5.

01 Approach to Patients with Jaundice, Abdominal

Swelling, and Ascites MEDICINE 1
Oscar Ty Cabahug, MD LE 05
18 February 2020 TRANS 01 (v 01)
7

■ Concentrated urine: bubbles formed from shaking the

OUTLINE
container are white because urochromes are
I. Causes Of Jaundice water-soluble and are not incorporated in the bubbles📣
A. Accumulation Of Bilirubin ● Urochromes - pigments which give urine its usual
II. Presentation Of Jaundice yellowish color
III. Bilirubin Production ■ Tea-colored urine: bubbles formed take a brownish
A. Bilirubin Synthesis yellowish or orange hue because of adherence of
B. Hepatic Metabolism bilirubin (which has a polar and a nonpolar end, thus
IV. Considerations In Jaundice incorporated in bubbles) to the bubbles 📣
V. Classifications ● Should be distinguished from carotenoderma
A. Overproduction Of Bilirubin ○ Due to an accumulation of the yellow pigment carotene📣
B. Decreased Hepatic Uptake Of Bilirubin ○ If the skin is yellow and the sclera of the patient is white
C. Decreased Hepatic Conjugation Of Bilirubin (spared) it is carotenoderma📣
D. Decreased Excretion Of Bilirubin ● Should be distinguished from intake of quinacrine
VI. Evaluation Of Jaundice ○ A drug used for treatment of malaria and SLE📣
A. History ○ You cannot simply distinguish it by the color of the sclerae
B. Physical Examination because quinacrine can also color the sclerae yellow even if
VII. Approach To The Patient With Abdominal Enlargement checking bilirubin in the blood will present normal levels📣
A. Evaluation Of Abdominal Enlargement
III. BILIRUBIN PRODUCTION
B. History
C. Physical Examination ● 80% from senescent RBCs
D. Laboratory Test ○ Old RBCs are degraded in the spleen📣
E. Endoscopic Procedures ○ The problem lies in metabolizing the hemoglobin, especially
References the heme part which is the precursor of the bilirubin📣
Review Questions ● 20% from ineffective erythropoiesis
Summary ○ Occurs in the bone marrow. RBCs are produced but do not
Need-to-know Concepts mature and become defective, and are subsequently
Concept Checkpoint destroyed inside the bone marrow 📣
● Bilirubin may also come from:
Objectives ○ Hepatic cytochromes
No objectives were given by the lecturer. ○ Muscle myoglobin
○ Other heme-containing enzymes
I. CAUSES OF JAUNDICE
A. BILIRUBIN SYNTHESIS
A. ACCUMULATION OF BILIRUBIN
● Excess production
● Decrease in metabolism (3 steps in metabolism of bilirubin)
○ Uptake: Liver
○ Conjugation: Liver
○ Excretion: Hepatocytes into biliary canaliculi
● Bilirubinuria indicates an elevation of the direct serum bilirubin
fraction and, therefore, the presence of liver or biliary disease
● Serum bilirubin levels increase when an imbalance exists
between bilirubin production and clearance
II. PRESENTATION OF JAUNDICE
● Serum bilirubin normally < 1 mg/dL (< 17 μmol/L)
○ Detected clinically when serum bilirubin exceeds 3 mg/dL
(51 μmol/L) (3 x 17 = 51) 📣
● Easily detectable in the sclerae
○ Because the sclera is white and there is an increased Figure 1. Bilirubin metabolism in the liver.
affinity of the bilirubin to the Descemet’s membrane in the ● Occurs in reticuloendothelial cells, primarily in the spleen & liver
sclerae 📣 ● The globin part of hemoglobin is a protein, so it is metabolized
● Causes “tea-colored” urine in the liver📣
○ Due to an increased level of the water soluble bilirubin ● STEPS:
📣 1. In the spleen, heme is converted to biliverdin (green pigment)
○ However, not all “tea-colored” urine is due to bilirubin. It by Heme Oxygenase
can be due to a concentrated urine due to urochromes 📣 ○ End products: Biliverdin, Carbon Monoxide, Iron📣
○ To differentiate the two, perform the Shake test 📣 2. Biliverdin is reduced to unconjugated bilirubin by Biliverdin
■ Shake test: distinguishes concentrated urine and Reductase (cytosolic)
tea-colored urine 📣

TRANS (13 & 15) Azis, Busog, Buzon, Cabujat, Casipit, Castillo, Castro CORE Borromeo, Biteng, San Juan 1 of 17
Butron - 63 917 776 0151 Banaga- 09271276274 Concepcion - 63 9176312197
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

○ Unconjugated bilirubin is non-polar, which means it is

○ Tea-colored urine: bubbles formed take a brownish
fat-soluble and cannot be dissolved in serum📣
yellowish or orange hue because of adherence of
3. In the hepatocytes, unconjugated bilirubin is conjugated through
bilirubin (which has a polar and a nonpolar end thus
UDP-Glucoronosyl Transferase, making it polar
incorporated in bubbles) to the bubbles
○ UDP-Glucoronosyl Transferase will attach 1-2 moieties of
● Heme is converted to biliverdin (green pigment) by Heme
glucuronide to convert it to the water-soluble conjugated
Oxygenase
bilirubin 📣
● Biliverdin is reduced to unconjugated bilirubin by Biliverdin
4. Conjugated bilirubin is excreted in the bile and reabsorbed in
Reductase
the intestines (duodenum), where it is reduced to urobilinogen
● In the hepatocytes, unconjugated bilirubin is conjugated
(colorless) via Bacterial β-Glucuronidase
through UDP-Glucoronosyl Transferase, making it polar
○ Some urobilinogen reabsorbed back into the systemic
● Inside the intestinal lumen, the urobilinogen can be acted
circulation and most of it will end in the liver, but some will be
upon by bacteria and oxidize it into urobilin(orange
excreted in the urine 📣
compound
5. Inside the intestinal lumen, the urobilinogen can be acted upon
by bacteria and oxidized into urobilin (orange compound;
CONCEPT CHECK
reason for color of the stool) 📣
1. What are the 3 steps in metabolism of bilirubin?
○ If you are excreting the conjugated bilirubin normally, the
2. What test distinguishes concentrated urine and tea-colored
stool will have a golden-brown color due to the color of
urine?
urobilin plus some conjugated bilirubin 📣
3. What reduces biliverdin to unconjugated bilirubin?
○ If you obstruct the flow of bile in the common bile duct, the
4. T or F. Heme oxygenase converts heme to bilirubin
stool will be clay-colored (darkish gray) due to the absence
5. T or F. Bilirubin may also come from hepatic cytochromes and
of urobilin and conjugated bilirubin 📣
muscle myoglobin.
6. Unconjugated bilirubin is tightly bound to albumin
___________________________________________________
○ Unconjugated bilirubin, because it is non-polar, cannot exist
in solution. It is like when you put oil in water. For it to exist in ANSWERS
1. Uptake, conjugation, and excretion
solution, it has to be tightly bound to albumin📣 2. Shake test
7. Conjugated bilirubin can also be bound to albumin, but it is 3. Biliverdin reductase
4. F. Heme oxygenase converts heme to biliverdin
usually: 5. T. Hepatic cytochromes, muscle myoglobin, and other heme-containing
○ Reversible, non-covalent enzymes are the other sources of bilirubin.
○ Irreversible, covalent: Delta bilirubin
○ Significance of delta bilirubin 📣 B. HEPATIC METABOLISM
■ When you have elevated bilirubin in the serum due to
obstruction of the bile duct and a procedure to relieve the
obstruction was performed, one of the first indications that
the obstruction was relieved is the change in the color of
urine into normal within a few hours
■ In a patient with cholangiocarcinoma, the bile duct is
obstructed and you put a stent to relieve the obstruction.
This will now enable bile to flow out to the intestine. 12
hours after putting a stent, the patient’s urine is expected
to be normal in color because the half-life of serum
bilirubin is only 4 hours. If the urine does not become
normal in color, it means that you did not relieve the
obstruction.📣 Figure 2. Bilirubin metabolism in the liver. 📍
■ In patients with a patent stent, once you take their blood, ● First, the heme is destroyed and released in the spleen. Then,
you will still notice a yellow color in the serum even if the the reticuloendothelial system of the spleen will release the
urine has a normal color due to the presence of delta unconjugated bilirubin is carried by albumin and taken up by the
bilirubin. The half-life of delta bilirubin is the same as the liver containing the ligandin 📣
half-life of albumin, which is 12-14 days. 📣 ○ Ligandin is responsible for holding the unconjugated
NEED-TO-KNOW bilirubin(2021B)
Causes of jaundice due to accumulation of bilirubin: ● Once inside the liver, it is acted upon by UDP-Glucuronosyl
● Excess production transferase and converted into conjugated bilirubin 📣
● Decrease in metabolism (3 Steps in Metabolism of bilirubin) ● Lastly, conjugated bilirubin is excreted out by hepatocytes into
○ Uptake: liver the biliary canaliculi. It travels down and mixes with the bile to
○ Conjugation: liver go into the small intestine 📣
○ Excretion: By hepatocytes into biliary canaliculi ● Process: UPTAKE → CONJUGATION → EXCRETION
● Serum bilirubin normally < 1 mg/dL (< 17 μmol/L) ○ Excretion is the most sensitive and rate-limiting step📍
○ Detected clinically when serum bilirubin exceeds 3 ■ First affected step when liver is damaged
mg/dL (51 μmol/L) (3 x 17 = 51)📣 ■ In viral hepatitis and cirrhosis:(2021B)
● Easily detectable in the sclerae ● Conjugated bilirubin is markedly increased which
● Shake test: distinguishes concentrated urine and tea-colored explains the presence of tea-colored urine a day before
urine📣 jaundice occurs
○ Concentrated urine: bubbles formed from shaking the ● Accumulation of conjugated bilirubin in the serum
container are white because of urochromes (pigments occurs because of impaired excretion
which gives urine its usual yellowish color) are
water-soluble and are not incorporated in the bubbles📣

