma

  1. Histo look
  2. What warrants investigation into follicular carcinoma on histo?
  3. What is seen on histo in Hurthle cell/oxyphil/oncocytic adenoma?
A
  1. neoplastic cells arranged in closely packed follicles;
    demarcated from adjacent thyroid parenchyma by a well defined capsule;
    uniform small follicles which contain colloid;
  2. extensive mitotic activity, necrosis, high cellularity;
  3. follicular adenoma w/ cells w/ abundant pink cytoplasm due to presence of many mitochondria (not clinically different from normal follicular adenoma)
35
Q

Follicular Adenoma

  1. What is the important feature?
  2. Why?
  3. What is required for accurate diagnosis?
  4. What can you say with a small sample?
A
  1. capsule
  2. differentiates adenoma from carcinoma (along w/ vascular invasion)
  3. histo exam of entire nodule; can’t use fine needle aspiration
  4. That it is a follicular neoplasm (can be adenoma or carcinoma)
36
Q

Follicular Adenoma

  1. How does it present?
  2. What is seen on radioactive iodine scan?
  3. What occurs rarely?
  4. Treatment?
  5. Prognosis
A
  1. painless asymptomatic mass, may produce local symptoms due to mass effect
  2. usually cold
  3. rarely is a functioning toxic adenoma
  4. lobectomy
  5. excellent, does not recur or metastasize
37
Q

Thyroid Carcinomas

  1. How common is it?
  2. Who gets it?
  3. Linked with what?
  4. Major subtypes
A
  1. uncommon
  2. female in middle age; males and females in childhood/late adult life
  3. ionizing radiation and dietary iodine deficiency; genetic events
  4. Papillary Carcinoma, Follicular Carcinoma, Medullary Carcinoma, Anaplastic Carcinoma
38
Q

Papillary Carcinoma

  1. How common is it?
  2. common presentation
  3. Etiology
  4. Gross look
  5. What does cut surface show?
A
  1. most common thyroid cancer
  2. 40 y/o female w/ neck mass; (age 25-50)
  3. accounts for majority of thyroid cancers associated with hx of radiation exposure
  4. solitary or multifocal; may be well encapsulated or infiltrative; has foci of fibrosis and calcification;
  5. papillary structures
39
Q

Papillary Carcinoma

  1. Histo look
  2. What does the nucleus look like? (3)
  3. What does the nucleolus look like?
  4. What else is present on histo?
A
  1. Branching papillae with fibrovascular cores lined by multiple layers of cuboidal to columnar epithelium
  2. longitudinal nuclear grooves (lines along long axis of nucleus);
    ground glass or Orphan Annie eyed nuclei (due to finely dispersed chromatin)
    Intranuclear cytoplasmic inclusions (invaginations of the cytoplasm into the nucleus)
  3. marginated to the periphery and close to nuclear membrane
  4. Psammoma bodies: calcifiled lamellated concretions seen in the cores of papillae
40
Q

Papillary Carcinoma

  1. What is the follicular variant (FVPTC)?
  2. What is the Tall Cell variant? Prognosis?
  3. Who gets the Diffuse Sclerosing variant?
  4. What is a papillary microcarcinoma?
A
  1. diagnosed based on nuclear features; usually encapsulated, lower incidence of LN invasion and metasasis; good prognosis
  2. tall columnar cells with intense eosinophilic cytoplasm lining the papillary structures, aggresssive
  3. occurs in younger individuals
41
Q

Papillary Carcinoma

  1. Presentation
  2. How is it diagnosed?
  3. Treatment?
  4. Prognosis?
  5. What does prognosis depend on?
  6. Genetic Mutations
A
  1. asymptomatic thyroid nodules, LN metastasis; cold on radioiodide uptake
  2. fine needle aspiration cytology
  3. Total thyroidectomy w/ excision of abnormal lymph nodes
  4. Good
  5. age, extrathyroid extension, distant mets; NOT isolated cervical lymph node metastasis
  6. RET/PTC (20-40%); BRAF (33-50%)
42
Q

Follicular Carcinoma

  1. How common?
  2. When does it present?
  3. HIgher in what areas?
  4. Gross look
A
  1. second most common thyroid cancer
  2. older, 40 to 60
  3. iodine deficient areas
  4. single, well circumscribed nodule, light tan appearance, may extend beyond capsule; may have area of hemorrhage
43
Q

