Term
| Types of ? type of communication: autocrine; paracrine; endocrine; neuroendocrine |
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Definition
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Term
| Cell sensitivity to a particluar hormone is RT ? |
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Definition
| total number of receptors per cell; cells can up-regulate or down-regulate the # of cells |
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Term
| Where do water soluble hormones interact with cells? |
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Definition
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Term
| Where do lipid soluble hormones interact with cells? |
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Definition
| Cross cell membrane by diffusion and bind with 4receptors in the cytoplasm or nucleus |
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
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Definition
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Term
| Highly vascular cells that allow regulation of secretory products, and drains into portal vein>liver |
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Definition
| Islets of Langerhans in the pancreas |
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Term
| Secretions of the pancreas |
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Definition
insulin Beta cells
glucagon Alpha cells
somatostatin D cells |
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Term
| Synthesized by B cells in pancrease |
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Definition
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Term
| Active form: alpha chain and beta chain |
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Definition
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Term
| Inactive form: C peptide joins the 2 active chains |
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Definition
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Term
| What is measured to study beta cell activity |
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Definition
| C-peptide: inactive form of insulin, and joins the 2 active chains (a and b) |
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Term
| Stored in secretory granules in B cells; pulsatile secretion, pre-formed then newly formed if stimulus continues; catabolized in the liver and kidney |
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Definition
| C-peptide, inactive form of insulin that joins the two active chains (a and b) |
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Term
What type of regulation of insulin?
increased GLUCOSE concentration stimulates the release on insulin; increased AA food products stimulates the release |
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Definition
| Metabolic Regulation of Insulin |
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Term
| The METABOLISM of glucose stimulates what release, not the glucose itself |
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Definition
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Term
| What type of regulation indirectly stimulates insulin by growth hormone and thyroxine, and INHIBITS insulin by somatostatin, insulin and catacholamine |
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Definition
| Endocrine regulation of insulin |
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Term
| Type of regulation that insulin release is ENHANCED by parasympathetic stimulation, and INHIBITED by sympathetic stimulation |
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Definition
| Neural regulation of insulin |
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Term
What do these do to insulin:
increased GLUCOSE concentrations, Increased AA food products; growth hormone and thyroxine; PARAsympathetic |
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Definition
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|
Term
What do these do to Insulin?
Somatostatin, insulin and catacholamines; SYMPathetic stimulation |
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Definition
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Term
| Where does insulin bind to alpha subunits on insulin receptors and activates multiple kinase pathways for GLUT-4 Transporter moves to surface to transport glucose across membrane |
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Definition
| insulin dependent skeletal muscle and adipose tissue |
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Term
| Where does insulin transport glucose into cells through GLUT-2 transporter, membrane protein that allows glucose movement across membrane |
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Definition
| Liver and pancreatic beta cells |
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Term
| Do you need insulin for the entry of glucose into all tissues? |
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Definition
| No. the brain is one. GLUT-1 transporter allows glucose into other tissues and does not require insulin. |
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Term
| Type of glucose transporter that is a transport protein and doesn't require insulin for production |
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Definition
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|
Term
| Glut-4 transporter is required for glucose to enter which cells |
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Definition
| Skeletal muscle and adipose tissue, insulin binds to alpha subunits |
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Term
