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NU 735 Fall Clinical > Acute Kidney Disease > Flashcards

Acute Kidney Disease Flashcards

1
Q

kidney where does blood reach each nephron

A

afferent tubulal : play a role in BP

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2
Q

Normal GFR patho

A

maintain in renal blood flow and relative resistance of the afferent and efferent arterioles

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3
Q

Efferent arterioles

A

carry blood away from the glomous that has been filtered maintains the GFR despite the fluctionation in BP

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4
Q

how much renal blood flow accounts for the amount of cardiac output

A

20% : renal vasoconstriction, salt, and water absorption occur as homeostatic responses to decreased effected circulating volume : mediators , ADH , vasopressin , angiotension II

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5
Q

AKI

A
  1. impaired kidney filtration and excretory function
    over days to weeks.
  2. Common causes:
    volume depletion , heart failure, medications, obstruction , malignancy, sepsis , surgical procedures, heart or liver failure, nephrotoxins
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6
Q

three categories of AKI

A

prerenal
intrinsic renal parenchymal disease
post-renal obstruction

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7
Q

KDIGO AKI definition

A
  1. increase in SC by > 0.3 within 48 hours
  2. increase in SC to > 1.5 x baseline, known or
    presumed to have occurred with in the prior 7 D
  3. urine volume < 0.5 ml kg h for 6 hours
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8
Q

Pre renal azotemia AKI

A

build-up of nitrogen in the blood
most common cause of AKI

no parenchymal damage of AKI
prolonged periods lead to AKI

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9
Q

Pre renal azotemia causes

A

hypovolemia

decreased CO

Medications interfere with renal autoregulatory response

NSAIDs - inhibit renal prostaglandin production and limit renal afferent vasodilation.

ACE i / ARBs- limit efferent vasoconstriction

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10
Q

Intrinsic AKI ( intrarenal)

A

50% of all AKI cases
pre and post-renal excluded

potential site of injury ;
tubules, interstitium, vasculature, and glomeruli

common causes
sepsis
ischemia
nephrotoxins
exogenous and endogenous

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11
Q

intrinsic AKI contribution problems

A

inflammation
apoptosis ( cellular death)
altered regional perfusion

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12
Q

causes of AKI

A

50% with severe sepsis
due to hemodynamic collapse
arterial dilation
renal vasoconstriction

tubular injury:
increase microvascular leukocyte
thrombosis
permeability
increase interstitial pressure
reduction in local flow to tubules
activation of reactive oxygen species -
manifested by urine tubular debris and casts

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13
Q

AKI contributing problems

A

inflammation
mitochondrial dysfunction
interstitial edema

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14
Q

Renal medulla :

A

most hypoxic region of the body
vulnerable outer medulla due to blood vessel architecture

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15
Q

Ischemic causes combined with limited renal reserve can cause AKI

A

independent ischemia is NOT sufficient to cause severe AKI

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16
Q

Causes of AKI

A

CKD
Sepsis
vasoactive or nephrotoxic drugs
surgery
burns and acute pancreatitits

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17
Q

Post operative AKI: intraoperative blood loss and hypotension

A

common procedure causing AKI:
cardiac surgery with cardiopulmonary bypass

valvular procedures with aortic cross-clamping

intraperitoneal procedures

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18
Q

cardiopulmonary bypass mechanisms; causing AKI

A

extracorporeal circuit activation: Leukocytes and inflammatory process

Hemolysis: pigment nephropathy

aortic injury: atheroemboli ( plaque rupture )

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19
Q

risk : AKI post-op

A

CKD
older age
diabetes
CHF
emergent procedures

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20
Q

other causes of AKI

A

fluid losses into the extravascular compartments: hypovolemia and decreased cardiac output

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21
Q

causes from hypovolemia and decreaseed cardiac output
other complications from AKI, ie, burns or acute pancreatitis

A

dysregulated inflammation
increased risk of sepsis
acute lung injury

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22
Q

Fluid resuscitation complication with AKI

A

abdominal compartement syndrome
intra abdominal > 20 mmHg =
renal vein compression and reduced GFR

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23
Q

kidney have high susceptibility to nephrotoxic agents

A

extremely high pressure perfusion
concentration of circultation subatances
all structures are vulnerable to toxic injury

