Thyroid Dysfunction Flashcards
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
- Autonomous activation of the TSH receptor (due to TSH receptor mutation) on hot nodules
- 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
- Autoimmune lymphocytic thyroiditis (Hashimoto’s Disease)