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Thyroid Basic and Clinical
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Thyroid from 02/09/2015 to 08/092015
• Covers basics - Anatomy, Physiology, Pathology and Pharmacology
• Clinical - Surgery, Medicine, Thyroid diseases in pregnancy, Pediatrics
1) Action(s) of thyroid hormone
a) Increases oxygen consumption
b) Accelerates LDL cholesterol degradation
c) Increases myocyte relaxation .
d) Alters SA node depolarization and repolarization
e) All of the above
e) All of the above
Thyroid hormone increases oxygen consumption and thermogenesis.
Thyroid hormone increases expression of the low-density lipoprotein (LDL) receptor, resulting in accelerated LDL cholesterol degradation.
T3 increases myocyte contractility and relaxation by altering myosin heavy chain and sarcoplasmic reticulum ATPase.
Thyroid hormone increases the heart rate by altering sinoatrial node depolarization and repolarization.
Other physiologic effects of thyroid hormone include increased mental alertness, ventilatory drive, gastrointestinal motility, and bone turnover. During fetal development, thyroid hormone plays a critical role in brain development and skeletal maturation.
ACTIONS OF THYROID HORMONE
• Increases oxygen consumption
• Increases carbohydrate and lipid catabolism
• Stimulates protein synthesis
• Increases basal metabolic rate
• Increases thermogenesis
• Increases expression of the low-density lipoprotein (LDL) receptor
• Accelerates LDL cholesterol degradation
• Increases myocardial contractility and relaxation
• Increases the heart rate
• Increases mental alertness
• Increases ventilatory drive
• Increases gastrointestinal motility
• Increases bone turnover
• Brain development and skeletal maturation during fetal development
2) Weight of thyroid gland ----------- grams
a) 5
b) 20
c) 45
d) 90
b) 20
It is normally 12 to 25 grams in size. It is slightly heavier in females. It enlarges during menstruation and pregnancy.
3) Isthmus
a) First tracheal ring
b) Second and third tracheal ring
c) Fourth and fifth tracheal ring
d) First to fifth tracheal ring
b) Second and third tracheal ring
The isthmus connects the lower parts of the thyroid lobes. It is usually anterior to the second and third tracheal cartilages. It may be higher or sometimes lower. Its site and size vary greatly. An accessory lobe, the pyramidal lobe may be present in up to 50% of the population. It usually arises from the thyroid isthmus
4) Thyroid gland is in level with
a) C2 - C5
b) C5 - T1
c) C2 - T2
d) T1 - T4
b) C5 - T1
The thyroid is ensheathed by the ## pretracheal layer of deep cervical fascia.
The pretracheal fascia binds the thyroid to the trachea, and it moves with the trachea on swallowing.
## When there is thyroid enlargement, the attachment of the sternothyroid muscle to the trachea limits upward expansion of each lobe.
Inferior expansion may extend into the superior mediastinum, compressing the trachea and veins at the thoracic outlet
THE THYROID EXAM
• Look at the thyroid region. If the gland is quite enlarged, you may actually see it.
• To find the thyroid gland, first locate the thyroid cartilage (Adams Apple). This is a mid-line bulge towards the top of the anterior surface of the neck. The thyroid gland lies approximately 2-3 cm below the thyroid cartilage.
• If you're unsure, give the patient a glass of water and have them swallow as you watch this region. Thyroid tissue, along with all of the adjacent structures, will move up and down with swallowing. The normal thyroid is not visible. It is not worth going through this swallowing exercise if you don't see anything on gross inspection.
• Anterior palpation can be performed by using the thumb of one hand. Posterior palpation is done standing behind the seated patient with the tip of index, middle and ring fingers.
• If enlarged
o Is it symmetrically enlarged?
o Is the enlargement unilateral or bilateral?
o Are there discrete nodules within either lobe? If nodules are palpated, determine their shape, size, position, translucency, and consistency.
o If the gland feels firm, is it attached to the adjacent structures (i.e. fixed to underlying tissue, consistent with malignancy) or freely mobile (i.e., moves up and down with swallowing)?
• If there is concern regarding malignancy, a careful lymph node exam is important.
• A midline mass high in the neck, which rises further when the patient extends the tongue, is typical of a thyroglossal duct remnant or cyst.
• A systolic or continuous bruit over the thyroid suggests Graves' disease.
5) Method of choice to accurately estimate size of the thyroid gland is
a) Palpation
b) Ultrasound
c) Radioiodine
d) TSH scanning
Size of the thyroid gland can be estimated by ultrasound. Nodules as small as 2-3 mm can be detected. The right lobe is normally slightly larger than the left.
6) What is the first branch of the external carotid artery?
a) Superior thyroid arteries
b) Inferior thyroid arteries
c) Arteria thyroidea ima
d) Lingual arteries
e) Thymic artery
...
7) The recurrent laryngeal nerves are closely related to ---------
a) Superior thyroid arteries
b) Inferior thyroid arteries
c) Arteria thyroidea ima
d) Lingual arteries
...
8) What is the cause of Pemberton's sign?
a) Hyperthyroidism
b) Hypothyroidism
c) Retrosternal goiter
d) Thyroid malignancy
...
9) The ligament of Berry - False statement(s)
a) Closely attached to the cricoid cartilage
b) Attached to the capsule
c) Related to the recurrent laryngeal nerve
d) All
e) None
...
10) The recurrent laryngeal nerve - False statement
a) Supplies the cricothyroid
b) Damage to one recurrent laryngeal nerve results in a normal, but weak voice
c) Bilateral damage cause airway obstruction
d) All
e) None
...
11) Thyroid gland develops during --------------- of gestation
a) Third week
b) 11 week
c) 6 months
d) 8 months
a) Third week
The thyroid gland develops from the floor of the pharynx during the third week of gestation. The gland migrates from the foramen cecum at the base of the tongue. It migrates along the thyroglossal duct to reach the neck. Rarely, ectopic location of thyroid tissue is found at the base of the tongue (lingual thyroid). In most of these cases this may be the only thyroid tissue that remains. Enlargement of a lingual thyroid can cause airway obstruction, dysphagia, or bleeding. Most lingual thyroid glands can be suppressed with thyroid hormone administration. Thyroglossal duct disappears by 8th week of intrauterine life.
Thyroid hormone synthesis normally begins at about 11 weeks of gestation.
• 8th week
- Thyroglobulin synthesis
- Thyroglossal duct disappears
• 11 th week
- Synthesis of thyroid hormones and calcitonin
• 12 th week
- Iodide trapping
• 20 th week
- Hypothalamic-pituitary axis]
12) Which can cross the placenta?
a) T 3
b) T4
c) T4 and T 3
d) TSH, T4 and T 3
e) None
e) None
TSH, T4 and T 3 do not cross the placenta. Fetal hypothalamic - pituitary axis functions by 20th week. It is independent of maternal endocrine status.
13) Which is the only component of the adult thyroid gland not of endodermal origin?
a) Isthmus
b) Pyramidal lobe
c) Calcitonin-producing C cells
d) Right lobe
e) Left lobe
During development the tissue that ultimately becomes the thyroid gland arises initially as a midline diverticulum in the floor of the pharynx. This tissue originates in the primitive alimentary tract. It consists of cells of endodermal origin. Calcitonin-producing C cells arise from the fourth pharyngeal pouch. They migrate from the neural crest into the lateral lobes of the thyroid. These cells are distributed among the follicles. These C cells are the only component of the adult gland not of endodermal origin.
14) Pyramidal lobe - True statement
a) Enlarged parathyroid
b) Distal end of the thyroglossal duct
c) Sign of malignancy
d) Large cyst
b) Distal end of the thyroglossal duct
The pyramidal lobe represents the most distal portion of the thyroglossal duct.
The thyroglossal duct is usually reabsorbed after 6 to 8 weeks of intrauterine life. The distal end of the thyroglossal duct remnant may occasionally be retained and mature as a pyramidal lobe in the adult thyroid
15) What does thyroid colloid contain in large amounts?
a) Free T3
b) Free T4
c) Thyroglobulin
d) All of the above
e) None of the above
c) Thyroglobulin
The thyroid is divided by thin fibrous septae into lobules composed of about 20 to 40 follicles. Each thyroid follicle contains a single layer of follicular epithelial cells (known as thyrocytes) surrounding a lumen containing colloid. The principal component of colloid is thyroglobulin
16) True about thyroglobulin-
a) Precursor of thyroid hormones
b) Synthesized by the follicular cells
c) Contains tyrosine residues
d) All of the above
d) All of the above
a) Precursor of thyroid hormones
Thyroglobulin is an iodinated glycoprotein. Thyroglobulin is a prohormone (precursor of thyroid hormones).]
b) Synthesized by the follicular cells
The follicular cells synthesize thyroglobulin and then secrete it into the colloid.
c) Contains tyrosine residues
Thyroglobulin contains 115 tyrosine residues. Each tyrosine residue is a site for iodination. Iodide is required to complete thyroglobulin formation. Iodine enters the follicular cells by active transport from the blood capillaries. The iodinated thyroglobulin is proteolysed in the cell to yield thyroid hormones, which are secreted into the bloodstream.
17) What regulates thyroid follicular activity?
a) TSH
b) Sympathetics
c) TRH
d) Thyroxine
e) Thyroglobulin
a) TSH
Follicular activity is mainly controlled by TSH secreted from the pituitary gland.
Catecholamines enhance the incorporation of iodine and synthesis of hormones. Adrenergic receptor blockers abolish these effects. Adrenergic receptor blockers do not affect the ability of cells to respond to TSH.
c) TRH
Thyrotropin-releasing hormone (TRH) is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus. TRH is transported to the anterior pituitary gland through the hypophysial portal system. TRH regulates TSH release from the pituitary.
d) Thyroxine
Thyroxine has a negative feed-back inhibition on the release of both TRH and TSH.
18) What is/are the effect(s) of high levels of circulating TSH?
a) Induce follicular hypertrophy
b) Progressive resorption of colloid
c) Increases vascularity of the thyroid
d) All of the above
d) All of the above
TSH stimulate the growth and invasive characteristics of some well-differentiated thyroid cancer cell lines.
Doppler ultrasound can detect increased vascularity of the thyroid.
There is also progressive resorption of colloid and increased stromal vascularity.
TSH stimulates thyroid cell growth and differentiation. TSH stimulates iodine uptake, organification and release of T3 and T4.
In the absence of TSH, the follicular cells are squamous and 'resting'.
Prolonged high levels of circulating TSH induce follicular hypertrophy and even hyperplasia.
19) TSH receptors are present on the
a) Basolateral surface of the follicular cells
b) Apical surface of the follicular cells
c) Both apical and basolateral surface of the follicular cells
d) Pituitary gland
a) Basolateral surface of the follicular cells
The basolateral surface of the thyroid follicular cells are opposed to the bloodstream. The apical surface faces the follicular lumen.
TSH receptors are present on the basolateral surface of the follicular cells.
When TSH binds with the TSH receptor, it is activated. The TSH receptor interacts with a guanine nucleotide-binding protein (G protein) and stimulates the production of cyclic AMP.
20) How does Iodide enter the follicular cells?
a) Passive diffusion from blood
b) Passive diffusion from lymph
c) Active transport from blood
d) Bound to TSH
c) Active transport from blood
Iodide enters the follicular cells across the basal plasmalemmal membrane of the thyrocytes (follicular cells) by active transport from the blood capillaries.
24) What is the normal T/S ratio?
a) 25:1
b) 1:25
c) 1:50
d) 50:1
a) 25:1
T/S ratio is ratio of iodide in thyroid to iodide in serum.
Thyroid gland, mammary gland, chorion, salivary gland and stomach can concentrate iodine against an electrochemical gradient.
T/S ratio reflects the activity of the thyroidal iodine transporter.
Thyroid is the only tissue that can oxidize iodine to a higher valence state. This step involves peroxidase. Thiourea drugs inhibit oxidation.
18) What is/are the effect(s) of high levels of circulating TSH?
a) Induce follicular hypertrophy
b) Progressive resorption of colloid
c) Increases vascularity of the thyroid
d) All of the above
d) All of the above
TSH stimulate the growth and invasive characteristics of some well-differentiated thyroid cancer cell lines.
TSH stimulates thyroid cell growth and differentiation. TSH stimulates iodine uptake, organification and release of T3 and T4. In the absence of TSH, the follicular cells are squamous and 'resting'. Prolonged high levels of circulating TSH induce follicular hypertrophy and even hyperplasia.
Doppler ultrasound can detect increased vascularity of the thyroid.
There is also progressive resorption of colloid and increased stromal vascularity.
19) TSH receptors are present on the
a) Basolateral surface of the follicular cells
b) Apical surface of the follicular cells
c) Both apical and basolateral surface of the follicular cells
d) Pituitary gland
a) Basolateral surface of the follicular cells
The basolateral surface of the thyroid follicular cells are opposed to the bloodstream.
The apical surface faces the follicular lumen.
TSH receptors are present on the basolateral surface of the follicular cells.
When TSH binds with the TSH receptor, it is activated. The TSH receptor interacts with a guanine nucleotide-binding protein (G protein) and stimulates the production of cyclic AMP
20) How does Iodide enter the follicular cells?
a) Passive diffusion from blood
b) Passive diffusion from lymph
c) Active transport from blood
d) Bound to TSH
Iodide enters the follicular cells across the basal plasmalemmal membrane of the thyrocytes (follicular cells) by active transport from the blood capillaries.
21) What is the location of the thyroid peroxidase?
a) Follicular basal plasmalemmal membrane
b) Follicular apical plasmalemmal membrane
c) Colloid
d) RBC
b) Follicular apical plasmalemmal membrane
Within the thyrocyte, iodide is rapidly oxidized by H2O2 in a reaction catalyzed by thyroid peroxidase. The thyroid peroxidase in the apical plasmalemma oxidizes iodide to iodine.
22) Organification
a) Monoiodotyrosine formed
b) diiodotyrosine formed
c) Both are formed
d) Neither are formed
Iodine is attached to the tyrosyl groups of the thyroglobulin to generate monoiodotyrosine and diiodotyrosine residues. This process is known as organification.
## Excessive circulating iodide may transiently inhibit thyroid hormone synthesis by disrupting organification.
Iodinated thyroglobulin is the precursor of thyroid hormones.
Thyroid peroxidase also catalyzes the coupling of the monoiodotyrosine and diiodotyrosine residues to generate thyroxine (T4) and triiodothyronine (T3).
## Excessive circulating iodide may also transiently inhibit secretion of T4 and T3 by inhibiting proteolysis of thyroglobulin.
23) Main hormone secreted by the thyroid
a) MIT
b) DIT
c) T3
d) T4
d) T4
Formation of T4 is the major pathway. Both T3 and T4 are bound to thyroglobulin and stored within the colloid. This allows quick secretion of the preformed hormones.
There is storage of about 2 weeks supply of thyroid hormone. The administration of antithyroid agents for as long as 2 weeks has little effect.
T3 is formed by coupling of a molecule of MIT with a molecule of DIT.
T4 is formed by coupling of two molecules of DIT.
MIT and DIT are biologically inert. Coupling of these two residues gives rise to the two biologically active thyroid hormones T4 and T3.
