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CSI- Winter > Jaundice and Ascites > Flashcards

Jaundice and Ascites Flashcards

1
Q

Jaundice/Icterus

A
  • Yellow pigmentation of skin, sclerae and mucus membranes resulting from elevated serum bilirubin levels
  • Typically levels above 3 mg/dL will lead to jaundice, icterus
  • Hyperbilirubinemia

-A sign of various illnesses, including liver disease and hematologic disorders

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2
Q

The liver has a large reserve capacity of enzymes and thus ______

A

liver function tests may remain relatively normal until liver dysfunction is severe!!

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3
Q

Liver function tests measure

A 
-Aspartate aminotransferase (AST)
(Aka - Serum glutamic oxaloacetic transaminase- SGOT) 
-Alanine aminotransferase (ALT)
(Aka - Serum glutamic pyruvic transaminase- SGPT)
-Serum albumin
-Prothrombin time
-Serum bilirubin
-Serum alkaline phosphatase
-Gamma-Glutamyl transferase (GGT)
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4
Q

Serum Albumin and Prothrombin time reflect

A

hepatic capacity for protein synthesis

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5
Q

Albumin levels fall with

A

prolonged liver dysfunction or in acute liver impairment
(Norm: 3.5-5.5 mg/dL)

*If pt has hypoalbuminemia and normal Prothrombin time – Consider malnutrition, renal or GI losses

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6
Q

Prothrombin time is dependent on

A

coagulation factors II, V, VII and X
(2, 5, 7, 10)

  • Norm = 10.5 to 13 seconds
  • Responds rapidly to altered hepatic function
  • However, these are dependent upon Vitamin K and a coexistent vitamin k deficiency must be ruled out.
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7
Q

Screening for hepatobiliary disease

A

Tests of biliary obstruction and cholestasis
Tests of hepatocellular damage

  • Important to realize lack of specificity of these tests
  • Primary use lies in overall pattern of tests as well as magnitude of abnormality
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8
Q

Serum Bilirubin reflects

A

balance between production, conjugation, and excretion into bile by the liver

  • Unconjugated (indirect) and Conjugated (direct)
  • Normal = 0.2 – 1 mg/dL
  • Conjugated (direct) represents up to 30% of total
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9
Q

Serum Alkaline phosphatase

is a group of isoenzymes derived from

A

Liver, bone, intestine and placenta

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10
Q

Elevation of Serum Alkaline phosphatase occurs in a variety of conditions:

A
  • Cholestasis, partial or complete bile duct obstruction
  • Bone regeneration
  • Pregnancy
  • Neoplastic, infiltrative, and granulomatous liver diseases
  • An isolated elevated alkaline phosphatase may be the only clue to pathology
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11
Q

Aspartate (AST/SGOT) and Alanine (ALT/SGPT) aminotransferases are

A

Intracellular amino-transferring enzymes in hepatocytes

  • After injury or death – these are released into the circulation
  • These aminotransferases are sensitive (not specific) for liver damage
  • Quantity of enzyme level correlates with the severity of hepatic necrosis
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12
Q

ALT

A
  • Found primarily in hepatocytes
  • More specific than AST for liver disease*
  • In most hepatocellular disorders, ALT is higher than AST
  • *Except in alcoholic liver disease (where its reversed)
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13
Q

AST

A
  • Found primarily in liver and cardiac muscle; but also in skeletal muscle, kidneys, brain, lungs pancreas, leukocytes, erythrocytes
  • *Will be higher than ALT in alcoholic liver disease
  • Usually 2 or 3 times that of ALT
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14
Q

GGT

A
  • Increased in any cause of acute damage to the liver or bile ducts
  • Not very specific and thus not really part of work-up for acute liver dysfunction/injury
  • Can be helpful in determining reason for elevation of Alkaline Phosphatase level in serum (see next slide)
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15
Q

