222 terms

Renal Internal

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How much of TBW is ICF? ECF? What are the main electrolytes in each?
2/3
1/3
ECF - Na
ICF - K
Measure of a solute concentration per unit volume of a solvent that takes into account all solute concentrations.
osmolarity
Measure of solute concentration per unit mass of solvent that is preferred unit of measurement bc it stays constant.
Osmolality
Measure of osmotic pressure gradient bw 2 solns. What is it influenced by?
Tonicity
Solutes that can cross the semipermeable membrane
What is plasma osmolality? What is normal pOsm?
ratio of plasma solutes and water
275-295
How do you measure osmolar gap? What should normal gap be?
Measured pOsm - expected pOsm
5-10 mOsm
What are some substances or situations that can cause an elevated osmolar gap?
Ethylene glycol, methanol, isopropyl etoh, ethanol
severe hyperlipidemia and severe elevations in free serum light chains aka myeloma
Plasma Osmolality ECF Osmolality and ICF Osmolality are the -- since cell membranes are freely permeable to --.
same
water
How do you calculate plasma tonicity? Does urea contribute to it?
2 x Na + glc/18
No bc it freely crosses the membrane
What is acute hyponatremia?
Drop in plasma tonicity due to ICF resulting in water movement into cells
What is acute hypernatremia?
Increase in plasma tonicity compared to ICF resulting in movement OUT of cells (dehydration)
What do we call the ability of plasma solutes to generate an osmotic force)?
tonicity
How does our body respond to increase in osmolality aka Na or glc?
Osmoreceptors in HT release aDH
When is ADH release suppressed?
Euvolemia pt resulting in water excretion and max dilute urine water
What are some ways our body regulates ECF volume esp in the setting of a low ECF? High ECF?
ADH is non-osmotically released in massive amounts when BP lowers
renal hypoperfusion of JGA leads to activation of RAAS
carotid sinus stim and increased SNS lead to retention of Na
drop in ANP
High ECF - decrease in RAAS and increase in ANP to retain water and Na
What are normal Na levels? Normal serum osmolality?
What is hyponatremia? hyper-?
135-145
275-295
Hypo <135
Hyper >145
What are the 2 things ADH is released in response to?
Increase osmolality via osmoreceptor and decreased volume aka baroreceptor
Name the ADH targets.
V1a, V1b, V2 receptors
What is the principal receptor located in the CD principal cells in hyponatremia?
V2
ADH stim V2 that leads to increased cAMP and expression of AQP2 receptor
JVP, skin turgor over forehead or sternum, edema, crackles and a hx of fluid loss and sx of vol overload would hint at what dx?
hyponatremia
Can serum osmolality be high in hyponatremia? Low?
Both - high is hyponatremia with hypertonicity and low is hypotonicity
Hypertonicity aka glc, mannitol, etc
What are some causes of SIADH?
CNS disorders or pulm tumors infxns/inflammatory disorders
What are some meds that cause SIADH?
SSRIs, antipsychotics, COX-2 inhibitors, opiates, and TCAs
What are some infections that can cause SIADH?
HIV and Rocky Mt SF
Nursing home pts with dementia, intubated pts, neglected infant, or pts with a lack of access to water would be like to present with which Na disorder?
hypernatremia
A solute diuresis of greater than 1000 would suggest what Na disorder?
Hypernatremia
Thirst, anorexia, ataxia, confusion, hyperreflexia, coma and rupture or bridging veins and intracranial hemorrhage would be indicative of what?
hypernatremia
Polyuria with dilute urine is a hallmark sign of --. But to make sure you need to exclude this dx of a sub acute --.
DI
psychogenic polydipsia
-- insipidus is due to the insufficient release of ADH; it is usually caused by CNS tumors. -- is due to a normal ADH release but an impaired renal response; it is usually caused by lithium use or congenital.
Central
nephrogenic
What is the confirmatory test for DI? What do you do if positive?