31) What is the half-life of TSH?
a) 30 seconds
b) 12 minutes
c) 50 minutes
d) 1.5 hours
c) 50 minutes
TSH variations are not much compared to other pituitary hormones. Therefore, single measurements of TSH are adequate for assessing its circulating level.
32) TSH measured using immunoradiometric assays can be used for the diagnosis of ------
a) Hyperthyroidism
b) Hypothyroidism
c) Both
d) Neither
TSH is measured using immunoradiometric assays. These assays are highly sensitive and specific. TSH can be used for the diagnosis of both hyperthyroidism (low TSH) and hypothyroidism (high TSH).
33) What % of administered radioactive 123 I taken up by normal thyroid?
a) Less than 10%
b) 25%
c) 60%
d) 90%
10 to 25% of radioactive tracer (e.g., 123I) is taken up by the normal thyroid gland over 24 h.
70 to 90% of radioactive tracer is taken up in Graves' disease.
34) Most common cause of preventable mental deficiency
a) Down's syndrome
b) Iodine deficiency
c) Birth injuries
d) Infections
Majority of cases of mental deficiency are idiopathic. Iodine supplementation of salt, bread, and other food substances has markedly reduced the prevalence of cretinism.
35) Recommended daily intake of iodine is ----------------- ug/d for adults
a) 25
b) 75
c) 150
d) 350
c) 150 ug/d
Recommended daily intake of iodine is 90 to 120 ug/d for children, and 200 ug/d for pregnant women. Increased iodine intake is associated with autoimmune thyroid disease
36) Recommended for surveillance of iodine deficiency is
a) Prevalence of goiter
b) Prevalence of cretinism
c) Urinary iodine excretion
d) Serum T4
e) Prevalence of neonatal hypothyroidism
Urinary iodine excretion is particularly recommended for surveillance of iodine deficiency. The objective of goiter control programme is to increase iodine intake.
Serum T4 is a more sensitive indicator of thyroid deficiency than T3.
What is Wolff-Chaikoff effect?
a) Excess iodide causes hyperthyroidism
b) Iodine deficiency increases thyroid blood flow
c) Excess iodide inhibits thyroid iodide organification
d) Iodide inhibits T4 release from the thyroid
c) Excess iodide inhibits thyroid iodide organification
Excess iodide transiently inhibits thyroid iodide organification. This phenomenon is known as the Wolff-Chaikoff effect. This stunning effect is transient.
Normal thyroid gland escapes from this inhibitory effect and iodide organification resumes.
The thyroid gland has an autoregulated process. When dietary iodide is excessive, there is inhibition of uptake of iodide into follicular cells. The reverse is true in iodide deficiency.
Iodine deficiency increases thyroid blood flow and stimulates uptake by the NIS. This is not Wolff-Chaikoff effect.Iodine supplementation can be used to treat hyperactivity of the gland in preparation for surgery.
T4 release from the thyroid cells is inhibited by iodide. Inhibition of hormone release is responsible for the rapid improvement that Iodide causes in hyperthyroid patients.
Oversupply of iodine, through supplements or foods enriched in iodine (e.g., shellfish, kelp), is associated with an increased incidence of autoimmune thyroid disease.
38) T4 circulate bound to
a) Thyroxine-binding globulin
b) Albumin
c) Transthyretin
d) All
Most T3 and T4 are bound to proteins so that free T4 constitutes less than 1% of peripheral hormone. Both hormones circulate bound to plasma proteins, including thyroxine-binding globulin (TBG), transthyretin (TTR or thyroxine-binding prealbumin ), and albumin.
TBG has high affinity and carries 80% of the bound hormones.
Albumin has low affinity for thyroid hormones but albumin has a high plasma concentration. Albumin binds up to 10% of T4 and 30% of T3
TTR also carries 10% of T4 but little T3.
T3 is less tightly bound than T4. Therefore, the amount of free T3 is more than free T4. Only the free hormone is active.
100% of T4 is from thyroid. Only 20% of T3 is from thyroid.
Most of T3 is formed by peripheral conversion of T4 to T3. This conversion is the result of deiodination, which takes place largely in the plasma and liver.
When the effects of the various binding proteins are combined, approximately 99.98% of T4 and 99.7% of T3 are protein-bound
39) Which Increase TBG levels?
a) Estrogens
b) Hepatitis
c) Tamoxifen
d) All of the above
Pregnancy and exposure to pharmacologic doses of estrogens can increase TBG levels. Because of this, total T4 level is increased in pregnancy.
Hepatitis and familial TBG excess increase TBG levels
Certain medications including 5-fluorouracil, tamoxifen, and methadone can increase TBG levels.
salicylates and salsaltes can displace thyroid hormones
from circulating binding proteins.
Mutations in TBG, TTR, and albumin that increase binding affinity for T4 and/or T3 cause disorders known as euthyroid hyperthyroxinemia or familial
dysalbuminemic hyperthyroxinemia (FDH).
The familial nature of the disorders, and the fact that TSH levels are normal rather than suppressed, should suggest the diagnosis. Free hormone levels (ideally measured by dialysis) are normal in FDH.
These disorders are usually dominantly transmitted and result in increased total T4 and/or T3, but free hormone levels are normal.
40) Glucocorticoids - True statement
a) Increase TBG levels
b) Inhibit peripheral conversion of T4 to T3
c) Lower serum TSH
d) All of the above
Exogenous glucocorticoids inhibit peripheral conversion of T4 to T3. This effectively lowers serum T3 levels. Steroids are used to rapid inhibit T3 formation in hyperthyroid conditions.
Steroids can also lower serum TSH.
Dopamine, glucocorticoids, and somatostatin suppress TSH but are not of major physiologic importance except when these agents are administered in pharmacologic doses.
Because of the rapid action of steroids, they are an important in the treatment of thyrotoxic crisis or resistant hyperthyroidism.
T4®T3conversion may be impaired by fasting, systemic
illness or acute trauma, oral contrast agents, and a variety of medications (e.g. propylthiouracil, propranolol, amiodarone, glucocorticoids)
41) X-linked TBG deficiency - True statement
a) Very low levels of total T4
b) Very low levels of total T 3
c) Euthyroid
d) TSH levels are normal
e) All
All true. X-linked TBG deficiency is associated with very low levels of total T 4 and T3. Free hormone levels are normal. Hence, patients are euthyroid and TSH levels are normal. The importance is not to try to make total T4 levels normal. This causes thyrotoxicosis. T4 level cannot be made normal because of rapid hormone clearance in the absence of TBG.
42) Estrogen - True statement
a) Delay TBG clearance
b) Increased total T4
c) Normal free T3
d) All
e) None
TBG is produced in the liver. Estrogen delays TBG clearance and increase TBG synthesis. Therefore, in pregnant women or in those taking estrogen-containing contraceptives, TBG levels are elevated. This increases total T4 and T3 levels. Free T4 and T3 levels are normal
43) What is the most important source of reverse T3?
a) Type 1 deiodinase
b) Type 2 deiodinase
c) Type 3 deiodinase
d) Type 4 deiodinase
c) Type 3 deiodinase
Type 3 deiodinase is present in the glial cells of the central nervous system. The type 3-deiodinase enzyme is the major T3 and T4 inactivating enzyme. Type 3 deiodinase converts T4 to inactive reverse triiodothyronine (rT3) and T3 to inactive diiodothyronine (T2). Type 3 deiodinase is the most important source of reverse T3 (rT3 ).
T4 is converted to T3 by the deiodinase enzymes. More than 80% of the T3 present in tissues is derived from T4 through the action of deiodinase enzymes.
Type 1 deiodinase is located primarily in thyroid, liver, and kidney.
Type 2 deiodinase is found primarily in the pituitary gland, brain, brown fat, and thyroid gland.
Type 4 deiodinase has not been described.
44) T4 to T3 conversion is impaired by
a) Fasting
b) Systemic illness
c) Oral contrast agents
d) Glucocorticoids
e) All
T4 to T3 conversion is impaired by systemic illness or acute trauma.
Glucocorticoids, propylthiouracil, propranolol, and amiodarone impair T4 to T3 conversion.
45) Thyroid hormone resistance - False statement
a) Autosomal dominant
b) Increased free thyroid hormone levels
c) Elevated TSH
d) Goiter
e) Severe hypothyroidism
e) Severe hypothyroidism
Thyroid hormone resistance is characterized by elevated free thyroid hormone levels and normal or elevated TSH. Increased levels of thyroid hormone compensate hormone resistance. Therefore, these patients are ** not hypothyroid.
The diagnosis is suspected when free thyroid hormone levels are increased without suppression of TSH.
## No treatment is indicated. The importance of making the diagnosis is to avoid inappropriate treatment of mistaken hyperthyroidism.
Resistance to thyroid hormone is an autosomal dominant disorder. Resistance is caused by mutations in the thyroid receptor gene.
46) A primary abnormality of thyroid function is excluded by
a) Normal TSH level
b) TRH stimulation test
c) Normal total T4
d) Normal free T3
e) Normal USS of thyroid
TSH levels change with any changes in free T 4 and T 3 levels. So, in suspected thyroid disease, first determine whether TSH is suppressed, normal, or elevated. A normal TSH level excludes a primary abnormality of thyroid function except in rare situations. If TSH level is abnormal, measure circulating thyroid hormone levels to confirm hyperthyroidism (suppressed TSH) or hypothyroidism (elevated TSH).
TRH stimulation test is not done now.
Serum total T 4 and total T 3 are measured by radioimmunoassays. T 4 and T 3 are highly protein-bound. Therefore, total T 4 and total T 3 levels are influenced by illness, medications, and genetic factors. It is more useful to measure the free or unbound hormone levels. Measure circulating thyroid hormone levels only if TSH levels measured using immunoradiometric assays are abnormal.
USS is most useful to detect anatomical abnormality. USS can detect nodules and cysts more than 3 mm. USS is useful for guiding FNA biopsies and for the aspiration of cystic lesions.
47) T3 thyrotoxicosis - True statement
a) Commonest type of thyrotoxicosis
b) Free T4 and T3 are raised
c) TSH levels are normal or high
d) None
All are false statements.
Less than 5% of patients with thyrotoxicosis have T3 toxicosis.
In T3 toxicosis, only elevated T3 level is elevated. T4 level is normal.
TSH is suppressed. Thus, free T3 levels should be measured in patients with a suppressed TSH but normal free T4 levels.
48) Which is not useful in suspected hypothyroidism?
a) TSH
b) Total T4
c) Free T4
d) Free T3
Free T 3 levels are normal in 25% with hypothyroidism. Therefore, T3 is not very useful in suspected hypothyroidism.
49) Most common cause of an elevated TSH level
a) Assay artifact
b) TSH-secreting pituitary tumor
c) Primary hypothyroidism
d) Thyroid hormone resistance
e) After treatment of hyperthyroidism
c) Primary hypothyroidism
TSH remains suppressed for several weeks after treatment of hyperthyroidism
50) Low TSH level
a) First trimester of pregnancy
b) High dose glucocorticoids
c) After treatment of hyperthyroidism
d) All
e) None
d) All
Low TSH level usually indicates thyrotoxicosis. Suppressed TSH level may also be seen during the first trimester of pregnancy and in response to certain medications (e.g., high doses of glucocorticoids or dopamine). TSH remains suppressed for several weeks after treatment of hyperthyroidism.
51) 50-year-old woman has been on treatment for angina for the past 5 years. She has low total T4 and TSH. How would you proceed?
a) Treat with low doses of thyroxine
b) Do TMT and echocardiography before giving thyroxine
c) Admit and give thyroxine under supervision
d) Do free T4
e) Take CT head
e) Take CT head
Low T4 and TSH suggest secondary hypothyroidism caused by hypothalamic-pituitary disease.
52) Major thyroid microsomal antigen
a) Thyroid receptor
b) TSH receptor
c) Thyroxine
d) Thyroid peroxidase
TPO is the major thyroid microsomal antigen.
53) Serum thyroglobulin levels are increased in
a) Thyrotoxicosis factitia
b) After total thyroidectomy
c) After radioablation of thyroid
d) All
e) None
All are false statements
Some iodinated thryoglobulin escapes intact from the follicles. They can be detected in blood by radioimmunoassay.
** Serum thyroglobulin levels are increased in all types of thyrotoxicosis except thyrotoxicosis factitia.
## The main role for thyroglobulin measurement is in the follow-up of thyroid cancer patients.
After total thyroidectomy and radioablation, thyroglobulin levels should be undetectable.
## If thyroglobulin can be detected, it suggests incomplete ablation or recurrent cancer.
54) Radioisotope used in thyroid scanning
a) 99 m Tc pertechnetate
b) 123 I
c) 125 I
d) 131 I
e) All
The thyroid gland selectively transports these radioisotopes of iodine.
## Hot nodules (i.e., with increased tracer uptake) are almost never malignant.
Cold nodules (i.e., with diminished tracer uptake) are also usually benign. However, these nodules are more likely to be malignant (5 to 10%).
Fine-needle aspiration is preferred to thyroid scans in the evaluation of solitary thyroid nodules. Thyroid scanning is also used in the follow-up of thyroid cancer.
After thyroidectomy and ablation using 131I, there is diminished radioiodine uptake in the thyroid bed. Whole-body scans using 131 I is performed to detect metastatic thyroid cancer deposits.
Technetium-99m (99mTc) pertechnetate is the most widely used thyroid-imaging agent. Pertechnetate is concentrated within the thyroid. Imaging begins 20 minutes after the intravenous injection of sodium pertechnetate. Normal uptake of the injected activity is 0.4 -4.0%.
Radioiodine uptakes are usually determined at 6 or 24 hours and range from 8 to 28%.
RADIOISOTOPE THYROID SCANNING
- Increased tracer uptake with homogeneous distribution - Graves' disease
- Focal areas of increased uptake, with suppressed tracer uptake in the remainder of the gland - Toxic adenomas
- Multiple areas of increased or decreased tracer uptake - Toxic multinodular goiter
- Very low uptake because of follicular cell damage and TSH suppression - Subacute thyroiditis.
Low uptake - Thyrotoxicosis factitia
23) Main hormone secreted by the thyroid
a) MIT
b) DIT
c) T3
d) T4
Formation of T4 is the major pathway. Both T3 and T4 are bound to thyroglobulin and stored within the colloid. This allows quick secretion of the preformed hormones. There is storage of about 2 week's supply of thyroid hormone. The administration of antithyroid agents for as long as 2 weeks has little effect.
T3 is formed by coupling of a molecule of MIT with a molecule of DIT. T4 is formed by coupling of two molecules of DIT.
MIT and DIT are biologically inert. Coupling of these two residues gives rise to the two biologically active thyroid hormones T4 and T3.
22) Organification
a) Monoiodotyrosine formed
b) diiodotyrosine formed
c) Both are formed
T [ Iodine is attached to the tyrosyl groups of the thyroglobulin to generate monoiodotyrosine and diiodotyrosine residues. This process is known as organification. Excessive circulating iodide may transiently inhibit thyroid hormone synthesis by disrupting organification. Iodinated thyroglobulin is the precursor of thyroid hormones. Thyroid peroxidase also catalyzes the coupling of the monoiodotyrosine and diiodotyrosine residues to generate thyroxine (T4) and triiodothyronine (T3). Excessive circulating iodide may also transiently inhibit secretion of T4 and T3 by inhibiting proteolysis of thyroglobulin. See figure above.
