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Endocrine > Non-neoplastic Thyroid Diseases > Flashcards

Non-neoplastic Thyroid Diseases Flashcards

1
Q

Where are the most common sites for ectopic thyroid tissue?

A

Base of the tongue

Pharynx/larynx

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2
Q

What secondary messenger system does thyroid hormone use?

A

Gs protein and AC/cAMP

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3
Q

Why is T4 found more in the blood, but is converted almost entirely to T3 inside cells?

A

T4 has a much longer half life and is more stable/harder to degrade

T3 however has a much higher activity when bound to THR’s and binds with 10x more affinity

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4
Q

Thyrotoxicosis

A

Also known as hyperthyroidism
- this is because the #1 cause is hyper function fo thyroid gland

Is a hyper metabolic state caused by increased circulating levels of free T3 and T4

  • *3 most common causes of thyrotoxicosis**
    1) Graves’ disease (85%)
    2) hyperfunctioning multi nodular goiter
    3) hyperfunctioning adenoma of thyroid gland
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5
Q

Common constitutional symptoms of hyperthyroidism

A

Soft warm and flushed skin w/ associated heat intolerance and excessive sweating
- caused by increased blood flow and peripheral vasodilation as well as increase BMR

Weight loss and increased appetite
- caused by increased sympathetic activity

Steatorrhea and DEAK deficency
- caused by hypermotility of GI tissues

Heart palpitations and tachycardia
- increased B1 adrenergic receptor activation in cardiac tissue as well as increased peripheral oxygen requirements

Proximal muscle weakness, tremors, anxiety
- caused by increased sympathetic

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6
Q

Ocular changes in hyperthyroidism

A

Causes a wide staring gaze and lid lag

  • this is due to excessive sympathetic stimulation to the superior tarsal muscle (mullers muscle)
  • this muscle works with levator palpabrae superioris to elevate eyelid
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7
Q

Thyroid storm

A

Caused by abrupt onset of severe hyperthyroidism

Most often seen in Graves’ disease and occurs due to acute elevation in catecholamines levels

Medical emergency since untreated = cardiac arrhythmias

Symptoms = all hyperthyroid symptoms except to the extreme

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8
Q

Apathetic hyperthyroidism

A

Thyrotoxicosis that occurs in older adults usually incidentally since the thyroid hormone effects are blunted

Usually only found with work up of unexplained weight loss or worsening CV disease

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9
Q

Lab values for hyperthyroidism

A

Low TSH is the most clinically relevant value

  • NOT T3/T4 since these values can be deceiving
  • however T4 is almost always increased when TSH is low (negative feedback)

Rare cases of 2nd or tertiary cause of hyperthyroidism = TSH may be normal or increased

After lab values, get a radioactive iodine uptake test

  • increased uptake diffusely = Graves’ disease most likely
  • increased up take localized = toxic adenoma
  • decreased uptake = thyroiditis
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10
Q

Causes of primary hypothyroidism

A

Congenital
- most common congenital = thyroid dysgenesis or dyshormorgentic goiter (non functional goiter)

Iatrogenic
- caused by surgical or radiation damage or bad ADRs from meds

Autoimmune (most common)

Improper iodine dietary (most common underdeveloped only)

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11
Q

What are the two most common clinical manifestations of severe hypothyroidism?

A

Cretinism (at birth)

  • more common in iodine Deficencies
  • shows: intellectual disability, short stature, coarse facial features, protruding tongues, umbilical hernias and CNS abnormalities
  • NOTE: mental disability is directly tied to time of onset of hypothyroidism (if mother has hypothyroidism before thyroid development = severe mental disability)

Myxedema (in adult hood)

  • generalized fatigue, mental sluggishness and apathy (mimics depression)
  • also shows decreased sweating, cold intolerance and constipation as well as decreased exercise capacity
  • shows increases in total cholesterol and low density lipoprotein levels (LDL)
  • in chronic stages = non pitting edema, enlargement of tongue, deepening of voice and coarse facial features (caused by accumulation of matrix substances in skin) n
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12
Q

Diagnosis of hypothyroidism

A

TSH levels will be elevated
- no feed back from T4 which is low

In secondary or tertiary however, TSH levels will be normal but T4 will still be low

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13
Q

3 most common causes of thyroiditis

A

1) hasimotos
2) granulomatous (De’Quervian)
3) subacute lymphocytic

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14
Q

Chronic lymphocytic hashimoto thyroiditis

A

Is the most common cause of hypothyroidism in areas where iodine is sufficient

Most prominent in women between ages 45-65
- can occur at any age and sex though

Pathogenesis: “antibody-dependent, cell mediated cytotoxicity
- autoimmune response with circulating autoantibodies that bring CD8Tcells to induce chronic fibrosis and infiltrates into thyroid parenchyma via

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15
Q

Genetics and hasimoto thyroidits

A

Heavily linked to genetics with 40% in monozygotic twins

Also 50% of siblings of infected kids also have anti-thyroid antibodies

Increased susceptibility = CTLA4 gene mutations
- normal gene codes for negative regulators of T-cell responses

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16
Q

Clinical features of hashimoto thyroiditis

A

Usually initially presents as mild transient and gradual hypothyroidism with a painless enlargement of thyroid gland
- enlargement is usually symmetric