Water deprivation test - pt admissted and water deprived and urine volume and osmolality measured hourly. Confirmatory for hypernatremia if urine osmolality is stable for 3 consecutive hrs despite rising plasma osmolality. Cofirm. Then give desmopressin and urine osmolality measured every 30 min. If it rises, central DI. If minimal change then nephrogenic
When do we use free water deficit?
How much water to replace clinically in hypernatremia
What does rapid correction of hyponatremia result in? hyper-?
osmotic demyelination syndrome aka locked in syndrome
cerebral edema
Why does water move into the brain with osmotic demyelination syndrome aka central pontine myelinosis?
Fall in serum tonicity causes water movement into brain
When do symptoms of CPM occur?
demyelination sx occur 2-6 days after rapid correction that exceeds >15 meq/L/day
What are the 3 ways in which we control the IC K: EC K ratio?
Na K ATPase, Na K 2Cl cotransporter, and K channels, colonic ability to absorb and secrete K, and kidney handling of K
Where is 90% of filtered K reabsorbed?
PT and LOH
Where does most K secretion occur?
principal cells and CD
How do the ENaC channels establish the gradient that promotes K secretion?
Na enters via ENac to generate a negative lumen that drives passive K exit thru apical K channels. Renal K excretion is enhanced by increased tubular fluid Na.
In principal cells, the -- channel moves K into and Na out of cells to generate a Na gradient for ENac.
Na K ATPase
How is K mainly secreted?
apical "small conductance K" SK channels (that are ROMK channel subtype aka renal outer medullary K channels)
Which type of K channels are activated by Ca and also aid in K secretion?
apical BK (big potassium) channels
Hyperkalemia induces -- release by the adrenal glands.
Aldosterone
Aldosterone increases expression of the -- in the CD.
ENac
Regardless of aldosterone, a high K diet will induce expression of the -- channel.
ROMK
pRBC and rhabdomyolosis are 2 ways to produce --.
hyperkalemia
What are 2 types of metabolic shifts that can induce hyperkalemia?
Acidosis and insulin deficiency
Forearm contraction during blood draw, fist clenching, tourniquet use, thrombocytosis, leukocytosis, acute anxiety, and cooling of blood are all examples of things that can induce --.
Pseudohyperkalemia
Why is hyperkalemia a medical emergency?
Bc of its effect on cardiac tissue- it depolarizes cardiac myocytes and increases cardiac excitability. Ascending paralysis and decreased ability to acidify urine
How do you tx hyperkalemia?
IV calcium for CV effects, sinulin and glc to shift K to SKM/hepatocytes, B agonist to activate Na K ATPase to shift it into the cell, Na HCO3-, and to remove the K use diuretics, mineralocorticoids, cation-exchange resins, and dialysis
Severe mm weakness, rhabdomyolosis, ECG changes, renal abnormalities, and glc intolerance are all signs of --.
Hypokalemia
What 2 diseases arise from ENac mutations?
Liddle syndrome and Pseudohypoaldosteronism type 1
Which pathologic state arises from a GOF mutation with Enac that increases Na reabsorption with susbequent K secretion and presents with HT and hypokalemia?
Liddle syndrome
Which disease presents as the opposite of Liddle syndrome aka Enac function decreased? How is it similar to Liddle syndrome?
Pseudohypoaldosteronism type 1
In both types pts have hypotension and hyper K but in pseudo they have high aldo as well
-- syndrome is an AR disease stemming from a defect in the -- in the distal tubule presenting with hypokalemia, -magesemia, and -CALCEMIA + metabolic alkalosis. Usually dx later in adolescence.
Gitelman
What channel does the AR disease Bartter syndrome have a defect in?
Na2KCl, ROMK or basolateral Cl channel in TALOH resulting in loss of NaCl uptake and hypokalemia, metabolic alkalosis, polyuria with possible increase in Ca excretion or decreased Mg
Hyperkalemic periodic paralysis is a familial disorder where pts develop hyperkalemia and present with -- in response to --.
