Exam 3 Flashcards

Question

Review of Renal Function What is needed to concentrate urine? What percent loss of nephrons results in inability to concentrate urine?

Answer 1

-Fluid and solute regulation -Conservation of plasma proteins -Waste removal -Acid-base balance -Synthesis functions Renal plasma flow = plasma flow to the glomerulus GFR is directly proportional to RPF Blood flow to the nephron -Renal artery and segmental branches -Afferent arteriole -Efferent arteriole -Vasa recta: vastly responsible for supplying O2 to the remaining nephron -Venous return -If segmental branch of the renal artery is occluded (embolism) the entire renal segment will eventually necroses. -There is no regeneration of renal parenchyma, remaining cells must undergo hypertrophy to retain GFR Glomerular filtration -Freely pass: water, Na, K, Cl, HCO3, Urea, Creatinine, Glucose, small proteins (light chains), conjugated bilirubin -Large stain in plasma: albumin, unconjugated bilirubin, immunoglobulins, lipoproteins, WBCs, RBCs, Platelets. **Kidneys can maintain H2O retention until ~66% of function is lost** **< 33% function = polyuria** Proximal Tubule -Most everything immediately resorbed -Renal threshold for Glucose Dogs: 180 mg/dl Cats: 280 mg/dl (200 mg/dl if diabetic) Horses: 160 mg/dl Cattle: 140 mg/dl Loop of Henle -Fluid solute regulation -Drops deep into the medullary gradient -Descending loop: water resorption along with urea, Na, Cl, enters filtrate. Reaches highest osmolarity at the bottom -Ascending limb: impermeable to water, lots of solute absorbed, reducing osmolality and adding to medullary gradient. Antidiuretic hormone (vasopressin) -Distal nephron site of important hormonal control -Produced in the hypothalamus, stored in the pituitary -Upregulates aquaporins - increase H2O reabsorption **Without it or if resistance to ADH = polyuria, diabetes insipidus** Aldosterone - Salt conservation: actively exchanges Na, K, and H, -Cl follows Na, water follows too (if ADH active) -If academia or hypokalemia are present, a separate pump results in HCO3 formation, K absorption, and excretion of Cl and H. What is needed to concentrate urine? 1. A medullary gradient 2. ADH 3. Tubules responsive to ADH What percent..? 66% = unable to concentrate urine 75% = Renal Azotemia

Answer 2

Produce -Vitamin D: Major exception horses, they lack 1-alpha-hydroxylase. Instead of calcitriol horses make small amounts of 24,25,-DHCC (vitamin D3). GI absorption of dietary calcium in horses is based on the amount consumed rather than vitamin D activity. -EPO (erythropoietin): mainly produced in response to hypoxia by renal peritubular interstitial cells. HIF-alpha is not degraded as it normally is when there is hypoxia, then it activates transcription of EPO. Rate of EPO transcription is inversely proportional to the O2 carrying capacity of blood. EPO acts as progenitor cells in bone marrow to stimulate increase of both red cell and platelet lineages. As erythrocytes increase the O2 carrying capacity increases and negative feedback for EPO occurs. -Production lost/decrease with chronic renal disease Conservation -Na, Cl: initiating stimuli is dehydration, Na deficiency or hemorrhage. -Ca: Mostly passively resorbed in the PCT. PTH promotes calcium resorption in the ascending limb of the loop of henle and the distal tubule. Renal calcium resorption promoted by calcitriol (minor effect). Exception horses, utilize the kidney as a major route of calcium excretion. -Albumin, antithrombin II: generally decrease with renal disease. Healthy animals pass a small trace amount but typically reabsorbed by PCT. Trace amounts on canine urine dipstick is OK. -Antithrombin II: Thrombotic disease- pulmonary thrombotic emboli, cerebral infarct, renal infarct, saddle thrombus (feline). Excretion -BUN -Creatinine -Phosphorus: Ruminants and equids exhibit extra renal excretion of phosphorus, primarily in saliva and the rumen of cattle. Carnivores take in more phosphorus therefore excrete more. -Potassium -Hydrogen -Lipase -Amylase -Generally increase with renal disease

