Pathophysiology- Chronic Liver Failure 2 Flashcards

1
Q

what are some of the proposed mechanisms of hepatic encephalopathy?

A
  • ammonia, nitrogenous wastes
  • increased intracellular glutamine
  • astrocyte swelling, cerebral edema
  • inflammatory cytokines alter blood-brain barrier
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2
Q

who notices changes in mental status for chronic hepatic encephalopathy?

A
  • often by family members but missed by coworkers or physicians
  • slow and subtle onset
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3
Q

what PE findings do you see with hepatic encephalopathy?

A
  • asterixis- hyperextended wrists with flapping movement, inability to perform the sustained grip of the hand
  • myoclonus- hyperextension of the ankle
  • absence of sensory, motor, or cerebellar deficit to suggest another etiology for altered mentation
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4
Q

is chronic hepatic encephalopathy reversible?

A
  • yes generally reversible with treatment
  • w/ long standing chronic hep encephalopathy–> permanent brain damage can occur
  • mild decrease in mentation, calculations
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5
Q

how do you treat chronic hepatitis encephalopathy?

A
  • treat the precipitating conditions like hypovolemia, hypokalemia, gi bleed, meds, exclude intracranial hemorrhage
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6
Q

what is lactulose?

A
  • poorly absorbable sugar
  • cathartic
  • decrease intestinal ph
  • decrease glutamine absorption
  • reduce syntehsis and absorption of nh3
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7
Q

what is zinc sulfate?

A
  • cofactor in NH3 metabolism
  • zinc deficiency is common in liver disease
  • correction of zinc is part of tx of excephalopathy
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8
Q

what do antibiotics do in terms of liver and gut

A
  • alter intestinal flora
  • decrease NH3
  • decrease intestinal mucosal glutaminase
  • decrease coliform bacteria which produce urease and convert urea to NH3
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9
Q

how to treat chronic liver failure?

A
  • nutrition
  • skeletal muscle metabolizes NH3. malnutrition is common in liver patients. Protein restriction is not helpful.
  • High veggie proteins with increased branched chain AA advised
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10
Q

what are some renal complications associated with liver disease?

A
  • hepatorenal syndrome
  • iga nephropathy
  • membranoproliferative glomerulonephritis
  • membranous glomerulonephritis
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11
Q

what is hepatorenal syndrome

A
  • liver failure cuase renal arterial vasoconstriction and renal failure
  • not associated with renal parenchymal abnormality
  • genreally reversed with correction of liver failure such as with transplantation
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12
Q

how to diagnose hepatorenal syndrome?

A
  • cirrhosis and ascites
  • no recent nephrotoxic drugs
  • no underlying renal disease ( >500mg protein/day, >50 RBCs/hpf), no improvement,
  • serum creatinine >1.5
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13
Q

how do you diagnose hepatorenal syndrome?

A
  • exclusion of other etiologies
  • lack of return of renal function with intravascular volume repletion
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14
Q

whats the difference between type 1 and type 2 hepatorenal syndrome?

A
  • type 1 is rapidly worsening or decrease in CrCl <20 ml/min within 2 weeks
  • type 2 is slow progression, often with worsening liver disease
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15
Q

tx or hepatorenal syndrome?

A
  • liver transplantation
  • hemodialysis until liver transplantation
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16
Q

what is the most common cause of IgA nephropathy?

A

liver disease

17
Q

what is IgA nephropathy?

A
  • increased deposition of IgA, c3, and other immunoglobulins in 35-90% of cirrhosis patients
  • decreased hepatic clearance of IgA with cirrhosis and portal hypertension(with collateral blood flow around the liver)
18
Q

what is membranoproliferative glomerulonephritis associated with?

A
  • chronic hep c
  • immune complex formation with chronic hep c
  • cryoglobulinemia- abnormal protein in the blood which precipitates with cold temp
19
Q

what is membranous glomerulonephritis associated with?

A

hep c and b

20
Q
A