| Glut-2 transporters is required for which cells to allow glucose to transport |
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Definition
| Liver and pancreatic BETA cells, type of protein transporter |
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Term
| What triggers beta cells to release insulin |
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Definition
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Term
| Glycolytic phosphorylation of glucose causes a rise in ATP:ADP ration, that inactivates K channel that depolarized membrane, causing Ca channel to open up and Calcium flows in.: What does all of this release |
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Definition
| Insulin by beta cells that is triggered by rising glucose levels, and phosphorylation begins |
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Term
| Major sites of insulin action |
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Definition
| Liver, muscle and adipose tissue |
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Term
| Does insulin activate or inhibit catabolism? |
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Definition
| Inhibits; by preventing the breakdown and release of fuel that is stored |
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Term
| What product metabolized does: stimulates glucose uptake in myos and fat and promotes storage; stimulates synthesis of glycogen in liver; INHIBITS hepatic glucose formation and glycogen breakdown? |
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Definition
| Carbohydrate metabolism--reaction to insul |
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Term
| What does insulin do to fat metabolism? |
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Definition
| insulin promotes fat storage and inhibits fat breakdown; stimulates lipogenesis, inhibits breakdown of FA to glucose |
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Term
| what does insulin do to protein metabolism |
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Definition
| promotes synthesis of protein and inhibits protein breakdown for gluconeogenesis |
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Term
| promotes synthesis of protein and inhibits protein breakdown for gluconeogenesis |
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Definition
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|
Term
| promotes fat storage and inhibits fat breakdown; stimulates lipogenesis, inhibits breakdown of FA to glucose |
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Definition
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Term
| Which cells produce glucagon |
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Definition
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Term
|
Definition
| high glucose levels and/or insulin, fatty acids and ketones |
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Term
|
Definition
| low glucose levels, amino acids, cortisol and catacholamines |
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Term
| What does the following: Maintains serum glucose levels, stimulates breakdown of hepatic glycogen stores and hepatic glucose synthesis; stimulates FA oxidation for fluconeogenesis; stimulates hepatic uptake of AA used to fuel gluconeogenesis |
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Definition
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|
Term
| Stimulates FA oxidation and hepatic uptake of AA for gluconeogenesis |
|
Definition
| glucagon-made by alpha cells |
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|
Term
| stimulates breakdown of hepatic glycogen stores and glucose syntesis in the liver |
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Definition
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|
Term
| Produced by D cells in the pancreas |
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Definition
|
|
Term
| What stimulates release of somatostain? |
|
Definition
| hi glucose, hi AA, growth hormone and thyroxine, parasympathetic (all same as insulin) |
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|
Term
| What inhibits somatostatin |
|
Definition
| somatostatin, insulin and catacholamines; Sympathetic (all same as insulin) |
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Term
|
Definition
| less glucagon, less insulin, less somatostatin |
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Term
|
Definition
| INHIBITS: glucagon, insulin, somatostatin |
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Term
|
Definition
fasting plasma >126 more than once
random glucose >200
plasma glucose >200 2 hours after oral glucose; A1C level of 6.5% (depends on ethnicity, and not same for kids) |
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|
Term
| Prediabetes plasma glucose: |
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Definition
|
|
Term
| Epidemiology :age < 30 years, peak 11-13, |
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Definition
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|
Term
Etiology: genetic, family hx. genetic mutation Class II MHC molecules (immune system mutation for self recognition);
possible environmental-previous infection, virus, or lack of infections |
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Definition
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|
Term
| Patho: deficiency of insulin caused by autoimmune destruction of pancreatic B cells: auto antibodies against beta cells and insulin in 70-80% |
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Definition
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|
Term
