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AAA-MEDICINE (ENDOCRINE) > THYROID DISORDERS 1.2 (based on T) > Flashcards

THYROID DISORDERS 1.2 (based on T) Flashcards

1
Q

What is thyrotoxicosis?

A

A state of thyroid hormone excess, which can originate from sources outside the thyroid gland (e.g., ectopic thyroid tissue, autoimmune disease).

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2
Q

What is hyperthyroidism?

A

A condition where excessive thyroid hormone is produced by the thyroid gland itself.

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3
Q

Can you have thyrotoxicosis without hyperthyroidism?

A

Yes, for example, thyrotoxicosis caused by exogenous excess thyroid hormone intake.

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4
Q

What are the major causes of thyrotoxicosis due to hyperthyroidism?

A

Graves’ disease, toxic multinodular goiter (MNG), and toxic adenoma.

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5
Q

What is a toxic adenoma?

A

A hyperfunctioning nodule within the thyroid gland that autonomously secretes excess thyroid hormones.

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6
Q

What are primary hyperthyroidism causes?

A

Graves’ disease, toxic multinodular goiter, toxic adenoma, functioning thyroid carcinoma metastases, activating mutations of TSH receptor or Gsa (McCune-Albright syndrome), struma ovarii, iodine excess (Jod-Basedow phenomenon).

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7
Q

What are the causes of thyrotoxicosis without hyperthyroidism?

A

Destruction of thyroid tissue (subacute thyroiditis, silent thyroiditis, amiodarone-induced, radiation, infarction of adenoma), ingestion of excess thyroid hormone (thyrotoxicosis factitia).

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8
Q

What are the causes of secondary hyperthyroidism?

A

TSH-secreting pituitary adenoma, thyroid hormone resistance syndrome, chorionic gonadotropin-secreting tumors (e.g., hydatidiform mole), gestational thyrotoxicosis.

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9
Q

What is the most common cardiovascular manifestation of thyrotoxicosis?

A

Sinus tachycardia.

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10
Q

What serious cardiac complication can occur in thyrotoxicosis?

A

Atrial fibrillation, which is more common in patients over 50 years old and can lead to ventricular tachycardia and arrest in severe cases like thyroid storm.

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11
Q

What are the most common symptoms of thyrotoxicosis?

A

Hyperactivity, irritability, heat intolerance, palpitations, fatigue, weight loss with increased appetite, diarrhea, polyuria, oligomenorrhea, and loss of libido.

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12
Q

What are the common signs of thyrotoxicosis?

A

Tachycardia, tremor, goiter, warm moist skin, muscle weakness, lid retraction or lag, gynecomastia.

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13
Q

What is the most common cause of primary hyperthyroidism?

A

Graves’ disease.

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14
Q

What percentage of thyrotoxicosis cases are caused by Graves’ disease?

A

60-80%.

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15
Q

What are the environmental and genetic risk factors for Graves’ disease?

A

Polymorphisms in HLA-DR, CTLA-4, CD25, PTPN22, FCRL3, CD226, high iodine intake, stress, and smoking.

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16
Q

What are the characteristic thyroid findings in Graves’ disease?

A

Diffuse thyroid enlargement (2-3x normal size), firm consistency, thrill or bruit due to increased vascularity.

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17
Q

What are the early manifestations of Graves’ ophthalmopathy?

A

Sensation of grittiness, eye discomfort, excessive tearing.

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18
Q

What is the most serious manifestation of Graves’ ophthalmopathy?

A

Optic nerve compression, which can cause papilledema, peripheral field defects, and permanent vision loss.

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19
Q

What is pretibial myxedema?

A

A form of thyroid dermopathy seen in <5% of Graves’ disease cases, characterized by non-pitting edema over the lower legs.

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20
Q

What is thyroid acropachy?

A

A rare (<1%) manifestation of Graves’ disease causing digital clubbing.

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21
Q

What is the typical TSH and thyroid hormone profile in Graves’ disease?

A

Suppressed TSH, increased total and free T4 and/or T3.

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22
Q

When should TSH receptor antibodies (TRAb) be measured?

A

When the clinical diagnosis of Graves’ disease is unclear, such as in cases with unilateral eye involvement.

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23
Q

What test differentiates Graves’ disease from destructive thyroiditis or ectopic thyroid hormone sources?

