Renal Flashcards
part of nephron
renal corpuscle (Bowman’s capsule and glomerulus)
proximal tubule
loop of Henle (descending and ascending portions)
distal tubule
feed into collecting ducts
metabolites filtered in glomerulus
creatinine
uric acid
urea
increased serum NaCl detected by JGA will lead to:
increased GFR and vasoconstriction to retain water
normal GFR
120-140 mL/min, 180 L/day
ADH effects on collecting ducts and urine
increases permeability of collecting ducts, which allows water to escape back into interstitium rather than being excreted (retains water)
aldosterone function
increases Na+ and K+ exchange in distal tubule of nephron: causes Na+ retention (and therefore, water retention), and K+ excretion
presence of protein in urine (above 150 mg/day) indicates:
increased glomerular permeability; always pathological!
normal urine specific gravity
1.020
normal urine pH
4.5-8.0
pH is always lowest at what time of day?
through the night, leading to lowest urine pH at first voidance in the morning
normal plasma creatinine
0.7-1.5 mg/100 mL
normal BUN
10-20 mg/dL
renal dysfunction/disease causes ___ in creatinine and BUN
increase
azotemia def
renal insufficiency –> nitrogenous substrates increased in the blood
morphologic examination of renal function
urine microscopy; urine bacteriologic exam; radiologic kidney exams
presence of cellular casts in urine indicates:
pyelonephritis
presence of red blood cells indicates:
glomerulonephritis
presence of fatty casts and/or protein in urine indicates:
nephrotic syndrome
lead nephropathy pathophysiology
causes interstitial nephritis –> inflammation impairs nephron function –> slow and progressive renal failure
stage I renal failure characteristics
decreased renal reserve, asymptomatic
stage II renal failure characteristics
renal insufficiency, azotemia; occurs after 75% of nephrons are destroyed/nonfunctional
stage III renal failure characteristics
end stage failure; occurs after 90% of nephrons are destroyed/nonfunctional; aka uremic syndrome
most common cause of stage III/end stage renal failure
diabetic nephropathy
(creatinine/BUN) is better indicator of renal function; why?
creatinine; because BUN is affected by dietary intake and so may not accurately represent extent of renal insufficiency
acute oliguric renal failure urine output
less than 400 mL/day
early symptoms of kidney disease are ___ and ___, caused by ___
polyuria; nocturia; inability of kidneys to concentrate urine, aka letting out a whole lot of water
uremia symptoms present when GFR falls to ___% of normal
5-10%
80% of UTIs are caused by
E. coli
predisposing factors for UTIs
urinary calculi; neurogenic bladder; bladder instrumentation (i.e. foley cath); prostatic hypertrophy
treatment of acute pyelonephritis
antibiotics – very effective!
glomerulonephritis is usually (bilateral/unilateral)
bilateral
patho of acute glomerulonephritis
usually follows b-hemolytic strep infection; antigen-antibody complexes form in glom basement membrane; phagocytes and lysosomes attack basement membrane directly
rapidly progressive glomerulonephritis prognosis
<2 years
patho of chronic glomerulonephritis
similar to acute, but due to a long-standing disease (i.e. diabetes); progresses gradually over time
hypertensive nephrosclerosis etio
arteriosclerosis of afferent arterioles (entering glomerulus) due to long-standing hypertension
nephritis resulting from SLE has similar clinical manifestations of ___
acute glomerulonephritis
gout etio
increased uric acid in plasma; deposits and crystallizes in joints and kidneys
uric acid calculi predisposing factors
gout
chemotherapy
> 90% of kidney stones contain ___
calcium
nephrotoxic substances
glycols
spot remover (inhalation) and beer
mercury bichloride
IV contrast media (in pts with preexisting renal insufficiency)
renal insufficiency (stage 2) effects: GFR? urine frequency? acid/base? sodium? potassium? toxins/nitrogenous substrates? CV function? respiratory changes? hematocrit?
GFR - slightly decreased urine frequency - polyuria/nocturia acid/base - mild acidosis sodium - decrease potassium - decrease toxins/nitrogenous substrates - increase CV function - none respiratory changes - mild tachypnea; compensatory response to mild acidosis hematocrit - minimal change
renal failure (stage 3) effects: GFR? urine frequency? acid/base? sodium? potassium? toxins/nitrogenous substrates? CV function? respiratory changes? hematocrit?
GFR - dramatically decreased (5-10% of normal) urine frequency - oliguria/anuria acid/base - moderate to severe acidosis sodium - increase potassium - increase toxins/nitrogenous substrates - increase CV function - HTN and arrhythmias respiratory changes - Kussmaul respirations hematocrit - decrease d/t diminished EPO
example of prerenal patho
CV disease: HTN, heart failure, atherosclerosis
example of renal patho
any disease that impacts the nephron and interstitial space itself: nephrotoxicity, glomerulonephritis
example of postrenal patho
any disease of urinary conduction tubes: calculi, infection, BPH
when a pt presents with anuria, start by doing assessments for ___ problems first
postrenal - obstructions, infections, etc
post obstructive diuresis def
after relief of obstruction, kidneys kick into diuresis and may cause hypovolemia
treat noninfective cystitis with:
muscle relaxants, anticholinergics, antiparasympathetics
noninfective pyelonephritis can be caused by:
radiation, chronic inflammation, chronic illness, infection elsewhere
glomerulonephritis patho
- increased glomerular permeability –> proteinuria, hematuria
- glomerular injury by immune complexes –> decreased GFR, oliguria
long-term manifestations of glomerulonephritis
HTN, edema, pleural effusion, ascites, electrolyte imbalances, CV sequelae
treatment goals of glomerulonephritis
stop inflammation, treat underlying inflammatory disease, restore fluid/electrolyte balance
two causes of acute tubular necrosis
ischemic, nephrotoxic
acute tubular necrosis def
dying tubular cells of nephrons, inability to concentrate urine
kidney disease 2 major problems
- unable to concentrate urine, for whatever reason – polyuria and nocturia, plus all the fluid/electrolyte and CV problems that go with it
- decreased GFR – result of RAAS kicking in to compensate for #1, or direct injury to glomeruli
short-term manifestations of glomerulonephritis
hematuria, proteinuria, decreased GFR, oliguria
most important treatment goal of managing acute tubular necrosis is:
maintaining fluid/electrolyte balance
(men/women) are more susceptible to renal cell carcinoma
men
renal cancer has (known/unknown) etiology
unknown
most common renal vascular anomaly
multiple renal arteries
a person on a low protein diet is unable to concentrate urine as well as a person on a high protein diet because:
decreased production of urea
factors that contribute to the development of congestive heart failure in chronic renal failure include:
anemia, sodium retention, HTN
major bladder cancer risk factor:
smoking
causes of hemolytic uremic syndrome
E. coli, shigella, drugs, tumors
renal cyst vs renal neoplasm
fluid densities are different
horseshoe kidneys are congenital anomalies associated with what disorder?
trisomies
true or false: cause of polycystic kidney disease is unknown
false
kidneys become (smaller/larger) in end-stage renal disease
smaller
Wilms tumor is the result of:
genetic defect on chromosome 11
common side effects of dialysis
hyperkalemia, hypotension, muscle cramps
