clin chem exam 1
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119 terms
Terms | Definitions |
|---|---|
 Clinical Chemistry | --analysis of body substances and interpretation of resultant data as an AID to dx, tx, prognosis --body substances = blood, serum, plasma, urine, CSF, transudates, exudates, feces, intestinal liquids, breath gases, amniotic fluids --induces that a pathologic change can be distinguished from a non-pathologic change --req. a point of reference to compare |
| Point of Reference = Reference interval | an interval of values within which a majority of healthy patient's values lie; used to make comparisons |
| Reference interval design | 1. set of selection criteria for reference individuals is chosen; only those individuals meeting the criteria are used and representative values are obtained from this reference population 2. reference interval includes 95% of the values obtained from the criteria-based poplulation; ~120 animals are tested if possible (rare); reference interval = mean +/- 2 SD of a bell-curve (Gaussian) distribution; 5% of healthy individuals have values outside the reference range; mathematical manipulation necessary to establish 95% interval for significantly non-Gaussian distributions |
| Potential Selection criteria: Animal Factors | 1. healthy (most common) 2. Population parameters --Species (most common): Hct higher in dogs vs. cats --Age : animal older than 1 year --Breed: active breeds have higher Hct --Sex: males have higher Hct 3. Environmental/Physiologic --Diet (BUN-->protein in diet) --fasted or not --pregnancy --excitement --body condition (CREA higher in well-muscled animals) --altitude (rbc increases with elevation) --meds (corticosteroids increase neutrophil and ALP) |
| Potential selection criteria: pre-analytical factors | Specimen handling and collection 1. collection site (capillary wbc higher than venous blood) 2. anticoagulant 3. sampling time 4. post-collection interval before testing 5. storage conditions (glu) |
| potential selection criteria: laboratory factors | 1. analytical factors-->may preclude use of another lab's ref ranges for your tests --instrumentation --methodology --reagents --instrument calibration standards 2. statistical method used to derive ref interval --bell-curve population : mean +/- 2 SD --skewed populations: transform data to obtain bell curve |
| Assumptions made when using ref interval | 1. reference population is representative of the patient population for important criteria 2. unused selection criteria (age, diet, etc.) cause only small variation in results 3. dz causes large changes in test results (vs. influence of unused criteria) so dz animals can be distinguished from healthy --these assumptions are not always valid-->ex. the assumption that age doesn't significantly influence test values in heatlhy cattle is wrong!!! liver tests change!!! |
| False + results | -false positive result = identifying a healthy individual as unhealthy -5% probability of a false positive result when running one test based on method of establishing ref. ranges -running multiple tests increases the change of obtaining a false + result |
| Differentiating the 3rd SD from pathologic values | 1. 3rd SD of healthy animals outside reference interval by only a small amount; diseased animals may have only small abnormalities, but unlikely that a healthy animal will have a large abnormality 2. 3rd SD values unlikely to occur in multiple tests for a similar function: abnormal values in multiple related tests supports a pathologic change (if both BUN and CREA elevated, probability that both are 3rd SD is small) 3. lack of clinical symptoms consistent with abnormal values suggest animal is probably healthy |
| Value of Sequential data | -"more diverse population parameters the wider the ref. interval" -wide ref. interval decrease sensitivity of dz detection; illness may change test results but magnitude of change may be less than the width of the reference interval -PRACTICE COMPARISON WITH SELF AS REFERENCE RATHER THAN WITH A GROUP REF INTERVAL |
