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ENDO Flashcards

1
Q

Most common causes of hypothyroidism in areas of iodine sufficiency (2)

A

autoimmune

iatrogenic

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2
Q

Most common cause of neonatal hypothyroidism

A

Thyroid gland dysgenesis – 80–85%

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3
Q

3 Causes of neonatal hypothyroidism

A

o Thyroid gland dysgenesis – 80–85%
o Inborn errors of thyroid hormone synthesis – 10–15%
o TSH-R antibody-mediated – 5%

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4
Q

Treatment of congenital hypothyroidism with dose

A

T4 dose of 10–15 μg/kg per day

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5
Q

If transient congenital hypothyroidism is suspected or with unclear diagnosis, when can you stop the treatment?

A

treatment can be stopped at age 3 y.o then with further evaluation

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6
Q

2 thyroiditis that may be associated with goiter

A

o Hashimoto’s thyroiditis

o Goitrous thyroiditis

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7
Q

Thyroiditis that may be associated with minimal residual thyroid disease (at the later stages)

A

Atrophic thyroiditis

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8
Q

Symptomatic hypothyroidis usually occurs at what TSH level

A

> 10 mIU/L

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9
Q

Mean age at diagnosis of autoimmune hypothyroidism

A

60 years

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10
Q

Annual risk of developing clinical hypothyroidism is about 4% when subclinical hypothyroidism is associated with what antibodies?

A

Thyroid peroxidase (TPO) antibodies

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11
Q

Pathology of Hashimoto’s (5)

A 
o	Marked lymphocytic infiltration of the thyroid with germinal center formation
o	Atrophy of the thyroid follicles
o	Oxyphil metaplasia
o	Absence of colloid
o	Mild to moderate fibrosis
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12
Q

Pathology of atrophic thyroiditis (3)

A

o More extensive fibrosis
o Less lymphocyte infiltration
o Thyroid follicles are almost completely absent

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13
Q

Usually represents the end stage of Hashimoto’s thyroiditis rather than a separate disorder

A

Atrophic thyroiditis

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14
Q

The best documented genetic risk factors for autoimmune hypothyroidism

A

HLA-DR polymorphisms

Especially HLA-DR3, DR4, and DR5

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15
Q

2 risk factors of autoimmune thyroiditis

A

o High-iodine or low selenium intake – increased risk of autoimmune hypothyroidism
o Smoking cessation – transiently increases incidence

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16
Q

T or F: Alcohol intake is a risk factor for autoimmune hypothyroidism

A

false. protective

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17
Q

Clinically useful markers of thyroid autoimmunity

A

Antiboidies to TPO and thyroglobulin (Tg)

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18
Q

Usual clinical manifestation of hashimoto’s thyroiditis (2)

A

goiter

pain - rare

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19
Q

Describe the goiter in hashimoto’s thryoiditis

A

Irregular and firm in consistency

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20
Q

Stage of hashimoto’s thyroiditis that present with signs and symptoms of hypothyroidism, dry skin, decreased sweating, thinning of the epidermis, and hyperkeratosis of the stratum corneum

A

Atrophic thyroiditis

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21
Q

Sin thickening without pitting with puffy face with edematous eyelids due to increased dermal glycosaminoglycan content trapping water

A

Myxedema

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22
Q

Clinical manifestations of myxedema (6)

A

o Puffy face with edematous eyelids
o Nonpitting pretibial edema
o Pallor, often with yellow tinge to the skin due to carotene accumulation
o Nail growth retardation
o Hair is dry, brittle, difficult to manage and falls out easily (diffuse alopecia)
o Thinning of the outer third of the eyebrows

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23
Q

Describe the speech in myxedema

A

hoarse voice and clumsy speech

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24
Q

Cardiovascular manifestations of myxedema (4)

A
  • reduced myocardial contractility
  • bradycardia
  • diastolic hypertension (increased peripheral resitance)
  • pericardial effusion
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25
Q

Pericardial effusions occur in how many percent of myxedema patients

A

30%

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26
Q

Steroid-responsive syndrome associated with TPO antibodies, myoclonus, and slow-wave activity on EEG

A

Hashimoto’s encephalopathy

Relationship with hypothyroidism and thyroid autoimmunity has not been established

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27
Q

Screening test used in autoimmune hypothyroidism

A

TSH

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28
Q

T or F:o Normal TSH level excludes primary and secondary hypothyroidism

A

False. Normal TSH level excludes primary (but not secondary) hypothyroidism

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29
Q

If there is elevated TSH, what test should you do in order to confirm presence of clinical hypothyroidism ?

A

Unbound T4

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30
Q

These antibodies are found in in >95% of autoimmune hypothyroidism

A

TPO and Tg antibodies

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31
Q

Differentiate the ultrasound findings of multinodular goiter, thyroid carcinoma, and Hashimoto’s thyroiditis

A
  • Multinodular goiter - multinodular
  • Thyroid carcinoma -solitary lesion
  • Hashimoto’s – heterogenous thyroid enlargement
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32
Q

In iatrogenic hypothyroidism, transient hypothyroidism in the first _______ after radioiodine treatment for Graves’ disease

A

3–4 months

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33
Q

Better measure of thyroid function than TSH in the months following radioiodine treatment

A

FT4

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34
Q

Cause of endemic goiter and cretinism

A

Iodine deficiency

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35
Q

T or F. Chronic iodine excess can also induce goiter and hypothyroidism

A

True

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36
Q

Psychiatric medication that can also cause iatrogenic hypothyroidism

A

Lithium

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37
Q

If there is no residual thyroid function, what is the dose of levothyroxine?

A

1.6 μg/kg body weight (typically 100–150 μg), ideally taken at least 30 min before breakfast

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38
Q

Dose of levothyroxine for iatrogenic hypothyroidism

A

Lower replacement doses (typically 75–125 μg/d)

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39
Q

Dose of levothyroxine in o adult patients under 60 years old without evidence of heart disease

A

50–100 μg levothyroxine (T4) daily

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40
Q

TSH monitoring should be done after how many month after instituting treatment of hypothyroidism

A

2 months

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41
Q

Patients treated with levothyroxine may experience full relief from symptoms only after ______

A

3-6 months after normal TSH levels are restored

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42
Q

T or F: Patients who miss a dose of levothyroxine can be advised to take two doses of the skipped tablets at once

A

True.Because T4 has a long half-life (7 days)

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43
Q

In the treatment of subclinical hypothyroidism, levothyroxine is recommended only in: (2)

A

o Woman who wishes to conceive or is pregnant

o TSH > 10 mIU/L

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44
Q

In subclinical hypothyroidism, trial of treatment with levothyroxine for TSH < 10mIU/L if with (3)

A

o Symptomatic
o Positive TPO antibodies
o Evidence of heart disease

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45
Q

In treatment of subclinical hypothyroidism, it is important to confirm that any elevation of TSH is sustained over a_____ period before treatment is given

A

3-month

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46
Q

Dose of levothyroxine in subclinical hypothyroidism

A

25–50 μg/d

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47
Q

Idiosyncratic reaction in children with levothyroxine treatment that occurs months after treatment has begun

A

Pseudomotor cerebri

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48
Q

In pregnant women or planning to conceive, thyroid function should be evaluated when?

A
  • immediately after pregnancy is confirmed
  • every 4 weeks during the first half of the pregnancy
  • every 6–8 weeks after 20 weeks’ gestation (every 6–8 weeks depending on whether levothyroxine dose adjustment is ongoing)
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49
Q

In pregnant women or planning to conceive, levothyroxine dose may need to be increased by up to

A

45%

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50
Q

Mortality rate of myxedema coma

A

20-40%

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51
Q

Clinical manifestations of myxedema coma (3)

A

 Reduced level of consciousness
 Seizures
 Hypothermia can reach 23°C (74°F)

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52
Q

Myedema coma is more common in this population

A

elderly

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53
Q

Causes of the clinical manifestations of myxedema coma (4)

A
  • sepsis
  • hypoventilation (leading to hypoxia and hypercapnia)
  • hypoglycemia
  • dilutional hyponatremia
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54
Q

Dose of levothyroxine in myxedema coma

A

A single IV bolus of 200–400 μg as loading dose

Daily oral dose of 1.6 μg/kg/d, reduced by 25% if administered IV

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55
Q

Supportive therapy for myxedema coma (8)

A
  • external warming
  • correct electrolytes
  • IV hydrocortisone 50 mg q6
  • treatment of precipitating factors
  • broad spectrum antibiotics
  • ventilatory syupport
  • hypertonic saline
  • IV glucose
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56
Q

State of thyroid hormone excess

A

Thyrotoxicosis

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57
Q

The result of excessive thyroid function

A

hyperthyroidism

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58
Q

T or F: Thyrotoxicosis is synonymous to hyperthyroidism

A

False

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59
Q

Accounts for 60–80% of thyrotoxicosis

A

Graves’ disease

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60
Q

Typical age of grave’s disease

A

20-50 years old

also occur in elderly

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61
Q

An important environmental factor contributing to Grave’s disease, presumably operating through neuroendocrine effects on the immune system

A

Stress

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62
Q

A minor risk factor for Graves’ disease and a major risk factor for the development of ophthalmopathy

A

Smoking

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63
Q

Occurrence of Graves’ disease in the postpartum period

A

threefold increase

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64
Q

The hyperthyroidism of Graves’ disease is caused by ________ that are synthesized in the thyroid gland as well as in bone marrow and lymph nodes

A

thyroid- stimulating immunoglobulin (TSI)

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65
Q

Thyroid stimulating Ig can be detected using what assay?