Answer 3

Azotemia (BUN & Creatinine) -Hyperkalemia: primarily with oliguria and anuria (obstruction) -May occur with acute or chronic renal disease -Bradyarrhythmia can be fatal (the blocked small cat/ruminant) -Metabolic acidosis -Potential misdiagnosis of pancreatitis (Amylase/Lipase) BUN -Blood Urea Nitrogen -Protein catabolism NH4 to UN in the hepatic urea cycle -UN is a small molecule that easily diffuses and equilibrates across total body water compartments (except parts of the nephron) -In most species BUN is primarily excreted renally **Ruminants: microflora degrade urea and assimilate as amino acids, urea is less reliable, favor creatinine, a similar mechanism occurs in equids but to a lesses extend** -Levels depend on renal function, hepatic function, hydration status, and renal perfusion. -Dietary protein intake and rate of protein catabolism **GI hemorrhage results in disproportionate often singular increase BUN** Creatinine -Synthesize in muscle from creatine and creatine phosphate at a fairly constant rate (qualities of a good renal biomarker) -Freely filters through the glomerulus -Proportional to muscle mass, greyhounds have slightly higher values -Not resorbed or secreted across tubules, more specifically correlates with GFR reduction than UN in all species. -Slower to equilibrate across total body water components (4hrs) than urea - better indicator of uroabdomen.

Answer 4

-Accumulation of nitrogenous waste (urea nitrogen and creatinine) -Reflects reduction in GFR; other decent GFR indicators = Phos, Mg, -Primary indicator of renal disease in veterinary medicine -Not synonymous with uremia -Uremia: clinical manifestation of chronic renal failure. Anemia, cachexia, fibrous osteodystrophy, gastritis, hypertension, stomatitis. Azotemia does not develop until renal functional capacity is reduced by 75% **Each doubling of elevated UN and creatinine reflects a 50% loss of remaining renal function** -Urine specific gravity needed: it varies with dehydration status -Dogs: 1.030 -Cats: 1.035 -Large animals: 1.025 -Hypersthenuric: higher than adequately concentrated urine -Hypoesthenuric: lower than adequately concentrated <1.008 -Isosthenuric range: 1.008-1.012 (66% function loss) -Gray zone: 1.013-1.029 Pre-Renal Azotemia -Dehydration artificially increases BUN & Creatinine - Azotemia detected -Many reasons for pre-renal azotemia but NOT renal disease Renal Azotemia -Trashmen don't pick up = Azotemia Post Renal Azotemia -Road is blocked, and trash backs up = Azotemia detected **The threshold for waste detection (azotemia) is static, regardless of which point along the axis the waste comes from; any combination of points may contribute**

Answer 5

-Mechanism: reduced renal blood flow -Reduced RPF = reduced GFR -Hopovolemia: dehydration very common -Shock: systemic vasodilation -Acute hemorrhage -Loss of colloidal osmotic pressure (COP) -Marked hypoalbuminemia Response -Increase release of ADH by hypothalamus -Increase USG -Increase H2O resorption in the distal nephron (sustained reduction of RPF will lead to renal hypoxia, acute renal injury, IV fluids needed). -Juxtaglomerular apparatus detects decrease RPF and triggers RAS -Aldosterone release from the adrenal glands -Renal absorption of Na and Cl increased -Renal plasma osmolality increased -**Stimulates thirst**

Answer 6

-Reflects 75% loss of renal function capacity -Any infrarenal disease that causes a major decrease in GFR -USG that is inadequately concentrated is suspicious -Isothenuric (1.008-1.012) is diagnostic -Same osmolality as ultra filtrate = no tubular alteration **Pre-renal azotemia may occur concurrently & tubules may still be somewhat responsive to ADH, partially masking isoestheouria; USG in that case will be in the "gray zone" of inadequately concentrated.

Answer 7

-Disease distal to the kidney -Urinary tract obstruction (very common in male cats and goats) -Urolithiasis -Mucoid plug -Neoplasia -Prostatic disease -Rapture or leak of post-renal structures, -Trauma such as foals increased abdominal pressure during parturition -Hyperkalemia due to reabsorption from the abdomen -Azomtemia may be moderate to marked (simulated anuria) -USG is variable - use clinical signs to help differentiate (stranguria, etc) -The resulting hyperkalemia can be fatal: Bradyarrhythmia -Post obstruction renal azotemia can develop, trend renal profiles after resolution of inciting cause.

