The document provides details about the anatomy, physiology, and common infections and lesions of the liver. It describes the liver's location, blood supply, segmentation, bile ducts and veins. It discusses the liver's roles in metabolizing drugs, processing nutrients, and maintaining glucose levels. Common infections covered include pyogenic abscesses, amebic abscesses, hydatid disease, ascariasis, and schistosomiasis. Benign lesions discussed are congenital cysts.

1. ‫الرحیم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬

2. Anatomy & Physiology of
Liver

3. Anatomy of Liver
• Largest organ in the body.
• Weighing 1500gr.
• In RUQ of abomen
• Beneath diaphragm and protected by rib cage.
• Surrounded by fibrous sheath known as Glisson’ capsule.

4. Ligaments of Liver
• Round lig. :remnant of umbilical vein
• Falciform lig. : separates the Lt. lobe of liver to Lt. lateral & Lt. medial
segments. Anchors the liver to ant. Abdominal wall.
• Ligamentum venosum(Aranitus lig.): between caudate lobe & Lt. lateral
segment
• Triangular lig. : Rt. & Lt.
secures 2 sides of liver to diaphragm
• Coronary lig. :extending from triangular lig. anteriorly. The Rt. Coronary lig.
Annchors the liver to Rt. retroperitoneum.
• Hepatodoudenal lig.(porta hepatis) :contains CBD, portal vein and hepatic
artery.
• Gastrohepatic lig.

7. Gastrohepatic
ligament
Hepatodoudenal
ligament(porta hepatis)
Foramen of
Winslow (epiploic
foramen):
Rt. Side and deep
to porta hepatis

8. Segmental Anatomy of Liver
• Liver grossly is separated to Rt. lobe( accounts for 60-70% of liver mass) &
Lt. lobe ( with caudate lobe accounts for remainder) by Cantlie’s line which
is a virtual plane from gall bladder fossa to IVC. The Lt. lobe is separated by
falciform lig. to Lt. medial and Lt. lateral sections.
• Liver is devided into 8 segments numbered in clockwise manner.
• Caudate lobe: segment 1
• Lt. lateral segment: segments 2 & 3
• Lt. medial segment: segment 4 (also known as Quadrate lobe which is an outdated term)
• Quadrate lobe: segment
• Rt. Anterior lobe: segments 5 & 8
• Rt. Posterior lobe: segments 6 & 7

10. Blood Supply of Liver
• Liver has dual blood supply consisting:
1. Hepatic artery almost dlivers ¼ of blood supply, arises from common
hepatic artery of celiac trunk. Gall bladder is supplied by cystic artery, a
branch of Rt. Hepatic artery.
2. Portal vein almost delivers ¾ of blood suuply.
Anatomical Variants of Hepatic Artery:
1. The most common: accessory or replaced Rt. hepatic artery from superior mesenteric artery.
2. Accessory or replaced Lt. hepatic artery from Lt. gastric artery.
3. Replaced both Rt. & Lt. hepatc artery or common hepatic artery coming off superior
mesenteric artery.
• Rt. Hepatic artery passes deep and posterior to CBD in 88% of the time but in 12% of time it
crosses anterior to CBD.

12. Portal Vein
• Formed by confluence of splenic vein, superior & mesenteric veins and drains
splanchnic blood from stomach, … & majority of the colon to liver.
• Portal Vein Branches:
1. Lt. portal vein: branches from main portal vein outside the liver with a sharp
bend to the Lt. & consists transverse portion followed by a 90˚ turn at the base
of umbilical fissure to become umbilical portion before entering the liver. This
branch has dominant inflow to caudate lobe.
2. Rt. Portal vein: Its devision occurs close to or inside the liver.
3. Superior pancreaticodoudenal branch
4. Short branch to caudate process on Rt. Side.(This branch must be ligated
during anatomic Rt. hemihepatectomy.)
• 20-35% of people have aberrant portal venous anatomy:
1. Portal vein trifurcation
2. Aberrant branch from the Lt. portal vein supplying the Rt. Anterior segments.

