A site for medical students - Practical,Theory,Osce Notes

Showing posts with label hepatology. Show all posts
Showing posts with label hepatology. Show all posts

How to elicit the signs of liver cell failure an OSCE guide

Following are the major signs of liver cell failure
3.Constructional Apraxia
Presence of a Button-like' breast tissue on palpation below the areola In a male suggests early gynaecomastla.
5.Testicular Atrophy
If the testis is less than 3.5 cm in length, and feels soft or
Flabby on  palpation, it suggests testicular atrophy.
6.Loss of Axillary and Pubic Hairs
They become sparse initially and are totally absent in later stages.

This is very important for those students preparing for USMLE and MRCP

How to elicit Asterlxis or Liver Flap an OSCE guide

Asterixis is also called as  Flapping Tremor
1. Explain procedure to the patient.
2. Ask the patient to fully extend his/her arms and dorsiflex his/her wrists.
3. His/her fingers are held widely separated.
4. Holds In the same position for a few seconds.
5. Comment as asterlxis present or not.
Alternate Method for elicitation of flapping tremor
Asterlxis can also be elicited in the legs, head and the trunk.
Note the following
  • The patient is elaborately positioned because the flap is best demonstrated in that position.
  • Asterlxis Is said to be present if the wrist and fingers Involuntarily flex abruptly and irregularly: fhe patient compensates by extending the wrist but the correction is only partial, tlcxion and partial extension occur alternately so that In the end the wrist comes to a flexed position.
  • Asterixis occurs because of non-rhythmic, transient loss of posture In the arms.

This sign is very important for those students who are preparing for USMLE and MRCP

How to examine for Spider Naevus an OSCE guide

Spider Naevus is a sign of liver cell failure.Sometime seen in healthy Individuals also.
1. Ask the patient to adequately expose.
2. Examine the- face. neck, arms and chest above the nipples
3. Blanch the spider naevus using the head of a pin or a glass slide.          
4. Release pressure to look for flushing.
5. Comment as present or not.
If present, significant or not significant.
Note the following
  • Count the naevi above the level of the nipples i.e. in the drainage area of the superior vena cava.
  • Less than 7 spider naevi are normal in young persons
  • More than 7 occur in liver cell failure pregnancy  or in persons on oral contraceptive
  • Spider naevus occurs because of the dilatation of a central arteriole (the body of the spider) which feeds the vessels radiating from it (the legs of the spider). If a red naevus does not blanch, it is purpura. Blanching occurs fully in erythema also and partially in telanglectasias.

These steps are very important for students preparing for USMLE and MRCP exams

How to examine the dilated vein ?

Examination of dilated vein 
How to know the presence of dilated and tortuous abdominal/chest wall veins ?
Method :
The patient is asked to sit with legs hanging from the bed (never examine in lying down position).
Then he / she is asked to cough or to perform the Valsalva manoeuvre. Cough makes the veins
prominent transiently while the Valsalva retains the prominence of veins so long the manoeuvre
is continued.
Proper light is necessary (patient facing the window) for demonstration.
What are the conditions associated with dilated chest wall veins ?
  • SVC obstruction is the commonest cause
  • Intrathoracic obstruction from any aetiology
  • IVC obstruction it is not uncommon
  • Severe congestive cardiac failure.
What is the difference between visible vein versus engorged vein?
Sometimes veins are visible normally in thin built persons (often in fair skinned Individuals) and is
usually present at the skin level. ie. flushed with the skin. But the engorged vein is a bit raised from the skin surface. Palpate the vein lightly by index finger and draw your Inference. Visibility of a vein does not indicate engorgement  moreover. TORTUOSITY indicate'its pathological
2.Detection of direction of blood flow 
How will you demonstrate the direction of venous flow ?
Method :
  • The veins are made prominent by the above mentioned method.
  • A tributory-free. long segment of vein (one inch or more) is selected for examination.
  • Stand on the right hand side of the patient and place the index finger of both hands side by side over the vein—the left above the right one. Now start milking the vein by movement of two index fingers in opposite direction.
  • The two ends of the bloodless vein is blocked with the pressure given by two index fingers. The left index finger is now removed and the rapidity of venous filling from above is noted. The same procedure is repeated after removal of the right index finger
  • You should notice the rapidity of venous filling from below is observed now. The rapidity of venous filling indicates the direction of blood flow.
Direction of venous blood flow
Normal direction of flow of blood in the veins over the abdomen is -
Above the umbilicus - Upwards
Below the umbilicus - Downwards
Thin veins over the subcostal margin are normal.
Venous flow in different conditions :
Normally — Away from the umbilicus (but one cannot see any venous prominence in health.
Portal hypertension — Away from the umbilicus.
IVC obstruction 
  • Above the umbilicus - Upwards and away from the umbilicus.
  • Below the umbilicus - Towards the umbilicus.
SVC obstruction — From above downwards
IVC obstruction features
Portal hypertension clinical features
SCV obstruction clinical features
  • Dilated veins seen over the abdomen and chest. 
  • Direction of flow is from above downwards.
  • Look for the direction of bloodflow above the umbilicus