Answer 8

Normal -SA: ~20:1 -LA: ~10:1 (GI metabolism) Increased BUN:Crea -Dehydration (BUN sooner than creatinine) -GI hemorrhage (creatinine doesn't increase) Decreased BUN:Crea -Fluid diuresis (decreed renal absorption of UN) -Non-creatinine chromogens falsely increased creatinine measurement. **Highest ratios occur with pre-renal causes: not very specific assessment**

Answer 9

Acute -Severity of azotemia does NOT differentiate -Acute kidney injury (AKI) -Abrupt renal dysfunction: may or may not be reversible -Faster rate of azotemia increase than chronic renal failure -Usually oliguric or anuric: little time for compensation by remaining nephrons -Labs resemble post-renal azotemia -USG can vary -Usual etiologies: toxins, ischemia, infractions Chronic renal disease (CKD) will lead to -Renal Secondary hyperthyroidism (except equids): Decrease calcitriol =decrease Ca = increase PTH -Mild to moderate non-regenerative anemia = decrease EPO -Severe azotemia does not differentiate -Slow, insidious onset: many nephrons have died off, remaining nephrons hypertrophy -Slow rate of Azotemia increase -Usually polyuric -USG dilute: more solute is presented to the remaining nephrons - solute diuresis. Medullary tonicity may be affected by the disease. Damaged distal nephron cells less responsive to ADH -Signs or uremic syndrome may develop: typically ANEMIA (all domestics) and HYPOCALCEMIA ( except horses). -Usually a life time of gradual renal insults **CKD eventually becomes oliguric then anuric** -Episodes of azotemia spikes with acute reduction in urine production in chronic renal disease - hyperkalemia develops 1. Renal insufficiency: GFR 20-50% 2. Renal failure: GFR <20-25% 3. End stage: GFR <5% **Disease in one part of the nephron will lead to disease in all other parts** -Glomerulus: glomerulonephritis, amyloidosis -Tubules: nephrosis -Interstitium: interstitial nephritis -Renal pelvis: pyelonephritis -Urine Protein:Creatinine: magnitude and significance of proteinuria -Run only when there is proteinuria in the absence of an active sediment (presence of RBCs, WBCs, or bacteria in the urine) -Ratio >0.5 abnormal -Glomerular proteinuria (more severe) assumed with ratio>2.0 and definitions at >5.0 -Acute tubular necrosis: damage from ischemia or toxins. Ischemia usually transient due to severe dehydration. Endogenous toxins: hemoglobin, myoglobin. Haptoglobin neutralizes what it can, then pigmentary nephropathy develops. Reversible if treated early on Early Biomarker of Decreased GFR -Symmetrical dimethylarginine. IDEXX

Answer 10

-Alternative metabolism of BUN and phosphorus in large animals (more so in ruminants than horses) less degree of elevation with renal disease -Calcium is usually decreased in CRF; horses often hypercalcemic (reduced renal clearance). -Cats are better at concentrating urine, may be >concentrated during CKD -Ferrets exhibit less extreme creatine increases than other species. Exertional Rhabdomylosis (ER) disease -Often in horses -Phatophysiology 1. Overworking of unconditioned muscles or trauma 2. Release of myoglobin filtered by the kidneys 3. Myoglobin toxic to renal tubules 4. Myoblobinuria (dark discolored urine clinal sign and UA). Nephrotic Syndrome Disease -Complication of protein-losing nephropathy -Hallmarks: 1. Proteinuria 2. Hypoalbuminemia 3. Hypercholesterolemia: decrease in oncotic pressure stimulates lipogenesis in liver to try to compensate 4. Edema: usually distal limbs

