primary: low T4/T3 from thryoid
secondary: low TSH from pituitary
tertiary: low TRH from hypothalamus
The most common cause of primary hypothyroidism is
chronic lymphocytic thyroiditis (also known as Hashimoto’s thyroiditis).
Explain pathogenesis of Chronic lymphocytic thyroiditis
Sensitization of the host’s own lymphocytes to various thyroidal antigens including thyroglobulin, thyroid peroxidase, and the TSH receptor.
What can we detect in pts serum to dx Chronic Lymphocytic Thyroiditis.
is this a genetic or environmental condition?
Antibodies to one or more of these antigens can be detected in many patients.
Environmental factors (viral or bacterial infection, or high iodine intake) and genetic factors (e.g. defects in suppressor T lymphocytes) may be responsible for initiating the autoimmune process.
what causes the glandular destruction seen in chronic lymphocitic thyroiditis?
Cytokine release and inflammation ultimately result in glandular destruction.
Causes of primary hypOthyroidism
Chrnic lyphocytic thyroiditis
reversible automimmne thyroiditis
iodine deficency or excess
drugs: antiT drugs or Lithium
Causes of secondary/tertiary Hypothyroidism
tumors, trauma, inflitrative disease, drugs (Dopaimne or Glucocorticoids)
inactivationg mutations in gens coding for various proteins in hypothalamic-pit-thyroid axis
Signs and symptoms of hypothyroidism
, including lack of facial expression, dry and pale skin, absence of hair on the lateral third of the eyebrow, and puffiness of the face and lips (due to accumulation of mucopolysaccharides in the dermis). The nose is broadened, the tongue is large, smooth, red, and clumsy, and there is drooping of the eyelids
Severe hypothyroidism, sometimes referred to as ________, can be life threatening. This scenario is characterized by multiorgan dysfunction, profound hypothermia, hypoventilation, and hypotension; central nervous system signs are evident on physical examination.
What is the first test we perform when we suspect individual has hypOthryoidism
What is the relationship between TSH and T4
log linear: small change in T4 shows BIG change in TSH
If TSH is abnormal, or there is a high clinical index of suspicion for a central disease process, a ____is ordered to further characterize the thyroid condition
how TSH can be ‘normal’ in secondary hypothyroidism?
With low free T4 and T3, the NORMAL response of the pituitary would be an increase in TSH. If TSH is NOT increased, it is considered “inappropriately normal”. The few remaining normal thyrotrophs are working as hard as they can to restore thyroid function, and the best they can do is maintain TSH within the reference range. However, it is not enough TSH to restore thyroid function.
TSH levels are elevated
Free T4 and T3 are LOW
see + thyroid peroxidase thyroglobulin antibodies
See decreased or normal TSH
LOW T3 and T4
negative for thryoid peroxidase antibodies
You find your patient has CENTRAL hypothyroidism (low or normal TSH and low Free T4)
what test/imaging should you get next?
order MRI of the pititary and hypothalamus
What is the treatement of Primary Hypothyroidism
Thyroid hormone is most often administered as T4 alone (levothyroxine
you start a pt on levothyroxine for primary hypothyroidism, when do you re-check their levels to judge effectiveness of treatement?
Because the half-life is approximately 7 days, we generally wait at least 5-6 half-lives before retesting and adjusting the thyroid hormone dose to achieve a TSH level between approximately 0.5 and 4 mU/L.
Why is Liothyronine not commonly prescribed to tx Primary hypothyroidism
Liothyronine (synthetic version of triiodothironine/T3) is also available, but not commonly used because T4 is converted to T3 in peripheral tissues, and T3 has a short half-life with a need for frequent dosing.
Common causes of HyPERthyroidism
The most common causes of primary hyperthyroidism are Graves’ disease (diffuse toxic goiter), toxic multinodular goiter, solitary toxic (follicular) adenoma, and “thyroiditis” (destruction d/t inflammation)
How does thyroiditits cause HYPERthryoidism if its destruction of the thryoid gland?
Hyperthyroidism results from release of preformed thyroid hormone in this setting.
Secondary hyperthyroidism is a very rare condition due to a
TSH-secreting pituitary adenoma.
Graves’ disease is an autoimmune condition of unknown cause. It is more common in____ and has a strong familial predisposition. Proposed environmental triggers include:
stress, tobacco use, infection, and iodine exposure
Proposed pathophysiology of Graves
pathophysiology of Graves’ disease involves a defect in suppressor T lymphocytes (Ts) that allows helper T lymphocytes (TH) to stimulate B lymphocytes (B) to synthesize thyroid autoantibodies.
What is the driving cause for thyrotoxicosis in Graves?
thyroid-stimulating immunoglobulin (TSI) is the driving force for thyrotoxicosis
Signs of HYPER thryoidism from Graves
1. Alertness, emotional lability, nervousness, irritability
2. Poor concentration
3. Muscular weakness, fatigability
5. Voracious appetite, weight loss
6. Increased frequency of bowel movements
7. Heat intolerance
Clincal signs of hyperthryoidism
1. Hyperkinesia, rapid speech 2. Proximal muscle weakness, fine tremor 3. Fine, moist skin; fine, abundant hair; onycholysis (separation of the nail from its bed); pretibial skin thickening 4. Lid lag, stare, chemosis, periorbital edema, proptosis 5. Accentuated first heart sound, tachycardia, atrial fib
Describe the dermatopathy associated with Graves
Marked thickening of the skin is noted, usually over the pretibial area. Thickening occasionally extends downward over the ankle and the dorsal aspect of the foot but almost never above the knee.
Proptosis is associated with what and how is it measured?
specifically with GRAVEs, not just hyperhthyroidism and use a Hertel exophthalmometer is used to measure the amount of proptosis.