Flaccid paralysis
cold weather, exercise, or fasting
Hypokalemic periodic paralysis is a rare syndrome that is strongly associated with hypokalemia and strongly associated with -- with a strong predisposition for (M/F) and (ethnic group).
hyperthyroidism, M and Asian
Elevated PTH activates -- to the active form of vitamin D ultiamtely leading to decreased -- loss and increased -- loss.
1 alpha hydroxylase
Ca, phosphate
-- syndrome is hypercalcemia with metabolic alkalosis and renal insufficiency from excessive intake of calcium carbonate antacids.
Milk Alkali
What granulomatous diseases cause hypercalcemia?
Sarcoidosis, TB, granulomatosis with polyangitis
What types of hyper vitaminoses cause hypercalcemia?
A and D
What should hypercalcemia workup begin with?
measurement of PTH
What is the range for normal serum calcium levels?
8.5-10.5 ng/dl
What 2 (physical) tests can you do to test for hypocalcemia?
Trousseau sign and Chvostek's sign
What is Trousseau's sign?
Sphyngomanometer inflated causing tetany of forearm mm
What is Chovstek's sign?
Tapping over facial nerve to produce facial mm twitching
Bisphophanates, calcitonin, cincalcet, citrate, foscarnet, phenytoin, and fluoride posioning are all drugs that can potentially cause --.
hypocalcemia
When does hypophosphatemia occurr?
phos <3.0 m/dl most commonly seen in chronic Etoh use, malnutrition, critical illness. Gets severe if less than 1.0 and sx are weakness, myalgia, HF, rhabdo, resp failure, seizures, and hemolysis
What diuretics cause hyophosphatemia?
Acetazolomide and metolazone
Hyperphosphatemia is classified as what? How do pts present?
>4.5 mg/dl and asx
What hormone regulates calcium and phosphorous? How is homeostasis achieved?
PTH
via kidney, bone, and gut
What is primary HT?
Pts who develop HT wo any risk factors like age obesity diet smoking sex DM fam hx and stress
If you are tx a pt with resistant HTN, what MUST be included in a regimen with 3+ drugs?
diuretic
If a pt has spontaneous hypokalemia or marked hypokalemia after initiation of a diuretic, they should be screened for --.
Secondary HT
-- results from aldosterone secretion WITHOUT response to FB loop mechanism. What causes this?
Primary hyperaldosteronism - FB response arising from high BP/baroreceptor response doesn't work bc of continuous aldosterone production without need for renin pathway
tumor producing aldosterone or adrenal hyperplasia
Why do you get hypokalemia in primary hyperaldosteronism?
Continued secretion of aldos - ongoing reabsorption of Na via Enac and ongoing secretion of K via ROMK --> hypokalemia
What are the 2 main clinical presentations of primary hyperaldosteronism?
hypokalemia and metabolic alkalosis
Why do you get metabolic alkalosis in primary hyperaldosteronism?
Hypokalemia results in K being pumped from inside cell to outside cell and in exchange Na and H are pumped into the cell. This stim H K ATPase to reabsorb K and in turn secrete H_ into the urine.
In primary hyperaldosteronism, Na reabsorption leads to hypernatremia and --, K secretion leads to hypokalemia, and secretion of -- in exchange of -- leads to metabolic alkalosis.
HT
H, K, metabolic acidosis
What does the serum aldosterone/renin ratio have to be greater than to suggest hyperaldosteronism?
>20
If the aldo/renin ratio is elevated, then perform a -- for confirmation.
salt loading
In a normal pt, Na loading should -- aldosterone production. In a pt with PH, aldosterone does not suppress and 24 hr urine will have elevated -- level despite the Na load.
decrease, aldosterone
How do you treat PH?
