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First Aid > Endocrine 3 > Flashcards

Endocrine 3 Flashcards

1
Q

What are the 5 P’s of episodic hyperadrenergic symptoms in pheochromocytoma?

A

Pressure (BP), Pain (headache), Perspiration, Palpitations (tachycardia), Pallor

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2
Q

What are the findings in pheochromocytoma?

A

Catecholamines & catecholamine metabolites (e.g., metanephrines) in urine & plasma.

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3
Q

What is the treatment for pheochromocytoma?

A

Irreversible α-antagonists (e.g., phenoxybenzamine) followed by β-blockers prior to tumor resection.

α-blockade must be achieved before giving β-blockers to avoid a hypertensive crisis– A before B.

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4
Q

What is VIPoma?

A

A rare neuroendocrine tumor that secretes vasoactive intestinal peptide (VIP).

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5
Q

Where does VIPoma most commonly arise?

A

In the pancreas.

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6
Q

What syndromes are associated with VIPoma?

A

Associated with MEN-1 & WDHA (Watery Diarrhea, Hypokalemia, Achlorhydria) syndrome.

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7
Q

What is the primary symptom of VIPoma?

A

Secretory diarrhea.

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8
Q

What are the metabolic findings in hypothyroidism?

A

Cold intolerance, ↓ sweating, weight gain (↓ basal metabolic rate→ ↓ calorigenesis), hyponatremia (↓ free water clearance).

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9
Q

What are the metabolic findings in hyperthyroidism?

A

Heat intolerance, ↑ sweating, weight loss (↑ synthesis of Na+-K+ ATPase → ↑ basal metabolic rate→ ↑ calorigenesis).

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10
Q

What are the skin/hair findings in hypothyroidism?

A

Dry, cool skin; coarse, brittle hair; diffuse alopecia; brittle nails; puffy facies & generalized nonpitting edema (myxedema).

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11
Q

What are the skin/hair findings in hyperthyroidism?

A

Warm, moist skin; fine hair; onycholysis; pretibial myxedema in Graves disease.

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12
Q

What are the ocular findings in hypothyroidism?

A

Periorbital edema.

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13
Q

What are the ocular findings in hyperthyroidism?

A

Ophthalmopathy in Graves disease (including periorbital edema, exophthalmos), lid lag/retraction.

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14
Q

What are the GI findings in hypothyroidism?

A

Constipation (↓ GI motility), ↓ appetite.

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15
Q

What are the GI findings in hyperthyroidism?

A

Hyperdefecation/diarrhea (↑ GI motility), ↑ appetite.

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16
Q

What are the musculoskeletal findings in hypothyroidism?

A

Hypothyroid myopathy (proximal weakness, ↑ CK), carpal tunnel syndrome, myoedema.

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17
Q

What are the musculoskeletal findings in hyperthyroidism?

A

Thyrotoxic myopathy (proximal weakness, normal CK), osteoporosis/↑ fracture rate.

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18
Q

What is the difference between hypothyroid and thyrotoxic myopathies?

A

Both exhibit proximal weakness, but in hypothyroid myopathy there is ↑ CK - in thyrotoxic myopathy there is proximal weakness with normal CK.

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19
Q

What are the reproductive findings in hypothyroidism?

A

Menorrhagia &/or oligomenorrhea; ↓ libido, infertility.

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20
Q

What are the reproductive findings in hyperthyroidism?

A

Oligomenorrhea or amenorrhea, gynecomastia, ↓ libido, infertility.

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21
Q

What are the neuropsych findings in hypothyroidism?

A

Hypoactivity, lethargy, fatigue, weakness, depressed mood, ↓ reflexes.

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22
Q

What are the neuropsych findings in hyperthyroidism?

A

Hyperactivity, restlessness, anxiety, insomnia, fine tremors, ↑ reflexes.

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23
Q

What are the cardiovascular findings in hypothyroidism?

A

Bradycardia, dyspnea on exertion.

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24
Q

What are the cardiovascular findings in hyperthyroidism?

A

Tachycardia, palpitations, dyspnea, arrhythmias, chest pain & systolic HTN.

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25
Q

Why is chest pain & systolic HTN seen in hyperthyroidism?

A

Due to ↑ # & sensitivity of β-adrenergic receptors, ↑ expression of cardiac sarcolemmal ATPase & ↓ expression of phospholamban.

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26
Q

What are the lab findings in hypothyroidism?

A

↑ TSH (if 1°), ↓ free T3 / T4, Hypercholesterolemia.

