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155 Cards in this Set
- Front
- Back
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Ways H2O and electrolytes can enter plasma:
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-alimentary tract
-cells -injections and infusions |
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How might Potassium be added to plasma or serum?
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-in vitro lysis of RBCs
-platelet activation |
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Ways H2O and electrolytes may leave the plasma and the body:
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-kidneys
-alimentary tract -respiratory tract -skin -extravascular sites (3rd space loss) |
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What electrolyte changes may occur in pairs?
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-inc. Na & inc. Cl
-inc. Cl & dec. HCO3 |
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Plasma [Na] is nearly equivalent to:
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ECF [Na]
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ECF [Na] is dependent on:
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-ratio of tbNa : tbH2O
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Serum [Na] is controlled by:
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-regulation of blood volume
-regulation of plasma osmolality |
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Hypovolemia effects on serum [Na]
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attempt to restore blood volume
-inc. RAS (inc. Na retention) -inc. ADH (inc. H2O retention) -dec. ANP (dec. Na excretion) |
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Increased Osmolality effects on serum [Na]
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attemp to dilute solutes
-inc. ADH (inc. H2O retention) -thirst centers (inc. H2O intake) |
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Normonatremia ratio:
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Hypernatremia ratio:
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Hyponatremia ratio:
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Pathologic dehydration
-definition |
-dec. in total body H20 characterized by either H2O loss or Na & H2O loss
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Normonatremic (Isotonic) dehydration effect on [Na]
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-lose isotonic fluid (H2O loss proportional to Na loss)
-[Na] in remaining fluid is the same but the animal is hypovolemic |
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Effect of drinking water after isotonic fluid loss
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-become hypotonic due to the dilution of electrolytes by the water
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Effect of losing pure water from the vasculature
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-become hypertonic due to increased electrolyte conc.
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Ways pure water can be lost
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-urine with a SG near 1.000
-water vapor in respiration |
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Fluid losses from blood can be either:
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-hypotonic
-isotonic -pure water |
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Most common cause for hypernatremia
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-dec. tb H2O (dehydration)
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Reasons for dec. tb H2O
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-dec. H2O intake
-inc. pure H2O loss -H2O loss > Na loss |
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Reasons for dec. H2O intake
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-restricted access to water
-defective thirst (occurs with continued daily loss of water) |
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Reasons for inc. loss of pure H2O
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-water vapor from hyperventilation, panting, fever (sweating)
-Diabetes insipidus |
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Reasons for H2O loss > Na loss
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-osmotic diuresis (glucose in tubular fluid)
-osmotic diarrhea (osmotic agents in alimentary system) |
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Causes of hyponatremia
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-H2O retention > Na retention (edematous state)
-Na loss > H2O loss (dehydration state) |
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Reasons for H2O retention > Na retention causing edema or transudates
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-heart failure
-cirrhosis -nephrotic syndrome |
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Reasons for Na loss > H2O loss causing hyponatremia
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Increased renal loss of Na
-hypoadrenocorticism -obligated loss with anions -diuretics -renal disease -osmotic diuresis (if concurrently drinking water) |
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Hypoadrenocorticism (addison's disease) causing hyponatremia
-pathogenesis |
-dec. aldosterone
-dec. renal conservation of Na -dec. tb Na -dec. cortisol -dec. inhibition of ADH release -inc. cortisol -inc. H2O retention -dilute remaining Na -hyponatremia |
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Conditions that will cause hyponatremia due to obligate Na loss with anions
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-ketosis (AcAc, beta-hydroxybutyrate)
-metabolic alkalosis (HCO3-) -Hypoxia (lactate) |
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Inc. intestinal loss of Na causing hyponatremia
-pathogenesis |
-Diarrhea and/or vomiting
-sequestration of fluid in the intestine (horse) -lose Na and H2O -dehydration -drink H2O -renal retention of H2O -hyponatremia |
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Inc. cutaneous loss of Na causing hyponatremia
-pathogenesis |
Sweating (only horses)
-increase Na and H2O los -dehydration -drink H2O -inc. renal retention of H2O -hyponatremia |
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3rd Space loss causing hyponatremia
-pathogenesis |
uroperitoneum
-Na poor urine enters the peritoneal cavity -plasma Na diffuses down the conc. gradient and into the peritoneal cavity -hyponatremia |
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General methods of Na loss leading to hyponatremia
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-renal loss
-intestinal loss -cutaneous loss -third-space loss |
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Blood glucose conc. to cause a H2O shift from ICF to ECF
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- > 400 mg/dl
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Marked Hyperglycemia causing hyponatremia
-pathogenesis |
-H2O leaves cells
-dilutes Na in ECF -hyponatremia -glucosuria -diuresis -inc. renal Na loss -hyponatremia |
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Mechanisms for Normonatremia disorders
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-inc. Na & H2O retention (edema and/or transudates)
-net Na & H2O loss from normonatremic dehydration |
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Reasons for inc. Na and H2O retention causing edema and/or transudates in normonatremia
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-heart failure
-cirrhosis -nephrotic syndrome |
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How do you differentiate normonatremic disorder and hyponatremic disorder with concern to inc. Na and H2O retention?
