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CSI > jaundice and ascites > Flashcards

jaundice and ascites Flashcards

1
Q

case w. jaundice ddx

A 
Liver cirrhosis
Liver neoplasm
Cholecystitis
Choledocholithiasis
Primary biliary cirrhosis
Hepatitis
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2
Q

what labs to get

A

CMP: some liver tests: ALT, AST, total bilirubin (may want fractionated also) , alk phos, albumin
hepatitis Abs
INR
CBC: anemia (hemolysis), thrombocytopenia
white count? not always indicates just infection

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3
Q

will see jaundice when levels are

A

-above 3 mg/dL will lead to jaundice, icterus

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4
Q

LFTs

A

-characterizes underlying liver disease
-Do not necessarily directly measure liver function
-measurements of serum levels of compounds that are:
Synthesized, metabolized, or excreted by the liver
-The liver has a large reserve capacity and thus liver function tests may remain relatively normal until liver dysfunction is severe

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5
Q

LFTs specifics

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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6
Q

Serum Albumin

A

Reflect hepatic capacity for protein synthesis

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

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7
Q

Prothrombin time

A

dependent on coagulation factors II, V, VII and X

  • Norm = 10.5 to 13 seconds
  • Responds rapidly to altered hepatic function
  • these are dependent upon Vitamin K and a coexistent vitamin k deficiency must be ruled out*
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8
Q

In light of hypoalbuminemia and normal Prothrombin time – Consider ??

A

malnutrition, renal or GI losses

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9
Q

screening for hepatobiliary disease

A

alk phos, ALT, AST
Tests of biliary obstruction and cholestasis and hepatocellular damage
-lack of specificity of these tests; look at overall pattern of tests as well as magnitude of abnormality

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10
Q

Serum Bilirubin

A

reflects balance btw production, conjugation, and excretion into bile by the liver
Normal = 0.2 – 1 mg/dL
-Conjugated (direct) represents up to 30% of total
-Evaluated in conjunction with other LFTs
-Once insult is resolved – bilirubin takes some time to return to normal levels

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11
Q

Serum Alkaline phosphatase

A

Group of isoenzymes derived from: Liver, bone, intestine and placenta
Elevation occurs in:
-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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12
Q

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

A

IC amino-transferring enzymes in hepatocytes
After injury or death- released into the circulation
-sensitive (not specific) for liver damage
-Quantity of enzyme level correlates with the severity of hepatic necrosis

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13
Q

ALT

A

-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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14
Q

AST

A

-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 3x ALT)

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15
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
  • helpful in determining reason for alk phos elevation in serum
  • If GGT is low or normal than elevation of Alk Phos is likely due to bone disease rather than liver injury or insult
  • A low level or normal level also makes it less likely that the person has consumed alcohol or has liver disease
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16
Q

jaundice: Most bilirubin (80%) is derived from the breakdown of ??

A

senescent red blood cells (RBCs)

  • 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

Hyperbilirubinemia:

Differentiated by the phase of hepatic bilirubin metabolism

A 
uptake, conjugation, excretion
also ategorized as:
Prehepatic
Hepatic
Posthepatic
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18
Q

Bilirubin is detected in biologic fluids by the

A

van den Bergh reaction
D=C, I=U
(total minus direct)

19
Q

Unconjugated hyperbilirubinemia

A

Primary mechanisms:
Overproduction, Impaired hepatic uptake, Decreased conjugation of bilirubin
*Not usually associated with significant hepatic disease

20
Q

Pre-Hepatic Etiology (UC bili):

Any condition that results in ??

A

excessive bilirubin production:
Hemolysis, Hematomas, PE
Genetic disorders, G6PD deficiency, SCD anemia
Spherocytosis, Infectious diseases (Malaria)

21
Q

Pre-Hepatic Etiology: mild or severe?

A

Jaundice resulting from hemolysis is usually mild

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

22
Q

Pre-Hepatic Etiology: Hemolysis can be investigated by examining ??

A
  • Peripheral blood smear (and bone marrow smear)
  • Measuring reticulocyte count, haptoglobin, lactate dehydrogenase (LDH), erythrocyte fragility and Coomb’s test (done by specialist, not PC)
23
Q

Unconjugated hyperbilirubinemia: Hepatic Etiology

Every condition resulting in hepatic injury can cause ??

A

hepatic jaundice:

  • Hepatitis: Infectious, toxic metabolites, drugs, auto-immune disorders, and liver tumors
  • Gilbert syndrome, Crigler-Najjar syndrome, Niemann-Pick disease type C
24
Q

UC hyperbili: Impaired Hepatic Uptake

A

Causes jaundice that occurs after administering certain drugs: Rifampin, Those involved in treating Gilbert syndrome

25
Q

UC hyperbili: Impaired Conjugation: can be due to ??

