Thyroid Flashcards
most sensitive indicator of mild thyroid dysfunction
MEASUREMENT OF TSH LEVELS (better marker than T4); most are primary disorders, with inverse relationship btw TSH and T4
- Hyperthyroidism: Low TSH
- Primary hypothyroidism: High TSH
TSH can be misleading if:
- TSH dependent hyperthyroid (i.e., at level of hypothalamus or pituitary): elevated T4 due to elevated TSH
- Secondary Hypothyroid: low T4 due to low TSH
Clinical situations in which TBG is increased (thereby increasing amount of bound T4)
Clinical situations where TBG is decreased
Increased TBG:
- Estrogen: i.e., pregnancy or OCPs
- Hepatitis: b/c TBG is made in the liver
Decreased TBG:
- Chronic liver failure
- chronic malnutrition
- protein loss
In general terms, a change in the TBG level will be associated with a change in the total thyroid levels, but not in amount of free/functional T4
- i.e., change in TBG levels does not cause hyper or hypothyroid
Thyroid Uptake and Scan
- Administer tracer dose of radioactive iodine-123
- measure the amount of iodide that the thyroid extracts from the blood as a percent of the total dose
- uptake of iodide is dependent on TSH
- can also see the distribution of Iodide in the gland and evaluate regional abnormalities
cold vs hot nodules
Cold Nodules: Do not take up iodine
Hot Nodules: Take up iodine
Causes of Increased Radioiodine Uptake
- Iodine deficiency
- Stimulation of the thyroid
» Thyroid stimulating immunoglobulins (Graves Disease)
» TSH
» hCG
• Autonomously functioning thyroid nodules
• Recovery phase of thyroiditis
Causes of Decreased Radioiodine Uptake
- Iodine excess • Defect in iodine uptake mechanism • Thyroid failure or ablation • Exogenous suppression of TSH • Active phase of thyroiditis
Thyroid Storm vs. Thyrotoxicosis
- Stress-induced catecholamine surge leading to death by arrhythmia
- a serious complication of Grave’s disease or other hyperthyroid disoders
CNS: Agitation, delerium, coma (vs. restlessness/tremor)
CV: Arrythmias, congestive heart failure (vs. tachycardia, a-fib)
Thermo: Hyperthemia (vs. heat intolerance)
GI: Diarrhea, vomiting, jaundice (vs. frequent defecation)
Etiology of Hyperthyroidism
Common:
- Graves disease
• Toxic multinodular goiter
• Solitary toxic nodule
Rare: - Neonatal Graves disease • Infantile “Familial” thyrotoxicosis • TSH-dependent thyrotoxicosis • CG-secreting neoplasm
- Hyperthyroidism responds to antithyroid drugs or radioiodine ablation
Graves Disease
- an autoimmune hyperthyroidism with thyroid-stimulating immunoglobulins
- presents with diffuse, painless goiter
- Elevated radioiodine uptake with diffuse
distribution of tracer
• Detectable thyroid stimulating
immunoglobulin (TSI); TSI is an IgG; could cross placenta and cause hyperthyroid in the fetus
Extra-thyroid symptoms (unique to Graves):
» Orbitopathy (Propotosis, EOM swelling)
» Pretibial myxedema
Treatment:
- surgery (b/c there is slight increase risk of thyroid cancer)
- radioactive iodide (contraindicated in pregnancy) (permanent hypothyroid is common)
- anti-thyroid drugs
Neonatal Graves Disease
- a pregnant woman with Graves disease passes TSI (IgGs) through the placenta to the baby –> baby develops form of Graves disease as a result of maternal antibodies
- can be treated with anti-thyroid drugs
- would expect condition to resolve as maternal antibodies are cleared
Toxic Multinodular Goiter
- Focal patches of hyperfunctioning follicular cells working independently of TSH due to mutation in TSH receptor (constitutively active) –> increased release of T3/T4
- Hot nodules (rarely malignant), with patches of cold nodules (compensating for the hot nodules)
- Peak age 5th -7th decade
• Insidious onset, may initially be present
as “sub-clinical hyperthyroidism”:
suppressed TSH, normal free T4
• May be exacerbated by acute iodine load,
for example IV contrast (Jod-Basedow phenomenon)
Subacute Thyroiditis
- Self-limited hypothyroidism, often following a flu-like illness
- may be hyperthyroid early in course
» Hard, tender, painful thyroid gland
» Constitutional symptoms
» Sedimentation rate elevated
Histo: granulomatous inflammation
Treatment
» Beta adrenergic blocking agents
» Anti-inflammatory drugs
» May require temporary thyroxine replacement during hypothyroid phase
Silent Thyroiditis
- Early hyperthyroidism, followed by hypothyroidism
- May be a variant of chronic (Hashimoto) thyroiditis
» Painless, non-tender thyroid
» Often noted in post-partum women (“postpartum thyroiditis”); may recur following
subsequent pregnancies
» High risk of permanent hypothyroidism
» Anti-thyroid peroxidase antibody often
detectable - Treatment: Beta adrenergic blocking agents
Etiology of Hypothyroidism
Goitrous
- Chronic thyroiditis
• Dyshormonogenesis
• Iodine deficiency
Non-Goitrous - Post-ablative • Atrophic thyroiditis • Developmental defects • Central hypothyroidism
Hashimoto’s Thyroiditis
- Most common cause of hypothyroidism
- An autoimmune disorder, with antibodies against thyroid peroxidase and and thyroglobulin
- presents with firm, irregular goiter
- May be associated with other autoimmune diseases, e.g., SLE, rheumatoid arthritis
- Associated with HLA-DR5
Histo:
- HURTHLE CELLS: cuboidal cells that ling the follicles, with abundant mitochondria, giving them a pink, granular appearance in sections
- lymphocytic infiltrate with germinal centers
Tx: administer PURE T4 to normalize TSH
Course: development of lymphoma of the thyroid
What is the gold standard treatment for hypothyroidism?