PHYSICAL DIAGNOSIS 2 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

Unconjugated Bilirubin vs Conjugated Bilirubin (PPT)

● You can only differentiate the two in patients with deep jaundice;
Table 1. Physical properties of unconjugated and conjugated bilirubin 📍 it is not really observable in patients with light jaundice. If you
cannot differentiate the two clinically, you have to rely on
Unconjugated Bilirubin (B1) Conjugated Bilirubin (B2)
biochemical analysis. 📣
Non-polar Polar
NEED-TO-KNOW
Lipophilic Lipophobic
● Excretion is the most sensitive and rate limiting step
Not water soluble Water soluble ● Physical properties of unconjugated and conjugated bilirubin
No renal excretion With renal excretion (see Table 1)
● Unconjugated bilirubin (B1) is non-polar → lipophilic → not
Indirect van den Bergh Direct van den Bergh water soluble, hence, no renal excretion → NEVER appear in
Not oxidized to biliverdin Oxidized to biliverdin the urine(2021B)
● Conjugated bilirubin (B2) is polar (due to the attachment of 2
Never appears in urine Appears in urine glucuronide moieties) → lipophobic→ water soluble, hence,
Yellowish Jaundice Greenish Jaundice with renal excretion
● In order to calculate for unconjugated bilirubin:
● Unconjugated bilirubin (B1) is non-polar → lipophilic → not ○ B1 = Total Serum Bilirubin - B2
water soluble, hence, no renal excretion → NEVER appears in
the urine(2021B)
CONCEPT CHECK
● Conjugated bilirubin (B2) is polar (due to the attachment of 2
1. What is the most sensitive and rate-limiting step of bilirubin
glucuronide moieties) → lipophobic → water soluble, hence,
metabolism?
with renal excretion(2021B)
2. T or F. Conjugated bilirubin is non-polar and lipophobic.
Van den Bergh Method ___________________________________________________
● Normal serum bilirubin concentration is between 17 & 26 ANSWERS
μmol/L (1 & 1.5 mg/dL)(2021B) 1. Excretion
2. F. Conjugated bilirubin is polar and lipophobic
● Only done in specialized laboratories, but they do not use it
anymore(2021B) IV. CONSIDERATIONS IN JAUNDICE
● Classic test to determine the fractional component of
● Bilirubin Fractionation is done in order to help us determine
bilirubin(2021B)
the possible diagnosis of the patient
● Serum is mixed with diazotized sulfanilic acid and if there is
bilirubin, it will change the color and using photocalorimetric NEED-TO-KNOW
methods, they can measure the amount of the substance(2021B) ● Unconjugated Hyperbilirubinemia
● Direct reacting Van den Bergh Test / Direct Bilirubin ○ > 80% B1 of the total bilirubin
○ The serum is tested directly ● Conjugated Hyperbilirubinemia
○ When you test it directly, you will only be able to test the ○ > 50% B2 of the total bilirubin
bilirubin dissolved in the serum. Bilirubin attached to the ● Indeterminate 📣
albumin will not be taken up ○ Does not fall into either categories
○ Unconjugated bilirubin is bound to albumin, hence ○ Bilirubin fractionation is not going to help us make a
conjugated bilirubin is also called Direct Bilirubin (B2) diagnosis
because it undergoes a direct Van den Bergh test(2021B) ● Example 📣:
○ Only conjugated bilirubin (B2) can be measured(2021B) ○ If B1 is 90 μmol/L and B2 is 10 μmol/L, you have a case
● Indirect Van den Bergh Test / Indirect Bilirubin of Unconjugated Hyperbilirubinemia
○ To measure the indirect bilirubin, you have to treat it first with ○ If B2 is 40 μmol/L and B1 is 20 μmol/L, you have a case
methanol to release the unconjugated bilirubin, which is of Conjugated Hyperbilirubinemia since 40+20 is 60 and
attached to the albumin. The amount that reacts to it is the 40 is more than 50% of 60
Total Serum Bilirubin 📣 ○ If B1 is 70 μmol/L and B2 is 30 μmol/L, it is
○ Unconjugated bilirubin (B1/Indirect Bilirubin) is calculated indeterminate because 70 μmol/L is not >80% B1 and 30
and not measured, thus an indirect Van den Bergh test(2021B) μmol/L is not > 50% B2
○ In order to calculate for unconjugated bilirubin: ○ If B1 is 7 μmol/L and B2 is 3 μmol/L, patient is normal
■ B1 = Total Serum Bilirubin - B2📍 because when it is less than 50 μmol/L, they do not have
● Conjugated bilirubin is a polar compound 📣 hyperbilirubinemia
○ Imagine bilirubin as a fat soluble substance that becomes
water soluble when a polar substance is added CONCEPT CHECK
○ It can be filtered out into the glomeruli and come out into the 1. What type of hyperbilirubinemia should have >80% of the total
urinary filtrate (urine). Since it is dissolved in the serum, it is bilirubin?
the only thing measured using the direct Van den Bergh test 2. If B1 is 40 μmol/L and B2 is 60 μmol/L, what kind of
Yellowish Jaundice vs Greenish Jaundice hyperbilirubinemia does it fall under? (2021B)
● Conjugated bilirubin can easily be re-oxidized to biliverdin, ___________________________________________________
unlike unconjugated bilirubin. ANSWERS
○ Unconjugated Hyperbilirubinemia (i.e. patients with 1. Unconjugated hyperbilirubinemia
2. Conjugated Hyperbilirubinemia because B1 is not >80% and B2 is >50% of the
hemolysis): sclerae will present with a bright-yellow hue total bilirubin (2021B)
because unconjugated bilirubin cannot be re-oxidized to
biliverdin V. CLASSIFICATIONS
○ Conjugated Hyperbilirubinemia: sclerae will present with a Table 2. Classification of jaundice📍
yellow-greenish hue because conjugated bilirubin can easily Classification Type of Hyperbilirubinemia
be oxidized back to biliverdin.
Overproduction Unconjugated Hyperbilirubinemia

PHYSICAL DIAGNOSIS 3 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites
Decreased hepatic uptake Unconjugated Hyperbilirubinemia
Decreased hepatic conjugation Unconjugated Hyperbilirubinemia
Decreased excretion Conjugated Hyperbilirubinemia
● If you develop acute viral hepatitis, wherein the liver does not
function very well, and you develop jaundice, what kind of
hyperbilirubinemia will you have? 📣
○ Conjugated Hyperbilirubinemia
○ Recall: Excretion is the most sensitive and regulating step
■ If you develop acute viral hepatitis and you have liver
dysfunction, it is the first affected process
○ Two reasons why it is conjugated hyperbilirubinemia
■ If you have a problem with excretion (rate-limiting and
sensitive step), you will have conjugated
hyperbilirubinemia
■ When you have viral hepatitis, you also have tea-colored
urine one day before you develop jaundice
● You cannot have tea colored urine if you have
unconjugated hyperbilirubinemia; only conjugated
hyperbilirubinemia has tea-colored urine
A. OVERPRODUCTION OF BILIRUBIN
● Causes unconjugated hyperbilirubinemia 📍
Hemolytic disorders
● Familial Hemolytic Disorders
○ Spherocytosis
■ RBCs are spherical instead of biconcave
■ Because it is spherical, it has problems going through the
microcirculation 📣
■ The body recognizes this so the spleen takes the cells up
and destroys them, releasing hemoglobin which leads to
the development of jaundice 📣
■ Exhibits extravascular hemolysis
● Occurs outside the systemic circulation and inside the
spleen via the reticuloendothelial system, wherein
monocytes and macrophages normally clear up old
and damaged RBCs(Hasudungan) 📣
● In hemolytic anemia, the reticuloendothelial system
works in overdrive, destroying more RBCs(Hasudungan)
● Because of this type of hemolysis, spherocytosis will
exhibit a deeper jaundice as compared to
paroxysmal nocturnal hemoglobinuria, which
causes intravascular hemolysis 📣
○ Sickle Cell Anemia
■ Only seen among Africans 📣
■ In Africa before, there were so many cases of malaria
which lead to the occurrence of a mutation wherein RBCs
of the Africans made a sickle cell shape, making them
more resistant to the disease 📣
■ Now that there’s not so much malaria present, it has
become a big burden to the population because there are
some people who are exposed to extreme cold and they
can die because of the sickle cell disease 📣
○ Thalassemia
■ Whether it is α-thalassemia or β-thalassemia, there is
something wrong with the hemoglobin 📣
■ Can also develop hemolysis 📣
○ RBC enzyme deficiency
■ Glucose-6-Phosphate Dehydrogenase (G6PD)
deficiency
● Whenever you have a patient with G6PD deficiency,
you have to make sure that you know what drugs
you’re giving to them 📣
● Giving them wrong drugs, especially the sulfa (i.e.
sulfonamides) drugs, cause them to develop severe
hemolysis and you can actually kill them 📣
PHYSICAL DIAGNOSIS
ver. 01
● Review the drugs that may potentially cause hemolysis
in patients with G6PD deficiency 📣
■ Pyruvate Kinase Deficiency
● May also develop hemolysis 📣
● Acquired Hemolytic Disorders
○ Microangiopathic Hemolytic Anemia
■ E.g. Hemolytic Uremic Syndrome 📣
● Seen mostly in the pediatric population 📣
● Not seen in adults 📣
○ Paroxysmal Nocturnal Hemoglobinuria (PNH)
■ Exhibits Intravascular Hemolysis 📣
● PNH and Plasmodium falciparum malaria are the
only 2 common entities that lead to this 📣📍
○ **According to other references, Microangiopathic Hemolytic Anemia also
causes intravascular hemolysis. But in the lecture, it was emphasized that
only PNH and Plasmodium falciparum malaria commonly cause it
● RBCs are destroyed not in the spleen but in the
systemic circulation 📣
● Has less jaundice than spherocytosis which causes
extravascular hemolysis, but causes hemoglobinuria
📣📍
○ Since hemoglobin is released into the bloodstream,
it can go out in the urine and cause the urine to
become black 📣
■ This is why Plasmodium falciparum malaria is
also called Blackwater fever 📣
■ Only Plasmodium falciparum malaria because it
is associated with massive hemolysis, releasing
so much hemoglobin in the systemic circulation
📣
○ Spur Cell Anemia
■ Extravascular hemolysis 📣
○ Immune Hemolysis
■ Coombs positive or Coombs negative hemolytic anemia
📣
■ Extravascular hemolysis 📣
Ineffective Erythropoiesis
● Cobalamin (Vitamin B12) deficiency
○ Megaloblastic anemia
■ Megaloblasts
● Vitamin B12 is needed for the normal division of RBCs.
Deficiency of this vitamin will prevent them from
dividing, causing them to be big.
● Do not go out into the systemic circulation 📣
○ Because most are destroyed inside the bone
marrow and the hemoglobin is released
○ Some RBCs that escape the bone marrow are
called macrocytes
● Folate deficiency
● Severe iron deficiency
○ There is not enough iron to form the right amount of
hemoglobin 📣
■ Leads to premature destruction of RBCs in the bone
marrow
B. DECREASED HEPATIC UPTAKE OF BILIRUBIN
● Causes unconjugated hyperbilirubinemia 📍
● Drugs
○ Rifampicin
■ Used in treatment of tuberculosis
■ Approach to patient who developed jaundice due to
quadruple-drug regimen of TB
● Quadruple-drug regimen
○ Rifampicin
○ Isoniazid (INH)
○ Pyrazinamide
○ Ethambutol
4 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

