Endocrine: thyroid disorders

Question 1

A 45-year-old woman presents with fatigue, weight gain, and cold intolerance. Physical exam reveals dry skin, coarse hair, and periorbital puffiness. TSH is 18 mIU/L (normal: 0.4–4.0 mIU/L), and free T4 is low. What is the most likely diagnosis?

Answer 1

Primary hypothyroidism
Rationale: Elevated TSH and low free T4 are hallmark features of primary hypothyroidism, most commonly due to autoimmune thyroiditis (Hashimoto’s thyroiditis).

Question 2

A 30-year-old woman presents with weight loss, heat intolerance, and palpitations. On examination, she has a diffusely enlarged thyroid and exophthalmos. Lab results show low TSH and elevated free T4. What is the most appropriate initial treatment?

Answer 2

Methimazole
R: Methimazole is the first-line treatment for Graves’ disease to reduce thyroid hormone synthesis.

Question 3

A 68-year-old woman is brought to the emergency department with confusion, bradycardia, hypothermia, and hypotension. Lab tests reveal TSH of 30 mIU/L and low free T4. What is the most likely diagnosis?

Answer 3

Myxedema coma
R: it is a manifestation of severe hypothyroidism characterized by mental status changes, hypothermia, and cardiovascular collapse.

Question 4

A 40-year-old man with a history of hypothyroidism treated with levothyroxine reports weight loss, palpitations, and tremors. Lab tests reveal TSH <0.01 mIU/L and elevated free T4. What is the next step in management?

Answer 4

decrease levothyroxine dose

Question 5

A 25-year-old woman presents with palpitations, weight loss, and irregular menstrual cycles. Her thyroid is diffusely enlarged and tender to palpation. Lab tests show low TSH and elevated free T4. Thyroid scintigraphy reveals decreased uptake. What is the most likely diagnosis?

Answer 5

Subacute thyroiditis
R: presents with tender thyroid, hyperthyroidism, low radioactive iodine uptake vs grave’s disease/toxic nodular goiter

Question 6

differentiate between central hypothyroidism and primary hypothyroidism using laboratory findings

Answer 6

Central hypothyroidism: Low free T4 with inappropriately normal or low TSH

Question 7

What is the pathophysiological basis for exophthalmos in Graves’ disease, and why is it absent in other causes of hyperthyroidism?

Answer 7

Exophthalmos occurs due to autoimmune-mediated inflammation and deposition of glycosaminoglycans in orbital tissues. It is specific to Graves’ disease because TSH receptor antibodies target orbital fibroblasts, a feature absent in other hyperthyroid conditions.

Question 8

Why is radioactive iodine uptake (RAIU) low in subacute thyroiditis but elevated in Graves’ disease?

Answer 8

In subacute thyroiditis, thyroid hormone release is due to glandular inflammation and leakage, not increased synthesis. In Graves’ disease, thyroid-stimulating antibodies drive excessive thyroid hormone synthesis, increasing RAIU.

Question 9

Why is levothyroxine preferred over liothyronine for treating hypothyroidism?

Answer 9

Levothyroxine (T4) provides a stable and long-lasting supply of thyroid hormone, allowing peripheral conversion to T3 as needed. Liothyronine (T3) has a shorter half-life, leading to fluctuating hormone levels.

Question 10

what clinical scenarios would you expect subclinical hypothyroidism to progress to overt hypothyroidism?

Answer 10

Progression is more likely in patients with elevated TSH (>10 mIU/L), positive thyroid peroxidase antibodies (TPO-Ab), or a history of autoimmune thyroid disease.

Question 11

What is the rationale for using beta-blockers in hyperthyroidism, and why don’t they address the underlying condition?

Answer 11

Beta-blockers reduce adrenergic symptoms like tachycardia and tremors by blocking beta-adrenergic receptors but do not affect thyroid hormone levels or synthesis.

Question 12

How does amiodarone therapy result in thyroid dysfunction, and how can you differentiate between amiodarone-induced hypothyroidism and hyperthyroidism?

Answer 12

Amiodarone affects thyroid function by iodine excess (Wolff-Chaikoff effect) and direct toxicity.

Question 13

Why is free T4 measurement more reliable than total T4 in patients with altered binding protein levels, such as in pregnancy or liver disease?

Answer 13

Total T4 levels are influenced by changes in thyroid-binding globulin (TBG), whereas free T4 reflects the biologically active hormone unaffected by binding protein fluctuations.

Question 14

What is the significance of thyroid-stimulating immunoglobulins (TSI) in Graves’ disease?

Answer 14

TSI stimulates the TSH receptor, causing excessive thyroid hormone production. It is diagnostic of Graves’ disease.

