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renal path

Terms in this set (61)

2 categories of renal disease
glomerulopathy and tubulointerstitial
_____________ disease can be caused by drugs, endogenous toxins, ischemia, immune processes, and/or infection
tubulointerstitial
the glomerulopathies are divided into two subcategories
nephrotic and nephritic
profound proteinuria without cellular inflammatory reaction; there is damage to the filtering mechanism of the glomerulus which leads to protein wasting in the urine (proteinuria)
nephrotic disease
the protein wasting associated with nephrotic syndrome decreases serum protein causing hypoproteinemia, which usually manifests as ____________
hypoalbuminemia
proteinuria associated with RBCs and WBCs in the urine; inflammation in the glomerulus leads to bleeding into the urine (hematuria).
nephritic disease
inflammatory response of nephritic syndrome controls the underlying process, but uncontrolled or prolonged inflammatory response can result in greater degree of destruction of the _________ architecture.
glomerular
part of kidney more susceptible to ischemic injury
renal medulla
prominent site of injury related to immune complex deposition and complement fixation
glomerulus
_________ factors regulating blood flow have profound effects on kidney; GFR depends on blood flow; kidney is susceptible to _______ injury
hemodynamic, hypoxic
the three classifications of acute renal failure
prerenal
intrinsic
postrenal
if the cause of renal failure is a decrease in blood supply to the kidneys (renal perfusion), this is called ________ failure
prerenal
if the cause of renal failure is a problem within the kidneys, this is ________ renal failure
intrinsic
________ failure is due to a problem in the collecting system (ureters/bladder/urethra), e.g: obstruction by stones or tumor
postrenal
failure to excrete urea results in a progressive __________ of BUN and creatinine, which can result in uremia (build up of toxins; chronic renal failure)
elevation
in prerenal failure, BUN:Creatine ratio is
>20:1
in prerenal failure, urine [Na+] is
<20meq/L
in prerenal failure, FENa is
<1%
in intrinsic renal failure, BUN:Creatinine ratio is
10-15:1
in intrinsic renal failure, urine [Na] is
>40meq/L
in intrinsic renal failure, FENa is
>2%
Clinical presentation of ______:

1) Rapid deterioration of renal function
2) Accumulation of nitrogenous waste in blood that would normally be excreted in urine
3) rapid rise in BUN and Cr
4) May have diminished urine volume (oliguria)
Acute Kidney Injury (AKI)
patients dependent on prostaglandin vasodilation to maintain renal perfusion can develop renal failure with use of ________; this is an example of prerenal failure
NSAIDs
Patients with renal hypoperfusion (renal artery stenosis, CHF)
that are dependent on angiotensin II mediated vasoconstriction may go into renal failure with _________ use; this is an example of prerenal cause of AKI
ACE inhibitor
toxic effects of amino glycoside antibiotics, rhabdomyolysis, and sepsis are all examples of ________ causes of AKI
intrarenal
regardless of origin, all forms of AKI, if untreated, result in ____________, death and sloughing of tubular epithelial cells
acute tubular necrosis
two theories regarding mechanism of AKI
tubular theory and vascular theory
disordered adhesion of renal tubular epithelial cells and dysregulation of elements that secure tubular cells together are consequences of __________
tissue hypoxia
renal damage is potentiated by _______ state of the renal medulla
hypoxic
clinical presentation of chronic renal failure
osteodystrophy
neuropathy
bilateral small kidneys
anemia
most common cause of chronic renal failure
diabetes mellitus
2nd most common cause of chronic renal failure
HTN
patho of CRF
irreversible loss of nephrons
____% of nephrons can be lost without any short term evidence of functional impairment
50%
________ is a serious problem in chronic renal failure
hyperkalemia
hyperkalemia is especially dangerous when GFR is
<5 ml/min
in ______________, antistreptococcal antibodies form secondary to strep infection and create an antigen/antibody complex, which lodges itself in the glomerular capillaries (then causes an inflammatory response in the glomeruli of both kidneys)
poststreptococcoal glomerulonephritis
signs and symptoms of post streptococcal glomerulonephritis
dark urine, facial and peri-orbital edema, flank pain
why edema in post streptococcal glomerulonephritis?
loss of proteins in urine = decreased oncotic pressure (leads to generalized edema)
why flank pain in post streptococcal glomerulonephrits?
stretch of kidney
BUN/Cr is __________ in poststreptococcal glomerulonephritis (decreased GFR)
elevated
poststreptococcal glomerulonephritis causes metabolic ________
acidosis
primary nephrotic dissuasion children ages 2-6 (minimal change disease)
lipoid nephrois
abnormality of the glomerular capillaries that increases permeability, allowing proteins (primarily albumin) to escape in filtrate
nephrotic syndrome
decreased oncotic pressure and generalized edema is a result of
hypoalbuminemia
in hypoalbuminemia, the liver tries to increase the production of serum proteins since they are being lost in the urine, and in so doing it also increases the production of ______
lipids
increased lipid production from the liver in response to hypoalbuminemia results in high cholesterol, or ____________
hyperlipidemia
marked proteinuria, lipiduria, casts, massive edema

these are signs/symptoms of
Poststreptococcal Glomerulonephritis
clinical presentation of flank pain and hematuria with or without fever
renal stones
75% of stones contain _____; most idiopathic is
calcium; hypocalciuria
caused by hypericuosuria, especially in patients with history of gout or excessive purine intake (organ meat)
uric acid stones
defective amino acid transport that can cause stone formation
cystinuria
composed of magnesium, ammonium, and phosphate salts;
result of chronic or recurrent UTI's by urease producing organisms (typically proteus)
struvite stones
Stones result from alterations in the solubility of various substances in urine; __________ and ___________ of salts
nucleation, precipitation
factors that can favor stone formation
dehydration, high protein diet, high Na+ diet
factors that can protect from stones
fluids, citrate, magnesium, dietary fiber
obstruction of renal stone in the ureter can cause the development of
hydronephrosis
in _____________, urine is continually forming, and the prolonged interference of outflow creates back pressure, dilating the ureter or kidney behind the obstruction; this distension of the capsule causes severe pain
hydronephrosis
stone formation in the renal pelvis is ________ until a fragment breaks off and travels down the ureter
painless
Hematuria and renal __________ can occur in the absence of pain
damage
_________ and ___________ are suggestive of bilateral obstruction or obstruction of a single functioning kidney
anuria and azotemia
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