Adrenalectomy or pharm blocking of aldosterone action like spironolactone/epelerenone
What is the triad of Liddle Syndrome
HT, hypokalemia, and metabolic alkalosis
Do pts with Liddle syndrome have an elevated aldo/renin ratio?
NO
How do you tx Liddle syndrome?
Inhibit ENac via amiloride or triamterene - no high aldo levels so no use in using spironolactone
-- is a genetic disorder that has a simiala presentation as PH.
Apparent Mineralocorticoid Excess
What other scenario leads to similar presentation as AME?
Chronic licorice ingestion
How does AME present?
hypercalciuria, nephrocalcinosis, and renal failure
What do you find in the lab results of pts with AME?
low serum renin and low serum aldo
What is the basis of the genetic mutation in AME?
def in 11 beta OH steroid dehydrogenase impairs cortisol to cortisone conversion. elevated cortisol leads to cortisol binding to mineralocorticoid receptor --> clinically presents as PH
What other syndrome presents similarly to AME?
Cushing's
-- is a catecholamine secreting tumor that arises from chromaffin cells of the adrenal medulla.
Pheochromocytoma.
What gene is associated with pheochromocytomas?
MEN2
What is the (rather uncommon) classic triad of pheochromocytomas?
episodic headache, sweating, tachy
What are the 3 hormones that are overproduced in pheos?
epi, norepi, and dopa
What lab measurements would you expect in a pheochromocytoma?
Plasma-fractionated metanephrines and urinary 24 h metanephrine and catecholamines
How do you tx a pheochromo?
Resect the tumor, combined alpha and beta adrenergic bockade COMBO (never beta alone) - phenoxybenzamine
In what subset of pts is renovascular HT increased?
pts w acute increase in BP, severe, or refractory HT
Due to the -- produced by the stenosis of the renal vasculature, -- production is increased and this activates the RAAS pathway leading to --.
iscemia, renin, HT
What cholesterol problem is related to renovascular HT?
Atherosclerotic disease
What disease (and subset of pts) should be on your diff dx list for renovascular HT?
Fibromuscular dysplasia in young female
What is the major complication gestational HT can lead to?
eclampsia
GO OVER SLIDE 20
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What meds must you avoid in pregnant women to prevent fetal defects? What do you rx instead?
Avoid ACE-I/ARB
methyldopa
Name some meds that cause HT.
OCPs, etoh, caffeine, NSAIDs
What is the endocrine function of the kidneys?
synthesis of EPO, renin, PGs, and 1-25 di OH vit D
What is the hallmark sign of kidney pathology?
Proteinuria
Urine specific gravity, urine osmolality, urine sodium and fractional excretion of filtered Na are renal function tests that assess what?
tubular function
In chronic renal failure, how do you assess GFR?
creatinine clearance and GFR
A symptom complex resulting from acute or chronic renal failure. Multi-system symptoms - acidosis, nausea, anemia, water & electrolyte imbalance, neuropsychological disorders
uremia
"Nitrogen in the blood" Refers to an increase in the non-protein nitrogen compounds (BUN, Creatinine, Uric acid).
azotemia
Are increased serum BUN and creatinine helpful?
No bc they lack sensitivity and specificity - aren't significantly increased until there is a significant reduction in renal function.
For oliguria/anuria/renal parenchymal pathology, which indicator do you use?
Proteinuria
How is urea metabolized in the kidneys and what is the reference range?
Filtered in the kidneys and partially reabsorbed in the PT.
7-22 mg/dl
How does GFR vary with BUN level?
Decreased GFR correlates to a higher serum BUN and an increased GFR correlates to a lower serum BUN
How does GFR vary with dietary protein?
