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N542 Physiology > Endocrine > Flashcards

Endocrine Flashcards

0
Q

What is the difference between endocrine hormones and neuroendocrine hormones?

A

Endocrine hormones are released by glands/cells into the blood and act on target organs/cells (ex: GH)
Neuroendocrine hormones are secreted by neurons into the blood and act on target organs/cells (ex: ADH)

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1
Q

What is a neurotransmitter, what is an example?

A

Comes from a nerve, released from an axon, acts locally

Ex: Neuropeptide Y helps with appetite

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2
Q

What is paracrine vs autocrine?

A

Paracrine: secreted by cells into extracellular fluid and affect neighboring target cells
Autocrine: secreted by cells into extracellular fluid and affect self-cells

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3
Q

Polypeptides are produced where? They tend to be preprohormones, which means what? What usually signals their release?

A

Produced on ER, go to golgi for packing into secretory vesicles, where they are stored.
They are preprohormones meaning they stay inactive in the cell.
Exocytosis usually due to calcium activating the cell.

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4
Q

Are steroids stored? If so, where? What are they synthesized from?

A

Unlike proteins, steroids are NOT stored. They are synthesized from cholesterol (the cell DOES store cholesterol).

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5
Q

What is the structure of a steroid?

A

Three cyclohexyl rings and one cyclopentyl ring

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6
Q

What are examples of amine hormones? What are they derived from?

A

Derived from Tyrosine
Adrenal medulla hormones (epi and norepi)
Thyroid hormones (T3,T4)
Dopamine

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7
Q

How are thyroid hormones released slowly and controlled?

A

Thyroid hormones bind to plasma proteins which release hormone to the target tissues, long duration of action

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8
Q

What is ultra-short negative feedback loop?

A

Hypothalamus tells itself that it produced enough of a hormone and stops
Hypothalamus - hypothalamus

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9
Q

What is a short negative feedback loop?

A

Anterior pituitary tells hypothalamus to stop producing a hormone
Hypothalamus - anterior pituitary

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10
Q

What is a long negative feedback loop?

A

Target organ signals to anterior pituitary or hypothalamus to stop producing a hormone
Hypothalamus - anterior pituitary - target organ

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11
Q

When a hormone (example: thyroid hormone) is carried by a plasma protein, when does it become activated?

A

When it LEAVES the protein, therefore, it has a longer duration of action

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12
Q

Which hormones have receptors on the surface of the cell membrane? In the cytoplasm? In the nucleus?

A

Cell membrane: catacholamines and proteins
Cytoplasm: Steroids
Nucleus: thyroid hormones

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13
Q

What are ways in which receptors are down-regulated? Why are receptors down-regulated?

A

If negative feedback isn’t adequately responding to high concentrations of a drug/hormone, receptors can be down-regulated by…
Inactivation of intracellular protein signaling molecules, sequestration of receptors away from site of action, destruction of receptors by lysosomes, decrease in production of receptors

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14
Q

How does intracellular signaling have an effect on the response of a hormone?

A

Hormone receptor complexes are formed: ion channel linked receptors (Ach/NE can cause channels to open/close so they have a postsynaptic effect) and G protein linked hormone receptors (trimeric subunits cause conformational change to effect downstream activity)
A hormone binding can cause enzyme activation/inactivation which has an effect on activation/repression of genes

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15
Q

How is the speed of response effected if the hormone is lipophilic?

A

The more lipophilic, the quicker and more potent the response

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16
Q

When phospholipase C is activated by a second messenger, what is the response?

A

It catalyzes the breakdown of PIP2 into IP3 and DAG. IP3 mobilizes calcium and DAG activates PKC which is a precursor for local hormones like prostaglandins

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17
Q

How can hormones alter the genetic activity of a cell (2 examples)?

A

Steroid hormones increase protein synthesis by binding to a receptor protein, transport to nucleus, and promote translation to form more proteins
Thyroid hormones can increase metabolic activity of a cell

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18
Q

The hypothalamus communicates with the anterior pituitary through CRH (corticotropin releasing hormone) and TRH (thyrotropin releasing hormone) to have an effect on which hormones and which target organs?

A

CRH to ACTH (Adrenocorticotropic hormone) to effect the adrenal cortex
TRH to TSH to the thyroid gland

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19
Q

The hypothalamus communicates with the anterior pituitary through GnRH (gonadotropin releasing hormone) to have an effect on which hormones and which target organs?

A

GnRH to FSH (follicle stimulating hormone) and LH (luteinizing hormone) to ovaries or testes

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20
Q

The hypothalamus communicates with the anterior pituitary through PIH/PRF (prolactin inhibitory/releasing hormone) and GHRH/SS(GHIH) (Growth hormone releasing hormone, Somatostatin) to have an effect on which hormones and which target organs?

