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NURS 3366 EXAM 4 100% VERIFIED LATEST UPDATE

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NURS 3366 EXAM 4 100% VERIFIED LATEST UPDATE


urine concentration decisions.

are made separately (not coordinating) in each nephron by two structures: the
glomerulus and the tubules



glomerulus affect on urine concentration

as blood enters glomerulus from afferent arteriole, it circulates in the glomerular
capillaries, which have basement membranes that serve as a screening, or filtration,
tool—this is called the glomerular membrane



first decision point of kidneys:

glomeruli are the first to "decide" what and how much to include as the beginning of
urine; done at the glomerular filtration rate (GFR)



glomerular membrane

where filtration occurs



glomerular filtration rate (GFR)

the volume of plasma filtered by all the functioning nephrons; the glomeruli filter approx.
180 liters ofplasma per day = normal GFR ~ 125ml /min



GFR is important because.

when a problem or disorder decreases the GFR we know the proper amount of water
and solutes are not being delivered into the urine, increasing risk of waste/water
accumulation within the body; decreases in GFR usually = decreased urine output



Decreased GFR means

,appropriate amount of water and solutes are not being delivered into the urine, thus
increasing risk of accumulation of wastes & water in the body



"decisions" of glomeruli and tubules aided by:

angiotensin II, aldosterone, ADH, & natriuretic peptides.



fluid deficit

low fluid sensed by kidneys > renin secreted by juxtaglomerular apparatus—area
around the glomeruli of each nephrons unit) > stimulates creation of angiotensin II >
peripheral vasoconstriction & aldosterone keeps Na+ and excretes K+



fluid deficit causes

oliguria (trying to conserve H2O) and what little urine is excreted will be small but
concentrated



fluid overload

BNP & ANP secreted by heart, go to renal tubules > stimulated to excrete more water
into the urine > you will void large amounts of more dilute urine (kidneys have gotten rid
of water to help your overloaded state)



when a person's GFR and/or waste product secretion decreases

we consider that person to be at some point on aspectrum from acute kidney injury
(AKI) to chronic kidney disease (CKD)




acute kidney injury (AKI)

acute but short-term; ex. glomerulonephritis, infection, trauma



chronic kidney disease (CKD)

slow developing but chronic, person considered to have renal insufficiency, scale of

,severity; AKI not resolved, PKD, diabetes mellitus, HTN, atherosclerosis



stage 1 CKD

kidney disease: kidney damage with normal or increased GFR (temporary increase is a
compensatory response



stage 2 CKD

mild reductionin GFR



stage 3 CKD

moderate reduction in GFR (25% of normal GFR, usually < 30mlof urine output/hour)



stage 4 CKD

severe reduction in GF



stage 5 CKD

full kidney failure—minimal or no GFR—sometimes called end-stage renal disease
(ESRD)--occurs when only ~ 10% renal function




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

Happens by direct tubular injury from the toxic substances or Unfixed tubular ischemia
coming from prerenal or post renal AKI

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