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Clin Med 3 > AKI - Exam 2 > Flashcards

AKI - Exam 2 Flashcards

1
Q

what is AKI?

A

Abrupt decline in renal function manifesting as reversible acute increase in nitrogenous wastes over hours to weeks

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2
Q

AKI is a precursor to what?

A

renal failure

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3
Q

BUN, Cr, and GFR in AKI?

A

BUN and Cr increase

GFR decreases

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4
Q

what is the RIFLE criteria?

A

” Classification system for the degree of insult to the kidney

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5
Q

are acute renal failure (ARF) and AKI the same?

A

NO!!!

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6
Q

3 graded levels of injury in RIFLE Criteria

A

risk, injury, failure

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7
Q

2 outcome measures of RIFLE Criteria

A

Loss of function
-total loss of kidney function (GFR < 15 for >4weeks) -> need dialysis for >4 weeks

End stage renal disease
-GFR < 15 for >3 months -> need dialysis for >3 months

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8
Q

RIFLE Criteria based on what?

A

Based on either degree of serum creatinine elevation or decrease in urine output

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9
Q

what conditions are at a higher risk for developing AKI?

A

HTN, DM (2 M/C)

CHF (chronic low flow to the kidneys = greater risk for AKI)

MM (have underlying kidney injury at baseline)

Chronic infection

Myeloproliferative disorder

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10
Q

3 etiologies of AKI?

A

pre-renal causes, intrinsic causes, post-renal causes

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11
Q

what are pre-renal causes of AKI?

A

low flow problem into kidney

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12
Q

what are intrinsic causes of AKI?

A

problem with kidney itself
-Problem with glomerulus, interstitial nephritis, tubules

-tubular problems are the M/C

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13
Q

what is the most common cause of intrinsic causes to the kidney? what is it due to?

A

tubular problems

-d/t vascular problems, ischemic problems, toxic problems, obstructive problems

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14
Q

what are post-renal causes of AKI?

A

anything that blocks off both ureters

ex: large bladder cancer, clot in bladder if someone on Coumadin and starts bleeding, problems with prostate

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15
Q

MAP and AKI

A

MAP < 80mmHg causes AKI to occur quickly

pre-renal cause of AKI

can occur in septic pts, cariogenic shock pts

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16
Q

examples of pre-renal causes of AKI?

A

pre-renal azotemia (increase in BUN/Cr w/out sx’s associated with it)

MAP <80mmHg then steep decline in GFR

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17
Q

most common cause of ARF?

A

renal blood flow problems (pre-renal causes)

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18
Q

intrinsic renal diseases affect what?

A

affecting small vessels, interstitial, glomeruli, or tubules

-most common is obstructive (acute tubular necrosis)

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19
Q

most common cause of tubular problems for AKI?

A

acute tubular necrosis - causes obstruction

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20
Q

post-renal processes of AKI

A

Obstruction or urine flow in ureters, bladder, or urethra

REVERSIBLE

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21
Q

how do NSAIDs affect the kidney?

A

NSAIDs are bad for kidneys (not toxic to kidney itself), but b/c they prevent the afferent arteriole from dilating to increase flow to kidney -> thus decreases flow to kidney -> increases likelihood of developing AKI

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22
Q

what is TTP-HUS-DIC?

A

all are coagulopathy disorders which can cause clots in the vessels and blockage of the vessels -> causing an ischemic kidney

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23
Q

pre-renal AKI etiology

A

Hypovolemia, decreased cardiac output, decreased effective circulating volume (CHF, liver failure/hepatorenal syndrome, sepsis, pancreatitis, nephrotic syndrome) -> all cause low flow through glomerulus

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24
Q

what is the most common cause of renal failure?

A

pre-renal injury

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25
Q

how is pre-renal injury reversed?

A

with restoration of renal perfusion/glomerular pressure (ex: with IVF, blood, vasopressors -> all improve volume thru kidneys)

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26
Q

BUN/Cr ratio for pre-renal injury

A

> 20:1 (dehydration ratio)

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27
Q

what do you see a decrease of in pre-renal injury?

A

fractional excretion of sodium (FeNa)

-activating RAAS -> holding onto fluid and sodium, so see decrease in FeNa

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28
Q

what does urinalysis for pre-renal injury reveal?

