propadeutics of hbs

1. PROPAEDEUTICS OF
HEPATOBILIARY SYSTEM
Harutyun S. Hovhannisyan, MD

2. Lecture plan
• Anatomy & topographic landmarks.
• History. Common signs & symptoms.
• Physical examination:
➢ Evaluation of ascites.
➢ Liver and gallbladder.
➢ Spleen.
• Paraclinical methods of HBS examination.
• Hyperbilirubinaemia & jaundice.

3. ANATOMY &
TOPOGRAPHIC LANDMARKS

5. The abdomen is generally divided into four
quadrants by two artificial lines that
intersect at the umbilicus
Other systems exist to further subdivide
these four quadrants into nine
regions/sections
RUQ LUQ
LLQ
RLQ
Epigastric
Right
Hypochondrium
Right
flank
Left
flank
Umbilical
Right
Iliac
Left
Iliac
Hypogastric
/ suprapubic
Left
Hypochondrium
Abdomen Topography

6. The liver and biliary system

9. Anatomy of Portal System
The portal vein
supplies 70% of the
blood flow to the
liver, but only 40% of
the liver oxygen
supply. The remainder
of the blood comes
from the hepatic
artery, and blood from
both of these vessels
mixes in the sinusoids.

10. Four ramus communicans between
portal and systemic circulations
esophageal and gastric veins
inferior rectal-anal veins
anterior abdominal wall veins
retroperitoneal venous plexus

13. Citation: Chapter 10 Pathology of the Liver, Gallbladder, and Extrahepatic Biliary Tract, Reisner HM. Pathology: A Modern Case Study; 2015. Available at:
https://accessmedicine.mhmedical.com/content.aspx?bookid=1569&sectionid=95970032 Accessed: March 20, 2023
Copyright © 2023 McGraw-Hill Education. All rights reserved
Anatomy of the hepatic lobule. (A) Depiction of multiple adjacent hepatic lobules. (B) Depiction of a portion of a hepatic lobule. (C) Photomicrograph of a
portal tract. Source: Figure 26.19 in McKinley & O'Loughlin's Human Anatomy, 2nd ed.)

16. What do we know about Portal Hypertension?

17. • The normal pressure of portal vein:
5-10mmHg (13~24 cmH2O)

18. Portal hypertension
• Portal hypertension is defined as a pressure > 12
mmHg.
• This increased pressure results from a functional
obstruction to blood flow from any point in the portal
system's origin (in the splanchnic bed) through the
hepatic veins (exit into the systemic circulation) or
from an increase in blood flow in the system.
P = F x R

21. HISTORY
COMMON SYMPTOMS &
SYNDROMES

22. Clinical features

24. Pathophysiology & Signs and Symptoms
due to PH
✓Congestive splenomegaly and hypersplenism
• Splenomegaly is defined as the spleen size >12cm in length.
• Hypersplenism is a type of disorder which causes the spleen to
rapidly and prematurely destroy blood cells
✓ Ramus communicans dilatation
✓ Ascites

25. Signs and Symptoms due to PH
• ramus communicans dilatation:
– esophageal and gastric veins: varices rupture and
gastrointestinal hemorrhage
– inferior rectal-anal veins: hemorrhoid & bleeding
– anterior abdominal wall veins: paraumbilical
varices (caput medusae)
– retroperitoneal veins plexus: dilatation &
congestion

38. JAUNDICE
• Yellow discoloration of the skin, sclerae and mucous
membranes (BIL> 50 μmol/L or >2.0-2.5 mg/dL).
• Hyperbilirubinaemia:
✓ Prehepatic (haemolysis, Gillbert’s syndrome)
✓ Intrahepatic (viral hepatitis, drugs, cirrhosis)
✓ Posthepatic (drugs, gallstones, cancer)

39. GASTROINTESTINAL EXAMINATION
General examination
– General inspection
– Hands and arms
– Face, eyes and mouth
– Neck
Abdominal examination
⚫ Inspection
⚫ Palpation
⚫ Percussion
⚫ Auscultation

