Clin Path- Urinary 3

drraythe's version from 2015-12-05 19:27

Part 2: Urine sediment findings

Question Answer
what is cylindruria?casts in urine
how do RBCs and WBCs look on an unstained microscopic examination of urine?WBCs are larger and grainy, RBCs are yellowish and smaller
note that the METHOD OF COLLECTION is important to know, to know the relevancy or specificity of your resultslike, if just voided, a WBC can be anywhere in the genito-urinary system, but if cytocentesis, you know it's either the bladder or the kidneys (or prostate, if male)
describe/explain crenationwhen RBCs get a ruffled appearance. it is an IN VIRTO change where the membrane changes/shrinks
how do you know if bacteria are a contaminant or a pathogen?If there are WBCs present, the body is fighting an infection so the bact are pathogenic. If there ARENT WBCs, they are probably a contaminant (like being cleared out after a dose of ampicillin killed them). (you can also determine by culture if there was a significant concentration to merit consideration---> 10^4 for robs, 10^5 for cocci
what are casts made of? if you want to look for casts, how must you handle your sample?usually made from protein/cells from tubule. needs to be a fresh sample, because casts deteriorate
what should we know about Hyaline casts?NOT pathogenic! aka Tamm-Horsfall mucoprotein
which casts implicate Active tubular degeneration (physiologic or pathologic)? (3)fine granular, coarse granular, and epithelial
how common/what does it mean if you see a leukocyte or erythrocyte cast?Cells trapped in mucoprotein(rare)
how common are waxy casts?very rare
what are the three types of epithelial cells you are likely to see in urine? where did they most likely come from?Squamous (prolly from distal urethra or genital tissues), transitional (Renal pelvis to urethra, Genito-urinary tissues), renal cells (tubular cells, RARE)
what are urine crystals made of?when ions combine into crystals
what are three major factors which affect the formation of crystals?concentration(high), pH(depends on crystal) and temp (usually low temp)
how does temp affect crystal formation?usually a dec in temp will cause an inc in crystal formation
what are some inhibitors of crystal formation?Tamm-Horsfall protein (from renal tubules), maybe other proteins
diff between crystals and uroliths?usually crystals have a definitie composition, whereas uroliths have variable compositions
which crystals tend to form in ACIDIC urine? (5)Ammonium biurate
Calcium oxalate
Uric acid
which crystals tend to form in BASIC urine? (3)Calcium carbonate
Calcium phosphate
Magnesium ammonium phosphate
Ammonium biurate crystalluria--> happens in who? what does it look like? When does it form?Happens in cats and dogs (esp Dalmatians, English bulldogs, black Russian terriers) when urine is acidic (<7). They look like "thorny apples" and are formed when NH4+ is crystalizing in urine
2 Situations:
(1) Urate receptor defect-->dec urate xport, so Less urate converted to allantoinin hepatocytes, so Less urate resorbed by renal tubules
(2) Hepatic dysfunction means more NH4+(instead of urea) and urates(instead of allantoin) are excreted from the kidney))
what is the difference between urea and urates?UREA is formed in the liver from ammonia, which came from proteins. URATES are formed from Nuclei degradation, Purines (adenine, guanine) and the liver converts the urates into allantoin (THIS DOESN'T HAPPEN IN PRIMATES, it stays as urates in them). Then the urea and allantoin are passed in the urine.
which animals don't convert urates(uric acid) into allantoin, and instead excrete urates?Primates, Birds, Reptiles, Dalmations, Eng. bulldogs, BR terrier