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24
Q

high concentrations of toxins

A

tubular interstitial and endothelial cells exposure

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25
occurrence of nephrotoxic injury
pharmacologic compound with diverse structures endogenous substances environmental exposures
26
risk factors for intrinsic AKI
old age CKD preenal azotemia
27
contrast-induced nephropathy
causes; hypoxia in the renal outer medulla tubular cytotoxic damage transient tubule obstruction
28
clinical presentaion of CIN
rise in creatinine in 24-48 hours peaking in 3-5 days resolving in a week treatment is IV hydration mucomist? no good data
29
Acute interstitial nephritis due to antibiotitc
Tubular necrosis: aminoglycosides and amphotericin Aminoglycosides: : filtered across glomerulus, accumulate in the renal cortex with high concentrations Features: manifest in 5-7 days and hypomagnesemia Amphotericin B: renal vasoconstriction, direct tubular toxicity mediated by reactive oxygen species : clinical features: polyurea, low mag, and ca+ , non-gap metabolic acidosis
30
chemotherapeutic agents and AKI
cause; necrosis apoptosis Ifosfamide : type 2 renal acidosis AKA Fanconis syndorme hemorrhagic cystitis polyurea hypokalemia drop in GFR Antiangiogenesis agents ( Avastin) : Injury to globular microvasculature proteinuria and hypertension Antineoplastic agents: thrombotic microangiopathy IE consider the chemo drug as the edeology of the AKI
31
toxic ingestion causing AKI
Ethylene glycol ( antifreeze) : renal injury once metabolized direct tubular injury tubular obstruction
32
Ethylene glycol ingestion
intoxicated WITH non-toxic blood alcohol concentration anion gap acidosis hypocalcemia urinary crystals Management: notify poison control antizol ( fomepizole) 15mg/kg IV x1 then 10mg kg iv q 12 hours x4 continue 15mg dosing until levels < 20 mg dl
33
AKI related endogenous compounds
internal vasoconstriction direct proximal tubular toxicity distal nephron lumen obstruction
34
Rhabdomyolysis
muscles sustain massive injury myoglobin released by injured muscle cells pigment nephropathy
35
massive hemolysis
hemoglobin released pigment nephropathy
36
initiation of cytotoxic therapy
Tumor lysis syndrome : hyperuricemia hyperkalemia hyperphosphatemia
37
Hyprcalcemia
intense renal vasoconstriction volume depletion
38
Post renal AKI
unidirectional flow of urine acutely blocked partially or completely : Increased retrograde hydrostatic pressure interference with GFR Functional or structural : renal pelvis to tip of urethra
39
Causes of post renal AKI
bladder neck obstruction: BPH or prostate CA ( common for 65 yer old and older) neurogenic bladder anticholinergic drugs foley cath blood clots calculi urethral strictures neoplasm abscess surgical damage
40
AKI work up
Collect history and physical exam Labs: CBC, CMP, UA FeNA : (urnie na /serum and Na+) ( urnie cr/serum cr ) x 100 < 1% FeNA prerenal > 1 % FeNA intrarenal uric acid Diagnostics: CT scan renal calculi protocol ( colicky pain ) renal US Procedures: renal bx
41
AKI clinical findings and complications
ATN: 85% of intrinsic AKI major causes is ischemia and nephrotoxins Uremia: manifested with elevated BUN mental status changes BUN > 100 bleeding complications Hypervolemia: ( oliguria) impaired Na+ and H20 excretion expansion of the extracellular fluid weight gain, dependant edema, increased JVD, pulmonary edema Hypovolemia: ( polyurea) retained urea and other waste products osmotic diuresis polyurea
42
AKI and potassium balance with renal dysfunction
Hyperkalemia: high risk in rhabdomyolysis hemolysis and tumor lysis muscle weakness Cardiac conduction: fatal arrhythmias spiked T wave Neuromuscular: generalized weakness muscle cramps paresthesia
43
Hyponatremia with AKI
Neurologic deficity seizures
44
Hypocalcemia ( Ca+)
paresthesia muscle cramps seizure prolong QT rhabdomyolysis or tumor lysis with hyperphophatemia
45
AKI complication
metabolic acidosis elevated anion gap
46
AKI urinalysis
easy to obtain limited sensitivity and specificity Oliguria : < 400 day associated with worse outcomes Proteinuria damage to the globular filtration barrier < 1mg day ischemia and nephrotoxic > 3.5 gr day glomerulonephritis, vasculitis, or medication toxins Urine eosinophils: Interstitial nephritis, pyelonephritis, cystitis, atheroembolic disease or glomerulonephritis Oxalate: Ethylene glycol toxicity Uric acid crystals: Tumor lysis syndrome Urine osmolality: > 500 in pre-renal azotemia urealiable with CKD and elderly patients
47
AKI imaging and procedures
Renal Ultra sound: normal size kidnes expeced in AKI shrunken kidneys with cortical thinning realated to CKD enalarged kidneys suggest acute interstitialnephritis or infiltrative disease CT scan obstruction: Dilation of collecting system hydroureteronephrosis MRI: caution advised gadolinium contrast nephrogenic systemic fibrosis , can cause other organ damage Renal BX definitive diagnosis high risk for bleeding
48
AKI treatment plan
management varies according to the underlying optimization of hemodynamics correction of fluid and electrolyte imbalance discontinuation of nephrotoxic agents dose adjustment of administered medications
49
AKI treatment with hypovolemia
volume challenge with isotonic crystalloid ( 9% NSS) watch for Hyperchloremic metabolic acidosis Anemia and hemorrhage : PRBC transfusion
50
AKI treatment severe hypovolemia with hypernatermia
Hypotonic crystalloids ( 0.45% NSS)
51
treatment with AKI Metabolic acidosis
bicarbonate
52
AKI treatment with Rhabdomyolysis and tumor lysis
agressive fluid management
53
AKI treatment with elevated uric acid
allopurinal
53
54
treatment of AKI with volume oveload
fluid and Na restricution diuretic
55
treatment of AKI hyponatremia
restrict enteral-free H20 isotonic fluid +/- minimize hypotonic solutions stop diuretics hypertonic rarely necessary vasopressin is generally not needed
56
treatment AKI hyperkalemia
restrict dietary K+ stop K+ sparing diuretics , ACEi /ARB, NSAIDs K binder ( kayelexate) emergent treatment regular insulin 10 units IV Amp D 50 amp NAHc03 ( ?) not shown to be effective inhaled beta agonists ( ie duoneb)
57
AKI treatment for Hyperphosphatemia
restrict dietary phosphate phosphate binder: aluminum hydroxide or calcium acetate
58
AKI treatment for hypocalcemia
calcium carbonate or calcium gluconate follow ionized calicium
59
Hypermagnesemia
discontinue Rx containing magnesium (mom)
60
AKI treatment : unable to manage electrolytes and or BUN cr worsen
consult nephrology CRRT hemodialysis

NU 735 Fall Clinical (40 decks)

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