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45 Cards in this Set
- Front
- Back
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3 drugs/chemicals inhibit creatinine secretion
and therefore _ plasma creatinine |
cimetidine
trimethoprim ketoacids elevate plasma creatinine |
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creatinine does not increase as expected
because of decreased creatinine production in these two conditions: |
muscle wasting
protein malnutrition |
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creatinine clearance is a worse than usual estimate of GFR
in what situation? why? |
if renal function has deteriorated,
secretion contributes proportionately more to total creatinine excretion [filtration from GFR has a smaller proportional contribution] --> we overestimate GFR |
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non-renal things that cause
BUN elevation |
protein catabolism
--fever --burns --glucocorticoid therapy GI bleeding tetracycline (it is anti-anabolic) |
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urea reabsorption...
is linked to ____ is stimulated by two hormones those two hormones act at what parts of the nephron? |
reabsorption of Na+ and H2O:
ATN II: Na+, H2O at proximal tubule vasopressin: H2O at medullary collecting duct |
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besides ATII and vasopressin,
something else affects BUN reabsorption |
åt low urine flow rates, urea reabsorption is 75%
at high urine flow rates, it's < 20% |
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BUN/creatinine ratio in
intrinsic kidney damage...? why? |
10:1-15:1
Na+ and H2O reabsorption are decreased throughout entire kidney --> tubular reabsorption of urea is also decreased [because urea reabsorption is linked to reabsorption of Na+ and H2O] BUN and creatinine are proportionately elevated |
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in decreased intravascular volume,
BUN/creatinine ratio is ____ because of two hormonal causes |
> 20:1
RAAS vasopressin |
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4 lab findings seen in
advanced acute kidney injury |
fluid retention
hyperkalemia metabolic acidosis nitrogenous wastes |
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specific causes of prerenal AKI, and the gist of how they do it
(11) |
decreased effective volume
--heart failure --cirrhosis --nephrotic syndrome decreased volume --hemorrhage --3rd degree burns --GI fluid losses decreased renal perfusion --renal artery stenosis --renal vein thrombosis decreased renal blood flow or GFR --NSAIDs --ACEs, ARBs --radiocontrast dyes |
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which patients are particularly vulnerable to
NSAID-induced prerenal azotemia? ACEs, ARBs - induced prerenal azotemia? |
heart failure
diabetes cirrhosis with ascites elderly heart failure diabbetes renal artery stenosis |
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decreased renal blood flow causes 3 physiological compensatory mechanisms to be engaged
____ ____ ____ |
sympathetic
RAAS vasopressin |
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efferent constriction in prerenal azotemia is caused by?
why? |
catecholamines
ATN II to raise FF and GFR |
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prerenal vs. intrinsic
BUN/creatinine ratio urine Na+ urine osmolality |
prerenal
> 20:1 < 20 mEq/L > 500 mosm/Kg intrinsic 10:1-15:1 >40 mEq/L 300 mosm/Kg (like plasma) |
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urine Na+ in prerenal is ____
because of hormones that cause ___ ___ what hormones? they act at what part of the nephron? |
< 20 mEq/L
Na+ reabsorption ATN II --proximal aldosterone --distal --cortical collecting |
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ischemic causes of ATN
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septic shock
postoperative multiple trauma (hypoperfusion) |
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ATN:
direct toxins vasoconstrictive toxins |
aminoglycosides
cisplatin NSAIDs cyclosporine A iodinated radiocontrast |
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what part of the kidney is most susceptible to
ischemic ATN? why? |
3rd portion of proximal
thick ascending limb metabolically active less O2 in the medulla |
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N-acetylcysteine is prophylaxis for...
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radiocontrast-induced ATN
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N-acetylcysteine
mechanism? how to administer it? |
anti-oxidant
increases bioavailability of NO --> renal vasodilation give with saline prehydration |
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decreased GFR in acute tubular necrosis is caused by...