HYPERTHYROIDISM (39 MCQs)
1) Causes of hyperthyroidism
a) Subacute thyroiditis
b) Thyrotoxicosis factitia
c) Struma ovarii
d) All
e) None
e) None
All these are causes of thyrotoxicosis, but not causes of hyperthyroidism
Thyrotoxicosis refers to the manifestations of excessive quantities of the thyroid hormones. The main causes of thyrotoxicosis are hyperthyroidism caused by Graves' disease, toxic multinodular goiter, and toxic adenomas.
## Thyrotoxicosis is not same as hyperthyroidism.
Hyperthyroidism is due to excessive thyroid function. Hyperthyroidism is thyrotoxicosis resulting from overproduction of hormone by the thyroid gland itself (e.g., Graves' disease). In thyroiditis (subacute or silent thyroiditis), presenting symptoms are those of thyrotoxicosis. Thyrotoxicosis in thyroiditis is due to the release of preformed thyroid hormones. True hyperthyroidism is absent since there is no overproduction of thyroid hormones. Radionuclide uptake is low in thyroiditis.
Thyrotoxicosis factitia is another cause of thyrotoxicosis with low or absent thyroid radionuclide uptake. Thyrotoxicosis factitia can be distinguished from thyroiditis by low levels of thyroglobulin.
Ectopic thyroid tissue, particularly teratomas of the ovary (struma ovarii ) and functional metastatic thyroid carcinoma also cause thyrotoxicosis with low or absent thyroid radionuclide uptake. Whole-body radionuclide studies can demonstrate ectopic thyroid tissue.
TYPES OF THYROTOXICOSIS
HYPERTHYROIDISM (RAIU increased except for iodine-induced hyperthyroidism)
1 Graves' disease
2 Toxic multinodular goiter
3 Toxic adenoma
4 Iodine-induced (Jod-Basedow)
5 Trophoblastic tumor
6 Increased TSH secretion
NO ASSOCIATED HYPERTHYROIDISM (RAIU decreased)
1. Thyrotoxicosis factitia
2. Subacute thyroiditis
3. hyroiditis with transient thyrotoxicosis
- Painless thyroiditis
- Silent thyroiditis
- Postpartum thyroiditis
4. Ectopic thyroid tissue
- Struma ovarii
- unfunctioning metastatic thyroid cancer
2) What is the most common cause of thyrotoxicosis?
a) Graves' disease
b) Toxic multinodular goiter
c) Toxic adenomas
d) Thyroiditis
a) Graves' disease
Graves' disease accounts for 60 to 80% of thyrotoxicosis
3) Thyroid stimulating immunoglobulins cause
a) Hyperthyroidism
b) Ophthalmopathy
c) Dermopathy
d) All
e) None
a) Hyperthyroidism
The hyperthyroidism of Graves' disease is caused by thyroid stimulating immunoglobulin (TSI). TSI bind to TSH receptors and stimulate it.
The extrathyroidal manifestations of Graves' disease (i.e., ophthalmopathy and dermopathy) are immunologically mediated.
T cells and macrophages infiltrate skin and extraocular muscles and secrete cytokines (IFN-alpha, tumor necrosis factor, IL-1). These cytokines activate fibroblasts and cause accumulation of glycosaminoglycans. Glycosaminoglycans cause trapping of water and edema. Later, fibrosis becomes prominent.
4) Major risk factor for Graves' disease
a) Smoking
b) Iodine deficiency
c) Iodine supplementation
d) Female sex
e) Viral infection
d) Female sex
Female sex is the chief risk factor for Graves' disease. Estrogen modulates the autoimmune response
Smoking is only weakly associated with Graves' hyperthyroidism. Smoking is strongly associated with the development of ophthalmopathy.
In regions of iodine deficiency, iodine supplementation precipitates hyperthyroidism, by means of the Jod-Basedow phenomenon.
Jod-Basedow phenomenon is excess iodine increasing thyroid hormone synthesis. Wolff-Chaikoff effect is excess iodine transiently inhibiting thyroid iodide organification.
There is no evidence that infection affects the susceptibility to Graves' hyperthyroidism or directly induces it.
Lid retraction and lid lag can occur in any form of thyrotoxicosis, regardless of the underlying cause. These ocular signs are due to sympathetic over activity. It is important to differentiate these ocular manifestations from those of ## infiltrative orbitopathy, which are characteristic of Graves' disease.
Retraction of the upper eyelid is detected by the presence of a rim of sclera between the lid and the limbus. Lid lag is the phenomenon in which the upper lid lags behind the eyeball when the patient is asked to look slowly downward.
5) Commonest sign of thyrotoxicosis in the elderly
a) Lid retraction
b) Proximal muscle weakness
c) Goiter
d) Tremor
e) Atrial fibrillation
e) Atrial fibrillation
In the elderly, the clinical features of thyrotoxicosis may be subtle. The elderly may present with fatigue and weight loss, leading to apathetic hyperthyroidism.
6) What is the most common cardiovascular manifestation of thyrotoxicosis?
a) Sinus tachycardia
b) Atrial fibrillation
c) Bounding pulse
d) Heart failure
a) Sinus tachycardia
Tachycardia is almost always present. Thyrotoxicosis results in hypermetabolism and increases circulatory demands. At rest, cardiac output is increased because of an increase in stroke volume and heart rate. The high cardiac output produces a bounding pulse, widened pulse pressure, and an aortic systolic murmur.
Atrial fibrillation is more common in patients older than 50 years.
7) In thyrotoxicosis there is
a) Hypercalcemia with hypercalcuria
b) Hypercalcemia with hypocalcuria
c) Hypocalcemia with hypercalcuria
d) Hypocalcemia with hypocalcuria
Thyrotoxicosis is usually associated with increased excretion of calcium and phosphorus in urine and stool. Thyroid hormones directly increase bone resorption. Osteopenia may occur in long-standing thyrotoxicosis. Mild hypercalcemia occurs in up to 20% of patients
8) Typical of Graves' disease
a) Diffuse goiter
b) Positive TPO antibodies
c) Pretibial myxedema
d) All of the above
d) All of the above
Remember that pretibial myxedema is seen in Graves' disease and not in myxedema (hypothyroidism)
GRAVES' DISEASE - DIAGNOSIS
1. Diffuse goiter
2. Thyrotoxicosis
3. Positive TPO antibodies
4. Infiltrative orbitopathy and ophthalmopathy
5. Infiltrative dermopathy
9) Specific to hyperthyroid Graves' disease
a) Thyroid peroxidase antibody
b) Thyroglobulin antibody
c) TSH Receptor antibody
d) All
e) None
c) TSH Receptor antibody
In autoimmune thyroid disease, antibodies against thyroid peroxidase, thyroglobulin, and the TSH-receptor are present in the serum. Autoimmune thyroid disease is also characterized by lymphocytic infiltration of the thyroid gland.
TSH-Receptor autoantibodies (TSHRAbs) are specific to hyperthyroid Graves' disease. 90% of untreated hyperthyroid patients with Graves' disease have detectable TSHR Abs. These antibodies compete with TSH for binding to the TSH receptor site in the cell membrane. After binding to TSHR, they can act as TSH agonists
10) Not detectable in the normal population
a) TSHRAbs
b) Tg antibodies
c) TPO antibodies
d) All
e) None
a) TSHRAbs
TSHRAbs are not detectable in the normal population. TSH receptor antibodies are very rare in patients without autoimmune thyroid disease. They occur in 90% of patients with Graves' disease. A positive test is therefore confirmatory, but a negative test does not exclude Graves' disease.
Other thyroid antibodies (e.g. anti-peroxidase and anti-thyroglobulin antibodies) are unhelpful in the differential diagnosis of thyrotoxicosis since they occur frequently in the population and are found with several of the disorders which cause thyrotoxicosis.
There is a high prevalence of Tg antibodies and TPO antibodies in the normal population.
11) The major antigen of Graves' disease
a) Acetyl choline receptors in ocular muscles
b) Thyroid receptors in ocular muscles
c) Thyroid receptors in follicular cells
d) Thyrotropin receptor
d) Thyrotropin receptor
The TSH-Receptor is the primary autoantigen of Graves' disease
12) Thyroid-stimulating antibodies are produced by
a) Thyroid
b) Lymph nodes
c) Bone marrow
d) All
Thyroid-stimulating antibodies are produced within and outside the thyroid gland. Thyroid-stimulating antibodies activate thyrotropin receptors and cause excess production of thyroid hormone. Antithyroid drugs decrease the production of thyroid-stimulating antibody (immunomodulatory effects)
13) Which cell is involved in the pathogenesis of Graves' ophthalmopathy?
a) Neutrophils
b) T cells
c) Gr-v cells
d) NK cells
There is an inflammatory-cell infiltrate in the extraocular muscles and orbital connective tissue. The cells are composed predominantly of activated T cells. The T cells localize in the orbit because of the presence of an orbital antigen that cross-reacts with a thyroid antigen. The activated T cells produce cytokines.
The cytokines activate fibroblasts, stimulating the production of glycosaminoglycans (mainly hyaluronate and chondroitin sulfate) and leading to edema and fibrosis.
14) What causes the clinical manifestations of Graves' ophthalmopathy?
a) Demyelination of optic nerve
b) Axonal degeneration of optic nerve
c) Increase in the volume of retrobulbar tissue
d) Papilledema
c) Increase in the volume of retrobulbar tissue
Graves' ophthalmopathy is characterized by edema and inflammation of the extraocular muscles and an increase in orbital connective tissue and fat. The edema is due to the hydrophilic action of glycosaminoglycans secreted by fibroblasts. The inflammation is due to infiltration of the extraocular muscles and orbital connective tissue by lymphocytes and macrophages.
The increase in the volume of retrobulbar tissue is responsible for most of the clinical manifestations of ophthalmopathy. The muscle cells are normal until the late stages of ophthalmopathy, when they may become atrophic or fibrotic.
15) Graves' ophthalmopathy is associated with
a) Hyperthyroidism
b) Normal thyroid function
c) Hypothyroidism
d) Any of the above
d) Any of the above
About 90 percent of patients with ophthalmopathy have hyperthyroidism. The remainder has autoimmune hypothyroidism or is euthyroid at presentation.
The onset of Graves' ophthalmopathy occurs within the year before or after the diagnosis of thyrotoxicosis in 75%. It can sometimes precede or follow thyrotoxicosis by several years, accounting for some cases of euthyroid ophthalmopathy.
Graves' disease is associated with specific eye signs (Graves' ophthalmopathy).
## It occurs without Graves' disease in 10%. Therefore, it is also called thyroid-associated ophthalmopathy.
The most frequent signs of ophthalmopathy are eyelid retraction or lag and periorbital edema. Lid retraction and lid lag can occur in any form of thyrotoxicosis, regardless of the underlying cause.
Graves' ophthalmopathy refers to clinical features of exophthalmos, and periorbital and conjunctival oedema, not simply the lid lag and lid retraction which can occur in all forms of thyrotoxicosis.
16) What is the earliest manifestation of Graves' ophthalmopathy?
a) Sensation of grittiness
b) Proptosis
c) Periorbital edema
d) Diplopia
a) Sensation of grittiness
The earliest manifestations of ophthalmopathy are a sense of irritation in the eyes, resembling that caused by a foreign body, and excess tearing.
About 35 % have proptosis. Exophthalmos is usually bilateral and is often asymmetrical in degree.
Periorbital edema, scleral injection, and chemosis are also frequent.
In less than 10%, the muscle swelling is severe and causes diplopia. Many patients with Graves' disease do not have much clinical evidence of ophthalmopathy.
USS, CT, or MRI of the orbits can detect orbital changes in virtually all patients with Graves' disease.
Orbital changes are swelling of extraocular muscles and increased retro-orbital fat.
The most serious manifestation is compression of the optic nerve at the apex of the orbit. This leads to papilledema and peripheral field defects. If untreated, permanent loss of vision results.
NO SPECS SCHEME FOR GRADING ORBITAL CHANGES OF GRAVES' DISEASE
0 - No signs or symptoms
1 - Only signs (lid retraction or lag), no symptoms
2 - Soft tissue involvement (periorbital edema)
3 - Proptosis ( >22 mm)
4 - Extraocular muscle involvement (diplopia)
5 - Corneal involvement
6 - Sight loss
17) What is the best screening test for the presence of hyperthyroidism?
a) Serum TSH
b) Serum total thyroxine and triiodothyronine
c) Serum free triiodothyronine
d) Serum thyroid hormone-binding proteins
Very small increases in thyroid secretion reduce the secretion of thyrotropin (TSH). Therefore, measurement of serum TSH is a useful screening test for the presence of hyperthyroidism.
The diagnosis of hyperthyroidism must be confirmed by the measurement of serum free thyroxine.
18) How can you confirm Graves' disease in a patient with thyrotoxicosis and diffuse goiter?
a) Raised T 4
b) Raised T 3
c) Raised T3 and T4 with suppressed TSH
d) Radionuclide scan
e) CT or MRI scan
d) Radionuclide scan
Diagnostic features of Graves' disease are biochemically confirmed thyrotoxicosis, diffuse goiter, ophthalmopathy, occasionally dermopathy, and positive TPO antibodies. The signs of ophthalmopathy or dermopathy are sufficient to confirm the diagnosis of Graves' disease in a patient with hyperthyroidism and a diffuse goiter.
When the diagnosis is unclear clinically, the presence of a high serum concentration of thyroid peroxidase antibody provides evidence of Graves' disease. It is present in about 75 percent of patients with Graves' hyperthyroidism.
For patients with thyrotoxicosis who lack these features, the most reliable diagnostic method is a radionuclide (99m Tc, 123 I, or 131 I) scan of the thyroid.
There is diffuse, high uptake in Graves' disease. Radionuclide scan can differentiate Grave's disease from nodular thyroid disease, destructive thyroiditis, ectopic thyroid tissue, and factitious thyrotoxicosis.
In secondary hyperthyroidism due to a TSH-secreting pituitary tumor, there is also a diffuse goiter. In secondary hyperthyroidism, TSH level is not suppressed. CT or MRI scan may show the pituitary tumor.
19) Specific to Graves' disease
a) Exophthalmos
b) Pretibial myxedema
c) Thyroid acropachy
d) TSH receptor antibody
e) All of the above
e) All of the above
All causes of thyrotoxicosis can cause lid retraction and lid lag due to potentiation of sympathetic innervation of the levator palpebrae muscles. Only Graves' disease causes other features of ophthalmopathy (periorbital oedema, conjunctival irritation, exophthalmos and diplopia)
Thyroid acropachy is a periosteal hypertrophy indistinguishable from finger clubbing. It is a rare manifestation
20) Low radioiodine uptake thyrotoxicosis
a) Graves' disease
b) Toxic nodular goiter
c) Thyroiditis
d) All of the above
e) None of the above
c) Thyroiditis
Low-uptake thyrotoxicosis is usually due to transient thyroiditis. Occasionally, it is due to 'factitious thyrotoxicosis' (consuming excessive amounts of a thyroid hormone). The exogenous thyroxine suppresses pituitary TSH secretion and hence iodine uptake and serum thyroglobulin.