If GGT is low or normal, then elevation of Alk Phose is likely due to

A

bone disease rather than liver injury or insult

-A low level or normal GGT level also makes it less likely that the person has consumed alcohol or has liver disease

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16
Q

Most bilirubin (80%) is derived from

A

the breakdown of senescent red blood cells (RBCs)

  • The remainder derives from ineffective erythropoiesis and catabolism of myoglobin and hepatic hemoproteins
  • Normal rate of production is about 4 mg/kg body weight daily
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17
Q

Bilirubin is detected in biologic fluids by the van den Bergh reaction:

A

Direct-reacting fraction -> Conjugated bilirubin

Indirect-reacting fraction -> Unconjugated bilirubin

Total minus direct= indirect

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18
Q

Causes of Unconjugated Hyperbilirubinemia

A
  • Overproduction
  • Impaired hepatic uptake
  • Decreased conjugation of bilirubin
  • *Not usually associated with significant hepatic disease
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19
Q

Pre-Hepatic Etiology of Unconjugated Hyperbilirubinemia

A
  1. Any condition that results in excessive bilirubin production
    (Hemolysis, Hematomas, Pulmonary emboli–>all things that break down RBCs and make bilirubin)
    -Genetic disorders: Glucose-6-phosphate dehydrogenase deficiency, Sickle cell anemia, Spherocytosis

-Infectious diseases (Malaria)

20
Q

Jaundice resulting from hemolysis is usually

pre hepatic

A

mild

-Serum bilirubin levels rarely exceed 5 mg/dL in the absence of coexisting hepatic diseases

21
Q

Hemolysis can be investigated by examining: (pre hepatic)

A
  • Peripheral blood smear (and bone marrow smear)

- Measuring reticulocyte count, haptoglobin, lactate dehydrogenase (LDH), erythrocyte fragility and Coomb’s test

22
Q

Unconjugated hyperbilirubinemia from Hepatic etiology:

A
  • anything causing hepatic injury can cause hepatic jaundice
  • Hepatitis (Any causes: Infectious, toxic metabolites, drugs, auto-immune disorders, and liver tumors)
  • Gilbert syndrome
  • Crigler-Najjar syndrome
  • Niemann-Pick disease type C
23
Q

Impaired Hepatic Uptake can cause jaundice and occurs after

A

administering certain drugs

  • Such as Rifampin
  • Those involved in treating Gilbert syndrome
24
Q

Impaired conjugation can be due to

A
  • Crigler-Najjar syndrome

- Acquired defects of UDP glucoronyl transferase induced by drugs such as chloramphenicol

25
Q

Two primary causes of neonatal jaundice

A

**Immature hepatic metabolic pathways are unable to conjugate bilirubin as efficiently and quickly as in adults
OR
-Bilirubin production is increase

26
Q

Increased bilirubin production in neonates leads to

A

unconjugated hyperbilirubinemia between 2nd and 5th day of life

  • Lasts until the 8th day in normal births or 14th day in premies
  • Usually harmless and doesn’t require any type of therapy
27
Q

Severe pathologic unconjugated hyperbilirubinemia in neonatal jaundice is usually caused by

A

hemolysis (due to blood group incompatibility) and defective conjugation

  • This is a serious condition which requires immediate attention
  • Can lead to severe hyperbilirubinemia which is a risk for permanent neurologic damage (Kernicterus)
  • *Phototherapy is the treatment of choice (If there is no response to phototherapy – seek another cause of the jaundice)
28
Q

Conjugated Hyperbilirubinemia is associated with

A

impaired formation or excretion of all components of bile (cholestasis)

  1. A defect in the excretion of bilirubin from hepatocytes into bile (intrahepatic cholestasis)
  2. A mechanical obstruction to the flow of bile through the bile ducts
29
Q

Impaired hepatic excretion (Intrahepatic cholestasis) during Conjugated Hyperbilirubinemia can be caused by