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constriction of afferent
tubular cell dysfunction and/or tubular cell obstruction |
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8 mechanisms of acute tubular necrosis
1 word or 1 line summary of each |
basolateral membrane dissociation of spectrin & Na/K ATPase
adenosine decreased NO synthesis tubules release ATN II but not PGE2 superoxide production casts and cell debris cell swelling Ca++ --> apoptosis |
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[from ATN horrible mechanisms page]
the 3 ATN mechanisms that cause afferent constriction |
adenosine
decreased NO ATN II, but lack of PGE2 release |
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ATN mechanisms page...:
what causes ATN II what does it cause (2) |
damaged tubular cells
release ATN II; fail to release PGE2 ATN II causes --afferent constriction --superoxide production |
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ATN mechanisms...:
what causes superoxide production what does it cause (4) |
ATN II causes superoxide production in the medulla
superoxides damage tubular cells, which detach obstruct the lumen form casts |
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ATN mechanisms
how does Na/K ATPase pump failure lead to apoptosis? (4) |
increased Na/Ca exchange
increased intracellular Ca++ caspase activation APOPTOSIS |
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ATN mechanims:
Na/K ATPase pump issues cause 3 big problems ____, ____, ____ |
adenosine
cell/tissue swelling apoptosis |
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ATN mechanisms:
how do Na/K ATPase issues cause adenosine production? (5) |
Na/K ATPase dissocates from spectrin at basolateral membrane
Na/K ATPase relocates to luminal membrane it pumps Na+ into lumen macula densa notices the increased Na+ and causes ADENOSINE production |
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what causes high-output ATN
how? |
aminnoglycosides
they damage tubular cells but don't cause afferent constriction |
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what's wrong in high-output ATN
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damaged tubules are unable to concentrate urine, so
each day they accumulate 300-400 mosms of urea and creatinine |
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urine sediment findings in
3 different conditions that cause AKI |
ATN:
muddy-brown granular casts epithelial cell casts glomerulonephritis: red cells red cell casts interstitial nephritis white cells white cell casts |
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two causes of bilateral kidney obstruction
other urinary tract obstructive processes |
** shed papillae during papillary necrosis **
ureteral compression by retroperitoneal neoplasia - - - - - - - - BPH catheter occlusion intratubular deposition of uric acid crystals |
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the most common cause of urinary tract obstruction
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BPH
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most common sites of kidney obstruction
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bladder neck (50%)
uretero-pelvic junction (27%) ureter (19%) |
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kidney obstruction causes what changes to the
pressure in bowman's space why? |
obstruction initially increases pressure in Bowman's space
- - - - - - - after 24-36 hours, the pressure becomes normal because obstruction causes **widespread vasoconstriction of afferent arterioles** [ by increased renal production of TXA2 and ATN II ] |
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kidney obstruction has two initial effects
and two other effects after a couple days |
initially:
obstruction causes increased pressure in Bowman's space ATN II production by tubules initially decreases urinary Na+ excretion -------- later on: pressure drops because obstruction causes vasoconstriction of afferent arterioles ATN II causes tubular inflammation and fibrosis --> increased urinary Na+ excretion |
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causes of anuria
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** obstruction **
cortical necrosis RPGN bilateral renal artery occlusion |
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kidney obstruction...:
obstruction --> elevated ATN II --> NF-kB --> (4) (inflammation diagram) |
--angiotensinogen --> ATN II
--fibroblast proliferation and differentiation --> fibrosis --tubule cells: macrophage chemoattractants --TNF-a->inflammation-->fibrosis |
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intrinsic AKI is potentially reversible when?
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initiation phase
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during the maintenance phase of intrinsic AKI
GFR? duration? |
GFR 5-10 ml/min
1-6 weeks long |
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intrinsic AKI causes symptoms in what body systems?
(5) |
metabolic
cardiovascular GI neurological mild anemia |
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metabolic sxs of intrinsic AKI
(5) |
volume overload
hyponatremia hyperkalemia metabolic acidosis hypocalcemia |
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cardiovascular sxs of intrinsic AKI
(5) |
arrhythmias
systolic and diastolic heart failure hypertension MI PE |
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GI sxs of intrinsic AKI
(4) |
anorexia
vomiting mucosal ulcerations --> blood loss |
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one manifestation of recovery phase of intrinsic AKI
why? |
brisk diuresis: 1 week
heavy solute load: BUN and creatinine that had built up |