Portal hypertension clinical features

  • Dilated veins are seen radiating from the umbilicus.
  • The direction of flow is away from the umbilicus.
  • Portosystemic anastomoses occurs between the paraumbilical vein of the left branch of portal vein to the anterior abdominal wall veins. 
  • Because of their engorged appearance, these vessel resemble medusa's hair after minerva had turned it into snakes and this sign is called caput medusae.
How abdominal wall veins are formed in portal hypertension ?
Dilated and tortuous veins suggest venous obstruction. They are formed due to blood passing
through a large umbilical or paraumbilical vein in the falciform ligament from the left branch of portal vein to the superior epigastric, internal mammary or inferior epigastric veins present in the abdominal wall (i.e. opening of anastomotic channels between portal and systemic veins)

Inferior venacaval obstruction clinical features

IVC obstruction features are the following
  • Dilated veins seen over the abdomen and chest. 
  • Direction of flow is from below upwards and look for the direction below the umbilicus. 
  • These represent dilated anastomotic channels between the superficial epigastric and circumflex iliac veins below, and the lateral thoracic veins above, they convey  the diverted blood from long saphenous vein to axillary vein
How abdominal wall wins are formed in IVC obstruction ?
These are dilated anastomotic channels formed between the superficial epigastric and circumflex
iliac vein below, and the lateral thoracic veins above, carrying blood from long saphenous vein to axillary vein. This Is why the direction of blood flow is from below upwards.

Signs of chronic liver disease

  • Alopecia
  • Foetor hepaticus: Sweetish, slightly faecal smell of breath similar to freshly opened corpse of mice, this is due to methyl mcrcaptan derived from methionine, occurring in hepatocellular failure
  • Jaundicce
  • Parotid swelling
  • Gynaecomastia, testicular atrophy, loss of secondary sexual characters
  • Spider naevi
  • Palmar erythema- link Reddening of palms of the hands affecting the thenar and hypothenar eminences
  • Dupuytren's contracture - This is a visible and palpable thickening of the palmar aponeurosis, most often of the ring finger, usually it is bilateral , occasionally affect the soles of the feet.
  • Loss of hair - Axillary and pubic
  • Muscle wasting
  • Testicular atrophy
  • Asterixis
  • Xanthelasma.
  • Look for signs of chronic cholestasis like scratch marks of pruritus and xanthelasma.
Stigmas of chronic compensated liver disease.
  • Parotidomegaly
  • Telangiectasia, spider naevi
  • Gynaecomastia
  • Palmar erythema 
  • Clubbing
  • Leukonychia 
  • Dupuytren's contracture - This is a visible and palpable thickening of the palmar aponeurosis, most often of the ring finger, usually bilateral , occasionally affect the soles of the feet.
  • Loss of hair - Axillary and pubic
  • Muscle wasting
  • Testicular atrophy
Stigmas of chronic decompensated liver disease. 
With the above features plus
  • Altered sensorium
  • Inversion of sleep rhythm 
  • Jaundice
  • Foetor hepaticus- Fetor hepaticus,sweetish, slightly faecal smell of breath similar to freshly opened corpse of mice due to methyl mercaptan derived from methionine, occurring in hepatocellular failure
  • Flapping tremor - Ask the patient to stretch out his arms, separate the fingers and extend the wrist. Jerky irregular flexion extension movements at the wrist and metacarpophalangeal joints are noted. This tremor is absent when coma supervenes. Flapping tremor is also seen in respiratory, renal failure, occasionally in hypoglycemia and barbiturate intoxication
  • Constructional apraxia
  • Ascites, edema
  • Hyperreflexia, extensor plantar.
Special stigmata of alcoholic cirrhosis 
  • Bilateral enlarged parotids
  • Gynaecomastia
  • Testicular atrophy with loss of body hair
  • Wasting of muscle mass
  • Dupuytrens ’s contracture
What is hepatic facies?
  • Hepatic facies is characterised by the following
  • Shrunken eyes.
  • Hollowed temporal fossa,
  • Pinched-up nose with malar prominences
  • Parched lips
  • Muddy complexion of skin
  • Shallow and dry face.
  • Icteric tinge of conjunctiva.