A

Radionuclide scan (Graves’ shows diffuse high uptake, whereas destructive thyroiditis shows low uptake).

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24
Q

What are the main treatment options for hyperthyroidism?

A

Antithyroid drugs (thionamides), radioactive iodine (RAI) therapy, thyroidectomy.

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25
What is the mechanism of thionamides (antithyroid drugs)?
They inhibit thyroid peroxidase, blocking iodine organification and coupling of iodotyrosine, thus reducing new thyroid hormone synthesis.
26
What is the first-line thionamide for Graves' disease?
Methimazole (MTZ).
27
What are the advantages of methimazole over propylthiouracil (PTU)?
Longer half-life, once-daily dosing, fewer severe side effects.
28
When is PTU preferred over methimazole?
In thyroid storm and the first trimester of pregnancy.
29
What are the major side effects of thionamides?
Hepatitis (PTU), cholestasis (MTZ, CBZ), vasculitis, agranulocytosis (low WBC and neutrophils, risk of severe infections).
30
What is the preferred treatment for symptomatic relief of thyrotoxicosis?
Beta-blockers (e.g., propranolol, which also inhibits T4 to T3 conversion).
31
When is radioactive iodine (RAI) therapy contraindicated?
Pregnancy, breastfeeding, severe ophthalmopathy (especially in smokers).
32
What is the expected outcome of radioactive iodine therapy?
Progressive thyroid destruction leading to hypothyroidism.
33
What are the absolute contraindications for thyroidectomy?
Uncontrolled hyperthyroidism, severe comorbidities that make surgery high-risk.
34
What is the major complication of thyroidectomy?
Damage to the recurrent laryngeal nerve, leading to hoarseness or voice loss.
35
What is the preferred treatment for hyperthyroidism in pregnancy?
PTU in the first trimester, then switch to methimazole after 16 weeks.
36
What congenital abnormalities are associated with methimazole use in early pregnancy?
Aplasia cutis, choanal atresia, tracheoesophageal fistula.
37
What is the typical clinical course of Graves’ ophthalmopathy?
Worsens over the first 3-6 months, plateaus for 12-18 months, then may improve spontaneously.
38
What is the first-line treatment for moderate-to-severe Graves’ ophthalmopathy?
Glucocorticoids (e.g., prednisone).
39
How is gestational thyrotoxicosis managed?
Supportive care; antithyroid drugs are not typically needed unless true Graves' disease is present.
40
What is thyroid storm?
A life-threatening exacerbation of hyperthyroidism characterized by fever, delirium, seizures, coma, vomiting, diarrhea, and jaundice.
41
What is the mortality rate of thyroid storm even with treatment?
0.3
42
What are the main causes of death in thyroid storm?
Cardiac failure, arrhythmia, or hyperthermia.
43
What are the common precipitating factors of thyroid storm?
Acute illness (e.g., stroke, infection, trauma, noncompliance with medications, diabetic ketoacidosis), surgery, or radioiodine treatment in partially treated hyperthyroidism.
44
What is the Burch-Wartofsky Point Scale used for?
Assessing the likelihood of thyroid storm.
45
What Burch-Wartofsky score indicates thyroid storm?
Greater than 45.
46
What Burch-Wartofsky score indicates impending thyroid storm?
25-45.
47
What Burch-Wartofsky score makes thyroid storm highly unlikely?
Less than 25.
48
What are the management objectives for thyroid storm?
Stop new hormone synthesis, halt release of stored hormones, prevent T4 to T3 conversion, control adrenergic symptoms, provide supportive care, and treat the underlying cause.
49
What is the drug of choice for thyroid storm?
Propylthiouracil (PTU).
50
What is the PTU dosing regimen for thyroid storm?
500-1000 mg loading dose, followed by 250 mg every 4 hours.
51
Why is PTU preferred over methimazole in thyroid storm?
PTU inhibits T4 to T3 conversion.
52
What is the role of beta-blockers in thyroid storm?
To control adrenergic symptoms and decrease T4 to T3 conversion (high-dose propranolol).
53
What is the role of glucocorticoids in thyroid storm?
Reduce inflammation and inhibit T4 to T3 conversion (e.g., hydrocortisone 300 mg IV bolus, then 100 mg every 8 hours).
54
What is the role of iodine therapy in thyroid storm?