| Profile or panel approach to biochemical analysis advantages vs. disadvantages | Biochemical profiliing = organization of clinical chemistry data into groups of related or complementary tests Advantages: 1. consistent, orderly approach to data interpretation 2. integration of data (interpret renal profile in light of lytes and acid-base data) 3. increase confidence in results (multiple tests supporting similar change) 4. increase discrimination (when similar tests are discrepant -high BUN, normal CREA?) Disadvantages: 1. increased probability of false positives 2. more tests = more money! |
| Sample types | --most commonly use serum (from clotted blood in red top tube) --heparinized samples (green top) for plasma-->used for LA for STAT! samples to avoid long clotting time (horse) --purple top prevents clotting by chelating calcium via edta and makes assay inaccurate |
| collection / handling | -fasted samples are preferred as it represents reference range --clean stick, let clot, and remove serum --cells continue to use glucose (glucose decreases 8-10% per hour) |
| interferences | --hemoglobinemia, lipemia (hemolysis due to membrane damage) --drugs, analytes (bromide-->halides identified by most lyte analyzers as high chloride levels) |
| Renal Functions | 1. regulation of water, electrolytes, and acid/base balance 2. excretion of metabolic wastes 3. excretion of foreign chemicals 4. regulation of arterial blood pressure 5. regulates rbc production 6. regulates vitamin D activity 7. gluconeogenesis **Processes** 1. filtration 2. active transport 3. osmosis |
| renal susceptibility to injury | 1. high metabolic rate (0.5% body weight, 10% of O2 consumption) so easier to damage if ischemic 2. high level of exposure to toxins because it filters |
| Reserve capacity of kidney | -66% nephron loss before loss of concentrating ability is detected (tubular dysfunction) -75% nephron loss before getting an increase in nitrogenous wastes (azotemia--glomerular dysfunction) Conclusions: 1. only 1/3-1/4 necessary for adequate function 2. lab assessment ~ insensitive!! 3. progression: dz-->lab change-->clinical signs 4. renal dz does NOT = renal failure!!!! (there can be extensive dz before signs of renal failure) |
| Nephron components | -segments are histologically and functionally distinct 1. bowmans capsule (renal corpuscle) 2. proximal convoluted tubule 3. loop of henle (descending/ascending) 4. distal convoluted tubule 5. distal collecting tubule 6. collecting ducts |
| Blood supply to kidney | 1. Nephron associated components: afferent arteriole, glomerular capillary tuft, efferent arteriole, vasa recta (all supply oxygenated blood) 2. fxns to inititate urine formation via glomerular filtration, supply metabolic needs, maintain medullary osmotic gradient, and recover components transported out of the urine and into the interstitium --in hypovolemia (shock), azotemia develops before ischemic injury bc bp in glomerulus must be greater than bowmans space to produce filtration, so as bp drops, wastes are not readily removed |
| Glomerulus anatomy | 1. endothelium = retains cells (60-100 nm) 2. basement membrane = retains large proteins 3. slit pores = retain most proteins (6-9 nm; alb ~7 nm) 4. sialoglycoprotein charge (negative)= repels proteins; albumin is negatively charged so that it stays on the plasma side; this charge is damaged in DM and amyloidosis |
| Glomerular filtration forces ( + vs -) | Positive = blood hydrostatic pressure (B-hp) Negative = Capsular hydrostatic pressure (C-hp) Blood oncotic pressure (B-op) |
| impact of CHF on glomerular filtration | drop Bhp because a drop in CO; drop net filtration and gfr |
| impact of severe hypoproteinemia on gf | drop in Bop causes an increase in net filtration |
| impact of obstructed ureters on gf | increase Chp and drop net filtration |
| impact of hypovolemic shock on gf | drop in Bhp drops net filtration |
| impact of polydipsia on gf | increase Bhp increases net filtration |
| major fxn of glomerulus | filtration |
| What is the major fxn of proximal tubules? | reabsorb nutrients, electrolytes, and glucose |
| What is the major fxn of the descending loop? | reabsorb water via osmosis |
| What is the major fxn of the ascending loop? | reabsorb sodium and chloride via active transport as they are moving against concentration gradient |