21) Which inhibit the function of TPO?
a) Propylthiouracil
b) Carbimazole
c) Methimazole
d) All
e) None
d) All
These drugs are actively concentrated by the thyroid gland against a concentration gradient. Their primary effect is to inhibit thyroid hormone synthesis by inhibiting the function of TPO.
This reduces oxidation and organification of iodide (iodination of tyrosine residues in thyroglobulin). These drugs also reduce thyroid antibody levels by an unclear mechanism and may alter the course of the underlying autoimmune process.
22) Which drug(s) impair the conversion of T4 to T3
a) Propylthiouracil
b) Carbimazole
c) Methimazole
d) All
e) None
a) Propylthiouracil
Large doses of propylthiouracil, but not methimazole or carbimazole, impair the conversion of T4 to T3 by deiodinase type 1 in the peripheral tissues.
Because of this additional action, large doses of propylthiouracil may provide rapid alleviation of severe thyrotoxicosis
23) Half-life of methimazole
a) 90 minutes
b) 6 hours
c) 24 hours
d) 5 days
b) 6 hours
Half-life of methimazole is 6 h. A single dose of methimazole exerts an antithyroid effect for longer than 24 hours.
Therefore, single daily dose of methimazole may be used for mild or moderate thyrotoxicosis. Once-daily dosing is possible after euthyroidism is restored.
Half-life of propylthiouracil is only 1.5 hours
24) What is the time taken to achieve euthyroidism by antithyroid drugs?
a) 24 to 48 hours
b) 5 to 10 days
c) 6 to 8 weeks
d) More than 6 months
c) 6 to 8 weeks
It takes 6 to 8 weeks for most patients to achieve euthyroidism. Antithyroid drugs inhibit the synthesis but not the release of hormone. Hence, reduction in the supply of hormone to the tissues does not occur until glandular hormone stores are depleted.
25) What is the most feared side effect of antithyroid-drug therapy?
a) Agranulocytosis
b) Thyrotoxic crisis
c) Seizures
d) Hypoglycemia
e) Interstitial nephritis
a) Agranulocytosis
It takes 6 to 8 weeks for most patients to achieve euthyroidism. Antithyroid drugs inhibit the synthesis but not the release of hormone. Hence, reduction in the supply of hormone to the tissues does not occur until glandular hormone stores are depleted.
26) Which of the following drugs can cause massive hepatic necrosis?
a) Propylthiouracil
b) Methimazole
c) Carbimazole
d) None of the above
In propylthiouracil-related hepatotoxicity, there is often markedly elevated aminotransferase levels and hepatic necrosis on biopsy.
Liver transplantation may be required. Asymptomatic elevations in serum aminotransferase levels occur frequently in untreated patients with hyperthyroidism. Therefore, routine monitoring of liver-function tests in patients being treated with propylthiouracil is generally not recommended.
The rare hepatic abnormalities associated with methimazole and carbimazole are typical of a cholestatic process. Complete, but slow, recovery is the rule after drug discontinuation. The mechanisms of hepatotoxicity for the two antithyroid drugs differ. The alternative agent could be used cautiously to treat the underlying hyperthyroidism in a patient with complicated thyrotoxicosis and drug-induced hepatic side effects
27) Which is not a contraindication for radioiodine treatment?
a) Pregnancy
b) Severe ophthalmopathy
c) Breast feeding
d) Children
b) Severe ophthalmopathy
The presence of severe ophthalmopathy requires caution. Some use prednisone at the time of radioiodine treatment to prevent exacerbation of ophthalmopathy
Risk of cancer after radioiodine treatment in adults is not increased. Many avoid radioiodine in children and adolescents because of the theoretical risks of malignancy
28) Radioiodine treatment - False statement
a) Useful for relapses after a trial of antithyroid drugs
b) Risk of thyrotoxic crisis
c) Antithyroid drugs must be continued during radioiodine administration
d) Avoid close contact with pregnant women for several days
e) Hyperthyroidism can persist for 3 months before radioiodine takes full effect.
c) Antithyroid drugs must be continued during radioiodine administration
Antithyroid drugs must be stopped 3 to 5 days before radioiodine administration to achieve optimum iodine uptake.
Patients should avoid close, prolonged contact with children and pregnant women for several days. There is the possibility of transmission of residual isotope and excessive exposure to radiation emanating from the gland.
Beta-adrenergic blockers or antithyroid drugs can be used to control symptoms during this interval.
## Persistent hyperthyroidism can be treated with a second dose of radioiodine, usually 6 months after the first dose. Most patients ultimately progress to hypothyroidism over 5 to 10 years.
29) What is the main side effect of radioactive iodine?
a) Hypothyroidism
b) Recurrent hyperthyroidism
c) Worsening of ophthalmopathy
d) Malignancy
e) Thyrotoxic crisis
a) Hypothyroidism
It may be transient when it occurs in the first few months after the administration of radioactive iodine. Some require a second treatment to cure their hyperthyroidism.
Radioactive iodine can induce or worsen ophthalmopathy, particularly in smokers. The worsening of ophthalmopathy is often transient and may be prevented by glucocorticoid therapy.
In patients who are treated with radioactive iodine, the risk of death from thyroid cancer and possibly other cancers is slightly increased. Whether this risk is related to Graves' disease or radioactive iodine is not known
There is a slight risk of the development of a thyrotoxic crisis soon after radioactive iodine administration. Patients with severe hyperthyroidism should be treated with an antithyroid drug for four to eight weeks before radioactive iodine is given. The antithyroid drug reduces thyroid secretion rapidly and thereby reduces the slight risk of the development of a thyrotoxic crisis. Patients with mild or moderate hyperthyroidism do not require treatment with an antithyroid drug before or after radioactive iodine therapy. Their symptoms can be adequately ameliorated with a beta-adrenergic antagonist until the radioactive iodine takes effect
30) Subtotal thyroidectomy - indication(s)
a) Relapse after antithyroid drugs
b) Young individuals
c) Large goiter
d) All
d) All
The surgical procedure of choice for the treatment of Graves' disease is a bilateral subtotal thyroidectomy. The high prevalence of postoperative hypothyroidism makes surgery an imperfect treatment.
Some recommend surgery in young individuals, particularly when the goiter is very large. Control thyrotoxicosis with antithyroid drugs before surgery to avoid thyrotoxic crisis.
Give potassium iodide before surgery to reduce the vascularity of the gland. Do not give iodine until a normal metabolic state has been restored by antithyroid drugs.
31) Indication(s) for surgery in Graves' disease
a) Obstructive symptoms
b) Very large goiters
c) Antithyroid drug allergy
d) All
e) None
Graves' disease is usually treated with antithyroid drugs, radio-iodine, or both. Most practitioners consider antithyroid drugs the treatment of choice for most young people with Graves' disease. Only a small percentage is recommended for surgery.
GRAVES' DISEASE - INDICATIONS FOR SURGERY
1. Patients requesting surgery
2. Antithyroid drug allergy
3. Cold nodule
4. Very large goiters
5. Need for a rapid return to normal activity
6. Obstructive symptoms
7. Cosmetic disfigurement
32) What is the best drug to manage Graves' disease in pregnancy?
a) Propylthiouracil
b) Carbimazole
c) Combination therapy with an antithyroid drug and thyroxine
d) Radio Iodine
a) Propylthiouracil
Propylthiouracil, carbimazole and methimazole cross the placenta. They can inhibit thyroid function in the fetus. Propylthiouracil is preferred because of relatively low transplacental transfer and its ability to block T 4 to T 3 conversion. Breast-feeding is safe with low doses of antithyroid drugs. Propylthiouracil is the drug of choice as it is excreted in the milk to a much lesser extent than carbimazole
Carbimazole and methimazole have been associated with rare cases of fetal aplasia cutis (single or multiple lesions of 0.5 to 3 cm at the vertex or occipital area of the scalp). The rare syndrome termed "methimazole embryopathy" is characterized by choanal or esophageal atresia. Methimazole may cross the placenta more readily than propylthiouracil, but both drugs have been used highly effectively in pregnancy
Combination therapy with an antithyroid drug and thyroxine must be avoided. The dose of antithyroid drug needs to be higher in patients who are also receiving thyroxine therapy. This results in fetal hypothyroidism, because little of the thyroxine reaches the fetus.
33) How can you assess risk of neonatal hyperthyroidism?
a) Fetal T4 and T3
b) Maternal free T4 and T3
c) Maternal serum thyrotropin-receptor antibodies
c) Maternal serum thyrotropin-receptor antibodies
Hyperthyroidism is present in the fetuses and neonates of 1 to 5 percent of women who have Graves' disease during pregnancy. It is caused by the transplacental passage of thyroid-stimulating antibodies.
## The risk of neonatal hyperthyroidism can be assessed by measuring maternal serum thyrotropin-receptor antibodies at the beginning of the third trimester.
34) Thyrotoxic crisis - False statement
a) Characterized by fever
b) No significant mortality
c) Thyrotoxic crisis is usually precipitated by acute illness
d) Radioiodine treatment may precipitate
e) None
b) No significant mortality
The mortality rate due to cardiac failure, arrhythmia, or hyperthermia is 30%, even with treatment.
Thyrotoxic crisis is usually precipitated by stroke, infection, trauma, diabetic ketoacidosis, surgery (especially on the thyroid), or radioiodine treatment of a patient with partially treated or untreated hyperthyroidism.
35) Not used in the management of thyrotoxic crisis
a) Oral propylthiouracil
b) Iodide
c) Propranolol
d) IV calcium
e) Dexamethasone
d) IV calcium
IV calcium is not indicated
Large doses of propylthiouracil should be given orally or by nasogastric tube or per rectum. Propylthiouracil is the agent of choice because it inhibits peripheral conversion of T 4 to T 3 in large doses.
## The major action of iodine is to inhibit hormone release.
Iodine acutely retards the rate of ## Secretion of T4. Iodine may also block thyroid hormone synthesis via the Wolff-Chaikoff effect (excess iodide transiently inhibits thyroid iodide organification).
## The rapid slowing of hormone release by iodine makes it more effective than the propylthiouracil when prompt relief of thyrotoxicosis is mandatory.
Iodine is given only one hour after the first dose of propylthiouracil. The 1-hour delay allows the antithyroid drug to prevent the excess iodine from being incorporated into new hormone. Iodine is also used in preparation for subtotal thyroidectomy, in severe thyrocardiac disease, and in acute surgical emergencies
Propranolol decreases tremulousness, palpitations, excessive sweating, eyelid retraction, and heart rate. High doses of propranolol decrease T 4 to T 3 conversion. Adrenergic antagonists are most useful in the interval when a response to thionamide or radioiodine therapy is being awaited.
Dexamethasone inhibits the secretion of thyroid hormone, inhibits the peripheral conversion of T4 to T3, and has immunosuppressive effects.
Concurrent administration of propylthiouracil, iodine, and dexamethasone to the patient with severe thyrotoxicosis causes a rapid reduction in serum T3 concentration. Additional therapeutic measures include antibiotics if infection is present, cooling, and intravenous fluids.
36) Which is not a treatment of orbitopathy?
a) Antibiotics
b) Oral glucocorticoid
c) Tarsorrhaphy
d) Orbital decompression
e) Total ablation of the thyroid gland
e) Total ablation of the thyroid gland
Infiltrative orbitopathy is not benefited by total ablation of the thyroid gland.
Ulceration and infection of the cornea should be treated with antibiotics, lubricants, and protective shields.
A trial of oral glucocorticoid therapy should be tried for patients with severe or progressive orbitopathy. If effective doses cannot be tolerated, a course of external radiation may be attempted if edema predominates.
Tarsorrhaphy (to oppose the eyelids by means of sutures) should be performed only by an experienced ophthalmologist because sutures may be torn out and cause scarring.
If glucocorticoid therapy and external radiation do not halt progression of the disease and if loss of vision is threatened, orbital decompression can be performed. Surgery almost invariably halts the progress of the disease and preserves vision if it is performed in time. See chart below.
37) Abnormality seen in sick euthyroid syndrome
a) Decrease in total T3 levels
b) Decrease in free T3 levels
c) Normal levels of T4
d) Normal levels of TSH
e) All of the above
e) All of the above
Any acute, severe illness can cause abnormalities of circulating TSH or thyroid hormone levels. The most common hormone pattern in sick euthyroid syndrome is a decrease in total and free T 3 levels (low T 3 syndrome) with ## normal levels of T4 and TSH
38) Present in both pregnancy and hyperthyroidism
a) Thyroid enlargement
b) Amenorrhea
c) Elevated total serum T4 and T3 levels
d) All
d) All
Both Pregnancy and hyperthyroidism are accompanied by thyroid enlargement, a hyperdynamic circulation, and hypermetabolism.
Amenorrhea may occur in thyrotoxicosis also.
In pregnancy, serum TBG levels are increased. Thus, in both pregnancy and hyperthyroidism, the total serum T4 and T3 levels are elevated. The most useful laboratory tests in their differentiation are measurement of the serum TSH and free T4 levels. Serum TSH is suppressed in hyperthyroidism in pregnant and in nonpregnant women.
39) What is the most common cause of thyrotoxicosis in childhood?
a) Excess iodine
b) Maternal thyrotoxicosis
c) Graves' disease
d) Pituitary tumor
e) Hypothalamic disorder
c) Graves' disease
Thyrotoxicosis in childhood and adolescence is almost always due to Graves' disease. Radioiodine is not used in the treatment of childhood thyrotoxicosis. Antithyroid drugs are more appropriate than surgery for most children
HYPOTHYROIDISM (26 MCQs)
1) What is the most common cause of hypothyroidism?
a) Hashimoto's thyroiditis
b) Treatment of hyperthyroidism
c) Iodine deficiency
d) Idiopathic
c) Iodine deficiency
Iodine deficiency is the most common cause of hypothyroidism. In areas where iodine deficiency is not present, autoimmune disease (Hashimoto's thyroiditis) and iatrogenic causes (treatment of hyperthyroidism) are the most common causes.
CAUSES OF HYPOTHYROIDISM
Primary (in 99%)
Iodine deficiency
Hashimoto thyroiditis (Autoimmune hypothyroidism)
Postablative - Following surgery, radioiodine therapy, or external radiation to the thyroid
Drugs (lithium, iodides, amiodarone, ethionamide, interferon alpha)
Congenital (thyroid dysgenesis)
Thyroid hormone resistance syndrome (TR-β mutations)
Congenital biosynthetic defect (dyshormonogenetic goiter)
Secondary
• Pituitary failure (TSH deficiency)
Tertiary
• Hypothalamic failure (rare)
Primary hypothyroidism is the etiology in 99% of cases of hypothyroidism. Less than 1% is due to TSH deficiency or other causes.
2) Which is not a cause of hypothyroidism?
a) Iodine deficiency
b) Chronic iodine excess
c) Anterior pituitary hormone deficiencies
d) Sheehan's syndrome
e) None of the above
e) None of the above. All are causes of hypothyroidism.