● Of the 4 drugs, only ethambutol does not cause liver

● In TB patients who developed jaundice due to 4-drug
dysfunction 📣
regimen:
● If a patient develops jaundice, you cannot stop all 4,
○ Ethambutol does not cause liver dysfunction
you should take out only the one that causes the
○ Pyrazinamide is stopped
hepatic dysfunction 📣
○ Rifampicin is still given at full dose
○ The most notorious of the 4 is pyrazinamide, so we
○ Isoniazid is reintroduced starting with a low dose
do not give it back 📣
until the highest dose that does not cause jaundice
● We try to give back rifampicin and INH 📣
is attained
○ Rifampicin causes idiosyncratic liver dysfunction
■ Probenecid
■ It does not matter whether you give 1mg or 450
mg because it’s idiosyncratic📣
CONCEPT CHECK
■ So when we give back the rifampicin, we give it at
1. What classification of jaundice causes conjugated
the full dose 📣
hyperbilirubinemia?
○ Toxicity of isoniazid (INH) to the liver is
2. Give two examples of familial hemolytic disorders that lead to
dose-related 📣
the overproduction of bilirubin.
■ When we bring back INH, we start with a low
3. What type of hemolysis causes hemoglobinuria?
dose, maybe 50, 100 and go up to 300 mg, and if
4. What 2 diseases cause intravascular hemolysis?
they develop jaundice we go back to 200 mg 📣
5. Which drug for tuberculosis causes idiosyncratic liver
■ We try to find the highest dose that will not cause
dysfunction?
jaundice 📣
___________________________________________________
● When giving pyrazinamide, you have to make sure that
you give at least two drugs, and then give another one ANSWERS
1. Decreased excretion
which is usually a second-line drug, and second-line 2. Spherocytosis, Sickle Cell Anemia, Thalassemia, RBC enzyme deficiency
drugs are very difficult to get in the Philippines 📣 3. Intravascular hemolysis
4. PNH and Plasmodium falciparum malaria
○ Probenecid 5. Rifampicin
■ This drug was previously used to try to prevent the
secretion of penicillin into the urinary filtrate in order to C. DECREASED HEPATIC CONJUGATION OF BILIRUBIN
reduce the amount of penicillin that you have to give 📣 ● Causes unconjugated hyperbilirubinemia 📍
■ Because of its effect on hepatic uptake, it is no longer ● Crigler-Najjar type I
used 📣 ○ Autosomal recessive
○ Complete absence of UDPGT
NEED-TO-KNOW
■ At an early age, they develop deep jaundice
● Overproduction of bilirubin, decreased hepatic uptake,
■ In the first weeks of life, the blood-brain barrier (BBB) is
and decreased hepatic conjugation
not yet competent 📣
○ Causes Unconjugated Hyperbilirubinemia
● If bilirubin is able to enter through the BBB, it can
● Only decreased excretion causes Conjugated
deposit in the brain to cause a condition called
Hyperbilirubinemia
kernicterus, which leads to death 📣
● Overproduction of bilirubin
○ Death in infancy or childhood
○ Hemolytic disorders
● Crigler-Najjar type II
■ Familial Hemolytic disorders:
○ Usually autosomal dominant
● Spherocytosis
○ Partial absence of UDPGT
● Sickle Cell Anemia
■ UDPGT production can be induced by phenobarbital
● Thalassemia
● Lessens jaundice but only used as maintenance 📣
● RBC enzyme deficiency
○ May survive into adulthood
○ G6PD deficiency
■ They develop jaundice but not kernicterus
○ Pyruvate Kinase deficiency
○ Patients are visibly yellow from afar because they have deep
■ Acquired Hemolytic disorders:
jaundice 📣
● Microangiopathic Hemolytic Anemia
○ Brain damage is dependent on how high the unconjugated
○ Eg. Hemolytic Uremic Syndrome
bilirubin was during infancy (2021B)
● Paroxysmal Nocturnal Hemoglobinuria
● Gilbert’s syndrome
● Spur Cell Anemia
○ Reduced UDPGT activity
● Immune Hemolysis
○ Affects not only bilirubin conjugation but also uptake
■ The only 2 common entities that lead to intravascular
○ Very common: 5% of the population, male predominance
hemolysis are PNH and Plasmodium falciparum
○ Jaundice is episodic and is induced or precipitated by:
malaria
■ Fasting (crash diets)
■ Extravascular hemolysis causes a deeper jaundice
■ Stress
than intravascular hemolysis
■ Alcohol drinking
■ Intravascular hemolysis causes hemoglobinuria
● NOT due to alcohol hepatitis but from the stress
○ Ineffective Erythropoiesis
related to drinking that makes their eyes yellow 📣
■ Cobalamin (Vitamin B12) deficiency
■ Lack of sleep
● Megaloblastic anemia
○ People who are exposed to precipitating factors can observe
■ Folate deficiency
themselves becoming yellow 📣
■ Severe iron deficiency
■ When you suspect a patient with Gilbert’s syndrome, test
● Decreased hepatic uptake of bilirubin
for the Bilirubin Fraction; it should be unconjugated
○ Drugs
hyperbilirubinemia
■ Rifampicin
■ If bilirubin levels are normal, patients are starved to induce
an increase in B1. After 1 or 2 days, they become yellow.

PHYSICAL DIAGNOSIS 5 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

These patients can now be diagnosed with Gilbert’s ● Acquired

syndrome. 📣 ○ Hepatitis (2021B)
● A simple history of being jaundiced after drinking ■ Causes conjugated hyperbilirubinemia
alcohol or stress is enough to make you suspect ■ In ordinary cases, should not develop pruritus
Gilbert’s syndrome. ■ Classic clinical presentation is first prodromal symptoms
● If B1 is high and there is no other indication of a liver of fever, anorexia, nausea, and sometimes right upper
disease, there is no need for liver biopsy or any other quadrant pain
work-up.(2021B) ■ Fever disappearance → tea-colored urine (next day) →
D. DECREASED EXCRETION OF BILIRUBIN jaundice (next day)
● This would help you strongly suspect the presence of
● Only condition that is associated with conjugated acute viral hepatitis
hyperbilirubinemia📍 ■ Cholestatic jaundice of acute viral hepatitis A (secondary
Decreased Hepatic Excretion complication)
● Genetically-Acquired ● Complication where swelling of hepatocytes blocks the
○ Dubin Johnson syndrome biliary canaliculi and bile does not flow, thus forming a
■ Altered excretion (cannot excrete) of conjugated bilirubin form of cholestasis with pruritus (without actual
into the bile ducts mechanical obstruction)
■ Dark or black hepatocytes upon liver biopsy ● Usually occurs about 48 weeks later after the bout of
■ Cannot visualize gallbladder in oral cholecystography acute hepatitis A
because the dye is not excreted into the gallbladder 📣 ○ Cirrhosis(2021B)
● Before, when a gallbladder stone is suspected, a dye is ■ Causes conjugated hyperbilirubinemia
taken orally in where it is absorbed, taken up by the ■ Patients with cirrhosis will not present with pruritus
bile, excreted into the bile and gets concentrated in the because they have no problem with excretion of bile (no
gallbladderThis is not done in the clinics anymore and cholestasis)
is replaced by ultrasonography 📣 ○ Drug-induced
■ Normal total urinary coproporphyrin, coproporphyrin I > ■ Androgens
80%, rise in plasma BSP at 90 minutes ● Used by bodybuilders
(bromosulfophthalein formerly used as sensitive indicator ● Affects heart and liver
of liver dysfunction but already withdrawn from the ■ Oral contraceptives
market)(2021B) ● 5% will develop cholestasis 📣
■ Defect: mutations in the gene for multiple drug resistance ● Recovery after discontinuation of drug
protein (2021B) ■ Chlorpromazine
○ Rotor Syndrome ● Antipsychotic drug
■ Problem with the hepatic storage of bilirubin ● Commonly used before
■ Normal-colored hepatocytes (liver cells are not ■ Erythromycin estolate
pigmented) ● Macrolide antibiotic that is not used anymore
■ Can visualize gallbladder in oral cholecystography 📣 ● Other erythromycin salts do not induce this
■ Increased total urinary coproporphyrin excretion, problem 📣
coproporphyrin I < 70%, no rise in BSP at 90 minutes(2021B)
NEED-TO-KNOW
○ Benign Recurrent Cholestasis
● Decreased hepatic conjugation of bilirubin
■ Manifestations: jaundice, skin excoriation and severe
○ Causes Unconjugated Hyperbilirubinemia
pruritus (due to accumulation and skin deposition of bile
○ Crigler-Najjar type I
acid)
■ Complete absence of UDPGT
■ Bile and bilirubin, cannot be excreted properly, and thus
■ Causes kernicterus, leading to death
bile acids and salts accumulate 📣
○ Crigler-Najjar type II
● Bile acids go back to the systemic circulation and get
■ Partial absence of UDPGT
deposited under the skin. This develops severe
● UDPGT production can be induced by phenobarbital
pruritus, which is classic of cholestasis
■ Survive into adulthood
■ Difference between cholestasis and mechanical bile duct
○ Gilbert Syndrome
obstruction: 📣
● Decreased excretion of bilirubin
● Both present with conjugated hyperbilirubinemia and
○ Causes Conjugated Hyperbilirubinemia
pruritus
○ Decreased Hepatic Excretion
● The difference is when you do an imaging, (e.g.
■ Familial
injecting a dye into the bile duct in cholestasis) no
● Dubin Johnson Syndrome
obstruction will be observed in the bile ducts because
● Rotor Syndrome
usually the obstruction is in the smaller ductules
● Benign Recurrent Cholestasis
● When you do an ERCP (Endoscopic Retrograde
● Progressive Familial Intrahepatic Cholestasis
Cholangio-Pancreatography), you will not see anything
■ Acquired
- classic of cholestasis
● Hepatitis
■ Recurrent attacks of jaundice and pruritus but will just
● Cirrhosis
spontaneously resolve
● Drug-induced
■ Does not lead to any hepatic damage
○ Androgens
○ Progressive Familial Intrahepatic Cholestasis
○ Oral Contraceptives
■ Idiopathic cause(2021B)
○ Chlorpromazine
■ Manifestations: jaundice, pruritus (2021B)
○ Erythromycin estolate
■ Eventually lead to liver damage or failure (sometimes
cirrhosis) 📣