13. Portal Vein
• Its Nl. pressure: 3-5mm Hg
• In the case of portal vein hypertension systemic circulation decompression
occurs through portocaval anastomoses most commonly via coronary
vein(Lt. gastric)

15. Hepatic Veins
• 3 hepatic veins pass obliquely through the liver to drain blood from liver to
IVC:
1. Rt. hepatic vein: drains segments 5,6,7 & 8.
2. Middle hepatic vein: drains segments 4,5 & 8.
3. Lt. hepatic vein: drains segments 2 & 3.
• 95% of the time Lt. & middle hepatic veins form a common trunk before
entering IVC.
• Venous drainage of caudate lobe directly enters IVC.
• There are few small, variable short hepatic veins that directly enter IVC
from undersurface of liver in addition to hepatic veins mentioned above.
• 15-20% of time a large inferior accessory Rt. hepatic vein runs in
hepatocaval ligament.( would be a cause of bleeding during Rt.
hepatectomy.)

17. Bile Ducts
• In general, the hepatic ducts follow the arterial branching pattern inside
the liver.
• Rt. hepatic duct:
1. Rt. anterior hepatic duct: enters liver above hilar plate.
2. Rt. posterior hepatic duct: dives behind the right portal vein and can be
found on the surface of the caudate process before entering the liver.
• Lt. hepatic duct: typically has a longer extrahepatic course before giving
off segmental branches behind the left portal vein at the base of the
umbilical fissure.
• Cystic duct: has a variable pattern of drainage into the common bile duct.
• would lead to potential injury or postoperative bile leakage during
cholecystectomy or hepatic resection.

19. Neural Innervation
• Parasympathetic innervation:
1. Anterior hepatic branch of Rt. vagus nerve.
2. Posterior hepatic branch of Lt. vagus neve.
• Sympathetic innervation:
1. Greater thoracic splanchnic nerve
2. Celiac ganglia
• the function of these nerves is poorly understood.
• The denervated liver after hepatic transplantation seems to function with normal
capacity.

21. Referred Pain From Liver
• A common source is the right phrenic nerve, which is stimulated by
tumors that stretch Glisson’s capsule or by diaphragmatic irritation.

22. Lymphatics
• Lymph is produced within the liver and drains via the perisinusoidal space of
Disse and periportal clefts of Mall to larger lymphatics that drain to the hilar
cystic duct lymph node as well as the common bile duct, hepatic artery,
retropancreatic, celiac lymph nodes and to the cardiophrenic lymph nodes(can
be pathologically identified on a staging CT or MRI scan)
• Hilar cholangiocarcinoma has a high incidence of lymph node metastases.

23. Physiology of Liver
Bilirubin Metabolism
Liver makes bilirubin water soluble my making conjugated with glucoronic
acid.
Conjugated Bilirubin:
1. The majority of it is excreted in intestine as waste(mucosa of intestine is
impermeable to conjugated bilirubin). Bacteria in intestine metabolizes
this product to unconjugated bilirubin and urobilinogen, then these
metabolites enter enterohepatic circulation.
2. A small amount of it dissolve in blood and excreted in urine.

24. Physiology of Liver
Formation of Bile
Bile is composed of water, electrolytes, bile salts, phospholipids &
cholesterol. Bile is produced by liver & stored in gall bladder(between meals)
and upon entry of food is released from gall bladder.
Bile Salts: Na & K salts of bile acids (derivative of cholesterol synthesized in
liver) conjugated to glycine and taurine. 1˚ bile salts enter intestine:
1. 90-95% are converted to 2˚ bile salts and reabsorbed in terminal ileum
(enterohepatic circulation)
2. 5-10% enter colon.
Roles of bile:
1. Digestion & absorption of lipids and lipid soluble vitamins.
2. Elimination of waste produtcs such as bilirubin and cholesterol and
metabolites of some of drugs.

25. Physiology of Liver
Drug Metabolism
Foreign molecules (xenobiotics) are eliminated from body by undergoing this
function of liver in smooth endoplasmic reticulum of hepatocytes. This
function has 2 main reactions:
1. Converting of lipophilic drugs to hydrophilic products (consists oxidation
performed by cytochrome P450 enzymes, reduction and hydrolysis)
2. Conjugation of the products of last reaction to glycine, glutathione &…

26. some drugs may be converted to active products by metabolism in the liver.
Normally, acetaminophen is conjugated by the liver to harmless water
soluble metabolites and eliminated in the urine. During an overdose, the
normal metabolic pathways are overwhelmed, and some of the drug is
converted to a reactive and toxic intermediate. Glutathione normally reacts
with this intermediate, leading to the production and subsequent excretion
of a harmless product. However, as glutathione stores are diminished, the
reactive intermediate cannot be detoxified and it combines with lipid
membranes of hepatocytes, which results in cellular necrosis. Thus,
treatment of acetaminophen overdoses consists of replenishing glutathione
stores by supplementing withsulfhydryl compounds such as acetylcysteine.