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-hyponatremic is due to H2O retention > Na retention
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Causes of normonatremic dehydration
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-renal loss (renal disease, diuretics, obligate loss with anions)
-intestinal loss (diarrhea, intestinal sequestration) -cutaneous loss (sweating in horses) |
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Most common type of dehydration
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-normonatremic dehydration
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Potassium concentration
-altered by |
-acid-base status
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Potassium shift with inorganic acidosis
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-accumulation of H+ in ECF
-H+ shift into cells for equilibration -K+ into blood to maintain electrical neutrality |
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Potassium shift with alkylosis
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-H+ in ECF reduced
-H+ leaves cells and enters plasma -K+ leaves plasma and enters cells to maintain electrical neutrality |
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Effect of excess Potassium loss on blood H+ concentration
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-decrease in K+
-shift of K+ from cells to ECF -H+ moves from blood to cells to maintain electrical neutrality -alkylemia occurs |
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Inorganic acids
-definition -examples |
-acids that do not contain carbon
-H3PO4, H2SO4, HCl |
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Reasons renal failure causes inorganic metabolic acidosis:
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-decreased excretion of H+ --> inc. H+
-dec. HCO3 (consumed to buffer inc. H+) -dec. excretion of H2PO4 & HPO4 --. hyperphosphatemia |
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Organic acids
-definition -examples |
-acids that contain carbon
-lactic acid -acetoacectic acid -beta-hydroxybutyruc acid |
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Effects that organic metabolic acidosis can have on potassium
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1) increased H+ and anion produced and enters blood
-both H+ and anion enter cells due to concentration gradient -electrical neutrality is maintained so K+ does not leave the cell 2) H+ and anion are both produced and enter the blood -H+ moves into the cell, and K+ leaves the cell and enters blood to maintain electrical neutrality -K+ is excreted renally with anion -no hyperkalemia occurs |
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Hyperkalemia occurs with
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-renal failure causing metabolic acidosis (oliguria)
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Regulation of Plasma K+
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-diet containing cells (K+)
-primary route of excretion = kidneys (inc. aldosterone --> inc. kidney loss of K) -insulin/epinephrine --> inc. K+ into cells |
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Major mechanisms for hyperkalemia
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-shift from cells
-inc. total body K+ (dec. renal loss) |
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Renal insufficiency causing hyperkalemia
-pathogenesis |
-Oliguria
-diminished rate of tubular flow through the nephron -secreted K+ accumulates in the tubular fluid, diminishing gradient -K+ secretion into the tubular fluid decreases and build up occurs in the plasma -hyperkalemia |
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Uroperitoneum causing hyperkalemia
-pathogenesis |
-urinary tract leakage
-K+ enters ECF -K+ can't be removed from the body -hyperkalemia |
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Hypoadrenocorticism causing hyperkalemia
-pathogenesis |
-adrenocortical hypoplasia decreases aldosterone and cortisol production
-hypoaldosteronemia -decreased activity of Na-K-ATPase pumps in collecting tubules -decreased resorption of Na & decreased secretion of K -increased K+ in blood -hyperkalemia |
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Pseudohyperkalemia
-causes |
-In vitro hemolysis (cattle, horses)
-Thrombocytosis (marked) |
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When can in vitro hemolysis cause pseudohyperkalemia?
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-when RBC [K+] > Plasma [K+]
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In what animals can In vitro hemolysis cause pseudohyperkalemia?
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-horses
-cattle |
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How does thrombocytosis causes a pseudohyperkalemia?
