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Endocrine - MSI Spring > Intro to Endocrinology > Flashcards

Intro to Endocrinology Flashcards

1
Q

What hormones does the hypothalamus produce?

A 
GnRH
CRH
TRH
PH
GHRH
Somatostatin 
Dopamine (PIH)
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2
Q

What hormones does the anterior pituitary produce

A 
FSH
LH
ACTH
TSH
Prolactin
GH
MSH
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3
Q

What hormones does the posterior pituitary release?

A

Oxytocin

ADH

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4
Q

What hormones does they thyroid release?

A

T3,T4

Calcitonin

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5
Q

What hormones does the parathyroid release?

A

PTH

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6
Q

What hormones does the pancreas release?

A

Insulin

Glucagon

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7
Q

What hormones does the adrenal medulla release?

A

NE and epinephrine

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8
Q

What hormones does the kidney release?

A

renin

1,25-dihydroxycholecalciferol

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9
Q

What hormones does the adrenal cortex release?

A

cortisol
aldosterone
adrenal androgens

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10
Q

What hormones does the testes release?

A

testosterone

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11
Q

What hormones does the ovaries release?

A

Estradiol and progesterone

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12
Q

What hormones does the corpus luteum release?

A

estradiol and progesterone

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13
Q

What hormones does the placenta release?

A

HCG
Estriol
Progesterone
HPL

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14
Q

What are the three classes of hormones?

A

Proteins/peptides
Amines
Steroids

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15
Q

How many a.a. differentiate a peptide hormone from a protein hormone

A

100 a.a

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16
Q

Describe protein/peptide hormones

A

water-soluble; most are peptides
DNA->mRNA->preprohormone
in ER signal peptide removed to produce prohormone
Packaged into vesicles in Golgi, cleaved by proteolytic enzymes to generate active form

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17
Q

What could be a stimulus for exocytosis of protein/peptide hormones?

A

increased intracellular Ca caused by membrane depolarization

Activation of GPCR followed by increased cAMP, and activation of PKA

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18
Q

Describe amine hormones

A

derived from tyrosine
Two groups:
- thyroid hormones: synthesized by thyroid gland and stored as thyroglobulin in follicles; cross cell membrane, act on nuclear receptors
- Catecholamine (epinephrine, NE, dopamine): synthesized in cytosol and secretory granules; act through cell-membrane associated receptors

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19
Q

Steroid hormones are all derivates of _______, modified how

A

cholesterol

*modified by removal or addition of side chains, hydroxylation, or aromatization of the steroid nucleus

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20
Q

What are the steroid hormones found in the body?

A

Cortisol, aldosterone, estradiol, estriol, progesterone, testosterone

1,25-dihydroxycholecalciferol (technically not a steroid but it is derived from cholesterol)

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21
Q

What are the two sources of cholesterol?

A

80% taken up as LDL particles through receptor-mediated endocytosis (diet)

De novo synthesis from acetyl coenzyme A (acetyl CoA)

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22
Q

What Apo protein can be found on LDL particle?

A

Apo B - 100

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23
Q

What stimulates the release of catecholamines into circulation?

A

Preganglionic sympathetic nerves synapse on adrenal gland to regulate release

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24
Q

What is the genomic action of steroid hormones?

A

Common theory - modulate gene transcription by interactions with intracellular, nuclear receptors