What are the causes of prolonged jaundice?

Jaundice present tor more than 6 months may be arbitrarily called as prolonged Jaundice'. The common causes are given below.
  • Cholestatic viral hepatitis.
  • Chronic hepatitis.
  • Cirrhosis of liver.
  • Carcinoma of liver (secondary).
  • Thalassaemia.
  • Drug-induced hepatitis (eg. rifampicin. INH. chlorpromazine).
  • Extrahepatic biliary obstruction (eg. stone, stricture, carcinoma of the head of pancreas).
  • Alcoholic hepatitis.
  • Wilson's disease.
  • Other causes like Gilbert's syndrome primary biliary cirrhosis, hereditary spherocytosis, sickle cell anaemia, autoimmune haemolytic anaemia, sclerosing cholangitis etc.

What is polycythemia?

Polycythemia is the excessive amount of RBC mass that leads to redness of conjunctiva, mucous membrane, skin and nailbed .
Polycythemia may be primary or secondary
Primary polycythemia 
Primary polycythemia  is a proliferative polycythemia is the malignant counterpart.
Secondary polycythemia 
Is a condition where you get it secondary to some systemic cause
This may be often accompanied by central cyanosis and clubbing as seen in congenital cyanotic heart disease and interstitial lung disease .This is called as secondary polycythemia
Laboratory criteria for polycythemia
In males
  • RBC mass is > 36 ml/kg
  • PCV > 55 %
In females
  • RBC mass > 32 ml/kg
  • PCV > 47 %
How to detect polycythemia?
Polycythemia is examined in the same manner as anemia.Examine the lower palpebral conjunctiva, longue, soft palate, nail beds, palms and soles, and general skin surface.The colour of the mucous membrane turns dusky-red. Patients with  polycythemia usually have facial plethora  and suffused conjunctiva, increased redness of lower palpebral conjunctiva and palmar erythema.
What are the common causes of polycythemia? 
  • COPD.
  • Congenital cyanotic heart diseases e.g. Fallot's tetralogy.
  • Right-to-lcft shunt in the heart.
  • Polycythemia rubra vera.
  • High altitude and severe dehydration  can produce relative polycythemia
Thrombosis and peptic ulceration (often with bleeding) are noted complications of polycythemia.
What is normal reticulocyte count. reticulocyte index and red cell mass 
Reticulocyte count- 0.2-2% of RBCs (increased in haemolyttc anaemia).
Reticulocyte Index— Reticulocyte % X Patient's PCV/Normal PCV
Red cell mass-in males Male is 30ml/kg of body weight.
Female - 25 ml/kg of body weight.
It is increased in polycythemia rubra vera

Difference between conjugated and unconjugated hyperbilirubinemia

Following are the difference between conjugated and unconjugated hyperbilirubinemia
                                               Unconjugated                                  conjugated                 
Water solubility                      0                                                        +
Affinity for lipids                      +                                                       0               
Renal excretion                         0                                                       +
Van den Bergh reaction     Indirect                                              Direct

