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39 Cards in this Set
- Front
- Back
- 3rd side (hint)
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What is the definition of a hormone?
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a chemical messenger secreted by a cell or group of cells (including neurons) into the blood for transport to a distant target. It exerts its effects at very low concentrations.
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What are some functions of Hormones on target cells?
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-They exert their effects by acting through various classes of receptors
- Alter membrane permeability and/or electrical state by activating 2nd messenger systems -regulate the transport of molecules across membranes -activate genes for transcription -induce exocytosis (secretory activity) |
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What are the three chemical classes of hormones? What types of chemicals to amines consist of?
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Peptides, Amines, and Steroids
- Amines consist of catecholamines and thyroid hormones |
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What is the parent amino acid for catecholamines and thyroid hormones? How do both hormones differ chemically?
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-Tyrosine!!
-Catecholamines are made by modifying the side groups of tyrosine. Thyroid hormones are synthesized from two tyrosines and iodine atoms. |
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How are Peptide hormones and Catecholamines similar? how do they differ?
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Ways they are similar
-Both are made in advance and stored in secretory vesicles -Both released from the parent cell through exocytosis -Both are hydrophilic and dissolve in blood plasma -Both have a short half-life -Both have receptors on the cell membrane -When they bind to receptors in ligand binding they both activate second messenger systems. (some ex of peptides are insulin and ACTH and some ex of catecholamines are E and NE.) Ways they are not alike -In their general target response peptides and catecholamines cause the modification of existing proteins while only peptides cause the induction of new protein synthesis. |
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How are Steroid and Thyroid Hormones similar? How do they differ?
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Ways they are similar
-They are released from parent cell through simple diffusion -they are both hydrophobic and bound to carrier proteins in blood plasma -they both have a long half life -They both cause the activation of genes for transcription and translation -both cause the induction of new protein synthesis ways they are different -Steroids are synthesized on demand from precursors while thyroid hormones are made in advance and stored in secretory vesicles. -Steroids have receptors that are located in the cytoplasm or nucleus (some have membrane receptors too) while Thyroid hormones have receptors in the nucleus. |
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What are the major functions of the Thyroid Hormones (TH)?
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-They are the major determinant of the rate at which the body produces heat during the basal metabolic rate.
(excess): high BMR, heat intolerance; increased food appetite, and increased catabolism of nutrients (deficiency): Low BMR, cold intolerance; decreased food appetite. -Also facilitates the activity of the Sympathetic nervous system by stimulating the synthesis of beta receptors for epinephrine and norepinephrine. (excess):symptoms similar to those observed with activation of the sympathetic nervous system(ex. increased HR) |
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How much does the Thymus weigh and what is it connected by?
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It weighs about 20g and is connected by the isthmus
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Give a broad outline of how TRH is converted to TSH
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First TRH is released from the hypothalamus and travels through the capillaries in th median eminence and portal vessels to the capillaries in the anterior pituitary. From there it binds to its receptors on anterior pituitary cells and than TSH is produced. TSH than goes on to stimulate the thyroid
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Describe the process of TRH binding to its receptor in the anterior pituitary
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When TRH binds to its receptor it activates a G-protein, Phospholipase C, IP3-DAG second messenger pathway. The production of IP3 causes the release of calcium from the ER which stimulates the exocytosis of TSH.
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Describe the process of TSH binding to its receptor on the thyroid gland
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When TSH binds to its receptor it activates a G-protein, Adenylyl cyclase, cAMP second messenger pathway. so then.....
1. TSH will increase the activity of a Na/I cotransporter on the basolateral membrane of the thyroid follicular cell. This will increase the ratio of follicular cell iodine to plasma iodine (the T/S ratio) 2. Iodination than occurs. This is when iodine is oxidized and attached to rings of tyrosines in thyroglobulin. 3. TSH than stimulates the conjugation of iodinated tyrosines to form T4 and T3 linked to thyroglobulin 4. Than endocytosis of thyroglobulin contains T3 and T4 from the lumen of the follicle cell (colloid) to the follicle cell takes place. 5. Lysosomal enzymes than release T3 and T4 from the TG through the process of proteolysis. 6. T3 and T4 are than secreted into circulation |
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How does T3 and T4 enter the cell? what % of T3 and T4 are bound to thyroxin-binding globulin (TBG)?
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-They enter the cell either through diffusion or through carrier-mediated transport.
- 99.5% of T3 is bound to TBG while 99.98% of T4 is bound to TBG |
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How is T4 converted to T3? What proteins are made in response to T3 binding to THR in the nucleus?
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- 5/3 monodeiodinase activity removes the 5 iodine, converting T4 to T3.
- The Na-K pump, gluconeogenic enzymes, respiratory enzymes, myosin heavy chain, B adrenergic receptors, and others. |
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What causes goiters?
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Too little or too much T3 and T4!!
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Describe Primary Hypothyroidism compared to secondary hypothyroidism.
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-In Primary hypothyroidism there is a decreased amount of T3,T4 which causes an up regulation of TSH which causes a goiter. (Also known as Hashimoto's disease)
-However secondary hypothyroidism is associated with a decrease in TRH which decreases TSH and T3,T4. (No goiter) |
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What are some of the effects of Hypothyroidism?