| What is the major fxn of the distal tubules? | reabsorb sodium under influence of aldosterone and K+ is secreted |
| What is the major fxn of the collecting ducts? | reabsorb water under influence of ADH from the pituitary gland to cause AQP to assemble into a pore; absorption of urea via passive diffusiong depending on flow rate (polyuric doesn't allow time for diffusion) |
| Primary Renal panel | 1. BUN 2. CREA 3. urine SG 4. urinalysis a. physical examination b. chemical examination c. urine sediment examination |
| Secondary renal panel | 1. electrolytes (calcium, P, Mg, Na, K, Cl) 2. acid-base (TCO2, AG, lytes, urine pH) 3. cholesterol |
| Creatinine sources | --purpose is to eliminate excess nitrogen (3) --endogenous production related to muscle mass --creatine phosphate = energy source for muscle contraction creatine + ATP <--> creatine-phosphate + ADP --creatinine is a degradation product of creatine; freely diffuses out of muscle cells and takes about 4 hours to equilibrate throughout body fluids (vs BUN 1.5 hours) --conditioning horses and rhabdomyolysis may be assoc. with increased values --dietary intake of meat is only a minor role but in strict carnivores accounts for up to 25% |
| creatinine excretion | --freely filtered by the glomerulus without reabsorption by the tubules --secreted by tubules in male dogs and humans; and very much so in goats (can't do creatinine clearance; use imulin) --minimal loss through gi and sweat (clinically insignificant) |
| Creatinine measurement and interpretation | --Jaffe's rxn (1886) is the oldest in use --potential interferences with non-creatinine chromagens; ketones are a main problem (use dry reagents to filter out) --generally as CREA rises, gf drops; as CREA drops, gf rises --then consider muscle mass and diet (minimal)-->creatinine drops in cachectic patients |
| BUN sources | protein catabolism (deamination) --protein breakdown-->ammonia--> urea (less toxic) -from normal turnover of tissues, corticosteroids, fever and dietary proteins |
| BUN non-renal + influences | 1. enteric hemorrhage (mod) 2. high protein diet (min) 3. terminal starvation (rare, mild) 4. severe burns (rare) |
| BUN non-renal - influences | 1. anorexia of 3-5 days (mild) 2. low protein diet (KD diet) 3. decreased liver fxn 4. anabolic steroid |
| excretion and interpretation of BUN | --all renal handling is by passive diffusion; freely filtered from the glomerulus, tubular reabsorption occurs depending on flow rate (40-60% in distal tubule); reabsorbed urea in renal medulla aids in water absorption osmotically --gi route is minor and of little influence on serum values; ruminants and azotemia-->bacterial degradation may keep BUN< CREA; not detected in feces --generally as BUN rises gf drops and as BUN drops gf rises; then consider diet/nutrition, liver |
| azotemia | -abnormal accumulation of nitrogenous wates in blood -may be asymptomatic and can occur without renal failure |
| uremia | clinical signs associated with renal failure --vomiting, anorexia, dh, gi ulcers, gi hemorrhage, mineralization of soft tissue, tachypnea, acidosis, lethargy |
| Isosthenuria | -urine solute concentration~ to plasma (no animal should have persistently) -measured by SG or osmolality -SG 1.008-1.012 -can occur in healthy pet (dogs) |
| Adequate urine concentration | minimum urine SG that is consistently attained in healthy animals when faced with a need for water conservation dog - >1.030 cat >1. 035 other > 1.025 |
| Prerenal azotemia | azotemia + adequate urine concentration; does not involve renal parenchymal changes in response to extrarenal changes --decreased blood flow to kidneys 1. decreased blood volume (dec. glomerular blood flow) from dehydration, vomit, dh, blood loss 2. altered blood flow (with normal or increased blood vol) due to decreased CO, neurogenic shock/vasodilation --increased production of nitrogenous wastes from high protein diet, gi hemorrhage; BUN not equal to CREA, SG variable and depends on other gf influences |
| Renal Azotemia | azotemia + inadequate urine concentration -often used interchangably with renal failure/renal insufficiency -2 Components!!! 1. BUN, CREA elevated-->localizes to glomerulus-->evaluates glomerular filtration/waste excretion 2. urine SG (dilute)-->localizes tubules-->evaluate water conservation |
