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Flashcards in jaundice and ascites Deck (43):
1

case w. jaundice ddx

Liver cirrhosis
Liver neoplasm
Cholecystitis
Choledocholithiasis
Primary biliary cirrhosis
Hepatitis

2

what labs to get

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

3

will see jaundice when levels are

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

4

LFTs

-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

5

LFTs specifics

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)

6

Serum Albumin

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)

7

Prothrombin time

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*

8

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

malnutrition, renal or GI losses

9

screening for hepatobiliary disease

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

10

Serum Bilirubin

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


11

Serum Alkaline phosphatase

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


12

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

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

13

ALT

-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)

14

AST

-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)

15

GGT

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

16

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

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

17

Hyperbilirubinemia:
Differentiated by the phase of hepatic bilirubin metabolism

uptake, conjugation, excretion
also ategorized as:
Prehepatic
Hepatic
Posthepatic

18

Bilirubin is detected in biologic fluids by the

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

19

Unconjugated hyperbilirubinemia

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

20

Pre-Hepatic Etiology (UC bili):
Any condition that results in ??

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

21

Pre-Hepatic Etiology: mild or severe?

Jaundice resulting from hemolysis is usually mild
-Serum bilirubin levels rarely exceed 5 mg/dL in the absence of coexisting hepatic diseases

22

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

-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

Unconjugated hyperbilirubinemia: Hepatic Etiology
Every condition resulting in hepatic injury can cause ??

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

24

UC hyperbili: Impaired Hepatic Uptake

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

25

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

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

26

Neonatal jaundice: Two primary causes??

*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

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

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

Conjugated Hyperbilirubinemia: associated with ??
two primary mechs??

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

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

-Drugs – can impair canalicular transport
-Destruction of intrahepatic bile ducts (Primary biliary cirrhosis)

30

Primary biliary cirrhosis

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

31

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

-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

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

most common causes??
other causes??

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

clinical approach to jaundice

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

ascites

most common cause??

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

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

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

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

500 mL
-Shifting dullness to percussion
-Ultrasound is able to detect smaller volumes (250 mL)

37

ascites overflow theory:

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

38

ascites underflow theory:

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

39

Intervention is typically done when ??
procedure of choice??

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


40

ascites flow chart

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

recurrent ascites-->diuretic: spironolactone and furosemide

41

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

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

if these fail, consider liver transplant

42

P of SOAP: workups of jaundice

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

43

how would you tx??

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