A

Thyrotropin-binding inhibitory immunoglobulin (TBII) assays

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66
Q

Antibodies that occur in up to 80% of cases of Grave’s disease (2)

A

thyroid peroxidase (TPO) and thyroglobulin (Tg) antibodies

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67
Q

Proposed pathogenesis of thyroid-associated ophthalmopathy

A

TSH-R is a shared autoantigen that is expressed in the orbit

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68
Q

In the elderly, features of thyrotoxicosis may be subtle or masked, and patients may present mainly with (2)

A

fatigue and weight loss

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69
Q

Type of thyrotoxicosis mostly seen in elderly that presents only as fatigue and weight loss

A

apathetic thyrotoxicosis

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70
Q

The most common cardiovascular manifestation of Grave’s disease

A

sinus tachycardia

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71
Q

Manifestations of high cardiac output in Grave’s disease (4)

A

Bounding pulse
Widened pulse pressure, Aortic systolic murmur
Worsening of angina or heart failure

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72
Q

Cardiac arrhythmia in Grave’s disease that is more common in patients >50 years of age

A

Atrial fibrillation

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73
Q

In Graves’ disease, the thyroid is usually_____ enlarged to ____ times its normal size. The consistency is____, but not_____.

A

diffusely
two to three
firm
nodular

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74
Q

PE finding in Grave’s disease that is due to the increased vascularity of the gland and the hyperdynamic circulation.

A

thrill or bruit, best detected at the inferolateral margins of the thyroid lobes

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75
Q

Clinical manifestation of ophthalmopathy in Graves’ disease (4)

A

lid retraction (staring appearance)
periorbital edema
conjunctival injection
marked proptosis

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76
Q

Thyroid-associated ophthalmopathy occurs in the absence of hyperthyroidism in___ of patients

A

10%

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77
Q

The earliest manifestations of thyroid-associated ophthalmopathy (3)

A

sensation of grittiness
eye discomfort
excess tearing

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78
Q

The most serious manifestation of thyroid-associated ophthalmopathy

A

compression of the optic nerve at the apex of the orbit, leading to papilledema; peripheral field defects; and, if left untreated, permanent loss of vision

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79
Q

Thyroid dermopathy occurs in ____ of patients with Graves’ disease, almost always in the presence of_____

A

<5%

moderate or severe ophthalmopathy

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80
Q

Most frequent involvement of thyroid dermopathy and the term associated with it

A

anterior and lateral aspects of the lower leg
pretibial myxedema

The typical lesion is a noninflamed, indurated plaque with a deep pink or purple color and an “orange skin” appearance.

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81
Q

Refers to a form of clubbing found in <1% of patients with Graves’ disease

A

Thyroid acropachy

It is so strongly associated with thyroid dermopathy

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82
Q

For patients with thyrotoxicosis who lack the typical features of Grave’s, the diagnosis is generally established by a

A

radionuclide (99mTc, 123I, or 131I) scan and uptake of the thyroid

distinguish the diffuse, high uptake of Graves’ disease from destructive thyroiditis, ectopic thyroid tissue, and factitious thyrotoxicosis, as well as diagnosing a toxic adenoma or toxic MNG

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83
Q

Group of drugs that inhibit the function of TPO, reducing oxidation and organification of iodide

A

Thionamides

PTU, carbimazole and methimazole (active metabolite)

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84
Q

Thionamide that has more adverse drug reaction especially hepatotoxicity

A

PTU

the U.S. Food and Drug Administration (FDA) has limited indications for its use to the first trimester of pregnancy, the treatment of thyroid storm, and patients with minor adverse reactions to methimazole

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85
Q

Dose of methimazole or carbimazole in Grave’s disease

A

10–20 mg every 8 or 12 h, but once-daily dosing is possible after euthyroidism is restored

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86
Q

Dose of PTU in Grave’s disease

A

100–200 mg every 6–8 h

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87
Q

Thyroid function tests and clinical manifestations are reviewed ____ after starting treatment for hyperthyroidism

A

4–6 weeks

TSH levels often remain suppressed for several months and therefore do not provide a sen- sitive index of treatment response

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88
Q

Most Grave’s disease patients do not achieve euthyroidism until _____ after treatment is initiated

A

6–8 weeks

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89
Q

Cholestasis is an adverse effect of thionamides that is more common in

A

Carbimazole or methimazole

Hepatotoxicity – PTU

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90
Q

Agranulocytosis is an ADR of thionamides that is seen in ____ of patient undergoing treatment

A

<1%

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91
Q

Rare but major side effects of thionamides (4)

A

Hepatitis
Vasculitis
Cholestasis
Agranulocytosis

It is essential that antithyroid drugs are stopped and not restarted if a patient develops major side effects

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92
Q

T or F. In patient on thionamide treatment for Grave’s disease, it is important to regularly monitor the blood counts to screen for agranulocytosis

A

False. It is not useful to monitor blood counts prospectively, because the onset of agranulocytosis is idiosyncratic and abrupt

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93
Q

Beta blockers used in Graves disease

A

Propranolol (20–40 mg every 6 h)
Atenolol - longer-acting selective β1 receptor blockers

may be helpful to control adrenergic symptoms

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94
Q

_____ causes progressive destruction of thyroid cells and can be used as initial treatment or for relapses after a trial of antithyroid drugs

A

Radioiodine

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95
Q

There is a small risk of thyrotoxic crisis after radioiodine, which can be minimized by

A

pretreatment with antithyroid drugs for at least a month before treatment

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96
Q

Carbimazole or methimazole must be stopped ____ before radioiodine administration to achieve optimum iodine uptake, and can be restarted ____ after radioiodine in those at risk of complications from worsening thyrotoxicosis.

A

2–3 days
3–7 days

Propylthiouracil appears to have a prolonged radioprotective effect and should be stopped for a longer period before radioiodine is given, or a larger dose of radioiodine will be necessary.

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97
Q

In general, patients who underwent radioiodine therapy need to avoid close, prolonged contact with children and pregnant women for _____ because of possible transmission of residual isotope and exposure to radiation emanating from the gland

A

5–7 days

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98
Q

Mild thyroid pain 1-2 weeks after radioiodine therapy

A

Radiation thyroiditis

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99
Q

Hyperthyroidism can persist for _____ before radioiodine takes full effect

A

2–3 months

β-adrenergic blockers or antithyroid drugs can be used to control symptoms during this interval

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100
Q

Persistent hyperthyroidism can be treated with a second dose of radioiodine, usually ____ after the first dose

A

6 months

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101
Q

Pregnancy and breast-feeding are absolute contraindications to radioiodine treatment, but patients can conceive safely ____ after treatment

A

6 months

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102
Q

T or F. Radioiodine should generally be avoided in those with active moderate to severe thyroid-associated eye disease

A

True

Prednisone, 30 mg/d, at the time of radioiodine treatment, tapered over 6–8 weeks may prevent exacerbation of ophthalmopathy

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103
Q

_____ is an option for patients who relapse after antithyroid drugs and prefer this treatment to radioiodine

A

Total or near-total thyroidectomy

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104
Q

The major complications of total or near-total thyroidectomy (4)

A

Bleeding
laryngeal edema
hypoparathyroidism
damage to the recurrent laryngeal nerves

unusual when the procedure is performed by highly experienced surgeons

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105
Q

Anti-thyroid drug that is used for hyperthyroid patient until 14-16 weeks AOG

A

PTU

Then converted to methimazole

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106
Q

Why is PTU preferred over Methimazole in pregnant women?

A

because of the association of rare cases of methimazole/ carbimazole embryopathy, including aplasia cutis and other defects, such as choanal atresia and tracheoesophageal fistulae

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107
Q

In euthyroid patients on low-dose PTU or methimazole that become pregnant, will you continue the medication?

A

No.

Recent recommendations suggest discontinuation of antithyroid medication in a newly pregnant woman with Graves’ disease, who is euthyroid on a low dose of methimazole (<5–10 mg/day) or PTU (<100–200 mg/day), after evaluating recent thyroid function tests, disease history, goiter size, duration of therapy, and TRAb measurement

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108
Q

What is the ratio of conversion from PTU to methimazole?

