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TEST BANK FOR PORTH'S PATHOPHYSIOLOGY CONCEPTS OF ALTERED HEALTH STATES 11TH EDITION BY TOMMIE L. NORRIS, VERIFIED CHAPTERS 1 - 52, COMPLETE NEWEST VERSION EXAM WITH ACTUAL QUESTIONS AND COMPLETE 100%CORRECT ANSWERS WITH VERIFIED AND WELL EXPLAINE $18.49   Add to cart

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TEST BANK FOR PORTH'S PATHOPHYSIOLOGY CONCEPTS OF ALTERED HEALTH STATES 11TH EDITION BY TOMMIE L. NORRIS, VERIFIED CHAPTERS 1 - 52, COMPLETE NEWEST VERSION EXAM WITH ACTUAL QUESTIONS AND COMPLETE 100%CORRECT ANSWERS WITH VERIFIED AND WELL EXPLAINE

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TEST BANK FOR PORTH'S PATHOPHYSIOLOGY CONCEPTS OF ALTERED HEALTH STATES 11TH EDITION BY TOMMIE L. NORRIS, VERIFIED CHAPTERS 1 - 52, COMPLETE NEWEST VERSION EXAM WITH ACTUAL QUESTIONS AND COMPLETE 100%CORRECT ANSWERS WITH VERIFIED AND WELL EXPLAINED RATIONALES ALREADY GRADED A+ BY EXPERTS |LATEST VE...

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  • PORTH'S PATHOPHYSIOLOGY CONCEPTS OF
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TEST BANK FOR PORTH'S
PATHOPHYSIOLOGY CONCEPTS
OF ALTERED HEALTH STATES
11TH EDITION BY TOMMIE L.
NORRIS, VERIFIED CHAPTERS 1 -
52, COMPLETE NEWEST VERSION
EXAM WITH ACTUAL QUESTIONS
AND COMPLETE 100%CORRECT
ANSWERS WITH VERIFIED AND
WELL EXPLAINED RATIONALES
ALREADY GRADED A+ BY
EXPERTS |LATEST VERSION 2024
WITH GUARANTEED SUCCESS
AFTER DOWNLOAD ALREADY
PASSED!!!!!!! (PROVEN ITS ALL
YOU NEED TO EXCEL IN YOUR
EXAMS




Page 1

,Page 2

, Chapter 1- Concepts of Health and Disease

GLUT stay Sequestered inside the cell and remains inactive until a signal from insulin is
received
Glucose Increases Transport of Glucose into Skeletal Muscle and Adipose Tissue
(GLUT-4)Increases Glycogen SynthesisDecreases Gluconeogenesis
Protein Increases Active Transport of Amino Acids in Cells Increases Protein Synthesis
Decreases Protein Breakdown
INSULIN'S ACTIONS ON FAT Promotes Fatty Acid and TG Synthesis Increases
Transport of Fatty Acids into Adipose Cells Increases Conversion of Fatty Acids to TGs
Maintains Fat Storage by Inhibiting Breakdown of Stored TGs by Adipose Cell Lipase
GLUCAGON Polypeptide Secreted by the Alpha Cells Maintains Blood Glucose Levels
Between Meals and During Fasting Periods Travels via the Portal Vein to Liver Site where it
exerts its main effects Initiates Glycogenolysis Promotes Gluconeogenosis by Increasing
Amino Acid Uptake by the Hepatocytes to be Converted Important in maintaining glucose
levels over time
GLUCAGON SECRETION Regulated by Blood Glucose Levels
When the blood glucose reaches hyperglycemia levels the secretion of glucagon is
decreased/inhibited
When the blood glucose reaches hypoglycemic levels there is an immediate increase in
glucagon secretion
glucagon Increases During Strenuous Exercise & Activation of the SNS ("Flight or
Fight") and Prevents Hypoglycemic Episodes
Amylin Suppresses post-prandial secretion of glucagon Slows gastric emptying/Increases
sense of satiety
Amylin mimetics (exogenous) Used in those unable to achieve glucose control with
insulin alone-acts synergistically with insulin
Somatostatin High-fat high-CHO & especially high-protein intake stimulate its release
Insulin inhibits its release Decreases GI activity after food consumption
"Incretin Effect" Stimulates Glucose-Dependent Insulin Release After Meals
Predominantly high-CHO Accounts for approximately 50% of the secreted post-prandial
insulin
Exogenous incretin mimetics bind to the Glucagon-like Peptide-1 (GLP-1) Receptor
Delays Gastric Emptying - Inhibits Post-Prandial Release of Glucagon & Suppresses
Appetite
Helps Maintain Blood Glucose Levels During Periods of Stress Fasting Exercise or
Hypoglycemia glucagon epinephrine GH Glucocorticoids
GLUCOSE METABOLISMMost Efficient Fuel Normal Brain Function Relies Exclusively
on Glucose Requires a continuous supply from the circulation Body Tissues Obtain Glucose
from Blood
When Glucose Levels Rise Insulin is Secreted




Page 3

, Glucose Not Needed for Immediate Energy is Stored in the Liver & Skeletal Muscle as
Glycogen
If Saturated Glucose will be Converted into Fatty Acids by Liver and Stored as
Triglycerides in Adipose Cells
Glycogenolysis breakdown of glycogen
Gluconeogenesis production of glucose from triglycerides and amino acids
FAT is the Most Dense Form of Fuel Storage
Use of Fats for Energy is Essential d/t High Portion Within Most Diets
Many CHO in Diet are fats are Converted to Triglycerides (TG) for Storage
fats are Broken down by adipose cell lipase into its 3 fatty acids & glycerol
Glycerol can enter the glycolytic pathway
Almost all body cells can use fatty acids as a fuel source
The liver converts fatty acids into ketones (organic acids) & releases them into the
bloodstream
Lipolysis breakdown o fatty acids to use for energy
PROTEIN METABOLISM is Essential for Formation of all Body Structures
Amino Acids are the Building Blocks
Body has Limited Storage Capacity of Amino Acids
Most amino acids contained in body proteins
Excess Amino Acids are Converted to Fatty Acids Ketones or Glucose and Stored or
Used as a Fuel Source
Amino Acids are Used as a Major Substrate for Gluconeogenesis when Glucose Needs >
Food Intake
Hormonal Regulation of Glucose is Primarily with the Endocrine Pancreas
Pancreas is Made Up of 2 Major Tissue Types Acini (exocrine) Islets of
Langerhans**(endocrine)
Each Islet cells is Composed of Alpha Cells Beta Cells Delta Cells
PHYSIOLOGY OF INSULIN Composed of 2 Polypeptide Chains - 'A' & 'B'
Proinsulin is the Immediate Precursor Consists of Insulin & Connecting Peptide C-Peptide
Runs from the A to B Chain of Insulin
Final Step in Insulin Synthesis is when C-Peptide is Enzymatically Removed from
Proinsulin
Plasma C-Peptide Levels Assess Residual Capacity for Insulin Synthesis
INSULIN is a Naturally occurring anabolic polypeptide hormone
insulin is Only hormone known to have a direct effect in lowering blood glucose levels
insulin Acts to regulate the metabolism of glucose and processes necessary for the
metabolism of fats carbohydrates & proteins
Insulin Promotes glucose uptake by target cells and provides for glucose storage as glycogen
insulin Prevents fat and glycogen breakdown and Inhibits gluconeogenesis and
increases protein synthesis
Blood glucose levels regulate release of insulin
Glucose enters the beta cell by a specific glucose transporter (GLUT-2)




Page 4

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