| Primary renal azotemia | decreased functional renal mass (most common) -loss of 75% of glomeruli and 67% tubules in both kidneys -prognosis generally guarded and depends on reversibility of the insult and compensatory ability of the remaining nephrons) |
| Secondary renal azotemia | less common; loss of fxnl ability but renal parenchyma may be relatively unaffected -decreased gfr (prerenal type) + secondary tubular dysfunction (not parenchymal loss) -Mechanisms for compromised tubular ability 1. ADH deficiency (DI) 2. tubules refractory to ADH (secondary DI): hypercalcemia interferes with ADH receptor and release; hypokalemia disrupts AQP assembly; pyometra toxins, pyelonephritis toxins, Cushings dz glucocorticoids interfere with ADH receptor 3. loss of medullary osmotic gradient Prognosis: (often favorable to excellent) depends on: 1. restoring renal blood flow to correct prerenal azotemia 2. recognizing as a secondary process!! 3. correcting the underlying primary process |
| Post- renal azotemia | azotemia + variable SG -can't be conclusively id by primary renal profile alone; dz depends on history, PE, imaging -obstruction/breach in post-renal urinary tract (urinary calculi, ruptured bladder, torn ureter/urethra, congenital malformation) |
| Secondary renal profile: cholesterol | increases seen in renal dz/failure; primarily associated with decreased albumin (glomerular lesions, nephrotic syndrome) -increases are seen in numerous organ/endogcrine pathologic states so it has limited usefulness -important ddx include: renal dz (protein losing nephropathies/nephrotic syndrome); hepatobiliary dz (cholestasis); pancreatitis; DM; Cushing's, hypothyroidism -decreases in chol commonly associated with decreased hepatic production (decreased liver mass from shunts, cirrhosis, cancer) |
| Name the 3 major parts of a complete urinalysis | 1. physical examination 2. sediment examination 3. chemical examination |
| List urinary components that can contribute to increased urine turbidity/cloudiness | cells, protein, mucus, crystals, lipid --normally in most spp is transparent --horses normally cloudy due to mucus /crystals (Ca carbonate crystals) --rabbits can look pyuric (carbonate and oxalate crystals) |
| Define adequate urine concentration and list cut-off value for dogs, cats, and other spp. | Adequate urine conc. is the minimum SG that should occur with the need to conserve fluid Dog >1.030 Cat > 1.035 other > 1.025 |
| Define urinary tract hemorrhage and distinguish it. | 1. increase in intact rbc in sediment 2. elevated occult blood on test strip 3. discoloration of the sample (pink/red) |
| Define urinary tract inflammation and distinguish it. | 1. increased number of wbc 2. wbc casts are present (if inflammation is in kidney parenchyma) 3. increase in turbidity |
| Define physiologic pre-renal proteinuria and distinguish | something is occurring extra-renally that is impacting protein handling 1. transiently increased glomerular permeability 2. seen more frequently 3. in assoc. with redness, swelling, increased vascular permeability of capillary tuft enabling more albumin to be released (systemic response) 4. shocky patients 5. should NOT see elevated wbc |
| Define overflow pre-renal proteinuria | exceeding tubular resorptive capacity 1. overlow proximal tubule capacity to absorb small MW proteins; assumes glomerular function is normal 2. Associated with multiple myeloma 3. Associated with rhabdomyolysis from spilowver of myoglobin into urine (dark brown color) |
| Define primary renal dz and distinguish | can be due to glomerular or tubular dysfunction-->glomerular is more common and a UPC may be helpful to confirm if its glomerular or tubular or a combination of the two |
| Describe the two main mechanisms by whcih glucosuria occurs and list examples of specific conditions/dz that lead to glucosuria by each mechanism | 1. exceeds renal threshold (DM) 2. damage/reduction in renal threshold with normal glucose (melamine toxicosis) |
| Name 3 ketone bodies and id one that is not routinely detected on the urinalysis chemistry strip | 1. acetone 2. acetoacetate 3. beta hydroxybutyrate beta hydroxybutyrate is commonly not detected |