40. General principles of exam
• Good light
• Relaxed patient in supine position
• Full exposure of abdomen
• Empty bladder
• Arms across chest, not above head.
• Ask patient where pain is, and examine last.
• If the patient is ticklish or frightened, initially use the patients hand
under yours as you palpate. When patient calms then use your
hands to palpate.
• Watch the patient’s face for discomfort

41. Equipment
• Examination gown and drape
• Examination gloves
• Examination light
• Stethoscope
• Skin marker
• Metric ruler
• Tissues
• Tape measure

42. • Nutritional state (wasting)
• Pallor
• Jaundice (liver disease)
• Pigmentation (hemochromatosis)
• Mental state (encephalopathy)
GENERAL INSPECTION

43. • Nails
– Clubbing
– Leuconychia
• Palmar erythema
• Dupuytren’s contractures
• Hepatic flap (asterixis)
HANDS

44. Clubbing

45. Clubbing

46. Clubbing - Schamroth’s sign
(loss of the subungual angle)

47. HANDS
Palmar erythema Dupuytren’s contractures

48. • Spider naevi (telangiectatic lesions)
• Bruising
• Wasting
• Scratch marks (chronic cholestasis)
ARMS

49. • Sclera: jaundice
• Cornea: Kaiser-Fleischer’s rings (Wilson’s disease)
• Xanthelasma (primary biliary cirrhosis)
• Parotid enlargement (alcohol)
FACE, EYES

50. Parotid enlargement
Xanthelasma

51. • Gynaecomastia
• Loss of hair
NECK, CHEST

52. ABDOMINAL EXAMINATION
Inspcetion

53. ABDOMINAL EXAMINATION
INSPECTION
 Shape and movements
 Scars
 Distension
⚫ Localised: mass, organomegaly
⚫ Generalized: 5 F’s
 Prominent veins (caput medusae)
 Striae
 Bruises
 Pigmentation
 Visible peristalsis

54. Ascitis & Caput Medusae

55. Tête de Méduse, by Peter Paul Rubens (1618)

56. Mechanisms of ascitis
1. disordered albumin synthesis and decreased plasma
colloid osmotic pressure caused by hepatocellular
function damage
2. increased capillary filter pressure due to increased
portal hypertension
3. lymph liquid leakage into abdominal cavity from
surface of the liver because of lymph back-flow
obstruction
4. salt and water retention by aldosterone and antidiuretic
hormones deactivation disturbance

57. ABDOMINAL EXAMINATION
Percussion

58. Percussion
• Assess density of
underlying tissue

59. Percussion notes
Percussion Note Description
Resonant Long, loud, low pitched, hollow
Dullness Medium in intensity and pitch,
moderate length
Stony dull Thudlike
Hyper-resonant Very loud, low pitched

60. ABDOMINAL EXAMINATION
PERCUSSION
 Dull sounds: solid or fluid-filled structures
 Resonant sounds: structures containing air or gas

61. Percussion pattern for ascites

62. Percussion pattern for ascites

63. Ascites

64. Ascites

65. ABDOMINAL EXAMINATION
Palpation

66. ABDOMINAL EXAMINATION
PALPATION
1. Ensure that your hands are warm
2. Stand on the patient’s right side
3. Help to position the patient
4. Ask whether the patient feels any pain
before you start
5. Begin with superficial examination
6. Move in a systematic manner through the
abdominal quadrants
7. Repeat palpation deeply.

67. Superficial (light) palpation of abdomen

68. Deep palpation of abdomen

69. ASCITIS
FLUID THRILL TEST
 Place the palm of your left
hand against the left side of the
abdomen
 Flick a finger against the right
side of the abdomen
 Ask the patient to put the edge
of a hand on the midline of
the abdomen
 If a ripple is felt upon flicking
we call it a fluid thrill = ascites