| Patho: cell mediated, T lymphocytes, CD4, Th1 , response against beta cells, CD8 mediated LOSS |
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Definition
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Term
| Pro-inflamm cytokine from T lymphocytes (CD4-Th1) , macrophage activation and more cytokinesm cause beta cells to injury and necrosis (insulitis), beta cell apoptosis |
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Definition
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|
Term
| Islet atrophy, fibrosis, insulin deficiency, GRADUAL progression, 90% of beta cells depleted before clinical |
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Definition
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Term
| Etiology: genetic and environmental: gene fefect to insulin receptor of insulin signaling pathway; physical inacitvity, diet and obesity |
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Definition
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|
Term
| Patho: combo peripheral tissue insulin resistance and inadequate insulin secretion |
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Definition
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|
Term
| Decreased ability of peripheral tissues to respond to insulin-due to abnormality of insulin molecure and low # of insulin receptors; defective receptors; problems with signal path; problems with GLUT 4 transporter |
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Definition
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|
Term
| Blood glucose high, not entering cells; get more gluconeogenesis, increase trigly, more FA metab, dysreg of adipolines |
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Definition
| Insulin resistance result of Type 2 DM |
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Term
| Increase glucose leads to modify protein synthe sis in cells, so insulin cells are not normal anymore, to will triccer T cell to change cell surface receptor |
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Definition
| Insulin resistance of Type 2 DM |
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|
Term
| patho: less uptake of glucose in muscle and adipose; can't suppress gluconeogenesis, more triglycerides and FA, dysregualtion of adipolines |
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Definition
| Result of insulin resistance |
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Term
| Insulin resistance can be measured when? |
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Definition
| up to 10 years before diagnosis of type 2 DM |
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Term
| Insulin resistance can be contributed to |
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Definition
| obesity, AGING; physical inactivity, diet |
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Term
| Role of obesity in insulin resistance |
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Definition
| hypersecrtion of insulin, beta cell dysfunction, beta cell hyperplasia to support the insuling hypersecretion; leads to beta cel exhaustion and cell loss |
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Term
| loss of pulsatile effect in secreting insulin, always trying to respond; down regulates teh number of insulin receptors in skeletal myo and adipose, so get insulin resistance; eventual beta cell death: hyposecretion of insulin |
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Definition
| B Cell exhaustion; follows beta cell hyperplasia in beta cell dysfunction hypersecretion |
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Term
| Patho: after B cell hypersecretion, then B cell exhaustion: this follows--lipidtoxicity with hi levels of FA inducing apoptosis; glucotoxicity |
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Definition
| Cell Loss in Type 2 diabetes |
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Term
| Too much sugar damages beta cells producing what |
|
Definition
| ROS damage then causes B cell dysfunction and loss, ongoing loss and damage. |
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Term
| When blood sugar not controlled, will have what type of cellular damage? |
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Definition
| ROX damage; with obesity will still have FA problems |
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Term
| What does hyperglycemia do with ROS? |
|
Definition
| excessive amounts form that continue to damage the B cells; it may alter genes tht produce insulin so the molecule is abnormal |
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Term
| Why are Islet cells at risk for damage by pro-oxidnt forces? |
|
Definition
| They do not make much antioxidant; ongoing beta cell loss, apoptosis, islet degeneration, deposition of amyloid |
|
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Term
| How long does the basal amount last in Type 2 diabetes? |
|
Definition
| 10-15 years, but it is not sufficient, so oral meds may be needed. |
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Term
| Epidemiology: 2nd half of gestation, resolves with delivery; affects 3-10% pg; risk factors, family hx ; obesity; hi maternal age |
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Definition
|
|
Term
| patho: caused by insulin resistance, impaired secretion and increased hepatic glucose production. get more progesterone, cortisol, prolactin and chorionic somatommotropin stimulate glucogenolysis and glyconeogensis |
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Definition
|
|
Term
| Patho: pg hormones interfere with action of insulin as it binds to receptor; insulin resistance usually compensated for by increase in insulin |
