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PCTH 325 > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

What is the endocrine system and why is it important?

A

A system of glands that produce and secrete hormones directly into the circulatory system to reach target tissues. It is important in maintaining homeostasis

NOTE: not all glands are a part of the endocrine system

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2
Q

Name 3 steroid and 2 peptide hormones

A

Steroids: cortisol, estrogen, progesterone

Peptides: insulin, oxytocin

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3
Q

4 reasons why it’s important to know the difference between different hormones?

A
  1. They are degraded differently
  2. They have different circulating half-lives
  3. They target different receptor types
  4. They have different mechanisms of action
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4
Q

What are the 4 characteristics of steroid hormones - clearance and half-life

A

They are very hydrophobic and are derived from cholesterol

  1. BOUND to carrier proteins
  2. PERMEATE cell membrane
  3. SLOW response rate - interacts with intracellular receptors and change transcription of target genes
  4. SLOW breakdown rate - most are bound to carrier proteins; only free hormones will be broken down
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5
Q

What are the 4 characteristics of peptide hormones - clearance and half-life

A

They are very hydrophilic (short proteins that are soluble in plasma)

  1. NOT bound to carrier proteins
  2. DON’T permeate cell membrane
  3. VERY FAST response rate - bind to cell surface receptors and change conformation rapidly
  4. FAST breakdown rate - enzymes cleave peptide hormones, leads to rapid inactivation
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6
Q

Steroid hormones receptor type

A

Bind to intracellular receptors, located inside target cells. The hormone-receptor complex interacts with DNA to influence transcription of target genes

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7
Q

Peptide hormones receptor type

A

Bind to cell surface receptors (transmembrane proteins). The hormone-receptor interaction initiates a conformational change in the receptor that alters signal transduction pathways

Very rapid - doesn’t require transcription of target genes

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8
Q

Give 2 examples of peptide hormone receptors

A
  1. G-protein coupled receptors - a conformational change –> dissociation of heterotrimeric G-proteins –> activation of downstream signaling cascades
  2. Receptor tyrosine kinase - conformational change –> dimerization, autophosphorylation –> recruitment and activation of downstream signaling molecules
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9
Q

What is feedback regulation?

A

(Normally negative feedback) Maintains homeostasis.

Stimulus occurs –> hormones released from endocrine glands –> physiological response exerts feedback regulation on the upstream control mechanism

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10
Q

Feedback regulation of cortisol release by HPA (hypothalamic-pituitary-adrenal) axis

A

CRH from the hypothalamus controls the release of ACTH from the anterior pituitary, which controls cortisol release form the adrenal cortex

Cortisol release exerts negative feedback, inhibiting release of ACTH and CRH on the anterior pituitary and hypothalamus

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11
Q

What is CRH-release influenced by?

A

Stress, circadian rhythm, and blood levels of cortisol

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12
Q

Feedback regulation of insulin release by circulating glucose

A

Increased level of circulating glucose activates insulin secretion –> reduces circulating glucose and reduced stimulus for further insulin release

Ex. of negative feedback

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13
Q

Feedback regulation of lactation by oxytocin and prolactin

A

Suckling by an infant triggers oxytocin release from the posterior pituitary –> milk ejection.

Ex. of positive feedback

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14
Q

Tertiary hypercortisolism vs. hypocortisolism

A

Defect further upstream

Tertiary hypercortisolism: over-secretion of CRH from the HYPOTHALAMUS

Tertiary hypocortisolism: under-secretion of CRH from the HYPOTHALAMUS

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15
Q

Secondary hypercortisolism vs. hypocortisolism

A

Defect in upstream control gland

Secondary hypercortisolism: over-secretion of ACTH from the ANTERIOR PITUITARY

Secondary hypocortisolism: under-secretion of ACTH from the ANTERIOR PITUITARY

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16
Q

Primary hypercortisolism vs. hypocortisolism

A

Defect in “primary” hormone secreting gland

Primary hypercortisolism: over-secretion of “primary” hormone from ADRENAL GLANDS

Primary hypocortisolism: under-secretion of “primary” hormone from ADRENAL GLANDS

17
Q

What causes too much hormone + what is a non-practical way to treat it and the most common intervention?

