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BMS 508

by: Jess Graff
Jess Graff

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About this Document

These notes cover the lecture from May 6
Human Anatomy and Physiology II
Mary Katherine Lockwood, PhD
Class Notes
anatomy, Physiology
25 ?




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This 4 page Class Notes was uploaded by Jess Graff on Thursday May 12, 2016. The Class Notes belongs to BMS 508 at University of New Hampshire taught by Mary Katherine Lockwood, PhD in Spring 2016. Since its upload, it has received 7 views. For similar materials see Human Anatomy and Physiology II in Biological Sciences at University of New Hampshire.

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Date Created: 05/12/16
BMS 508.03 5/6/2016 Chapter 27 (cont) Electrolyte and Acid Base Balance Acid-Base Balance • Renal Compensation • Is a change in rates of H and HCO secreti3n or reabsorption by kidneys in response to changes in plasma pH • The body normally generates enough organic and fixed acids each day to add 100 mEq of H to ECF+ • Kidneys assist lungs by eliminating any CO that: 2 • Enters renal tubules during filtration • Diffuses into tubular fluid en route to renal pelvis • Hydrogen Ions • Are secreted into tubular fluid along: • Proximal convoluted tubule (PCT) • Distal convoluted tubule (DCT) • Collecting system • Buffers in Urine • The ability to eliminate large numbers of H in a normal volume of urine depends on the presence of buffers in urine • Carbonic acid–bicarbonate buffer system • Phosphate buffer system • Ammonia buffer system • Major Buffers in Urine • Glomerular filtration provides components of: • Carbonic acid–bicarbonate buffer system • Phosphate buffer system • Tubule cells of PCT • Generate ammonia • Renal Responses to Acidosis • Secretion of H + • Activity of buffers in tubular fluid • Removal of CO 2 • Reabsorption of NaHCO 3 • Renal Responses to Alkalosis • Rate of secretion at kidneys declines • Tubule cells do not reclaim bicarbonates in tubular fluid • Collecting system transports HCO into tub3lar fluid while releasing strong acid (HCl) into peritubular fluid Acid-Base Balance Disturbances • Acid–Base Balance Disturbances • Disorders • Circulating buffers • Respiratory performance • Renal function • Cardiovascular conditions • Heart failure • Hypotension • Conditions affecting the CNS • Neural damage or disease that affects respiratory and cardiovascular reflexes • Acute Phase • The initial phase • pH moves rapidly out of normal range • Compensated Phase • When condition persists • Physiological adjustments occur • Respiratory Acid–Base Disorders • Result from imbalance between: • CO 2eneration in peripheral tissues • CO 2xcretion at lungs • Cause abnormal CO levels2in ECF • Metabolic Acid–Base Disorders • Result from: • Generation of organic or fixed acids • Conditions affecting HCO conce3tration in ECF • Respiratory Acidosis • Develops when the respiratory system cannot eliminate all CO 2 generated by peripheral tissues • Primary sign • Low plasma pH due to hypercapnia • Primary cause • Hypoventilation • Respiratory Alkalosis • Primary sign • High plasma pH due to hypocapnia • Primary cause • Hyperventilation • Metabolic Acidosis • Three major causes • Production of large numbers of fixed or organic acids + • H overloads buffer system • Lactic acidosis • Produced by anaerobic cellular respiration • Ketoacidosis • Produced by excess ketone bodies • Impaired H excretion at kidneys • Severe bicarbonate loss • Combined Respiratory and Metabolic Acidosis • Respiratory and metabolic acidosis are typically linked • Low O ge2erates lactic acid • Hypoventilation leads to low P O2 • Metabolic Alkalosis • Is caused by elevated HCO concentrations 3 + • Bicarbonate ions interact with H in solution • Forming H CO 2 3 • Reduced H causes alkalosis • The Detection of Acidosis and Alkalosis – • Includes blood tests for pH, P CO2’and HCO lev3ls • Recognition of acidosis or alkalosis • Classification as respiratory or metabolic


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