PHYSICAL DIAGNOSIS 6 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

CONCEPT CHECK ○ Somatic Pain - the gallbladder becomes inflamed, and

1. Ultrasonography is used for diagnosing what familial syndrome irritates the overlying parietal peritoneum that is supplied by
that causes decreased hepatic excretion? the somatic nerve; felt in the right upper quadrant📣
2. T/F. Alcohol induced Gilbert syndrome is because of sudden ○ Only 10% of patients with gallbladder stone will need an
onset of alcohol hepatitis. operation. These are the patients who have fat intolerance to
3. What drug can induce UDPGT production? avoid these complications: 📣
4. Which disease which causes decreased hepatic conjugation of ■ Acute cholecystitis (when stuck in the cystic duct)
bilirubin causes kernicterus? ■ Jaundice → Ascending cholangitis (outside the cystic duct
___________________________________________________ and blocks the ampulla)
○ Primary stones – stone formed de novo as in biliary stasis
ANSWERS
1. Dubin Johnson Syndrome ○ Secondary stones – stone from gallbladder that pass
2. False. through the cystic duct but get stuck in distal common bile
3. Phenobarbital
4. Crigler-Najjar type I
duct which has a smaller papilla
○ Easily be removed by surgery or endoscopic retrograde
Extrahepatic Biliary Obstruction cholangiopancreatography (ERCP)
● Caused by mechanical type of obstruction outside the liver ■ Promotes bile flow and prevents death from ascending
● Can be intraductal (inside) or extraductal (outside) 📣 cholangitis by putting a stent, thus prolonging life(2021B)📍
● Malignancy
○ Common in elderly
○ Obstruction occurs slowly, and have painless jaundice
○ Most due to cholangiocarcinoma
■ Most cases like intrahepatic bile tumors are inoperable,
since surgery is associated with faster mortality.
■ Some are operable when the tumor is still small and
located at the distal part upon CT scan(2021B)📍
○ Klatskin tumor – hilar cholangiocarcinoma occurring at the
bifurcation of left and right hepatic bile ducts
○ Patient will die in 6 to 12 months
○ More life-threatening
○ Painless jaundice in >60 y/o - almost always
cholangiocarcinoma 📣
● Strictures
○ Only occurs when the bile duct is injured.📣
■ From previous surgeries or can be a stone that passed
Figure 3. Anatomy of the Biliary Tree. through it before
The left and right hepatic ducts are inside the liver. Most part of the common ○ Usually it is post-operative – manipulation or trauma of the
hepatic duct is still inside the liver but part of it is already outside the liver. Then,
area causes devascularization of the biliary tree, leading to
it is joined by the cystic duct, it now becomes the common bile duct. and the
common bile duct will now drain into the duodenum in the papilla. 📣 low-grade ischemia then fibrosis and stricture formation
○ Second operation of gallbladder is more difficult if the small
● Intraductal - inside the bile duct
bile duct has also undergone fibrosis
○ CBD stones
○ Treatment: Stents – rubber, metallic (usual)
○ Malignancy
■ Patients who did not have previous surgeries may have
○ Strictures
fibrosis due to previous passage of stones down the bile
○ Parasitic Infestation (Ascaris, Clonorchis)
duct
○ Sclerosing cholangitis
■ Shorter strictures are usually benign, while longer ones
○ Blood clots
are usually malignant
● Extraductal - outside the bile duct
● Parasitic Infestation
○ Malignancy
○ Clonorchis sinensis
○ Tuberculosis
○ Ascaris
○ Inflammation
■ Very common cause of biliary obstruction in the
Intraductal Compression Philippines
● Common Bile Duct Stones ■ Unlike immobile stones, ascaris moves forward causing
○ Common especially in the younger individuals📣 severe pain worse than stones, and cannot swim
○ Stone formed in the gallbladder goes out into the common backwards (2021B)
bile duct, blocking the flow of bile(2021B) ■ It pushes itself against the action of the body (i.e.
■ The stones stay in the common bile duct since the swimming upwards in the bile duct when the gallbladder
ampulla (of Vater) has a smaller diameter than the contracts to secrete contents)
common bile duct 📣 ■ Diagnosis and Treatment: ERCP - best performed if the
■ If it is already symptomatic, then it means that you already ascaris is not fully inside the bile duct
developed fat intolerence; when you eat fatty food, there ■ If the worm dies within the bile duct, it is removed piece by
is a feeling of bloatedness as if you want to burp but you piece to avoid stone formation
are unable to. 📣
○ With fat intake, gallbladder contracts to release bile. Thus, NICE-TO-KNOW
this is associated with painful jaundice.(2021B) ● Which do you think is more painful obstruction in the
○ Visceral Pain - produced when the gallbladder cannot bile duct? an ascaris or a stone? - When you remove/pull
contract due to a stone stuck in gallbladder; pain is felt at the down the Ascaris it will swim back. Thus more painful and
center 📣 difficult to remove than common bile duct stones. 📣

PHYSICAL DIAGNOSIS 7 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites
● Sclerosing Cholangitis
○ Associated with ulcerative colitis and Crohn’s disease
○ Intermittent attacks of pruritus, jaundice, pain, and fever
○ Multiple strictures all over the bile duct (beaded appearance
of bile ducts upon imaging)
○ No treatment or surgery; management includes trying to
alleviate obstruction during attacks
● Blood Clot
○ It can happen after a liver biopsy. 📣
■ Injury to a small vessel that connects to the a bile duct
may allow blood to flow along the bile duct and form a
blood clot
○ In hemophilia, blood flows down the bile duct, thus clot
formation will block flow
○ Patients who have undergone liver biopsy may experience
bleeding that may clot and cause bile duct obstruction.
Extraductal Compression
● Malignancy
○ Periampullary cancer can be 1 of 4 entities:
■ Pancreatic Head Carcinoma
● Most common cause of extraductal compression that is
due to malignancy 📣
● Very close to distal common bile duct, thus cancer of
the pancreatic head may cause blockage of flow
■ Distal Common Bile Duct Cancer
(Cholangiocarcinoma)
■ Duodenal Cancer
■ Ampullary Cancer
○ All 4 of these will usually lead to early jaundice due to
obstruction of bile flow
○ Normally present with similar manner and cannot be
distinguished using biopsy because all are adenocarcinoma
○ Treatment: Whipple’s Procedure
■ Also known as pancreaticoduodenectomy
■ The operation done to relieve pancreatic cancers
■ Removal of the pancreas, gallbladder, part of common bile
duct, and part of the duodenum and connect them
together
○ In the porta hepatis, obstruction of common hepatic duct
may occur due to enlarging lymph nodes (can be seen in
patients with tuberculosis or metastatic cancer)
● Tuberculosis
○ Can be biliary tuberculosis or tuberculous cholangitis
○ Can involve the lymph node in porta hepatis
● Inflammation
○ Acute pancreatitis can cause temporary but mild jaundice
because of the compression of common bile duct
NEED-TO-KNOW
● Pancreatic Head Cancer is the most common cause of
extraductal compression that is due to malignancy.
● Common bile duct obstruction is common among younger
individuals.
● Cholangiocarcinoma is the most common cause of
intraductal compression seen among elderly.
CONCEPT CHECK
1. Most common cause of extraductal compression that is due
to malignancy??
2. Most common cause of intraductal compression that is due
to malignancy in elderlies?
3. Treatment for patients with fat intolerance secondary to
common bile duct obstruction?
___________________________________________________
ANSWERS
1. Pancreatic Head Cancer
2. Cholangiocarcinoma
PHYSICAL DIAGNOSIS
ver. 01
3. Surgery
VI. EVALUATION OF JAUNDICE
A. HISTORY
● History is used to diagnose while the laboratory tests are used
to confirm.📣
● When we take the history, we have to determine the exposure, if
there is a history of:
○ Transfusions
■ Test for possibility of Hepatitis B or C and HIV
○ IV drug use (possible risk of HIV infection)
■ Because of needle sharing (2021B)
○ Tattoos (Hepatitis B, C risk)
■ If needles are not properly sterilized (2021B)
○ Sexual promiscuity
■ Test for HIV, syphilis, Hepatitis B, and Hepatitis C
because they can be transmitted sexually.
○ Ethanol use
■ For men, you have to drink 60g to 80g of alcohol to
develop alcohol-induced liver disease (4 bottles of beer
everyday) 📣
■ Drinking consistently over a long period of time puts you
at risk for alcoholic cirrhosis(2021B)
■ NTK: Binge drinking allows your liver to recover(2021B)
○ Travel
■ Recent travel to India can suggest Hepatitis E
● History of fever, abdominal pain, arthralgia/myalgia
CASE 1📣
● A young medical student presents with jaundice that occured
1 day PTC and tea-colored urine that occured 2 days PTC.
Based on the history, what is your impression?
● Impression: Acute Hepatitis A
● Rationale: The patient is a medical student so she most likely
is financially well-off and not exposed to possible carriers of
Hepatitis A virus while growing up. Now that she is a medical
student and studying in UERM where street food vendors
exist, her risk of exposure has significantly increased
especially since she hasn’t yet developed immunity against
the virus due to her lack of exposure in the previous years. If
the patient grew up in a different environment (eg. Tondo), the
impression would not be Hepatitis A because at the age of 9,
almost all children would have already been exposed to
Hepatitis A virus and would have developed immunity.
CASE 2📣
● A surgeon presents with an icteric sclera, tea-colored urine,
and fever that disappeared when jaundice appeared. What is
your impression?
● Impression: Acute Hepatitis B
● Rationale: He is a surgeon who has high risk of exposure (eg.
needle-prick during operation).
CASE 3📣
● A second year medical student presents with jaundice and
persistent fever. What is your impression?
● Impression: Amoebic liver abscess, ascending cholangitis, or
typhoid hepatitis
● Rationale: It is not acute hepatitis because the fever should
have disappeared by the time the jaundice appeared. Since
the fever is persistent, you should think about conditions that
will cause fever and jaundice at the same time.
● Drug use (e.g. acetaminophen, INH, chlorpromazine)
○ 12 g or 24 tablets of acetaminophen is hepatotoxic📣
● Previous biliary surgeries
○ If jaundice occurs immediately after surgery: accidental
ligation of common bile duct 📣
8 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