Hi protein diet correlates to a higher serum BUN and a lower protein diet correlates to a lower serum BUN
What happens to BUN levels in the setting of increased aa degradation?
higher serum BUN
What happens to BUN levels in the setting of liver damage/dysfunctional urea cycle?
lower serum bun
Prerenal hypoperfusion (CH, shock, bleeding) lead to a -- GFR with -- proximal reabsorption of urea lead to an increased serum BUN
Decreased, increased
Acute tubular necrosis leads to a -- GFR without -- PT reabsorption of urea leads to an increased serum BUN.
decreased, increased
Postrenal obstruction leads to a decreased GFR with back diffusion of urea with -- PT reabsorption of urea that leads to an increased serum BUN.
increased
Chronic renal failure leads to a -- GFR which leads to an increased --.
decreased
serum BUN
How does increased tissue catabolism in 3rd degree burns or a postoperative state lead to an increased BUN?
increased aa degradation
How does increased dietary protein lead to increased serum BUN?
increased aa degradation
How does dehydration without renal failure lead to an increased serum BUN?
decreased GFR with increased proximal reabsorption of urea
Increased plasma volume in the setting of SIADH or pregnancy leads to -- that results in a decreased serum BUN
increased GFR
How do hepatic alterations leads to a decreased serum BUN?
Cirrhosis, liver disease, dysfunctional urea cycle
Why does malnutrition lead to a decreased serum BUN?
decreased amino acid degradation
Is serum creatinine affected by diet or degree of hydration like BUN? How does its stability compare?
NO
Increases more slowly than BUN and constancy of production more stable than BUN = more reliable than BUN as an index of renal function
What is the reference range of serum creatinine?
0.7 - 1.5 mg/dl
When do we see significant increase in serum creatinine?
50% reduction in renal function
Where along the nephron is serum creatinine absorbed?
filtered in the kidneys without reabsorption
How is serum creatinine secreted?
Depends on the GFR - as GFR decreases, creatinine secretion into tubules increase
How do creatinine levels vary with GFR?
Increased GFR means lower creatinine and vv
How does GFR change with age?
Decreased mm mass associated with aging results in reduced production of creatinine but the concurrent reduction in GFR itself results in a net increase in serum creatinine with age
Name 2 drugs that block tubular secretion. How do they affect creatinine levels?
Cimetidine and trimethoprim result in increased creatinine
What are some situations that would cause falsely elevated serum creatinine?
ketoacidosis and cephalosporins
What is the normal BUN/Cr ratio?
10:1 but ranges from 12-16
What pathologies are present with the BUN/Cr ratio is less than 10? greater than 10?
Acute tubular necrosis, prolonged postrenal with tubular dysfunction failure

Prerenal and postrenal failure
What do Bun/Cr ratios less than 10 indicate?
tubule dysfunction/necrosis
How does the BUN/Cr ratio adjust to prerenal hypoperfusion like in CHF, shock, bleeding?
ratio >10 and PT still functioning so it increases resoprtion of BUN into the blood and increases secretion of creatinine into urine resulting in the ratio
When the PT isn't functioning, what happens to the resorption of BUN into the blood?
does not get resorbed and creatinine secretion is not increased; Bun/Cr ratio is less than 10
The proximal tubule is still functioning so it increases resorption of BUN into the blood and increases secretion of Creatinine into the urine resulting in a BUN/Cr ratio >10
postrenal obstruction with good tubular function (acute)
The proximal tubule is NOT FUNCTIONING so it does not increase resorption of BUN into the blood and does not increase secretion of Creatinine into the urine resulting in BUN/Cr ratio <10
Prolonged Postrenal obstruction with tubular dysfunction
BUN/Creatinine ratio is good to categorize -- renal failure.
acute
-- reflects the relative concentration of the urine and is the ratio of the density of a substance to the density of a standard usually water for a liquid or solid and air for a gas.
Specific gravity
What urine mOsm indicates tubular dysfunction?
<300 mOsm
What UNa indicates tubular dysfunction?
>40 mEg/L
What fractional excretion of filtered sodium indicates tubular dysfunction? What is FENa?
% of Na filtered by the glomerulus NOT reabsorbed by the tubule
>2%
What is FENa most sensitive and specific for?