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Definition
|
|
Term
| patho: increased risk for Type 2 later in life |
|
Definition
|
|
Term
| Ptho: hormones interfere with action of insulin as it binds to receptor; resistance in pg, is usually compensated by increase in insulin secretion. |
|
Definition
|
|
Term
| Clinical: hyperglycemia, at first postprandial, then both fasting the PP; glcosuria; polyuria, polydipsia, polyphagia-lesss activity in satiety center in hypothalamus; more glucagon, ketosis, VLDL levels rise from fatty acids; also increases VLDL |
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Definition
| Diabetes, also negative nitrogen balance and more protein wasting |
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Term
|
Definition
| Sx first due to catecholamine release (autonomic); altered CNS function; nocturnal hypoglycemia |
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Term
| Caused by low insulin levels, stressful situation such as infection, trauma, emotional stress not taking meds |
|
Definition
| clinicals of ketoacidosis, hyperglycemia |
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|
Term
| Sx first due to catecholamine release (autonomic); altered CNS function; nocturnal hypoglycemia |
|
Definition
|
|
Term
| in adipose tissue: gluconeogenesis from lipolysis releases free FA (FFA) taken up by liver when insulin is low: ketones deplete buffering , get acidosis |
|
Definition
| keotacidosis in hyperglycemia |
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|
Term
| Advanced glycosylation end products, Polyol (sorbital) pathway, Protein Kinase C: Why are these activated? |
|
Definition
| Too much glucose inside the cell for the cell to use., shunted along different pathways in normal settings |
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Term
| Too much glucose first reacts with REVERSIBLY with AA on cellular proteins to form an intermediate; This develops from direct action of sugars on proteins |
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Definition
| AGE; Advanced glycosylation end products, sugars attach to proteins |
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Term
| Intermediate (schiff base) formed from sugar with cell proteins; then does an internal rearrangement to form ADvanced glycosylation end PRoduct |
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Definition
| Patho of AGE pathway from too much sugar that attaches to protein |
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Term
| A1C levels: do they indicate reversible or irreversible portion of AGE path |
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Definition
|
|
Term
| AGE: reversible or irreversible ? |
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Definition
| Irreversible, forms from reaction of too much sugars and proteins in AGE path |
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Term
| Index of glycemic control over the preceeding 203 months. |
|
Definition
| A1C; RBC's form an AGE, an altered protein from too much sugar |
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|
Term
| AGE causes a disruption in what? |
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Definition
|
|
Term
| Effects of what? On collagen-abnormal cross links of matrix, vascular thickening/stiffness; traps plasma and interstitial proteins, such as LDL in arterial walls-atheroscl and membrane thickening of GBM; GENERATES ROS: inflam |
|
Definition
|
|
Term
| conversion of glucose>sorbital>fructose: enzyme process using cofactor NADPH (comes from liver) needed to make glutathione |
|
Definition
| Normal Polyol (sorbital) pathway |
|
|
Term
| What drugs decrease NADPH, needed for glutathione |
|
Definition
|
|
Term
| DM that doesn't require GLUT2 or 4 transport--excess sorbital leads to? |
|
Definition
| cellular injury; decreased levels of cofactor needed to make glutathione> will get oxidative stress: ROS injury |
|
|
Term
| Too much ?? in glucose pathways abnormalities will affect which tissues |
|
Definition
| nerves, lenses, kidneys, blood vessels |
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|
Term
| What does intracellular endothelial hyperglycemia activate? |
|
Definition
| Proein Kinase C activation: protein involved in signal transduction. Stimulates endothelial growth factor production, causing neovascularization. |
|
|
Term
| Thickening of extracellular matrix in cap basement membrane; Stimulates inflamm response with release of proinflamm cytokines: ROS injury |
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Definition
| Protein Kinase C activation-protein involved in signal transduction. Changes transcription due to AGE; activated by hi BS. Changes cap perm, new vessels change perm |
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|
Term
| What pathway affects excessive glucose shunting--affects insulin signaling and unductin of insulin resistance; stim expression of protein that interferes with protein |
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Definition
|
|
Term
| capillary cell damage; basement membrane thickeing resulting in macular edema and retinal ischemia and/or protein kinase C; growth factors |
|
Definition
| Retinopahy. too many vessels formed and are leaky so don't function well. Extracellular matrix thick |
|
|
Term
| Which retinopathy? Macular vessel abnormalities, microaneurysms (TINY DOTS), more vascular perm , macular edeam |
|
Definition
| Non proliferative retinopathy |
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|
Term
| Which retinopathy? COTTON WOOL SPOTS from infarcts of nerve fiber secondary to retinal ischemia |