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-blood collected
-marked coagulation occurs -clotting causes K+ to enter serum -pseudohyperkalemia |
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General 2 ways that hypokalemia will occur
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-K+ shift into cells
-dec. in total body K+ |
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Ways to decrease total body K+
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Dec. Intake:
-anorexia Inc. Loss: -renal -intestinal -cutaneous |
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Shift of K+ into cells causing hypokalemia
-pathogenesis |
metabolic alkalosis
-hypovolemia activates RAAS increasing renal secretion a K+ -bicarbonaturia causes renal excretion of cations including K+ -decreased dietary intake |
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anorexia leading to hypokalemia
-pathogenesis |
-anorexia
-dec. K+ intake with concurent daily loss of K+ via kidneys & intestine -dec. total body K+ -hypokalemia |
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Length of time for hypokalemia to develop in food restricted:
-dogs and cats -herbivores |
-dogs and cats: 2-3 days
-herbivores: longers |
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Ways increased renal excretion can cause hypokalemia
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-polyuria
-ketonuria (anions cause the obligate excretion of cations/K+) |
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Ways increased intestinal loss can cause hypokalema
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-diarrhea
-sequestration of intestinal fluid (equine) |
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Inc. cutaneous sweat
-pathogenesis |
Cutaneous loss
-inc. K+ loss -hypokalemia -inc. H2O loss -dehydration -stimulate thirst -stimulate ADH -H2O dilutes K+ -hypokalemia |
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In what animal is [K+] higher in sweat than in plasma
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-horse
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When does normokalemia typically occur
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Acidotic states
-dec. tb K+ -acidosis --> K+ shift from ICF to ECF |
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Sodium Potassium ratio
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Classic cause for a decreased Na/K ratio
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-hypoadrenocorticism (inc. Na loass w/ inc. K retention)
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Reasons for a decreased Na/K ratio
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-hypoadrenocorticism
-diarrhea/hemorrhage -renal failure -urinary tract obstruction -diabetes millitus with ketonuria -3rd space loss of Na -other |
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Ways [Cl-] is controlled
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-renal resorption and excretion
-alimentary tract function |
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Renal effects on [Cl-] control
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-Na+ and Cl- resorption
-NH4+ and Cl- secretion -HCO3- and Cl- exchange |
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Alimentary Tract effects on [Cl-] control
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-H+ and Cl- resorption and secretion
-Na+ and Cl- resorption -HCO3- and Cl- exchange |
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General reasons why hyperchloremia may occur
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-[Na+] goes up --> expect inc. [Cl-]
-[HCO3-] goes down --> expect inc. [Cl-] or increased [anion conc.] |
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Hyperchloremia due to Hypernatremia
-reasons |
-Loss of H2O with Na content (diabetes insipidus, osmotic diuresis, osmotic diarrhea)
-pure H2O loss as water vapor |
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Hyperchloremia due to Proximal Renal Tubular Acidosis
-pathogenesis |
-Proximal tubular defect
-HCO3- lost in urine -Acidosis from loss of HCO3- -Cl- retained to maintain electrical neutrality -Hyperchloremic metabolic acidosis |
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Hyperchloremia due to Distal Renal Tubular Acidosis
-pathogenesis |
-Distal tubular defect
-impaired H+ excretion -HCO3- consumption for buffer -Reduced Cl- excretion for electrical neutrality -Hyperchloremic metabolic acidosis |
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Hyperchloremia due to diarrhea
-pathogenesis |
-secretions contain Na+ and HCO3-
-fluid loss -HCO3- depeletion -Cl- fluid left behind -hyperchloremia |
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In what animals is diarrhea and important cause of hyperchloremia?