Answer 11

1. Central Diabetes Insipidus -Lack of ADH production by the hypothalamus -Marked polyuria and polydipsia 2. Nephrotic Diabetes INsipidus -ADH resistance Collecting duct -Damaged to distal nephrons cells (CKD decreased polyuric), hypercalcemia, corticosteroids, endotoxemia, hypokalemia, hyperammonemia. 3. Medullary Washout -Disruption to the medullary gradient -Prolonged pr marked fluid diuresis (iatrogenic) -Osmotic diureses (mannitol) -Hypoadrenocortisim (Addison's disease) -Hepatic insufficiency

Answer 12

Recognize the electrolytes commonly measured with routine biochemical testing Learning Objectives * Identify common electrolyte abnormalities in domestic animals Presented by: * Discuss pathophysiology of common electrolyte derangements

Answer 13

A. Electrolyte Entry and Exits -Lytes: Na, K, Cl, and HCO3- -Pets eating main source of electrolytes -Hospitalized patients usually on Isotonic saline to match plasma -Hypertonic NaCl; the artificial RAASzle dazzle -Supplemental KCl -Medications such as KBr interfere = falsely detected as Cl. -Excretion of excess via GI and kidneys -Disease may result in either excess of decreased excretion -Routes of excretion: Renal, GI, cutaneous, cavitary, respiratory. -PE important to confirm or rule out deficiency, dehydration B. Fluid Compartments -ECF: 20% -ICF: 40% -Plasma: 5% -Interstitial: 15% -Blood volume: 8-9% of BW in dogs. Cats: 6-7% of BW -Water: 60% of BW C. Electroneutrality -Balance between cations and anions -Electrolyte shifting: K, Na, H, like to exchange. Cl and HCO3 like to exchange -As an anion species increases, other anions must decrease, or cations must increase, vice versa if cation species increases. -IC or EC location of electrolytes gradient maintenance thanks to ATPases -Interstitial and vascular compartments are practically continuous with one another -Exchanges generally occur within capillary beds. -Proteins remain within the vascular space, exerts colloidal osmotic pressure. -Proteins add only minimally to osmolality. D. Measurement -We measure electrolytes with serum samples. **Don't delay separation** -Falsely increase K: thrombocytosis with PLT activation or leukemia with cell lysis in vitro. -In vitro hemolysis will increase K in cetrain breeds with increased within RBCs potassium. Japanese dog breeds (Akita, Shiba inu), Horses, pigs, most cattle, some sheep. a. Direct potentiometry: I-stat, Catalyst, no dilution step. They measure lytes in only the aqueous portion of plasma, thus no interference with marked lipemia or hyperproteinemia. -Representative of ECF lytes b. Indirect potentiometry: automated chemistry analyzers at reference labs; require dilution steps. Measure lytes based on total plasma volume; hyperlipemic/proteinemic interference due to reduced aqueous phase. Results in falsely decreased lytes values (pseudohyponatremia/chloremia) E. Points of Regulation -ECF is regulated by osmoreceptors and baroreceptors -In most disease states, fluid initially lost from ECF compartment -Water or solutes from ICF move to ECF to maintain tonicity -Exception: external hemorrhage, the compartments remain isotonic to each other. No shifting occurs, hypovolemia will result. Initially HCT does not change as the proportion of RBCs to plasma remains constant. -Once Hypovolemia is corrected by ADH, thirst and RAAS, HCT will be decreased, reflective of hemorrhage. -Hypervolemia: inhibition of ADH release, inhibit thirst, pressure natriuresis (independent of hormones, excrete Na and H2O). Release of atrial natriuretic peptide, which counteracts RAAS. -Fluid loss is characterized by the solute concentration of the lost fluid. -Hypertonic (electrolyte rich), isotonic (neutral), hopotonic (electrolyte poor) **hypotonic fluid loss is the most common. ** Diabetes insipidous -Loss of hypotonic fluid results in hypertonic dehydration (remaining ECF became hypertonic). Water moves from ICF to ECF When contradicting responses occur there is an order of precedence 1. Hypovolemic response 2. Hyperosmolality response 3. Hypervolemic response **Low circulating volume is corrected first**

