Endocrine Pharmacology

Question 1

Endocrine and exocrine example

Answer 1

Pancreas is exocrine (secretes digestive enzymes into GI tract), and an endocrine (secretes insulin, glucagon into blood)

Question 2

steroird examples

Answer 2

cortisol
aldosterone
testosterone
estrogen
progesterone

Question 3

peptide examples

Answer 3

insulin
glucagon
parathyroid hormone
GH
LH
OT

Question 4

tyrosine derivatives

Answer 4

EP
NE
DA
Thyroid

Question 5

steroid hormones, bindding and breakdown

Answer 5

hydrophobic.
bound to carrier proteins
can permeate cell membrane
slow response: bind intracellular receptors, cause change in transcription (min-hours)
breakdown is slow: (Large fraction is bound to carrier, so there is large reserve of steroid in system, therefore breakdown is slow because only unbound are metabolized)

Question 6

Peptide hormones, binding, breakdown

Answer 6

hydrophillic
not bound to carrier proteins. circulating [] reflects “active” []
cannot permeate PM
response very fast-bind cell surface receptors
breakdown fast- specific enzymes cleave

Question 7

steroid hormone receptor

Answer 7

intracellular
have hormone binding domain and DNA binding domain
hormone-receptor complex interacts with DNA to influence transcription
ex: glucocorticoid receptor, estrogen receptor, thyroid hormone

Question 8

GPCR

Answer 8

peptide hormone.
conformational change causes dissociation of G protein, signalling cascade.
ex: OT receptor, TSH, FSH

Question 9

Receptor TK

Answer 9

peptide
conformational change causes dimerization, autophosphorylization, followed by recruitment downstream signalling molecules

ex: insulin receptor, GH

Question 10

HPA axis-cortisol release

Answer 10

CRH from HTh controls ACTH release from anterior pituitary which controls release of cortisol from adrenal cortex

CRH is principle regulator

Question 11

Insulin release control by circulating glucose

Answer 11

elevation of BG activates beta cells to secrete insulin. insulin reduces glucose (uptake/storage in liver, muscle etc), which reduces the stimulus for further insulin release

Question 12

feedback

Answer 12

hormone released following stimulus

hormone response exerts feedback regulation on upstream control mechanism

Question 13

control of lactation

Answer 13

suckling triggers OT release from posterior pituitary, leading to milk ejection and prolactin release from anterior pituitary leading to milk production. milk is released, baby continues feeding

POSITIVE FEEDBACK

Question 14

Classifications of hypercortilism

Answer 14

tertiary: over secretion CRH from HTh
secondary: over secretion ACTH from anterior pituitary

primary: defect in primary hormone gland (adrenal)

Question 15

treatment for hypersecretion

Answer 15

often tumor/intrinsic defect

theoretically-drug that blocks hormone receptor or synthesis of hormone.Not effective bc the drugs are expensive, not specific, too many SE

common- remove/ablate endocrine gland with surgery/radiation

Question 16

treat hyperthyroidism

Answer 16

drugs that inhibit synthesis of thyroid hormones (thioamides) or radiation (radioactive iodine) to destroy cells in thyroid gland

Question 17

treat: hyperaldosteronism

Answer 17

removal adrenal gland, drugs that block mineralcorticoid receptor (adlosterone antagonists) sometimes

Question 18

treating hyposecretion of hormone

Answer 18

hormone replacement

Question 19

hypoinsulinism (diabetes)

Answer 19

Insulin replacement throughout day to mimic natural release
Rapid/short acting insulin reaches peak formation quickly, used before meals
Intermediate/long acting ones used to control blood glucose over night or in btw meals

Question 20

Growth hormone deficiency (pituitary dwarfism)

Answer 20

defects in pituitary gland = inadequate secretion of GH, slower bone growth and muscle development. replaced with injection SQ once day

Question 21

Hypocortilism or chronic adrenal insufficiency (Addison’s disease)

Answer 21

symptoms: weight loss, hypoglycemia, hypotension, change in pigment, GI distrurbamce, change in hair distribution, can lead to adrenal crisis

defects in adrenal gland lead to insufficient production of corticosteroids including cortisol. can be treated by administering exogenous glucocorticoids (hydrocortisone, prednisone) to bring circulating levels closer to normal

Question 22

ovarian cycle

Answer 22

1. Follicular phase: E released by developing follicle, exerts neg FB on GnRH and FSH
2. Ovulation: E levels cross threshold, begin to exert + FB on LH secretion, promoting LH surge and ovulation.
3. Luteal Phase: follicle develops into corpus luteum, secreting high levels of E and P which exert - FB on GNRH,FSH,LH
4. Menses: breakdown corpus lutuem, due to dimishing levels FSH/LH, causes shedding uterus lining

Question 23

birth control pill

Answer 23

most combined=combined oral contraceptive (E+P)

exert - FB on GnRH, FSH, LH secretion
= no follicular development
= LG surge inhibited, no ovulation

tricks pituitary into thinking ovulation has occured. stops the release of FSH and LH, prevents development of follicle and ovulation. prevents normal release of hormones (e and P) from follicle and corpus luteum bc they dont develop

Question 24

P only pill

Answer 24

thickens cervical lining

inhibit LH surge

Question 25

Glucocorticoids

and SE from stopping

Answer 25

modulate HPA axis. often used to treat non-adrenal disorders bc anti-inflammatory and immunosuppresive action

SE: acute adrenal insuficiency “Farquharson Phenomen”- introduction of continuous exogenous hormone leads to atrophy in producing organ bc it suppresses natural production of that hormone.

so if stop, there is temporary atrophy of adrenal gland. develop addison disease symptoms

need to taper