Endocrine

Endocrine

Hypothalamic Control Mechanisms

Basic Anatomy

Anterior Pituitary

Posterior Pituitary

Peptide vs. Steroid Hormones

Blood Sugar Regulation

Calcium Regulation

Calcitonin

Parathyroid Hormone & Vitamin D

Blood Volume Regulation

Hypothalamic Control Mechanisms

Basic Anatomy

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Image above originally from Anatomy & Physiology, Connexions Website. Modified via Creative Commons Attribution 3.0 License.

Anterior Pituitary

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Sunflowers: Grow towards the sun (Phototropism = Light + growing)

Tropism = Growth

Tropic Hormones target Endocrine Glands, and cause their follicles to grow.

- The picture below shows the follicles of the Thyroid (rings/spherical shells of follicular cells secreting a colloid of thyroglobulin [Protein that binds Thyroid Hormone, aka Thyroxine] into the center of the follicle.) The thyroid is the classic example of a gland ruled by the hypothalamic-pituitary axis.

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Releasing Hormones: Made by the Hypothalamus, go down the portal vein to the Ant. Pituitary. They cause the Ant. Pituitary to RELEASE Tropic Hormones.

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Portal system - any veins that connect two beds of capillaries. In the brainn, this is between the hypothalamic capillaries and those in the anterior pituitary. In the gut, this is between the capillaries in the gut and the capilaries in the liver (hepatic portal vein).

Releasing Hormones - released by the Hypothalamus, and carried down the hypophyseal (hypothalamic) portal system. They cause the release of tropic hormones from the anterior pituitary.

Tropic Hormones - Hormones with other glands as their target. They cause the target gland’s follicles to replicate and become more functional. (Tropism = growth)

        LH ---gonads---> sex hormones (Testosterone in men, Estrogen in women)

MSH - Cosecreted with ACTH as a propeptide that gets cleaved to form a final product:

Proopiomelanocortin ---(cleaved to)---> MSH + ACTH + Endorphin. So, pituitary tumors that oversecrete ACTH can cause skin darkening. 

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Posterior Pituitary

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Stupid Mnemonic for Posterior Pituitary Hormones: The Anterior Pituitary wears the hypothalamus like a mullet! They are a party in the back! And what happens at parties? You get dehydrated and pregnant! So, the Posterior Pituitary produces ADH to deal with the dehydration, and Oxytocin to push the baby out, and to feed it milk. Dumb, not P.C., I know, but … mnemonics that are silly work better!

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ADH = Anti-Diuretic Hormone. (Diuresis (Gr.) = Through + Urine)

Silly mnemonic = Anti-Diuretic Hormone ≅ Anti-Diarrheal Hormone (Because Diarrhea is watery. So, Anti-Diarrheal Hormone makes your pee not watery)

ADH (a.k.a. Vasopressin [artery-squeezer]) has 2 effects, depending on the receptor to which it binds:

        V1 - arteries ⇒ squeezing

        V2 - kidneys ⇒ aquaporins get exocytosed to membrane

The control of ADH is mostly governed by the Plasma Osmolarity. Since ADH serves to dilute the blood, a hyperconcentrated serum will trigger its release. If your blood is really dilute (<280 mOsm), you produce none at all, and pee out urine that is isosmotic to your blood. In normal osmolarity ranges, you are always losing more free water than solute (due to breathing), so you need to constantly add pure solvent, so you make some ADH. Blood volume is a far less effective trigger for ADH production. By the time low blood pressure stimulates ADH secretion, you have lost >15% of your blood volume (~1L out of 5L), and are in the first stage of shock!

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Peptide vs. Steroid Hormones

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Peptide Hormones act FAST (seconds to minutes)

Steroid Hormones act SLOWLY (days to weeks)

Act via a 2nd Messenger Pathway, after binding to a transmembrane receptor.

Act via intranuclear Steroid Receptors, which either themselves are Transcription Factors, or which bind to and active TFs.

USEFUL TIP: Since Steroid hormones all come from Cholesterol, they all have some version of the word rood “-ster” in their names. (See the chart below)

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Blood Sugar Regulation

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The major effectors are peptide hormones secreted by the islet cells of the pancreas.

glucagon (glucose + agonist): acts to increase [glucose] in the blood, so it will stimulate glycogenolysis (glycogen + splitting - into the component glucose monomers), and it will also increase de novo glucose synthesis (gluconeogenesis). Produce by alpha cells.

insulin (mnemonic: in-“cell”-in): acts to put the glucose into the cells. This will decrease the [glucose] in the blood. Produced by beta cells.

*Note: Glucocorticoids (made by the adrenal cortex) are stress hormones - In response to a stressor (a bear shows up behind you!), you need to be able to respond to the stress, so an increase in the blood sugar will help. Thus, glucocorticoids act like glucagon.

Calcium Regulation

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The fraction of Calcium floating free in the serum is really tiny (1 mM), but it is even less inside the cytoplasm (10-4 mM). This is why Calcium is such a good part of the second-messenger pathway (the signal:noise ratio is enormous), and why it is used to tell neurons that an action potential has reached the synaptic bouton.

The major storehouse of Calcium in the body is the bones. The Calcium there is bound to an anion that makes a relatively insoluble substance.  Osteoblasts (bone + seeds) take serum calcium and put it into the bone. Osteoclasts (bone+breakers) digest the bone and release it into the serum. Both processes happen simultaneously. This lays down bone along the lines of force (for example, from the round femoral head, curving down into the shaft), and removes areas where microfractures have occurred, much like scraping up the road to replace potholes.

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Short-term, the quickest way to increase serum calcium concentration is to ramp up osteoclast activity, and dissolve the bone. Long-term, this would lead to weak bones, so the body also has to bring in more calcium from the environment, which it does by increasing Calcium absorption from food in the gut, under the aegis of Vitamin D3 (the active form of Vitamin D).

Calcitonin

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There are hormones that raise the Calcium, and one that lowers it. Calcium regulation is easier to learn by memorizing the mnemonic for the calcium-lowering hormone:

Calcitonin = “Calci-bone-in.

Calcitonin takes serum calcium and puts it into the bone by ramping up osteoblast activity. This leads to a  decrease in the serum calcium concentration, which takes the accelerator off the production of calcitonin by the C-cells (aka parafollicular, or beside-the-follicle) cells of the thyroid.

Parathyroid Hormone & Vitamin D

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PTH and Vitamin D work synergistically. Both have 2 actions, one for short-term, and one for long-term raising of the serum [Ca++]. Short term, both increase osteoclast activity. To fix this deficit long-term, as mentioned above, Vitamin D directly leads to the uptake of Calcium from the food in the gut. PTH activates the enzyme 1,25 Hydroxylase in the kidney, which converts Vitamin D2 into Vitamin D3 (the subscript refers to the number of hydroxyl groups, therefore Vitamin D3 is also known as calcitriol). [Beyond the scope of the MCAT: We get Vitamin D1 from food, and from our Skin, in response to UV light. The liver converts Vitamin D1 to Vitamin D2. Lack of UV exposure in Northern climates is the reason largely thought responsible for the evolution of pale humans, or Caucasians.]

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Blood Volume Regulation

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For the MCAT, know the horizontal line in the middle of the following diagram, from the liver making Angiotensinogen to the secretion of Aldosterone by the Adrenal Cortex. Like other products of the Adrenal Cortex, Aldosterone is a steroid hormone. All the other parts of the RAAS are peptides.