Fractions of normal bilirubin
Normal serum bilirubin level is 0.3-1.0 mg/dl.
Conjugated fraction is 0.1-0.3 mg/dl and
Unconjugated fraction is 0.2-0.7 mg/dl.
What are the conditions which produce predominantly conjugated and unconjugated hyperbilirubinemia?
Conjugated hyperbilirubinaemia is said to occur with > 50% conjugated fraction of bilirubin is conjugated
Causes of conjugated hyperbilirubinemia
  • Viral or drug-induced hepatitis.
  • Drug-induced cholestasis.
  • Cholestatic jaundice of pregnancy.
  • Cirrhosis of liver.
  • Dubin-Johnson syndrome.
  • Rotor syndrome.
  • Secondary carcinoma of liver.
Causes of unconjugated hyperbilirubinemia
Unconjugated hyperbitirubinaemia is said to occur when the unconjugated fraction is > 80%
Causes of conjugated hyperbilirubinemia
  • Haemolysis.
  • Ineffective erythropoiesis.
  • Prolonged fasting (<300 cal/day).
  • Gilbert's syndrome and rarely Crigler-NaJ|ar syndrome
  • Neonatal jaundice.

What is Jaundice?

Jaundice is defined as yellowish discoloration of sclera, mucous membrane, nailbed of skin due to excess amount of serum bilirubin of > 2 mg/dl. 
Subclinical jaundice -Serum bilirubin 1-2 mg/dl 
Normal -  serum bilirubin  < 1 mg/dl
What is latent jaundice?
The normal serum bilirubin level is 0.3-1.0 mg/dl. Clinical jaundice is evident only when scrum bilirubin exeeds  2.5 mg/d .Jaundice is said to be latent, i.e. when it is clinically non-evident and detected only by serum analysis.This is seen when the serum bilirubin level is in between l-2.5mg/dl.
What are the sites you should examine for jaundice ?
Upper bulbar conjunctiva is examined after retract the uppereyelid and ask the patient to look downwards both eye should be examined at a time 
  • Undersurface of tongue.
  • Soft palate.
  • Palms and soles.
  • General skin surface.
How to examine for jaundice ?
While examining for jaundice first elevate the upper eyelid, Then ask the patient to look down and then look at the periphery of the sclera in bright natural day light
As in the artificial light you cannot detect the light yellow discolouration of sclera always examine the patient in the natural light.You should take the patient in front of an open window for examination of jaundice.
Why the upper bulbar conjunctiva is selected for examination of jaundice?
  • A white background is formed by sclera.
  • Sclera of eye is rich in elastic fibers.Serum bilirubin has affinity to elastic fibers. Periphery of the sclera is  thick  with more elastic fiber so  early staining by bilirubin will occur at the periphery. In case of marked hyperbilirubinemia, all tissues except the brain is stained by bilirubin, the brain is not stained due the blood-brain barrier block the bilirubin staining of the brain.
What are the three types of jaundice?
Hemolytic anemia —This is a lemon yellow jaundice, Urine colour is normal no yellowish discolouration of urine hence called acholuric jaundice.
Hepatocellular jaundice jaundice- Hyper bilirubinuria with other stigmas of hepatocellular damage and other features of primary liver disease may be seen.
Obstructive jaundice –is characterised by greenish dark yellow jaundice, pruritus, pale stool, palpable gallbladder. 
This is seen in either intra-or extra- hepatic cholestasis.
Differential diagnosis of jaundice
Carotinemia is a condition characterized by yellowish discoloration of skin (carotenoderma) that spare the sclera and mucous membrane.
What are the diseases commonly present as latent jaundice?
  • Mitral stenosis (passive venous congestion of liver).
  • Myocardial infarction.
  • Cirrhosis of liver.
  • Pernicious anaemia.
  • Acute pancreatitis.
  • Pulmonary infarction (acute pulmonary thromboembolism).
  • Congestive cardiac failure.
What are the causes of familial non-haemolytic hyperbilirubinaemias?
Gilbert's syndrome.
Crigler-Najjar syndrome.
Dubin-Johnson syndrome.
Rotor syndrome.