Answer 14

A. Sodium Overview -Plasma Na is predominantly governed by blood volume and plasma osmolality. -Hypovolemia - RAAS initiates additional Na retention. -Hypervolemia - ANP promotes renal Na wasting, inhibits renin and angiotensisn II -Na must be interpreted in light of patient's hydration status. PE very important, skin tenting, CRT. -Na and glucose are effective osmoles, cell membrane is impermeable, can't cross and exist in large amounts -BUN is only effective in parts of the renal tubules Osmolality = 2(Na + K) +(glucose/18) + (UN/2.8) -Rapid and prolonged elevations in effective osmoles can both lead to neurological disease, so determining effective osmolality is clinically useful Effective osmolality = 2 (Na+K) + (glucose/18) for ease of use = 2(Na) -Rapid elevations in effective osmoles: water leaves cells, including neurons, neuronal shrinkage occurs, neuro signs development. Head pressing. Ex: hypergycemic hyperosmolar syndrome, severe type of diabetes. -Prolonoged elevations in effective osmoles: cells create cytosolic idogenic osmoles to counter ECF osmolarity. Taurine, glycine, glutamine, sorbitol, inositol. If hypotonic fluids are given to an animal with idogenic osmoles, cerebral edema will develop. B. Hypernatremia -Decreased free water intake, frozen, inaccessibility, etc. Primary adipsia/hypodipsia (corpus collosal abnormalily, but rare) -Hypotonic fluid loss: pyrexia, tachypnea, increase insensible losses. Renal: diabetes insipidus (central or nephrogenic), osmotic diuresis. GI: diarrhea and vomiting, osmotic cathartics (sorbitol, phosphate enemas, paintball consumption) -Activated charcoal with sorbitol, repeated dose = hypernatremia. -Excess Na: salt toxicity. pronounced in pigs. Decrease renal excretion Na. Primary hyperaldosteronism (Conn's syndrome, very rare except in cats) C. Hyponatremia -Na deficit with dilution (loss Na containing fluids with subsequent water rehydration) -Renal: hypoadrenocorticism, prolonged diuresis (high fluid rates, diuretics), ketonuria (anion effect), PT dysfunction. -GI: diarrhea, whipworms, pseudo-Addison's. Vomiting, sequestration, pytalism. -Cutaneous: sweating (horses only) -Repeated drainage of cavity effusions. -Edematous disorders: commonly masked by dehydration (Na WRI). Include edema formation due to congestive heart failure, cirrhosis, PLN/PLE, bovine high-mountain disease (bovine CHF, "brisket disease") -Severe burns: loss of lytes and proteins. Shifting: marked hyperglycemia pulls water from ICF to ECF, diluting NA. Glucose of 62 mg/dl = 1 mmol/L Na decrease. Rhabdomylosis = shifting ECF to ICF when many cell membranes are damaged. -Na poor uroabdomen can draw Na from intravascular fluid into the effusion. Na may replace K in ICF during hypokalemia. D. Potassium Overview -Tightly regulated due to narrow range compatible with life -Evaluate in conjunction with acid-base status as shifting relative to H is a critical theme. -If acid-base status is normal serum K tends to reflect total body K. -Sample handling is critical to prevent false increased K. **Do not analyze K if samples collected in K-DETA tubes** -Aldosterone is directly stimulated by hyperkalemia, however, hypokalemia does not inhibit aldosterone secretion. Rather in hypokalemic states, an alternative pump is activated that reduces renal excretion of K. **Recall hyperkalemia can lead to bradyarrhythmia** E. Hyperkalemia -Shifting (ICF to ECF): inorganic metabolic acidosis as H builds up it enters the cell and K moves out. -Rhabdomylysis. -Tumor lysis syndrome -Marked intravascular hemolysis in K rich species and breeds. -Insulin moves K into cells, so insulin deficiency (Type I DM) and resistance (Type II DM), insulin resistance in horses, may result in hyperkalemia -Increase in total body K: decrease renal excretion in distal tubules. Hypoadrenocorticism, oliguric or anuric renal disease, urinary tract obstruction, urinary track leakage within the body. -Oversupplementation with K rich fluids -Na:K ratio <27 suggestive of hypoadrenocorticism. -Severe diarrhea, whipworms in SA (pseudo-Addison's); HCO3 loss, acidemia contributes to K increase. -Anuric/oliguric renal failure or urethral obstruction. -Diabetes mellitus with ketonuria. Glucose draws water out of cells diluting Na, which is also lost in urine due to anion effect and osmotic diuresis F. Hypokalemia -Shifting ECF-ICF. Metabolic alkalosis: H leaves the cell, exchanging for K; additionally, most alkaloses present with hypovolemia, so RAAS promotes renal K wasting. -Insulin activity increase drives K into cells: insuloma (ferrets), insulin overdose (wrong insulin syringe) -Decrease total body K: anorexia, as most diets are K rich, voluntary or involuntary anorexia leads to hypokalemia; typically mild, may be more pronounced in large animals. -Increase K renal loss: Increase renal excretion with anions (anion effect; occurs with some organic metabolic acidosis). -Polyuria: decrease lectrolytes -Loop and thiazine diuretics -Primary hyperaldosteronism - CATS! -Increase GI loss: vomiting diarrhea, sequestration, ptyalism = especially relevant in large animals, "choke" in horses. Sweating in horses.

