Endocrine Flashcards

1
Q

Which hormones are secreted by the pituitary?

A

Posterior Pit

GH

PRL

ACTH

LH

FSH

TSH

Anterior Pit

ADH

Oxytocin

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2
Q

Compare the signs of pituitary hyperfunction in children and adults.

A

Prepubertal = giantism

Post-pubertal = acromegaly

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3
Q

What are the signs of pituitary hypofunction?

A

General weakness, cold intolerance, poor appetite, weight loss, hypotension, amenorrhea (w), impotence (m), dwarfism (children)

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4
Q

What are the causes of hyperthyroidism?

A

1) graves disease
2) nodular goiter
3) toxic adenoma
4) exogenous thyroid medication
* T3 and T4 normally inhibit secretion of TSH, which accounts for the low concentraiton of TSH in these forms of hyperthyroidism.*

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5
Q

What are the clinical features of hyperthyroidism?

A
  • restlessness, nervousness
  • emotional lability
  • sweating
  • tachycardia, palpitations
  • muscle tremor
  • diarrhea, weigh loss
  • exopthalmoos
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6
Q

What are the causes of hypothyroidism?

A
  • developmental defects
  • thyroiditis (immune)
  • hashimotos’ thyroiditis (most common)
  • thyroidectomy
  • iodine deficiency
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7
Q

What are the clinical features of hypothyroidism?

A

Children: cretinism (mental retardation) and dwarfism

  • myxedema
  • fatigue
  • bradycardia
  • constipation
  • myalgia, weakness, stiffenss
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8
Q

Correlate the pathologic and clinical features of nodular goiter.

A

Nodules consist of thyroid follicles . . . between nodules vessels and collagen fibers infiltrated with lymphocytes and macrophages. May have calcification, hemorrhage, and atrophy.

Compression of adjacent structures >> coughing, hoarseness

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9
Q

List the most important thyroid neoplasms and discuss their prognosis.

A

Papillary

80%, 4x more common in women, favorable prognosis

Follicular

most > 40 yrs, can be treated with radioactive iodine

Medullary

derived from C cells, produce calcitonin, can be inherited MEN2

Anaplastic

very unfavorable prognosis

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10
Q

What are the causes of hyperparathyroidism?

A

Adenomas (80%)

Hypocalcemmia

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11
Q

What are the clinical features of hyperPTH?

A
  • Decalcification >> fractures
  • deposition of calcium salts >> nephrocalcinosis, urolithiasis
  • lethargy, muscle weakness, arrhythmias
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12
Q

What are the metabolic consequences of hyperparathyroidism?

A

Stimulates osteoclasts, leading to bone resorption and release of calcium into circulation. In kindeys promotes resorption of CA in urine and formation of active vitamin D.

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13
Q

Compare the clinical features of hyperparathyroidism and hypoparathyroidism.

A
  • neuromuscular excitability and muscular contraction
  • tetany
  • arrhythmias
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14
Q

What are the causes of adrenocortical hyperfunction?

A

Hypersecretion of mineralocorticoids, glucocorticoids, sex steroids. Can be caused by hyperplasia or neoplasia.

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15
Q

Describe the clinical features of the three most important syndromes caused by adrenocortical hyperfunction.

A
  • Hyperaldosteronism (Conn’s syndrome)
  • Cushings syndrome
  • Adrenogenital syndrome
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16
Q

What are the clinical features adrenocortical hyperfunction?

A

hypercortisolism: central obesity, moon face, buffalo humb, plethora, HTN, thin skin, glucose intolerance, fatigue, weakness

Androgenital: *virilization, *

17
Q

What are the causes of adrenocortical hypofunction?

A

Usually caused by adrenal destruction

acute >> waterhouse-friderichsen (meningococcal septicemia)

chronic >> autoimmune

18
Q

Compare neuroblastoma and pheochromocytoma.

A

Neuroblastoma

undifferentiated precursors of neural cells that are precursors of normal adrenal medullary cells. occur mostly in young children, fast growing abdominal masses, produce VMA

Pheochromocytoma

polygonal cells resembling normal adrenal medulla, adults, secrete catecholamines, elevated VMA