What are the clinical fatures of of obstructive jaundice ?

Following are the features of obstructive jaundice
Urine colour is yellow or mustard oil-like colour (due to conjugated bilirubin).
Stool is clay coloyred coloured (china-clay) with steatorrhoea (steatorrhoea means frothy bulky soft ,greasy  and offensive .This is due to absence of bile pigment in the stool.
Jaundice is greenish yellow due to due to oxidation of bilirubin to biliverdin
Generalised pruritus with scratch marks and shiny nails are seen in obstructive jaundice because the bile acids irritate the free nerve endings.
Sinus bradycardia occurs as bile salts directly inhibit the sinoatrial node.
Xanthelasma near eye and xanthoma in knees, buttocks may be seen due to hypercholestrolemia.
Deficiency of fat soluble vitamin produce 
  • Petechiae, purpura or ecchymosis are seen due to vitamin K deficiency as lack of bile salts produces malabsorption produces
  • Prolonged obstructive jaundice can produce osteomalacia- bonePain. bone fracture due to vitamin D deficiency this is due to malabsorption or steatorrhea and it is called as hepaticosteodystrophy
Gall bladder may be palapable. If it is palpable it indicate that the site of obstruction is bile dut and it is due to carcinoma head of pancreas and not due to choledocholithiasis according to Courvoisiers law
What are the causes of obstructive jaundice?
Obstructive jaundice can be intrahepatic or extrahepatic
Intrahepatic (medical) causes of jaundice are 
  • Cholestatic viral hepatitis.
  • Chronic active hepatitis.
  • Cirrhosis of liver (specially primary biliary cirrhosis).
  • Lymphoma.
  • Drugs azole. methyl testosterone, anabolic steroids.
  • Secondary carcinoma of liver (jaundice is rarely seen in hepatoma).
Extrahepatic /surgical causes of jaundice
  • Gall stone impaction in CBD.
  • Carcinoma of the head of pancreas.
  • Carcinoma of gall bladder.
  • Stricture of CBD.
  • Enlarged glands at porta hepatis
  • Sclerosing cholangitis from inflammatory bowel disease.
What are the medical causes of extrahepat1c obstruction

  • Sclerosing cholangitis in ulcerative colitis.
  • Obstruction by round worm in CBD.
  • Enlarged Iymph nodes at porta hepatis in lymphoma.

Features of hepatocellular jaundice

Features of hepato cellular jaundice  are given below
  • There is yellowish discolouration of urine.
  • Stool is high coloured and become pale if there is obstruction due to cellular odema
  • Orange yellow tinge of bulbar conjunctiva
  • Anorexia ,nausea and vomiting is present before the appearance of jaundice
  • Tender hepatomegaly is frequent.
Causes of Hepatocellular jaundice
  • Viral hepatitis (type A and E commonly).
  • Drugs — Rifampicin. INH, after halothane anaesthesia.
  • Poisons - Copper sulphate.
  • Pregnancy — Acute fatty liver of pregnancy.
  • Alcoholic hepatitis.
  • Weil s disease.

What are the clinical features of haemolytic jaundice?

Following are the clinical feaatures of hemolytic jaundice
  • Acholuric  urine means freshly passed urine is of normal colour as there is no bilirubin in urine but if the urine sample is kept for sometime, this will turn dark yellow due to conversion of urobilinogen to urobilin by oxidation.
  • Stool is high-coloured due to excess amount of stercobilinogen and stercobilin.
  • Jaundice is usually mild and there is lemon-yellow tinge of bulbarconjunctlva. 
  • Serum bilirubin is usually less than 6 mg/dl and this is predominantly of unconjugaled variety.
  • Anaemia is present .It can be mild, moderate or severe, according to the degree of haemolytic process.
  • Splenomegaly, is very characteristic of haemolytic anemia
What are the causes of  Haemolytic jaundice?
Following are the common causes of haemolytic jaundice
  • Thalassaemia.
  • Mismatched blood transfusion.
  • Snake bite (Viperidae group).
  • Malaria (specially falciparum malaria).
  • Rh incompatibility.
  • Primaquine or sulphonamide-induced (in GePD deficiency).