|
Definition
| Preproliferative retinopathy |
|
|
Term
| Type of retinopathy? neovascularization, angiogenesis of vessels, hemorrhage, RETINAL DETACHMENT, Neovascular glaucoma |
|
Definition
| Proliferative retinopathy |
|
|
Term
| new vessels sprout from exiting vessels at optic nerve. Protein kinase C plays role in new vessel forming. |
|
Definition
| Retinopathy-chronic diabetes complication. |
|
|
Term
| Patho: AGE or sorbital products and activation of Protein kinase C causing thick matrix |
|
Definition
| nephropathy-chronic diabetes complication |
|
|
Term
| 60% of death in Type 2 DM, due to hi trigly, VLDL, LDL, LDL trapping |
|
Definition
| Premature atherosclerosis-chronic diabetes complication |
|
|
Term
| Diffuse thickening of basement membranes, type IV collagen in arterial walls |
|
Definition
| Microangiopathy-chronic diabetes complication |
|
|
Term
| Due to alterations to fibrin, collagen, elastin in arteries secondary to AGE; ROS damage to endothelial cells which alter vessel function |
|
Definition
| HTN-chronic diabetes complications |
|
|
Term
| Hi BS>metabolic pathway>ROS>neuronal injury>impairs nerve function, neuronal cell death; due to cell injury secondary to microcirculatoin, peripheral and Autonomic NS |
|
Definition
| Diabetic neuropahy-chronic diabetes complication; Change to nerve functions and ability of nerves to be normal |
|
|
Term
| Why are diabetics prone to infections |
|
Definition
| altered neutrophil chemotaxis and phagocytosis because of AGE alteration to circulating plasma proteins |
|
|
Term
| Stimulates separate set of GLUT4 transporters thru a SEPARATE cellular signal pathway to move to myo cell membrane for glucose transport. |
|
Definition
| Exercise and insulin resistance: Exercise stimulates separate pathway. SO important alone. |
|
|
Term
| Can stimulate glucose transport to move |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Receives neural input from many different parts of CNS; receives hormonal input from vasculature (neg and others); secretions are pulsatile |
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Definition
| Hypothalmus==floor and lateral walls of 3rd ventricle |
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|
Term
| Secretions from ? that go to the posterior pituitary gland |
|
Definition
| Hypothalamus: Oxytocin, ADH (vasopressin) |
|
|
Term
Oxytoxin
ADH (vasopressin) |
|
Definition
| hypothalamus secretions that travel to posterior pituitary |
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|
Term
| Receives oxytoxin and ADH from the hypothalamus |
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Definition
|
|
Term
| Secretions going to ANT pituitary from ? |
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Definition
| From hypothalamus secreted to ANT pituitary: Corticotropin-releasing; thyrotropin-releasing; gonadotropin-releasing, growth hormone-releasing; somatostatin: prolactin releasing (substance P) |
|
|
Term
| Corticotropin-releasing hormone (CRH) from hypothalamus to the ant pituitary stimulates? |
|
Definition
| adrenocorticotropic hormone (ACTH) in ANT pit. |
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|
Term
| Thyrotropin -releasing hormone (TRH) from hypothalamus to the ant pituitary stimulates? |
|
Definition
| Thyrotropin secreting hormone (TSH) in ANT pit; TRH comes from hypothalamus |
|
|
Term
| Gonadotropin -releasing hormone (GnRH) from hypothalamus to the ant pituitary stimulates? |
|
Definition
| stimulates leutinizing hormone (LH) and gollicule stim hormone (FSH) secretion in ANT pit |
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|
Term
| Somatostatin-secretion from hypothalamus to the ant pituitary stimulates? |
|
Definition
| Growth hormone inhibiting factor>halts function in ANT pit |
|
|
Term
| Released by hypothalamus to ANT pit |
|
Definition
| Prolactin releasing factor-substance P |
|
|
Term
| What releases releasing hormones? |
|
Definition
| Hypothalmus send them to the ANT pituitary |
|
|
Term
| What secretes oxytocin and ADH |
|
Definition
| Hypothalamus, go to POST pituitary |
|
|
Term
|
Definition
| Posterior oxytocin ADH hypothalmus |
|
|
Term
|
Definition
| Anterior releasing hormones from hypothalamus |
|
|
Term
| Regulated by hypothalamus; negative feedback from circulating hormones |
|
Definition
|
|
Term
| Posterior pituitary hormones |
|
Definition
oxytocin and ADH
Smooth myo contraction in breast feeding, contracts uteus; ADH-binds to receptors on cells in collecting ducts, REABSORBS water |
|
|
Term
| ANTERIOR pituitary hormones |
|
Definition
| Contains 5 cells, all diff hormones; ACTH, TSH, GH, Prolactin, gonadotropins |
|
|
Term
|
Definition
| melanocyte stimulating-increases skin pigmentation |
|
|
Term
| Way to remember disorders of brain hormones |
|
Definition
| separate primary (happens to cells) from secondary (what is along the pathway to affect it?) |
|
|
Term
| etiology: pituitary cell hyperplasia, pituritary adenoma (MOST common), 10% intracranial neoplasm; impinges surroundin gcells; Rare CA pituitary; |
|
Definition
|
|
Term
| Diseases in hypothalamus with overproduction of releasing hormones, so too much pituitary |
|
Definition
| Hyperpituitarism-secondary |
|
|
Term
| Patho of pituitary adenoma |
|
Definition
| ANTERIOR most common; single cell type produces singe predominent hormonal excess; MOST are prolactin secreting (amenorrhea,HA, breast milk, infertile): Also Growth hormone adenoma: acromegaly |
|
|
Term
| Clinial: xray changes in sella turcica; visual field abnormalities from optic nerve compression; ICP, inc; HA, N/V, LOC chang, endocrine abnormalities |
|
Definition
|
|
Term