A

hyaline casts

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29
Q

FeNa <1% is suggestive of what?

A

pre-renal azotemia

-Kidney is working well, it’s trying to hold onto sodium with aldosterone and also water, so have less Na being secreted, so < 1% FeNa

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30
Q

FeNa >1% is suggestive of what?

A

intrinsic renal failure

-kidney is losing Na, it can’t hold onto it

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31
Q

FeNa >4% is suggestive of what?

A

post-renal failure

-Early on the FeNa will be lower than 4%, but later on it will rise b/c later on you don’t make as much urine, so have a lot of Na just sitting around in the little bit of urine that you do make (urine is super concentrated with Na)

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32
Q

when is FeNa not accurate?

A

when pt is on diuretics - can’t do FeNa if have taken diuretics w/in past 24hrs

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33
Q

can have increase in FeNa and be pre-renal if ___

A

on diuretics, have CKD and baseline FeNa is already baseline high

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34
Q

what is an alternative to FeNa?

A

FeUrea or FeUA

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35
Q

FeUrea/FeUA is not influenced by what?

A

not influenced by diuretics like FeNa is

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36
Q

FeUrea < 35% or an FeUA < 9-10% suggests?

A

a prerenal etiology of ARF

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37
Q

FeUrea > 50% or an FeUA > 10-12% suggests?

A

ATN (intrinsic cause) - acute tubular necrosis

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38
Q

pre-renal labs

A

elevated H/H, albumin, Ca (b/c pts are dry)

elevated Na, BUN, Cr

Decreased CO/effective arterial volume -> have edema

Urine output - oliguria (<500ml/day) or anuria (<100ml/day); low urine Na (<20 mEq/L)

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39
Q

what is the urine output like in pre-renal AKI?

A

OLIGURIA (< 500ml/day) or anuria (<100ml/day)

Low urine Na (<20 mEq/L)

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40
Q

if a male has anuria, what is the first thing to think about?

A

their prostate

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41
Q

if not making any urine, then what is usually the cause?

A

an obstruction of some kind

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42
Q

pre-renal tx

A

volume depletion
-NS and titrate

decreased CO/effective circulating volume
-diuretics (high dose IV), nitrates, dobutamine

all meds cleared by renal excretion should be avoided or doses adjusted

if pt volume depleted -> do not give diuretics

43
Q

what meds are never given to a person that anuric?

A

diuretics

44
Q

why give high dose IV diuretics for pre-renal tx?

A

to get the volume off, so give something nephrotoxic

treating like severe CHF pts with low volume

45
Q

what is acute interstitial nephritis?

A

ALLERGIC reaction to medication (usually a new drug)

intrinsic renal cause

46
Q

classic presentation of acute interstitial nephritis?

A

after recent new drug exposure

peripheral eosinophilia

***More commonly, pts are found incidentally to having rising serum creatinine after initiation of new med

47
Q

most common meds associated with causing acute interstitial nephritis?

A

antibiotics

-Beta-lactams, sulfonamides, vancomycin, erythromycin, rifampin

48
Q

what does urinalysis in acute interstitial nephritis show?

A

WBC casts (PATHOGNOMONIC)

49
Q

treatment of acute interstitial nephritis?

A

D/C offending agent -> leads to reversal of renal injury

Glucocorticoids (can accelerate renal recovery) - 6wk taper prednisone or IV methylprednisolone x 3 days

50
Q

can damage be permanent in acute interstitial nephritis?

A

yes, if long duration of exposure

51
Q

is acute tubular necrosis reversible?

A

yes, unless severe/prolonged injury to tubular cells

52
Q

causes of acute tubular necrosis?

A
  1. Ischemia (protracted pre-renal condition like AAA and have to clamp aorta -> causing low flow to both kidneys)
  2. Sepsis
  3. Toxins

(sepsis and toxins b/c of poor renal perfusion)

53
Q

toxins that cause acute tubular necrosis

A

exogenous nephrotoxins (meds, poison)

endogenous nephrotoxins

54
Q

what are some endogenous nephrotoxins that cause acute tubular necrosis?

