13-14 Flashcards

1
Q

Prerenal or functional renal failure is caused by a reduction in ___

A

Glomerular perfusion

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2
Q

Most prerenal ARF is caused by a decrease in ___

A

Effective intra-arterial volume

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3
Q

RBF remains remarkably constant through autoregulation despite wide variations in ____

A

BP and renal perfusion pressure from 70-150 mmHg

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4
Q

Maintenance of GFR is by combined ___

A

Afferent arteriolar vasodilation and efferent arteriolar vasoconstriction, which increases FF contributing to Na ad H2O retention

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5
Q

___ constructs the efferent arteriole and is the predominant influence in maintaining GFR

A

Ang II

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6
Q

BUN:Cr in acute renal failure (ARF)

A
>20:1  = prerenal failure
<5-10:1 = liver disease
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7
Q

Muddy brown, dirty brown casts, DARK, think ___

But no blood or protein

A

Acute tubular necrosis

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8
Q

With prerenal azotemia and ATN what will you find with US?

A

Normal kidneys

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9
Q

What segments in the kidney are most susceptible to ischemia and nephrotoxins

A

PT

Thick a limb

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10
Q

3 phases of ATN

A
  1. Initial: ischemia or toxin exposure
  2. Maintenance: injury is established. GFR stabilizes at 5-10 urine output is lowest at this point
  3. Recovery: gradual rise in urine output and decrease in Cr caused by diuresis from salt and water accumulation
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11
Q

Tx of acute kidney injury:
Intravascular volume depletion:
___ is the replacement fluid of choice until stabilized.

A

NaCl - 0.9% - normal saline

Crystalloids

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12
Q

Tx of acute kidney injury:
Decreased Effective Volume:
Bacterial sepsis causes excessive ___ and ____. Treatment includes ____ and _____

A

Vasodilation and intrarenal vasoconstriction

Tx: NaCl and vasopressors

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13
Q

Tx of acute kidney injury:
Decreased Effective Volume:
Cirrhosis tx:

A

Lasix

Spironolactone

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14
Q

I’m treatment of impaired renal compensatory responses, stop use of ____

A

NSAIDs and ACEI

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15
Q

Pharmacological therapy for ATN:

What not to use/do

A
Dopamine
Loop diuretics
ANP 
Fenoldopan
Acetylcysteine
Protein restriction
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16
Q

therapy for ATN:

Keep blood sugar between ____

A

110-149 mg/dL

17
Q

Profound renal vasoconstriction in the setting o histologically normal kidneys

A

Hepatorenal syndrome

18
Q

Hepatorenal syndrome resembles prerenal azotemia. The defining feature is ___

A

Lack of improvement with volume expansion. Improves with liver transplant

19
Q

Hepatorenal syndrome pathogenesis:

*primary mechanism is decrease in ____ which leads to hyperdynamic circulation and activation of vasoconstrictor systems

A

Impaired Na and H2O handling leads to fluid retention causing ascites and edema.
*splanchnic and systemic vascular resistance

20
Q

Pathophys of HRS:
- a reduction in ____ due to ____ in the splanchnic circulation, triggered by ____. Caused by increased production or activity of ____, such as ____

A
  1. SVR
  2. Primary arterial vasodilation
  3. Portal HTN
  4. Vasodilator factors
  5. NO, Carbon monoxide, endogenous cannabinoids
21
Q

HRS has a ___ survival rate

A

Very low

22
Q

HRS
Stage 1
Stage 2

A
  1. Portal HTN is moderate, increased Cardiac output increases to compensate for decreased vascular resistance
  2. Severe portal HTN, cardiac output cannot compensate, vasoconstrictors are activated.
23
Q

HRS

Causes ____ retention which leads to ascites and edema. This leads to renal failure by causing ____

A

Na and H2O

Cortical vasoconstriction and hypoperfusion

24
Q

Renal failure rarely occurs in cirrhosis without ___

A

Ascites

25
Q

HRS

Type I

A

Rapid decline in renal function
At least double Cr >2.5 or reduction of Clearance of Cr by 50% or more to <20ml/min over duration of <2 weeks
Bad prognosis

26
Q

Type I HRS is usually seen in which patients?

A

Hospitalized with advanced cirrhosis or fulminate hepatic failure

27
Q

HRS

Type II

A
Moderate or stable reduction in GFR 
Cr=2
Insidious onset
Slow progression 
Better prognosis