Hypothyroidism Practice Quiz (27 questions)

1. What best defines hypothyroidism?

A. Reduced thyroid function that slows cellular activities

B. Inflammation that increases thyroid hormone release

C. Excess thyroid function that accelerates cellular activities

D. Tissue resistance to thyroid hormones despite normal production

Answer: (A)

Explanation

Hypothyroidism is thyroid hypofunction, commonly caused by decreased thyroid hormone production, and it slows cellular activity. Resistance to thyroid hormones is a disorder of tissue response rather than reduced thyroid function.

2. Which laboratory pattern most strongly suggests central hypothyroidism?

A. Elevated TSH with reduced thyroid function originating in the thyroid

B. Elevated TSH caused by excess thyroid hormone production

C. Low or inappropriately normal TSH with reduced thyroid function

D. Normal TSH with increased thyroid hormone production

Answer: (C)

Explanation

Central hypothyroidism arises from the pituitary or hypothalamus, so TSH is typically low or inappropriately normal despite reduced thyroid function. Elevated TSH is more characteristic of primary hypothyroidism originating in the thyroid.

3. Which complication can result from untreated hypothyroidism?

A. Myxedematous coma

B. Primary hyperparathyroidism

C. Excessive thyroid hormone production

D. Acute adrenal crisis

Answer: (A)

Explanation

Untreated hypothyroidism can produce severe complications, including myxedematous coma, along with cardiovascular, metabolic, hematopoietic, and developmental effects. Adrenal crisis and hyperparathyroidism are different endocrine disorders.

4. How does the prevalence of adult hypothyroidism generally change with age?

A. It remains stable with age and is approximately 20% worldwide

B. It decreases with age and remains below 1% worldwide

C. It increases with age but occurs in less than 0.1% worldwide

D. It increases with age and is approximately 1–10% worldwide

Answer: (D)

Explanation

Adult hypothyroidism becomes more prevalent as age increases, with an estimated worldwide prevalence of approximately 1–10%. The prevalence is therefore not stable or consistently below 1%.

5. In an iodine-deficient region, which cause most commonly accounts for hypothyroidism?

A. Iodine deficiency

B. Pituitary adenoma

C. Hashimoto thyroiditis

D. Resistance to thyroid hormones

Answer: (A)

Explanation

Iodine deficiency is the leading cause of hypothyroidism in areas where iodine intake is insufficient. Hashimoto thyroiditis is the most frequent cause among adults more broadly, but it does not replace iodine deficiency as the predominant cause in iodine-deficient regions.

6. Which comparison of congenital hypothyroidism frequencies is accurate?

A. General congenital hypothyroidism occurs in about 1 in 50,000 births, while central congenital hypothyroidism occurs in about 1 in 3,000–4,000

B. Both forms occur at approximately 1 in 50,000 births

C. Both forms occur at approximately 1 in 3,000 births

D. General congenital hypothyroidism occurs in about 1 in 3,000–4,000 births, while central congenital hypothyroidism occurs in about 1 in 50,000

Answer: (D)

Explanation

Congenital hypothyroidism overall occurs in approximately 1 in 3,000–4,000 births, whereas the central form is much less frequent, at approximately 1 in 50,000 births. Reversing these frequencies would substantially overestimate central congenital hypothyroidism.

7. What metabolic effect is expected when hypothyroidism slows cellular activity?

A. Increased energy consumption with enhanced conversion of T4 and T3

B. Reduced energy consumption with altered availability of T4 and T3

C. Unchanged energy consumption with increased thyroid hormone synthesis

D. Reduced energy consumption with increased thyroid hormone release

Answer: (B)

Explanation

Hypothyroidism slows metabolism, reducing energy consumption and altering the availability of the thyroid hormones T4 and T3. Increased energy use would reflect a metabolic state opposite to the mechanism described.

8. What causes the characteristic tissue changes of myxedema?

A. Infiltration by extracellular matrix rich in acidic polysaccharides

B. Reduced cellular energy use without tissue infiltration

C. Loss of thyroid tissue through autoimmune destruction

D. Accumulation of intracellular fat from increased metabolism

Answer: (A)

Explanation

Myxedema results when the skin and subcutaneous tissues become infiltrated by extracellular matrix containing acidic polysaccharides. Reduced cellular energy use describes hypometabolism, which is related to hypothyroidism but does not itself define the tissue infiltration of myxedema.

9. Why is untreated hypothyroidism particularly harmful during childhood?

A. Thyroid hormones are essential for bone growth and nervous-system development

B. Thyroid hormones mainly control skin pigmentation during early development

C. Thyroid hormones prevent iodine deficiency by increasing intestinal absorption

D. Thyroid hormones primarily regulate adult blood pressure and cardiac rhythm

Answer: (A)

Explanation

During childhood, thyroid hormones support bone growth and nervous-system development, especially brain growth, so deficiency can cause short stature and severe developmental impairment. The other choices assign thyroid hormones functions that do not explain the characteristic childhood consequences.