70.  Pain in RUQ
 Inflammation of gallbladder
(cholecystitis)
 Courvoisier's law
ABDOMINAL EXAMINATION
MURPHY’S SIGN

71. Liver palpation and percussion

72. Liver palpation methods
1. Classical
2. Dipping
3. Hooking

73. ABDOMINAL EXAMINATION
PALPATION OF THE LIVER
1. Start palpating in the right iliac fossa
2. Ask the patient to take a deep breath in
3. Move your hand progressively further up the abdomen
4. Try to feel the liver edge

74. Palpation of the liver

78. Liver palpation

85. ABDOMINAL EXAMINATION
PALPATION OF THE SPLEEN
1. Roll the patient towards you
2. Palpate with your left hand while using your right hand to
press forward on the patient’s lower ribs from behind
3. Feel along the costal margin

86. Palpation of the spleen

87. PARACLINICAL METHODS OF
EXAMINATION

88. Laboratory Tests
• CBC : WBC↓, Plt↓
• Elevated serum enzyme tests usually indicate liver injury earlier than do
other indicators of liver function.
• The key enzymes are ALT and AST, which are present in hepatocytes.
• In most cases of liver damage, there are parallel increases in ALT and
AST. The most dramatic rise is seen in cases of acute hepatocellular
injury: viral hepatitis, hypoxic or ischemic injury, and acute toxic injury.
• The liver’s synthetic capacity is reflected in measures of serum protein
levels and prothrombin time (i.e., synthesis of coagulation factors):
albumin↓, A/G ratio reversing, prothrombin time↑
• Serum bilirubin, γ-glutamyltransferase (GGT), and alkaline phosphatase
(ALP) measure hepatic excretory function.
• Markers of viral hepatitis (e.g. HBV, HCV, HDV)

89. Images
✓Ultrasound
✓CT/MRI
✓Esophageal endoscopy
✓Esophageal barium swallow
✓Selective angiography
✓Liver biopsy

90. Images
Ultrasound and Doppler: cirrhosis, splenomegaly, ascites,
thrombosis and occlusion of the portal, superior mesenteric
and splenic vein, enlargement of portal vein>13mm and of
splenic vein>10mm

91. Images
CT scan

92. Splenomegaly

93. Splenomegaly

94. Images
Esophageal endoscopy:
white, pink, red, cherry red varices

95. Images
Esophageal barium swallow
multiple irregular filling
defects as “string of beads”
or “earthworm”

96. Normal Portal hypertension
Angiography
Images

97. Bile production
⚫ The secretion of bile, approximately 600 to 1200 mL daily, is one of
the many functions of the liver.
⚫ Bile functions in the digestion and absorption of fats and fat-soluble
vitamins from the intestine, and it serves as a vehicle for excretion of
bilirubin, excess cholesterol, and metabolic end-products that cannot
be eliminated in the urine.
⚫ Bile contains water, electrolytes, bile salts, bilirubin, cholesterol, and
certain products of organic metabolism.
⚫ Approximately 94% of bile salts that enter the intestine are
reabsorbed into the portal circulation by an active transport process
that takes place in the distal ileum. From the portal circulation, the
bile salts pass into the liver, where they are recycled. Normally, bile
salts travel this entire circuit approximately 18 times before being
expelled in the feces.
⚫ This system for recirculation of bile is called the enterohepatic
circulation.

98. Jaundice (icterus)
• Jaundice (i.e., icterus), which results from an abnormally high
accumulation of bilirubin in the blood, is a yellowish discoloration
to the skin and deep tissues.
• Jaundice becomes evident when the serum bilirubin levels rise
above 2.0 to 2.5 mg/dL.
• Bilirubin has a special affinity for elastic tissue. The sclera of the
eye, which contains considerable elastic fibers, usually is one of
the first structures in which jaundice can be detected.

99. Bilirubin elimination

100. Bilirubin elimination
⚫ Bilirubin is formed during the breakdown of senescent red blood
cells.
⚫ In the process of degradation, the heme portion of the hemoglobin
molecule is oxidized to form biliverdin, which is then converted to
free bilirubin.
⚫ Free bilirubin, which is insoluble in plasma, is transported in the
blood attached to plasma albumin. Even when it is bound to
albumin, this bilirubin is still called free bilirubin.
⚫ As it passes through the liver, free bilirubin is released from the
albumin carrier molecule and moved into the hepatocytes. Inside the
hepatocytes, free bilirubin is converted to conjugated bilirubin,
making it soluble in bile.
⚫ Conjugated bilirubin is secreted as a constituent of bile, and in this
form it passes through the bile ducts into the small intestine.

