Endocrinology Flashcards

1
Q

3 major classes of hormones

A

peptides, amines, steroids

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2
Q

peptides

A
  • water soluble, don’t require carrier proteins
  • usually fast onset but short acting response
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3
Q

amines

A
  • synthesized from tyrosine
  • cathecolamines (NE, epi) water soluble
  • thyroid hormone, not water soluble, requires a carrier protein
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4
Q

steroids

A
  • synthesized from cholesterol
  • lipid soluble
  • slow onset but last lasting response because requires altered gene expresion
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5
Q

metabolic clerance rate

A

volume of plasma cleared of a hormone per minute
* hormones removed by metabolism.binding in the tissues, hepatic, and renal excretion

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6
Q

measuirng hormone levels

A
  • radioimmunoassay (RIA)
  • ELISA
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7
Q

G-protein coupled receptors

A

most targeted by current drugs, activate signals by conformational change

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8
Q

ligand gated ion channels

A

important in PNS, CNS, and excitable tissues

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9
Q

receptor tyrosine kinase

A

GF, cytokine receptors

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10
Q

nuclear hormone receptors

A
  • located in cytosol, translocate to nuclease
  • typically ligand activated transcription factors
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11
Q

eicosanoid second messengers

A
  • binding of first hormonal messenger to its receptor can result in generation of second messenger
  • eicosanoids are group second messengers that are derived from arachidonic acid (pathway serves as targer for many drugs)
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12
Q

primary hormones that affect glucose levels

A

insulin, glucagon, somatostatin

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13
Q

secondary hormones that affect glucose levels

A

incretins, GH, CORT, cathecholamines

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14
Q

alpha cells

A

in the periphery and secrete glucagon

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15
Q

beta cells

A

located in the center and secrete insulin

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16
Q

delta cells

A

secrete somatostatin

17
Q

when do insulin levels increase?

A
  • after eating a carb rich meal
  • supposed to go down after meal
  • if there isn’t enough insulin ou will still have glucose in your body
18
Q

when do glucagon levels increase?

A
  • increase when you haven’t eaten
  • increase glucose production to feed cells and brain
  • glucagon stimulates insulin because of glucose production
19
Q

what does somatostatin do?

A

inhibits insulin and glucagon

20
Q

insulin synthesis and secretion

A
  • proinsulin synthesized first with three domains: A, B, C
  • a and b chains of proinsulin are joind by disulfide bridges to form insulin
21
Q

insulin

A
  • peptide hormone synthesized by beta cells
  • cleaved into active precursor
22
Q

insulin effects

A
  • increases glucose entry into muscle and fat tissues
  • increase glycogen in liver and muscle
  • increases expression of enzyme endothelial lipoprotein lipase –> releases fatty acids and glycerol from circulating triglycerides
  • inhibits hormone sensitive lipase
  • increases aa uptake-protein synthesis
23
Q

control of insulin secretion

A
  • glucose is taken up via GLUT2 and oxidized to produce ATP
  • increase in cellular ATP and ADP concentration inhibits ATP-sensitive K+ channels resulting in depolarization of beta cell membrane potential
  • depolarization activates the voltage gated sensitive Ca++ channels cuaing influx in Ca++
  • Ca++ induced release augements an increase in intracellular Ca++ triggers exocytosis of secretory granules containing insulin
24
Q

situations requiring increased insulin

A

pregnancy, thyrotoxicosis, fever, stress

25
Q

glucagon

A
  • antagonizes the actions of insulin to increase blood glucose concentration
  • transcription and translation of glucagon occurs in alpha cells
26
Q

glucagon actions and control

A
  • main target organ for glucagon is the liver
  • effects are to increase hepatic production of glucose and ketones (beta hydroxybutyrate and acetoacetic acid) because ketones provide an alternative energy source to glucose in many tissues
  • high conentartions stimulate lipolysis and proteolysis to maintain a supply of substrates required for cellular energy metabolism
  • protein rich meal stimulates glucagon secretion
27
Q

incretin hormones

A
  • GLP-1 stimulates insulin secrtion, inhibits gastric emptying, inhibits glucagon secretion
  • GIP: gastric inhibitory peptide
  • both promote beta-cell proliferation in the pancreas and inhibit apoptosis
  • release is stimulated by nutrient ingestion and peptides are degraded by DPP-4
28
Q

somatostain tumor

A
  • will inhibit production of insulin therefore decreased insulin levels
  • however because insulin inhibits glucagon and there is no levels of glucagon increase
  • increase glucagon therefore increase glucose
    decreased insulin, increased glucagon, increased glucose
29
Q

diabetes mellitus

A
  • group of disorders involved in regulation of insulin production/secretion or in the cellular actions of insulin –> hyperglycemia
  • diabetes leading cause of blindess, nontraumatic lower extremity amputation, end stage renal disease
30
Q

how is diabetes and pre-diabetes diagnosed?

A
  • A1C test
  • fasting blood sugar test
  • oral glucose tolerance test
31
Q

A1C test

A
  • measures percentage of blood sugar attached to oxygen carrying protein in RBC
  • the higher your blood sugar levels the more hemoglobin you’ll have with sugar attached
  • 5.7% is normal
  • between 5.7 and 6.4% is prediabets
  • 6.5% or higher on 2 separate tests indicates type 2 diabetes
32
Q

fasting plasma glucose test

A

testing how fast body processes sugar
* when fasting glucagon increase so CORT increase and BP while insulin decreases

33
Q

oral glucose tolerance test

A
  • used to diagnose diabetes only during pregnancy
  • blood sample taken after you fast then given a sugar solution and measure blood sugar level