if there were too few hepatocytes, what would be excreted in urine?ammonia(from protein) wouldn't be converted into urea (so ammonia excreted) and urates wouldn't be converted to allantoin, so urates would be excreted (this is normal for Primates, Birds, Reptiles, Dalmatians, Eng. bulldogs, BR terrier)
Bilirubin crystalluria--> happens in who? why does this happen? what does it look like? what will tests look like?happens in dogs (esp healthy dogs w concentrated urine) and cats, and looks like little bundles of thorns. It happens when there is Increased renal excretion of bilirubin (Hemolytic icterus disorders, Cholestatic icterus disorders). You can expect Expect concurrent (+) bilirubin reaction, but the reagent pad wont detect the biilrubin in the crystals themselves
Calcium oxalate crystalluria--> when does this happen? what are the two types?happens when there is too much calcium (due to hypercalcemia) and oxalate, and when the pH is less than or equal to 7. the two types are Calcium oxalate monohydrate and Calcium oxalate dihydrate (more on these in other cards)
Calcium oxalate crystalluria--> Calcium oxalate monohydrate--> what situations cause the monohydrate crystals? what do they look like?Ethylene glycol toxicosis, or a Ruminant diet (plants). look cylindrical, might have points (look like typical crystal point shape)
Calcium oxalate crystalluria--> Calcium oxalate dihydrate--> what situations cause the dihydrate crystals? what do they look like?Healthy dogs with concentrated urine, Ethylene glycol toxicosis, Ruminant diet (plants), Equine diet (plants). They look like envelopes (square to rectangular with an x on them)
*LOOK AT THE CRYSTAL PICTURESat least theyre pretty
Urate or uric acid crystalluria happens at what pH, and is due to what? what do they look like?pH less than or equal to 7 (acidic urine). happens when there is an inc in the excretion of urates or uric acid. looks like hexagons (i think they can look like fish scales too)
which crystal can be normal in small amounts in healthy animals?urate/ uric acid crystalluria
what are the species/breed dispositions for Urate or uric acid crystalluria?canine breed dispositions are dalmations, English bulldogs & black Russian terriers
in what dz processes do you see urate/uric acid crystals? explain whyusually see in end-stage liver dz, and in portosystemic shunts. This is bc there is hepatic dysfunction, less hepatocytes fxning means dec conversion of uric acid to allantoinby hepatocytes, so there is an inc in renal excretion of urates
Calcium carbonate crystalluria happens at what pH, in who? what does it look like?happens in alkaline urine (pH greater than or equal to 7). COMMON IN HERBIVORES! looks like radiating pattern in a circle, like wheel spokes but many spokes
Calcium phosphate crystalluria happens at what pH, in who? Why does this happen? what do they look like?happens in healthy dogs with alkaline urine (pH greater than or equal to 7). This can be the result of a UTI causing alkaline urine, or can be from hypercalcemia-->hypercalceuria. look like spikes radiating out at all angles, like those poof flowers
Magnesium ammonium phosphate crystalluria is aka? happens at what pH? Happens in who, and why? what do they look like?aka: struvite, triple phosphate (also Ca2+present). Happens in alkaline urine, in mostly dogs and cats. This is because of their carnivore diet being high in Mg and PO4 (constituents of protein). It is also common with the degradation of urea, which happens with certain Urease-producing bacteria, OR if you delay the urinalysis. Look like gemstones.

