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Endocrine > thyroid > Flashcards

thyroid Flashcards

1
Q

Thyrotoxicosis:

A

Thyrotoxicosis: hypermetabolic state caused by elevated circulating levels of free T3 and T4

– Most commonly from hyperthyroidism
– Can also be from excessive release of preformed thyroid hormone (e.g., in thyroiditis)

– Extrathyroidal source

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2
Q

most common causes of hyperthyroidism

A
  1. Diffuse hyperplasia (Graves disease)
  2. Hyperfunctioning (“toxic”) multinodular goiter
  3. Hyperfunctioning (“toxic”) adenoma
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3
Q

What are the primary causes of hyperthyroidism?

A

Primary:

  1. Diffuse hyperplasia (Graves disease)
  2. Hyperfunctioning (“toxic”) multinodular goiter
  3. Hyperfunctioning (“toxic”) adenoma
  4. Iodine‐induced hyperthyroidism
  5. Neonatal thyrotoxicosis associated with maternal Graves disease
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4
Q

Secondary causes of hyperthyroidism

A

Secondary:
– TSH‐secreting pituitary adenoma (rare)

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5
Q

Disorders of THYROTOXICOSIS thare ARENT associated with hyperthyroidism?

A
  1. Granulomatous (de Quervain) thyroiditis (painful)
  2. Subacute lymphocytic thyroiditis (painless)
  3. Struma ovarii (ovarian teratoma with ectopic
  4. thyroid)
  5. Factitious thyrotoxicosis (exogenous thyroxine intake)
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6
Q

Name the 4 cardiac symptoms related to thyrotoxicosis

A
  1. Tachycardia, palpitations, and cardiomegaly common
    1. From elevated cardiac contractility and cardiac output
      1. response to increased peripheral oxygen requirements
  2. Arrhythmias particularly atrial fibrillation
    1. occur frequently esp. in older patients
  3. Congestive heart failure in those with preexisting cardiac disease
  4. Thyrotoxic or hyperthyroid cardiomyopathy
    1. Reversible left ventricular dysfunction and “low‐output” heart failure
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7
Q
A

hyperthyroidism

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8
Q

Advanced age and co‐morbidities may blunt features that typically bring younger patients to attention

A

apathetic hyperthyroidism

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9
Q

most useful single screening test for hyperthyroidism. how is the test subsequently confirmed?

A

TSH, followed by free T4 (will be increased)

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10
Q

how would you test for a secondary cause of hyperthyroidism?

A
  1. Rare secondary cause is pituitary‐associated): TSH levels are either normal or raised
  2. Thyrotropin‐releasing hormone (TRH) stimulation test
    1. ​A normal rise in TSH after administration of TRH excludes secondary hyperthyroidism
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11
Q

Radioactive iodine test for

  1. grave’s
  2. toxic adenoma
  3. thyroiditis
A
  1. Diffusely increased uptake in the whole gland (Graves disease)
  2. Increased uptake in a solitary nodule (toxic adenoma)
  3. Decreased uptake (thyroiditis)
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12
Q

Treatments for hyperthyroidism

A
  1. B blockers to tx symptoms
  2. thionamide to block hormone synthesis
  3. iodine to prevent release of thyroid hormone
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13
Q

Causes of Primary Hypothyroidism

A
  1. Causes of Primary Hypothyroidism
    1. Autoimmune: Hashimoto thyroiditis
    2. Iodine deficiency
    3. Iatrogenic (postablative): surgery, radioiodine therapy, external radiation
    4. Drugs: Lithium, iodines, p‐aminosalicylic acid
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14
Q

drugs associated with primary hypothyroidism

A

Lithium, iodines, p‐aminosalicylic acid

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15
Q

The RARE causes of primary hypothyroidism and secondary causes

A
  1. Rare
    1. Thyroid hormone resistance syndrome (THRB mutations)
    2. Congenital biosynthetic defect (dyshormonogenetic goiter)
    3. Genetic defects in thyroid development (PAX8, FOXE1, TSH receptor mutations)
  2. Secondary
    1. rare: Pituitary or hypothalamic failure
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16
Q

cretinism

A
  1. Cretinism:
    1. Hypothyroidism in infancy or early childhood
    2. Found where dietary iodine deficiency is endemic
      1. Himalayas, inland China, Africa, and other mountainous areas
    3. Much less prevalent due to iodine food supplementation
    4. Rarely from dyshormonogenetic goiter
      1. Genetic defects that interfere with the biosynthesis of thyroid
    5. hormone
      1. 0rMaternal T3 and T4 cross the placenta and are critical for fetal brain development
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17
Q