Follicular Carcinoma

  1. Microscopic look
  2. Possible variants
  3. What does it look like when it invades?
  4. It is significant if the tumor invades what?
A
  1. fairly uniform follicular cells forming follicles containing colloid; may have nests of cells w/ less apparent follicular differentiation; no psammoma bodies
    2 . Hurthle cell or oncocytic variant (granular pink cytoplasm)
  2. mushrooming of the tumor through the full thickness of the capsule; requires extensive sampling of the tumor capsule interface;
  3. vessels in the capsule or beyond; not if it invades vessels w/in the tumor
44
Q

Follicular Carcinoma

  1. Presentation
  2. How does it spread? Where?
  3. Treatment
  4. What does prognosis depend on?
  5. Prognosis
  6. Genetic Events
A
  1. slowly enlarging painless nodule; cold on scintiscans
  2. hematogneous to bone, lungs, liver
  3. total thyroidectomy w/ radioactive iodine
  4. extent of invasion
  5. > 90% have 10 yr survival
  6. PI3K/AKT (33-50%); PAX8/PPARG fusion product (33-50%)
45
Q

Medullary Carcinoma

  1. What kind of neoplasm? Derived from what cells?
  2. How common?
  3. What can it do?
  4. What causes 30% of them?
  5. When do these 30% present?
  6. How do these 30% present?
A
  1. neuroendocrine; parafollicular or C cells
  2. 5% of thyroid neoplasms
  3. secrete calcitonin or other polypeptide hormones like ACTH or VIP
  4. MEN syndrome 2A or 2B
  5. first decade (sporadic- 4th or 5th decade)
  6. multiple; sporadic-single
46
Q

Medullary Carcinoma

  1. Gross look
  2. Histo look
  3. What do familial medullary cancers have?
  4. What does Congo Red Stain do?
A
  1. solid grey-tan tumor w/o well defined capsule; infiltration of adjacent thyroid parenchyma; larger lesions w/ foci of hemorrhage and necrosis
  2. spindle cells forming nests; acellular amyloid deposits derived from calcitonin;
  3. prominent clusters of C cells
  4. demonstrates amyloid; imparts reddish color; gives an apple green birefringence under polarized light
47
Q

Medullary Carcinoma

  1. Presentation
  2. How may people with MEN present?
  3. When is it more aggressive?
  4. Treatment
  5. 2 Tumor Markers
  6. What may be done in asymptomatic MEN pts?
A
  1. mass, may be asymptomatic; may present w/ paraneoplastic syndromes like diarrhea (VIP), Cushing syndrome (ACTH)
  2. may have endocrine neoplasms in other organs
  3. when it arises in MEN 2B pts
  4. total thyroidectomy
  5. Calcitonin (does not cause hypocalcemia) and CEA (used as tumor markers)
  6. prophylactic thyroidectomy
48
Q

Anaplastic Carcinoma

  1. Age it shows up?
  2. Prognosis
  3. Histo look
  4. What immunohistochemical stain is used?
A
  1. mean is 65 years
  2. poor; mortality is almost 100% in 1 year
  3. highly anaplastic cells: spindle cells, giant cells; foci of papillary or follicular differentiation may be present; mitotic figures
  4. stain for cytokertain; may not stain for thyroglobulin
49
Q

Anaplasit Carcinoma

  1. Presentation
  2. How far has it spread at presentation?
  3. Symptoms
  4. Therapy
  5. When does death occur?
  6. Genetic event
A
  1. rapidly enlarging bulky mass
  2. beyond thyroid into adjacent structures
  3. dyspnea, dysphagia, hoarseness, cough (Due to compression of neck structures)
  4. no effective therapy
  5. usually within 1 year due to compromise of vital structures
  6. inactivation of p53 or activating mutations of beta catenin
50
Q

Thyroglossal duct/cyst

  1. Define
  2. How does it present?
  3. Histo look
  4. complication?
A
  1. incomplete atrophy of the duct where thyroid began in fetus
  2. as a midline cyst/anterior mass; at any age
  3. lined w/ benign epithelium; normal thyroid and lymphocytes in the wall
  4. infection w/ risk of abscess formation

MHD II Test 3 (14 decks)

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