○ If jaundice occurs weeks or months later after the surgery: ■ Dullness indicates mild splenomegaly or hepatomegaly
stenosis📣 ● Skin
● Pruritus 📣 ○ Excoriations on the skin may be a manifestation of pruritus
○ Decreased bile excretion 📣
○ Cholestasis will cause pruritus ● Signs of portal hypertension 📣
○ Cholangiocarcinoma will cause pruritis due to mechanical ○ Ascites
bile duct obstruction ○ Caput Medusae
○ Clonorchis has pruritus
● Acholic stools
○ Due to either cholestasis or mechanical bile duct obstruction
○ Pruritus is expected
● Other conditions
○ Pregnancy
■ Continuing pregnancy when the patient has fatty liver
may be fatal to the patient. 📣
○ Inflammatory Bowel Disease
■ Examples are ulcerative colitis and Crohn’s disease.
■ Development of jaundice in these conditions is rare 📣
Figure 6. Percussion findings in ascites. (Bates)
○ Congestive heart failure
■ Multiple cardiac sclerosis or chronic passive congestion
may lead to development of jaundice 📣
○ Septicemia - associated with jaundice
B. PHYSICAL EXAMINATION
● Palpation of liver edge 📣
○ It should be non-tender, sharp, and firm.
○ In cancer, it becomes nodular and hard.
○ In cirrhosis, the liver is usually not palpable because the liver
is smaller.
○ In viral hepatitis, the liver edge is sharp, soft, and tender.

Figure 7. Caput Medusae. (Bates)

● Signs of decreased hepatic function 📣
○ Most of the signs of decreased hepatic function is because of
hyperestrinism
■ There is an increased level of estrogen due to the inability
of the liver to metabolize estrogen’s precursor
● Patient with ovaries - estradiol
● Patient with placenta- estriol
● Male patient - estrone
■ Cirrhotic patients with hyperestrinism presents with palmar
erythema, telangiectasia, gynecomastia, testicular
Figure 4. One maneuver to palpate the liver is by placing your left hand atrophy, sparse axillary hair.
behind the patient, parallel to the 11th and 12th ribs adjacent to the soft
tissues below. By pressing your left hand upward, the patient’s liver may be
● Virchow’s Node 📣
felt more easily by your other hand.(Bates) ○ Also called Sentinel node
○ In abdominal malignancies, palpate on the left clavicle (left
supraclavicular lymph nodes)
● Sister Mary Joseph’s Nodule 📣
○ Palpate nodule at the umbilicus
○ Indication of abdominal malignancy
● Signs of Inflammation 📣
○ Murphy’s Sign - classic sign of acute cholecystitis
■ Ask the patient to breathe in while you press on the right
upper quadrant of the abdomen.
■ (+) Murphy’s Sign = inspiratory arrest
○ Percussion or point tenderness
● Lymphadenopathies
● Specific findings
Figure 5. Another maneuver is the “hooking technique” which is done by ○ Hemochromatosis
standing to the right of the patient’s chest and placing both hands on the right
abdomen below the border of liver dullness. Ask the patient to take a deep ■ Hyperpigmentation
breath and press in with your fingers and up toward the costal margin.(Bates) ○ Primary Biliary Cirrhosis
■ Xanthomata
● Palpation of spleen 📣
■ Xanthelasma - eyelid 📣
○ If spleen is palpable, it means it is enlarged (moderate
○ Wilson’s Disease
splenomegaly).
■ Kayser-Fleischer rings - around the cornea 📣
○ Percussion of the Traube’s space
■ Normally tympanitic

PHYSICAL DIAGNOSIS 9 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

○ CT scan can be used to identify choledocholithiasis in distal

common bile duct
○ Triphasic CT Scan 📣
■ They inject a dye, measure the arterial and post venous
phase to determine if mass is malignant
● MRI
○ MRI is the preferred test for brain and spine problems
● Magnetic Resonance Cholangio-Pancreatography (MRCP)
○ Can trace the bile duct very cleary 📣
● Endoscopic Retrograde Cholangio-pancreatography
(ERCP)
Figure 8. Kayser-Fleischer rings. A golden to red brown ring, sometimes ○ Catheter is inserted in the papilla
shading to green or blue, from copper deposition in the periphery of the ○ Gold standard in biliary imaging
cornea found in Wilson’s Disease.(Bates)
○ Have therapeutic options
C. LABORATORY TESTS ■ Stone extraction, stenting, etc
● Percutaneous Transhepatic Cholangiography 📣
● Serum Transaminases (AST vs ALT) (2021B)
○ Used when catheter cannot be inserted inside the papilla
○ AST (aspartate transaminase) or SGOT (serum
○ Not done blindly anymore
glutamic-oxaloacetic transaminase)
■ More sensitive, but less specific than ALT
■ Less specific because RBCs, muscles, and heart can also
produce AST
■ Used to decrease the chance of false negative result
○ ALT (alanine transaminase) or SGPT (serum glutamic
pyruvic transaminase)
■ More specific because it is only produced in the liver
○ AST/ALT > 0.7 - more severe liver disease
■ Indicator of liver injury
■ ALT is found more in the cytoplasm while AST is found in
the organelles
○ In liver injury, SGPT/SGOT ratio levels go up; in viral injuries,
these go the highest/high normal (SGPT/SGOT value of
>400) this indicates acute viral hepatitis. To test a patient Figure 9. Stone in common bile duct that is detected by endoscope (2021B)
suspected to have hepatitis, don’t ask for the hepatitis profile
but rather the SGPT/SGOT levels. SGOT goes up first
because it is more sensitive (might come from other parts of
the body); SGPT rather is more specific (only from liver). 📣
● Alkaline Phosphatase
○ Elevated due to two conditions:
■ Infiltration of the liver
■ Blockage of bile ducts
○ Production in the biliary epithelium of the bones
○ Extreme elevations (>7x the upper limit of normal)
■ Cholestasis or extrahepatic biliary obstruction
○ In children, ALP is higher than in adults and may rise due to
bone problems
Tests for Hepatic Functional Reserve Capacity (2021B)
● Serum Albumin
○ Low in chronic conditions (cirrhosis, cancer)
○ Normal in acute processes (viral hepatitis, choledocholithisis) Figure 10. Different endoscopes. Gastroscope lenses on top and forward
○ Due to long half life, you have to wait for 14 days for the viewing (top and bottom left); Duodenoscope with lenses on the side for side
value to go down 📣 viewing (top and bottom right). (2021B)
● Prothrombin Time
○ More sensitive because clotting factor VII has a half life of
12 hours
○ More specific because an abnormal clotting time may be due
to problem in factors VIII and IX (Hemophilia A and B)
○ Prothrombin time - extrinsic pathway
○ Clotting time - intrinsic pathway 📣
D. HEPATOBILIARY IMAGING
● Ultrasonography
○ Limitation: best used to detect differences in echogenicity
(e.g. from solid against liquid, or air in solid)
■ Can be used in amoebic liver abscess 📣
■ Cannot detect stone in bile duct because both are solid Figure 11. ERCP.
● CT scan
○ More sensitive than ultrasonography but more expensive