17
Q

Other diseases that hashimoto is related to

A

Almost always presents with other autoimmune conditions

Increased risk for B-cell non-Hodgkin lymphomas

Is believed to be tied in some way to increased risks of papillary carcinomas of the thyroid

18
Q

Subacute granulomatous thyroiditis

De’Quervian

A

Much less common than hashimoto

More common in 30-50 aged women
- can be anyone though

  • is believed to be initiated via a viral infection or inflammatory processes (NOT AUTOIMMUNE)*
  • many patient’s have a PMH of URI’s shortly before onset

this process spontaneously resolves on its own

Histologically:

  • shows disruption of thyroid follicles which initially have neutrophils built are replaced with macrophages and plasma cells over time
  • also presents with granulomatosis giant cells via colloid reactions and mononuclear infiltrates
  • gross anatomy shows firm enlarged thyroid
19
Q

Clinical features of De’Quervian thyroiditis

A

Is often acute and initially characterized by neck pain (especially with swallowing) fever, malaise and enlargement of thyroid

Also shows transient hyperthyroidism initially and then with progression shows transient hypotension

Also leukocyte and ESR are elevated

Is self-limiting most of the time within 6-8 weeks

20
Q

Subacute lymphocytic thyroidits

Painless/silent thyroiditis

A

Most often precedes pregnancy
- hence why also nicknamed “postpartum thyroiditis”

Is autoimmune etiology and most commonly affects middle-aged women

Always presents with PAINLESS neck masses and hyperthyroidism symptoms
- the thyroid for the most part is NOT enlarged

Is also self-limiting and takes a few months to return to normal

21
Q

Riedel thyroiditis

A

Rare disorder that is a IgG4-related thyroiditis that causes extensive fibrosis of the thyroid and surrounding neck structures

Will simulate a thyroid neoplasm on palpation and often presents with hyperthyroidism first

22
Q

Graves’ disease

A

MOST common cause of endogenous hyperthyroidism
- effects 3% of women in the entire US

Characterized by a triad of

1) thyrotoxicosis
2) infiltrative opthalmopathy with orbital edema and exophthalmos in 40% of patients
3) localized myxedema usually pretibial

Peaks around 20-40 years of age and much more common in women

Very genetic concordance rates in monxygotic twins = 60%
- HLA-DR3 antigens and CTLA-4 (inhibitory T-cell receptor) /PTPN22 (tyrosine phosphatase) genetic mutations all lead to increased

Gross Histology shows symmetrically enlarged thyroid gland with diffuse hypertrophy and hyperplasia of follicular cells
- capsule is still intact though

Microscopic histology shows small papillae in the follicular lumen and tall columnar follicular epithelial cells with a pale staining follicular lumen
- lymphoid infiltrates of primarily T cells is also present through the interstitum

23
Q

Pathogenesis of Graves’ disease

A

Presence of thyroid stimulating immunoglobulin antibody (TSI)
- seen in 90% of patients

This antibody not only destroys circulating TSH, built also binds to TSH receptors and chronically activates them
- this produces hyperthyroidism without elevated T3/T4

Opthalmopathy and orbital edema seen in Graves’ disease is caused by the following:

1) marked infiltration of the retroribtal space by mononuclear cells (predominantly T-cells)
2) inflammatory edema and swelling of extraocular muscles
3) accumulation of extracellular matrix components (especially hyaluronic acid and chondroitin sulfate)
4) increased number of adipocytes

24
Q

What autoimmune diseases are seen in high frequency with graves and hasimotos?

A

SLE

Pernicious anemia

Type 1 diabetes

Addison disease

25
Q

Pathogenesis of dermopathy in Graves’ disease

A

Glycosaminoglycans and T-cell lymphocyte infiltration

Manifests as thickening and scaling fo the skin
- skin also may be slightly pigmented with orange papules

26
Q

Lab values of Graves’ disease

A

Elevated serum T3/T4 With lowered TSH

If using radioactive iodine however, its uptake will be increased compared to normal, even with elevated T3/T4

27
Q

Goiter

A

Enlargement of the thyroid
- mostly common form of all thyroid abnormalities

Diffuse and multi nodular goiters are most common subtypes and are a result of impaired synthesis of thyroid hormones
- most common underlying cause = iodide deficiency

Enlargement of the thyroid is caused by excess TSH being bound to thyroid which induces Hypertrophy of the thyroid

  • if mild = goiter is enough to restore euthyroid
  • if severe = goitrous hypothyroidism
28
Q

Sporadic goiters

A

Less frequent than endemic (iodide induced) goiters

Are more common in females than males and is seen more in puberty/young adulthood

Caused by several conditions including:

  • excessive ingestion of cabbage and cauliflower
  • anything that blocks thyroid hormone synthesis
  • enzyme defects

in most cases = not apparent

29
Q

Multi Nodular goiters

A

Are caused by recurrent episodes or hyperplasia and involution of goiters

Results in long-standing goiters that are massive and ASYMMETRIC

Most commonly are known for causing mass effects

  • airway obstruction
  • dysphagia
  • “superior vena cava syndrome”

If the goiter causes thryotoxicosis = Plummer syndrome
- DOENST show infiltration opthalmopathy

Need to surgically removes these usually

30
Q

What are red flag signs for thyroid malignancies associated with goiters

A

Sudden abrupt enlargement or mass effect symptoms

- especially hoarseness

Endocrine (46 decks)

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