L5 Endocrine Flashcards

(59 cards)

1
Q

Hypophysiotropic hormones

A

TRH
CRH
GnRH
GHRH
Somatostatin
Dopamine

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2
Q

Chemical classifications of hormones

A

Amines
Peptides
Glycoproteins
Steroids

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3
Q

Amine Hormones

A

all are derivatives of the nonessential AA tyrosine

Thyroid hormones: T4, T3
Adrenal Medulla hormones: epinephrine, norepinephrine, dopamine

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4
Q

Catecholamines

A

Epinephrine
Norepinephrine
Dopamine

Lipophobic, they do not need a carrier to travel in the blood

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5
Q

Thyroid hormones

A

Lipophilic, need a protein carrier to travel in the blood

Thyroxine
Triidothronine

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6
Q

Peptide Hormones

A

Chains of amino acids

Initially synthesized as larger preprohormones in the ribosomes, which then are cleaved onto prohormones by enzymes in the ER

Then the golgi apparatus packages them into vesicles, and they are attached to active hormone

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7
Q

Peptide hormone examples

A

ADH/vasopressin
Insulin

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8
Q

Preprohormone

A

prohormone from even larger precursor molecule

synthesized on ribosomes, cleaved to prohormones on ER

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9
Q

Prohormones

A

long-chained precursor that is cut and spliced to make the active hormone

occurs in golgi apparatus

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10
Q

Example of synthesis of peptide hormone

A
  1. Preproinsulin: a, b chains and connecting peptide are made on ribosomes
  2. Proinsulin: Preproinsulin is cleaved to proinsulin in ER
  3. Insulin: Proinsulin is cleaved to insulin in golgi apparatus
  4. Secretory vesicles contain and release insulin and C-peptide
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11
Q

Glycoprotein hormones

A

Long polypeptides bound to one or more carbohydrate groups

examples are FSH and LH

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12
Q

Steroid Hormones

A

all synthesized from cholesterol
they are lipophilic, meaning they need a protein carrier to travel in the blood

Adrenal cortex, Gonads, and Placenta hormones are examples

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13
Q

Corticosterioids

A

Aldosterone
Cortisol
Dehydroepiandrosterone and androstenedione

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14
Q

Aldosterone

A

mineralcorticoid
Na+ reabsorption in exhange for K+ or H+ secretion by kidneys

part of the renin-angiotensis-aldosterone system
low blood pressure is a trigger
resides in zona glomerulosa

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15
Q

Cortisol

A

glucocorticoid
helps with metabolism, response to stress, immune modulation
resides in zona fasiculata/reticularis

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16
Q

DHEA

A

similar effects to testosterone, much less potent
resides in zona fasiculata/reticularis

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17
Q

Synergistic hormonal interaction

A

> 2 hormones work together to produce a result
can be additive or complementary

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18
Q

Additive Synergistic hormonal interaction

A

each hormone separately produces a response, but together they produce a greater effect

ex: NE and E on the heart

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19
Q

Complementary Synergistic hormonal interaction

A

each hormone stimulates a different step in the process

ex: FSH and testosterone on sperm production

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20
Q

Permissive hormonal interaction

A

1 hormone enhances the effectiveness of a 2nd hormone to produce a specific result

ex: thyroid hormone and epinephrine on rate of lipolysis

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21
Q

Antagonistic

A

2 hormones produce opposite effects

ex: insulin and glucagon

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22
Q

Hormone plasma concentration

A

Plasma concentration reflects the rate of secretion. Most do not accumulate in the blood because they have short half lives.

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23
Q

Hormone effects and concentration

A

Effects are very dependent on concentration
physiological concentrations produce normal tissue responses
Deficit/excess of hormone produces pathological responses

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24
Q

Hormone release

A

SECRETION
usually released in short bursts, plasma concentration can change rapidly over brief time