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-Low BMR
-feeling of no energy -feeling cold -lethargy -sleepiness -mental sluggishness -impaired memory -slowed speech -slowed reflexes |
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Describe the two different forms of primary hyperthyroidism
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-The first is due to a tumor that stimulates T3,T4 production but which decreases TSH. There is no goiter.
-The second is called Graves' disease. This increases T3,T4, decreases TSH but increases TSI which is a thyroid stimulating Immunoglobulin. This produces TSH receptor antibodies that stimulate the TSH receptor. This results in a goiter |
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Describe secondary hyperthyroidism
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There is an increase in TRH, T3,T4, and TSH.
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What are the effects of Hyperthyroidism?
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-High BMR
-Restlessness -Hyperexcitable -sweating -weight loss despite ample food -increases HR -increased contractile force -exaggerated responses to stimuli in the environment -Nervousness -Irritability |
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What are the most common among the endocrine diseases?
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Thyroid disease
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describe the process of how insulin is created in a pancreatic B cell
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1. Glucose enters the cell through the GLUT2 transporter
2. Glucose metabolism creates an increase in ATP which than inhibits the K(ATP) channel. 3. This depolarizes the cell which than activates the voltage gated ca2+ channel. 4. This evokes ca2+ induced ca2+ release. 5. The release of ca2+ than leads to the exocytosis of insulin |
other modulaters of secretion act via the adenylyl cyclase cAMP, protein kinase A pathway, and the phospholipase C pathway.
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What happens to (adipocytes and muscle) and the liver during Insulin release?
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-there is an increase in glucose uptake in Adipocytes and muscle
- there is a cessation of glucose output *This aids in the restoration of plasma glucose to normal* |
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Where are the alpha and beta regions of a Tyrosine kinase receptor located?
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The alpha subunit is located on the membrane and the beta subunit is in the cytoplasm.
(the alpha subunit contains the Glycosylation site and the beta subunit contains the phosphorylation sites and the tyrosine kinase domain) |
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describe the action that takes place when insulin binds to a tyrosine kinase receptor
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receptor tyrosine kinase proteins start off as inactive monomers. But once insulin binds to them they dimerize and than the activated tyrosine is phosphorylated by ATP and becomes fully activated. Than Insulin Receptor Substrate proteins (IRS) bind to the tyrosines and promote different cellular responces.
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So how does insulin really lower blood glucose levels?
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Through GLUT-4 transporters!!! Insulin causes the insertion of GLUT-4 transporters into the cell membrane which than diffuse glucose into the cell.
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What is the benefit of having increased glucose enter cells?
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There will be an increase in glycogen, lipid, and protein synthesis
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What is the main cause of Diabetes Mellitus (Type 1DM)?
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the destruction of beta cells in the pancreas due to an autoimmune disease.
*This effects 10% of diabetics* |
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What is the danger of polyphagia in 1DM?
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Your body being hungry all the time means that your body isnt absorbing the glucose it just ate. B/c of this your body starts to break down fats which produce ketones and increase your blood pH.
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What are some other effects of increase in plasma ketones and plasma glucose?
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-Decrease in arterial blood pressure which causes a decrease in brain blood flow.
(This can result in impaired brain function, coma, and death) |
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What is the kidneys limit in terms of glucose reabsorption?
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They can only reabsorb 200-300mg/100ml. The rest is filtered out.
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What is the pathological result of fat metabolism in 1DM?
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Fat metabolism leads to increased plasma fatty acids due to the increase in the breakdown of fat. This breakdown of fat contributes to tissue loss.
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What is the pathological result of protein metabolism in 1DM?
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The breakdown of protein means a decrease in amino acid uptake by most cells and an increase in plasma amino acids. The protein breakdown also leads to tissue loss
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what is a direct result of the circulatory failure that often comes from 1DM?
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-Anaerobic metabolism will take place which causes lactic acid production. This leads to metabolic acidosis which increases ventilation. Also results in urine acidification and hyperkalemia
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What is the treatment for insulin shock: (hypoglycemia)?
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About 10 snickers bars and a liter of coke. lol. (Just intake some sugar)
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Type 2 diabetes (T2DM)
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-a diseased caused by being a fatty McPatty
-effects 90% of all diabetics. -It increases with age but is not age dependent -characteristics include insulin resistance and defects in beta cells ability to secrete insulin in response to increased plasma glucose. -about 1/3 of patients require insulin -70% die from cardiovascular disease |
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What is the most effective treatment for T2DM? what oral drugs can be taken to treat hyperglycemia?
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-Diet and exercise!!
- Sulfonylureas (these increase insulin release from beta cells in the pancreas) |
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What causes Gestational Diabetes and what are its effects?
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It is thought that it is related to the elevated levels of progesterone and cortisol.
-Peptide hormone hPL (human placental lactogen) implicated due to its ability to alter glucose and fatty acid metabolism to support fetal growth and to decrease effectiveness of insulin. -if untreated it can lead to fetal hyperglycemia, hyperinsulinemia and macrosomia (fat babies) -fat babies are at a risk to be obese and contract T2DM as adults. |
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What is the effect of glucagon release from alpha cells in the pancreas?
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There is an increase in glycogenolysis, gluconeogenesis, and ketone synthesis.
- This increases plasma glucose and ketones |
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What is the half-life of glucagon and what is its target receptor/second messenger pathway?
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-about 4-6 minutes
- It targets the liver primarily and acts on a G protein coupled receptor linked to cAMP |
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