| Explain why ketones are forming in the body | negative energy balance and body is breaking down fatty acids for energy |
| List clinical conditions/dz associated with increased ketone formation | DM, parturition, lactation, starvation |
| Name a single additional change/finding in the UA that would stronly support that ketonuria was due to DM | glucose on the UA |
| Explain the term renal threshold. What is it for dogs, cats and cows? | renal threshold = the amount of glucose that can be reabsorbed by the proximal tubules dogs/others == 180 cow= 100 cat= 280 |
| Name the form of bilirubin present in urine, and explain why only this form is present compared to the other forms of bilirubin | only conjugated bilirubin is excreted because unconjugated bilirubin is protein bound and therefore too large to be filtered. Although delta bilirubin is also conjugated, it is also protein bound and therefore too large to be filtered |
| Name the form of bilirubin detected by urine chemistry test strip. What is the confimratory tablet test for bilirubin called? | conjugated bilirubin is sensed by chem strips The confirmatory tablet test for bilirubin is the ictotest which is more sensitive because it turns purple and easier to interpret with dark urine samples |
| List the 3 primary things that are detected by urine occult blood test strips and the process that each item typically represents. | 1. Hemoglobin--hemolysis, spill over after IV hemolysis (may contribute to protien, check HCT, rbc morph, pink/red serum as haptoglobin is saturated) 2. myoglobin--rhabdomyolysis (history, PE, clear serum, spectrophotometry, CK, AST) 3. rbc--hemorrhage (patchy chem strip distribution, recheck supernatant should be clear after spinning, examine sediment) |
| Identify the change in pH that occurs over time as a urine sample is stored and explain why. | alkalinization occurs over time as samples are stored because carbon dioxide is lost if the sample is not sealed; also bacteria with urease breaks down urea and the resulting ammonia alkalinizes the urine in vitro |
| Explain the mechanism by which certain bacteria can cause urine to become more alkaline. | bacteria with urease breaks down urea and the resulting ammonia alkalinizes the urine in vitro |
| List alterations in the urine/urinalysis that may occur if the urine pH is alkaline. | breaks down organic components and can falsely elevated protein values suggesting proteinuria |
| Id the section of the urinary tract in which urinary casts are formed. | distal tubules and ascending loop |
| Name the mucoprotein that forms the matrix for casts. | Tamm-Horsfall mucoprotein secreted by DCT epithelial cells |
| Name the process indicated by the presence of epithelial, granular, or waxy casts. | epithelial-->dilated tubules with severe renal disease/failure granular--> tubular degeneration; always considered pathologic Waxy casts--> tubular degeneration; +-slowed transit |
| Explain how pyelonnephritis may be distinguished from cystitis solely from UA results | if rbc and wbc CASTS are seen, this localizes to renal inflammation and hemorrhage (glomerular/tubular) rather than resulting from cystitis |
| Name two urine crystals that are naturally pigmented | leucine and urate crystals bilirubin and sulfa-type drugs |
| Name urine crystal commonly found in Dalmations | Ammonium urate (biurate) |
| Name and recognize the crystals associated with: 1. ethylene glycol 2. hepatic insufficiency 3. cholestasis | 1. ethylene glycol = calcium oxalate (monohydrate form) 2. hepatic insufficiency = Ammonium urate (biurate) 3. cholestasis = bilirubin granules/clusters |
| Name the dumbell-shaped crystal commonly seen in health LA | calcium carbonate |
| List the blood gas parameters that are measured and calculated | 1. pO2 2. pCO2 3. pH 4. HCO3 (calculated) 5. TCO2 |
| Explain the relationship btw TCO2 and HCO3 | ... |
| Define acidemia | a decrease in blood pH |
| Define alkalemia | an increase in blood ph |
| Define acidosis | condition leading toward a decrease in blood ph |
| Define alkalosis | a condition leading toward an increase in blood pH |
| Id blood gas parameters that are primarily assoc with metabolic disorders | HCO3 |