Iodine deficiency is responsible for endemic goiter and cretinism. It is an uncommon cause of adult hypothyroidism.
Paradoxically, chronic iodine excess can also cause goiter and hypothyroidism. Mechanism is unclear.
## Patients with autoimmune thyroiditis are especially susceptible. Amiodarone causes hypothyroidism in up to 13%. Amiodarone contains lot of iodide and iodine excess is responsible for hypothyroidism caused by amiodarone. Lithium may also cause hypothyroidism.
TSH levels may be low, normal, or even slightly increased in secondary hypothyroidism. Increased TSH is due to secretion of TSH which is immunoactive but not active physiologically. The diagnosis is confirmed by detecting a low free T 4 level.
3) Drug induced hypothyroidism
a) Lithium
b) Contrast media
c) Amiodarone
d) Interferon alpha
e) All
e) All
Lithium interferes with the synthesis and release of thyroid hormones. Approximately 5% of patients taking lithium for more than 18 months develop hypothyroidism
Contrast media contain iodine. Excess iodine may cause hypothyroidism.
Amiodarone is a structural analog of thyroid hormone. Chronic therapy can cause both hypothyroidism and hyperthyroidism.
Interferon alpha can cause autoimmune thyroiditis. This complication is not reversible upon cessation of therapy.
4) What is the most common cause of neonatal hypothyroidism?
a) Thyroid gland dysgenesis
b) Inborn errors of thyroid hormone synthesis
c) TSH-R antibody-mediated
d) Antithyroid drugs in mother
Thyroid gland dysgenesis accounts for about 85% of neonatal hypothyroidism. The majority of infants appear normal at birth.
Diagnosis is by TSH or T 4 levels in heel-prick blood specimens.
Inborn errors of thyroid hormone synthesis accounts for about 12% of neonatal hypothyroidism.
TSH-R antibody-mediated accounts for about 5%.
5) What is the earliest sign of congenital hypothyroidism?
a) Patent posterior fontanel
b) Coarse facial features
c) Hypertrophied muscle
d) Delayed relaxation of knee jerk
e) Bradycardia
a) Patent posterior fontanel
Patent posterior fontanel is the earliest sign of congenital hypothyroidism. It is due to wide-open cranial sutures due to lag in skeletal maturation in utero.
Coarse facial features appears by 8 to 10 weeks.
Hypertrophied muscles are seen rarely in long standing untreated cases
6) What causes thyroid follicular destruction in Hashimoto's thyroiditis?
a) B cells
b) T cells
c) Antibodies
d) Inhibition of thyroid cell function
e) Complement
Thyroid follicular destruction is predominantly by T cell mediated mechanisms
Antibodies may also contribute to thyroid dysfunction by complement fixation or inhibition of thyroid cell function.
7) What is the most common symptom of hypothyroidism?
a) Weakness
b) Hair loss
c) Poor memory
d) Constipation
e) Weight gain
Weakness and dry skin are the most common symptoms.
Hair is dry, brittle and falls out easily. There may be diffuse alopecia and thinning of the outer third of the eyebrows.
Poor memory and difficulty concentrating are common. Rare neurologic problems include reversible cerebellar ataxia, dementia, psychosis, and myxedema coma.
Peristaltic activity is decreased and constipation is common. It may lead to fecal impaction (myxedema megacolon)
8) What is the most common sign of hypothyroidism?
a) Carpal tunnel syndrome
b) Delayed relaxation of tendon reflexes
c) Peripheral edema
d) Bradycardia
e) Coarse skin
e) Coarse skin
Carpal tunnel and other entrapment syndromes are common. It is due to compression of the median nerve in the carpal tunnel by glycosaminoglycan deposits.
There may be slow relaxation of tendon reflexes ("hung-up reflexes") and pseudomyotonia. These are due to a decrease in the rate of muscle contraction and relaxation rather than a delay in nerve conduction
Myocardial contractility and pulse rate are reduced. This causes reduced stroke volume. Peripheral resistance is increased and may cause hypertension, particularly diastolic.]
9) Not a feature of hypothyroidism
a) Pericardial effusion
b) Hoarse voice
c) Menorrhagia
d) Decreased prolactin
Prolactin levels are often slightly increased. Galactorrhea may develop.
Pericardial effusion occurs in up to 30%. Cardiomyopathy is unusual. Fluid may also accumulate in other serous cavities and in the middle ear, giving rise to conductive deafness.
Fluid accumulation in the vocal cords and tongue cause hoarse voice.
Another feature of hypothyroidism is menorrhagia and later amenorrhea. Fertility is reduced and the incidence of miscarriage is increased.
10) What is the cause of myxedema?
a) Subclinical hypothyroidism
b) Hyaluronic acid
c) Sodium
d) Cardiac failure
b) Hyaluronic acid
Myxedema is seen in severe hypothyroidism. Hypothyroidism causes an accumulation of hyaluronic acid (type of glycosaminoglycan) in the dermis and other tissues. This material is hygroscopic and causes non-pitting mucinous edema. This is responsible for the thickened skin and puffy appearance (myxedema) seen in severe hypothyroidism.
Myxedematous tissue is nonpitting and is seen around the eyes, on the dorsa of the hands and feet, and in the supraclavicular fossae. It causes enlargement of the tongue (macroglossia) and thickening of the pharyngeal and laryngeal mucous membranes (hoarseness of voice). A histologically similar deposit may occur in Graves' disease, usually over the pretibial area (pretibial myxedema).
11) CNS change(s) in hypothyroidism
a) Dementia
b) Psychiatric disorders
c) Stupor
d) Cerebellar ataxia
e) All of the above
e) All of the above
All intellectual functions, including speech, are slowed in thyroid hormone deficiency. Loss of initiative is present and memory defects are common. Lethargy and somnolence are prominent. Dementia in elderly patients may be mistaken for senile dementia.
Psychiatric disorders are common. They are usually of the paranoid or depressive type and may induce agitation (myxedema madness). Headaches are frequent.
Cerebral blood flow is reduced. Cerebral hypoxia may predispose to confusional attacks and syncope, which may be prolonged and lead to stupor or coma. Other factors predisposing to coma in hypothyroidism include exposure to severe cold, infection, trauma, hypoventilation with carbon dioxide retention, and depressant drugs.
Body movements are slow and clumsy, and cerebellar ataxia may occur.
12) Which is not a feature of Hashimoto's thyroiditis?
a) Puffy face
b) Edematous eyelids
c) Nonpitting pretibial edema
d) Pretibial myxedema
e) Obstructive sleep apnea
d) Pretibial myxedema
Pretibial myxedema is typical of Graves disease. The typical lesion has an "orange-skin" appearance. It is most common over the anterior and lateral aspects of the lower leg. Hence, it is called pretibial myxedema.
Obstructive sleep apnea is common in hypothyroidism. It is reversible with restoration of a euthyroid state
13) Hashimoto's encephalopathy - True statement
a) Myoclonus
b) Steroid-responsive
c) May occur without hypothyroidism
d) All of the above
d) All of the above
Hashimoto's encephalopathy is a rare syndrome. It is associated with myoclonus and slow-wave activity on electroencephalography. It can cause coma and death.
It is steroid-responsive.
It may occur in autoimmune thyroiditis without hypothyroidism.
14) Which of the following is not associated with autoimmune hypothyroidism?
a) Vitiligo
b) Pernicious anemia
c) Type 2 diabetes mellitus
d) Celiac disease
e) Thyroid-associated ophthalmopathy
c) Type 2 diabetes mellitus
Autoimmune hypothyroidism may be associated with signs or symptoms of other autoimmune diseases, particularly vitiligo, pernicious anemia, Addison's disease, alopecia areata, and type 1 diabetes mellitus
Less common associations include celiac disease, dermatitis herpetiformis, chronic active hepatitis, rheumatoid arthritis, SLE, and Sjogren's syndrome.
Thyroid-associated ophthalmopathy usually occurs in Graves' disease. It also occurs in 5% with autoimmune hypothyroidism.
15) What is the best screening test in suspected hypothyroidism?
a) TSH
b) Free T4
c) Free T3
d) TPO antibodies
e) Creatine phosphokinase
A normal TSH level excludes primary (but not secondary) hypothyroidism.
If the TSH is elevated, do a free T 4 level to confirm clinical hypothyroidism. Free T 4 is inferior to TSH as a screening test. It will not detect subclinical or mild hypothyroidism.
## Circulating free T 3 levels are normal in 25%. Therefore, T 3 measurements are not indicated in suspected hypothyroidism.
After hypothyroidism is confirmed, TPO antibodies determine the etiology. They are present in more than 90% with autoimmune hypothyroidism. If there is any doubt about the cause of a goiter associated with hypothyroidism, do FNA biopsy to confirm autoimmune thyroiditis.
Other abnormal laboratory findings in hypothyroidism include increased creatine phosphokinase, elevated cholesterol and triglycerides, and anemia (usually normocytic or macrocytic).
16) T4 level in subclinical hypothyroidism
a) Normal
b) Low
c) Raised
d) Normal or raised
a) Normal
In subclinical hypothyroidism, T 4 is normal with raised TSH. Do thyroid peroxidase antibodies. If peroxidase antibodies are positive, or patient is symptomatic, treat with thyroxine.
If TPO Ab are negative or the patients is asymptomatic, do yearly follow up.
If T4 is reduced with raised TSH, then it is clinical hypothyroidism. Do TPO antibodies test. If positive, autoimmune hypothyroidism is confirmed. If negative, look for other causes of hypothyroidism.
17) TSH is normal and T4 is low. What is the diagnosis?
a) Pituitary disease
b) Drug effect
c) Sick euthyroid syndrome
d) All
d) All
18) How is dose of levothyroxine adjusted in hypothyroidism?
a) T4
b) T3
c) Free T3
d) TSH
d) TSH
The goal of treatment is a low normal TSH. TSH responses are gradual. TSH should be measured about 2 months after instituting treatment or after any subsequent change in levothyroxine dosage. Patients may get full relief from symptoms only 3 to 6 months after restoring normal TSH levels. It patients are over treated with T4, they have an increased risk of atrial fibrillation and reduced bone density.
19) What is the best test of thyroid function 2 months after radioiodine treatment of Graves' disease?
a) TSH
b) TRH stimulation test
c) Free T4
d) Free T3
e) Radio iodine uptake
Hyperthyroidism suppress TSH secretion. TSH remains suppressed for few months even after treatment of hyperthyroidism.
So, free T 4 levels are a better measure of thyroid function than TSH in the months following radioiodine treatment.
3 to 4 months after radioiodine treatment, transient hypothyroidism may occur. Iatrogenic hypothyroidism is a common cause of hypothyroidism. Hypothyroidism is due to reversible radiation damage rather than to cellular destruction. Give low-dose thyroxine until recovery occurs.
20) A 50-year-old woman with normal body weight is on 200 ug of levothyroxine per day for hypothyroidism and insulin for DM. TSH level is elevated. Free T4 levels are high. What is the next step?
a) Increase levothyroxine dose
b) Decrease levothyroxine dose
c) Continue same treatment
d) Suspect noncompliance
e) Check serum proteins
High TSH levels despite a constant levothyroxine dosage is due to poor compliance. Such patients often have normal or high free T 4. This is because they take medication for a few days before testing. This normalizes T 4 but not TSH levels.
Other causes of increased levothyroxine requirements must be excluded, particularly malabsorption (e.g., celiac disease, small-bowel surgery) and drugs that interfere with T 4 absorption or clearance (e.g., cholestyramine, ferrous sulfate, calcium supplements, lovastatin, aluminum hydroxide, rifampicin, amiodarone, carbamazepine, and phenytoin
21) Half-life of T 4
a) 12 hours
b) 24 hours
c) 3 days
d) 7 days
e) 3 weeks
T 4 has a long half-life of 7 days. Therefore, patients who miss doses can take up to three doses of the skipped tablets at once
22) Which of the following has a major role in myxedema coma?
a) Hypoventilation
b) Hypoglycemia
c) Hyponatremia
d) Heart failure
e) Exposure to cold
Myxedema coma is the final stage of severe longstanding hypothyroidism and is associated with a high mortality rate. Hypoventilation plays a major role in pathogenesis of myxedema coma. Hypoventilation causes hypoxia and hypercapnia. It is usually precipitated by drugs that impair respiration (e.g., sedatives, anesthetics, antidepressants)
Hypoglycemia and dilutional hyponatremia also contribute to the development of myxedema coma.
Other precipitating causes are pneumonia, heart failure, myocardial infarction, gastrointestinal bleeding, cerebrovascular accidents and sepsis.
Exposure to cold is also a risk factor. Myxedema coma almost always occurs in the elderly. Myxedema coma has a high mortality rate even with intensive treatment
23) Which is not indicated in the treatment of myxedema coma?
a) IV levothyroxine
b) IV liothyronine
c) Hydrocortisone
d) External warming in all
e) Ventilatory support
d) External warming in all
External warming is indicated only if the temperature is less than 30 degree C. It can cause cardiovascular collapse
Levothyroxine can be administered as a single IV bolus. If IV preparation is not available, levothyroxine can be given by nasogastric tube, though absorption may be impaired in myxedema.
T3 also can be given IV or via nasogastric tube.
There is impaired adrenal reserve in severe hypothyroidism. Therefore, give parenteral hydrocortisone. Hypertonic saline may be needed if there is hyponatremia. Avoid hypotonic IV fluids. Hypotonic IV fluids may exacerbate water retention secondary to reduced renal perfusion and inappropriate vasopressin secretion.
24) Subclinical hypothyroidism
a) Low T4 and T3 with normal TSH
b) Low T4 with normal T3 and TSH
c) Low T3 with normal T4 and TSH
d) Raised TSH with normal T4 and T3
e) Very low T4 with raised TSH
d) Raised TSH with normal T4 and T3
Subclinical hypothyroid disease is a laboratory diagnoses. Undetected subclinical hypothyroidism during pregnancy may adversely affect the fetus and be associated with hypertension and toxemia. Therefore, screening of pregnant women has been advocated.
Subclinical hypothyroidism is associated with ovulatory dysfunction and infertility. Screening may be useful in this population also.
Women who are pregnant or who have ovulatory dysfunction and infertility should be treated regardless of the presence or absence of symptoms, antibody status, or serum lipid levels.
RISK FACTORS FOR SUBCLINICAL HYPOTHYROIDISM
1. Treated hyperthyroidism
2. History of neck irradiation
3. Postpartum thyroiditis
4. Autoimmune disorders, especially type 1 diabetes
5. Amiodarone
6. Lithium
7. Interferon alfa
25) Pendred syndrome - True statement
a) Thyroid organification defect
b) Hearing loss
c) Hypothyroidism
d) All of the above
Organification of iodine involves binding of oxidized iodide with tyrosyl residues in thyroglobulin. This process is deficient in Pendred syndrome. The abnormality is in the gene encoding pendrin. Pendrin is involved in the apical secretion of iodide into the follicular lumen.
