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Thyroid Flashcards

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1
Q

Thyroid Hormone

A
  • Affects function of every organ system
  • Critical for normal growth and development in childhood
  • Maintains metabolic stability in adults
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2
Q

Active unbound (free) thyroid hormone

A
  • Diffuses into cells
  • Elicits biologic effects
  • Regulates thyrotropin/thyroid stimulating hormone (TSH) secretion (involves in negative feedback)
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3
Q

T4

A

ONLY source is secretion from thyroid gland

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4
Q

5’ monodeidonase enzymes

A
  • Catalyzes T4 to T3 in extra-thyroid peripheral tissues
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5
Q

Type 1 5’-monodeidonase enzymes

A
  • Converts T4 to T3 in **liver **
  • Also present in kidney and thyroid
  • Predominant extrathyroidal source of T3
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6
Q

Type 2 5’-monodeidonase enzymes

A
  • Converts T4 and T3 in **pituitary **
  • Also present in thyroid, CNS, and borwn adipose tissue
  • Intracellular T3 production -** important in hypothyroidism/iodine deficiency **
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7
Q

Type 3 5’-monodeidonase enzymes

A

Present in placenta, developing brain, and skin

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8
Q

HPA

A
  • Highly sensitive to small changes in circulating thyroid hormone concentrations
  • Alterations in thyroid hormone secretion maintain peripheral free thyroid hormone levels within a narrow range
  • Recall that this is influenced by negative feedback
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9
Q

Thyroid Hormone Transport Proteins

A
  • Transport T4 and T3 in the bloodstream
  • Assure minimal urinary loss of iodine (one of the trace elements)
  • Provide mechanism for uniform tissue distribution of free hormone
  • Transport hormones into CNS
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10
Q

What are the transport proteins?

A
  • Thyroxine-binding globulin (TBG)
  • Transthyretin (TTR)
  • Albumin
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11
Q

What blocks the transfer of iodine transfer into thyroid?

A
  • Bromine
  • Fluorine
  • Lithium – under certain circumstances
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12
Q

What inhibits thyroid hormone secretion?

A
  • Iodine – in large doses
  • Lithium
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13
Q

What impairs organification and coupling of thyroid hormones?

A
  • Thioamides
  • Sulfonamide
  • Salicylamide
  • Antipyrine
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14
Q

Iodine deficiency

A

Causes INCREASE in MIT:DIT ratio–> relative INCREASE in T3

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15
Q

What competitively inhibits transport (structurally related)?

A
  • Thiocyanate
  • Perchlorate
  • Pertechnetate
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16
Q

What is extrathyrodial deiodination of T4 and T3 impacted by?

A
  • Nutrition
  • Nonthyroidal hormones
  • Ambient temperature
  • Drugs
  • Illness
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17
Q

Thyrotoxicosis

A

Caused by tissue exposure to excessive levels of T4, T3, or both

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18
Q

Radioactive iodine uptake (RAIU)

A
  • Measurement of radioactive iodine uptake (RAIU)
  • Normal 24-hour range 10-30%
  • Elevated RAIU indicates endogenous hyperthyroidism – thyroid gland actively overproducing T4 or T3
  • Low RAIU in absence of iodine excess indicates that high levels of thyroid hormone are not a consequence of thyroid gland hyperfunction
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19
Q

What is the diagnostic criteria?

A
  • Low serum TSH
  • Elevated serum free and total T4 and T3
  • RAIU
    • Elevated uptake by thyroid gland when hormone is being overproduced
    • Suppressed uptake in thyrotoxicosis due to thyroid inflammation (thyroiditis)
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20
Q

What are some other test for thyrotoxicosis?

A
  • Thyroid-stimulating antibodies (TSAbs)
    • Differentiates autoimmune thyrotoxicosis (Graves’ disease) and everything else
  • Thyroglobulin
  • Thyrotropin receptor antibodies
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21
Q

What are some symtpoms of thyrotoxicosis?

A
  • Hyperactivity/irritability/dysphoria
  • Heat intolerance/sweating
  • Palpitations
  • Fatigue/weakness
  • Weight loss with increased appetite
  • Diarrhea
  • Polyuria
  • Menstrual disturbances of libido
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22
Q

What are signs of thyrotoxicosis?