ATN (acute tubular necrosis)/tubular damage
When do we see epithelial casts?
Intrinsic renal/acute tubular necrosis
What are the primary causees of chronic renal disease?
DM, HT, chronic glomerulonephritis, and cystic renal disease + small sized kidneys
What BUN/Cr ratio indicates severely damaged/dysfunctional tubules?
<15
Normocytic anemia in the context of chronic renal disease would indicate what?
normocytic anemia and decreased EPO
What are the lab findings in chronic renal disease?
Hyperkalemic metabolic acidosis, HYPOCALCEMIA, and hyperphosphatemia
Why do we see metabolic acidosis in chronic renal disease?
impaired excretion of K adn H in exchange for NA and retention of organic acids
Why do we see hypocalcemia in chronic renal disease?
CRF leads to decreased vit D that leads to decreased serum calcium. This will cause secondary hyperPTH producing bone lysis
Why do we see hyperphosphatemia?
decreased excretion of phosphate
What condition do you also see hyperkalemia, metabolic acidosis, and hyperphosphatemia?
acute renal failure, esp ATN
Is creatinine filtered? reabsorbed? secreted?
yes, no, minimal
Why is creatinine used to assess GFR?
creatinine production and excretion is relatively constant
What is the FR for kidney failure?
<15
eGFR is best for estimating what?
reduced renal function with values under 60 ml/ min
What 2 variables are not taken into account in eGFR and may skew the readings?
dietary intake and mm mass
Which component of a routine urinanalysis should be centrifuged?
microscopic examination
Do we have detectable glucose in our urine normally?
NO
What biochemical reaction do we test for to see if we have glc in our urine?
Glucose oxidase - doesn't react with other sugars or reducing substances; do this for DM pts
What kind of conditions are associated with glucosuria?
DM, gestational diabetes, endocrine disorders, disturbances in metabolism
Would you detect bilirubin in a urine sample of a healthy pt? How does bilirubin appear?
NO
Color intensity is roughly proportional to concentration of bilirubin
How does urobilinogen appear in the urine?
Normally present in small amounts in a healthy adult
What is urobilinogen?
colorless product of bilirubin reduction formed in the intestines by bacterial action
What kind of healthy pts secrete large amounts of ketones?
those on restricted carbohydrate diets
Diabetic pts with prolonged stress, acute infections, surgery, and GI disturbance and in general poor control might present with --.
Ketonuria
What is the biochemical reaction for the presence of blood in urine based on?
peroxidase activity of HGB; method is sensitive to intact and lytsed RBC - free HGB and myoglobin will also react
What is the main protein detected in a urinanalysis?
albumin
What is microalbuminuria? macroalbuminuria? What is the minimal detection limit?
30-300 mcg/L
>300
10-20 mg/dl
According to the American Diabetes Association, what should serum creatinine be used to estimate?
GFR and stage the level of chronic kidney disease
What is the single leading cause of end-stage renal disease in diabetics?
diabetic nephropathy
-- has been shown to be the earliest stage of diabetic nephropathy in type 1 diabetes and a marker for development of nephropathy in type 2 diabetes. It is also a well established marker of CVD risk.
Microalbuminuria
What should be used in the treatment of microalbuminuria (or albuminuria) to delay progression to diabetic nephropathy ?
ACE inhibitors or ARBs
What is used as an indrect screening method for bacteriuria? Why is it limited?
nitrite - reduction of nitrate by bacteria containing reductase enzymes
Bacterial species must be one that contains reductase enzymes
What solid elements are we looking for in microscopic examination?
cells, casts, crystals, and microorgs
RBC casts are almost dx of -- injury.
glomerular
Casts only come from --.
renal tubules
Hematuria without proteinuria hints towards.
