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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
Q

What is the nongenomic actions of steroid hormones

A

Rapid steroid actions

Specific-receptor-mediated actions or direct steroid-membrane interactions

26
Q

Compare and contrast the half lives and metabolic clearance of thyroid, steroid, and protein hormones

A

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
Q

Metabolic clearance = ?

A

(mg/minute removed)/(mg/ml of plasma) = ml cleared/min

28
Q

Describe neural mechanism of endocrine regulation

A

Neuronal input to an endocrine cell increases or decreases hormonal secretion

29
Q

Describe feedback mechanism of endocrine regulation

A

More common than neural mechanism

Negative feedback predominate

30
Q

Describe positive feedback mechanisms

A

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
Q

What is the long-loop feedback?

A

negative feedback: hormone released from 3rd tier (peripheral endocrine gland) feeds back all the way to 1st tier (hypothalamus) and 2nd tier (pituitary)

32
Q

What is short-loop feedback?

A

negative feedback: hormone secreted from 2nd tier (pituitary) to 1st (hypothalamus)

33
Q

What is ultra short-loop feedback?

A

negative feedback: gland inhibits its own secretions

34
Q

What are the endocrine axes?

A

Hypothalamus - pituitary - adrenal gland (HPA) axis
Hypothalamus - pituitary - thyroid gland (HPT) axis
Hypothalamus - pituitary - gonads (HPG) axis

35
Q

What is physiological response-driven negative feedback?

A

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
Q

How is the first tier of the endocrine axes highly regulated?

A

by descending and ascending neural inputs

  • suprachiasmatic nucleus
  • pineal gland

physiological stress influences the release of hormones from the hypothalamus

37
Q

What is the role of suprachiasmatic nucleus in regulation of 1st tier?

A

impose a circadian rhythm on the secretion of hypothalamic releasing hormones and endocrine axes

38
Q

What is the role of the pineal gland in regulated 1st tier?

A

releases melatonin which feedback to the SCN information about day-night

39
Q

What is responsive sensitivity?

A

Hormone concentration that produces 50% of maximal response (EC50)

40
Q

How can responsiveness be changed?

A

changing # of receptors

Changing affinity of receptors for hormone

41
Q

Describe upregulation

A

increase receptor # or sensitivity of target tissue when hormone levels are low

  • increase synthesis of new receptors
  • decrease degradation of receptors
  • activate
42
Q

Describe down-regulation

A

reduce receptor # or sensitivity of the target tissue when hormone levels are high for an extended period of time

43
Q

Describe the adenylyl cyclase mechanism

A

1st messenger: hormones (FLAT, glucagon, PTH, calcitonin, HCG, MSH, CRH)
primary effector: adenylyl cyclase
2nd messenger: cAMP
secondary effector: PKA

44
Q

Describe the phospholipase C mechanism

A

1st messenger: hormones (GnRH, TRH, GHRH, Oxytocin)
1* effector: Phospholipase C
2nd messenger: IP3/DAG/Ca
2* effector: PKC or calmodulin

45
Q

Describe steroid hormone mechanism

A

Hormone: thyroid, glucocorticoids, aldosterone, estrogen, testosterone
No second messenger
act through cytosolic/nuclear receptors
hormone-receptor complex acts as transcription factor

46
Q

What enzyme deactivates cAMP?

A

phosphodiesterase

47
Q

Describe the steroid receptor

A

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
Q

Describe the guanylyl cyclase mechanism

A

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
Q

Describe the RTK mechanism

A

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
Q

Describe tyrosine kinase-associated receptors

A

JAK-STAT

associate non-covalently to proteins that have tyrosine kinase activity

51
Q

Describe hypofunction of endocrine

A

Reduced production of specific hormones

52
Q

Describe hyperfunction of endocrine

A

increased production of specific hormones

53
Q

Describe mass lesions with endocrine disorders

A

Enlargement of the endocrine organ due to an underlying neoplasia or hyperplasia

54
Q

What are the disorders of endocrine hyperfunction?

A

Neoplastic: benign (adenoma), malignant (adrenal cancer), or ectopic (SIADH)
Autoimmune: Graves’ disease
Latrogenic: cushings
Infectious/inflammatory: subacute throiditis
Activating receptor mutations: TSH

55
Q

Disorders of endocrine hypofunction

A

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
Q

What is the primary main cause of endocrine disorder?

A

Low or high levels of hormone due to defect in peripheral endocrine gland

thyroid

57
Q

What is the secondary main cause of endocrine disorders?

A

Low or high levels of hormone due to defect in pituitary gland

58
Q

What is the tertiary main cause of endocrine disorders?

A

low or high levels of hormone due to defect in hypothalamus

59
Q

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?

A

Adipose tissue, heart, liver, kidney and GI tract

Endocrine - MSI Spring (15 decks)

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