What is alcoholic hepatitis?

Alcoholic hepatitis is a very common cause of liver injury. It is caused by excessive alcohol consumption.Typically there will be steatosis of the liver.In Steatosis pathological fat globules begin to accumulate in the cytoplasm of liver cells.Sometimes this can be pretty harmless, and as a result, steatosis is not very specific for predicting if the liver will develop cirrhosis.
Mallory’s hyalin is an aggregate of filament found in the hepatocytes.If present it indicate a risk of irreversible changes in hepatocytes(livercell).It may ultimately lead to cirrhosis. Mallory’s hyalin is not specific for alcoholic liver disease.
Ethanol(alcohol)after consumption is oxidised to acetaldehyde. Acetaldehyde is then converted to acetate by the mitochondria of liver cells.90% of this conversion is seen in liver.Acetate is then released into the bloodstream and it is taken up by peripheral tissues.In the peripheral tissue acetate is metabolised to carbon dioxide, fatty acids and water 
Epedemiology of alcoholic hepatitis
10-30% of heavy drinkers will ultimately develop cirrhosis and 50% of alcoholic will have fatty liver.
Role of nutritional factors are controversial, although it is possible that obesity and malnutrition both contribute to liver damage. 
The risk of hepatitis is increased by high alcohol consumption combined with hepatitis C infection. 
In males with alcoholic hepatitis, average alcohol consumption was about 16 units/day over a period of 8 years. However,the amount is highly variable.In females,the corresponding dose was 11 units/day. 
Why alcohol is  is toxic to liver cells?
The first sign of alcoholic hepatitis is fatty liver.This can occurs in most heavy drinkers at some time, but it is completely reversible upon cessation of alcohol consumption.
1.The hepatocytes have to metabolise the alcohol which is done at the expense of metabolising fats.As a result, fat metabolism is altered which results in fat deposits inside the cells.More fat is released into the blood stream (fatty acids) as well as within the hepatocytes.Due to the elevated levels of fatty acids there is increased synthesis of triglycerides and fatty acids.
2.The product of alcohol metabolism ,Acetaldehyde binds to liver cell proteins, and causes hepatocytes injury, leading to inflammation.This inflammation may be a causatory factor in liver cirrhosis. 
3.Alcohol stimulates collagen synthesis by fibroblasts and also  fibroblast proliferation.Finally, the fibrosing process will end up linking hepatic veins to portal veins, cell regeneration  occur at these areas resulting in  nodules formation – this is the start of the process of cirrhosis.
What are the clinical sign of chronic  liver disease
1.Very thin arms and legs(due to muscle wasting)
2.Swollen abdomen
3.Red tongue (iron-deficiency anaemia)
4.Dry scaly cracked skin (due to zinc /fatty acid deficiency)
Endocrine manifestation of chronic liver disease
2.Testicular atrophy
3.Loss of body hair
4.Signs of 'pseudo-Cushings’ (red face, hump, striae)
Face /skin manifestations of chronic liver disease
1.Parotid enlargement
2.Spider naevi
3.Easy bruising
4.Dupuytren’s contracture
Neuromuscular manifestations
2.Memory loss / cognitive impairment
3.Peripheral myopathy- degradation of muscle
5.Wernicke-Korskoff syndrome
Cardiovascular manifestations
3.Hyperdynamic circulation
1.Rib fractures on CXR
2.Spinal osteoporosis (particularly in men)
Generally, patients with fatty liver are asymptomatic or have few symptoms, however they may notice nausea and malaise. Mild alteration in LFT’s 
Mild alcoholic hepatitis is indistinguishable from fatty liver disease- and the two may co-exist. The symptoms of mild alcoholic hepatitis are more severe include Anorexia,Nausea ,Abdominal pain Weight loss