A

15–20 mg of propylthiouracil to 1 mg of methimazole

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109
Q

Antithyroid drugs given to the mother can be used to treat the fetus and may be needed for ___ after delivery, until the maternal antibodies disappear from the baby’s circulation

A

1–3 months

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110
Q

T or F. Breast-feeding is safe with low doses of antithyroid drugs

A

True

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111
Q

Rare and presents as a life-threatening exacerbation of hyperthyroidism, accompanied by fever, delirium, seizures, coma, vomiting, diarrhea, and jaundice

A

Thyrotoxic crisis, or thyroid storm

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112
Q

Most common causes of mortality in thyroid storm (3)

A

Cardiac failure
Arrhythmia
Hyperthermia

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113
Q

Thyrotoxic crisis is usually precipitated by (3)

A
  1. acute illness (e.g., stroke, infection, trauma, diabetic ketoacidosis)
  2. surgery (especially on the thyroid)
  3. radioiodine treatment of a patient with partially treated or untreated hyperthyroidism
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114
Q

Dose of PTU in thyroid storm

A

Propylthiouracil 500–1000 mg loading dose and 250 mg every 4 h

Alternative: Methimazole 20 mg every 6 h

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115
Q

Antithyroid drug of choice for thyroid storm

A

PTU

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116
Q

In the management of thyroid storm, ___ hour after the first dose of propylthiouracil, ____ is given to block thyroid hormone synthesis via the Wolff-Chaikoff effect

A 
One 
stable iodide (5 drops SSKI every 6 h)
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117
Q

Dose of propranolol in thyroid storm

A

60–80 mg PO every 4 h; or 2 mg IV every 4 h

high doses of propranolol decrease T4 → T3 conversion, and the doses can be easily adjusted.

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118
Q

Dose of hydrocortisone in thyroid storm

A

300 mg IV bolus, then 100 mg every 8 h

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119
Q

Drugs that may be given to sequester thyroid hormones

A

Cholestyramine

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120
Q

Management of severe thyroid ophthalmopathy, with optic nerve involvement or chemosis resulting in corneal damage

A
  1. refer to ophthalmologist
  2. Pulse therapy with IV methylprednisolone (e.g., 500 mg of methylprednisolone once weekly for 6 weeks, then 250 mg once weekly for 6 weeks)
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121
Q

Typically presents with a short thyrotoxic phase due to the release of preformed thyroid hormones and catabolism of Tg

A

Destructive thyroiditis (subacute or silent thyroiditis)

True hyperthyroidism is absent, as demonstrated by a low radionuclide uptake

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122
Q

Amiodarone treatment is associated with thyrotoxicosis in up to ___ of patients, particularly in areas of low iodine intake

A

10%

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123
Q

A rare cause of thyrotoxicosis that is characterized by the presence of an inappropriately normal or increased TSH level in a patient with hyperthyroidism, diffuse goiter, and elevated T4 and T3 levels

A

TSH-secreting pituitary adenoma

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124
Q

Supports the diagnosis of TSH-secreting pituitary adenoma

A

Elevated levels of the α-subunit of TSH

released by the TSH-secreting adenoma

confirmed by demonstrating the pituitary tumor on MRI or CT scan

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125
Q

Ρare and due to suppurative infection of the thyroid

A

Acute thyroiditis

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126
Q

Μost common cause of acute thyroiditis ins children and young adults

A

presence of a piriform sinus

Such sinuses are predominantly left-sided

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127
Q

Remnant of the fourth branchial pouch that connects the oropharynx with the thyroid

A

piriform sinus

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128
Q

The patient presents with abrupt onset thyroid pain, often referred to the throat or ears, and a small, tender goiter that may be asymmetric. Fever, dysphagia, and erythema over the thyroid are common, as are systemic symptoms of a febrile illness and lymphadenopathy

A

Acute thyroiditis

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129
Q

In acute thyroiditis, thyroid function is low, normal, or high?

A

Normal

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130
Q

Other terms for subacute thyroiditis (3)

A

de Quervain’s thyroiditis
granulomatous thyroiditis
viral thyroiditis

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131
Q

Peak incidence of subacute thyroiditis and sex predilection

A

30–50 years

women are affected three times more frequently than men

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132
Q

The patient usually presents with a painful and enlarged thyroid, sometimes accompanied by fever. There may be features of thyrotoxicosis or hypothyroidism, depending on the phase of the illness. Malaise and symptoms of an upper respiratory tract infection may precede the thyroid-related features by several weeks.

A

Subacute thyroiditis

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133
Q

The patient typically complains of a sore throat, and examination reveals a small goiter that is exquisitely tender. Pain is often referred to the jaw or ear

A

Subacute thyroiditis

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134
Q

Usual outcome of subacute thyroiditis

A

Complete resolution

but late-onset permanent hypothyroidism occurs in 15% of cases, particularly in those with coincidental thyroid autoimmunity

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135
Q

In subacute thyroiditis, thyroid function tests characteristically evolve through three distinct phases over about____ : (1)____, (2)______, and (3) ____

A

6 months

thyrotoxic phase
hypothyroid phase
recovery phase

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136
Q

Cause of thyrotoxic phase in subacute thyroiditis

A

Discharge of hormones from damaged thyroid cells

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137
Q

Treatment of subacute thyroiditis

A
  1. Aspirin 600 mg every 4-6 h
  2. NSAIDs

sufficient to control symptoms in many cases. If not, may give glucocorticoids

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138
Q

Dose of glucocorticoids in subacute thyroiditis

A

15–40 mg of prednisone gradually tapered over 6–8 weeks. . If a relapse occurs during glucocorticoid withdrawal, the dosage should be increased and then withdrawn more gradually

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139
Q

Thyroid function monitoring in subacute thyroiditis during treatment

A

TSH and FT4 every 2-4 weeks

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140
Q

T or F. PTU and methimazole may be used in the thyrotoxic phase of subacute thyroiditis

A

False. antithyroid drugs play no role in treatment of the thyrotoxic phase

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141
Q

Treatment of hypothyroid phase of subacute thyroiditis

A

Levothyroxine replacement 50–100 μg daily

Low dose is given to allow TSH-mediated recovery

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142
Q

Painless thyroiditis

A

“silent” thyroiditis

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143
Q

Postpartum thyroidiris

A

“silent” thyroiditis

The condition occurs in up to 5% of women 3–6 months after pregnancy and is then termed postpartum thyroiditis

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144
Q

Silent thyroiditis is associated with the presence of ___ antibodies antepartum

A

TPO

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145
Q

Silent thyroiditis is three times more common in

A

women with type 1 diabetes mellitus

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146
Q

Difference between silent and subacute thyroiditis (4)

A

Silent:

  1. Painless
  2. Normal ESR
  3. Presence of TPO
  4. No response to glucocorticoids
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147
Q

Severe thyrotoxic symptoms of silent thyroiditis can be managed with

A

Brief course of propranolol, 20–40 mg three or four times daily

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148
Q

Thyroxine replacement may be needed for the hypothyroid phase of silent thyroiditis but should be withdrawn after ____, as recovery is the rule

A

6–9 months

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149
Q

Drug-induced thyroiditis is caused by (4)

A
  1. IFN-alpha
  2. IL-2
  3. TKI
  4. Amiodarone
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150
Q

The most common clinically apparent cause of chronic thyroiditis

A

Hashimoto’s thyroiditis

An autoimmune disorder that often presents as a firm or hard goiter of variable size

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151
Q

A rare disorder that typically occurs in middle-aged women and presents with an insidious, painless goiter with local symptoms due to compression of the esophagus, trachea, neck veins, or recurrent laryngeal nerves

A

Riedel’s thyroiditis

Goiter is hard, nontender, often asymmetric, and fixed, leading to suspicion of a malignancy

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152
Q

Dense fibrosis disrupts normal thyroid gland architecture and can extend outside the thyroid capsule. This is seen in

A

Riedel’s thyroiditis

Despite these extensive histologic changes, thyroid dysfunction is uncommon

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153
Q

Any acute, severe illness can cause abnormalities of circulating TSH or thyroid hormone levels in the absence of underlying thyroid disease, making these measurements potentially misleading. This is called

A

Sick euthyroid syndrome

Unless a thyroid disorder is strongly suspected, the routine testing of thyroid function should be avoided in acutely ill patients.

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154
Q

The major cause of these hormonal changes is the release of cytokines most especially

A

IL-6

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155
Q

The most common hormone pattern in sick euthyroid syndrome (SES), also called nonthyroidal illness (NTI), is a decrease in _____ with normal levels of _____

A

Decrease total and unbound T3 levels (low T3 syndrome)

normal T4 and TSH

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156
Q

Which SES syndrome has poorer prognosis?

A

Low T4 syndrome – in very sick patients

dramatic fall in total T4 and T3 levels

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157
Q

Amiodarone is what type of antiarrhythmic drug?

