Clinical Presentation of Liver Disease Flashcards

1
Q

What are some complications of chronic liver disease?

A
  • ascites (most common cause is hepatic cirrhosis).
  • spontaneous bacterial peritonitis
  • portal hypertension
  • variceal bleeding
  • hepatorenal syndrome
  • hepatic encephalopathy
  • coagulation abnormalities
  • bone disease
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2
Q

What causes ascites?

A

cirrhosis leads to portal hypertension, leading to splanchnic vasodilation, increased pressure, arterial underfilling, and activation of vasoconstrictors and antinatiruretic factors leading to sodium retention and plasma volume expansion

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3
Q

What is Meigs syndrome?

A

triad of ascites, pleural effusion, and benign ovarian tumor (most common fibroma).
*resolves with removal of tumor

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4
Q

How do we analyze ascitic fluid?

A

via PARACENTESIS, and evaluating:

  • macroscopic appearance (straw color, turbid, bloody, chylous…).
  • cell count
  • chemistry profile (protein, albumin, amylase).
  • cytology
  • gram stain and bacterial culture
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5
Q

What gradient will we look at to evaluate ascites?

A
  • serum ascites albumin gradient (SAAG)=
    Serum albumin - albumin level of ascitic fluid.
    *HIGH gradient= > 11 g/L or 1.1 g/dL (think PORTAL HTN)
    *LOW gradient= less than 11/g/L
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6
Q

What is the most important initial treatment for ascites?

A
  • salt restriction and diuretic therapy (spironolactone; aldosterone antagonist, and furosemide; loop diuretic).
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7
Q

If initial ascites treatment options fail, what then can we do?

A
  • serial therapeutic paracentesis, peritoneovenous shunt, TIPS, or liver transplantation
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8
Q

What is transjugular intrahepatic portosystemic shunt (TIPS)?

A

pass a needle catheter via the transjugular route into the hepatic vein and wedge it there. The needle is then extruded and advanced through the liver parenchyma to the intrahepatic portion of the portal vein and a stent is placed between the portal and hepatic veins; aka you open up the damn to reduce the pressure. This is just done to mitigate the symptoms; not a fix-all situation.
*does not require anesthesia.

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9
Q

What is spontaneous bacterial peritonitis (SBP)?

A
  • a common and sever complication of ascites characterized by spontaneous infection of the ascitic fluid WITHOUT an intraabdominal source. Aka you’re getting bacteria into the peritoneal fluid.
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10
Q

What is the most common organism of spontaneous bacterial peritonitis?

A
  • E. coli

* treat with Abx (cefotaxime) before cultures even come back if suspicious.

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11
Q

How do you diagnose SBP?

A
  • paracentesis with fluid sample having absolute neutrophil count >250/uL
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12
Q

How do pts with SBP present?

A

fever, altered mental status, elevated WBC, and abdominal pain.
*or they may present without any of these.

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13
Q

What is NORMAL portal vein pressure vs. portal HTN?

A
  • NORMAL= 5 mm Hg

- portal HTN= >12 mm Hg

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14
Q

What are the clinical signs of portal HTN?

A

esophageal varices, ascites, caput medusae, hemorrhoids, palmar erythema

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15
Q

How do you treat esophageal varices due to portal HTN?

A
  • 5% dextrose and colloid solutions until blood is available.
  • packed RBCs, FFP, or vitamin K to replenish clotting factors.
  • octreotide (somatostatin analog)= reduces splanchnic pressure.
  • beta blockers
  • sclerotherapy and band ligation
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16
Q

What is hepatorenal syndrome?

A
  • increased renal vascular resistance and a reduced systemic vascular resistance, but poorly understood.
17
Q

What are the clinical manifestations of hepatorenal syndrome?

A
  • jaundice
  • clubbing
  • palmar erythema
  • spider nevi
  • low BP, wide pulse pressure (difference between systolic and diastolic), and bounding pulses
  • decreased GFR (after diuretic withdrawal) and decreased urine output.
  • urine osmolality > plasma osmolality
18
Q

What will serum creatinine and creatinine clearance be in hepatorenal syndrome, respectively?

A
  • creatinine= greater than 133 umol/L

- creatinine clearance= less than 40 cc/min

19
Q

What is type 1 hepatorenal syndrome?

A
  • rapid progressive impairment of renal function with doubling of serum creatinine (>221 umol/L in less than 2 weeks).
  • Low GFR (creatinine clearance less than 20 cc/min)
20
Q

What is type 2 hepatorenal syndrome?

A

slower and more insidious than type 1

21
Q

How do you treat hepatorenal syndrome type 1?

A
  • fluids
  • diuretics cautiously
  • vasopressin analouges or albumin
  • dialysis
  • TIPS or liver transplant
22
Q

How do you clinically diagnose hepatic encephalopathy?

A
  • mental status change and asterixis
  • best marker for maximum cirrhosis progression
  • hepatic encephalopathy is required for dx fulminant liver failure.
23
Q

Is there a correlation between ammonia level and severity of disease in hepatic encephalopathy?

A

NO

24
Q

How do you treat hepatic encephalopathy?

A
  • identify the precipitating factors (low protein diet, stop diuretics…)
  • lactulose= non-absorbable disaccharide that causes colonic acidification and elimination of nitrogenous products.
  • if that fails, use poorly absorbed antibiotics (neomycin and metronidazole, or rifaximin)
25
Q

Why is bone disease associated with liver disease?

A
  • osteoporosis is common due to malabsorption of vitamin D (due to lack of bile production to absorb the fat soluble vitamin) and decreased liver synthesis of vitamin D.
  • can treat with bisphosphonates (controversial)
26
Q

How can you screen a pt suspected to have bone disease due to liver disease?

A

DEXA scan

27
Q

Why do coagulation abnormalities occur in most pts with liver disease?

A
  • decreased synthesis of clotting factors
  • impaired clearance of anticoagulants
  • thrombocytopenia from hypersplenism due to portal HTN.