| Id blood gas parameters that are primarily associated with respiratory disorders | pCO2 |
| id whether compensation of blood gas abnormailities involves movement of respiratory and metabolic parameters in the same or opposite directions and explain | when one parameter becomes altered, the body compensates by changing the other parameter in the SAME DIRECTION to maintain the 20:1 ratio, or ph 7.4 |
| List ex. of conditions leading to respiratory acidosis | anesthesia, CNS dz, or severe pulmonary dz with diffusion rates of CO2 20x>>O2 |
| List. .ex. of conditions leading to respiratory alkalosis | fear/pain, moderate pulmonary dz, iatrogenic increased bagging during anesthesia |
| list ex of cond. leading to metabolic acidosis | secretional gi or renal loss |
| list ex of cond leading to metabolic alkalosis | H+ loss or sequestration, iatrogenic, hypokalemia with dehydration |
| provide the anion gap formula from memory | AG = (Na+ + K+) - (HCO3- + Cl-) |
| list two unmeasured cations and at least 5 unmeasured anionsthat may be found in blood in health or dz | unmeasured cations = Ca++, Mg++ unmeasured anions= lactate, phosphate, albumin, sulfate, ketones |
| id the specific type of acid-base distubanc e most commonly associated with increased anion gap. List the 5 specific causes for this type of acid-base distrubance as listed in class | Titrational metabolic acidosis Endogenous Anions 1. uremic acids (renal azotemia) 2. lactic acids (lactic acidosis) 3. ketoacids (ketoacidosis from pregnancy, lactation) Exogenous Anions 4. ethylene glycol intoxication (glycoaldehyde-->glycolic acid, glyoxylic acid, oxalic acid) 5. salicylate (aspirin) intoxication |
| id the most common cause for a decrease in anion gap; what causes a negative anion gap? | decreased ag= hypoalbuminemia neg AG consider bromide from KBr for seizures because the bromide is mistaken for chloride and gives a non-physiological increase in chloride |
| id which change in anion gap is likely to be of greater clinical significance: an increase or decrease and explain | Increase: because that would indicate more pathologic changes in the body. Whereas decreased AG only really indicates hypoalbuminemia or a change in Br-. |
| List 3 ways of detecting metabolic acidosis on chem panel w/o blood gas. | decreased TCO2, increased anion gap, little change in Cl- vs. Na+ --> Titrational decreased TCO2, little change in anion gap, increased Cl- vs. Na+ --> Secretional so the 3 ways to detect are TCO2, anion gap, and Cl- vs. Na+ |
| Explain the mechanistic difference between a "secretion" and a "titration" metabolic acidosis; how does each occur? | Secretional = bicarbonate loss from upper gi dh or salivation in ruminants Titrational Metabolic Acidosis = occurs in presence of organic acid excess from renal azotemia, lactic acidosis, ketoacidosis |
| Use lab data to correctly differentiate between secretional and titrational acidosis (AG; Cl-; TCO2) | Secretional: --AG = normal --Cl- = increased relative to sodium --TCO2 = decreased Titrational : --AG = high/elevated --Cl- = no change --TCO2= decreased |
| Explain how blood pH affects serum K+ levels | as blood pH decreases to become more acidic; H+ will move into cells. In order to maintain electroneutrality, K+ must leave the cells causing a normal to hyperkalemia to be present |
| Identify chemistry data patterns for chloride that indicate an abnormal acid-base balance | *Chloride should always follow sodium, and if not consider an acid-base disturbance!** Chloride increased relative to sodium suggests a decrease in TCO2 and is interpreted as evidence for metabolic acidosis. Chloride decreased relative to sodium suggests an increase in TCO2 and is interpreted as evidence for metabolic alkalosis. Chloride should follow +/- 3 units!! |
| Correctly id "paradoxical aciduria" from laboratory data. | --alkalemia with aciduria |