Question 15

Why is subclinical hypothyroidism more likely to progress to overt hypothyroidism in the presence of thyroid peroxidase antibodies (TPO-Ab)?

Answer 15

TPO-Ab indicates ongoing autoimmune thyroid destruction, increasing the likelihood of progression.

Question 16

What factors influence the decision to treat subclinical hypothyroidism?

Answer 16

Treatment is recommended for TSH >10 mIU/L, symptoms of hypothyroidism, positive TPO-Ab, or high cardiovascular risk.

Question 17

Why is methimazole preferred over propylthiouracil (PTU) for most cases of hyperthyroidism?

Answer 17

Methimazole has a longer half-life for long-term management, fewer side effects, and better efficacy, except in the first trimester of pregnancy or thyroid storm.

Question 18

How does amiodarone-induced thyroid dysfunction differ between Type 1 and Type 2 hyperthyroidism?

Answer 18

Type 1: Iodine-induced hormone overproduction in preexisting thyroid disease.
Type 2: Destructive thyroiditis releasing stored hormones.

Question 19

What is the primary indication for thyroidectomy in hyperthyroidism?

Answer 19

Indications include large goiters, obstructive symptoms, pregnancy (when radioactive iodine is contraindicated), or suspected malignancy.

Question 20

How does iodine administration help in thyroid storm?

Answer 20

high-dose iodine inhibits thyroid hormone release (Wolff-Chaikoff effect)

Question 21

Why is TSH measurement alone insufficient in diagnosing secondary hypothyroidism?

Answer 21

In secondary hypothyroidism, TSH may be low or normal despite low free T4 due to pituitary dysfunction.

Question 22

How do glucocorticoids impact thyroid function tests in critically ill patients?

Answer 22

Glucocorticoids suppress TSH secretion, potentially leading to low TSH and low free T4 (euthyroid sick syndrome).

Question 23

most accurate tool to measure thyroid volume, nodularity and assess goiter in iodine-deficient regions

Answer 23

ultrasound

Question 24

most common cause of hypothyroidism

Answer 24

iodine deficiency

Question 25

marked lymphocytic infiltration with germinal center formation, atrophy of thyroid follicles, absence of colloid & fibrosis

Answer 25

Hashimoto’s thyroiditis

Question 26

When ACTH level is normal or high
>15pg/ml, what is the possible cause?

Answer 26

ACTH-dependent cushing’s

Question 27

When ACTH is suppressed to <5pg/ml, what is the possible cause?

Answer 27

ACTH-independent cushing’s

Question 28

A patient presents with hypertension, moon facies, and central obesity. Plasma cortisol levels are elevated, but ACTH levels are undetectable. What test should be performed next?

Answer 28

CT scan of the adrenal glands
R: Undetectable ACTH suggests an adrenal source of cortisol overproduction, warranting imaging to identify an adrenal adenoma or carcinoma (ACTH-independent cushing’s)

Question 29

late-night salivary cortisol is a useful screening test for Cushing’s syndrome since it ________

Answer 29

detects loss of diurnal cortisol variation

Question 30

mechanism of dexamethasone supression test in diagnosing

Answer 30

failure to supress cortisol indicates Cushing’s s.
R: exogenous dexamethason supresses ACTH and cortisol secretion in healthy indv’s

Question 31

glucocorticoids contribute to hypertension in Cushing’s s. by ______

Answer 31

enhance vascular sensitivity to catecholamines and increased sodium retention

Question 32

Hyperaldosteronism vs Cushing’s syndrome in terms of electrolyte imbalance

Answer 32

(1) causes hypokalemia since aldosterone promotes potassium excretion

Question 33

test confirming mineralocorticoid excess in HPN patient w/ hypokalemia

Answer 33

Plasma aldosterone-renin ratio (ARR)
R: HIGH ARR = primary aldosteronism

Question 34

In spironolactone, mineralocorticoid receptor blockade help manage HPN in cushing’s syndrome by ______

Answer 34

counteracting sodium retention and volume expansion

Question 35

what class of agents are not effective in Cushing’s syndrome?

Answer 35

Beta-blockers
R: less effective against cortisol-induced HPN

Question 36

mechanism of amiloride in managing HPN in Cushing’s syndrome

Answer 36

inhibits epithelial sodium channels in kidney

Question 37

mechanism of Metyrapone in Cushing’s syndrome

Answer 37

inhibits 11B-hydroxylas = reducing cortisol synthesis

Question 38

mechanism of Mitotane in adrenal carcinoma causing cushing’s syndrome

Answer 38

selectively destroys adrenal cortical cells
R: reduces tumor-rel cortisol production

Question 39

Patient presented with uncontrolled hypertension and elevated ACTH levels. What is the appropriate next step?

Answer 39

get an MRI imaging to confirm ACTH-dependent cushing’s syndrome