10. Which pattern is most characteristic of typical hypothyroidism?

A. Weight gain despite reduced appetite with psychomotor slowing

B. Weight loss despite increased appetite with psychomotor slowing

C. Weight loss with reduced appetite and persistent tachycardia

D. Weight gain with increased appetite and marked hyperreflexia

Answer: (A)

Explanation

Hypothyroidism commonly produces fatigue, cold intolerance, constipation, weight gain despite reduced appetite, slowed thinking, bradycardia, and delayed reflex relaxation. Increased appetite with weight loss is more consistent with a hypermetabolic state than with the described hypothyroid pattern.

11. Which finding is specifically associated with myxedematous infiltration in hypothyroidism?

A. Oily skin accompanied by tremor and distal muscle fasciculations

B. Dry skin accompanied by hoarseness and carpal-tunnel paresthesia

C. Flushed skin accompanied by exophthalmos and persistent tachycardia

D. Warm skin accompanied by diarrhea and proximal muscle weakness

Answer: (B)

Explanation

Myxedematous infiltration can cause dry skin, hoarseness, hearing loss, snoring, sleep apnea, myalgia, arthralgia, and carpal-tunnel paresthesia. Tremor, warm skin, and tachycardia are not the characteristic infiltrative findings described here.

12. How is subclinical hypothyroidism distinguished from overt hypothyroidism by laboratory findings?

A. TSH is elevated while peripheral thyroid hormone levels remain normal

B. TSH is elevated while peripheral thyroid hormone levels are reduced

C. TSH is normal while peripheral thyroid hormone levels are reduced

D. TSH is reduced while peripheral thyroid hormone levels remain normal

Answer: (A)

Explanation

Subclinical hypothyroidism is defined by elevated TSH with normal peripheral thyroid hormone levels, often producing no symptoms or only mild symptoms. Reduced peripheral hormone levels indicate overt hypothyroidism rather than the subclinical form.

13. A young patient has subclinical hypothyroidism with TSH above 10 mIU/L. Which long-term risk is associated with this condition?

A. Reduced risk of dyslipidemia and type 2 diabetes

B. Increased risk of coronary disease and heart failure

C. Reduced risk of vascular disease through lower blood pressure

D. Increased risk of acute asthma and bacterial pneumonia

Answer: (B)

Explanation

In young patients with TSH above 10 mIU/L, subclinical hypothyroidism is associated with coronary disease, heart failure, dyslipidemia, and type 2 diabetes. The condition therefore does not imply protection from cardiovascular or metabolic disease.

14. Which prevalence comparison between pregnancy-related forms of hypothyroidism is correct?

A. Both overt and subclinical hypothyroidism affect about 2%

B. Both overt and subclinical hypothyroidism affect about 0.5%

C. Overt hypothyroidism affects about 0.5%, whereas subclinical hypothyroidism affects about 2%

D. Overt hypothyroidism affects about 2%, whereas subclinical hypothyroidism affects about 0.5%

Answer: (C)

Explanation

During pregnancy, overt hypothyroidism affects approximately 0.5% of women, while subclinical hypothyroidism affects approximately 2%. Maternal complications can include miscarriage, anemia, hypertension, placental abruption, premature membrane rupture, and postpartum hemorrhage.

15. Why is early treatment particularly important in congenital hypothyroidism?

A. Treatment begun after 3 months mainly produces irreversible renal impairment

B. Treatment begun after 3 months can be followed by irreversible neurological sequelae

C. Treatment begun after 3 months primarily causes permanent thyroid enlargement

D. Treatment begun after 3 months is associated with persistent hyperthyroidism

Answer: (B)

Explanation

Untreated congenital hypothyroidism threatens psychomotor and mental development, and treatment delayed beyond 3 months may result in irreversible neurological sequelae. The major concern is neurodevelopmental injury rather than thyroid enlargement or hyperthyroidism.

16. Which condition is classified as a cause of adult primary hypothyroidism?

A. Hashimoto thyroiditis affecting the thyroid gland

B. A congenital TRH defect affecting hypothalamic signaling

C. A hypothalamic tumor reducing central stimulation

D. Pituitary irradiation impairing TSH production

Answer: (A)

Explanation

Adult primary hypothyroidism arises from disease or damage within the thyroid and may be autoimmune, iatrogenic, nutritional, medication-related, or due to other thyroid processes such as Hashimoto thyroiditis. Hypothalamic and pituitary disorders cause central hypothyroidism instead.

17. Which statement correctly distinguishes central from primary hypothyroidism?

A. Central hypothyroidism is usually autoimmune thyroiditis, whereas primary hypothyroidism reflects congenital TRH defects

B. Central hypothyroidism results from pituitary-hypothalamic disease, whereas primary hypothyroidism results from thyroid disease

C. Central hypothyroidism results from thyroid disease, whereas primary hypothyroidism results from pituitary-hypothalamic disease

D. Central hypothyroidism is caused by iodine deficiency, whereas primary hypothyroidism is caused by pituitary tumors

Answer: (B)

Explanation

Central hypothyroidism results from acquired or congenital defects involving the hypothalamus or pituitary, including tumors, irradiation, surgery, trauma, and rare TRH or TSH defects. Primary hypothyroidism originates in the thyroid itself, such as with autoimmune thyroiditis or iodine deficiency.