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-horses
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General reasons for hypochloremia
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-hyponatremia
-increased bicarbonate -increase in unmeasured anions |
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Hypochloremia from hyponatremia can be due to
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-edematous disorder
-dehydration disorder -uroperitoneum -marked hyperglycemia |
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Hypochloremia due to an edematous disorder
-pathogenesis |
-retention of H2O
-dilution of Na+ & Cl- |
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Routes that dehydration can occur
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-renal loss
-intestinal loss -cutaneous loss (sweating in horses) |
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Hypochloremia due to a dehydration disorder
-pathogenesis |
-excretion of Cl- with Na+ and H2O via kidneys, intestines, skin
-H20 moves into vasculature to compensate for hypovolemia -dilution of electrolytes -hypochloremia |
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Hypochloremia due to uroperitoneum
-pathogenesis |
-Na+ and Cl- reabsorbed in the renal tubules
-low Cl- content in urine -urine into peritoneal cavity -Cl- diffuses from the blood and into the peritoneal cavity -hypochloremia |
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Electrolyte balance by the stomach/abomasum
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-H+ secretion
-Cl- secretion -HCO3- production |
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Hypochloremic metabolic acidosis due to vomiting
-pathogenesis |
-Cl- secreted by the stomach mucosa
-vomiting does not allow Cl- to enter the intestine -dec. Cl- in the blood -increase in HCO3- |
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How does vomiting cause paradoxical aciduria?
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-Vomiting causing loss of Cl-
-inc. in HCO3- in plasma -animal becomes hypovolemic -RAS system acitvated -inc. aldosterone production -inc. excretion of K+ and H+ |
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Paradoxical Aciduria
-definition |
-aciduria in the presence of alkalosis
-excretion of hydrogen even though the body is alkalotic |
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hypochloremia due to a metabolic acidosis
-pathogenesis |
-ketoacidosis/lactic acidosis
-increased filtration of unresorbable anions from plasma -Na+ excreted to maintain electrical neutrality -Cl- follows -hypochloremia & inc. HCO3- |
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What can give a falsely high chlorine concentration in a sample?
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-bromide
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[HCO3-] is proportional to
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-[tbCO2]
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Carbonic Anhydrase locations
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-erythrocytes
-renal epithelial cells -gastric parietal cells |
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Inc. [HCO3-]
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-metabolic alkylosis
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Metabolic alkylosis causes
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-conservation by the kidney
-abomasal (displacement, torsion, etc.) -vomiting (pyloric obstruction, etc.) |
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Ways H+causing acidosis is removed from the body
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-buffered by HCO3- and blown off as water w/ CO2 by the lungs
-form ammonium --> released by kidneys -form HPO3- --> releaased by kidneys -H+ --> released by kidneys |
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How is urine pH measured?
-why is this important |
-measured by the amount of free H+ in the urine
-need to remember that that is H+ that is not counted bound to other molecules |
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dec. [HCO3-]
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-metabolic acidosis
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dec. [HCO3-] mechanisms
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-dec. renal loss of H+
-inc. H+ production -inc. HCO3- loss |
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Dec. loss in H+
-causes |
-dec. renal loss (renal failure, urinary obstruction, uroperitoneum)
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Inc. H+ production
-causes |
-hypoxia
-inc. beta-oxidation of fatty acids |
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Dec. [HCO3-] due to hypoxia
-pathogenesis |
-hypoxia
-anaerobic glycolysis -lactic acidosis -increased degredation of ATP -inc. H+ |
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Inc. HCO3- loss
-causes |
-renal tubular acidosis
-diarrhea (horses) -ruminant choke (can't swallow saliva) |
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metabolic acidosis due to Inc. HCO3- loss can also be called
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-secretory acidosis
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Anion gap
-purpose |
-detect an increase in unmeasured anions
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Anion gap
-equation |
Anion gap = [mC+] - [mA-] = ([Na+] + [K+]) - ([Cl-] + [HCO3-])
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Major cations
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-sodium
-potassium |
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Major anions
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-Chloride
-Bicarbonate |
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Unmeasured anions
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-proteins
-organic anions -phosphates -sulfates |
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Why is a normal anion gap near 16-20 mmol/L?
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-protein
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Effect of hypoalbuminemia and hypoproteinemia on anion gap
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-dec. anion gap
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Organic Anions
-examples |
-lactate-
-ketone bodies -ethylene glycol |
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What must be true if there is no change in the [cations] and there is an increase in the [organic anions]?