A
  • Tachycardia – atrial fibrillation in elderly
  • Tremor (fine tremor of protruded tongue/outstretched hands)
  • Thyromegaly/goiter
  • Warm, moist skin
  • Muscle weakness/proximal myopathy
  • Lid retraction/lag
  • Gynecomastia
  • Fine hair
  • Onycholysis
  • Cardiovascular: tachycardia at rest, widened pulse pressure, systolic ejection murmurHyperactive deep tendon reflexes
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23
Q

What are the signs of Graves’ disease?

A
  • Ophthalmopathy/exophthalmos
  • Pretibial myxedema
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24
Q

What are the presentation of thyrotoxicosis dependent on?

Study These Flashcards
A
  • Thyrotoxicosis severity
  • Duration
  • Individual susceptibility to excess thyroid hormone
  • Patient age
    • Elderly: symptoms may be masked, patients may present with fatigue and weight loss
25
What are the presentations of Thyroid storm?
* Tachycardia * Heart failure * Psychosis * Hyperpyrexia * Coma
26
What are some causes of Primary Hyperthyroidism?
*** Graves’ disease * Toxic multinodular goiter * Toxic adenoma ** * Functioning thyroid carcinoma metastases * Activating mutation of TSH receptor * Activating mutation of GSalpha * Struma ovarii * Drugs: iodine excess
27
What are the causes of thyrotoxicosis without hyperthyroidism?
* Subacute thyroiditis * Silent thyroiditis * Thyroid destruction: - Amiodarone - Radiation - Infarction of adenoma * Ingestion of excess thyroid hormone (thyrotoxicosis factitial) or thyroid tissue
28
What are the causes of secondary hyperthyroidism?
* TSH-secreting pituitary adenoma * Thyroid hormone resistance syndrome - Occasional patients may have features of thyrotoxicosis * Chronic gonadotropin-secreting tumors * Gestational thyrotoxicosis
29
Primary thyrotoxicosis
Low TSH and high unbound T4
30
Secondary thyrotoxicosis
TSH normal or elevated, high unbound T4
31
Graves' Disease
Autoimmune syndrome causing hyperthyroidism due to action of thyroid-stimulating antibodies (TSAbs) directed against thyrotropin receptor on surface of thyroid cell
32
What are the classical findings of Graves' Disease
* Hyperthyroidism * Diffuse thyroid enlargement * Exophthalmos * Less commonly expressed as: - Pretibial myxedema - Thyroid acropachy
33
What are some characteristics of Graves' Disease
* Thyroid gland diffusely enlarged * Gland surface can be smooth or bosselated * Consistency varies from soft to firm * Thrill/systolic bruit may be present in severe disease - Increased vascularity with hyperplasia
34
What are some laboratory findings of Graves' disease?
* Increase in T3 relative to T4 (increase ratio) * T3 toxicosis * T4 toxicosis * Saturation of TBG increased * TSH levels suppressed or undetectable *** TRAbs **
35
How do you diagnose Graves' disease?
1) Measure serum-free T4, total T4, total T3 and TSH to confirm diagnosis of thyrotoxicosis 2) 24-hr RAIU when diagnosis is uncertain AND patient is not pregnant/lactating 3) Measure TRAb to differentiate Graves disease from other causes of thyrotoxicosis
36
What is the treatment of Graves' Disease?
* Antithyroid medications * Radioactive iodine * Surgery
37
When does Graves' Opthalmopathy occur?
Within the year before or after diagnosis of thyrotoxicosis in 75% of patients
38
What are some features of Graves' Ophthalmopathy?
* Lid retraction * Periorbital edema * Chemosis * Conjunctival injection * Proptosis – abnormal protrusion/displacement of eye (bug eye)
39
What are some early manifestations of Graves' Ophthalmopathy?
* Grittiness * Eye discomfort * Excess tearing
40
What is the pathway to Graves' Ophthalmopathy?
1) Extraocular muscle infiltrated by activated T cells 2) Cytokines released 3) Fibroblast activation 4) Increased synthesis of glycosaminoglycans 5) Increased water leads to muscle swelling
41
Toxic Adenoma
* Autonomous thyroid nodule – discrete thyroid mass functioning **independent** of pituitary and TSH control * Hot nodule * Benign tumors that produce thyroid hormone
42