27. Physiology of Liver
Processing of absorbed nutrients
Playing role in maintaining glucose concentration in normal range
Matabolism aof aminoacids
Metabolism and storage of fat
Metabolism and storage of sugar
Producing albumin, proteins involved in immune processes ,factors of
coagulation

28. Infections of Liver

29. Pyogenic Liver Abscess
• More frequently found in Rt. lobe.
• Resulted from: diverticulitis, appendicitis, impaired biliary drainage, subacute bacterial
endocarditis, infected indwelling catheters, Crohn’s disease & ….
• Infecting agents: E.Coli (most commonly), Klebsiella, Proteus Vulgaris, S.Fecalis &
Bacteroides Fragilis
• Presentations: RUQ pain, Fever, Jaundice
• Lab data: Leukocytosis, ↑ ESR, ↑ALP
• Imaging: round or oval hypoechoic with well defined border by US, hypodense with
peripheral enhancement by CT (if containing air-fluid level indicates gas-producing
organisms)
• Treatment:
1. IV AB therapy (should cover G- & anaerobic bacteria) for at least 8 weeks
2. Surgical drainage if initial therapy fails.
most pyogenic abscesses are quite viscous & catheter drainage is ineffective.

30. Amebic Abscess
• The most common type of liver abscess.
• Caused by Entamoeba Hystolytica (endemic worldwide, most commonly in subtropical
climates) which may cause brain or lung abscess.
• Most commonly involves superior-anterior aspect of Rt. Lobe of liver
• Has necrotic central portion containing thick, pus-like material likened to chocolate sauce.
• Presentations: RUQ pain, Fever, hepatomegaly but jaundice in unusual.
• Lab data: Leukocytosis, ↑ALP, positive Ab test for E.Hystolytica
• Imaging: round hypoechoic with well defined border by US, hypodense with peripheral
enhancement by CT & somewhat ragged in appearance with peripheral zone of edema &
septations in central cavity.
• Treatment:
1. Metronidazole 750mg tid for 7-10 days
2. Aspiration is needed for Pt. with large abscess, no respond to medical therapy,
superinfection of abscess & for abscess in Lt. lobe (may rupture into pericardium)

31. Hydatid Disease
• Caused by tapeworm Echinococcus granulosus (most common in sheep raising area) or
Echinococcus multilocularis (occurs in northern hemisphere)
• Echinococcus granulosus also may form cysts in brain, lung, spleen & bone.
• Echinococcus multilocularis also may form multilocular cyst in lung in addition to liver.
• Most commonly involves inferior-anterior or inferior-posterior segments
• Presentations: dull RUQ pain, allergic or anaphylactic reaction in the case of rupture.
• Lab data: positive ELISA test for echinococcal Ags, eosinophilia, but ELISA test may be
negative if cyst does’nt leak or does’nt contain the parasite.
• Imaging: well defined hypodense with distinct wall by CT, calcification of pericyst, daughter
cysts occur in peripheral location within main cyst and are more hypodense than mother
cyst. If the entire cyst is calcified it means the cyst id dead.
• Treatment: Surgical based
1. Albendazole or Mebendazole, AB therapy depends on diffusion of AB through cyst
membrane (only if the cyst are small and the Pt. is’nt a suitable candidate for surgery)

32. Hydatid Disease
• Treatment: Surgical based
2. Removal of cysts by open or laparascopic surgery with instillation of scolocidal agents.
During surgical resection, caution must be exercised to avoid rupture of the cyst because
by release of protoscolices into the peritoneal cavity Peritoneal contamination can result in:
1. acute anaphylactic reaction
2. peritoneal implantation of scolices with daughter cyst formation.

33. Ascariasis
• Caused by roundworm Ascaris lumbricoides arrive in liver by retrograde locomotion in bile
ducts
• Causing partial bile duct obstruction, cholangitis due to partial obstruction, the worm may
serve as nidus for development of intrahepatic gall stone
• Presentations: biliary colic, acute cholecystitis, acute pancreatitis, hepatic abscess
• Imaging: linear filling defects by plain radiograph, US or ERCP.
• Treatment:
1. Albendazole or mebendazole or piperazine in combination with endoscopic resection of
worms.
2. Surgical intervebtion if worms can’t be removed by ERCP.