A

Type III

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158
Q

Amiodarone is structurally related to thyroid hormone and contains ___ iodine by weight

A

39%

Thus, typical doses of amiodarone (200 mg/d) are associated with very high iodine intake, leading to greater than fortyfold increases in plasma and urinary iodine levels

Moreover, because amiodarone is stored in adipose tissue, high iodine levels persist for >6 months after discontinuation of the drug

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159
Q

Amiodarone has the following effects on thyroid function

A
  1. acute, transient suppression of thyroid function
  2. hypothyroidism in patients susceptible to the inhibitory effects of a high iodine load
  3. thyrotoxicosis that may be caused by either a Jod-Basedow effect from the iodine load, in the setting of MNG or incipient Graves’ disease, or a thyroiditis-like condition
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160
Q

Iodide- dependent suppression of the thyroid is called

A

Wolff-Chaikoff effect

161
Q

hyperthyroidism following administration of iodine or iodide, either as a dietary supplement or as iodinated contrast for medical imaging

A

Jod-Basedow phenomenon

162
Q

Type of amiodarone-induced thyrotoxicosis that is associated with an underlying thyroid abnormality (preclinical Graves’ disease or nodular goiter). Thyroid hormone synthesis becomes excessive as a result of increased iodine exposure (Jod-Basedow phenomenon)

A

Type 1 AIT

Increased vascularity

163
Q

Type of amiodarone-induced thyrotoxicosis that occurs in individuals with no intrinsic thyroid abnormalities and is the result of drug-induced lysosomal activation leading to destructive thyroiditis with histiocyte accumulation in the thyroid; the incidence rises as cumulative amiodarone dosage increases

A

Type 2 AIT

Decreased vascularity

164
Q

Treatment of type 1 AIT (3)

A
  1. discontinuation of amiodarone
  2. potassium perchlorate 200 mg every 6 h - reduce thyroidal iodide content
  3. Near-total thyroidectomy
165
Q

Treatment of type 2 AIT (4)

A
  1. discontinuation of amiodarone
  2. glucocorticoids – modest benefit
  3. Lithium
  4. Near-total thyroidectomy
166
Q

An autosomal dominant syndrome that causes inappropriate PTH secretion and increased renal tubular calcium reabsorption

A

Familial hypocalciuric hypercalcemia (FHH)

167
Q

Familial hypocalciuric hypercalcemia that involve inactivating mutations in the calcium sensor receptor (CaSR)

A

FHH type 1

168
Q

Familial hypocalciuric hypercalcemia that involve mutations in the G11 protein (GNA11)

A

FHH type 2

169
Q

Familial hypocalciuric hypercalcemia that involve mutation in the adaptor-related protein complex 2, -2 subunit (AP2S1)

A

FHH type 3

170
Q

Many solid tumors produce this protein that mimick effects of PTH on bone and the kidney

A

PTH-related peptide (PTHrP)

PTH levels are suppressed by the high serum calcium levels

171
Q

Value of mild hypercalcemia

A

up to 11–11.5 mg/dL

172
Q

Value of severe hypercalcemia

A

> 12–13 mg/dL

May result in lethargy, stupor, or coma, gastrointestinal symptoms (nausea, anorexia, constipation, or pancreatitis

173
Q

ECG changes in hypercalcemia (3)

A
  • Bradycardia
  • AV block
  • Short QT interval
174
Q

First step in the approach to hypercalcemia

A

Ensure that the alteration in serum calcium levels is not due to abnormal albumin concentrations

About 50% of total calcium is ionized – may be directly measured but may be influenced by collection methods and other artifacts. The rest is bound principally to albumin

175
Q

Corrected calcium formula if with low albumin

A

Total calcium + (0.2 mM (0.8 mg/dL) * every decrement in serum albumin of 1.0 g/dL below the reference value of 4.1 g/dL for albumin

176
Q

Most common cause of chronic hypercalcemia

A

Primary hyperparathyroidism

177
Q

Second most common cause of hypercalcemia

A

Hypercalcemia of malignancy

178
Q

Second most important laboratory test once true hypercalcemia is established

A

PTH level

179
Q

PTH, Ca, and phosphorus are low or high in primary hyperthyroidism

A

Increased PTH, elevated calcium, low phosphorus

180
Q

Calcium/creatinine clearance ratio that suggest FHH

A

<0.01

Calcium/creatinine clearance ratio – urine/serum Ca divided by urine/serum crea

181
Q

Most common cause of low PTH, elevated Ca

A

Malignancy

182
Q

Hypercalcemia in granulomatous disorders is caused by

A

Increased Serum 1,25(OH)2D levels

183
Q

Initial therapy of significant, symptomatic hypercalcemia

A

volume expansion

4–6 L of IV saline may be required over the first 24 h
Underlying comorbidities may require the use of loop diuretics to enhance Na and Ca excretion

184
Q

Commonly used drug for the treatment of hypercalcemia of malignancy

A

Bisphosphonates

  • Zoledronic acid – 4 mg IV over 30 mins
  • Pamidronate – 60-90 mg IV over 2-4 h
  • Ibandronate – 2 mg IV over 2 h
185
Q

Potent inhibitor of bone resorption that treat hypercalcemia that is refractory to bisphosphonates

A

Denosumab – 120 mg SQ on days 1, 8, 15, and 29 and then every 4 weeks

186
Q

Preferred therapy in patients with 1,25(OH)2D-mediated hypercalcemia

A

Glucocorticoids

  • IV hydrocortisone – 100-300 mg daily
  • Oral prednisone – 40-60 mg daily for 3-7 days
187
Q

Low calcim, high PTH

A

secondary hyperparathyroidism

188
Q

Most common causes of hypocalcemia (2)

A

Impaired PTH production

Impaired Vitamin D production

189
Q

Twitching of the circumoral muscles in response to gentle tapping of the facial nerve just anterior to the ear

A

Chvostek’s sign

190
Q

Carpal spasm induced by inflation of a blood pressure cuff to 20 mmHg above the patient’s systolic blood pressure for 3 min

A

Trousseau’s sign

191
Q

Treatment of acute, symptomatic hypocalcemia

A

Calcium gluconate – 10 mL 10% wt/vol (90 mg or 2.2 mmol) IV, diluted in 50 mL of 5% dextrose or 0.9% sodium chloride, given intravenously over 5 min

May need constant IV infusion if with continuing hypocalcemia  10 amp of Ca gluconate or 900 mg of calcium in 1 L of 5% dextrose or 0.9% sodium chloride administered over 24 h

Magnesium supplement – if with hypomagnesemia

192
Q

Recently been approved by the FDA for the treatment of refractory hypoparathyroidism

A

PTH (1-84) (Natpara)

193
Q

Dose of vitamin D supplementation if vitamin D deficiency is due to nutritional deficiency

A

Vitamin D 50,000 U, 2–3 times per week for several months

194
Q

Dose of vitamin D supplementation if vitamin D deficiency is due to malabsorption of Vit D

A

Vitamin D 100,000 U/d or more

195
Q

Primary hyperparathyroidism often presents in its severe form with skeletal complications

A

osteitis fibrosa cystica

196
Q

Long-term stimulation of PTH secretion in renal insufficiency

A

Tertiary hyperparathyroidism

197
Q

Neurohypophysis is also known as the

A

Posterior pituitary

198
Q

Neurohypophysis produces two hormones

A
  1. arginine vasopressin (AVP)

2. oxytocin

199
Q

A deficiency of AVP secretion or action causes

A

diabetes insipidus (DI)

200
Q

A syndrome characterized by the production of large amounts of dilute urine

A

diabetes insipidus

201
Q

AVP secretion is regulated primarily by the

A

“effective” osmotic pressure of body fluids

202
Q

Specialized hypothalamic cells which are extremely sensitive to small changes in the plasma concentration of sodium and its anions but normally are insensitive to other solutes such as urea and glucose

A

osmoreceptors

203
Q

The average threshold, or set point, for AVP release corresponds to a plasma osmolarity of ____ and sodium level of ________

A

280 mosmol/L

135 meq/L

levels only 2–4% higher normally result in maximum antidiuresis

204
Q

The set point of the osmoregulatory system can be lowered by (4)

A
  1. Pregnancy
  2. Menstrual cycle
  3. Estrogen
  4. Relatively large, acute reductions in blood pressure or volume
205
Q

Stimuli that is extremely potent that they typically elicit immediate, 50- to 100-fold increases in plasma AVP

A

Nausea / emesis

act via the emetic center in the medulla

AVP secretion also can be stimulated by nausea, acute hypoglycemia, glucocorticoid deficiency, smoking, and, possibly, hyperangiotensinemia

206
Q

The most important, if not the only, physiologic action of AVP is to

A

reduce water excretion by promoting concentration of urine

207
Q

AVP acts on what part of the kidney (2)

A

distal tubule and medullary collecting ducts

In the absence of AVP, these cells are impermeable to water and reabsorb little, if any, of the relatively large volume of dilute filtrate that enters from the proximal nephron

In the presence of AVP, these cells become selectively permeable to water, allowing the water to diffuse back down the osmotic gradient created by the hypertonic renal medulla

208
Q

Like AVP, thirst is regulated primarily by an osmostat that is situated in the _______ and is able to detect very small changes in the plasma concentration of sodium and its anions.