What are some treatment options of toxic adenoma?
* Surgical resection * Antithyroid drugs * Percutaneous ethanol injection (not often used in practice) - Associated with pain and damage to surrounding extrathyroid tissue * Radioactive iodine ablation - Rarely associated with thyroid cancer * Conservative management possible if nodule not large enough to cause thyrotoxicosis
43
What do you give a patient when he/she is euthyroid who have goiter?
* Thioamides - Dosed to suppress TSH levels to: - Slow goiter growth - Cause shrinkage | Therapy goal is to reduce goiter size and mass-related dysphagia
44
What is the preferred treatment of multinodular goiter?
* RAI (radioactive iodine) * Surgery appropriate - Younger patients - Goiter is impinging on vital organs * Alternate treatment: percutaneous injection of 95% ethanol to destroy single/multinodular adenomas (not often used in practice) - 5-year success rate approaches 80%
45
What are the less common causes of thyrotoxicosis?
* Trophoblastic disease * TSH-induced hyperthyroidism * Pituitary resistance to thyroid hormone * Subacute thyroiditis * Painless thyroiditis * Thyroid cancer * Struma Ovarii
46
Trophoblastic disease
**Human chorionic gonadotropin (hCG)** is a stimulator of TSH receptor and may cause hyperthyroidism due to similarities in alpha subunits (the two hormones have unique beta subunits)
47
What is the criteria for diagnosis of TSH-induced hyperthyroidism?
* Evidence of peripheral hypermetabolism * Diffuse thyroid gland enlargement * Elevated free thyroid hormone levels * **Elevated or inappropriately “normal” serum immunoreactive TSH concentrations**
48
TSH-secreting pituitary adenoma
* Occurs sporadically - Release biologically active hormones unresponsive to normal feedback control - Co-secrete prolactin or growth hormone - Patients may present with amenorrhea/galactorrhea or signs of acromegaly
49
What is the presentation of TSH-secreting pituitary adenoma?
* Visual field defects – tumor impingement of optic chiasm by tumor
50
What is the diagnosis of TSH-secreting pituitary adenoma?
* Demonstration of a lack of TSH response to THR stimulation - Lack of routine availability of TRH * Inappropriate TSH levels * Elevate alpha-subunit levels * Radiologic imaging
51
What is the treatment of TSH-secreting pituitary adenoma?
**Transsphenoidal pituitary surgery is treatment of choice** * Pituitary gland irradiation often given post surgery to prevent tumor recurrence * Medications: dopamine agonists and octreotide have been used to treat tumors - Especially when prolactin is co-secreted
52
Subacute Thyroiditis
* Painful subacute thyroiditis often develops after viral syndrome * Genetic predisposition – higher risk for patients with **HLA-Bw35 antigen **
53
What are the presentations of subacute thyroiditis?
* Systemic symptoms: fever, malaise, myalgia * Typical thyrotoxicosis signs and symptoms * Severe pain in thyroid region - May extend to ear on affected side - Pain migrates from one side of gland to other with time * Physical exam: thyroid gland firm and exquisitely tender
54
What is the treatment for subacute thyroiditis?
* Thyrotoxic symptoms may be relieved with beta-blocker * Pain: NSAIDs * Prednisone (30-40 mg daily) may be used to suppress inflammatory process if needed * Anti-thyroid drugs NOT indicated – do NOT decrease release of preformed thyroid hormones
55
Postpartum thyroiditis
* Development of lymphocytic thyroiditis during the first 12 months AFTER end of pregnancy
56
What is the treatment of painless thyroiditis?
* Propranolol/metoprolol – adrenergic symptoms * Anti-thyroid drugs not indicated as they do NOT DECREASE release of performed thyroid hormones
57
Thyrotoxicosis factitial
Hyperthyroidism due to ingestion of thyroid hormone
58
What medications induce thyrotoxicosis?
* Amiodarone * Biotin
59
Amiodarone
* Thyrotoxicosis: 2-3% * Overt hypothyroidism: 5% * Subclinical hypothyroidism: 25% * Euthyroid hyperthyroxinemia * Contains 37% iodine by weight

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