34. Schistosomiasis
• Cause hepatic fibrosis followed by perisinusoidal portal hypertension. Liver shrinks, but the
liver function is preserved.
• Causing partial bile duct obstruction, cholangitis due to partial obstruction, the worm may
serve as nidus for development of intrahepatic gall stone
• Lab data: ↑ALP, hypoalbuminemia as the result of frequent GI bleeding and malnutrition
• Treatment:
1. Praziquantel 40-75mg single dose
2. If refractory GI portal hypertensive bleeding: distal splenorenal shumt or gastric
devascularization.

35. Virla Hepatitis
• Hepatitis A: usually acute self-limited illness which rarely leads to fulminant hepatic failure.
treatment is usually supportive except for who develop fulminant hepatitis.
• Hepatitis B or C: lead to chronic liver disease, cirrhosis or HCC. Treatment of chronic hepatitis
B is viral suppression by pegilated INF (may cause flu-like symptoms, fatigue, bone marrow
suppression or autoimmunity) or tenofovir to prevent development of cirrhosis, liver failure
or HCC.
• acute hepatitis C develops 2-6 weeks after exposure to the virus. Usually the Pt. is
asymptomatic. The Pt. presents with jaundice, dark urine, RUQ pain and nausea. Diagnosis is
confirmed by PCR of HCV RNA (detectable within few days following exposure) or HCV Ab
(detectable 2-6 months after exposure). Treatment is started if the virus is’nt cleared within
12 weeks after diagnosis and is performed by pegilated INF monotherapy.
• to treat chronic hepatitis C:
• Genotype1: pegylated INF, ribavirin & telaprevir
• Genotypes 2, 3 & 4: pegylated INF & ribavirin
• Genotypes 2 & 3 are more responsible to treatment than genotypes 1 & 4.

36. Benign Liver Lesions

37. Congenital Cyst
• Most common benign lesion of liver.
• Commonly found incidentally, usually is asymptomatic.
• Higher prevalence in women.
• Simple cysts are result of excluded hyperplastic bile duct rests.
• Presentations: abdominal pain, epigastric fullness & early satiety only if large size.
• Imaging: thin-walled, homogenous, fluid-filled with few to no septation.
• Treatment:
1. Coservatively if asymptomatic.
2. If symptomatic, US or CT-guided percutaneous aspiration followed by sclerotherapy.
• Laparascopic or open surgery cyst fenestration if aspiration is’nt available or effective. The
excised cyst wall is sent for pathologic analysis to exclude the presence of carcinoma, and the
remaining cyst wall must be carefully inspected for evidence of neoplastic change. If such
change is present, complete resection is required, either by enucleation or formal hepatic
resection.

38. Polycystic Liver Disease
• Adult PCLD is an autosomal dominant & usually presents in the 3rd decade of life.
• Mutations in PKD1 or PKD2.
• Higher prevalence in women, increases with age advancing & increasing severity of renal
cystic disease and renal dysfunction.
• In most Pt.s liver synthetic function is preserved and liver decompensation occurs rarely. But
disease progression results in renal failure.
• May be complicated due to intracystic hemorrhage, infection or posttraumatic rupture.
• Presentations: Pt. with many or large cyst (>2cm) or with
𝑐𝑦𝑠𝑡 𝑣𝑜𝑙𝑢𝑚𝑒
𝑝𝑎𝑟𝑒𝑛𝑐ℎ𝑦𝑚𝑎 𝑣𝑜𝑙𝑢𝑚𝑒
>1 develops
abdominal pain, distension, shortness of breath or early satiety. Pt. with amall number or
small cyst (<2cm) remains asymptomatic.
• Lab data: ↑GGT
• Imaging: polycystic appearance of liver.