Administered one hour after PTU to block thyroid hormone synthesis via the Wolff-Chaikoff effect.
55
What is the role of cholestyramine in thyroid storm?
Sequesters thyroid hormones to reduce their effects.
56
What are supportive therapies for thyroid storm?
Cooling, oxygen, IV fluids, and antibiotics if an infection is present.
57
What are the non-hyperthyroid causes of thyrotoxicosis?
Thyroiditis, amiodarone-induced thyroiditis, sick euthyroid syndrome.
58
What are the causes of acute thyroiditis?
Bacterial (Staphylococcus, Streptococcus, Enterobacter), fungal (Aspergillus, Candida, Coccidioides), and radiation thyroiditis.
59
What is the most common cause of acute thyroiditis in children/young adults?
Presence of a pyriform sinus, a remnant of the fourth branchial pouch.
60
What are the clinical features of acute thyroiditis?
Thyroid pain, fever, dysphagia, erythema over the thyroid, and systemic symptoms like fever and lymphadenopathy.
61
How is acute thyroiditis managed?
Antibiotics and surgical drainage if an abscess is present.
62
What is subacute thyroiditis also known as?
De Quervain's thyroiditis, granulomatous thyroiditis, or viral thyroiditis.
63
What is the typical etiology of subacute thyroiditis?
Viral (e.g., mumps, coxsackie, influenza, adenoviruses, echoviruses, and SARS-CoV-2).
64
What is the hallmark symptom of subacute thyroiditis?
Painful, enlarged thyroid with pain radiating to the jaw or ear.
65
What is the typical progression of thyroid function in subacute thyroiditis?
Thyrotoxic phase (6-8 weeks) → hypothyroid phase (3-6 months) → recovery phase.
66
What is the treatment for subacute thyroiditis?
NSAIDs or high-dose aspirin for pain relief; steroids if symptoms are severe.
67
What is painless (silent) thyroiditis?
A transient thyroiditis seen in autoimmune disease, postpartum women, or drug-induced cases.
68
What is the key difference between painless thyroiditis and subacute thyroiditis?
Painless thyroiditis has no thyroid pain or tenderness, whereas subacute thyroiditis is painful.
69
What are the phases of painless thyroiditis?
Thyrotoxic phase (2-4 weeks), hypothyroid phase (4-12 weeks), then recovery.
70
What is postpartum thyroiditis?
A variant of painless thyroiditis occurring in 5% of women 3-6 months after pregnancy.
71
What is the most common thyroid function pattern in sick euthyroid syndrome?
Low total and free T3, normal T4, normal TSH (low T3 syndrome).
72
What are the thyroid effects of amiodarone?
Can cause hypothyroidism or thyrotoxicosis due to its high iodine content.
73
What are the two types of amiodarone-induced thyrotoxicosis (AIT)?
Type 1 AIT (iodine-induced hyperthyroidism in pre-existing thyroid disease) and Type 2 AIT (destructive thyroiditis in normal thyroids).
74
How does amiodarone affect thyroid function tests?
Increases T4, decreases T3, increases rT3, transiently increases TSH.
75
How is Type 1 AIT treated?
Thionamides (e.g., methimazole or PTU).
76
How is Type 2 AIT treated?
Glucocorticoids (e.g., prednisone).
77
What is Riedel’s thyroiditis?
A rare, fibrotic thyroid disorder causing a hard, fixed goiter that mimics malignancy.
78
What is the management of Riedel’s thyroiditis?
Surgical decompression and tamoxifen therapy.
79
What is sick euthyroid syndrome?
Thyroid function abnormalities in severe illness without underlying thyroid disease.
80
What lab findings suggest sick euthyroid syndrome?
Low T3, normal T4, normal or low TSH.
81
When should thyroid function tests be avoided in hospitalized patients?
Unless there is a strong suspicion of true thyroid dysfunction, as sick euthyroid syndrome may cause misleading results.
82
What is the role of cytokines in sick euthyroid syndrome?
IL-6 and other cytokines alter thyroid hormone metabolism.
83
How does acute liver disease affect thyroid function?
Initially increases total T3 and T4 due to TBG release, but later decreases as liver failure progresses.
84
What are the thyroid effects of HIV?
Early HIV increases T3 and T4; advanced AIDS decreases T3.
85
How does renal disease affect thyroid function?
Causes low T3 but normal rT3.

AAA-MEDICINE (ENDOCRINE) (10 decks)

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