endocrine 3/26/13

Question 0

what is DHEA and who is it important to?

Answer 0

DHEA is responsible for the creation of testestorone in females and thus gives them their libido; for men, it is no big deal “nipples on a man”

Question 1

name the 3 zones of the adrenal medulla and what each one manufactures (from outermost to innermost):

Answer 1

from outermost to innermost:

1. Zona Glumerulosa: manufactures mineralcorticoids (90% of which is aldosterone); tissue appears convoluted like glumeruli
2. Zona Fasciculata: manufactures corticoids (95% of which is cortisol); tissure resembles rows of fascicles
3. Zona Reticularis: manufactures androgens (most of which is DHEA); tissue resembles a net (reticuli)

Question 2

how are corticosteroids made:

1. what is the receptor that the LDL uses to get into the cell membrane?
2. what process brings the LDL in?
3. what is the “figure” that is formed and what is the “pit” that comes next?
4. what does LDL merge with? what is released? where does it go?
5. what is the enzyme that is the rate limiting factor? what does it cause to be formed? where does it go?
6. what happens to it next (what 2 pathways)? what is the enzyme that causes a different pathway?

Answer 2

1. B100 receptor for LDL
2. endocytosis
3. Omega figure; clathrine pit
4. merges with a lysosome and cholesterol is released; goes to mitichondria
5. inside the mitichondria is cholesterol desmolase (rate limiter) which turns cholesterol into pregnalone (preg-na-lone) which is released and goes to smooth ER
6. in the smooth ER, pregnalone is converted to progestagen (pro-gest-a-gen); it is either converted to androgens which can become estrogen; or via 21 Hydrolase can become a mineral or gluco-corticoid.

Question 3

negative feedback of the cortisol hormones:

1. ___ ___ of hypothalamus releases what? which goes where?
2. ___ ___ releases what from its ___ (receptor cells) and this hormone goes 2 places; where? why?
3. this (_____) goes to where causing the ___ ___ to release cortisol.
4. cortisol goes 2 places; where? why?

Answer 3

1. MEDIAN PROMINENCE of hypothalamus releases cortocotripic releasing hormone which goes to eht anterior pituitary
2. ANTERIOR PITUITARY releases ACTH from its corticotropes which;
   a. negatively feeds back to hypothalamus telling it to stop releasing corticotropic releasing hormone and
3. ACTH goes to adrenal gland and tells zona fasciculata to make cortisol.
4. cortisol goes to the anterior pituitary and hypothalamus telling them both to stop putting out stimulating hormones.

Question 4

what does ACTH do to the adreal cortex in terms of releasing aldosterone?

Answer 4

primes the adrenal cortex to be able to release aldostorone (cannot do it without being primed).

Question 5

what is growth hormones main job?

Answer 5

cause protein synthesis using carbs and fats for fuel

Question 6

what does T3 (also T4) do with metabolism???

Answer 6

-increases # of Na/K pumps which increases increased heat
-increases # of cristae in each mitochondria; increasing mitochondria size
all increases metabloism

Question 7

what is cortisol?

Answer 7

it is a stress hormone but also a primer for GH

Question 8

how are carbohydrates (namely glucose) utilized under stress (when cortisol is in the system)

Answer 8

cortisol tells liver to slow down on using glucose and make fuel using alternative means (gluconeogenesis)

Question 9

what is gluconeogenesis:

Answer 9

making fuel from proteins or fatty acids:
A-protein is broken down (by liver) into acetyl group and ammonia; ammonia is turned to urea by liver and excreted by kidneys; the acetyl group can be put into the kreb’s cycle
B-fatty acids are broken into (by liver) via beta oxidation into an acetyl group which is combined to form acetyl acetic acid (ketone) which can be used as fuel in the kreb’s cycle.

Question 10

what else besides pancreatic issues can cause diabetes

Answer 10

cortisol or GH issues

Question 11

1. what is cortisol’s affect on protein

2. why is the liver spared from catabloic activity?

Answer 11

1. all organs except for liver begin to catabloize (including muscles),
   - this causes an increase in plasma amino acids which the liver can use for gluconeogenesis or wound repair.
2. the liver is spared because it if the protein factory which makes albumin, clotting and anti-clotting the body needs to heal.

Question 12

what happens to fats in the presence of cortisol release?

Answer 12

fats are mobilized from the legs and end up causing moon face and buffalo hump.

Question 13

how cortisol affects the immune system

2 theories:

Answer 13

1. causes wbcs to go their posts; leaving the circulation and causing decreased counts. the wbcs die after 1-2 weeks and the numbers really drop
2. cortisol down regulates the immune response;
   
   • stabilizes mast cell membranes
   • stops lysosome action of leaking free radicals
   • decreases capillary permeability
   • blocks IL4 to cap fevers

Question 14

how does aldosterone work in the kidneys?

1. what is its job and where in the kidneys?
2. too much?
3. too little?

Answer 14

• it is the “fine tuner”; works on the DCT and cortical collecting ducts (cortisol works on cortical…)
• causes Na+ reabsorption; too little and sodium is lost (along with water) while K+ or H+ is retained (leading to hyperkalemia or acidosis)
• too much and you retain Na+ (along with water) causing increased volume and BP which leads to “aldosterone escape”

Question 15

what is aldosterone escape?

Answer 15

pressure diuresis & naturesis d/t increased volume and sodium levels from hyperaldosteronemia

Question 16

cortico hyperplasia:

1. what is the old school name?
2. what causes it?
3. what are the effects?
4. since cortisol can do some of what ____ can do, what are other side effects?

Answer 16

1. Cushings disease
2. hypersecretion of cortisol
3. causes:
   a. muscle wasting d/t increased gluconeogenesis
   b. fat mobilization (moon face, buffalo hump)
   c. hyperglycemia
4. cortisol and aldosterone have similar makeup therefore you see s/s of hyperaldosteronemia which are:
   a. increased sodium reabsorption
   b. increased fluid retention
   c. increased BP
   d. hypokalemia or alkalosis
   e. increased DHEA= male sex characteristics on females (hirstutism (hairiness), deep voice)etc.

Question 17

adrenal insuffeciency:

1. what is old school name?
2. what is it?
3. what are side effects?

Answer 17

1. Addison’s disease
2. adrenal insuffeciency (decreased cortisol)
3. decreased cortisol=decreased aldosterone:
   a. decreased BP
   b. decreased sodium leading to increased neural excitability
   c. acidosis (d/t retained H+) or
   d. hyperkalemia (d/t retained K+)
   e. increased ACTH which leads to more melanocyte stimulating hormone leading to hyperpigmentation

Question 18

insulin:

1. where is it from?
2. what does it do?
3. how is it received at the cell membrane?

Answer 18

1. released from beta cells at islets of Langerhan
2. it is a storage hormone (tells cells to store glucose, AAs, fats etc).
3. insulin receptor on membrane is a Kinase (it adds phosphate)

Question 19

glucagon:

1. what cells does it come from?
2. what is its job?
3. what is the __ sparing that it does.

Answer 19

1. from alpha cells in pancreas
2. tells body to release glucose (for the brain only), AAs and FAs into the blood (the antithesis of insulin).
3. Glucose sparing is done so that the glucose released is only for the brain, FAs are released as Ketones for the rest of the body (“Hamburger for the masses”).