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27
Q

What are the lab findings in hyperthyroidism?

A

↓ TSH (if 1°), ↑ free T3 / T4, ↓ LDL, HDL, & total cholesterol.

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28
Q

What is the most common cause of hypothyroidism in iodine-sufficient regions?

A

Hashimoto thyroiditis.

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29
Q

What is Hashimoto thyroiditis?

A

An autoimmune disorder with antithyroid peroxidase & antithyroglobulin antibodies.

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30
Q

What are the histological findings in Hashimoto thyroiditis?

A

Hürthle cells, lymphoid aggregates with germinal centers.

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31
Q

What are the clinical findings in Hashimoto thyroiditis?

A

Moderately enlarged, nontender thyroid.

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32
Q

What is postpartum thyroiditis?

A

Self-limited thyroiditis arising up to 1 year after delivery.

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33
Q

What are the findings in congenital hypothyroidism (cretinism)?

A

Pot-bellied, Pale, Puffy-faced child, Protruding umbilicus, Protuberant tongue, Poor brain development.

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34
Q

What is subacute granulomatous thyroiditis (de Quervain)?

A

Self-limited disease often following flu-like illness.

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35
Q

What are the findings in subacute granulomatous thyroiditis?

A

↑ ESR, jaw pain, very tender thyroid.

36
Q

What is Riedel thyroiditis?

A

Thyroid replaced by fibrous tissue with inflammatory infiltrate.

37
Q

What are the clinical findings in Riedel thyroiditis?

A

Fixed, hard (rock-like), painless goiter.

38
Q

What are the other causes of hypothyroidism?

A

Iodine deficiency, goitrogens (e.g., amiodarone, lithium), Wolff-Chaikoff effect.

39
Q

What is the most common cause of hyperthyroidism?

A

Graves disease.

40
Q

What is the pathogenesis of Graves disease?

A

Thyroid-stimulating immunoglobulin stimulates TSH receptors on thyroid.

41
Q

What is the histology of Graves disease?

A

Tall, crowded follicular epithelial cells; scalloped colloid.

42
Q

What is toxic multinodular goiter?

A

Focal patches of hyperfunctioning follicular cells working independently of TSH.

43
Q

What is thyroid storm?

A

A serious complication of untreated hyperthyroidism that worsens with acute stress.

44
Q

What is the treatment for thyroid storm?

A

4 P’s: β-blockers, Propylthiouracil, corticosteroids, Potassium iodide.

45
Q

What is the Jod-Basedow phenomenon?

A

Thyrotoxicosis if a patient with iodine deficiency is made iodine replete.

46
Q

What are the causes of smooth/diffuse goiter?

A

Graves disease, Hashimoto thyroiditis, Iodine deficiency, TSH-secreting pituitary adenoma.

47
Q

What are the causes of nodular goiter?

A

Toxic multinodular goiter, Thyroid adenoma, Thyroid cancer, Thyroid cyst.

48
Q

What is thyroid adenoma?

A

Benign solitary growth of the thyroid.

49
Q

How is thyroid cancer diagnosed and treated?

A

Typically diagnosed with fine needle aspiration; treated with thyroidectomy.

50
Q

What are the complications of thyroidectomy?

A

Hoarseness due to recurrent laryngeal nerve damage, hypocalcemia due to removal of parathyroid glands.

51
Q

What is the most common type of thyroid cancer?

A

Papillary carcinoma: excellent prognosis.

52
Q

What are the histological features of papillary carcinoma?

A

Empty-appearing nuclei with central clearing (‘Orphan Annie’ eyes), psammoma bodies.

53
Q

What factors increase the risk of developing papillary carcinoma of the thyroid?

A

RET/PTC rearrangements, BRAF mutations, childhood irradiation.

54
Q

What is follicular carcinoma of the thyroid?

A

Good prognosis, invades thyroid capsule/vasculature.

55
Q

What genetic abnormalities are associated with follicular carcinoma of the thyroid?

A

RAS mutation & PAX8-PPAR-γ translocations.

56
Q

What is medullary carcinoma of the thyroid?

A

From parafollicular ‘C cells’, produces calcitonin.

57
Q

What genetic abnormalities are associated with medullary carcinoma of the thyroid?

A

Associated with MEN 2A & 2B (RET mutations).

58
Q

What is undifferentiated/anaplastic carcinoma of the thyroid?

A

Invades local structures, very poor prognosis.

59
Q

What condition is lymphoma of the thyroid associated with?

A

Hashimoto thyroiditis.