PHYSICAL DIAGNOSIS 10 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites
Figure 12. Filling defects.
Figure 13. Narrowing.
PATIENT WITH ABDOMINAL ENLARGEMENT
A. EVALUATION OF ABDOMINAL ENLARGEMENT
● It is a manifestation of numerous diseases
● Complaints may be abdominal fullness or bloating and may note
increasing abdominal girth on the basis of increasing clothing or
belt size
Figure 14. Causes of protuberant abdomen
Causes (Harrison’s 20th ed)
● Fat
○ Weight gain with an increase in abdominal fat can result in
an increase in abdominal girth which may be perceived as
abdominal swelling
○ May be caused by an imbalance between caloric intake and
energy expenditure associated with a poor diet and
sedentary lifestyle
○ Can be manifestation of certain diseases, such as Cushing’s
syndrome
○ Excess abdominal fat has been associated with an increased
risk of insulin resistance and cardiovascular disease
● Fetus
PHYSICAL DIAGNOSIS
ver. 01
○ Pregnancy, noted at 12-14 weeks of gestation
○ Abdominal distention may be seen before this point as a
result of fluid retention and relaxation of the abdominal
muscles
● Flatus
○ Normal level of intestinal gas is ~200mL, which is made of
nitrogen, oxygen, carbon dioxide, hydrogen, and methane
○ Increase in intestinal gas can be due to aerophagia
(increased swallowing of air) or increased bacterial
metabolism
● Fluid
○ Often known as ascites, accumulation of fluid results in
abdominal distension
● Feces
○ Severe constipation or intestinal obstruction
○ Accompanied by abdominal discomfort, pain, nausea, and
vomiting
● Fatal Growth
○ Neoplasms, abscesses, or cysts
○ Enlargement of intra abdominal organs like the liver or
spleen, or an abdominal aortic aneurysm
NEED-TO-KNOW
● 6 F’s of Abdominal swelling: fat, fetus, flatus, fluid, feces and
fetal growth (often a neoplasm)(Harisson’s 20th ed)
B. HISTORY
● Determine temporal relationship between abdominal
enlargement and pedal edema
○ CHF: if pedal edema comes first then abdominal
enlargement
○ Cirrhosis: if abdominal enlargement comes first before pedal
edema due to secondary hyperaldosteronism
○ Malignant ascites if with abdominal enlargement without
pedal edema
■ In females: ovarian cancer
■ In males: pancreatic, gastric or colon cancer
○ These are the causes of edema: liver, heart or kidneys (has
both pedal and orbital edema, e.g. nephrotic syndrome)
● Symptoms suggestive of malignancy like weight loss, night
sweats, and anorexia
● Ask about risk factors for or symptoms of chronic liver disease,
including alcohol abuse and jaundice which suggest of ascites
● Ask about other symptoms of medical conditions, including
heart failure and tuberculosis, which may also cause
ascites.(Harrison’s 20th ed)
● History of orthopnea, PND, exertional dyspnea
○ Orthopnea – cardiac problem
○ PND – comes first in cardiac failure before orthopnea due to
decrease in oxygen drive
○ Exertional dyspnea – sign of CHF
● History of urinary symptoms, periorbital edema
○ Fluid accumulates in the periorbital edema as it is the loosest
tissue in the body
● History of hematemesis, melena, jaundice, sleep
disturbances
○ This is associated to cirrhosis
● Weight loss, constipation, hematochezia, abdominal pain,
postprandial vomiting
○ Inability to pass stool or flatus together with nausea or
vomiting suggests bowel obstruction, severe constipation, or
an ileus (lack of peristalsis) (Harrison’s 20th ed)
○ Increased eructation and flatus may point toward aerophagia
or increased intestinal production of gas.(Harrison’s 20th ed)
○ Weight loss – if greater than 5 kg in 3 months, think cancer if
DM and hyperthyroidism are ruled out
○ Constipation – colon cancer in patients older than 45 years
old (colonoscopy)
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5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

○ Hematochezia – colon cancer ● Direction of flow of abdominal veins (2020A)

○ Abdominal pain – pancreatic and intestinal cancer ○ Umbilicus as the delineation

○ Postprandial vomiting – gastric malignancy ○ Inferior vena caval obstruction – flow of veins goes up from
C. PHYSICAL EXAMINATION umbilicus
○ Caput medusa – flow of veins goes down from umbilicus
● Inspection for the presence of uneven distention or an obvious ● This should include assessment for signs of systemic diseases
mass. (Harrison’s 20th ed) ● (+) Lymphadenopathy especially supraclavicular
● (+) Spider angiomas, palmar erythema, dilated superficial veins lymphadenopathy (Virchow’s Node) suggests metastatic
around the umbilicus (caput medusae) and gynecomastia abdominal malignancy (Harrison’s 20th ed)
suggest chronic liver disease (Harrison’s 20th ed) ● Palpate for the ff: (Harrison’s 20th ed)
● Check for pallor, periorbital edema ○ Tenderness
● Care should be taken during cardiac evaluation to evaluate for ○ Abdominal masses
the following: (Harrison’s 20th ed) ○ Enlargement of liver or spleen
○ Elevation of JVP ● Rectal examination
○ Kussmaul’s sign – elevation of JVP during inspiration ● Pelvic examination
○ Pericardial knock - seen in heart failure or constrictive
pericarditis D. LABORATORY TEST
○ Murmur of tricuspid regurgitation ● Liver function test
● Assess for cardiomegaly, basal crackles, elevated central ● Tumor markers (used for monitoring, not diagnosis)
venous pressure ○ CA 19-9 (pancreatic cancer)
● Bowel sounds (Harrison’s 20th ed) ○ CA 125 (ovarian cancer)
○ Absence of bowel sounds, or presence of high-pitched ○ CEA (colon cancer)
localized bowel sounds points toward an ileus or intestinal ○ Alpha-fetoprotein (AFP) (liver cancer) – greater than 500
obstruction ng/mL
○ Umbilical venous hum – presence of portal hypertension ● Plain abdomen, barium enema, ultrasound, CT-scan/MRI/
○ Harsh bruit over the liver – rarely heard in patients with ● Diagnostic paracentesis
hepatocellular CA or alcoholic hepatitis ○ Serum ascites albumin gradient (SAAG)
● Note signs of decreased hepatic function and portal ■ Transudative (>1.1 g/dL) – portal hypertension, CHF
hypertension ● When ascitic albumin is low
● Percussion: (Bates 11th ed) ● Serum albumin > Ascitic albumin
○ Protuberant abdomen that is tympanitic throughout suggests ■ Exudative (<1.1 g/dL) – TB, CA, peritonitis, pancreatitis,
intestinal obstruction nephrotic syndrome
○ Dull - solid mass or ascitic fluid (minimums of 1500mL) ● Serum albumin < Ascitic albumin
● Palpation of liver edge (2020A) ● Serum amylase and lipase levels (Harrison’s 20th ed)
○ Reveals hepatomegaly, maybe due to chronic passive ○ Acute pancreatitis
congestion ● Urinary protein quantitation (Harrison’s 20th ed)
● Fluid wave (Bates 11th ed) ○ Indicated when nephrotic syndrome, which may cause
ascites, is suspected.
● Hepatic venous pressure gradient (Harrison’s 20th ed)
○ Cannulation of the hepatic vein to confirm that ascites is
caused by Cirrhosis.
● Liver biopsy may be necessary to confirm cirrhosis(Harrison’s 20th ed.)
E. ENDOSCOPIC PROCEDURES (2021B)
● Gastroscopy (lens forward viewing) & Duodenoscopy (lens
side viewing)
○ Stomach or duodenum
● Colonoscopy
○ Ileum to colon
● Laparoscopy with biopsy
○ Bile duct or pancreatic duct
● Endoscopic Retrograde Cholangio-pancreatography
(ERCP)
○ Remove stones
Figure 15. Test for ascites ● Percutaneous Transhepatic Cholangiography
● Shifting dullness (Bates 11th ed) ○ Biliary obstruction if ERCP cannot be done/failed
● Double-balloon Enteroscopy
● Video-capsule Endoscopy
○ Lesions in the mucosa seen by swallowing a capsule-sized
camera that takes images while going down the GI tract

NEED-TO-KNOW
● Temporal relationship of abdominal enlargement with pedal
edema
○ CHF: if pedal edema comes first then abdominal
enlargement
○ Cirrhosis: if abdominal enlargement comes first before
pedal edema due to secondary hyperaldosteronism
Figure 16. Test for ascites