26) Thyroid hormone resistance syndrome - True statement
a) Autosomal-dominant
b) High T3 and T4
c) High TSH
d) All
Thyroid hormone resistance syndrome is a rare autosomal-dominant disorder. It is caused by inherited mutations in the thyroid hormone receptor. The receptors are unable to bind thyroid hormones. Therefore, there is resistance to thyroid hormone, despite high circulating levels of T3 and T4 . The pituitary is also resistant to feedback from thyroid hormones. Therefore, TSH levels tend to be high as well
6) What causes thyroid follicular destruction in Hashimoto's thyroiditis?
a) B cells
b) T cells
c) Antibodies
d) Inhibition of thyroid cell function
e) Complement
...
NEOPLASMS OF THE THYROID (20 MCQs)
1) Adenomas of the thyroid - True statement
a. Derived from follicular epithelium
b. Most follicular carcinomas arise in preexisting adenomas
c. Most have subclinical thyrotoxicosis
d. All of the above
e. None of the above
1) Adenomas of the thyroid - True statement
a. Derived from follicular epithelium T [ Adenoma is the most common thyroid neoplasm. Adenomas of the thyroid are typically discrete, solitary masses, derived from follicular epithelium. Hence they are also known as follicular adenomas.]
b. Most follicular carcinomas arise in preexisting adenomas [ Follicular adenomas are not precursors of carcinomas. Only a subset of follicular carcinomas arises in preexisting adenomas.]
c. Most have subclinical thyrotoxicosis [ The vast majority of adenomas are nonfunctional. Only a small proportion produces thyroid hormones and causes clinically apparent thyrotoxicosis ("toxic adenomas").]
d. All of the above
e. None of the above
2) Follicular adenoma - True statement
a. Has a well-formed capsule
b. No capsular invasion
c. Microscopy shows well-differentiated follicles resembling normal thyroid parenchyma
d. Areas of hemorrhage are common
e. All of the above
2) Follicular adenoma - True statement
a. Has a well-formed capsule [ The typical thyroid adenoma is a solitary, spherical, encapsulated lesion that is well demarcated from the surrounding thyroid parenchyma. The hallmark of all follicular adenomas is an intact, well-formed capsule encircling the tumor. The capsule that is grossly and microscopically complete.]
b. No capsular invasion [ The neoplastic cells are demarcated from the adjacent parenchyma by a well-defined, intact capsule. Follicular carcinomas demonstrate capsular and/or vascular invasion. Careful evaluation of the capsule is important for distinguishing follicular adenomas from follicular carcinomas.]
c. Microscopy shows well-differentiated follicles resembling normal thyroid parenchyma
d. Areas of hemorrhage are common [ Areas of hemorrhage, fibrosis, calcification, and cystic change are common in follicular adenomas, particularly within larger lesions.]
e. All of the above T [ All are true statements. Follicular adenomas present as a unilateral painless mass, often discovered during a routine physical examination. Larger masses may produce local symptoms, such as difficulty in swallowing.]
3) What is the treatment of suspected follicular adenoma?
a. Observation
b. Thyroxine
c. Radioiodine
d. Surgery
3) What is the treatment of suspected follicular adenoma?
a. Observation
b. Thyroxine
c. Radioiodine
d. Surgery T [ A definitive diagnosis of adenomas can be made only after careful histologic examination of the resected specimen because of the need for evaluating capsular integrity. Suspected adenomas of the thyroid are therefore removed surgically to exclude malignancy. Follicular adenomas have an excellent prognosis and do not recur or metastasize.]
4) What is the most common type of thyroid carcinoma?
a. Papillary carcinoma
b. Follicular carcinoma
c. Medullary carcinoma
d. Anaplastic (undifferentiated) carcinoma
4) What is the most common type of thyroid carcinoma?
a. Papillary carcinoma T [ Papillary carcinomas are the most common form of thyroid cancer (85%). Activation of the MAP kinase pathway is a feature of most papillary carcinomas. Most thyroid carcinomas (except medullary carcinomas) are derived from the thyroid follicular epithelium. The vast majority are well-differentiated lesions.]
b. Follicular carcinoma [ 5% to 15% of cases.]
c. Medullary carcinoma [ 5% of cases.]
d. Anaplastic (undifferentiated) carcinoma [ <5% of cases.]
5) Not a carcinoma arising from the follicular cells
a. Papillary
b. Follicular
c. Anaplastic
d. Medullary carcinoma
5) Not a carcinoma arising from the follicular cells
a. Papillary
b. Follicular
c. Anaplastic
d. Medullary carcinoma T [More than 90% of thyroid cancers arises from the follicular cells. Medullary carcinoma arises from the parafollicular C cells.]
6) The major risk factor predisposing to thyroid cancer
a. Deficiency of dietary iodine
b. Hashimoto's thyroiditis
c. Ionizing radiation
d. Smoking
e. Female sex
6) The major risk factor predisposing to thyroid cancer
a. Deficiency of dietary iodine [ Deficiency of dietary iodine and goiter is linked with a higher frequency of follicular carcinomas.]
b. Hashimoto's thyroiditis
c. Ionizing radiation T [ The major risk factor predisposing to thyroid cancer is exposure to ionizing radiation, particularly during the first 2 decades of life. The majority of thyroid carcinomas associated with previous exposure to ionizing radiation is papillary carcinoma.]
d. Smoking
e. Female sex
7) Papillary carcinomas - True statement
a. May be multifocal
b. May be well circumscribed
c. Often cystic
d. All of the above
e. None of the above
7) Papillary carcinomas - True statement
a. May be multifocal [ Papillary carcinomas are solitary or multifocal lesions.]
b. May be well circumscribed [ Some tumors may be well circumscribed and even encapsulated; others may infiltrate the adjacent parenchyma with ill-defined margins.]
c. Often cystic [ The lesions may contain areas of fibrosis and calcification and are often cystic. The cut surface sometimes reveals papillary foci that may point to the diagnosis.]
d. All of the above T
e. None of the above
8) Orphan Annie eye nuclei is diagnostic of
a. Follicular carcinoma
b. Medullary carcinoma
c. Papillary carcinoma
d. Anaplastic (undifferentiated) carcinoma
8) Orphan Annie eye nuclei is diagnostic of
a. Follicular carcinoma
b. Medullary carcinoma
c. Papillary carcinoma T [ The diagnosis of papillary carcinoma depends on some abnormalities in the nucleus. The nuclei of papillary carcinoma cells contain finely dispersed chromatin. This gives an empty appearance called as ground-glass or Orphan Annie eye nuclei.]
d. Anaplastic (undifferentiated) carcinoma
9) Which is not a microscopic hallmark of papillary neoplasms?
a. Orphan Annie eye nuclei
b. Psammoma bodies
c. Lymphatic invasion
d. Intranuclear grooves
e. Involvement of blood vessels even in a small lesion.
9) Which is not a microscopic hallmark of papillary neoplasms?
a. Orphan Annie eye nuclei
b. Psammoma bodies [ Psammoma bodies are calcified clumps of cells often present within the papillae. Psammoma bodies and most likely caused by sloughed papillary projections. These are almost never found in follicular and medullary carcinomas. Therefore, when they are present in fine-needle aspiration material, they are diagnostic of papillary carcinoma.]
c. Lymphatic invasion [ Lymphatic invasion by tumor is often present. Metastases to adjacent cervical lymph nodes are common (50%).]
d. Intranuclear grooves [ Invaginations of the cytoplasm may in cross-sections give the appearance of intranuclear grooves or inclusions ("pseudo-inclusions"). See figure below. Inclusion bodies and cellular grooving allow the diagnosis of papillary carcinoma by FNAC.]
e. Involvement of blood vessels even in a small lesion.] T [ Involvement of blood vessels is relatively uncommon, particularly in smaller lesions.]
10) How does papillary carcinomas present?
a. Asymptomatic benign nodule
b. Enlarged cervical lymph node
c. Hoarseness
d. Lung metastases
e. Any of the above
10) How does papillary carcinomas present?
a. Asymptomatic benign nodule [ Most papillary carcinomas present as an asymptomatic thyroid nodule. It moves freely during swallowing and is not distinguishable from a benign nodule.]
b. Enlarged cervical lymph node [ The first manifestation may be a mass in a cervical lymph node. Even with isolated cervical nodal metastases, prognosis is good.]
c. Hoarseness [ Hoarseness, dysphagia, cough, or dyspnea suggests advanced disease.]
d. Lung metastases [ In a minority of patients, hematogenous metastases are present at the time of diagnosis, most commonly in the lung.]
e. Any of the above T [ Papillary thyroid cancers have an excellent prognosis, with a 10-year survival rate > 95%.]
FINDINGS IN FAVOR OF MALIGNANT THYROID NODULES
Historical features
• Young (<20 years old) or old (>60 years old) age
• Male sex
• Neck irradiation during childhood or adolescence
• Rapid growth
• Symptoms of compression - Recent changes in speaking (hoarseness or dysphonia), breathing (dyspnea), or swallowing (dysphagia)
• Family history of thyroid malignancy
Physical examination
• Hard nodule
• Fixation to adjacent tissues
• Vocal cord paralysis
• Regional lymph adenopathy
Ultrasound findings
• Hypoechoic lesions
• Irregular margins
• Presence of calcifications
• Absence of halo
• Internal or central blood flow
High suspicion
• Family history of medullary thyroid carcinoma or multiple endocrine neoplasia
• Rapid tumor growth, especially during levothyroxine therapy
• Very firm or hard nodule
• Fixation of the nodule to adjacent structures
• Paralysis of vocal cords
• Regional lymphadenopathy
• Distant metastases
11) Which is a reliable test for distinguishing between benign and malignant nodules?
a. Scintiscans
b. Fine-needle aspiration cytology
c. CT
d. MRI
11) Which is a reliable test for distinguishing between benign and malignant nodules?
a. Scintiscans [ Papillary carcinomas are cold nodules on scintiscans.]
b. Fine-needle aspiration cytology T [ FNAC is a reliable test for distinguishing between benign and malignant nodules. The nuclear features are often well demonstrable in aspirated specimens.]
c. CT
d. MRI
12) Treatment of papillary carcinoma
a. Surgery
b. Radioiodine
c. Thyroxine
d. TSH antibodies
12) Treatment of papillary carcinoma
a. Surgery T [ For lesions smaller than 1 cm, lobectomy plus isthmectomy may be appropriate. If lesion is larger than 2 cm, total thyroidectomy is considered. Controversy exists about the use of total thyroidectomy versus lobectomy and isthmectomy in adults with a 1- to 2-cm papillary carcinoma. The advantage of total thyroidectomy is that radioiodine treatment is possible. Radioablation is much less effective and requires a larger dosage if residual thyroid exists as in lobectomy. Surgery of lymph nodes is routinely performed in patients with papillary carcinoma.]
b. Radioiodine
c. Thyroxine
d. TSH antibodies
13) Follicular carcinomas - True statement
a. More common in women
b. Present at an older age than do papillary carcinomas
c. More frequent in areas with dietary iodine deficiency
d. All of the above
13) Follicular carcinomas - True statement
a. More common in women [ Follicular carcinomas account for 5% to 15% of primary thyroid cancers. They are more common in women (3:1).]
b. Present at an older age than do papillary carcinomas [ Peak incidence is between 40 and 60 years of age.]
c. More frequent in areas with dietary iodine deficiency
d. All of the above T [ Microscopically, most follicular carcinomas are composed of small follicles with colloid, similar to normal thyroid. The nuclei do not have the typical features of papillary carcinoma (Orphan Annie eye nuclei). Psammoma bodies are not present.]
14) Hürthle cell carcinoma
a. Follicular carcinoma
b. Papillary
c. Medullary
d. None
14) Hürthle cell carcinoma
a. Follicular carcinoma T [ Hürthle cell carcinoma is a subtype of follicular carcinoma. It consists of oxyphilic cells and tends to occur in older patients, usually 60 to 75 years of age.]
b. Papillary
c. Medullary
d. None
15) Helpful in definitely distinguishing papillary from follicular neoplasms
a. Capsular invasion
b. Lymphatic invasion
c. Vascular invasion
d. Psammoma bodies
e. None of the above
15) Helpful in definitely distinguishing papillary from follicular neoplasms
a. Capsular invasion
b. Lymphatic invasion [ Follicular carcinomas do not usually invade lymphatics. Therefore, regional lymph nodes are not commonly involved. Papillary carcinomas usually invade lymphatics.]
c. Vascular invasion [ Vascular (hematogenous) dissemination is common in follicular carcinomas , with metastases to bone, lungs, liver, and elsewhere.]
d. Psammoma bodies T [ Psammoma bodies are concentrically calcified structures often present within the papillae. These are almost never found in follicular and medullary carcinomas. Therefore, when they are present in fine-needle aspiration material, they indicate papillary carcinoma.]
e. None of the above
16) Helpful in distinguishing follicular adenomas from minimally invasive follicular carcinomas
a. Psammoma bodies
b. Orphan Annie eye nuclei
c. Intranuclear grooves
d. Capsular invasion
16) Helpful in distinguishing follicular adenomas from minimally invasive follicular carcinomas
a. Psammoma bodies [ Nuclear features and Psammoma bodies are helpful in distinguishing papillary from follicular neoplasms. They are of no value in distinguishing follicular adenomas from minimally invasive follicular carcinomas. This distinction requires extensive histologic sampling of the tumor-capsule-thyroid interface to exclude capsular and/or vascular invasion.]
b. Orphan Annie eye nuclei
c. Intranuclear grooves
d. Capsular invasion T [ Follicular adenoma is surrounded by a thin fibrous capsule. Compressed normal thyroid parenchyma is usually present external to the capsule and there is no capsular invasion. In contrast, follicular carcinomas demonstrate capsular invasion. The presence of vascular invasion is another feature of follicular carcinomas. FNAC is not useful in the diagnosis of FTC. Diagnosis of FTC requires demonstration of invasion of the capsule or vascular or lymphatic channels. Invasion cannot be determined with the FNAC.]
17) Treatment of follicular carcinomas
a. Total thyroidectomy
b. Radioactive iodine
c. Thyroid hormone
d. All of the above
17) Treatment of follicular carcinomas
a. Total thyroidectomy [ Follicular carcinomas are treated with total thyroidectomy followed by the administration of radioactive iodine. Metastases take up the radioactive iodine.]
b. Radioactive iodine [ It is used to identify and ablate metastatic lesions.]
c. Thyroid hormone [ Residual follicular carcinoma may respond to TSH stimulation. Therefore, thyroid hormone is given after surgery to suppress endogenous TSH.]
d. All of the above T [ Serum thyroglobulin levels are used for monitoring tumor recurrence.]