A

myoglobinuria (rhabdo)

severe transfusion rx (get hemolysis) -> hemoglobinuria

uric acid (tumor lysis syndrome)

light chains (multiple myeloma)

55
Q

exogenous nephrotoxins that cause acute tubular necrosis

A

NSAIDs, chemotherapeutic agents, ahminoglycosides (GN’s), amphotericin (anti-fungal), Vancomycin, radio contrast dye, poison (ethylene glycol -> alcoholics)

56
Q

what is seen on urinalysis for acute tubular necrosis?

A

pigmented granular casts (muddle-brown casts) - PATHOGNOMONIC

57
Q

what is the first thing to do when treating pt with acute tubular necrosis?

A

aggressive volume replacement (hydrate!!!) (esp if nephrotoxic agent, volume depletion)

58
Q

what can you consider giving a pt with acute tubular necrosis?

A

high dose loop diuretics (100-200mg Lasix) to improve urine output if oliguria is present and extracellular-volume normalized

59
Q

restrict what fr any pt with renal disease and for acute tubular necrosis?

A

Protein restriction

60
Q

what examples of glomerular diseases?

A

Infectious Disease associated Syndromes
-Post-streptococcal glomerulonephritis - M/C (group strep A)

Nephrotic syndrome
-Minimal change disease (pediatric version of nephrotic syndrome)

Membranous glomerulonephritis

IgA nephropathy

Henoch-Schonlein Purpura

Goodpasture syndrome

Diabetic nephropathy

Hypertensive nephropathy

Progressive Glomerulonephritis

Polycystic kidney disease

61
Q

which glomerular diseases are d/t chronic renal failure?

A

Goodpasture syndrome, Diabetic nephropathy, Hypertensive nephropathy, Progressive Glomerulonephritis, Polycystic kidney disease

62
Q

what is post-strep glomerulonephritis?

A

immune-mediated disease
-Immune complex containing strep Ag deposited in affected glomeruli -> body keeps attacking the antigen and thus causes inflammation -> causes glomerular nephritis

63
Q

post-strep glomerulonephritis caused by what and occurs when?

A

Caused by the infection, but occurs 7-12 days following the infection/sore throat/impetigo (usually untreated infection)

64
Q

color of urine in post-strep glomerulonephritis?

A

cola colored urine (blood degraded/hematuria/RBC casts)

65
Q

classic sign of post-strep glomerulonephritis?

A

HTN (salt and fluid retention) in the child

66
Q

post-strep glomerulonephritis is the M/C of what? occurs where?

A

AKI in children globally

M/C in developing countries

67
Q

post-strep glomerulonephritis highest risk at what age?

A

children 5-12 y/o

68
Q

what does urinalysis show for post-strep glomerulonephritis?

A

RBC casts - PATHOGNOMONIC

-also have proteinuria, hematuria, pyuria (all b/c glomerulus is leaking everything)

69
Q

if see a lot of sediment on urinalysis and maybe no infection, but child has HTN what should you think?

A

PSGN

70
Q

what will pts with post-strep glomerulonephritis have elevated?

A

elevated titers of antibodies to strep

ELEVATED anti-streptolysin (ASO)

71
Q

post-strep glomerulonephritis tx

A

PCNs if there is infection

symptomatic tx if no infection (anti-HTNs, Na restriction, diuretics)

children usually recover, adults can progress to permanent kidney damage

72
Q

what is IgA Nephropathy?

A

IgA deposition in glomerulus (like PSGN), but NOT INFECTIOUS

73
Q

IgA nephropathy often following?

A

URI

74
Q

color of urine in IgA nephropathy?

A

red or Coca Cola 1-2 days s/p onset

75
Q

IgA nephropathy dx?

A

renal bx

76
Q

IgA nephropathy tx?

A

ACEI/ARB

steroids

renal transplant (will need this eventually)

77
Q

what is Henoch Schonlein Purpura?

A

small vessel vasculitis w/IgA complex deposition (related to IgA)

PEDIATRIC VERSION OF IgA Nephropathy

Same IgA complex deposited at glomerulus and in small vessels -> so causes vasculitis/inflammation of vessels -> causes ischemic state

78
Q

who is affected in Henoch Schonlein Purpura?

A

children about 6 y/o

79
Q

Classic presentation of Henoch Schonlein Purpura?

A

Rash - esp LE’s and buttocks

Severe abdominal pain/vomiting

(can also have arthralgia in knees, ankles)

80
Q

Henoch Schonlein Purpura tx?