Answer 15

A. Chloride Overview -Mostly does whatever CL is doing -Whenever Na and Cl are disproportionate to each other relative to their reference intervals, there's an acid/base trickery afoot. -Sometimes the disparity is obvious. Often we need to calculate corrected chloride 1. Find the mean Na. Upper value RI minus low value, divided by 2, then add to lower value. 2. Divide mean by the measure valued of Na 3. Multiply that value with the measured value of Cl B. Hyperchloremia -When following Na, causes for hyperchloremia are the same as for hypernartremia. -Disproportionate increase in Cl relative to Na = hyperchloremic metabolic acidosis. GI loss of HCO3 and Na due to secretory diarrhea (common in calve scours) or salivary loss (cattle). Renal loss: HCO3 due to proximal or distal renal tubular acidosis (Cl retained). False with increase KBr. C. Hypochloremia -When following Na, causes for hypochloremia are the same as for hyponatremia. -When there is a disproportionate decrease in Cl relative to Na = hypochloremic metabolic alkalosis. GI sequestration of CL due to vomiting, displaced abomasum, gastric reflux (horses), pyloric outflow obstruction; HCO3 serves as the anion for Na absorption instead of Cl. -Renal wasting chloride due to loop or thiazine diuretics. -Hypochloremia can also develop with certain acidosis -Filtered lactate, ketones, ethylene glycol metabolites are unable to be resorbed in the renal tubules. -By anion effect, they drag Na along and reduce the gradient Cl relies on for resorption, encouraging excretion. -Additionally the hypokalemia pump from before activates during acidemia and excretes Cl in order to conserve HCO3, H is excreted and balances Cl. D. Bicarbonate -HCO3 is a base; it functions as a buffer to maintain pH. -H+HCO3 -H2CO3 - H2O + CO2 -Made from water and CO2 in cells that express CA (carbonic anhydrase), proximal renal tubular cells, intercalated cells of the collecting ducts, parietal cells of gastric and abomasal epithelium, exocrine pancreatic epithelial cells. RBCs. -HCO3 and TCO2 are used interchangeably to assess metabolic acid-base status -95% of CO2 and HCO3 formed at pH 7.4

Answer 16

Osmolal Gap -Need special equipment -The difference between measured osmolality and calculated osmolality Osmolal gap = mOSMO - cOSMO -Recall calculated osmolality takes into consideration Na, K, BUN, glucose. -The osmolal gap increases when a non-ionic osmole is present -Pseudohyponatremia from a markedly lipemic or hyperproteinemic sample measured with indirect potentiometry will also result in falsely increased osmolal gap. -Normal osmolal gap is < 10mOsm/kg -If pseudohyponatremia has been ruled out, a result > 10 mOsm/kg indicates presence of non-ionic osmole such as: Mannitol Ethylene glycol Ethanol Methanol Contrast media (radiographs) **only detects non-ionic osmoles because changes in ionic compounds is always balanced, resulting in unchanged osmolality** Anion Gap -The difference between measured cations and measured anions. Anion gap = (Na+K) - (Cl + HCO3) -When increased beyond the upper RI limit, there are more unmeasured anions that under physiological conditions. Occurs when accompanying decrease in HCO3. This represents a high anion gap metabolic acidosis -Increases in proteins will mildly increase the anion gap; likewise decreases in proteins will midly decrease the anion gap. -The main unmeasured include: Ketones Lactate Uremic acids Metabolites of ethylene glycol Salicylic acid (aspirin). -Decrease anion gap values are not clinically significant and usually reflect hypoproteinemia