25
What is the nongenomic actions of steroid hormones
Rapid steroid actions | Specific-receptor-mediated actions or direct steroid-membrane interactions
26
Compare and contrast the half lives and metabolic clearance of thyroid, steroid, and protein hormones
Thyroid: 1-6 days plasma half life; 1-20 ml/m metabolic clearance Steroids: 25-100 min plasma hl; 200-1000 ml/m Proteins: 10-50 min hl; 50-600 ml/m
27
Metabolic clearance = ?
(mg/minute removed)/(mg/ml of plasma) = ml cleared/min
28
Describe neural mechanism of endocrine regulation
Neuronal input to an endocrine cell increases or decreases hormonal secretion
29
Describe feedback mechanism of endocrine regulation
More common than neural mechanism | Negative feedback predominate
30
Describe positive feedback mechanisms
self-augmenting leads to an explosive event rarely used to maintain homeostatic function - menstrual cycle: estrogen, increase FSH and LH release to increase estrogen for ovulation - delivery of a fetus: oxytocin
31
What is the long-loop feedback?
negative feedback: hormone released from 3rd tier (peripheral endocrine gland) feeds back all the way to 1st tier (hypothalamus) and 2nd tier (pituitary)
32
What is short-loop feedback?
negative feedback: hormone secreted from 2nd tier (pituitary) to 1st (hypothalamus)
33
What is ultra short-loop feedback?
negative feedback: gland inhibits its own secretions
34
What are the endocrine axes?
Hypothalamus - pituitary - adrenal gland (HPA) axis Hypothalamus - pituitary - thyroid gland (HPT) axis Hypothalamus - pituitary - gonads (HPG) axis
35
What is physiological response-driven negative feedback?
also known as response-driven feedback Secretion of a hormone is stimulated or inhibited by a change in the level of a specific extracellular signal ex. insulin: regulates blood glucose levels, blood glucose concentration turns on or off insulin secretion
36
How is the first tier of the endocrine axes highly regulated?
by descending and ascending neural inputs - suprachiasmatic nucleus - pineal gland physiological stress influences the release of hormones from the hypothalamus
37
What is the role of suprachiasmatic nucleus in regulation of 1st tier?
impose a circadian rhythm on the secretion of hypothalamic releasing hormones and endocrine axes
38
What is the role of the pineal gland in regulated 1st tier?
releases melatonin which feedback to the SCN information about day-night
39
What is responsive sensitivity?
Hormone concentration that produces 50% of maximal response (EC50)
40
How can responsiveness be changed?
changing # of receptors | Changing affinity of receptors for hormone
41
Describe upregulation
increase receptor # or sensitivity of target tissue when hormone levels are low - increase synthesis of new receptors - decrease degradation of receptors - activate
42
Describe down-regulation
reduce receptor # or sensitivity of the target tissue when hormone levels are high for an extended period of time
43
Describe the adenylyl cyclase mechanism
1st messenger: hormones (FLAT, glucagon, PTH, calcitonin, HCG, MSH, CRH) primary effector: adenylyl cyclase 2nd messenger: cAMP secondary effector: PKA
44
Describe the phospholipase C mechanism
1st messenger: hormones (GnRH, TRH, GHRH, Oxytocin) 1* effector: Phospholipase C 2nd messenger: IP3/DAG/Ca 2* effector: PKC or calmodulin
45
Describe steroid hormone mechanism
Hormone: thyroid, glucocorticoids, aldosterone, estrogen, testosterone No second messenger act through cytosolic/nuclear receptors hormone-receptor complex acts as transcription factor
46
What enzyme deactivates cAMP?
phosphodiesterase
47
Describe the steroid receptor
Monomeric phosphoproteins Each receptor has 6 domains (A-F) - E domain: steroid hormone binding domain - C domain: highly conserved, has 2 zinc fingers, responsible for DNA binding
48
Describe the guanylyl cyclase mechanism
1st messenger: hormones - ANP: acts through receptor w guanylyl cyclase activity - NO diffuses to cytosol and activates cytosolic guanylyl cyclase 1* effector: guanylate cyclase 2nd messenger: cGMP 2* effector: PKG
49
Describe the RTK mechanism
Have intrinsic tyrosine kinase activity w/i the receptor molecule When activated, the intrinsic tyrosine kinase phosphorylates itself and other proteins ex. Nerve, epidermal, insulin and insulin-like growth factors receptors
50
Describe tyrosine kinase-associated receptors
JAK-STAT | associate non-covalently to proteins that have tyrosine kinase activity
51
Describe hypofunction of endocrine
Reduced production of specific hormones
52
Describe hyperfunction of endocrine
increased production of specific hormones
53
Describe mass lesions with endocrine disorders
Enlargement of the endocrine organ due to an underlying neoplasia or hyperplasia
54
What are the disorders of endocrine hyperfunction?
Neoplastic: benign (adenoma), malignant (adrenal cancer), or ectopic (SIADH) Autoimmune: Graves' disease Latrogenic: cushings Infectious/inflammatory: subacute throiditis Activating receptor mutations: TSH
55
Disorders of endocrine hypofunction
Hemorrhage: Adrenal insufficiency Nutritional: vit D Enzyme defects: 21-hydroxylase deficiency Autoimmune: addisons, hashimotos, type i DM Latrogenic: hypothyroidism Infectious/inflammatory: adrenal insufficiency Hormone mutations: GH, AVP
56
What is the primary main cause of endocrine disorder?
Low or high levels of hormone due to defect in peripheral endocrine gland thyroid
57
What is the secondary main cause of endocrine disorders?
Low or high levels of hormone due to defect in pituitary gland
58
What is the tertiary main cause of endocrine disorders?
low or high levels of hormone due to defect in hypothalamus
59
In addition to hormones secreted by classic endocrine glands, there are hormones synthesized by endocrine cells within organs whose primary function is not endocrine. Where are these cells?
Adipose tissue, heart, liver, kidney and GI tract

Endocrine - MSI Spring (15 decks)

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