60
Q

What is hypoparathyroidism due to?

A

Accidental surgical excision of parathyroid glands, autoimmune destruction, or DiGeorge syndrome.

61
Q

What signs indicate hypoparathyroidism?

A

Chvostek sign, Trousseau sign.

62
Q

What is Pseudohypoparathyroidism type 1A?

A

Unresponsiveness of kidney to PTH → hypocalcemia despite ↑ PTH levels.

63
Q

What is the presentation of Pseudohypoparathyroidism type 1A?

A

Constellation of physical findings known as Albright hereditary osteodystrophy.

64
Q

What is Pseudopseudohypoparathyroidism?

A

Physical exam features of Albright hereditary osteodystrophy but without end-organ PTH resistance.

65
Q

What is the primary cause of primary hyperparathyroidism?

A

Usually due to parathyroid adenoma or hyperplasia.

66
Q

What is the presentation of primary hyperparathyroidism?

A

Hypercalcemia, hypercalciuria, polyuria, hypophosphatemia, often asymptomatic.

67
Q

What will be elevated in urine in primary hyperparathyroidism?

A

↑ PTH, ↑ ALP, ↑ cAMP.

68
Q

What is osteitis fibrosa cystica?

A

Cystic bone spaces filled with brown fibrous tissue due to PTH.

69
Q

What is secondary hyperparathyroidism?

A

2° hyperplasia due to Ca2+ absorption &/or PO43−, most often in chronic renal disease.

70
Q

What is the presentation of secondary hyperparathyroidism?

A

Hypocalcemia, hyperphosphatemia in chronic renal failure, ↑ ALP, ↑ PTH.

71
Q

What is renal osteodystrophy?

A

Renal disease leading to 2° & 3° hyperparathyroidism and bone lesions.

72
Q

What is tertiary hyperparathyroidism?

A

Refractory (autonomous) hyperparathyroidism resulting from chronic renal disease.

73
Q

What is familial hypocalciuric hypercalcemia?

A

Defective G-coupled Ca2+-sensing receptors in multiple tissues.

74
Q

What is the phosphate level in chronic renal failure?

A

Hyperphosphatemia

Unlike hypophosphatemia seen in most other causes.

75
Q

What are the lab findings in chronic renal failure?

A

↑ ALP and ↑ PTH

76
Q

What causes renal osteodystrophy?

A

Renal disease leading to secondary and tertiary hyperparathyroidism, resulting in bone lesions.

77
Q

What is tertiary hyperparathyroidism?

A

Refractory (autonomous) hyperparathyroidism due to chronic renal disease

Characterized by ↑↑ PTH and ↑ Ca2+.

78
Q

What is familial hypocalciuric hypercalcemia?

A

A condition caused by defective G-coupled Ca2+-sensing receptors in multiple tissues.

Results in higher than normal Ca2+ levels needed to suppress PTH, excessive renal Ca2+ reuptake, mild hypercalcemia, and hypocalciuria with normal to ↑ PTH levels.

79
Q

What is Nelson syndrome?

A

Enlargement of an existing ACTH-secreting pituitary adenoma after bilateral adrenalectomy for refractory Cushing disease.

Occurs due to the removal of the cortisol feedback mechanism.

80
Q

What are the symptoms of Nelson syndrome?

A

Hyperpigmentation, headaches, and bitemporal hemianopia.

81
Q

What is acromegaly?

A

Excess growth hormone (GH) in adults, typically caused by a pituitary adenoma.

In children, excess GH leads to gigantism and increased linear bone growth.

82
Q

What are the findings in acromegaly?

A

Large tongue with deep furrows, deep voice, large hands and feet, coarsening of facial features, frontal bossing, diaphoresis, impaired glucose tolerance, hypertension, and increased risk of colorectal polyps and cancer.

83
Q

How is acromegaly diagnosed?

A

↑ serum IGF-1, failure to suppress serum GH following oral glucose tolerance test, and pituitary mass seen on brain MRI.

84
Q

What is the treatment for acromegaly?

A

Pituitary adenoma resection. If not cured, octreotide (somatostatin analog), pegvisomant (GH receptor antagonist), or dopamine agonists (e.g., cabergoline).

85
Q

What is Laron syndrome?

A

A form of dwarfism caused by defective growth hormone receptors leading to decreased linear growth.

Characterized by ↑ GH, ↓ IGF-1, short height, small head circumference, characteristic facies, delayed skeletal maturation, and small genitalia.

First Aid (18 decks)

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