A

anteromedial hypothalamus

209
Q

The thirst osmostat appears to be “set” about ____ higher than the AVP osmostat

A

3%

This arrangement ensures that thirst, polydipsia, and dilution of body fluids do not occur until plasma osmolarity/sodium starts to exceed the defensive capacity of the antidiuretic mechanism

210
Q

A decrease of _____ in the secretion or action of AVP usually results in DI

A

75% or more

211
Q

In DI, the 24-h urine volume exceeds______, and the osmolarity is ______

A

40 mL/kg body weight

<300 mosmol/L

212
Q

A primary deficiency of AVP secretion usually results from agenesis or irreversible destruction of the neurohypophysis. It is referred to as

A

central DI

Also known as neurohypophyseal DI, neurogenic DI,
pituitary DI, cranial DI,

usually idiopathic

213
Q

Pituitary DI caused by surgery in or around the neurohypophysis usually appears within

A

24 h

After a few days, it may transition to a 2- to 3-week period of inappropriate antidiuresis, after which the DI may or may not recur permanently

214
Q

Most common genetic form of DI is an autosomal _____ and is caused by diverse mutations in the coding region of one allele of the ____

A

Dominant

AVP– neurophysin II (or AVP-NPII) gene

215
Q

Form of pituitary DI that is caused by mutations of the WFS 1 gene

A

Wolfram’s syndrome

216
Q

Wolfram’s syndrome is composed of (4)

A

DIDMOAD

DI
Diabetes Mellitus
Optic Atrophy
Neural Deafness

217
Q

A primary deficiency of plasma AVP also can result from increased metabolism by an N-terminal aminopeptidase produced by the placenta

A

gestational DI

signs and symptoms manifest during pregnancy and usually remit several weeks after delivery

218
Q

Secondary deficiencies of AVP secretion result from inhibition by excessive intake of fluids. This is called

A

primary polydipsia

219
Q

3 categories of primary polydipsia

A

dipsogenic DI
psychogenic polydipsia
iatrogenic polydipsia

220
Q

Form of DI characterized by inappropriate thirst caused by a reduction in the set of the osmoregulatory mechanism. It sometimes occurs in association with multifocal diseases of the brain such as neurosarcoid, tuberculous meningitis, and multiple sclerosis but is often idiopathic.

A

dipsogenic DI

221
Q

Primary deficiencies in the antidiuretic action of AVP

A

nephrogenic DI

222
Q

Most common genetic form of nephrogenic DI

A

semirecessive X-linked caused by mutation in the coding region of the the V2 receptor

223
Q

When will hypernatremia and other overt physical or laboratory signs of dehydration develop in patients with DI?

A

If patient also has a defect in thirst or fails to increase fluid intake for some other reason

polyuria results in a small (1–2%) decrease in body water and a commensurate increase in plasma osmolarity and sodium that stimulates thirst and a compensatory increase in water intake

224
Q

In the approach to patients with DI, if basal plasma osmolarity and sodium are within normal limits, the traditional approach is to determine the effect of (2) ______ on urine osmolarity

A

fluid deprivation

injection of antidiuretic hormone

225
Q

Test that differentiate pituitary and nephrogenic DI once primary polydipsia has been ruled out

A

2 μg of the AVP analogue, desmopressin

this approach is of little or no diagnostic value if fluid deprivation results in concentration of the urine because the increases in urine osmolarity achieved both before and after the injection of desmopressin are similar in patients with partial pituitary DI, partial nephrogenic DI, and primary polydipsia

226
Q

Effect of fluid deprivation in DI

A

raises plasma osmolarity and sodium without inducing concentration of the urine

227
Q

A simpler, and less stressful, but equally reliable way to differentiate between pituitary DI, nephrogenic DI, and primary polydipsia is measure

A

Basal plasma AVP and urine osmolarity under conditions of unrestricted fluid intake

228
Q

If AVP is normal or elevated (>1 pg/mL) and the concurrent urine osmolarity is low (<300 mosm/L)

A

nephrogenic DI

229
Q

If basal plasma AVP is low or undetectable (<1 pg/mL), what is the next step?

A

MRI of the brain

to differentiate pituitary DI from primary polydipsia

230
Q

Difference in the MRI of primary polydipsia and pituitary DI

A

primary polydipsia – presence of bright spot (normal)

pituitary DI – absent or abnormally small bright spot

231
Q

Medical treatment of pituitary DI

A

desmopressin (DDAVP)

232
Q

DDAVP acts selectively at ___receptors to ______ urine concentration and _____ urine flow in a dose- dependent manner

A

V2

Increase

Decrease

233
Q

Onset of antidiuresis of IV DDAVP and oral DDAVP

A

Rapid.
15 min after IV
60 min after oral

234
Q

Effect of desmopressin test if the diagnosis is primary polydipsia

A

Hyponatremia

235
Q

T or F. Primary polydipsia can be treated with desmopressin

A

False. Primary polydipsia cannot be treated safely with DDAVP or any other antidiuretic drug because eliminating the polyuria does not eliminate the urge to drink. Therefore, it invariably produces hyponatremia and/or other signs of water intoxication, usually within 8–24 h if urine output is normalized completely

236
Q

Management of nephrogenic DI (3)

A

Management of nephrogenic DI (3)

237
Q

The most common cause of an increase in total body sodium

A

primary hyperaldosteronism

238
Q

form of hypernatremia due to a primary defect in the thirst mechanism

A

hypodipsic hypernatremia

239
Q

a syndrome characterized by chronic or recurrent hypertonic dehydration

A

hypodipsic hypernatremia

240
Q

Most common cause of hypodipsia

A

hypogenesis or destruction of the osmoreceptors in the anterior hypothalamus that regulate thirst

These defects can result from various congenital malformations of midline brain structures or may be acquired due to diseases such as occlusions of the anterior communicating artery, primary, or metastatic tumors in the hypothalamus, head trauma, surgery, granulomatous diseases such as sarcoidosis and histiocytosis, AIDS, and cytomegalovirus encephalitis

241
Q

Management of hypodipsic hypernatremia

A
  1. oral water

2. hypotonic IV fluids

242
Q

An increase in total body water that exceeds the increase in total body sodium

A

hypervolemic hyponatremia (type 1)

243
Q

A decrease in body sodium greater than the decrease in body water

A

hypovolemic hyponatremia (type 2)

244
Q

an increase in body water with little or no change in body sodium

A

euvolemic hyponatremia (type 3)

245
Q

Causes of hypervolemic hyponatremia (2)

A
  1. severe congestive heart failure

2. cirrhosis

246
Q

Causes of hypovolemic hyponatremia (3)

A
  1. severe diarrhea
  2. diuretic abuse
  3. mineralocorticoid deficiency
247
Q

Causes of euvolemic hyponatremia

A
  1. defect in the osmotic suppression of AVP

Defect in the osmotic suppression of AVP can have either of two causes

  • nonhemodynamic stimulus such as nausea or a cortisol deficiency, which can be corrected quickly by treatment with antiemetics or cortisol
  • primary defect in osmoregulation caused by another disorder such as malignancy, stroke, or pneumonia that cannot be easily or quickly corrected (SIADH)
248
Q

primary defect in osmoregulation caused by another disorder such as malignancy, stroke, or pneumonia

A

SIADH

249
Q

In acute symptomatic SIADH, the aim of therapy should be to ______ plasma osmolarity and/ or plasma sodium at a rate ____ an hour until they reach levels of _____ or_____, respectively

A

Raise
~1%
~270 mosmol/L
130 meq/L

250
Q

Medical treatment of acute, symptomatic SIADH

A

AVP receptor-2 antagonist (vaptan)

251
Q

Vaptan that has a combined V2/V1a antagonist action that has been approved for short-term, in-hospital IV treatment of SIADH

A

Conivaptan

252
Q

Oral vaptan

A

Tolvaptan

253
Q

Acute, potentially fatal neurologic syndrome characterized by quadriparesis, ataxia, and abnormal extraocular movements that occurs during correction of hyponatremia when Na is raised faster than 1mEq/L per hour

A

central pontine myelinolysis

254
Q

In chronic and/or minimally symptomatic SIADH, the hyponatremia can and should be corrected more gradually by restricting total fluid intake to less than the sum of urinary and insensible losses. The aim should be to reduce total discretionary intake (all liquids) to _____ less than urinary output

A

~500 mL

Because the water derived from food (300–700 mL/d) usually approximates basal insensible losses in adults, t

255
Q

The best approach for treatment of chronic SIADH is the administration of

A

Tolvaptan (oral vaptan)

Other drugs:
Demeclocycline
fludrocortisone

256
Q

A selective AVP V2 antagonist that also increases urinary water excretion by blocking the antidiuretic effect of AVP

A

Tolvaptan

257
Q

Treatment of hyponatremia in SIAD due to an activating mutation of the V2 receptor