18. What accounts for most permanent cases of congenital primary hypothyroidism?

A. Maternal antithyroid medication causing transient hormone suppression

B. Central pituitary dysfunction from congenital TSH deficiency

C. Thyroid dysgenesis, including ectopia, athyreosis, or hypoplasia

D. Childhood autoimmune thyroiditis developing after normal thyroid formation

Answer: (C)

Explanation

Thyroid dysgenesis accounts for approximately 70–80% of permanent congenital primary hypothyroidism, with ectopia representing most dysgenetic cases. Maternal medications and antibodies can cause transient disease, while pituitary dysfunction is a central rather than primary cause.

19. A patient is suspected of having primary hypothyroidism. Which laboratory test should be ordered first?

A. Free T4

B. Serum TSH

C. Thyroid ultrasound

D. Free T3

Answer: (B)

Explanation

TSH is the first-line test for suspected primary hypothyroidism and is elevated in both overt and subclinical primary disease. Free T4 is particularly important when central hypothyroidism is suspected, because TSH may be inappropriately normal or low in that condition.

20. Which test is essential for confirming central hypothyroidism and assessing the depth of hormone deficiency?

A. Urinary iodine testing

B. Free T3 measurement

C. Free T4 measurement

D. Anti-thyroid peroxidase antibodies

Answer: (C)

Explanation

Free T4 confirms central hypothyroidism and helps assess the severity of hormone deficiency, while also helping interpret possible subclinical primary hypothyroidism alongside TSH. Free T3 is considered unnecessary for this assessment.

21. Which cardiac consequence of hypothyroidism is described as potentially reversible after treatment?

A. Established coronary plaque

B. Systolic and diastolic dysfunction

C. Irreversible coronary narrowing

D. Silent coronary atherosclerosis

Answer: (B)

Explanation

Hypothyroidism can produce systolic and diastolic dysfunction that may reverse with treatment. Silent coronary atherosclerosis, in contrast, is described as irreversible rather than a transient cardiac functional change.

22. A patient with deep, neglected hypothyroidism develops myxedematous coma. Which precipitating factor is most characteristic?

A. Brief dietary carbohydrate restriction

B. A high-iodine diet

C. Exposure to cold

D. Moderate physical exercise

Answer: (C)

Explanation

Cold triggers approximately 95% of cases of myxedematous coma, although infection, stress, medications, and overhydration may also contribute. A high-iodine diet is not identified as the characteristic precipitant of this emergency.

23. What mortality rate is associated with myxedematous coma?

A. Approximately 20%

B. Approximately 5%

C. Approximately 80%

D. Approximately 50%

Answer: (A)

Explanation

Myxedematous coma causes death in about 20% of cases, making it a rare but serious complication of profound untreated hypothyroidism. Rates near 50% or 80% overstate the reported mortality, while 5% understates it.

24. How should levothyroxine generally be taken to promote consistent absorption?

A. Immediately after dinner with other medications and supplements

B. With breakfast and coffee to reduce gastrointestinal discomfort

C. At varying times each day according to symptoms

D. Fasting 30–60 minutes before breakfast or at bedtime two hours after the last meal

Answer: (D)

Explanation

Levothyroxine should be taken under consistent daily conditions, either fasting 30–60 minutes before breakfast or at bedtime two hours after the last meal. Taking it with meals, coffee, or changing schedules can make absorption and dosing less consistent.

25. How should levothyroxine dosing generally change when comparing pregnancy with older age?

A. The dose usually decreases by 30–50% in pregnancy and is higher in older adults

B. The dose increases in older adults and decreases during pregnancy to reduce cardiac stress

C. The dose usually increases by 30–50% in pregnancy and is lower in older adults

D. The dose remains similar in pregnancy and older adults at about 1.5–1.8 μg/kg/day

Answer: (C)

Explanation

Pregnancy generally requires a 30–50% levothyroxine dose increase, whereas older adults typically receive a lower dose of about 1.1–1.3 μg/kg/day. The opposite pattern would confuse the distinct dosing adjustments for these populations.

26. What is the appropriate initial levothyroxine strategy for a fragile elderly patient with longstanding severe hypothyroidism?

A. Start immediately at the standard calculated adult dose and reassess after several months

B. Start with 12.5–25 μg and increase gradually with clinical, hormonal, and electrocardiographic monitoring

C. Begin with a high loading dose and stop monitoring once symptoms improve

D. Use a fixed pediatric dose until TSH becomes normal

Answer: (B)

Explanation

Fragile or elderly patients and those with deep or longstanding hypothyroidism should begin with 12.5–25 μg, followed by gradual increases and clinical, hormonal, and electrocardiographic monitoring. Immediate full-dose treatment can increase risk in these vulnerable patients.

27. When should TSH generally be reassessed during levothyroxine dose adjustment?

A. Every 6–8 weeks

B. Every 6–12 months during each adjustment

C. Every 24 hours

D. Once after the initial prescription

Answer: (A)

Explanation

TSH is reassessed every 6–8 weeks while the dose is being adjusted, allowing time for the hormone axis to respond. Once TSH is stable and normal, monitoring can be extended to every 6–12 months.