39. Polycystic Liver Disease
• Treatment: the principal aim is to ameliorate symptoms by decreasing liver volume.
1. Medical therapy: by somatostatin analogs (octreotide) or rapamycin inhibitors which has
antiproliferative effect (sirolimus).
2. If Pt. has one or few dominant cyst each measuring >5cm: cyst aspiration and
sclerotherapy by ethanol, minocycline or tetracycline which damages epithelium of cysts
which have the role fluid secretion.
3. If Pt. is symptomatic: cyst fenestration or surgical unroofing the cyst. But this procedures
may cause complications such as ascites, pleural effusion, hemorrhage or biliary leakage.
4. If the Pt. has massive hepatomegaly specially his liver has at least 1 spared segment with
predominantly normal liver parenchyma: hepatic resection. Comolications such as
adhesion band formation

40. Biliary Cystadenoma
• Most commonly occurs in Rt. lobe.
• Slow-growing, unusual, benign lesions.
• Usually are benign may undergo malignant transformation.
• Walls are thicker than simple cysts with soft tissue nodules and septations.
• Presentations: abdominal pain or mass or both.
• Treatment:
1. Surgical resectin.

41. Caroli’s Disease
• syndrome of congenital ductal plate malformations of the intrahepatic bile ducts and is
characterized by segmental cystic dilatation of the intrahepatic biliary radicals. It usually
occurs in the absence of cirrhosis.
• Associated with: biliary lithiasis, cholangitis, biliary abscess formation.
• Presentations:
1. Usually by the age of 30 and includes: fever, chills & abdominal pain.
2. Later in life with complications portal hypertension.
• Imaging: MRCP, ERCP, PTC. Imaging solidifies the diagnosis by confirming the communication
of intrahepatic cysts with biliary tree.
• Treatment:
1. Biliary drainage by PTC or ERCP as first line treatment.
2. Hepatic resection for: hepatic decompensation, unresponsive recurrent cholangitis or Pt.
with small cholangiocarcinoma.

42. Hepatic Cysts
• Primary: congenital cysts
• Secondary: from trauma (biloma or seroma), infection or neoplasms.
• Primary cyst are differntiated from secondary cysts in that primary cysts have well-defined
thin wall, are filled by homogenous, clear fluid & don’t have solid component.

43. Hemangioma
• Most common solid benign mass.
• Congenital vascular lesions that contain fibrous tissue & small blood vessels.
• Higher prevalence in women.
• Presentations: Usually asymptomatic, may be symptomaticas aa result of compression of
adjacent organs if:
1. being large size
2. Intermittent thrombosis which results in further expansion.
• Imaging: asymmetrical nodular peripheral enhancement which is isodense with large vessels
& centripetal enhancement fill-in over time by biphasic CT, hypointense in T1-weighted &
hyperintense in T2-weighted MRI.
caution should be exercised in ordering a liver Bx because of risk of bleeding from site of
Bx.
• Treatment: surgical resection if the Pt. is symptomatic.

44. Adenoma
• Most commonly seen in premenopausal women older than 30 Y/O.
• Use of estrogens (OCP) is a clear risk factor.
• Encapsulated & soft in gross examination.
• Lack bile ducts & Kupffer cells, have no true lobule, have vacuolated hepatocytes due to
glycogen deposition.
• Significant risk of spontaneous rupture, intraperitoneal bleeding & also risk of malignant
transformation.
• Presentations: abdominal pain
• Imaging: by using MRI contrast agent gadobenate dimeglumine easily distinguished from
other lesions that have bile ducts, Hypervascular enhancement by arterial phase &
hypodense by venous phase of CT, Hyperintense by T1-weighted MRI
• Treatment: surgically resected once diagnosed.

45. Follicular Nodular Hyperplasia
• Solid benign lesion which is believed to be a hyperplastic response to an anomalous artery.
• Well circumscribed mass with central scar & fibrous septa extending from central scar.
• More common in women of childbearing age.
• Use of estrogens (OCP) is a not clear risk factor.
• No risk of spontaneous rupture, intraperitoneal bleeding & also no risk of malignant
transformation.
• Presentations: abdominal pain
• Imaging: Homogenous enhancement by arterial phase & hypodense by venous phase of CT,
Hypointense by T1-weighted & hyperintense by T2-weighted MRI.
• Treatment:
1. Reassurance & prospective observation.
2. Surgical resection is recommended only when Pt. is symptomat or HCC can’t be excluded.

46. Bile Duct Hamartoma
• Typically small liver lesions, 2-4mm in size, visualized on the surface of liver.
• Firm, smooth & whitish yellow in appearance.
• Treatment: Excisional biopsy often is required to establish the diagnosis as being difficult to
differentiate from small metastatic lesions.