| Etiology: primary: benign lesions, tumors, trauma, hemorrhage ischemic necrosis, injury surgery: causing low secretion |
|
Definition
|
|
Term
| Etiology: secondary, diseases of hypothalamus, causing low secretions |
|
Definition
|
|
Term
| Clinical: most important Adrenal insufficiency, hypothyroidism and diabetis insipidus; amenorrhea, impotence |
|
Definition
|
|
Term
| Etiology: central: loss of>85% of vasopressin secreting cells in hypothalamus from trauma, inflamm, edema; nephrogenic (kidneys not responding to circ ADH), Pregnancy, |
|
Definition
| Posterior Pituitary Syndromes: Diabetes Insipidus |
|
|
Term
| Clinical: Hypernatremia; increased Urine, Vasopressin will show response |
|
Definition
| Posterior Pituitary: Diabetes Insipidus |
|
|
Term
| What stimulates the Thyroid secretion |
|
Definition
| Thyrotropin (TSH) from ant pit, binds to TSH receptor |
|
|
Term
| TSH from ant pit binding to TSh results in: |
|
Definition
| iodide uptake; T3 and T4 syntesis and secretion by thyroid gland., most reversibly bound to plasma protein. |
|
|
Term
| thyrogloculin helps store what? until its converted? |
|
Definition
|
|
Term
| What is a prohormone for T3 |
|
Definition
|
|
Term
| What inhibits or is a negative feedback for thyroid secretion? |
|
Definition
| T3 and T4 inhibit TSH directly, and thus TSH indirectly |
|
|
Term
| What inhibits or is a negative feedback for thyroid secretion? |
|
Definition
| T3 and T4 inhibit TSH directly, and thus TSH indirectly |
|
|
Term
| what hormones are stimulatory in nature |
|
Definition
|
|
Term
| hormone that increase activity of membrane bound Na, K, ATPas, increases basal metabolic rate, heat production and stimulates O2 consumption |
|
Definition
|
|
Term
| Hormone that promotes bone and brain G and D; increases rate of carb absorptoin, protein synthesis and lipid catabolism stimulates NS and HR/contractility |
|
Definition
|
|
Term
| C cells scattered in follicles |
|
Definition
| Thyroid, C cells secrete calcitonin |
|
|
Term
|
Definition
| Secrete calcitonin, inhibits osteoclastic bone reabsorption: FROM thyroid |
|
|
Term
| What stimulates the release of calcitonin from the C cells in the thyroid |
|
Definition
|
|
Term
| Etiology: Primary: AUTOIMMUNE; stimulates too much thyroid; breakdown of T helper cell tolerance; autoantibodies to TSH to the receptor: TYPE II hypersensitivity |
|
Definition
| Graves disease : primary etiology and patho |
|
|
Term
| hyperfunctional multinodular goiter, hyperfunctional adenomas: stimulate T3 and T4. Attaches itself to receptors to produce too much |
|
Definition
| Graves Disease primary etiology |
|
|
Term
| Etiology: secondary: exogenous thyroid hormone intake (pills), TSH secreting pituitary adenoma |
|
Definition
| Graves disease, too much thyroid |
|
|
Term
| clinical: suppressed TSH, hi T4, T3, **high % uptake of iodine**, hi TSH-R antibody ; increased metabolic rate-heat intolerance; appetite with wt loss |
|
Definition
|
|
Term
| clinical: overactivity of SYMPathetic : cardiac output hi, palpitations, tachy, a-fib, cariomegaly, nervous, poor concentration, hyperkinesia, insomnia, myo weak and tremor |
|
Definition
|
|
Term
| Clinicals: altered skeletal due to bone reabsorption, hi number and size of follicles with lymphocytes, scanty colloid; exopthalamosis: infiltration fo retro orbital space by leukocytes, edema |
|
Definition
|
|
Term
| patho: autoimmune destruction of thyroid so can't produce; breakdown of helper T toleracne, autoantibodies TSH receptors: thyroid follicular cell membrane. |
|
Definition
Hashimotos thyroiditis
autoantibody binds to block stimulation of T4 and #. CD* T cell destroys thyroid cells replaced by infilt and fibrosis |
|
|
Term
| Other etiology (besides autoimmune antibodies); iodine deficieincy, thyroid ablation, genes, drugs (lithium, antithyroid) |
|
Definition
|
|
Term
| Clinical: low serum T4 and T3; feedback loop stimulate hypothalamus and sim more SH, even tho TSH is HI, won't produce T3, T4, as it's broke |
|
Definition
|
|
Term
| Most sensitive test for early hypothyroidism |
|
Definition
|
|
Term
| Secondary hypothyroidism? lo or hi TSH |
|
Definition
|
|
Term
| Impaired development of skeletal system-short stature, coarse facial features, mental retardation |
|
Definition
| Cretinism (low thyroid)infants, young child |
|
|
Term
| Hypothermia, cold intolerance, low basal metabolic rate, round puffy face, periorbital edema, big tongue, wt gain, myo weak, cramps, stiffness, slow thinking, lethargy, depression, apathy |
|
Definition
| Myxedema (low thyroid in older children, adults) |
|
|
Term
| Diffuse enlargement of the thyroid gland that reflects impaired synthesis of thyroid hormone |
|
Definition
|
|
Term
| etiology: hypo or hyper thyroidism; dietary iodine deficiency, ingestion of goitrogens=things that block thyroid hormone synthesis in foods or meds |
|
Definition
|
|
Term
|
Definition
diffuse nontoxic simple
single and multiple nodes |
|
|
Term
| two small glands close to each thyroid lobe, contains chief cells(most) and oxyphil cells |
|
Definition
|
|
Term
| Where is parathyroid hormone secreted |
|
Definition
|
|
Term
Regulation of :
Ca levels, phosphate levels, |
|
Definition
| parathyroid hormone (PTH) |
|
|
Term
| decreased Ca+ stimulates what hormone |
|
Definition
| PTH synthesis and secretion |
|
|
Term
| Increased Ca levels inhibits what? |
|
Definition
| Parathyroid hormone: stimulate calcitonin release |
|
|
Term
| PTH does what in regulating calcium |
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Definition
| stimulates Ca release from bone; increases renal tubular reabsorption of Ca, stimulates renal conversion of Vit D; augments Calcium absorption in the gut |
