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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
Q

occurrence of nephrotoxic injury

A

pharmacologic compound with diverse structures
endogenous substances
environmental exposures

26
Q

risk factors for intrinsic AKI

A

old age
CKD
preenal azotemia

27
Q

contrast-induced nephropathy

A

causes;
hypoxia in the renal outer medulla
tubular cytotoxic damage
transient tubule obstruction

28
Q

clinical presentaion of CIN

A

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
Q

Acute interstitial nephritis due to antibiotitc

A

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
Q

chemotherapeutic agents and AKI

A

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
Q

toxic ingestion causing AKI

A

Ethylene glycol ( antifreeze) :
renal injury once metabolized
direct tubular injury
tubular obstruction

32
Q

Ethylene glycol ingestion

A

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
Q

AKI related endogenous compounds

A

internal vasoconstriction
direct proximal tubular toxicity
distal nephron lumen obstruction

34
Q

Rhabdomyolysis

A

muscles sustain massive injury
myoglobin released by injured muscle cells
pigment nephropathy

35
Q

massive hemolysis

A

hemoglobin released
pigment nephropathy

36
Q

initiation of cytotoxic therapy

A

Tumor lysis syndrome :
hyperuricemia
hyperkalemia
hyperphosphatemia

37
Q

Hyprcalcemia

A

intense renal vasoconstriction
volume depletion

38
Q

Post renal AKI

A

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
Q

Causes of post renal AKI

A

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
Q

AKI work up

A

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
Q

AKI clinical findings and complications

A

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
Q

AKI and potassium balance with renal dysfunction

A

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
Q

Hyponatremia with AKI

A

Neurologic deficity
seizures

44
Q

Hypocalcemia ( Ca+)

A

paresthesia
muscle cramps
seizure
prolong QT
rhabdomyolysis or tumor lysis with hyperphophatemia

45
Q

AKI complication

A

metabolic acidosis
elevated anion gap

46
Q

AKI urinalysis

A

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
Q

AKI imaging and procedures

A

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
Q

AKI treatment plan

A

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
Q

AKI treatment with hypovolemia

A

volume challenge with isotonic crystalloid ( 9% NSS) watch for Hyperchloremic metabolic acidosis

Anemia and hemorrhage :
PRBC transfusion

50
Q

AKI treatment severe hypovolemia with hypernatermia

A

Hypotonic crystalloids ( 0.45% NSS)

51
Q

treatment with AKI Metabolic acidosis

A

bicarbonate

52
Q

AKI treatment with Rhabdomyolysis and tumor lysis

A

agressive fluid management

53
Q

AKI treatment with elevated uric acid

A

allopurinal

53
Q
A
54
Q

treatment of AKI with volume oveload

A

fluid and Na restricution
diuretic

55
Q

treatment of AKI hyponatremia

A

restrict enteral-free H20
isotonic fluid +/-
minimize hypotonic solutions
stop diuretics
hypertonic rarely necessary
vasopressin is generally not needed

56
Q

treatment AKI hyperkalemia

A

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
Q

AKI treatment for Hyperphosphatemia

A

restrict dietary phosphate
phosphate binder: aluminum hydroxide or calcium acetate

58
Q

AKI treatment for hypocalcemia

A

calcium carbonate or calcium gluconate
follow ionized calicium

59
Q

Hypermagnesemia

A

discontinue Rx containing magnesium (mom)

60
Q

AKI treatment : unable to manage electrolytes and or BUN cr worsen

A

consult nephrology
CRRT
hemodialysis

NU 735 Fall Clinical (13 decks)

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