Unit 2 [Thyroid Dysfunction and Endocrine Response to Stress] Flashcards

(9 cards)

1
Q

hypothyroidism

A
  • too little TH
  • characterized by plasma concentrations of thyroid hormone chronically BELOW normal
  • causes: iodine deficiency, thyroid damage, autoimmune destruction (rarely pituitary or hypothalamus destruction)
  • symptoms: low metabolism, weight gain, coldness, low blood pressure/HR, stunted growth
  • goiter
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2
Q

hyperthyroidism

A
  • conditions characterized by plasma concentrations of TH that are chronically ABOVE normal
  • causes: tumors or autoimmune disease, Graves’ for example (TSI antibodies stimulate the TSH receptor on the thyroid gland and have no negative feedback)
  • symptoms: high metabolism, weight loss, more appetite, running hot/increased HR, anxiety, GOITER
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3
Q

goiter

A
  • hypothyroidism: TSH is tropic/trophic, meaning less negative feedback will be sent to hypothalamus
  • enlarged thyroid gland due to increase in size and # of follicular cells
  • excess TSH receptor activation (DIETARY IODINE DEFICIENCY IN MOTHER)
  • hyperthyroidism can also result in this, lack of negative feedback!
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4
Q

stress

A
  • in physiologic terms, refers to any real or potential threat to homeostasis in the body
  • ex: surgery, temperature drops, exercise, shock, starvation, fear…
  • adrenal glands secrete hormones involved in the stress response
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5
Q

adrenal gland location and anatomy

A
  • below the lungs and above the kidneys
  • have a cortex and medulla
  • cortex split into zonas glomerulosa, fasciculata, and reticularis (all of which secrete steroids, while medulla secretes catecholamines)
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6
Q

zona glomerulosa

A
  • secretes aldosterone (mineralocorticoid), which regulates concentrations of sodium and potassium and thereby blood volume
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7
Q

zona fasciculata

A
  • mostly glucocorticoids (CORTISOL)
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8
Q

zona reticularis

A
  • secretes sex steroids (androgens), contributing to puberty and sex characteristics
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9
Q

adrenal medulla and amine hormones

A
  • adrenal catecholamines
  • modified sympathetic ganglion without postganglionic fibers
  • releases directly into the bloodstream!
  • still binds to alpha (smooth muscle contraction), beta 1 (cardiac muscle), and beta 2 (smooth muscle relaxation) adrenergic receptors
  • neurohormones result in delayed onset action
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