Lower UTI bleeding and inflammation
Moderate to marked hematuria can cause proteinuria in the absence of -- due to the presence of other proteins in blood not of renal origin.
casts
-- is common after strenuous exercise, catheterization, acute febrile illness, contamination from vulva.
benign transient hematuria
Multilobed nucleus, granular looking appearing singly or in clumps indicating acute infection
WBCs
If WBCs are present in significant numbers, -- on the reagent strip should be positive.
leukocyte esterase
Large, flat cuboidal cells with small nucleus surrounded by abundant cytoplasm indicative of improper specimen collection.
Squamous epithelial cells
Larger nucleus and less cytoplasm when compared to squamous epithelial
urothelial epithelial cells
Single -- are very difficult to identify in urine. They are seen and identified howevas inclusions in casts in certain renal diseases.
Renal tubular cells
Is the identification of malignant cells part of the routine analysis?
no - request separately and send to cytology examination and analysis
What kind of cast doesn't warrant further investigation?
hyaline
How are coarse granular casts formed?
Normal flow of cellular casts thru the nephrons is slowed down enough to allow disintegration of the cells into coarse granules.
What kind of casts are the result of prolonged stasis associated with chronic renal diseases?
Waxy casts
Colorless, homogenous casts with rounded ends and most frequently observed in normal urine after physical exercise and dehydration
hyaline casts
What is the most abundant protein in normal urine and forms the transparent matrix of hyaline casts?
Tamm-Horsfall protein
-- formation occurs when glomeruli are damaged, most frequently due to immune injury (reaction to recent infection by Group A streptococci).
RBC cast
What is the clinical significance of RBC casts?
dx of glomerular disease or renal parenchymal bleeding - think post strep glomerulonephritis
Exudation of PMNs into the neprhon in inflammatory renal disease is most likely to result in what?
WBC cast formation
Presence of WBC casts hint at a dx of --
Pyelonephritis, nephrotic syndrome, or glomerulonephritis
Renal tubular casts are seen after extensive sloughing of renal tubule epi cells following --.
ischemic, toxic, inflammatory, or metabolic damage
Epithelial cell casts indicate what?
massive damage and desquamation in the renal tubules, acute renal failure/acute tubular necrosis or post renal transplant (aka allograft rejection)
-- are formed when lipid particles (oval fat bodies) become embedded in the hyaline-protein matrix.
fatty casts
What are fatty casts made of?
Degenerative products of autolytic changes that occur in lipid laden renal tubular epithelial cells
What is a characteristic feature of nephrotic syndrome?
lipiduria with marked proteinuria
How is nephrotic syndrome usually characterized?
lipiduria, hypoalbuminemia, and hypercholesterolemia
-- and -- are also found in the urine of pts with fatty degenerative tubular diseases, such as diabetes.
fatty casts and oval fat bodies
Why are broad waxy casts bad news?
imply advanced tubular atrophy and/or dilation associated with end-stage renal disease; fairly severe localized nephron obstruction and oliguria or anuria
Which two crystals represent non pathologic findings of acidic pH?
calcium oxalate, uric acid
Which crystals represent non pathologic findings of alkaline pH?
triple phosphate (coffin lids), ammonium biurate (thorn apples) and calcium carbonate (bow ties)
Abnormal (aka pathologic) crystals in urine all occur only in -- pH urine
acid
-- seen in liver disease associated with bilirubinemia (+ dipstick) - such as obstruction to bile flow, cholestasis, or hepatitis.
Bilirubin crystals
Rare, associated with nephrotic syndrome - excretion of oval fat bodies and fatty casts.
cholesterol crystals
To prevent precipitation of crystals that could cause formation of calculi during the therapeutic period, patients may be placed on diets that produce -- urine.
alkaline
GO OVER CLINORIL
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Bacteria and yeast are usually accompanied by the presence of increased numbers of --.
WBC
What bacteria, indicative of vaginitis in women or urethritis/prostatis in men, resembles WBCs?
trichomonas vaginalis
This trematode is common in the middle east
Schistoma haematobium
What is the most common helminth infection in the US?
pinworm - enterobius
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