PURE T4
- combination therapies will not be the right answer
Neonatal Hypothyroidism
• Incidence (U.S.):
» Caucasian 1:5,500 births
» African-American 1:32,000 births
• Etiology » In-born errors of hormone synthesis or iodine uptake » Thyroid agenesis » Ectopic thyroid » TSH receptor mutations » Thyroid hormone resistance
• Screening: Neonatal TSH and T4
• Treatment:
» Thyroxine 6-8 mcg/kg/d
» TSH may not normalize immediately
• Neuropsychological outcome » IQ generally normal if treatment is started within the first three months of life » Outcome dependent on severity of hypothyroidism in utero and at time of diagnosis
Iodine Deficiency Disorders
• Goiter • Childhood and adult hypothyroidism • Neonatal hypothyroidism • Cretinism • Worsened public health » Infant mortality » Growth retardation » Diminished intelligence
Cretinism
- due to severe fetal hypotyroidism, often occuring where endemic goiter is prevalent (iodine deficiency)
- sporadic cretinism is due to defect in T4 formation or developmental failure in thyroid formation
Findings:
- Pot-bellied
- Pale
- Puffy-faced child
- Protruding umbilicus
- Protuberant tongue
- Myxedema
- Delayed sexual maturation
Neurologic » Severe mental retardation » Deaf mutism » Spastic paresis » Gait disturbance » Oculomotor dysfunction
Multinodular Goiter
• May be asymptomatic • Obstructive symptoms: compress recurrent laryngeal nerve » Neck discomfort » Dysphagia » Stridor » Voice change • Thyrotoxicosis (Toxic multinodular goiter) » Symptomatic » Subacute » Iodine-induced
Treatment for non-toxic multinodular goiter:
• Observation
• Surgery
• Radioactive iodine
• Thyroxine suppression (Generally not effective): give exogenous thyroxine to suppress thyroid activity
» May be helpful if TSH is elevated
» Do not suppress if TSH is below normal
Solitary Thyroid Nodules
• Benign or malignant?
» Approximately 5-10% of solitary thyroid nodules will prove to be malignant
• Functioning or nonfunctioning?
» 80% to 90% of solitary nodules are nonfunctioning (“cold”)
» Hot nodules are virtually never malignant
• Local effects
» Discomfort
» Appearance
Thyroid Cancer / Malignancies
Tumors of Follicular Cells:
- Papillary carcinoma
- Follicular carcinoma
- Anaplastic carcinoma
Tumors of C Cells:
4. Medullary carcinomas
Other:
- Lymphoma
- Squamous cell carcinoma
- Metastatic
Papillary Carcinoma
- most common thyroid cancer
- Head & neck radiation during childhood is greatest risk factor
- excellent prognosis
- Often multifocal or bilateral
- Spread is by local lymphatics and by direct
invasion of surrounding structures
Histo:
- Ophan Annie Nuclei: empty-appearing nuclei
- Psammoma bodies
- Nuclear grooves
Prognostic Factors: - Age: good prognosis if < 40 yo - Sex: male sex is worse • Local invasion • Distant metastases • Tumor size
Follicular Carcinoma
- Presents with uniform follicles
- More common in areas of chronic iodine
deficiency
• Distant metastases: lung, bone liver,
brain
• Follicular cancer cannot be distinguished from follicular adenoma by fine needle aspiration cytology
Hurthle cell carcinoma
» Variant of follicular cancer
» Usually does not take up radioiodine