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Term
| How does PTH regulate Phosphate |
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Definition
| Increases phosphate excretion in kidneys |
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Term
| patho: decreased bone formation, incr bone reabsorp of combo : imbalance in osteoblast and osteoclast activity; estrogen def and low testosterone levels allow incr osteoclasts |
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Definition
| Osteoporosis: low osteoblasts replication, slo manufacture of Vit D in skin; decreased renal mass with age, from activated Vit D |
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Term
| Patho: less Ca absorption from gut, low Ca and Vit D intake stimulates bone reabsorptoin, glucocorticoids, immobilization. HIGH TRABECULAR BONES |
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Definition
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Term
|
Definition
bone density 1-2.5 SD below peak bone mass
osteoporosis |
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Term
|
Definition
bone density >2.5 SD below peak bone mass
osteoporosis |
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Term
| Clinical:osteopenia or porosis, fx of vertebral column, hip, wrist; increased hyphosis from small fx in vertebral column |
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Definition
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Term
| Three zones: zona glomerulosa, zona faciculata, zona faciculata and reticularis |
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Definition
| Outer layer of Adrenal gland |
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|
Term
| aldoserone, cortisol, corticosteroids, androgens and estrogens |
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Definition
| hormones from adrenal gland |
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Term
Norepinephrine
epinephrine |
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Definition
|
|
Term
| Primary mineralocorticoids |
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Definition
|
|
Term
| Function of what hormone?: increases Na reabsorption from tubules; and from colonic fluid, saliva and sweat |
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Definition
| Aldosterone (from adrenal gland outer cortex, zona glomerulosa-most outer) |
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Term
| What does this regulate: renin-angiotensin system, angiotensin II binds to receptors in zona glomerulosa, ACTH (ant pit), Na, K, low levels of Na/ hi K |
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Definition
| Regulates Aldosterone (adrenal gland) |
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|
Term
| Type of hormonal glucocorticoids |
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Definition
|
|
Term
| Function of what? regulates metab of fat, carbs, protein to maintain GLUCOSE GLUCONEOGENESIS; effect of myo and fat, but promote uptake of carbs, acids, and FA; suppresses normal G and D; adaptation to stress, increases release of CRH< ACTH and cortisol |
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Definition
| Cortisol/corticosterone: adrenal gland secretion from mid layer of cortex, faciculata |
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Term
| What regulates glucocoricoids -cortisol/cortisosterone from the adrenal glands |
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Definition
| ACTH secreted by the ANT pit. regulted by CRH secreted by hypothalamus; in epidsodic bursts from low levels of cortisol;diurnal rhythm |
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Term
| Prolonged stress will change corticol secretion and ACTH in what way? |
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Definition
|
|
Term
|
Definition
| increased levels of cortisol, exogenous corticol |
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Term
| adrenal precursor steroid (androsenedrioine, DHEA, and DHEA-S); |
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Definition
| Androgens, secreted by adrenal gland |
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|
Term
| Effects of what hormone? stimulates protein synthesis , development of growth of male sex charac; required for female libido |
|
Definition
| Androgens from adrenal gland (inner layer of cortex) |
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|
Term
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Definition
| chromaffin cells, secretes epi and norepi (catacholamines), 90% epinephrine secreting. center of adrenal gland |
|
|
Term
| What regulates the adrenal cortex (epi and norepi) |
|
Definition
| innervated by preganglionic nerve fibers in SYMP NS |
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|
Term
| Function of adrenal medulla |
|
Definition
| interacts with alpha and beta adrenergic receptors, increases contractitliy of cardiac and smooth myo and neurotransmissions and VC |
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Term
|
Definition
| Cushing Syndrome: too much cortisol |
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|
Term
| Hypersecretion of ACTH (primary, > 50% |
|
Definition
| Cushing syndrome-too much cortisol from adrenal gland, often due to ingestin of exogenous glucocorticoids |
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|
Term
| Etiology of Cushing Syndrome: anterior pituitary ACTH producing adenoma, or ant pit hyperplasia, hypothalamic corticotropin Rele tumor |
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Definition
| Cushing Syndrom: excess cortisol projection of adrenal gland |