PHYSICAL DIAGNOSIS 12 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

d. Unconjugated hyperbilirubinemia
○ Malignant ascites if with abdominal enlargement without
5. Jaundice with a greenish hue seen in patients with
pedal edema
obstructive type of jaundice is due to which of the
● A protuberant abdomen with bulging flanks suggests possible
following substances?
ascites
a. Biliverdin
● Percussion:
b. Conjugated bilirubin
○ Protuberant abdomen that is tympanitic throughout
c. Delta bilirubin
suggests intestinal obstruction
d. Urobilinogen
○ Dull - solid mass or ascitic fluid (minimums of 1500mL)
6. Which of the following conditions is expected to have
● (+) Spider angiomas, palmar erythema, dilated superficial
abnormal findings on cholangiography with ERCP?
veins around the umbilicus (caput medusae) and
a. Chlorpromazine-induced cholestasis
gynecomastia suggest chronic liver disease
b. Dubin Johnson syndrome
● (+) lymphadenopathy especially supraclavicular
c. Rotor syndrome
lymphadenopathy (Virchow’s Node) suggests metastatic
d. Sclerosing cholangitis
abdominal malignancy
7. Which of the following clinical manifestations will
● Tumor markers
distinguish intrahepatic cholestasis from decreased
○ CA 19-9 (pancreatic cancer)
hepatic excretion of bilirubin?
○ CA 125 (ovarian cancer)
a. Alcoholic stools
○ CEA (colon cancer)
b. Right upper quadrant pain
○ Alpha-fetoprotein (AFP) (liver cancer) – greater than 500
c. Pruritus
ng/mL
d. True-colored urine
8. 21/F, post-cholecystectomy developed fever, myalgia, and
CONCEPT CHECK
abdominal pains 5 days prior to consult. Tea-colored urine
1. T or F. Tumor markers are used for diagnosis.
and defervescence occurred 2 days prior, followed by
2. T or F. Kussmaul’s is seen during expiration
jaundice one day prior to consultation. What is the primary
3. T or F. IIn ascites, dullness shifts to the more dependent side,
impression?
whereas tympany shifts to the top.
a. Acute viral hepatitis
4. T or F. Weight gain with an increase in abdominal fat can
b. Amebic liver abscess
result in an increase in abdominal girth which may be
c. Ascending cholangitis
perceived as abdominal swelling
d. Typhoid hepatitis
___________________________________________________
9. Which of the following conditions may cause extraductal
ANSWERS
biliary compression resulting in obstructive type of
1. F
2. F jaundice?
3. F a. Cholangiocarcinoma
4. T
b. Clonorchis sinensis
REFERENCES c. Ascariasis
d. Pancreatic head cancer
Kasper, D. L., & Harrison, T.R. (2018). Harrison’s Principles of Internal
Medicine. New York: McGraw-Hill, Medical Pub. DIvision. 10. What is the most likely diagnosis in a 40/M patient with
Cabahug, O. (2020). Approach to the patient with jaundice [lecture intermittent pruritus, excoriations and jaundice on
powerpoint]. physical examination but normal cholangiography on
2020 A and 2021B lecture transcriptions ERCP?
REVIEW QUESTIONS a. Benign recurrent cholestasis
b. Biliary ascariasis
2020 Feedback (same lecturer)
c. Biliary tuberculosis
1. Which of the following is true of delta biliverdin? d. Choledocholithiasis
a. covalently bound to albumin ..........................................................................................................
b. Rendered hydrophobic by 4 water molecules Answers: (1) a, (2) b, (3) a, (4) d, (5) a, (6) d, (7) c, (8) a, (9) d, (10) a
c. Deconjugated
d. Has 3 moieties of glucuronide 2020 Quiz
2. What is the rate limiting step in bilirubin metabolism that is 11. What is the rate-limiting step in bilirubin metabolism and
affected first in diffuse inflammatory conditions of the is the first to be affected in acute viral hepatitis?
liver? a. Hepatic Conjugation
a. Conjugation b. Hepatic Excretion
b. Excretion c. Hepatic Uptake
c. Uptake d. Serum Transport
d. Transport 12. Which of the following statements is true?
3. What feature of unconjugated bilirubin differentiates it from a. Unconjugated bilirubin is nonpolar
conjugated bilirubin? b. Glucuronide attaches to unconjugated bilirubin in a
a. Not excreted in the urine reversible, non-covalent bond
b. Has a direct reaction to the Van der Berghi test c. Urine from patients with viral hepatitis and cirrhosis is not
c. Polar and readily dissolves in the serum usually tea-colored
d. Readily oxidized back to biliverdin d. Increase in bilirubin excretion, and hepatocyte swelling
4. A patient with a total bilirubin level of 50 umol/L and a causes cholestatic jaundice in patients with hepatitis A.
conjugated bilirubin level of 8 umol/L has which of the 13. Which of the following is not a characteristic of
following? unconjugated bilirubin?
a. Conjugated hyperbilirubinemia a. No renal excretion
b. Indeterminate hyperbilirubinemia b. Direct van den bergh test
c. Normal bilirubin levels c. Cannot be re-oxidized to biliverdin

PHYSICAL DIAGNOSIS 13 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

d. Causes yellow jaundice d. Visualization of the gallbladder on oral cholecystography

For 14-17 6. Which of the following diagnostic tests will distinguish
A: Unconjugated Hyperbilirubinemia intrahepatic cholestasis from extrahepatic biliary
B: Conjugated Hyperbilirubinemia obstruction?
14. Overproduction a. Duodenoscopy
15. Decreased Excretion b. Serum bilirubin
16. Decreased Hepatic Uptake c. Serum transaminases
17. Liver Cirrhosis d. Ultrasound
18. Which of the following does not cause abdominal 7. What is the MOST LIKELY diagnosis in a patient who had
enlargement? cholecystectomy 2 years ago, presenting with fever and
a. Fat abdominal pain 5 days prior to consultation followed by
b. Fever tea-colored urine and disappearance of the fever 2 days
c. Flatus prior and jaundice one day prior to consultation?
d. Fetus a. Acute viral hepatitis
19. Which of the tumor is matched with the correct cancer? b. Amoebic liver abscess
a. CA 125-Ovarian Cancer c. Ascending cholangitis
b. AFP- Pancreatic Cancer d. Typhoid hepatitis
c. CA 19-9- Colon Cancer 8. What is the MOST LIKELY diagnosis in a 20M with
d. CEA - Liver Cancer intermittent jaundice after prolonged fasting but NOT
20. Which of the following statements is correct? ASSOCIATED with pruritus or tea-colored urine?
a. Spur cell anemia is a type of familial hemolytic disorder a. Crigler-Najar syndrome type I
b. Intravascular hemolysis can cause hematuria b. Gilbert’s syndrome
c. Spherocytosis causes hematuria c. Rotor syndrome
d. Paroxysmal nocturnal hemoglobinuria causes extravascular d. Sickle cell anemia
hemolysis 9. The Sister Mary Joseph nodule that is indicative of an
......................................................................................................... intra-abdominal malignancy is detected in which of the
Answers: (11) b, (12) a, (13) b, (14) a, (15) b, (16) a, (17) b, (18) b, (19) a, (20) b
following:
2021 Feedback (same lecturer) a. Left supraclavicular area
b. Periumbilical area
1. What is the rate-limiting step in bilirubin metabolism and c. Right inguinal area
is the first to be affected in acute viral hepatitis? d. Right upper quadrant of the abdomen
a. Hepatic Conjugation 10. Which of the following laboratory tests will give an
b. Hepatic Excretion indication of the hepatic functional reserve capacity in
c. Hepatic Uptake patients with cirrhosis?
d. Serum Transport a. Alanine aminotransferase
1. Which of the following properties will distinguish b. Albumin
unconjugated from conjugated bilirubin? c. Alkaline phosphatase
a. Excreted in the urine through glomerular secretion d. Globulin
b. Only calculated and has an indirect reaction to the Van den 11.Which of the following is a sign of decreased hepatic
Bergh test function?
c. Polar and readily dissolved in the serum a. Ascites
d. Polar and readily dissolved in the serum b. Caput medusae
2. A patient with a total bilirubin level of 100 umol/L and an c. Palmar erythema
unconjugated bilirubin level of 40 umol/L has which of d. Splenomegaly
the following? 12. Which of the following laboratory tests is correctable with
a. Conjugated hyperbilirubinemia the administration of Vitamin K in patients with biliary
b. Indeterminate hyperbilirubinemia obstruction?
c. Normal bilirubin levels a. Bleeding time
d. Unconjugated hyperbilirubinemia b. Prothrombin time
3. Which of the following deficiencies will lead to c. Serum albumin
overproduction of bilirubin due to ineffective d. Serum bilirubin
erythropoiesis? 13. Which of the following conditions is associated with
a. Copper moderate to extreme elevations in the serum alkaline
b. Folate phosphatase?
c. G6PD a. Biliary ascariasis
d. UDP glucuronosyltransferase b. Crigler Najjar syndrome type II
4. Which of the following conditions is expected to have c. Hepatocellular carcinoma
abnormal findings on cholangiography with ERCP? d. Septic hepatitis
a. Chlorpromazine-induced cholestasis 14. Which of the following forms of biliary imaging is
b. Dubin Johnson syndrome non-invasive?
c. Progressive familial intrahepatic cholestasis a. Endoscopic retrograde cholangio-pancreatography
d. Sclerosing cholangitis b. Endoscopic ultrasonography
5. Which of the following features will differentiate the c. Magnetic resonance cholangio-pancreatography
Rotor syndrome from the Dubin Johnson syndrome? d. Percutaneous trans-hepatic cholangiography
a. Higher level of serum transaminases 15. Which of the following procedures is capable of removing
b. Lower level of serum bilirubin the stones in the common bile duct?
c. Presence of pigment in the hepatocytes a. Endoscopic retrograde cholangio-pancreatography

PHYSICAL DIAGNOSIS 14 of 17
 5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

b. Endoscopic ultrasonography
c. Magnetic resonance cholangio-pancreatography
d. Percutaneous trans-hepatic cholangiography
16. Which of the following tumor markers is associated with
hepato-cellular carcinoma?
a. Alpha fetoprotein
b. CA 125
c. CA 19-9
d. Carcino-embryogenic antigen
17. Which of the following will have a serum ascites albumin
gradient (SAAG) of more than 1.1?
a. Acute pancreatitis
b. Bacterial peritonitis
c. Cirrhotic ascites
d. Peritoneal carcinomatosis
18. Which of the following entails the use of an endoscope?
a. Double balloon enteroscopy
b. Laparoscopy
c. Percutaneous trans-hepatic cholangiography
d. Video capsule endoscopy
Answers: (1) b, (2) b, (3) a , (4) b , (5) d, (6) d, (7) d , (8) b, (9) b , (10) b , (11) c, (12)
b, (13) a , (14) c , (15) a , (16) a , (17) c , (18) a ,

