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NURS 3366 University Of Texas - Arlington -NURS 3366 - Exam 4 Questions With Complete Solutions

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NURS 3366 University Of Texas - Arlington -NURS 3366 - Exam 4 Questions With Complete Solutions

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NURS 3366 - Exam 4 Questions With Complete Solutions


S&S of AKI
abrupt (occurs over <48hrs) decreasd GFR > decreased urine
output (oliguria), and acute increase in serum creatinine
3 types of AKI
1. prerenal
2. intrarenal
3. postrenal
prerenal AKI
sudden and severe drop in blood pressure (shock) or interruption
of blood flow to the kidneys from severe injury or
illness; causes intrarenal AKI due to ATN, most common
intrarenal AKI
direct damage to the kidneys/nephrons/glomerulus/tubules by
inflammation, toxins, drugs, infection, or reduced blood supply
S&S of intrarenal AKI
glomerulonephritis and/or ATN > blood/protein/casts in urine >
can lead to CKD
glomerulonephritis
post-streptococcal antibodies attack glomerular membranes,
inflammation, vasodilation, protein and blood leak into urine
acute tubular necrosis causes

,occurs due to direct tubular injury from toxic substances or
unfixed tubular ischemia from prerenal or postrenal AKI
patho of ATN
tubular cells die from reduced blood flow (ischemia) or direct
injury, slough off and form cast (abnormal clumps), casts cause
blockage and sluggish urine flow, creates pressure on Bowman's
capsule & glomerular capillaries, eeduced GFR, oliguria &
decreased ability to excrete creatinine
tubular casts
Tightly packed collections of proteins, lipids, or cellular debris
that precipitate in renal tubules or collecting ducts and are
washed out by the flow of urine
postrenal AKI
sudden obstruction of urine flow due to enlarged prostate,
kidney stones, bladder tumor, or injury; causes intrarenal AKI
from hydronephrosis
all AKI injuries cause
decreased GFR, oliguria, and elevated serum creatine
chronic kidney disease
can be congenital (PKD) or acquired (athero, DM, HTN)
polycystic kidney disease (PKD)
an autosomal dominant inherited disease in which cysts
throughout the kidneys interfere with normal renal function
CKD causes

,imbalance in fluid & solute status and decreased metabolic
activity > results in fluid overload and high waste levels
(hypernatremia/phosphatemia/kalemia)
patho of CKD
RAAS overactivated, fluid overload increases, GFR
oliguria/anuria > hypertension due to increased hydrostatic
pressure, low serum osmolality > B -> T (peripheral and
pulmonary edema)
anuria
absence of urine
blood urea nitrogen
measurement of urea levels in blood, >25 could possibly be
renal issue or high meat diet
azotemia
high levels of waste like urea nitrogen and creatinine in the
blood
uremia
azotemia (high waste) +
pruritis
itching from deposition of urea on skin
uremic encephalopathy
neurological changes due to toxic levels of waste in blood--
confusion, decreased LOC, seizures

, when pt reaches CDK
kidneys are definitely not concentrating urine properly/getting
rid of waste
specific gravity
measures the concentration of urine
if pt dehydrated
very little urine, high concentration (oliguria, not trying to give
away more O2)
if pt over-hydrated
lots or urine output and very diluted
if pt kidneys sick
waste and fluid retention so little water and waste output
(oliguria, azotemia)
creatinine clearance urine test
measures 24 hours worth of creatinine excreted in urine &
compares it to serum creatinine, truly reflects GFR,
CKD also causes
hypocalcemia (less vitamin D activation) > hyperexcitable cells
> tetany, positive Chvostek's sign > osteoporosis fractures due
to lack of calcium
to treat oliguria and fluid volume overload
diuretics; an attempt to“encourage” the kidney to removewater
to treat azotemia and uremia

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