A

PIH/PRH to PRL (prolactin) to the mammary glands

GHRH/SS to GH (growth hormone) to skeletal muscle and bone

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21
Q

What are the two posterior pituitary hormones and what are their target organs?

A

ADH to the kidney tubules

Oxytocin to the mammary glands and uterine muscles

22
Q

What does growth hormone do?

A

Increases cell size, mitosis, and differentiation, increases protein synthesis, increases mobilization of fatty acid, DECREASES glucose utilization (so the muscles can have it) and INCREASES gluconeogenesis in the liver, which increases blood sugar (Note: athletes taking too much GH will damage the liver)
So, in all, it enhances protein, uses up fat, and conserves carbs

23
Q

What stimulates growth hormone?

A

Starvation (especially of protein), hypoglycemia, exercise, excitement, trauma, ghrelin (secreted before meals)

24
Q

How do GHRH, GHIH (somatostatin), Ghrelin, and IGF-1 regulate growth hormone?

A

GHRH stimulates ant pituitary to release GH
GHIH inhibits ant pituitary from releasing GH
Ghrelin stimulates ant pituitary to release GH
IGF-1 (insulin-like growth factor) stimulates GHIH or directly inhibits ant pituitary from releasing GH

25
Q

Is there more T3 or T4 in the body? Which is more potent?

A

93% thyroid hormone is T4
T3 is four times as potent
Most of T4 converts to T3
Note: T3 is triiodothyronine, T4 is thyroxine

26
Q

Specifically, where in the thyroid gland are the thyroid hormones?

A

The thyroid gland is made of follicles filled with colloid which is made of thyroglobulin. The thyroglobulin contains thyroid hormone. The cuboidal epithelial cells secrete the hormone into the follicles.

27
Q

How is thyroid hormone formed?

A

First, iodine is needed. The NIS (sodium iodide symporter) uses active transport for iodide to enter the cell. Peroxidase is an enzyme that oxidizes iodide (I) to iodine (I2), so it can combine with thyroglobulin. Thyroglobulin contains the tyrosine amino acid. Tyrosine combined with iodine go through iodination and coupling to form thyroid hormones.
Pendrin is another active transporter that exchanges iodide for chloride

28
Q

99% of thyroid hormones combine with what? When they are combined, are they activated?

A

99% of thyroid hormones combine with plasma proteins. They are NOT activated yet.
Specific plasma proteins: thyroxine-binding globulin, thyroxine-binding prealbumin, and albumin

29
Q

When someone has liver problems, they have thyroid hormone problems, WHY?

A

99% of thyroid hormones are carried around by plasma proteins which are synthesized in the liver. If the liver isn’t working properly, the thyroid hormones can’t get to the target organ.

30
Q

How does thyroid hormone work cellularly to have an effect on synthesis of new proteins?

A

Thyroid hormone receptors (THR) in the nucleus form a heterodimer with retinoid X receptor (RXR) at specific thyroid hormone response elements (THRE) on the DNA. When T4 enters the cell it oxidizes to T3, or T3 enters the cell. T3 binds to the THR (which is bound to RXR on THRE on the DNA), new mRNA is formed, new transcription takes place to form different proteins.

31
Q

When thyroid hormone synthesizes new proteins, what effect can that have on the body?

A

Growth, CNS development, cardiovascular (increase CO, increase blood flow, increase HR, increase strength, increase respiration), and boosts metabolism (increase mitochondria, increase NaK ATPase, increase oxygen consumption, increase glucose absorption, increase gluconeogenesis, increase glycogenolysis, increase lipolysis, increase protein synthesis, increase BMR)

32
Q

How is thyroid hormone regulated? Talk about the steps from the hypothalamus to the target tissues, what is released, where does it go?

A

Hypothalamus releases TRH to the anterior pituitary which releases TSH to the thyroid gland which releases T3 and T4 to the target tissues.
Regulation is mostly by negative feedback of T3 (and T4) back on the anterior pituitary and hypothalamus, some positive feedback (feed-forward) to the target tissues by T3 (released by target tissues)

33
Q

Where in the adrenal gland are hormones produced? (Aldosterone, cortisol, androgens, catecholamines?)

A

Medulla: catecholamines
Cortex: Zona glomerulosa (outer layer) makes aldosterone (mineralocorticoid)
Zona fasciculata and zona reticularis (inner layers) make cortisol (corticosteroid) and androgens

34
Q

What two events stimulate aldosterone release and what effect does aldosterone have in these two cases? Which case causes direct and which causes indirect release of aldosterone?

