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Endocrinology > Thyroid > Flashcards

Thyroid Flashcards

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?

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
Q

What are the presentations of Thyroid storm?

A
  • Tachycardia
  • Heart failure
  • Psychosis
  • Hyperpyrexia
  • Coma
26
Q

What are some causes of Primary Hyperthyroidism?

A

*** 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
Q

What are the causes of thyrotoxicosis without hyperthyroidism?

A
  • Subacute thyroiditis
  • Silent thyroiditis
  • Thyroid destruction:
    • Amiodarone
    • Radiation
    • Infarction of adenoma
  • Ingestion of excess thyroid hormone (thyrotoxicosis factitial) or thyroid tissue
28
Q

What are the causes of secondary hyperthyroidism?

A
  • TSH-secreting pituitary adenoma
  • Thyroid hormone resistance syndrome
    • Occasional patients may have features of thyrotoxicosis
  • Chronic gonadotropin-secreting tumors
  • Gestational thyrotoxicosis
29
Q

Primary thyrotoxicosis

A

Low TSH and high unbound T4

30
Q

Secondary thyrotoxicosis

A

TSH normal or elevated, high unbound T4

31
Q

Graves’ Disease

A

Autoimmune syndrome causing hyperthyroidism due to action of thyroid-stimulating antibodies (TSAbs) directed against thyrotropin receptor on surface of thyroid cell

32
Q

What are the classical findings of Graves’ Disease

A
  • Hyperthyroidism
  • Diffuse thyroid enlargement
  • Exophthalmos
  • Less commonly expressed as:
    • Pretibial myxedema
    • Thyroid acropachy
33
Q

What are some characteristics of Graves’ Disease

A
  • 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
Q

What are some laboratory findings of Graves’ disease?

A
  • Increase in T3 relative to T4 (increase ratio)
  • T3 toxicosis
  • T4 toxicosis
  • Saturation of TBG increased
  • TSH levels suppressed or undetectable
    *** TRAbs **
35
Q

How do you diagnose Graves’ disease?

A

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
Q

What is the treatment of Graves’ Disease?

A
  • Antithyroid medications
  • Radioactive iodine
  • Surgery
37
Q

When does Graves’ Opthalmopathy occur?

A

Within the year before or after diagnosis of thyrotoxicosis in 75% of patients

38
Q

What are some features of Graves’ Ophthalmopathy?

A
  • Lid retraction
  • Periorbital edema
  • Chemosis
  • Conjunctival injection
  • Proptosis – abnormal protrusion/displacement of eye (bug eye)
39
Q

What are some early manifestations of Graves’ Ophthalmopathy?

A
  • Grittiness
  • Eye discomfort
  • Excess tearing
40
Q

What is the pathway to Graves’ Ophthalmopathy?

A

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
Q

Toxic Adenoma

A
  • Autonomous thyroid nodule – discrete thyroid mass functioning independent of pituitary and TSH control
  • Hot nodule
  • Benign tumors that produce thyroid hormone
42
Q

What are some treatment options of toxic adenoma?

A
  • 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
Q

What do you give a patient when he/she is euthyroid who have goiter?

A
  • Thioamides
    • Dosed to suppress TSH levels to:
      • Slow goiter growth
      • Cause shrinkage

Therapy goal is to reduce goiter size and mass-related dysphagia

44
Q

What is the preferred treatment of multinodular goiter?

A
  • 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
Q

What are the less common causes of thyrotoxicosis?

A
  • Trophoblastic disease
  • TSH-induced hyperthyroidism
  • Pituitary resistance to thyroid hormone
  • Subacute thyroiditis
  • Painless thyroiditis
  • Thyroid cancer
  • Struma Ovarii
46
Q

Trophoblastic disease

A

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
Q

What is the criteria for diagnosis of TSH-induced hyperthyroidism?

A
  • Evidence of peripheral hypermetabolism
  • Diffuse thyroid gland enlargement
  • Elevated free thyroid hormone levels
  • Elevated or inappropriately “normal” serum immunoreactive TSH concentrations
48
Q

TSH-secreting pituitary adenoma

A
  • 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
Q

What is the presentation of TSH-secreting pituitary adenoma?

A
  • Visual field defects – tumor impingement of optic chiasm by tumor
50
Q

What is the diagnosis of TSH-secreting pituitary adenoma?

A
  • 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
Q

What is the treatment of TSH-secreting pituitary adenoma?

A

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
Q

Subacute Thyroiditis

A
  • Painful subacute thyroiditis often develops after viral syndrome
  • Genetic predisposition – higher risk for patients with **HLA-Bw35 antigen **
53
Q

What are the presentations of subacute thyroiditis?

A
  • 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
Q

What is the treatment for subacute thyroiditis?

A
  • 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
Q

Postpartum thyroiditis

A
  • Development of lymphocytic thyroiditis during the first 12 months AFTER end of pregnancy
56
Q

What is the treatment of painless thyroiditis?

A
  • Propranolol/metoprolol – adrenergic symptoms
  • Anti-thyroid drugs not indicated as they do NOT DECREASE release of performed thyroid hormones
57
Q

Thyrotoxicosis factitial

A

Hyperthyroidism due to ingestion of thyroid hormone

58
Q

What medications induce thyrotoxicosis?

A
  • Amiodarone
  • Biotin
59
Q

Amiodarone

A
  • Thyrotoxicosis: 2-3%
  • Overt hypothyroidism: 5%
  • Subclinical hypothyroidism: 25%
  • Euthyroid hyperthyroxinemia
  • Contains 37% iodine by weight

Endocrinology (10 decks)

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