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|
Term
| clinical: hi cortisol levels and HIGH ACTH levels; |
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Definition
| Primary hypothalamic-Pituitary Cushing Syndrome >50% |
|
|
Term
| High corisol and low ACTH levels |
|
Definition
| hypersecretion of cortisol BY adrenal adenomas |
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|
Term
| hypersecretion that is disorderly ,episodic and random, loss of kiurnal rhythm, may have pos and neg feedback loops |
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Definition
| Endogenous Cushing Syndrome (either from primary hypothalamus or primary adrenal cusing syndrome |
|
|
Term
| patho for exogenous Cushing SYndrom |
|
Definition
| hyposecretion and zone fasciculata and reticularis atrophy |
|
|
Term
| patho for endogenous and exogenous cushing |
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Definition
| pituitary and adrenal glands fail to respond normally to stress |
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|
Term
| Clinical: central obesity, moon facies, thin extremities, fatigue and weak, oseoporosis, mentrual abnormalities, edema, thin skin, hyperglycemia glucose intolerance. |
|
Definition
| Hypercortisolism: cushing syndrome |
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Term
| Etiology: sudden withdrawal of long term cortical therapy, adrenal hemorrhage, Addison's disease (primary chronic adrenocortical insufficient), autoimmune destruction of adrenal cortex (60-70%), infections, infiltrative disease |
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Definition
| Primary adrenalcortical Insufficiency |
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|
Term
| Etiology: pituitary or hypothalamic hypofunction |
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Definition
| Secondary Adrenocortical INsufficiency |
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|
Term
| Clinicals: due to deficiency of glucocorticoids and androgens |
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Definition
| Secondary Adrenocortical Insufficiency |
|
|
Term
| decreased ACTH and endogenous corticol levels, aldosterone secretion is normal, no hyperpigmentation, decreased libido |
|
Definition
| Secondary Adrenocorical Insufficiency |
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|
Term
| Etiology: primary: autonomous overproduction of aldosterone |
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Definition
|
|
Term
| Clinicals: hypernatremia, hypokalemia, hypertension; myo weakness, cardiac dysarrhythmisas, visual disturbances |
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Definition
|
|
Term
| thyroid diseases are usually |
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Definition
|
|
Term
| Autoimmune inflamm response against RECEPTORS on cell |
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Definition
|
|
Term
|
Definition
|
|
Term
| Clinical: due to low glucocorticoids and mineralcorticoids |
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Definition
| primary adrenal corticoco insufficiency |
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|
Term
|
Definition
|
|
Term
|
Definition
|
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Term
|
Definition
| Catabolic: fight or flight;breakdown protein or fat for glucose, halts normal function, produces products for F or F |
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|
Term
| Mediate adaptation to stress |
|
Definition
| function of glucorticoids |
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|
Term
|
Definition
| Cushing syndrom: due to taking cortisol (exogenous or iatrogenic) |
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|
Term
| Primary hypothalamic-Pituitary: assoc with hypersecretin of ACTH |
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Definition
|
|
Term
| Primary adrenal cushing syndrom |
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Definition
| comes from adrenal galnd itself, hyper of cortisol by ADRENAL adenomas or CA |
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|
Term
| etiology: sudden withdrawal of corticoid therapy; massive adrenal hemorrhage; long stress |
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Definition
| Primary ACUTE adrenalcorticol unsufficiency |
|
|
Term
| etiology: autoimmune destruction, Infections of adrenal gland, |
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Definition
| Chronic adrenalcortico etiology |
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|
Term
|
Definition
|
|
Term
| Primary neurotransmmitter para |
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Definition
|
|
Term
| Clincal: GI anorexia, N/V, wt loss, lethargy, eak, hyperpigmentation with hih ACTH, leading to hi melanocyte stimulating; low corticol levels, hi ACTH, |
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Definition
| PRIMARY adrenocortical insuff |
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|
Term
| Etiology: pituitary or hypothalamic hypofunction |
|
Definition
| Secondary Adrenalcortico etio |
|
|
Term
| Low glucocorticoids and androgens |
|
Definition
| Secondary Adrenocortical insuff |
|
|
Term
| Clinicals: NO PIGMENT; decreased libido, low ADTH and endogenous cortisol, aldosterone normal |
|
Definition
| SECONDary adrenocortical insuff |
|
|
Term
| etiology: Primary: autonomous overproduction of aldosterone, CONN syndrom ,a of adrenocortical adenoma, genetic alteration |
|
Definition
|
|
Term
| Clinical: hypernatremia, hypokalemia, hyperstension; myo eak, cardiaca arr, visual disturance |
|
Definition
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