Anatomy of human liver

It is the largest of viscera of humanbody
Human liver consists of about 2.5% of body weight
Liver is completely covered by Glisson’s Capsule and incompletely by the peritoneum.
Measurements of human liver are the following
21 – 23 cm transversely
15 – 18 cm superior to inferior
10 – 13 cm anterior to posterior
Location of liver
Located in the right hypochondrium and the epigastrium.It is mostly covered by ribs.It Contains numerous vascular structures
Detailed Anatomy
Liver has four lobes.Divisions are based on blood supply anb bile drainage.Anatomical lobes are divided by falciform ligament. Functional Lobes the right and left lobes separated by imaginary line from fossa for Gall bladder to IVC .Right lobe contains caudate process and left contains Caudate lobe and Quadrate lobe
Fissures of liver
Right sagittal (main)
Left sagittal (accessory)
Right oblique intersegmental
Lateral intersegmental
Main lobar fissure is located in the boundary between right and leftlobes. In ultrasound scan it is seen as hyperechoic line from Portal vein to neck of Gall bladder.It is used to identify GB when it is packed with stones
Portal fissure
Portal fissure is created by portal veins (triads)
Segments of the Liver
Hepatic segments
I = caudate lobe
II & III = superior and inferior lateral segments, Left lobe
IV = medial segment, Left lobe
V & VI = caudal to transverse plane
VII & VIII = cephalad to transverse plane  
Fossae (Superficial) or the following are seen
IVC – posterior
Portal Vein – inferior
Gallbladder – inferior
Falciform is the most superficial ligament anteriorly.It divides left lobe into two sections
anatomical left lobe 
Caudate & quadrate lobes
Ligamentum teres hepatis 
Ligamentum venosum 
Right/Left Coronary Ligaments      
Hepatophrenic & Hepatorenal  ligaments are subdivisions of right coronary ligament hepatophrenic ligament is superior and hepatorenal. 

Pathogenesis of hepatic encephalopathy

Hepatic encephalopathy is a complex neuro psychiatric syndrome that is caused by liver disease. 
This will manifests as disturbances in
1.Consciousness and behaviour.
2.Personality changes.
4.Distinctive electroencephalographic changes
It may present as 
Acute and reversible form
Chronic and progressive form
Severe cases  may leads to coma, later on death 
Occur in severe hepatocellular dysfunction.

Main  mechanism of hepatic encephalopathy is porto systemic shunting of blood.
This is a complication of portal HTN.
There is obstruction to the passage of blood  absorbed from the intestine to go through liver. As there is no valves in the portal venous system it will facilitates retrograde blood flow to the lower pressure systemic venous circulation. So the portal blood bypass the liver and it reaches the systemic circulation without undergoing the 1st pass detoxification. There is portal systemic collateral formation.The major sites of collateral are Gastro oesophageal junction, umbilicus, anal canal and posterior abdominal wall.

Toxic substances accumulated in hepatic encephalopathy are
False neurotransmitters
Mercaptans(methionine metabolism)
Short chain fatty acids
GABA(Gama-aminobutyricacid) inhibitory neurotransmitter
Endogenous benzodiazepine acting through GABA receptors 
What these neurotransmitters will do?
1. These neurotransmitters will causes the supporting cells of the brain (astrocytes) to swell. Which inturn increases the intracranial pressure, leading  to herniation of brainstem and death
2. There will be disruption of the blood brain barrier leading to cerebral edema. 

Factors precipitating hepatic encephalopathy

Patients with chronic liver disease are prone to hepatic encephalopathy which manifest as altered sensorium. It may be precipitated by a variety of causes which can be prevented.

1. Increased nitrogen load
Increased nitrogen load is seen in the following conditions
Gastrointestinal bleeding, since the blood contain large quantity of proteins when there is GI bleed, there will be protein load in intestine.It is acted upon by intestinal bacteria leading to  increased NH3
Excess dietary protein intake.

2. Electrolytic imbalances
Hypokalemia(secondary to diuretic therapy, paracentesis,vomiting) stimulates renal NH3 production.
Systemic alkalosis.

3. Drugs
Diuretics produce electrolyte imbalance
Narcotics, sedatives

4. Infections
Superimposed acute viral hepatitis
Alcoholic hepatitis
Extrahepatic bileduct obstruction

5. Surgeries