PPY 2540 Study Guide - Midterm Guide: Adrenal Medulla, Anterior Pituitary, Posterior Pituitary
19 Oct 2016
School
Department
Course
Professor
Exam 2 Review
12 Endocrine
18 CNS/PNS
18 Resting Potential
Action Potential
Synapses
1. Get an action potential and release a neurotransmitter
a. In vesicles
2. Protein/peptide hormones - stored in vesicles leave by calcium exocytosis
a. Bind to cell surface receptors
3. T3, T4, TGT2- nonpolar
a. Polar stored in vesicles
b. Prostaglandins nonpolar
4. Hypothalamus - TRH (was in vesicles) released into portal vein thru fenestrated
capillaries
a. Bind to g-protein coupled receptors or anterior pituitary
b. Release TSH (polar so in vesicles, need calcium up to release, G-Q to give IP3)
c. T3 and T4 in colloid
5. Neuron to hypothalamus to posterior pituitary, no need to bind, ADH released
a. Does not bind to receptor and released in posterior pituitary
b. Responds to dehydration (high osmolality)--signal for ADH
i. Made in hypothalamus and released in post. Pituitary
6. PTH (parathyroid hormone) - responds to low Ca
a. Kidney stimulation, reuptake Ca
b. Causes breakdown of bone- osteoclasts
c. Homeostatic
d. Want to get Ca in blood
e. Osteoblast to stimulate bone/make bone, opposite of osteoclasts
7. GH
a. To Liver and to tissues
b. Growth factor
c. Many tissues, inhibits glucose utilization, no more glucose in blood
d. IGF (insulin-like growth factor)
e. “Glucose utilization”
8. Hypothalamus with CRH to Anterior Pituitary with ACTH to Adrenal cortex with Cortisol
a. ACTH binds to adrenal cortex to stimulate the synthesis of GC cortisol
i. Gluconeogenesis - make new glucose
ii. Lipolysis - breakdown of fats
iii. Glycogenolysis - increases glucose in blood
b. Look at negative feedback model with Hypothalamus
c. Cortisol is nonpolar
9. Epinephrine
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a. Blood glucose by glycogenolysis stimulated by sympathetics from adrenal
medulla
b. Response to acute stress
c. Sympathetics
d. High blood glucose to increase heart rate
e. Released from adrenal medulla
f. Break down in glycogen
10. TRH binds to receptors
a. Anterior pituitary need to release TSH in vesicles
b. Need calcium to release-- calcium release causes TSH release
c. TSH goes to thyroid
i. Follicle cells surround colloid and colloid is in thyroid -- colloid is storage
place for protein- thyroglobulin
ii. T3 and T4 and thyroglobulin in colloid (nonpolar but don’t diffuse bc
attached to protein) -- need to degrade thyroglobulin
1. Lysosome breaks down proteins in follicle cell
2. Fuse T3 and T4 with lysosomes, then leave cell by diffuse
because they are nonpolar out of cell
iii. TSH binds to g protein receptor and stimulate Gs
1. Get cAMP and PKA
d. NO QUESTION ON T3 T4
e. Resynthesis thyroglobulin
i. Transport ions in cell, active secondary symport with potassium
f. T3 and T4
i. Increases basal metabolism - increase Na/K ATPase
ii. Increase MIT
iii. Cold tolerance
11. Melatonin increases drowsiness in the night
12. Glucose and glucagon
a. Yin and yang of homeostasis
b. Glucose in vesicles, increases ATP
c. Release beta cells in pancreas, in vesicles
i. Need calcium up, from ER or voltages gated protein channel
ii. Can’t be IP3, need voltage gated channel
d. Glucose in, leak channel ATP shuts, depolarizes
i. Calcium channel in, insulin released from vesicles
e. Insulin binds to Tyrosine kinase receptors, IP3 mechanism, calcium channel
i. Transporters ON vesicles and fuse in liver with higher rate of transport
f. WOULD NOT STOP TALKING ABOUT 60s MUSIC AT THIS POINT
g. Homeostasis mechanism continues with glucagon (g coupled protein receptor)
i. Release of alpha cells
ii. Glucagon response to low blood glucose -- more insulin, glucgon goes
down
iii. In liver, break down of glycogen (glycogenolysis)
find more resources at oneclass.com
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Document Summary
Follicle cells surround colloid and colloid is in thyroid -- colloid is storage place for protein- thyroglobulin. Tsh binds to g protein receptor and stimulate gs: get camp and pka, no question on t3 t4, resynthesis thyroglobulin. Transport ions in cell, active secondary symport with potassium: t3 and t4. In liver, break down of glycogen (glycogenolysis: glycogen synthase w. pka phosphorylating, pka inhibits glucose to glycogen. Inactivate the sodium channel and open the potassium channel for repolarization: hyperpolarization to resting potential, caused by potassium channel being shut slowly. First, the electrical component is caused by a charge difference across the lipid membrane. Second, a chemical component is caused by a differential concentration of ions across the membrane: definitions, not equal +/- then electrical gradient, epinephrine, norepinephrine, acetylcholine is cholinergic -- can bind to ionotropic or metabotropic. Into it: scn , crh to acth to cortisol, glucocorticoids.