18) Anaplastic carcinomas of the thyroid - True statement
a. Rare
b. Aggressive
c. Present as a rapidly enlarging bulky neck mass
d. No effective therapy
e. All of the above
18) Anaplastic carcinomas of the thyroid - True statement
a. Rare [ Anaplastic carcinomas are undifferentiated tumors of the thyroid follicular epithelium, accounting for less than 5% of thyroid tumors.]
b. Aggressive [ Mortality rate is almost 100%. Patients with anaplastic carcinoma are older than those with other types of thyroid cancer, with a mean age of 65 years.]
c. Present as a rapidly enlarging bulky neck mass [ Anaplastic carcinomas usually present as a rapidly enlarging bulky neck mass. Symptoms related to compression and invasion, such as dyspnea, dysphagia, hoarseness, and cough, are common.]
d. No effective therapy [ In most cases, the disease has already spread beyond the thyroid capsule into adjacent neck structures or has metastasized to the lungs at the time of presentation. There are no effective therapies. The disease is almost uniformly fatal.]
e. All of the above
19) Medullary carcinomas of the thyroid - False statement
a. Arise from parafollicular cells
b. Calcitonin is useful in diagnosis
c. 99% are associated with MEN syndrome
d. Mutations in the RET protooncogene play an important role
19) Medullary carcinomas of the thyroid - False statement
a. Arise from parafollicular cells [ Medullary carcinomas of the thyroid are neuroendocrine neoplasms derived from the parafollicular cells (C cells) of the thyroid. They account for 5% of thyroid neoplasms.]
b. Calcitonin is useful in diagnosis [ Medullary carcinomas secrete calcitonin, similar to normal C cells. Measurement of calcitonin is important for both diagnosis and postoperative follow-up.]
c. 99% are associated with MEN syndrome F [ False statement. About 70% arise sporadically. 30% occurs in the setting of MEN syndrome 2A or 2B or as familial tumors without an associated MEN syndrome. Sporadic medullary thyroid carcinomas present as a solitary nodule. In contrast, bilaterality and multicentricity are common in familial cases.]
d. Mutations in the RET protooncogene play an important role [ Activating point mutations in the RET protooncogene play an important role. All asymptomatic MEN-2 family members carrying RET mutations are offered prophylactic thyroidectomy as early as possible to protect against the inevitable development of medullary carcinomas.]
20) Not a prominent feature of sporadic medullary carcinoma
a. Mass in the neck
b. Paraneoplastic syndrome
c. Hypocalcemia
d. Raised carcinoembryonic antigen
20) Not a prominent feature of sporadic medullary carcinoma
a. Mass in the neck [ Sporadic cases of medullary carcinoma often present with a mass in the neck, sometimes associated with local effects such as dysphagia or hoarseness.]
b. Paraneoplastic syndrome [ Some cases present with a paraneoplastic syndrome, caused by the secretion of a peptide hormone (e.g., diarrhea due to the secretion of VIP, or Cushing syndrome due to ACTH).]
c. Hypocalcemia T [ Hypocalcemia is not a prominent feature, despite the presence of raised calcitonin levels.]
d. Raised carcinoembryonic antigen [ Carcinoembryonic antigen secreted by the neoplastic cells is a useful biomarker in addition to circulating calcitonin. It is especially useful in calcitonin-negative tumors and for presurgical assessment of tumor load.]
1) Most common cause of pancreatic injury
a) Penetrating trauma
b) Blunt abdominal trauma
c) Automobile seatbelts
d) Bicycle handlebars
1) Most common cause of pancreatic injury
a) Penetrating trauma T [ Two thirds of pancreatic injuries are the result of penetrating trauma.]
b) Blunt abdominal trauma [ The remaining one third is due to blunt trauma. Automobile seatbelts or bicycle handlebars may cause blunt injury. The neck and body of the pancreas can be injured as they pass over the vertebral column.]
c) Automobile seatbelts
d) Bicycle handlebars
2) Most frequent presentation of blunt pancreatic trauma
a) Pseudocyst
b) Epigastric pain
c) Hematemesis
d) Fistula
e) Malabsorption
...
3) Which is best to evaluate suspected pancreatic trauma?
a) Serum amylase levels at the time of hospital admission
b) Serum lipase
c) Contrast-enhanced CT
d) Ultrasound
3) Which is best to evaluate suspected pancreatic trauma?
a) Serum amylase levels at the time of hospital admission [ Serum amylase levels are elevated in most patients with significant pancreatic trauma. They are also increased in up to 90% of severe abdominal trauma patients who do not have pancreatic injury. Thus, measurement of amylase at the time of hospital admission is not helpful in identifying those with pancreatic injury. A progressive rise in serum amylase activity is a more specific indicator of pancreatic injury.]
b) Serum lipase
c) Contrast-enhanced CT T [ In a patient who is hemodynamically stable, a CT scan provides the safest and most comprehensive means of diagnosis of pancreatic injury. Sensitivity is reported only to be in the range of 40-68%. CT scan is contraindicated in patients who are hemodynamically unstable. In the patient who is unstable, operative exploration provides the optimal diagnostic tool for pancreatic injury.]
d) Ultrasound [ USS is also very useful to evaluate abdominal trauma, but CT is better.]
4) A patient with suspected pancreatic injury has persistent abdomi¬nal pain with signs of peritonitis. What should be done?
a) Do immediate ERCP
b) Start IV fluids
c) Arrange for immediate operation
d) Fix date for MRI and cholangiography
4) A patient with suspected pancreatic injury has persistent abdomi¬nal pain with signs of peritonitis. What should be done?
a) Do immediate ERCP [ ERCP is increasingly being used to diagnose pancreatic ductal injuries.]
b) Start IV fluids T [ Start IV fluids. Maintain nil oral. Do urgent ultrasound. After ascertaining the damage, undertake appropriate action. The management of pancreatic injuries depends on the presence of pancreatic duct disruption, major associated vascular injury, and/or significant injury to peripancreatic organs, especially the duodenum.]
c) Arrange for immediate operation [ Operation is indicated only if there is disruption of the main pancreatic duct. Almost all other patients will resolve with conservative management.]
d) Fix date for MRI and cholangiography
5) What is the most common cause of death in the immediate period after pancreatic injury?
a) Pseudocyst
b) Pancreatic duct stricture
c) Bleeding
d) Peritonitis
5) What is the most common cause of death in the immediate period after pancreatic injury?
a) Pseudocyst [ The major delayed complications of severe pancreatic injuries are the development of pseudocysts or a pancreatic duct stricture.]
b) Pancreatic duct stricture [ This is a delayed complication.]
c) Bleeding T [ Once the acute phase has passed the mortality and morbidity should be minimal with a complete return to normal activity.]
d) Peritonitis
6) What is the most common cause pancreatic fistula?
a) Operative trauma to the gland
b) Complication of acute pancreatitis
c) Complication of acute pancreatitis
d) Complication of pancreatic cancer
6) What is the most common cause pancreatic fistula?
a) Operative trauma to the gland T [ The danger of a pancreatic fistula is digestion of surrounding structures by activated pancreatic enzymes causing local damage, perforation, bleeding and digestion of the skin.]
b) Complication of acute pancreatitis
c) Complication of acute pancreatitis
d) Complication of pancreatic cancer
7) How can you obtain immediate control of the fistula?
a) Nil by mouth regime
b) Octreotide
c) Adequate drainage of the fistula
d) All of the above
7) How can you obtain immediate control of the fistula?
a) Nil by mouth regime
b) Octreotide
c) Adequate drainage of the fistula
d) All of the above T [ As a principle, in the management of any fistula, the underlying cause for the fistula must be treated before closure will be effective.]
e) None
Management of the Injured Patient > D. Pancreatic Injuries
o CURRENT Diagnosis & Treatment: Surgery, 14e
Torso Trauma > PANCREATIC INJURIES
o Principles of Critical Care, 4e
Chapter 251. Trauma in Children > Pancreatic Trauma
o Tintinalli's Emergency Medicine
THYROID NODULE (7 MCQs)
1) Thyroid nodules - True statement
a. Increase in frequency with age
b. Only about 5% of cases are due to thyroid carcinoma
c. May cause pressure symptoms
d. All of the above
e. None of the above
) Thyroid nodules - True statement
a. Increase in frequency with age [ Nodules are more common in women and increase in frequency with age and with decreasing iodine intake. Nodules detected by ultrasonography (not by palpation) are very common after the age of 60 years.]
b. Only about 5% of cases are due to thyroid carcinoma [ The most common diagnoses are colloid nodules, cysts, and thyroiditis (in 80 percent of cases); benign follicular neoplasms (in 10 to 15 percent); and thyroid carcinoma (in 5 percent).]
c. May cause pressure symptoms [ Most nodules are incidental, asymptomatic, small, and solitary. Large, partly intrathoracic nodule may cause pressure symptoms. In such cases, treatment is warranted regardless of cause.]
d. All of the above T
e. None of the above
2) Finding(s) suggestive of thyroid carcinoma in a patient with solitary nodule-
a. Family history of medullary thyroid carcinoma
b. Rapid tumor growth during levothyroxine therapy
c. Hard nodule
d. Regional lymphadenopathy
e. All of the above
2) Finding(s) suggestive of thyroid carcinoma in a patient with solitary nodule-
a. Family history of medullary thyroid carcinoma
b. Rapid tumor growth during levothyroxine therapy
c. Hard nodule
d. Regional lymphadenopathy
e. All of the above T [ See table below. Biopsy is useful to guide the type of surgery.]
CLINICAL FINDINGS SUGGESTING CARCINOMA IN A EUTHYROID PATIENT WITH A SOLITARY NODULE
High suspicion
• Family history of medullary thyroid carcinoma or multiple endocrine neoplasia
• Rapid tumor growth, especially during levothyroxine therapy
• Very firm or hard nodule
• Fixation of the nodule to adjacent structures
• Paralysis of vocal cords
• Regional lymphadenopathy
• Distant metastases
Moderate suspicion
• Age of either <20 years or >70 years
• Male sex
• History of head and neck irradiation
• A nodule >4 cm in diameter or partially cystic
• Symptoms of compression
o Dysphagia
o Dysphonia
o Hoarseness
o Dyspnea
o Cough
3) Which of the following is least useful in the evaluation of solitary thyroid nodule?
a. TSH
b. Antithyroperoxidase antibody
c. Fine-needle aspiration biopsy
d. Serum calcitonin level
3) Which of the following is least useful in the evaluation of solitary thyroid nodule?
a. TSH [ Clinical examination is not sensitive for identifying thyroid dysfunction (neither hypothyroidism nor hypothyroidism). Therefore, measurement of the serum TSH level is needed. Nearly all patients with thyroid cancer are euthyroid.]
b. Antithyroperoxidase antibody [ If TSH level is subnormal, measure free thyroxine or free triiodothyronine to confirm hyperthyroidism. If the TSH concentration is elevated, do a serum antithyroperoxidase antibody level to confirm Hashimoto's thyroiditis.]
c. Fine-needle aspiration biopsy [ A fine-needle aspiration biopsy is needed even if TPO antibody levels are elevated to exclude a coexisting cancer, including lymphoma. It accounts for only 5 percent of thyroid cancers but is associated with Hashimoto's thyroiditis.]
d. Serum calcitonin level T [ If a patient has a family history of medullary thyroid cancer or multiple endocrine neoplasia type 2, obtain a basal level. An elevated level suggests medullary thyroid cancer. Serum calcitonin is not routinely measured in patients who have no suggestive family history.]
4) Which one of the following can most reliably rule out malignancy?
a. USS
b. Functioning nodule on radionuclide scanning
c. FNAB
d. TPO antibodies
4) Which one of the following can most reliably rule out malignancy?
a. USS [ Ultrasonography can accurately detect nonpalpable nodules and measure the size of the nodule. USS can differentiate simple cysts from solid nodules. Simple cysts have a low risk of being malignant. Solid nodules or mixed cystic and solid nodules have a 5 percent risk of being malignant. Sonographic findings cannot reliably distinguish between benign and cancerous lesions. Ultrasonography also provides guidance for diagnostic procedures (e.g., fine-needle aspiration biopsy) as well as therapeutic procedures (e.g., cyst aspiration, ethanol injection, or laser therapy).]
b. Functioning nodule on radionuclide scanning T [ Radionuclide scanning is not routinely recommended. Radionuclide scanning may be used to identify whether a nodule is functioning. A functioning nodule is nearly always benign. 90 percent of nodules are nonfunctioning and has a 5 percent risk of being malignant.]
c. FNAB [ In the case of a strong clinical suspicion of cancer, surgery is recommended, regardless of the results of fine-needle aspiration biopsy.]
d. TPO antibodies [ It is associated with Hashimoto's thyroiditis.]
5) When is CT indicated in the evaluation of goiters?
a. To differentiate between malignant and benign nodules
b. In the evaluation of substernal goiters
c. To identify nodules for biopsy
d. To detect enlarged lymph nodes
5) When is CT indicated in the evaluation of goiters?
a. To differentiate between malignant and benign nodules [ CT and MRI also cannot reliably differentiate between malignant and benign nodules. These tests are not usually indicated in the evaluation of a nodule.]
b. In the evaluation of substernal goiters T [ CT and MRI is indicated in the diagnosis and evaluation of substernal goiters, since these imaging techniques can assess the extent of the goiter more precisely than can other techniques and can evaluate tracheal compression.]
c. To identify nodules for biopsy
d. To detect enlarged lymph nodes
6) What is the treatment of a benign nonfunctioning nodule in female of 65 years?
a. Lifelong follow-up
b. Levothyroxine
c. Iodine-131
d. Surgery
6) What is the treatment of a benign nonfunctioning nodule in female of 65 years?
a. Lifelong follow-up T [ Periodic lifelong follow-up every 6 to 24 months is the recommended option. This includes measurement of serum thyrotropin levels, neck palpation, and fine-needle aspiration in case of growth or other suspicious signs.]
b. Levothyroxine [ For a nonfunctional benign nodule, there is no clear recommendation on the use of levothyroxine.]
c. Iodine-131 [ Iodine-131 is considered the treatment of choice for a functioning benign nodule.]
d. Surgery [ The main indications for surgical treatment of thyroid nodules are malignancy or indeterminate cytology on FNA, and suspicious history and physical examination. Surgery is an option, especially if the nodule is very large or partly cystic or if the patient is young.]
7) A 42-year-old woman presents with a palpable mass on the left side of her neck. She has no neck pain and no symptoms of thyroid dysfunction. Ultrasound examination reveals a solid, solitary, mobile thyroid nodule, 2 cm by 3 cm, without lymphadenopathy. The patient has no family history of thyroid disease and no history of external irradiation. What should be done?
a. Repeat ultrasonography after 1 year
b. Give levothyroxine
c. Hemithyroidectomy
d. Iodine-131
7) A 42-year-old woman presents with a palpable mass on the left side of her neck. She has no neck pain and no symptoms of thyroid dysfunction. Ultrasound examination reveals a solid, solitary, mobile thyroid nodule, 2 cm by 3 cm, without lymphadenopathy. The patient has no family history of thyroid disease and no history of external irradiation. What should be done?
a. Repeat ultrasonography after 1 year T [ The main concern is to exclude thyroid cancer. The initial evaluation should include measurement of the serum thyrotropin level and a fine-needle aspiration, preferably guided by ultrasonography. The usual approach after documenting benign cytology is to follow the patient yearly with neck palpation and measurement of the serum thyrotropin level, with repeated ultrasonography and fine-needle aspiration if there is evidence of growth of the nodule.]
b. Give levothyroxine [ Levothyroxine is not the recommended therapy to shrink or prevent growth of benign nodules because of the drug's low efficacy and potential side effects.]
c. Hemithyroidectomy [ In patients less than 20 years old, and in the case of a high clinical suspicion for cancer (e.g., follicular neoplasia as diagnosed by fine-needle aspiration and a nonfunctioning nodule revealed on scanning), the patient should be offered hemithyroidectomy regardless of the results of fine-needle aspiration.]
d. Iodine-131 [ In the case of a functioning benign nodule, iodine-131 is the therapy of choice, independent of concomitant hyperthyroidism.]