A
  • Crigler-Najjar syndrome

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

26
Q

Neonatal jaundice: Two primary causes??

A

Immature hepatic metabolic pathways are unable to conjugate bilirubin as efficiently and quickly as in adults
Bilirubin production is increase, leads to UC bili btw day 2-5, last until day 8 (normal), day 14 in premies, typ. harmless and doesn’t need tx

put on bililytes? if more severe, electrophoresis

27
Q

neonatal jaundice: Severe pathologic UC bili: usually caused by ??

A

hemolysis (due to blood group incompatibility) and defective conjugation
-serious condition which requires immediate attention
Can lead to severe hyperbili; risk for permanent neurologic damage (Kernicterus)
tx of choice: Phototherapy
-If there is no response to phototherapy – seek another cause of the jaundice

28
Q

Conjugated Hyperbilirubinemia: associated with ??

two primary mechs??

A

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

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

C bili: Impaired hepatic excretion (Intrahepatic cholestasis)
Caused by many conditions

A
  • 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

drugs that can induce cholestasis (impaired hepatic excretion, C bill)

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

ALSO Post-operative Jaundice:
Occurs 1-10 days after surgery, 15% incidence after heart surgery

32
Q

Post-hepatic (Obstructive jaundice, C bili): Due to partial or complete ??

most common causes??
other causes??

A

obstruction of intrahepatic or extrahepatic bile ducts

  • Gallstones in the common bile duct, Pancreatic head tumors
  • others: Biliary atresia, ductal carcinoma, strictures of the common bile duct, Pancreatitis, pancreatic pseudocysts, or liver flukes (parasites)
33
Q

clinical approach to jaundice

A

good hx (esp. social, travel) and PE
lab tests: Comprehensive metabolic panel [electrolytes, liver enzymes (including direct and indirect-bilirubin)], lipase, complete blood count
imaging: US, CT, MRI, MRCP, ERCP
MRCP: looking at GB, pancreas, biliary duct system, purely diagnostic
ERCP: endoscopy, can go in and remove stone if see it

34
Q

ascites

most common cause??

A

Accumulation of excess fluid in the peritoneal cavity

  • Liver cirrhosis
  • high albumin (greater than 1.1 g/dL): cirrhosis, chronic hep congestion, RVHF, Budd-Chiari, constrictive pericarditis, massive liver metastasis, mycetoma, mixed ascites
  • low albumin (less than 1.1 g/dL): peritoneal carcinomatosis, peritoneal TB, pancreatic/biliary disease, nephrotic syndrome
35
Q

The ?? has replaced the exudative-transudative classification of ascites
an elevated gradient signifies ??

A

serum ascites-albumin gradient
-An elevated serum ascites-albumin gradient (more than 1.1 g/dL) signifies the presence of portal HTN

-typically ascites is transudative

36
Q

Ascites becomes clinically detectable with fluid accumulation of greater than ??
most sensitive sign of ascites??
imaging for smaller volumes??

A

500 mL

  • Shifting dullness to percussion
  • Ultrasound is able to detect smaller volumes (250 mL)
37
Q

ascites overflow theory:

A

Overflow of fluid into the peritoneum resulting from portal HTN and splanchnic vasodilation: Excess renal sodium, Water retention

38
Q

ascites underflow theory:

A

Decreased effective circulating BV from systemic arterial vasodilation leading to activation of neurohumoral systems: Sodium and water retention

39
Q

Intervention is typically done when ??

procedure of choice??

A

symptomatic: I.e. dyspnea, abdominal pain, etc
Paracentesis: Usually done under ultrasound, Can drain as much as 5-8 liters of fluid

40
Q

ascites flow chart

A

hyponatremia–>Na+ and H2O restriction
normal Na+–>Na+ restriction

recurrent ascites–>diuretic: spironolactone and furosemide

41
Q

ascites flow chart: if refractory ascites despite max diuretic dose OR e-lyte abnormality/renal dysfunction at submax dose

A
  • large-volume paracentesis w. colloid expansion (IV albumin)
  • shunt placement: TIPS/sx shunt
  • aquaretics?

if these fail, consider liver transplant

42
Q

P of SOAP: workups of jaundice

A 
Complete blood count
Comprehensive metabolic panel
Direct and indirect bilirubin
Hepatitis panel
Prothrombin time
RUQ ultrasound ??
CT scan of abdomen ??
43
Q

how would you tx??

A
  • abx: cephalosporin, usyn, augmentin

- remove stone: cholecystectomy w. intraoperative cholangiagram (look to see if stone), ERCP

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