Answer 17

Recommend appropriate tests to evaluate for acid-base disorders Click to add subtitle Learning Objectives * Identify common acid-base abnormalities in domestic animals Date: * Discuss pathophysiology of common acid-base disorders

Answer 18

Introduction -The overall acid-base status is evaluated by measuring pH -pH is the negative log of [H+]. Thus pH scale relates inversely with [H+]. It takes large changes in hydrogen concentration to change the pH. -Normal blood pH is physiologically 7.4-7.5 -Slight variations occur between species and diets. -Blood pH <7.4 = acidemia -Blood pH >7.5 = alkalemia -Changes in pH may reflect changes in H+ production, excretion, and/or buffering -H is removed from plasma by buffers -HCO3 (H2CO3) is the main buffer, though other buffers contribute PO4, NH3, Sulfates, Hemoglobin, Albumin. - Acid/base primarily regulated by kidneys and lungs -Kidneys: PO4 and NH3 for excretion. Dogs have been shown to increase production of NH3 during acidemia. HCO3 is filtered freely and efficiently conserved. Acidemia stimulates aldosterone to excrete H+ and intercalated cells respond to states of acidemia with HCO3 synthesis. -Lungs: expiration of CO2 drives H+ buffering. This process consumes HCO3 as well, but there's significantly more HCO3 available than H+ that needs to be buffered. Because CO2 expiration drives H+ buffering, then partial pressure of CO2 (PCO2) can be used to assess respiratory acid status. -Henderson-Hasselbalch: as ventilation increases, more CO2 is expired, H decreases alongside PCO2. As ventilation decreases less CO2 is expired, H increases alongside PCO2. -Acid-base status is only completely assessed when arterial blood samples in conjunction with serum biochemistry. -Blood gas does not tell you about mixed acid-base disturbances. -Serum alone will only give an idea on metabolic side -With renal and tubular acidosis urinalysis is additionally needed. -Venous samples acceptable but can't assess oxygenation (decrease pH and increased POC2) -Arterial blood samples should be collected in a heparinized syringe, no air in the syringe. Tests and Terms -pH provides overall acid-base status -PaCO2/PCO2: partial pressure of CO2 (a= arterial); represents the respiratory acid, use to interpret respiratory acid-base status. -TCO2/HCO3: main base of the extracellular fluid, usually given as TCO2 on blood gas; represents the metabolic base, use to interpret metabolic acid-base status. -PaO2: partial pressure of O2; idea of oxygenation -BE: base excess, redundant when TCO2/HCO3 Simple Acid-Base disturbances -Have a single primary disturbance (metabolic or respiratory), usually with compensatory response by the alternate system -A primary respiratory disturbance is met with a compensatory metabolic response and vice versa. -Note: compensatory response is almost never enough to normalize pH, except if the respiratory insult is chronic and mild. **If the untreated pH is normal you should consider the possibility of two primary opposing disturbances. -Respiratory compensation begins immediately. Metabolic within hours but takes days to reach a peak response, but generally more effective -In simple acid-base disturbances the pH matches the system abnormality and represents the primary disturbance, the arrows are in same direction.