A
  • many things
  • Drugs – can impair canalicular transport
  • Destruction of intrahepatic bile ducts (Primary biliary cirrhosis)
30
Q

Primary biliary cirrhosis

A
  • Chronic, progressive liver disease
  • Occurs primarily in women
  • Destroys small lobular bile ducts
  • Leads to progressive cholestasis
  • > portal inflammation -> fibrosis -> cirrhosis
31
Q

Drug-induced cholestasis (Intrahepatic cholestasis) during Conjugated Hyperbilirubinemia can be caused by

A

A wide array of drugs

  • Nitrofurantoin, oral contraceptives, anabolic steroids
  • Erythromycin, cimetidine, chlorpromazine
  • Prochlorperazine, imipramine, sulindac, and Penicillins

-Post-operative Jaundice, occurs 1-10 days after surgery, 15% incidence after heart surgery

32
Q

Post-hepatic (Obstructive jaundice) during Conjugated Hyperbilirubinemia can be caused by

A

partial or complete obstruction of intrahepatic or extrahepatic bile ducts

-Most common causes are:
Gallstones in the common bile duct, Pancreatic head tumors

  • Other causes include: Biliary atresia, ductal carcinoma, strictures of the common bile duct
  • Pancreatitis, pancreatic pseudocysts, or liver flukes (parasites)
33
Q

Lab tests to order when you suspect jaundice

A

Comprehensive metabolic panel (CMP) [electrolytes, liver enzymes (including direct and indirect-bilirubin)], lipase, complete blood count

-Also ultrasound, CT scan, MRI, MRCP, ERCP,

34
Q

When you suspect jaundice, always ask yourself…

A

Is the patient on a medication that can be causing things? chart slide 47

35
Q

Ascites

A
  • Accumulation of excess fluid in the peritoneal cavity

- Liver cirrhosis is the most common cause

36
Q

The ________ has replaced the exudative-transudative classification of ascites

A

serum ascites-albumin gradient

37
Q

An elevated serum ascites-albumin gradient (>1.1 g/dL) signifies

A

the presence of portal hypertension

38
Q

Ascites becomes clinically detectable with fluid accumulation of greater than ______

A

500 mL

  • *Shifting dullness to percussion is the most sensitive clinical sign of ascites
  • Ultrasound is able to detect smaller volumes (250 mL)
39
Q

Ascites Overflow theory

A
  • Overflow of fluid into the peritoneum resulting from portal hypertension and splanchnic vasodilation
  • Excess renal sodium
  • Water retention
40
Q

Ascites Underflow Theory

A
  • Decreased effective circulating blood volume resulting from systemic arterial vasodilation leading to activation of neurohumoral systems
  • Sodium and water retention
41
Q

Intervention is typically done when symptomatic, procedure of choice is

A

(symptoms are dyspnea, abdominal pain, etc…)

  • Paracentesis is procedure of choice
  • Usually done under ultrasound
  • Can drain as much as 5-8 liters of fluid
42
Q

Ascites with hyponatremia?

A

restrict dietary sodium AND fluids

43
Q

Ascites with normal serum sodium?

A

restrict dietary sodium only

(

44
Q

If you have recurrent ascites after sodium restriction, try _________

A

Diuretic therapy (Spironolactone and Furosemide)

45
Q

Diuretic therapy (Spironolactone and Furosemide) doesn’t work and pt has refractory ascites despite max diuretics or pt has electrolyte abnormalities/renal dysfunction try these 3 things:

A
  1. Large volume paracentesis with colloid expansion (IV albumin)
  2. Shunt placement (TIPS/surgical shunt)
  3. Aquaretics? (class of drug that is used to promote aquaresis, the excretion of water without electrolyte loss, increase urine output and renal blood flow but maintain electrolytes in body)
46
Q

If surgical shunt/paracentesis/aquaretics don;t help ascites

A

Consider liver transplant

CSI- Winter (44 decks)

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