A

Caused by a tumour or other intrinsic defect of the endocrine gland

Not practical - treat with a drug that blocks the hormone receptor or interferes with the synthesis of the hormone

Most common intervention is to remove all/part of the endocrine gland through surgery or radiation therapy

18
Q

2 examples of defects resulting in too much hormone

A
  1. Hyperthyroidism
  2. Hyperaldosteronism
19
Q

How is hyperthyroidism treated (2)?

A
  1. Drugs inhibit synthesis of thyroid hormones (thioamides)
  2. Radiation (radioactive iodine) to destroy cells in the thyroid gland
20
Q

How is hyperaldosteronism treated (2)?

A
  1. Surgical removal of the adrenal gland
  2. Drugs that block the mineralocorticoid receptor (aldosterone antagonists)
21
Q

3 examples of defects resulting from hormone deficiency

A
  1. Hypoinsulinism (aka diabetes) - insulin is administered parenterally
  2. Growth hormone deficiency (pituitary dwarfism) - defects in the pituitary gland –> leads to inadequate secretion of growth hormone, causing slower bone growth and muscle development
  3. Hypocortisolism/chronic adrenal insufficiency (Addison’s disease) - defects in the adrenal gland –> leads to insufficient production of corticosteroids, including cortisol
22
Q

How can growth hormone deficiency (pituitary dwarfism) be treated?

A

Growth hormone can be replaced with injections of synthetic/recombinant forms of the hormone in children

23
Q

How can hypocortisolism/chronic adrenal insufficiency (Addison’s disease) be treated?

A

Administering exogenous glucocorticoids to bring circulating levels closer to normal

24
Q

How does estrogen and progesterone play a role in the modulation of the endocrine system?

A

Estrogen and progesterone are important in feedback regulation. Negative feedback is the dominant effect in the ovarian/menstrual cycle, but positive feedback occurs to induce ovulation

25
Q

What is the most common form of oral contraceptives?

A

Combined oral contraceptive (pill), which is a combination of synthetic estrogen and progesterone

26
Q

How do oral contraceptives modulate the ovarian/menstrual cycle? (ex. of a modulation of the endocrine system)

A
  1. Exogenous estrogen and progesterone trick the pituitary into thinking that ovulation has already occurred
  2. Stops release of FSH and LH
  3. Prevents development of a follicle and thus ovulation
  4. Negative feedback: Follicle and corpus luteum not developed = non-normal release of estrogen and progesterone
27
Q

MOA of birth control pills

A

MOA: exerts negative feedback on GnRH, FSH, and LH secretion. Results in:

  1. Follicular dev. inhibited (no egg)
  2. LH surge inhibited (no ovulation)
28
Q

What are glucocorticoids and what are they used for? (ex. of a modulation of the endocrine system)

A

Similar to endogenous cortisol, therefore, can modulate the HPA axis

Used in the treatment of “non-adrenal” disorders because of their anti-inflammatory and immunosuppressive abilities

29
Q

Side effect of stopping glucocorticoids too quickly?

A

Acute adrenal insufficiency (symptoms similar to Addison’s disease).

The negative feedback from glucocorticoid administration will suppress CRH and ACTH production - adrenal glands can’t produce sufficient levels of cortisol (ex. of Farquharson Phenomenon)

30
Q

Farquharson Phenomenon

A

Continuous exogenous hormone suppresses the natural production of that hormone, which causes temporary atrophy in the producing organ

31
Q

How to treat the effects of stopping glucocorticoids too quickly?

A

Tapering - helps with stopping long-term glucocorticoid therapy because of the temporary atrophy of the adrenal glands due to endogenous CRH and ACTH suppression

PCTH 325 (19 decks)

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