Serum TSH in primary hyperthyroidism and secondary hyperthyroidism

A

serum TSH is either HIGH (rare- indicates secondary hyperthyroidism, which would be a TSH-secreting tumor) or LOW (expecte because of negative feedback in primary hyperthyroidism)

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18
Q

myxedema

A

Myxedema: Hypothyroidism in older child or adult

  1. Broadening and coarsening of facial features
  2. Enlargement of the tongue
  3. Deepening of the voice
  4. Generalized fatigue, apathy, and mental sluggishness (can mimic depression)
  5. Speech and intellectual functions are slowed
  6. Listless, cold intolerant, and frequently overweight
  7. Decreased sympathetic activity → constipation and decreased sweating
    8.
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19
Q

nonpitting edema

A

myxedema- hypothyroidism in grown children or adults

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20
Q

total cholesterol and LDL levels in hyperthyroidism

A

increased

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21
Q
A

hypothyroidism

22
Q

account for the majority of hypothyroid cases

A

hoshimoto’s thyroiditis and postablative hypothyroidism

23
Q

Serum TSH levels: high, normal, low

A

high: either primary hypothyroidism or the rare TSH secreting pituitary adenoma causing secondary hyperthyroidism

Normal: normal or secondary hypothyroidism

low: primary hyperthyroidism

24
Q

T3 and T4 levels in hyper/hypothyroidism

A

increased in all cases of hyperthyroidism, decreased in all cases of hypthyroidism

25
Q

Hashimoto Thyroiditis: relative frequency, peak incidence, age preferences? what is it?

A
  1. Hashimoto Thyroiditis
    1. Most common cause of hypothyroidism in areas of the world where iodine levels are sufficient
    2. Peaks between 45 and 65 yrs
    3. W >>> M (ratio of 10 : 1 to 20 : 1) – Can occur in children
    4. Autoimmune destruction of the thyroid gland
    5. Gradual and progressive thyroid failure
26
Q

Hashimoto Thyroiditis

What causes it, genetics

A

Hashimoto Thyroiditis

  1. Most common cause of hypothyroidism in areas of the world where iodine levels are sufficient
  2. Peaks between 45 and 65 yrs
  3. W >>> M (ratio of 10 : 1 to 20 : 1)
  4. Can occur in children
  5. Autoimmune destruction of the thyroid gland
  6. Gradual and progressive thyroid failure

Autoantibodies

  1. Anti‐microsomal
  2. antithyroid peroxidase
  3. antithyroglobulin
  4. Strong genetic association with polymorphisms in both CTLA4 and PTPN22 • Type 1 Diabetes is too
27
Q

Hoshimoto Morphological changes

A
  1. Thyroid is typically diffusely enlarged (goitrous)
  2. Prominent mononuclear inflammatory infiltrate:
    1. Lymphocytes, plasma cells, and germinal centers
  3. Thyroid follicles are atrophic/lost
  4. Areas with “Hürthle cell” metaplasia
  5. Epithelial cells with abundant eosinophilic, granular cytoplasm
  6. Fibrosis: Does not extend beyond the capsule of the gland
28
Q

clinical course of hoshimoto

A

usually comes to attention because of painless enlargement.

usually symmetric and diffuse

usually produces hypothyroidism

in some it is preceded by thyrotoxicosis “hyperthroidism–> subsequent hypothyroidism” “hoshitoxicosis”

29
Q

“hashitoxicosis”

A

Disruption of thyroid follicles–> release of thyroid hormones (“hashitoxicosis”)–> free T4 and T3 levels elevated–>TSH is diminished–>radioactive iodine uptake is decreased

30
Q
  1. Typically presents with painless mild hyperthyroidism and/or goitrous enlargement
    1. Most common age group
    2. Most common gender
    3. Variant
A

