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DEMS: Unit III > Thyroid Dysfunction > Flashcards

Flashcards in Thyroid Dysfunction Deck (25)
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Major signs and symptoms of hyperthyroidism

  • Nervousness, anxiousness, restlessness, hand tremor
  • Irritability
  • Heat intolerance
  • Increased sweating
  • Increased appetite
  • Increased frequency of bowel movements
  • Weight loss
  • Muscle weakness
  • Exophthalmos and rapid heart beat


Disorders leading to hyperthyroidism

  • Graves Disease - 0.5% of the population
  • Iatrogenic
  • Hot nodule / toxic adenoma
  • Toxic / multinodular goiter
  • Subacute thyroiditis
  • Silent (postpartum) thyroiditis
  • Pituitary TSH overproduction
  • Other: 
    • Struma ovarii
    • Jod Basedow
    • Molar pregnancy


Graves Disease: etiology

  • Most common form of hyperthyroidism - occurs in 0.5% of the population
  • Etiology
    • Autoimmune disease (Type II hypersensitivity) - circulating IgG directed at TSH receptor --> IgG interact with TSH receptor, stimulate thyroidal function
    • Neonatal Graves: hyperthyroid infant born to mother with Graves disease; infant's hyperthyroidism disappears over several months (disappearance of maternal IgG)


Graves Disease: clinical presentation and lab tests

  • Clinical triad often presents during stress:
    • Hyperthyroidism: diffuse hyperfunctional enlargement of thyroid (toxic diffuse goiter with bruit)
    • Infiltrative ophthalmopathy with resultant exophthalmos (bulging of eye anteriorly)
    • Localized, infiltrative dermopathy (pretibial myxedema) in a minority of patients
  • Lab tests:
    • Increased T3/T4
    • Decreased TSH
    • Increased radioactive iodine uptake (RAIU)


Factitious/iatrogenic thyrotoxicosis: etiology, clinical presentation, lab tests

  • Etiology:
    • Exogenous TH shuts off pituitary TSH production/release --> causes thyroid gland to atrophy
  • Clinical presentation: 
    • Thyrotoxicosis (aka hyperthyroidism)
  • Lab tests:
    • Increased T3/T4
    • Decreased TSH
    • Majorly decreased RAIU (may be zero)


Toxic adenoma (hot nodule): etiology, clinical presentation, lab tests

  • Etiology:
    • AKA autonomous adenoma
    • Cells are clonal expansion of single mutated cells
    • Ex. TSH receptor gain of function mutation --> constitutively active thyroid follicle cells
    • Mutated cells lead to increased growth and increased hormone production
    • Overproduction of TH by nodule suppresses pituitary TSH --> remainder of thyroid gland shrinks
  • Clinical presentation:
    • Thyrotoxicosis (hyperthyroidism)
  • Lab tests:
    • Increased T3/T4
    • Decreased TSH
    • Increased RAIU localized at area of nodule


Toxic nodular goiter (toxic multinodular goiter): etiology, clinical presentation, lab tests

  • Etiology:
    • Autonomous activation of the TSH receptor (due to TSH receptor mutation) on hot nodules
      • Focal patches --> hyperfunctioning follicular cells
    • Iodine is substrate for unregulated thyroid hormone synthesis
    • Multiple areas of autonomy may exist surrounded by non-functioning areas + suppressed normal thyroid tissue
  • Clinical presentation: 
    • Thyrotoxicosis which may develop slowly over a number of years
    • Goiter
    • Hyperthyroidism can be induced by injudicious administration of TH if areas of thyroid are autonomous, but not sufficiently active to produce toxicity
  • Lab tests:
    • Increased T3/T4
    • Decreased TSH
    • Increased RAIU in some "hot areas"
    • Decreased RAIU in "cold areas"


Subacute thyroiditis (giant cell thyroiditis, De Quervain's thyroiditis): etiology

  • Viral infection causes viral or thyroid antigen, released secondary to virus-induced host tissue damage
  • Antigen stimulates cytotoxic T lymphocytes --> damage thyroid follicular cells
  • In contrast to autoimmune disease: this immune response is virus-initiated, non-self-perpetuated --> process is limited
  • Thyroid gland leaks T3, T4, and inactive iodinated compounds


Subacute thyroiditis: clinical presentation and lab tests

  • History of viral URI that spreads to thyroid --> externally sore throat (neck) & radiation of pain to neck and ears
  • Swollen and tender thyroid gland, fever, hypermetabolism
  • Course: initially hyperthyroidism, as it subsides --> euthyroidism, hypothyroidism, finally euthyroidism
    • May subside over months
  • Course is important to know to not confuse with early Graves or late Hashimoto
  • Lab tests:
    • Increased T3/T4 (during hyperTH phase)
    • Decreased TSH
    • Decreased RAIU
    • Increased ESR


Silent thyroiditis: etiology, clinical presentation, lab tests

  • Etiology:
    • Likely autoimmune --> lymphocytic thyroiditis and autoAbs present in 50-75% of cases
    • 5-8% of pregnancies followed by silent thyroiditis, especially in patients with other autoimmune disease like T1D
  • Clinical presentation:
    • Mild hyperthyroidism, non-tender enlargement of thyroid gland
    • Hypothyroidism may follow before return to euthyroid state is achieved
    • Clinical course may be recurrent over a matter of years - predilection for postpartum occurrence of this entity
  • Lab tests:
    • Increased T3/T4
    • Decreased TSH
    • Decreased RAIU
    • Normal ESR
    • Lymphocytic pathology