A

Hypovolemia: cardiac stretch receptors detect low fluid volume. Renin is released from kidney, ACE converts Angiotensin 1 to Angiotensin 2 in the lung, this causes K excretion into the urine (not as much as next scenario), Na reabsorption (water follows), and aldosterone release. INDIRECT Aldosterone release from adrenal cortex causes Na and Cl reabsorption via a sodium-chloride symporter.
Hyperkalemia: DIRECTLY causes release of aldosterone which causes Na reabsorption and K excretion, some indirect Na and Cl reabsorption as well

35
Q

What is the pathway from hypothalamus to target organs for cortisol to be released?

A

Hypothalmus releases CRH which stimulates the release of ACTH by the anterior pituitary.. This causes the adrenal cortex to release cortisol to act on the target tissues.

36
Q

What are the four areas that cortisol acts on? What effect does cortisol have on these areas?

A

Immune system- suppresses function, fever
Liver- gluconeogenesis
Muscle- protein catabolism
Adipose tissue- lipolysis

37
Q

Besides the hypothalamus causing CRH release, what two factors also cause CRH to be released?

A

Circadian rhythm (peaks at 8am) and stress

38
Q

How do the half-life of cortisol and aldosterone differ?

A

Cortisol has a longer half-life of 60-90 min (also peaks longer), aldosterone’s half-life is shorter at 20 min

39
Q

How are cortisol and aldosterone transported?

A

90% of cortisol is transported by plasma proteins (cortisol-binding globulin/transcortin and sometimes albumin)
Only 60% of aldosterone is transported by plasma proteins, this is only to serve as a reservoir to lessen rapid fluctuations in aldosterone

40
Q

What percent of epi and norepi does the adrenal medulla release?

A

80% epi

20% norepi

41
Q

How is norepi’s action terminated?

A

Reuptake: 80% can be reused
Metabolism: enzymes MAO in cytoplasm, and COMT in liver

42
Q

How is epi’s action terminated?

A

MAO and COMT (like norepinephrine, but relies more on COMT because it has a longer halflife)

43
Q

What response can norepinephrine and epinephrine have once they are released from the adrenal medulla (or once NE is released from postganglionic SNS nerve stimulation)?

A

Adrenergic response. This can be alpha 1/2 or beta 1/2. The specific reaction is determined by which cells are stimulated and secondary messengers.

44
Q

Why is ionized calcium measured, what is the normal value? How does it compare to total plasma concentration?

A

Ionized calcium is the amount of calcium in the plasma and interstitial fluid that is not bound to proteins and is filtered through the glomerulus, normal value is 1.2 mmol/L. This form of calcium is important for body functions such as the heart, nervous system, and bone formation. Ionized calcium is HALF of total plasma calcium concentration.

45
Q

PTH have calcium-sensitive receptors that detect calcium levels. Do high or low blood calcium levels inhibit/stimulate PTH?

A

Decreased blood calcium levels stimulate PTH secretion

Increased blood calcium levels inhibit PTH secretion

46
Q

When PTH is released, what three areas of the body does it work on, and what are the effects?

A

Bone: increased bone reabsorption, releases calcium (bone mass remains constant)
Kidney: increase 1,25 dihydroxychlecaciterol (vitamin D), increase calcium reabsorption (conservation of calcium), decrease phosphate reabsorption
Intestine (indirect response from kidney): Increase calcium reabsorption, increase phosphate reabsorption

47
Q

What are the effects of excess PTH and hypofunction of PTH?

A

excess PTH: rapid absorption of calcium salts resulting in hypercalcemia in ECF
hypofunction of PTH: hypocalcemia resulting in tetany

48
Q

What is calcitonin, where is it secreted?

A

Calcitonin is a peptide hormone secreted by the thyroid gland

49
Q

How does calcitonin work?

A

Increase plasma calcium stimulates calcitonin secretion, decreased plasma calcium inhibits calcitonin secretion. This works in opposition to PTH, but is not as strong

50
Q

Where and how long can thyroid hormones be stored?

A

Each thyroglobulin molecule can store some thyroid hormones in its follicles (about 30 hormones per thyroglobulin molecule) for 2-3 months

51
Q

Excess aldosterone can cause what? Too little aldosterone can cause what?

A

Excess: hypokalemia, muscle weakness and alkalosis (due to too much H ion secretion)
Too little: hyperkalemia and cardiac toxicity

52
Q

In order for Vitamin D to be effective, why do the kidneys need to be working properly?

A

Conversion to 1,25-dihydroxycholecalciferol happens in the kidneys, this is the most active form of vitamin D. Also, calcium helps this conversion happen.

N542 Physiology (9 decks)

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