A

osmotic diuretic such as urea

258
Q

When diffuse enlargement of the thyroid occurs in the absence of nodules and hyperthyroidism, it is referred to as

A

diffuse nontoxic goiter

259
Q

diffuse nontoxic goiter is also known as (2)

A 
simple goiter(absence of nodules)
colloid goiter (presence of uniform follicles that are filled with colloid)
260
Q

Diffuse goiter is termed as endemic goiter when it affects ____ of the population

A

> 5%

261
Q

Thyroid enlargement in teenagers

A

juvenile goiter

262
Q

Examples of environmental goitrogens

A
  1. cassava root (contains thiocyanate)
  2. cruciferous vegetables (Brussels sprouts, cabbage, and cauliflower)
  3. milk from regions where goitrogens are present in grass
263
Q

Examination reveals a symmetrically enlarged, nontender, generally soft thyroid gland without palpable nodule, with a lateral lobe with a volume greater than the thumb of the individual being examined

A

Diffuse nontoxic goiter

264
Q

On ultrasound, total thyroid volume exceeding ____ is considered abnormal

A

30 mL

265
Q

Goiter that may obstruct the thoracic inlet

A

Substernal goiter

266
Q

Refers to facial and neck congestion due to jugular venous obstruction when the arms are raised above the head, a maneuver that draws the thyroid into the thoracic inlet

A

Pemberton’s sign

267
Q

A low TSH with a normal free T3 and free T4, particularly in older patients, suggests the possibility of thyroid autonomy or undiagnosed Graves’ disease, and is termed

A

subclinical thyrotoxicosis

268
Q

T or F. Treatment of subclinical hyperthyroidism is not recommended in the elderly

A

False. Increasingly recommended to reduce the risk of atrial fibrillation and bone loss

269
Q

Usual reason for surgery in diffuse nontoxic goiter (2)

A
  1. Compressive symptoms or obstruction of the thoracic inlet
  2. Cosmetic reasons

Surgery is rarely indicated for diffuse goiter
Subtotal or near-total thyroidectomy

270
Q

Aim of levothyroxine treatment post surgery of DNTG

A

keep the TSH level at the lower end of the reference interval to prevent regrowth of the goiter

271
Q

Usual clinical manifestation of multinodular goiter

A

asymptomatic and euthyroid

272
Q

Sudden pain in an MNG is usually caused by (2)

A
  1. hemorrhage into a nodule

2. Possibility of invasive malignancy

273
Q

Hoarseness, reflecting laryngeal nerve involvement, in MNG suggests

A

malignancy

274
Q

In MNG, tracheal deviation is common, but compression must usually exceed ____ of the tracheal diameter before there is significant airway compromise

A

70%

275
Q

T or F. The risk of malignancy in MNG is similar to that in solitary nodules

A

True

276
Q

Medication that may cause acute, subacute or chronic thyroiditis

A

Amiodarone

277
Q

Most common bacteria associated with acute thyroiditis (3)

A

Staphylococcus, Streptococcus, and Enterobacter

278
Q

In MNG, contrast agents and other iodine-containing substances should be avoided because of the risk of inducing the

A

Jod-Basedow effect

enhanced thyroid hormone production by autonomous nodules

279
Q

Toxic MNG is more common in what population

A

Elderly

May present with atrial fibrillation or palpitations, tachycardia, nervousness, tremor, or weight loss

280
Q

Thyroid scan of toxic MNG shows

A

heterogeneous uptake with multiple regions of increased and decreased uptake

281
Q

“Cold” nodules in thyroid scan

A

Decreased uptake

If present, fine-needle aspiration (FNA) may be indicated based on sonographic patterns and size cutoffs

282
Q

“Hot” nodules in thyroid scan

A

Increased uptake

Usually benign

283
Q

Treatment of choice for toxic MNG

A

Radioiodine

it treats areas of autonomy as well as decreasing the mass of the goiter by ablating the functioning nodules. Sometimes, however, a degree of autonomy may persist, presumably because multiple autonomous regions may emerge after others are treated, and further radioiodine treatment may be necessary

284
Q

Definitive treatment of underlying thyrotoxicosis as well as goiter in toxic MNG

A

Surgery

Patients should be rendered euthyroid using an antithyroid drug before operation

285
Q

A solitary, autonomously functioning thyroid nodule is referred to as

A

toxic adenoma

286
Q

Most patients with solitary hyperfunctioning nodules have acquired somatic, activating mutations in the

A

TSH-R

Less commonly, somatic mutations are identified in G.Sα, same mutations with McCune-Albright syndrome.
In most series, activating mutations in either the TSH-R or the GSα subunit genes are identified in >90% of patients with solitary hyperfunctioning nodules.

287
Q

Thyrotoxicosis in solitary hyperfunctioning nodule is usually mild and is generally only detected when the size of the nodule is

A

> 3 cm

288
Q

Provides a definitive diagnostic test for hyperfunctioning solitary nodule

A

Thyroid scan

Demonstrating focal uptake in the hyperfunctioning nodule and diminished uptake in the remainder of the gland, as activity of the normal thyroid is suppressed

289
Q

usually the treatment of choice for hyperfunctioning solitary nodule

A

Radioiodine ablation

131I is concentrated in the hyperfunctioning nodule with minimal uptake and damage to normal thyroid tissue

290
Q

Surgery for hyperfunctioning solitary nodule

A

Lobectomy

preserving thyroid function and minimizing risk of hypoparathyroidism or damage to the recurrent laryngeal nerves

291
Q

Thyroid nodules that reflect a combination of both macro- and microfollicular architecture and appear as mixed cystic/ solid or spongiform lesions on ultrasound

A

Hyperplastic

292
Q

Thyroid nodules that generally have a more monotonous microfollicular pattern

A

neoplastic, encapsulated adenomas

293
Q

If the thyroid adenoma is composed of oncocytic follicular cells arranged in a follicular pattern, this is termed

A

Hürthle cell adenoma

294
Q

The definition of spongiform requires the presence of microcystic areas comprising ____ of the thyroid nodule volume, with the concept that this microcystic sonographic pattern recapitulates the histology of ______

A

> 50%

macrofollicles containing colloid

295
Q

T or F. Majority of solid thyroid nodules (whether hypo-, iso-, or hyperechoic) are benign

A

True

296
Q

Diagnostic procedure of choice to evaluate thyroid nodules

A

Ultrasound-guided FNA

297
Q

In relative iodine deficiency, both ____ and ____ therapy have been demonstrated to decrease thyroid nodule volume

A

Iodine
Levothyroxine
If the nodule has not decreased in size after 6–12 months of therapy, treatment should be discontinued because little benefit is likely to accrue from long-term treatment
TSH suppression with levothyroxine therapy does not decrease thyroid nodule size in iodine-sufficient populations.

298
Q

Most common malignancy of the endocrine system

A

Thyroid carcinoma

299
Q

T or F. Thyroid cancer is twice as common in women as men and is associated with a worse prognosis in women

A

False. Thyroid cancer is twice as common in women as men, but male gender is associated with a worse prognosis

300
Q

Serum markers used to detect residual or recurrent medullary thyroid CA

A

Calcitonin

301
Q

T or F. Higher serum TSH levels, even within normal range, are associated with increased thyroid cancer risk in patients with thyroid nodules

A

True. These observations provide the rationale for T4 suppression of TSH in patients with thyroid cancer

302
Q

RET/PTC and PAX8-PPARg1 rearrangements, are relatively specific for

A

thyroid neoplasia.

303
Q

Activation of the _______ is seen in up to 70% of papillary thyroid carcinomas

A

RET-RAS-BRAF signaling pathway

simultaneous RET, BRAF, and RAS mutations rarely occur in the same tumor, suggesting that activation of the MAPK cascade is critical for tumor development, independent of the step that initiates the cascade

304
Q

Most common genetic alteration in PTC

A

BRAF V600E mutations

305
Q

Mutations in_____ , occur in about two-thirds of ATCs, but not in PTC or FTC

A

CTNNB1, which encodes β-catenin

306
Q

Mutations of the tumor-suppressor ____ play an important role in the development of ATC

A

P53

Because P53 plays a role in cell cycle surveil- lance, DNA repair, and apoptosis, its loss may contribute to the rapid acquisition of genetic instability as well as poor treatment responses

307
Q

Medullary thyroid carcinoma, when associated with multiple endocrine neoplasia (MEN) type 2, harbors an inherited mutation of the

A

RET gene

Unlike the rearrangements of RET seen in PTC, the mutations in MEN 2 are point mutations that induce constitutive activity of the tyrosine kinase

308
Q

The most common type of thyroid cancer

A

Papillary thyroid carcinoma

80–85% of well-differentiated thyroid malignancies

309
Q

Large, clear nuclei with powdery chromatin with nuclear grooves and prominent nucleoli seen in FNA of thyroid. What do you call this feature and what disease do you see this feature?