Part 3: Polyuria/Polydipsia disorders

Question Answer
how does chronic renal failure cause polyuria?Too few functional nephrons (solute diuresis & polyuria)
how does Acute renal failure cause polyuria?Tubules not responding to ADH
how does Post-obstructive diuresis cause polyuria?Tubules not responding to ADH & solute diuresis
how does Diabetes mellitus cause polyuria?Solute diuresis (possible dec in medullary tonicity)
how does Hypercalcemia cause polyuria?Ca2+interferes with tubule response to ADH
how does Canine pyometra cause polyuria?Tubules not responding to ADH
how does Hypokalemia cause polyuria? Tubules not responding to ADH
how does Hypoadrenocorticism cause polyuria?dec medullary tonicity &/or dec release of ADH
how does Liver failure cause polyuria?dec medullary tonicity &/or NH4+interferes with ADH
how does Central diabetes insipidus cause polyuria?dec release of ADH
how does Hyperadrenocorticism cause polyuria?cortisol--> dec in ADH
how does Psychogenic polydipsia cause polyuria?dec Plasma osmolality --> dec release of ADH
what are the 4 major pathogenic mechanisms of polyuria?solute diuresis, dec in tubular response to ADH, dec in medullary tonicity, and a dec in ADH
what are the three dzs which cause a solute diuresis?chronic renal failure, Post-obstructive diuresis, Diabetes mellitus
what are the three dzs which cause a dec in medullary tonicity?Chronic renal failure, Hypoadrenocorticism, liver failure
what is Isosthenuria?State in which urine osmolality= plasma osmolality
explain how the term isosthenuria can have some "wiggle room" in the exact definition. what is the usual specific gravity of isosthenuria?it is NOT a fixed specific gravity, rather, can be +/- 100 mosm/kg. so usually 1.007 –1.013 (which is 200-400 mmol/kg, where plasma is 300,so this is within the plus or minus 100 rule), or, sometimes 1.008-1.012 or sometimes 1.007-1.017, if the urine contains +3 or +4 glucose or protein, since these can affect the SG even though it would still be considered isosthenuria
what is the specific gravity of isosthenuria?trick question! NOT A FIXED SG. It is a range. can be +/- 100mosm/kg of the plasma mosm/kg(which is 300) and still be considered iso. the average SG RANGE is 1.007 –1.013. if the urine contains +3/+4 glucose or protein, the range will be heavier but still considered iso (1.008-1.017)
what is the USGref of Hyposthenuria?USGref< 1.007 (plasma is mmol/kg, and in this case, the urine is <200mmol/kg)
what is going on in the proximal tubule? what is the SG like? in what situation in the prox tubule can cause polyuria?in the PCT, there is the reabsorption of H2O (75% of it) which is done by having the peritubular osm > tubular osm. However, the solute concentration DOESNT CHANGE, and is isosthenuric (apprx 1.010) because an equal proportion of solute is absorbed as well. POLYURIA can happen here if there is TOO MUCH solute, which means there is less of an osmotic gradient to pull water towards the interstitium, so less H2O is resorbed
explain how chronic renal failure and solute diuresis relateToo much solute for remaining functional nephrons
explain how post-obstructive diuresis and solute diuresis relateSolute accumulates during obstruction --> overloads nephrons after removing obstruction
explain how diabetes mellitus and solute duiresis relateGlucose in tubular fluid reduces osmotic gradient
what is going on in the loop of henle? what is the SG like? in what situation in the loop of henle can cause polyuria?entering the LOH from the PCT, the SG is 1.010. in the descending LOH, H2O IS REMOVED, solute remains. at this point the SG is >1.040. Then, In the ascending LOH, the H2O REMAINS, and the SOLUTE is REMOVED. After this, the SG is apprx 1.003. This means in the LOH there is an overall DEC in SOLUTE CONC. This is bc the peritubular osm>>> tubular osm. POLYURIA from the LOH can be caused by Too much tubular solute OR by Too little interstitial solute. So, less H2O is resorbed b/c of messed up osmotic gradient
explain how chronic renal failure and a decrease in medullary tonicity relateDamaged medullary tissue or poor blood flow. dec in Na+ and Cl- transport in ascending limb (also solute diuresis)
explain how diabetes mellitus and a dec in medullary tonicity relate*persistent diuresis (solute overload) --> “medullary washout”
explain how Hypoadrenocorticism and a dec in medullary tonicity relatePersistent hyponatremia & hypochloremia --> dec dec in Na+ and Cl- transport in ascending limb
explain how liver failure and a dec in medullary tonicity relatedec in urea synthesis --> dec urea delivery to renal medulla
explain what is going on in the distal nephron (DCT and collecting tubule). What is the SG like and how does it change, and in what situation in this area can cause polyuriaThis is the portion of the nephron that is dependent on ADH. the SG starts where it ended in the LOH, at 1.003. provided there is ADH stimulus, there will be a dec in tubular fluid volume (because it is being resorbed) and thus the solute conc will increase, because there is less water to dilute it. Usually the SG is then 1.040. This is because ADH is aiming to conserve water, why absorbing more of it back up into the body (this works by ADH opening aquaporins, and then the high tonicity of the medulla draws the water out of the tubule). POLYURIA could occur in this segment if there is no ADH, a poor cellular response to ADH, or a reduced gradient.
chronic and acute renal failure, and post obstructive diuresis are all related to a dec in tubular response to ADH how?there are damaged renal tubular cells, so they cant respond. She also said "and previous mechanisms" which i assume means solute diuresis, etc
how does hypercalcemia relate to a dec in tubular response to ADH?Free Ca2+interferes with ADH activity
how does canine pyometra relate to a dec in tubular response to ADH?she had "??? maybe endotoxins interfere with ADH activity"
how does hypokalemia relate to a dec in tubular response to ADH?a dec in K+ directly leads to the tubules being less responsive to ADH (prolly has to do with an exchanger pump or sthing)
explain how liver failure relates to a dec in tubular response to ADH?an increase in NH4+ might make the tubules less responsive to ADH
how does Hypoadrenocorticism relate to dec ADH?it may or may not have an effect. If it does, a dec [Na+] and a dec [Cl-]--> hyposmolar plasma --> less stimulus for ADH released
explain how central diabetes insipidus relates to a dec in ADH?brain/pituitary dz-->dec ADH secretion directly.
explain how Hyperadrenocorticism relates to a dec in ADH?there is an inc in cortisol which inhibits ADH secretion
explain how Psychogenic polydipsia relates to a dec in ADH?an inc in H2O consumption dilutes plasma solutes, which leads to hyposmolar plasma, which means there is less stimulus for ADH release.

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