Answer 19

Metabolic acidosis -Decrease TCO2 or HCO3 -Primary metabolic acidosis if decrease pH matches an acidemia -Respiratory compensation decrease PCO2, increased expiration = increased H+ buffering. Tachypnea expected. **Primary metabolic acidosis with compensatory respiratory alkalosis** Major metabolic acidosis -Titrational metabolic acidosis: a.k.a HIGH ANION GAP metabolic acidosis. Indicates increase in unmeasured anions that are acidic species. Ketoacids, lactic acids, uremic acids, ethylene glycol metabolites, salicylic acid. KLUES. **Diagnosis hinges on increased anion gap** Organic acids are less likely to cause H+ shifts (all listed except salicylic acid). -Ex: diabetic cat with ketoacidosis = tritational metabolic acidosis. -Secretional metabolic acidosis a.k.a hyperchloremic metabolic acidosis and normal anion gap metabolic acidosis. -Characterized by loss of HCO3. GI origin, diarrhea (calf scours), LA salivary loss, vomiting of intestinal contents (rare). Renal origin, renal tubular acidosis HCO3 loss in proximal tubular or lack of synthesis in the distal tubules; necessitates Cl retention. **Diagnosis hinges on a disproportionately increased Cl and Na, recall corrected chloride. Minor metabolic acidosis -Dilution metabolic acidosis (FYI) -A small acidic effect that results from dilution of plasma with free water gains or rapid IV fluid infusion. Negligible.

Answer 20

-Increased TCO2 or HCO3 -Increased pH when it matches an alkalemia -Increased PCO2 decreased expiration = decreased H+ buffering. Bradypnea expected. -Primary metabolic alkalosis with compensatory respiratory acidosis Major metabolic alkalosis -Hypochloremic metabolic alkalosis Minor metabolic alkalosis (FYI) -Contraction alkalosis: increased HCO3 due to loss of HCO3 poor fluid commonly with hypochloremic -Renal loss of H+ loop or thiazine diuretics. Hypokalemia K resorption costs H+ -Intracellular shifting of H+ during hypokalemia. Hypochloremic metabolic alkalosis -Occurs due to loss or sequestration of HCL -Companion animals typically due to vomiting or pyloric outflow obstruction -Cattle: abomasal sequestration -Horses: esophageal reflux, ileus -May present with paradoxical aciduria: may occur with concurrent hypovolemia. Under RAAS influence Cl typically is absorbed along with Na, but with previous loss of HCl, Cl is temporarily sparse in the urine. **H+ and K are lost to maintain electroneutrality, thus the urine is acidic despite alkalemia**

Answer 21

-Increase PCO2 decreased expiration = decreased H+ buffering -Primary respiratory acidosis when pH decreased -Compensation: Increased TCO2 or HCO3 Primary respiratory acidosis with compensatory metabolic alkalosis. -Hypoventilation: includes decreased respiratory rate, but also other factors - dead space, functional alveoli, etc. -Diseases that impair alveolar gas exchange: infection, pneumothorax (spontenous in Huskies!), pulmonary fibrosis (WHWTs!), tracheal collapse, pleural effusion, neoplasia, diaphragmatic hernia. -Respiratory muscles inhibition: tetanus, botulism, tick paralysis, severe hypokalemia, myasthenia gravis. -Drugs, anesthetics, sedatives, narcotics -Brain stem disease.

Answer 22

-Decrease PCO2, increased inspiration = increased H+ buffering -Increase pH -Compensation: decreased PCO2 or HCO3 -Note: with chronicity this compensation may normalize pH -Primary respiratory alkalosis with metabolic compensatory metabolic acidosis. -Occurs with hyperventilation: hypoxemia, altitude sickness, severe anemia. -Heat stroke, septicemia, drugs (salicylates) and aminophylline. -CNS disease -Pain/anxiety

Answer 23

-Consist of two or three primary disturbances -May include any combination 1. Respiratory acidosis or alkalosis 2. Metabolic acidosis 3. Metabolic alkalosis -Mixed metabolic acid-base disturbances are fairly common in companion animals and ruminants, especially with particular disease processes: -Companion animals: vomiting with renal disease, vomiting with diabetic ketoacidosis -Ruminants: displaced abomasum with lactic acidosis, calf scours with lactic acidosis. When to suspect mixed disturbances -Unexpected pH - normal in the presence of altered PCO2 and/or TCO2. -Change is pH is greater than expected: may indicate compounding primary disturbances -PCO2 and TCO2 increase/decrease opposite to the other: compensatory response should be parallel to change -Compensation is inadequate or hasn't occurred within the expected time frame. Respiratory immediately, metabolic hours to days

Exam 3 Flashcards

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