Subacute Lymphocytic Thyroiditis

  1. Painless
  2. Typically presents with:
  3. Mild hyperthyroidism and/or – Goitrous enlargement
  4. Most common in middle‐aged pts (can occur at any age)
  5. W>M
  6. Postpartum thyroiditis: ~5% women postpartum
    1. Variant of autoimmune thyroiditis
    2. Most have circulating antithyroid peroxidase antibodies or a family history of other autoimmune disorders
    3. Up to 1/3 evolve into overt hypothyroidism
31
Q

distinguishing Subacute Lymphocytic Thyroiditis from Hoshimoto

A

Lymphocytic infiltration with large germinal centers, p**atchy disruption<strong> </strong>and collapse of thyroid follicles

No fibrosis or Hürthle cell metaplasia: differentiates it from Hashimoto thyroiditis

32
Q

Granulomatous Thyroiditis aka De Quervain thyroiditis

age, gender, etiology, common association

A

Granulomatous Thyroiditis aka De Quervain thyroiditis

  1. Typically affects pts 40‐50 yrs
  2. W> M
  3. Thought to be from an immune response triggered by a viral infection
    1. Majority of patients have a hx of an URI just before the onset of thyroiditis
  4. Seasonal incidence, with occurrences peaking in the summer
  5. Self‐limited
33
Q
  1. Unilaterally or bilaterally enlarged and firm
  2. Capsule is intact, but may be stuck to surrounding structures
  3. Histology varies and can be patchy

Early: Neutrophilic microabscesses in damaged follicles

– Later: aggregates of lymphocytes, macrophages, and plasma cells associated with damaged follicles

  • Multinucleated giant cells around colloid • Fibrosis may replace the foci of injury
  • Different histologic stages are sometimes found in the same gland, suggesting waves of destruction over a period of time
A
  1. Unilaterally or bilaterally enlarged and firm
  2. Capsule is intact, but may be stuck to surrounding structures
  3. Histology varies and can be patchy

Early: Neutrophilic microabscesses in damaged follicles

Later: aggregates of lymphocytes, macrophages, and plasma cells associated with damaged follicles

Multinucleated giant cells around colloid • Fibrosis may replace the foci of injury

Different histologic stages are sometimes found in the same gland, suggesting waves of destruction over a period of time

34
Q

Most common cause of thyroid pain

A

granulomatous thyroiditis

35
Q

clinical course of Granulomatous Thyroiditis

A

most common cause of painful thyroid

Variable enlargement of the thyroid

Inflammation and hyperthyroidism are transient: diminish 2 to 6 weeks even without treatment–> normal thyroid function after 6‐8 weeks

High serum T4 and T3 levels and low serum TSH levels

Radioactive iodine uptake is diminished

– Unlike Graves disease

36
Q
A

hoshimoto’s, would need more to differentiate it from Subacute Lymphocytic Thyroidits

37
Q
A

Granulomatous Thyroiditis

38
Q

a thyroid inflammatory condition that mimics thyroid carcinoma

A

Reidel’s thyroiditis

  1. Rare
    1. Extensive fibrosis of the thyroid and
    2. Surrounding structures
  2. Clinically mimics thyroid carcinoma
    1. A form of systemic autoimmune IgG4‐related sclerosing disease
  3. Can affect other organs
39
Q

Most common cause of endogenous hyperthyroidism

A

grave’s

40
Q

Most common cause of endogenous hyperthyroidism

incidence, gender, age, clinical description, cause

A

Grave’s Most common cause of endogenous hyperthyroidism

~ 2% of US women (W>>>>M)

Peaks 20‐40 yrs

  1. Triad of clinical findings:
    1. Hyperthyroidism and thyrotoxicosis
      1. associated with diffuse enlargement of the gland
    2. Infiltrative ophthalmopathy
      1. ​resultant exophthalmos
    3. Localized infiltrative dermopathy: pretibial myxedema
      1. only in a minority of patients
41
Q

Pathogenesis of Grave’s

A

Multiple autoantibodies but 90% of pts have thyroid‐stimulating immunoglobulin (TSI): most important and specific one

TSI: Binds to the TSH receptor and mimics its actions → release of thyroid hormones