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-decrease in either [Cl-] or [Hcl-]
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Normochloremic Metabolic Acidosis
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-hypochloremic metabolic acidosis
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-hypochloremic metabolic alkalosis
(occurs with vomiting or GI sequestration of H+ and Cl-) |
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-hyponatremia and hypochloremia
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-hypoproteinemia
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-pseudo-metabolic acidosis
-falsely increased AG |
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Conditions causing an increased AG
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Metabolic acidoses:
-lactic acidosis -ketoacidosis -renal failure -ethylene glycol (glycolate, oxalate) |
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Lactate sink
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-erythrocytes
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major source of lactate in health
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-muscles breaking down glucose
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Cori cycle
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-glucose to lactate via anaerobic glycolysis in peripheral tissue/skeletal muscle
-lactate to glucose via gluconeogenesis in the hepatocytes |
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Formation of Lactate and Acidemia during hypoxia
-pathogenesis |
hypoxia
-anaerobic glycolysis -increased lactate production -production of lactate > liver use -increased [lactate] Hypoxia -anaerobic glycolysis -inadequate ATP production -ATP degredation -inc. H+ production -acidemia |
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How should L-lactate in blood be measured?
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-either using blood or plasma
-process it quickly so that erythrocytes do not add more L-lactate to the sample -decrease L-lactate production by collecting into a tube with NaF or by chilling -collect from free flowing blood to decrease lactate collection from stagnant blood |
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Hyperlactemia
-causes |
-hypoxia disorder
-metabolic disorder -In vitro |
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Hypoxia disorders that result in hyperlactemia
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-stagnant hypoxia (shock, blood vessel occlusion)
-demand hypoxia (strenuous exercise, struggling in restraint) -hypoxemia (respiratory disorder) -hemoglobic hypoxia (anemia, methemoglobinemia) |
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Lactic Acidosis
-definition |
-Lactate + H+ produced from the use of ATP
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Metabolic disorders that result in hyperlactemia
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-grain overload
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Grain overload causing hyperlactemia
-pathogenesis |
-Excess starch intake
-increased formation of L-lactate by ruminal bacteria -increased lactate absorption by ruminal mucosa -increased plasma [L-lactate] |
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In vitro hyperlactemia
-pathogenesis |
-stored blood
-erythrocytes continue glycolysis during storage -L-lactate production -inc. plasma [L-lactate] |
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How a beta-hydroxybutyrate and acetoacetate produced?
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-ketogenesis in the liver
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Beta-hydroxybutyrate
-samples for assays |
-serum
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Acetoacetate
-samples for assays |
-urine
-blood -serum -milk |
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Clinical disorder involving increased ketone bodies
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-ketosis
-ketonemia (blood) -ketonuria (urine) |
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Conditions causing ketonemia
-all mammals |
-starvation
-prolonged anorexia -diabetes mellitus |
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Conditions causing ketonemia
-cattle |
-high energy demands (lactation, lipidosis, diabetes mellitus)
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Conditions causing ketonemia
-dogs |
-high energy demands (lactation, Diabetes mellitus, endurance)
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Conditions causing ketonemia
-horses |
-Diabetes mellitus
-endurance racing |
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Starling's Law
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Pressure gradient = (Pcap - Pif) - (Oncotic cap - Oncotic if)
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Why does water and electrolytes leave arterial capillaries?
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-hydraulic pressure > oncotic pressure
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Why does water and electrolytes enter venous capillaries?
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-oncotic pressure > hydraulic pressure
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Why is the osmolarity of the peripheral capillary bed not very different?
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-difference is only really due to proteins
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What are the biggest contributors to osmolarity?
|
-electrolytes
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Increases in what can cause an increase osmolality (hyperosmolality)?
|
-inc. [Na] & inc. [Cl]
-inc. [urea] and/or inc. [glucose] -foreign substance |
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Instrument used to measure osmolality
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-freezing point osmometer
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How does a freezing point osmometer work?
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-the more solute that is present in the sample, the lower the freezing point will be
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Hypoosmolality can be due to:
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-dec. Na
-dec. Cl |
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How can osmolality be calculated?
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Osmc = 2[Na] + ([UN]/3) + ([glucose]/20)
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In calculating osmolality, what does 2[Na] represent?
|
contribution of all electrolytes toward osmolality
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Assays that measure Na+
|
-direct potentiometry
-indirect potentiometry |
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Direct potentiometry
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-no dilution of sample used for analysis
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Indirect potentiometry
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-dilution of sample during analysis
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Pseudohyponatremia can be caused by:
|
-lipemia
-inc. [TP] |
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How can lipemia or inc. [TP] cause a pseudohyponatremia?
|
-occurs in indirect potentiometry
-lipemia or inc. [TP] causes there to be less water in the sample -H2O portion of the sample becomes more diluted for analysis -same dilution factor is used from a sample w/o lipemia -hyponatremia |
