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Urinary Balances Review

by: Kiara Scheuer

Urinary Balances Review NTDT 20403

Kiara Scheuer

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About this Document

Gives the important points that will be on the test. Simply explains the major things to remember for the exam.
Dr. Powell
Study Guide
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This 5 page Study Guide was uploaded by Kiara Scheuer on Friday September 9, 2016. The Study Guide belongs to NTDT 20403 at Texas Christian University taught by Dr. Powell in Fall 2016. Since its upload, it has received 3 views. For similar materials see Nutrition in Nutrition at Texas Christian University.


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Date Created: 09/09/16
Glycolysis: 2 ATP & 2 NADH + H Anaerobic fermentation­ oxidizes 2 NAD for another glycolysis cycle Krebs= 2 ATP, ETT= 28 ATP, all together= 30 ATP, 10 NADH + H X 2.5 ATP, 2 FADH2 X 1.5 ATP Krebs= pyruvic to acetyl CoA during transitional phase, NAD reduced to NADH + H, COA + oxalacetic  acid=citric acid, 2 Co2, 4 NADH + H, 1 FAD reduced to 1 FADH2 ATP synthase= driven by proton gradient ETC order= 1,2,coQ,3, cytochrome  Storing glucose as glycogen thru glycogenesis requires hexokinase Excess Acetyl CoA converted to fatty acid thru beta oxidation Transamination forms keto acid Oxidative deamination forms ammonia, combines with CO2 to form urea Rising amino acid lvls can trigger insulin, stimulated translocation of 4 glucose transporter protein Post absorptive state: catabolic, goal­ to maintain blood glucose lvls Glucose harvested from glycogenolysis in lover, the skeletal muscles, then lipolysis, then catabolism of  proteins Absorptive State: Formation of polypeptides by amino acids, formation of triglycerides from glycerol & fatty  acids, secretion of insulin Beta oxidation in liver forms keto acids Corticotropin hormone: appetite suppressant Nueropeptide Y & Agouti enhance hunger Renal ptosis results in hydronephrosis PCT has microwili Ascending loop is permeable to water Collecting duct merges to form papillary duct Renal artery bp­ 95, vein­ 8 Glomerulus forms initial stages of filtrate Peritubular – pourous , pressure is 8, surrounds pct & dct vasa recta­ surrounds LOH in juxtamedullary nephrons, concentrated urine both peritubular & vasa return blood to cortical radiate veins glomerular filtration is passive podocytes in visceral layer of glomerular capsule basement membrane prevents negative charged particles GFR influences by surface area, permeability, net filtration pressure Glomerular HP highest (55), glomerular OP 30), Capsular HP (15) Extrinsic prevents filtrate formation, increases blood volume/pressure (results in anuria) Intrinsic: myogenic (afferent) & tubuloglomerular (ascending), NaCl lvls rise when GFR is high, triggers  macula densa to constrict to reduce GFR Extrinsic: sympathetic (vasoconstrict, inhibit filtrate formation & renin angiotensin, angiotensin II fxns— induces aldosterone & ADH, vasoconstriction to increase BP, reduced GFR by reducing surface area Most reabsorption in PCT Sodium reabsorption: everywhere except descending LOH, active, transcellular, aldosterone triggers it in the DCT, Collecting Duct, and ascending LOH Chloride/potassium reabsorption: paracellular, passive, set by Na, cotransport in ascending LOH reabsorbs  Na, Cl, and K Water reabsorption: hypertonic creates osmotic gradient, transceullar in PCT, obligatory—must absorb  water wherever aquaporins, facultative—ADH makes more aquaporins in collecting duct & DCT, transports  K, Mg, phosphate Lipid reabsorption—simple diffusion, east in PCT Ca reabsorption—both paracellular and transcelluar, does not require hormones in PCT, requires  parathyroid hormone to trigger reabsorption in DCT & ascending LOH Glucose reabsorption—PCT via sodium glucose transporter, all is reabsorbed Nitrogenous wastes reabsorption—creatine not reabsorbed, all uric acid in PCT, ½ urea in PCT Co2 reabsorption—in PCT have carbonic anhydrase, converted to bicarbonate Transport max—max absorption, reached when saturated, leads to glycosuria in diabetes mellitus In glomerular filtration, water/solutes go from glomerulus to bowmans capsule Potassium & hydrogen use Na antiport ADH­ triggers reabsorption of water in collecting duct (descending LOH) Main site for secretion: PCT Aldosterone: elimination of K in DCT & collecting ducts H secreted into if pH is higher than 4.5 Medullary Osmotic gradient: regulated urine concentration/volume, countercurrent multiplier (establishes  osmotic gradient), and exchanger (maintains osmotic gradient), part of juxtamedullary nephrons Body fluid osmosis—300 Osmolality of filtrate entering PCT is isosmotic Osmolality higher in medulla 500ml of urine excreted daily Descending LOH: permeable to water, not NaCl, water moves passively to hypertonic, concentrates