GOITER AND MNG (12 MCQs)
1) What is the most common manifestation of thyroid disease?
a. Hypothyroidism
b. Hyperthyroidism
c. Goiter
d. Abnormal thyroid function tests
1) What is the most common manifestation of thyroid disease?
a. Hypothyroidism
b. Hyperthyroidism
c. Goiter T [ Goiter is enlargement of the thyroid. Goiter is the most common manifestation of thyroid disease. 4 questions have to be answered 1. Is the goiter diffuse or nodular? 2. Is it nontoxic or toxic? 3. Is it causing any local compressive or cosmetic problems? 4. Is it benign or malignant?]
d. Abnormal thyroid function tests
CAUSES OF THYROID ENLARGEMENT
Diffuse goiter
• Iodine deficiency (endemic goiter)
• Simple goiter
• Hashimoto's thyroiditis
• Graves' disease
• Transient thyroiditis
• Drugs
o Iodine, amiodarone, lithium
• Suppurative thyroiditis
• Dyshormonogenesis
• Riedel's thyroiditis
Multinodular goiter
Solitary nodule
• Colloid nodule - most common and do not have an increased risk of malignancy
• Simple cyst
• Follicular adenoma - Most follicular adenomas are benign
• Carcinoma
• Lymphoma
• Thyroiditis
2) What causes diffuse nontoxic (simple) goiter?
a. Viral thyroiditis
b. Euthyroid Graves' disease
c. Dietary iodine deficiency
d. Colloid goiter
e. Adolescence
2) What causes diffuse nontoxic (simple) goiter?
a. Viral thyroiditis
b. Euthyroid Graves' disease
c. Dietary iodine deficiency T [ Diffuse goiter is most commonly caused by dietary iodine deficiency resulting in impaired synthesis of thyroid hormone. A compensatory rise in the serum TSH level causes hypertrophy and hyperplasia of thyroid follicular cells and enlargement of the thyroid gland. The compensatory increase in functional mass of the gland may overcome the hormone deficiency, ensuring a euthyroid metabolic state. The degree of thyroid enlargement is proportional to the level and duration of thyroid hormone deficiency.]
d. Colloid goiter [ Diffuse goiter (also called simple goiter) causes enlargement of the entire gland. The enlarged follicles are filled with colloid. Therefore, it is also called colloid goiter. With time, recurrent episodes of hyperplasia and involution produce an irregular enlargement of the thyroid and nodule formation (termed multinodular goiter). A thyroid nodule is a lesion in the thyroid gland due to an abnormal focal growth of thyroid cells. All long-standing simple goiters convert into multinodular goiters.]
e. Adolescence [ There is no physiologic increase in thyroid volume during normal adolescence. Development of a goiter during adolescence is a pathologic rather than a physiologic process.]
3) Colloid goiter (diffuse nontoxic simple goiter) - True statement
a. Usually presents between the ages of 15 and 25 years
b. Mild tenderness is common
c. TSH is only mildly elevated
d. All of the above
e. None of the above
3) Colloid goiter (diffuse nontoxic simple goiter) - True statement
a. Usually presents between the ages of 15 and 25 years T [ This form of goiter usually presents between the ages of 15 and 25 years, often during pregnancy.]
b. Mild tenderness is common [ The goitre is soft and symmetrical. There is no tenderness, lymphadenopathy or overlying bruit.]
c. TSH is only mildly elevated [ Concentrations of T3, T4 and TSH are normal and no thyroid autoantibodies are detected in the serum. In most cases the goitre regresses without any treatment. In some, the gland becomes multinodular as a result of recurrent episodes of hyperplasia and involution during the following 10-20 years.]
d. All of the above
e. None of the above
4) What causes endemic goiter?
a. Iodine deficiency
b. Goitrogens
c. Thiocyanate
d. Hereditary enzymatic defects
e. Not known
...
5) What causes MNG?
a. Mutation in TSH receptor
b. Chronic deficient iodine intake
c. Estrogen sensitivity
d. Autoimmune phenomena
...
6) Histological picture of MNG
a. Hypercellular areas
b. Cystic areas filled with colloid
c. Fibrosis
d. Lymphocytic infiltration
e. All of the above
...
7) How does MNG usually present?
a. Goiter
b. Dysphagia
c. Pain in the neck
d. Hoarseness
e. Change in TSH level
...
8) How substernal extension is best evaluated?
a. Clinical examination
b. MRI
c. Barium sallow
d. Biopsy
e. Mediastinoscopy
...
9) What is the treatment of a small asymptomatic benign diffuse goiter?
a. Periodical evaluation
b. Thyroxine
c. Surgery
d. Radioiodine
...
10) What is the best treatment to reduce the size of MNG?
a. Thyroxin
b. Radioiodine
c. Surgery
d. Antithyroid drugs
e. Steroids
...
11) What is the treatment of choice for most patients with toxic multinodular goiter?
a. Radioiodine
b. Antithyroid therapy
c. Surgery
d. Amiodarone
...
12) Toxic adenoma - True statement
a. Due to a mutation in the TSH-R
b. Causes severe thyrotoxicosis
c. Definitive diagnostic test is FNAC and cytological studies
d. Best treated with antithyroid drugs and beta blockers
e. All of the above
...
AMIODARONE INDUCED THYROID DISEASE
(3 MCQs)
1) Amiodarone
a. High iodine levels persist for > 6 months even after discontinuation
b. May cause hypothyroidism
c. Amiodarone inhibits deiodinase activity
d. May cause thyrotoxicosis
e. All of the above
1) Amiodarone
a. High iodine levels persist for > 6 months even after discontinuation [ Amiodarone contains 40% of iodine by weight. Thus, typical doses of amiodarone (200 mg/d) are associated with very high iodine intake. Amiodarone is stored in adipose tissue. Therefore, high iodine levels persist for > 6 months after discontinuation of the drug.]
b. May cause hypothyroidism [ Excess iodide transiently inhibits thyroid iodide organification. This phenomenon is known as the Wolff-Chaikoff effect. In normal individuals, the thyroid gland escapes from this inhibitory effect and iodide organification resumes. The suppressive action of high iodide may persist in patients with underlying autoimmune thyroid disease. Amiodarone may cause hypothyroidism in such patients susceptible to the inhibitory effects of a high iodine load. Amiodarone-associated hypothyroidism is more common in women and individuals with positive TPO antibodies. It is usually unnecessary to discontinue amiodarone for this side effect. Levothyroxine can be used to normalize thyroid function.]
c. Amiodarone inhibits deiodinase activity [ Amiodarone first causes a transient decrease of T4 levels. This is due to Wolff-Chaikoff effect (i.e., the inhibitory effect of iodine on T4 release. Soon, most escape from this iodide-dependent suppression of the thyroid. Later, the inhibitory effects of amiodarone on deiodinase activity and thyroid hormone receptor action become predominant. This effects lead to increased T4, decreased T3, increased rT3, and a transient increase of TSH. TSH levels normalize or are slightly suppressed after about 1 to 3 months.]
d. May cause thyrotoxicosis [ Jod - Basedow phenomenon is thyroid hormone synthesis becoming excessive as a result of increased iodine exposure. Amiodarone-induced thyrotoxicosis is far more prevalent in iodine-deficient regions.]
e. All of the above T [ Amiodarone may also cause a thyroiditis-like condition.]
2) Amiodarone-induced thyrotoxicosis (AIT) - True statement
a. Type 1 AIT is associated with an underlying thyroid abnormality
b. Type 2 amiodarone-induced thyrotoxicosis is a destructive thyroiditis
c. There is increased vascularity in type 1 AIT
d. All of the above
2) Amiodarone-induced thyrotoxicosis (AIT) - True statement
a. Type 1 AIT is associated with an underlying thyroid abnormality [ There are two major forms of AIT (amiodarone-induced thyrotoxicosis). Type 1 amiodarone-induced thyrotoxicosis is due to release of excessive thyroid hormone. It is iodine-induced. Type 1 AIT 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).]
b. Type 2 amiodarone-induced thyrotoxicosis is a destructive thyroiditis [ Type 2 amiodarone-induced thyrotoxicosis is a destructive thyroiditis that causes the release of preformed thyroid hormone from the damaged thyroid gland. Type 2 AIT occurs with no intrinsic thyroid abnormalities. It is due to drug-induced lysosomal activation leading to destructive thyroiditis.]
c. There is increased vascularity in type 1 AIT [ Distinguishing between the two forms of amiodarone induced thyrotoxicosis is difficult, especially since some patients have both types. Color-flow Doppler thyroid scan shows increased vascularity in type 1 but decreased vascularity in type 2 AIT.]
d. All of the above
3) What is the most effective long-term solution for amiodarone-induced thyrotoxicosis?
a. Stop amiodarone
b. Antithyroid drugs
c. Glucocorticoids
d. Lithium
e. Near-total thyroidectomy
3) What is the most effective long-term solution for amiodarone-induced thyrotoxicosis?
a. Stop amiodarone [ This is often impractical because of the underlying cardiac disorder. Discontinuation of amiodarone will not have an immediate effect because of its storage and prolonged half-life.]
b. Antithyroid drugs [ Type 1 amiodarone-induced thyrotoxicosis is best treated with high doses of antithyroid drugs (methimazole or propylthiouracil). High doses of antithyroid drugs can be used in type 1 AIT but are often ineffective.]
c. Glucocorticoids [ Type 2 amiodarone-induced thyrotoxicosis responds to high-dose corticosteroids.]
d. Lithium [ It blocks thyroid hormone release and can provide modest benefit in type 1 AIT .]
e. Near-total thyroidectomy T [ Near-total thyroidectomy rapidly decreases thyroid hormone levels if the patient can undergo the procedure safely. Near-total thyroidectomy is the most effective long-term solution for amiodarone-induced thyrotoxicosis.]
THYROIDITIS (14 MCQs)
1) Most common type of thyroiditis
a. Hashimoto's thyroiditis
b. Painless sporadic thyroiditis
c. Painless postpartum thyroiditis
d. All of the above
1) Most common type of thyroiditis
a. Hashimoto's thyroiditis T [ This is the most common type of thyroiditis. In Hashimoto's thyroiditis, the antithyroid immune response begins with activation of helper T cells that that are specific to a thyroid antigen (e.g., thyroid peroxidase and thyroglobulin.). Once helper T cells are activated, they induce B cells to secrete thyroid antibodies.]
b. Painless sporadic thyroiditis
c. Painless postpartum thyroiditis [ Painless postpartum thyroiditis is induced by the accumulation of fetal cells in the maternal thyroid gland during pregnancy.]
d. All of the above
CAUSES OF THYROIDITIS
1. Hashimoto's autoimmune thyroiditis
2. Postpartum, silent, or painless thyroiditis
3. Subacute (nonsuppurative) thyroiditis
4. Acute infectious thyroiditis
5. Riedel's thyroiditis
6. Postirradiation
7. Amiodarone induced
2) Preferentially elevated in thyrotoxicosis due to thyroiditis
a. Serum T3
b. Serum T4
c. TSH
d. All of the above
2) Preferentially elevated in thyrotoxicosis due to thyroiditis
a. Serum T3
b. Serum T4 T [ Inflammatory destruction of the thyroid may release preformed thyroid hormones from the damaged gland and lead to transient thyrotoxicosis. As thyroid hormone stores are depleted, there is often a progression through a period of euthyroidism to hypothyroidism. Serum T4 concentrations are proportionally higher than T 3 concentrations, reflecting the ratio of stored hormone in the thyroid gland. In Graves' disease and in toxic nodular goiter, T3 is preferentially elevated. The signs and symptoms of thyrotoxicosis due to thyroiditis are usually not severe.]
c. TSH
d. All of the above
3) What is the most common cause of chronic thyroiditis?
a. Hashimoto's thyroiditis
b. Riedel's thyroiditis
c. Viral thyroiditis
d. TB
e. Fungal infection
3) What is the most common cause of chronic thyroiditis?
a. Hashimoto's thyroiditis T [ This is an autoimmune disorder. It presents with a firm or hard goiter of variable size. Hashimoto's thyroiditis is the most frequent cause of hypothyroidism and goiter.]
b. Riedel's thyroiditis
c. Viral thyroiditis
d. TB [ TB may cause a subacute thyroiditis.]
e. Fungal infection [ Aspergillus, candida and pneumocystis produce acute thyroiditis. Parasites like ecchinococcus, strongyloidis and cysticerci may cause chronic thyroiditis.]
4) What is the most common clinical finding in Hashimoto's thyroiditis?
a. Painless goiter
b. Atrophic thyroid glands
c. High serum thyroid peroxidase antibody concentrations
d. High serum thyroglobulin antibody concentrations
...
5) Hurthle cells are typical of
a. Papillary carcinoma
b. Follicular carcinoma
c. Anaplastic carcinoma
d. Hashimoto's thyroiditis
e. Lymphoma within the thyroid gland
...
6) Painless postpartum thyroiditis - True statement
a. Thyrotoxicosis begins one to six months after delivery
b. Antithyroid drug therapy is indicated
c. Hypothyroidism never occur
d. No recurrence with subsequent pregnancies
e. No TPO antibodies
...
7) Post - partum thyroiditis - False statement
a. Severe thyroid tenderness
b. TPO antibodies are absent
c. Glucocorticoid is the treatment of choice
d. Permanent hypothyroidism almost always follow
e. All
...
8) de Quervain's thyroiditis (Painful subacute thyroiditis) - False statement.
a. Equally common in men and women
b. Granulomas are present
c. T 4 may be increased with low radioactive iodine uptake
d. TSH may be increased with increased radioactive iodine uptake
e. All
...
9) Goiter in de Quervain's thyroiditis is typically
a. Large
b. Nontender
c. Symmetric
d. Any of the above
e. None of the above
...
10) Thyroid function tests in de Quervain's thyroiditis may show
a. Thyrotoxicosis
b. Hypothyroidism
c. Normal thyroid function
d. Any of the above
...
11) The hallmark of painful subacute thyroiditis
a. Low TSH
b. Low T4
c. Normal T3
d. High titer of thyroid antibodies
e. Elevated erythrocyte sedimentation rate
...
12) Which drug is not used in the treatment of de Quervain's thyroiditis?
a. Aspirin
b. Prednisone
c. Beta-adrenergic blockers
d. Antithyroid drugs
e. Levothyroxine
...
13) Riedel's thyroiditis - True statement
a. Typically presents with thyroid dysfunction
b. Tender goiter
c. Diagnosis is by FNA biopsy
d. Treatment is surgical
e. No association with lung fibrosis
...
14) Suppurative thyroiditis - True statement
a. Rare
b. Pyriform sinus fistula is the most common source of infection in children
c. Fine-needle aspiration biopsy with Gram's staining and culture is the diagnostic test of choice
d. May be fatal
e. All of the above
...
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