Introduction to Endocrine Physiology Flashcards
1
Q
- What are the mechanisms of cellular communication?
A
- Autocrine
- Paracrine
- Endocrine
- Neuroendocrine
2
Q
- In addition to hormones secreted by classic endocrine glands, there are:
A
- Hormones synthesized by endocrine cells w/ organs whose PRIMARY function is not endocrine (Heart, Liver, Kidney, GI Tract, Adipose Tissue)
- Hormones modified by peripheral conversion (Angiotensin II, Vitamin D)
3
Q
- What hormones does the hypothalamus secrete?
A
- TRH
- CRH
- GHRH
- GnRH
- Somatostatin
- Dopamine
4
Q
- What hormones does the anterior pituitary secrete?
A
- TSH
- FSH
- LH
- ACTH
- MSH
- GH
- Prolactin
5
Q
- What hormones does the posterior pituitary secrete?
A
- ADH
- Oxytocin
6
Q
- What hormones does the thyroid secrete?
A
- T3,T4
- Calcitonin
7
Q
- What hormones does the parathyroid gland secrete?
A
- PTH
8
Q
- What hormones does the pancreas secrete?
A
- Insulin
- Glucagon
9
Q
- What hormones does the adrenal medulla secrete?
A
- NE
- Epi
10
Q
- What hormones does the kidney secrete?
A
- Renin
- 1,25-Dihydroxycholecalciferol (Calcitriol)
- EPO
11
Q
- What hormones does the adrenal cortex secrete?
A
- Cortisol
- Aldosterone
- Adrenal androgens
12
Q
- What hormones do the testes secrete?
A
- Testosterone
13
Q
- What hormones do the ovaries secrete?
A
- Estradiol
- Progesterone
14
Q
- What hormones does the corpus luteum secrete?
A
- Estradiol
- Progesterone
15
Q
- What hormones does the placenta secrete?
A
- HCG: Human chorionic gonadotropin
- hPL: Human placental lactogen
- Progesterone
- Estradiol
16
Q
- What are the three general classes of hormones?
A
- Proteins and peptides (stored in secretory vesicles until used)
- AA < 100 length are peptides
- AA > 100 length are proteins
- Water soluble
- Amines
- Tyrosine derived
- Steroids
- Not stored
- Made from cholesterol
- Lipid-soluble
17
Q
- How are protein/peptide hormones synthesized?
- What are the stimuli for exocytosis?
A
- Made as preprohormone (not active)
- Signal peptide removed in ER to make PROHORMONE
- Packed into vesicles in Golgi
- Cleaved by proteolytic enzymes and generated to active form
-
Stimuli for exocytosis:
- Increase in intracellular Ca2+ caused by depolarization
- Activation of GPCR (increase in cAMP and activation of PKA)
18
Q
- What are the steroid hormones?
- Where are they made?
- How are they modified?
A
- Hormones:
- Cortisol
- Aldosterone
- Estradiol/Progesterone
- Testosterone
- 1,25-dihydroxycalciferol
- Synthesized in:
- Adrenal cortex
- Gonads
- Corpus Luteum
- Modification:
- Removal of side chains
- Addition of side chains
- Hydroxylation of steroid nucleus
- Aromazation of steroid nucleus
19
Q
- What are the two sources of cholesterol?
A
- 80% taken up via receptor mediated endocytosis of LDL
- De novo synthesis from acetyl CoA
20
Q
- What are the genomic actions of steroid hormones?
A
- Modulate gene transcription by interaction w/ intracellular nuclear receptors
21
Q
- What are the nongenomic actions of steroid hormones?
A
- Specific-receptor mediated actions or direct-steroid membane interactions
22
Q
- Amine hormones are derived from what amino acid?
- What are the two groups of amine hormones and where are they synthesized?
- Which has a longer half life?
- Which category has a faster clearance rate?
A
- Tyrosine
- Catecholamines
- Made in cytosol and secretory granules
- Act thru cell-membrane associated receptors
- Thyroid hormones
- Made by thyroid
- Stored within follicles
- Cross cell membrane and act thru nuclear receptors
- Thyroids have longest half life
- Catecholamines have faster clearance rate
23
Q
- How are the secretions of hormones turned on and off?
