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Family Medicine Clerkship- Case files > Thyroid/ Parathyroid > Flashcards

Thyroid/ Parathyroid Flashcards

1
Q

What are the distinguishing features of Grave’s disease?

A
  • Nervousness
  • Palpitations
  • Weight loss
  • Fine resting tremor
  • Dyspnea on exertion
  • Difficulty concentrating
  • Tachycardia
  • Hypertension
  • Heat insensitivity
  • Exophthalmos
  • Dry skin
  • Amenorrhea
  • Atrial fibrillation (irregular heart rate)
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2
Q

What is the most appropriate imaging in suspected Grave’s?

A
  • Nuclear medicine thyroid scan with uptake
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3
Q

What is the definitive nonsurgical treatment of Grave’s?

A
  • Thyroid ablation with radioactive iodine and often times thyroid hormone replacement
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4
Q

Describe the pathophysiology behind Grave’s disease.

A
  • Autoimmune thyroid disorder where autoantibodies agains TSH receptors on the thyroid gland result in hyper functioning of the gland
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5
Q

What is common the demographic for Grave’s disease?

A
  • Reproductive age females
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6
Q

What are the treatments for Grave’s disease?

A
  • Antithyroid drugs => propylthiouracyl and methimazole

- Beta blockers to block the peripheral effects of excessive thyroxine

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7
Q

Who is radioactive iodine contraindicated in the treatment of Graves/hyperthyroidism?

A
  • Pregnant women (these patients undergo thyroidectomy)
  • Breastfeeding women
  • Children
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8
Q

What are the most dangerous consequences of thyroid storm?

A
  • Altered mental status, coma, seizures
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9
Q

What are the symptoms of thyroid storm?

A
  • Fever
  • Confusion
  • restlessness
  • Psychotic behavior
  • Tachycardia
  • Elevated BP
  • Dyspnea on exertion
  • Peripheral vasoconstriction
  • Cerebral or cardiac ischemia
  • Altered mental status, coma, seizures
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10
Q

What lab results would indicate hyperthyroidism?

A
  • High free thyroxine

- Low TSH

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11
Q

How would Graves differ from thyroiditis on radio nucleotide imaging?

A
  • Grave’s => Diffuse hyperactivity with large amounts of uptake due to presence of new hormone
  • Thyroiditis => patchy uptake with overall reduced activity, reflecting the release of existing hormone rather than over production
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12
Q

How do propylthiouracil and methimazole work?

A
  • PTU => inhibit the organification of iodine AND prevents the peripheral conversion of T4=> T3
  • Methimazole => inhibit the organification of iodine
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13
Q

What is the most risky potential side effect of PTU and methimazole?

A
  • Agranulocytosis
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14
Q

What is the treatment in thyroid storm?

A
  • PTU
  • Beta blockers
  • Hydrocortisone to prevent adrenal crisis
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15
Q

What symptoms are observed in patients who are hypothyroid?

A
  • Lethargy
  • Weight gain
  • Hair loss/thinning
  • Dry skin
  • Slowed mentation or forgetfulness
  • Constipation
  • Cold intolerance
  • Depressed affect
  • Low BP
  • Bradycardia
  • Myxedema
  • Diminished relaxation of reflexes
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16
Q

What is the most common cause of hypothyroidism in the U.S.?

A
  • Hashimoto thyroiditis
17
Q

How would labs be different in primary hypothyroid and secondary hypothyroid?

A
  • Primary hypothyroid => elevated TSH and low free thyroxine

- Secondary hypothyroid => lower TSH; work up to see if hypothalamic or pituitary in etiology (TRH test)

18
Q

What are thyroid nodules associated with?

A
  • Iodine deficiency
  • Ingestion of goitrogens
  • Increased number of pregnancies
19
Q

Which type of thyroid nodule is rarely malignant?

A
  • Hyperfunctional(hot) nodules are rarely malignant
20
Q

How should nonfunctioning nodules be biopsied?

A
  • Fine needle aspiration
21
Q

Differentiate hyperparathyroidism from secondary hyperparathyroidsim, and tertiary hyperparathyroidism.

A
  • Hyperparathyroidism: Elevated parathyroid hormone usually due to excess production by the parathyroid, leading to hypercalcemia
  • Secondary hyperparathyroidism: Parathyroid glands overproduce PTH to respond to low serum calcium levels (could be due to low calcium intake or vitamin D)
  • Tertiary hyperparathyroidism: Elevated PTH in patients who have renal failure
22
Q

What are the cause of hypercalcemia?

A
  • increase in calcium resorption from bone
  • decreased renal excretion of calcium
  • increase absorption form the GI tract
23
Q

What is the role of calcitonin in calcium homeostasis?

A
  • Calcitonin responds to increased levels of calcium and attempts to lower calcium through renal excretion and by opposing osteoclast activation
  • Calcitonin in produced by the parafollicular cells of the thyroid
24
Q

What is the role of PTH in calcium homeostasis?

A
  • PTH responds to low levels of calcium by promoting osteoclast activation and increases calcium resorption from the kidneys
  • PTH increases serum calcium levels but decreases phosphate levels (promotes phosphate excretion renal)
  • PTH increases calcitriol (Vit D) levels which act in the GI tract to promote calcium and phosphate absorption
25
Q

What is the most common cause of hypercalcemia?

A
  • Hyperparathyroidism (in the ambulatory patient)

- Cancer is second

26
Q

What are the 5 main etiologies of hypercalcemia?

A
  • PTH related
  • Malignancy
  • Renal failure
  • High bone turnover
  • Vit D
27
Q

What are the classic signs of hypercalcemia?

A
  • Stones (nephrolithiasis)
  • Bones ( bone pain)
  • Psychiatric groans (poor concentration, weakness, fatigue, stupor, coma)
  • Abdominal moans (abdominal pain, constipation, nausea, vomiting, pancreatitis, anorexia)
  • Shortened QT
  • Arrhythmias
28
Q

What are examples of primary hyperparathyroidism?

A
  • MEN I or II ( multiple endocrine neoplasia)
29
Q

What types of cancers cause hypercalcemia?

A
  • lung tumors (tumor secretes PTH-rP)
  • squamous carcinoma of the head and neck
  • renal carcinoma
  • breast cancer
  • multiple myeloma
  • prostate cancer
30
Q

How does vitamin A lead to hypercalcemia?

A
  • Vitamin A (and analogs used to treat acne) causes increased bone resorption
31
Q

How does granulomatous disease cause hypercalcemia?

A
  • Granulomatous disease (TB, sarcoidosis, hodgkin disease) cause extra renal conversion of Vit D to calcitriol
32
Q

Describe the labs of a patient with renal failure causing tertiary hyperparathyroidism.

A
  • Hypocalcemia
  • Hyperphosphatemia
  • Low vitamin D levels
  • can lead to increased PTH and hypercalcemia if left untreated
33
Q

What medications are associated with hypercalcemia?

A
  • Thiazides and Li+

Family Medicine Clerkship- Case files (13 decks)

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