A

orphan Annie eye” appearance

Papillary thyroid carcinoma

The histologic finding of these cells arranged in either papillary structures versus follicles distinguishes the classic and follicular variants of PTC, respectively

310
Q

PTC has a propensity to spread via the lymphatic system but can metastasize hematogenously as well, particularly to

A

Bone and lung

Because of the relatively slow growth of the tumor, a significant burden of pulmonary metastases may accumulate, sometimes with remarkably few symptoms

311
Q

Micrometastases of PTC is defined as ____ of cancer in a lymph node

A

<2 mm

do not affect prognosis

312
Q

Gross PTC metastatic involvement of multiple ____ lymph nodes indicates a 25–30% chance of recurrence, and may increase mortality in older patients

A

2–3 cm

313
Q

Follicular thyroid CA is more common in iodine-deficient or sufficient areas?

A

Deficient

314
Q

Follicular carcinoma is different histologically to follicular adenoma because of the presence of

A

capsular and/or vascular invasion

315
Q

FTC tends to spread by hematogenous routes leading to this most common sites (3)

A

bone, lung, and central nervous system

316
Q

Poor prognostic features of FTC (5)

A
  1. distant metastases
  2. age >50 years
  3. primary tumor size >4 cm
  4. Hürthle cell histology
  5. Marked vascular invasion
317
Q

All well-differentiated thyroid cancers with the size of ____ should be surgically excised although active surveillance may be an option for _______ without metastases

A

> 1cm (T1b or larger)

small intrathyroidal micropapillary thyroid cancers (T1a)

318
Q

Initial surgical procedure for patients with intrathyroidal cancers >1 cm and <4 cm (T1b and T2 tumors) in the absence of metastatic disease

A

unilateral (lobectomy) or bilateral (near total thyroidectomy)

319
Q

Surgey for thyroid tumors >4 cm or in the presence of metastases or clinical evidence of extrathyroidal invasion

A

near-total thyroidectomy

For patients at high risk for recurrence, bilateral surgery allows administration of radioiodine for remnant ablation and potential treatment of iodine-avid metastases, if indicated, as well as for monitoring of serum Tg levels

320
Q

Medical therapy that is a mainstay of thyroid cancer treatment

A

levothyroxine suppression of TSH

Because most tumors are still TSH-responsive

321
Q

In thyroid caner, or patients at low risk of recurrence, TSH should be maintained at the ______. For patients either at intermediate or high risk of recurrence, TSH levels should be kept to _____ and____, respectively, if there are no strong contraindications to mild thyrotoxicosis. TSH should be _____ for those with known metastatic disease

A

Low-risk: lower normal limit (0.5–2.0 mIU/L)

Intermediate: 0.1 to 0.5 mIU/L

High: <0.1 mIU/L

Metastatic: <0.1 mIU/L

322
Q

After near-total thyroidectomy, ____of thyroid tissue remains in the thyroid bed. This residual thyroid is eliminated by ____

A

<1 g

Postsurgical radioablation

use 131I for thyroid ablation should be coordinated with the surgical approach, because radioablation is much more effective when there is minimal remaining normal thyroid tissue.

323
Q

Indications of radioablation therapy of well-differentiated thyroid CA (5)

A
  1. larger tumors
  2. more aggressive variants of papillary cancer
  3. tumor vascular invasion
  4. extrathyroidal invasion
  5. presence of large-volume lymph node metastases
324
Q

Radioiodine is administered after (what diet) and in the presence of _______to stimulate uptake of the isotope into both the remnant and potentially any residual tumor

A

iodine depletion (patient follows a low-iodine diet for 1–2 weeks)

elevated serum TSH levels

325
Q

To achieve high serum TSH levels prior to radioablation, there are two approaches:

A
  1. withdraw thyroid hormone

2. treat with liothyronine 25 μg qd or bid followed by thyroid hormone withdrawal for 2 weeks

326
Q

A sensitive marker of residual/recurrent thyroid cancer after ablation of the residual postsurgical thyroid tissue

A

Serum thyroglobulin

327
Q

When do you perform neck ultrasound after thyroid ablation?

A

After 6 months

Because the vast majority of PTC recurrences are in cervical lymph nodes

328
Q

Aside from radioiodine, this therapy can also be used to treat gross residual neck disease or specific metastatic lesions, particularly when they cause bone pain or threaten neurologic injury

A

external beam radiotherapy

329
Q

Group of drugs that are being explored as a means to target pathways known to be active in thyroid cancer, including the RAS, BRAF, RET, EGFR, VEGFR, and angiogenesis pathways

A

Kinase inhibitors

Sorafenib

330
Q

Poorly differentiated and aggressive thyroid cancer

A

Anaplastic Thyroid Cancer

331
Q

The prognosis of ATC is poor, and most patients die within ____ of diagnosis

A

6 months

332
Q

Because of the undifferentiated state of these tumors, the uptake of radioiodine is usually_____

A

Negligible

but it can be used therapeutically if there is residual uptake

333
Q

Lymphoma in the thyroid gland often arises in the background of

A

Hashimoto’s thyroiditis

334
Q

A rapidly expanding thyroid mass that occurs with Hashimoto’s thyroiditis is suggestive of

A

Thyroid Lymphoma

335
Q

Most common type of lymphoma in the thyroid

A

Diffuse large-cell lymphoma

336
Q

Thyroid biopsies reveal sheets of lymphoid cells that can be difficult to distinguish from small-cell lung cancer or ATC.

A

Thyroid Lymphoma

337
Q

Treatment of thyroid lymphoma

A

External beam radiation

Surgical resection should be avoided as initial therapy because it may spread disease that is otherwise localized to the thyroid. If staging indicates disease outside of the thyroid, treatment should follow guidelines used for other forms of lymphoma

338
Q

3 familial forms of medullary thyroid carcinoma

A

MEN 2A
MEN 2B
Familial MTC without other features of MEN

339
Q

Which is more aggressive? MTC secondary to MEN2B or MEN 2A? And familial or sporadic?

A

MEN2B > MEN 2A

Familial > sporadic MTC

340
Q

All patients with MTC should be tested for what mutations

A

RET mutations

because genetic counseling and testing of family members can be offered to those individuals who test positive for mutations.

341
Q

Management of MTC is primarily

A

Surgical

External radiation treatment and targeted kinase inhibitors may provide palliation in patients with advanced disease

342
Q

Prior to surgery for MTC, this condition should be excluded in all patients with a RET mutation

A

pheochromocytoma

343
Q

Does MTC tumors take up radioiodine?

A

No. Unlike tumors derived from thyroid follicular cells, these tumors do not take up radioiodine.

344
Q

First diagnostic test in thyroid nodules

A

TSH

345
Q

If TSH is suppressed in thyroid nodule, what is the next step?

A

radionuclide scan

determine if the identified nod- ule is “hot,” as lesions with increased uptake are almost never malignant and FNA is unnecessary

346
Q

2015 ATA guidelines do not recommend FNA for any thyroid nodule ____ unless metastatic cervical lymph nodes are present

A

<1 cm

347
Q

Widely used to provide more uniform terminology for reporting thyroid nodule FNA cytology results

A

Bethesda System

348
Q

Grayscale sonographic features associated with thyroid cancer (6)

A
  1. Hypoechoic compared with surrounding thyroid
  2. Marked hypoechogenicity
  3. Microcalcifications
  4. Irregular, microlobulated margins
  5. Solid consistency
  6. Taller than wide shape on transverse view
349
Q

If TSH is normal or high in thyroid nodule, what is the next step?

A

Ultrasound for LN assessment

350
Q

If thyroid nodule is not functional on radionuclide scan with suppressed TSH, what is the next step?

A

Ultrasound for LN assessment

351
Q

After ultrasound with confirmation of presence of thyroid nodules, what is the next step?

A

FNA based on features and cutoffs

352
Q

If initial FNA of thyroid nodule is not diagnostic, what is the next step?

A

Repeat USD-guided FNA

353
Q

If FNA of thyroid nodule is suggestive of follicular neoplasm, what is the next step?

A

Molecular testing

354
Q

If FNA of thyroid nodule is suggestive of atypia or follicular lesion of undetermined significance, what is the next step?

A

Repeat USD-guided FNA or consider molecular testing

355
Q

If FNA of thyroid nodule is suggestive of benign lesion, what is the next step?

