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71 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 when...
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if renal function has deteriorated,
creatinine secretion contributes proportionately more to overall creatinine excretion --> we overestimate GFR |
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BUN vs creatinine: are they
filtered, secreted, reabsorbed...? |
BUN:
--filtered --flow-rate dependent reabsorption creatinine --filtered --slightly secreted |
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creatinine normal range
BUN normal range |
0.6-1.2 mg/dL
7-18 mg/dL |
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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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things that cause
low BUN |
severe liver failure
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urea reabsorption is stimulated by these two hormones.
exactly where do they operate, and what else are they doing at those locations? |
urea reabsorption is linked to reabsorption of...:
AT 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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two big picture, general situations that cause
BUN:creatinine ratio is > 20:1 |
decreased renal perfusion
decreased real or effective intravascular volume |
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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 BUN and creatinine are proportionately elevated |
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in decreased intravascular volume,
BUN/creatinine ratio is ____ because of two things |
> 20:1
RAAS vasopressin |
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two main ways we can detect acute kidney injury clinically
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elevated creatinine clearance indicates a decreased GFR
oliguria <500 mL/day anuria <50 mL/day |
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4 lab findings seen in
advanced acute kidney injury |
fluid retention
hyperkalemia metabolic acidosis nitrogenous wastes |
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3 broad categories of acute kidney injury...
in order from most common |
prerenal
intrinsic / [intrarenal] postrenal |
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3 main types of
acute intrinsic kidney injury |
acute:
tubular cell injury interstitial nephritis glomerulonephritis |
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the causes of tubular cell injury
(broad categories and subcategories) |
ischemia and inflammation
toxins --direct --vasoconstrictive |
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the most common cause of acute kidney injury
and its mechanism |
decreased renal perfusion
decreased hydrostatic pressure --> decreased GFR |
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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 " ? |
heart failure
diabetes cirrhosis with ascites elderly heart failure diabbetes renal artery stenosis |
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how can NSAIDs cause prerenal azotemia?
they can cause... |
decreased renal prostaglandin production
thereby limiting how much afferent dilation can compensate for decreased renal blood flow |
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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
AT II to raise FF and GFR |
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filtration fraction =
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GFR/RBF
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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 what hormones? where do they act? |
< 20 mEq/L
Na+ reabsorption caused by ATII --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 kiidney 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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direct toxins that cause ATN
where do they act? |
cisplatin
aminoglycosides proximal |
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how do iodinated radiocontrast agents cause ATN?
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vasoconstrict afferent
occlude small vessels in medulla |
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N-acetylcysteine is prophylaxis for...
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radiocontrast-induced ATN
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N-acetylcysteine
mechanism? administration? |
anti-oxidant
increases bioavailability of NO --> renal vasodilation give with saline prehydration |
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decreased GFR in ATN is caused by...
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constriction of afferent
tubular cell dysfunction and/or tubular cell obstruction |
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8 multiple mechanisms of ATN
1 line each |
spectrin & Na/K ATPase dissociate
adenosine decreased NO synthesis tubules release ATII but not PGE2 superoxide production casts and cell debris cell swelling Ca++ --> apoptosis |
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ATN mechanisms:
dissociation of spectrin and Na/K ATPase --> (2) which then causes... |
proximal tubules:
loss of cell polarity. Na/K ATPase pumps relocate to luminal membrane Na+ enters cells and gets pumped back into tubular lumen increased Na+ delivered to macula densa --> adenosine production |
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ATN mechanisms...:
adenosine --> |
afferent constriction
--> decreased GFR |
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the ATN mechanisms that cause afferent constriction
(which causes decreased GFR) |
adenosine
decreased NO ATII, but lack of PGE2 release |
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ATN mechanisms...:
what causes AT II what does it cause |
damaged tubular cells
release AT II; fail to release PGE2 ATII causes --afferent constriction --superoxide production |
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ATN mechanisms...:
what causes superoxide production what does it cause |
ATII 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) |
dissociation with spectrin at basolateral membrane
Na/K ATPase relocates to luminal membrane Na+ pumped into lumen macula densa notices Na+ 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 with high-output ATN
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they're unable to concentrate their urine, so
each day they accumulate 300-400 moosms of urea and creatinine |
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one kind of ATN has a better prognosis
why |
high-output, aka non-oliguric
- - - - - - fluid overload hyperkalemia are less likely |
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one really quick urinalysis way to distinguish
ATN vs. prerenal |
ATN has
muddy-brown granular casts epithelial cell casts |
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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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uremia only occurs if there is obstruction of...
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both kidneys
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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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intratubular deposition of uric acid crystals occurs in the setting of
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chemo for lymphoproliferative and hematologic malignancies
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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 |
pressure 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 ATII ] |
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kidney obstruction has two initial effects
and two other effects after a couple days |
initially, increased pressure in Bowman's space
then, vasoconstriction of afferent arterioles - - - - - - - - - - - - ATII production by tubules, which initially decreases urinary Na+ excretion then, ATII 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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_ is highly sensitive and specific for diagnosing renal obstruction
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anuria and
hydronephrosis on renal ultrasound |
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kidney obstruction...:
obstruction --> elevated ATII --> NF-kB --> (4) (inflammation diagram) |
--angiotensinogen --> AT II
--fibroblasts -->fibrosis --tubule cells: macrophage chemoattractants --TNF-a->inflammation-->fibrosis |
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intrinsic AKI
low-dose dopamine's effects |
increases renal blood flow
contraindicated because --medullary hypoxemia --reduces gastric blood flow --intestinal ischemia --euthyroid sick syndrome --decreases immune function |
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the phases of intrinsic AKI
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initiation
maintenance recovery |
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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
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volume overload
hyponatremia hyperkalemia metabolic acidosis hypocalcemia |
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intrinsic AKI's hypocalcemia is due to (3)
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elevated phosphate
resistance to PTH decreased production of vitamin D |
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cardiovascular sxs of intrinsic AKI
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arrhythmias
systolic and diastolic heart failure hypertension MI PE |
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GI sxs of intrinsic AKI
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anorexia
vomiting mucosal ulcerations --> blood loss |
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neurological sxs of intrinsic AKI
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altered consciousness
asterixis seizures may lead to full-blown uremic encephalopathy: --dementia --stupor --coma |
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mild anemia in intrinsic AKI is because...
(4) |
inhibition of erythropoiesis
hemolysis/reduced RBC survival bleeding hemodilution |
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one manifestation of recovery phase of intrinsic AKI
why? |
brisk diuresis: 1 week
heavy solute load: BUN and creatinine |
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prognosis for ATN
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50% mortality in elderly following surgery or trauma
10-20% in young, in spite of dialysis |