PHYSICAL DIAGNOSIS 15 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

SUMMARY
NEED-TO-KNOW CONCEPTS
PRESENTATION OF JAUNDICE ○ If B1 is 90 μmol/L and B2 is 10 μmol/L, you have a case
Causes of jaundice due to accumulation of bilirubin of Unconjugated Hyperbilirubinemia
● Excess production ○ If B2 is 40 μmol/L and B1 is 20 μmol/L, you have a case
● Decrease in metabolism (3 Steps in Metabolism of of Conjugated Hyperbilirubinemia since 40+20 is 60
bilirubin) and 40 is more than 50% of 60
○ Uptake: liver ○ If B1 is 70 μmol/L and B2 is 30 μmol/L, it is
○ Conjugation: liver indeterminate because 70 μmol/L is not >80% B1 and 30
○ Excretion: By hepatocytes into biliary canaliculi μmol/L is not > 50% B2
● Serum bilirubin normally < 1 mg/dL (< 17 μmol/L) ○ If B1 is 7 μmol/L and B2 is 3 μmol/L, patient is normal
○ Detected clinically when serum bilirubin because when it is less than 50 μmol/L, they do not have
exceeds 3 mg/dL (51 μmol/L) (3 x 17 = 51) hyperbilirubinemia
● Easily detectable in the sclerae CLASSIFICATIONS
● Shake test: distinguishes concentrated urine and Table 2. Classification of Jaundice with respectd to Bilirubin(2021B) 📍
tea-colored urine Classification Type of Hyperbilirubinemia
○ Concentrated urine: bubbles formed from
shaking the container are white because of Overproduction Unconjugated Hyperbilirubinemia
urochromes (pigments which gives urine its Decreased hepatic uptake Unconjugated Hyperbilirubinemia
usual yellowish color) are water-soluble and are
not incorporated in the bubbles Decreased hepatic Unconjugated Hyperbilirubinemia
conjugation
○ Tea-colored urine: bubbles formed take a
brownish yellowish or orange hue because Decreased excretion Conjugated Hyperbilirubinemia
of adherence of bilirubin (which has a polar and
a nonpolar end thus incorporated in bubbles) to Overproduction of Bilirubin
the bubbles ● Hemolytic disorders
○ Familial Hemolytic disorders:
BILIRUBIN PRODUCTION ■ Spherocytosis
Bilirubin Synthesis ■ Sickle Cell Anemia
● Heme is converted to biliverdin (green pigment) by Heme ■ Thalassemia
Oxygenase ■ RBC enzyme deficiency
● Biliverdin is reduced to unconjugated bilirubin by ● G6PD deficiency
Biliverdin Reductase ● Pyruvate Kinase deficiency
● In the hepatocytes, unconjugated bilirubin is conjugated ○ Acquired Hemolytic disorders:
through UDP-Glucoronosyl Transferase making it polar ■ Microangiopathic Hemolytic Anemia
● Inside the intestinal lumen, the urobilinogen can be acted ● Eg. Hemolytic Uremic Syndrome
upon by bacteria and oxidized into urobilin (orange ■ Paroxysmal Nocturnal Hemoglobinuria
compound) ■ Spur Cell Anemia
● Significance of Delta Bilirubin ■ Immune Hemolysis
○ When you have elevated bilirubin in the serum ○ The only 2 common entities that lead to intravascular
due to obstruction of the bile duct and then you hemolysis are PNH and Plasmodium falciparum
performed a procedure to relieve the malaria
obstruction, one of the first indications that the ○ Extravascular hemolysis causes a deeper jaundice than
obstruction was relieved is the change in the intravascular hemolysis
color of urine into normal within a few hours. ○ Intravascular hemolysis causes hemoglobinuria
Hepatic Metabolism ● Ineffective Erythropoiesis
● Excretion is the most sensitive and rate limiting step ○ Cobalamin (Vitamin B12) deficiency
● Physical properties of Unconjugated and conjugated ■ Megaloblastic anemia
bilirubin (see table 1) ○ Folate deficiency
● Unconjugated bilirubin (B1) is non-polar → lipophilic → ○ Severe iron deficiency
not water soluble, hence, no renal excretion → NEVER Decreased Hepatic Uptake of Bilirubin
appear in the urine(2021B) ○ Drugs
● Conjugated bilirubin (B2) is polar (due to the ■ Rifampicin
attachment of 2 glucuronide moieties) → lipophobic → ■ In TB patients who developed jaundice due to 4-drug
water soluble, hence, with renal excretion regimen:
● In order to calculate for unconjugated bilirubin:
● Ethambutol does not cause liver dysfunction
○ B1 = Total Serum Bilirubin - B2
● Pyrazinamide is stopped
CONSIDERATIONS IN JAUNDICE ● Rifampicin is still given at full dose
● Unconjugated Hyperbilirubinemia ● Isoniazid is reintroduced starting with a low dose
○ > 80% B1 of the total bilirubin until the highest dose that does not cause jaundice
● Conjugated Hyperbilirubinemia is attained
○ > 50% B2 of the total bilirubin Decreased Hepatic Conjugation of Bilirubin
● Indeterminate ● Causes Unconjugated Hyperbilirubinemia
○ Doesn’t fall into either categories ● Crigler-Najjar type I
○ Bilirubin fractionation is not going to help us make a ● Crigler-Najjar type II
diagnosis ● Gilbert Syndrome
● Examples: Decreased Excretion of Bilirubin

PHYSICAL DIAGNOSIS 16 of 17
5.01 Approach to Patients with Jaundice, Abdominal Swelling, and Ascites ver. 01

● Causes Conjugated Hyperbilirubinemia ○ CHF: if pedal edema comes first then abdominal
● Decreased Hepatic Excretion enlargement
○ Familial ○ Cirrhosis: if abdominal enlargement comes first before pedal
■ Dubin Johnson Syndrome edema due to secondary hyperaldosteronism
■ Rotor Syndrome ○ Malignant ascites if with abdominal enlargement without
■ Benign Recurrent Cholestasis pedal edema
■ Progressive Familial Intrahepatic Cholestasis ● A protuberant abdomen with bulging flanks suggests possible
○ Acquired ascites
■ Hepatitis ● Percussion:
■ Cirrhosis ○ Protuberant abdomen that is tympanitic throughout suggests
■ Drug-induced intestinal obstruction
● Androgens ○ Dull - solid mass or ascitic fluid (minimums of 1500mL)
● Oral Contraceptives ● (+) Spider angiomas, palmar erythema, dilated superficial veins
● Chlorpromazine around the umbilicus (caput medusae) and gynecomastia
● Erythromycin estolate suggest chronic liver disease
● Pancreatic Head Cancer is the most common cause of ● (+) lymphadenopathy especially supraclavicular
extraductal compression that is due to malignancy. lymphadenopathy (Virchow’s Node) suggests metastatic
● Common bile duct obstruction is common among younger abdominal malignancy
individuals. ● Tumor markers
● Cholangiocarcinoma is the most common cause of ○ CA 19-9 (pancreatic cancer)
intraductal compression seen among elderly. ○ CA 125 (ovarian cancer)
APPROACH TO THE PATIENT WITH ABDOMINAL ○ CEA (colon cancer)
ENLARGEMENT ○ Alpha-fetoprotein (AFP) (liver cancer) – greater than 500
Evaluation of Abdominal Enlargement ng/mL
● 6 F’s of Abdominal swelling: fat, fetus, flatus, fluid, feces and
fetal growth (often a neoplasm)
● Temporal relationship of abdominal enlargement with pedal
edema
CONCEPT CHECKPOINT
BILIRUBIN PRODUCTION 4. What 2 diseases cause intravascular hemolysis?
1. What are the 3 steps in metabolism of bilirubin? ○ PNH and Plasmodium falciparum malaria
○ Uptake, conjugation, and excretion 5. Which drug for tuberculosis causes idiosyncratic liver
2. What test distinguishes concentrated urine and tea-colored dysfunction?
urine? ○ Rifampicin
○ Shake test 6. Ultrasonography is used for diagnosing what familial syndrome
3. What reduces biliverdin to unconjugated bilirubin? that causes decreased hepatic excretion?
○ Biliverdin reductase ○ Dubin Johnson Syndrome
4. T or F. Heme oxygenase converts heme to bilirubin 7. T/F. Alcohol induced Gilbert syndrome is because of sudden
○ F. Heme oxygenase converts heme to biliverdin onset of alcohol hepatitis.
5. T or F. Bilirubin may also come from hepatic cytochromes and ○ False
muscle myoglobin. 8. What drug can induce UDPGT production?
○ T. Hepatic cytochromes, muscle myoglobin, and other ○ Phenobarbital
heme-containing enzymes are the other sources of bilirubin 9. Which disease which causes decreased hepatic conjugation of
6. What is the most sensitive and rate-limiting step of bilirubin bilirubin causes kernicterus?
metabolism? ○ Crigler-Najjar type I
○ Excretion 10. Ultrasonography is used for diagnosing what familial syndrome
7. T or F. Conjugated bilirubin is non-polar and lipophobic. that causes decreased hepatic excretion?
○ F. Conjugated bilirubin is polar and lipophobic. ○ Dubin Johnson Syndrome
CONSIDERATIONS IN JAUNDICE 11. T/F. Alcohol induced Gilbert syndrome is because of sudden
1. What type of hyperbilirubinemia should have >80% of the total onset of alcohol hepatitis.
bilirubin? ○ False
○ Unconjugated Hyperbilirubinemia EVALUATION OF ABDOMINAL ENLARGEMENT
2. If B1 is 40 μmol/L and B2 is 60 μmol/L, what kind of 1. T or F. Tumor markers are used for diagnosis.
hyperbilirubinemia does it fall under? ○ F
○ Conjugated Hyperbilirubinemia because B1 is not >80% and 2. T or F. Kussmaul’s is seen during expiration
B2 is >50% of the total bilirubin ○ F
CLASSIFICATIONS 3. T or F. In ascites, dullness shifts to the more dependent side,
1. What classification of jaundice causes conjugated whereas tympany shifts to the top.
hyperbilirubinemia? ○ F
○ Decreased Excretion 4. T or F. Weight gain with an increase in abdominal fat can result
2. Give two examples of familial hemolytic disorders that lead to in an increase in abdominal girth which may be perceived as
the overproduction of bilirubin. abdominal swelling
○ Spherocytosis, Sickle Cell Anemia, Thalassemia, RBC ○ F
enzyme deficiency
3. What type of hemolysis causes hemoglobinuria?
○ Intravascular hemolysis

PHYSICAL DIAGNOSIS 17 of 17