A
-
Neural mechanism
- Neuronal input to an endocrine cell increases or decreases hormonal secretion
-
Feedback mechanism
- More common
- Some element of the physiological response feeds back to act directly or indirectly on endocrine gland to increase or decrease secretion rate
- Negative feedback mech predominates
24
Q
-
Positive feedback mechanisms:
- Characteristics
- Examples
A
- Rare
- Self-augmenting
- Leads to explosive event
- Rarely used to maintain homeostatic functions
- Examples:
- Menstrual cycle (estrogen stimulates FSH and LH, further increasing estrogen level)
- Delivery of baby (oxytocin)
25
* ***Negative feedback mechanisms:***
* ***Characteristics***
* ***Types***
* Underlies homeostatic regulation of organ systems
* Types:
* Long loops
* Short-Loop feedback
* Ultra short loop
26
* Long loop feedback
Hormone released from third tier (peripheral endocrine gland) feeds back to the 1st tier
27
* Short loop feedback
* Hormone secreted from the 2nd tier feeds back and inhibits 1st tier
28
* Ultra short loop feedback
* Gland inhibits its own secretion
29
* What are the three endocrine axes?
* HPA (hypothalamic-pituitary adrenal gland axis)
* HPT (hypothalamus-pituitary-thyroid gland axis)
* HPG (hypothalamus-pituitary-gonads axis)
30
* Physiological response driven negative feedback loops
* Response driven feedback
* Secretion of a hormone is stimulated or inhibited by a change in level of extracellular signal
* EX:
* Insulin regulates BGL; BG concentration turns on or off insulin secretion
* Turned on in high blood glucose
* Decreases in low blood glucose levels
31
* ***Two major inputs that control first tier of the endocrine axes (hypothalamus)***
* **Pineal gland**
* Melatonin
* **SCN**
* Circadian rhythms on secretion of hypothalamic releasing hormones and endocrine axes
32
* Identify sensitivity of a hormone
* How can responsiveness of a hormone be changed?
* Sensitivity-hormone concentration that produces 50% of maximal response
* Changing the number of receptors or receptor affinity for the hormone
33
* Up-regulation
* Increase receptor number or sensitivity of target tissue when hormone levels are low
* Increase in synthesis in new receptors
* Decrease in degradation of existing receptors
* Activating receptors
34
* Down-regulation
* Reducing receptor number or sensitivity of target tissue when hormone levels are high or for an extended period of time
* Decrease in synthesis of new receptos
* Increase in degredation of existing receptors
* Inactivating/desensitizing receptors
35
* ***Adenylyl cyclase MOA***
* 1st messenger
* Primary effector
* 2nd messenger
* Secondary effector
* 1st messenger-hormones (ACTH, LH, FSH, TH, Glucagon)
* Primary effector: Adenylyl Cyclase
* 2nd messenger: cAMP
* Secondary effector: PKA
36
* ***Phospholipase C Mechanism of Action***
* ******1st messenger
* primary effector
* 2nd messenger
* secondary effector
* 1st messenger: hormone (GnRH, TRH, Oxytocin)
* Primary effector: Phospholipase C
* 2nd messenger: IP3/DAG/Ca2+
* Secondary effector: PKC or calmodulin
37
* ***Guanylyl Cyclase MOA ***
* ***1st messenger***
* ***Primary effector***
* ***2nd messenger***
* ***Secondary effector***
* 1st messenger
* Hormones
* ANP-thru receptor
* NO-can pass thru cytosol
* Primary effector
* Guanylate cyclase
* 2nd messenger
* cGMP
* Secondary effector
* PKG
38
* ***Steroid hormones (Thyroid hormone, glucocorticoids, aldosterone, estrogen, testosterone, etc.) MOA***
* Act thru cytosolic/nuclear receptors
* Receptors are monomeric proteins w/ 6 domains (A-f)
* E domain: **steroid binding domain-closer to C terminus**
* **C domain: 2 zinc fingers, binds DNA, highly conserved-closer to N terminus**
* **Hormone receptor complex works as a transcription factor that regulates the rate of transcription of a gene**
* **Nature of the new protein is SPECIFIC to the hormone**
39
* What are the two categories of tyrosine kinases?
* Receptor tyrosine kinases
* Tyrosine kinase associated receptors
40
* Receptor tyrosine kinases
* Have intrinsic tyrosine kinase activity within receptor
* When activated, **phosphorylates itself and other proteins**
* EX: Nerve growth factor w/ epidermal growth factor receptors or insulin w/ insulin like growth receptor
41
* Tyrosine kinase associated receptors
* Associate non-covalently to proteins that have tyrosine kinase activity
* EX: JAK
42
***GHRH is a _ that after receptor activation, stimulates intracellular _ production***
* GPCR (Gs), cAMP
43
* Mass lesions
* Enlargement of the endocrine organ due to an underlying neoplasia or hyperplasia