Some also have TSH receptor blocking antibodies in the circulation

Can lead to hypothyroidism in a minority of pts

Genetic susceptibility linked to polymorphisms in immune‐function genes CTLA4 and PTPN22 and the HLA‐DR3 allele

42
Q
A

Grave’s, scaloped margins and papillae w/out a fibrovascular core

43
Q

Graves

  1. Thyroid gland:
  2. Follicular cells:
  3. Colloid:
  4. Immune cells:
A
  1. Thyroid gland
    1. symmetrically enlarged
    2. Diffuse hypertrophy and hyperplasia of thyroid
  2. follicular epithelial cells
    1. Follicular cells are tall and more crowded
    2. Can even form small papillae that project into the lumen
      1. Lack fibrovascular cores (in contrast to papillary carcinoma)
  3. Colloid is pale with scalloped margins
  4. Inflammatory infiltrates of
    1. lymphocytes and plasma cells
    2. Germinal centers are common
44
Q

Sx associated with graves

Sx associated uniquely with Graves disease:

A

thyrotoxicosis, degree varies

Sx associated uniquely with Graves disease:

  1. Diffuse hyperplasia of the thyroid, ophthalmopathy, and dermopathy
  2. Increased blood flow through the hyperactive gland can produce an audible “bruit”
45
Q

Graves: opthalmopathy, surprising reversal of thyroid function, risk for other conditions

A

Exophthalmos may persist or progress despite successful treatment of the thyrotoxicosis

Sometimes pts spontaneously develop thyroid hypofunction

Increased risk for other autoimmune diseases

  1. Systemic lupus erythematosus
  2. Pernicious anemia
  3. type 1 diabetes
  4. Addison disease
46
Q

Lab findings in Graves

A

Low TSH levels

High free T4 and T3 levels

Radioiodine shows diffusely increased uptake

47
Q

how do goiters form?

A

decreased iodine –> decreased thyroid hormone produced –> increased thyroid stimulating hormone -> increased folliciular hyperplasia/hypertrophy –> increased thyroid mass

48
Q

Sporadic Goiter: peak, preferrence, cause, clinical

A

Sporadic Goiter (less frequent)

  1. Peaks at puberty or in young adult life
  2. F>>>> M
  3. Causes:
    1. Ingestion of substances that interfere with thyroid hormone synthesis
    2. Hereditary enzymatic defects that interfere with thyroid hormone synthesis
    3. Mostly unknown
  4. Clinical:
    1. Majority are euthyroid although TSH is ususaly elevated (and T3 and T4 levels are normal)
    2. Symptoms are from mass effects
49
Q

multi nodular goiter

  1. how they arise
  2. settings in which they arise
  3. common clinical confusion
  4. sporadic vs endemic
A

Simple goiter→ multi nodulargoiter

  1. Recurrent episodes of hyperplasia and involution
  2. Virtually all long‐standing simple goiters convert into multinodular goiters
  3. Produces the most pronounced thyroid enlargements
  4. Can be mistaken for neoplasms
  5. Occur in both sporadic and endemic forms
50
Q

Clincai manifestations of multinodular goiter, related syndromes

A

Most symptoms are from:

  1. mass effects, cosmetic concerns
  2. airway obstruction, dysphagia
  3. Most pts are euthyroid
  4. Plummer syndrome: autonomous nodule develops in a long‐standing goiter and produces hyperthyroidism (toxic multinodular goiter)
    1. ~10% of multinodular goiters over 10 yrs
  5. superior vena cava syndrome: compression of large vessels in the neck and upper thorax
  6. Incidence of malignancy in long‐standing multinodular goiters <5%
  7. Dominant nodule can show up as a “solitary thyroid nodule”
    1. Mimics a thyroid neoplasm
51
Q

multinodular goiter work up (so a patient comes into the office exhibiting a large thyroid/neck mass

A
  1. radioiodine scan
    1. Uneven iodine uptake and sometimes a “hot” nodule
      1. From an admixture of hyperplastic and involuting nodules
  2. A fine‐needle aspiration can be helpful in evaluating a dominant nodule to distinguish between hyperplasia vs neoplasm

Endocrine (20 decks)

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