| Characterize the fluid and electrolyte alterations that lead to paradoxical aciduria. | --Driving forces are: need for sodium resorption (dehydration, hyponatremia) and alkalosis --hypochloridemia and hypokalemia are contributing factors 1. Hypochloridemia = Cl- is reabsorbed from the urine with Na+ to maintain electroneutrality; however, if P is hypochloremic, HCO3- will be resorbed in place of Cl-; urine pH drops and reabsorbed HCO3- increases pH to exacerbate alkalemia 2. Hypokalemia = as Na+ is reabsorbed from urine; K+ is secreted from blood to maintain electroneutrality; however, if P is hypkalemic, body compensates by secreting H+; this causes blood to become alkalemic and urine more acidic --typically associated with upper gi obstruction/gastric vomitin and displaced abomasum |
| Correctly id the type of acid-base distrubance characterized by increased AG without concurrent decrease in TCO2. | ...Mixed metabolic alkalosis and titration metabolic acidosis |
| What is the initial reversible impact of hypercalcemia on renal function? What clinical sign is likely to be associated with this change? | inhibits ADH--> POLYURIA |
| Describe 3 mechanisms by which renal failure in dogs and cats may contribute to hypocalcemia. | 1. Mass Action: PxCa=<75; body won't handle high concentrations of both, so Ca++ will precipitate out 2. High P inhibits 1a hydroxylase which normally converts vit D to its active form 3. Decreased functional mass of kidney leads to decreased ability to produce adequate amounts of 1 a hydroxylase |
| Why is hypocalcemia more significant if an animal is alkalotic. What is the clinical manifestation of hypocalcemia in cows?...dogs? Why are they different? | --low calcium is more significant in alkalotic P because less H+ will be protein bound, thereby allowing more Ca++ to bind to protein; the increase in protein bound Ca++ may mask the degree of hypocalcemia --Cows= flaccid paralysis; decreased neuronal firing due to decreased calcium-inducined acetylcholine release from NMJ --Dogs=tetanic paralysis; low interstitial ionized calcium concentration increases neuronal sodium permeability allowing easy initiation of action potentials |
| List 2 primary endocrine diseases that are commonly associated with hypercalcemia. | Primary hyperparathyroidism Addisons's disease |
| Why is hypomagnesemia often accompanied by hypocalcemia? | Mg++ is required for PTH release from the parathyroid gland; so without Mg++, PTH can't elevate blood calcium levels |
| Alterations in serum phosphorus are most commonly a reflection of what renal parameter? | gfr |
| What is the major clinical consequence of severe hypophosphatemia? At what serum concentration of P does this consequence become of high concern? | Hemolysis! if P<1.0 mg/dl because rbc require ATP to maintain membrane structure and will lyse if not enough |
| Describe the role of hyperphosphatemia in the pathogenesis of renal secondary hyperparathyroidism. | Hyperphosphatemia inhibits the function of 1 a hydroxylase, which normally functions to convert vit D to its active form in the kidney; without vit D, Calcium is not absorbed; hypocalcemia triggers the release of PTH which causes Ca mobilization from bone stores |
| In renal failure, total body sodium is often very low while serum concentration are often normal. Explain. | dehydration |
| Explain the significance of severe hyponatremia in association with renal azotemia in most species. | ...if you see hyponatremia with renal azotemia, think about Secondary Renal Azotemia characterized by medullary washout |
| Large decreases in serum sodium can be typical of renal failure in which common domestic species? Provide 2 reasons for this. | ...Bovine can have decreases in serum sodium due to (1.) greater renal loss of Na (2.) GI sequestration secondary to ileus |
| Explain why serum K+ is often a poor indicator of total body K+. | ...most K+ is intracellular |
| List two mechanisms by which serum K can be elevated in renal disease? | ...hypoaldosteronism --> retention of K+ at DCT because there is no aldosterone to signal K+ exchange with Na 2.Anuria, oliguria, obstructive dz leads to marked hyperkalemia beca use if animal can't excrete K+ and body absorbs from gut it can reach very high levels |
| Explain why hypokalemia is more significant if there is concurrent metabolic acidosis. What organ system is most likely to be clinically affected by hypokalemia? | ...muscles affected most; total body loss because in metabolic acidosis you would expect hyperkalemia |
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