101. Bilirubin elimination
⚫ In the intestine, approximately one half of the bilirubin is converted
into a highly soluble substance called urobilinogen by the intestinal
flora.
⚫ Urobilinogen is either absorbed into the portal circulation or excreted
in the feces.
⚫ Most of the urobilinogen that is absorbed is returned to the liver to
be re-excreted into the bile.
⚫ A small amount of urobilinogen, approximately 5%, is absorbed into
the general circulation and then excreted by the kidneys.
⚫ Usually, only a small amount of bilirubin (0.1 to 1.2 mg/dL) is found
in the blood. Laboratory measurements of bilirubin usually measure
the free and the conjugated bilirubin as well as the total bilirubin.
These are reported as the direct (conjugated) bilirubin and the
indirect (unconjugated or free) bilirubin.

102. Causes of jaundice
• 4 major causes of jaundice are:
– Excessive destruction of RBCs
– Impaired uptake of bilirubin by hepatocytes
– Decreased conjugation of bilirubin
– Obstruction of bile flow in the canaliculi of the
hepatic lobules or in the intrahepatic or extrahepatic
bile ducts.
• From an anatomic standpoint, jaundice can be
categorized as:
– Prehepatic /flavin icterus/
– Intrahepatic /rubin icterus/
– Posthepatic /verdin icterus or melas icterus/

103. Causes
• Prehepatic (Excessive RBC destruction)
– Hemolytic blood transfusion reaction
– Hereditary disorders of the red blood cell
– Sickle cell anemia
– Thalassemia
– Spherocytosis
– Acquired hemolytic disorders
– Hemolytic disease of the newborn
– Autoimmune hemolytic anemias
UGT (Uridine diphosphate
glucuronosyltransferase) deficiencies
– Gilbert syndrome
– Crigler-Najjar syndromes (I and II)
• Intrahepatic
– Decreased bilirubin uptake by the
liver
– Decreased conjugation of
bilirubin
– Hepatocellular liver damage
– Hepatitis
– Cirrhosis
– Cancer of the liver
– Drug-induced cholestasis
• Posthepatic (Obstruction of bile
flow)
– Structural disorders of the bile
duct
– Cholelithiasis
– Congenital atresia of the
extrahepatic bile ducts
– Bile duct obstruction caused by
tumors

104. Manifestations
• Prehepatic jaundice is:
– Mild jaundice
– The unconjugated bilirubin is elevated
– The stools are of normal color
– There is no bilirubin in the urine
• Intrahepatic jaundice usually interferes with all phases of bilirubin
metabolism—uptake, conjugation, and excretion:
– Both conjugated and unconjugated bilirubin are elevated
– The urine often is dark because of the presence of bilirubin
• Posthepatic or obstructive jaundice, also called cholestatic jaundice, occurs
when bile flow is obstructed between the liver and the intestine:
– Conjugated bilirubin levels usually are elevated
– The stools are clay colored because of the lack of bilirubin in the bile
– The urine is dark
– The levels of serum alkaline phosphatase are markedly elevated
– The aminotransferase levels are slightly increased
– Blood levels of bile acids often are elevated in obstructive jaundice. As
the bile acids accumulate in the blood, pruritus develops.

105. Child-Pugh classification of liver function
Child-Pugh classification is a scoring system developed
for evaluating surgical risk in patients with cirrhosis.
Child’ grade 1 point 2 points 3 points
Serum bilirubin (umol/L) <34.2 34.2-51.3 >51.3
Albumin (g/l) >35 30-35 <30
Prothrombin (s' prolonged) 1-4 4-6 >6
Ascites absent slight moderate
Encephalopathy none
none or
minimal
coma

106. Questions?