most have a 24 hour cylical behavior due to variations in neural paths

cortisol is low late at night and high in the morning

25
Hormone receptors
ability of any target tissue to respond to a hormone depends on the presence of specific receptors on the cell surface or inside the cell a hormone can influence its target cells' ability to respond by regulating the receptors
26
Up-regulation
increase in number of receptors usually results from prolonged exposure to low hormone concentrations
27
Down-regulation
decrease # of receptors usually results from exposure to high concentration of hormone
28
Properties of receptors
Specificity High Affinity/bond strength Low Capacity/saturation
29
Lipophilic hormones
cortisol/steroids, thyroid hormones receptors are inside the cytoplasm or nucleus, need a protein carrier
30
Lipophobic hormones
receptors are on the cell membrane
31
Mechanism of action for lipophilic hormones
1. Hormones bind to specific carrier proteins in plasma 2 Hormone dissociates from carrier protein to pass through lipid bilayer of target cell membrane 3. Hormone binds to a receptor that is inside of the cell 4. Steroid-receptor complex translocates to nucleus 5. DNA-binding domain of receptor binds to DNA inside cell 6. Dimerization occurs, stimulates gene transcription 7. Hormone binding results in activation of particular genes resulting in changes in protein synthesis 8. Activation of receptor results in delayed responses
32
Hormones and 2nd messenger systems
peptides, glycoproteins, catecholamines bind to receptors in the cell membrane extracellular hormones are transduced into intracellular 2nd messengers can impact ion channels, enzyme activity, G-proteins
33
What is important for PTs with 2nd messenger systems?
1. Many drugs bind to signaling cascades 2. One hormone can have different effects depending on receptor subtype it binds to 3. Drugs can have the same effects as NT or hormones by impacting the downstream of the 2nd messenger system (backdoor activation) 4. If a drug acts on multiple 2nd messenger systems, it will have a broad unanticipated impact
34
Main classes of 2nd messenger systems
Adenylate cyclase Phsopholipase C Tyrosine Kinase
35
Adenylate Cyclase-cAMP
most common, enzyme system that always requires a G protein 1. hormone binds to G protein 2. beta-2 subunit dissociates and activates AC 3. cAMP activates protein kinases (adds a phosphate) 5. cAMP is inactivated by phosphodiesterase (PDE)
36
Caffeine and cAMP
caffeine inhibits the action of cAMP PDE, which ultimately prevents the breakdown and inactivation of cAMP cAMP concentration inside cells stays higher for longer
37
Phospholipase C
1. Binding of epinephrine to alpha 1-adrenergic receptor activates G-protein that is coupled to PLC 2. PLC splits phospholipid into IP3 and DAG (2nd messengers) 3. IP3 opens CA2 channels in ER 4. Influx of Ca2, Ca2 binds to calmodulin 5. Calmodulin activates specific protein kinases that modify enzymes
38
Epinephrine and 2nd messenger systems
Can act through two second messenger systems Allows for a graded response stimulate alpha 1 and higher levels stimulates beta 2 cells, at low levels
39
alpha 1 cells
coupled to PLC, IP, Ca most vascular smooth muscle pupillary dilator muscle liver (increases glycogenolysis)
40
Alpha 2 cells
activation leads to decreased AC/cAMP inhibits NT release
41
Beta 1 cells
activation leads to increase AC/cAMP increase HR and contractility
42
Beta 2 cells
activation leads to increase AC/cAMP vascular smooth muscle vasodilation bronchodilation gluconeogenesis, glycogenolysis
43
Beta 3 cells
activation leads to increase AC/cAMP lipolysis
44
Tyrosine Kinase
no G protein main system for insulin have receptor proteins in plasma membrane, that add phosphate groups to residue tryosine 1.Receptor has 2 units that come together (dimerization), activating enzymatic portion of tyrosine kinase 2. Receptor autophosphorylates, increasing own activity 3. Receptor phosphorylates other signaling molecules
45
Hormones are metabolized by
1. Target cell 2. Peptide hormones bound to receptors are removed by endocytosis 3. Depends on secretion and rate of removal
46
Inputs that act directly on endocrine cells
ions or nutrients neurotransmitters hormones
47
Ions or nutrients and hormone secretion
1. Some hormones are directly controlled by plasma concentration of specific ions and nutrients 2. These hormones will regulate w/negative feedback, the concentration of the nutrient/ion
48
Neurons and hormone secretion
1. hormones of the hypothalamus and post pituitary are controlled by the CNS 2. Adrenal medulla is stimulate by sympathetic preganglionic fibers
49
Other hormones and hormone secretion
1. hormone secretion is controlled by negative feedback 2. Ant. pituitary and hypothalamic secretions are controlled by the target organs they regulate 3. Feedback loops maintain normal hormone concentrations hormones can provide negative feedback for other hormones
50
Posterior Pituitary gland
outgrowth of the hypothalamus neural and vasculature connections ADH/Oxytocin hormones are produced in the hypothalamus and then are released in vasculature in the posterior pituitary or they are stored here secreted hormones go to a capillary bed that leads to the main bloodstream
51
Anterior Pituitary
no neural connections to the hypothalamus blood from the median eminence (hypothalamus) flow into the anterior pituitary hormones from the hypothalamus cause the production of new hormones from the anterior pituiatry, which are released into the blood hormones are released into MAIN BLOODSTREAM
52
Hormones of the anterior pituitary
FSH, LH = gonads Growth Hormone = Liver, tissues, organs TSH = thyroid Prolactin = breasts ACTH = adrenal cortex
53
Trophic effects and anterior pituitary
hormones from the AP have trophic effects on target gland health of target glands depends upon stimulation by anterior pituitary for growth
54
Hypophysiotropic hormones
=made in the hypothalamus and control secretion of AP hormones =called either releasing or inhibiting hormones =transported down axons which terminate in the median eminence =usually a part of a 3 hormone sequence
55
Growth hormone releasing hormone
stimulates GH which stimulates liver to secrete IGF or metabolism
56
Thyroid releasing hormone
stimulates thyroid stimulating hormone stimulates T3 and T4
57
Somatostatin
inhibits GH secretion
58
Corticotropin releasing hormone
stimulates ACTH release stimulates cortisol release
59
The hypothalamus receives...
Inhibitory and stimulatory input from ALL areas of the CNS