Pituitary overproduction of TSH: etiology, clinical presentation, lab tests

  • Etiology:
    • Pituitary tumor that secretes TSH or pituitary resistance to T3 --> relative excess of TSH & overproduction of thyroid hormones that cause hyperthyroidism
    • Very rare
    • Thyroid hormone resistance due to mutations in TRb receptor in ligand binding domain
  • Clinical presentation:
    • Thyrotoxicity
  • Lab tests:
    • Increased T3/T4
    • Increased TSH


Other causes of hyperthyroidism (3)

  • Struma ovarii
    • Hyperfunctioning thyroid tissue found in ovaries
    • Increased RAIU in pelvis
  • Jod-Basedow
    • Iodide induced hyperthyroidism, particularly in areas of iodide deficiency
    • Recently noted with multinodular goiters as well
  • Molar pregnancy
    • Hyperthyroidism
    • Possibly hCG stimulates thyroid (same a-subunit as TSH)


Major signs/symptoms of hypothyroidism

  • Metabolic pathways slow down
  • Every organ system malfunctions
  • Myxedema includes all hypothyroid symptoms
    • Fatigue
    • Somnolence
    • Decreased appetite
    • Weight gain
    • Dry skin
    • Brittle hair and anils
    • Cold intolerance
    • Constipation
    • Muscle cramps
    • Headaches
  • Patients appear sluggish and puffy, with cool dry skin and slow heart rate
  • Myxedema coma --> severe hypothyroidism leads to decreased mental status & hypothermia


Lab tests for hypothyroidism

  • Decreased T4 and decreased free T4
  • RAIU and TSH used to narrow differential diagnosis


Primary hypothyroidism: etiology

  • Pathology interfering with thyroid gland function --> decreased release of thyroid gland
  • Two most common causes:
    • Autoimmune lymphocytic thyroiditis (Hashimoto's Disease)
      • Very common
      • Seen in 5-10% of the population, incidence increases with age
      • Patient has circulating autoantibodies against thyroglobulin and/or thyroid peroxidase
    • Radioactive iodine ablation of the thyroid
      • Common treatment for Graves' Disease, hot nodule, and multinodular goiter


Primary hypothyroidism: clinical presentation

  • Goiter: 
    • When thyroid fails, pituitary increases production of TSH to compensate --> goiter
    • But if abnormality is destructive, goiter may not appear or may disappear in late course of disease
  • Hypothyroidism/myxedema
  • Onset of Hashimoto's disease is gradual
    • May be preceded by transient thyrotoxicosis caused by disruption of thyroid follicles w/ secondary release of thyroid hormones


Primary hypothyroidism: lab tests

  • Primary hypothyroidism:
    • Decreased T3/T4
    • Increased TSH
    • Decreased RAIU
  • Transient thyrotoxicosis:
    • Increased T3/T4
    • Decreased TSH
    • Decreased RAIU


Secondary (pituitary) hypothyroidism: etiology, clinical presentation, lab tests

  • Etiology:
    • Pituitary insufficiency (due to a variety of causes)
  • Clinical presentation:
    • Hypothyroidism/myxedema 
    • Accompanied by multiple hormone deficiencies
    • Occasionally TSH deficiency may be isolated
  • Lab tests:
    • Decreased T3/T4
    • Decreased TSH
      • Responds poorly to TRH stimulation
    • Decreased RAIU


Tertiary (hypothalamic) hypothyroidism: etiology, clinical presentation, lab tests

  • Etiology:
    • Hypothalamic failure (due to a variety of causes)
  • Clinical presentation:
    • Hypothyroidism/myxedema accompanied by multiple trophic hormone failure
  • Lab tests:
    • Decreased T3/T4
    • Decreased TSH
      • Responds well to TRH stimulation


Distinction between primary and secondary hypothyroidism

  • Critical
  • 2ndary hypothyroidism: 
    • Therapy with TH may unmask latent pituitary ACTH deficiency (accelerates cortisol metabolism) --> precipitate acute adrenal insufficiency
    • Always administer cortisol first (before TH)


Tests used to evaluate thyroid function: serum thyroxine

  • Total T4
  • Major hormone produced by thyroid gland
  • Important to remember that bound hormone comprises 99.975% of circulating hormone
    • Free hormone is metabolically active
  • Normal: 4-12 ug/dL
  • Influenced by thyroidal secretion and level of thyroxine binding proteins in circulation
    • Pregnancy: Increased TBG --> increased total T4
      • Patient is euthyroid because serum free T4 is normal
    • HyperTH: increased total T4 and increased free T4
    • Decreased TBG: decreased total T4 and normal free T4 --> euthyroid


Tests used to evaluate thyroid function: free thyroxine

  • Not really well measured due to low concentration
  • Normal: 0.58 - 1.64 ng/dL


Tests used to evaluate thyroid function: triiodothyroxine

  • Levels measured by radioimmunoassay
  • Active TH in circulation
  • Normal: 90-190 ng/dL


Tests used to evaluate thyroid function: serum TSH

  • Accurate measurements are most valid and important assessments of thyroid function
  • Normal: 0.5 - 5.0 ug/mL
    • 1ary hypoTH: increased TSH
    • 2ndary hypoTH: decreased TSH
  • Increased TSH may be first sign of thyroid failure
  • Increased TSH --> inadequate T3/T4 production
  • HyperTH: decreased TSH 
    • Unless pituitary in origin --> increased TSH


Tests used to evaluate thyroid function: serum thyroglobulin (TG)

  • Not a measure of thyroid hormones
  • Measure of thyroidal protein secretion
  • Used to follow thyroid cancer patients - TG is tissue-specific marker for thyroid disease
    • Reverse T3: recent data suggest conversion of T4 to T3 or rT3 is important branch point, under metabolic control
    • Starvation/steroid administration/severe illness: T4 preferentially inactivated to rT3 in lieu of active T3
    • Euthyroid sick syndrome or non-thyroid illness