A

Follow-up

356
Q

Diagnostic categories of Bethesda Classification for Thyroid Cytology and the risk of malignancy. (6)

A

I. Nondiagnostic or unsatisfactory - 1–5%
II. Benign - 2–4%
III. Atypia or follicular lesion of unknown significance (AUS/FLUS) - 5–15%
IV. Follicular neoplasm - 15–30%
V. Suspicious for malignancy – 60-75%
VI. Malignant - 97–100%

357
Q

ACTH-producing corticotrope adenoma of the pituitary

A

Cushing’s disease

Majority of patients with Cushing’s disease

358
Q

Most common cause of Cushing’s syndrome

A

Medical use of glucocorticoids

359
Q

hyperpigmentation of the knuckles, scars, or skin areas exposed to increased friction due to stimulation of melanocyte pigment production

A

ectopic ACTH syndrome

360
Q

Weight gain, central obesity, rounded face, fat pad on back of neck (“buffalo hump”), Facial plethora, thin and brittle skin, easy bruising, broad and purple stretch marks, acne, hirsutism, Osteopenia, osteoporosis (vertebral fractures), decreased linear growth in children are symptoms of

A

Cushing’s syndrome

361
Q

Myopathy in Cushing’s syndrome

A

proximal

prominent atrophy of gluteal and upper leg muscles with difficulty climbing stairs or getting up from a chair

362
Q

Diagnostic tests for Cushing’s syndrome

A

Increased 24-h urinary free cortisol excretion in three separate collections

Failure to appropriately suppress morning cortisol after overnight exposure to dexamethasone

Evidence of loss of diurnal cortisol secretion with high levels at midnight

363
Q

T or F. Imaging should only be used after it is established whether the cortisol excess is ACTH-dependent or ACTH-independent

A

True

If with confirmed ACTH-independent cortisol excess
Adrenal imaging is indicated with unenhanced CT scan (helps to distinguish between benign and malignant adrenal lesions)

364
Q

Used in diagnosis of glucocorticoid excess

A

Dexamethasone Suppression Test

365
Q

If cortisol production is autonomous, what is the effect of dexamethasone

A

Little additional effect

366
Q

If cortisol production is driven by an ACTH-producing pituitary adenoma, what is the effect of dexamethasone

A

Ineffective at low doses but usually induces suppression at high doses.

367
Q

If cortisol production is driven by an ectopic source of ACTH, what is the effect of dexamethasone

A

Resistant to dexamethasone suppression

368
Q

Diagnostic test for ectopic ACTH syndrome:

A

High-resolution, fine-cut CT scanning of the chest and abdomen (for scrutiny of the lung, thymus, and pancreas)

369
Q

Treatment of choice for Cushing’s disease

A

Selective removal of the pituitary corticotrope tumor (endoscopic transsphenoidal approach)

370
Q

Drugs used in Cushing’s syndrome that inhibits cortisol synthesis at the level of 11β-hydroxylase

A

Metyrapone 500 mg/tab TID (maximum dose, 6 g)

371
Q

Antifungal drug used in Cushing’s syndrome that inhibits the early steps of steroidogenesis.

A

ketoconazole

372
Q

A derivative of an insecticide which is an adrenolytic agent used in adrenocortical carcinoma

A

Mitotane

373
Q

Ectopic ACTH production is predominantly caused by

A

occult carcinoid tumors, most frequently in the lung

but also in thymus or pancreas

Advanced small-cell lung cancer can cause ectopic ACTH production. In rare cases, ectopic CRH and/or ACTH production has been found to originate from medullary thyroid carcinoma or pheochromocytoma

374
Q

A rare cause of ACTH-independent Cushing’s that is also associated with polyostotic fibrous dysplasia, unilateral cafe-au-lait spots, and precocious puberty

A

McCune-Albright syndrome,

375
Q

Caused by activating mutations in the stimulatory G protein alpha subunit 1, GNAS-1.

A

McCune-Albright syndrome,

376
Q

The most important first step in the management of patients with suspected Cushing’s syndrome

A

establish the correct diagnosis

377
Q

the time of the physiologically lowest secretion of cortisol

A

midnight

378
Q

For ACTH-dependent cortisol excess, the imaging of choice is

A

MRI of the pituitary

379
Q

If dexamethason suppression and CRH responsiveness test show discordant results, the differential diagnosis for Cushing’s can be further clarified by performing

A

bilateral inferior petrosal sinus sampling (IPSS) with concurrent blood sampling for ACTH in the right and left inferior petrosal sinus and a peripheral vein

380
Q

Another test that can be done in in ectopic ACTH syndrome is the_____ which can be helpful in some cases because ectopic ACTH-producing tumors often express somatostatin receptors.

A

octreotide scintigraphy

381
Q

an anesthetic agent, can be used to lower cortisol in severe cases of cortisol excess

A

etomidate

by continuous IV infusion in low, nonanesthetic doses.

382
Q

Primary adrenal insufficiency is most commonly caused by

A

autoimmune adrenalitis

383
Q

transmitted in an autosomal recessive manner and is caused by mutations in the autoimmune regulator gene AIRE

A

autoimmune polyglandular syndrome 1

APS2 is much more prevalent and is of polygenic inheritance, with confirmed associations with the HLA-DR3 gene region in the major histocompatibility
complex and distinct gene regions involved in immune regulation.

384
Q

Cause of primary adrenal insufficiency characterized by alacrima, achalasia, and neurologic impairment

A

Triple A syndrome

385
Q

Cause of primary adrenal insufficiency characterized by progressive external ophthalmoplegia, pigmentary retinal degeneration, cardiac conduction defects, gonadal failure, hypoparathyroidis and type 1 diabetes

A

Kearns-Sayre syndrome

mitochondrial DNA deletions

386
Q

Characterized by the abrupt onset of fever, petechiae, arthralgia, weakness, and myalgias, followed by acute hemorrhagic necrosis of the adrenal glands and severe cardiovascular dysfunction

A

Waterhouse-Friderichsen syndrome

387
Q

primary adrenal insufficiency is also known as

A

Addison’s disease

388
Q

Adrenal insufficiency where there is loss of both glucocorticoid, mineralocorticoid secretion, and androgen secretion

A

Addison’s disease

In secondary adrenal insufficiency, on the other hand, only glucocorticoid deficiency is present, as the adrenal itself is intact and thus still amenable to regulation by the RAA system. Adrenal androgen secretion is disrupted in both primary and secondary adrenal insufficiency.

389
Q

A distinguishing feature of primary adrenal insufficiency

A

hyperpigmentation

caused by excess ACTH stimulation of melanocytes. It is most pronounced in skin areas exposed to increased friction or shear stress. It is also increased by sunlight.

On the other hand, in secondary adrenal insufficiency, the skin has an alabaster-like paleness due to lack of ACTH secretion.

390
Q

a characteristic biochemical feature in primary adrenal insufficiency and is found in 80% of patients at presentation

A

hyponatremia

Hyperkalemia is present in 40% of patients at initial diagnosis.

391
Q

The diagnosis of adrenal insufficiency is established by

A

short cosyntropin test

ACTH stimulation of cortisol production

administration of cosyntropin (ACTH 1-24), 0.25 mg IM or IV, and collection of blood samples at 0, 30, and 60 min for cortisol

392
Q

A normal response to cosyntropin test is defined as a cortisol level _______ 30–60 min after cosyntropin stimulation

A

> 20 μg/dL (>550 nmol/L)

393
Q

During the early phase of HPA disruption or within 4 weeks of pituitary insufficiency, patients may still respond to exogenous ACTH stimulation. In this circumstance, the _______ is an alternative choice but is more invasive.

A

Insulin tolerance test

It involves injection of insulin to induce hypoglycemia, which represents a strong stress signal that triggers hypothalamic CRH release and activation of the entire HPA axis. The ITT involves administration of regular insulin 0.1 U/kg IV (dose should be lower if hypopituitarism is likely) and collection of blood samples at 0, 30, 60, and 120 min for glucose, cortisol, and growth hormone (GH), if also assessing the GH axis. Oral or IV glucose is administered after the patient has achieved symptomatic hypoglycemia
(usually glucose <40 mg/dL).

394
Q

A normal response to Insulin tolerance test

is defined as a cortisol ____ and GH _______

A

> 20 μg/dL

> 5.1 μg/L

395
Q

Once adrenal insufficiency is confirmed, measurement of _____ is the next step

A

plasma ACTH

with increased levels defining primary and inappropriately low levels defining the secondary origin of disease

396
Q

Management of acute adrenal insufficiency (3)

A
  1. hydration
  2. bolus injection of 100 mg hydrocortisone, followed by the administration of 100–200 mg hydrocortisone over 24
  3. mineralocorticoid (once hydrocortisone dose is given at <50mg
397
Q

Glucocortcoid replacement in chronic adrenal insufficiency

A

15–25 mg hydrocortisone in two to three divided doses

Long-acting glucocorticoids such as prednisolone or dexamethasone are not preferred because they result in increased glucocorticoid exposure due to extended glucocorticoid receptor activation at times of
physiologically low cortisol secretion.

398
Q

Mineralocorticoid replacement in primary adrenal insufficiency

A

100–150 μg fludrocortisone

In patients living or traveling in areas with hot or tropical weather conditions, the fludrocortisone dose should be increased by 50–100 μg during the summer. Mineralocorticoid dose may also need to be adjusted during pregnancy, due to the anti-mineralocorticoid activity of progesterone, but this is less often required than hydrocortisone dose adjustment

PSBIM (12 decks)

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