filtrate,  highest at 1200 Ascending LOH: impermeable to water, active transport of Na, K, and Cl, high osmolality est positive  feedback= attracts water from descending LOH, filtrate 100 at top (hypotonic) Vasa Recta: surrounds juxtamedullary nephrons, maintains osmotic gradient, removes water from ECF,  freely permeable to water and NaCl, loose water as move deeper into medulla, more concentrated in  medulla, has higher blood volume at end ADH: makes pee more yellow, increases water reabsorption, causes aquaporins in DCT & collecting duct,  determines # of channels, facultative water reabsorption Diuretics: increase urine volume, glucose is osmotic diuretic (not reabsorbed, carries water out with it,  alcohol inhibits ADH release, caffeine/hypertension inhibits Na reabsorption (obligatory), loop diuretics inhibit medullary osmotic gradient Nocturnal Enuresis: primary—common, not enough ADH, small bladder, secondary—psychological Nonelectrolytes: covalent bonds, glucose/phospholipids/cholesterol/triglycerides/creatine/urea, large  molecules, make up bulk Electrolytes: dissociate in water, ions, salts/acids/bases/proteins), electrolytes are most determining agent of osmotic pressure because  dissociate into 2 ions, charger ions can conduct electrical current, have great  ability to cause fluid shifts (toward area of higher osmolality) Water intake=2500 Ml Insensible water loss= vaporized out of lungs/diffused thru skin, sensible water loss= urine excretion Blood volume/pressure—baroreceptors in carotid arteries & aorta, osmotic pressure—osmoreceptors in  hypothalamus Body water tonicity= 280­300 ADH, aldosterone & angiotensin II all increase body water, Atrial natriuretic peptide=decreases body water Less solutes (decreased osmolality)—ADH stops More solutes (increased osmolality)—ADH released No receptors used to monitor sodium lvls, all sodium can be reabsorbed, sodium is never secreted into Aldosterone= most important renal sodium regulator, trigger is renin­angiotensin, effects are to stop urinary  output and increase blood volume, slow Atrial Natriuretic peptide: from heart, reduced blood pressure/volume by stopping vasoconstriction and  Na/water retention, promotes Na excretion by inhibits reabsorption at collecting ducts & suppresses  ADH/Renin/aldosterone Estrogens: enhance Na reabsorption, progesterone: promotes Na/water loss Glucocorticoids: enhance reabsorption of sodium, edema Hypovolemia: loss of water/electrolytes, hemorrhage, osmolarity isotonic, not enough sodium & proteins Osmolality= solutes dissolved in 1 kg of water, solutions ability to cause osmosis Osmolarity: solutes present in 1 liter Hypotonic Hydration: promotes osmosis of water from ECF into tissue cells, intravenous hypertonic saline  reverses Electrolyte balances associated with addison’s (hyperaldosteronism) and pica, regulation of Na, K, Ca,  anions Sodium: most abundant cation in ECF, electric potentials, osmotic gradients, Ph buffer, too much sodium –  water retention/edema, hypertension, results from hypotonic hydration, not enough sodium—excess body  water, corrected by elimination of excess water Potassium: main intracellular cation, excess in ECF= depolarization, reduced excitement, low K=  hyperpolarization & nonresponsivness, PCT reabsorbs most, LOH the rest, collecting ducts alter amount of  potassium secreted, controls its own ECF via feedback reg of aldosterone, adrenal cortex cells sensitive to  K in ECF=trigger aldosterone release, aldosterone increases K secretion in collecting ducts, too much k— rapid type increases resting mom potential (excited cells), slow type prolongs refractory period (less  excited), acidosis, not enough k—hyperpolarization & nonresponsiveness, alkalosis Acidosis= hyperkalemia, alkalosis= hypokalemia Chloride: most abundant anion in ECF, HCL production/chloride shift/ pH balance, regulated by Na balance,  too much chloride—fried dietary excess or intravenous saline, not enough—ass with not enough sodium,  can result from too much potassium or acidosis nd Calcium: ass with bone hardness/muscle contraction/neurotransmitter exocytosis, 2  messenger, blood  clothing, too much calcium—from alkalosis, hyperparathyroidism & hyperthyroidism, reduces permeability,  inhibits depolarization, results in weak muscles/slow reflexes/arrhythmia, not enough calcium­­­ from vit d  deficiency/pregnancy/lactation/acidosis/hypoparathyroidism, hypothyroidism, increases permeability (more  excitable), results in tetany Phosphate: lots of ICF, part of ATP, RNA/DNA, phospholipids & creatine, activating enzymes, buffer Ph,  body can tolerate large fluctuations, parathyroid hormone= lowers phosphate lvls to prevent Ca & phosphate crystallization  Anions: Chloride maintains osmotic pressure, 99% reabsorbed, during acidosis= body reabsorbs more  HCO3, secretes Cl in exchange


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