A

Mostly supportive (immunosuppressants and/or plasmapheresis for worsening disease)

Excellent prognosis

Recover spontaneously in weeks (if not then use immunosuppressants)

81
Q

nephrotic syndrome can be problem with what?

A

primary (problem with kidney) or secondary

82
Q

type of nephrotic syndrome?

A

minimal change disease (pets version of nephrotic syndrome)

83
Q

what is seen in nephrotic syndrome?

A

***Heavy proteinuria (> 3.5g/24hrs) -> foamy urine

***Hypoalbuminemia (< 3 g/dL)

***Peripheral edema

Hypercoag state (DVT, PE may be first presentation)

Bland urinary sediments (not many cells or casts)

84
Q

what is minimal change disease?

A

nephrotic syndrome in children

85
Q

what is the characteristic histologic finding for minimal change disease?

A

diffuse effacement of the epithelial cell foot processes on electron microscopy

86
Q

abrupt onset what for minimal change disease?

A

edema & nephrotic syndrome

87
Q

Minimal change disease tx

A

all children treated with PREDNISONE (steroids) for 8-16 weeks (most have complete remission after 8 weeks of steroids)

PREDNISONE!!! (up to 16 weeks of therapy)

88
Q

urine sediment in nephrotic syndrome?

A

heavy proteinuria

89
Q

what is vascular AKI?

A

intrinsic use of AKI

d/t:

  • renal artery obstruction from thrombus, embolus, dissection, vasculitis
  • renal vein obstruction
  • microangiopathy (TTP, HUS, DIC)
  • scleroderma renal crisis
90
Q

vascular AKI sx’s?

A

LE rash, lived reticularis, urine eosinophils

91
Q

tx for vascular AKI?

A

no tx just BP control and symptomatic management

92
Q

common cause of post-renal failure?

A

bladder outlet obstruction
-check with bedside U/S -> see no urine output

d/t:
-prostatic obstruction, bladder Ca, stone, clots

93
Q

treatment for bladder outlet obstruction/post-renal failure (d/t obstruction)?

A

relief of obstruction -> bladder catheterization

94
Q

what is polycystic kidney disease?

A

Multisystem and progressive genetic d/o w/cyst formation and enlargement of the kidney (and other organs i.e. Pancreas, liver, spleen)

95
Q

where are cysts predominantly in polycystic kidney disease?

A

in the kidney (but can be in other organs like pancreas, liver, spleen)

96
Q

pt with polycystic kidney disease may come in with what and at 2x the risk of what?

A

May come in with worst headache of their life

-at 2x the risk of intracranial aneurysm

97
Q

polycystic kidney disease significant association with?

A

ESRD

98
Q

polycystic kidney disease signs and sx’s?

A

Pain (M/C) - abd, flank, back d/t enlargement of cysts, bleeding of cysts, kidney stones, infections

Hypertension

99
Q

need to image polycystic kidney disease pts for what?

A

for bleeding from the cysts

100
Q

polycystic kidney disease are on a lot of what for their pain?

A

narcotics -> need chronic pain management

101
Q

diagnostic for polycystic kidney disease?

A

U/S - see multiple cysts in the kidney

Urinalysis - hematuria (d/t bleeding cysts)

102
Q

polycystic kidney disease tx

A

BP management (ACEI/ARB - slows progression of disease)

Pain control -> use narcotics

  • AVOID NSAIDs b/c promote bleeding and suppress auto-regulation
  • AVOID Tylenol b/c of liver cysts
  • surgical cyst decompression (done by IR)
  • Nephrectomy = LAST LINE

Hematuria

  • hydrate and if a lot then transfuse
  • can bleed a lot
103
Q

when to dialyze?

A 
Acidosis Electrolytes (can't fix them)
-***hyperkalemia***, hyperphosphatemia, hypocalcemia

Ingestions: OD

Overload:
-severe volume overload, esp on many IVs + anuria (on diuretics, but not peeing -> dialysis)

Uremia
-many sx’s:
CNS (asterixis, seizures, coma), platelet dysfxn (gi bleed, diathesis, coagulopathies), infectious risk, pleuritis/pericarditis (friction rub), pericardial effusion

Clin Med 3 (21 decks)

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